Airway Devices and Anesthetics Impact on Hemodynamic Responses during Intubation, Resúmenes de Medicina

¡Descarga Airway Devices and Anesthetics Impact on Hemodynamic Responses during Intubation y más Resúmenes en PDF de Medicina solo en Docsity! Chapter 7 Physiologic and Pathophysiologie Responses to Intubation AARON M. JOFFE | STEVEN A. DEEM . Background . Cardiovascular Responses During Airway Monipulation Cardiovascular Reflexes E Intubation in the Presence of Cardiovascular Disease C. Implications for Patients with D, Neurovascular Disease Intubation in Patients with Neuropathologic Disorders E. Neuromuscular Blocking Drugs and Cardiovascular Responses F. Cardiopulmonary Consequences of Positive-Pressure Ventilation Prevention of Cardiovascular Responses A. Technical Considerations: Minimizing Stimulation of Airway Proprioceptors Topical and Regional Anesthesia Inhalational Anesthetics Intravenous Agents Nonanesthetic Adjuvant Agents IV. Airway Effects of Endotracheal Intubation A. Upper Airway Reflexes B. Dead Space mOoOw l. BACKGROUND Laryngoscopy, endotracheal intubation, and other airway manipulations (e.g., placement of a nasopharyngeal or oropharyngeal supralaryngeal airway) are noxious stimuli that may induce profound changes in cardiovas- cular physiology, primarily through reflex responses. Although these responses may be of short duration and of little consequence in healthy individuals, serious complications can occur in patients with underlying coro- nary artery disease,'? reactive airways,** or intracranial neuropathology.>* 184 Upper Airway Resistance Lower Airway Resistance Endotracheal Tube Resistance and Exhalation F. Functional Residual Capacity 6. Cough H. Humidification of Gases mouO V. Control and Treatment of the Respiratory Responses to Airway Instrumentation A. Preventing Upper Airway Responses cal Considerations: Minimizing cal Anesthesia 3 intra wenous Agents B. Preventing Bronchoconstriction lerations: Minimizing A Anesthesia Agents ETS MI. Conclusions VII. Clinical Pearls II. CARDIOVASCULAR RESPONSES DURING AIRWAY MANIPULATION A. Cardiovascular Reflexes The cardiovascular responses to noxious airway manipu- lation are initiated by proprioceptors responding to tissue irritation in the supraglottic region and in the trachea.” Located in close proximity to the airway mucosa, these proprioceptors consist of mechanoreceptors with small- diameter myelinated fibers, slowly-adapting stretch receptors with large-diameter myelinated fibers, and polymodal endings of nonmyelinated nerve fibers.* (The CHAPTER 7 Physiologic and Pathophysiologic Responses to Intubation | 185 superficial location of these proprioceptors and their nerves explains why topical local anesthesia of the airway is such an effective means of blunting cardiovascular responses to airway interventions.) The glossopharyngeal and vagal afferent nerves transmit these impulses to the brainstem, which, in turn, causes widespread autonomic activation through the sympathetic and parasympathetic nervous systems. Bradycardia, often elicited in infants and small children during laryngoscopy or intubation, is the autonomic equivalent of the laryngospasm response. Although seen only rarely in adults, this reflex results from an increase in vagal tone at the sinoatrial node and is virtually a monosynaptic response to a noxious stimu- lus in the airway. In adults and adolescents, the more common response to airway manipulation is hypertension (HTN) and tachycardia mediated by the cardioaccelerator nerves and sympathetic chain ganglia. This response includes wide- spread release of norepinephrine from adrenergic nerve terminals and secretion of epinephrine from the adrenal medulla.? Some of the hypertensive response to endotra- cheal intubation also results from activation of the renin- angiotensin system, including release of renin from the renal juxtaglomerular apparatus, which is innervated by P-adrenergic nerve terminals. In addition to activation of the autonomic nervous system, laryngoscopy and endotracheal intubation result in stimulation of the central nervous system, as evidenced by increases in electroencephalographic (EEG) activity, cerebral metabolic rate, and cerebral blood flow (CBF).'” In patients with compromised intracranial compliance, the increase in CBF may result in elevated intracranial pressure (ICP), which, in turn, may result in herniation of brain contents and severe neurologic compromise. The effects of endotracheal intubation on the pul- monary vasculature are probably less well understood than the responses elicited in the systemic circulation. They are often coupled with changes in airway reactiv- ity associated with intubation. Acute bronchospasm or a main stem bronchial intubation results in a marked maldistribution of perfusion to poorly ventilated lung units, causing desaturation of pulmonary venous blood and subsequent reduction in systemic arterial oxygen (O») tension. In addition, institution of positive end- expiratory pressure (PEEP) after endotracheal intuba- tion causes a reduction in cardiac output related to impaired venous return to the left side of the heart from the pulmonary circulation. The impact of these changes can be profound in patients with severely com- promised myocardial function or intravascular volume depletion. B. Intubation in the Presence of Cardiovascular Disease Myocardial ischemia results when there is an imbalance between myocardial O, supply and demand. In the pres- ence of a stable O, content of whole blood (the product of hemoglobin concentration and saturation, with a minor contribution from dissolved O»), the myocardial O, supply is almost entirely determined by coronary blood flow and distribution, because O, extraction at the cellular level is at or near maximum even under resting conditions. The chief components on the demand side of the myocardial O, balance equation are beat frequency or heart rate (HR) and myocardial wall tension. Of the two, increases in HR are of greatest concern, because cardiac inotropism (contractility) subserves cardiac chronotro- pism (rate). Not only does tachycardia increase myocar- dial O, consumption per minute at constant wall tension, but elevations in rate effectively reduce the diastolic period. Because full diastolic relaxation may be impaired, a subsequent increase in resting wall tension will impair subendocardial blood flow, thereby reducing myocardial O, supply. Concomitantly, the rate of intraventricular pressure development in systole (dP/dT), a measure of myocardial contractility and another determinant of myocardial O, demand, will also increase. It follows, then, that neuroendocrine responses to airway manipulation resulting in tachycardia and HTN may result in a variety of complications in patients with cardiac disease, myocardial ischemia chief among them. This set of circumstances is responsible for episodes of ischemic electrocardiographic STsegment depression and increased pulmonary artery diastolic blood pressure (BP) that may be seen when intubation is performed in patients with arteriosclerosis; occasionally, these episodes presage the occurrence of a perioperative myocardial infarction? However, short ischemic episodes (<10 minutes) evidenced by electrocardiographic ST-segment depression, such as those that may be experienced only during airway manipulation, have not been shown to correlate with postoperative myocardial infarction. In contrast, ST-segment changes of a single duration lasting longer than 20 minutes (mean SD 20 + 30 minutes) or cumulative durations of longer than 1 hour (mean SD 1 +2 hours) do seem to be an important factor associated with adverse perioperative cardiac outcomes.!!*? Patients with aneurysmal disease of the cerebral and aortic circulation may also be at particular risk of com- plications related to a sudden increase in BP during airway instrumentation. Laplace's law defines the trans- mural wall tension of a blood vessel (the determinant of its likelihood of rupture) as the product of the pressure inside the vessel and its radius divided by the wall thick- ness. The presence of a thin-walled vascular aneurysm (higher transmural wall tension at baseline) combined with a sudden increase in intraluminal pressure can lead to rupture of the affected vessel and abrupt deterioration in the patient's status. Leaking aortic aneurysms are par- tially tamponaded by intra-abdominal pressure but can suddenly expand into the retroperitoneal space during arterial HTN. The results are significant blood loss and additional technical problems for the surgeon trying to resect the lesion and insert a vascular prosthesis. C. Implications for Patients with Neurovascular Disease Intracranial aneurysms and arteriovenous malformations (AVMs) often arise with a small “sentinel” hemorrhage that serves as a warning of worse things to come. During subsequent periods of elevated arterial BP, these lesions 188 PART 1 Basic Clinical Science Considerations 35.0 30.0 25.0 20.0 15.0 10.0 5.0 0.0 =5.0 10.0 15.0 10.0 5.0 0.0 5.0 10.0 15.0 20.0 25.0 30.0 35.0 Change in HR (%) Change in MAP (%) BL INDINT 11 2 3 4” 5 Intubation time course (min) Airway scope =4= GlideScope -9- Macintosh *=P<0.05 ** = P<0.01 Intubation time course (min) Figure 7-2. Percentage change from baseline in heart rate (HR, lef) and mean arterial pressure (MAP, right) associated with endotracheal infubation using an Alway Scope, GlideScope, or Macintosh laryngoscope. Data values are presented as mean + standard error. *P < 0.05 compared to Macintosh group. **P < 0.01 compared to Macintosh group. BL Baseline; IND, 1 minute after induction; INT, at intubation; 1” through $, minutes after endotracheal intubation. (| way scope, less effective than systemic administration of lidocaine. During general anesthesia, rigid laryngoscopy and instil- lation of lidocaine solution initiate the same adverse reflexes caused by placement of an ETT (Fig. 7-3).7 Furthermore, a laryngotracheal spray of lidocaine solu- tion may, in itself, produce profound cardiovascular —> < Larngoscopy and intubation Lidocaine 40 3 8 MAP (% change from control) 3 $ Mean +SE «=P< 05 vs Control += P< 05 vs IV Lidocaine Time (min) Figure 7-3. Mean arterial pressure (MAP) response to endotracheal intubation after either Intravenous (1) or intratracheal (LTA) lidocaine instillation. (+: r DC, 1 Tsai P, Chen B: Her al intut paring the stimulation in adults, and in children it may produce the same sort of bradycardic response associated with endo- tracheal intubation.** If topical lidocaine is administered to the upper airway, there should be an intervening period of at least 2 minutes to allow initiation of anes- thetic effect before airway instrumentation begins. Excellent topical anesthesia of the airway obtained before awake flexible fiberoptic intubation was respon- sible for reports suggesting that there was less cardiovas- cular stimulation after this procedure than after intubation with a rigid laryngoscope.”” Later studies performed with patients under general anesthesia demonstrated no differ- ence between the two modes of intubation with regard to hemodynamic impact, probably because the more pro- found stimulus results from placement of the ETT below the level of the glottis.*!** Increasing the concentration of lidocaine used, and thus the total dose, also does not appear to mitigate this effect, although it may improve intubating conditions during awake flexible fiberoptic intubation.***” Although both 2% and 4% lidocaine administered through an epi- dural catheter in the working channel of the flexible fiberoptic bronchoscope by a “spray-as-you-go” technique provided similar intubating conditions and hemodynamic profiles, the former resulted in a smaller overall dose, lower plasma levels, and therefore less chance for toxicity reactions.*” Lower concentrations of lidocaine (1%) pro- vided lower plasma levels and similar hemodynamics but appeared to provide less optimal intubating conditions than atomized 2% lidocaine when used for topical anes- thesia before airway manipulation.* In contrast to topical anesthesia of the airway, which appears to provide inconsistent benefit, regional nerve blocks involving the sensory pathways from the airway prevent hemodynamic responses to intubation. The supe- rior laryngeal nerve (SLN) innervates the superior surface of the larynx, and the glossopharyngeal nerve innervates the oropharynx. Depositing local anesthetic on each CHAPTER 7 Physiologic and Pathophysiologic Responses to Intubation 189 cornu of the hyoid bone can block the SLN. Blockade of the glossopharyngeal nerve at the tonsillar pillars (sensory distribution above the level of the epiglottis) potentiates this effect by decreasing the stimulus of laryngoscopy.*” The inferior surfaces of the larynx and trachea require topical anesthesia, however, because they are innervated by the recurrent laryngeal nerve and the vagus, which cannot be directly blocked. With the preceding combina- tion, awake patients exhibit little response as the ETT is inserted. Instillation of lidocaine via an ETT to prevent altera- tions in cerebrovascular hemodynamics in patients with severe head injury may be of some benefit. A dose of 1.7 mg/kg lidocaine instilled at body temperature given slowly (1 mL/sec) through a fine tube advanced to the end of the ETT but not in contact with the tracheal mucosa was reported to be efficacious in half of the patients treated.** C. Inhalational Anesthetics Defining the anesthetic dose requirement for effectively blocking (or even blunting) hemodynamic and ICP responses to endotracheal intubation has remained an elusive goal. Airway maneuvers are typically brief inter- ventions that produce short-lived responses during a dynamic perioperative period, with drug concentrations rapidly fluctuating both in blood and at effect sites. Agents that are capable of preventing responses may also produce profound cardiovascular depression before and after the stimulation of endotracheal intubation. Accord- ingly, there are relatively few well-controlled dose- response studies, and those that are available often give information that is not useful for the clinical anesthesiologist. For inhalational anesthetics, endotracheal intubation using doses in the range of the minimum alveolar con- centration (1 MAC) resulted in marked cardiovascular stimulation during anesthesia with nitrous oxide (N¿0) supplemented with either halothane or morphine.*” It should not be surprising that 1 MAC is insufficient, because it is known that approximately 1.5 to 1.6 MAC is needed to block the adrenergic and cardiovascular responses to a simple surgical skin incision (MAC- BAR)" The dose of anesthetic required to prevent coughing during endotracheal intubation with sevoflu- rane may exceed MAC by a factor of 2.86 in adults,” although this factor appears to be close to 1.3 in children.” Accordingly, it appears that the dose of volatile anes- thetic required to block the cardiovascular response to endotracheal intubation must be inordinately high, result- ing in profound cardiovascular depression before endo- tracheal intubation.** From a cerebrovascular viewpoint, this approach is totally impractical, because high doses of volatile anesthetics cause cerebral vasodilation and marked increases in ICP in patients with compromised intracranial compliance. Furthermore, from a cardiovas- cular point of view, the arterial hypotension and reduced cerebral perfusion pressure before intubation would be entirely unacceptable for patients with cerebrovascular disease or brain injury. D. Intravenous Agents Propofol, barbiturates, and benzodiazepines are all associ- ated with profound hypotension at doses that suppress the hemodynamic and ICP responses to intubation.*+?* In the case of etomidate, the effective dose for blocking the cardiovascular response to intubation can be identi- fied by a burst-suppression pattern on the cortical surface EEG, indicating fairly deep cerebral depression.” Because etomidate supports BP at such deep levels of anesthesia, itis probably the only contemporary agent that, by itself, can achieve suppression of cardiovascular responses without first producing undue arterial hypotension and compromise of coronary and cerebral perfusion. Because it is clinically impractical to achieve sufficient anesthetic depth for preventing a hyperdynamic response to intubation solely with an intravenous (IV) or inhala- tional agent (etomidate excepted), a wide variety of anes- thetic drug combinations, adjuvants, or both have been used in attempts to potentiate anesthetic effects while minimizing hemodynamic depression. Opioids are the adjuvants most commonly adminis- tered in addition to other IV or inhaled agents to facili- tate induction of anesthesia and subsequent airway manipulation. Their use in this capacity relates to their historical use as part of a N¿O-narcotic anesthetic often used in patients with marginal cardiac reserve. For example, Bennet and Stanley compared the cardiovascu- lar responses after administration of N20O-morphine 0.4 mg/kg versus N20O-fentanyl 4 ug/kg 10 minutes before intubation. The HR, cardiac output, and systolic and mean BP were reduced compared to baseline and remained unaffected by intubation in the N¿O-fentanyl group, but these parameters were all significantly elevated compared with preanesthetic controls in the N20- morphine group.” Whereas the assumed potency of fen- tanyl in this study was 100 times that of morphine, the lack of effect of morphine suggests that, with respect to suppression of pressor responses to laryngotracheal manipulation, fentanyl is more than 100 times as potent. As reported by Bennett and Stanley” and later by other investigators,”? fentanyl may not achieve its peak central nervous system effect until 10 minutes after bolus IV injection. Fentanyl appears to provide blunting of hemodynamic responses in a graded manner: 2 1g/kg IV given several minutes before induction only partially prevented HTN and tachycardia during an RSI with thiopental and succinylcholine. In this situation, 6 ug/kg was considerably more effective. Chen and coworkers reported almost complete suppression of hemodynamic response to intubation with both 11 and 15 hg/kg of IV fentanyl, whereas higher TV doses (30 to 75 1g/kg) allowed only a very occasional response to intubation.** In doses that prevent hemodynamic response to intu- bation, however, fentanyl is not a short-acting agent, and the risk of prolonged postoperative respiratory depression must be weighed against the advantages of perioperative cardiovascular stability. With this risk in mind, it has been observed that pretreatment with 2 g/kg IV fentanyl given 10 minutes before intubation during an infusion of propofol sufficient to reduce the Bispectral Index Score to 45 prevented a significant increase in HR or BP 190 | PARTI Basic Clinical Science Considerations compared with awake preanesthetic values.” Similar results were observed when intubation was performed after administration of fentanyl, 2 1g/kg, and propofol bolus doses of 2.0 to 3.5 mg/kg.'” Fentanyl and propofol require 6.4 and 2.9 minutes, respectively, to achieve effect-site equilibrium after IV bolus administration.'” Therefore, the common practice of administering 1 to 2 mL (50 to 100 ug) just before or almost simultaneously with other induction medications would not be expected to have any effect based on inad- equate dose and inappropriate timing of administration. Rather, this may provide a more plausible explanation for hypotension during the minutes-long quiescent period between endotracheal intubation and actual surgical inci- sion. It is strongly recommended that laryngoscopy and intubation be timed to coincide with the peak effect of these agents. Opioids with shorter onset and offset times have some advantages over fentanyl for modulating circulatory responses to intubation. Alfentanil has a smaller steady- state distribution volume and shorter terminal elimina- tion half-life than fentanyl.? Ausems and colleagues demonstrated that an alfentanil plasma concentration of 600 ng/mL effectively prevented hemodynamicresponses to intubation during induction of N20 anesthesia.” This was achieved by a 30-second infusion of alfentanil at 150 u1g/kg. During this induction period, N20 and suc- cinylcholine were also administered. Only 5 of the 35 patients studied sustained an increase in HR or BP greater than 15% above preinduction values. Remifentanil has been found to be highly effective in preventing hemodynamic responses to intubation, albeit always with the cost of impressive bradycardia or hypo- tension, or both, before and after airway manipulation.** Many studies have used vagolytic agents to avoid brady- cardia, at the risk of an elevated HR response after intu- bation. Remifentanil's half-time for equilibration between blood and effect site is 1.3 minutes,” and it has a brief half-life of 3 to 5 minutes due to hydrolysis by tissue and blood esterases.*” Typical remifentanil infusion rates used for blunting hemodynamic responses are 0.25 to 1.0 ug/ kg/min in association with cautious propofol administra- tion and nondepolarizing neuromuscular blockade.*” For RSI with thiopental and succinylcholine, the optimal dose of remifentanil appears to be 1.0 ug/kg adminis- tered over 30 seconds, with laryngoscopy performed 1 minute after induction. A bolus dose of 1.25 Lig/kg was associated with unsatisfactory bradycardia, whereas 0.5 18/kg resulted in excessive cardiovascular stimula- tion.* This dosing recommendation is supported by another report that found remifentanil 1 g/kg given over 30 seconds, followed by thiopental 5 mg/kg and rocuronium 1 mg/kg 100 seconds later, was more effec- tive than lidocaine and esmolol in attenuating the hemo- dynamic response to RSI.” IV lidocaine may also blunt hemodynamic and cere- brovascular responses to intubation. When given in a bolus of 1.5 mg/kg IV, it adds approximately 0.3 MAC of anesthetic potency.”” Significant reductions in hemo- dynamic response to endotracheal intubation have been noted when lidocaine (3 mg/kg) was used as an adjunct to high-dose fentanyl anesthesia,”! as well as during other light anesthetic techniques, such as thiopental-N30-0».? However, smaller doses of lidocaine (1.5 mg/kg) have not been consistently reported to be effective in reducing the hemodynamic response to laryngoscopy and endotra- cheal intubation.”?”* The general anesthetic properties of lidocaine tend to reduce cerebral metabolic rate for Oz and CBE, thus lowering ICP in patients with compromised intracranial compliance.”* Theoretically, these properties of lidocaine might be exploited to mitigate rises in ICP during airway manipulation in those patients with acute intracranial pathology or compromised intracranial compliance. However, only a single human study has been reported specifically evaluating the ability of IV lidocaine to blunt intubation-related elevations in ICP. Bedford and col- leagues compared 1.5 mg/kg IV lidocaine with placebo in 20 patients diagnosed with brain tumor. When admin- istered 2 minutes before intubation, lidocaine failed to prevent a rise in ICP from the preanesthesia baseline, although the increase was more modest than that observed with the placebo (-12.1 mm Hg; 95% confidence inter- val, -22.8 to —1.4 mm Hg; P = 0.03). This dearth of direct benefit was underscored by a systematic review that also failed to identify any evidence that pretreatment with IV lidocaine before RSI consistently reduced ICP or positively affected neurologic outcome.” This review is now more than a decade old, but because no new direct evidence has been published in the interim, its conclusion remains valid. With regard to the patient at risk for intracranial H'TN, it is important that agents used to control cardiovascular responses to intubation also have a minimal adverse impact on ICP. Agents that act as cerebral vasodilators, such as volatile anesthetics, nitroglycerin, nitroprusside, or hydralazine, are generally avoided if there is a serious risk of intracranial HTN. E. Nonanesthetic Adjuvant Agents A final means for modifying the cardiovascular responses to endotracheal intubation is prophylactic administration of vasoactive substances that directly affect the cardio- vascular system. This approach was introduced in 1960 by DeVault and associates, who found that pretreatment with phentolamine, 5 mg IV, prevented the hypertensive- tachycardic response to endotracheal intubation during « a light barbiturate-succinylcholine anesthetic technique.”* Since then, a large number of articles have appeared advocating. the use of various vasodilators and adren- ergic blocking agents as pretreatment before endotra- cheal intubation, including diltiazem, verapamil, and nicardipine””*?; hydralazine”; nitroprusside**; nitroglyc- erin**; labetalol*; esmolol**97%%; and clonidine% Virtu- ally all of these agents appear to be somewhat effective when compared to placebo, particularly when used in high doses. Esmolol is the best studied of the group. In a large, multicenter, placebo-controlled trial, esmolol at doses of 100 or 200 mg suppressed the hemodynamic response to endotracheal intubation, particularly when combined with a moderate-dose opiate.*” However, esmolol doses of 200 mg were associated with a doubling of the CHAPTER 7 Physiologic and Pathophysiologic Responses to Intubation | 193 CONTROL INTUBATION 100 Y 4 c Pressure (om H20) 3 , y Flow (Usec) VaoooS pass y T T T T T T B 1 2 3 B Time (sec) » (7) Figure 7-5 Pressure and fiow curves (abeled A and B respectively) generated during a burst of three successive coughs (C) by a vol unteer before (control) and after endotracheal intubation. Notice Ihathe fows nd pressres generotedare oriy modestiy cinta after intubation. (Hom E | intut ler agonist (albuterol) or an inhaled anticholinergic agent (ipratropium bromide), measured airway resistance after intubation was markedly lower compared with placebo treatment (Fig. 7-6). Increases in airway resistance may result from changes in intrinsic smooth muscle tone, airway edema, or intra- luminal secretions. These factors are, in turn, controlled by a series of intracellular and extracellular events, 16 sa EPlacebo Hipratropium [E Albuterol 12 10 Ru (cm H2O+L-Tesec”1) o onao 2 5 15 Time postintubation (min) Figure 7-6 Lung resistance (R)at 2. 5, and 15 minutes after Intuba- tion in patients pretreated with either a placebo, the f-adrenergic agonist albuterol, or the anticholinergic drug ipratroplum bromide. Each of the drugs markediy diminished lung resistance for longer than 15 minutes ato endotracheal intubation under thiopentat- narcotic anesthesia. including neural and hormonal factors. Rapid changes in airway caliber after airway instrumentation are thought to result largely from parasympathetic nervous system activation of airway smooth muscle.!!*!1* Cholinergic innervation predominates in the larger central airways, with efferent nerves arising in the vagal nuclei of the brain stem and synapsing with ganglia in the airway walls. Postganglionic parasympathetic nerves release acetylcho- line, activating muscarinic receptors on airway smooth muscle that lead to smooth muscle constriction. Such responses can be blocked via muscarinic blockade, using either systemic or inhaled anticholinergic agents. Endotracheal intubation also may induce broncho- spasm by causing coughing. A cough reduces lung volume, which in turn markedly increases bronchoconstriction in response to a stimulus.'”” In the patient with known reac- tive airways, prevention of coughing at the time of endo- tracheal intubation by use of either a deep level of anesthetic or a muscle relaxant may help to minimize the likelihood of bronchospasm. E. Endotracheal Tube Resistance and Exhalation In normal patients breathing at moderately elevated minute ventilation, exhalation is usually completed well before the next inhalation begins. By contrast, patients with obstructive airways disease may not complete full exhalation before the start of the next inhalation. In other words, inhalation begins before exhalation to functional residual capacity (FRC), resulting in persistent positive pressure in the alveoli. This phenomenon has been called auto-PEEP or dynamic hyperinflation, and it results in air trapping, elevated intrathoracic pressure, and hemody- namic compromise.!** Auto-PEEP most commonly occurs in patients with obstructive lung disease and high minute ventilation, but it may also rarely occur in patients with relatively normal airways who are ventilated at very high minute ventila- tion. This has been observed in patients with burns or sepsis, who may require as much as 30 to 40 L of minute ventilation. Under these circumstances, the resistance of the ETT may limit expiratory flow so that full exhalation does not occur. This has been demonstrated experimen- tally, with the magnitude of the auto-PEEP correlating directly with the resistance ofthe ETT.''” Among patients under anesthesia, major resistance to exhalation caused by the ETT is of no consequence in routine cases and is only rarely seen in critically ill patients. However, low levels of auto-PEEP due to tube resistance probably occur frequently in patients with high minute ventila- tion'*% and during single-lung ventilation via a double- lumen ETT. F. Functional Residual Capacity The effect of endotracheal intubation on FRC has been a subject of considerable controversy. Intensivists are well aware of patients recovering from respiratory failure in whom oxygenation improved after extubation. The improvement has been attributed to “physiologic PEEP"— the presumption that a small positive pressure is 194 | PARTI Basic Clinical Science Considerations normally created by the glottis and that this leads to breathing at a higher lung volume. The assumption is that an ETT removes the glottic barrier and may, therefore, lower lung volume. However, the existence of positive intratracheal pressure has never been documented, and in a study of volunteers who underwent awake intuba- tion, no consistent changein FRC could be measured. 2012 By contrast, a different conclusion was reached in a series of patients who were studied just before and after extubation following recovery from respiratory failure. In this situation, both FRC and arterial oxygen tension (PaO,) were found to increase after extubation, support- ing the concept that the presence of an ETT decreases FRC.'? Resolution of these disparate results was sug- gested by a rabbit study in which normal rabbits did not demonstrate a difference in oxygenation or tracheal pres- sure after intubation, but after respiratory failure was induced, endotracheal intubation worsened oxygen- ation.!'? These results suggest that the rabbits compen- sated for respiratory failure by using glottic closure to maintain a positive intratracheal pressure and that the effect of an ETT on FRC depends on that underlying respiratory state. G. Cough Although it is widely recognized that cough efficiency is reduced whenever an ETT is in place, it is a common observation that a disconnected ETT is likely to produce a plug of sputum whenever the patient is stimulated to cough. In awake intubation volunteers, peak airway flow was reduced but was still adequate to enable secretion clearance.!'* However, the ETT prevented collapse of the trachea by acting as a stent. Therefore, although secre- tions could be moved to the central airways, the ETT prevented maximum efficiency of expectoration. Large airway collapse is important for producing maximum force against secretions, and this explains why moving secretions from the trachea out through the ETT often requires the use of a suction catheter. Under normal circumstances, the upper airway warms, humidifies, and filters 7000 to 10,000 L of inspired air daily, adding up to 1 L of moisture to the gases. When the upper airway is bypassed by intubation, the gas must be warmed and humidified in the trachea if it is not adequately humidified before inhalation. In an anesthe- tized patient breathing dry gases, up to 10% of the average metabolic rate may be required to perform these tasks.!2 Delivery of cool, dry gases may also have a significant effect on mucociliary transport, a critical defense mecha- nism of the respiratory tract. Inhalation of unconditioned gas rapidly leads to abnormal mucosal ciliary motion, with subsequent encrustation and inspissation of tracheal secretions.!**12" These changes occur as early as 30 minutes after intubation and, theoretically, may lead to an increase in postoperative complications in patients with limited chest excursion. Accordingly, assurance of adequate gas conditioning should be standard in all but very brief endotracheal intubations. V. CONTROL AND TREATMENT OF THE RESPIRATORY RESPONSES TO AIRWAY INSTRUMENTATION A. Preventing Upper Airway Responses Cough and laryngospasm in response to intubation appear to be sound protective reflexes. Under most circum- stances, the body needs to prevent further intrusion by a foreign body and to expel it from the airway. However, these responses can be troublesome during induction of anesthesia or at the time of extubation. Cough can lead to bronchospasm as lung volume is reduced, and it can also result in desaturation as the lung volume drops to residual volume. Laryngospasm may result in life- threatening abnormalities of blood gases. Consequently, anesthesiologists routinely try to prevent these responses with the use of medications delivered topically, via inha- lation, or intravenously. Inhibition of upper airway reflexes can certainly be accomplished by performing endotracheal intubation after the administration of NMB agents. However, both laryngeal and tracheal reflexes are difficult to inhibit by deep levels of general anesthesia alone.'* When circum- stances preclude the use of NMB agents, the clinician must give consideration to how best to prevent discom- fort, gagging, coughing, and laryngospasm during endo- tracheal intubation: avoidance of endotracheal intubation, use of regional and topical anesthesia, very deep general anesthesia, or a combination of all modalities. 1. Technical Considerations: Minimizing Airway Stimulation Although placement of an LMA is likely to be less noxious than direct laryngoscopy and endotracheal intu- bation, it remains a highly stimulating procedure. For example, Scanlon and colleagues found a 60% incidence of gagging, a 30% incidence of laryngospasm, and a 19% incidence of coughing when the LMA was placed after induction with thiopental 5 mg/kg.” Induction with propofol 2.5 mg/kg reduced these events by two thirds but did not ablate them. Therefore, instrumentation of the upper airway by any technique will illicit protective reflexes that must be obtunded with local or general anesthesia (or both). 2. Regional and Topical Anesthesia The surfaces of the mouth and nose are easily anesthe- tized with topical anesthetic sprays or gels. Lidocaine is equally effective as cocaine and less toxic; it can be com- bined with a vasoconstrictor to give equivalent intubating conditions.!**!% Administration of an antisialagogue 30 to 60 minutes before application of the topical anesthetic results in better anesthesia as well as better intubating conditions. The lack of secretions probably minimizes dilution of the applied anesthetic and also results in better intubating conditions. The mouth and pharynx derive their sensory innerva- tion from the trigeminal and glossopharyngeal nerves. The supraglottic larynx derives its sensory innervation from the SLN, a branch of the vagus, and intubation can be facilitated by blocking it bilaterally.!'** The nerve block CHAPTER 7 Physiologic and Pathophysiologic Responses to Intubation 195 relies on the consistent relationship of the SLN to the lateral horns of the hyoid bone. When combined with topical anesthesia of the nose or mouth and adequate anesthesia of the infraglottic larynx, the nerve block pro- vides excellent intubating conditions, and most patients are able to accept an ETT without cough, gag, or laryn- gospasm. Equal success in blunting upper airway reflexes can be achieved by careful spraying of the larynx with topical anesthesia. A nasal trumpet helps ensure that solution reaches the larynx. Topical anesthesia spares the patient the need for two injections. The infraglottic larynx derives sensory innervation from the recurrent laryngeal nerves, which run along the posterolateral surfaces of the trachea. Again, topical anes- thesia rather than nerve block is the method of choice for obtunding reflexes. Injection of several milliliters of 4% lidocaine via the cricothyroid membrane routinely results in excellent blockade of sensation. The efficacy of topical and nerve block anesthesia at suppressing airway reflexes during intubation is evident. Several studies have documented that topical anesthesia applied preoperatively (for brief cases) or intraopera- tively can suppress cough and laryngospasm at the time of extubation.'** A randomized study of patients under- going tonsillectomy found that the incidence of stridor or laryngospasm at the time of extubation could be reduced from 12% to 3% by application of topical lido- caine at the time of intubation.*** The LITA endotracheal tube (Laryngotracheal Instillation of Topical Anesthetic, Sheridan Corporation, Argyle, NY) contains a small channel that can be used to spray the upper airway while an ETT is in place. When this method was used to spray the ETT before extubation, coughs were reduced by more than 60%, and the severity of the coughing was decreased.'* The use of liquid, in the form of a lidocaine-bicarbonate mixture, rather than air to inflate the cuff of the ETT after intubation has also been reported to be effective in diminishing emergence phenomena.!*”*% Inflating the ETT cuff with 40 mg of lidocaine (2 mL of 2% solution) and then adding 3 to 7 mL of 8.4% sodium bicarbonate (NaHCO») until no cuff leak was present resulted in significant reductions in coughing, restlessness, and BP during emergence. In addition, sore throat complaints assessed at 15 minutes and at 1, 2, 3, and 24 hours post- operatively; postoperative dysphonia; and hoarseness after extubation were all reduced when compared to cuff inflation with air. When this technique was used, more than 50% of the original 40 mg of lidocaine still remained in solution at 2 hours after inflation of the cuff, and only about 75% was released even after 6 hours of surgery (Fig. 7-7). Because standard 8.4% NaHCO) is a basic solu- tion with a calculated pH of 7.8 (range 7 to 8.5), the addition of more than 2 mL of bicarbonate to the 2 mL of 2% lidocaine (calculated pH 6, range 5 to 7) already injected into the ETT cuff results in a solution with a pH 7.95 to 8.09; this leads to concern about tracheal mucosal damage from flash burn injury in the event of a cuff rupture. However, a direct comparison between solutions of2 mL of 2% lidocaine with 8.4% versus 1.4% bicarbon- ate reported similar efficacy in reducing postoperative sore throat complaints and the occurrence of various 75 Percent released 25 o 60 120 180 240 300 360 Time (min) Figure 7-7 Percentage of lidocaine released in vitro as a function of time from an endotracheal tube (ETT) cuff filled with 40 mg lidocaine hydrochloride and additional 8.4% sodium bicarbonate solutlon equal to 0, 3 4,5, 6, or 7 mL. (From Es: JP, 2002) emergence phenomena.!* Therefore, in actual clinical practice, a favorable risk-benefit balance can be achieved by using the following combination in a 10-mL syringe: 5 mL 1% lidocaine, 1 mL 8.4% NaHCO, solution, and 4 to 5 mL of sterile diluent (J.P. Estebe, personal commu- nication, 2010). 3. Intravenous Agents Given a high enough dose, virtually all agents used as IV anesthetics will suppress the cough response to intuba- tion. However, different agents appear to vary in their ability to inhibit upper airway reflexes when judged on the basis of equal potency in depressing consciousness and in depressing the cardiovascular system. Propofol/ narcotic anesthesia may be adequate for intubating the trachea in some patients even without the use of muscle relaxants.'* On the other hand, ketamine clinically appears to enhance laryngeal reflexes at doses that provide adequate anesthesia for surgery. IV lidocaine is frequently used to prevent cough and laryngospasm at the time of intubation or extubation. Although the studies are not uniform in documenting efficacy, the preponderance of evidence supports the use of lidocaine.'*”!* Studies that did not document efficacy are sometimes flawed by the lack of documentation that adequate serum levels were reached. The maximal eff- cacy of IV lidocaine occurs 1 to 3 minutes after injection and requires a dose of 1.5 mg/kg or more. This corre- sponded to a plasma level in excess of 4 1g/mL. The ability of IV lidocaine to suppress cough appears to be related to factors beyond induction of general anes- thesia, because cough suppression occurs at levels rou- tinely seen in awake patients being treated with the drug. 198 | PARTI Basic Clinical Science Considerations 5. Choice of Neuromuscular Blocking Drug The choice of muscle relaxants can influence bronchial tone after endotracheal intubation. Rapacuronium was withdrawn from the market after a number of reports of severe bronchospasm, most likely due to antagonism at the M) receptor.'*" Mivacurium releases significant amounts of histamine and leads to mast cell degranulation; it should be used extremely cautiously, if at all, in patients with a history of atopy or asthma.'*” Studies in France and Norway have suggested a high incidence of anaphylaxis with rocuronium, although this finding does not appear to be supported in literature from other countries. VI. CONCLUSIONS Airway manipulations of any kind can result in reflex- mediated changes in cardiopulmonary physiology. The type and depth of anesthesia provided must be individu- alized for the type of airway being used and the clinical situation for which it is required. Additionally, airway managers should be prepared to treat profound altera- tions in HR, BP, airways resistance, or ICP occurring during or immediately consequent to airway manipula- tion. Although these responses may be of short duration and of little consequence in healthy individuals, serious complications can occur in patients with underlying coronary artery disease, reactive airways, or intracranial neuropathology. VII. CLINICAL PEARLS + Laryngoscopy can induce bradycardia, by increasing vagal tone at the sinoatrial node, or HTN and tachy- cardia mediated by the cardioaccelerator nerves and sympathetic chain ganglia. The former is most common in infants and children, whereas the latter is typical for adolescents and adults. Laryngoscopy and intubation result in stimulation of the CNS and may increase cerebral blood flow (CBF), which may result in elevation of intracranial pressure (ICP) and brain herniation. Ischemic electrocardiographic changes lasting less than 10 minutes during airway manipulation have not been shown to correlate with postoperative myocardial infarction. Succinylcholine is associated with bradycardia in chil- dren, particularly when doses are repeated, but it is a cardiovascular stimulant in adults. Succinylcholine may directly elevate CBF and ICP, an effect that can be blunted by pretreatment with a nonde- polarizing agent and strict maintenance of normocapnia. The application of cricoid pressure can result in greater HR and BP response to endotracheal intubation than when it is not used, and it should be considered when estimating the risk-benefit ratio of this procedure in individual patients. + Fentanyl provides a graded response in blunting hemo- dynamic responses to intubation, with 2 1g/kg IV fentanyl given several minutes before induction only partially preventing hypertension and tachycardia during a rapid-sequence intubation (RSI). Fentanyl and propofol require 6.4 and 2.9 minutes, respectively, to achieve effect-site equilibrium after IV _bolus administration. Therefore, the commonly observed practice of administering 1 to 2 mL of fen- tanyl (50 to 100 ug) just before or almost simultane- ously with administration ofotherinduction medications would not be expected to have any effect based on inadequate dose and inappropriate timing of administration. + When given in a bolus of 1.5 mg/kg IV, lidocaine adds approximately 0.3 MAC of anesthetic potency, but it is not reliable at blunting the cardiovascular or airway response to laryngoscopy or intubation. Additionally, pretreatment with IV lidocaine before RSI does not consistently reduce ICP or positively affect neurologic outcome. For surgeries lasting longer than 2 hours, cough and throat complaints may be decreased by inflating the cuff of the ETT with a buffered solution containing 40 mg of lidocaine. This can be accomplished by using a 10-mL syringe containing 5 mL 1% lidocaine, 1 mL 8.4% NaHCO; solution, and 4 to 5 mL of sterile diluent and inflating the cuff until no leak is present. 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