Physician Assistant National Certifying Examination (PANCE) Cardiovascular System Syllabus

Describe the ECG findings of atrial fibrillation versus atrial flutter.

Atrial fibrillation: irregularly irregular rhythm with absent P waves and a fibrillatory baseline. Atrial flutter: regular sawtooth flutter waves (atrial rate $\approx 300\,\text{bpm}$) with a regular ventricular response, classically $2{:}1$ conduction giving $\approx 150\,\text{bpm}$.

What are the rate-control and rhythm-control options for atrial fibrillation?

Rate control: beta-blockers or non-dihydropyridine calcium channel blockers (diltiazem/verapamil); digoxin as adjunct. Rhythm control: electrical/pharmacologic cardioversion (must anticoagulate or exclude thrombus with TEE if onset $>48$ h), antiarrhythmics (amiodarone, flecainide), or catheter ablation.

What is the most common type of paroxysmal supraventricular tachycardia (SVT) and its acute treatment?

AV nodal reentrant tachycardia (AVNRT)—a regular, narrow-complex tachycardia ~150–250 bpm with no visible P waves. Acute treatment: vagal maneuvers first, then IV adenosine; if unstable, synchronized cardioversion.

What is Wolff-Parkinson-White (WPW) syndrome and why is it dangerous in atrial fibrillation?

A congenital accessory pathway (bundle of Kent) producing a short PR interval, a delta wave, and a wide QRS. In AF, AV-nodal blockers (adenosine, beta-blockers, CCBs, digoxin) can accelerate conduction down the accessory pathway, risking ventricular fibrillation; use procainamide or cardioversion instead.

How do you distinguish and treat monomorphic ventricular tachycardia in a stable versus unstable patient?

Monomorphic VT is a regular, wide-complex ($>120\,\text{ms}$) tachycardia. Stable: IV antiarrhythmics (amiodarone, procainamide, or lidocaine). Unstable (hypotension, ischemia, altered mental status): immediate synchronized cardioversion. Pulseless VT is treated like VF.

What is the immediate management of pulseless ventricular tachycardia or ventricular fibrillation?

Immediate unsynchronized defibrillation plus high-quality CPR. Continue ACLS: epinephrine every 3–5 minutes, and amiodarone (or lidocaine) for refractory shockable rhythms. Identify and treat reversible causes (Hs and Ts).

What is torsades de pointes and how is it treated?

A polymorphic ventricular tachycardia with a twisting QRS axis occurring in the setting of a prolonged QT interval. Treatment: IV magnesium sulfate, correct electrolytes, stop offending drugs, and use overdrive pacing or isoproterenol for bradycardia-dependent cases; defibrillate if pulseless.

Classify the AV blocks by their ECG features.

First-degree: PR $>200\,\text{ms}$, all P waves conduct. Mobitz I (Wenckebach): progressive PR lengthening until a dropped beat. Mobitz II: constant PR with sudden dropped QRS (His-Purkinje disease, risk of progression). Third-degree (complete): AV dissociation with independent atrial and ventricular rates.

Which bradyarrhythmias require a permanent pacemaker?

Symptomatic sinus node dysfunction, Mobitz type II second-degree AV block, high-grade or third-degree (complete) AV block, and symptomatic bradycardia not from reversible causes. Mobitz I and first-degree block usually do not require pacing if asymptomatic.

What is congenital long QT syndrome and the main risk it carries?

An inherited channelopathy (commonly LQT1, LQT2 potassium-channel and LQT3 sodium-channel mutations) causing prolonged ventricular repolarization. It predisposes to torsades de pointes, syncope, and sudden cardiac death. Beta-blockers are first-line; avoid QT-prolonging drugs.

How is the QT interval corrected for heart rate (Bazett's formula)?

$$QT_c = \frac{QT}{\sqrt{RR}}$$ where QT and RR are in seconds. A $QT_c > 450\,\text{ms}$ in men or $> 460\text{–}470\,\text{ms}$ in women is prolonged; $QT_c > 500\,\text{ms}$ markedly increases torsades risk.

Name two inherited channelopathies besides long QT syndrome and a hallmark feature of each.

Brugada syndrome: sodium-channel (SCN5A) mutation with coved ST elevation in $V_1\text{–}V_2$ and risk of VF/sudden death, classically during sleep/fever. Catecholaminergic polymorphic VT (CPVT): ryanodine receptor mutation causing exercise/emotion-induced bidirectional VT.

Describe the murmur and key features of aortic stenosis.

A harsh crescendo-decrescendo (diamond-shaped) systolic ejection murmur at the right upper sternal border radiating to the carotids, with a delayed/weak carotid upstroke (pulsus parvus et tardus). Classic triad: angina, syncope, and exertional dyspnea (heart failure).

What defines severe aortic stenosis hemodynamically, and what is the definitive treatment?

Severe AS: aortic valve area $< 1.0\,\text{cm}^2$, mean gradient $\geq 40\,\text{mmHg}$, or peak jet velocity $\geq 4\,\text{m/s}$. Definitive treatment of symptomatic severe AS is valve replacement (surgical AVR or TAVR); medical therapy does not change the natural history.

Describe the murmur of chronic aortic regurgitation and its peripheral signs.

An early decrescendo diastolic blowing murmur at the left sternal border, best heard sitting forward in expiration, with a wide pulse pressure. Peripheral signs include water-hammer (Corrigan) pulse, head bobbing (de Musset), and Quincke pulses; treat with afterload reduction and surgery for symptoms/LV dysfunction.

Describe the murmur and most common cause of mitral stenosis.

A low-pitched mid-diastolic rumble with an opening snap at the apex, best heard in left lateral decubitus; a loud S1 is typical. The most common cause worldwide is rheumatic heart disease. It can cause left atrial enlargement, atrial fibrillation, and pulmonary hypertension.

Contrast the murmurs of acute versus chronic mitral regurgitation.

Chronic MR: holosystolic murmur at the apex radiating to the axilla, often well tolerated due to LA compliance. Acute MR (e.g., papillary muscle rupture, endocarditis): early/decrescendo systolic murmur with abrupt pulmonary edema and cardiogenic shock requiring urgent surgery.

What are the Duke criteria categories used to diagnose infective endocarditis?

Diagnosis requires combinations of major and minor criteria. Major: positive blood cultures with typical organisms, and echocardiographic evidence of endocardial involvement (vegetation, abscess, new valve regurgitation). Minor: predisposing condition, fever $\geq 38^\circ\text{C}$, vascular phenomena, immunologic phenomena, and suggestive microbiology.

Which organisms most commonly cause infective endocarditis in different settings?

Staphylococcus aureus: most common overall and in acute IE and IV drug users (often tricuspid). Viridans streptococci: subacute IE on previously damaged native valves. Staphylococcus epidermidis: prosthetic valves. Enterococci: post-GU/GI procedures; HACEK organisms cause culture-negative cases.

List the classic peripheral stigmata of infective endocarditis.

Janeway lesions (painless palms/soles, septic emboli), Osler nodes (painful pulp of fingers, immune complexes), Roth spots (retinal hemorrhages with pale centers), splinter hemorrhages, and petechiae. New murmur, fever, and embolic phenomena complete the picture.

What are the Jones criteria for diagnosing acute rheumatic fever?

Following group A streptococcal pharyngitis: diagnosis needs 2 major or 1 major + 2 minor criteria plus evidence of prior strep infection. Major (JONES): Joints (migratory polyarthritis), carditis (O = heart), Nodules (subcutaneous), Erythema marginatum, Sydenham chorea. Minor: fever, arthralgia, elevated ESR/CRP, prolonged PR.

Which valve is most affected by rheumatic heart disease and what is the prevention?

The mitral valve is most commonly affected (mitral stenosis/regurgitation), followed by the aortic valve. Prevention is prompt treatment of streptococcal pharyngitis with penicillin and long-term secondary antibiotic prophylaxis to prevent recurrent rheumatic fever.

How is hypertension classified by the ACC/AHA 2017 guideline?

Normal: $<120/<80$. Elevated: $120\text{–}129/<80$. Stage 1: $130\text{–}139$ or $80\text{–}89$. Stage 2: $\geq 140$ or $\geq 90\,\text{mmHg}$. Diagnosis requires confirmation on $\geq 2$ readings on $\geq 2$ occasions.

What distinguishes essential (primary) from secondary hypertension?

Essential hypertension (~90–95% of cases) has no single identifiable cause and is multifactorial (genetics, sodium, obesity, age). Secondary hypertension has an identifiable cause and is suggested by young age, abrupt onset, severe/resistant HTN, or specific clues (e.g., hypokalemia, abdominal bruit).

List common causes of secondary hypertension and a clue for each.

Primary hyperaldosteronism (hypokalemia, metabolic alkalosis), renal artery stenosis (abdominal bruit, rise in creatinine after ACEi), pheochromocytoma (episodic headache/palpitations/sweating), Cushing syndrome, obstructive sleep apnea, hypo/hyperthyroidism, and coarctation of the aorta (arm-leg BP gradient).

What are the first-line antihypertensive drug classes for essential hypertension?

Thiazide diuretics, ACE inhibitors, ARBs, and dihydropyridine calcium channel blockers. In Black patients without HF/CKD, thiazides or CCBs are preferred initially; ACEi/ARB are favored with diabetes, CKD, or HFrEF.

Distinguish a hypertensive urgency from a hypertensive emergency.

Both involve severely elevated BP (often $>180/120\,\text{mmHg}$). Emergency: presence of acute target-organ damage (encephalopathy, stroke, MI, aortic dissection, pulmonary edema, AKI, eclampsia)—requires IV agents with controlled BP lowering. Urgency: no acute organ damage—lower BP gradually with oral agents.

What is the cardiac output equation and how does it relate to blood pressure?

$$CO = HR \times SV$$ and mean arterial pressure $$MAP = CO \times SVR.$$ Blood pressure is therefore the product of cardiac output and systemic vascular resistance, which is why antihypertensives target heart rate, contractility, volume, or vascular tone.

How is the ejection fraction calculated and what is the normal range?

$$EF = \frac{SV}{EDV} \times 100\% = \frac{EDV - ESV}{EDV} \times 100\%$$ where EDV is end-diastolic and ESV is end-systolic volume. Normal LVEF is approximately $55\text{–}70\%$; $\leq 40\%$ defines reduced EF heart failure.

What is restrictive cardiomyopathy and a classic systemic cause?

A non-dilated, rigid ventricle with impaired diastolic filling and preserved systolic function, producing right-sided heart failure with elevated filling pressures. A classic cause is cardiac amyloidosis (also hemochromatosis, sarcoidosis, endomyocardial fibrosis); it must be distinguished from constrictive pericarditis.