4 Respiratory Distress

Question 1

remarks on ABG

Answer 1

ABG analysis that exhibits no evidence of hypoxemia or pulmonary disease suggests hyperventilation from metablolic disease

Question 2

most common causes of dyspnea in the ED

Answer 2

asthma/COPD
ADHF / cardiogenic pulmonary edema
ACS

pneumonia
psychogenic

Question 3

most immediately life-threatening causes of dyspnea in the ED

Answer 3

upper airway obstruction
tension pnuemonthorax
pulmonary embolism

neuromuscular weakness: MG, GBS
fat embolism

Question 4

remarks on BNP / NT pro-BNP

Answer 4

elevated with any cause of ventricular overload, such as
heart failure and strain (both right and left sided)
myocardial ischemia
PE
sepsis
COPD

A normal BNP (<100 pg/mL) or NTproBNP <300 pg/mL exludes heart failure in low and moderate pretest probability patients outside of “flash” pulmonary edema settings

BNP values between 100 and 500 pg/mL have no utility in excluding or including heart failure in the dyspneic patient

BNP measurement is best used when diagnostic uncertainty is present rather than routinely

Question 5

In severe dyspnea, the initial treatment goal is

Answer 5

maintainance of the airway and oxygenation, seeking an arterial oxygen partial pressure (PaO2) >60 mmHg (>8 kPa) and/or arterial oxygen saturation (SaO2) ≥90%

Question 6

formula for A-a gradient

Answer 6

149 - PaCO2/0.8 - PaO2

a simplified formula:
145 - PaCO2 - PaO2

A normal gradient is <10 mm Hg in young, healthy patients and increases with age, predicted by the formula

=2.5 + 0.21 (age in years) (+/- 11)

The supine position and many chronic cardiac and pulmonary diseases may raise the gradient. The supine position is a common ED patient position, impairing the assessment

Question 7

5 mechanisms of hypoxemia

Answer 7

hypoventilation
right-to-left shunt
V/Q mismatch
diffusion impairment
low inspired oxygen

Question 8

remarks on right-to-left shunts

Answer 8

occurs in
- congenital cardiac malformation
- acquired pulmonary disorders
* pulmonary consolidation
* pulmonary atelectasis

always associated with an increase in the A-a O2 gradiant

a hallmark of significant right-to-left shunting is the failure of arterial oxygen levels to increase in response to supplemental oxygen

Question 9

remarks on compensatory mechanisms for hypoxemia

Answer 9

acute:
* Minute Ventilation increases
* pulmonary arterial vasoconstriction (may lead to acute right heart failure)
* increase in cardiac output

chronic:
* increased RBC mass
* decreased tissue O2 demands

“Acute compensatory mechanisms are always activated when PaO2 reaches 60 mmHg and compensatory mechanisms fail when PaO2 falls below 20 mmHg (2.67 kPa)

Question 10

central depression of respiration occurs when?

Answer 10

PaO2 is <20 mmHg

Question 11

remarks on hypercapnia

Answer 11

hypercapnea is exclusively caused by alveolar hypoventilation and is defined as a PaCo2 >45 mmHg (>6 kPa)

causes include
* rapid shallow breathing
* small tidal volumes
* underventilation of the lung
* reduced respiratory drive

Hypercapnia never results from increased CO2 production alone

Question 12

some causes of hypercapnia

Answer 12

depressed central respiratory drive
drug depression of respiratory center (opioids, sedatives, anesthetics)
endogenous toxins (tetanus)

kyphoscoliosis
morbid obesity
neuromuscular disease (MG, GBS)
neuromuscular toxin (organophosphate poisoning, botulism)

COPD
UAO

Question 13

consequences of hypercapnia

Answer 13

acute elevations increase intracranial pressure, and patients may have headache, confusion, or lethargy

severe hypercapnia can trigger seizures and coma

extreme hypercapnia can result in cardiovascular collapse, but is usually seen only with acute elevations of PaCO2 >100 mmHg

as opposed to acute hypercapnia, chronic hypercapnia, even >80 mmHg, may be well tolerated

Question 14

bicarbonate response to hypercapnia

Answer 14

acute: bicarbonate increases about 1 mEq/L for each increase of 10 mmHg in the PaCO2

chronic: bicarbonate increases about 3.5 mEq/L for each increase of 10 mmHg in the PaCO2

Question 15

remarks on acute bronchitis

Answer 15

a productive cough is the hallmark of acute bronchitis

Although pneumonia generally produces a cough, pulmonary secretions may be scant and the cough nonproductive

naproxen reduces coughing in patients with acute bronchitis

Question 16

most likely cause of subacute cough

Answer 16

postinfectious

Question 17

remarks on smoking-induced coughing

Answer 17

usually worse in the morning and, with chronic bronchitis, usually productive

Question 18

remarks on chronic cough from asthma

Answer 18

usually worse at night, exacerbated by irritiants, and associated with episode wheezing and dyspnea

Question 19

remarks on cough from GERD

Answer 19

has a history of heartburn, is worse when lying down, and improves with anti-acid therapy

Question 20

pathophysiology of ACEi-induced cough

Answer 20

Accumulation of bradykinin and substance P,
which stimulate the pulmonary cough receptors
and enhance the formation of irritating prostaglandin metabolites

cough typically resolves in 1-4 weeks after ACEi/ARB is stopped
but may linger up to 3 months*

Question 21

for intractable coughing paroxysms in the ED, some patients respond to

Answer 21

4 mL of 1-2% preservative-free lidocaine (40-80 mg) by nebulization
- causes transient suppression of the gag reflex due to posterior pharyngeal anesthesia

for patients with refractory chronic cough, moderate reduction in cough severity has been observed with opioid antitusives, dextromethorphan, moguisteine, gabapentin, and pregabalin