USMLE Step 3 Cardiology

Table Of Contents
1 Community Health Centers
2 Office
3 Inpatient Facility
4 Emergency Department

Community Health Centers

  • LDL levels:
    • keep < 100 in pt w/ known CHD risk equivalent (CAD, MI, PVD, or inpatient DM).
    • If pt has none of these problems, can keep below < 160 if 0-1 RF, < 130 if >=2 RF.
    • Consider drug therapy only day 30 above the threshold, unless > 2 RF.
  • Initial DOC for newly diagnosed HTN:
    • is thiazide diuretic.
    • A common side effect is photosensitivity, leading to a rash in sun-exposed areas.
    • Rx by stopping med, or avoid sun exposure.
    • Thus, this is a common side efx of meds in newly diagnosed HTN.
  • Best RF to modify to reduce risk of CAD:
    • is LDL.
    • HTN is also good but not as good as LDL.
    • Other stuff helps too (exercise, stop smoke, control DM), but they don’t lower risk as much as LDL and HTN.
  • Secondary HTN:
    • Consider it in a young patient w/ high blood pressure.
    • 90% of secondary HTN is d/t unidentified cause.
    • Otherwise, the MCC is renovascular HTN.
    • Look for abd or flank bruit in pt with renovascular HTN.
    • Other causes: pheno (headaches, tachy), Cushing’s disease (edema), advanced renal disease (edema).
  • Retinal abnormalities:
    • is a long term effect of HTN, not seen early in disease.
  • DM
    • is the single most important predictor of adverse CV outcomes.
    • Such a good predictor that DM is considered a CHD equivalent.
    • In women, the prediction is even more important.
  • For people with DM
    • keep BP < 130/85, versus 140/90 in a healthy person.
  • AAA:
    • Cutoff for surgery is > 5 cm diameter.
    • If smaller, do periodic imaging.
    • Rapid growth can also need surgery.
    • Big time RF is smoking.
    • Other RF don’t have as much impact as smoking cessation does.

Office

  • Amlodipine side efx:
    • fluid retention and urticarial rash.
  • ACEI side efx:
    • angioedema, urticaria.
    • Rash is usually psoriatic, not photosensitivity in nature.
    • Note that ARB might also cause angioedema if a pt has bad experience w. ACEI.
  • Paroxysmal a fib:
    • present w/ EPISODIC palpitation possibly associated w/ symptoms.
    • Same CVA risk as normal afib, so need warfarin.
    • Either rate or rhythm control is effective if asymptomatic.
    • If there are marked or persistent symptoms (palpitation, dizzy, dyspnea) rhythm control is better.
    • Amiodarone is the preferred drug for rhythm control if pt also has some other structural heart disease
      (cardiomyopathy, CHF, CAD).
    • Flecainide can work ONLY if pt has NO structural heart disease. It can lead to fatal arrhythmias if you give it to pt w/ structural heart disease.
  • Ibutilide:
    • use for acute termination of a-fib.
  • Fibrinogen:
    • associated w/ increased CV risk. > 3.43 is a double risk. > 2.7 is high.
    • Drug therapy to decrease fibrinogen hasn’t been shown to be preventative.
    • However, stopping further increase helps.
  • Within statins,
    • lovastatin and atorvastatin increase levels, while prava and simva don’t increase.
    • Thus, if someone is at a high level for fibrinogen, must think about which statin to use if pt also has high LDL.
  • Nonsusstained ventricular tachy:
    • >=3 consecutive ventricular beat w/ rate > 120, and the episode lasts < 30 sec.
    • If you see this, pt most likely has structural heart disease. Ex. Prior MI scarring, ventricular hypertrophy, mitral valve prolapse (midsystolic click).
    • If you pick up this rhythm on EKG, next step is to get echo and stress test to r/o ischemia.
  • CHF:
    • ACEI are the main therapy.
      • Improve survival and delay progression of disease.
      • Indicated even if pt is asymptomatic.
      • Only contraindications are poor tolerance to drug, or renal failure or hyperkalemia.
  • CHF:
    • standard therapy is diuretic, ACEI, bb, digoxin, or spironolactone.
    • ACEI is the best, and won’t exacerbate confusion in a pt.
    • digoxin could worsen confusion.
  • If ACEI isn’t well tolerated (angioedema),
    • then hydralazine and isosorbide dinitrate is a common combination.
    • Side efx might include drug-induced lupus.
      • Manifest as flu-like symptoms (fever, malaise, myalgia, facial rash). LAD, splenomegaly can also happen.
      • Antihistone antibody is marker of drug induced lupus.
      • Rx is to stop drug.
      • Hydralazine is safe in pregnancy (as are dopa, labetalol)
  • CHF as a cause of hypoNa.
    • The decreased CO and SBP decreases perfusion at carotid baroreceptor, so body stimulates ADH and renin angiotensin despite volume overload.
    • This causes even more fluid retention, leading to hypoNa.
    • Must correct levels gradually, not acutely.
    • Best Rx is water restriction.
  • CHF:
    • syndrome which results from impaired ventricular emptying (systolic) or relaxation (diastolic).
    • Symptoms:
      • fatigue, weakness (d/t reduced CO), edema (d/t fluid retention).
      • Exertion exacerbates all symptoms.
      • Its’s a syndrome, so it’s a clinical diagnosis based on H and P. 
    • Dx is 2 major or 1 major + 2 minor. Minor criteria:
      • PND, orthopnea, raised JVP, rales, S3, CXr findings (increased vascular congestion or silhouette) are major criteria.
      • bilateral LE edema, hepatomegaly, dyspnea on exertion, nocturnal cough).
  • Digoxin toxicity:
    • N/V, anorexia, confusion, visual disturb, cardiac abnormalities. Drugs that can cause toxicity: verapamil, quinidine, amiodarone, spironolactone.
  • Hypercholesteremia + hypertriglyceridemia (>200):
    • DOC is a statin.
    • If statin isn’t good alone add gemfibrozil or niacin.
  • Lone a fib:
    • a-fib which occurs w/o any other signs of clinical heart disease (r/o CAD, TH, PE, HTN, DM, CHF). Warfarin is not necessary, just aspirin is good enough.
  • Unstable angina:
    • no matter what, need a coronary angio ASAP to look at blockage and see it’s severity.
    • If angio reveals pt to be high risk, consider percutaneous coronary intervention (PCI) or CABG.
    • Remember that DM will increase rate of progression a lot.
    • Evaluating heart ischemia in pt w/ prior CABG, poor heart function, or if there already exist baseline
  • EKG changes:
    • use adenosine or dipyramidole to induce ischemia and watch the technetium-99. (sestamibi).
    • Stress echo should only be done if adenosine cant be used for some reason.
    • Remember that arthritis can also impair exercise.
  • Adenosine
    • can induce bronchospasm, so if pt has COPD or asthma, adenosine is contraindicated.
    • Use dobutamine instead.
  • Orthostatic hypotension dx
    • with fall or 20 SBP or 10 DBP.
    • Can happen after standing up or even eating.
    • Drop in BP must happen within 2-5 min of standing.
  • 2 MCC ortho hypo:
    • autonomic dysfunction or intravascular volume depletion.
    • Autonomic dysfunction (DM neuropathy).
    • Drugs: antihypertensives, vasodilators, anti-angina drugs.
  • Ca channel blocker:
    • peripheral edema is common side efx.
    • The –dipines are common, but diltiazem can also cause it.
  • Exercise stress test
    • is FSOM in pt w/ angina symptoms..
  • Weight loss
    • is the best non-drug way to decrease BP.
    • Benefit in overall CV risk is unclear but probably helps.
  • Other first-line drug for HTN besides ACEI
    • is b-blocker.
  • Positive stress test:
    • > 1 mm downsloping ST depression.
    • NSOM is to do a cardiac cath to see where the lesions are and to possibly to balloon stenting.
  • Right-sided endocarditis:
    • commonly see R sided involvement or septic pulmonary emboli.
    • Septic emboli manifest as scattered bilateral rales.
    • Pulmonary infiltrates on both sides.
    • IVDU is the likely cause.
    • Otherwise, R sided disease is very uncommon.
  • Coumadin management:
    • If INR > 3 but < 5, just hold drug for a few days to get level to therapeutic.
    • If INR > 5 but < 9, stop the drug and give small dose of vit K (1-2 mg).
    • If > 9 but < 20, higher dose of vit K.
    • If > 20, consider FFP.
    • If at anytime pt is bleeding, give FFP.
  • Drug interaction w/ warfarin:
    • Amiodarone increases warfarin action. If need to have the two together, reduce warfarin by 25%.
  • MVP:
    • MC valve abnormality in industrialized nations. Mid to late systolic click, most easily heard over LV.
  • Mitral regurg:
    • holosystolic decrescendo murmur (can be 2ndary to MVP) heard in apex, radiates to axilla.
    • Increases w/ grip, decrease w/ Valsalva.
  • Systolic murmur in LU sternal border:
    • pulmonic stenosis.
  • Mitral stenosis:
    • low pitched diastolic rumble heard over the apex best when pt is lying L lat decubitis.
    • The narrowing of the valve leads to increased P in LA, which backflows into increased P in pulmonary vasculature and R side of heart.
    • MCC is rheumatic fever.
    • May present as hemoptysis.
    • LA can enlarge, leading to elevation of L mainstem bronchus, and flattening of L heart border.
    • Mitral stenosis: opening snap with diastolic rumble. Best heard mid clavicular on L side between 5th and 6th ribs.
  • MC congenital heart malformation:
    • VSD.
    • If large enough may be symptomatic.
    • Murmurs is pansystolic murmur at LL sternal border.
    • Should get an echo.
    • VSD is not congenitally cyanotic, only if its big enough.
  • Polypharmacy:
    • Using too many diuretics, a-blocker, or nitrates can induce ortho hypo.
  • MCC perioperative mortality:
    • cardiac death.
    • Highest risks: unstable angina and critical aortic stenosis.
    • Exercise angina and MI < 6 mo ago are also decently big RF, but less than the other two.
  • Amiodarone induced lung toxicity:
    • MC presentation is as a chronic interstitial pneumonitis.
    • Nonprod cough, fever, pleuritic CP, focal or diffuse interstitial opacity on CXR.
    • Rx with d/c drug.
    • If really bad, consider steroids.

Inpatient Facility

  • Metformin:
    • higher chance of lactic acidosis (contraindicated) if renal insufficiency, hepatic dysfunction, or CHF.
    • Thus, if pt goes to a procedure that needs contrast (ex. Cardiac cath), you must d/c metformin a bit before the procedure.
  • Acute MI:
    • sinus bradycardia could happen after MI.
    • FSOM is IV atropine. If that doesn’t work, then must intervene w/ thrombolysis or PCA (angio).
    • In the meantime, probably need to do transvenous cardiac pacing while setting up the thrombolysis .
    • Remember that thrombolysis is contra in recent abd surgery (2 wks).
  • If need to intervene in CAD in a pt with DM,
    • CABG is better than angio.
    • DM has a higher chance of restenosis, so angio or balloon + stent isn’t good enough.
  • Multifocal atrial tachy:
    • > 3 P waves of different morphologies. Narrow QRS, variable PR segment.
    • MCC is hypoxia and COPD.
    • Thus, someone showing this arrhythmia must first analyze their O2 status, since correction may eliminate the arrhythmia.
    • Other causes are hypoK and hypoMg.
    • Rx is always reverse the cause.
    • If the initial therapy doesn’t work, try bb or verapamil if bb is contra (COPD, asthma).
  • Acute heart failure:
    • MCC are papillary m. rupture, infective endocarditis, chordae tendinae rupture, and chest wall trauma.
    • A mitral regurg makes you think of ruptured chordae tendinae.
    • Dx DDx for chordae tendinae rupture: IE, ischemia, MV rupture.
  • Ehlers Danlos syndrome:
    • mitral valve degeneration can happen, leading to chordae rupture.
    • Pes planus and scoliosis are common findings.
    • Joint hypermobility, hyperextensibility. Marfans can also cause a rupture.
  • Anticoagulation for mechanical valves:
    • mechanical mitral and aortic valves need INR between 2.5-3.5.
  • Torsades de pointes:
    • look for an EKG showing a QT interval prolongation, followed by some sort of clear arrhythmia.
    • Frequent variation in QRS morphology is more likely torsades.
    • Rx for torsades with hemodynamic compromise is immediate defibrillation.
    • Once pt is stable, then give MgSO4.
    • Remember that the lab value for Mg is unreliable, so just give it regardless of levels.
    • If Mg therapy fails, then do a temporary transvenous pacemaker.
  • Synchronized cardioversion:
    • for v-tach, a fib.
  • s/p MI,
    • best to hold sexual activity for 6 weeks after the event.
    • If there were complications because of the MI, need to further evaluate.
  • A-fib:
    • First line for rate control is Ca channel blocker. Diltiazem is good.
    • Propranolol is good alternative if diltiazem is contra (significant CHF, cardiac conduction system disease).
  • Cancer drugs w/ CV side efx:
    • -rubicin and mitoxantrone.
    • These are cardiotoxic, so should get baseline radionuclide ventriculography (RVG) can detect early toxicity.
    • This can do noninvasive serial monitoring of cardiac function.
    • Multiple gated blood pool (MUGA) is also good.
    • Echo isn’t good enough because can’t do serial evals.
    • Used more in kids getting chemo, to avoid radiation exposure.

Emergency Department

  • If someone presents with cardiac symptoms, but all the first-line tests come back negative,
    • consider doing continuous EKG monitor for 24 h to evaluate for arrhythmias.
  • Stress test with radioactive stuff:
    • a perfusion defect is a place where blood flow is not the same as elsewhere.
    • Lateral wall of LV is supplied by L circumflex, so defect there is likely this vessel.
  • In a pt with acute MI,
    • Ca channel blockers may actually be harmful.
    • Think about this b/c often they might be on the drug to control HTN.
    • In contrast, bb, ACEI, and statins can help prevent CAD.
  • 2nd degree AV block:
    • Rx with permanent cardiac pacemaker insertion. (aka transvenous pacemaker).
    • This helps prevent progression to Type III block.
    • Remember that 3rd degree block is a random, no relationship at all btw A and V beating on EKG.
  • Acute MI management:
    • FSOM includes O2, IV access and give aspirin and nitro.
    • ACEI aren’t used acutely but reduces mortality if taken for the weeks after an MI.
    • bb helps w/ decrease myocardial demand and controls HR.
    • Can give after aspirin, nitro, and morphine.
  • Acute MI:
    • If EKG shows ST-segment elevation in 2 contiguous leads,
      • then thrombolytics are indicated, and if pt presents within 12-24 h of symptoms.
      • Must give NO before getting the EKG.
      • Contra for thrombolytics are active bleed, any intracranial event (bleed, ischemia, neoplasm), SBP > 180, or trauma.
      • Don’t confuse with ST-segment depression, which is just ischemia.
  • Flash pulmonary edema:
    • Presents w/ acute onset of SOB.
    • No previous history necessary.
    • Hypertensive crisis can cause it, so look for a very high BP.
    • CXR looks like lots of edema, and there will be diffuse crackles.
    • FSOM in any flash pul edema is give O2 (O2 sat will be low), morphine, and IV furosemide (loop diuretics).
    • If the cause is HTN crisis, the preferred drug to give is IV NO or nitroprusside.
  • Other causes of flash pul edema:
    • mitral stenosis or acute aortic/mitral regurg.
    • Thus, after someone has an episode of this, get an echo.
    • Bb are CONTRAINDICATED in acute heart failure, can slow heart too much, and lead to death.
  • Cardiogenic pulmonary edema:
    • Initial Rx is similar: O2, morphine (reduces work of breathing), and a loop diuretic.
  • Cardiogenic shock complicated by hypotension:
    • dopamine is a good choice.
  • Acute pericarditis:
    • can be infarct associated, and happen after an MI (esp. transmural).
    • The associated CP depends on position, and worsens w/ deep inspiration.
    • EKG has diffuse ST elevation w/ PR depression.
    • Rub is heard over L sternal border (a scratchy sound), which gets louder as pt leans forward.
    • Rx is NSAIDS (or anything for pain).
  • Dressler’s syndrome:
    • happens in MI pt and after cardiac surgery.
    • Usually develops weeks/months after MI not days.
    • Presents w/ fever, leukocytosis, pleuritic chest pain, and pericardial rub.
    • Thus, very similar to pericarditis, but look at the time course.
    • Q waves are indicative of old infarct (days old sometimes)
  • Aortic stenosis:
    • Area of aortic valve < 1 cm, 2 is considered severe stenosis.
    • Onset of symptoms has a big effect on prognosis, so prompt intervention is important in symptomatic aortic stenosis (syncope,
      angina, dyspnea).
    • Rx w/ aortic valve replacement will reduce mortality.
    • Balloon valvulotomy has only transient efficacy, and high procedural morbidity.
  • Carotid artery dissection:
    • presents w/ unilateral headache + associated Horner’s syndrome (miosis, ptosis, and anhidrosis) on the affected side only.
    • Thus, the symptoms aren’t bilateral.
    • Some causes are trauma, CT disease, smoking, seatbelts in MVA.
    • Dx is MRA.
    • If MRA fails, then catheter angio is definitive test.
    • Rx is with anticoagulation w/ heparin or platelet agents.
    • Pt with this dissection is at high risk of developing cerebral infarction.
  • MCC of CHF
    • is ischemic heart disease.
    • Thus, if you diagnose a new case of CHF, and are still trying to look for etiology, first r/o coronary lesions with a cardiac stress test.
    • Other causes of CHF are HTN, and valve or renovascular disease.
    • BNP is not useful in this case.
    • BNP’s main purpose is to distinguish between cardiogenic pulmonary edema from primary pulmonary conditions.
  • Acute aortic dissection:
    • Usually presents in older male with long history of HTN and atherosclerosis.
    • In younger pt, think CT disease (Marfan, Ehler Danlos), inflammatory vasculitis, aortic valve problem, or cocaine.
    • Presents w/ sudden onset of sharp tearing chest or back pain.
    • If tear happens in ascending aorta, pt may develop acute aortic insufficiency, causing acute heart failure.
    • Dissection could also extend into coronary vessels, leading to cardiac tamponade or hemothorax.
    • PE shows difference in BP between 2 arms.
    • CXR can show mediastinal widening.
    • TEE is Dx of choice.
    • FSOM is to give bb to lower SBP and LV contractility to < 100-120 mmHg and < 60 bpm.
    • If bb is not enough to lower BP, give sodium nitroprusside.
    • After this is achieved, go to surgery right away.
  • Syncope w/o any apparent cause
    • is most likely neurocardiogenic.
    • Prodrome of nausea, lightheadedness, pallor, and diaphoresis.
    • Precipitating events include prolonged standing, exertion, venipunture, or painful stimulus.
  • Ventricular tachy vs. sus supraventricular tachy:
    • supra has regular, narrow QRS complexes.
    • Ventricular tachy has wide QRS complexes.
  • A flutter
    • is in a sawtooth pattern.
  • WPW syndrome:
    • delta wave is a upstroke of QRS that is slurred.
    • It may present as SVT.
    • If verapamil or bb are given to WPW pt, v fib may occur d/t increased accessory pathway conduction.
  • Pericardial effusion:
    • can happen in response to pericarditis or any malignancy.
    • If too much fluid gets out, and tamponade develops,
    • presents as Beck’s triad: hypotension, muffled heart sounds, and elevated JVP. SOB is present.
    • Dx is echo emergently and Rx is surgery.
    • Equal diastolic P on all chambers on cardiac cath is also present.
    • Pericardiocentesis is life-saving.
  • Chest pain relieved by NO
    • is probably cardiogenic.
    • Get cardiac enzymes.
  • A-fib which is hemodynamically unstable:
    • Must do synchronized cardioversion. (in sync w/ the R wave).
    • If pt is stable, then you can convert to normal w/ drug (amiodarone, sotalol).
    • These agents aren’t for long term rate control.
    • Long term rate control is with diltiazem or metoprolol.
  • Asynchronized cardioversion
    • is TOC for ventricular fibrillation
  • Acute arterial occlusion:
    • MCC are recent MI and afib.
    • Presents as sudden symptoms usually in LE (numbness, coldness, delayed capillary refill, pulse deficit in distal arteries).
    • Very important to tx with immediate IV heparin followed by continuous heparin infusion.
  • Cocaine-induced myocardial ischemia:
    • Initial Rx is nitrates, benzos, or Ca channel blocker.
    • If no improvement with these (d/t possibility of coronary artery thrombosis), then do immediate coronary
      angiography.
    • A distinct feature of cocaine-induced vasospasm is that it might lead to coronary artery thrombosis.
  • Acute coronary syndrome:
    • STEMI on EKG requires an urgent cardiac cath.
    • Non-STEMI can be managed with serial cardiac enzymes, as can unstable angina without any EKG changes.
  • TCA overdose:
    • hypotension, anticholinergic effects, CNS symptoms, cardiac arrhythmia.
    • Can lead to QRS prolongation and reentry arrhythmia (v-tach, vfib, torsades).
    • Best agent for TCA induced cardiotoxicity is sodium bicarbonate.
    • Lidocaine is the best anti-arrhythmic for TCA induced arrhythmias.
  • Syncope
    • can be diagnosed by EKG + H/P in 70% of cases.
    • FSOM in a new syncopal episode is EKG.
    • Neurological testing (CT head EEG) are usually not valuable unless something in the H and P clearly shows that it’s a neurological etiology.