Heart failure with preserved ejection fraction (HFpEF) develops when the LV does not fill up easily (diastolic dysfunction). The EF in HFpEF may be in the normal range, but inadequate filling means the actual stroke volume is insufficient to generate enough cardiac output. Even before cardiac output drops, signs and symptoms of heart failure can develop as higher atrial pressure becomes necessary to fill the LV. Diastolic dysfunction can occur alone or alongside systolic dysfunction with reduced ejection fraction. If both are present, treatment should focus on the systolic dysfunction because it requires a more specific therapeutic approach discussed previously.
After the LV contracts, early filling is driven by the rapid energy-intensive deactivation of myofilaments. High afterload from hypertension, aortic stenosis, or a stiff aorta can delay and slow this initial relaxation. Unsynchronized ventricular depolarization due to a bundle-branch block or ventricular rhythm can also slow the deactivation rate. After relaxing, the contracted LV wall recoils with elastic properties to create a relative vacuum force proportional to how much it has contracted past its equilibrium state. Higher end-systolic volume from low contractility, severe tachycardia, high preload, or high afterload diminishes this elastic restorative force. There may be no restorative force if the LV is still overloaded by the end of systole.
Late-diastolic filling is driven by higher pressure in the LA, especially when it contracts, which stretches out the LV wall. Aging, amyloid accumulation, and the degree of blood vessel pressurization in the ventricle all influence intrinsic LV wall compliance or stiffness. This intrinsic compliance and LV geometry determine how easily the LV stretches and fills past its equilibrium state. LV geometry that favors emptying and coping with high afterload (thicker wall and smaller chamber) has the tradeoff of making LV filling more difficult. In addition, external forces like pericardial or thoracic pressure influence LV expansion. These conditions are discussed separately in the chapters addressing right heart failure and pericardial disease. Mitral stenosis also impairs LV filling and is addressed separately in the chapter on valvular heart disease.
Image 7.1 Apical 4-chamber views comparing heart failure with reduced EF (A) to heart failure with preserved EF (B).
With various etiologies, patients with HFpEF are a heterogeneous group. Many patients with HFpEF are asymptomatic at rest or without sufficient exacerbating factors. PoCUS alone cannot rule in or out the diagnosis of HFpEF. Unless advanced echocardiographic or invasive measurements are available, the diagnosis is one of exclusion. Thus, consider HFpEF in patients with signs and symptoms of heart failure who lack systolic dysfunction, and a thorough workup has not revealed an alternative cause. PoCUS findings, such as ejection fraction, can change in acute settings, so consider repeating the exam after initial treatments. A thorough workup may include natriuretic peptide levels. However, natriuretic peptide levels can be normal with HFpEF, especially when compensated, and repeat measurements vary significantly in individuals with stable physiology.1 Therefore, natriuretic peptide levels are only helpful if significantly elevated or in follow-up if they change by a factor of two or more.
Image 7.2 PLAX (A), A4C (B), and SC4C (C) views revealing dilated atria in the setting of preserved LVEF. Notice that the 4-chamber views reveal atria that are grossly as large or larger than the ventricles.
PoCUS can identify LA enlargement when the LA appears as large or larger than the LV in the A4C view. Severe LVH may also be apparent. However, none of these findings are sensitive or specific. Thus, refer to them as potential clues. Consider HFpEF as a diagnosis of exclusion that requires a constellation of signs and symptoms, including PoCUS findings consistent with heart failure with no alternative cause, such as significant systolic, valvular, pericardial, pulmonary, renal, or hepatic dysfunction or anemia. Advanced echocardiographic techniques combined with stress testing can provide a more sensitive and specific assessment of diastolic function and, when available, should be considered in patients with suspected HFpEF.1
Acute treatment should address the triggers and complications listed above, but cautiously, because patients with significant HFpEF have limited reserve to increase cardiac output (stroke volume and heart rate). When LV filling is the primary problem, aggressive treatment with diuretics or vasodilators can lead to hypotension and end-organ dysfunction more readily than in patients whose primary problem is emptying (systolic heart failure).2–4
Medical therapy for HFpEF aims to address the underlying risk factors listed above. Data suggests that aldosterone-receptor antagonists like spironolactone should be used to treat hypertension in HFpEF, especially if poorly controlled despite multiple other agents.5 The sodium-glucose cotransporter 2 (SGLT2) inhibitors like dapagliflozin and empagliflozin may also be particularly helpful.6,7 In addition, all heart failure patients deserve adequate education on the disease process, specific medications like diuretics, the impact of lifestyle, symptom and weight monitoring, and other necessary self-care.
HFpEF is associated with a wide range of underlying conditions and is a diagnosis of exclusion. Treatment should address the acute triggers and underlying conditions involved. Use caution to avoid hypovolemia-associated hypotension, which may be more prominent compared to patients with other forms of heart failure.