Ventilation Mechanisms and Pulmonary Hypertension PDF

‫‪Ventilation‬‬ ‫دکتر مريم بنی عقیل‬ ‫فلوی فوق تخصص ریه‬  21% 760 mmhg 74 mmhg 0.8 Mechanisms of hypoxemia  Hypoventilation  V/Q mismatch  Right to left shunt Anatomic Physiologic  Diffusion limitation  Reduced impaired o...

‫‪Ventilation‬‬ ‫دکتر مريم بنی عقیل‬ ‫فلوی فوق تخصص ریه‬  21% 760 mmhg 74 mmhg 0.8 Mechanisms of hypoxemia  Hypoventilation  V/Q mismatch  Right to left shunt Anatomic Physiologic  Diffusion limitation  Reduced impaired oxygen tension  Mechanisms of hypoxemia  Hypoventilation Mechanisms of hypoxemia  Hypoventilation SHUNT & v/q miss-match Shunt P O2 does not rise with administration of 100% oxygen perfusion  Pulmonary circulation is a low pressure  system  Syst. pr======25 mmHg  Diast. pr======8 mmHg  Mean pr.======15 mmHg  When cardiac o utput increases, as occurs during exercise the pulmonary responding to the increase in flow with a decrease in pulmonary vascular resistance. In consequence, the increase in mean pulmonary arterial pressure (PAP), even with a three- to fourfold increase in cardiac output , is small pvr PVR = 80(PAP – PCW)/CO PVR = pulmonary vascular resistance (dyn · s/cm5); PAP = mean pulmonary arterial pressure (mmHg); PCW = pulmonary capillary wedge pressure (mmHg); CO = cardiac output (L/min). The normal value for pulmonary vascular resistance is ~50–150 dyn · s/cm5.  Mechanisms of increased PVR  PVR may increase by a variety of mechanisms :  Pulmonary arterial and arteriolar vasoconstriction is a prominent response to alveolar hypoxia.  PVR also increases if intraluminal thrombi or proliferation of smooth muscle in vessel walls diminishes the luminal cross-sectional area.  If small pulmonary vessels are destroyed, either by scarring or by loss of alveolar walls (as in chronic obstructive lung disease), the total cross-sectional area of the pulmonary vascular bed diminishes, and  pulmonary hypertension 39 All diseases of the respiratory system causing hypoxemia are potentially capable of increasing PVR, since alveolar hypoxia is a very potent stimulus for pulmonary vasoconstriction. The more prolonged and intense the hypoxic stimulus, the more likely it is that a significant increase in PVR producing pulmonary hypertension will result. In practice, patients with hypoxemia caused by chronic obstructive lung disease, interstitial lung disease, chest wall disease, and the obesity hypoventilation–sleep apnea syndrome are particularly prone to developing pulmonary hypertension. Dr Yahyapour ‫باتشکر از توجه‬ ‫شما‬