(Chest. 2003;124:1160-1163.)
© 2003
American College of Chest Physicians
Cardiovascular Collapse in a 77-Year-Old-Woman With an Asthma Exacerbation Following Bronchodilator Treatment*
Markus F. Meyer, MD;
William E. Hopkins, MD and
David A. Kaminsky, MD
* From the Department of Medicine (Dr. Meyer), and Divisions of Cardiology (Dr. Hopkins) and Pulmonary Disease and Critical Care Medicine (Dr. Kaminsky), Fletcher Allen Health Care, University of Vermont College of Medicine, Burlington, VT.
Correspondence to: David A. Kaminsky, MD, Associate Professor of Medicine, Pulmonary Disease and Critical Care Medicine, University of Vermont College of Medicine, Given C-317, Burlington, VT 05405; e-mail: dkaminsk{at}zoo.uvm.edu
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Introduction
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A 77-year-old woman presented to the walk-in clinic with a 1-week history of increasing dyspnea and wheezing. She had a history of frequent episodes of shortness of breath triggered by various irritants such as dust and fumes, and asthma was diagnosed 12 years earlier. Recent pulmonary function studies showed a reduced FEV1 and FVC but a preserved ratio. Lung volumes showed a normal total lung capacity but elevated residual volume/total lung capacity ratio consistent with airtrapping; specific airway conductance was normal and a methacholine challenge test had not been done.
In the clinic, she was treated with nebulized albuterol and ipratropium and was sent home with the advice to continue her albuterol inhaler as needed. The next day, she presented again with worsening symptoms despite the frequent use of albuterol. The patient was found to have severe wheezing bilaterally. Shortly after another treatment with nebulized albuterol and ipratropium was started, worsening dyspnea and hypotension developed. She received IV methylprednisolone and was transferred via ambulance to the hospital. She had a history of mild hypertension for which she was started on hydrochlorothiazide 2 months ago.
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Physical Examination
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On arrival in the emergency department, the patient was unresponsive and hypothermic at 34°C. BP was 59/24 mm Hg, with an irregular heart rate of 110 beats/min. Her respiratory rate was 20 breaths/min, and oxygen saturation by pulse oximeter was 87% on oxygen delivered by a nonrebreather facemask. Cardiopulmonary auscultation confirmed severe bilateral expiratory wheezes and a new 4/6 systolic ejection murmur best heard at the left sternal border. The patient’s extremities were cool with diminished peripheral pulses.
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Laboratory Findings
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CBC count, renal function, and liver function were all normal. Her electrolytes were notable for the following: sodium, 133 mEq/L; potassium, 2.6 mEq/L; chloride, 101 mEq/L; and bicarbonate, 22 mEq/L. An arterial blood gas analysis obtained on 100% oxygen via a nonrebreather mask revealed pH 7.38, PCO2 of 38 mm Hg, PO2 of 52 mm Hg, and HCO3 of 24 mEq/L. Cardiac enzymes were normal. D-dimer was 3.7 µg/mL (normal < 0.5 µg/mL), and lactic acid was 1.4 mEq/L.
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Hospital Course
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The patient was treated with oxygen, normal saline solution, and dopamine. Because of the hypotension and new systolic murmur, bedside echocardiography was performed in the emergency department (Fig 1
), revealing hyperdynamic ventricles with obliteration of the left ventricular cavity during systole and associated systolic anterior motion of the mitral valve. A left ventricular outflow tract gradient of at least 75 mm Hg was recorded. There was mild concentric left ventricular hypertrophy and slight asymmetric hypertrophy of the basal septum. Following the echocardiographic results, dopamine was immediately discontinued and a total of 3 L of normal saline solution was administered. Within 1 h, the murmur and wheezing had resolved, and the patient regained a normal BP and mental status. Oral verapamil was started. A ventilation-perfusion scan was read as low probability for pulmonary embolism. The patient was started on inhaled corticosteroids, had no further episodes of shortness of breath, and was discharged home.
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Figure 1.. Top: Parasternal short-axis images in end-diastole and end-systole. The left ventricle is hyperdynamic with cavity obliteration. Bottom: Continuous-wave Doppler echocardiographic envelopes in the left ventricular outflow tract (LVOT). The velocity is markedly increased, and the "dagger" shape of the flow pattern is pathognomonic for dynamic outflow tract obstruction.
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What is the most likely diagnosis?
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Diagnosis: Cardiovascular collapse triggered by volume depletion and ß-agonist-induced left ventricular outflow tract obstruction
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The most common cause of left ventricular outflow tract obstruction is hypertrophic obstructive cardiomyopathy (HOCM) associated with systolic anterior motion of the mitral valve. During conditions of increased contractility or reduced left ventricular volume, the anterior mitral valve leaflet can move into the left ventricular outflow tract during systole and obstruct blood flow. Echocardiography is the diagnostic test of choice, because it directly reveals the severely constricted ventricular cavity and the systolic anterior movement of the mitral valve. In addition, Doppler echocardiography allows for measurement of the gradient across the left ventricular outflow tract. Echocardiographic evaluation of patients with a significant left ventricular pressure gradient with and without overt HOCM has shown that small chamber size and hypertrophy increase the probability of obstruction. Multiple factors determine left ventricular chamber size, but hypovolemia as induced by diuretic agents, or a reduction in preload and afterload by nitrates, are clinically relevant triggers.
ß-Adrenergic agonists, because of their chronotropic and inotropic effects, can also induce left ventricular outflow tract obstruction. This has been observed in patients during stress echocardiography with dobutamine in which up to one of five patients acquired a significant left intraventricular pressure gradient > 25 mm Hg. The majority of patients who acquire a significant gradient with dobutamine also acquire variable degrees of arterial hypotension.
To our knowledge, only one study has described the effects of inhaled albuterol, a ß2-selective ß-agonist, in a patient with HOCM. A 22-year-old man with HOCM showed no effect on the left ventricular outflow tract gradient following two inhalations of albuterol; however, our patient received numerous inhalations of albuterol. We hypothesize that the repeated doses of albuterol allowed ß1-receptor effects to become manifest and lead to worsened left ventricular outflow tract obstruction. Our patient may have been further predisposed to obstruction because she had also recently been started on diuretics, which may have reduced left ventricular volume.
The symptoms in patients with HOCM are variable and only partly related to the direct effects of outflow tract obstruction. During rest, a pressure gradient is present in approximately 25% of patients with HOCM, and there is a good correlation between symptoms and the degree of outflow tract obstruction. Ninety percent of patients complain of intermittent dyspnea on exertion, which is the most prominent symptom in HOCM. Chest pain, which occurs in approximately 30% of patients with HOCM, is the result of local cardiac ischemia secondary to elevation in left ventricular pressure. Wheezing and other asthma-associated symptoms have been reported in some patients but are not common. In the 19th century, this entity of asthma-like symptoms in patients with underlying cardiac disease was termed cardiac asthma. Cardiac asthma appears to be due to airflow limitation and bronchial hyperreactivity induced by pulmonary vascular congestion as a result of elevated left ventricular filling pressures. In addition, recent work has suggested that pulmonary ß-receptor down-regulation occurs in chronic heart failure and may contribute to increased airway constriction.
The treatment of choice for patients with left ventricular outflow obstruction is pharmacologic. Treatment is primarily aimed at slowing the heart rate to increase ventricular filling time, which will increase end-diastolic volume. Since increased end-diastolic volume will increase contractility via the Frank-Starling mechanism, it is also desirable to reduce cardiac contractility. Both beta-blockers and calcium antagonists with a predominant cardiac effect, such as verapamil, fulfill these requirements. The additional negative dromotropic effect of both drugs also helps to prevent ventricular obstruction by slowing ventricular conduction, which leads to a more favorable sequence of myocardial excitation. However, in patients with airway hyperresponsiveness, ß-blockers should be used cautiously and verapamil may be a better choice. Diuretics are contraindicated, and a sufficient intravascular volume status should be maintained. Concurrent hypertension needs to be treated, since additional hypertrophy may further worsen the outflow tract obstruction and diastolic dysfunction. This can usually be achieved by maximizing the doses of ß-blockers or verapamil and adding angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists, as necessary.
We believe that our patient had bronchial asthma because of her long history of frequent episodes of shortness of breath in association with typical respiratory irritants; however, it is likely that her more recent symptoms were due, in part, to transient episodes of cardiac asthma from left ventricular outflow tract obstruction induced by heavy use of inhaled ß-agonists in the setting of intravascular volume depletion. In addition to not receiving diuretics and receiving verapamil, the patient is now maintained on inhaled steroids and has been instructed to use limited inhalations of albuterol or nebulized levalbuterol for acute episodes of shortness of breath.
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Clinical Pearls
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- Left ventricular outflow tract obstruction should be suspected in a patient with a new systolic murmur with paroxysmal worsening of wheezing and dyspnea following ß-agonist therapy.
- In patients with known HOCM, inhaled ß-agonists, especially in high doses, may cause or worsen "asthma."
- In patients with HOCM, diuretics are contraindicated and intravascular volume depletion should always be avoided, as it will worsen left ventricular outflow obstruction.
- A calcium-channel blocker, with a predominant cardiac effect, such as verapamil, is the drug of choice in HOCM, as it will slow heart rate and increase end-diastolic volume, while reducing cardiac contractility.
Received for publication January 16, 2003.
Accepted for publication February 28, 2003.
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Suggested Reading
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- Borst, MM, Beuthien, W, Schwencke, C, et al (1999) Desensitization of the pulmonary adenylyl cyclase system: a cause of airway hyperresponsiveness in congestive heart failure? J Am Coll Cardiol 34,848-856[Abstract/Free Full Text]
- Cabanes, LR, Weber, SN, Matran, R, et al Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function. N Engl J Med 1989;320,1317-1322[Abstract]
- Fishman, AP Cardiac asthma: a fresh look at an old wheeze. N Engl J Med 1989;320,1346-1348[ISI][Medline]
- Smith, SC, Spector, SL Cardio-selective ß-adrenergic therapy in a patient with asthma and hypertrophic obstructive cardiomyopathy. Chest 1981;80,103-105[Free Full Text]
- Sorrentino, MJ, Marcus, RH, Lang, RM Left ventricular outflow tract obstruction as a cause for hypotension and symptoms during dobutamine stress echocardiography. Clin Cardiol 1996;19,225-230[ISI][Medline]
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Introduction
Physical Examination
