Medical Pharmacology Chapter 25: Pulmonary Pharmacology--Asthma
Asthma: Systems Pathophysiology
Airway diameter reduction, caused by smooth muscle contraction, vascular congestion, bronchial wall edema and thick, tenacious secretion.
Increased airway resistance
Decreased forced expiratory rates
Increased work of breathing
Changes in respiratory muscle function
Changes in elastic recoil
Abnormal ventilation/pulmonary blood flow distribution
Lung and thorax hyperinflation
ECG changes indicative of right ventricular hypertrophy and pulmonary hypertension
vital capacity < 50% of normal
1 - second forced expiratory volume (FEV1): reduced to 30% of expected
maximum/a minimum midexpiratory flow rates: reduced to 20% or less of expected
In acute illness: residual volume (RV): may approach 400% of normal; functional residual capacity doubles
Patients report that the attack has ended clinically when RV has fallen to 200% of expected and FEV1 reaches 50% of expected level
Very common finding during acute phase
Respiratory failure -- relatively uncommon: 10% to 15% of presenting patients
Respiratory alkalosis: common
Normal arterial carbon dioxide tension but severe airway obstruction present is suggestive of possibly impending respiratory failure
Metabolic acidosis in acute asthma with severe obstruction
Clinical presentations may not correlate with blood gas data; however, estimating patient's ventilatory state solely on clinical presentation may be dangerous
Patients with possible alveolar hypoventilation should have arterial blood gas tension measurements
Cyanosis: -- very late sign; suggestive that extreme hypoxia may go undetected.
There are three principal symptoms that characterize asthma. These are dyspnea, cough, and wheezing with wheezing being particularly prominent.
As we have noted earlier, asthma is an episodic disorder with the above symptoms commonly exhibited.
Initially patients experienced chest constriction perhaps with a nonproductive cough.
Audibly harsh, wheezing respiration is then noted; expiration is prolonged and difficult.
Tachypnea, mild systolic hypertension and tachycardia are frequent presentations.
Lung overinflation is typical in the anterioposterior thoracic dimension (diameter) increases.
Severe or prolonged asthma attacks are associated with a loss of adventitial breath sounds along with notably high pitched wheezing.
Respiratory accessory muscles become more prominent as well as paradoxical pulse-signs indicative of severe obstruction with impaired, significantly impaired pulmonary function.
Paradoxical pulse requires significantly large negative intrathoracic pressures; therefore, with shallow breathing, condition which does not favor development of large negative intrathoracic pressures, significant obstruction can be present even in the absence of paradoxical pulse.
[Paradoxical pulse definition: Inspiratory decrease in arterial pressure >10 mm Hg with Inspiratory venous pressure unchanged (Kussmaul's Sign); Paradoxical pulse signs: Palpable decrease in pulse with inspiration Inspiratory systolic blood pressure decreased over 10 mm Hg less than expiratory pressure]. Significant disease may remain if the endpoints are only an a reduction in wheezing and the resolution of subjective complaints.
The conclusion of an asthmatic episode may be associated with coughs producing a thick, stringy me at this in the form of distal airway casts (Curschmann's spirals) which when microscopically evaluated shows the presence of eosinophils and Charcot-Leyden crystals.
Severe mucus plugging with possibly imminent suffocation may occur and in this case the cough would be ineffective and the patient will be gasping. Such circumstances may necessitate mechanical ventilation. Atelectasis (collapsed lung) may also occur in asthma.
Bronchial wall characteristics during an acute asthma attack:
Animation of asthmatic breathing cycle noting residual lung volume (copyright (C) 1996, Stephen M. Borowitz)
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