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nerve, the skin and abdominal vessels contract while coronary vessels dilate ? Severe hypoxia and hypercapnia → directly inhibit cardiovascular center → depressed cardiac function, dilated vessels → BP↓, arrhythmia ? Acute severe hypercapnia → ventricular fibrillation or cardiac arrest especially during intubation procedure ? PaCO2 enhance cardiac inhibition by vagus 28 Influence of hypercapnia Respiratory system ? Stimulate respiratory center → strengthen respiratory movement, Ventilation ? ? (PaCO2 ? kPa, Ventilation volume? 2 L/min) ? Slight contraction of small pulmonary arteries ? Directly relax the bronchial smooth muscle ? PAO2? ? PaCO2? → rightward shift of the oxyhaemoglobin dissociation curve (ODC) 29 pH? pH ? 30 Influence of hypercapnia urinary system ? Mild CO2 retention →dilation of renal blood vessels → renal blood flow? → urine ? ? PaCO2 8 kPa, pH ? ? →renal blood vessels spasm → renal blood flow ? ? HCO3 and Na+ reabsorption? → urine ? 31 Influence of hypoxemia amp。 hypercapnia Acidbase balance and electrolytes ? Severe hypoxia → inhibition of cellular energy metabolism → insufficient energy production, production of lactic acid ↑ → sodiumpotassium pump failure → metabolic acidosis, hyperkalemia → PCO2↑ ? Respiratory acidosis and metabolic acidosis ? pH is determined by HCO3/PaCO2 ratio ? Slow CO2 retention → pensated by kidney, decreased elimination of HCO3- (It takes 1 ~ 3 days for kidney to pensate) pH = HCO3 PaCO2 32 Clinical manifestation Acute respiratory failure (1) Dyspnea ? Dyspnea is a early symptom of respiratory failure. ? Increased breath rates ? Change in breath rhythm: CheyneStokes respiration, Biot’s respiration ? Accessory respiratory muscles involved in breathing → ―three depressions sign‖ 33 Cyanosis: ? Cyanosis is a typical sign of hypoxia, indicating arterial oxygen saturation lower than 90%. ? The extent of cyanosis is associated with content of reduced hemoglobin. So it is less readily detectable if anemia is present and more readily seen in polycythemia. ? Peripheral cyanosis is associated with stasis, in which oxyhemoglobin is reduced more than it normally is because of the prolonged peripheral blood transit time, while the PaO2 could be normal. ? Central cyanosis results from arterial hypoxemia. Clinical manifestation Acute respiratory failure (2) 34 Neuropsychic symptoms: ? Mental disorder, mania, a, convulsion Circulatory system: ? Tachycardia, myocardial impairment, peripheral circulatory failure, hypotension, arrhythmia, cardiac arrest. Digestive system : ? Hepatic function impairment: ALT↑ ? Gastrointestinal tract: mucosal erosion, stress ulcer, gastrointestinal bleeding Urinary system: ? Renal function impairment: BUN↑ ? Proteinuria, hematuria, casts in urine Clinical manifestation Acute respiratory failure (3) 35 Clinical manifestation Chronic respiratory failure Dyspnea: ? Excessive respiratory effort, prolonged expiration——rapid shallow breathing——slow shallow breathing, CheyneStokes breathing (CO2 narcosis, severe respiratory depression) Neuropsychic symptoms: ? Irritation caused by increased PaCO2 in early stage: insomnia at night, drowsiness during the day ? Depression caused by pulmonary encephalopathy in late stage: apathy, convulsion, a, tendon reflex weakened or disappear Circulatory system: ? Peripheral vesodilation, skin congestion, warm and sweaty extremities, BP↑, CO↑, pulsus magnus, HR↑, pulsatile headache 36 Diagnostic criteria ? History of respiratory dysfunction that severely affects the lung’s ability to maintain arterial oxygenation or carbon dioxide elimination ? Clinical manifestation of dyspnea and cyanosis ? Blood gas analysis ? PaO2 60 mmHg, or plus ? PaCO2 50 mmHg ? Breathing air on sea level and standard atmosphere pressure at rest ? Exclude intracardiac shunt and decreased cardiac output, such as ventricular septal defect ? In fact it is a pathophysiology amp。 laboratory Diagnosis 37 Diagnostic criteria The acute respiratory distress syndrome (ARDS) ARDS is a process of nonhydrostatic pulmonary edema and hypoxem