A 54-year-old woman presented to the telemetry floor with shortness of breath (SOB) for 4 months that progressed to an extent that she was unable to perform daily activities. She also used 3 pillows to sleep and often woke up from sleep due to difficulty catching her breath. Her medical history included hypertension, dyslipidemia, diabetes mellitus, and history of triple bypass surgery 4 years ago. Her current home medications included aspirin, atorvastatin, amlodipine, and metformin. No significant social or family history was noted. Her vital signs were stable. Physical examination showed bilateral diffuse crackles in lungs, elevated jugular venous pressure, and 2+ pitting lower extremity edema. ECG showed normal sinus rhythm with left ventricular hypertrophy. Chest x-ray showed vascular congestion. Laboratory results showed a pro-B-type natriuretic peptide (pro-BNP) level of 874 pg/mL and troponin level of 0.22 ng/mL. Thyroid panel was normal. An echocardiogram demonstrated systolic dysfunction, mild mitral regurgitation, a dilated left atrium, and an ejection fraction (EF) of 33%. How would you manage this case?

Case Review

In this case, a patient with known history of coronary artery disease presented with worsening of shortness of breath with lower extremity edema and jugular venous distension along with crackles in the lung. The sign and symptoms along with labs and imaging findings point to diagnosis of heart failure with reduced EF (HFrEF). She should be treated with diuretics and guideline-directed medical therapy for congestive heart failure (CHF). Telemetry monitoring for arrythmia should be performed, especially with structural heart disease. Electrolyte and urine output monitoring should be continued.

Case Discussion

In the initial evaluation of patients who present with signs and symptoms of heart failure, pro-BNP level measurement may be used as both a diagnostic and prognostic tool. Based on left ventricular EF (LVEF), heart failure is classified into heart failure with preserved EF (HFpEF) if LVEF is >50%, HFrEF if LVEF is <40%, and heart failure with mid-range EF (HFmEF) if LVEF is 40% to 50%. All patients with symptomatic heart failure should be started on an angiotensin-converting enzyme (ACE) inhibitor (or angiotensin receptor blocker if ACE inhibitor is not tolerated) and β-blocker, as appropriate. In addition, in patients with New York Heart Association functional classes II through IV, an aldosterone antagonist should be prescribed. In African American patients, hydralazine and nitrates should be added. Recent recommendations also recommend starting an angiotensin receptor-neprilysin inhibitor (ARNI) in patients who are symptomatic on ACE inhibitors.

Alternatively, ARNI could be started instead of ACE inhibitors or ARBs. Loop diuretics may be added to relieve symptoms of congestion. They help in improving quality of life by decreasing fluid retention and thus relieving symptoms but have shown no mortality benefit. Medications should be started at low doses and gradually titrated up to recommended target doses. Digoxin can also be considered in patients who are symptomatic despite being on ACE inhibitors/ARBs, β-blockers, and mineralocorticoid receptor antagonists (MRAs) to reduce the risk of hospitalization. Ischemia evaluation can be considered in patients with angina symptoms.

In patients who can tolerate neither ACE inhibitors nor ARBs (or for patients in whom they are contraindicated), the combination of hydralazine and isosorbide dinitrate may be considered.

Early follow-up within a week is recommended for all patients with heart failure after hospital discharge. Educating patients about dietary habits, adherence to medications, and lifestyle modification is an important component of managing heart failure.

A 56-year-old man presented to emergency department with complaints of shortness of breath that have progressively worsened over the past 2 months. At baseline, on a flat surface, he could walk 6 blocks, but at presentation, this decreased to 2 blocks. He stated that he has gained 10 pounds and has increased swelling of his feet. His medical history included asthma, hypertension, dyslipidemia, and obesity. He is a smoker and works as an office manager. He had seen his primary care physician who suggested that his asthma might be causing his symptoms, and he was asked to take albuterol as needed, which did not improve his symptoms. He appeared to be in mild distress with stable vital signs and had jugular venous distension. He also had bibasilar crackles in the lungs, an S₃ heart sound, and bilateral pedal edema. His ECG showed Q waves, nonspecific ST changes, and left ventricular hypertrophy. His troponin levels were elevated but not trending up. Pro-B-type natriuretic peptide was 680 pg/dL. He was started on intravenous furosemide and noninvasive positive-pressure ventilation. Th next day, his echocardiography showed a left ventricular ejection fraction (LVEF) of 32% and regional wall motion abnormalities. How would you manage this case?

Case Review

This patient had suspected ischemic cardiomyopathy. He underwent coronary angiography and was found to have a mid-left anterior descending artery lesion for which percutaneous coronary intervention (PCI) was performed. The patient was started on dual antiplatelet therapy along with a statin. In addition, he was discharged on an angiotensin-converting enzyme inhibitor (ACEI), mineralocorticoid receptor antagonist (MRA), and β-blocker and advised to follow up in the cardiology clinic within a week. He was also provided with an external wearable defibrillator.

Case Discussion

The etiology of heart failure with reduced ejection fraction includes coronary artery disease (CAD), valvular heart disease, arrhythmias, and high-output heart failure. Myocardial ischemia is associated with cardiac remodeling, leading to progressive changes in shape and size of the heart. Patients with ischemia as an underlying etiology of heart failure can present with angina or its equivalents, along with ischemic ECG changes. Echocardiography can help to determine the etiology, such as valvular disorders or wall motion abnormities. Patients with angina symptoms or hemodynamic instability in association with acute EKG changes suggestive of ACS should undergo urgent coronary angiogram. Cardiac catheterization is also indicated if high-risk factors for CAD such as dyslipidemia, cocaine abuse, and obesity are present with positive stress testing. PCI should be performed if any evidence of coronary occlusion is present. In such cases, dual antiplatelet therapy should be continued along with guideline-directed medical therapy (GDMT) for heart failure. Ischemic cardiomyopathy is associated with higher risk of fatal ventricular arrhythmias, and in order to prevent sudden cardiac death, an external wearable defibrillator is advised until improvement in ejection fraction is seen. An implantable cardioverter-defibrillator should be considered after PCI if ejection fraction does not improve after 3 months of optimized GDMT. GDMT consists of ACEIs/angiotensin receptor blockers, β-blockers, MRAs, and angiotensin receptor-neprilysin inhibitors, with patient education and lifestyle modifications to control the risk factors.

A 62-year-old woman presented to the emergency department (ED) with sudden onset of palpitations that started while gardening. She had been having similar episodes for the past 4 to 5 months that lasted for few minutes and resolved on their own. Recently, she started having shortness of breath on exertion, which had been progressively worsening. She had become unable to lay flat, and her exercise tolerance had decreased from 5 blocks to 1 block. She stated that she drinks 5 cups of caffeinated beverages daily. She denied having any chest pain, dizziness, or syncope. Her medical comorbidities included hypertension and anxiety disorder. She denied taking any over-the-counter supplements or drugs. She had no family history of heart disease and had never smoked or used any recreational drugs. In the ED, her vital signs showed a blood pressure of 140/84 mm Hg and a pulse of 180 bpm. On physical examination, she was in mild respiratory distress with jugular venous distension. On lung examination, she had coarse bibasilar crackles bilaterally. No pedal edema was noted. Chest radiography showed pulmonary vascular congestion and right basal infiltrates. Pro-B-type natriuretic peptide and troponin levels were elevated but not trending up. Her ECG showed supraventricular tachycardia, no P waves, and narrow QRS complexes. To determine the underlying rhythm, a vagal maneuver was attempted that slowed down the rate, and the rhythm was determined as atrial flutter. She was admitted to the telemetry floor, where rate was controlled by metoprolol. Echocardiography showed a left ventricular ejection fraction of 30% with no wall motion or valvular abnormalities. She underwent catheter ablation of the ectopic focus and was converted to sinus rhythm. She was discharged and was seen in clinic in 2 weeks later, where repeat echocardiography showed an ejection fraction of 62% with cardiac dilatation.

Case Review

The patient presented with palpitations and acute onset of dyspnea and was found to have tachycardia; in addition, the ECG showed atrial flutter with rapid ventricular rate. Her cardiomyopathy is most likely tachycardia induced. With rate control or cardioversion, cardiomyopathy can be reversed, thus treating the underlying cause.

Case Discussion

Tachycardia-induced cardiomyopathy is a reversible form of cardiomyopathy that can manifest from months to years after tachycardia onset. It is usually observed in supraventricular tachycardia and can be precipitated by a high burden of premature ventricular contractions, such as bigeminy. It is highly dependent on the ventricular rate, but no cutoff rates have been established. The hallmark feature is restoration of rate and rhythm, leading to normalization of left ventricular function and ejection fraction. The main principle in management of tachycardia-induced cardiomyopathy causing heart failure with reduced ejection fraction is heart rate normalization, either with rate or rhythm control. The decision to pursue an ischemic workup should be based on clinical suspicion and risk factors, but in general, it is not necessary.

Treatment of the underlying etiology is the cornerstone of therapy. There may be no underlying structural heart disease primarily responsible for the cardiac dysfunction. Thyroid function should be tested, and urine drug screen should be performed. Caffeine intake and other caffeinated beverages should be restricted. Long-term treatment may include diuretics such as furosemide, angiotensin-converting enzyme inhibitors, β-blockers, and, in some cases, ablation. Usually ejection fraction improves as early as 1 week after treatment, and complete resolution occurs in 4 to 6 weeks.

A 70-year-old man presented to the emergency department (ED) with complaints of dyspnea for 4 weeks, which had been progressively worsening, limiting his exercise tolerance from 4 blocks to half a block. He did not complain of chest pain or palpitations. His medical history included hypertension, paroxysmal atrial fibrillation, coronary artery disease status post percutaneous coronary intervention (PCI) to mid-left anterior descending artery (LAD) 2 years ago, and heart failure with reduced ejection fraction (HFrEF) (left ventricular ejection fraction, 40%). His medications included furosemide 40 mg once a day, metoprolol succinate, aspirin, dabigatran, and atorvastatin. He admitted to smoking crack cocaine and drinking alcohol every day. In the ED, vital signs were stable, with a blood pressure of 110/70 mm Hg, pulse of 70 bpm, and respiratory rate of 20 breath/min. On physical examination, the patient was in respiratory distress using accessory muscles of respiration. He had bibasilar crackles on examination, no murmurs, loud S₃, abdominal distension, and positive hepatojugular reflex. He also had pedal edema extending to mid-thigh. His ECG showed left ventricular hypertrophy with left axis deviation. Chest radiography showed bilateral congestion. Pro-B-type natriuretic peptide and troponin levels were elevated but not trending up. His creatinine was elevated from baseline. He was initiated on intravenous furosemide and bilevel positive airway pressure therapy. How would you manage the case on the telemetry floor?

Case Review

This patient with known HFrEF who has been on diuretic therapy appears to be experiencing an exacerbation of heart failure. He is wet and warm in terms of volume status and perfusion and hence can be treated with diuretics. His urine output should be strictly quantified along with daily weight and monitoring of electrolytes. Diuretics should be titrated based on volume status and improvement in clinical status. Creatinine usually improves with improvement in renal congestion. Education regarding avoiding cocaine and remaining adherent to the medication regimen should be provided.

Case Discussion

The goal of acute heart failure exacerbation management is not only to excrete salt, but also to maintain a net negative water balance. First and foremost, the patient’s adherence to diet and medications needs to be assessed. Elderly patients often take over-the-counter nonsteroidal anti-inflammatory drugs and should be educated to avoid such medications. The cornerstone of treatment of acute heart failure syndrome (AHFS) is diuretics, and the most commonly used agents are loop diuretics due to their greater efficacy. Furosemide, bumetanide, and torsemide are loop diuretics used for diuresis in routine practice. AHFS management can also be guided by the following algorithm using volume and perfusion status.