Respiratory/Pulmonary Emergencies - Boston University
Respiratory/Pulmonary Emergencies Hap Farber Pulmonary Center Boston University School of Medicine Respiratory Failure 1) ABG single most important laboratory test for evaluating of respiratory disorders. 2) Respiratory failure: ABG w/ pCO2 > 50 and/or pO2 <60
Normal Individuals 1) Normal pO2 depends on age and position; normal pCO2 is unaffected by age or position. 2) To interpret any decrease in pO2, must know difference between alveolar (A) and arterial (a) pO2 (A-a gradient). 3) Characterize A-a gradient as normal or abnormally elevated. A-a= 150-(paO2 + pCO2 /R) for 21%O2; R=0.8. A-a (21%O2) <15 (20 at any age)
Normal Individuals 4) A-a gradient most sensitive indicator of respiratory disease interfering with gas exchange. 5) A-a gradient differentiates intrapulmonary and extrapulmonary causes of hypercapnia and hypoxemia. 6) A-a gradient must be measured with patient either breathing room air or intubated Hypoventilation
1) Decrease in alveolar ventilation for given level of carbon dioxide production due to decrease in minute ventilation from extrapulmonary dysfunction 2) If no abnormality in distal gas exchange, A-a gradient will be normal 3) Usual mechanism for impaired gas exchange in extrapulmonary respiratory failure, e.g. drug overdose (7.27/56/70; A-a=10) V/Q Mismatch
1) Areas with low V/Q; inadequate ventilation for given level of perfusion: decreased pO2 and O2 content (% saturation) 2) Areas with high V/Q; excessive ventilation for given level of perfusion yields higher level pO2 than normal but only minimal improvement in O2 content (% sat b/o Hb curve - sigmoid) 3) Low V/Q decreases oxygen transfer into blood far more than high V/Q increases it; results in decreased pO2 and increased A-a gradient Right to Left Shunt
1) Deoxygenated blood going directly to arterial circulation w/o exposure to alveolar gas: decreased pO2 and O2 content 2) A-a gradient always greatly increased Types: cardiac or great vessel (ASD/VSD) pulmonary vascular (AVM/fistula) pulmonary parenchymal (collapsed or filled alveoli) Hypoxemia (summary)
To determine whether hypoxemia is caused by hypoventilation, V/Q mismatch, or R-L shunt, look at pCO2, A-a gradient and sometimes response to 100% oxygen 1) hypoventilation: increased pCO2; normal A-a; if given 100% (pO2>500) 2) V/Q mismatch: normal or increased pCO2: increased A-a; moderate response to 100% 3) R-L shunt: normal or decreased pCO2; large A-a; small or no response to 100% Hypercarbia
1) Hypoventilation - inadequate alveolar ventilation for level of CO2 production (consider temperature and caloric intake) 2) Severe V/Q mismatch - major mechanism for development of hypercapnia if parenchymal lung disease. Via low V/Q areas: substantially more low V/Q areas must be present to cause arterial hypercapnia than to cause hypoxemia. CO2 dissociation curve more nearly linear; thus, high V/Q areas can increase CO2 elimination much more effective than O2. Occurs if few high V/Q remain or when respiratory muscle fatigue limits increased minute ventilation to high V/Q 3) Combined (hypoventilation and V/Q mismatch) when respiratory muscle dysfunction/fatigue imposed on V/Q mismatch.
Respiratory Acid-Base 1) Is it a respiratory disturbance (pCO2) or metabolic disturbance (HCO3) 2) Is it simple or complicated 3) Is it acute or chronic Respiratory Acidosis
1) pCO2 increases b/o respiratory dysfunction 2) important to determine length of time present (relation between pCO2 and pH; 10pCO2/0.8pH: remember that renal response to increased pCO2 - bicarbonate retention - requires several days) 3) can have normal or increased A-a gradient 4) major decision is whether to intubate Respiratory Alkalosis 1) pCO2 decreases b/o increased central
drive 2) Similar as respiratory acidosis (reverse) 3) is it a respiratory disturbance (pCO2) or metabolic disturbance (HCO3) 4) is it simple or complicated 5) is it acute or chronic 6) normal or increased A-a gradient Etiology of Respiratory Failure 1) Extrapulmonary vs pulmonary (dysfunction in
any component can cause respiratory failure) 2) Extrapulmonary d/t decreased gas exchange between atmosphere and distal airways/alveoli 3) Pulmonary d/t decreased gas exchange between distal airways and capillary blood 4) For diagnostic/therapeutic reasons can be termed hypercapnic or nonhypercapnic Hypercapneic Respiratory Failure : a. hypoventilation - extrapulmonary b. severe V/Q - pulmonary
c. combination Major problem is elevated pCO2 and resultant respiratory acidosis. pCO2 can be decreased either by increasing CO2 elimination or by decreasing CO2 production. Key initial decision is INTUBATION. Nonhypercapneic Respiratory Failure a. V/Q mismatch b. R to L shunt c. never from extrapulmonary source Major problem: low pO2. Supplemental O2
(intubation not immediate). Asthma Red flags for a bad exacerbation 1) days to weeks of increased unrelenting symptoms followed by rapid deterioration 2) lack of response to previously effective medication 3) history of longstanding, poorly controlled disease
4) previous admissions to an ICU, especially if intubation 5) significant accessory muscle use 6) pulsus paradoxus >10 7) patient sitting upright and/or stating fatigue (I need to be intubated) 8) CO2 retention Asthma Physician examining an asthmatic for the first time is far worse at predicting the severity of attack than the patient! Why are asthmatics dying: (1-2%; >9000 deaths/year; almost all avoidable)
Asthma 1) patient delay in seeking treatment (25% of deaths occur within 30min of onset of symptoms) 2) inadequate or inaccurate physician assessment 3) sedation 4) overuse/misuse of beta-agonists
3) respiratory rate as low as possible 4) permissive hypercapnea: bicarbonate 5) inspiratory flow to accommodate expiratory phase 6) sedation/paralysis COPD 1) Differential diagnosis of acute decompensation large (most commonly: viral respiratory tract infection) 2) Increased pCO2 and decreased pO2
3) Think PE if drop in pO2 with unexpected finding of acute respiratory alkalosis 4) INTUBATION most critical decision COPD (INTUBATION) While wanting to avoid intubation, should not allow situation to deteriorate to emergency intubation! CO2 retention present? acute, acute on chronic, or chronic? how acidemic? acceptable pO2(>50) without unacceptable rise in pCO2 what is trend? respiratory muscle fatigue (paradox)?
1) Oxygen: ?rise in pCO2 (don't worry unless pCO2 >10; pH>0.05). If so, decrease O2 slowly, not abruptly since abrupt decrease or cessation of O2 may not cause prompt increase in ventilation 2) Antipyretics (CO2 production increases 13%/1oC above normal) 3) Bronchodilators 4) Steroids 5) Antibiotics? 6) Phlebotomy if Hct > 55 7) Diuretics ARDS
1) Etiologies both pulmonary and nonpulmonary 2) Normal lungs are not dry, but in ARDS "loose" junctions allow liquid and solutes much greater access to interstitium. Overwhelms lymphatics ability to remove fluid from the interstitium 3) Pulmonary edema results via several possible mechanisms: Increased capillary hydrostatic pressure (PCWP) Decreased colloid oncotic pressure - worsens other mechanisms
Decreased interstitial pressure Increased interstitial colloid oncotic pressure Primary lymphatic insufficiency Alveocapillary membrane permeability ARDS 4) Cardiogenic vs. noncardiogenic edema: can determine if PCWP/LV function known. Measure ratio of total protein (sputum)/total protein (serum): If >0.75 ARDS, if <0.50 CHF 5) ARDS vs. bad pneumonia: semantics ARDS (Treatment)
1) Reverse initiating disorder 2) Block mechanism of alveocapillary injury: STEROIDS DON'T HELP! 3) Minimize pulmonary edema or deleterious effects of the edema 4) Ventilatory support/PEEP/PCV/APRV: small tidal volumes (no differences with different levels of PEEP) remember CPAP/BiPAP 5) Permissive hypercapnea 6) Surfactant?
7) Prevention of nosocomial infection ARDS (Treatment) 8) Prevention of multisystem organ failure 9) Cytokine antagonists? 10) Steroids? (during proliferative phase NOT HERE EITHER!) 11) Inhaled NO? Inhaled prostacyclin? 12) ECMO?
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