Hemodynamic effects of Laryngoscopy and TI
Autonomic innervation and response of the airway:
➧ The area of the trachea and pharynx is richly innervated and involves both the parasympathetic and sympathetic nervous systems.
➧ Following the mechanical stimulation of the upper respiratory tract (URT) (i.e. nose, epipharynx, laryngopharynx), the afferents are carried by the glossopharyngeal nerve and from the tracheobronchial tree via the vagus nerve which enhances the activities of the cervical sympathetic afferent fibers resulting in a transient rise in heart rate (HR) and blood pressure (BP).
➧ The lower respiratory tract (LRT) is protected by reflex arcs from both the upper and lower airways. The afferent pathways are comprised of the glossopharyngeal nerves in the oropharynx, superior to the anterior surface of the glottis, and the superior and recurrent laryngeal nerves for the posterior and inferior glottis, whereas the efferent pathway is controlled by the vagus.
➧ Afferent stimuli can therefore trigger cardiac, airway, cerebral, neuromuscular, and adrenal responses.
➧ The hemodynamic responses to orotracheal intubation have two components. The first is the response to laryngoscopy and the second is the response to tracheal intubation (TI).
➧ Tachycardia and hypertension have been reported since 1950 during intubation under light anesthesia as TI causes a reflex increase in sympathetic activity.
➧ The hemodynamic responses are due to reflex sympathoadrenal discharge provoked by epilaryngeal and laryngotracheal stimulation after laryngoscopy and TI, this results in hypertension, tachycardia, arrhythmia, and a change in plasma catecholamine concentrations.
➧ Translaryngeal intubation of the trachea stimulates laryngeal and tracheal receptors, resulting in a marked increase in the elaboration of sympathomimetic amines. This sympathetic stimulation results in tachycardia and a rise in BP.
➧ In normotensive patients, this rise is approximately 20-25 mmHg; it is much greater in hypertensive patients. Nasopharyngeal intubation causes a significant pressor response.
➧ Stimulation of the larynx and trachea by the passage of the tracheal tube, but not direct laryngoscopy, causes a significant increase in this response. Direct stimulation of the trachea appears to be a major cause of the hemodynamic changes associated with TI.
➧ The extent of the reaction is affected by many factors: the technique of laryngoscopy and intubation, and the use of various airway instruments. Laryngoscopy itself is one of the most invasive stimuli during orotracheal intubation.
➧ Many anesthesiologists agree that applying a small force to the patient’s larynx when using a laryngoscope might prevent excessive hyperdynamic responses to orotracheal intubation.
➧ In infants, laryngoscopy and TI often result in bradycardia from vagal stimulation. Administration of anticholinergic agents such as atropine can block this response. In older children or adults, this vagal response is rarely observed. Although bradycardia can develop in up to 10% of patients undergoing TI, the typical result is tachycardia and hypertension, leading to an increase in myocardial oxygen consumption. It has been shown that up to 15% of patients undergoing TI under general anesthesia will have ventricular arrhythmias, with the majority of events occurring at the time of tube insertion, as opposed to at the time of laryngoscopy.
➧ The rise in HR and BP occurs about 14 sec. after the start of direct laryngoscopy and becomes maximal after 30-45 sec. Prolonged intubation time in difficult airways, in addition, induces hypercarbia and decreases anesthetic gas concentration, resulting in tachycardia and hypertension. These responses are usually transient and innocuous.
Cardiac Patients:
➧ In patients with co-existing hypertension or ischemic heart disease, these may be exaggerated or may jeopardize the balance between myocardial oxygen requirements and delivery. In these patients, it is important to minimize the duration of direct laryngoscopy, if possible, to less than 15 sec.
➧ During and immediately following TI associated with tachycardia and hypertension, there is a decrease in the left ventricular ejection fraction (stroke volume/end-diastolic volume). This is particularly marked in patients with coronary artery disease.
➧ Increases in HR may be associated with ST-segment changes that indicate myocardial ischemia.
➧ The cardiovascular response to TI can be problematic if the patient suffers from cardiac disease, cerebrovascular or abdominal-vascular disease in which hypertension may lead to hemorrhage.
Hypertensive Patients:
➧ Hypertensive patients are prone to greater and exaggerated circulatory responses after laryngoscopy and TI, because of long-term persistent vascular hyperreactivity, than normotensive patients. An increase in BP associated with TI is dangerous and may cause complications, including pulmonary edema, heart failure, and cerebrovascular hemorrhage. Therefore, prevention of these pressor responses is of particular importance in hypertensive patients.
Elderly Patients:
➧ Transient tachycardia and hypertension associated with laryngoscopy and TI are probably of little consequence in young healthy patients, but either or both may be hazardous to elderly patients, especially to those with hypertension or myocardial insufficiency. Elderly patients have a high incidence of clinical and occult coronary artery disease, and age is a major risk factor for perioperative cardiac morbidity. This risk may be minimized by the maintenance of a balance between myocardial oxygen supply and demand. Thus, the maintenance of hemodynamic stability during TI is of particular clinical importance in elderly patients with hypertension.
Intracranial Pressure (ICP):
➧ Sympathetic stimulation from TI also increases ICP; this can be harmful in patients with intracranial mass lesions or increased ICP from other pathology. The patient with elevated ICP who has a minimum reserve in intracranial compliance is actually at risk for brain-stem herniation and sudden death during laryngoscopy and TI. Instrumentation of the airway may result in a sudden increase in cerebral blood flow due to increases in cerebral metabolic activity and systemic cardiovascular effects. The normal autoregulation mechanism may not be effective because of disease or because its upper-pressure limit (normally, mean arterial pressure 150 mmHg) may be exceeded. Coughing or bucking will decrease venous return from the head and may increase ICP as well.
Intraocular Pressure (IOP):
➧ The mechanism of IOP rise is secondary to increased sympathetic activity. Adrenergic stimulation causes vaso- and veno-constriction, and an increase in central venous pressure, which has a close relationship with IOP.
➧ In addition, adrenergic stimulation can also produce an acute increase in IOP, by increasing the resistance to the outflow of aqueous humor in trabecular meshwork between the anterior chamber and Schlemm’s canal.
➧ The acute increase in IOP may be dangerous for patients with impending perforation of the eye, perforating eye injuries, and glaucoma.
➧ Control of IOP during ophthalmic surgery or diagnostic tonometry is clinically important, because uncontrolled IOP increases induced by airway manipulation may worsen ocular morbidity or produce misleading results.
Read more ☛ Complications while ETT is in place
Read more ☛ about Traumatic Complications of TI
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