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CHAPTER 55: Status Asthmaticus 497

The objective of this chapter is to review the pathophysiology, assess- airflow obstruction. In ventilated patients, end-expiratory alveolar
27
ment, and management of patients with severe asthma exacerbation, pressure is not reflected at the airway opening if the expiratory port
which is signaled by many, but not necessarily all of the following of the ventilator is open (which allows airway-opening pressure to
features: resting dyspnea, upright positioning, monosyllabic speech, approach atmospheric pressure or the level of ventilator-applied positive
respiratory rate >30 bpm, accessory muscle use, pulse >120/min, pulsus end-expiratory pressure [PEEP]). If the expiratory port is closed at end
paradoxus >25 mm Hg, peak expiratory flow rate <40% of predicted or expiration, central airway pressure generally equilibrates with alveolar
personal best, minimal or no relief from short-acting β-agonists, hypox- pressure, permitting measurement of intrinsic PEEP (PEEPi), which
emia, and eucapnia or hypercapnia. Altered mental status, paradoxical is also referred to as auto-PEEP. This measurement is most accurate
1
breathing, bradycardia, a quiet chest, and absence of pulsus paradoxus in sedated and/or paralyzed patients, since expiratory muscle contrac-
from respiratory muscle fatigue identify imminent arrest. tion elevates end-expired pressure. Importantly, however, PEEPi can
underestimate the degree of lung hyperinflation in patients with poorly
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PATHOPHYSIOLOGY communicating airspaces. 28
The pressure-volume relationship of the lung demonstrates that lung
Typical asthma exacerbations often evolve over hours to days in hyperinflation decreases static compliance. However, lung compliance
response to infections, irritants, allergens, or air pollution. While this may be normal despite hyperinflation, suggesting a stretch-relaxation
9,10
allows for ample time to intervene early with systemic corticosteroids, response in parenchymal tissue. This state is not favorable for expira-
29
many patients rely on increasing doses of inhaled β-agonists, eventu- tory flow, but may protect against complications of lung hyperinflation.
ally to no avail. These patients invariably have airway inflammation
and mucus plugs that can be quite striking on postmortem analysis. ■ CIRCULATORY EFFECTS OF SEVERE AIRWAY OBSTRUCTION
11
A smaller subset of patients develop sudden-onset attacks that appear
to stem from a more pure form of smooth muscle–mediated broncho- Circulatory abnormalities reflect a state of cardiac tamponade result-
ing from dynamic hyperinflation (DHI) and pleural pressure changes
spasm. While these attacks can be lethal, they can also respond quickly
to bronchodilators. 10,12,13 Triggers of sudden attacks include allergen associated with breathing against obstructed airways. During expi-
ration, elevated intrathoracic pressures decrease right-sided filling.
and irritant exposures, exercise, stress, sulfites, use of nonsteroidal
anti-inflammatory agents and β-blockers in susceptible patients, and Vigorous inspiration augments right ventricular filling and shifts the
intraventricular septum leftward to cause a conformational change in
inhalation of crack cocaine or heroin. 14-17 Infections are not a common
trigger of sudden-onset attacks. However, during pandemics such as the left ventricle (LV), diastolic dysfunction, and incomplete LV filling.
18
Additionally, large negative pleural pressures directly impair LV emp-
those resulting from H1N1 influenza, large numbers of patients with
exacerbations of asthma may be encountered and appropriate treatment tying, which under extreme conditions can even cause pulmonary
edema.
Finally, lung hyperinflation increases RV afterload and
30,31
algorithms for documented pathogens should be applied. 19 may cause transient pulmonary hypertension. The net effect of these
■ ABNORMALITIES OF GAS EXCHANGE cyclical events is to accentuate the normal inspiratory reduction in
32
. .
Airway obstruction causes ventilation-to-perfusion (V/Q) mismatch. stroke volume, a phenomenon termed pulsus paradoxus (PP). Pulsus
paradoxus is a marker of asthma severity ; however, the absence of a
33
Intrapulmonary shunting is trivial, so modest enrichment of oxygen (eg, widened PP does not ensure a mild attack. The PP falls in improving
34
1-3 L/min by nasal cannula) generally corrects hypoxemia. Refractory patients, but also in the fatiguing asthmatic no longer able to generate
20
hypoxemia is rare and suggests other conditions such as pneumonia, large swings in pleural pressure.
atelectasis, or pneumothorax. Hypoxemia correlates with the forced
expiratory volume in 1 second (FEV ) and peak expiratory flow rate ■ PROGRESSION TO VENTILATORY FAILURE
1
(PEFR); however, there is no cutoff value for spirometry that accurately
predicts hypoxemia. 21,22 Airflow rates commonly increase before oxy- Several pathophysiologic mechanisms appear to be responsible for ven-
genation in improving patients, possibly because large airways recover tilatory failure in acute asthma. Intrinsic PEEP is a threshold pressure
quicker than smaller airways. 23,24 that must be overcome before inspiratory flow occurs, increasing inspi-
Supplemental oxygen improves oxygen delivery to tissues, including ratory work of breathing. Increased airway resistance and decreased
the exercising respiratory muscles. It also protects against β-agonist– lung compliance further increase work.
induced hypoxemia resulting from pulmonary vasodilation and Increased mechanical loads are placed on a diaphragm that is placed
. .
increased blood flow to low V/Q units. 25,26 in a disadvantageous position by lung hyperinflation, and at the same
Respiratory alkalosis is common in early and mild attacks. If present time circulatory abnormalities may result in hypoperfusion of the
for many hours to days, there is compensatory renal bicarbonate wasting exercising respiratory muscles. In the end, strength is inadequate for
that may subsequently manifest as a normal anion-gap metabolic aci- load and hypercapnia ensues, which further decreases diaphragm force
dosis (ie, posthypocapnic metabolic acidosis). As the severity of airflow generation. 35,36
obstruction increases, the partial pressure of arterial carbon dioxide
) generally increases as well due to inadequate alveolar ventilation
(Pa CO 2 CLINICAL PRESENTATION, DIFFERENTIAL DIAGNOSIS,
(reflecting a decrease in minute ventilation as the patient nears respira- AND ASSESSMENT OF SEVERITY
tory arrest) and possible elevated CO production from increased work
2
of breathing. Hypercapnia usually does not occur unless the FEV is Multifactorial analysis including the history, physical examination, mea-
1
less than 25% of predicted. Increase in dead space might also occur sures of airflow obstruction, response to therapy, and in selected patients
21
if hyperinflated lung limits blood flow to create West’s zone 1 condi- arterial blood gases and chest radiography is required to assess severity
tions (where alveolar pressure exceeds pulmonary capillary pressure). and the risk for deterioration. 37
23
However, multiple inert gas elimination technique (MIGET) analysis
. .
demonstrates only small areas of high V/Q and slightly increased dead ■ MEDICAL HISTORY
space in acute asthma. 20,26 Importantly, the absence of hypercapnia does Characteristics of prior exacerbations that predict a fatal or near fatal attack
not preclude a severe attack or impending arrest. 22 include intubation, hypercapnia, barotrauma, hospitalization despite
■ LUNG MECHANICAL ABNORMALITIES corticosteroids, psychiatric illness, and medical noncompliance. 1,9,38-40
Substance abuse, alcohol ingestion, and excessive, long-term use of
Incomplete exhalation and the formation of positive end-expiratory β-agonists are also associated with mortality. 16,41 Pharmacogenetic
alveolar pressure are hallmarks of the tachypneic patient with expiratory studies have suggested an association between polymorphisms of
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