Respiratory Failure

Respiratory Failure

PiO2 150mmHg Externel respiration Ventilation PAO2 100 PACO2 40 Gas exchange PvO2 40mmHg PvCO2 46mmHg PaO2 100mmHg PaCO2 40mmHg

Concept External respiratory dysfunction → PaO2＜60mmHg（at sea level） Hypoxemic Type I ----- No hypercapnia Hypercapnic Type II -- PaCO2＞50mmHg Differential diagnosis

Etiology and Pathogenesis 1. Ventilatory disorder -----hypoventilation 1) Paralysis of respiratory muscle 2) Low compliance of chest wall 3) Low compliance of lung 4) Hydrothorax or pneumothorax • Restrictive —— restricted inspiration

• Obstructive----airway obstruction due to: congestion, edema of mucous membrane bronchial spasm airway space obstruction Dyspnea ----inspiratory or expiratory Forced expirationclosure of airway

Expiration Inspiration Expiration Inspiration Dyspnea due to intrathoracic and extrathoracic airway obstruction

0 0 +5 +10 +10 +20 +20 +20 +30 +20 +20 +20 +35 +25 +20 +20 +20 +20 Normal emphysema Equal pressure point shifted up  airway closure during forced expiration PA = Ppl + PER

PaO2 100% 13.3 PaCO2 PaO2 （kPa） SaO2 SaO2 7.6 Arterial blood pH 75% 10.7 pH 7.4 50% 8.00 7.2 PaCO2 25% 5.33 N Alveolar ventilation (L/min)

PACO2×VA （PiO2-PAO2）×VA R= Blood gas alterations Alveolar hypoventilation ↑ d PaCO2 ↓ d PaO2 = R • • PACO2 PAO2 = PiO2 R PaCO2 the best index of alveolar ventilation 0.863×VCO2 VA PACO2 = •

二. Diffusion disorder 1, Surface area of diffusion membrane↓ 2, Thickness of diffusion membrane ↑ + Increased blood flow Blood gas variations : PaO2 ↓ PaCO2 N or ↓

2. Diffusion disorder • ↓ Surface area of diffusion membrane • ↑ Thickness of diffusion membrane + increased blood flow Blood gas variations : ↓ PaO2 N or ↓ PaCO2

PCO2( kPa ) PO2 13.33 PaO2 PvCO2 10.67 6.13 8.00 PvO2 5.33 PaCO2 2.67 0.75 s 0 0.50 0.25 Variation of blood gas in alveolar capillary -----------by patient with diffusion disorder

3. Ventilation-perfusion imbalance 4L VA Normal 0.8 = = Q 5L ＜﹣ 10cmH2O 50% -10 0 -20 -30 ＞ - 2.5cm H2O

Normal ventilation and blood flow distribution in lung

•Local hypoventilation functional shunt diseased normal total lung VA/Q ＜0.8 ＞0.8 =0.8 >0.8 <0.8 PaCO2 ↑↑ ↓↓ N ↓ ↑ CaCO2 ↑↑ ↓↓ N ↓ ↑ PaO2 ↓↓ ↑↑ ? CaO2 ↓↓ ↑ ↓

• Local hypoperfusion  dead space like ventilation diseased normal total lung VA/Q PaCO2 CaCO2 PaO2 CaO2 ?

2、Local hypoperfusion → dead space like ventilation diseased normal total lung VA/Q ＞0.8 ＜0.8 =0.8 PaCO2 ↓↓ ↑↑ N PaO2 ↑↑ ↓↓ ↓ CaO2 ↑ ↓↓ ↓ CaCO2 ↓↓ ↑↑ N

4. Anatomic shunt Bronchial vein Pulmonary vein Pulmonary artery

Acute respiratory distress syndrome（ARDS） Acute lung injury inflammation bronchospasm vasoconstrction thrombosis pulm.edema atelectasis dead space like ventilation diffusion disorder functional shunt hypoxemia

Metabolic and functional alterations PaO2 ＜ 60mmHg compensation ＜ 30mmHg disturbances PaCO2＞ 50mmHg compensation ＞ 80mmHg disturbances See chapter “Hypoxia” and “Respiratory acidosis”

Principles of Treatment • Treating causes • Increasing PaO2 • Decreasing PaCO2 • Correcting metabolic and functional disturbances The difference of oxygen therapy between type I and type II respiratory failure ?

48岁，男，因气促、神志模糊送来急诊 活动时呼吸困难已数年，夜间有时感觉憋气，近来活动减少，医生说他有心扩大和高血压，用过利尿剂和强心药。数次急诊为“支气管炎和肺气肿”吸入平喘药，一天吸烟一包已20年，一向稍胖，近6个月长40磅。检查: 肥胖、神志恍惚、反应迟钝、不回答问题，无发热，脉搏110，血压 170/110mmHg，呼吸18，打磕睡时偶闻鼾声，肺散在哮鸣音、心音弱，颈静脉怒张，外周水肿。动脉血PaO2 50、PaCO2 65、pH 7.33，Hct 49% ,WBC计数分类正常, X光肺野清晰，心脏大，肌酐2.6mg/dl（1-2），BUN 65mg/dl（9-20）。

吸氧，用平喘药，作气管插管后送ICU。因发作性呼吸暂停伴血氧降低, 行机械通气。超声心动图见右心肥大与扩大，室间隔运动减弱。肺动脉收缩压70mmHg。在ICU头二天尿增多，BUN及肌酐下降。第三天清醒能正常回答问题。第4天拔去插管，用多导睡眠图测得入睡数分钟出现阻塞性和中枢性呼吸暂停，约每小时30次，最长停38s（15s），SaO2常降至58%。持续正压通气可解除阻塞，中枢性呼吸暂停和低氧血症仍存在。再增加吸氧则消除低氧血症。转入普通病房及回家后，每晚仍用持续正压通气和氧疗, 神经症状改善，继续尿多、体重下降。三个月后超声心动图右心已缩小，室间隔运动正常，肺动脉压45/20mmHg。

问题：1、病人患什么病？有哪些合并症？诊 断依据？ 2、有无呼衰？发生机制？ 3、病人肺动脉高压发生机制? 4、有关心衰？发生机制？ 5、神志恍惚、反应迟钝机制？ 6、肌酐、BUN变化机制? 7、病人酸碱紊乱类型? 8、病人有高血压和水肿，为何不用利尿剂？ 9、疗效显著，为什么？

Respiratory Failure