When the left ventricle cannot sufficiently contract and empty during systole, it's known as systolic heart failure or heart failure with reduced ejection fraction (HFrEF). In this condition, regardless of the initial cause, maladaptive neurohormonal positive feedback can accelerate systolic dysfunction by increasing intravascular volume, raising arterial blood pressure, and directly injuring the myocardium.1 Subsequent progressive chamber overload leads to dilated cardiomyopathy. The initial cause is often not identified, but conditions associated with systolic heart failure and dilated cardiomyopathy include hypertension, coronary artery disease, current or recent pregnancy, some infections, metabolic derangements such as hypothyroidism, and substances such as alcohol, cocaine, and certain chemotherapy drugs.
Image 2.1 Chronic maladaptive changes triggered by inadequate LV systolic contraction (emptying). Specific treatments for systolic heart failure are highlighted in green.
Due to this unique pathophysiology, it's essential to differentiate LV systolic dysfunction from other pathology. Unfortunately, HFrEF has non-specific signs and symptoms, including fatigue, early satiety, shortness of breath with exertion or lying flat, peripheral edema, jugular venous distention, extra heart sounds, abnormal lung sounds, and cardiomegaly. Signs of pulmonary edema are not very sensitive either because substantial lymphatic drainage may prevent patients with HFrEF from developing pulmonary or peripheral edema. Decompensated HFrEF overloads heart chambers and central veins, leading to pulmonary edema, pleural effusions, pericardial effusion, ascites, and injury to dependent flow-sensitive organs like the liver and kidneys. In addition, without sufficient peripheral vascular resistance, limited cardiac output will cause hypotension. Dilated cardiomyopathy can also lead to arrhythmias and thromboembolic disease. With training, generalists can use PoCUS to identify LV systolic dysfunction2–7and to assess for alternative diagnoses and complications of HFrEF.8
PoCUS evaluates ejection fraction (EF) as a surrogate for systolic function. EF is the percent change in LV volume between end-diastole and end-systole. PoCUS uses LV cross-sectional area as a rough surrogate for volume and simple visual estimation to qualitatively estimate the percent LV volume change between end-diastole and end-systole. Normal EF ranges from 52-72% for men and 54-74% for women. Instead of defining the EF as an exact percentage, which may overstate the precision of the finding, PoCUS should distinguish patients whose EF is either severely reduced, mild to moderately reduced, or at least near-normal. These categories can be defined as <30%, 30-50%, and >50% respectively. It is important to document if there is additional uncertainty, such as when image quality is poor. For example, write, "Poor image quality, but suspect LVEF >50%."
Heart failure with reduced ejection fraction (HFrEF) is defined as LVEF ≤40%.9 Assessing LVEF using PoCUS is largely qualitative and often performed during an acute illness when LVEF may be transiently higher or lower than baseline. LVEF can change from 40-50% to 30-40% or vice versa within a year10, and evidence suggests that treatments such as spironolactone or an angiotensin receptor blocker may benefit those with heart failure mildly-reduced EF (HFmrEF) 41-50%.11,12 The 30-50% category acknowledges the limitations of PoCUS. It provides a middle ground that errors on the side of giving more patients neurohormonal treatments or additional workup, if available, before ruling out HFrEF.
To visually estimate LVEF, look at two or more views, including at least one long-axis and one short-axis view. The subcostal four-chamber view often cuts the heart unevenly, so don’t use it to assess LVEF when other views are available. Short-axis views to assess LVEF should cut the LV at the mid-papillary muscles. Pay close attention to the myocardium during systole. Look specifically at 1) wall thickening, 2) inward motion of LV myocardium, and 3) anterior motion of the anterior mitral-valve leaflet during diastole. Be aware that foreshortened or oblique-plane imaging of the LV can exaggerate inward wall motion. In addition, the anterior mitral valve leaflet's anterior motion during diastole can be magnified with septal hypertrophy or suppressed in severe aortic regurgitation, mitral stenosis, or after mitral valve surgery.
Image 2.2 Comparing LVEF >>50% (A), >50% (B), 30-50% (C), <30% (D). Images with different depths are scaled for comparison.
Image 2.3 Comparing LVEF >50% (A) with LVEF <50% (B, C). Do not rely on the SC4C view alone to assess LVEF. If the subcostal window is the only window available, then obtain a subcostal short-axis view (C).
Acute physiologic changes can impact the EF and affect the false negative and false positive rates for identifying systolic heart failure. Review the factors below that can acutely change LVEF. If the estimated LVEF is >50% despite a predominance of factors that decrease LVEF, one can be confident that systolic function is preserved. However, if the estimated LVEF is >50%, but acute changes increase LVEF, reassess LVEF after the acute changes stabilize. Conversely, when systolic function appears reduced despite acute factors that increase LVEF, like hypotension, one can be more confident that systolic function is present. However, if the estimated LVEF is <50%, but most acute changes decrease LVEF, one should assess again after something like a hypertensive crisis or tachyarrhythmia stabilizes.
* If initially low, additional preload can increase cardiac output while lowering LVEF from a hyperdynamic state.
† Mitral valve regurgitation may decrease LV afterload but only to generate reverse flow, which increases vascular congestion and does not improve cardiac output.
** Decreasing preload can decrease cardiac output while increasing LVEF to a hyperdynamic state.
Image 2.4 Reduced LVEF with PSAX view (A) and PLAX view (B) in the setting of a tachyarrhythmia. Ideally, the LVEF should be assessed again after the heart rate stabilizes.
The DOSE trial compared high to low-dose IV diuretic strategies for patients with acute decompensated heart failure. The high-dose strategy did not increase the overall incidence of worsening renal function.13 However, a sub-group analysis of this study showed that only those with reduced LVEF who received the high-dose strategy had a significantly higher incidence of being dyspnea-free at 72 hours, more fluid loss overall, and a lower composite outcome of death, total hospitalizations, and unplanned clinic visits at three months.14 This suggests that HFrEF, more so than heart failure with preserved EF (HFpEF), benefits from an abrupt decrease in preload and suggests that PoCUS can help identify which patients with acute decompensated heart failure would benefit from a more aggressive diuretic strategy.
The LV wall can sometimes thicken and contract asymmetrically. Acute or prior coronary ischemia may cause this, but so can conduction abnormalities (i.e., left bundle branch block), interventricular interdependence, Takotsubo cardiomyopathy, and other focal cardiac pathology. Interpreting focal wall-motion changes is outside the scope of most PoCUS users, and PoCUS should never be used to rule out coronary ischemia. However, if not already known, finding significant focal wall-motion abnormalities should prompt consideration of coronary artery disease.
Image 2.5 Parasternal short-axis view revealing significant focal wall-motion changes in a patient with known coronary artery disease.
PoCUS or other cardiac imaging is essential to identify HFrEF patients and direct them to specific long-term medical therapy. Whether decompensated or not, identifying HFrEF and providing neurohormonal blockage therapy can be lifesaving. In addition, loop diuretics, carvedilol, enalapril/losartan, and spironolactone are relatively cheap, extremely effective, and feasible to prescribe in most healthcare settings. Therefore, don't pass up a chance to incorporate PoCUS in settings where HFrEF patients may be overlooked, misdiagnosed, or inadequately treated because of diagnostic uncertainty. A comprehensive discussion of relative benefits, specific dosing, and indications for additional therapies is beyond the scope of this material. Consider reading the following for further reference.15,16