Diagnosis

Clinical Presentation

History

  • Afflicted patients most commonly present with the following symptoms:
    • Dyspnea (on exertion and/or at rest)
    • Fatigue
    • Exercise intolerance
    • Orthopnea, paroxysmal nocturnal dyspnea
    • Bendopnea (dyspnea when leaning forward)
    • Systemic or pulmonary venous congestion (lower extremity swelling or cough/wheezing)
    • Presyncope, palpitations, and angina may also be present
  • Other possible presentations include incidental detection of asymptomatic cardiomegaly or symptoms related to coexisting arrhythmia, conduction disturbance, thromboembolic complications, or sudden death.
  • Clinical manifestations of HF vary depending on the severity and rapidity of cardiac decompensation, underlying etiology, age, and comorbidities of the patient.
  • Extreme decompensation may present as cardiogenic shock (resulting from both low arterial and high venous pressures), characterized by hypoperfusion of vital organs, renal failure (decreased urine output), mental status changes (confusion and lethargy), or “shock liver” (elevated liver function tests).

Physical Examination

  • The goal of the physical examination in HF is to estimate intracardiac pressures, cardiac output, and end-organ perfusion.
  • Elevated right-sided pressures result in lower extremity edema, jugular venous distension (JVD), abdominojugular reflux, pleural and pericardial effusions, hepatic congestion, and ascites.
  • JVD is the most specific and reliable physical examination indicator of right-sided volume overload and is representative of left-sided filling pressures except in cases of disproportionate right heart dysfunction (e.g., pulmonary hypertension, severe tricuspid regurgitation, and pericardial disease).
  • JVD is best visualized with oblique light and the patient at 45 degrees. Venous pulsations are differentiated from carotid pulsation by their biphasic nature, respiratory variability, and compressibility.
  • Abdominojugular reflux suggests an impaired ability of the right ventricle to handle augmented preload and may be due to constriction or pulmonary hypertension in addition to myocardial disease.
  • Elevated left-sided pressures may result in pulmonary rales, but rales are absent in the majority of HF patients with elevated left-sided filling pressures.
  • In the setting of systolic dysfunction, a third (S3) or fourth (S4) heart sound as well as the holosystolic murmurs of tricuspid or mitral regurgitation (MR) may be present; carotid upstrokes may also be diminished.
  • Low cardiac output is suggested by a proportional pulse pressure (pulse pressure/diastolic blood pressure) ≤25%, diminished carotid upstroke, and cool extremities.

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