Pulmonary Medicine Q: 27 y/o women comes to ER w/pleuritic chest pain for hrs, non smoker, but OCPs; CXR

splinting w/deep inspirations; ABGs showed pH 7.45, PaCO2 31, HCO3 21, paO2 83 (breathing ambient air, PB 747) A: diagnostic imaging to exclude PE; clue is OCPs

Gas Exchange: At alveoli pO2 = 100 pCO2 = 40 A/f tissue pO2 =40 pCO2 = 46

Hemoglobin (Hb) and O2 transport DO2 = CO X CaO2 (oxygen content of arterial blood) CaO2 = (1.34 X hb X SaO2) + 0.003 X PaO2 Biggest compoments of oxygen delivery are hemoglobin and CO

Hemoglobin-O2 Binding Curve @14:40 At saturation of 90%, PaO2 is 60 Blood Gas Report Ph PaCO2 PaO2 HCO3 B.E. O2 sat

7.35-7.45 35-45 110-0.5(age) 22-26 -2 to 2 >90%

Analysis of Oxygenation Alveolar Gas Equation PAO2 = FiO2(PB -47)-1.2(PaCO2) Pb is barometric, unless said otherwise, assume at sea level PAO2 defines upper limit of PaO2 Ambient FiO2 is 21% at all altitudes Factor 1.2 determined by RQ varies with FiO2 PAO2 = 150 1.2(PaCO2) at room air -how you get alveolar oxygen Alveolar-Arterial PO2 Gradient A-aDO2 = PAO2 PaO2 (from ABG) Insight into the patients state of gas exchange -If elevated (>15), defect in gas exchange Ideal conditions PAO2 = PaO2 -Every alveolus perfectly ventilated -No diffusion impairment -All pulmonary capillaries perfused -No shunt present Mechanisms of Hypoxemia See notes Hypoventilation -not fast enough or tidal volume is low -A-a gradient normal, really problem with central drive -If give them oxygen, arterial oxygen goes up Diffusion -if give oxygen, will improve arterial oxygen Shunt -Gets high FiO2, but oxygen levels do not change much, think shunt Va/Q Imbalance -most common cause of hypoxemia Alveolar Hypoventilation Muscle weakness Neuromuscular junction disease Reduced respiratory drive Chest wall elastic loads -abdominal ascites -big belly from pregnancy

V/Q Mismatch Asthma COPD Pneumonia Pulmonary Embolism Pulmonary Edema Ventilation Perfusion Ratios See diagram @24.50 and notes Reduced Diffusion Capacity Interstitial Lung Disease Pulmonary Edema Reduced Lung Volume Emphysema Pulmonary Resection Anemia Shunt Intrapulmonary -ARDS -Pneumonia -Pulmonary Edema (all these, big segments of alveoli not involved in gas exchange) Extrapulmonary -Congenital Heart Disease -Pulmonary Vascular Disease Problems: Oxygenation Room Air, PaO2 = 45 (hypoxemia), PaCO2 = 30 -PAO2 = 150 1.2(30) = 114 mmHg -A-aDo2 = 114 45 = 69 elevated (N < 15) So have hypoxemia from elevated A-a gradient, from V/Q mismatch, shunt, or diffusion abnormality 100% O2, PaO2 = 65, PaCO2 = 32 -minimal elevation in PaO2 -shunt major cause of hypoxemia

Problems: Oxygenation Room Air, PaO2 = 45 hypoxemia, PaCO2 = 45 -PAO2 = 150 1.2(45) = 96 -A-aDO2 = 96 45 = 51 elevated (N < 15) 100% O2, PaO2 = 555 dramatic increase, excludes shunt, PaCO2 = 48 -V/Q mismatch or diffusion? V/Q mismatch b/c more common -PAO2 = 1.0(760-47) 1.2(48) = 655 -A-aDO2 = 655 555 = 100 -Dramatic increase in PaO2 -V/Q mismatch major cause of hypoxemia

Oximetry Binding sites for O2 are heme groups OXYGEN SATURATION -% of all heme sites saturated with O2 Oximetry measures absorption of 2 wavelenghts of light SpO2 = (Oxy Hb)/ (Oxy Hb + Deoxy Hb) X 100 ABG SaO2 is calculated value from PaO2 -If get ABG, it takes PaO2, plots saturation, if PaO2 is 60, thinks sat is probably 90%

Q: 54 yo man came to the ER c/o headaches and SOB. RA ABG: PaO2 was 89, PaCO2 38, pH 7.43; HCT was 44%. SaO2 was not directly measured but instead calculated at 98% for this PaO2. After some improvement, he was scheduled for a brain CAT scan, two days later and discharged. He was brought back to the ER, unconscious; His carbon monoxide, SaO2 and ABGs measured; Results: PaO2 79, PaCO2 31, pH 7.36, SaO2 53%, carboxyhemoglobin 46% Oximetry Carboxyhemoglobin: Hb + CO -Hb binds to CO more avidly, but pulse ox does not recognize CO from O2, And thus overestimates O2 sat -So if measured SatO2 is much lower than PaO2, think CO -Does not affect PaO2, only SaO2 -Pulse oximetry reads CO-HB as OxyHB Follow Up: -PaO2 = 79, PaCO2 = 31, SpO2 = 53% (measured), pH = 7.36 -CO-Hb 46% measured by CO-Oximeter -CO-Oximeter measures 4 wavelengths

Problem: 42 yo HIV pt w/fever, chills, SOB, cough -taking dapsone for PCP prophylaxis -ABG: PaO2 82.5, PaCO2 35.2, pH 7.43, SaO2 89% -PCP pneumonia, started on primaquine, clinda, and prednisone -ABG (after exogenous O2): PaO2 378, PaCO2 of 35, pH 7.42, SaO2 80% (does not correlate w/PaO2!) -What is happening? Methemoglobin Oxidation of Fe++ to Fe+++ state Unlike Co-Hb, Met-Hgb does depress the SpO2 reading (reinforce: w/CO, if get calculated O2 saturation, it will be appear normal, but measured O2 sat will be markedly different than what the arterial PaO2 would indicate if you plotted it on graph) Both dapsone and primaquine are oxidants Met-Hb depresses the SpO2 to 80s -Durther increases in Met-Hb do nto depress SpO2 Methylene blue administration is Rx Ventilation and Acid-Base Balance Ventilation usually adjusts to metabolic rate to maintain normal CO2 levels Analysis of Ventilation PaCO2 = (VCO2 x K)/VA VCO2 is what makes CO2, and it goes up w/fever, pneumonia VA is alveolar ventilation, which is what rids of CO2, and when sick, should breath faster or deeper

VA = VE VD VE is minute ventilation VD is dead space Hypercapnia > 45 mmHg Hypocapnia < 35

Dead Space Pathology Anatomic -trachea and bronchi are not involved in ventilation, only when get to alveoli -Rapid shallow breathing Alveolar Dead space -Acute pulmonary embolus -Decrease cardiac output -Acute pulmonary ventilation Positive Pressure Ventilation Alveolar Septal Destruction (COPD) Pulmonary Function Testing Q: which does not cause a decrease in DLCO? A. Emphysema -ability of CO across membrane, here alveolar destruction, so does not go through B. Pulmonary arterial hypertension -inc. resistance, less volume that gets to capillary, no less diffusion C. Anemia -less hb for oxygen to bind to, so less diffusion D. Erythrocytosis -more blood to exchange E. Pulmonary embolus -less blood to exchange, so less diffusion Spirometry: Normal person should be able to blow out majority, say 70%, of their expired air, within the first second FEV1/FVC < 70% defines obstruction Lung Volumes: Vital capacity: air forcefully exhales a/f a maximum inhalation; excludes residual volume In COPD, hyperinflated lungs, over time, residual volume goes up Not all volumes are measured directly FRC is measured directly Combined w/SVC, so you can then measure IC and ERV RV = FRC ERV TLC = FRC + IC Predicting Normal Values Consider range of 80% to 120% predicted to be normal for FEV1 and FVC

Obstructive Disease FEV1/FVC < 70% Restrictive Pattern Normal or high FEV1/FVC ratio Low FEV1 or FVC suggests restriction Lung volumes necessary to confirm true restrictive dysfunction TLC, RV, FRC, SVC will be reduced Severity based on TLC -Mild: 70-80% -Moderate: 60-69% -Severe < 60% Flow-Volume in UAO See notes for diagram Dynamic Intrathoracic: Obstruction with expiration -tracheal tumor/foreign body Dynamic Extrathoracic: Obstruction on inspiration: -Tracheomalacia -vocal cord problem Fixed Upper Airway Obstruction Both inspiratory and expiratory loops are flattened -compressive tumors -tracheal stenosis- prolonged intubation Bronchodilator Response Asthma vs COPD FEV1 or FVC improvement > 12% predicted and 200 ml Other markers: -reduced TLC, FRC, RV- decreased hyperinflation with BDs -FEF 25-75% improvement >35% suggests BD response Changes in DLCO Decreased in conditions that disrupt alveolar: capillary surface gas transfer Emphysema, interstitial inflammation and fibrosis, edema, infections Reduced capillary lung volumes -Pulm. HTN, PE, PPH Increased in conditions that recruit pulmonary vascular bed and increase blood volume -Exercise, mild CHF (due to back pressure from L heart to R heart), asthma -Increase Hb-erythrocytosis, pulm. Hemorrhage

Stopped at 1:08 See problems @1:05