4 - Toronto Notes 2011 - Cardiology - and - Cardiovascular - Surgery

c
Cardiology and Cardiovascular Surgery

Mark Dam, Shiying Liu and Michael Ward. chapter editors Doreen Ezeife and Nigel Tan, associate editors Stnen Wong, EBM editor Dr. Chi-Ming Chow, Dr. Andrew Dueck and Dr. Anna Woo, staff editors With contributions from Dr. Young Kim
Basic Anatomy Review .. 2 Coronary Circulation Cardiac Anatomy Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Chest Pain Syncope Local Edema Generalized Edema Palpitations Dyspnea Cardiac Diagnostic Tests .................. 5 Electrocardiography (ECG) Basics Approach to ECGs Rate Rhythm Axis Intraventricular Conduction Abnormalities Hypertrophy and Chamber Enlargement Ischemia/! nfarction Miscellaneous ECG Changes Other Cardiac Diagnostic Tests Cardiac Biomarkers Ambulatory ECG Echocardiography Stress Testing Nuclear Cardiology Cardiac Catheterization and Angiography Contrast-Enhanced CT Coronary Angiography Magnetic Resonance Imaging (MRI) CARDIAC DISEASE Arrhythmias ........................... 12 Mechanisms of Arrhythmias Bradyarrhythmias AV Conduction Blocks Supraventricular Tachyarrhythmias Pre-Excitation Syndromes Ventricular Tachyarrhythmias Electrophysiology (EPS) Studies Electrical Pacing Implantable Cardioverter Defibrillators (ICDs) Catheter Ablation Ischemic Heart Disease (IHD) ............. 22 Chronic Stable Angina Acute Coronary Syndromes (ACS) Unstable Angina (UA)/Non-ST Elevation Ml (NSTEMI) ST-Eievation Myocardial Infarction (STEMI) Treatment Algorithm for Chest Pain Sudden Cardiac Death Coronary Revascularization Percutaneous Coronary Intervention (PCI) Coronary Artery Bypass Graft (CABG) Surgery Off Pump Coronary Artery Bypass (OPCAB) Surgery Heart Failure. . . 32 Congestive Heart Failure (CHF) Sleep-Disordered Breathing Cardiac Transplantation ................. 35 Ventricular Assist Devices (VADs) Myocardial Disease ..................... 36 Myocarditis Dilated Cardiomyopathy (DCM) Hypertrophic Cardiomyopathy (HCM) Restrictive Cardiomyopathy (RCM) Valvular Heart Disease .................. 40 Infective Endocarditis (IE) Rheumatic Fever Choice of Valve Prosthesis Summary of Valvular Disease Pericardia! Disease...................... 44 Acute Pericarditis Pericardia! Effusion Cardiac Tamponade Constrictive Pericarditis VASCULAR DISEASE Peripheral Arterial Disease ............... 46 Acute Arterial Occlusion/Insufficiency Chronic Arterial Occlusion/Insufficiency Hypertension .. FM35 Pulmonary Hypertension ............... R16 Carotid Artery Disease ................ NS21 Aortic Disease ......................... 48 Aortic Dissection Aortic Aneurysm Peripheral Venous Disease .. 51 Deep Venous Thromboembolism Superficial Thrombophlebitis Varicose Veins Chronic Venous Insufficiency Lymphedema Common Medications ................... 54 Landmark Cardiac Trials ................. 57 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
Toronto Notes 2011
Cardiology and CV Surgery Cl
C2 Cardiology and CV Surgery
1'oroDio
2011
Basic Anatomy Review

Coronary Circulation
conventional arterial supply to the heart arises from the right and left coronary arteries, originating from the root ofthe aorta (see Figure I) right coronary artery (RCA)
acute marginal branches atrioventricular (AV) nodal artery posterior Interventricular artery (PIV) = posterior descending artery (PD) Left main coronary artery (LCA): two major branches left anterior descending artery (LAD) - septal branches
dominance ofdrculatlon
- diagonal branches left drcumfleJ: artery (I.Cx) - obtuse marginal branches
right-dominant circulation: PIV and at least one posterolateral branch arise from RCA (8096) Left-dominant circulation: PIV and at least one posterolateral branch arise from LCx (1596) balanced cin::ulation: dual supply ofposteroinferior LV from RCA and LCx (596) the sinoatrial (SA) node ia supplied by the SA nodal artery, which may arise from the RCA (60%) or LCA (40%) most venous blood from the heart drains into the RA through the coronary a:lnns, although a small amount drains through Th.ebesian veins into all four chambers, contributing to the
physiologic R-L shunt
Laft IDDI' dncending (LAD)
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Aare 1. Anatomy of tile Coronary Arterl11 (llgld: alterlor oblque pro)ecGon)
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Flg1re Za. Cardiac Cycle
Flgere 2b. Canllac Cycle. JVP Pulle and Cai'GIId Pllsa
'IbroDlo Nota 2011
Buic Anatomy Review
Cardiology and CV SUJ'8ery C3
Cardiac Anatomy
layen of the heart endocardium myocardium epicardium =visceral pericardium
pericardia! space parietal pericardium
"Y&lves tricuspid valve (TV): separate.. RA and RY pubrulDic valve (PV): separates RY and pulmonary artery (PA) mitral valve (MV): separates LA and LV aortic valve (AV): separates LV and ucending aorta oonchu:tion aydem impulses travel from: SA AV bundle: of His LBB/RBB -+ Purkinje fibres SA node governs pacemaking control anterior-, middle- and posterior-internal nodal tracts carry impulses in the right atrium and along Ba.chmann's bundle In the left atrium atrial impulses converge at the AV node the AV node is the only conducting tract from the atria to the ventricles because of electrical isolation by the annulus fibrosis (except when accessory pathways are present) the bundle of His bifurcates into left and right bundle bl'llllCbes (LBB and RBB)
LBB further splits into anterior and posterior fascicles RBB and fasdclt:s ofLBB give o1fPurkinje fibres which conduct impulses into the ventricular
myocardium canllovascular lnncmdio.n
lfiiiP8thet:lc nerves innervate the sinoatrial node (SAN), atroventricular node (AVN), ventricular myocardium and vasculature SAN (pl) fibres increase pacemaking activity (chronotropy) cardiac muscle fibres increase contractllity (inotropy) to help increase cardiac output stimulation of IH- and IJ2-receptora in the W:1.etal and coronary c.ln:ulation causes vasodllatation
parasympathetic nenes Innervate the SAN, AVN, atrial myocardium but few vascular beds basal vagal tone dominates the tonic sympathetic stimulation of the SAN and AVN resulting in slowing of pacemaking activity and condw:tion (ie. reduced chronotropy and drmnotropy) parasympathetic& have very little impact on total peripheral vascular resistance
lknlla
- Middle1rlct
- Posteriorlrlle:t
aiHII
Cl Ytulg M. IGm 2010
Figun 3. Conduction Systam of the Heart
Differential Diagnose5 of Common Presentations
Toronto Notes 2011
Differential Diagnoses of Common Presentations

Note: bold text indicates most common, underlined text indicates life threatening
Chest Pain
Pulmonary pneumonia pulmonary embolism (PEl pneumothorax/hemothorax, tension pneumothorax empyema pulmonary neoplasm bronchiectasis
TB
Generalized Edema
Increased hydrostatic pressure increased fluid retention cardiac causes e.g. CHF hepatic causes e.g. cirrhosis renal causes e.g. acute and chronic renal failure vasodilators (especiallyCCBs) refeeding edema Decreased oncotic pressure hypoalbuminemia Hormonal hypothyroidism exogenous steroids pregnancy estrogens
Cardiac Ml/angina myocarditis pericarditis/Dressier's syndrome cardiac tamJonade Gastrointestin esophageal: spasm, GERD, esophagitis, ulceration, achalasia, neoplasm, Mallory-Weiss syndrome PUD gastritis pancreatitis biliary colic Mediastinal lymphoma thymoma Vascular dissecting aortic aneurysm Surface structures costochondritis rib fracture skin (bruising, shingles) breast
Palpitations
Cardiac arrhythmias (PAC, PVC, SVT, VT) mitral valve prolapse valvular heart disease J:m>ertrophic obstructive cardiomyqpatby Endocrine thyrotoxicosis pheochromocytoma hypoglycemia
Systemic
Syncope
Hypovolemia Cardiac structural or obstructive causes myocardial disease (e.g. acute coronary syndrome) aortic stenosis hypertrophic cardiomyopathy (HCM) cardiac tamponade/constrictivt: pericarditis arrhythmias (sc:c: arrhythmia section) Respiratory massiyePE pulmonary hypertension hypoxia
hypercapnia
fever anemia Drugs tobacco, caffeine, alcohol, epinephrine, ephedrine, aminophylline, atropine Psychiatric panic attack
Dyspnea
Cardiovascular acuteMI CHF/LV failure aortic stenosis/mitral stenosis cardiac elevated p onary venous pressure Respiratory airway disease asthma COPD exacerbation upper airway obstruction (anaphylaxis, foreign body, mucus plugging) parenchymal lung disease ARDS pneumonia interstitial lung disease pulmonary vascular disease pulmonary embolism pulmonary HTN pulmonary vasculitis pleural disease pneumothorax pleural effusion Neuromuscular and chest wall disorders C-spine injury polymyositis, myasthenia gravis, Guillain-Barre syndrome kyphoscoliosis Anxiety/psychosomatic Severeanemia
Neuio1ogic
stroke/TIA (esp. vt:rtebrobasilar insufficiency) migraine seizure vuovagal Metabolic anemia hypoglycemia Drugs antihypertensives antiarrhythmics beta-blockers, CCBs Psychiatric panic attack
Local Edema
Inflammation/infection Venous or lymphatic obstruction thrombophlebitis/deep vein thrombosis chronic lymphangitis venous insufficiency filariasis
'IbroDlo Nota 2011
Cardiac Diagnostic Testl

O..nrillw flf DiatiDSiic r.... Cmilc IHrurllllra (Tn. CK-MB)- in -vmptullllllie IIBbl ECG-atrwt. wi11ulnl-. orin -vmptullllllie IIBbl 811811. or with
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Cardiac Diagnostic Tests

Electrocardiography (ECG) Basics
the electrocardiogram (ECG) is a graphic representation of the electrical activity of the heart recorded from the surface of the body on the ECG graph the horizontal axis represents time 1 mm. (I small square)= 40 msec 5 mm. (I large square) = 200 .l1lllec (at paper speed 25 mmlaec) the vertical axis represents voltage 1 mm. (I small square) = 0.1 m V 10 mm. (2large squares)= 1 mV (at standard gain setting) leads standard 12-leadECG Umb leads: I. II, DI. aVI., aVR. aVF precordial leads: VI-V6 (VI-V2 septal, V3-V4 anteriol; VS-V6lateral) additional leads right-sided leads: V3R-V6R (useful in RV infarction and dmrocardia) lateral =I, aVL, V5, V6; inferior =II, Til, aVF; &ontal =VI-V4
....
CTA
MIIAIM!I
Figura 4. ECG WHeferma 11d Nannll Values
Approach to ECGs
Rate
111118 Cllculltianl Examples
normal =60-100 bpm (atrial mre: IS0-250 bpm =paroxsyma1 tachycardia, 250-350 bpm =atrial flutter, >350 bpm = atrial fibrillation regular rhythm to calculate the rate, divide 300 by number of large squares between 2 QRS complexes (there are 300 large squares in 1 minute: 300 x 200 maec = 60 sec) or remember 300-150-100-75-60-5()....43 (rate falls in this sequence with the number of additional large squares between QRS) irregu1a.r rhythm rate = 6 x number ofR-R intervals in 10 seconds (the '"rhythm strips" are 10 second recordings) types: wandering pacemaker, multifocal atrial tachycardia. atrial fibrillation atrial escape = 60-80 bpm; Junctional escape = 40-60 bpm; ventricular escape = 20-40 bpm
Rhythm regular = R-R interval is the same aaoss the tracing irregular= R-R interval va.rl.es across the tradng regularly-irregula.r = repeating pattern of varying R-R intervals irregularly irregular = R-R intervals vary erratically normal sinus rl:rythm (NSR) P wave precedes each QRS; QRS follows each P wave P wave axis is normal (positive in leads I, aVF) rate between 60-100 bpm
Practice
....
AJtnuh ta EC&I &IIIIIIIY
Rail Rhythn Axis Conducti111
Clwmbar rRIII!IIII&ntfhypatrophy lschami.-'lnhuctian
Milcelllneoua
Far mara
111d
'iisit
Axis mean axis indicates the direction of the mean vector can be determined for any waveform (P, QRS, T) the standard ECG reported QRS axis usually refers to the mean axis of the frontal plane; it indicates the mean direction ofventricular depolarization forces QRS axis in the horizontal plane is not routinely calculated; it Is directed posteriorly and to the
left the transition from negative to poaltive is usually In lead V3 QRS axis in the frontal plane (see Flgure 5) normal uis: -300 to 90" (i.e. posltive QRS in leads I and II) left axis deviation (LAD): axis <-300 right axis deviation (RAD): axis >90<>
L8ft Ant. Hemiblack lnlllriorMI WPW
RV Pacing
N0111111IYariant
RVH l..aftl'oat Hamibhx:k PE
dafacl
BIMdlld llillplngm Llad Mispl-mant Endocardial CUIIian
COPD
t..1anll Ml WF'W Dllldracanlill
Sapbll Dahn:1a
Cardiac Diagnostic Teats
Toronto Notes 2011
Intraventricular Conduction Abnormalities

Right Bu1dla BI'IIICh Block (RBBBJ
CampiBIB RBBB QRS duration >120 msec

Positive ORS in lead V1 (rSR' or occasionally broad Rwave] Broad Swaves in leads I, VS-6 (>40 msecl Usually secondll'fTWIIW inversion i'lleads V1-2
Lift Bundl1 B111nch Block (LBBBJ Ca11platll LIBB QRS dLnlion >120 msec Broad notched or slurred Rwaves in leads I, aVI.. and usually
V5andV6
Deep broad Swaves in leads V1-2
Figure 5. Axial Reference System Elldlilld conlliis I+) Bill dispid by 1hi!DI
llmiWI. lirpJEstllllei"-J toward the plllitM
Secondlry ST-T changes (-vein leads with broad RWIIWS, +vein V121 are usually present LBBB usually masks ECG signs Df myocardial inlan:tion
ol1flllllll rlllllts in Ill upMtd dallection il thatilld. NonriiQRS IIliis is between -30'111d +90'.
(Left Antcrill' Hemibloc:kl
Left Anllriar Fudc:ullr Bloc:k (LAFBI LBft l'oltlriar F.c:ic:ullr Bloc:k (LPFBI Biflldc:ullr Bloc:k {Left Pauiar Hemibloc:kl Left axis deviation (-30" 1D -911"1 Right axis deviation ( 11 II" 1D 1811"1 RBBB pattern Small q and prominent Rin Small r and prominant S i1 Small q and prominent R
leads I and aVL Small r and prominent Sin leads II. IlL and aVF leads I and aVL Small qand prominent Rin leads 11,111, and aVF The first 60 msec (1 .5 small squares] Dlthe ORS shows the pattern Dl LAFB or LPFB Bilascicular block refers 1D impaired conduction in two of the three fascicles, most commonly a RBBB and left anterior hemiblock; the appearance on an ECG meets the criteria fur bDih types of blocks
Laft Bundla
Right Bundle
Lift Ventricular
Right Ventricular
Figura 6. Complete LBBB. RBBB. LVH and RVH (only samples, please see online examples for the full range of waveforms and the text for additional characteristicsI
lll'lllilt
Nonspecific Intraventricular Block QRS duration >120 msec absence of criteria for LBBB or RBBB Hypertrophy and Chamber Enlargement left ventricular hypertrophy (LVH) Sin V1 + Rin V5 orV6 >35 mmabove age40, (>40 mmforage 31-40, >45 mmforage 21-30) RinaVL>llmm Rin I+ Sin III >25 mm additional criteria: LV strain pattern (ST depression and T wave Inversion in leads I, aVL, V4-V6) left atrial enlargement right ventricular hypertrophy (RVH) right axis deviation R/S ratio >I or qRin lead VI RV strain pattern: ST segment depression and T wave inversion in leads VI-2 left atrial enlargement (LAE) biphasic P wave with the negative terminal component of the P wave in lead VI ;<:I mm wide and :2:1 mm deep P wave >I20 msec, notched in lead II ("P mitraleD) right atrial enlargement (RAE) P wave >2.5 mm in height in leads II, III, or aVF ("P pulmonalea) Laft Atrial Enlargement
Right Atrial Enlargement
Figura '1. LAE, RAE (only samples, please see online examples and text above for characteristics]
mmmm
'IbroDlo Nota 2011
Cardiac Diagnoslic Testl
lschamia/lnfrction look fur the anatomic distribution of the following ECG abnormalities (see Table 1) iachemia ST segment depression T wave l.nversion (most commonly in Vl-V6)
injury
,,
IIIJ!IIIclllt EC& ClllngM
tra.nsmura.l (involving the eplcardium) - ST elevation in the leads fadng the area injured/ infarcted; transient ST elevation may occur in patients with coronary artery spasm (e.g. Prinzmetal angina) can be slight or prominent (>10 mm) I!Ubendocardial- marked ST depression in the leads facing the affected area; it may be accompanied by enzyme changes and other signs of myocardial infarction; may also occur
with angina
Look for ST It 80 mc from J pam J point - the junction betw8111 th1 QRS eompleot and the ST llllment ST aiiMIIion: lit laut 1mm il 2 14acant inb lalds, Dr lit least 1-2 rnm in ldjacllll precordilllds
ST prweion: diiWI!IIgpilg Dr
harimntlll
Q WIIVI; pllh*9icll if CIIISO!:lsmall
11111111lRS
mwcl or >3B of the
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Q. _
Sepllll depollrimli1111 by the 11ft bundle Seen in leads I, II, Ill, aVL.. VS, Vl5
<40 mMC
Figure I. ECG CIJanu wiUJ lm.ctiun
....
evolving infarction (ST elevation in contiguous leads = acute MI) typical" sequential changes of evolving myocardial infarction
lilt
'..
L.BBB
Acut81'11ric:.-dilia(diflu.. d&I;N) llchamill w/racipmcal changa
3rd
hyperacute T waves (tall. symmetric T waves) in the leads facing the infarcted area, with or without ST elevation 2nd ST elevation (injury pattern) in the leads facing the lnfarcted area usually 1n the first hOUIS post Infarct in acute posterior infarction. there is ST depression in Vl-V3 {reciprocal to ST elevation in the posterior leads, that are not recorded in the standard 12-lead ECG)
lliffllllllill rl ST Slg..rt n Ellvdan Aculll S'IIMI Vantricl.61r
Post-MI
(Pri1'1D118111r) angina
Hypgthmmia (Diboma WIIVBI)
MBCI old ECG'1)
&n1y rapDIIIrillllion (Normal variant
significant Q waves: >40 msec or >113 of the total QRS (hours to days post-infarct) 4th inverted T waves (one day to weeks after infarction) this classical sequence, however. does not always occur, e.g. Q waves of infarction may appear in the very early stages, with or without ST cha.ngea non-Q wave iDfarction: there may be only ST or T changes, despite clinical evidence of infarction
completed infarction abnormal Q (note that wide Q waves may be found in m and aVL in normal individuals) duration >40 msec (>30 msec in aVF for inferior Infarction) QIQRS voltage ratio is >3396 abnormal R waves (RIS ratio >1, duration >40 msec) in VI and more frequently 1n V2 are found in posterior infarction (usually in association with signs of inferior andJor lateral
nDe,....IDII
Ac:UI8 NSTEMI Dr illehlllrlil LVH or RVH with lllrlil
Post-MI STEMI with 111Ciprocal L8ft Dr flight BBB

WDiff.Minsgr..\Nhita syndrom
infarction)
Tillie 1. Area af lnflln:tion{O wava}/lllchamia (right daminant aiii'IDmy)

Leltar*rior descending (lAD)
Anl!mseplal Anlarior Anlllnllltlnl VI,V2
......
Circumflex
Extensivurariar Right verm:le faltsrill" Ml (lillie. with n. Mil
V3, V4 aVL, V3-t I, aVL, Vl-t

II,IILaVF
V3R, V4R (right sided chest leads) VI, V2 fptrilant: RWIVII) V5-t VI, V2 fptrilant: RWIVII)
Lltlnl lsdatad postarior Ml
1'oroDio
2011
MISCEUANEOUS ECG CHANGES
Electrolyte Disturbances
hyperkalemia (see Figure 9)
....
,,
mild to moderate (K 57 mmoVL): tall peaked T waves severe (K >7 mmoVL): progressive changes whereby P waves flatten and disappear, QRS widens and may show bizarre patterns, axis shifts left or right, ST sblft wltb. tall T waves
hypokalemia (see Figure 10)
ST segment depression, prolonged QT interval., low T wwes, prominent U waves (U>T) enhances the mxic effects ofdigitalis
'-Vullaae
PIICordillleldl < ID rrm ..d linb lelldii<Smm Diffarsntill lillgnasil MyoCMIII d i IIIChemia
C..Ornyopalf1y [u.ualy infllrlliva type).
Dafinilion: IDIIII ORS ha9JI in
1 -Ji-1 -L
Hypothermia s1nU8 bradycardia
STsegmmt
hypercalcemia: shortened QT interval hypocalcemia: prolonged QT interval
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+-
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F"1111ra 11. Oabarna J W1V81 af a
when severe, prolonged QRS and QT intervals atrial fibrillation with slow venlricular response and other alrlallvenlricular dysrhythmias Osborne J waves (see Figure 11): "bump-like" waves at the junction of the J point and the
Pericarditis
early- diffuse ST segment elevation PR segment depression. upright T waves lllter - iscelectric ST segment, flat or inverted T waves low voltage ifchronic coD.St:rictive pericarditis tachycardia
....
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liD EllllcW
Drug Effects digitalis
hlllucilltions. confulion n d.-ion.
Palpilllliol'l8. fidigue, viul chang (ytlllow vision). appalilll,
therapeutic levels may be associated with Kdigitalis dfea- (see Figure 12): !IT downtdoping or "scooping'"
T wave depression or inversion QT shortening U waves slowing ofventricular rate in atrial fibrlllation toxic levels associated with: arrhythmias: paroxysmal atrial tachycardia (PAT) with conduction bWcks, severe bradycardia in atrial fibrillation, accelerated junctional rhythms, PVCs, ventricular tachyt:ardia (seeArrlJythmiru, C12) "regularization" ofventricular rate in atrial fibrillation due to a junctional rhythm and AV dissociation amiodarone, quinidine, phenotbiaziru:s, bicyclic antidepressants, antipsychotics, some antihistamiD.es, some antibiotics: prolonged QT interval, U waves
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Prolonged
ar
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PlclnU.11 Demend PICIIIllbr hll diachlrge (IIIITDW v.ticalapillll on ECG llripJ

piurtoQRS
Atrial pacemabr has disdllrga prior tDPwave Trilllll"d pacarnalc8r haa a dill:harge fllllowilg lha P W8VI but prior tD 1ha QRS Alrial ..d Y8111Jic:ulu piCitg hm dilcharged bafurs tha P wavelllld ORSWIMI
12. Atrial Fllrillation. IT a ..ga duatD Digitalis ("diaitalis aHacr)

Pulmonary Disorders
cor pulmonale (often secondary to COPD) low voltage, RAD, poor R wave progression RAE and RVH with strain multifocal atrial tachycardia (MAT) massive pulmonary embolism (PE)
sinU8 tachycardia and atrial fi.brlllatlon/atrial flutter are the most common arrhytbmlas RAD, RVH with strain - most specific sign is SIQ3T3 (Sin I. Q and inverted T wave in
rm
'IbroDlo Nota 2011
Cardiac Diagnostic Testl
Cardiology and CV SUJ'8ery QJ
Cardiac Biomarkers
provide diagnostic and prognomc infonnati.on and identify increased risk of mortality in acute coronary syndromes
Tallie 2. CM!Iac Enzyna
lllnllal EIMIIId
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Tropanin Tropanil T
1-2 days
1day
3days
Myocardial inlllrctian. mytJcarditis. pericllllitis. ITU!IClllar dysbaphy,

Cll'dilc dalirlll:ian. ale.
check troponin I at presentation and 8h later creatine kinase-MB (CK-.MB, depends on local laboratory protocol) new CK-MB elevation can be wed to diagnose reinfarction, troponin cannot other biomarkers ofcardiac disease: AST and LDH also increased in myocardial infarction (low specificity) BNP and NT-proBNP - secreted by ventricles in response to increased end-diastolic pressure and volume DDx: CHF. AF. PE, COPD exacerbation, pulmonary hypertension
Figure 13. Cardiac EnQII'Ia
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indications fur outpatient management: palpitations, syncope, antiarrhythmic drug monitoring, and arrhythmia surveillance in patients with docwnented or potentially abnormal rhythms. surmllance of non-sustamed arrhythmias that c::an lead to prophylactic intervention available technologies Holter monitor battery operated, continually records up to 3 leads hn symptoms remrded by patient on Holter clock fur mrrelation with ECG findings continuous loop recorder (diagnostic yield 66-8396) worn continuously and can record data before and after patient activation fur symptomatl.c episodes (usually worn fur 2 weeks) external and implantable devices external devices can be tran.stelephonically downloaded implantable loop recorder (ll.R) -implanted subcutaneously to the right or left of the sternum; triggered by placing an activator aver it; anterograde and retrograde recording time is programmable; cannot be tran8telephonically downloaded; left in place for 14 to 18montlu
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Echocardiography
Transthoracic Echocardiogrephy (TTE) ultrasound beams are directed across the chest wall to obtain images of the heart indications: evaluation ofleft ventricular ejection fraction (LVEF), wall motion abnormalities, myocardJal ischemia and compllcations of MI, chamber sizes, wall thickness, valve mozphology, pranmal great vessels. pericardia! effusion. unexplained hypotension, murmurs, syncope,
congenital heart disease use with Doppler, which is used to quantify degree ofvalvular stenosis or regurgitation
Trensoeaophageal Echocardiography (TEE) ultrasound probe inserted into the esophagus to allow fur better resolution of the heart and its structures
better visualization of posterior structures, such as left atrium, mitral and aortic valves, interatrialaeptum invasive procedure, used to complement transthoracic echocardiography indications: intracardiac thrombi, tumours, valvular vegetations (infective endocarditis), aortic dissection, aortic atheromas, prosthetic valve function, shunts, technically inadeqwrte transthoracic studies use with Doppler, which is used to quantify degree ofvalvular stenosis or regurgitation
Stress Ec:hocardlography echocardiography in combination with either physiologic (exercise treadmill or bike testing) or pharma.cologic (dobutamine infusion) stress validated in demonstrating myocardial ischemia and 8S8e&Sing viability provides i.nfonnation on the global left ventricular .reaponse to exercise regional wall motion is analyzed at rest and with stress used for valvular heart disease evaluation
CIO Cardiology and CV Surgery
Cardiac Diagnostic Teats
Toronto Notes 2011
Contrast Echocarcl iography

contrast agents injected into the bloodstream to improve imaging of the heart conventional agent: agitated saline (contains microbubbles of air) allows visualization of right heart and intracardiac shunts, most commonly patent foramen ovale (PFO) and sometimes intrapulmonary shunt newer contrast agents are capable of crossing the pulmonary bed and achieving left heart opacification following intravenous injection; these contrast agents improve visualization of endocardial borders and enhance evaluation of ejection fraction
...,,
Most CDIIIIIIODiy Ulllll T.-lmill ltnw Tell: PnrtDoall The lkucl PrltDcol - 7 stage test with each stage lasting 3 minutes. Wdh each IIUCCNSiVIJ llbge, 1he
1relldmll increa- in both speed IJid
Stress Testing
exercise testing is a cardiovascular stress test using treadmill or bicycle exercise with electrocardiographic and blood pressure monitoring guidelines for use: patients with intermediate ( 10-90%) pretest probability of CAD based on age, gender and symptoms complete RBBB ST depression <1 mm at rest exercise test results stratify patients into risk groups: low risk patients can be treated medically without invasive testing intermediate risk patients may need additional testing in the form of exercise imaging studies or cardiac catheterization high risk patients should be referred for cardiac catheterization
gredient. For old individuals or those with limibJd exen:ise capacity: eilher The Modifild Bruce or The Modihd Naughtun l'rotDcol
...,,
Important ContrlindicatiDns ta
Exen:ile luling Acute Ml, eartic dissection, pericerditis, myocarditis, pumanary embalism Severe AS, arllllilll HTN to exen:iaa adaqulll&ly
Indications for Terminating Exercise Stress Test

drop in systolic blood pressure of>10 mmHg from baseline despite an increase in workload, when accompanied by other evidence ofischemia moderate to severe angina ST elevation (> 1 mm) in leads without diagnostic Q-waves (other than Vl or aVR) increasing nervous system symptoms (e.g. ataxia, dizziness, or near syncope) signs of poor perfusion (cyanosis or pallor) technical difficulties in monitoring ECG or systolic blood pressure patient's desire to stop sustained ventricular tachycardia
...,,
Most lmpartut Prognostic Futort il Exercise luling
Sldlpmsian ST ahrVIIIion
liload PfiiSII8 compensetion
Interpretation
the most commonly used ECG criteria for a positive exercise test: mm of horizontal or downsloping ST-segment depression or elevation (at least 60 to 80 msec after the end ofthe QRS complex)
NUCLEAR CARDIOLOGY myocardial perfusion imaging {MPI) with ECG-gated single photon emission computed tomography (SPECT), using radiolabelled tracer role in evaluating myocardial viability, detecting ischemia, and simultaneously assessing perfusion and left ventricular function the degree of severity shown on the scan reveals the likelihood of further cardiac event rates independent ofthe patient's history, examination, resting ECG, and stress ECG result often denoted as MIBI scan with reference to radiolabelled tracer user exercise treadmill test (unless contraindicated) vasodilator stress with intravenous drugs dipyridamole (Persantine), adenosine act to increase coronary flow by vasodilation of arterioles (the resistance vessels) images of the heart obtained during stress and at rest 3-4h later fixed defect - impaired perfusion at rest and during stress (infarcted/hibernating) reversible defect - impaired perfusion only during stress (ischemic)
...,,
Dulal Trudmill Saare Weighted index combining: 1. TraadmiU IIX8rcise time using standard Bruce protocol 2. Maximum net ST segment deviation
(dlpmsion or eiiVIItion)
3. Exen:in-inducad angina
Provides diagnostic 1nd prognostic
information (IIUCh u 1-y&lr morlllity)
....
,
,
Pltients with normal parfusion 51udi81

ltpukstmlhiVIJa incidanca of dalth or nonfatal Ml and
are 1hus often spared furth inVIIsive evaluation for assessment of their symptoms.
....
Tracers
thalliwn-201 (201Tl, a K analogue) technetiwn-99 (99Tc)-labelled tracer (sestamibi/Cardiolite or hexamibi/Myoview-)
ACC/AHA zaaz Guidelines for Use Stabbl angina, baseline ECG

abnormalities, post-rwac:IArization
Summary of Stress Testing

Exercise ECG initial evaluation in patients without hard-to-interpret ECGs who are able to exercise Exercise Stress Echo when ECG is uninterpretable intermediate pre-test probability with normal/equivocal exercise ECG post-ACS when used to decide on potential ef1icacy of revascularization to evaluate the clinical significance of valvular heart disease
assessment. heart h.ilure, patients Ulllble to exercise, preoperative risk assessment for patients undergoing nancanl wrgery.
'IbroDlo Nota 2011
Cardiac Diagnoslic Testl
Cardiology and CV Surgery Cll
Dobutamine Stress Echo in patients unable to aerdse, with the same lndlcatlons as aerdse stress echo to assess tissue viability o Exeidse Myocardial Perfusion Imaging (MPI) when ECG is uninterpretable intermediate pre-test probability with normal/equivocal exercise ECG in patients with previOUI imaging whose symptoms have changed to diagnose iachemla Dipyridamclel.Adenosine MPI to diagnose CAD in possible ACS patients with non-diagnostic ECG and negative serum
,, ,
liellltlwlly 1111 &peclllclty Ill Vll'loul 111Mtlldq Exarcila ECG (Sn 611; Sp 71) Stms (Sn 71; Sp 881
PET -..inu!Sn 81; Sp 82) MIBI acannllg (Sn BB; Sp 77)
biomarkers when ECG is uninterpretable due to LBBB or V-paced rhythm in patients unable to aercise, with the same indications as exercise :MPI
Cardiac Catheterization and Angiography

invasive: catheters are introduced peu:utaneously intJJ arterial and venous circulation under conscious sedation and contrast ia injected arterial access most commonly through the femoral artery. radial approach gaining favour especJally for obese patients and outpatients dependent on driving and ambulation (occupational requirements) venous access through the femoral vein or internal jugular vein
o
same day procedure as outpatient
indications for prehospitalization: anticoagulation therapy, renal failure, diabetes, contrast allergy catheterization permits direct meamrement of intracardiac pn:llllures, transvalvular and mean peak pressure gradients, valve areas, cardiac output, shunt dam. oxygen saturations, and visualization of coronary arteries, cardiac chambers and great vessels
Right Heart Catheterization (Swan-Ganz catheter) right atrial. right ventricular. pulmonary artery pressures are recorded o Pulmonary Capillary Wedge Pressure obtained by advancing the catheter to wedge into the di.stal pulmonary artery records pressures measured from the pulmonary venous system in the absence of pulmonary venous di&ease, will rdlect left atrial pressure
Left Heart Catheterization systolic and end-diasto1ic pressure tracings recorded; left ventricular size, wall motion and ejection fraction can be assessed by injecting contrast Into the left ventricle (left ventriculography) cardiac output (measured by the Pick oxygen method or the indicator dilution method) Coronary Angiography coronary vasculature accessed via the coronary ostium conttaindicated with severe renal failure (due to contrast agent toxicity), must check renal status
..... 1
,}---------, ACCIAHA 2002 .._..lllllld.. lndlml- fur c-ay Disebling (CCS c:luses Ill end M chronic llllble enain diiPite medical tharapy critaia on clilir:ll essmment or nor.-ilvaiva Wli1;
Ana-...,
1-.........
2 -lnflnlplcal
- AnllrDipical
i - Anllnlllllal
SUdden cardiac dlllllh. ..-icu vanbi1D1r arrhythmia. or CHF Uncartlin dilpsis or prognosisaftar non-invuive tailing
lllllbilily to
liSting
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" c__,= acuta marginal.
Gold standlrd far localizing nl q111ntifyilg CAD.
Figure 14. Coronary Angiogram Sclllmltic {RCA = right coronary artBry, AM LAD left antariar dascending, OM obtuse marginal!
,.--------------.
Hamodynlmicaly significant llanosis is dllil'lld q 711'1 or more narrowing Gf1he
dilnllblr.
Prognosticators
o
angiograpbic variables may provide valuable information regarding lesion severity, complexity, locatl.on and progno!lis
Cl2 Cardiology and CV Surgery
Cardiac Diagnostic Tests/Arrhythmias
Toronto Notes 2011
Diagnostic Catheterization outcomes related to complications for diagnostic catheterization should be <1% procedure related complications: vascular injury, renal failure, stroke, MI mortality rate 0.1-0.2% inadequate diagnostic procedures should occur in far fewer than 1% of cases provocative pharmacological agents can be used to unmask pathology fluid loading may unmask latent pericardia! constriction afterload reduction or inotropic stimulation may be used to increase the outflow tract gradient in hypertrophic cardiomyopathy coronaryvasoreactive agents (e.g. methylergonovine, acetylcholine) a variety of pulmonary vasoreactive agents in primary pulmonary hypertension (e.g. oxygen, calcium channel blockers, adenosine, nitric oxide, or prostacyclin)
Contrast-Enhanced CT Coronary Angiography

fast ECG-synchronized multi-slice CT image acquisition in the heart has enabled non-invasive imaging of the coronary arterial tree often used to assess coronary artery and previous graft stenosis/viability that could not be seen during coronary angiography sensitivity= 85%, specificity= 90% for the diagnosis of obstructive coronary disease with >50% stenosis
Magnetic Resonance Imaging (MRI)

offers high spatial resolution, eliminates the need for iodinated contrast, and does not involve exposure to ionizing radiation valuable in assessment of congenital cardiac anomalies, abnormalities of the aorta, and assessment ofviable myocardium
CARDIAC DISEASE Arrhythmias

Mechanisms of Arrhythmias
(I} Alterations in Impulse Fonnation
1his can occur due to:

A. Abnonnal Automaticity
automaticity is a property of certain cardiomyocytes to depolarize themselves to their threshold voltage so as to spontaneously generate action potentials in a rhythmical fashion under normal circumstances, only cells at the specialized conduction system (SAN, AVN and ventricular conduction system) exhibit natural automacity and are thus pacemaking cells - the automaticity of these pacemakers can either become abnormally increased or decreased cells in the myocardium outside the conduction system in disease (e.g. post-MI ventricular ischemia) may inappropriately acquire the property of automaticity and contribute to abnormal depolarization. If these ectopic generators depolarize at a rate that is greater than the SAN, they assume pacemaking control and become the source of abnormal rhythm automaticity can be influenced by: neurohormonal tone (sympathetic and parasympathetic stimulation) abnormal metabolic conditions (hypoxia, acidosis, hypothermia) electrolyte abnormalities drugs (e.g. digitalis) local ischemia/infarction other cardiac pathology this mechanism is responsible for the accelerated idioventricular rhythm and ventricular tachycardia that often occurs 24 to 72 hours post myocardial infarction
'IbroDlo Nota 2011
CardioloBf and CV Surgery Cl3
B. Trigcred Adtrily due to AftcrdepoJ.arizations
There are two types of triggered activity:

1. Early AfterdepolarhatioM occur in the conten action potential prolongation consequence of the membrane potential becoming more positive during repolarization result in self-maintaining depolarizing oscillations of action potential, generating a ta.chyarrhythmia. basis for the degeneration ofQT prolongation. either congenital or acquired. into Torsades de Pointe& 2. Delayed Afterdepolarizaons occur after the action potential has fully repolarized, but before the next usual action potential. thus called a delayed afterdepolarization commonly occurs in situations of high intracellular calcium (digitalis intoxication, ischemia) or during enhanced catecholamine stimulation
(II) Alterations in Impulse Conduction
'Ibis can occur due to:

A. Re-Entry C1rcuit8 (see Figure 15 for detailed descrl.ptl.on) the presence ofself-sustaining re-entry circuit causes rapid repeated depolarizations in a region of myocardium e.g. myocardium that has infarcted and become ischemic will consist of non-excitable and partially excitable zones which will promote the fOrmation of re-entry circuits
Rgurt 15. Mecllanlun of Reentry
Requii'8B both unidirectional block (11and slowed ratrugrada cDnlbction (21. When an action potential raachas a division in the conduction path (anywhara in the myacardiuml, the impulse proceeds II'Ound and stirrdates dstal rnyocmdium. If the action patantial propagatas through a block (rafractary tissual in 1ha retrograde diractian but nllt in 1ha foTward diraction,. unidiFICtianal block is p111S1nt 111. This can occur as a rasult af calular dysfunction with changes in cellwar refractoriness. Slowed retrograde conduction of the action potential'lllrough B (datted lne) encounters excitable tissue in A because these myacytes have had sufficient time to repolarise by this time paint. and now the impulsa is free to excite A again thus generating a raantJy circuit.
B. Conduction Block
ischemia, fibrosis, trauma and drugs can cause transient, permanent, unidirectional or bidirectional block most common cause of block is due to refractory myocardium (cardiomyocytes are in refractory period or zone of myocardium unexcitable due to fibrosis) ifblock OCCill'll along the specialized conduction system, distal zones of the conduction system can assume pacemaking control conduction block can not only lead ro bxadyaudia, but also tachyc:ardl.a when impaired conduction leads to re-entry phenomenon
C. Bypua 'lradl
normally the only conducting tra<:t from the atria to the ventricles is the AVN congenital development of additional, or acce!iiKlrf conducting tracts bypa&s the AVN and fadlitrte premature ventrkular activation before normal AVN conduction seePre-Exdtlltioll Sytulromes. Cl9
Cl4 CardiologyandCVSurgery
Arrhythmias
Toronto Notes 2011
Bradyanhythmias I<60 bpm)

Sinus bradycardia Sinoatrilll {SA) block Sinus arrast AV block {2nd & 3rd degree) Junctional rllylhm ldiovanlricular rllylhm
Anhythmias
Regular
Tadlyanhythmias(>1DD bpm)
NanawORS
Sinus tachycardia Atrial tachycardia Junctionallllchycardia
WideORS SVT with abarrancy/BBB

Ventricular tachycardia
lnagular
Atriallbrillation
A. flutter withllllriabla block Multifocal atrial tilchycardia
AVNRT
AVRT Atrial ftuttar
Figura 16. Clinical Approach to Arrhydlmill

Bnulyanhythmias
Examples
Bradyarrhythm ias
SA NODAL DYSFUNCTION Sinus Bradycardia P axis normal (P waves positive in I and aVF) rate <60 bpm marked sinus bradycardia {<50 bpm) may be seen in normal adults, particularly athletes, and in elderly individuals caused by increased vagal tone or vagal stimulation vomiting episodes of myocardial ischemia or infarction {inferior MI) sick sinus node increased intracranial pressure hypothyroidism hypothermia drugs (beta-blockers, calcium blockers, etc.) treatment: if symptomatic, atropine during acute episodes; pacing for sick sinus node syndrome; if drug-induced, reduction or withdrawal of drugs Sinus Block. Pause, and Arrest three disorders involving the SA node; the sinus pacemaker fires but impulse fails to depolarize the atrial myocardium, resulting in no initial P wave (and consequently no QRS complex. ST segment or T wave) sinus block: also SA block, a complete block or failure of the sinus node to depolarize the atria; the block can last one or more cardiac cycles and is a multiple of the normal P-P interval sinus pause: a delay in the formation of a sinus impulse in the SA node, resulting in a temporary pause (usually>3 sec) sinus arrest: a longer delay in the formation of a sinus impulse in the SA node there is no clear cut-offbetween sinus pause: vs. arrest, however, if the: pause lasts greater than 3x the normal P-P interval, then it may be called an arrest the P-P prolongation is not phasic or gradual (unlike sinus arrhythmia) and is not a multiple of the normal P-P interval (unlike sino-atrial block) escape beats or rhythm may occur: atrial escape: P waves with abnormal morphology junctional escape: P waves not seen, or follow the QRS {retrograde P), rate 40-60 bpm ventricular escape: no P wave; wide, abnormal QRS; slow rate 20-40 bpm Sick Sinus Syndrome (SSS) characterized by sinus node dysfunction (marked bradycardia. sinus pause/arrest. sinoatrial block) when symptomatic, electronic pacemaker is indicated frequently associated with episodes of atrial tachyarrhythmias ("tachy-brady syndrome) usually require a combination of a pacemaker for bradycardia and medications {beta-blocker, calcium channel blocker, and/or digoxin, initiated after pacemaker insertion) for tachycardia
....
lin Arrhytbmi1
Normal PW.V., 1111riatian of !he P-P int8rval by > 120 msec due to lllll'(ing rate of SA node
.........ry SA": Seen moru oftun in young lldulb

{ <31 Y18fS old) NorTIIIII, mulbi frum in autonomic tone during raspiratory cycle Rate increases inspiration, slows witt1 expirltion
"N-r!*81ory SA": Seen more often in the elderly

Can occur in !he norTIIIII heart; if marked, may be due to sirws node d.,.tunction {e.g. in hellll: dilleQII, or lifter digitillis tmcicity) U.U.IIy do111 not rvquira treltmant
'IbroDlo Nota 2011
Cardiology and CV Surgery ClS
AV Conduction Blocks
1st Degree AV Block prolonged PR interval (>200 msec) frequently found o..mong otherwise healthy adults no treatment required
2nd Degree AV Block some of tbe atrial impulses are not conducted to the ventricles c:an describe block by ratio ofP waves to# ofQRS (e.g. 2: l, 3: l, 4:1 increases in severity) second degree AV block is further subdivided into: Type I (Mobitz I) 2nd Degree AV Block a gradual prolongation of the PR interval precedes the fallw:e of conduction of a P wave (Wenc:kebach phenomenon) AV block ls usually in AV node (proximal) - triggers (usually reverslble): Increased vagal tone (eg. following surgery),
RCA-mediated ischemia - not an indication fur temporary or permanent pacing
) Fiare 17. Secand D11re1 AV llack with Wencklblch l'llllom8lllln (Mabib: I) (4:3 canductian)(I.Hd V1
Type D (MobJtz II) 2nd Degree AV Block. tbe PR interval is constant; there I& an abrupt failure ofconduct:lon of a P wave AVblock is usually distal to tbe AV node (I.e. His bundle) increased risk ofhigh grade or 3rd degree AV block
"' ,
'JWe II (llollllz Ill 'r Typa II AV bla'* ilan indiCIIIian fllr pemwulllt piCina.
Figure 1I. Sacand Dagna AV Black (Mollitz II) (3:2 cand1ctian) (Lead V1)
2:1 AV Block often not possible to determine whether the block is type I or type II prolonged or repeated recordings may clarify the diagnosis
Figure 19. 2:1 AV Black (Lead II) 3rd Degree AV Block complete failure ofconduction of the supraventricular impulses to the ventricles ventricular depolarization initiated by an escape pacemaker distal to the block QRS can be narrow or wide Ounctional va. ventricular escape rhythm) PP and RR intervals are constant, variable PR intervals no relationship between P waws and QRS complexes (P tltrrJUWl) management (see &ctricalPacing. C21)
Figure 20. Third Degree AV Block (Comp1818 Heart Blo-*) (Lead II)
C16 CardioloBY aod CV Suqp:ry
10ronto Nota 2011
Supraventricular Tachyarrhythmias
Presentation for SVT (and pra-axcltatlon syndromes) symproms can include: palpitations, dizziness, dyspnea. chest discomfort, presyncopelsyncope me;y precipitate congestive heart failure (CHF), hypotension, or ischemia in patients with
underlying disease untreated tachycardJas can cause cardiomyopathy (rare. potentially reveraJble with treatment of SVT's) includes supraventricular and ventricular rhythms
o
Supraventricular Tachyanhythmlu (SVT) tachyarrhythmias that originate in the atria or AV junction this term is used when a more specific diagnosis of mechanism and site oforigin cannot be made characterlzed by narrow QRS, unless there is pre-existing BBB or aberrant ventr:icul.ar c:onductl.on (abnormal conduction due to a change in cycle length)
Sinus Tachycardia sinus rhythm with rate> 100 bpm o occurs in normal subjects with increased sympathet1.c tone (exerc.l.se, emotions, pain), alcohol use, caffeinated beverages, drugs (e.g. beta-adrenergic agonists, anticholinergic drugs, etc.) etiology: fever, hypotension, hypovolemia. anemia, thyrotoxicosis, heart failure, MI. shock, pulmonary embolism, etc. treatment: treat underlying disease; consider beta-blocker if symptomatic, CCB ifbeta-blockers
contraindicated
Premature Beats o premature atrial contraction {PAC. Figure 25) ectopic supraventricular beat originating in the atria P wave morphology of the PAC usually ditrera from that ofa normal sinus beat junctlanal premature beat ectopic supraventricular beat that originates in the vicinity ofthe AV node P wave is usually not seen or an inverted P wave is seen and me:y be before or closely follow the QRS compleJ: treatment uauall.y not required
Atrial Flutter
Figura .Z1 . Abill Flutter wid! V.riabla Block
rapid, :regular atrial depolarization from a maao re-entry drcuit within the atrium (molt commonly the right atrium) atrial rate 250-350 bpm, usually 300 bpm AV block UBUally occurs; it may be fixed (2:1, 3:1,4:1, etc.) or variable etiology: CAD, thyrotoxicosis, MV disease. cardiac swgery, COPD, pulmonary embolism, pericarditis ECG: sawtooth flutter wava (most common type of flutter) in inferior leads (II, m, aVF); narrow QRS (unless aberrancy) in atrial flutter with 2:1 block, carotid sinus massage (first check for bruits), Valsalva maneuver or adenosine may decrease AV conduction and bring out flutter waves o treatment acute: ifunstable (e.g. hypotension, CHF, angina): electrical cardioversion ifstable (1) rate control: beta-blocker, diliiazem, verapamJl, or digoxin (2) chemical cardioversion: sotal.ol, amiodarone. type I antiarrbythmics or electrical cardioversion anticoagulation guidelines same as for patients with AF (see Alrlal Ftbrlllatlon, C17) long-term: antiarrhythmic:&, catheter radl.ofrequency (RF) ablation (success rate dependent on site of origin ofatrial flutter)
Multlfocal Atrial Tachycardia (MAT) irregular rhythm caused by presence of 3 or more atrial foci (may mimic AF) atrial rate 100-200 bpm; at least 3 distinct P wave morphologies and PR intervals vary, some P waves may not be conducted o occurs more commonly in patients with COPD, and hypoxemia; less commonly in patients with hypokalemia, hypomagnesemia. sepsis, theophylline or digital.la toxicity treatment: treat the underlying cause; CCBs may be used (e.g. diltiazem, verapamil), beta-blockers may be contraindicated because ofsevere pulmonary disease no role for electrical cardioversion, antiarrhythmics or ablation
'IbroDlo Nota 2011
CardiologyandCVSuqery Cl7
Atrial Fibrilllltion (Af)

most common sustained arrhythmia
incidence lnaeases with age (10% of population >80 years old) symptoms: palpitations, fatigue. syncope and may precipitate or worsen heart failure may be associated with thromboembolic events (4%/year In nonvalvular AF)
IDitlation
9lng].e circuit re-entry and/or ectopic fod act as aberrant generatois producing atrial tachycardia {350-600) impul&e& then conduct irregularly acro&S the atrial myocardium to give rise to fibrillation in some cases, ectopic foci have also been mapped to the pulmonary vein ostia and can be ablatEd
maiutnaoce
the tachycardia causes atrial structural and electropbysl.ol.oglcal remodelling changes that further promote AF; thus the longer the patient is in AF, the more difficult it is to convert back to sinus rhythm the AV node Irregularly filters incoming atrial impulses producing an Irregular ventricular response of <200 bpm and the tachycardia leads to suboptimal cardiac output fibrillatory conduction of the atria promotes blood stasis increasing the risk ofthrombus furmation - AF is an imporbmt risk filctor for stroke
Tillie 3. CHADSZ Risk PrGIIidian fur Na..v.lvullr AF

Cco;ill6tillll Haart Faim
ll)1lel1enlian
1.9-2.8 (low)
aspirin 81-325
daly
2-3
Age>75
IliaballS
4.1).5.9 (mod) 8.5-1 8.2
caurradin (INR 2-3) caurradin IINR 2-3)
Slnia'TIA. (flill')
AFonECG no organized P waves due to zapid atrial activtty {350-600 bpm) causing a cbaotlc fibrillatory baseline Irregularly Irregular ventricular response (typically 100-lSObpm), narrow QRS {unless aberrancy or previous BBB) wide QRS compleus due to aberrancy may occur following a long-short cycle sequence ("Ashman phenomenonj loss of atrial contraction. thus no wave seen In ]VP, no S4 on auscultation
Figure 22. Abill Fibrillllion (Laad II)

Management (adapted &om ACC/AHAJESC pidelinal006) Major objectiftl {RACE) 1. Rate control: beta-blockers, diltiazem, verapamil (in patients with heart allure: digoxin,
amiodarone)
Milllill*l-m.ITrial N1112002; 3U:1B33

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2. Anti-coaguhn:ion: prevmt thromboembolism assess stroke risk: determine CHADS2 score in patients with nonvalvular AF if no risk factors. ASA 81-325 mg dafly I moderate risk factor, ASA or warfarin (INR2.0-3.0, target 2.5) moderate risk factors or any high risk factor (prior stroke. TIA or embolism. mitral stenosis, prosthetic valve), warfarin 3. Cardioversion {electrlcal) ifAF <24-48 hrs, can usually cardiovert without anticoagulation ifAF >24-48 hrs, anticoagulate fur 3 weeks prior and 4 weeks after cardioversion ifpatient unstable (hypotensive, active angina due 1D tachycardia, uncontrolled heart failure), should cardiovert immediately 4.Etiology HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocardlti&, ASD, following surgery. PE. COPD, thyrota:ncosls, SSS (Sick Sinus Syndrome), alcohol ("holiday heart") may present in young patients without demonstrable disease ("lone .AF") and in the elderly without underlying heart <Wease restore normal sinus rhythm iffeasible
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CIS Carcliolosrand CV Surgery
A:rrhythmiu
1'oroDio
2011
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Additio1111l Management Pointa Regarding Atrial Fibrillation recent studies of patienb with atrial fibrillation suggest that there is no difference in long-term survival when treating patients with a rhythm-control ver8118 rate-control strategy however, many patients with a significant underlying structural heart lesion (e.g, acute MI. history ofcongestive heart fallure), valvular lesions (mitral stenosis, mitral regurgitation, aortic stenosls), hypertrophic cardlomyopathy, cardJ.ac amyloid. other cardiomyopathies, pericardial disease, congenital heart lesions) will not tolerate atrial fibrillation well (since many dependent on atrial kick.) and these patients should be cardiaverted (chemical or electrical) as soon as possible
Newly Discovered AF anticoagulants may be benefi.dal ifhigb. risk for stroke lfthe episode is selflimited and not associated with severe symptoms. no need for
Dibrnl: lllllnllll.. . . . dad!, rn,acardll imtlins. llldl: aiJ!Ib!ctt 11111111alma (OR 0.68, MO.M0.115). ildlaric lllnlla ((1110.53, !IS0.41 -ILIB). 1111 r,Qnil: lridi181:1[11 0.48.115'10.25
- 0.10). lhlfUIIII fiUigrbtttfilren:e in flld
antlar.rhythmic drugs
lfAF persists, 2 options: 1. rate control and anticoagulation {as indicated above) 2. cardioversion (as above)
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Recurrent AF/Pennanant AF
lfepisodes are brief or minimally symptomatic, antiarrhythmic drug may be avoided; rate
control and anticoagulation are appropriate patients who have undergone at least one attempt to restore sinus rhythm may remain in AF after recurrence: permanent AF may be accepted (with rate control and antithrombotics as indicated by CHADS2 score) in certain clinical situations ifsymptoms are bothersome or episodes are prolonged, antiarrhythmic drugs should be used no or minimal heart disease: ftecainide, pmpafenone or sotalol LV dysfunction: amiodarone
CAD: beta-blockers. amiodarone
AV Nodal Re-Entrant Tachycardia (AVNRT) re-entrant clrcuit using the dual pathways (Cut conducting beta fibres and slow conducting alpha fibres) within or near the AV node; often found in the absence of structural heart disease; cause is commonly idiopathic, although familial AVNRT has been reported sudden onset and offset
usually initiated by a supraventricular or ventricular premature beat AVNRT accounts for 60-7096 of all paroxysmal SVTs retrograde P waves may be seen but are usually lost In the QRS complex treatment acute: Valsalva or carotid massage. adenosine is first choice ifUDreSponsive to vagal maneuvers; ifno response, try metoprolol, digoxin, diltiazem; electrical cardiaversion if patient hemodynamically unstable (hypotension, angina or CHF) long-term: lst line: beta-blocker, diltiazem, digoxin, 2nd: anti-arrhythmic d.nJw!
(flecainide. propafenone), 3rd: catheter ablation fast resuJar rhythm; rate 150-250 bpm
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against1hl CIIV!id artav for 5-10 11conds.. Nwr{lliltlln for bnihl

. . . . palpation.
lhe cntid llllltiGB i1111lually a cOIIIbml prenura diral:lad pollariorly
2. An alrial pranlllura bllllt (APBJ llflar 11narmlll
deponing bllld conducu through A

(ainCII npallrilad) but nat B (still rafractury -
11111 proUina unidirec:tiallll block)

lha i11110181nMIIa along Aand n111ChB1 the diltlll and of B which hu now npalarilad, allowing 18?rogl'lfle coiiiM:Iian to IIS!IIblish a18811?ry circuit
iE
1. for AVNRT: Praunce of fulllld algw tnll:ll in AV node
12
i
0
:::E
F'ra Z1 Macllani1111 far AV Nollll A..&try
'IbroDlo Nota 2011
CardiologyandCVSuqery Cl9
a.d.tK.nl
or laft ha.t
Pre-Excitation Syndromes
refer to a subset ofsupraventricular tachyarrbythmiu, mediated by an accasory pathway, which c:an lead to vmtricular pre-excitation
Wolff-Parkinson-White fWPW) Syndrome congenital defect present in 1.5-2/1000 of the general population an accessory conduction tract (Bundle of Kent; can be in right or left atrium) abnormally allows early electrical activation of part ofone ventricle impulses travel at a greater conduction velocity across the Bundle of Kent thereby effectively 'bypassing' AV node since the ventricles are a.ctivated earlier, the ECG shows early wntricu1ar depolarization in the furm of initial slurring of the QRS complex - the so called delta wave atrial impulses that conduct to the ventricles through both the Bundle of Kent and the normal AV nodeJHis-Purkinje system generate 11 broad "fusion complex" ECG features ofWPW PR Interval <120 msec "delta wave": slurred upst:mla: of the QRS (the leads with the delta wave vary with site of bypass) widening of the QRS complex due tD the premature activation secondary ST segment and T wave changes tllchyarrhythmia.s may occur, most often AVRT and AF
Can IDiilll in rVIt
,, I
J ..
C YOII'III M.Kim ZD11
Figu111 24. Acceuary pathway caniiiUGiian in WPW causes 8llly venbiciAr actintian lllna tD tiJa appe. .nca al 1 daltB wave {llurred gpstrelre of tha DRS) a tha ECG Wore unll canduction occurs acraa the AVN
AF In WPW Patients AF Is the index arrhythmia in up to 20 percent ofpatients with WPW syndrome it Is usually Intermittent rather than persistent or permanent rapid atrial depolarizations In AF are conducted through the bypa88 tract which is not able to filter impulses like the AVN consequently, the ventricular rate becomes extremely (>200 bpm) and the QRS complex
widens
treatment: electrical cardioversion. IV procainam!de or IV amiodarone do not use drugs that &low AV node conduction (digoxin, beta blockers) as this may cause
preferential conduction through the bypass tract and then precipitate VF long-term: ablation of bypass tract when possible
AV ReEntnmt Tachycardia (AVRT) re-entrant loop via accessory patbwa.y and normal conduction system
initiated by a premature atrial or ventricular complex orthodromic AVIIT: stimulus from a premature romplatravds up the bypass tmct 0/ID A) and down the AV node (A to V) with narrow QRS complex (no delta wave because stimnlus travels tluough normal conduction system) comprille& 95 percent ofthe reentrant tachycardias associated with WPW syndrome antidromic AVRT: more rarely the stimnlus goes up the AV node (V to A) and down the bypass tract (A to V); wide and abnormal QRS as ventricular activation is only via the bypass tract treatment acute: similar to AVNRT acept avoid long-acting AV nodal blockers, e.g. digoxin and verapamil long-term: for recurrent arrhythmias, ablation of the bypass tract Is recommended drugs such as flecalnide and procainamide can be used
Ventricular Tachyarrhythmias
Premature Ventricular Contraction (PVC) or Ventricular Premature Beat (VPB) QRS width >120 msec, no preceding P wave, bimrre QRS morphology origin: LBBB pattern = RV site; RBBB pattern = LV site PVCs may be benign but are usually signifi.c:ant in the following situations: consecutive = VT) or multiform (varied origin) PVC falling on the T wave ofthe previous beat ("Ron T phenomenonj: may precipitate ventricular tachycardia or VF
Accelerated ldloventrlculer Rhythm ectopic ventricular rhythm with rate 50-100 bpm more frequently occurs in the presence ofsinus bradytardia, and is easily overdriven by a faster supraventricular rhythm frequently OCCill'll in p11tientll with acute myocardial infarction or other types ofheart disease (cardiomyopathy. hypertensive. valvular) but it does not affect prognosis and does not usually require t:reat:ment
l'nlmature VenbiciW CGntractiCII !PVC)
Pr urtura Alrial ConiiKiion (PAC) ..

NDIB: Thil dilgrlm 111D show& rr..tedT--
Figu111 ZS. PVC (with bigaminy

pattern) 11'111 PAC
C20 Carcliolosrand CV Surgery
1'oroDio
2011
'' ,
1M4t lUll 'lllchyoanla
Venb'ic:ular Tac:hycardia (VT)

I
Arrl!rlllnlll IIIII llay l'rMIIIt U

Vantriculllr illl:hyaldill
SVT with ab..-.nt conduction (1'111 rell18d) SVTwith prwuilting BBB or

nlllllp8cific iltmlnlric.ar condulrtiDn d8tilct
AV cordlction through a bypaN tnllrt in Wf'W plllianb wring .. lllrilll
3 or more consecutive ectopic ventricular complexes (Figure 26) rate >100 bpm (usually 14{)..200) ventricular flutter: ifrate >200 bpm and complexes resemble a sinusoidal pattern '"8U8tal.ned ifit lasts longer than 30 sec
tachywlhythmia (a.g. lllrilll flllt8r,

atrialllll:hyaldia) AniDIImic AVRT il Wf'W pdanbl
ECG characteristics: wide regular QRS tachycardia (QRS usually >140 msec); AV dJssodatlon; bizarre QRS pattern. Also favour Ih ofVT: left axl.s or right am deviation, nonspecific intraventricular block pattern, monophasic or bipbasic QRS in Vl with RBBB, QRS concordance in Vl-V6 occasionally during VT supraventricular impulses may be conducted to the ventricles genenrting QRS complexes with normal or aberrant supraventricular morphology ("ventricular capture") or sUDUilatl.on pattern ("fusion complexes") m.onomorplW: VT identical complaes with uniform morphology more common than polymorphic VT typically result from Intraventricular re-entry drcuit potential causes: chronic infarct scarring, acute MI/isdtemia, cardiomyopathies, myocarditis, arrbythmogenic right ventricular dyapluia, idiopathic, drugs (e.g. cocaine), electrolyte disturbances polymorphic VT compleus with constantly changing morphology, amplltude, and polarity more frequently aasodated with hemodynamic instability due to faster rates (typically 200-250 bpm) vs. monomorphic VT potential causes: acute myocardial infarction, severe or silent ischemia, and predisposing facoors fur QT prolongation (see below in Torsades de Pointes) treatment sustained VT (loDger than 30 seconds) is an emergency, requiring immediate treatment hemodynamic compromise - electrical cardioversion no hemodynamic compromise- electrical cardioversion, lidocaine, amlodarone, type Ia agents (procainamide, quinidine)
vr
F'1111r1 26. Ventricullr Tachycanla(MDDomurphic)
Tabla 4. Wida Camplax Tachycanlia: Cluaa fDr Diffarallilling VT n. SVT with Abarrancy*
PresBJiir.l S\'llpbml Hislay a! CAD and praviaus Ml Plft&cal xlm

Cslllllll y WIIV8I
vr vr
Nat helplul
AV clssacidian
YariableS1 c.utid sinus IIIIIS\111111!/Dnosile tllminltalardlytlmia
(left or rVt sLperior axis) Fositive ORS CliiCOrdln:e SVT"" (A WIV8 ICI'OII chast: llllds) Nagltiw QIIS concordance {S WIIV8 acroa chest leads) Axis an11ythmia "H 1111i111t >8511111!11iiM Mill' llllllcllnl1art lillllltlhm dalceII Vf >95'1. "Mrt tlmiwle vr iliiiiiW no IIIUcllnlhiWIdiaa
VT
Exbwna axis daviati111
Clplure or flllilll QIIS widlh >140 msa:
vr vr vr
VT
vr May suggast: vr vr (polymalplic)
_..willl
Torsadea de Polntes
a variant of polymorphic VT that occun In patients with baseline QT prolongation- "'twisting ofthe points" (Figure 27) looks like usual VT acept that QRS complexes "rotate around the baseline" changing their axis and amplitude vmtricular rate greater than 100 bpm. usually 150-300 bpm etiology: patients with prolonged QT intervala are predisposed
congenital long QT syndromes drugs- e.g. Class lA (quinidine), Class Ill (sotal.ol), phenothia.zl.nes (TCAs), erythromycin. quinolones, antlhistam.ines electrolyte distw:bances - hypokalemia, hypomagnesemia nutritional defidend.es causing above electrolyte abnormalities
treatment IV magnesium, temporary pacing, isoproterenol and correct underlying cause of prolonged QT, electrical cardioversion ifhemodynamic compromise
'IbroDlo Nota 2011
Cardiology and CV Surgery Clt
Figura 27. Tarud da Pailtal

Ventricular Abrlllatlon (VAb) chaotic ventricular arrhythmia, with very rapid irregular ventricular fibrillatory waves of varying morphology {Pigure 28) terminal event, unless advanced cardiac life-support (ACLS) procedures are promptly init:i..ed ID maintain vent:ilation and cardiac output. and electrical defi.brillation is carried out most frequent cause ofsudden death refer to ACLS algorithm for complete therapeutic guldellnes
r 'f
Figura Zl. v..bic..ar Fir..lltian
L,.
,; 1
'":1
Electrophysiology (EPS) Studies

invasive test fur the investigation and treatment of cardiac rhythm disorders using iotn!cardi.ac catheters provide detailed analysis ofthe arrhythmia mechanism and precise site oforigin when ECG data are nondiagnostic or unobtainable bradyarrhytbmias: define the mechanisms ofsinus node dysfunction and localize site of AV
conduction block. tachyarrhythmias: map fur possible ablation or to assess indudbllity of ventricular tachycardia
Electrical Pacing
the decision to implant a pacemaker usually is based on symptoms ofa bradyarrhythmia or tachyanhythmia in the setting ofheart: disease
Pacemaker Indications SA node dysfunction (most common): symptomatic bradyt:ardia hemodynamic instability common manifestations include: syncope. near syncope. transient Ught:headed:nes. or severe fatigue SA node dysfunction is commonly caused by: intrinsic disease within the sinus node (e.g, idiopathic degeneration, fibrosis, ischemia, or surgical trauma), abnormalities in autonomic nervous system function. and drug effects AV nodal-infranodal block: Mobitz II, complete heart block
Pacing Techniquea temporary: transvenous (jugulaJo subclavian. femoral) or eDernal pacing permanent: transvenous iniD RA, apex ofRV or both can sense and pace atrium, wntricle or both new generation: rate responsive. able to respond to physiologic demand biventrlcular
Tallie 5. Pacemakar Nonaclature
1'111111111 I
CllanOr paced
0 = Nana A= AlrUn v= v.ntri:IIJ D= lklai(A+V)
I'DIIIIal I ChltM lensed

0 = None A= Atriun v= Ventricle D=Dual (A+V)
1'111111111. Reapcnae tD 1181'11ing

0 =None I= lnhlitad T= Tri!prad
I'DIIIIIIIIV
Pnlpnmability 0 =None R= Rata rnoct.da1im
Tactryanhythmia como!
S =Shock D= Dual (P+SI
0 = NIIIB P = Paca
examples ofcommonly used pacemakers VVI: single lead in ventricle. pacemaker inhibited in response to a sensed beat in ventricle;
protect patient from bradycardia
DDD: separate leads in atrium and ventricle; pace atrium if atrium does not contract; once an atrial event has occurred (whether paced or native) device will ensure that ventricular contraction follows; device is inhibited in the presence ofsinus rhythm and normal AV ronduction, provides physiologic pacing
Arrhythmiu/lschem.ic: Heart Disease (IHD)
Toronto Notes 2011
................... c.d.....
t.AIUII wilb Lllt'IIIIMidu . , . . o,M:tilll AnnllllemMed21X11; 147:25162 Studr: Mela-!Mw of 12 RCTs used for lmpilnllbll CltdiMIW llllillillltDr (ICDI mcy, 5RCTs IUid 48 DbseMdilllll Allfiesfor 111d 21 RCTs1nd 43 DbnmliDI'III sludiesfor Sllely rMiw. 8516 b' ICDeflicq 26 840
Implantable Cardioverter Defibrillators (ICDs)

sudden cardiac death (SCD) usually results from ventricular fibrillation (VFib), sometimes preceded by monomorphic or polymorphic ventricular tachycardia (VT) ICDs detect ventricular tachyarrhytlunias and are highly effective in terminating VT NFib and in aborting SCD several studies demonstrate mortality benefit vs. antiarrhythmics in 2 prevention (AVID, CASH,CIDS) benefit fur 1o prevention of SCD in patients with ischemic and non-ischemic cardiomyopathy, depressed left ventricular ejection fraction (LVEF), prolonged QRS see Heart Failure, C32 for current treatment recommendations
far ..r.ty IIYiiiW Ylitb 11ft Wll1lricUir ljac:tian hlction Qllntlllle Cardiomler Delldllw
implllrotian. Aklllle martll!y lllllllvne eveJ'G a.ulll: ICDs radUCid morlllly by 20'Jo
nMb:lian (54\l in suddan Clldi.: dlllh 1Q. 37\. 63%; hid I rab:ed relltiw risk rl 0.54 fur ll.ggse mllltJIIy
1 1 =44.4\IMI!grnlnt
Catheter Ablation
Techniques
radiofrequency (RF) energy: a low-voltage high-frequency form of electrical energy (similar to cautery). RF energy produces small, homogeneous, necrotic lesions approximately 5-7 mm in diameter and 3-5 mm in depth
RCTs (CI 0.43 D.58.11=60.4llj.llltM of success of lCD n,lllllllian were 99\ ta 98.8% 99.3'11j willla 1.2\ (CI O.B 1.5\1 clwa ofperiirnpllllllltian COIIII*Itialls!pel'100patient-yam)WIII'II: 1.4(CI 1.5(CI1.31.811ead prablllrl; O.i (CI 0.5 0.111 ilflmt sill irlaclian; and 19.1 (CI 1U 22.01 il1l!llllllPiJII dilclllrgls il RCTI111111111'1tSofU(CI4.5-5.3Iilllfiiii'Dilril il DbaaMIIilllll ftldiiS. ICDs 11e saltllld &lleciNe in rWilg morlllly il aclil ]lltilra l'lilll LV iYIIaic dylb1cliDn. but cany l!irP'i1311rilb of inlpJIIIIJirilla 6sdi1JQ8I.IiiiNncls RCTsllld Dlialrvatioraln.danwthatirnp!Md risk lll'ltilicllion of pllim lillY Utlw impiiMI lllll:amlld llll!CIIIIImsa Milts. -
Indications
paroxysmal SVT AVNRT: accounts for more than half of all cases accessory pathway (orthodromic reciprocating tachycardia): 30% of SVT re-entrant rhythm, with an accessory AV connection as the retrograde limb corrected by targeting the accessory pathway atrial flutter: flutter focus in RA atrial fibrillation: potential role fur pulmonary vein ablation ventricular tachycardia: commonly arises from the right ventricular outflow tract and less commonly originates in the inferoseptalleft ventricle near the apex (note: majority of cases of VT are due to scarring from previous MI and cannot be ablated)
Major Complications
approximately 1% of patients death: 0.1-0.2% cardiac: high grade AV block requiring permanent pacemaker, tamponade, pericarditis vascular: hematoma, vascular injury, thromboembolism, TIA/stroke pulmonary: pulmonary embolism
Ischemic Heart Disease (IHD)

Epidemiology
most common cause of cardiovascular morbidity and mortality atherosclerosis and thrombosis are the most important pathogenetic mechanisms male:female ratio= 2:1 with all age groups included (Framingham study), 8:1 for age <40, 1:1 forage >70 peak incidence of symptomatic HID is age 50-60 (men) and 60-70 (women) for primary prevention of ischemic heart disease, please see Family Medicine, FM17
Tabla &. Risk Factors for Atharosclerotic Heart Disease

Mljar Rislr: FIU:bn Milar Risk Factan Male, pos1menopausal female
Smoking
Diabetes mellitus {DM)
Hypsrbn&ion (HlN) Ftrnily history (FHx) Dl Ml

Fim degree male rei alive <55 Fim degree female relative <65 Hypaltipidemia
Obesity SedBirtary life&tyte Hypelhomocysteinemia
Toronto Notes 2011
Cardiology and CV Surgery C23
HTN Hypercholesterolemia Cigaratl8s
Endothelial injury
Macrophage influx - - - - - - - - + F o a m calls

Dlcidized LDL
Flllty slruaks
4Jid core
...
Endothelial damage
Smooth mu8Cie
Fibror cap
Growth -----------+AthertJIIIil
Lumen murowilg
Ruplln
CalcffiCIIIion
Figure 29. Pathophysiology of Atherosclerosis

i-
Cytoki1as
Chronic Stable Angina

Definition symptom complex resulting from an imbalance between oxygen supply and demand in the myocardium factors influencing supply luminal diameter (most important factor) duration of diastole (important fur coronary artery perfusion) hemoglobin Sa02 factors influencing demand heart rate contractility wall stress Etiology and Pathophysiology decreased myocardial oxygen supply atherosclerosis, vasospasm tachycardia (decreased duration of diastolic coronary perfusion) anemia hypoxemia congenital anomalies increased myocardial oxygen demand tachycardia hyperthyroidism (increased contractility, increased HR} myocardial hypertrophy, aortic stenosis Signs and Symptoms typical: retrosternal chest pain, tightness or discomfort radiating to left ( right) shoulder/arm/ neck/jaw, associated with diaphoresis, nausea, anxiety predictably precipitated by the "3 E's: Exertion, Emotion and Eating brief duration, lasting< 10-15 minutes and typically relieved by rest and nitrates Levine's sign: clutching :fist over sternum when describing chest pain anginal equivalents: dyspnea, acute left ventricular failure, flash pulmonary edema Clinical Assessment history, physical and directed risk factor assessment labs: Hb, fasting glucose, fasting lipid pro:file ECG (at rest and during episode of chest pain if possible) CXR (suspected heart failure, valvular disease, pericardia! disease, aortic dissection/aneurysm, or signs or symptoms of pulmonary disease) stress testing (see Cardiac Diagnostic Tests, CS} or angiography echocardiography to assess systolic murmur suggestive of aortic stenosis (AS), mitral regurgitation (MR) and/ or hypertrophic cardiomyopathy (HCM) to assess LV function in patients with Hx of prior Ml, pathological Q waves, signs or symptoms of congestive heart failure (CHF)
.....
,,
Chronic stable angi1111 is most often

due to a fixed siBnosis clllll8d by an
atheroma.
mutt of
Acuts coronary syndromaa ara tha
....
,,
Can.dian Cardion_..,
ICCSI hnctillnal C._lilic1tian Df
Anatn
Cllst 1: ordinary physical ectivity (walking, climbing stairs) does not CllllH angina; angina with rtnnuous, rapid, or prolonged ectivity. Clla II: slight limitation Df on!ilary
activity: angina brought m> 2 blocks on level or climbing > 1 flight of stair11 or by emotional rlnll. Cllss Ill: marked limitation of ordillllry ectivity: engi1111 brought on at <2 blocks on level or climbing <1 flight ohtairs. Cll IV: inability to CIITY out any physical activity without discomfort; angil'lll may be present at rest.
Toronto Notes 2011
Differential Diagnosis cardiovascular aortic dissection pericarditis myocardial infarction (MI) respiratory (e.g. PE, pneumothorax, pneumonia) gastrointestinal (e.g. peptic ulcer disease, gastroesophageal reflux disease, esophagitis, gastritis, esophageal spasm, esophageal rupture) musculoskeletal (e.g. rib fracture, costochondritis, muscle spasm) neurological (e.g. herpes zoster) psychiatric (e.g. anxiety)
Optilllllhllcallhlpy with ....... Pl:lt. Stllilel:aranuy .._COURAGE Trill NU.f2007; 356:1503-16
l1udr. lllncloniled. CCIII1IIIed iilll'oitll me11ian
l'llldltim 2287 petimll MID llld alijeclive IYidara gf llrjiCII"dill ia:larillllld 19iblt
lllhllcoronll'f lll8ly disa11a. 1...-. l'llierQwellllllldonilld 111 IIIC8ive inllnsivl phnllcolagic llllrepy lll1d lillllytl iniiMOOan Mil orl'oitllout pen:ibreu COI'OOIIV inlllwrDln (Fa). l'limlryou1comewulkue mollllily IIIII nonfllll mvoCIIIill inlln:lioa (MQ. Secondlly lllk:ome hid llllillianil mmtJ alllrab, Ml111d lapiiJimlior1 fDJ ualllbla 11911 willlliiQIIivB bilnltkm. llelulll:n..wunoliQnifil:lrt._cein prinwy (ooqJSIId hmnllllio: 1.05; 01 Slmldll'f IMI:Oines (hmrd ratio: 1.05; P=0.62) bltwean the PCIIIId iiiiMitioiiPJPL The PCI P4> hill liJtler Ales of '-CI.IIIrimlion 114.6Y81Q alfvlkM-11p (lllmd lllie 0.60, P<O.OOIIIIId WIS I11IR in the fnt 4 C...._.ll: PCI111n adjunct in initial
Treatment of Chronic Stable Angina 1. General measures goals: to reduce myocardial oxygen demand and/or increase oxygen supply lifestyle modification treatment of risk factors: statins (see EndocrinoloB)'. E2, Family Medicine. FM6 for target lipid guidelines), anti-hypertensives, etc. exercise program
2. Anti-platelet therapy (first line therapy) enteric coated ASA (ECASA) clopidogrel when ASA absolutely contraindicated 3. (first line therapy- decrease overall mortality) increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload) cardioselective agents preferred (e.g. metoprolol, atenolol) to avoid peripheral effects (inhibition of vasodilation and bronchodilation via receptors) avoid intrinsic sympathomimetics (e.g. acebutolol) which increase demand
file
4. Nitrates (symptomatic control, no clear impact on survival) decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary perfusion maintain daily nitrate-free intervals to prevent tolerance (tachyphylaxis) 5. Calcium channel blockers (CCBs, second line or combination) increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload) caution: verapamil/diltiazem combined with beta-blockers may cause symptomatic sinus bradycardia or AV block 6. ACE inhibitors (ACEis, not used to treat symptomatic angina) angina patients tend to have risk factors for CV disease which warrant use of an ACEI (e.g. hypertension, diabetes, proteinuric renal disease, previous MI with LV dysfunction) class Ila evidence of benefit in all patients at high risk for CV disease class I evidence in patients with concomitant DM, renal dysfunction or LV systolic dysfunction angiotensin II receptor blockers (ARBs) when ACEis contraindicated (e.g. hypersensitivity, angioedema) 7. Invasive Strategies revasculari2ation (see Coronary Revascularization and COURAGE trial)
in CIIIIIIIIIY lfllry di- doll not lillie mollllly, Ml strolll 01 far AI:S, 1M dOll pr!Nide fllialllld NlliCid rist al TMSCI.IIIrizllilm.
VARIANT ANGINA (Prinzmetal's Angina) myocardial ischemia secondary to coronary artery vasospasm, with or without atherosclerosis uncommonly associated with infarction or LV dysfunction typically occurs between midnight and 8 AM, unrelated to exercise, relieved by nitrates typically ST elevation on ECG diagnosed by provocative testing with ergot vasoconstrictors (rarely done) treat with nitrates and CCBs SYNDROME X typical symptoms of angina but normal angiogram may show definite signs of ischemia with exercise testing thought to be due to inadequate vasodilator reserve of coronary resistance vessels better prognosis than overt epicardial atherosclerosis
Toronto Notes 2011
Acute Coronary Syndromes (ACS)

Definition coronary atherosclerosis with superimposed thrombus on ruptured plaque: other causes of unstable angina: coronary thromboembolism (e.g. infective endocarditis, intracavitythrombus, paradoxical embolism) or cholesterol embolism severe coronary vasospasm coronary dissection increased demand can also contribute (e.g. tachycardia, anemia)
Spectrum of ACS unstable angina (UA)/non-ST elevation myocardial infarction (NSTEMI) ST elevation myocardial infarction (STEMI) sudden cardiac death
llllii!'IW Bm. I ..,_..illllfln:llll7 JWA 1118; 2lllt1 Z56-63 The -.,st r.tures 11111 inc:lelse lhe llllllillaad a1 111m sr...-IIMtion.n-. c11111 ]llin lldiJting 1o bath the riilt 11111 111ft ann sindlneollly, pre- al111 S3111d
The -.,st r.tures 11111 decrease lhe lcllillaad al Ill 111 nDmlll ECG "11011. pluilic c:lllll!plin, an or Sllbllilg cllalt plil.llld positillnll dl8lt plin.
Investigations history and physical note that up to 30% of Mis are umecognizc:d or "silent" due: to atypical symptoms - more common in women, DM, elderly, post-heart transplant (because of denervation) ECG,CXR labs serum cardiac biomarkers for myocardial damage (repeat 8 hours later) (see Cardiac Biomarkers, C9) CBC, INR/aPTT, electrolytes and magnesium, creatinine. urea, glucose, serum lipids draw serum lipids within 24-48 hours because values are unreliable from 2 to 48 days post-MI
Unstable Angina (UA)/Non ST Elevation Ml (NSTEMI)

Definition syndrome of acute plaque rupture and thrombosis with incomplete or transient vessel occlusion unstable angina is clinically defined by any ofthe following: accelerating pattern of pain: increased frequency, increased duration, with decreased exertion, decreased response to treatment angina at rest new onset angina angina post-MI or post-procedure (e.g. percutaneous coronary intervention [PCI], coronary artery bypass grafting [CABG]) NSTEMI is clinically defined by the presence of 2 of 3 criteria: symptoms of angina/ischemia rise and fall of serum markers of myocardial necrosis evolution of ischemic ECG changes (without ST elevation or new LBBB) acute phase ofUAJNSTEMI risk of progression to MI or the development of recurrent MI or death is highest in the early period at 1 to 3 months after the acute phase. most patients resume a clinical course similar to that in patients with chronic stable coronary disease majority of NSTEMis do not result in the development of Q waves
TIMI Rillk
far UNNSTEMI
a..t.lllb
1'11111
lilblriell
ri8: fdDrs fur CAD ICooMI CAD ISIInolis Aspirinu. inplll7da\'J
RKint IS24 hrl-. angina ST-segrrert dellillion 0!:0.5 mm
iiiCIIIIId Clldlc rnmbll II& TDIIII'oilll qi0Q11Phy CAD COIOfiiUY lf1lly llseue
NSTIMI nan STIIgllllnllllvllian myaclllill inflln:tian T M 1ilurilalylil in myac:ardilll irOn:tion UA =II!SIIIIIe.,P .lAMA 2UOO; 284:m-842
ST Elevation Myocardial Infarction (STEMI)

Definition syndrome of acute plaque rupture and thrombosis with total coronary occlusion resulting in myocardial necrosis STEMI is clinically defined by new ischemic ECG changes plus one or both of ischemic symptoms and elevated cardiac enzymes ECG criteria (see Approach to ECGs, CS) ST elevation in 2 contiguous leads mm in limb leads or nun in precordial leads) or new BBB (either LBBB or RBBB) Acute Management of STEMI after diagnosis of STEMI is made, do not wait for results of further investigations before implementing reperfusion therapy goal is tore-perfuse artery: thrombolysis (EMS-to-needle) within 30 minutes or primary PCI (EMS-to-balloon) within 90 minutes (depending on capabilities of hospital)
lf11.tmtnt of NSTEMI
IIEMDAN
Enolll!larin
Morphine
Ot
Nitnd

MANAGEMENT OF ACUTE CORONARY SYNDROMES
Toronto Notes 2011
a.m
lllflldi. NfJM 2006; 354:1417-811 Studr. Pros,ective. 11llllorrized. controlled nUiiclntrllrill. l'ilil* 20,419 prtients (ITIIIW IQll 60 1111111el with Simi wiD W81111C.'1181Uad to llllargo lbilat,'sis. l'llierQW81111111doniledto IIICIINt litMr IIIJlllllrin or Wligld bald lllillclioniiJd hlplrin in llddililn 1nd lllndlld
thapiel. DIDin: Dedi oroomntnorntal Ml ll diJyl pasiMit.
I. General measures
ABCs: assess and correct hemodynamic status first bed rest, cardiac monitoring, oxygen nitroglycerin SL followed by IV morphine IV
a-11111: ThecaufOIIeprinlryaull:ame IJCQIII8I( ""' altai in tile IIIOXI()Irin compll1d witli those wllo received lllfnlctioalled hq)uin (UI
WI. 12.1)!., p<0.001, NNT =47). Tlirla I&(IIIIIBiy, lhR wu ltrlnd IIJMid l'ltb:ld mar111ty (&.91 w. 7.51, p=0.11 I lind il naafltllllitan:tiill(3.0'hs. p<0.001) in the _...m gnq,. The risk rJ llllljoriJieeiiv WU igniliclntlv ii1CIIIIId in hiAIIXI(IIIil graup (2.11vs. 1.4\, p<0.001, tH1=142). CllldlliD1: In plliiAts willl mMIIDMng enoxapn, is superior to IIRtionltad bapllil in pfllloring IIWII'1IAt naafltll r.t 111'111 lillY illd to 1Sllllll'llll:tion in
mortJiy.
2. Anti-platelet and anticoagulation therapy ASA 162-325 mg chewed NSTEMI clopidogrel300 mg loading dose, then 75 mg QD in addition to ASA or if ASA contraindicated subcutaneous Low Molecular Weight Heparin or IV unfractionated heparin (UFH) (LMWH preferable, except in renal failure or if CABG is planned within 24h) ifPCI is planned: clopidogrel300 mg loading dose and IV GP lib/Ilia inhibitor (e.g. abdxi.mab) anticoagulation options depend on reperfusion strategy: primary PCI: UFH during procedure; bivalirudin possible alternative thrombolysis: LMWH (enoxaparin) until discharge from hospital; can use UFH as alternative because of possible rescue PCI no re-perfusion: LMWH (enoxaparin) until discharge from hospital continue LMWH or UFH followed by oral anticoagulation at discharge if at high risk for thromboembolic event (large anterior MI, AFib, severe LV dysfunction, CHF, previous DVT or PE, or echo evidence of mural thrombus)
3. Beta-blockers first dose IV followed by oral administration non-dihydropyridine CCB (e.g. diltiazem., verapamil) in absence of severe LV dysfunction in patients with continuing or frequently recurring ischemia when beta-blockers are contraindicated (evidence suggests that CCBs do not prevent MI or decrease mortality) STEMI: if bradycardia is present, consider administering atropine (increased mortality in patients with hemodynamic compromise with early IV beta-blockers)
4. Invaaive strategies and reperfuaion options UAJNSTEMI: early coronary angiography revascularization ifpossible is recommended with any of the following high-risk indicators (class 1): recurrent angina/ischemia at rest despite intensive anti-ischemic therapy CHF or LV dysfunction hemodynamic instability high (;;::3) TIMI risk score (tool used to estimate mortality following an ACS) sustained ventricular tachycardia dynamic ECG changes high-risk findings on non-invasive stress testing PCI within the previous 6 months repeated presentations fur ACS despite treatment and without evidence of ongoing ischemia or high risk features (class IIa) note: thrombolysis is NOT administered for UAJNSTEMI STEMI Percutaneous Coronary Intervention (PCI) - early PCI (:5;12 hrs after symptom onset and <90 mins after presentation) improves mortality w. thrombolysis with fewer intra-cranial hemorrhages and re-current Mis - primary PCI: without prior thrombolytic therapy - method of choice for re-perfusion in experienced centres UAMA 2004; 291:736-39) - rescue PCI: following failed thrombolytic therapy (diagnosed when, following thrombolysis, ST segment elevation fails to resolve below half its initial magnitude and patient still having chest pain) Thrombolysis hrs of symptom onset, and <30 min after - preferred if patient presents presentation to hospital, has contraindications to PCI, or PCI cannot be administered within 90 min by a skilled practitioner
Toronto Notes 2011
STEMI: on&&! of pain <3 hili
Catheter team
Diqnolis STlMI: lie tr111tment
in < 1 hr'l
,.. . . .,.
t
Medical
Contraindic:ations to Thrombolysis?
L . __
Yeo
GB lib/lila receptor anlllgonists <1101111-.:..::..--'
Yes
management
Thrombolysis -----,... (bafora admission! ------"-1neffect'lve --'----- E mergent C oronary Ang1ogra phy Effuctive
Early Coronery Angiogaphy
Figura 30. Raparfusion Stl'l'lllgy in STEMI Tabla7. Contraindications and Cautions for Thrombolysis in STEMI
Absallllll
+ PCI
Rllllliva
Chronic, severe, poorly controlled hypertension Uncontrolled hypertEnsion (sBP> 180, dBP> 11 0) Currant anticDagulation
Prior inlraC18nial hemonhage Known sbuclural cerebral vascular lesion Known malignant IC nBOplasm Significant closed-head or facial tiiiWila Ischemic stnJke months) Active bleeding Suspected aortic dissection
vascular punctures
Ischemic stnJke (:<:3 months) Recent internal bleeding (s2-4 weeks)
Prolonged CPR or major surgery (..;3 weeks)

Pregnancy
Active peptic ulcer
Long-Term Management ACS (post-disc:harge) pre-discharge: ECG (if not fully revascularized) and echo drugs required in hospital to control ischemia should be continued after discharge in all patients (class Ila) including patients with LV dysfunction, CHF, and diabetics (class I) and all patients who did not undergo revascularization
1. General Measures education risk factor modification
2. Anti-platelet and Anti-Coagulation Therapy ECASA 81-162 mg QD clopidogrel75 mg QD (at least 1 month, up to 9-12 months, ifstent placed at least 12 months) warfarin x 3 months if high risk (large anterior Ml, LV thrombus, LVEF <30%, history of VTE, chronic AF)
3. Beta-Blockers (e.g. metoprolol25-50 mg bid or atenololS0-100 mg QD)
4.Nitrates alleviate ischemia but do not improve outcome use caution in right-sided MI patients who are preload dependent
5. Calcium Channel Blockers (NOT recommended as first line treatment, consider as alternative to beta-blockers)
6. Angiotensin-Converting Enzyme Inhibitors (ACm) prevent adverse ventricular remodelling recommended for asymptomatic patients, even ifLVEF >40% recommended for symptomatic CHF, reduced LVEF (<40%), anterior MI use ARBs in patients who are intolerant ofACEis
7. Aldosterone Antagonists
if on ACEI and beta-blockers and LVEF <40% and CHF or DM significant mortality benefit shown with eplerenone by 30 days 8. Statins (early, intensive, irrespective of cholesterol level; e.g. atorvastatin 80 mg QD) 9. Invasive (risk stratification, see Figure 31)
Toronto Notes 2011
Hiah Risk !30-35%1 Prior Ml
CHF Ruc:ummt ll;cllemia

Higll-Risk Arrhy1mia
Poll-Infarction Risk Slntification r
Intermediate/Low-Risk 165-70'5\
Non-Invasive Stress TliSting
+ +
I
Ischemia or Poor
Functional Sllrtus
Nonnal Results
No further tasting
Cardiac Cathatarization . . . - - - - - - - - - - '

ECHO dorerautirelypost-MI
at this tine
+ +
Figure 31. Post-MI Risk Stratification
.....
,.. ,
Resting LVEF is a useful progno5tic factor.
Prognosis following STEM I 5-15% of hospitalized patients will die risk factors infarct size/severity
age
co-morbid conditions development ofheart failure or hypotension post-discharge mortality rates 6-8% within first year, half ofthese within first 3 months 4% per year following first year risk factors LV dysfunction residual myocardial ischemia ventricular arrhythmias history of prior MI
Teble 8. Complications of Myocerdiellnferction

CampliCition Anhythmia t Tachycardia 2_ Bradycll"dia
Compkmon of Ml
Etiolarw Sinus. AF, VT, VFib Sinus. AV block
Presentalian
Fm48hrs Fm48hrs
1-7 days 1-7 days 1-7 days Within 48 hours Anytime Anytime 7-10days, up to 6 months 17 days
Tb. .Pr See.AnfJythmias, C1 2
CRASH PAD Cardiac Ruplln

Anhytlunia
Myacardill Ruptu.. Transmural infarction 1.LV free wall 2. Papillary llll&cla MR) Inferior infarction J_ Ventricular septum(-+ \lSD) Septal infarction SHckfCHF Post-lnfln:t Angina Infarction or ana.trysm Persistent coronary stenosis multivessel disease Reoccklsion MuraVapicallhrombus DVT lnll111111181ory AutoimmWll!
Surgery Surgery Surgery lnotropes, intra-aortic balloon pump Aggressive medical therapy PCI orCABG See above Anticoagulation ASA
Shock Hypertensionllleart failure Pericardilifll'ulmonary emboli AMuryam

DVT
IIICiftlllt Ml
Tbrombolmbalism
Pail:llditis
(Dnlllllr'l synlhml
2-aweeks
Toronto Notes 2011
Treatment Algorithm for Chest Pain

Chilli Pain
1. Morphina PAN
2. 0, 3. ASA 162-325 mg cllewed 4. Nitroglycurin SL 5. ECG 6. CIWdiac Enzymas
...
Initial enzymes normal No ischemic ECG cllanges
ST aagment deprassion (UA) Positiva enzymes with no ECG changes (NSTEMI)
STEMI
Obsstve:
Sari& ECGs and enzymas
pm
--+
_____.. Rucummt pain, serial studies positive

Pain resolves, Serial studies nonnal
low risk
1. Beta-blockllr 2. EIIOX.IIparin (LMWH) 3. Morphine pm 4. Oxygan 5. ASA [if not alraady given) 6. Nitroglycarin IV
Ri1kl111"11ifv
Initially traet asperUA/ NSTEMI
I I
High risk
Stress Test
Stress Tell
....
+ve
L ..
-ve
GPIIIrlllla intibitor, Clopidogrel
Com;idur rspurfu&ion options

PCI
I
Hf
lhrvmbolysis
Post-inWct risk-stllllify+<
low
!-VI
J Canlilc Ctheterilation I "1 Corvnary Revascularization
risk+
Stress Test
Consider other causas of chest pain
Risk Factor and lif&-long lllti-anginal therapy
Seal/6pfuuiat Shf8gy in S1fMI, Figure 3D S Post-MI Risk Slnttificlfion. FlgU11131
Figure 32. Treltment Algorithm for Chest Pain

AdllptBd tram Cecil fmlllillsotMedir:ine 6th Ed. Andreoli IIIII Clrpelder. p.1011Z0041with pemimian fram ElseYier
Sudden Cardiac Death

Definition
unanticipated, non-traumatic cardiac death in stable patient, within 1 hour of symptom onset; ventricular fibrillation is most common cause
Etiology
primary cardiac pathology ischemia/MI LV dysfunction severe ventricular hypertrophy hypertrophic cardiomyopathy (HCM)
AS
long QT syndrome congenital heart disease
Management
acute: resuscitate with prompt CPR and defibrillation investigate underlying cause (cardiac catheterization, electrophysiologic studies) treat underlying cause anti-arrhythmic drug therapy: a.miodarone, beta-blockers implantable cardioverter defibrillator (lCD)
Toronto Notes 2011
Percutaneous Coronary Intervention (PCI)

Wltrlllll ... IIIII Stlnll Cin:liRm 21lll8; 111;311&1206 Studr: t.lllla-nysis of RCTs lfld obii8Miional studies. 22 ACTs a 34 abeeMiioall sllllles. 1,47011111 182,1)1 pllilntsil RCTs llld allleMitianllllbdnmpecMtfiWD llldniiJI p8!QIIInBOUI CUiamy illaMnion. DNo-EUiilg S1ln1s IDES)- Bale
Outall: J11Crill iArction (MI), lf'ld llrgatYIR8IIMitUIIrilltion ._..: No4ilnlce in mor11ity-bmd betweea DES w. BMS II ACTs. while e.mtionli stlldillllllawlll iQnificlnttr IIMII in DES-11111ed patieull (lard rllio (HA) 0.78, p<0.001 1- No lilnu in Ml incidinCI-bnl in RCTs, 1\tie l:iwer incidences of Ml were fruld in obwvllionlltlldi81 {HA 0.87, DES lu 1 i!Jiificlnllv lawlr Ml rlfl in boll! ACT (HII 0.45, p<0.001] lf'ld obAMtionll stlldiul {HR 0.46, p<0.001lliS re!U:esas of lVR Cllft1IRd tD 114 Aldlougllllllfl is no lifllrlnCI in mollalty 01 M1 incidence u fruld by IICT5. abllmlionll5lulial..-klwunld mnlty llld Ml rilles in P1tia11s wMh DES over BMS.
S18IQ IBMSl.
----
interventional technique aimed at relieving significant coronary stenosis main techniques: balloon angioplasty, stenting less common techniques: rotationaUdirectional/extraction atherectomy
Indications medkally refractory angina NSTEMI/UA with high TIMI risk score within 90 min of presentation primary/rescue PCI for STEMI Balloon Angioplasty and lntracoronary Stenting coronary lesions dilated with balloon inflation major complication is restenosis, felt to be due to elastic recoil and neointimal hyperplasia majority ofpatients receivt: intracoronary stent(s) to prevent restenosis bare metal stent (BMS) drug-eluting stent (DES) coated with antiproliferative drugs (sirolimus, paclitaxel} reduced rate of neointimal hyperplasia and restenosis compared to BMS (5% vs. 20%) complication: late stent thrombosis (5 events in 1000 stents implanted) Adjunctive Therapies ASA and heparin decrease post-procedural complications further reduction in ischemic complications has now been demonstrated using GPIIb/llla inhibitors (abciximab, eptifibatide, tirofiban) in coronary angiography and stenting following stent implantation dual antiplatelet therapy (ASA and dopidogrel) for 1 month with BMS or <: 12 months with DES Procedural Complications mortality and emergency bypass rates < 1% nonfatal Ml: approximately 2-3%
Table 9. Choice of RevasculariZIItion Procedure
PCI
Advantages Less invasive technique Less periprocedura1 marbicity and mortality Shorter periprocedural hospitalization
c..-..:
CABG
Greater ability ID achieve complete revascularimtian Less need for repealed revascularimtion procecklres
Indications
Single or double-vessel disease nabiity ID talara111 surgery
Triple-vessel or left main disease Diabetes rnalitus Plaque morphology unlavoLillble for PCI
Coronary Artery Bypass Graft (CABG) Surgery
,._.._.c._,.... _
r:.-y "'-' ...._ SYIITAlllrill
..... GnllqforiMn
NEIU21109; 381(10);961-972 llldy: randorrimd conlrollad1riiL I'I!UIIIan: 1800 PllilrD with urG8111d tlntvestel or left artery disease and lllltllmilllllv .P.IInt lor bodii'IR:ullnlaus {PCQ RICalnry Miry l!\1llss Glllt{CABG]. m....-n: PCivenus CABG.
the objectivt: of CABG is complete reperfusion ofthe myocardium; goals include relieving symptoms (angina, heart failure) and thus improving quality oflife, and/or prolonging life
inllrt1ion. Cl' rtplll rMSCullrilltion il121110rh poll-illllwmn lllsulll: ..cidlnca of prinuny Dlitllma- bMr in 1he CABO in1ertelllilrrvs. PCI vs. 17.8\ P=0.002. PCI-.aciltldwilll liiJiilicrir hiuhil rms of ..,..t revuc:ului1JtiJ (115'Jovs. 5.1\.P<0.001] and c:atdilc d8llll (3J\ vs. CABG had !iPr IRs of lllnll8(2.2\w.D.&li.P=DJl3). Can.._: .. pa1ilnll wi1h dna-wall II' 11ft CABO ID PCI in prMrmng mljor adwrla canliovatculr llld cerebrowuculu eventswilllin 12 months of irDMnlion.
l:lliSI, . . rn,andill
Indications Class I recommendations CABG significant left main artery disease triple vessel disease, survival benefit greatest in patients with abnormal LV function (EF<50%) two-vt:ssel disease with significant proximal left anterior descending (LAD) disease and with abnormal LV function (EF <50%) or demonstrable ischemia on noninvasivt: testing one or two vessel disease without significant LAD disease who have survived sudden cardiac death or sustained VT CABGorPCI patients with one or two vessel disease without significant LAD disease but with a large area ofviable myocardium and high risk criteria on noninvasive testing recurrent stenosis associated with a large area of viable myocardium or high risk criteria on noninvasive testing Class II recommendations CABGorPCI one vt:ssel disease with significant proximal LAD repeat CABG for multiple saphenous vein graft stenosis, with high risk criteria on noninvasivt: testing, especially when LAD graft at risk. PCI may be appropriate for focal lesions, or multiple lesions in poor surgical candidates one or two vessel disease without significant proximal LAD disease but with a moderate area ofviable ischemia on noninvasivt: testing
Toronto Notes 2011
Operative Issues
isolated proximal disease in large coronary arteries (> 1.0-1.5 mm) is ideal for bypass surgery; small, diffusely diseased coronary arteries are not suitable for bypass surgery arteries with severe stenoses (>50% diameter reduction) are bypassed, except those of small calibre (<1 mm in diameter) Table 1D. Risk Factors far CABG Mortality and Morbidity
Rille. flctol'l for CABG Mortality (dec1811Sing order of significanceI
Urgency of surgBI'f (emergent or urglllltl Reoperation Olderage Poor left wnbicular function (sae below] Famalegender Left main disease Others include catastrophic conditions (cardiogenic shock, wnbicular septal rupture, ongoing CPR], diMy&is-dapandent nmal faiura, and-rlllge COPD, diabetes, cBrebrovascLJar disease, and peripheral vascLJar disease Risk Factan for CABG Pomp Morbidity or Length of S1ay (decraasing order of significanca] ReopBnllion Emergent procedure Preoperative inlrll-aortic balloon pu1111 (IABP} Congestive hat failure CABG + wlw surgery Older age Renal dysfunction CDPD Diabllles Cen!brovascular disease
left ventricular (LV) function is an important determinant of outcome of all heart diseases
patients with severe LV dysfunction usually have poor prognosis, but surgery can sometimes dramatically improve LV function assess viability of non-functioning myocardial segments using delayed thallium myocardial imaging, PET scanning or MRI Tabla 11. Conduits fur CABG
Gn*
Saphenoi!S Veil Gnlts(SVG]
OcdlllicQ'Patency Rite Considenticm At 10years, 50% occilded, Usad when a18rial gl'llfts ara not available or many gl'llfts 25% stenotic, 25% angiDIJ'Ilphically normal are required. such as 1riple or quadruple bypass 91)..95% patency 11115 yuars Most pruferrad option because of IIICcallllllt patency IIJ1li'OVI!d event-he survival (angin11, Mil Decreased late cardiac events No increase in opBnlliva risk
Lift lnllmal
Tha1'1Cic:/M111mary Artery {UTMIMA} (UMAtulAD]
Right lntBmal
Tharacic:/Ma11mary Artery (RITP.'WIMA) Radial Arllry (frail PI)
Pedicled RIMA plllency comparable to UMA free RIMA patency less 85-90% patency at 5 years 81)..90% patency 1115 years
Used in bilateral ITA grafting Patients receiving bilateraiiTAs have less risk of recurrent angina, late myocardial infarction, r.gioplasty Prone to severe vasospasm postoperatively due to muscular
wall
Primarily used as an in situ graft to bypass the RCA Use limited because of the fragile quality of the artery, other tactrical issues, incraasad operative time (laparotomy incision] and incisional discomfort with aSSDCiated il8118 For young111 patients (<60 years of agel Is preferred due to longer term graft patency Dpaf'llliva mortality 2-3 times hijlar than first operation 10% perioperative Ml rate Reoperation undertaken only in symptomatic plllients who have failed medical therapy and in whom angiography has documented progression of the disease Increased risk with redo-sternotumy secondary to adhesions which may result in laceration to aorta, RIJ, IMA and other bypass gl'llfts
Right GIJ!roepiploic
Artery
Complete Artlrial
Revllc:llllriDtion
Rado Bypa Grafting
Off-Pump Coronary Artery Bypass (OPCAB) Surgery

complications of CABG with cardiopulmonary bypass (CPB) stroke and neurocognitive defects (microembolization of gaseous and particulate matter) immunosuppression systemic inflammatory response leading to: myocardial dysfunction renal dysfunction neurological injury respiratory dysfunction coagulopathies
Ischemic Heart Disease (IHD)/Heart Failure
Toronto Notes 2011
Procedure
OPCAB avoids the use of CPB by allowing surgeons to operate on a beating heart stabilization devices (e.g. Genzyme Immobilizer) hold heart in place allowing operation while positioning devices (Medtronic Octopus and Starfish system) allow the surgeon to lift the beating heart to access the lateral and posterior vessels procedure is safe and well tolerated by most patients; however, OPCAB surgery remains technically more demanding
Indications
used in poor candidates for CPB who have: calcified aorta, poor LVEF, severe peripheral vascular disease (PVD), severe COPD, CRF, coagulopathy, transfusion issues (e.g. Jehovah's Witness), good target vessels, anterior/lateral wall revascularization, target revascularization in older, sicker patients absolute contraindications: hemodynamic instability, poor quality target vessels including intramyocardial vessels, diffusely diseased vessels and calcified coronary vessels relative contraindications: cardiomegaly/CHF, critical left main disease, small distal targets, recent or current acute MI, cardiogenic shock, LVEF <35%
Outcomes
OPCAB decreases in-hospital morbidity (decreased incidence of chest infection, inotropic requirement, supraventricular arrhythmia), blood product transfusion, ICU stay, length of hospitalization, and decreased CK-MB and troponin I level no significant difference in terms of survival at 2 years, frequency of cardiac events (MI, PCI, CHF, recurrent angina, redo CABG) or medication usage compared to on-pump CABG
Heart Failure
Congestive Heart Failure (CHF)
Definitions
',, ..
Dlchlllllmles Ill Hurt FaiU8
FOIWllrd vs. Backw1rd
Lift-sided vs. RictTt-sidad Systolic dysfunction vs. Dilstolic

dysfunction Low autput vs. High output
heart failure: a complex clinical syndrome, resulting from almost any cardiac disorder that impairs the ability of the ventricle to fill with or eject blood forward heart failure: heart unable to maintain adequate cardiac output to meet demand and/or able to do so only by elevating filling pressure backward heart failure: heart unable to accommodate venous return resulting in elevated filling pressures and vascular congestion (systemic or pulmonary) heart failure can involve left side of heart (left heart failure), right side (right heart failure) or both (biventricular failure) (see Table 12) heart failure can also have components of ineffective ventricular filling (diastolic dysfunction) and/or contraction (systolic dysfunction) most cases associated with poor cardiac output (low-output heart failure); however, some not due to intrinsic cardiac disease but instead due to increased demand (high-output heart failure)
Pathophysiology
primary insults (myocyte loss, overload) -+ pump dysfunction, which leads to: remodeling (dilatation, hypertrophy) neurohumoral activation -+ necrosis and apoptosis both pathways result in further damage (re-starting the cycle), edema, tachycardia, vasoconstriction, congestion compensatory response to myocardial stress (perpetuate disease process) increased end-systolic ventricular pressure (pressure overload) e.g. HTN, aortic stenosis -+ hypertrophy increased end-diastolic ventricular volume (volume overload) e.g. aortic regurgitation -+ cardiac dilatation systemic response to ineffective circulating volume activation of sympathetic nervous and renin-angiotensin-aldosterone systems results in: salt and water retention with intravascular expansion increased heart rate and myocardial contractility increased afterload
',, ..
IIH Ejecdcm FrudDn ta Gnlde LV Dylfnction Grade I (EF (NormalI Grade II (EF = 40-59%1 Grade Ill (EF = 21-39%1 Grade IV (EF
Systolic Dysfunction {impaired ventricular ejection)

impaired myocardial contractile function -+ decreased ejection fraction (LVEF) and stroke volume (SV)-+ decreased cardiac output (CO) findings: apex beat displaced, S3, increased heart size on CXR, decreased LVEF, LV dilatation causes: ischemic (e.g. extensive CAD, previous MI) non-ischemic hypertension diabetes mellitus alcohol (and other toxins) myocarditis dilated cardiomyopathy
Toronto Notes 2011
Heart Failure

...._ \ I
Diastolic Dysfunction (impaired ventricular filling) at least 1/3 of all HF patients have nonnal systolic function (i.e. nonnal ejection fraction);
prevalence higher in older patients increased LV filling pressures produce venous congestion upstream (ie. pulmonary and systemic venous congestion) findings: H1N, apex beat sustained, S4, nonnal-sized heart on CXR. LVH on ECG/echo, normal
9,}-----------------.
NIW Yark Hurt ARecidon INYHAI funeti01111l Cl-ificrion of H.-rt

failllnl
LVEF
causes of decreased compliance: transient: ischemia (relaxation of myocardium is active and requires ATP) permanent severe hypertrophy (HTN, AS, HCM) restrictive cardiomyopathy (RCM)
. a- 1: ordillllry physical activity does not ceusa symptoms of HF a- II: comfortBble lit nJSt, ordinlll'(
a- ID: marked limitation of
physicniiiC!ivity rnults in rymptoms
a-
MI
High-Output Heart Failure caused by demand for increased cardiac output
often exacerbates existing heart failure or decompensates a patient with other cardiac pathology differential diagnosis: anemia, thiamine deficiency (beriberi), hyperthyroidism, A-V fistula or L-R shunting, Paget's disease, renal disease, hepatic disease
ordinary activity: less then ordinary physicniiiC!ivity results in rymptoms N: inability to carry out any physicniiiC!ivity without discomfort; rymptoms may be pmsnt at rust
.....
'.,.-----------------, ,
What ... thl Fi11 Most CDIIIIDIRI C.UielofCHF?
1. CoroniiV lltery disease {61HO'Yo)

2. HTN 3. Idiopathic {often in the fonn of dilated
cardiomyopathy) 4. Valvul.-{e.g_ AI., AR and MRI 5. Alcohol {may CMJSB dilllllld cardiomyopathy)
Etiologies of Primary Insults consider predisposing, precipitating and perpetuating factors most common causes see sidebar less common causes of CHF toxic e.g. anthracyclines, radiation, uremia, catecholamines infectious e.g. Chagas' disease (common cause in South America), Coxsackie virus, HIV endocrine e.g. hyperthyroidism, DM, acromegaly infiltrative e.g. sarcoidosis, amyloidosis, hemochromatosis genetic e.g. HCM, Friedreich's Ataxia, muscular dystrophy congenital heart disease metabolic e.g. thiamine deficiency, selenium deficiency peripartum
Preclpillntll of llllut hilur1
HEART FAILED
Hypertension (common) fndocerditir,/snvironmsnt {e.g_ hset Anemia humlltic h..n diull11 and othlr valwlar disease Thyrotoxicosis Failure to take meds {very common) Antlythmia {common) lnfectionlischemi.tlnfllrction (common) Lung problems {PE, pneumonia. COPD) Endocrine (pheochromocytomlr, hyperaldosteronism) Di11111ry ildiscrwtions {common)
WliVel
Precipitants of Symptomatic Exacerbations

consider natural progression of disease vs. new precipitant always search for reversible cause see side bar ("HEART FAILED") differential can also be organized as follows: new cardiac insult/disease: Ml, arrhythmia, valvular disease new demand on CV system: hypertension, anemia, thyrotoxicosis, infection, etc. failure to take medications as prescribed
Tabla 12. Signs and Symptoms of Left vs. Right Heart Failure
Lift Failure
Law canlilc output
Right Failure
(farwanll
Fatigue Syncope
Sy&temic hypoten&ian
Right heart failure can mimic mast Df the symptoms Df forward left heart failure if decreased RV output leads to LV underfilling
Coal extremities Slaw capiiiiiY refill Peripheral cyanosis Pulsus aiiBmans Mitral regurgitatian 83
Dyspnea. orthopnea. PND
....
Tricuspid regurgitation
'9J-----------------. ,
S3 (right-sidedl Peripheral edema Bevated .NP with AJR and Kussmaul's sign Hepalllmegmy Publllile liwr
Mnsurlng NT11f8 BNP BNP is 158C1'818d by ventricles due to LV llnlll:h end Wlll1llnlion.
Cardiomyocytn semll BNP priCIIISOI
Cough Crackles
that is claaved iniD proBNP. After

secretion into ventricles. proBNP is cl811'18d into the IIC!ive C-111nninal portion end the inar:tive NT-proBNP portion. Nf.tlroBNP levlls (pa/lal.)
Ag1
Investigations
identify and assess precipitating factors and treatable causes of CHF blood work: CBC, electrolytes (including calcium and magnesium), BUN, creatinine, fasting blood glucose, HbAl C. lipid profile, liver function tests, serum thyroid-stimulating hormone, ferritin, BNP. uric add (associated with prognosis ofHF in Seattle HF Score) ECG: look for chamber enlargement, arrhythmia, ischemia/infarction CXR: cardiomegaly, pleural effusion, redistribution, Kerley B-lines, bronchiolar-alveolar cuffing echocardiography: LVEF, cardiac dimensions, wall motion abnonnalities, valvular disease, pericardia! effusion radionuclide angiography (MUGA): LVEF myocardial perfusion scintigraphy (thallium or sestamibi SPECT)
<50 50-75 >75
HF wry liklly >450 >900 >1800
Umillllions - Age, body habitus, renal function. pulmonary 1111bolism
Heart Failure
Toronto Notes 2011
Acute Treatment of Pulmonary Edema

It'
F...,_ -' Hrl hilun1 gn CXR

HERB-8
Heart enlarvament (cardiothcncic ndio
>0.50) Pleural Effusion Ra-diSlribution (alveolar ed.ma)

Kerley &-tine Bronchiollll"llivllolar culling
treat acute precipitating factors (e.g. ischemia. arrhythmias) L(furosemide) 40-500 mg IV M -morphine 2-4 mg IV- decreases anxiety and preload (venodilation) N- nitroglycerin- topica1/IV/SL 0- oxygen P- positive airway pressure (CPAP/BiPAP)- decreases preload and need for ventilation P - position - sit patient up with legs hanging down unless patient is hypotensive
in ICU setting or failure ofLMNOP, other interventions may be necessary nitroprusside (IV) hydralazine (PO) sympathomimetics dopamine - low dose: selective renal vasodilation (high potency D 1 agonist) - medium dose: inotropic support (medium potency agonist) - high dose: increases SVR (low potency agonist), which is undesirable dobutamine - selective inotrope agonist) and arterial vasodilator antagonist) phosphodiesterase inhibitors (milrinone) - inotropic effect and vascular smooth muscle relaxation (decreased SVR), similar to dobutamine - adverse effect on survival when used as long-term oral agent consider PA catheter to monitor pulmonary capillary wedge pressure (PCWP) if patient is unstable or a cardiac etiology is uncertain (PCWP >18 indicates likely cardiac etiology) mechanical ventilation as needed rarely used, but potentially life-saving measures: intra-aortic balloon pump (IABP) left or right ventricular assist device (LVAD/RVAD) cardiac transplant
Long Term Management

Conservative Meuura 1. Symptomatic measures: oxygen in hospital, bedrest, elevation of head of bed 2. Lifestyle measures (grade B evidence): diet, exercise, DM control, smoking cessation, decrease alcohol consumption, patient education, sodium and fluid restriction 3. Multidisciplinary heart failure clinics (grade B evidence): for management of individuals at higher risk, or with recent hospitalization Pharmacological Therapy I. Vuodilators a. ACEis: standard of care - slow progression of LV dysfunction and improve survival all symptomatic patients functional class II-IV (grade A) all asymptomatic patients with LVEF <40% (grade A) post-MI target dose as used in mortality trials, or maximum tolerated dose b. angiotensin II receptor blockers (ARBs) second line to ACEI if not tolerated (grade B), or as adjunct to ACEI if beta-blockers not tolerated (grade A) c. hydralazine and nitrates (Ve-HeFT-1 trial) second line to ACEI, decrease in mortality not as great as with ACEI may consider in acute renal failure until creatinine stabilizes 2. Beta-blocker&: slow progression and improve survival class I-III with LVEF <40% (grade A) stable class IV patients (grade A) note: should be uaed cautiously, titrate &lowly because may initJally woraen CHF 3. Diuretic:&: symptom control, management of fluid overload furosemide (40-500 mg OD) for potent diuresis metolazone may be used with furosemide to increase diuresis furosemide, m.etalozone, and thiazi.des oppose the hyperkalemia induced by beta-blockers, ACEis, ARBs, and aldosterone antagonists
4. Aldosterone antagonist&: mortality benefit in severe CHF spironolactone for class Illb and IV CHF already on ACEI and loop diuretic (grade A) eplerenone may be considered if intolerable endocrine side effects note: potential for life threatening hyperkalemia monitor K after initiation and avoid if Cr >220 filllOl/L or K >5.2 mmol/L
..111M 1997; 277:1712-19 1ba beslliDilgs far dlllding incrnsed 111111

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hell!
....
, ...----------------.
C llllic Tr..ment-' CHF ... ACE inhibi1Dr5* Beta blockers* Aldonlronuntagonim*

(if IIYirl CHF) Diurvtic lnotropa
Antiarrythmic Anticoagulant
* = Mortality Benflfit
....
,,
Mllllcllllons Contralndlcmd In CHF NSAJDS -may increese BP Clanl/ID antilllhythmics

Metformin - Cll in severe HF Thiazolidinedionas- increase ed.ma cGMP phosphodiestel'lllse (e.g. sildllllllfil) with basalina low BP
Toronto Notes 2011
Heart Failure/Cardiac Transplantation
5. lnotropes: digoxin improves symptoms and decreases hospitalizations, no effect on mortality indications: patient in sinus rhytlun and symptomatic on ACEI (grade A), or CHF and atrial fibrillation (grade B) patients on digitalis glycosides may worsen if these are withdrawn
6. Anti-arrhythmic drugs: for use in CHF with arrhythmia can use amiodarone, beta-blocker, or digoxin (grade B)
7. Anticoagulants: warfarin for prevention of thromboembolic events prior thromboembolic event or atrial fibrillation (grade B), presence of LV thrombus on echo possible benefit in other patients with LVEF <30% (controversial)
8. CCBs (equivocal effect on survival): not currently recommended
Procedural Interventions resynchronization therapy: symptomatic improvement with biventricular pacemaker consider ifQRS >130 ms, LVEF <35%, and severe symptoms despite optimal therapy (grade B) greatest benefit likely with marked LV enlargement. MR, QRS >150 ms, high diuretic requirement lCD: mortality benefit in 1c and 2c prevention of sudden cardiac death prior MI, optimal medical therapy, LVEF <30%, clinically stable (grade B) prior MI, NSVT, LVEF 30-40%, EPS inducible VT (grade B) LVAD/RVAD (see Ventricular Assist Devices, C36) cardiac transplantation (see Cardiac Transplantation, C35) valve repair if patient is surgical candidate and has significant valve disease contributing to CHF (see Valvular Heart Disease, C40)
Sleep-Disordered Breathing
45-55% of patients with CHF have sleep disturbances, including Cheyne-Stokes breathing and sleep apnea (central or obstructive) associated with a worse prognosis and greater LV dysfunction nasal continuous positive airway pressure (CPAP) is effective in treating Cheyne-Stokes respiration/sleep apnea with improvement in cardiac function and symptoms
Cardiac Transplantation
for end-stage heart disease; due to ischemic cardiomyopathy (60%), idiopathic cardiomyopathy (20%), and minority due to valvular or congenital problems worldwide 1-year survival is 79%, 5-year survival about 60%, annual mortality rate of 4% donor hearts are considered from patients up to age 50-55 matching is according to blood type, body size and weight (should be within 25%), and HLA tissue matching {if time allows)
Indications for Surgery severe cardiac disability despite maximal medical therapy (recurrent hospitalizations for CHF, NYHA ill or IV; peak metabolic oxygen consumption <14 ml/kglmin in absence ofbeta-blocker) symptomatic cardiac ischemia refractory to conventional treatment (unstable angina not amenable to CABG or angioplasty with LVEF <30%; recurrent, symptomatic ventricular arrhythmias) exclusion of all surgical alternatives to cardiac transplantation (revascularization for significant reversible ischemia, valve replacement for critical aortic valve disease, valve replacement or repair for severe MR) Prerequisites emotionally stable with social support medically compliant and motivated contraindications: incurable malignancy, major systemic illness, irreversible major organ disease (e.g. renal, hepatic), active systemic infection (e.g. Hep C, HIV), obesity, irreversible pulmonary hypertension (pulmonary vascular resistance [PVR] >6 Wood units), severe COPD (FEV1 <1 L), or active drug addiction or alcoholism typically age <70 years Complications rejection common, however less than 5% have serious hemodynamic compromise gold standard to detect rejection: endomyocardial biopsy no noninvasive tests to detect rejection risk of acute rejection is greatest during the first 3 months after transplant
Cardiac TranaplantationJMyocardial Diseue
Toronto Notes 2011
infection leading cause of morbidity and mortality after cardiac transplantation risk peaks early during the first few months after transplantation and then declines to a low persistent rate allograft coronary artery disease approximately 50% develop graft CAD within 5 years oftransplantation the most common cause oflate death following transplantation
malignancy
develop in 15% of cardiac transplant recipients second most common cause of late death following transplantation cutaneous neoplams most common, followed by non-Hodgkin's lymphoma and lung cancer immunosuppressive medication side effects (prednisone. cyclosporine. tacrolim.us, sirolim.us)
Prognosis the Heart Failure Survival Score (HFSS) uses 7 prognostic variables - ischemic cardiomyopathy; resting heart rate. LVEF, mean BP, QRS >120ms, serum Na, peak V0 2 -to stratify patients into low, medium, and high risk categories; one-year survival rates without transplant for these three strata were 88, 60, and 35%, respectively
Ventricular Assist Devices (VADs)

REMATCH Trill 1>1111 Jlicnc 1999; 67:723-730 lncallld III1MI al 23'1. 111. LVAD VI. 1111di:llll111111Q111Ef11 ol belllfaiknlf!Br 2
8'li.
HelllmlllVAD ha 1 biqic: lll.lla,1llillbv
l9rlr rilk al irQction.
does not require 10110"tmm
works to unload the ventricle while maintaining its output; also results in decreased myocardial oxygen consumption, permitting recovery of the myocardium that is not irreversibly injured can support the left (LVAD), right (RVAD) or both ventricles (BiVAD) indications bridge to transplantation postoperative mechanical support when unable to separate from cardiopulmonary bypass despite inotropic and Intra-Aortic Balloon Pump (IABP) support IABP is a catheter based device inserted into the aorta via the femoral artery that decreases myocardial 0 2 demand and increases blood flow to coronary arteries postoperative cardiogenic shock
Myocardial Disease
Definition of Cardiomyopathy (CMP) intrinsic or primary myocardial disease not 2 to congenital, hypertensive, coronary, valvular, or pericardia! disease functional classification: dilated, hypertrophic or restrictive LV dysfunction 2 to MI often termed "ischemic cardiomyopathy", but is not a true cardiomyopathy (Le. primary myocardial disorder) since the primary pathology is CAD
Myocarditis
Definition inflammatory process involving the myocardium ranging from acute to chronic; an important cause of dilated cardiomyopathy Etiology idiopathic infectious viral (most common): coxsackie B, echovirus, poliovirus, HIY, mumps bacterial: S. aureus, C. perfringens, C. diphtheriae, Mycoplasma, Rickettsia fungi spirochetal (Lyme disease - Borrelia burgdorftn) Chagas disease (Trypanosoma cruzi), toxoplasmosis toxic: catecholamines, chemotherapy; cocaine hypersensitivity, eosinophilic: drugs (antibiotics, diuretics, lithium, clozapine), insect/snake bites systemic diseases: collagen vascular diseases (SLE, RA, others), sarcoidosis, autoimmune other: giant cell myocarditis, acute rheumatic fever Signs and Symptoms constitutional symptoms acuteCHF chest pain - due to pericarditis or cardiac ischemia arrhythmias systemic or pulmonary emboli sudden death
Toronto Notes 2011
Myocardial Disease
Investigations ECG: non-specific ST-T changes conduction defects bloodwork increased CK, troponin, LDH, and AST with acute myocardial necrosis increased WBC, ESR, ANA, rheumatoid factor, complement levels blood culture, viral titres and cold agglutinins for Mycoplasma CXR: enlarged cardiac silhouette echo: dilated, hypokinetic chambers, segmental wall motion abnormalities myocardial biopsy Management supportive care restrict physical activity treatCHF treat arrhythmias anticoagulation treat underlying cause if possible Prognosis usually self-limited and often unrecognized, many recover sudden death in young adults may progress to dilated cardiomyopathy few may have chronic myocarditis
Table 13. Summary Table for CH F and Myocardial Disease
SYSTOLIC HEART FAIWRE
Dilalad
Secondary CauHs
DIASTOLIC HEART FAIWRE

Hypallnlphic
Rasbictive
SacandiiJ Causes
Cardiomropallly Idiopathic, infectious

(e.g. myocarditis),
Cardiomyopathy
Caniomyopallrr
Amyloidosis, sarcoidosis,
alcohol, fllmiial, collagen vascular

disease, etc.
Coronary artery Genetic disorder affecting disease, Ml, diabetes, cardiac sarcomeres vnlar (e.g. AR, MR) (most common cause of sudden cardiac death il
young athletes)
Hypertension. diabetes,
valvular {e.g. AS), post-MI, transiently
sderoderrna. h111110clromatosis, Fab!J's. Pompe's
Disease, Loefller's, etc.
by ischemia, etc.
Dilated Cardiomyopathy (DCM)

Definition unexplained dilation and impaired systolic function of one or both ventricles
Etiology idiopathic (presumed viral or genetic) -50% ofDCM alcohol familial uncontrolled tachycardia (e.g. persistent atrial fibrillation) collagen vascular disease: SLE, PAN, dermatomyositis, progressive systemic sclerosis infectious: viral (coxsackie B, HIV), Chagas disease, Lyme disease, Rickettsial diseases, acute rheumatic fever, toxoplasmosis neuromuscular disease: Duchenne muscular dystrophy, myotonic dystrophy, Friedreich's ataxia metabolic: uremia, nutritional deficiency (thiamine:, selenium, carnitine) endocrine: hyper/hypothyroidism, DM, pheochromocytoma peripartum toxic: cocaine, heroin, organic solvents drugs: chemotherapies (doxorubicin, cyclophosphamide), anti-retrovirals, chloroquine, clozapine, TCA radiation induced Signs and Symptoms may present as CHF systemic or pulmonary emboli arrhythmias sudden death {major cause of mortality due to fatal arrhythmia)
....
,,
M-iof Risks Factars hr DCM Alcohol, cocaine, family history and obesity.
Myocardial Diseue
Toronto Notes 2011
.....
High 8NP High Cr High LFTa low Bicarb lowNa
Allnonnal Lalli in DCM
Investigations bloodwork: CBC, electrolytes, Cr, bicarbonate, BNP, CK, troponin, LFfs, TSH, TIBC ECG: variable ST-T wave abnormalities, poor R wave progression, conduction defects (e.g. BBB), arrhythmias (non-sustained VT) CXR: global cardiomegaly (globular heart), signs of CHF, pleural effusion echocardiography: chamber enlargement. global hypokinesis, depressed LVEF, MR and TR, mural thrombi endomyocardial biopsy: not routine, used to rule out a treatable cause angiography: in selected patients to exclude ischemic heart disease Management treat underlying disease: e.g. abstinence from EtOH treat CHF: see Heart Failure. C32 thromboembolism prophylaxis: anticoagulation with warfarin indicated for: AF, history ofthromboembolism or documented thrombus LVEF <30% (controversial) treat symptomatic or serious arrhythmias immunize against influenza and S. pneumoniae consider surgical options (e.g. LVAD, transplant. volume reduction surgery) in appropriate candidates with severe, refractory disease consider lCD among patients with a LVEF <30% Prognosis depends on etiology better with reversible underlying cause, worst with infiltrative diseases, HIY, drug-induced cause of death usually CHF (due to pump failure) or sudden death 2 to ventricular arrhythmias systemic emboli are significant source of morbidity 20% mortality in 1st year, 10% per year after
Hypertrophic Cardiomyopathy (HCM)
---------------------
Definition defined as unexplained ventricular hypertrophy (not due to systemic liTN or AS) most causes involve asymmetric pattern of hypertrophy (septal hypertrophy most common) Etiology and Pathophysiology histopathologic features include myocyte disarray, myocyte hypertrophy, and interstitial fibrosis cause is felt to be a genetic defect involving one of the cardiac sarcomeric proteins (>200 mutations associated with autosomal dominant inheritance, incomplete penetrance) prevalence of 1/500-1/1000 in general population presents as early as 20-40 yrs old Hemodynamic Classification hypertrophic obstructive cardiomyopathy (HOCM): dynamic LV outflow tract (LVOT) obstruction, either at rest or with provocation non-obstructive hypertrophic cardiomyopathy: no LVOT obstruction many patients have diastolic dysfunction (impaired ventricular filling secondary to LV hypertrophy which decreases compliance) Signs and Symptoms (of HCM) clinical manifestations: asymptomatic (conunon, therefore screening is important), SOBOE, angina, presyncope/syncope (due to LV outflow obstruction or arrhythmia), CHF, arrhythmias, sudden cardiac death (SCD) pulses: rapid upstroke, bifid carotid pulse (in HOCM) precordial palpation: PMI localized, sustained, double impulse, 'triple ripple' (triple apical impulse in HOCM), LV lift precordial auscultation: normal or paradoxically split S2, S4, harsh systolic diamond-shaped murmur at LLSB or apex, enhanced by squat to standing or Valsalva (murmur secondary to LVOT obstruction as compared to aortic stenosis); often with pansystolic murmur due to mitral regurgitation Investigations ECG: LVH, high voltages across precordium, prominent Q waves (lead I, aVL, V5, V6), tall R wave in Vl, P wave abnormalities echo: asymmetric septal hypertrophy (less commonly apical), systolic anterior motion of mitral valveandMR cardiac catheterization (usually performed only when patient being considered for invasive therapy}
Toronto Notes 2011

Management
Myocardial Disease
avoid factors which increase obstruction, including volume depletion and strenuous exertion treatment ofHOCM (with LVOT obstruction) medical agents: beta-blockers, disopyramide, verapamil (only in patients without resting or provocable obstruction) avoid nitrates, diuretics and ACEI as they decrease outflow tract diameter and worsen symptoms patients with drug-refractory symptoms surgical myectomy septal ethanol ablation dual chamber pacing treatment of ventricular arrhythmias: amiodarone or ICD first-degree relatives of patients with HCM should be screened annually during adolescence (physical, ECG, 2D echo), then serially every 5 years
Prognosis
potential complications: AF, VT, CHF, sudden death (most common cause ofSCD in young athletes) major risk factors for sudden death (consider lCD placement) history of survived cardiac arrest/sustained VT family history of multiple premature sudden deaths other factors associated with increased risk of sudden cardiac death syncope non-sustained VT on ambulatory monitoring mrn) marked ventricular hypertrophy (maximum wall thickness abnormal BP in response to exercise (in young patients with HCM)
Restrictive Cardiomyopathy (RCM)

Definition
-------------------
impaired ventricular filling with usually intact systolic function in a non-dilated, non-hypertrophied ventricle 2 to myocardial abnormality (stiffening, fibrosis and/or decreased compliance) usually with intact systolic function initially
Etiology
infiltrative: amyloidosis, sarcoidosis non-infiltrative: scleroderma, idiopathic myocardial fibrosis storage diseases: hemochromatosis, Fabry's disease, Gaucher's disease, glycogen storage diseases endomyocardial endomyocardial fibrosis, Loeffler's endocarditis or eosinophilic endomyocardial disease radiation heart disease carcinoid syndrome (may have associated TV or PV dysfunction) CHF (usually with preserved LV systolic function), arrhythmias elevated JVP with prominent x and y descents, Kussmaul's sign S3, S4, MR, TR thromboembolic events ECG: low voltage, non-specific, diffuse ST-T wave changes non-ischemic Q waves CXR: mild cardiac enlargement echo: LAE, RAE; specific Doppler finding with no significant respiratory variation cardiac catheterization: increased end-diastolic ventricular pressures endomyocardial biopsy: to determine etiology (especially for infiltrative RCM) exclude constrictive pericarditis treat underlying disease: control HR, anticoagulate if atrial fibrillation supportive care and treatment for CHF, arrhythmias heart transplant: might he considered for CHF refractory to medical therapy
Clinical Manifestations
Investigations
Management
Prognosis
depends on etiology
Valvular Heart Disease
Toronto Notes 2011

Infective Endocarditis (IE)
see Infectious Diseases. ID14 AHA 2007 guidelines recommend IE prophylaxis only for patients with prosthetic valve material, past history of IE, certain types of congenital heart disease or cardiact transplant recipients who develop valvulopathy only for the following procedures dental respiratory tract procedures on infected skin/skin stru.ctures/MSK structures + not GI/GU proudura specifically
Rheumatic Faver
see Pediatrics, P57
Prognosis
acute complications: myocarditis (DCM/CHF), conduction abnormalities (sinus tachycardia, AF), valvulitis (acute MR), acute pericarditis (not constrictive pericarditis) chronic complications: rheumatic valvular heart disease - fibrous thickening, adhesion, calcification ofvalve leaflets resulting in stenosis/regurgitation, increased risk of IE thromboembolism onset of symptoms usually after 10-20 year latency from acute carditis of rheumatic fever mitral valve most commonly a1fected
Choice of Valve Prosthesis

Etdlells E. Glnns V, Shldowilz S. Bel C. SiJ S. JS.SIIIf8mu.lll8811; 131101:6K-'104. Dljiii1NIIII Mldicinl, TGRHlbl Haspilll, ON.
........ c-a.
........ C..i:ll ,... . bllflrlllllctq
.....
Tabla 14. Mechanical Valva vs. Bioprosthatic Valva

Machanical Vllva
o o o
BiDprostllllic Valva
o o o
Good durability Less prefi!IT!d in small acrtic root (stl!lloticl Increased risk of thromboembolism (1 anticoagulation with coumadin
Limited long-term durability (milral<aorticl Good flow in small acrtic root sizes Decreased risk of thromboembolism: needed for aortic valves anticoagulation not
Bhled CIOIS taetionaiiiUdy. Mil: 1 PlllieniJ Z4 uurrmulmy canioloa
clnic.l'llilnll wmmminld fllr: I) nunu DVII the right cliMcle 2) nunu loudest llsecurat rigli imollaiiJliC13) llducad i1lllllityof S2 4) !educed volume 11111e Cldlldse 51 deiiYI!d
. . . . l'ldilnll Wllllllllllinld by blindld iwalligllm, and the Cliliclllllllmi'illiDII findings Will compnl fD finlilgs on !l6slquant
Clllllidi4JSinlll.
Target INR aortic valves: 2.1h!.D mitral valves: 2.5-3.5

Increased risk of hemonhage: 1-2"1Vyear
Some reconmendation for limited anticoagulation far mitral vaM!s
Decreased risk of hemollhage
lllnlllil-dlfinld 'IIM-<Ilcrnlora pelk inbmsty grldild II >25 ITIT1Hq. Rllulll: Abearafla nunu DVII the rigli cBvicle 1\ild out aortic stlllotis wflile affla 4 111Cii1Bd in lllltic s11nosis Cam:lllianl: lled!idlllehnitJBI C8111CCU!It81y rula in and rula out rnodarlll _, - lllnosil.
Modellle" - -
Toronto Notes 2011
Summary of Valvular Disease

Table 15. Valvular Heart Disease
AS
click
AR
Etiology Supravalvular: aortic root disease (Marian's, atherosclerosis and dissecting aneurysm, connective tissue disease) s, s, s, Valwlar: congenital (bicuspid AV. Anas Nader 2009 large VSD), IE Acute Onset: IE, aortic dissection, trauma, failed prosthetic valve Pathophysiology Volume overload -+ LV dilatation -+ increased SV, high sBP and low dBP -+ increased wall tension -+ pressure overload -+ LVH (low dBP -+ decreased coronary perfusion) Symptoms Usually only becomes symptomatic late in disease when LV failure develops Dyspnea, orthopnea, PND, syncope, angina Physical Exam Waterhammer pulse, bisleriens pulse, femoral-brachial sBP > 20 (Hill's test wide pulse pressure), hyperdynamic apex, displaced PM I, heaving apex Auscultation: early decrescendo diastolic murmur at LLSB (cusp) or RLSB (aortic root), best heard sitting, leaning forward, on full expiration, soft S1, absent S2, S3 (late) Investigations ECG: LVH, LAE CXR: LVH, LAE, aortic root dilatation Echo/TTE: quantffy AR, leaflet or aortic root anomalies Cath: ff >40 yrs and surgical candidate-to assess for ischemic heart disease Exercise testing: hypatension with exercise Treatment Asymptomatic: serial Echos, afterload reduction (e.g. ACEis, niledipine, hydralazine) Symptomatic: avoid exertion, treat CHF Surgery if: NYHA class III-IV CHF. LVEF <50% with/without symptoms, increasing LV size Surgical Options Valve replacement: most patients Valve repair: very limited role Aortic root replacement (Bentall procedure): - When ascending aortic aneurysm present, valved conduit used
Etiology Congenital (bicuspid, unicuspid valve), calcification (wear and tear), rheumatic disease Aortic valve area: N=34 cm2 s, s, s, Mild AS 1.5 to 3 cm2 Anas Nader 2009 Moderate AS 1.0 to 1.5 cm 2 Severe AS < 1.0 cm2 Critical AS <0.5 cm 2 Pathophysiology Outflow obstruction -+ increased EDP -+ concentric LVH -+ LV failure -+ CHF. subendocardial ischemia Symptoms Exertional angina, syncope, dyspnea, PND, orthopnea, peripheral edema Physical Exam Narrow pulse pressure, brachial-radial delay, pulsus parvus et tardus, sustained PMI Auscultation: crescendo-decrescendo SEM radiating to Rclavicle and caratid, musical quality at apex (Gallavardin phenomenon), S4, soft S2 w/paradoxical splitting, S3 (late) Investigations ECG: LVH and strain, LBBB, LAE, AF CXR: post-stenatic aortic root dilatation, calcified valve, LVH, LAE, CHF ECHO: reduced valve area, pressure gradient, LVH, reduced LV function Treatment Asymptomatic: serial Echos, avoid exertion Symptomatic: avoid nitrates/arterial dilators and ACEis in severe AS Surgery ff: symptomatic or LV dysfunction Surgical Options Valve replacement: aortic rheumatic valve disease and trileaflet valve -Pregnancy - Balloon valwloplasty (in very young)
MS
Etiology Rheumatic disease most common cause; congenital (rare) Severe MS is MVA < 1.2 cm2
MR
Etiology Mitral valve prolapse Congenital cleft leaflets, LV dilatatiorv'aneurysm (CHF. DCM, s, s, s, s, s, OS s, myocarditis), IE abscess, Marian's Anas Nader 2009 Pathophysiology Anas Nader 2011 syndrome, HOCM, acute Ml, myxoma, MV annulus calcffication, MS -+ fixed CO and LAE -+ increased LA pressure -+ pulmonary chordae/papillary muscle trauma/ischemia/rupture, rheumatic disease vascular resistance and CHF; worse with AF (no atrial kick), tachycardia Pathophysiology (decreased atrial emptying time) and pregnancy (increased preload) Reduced CO -+ increased LV and LA pressure -+ LV and LA dilatation -+ Symptoms CHF and pulmonary HTN SOBOE, orthopnea, fatigue, palpitations, peripheral edema, malar flush, Symptoms pinched and blue facies (severe MS) Dyspnea, PND, orthopnea, palpitations, peripheral edema Physical Exam Physical Exam AF. no a wave on JVP. left parastemallift, palpable diastolic thrill at apex Displaced, hyperdynamic apex, left parastemallift, apical thrill Auscultation: mid-diastolic rumble at apex, best with bell in LLD position following Auscultation: holosystolic murmur at apex, radiating to axilla mid-diastolic rumble, loud exertion, loud S1, OS following loud P2 (heard best during expiration), long murmur S2 (if pulmonary HTN), S3 and short A2 -OS interval correlate with worse MS Investigations Investigations ECG: LAE, left atrial delay (bifid Pwaves), LVH ECG: NSR/AF. LAE (P mitrale), RVH, RAD CXR: LVH, LAE, pulmonary venous HTN CXR: LAE, CHF, MV calcification Echo: severity of MR, LV function, leaflets Echo/TTE: restricted opening of MV Swan-Ganz: prominent LA v wave Cath: concurrent CAD if >40 yrs (male) or >50 yrs (female) Treatment Treatment Asymptomatic: serial Echos, Avoid exertion, fever (increased LA pressure), treat AF and CHF, increase diastolic Symptomatic: decrease preload (diuretics), decrease afterload (ACEis) for severe MR and filling time (beta-blockers, digitalis) Surgery if: NYHA class III-IV CHF and failure of medical therapy (usually MVA < 1.2 cm2 poor surgical candidate; stabilize acute MR with vasodilators before surgery ) Surgery if: acute MR with CHF. papillary muscle rupture, NYHA class III-IV CHF. AF, LVEF Invasive Options Percutaneous balloon valwloplasty: young rheumatic pts and good leaflet morphology, <60%, increasing LV size, earlier surgery ffvalve repairable Surgical Options asymptom pts with mod-sev MS, new-onset AF. pulmon HTN Valve repair: > 75% of pts with MR and myxomatous MV disease (MVP) Contraindication: Left atrial thrombus, moderate MR - annuloplasty rings, leaflet repair, chordae transfers/shorterv'replacement Open Mitral Commissurotomy: If mild calcif + leaflet/chordal thickening Valve replacement: failure of repair, heavily calcffied annulus - restenosis in 50% pts in 8 yrs Advantage of repair: low rate of endocarditis, no anticoagulation, less chance of reValve replacement: mod-sev calcif and sev scarred leaflets operation

Table 15. Valvular Heart Disease (continued)
Toronto Notes 2011
TS
Etiology Rheumatic disease, congenital, carcinoid, fibroelastosis; usually accompanied by MS Pathophysiology s, S, OS s, Increased RA pressure -+ right heart Anas Nader 2011 failure -+ decreased CO and fixed on exertion Symptoms Peripheral edema, fatigue, palpitations Physical Exam Prominent a waves in JVP, +ve abdominojugular reflex, Kussmaul's sign, diastolic rumble 4th left intercostal space Investigations ECG: RAE CXR: dilatation of RA without pulmonary artery enlargement Echo: diagnostic Treatment Preload reduction (diuretics) Surgery if: usually only ff other surgery needed (e.g. MVR) Surgical Options Valve Replacement: -If severely diseased valve - Bioprosthesis preferred
TR
Etiology RV dilatation, IE (IV drug use), rheumatic disease, congenital (Ebstein anomaly), carcinoid s, s, s, Pathophysiology Anas Nader 2009 RV dilatation -+ TR -+ further RV dilatation -+ right heart failure Symptoms Peripheral edema, fatigue, palpitations Physical Exam cv waves in JVP. +ve abdominojugular reflux, Kussmaul's sign, holosystolic murmur at LLSB accentuated by inspiration, left parastemallift Investigations ECG: RAE, RVH, AF CXR: RAE, RV enlargement Echo: diagnostic Treatment Preload reduction (diuretics) Surgery if: usually only ff other surgery needed (e.g. MVR) Surgical Options Annuloplasty, i.e. repair (rarely replacement)
PS
click
PR
Etiology Pulmonary HTN, IE, rheumatic disease, tetralogy of Fallot (post-repair) Pathophysiology s, s, s, Increased RV wlume -+ increased wall tension -+ Anas Nader 2009 RV hypertrophy -+ right heart failure Symptoms Chest pain, syncope, fatigue, peripheral edema Physical Exam diastolic murmur at LLSB, Graham Steell (diastolic) murmur 2nd and 3rd LICS increasing with inspiration Investigations ECG: RVH CXR: prominent pulmonary arteries ff pulmonary HTN; enlarged RV Echo: diagnostic Treatment Rarely requires treatment; valve replacement ff severe Surgical Options Pulmonary valve replacement
Etiology Usually congenital, rheumatic disease (rare), carcinoid Pathophysiology s, s, s, Increased RV pressure -+ Anas Nader 2009 RV hypertrophy -+ right heart failure Symptoms Chest pain, syncope, fatigue, peripheral edema Physical Exam Systolic murmur at 2nd LICS accentuated by inspiration, pulmonary ejection click. right-sided S4 Investigations ECG: RVH CXR: prominent pulmonary arteries enlarged RV Echo: diagnostic Treatment Balloon valvuloplasty if severe symptoms Surgical Options Percutaneous or open balloon valwloplasty
Mitral Valve Prolapse

Etiology Myxomatous degeneration of chordae; thick. bulky leaflets that crowd orifice; Marian's syndrome; pectus excavatum, straight back syndrome, other MSK abnormalities; <3% of population Pathophysiology MV displaced into LA during systole; no causal mechanisms found for symptoms Symptoms Prolonged, stabbing chest pain, dyspnea, anxiety/panic, palpitations, fatigue, presyncope Physical Exam Ausculation: mid-systolic click (billowing of mitral leaflet into LA; tensing of redundant valve tissue); mid to late systolic murmur at apex, accentuated by Valsalva or squat-to-stand maneuvers Investigations ECG: non-specffic ST-Twave changes, paroxysmal SVT, ventricular ectopy Echo: systolic displacement of thickened MV leaflets into LA Treatment Asymptomatic: no treatment; reassurance Symptomatic: beta-blockers and avoidance of stimulants (calfeine) for significant palpitations, anticoagulation if systemic emboli Surgical Options Mitral valve surgery (repair fawured over replacement) ff symptomatic and significant MR
'IbroDlo Nota 2011
Valvular Heart Diseaae
CardioloBf and CV Surgery C43
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\ PRESSURE
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:r
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\1:
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nME
/ \ l
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TIME SZ
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s\
IIIII 1
IZ
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IEART SOUNDS:
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Figure 33. Hemodynamics Df Aortic
Stenosis across the aortic valva res!Ms in the generation af a significant pressure gradient between the laft ventricle and the aorta and a aascendo-(Jecrescendo munnur during systolic contraction. The stenosis decreases the intllnsity af aortic valve closure hance dimirishing S2.
Figure 34. HemiMipllllllcs of Aortic Ragu.,;tmo. Regurgitation across the aortic valve during diastnle causes tha aortic pressure to rapidly decrease and a decrescendo munnur can be heard at the onset of diastole Iafter S2 is audible). The presence af regurgitant blood from the aorta incraasas laft-ventricular and-(Jiastolic volume.
Figura 35. Hemodynllllllcs of Acnl Mitral Regurgitation During systolic contraction, blood 111!1Urgitates from the Iaft ventricle into tha 111ft a1rium across tha incompetent mitral valve resulting in an audible holosystolic munnur batwean S1 and S2. The portion af left ventricular end diastolic volume that regurgitates into the 111ft a1rial myocardium inaeases laft a1rial preSSII"es resulting in a tal V-wava.
iii
I;!
Cl
Ill 'SII81 li
.!.
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Sl
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Figure 3&. Hemodynamics Df Mitral Stenosis Fir.rt nota that tha 111ft atrial pressure exCBBds the 111ft ventriwar pressure during diastole dua to mitral stenosis and 1he consequent generation af a pressure gradient across the left atrium and left ventricle. In diastola, the stenotic mitral valve opens which cotTBiponds to the opening snap (OS) and the paBSige of blood across tha rritral stanosis results in an audible dacrescendo munnur. Laft a1rial contraction prior to S1 inCT1111SB& tha preSSII"B gradient resulting in accantuation of tha munnur before S1 is audible.
Pericardial Disease
Toronto Notes 2011
Pericardial Disease
Acute Pericarditis
Etiology of Pericarditis/Pericardia! Effusion
idiopathic is most common: usually presumed to be viral infectious viral: Coxsackie virus A, B (most common), echovirus bacterial: S. pneumoniae, S. aureus TB fungal: histoplasmosis, blastomycosis post-MI: acute (direct extension of myocardial inflammation, 1-7 days), Dressler's syndrome (autoimmune, 2-8 weeks) post-cardiac surgery (e.g. CABG), other trauma metabolic: uremia (common), hypothyroidism neoplasm: Hodgkin's, breast, lung, renal cell carcinoma, melanoma collagen vascular disease: SLE, polyarteritis, RA, scleroderma vascular: dissecting aneurysm other: drugs (e.g. hydralazine), radiation, infiltrative disease (sarcoid)
.....
,,
Signs and Symptoms

diagnostic triad: chest pain, friction rub, and ECG changes pleuritic chest pain - alleviated by sitting up and leaning forward pericardia! friction rub- may be uni-, bi- or triphasic fever, malaise
Acull PeriCinltil
Chest Pain
Friction Rub ECG Chanv-s
Investigations
ECG: initially diffuse elevated ST segments depressed PR segment, the elevation in the ST segment is concave upwards -+ 2-5 days later ST isoelectric with T wave flattening and inversion CXR: normal heart size, pulmonary infiltrates echo: assess pericardia! effusion
Treatment
treat the underlying disease anti-inflammatory agents (high dose NSAIDs/ASA, steroids if severe or recurrent); analgesics
Prognosis
complications: recurrence, atrial arrhythmia, pericardia! effusion, tamponade, constrictive pericarditis
Pericardial Effusion
Etiology
transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism exudative (serosanguinous or bloody) causes similar to the causes of acute pericarditis may develop acute effusion secondary to hemopericardium (trauma, post-MI myocardial rupture, aortic dissection) physiologic consequences depend on type and volume of effusion, rate of effusion development, and underlying cardiac disease
.....
,,
Ewn'sSign llronchill brelltiJing and dulmss to percussion at til& lower lllgla of til& left scapula in periclrdilll ellusion due 1D affusion compressing Iaft lower lobs
Signs and Symptoms may be asymptomatic or similar to acute pericarditis

dyspnea, cough extra-cardiac (esophageal/recurrent laryngeal nerve/tracheo-bronchial/phrenic nerve irritation) ]VP increased with dominant Y descent arterial pulse normal to decreased volume, decreased pulse pressure auscultation: distant heart sounds rub ECG: low voltage, flat T waves CXR: cardiomegaly, rounded cardiac contour echo (procedure of choice): fluid in pericardia! sac pericardiocentesis: definitive method of determining transudate vs. exudate, identify infectious agents, neoplastic involvement
of lung.
Investigations
Treatment
mild: frequent observation with serial echocardiograms, treat underlying cause, antiinflammatory agents for inflammation severe: may develop cardiac tamponade
Toronto Notes 2011
Perlcardial Diaeaae
Cardiology and CV Surgery C4S
Cardiac Tamponade
--------------------------------------
Etiology major complication of rapidly accumulating pericardia! effusion; cardiac tamponade is a clinical diagnosis any cause of pericarditis but especially trauma, malignancy, uremia, idiopathic, proximal aortic dissection with rupture Pathophysiology high intra-pericardia! pressure -+ decreased venous return -+ decreased diastolic ventricular filling -+ decreased CO -+ hypotension and venous congestion Signs and Symptoms tachypnea, d}'lipnea, shock, muffled heart sounds pulsus paradoxus (inspiratory fall in S}'litolic BP >10 mmHg during quiet breathing) JVP "xD descent only, absent Y descent hepatic congestion/peripheral edema Investigations ECG: electrical alternans (pathognomonic variation in Rwave amplitude), low voltage echo: pericardia! effusion, compression of cardiac chambers (RA and RV) in diastole cardiac catheterization Treatment pericardiocentesis - echo- or ECG-guided pericardiotomy avoid diuretics and vasodilators (these decrease venous return to already under-filled RV -+ decrease LV preload-+ decrease CO) fluid administration i.e. saline load may temporarily increase CO treat underlying cause
.....
, _._______________
Classic quartet of bmponade: hypotansion, incraased JVP, tachyclll'dia, pulsus paradoxus.
.....
, _._______________
(a.v.llllhm)
DDx PuiiiUI Plll'ldoxul

Con5trictiv j)llricarditis
Sw.. obstructive pumonary diusa

Tension Pneumothorax Pulmonary embolus Cllllioguic ahock
Constrictive Pericarditis
Etiology chronic pericarditis resulting in fibrosed, thickened, adherent, and/or calcified pericardium any cause of acute pericarditis may result in chronic pericarditis major causes are idiopathic, post-infectious (viral, TB), radiation, post-cardiac surgery, uremia, MI Signs and Symptoms dyspnea, fatigue, palpitations abdominal pain may mimic CHF (especially right-sided HF) ascites, hepatosplenomegaly, edema increased ]VP, Kussmaul's sign (paradoxical increase in JVP with inspiration), Friedreich's sign (prominent Y descent) BP usually normal (and usually no pulsus paradoxus) precordial examination: pericardia! knock (early diastolic sound) see Table 16 for differentiation from cardiac tamponade Investigations ECG: non-specific: low voltage, fiat T wave, AF CXR: pericardia! calcification, effusions echo/CT/MRI: pericardia! thickening cardiac catheterization: equalization of end-diastolic chamber pressures (diagnostic) Treatment medical: diuretics, salt restriction surgical: pericardiectomy (only if refractory to medical therapy) prognosis best with idiopathic or infectious cause and worst in post-radiation with death resulting from heart failure
Table 1&. Differentiation of Constrictive Pericarditis n.. Cardiac Tamponade

Charac:terillic
COIIIIrictive Pericarditis Tamponade
M
Kussmaurs sign
Pulsus paradoxus
Y>Y Present
UncolllllOn
Y>Y
Absent
/lJwsys
Pericardia! knock
Hypotension
Present
Variable
Absent
Severe
Peripheral Arterial Disease
Toronto Notes 2011
VASCULAR DISEASE Peripheral Arterial Disease

Acute Arterial Occlusionnnsufficiency
-------------
Definition acute occlusion/rupture of a peripheral artery urgent management required: >6 hours results in irreversible ischemia and myonecrosis lower extremity> upper extremity; femoropopliteal > aortoillac
....
Dilfllrentill of Claudicdan
V.scular Atherosclerotic disease
Vasculitis (e.g. Buerver's dis-.

Takayasu's lllteritist
Venous disease (e.g. DVT. varicou

Popliteal entnlpment syndrome
vain&I
Dillbelic neuropathy
Neurospinll disease (e.g. spinal

atenosist
dystrophy
Etiology embolus cardiac embolus (80-90%): history of MI <3 months, valvular disease, AF, cardiomyopathy, endocarditis, atrial myxoma arterial embolus: proximal arterial aneurysm, atheroembolism venous embolus (intracardiac shunt); may have Hx of OCP use Hx ofTIAs/strokes thrombus atherosclerotic, congenital anomaly, infection, hematological disorders and stasis trauma arterial catheterization, intra-arterial drug injection induced, aortic dissection, severe venous thrombophlebitis, prolonged immobilization idiopathic Clinical Features general pain in lower extremity progressing within hours to a feeling of cold, numbness, loss of function and sensation symptoms (6 P's)- all may not be present Pain: absent in 20% of cases due to prompt onset of anesthesia and paralysis Pallor: within a few hours becomes mottled cyanosis Paresthesia: light touch (small fibres) lost first then sensory modalities (large fibres) Paralysis/Power loss: most important, heralds impending gangrene Polar (cold) Pulselessness: not reliable embolus vs. thrombus - dramatically different treatment (see Table 17) Investigations CXR, ECG, arteriography Treatment immediate heparinization with 5000 IU bolus and continuous infusion to maintain PTT >60 seconds absent power and sensation - emergent revascularization present power and sensation -work-up (including angiogram) definitive treatment embolus: embolectomy thrombus: thrombectomy graft, bypass irreversible ischemia: amputation identify and treat underlying cause continue heparin post-op, start warfarin post-op day 1 for 3 months
Table 17. Diffarentiation of Arterial Embolism and Thrombosis
MSK
Osteoarthritis
Rhematoid arthritirlconnective tiaau&
Remota ll'lluma
di-
Dnslll
l.o&& of lunctionl&lllllation
Hx of ciMJdcatian
Aculll
Prominllllt No No
Yes
Th111mbus Progressiw, aculll-cnduonic

LilliS profoWJd
Yes Yes Decreased or absent
A1rophic changes Conlnllaterallinb pulses
Complications compartment syndrome with prolonged ischemia; requires fasciotomy renal failure and multi-organ failure due to toxic metabolites from ischemic muscle Prognosis 12-15% mortality rate 5-40% morbidity rate (amputation)
Toronto Notes 2011
Peripheral Arterial Disease
Chronic Arterial Occlusionnnsufficiency- - - - --Etiology
predominantly due to atherosclerosis: primarily lower extremities with symptoms related to the location of obstruction
Risk Factors
major: smoking, DM, hyperhomocysteinemia minor: HTN, hyperlipidemia, family history, obesity, sedentary lifestyle, male gender
Clinical Features
claudication 1. pain with exertion: usually in calves or any exercising group 2. relieved by short rest: 2 to 5 minutes, and no postural changes necessary 3. reproducible: same distance to elicit pain, same location of pain, same amount of rest to relieve pain pulses may be absent at some locations, bruits may be present signs of poor perfusion: hair loss, hypertrophic nails, atrophic muscle, skin ulcerations and infections, slow capillary refill, prolonged pallor with elevation and rubor on dependency, venous troughing (collapse of superficial veins of foot) other manifestations of atherosclerosis: CVD, CAD, impotence, splanchnic ischemia
Differential Diagnosis
Signs "'rip"-1 V.e.m.r lnsuflici_.,
..r
SICVD
Symmetry of lag musculature Integrity of skil
Colour of tlltl nails Vlllicose veins

Distribution
..r hair
osteoarthritis (OA): worse at night and varies day-to-day neurogenic claudication: due to spinal stenosis or radiculopathy; pain very similar but relieved by longer rest and postural changes varicose veins: localized pain, typically less severe, after exercise and never at rest; related to the presence and site of varices inflammatory processes: Buerger's disease, Takayasu's arteritis other: popliteal entrapment (e.g. tumour, Baker's cyst), radiation injury, remote trauma
Investigations
non-invasive ankle-brachial index (ABI) (grade lA recommendation): measure brachial and ankle pressures bilaterally (use highest value) generally, ABI <0.90 abnormal, rest pain appears at <0.3 (see Table 18) CTA and MRA - excellent correlation with arteriography, where available, can replace it for intervention planning (grade lA recommendation) Doppler segmental pressures and pulse volume recordings, transcutaneous oxygen studies (photoplethysmography) treadmill exercise claudication test and real-time duplex scanning considered by vascular specialist (grade 3C) invasive arteriography (gold standard): defines site and size of occlusion, and collateral flow status, operative planning tool
Table 1B. Ankle-Brachial Indices and Degrees of Ischemia ABI rtcerdilg
>0.95 0.85-0.94 0.50-0.84 0.26-0.49 <0.25
Degree of lscllemia Normal/no ischemia Mild ModenJte

Severe
Consider lirrt s!Mige

Suspect wall calcification {most common in diabeticsl
>1.2
Treatment (see Figure 37)
conservative risk factor modification (smoking cessation improves prognosis, treatment ofHTN, hyperlipidemia and/or DM) exercise program - develops collateral circulation, improves exercise tolerance foot care (especially DM) pharmacotherapy anti-platelet agents (ECASA, clopidogrel or more rarely ticlopidine) cilostazol (cAMP-phosphodiesterase inhibitor with anti-platelet and vasodilatory effects) pain relief: opiate analgesia (morphine sulphate), supplemented by NSAIDs; if opiate analgesia inadequate, possibility oflumbar sympathectomy
C48 Carcliolosrand CV Surgery
Peripheral Arterial DileudAortic Dlleue

surgical/lnlervelrtional
1'oroDio
2011
indications: claudication interfering with lifestyle, rest pain. pre-gangrene, gangrene surgical options: endovascular (stentinglangioplasty) or arterial bypass grafts bypass graft sites: aortofemoxal, axlllofemoxal, femoropopliteal, distal arterial graft choices: in situ graft - reversed vein graft, synthetic - polytetrafluoroethylene graft
(Goror Dacron amputllli.oll! ifnot suitable for revascularization and persistent serious infections and/or
gangrene
Prognosis
conservative therapy: 60-8096 improve, 20-30% stay the same, 5-1096 deteriorate, 596 will require Intervention within 5 years, <496 will require amputation A
Criticllllimb illchamia
nl cmaiMir graft
angioplqty
Aulblbihunoral bypaa .,aft
Axilloblemoral bypaa graft
F"1111r 3'1. TI1Nitmlllt Options fur Critical Limit lscllenH (AI Algorithm for the treatment of critical limb ischemia (BI Surgical treatment options for the treatment of aortoiliac disease MadFalfmm a.nl.ll. t:mn: iowa' .,.. idllnia. BIIJ. 2IIXI;
Hypertension
see Family Medtdpe. FM3S
Pulmonary Hypertension
see Re$l)iroloD Rl6
Carotid Artery Disease

see Neurosw::gccy;. NS2l
Aortic Disease
Aortic Dissection
Definition
tear In aortic intima allowing blood to dissect Into the media; acute <2 weeks {lnltlal mortality 196 per hour), chronic >2 weeks (mortality levels off to 75-8096) ClassifiCation (see Figure 38) Stanford Type A: involves ascending aorta aortic arch; requires emergency surgery Type B: only involves aorta distal to subclavian artery; emergency surgery only lf complications of dissection (requires long-term follow-up to assess aneurysm sJze)
'IbroDlo Nota 2011
Aortic Dlleale
DeBakey 'JYpe I: involves aacending and descending aorta, 50% of patients Type TI: ascending aorta only (stops at the innominate artery), 35% of patients 'JYpe TIIA: descending thoraclc aorta only (distal to left subclavian artery and proxlmal to diaphragm), 15% of patients (including Type mB) Type TIIB: Type TIIA plus abdominal aorta
Debakey: Slanfanl;
Type I
L - TJPI A
Type II
___J
Dabakey: Slanfanl;
Type IIA
L - TJPI B
Type 1118
___J
Figun 31. a...mc.tion af ADrtic Diuactian
Etiology most common: damage to aortic media (smooth muscle and elastl.c tl.!sue), leading to degenerative/cystic changes due to hypertension other: cystic medial necrosis, atherosclerosis, connective tissue disease (Marfun's, Hhlers-Danlos), congenital conditiom (coan::brtion of aorta, bicuspid aortic valves, patent ductus arteriosus), infe<:tion, trauma, arteritis (Takayasu's) Epidemiology incidence of 5.2 in 1 000 000 male:female = 3.2:1 small increased incidence in African-Canadians (related to higher incidence ofhypertension) lowest lncidence !n Asla.ns peak incidence 50-65 yrs old; 20-40 yrs old with conne<:tive tissue diseases Clinical Features sudden onset tearing chest pain that radiates to back. with hypertension (75-85% of patients) asymmetric BPs and pulses between arms (>30 mmHg difference indicates poor prognosis) ischemic syndromes due to occlusion of aort1.c branches: coronary (MI), carotids (ischemic stroke, Horner's syndrome), splanchnic (ischemic gut) "'unseating" ofaortic valve cusps (new diastolic murmur in 20-3096) rupture into pleura (dyspnea. hemoptysis) or peritoneum (hypotension, shock) or pericardium (cardiac tamponade) renal insufficiency lower limb ischemia (cold legs)
syncope
Investigations
CXR
pleural cap (pleural effusion in lung apices)
widened mediastinum left pleural effusion with extravasation of blood TEE: can visualize aortic valve and thoracic aorta but not abdominal aorta ECG: LVH, MI, pericarditis, heart bWck.
CT, aortcgrapby, MRA: 100% sensl.tive and spedftc bloodwork: LDH (r/o ischeml.c gut), amylase (r/o pancreatitis), tropon!n (r/o Ml)
Treatment
pharmacologic sodium nitroprusside and beta-bl.oc:ker to lower BP and decrease cardiac contractility beta-blocker given first to blunt refla tachycardia and lnotropy that will occur with sodium nitroprusside (vasodilator) then lower sBP with nitroprusside target sBP of llOmmHg and HR of 60 bpm
CSO Cardiology and CV Surgery
Aortic Disease
Toronto Notes 2011
surgical resection of intimal tear, reconstitution of flow through true lumen, replacement of the affected aorta with prosthetic graft. correction of any predisposing factors (e.g. bicuspid aortic valve, PDA, etc.) post-operative complications: renal failure, intestinal ischemia, stroke, paraplegia, persistent leg ischemia, death 2/3 of patients die of operative or post-operative complications Type A:. requires emergent surgery with cardiopulmonary bypass, may require hypothermic circulation for transverse arch dissections, valve replacement and coronary re-implantation for aortic root involvement, initial mortality rate without surgery is 3% per hour for first 24 hours, 30% 1 week, 80% 2 weeks Type B: initially managed medically- 10-20% require urgent operation for complications (expansion, rupture, compromise of branch arteries, refractory H1N, or ongoing pain) with treatment, 60% 5 yr survival, 40% 10 yr survival
Aortic Aneurysm
.....
,t----------------. ,
,...----------------. ,
----------------------------------------
Definition of Aneurysm localized dilatation of an artery having a diameter at least 1.5 times that of the expected normal
diameter ofthat given aortic segment true aneurysm: involving all vessel wall layers (intima, media and adventitia} false aneurysm: disruption of the aortic wall or the anastomotic site between vessel and graft with containment of blood by fibrous capsule made of surrounding tissue aneurysms can rupture, thrombose, embolize or erode and fistulize
ACCIAHA 2005 Guidalinas dufinu 1111 AAA when the minimum AP diamatw of bdomilllllaorlll em.
.....
Classification
thoracic (TAA): ascending, transverse arch, descending thoracoabdominal abdominal (AAA): 90-98% are infrarenal
Cllulc Triatl of Rupturlcl AAA Pain

Hypotension Pulsatile abdominal mass
.....
,,
.......
Etiology
degenerative atherosclerotic traumatic mycotic (Salmonella, Staphylococcus, usually suprarenal) connective tissue disorder (Marfan syndrome, Ehlers-Danlos)
ACC/AHA 2005
1. Men Yl1 with AAA in relative nuld have LVS fDrAAA. 2. Men 60-75 yr1 who hBV&BVer smoked should haV& anubne LVS screenilg fDr AAA.
vasculitis
infectious (syphilis, fungal) ascending thoracic are associated with bicuspid aortic valve risk factors: smoking, liTN, age >70, family history
Epidemiology
incidence 4.7 to 31.9 per 100 000 for AAA and 5.9 per 100 000 forTAA high risk groups 65 years and older male:female = 3.8:1 PVD, CAD, CVD family history of AAA
Clinical Features
common presentation: due to acute expansion or disruption of wall syncope pain (chest, abdominal, flank, back) hypotension palpable pulsatile mass above the umbilicus, pulsatile abdominal mass in two directions airway or esophageal obstruction, hoarseness (left recurrent laryngeal nerve paralysis), hemoptysis, or hematemesis distal pulses may be intact 75% asymptomatic (discovered incidentally) uncommon presentation partial bowel obstruction ureteric obstruction and hydronephrosis GI bleed (duodenal mucosal hemorrhage, aortoduodenal fistula) aortocaval fistula distal embolization (blue toe) associated diseases hypertension, PVD, CAD, COPD, renal insufficiency most commonly in the abdominal aorta (50% abdominal aorta, 40% thoracic aorta, 10% ascending aorta)
Toronto Notes 2011
Aortic: Disease/Peripheral VenoWI Disease
Cardiology and CV Surgery CSI
Investigations
bloodwork: CBC, electrolytes, urea. creatinine, PTT, INR, type and cross abdominal U/S (100% sensitive. up to 0.6 em accuracy in size determination) CT (accurate visualization, size detennination) MRI (accurate visualization, limited access) aortogram Doppler/duplex (r/o vascular tree aneurysms elsewhere)
Treatment
Conservative cardiovascular risk factor reduction: smoking cessation, HTN control, DM and hyperlipidemia control regular exercise watchful waiting, U/S every 6 months to 3 years depending on size and location
....
,,
Surgical when risk of rupture greater than or equal to risk of surgery (>5.5em) risk of rupture depends on
size
Manqemant of Rapturwd AAA Noimqing Straight to DR {confirm diagnosis by laparotomy) CI'0$$111111c;h 10 unit$ PRBCs Start possible
rate of enlargement >0.4 cm/yr symptoms, comorbidities (HTN, COPD, dissection), smoking elective AAA repair mortality 2-5%; elective TAA repair mortality <10% (highest with proximal aortic and thoracoahdominal repairs) consider revascularization for patients with CAD before elective repair of aneurysm indications general: ruptured, symptomatic, mycotic, associated with acute Type A dissection or complicated Type B dissection or when risk of rupture is greater than risk of surgery (size >5.5 em or >2x normal lumen size) ascending thoracic aortic aneurysms symptomatic, enlarging, diameter >5.5 em or >2x normal lumen size, >4.5 em and aortic regurgitation (annuloaortic ectasia); em in Marfan syndrome contraindications: life expectancy <1 year, terminal disease (e.g. cancer), significant co-morbidities (recent Ml, unstable angina), decreased mental acuity, advanced age surgical options open surgery (laparotomy) with graft replacement possible complications - early: renal failure, spinal cord injury (paraparesis or paraplegia), impotence, arterial thrombosis, anastomotic rupture or bleeding, peripheral emboli -late: graft infection/thrombosis, aortoenteric fistula, anastomotic (pseudo) aneurysm endoluminal graft placement under image guidance newer procedure; high success rates in patients with suitable anatomy and experienced centres advantages: decreased morbidity and mortality, procedure time, need for transfusion, ICU admissions, length ofhospitalization, and recovery time disadvantages: endoleak rates as high as 20-30%, device failure increasing as longer follow-up periods are achieved, re-intervention rates 10-30%, cost-effectiveness is an issue {devices are very expensive) complications - early: immediate conversion to open repair, groin hematoma. arterial thrombosis, iliac artery rupture. and thromboemboli - late: endoleak, severe graft kinking, migration. thrombosis, rupture of aneurysm
....
,,
1"fUr rupture risk
IIIII of AAA Rupblre

SIZII
<4em 4-4.9 em S-5.9em &-6.9 em 7-7.9 em
D'l(, 1% S-1D'l(, 1G-20% 2G-4D'l(,
....
,,
Replir of AaympiDmatia AAA is Nat JllltliMI fllr: Mlllll <5.0 em Females <4.5 em
Peripheral Venous Disease

Deep Venous Thromboembolism
see Hematology. H31
-------------------
Superficial Thrombophlebitis
Definition
erythema, induration, and tenderness along the superficial vein; usually spontaneous but can follow venous cannulation

Etiology
Peripheral Venous Diaease
Toronto Notes 2011
infectious: suppurative phlebitis (complication of intravenous cannulation; associated with fever,

chills)
trauma inflammatory: varicose veins, migratory superficial thrombophlebitis, Buerger's disease, SLE hematologic: polycythemia. thrombocytosis neoplastic: occult malignancy (especially pancreatic) idiopathic
', ,
Clinical Features
most common in greater saphenous vein and its tributaries 9}-----------------, pain and cord-like swelling along course of involved vein areas of induration, erythema and tenderness correspond to dilated and often thrombosed Mignrtorv tl4)elficial1hrombophlebitis superficial veins is ofbJn a sign of underlying malignancy {"Trouss1181l's disellse"). complications simultaneous DVT (up to 20% of cases), pulmonary embolus (rare unless DVT) recurrent superficial thrombophlebitis
Investigations
non-invasive tests (e.g. Doppler ultrasonography) to exclude associated DVT

Treatment
conservative bedrest and elevation of limb moist heat, compression bandages, mild analgesic, anti-inflammatory and anti-platelet (e.g. ASA), ambulation surgical excision of involved vein indication: failure of conservative measures (symptoms that persist over 2 weeks) suppurative thrombophlebitis: broad-spectrum IV antibiotics and excision
Varicose Veins
Definition
distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial, or perforator systems distribution: greater saphenous vein and tributaries (most common), esophagus, anorectum, scrotum
Etiology primary main factor: inherited structural weakness of valves
contributing factors: increasing age, female gender, OCP use, occupations requiring long hours of standing, pregnancy, obesity secondary malignant pelvic tumours with venous compression congenital anomalies - arteriovenous fistulae
Epidemiology
most common form ofvenous disorder oflower extremity 10-20% of population

Clinical Features
diffuse aching, fullness/tightness, nocturnal cramping aggravated by prolonged standing (end of day), premenstrual visible long, dilated and tortuous superficial veins along thigh and leg ulceration, hyperpigmentation, and induration (secondary varicosities) associated esophageal varices (GI bleed), hemorrhoids, varicocele Brodie-Trendelenberg test (valvular competence test) with patient supine, raise leg and compress saphenous vein at thigh; have patient stand; if veins fill quickly from top down then incompetent valves; use multiple tourniquets to localize incompetent veins
Complications
recurrent superficial thrombophlebitis hemorrhage: external or subcutaneous ulceration, eczema, lipodermatosclerosis, and hyperpigmentation
Treatment
largely a cosmetic problem conservative: elevation ofleg and/or elastic stockings surgical: high ligation and stripping ofthe long saphenous vein and its tributaries, sclerotherapy, endovenous laser therapy (EVLT)
Toronto Notes 2011
Peripheral Venoua Disease
Prognosis natural history benign, slow with predictable complications almost 100% symptomatic relief with treatment if varicosities are primary good cosmetic results with treatment significant post-operative recurrence, especially with sclerosing agent injection
Chronic Venous Insufficiency

Definition chronic elevation of deep venous pressure and blood pooling in lower extremities Etiology calfmuscle pump dysfunction and valvular incompetence (valvular reflux) due to phlebitis, varicosities, or DVT venous obstruction AV fistulas, venous malformations Clinical Features pain (most common), ankle and calf edema - relieved by foot elevation pruritis, brownish hyperpigmentation (hemosiderin deposits) stasis dermatitis ulceration: shallow, above medial malleolus, weeping (wet), painless, irregular outline signs ofDVT/varicose veins/thrombophlebitis Investigations ambulatory venous pressure measurement (gold standard) Doppler U/S (most commonly used) photoplethysmography Treatment conservative elastic compression stockings, leg elevation, avoid prolonged sitting/standing ulcers: zinc-oxide wraps, split-thickness skin grafts, antibiotics, debridement surgical if conservative measures fall, or if recurrent/large ulcers surgical ligation of perforators in region of ulcer, greater saphenous vein stripping venous bypass if short segment obstruction
Lymphedema
Definition obstruction oflymphatic drainage resulting in edema with high protein content Etiology primary: Milroy's syndrome secondary infection: filariasis (#1 cause worldwide), post-operative malignant infiltration: axillary, groin or intrapelvic radiation/surgery (axillary, groin lymph node removal): #l cause in North America Clinical Features classically non -pitting edema impaired limb mobility; discomfort/pain; psychological distress Treatment avoid limb injury (can precipitate or worsen lymphedema) skin hygiene daily skin care with moisturizers topical treatment of fungal infection; systemic treatment of bacterial infection external support intensive: compression bandages maintenance: lymphedema sleeve exercise gentle daily exercise of affected limb, gradually increasing ROM must wear a sleeve/bandages when doing exercises massage and manual lymph drainage therapy Prognosis if left untreated, becomes resistant to treatment due to subcutaneous fibrosis cellulitis causes rapid increase in swelling: can lead to sepsis and death
_._______________
Pittilg edema -+ vucLJar Non-pitting adema -+ lymphatic
Common Medications
Toronto Notes 2011
Common Medications
Tabla 19. Commonly Used Cardiac Therapeutics
Drug Class Examples Madlanism of Action Side Eflecls CalllnindicidiiiiS Bilateral renal artery stenosis, pregnancy, caution i1 decreased GFR ANGIOTENSIN CONVERnNG ENZYME INHIBITORS (ACEISJ enalapril (Vasotec411 J. Inhibit ACE-mediated HTN. CAD. CHF. post-Ml perindopil (CoversyPJ, conversion of angiotensin I DM ramipril (AIIacel to angiotensin II (AT II), lisinopril causing peripheral vasodilation and decreased aldDS!EnJne synthesis ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS) candesartan, irbesartan, Block AT II receptors, valsarlan causing similar effects to ACEis II-BLOCKERS Ill antagonists
Dry cough. 10% hypotension. fatigue, hyperkalemia, renal insufficiency, angioedema
Same as ACBs, although Similar to ACEis, but do not evidence is generally less cause cough fur ARB&. Dfta1 used when ACEis are not tolerated.
av
SameasACEis
atnlol, mBIIlprOiol bisoprolol propranolol f1Jll2 antagonists aJIIJII2 antagonists labetalol, carvedilol 11 1 antagonists with ISA acebutalol
Block jl-adranargic HTN, CAD, acute Ml, recaptors, d8Cillllsing HR, post-MI. CHF (start low BP, contractility, and and go slow!, AF, SVT myocardial oxygen demand, slow conooction 11nugh theAVnode
HypOillnsion, fltiiJI&, light headedness. deprassian. bradycardia, hyperkalemia, bronchospasm, impotence, depression of counte11'8gulatory response to hypoglycemia. I!X8cerilation of Raynaud's phenomenon and claudication
Si1us bradycardia, 2nd or 3rd dagree heart block. hypotension, WPW. Caution in asthma, claudication, Raynaud's phenomenon. and
CALCIUM CHANNa BLOCKERS (CCBSJ Benzothiazepines dillimem Phenylalkylaminas varapamil (non-dihydropyridinesl
Block smooth muscle and myocardial calcium channels causing effects similar to Also wsodilate Block smooth musde cak:ium channels causing vasodilation
HTN, CAD, SVT, diastolic dysfunction
Hypotension, bradycardia, edema Si1us bradycardia, 2nd or Negative inotrope 3rd dagree heart block, hypotension, WPW, CHF
Dihydropyridi1es
lll'llodipine nifl!dipine felodipile (Piendii-J hydrochlorthil2ide, chlorthalidone metoiBZOne furosemide (Lasix411J spironolactone. eplenerone digoxin (lanoxinJ
HTN
Hypotension, edema, flushing. headeche, light-headedness
Severe aortic stenosis and liver failure
DIUIIETICS Thi12ides
Reduce Na reabsorption in HTN (drugs of choice fur theDCT uncomplicated HTNJ Blocks N!VX-AlPase in the CHF. pulmonary or loop of Henle peripheral edema Antagooize aldosterone receptors HTN, CHF. hypokalemia
Hypotension, hypokalemia,
Sulfa allergy, pregnancy
polyuria
Hypovolemia. hypokalemic metabolic alkalosis Edema. hyperkalemia, gynecomastia Hypovolemia. hypokalemia Renal insufficiency, hypllkalemia, pregnancy
Loop dUetics
Aldosterone receptor antagonists INDTRDPES
NWIC-ATPase, CHF.AF leading to increased intracellular Na and Ca concantration and inCIIIIISed myocardial contractility. Also slows conduction through the AV node Antagooizes vitamin K. Abial fibrilllltion, LV leading to decreased dysfunction, prosthetic synthesis of clotting factors viMs II, VII, IX. and X Antithrombin Ill agonist. leading to decreased clotting factor activity
AV lllchyarrhythmias, 2nd or 3rd degree AV block. bnldyanhythmias, blurred or hypoklllemia, WPW yellow vision (van Gogh syndrome), ano11111ia, neusea and vomitilg
ANTICOAGULANTS Coumarins
wlriarin (Coumadin-)
Bleedi1g (by far the most Recent surgery or bleeding. impol'llrlt side effect), paradoxical bleeding diathesis. thrombosis, skin necrosis prag1111ncy Recent surgery or bleeding. bleeding diathesis. thrombocytopenia, renal i1sufficiency (fur LMWHs)
Heperins
unfractionatad heparin low molecular weight heparins {LNIWHsJ: dalteparin, enoxaparin, tinzap!lin
Acute Ml; when irrmediate Bleadi1g. osteoporosis. hepam. anticoagulant effect needed induced thrombocytopenia (less in LMWHsl
Toronto Notes 2011
Common Medications
Table 19. Commonly Used Cardiac Therapeutics (continued)
Drug Class
ANTIPLATELETS Salic:ylates
Examples
Meclllnism of Aclian I11'1M!rsibly acetylates platelet COX-1, preventing tlv'ontoxana A2-mediated platelet IIIIQ18QIIlion
lndiCIIions
CAD. acute MI. post-MI. post.PCI and CABG
Side Efflcts
Bleeding. Gl upset gastmintestinal ulceration, impaired 181'1BI perfusion Bleeding. tlromblllic thrombocytopenic purpwll, neutropenia (ticlopidine)
WPCI Bleeding
Colllnlinlic:llions Active bleeding or peptic ulcer disease (PUll)
Thienopyridine&
clopidogral ticlopidine [Ticli!P) eptifibBiide, tirufib111. abciximab alteplase, tenecteplase, straptokinasa nitroglycerin
Block plirtelst ADP receptors Block binding of fibrinogen 1D Gpllll/llla
Acul8 Ml, post-MI, post.PCiand CABG Acute is planned
Active blaading or PUD
GPIII:VIIIa THROMBOLYTICS
Recent surgery or bleeding.

dathesis See Table 7, C27
Convert circulating AcuteSTEMI plasminogen to plasmin. which lyses crossMcad fibrin Relax wscular smooth muscle, producing venous and arteriolar dilation CAD, Ml, CHF [isosorbide plus hydralazine)
Bleeding
NI111ATES
Headache, dilziness, weakness, Concurrent use of cGMP posb.lral hypotension phosphodiesterase angle closure glaucoma. increased ICP Liver or muscle disease
UPID LOWERING AGENTS
Statins
hytoxymethylgluturyt Dyslipidemia (1" prevention Myalgia, rhabdomyolysis, atorvastllin pravestllin (Pravachol), CoA reductase, which of CAD}, CAD, post-MI abdominal pain rosuwstatin (Crestor0), catalyzes the rate-limililg simVIIstatin {lllcar), step in cholesterol synthesis lovastatil (Meracor)
Antiarrhythmic&
:<i!
"Cl
"' a']
_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ _
!:!!! c a:
TIME
Figure 39. Representl'tive Action Potential

Table 20. Antianhythmic Drugs (Vaughn-Williams Classification) Class A4111111
Ia
quinidine procainamide disopyramida lilklcaine mexiletine propalenone flecainide encainide propranolol metoprolol, etc. niodnne sotalol lndic:llions SVT, VT Side Efflcb Torsades de Pointes (all Ia], dilllhea syndrome Anti-cholinergic sflacts Confusion, stupor, seiZllniS Gl upset 1remor Exacerbation of VT (aile) Negative inotroll'f (alllc) Bradycardia and heart block (alllc) Bronchospasm, negative inD1rDpy, bradycardia, AV block, implllence, fatigue Photosensitivity, pulmonary toxicity, hepatotoxicity, thyroid disease, increased INR Tol88des de Pointes, bradycardia, heart block and bet!HJiocker side effects Bradycardia, AV block Hypotension Mechanism of Al:tioo Moderate Na channel blockade Slows phase 0 upstroke Prolongs rapolarillltion, slowing conduction Mild Na channel blockade Shortens phase 3 repolarillltion Marked Na channel Markedly slows phase Dupstroke
Anii-Arrydlmlc Drug Ca.llllclldon:
Some Block Plllllssiurn Ch111nels

I - SodmCB II - 11-llocker Ill - Potassi..n CB
IV- CCB
lb
lc
VT
svr. vr
AF SVT,AF SVT, VT AF SVT, VT,AF
II
Beta-blocker
Decreases phase 4depolarization Blocks Kchamel Prolongs phase 3 repolarization, which prolongs refractory period
Ill
IV
verapamil
svr
AF
CCB
Slows phase 4 spontaneous depolllizalion, slowing AV node conduction
'AI anti11111ythmics hM potBntiii1D be prolllhytMi:
'*Amodnne Ills clllss I, I. II, and IV]liUplltias
Common Medications
Toronto Notes 2011
Table 21. Actions of Alpha and Beta Adrenergic Receptors

ALPHA RECEPTORS
Alpha1
CardiiiVISCullr
BETA RECEPTORS
Belli Increased myocardial contractility Accelerate SA node Accelerate ectopic pBcemakel$
Alpha2
Betll2
Decreased vascular smooth muscle tone
Constriction of vascular sroooth muscle Constriction of skin. skeletal muscle and splanchnic vessels Increased myocardial Paipherally act to contractility modulate vessel tone Decreased heart rata Vasoconsbict and dilate; owase Alpha 1 vasoconsbictor activity Pilomotor sroooth muscle cantraction Apocrine consbiction Radial rruscle contraction Inhibition Ill myentl!ric plexus Anal &phinctllr contraction
RllpiratDry
Bronchodilation
01111111
Ocular Gaatnin1111tinll
Ciliary muscle relaxation
Ganitaumuy
PragrBJI uterine
contraction Penile and seminal vesicle ejaculation Urinary bladder contraction
Stimulation of ranal renin release Smooth muscle wall relaxation
Bladder walralaxation Uterine relaxation
Metabolic
Stimulate gluconeogenesis and glycogenolysis at the liver Fat cell lipolysis
Fat cell lipolysis

Glycogenolysis
Gluconeogenesis
Adlp!Bd fnlm tlw Fllliy l'llctice NDIBboli
Table 22. Commonly Used Drugs thl1 Act on Alpha and Beta Adrenergic Receptors
ALPHA RECEPTORS
Machlnilm Ill Action Alp.l1
Phenylephrine MethDXIlllline Pramsin Phenoxybenzamile Alphl1 and Alpha2 Epilephrine Norepinephrine Phentolamine
BETA RECEPTORS
AlphaZ
Clonidine Yohimbine
Bltll1
Norepinephrine Dobutamine Metoprolol Aceilutolol Alprenolol Ate noloI Esmolol
Bltll1 and BIIIZ

Isoproterenol Epinephrine Propranolol TinlDiol Nadolol Pindolol Carvedilol
BltaZ
Albuterol Terblllaline Butaxamine
AGonilt
Altagoailt
Adlp!Bd fnlm tlw Fllliy l'llctict N!Ohool:
Toronto Notes 2011
Landmark Cardiac Trials

Trill
lklfl1111c:1
Results
In patients 111gina or previoos Ml and high total cholesll!llll, simvastatin reduced: all-cause mortality, fatal and nonfatal CDI'Dnary events, need for coronary artary bypass surgery or angioplasty
ISCHEMIC HEART DISEASE
4S
l.anr:st 1994; 344:1383-89
Ato Z: Phase Z J4MA 2004; 292:1307-16 ALIJIAT J4MA 2002; 288:2981-97
Early of aggressive simvastatin regimen resulted in a trend towards reduced major cardiovascular events
In hypertensive patients with <! 1risk factors for CHD, amlodipine nor fatal CHD and nonfatal Ml or morllllity when compared with chlorthalidane (thiazide duratics) In hypertensive patim with ria facto!$ for CHD and avaraga or below-avarage cholesterol, atorvasbrtin reduced ntllfatBI Ml, fatal CHD, fataVnonlatal stroke. coronary events but not all-cause mortality In acute MI. reduced all-cause mortality, cardiovascular death 111d sudden death from athelllsclerotic heart disease In atherosclerotic vascular disease. clopidogra reduced the primary combined endpoint crf stroke, Ml or vascular death and inproved peripheral arterial disease compared to aspirin Pravasllltin reduced Ml and stroke in patients with previous Ml111d average cholesterol Compared with optimal medcal therapy alone, PCI + medical therapy did not reduce all-cause mortality and non-fatal ML and it did not reduce the incid111ce of major cardiovascular events Clopidogra plus aspirin reduced death from c:-J causes. non-fatal MI. or stroke but increased bleedilg complications
ASCOT-LLA
lilncet 2003; 361 :114&-58
BHAT
CAPRIE
J4MA 1982; 247:1707-14
l.anr:st 1996; 348:132&-39
CARE
COURAGE
NEJM 1996; 335:1001-9 NEJM ZOOS; 358:1887-98
CURE EUROPA FRISC II FRISC II
NEJM 2001; 345:494-502

l.anr:st 2003; 362:782-88
Wrth stable CAD 111d no CHF, perindopril reduced cardiovascular death. Ml and total mortality
lowers risk of death, Ml and the need lor revascularization dlling the
Lancet 1999; 354:701-7 Lancet 1999; 354:70S.15 lilncet 1994; 343:1,, S.22
first month. These benefits are not sustained during longer term follow up
Benefit crf earty invasive treatment in reduction crf death or Ml significarrt Ill 6 months
In acute Ml (<24 hours),lisilopril reduced mortality and severe ventricular dy&function. Nitrate conferred no b-'it excuptwhan combiled with lisinapril Although there was an excess crf hemonhagic stroke with t-PA plus heparin, compared with the other RJgim111s, the combined 30-day endpoint of death or disabling stroke was sigrificantly lower with acceleratEd t-PA In hii#J.fisk patients without low LVEF or CHF. ramipril reduced rates of death, MI. stroke,revasculurization. new diagnosis of diubelel and complications due to diabetes. V"rtamin Ehad no effect on ootcomes. In hii#J.fisk patients with various cholesterol values, simvastatin reduced all-cause mortality, coronary deaths and major vascular evants
GISSI-3
GUSTO-I
NEJM 1993; 329:673-82
HOPE
NEJM 2000; 342:154-60
HPS ISIS-2
lancet 2002; 360:7-22 lancet 1988; 2:349-60
Early therapy with SK and ASA in patients with Ml individually and in combination significantly reduced all-cause mortality and in combination dernons1rated additive
effect
ISIS-4 LIPID OASIS-5 OPllMAAL PROVE ITTIMI22 SYNTAX
lilnm 1995; 345:669-85
In patients suspected or acute Ml, earty treatment with captopril reduced al-c:ause mortality at 35 days and during long-term follow up Pravasllltin reduced both mortality due to CHD and ovarall mortality and had benefit for patim unstable 111gina Compared to enoxaparin. fondapariiiiX reduced mortality rates. major bleeds at 9 and Ml at 30d 111d 18Dd Losartan 50 mg daily conferred no benefit in
NEJM 1998; 339:1349-57 NEJMZ006; 354:1464-76

l.ancst 2002; 360:752-60
with captopri
NEJMZ004; 350:1495-1504 In patim hospitalized lor ACS, higft.dosa atorvastatin reduced al-c:ausa mortality,
MI. unstable 111gina. revascularization 111d stroke CDIIlHired with pravastatin
NEJM ZOOS; 360:961-972
CABG has lower rate of major cardiac or cerebrovascular IIV8nts. The rate of stroke was increased with CABG, whereas the rate of repeat revascularization was increased with PCI Lipid-lowering therapy with atorvastatin 80 mgfday il patients provides clinical benefit beyond atDI'VIstatin 10mgfday stable CHD
TNT WOSCOPS
NEJM 2005; 352:1425-35 NEJM 1995; 333:1301-7
Pravasllltin reduced nonfatal Ml or death from CHD and need for myocardial revascularization procedures in patients hyparcholasterolamia and no Ml

Trial
HEART FAIWRE AIRE CHARM CIBISII COMET CONSENSUS COPERNICUS I-PRESERVE MERIT-HF
Toronto Notes 2011
l..ancvt 1993; 342:821-8

Lancvt 2003; Lane 1999; 353:9-13 Lane 2003; 362:7-13
Rnipril commiiiiC8d 3-1 0 day$ aftur Ml and continued fur am1151 15-monlh period significllllly reduced mortality in patients with non-severe CHF Cand88Brl!n reduced OYlllllll mortlllity, cardiovascular d8Bih and CHF hospitalizations Bisoprolol reduced mortality, cardiovascular death. all-cause hospitalization and CHF hospitalization Carvecilol was associated with areductioo in all cause mortlllity compared with metoprolol Enalapril reduced mortlllity, death due to prtVeSSion of heart failure Carvecilol il addition to standard trelllment significantly reduced the risk of death or hospitalization in patients with severe CHF In patients with CHF and normal LVEF, treatment with ARB (irbesartllnl did nat if11)1UVe mortality or cardiovascular morbidity compared to placebo MeiDpnllol CR/XL daily in addilioo to optirnJm standard therapy improved survival in clinically stable patients, equaling to prevention of 1 death per 27 patiants 1niBted per 'fllllr In 58\181'8 CHF and LVEF <35%, spironolactone reduced all-causa mol'llllity, sudden death and death due to progression of heart lailura
NEJM 1987; 316:1429-35 NEJM 2001; 344:1651-8 NEJM 2008; 359:2456-2467

Lancet 1999; 353:2001-7
RALES SAVE
NEJM 1999; 341:709-17 NEJM 1992; 327:669-77
Pllliants with LV dysfunction post-MI. long-1Brm captopri 0\181' 3.5y raducad the risk of death due to cardiovascular causes. racurrant Ml, diMIIopment of severe CHF and CHF hospitalization
In mild-to-moderate CHF. shock-art, lCD significantly reduces risk of death_ Amiodarone had no benefit compared with placebo in treating patients with mild-to-moderate CHF In stable chronic CHF with decreased LVEF ( <0.351, long-tenn enelapril reduced death due to al cauS81i and death or hospitalization dua to CHF In patients with LV dysfunction post-MI, long-tenn trandolapril reduced the risk
SCD-HeFT
NEJM 2005; 352:225-237
SOLVD lRACE V-HeFT II
NEJM 1991; 32S:293-302 NEJM 1995; 333:1670-6 NEJM 1991; 32S:303-10
of death or prograssion to severe CHF and reduced risk of sudden death

In chronic CHF, enalapril reduced mortlllity more than hydralazine-isosorbide for at least 2y. Treatment with eilhar enalapril or hydralazin&-isosoltide increased LVEF AtoMstlllin reduces the risk of cardiovascular avants in patients with type 2
DIABETES
CARDS ONTARGET
Lancet 2004; 264:685-96
dabetas
NEJM 2008; 358:154759
In patients with vascular disaase or dillbates without CHF, ternisartan is equally as effective as ramipril with telmisartlln causing a reduced risk of and angioedema, and an inCII!Ised risk of hypotensive symptoms. Contination therapy offers no advallage No significllll di!flJrenca in mortality rates blllwaan rate or rhythm control Encainida or flacainide startlld -15d aftur Ml caused axcas&iva mortality risk. excessive risk of death from arrhythmia in asymptomatic or mildly symptomatic ventricular arrhyttmias after Ml In hypertensive patients >80 y, treatment with indapamide. with or without perindopril, showed atrend towards relative risk of fatal or nan-fatal stroke Hypertensive patients with OM and tight BP control at < 1511/85 mmHg by use of ACEi or beta-blocker reduced risk of diabetic complications and death related to diabetes and reduced risk of end-o111an damage Valsartan group had incidence of Ml than amlodipine IJ"Oup, whereas amlodipine had ahigher incidence of naw onsat diabetes
ARRHYTHMIA
AFFIRM
NEJM 2002; 347:1825-33 NEJM 1989; 321:406-12
CAST
HYPERTENSION
HYVET
NEJM 2008; 358:1887-98
UKHDS (UKPDSI
BMI 1998; 317:703-13
VAWE
lancet 2004; 363:2022-2031
MISCELlANEOUS
JUPITER
NEJM 2008; 359:21952207
Wrlh low to nonnallDL.C and elevated hsCRP, trelllment with rosuvastlllin

sigrificently reduced major cardiovascular avants. NNT with rosuvasllllin for 2 yaars to prevent one primary endpoint = 95
WHI
JAMA 2002; 288:321-333
Estrogan plus progestin tharapy is associated with increased risks of cardiovascular disease and breast cancer but decreased risks of hip fracture and colorectal cancer in postmenopausal women
Toronto Notes 2011
References
References
lllilmic Hlllt U..a Cannon CP., atli.lntBnsivlwrwJs modmltl lipid lllwllrq with llltinslfur IWIII CO!IIIIIry syndmmas.IN 2004;350(15]:141&.504. lindat-1, B, alii. Mnn rJ Mygclnlialllllmage and Inflammation il Relllion to long-Term Mortality in U11513ble CoronJY Arl81y lilee. New England Journal rJ Mlclcina. iml; 343:11391147. at Ill Eplare110111, 1181eetivu in pllianbi wi1h laltwntriwllr dylfunction lflur nnrction.I>EJM 2003; 348(14):130121. llluch, U. et 11. Thrombus Farmlltion on the Alheralicletutic l'lllques: l'lthagenesis and Clrical Coosecpnces. Annlls of Internal Medicine. ZOO I; 134: ZZ4238. Thl Alllrillllsvua6!rimlian Thlrl!ill SUiy lirtUp. eom,.rilon rt CllrOIII1YATIBJY Bypass Slrrllary and Sllllling lor tha Tfllllnlnt of Mulliwllll Dil81st. NIW England Junal rl Madicina. 2001; 344:1 117-1124. TIIJ)ie, A. G. G. and Antrran, E. M.low-Molec:uiiTWeiglrl Hepllrins in the Treltment ol Ai:uleCoronary Syndromes. Arcllioles of Internal Medicine. 2001; 161: 14841490. Yeglimriln1, Y., Brlunllain, J. B., Aibri, A, and Stone, P. H. RIMIM' Article: l)Jmble Anginll'eclllris. Nlw Englllld Journal rl Medicine. 21KKl; 342:101114.
llll:lelrCinlialogy LeeTH and lloul:ller CA. Nori-ive 11151$ in petiente wi1h dlble coronJY TIBrV di !Reviewi.IN 2!KKl;344:1840.5.
Fetlman IW.IIII McNurm. D. MyaciTditis {Review]. NEJM 2000; 343:1388-98.
.....rill
AWAHAZOOZ
percullneoos coranuy intel\1ilrtion. Cin:ulltion. 2001;103:301 H041. ml1'llqlmlll!cipltiiiiiJMth . . . and non-STgmantiiiiVIIion myocardial inflrc1iln (INaillhle at: httpi/wwl't
ICC.CJ19) ACCF/AIIA ZOOI FocUied Update 111 the &idelinesfor the DillgnOiisand Management of lleert Failu11 in AdultJ. Ciralllllim 2009; 119:197721116. AWAHA !Jidllinas furthl m.-gamant rt pltiantl with ST-tlmtion myocardial irrfln:tian: 1 rlpOII ci tha American Collegl of CITdiology/Arrwican HrtAIIociltian Tilt Rlrc;e onl'llclice &idefnee !Cormitt8e to &idainas for tha M1ragernent of Pltianll with Acute Cin:ulltian 2004;
11 O(l]:e8z.292. Antnwl EM at al. Al:.t/AIIA &idalinls for the of Patianll with STaiMtion MyaciTdial HarctiMI surnmuy: ARaport oftlia Amarican College rl C.diology. Ameril:lin He.t Association TIISkFon:e llll'rllctice &idelnes. Cin:ulltion. 2004; 110-588. CCS. ZOO I Canadian cardilll'llc* sociaty con1111u guidalna updata for 1hl1111111gamantand priVInlion ci hllllrtfliU.. Canadian Journal of Cardilklgy. 2001;11(auppE):S.24. GP etal. Clnical Fractice, Diastulic Heertfaii.Jre. NEJM 2004; 351:1097. www.acc.org-The American Colege ci Cardiology (clinicli guidaliles, ate]. www.ccs.ca- CanllliM C.-di01111SCUIIT Sociaty 2005 Co1118naus Confarance Atarial Daa (Draft). www.thahllllrtorv- Cardiololll' Onina ragimtiCII]. www.hllllrMIIwrepeir.nat- Heut VIM Rrpair Online. Beard JD. Clnunic lowar limb ilchanil. BMJ. Fuchs JA. Atherogenesis 1nd the Medal Mlllagemerrt of Atherosclerosis. In Vuc:W1r Suverv 4th edition, Rollert B. Rutherfunl Ell. 1915. WB. Suiders Co, Toronto. pp 222234. Harrilgton RAet al. AntitiiRIIIDitic Tharapylor CoroniJY Artery lilease: tha Saventh ACCP Conlwca an Antithrontoti: 1111 Tlrrornbolytic ThlniP'f. Cllast. Z004; 126 (3suppl]:513a-584a. May J, Whilll GH, end Hlrlis JP. diMinlida ofand1Mscui1T1111Upias. Adv Slrr1135: 153-72. 2001. Schnieder FA and Comero1J. AJ.Intermillent claudication: rt the p!Oblem, petient ei'IUI!ion, end therapeutic str111gies. Am J Card 87 (Supplj: 30-130, 2001. Way LW,IIohartyliM, aditon. Cummt Surgicel Diagnosis lid Tnlltmant, 11th aditiln. Mldcal Bookr,t.lc:Grlw-Hil 2004. SC, C1marun DE. adi1Dn1. Currarll tharepy in thrncjc and cardiCIVUCUIIr mlllbrl. Mc!irMHlilllr1;, 21104.
w-.yECt
Zinelblum, P. JDSellhson. M.lhe EvoMng Role ci AndltDry Arrhythrri1 Monitoring in General Clriiclill'nletie. Annals of lntemll Medicine. 130 (10]. 1911. lradilh AH. lllDcton Ai, HL. AWAHA cilical compatanca Sllt8rnant 111 and entlllltDry a naport oflhl AWAHN ACP-ASI'.'I tiSic.forca on cilical compatanca. Ci'cu11ti011. 104:3161-3118. 2001. Krahn, A, Klein, li, Simes, A. Vee, R. loop Recorder Use for Detection ollntermillent Arrhythrriu. Pacilg and Clinical Electrophysiology 27 (5]. 2004. V., Squires, R, Weistlet A. 1196 Mayo
SlriiiWng AllOT!, T. Bardsley, W, Behrenbeck, T, Christian, T., Clements, 1., Edwards, B., Gibbons, R, Mler, T, Oh, J, l'elikb, P., Foundation forMadical Ellucation and Rll88an:h. 71(1): 43-52. 1996. Gibbon dill. &sn:iA Taring &ideilas. JACe. 30 (I ):ZW-315. 1817.
El:hll:lldiolnphr Pl131o, E. SUess Et:hDCIIdiog!1phy: AhistDrical pqective. AmJ Med. 114;12l-130. 2003. Haatlil, G., Gil as, M. Et:hDCIIdiog!1phy and 1hl gnral plfisician.l'oslgrad Mad. J. IIU;84-88. 2004. Chaitlin, M. ACC/AHA/ASE 2003 Guidalina UpdatB for111a Clinical Applicalim of Echocudiogrlohy: &mnary Articla. Journal rlthi.AmariciJI Sociat.y of Edloclrdiography. 16(10]. 2003. liowd11, R. Khn I. SacchL Uatal R. HisiDry cithl avolub af achocardilgRjllry.lnllrnlltiionli Journal ol Cardiology. 87 (I): 16. 2004.
llll:lelrCinlialogy Sahharwal N. Llhiri, A. Role of m,ocardial parfusiOII rist stratiication il suspactlld or known coroniJY artily di Hllrt. 89:1 2911297. 2003. Baler, G., Zlrat, B. ContriiUin rJ Nuclear Clnliologv to lhgnolii and Prognllliis ol Patian11 wi1h Cornry Arl81y Di111111. Cin:ulation. m.
IR
Kim, WY, atal. CoronaJY magnetic r..onanceangiographylorllla dfldOII of coronBJY "'"" NEJM. 345(26]:1 BSH 2001. Danias, P.,I!OIIssakis, A. loannidis J. Cardiac imaging Diagnostic [)1118nnanca ci coranary magnatic rasonenca angiography as CIIIJ'Illlld against c0111111111io11a rav Amata-nlylis Joulllll of1ha American Colaga rl Clnliologv 44(2]: 1867-1876. 2004.
t:T Milar JM atai.II!Qnoatic of coronary engii!QIIIIhy by &c.- CT. NEJM. 359(22):232436. ZOOS. Schoepf, J., Becker. C., Ohnesorge. B., 'ftlcel K. CT ofCoronuy Artery Disease. Radiology 232:1 &-37. 2004. Sombarg. J. Arrtlytlma Thlnpy.lippincott Wilams & 9(6): 537-542. 2002.

CatiVEPS Hayn, D.. Fu1111111, S. Cardiac Pacing:
References
Toronto Notes 2011
Stnd, Wlllra Wa All, Whn WaAra Going. Joumal oiCardiavucullr 151512004. Zipaa II al. ACC,IAHA Task Farca Raport mr Clinicallntracanliac Bactruphysiolllgicalllld Cathlllllr Ablation l'roc:aUaa. JACC. 26121: 555-513. 1115. Welens, J. CardiiC Anflyt!mias: fur a cure. Journal of tile Ameri:an Colege of Cardii*Jw. 44161: 11551163. 2004. Conti, J. ACC 2005 Anrull Saalion Higillgltt. Criac ArrflythmiiL J011mal al the American Colage of Cartilgy. 451111:1130-1!32. 2005. Kaane, D. NIIW Catheta' Abllltion filrtha T..tmant of Cardiac Anhythmilla. Canliac Bsetrophysiology RIMM. 6:341-348. 2002. Skilnes,A., G.. Krllin, A. Yee, H. Cryallblllion: l'atlntials and l'llllllls.J Cardiavuc 2004. l'llcbt D. Ewlution og Mapping IIIII Allllanic Imaging of Cardiac Arrhy1llriu. Jaumal of Canlowscular Bsetrophysiollgy. 15111. 2004. Zipaa, D. Thayaar in slllclmpllysiology: Joumal altha AmariCUI Collllga of Cardiology. 4317]:1306-1324. 2004. Ryan TJ, fUCIII DP, Gunnar RM, et al. Guidelines for perQjtlneous 11ansum.l lllllioJIIIsty. Are!)Cirt of the American Colege of Cardiolocw!Ameri:an Heart Allocil1ion Task Fan:e on Assaaamant of Dilgnostic and Tllarapeutic C.4iavascul ProcailJRIS 1Subconmt18s on Parcutnous Transum.J Conmaiy Angioplastyl. Cin:uhllion 7812):486-502. 1B88. Bernstein AD. The NASPWBl f'lc:emabrCode. Tl!lC Heart tlstJ.1991; 18141: 21Hll. Garcia TB ud Miller GT. Arrllyttma llecognition: The Art of ln18rprmtion. 2004. Jo1111 & Blrdll:t Publshars, Sud wry, MA. l'ryst!rNsky EN. Bsetropllysiology and Pacing. In: Textboak of CardiMSCUiar Mlllicile Tlird Ecition, Tapa IEJ, HM, l'rystawsky EN, Th1111'11S JD, 2001. W.ms & Wilkins, Phi..._,lil. PA.
PD Eds
l'lrcuWI1011 AII.....IIWI'CI
Glidehs for pertWriaws transliminal coronary angioplalty: a raport of1he American Collga of Cardiology/Am HIITI.Associllion Taak Fon:e on Aslessmant of lliagnoltic and llllrlpautic Cardiovascular l'roc:aUaa Subcommitllla on l'a'eullnllous Transliminal Coronary angiopllllllyl. J Am Call Cardioi.12:5Z9-,'i45. 1988. O'Nail W.lban, S., Grin111, C. Tile in irtBMntional cardiology. J011mal al the American College of Cartilgy. 45 !71:11111134. 2005. Bulae at II. AWSCA&IIXjlllrt coliCirl dacumalll AmariCIII Collllga of Cardiology/Sol:illly for Canlilc Angiography and hlrwntions Clinical Explrt Cansnus Document on Cardiac Cathat8rizlltion l.abolltory smldards. Joumal oltha Amari CUI Collllga of Cardiology. 31181:21702214. 2001. Baim, D. New devices for pen:utlneous coronary iltel'lention are bypaas UQeiY obsolete. lippincott Wluns & 593-517. 2004. Sarruys PW 11: al.l'en:ullna1111s C0Jm11V intaMnlion vmus coronary-llllry hypess QI6'G for IBVfi COIIl!Vf l1llrY disaaaa. Nf.JM. 3601101:96112. 2009. WMY.accJug- The AmariCIII College of lcili:al glidalin111, atcl WMY.theheut.org- CartiJgy Online HIITI Valva lllpeir Dnlina AIIIXIndar Pand Giangola G. Daap wnws thronilolilllld BITIXIIilm: Diagnosis, p1ophyllxil, end traatmant. AM Vase &rg 13: 3111-27, 1191. Beard JD. Chronic bNar iml iidlarnia. BMJ. 2000;320:854.ai7. Bajar HM. Manual of periJpn1ive care in cardiac 3rd ecltion. Maaclllsetls: lllackw!l Si:ielice tic., 1999. Chang DCH, llllrid TE ads. cara in canliac anedh81i and wrgery. Austin: LJndes Bioance, IM. Coularn C/1 and IIIDI Ill Acute lOrtie abnonmities. Semin Roentgenol36: 148-44, 2001. Crawford ES and Crawfurd JL Tluncollbdominll Aartic Aneurysm. In: Vascular surgary: Principles ud Practica 2nd dian, Vaith F.t Hobson RW, Wluns RA,IIIII Wlion SE Edi 1994. MclirwtHilllne, Trndo. Fui:bs JA. Atlle!agenesis d tile Medical Mngement ol Atlierosclerasis. tl VIKullr 4tll edition, Raber! B. Rutherford Ed. 1995. WB Samders Co. Tcronto. pp222234. FniischiiQ JA. Alldoninal Aortic Aneurysms. In: Vucular Principles and Practice 211d elition, Veith F.! Habson RW, Wiliams RA, and Wison SE Eds 11M. McGnrN-IIilllne, Toronto. Hlllatt JN Jr. Alldoninel aortic ll*rfSm: n11urallistory and IJ8IImant. Heart Dis Stroke 1: 3DU, 1992. Hallatt JN Jr. Managsmant of abdominalaortie lii8Ury11111. Mayu Clin Proc 15: 39H, ZDOO. Hlln llJ, Starr A, lluwin FM.Iustrated handbook II canlilll: New York: Sprirver.llerlag tic. 1996. May J, 'Miill GH, and llarrisJP. The complicatione and d!Mnsida ol111diiWIKlilr tharapiaa. Adv Surg35: 15312. 2001. Pitt MPIIlld RS. The nllturallislory oftllOIICic aortic aneurysm disease: An Mrl'iew. J Canl 27G-a 1997. Powall JT ud Brown LC. Thallllurai!Wry of abdominal aortic uaurysma and llllir risk of r\flllll. Adv &nil 35: 113-85, 2001. Roeen CL end Tracy JA. The of lowwllldl'llmity daap venous thrombosis. Em Mad Clin NAm 11: 88S-112. 2001. Schmieder FA and Comenltl AJ. lntemittent cleudic:alian: of the prabhm, patillrl mlllltion, and therlpeutic strdeQies. Am J Canl871Siqlll: 3[}.130, 2001. Venne S. Smilko PE, et al. Clnician Updall1: Shedd radialarbiries be used laWnely far coronary ulely lrt'Pss grafting? 2004;110:e4D-e46. LW, DohertyGM, lliiDI1. CUrrantSuQicalllagnosis and T1111mlnt II til ICition. Lange Medical BookwT'IIcGIIwIIIL 2004. Yang SC, Cameron DE.IChn. CurNnt1herapy in 1hcncic end caniovaacular madicina. McGraw-Hillnc, 2004.
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4 - Toronto Notes 2011 - Cardiology - and - Cardiovascular - Surgery

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c

Cardiology and Cardiovascular Surgery

Toronto Notes 2011

Cardiology and CV Surgery Cl

C2 Cardiology and CV Surgery

Basic Anatomy Review

- diagonal branches left drcumfleJ: artery (I.Cx) - obtuse marginal branches

physiologic R-L shunt

Laft IDDI' dncending (LAD)

Aare 1. Anatomy of tile Coronary Arterl11 (llgld: alterlor oblque pro)ecGon)

PIN- milrlll valva

Camoll- 3ft! dep l'elltblodt JVP tv_..: eii.Mbd

AblaJtI -AliiII A brillion

c Anll .... 211011

CardII: r....-: xdlant anly, llbsarty dMclnt l'rl!rrirrtyd8Qrt. runn.urs 1191

Flg1re Za. Cardiac Cycle

Flgere 2b. Canllac Cycle. JVP Pulle and Cai'GIId Pllsa

'IbroDlo Nota 2011

Buic Anatomy Review

Cardiology and CV SUJ'8ery C3

myocardium canllovascular lnncmdio.n

Cl Ytulg M. IGm 2010

Figun 3. Conduction Systam of the Heart

C4 Cardiology and CV Surgery

Differential Diagnose5 of Common Presentations

Toronto Notes 2011

Differential Diagnoses of Common Presentations

'IbroDlo Nota 2011

Cardiac Diagnostic Testl

Cardiology and CV SUJ'8ery C5

Cardiac Diagnostic Tests

Figura 4. ECG WHeferma 11d Nannll Values

111118 Cllculltianl Examples

Clwmbar rRIII!IIII&ntfhypatrophy lschami.-'lnhuctian

L8ft Ant. Hemiblack lnlllriorMI WPW

RVH l..aftl'oat Hamibhx:k PE

BIMdlld llillplngm Llad Mispl-mant Endocardial CUIIian

t..1anll Ml WF'W Dllldracanlill

C6 Cardiology and CV Surgery

Cardiac Diagnostic Teats

Toronto Notes 2011

Intraventricular Conduction Abnormalities

CampiBIB RBBB QRS duration >120 msec

Deep broad Swaves in leads V1-2

(Left Antcrill' Hemibloc:kl

'IbroDlo Nota 2011

Cardiac Diagnoslic Testl

Cardiology and CV SUJ'8ery C7

mwcl or >3B of the

Figure I. ECG CIJanu wiUJ lm.ctiun

lliffllllllill rl ST Slg..rt n Ellvdan Aculll S'IIMI Vantricl.61r

&n1y rapDIIIrillllion (Normal variant

Ac:UI8 NSTEMI Dr illehlllrlil LVH or RVH with lllrlil

Post-MI STEMI with 111Ciprocal L8ft Dr flight BBB

Tillie 1. Area af lnflln:tion{O wava}/lllchamia (right daminant aiii'IDmy)

Extensivurariar Right verm:le faltsrill" Ml (lillie. with n. Mil

V3, V4 aVL, V3-t I, aVL, Vl-t

Lltlnl lsdatad postarior Ml

C8 Cardiology and CV Surgery

MISCEUANEOUS ECG CHANGES

Dafinilion: IDIIII ORS ha9JI in

hypercalcemia: shortened QT interval hypocalcemia: prolonged QT interval

Thick dl8ll waiVblnwl 4:11811: COPD, obity llenllllizld llde1111 Hypothyrvidi"''frnYodemm