A 73-year-old man with history of hypertension and osteoarthritis is evaluated for gradually increasing dyspnea over the preceding 6 weeks. He takes metoprolol for hypertension and naproxen for the arthritis. He has occasionally awakened in the night with mild dyspnea relieved by sitting up but has not noticed edema. Physical examination shows BP of 148/94, HR 96, and RR 16. O2 saturation is 92%. Neck veins show the jugular column 7 cm above the sternal angle. Lung examination reveals mild basilar crackles but no wheezing. Cardiac examination shows sustained apex impulse, S4 gallop, and no murmur. There is no peripheral edema. ECG shows stable left ventricular hypertrophy; no Q waves are seen. Chest x-ray shows increased interstitial markings and some cephalization of flow to the upper lobe vessels. The cardiac silhouette is boot-shaped, but there is no definite cardiomegaly. Echocardiogram shows left ventricular hypertrophy and LV ejection fraction of 55% (normal 50%-70%). What is the likely pathogenesis of this patient's dyspnea?
The most likely explanation for this patient's presentation is heart failure with preserved ejection fraction (HFPEF), also known as diastolic dysfunction. As many as 50% of patients presenting with definite HF (Heart failure) will have an ejection fraction above 50%. HFPEF is more common in the elderly, in women, and those with conditions (especially hypertension) that lead to LV hypertrophy. Often the echocardiogram will show evidence of impaired relaxation or increased stiffness of the LV (the latter often suggested by decreased flow across the MV during atrial systole, giving the so-called reversed e/a flow ratio). Tachycardia, by decreasing diastolic filling time, will often worsen HF symptoms in diastolic dysfunction. As opposed to systolic HF, beta-blockers and ACE inhibitors have not demonstrated long-term survival benefit. Management focuses on controlling BP, preventing tachycardia, and treating pulmonary and peripheral fluid overload with diuretics; so many of the modalities used in systolic HF are also employed in HFPEF, just without proof of survival benefit.High output HF due to an AV fistula, Paget disease, or hyperthyroidism can mimic diastolic HF, but the patient usually has evidence of a hyperdynamic circulation (tachycardia, wide pulse pressure, hyperdynamic precordium). Occult CAD should be considered in patients with exertional dyspnea (which can be an angina equivalent), but this patient's rest symptoms and pulmonary vascular congestion would be unusual. In HF due to coronary artery disease, there is almost always evidence of prior MI or ischemic change on ECG. Nevertheless, a stress test is often obtained in patients with unexplained HF to rule out this possibility. Interstitial lung disease can cause rales and interstitial changes on CXR but would not explain the cephalization of flow nor the elevated venous pressure. Measuring B-type natriuretic peptide (BNP) will resolve the issue in equivocal cases; BNP will be elevated in HF and normal or minimally elevated in ILD. Anemia can cause fatigue and exertional dyspnea and, rarely, even overt HF, but to cause HF the anemia would have to be very severe (usually Hb 7 g/dL or below) and should be apparent from the physical examination. In addition, severe anemia would usually cause evidence of hyperdynamic circulation as seen in high-output HF.
Increased metabolic demands leading to high-output heart failure (HF)
Occult coronary artery disease with dyspnea as an angina equivalent
Impaired diastolic relaxation and filling
Interstitial lung disease (ILD) mimicking pulmonary vascular congestion
C.V.S.