here - Boston University Medical Campus

Report
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
5) withholding/delaying steroids
6) inadequate observation
7) pneumothorax
Asthma (Treatment)









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
2) pressure regulated ventilation
(PRVC/APRV)
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)?
significant CNS and/or cardiovascular dysfunction







COPD (Treatment)







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?
13) Liquid ventilation?
14) Prone position?

similar documents