الفهرس 
Anatomy and Physiology of the Pulmonary Circulation
List of AbbreviationsOnly 14 pages are availabe for public view
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Abstract
Pressures in the pulmonary circulation are about one-fifth those present in the systemic circulation. The normal pressure in the pulmonary artery is about (22/8 mm Hg), with a mean pulmonary artery pressure of (13 mm Hg). Blood volume in the lungs is about 450ml. Cardiac output can increase nearly four times before pulmonary artery pressure becomes increased, due to opening of previously collapsed pulmonary capillaries. This is a protective mechanism against pulmonary edema and right ventricular failure. Pulmonary blood flow distribution is governed by the effect of gravity and other factors as cardiac output, alveolar hypoxia, lung volume, neural regulation, nitric oxide, prostaglandins and other vasoactive substances. Alveolar hypoxia may directly cause ion fluxes, which cause or contribute to the pulmonary vasoconstriction or indirectly cause vasoconstriction through release of vasoactive mediators (e.g. Leukotrienes, Prostaglandins, Catecholammes, Serotonin, Histamine, Bradykinin.). Pulmonary hypertension is defined as mean pulmonary artery pressure (>25mmHg) at rest or >30mm Hg with exercise. The estimated incidence of Primary Pulmonary Hypertension (PPH) is (1-2 cases per million). Secondary Pulmonary Hypertension (SPAH) is relatively common, but under diagnosed. In PPH the pulmonary vasculature is the exclusive target of the disease. Many studies point to abnormalities in pulmonary endothelial cell function, which maintains pulmonary vascular smooth muscle in a state of relaxation under normal condition. Reduced expression of Nitric oxide, Prostacyclin, and increased endothelin production by the pulmonary vascular endothelium increased pulmonary vascular tone. This form of endothelial dysfunction with intimal and medial proliferation and in-situ thrombosis are contributing to the pathogenesis of primary pulmonary hypertension.
On the other hand SPAH is the sequel of: 1) hypoxic vasoconstriction secondary to COPD, sleep-disordered breathing, interstitial lung disease alveolar hypoventilation disorders 2) obliteration of pulmonary vasculature 3) volume and pressure overload 4) pulmonary venous obstruction. The continuous pressure gradient between the aorta and the right ventricle (RV) (coronary perfusion pressure) is responsible for the coronary blood flow to the RV free wall throughout systole and diastole. Therefore, systemic hypotension or increased RV pressure results in a decreased RV coronary perfusion pressure. RV function is sensitive to increases in afterload. Acute increase in mean pulmonary artery pressure (PAP) above (40 mmHg) results in significant decrease in right ventricular ejection fraction. Two important principles emerged in the management of right heart failure: First, RV afterload must be reduced and second, systemic pressure must be maintained or increased. Some risk factors may exist prior to diagnosis of PPH e.g. ingestion of appetite suppressants. PPH is characterized by non specific signs and symptoms (e.g. dyspnea, fatigue, dizziness, syncope, palpitation, cough, hoarseness and chest pair). SPAH the clinical manifestation may be masked by the underlying etiology.
Right heart catheterization is a valuable test for the diagnosis, quantification and characterization of Pulmonary Arterial Hypertension (PAH) also left heart dysfunction and intracardiac shunts can be excluded, and the cardiac output can be measured. The Doppler echocardiography is the most reliable non-invasive method to estimate PAH.
Anticoagulant therapy and vasodilator therapy are the mainstays of treatment in patients with PPH. Calcium channel blockers appear to have the widest usage. Patients with PPH who are challenged with very high doses of calcium channel blockers may manifest dramatic reduction in Pulmonary artery pressure, the patient’s quality of life is restored with improved functional class. Prostacyclin infusion therapy in patients with PPH also improved their symptoms, exercise tolerance, hemodynamicssurvival. The treatment of SPAH is primarily directed at the underlying disease, general supportive therapy consisting of: oxygen therapy, medications (anticoagulants, calcium channel blockers, peripheral vasodilators, cardiac glycosides, diuretics and endothelin-receptor antagonists) can be applied. Corrective surgery on the mitral valve, thrombo end- arterectomy, lung volume reduction surgery and lung transplantation are performed to eliminate the primary pathological process.
RV decompensation as a sequel of pulmonary hypertension requires optimization of RV preload. Reduction of RV afterload, enhancement of right coronary perfusion pressure, and improvement of RV contractility. We should emphasize the value of preoperative pulmonary vasodilator testing oxygen, intravenous nitroglycerine, inhaled nitric oxide, and prostacyclin analogues, may be of value in the short-term assessment of pulmonary vasodilator reserve, and can be continued throughout the surgical procedure and in the early postoperative period to avoid rebound pulmonary hypertension (hypertensive crisis). Perioperative optimization of acid-base status, oxygenation, ventilation, temperature, and the level of anesthesia are important to avoid precipitants of increased pulmonary arterypressure. Deaths of patients with pulmonary hypertension undergoing surgery often occur during the first several postoperative days. To minimize the risk, it is recommended to treat these patients’ first postoperative 48hrs as an extended operative period. Patients who experience stormy Intraoperative course, with difficulty to control PAP and to maintain hemodynamic stability, should be transferred to postoperative Intensive Care Unit sedated and mechanically ventilated with careful handling during weaning.