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Cardiology Review: Murmurs, Exams, Pericarditis to Atrial Fibrillation

Cardiac Exam: Murmurs, Sounds, and Basic Cardiac Anatomy

  • Palpation findings you should recall during a cardiac exam:

    • Thrill: a palpable vibration felt over the chest, like a motor purring; often graded on a 0–6 scale, with a 4/6 being described here as a loud thrill. May be present with shunts like a ventricular septal defect (VSD).

    • Lift or heave: a sustained impulse felt or seen on inspection, suggesting ventricular hypertrophy or dilated cardiomyopathy (enlarged heart chambers).

    • Murmur grading realism: in early PA practice, many appear normal; over time, you learn to distinguish louder vs softer murmurs and when a thrill is present.

  • Palpation and auscultation locations for murmurs:

    • Aortic area: 2nd right intercostal space (ICS)

    • Pulmonic area: 2nd left ICS

    • Tricuspid area: 4th left ICS

    • Mitral area: 5th left ICS at the midclavicular line

    • Murmurs radiate to other areas depending on the valve involved; the sound radiates rather than being exactly over the valve.

    • A helpful reminder: murmurs are often best heard in the area where the sound radiates, not necessarily at the valve’s exact location.

    • Clinicians: when a question says, for example, a systolic murmur at the second intercostal space on the right, think aortic valve involvement; questions are often worded to help you narrow the valve.

  • Basic flow of blood through the heart (overview for orientation):

    • Systemic venous return via the superior and inferior vena cavae drains into the right atrium (RA).

    • RA → tricuspid valve → right ventricle (RV) during diastole.

    • RV → pulmonic valve → pulmonary arteries → lungs for oxygenation.

    • Oxygenated blood returns via the pulmonary veins → left atrium (LA).

    • LA → mitral valve → left ventricle (LV) during diastole.

    • LV → aortic valve → aorta → systemic circulation.

  • A note on pulmonary embolism (PE) anatomy:

    • Saddle PE occurs at the bifurcation of the pulmonary arteries and can cause obstructive shock.

  • Core heart sounds and their timing:

    • S1: occurs when the mitral and tricuspid valves close; marks the beginning of systole (ventricular contraction and ejection).

    • S2: occurs when the aortic and pulmonic valves close; marks the beginning of diastole (ventricular filling).

    • LV/RV valves (aortic and pulmonic) close at about the same time; AV valves (mitral and tricuspid) close almost simultaneously.

    • S2 is loudest at the base of the heart; S1 at the apex.

  • Normal vs abnormal S2 splitting:

    • Normal physiological S2 split: during inspiration, the pulmonic valve closes slightly later than the aortic valve, widening the split. This is normal and should be heard with deep inspiration.

    • Fixed split S2: does not vary with respiration and is associated with an atrial septal defect (ASD); the split persists on inspiration and expiration.

  • S3 and S4 gallops (timing and clinical significance):

    • S3 gallop: early diastole, after S2; associated with volume overload and congestive heart failure (CHF) in adults; can be normal in young athletes (athletic heart). Remember the phrase: "sloshing in" (S1, S2, S3 – diastolic filling time).

    • S4 gallop: late diastole, just before S1; indicates a stiff ventricle (e.g., longstanding hypertension with LV hypertrophy or post-MI scar); never normal.

    • Mnemonic memory aids: S3 associated with CHF or athletic heart; S4 with stiff ventricle (stiff wall).

  • Functional (physiologic) murmurs:

    • Occur in states of high cardiac output with no primary valve pathology.

    • Typical scenarios: pregnancy, anemia, young athletes with increased flow.

    • These murmurs are not due to structural valve disease; they arise from increased flow across a normal valve.

  • Murmur timing reminder:

    • Systolic murmurs occur between S1 and S2.

    • Diastolic murmurs occur between S2 and S1.

    • If unsure of a murmur’s timing, palpate the carotid pulse or the point of maximal impulse (PMI) to correlate with murmur timing (if the murmur coincides with the pulse, it’s typically systolic).

  • Four systolic murmurs and two diastolic murmurs to know for boards (brief overview):

    • Systolic murmurs: Mitral regurgitation (MR), Aortic stenosis (AS), Tricuspid regurgitation (TR), Pulmonic stenosis (PS).

    • Diastolic murmurs: Aortic regurgitation (AR), Mitral stenosis (MS).

    • Mnemonic for diastolic murmurs: ARMS (Aortic regurgitation, Mitral stenosis).

  • Systolic murmur details and pathophysiology

    • Mitral regurgitation (MR):

    • Timing: holosystolic (throughout S1–S2).

    • Location/quality: apical, radiates to the axilla; blowing quality; best heard at the apex.

    • Etiology: mitral valve prolapse (MVP), LV dysfunction with dilation, ischemic heart disease, papillary muscle rupture (post-MI, acute MR).

    • Clinical notes: volume overload; S3 may be present; may lead to pulmonary edema.

    • Treatment: valve repair preferred if possible; if not, valve replacement.

    • Aortic stenosis (AS):

    • Timing: systolic murmur; harsh, crescendo-decrescendo pattern; best heard at the 2nd right ICS.

    • Radiation: to the carotids.

    • Etiology: congenital bicuspid aortic valve or calcific degeneration with age.

    • Symptoms/signs: syncope with exertion, angina, dyspnea on exertion; beware exercise stress testing if unaddressed AS.

    • Management: aortic valve replacement (AVR) or transcatheter aortic valve replacement (TAVR).

    • Tricuspid regurgitation (TR):

    • Timing: holosystolic/pansystolic murmur; best heard at left lower sternal border.

    • Radiation: may radiate to the right or lower sternum; louder with inspiration (Carvallo’s sign).

    • Etiology: pulmonary hypertension, rheumatic disease, IV drug use with endocarditis, Ebstein anomaly.

    • Clinical notes: signs of right-sided failure (JVD, edema, ascites).

    • Treatment: diuretics; valve repair or replacement if severe.

    • Pulmonic stenosis (PS):

    • Timing: systolic murmur; best heard at the 2nd left ICS.

    • Etiology: often congenital.

  • Diastolic murmurs details

    • Aortic regurgitation (AR):

    • Timing: blowing, decrescendo diastolic murmur; best heard at left sternal border (Erb’s point, 3rd ICS); may be accentuated when leaning forward and holding breath.

    • Etiology: hypertension with aortic root dilation, aortic dissection, Marfan syndrome.

    • Physical findings: wide pulse pressure (e.g., 150/40); Corrigan (water-hammer) pulse; Traube sign; pistol-shot femoral pulses (Traube sign).

    • Symptoms: angina, dyspnea due to volume overload.

    • Treatment: aortic valve replacement.

    • Mitral stenosis (MS):

    • Timing: diastolic rumble with an opening snap after S2 (hard to hear but classic when present).

    • Etiology: typically rheumatic heart disease following untreated group A streptococcal infection.

    • Clinical notes: risk of atrial fibrillation due to LA enlargement.

    • Treatment: valve replacement when indicated; manage AFI risk.

  • Valve repair versus replacement concepts

    • Valve repair: leaves existing leaflets intact; ring annuloplasty to tighten the valve and improve coaptation.

    • Valve replacement: replace with a tissue valve (bovine or porcine) or a mechanical valve.

    • Anticoagulation implications:

    • Tissue valves: typically anticoagulation for ~1–2 months post-operation; then may discontinue.

    • Mechanical valves: long-term anticoagulation required due to thrombosis risk.

    • Anticoagulation specifics:

    • Warfarin: vitamin K antagonist; INR target typically between 2.0\le INR\le 3.0.

    • Reversal: vitamin K; fresh frozen plasma (FFP) for urgent reversal in active bleeding; dietary considerations with leafy greens.

    • Drug interactions: grapefruit juice and alcohol can increase INR; various drugs can affect warfarin metabolism.

  • Hypertrophic obstructive cardiomyopathy (HOCM)

    • Pathophysiology: thickened interventricular septum causing dynamic LV outflow tract obstruction; linked to sudden cardiac death in athletes.

    • Physical exam concepts: murmur that worsens with decreased preload; dynamic obstruction.

    • Maneuvers that affect preload and murmur intensity:

    • Squatting increases preload; often reduces murmur intensity.

    • Standing and Valsalva reduce preload; murmur intensity increases.

    • Handgrip (not emphasized here) can also affect murmur depending on afterload.

    • Clinical approach: differentiate from AS; consider sports physicals for athletes; echocardiography for diagnosis.

  • Mitral valve prolapse (MVP)

    • Features: midsystolic click with or without late systolic murmur; palpitations and dysautonomia symptoms in some patients.

    • Valsalva/standing effects: murmur can be accentuated with standing or Valsalva due to decreased preload.

    • Management: beta-blockers for symptoms; echo to confirm; repair if severe regurgitation.

  • Inflammation and infection in the heart

    • Pericarditis (inflammation of the pericardium):

    • Causes: viral infections, TB, cancer, lupus, rheumatoid arthritis; drugs (minoxidil, penicillin, chemotherapy).

    • Dressler syndrome (post-MI or post-CABG pericarditis): common after MI or bypass surgery; fibrinous pericarditis.

    • Symptoms: sharp chest pain, worse with inspiration and lying flat; friction rub (sound like boot scraping in snow) is highly specific.

    • EKG findings: PR depression; diffuse concave upward ST elevations; J point notching occasionally.

    • Labs: ESR elevated; CRP elevated.

    • Treatment: NSAIDs (e.g., ibuprofen, indomethacin, naproxen) plus colchicine for ~3 months; avoid steroids due to recurrence risk.

    • Pericardial effusion and tamponade

    • Pathophysiology: buildup of fluid in the pericardial space compressing the heart and impairing diastolic filling.

    • Beck’s triad: hypotension, JVD, muffled heart tones.

    • Kussmaul sign: JVP increases on inspiration (noted in some cases).

    • Pulsus paradoxus: >10 mmHg drop in systolic BP with inspiration; observed as a sign of tamponade.

    • Electrical alternans on EKG: beat-to-beat QRS amplitude variation due to heart swinging in fluid.

    • Management: urgent pericardiocentesis with ultrasound guidance if unstable; pericardial window or drain if stable but large effusion; send fluid for pathology to assess malignancy or infection.

    • Myocarditis (inflammation of the heart muscle)

    • Etiology: usually viral; can be hypersensitivity or autoimmune; sometimes associated with vaccines.

    • Presentation: flu-like symptoms followed by dyspnea and possible heart failure signs; tachyarrhythmias.

    • Lab/EKG: elevated ESR/CRP; troponin elevated; ECG may show diffuse ST elevations similar to pericarditis but without STEMI features; heart blocks or ventricular arrhythmias possible.

    • Imaging/diagnosis: echocardiography to assess wall motion; cardiac MRI helpful; definitive etiology often from endomyocardial biopsy.

    • Treatment: heart failure management; avoid NSAIDs (can worsen heart failure); restrict activity for 3–6 months; monitor arrhythmias; treat underlying cause.

    • Infective endocarditis (IE)

    • Risk factors: prosthetic valves, IV drug use, pacemaker/ICD leads, prior valve disease, immunosuppression, dental or other procedures with potential bacteremia.

    • Presentation: fever, malaise; murmur; possible glomerulonephritis; vascular phenomena; rare findings such as splinter hemorrhages, Janeway lesions, Osler nodes, Roth spots.

    • Diagnosis: positive blood cultures; echocardiography (TEE is common for detection of vegetations).

    • Common pathogen: Staphylococcus aureus.

    • Treatment: antibiotics for roughly 2–6 weeks (often 4–6 weeks for native valves; longer for prosthetic valves).

    • Prophylaxis: antibiotic prophylaxis for dental work, certain GI/ GU procedures when bacteremia risk is high in patients with prosthetic valves or prior IE or certain high-risk conditions.

  • Rheumatic heart disease and related issues

    • Etiology: sequela of untreated group A streptococcal pharyngitis; rheumatic fever can affect joints and heart.

    • Cardiac impact: mitral valve most commonly affected in rheumatic disease; mitral stenosis is a classic worldwide complication.

    • Prevention and treatment: primary penicillin prophylaxis; valve surgery if severe.

  • Atrial fibrillation (A-fib) overview for exam prep

    • Pathophysiology: chaotic atrial activity with multiple foci leading to irregular, often rapid ventricular response; AV node reduces conduction to pacing rate.

    • Typical presentation: irregularly irregular rhythm; absence of discrete P waves; variable R-R intervals; tachycardia range often around 110–140 bpm in acute presentations.

    • Classifications: paroxysmal (terminates within 7 days), persistent (>7 days, may require cardioversion), permanent (accepted long-standing AF with no sinus rhythm).

    • Duration and thromboembolism risk: the 48-hour rule is a practical guide—AF lasting >48 hours increases risk of left atrial thrombus; risk stratification is essential for management decisions.

    • Initial evaluation and workup: history, ECG, baseline labs, echocardiography to assess atrial size and cardiomyopathy, assess for valvular disease; evaluate for precipitating factors (e.g., hyperthyroidism, sleep apnea, caffeine or energy drinks intake).

    • Rate control vs rhythm control:

    • Rate control options: beta blockers, calcium channel blockers, and digoxin.

    • Rhythm control options: antiarrhythmic drugs or electrical cardioversion; urgent if unstable.

    • Anticoagulation and stroke prevention:

    • CHADS-VASc score helps determine need for anticoagulation; general guidance from the lecture:

      • If CHADS-VASc = 0: no anticoagulation.

      • If CHADS-VASc = 1 (men) or 2 (women): consider none or anticoagulation; aspirin alone is not indicated for AF stroke prevention in this scenario.

      • If CHADS-VASc >= 2 (men) or >= 3 (women): anticoagulation indicated.

    • Anticoagulation options:

      • Warfarin (vitamin K antagonist): INR target ~2.0 ext{ to } 3.0; interactions with diet (vitamin K), drugs, and foods; reversal with vitamin K; FFP for urgent reversal in active bleeding; not recommended in pregnancy.

      • DOACs (direct oral anticoagulants): rivaroxaban, apixaban, edoxaban (Factor Xa inhibitors); preferred over warfarin in non-valvular AF without mitral stenosis; require dose adjustment for renal impairment; do not require routine INR monitoring; reversal agents exist but with varying accessibility.

      • Important caveat: DOACs are not used with significant mitral stenosis; warfarin remains preferred for AF with mitral stenosis.

    • Rhythm control strategies and procedures:

    • Direct current cardioversion (DCCV) when indicated; if AF duration >48 hours, anticoagulation for ~3 weeks before cardioversion or seek TEE-guided cardioversion to exclude LA thrombus; if unstable, cardioversion is urgent.

    • Pulmonary vein isolation (PVI) via catheter ablation as a curative approach for paroxysmal or some persistent AF.

    • Practical antiarrhythmics for AF (sample drugs):

    • Amiodarone (Class III): effective but notable toxicities (thyroid, liver, pulmonary toxicity); requires baseline and periodic monitoring; can prolong QT; pulmonary toxicity can be irreversible.

    • Sotalol (Class III with beta-blocker effect): QT prolongation risk; monitor QT.

    • Flecainide and Propafenone (Class Ic): require normal LV function and no significant CAD; use with caution in patients with structural heart disease.

  • Practical clinical question highlights (from the end of the lecture)

    • Pericarditis presentation with pleuritic chest pain and a friction rub; NSAIDs and colchicine are mainstays; avoid steroids due to recurrence risk; Dressler syndrome as a post-MI pericarditis variant.

    • Amiodarone pulmonary toxicity: consider in AF patients with pulmonary fibrosis on imaging or restrictive patterns on PFTs.

    • Tamponade signs: hypotension, JVD, muffled heart sounds; pulsus paradoxus; electrical alternans on EKG; management includes urgent pericardiocentesis if unstable, possibly pericardial window for ongoing effusion.

    • AF management in unstable patients: immediate synchronized cardioversion; if unstable, do not delay for anticoagulation.

    • Brief sample exam-style questions reviewed in class and their rationale (pericarditis treatment, amiodarone toxicity, tamponade, unstable AF management).

Key formulas, numbers, and clinical thresholds to memorize

  • Anticoagulation decision rule for AF (summary from CHADS-VASc):

    • If CHADS ext{-}VASc = 0: no anticoagulation.

    • If male with CHADS ext{-}VASc = 1 or female with CHADS ext{-}VASc = 2: consider no anticoagulation vs. anticoagulation; aspirin not routinely recommended for stroke prevention in AF.

    • If CHADS ext{-}VASc ext{ is }
      promote 2 ext{ in men or }
      promote 3 ext{ in women}: anticoagulation indicated.

  • Warfarin INR target: 2.0 \le INR \le 3.0.

  • Bypass/acute management notes:

    • If AF duration > 48 hours, anticoagulation for ~21 days (3 weeks) before cardioversion or perform TEE-guided cardioversion to exclude left atrial thrombus.

    • If AF duration < 48 hours and patient is unstable: proceed to synchronized cardioversion without waiting for anticoagulation.

  • Valve replacement choices and anticoagulation implications:

    • Tissue valve: typically short-term anticoagulation; often discontinue after 1–2 months.

    • Mechanical valve: long-term anticoagulation required (lifelong).

  • Classic murmurs location quick references (non-exhaustive):

    • Aortic stenosis: harsh systolic murmur at the 2nd right ICS radiating to the carotids.

    • Mitral regurgitation: holosystolic murmur at the apex radiating to the axilla.

    • Tricuspid regurgitation: pansystolic murmur best heard at the left lower sternal border; louder with inspiration.

    • Aortic regurgitation: diastolic blowing decrescendo murmur best heard at the left sternal border with patient in a leaning-forward position.

  • Be mindful of red flags in quarterback-style questions:

    • A-fib with murmur radiating to the neck suggests AS in the appropriate context.

    • Shortness of breath with prior MI and a new holosystolic murmur at the apex suggests MR due to LV dilation or papillary muscle dysfunction.

    • A mid-systolic click with a murmur that worsens with standing suggests MVP.

Connections to practice and real-world relevance

  • The timing and radiation of murmurs help distinguish valve pathologies in clinical exams and guide when to order further imaging (e.g., echocardiography) or consider surgical interventions.

  • Understanding preload effects on HOCM and MVP helps explain why certain physical maneuvers either worsen or improve the murmur, guiding recommendations for athletes and physical exams.

  • Recognizing pericarditis, pericardial effusion, and tamponade is crucial in acute care; prompt management can be life-saving, particularly in tamponade where hemodynamic collapse can occur rapidly.

  • AF management hinges on stroke risk (CHADS-VASc) and hemodynamic stability; choosing rate vs rhythm control and selecting anticoagulation strategy (warfarin vs DOACs) depends on valvular disease and patient-specific factors.

  • Infections (infective endocarditis) and rheumatic heart disease remain important globally; prophylaxis guidelines influence dental and invasive procedures for high-risk patients.

  • The evolving role of TAVR for aortic stenosis reflects less invasive options with favorable short-term outcomes and expanding indications.

  • The emphasis on not using NSAIDs in myocarditis and heart failure highlights nuanced aspects of pharmacotherapy in cardiology.

  • Recognizing the implications of rheumatic disease globally helps in understanding patient histories and anticipating valve involvement in younger patients.

If you want, I can convert these notes into a concise study sheet focused on specific exam-style questions or create a quick-reference card for how to approach auscultation and differentiating murmurs in a high-yield, exam-ready format.