Acute Shortness of Breath


Emergency Medical

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A 40-year-old woman arrives at the emergency department with a markedly panicked appearance, screaming, "I can't breathe!" She is anxiously flailing her arms and appears tachypneic and pale. Six nurses are needed to obtain her vital signs and to place an intravenous (IV) line. The patient's heart rate is 120 beats per minute (bpm) with a blood pressure of 200/88 mm Hg, a respiratory rate of 50 breaths per minute, and oxygen saturation of 79% with the patient breathing room air. She is unable to cooperate with history taking and physical examination, and she repeatedly removes her oxygen mask and monitoring equipment. She is intubated on an emergency basis by using rapid-sequence induction.

After the patient is adequately sedated, physical examination is possible. The ventilator is set on assist-control mode at a rate of 16 bpm, tidal volume of 600 mL, positive end-expiratory pressure (PEEP) of 5 cm H2O, and a fraction of inspired oxygen (FiO2) of 100%. Her vital signs include a rectal temperature of 37.1C with a heart rate of 110 bpm, ventilator-assisted respiratory rate of 16 breaths per minute, blood pressure of 183/100 mm Hg, and O2 saturation of 100%. Her pupils are equal, round, and reactive to light. She has no jugular venous distension or tracheal shift. Her heart rate is a regular rhythm with no appreciable murmurs, rubs, or gallops. She has coarse breath sounds with bibasilar rales. Abdominal examination reveals linea nigra, and moderate distension is noted, but palpation yields softness without any masses. She has no lower-extremity edema or rashes.

The patient's husband arrives and provides additional history. They had a baby by means of normal spontaneous vaginal delivery 2 months ago with no complications. Three days ago, the patient began having shortness of breath, which was worst at night and when she was lying flat or exerting herself. She has been using an over-the-counter epinephrine inhaler (0.22 mg, Primatene Mist), with no improvement. She has no notable medical history of asthma, chronic obstructive pulmonary disease (COPD), or other respiratory problems. He denies any knowledge of drug or alcohol use.

An ECG shows sinus tachycardia with frequent premature ventricular contractions (PVCs). The patient has no ST-segment or T-wave changes and no S1Q3T3 pattern.

A portable postintubation chest radiograph is obtained (see Image 1). Bedside abdominal and cardiac ultrasonographies are performed in the emergency department. The sonogram of her abdomen shows no free fluid and a nongravid uterus. Images 2-4 are her cardiac sonograms.

What is the diagnosis and treatment?







Peripartum cardiomyopathy (PPCM): The radiographic findings of acute congestive heart failure coupled with the patient's history of recent pregnancy suggest PPCM as the cause of her respiratory distress. The echocardiographic images show a dilated left ventricle (LV) with global hypokinesis (Images 2-3, Video 1), no evidence of a significant or compromising pericardial effusion (Image 3, Video 1), and lack of respiratory-associated changes in the diameter of the IVC, suggesting fluid overload and associated congestive heart failure (Image 4, Video 2).

PPCM is a rare cause of heart failure with 4 diagnostic criteria: (1) echocardiographic evidence of heart failure (ie, ejection fraction <45%), (2) onset between the last month of pregnancy and 5 months after pregnancy, (3) no other identifiable causes of heart failure, and (4) no preexisting heart disease before the last month of pregnancy. The incidence is 1 case per 299 live births in Haiti, 1 case per 1,000 live births in South Africa, and 1 case per 2289-4000 live births in the United States (Sliwa, 2006). Reasons for these geographic variations are not well understood.

The etiology of PPCM is currently unknown (Sliwa, 2006). Several possible causes have been hypothesized, including increased inflammatory cytokines, viral infection, myocarditis, a maternal immunologic response to fetal cells in maternal blood, and pregnancy-related hemodynamic changes. Although no causal links have been identified to date, the following factors have been associated with an increased risk: age over 30 years; multiparity; African descent; multiple-gestation pregnancy; maternal cocaine abuse; and history of preeclampsia, eclampsia, or postpartum hypertension.

Patients with PPCM may present with classic signs and symptoms of heart failure. Their histories are commonly notable for dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and cough. Physical examination may reveal a displaced apical impulse, an S3 heart sound, and heart murmurs. Patients frequently present with severe heart failure, ie, New York Heart Association (NYHA) functional class III or IV, as did this patient.

Left ventricular (LV) stasis from severe heart failure and current or recent pregnancy place patients with PPCM at high risk for cardiac thrombosis and subsequent peripheral embolization (Sliwa, 2006). Therefore, patients with PPCM may present with lower-extremity arterial occlusion, cerebrovascular accident, mesenteric ischemia or infarct, and pulmonary embolism. Clinicians must have a high index of suspicion for underlying PPCM when they encounter patients with these embolic diseases.

The differential diagnosis for PPCM is extensive. Life-threatening differential diagnoses include exacerbations of asthma or COPD, pneumonia, pleural effusion, pneumothorax, pulmonary embolism, acute congestive heart failure, acute myocardial infarction, an incompetent cardiac valve, endocarditis, anaphylaxis, and subarachnoid hemorrhage (SAH) leading to flash pulmonary edema.

Minimal diagnostic evaluation should include ECG and echocardiography. The ECG may show sinus tachycardia or atrial fibrillation with nonspecific ST- and T-wave changes. Additionally, as in this case, the echocardiogram may show LV enlargement and a global reduction in contractility without signs of LV hypertrophy. Other studies, such as chest radiography, chest CT, cardiac catheterization, and myocardial biopsy should be performed on an individual basis as needed to rule out other conditions.

The treatment of PPCM is similar to that of other causes of heart failure. In the setting of acute pulmonary edema, urgent afterload and preload reduction is required (Tintinalli, 2004). IV nitroglycerin or nitroprusside infusions can be uptitrated until BP is controlled. Diuretics, such as IV furosemide, help lower BP and cardiac filling pressures. Morphine is a potent venodilator and helps reduce preload and alleviate respiratory distress. Immunosuppressive agents, such as azathioprine and steroids, as well as IV immunoglobulin (IVIG) have shown mixed results in small clinical trials and are not the standard of care at this time (Sliwa, 2006). If these therapies are not effective, intra-aortic balloon pump, LV assist devices, and a heart transplant may be necessary.

Maintenance therapy for PPCM is the same as for heart failure of another etiology and may include diuretics, digoxin, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors. If the patient is pregnant, ACE inhibitors should not be given because of the risk of oligohydramnios, fetal renal damage, or fetal death. Hydralazine with nitrates can be substituted for ACE inhibitors.

Anticoagulation should be considered because patients with PPCM are at high risk for thromboembolism given their hypercoagulable state of pregnancy and for LV stasis from severe LV dysfunction. The decision to provide anticoagulants should be made in conjunction with specialists and after other life-threatening etiologies that may deteriorate with anticoagulation (eg, SAH) are appropriately ruled out (verbal communication, Eric Savitsky, MD).

Many women with PPCM have spontaneous recovery of LV function. This occurrence is distinct from outcomes with other causes of dilated cardiomyopathy. A retrospective study of 123 women in the United States with PPCM showed that mean LV ejection fractions increased from 29% to 48% over 1 year (Elkayam, 2005). This same series showed an overall transplantation rate of 4% and a mortality rate of 9%.

Several studies have shown that patients with a history of PPCM are at risk for severe LV dysfunction if they become pregnant again. A recent study showed that, of 9 patients with a history of PPCM that became pregnant again, 5 (56%) died from severe heart failure (Mishra, 2006). Patients must be clearly advised of the risks of subsequent pregnancy.

The patient in this case was extubated on hospital day 3 and discharged home on day 7. As of this report, the patient is doing well with a maintenance regimen of isosorbide mononitrate, hydralazine, carvedilol (Coreg), benazepril, and spironolactone (Aldactone). She is awaiting a repeat echocardiogram to reassess her cardiac function.

Image Legends

Image 1. Chest radiograph shows appropriate placement of an endotracheal tube and a central line in the left internal jugular vein. Image also shows cardiomegaly, bilateral pulmonary congestion, and cephalization of vessels.

Image 2. Apical 4-chamber cardiac sonogram shows a dilated left ventricle (LV) with decreased wall motion and an estimated ejection fraction of 10-15%. The septum, inferior wall, and lateral wall are all hypokinetic, a finding that suggests a global cause rather than a local infarct. Likewise, the lack of right ventricular (RV) dilatation suggests something other than a massive pulmonary embolus. LA = left atrium; RA = right atrium.

Image 3. Long-axis parasternal view shows a dilated left ventricle (LV) with decreased wall motion, normal right ventricular (RV) size, and lack of clinically significant or compromising effusion. LA = left atrium; RA = right atrium. For the corresponding movie clip, see Video 1.

Image 4. Image shows the inferior vena cava (IVC) as it inserts into the heart. Key findings are lack of respiratory associated changes in the diameter of the IVC. These results indicate fluid overload and congestive heart failure. For the corresponding movie clip, see Video 2.


  • Elkayam U, Akhter MW, Singh H, et al. Pregnancy-associated cardiomyopathy: clinical characteristics and a comparison between early and late presentation. Circulation 2005;111:2050-5.
  • Mishra TK, Swain S, Routray SN. Peripartum cardiomyopathy. Int J Gynecol Obstet 2006 Nov;95(2):104-9.
  • Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet 2006;368:687-93.
  • Tintinalli J. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:367-8.


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