Cardiogenic pulmonary edema.
The other clinical form of pulmonary edema is non-cardiogenic pulmonary edema, which results from conditions that have no cardiac origin, including smoke inhalation, near drowning, oxygen toxicity, acute pancreatitis, and sepsis. The term permeability pulmonary edema describes this type of pulmonary edema. In permeability pulmonary edema, pathophysiological disruption of the alveolar-capillary membrane is the basis for the exudation of fluid into the pulmonary interstitium and ultimately into the lungs.
In addition to pulmonary edema having these two pathophysiological forms, the edema fluid itself differs between these two types of pulmonary edema. The fluid that accumulates in the lungs during cardiogenic pulmonary edema has low protein (lactic dehydrogenase) content and is called a transudate. The fluid associated with the non-cardiogenic form of pulmonary edema contains greater protein content and is termed an exudate.
Mechanisms of Cardiogenic Pulmonary Edema
As long as the cardiac output of the left ventricle keeps pace with the volume and rate of blood flowing to the left atrium, essentially the right ventricular cardiac output, blood will not accumulate in the pulmonary vasculature and vascular pressures remain normal. However, when the right heart output exceeds the output of the left ventricle, the pulmonary circulation becomes congested with blood and the blood pressure (hydrostatic pressure) in the pulmonary vasculature increases. Ordinarily the vascular pressures within the pulmonary vessels are low, e.g., mean pulmonary artery pressure is 12 mm Hg and pulmonary capillary wedge pressure is 8 mm Hg.
A number of factors can cause the elevation of the pulmonary vascular pressures. They include myocardial infarction, cardiac dysrhythmias, mitral stenosis, and systemic hypertension. These conditions will produce cardiogenic pulmonary edema whenever they cause the pulmonary capillary wedge pressure to exceed the value of the colloid osmotic pressure in the pulmonary capillaries, which normally is around 25 mm Hg.
When cardiogenic pulmonary edema develops, the extravasation of fluid from the pulmonary vasculature into the lungs generally occurs because of a disturbance of the pressures associated with Starling's law of the capillaries. The pressures involved in the Starling equation are (1) hydrostatic pressure in the pulmonary capillary, (2) colloid osmotic pressure in the pulmonary capillary, (3) hydrostatic pressure in the pulmonary interstitium, and (4) colloid osmotic pressure in the pulmonary interstitium. These pressures are normal, fluid is filtered through the "arterial ends" of the pulmonary capillaries and is reabsorbed along the "venous ends" of the pulmonary capillaries. A slightly larger volume of fluid is filtered compared to the volume reabsorbed. However, the pulmonary lymphatics normally siphon off excess fluid at a rate of 10 to 20 ml per hour, preventing fluid from accumulating and edema from forming.
Interestingly, patients who experience chronic left ventricular failure have enlarged lymphatic vessels and lymph fluid flows as high as 200 ml per hour. These compensatory developments prevent pulmonary edema from developing despite increased pulmonary capillary hydrostatic pressure and increased fluid filtration into the pulmonary interstitium. Amazingly, such patients have been known to generate pulmonary capillary wedge pressures as high as 40 mm Hg without having pulmonary edema.
Left Ventricular Systolic Dysfunction
Systolic dysfunction represents decreased myocardial contractility with subsequent decreased cardiac output. The decreased cardiac output stimulates sympathetic activity and blood volume expansion via the activation of the reninangiotensin-aldosterone axis. These responses decrease left ventricular filling and increase pulmonary capillary hydrostatic pressure, and ultimately produce pulmonary edema. Once the reninangiotensin-aldoslerone system activates and pulmonary edema begins to occur, a vicious cycle perpetuates throughout the cardiopulmonary system. Circulating angiotensin II causes systemic vasoconstriction and vascular resistance to increase, producing increased myocardial wall tension, myocardial ischemia, worsened left ventricular dysfunction, and further decreased cardiac-output. The increased myocardial wall tension (increased after-load) causes left ventricular diastolic dysfunction, which further elevates pulmonary artery and pulmonary capillary pressures. Consequently, these higher pulmonary vascular pressures cause more fluid to leave the pulmonary vasculature; thus, perpetuating the cycle. Common causes of systolic dysfunction include coronary artery disease, myocardial infarction, and dilated cardiomyopathy.
Left Ventricular Diastolic Dysfunction
Diastolic dysfunction is characterized by a stiffer (less compliant) ventricular wall. What results from diastolic dysfunction is inadequate filling of the vbentricle, which leads to decreased stroke volume and lower cardiac output. The low ventricular compliance elevates left ventricular end-diastolic pressures, promoting increased pulmonary vascular pressures and pulmonary edema. In the presence of diastolic dysfunction, left ventricular contractility may be preserved; however, cardiac output still falls because of inadequate left ventricular filling. Causes of diastolic dysfunction include restrictive cardiomyopathy and aortic stenosis.
Clinical Manifestations of Pulmonary Edema
Patients will often complain of sudden onset of difficulty breathing, shortness of breath, and anxiety. Patients will also experience varying degrees of orthopnea. In other words, when lying down, these patients will literally feel as though they are drowning because of the accumulation of fluid in their lungs. The symptoms of mild pulmonary edema may be relieved to various degrees by sleeping in a semi-recunbant position. Paroxysmal nocturnal dyspnea, the complaint of frequently awakening with shortness of breath and coughing during the night, is common. Coughing is a sign of worsening pulmonary congestion. When pulmonary edema becomes severe, patients will expel pink, frothy sputum from their lungs. Chest pain may be present, indicating a possible myocardial infarction.
Tachycardia and tachypnea are both present, as is diaphoresis. Auscultation of the thorax reveals inspiratory crackles caused by air flowing through fluid-filled airways and alveoli. Wheezes may be heard in some instances resulting from air flowing at high velocities through narrowed airways. Because of impaired gas exchange, patients may demonstrate cyanosis or complain of lightheadedness resulting from hyperventilation.
Obtaining hemodynamic data from a pulmonary artery catheter helps differentiate cardiogenic pulmonary edema from non-cardiogenic pulmonary edema. The pathophysiology of these two clinical conditions is different despite both manifesting fluid in the pulmonary interstitium and in the lungs. Cardiogenic pulmonary edema is secondary to higher than normal vascular pressures throughout pulmonary circulation; non-cardiogenic pulmonary edema results from disruption of the pulmonary capillary endothelium (i.e., leaky capillary). In terms of hemodynamic measurements, differentiation between these two types of pulmonary edema is based on the measurement of the pulmonary capillary wedge pressure (PCWP). The PCWP is generally greater than 18 mm Hg in cardiogenic pulmonary edema, and lower than 18 mm Hg in non-cardiogenic pulmonary edema. However, a superimposed chronic pulmonary disease (e.g., severe COPD) with pulmonary hypertension can cloud this differentiation.
Treatment of Cardiogenic Pulmonary Edema
Supplemental oxygen at high concentrations via partial rebreathing mask or non-rebreathing mask is often administered. These patients may be treated with non-invasive positive pressure ventilation (NPPV), e.g., mask CPAP, to avoid endotracheal intubation and mechanical ventilation. The decision to abort NPPV for endotracheal intubation and mechanical ventilation will be dictated by worsening acidosis, hypercapnia, and hypoxemia.
At the same time, these patients often receive (1) a positive inotrope to improve myocardial contractility, (2) an anti-hypertensive drug to reduce left ventricular afterload, and (3) a diuretic to reduce venous return and to reduce preload. The purpose of these three pharmacological approaches is to increase the cardiac output. Patients who are hypotensive and have valve disorders will likely not tolerate medications intended to reduce afterload and preload. In these patients, providing positive inotropes to enhance myocardial contractility is paramount.
Overall, the mortality rate associated with cardiogenic pulmonary edema seems to range between 15% and 20%. When cardiogenic pulmonary edema results from a myocardial infarction, the mortality rate becomes as high as 40%. Furthermore, the mortality rate approaches 80% if the patient is also hypotensive.
William Wojciechowski, MS, RRT, is chair and associate professor in the department of cardiorespiratory care at the Univ of S. Alabama, Mobile.
by Bill Wojciechowski, MS, RRT
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|Title Annotation:||RESPIRATORY CLINICAL KEEPER|
|Publication:||FOCUS: Journal for Respiratory Care & Sleep Medicine|
|Date:||Sep 1, 2010|
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