The heart and lungs are intimately linked by the pulmonary vasculature; thus, it is not surprising that the pulmonary vasculature is most commonly affected by left-heart disease. Any process that raises left ventricular (LV) end-diastolic pressure or left atrial pressure will result in elevated pulmonary venous pressure (PVP). Such processes include diseases that reduce LV contractility, such as ischemic heart disease, mitral regurgitation, or cardiomyopathy, as well as processes that decrease LV compliance, such as ischemic heart disease, aortic stenosis, and hypertension. Mitral stenosis results in elevated left atrial pressures. In all of these circumstances, PVP is increased and leads to elevations of pulmonary capillary and pulmonary arterial pressures.
What are the mechanical effects of the heart on the lungs?
The heart and lungs both occupy an enclosed space within the thoracic cavity. Any process that results in changes in the size or position of the heart may alter pulmonary function. Cardiomegaly may produce pulmonary symptoms such as cough, dyspnea, and wheezing by compressing mediastinal structures such as the trachea or bronchi. A dilated main pulmonary artery or enlarged left atrium may cause gas trapping and hyperinflation by occluding bronchi. Massive cardiomegaly or pericardial effusion may cause left lower lobe atelectasis.
Describe the pulmonary vascular consequences of elevations in PVP.
Pulmonary capillary pressures are elevated in the setting of increased PVP. Normal Starling forces in the alveolar interstitium yield a net filtration force of 4 mmHg outward from the pulmonary capillaries to the interstitium. However, net fluid accumulation does not occur due to the absorbtive capacity of the pulmonary lymphatics, which may increase fluid transport 5- to 10-fold in response to increased fluid formation. Eventually, the lymphatics reach their limit, and net fluid formation in the form of interstitial edema occurs, usually at capillary pressures 20 mmHg. Alveolar flooding, or pulmonary edema, may be seen with elevations in pressure 25 mmHg. While these pressure limits apply to acute pulmonary edema, situations in which PVP is chronically elevated, such as mitral stenosis, may require much higher pressures before alveolar edema occurs.
What are the two primary diagnoses to consider when Kerly B lines are seen on chest x-ray?
Left-heart disease (congestive heart failure or mitral stenosis) and lymphangitic carcinomatosis. Radiographically, pulmonary congestion, with redistribution of flow to the upper zones of the lung, is typically seen with pulmonary capillary pressures of 18-20 mmHg. As pressure increases further, interstitial edema occurs with the appearance of perihilar haze, peribronchial cuffing, and Kerly B lines. So-called periacinar rosettes, or radiolucent grapelike clusters surrounded by radiodense fluid, may appear as fluid encroaches upon the alveolar space. At 25-30 mmHg pressure, frank pulmonary edema occurs, with fluffy alveolar infiltrates typically in a perihilar distribution. Fairly accurate assessments of true pulmonary capillary pressures, as measured by Swan-Ganz catheter readings, can be made if one looks closely at the chest radiograph.
Describe the pulmonary function abnormalities associated with elevations in PVP due to cardiac disease.
Patients with elevated PVP, such as seen in chronic congestive heat failure, may show a combined restrictive and obstructive ventilatory defect on pulmonary function testing. Restriction occurs as a result of loss of lung volume due to increased blood and fluid within the interstitial and alveolar spaces; compliance is reduced.
Airflow limitation is evident as a fall in forced expiratory volume in the first second (FEV,) and forced vital capacity (FVC). Since both FEV: and FVC fall, the ratio of FEV/FVC may be normal. A very low ratio usually implies the concurrence of additional airways disease, such as chronic obstructive pulmonary disease (COPD). Increased airway resistance due to elevations of PVP occurs predominantly in the lung periphery.
Diffusing capacity for carbon monoxide (DLCO) may be increased early on due to increased pulmonary blood volume, but with worsening interstitial edema and ultimate injury to the pulmonary vessels, DLCO normalizes and is then reduced.
How can diseases of the left heart affect the lungs? Photo Gallery
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