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Respiratory Failure. 男性 , 50 岁 , 患喘息性支气管炎 30 年 , 三年来常下肢浮肿 . 三天前因受凉发烧 , 咳嗽加重 , 咳黄痰 . 当日上午患者神志恍惚 , 嗜睡 . 查 : T 38℃, 颈静脉充盈 , 肝大 , 双下肢凹陷性水肿 . 血气分析 : pH7.29, PaCO 2 10.7kPa(80mmHg), PaO 2 7.33kPa(55mmHg). BE -5mmol/L 血清钾 5.5mmol/L. RESPIRATION 4 distinct mechanisms: Ventilation
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男性, 50岁, 患喘息性支气管炎30年, 三年来常下肢浮肿. 三天前因受凉发烧, 咳嗽加重, 咳黄痰. 当日上午患者神志恍惚, 嗜睡. 查: T 38℃, 颈静脉充盈, 肝大, 双下肢凹陷性水肿. 血气分析: pH7.29, PaCO2 10.7kPa(80mmHg), PaO2 7.33kPa(55mmHg). BE -5mmol/L血清钾 5.5mmol/L.
RESPIRATION 4 distinct mechanisms: Ventilation Gas exchangeExternal respiration Transportof oxygen and carbon dioxide in the blood Internal respiration
The Process of External Respiration PiO2 159mmHg Pulmonary ventilation PAO2 102mmHg PACO2 40mmHg Pulmonary gas exchange PaO240mmHg PaCO2 46mmHg PvO2 100mmHg PvCO2 40mmHg
Definition of RF Disorders of external respiratory function PaO2 <60 mmHg (8.0kpa) while breathing air at rest, with or withoutPaCO2 >50 mmHg(6.67kpa). judgment standard: PaO2 <60 mmHg , PaCO2 >50 mmHg hypotonic hypoxia with (or without) respiratory acidosis
respiratory insufficiency: It is a condition in which respiratory function is inadequate to meet body’s needs during exertion. However, respiratory failure does so in rest. a kind of respiratory insufficiency a severe respiratory insufficiency
Classification 1. According to blood gas: 1) typeⅠ(hypoxemic RF) : PaO2 <60 mmHg (8.0kpa) 2) type Ⅱ (hypercapnic RF) : PaO2 <60 mmHg (8.0kpa) , with PaCO2 >50 mmHg(6.67kpa)
2. According to primary site central peripheral 3. According to duration acute chronic
Conducting Airways Lungs Gas Exchange Chest Wall (muscle, ribs) Diaphragm (muscle) Pe Pi
Pathogenesis of RF: Disorders of external respiratory functionpulmonary ventilation disturbance pulmonary gas exchange disturbance
Causes of RF Disorders of: Central Nervous System Spinal Cord Neuromuscular System the chest wall and pleura the airway
Ⅰ.pulmonary ventilation disturbance i.Types and Causes restrictive hypoventilation obstructive hypoventilation
Rib Cage Contract IntercostalsContractto Lift Spine Rib Diaphragm Volume Volume Ribs Mechanisms of Breathing: • Diaphragm • External Intercostal Muscles
component elements causing ventilation disturbance Airway straitness or block thorax wall damaged Inhibition of R. center High spinal cord damaged weakness of R. M Anterior angle cell damaged phrenic nerve damaged Lung elastic resistance increased
Restrictive hypoventilation: Causes and mechanisms: • impaired activity of respiratory muscle (dysfunction of CNS, neural, muscleetc.) • decreased compliance of thorax (chest malformation , pleura fibrosis) • decreased compliance of lungs (pulmonary edema , inflammation , fibrosis, insufficient surfactant) • thorax fluidify or pneumothorax
2. Obstructive hypoventilation : central airway obstruction peripheral airway obstruction
1) central airway obstruction: above the forfication (between the glottis and the carina) obstruction locates out of thorax( paralysis, edemaor inflammation of vocal cords ) inspiratory dyspnea obstruction locates within thorax expiratory dyspnea why?
Phase of inspiration (Ptr <Patm) Phase of expiration (Ptr<Ppl) Phase of inspiration (Ptr>Ppl) Phase of expiration (Ptr > Patm) Patm Patm Ptr Ptr Ptr Ptr Ppl Ppl The effects on the phase of respiration on an extrathoracic variable obstruction The effects on the phase of respiration on an intrathoracic variable obstruction Ptr—intratrachel pressure Ppl—pleural pressure Patm—atmospheric pressure
2) peripheral airway obstruction(diameter<2mm): • peripheral airway character: • Wall: thin,without cartilage support; • Diameter changes with respiration; • keep tight connection to surrounding alveoli
causes and mechanism: chronic obstructive pulmonary disease (chronic bronchitis,emphysema), severe pneumonia, atelectasis ,etc. → equal pressure point is moved up expiratory dyspnea
point that Intra-airway pressure = extra-airway pressure Equal pressure point normal person makes forced expiration Emphysema patients makes forced expiration
Mechanism of chronic obstructive pulmonary disease (COPD) 1. inflammation stimulation, airway wall became thickening 2. Airway smooth muscle contraction 3. Retentionof inflammatorysecretion in airway →inelastic resistance ↑ → a great amount of gas keep in alveoli 4. Alveolar wall was damaged → elastic pull to peripheral airway ↓,collapse occur in forced expiration. →expiratory dyspnea
ii. Alteration of PaO2 ,PaCO2 in pulmonary ventilation disturbance PaO2↓ PaCO2↑ (type II RF)
Ⅱ . Pulmonary gas exchange disturbance
Pulmonary gas exchange disturbance diffusion impairmentVA / Q mismatch anatomic shunt
i. Diffusion impairment Causes: area of R-M thickness of R-M diffusion time
1. Area of R-M Normal adult R-M: 80 m2 At rest, used R-M:35~40 m2 area of R-M : atelectasis,pulmonary consolidation,lobar resection, emphysema
2. Thickness of R-M : pulmonary edema, fibrosis, formation of pulmonary hyaline membrane, hydremia
Alteration of PaO2 , PaCO2 PaO2↓ PaCO2 : N or ↓ according to compensatory ventilation why?
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 Blood gas change when blood circulating through lungs Real line stands for normal person; broken line stands for patients with increased thickness of R-M
CO2 diffusivity is higher than O2 • CO2 O2 CO2/ O2 • Solubility 51.5 2.14 24 • Molecular weight 44 32 • square rootof MW 6.63 5.66 1.17 • Diffuse coefficient ratio20/1
ii. Ventilation-Perfusion Mismatch At rest: (VA): ~ 4L (Q) : ~ 5L VA/Q : 0.8 ratio
1.Types and Causes 1) Hypoventilation of Partial alveoli (VA/Q↓) functional shunt or venous admixture Causes:Disorders of trachea or alveolus
functional shunt : alveolar Ventilation (VA ), alveolar Perfusion (Q) have not VA /Q accordingly , even due to inflammation venous blood flowing through these units have not been totally arterialized and mixes into arterial blood, this process is called as functional shunt, also as venous admixture.
O 2 CO 2 A血 V血
V血 O 2↓ CO 2 V血
2) Low perfusion of Partial alveoli (VA/Q↑) dead space like ventilation: alveoli at diseased region have low perfusion,while ventilation is not decreased, alveolar ventilation can not be fully used. • causes:Disorders of pulmonary vessel(vessel inflammation, occlusion,spasm)
O 2 CO 2 A血 V血
O 2 CO 2 A血 V血
2. Alteration of PaO2 ,PaCO2 PaO2 ? N PaCO2
1) blood gas change in functional shunt Asthma C.bronchitis VA / Q functional shunt PaO2 ,PaCO2 compensatory respiration ventilation health region diseased region VA / Q VA / Q PaO2 ↑ , CaO2+, PaO2 ↓ , CaO2 ↓ PaCO2 ↓ CaCO2 ↓ PaCO2 ↑ ,CaCO2 ↑ PaO2 ↓, PaCO2 ? C . O2 and CO2 (ml/dl) PO2 and PCO2 Dissociation curve of O2 and CO2
2) blood gas change in dead space like ventilation p. embolism P. arteritis, DIC VA / Q dead space like ventilation other region Q functional shunt health region diseased region VA / Q VA / Q PaO2 ↓ , CaO2 ↓PaO2 ↑ , CaO2 + PaCO2 ↑ ,CaCO2 ↑ PaCO2 ↓ CaCO2 ↓ PaO2 ↓, PaCO2 ? C . O2 and CO2 (ml/dl) PO2 and PCO2 Dissociation curve of O2 and CO2
iii. anatomic shunt(true shunt) 1、Under physiological condition anatomic shunt: bronchia vein venous bloodpulmonary vein A-V communicating branch true shunt: there are totally no gas exchange in the blood flowing through anatomic shunt, so anatomic shunt also called as true shunt. N: 2%-3%
2、Under pathological condition bronchiectasis flow of bronchial vein shock flow of A-V shunt true shunt atelectasis Consolidationlike true shunt of lung PaO2 PaCO2± or or