Congestive heart failure has been defined as a clinical syndrome that occurs when the heart is unable to meet the demands of actively metabolizing tissue without increasing filling pressures. Myocardial causes of heart failure (HF) may be systolic and/or diastolic. The versatile, noninvasive nature of echocardiography means that it plays a part in the diagnosis, determining the etiology, and noninvasive evaluation of HF guide management. This chapter will highlight the role of echo in evaluating a few cases of systolic dysfunction and diastolic dysfunction.
Mrs. LH is a 66-year-old woman who uses a wheelchair. She has a past history of recent myocardial infarction s/p percutaneous coronary intervention (PCI) to a large left anterior descending artery (LAD) (Video 21-1*, Figure 21-1, Video 21-2, Video 21-3) and left circumflex artery (LCX), and history of congestive heart failure (CHF) with medical noncompliance, hypertension (HTN), and hyperlipidemia. Mrs. LH was seen in clinic with worsening pedal swelling and decreased ability to lie down flat at night. She had a history of dietary and medical noncompliance and was brought in by her husband who complained that his wife was getting worse. She denied new onset of chest pain but admitted that she had not been compliant with her carvedilol medication out of concerns that it may precipitate an undue drop in blood pressure.
On examination, Mrs. LH’s jugular venous pressure was elevated with a prominent V wave and she had a soft systolic murmur over her tricuspid area, which got louder with inspiration. Also present was a soft S1 with a prominent third heart sound. She also had bilateral crackles over her lung bases, bilateral pedal edema, and chronic stasis dermatitis. Her electrocardiogram (ECG) was unchanged from her previous ECGs and 3 sets of troponins were negative. Echocardiography revealed an ejection fraction (EF) of 32% with anterior wall motion abnormalities and a prominent left ventricular thrombus at the apex (Video 21-1, Video 21-4, Video 21-5). She was then admitted and maintained on oral lisinopril daily, intravenous (IV) frusemide, and IV heparin with warfarin. She was eventually discharged after achieving euvolemic status on the same medicines with aspirin 81 mg daily, atorvastatin 40 mg daily, carvedilol 12.5 mg twice daily and spironolactone 25 mg daily. Her discharge INR was 2.6 and she was asked to follow up with her cardiologist for consideration of stress testing and implantable cardioverter defibrillator (ICD) placement.
The signs and symptoms are at first predominantly that of coronary artery disease (CAD) but also include signs and symptoms of CHF.
May present with classic signs of chest pain radiating to the left arm, jaw, or neck.
Women tend to have atypical symptoms.
Pain is usually described as crushing.
Associated nausea or vomiting may be present.
May be asymptomatic. This is more common in:
The elderly
Patients with diabetes mellitus
Women
Lightheadedness and dizziness may be a feature.
Shortness of breath
Leg swelling
Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal dyspnea
Signs include:
Pedal edema
Raised jugular venous pulse (JVP)
Displaced apex beat
A third heart sound that may be due to ischemic mitral regurgitation or systolic dysfunction.
According to the NHANES study, 13,643 men and women were followed up for 19 years and 1382 developed congestive cardiac failure. Of these, CAD was associated with a RR of 8.1 and a population-attributable risk of 62%.1 The resulting cardiomyopathy after a coronary insult may be due to:
Irreversible loss of myocardium after an ischemic insult.
Stunned or hibernating myocardium.
Stunned myocardium refers to transient post ischemic dysfunction, whereas hibernating myocardium refers to contractile dysfunction that improves after revascularization.
Multiple factors contribute to the development of the atherosclerotic plaque from formation of fatty streaks in childhood to eventual development of a fibrous plaque and neovascularization as well as inflammation. An acute obstruction may be due to rupture of vulnerable plaque with eventual platelet activation, adhesion, and aggregation leading to occlusion of the vessel wall. Plaque erosion may also lead to platelet aggregation.
Major risk factors for atherosclerosis include:
HTN
Diabetes mellitus
Cigarette smoking
Hyperlipidemia
Family history of premature CAD
*Videos available on www.BaligaHeartFailureCh21.com.
This usually involves some form of ischemic evaluation. These include:
Stress testing
Computed tomography (CT) angiography
Coronary angiography
Echocardiogram may demonstrate wall motion abnormalities suggesting ischemia. The presence and location of wall motion abnormalities also give clues about the location of the coronary insult. Due to its noninvasive nature and lack of need for radioactive contrast, echocardiography is widely used to determine the EF and can also give useful information about myocardial viability. The presence of end-diastolic wall thickness <0.6 cm (Video 21-6 and Figure 21-2) excluded the potential for functional recovery with a sensitivity of 94% and a specificity of 49%,2 while a deceleration time >150 ms predicted an increase in EF after coronary artery bypass grafting (CABG) with sensitivity and specificity of 80%.3 Echocardiography may also show complications of a myocardial infarction such as:
Ventricular septal defect (VSD)
Pericardial effusion (Figure 21-2)
Ruptured papillary muscle and severe mitral regurgitation
Cardiac rupture
Other findings would include a B bump to suggest an elevated Left ventricular end diastolic pressure (LVEDP),4 increased E-point septal separation (EPSS) suggesting decreased stroke volume, and/or a dilated left ventricle and increased E/e’ ratio with bulging of the interatrial septum to the right suggesting increased left atrial pressure.5
ECG may show evidence of ischemia or Q waves correlating with a coronary artery distribution.
This involves treatment of the CHF as well as the underlying CAD with coronary artery revascularization either percutaneously or by surgery. Patients need to be on
Aspirin
Beta blocker
Angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB) or sacubitril/valsartan.
Statin: For secondary prevention of myocardial infarction. The high-intensity statins are preferred.
Spironolactone: For patients with NYHA class II-IV symptoms and EF <35% who have normal renal function and normal potassium concentration.
Loop diuretic: This provides a symptomatic benefit.
ICD or cardiac resynchronization therapy.
Mr. BB is a 43-year-old man who presented to the hospital with shortness of breath and leg swelling. He had a flu-like illness 3 weeks prior. He said the “flu” never got better, but was now associated with worsening shortness of breath on exertion and he had been unable to sleep for 3 days. He also described progressive leg swelling and early satiety. On examination, he had a jugular venous pulse which was raised all the way to the jaw, a displaced apex beat, and a soft systolic murmur over his tricuspid and mitral areas, which increased with inspiration and radiated to his axilla respectively. Abdominal examination demonstrated a fluid thrill by examination and he had 1+ pedal edema. Echocardiography showed a dilated left ventricle measuring 6.5 cm with a reduced EF of 30% (Figure 21-3, Figure 21-4, Video 21-7, Figure 21-5, Figure 21-6, Video 21-8, Figure 21-7), a B bump and increased EPSS on M mode (Figure 21-8) with an E/e’ of 18. M mode through the base of the heart at the level of the aorta also demonstrated minimal movement of the aortic root (Figure 21-9). Spectral Doppler showed mild pulmonic and tricuspid regurgitation with elevated right ventricular (RV) systolic pressures (Figures 21-10 and 21-11). His atria were mildly dilated and his inferior vena cava (IVC) was dilated with minimal compressibility with sniff (Video 21-9). His hepatic veins showed diastolic predominance of hepatic flow. A left and right heart catheterization was performed. These showed luminal irregularities in his coronaries and right atrial (RA) pressure of 19 mm Hg, RV pressure of 50/19 mm Hg, pulmonary artery (PA) pressures of 50/23 mm Hg, and a wedge pressure of 21 mm Hg. His cardiac index (CI) was 2.0 L/min/m2. He was subsequently started on IV doses of a loop diuretic and an oral ACE inhibitor. He was net negative 8.0 L over the course of his admission and was discharged on furosemide, lisinopril, carvedilol and spironolactone, to follow up with his outpatient cardiologist for consideration of ICD placement if his EF failed to improve (Figure 21-12).
Symptoms
Shortness of breath
Leg swelling
Orthopnea
Paroxysmal nocturnal dyspnea
Early satiety
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