Acute Pulmonary Edema

Acute pulmonary edema is a life-threatening condition that can occur suddenly and at any time during a cardiac catheterization procedure. It is also commonly referred to as “flash” pulmonary edema. The cath lab team must recognize the symptoms, diagnose the cause, and treat the condition in a rapid fashion to stabilize the patient. In this article, we will explain the causes and treatments of flash pulmonary edema for patients under going cardiac catheterization.

Flash pulmonary edema is the development of respiratory distress related to the rapid accumulation of fluid within the lung interstitium (the tissue and space around the air sacs of the lungs) secondary to elevated cardiac filling pressures.  Flash pulmonary edema results when certain medical conditions occur which in turn produce sudden lung congestion. Flash pulmonary edema may also occur as a consequence of disruption in the normal pressure-volume relationship during the cardiac cycle.

Normally, the alveolar bed within the lungs serves to protect from fluid accumulation. Alveoli have very low permeability for fluid and protein. Any fluid accumulated in the alveoli is continuously absorbed back into the interstitium by the alveolar epithelial cells and drained from the pulmonary interstitium by lymphatic vessels. When flash pulmonary edema occurs, there is a compromise in the permeability of the alveolar bed. The alveolis become more permeable, allowing fluid to enter the alveoli space.

Causes

Causes of flash pulmonary edema include:

• Heart failure by either systolic or diastolic dysfunction

Systolic dysfunction occurs when there is less forward movement of blood, prompting an increase in diastolic volume and diastolic pressure that precipitates pulmonary vascular congestion and leads to pulmonary edema. Diastolic dysfunction occurs when the myocardium is less compliant. This left ventricle relaxation abnormality results in increased end diastolic pressure that causes an increase in venous pressure and results in pulmonary vascular congestion.

• Coronary ischemia

Coronary ischemia can cause systolic and diastolic dysfunction, or acute mitral valve regurgitation.

• Acute myocardial infarctions with elevated end diastolic pressures and low ejection fractions
• Hypertension

Hypertension may cause an exacerbation of diastolic dysfunction.

• Rapid heart rhythms
• Acute aortic regurgitation
• Acute mitral valve regurgitation
• Pickering’s syndrome (bilateral renal stenosis)
• End stage renal disease

Bilateral renal artery stenosis and advanced renal disease may lead to fluid retention and elevated blood pressure, predisposing the patient to flash pulmonary edema.

Symptoms

Symptoms in a patient who is developing flash pulmonary edema may include frothy sputum, cough, dyspnea, tachypnea, diaphoresis, altered mental status, falling oxygen saturations, and a sense of impending doom or drowning. 

Treatment

The goal of treatment in cardiogenic flash pulmonary edema includes efforts to maximize heart function by decreasing cardiac work and intravascular volume. The following treatments will decrease the intrapulmonary pressures, allowing the lymphatic system to clear fluid from the alveolar space.

Drug treatment for flash pulmonary edema includes furosemide, nitroglycerin, nitroprusside, morphine, and oxygen. Furosemide acts both as a vasodilator and diuretic. Nitroglycerin is a vasodilator that reduces preload and, at higher doses, can cause decreased afterload, improving cardiac output. Nitroprusside is a balanced venous and arterial dilator that decreases preload and afterload, and therefore, blood pressure. Morphine reduces pulmonary edema and blood pressure through venous dilation. Morphine should be used with extreme caution because it can lead to respiratory depression. A non-rebreather O2 face mask at 15 liters can improve oxygen saturation. Assistance with airway management may be needed if the patient does not respond to aggressive medical management.

Summary

Flash pulmonary edema is a medical emergency in the cardiac catheterization lab that can quickly lead to respiratory failure, cardiac arrest, and death. The cath lab team must be able to recognize and treat flash pulmonary edema rapidly, as the patient’s life may depend on it.

Acknowledgments. Special thanks to Dr. David Burkey and Lisa Dittrich, RCIS, for their help in fine-tuning this article.

Donna Gagne can be contacted at donnagagne@me.com.

References

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3. Messerli FH, Bangalore S, Makani H, ET al. Flash pulmonary oedema and bilateral renal artery stenosis:  the Pickering syndrome.  Eur Heart J 2011; 32: 2231.
4. Pierard LA, Lancellotti P.  The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema. N Engl J Med 2004; 351: 1627.