127 questions

SILVERSTIEN
1. Fixed Splitting = ASD
2. Continuous machine-like murmur = PDA
3. S3: rapid ventricular filling tensed mitral chordae tendinae. Assoc w Volume Overload, Systolic dysfunction, DCM, MR, TR.
note: S3 is NORMAL in CHILDREN.
4. S4: atrial contraction against stiff ventricle. Hear S4 gallop in diastolic dysfunction, LVH, ischemia, HCM.
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10. Young woman atypical/non-cardiac chest pain--no stress test bc poor positive predictability; also: if rhythm is normal during
palpitations, just reassure.
11. Is chest pain exertional? Orthopnea.
12. do a pre-op stress test on patients who are at a lower functional status and are getting an elective surgery
ISCHEMIA [Silverstein]
1. RCA infarct: ST elevation II, III, aVF. (reciprocal depressions @ I and aVL). Inferior infarct, may affect SA and AV node (sinus
bradycardia, AV block), RV infarct, posteromedial papillary rupture.
2. In a STEMI, once you see ST elevation on EKGNEXT BEST STEP is to open up the artery (Heart Cath)
3. 1st line anti-anginal: BETA BLOCKERS (to reduce contractility, HR and increase time in diastole for greater coronary flow)
4. Myocardial Perfusion imaging stress test (exercise or adenosine for vasodilation)
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HEART FAILURE [Silverstein]
1. LEFT SIDED HF: dyspnea, orthopnea, PND, fatigue, pulmonary rales/crackles, LOUD P2 (pulmonary HTN), S3 gallop (if
systolic), cephalization on XCR,
2. EKG shows biphasic P-waves=LAE. Chronic left atrial overload (eg MS): LVEDP LA pressure pulm vasc congestion
3. BNP levels: >900 pg/mL is SEVERE HF.
4. Persistently symptomatic African American patient with HFrEF (systolic dysfunction): Hydralazine and Nitrates.
5. NYHA Class II - IV patients: ACEi + B-Blocker + Spirinolactone (provided that they have OK renal function & normal K), add
furosemide if volume overloaded.
6. Cor Pulmonale = right sided HF due to long-term pulmonary hypertension
7. acute increase in creatinine indicates renal failure probably means acutely decomensated heart failure.
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CARDIOMYOPATHY & PERICARDIAL DISEASE [Silverstein]
1. CHAGAS: Trypanosoma cruzi. LBBB + LAD, apical aneurysm, systolic dysfunction (HFrEF), S3, fibrinous myocarditis, dilated
cardiomyopathy. Tx acute phase: Amiodarone (anti-trypanosomal)
2. HYPERTROPHIC CARDIOMYOPATHY: asymmetrical septum, LV outflow obstruction, Diastolic dysfunction (HFpEF),
cresendo-decrescendo @ LLSB that worsens with valsalva/standing ( venous return worsens obstruction). Sx management:
ECHO, B-Blockers, CCBs, DISOPYRAMIDE (Type IA)-negative inotropy. AVOID nitrates/digoxin!
3. CONSTRICTIVE PERICARDITIS: pericardial thickening/calcification 2' to inflamm of virus/TB/SLE/procainamide/post-op.
Friction rub, Kussmaul's sign, PERICARDIAL KNOCK, STEEP Y DESCENT, diffuse ST elevations, , equalized EDP in all 4
chambers

4. CARDIAC TAMPONADE: pericardial effusion, fluid compresses heart CO. Beck Triad: (1) JVD elevation; (2) muffled heart
sounds; (3) hypotensive. PULSUS PARADOXUS, electrical alternans & low voltage ekg. Steep X & BLUNTED Y descent. Dx:
ECHO then heart cath. Tx: pericardiocentesis.
5. Young pt athlete with syncopeNEXT best test to do is an ECHO
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VALVULAR DISORDERS
1. MITRAL STENOSIS: @ Apex, Diastolic Decrescendo w OPENING SNAP. Loud S1. 2' to Rheumatic Heart Disease.
Complications due to HIGH LA PRESSURES: pulmonary congestion/HTN (orthopnea/hemoptysis), LAE (A-Fib/thrombi/stroke)
2. MITRAL REGURGITATION
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PERIPHERAL VASCULAR DISEASE [D'AMICO 2 hrs]
1. 40% of peripheral vascular disease patients are ASYMPTOMATIC
2. PAD Pathogenesis: FOAM cell FATTY streak Intermed lesion ATHEROMA Fibrous plaquecomplicated lesion/rupt
3. Femoropopliteal occlusive disease: Most COMMON site for LE atherosclerosis is DISTAL SUPERFICIAL FEMORAL A.
4. Thromboangitis Obliterans (Beurger Disease): YOUNG MALE SMOKERS especially effecting ARTERIES: RADIAL & TIBIAL A.
5. Picture of angiogram: top arrow= superficial femoral A; bottom arrow: Distal Popliteal Artery (before trifurcation)
6. RAYNAUD DISEASE: @ Fingers & Toes (white/red/blue)
In evaluating coronary disease or PAD, the NEXT versus BEST is an important distinction because you would do the less risky non-invasive test
(ABI) before proceeding to the gold standard test (angiogram) that is more costly and has additional risks.

FOLEY
1. Angiotensin II, Aldosterone & Endothelin-1 promote ventricular remodeling & concentric hypertrophy in the failing heart
decreased contractility & efficiency
2. Frank Starling curve is shifted DOWNWARD & to the RIGHT in heart failure (decreased compliance, increased LV EDV)
3. Decreased Baroreceptor stim transmits to medullary CV area which increases sympathetics: (1) increased NE (2) increased HR
& contractility (3) vasoconstriction (4) renin/AII/Aldosterone; also transmits to hypothalamus which stimulates ADH secretion
from posterior pituitary.
4. In HF, abnormally high capillary hydrostatic pressure (Pc) causes NET FILTRATION into interstitium. This is compounded by the
net rate of capillary filtration exceeding that of lymphatic flow EDEMA formation.
5. Endothelin-1 responds to hypoxia/sympathetics detrimental effects in CHF.
6. BNP secreted in response to distention of ventricle causes vasodilation & Na excretion, but in HF, kidneys become less
responsive to ANP & BNP, so retention of sodium & water persists in HF patients
7. Reactive Hyperemia: following transient obstruction of blood, there's compensatory increase in blood flow to organ/tissue
8. Mechanical compression during systole mostly affects ENDOCARDIAL layer, there will be enhanced flow during diastole (note:
CAD can especially restrict endocardial flow)
9. Resistance, R = 8nL/pi*r^4
10. Coronary blood flow is dominated by vasodilation necessary for cardiac metabolism; overpowers neural vasoconstriction
11. CO = HR * SV; SV=EDV-ESV; PP = systolic-diastolic; MAP = 2/3*diastolic + 1/3*systolic
12. Myocardial Oxygen Demand: Wall stress (ventricle diameter, wall thickness), afterload, heart rate, contractility.
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FUCHS
1. Nitroglycerine MOA: cGMP dephosphorylation of myosin light chain Ca2+ VENODILATION ( preload). Sides:
inhibits platelet aggregation, makes methemoglobin (tissue hypoxia/death), reflex tachycardia, HA, Tolerance.
2. Nitroprusside Side effect =Cyanide poisoning
3. CCBs Verapamil & Diltiazem = NEGATIVE INOTROPY (reduced contractility). Use: Angina, A-Fib and HTN
4. Atenolol: cardioselective Beta-Blocker (OK for pulm dz's), excreted by kidneys (renal failure will increase its half life)
5. LMW Heparin advantages: bioavail/duration, fixed dosages, no monitoring, less likely to cause HIT, LESS bone loss.
6. Ranolazine: for Chronic Angina only. inhibits late Na phase, reduces intracell calcium, reduces vent tension, less O2 demand.
Sides: QT prolongation, risk torsades de pointes, constipation/nausea/dizziness.
7. Warfarin: inhibits production of VII, IX, X, Prot C and Prot S. Cutaneous necrosis, tissue infarct, bleeding. TERATOGENIC.
8. Nesiritide: recomb BNP for vasodilation, natriuresis and diuresis. for Acute decomp HF. SIDES: Renal damage, HoTN, HA
9. Dobutamine/Dopamine: B agonists for Acute decomp HF. Non-selective B activation: stimulates all things in heart, also
bronchodilates, glycogenolysis, glucagon release, renin release, vasodilation. NOTE! Dopamine specifically helps the kidneys out
and increases renal perfusion. SIDES: arrhythmia, angina, HA and tremor.
10. Risk of Thrombocytopenia: Bypryidines (Inamrinone and Milrinone) and also Heparin (specifically Unfractionated)
11. Spirinolactone & Eplerenone: Aldosterone Antagonists that decrease ENaC @ DT & CD. potassium sparing.
12. Digoxin toxicity occurs in hypokalemia, renal failure, or in combo w verapamil/amiodarone/quinidine. Tx: Magnesium or antidigoxin Fab (Digibind)
SORWEIDE
1. NEW LBBB is a MI until proven otherwise
2. LBBB absolutely require WIDE QRS > 0.12 sec, deep S in V1.
3. HYPERKALEMIA = Peaked T waves (most dangerous acute EKG abnormality)
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PUMERANTZ
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2. GPC, OPTOCHIN RESISTANT, DEXTRAN, BILE-SOLUBLE, alpha-hemolytic = STREP VIRIDANS @ MITRAL VALVE
(manuever: . subacute IE. Penicillin + ceftriaxone (susceptible) OR penicillin + gentamicin (some resistance)
3. Time dependent killing: T<MIC = beta lactams (penicillin)
4. Penicillin G in high doses in setting of renal failure = seizures
5. GPC, Cat+, Coag+, beta-hemolysis, Clumping factor A = STAPH AUREUS (IV drug user) @ TRICUSPID VALVE (murmur @
LLSB that increases with inspiration)
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KANDPAL
1. CARNITINE DEFICIENCY: Dilated Cardiomyopathy and cardiact arrest. Inability to transport LCFAs into mitochondria
2. Carnitine Palmitoyl Transferase 2 deficiency = cardiac hypertrophy.
3. Reperfusing ischemic heart increases FA oxidation accumulated Acetyl CoA triggers neg feedback on pyruvate DH
increased lactate levels pH acidosis. Damaging! want to administer partial FA oxid inhibitor to prevent this.
PARSA
1. 7-10 days post-MI: increased macrophages (appears yellow), complications: free wall rupture (TAMPONADE), Papillary
rupture (Mitral Regurgitation), interventricular septum rupture due to macrophage-mediated destruction
2. Troponins rise @ 4 hrs, peak @ 24-48 hrs, remain elevated for 7-10 days post-MI.
3. Most dangerous plaques: soft, partially necrotic thin capped plaque: most susceptible to ACUTE PLAQUE CHANGE
transmural MI
4. PIC: Adhesive Pericarditis
5. PIC: Myxoma @ Left Atrium (benign)
6. Restrictive Cardiomyopathy = AMYLOID HEART , diastolic dysfunction due to stiff ventricular walls.
GUO
1. HIGH YIELD CONCEPT in clinical scenario
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MESA
1. Aortic Dissections: Type I debakey starts before arch & extends down abd. Type II debakey=only before arch. Type III
debakey=only AFTER arch.
2. Modifiable factors in Atherosclerosis: hyperlipidemia, DM, Smoking, HTN
3. KAWASAKI DISEASE: young asians. anti-endothelial antibodies acquired heart dz in children. Tx: IVIG + Aspirin
4. THROMBOPHLEBITIS: affects deep veins of legs (usually asymptomatic), most severe complication = pulmonary embolism
YASMER
1. HOW TO USE MODALITIES (MRI, perfusion, CT)
2. Rest vs stress PIC
3.