Flashcards Internal Medicine EOR: Cardiovascular (2026) (Smarty PANCE) | Quizlet

What is atrial arrhythmia?

A supraventricular tachyarrhythmia originating in atrial tissue above the AV node, including atrial fibrillation, atrial flutter, and atrial (including multifocal) tachycardia.

What are the ECG findings of atrial fibrillation?

Irregularly irregular rhythm with absent P waves and a fibrillatory baseline.

What is the ECG hallmark of atrial flutter?

Regular sawtooth flutter (F) waves, classically at an atrial rate near 300 bpm with 2:1 conduction giving a ventricular rate near 150 bpm.

What tool guides anticoagulation decisions in nonvalvular atrial fibrillation?

The CHA2DS2-VASc score; anticoagulation is generally recommended at a score of 2 or more in men and 3 or more in women.

What is the difference between rate control and rhythm control in AFib?

Rate control slows the ventricular response (beta-blockers, nondihydropyridine CCBs); rhythm control restores/maintains sinus rhythm (antiarrhythmics, cardioversion, ablation).

What arrhythmia shows 3 or more distinct P-wave morphologies and is associated with COPD?

Multifocal atrial tachycardia.

How is unstable atrial fibrillation managed?

Immediate synchronized cardioversion.

What is a heart block?

A disorder of impulse conduction through the AV node or His-Purkinje system, ranging from delayed conduction to complete AV dissociation.

What defines first-degree AV block?

A fixed prolonged PR interval greater than 200 ms with every P wave conducting to a QRS.

What characterizes Mobitz I (Wenckebach) second-degree AV block?

Progressive PR prolongation until a beat is dropped, then the cycle repeats.

What characterizes Mobitz II second-degree AV block?

Constant PR intervals with intermittent non-conducted P waves and dropped QRS complexes, carrying high risk of progression to complete block.

What defines third-degree (complete) AV block?

Complete AV dissociation with independent atrial and ventricular rates and no relationship between P waves and QRS complexes.

Which AV blocks typically require a permanent pacemaker?

Mobitz II and third-degree AV block (and symptomatic high-grade block).

What is the acute treatment for symptomatic bradycardia from heart block?

Atropine first, then transcutaneous pacing or chronotropic infusions (dopamine/epinephrine) as a bridge to a pacemaker.

What is a junctional arrhythmia?

A rhythm originating from the AV junction (pacemaker tissue near the AV node) when it takes over due to SA node failure or enhanced junctional automaticity.

What are the ECG findings of a junctional rhythm?

Narrow QRS with absent, inverted, or retrograde P waves (before, during, or after the QRS), typically at 40–60 bpm.

What is the typical rate of an accelerated junctional rhythm versus junctional tachycardia?

Accelerated junctional rhythm is 60–100 bpm; junctional tachycardia exceeds 100 bpm.

What classic condition causes junctional rhythm with possible junctional tachycardia?

Digoxin toxicity.

How is a symptomatic slow junctional escape rhythm treated?

Atropine and treatment of the underlying cause; pacing if refractory.

What are premature beats?

Early ectopic depolarizations arising from the atria (PACs) or ventricles (PVCs) that interrupt the underlying sinus rhythm.

What are the ECG findings of a premature atrial contraction (PAC)?

An early P wave with abnormal morphology followed by a narrow QRS, often with an incomplete compensatory pause.

What are the ECG findings of a premature ventricular contraction (PVC)?

An early, wide, bizarre QRS with no preceding P wave, usually followed by a full compensatory pause.

What is the general management of asymptomatic PACs and PVCs in a structurally normal heart?

Reassurance and reduction of triggers (caffeine, alcohol, stimulants, stress); no specific therapy needed.

What patterns of PVCs are described by bigeminy and a couplet?

Bigeminy is a PVC after every sinus beat; a couplet is two consecutive PVCs.

When are PVCs concerning?

When frequent, complex, symptomatic, or associated with structural heart disease or reduced ejection fraction (risk of PVC-induced cardiomyopathy).

What is a ventricular arrhythmia?

A tachyarrhythmia originating below the AV node in the ventricles, including ventricular tachycardia and ventricular fibrillation.

What are the ECG findings of monomorphic ventricular tachycardia?

A regular wide-complex tachycardia (QRS >120 ms) with uniform QRS morphology, usually faster than 100 bpm.

What is torsades de pointes and what predisposes to it?

A polymorphic VT with QRS amplitude twisting around the baseline, precipitated by a prolonged QT interval (drugs, hypokalemia, hypomagnesemia, congenital long QT).

What is the treatment for torsades de pointes?

IV magnesium sulfate, correction of electrolytes, and removal of offending agents.

How is pulseless VT or ventricular fibrillation treated?

Immediate defibrillation and CPR per ACLS.

How is stable, sustained monomorphic VT with a pulse managed?

Antiarrhythmics such as amiodarone or procainamide, with synchronized cardioversion if the patient becomes unstable.

What is the most common cause of sudden cardiac death in adults?

Ventricular fibrillation, usually in the setting of ischemic heart disease.

What is dilated cardiomyopathy?

A cardiomyopathy defined by ventricular dilation and impaired systolic contraction, producing a dilated, weakly pumping heart.

What is the most common cause of dilated cardiomyopathy?

Idiopathic, though ischemic disease, alcohol, viral myocarditis, peripartum state, and chemotherapy (doxorubicin) are common identifiable causes.

What are the typical clinical features of dilated cardiomyopathy?

Signs of systolic heart failure with an S3 gallop, displaced PMI, and frequently mitral/tricuspid regurgitation murmurs.

What is the characteristic echocardiographic finding in dilated cardiomyopathy?

Left ventricular dilation with a globally reduced ejection fraction.

What is the management of dilated cardiomyopathy?

Guideline-directed heart failure therapy (beta-blocker, ACE inhibitor/ARB/ARNI, MRA, SGLT2 inhibitor) plus treatment of the underlying cause.

What is hypertrophic cardiomyopathy?

An autosomal dominant cardiomyopathy of inappropriate myocardial hypertrophy (often asymmetric septal) that can cause left ventricular outflow tract obstruction.

What is the most common cause of sudden cardiac death in young athletes?

Hypertrophic cardiomyopathy.

What murmur is heard in hypertrophic cardiomyopathy and how does it change with maneuvers?

A harsh crescendo-decrescendo systolic murmur at the left lower sternal border that increases with decreased preload (Valsalva, standing) and decreases with increased preload (squatting, handgrip).

What ECG findings are typical in hypertrophic cardiomyopathy?

Left ventricular hypertrophy with deep, narrow ("dagger-like") Q waves in the inferior and lateral leads.

What medications should be avoided in obstructive hypertrophic cardiomyopathy?

Preload/afterload reducers such as nitrates, diuretics, and other vasodilators (they worsen outflow obstruction).

What is first-line medical therapy for symptomatic hypertrophic cardiomyopathy?

Beta-blockers (or nondihydropyridine calcium channel blockers); avoidance of dehydration and intense exertion.

What is restrictive cardiomyopathy?

A cardiomyopathy in which stiff, noncompliant ventricular walls impair diastolic filling while systolic function and chamber size remain relatively preserved.

What are common causes of restrictive cardiomyopathy?

Infiltrative and storage diseases—amyloidosis, sarcoidosis, hemochromatosis, and endomyocardial fibrosis.

What is the predominant type of dysfunction in restrictive cardiomyopathy?

Diastolic dysfunction (impaired relaxation/filling) with preserved ejection fraction.

How is restrictive cardiomyopathy distinguished from constrictive pericarditis?

Both cause diastolic heart failure, but echo/MRI show thickened myocardium in restriction versus a thickened pericardium in constriction; the distinction often requires imaging and hemodynamic study.

What is the management of restrictive cardiomyopathy?

Treat the underlying disease and manage congestion cautiously with diuretics; outcomes are often poor.

What is acute coronary syndrome?

A spectrum of acute myocardial ischemia caused by plaque rupture and coronary thrombosis, comprising unstable angina, NSTEMI, and STEMI.

How are unstable angina, NSTEMI, and STEMI distinguished?

Unstable angina has ischemic symptoms with normal troponin and no ST elevation; NSTEMI has elevated troponin without ST elevation; STEMI has ST elevation with elevated troponin.

What ECG finding defines STEMI?

ST-segment elevation in 2 or more contiguous leads (or new LBBB with ischemic symptoms).

What are the inferior, anterior, and lateral ECG lead groupings and their vessels?

Inferior = II, III, aVF (RCA); anterior = V1–V4 (LAD); lateral = I, aVL, V5–V6 (left circumflex).

What is the reperfusion goal for STEMI?

Primary PCI within 90 minutes of first medical contact, or fibrinolytics within 30 minutes if timely PCI is unavailable.

What is the initial pharmacologic management of ACS?

Aspirin, a second antiplatelet (P2Y12 inhibitor), anticoagulation, nitrates, high-intensity statin, and beta-blocker, with oxygen only if hypoxic.

Why should nitrates be used cautiously in inferior MI?

An associated right ventricular infarction is preload-dependent, so nitrates can cause profound hypotension.

What is stable angina?

Predictable, exertional chest discomfort due to a fixed coronary stenosis that is relieved by rest or nitroglycerin and lasts only a few minutes.

What is the classic description of stable angina?

Substernal pressure provoked by exertion or emotional stress and relieved within minutes by rest or nitroglycerin.

What is the initial diagnostic test for suspected stable angina?

Exercise (or pharmacologic) stress testing; coronary angiography for high-risk or diagnostic uncertainty.

What is first-line medical therapy for stable angina?

Antianginal therapy with beta-blockers plus sublingual nitroglycerin for episodes, along with aspirin and a statin for risk reduction.

What lifestyle and risk-factor measures are key in stable angina?

Smoking cessation, blood pressure and lipid control, diabetes management, exercise, and weight optimization.

What is vasospastic (Prinzmetal) angina?

Angina caused by transient coronary artery spasm, producing chest pain at rest with reversible ST elevation and typically normal or minimally diseased coronaries.

When does vasospastic angina classically occur?

At rest, often at night or in the early morning, and it may be triggered by smoking, cocaine, or stimulants.

What ECG change occurs during a vasospastic angina episode?

Transient ST-segment elevation that resolves as the spasm and pain subside.

What is the treatment of choice for vasospastic angina?

Calcium channel blockers (and nitrates); beta-blockers and triggers like cocaine should be avoided.

What is heart failure?

A clinical syndrome in which the heart cannot pump or fill adequately to meet the body's metabolic demands, leading to congestion and/or hypoperfusion.

How are HFrEF and HFpEF defined?

HFrEF is heart failure with ejection fraction 40% or less (systolic dysfunction); HFpEF is heart failure with ejection fraction 50% or greater (diastolic dysfunction).

What distinguishes left-sided from right-sided heart failure symptoms?

Left-sided failure causes pulmonary congestion (dyspnea, orthopnea, rales); right-sided failure causes systemic congestion (JVD, peripheral edema, hepatomegaly).

What lab test helps diagnose heart failure?

BNP or NT-proBNP, which is elevated in decompensated heart failure.

What classes of medication reduce mortality in HFrEF?

Beta-blockers, ACE inhibitors/ARBs/ARNI, mineralocorticoid receptor antagonists, and SGLT2 inhibitors.

What is the role of diuretics in heart failure?

Loop diuretics relieve congestion and improve symptoms but do not reduce mortality.

What is primary (essential) hypertension?

Chronically elevated blood pressure with no identifiable secondary cause, accounting for the large majority of hypertension cases.

How is hypertension defined by current ACC/AHA thresholds?

Stage 1 is 130–139/80–89 mmHg and stage 2 is 140/90 mmHg or higher, based on properly averaged readings.

What are first-line medications for primary hypertension?

Thiazide diuretics, ACE inhibitors or ARBs, and dihydropyridine calcium channel blockers.

What is the preferred initial antihypertensive in a patient with diabetes and proteinuria?

An ACE inhibitor or ARB.

What lifestyle modifications lower blood pressure?

The DASH diet, sodium restriction, weight loss, exercise, alcohol moderation, and smoking cessation.

What is secondary hypertension?

Hypertension caused by an identifiable underlying condition, often suggested by early/late onset, severe or resistant disease, or specific clinical clues.

What is the most common cause of secondary hypertension?

Renal parenchymal disease; primary aldosteronism is the most common endocrine cause.

What clues suggest renal artery stenosis as a cause of secondary hypertension?

Resistant hypertension, an abdominal bruit, or an acute rise in creatinine after starting an ACE inhibitor or ARB.

What triad suggests pheochromocytoma?

Episodic headache, palpitations, and sweating with paroxysmal hypertension.

What lab pattern suggests primary hyperaldosteronism?

Hypertension with hypokalemia and an elevated aldosterone-to-renin ratio.

What is severe asymptomatic hypertension (hypertensive urgency)?

Blood pressure of 180/120 mmHg or higher without evidence of acute target-organ damage.

How does hypertensive urgency differ from hypertensive emergency?

Both have BP 180/120 mmHg or higher, but emergency has acute target-organ damage (encephalopathy, MI, stroke, pulmonary edema, AKI) while urgency does not.

How is hypertensive urgency managed?

Gradual blood pressure lowering with oral agents over hours to days, restarting or adjusting outpatient medication, without rapid IV reduction.

Why should blood pressure not be lowered too rapidly in severe asymptomatic hypertension?

Rapid reduction can cause cerebral, coronary, or renal hypoperfusion and ischemia.

What is hypotension?

Abnormally low blood pressure, generally a systolic pressure below 90 mmHg or a mean arterial pressure low enough to impair tissue perfusion.

What symptoms suggest symptomatic hypotension?

Lightheadedness, dizziness, syncope, fatigue, blurred vision, and signs of poor perfusion.

What are broad categories of hypotension causes?

Hypovolemia, cardiogenic causes, distributive (vasodilatory) causes, and medication effects.

What is the initial evaluation of a hypotensive patient?

Assess perfusion and volume status, review medications, and identify reversible causes while supporting circulation.

What is orthostatic hypotension?

A fall in systolic blood pressure of at least 20 mmHg or diastolic of at least 10 mmHg within 3 minutes of standing.

What symptoms accompany orthostatic hypotension?

Positional lightheadedness, dizziness, or syncope on standing.

What are common causes of orthostatic hypotension?

Volume depletion, medications (diuretics, alpha-blockers, antihypertensives), and autonomic dysfunction (e.g., diabetes, Parkinson disease).

What is the management of orthostatic hypotension?

Volume repletion, slow position changes, compression stockings, medication review, and fludrocortisone or midodrine if refractory.

What is vasovagal hypotension?

A transient drop in blood pressure (often with bradycardia) from a reflex autonomic response, the most common cause of syncope.

What are typical triggers of vasovagal syncope?

Prolonged standing, pain, emotional distress, heat, or the sight of blood.

What prodromal symptoms precede vasovagal syncope?

Nausea, diaphoresis, warmth, pallor, and tunnel vision before brief loss of consciousness with rapid recovery.

How is vasovagal syncope managed?

Reassurance, trigger avoidance, adequate hydration and salt, and physical counterpressure maneuvers.

What are lipid disorders?

Abnormal levels of plasma lipids—elevated LDL, elevated triglycerides, or low HDL—that increase atherosclerotic cardiovascular risk.

What is the primary lipid target for cardiovascular risk reduction?

LDL cholesterol.

Which patients warrant high-intensity statin therapy?

Those with clinical ASCVD, LDL 190 mg/dL or higher, or many diabetics and high 10-year-risk patients aged 40–75.

What complication is associated with very high triglycerides (over 500 mg/dL)?

Acute pancreatitis.