4.1.1 What Are the Physiological Responses to Tracheal Intubation?
The goal of tracheal intubation is to provide a secure, definitive airway. Unfortunately, laryngoscopy and intubation can result in a cascade of physiological and pathophysiological reflex responses. These responses are initiated by stimulation of afferent receptors in the posterior pharynx supplied by the glossopharyngeal and vagus nerves. The central nervous system (CNS), cardiovascular system, and respiratory system all respond predictably to these afferent stimuli, and in selected patients the resultant physiologic manifestations may adversely affect the patients' outcome. Though no data exist to suggest that patient outcomes are altered by attenuating the increases in intracranial pressure (ICP), stimulation of the autonomic nervous system with increases in the heart rate and blood pressure, and stimulation of the upper and lower respiratory tract resulting in increases in airway resistance, in light of the possible adverse effects in a compromised patient, it seems both reasonable and logical to attempt to attenuate these responses.
The CNS responds to airway manipulation by increasing cerebral metabolic oxygen demand (CMRO2) and cerebral blood flow (CBF). If the intracranial compliance is decreased (tight brain), the increase in CBF may increase the ICP further. This response is important in situations in which there is a loss of autoregulation such that blood flow to the brain, or regions of the brain, becomes pressure-passive (ie, increases in blood pressure result in increases in ICP).
Laryngoscopy stimulates protective reflexes and predictably leads to cardiovascular and respiratory system responses mediated by the sympathetic nervous system. In children, this process is believed to be primarily a monosynaptic reflex promoting vagal stimulation of the sinoatrial node, resulting in bradycardia. In adults, a polysynaptic event predominates whereby impulses travel afferently via the 9th and 10th cranial nerves to the brain stem and spinal cord. An efferent sympathetic response results in norepinephrine release from adrenergic nerve terminals, epinephrine release from the adrenal glands, and activation of the renin–angiotensin system leading to tachycardia and hypertension. These responses may be detrimental in patients with myocardial ischemia (tight heart), known intracerebral or aortic aneurysms, major vessel dissection, or those with major vascular injuries. Hypertension may also lead to significant increases in ICP if autoregulation has been lost (eg, acute severe head injury or intracranial hemorrhage).
The respiratory system may respond in three important ways to laryngoscopy and intubation: activation of the upper airway reflexes leading to laryngospasm; coughing; and bronchospasm (tight lungs). Laryngospasm, a forceful involuntary spasm of the laryngeal musculature, may produce difficulty with intubation as well as ventilation. Persistent and life-threatening laryngospasm is treated with a gentle continuous positive airway pressure with 100% oxygen, intravenous lidocaine (1.5 mg·kg−1), or if persistent, neuromuscular blockade (eg, succinylcholine at 10% of the intubating dose). Negative intrathoracic pressure created by inspiration attempts against a closed glottis (laryngospasm) may result in negative pressure pulmonary edema (see Chapter 58).