Page 4 - The 5-Minute Clinical Consult 2021 29th Edition

PHYSICAL EXAM
Increased filling pressures: rales and sometimes wheezing, peripheral edema, S gallop,
3
hepatomegaly, jugular venous distention, hepatojugular reflux, ascites
Remodeling: enlarged or displaced point of maximal impulse
Poor cardiac output: hypotension, pulsus alternans, tachycardia, narrow pulse pressure, cool
extremities, cyanosis

DIFFERENTIAL DIAGNOSIS
Simple dependent edema, pulmonary embolism, exertional asthma, cardiac ischemia,
asthma/chronic obstructive pulmonary disease, constrictive pericarditis, nephrotic syndrome,
cirrhosis, venous occlusive disease with subsequent peripheral edema, high-output states:
anemia, sepsis, hyperthyroidism, lymphedema, tamponade

DIAGNOSTIC TESTS & INTERPRETATION
Diagnosis should be primarily clinical, with laboratory data as adjunctive and indicative of
complications.
Initial Tests (lab, imaging)
β-Type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-BNP) are helpful in the acute
setting to differentiate the cause of dyspnea (BNP <100 essentially rules out HF). A BNP level
in those with risk factors for developing HF or with structural heart disease but no symptoms
of HF can help predict the development of symptomatic HF (1)[A]. Other, non-HF conditions,
such as pulmonary embolism, renal failure, and acute coronary syndromes, may cause elevated
BNP. Of note, sacubitril/valsartan (Entresto), an angiotensin receptor blocker and neprilysin
inhibitor can raise BNP levels but has less impact on NT-proBNP levels. Obesity may lower
BNP levels. The use of BNP-guided therapy in chronic HF and acutely decompensated HF is
not well established, although a predischarge BNP can predict risk of readmission and survival
(1)[A].
Lab findings include respiratory alkalosis, mild azotemia, decreased erythrocyte sedimentation
rate, proteinuria (usually <1 g/day), elevated creatinine (cardiorenal syndrome), dilutional
hyponatremia (poor prognosis), hyperuricemia, and hyperbilirubinemia.
Chest x-ray (changes lag clinical symptoms by up to 6 hours): increased heart size, vascular
redistribution (cephalization) with “butterfly” pattern of pulmonary edema, interstitial and
alveolar edema, Kerley B lines, and pleural effusions. Findings of pulmonary edema may be
absent in long-standing HF.

Diagnostic Procedures/Other
Determination of left ventricular ejection fraction (LVEF) is critical to proper diagnosis and
management:
Echocardiogram is the most useful test to determine LVEF, RV function, diastolic dysfunction,
ventricular size, wall thickness, and valvular abnormalities; may be repeated if change
suspected in underlying cardiac status
Nuclear imaging to estimate ventricular sizes; assess for ischemia or infarction, ATTR wild-
type amyloidosis, and systolic function.
Cardiac MRI can be considered in select circumstances: suspicion of cardiac sarcoidosis,
arrhythmogenic RV CM, acute myocarditis, amyloidosis, and hemochromatosis.
Cardiac catheterization is important for excluding CAD as an etiology in the setting of risk