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The pulmonary embolism rule-out criteria (PERC) helps assess people in whom pulmonary embolism is suspected, but unlikely. Unlike the Wells score and Geneva score , which are clinical prediction rules intended to risk stratify people with suspected PE, the PERC rule is designed to rule out the risk of PE in people when the physician has already ...
Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term disease caused by a blockage in the blood vessels that deliver blood from the heart to the lungs (the pulmonary arterial tree). These blockages cause increased resistance to flow in the pulmonary arterial tree which in turn leads to rise in pressure in these arteries ...
Pulmonary hypertension is defined as a mean PAP of at least 20 mm Hg (3300 Pa) at rest, and PAH is defined as precapillary pulmonary hypertension (i.e. mean PAP ≥ 20 mm Hg with pulmonary arterial occlusion pressure [PAOP] ≤ 15 mm Hg and pulmonary vascular resistance [PVR] > 3 Wood Units). [58]
Lung infarction or pulmonary infarction occurs when an artery to the lung becomes blocked and part of the lung dies. [1] It is most often caused by a pulmonary embolism . Because of the dual blood supply to the lungs from both the bronchial circulation and the pulmonary circulation , this tissue is more resistant to infarction .
Pulmonary embolism similarly presents with shortness of breath and hypoxia. Chest pain worse with inspiration is frequently seen. Chest pain can also be similar to a heart attack. This is due to the right ventricular stress and ischemia that can occur in PE. [13] Other symptoms are syncope and hemoptysis. [14] DVT is a common cause.
An abrupt stop of pulmonary gas exchange lasting for more than five minutes may permanently damage vital organs, especially the brain. Lack of oxygen to the brain causes loss of consciousness. Brain injury is likely if respiratory arrest goes untreated for more than three minutes, and death is almost certain if more than five minutes.
The pathophysiology of pulmonary heart disease (cor pulmonale) has always indicated that an increase in right ventricular afterload causes RV failure (pulmonary vasoconstriction, anatomic disruption/pulmonary vascular bed and increased blood viscosity are usually involved [1]), however most of the time, the right ventricle adjusts to an overload in chronic pressure.
As the left ventricle becomes unable to compensate for an acute rise in systemic vascular resistance, left ventricular failure and pulmonary edema or myocardial ischemia may occur. [ 6 ] In the kidneys, chronic hypertension has a great impact on the kidney vasculature, leading to pathologic changes in the small arteries of the kidney .