Distribution of ventilation is uneven due to different degrees of bronchial obstruction. Impairment of circulation may occur in overdistended areas. Some alveoli are poorly ventilated and normally perfused (low ventilation-perfusion ratio) and lead to hypoxemia. In completely obstructed areas, normal perfusion would constitute a true shunt. However, a small collateral ventilation of these alveoli accounts for the absence of true shunt. Other alveoli are overinflated, compress capillaries, and increase the dead-space. Evidence for the ensuing ventilation-perfusion imbalance is provided by blood gas analysis.
The increased minute ventilation following the stimulation of ventilatory drive reduces PaCO2, creating respiratory alkalosis (Table 1, stages I and II). In more severe asthma, hypoxemia may develop associated with respiratory alkalosis. With progression of obstruction, there is a decrease in tidal volume and an increase in respiratory rate. PaCO2 increases due to alveolar hypoventilation and concomitant increased CO 2 production, resulting in respiratory acidosis (stage IV). In severe forms, metabolic acidosis develops which can sometimes be attributed to a lactic origin. The explanation of this is still debated; it is probably due to tissue hypoxia, lactate production by respiratory muscles, and/or intracellular alkalosis.
Hypoxemia and hypercapnia account for cyanosis, diaphoresis, tachycardia, unconsciousness, and coma. Clinical signs
Clinical signs are derived from the pathophysiological changes following bronchial obstruction ( Fig, 4).
The patient experiencing a severe asthma attack remains seated, avoids speaking, and is dyspneic with profuse diaphoresis and cyanosis. The respiratory rate is increased (above 30 breaths/min). Prolonged and active expiration is covered by musical wheezes. The patient breathes with effort, using accessory muscles. Contraction of the sternocleidomastoid muscle, tracheal tug, and inward movement of the thoracic cage during inspiration may be noted. With fatigue, there may appear a paradoxical respiration, bradypnea, and respiratory pauses. These signs or the appearance of a silent chest indicate imminent respiratory arrest. Complications such as pneumothorax or pneumomediastinum may occur any time.
The cardiopulmonary interaction promotes first a tachycardia in an attempt to maintain cardiac output despite reduced preload. A heart rate above 120 beats/min and pulsus paradoxus are severity criteria. Hypotension with more severe tachycardia and/or arrhythmias appear in more compromised stages. Cardiocirculatory collapse and shock are warning signs of impending cardiac or cardiorespiratory arrest, as are altered consciousness or coma reflecting impaired gas exchange.
If, at first sight, the patient is sitting, cyanotic, and sweating, most of the severity signs described above will be present.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.