Congestive heart failure/pulmonary edema case file

Congestive Heart Failure/Pulmonary Edema Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 38

A 63-year-old woman arrives in the emergency department (ED) in respiratory distress. The paramedics who transported her were not able to obtain any information about her past medical history but did bring her bag of medications, which includes furosemide.

On examination, her temperature is 37.5°C (99.5°F), blood pressure 220/112 mm Hg, heart rate 130 beats per minute, respiratory rate 36 breaths per minute, and oxygen saturation 93% on high-flow oxygen. The patient’s skin is cool, clammy, and diaphoretic. She is alert but can only answer yes-or-no questions because of dyspnea. She has jugular venous distension to the angle of the jaw, rales in both lung fields, and +2 pretibial edema bilaterally. Her heart sounds are regular although tachycardic with an S3/S4 gallop.

⯈ What is the most likely diagnosis?

⯈ What is the most appropriate next step?

ANSWER TO CASE: 38

Congestive Heart Failure/Pulmonary Edema

Summary: This is a 63-year-old woman in respiratory distress with signs of pump failure and fluid overload.

• Most likely diagnosis: Congestive heart failure (CHF) and pulmonary edema
• Most appropriate next step: Management of the ABCs, preload and afterload reduction, and diuresis

ANALYSIS

Objectives

1. Recognize the clinical presentation and complications of CHF.
2. Understand the diagnostic and therapeutic approach to suspected CHF.

Considerations

This 63-year-old woman is brought into the ED with signs of severe CHF: dyspnea, tachypnea, hypoxia, hypertension, and tachycardia. Her medications include furosemide, strongly suggesting a history congestive heart failure. This clinical presentation is classic for a CHF exacerbation. Rapid assessment of the ABCs, IV access, and prompt initiation of preload and afterload reduction and diuresis are the mainstays of therapy. Supplemental oxygen should be administered. Noninvasive positive pressure ventilation (NIPPV) or endotracheal intubation may be necessary for severe cases as well as those refractory to treatment. Once the patient is stabilized, it is important to try to identify any precipitants of the exacerbation. Diagnostic tests should be directed at excluding myocardial infarction, a common cause of worsening CHF.

Approach To:

Congestive Heart Failure/Pulmonary Edema

CLINICAL APPROACH

Emergency physicians must be comfortable identifying and treating patients with heart failure (HF) as this condition is the most common reason for hospitalization of patients older than 65 and is increasing in prevalence. In addition, HF is associated with a significant morbidity and mortality. Patients with HF have a 50% mortality rate at 4 years after the onset of symptoms.

The right side of the heart receives blood from the peripheral circulation and sends it to the lungs for oxygenation. The left side subsequently receives oxygenated blood from the lungs and pumps it back into the circulation. Disruption of these functions leads to loss of normal contractile ability and HF. After HF occurs,

the heart cannot provide enough blood to meet the body’s metabolic needs or must maintain elevated ventricular filling pressures to do so. The term “congestive” refers to abnormal fluid retention resulting from this loss of contractility. There are many causes of HF, the most common of which are coronary artery disease and hypertension.

Failure of the right side of the heart results in increased systemic venous pressures while left-sided failure causes increased pulmonary venous pressures. Each has different symptoms and physical findings (Table 38–1), although the two conditions often occur concomitantly.

This condition can also be divided into HF due to systolic dysfunction (impaired contractility) versus failure resulting from diastolic dysfunction (impaired ventricular relaxation and filling). Although patients with HF commonly have both types of dysfunction, distinguishing between the two can be important because patients with diastolic dysfunction are preload dependent. As a result, they may be sensitive to reductions in diastolic filling volumes (due to aggressive diuresis or venodilation) and become hypotensive.

Clinical Evaluation

During the evaluation, the clinician must be able to distinguish patients with CHF from those with other conditions with similar clinical presentations such as pneumonia, pneumothorax, pulmonary embolus, and exacerbation of chronic obstructive pulmonary disease (COPD) (Table 38–2). In addition, the clinician must try to determine what caused the patient’s condition to decompensate. The most common precipitants are cardiac causes (eg, myocardial ischemia or infarction) and noncompliance with medications or dietary restrictions. Other causes include uncontrolled hypertension, valvular dysfunction, arrhythmia, infection, volume overload, pulmonary embolism, thyrotoxicosis, and iatrogenic etiologies.

The sequence of the clinical evaluation depends on the patient’s clinical status. Those with significant respiratory distress require aggressive interventions while a focused history, physical examination, and diagnostic testing are performed simultaneously. If the patient is stable, a more detailed history can be obtained. Important historical points include the onset, duration, and character of respiratory complaints; any associated symptoms (such as chest pain or fever); past medical history (including prior heart disease and cardiac workup); and current medications (including recent changes in doses and any missed doses).

On examination, patients with CHF may show signs of hypoperfusion: clammy skin, delayed capillary refill, and thready pulses. If the patient is hypotensive, intraarterial blood pressure monitoring is important because noninvasive measurements are often inaccurate in vasoconstricted individuals. Patients may have crackles, rales, or wheezes on auscultation. An S3 or S4 is common but may be difficult to hear in a busy ED. The cardiac examination may also reveal the murmur of a ventricular septal defect or acute mitral regurgitation or the irregularly irregular rhythm of atrial fibrillation—all of which can precipitate acute pulmonary edema. The ED physician should also note any jugular venous distention or peripheral edema.

Although x-ray findings may lag behind clinical symptoms by up to 6 hours, chest radiography still provides valuable information for the clinician. In early CHF, the chest x-ray shows upper zone vascular redistribution (cephalization). As the pulmonary congestion increases, interstitial edema and Kerley B lines become prominent, followed by opacification of the air spaces with alveolar edema. Other findings may include cardiomegaly and pleural effusions. The x-ray may also help exclude other causes of dyspnea and respiratory distress (eg, pneumothorax or pneumonia).

Laboratory studies should include complete blood count, electrolytes, blood urea nitrogen/creatinine, and urinalysis. If there is a suspicion of acute coronary syndrome, cardiac enzymes should be sent. The B-type natriuretic peptide (BNP) is a hormone released from the ventricles in response to stretch. It is most useful in patients with a mixed clinical picture (eg, a patient with CHF and COPD). Levels less than 100 pg/mL make HF unlikely and those greater than 500 pg/mL make it highly likely. Levels between these two extremes are indeterminate. The BNP level also has prognostic significance and can be used to monitor response to therapy. In obese patients, BNP levels tend to be lower than expected based on the observed symptoms. Furthermore, BNP levels may lag behind the patient’s clinical picture. Electrocardiograms (ECGs) are helpful in detecting evidence of cardiac ischemia or infarction and arrhythmias. Liver enzymes may be of use in patients with hepatomegaly, and lactate levels in those with suspected cardiogenic shock.

Treatment

Treatment of cardiogenic pulmonary edema consists of oxygenation, vasodilation, diuresis, and augmentation of cardiac contractility if needed. High-flow oxygen should be the first intervention. Noninvasive positive-pressure ventilation via continuous or biphasic positive airway pressure may be necessary if hypoxia continues. Ultimately, the patient may require intubation if refractory to the aforementioned interventions. Vasodilation is obtained by reducing preload. This is most effectively and rapidly achieved with nitroglycerin, which can be given via sublingual, topical, or intravenous routes. In the critically ill patient, intravenous nitroglycerin is best. Diuresis with furosemide or bumetanide effectively reduces intravascular volume and preload, thus reducing pulmonary congestion. In addition, angiotensin-converting enzyme (ACE) inhibitors may play a role in preload reduction and in the treatment of CHF. Morphine is no longer recommended as standard therapy for CHF due to an association with increased rates of intubation and ICU admission. If patients do not improve with this therapy, an inotrope, such as dobutamine, may be given to increase myocardial contractility. If the patient is hypotensive, dopamine is a useful vasopressor.

COMPREHENSION QUESTIONS

38.1 A 62-year-old woman is sent to the ED from her primary physician’s office with worsening heart failure. The patient has had congestive heart failure, previously controlled with oral digoxin and furosemide. Which of the following is the most likely reason for the exacerbation of her CHF?

A. Valvular dysfunction

B. Arrhythmia

C. Myocardial ischemia and infarction

D. Thyrotoxicosis

38.2 A 55-year-old man has symptoms of worsening orthopnea, tachypnea, and rales on pulmonary examination. The liver is percussed at 6 cm at the midclavicular line. His jugular vein is at +2 cm at 45 degrees. Which of the following is the best description of this patient’s disease process?

A. Right-sided heart failure

B. Left-sided heart failure

C. Biventricular heart failure

D. Acute respiratory distress syndrome

38.3 A 58-year-old man is brought into the ED by paramedics because of worsening dyspnea. He has congestive heart failure due to cardiovascular disease. On examination, his blood pressure is 150/100 mm Hg and heart rate 104 beats per minute. He has jugular venous distension and rales in both lung fields. Which of the following is the most effective and most rapid method of reducing preload in this patient?

A. Diuretics

B. Nitroglycerin

C. Dobutamine

D. Morphine

38.4 A 54-year-old man complains of acute onset of worsening fatigue and dyspnea. He has alcohol-induced cardiomyopathy and congestive heart failure. Which of the following is the best workup for his CHF exacerbation?

A. Chest x-ray, cardiac enzymes, ECG

B. Computed tomography (CT) scan of the chest, ECG, D-dimer test

C. Echocardiogram, ECG, thallium stress test

D. Arterial blood gas, cardiac enzymes, pulmonary angiography

ANSWERS

38.1 C. Myocardial ischemia and infarction is one of the most common precipitants of a CHF exacerbation (as well as noncompliance with medications).

38.2 B. Left-sided heart failure can present with dyspnea, orthopnea, paroxysmal nocturnal dyspnea, tachypnea, crackles or wheezes, and an S3 or S4 gallop. The lack of jugular venous distension and/or hepatomegaly suggests absence of right-sided heart failure.

38.3 B. Nitroglycerin is the most effective and most rapid means of reducing preload in the patient with CHF.

38.4 A. The workup of a CHF exacerbation includes chest x-ray, ECG, electrolytes, BUN/creatinine, and cardiac enzymes. A BNP level may also be sent.

CLINICAL PEARLS

⯈ The most common causes of CHF include coronary artery disease and hypertension while the most common causes of an acute exacerbation are myocardial ischemia or infarct and noncompliance.

⯈ BNP is a hormone released by the ventricles in response to stretch. It can be useful as a marker for heart failure.

⯈ Treatment of CHF includes oxygenation, correction of the underlying cause, and relief of symptoms by vasodilation, diuresis, and possibly inotropic support.

References

Collins SP, Ronan-Bentle S, Storrow AB. Diagnostic and prognostic usefulness of natriuretic peptides in emergency department patients with dyspnea. Ann Emerg Med. 2003;41:532-544. 

Humphries RL. Chapter 32: Cardiac emergencies. Stone CK, Humphries RL. Current Diagnosis and Treatment: Emergency Medicine. 6th ed. Available at: http://www.accessmedicine.com/content. aspx?aID=3106633. 

Kosowsky JM, Kobayashi L. Acutely decompensated heart failure: diagnostic and therapeutic strategies for the new millennium. Emerg Med Pract. 2002;4(2):1-28. 

Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161-167. 

Niemann JT. Congestive heart failure and cor pulmonale. Harwood Nuss’ Clinical Practice of Emergency Medicine, 4th ed. 2005. 

O’Brien JF, Falk JL. Heart failure. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby Elsevier; 2009: Chapter 79. 

Peacock WF. Congestive heart failure and acute pulmonary edema. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011: Chapter 57.

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