Hap FarberPulmonary CenterBoston University School of Medicine
1) ABG single most important laboratory test for evaluating of respiratory disorders.2) Respiratory failure: ABG w/ pCO2 > 50 and/or pO2 <60
1) Normal pO2 depends onageandposition;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)
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
1) Decrease in alveolar ventilation for given level of carbon dioxide production due to decrease in minute ventilation from extrapulmonary dysfunction2)If no abnormality in distal gas exchange, A-a gradient will be normal3) Usual mechanism for impaired gas exchange in extrapulmonary respiratory failure, e.g. drug overdose (7.27/56/70; A-a=10)
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 content2) A-a gradient always greatly increasedTypes:cardiac or great vessel (ASD/VSD)pulmonary vascular (AVM/fistula)pulmonary parenchymal (collapsed or filled alveoli)
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% oxygen1) 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%
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/Q3) Combined (hypoventilation and V/Q mismatch) when respiratory muscle dysfunction/fatigue imposed on V/Q mismatch.
1) Is it a respiratory disturbance (pCO2) or metabolic disturbance (HCO3)2) Is it simple or complicated3) Is it acute or chronic
1) pCO2 increases b/o respiratory dysfunction2) 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 gradient4) major decision is whether to intubate
1) pCO2 decreases b/o increased central drive2) Similar as respiratory acidosis (reverse)3) is it a respiratory disturbance (pCO2) or metabolic disturbance (HCO3)4) is it simple or complicated5) is it acute or chronic6) 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/alveoli3) Pulmonary d/t decreased gas exchange between distal airways and capillary blood4) For diagnostic/therapeutic reasons can be termed hypercapnic or nonhypercapnic
Hypercapneic Respiratory Failure
: a. hypoventilation - extrapulmonaryb. severe V/Q - pulmonaryc. combinationMajor 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 mismatchb. R to L shuntc. never from extrapulmonary sourceMajor problem: low pO2. Supplemental O2 (intubation not immediate).
Red flags for a bad exacerbation1) days to weeks of increased unrelenting symptoms followed by rapid deterioration2) lack of response to previously effective medication3) history of longstanding, poorly controlled disease4) previous admissions to an ICU, especially if intubation5) significant accessory muscle use6) pulsus paradoxus >107) patient sitting upright and/or stating fatigue (I need to be intubated)8) CO2 retention
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)
1) patient delay in seeking treatment (25% of deaths occur within 30min of onset of symptoms)2) inadequate or inaccurate physician assessment3) sedation4) overuse/misuse of beta-agonists5) withholding/delaying steroids6) inadequate observation7) pneumothorax
1) Beta-adrenergic agents2) Steroids3) Atropine derivatives4) magnesium?5) theophylline?6) acetylcysteine?7) isoproterenol?8) mechanical ventilation9) general anesthesia
1) large endotracheal tube2) pressure regulated ventilation (PRVC/APRV)3) respiratory rate as low as possible4) permissive hypercapnea: bicarbonate5) inspiratory flow to accommodate expiratory phase6) sedation/paralysis
1) Differential diagnosis of acute decompensation large (most commonly: viral respiratory tract infection)2) Increased pCO2 and decreased pO23) Think PE if drop in pO2 with unexpected finding of acute respiratory alkalosis4) INTUBATION most critical decision
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 pCO2what is trend?respiratory muscle fatigue (paradox)?significant CNS and/or cardiovascular dysfunction
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 ventilation2) Antipyretics (CO2 production increases 13%/1oC above normal)3) Bronchodilators4) Steroids5) Antibiotics?6) Phlebotomy if Hct > 557) Diuretics
1) Etiologies both pulmonary and nonpulmonary2) 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 interstitium3) Pulmonary edema results via several possible mechanisms:Increased capillary hydrostatic pressure (PCWP)Decreased colloid oncotic pressure - worsens other mechanismsDecreased interstitial pressureIncreased interstitial colloid oncotic pressurePrimary lymphatic insufficiencyAlveocapillary membrane permeability
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 CHF5) ARDS vs. bad pneumonia: semantics
1) Reverse initiating disorder2) Block mechanism of alveocapillary injury: STEROIDS DON'T HELP!3) Minimize pulmonary edema or deleterious effects of the edema4) Ventilatory support/PEEP/PCV/APRV: small tidal volumes (no differences with different levels of PEEP) - remember CPAP/BiPAP5) Permissive hypercapnea6) Surfactant?7) Prevention of nosocomial infection
8) Prevention of multisystem organ failure9) Cytokine antagonists?10) Steroids? (during proliferative phase – NOT HERE EITHER!)11) Inhaled NO? Inhaled prostacyclin?12) ECMO?13) Liquid ventilation?14) Prone position?