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Physical Examination of the Cardiovascular System

Chapter 246 | Harrison's 22e · Part 6 – Cardiovascular Disorders · Chapter 246

Key Clinical Points

  1. Physical examination remains a critical tool for bedside risk assessment (heart rate, blood pressure, signs of pulmonary congestion, and mitral regurgitation) even when imaging is available.
  2. JVP and the presence of an S3 heart sound are key predictors of heart failure prognosis.
  3. Carotid pulse morphology provides specific clues to aortic and pulmonic valve pathologies.
  4. S2 splitting patterns (fixed, wide, paradoxical, narrow) identify congenital defects and conduction blocks.
  5. Skin findings like cyanosis types and telangiectasias can indicate systemic diseases or specific cardiac conditions.
  6. Murmurs are hemodynamically driven by pressure gradients; their behavior during maneuvers (ValsManeuver, squatting) helps differentiate HOCM from MVP.
  7. S1 and S2 heart sounds provide the timing framework for identifying murmurs and valvular issues.
  8. The 'polypill' (aspirin, statin, antihypertensive) is a low-cost intervention for primary/secondary prevention.

INTRODUCTION

• Context: Physical examination remains a critical tool for establishing the presence, severity, and prognosis of cardiovascular diseases. • Clinical Utility: Findings such as heart rate, blood pressure, signs of pulmonary congestion, and mitral regurgitation (MR) inform bedside risk assessment before results from cardiac biomarker testing are known. • Prognostic Indicators: ◦ JVP: Predicts heart failure prognosis. ◦ S3 Heart Sound: Predicts heart failure prognosis. ◦ diac Murmurs: Provide insight into the natural history of many valvular and congenital heart lesions. • Innovation & Prevention: Low-cost interventions (e.g., "polypill" — a regimen of aspirin, a statin, and an antihypertensive) and hand-held ultrasound are increasingly integrated into care to improve outcomes in both primary and secondary prevention.

CLINICAL FEATURES

General Physical Examination

• Initial Assessment: Note age, posture, demeanor, and overall health status. • Patient State: Assess for pain, distress, diaphoresis, or specific behaviors (e.g., avoiding certain body positions to reduce pain in suspected acute pericarditis). • Respiratory Clues: Look for barrel chest deformity (increased anterior-posterior diameter), tachypnea, and pursed-lip breathing (suggesting pulmonary causes). • Anthropometrics: Measure height, weight, BMI, and body surface area; use waist circumference and waist-to-hip ratio to predict long-term cardiovascular risk. • Mental Status: Assess level of alertness and mood continuously during the interview and examination.

Skin Findings

• Cyanosis: ◦ Central: Indicates significant right-to-left shunting at the heart or lung level. ◦ Peripheral/Acrocyanosis: Related to reduced extremity blood flow or small vessel constriction; can be exacerbated by β-blockers with unopposed α-mediated vasoconstriction. ◦ Differential Cyanosis: Isolated cyanosis of lower extremities; suggests a large patent ductus arteriosus (PDA) and secondary pulmonary hypertension. • Telangiectasias: ◦ Lips, tongue, mucous membranes: Suggest Osler-Weber-Rendu syndrome; also seen in mitral stenosis (MS) or scleroderma. ◦ Malar telangiectasias: Seen in advanced mitral stenosis (MS) or scleroderma. • Discoloration: ◦ Bronze/Tan skin: Suggests hemochromatosis associated with systolic heart failure. • Jaundice: May be visible first in the sclerae; indicates advanced right heart failure and congestive hepatomegaly. • Other Signs: ◦ Subcutaneous xanthomas (tendon sheaths): Indicate hereditary lipid disorders. ◦ Ascites: Non-specific finding.

DIAGNOSTIC APPROACH

1. Carotid Pulse Morphology (Figure 1)

Evaluate the systolic upstroke and dicrotic notch to differentiate conditions: • Normal: Single systolic peak with a clear dicrotic notch. • Aortic Stenosis: Pulsus tardus → slow, rounded systolic up1upstroke; parvus → reduced peak; diminished/delayed dicrotic notch. • Severe Aortic Regurgitation: Bisferiens pulse → two distinct peaks in systole (rarely seen in severe AR). • Hypertrophic Obstructive Cardiomyopathy (HCM): Bisferiens pulse → rapid upstroke to first peak (percussion wave) and slower rise to second peak (tidal wave). • Sepsis or Intra-aortic Balloon Counterpulsation: Dicrotic pulse → peaks in both systole and diastole (often with IABP inflation just after the dicrotic notch).

2. Jugular Venous Pulse (JVP) (Figure 2)

The JVP reflects right atrial and ventricular pressures: • A wave: Represents right atrial presystolic contraction; enlarged/accentuated → reduced right ventricular compliance (also suggested by a right-sided S4). • C wave: Reflects carotid pulsation or early systolic increase in right atrial pressure. • v wave: Represents atrial filling during ventricular systole; peaks at S_2. • y descent: Follows A wave as atrial pressure falls (corresponds to tricuspid valve opening).

3. S2 Splitting Patterns (Figure 3)

The timing between the aortic (A_2) and pulmonary (P_2) components of S_2 identifies specific pathologies: • Atrial Septal Defect (ASD): Fixed splitting → constant volume in right heart. • Right Bundle Branch Block (RBBB): Wide splitting (increases with inspiration). • Left Bundle Branch Block (LBBB): Paradoxical/reversed splitting (P_2 occurs before A_2). • Pulmonary Hypertension: Narrow or absent split → high pressure causes rapid P_2 closure.

4. Hemodynamics of Heart Murmurs (Figure 4)

Murmurs are identified by the specific pressure gradients during the cardiac cycle: • Mid-systolic Murmur (MSM): Caused by systolic pressure gradient between left ventricle and aorta (e.g., mitral regurgitation). • Presystolic Murmur (PSM) & Mid-diastolic Murmur (MDM): Caused by diastolic pressure gradients (e.g., mitral stenosis).

5. Mitral Valve Prolapse (MVP) Dynamics (Figures 5, 6, 7)

The timing of the click (C) and murmur (M) changes with loading: • Decreased Volume/Impedance (e.g., Standing): Click and murmur move closer to S_1. • Increased Volume/Impedance (e.g., Squatting): Click and murmur move away from S_1 toward S_2.

6. Physiological Maneuvers (Table 246-1)

Clinical maneuvers provide specific diagnostic clues: • Respiration: ◦ Right-sided murmurs/sounds \uparrow with inspiration (except PES). ◦ Left-sided murmurs/sounds \uparrow during expiration. • Valsalva Maneuver: ◦ Most murmurs decrease in length and intensity. ◦ Exceptions: HOCM (\uparrow intensity), MVP (longer, often \uparrow intensity). • Post-VPB or AF: ◦ Semilunar valve murmurs \uparrow in the cardiac cycle. ◦ AV regurgitation murmurs do not change or become shorter (MVP). • Positional Changes: ◦ Standing: HOCM \uparrow; MVP lengthens/intensified. ◦ Squatting: HOCM and MVP soften or disappear. • Exercise: ◦ PS, MS, MR, VSD, AR \uparrow with hand grip. ◦ HOCM \downarrow with maximum hand grip.

Reference Tables

TABLE 246-1 Effects of Physiologic Interventions on the Intensity of Heart Murmurs and Sounds Respiration Right-sided…

Harrison's 22e, p.1867

  • Respiration
  • Right-sided murmurs and sounds generally increase with inspiration, except for
    the PES. Left-sided murmurs and sounds are usually louder during expiration.
  • Valsalva Maneuver
  • Most murmurs decrease in length and intensity. Two exceptions are the systolic
    murmur of HOCM, which usually becomes much louder, and that of MVP, which
    becomes longer and often louder. After release of the Valsalva maneuver,
    right-sided murmurs tend to return to control intensity earlier than do left-sided
    murmurs.
  • After VPB or AF
  • Murmurs originating at normal or stenotic semilunar valves increase in the
    cardiac cycle after a VPB or in the cycle after a long cycle length in AF. By
    contrast, systolic murmurs due to AV valve regurgitation do not change or
    become shorter (MVP).
  • Positional Changes
  • With standing, most murmurs diminish, with two exceptions being the murmur
    of HOCM, which becomes louder, and that of MVP, which lengthens and often
    is intensified. With squatting, most murmurs become louder, but those of HOCM
    and MVP usually soften and may disappear. Passive leg raising usually produces
    the same results.
  • Exercise
  • Murmurs due to blood flow across normal or obstructed valves (e.g., PS,
    MS) become louder with both isotonic and submaximal isometric (hand grip)
    exercise. Murmurs of MR, VSD, and AR also increase with hand grip exercise.
    However, the murmur of HOCM often decreases with nearly maximum hand
    grip exercise. Left-sided S and S sounds are often accentuated by exercise,
    4 3
    particularly when due to ischemic heart disease.