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Cardiology Flashcards

1
Q

Viruses implicated in dilated cardiomyopathy

A

1) Coxsackie B. Also parvovirus B19, HHV6, adenovirus and enterovirus.

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2
Q

Cardiac problem that results in an S3? S4?

A

S3 = volume overloaded state, causing eccentric hypertrophy and an extra sound when atrial blood hits blood already in the ventricle.

S4 = pressure overloaded state, causing concentric hypertrophy and an extra sound when atrial blood hits a stiffened ventricle.

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3
Q

Sensitivity, specificity and predictive accuracy for diagnosing heart failure in a patient with a BNP > 100

A

90, 76 and 83%

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4
Q

Electrolyte abnormality that is an important predictor of adverse clinical outcomes in patients with CHF?

A

Hyponatremia, it typically parallels the severity of disease. It occurs due to decreased intravascular volume, ADH release and free water retention

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5
Q

Treatment of CHF-related hyponatremia

A

Free water restriction

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6
Q

Drug typically given in the setting of acute MI that is contraindicated if the patient also has pulmonary edema

A

Beta-blockers, these are contraindicated in patients with acute decompensated heart failure because the increased heart rate is essential to adequate tissue perfusion.

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7
Q

Drugs given for initial stabilization of a patient with acute MI. What adjuncts can be given if the patient has persistent pain, hypertension, heart failure, bradycardia or pulmonary edema despite initial treatment?

A

Beta-blocker (unless hypotensive, bradycardic, heart failure or heart block)

Aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor)

Statin

Heparin

Oxygen

Nitrates (avoid this and diuretics if RV infarct)

Persistent pain, hypertension or heart failure = nitrates +/- morphine for pain.

Bradycardia = atropine

Pulmonary edema = furosemide

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8
Q

Cardiac, pulmonary, GI, endocrine, ocular, dermatologic and neurologic side effects of amiodarone.

A

Cardiac = sinus brady, heart block and long QT

Pulmonary = chronic interstitial pneumonitis

GI = hepatitis and transaminitis

Endocrine = hypothyroidism, hyperthyroidism

Ocular = corneal deposits, optic neuropathy

Derm = blue-grey skin discoloration

Neuro = peripheral neuropathy

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9
Q

Arteries most commonly involved in patients with fibromuscular dysplasia

A

Renal, carotid and vertebral arteries

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10
Q

Diagnosis and treatment of fibromuscular dysplasia

A

Diagnosed with CT angiography, catheter-based digital subtraction arteriography if CT angio is inconclusive.

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11
Q

Aldosterone concentration : renin activity in fibromuscular dysplasia? What about with adrenal hyperplasia/adenoma?

A

~10 in fibromuscular dysplasia. > 15 in primary hyperaldosteronism.

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12
Q

ECG characteristics of PAC’s

A

Unusual P-wave morphology because the impulse is coming from somewhere other than the SA node in the atria. Early contractions are also present.

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13
Q

Treatment of symptomatic PAC’s

A

Low dose beta-blockers, decrease stress and cessation of tobacco, alcohol and caffeine.

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14
Q

Indication for fibrinolysis in patient with MI

A

Within 12 of hours of onset of symptoms and unable to undergo PCI

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15
Q

How long should you continue aspirin and P2y12 receptor blockers after drug-eluting stent placement?

A

12 months

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16
Q

Milrinone mechanism of action

A

PDE inhibitor that increases myocardial contractility

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17
Q

Desired CXR location of central venous catheter

A

Angle between the trachea & right mainstem bronchus or proximal to the cardiac silhouette

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18
Q

Congenital causes of high-output heart failure

A

PDA, angioma, pulmonary/CNS AVF

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19
Q

Acquired causes of high-output heart failure

A

Trauma, iatrogenic, atherosclerosis (aortocaval fistula) and cancer.

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20
Q

Side effects and electrolyte changes seen in patients taking thiazide diuretics

A

Hyponatremia, hypokalemia, hypercalcemia, hyperglycemia, hyperuricemia and elevated LDL cholesterol.

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21
Q

Electrolyte abnormalities that put patients at risk for VT when taking furosemide

A

Hypokalemia and hypomagnesemia

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22
Q

Basic lab analysis for a patient presenting with hypertension

A

Rule out other causes of hypertension with:

UA, BMP, lipid profile and baseline ECG

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23
Q

Signs and symptoms of secondary hypertension

A

Malignant hypertension, HTN requiring 3+ drugs, sudden rise in BP with previously normal values and onset at

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24
Q

Causes of secondary hypertension

A

Renal parenchymal disease, renovascular disease, primary hyperaldosteronism, pheochromocytoma, Cushing syndrome, hypothyroidism, primary hyperparathyroidism and aortic coarctation.

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25
Q

Treatment of beta-blocker or CCB toxicity

A

IV glucagon

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26
Q

Most common cause of aortic regurgitation in developed vs. undeveloped countries.

A 
Developed = bicuspid valve
Undeveloped = rheumatic heart disease
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27
Q

Indications for carotid endarterectomy

A

Men: asymptomatic and > 60% stenosed, symptomatic and > 50% stenosed.

Women: symptomatic or asymptomatic and > 70% stenosed.

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28
Q

Management of aortic dissections

A

IV labetolol. Surgery is only indicated for type A dissections.

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29
Q

Why patients with aortic stenosis get angina?

A

LV hypertrophy results in increased myocardial oxygen demand.

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30
Q

Common causes of constrictive pericarditis

A

Idiopathic or viral, radiation, cardiac surgery, connective tissue disorders and Tb.

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31
Q

Management of patients with claudication

A

Low-dose aspirin and statin therapy + 12 weeks of exercise for 30-45 minutes 3x per week. Add cilostazol if symptoms persist afterwards. Consider vascular consult if ABI

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32
Q

Management of cocaine-related STEMI

A

Same as regular STEMIs except: avoid beta-blockers. Also add IV benzodiazepine, CCB or alpha-blocker to reduce vasospasm.

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33
Q

Management of hypertensive emergency

A

MAP lowered by 10-20% in 1st hour and 5-15% over next 23 hours.

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34
Q

Types of heparin-induced thrombocytopenia (HIT)

A

Type 1 HIT: non-immune direct effect of heparin on platelet activity within first 2 days of exposure. Platelet count normalizes with continued therapy and there are no clinical consequences.

Type 2 HIT: immune-mediated due to anti-platelet factor 4 antibodies complexed with heparin. This causes thrombocytopenia around 30k-60k and thrombosis 5-10 days after starting heparin. This can be life threatening.

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35
Q

Hypertensive urgency vs. emergency

A

Urgency = > 180/120 without symptoms or signs acute end-organ damage

Emergency = MH (retinal hemorrhages, exudates and papilledema) and encephalopathy (cerebral edema and non-localizing neurologic signs and symptoms)

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36
Q

Phases of post-MI arrhythmia

A

1a = immediate arrhythmia within 10 minutes of coronary occlusion due to ischemia-related areas of heterogeneous conduction causing re-entrant arrhythmias.

1b = delayed arrhythmias due to abnormal automaticity 10-60 minutes after MI

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37
Q

Lab studies present in a patient with recent atheroembolism from coronary vascularization

A

Eosinophilia, eosinophiluria and hypocomplementemia with renal dysfunction that can persist beyond 2 weeks.

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38
Q

Lab studies present in a patient with contrast-induced nephropathy

A

Muddy-brown granular and epithelial cell casts 3-5 days after exposure and resolution within 1 week.

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39
Q

Mechanisms of niacin-induced peripheral vasodilation

A

Drug-induced release of histamine and prostaglandins. This is why it can be treated with low-dose aspirin 30-minutes before taking niacin and improvement 2-4 weeks later.

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40
Q

CXR sign for pericardial effusion

A

Water bottle sign with clear lung fields

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41
Q

Treatment of stable angina

A

1st line = beta-blockers. CCB or long-acting nitrates can be used if beta-blockers are contraindicated, poorly tolerated or are ineffective.

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42
Q

Osler nodes vs. Janeway lesions

A

Janeway lesions are non-tender lesions on the palms and soles due to vascular phenomena associated with infective endocarditis.

Osler nodes are painful lesions on the fingertips and toes due to immunologic phenomena associeated with infective endocarditis.

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43
Q

Patient has recurrent high fevers, arthritis and a maculopapular, nonpruritic rash affecting the trunk and extremities only during febrile episodes.

A

Adult Still’s disease.

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44
Q

Common presentation of uremic pericarditis? Treatment?

A

BUN > 60 and ECG not consistent with classic pericarditis. Treat with dialysis and avoid heparin (risk of hemorrhage).

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45
Q

Indications for urgent dialysis

A

Acidosis = pH 6.5 refractory to medical therapy

Ingestion = methanol, ethylene glycol, salicylate, Li, sodium valproate, carbamazepine

Overload = fluid retention refractory to diuretics

Uremia = encephalopathy, pericarditis and bleeding.

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46
Q

Risks for ascending aortic aneurysms? Descending?

A

Ascending = cystic medial necrosis (aging) and connective tissue disorders.

Descending = atherosclerosis (HTN, hypercholesterolemia and smoking)

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47
Q

Conditions included is atherosclerotic cardiovascular disease (ASCVD)

A

ACS, MI, angina, hx of arterial revascularization, stroke/TIA or PAD.

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48
Q

Recommendation for bystander CPR

A

Compression-only CPR

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49
Q

When to use immersion cooling vs. evaporative cooling for heat stroke.

A

Exertional heat stroke = immersion. Non-exertional (typically elderly) = evaporative.

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50
Q

Drugs to avoid in patients with RV MI.

A

Those that reduce preload (nitrates, diuretics and opioids) and those that slow heart rate (beta blockers) or decrease contractility (CCBs)

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51
Q

AVNRT pathophysiology and ECG findings

A

2 conducting pathways, one fast and one slow, form within the AV node and cause a rapid, regular rhythm with narrow QRS and buried P waves.

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52
Q

Atrial flutter pathophysiology and ECG findings

A

Caused by a re-entrant circuit around the tricuspid annulus. ECG shows rapid sawtooth flutter waves.

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53
Q

2nd line medication to terminate SVT if adenosine fails

A

Verapamil

54
Q

Management of pulmonary hypertension secondary to severe HFrEF with pulmonary edema? Idiopathic pulmonary hypertension? Pulmonary HTN due to chronic lung disease? Chronic thromboembolism?

A

Loop diuretics, ACE-I, beta-blockers and aldosterone antagonists (treat the CHF to treat PH).

Oxygen + bronchodilators if due to chronic lung disease.

Endothelin receptor antagonists (bosentan), PDE-5 inhibitors (sildenafil) and/or epoprostenol for idiopathic PH.

Warfarin for chronic thromboembolism

55
Q

When is endovenous ablation indicated for chronic venous stasis?

A

Persistent symptoms despite conservative treatment and documented reflux.

56
Q

Signs of scleroderma renal crisis

A

Sudden onset renal failure, MH, mild proteinuria, MAHA/DIC and thrombocytopenia

57
Q

Cause of paradoxical splitting with aortic stenosis

A

Delayed myocardial relaxation and delayed closure of the aortic valve.

58
Q

Anti-arrhythmic with side effects of diarrhea, tinnitus, QT prolongation, torsades de pointes, hemolytic anemia and thrombocytopenia.

A

Quinidine

59
Q

CHA2DS2VASc

A

CHF

HTN

Age > 75

DM

Stroke/TIA/Thromboembolism

Vascular disease (MI, PAD, aortic plaque)

Age 65-74

Sex category

60
Q

Arrhythmia most specific for digitalis toxicity

A

Atrial tachycardia (150-250) with AV block

61
Q

Meds to withhold prior to stress testing

A

Hold for 48 hours: beta-blockers, CCB and nitrates.

Hold for 48 hours prior to pharm-stress test: dipyridamole

Hold for 12 hours prior to pharm-stress test: caffeine

Continue ACE-I, ARB, digoxin, statin and diuretics.

62
Q

CYP450 Inhibitors

A

Acetaminophen (>2g/d), NSAIDs

Antibiotics, antifungals (metronidazole)

Amiodarone

Cimetidine

Cranberry juice, Ginkgo biloba, vitamin E

Omeprazole

Thyroid hormone

SSRIs

63
Q

CYP450 Inducers

A

Carbamazepine

Ginseng

Green vegetables

Oral contraceptives

Phenobarbital

Rifampin

St. John’s wort

64
Q

Treatment for patients with lone atrial fibrillation

A

None. Their CHADSVAsc score is typically 0, they have no cardiopulmonary or structural heart disease and do not require anticoagulation.

65
Q

Drug options for oral anticoagulation in patients with a-fib

A

Warfarin, factor Xa inhibitors (rivaroxaban, apixaban) and direct thrombin inhibitors (dabigatran)

66
Q

Beta-blocker mechanism in symptomatic management of hyperthyroidism

A

Reduce sympathetic stimulation from the increased beta-adrenergic receptors and block peripheral conversion of T4 to T3

67
Q

Chronic vs. acute mitral regurgitation symptoms

A

Acute mitral regurgitation leads to abrupt and excessive volume overload with increased filling pressures and pulmonary edema. Chronic mitral regurgitation does not cause significant change in left atrial or ventricular size/compliance

68
Q

When is urine sodium not a reliable indicator of hypovolemia?

A

When patients are taking diuretics

69
Q

Indications for temporary intravenous cardiac pacing?

A

Sick sinus syndrome or symptomatic second and third degree heart block

70
Q

Calcium channel blockers that commonly cause peripheral edema? Combination of these with what medications can reduce the edema?

A

Dihydropyridines (amlodipine and nifedipine). Combining them with ACE-I, which have post-capillary venodilatory effect, can resolve the edema.

71
Q

Cardiac condition to watch out for in Hodgkin’s survivors even 10-20 years down the road

A

Constrictive pericarditis can arise late in patients who received XRT and/or anthracycline chemotherapy.

72
Q

Maneuvers that increase the murmur of hypertrophic cardiomyopathy and mitral valve prolapse? What maneuvers decrease it?

A

Increase: Valsalva, abrupt standing and nitroglycerin (all decrease preload)

Decrease: hand grip (does not increase MVP, increased afterload), passive leg raise (increased preload) and squatting (increased preload and afterload)

73
Q

Treatment of infective endocarditis in patient with penicillin-sensitive S. viridans

A

IV Penicillin G or IV Ceftriaxone x 4 weeks

74
Q

Murmur of aortic dissection

A

Diastolic decrescendo murmur at the right sternal border

75
Q

Types of systemic amyloidosis

A

Primary (AL) or secondary (AA) due to chronic inflammatory conditions.

76
Q

Primary anti-ischemic effects of nitrates

A

Decreased preload causes decreased left ventricular end diastolic volume and wall stress, reducing myocardial oxygen demand.

77
Q

Studies to order in patients with new-onset a-fib

A

fT4 and TSH, echo, tox screen, BMP and screen for PE and OSA.

78
Q

When to use immediate synchronized cardioversion

A

Sustained monomorphic VT unresponsive to antiarrhythmics and unstable a-fib with RVR

79
Q

ECG characteristics of PVCs

A

QRS > 120msec

Bizarre morphology not representing any conduction abnormality

T-wave in opposite direction of QRS

Compensatory pause

80
Q

First line treatment for patients with frequent and symptomatic PVCs

A

Escalating doses of beta-blockers or CCBs

81
Q

Anti-arrhythmics with the use dependence phenomenon.

A

Class IC (flecainide and propafenone) and IV (CCBs) antiarrhythmics have the slowest rate of drug binding and dissociation. Consequently, when patients have increased heart rate, there is less time to dissociate and more sodium channels become blocked resulting in widening of the QRS.

82
Q

Digoxin mechanism of action

A

Inhibits the Na-K pump, resulting in increased intracellular Na+ levels that simultaneously causes increased intracellular Ca2+ levels and increased contractility.

Additionally it enhances vagal tone and slows AV node conduction.

83
Q

Most common cause of chronic mitral regurgitation in developed countries

A

Mitral valve prolapse

84
Q

Medications than can reduce the responsiveness of blood pressure to anti-hypertensive medications

A

NSAIDs, decongestants and glucocorticoids

85
Q

Management of PACs

A

If infrequent, just reassure that they’re benign.

If frequent, get TTE to rule out underlying heart disease and treat with low-dose beta-blocker

86
Q

PAC ECG

A

Abnormal p-wave morphology due to impulse coming from location other than SA node in atria + irregular rhythm.

87
Q

Drugs to stop in a patient with digoxin toxicity

A

Loop diuretics. They can cause hypokalemia, which adds to the cardiac effects of digoxin.

88
Q

Treatment of stable a-fib in patients with WPW

A

IV ibutilide or procainamide. Don’t use beta-blockers, CCBs, adenosine or digoxin in these patients because they promote conduction across the accessory pathway and can lead to degeneration to v-fib.

89
Q

Modified Wells criteria for DVT

A 
Bedridden > 3 days
Immobilization
Tender veins
Cancer active
History of DVT
Pitting edema
Unilateral swelling > 3cm
Swollen leg
Superficial non-varicose veins

More likely alternate dx = -2 points

score

90
Q

Next step if modified Wells criteria for DVT is 1?

A

1 = compression ultrasonography, repeated in 5-7 days if initially negative.

91
Q

Who gets a high-intensity statin?

A

Clinically significant ASCVD (ACS, MI, angina, TIA, stroke, PAD, hx of revascularization) and age

92
Q

Definition of orthostatic hypotension

A

Drop > 20mmHg systolic or > 10mmHg diastolic

93
Q

BP difference in arms when you worry about aortic dissection

A

> 20mmHg SBP difference

94
Q

Definition of pulsus paradoxus

A

> 10mmHg SBP drop during inspiration

95
Q

1st line drugs for patients with hypertrophic cardiomyopathy

A

Beta-blockers or CCBs because the promote diastolic relaxation, increased filling and decreased outflow obstruction.

96
Q

Medication recommendations for patients with reversible ischemia seen on stress testing

A

Aspirin + beta-blocker + lifestyle changes

97
Q

Auscultatory finding very specific for renal artery stenosis

A

Systolic-diastolic abdominal bruit

98
Q

Anti-platelet and anti-coagulant to give in patients with suspected ACS

A

Aspirin if low-probability for dissection

Heparin once ECG confirms STEMI

99
Q

Modified Wells criteria for PE

A

3 points = clinical signs of DVT and no other etiology is more likely than PE

1.5 points = prior PE/DVT, HR > 100, recent surgery/immobilization

1 point = hemoptysis, cancer

> 4 points = PE likely

100
Q

Aortic regurgitation murmur when it is due to root disease vs. valvular disease

A

Root disease = RLSB

Valvular disease = LLSB

101
Q

Signs of right ventricular heart failure

A

Elevated JVP

Right ventricular third heart sound

Tricuspid regurgitation

Hepatomegaly with pulsatile liver

LE edema, ascites and/or pleural effusions

Confirmed with pulmonary artery systolic pressures > 25mmHg

102
Q

Hallmark ECG findings in left ventricular aneurysms

A

Persistent STEMI after MI and deep Q waves in the same leads

103
Q

Cutoff for ST depression

A

1mm or greater

104
Q

Adverse side effects of PDE-5 inhibitors

A

Hypotension, blue vision discoloration, ischemic optic neuropathy, priapism, flushing, HA and hearing loss.

105
Q

Medications that can prolong the QT interval

A

Diuretics (low K, Mg or Ca)

Antiemetics

Antipsychotics

TCAs

SSRIs

Antiarrhythmics (sotalol, amiodarone, flecainide)

Antianginal (ranolazine)

Anti-infectives (macrolides, fluoroquinolones and antifungals)

106
Q

Treatment of patients in torsades de pointes

A

Stable = IV Mg.
Unstable = immediate defibrillation.
Quinidine/TCA related = sodium bicarbonate

107
Q

Physical exam findings in patients with severe aortic stenosis

A

Pulsus parvus et tardus
Mid-late systolic murmur (early peak = mild-moderate stenosis)
Soft, single 2nd heart sound due to delayed closure

108
Q

Diagnosis and treatment of autosomal dominant polycystic kidney disease

A

Dx: u/s
Tx: ACE-I for hypertension, close monitoring of renal function and ultimately dialysis or transplant

109
Q

Pathophysiology of isolated systolic hypertension in the elderly? Treatment?

A

Pathophys: loss of arterial wall elasticity
Tx: monotherapy with thiazide, ACE-I or CCB

110
Q

ECG characteristics of supraventricular arrhythmias

A

Narrow QRS + tachycardia

P-waves buried within QRS

Retrograde p-waves (inverted p-waves after QRS or spikes on the QRS)

111
Q

Rhythms included in the domain of supraventricular arrhythmias

A

Sinus tachycardia

Multifocal atrial tachycardia

Atrial flutter

Atrial fibrillation

AVNRT

AVRT

Junctional tachycardia

112
Q

Rhythms included in the domain of paroxysmal supraventricular tachycardia

A

AVNRT (most common), AVRT, atrial tachycardia and junctional tachycardia all have abrupt onset and resolution.

113
Q

Murmur heard in patients with atrial septal defects

A

Significant left to right shunting leads to increased flow across the tricuspid valve, resulting in a mid-diastolic flow murmur at the RLSB.

114
Q

PR interval cutoff for 1st degree heart block

A

> 200msec

115
Q

Uses of N-acetylcysteine

A

Mucus dissolution
Protection against contrast-induced renal failure
Acetaminophen overdose

116
Q

2 murmurs that get softer with the handgrip maneuver

A

Aortic stenosis and hypertrophic cardiomyopathy

117
Q

Murmurs that get louder with squatting and handgrip maneuvers?

A

These increase afterload and consequently increase the murmurs of AR, MR and VSD.

118
Q

Lifestyle factor associated with the highest risk of AAA expansion and rupture

A

Smoking

119
Q

Indications for endovascular or operative repair of AAA

A

Size > 5.5 or rapid expansion (>0.5cm in 6 months or >1cm in 1 year)

120
Q

Differences between Mobitz I and II heart block

A

Mobitz I: progressive prolongation of PR leading to a dropped beat due to abnormality in AV node. Typically benign, improves with exercise/atropine, worsens with vagal maneuvers and has narrow QRS.

Mobitz II: random dropped beats without PR prolongation due to abnormality below AV node. Exercise/atropine worsen the block, vagal maneuvers improve it and these patients need a pacemaker.

121
Q

Management of patients with renovascular hypertension/renal artery stenosis.

A

ACE-I/ARB, aspirin and aggressive risk factor reduction.

Renal artery stenting is reserved for those who are non-responsive to medical therapy, have flash pulmonary edema or refractory heart failure due to severe HTN.

122
Q

Treatment of patients with sustained monomorphic VT

A

Unstable = electrical synchronized cardioversion

Stable = IV amiodarone (may also use procainamide or lidocaine)

123
Q

Medications with mortality benefit for patients with CHF

A

Beta-blockers

ACE-I/ARBs

Spironolactone

124
Q

ECHO in patients with cardiac amyloidosis

A

Ventricular wall thickening with normal sized chambers

125
Q

Causes of secondary hypertension

A

Renal parenchymal disease: proteinuria, RBC casts and elevated serum Cr

Renovascular disease: severe HTN, age > 55, diffuse atherosclerosis, unilateral renal atrophy, resistant heart failure, flash pulmonary edema, abdominal bruit and elevated serum Cr

Primary aldosteronism: adrenal incidentaloma, hypokalemia and mild hypernatremia

Pheo: adrenal incidentaloma, paroxysmal tachycardia, headaches, flushing and diaphoresis

Cushing’s: central obesity, plethora, proximal muscle weakness, abdominal striae, ecchymosis, amenorrhea/erectile dysfunction

Hypothyroidism: fatigue, dry skin, cold intolerance, constipation, weight gain and bradycardia

Primary hyperparathyroidism: stones, bones, abdominal moans and psych overtones with elevated Ca

Coarctation: brachial femoral pulse delay

126
Q

Lab findings in patients with Cushing’s

A

Hyperglycemia, hypokalemia, leukocytosis and lymphocytopenia

127
Q

Next step for a young patient with a soft mid-systolic murmur

A

Reassurance

128
Q

Meds used for cardiac stress testing

A

Dipyramidole and adenosine are coronary vasodilators that result in coronary steal from ischemic myocardium

129
Q

High risk for thromboembolism threshold in patients with a-fib

A

A-fib lasting > 48 hours without adequate anticoagulation

130
Q

CK-MB vs. troponin

A

CK-MB normalizes within 1-2 days, troponin takes 10 days to normalize

Step 2 CK (14 decks)

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