RespiratoryPulmonary Emergencies Hap Farber n Pulmonary Center n

Respiratory/Pulmonary Emergencies Hap Farber n Pulmonary Center n Boston University School of Medicine n

Respiratory Failure 1) ABG single most important laboratory test for evaluating of respiratory disorders. n 2) Respiratory failure: ABG w/ p. CO 2 > 50 and/or p. O 2 <60 n

Normal Individuals n n 1) Normal p. O 2 depends on age and position; normal p. CO 2 is unaffected by age or position. 2) To interpret any decrease in p. O 2, must know difference between alveolar (A) and arterial (a) p. O 2 (A-a gradient). 3) Characterize A-a gradient as normal or abnormally elevated. A-a= 150 -(pa. O 2 + p. CO 2 /R) for 21%O 2; R=0. 8. A-a (21%O 2) <15 (20 at any age)

Normal Individuals n n n 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 n 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 n n n 1) Areas with low V/Q; inadequate ventilation for given level of perfusion: decreased p. O 2 and O 2 content (% saturation) 2) Areas with high V/Q; excessive ventilation for given level of perfusion yields higher level p. O 2 than normal but only minimal improvement in O 2 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 p. O 2 and increased A-a gradient

Right to Left Shunt n n 1) Deoxygenated blood going directly to arterial circulation w/o exposure to alveolar gas: decreased p. O 2 and O 2 content 2) A-a gradient always greatly increased n n Types: cardiac or great vessel (ASD/VSD) pulmonary vascular (AVM/fistula) pulmonary parenchymal (collapsed or filled alveoli)

Hypoxemia (summary) n n To determine whether hypoxemia is caused by hypoventilation, V/Q mismatch, or R-L shunt, look at p. CO 2, A-a gradient and sometimes response to 100% oxygen 1) hypoventilation: increased p. CO 2; normal A-a; if given 100% (p. O 2>500) 2) V/Q mismatch: normal or increased p. CO 2: increased A-a; moderate response to 100% 3) R-L shunt: normal or decreased p. CO 2; large A-a; small or no response to 100%

Hypercarbia n n n 1) Hypoventilation - inadequate alveolar ventilation for level of CO 2 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. CO 2 dissociation curve more nearly linear; thus, high V/Q areas can increase CO 2 elimination much more effective than O 2. 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 (p. CO 2) or metabolic disturbance (HCO 3) n 2) Is it simple or complicated n 3) Is it acute or chronic n

Respiratory Acidosis n n 1) p. CO 2 increases b/o respiratory dysfunction 2) important to determine length of time present (relation between p. CO 2 and p. H; 10 p. CO 2/0. 8 p. H: remember that renal response to increased p. CO 2 - bicarbonate retention - requires several days) 3) can have normal or increased A-a gradient 4) major decision is whether to intubate

Respiratory Alkalosis 1) p. CO 2 decreases b/o increased central drive n 2) Similar as respiratory acidosis (reverse) n 3) is it a respiratory disturbance (p. CO 2) or metabolic disturbance (HCO 3) n 4) is it simple or complicated n 5) is it acute or chronic n 6) normal or increased A-a gradient n

Etiology of Respiratory Failure n n 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 n n : a. hypoventilation - extrapulmonary b. severe V/Q - pulmonary c. combination Major problem is elevated p. CO 2 and resultant respiratory acidosis. p. CO 2 can be decreased either by increasing CO 2 elimination or by decreasing CO 2 production. Key initial decision is INTUBATION.

Nonhypercapneic Respiratory Failure n n a. V/Q mismatch b. R to L shunt c. never from extrapulmonary source Major problem: low p. O 2. Supplemental O 2 (intubation not immediate).

Asthma n n n n n 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) CO 2 retention

Asthma n Physician examining an asthmatic for the first time is far worse at predicting the severity of attack than the patient! n Why are asthmatics dying: (1 -2%; >9000 deaths/year; almost all avoidable)

Asthma n n n n 1) patient delay in seeking treatment (25% of deaths occur within 30 min of onset of symptoms) 2) inadequate or inaccurate physician assessment 3) sedation 4) overuse/misuse of beta-agonists 5) withholding/delaying steroids 6) inadequate observation 7) pneumothorax

Asthma (Treatment) n n n n n 1) Beta-adrenergic agents 2) Steroids 3) Atropine derivatives 4) magnesium? 5) theophylline? 6) acetylcysteine? 7) isoproterenol? 8) mechanical ventilation 9) general anesthesia

Asthma (Intubation) 1) large endotracheal tube n 2) pressure regulated ventilation (PRVC/APRV) n 3) respiratory rate as low as possible n 4) permissive hypercapnea: bicarbonate n 5) inspiratory flow to accommodate expiratory phase n 6) sedation/paralysis n

COPD 1) Differential diagnosis of acute decompensation large (most commonly: viral respiratory tract infection) n 2) Increased p. CO 2 and decreased p. O 2 n 3) Think PE if drop in p. O 2 with unexpected finding of acute respiratory alkalosis n 4) INTUBATION most critical decision n

COPD (INTUBATION) n While wanting to avoid intubation, should not allow situation to deteriorate to emergency intubation! n CO 2 retention present? acute, acute on chronic, or chronic? how acidemic? acceptable p. O 2(>50) without unacceptable rise in p. CO 2 what is trend? respiratory muscle fatigue (paradox)? significant CNS and/or cardiovascular dysfunction n n n

COPD (Treatment) n n n n 1) Oxygen: ? rise in p. CO 2 (don't worry unless p. CO 2 >10; p. H>0. 05). If so, decrease O 2 slowly, not abruptly since abrupt decrease or cessation of O 2 may not cause prompt increase in ventilation 2) Antipyretics (CO 2 production increases 13%/1 o. C above normal) 3) Bronchodilators 4) Steroids 5) Antibiotics? 6) Phlebotomy if Hct > 55 7) Diuretics

ARDS n n n 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: n n n n 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 n 5) ARDS vs. bad pneumonia: semantics n

ARDS (Treatment) n n n n 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/Bi. PAP 5) Permissive hypercapnea 6) Surfactant? 7) Prevention of nosocomial infection

ARDS (Treatment) n n n n 8) Prevention of multisystem organ failure 9) Cytokine antagonists? 10) Steroids? (during proliferative phase – NOT HERE EITHER!) 11) Inhaled NO? Inhaled prostacyclin? 12) ECMO? 13) Liquid ventilation? 14) Prone position?