Flashcards in Cardiology Deck (130):
Viruses implicated in dilated cardiomyopathy
#1) Coxsackie B. Also parvovirus B19, HHV6, adenovirus and enterovirus.
Cardiac problem that results in an S3? S4?
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.
Sensitivity, specificity and predictive accuracy for diagnosing heart failure in a patient with a BNP > 100
90, 76 and 83%
Electrolyte abnormality that is an important predictor of adverse clinical outcomes in patients with CHF?
Hyponatremia, it typically parallels the severity of disease. It occurs due to decreased intravascular volume, ADH release and free water retention
Treatment of CHF-related hyponatremia
Free water restriction
Drug typically given in the setting of acute MI that is contraindicated if the patient also has pulmonary edema
Beta-blockers, these are contraindicated in patients with acute decompensated heart failure because the increased heart rate is essential to adequate tissue perfusion.
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?
Beta-blocker (unless hypotensive, bradycardic, heart failure or heart block)
Aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor)
Nitrates (avoid this and diuretics if RV infarct)
Persistent pain, hypertension or heart failure = nitrates +/- morphine for pain.
Bradycardia = atropine
Pulmonary edema = furosemide
Cardiac, pulmonary, GI, endocrine, ocular, dermatologic and neurologic side effects of amiodarone.
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
Arteries most commonly involved in patients with fibromuscular dysplasia
Renal, carotid and vertebral arteries
Diagnosis and treatment of fibromuscular dysplasia
Diagnosed with CT angiography, catheter-based digital subtraction arteriography if CT angio is inconclusive.
Aldosterone concentration : renin activity in fibromuscular dysplasia? What about with adrenal hyperplasia/adenoma?
~10 in fibromuscular dysplasia. > 15 in primary hyperaldosteronism.
ECG characteristics of PAC's
Unusual P-wave morphology because the impulse is coming from somewhere other than the SA node in the atria. Early contractions are also present.
Treatment of symptomatic PAC's
Low dose beta-blockers, decrease stress and cessation of tobacco, alcohol and caffeine.
Indication for fibrinolysis in patient with MI
Within 12 of hours of onset of symptoms and unable to undergo PCI
How long should you continue aspirin and P2y12 receptor blockers after drug-eluting stent placement?
Milrinone mechanism of action
PDE inhibitor that increases myocardial contractility
Desired CXR location of central venous catheter
Angle between the trachea & right mainstem bronchus or proximal to the cardiac silhouette
Congenital causes of high-output heart failure
PDA, angioma, pulmonary/CNS AVF
Acquired causes of high-output heart failure
Trauma, iatrogenic, atherosclerosis (aortocaval fistula) and cancer.
Side effects and electrolyte changes seen in patients taking thiazide diuretics
Hyponatremia, hypokalemia, hypercalcemia, hyperglycemia, hyperuricemia and elevated LDL cholesterol.
Electrolyte abnormalities that put patients at risk for VT when taking furosemide
Hypokalemia and hypomagnesemia
Basic lab analysis for a patient presenting with hypertension
Rule out other causes of hypertension with:
UA, BMP, lipid profile and baseline ECG
Signs and symptoms of secondary hypertension
Malignant hypertension, HTN requiring 3+ drugs, sudden rise in BP with previously normal values and onset at
Causes of secondary hypertension
Renal parenchymal disease, renovascular disease, primary hyperaldosteronism, pheochromocytoma, Cushing syndrome, hypothyroidism, primary hyperparathyroidism and aortic coarctation.
Treatment of beta-blocker or CCB toxicity
Most common cause of aortic regurgitation in developed vs. undeveloped countries.
Developed = bicuspid valve
Undeveloped = rheumatic heart disease
Indications for carotid endarterectomy
Men: asymptomatic and > 60% stenosed, symptomatic and > 50% stenosed.
Women: symptomatic or asymptomatic and > 70% stenosed.
Management of aortic dissections
IV labetolol. Surgery is only indicated for type A dissections.
Why patients with aortic stenosis get angina?
LV hypertrophy results in increased myocardial oxygen demand.
Common causes of constrictive pericarditis
Idiopathic or viral, radiation, cardiac surgery, connective tissue disorders and Tb.
Management of patients with claudication
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
Management of cocaine-related STEMI
Same as regular STEMIs except: avoid beta-blockers. Also add IV benzodiazepine, CCB or alpha-blocker to reduce vasospasm.
Management of hypertensive emergency
MAP lowered by 10-20% in 1st hour and 5-15% over next 23 hours.
Types of heparin-induced thrombocytopenia (HIT)
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.
Hypertensive urgency vs. emergency
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)
Phases of post-MI arrhythmia
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
Lab studies present in a patient with recent atheroembolism from coronary vascularization
Eosinophilia, eosinophiluria and hypocomplementemia with renal dysfunction that can persist beyond 2 weeks.
Lab studies present in a patient with contrast-induced nephropathy
Muddy-brown granular and epithelial cell casts 3-5 days after exposure and resolution within 1 week.
Mechanisms of niacin-induced peripheral vasodilation
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.
CXR sign for pericardial effusion
Water bottle sign with clear lung fields
Treatment of stable angina
1st line = beta-blockers. CCB or long-acting nitrates can be used if beta-blockers are contraindicated, poorly tolerated or are ineffective.
Osler nodes vs. Janeway lesions
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.
Patient has recurrent high fevers, arthritis and a maculopapular, nonpruritic rash affecting the trunk and extremities only during febrile episodes.
Adult Still's disease.
Common presentation of uremic pericarditis? Treatment?
BUN > 60 and ECG not consistent with classic pericarditis. Treat with dialysis and avoid heparin (risk of hemorrhage).
Indications for urgent dialysis
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.
Risks for ascending aortic aneurysms? Descending?
Ascending = cystic medial necrosis (aging) and connective tissue disorders.
Descending = atherosclerosis (HTN, hypercholesterolemia and smoking)
Conditions included is atherosclerotic cardiovascular disease (ASCVD)
ACS, MI, angina, hx of arterial revascularization, stroke/TIA or PAD.
Recommendation for bystander CPR
When to use immersion cooling vs. evaporative cooling for heat stroke.
Exertional heat stroke = immersion. Non-exertional (typically elderly) = evaporative.
Drugs to avoid in patients with RV MI.
Those that reduce preload (nitrates, diuretics and opioids) and those that slow heart rate (beta blockers) or decrease contractility (CCBs)
AVNRT pathophysiology and ECG findings
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.
Atrial flutter pathophysiology and ECG findings
Caused by a re-entrant circuit around the tricuspid annulus. ECG shows rapid sawtooth flutter waves.
2nd line medication to terminate SVT if adenosine fails
Management of pulmonary hypertension secondary to severe HFrEF with pulmonary edema? Idiopathic pulmonary hypertension? Pulmonary HTN due to chronic lung disease? Chronic thromboembolism?
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
When is endovenous ablation indicated for chronic venous stasis?
Persistent symptoms despite conservative treatment and documented reflux.
Signs of scleroderma renal crisis
Sudden onset renal failure, MH, mild proteinuria, MAHA/DIC and thrombocytopenia
Cause of paradoxical splitting with aortic stenosis
Delayed myocardial relaxation and delayed closure of the aortic valve.
Anti-arrhythmic with side effects of diarrhea, tinnitus, QT prolongation, torsades de pointes, hemolytic anemia and thrombocytopenia.
Age > 75
Vascular disease (MI, PAD, aortic plaque)
Arrhythmia most specific for digitalis toxicity
Atrial tachycardia (150-250) with AV block
Meds to withhold prior to stress testing
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.
Acetaminophen (>2g/d), NSAIDs
Antibiotics, antifungals (metronidazole)
Cranberry juice, Ginkgo biloba, vitamin E
St. John's wort
Treatment for patients with lone atrial fibrillation
None. Their CHADSVAsc score is typically 0, they have no cardiopulmonary or structural heart disease and do not require anticoagulation.
Drug options for oral anticoagulation in patients with a-fib
Warfarin, factor Xa inhibitors (rivaroxaban, apixaban) and direct thrombin inhibitors (dabigatran)
Beta-blocker mechanism in symptomatic management of hyperthyroidism
Reduce sympathetic stimulation from the increased beta-adrenergic receptors and block peripheral conversion of T4 to T3
Chronic vs. acute mitral regurgitation symptoms
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
When is urine sodium not a reliable indicator of hypovolemia?
When patients are taking diuretics
Indications for temporary intravenous cardiac pacing?
Sick sinus syndrome or symptomatic second and third degree heart block
Calcium channel blockers that commonly cause peripheral edema? Combination of these with what medications can reduce the edema?
Dihydropyridines (amlodipine and nifedipine). Combining them with ACE-I, which have post-capillary venodilatory effect, can resolve the edema.
Cardiac condition to watch out for in Hodgkin's survivors even 10-20 years down the road
Constrictive pericarditis can arise late in patients who received XRT and/or anthracycline chemotherapy.
Maneuvers that increase the murmur of hypertrophic cardiomyopathy and mitral valve prolapse? What maneuvers decrease it?
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)
Treatment of infective endocarditis in patient with penicillin-sensitive S. viridans
IV Penicillin G or IV Ceftriaxone x 4 weeks
Murmur of aortic dissection
Diastolic decrescendo murmur at the right sternal border
Types of systemic amyloidosis
Primary (AL) or secondary (AA) due to chronic inflammatory conditions.
Primary anti-ischemic effects of nitrates
Decreased preload causes decreased left ventricular end diastolic volume and wall stress, reducing myocardial oxygen demand.
Studies to order in patients with new-onset a-fib
fT4 and TSH, echo, tox screen, BMP and screen for PE and OSA.
When to use immediate synchronized cardioversion
Sustained monomorphic VT unresponsive to antiarrhythmics and unstable a-fib with RVR
ECG characteristics of PVCs
QRS > 120msec
Bizarre morphology not representing any conduction abnormality
T-wave in opposite direction of QRS
First line treatment for patients with frequent and symptomatic PVCs
Escalating doses of beta-blockers or CCBs
Anti-arrhythmics with the use dependence phenomenon.
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.
Digoxin mechanism of action
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.
Most common cause of chronic mitral regurgitation in developed countries
Mitral valve prolapse
Medications than can reduce the responsiveness of blood pressure to anti-hypertensive medications
NSAIDs, decongestants and glucocorticoids
Management of PACs
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
Abnormal p-wave morphology due to impulse coming from location other than SA node in atria + irregular rhythm.
Drugs to stop in a patient with digoxin toxicity
Loop diuretics. They can cause hypokalemia, which adds to the cardiac effects of digoxin.
Treatment of stable a-fib in patients with WPW
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.
Modified Wells criteria for DVT
Bedridden > 3 days
History of DVT
Unilateral swelling > 3cm
Superficial non-varicose veins
More likely alternate dx = -2 points
Next step if modified Wells criteria for DVT is 1?
1 = compression ultrasonography, repeated in 5-7 days if initially negative.
Who gets a high-intensity statin?
Clinically significant ASCVD (ACS, MI, angina, TIA, stroke, PAD, hx of revascularization) and age
Definition of orthostatic hypotension
Drop > 20mmHg systolic or > 10mmHg diastolic
BP difference in arms when you worry about aortic dissection
> 20mmHg SBP difference
Definition of pulsus paradoxus
> 10mmHg SBP drop during inspiration
1st line drugs for patients with hypertrophic cardiomyopathy
Beta-blockers or CCBs because the promote diastolic relaxation, increased filling and decreased outflow obstruction.
Medication recommendations for patients with reversible ischemia seen on stress testing
Aspirin + beta-blocker + lifestyle changes
Auscultatory finding very specific for renal artery stenosis
Systolic-diastolic abdominal bruit
Anti-platelet and anti-coagulant to give in patients with suspected ACS
Aspirin if low-probability for dissection
Heparin once ECG confirms STEMI
Modified Wells criteria for PE
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
Aortic regurgitation murmur when it is due to root disease vs. valvular disease
Root disease = RLSB
Valvular disease = LLSB
Signs of right ventricular heart failure
Right ventricular third heart sound
Hepatomegaly with pulsatile liver
LE edema, ascites and/or pleural effusions
Confirmed with pulmonary artery systolic pressures > 25mmHg
Hallmark ECG findings in left ventricular aneurysms
Persistent STEMI after MI and deep Q waves in the same leads
Cutoff for ST depression
1mm or greater
Adverse side effects of PDE-5 inhibitors
Hypotension, blue vision discoloration, ischemic optic neuropathy, priapism, flushing, HA and hearing loss.
Medications that can prolong the QT interval
Diuretics (low K, Mg or Ca)
Antiarrhythmics (sotalol, amiodarone, flecainide)
Anti-infectives (macrolides, fluoroquinolones and antifungals)
Treatment of patients in torsades de pointes
Stable = IV Mg.
Unstable = immediate defibrillation.
Quinidine/TCA related = sodium bicarbonate
Physical exam findings in patients with severe aortic stenosis
Pulsus parvus et tardus
Mid-late systolic murmur (early peak = mild-moderate stenosis)
Soft, single 2nd heart sound due to delayed closure
Diagnosis and treatment of autosomal dominant polycystic kidney disease
Tx: ACE-I for hypertension, close monitoring of renal function and ultimately dialysis or transplant
Pathophysiology of isolated systolic hypertension in the elderly? Treatment?
Pathophys: loss of arterial wall elasticity
Tx: monotherapy with thiazide, ACE-I or CCB
ECG characteristics of supraventricular arrhythmias
Narrow QRS + tachycardia
P-waves buried within QRS
Retrograde p-waves (inverted p-waves after QRS or spikes on the QRS)
Rhythms included in the domain of supraventricular arrhythmias
Multifocal atrial tachycardia
Rhythms included in the domain of paroxysmal supraventricular tachycardia
AVNRT (most common), AVRT, atrial tachycardia and junctional tachycardia all have abrupt onset and resolution.
Murmur heard in patients with atrial septal defects
Significant left to right shunting leads to increased flow across the tricuspid valve, resulting in a mid-diastolic flow murmur at the RLSB.
PR interval cutoff for 1st degree heart block
Uses of N-acetylcysteine
Protection against contrast-induced renal failure
2 murmurs that get softer with the handgrip maneuver
Aortic stenosis and hypertrophic cardiomyopathy
Murmurs that get louder with squatting and handgrip maneuvers?
These increase afterload and consequently increase the murmurs of AR, MR and VSD.
Lifestyle factor associated with the highest risk of AAA expansion and rupture
Indications for endovascular or operative repair of AAA
Size > 5.5 or rapid expansion (>0.5cm in 6 months or >1cm in 1 year)
Differences between Mobitz I and II heart block
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.
Management of patients with renovascular hypertension/renal artery stenosis.
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.
Treatment of patients with sustained monomorphic VT
Unstable = electrical synchronized cardioversion
Stable = IV amiodarone (may also use procainamide or lidocaine)
Medications with mortality benefit for patients with CHF
ECHO in patients with cardiac amyloidosis
Ventricular wall thickening with normal sized chambers
Causes of secondary hypertension
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
Lab findings in patients with Cushing's
Hyperglycemia, hypokalemia, leukocytosis and lymphocytopenia
Next step for a young patient with a soft mid-systolic murmur
Meds used for cardiac stress testing
Dipyramidole and adenosine are coronary vasodilators that result in coronary steal from ischemic myocardium
High risk for thromboembolism threshold in patients with a-fib
A-fib lasting > 48 hours without adequate anticoagulation