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Coronary Artery Disease (CAD)
o Accumulation of atheromatous plaques within walls of coronary arteries that supply O2 to myocardium
+ Blood flow causes ischemia of myocardial cells due to lack of oxygen
- Effects of ischemia reversible if blood flow to heart improved
Complete occlusion of artery causes irreversible cell death called myocardial infarction
o Risk Factors:
DM, HTN, tobacco, age >45, hyperlipidemia, | LDL, + HDL,| homocysteine
FHx of premature CAD or MI in 1
-degree relative men <45yrs & women <55yrs
o Clinical Presentation Asymptomatic, stable angina, unstable angina, MI, sudden cardiac death
o Canadian Cardiovascular Society (CCS) Angina Classification:
Class I Angina w/strenuous or rapid activity no angina from ordinary physical activity
Class II Slight limitation of ordinary activity angina after >2 blocks or >1 flight of stairs
Class III Marked limitation of ordinary activity angina after <2 blocks or <1 flight of stairs
Class IV Any physical activity causes discomfort angina may be present at rest
o Diagnosis:
Resting ECG:
- Prior MI Q waves
- UA ST segment or T-wave abnormalities seen during episode of chest pain
Stress ECG:
- Recording ECG before, during & after exercise on treadmill
- 75% sensitive only if able to exercise sufficiently to reach 85% of predicted maximum HR
o Predicted maximum HR = 220 Patients age
- Should undergo cardiac catheterization if results from stress test
- Positive findings for CAD:
o ST elevation Transmural infarct
o ST depression Subendocardial ischemia
o Failure to exercise >2mins due to symptoms
o Hypotension
o Ventricular arrhythmia
Stress Echocardiography:
- Performed before & immediately after exercise preferred over stress ECG
- More sensitive in detecting ischemia, can assess LV size, EF & diagnose valvular disease
- Ischemia evidenced by wall motion abnormalities not seen at rest akinesis or dyskinesis
- Should undergo cardiac catheterization if test results
Myocardial Perfusion Imaging (MPI):
- Stress test preformed after injection w/radioisotope Thallium-201 or Technetium-99
- Nuclear imaging obtained immediately after exercise & again after 4hrs
- Viable cells extract radioisotope from blood no uptake means no perfusion to area
- MPI can assess myocardial viability by detecting perfusion, ventricular volume & EF
o Reversible ischemia Impaired perfusion only during stress
o Infarction Impaired perfusion at rest & during stress
- MPI has best sensitivity & specificity of exercise stress tests but more expensive
Pharmacologic Stress:
- If unable to exercise administer IV agents to stimulate myocardial function
- Dobutamine | Myocardial O2 demand by | HR, | BP & | contractility
- Adenosine & Dipyramidole Vasodilation actually causes + flow to coronary arteries
Holter Monitoring Ambulatory ECG useful in detecting silent ischemia
Cardiac Catheterization & Coronary Angiography:
- Most accurate way of identifying severity of vessel involvement indicated in following:
o After positive results from any stress test
o If revascularization or other surgical intervention being considered
o Angina difficulty diagnosing, refractory to medical therapy, occurring after MI
o Severely symptomatic requiring urgent diagnosis & management
o Evaluation of valvular disease to determine need for surgical intervention

o Treatment:
Risk Factor Modification:
- Smoking cessation 50% reduction in CAD risk 1yr after quitting
- HTN control esp. diabetics
- Hyperlipidemia low-fat diet & HMG-CoA reductase inhibitors
- DM strict glycemic control to reduced vascular disease risk
- Exercise & Weight loss also modifies other risk factors like DM, HTN, hyperlipidemia
- Diet + intake of saturated fat (<7% total calories) & + cholesterol (<200 mg/day)
Pharmacologic Management:
- Aspirin + Morbidity & + risk of MI indicated in all pts. w/CAD
o Clopidogrel If ASA contraindicated or in combination w/ASA
- -blockers + O2 demand via + HR, + contractility, + BP
o + Mortality risk shown to reduce frequency of coronary events
o Cardioselective agents preferred Metoprolol, Atenolol, Carvedilol
Avoids inhibition of peripheral vasodilation & bronchodilation via |2
- Nitrates + O2 demand via vasodilation + preload, + afterload, | coronary perfusion
o Symptomatic control of angina only no impact on survival
o Tachyphylaxis prevent tolerance by maintaining daily nitrate-free intervals
- CCBs + O2 demand via coronary vasodilation + afterload, | coronary perfusion
o 2
line when -blockers or Nitrates not fully effective
o Caution: Verapamil/Diltiazem + |-blockers may cause bradycardia or AV block
- ACEIs Not used to treat symptomatic CAD indicated in CHF, HTN, DM, LV dysfunction
- Percutaneous Coronary Intervention (PCI):
o PTCA indicated in moderate one- or two-vessel disease w/normal EF:
Medically refractory angina
NSTEMI/UA w/TIMI risk score 3
Primary PCI for STEMI
o Restenosis rates up to 40% within first 6 months stents significantly + rates
- Coronary Artery Bypass Grafting (CABG):
o Indicated in severe multi-vessel disease w/+ EF or comorbid DM:
Left main artery disease
Triple-vessel disease w/+ LV function
Two-vessel disease w/proximal LAD stenosis
Failed or contraindicated PTCA
- Thrombolysis t-PA, Streptokinase, Urokinase, Anistreplase, Alteplase, Reteplase
o Indications STEMI <12hrs after symptom onset or when PCI not viable option
Administer as soon as possible preferably 3hrs after onset
Not indicated for NSTEMI or UA as artery not occluded
o Absolute contraindications:
Active bleeding - Malignant IC neoplasm
Prior intracranial hemorrhage - Prior stroke (3 months)
Recent head trauma (3 months) - Suspected aortic dissection
o Relative contraindications:
HTN sBP >180 or dBP >110 - Current anticoagulation use
Recent major surgery (3wks) - Active peptic ulcer

Chronic Stable Angina
o Symptom complex resulting from imbalance between oxygen supply & demand in myocardium
o Often due to fixed stenosis caused by atheroma O2 demand exceeds available blood supply
Goal of treatment to + myocardial O2 demand & | O2 supply
o Pathophysiology:
Factors influencing supply Luminal diameter (most important), duration of diastole, Hb, SaO2
- + Myocardial O2 supply atherosclerosis, vasospasm, hypoxemia, tachycardia, anemia
Factors influencing demand HR, contractility, wall stress
- | Myocardial O2 demand tachycardia, AS, myocardial hypertrophy, hyperthyroidism
o Clinical Presentation:
Chest pain Retrosternal tightness radiating to left ( right) shoulder, arm, neck or jaw

- Precipitated by the 3 Es 1) Exertion, 2) Emotion, 3) Eating
- Brief duration pain lasts <15mins w/relief after rest or nitrates
Anginal equivalents Dyspnea, diaphoresis, acute LVF, flash pulmonary edema
Levines sign Clutching fist over sternum when describing chest pain
o Diagnosis Resting ECG Normal
o Treatment See Pharmacologic Management of CAD

Unstable Angina (UA)
o Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion
Oxygen demand unchanged but + O2 supply 2
to reduced resting coronary flow
o UA defined by any of the following:
Angina at rest
New-onset angina
Accelerating pain pattern | frequency, | duration, | pain intensity
o Diagnosis & Treatment See NSTEMI section below

Prinzmetals (Variant) Angina
o Transient coronary vasospasm 75% ass. w/fixed atherosclerotic lesion
o Clinical Presentation Intermittent angina at rest pain not provoked by exertion
o Diagnosis:
ECG Hallmark is transient ST elevation during chest pain represents transmural ischemia
Coronary Angiography Definitive test shows coronary vasospasm after IV Ergonovine
o Treatment Vasodilation via Nitrates & CCBs

Myocardial Infarction (MI)
o Due to coronary atherosclerosis w/superimposed thrombus on ruptured plaque
o Classification:
1) Non-ST Elevation Myocardial Infarction (NSTEMI):
- Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion
- Oxygen demand unchanged but + O2 supply 2
to reduced resting coronary flow
- Defined by presence of 2/3 criteria:
o Symptoms of angina or ischemia
o Rise & fall of serum MI markers absent enzyme markers in UA
o Ischemic ECG changes without ST elevation or new LBBB
- NSTEMI & UA categorized together due to similar etiology & presentation
2) ST Elevation Myocardial Infarction (STEMI):
- Acute plaque rupture & thrombosis w/total vessel occlusion causing myocardial necrosis
- Defined by new ischemic ECG changes + 1 or both of ischemic Sx. & | cardiac enzymes
o ECG ST elevation in 2 contiguous leads or new BBB either LBBB or RBBB
o Clinical Presentation:
Chest pain, dyspnea, diaphoresis, weakness, fatigue, N/V
- Pain similar to angina but more intense & longer duration
- Up to 1/3 asymptomatic painless infarcts
o Diagnosis:
ECG Markers for ischemia/infarction include:
- Peaked T-waves occur very early & may be missed
- ST elevation transmural injury of entire wall thickness (can be Dx. of acute infarct)
- ST depression subendocardial injury involving inner half of wall
- Q-waves seen later as specific evidence of necrosis (not seen w/NSTEMI)
- T-wave inversion sensitive but not specific
Cardiac Enzymes Diagnostic gold standard for myocardial injury
- Creatine Kinase-MB (CK-MB):
o | CK-MB within 4-8hrs w/peak at 24hrs returns to normal after 48-72hrs
o Sensitivity & specificity >95% if measured within 24-36hrs of onset of chest pain
o CK & CK-MB should be measured on admission & every 8hrs over 24hr period
- Troponin I & T:
o | Troponin within 3-5hr w/peak at 24-48hrs returns to normal after 5-14 days
o Greater sensitivity & specificity than CK-MB for myocardial injury

Troponin I can be falsely elevated in renal failure
o Troponin should be measured on admission & every 8hrs over 24hr period
- Creatinine Phosphokinase (CPK) Elevated within 4-8hrs but nonspecific
- Myoglobin Elevated within 1hr but nonspecific
o TIMI Risk Score:
1 point for each criteria met:
- Age >65 yrs - At least 2 anginal episodes in last 24hrs
- | Serum cardiac biomarkers - ASA use in prior 7 days
- Presence of 3 or more CAD risk factors - Prior coronary stenosis 50%
- ST segment deviation on admission ECG
Risk of all cause mortality at 14 days:
- 0-1 points = 4.7%
- 2 points = 8.3%
- 3 points = 13.2 %
- 4 points = 19.9%
- 5 points = 26.2%
- 6-7 points = 40.9%
o Treatment:
Management of NSTEMI:
- Initial O2 + NTG + |-blockers + ASA Morphine
- Clopidogrel Initiate w/ASA 300mg loading dose & 75mg daily
o Avoid use if emergency CABG likely discontinue 5 days before CABG
- Heparin For all pts. w/MI does not dissolve clots only prevents future formation
o LMWH preferred except in renal failure or if CABG planned within 24hrs
- GP IIb/IIIa inhibitors Abciximab, Eptifibatide, Tirofiban
o If undergoing PCI or at high-risk ex. | Troponin, TIMI >4, DM
- Invasive Early coronary angiography & revascularization
o Indicated w/following high-risk indicators:
Recurrent or persistent pain refractory to medical therapy
LV dysfunction EF <40%
TIMI risk score 3
Sustained VT or dynamic ECG changes
High-risk findings on non-invasive stress testing
PCI within previous 6 months
o Thrombolysis is NOT indicated for NSTEMI or UA!
Management of STEMI:
- Initial O2 + NTG + |-blockers + ASA Morphine
- Invasive Emergency reperfusion indicated if <12hrs from symptom onset
o PCI Preform <90mins (EMS-to-balloon) after first medical encounter
Advantages over thrombolysis:
- + Mortality rate & + rate of MI reoccurrence
- + Risk of intracranial hemorrhage
- 90% success rate vs. 60% w/thrombolytics
o Thrombolysis Preform <30mins (EMS-to-needle) after first medical encounter
Generally preferred if given <3hrs after symptom onset
Indicated if PCI contraindicated or unable to preform PCI within 90mins
o CABG Indicated if >12hrs after symptom onset or failed PCI
- Adjunctive medical therapy:
o Clopidogrel 300-600mg loading dose & 75mg daily
Avoid use if emergency CABG likely discontinue 5 days before CABG
o Heparin Initial bolus of UF advised while in transit to catheterization lab
LMWH preferred except renal failure or if CABG planned within 24hr
o GP IIb/IIIa inhibitors If undergoing primary PCI
Avoid use if initiating thrombolytic therapy due to | risk of bleeding
Outpatient Management:
- Aspirin 81-162mg QD
- |-blockers Metoprolol 25-50mg BID or Atenolol 50-100mg QD
o CCBs If |-blockers contraindicated in absence of severe LV dysfunction
Use non-dihydropyridine CCBs Diltiazem or Verapamil
- Clopidogrel 75mg QD x 1-12 months at least 12 months if stent placed
- Nitrates Alleviates pain caution in right-sided MI pts. who are preload dependent

- Warfarin If high risk of systemic thromboembolism A-Fib, CHF, LV thrombus
- ACEIs Prevents adverse ventricular remodeling CHF, + LVEF <40%, anterior MI
o ARBs if contraindicated or intolerant to ACEIs
- Statins Early & intensive therapy
o Complications:
CHF MCC of in-hospital mortality if severe may lead to cardiogenic shock
Myocardial ruptures:
- Free wall rupture 90% occur within 2wks MC after 1-4 days w/90% mortality rate
o Often leads to hemopericardium & cardiac tamponade
o Treat w/immediate pericardiocentesis & surgical repair
- Interventricular septum rupture Occurs within 10 days after MI
o Emergent surgery indicated likelihood of survival correlates w/size of defect
- Papillary muscle rupture Leads to MR if suspected obtain ECHO immediately
o Emergent surgery & mitral valve replacement usually necessary
o Reduce afterload via Sodium nitroprusside or intra-aortic balloon pump (IABP)
- Ventricular pseudoaneurysm Incomplete free wall rupture contained by pericardium
o Surgical emergency likely to progress to free-wall rupture
- Ventricular aneurysm Rarely rupture in contrast to pseudoaneurysms
o Associated w/| incidence of ventricular tachyarrhythmias
o Medical management may be protective or surgery if aneurysm severe
- VT Within 48hrs of MI usually due to myocardium reperfusion
- Bradycardia Usually from inferior wall MI seen in early stages
o May be protective mechanism causing + O2 demand treat w/Atropine
- AV block Due to ischemia of conduction tracts
o Inferior wall MI 1
degree or 2
degree (type I) block no treatment
o Anterior wall MI 2
degree (type II) or 3
degree block requires pacemaker
Recurrent infarction Extension of existing infarction or re-infarction of new area
- Suspect if repeat ST elevation on ECG within first 24hrs after infarction
Acute pericarditis Treat w/Aspirin
Dressler's syndrome Autoimmune inflammatory reaction occurring weeks to months after MI
- Consists of fever, malaise, pericarditis, leukocytosis & pleuritis treat w/NSAIDs

Congestive Heart Failure (CHF)
o Failure of heart to pump blood effectively to tissues heart can not meet demand of body
o Pathophysiology:
Systolic dysfunction Impaired ventricular ejection + LVEF + + SV = + CO
- Findings apex beat displaced, S3, cardiomegaly, + LVEF, LV dilatation
- Due to impaired myocardial contractility MI, HTN, DM, alcohol, myocarditis, DCM
Diastolic dysfunction Impaired ventricular filling during diastole w/normal EF MC in elderly
- | LV filling pressures produce upstream pulmonary & systemic venous congestion
- Findings HTN, apex beat sustained, S4, normal-size heart, LVH, normal LVEF
- Due to decreased compliance:
o Transient Ischemia relaxation of myocardium is active & requires ATP
o Permanent Hypertrophy (HTN, AS, HCM), RCM, MI
High-Output HF | CO demand + thiamine, hyperthyroid, A-V fistula, L-R shunt, Pagets, CRF
o Etiology:
Most common CAD, HTN, valvular (AS, AR, MR), EtOH (DCM)
Less common:
- Toxic anthracyclines, radiation, uremia, catecholamines
- Infectious Chagas, Coxsackie, HIV
- Endocrine Hyperthyroidism, DM, acromegaly
- Infiltrative sarcoidosis, amyloidosis, hemochromatosis
- Genetic HCM, Friedreichs ataxia, muscular dystrophy, congenital heart disease
- Metabolic thiamine or selenium deficiency

o Clinical Presentation:
LHF Pulmonary venous congestion
- Cool extremities, slow capillary refill, peripheral cyanosis
- Syncope, DOE, systemic hypotension, tachycardia, pulsus alternans
- Orthopnea SOB while laying flat & relived by elevation of head w/pillows
- Paroxysmal nocturnal dyspnea (PND) causes night time awakenings
- Auscultation:
o Displaced PMI usually to left due to cardiomegaly
o S3 ventricular gallop due to rapid filling into noncompliant LV
May be normal finding in children
o Crackles/rales at lung bases indicates pulmonary edema
o Dullness to percussion & + tactile fremitus of lower lung due to pleural effusion
RHF Systemic venous congestion
- MCC of RHF is LHF can mimic LHF if + RV output leads to LV under-filling
- Cyanosis, peripheral edema, JVD, Kussmauls sign
- Nocturia due to | venous return w/elevation of legs
- Hepatomegaly hepatojugular reflex RUQ pain due to hepatic congestion
- Auscultation S3 (right-sided), right ventricular heave, tricuspid regurgitation
- RHF can present similar to cirrhosis but w/cirrhosis no JVD or trouble lying flat
o New York Heart Association (NYHA) Classification:
Class I Nearly asymptomatic symptoms only w/vigorous activities
Class II Slight limitation of activities symptoms w/moderate exertion (ex. climbing stairs)
Class III Markedly limiting symptoms w/normal activities of daily living (ex. walking)
Class IV Incapacitating symptoms occur at rest
o Diagnosis:
CXR Cardiomegaly, pleural effusion, Kerley B-lines, bronchiolar-alveolar cuffing
ECHO Assess LV function via LVEF helps distinguish systolic from diastolic dysfunction
- Initial test of choice preform when CHF suspected based on PE findings or CXR
ECG Nonspecific may show chamber enlargement, arrhythmia, ischemia/infarction
Radionuclide Angiography (MUGA) Precise measurement of left & right ventricular EF
- RBCs tagged w/radioisotope & imaged during exercise & rest
- Useful when ECHO suboptimal or more precise assessment of LVEF needed
- Can also assess wall motion abnormalities in ischemic heart disease
| BNP Secreted by ventricles due to LV stretch & wall tension
- Basic natriuretic peptide precursor cleaved into proBNP & secreted into ventricles
- proBNP cleaved into active C-terminal portion & inactive NT-proBNP portion
o HF suggested if NT-proBNP >450pg/mL
o Treatment:
Diet Sodium restriction initially <4g/day
Diuretics No effect on prognosis or mortality Furosemide is most potent diuretic
ACEIs + Mortality & prolongs survival venous & arterial dilation = + preload & + afterload
- Diuretics + ACEI is initial treatment in most symptomatic cases
- ACEIs given to all pts. w/systolic dysfunction even if asymptomatic
- Start w/low dose to prevent hypotension monitor BP, K
, BUN, Cr
-Blockers + Mortality in pts. w/post-MI heart failure
- Slows progression of heart failure by slowing down tissue remodeling
- Use cautiously & titrate slowly as may initially worsen CHF
ARBs 2
line only if unable to tolerate ACEIs
Hydralazine & Isosorbide Dinitrates 2
line only if unable to tolerate ACEIs
- Less effective on reducing mortality compared to ACEIs
Digitalis No effect on mortality only symptomatic relief
- Consider use if EF <30%, severe CHF, or severe A-fib
o Management Guidelines:
Mild (NYHA Class I to II) Na
restriction + ACEI Loop diuretic
Moderate (NYHA Class II to III) Loop diuretic + ACEI |-blocker
Severe (NYHA Class III to IV) Loop diuretic + ACEI + Digoxin
- Add Spironolactone if class IV & still symptomatic despite above treatment

o Complications:
Acute Pulmonary Edema (APE) Caused by rapid decompensation of LV function
- Precipitants dysrhythmias, MI, medication noncompliance, | Na
load, + inotropy
- Treatment NOMAD: NTG, Oxygen, Morphine, Aspirin, Diuretic
Paroxysmal Nocturnal Dyspnea (PND) Brief SOB that awakens pt. from sleep treat w/NOMAD
- Due to | volume load when lying horizontal or sudden + in myocardial contractility
o Results in pulmonary edema causing impaired exchange of oxygen
- Improvement w/walking & no response to bronchodilators differentiates from asthma

o Etiology:
Viral Coxsackie B (MCC), Echovirus, HIV, CMV, Influenza, EBV, HBV, Adenovirus
Bacterial S. pyogenes, C. diphtheriae, Meningococcus, B. burgdorferi, M. pneumoniae
Parasitic T. cruzi (Chagas), Toxoplasma, Trichinella, Echinococcus
Systemic Kawasakis, SLE, sarcoidosis, acute RF
Toxic Catecholamines, chemotherapy, cocaine
Hypersensitivity Antibiotics, diuretics, lithium, clozapine, insect/snake bites
o Clinical Presentation:
Varies from asymptomatic to fulminant cardiac failure & death
- Acute CHF dyspnea, rales, peripheral edema, JVD
- Chest pain due to pericarditis or cardiac ischemia
- Fever, preceding URI, palpitations, arrhythmias, syncope
Auscultation S3/S4, MR, TR, friction rub if pericardium involved
o Diagnosis:
Labs Leukocytosis, | ESR, | CK, | Troponin I check cultures, viral titers & cold agglutinins
ECG ST changes, dysrhythmias, conduction disturbances
CXR Often normal cardiomegaly or pulmonary venous congestion
ECHO Dilated chambers, hypokinetic wall movements, pericardial effusion
Myocardial Biopsy
o Treatment:
CHF ACEIs + necrosis & inflammation also address any underlying causes
Dysrhythmias Digoxin use cautiously as effects may be exaggerated by inflamed myocardium
IVIG May be of benefit
Contraindicated Immunosuppressives (ex. steroids, cyclosporine, NSAIDs)

Dilated Cardiomyopathy (DCM)
o Dilation & impaired systolic function of one or both ventricles MC type of cardiomyopathy
o Etiology:
MCC CAD w/prior MI
Infectious Coxsackie B, HIV, chagas, lyme disease, rickettsial, acute RF, toxoplasmosis
Toxic Alcohol, cocaine, doxorubicin, chloroquine, clozapine, heavy metals (Pb, Hg, Cb)
Endocrine DM, hyper/hypothyroidism, pheochromocytoma, acromegaly
Metabolic Uremia, hypocalcemia, hypophosphatemia, + thiamine (wet-beriberi), + selenium
Neuromuscular Duchennes, myotonic dystrophy, Friedreichs ataxia
Collagen SLE, PAN, dermatomyositis, progressive systemic sclerosis
Other Uncontrolled tachycardia (persistent A-Fib), peripartum cardiomyopathy, FHx in 20%
o Clinical Presentation:
CHF dyspnea, rales, peripheral edema, JVD
Arrhythmias can be fatal causing sudden death
Angina due to | O2 demands of enlarged ventricles
Emboli systemic or pulmonary & may present w/neurologic deficits
Auscultation S3/S4 gallop (stiffened ventricular walls), regurgitant valves (MR, TR), rales
o Diagnosis:
Labs | BNP, | Cr, | LFTs, + HCO3, + Na

ECG ST & T-wave abnormalities, conduction defects (BBB), arrhythmias (VT, A-Fib)

CXR Global cardiomegaly & pleural effusion
ECHO Enlarged chambers, global hypokinesis, + LVEF, MR, TR, mural thrombi
Angiography To exclude ischemic heart disease in certain cases
o Treatment:
Initial Address underlying cause & treat CHF accordingly
Warfarin Thromboembolism prophylaxis indications:
- A-Fib, previous thromboembolism, documented thrombus, LVEF <30% (controversial)
ICD Consider if life-threatening dysrhythmias
Surgical Consider in severe, refractory cases ex. LVAD, volume reduction, heart transplant
Vaccination Influenza & S. pneumoniae
o Prognosis 20% mortality in 1
year & 10% per year after often due to CHF, arrhythmias or emboli

Restrictive Cardiomyopathy (RCM)
o Impaired ventricular filling 2
to myocardial stiffening, fibrosis or + compliance
Usually intact systolic function w/non-dilated & non-hypertrophied ventricle
o Etiology:
Cardiac Endomyocardial fibrosis, Loefflers endocarditis, radiation heart disease
Other Carcinoid syndrome, amyloidosis, sarcoidosis, hemochromatosis, Gauchers, Hurlers
o Clinical Presentation:
CHF commonly present w/dyspnea & exercise intolerance (RHF usually predominates)
- Arrhythmias, | JVP, Kussmauls sign, thromboembolic events
Auscultation S3, S4, MR, TR
o Diagnosis:
ECG Low voltage, non-specific ST/T-wave changes, conduction abnormalities (left BBB)
CXR Enlarged atria & pulmonary venous congestion
ECHO LAE, RAE, normal sized ventricles, thicken myocardium, MR or TR
- May see speckled appearance if amyloid cause
Cardiac Catheterization Reveals | end-diastolic ventricular pressures
Endomyocardial Biopsy May detect eosinophilic infiltration or myocardial fibrosis
- Can also help distinguish RCM from constrictive pericarditis
o Treatment:
Initial Address underlying cause & treat CHF accordingly
A-Fib Anticoagulation + HR control
Permanent pacemaker If complete heart block
Heart transplant Consider in refractory cases

Hypertrophic Cardiomyopathy (HCM)
o Unexplained ventricular hypertrophy not caused by systemic HTN or AS
Often involve asymmetric pattern of hypertrophy MC is septal hypertrophy
o Etiology 50% inherited defect in cardiac sarcomeric proteins auto. dominant w/variable penetrance
o Pathophysiology:
Hypertrophic Obstructive Cardiomyopathy (HOCM) Dynamic LVOT obstruction
- Systolic flow draws anterior leaflet of mitral valve into tract via Bernoulli effect
o Causes dynamic left ventricular outflow tract obstruction
- Outflow obstruction can cause left atrial dilatation, A-Fib, CHF, RHF
- | LVEDV = + Obstruction | Blood volume, negative inotropes, | peripheral resistance
Diastolic dysfunction Impaired ventricular filling 2
to LVH which reduces compliance
o Clinical Presentation:
Asymptomatic Screening important
Angina At rest or during exercise usually unresponsive to NTG
- May respond to recumbent position pathognomonic (but rare)
Syncope After exertion or Valsalva maneuver
CHF Dyspnea, rales, peripheral edema, JVD
Arrhythmias A-Fib or VT sudden death in HCM usually due to arrhythmia
- Harsh systolic ejection murmur at LLSB w/S4 2
to LVOT obstruction
o Enhanced by + LVEDV Standing position or Valsalva maneuver

HCM is one of few murmurs that diminishes w/squatting (| LVEDV)
- Paradoxical splitting of S2 Pulmonic valve closes before aortic valve
o Inspiration will delay pulmonic closure & cause paradoxical narrowing of split
- Pansystolic murmur due to MR
Pulses Rapid upstroke & bifid carotid pulse
Precordial palpation PMI localized & triple apical impulse
o Diagnosis:
ECG LVH, PVCs, A-Fib, prominent Q-waves, high voltages across precordium
ECHO Septal hypertrophy, LVH, systolic anterior motion of mitral valve, MR
Cardiac Catheterization Preform if considering invasive therapy
o Treatment:
Preventative Avoid factors that | obstruction esp. volume depletion & strenuous exertion
Pharmacologic management:
- |-blockers Disopyramide + HR, | LV filling time, + inotropy
- CCBs (Verapamil) 2
line only in pts. without resting or provocable obstruction
- Avoid ACEI, Nitrates, Diuretics + preload will worsen obstruction & symptoms
Refractory cases Septal myectomy or Septal ethanol ablation or Dual chamber pacing
Ventricular arrhythmias Amiodarone or ICD
Screening 1
degree relatives of HCM pts. screened via physical, ECG & 2D-ECHO
- Screen annually during adolescence then serially every 5yrs
o Complications:
MCC of sudden cardiac death (SCD) in young athletes
- Factors ass. w/| risk of SCD:
o Syncope or non-sustained VT
o Marked ventricular hypertrophy max. wall thickness 30mm
o Abnormal BP response to exercise in young pts.

o Etiology:
Idiopathic Usually presumed to be viral MCC is Coxsackie virus
Infectious Coxsackie, Echovirus, S. pneumoniae, S. aureus, TB, Histoplasmosis, Blastomycosis
Acute post-MI Direct extension of myocardial inflammation seen after 1-7 days
Dresslers syndrome Autoimmune response to infarcted myocardium seen after 2-8wks
Trauma Post-cardiac surgery (ex. CABG)
Metabolic Uremia (common), hypothyroidism
Malignancy Hodgkins, breast, lung, renal cell carcinoma, melanoma
Collagen SLE, polyarteritis, RA, scleroderma
Drugs Hydralazine, Procainamide, Isoniazid
Other Radiation, dissecting aneurysm
o Clinical Presentation:
Recent viral URI fever
Pleuritic chest pain alleviated by sitting up & leaning forward
- Does not respond to NTG pain aggravated by lying supine, coughing, swallowing
Auscultation pericardial friction rub on expiration is pathognomonic (but variably present)
o Diagnosis:
ECG Diffuse ST elevations, PR depressions (specific), low voltage
CXR Normal sized heart & pulmonary infiltrates
ECHO To assess for pericardial effusion
Diagnostic triad 1) Chest pain, 2) Friction rub, 3) ECG changes
o Treatment:
Self-limited Most cases resolve in 2-6wks
NSAIDs Mainstay of therapy to relieve pain & + inflammation
Steroids For intractable cases (ex. Dresslers)
o Complications Recurrence, atrial arrhythmia, pericardial effusion, tamponade, constrictive pericarditis


Pericardial Effusion
o Etiology:
Transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism
Exudative (serosanguinous or bloody) Causes similar to acute pericarditis
- May develop acute effusion 2
to hemopericardium trauma, post-MI rupture, dissection
o Clinical Presentation:
Asymptomatic can also present similar to acute pericarditis
Dyspnea, cough, | JVP w/dominant x descent, + pulse pressure
Esophageal/recurrent laryngeal/tracheo-bronchial/phrenic nerve irritation
Auscultation distant heart sounds rub
o Diagnosis:
ECHO Procedure of choice shows fluid in pericardial sac
ECG Low voltage & flat T-waves
CXR Cardiomegaly, rounded cardiac contour (water bottle appearance)
Pericardiocentesis Identify transudate vs. exudate, infectious agents, neoplastic involvement
o Treatment:
Mild effusion Frequent observation w/serial ECHOs + Anti-inflammatory agents
Severe effusion Pericardiocentesis may develop cardiac tamponade

Pericardial Tamponade
o Due to rapid accumulation of fluid in pericardial sac impairs cardiac filling leading to + CO
o Etiology Pericarditis, trauma, post-MI rupture, aortic dissection w/rupture, malignancy, uremia
o Clinical Presentation:
Becks Triad 1) Hypotension, 2) Muffled heart sounds, 3) JVD
Other dyspnea, tachypnea, tachycardia, peripheral edema
Pulsus Paradoxus + sBP by >10 mmHg w/inspiration due to + stroke volume
- Transiently enlarged RA bulges leftward causing + LV volume & output
Auscultation distant heart sounds
o Diagnosis:
ECG Electrical alternans pathognomonic variation in R-wave amplitude
ECHO Pericardial effusion & compression of cardiac chambers (RA & RV) in diastole
o Treatment:
Pericardiocentesis Preform immediately if unstable
| Fluids To expand volume & | CO avoid diuretics & vasodilators
Pericardiotomy Pericardial window created to allow drainage

Constrictive Pericarditis
o Chronic pericarditis resulting in fibrosed, thickened, adherent or calcified pericardium
o Etiology Any cause of acute pericarditis may result in chronic pericarditis
Idiopathic, viral, TB, radiation (worst prognosis), post-cardiac surgery, uremia, MI
o Clinical Presentation:
Dyspnea, tachycardia, palpitations, JVD, normal BP, absent pulsus paradoxus
Kussmauls sign failure of jugular venous pressure to fall during inspiration
May mimic CHF (esp. RHF) ascites, hepatosplenomegaly, edema
Auscultation distant heart sounds
Precordial pericardial knock (early diastolic sound)
o Diagnosis:
ECG Low voltage, T-wave flattening or inversion, notched P-waves
CXR Pericardial calcification & effusions
ECHO/CT/MRI Pericardial thickening
Cardiac Catheterization Equalization of end-diastolic chamber pressures diagnostic
o Treatment Diuretics + Na
restriction if unresponsive consider Pericardiectomy

Mitral Stenosis (MS)
o Etiology MCC is RHD MC in females & congenital MS rare cause
o Clinical Presentation:
DOE, orthopnea, fatigue, palpitations, PND
Pulmonary HTN peripheral edema, cough, hemoptysis
Dysphagia & hoarseness enlarged LA impinging on esophagus & recurrent laryngeal nerve
A-Fib dilation of left atrium major cause of A-fib
Systemic emboli due to blood stagnation in enlarged LA
Absent a wave on JVP, sternal lift due to RVH, + pulse pressure, loud
Auscultation OS after S2 w/mid-diastolic rumble at apex best heard over LSB
- Murmur enhanced by | LA return esp. expiration
- Long murmur & short A2-OS interval correlate w/severe MS
o Diagnosis:
ECHO Thickening of MV leaflets
CXR LAE w/straight left heart border, kerley B-lines (pulmonary effusion), large PA
o Treatment:
Diuretics & Na
Digitalis To control ventricular rate in A-Fib
Anticoagulation If atrial thrombus or A-Fib present
Balloon valvuloplasty Standard of care indicated in symptomatic pts. w/orifice 1.2cm

- Alternatives Mitral commissurotomy or Valve replacement

Mitral Regurgitation (MR)
o MR + CO | LV/LA pressure LV/LA dilatation CHF + Pulmonary HTN
o Etiology:
MCC is mitral valve prolapse (MVP)
Endocarditis, rheumatic fever, LV dilatation/aneurysm, Marfans, HOCM
MV annulus calcification or chordae/papillary muscle rupture
o Clinical Presentation:
Dyspnea, PND, orthopnea, palpitations, peripheral edema, cough
Auscultation loud holosystolic murmur at apex w/radiation to axilla & S3
- Murmur enhanced by expiration or | TPR
o Diagnosis:
ECHO Shows diseased or prolapsed valve
Swan-Ganz Catheterization Prominent V wave due to systolic overload on LA
o Treatment:
Asymptomatic Serial ECHOs
Diuretics To + preload & improve CO
Vasodilators To + afterload which favors aortic exit esp. ACEIs
Surgery Indicated in acute MR w/CHF or if signs of LV dysfunction
- Valve repair Annuloplasty rings, leaflet repair, chordae transfers/shorten/replacement
o Advantages low rate of endocarditis, no anticoagulation & less reoperation
- Valve replacement If failed repair or heavily calcified annulus

Mitral Valve Prolapse (MVP)
o MV displaced into LA during systole MC valvular disorder w/90% of cases in women
o Pathophysiology:
Myxomatous degeneration of chordae due to defect in connective tissue proteins
- Due to Marfans, Ehlers-Danlos, RHD, pectus excavatum
o Clinical Presentation:
Asymptomatic Stabbing chest pain, dyspnea, palpitations, presyncope, systemic emboli
Auscultation Mid-systolic click followed by late-systolic high-pitched murmur at apex
- Murmur enhanced by + venous return valsalva or squat-to-stand maneuver
- Click due to tensing of mitral leaflet - + preload will move click closer to S1

- Other findings Wide splitting of S2 or S3
o Diagnosis:
ECG Non-specific ST & T-wave changes, paroxysmal SVT, ventricular ectopy
ECHO Systolic displacement of thickened MV leaflets into LA
o Treatment:
Asymptomatic No treatment
Symptomatic |-blockers & avoidance of stimulants ex. caffeine
Anticoagulation If systemic emboli
Endocarditis prophylaxis If murmur audible or if myxomatous leaflet
Surgical MV repair favored over replacement if significant MR

Aortic Stenosis (AS)
o AS Outflow obstruction | EDP Concentric LVH LVF
o Normal AV area = 34cm
Severe AS = <1cm
& critical AS = <0.5cm

o Etiology:
Degenerative calcification idiopathic & seen in older population
Bicuspid AV MC congenital valve abnormality & ass. w/early calcific AS by age 60-70yrs
Rheumatic heart disease
o Clinical Presentation:
Dyspnea, PND, orthopnea, peripheral edema
Exertional angina & syncope CO cannot maintain BP causing syncope & angina
Parvus et Tardus pulses weak compared to heart sounds
Narrow pulse pressure, brachial-radial delay & sustained PMI
- Crescendo-decrescendo SEM radiating to carotid arteries best over right 2
o Gallavardin phenomenon musical quality at apex
- S4, late S3 & paradoxical splitting of S2 delayed AV opening causes closure after PV
o Diagnosis:
ECG LVH & strain, LBBB, LAE
ECHO Reduced valve area, pressure gradient, LVH, + LV function
CXR Calcified valve & post-stenotic aortic root dilatation
o Treatment:
Asymptomatic Serial ECHOs avoid exertion, nitrates, arterial dilators & ACEIs
Surgery If severe AS or LV dysfunction
- Valve replacement definitive therapy
- Valvuloplasty temporary improvement as rate of restenosis very high

Aortic Regurgitation (AR)
o AR LV dilatation |SV + |sBP + +dBP | Wall tension Pressure overload LVH
o Etiology:
Aortic root Marfans, EhlersDanlos, dissecting aneurysm, syphilis, CT disease, HTN
- Associated w/cystic medial necrosis
Valvular Congenital bicuspid AV, Turners syndrome, large VSD, RHD, endocarditis
Acute AR IE, aortic dissection, trauma, failed prosthetic valve
o Clinical Presentation:
Asymptomatic Until late LVF develops dyspnea, orthopnea, PND
Angina Low pressure in aortic root causes + diastolic coronary blood flow
Pulses Wide pulse pressure & bounding/waterhammer pulse
- Pulsus Bisferiens dicrotic pulse w/2 palpable waves in systole
- Duroziez sign diastolic femoral bruit when femoral artery compressed
- Hills sign sBP in legs >20 mmHg higher than arms
- Quinckes sign alternating blushing & blanching of fingernails when pressure applied
- De Mussets sign bobbing of head w/heartbeat
Precordial Hyperdynamic apex & laterally displaced PMI due to LVE
Auscultation Early decrescendo diastolic murmur at LLSB (cusp) or RLSB (aortic root)
- Best heard sitting, leaning forward & on full expiration
- Soft S1, absent S2 & late S3

- Austin Flint murmur low-pitched diastolic rumble heard in severe regurgitation
o Due to regurgitated blood striking anterior mitral leaflet similar sound to MR
o Diagnosis:
ECHO To identify leaflet or aortic root anomalies
CXR LVH, aortic root dilation
Stress Test Hypotension w/exercise
o Treatment:
Asymptomatic + Afterload w/ACEIs, Nifedipine, Hydralazine avoid exertion
Surgery Indicated in severe cases w/LVEF <50%
- Valve replacement only definitive treatment
- Bentall procedure aortic root replacement

Tricuspid Stenosis (TS)
o Etiology RHD, congenital, carcinoid rare valvular defect
o Clinical Presentation:
Peripheral edema, JVD, palpitations, Kussmauls sign, abdominojugular reflex (AJR)
Auscultation Rumbling diastolic murmur best heard over LSB between 4
o Diagnosis:
ECHO Diagnostic
CXR RA dilation without pulmonary artery enlargement
o Treatment Diuretics (+ preload) or Valve replacement (if severe TS)

Tricuspid Regurgitation (TR)
o Right ventricle dilatation TR Further RV dilatation RHF
o Etiology RHD, IE (IV drugs), RV dilation, | PA pressure (LHF, MS, MR), Ebstein anomaly
o Clinical Presentation:
Peripheral edema, JVD, palpitations, Kussmauls sign, AJR
Auscultation Holosystolic murmur heard best at LLSB accentuated by inspiration
o Diagnosis ECHO is diagnostic ECG shows RAE, RVH, A-Fib
o Treatment Diuretics (+ preload) + Annuloplasty (repair) + Endocarditis prophylaxis

Pulmonic Stenosis (PS)
o Etiology Congenital (MCC) or RHD (rare)
o Clinical Presentation:
Chest pain, syncope, fatigue, peripheral edema, right-sided S4
Auscultation Systolic murmur w/pulmonary ejection click
- Best heard at 2
LICS & accentuated by inspiration
o Diagnosis ECHO is diagnostic ECG shows RVH
o Treatment Balloon valvuloplasty if severe symptoms

Pulmonic Regurgitation (PR)
o Etiology Pulmonary HTN, IE, RHD, Tetrology of Fallot (post-repair)
o Clinical Presentation:
Chest pain, syncope, fatigue, peripheral edema
Auscultation Graham Steell diastolic murmur at 2
LICS accentuated by inspiration
o Diagnosis ECHO is diagnostic ECG shows RVH
o Treatment Rarely requires treatment valve replacement if severe

Infective Endocarditis
o Infection of cardiac endothelium, characterized by vegetations involving valve leaflets or walls
Leaflet vegetation Platelet-fibrin thrombi, WBCs & bacteria
Valve involvement MV >> AV > TV > PV
o Classification:
Acute Bacterial Endocarditis (ABE):
- Infection of healthy valves MCC is S. aureus
- Produces metastatic foci & usually fatal if not treated within 6wks
Subacute Bacterial Endocarditis (SBE):

- Seeding of previously damaged valves (RHD, CHD) MCC is S. viridans
- Does not produce metastatic foci
o Etiology:
ABE S. aureus, GNs
SBE S. viridans, oral flora, GAS, Enterococci, S. epidermidis
IVDU S. aureus, Streptococci, Enterococci, Candida
- Dont TRI drugs ABE often affects tricuspid valve in IV drug users
Prosthetic valves (<20%) S. aureus, S. epidermidis, GN bacilli, fungi
Nosocomial Indwelling venous catheters, hemodialysis, CT surgery
o Clinical Presentation:
Systemic Fever, chills, rigors, night sweats, anorexia, weight loss
Cardiac New-onset regurgitant murmur, dyspnea, chest pain
- Petechiae Multiple nonblanching red macules on upper chest & mucous membranes
- Janeway lesions Multiple hemorrhagic nontender macules on palms & soles
- Splinter hemorrhages Fine linear hemorrhages in middle of nailbed
- CNS emboli Focal neurological signs
- Renal emboli Microscopic hematuria, flank pain
- Septic pulmonary emboli
- Oslers nodes Tender raised subcutaneous nodules on fingers & toes
- Roths spots Retinal hemorrhages w/pale center seen on fundoscopy
- Glomerulonephritis & arthritis
SBE specific Splenomegaly & clubbing
o Diagnosis:
Dukes Criteria 2 major or 1 major + 3 minor or 5 minor criteria
- Major criteria:
o Blood Cx. 2 cultures 12hrs apart, or 3 taken at least 1hr apart
o ECHO Vegetations pathognomonic but absence doesnt R/O endocarditis
Transesophageal ECHO more sensitive
- Minor criteria:
o Predisposing valve lesion or IVDU
o Fever >38C
o Vascular Arterial emboli, septic pulmonary infarcts, Janeway lesions
o Immunologic Oslers nodes, Roths spots
o Blood cultures but not meeting major criteria
o ECHO suspicious for endocarditis but not meeting major criteria
o Treatment:
Antibiotics 1
line = Cloxacillin + Gentamicin minimum 4wks
- Ampicillin add if native valve & non-IVDU
- Rifampin add If prosthetic valve
Prophylaxis For high-risk pts. ex. VHD or previous H/O endocarditis
- Dental/respiratory procedures Amoxicillin 30-60min prior
o Clindamycin if penicillin-allergic

Rheumatic Fever
o Inflammatory disease due to antibody cross-reactivity following GAS infection
o Diagnosis 2 major criteria or 1 major + 2 minor criteria w/recent strep infection
Major criteria:
- Arthritis Migratory, multiple joints, very warm, tender
- Pancarditis Involving pericardium, myocardium, endocardium
- Erythema marginatum Pink macules w/central blanching & nonpruritic
- Subcutaneous nodules Pea-sized, firm, non-tender nodules (often extensor surfaces)
- Sydenhams chorea Clumsiness, difficulty w/handwriting
Minor criteria:
- H/O RF or RHD - |ESR or |CRP or Leukocytosis
- Fever - Prolonged PR interval

- Polyarthralgia - Recent streptococcal pharyngitis
o Treatment:
Penicillin or Erythromycin For 10 days to eradicate throat carriage of GAS
ASA For arthritis
Prednisone If severe carditis
Prophylaxis Daily Penicillin or Erythromycin
- No carditis 5yrs or until 21yrs old (whichever is longer)
- Carditis but no RHD 10yrs or longer
- Carditis w/RHD minimum 10yrs since last episode (sometimes life long)
o Complications:
Acute Myocarditis, A-Fib, acute MR, pericarditis
Chronic Rheumatic heart disease (RHD)
- Valvular abnormalities due to IC deposition in valve leaflets
o Fibrous thickening, adhesion & calcification resulting in stenosis or regurgitation
o Valve involvement MV > AV > TV
- Onset usually after 10-20yr latency from acute carditis of rheumatic fever
- | Risk of IE & thromboembolism

Alterations in Impulse Formation
o Abnormal Automaticity:
Normally only specialized cells of conduction system exhibit automacity & are pacemaking cells
- Cells found in SA node, AV node & ventricular conduction system
Cells in myocardium outside conduction system may inappropriately acquire automaticity
- Often seen in diseased cells ex. Post-MI ventricular ischemia
Ectopic generators assume pacemaking control if they depolarize at rate greater than SA node
Automaticity can be influenced by:
- Sympathetic & parasympathetic stimulation
- Abnormal metabolic conditions hypoxia, acidosis, hypothermia
- Electrolyte abnormalities or drugs (ex. digitalis)
- Local ischemia/infarction
o Early After-depolarizations:
Due to membrane potential becoming more positive during repolarization
Tachyarrhythmia results from self-maintained depolarizing oscillations of action potential
Basis for degeneration of QT prolongation into Torsades de Pointes
o Delayed After-depolarizations:
Occurs after AP has fully repolarized, but before next normal AP delayed after-depolarization
Seen w/| intracellular Ca
(digitalis toxicity, ischemia) or w/catecholamine stimulation

Alterations in Impulse Conduction
o Re-entry Circuits:
Self-sustaining re-entry circuit causes rapid repeated depolarizations in region of myocardium
Infarcted myocardium w/ischemia will consist of non-excitable & partially excitable zones
- These zones promote formation of re-entry circuits
o Conduction Block:
Ischemia, fibrosis, trauma & drugs can cause transient, permanent, uni- or bi-directional block
MCC is refractory myocardium cells in refractory period or unexcitable due to fibrosis
If block occurs along conduction system, distal conduction zones can assume pacemaking control
Can lead to bradycardia but also tachycardia if impaired conduction leads to re-entry
o Bypass Tracts:
Normally AV node only conducting tract from atria to ventricles
Development of additional or accessory conducting tracts can bypass AVN
- Facilitates premature ventricular activation before normal AVN conduction
Sinus Bradycardia
o HR <60 bpm w/normal P-waves & PR intervals
o Precipitants | Vagal tone, anti-arrhythmics, vomiting, inferior MI, | ICP, hypothyroidism, hypothermia

o Normal variant Bradycardia may be seen in normal adults esp. athletes & elderly
o Asymptomatic May have light-headedness or possible syncope
o Treatment Atropine pacing or pressors for hypotension only if symptomatic

Sinus Block, Pause & Arrest
o 3 disorders involving SA node sinus pacemaker fires but impulse fails to depolarize atrial myocardium
Results in no initial P wave & consequently no QRS complex, ST segment or T wave
o Sinus (SA) Block Complete block or failure of sinus node to depolarize atria
Block can last one or more cardiac cycles & is multiple of normal P-P interval
o Sinus Pause Delay in formation of sinus impulse in SA node causes temporary pause (usually >3 sec)
If pause >3x the normal P-P interval it may be called sinus arrest
o Sinus Arrest Longer delay in formation of sinus impulse in SA node
P-P prolongation not gradual (unlike sinus arrhythmia) & not multiple of P-P (unlike SA block)
o Escape beats or rhythm may occur:
Atrial escape P-waves w/abnormal morphology
Junctional escape P-waves not seen or follow QRS (retrograde P) rate 40-60 bpm
Ventricular escape No P-wave & wide abnormal QRS slow rate 20-40 bpm

Sick Sinus Syndrome (SSS)
o Sinus node dysfunction Marked bradycardia, sinus pause/arrest, sinoatrial block
o Frequently ass. w/episodes of atrial tachyarrhythmias tachy-brady syndrome
o Treatment Electronic pacemaker indicated if symptomatic bradycardia
|-blocker, CCB, Digoxin Often initiated after pacemaker insertion for tachycardia

AV Conduction Blocks
o Precipitants Inferior wall MI, Digitalis toxicity, | vagal tone, conduction system disease
o 1
Degree AV Block Prolonged PR interval >0.20s benign & no treatment required
o 2
Degree AV Block:
Mobitz Type I (Wenckebach):
- Progressive PR prolongation followed by failure of P-wave conduction
- AV node is MC site of block benign & no treatment required
Mobitz Type II:
- P-wave suddenly fails to conduct without prior PR prolongation QRS drops suddenly
- Site of block within His-Purkinje system requires permanent pacemaker
o Treat quickly as it can progresses to 3
degree complete heart block
o 3
Degree AV Block (Complete Heart Block):
Failure of atrial impulse conduction to ventricles independent atrial & ventricular activity
No relationship between P-waves & QRS complexes always requires pacemaker implantation

Premature Complexes
o Premature Atrial Complexes (PACs):
Ectopic supraventricular beat originating in atria
ECG Early P-waves that differ in morphology from normal sinus P-waves
- Difference is because PACs originate within atria & not sinus node
- Normal QRS complex because conduction below atria is normal
Asymptomatic but may cause palpitations or give rise to PSVTs
PACs found in >50% of normal adults Tx. w/-blockers if symptomatic
o Premature Ventricular Complexes (PVCs):
Early beat fires independently from focus in ventricle & spreads to other ventricle
Conduction not through normal pathway but through slower ventricular muscle
- Slower conduction causes wide QRS complexes >120msec w/bizarre morphology
- No preceding P-wave seen its hidden within wide QRS complex
- Couplet 2 successive PVCs
- Bigeminy Sinus beat followed by PVC
- Trigeminy Sinus beat followed by 2 PVCs
PVCs seen in >50% of men w/Holter monitoring usually asymptomatic & benign
PVC significant in following situations:
- Consecutive (3 = VT) or Multiform (varied origin)

- R on T phenomenon PVC falling on T-wave of previous beat
o May precipitate VT or V-Fib can potentially cause sudden death
-blockers May benefit if symptomatic also order EP study to assess benefit of ICD
Studies shown | risk of death if antiarrhythmic drugs used to suppress PVCs after MI

Atrial Fibrillation (A-Fib)
o Disorganized electrical activity of atrial myocardium causing atrial quiver & rapid ventricular rate
o Pathophysiology:
Initiation Single circuit re-entry or ectopic foci produce atrial tachycardia 350-600 bpm
- Impulses then conduct irregularly across atrial myocardium to give rise to fibrillation
Maintenance Tachycardia causes atrial structural & EP changes which further promotes A-Fib
- Longer pt. remains in AF the more difficult to convert back to sinus rhythm
AV node blocks most incoming atrial impulses producing ventricular rate <200 bpm
- Tachycardia leads to suboptimal cardiac output
o Etiology:
CAD, MI, HTN, RHD, pericarditis, pulmonary disease, PE, post-op stress
Sepsis, hyper-/hypothyroidism, pheochromocytoma, sick sinus syndrome
Excessive alcohol ex. "holiday heart syndrome"
o Clinical Presentation:
Fatigue, exertional dyspnea, palpitations, dizziness
Irregularly irregular pulse, angina, syncope
Stroke or TIA 2
to embolizing thrombi due to atrial stasis
o Diagnosis:
- No identifiable P-waves due to tachycardia chaotic fibrillatory baseline
- Irregular RR intervals due to irregular impulse conduction to ventricles 100-180 bpm
- Narrow QRS complexes unless aberrancy or previous BBB
- Ashman phenomenon wide QRS complexes following long-short RR interval
ECHO Can identify presence of clot in left atrium
Other Absent S4 on auscultation & absent a wave in JVP due to loss of atrial contraction
o Treatment:
Rate control Nondihydropyridine CCBs or -blockers target pulse rate 60-100 bpm
- Consider using Digoxin or Amiodarone in pts. w/HF
Cardioversion Convert back to sinus rhythm after rate control achieved
- Electrical cardioversion indications:
o Hemodynamically unstable Immediate electrical cardioversion
o A-Fib <48hr Usually can cardiovert without anticoagulation
o A-Fib >48hr Risk of embolization during cardioversion rises to 2-5%
Anticoagulate for 3wks before & 4wks after electrical cardioversion
- Pharmacologic cardioversion Only used if electrical conversion fails or unfeasible
o Agents Ibutilide, Procainamide, Flecainide, Sotalol, Amiodarone
Anticoagulation To prevent embolic CVA target INR of 2-3
- A-Fib >48hrs Obtain Transesophageal ECHO (TEE) to R/O thrombus in LA
o If no thrombus seen Start IV Heparin & perform cardioversion within 24hrs
TEE avoids need for 3wk wait prior to starting anticoagulation
o Anticoagulation for 4wks after cardioversion still required
Chronic A-Fib CCB or -blocker (rate control) + Warfarin (chronic anticoagulation)
"Lone" A-Fib Pts. < 60yrs w/A-Fib in absence of underlying CV risk factors
- Do not require anticoagulation due to low risk for embolization

Atrial Flutter
o Rapid, regular atrial depolarization from macro re-entry circuit within atrium MC site is RA
o Pathophysiology:
Irritable automaticity focus in atria fires giving rise to regular atrial contractions 250-350 bpm
Ventricular rate 30-50% of atrial rate difference due to long refractory period in AV node
- AV node allows only 1 out of every 2 or 3 flutter waves to conduct to ventricles
- AV block may be fixed (2:1, 3:1, 4:1) or variable
o Etiology COPD, CAD, MV disease, ASD, CHF, cardiac surgery, PE, pericarditis, thyrotoxicosis

o Diagnosis:
ECG Sawtooth flutter baseline in inferior leads (II, III, aVF)
- Narrow QRS after every second or third tooth P-wave
o Treatment:
Rate control |-blocker, CCB, Digoxin
Cardioversion Preform immediate electrical cardioversion if unstable
- Chemical cardioversion Sotalol, Amiodarone, Type I antiarrhythmics
Anticoagulation Same guidelines as A-Fib
Long-term Catheter radiofrequency (RF) ablation success rate dependent on site of origin

Multifocal Atrial Tachycardia (MAT)
o Irregular rhythm caused by 3 or more atrial foci w/atrial rate 100-200 bpm may mimic AF
o Etiology COPD (MCC), hypokalemia, sepsis, theophylline or digitalis toxicity
o Diagnosis ECG at least 3 distinct P-wave morphologies w/variable PR & RR intervals
o Treatment:
Normal LV function CCBs, -blockers, Digoxin, Amiodarone, IV Flecainide, IV Propafenone
- |-blockers may be contraindicated in severe pulmonary disease
+ LV function Digoxin, Diltiazem, Amiodarone
Electrical cardioversion Ineffective & should not be used

Paroxysmal Supraventricular Tachycardia (PSVT)
o Etiology:
Ischemic heart disease or excessive caffeine/alcohol consumption
Digoxin toxicity MC arrhythmia is paroxysmal atrial tachycardia w/2:1 block
AV node reentry or AV reciprocating tachycardia (accessory pathway)
Atrial flutter w/rapid ventricular response
o Classification:
AV Nodal Reentrant Tachycardia (AVNRT):
- Accounts for 60-70% of all PSVTs & often found in absence of structural heart disease
- Re-entrant circuit using dual pathways within AV node fast |-fibers & slow -fibers
- Usually initiated by premature atrial or ventricular contractions
- Sudden onset & offset, fast regular rhythm w/rate between 150-250 bpm
- ECG No discernible P-waves buried within narrow QRS complexes
o Rapid conduction causes impulses to activate atria & ventricles simultaneously
AV Reentrant Tachycardia (AVRT):
- Re-entrant loop via accessory pathway between atria & ventricle conducts retrogradely
o Initiated by a premature atrial or ventricular complex
- Orthodromic AVRT Stimulus travels up bypass tract (V to A) & down AV node (A to V)
o Accounts for 95% of reentrant tachycardia associated w/WPW syndrome
o ECG narrow QRS no delta wave
- Antidromic AVRT Stimulus goes up AV node (V to A) & down bypass tract (A to V)
o ECG wide & abnormal QRS due to ventricular activation via bypass tract
o Treatment:
Vagal stimulation Delays AV conduction & blocks reentry mechanism
- Valsalva, carotid sinus massage, breath holding, head immersion in cold water/ice
IV Adenosine 1
line if no response to vagal maneuvers
- Works by + SA & AV nodal activity w/short duration of action
CCB, -blocker, Digoxin Alternatives if LV function preserved
Electrical cardioversion If drugs not effective or if unstable almost always successful
Long-term prevention:
- 1
line Digoxin (preferred), |-blocker, CCB
- 2
line Anti-arrhythmics Flecainide or Propafenone
- 3
line Radiofrequency catheter ablation of either AV node or accessory tract

Wolff-Parkinson-White Syndrome (WPW)
o Accessory conduction tract from atria to ventricles causing premature ventricular excitation

Bundle of Kent abnormal fast conducting fibers that bypass AV node found in either LA or RA
o Etiology Congenital defect seen in 1.5/1000 of general population
o Can lead to paroxysmal tachycardia via 2 possible mechanisms:
Orthodromic AVRT:
- Impulse travels through AV node (anterograde) & depolarizes ventricles
- Then travels back through accessory pathway (retrograde) & re-depolarizes atria
- Absent delta waves because conduction occurs retrograde over accessory pathway
SVT (A-Fib or Atrial flutter):
- Accessory pathway allows all or most impulses to pass causing | ventricular rate
o Normally, AV node allows only certain impulses to ventricles
o Diagnosis:
ECG Wide QRS complex w/slurred upstroke (delta wave) & PR interval <120 msec
- Tachyarrhythmias most often AVRT or AF
o Treatment:
Electrical cardioversion If A-Fib w/rapid ventricular response
Surgical Radiofrequency catheter ablation of bypass tract effective treatment
Pharmacologic Amiodarone, Flecanide, Procainamide, Propafenone, Sotalol
|-blockers, CCBs, Digoxin Contraindicated due to conduction blockage at AV node
- Allows unopposed conduction down accessory bypass tract

Torsades de Pointes
o Variant of polymorphic VT occurring in pts. w/baseline QT prolongation ventricular rate 150-300 bpm
o Etiology:
Congenital long QT syndromes
Drugs Class IA (Quinidine), Class III (Sotalol), Phenothiazines (TCA), Erythromycin, Quinolones
Electrolytes Hypokalemia or hypomagnesemia
o Diagnosis ECG QRS complexes rotate around baseline changing their axis & amplitude
o Treatment IV Magnesium, temporary pacing, Isoproterenol & correct underlying cause of prolonged QT

Ventricular Tachycardia (VT)
o Rapid & repetitive firing of 3 or more consecutive PVCs originates below the bundle of His
o Etiology:
CAD w/prior MI (MCC), active ischemia, hypotension, cardiomyopathies
Prolonged QT syndrome, drug toxicity, congenital defects
o Classification:
Sustained VT Lasts >30secs almost always symptomatic
- Life-threatening arrhythmia can progress to V-fib if untreated
- Often ass. w/hemodynamic compromise or development of myocardial ischemia
Nonsustained VT Brief, self-limited runs of VT usually asymptomatic
- | Risk for sudden death if CAD & LV dysfunction present
o Clinical Presentation:
Palpitations, dyspnea, light-headedness, angina, impaired consciousness, syncope
o Diagnosis:
ECG Wide QRS tachycardia may be monomorphic or polymorphic
- Monomorphic VT MC type identical complexes w/uniform morphology
- Polymorphic VT Constantly changing morphology, amplitude & polarity
- Other AV dissociation sinus P-waves continue their cycle unaffected by tachycardia
o Treatment:
Sustained VT:
- Hemodynamically stable IV Amiodarone, IV Procainamide, IV Sotalol
- Hemodynamic compromise Immediate electrical cardioversion
o Follow w/IV Amiodarone to maintain sinus rhythm
Nonsustained VT Do not treat if asymptomatic w/no underlying heart disease

Ventricular Fibrillation (V-Fib)
o Multiple foci in ventricles fire rapidly leads to chaotic quivering of ventricles & no cardiac output

Most episodes begin w/VT except in setting of acute ischemia/infarction
o Etiology:
MCC Ischemic heart disease
Prolonged QT torsades de pointes, anti-arrhythmic drugs
WPW w/A-Fib + rapid ventricular response
o Clinical Presentation:
Loss of consciousness if V-Fib >5-6 secs if untreated can lead to sudden cardiac death
BP immeasurable, absent heart sounds & pulse
o Diagnosis ECG QRS & P-waves both unidentifiable
o Treatment:
Medical emergency Immediate defibrillation & CPR
- Unsynchronized DC cardioversion up to 3 sequential shocks to establish rhythm
If V-Fib persists IV Epinephrine 1mg bolus initially & then every 3-5 mins
- Causes | myocardial & cerebral blood flow also reduces defibrillation threshold
- Attempt to defibrillate again 30-60secs after first epinephrine dose
Refractory V-Fib IV Amiodarone followed by shock
- 2
line Lidocaine, Bretylium, Magnesium, Procainamide
Chronic therapy ICD is mainstay alternative is long-term Amiodarone
o Prognosis:
V-Fib not ass. w/acute MI | Recurrence rate up to 30% within first year
- Require chronic therapy ICD or prophylactic Amiodarone
V-Fib within 48hrs of acute MI Low recurrence rate 2% within first year

Hypertension (HTN)
o Classification:
HTN Pre-HTN: 120/89, Stage 1: 140/90, Stage 2: 160/100
Isolated Systolic HTN sBP 140 & dBP <90 often develops in 5
- Associated w/progressive reduction in vascular compliance
Hypertensive Urgency sBP >210 or dBP >120 w/absent end-organ damage
Hypertensive Emergency sBP >220 or dBP >120 + acute end-organ damage
- Papilledema, retinal hemorrhages, bulging discs, mental status changes, | Cr
o Etiology:
(Essential) HTN MCC of HTN (>90%) unknown cause
- Renal renal failure, glomerulonephritis, renal artery stenosis
- Endocrine cushings syndrome, 1
hyperaldosteronism, pheochromocytoma
- Other coarctation of the aorta or drug-induced (cocaine, amphetamines)
o Risk Factors FHx, obesity, smoking, DM, high Na
/fat diet, alcohol, black race, male gender
o Clinical Presentation Asymptomatic light-headed, occipital headache, epistaxis, hematuria, vision
o Diagnosis:
Fundoscopic Check for AV nicking, hemorrhage or papilledema
Auscultation Check for renal artery bruits
ECG May show LVH or left ventricular strain
o Treatment:
Lifestyle modification Na
restriction, low-fat diet, weight loss, exercise, smoking cessation
Pharmacologic Thiazides (preferred), ACEIs, CCBs, |-blockers
Hypertensive Emergency + MAP by 25% in 1-2hrs gradually reduced BP back to normal
- Severe HTN IV agents Nitroprusside, Labetalol, Nitroglycerin
- No immediate danger Oral agents Captopril, Clonidine, Labetalol, Diazoxide
Hypertensive Urgency + BP within 24hrs via oral agents

Aortic Dissection
o Tear in aortic intima allowing blood to dissect into aortic media
Acute dissection < 2wks initial mortality 1% per hour

Chronic dissection >2wks mortality levels up to 75-80%
o Etiology:
Cardiac HTN (longstanding in 70% of cases), bicuspid AV, coarctation of the aorta, PDA
Other Marfans, EhlersDanlos, syphilis, trauma, 3
trimester pregnancy, cocaine
o Classification:
- Type I Ascending & descending aorta MC type 50%
- Type II Ascending aorta only stops at innominate artery
- Type IIIA Descending thoracic aorta only proximal to diaphragm
- Type IIIB Type IIIA + abdominal aorta
- Type A (Proximal) Ascending aorta aortic arch requires emergent surgery
o Mortality rate w/o surgery is 3% per hour for first 24hrs & 80% at 2wks
- Type B (Distal) Descending aorta only distal to subclavian artery
o Clinical Presentation:
HTN (75%) syncope
Chest pain sudden onset, tearing or stabbing pain w/radiation to back
- Anterior chest pain more common w/proximal dissection (type A)
- Interscapular back pain more common w/distal dissection (type B)
Asymmetric BP & pulses between arms poor prognosis if >30 mmHg difference
Aortic regurgitation w/new diastolic murmur esp. w/proximal dissection
o Diagnosis:
CXR Widened mediastinum & pleural capping (effusion in lung apices)
TEE Can visualize AV & thoracic aorta but not abdominal aorta
- Preferred test in acute setting alongside CT due to high sensitivity & specificity
- Ideal test for unstable pts noninvasive & preformed at bedside
CT/MRI Both highly accurate MRI not ideal in acute setting due to longer time
Angiography Invasive but best test for determining extent of dissection for surgery
o Treatment:
Immediate BP control:
- IV |-blockers To + HR & diminish force of LV ejection
- IV Sodium Nitroprusside To + sBP below 120mmHg
Surgical Resection of intimal tear & replacement of affected aorta w/prosthetic graft
- High morality rate due to operative or post-op complications
Type A Requires emergent surgery w/cardiopulmonary bypass
- Hypothermic circulation for transverse arch dissections
- Valve replacement & coronary re-implantation for aortic root involvement
Type B Managed medically 10-20% may require urgent surgery for complications
o Complications:
Ischemic syndromes Due to dissection or occlusion of aortic branches
- Coronary (MI), Carotids (stroke, hemiplegia, horners), Splanchnic (ischemic gut)
AR Due to dissection through aortic root w/unseating of AV cusps
Cardiac Tamponade Due to dissection into pericardium
Rupture Pleural (dyspnea, hemoptysis) or Peritoneum (hypotension, shock)

Aortic Aneurysm
o Localized dilatation aortic segment w/diameter at least 1.5x that of normal
o True aneurysm Involves all vessel wall layers intima, media, adventitia
o False aneurysm Disruption of aortic wall or anastomotic site between vessel & graft
Containment of blood by fibrous capsule made of surrounding tissue
o Classification:
Thoracic (TAA) ascending, transverse arch, descending
Abdominal (AAA) 90% infrarenal & MC between renal arteries & iliac bifurcation

o Etiology:
Degenerative, atherosclerotic, trauma, vasculitis, bicuspid AV
Marfans, EhlersDanlos, infectious (syphilis, fungal), mycotic (Salmonella, Staph)

o Risk Factors Smoking, HTN, age >65, FHx, M>W, CAD
o Clinical Presentation:
Asymptomatic (75%) discovered incidentally due to pain in chest, abdomen, flank or back
- Syncope, hypotension, palpable pulsatile abdominal
- Airway or esophageal obstruction hoarseness, hemoptysis, hematemesis
Uncommon presentation:
- Partial bowel obstruction or ureteric obstruction w/hydronephrosis
- GI bleed duodenal mucosal hemorrhage, aortoduodenal fistula
- Aortocaval fistula or distal embolization (blue toe)
o Diagnosis:
U/S Test of choice to evaluate size & location of aneurysm 100% sensitive
CT 100% sensitive but longer time to preform than U/S
AXR May show calcifications of dilated segment allowing measurement of aortic diameter
- But not used to R/O aneurysm only for quick assessment
o Treatment:
Conservative management:
- + Risk factors Smoking cessation, HTN/DM/hyperlipidemia control, exercise
- U/S Every 6 months to 3yrs depending on size & location
Surgical indications:
- Risk of rupture Risk of surgery size >5.5cm or >2x normal lumen size
- Symptomatic, ruptured or mycotic aneurysm
- Acute type A dissection or complicated type B dissection
- Ascending thoracic aortic aneurysms
Surgical procedures:
- Laparotomy w/graft replacement
- Endoluminal graft placement under image guidance
o Newer procedure w/+ mortality, + procedure time & + recovery time
o Disadvantages endoleak rates up to 20-30% & high-cost for device
o Complications:
Rupture of AAA Emergent laparotomy indicated crossmatch 10 units PRBCs
- Triad of 1) Abdominal pain, 2) Hypotension, 3) Palpable pulsatile abdominal mass
o No further diagnostic testing needed w/triad of symptoms
- CV collapse & syncope 2
to sudden hemorrhage
- Signs suggesting expansion & impending rupture:
o Sudden onset of severe pain in back or abdomen & radiating to groin/legs
o Grey Turner's sign Ecchymoses on back & flanks
o Cullen's sign Ecchymoses around umbilicus

Peripheral Vascular Disease (PVD) Chronic Arterial Insufficiency
o Occlusive atherosclerotic disease of LE w/symptoms related to site of obstruction
MC site of occlusion is superficial femoral artery in Hunter's canal also popliteal & aortoiliac
o Risk Factors DM, smoking, CAD, hyperlipidemia, HTN, hyperhomocystinemia
o Clinical Presentation:
Intermittent claudication Leg pain reproduced in same location by same walking distance
- Pain completely relieved by rest
- Femoral or popliteal occlusion causes calf claudication
- Aortoiliac occlusion causes buttock, hip & calf claudication
Rest pain Continuous & typically felt over distal metatarsals
- Often prominent at night awakens pt. from sleep
- Pain relieved by hanging foot over side of bed or standing | perfusion due to gravity
- Rest pain suggests severe ischemia & possible progression to gangrene
Pulses May be diminished or absent
Signs of + perfusion:
- Muscular atrophy, + hair growth, thick toenails, | capillary refill, + skin temp.
- Pallor of elevation & rubor of dependency skin color change w/leg elevation
- Skin ulceration MC in toes & 2
to local trauma that does not heal
- End-stage disease tissue infarction & gangrene

o Diagnosis:
ABI Ratio of sBP at ankle to sBP at arm is normally 1.0
- Claudication = ABI <0.7 & Rest pain = ABI <0.4
- False ABI seen w/calcified arteries as vessels not compressible esp. DM
Pulse volume recordings Noninvasive assessment of segmental limb perfusion
- Pulse wave forms represent volume of blood per heart beat at sequential sites down leg
- Large wave form indicates good collateral blood flow
Arteriography Gold standard for diagnosing & locating site of occlusion
- Invasive & only needed if considering surgery/revascularization
o Treatment:
Conservative management:
- Smoking cessation Smoking causes vasoconstriction & progression of atherosclerosis
- Exercise Develops collateral circulation & improves exercise tolerance
- Atherosclerotic risk factor reduction Control of hyperlipidemia, HTN, DM, weight
- Avoid extremes of temperature esp. extreme cold
- Foot care esp. in diabetics
Pharmacologic management:
- Anti-platelets ECASA, Clopidogrel rarely Ticlopidine
- Cilostazol cAMP-phosphodiesterase inhibitor w/anti-platelet & vasodilatory effects
- Pain relief Morphine sulphate supplemented w/NSAIDs
o If opiate analgesia inadequate consider lumbar sympathectomy
Surgical indications Claudication interfering w/lifestyle, rest pain, pre-gangrene, gangrene
Surgical procedures:
- Endovascular stenting/angioplasty
- Arterial bypass grafts reversed vein graft or synthetic graft (Gor-Tex, Dacron)
o Bypass graft sites aortofemoral, axillofemoral, femoropopliteal, distal arterial
- Amputation if not suitable for revascularization and/or gangrene

Acute Arterial Occlusion
o Acute occlusion/rupture of peripheral artery MC in LE femoropopliteal > aortoiliac
o Urgent management required Irreversible ischemia & myonecrosis results >6hrs
o Etiology:
Cardiac emboli (MCC 80%) A-Fib, post-MI, VHD, endocarditis, atrial myxoma
Arterial emboli Proximal arterial aneurysm, atheroembolism
Thrombi Atherosclerotic, trauma, hematological disorders & stasis
o Clinical Presentation:
6 Ps but all may not be present:
- Pain in LE progressing within hrs to feeling of cold, numbness & loss of function
o Pain absent in 20% of cases due to prompt onset of anesthesia & paralysis
- Pallor within few hrs becomes mottled cyanosis
- Paresthesia light touch (small fibers) lost first, then sensory (large fibers)
- Paralysis loss of power most important because it indicates impending gangrene
- Polar cold
- Pulselessness not reliable
o Diagnosis:
Arteriogram To define site of occlusion
ECG Check for A-Fib or MI
ECHO For evaluation of valves, clot or MI
o Treatment:
IV Heparin Immediate bolus w/continuous infusion to maintain PTT >60secs
Embolectomy via Fogarty balloon catheter
Thrombectomy graft bypass
Amputation If irreversible ischemia

Deep Venous Thrombosis (DVT)
o Thrombus formation & subsequent inflammatory response in superficial or deep vein
o Thrombi propagate in direction of blood flow MC in LE originating in calf veins

o Most important complications are PE (50% risk w/proximal DVT) & chronic venous insufficiency
o Virchows Triad:
1) Endothelial damage Leads to + inhibition of coagulation & local fibrinolysis
- Trauma, major surgery, pelvic procedures
2) Venous stasis Immobilization inhibits clearance & dilution of coagulation factors
- Prolonged bed rest, long flights, orthopedic casts, CHF
3) Hypercoagulability Hereditary states, OCP, malignancy
o Clinical Presentation:
Asymptomatic esp. if superficial venous system patent allowing blood drainage
Classic findings Seen in 50% but all have low sensitivity & specificity:
- Unilateral LE pain, edema & erythema improves w/rest or elevation
- Homans sign pain w/foot dorsiflexion
- Palpable cord due to thrombosed vein
Phlegmasia alba dolens White leg w/no ischemia
Phlegmasia cerulea dolens Cyanotic leg w/severe pain & ischemia
Post-phlebitic (post-thrombotic) syndrome Pain, edema, hyperpigmentation & skin ulceration
- MC complication in up to 2/3 of DVT cases due to small obstructions still remaining
o Diagnosis:
vDuplex U/S Initial test for DVT high sensitivity & specificity
- Only for detecting proximal thrombi (popliteal, femoral) not distal (calf vein) thrombi
- vDuplex leg symptoms Rules in proximal DVT
- C vDuplex w/o leg symptoms Does not R/O DVT!
Venography Best test for diagnosis of distal calf vein thrombi but invasive & rarely used
- Visualize deep & superficial venous systems assesses patency & valvular competence
Impedance Plethysmography Noninvasive alternative to doppler U/S
- High sensitivity for proximal DVT only but poor specificity due to | false positive rate
D-dimer Low specificity may be elevated in MI, CHF, pneumonia, post-operative state
- Must be combined w/Doppler to R/O DVT
o Treatment:
Acute anticoagulation Unfractionated Heparin or LMWH
- IV Heparin Bolus w/continuous infusion for 5-10d goal is aPTT of 1.52.5x control
- LMWH (Dalteparin, Enoxaparin) No lab monitoring, better bioavailability & as effective
Chronic anticoagulation Warfarin continue for 3-6 months or more based on risk factors
- Start w/Heparin & overlap for 5+ days until therapeutic INR of 2-3 reached
Thrombolytics Streptokinase, Urokinase, TPA indicated in massive PE or RHF
- Speeds up lysis of clots but no improvement in survival
IVC Filter Indications for Greenfield filter placement:
- Contraindication to anticoagulation in documented DVT or PE
- Failure of adequate anticoagulation as reflected by recurrent DVT or PE
- Low pulmonary reserve w/high risk of death from PE
Preventative Leg elevation, pneumatic compression boots, compression stockings

Chronic Venous Insufficiency (CVI) Post-Phlebitic Syndrome
o Pathophysiology:
Superficial & deep venous systems connected by perforating veins
- Valves allow flow from superficial to deep veins but not vice versa
Prior DVT is underlying cause in many cases w/2 major effects:
- Destruction of valves in deep venous system causing valvular incompetence
- Valves in perforator veins also damaged 2
to chronically elevated deep venous pressure
o Inhibits normal transmission of blood from superficial to deep system
Ambulatory venous HTN Interstitial fluid accumulation resulting in edema
- Extravasation of plasma proteins & RBCs into subcutaneous tissues
o Results in brawny induration & dark pigmentation due to hemosiderin deposits
Eventual + capillary blood flow w/tissue hypoxia mild trauma may cause ulcer formation
- Venous ulcers MC at medial malleolus overlying incompetent perforator vein
o Ulcer formation directly proportional to amount of swelling present
o Clinical Presentation:

Pain Aching or tightness of involved leg often worse at end of day
Edema Lower leg & relieved by elevation opposite is true in arterial insufficiency
Skin Stasis dermatitis, pruritus, hyperpigmentation, venous ulcers
o Diagnosis:
Doppler U/S Most commonly used imaging technique
Ambulatory Venous Pressure (AVP) Gold standard but invasive & rarely done
Plethysmography Noninvasive
o Treatment:
Conservative Elastic compression stockings, leg elevation, avoid prolonged sitting/standing
Surgery If conservative measures fail or recurrent/large ulcers
- Ligation of perforators in region of ulcer
- Greater saphenous vein stripping
- Venous bypass if short segment obstruction
Ulcers Wet-to-dry saline dressings, zinc-oxide wraps, antibiotics, debridement, unna boot
- Split-thickness skin grafts if unna venous boot (external compression stocking) fails

Superficial Thrombophlebitis
o Erythema, induration & tenderness along superficial vein MC in greater saphenous system
MC at sites of IV infusion in upper extremities & usually ass. w/varicose veins in lower extremities
o Etiology:
Infectious Suppurative phlebitis due to complication of IV cannulation
Inflammatory Varicose veins, Buergers disease, SLE, trauma
Other Polycythemia, thrombocytosis, occult malignancy (esp. pancreatic)
o Clinical Presentation:
Pain w/cord-like swelling along course of involved vein
Induration, erythema & tenderness corresponds to dilated & often thrombosed veins
o Diagnosis R/O associated DVT w/non-invasive tests
o Treatment:
Conservative Bed rest, limb elevation, heat, compression bandages, ASA
Suppurative thrombophlebitis IV Antibiotics + I&D of involved vein
o Complications Simultaneous DVT (<20%) or recurrent superficial thrombophlebitis

Varicose Veins
o Distention of tortuous superficial veins resulting from incompetent valves in venous system
Often due to inherited structural valve weakness important risk factor

o MC in greater saphenous system dilated, tortuous superficial veins along thigh & leg
Also in esophagus, anorectum, scrotum esophageal varices (GI bleed), hemorrhoids, varicocele
o Risk Factors Age, females, OCP, occupations requiring standing, pregnancy, obesity, pelvic tumors
o Clinical Presentation:
Diffuse aching pain & nocturnal cramping aggravated by prolonged standing
Ulceration, hyperpigmentation & induration
Brodie-Trendelenberg test Raise leg, compress saphenous vein at thigh & then have pt. stand
- If veins fill quickly from top down Test for incompetent valves
o Treatment:
Conservative management Elevation of leg or elastic stockings
Surgical Stripping of long saphenous vein, Sclerotherapy or Endovenous laser therapy (EVLT)
o Complications Recurrent superficial thrombophlebitis, hemorrhage, ulceration, eczema

o Obstruction of lymphatic drainage resulting in non-pitting edema w/high protein content
Primary Milroys syndrome
Secondary Filariasis (MCC worldwide), LN removal (MCC in US), malignant infiltration
o Clinical Presentation Non-pitting edema, + limb mobility, discomfort/pain
o Treatment Compression bandages/sleeve, skin hygiene, manual lymph drainage, low-intensity exercise
If untreated, may become resistant to treatment due to subcutaneous fibrosis

- Prenatal Circulation
o Circulation before birth:
Placenta Umbilical vein Ductus venosus IVC RA FO LA LV Aorta
Fetal lungs bypassed via following fetal shunts:
- Shunting of deoxygenated blood:
o Ductus Arteriosus Connection between pulmonary artery & aorta
- Shunting of oxygenated blood:
o Foramen Ovale (FO) Connection between RA & LA
o Ductus Venosus Connection between umbilical vein & IVC
o Circulation after birth:
With first breath, lungs open & pulmonary resistance + allowing pulmonic blood flow
Systemic circulation becomes high resistance system causes ductus venosus closure
| Pulmonic flow causes | left atrial pressures causes foramen ovale closure
| O2 concentration after first breath cause + prostaglandins causes ductus arteriosus closure

- Congenital Heart Disease (CHD) Cyanotic vs. Acyanotic
o Most critical period of heart development between 3-8wks gestation most susceptible to insult
o Acyanotic CHD:
Left-to-Right shunts ASD, VSD, PDA
- Cause | pulmonary blood flow leading to | pulmonary pressures
- If untreated can lead to Eisenmenger's syndrome reversal of shunt (right-to-left)
Obstruction Coarctation, aortic stenosis, pulmonary stenosis
- Present w/pallor, + urine, cool extremities, poor pulses, syncope
o Cyanotic CHD:
Right-to-Left shunts TOF or Ebsteins anomaly
Other TGA, hypoplastic left heart, TAPV, truncus arteriosus
Hyperoxic Test To determine if cyanosis is cardiac in origin
- Obtain preductal, right radial ABG repeat ABG after child inspires 100% O2
- If PaO2 improves >150mmHg then cyanosis not cardiac in origin

- Atrial Septal Defect (ASD)
o Classification:
Ostium Primum Presents in early childhood ass. w/Downs syndrome
- Findings include murmur or fatigue w/exertion
Ostium Secundum MC type tends to present in late childhood or early adulthood
Sinus Venosus Defect located at entry of SVC into RA
o Clinical Presentation:
Asymptomatic easy fatigability, frequent respiratory infections, FTT
Systolic ejection murmur (SEM) grade 3/6 pulmonic outflow murmur
- Wide & fixed split S2 w/right ventricular heave
- May also present w/mid-diastolic rumble at LLSB
If ASD remains patent CHF & pulmonary HTN can develop in adult life
o Diagnosis:
ECHO w/color-flow Doppler Reveals blood flow between atria diagnostic
- Also shows paradoxical ventricular wall motion & dilated RV
ECG Right axis deviation (RAD), RVH, PR prolongation
CXR Cardiomegaly & | pulmonary vasculature
o Treatment:
Spontaneous closure rate >80% If ASD diameter <8 mm
Surgical closure Indicated in CHF or >2:1 ratio of pulmonary to systemic blood flow
o Associations Holt-Oram syndrome, downs, fetal alcohol syndrome

- Ventricular Septal Defect (VSD)
o Clinical Presentation:
Small defects Asymptomatic at birth & often normal development
- Harsh, high-pitched holosystolic murmur over LLSB

Large defects Dyspnea w/respiratory distress, | URTIs, FTT, CHF
- Soft, blowing holosystolic murmur w/systolic thrill & loud P2
- Mid-diastolic apical rumble reflects | flow across mitral valve
- Size of VSD inversely related to intensity of murmur
o Diagnosis:
ECHO Diagnostic
ECG May show LVH, LAH & RVH
CXR May show | pulmonary vascular, cardiomegaly & CHF
o Treatment:
Small defects Most close spontaneously in first 1-2yrs monitor via ECHO
Surgical repair indications:
- Symptomatic w/failed medical management
- Children <1yr w/signs of pulmonary HTN
- Older children w/larger VSDs not reducing in size over time
o Associations Aperts, downs, fetal alcohol, TORCH, cri du chat, trisomy 13 or 18

- Patent Ductus Arteriosus (PDA)
o Failure of ductus arteriosus to close in first few days of life
Leads to left-to-right shunt from descending aorta to left pulmonary artery
o Risk Factors 1
trimester rubella infection, prematurity, female gender
o Clinical Presentation:
Often asymptomatic may have apneic or bradycardic spells, poor feeding, accessory muscle use
- Large defects may present w/FTT, recurrent respiratory infections & CHF
Continuous machinery murmur at sternal border of 2
left intercostal space & loud S2
Wide pulse pressure, bounding pulses, hyperactive precordium
o Diagnosis:
ECHO w/color-flow Doppler Diagnostic
ECG May show LAE, LVH or RVH
CXR May show cardiomegaly & | pulmonary vasculature
o Treatment:
Indomethacin Induces closure of PDA
- Contraindicated if PDA needed for survival:
o Transposition of the great vessels, tetralogy of fallot, hypoplastic left heart
Surgical closure If indomethacin fails or if child >68 months of age

- Coarctation of the Aorta
o Narrowing of aorta almost always at level of ductus arteriosus occurs just below left subclavian artery
Associated bicuspid aortic valve seen >2/3 of pts.
o Clinical Presentation:
Asymptomatic few pts. have HTN in infancy
Classic finding systolic BP higher in upper extremities (140-145mmHg)
- Difference in BP between left & right arm can indicate point of coarctation
Weak/absent pulses in lower extremities & radial-femoral delay
Differential cyanosis + O2 saturation in left arm & LE (postductal) compared to right arm
Short systolic murmur w/late peak at apex, left axilla & left back
May also have LE claudication, syncope, epistaxis or headache
Critical coarctation in infancy requires patent PDA for survival
- Closure of ductus may cause shock in first few weeks of life
o Diagnosis:
ECHO w/color-flow Doppler Diagnostic
ECG RVH (infancy) & LVH (late)
CXR Cardiomegaly & pulmonary congestion
- 3 sign due aortic wall indentation at site of coarctation
- Rib notching due to collateral circulation via intercostal arteries
o Treatment:
PGE1 Keeps ductus arteriosus patent for severe coarctation in infancy
Surgical correction or Balloon angioplasty (controversial)
o Associations Turners syndrome (35%), berry aneurysms, aortic dissection

- Transposition of the Great Vessels
o Parallel pulmonary & systemic circulations aorta connected to RV & pulmonary artery to LV
Incompatible w/life without ASD, VSD or PDA - ass. w/maternal diabetes & rarely DiGeorges
o Clinical Presentation:
Critical illness & early cyanosis occur immediately after birth
Unresponsive to O2 as ductus arteriosus closes can cause severe hypoxemia, acidosis & death
Single loud S2 but no murmur heard if VSD not present
If VSD present cyanosis not prominent & presents w/CHF after few weeks of life
Reverse differential cyanosis may be seen if LV outflow tract obstruction present coarctation, AS
o Diagnosis CXR egg on a string egg-shaped heart w/narrow mediastinum & ECG RAD & RVH
o Treatment:
IV PGE1 To maintain or open PDA
Surgical correction Arterial or atrial switch
Balloon atrial septostomy To create or enlarge ASD last resort if above measure fail

- Tetralogy of Fallot
o PROV Pulmonary stenosis, Overriding aorta, RVH & VSD
o Early cyanosis results from right-to-left shunt across VSD due to pulmonary stenosis
o Risk Factors Maternal PKU & DiGeorge syndrome
o Clinical Presentation:
Tet spells Hypoxia leads to | pulmonary vascular resistance (PVR) & + systemic resistance
- Occurs in exertional states (crying, playing) peak incidence at 2-4 months of age
- Squatting (| vascular resistance) often seen during hypoxemic episodes
- Hyperpnea paroxysm of rapid & deep breathing
Cyanosis Often not present in infancy but develops over first 2 yrs of life
- | Cyanosis often leads to deep sleep & + murmur intensity
Murmur Systolic ejection murmur at LSB & single loud S2 due to RV outflow tract obstruction
- RVOTO is progressive resulting in | right-to-left shunt
Hypoxemia May cause FTT or AMS if severe seizures or loss of consciousness
o Diagnosis:
CXR Boot-shaped heart due to small PA & RVH & + pulmonary vascular markings
o Treatment:
Severe pulmonary stenosis PGE1 to maintain PDA along w/urgent surgical consultation
Tet-spells O2, Propranolol, Phenylephrine, Morphine squatting & fluids also help
Blalock-Taussig shunt Definitive surgical correction

- Ebsteins Anomaly
o Congenital defect of tricuspid valve septal & posterior leaflets are malformed & displaced into RV
RA massively enlarged & patent foramen ovale often exists allowing R-to-L shunt
TR & accessory conduction pathways (WPW) often present & ass. w/arrhythmias
o Treatment Surgical tricuspid valve repair or replacement
o Associations Lithium or Benzodiazepine use in 1

- Hypoplastic Left Heart Syndrome
o Severe hypoplasia of LV MCC of death from CHD in first month of life
o Systemic circulation dependent on ductus patency closure causes circulatory shock & metabolic acidosis
Treat w/intubation, IV PGE1 & correct metabolic acidosis
o Treatment Surgical correction (50% survival to late childhood) or heart transplant

- Total Anomalous Pulmonary Venous Connection (TAPVC)
o Characterized by all pulmonary veins draining into right-sided circulation
No direct oxygenated pulmonary venous return to left atrium
o ASD must be present to allow blood to shunt into LA & systemic circulation treat w/surgical repair

- Truncus Arteriosus
o Single great vessel gives rise to aorta, pulmonary & coronary arteries truncal valve overlies a large VSD
o Treatment Surgical repair within first 6 months of life