i. Zone 1 = dead space ii. Zone 2 = ventilation = perfusion (ideal situation) iii. Zone 3 = shunt

Transcription

1 Respiratory Review I. Oxygen transport a. Oxygen content of blood i. Dissolved oxygen =.003 x PaO 2, per 100 ml plasma 1. Henry s Law ii. Oxygen on hemoglobin = 1.34 ml x sat x Hgb iii. CaO 2 = Dissolved O 2 + O 2 on hemoglobin iv. Arterial blood O 2 content = 20 ml/dl v. Venous blood O 2 content = 15 ml/dl b. Oxy-hemoglobin dissociation Curve i. ii. 40, 50, 60% = 70, 80, 90 PaO 2 iii. P50 = 27 mmhg iv. Factors causing leftward shift of curve 1. hypothermia 2. decreased 2,3-DPG 3. hypocarbia 4. increased ph 5. fetal hemoglobin 6. methemoglobin 7. carboxyhemoglobin v. Factors causing rightward shift of curve 1. hyperthermia 2. increased 2,3-DPG 3. decreased ph (Bohr effect) 4. sickle cell hemoglobin c. Oxygen delivery i. O 2 content x cardiac output = 1000 ml/min d. Oxygen consumption i. A V difference x cardiac output = 250 ml/min ii. Fick equation cardiac output can be calculate by knowing the A-V difference and assuming a 250 ml/min consumption e. Respiratory quotient i. CO 2 production / O 2 consumption = 0.8

2 II. III. IV. f. Alveolar / Arterial (A/a) gradient i. Typically 4 10 mmhg ii. Secondary to physiologic shunt and return of deoxygenated blood from bronchial & Thebesian veins and intrapulmonary shunting 1. Typically 2 3% of blood is shunted iii. Shunt increases with age 1. Shunt = (age +10)/4 iv. A-a gradient increases with age, lung disease, right-to-left intracardiac shunting Carbon dioxide transport a. Most CO 2 transported as bicarbonate (73%) b. Some attached to hemoglobin as carbamino compounds c. Some dissolved in plasma d. Oxygen consumption frees space on hemoglobin for CO 2 transport (Haldane effect) ABGs a. Normal arterial values i. ph ii. PaO mmhg iii. PaCO iv. Bicarb meq/l v. Sat >= 95% vi. Base excess b. Normal mixed venous values i. ph ii. PvO mmhg iii. PvCO mmHg iv. Sat 72 75% c. Interpretation of ABGs CO2 changes i. For every decrease of 10 mmhg, ph will rise 0.1 ii. For every increase of 10 mmhg, ph will fall 0.05 iii. For every decrease of 10 mmhg, bicarb will fall 2 meq/l iv. Ability to buffer acidity is greater Acid-base balance a. Ventilation can produce a rapid change in ph b. Chemosensitive areas in the medulla detect changes in ph and alter ventilation to correct. c. Bicarbonate / carbonic acid is the major buffer system in body d. Normal ratio of bicarbonate : CO 2 is 20:1 e. Renal regulation of ph i. 90% of bicarbonate is reabsorbed in proximal tubule ii. Carbonic anhydrase catalyzes reaction and aids in bicarbonate reabsorption iii. Excess hydrogen ions excreted free and as ammonium f. Anion gap

3 i. Difference between cations and anions ii. Normally 12 meq/l iii. Acidosis with normal anion gap implies hyperchloremia iv. Wide anion gap acidosis from: ketoacidosis, ASA, ETOH, lactic acid, renal failure v. Narrow anion gap acidosis from: renal tubular acidosis, diarrhea, carbonic anhydrase inhibitors, hypoaldosteronism, vi. high chloride intake Metabolic alkalosis from: volume contraction, hyperaldosteronism, vomiting vii. Physiologic effects of acidosis: increased potassium, vasodilation, myocardial depression, right shift of oxyhemoglobin curve viii. Physiologic effects of alkalosis: decreased potassium, decreased ionized calcium, vasoconstriction, bronchochonstriction, left shift of oxy-hemoglobin curve V. Lung volumes a. Tidal volume (TV) volume of air moved in or out during each ventilation. Typical volume is 7 10 ml/kg and does not change throughout life b. Inspiratory reserve volume (IRV) the additional volume of air that can be forcibly inhaled after a normal inspiration. Typical volume is 3000 ml c. Expiratory reserve volume (ERV) the additional volume of air that can be forcibly exhaled after a normal exhalation. Typical volume is 1100 ml d. Residual volume (RV) the volume of air remaining in the lungs after forced exhalation. Typical volume is 1200 ml e. Minute volume = tidal volume x rate f. Dead space i. Anatomic upper airway structures down thru terminal bronchiole (division 16 of 23) ii. Physiologic all ventilate and non-perfused areas. Normally in adult about 150 ml VI. Lung Capacities a. Capacities are the sum of two or more volumes i. Vital Capacity = TV + IRV + ERV ii. Functional residual capacity (FRC) = ERV + RV iii. Total lung capacity = FRC + TV + IRV

4 iv. VII. v. Closing volume & closing capacity 1. During forced exhalation, small airways begin to close. The remaining volume that can be exhaled is called the closing volume 2. Closing capacity = closing volume + RV 3. If closing capacity exceeds FRC, shunting ensues Pulmonary function testing & volume loops a. PFTs are typically report in both absolute values and as a predicted percentage of normal b. Maximum breathing capacity maximum volume that can be exhaled per minute (test done over 15 secs and multiplied by 4) c. Forced expiratory volume 1 (FEV 1 ) volume forcibly exhaled in 1 second d. Forced vital capacity (FVC) volume forcibly exhaled e. FEV 1 / FVC normal values > 80% f. Forced expiratory flow (FEF 25-75) average forced expiratory flow during the mid (25-75%) of the FVC. Less effort dependent g. Peak expiratory flow rate just what it says

5 h. Flow volume loop i. Abnormal loops j. Zones of the lung (West Zones) i. Zone 1 = dead space ii. Zone 2 = ventilation = perfusion (ideal situation) iii. Zone 3 = shunt

6 k. VIII. IX. l. Carbon dioxide elimination not affected by shunt because of the increased diffusion rate of CO 2 as compared to O 2 (20:1) COPD a. Pathophysiology i. Loss of lung elasticity ii. Breakdown of parenchyma with formation of blebs iii. Exhalation more profoundly affected than inspiration iv. Increased FRC, CC. Decreased FEV 1 b. Categories i. Pink Puffer 1. Has intact CO 2 response and maintains oxygenation 2. More commonly associated with emphysema 3. Usually not responsive to bronchodilators 4. Associate with greater parenchymal damage ii. Blue Bloater 1. Lost CO 2 response lives on O 2 drive 2. More commonly associated with chronic bronchitis 3. Responsive to bronchodilators 4. May lose ventilatory drive with supplemental oxygen c. Asthma i. Reactive airway disease ii. Expiratory obstruction iii. Responsive to bronchodilators Restrictive airway disease a. Pulmonary sarcoidosis, asbestosis, pneumonitis

7 b. Extra-pulmonary kyphoscoliosis, scleraderma, obesity c. Decreases TLC, VC, and FEV 1 d. FEV 1 / FVC usually normal X. ARDS a. Lung capillaries have increased permeability b. Leakage of plasma proteins into alveoli c. Increases shunt with hypoxemia d. Decreased FRC e. Increased PVR f. Anything can cause ARDS burns, shock, transfusion, sepsis, etc XI. Lung Cancer a. 4 major types i. Adenocarcinoma ii. Sqamous cell carcinoma (bronchogenic) iii. Undifferentiated cell (large and small cell) carcinoma iv. Alveolar cell carcinoma b. Associated co-morbidities common COPD, atalectasis, pleural effusions, pulmonary HTN, pneumonia c. Small cell carcinoma associated with paraneoplastic syndromes Cushings syndrome, SIADH, Eaton-Lambert syndrome XII. Pneumonectomy a. Predictors of tolerance i. CO 2 < 45 ii. FEV 1 > 2L iii. FEV 1 /FVC > 50% iv. Max VO 2 > 10mL/kg/min b. One-lung anesthesia i. Done with double-lumen tube or bronchial blocker ii. Easier to place DLT on left left main stem bronchus has a steeper angle (45 o vs 25 o ), however the cephalad location of the RUL bronchus makes right DLT placement difficult iii. Primary concern is shunt with hypoxia 1. Non-dependent lung reinflation or CPAP most effective treatment 2. Dependent lung PEEP may provide minimal treatment 3. Shunt disappears with ligation of pulmonary artery c. Acute lung injury (ALI) following thoracotomy i. Pulmonary edema occurring 0 3 days after thoracotomy ii. Predictors of ALI: pneumonectomy (particularly right), excessive intravenous hydration, high intraop ventilating pressures, alcohol abuse iii. Overall incidence 3% XIII. Pneumothorax a. Collection of gas in the space between the parietal and visceral pleurae resulting in lung collapse

8 XIV. b. Tension pneumothorax gas in space under pressure causing displacement of mediastinal structures and depressed cardiopulmonary function c. Definitive treatment is decompression. Discontinue nitrous oxide if in use Non-cardiogenic pulmonary edema a. Occurs following acute and complete upper airway obstruction b. Believed secondary to forceful inspiratory efforts against a closed glottis c. Treatment is supportive. Diuretics used, but of questionable efficacy