【正文】 ormality (彌散障礙 ) ? The factors that influence rate of gas diffusion across the respiratory membrane include: ? the partial pressure difference of the gas between the two sides of the membrane, ? the surface area of membrane ? the time of contact between blood and alveoli ? the permeability of the membrane ? Diffusion abnormality manifested as hypoxemia 100 80 60 40 動脈氧分壓 血液通過肺泡毛細(xì)血管時(shí)間 17 Mechanisms of hypoxemia ? Ventilation/perfusion mismatch（ 通氣 /灌流失衡 ） ? Shunt（肺動 靜脈分流） V/Q= V/Q V/Q Q V (AV shunt) Normal V Q (dead space effect) 18 (二 )通氣 /血流比例 V/Q 肺泡死腔通氣 V/Q 靜 動脈分流 V/Q 正常通氣 /血流 V/Q VD PaCO2－ PeCO2 VT PaCO2 Qs CcO2 － CaO2 QT CcO2 － CvO2 VA (, ) Q (, ) 見于肺不張， ARDS 見于 COPD 正常 Mechanisms of hypoxemia 19 Mechanisms of hypoxemia ? Oxygen consumption, (VO2 ) ↑: fever, chill, dyspnea, twitch (eg, 500ml/min) ? Oxygen delivery (DO2）↓, Palev O2 ↓ 800 100 20 10 肺泡氧分壓 2 4 6 8 10 肺泡通氣量 (l/min) 400 動脈氧分壓(kPa) 20 Mechanisms of hypercapnia ? CO2 production↑: ? fever, infection, sepsis, epilepsy ? Alveolar ventilation ↓ ? neuromuscular diseases or fatigue of respiratory muscles ? obstructive ventilation disorder 21 Influence of hypoxemia Central nervous system ? Oxygen consumption of brain3 ml/100g O2 Delivery capacity ? ? blood viscosity ?， blood stream resistance? → cardiac load amp。 Digestive system ? Renal blood vessels contraction, blood supply ↓when acpany with hypotension, DIC → Renal failure ? Gastric mucosal erosion, necrosis, ulcer and bleeding Hepatic cell impairment by hypoxia → ALT↑， jaundice 26 Influence of hypercapnia Central nervous system ? Cerebral blood flow: PaCO2?， blood flow? 4% → headache, intracranial pressure? ? Cerebrospinal fluid: H+、 HCO CO2enter bloodbrain barrier →[H+] ? →stimulate subcortex 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: