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Cardiac patients presenting for emergency noncardiac surgery have higher risk for perioperative morbidity and mortality. Emergency surgeries are associated with two to five times the risk of major adverse cardiac events compared with elective procedures. Preoperative evaluation and patient optimization are limited by the nature of emergency surgery.
The main anesthetic goals in patients with cardiac disease undergoing emergency noncardiac surgery are prevention, detection, and treatment of myocardial ischemia by optimization of myocardial oxygen (O 2 ) supply and demand.
The older trauma patients have higher rates of established cardiac disease than younger patients; hence, they are more susceptible to the effects and vicissitudes of trauma. A second significant population that may be encountered in the trauma arena are adults with uncorrected or corrected congenital heart disease.
The central pathophysiology involved in most trauma involves hemorrhage and resultant hypovolemia. Uncontrolled hemorrhage progresses to hypovolemic shock, which results in a constellation of physiologic and organ-related perturbations.
Neurosurgical emergencies that require emergent surgery and care by an anesthesiologist are mostly caused by head or spinal cord trauma, rupture of cerebral aneurysms or arteriovenous malformations, hematomas, acute hydrocephalus, and intracranial tumors with possible brain herniation.
Patients with severe traumatic brain injury or spinal cord injury (SCI) also tend to have other injuries. In addition, if these patients also have significant cardiac disease, management is complex and requires a multidisciplinary approach.
Vascular surgical procedures are associated with a two- to fourfold higher risk of adverse cardiac events (myocardial infarction, cardiac death) compared with other types of noncardiac operations. Coronary artery disease (CAD) shares similar risk factors with noncoronary vascular disease, with atherosclerosis the most common pathologic process affecting coronary arteries, cerebral arteries, the aorta, and peripheral arteries. Consequently, as many as 50% of patients with atherosclerotic disease in one vascular distribution have concomitant disease in at least one other location.
The vascular procedure with the highest associated mortality rate is open surgical repair of abdominal aortic aneurysmal rupture (rAAA), followed by elective thoracoabdominal aortic replacement, lower extremity arterial bypass, and carotid endarterectomy. In addition, patients requiring lower extremity amputation frequently have diffuse and severe CAD.
rAAA is a surgical emergency that requires rapid diagnosis, efficient preoperative evaluation, and prompt transfer to the operating room for open or endovascular repair. The mortality rate of patients with rAAA who reach the hospital has not changed significantly over the past few decades and still approaches 50% compared with 6% for elective repair.
Emergency abdominal surgeries, commonly encountered in practice, include, but are not limited to, cholecystectomy, appendectomy, acute intestinal obstruction from a variety of causes, and acute abdomen caused by perforated bowel and intraabdominal sepsis.
The unique risks associated with emergency abdominal surgeries include abdominal distention causing cardiovascular and respiratory issues, risk of aspiration of gastric contents, rapid fluid shifts, electrolyte and acid-base changes, and increased risk of associated sepsis.
The most common types of surgical orthopedic emergencies are spine injury with spinal cord compromise, open fractures, septic joints, and acute compartment syndrome. These orthopedic emergencies range in acuity from needing immediate operative management versus waiting up to 24 hours. When time is available regarding the cardiac patient, as much of the preoperative history, physical examination including airway examination, laboratory analysis, and other studies (electrocardiography, chest radiography, echocardiography) should be obtained.
The majority of truly emergent otolaryngologic surgeries involve processes that immediately threaten the patient's airway and include emergency tracheostomy, emergencies of airway compromise (Ludwig angina, postoperative hematoma, acute epiglottitis, angioedema), and neck dissections for neck abscesses. Emergency otolaryngologic surgery ranges in acuity from the need for operative management in minutes to seconds (emergency tracheostomy, postoperative hematoma compressing the airway) to potentially several hours (posttonsillectomy hemorrhage, malignant otitis externa [MOE]). When possible, especially regarding cardiac patients, as much preoperative information should be gathered as possible.
Ophthalmologic emergencies occur relatively infrequently on the spectrum of emergency surgery; however, these patients often require prompt operative intervention to preserve vision in the affected eye. Patients requiring emergency eye surgery have most often sustained trauma to the eye (ruptured globe) or have been affected by an ongoing or suddenly acute disease process (acute glaucoma, retinal detachment, infection).
Cardiac patients undergoing emergency surgery are at increased risk of perioperative cardiovascular events compared with those undergoing elective surgery. A decision has already been made to proceed with surgery as soon as possible, thereby limiting preoperative evaluation, risk stratification, and optimization. The 2014 American College of Cardiology/American Heart Association (ACC/AHA) guidelines clearly mention that patients must proceed to the operating room (OR) if surgery is deemed emergent (defined as a situation that is limb or life threatening if surgery is not performed promptly, typically within 6 hours) mandating the perioperative team to anticipate and be prepared to manage adverse cardiovascular events in case they arise. Emergency surgeries are associated with two to five times the risk of major adverse cardiac events (MACEs), including myocardial ischemia, heart failure, cardiac arrest, conduction abnormalities, and death, compared with elective procedures.
This section focuses on anesthetic implications in cardiac patients undergoing emergency abdominal surgeries that are commonly encountered in practice, which include but are not limited to cholecystectomy, appendectomy, acute intestinal obstruction from a variety of causes, and acute abdomen caused by perforated bowel or intraabdominal sepsis. The general principles included in this section are also applicable to urogynecologic emergencies such as acute ovarian or testicular torsion or urosepsis that typically present as an acute abdomen. Vascular emergencies such as abdominal aortic aneurysm rupture (rAAA), acute mesenteric arterial occlusion, and abdominal trauma are covered elsewhere in this chapter. Although transplant of abdominal organs such as the liver, kidney, pancreas and intestine are technically emergent surgeries, they differ in that patients often have undergone extensive workup to determine their candidacy for transplant. Transplant surgery in cardiac patients is discussed elsewhere in this text.
Emergency abdominal surgeries are associated with certain unique risks, including:
An advanced age population with multiple comorbidities. Aging and chronic illness deplete physiologic reserve, and superimposed acute illness potentially shifts them to a state of critical illness.
Risk of aspiration of gastric contents
Rapid fluid shifts. An acute abdomen is a state of absolute hypovolemia in both extracellular and intracellular compartments, with an increase in the release of stress hormones such as vasopressin (antidiuretic hormone) and activation of the renin–angiotensin–aldosterone axis that conserve salt and water. To maintain circulating volume, there are increases in myocardial work and cardiac output (CO) driven by catecholamines and widespread capillary leak.
Electrolyte and acid-base changes
Increased risk of associated sepsis
Abdominal distention causing cardiovascular and respiratory issues
The AHA/ACC guidelines recommending proceeding with surgery also recommend assessing clinical risk factors, collecting information about preexisting cardiac illness, and incorporating them to help determine the surgical strategy and to optimize perioperative monitoring and management. In reality, most of the time, the cardiac status of these emergent patients is unknown or possibly manifested intraoperatively with unstable hemodynamics (which may be an indicator of an underlying cardiac condition). In such instances, evaluation and management must go hand in hand, preferably in the hands of an anesthesia provider capable of performing and interpreting point-of-care procedures such as bedside echocardiography or pulmonary artery catheter (PAC) data.
A prudent approach includes aggressive perioperative medical management of the unstable cardiac condition with a goal to shift cardiac interventional therapies, if deemed required, to the immediate postoperative period. In such instances, the conflicting risks and benefits of emergent surgery versus the unstable cardiac condition could put immense pressure on the entire perioperative team with implications on outcomes. A multidisciplinary approach is best if implemented at the time of initial evaluation and must involve all persons available, including the patient, family, surgical team, cardiology and primary care team, if possible.
In most emergency situations, it is often possible to obtain available clinical information and perform a rapid history and physical examination. Additionally, available laboratory and diagnostic data should be reviewed. Routine blood work, if already not sent, should be drawn at the time of intravenous (IV) catheter placement. Coagulation studies and blood type and crossmatch should be included. If required, anticoagulation reversal should be initiated ( Table 16.1 ).
Agent | Notes |
---|---|
Antiplatelet agents (e.g., clopidogrel, prasugrel, ticagrelor, eptifibatide) | Platelet transfusion may be required for reversal |
Warfarin or coumadin |
|
Unfractionated heparin | Protamine |
LMWH: enoxaparin | Protamine a |
Direct thrombin inhibitors |
|
Direct factor Xa inhibitors (e.g., apixaban, edoxaban, rivaroxaban) | PCC b |
a Per American College of Chest Physicians recommendation to be administered to a bleeding patient if LMWH has been given for less than 8 hours. Only incompletely reverses LMWH and ineffective in case of fondaparinux.
b High-dose four-factor PCC is possibly effective but remains an off-label use because there is no Food and Drug Administration–approved reversal agent yet available.
Monitoring needs will depend on the patient's cardiac disease and clinical state. Invasive monitoring, if required, may include an arterial catheter or central catheter. Placement of an introducer sheath allows for both volume resuscitation as well as potential PAC placement if indicated. If clinically indicated, invasive monitoring may be placed preoperatively and is usually well tolerated by most conscious patients under adequate local anesthesia and ultrasound guidance. Handheld ultrasound or bedside echocardiography permits easy and prompt recognition of significant cardiac lesions, and such information provides the operating team an opportunity to incorporate measures to optimize perioperative outcomes. It has been shown that use of such devices can recognize major cardiac abnormalities, especially the presence of unrecognized left ventricular (LV) systolic dysfunction or valvular heart disease.
A significant number of patients presenting for emergency abdominal surgery present with systemic inflammatory response syndrome, sepsis, or septic shock. Early antibiotic administration and goal-directed resuscitation must be initiated when indicated. Significant intracellular and interstitial fluid depletion may exist despite the appearance of normal cardiovascular measurements (blood pressure, CO, stroke volume). Patients typically require administration of resuscitation fluids to maintain blood pressure and circulating volume during emergency abdominal surgery, but must be performed judiciously in a cardiac patient to prevent pulmonary edema or acute ventricular dysfunction. Also, electrolyte and acid–base abnormalities should be corrected. Occasionally, after relieving obstruction (in cases of urosepsis, obstructive jaundice, or intestinal obstruction), there is a potential for patients to become overtly septic or prone to arrhythmia.
Antiaspiration prophylaxis in the form of nonparticulate antacid and, if time permits, an H 2 blocker or proton pump inhibitor, must be administered to reduce risk of aspiration. Metoclopramide, because of its prokinetic properties, is best avoided in emergency abdominal surgery.
Overall, there is no specific anesthetic technique recommended. General anesthesia (GA) is typically indicated because of the emergent nature of the case, with an open abdomen and likelihood of hemodynamic instability with attendant need for ongoing resuscitation. Anticipation of increased sensitivity to anesthetic agents and hemodynamic perturbations is essential. Decreased doses and gently titrated anesthetic agents with close monitoring of the hemodynamics are required.
After initiating emergency fluid resuscitation as needed and placement of appropriate monitors, a modified rapid-sequence induction often balances the risk-to-benefit equation of competing goals of preventing aspiration versus cardiovascular stability. Agents that minimally depress the cardiovascular system (judicious propofol, etomidate, or ketamine for induction and high-dose rocuronium for intubation) are recommended to achieve this goal.
Patients undergoing emergency abdominal surgeries are prone to volume shifts, and use of the arterial tracing for evaluation of systolic pressure or pulse pressure variation is predictive of fluid responsiveness. A goal-directed fluid therapy approach may assist in appropriate fluid resuscitation. A respiratory-related change of more than 13% suggests that the patient would be fluid responsive. A change of 9% to 13% has been shown to reflect an intermediate range of predictability, a gray zone, in which the patient may be fluid responsive. If the systolic pressure or pulse pressure variation is less than 9%, it is unlikely that the patient would be fluid responsive.
In patients with coronary artery disease (CAD), it is important to avoid excessive myocardial oxygen demand (MVO 2 ), which could elicit or exacerbate myocardial ischemia. Elevated heart rate (HR) can be controlled with a short-acting β-blocker, such as esmolol, especially to blunt the sympathetic response during laryngoscopy, surgical stimulation, and emergence from GA. Nitroglycerin can also be useful to treat hypertension, especially if the HR is low and hypertension persists. Nitroglycerin can provide both venodilation and dilation of coronary arteries. In addition to demand-related ischemia, adequate supply of oxygen to the myocardium must be maintained in the form of correction of anemia, hypovolemia, and prevention of desaturation. Vasopressor or inotropic infusion might be necessary with the anesthetic agents to maintain an adequate perfusion pressure or if cardiomyopathy is severe. A central venous catheter (CVC) can be placed to provide central access for the administration of a vasopressor or inotrope. Patients with cardiomyopathies may not tolerate rapid fluid shifts during emergency abdominal surgeries and therefore may need monitoring of mixed venous oxygen saturation or CO to direct vasoactive agent therapy. Because of third spacing, frequent monitoring and replacement of electrolytes is necessary. Severe hyperglycemia should be controlled with IV insulin, and hypothermia must be prevented.
Patients with coexisting valvular heart disease need special consideration, particularly patients with aortic stenosis who require maintenance of cardiac preload, systemic vascular resistance (SVR), and myocardial contractility. Rapid correction of arrhythmias is necessary because patients with aortic stenosis and associated LV hypertrophy are likely to poorly tolerate such arrhythmias. Although the usage of PACs is declining, the presence of severe pulmonary hypertension (PH) or severe LV or right ventricular (RV) dysfunction may be an indication for monitoring with a PAC to guide the administration of nitric oxide or other pulmonary vasodilators.
Transesophageal echocardiography (TEE) is used for real-time evaluation of cardiac function and restrictive fluid management during surgery. Perioperative hemodynamic management with TEE may be useful for gastrointestinal tract surgeries in patients with severe cardiac disease. See Chapter 10 for an approach to using TEE for fluid resuscitation.
Despite maximal medical management, if a patient continues to be unstable during emergency abdominal surgery, mechanical support for the ventricle (e.g., intraaortic balloon pump [IABP] or percutaneous ventricular assist device [VAD]) or venoarterial extracorporeal membrane oxygenator (ECMO) can be initiated intraoperatively to facilitate successful completion of surgery and hemodynamic stabilization. This requires resources, early planning, and communication with various teams. Additionally, there is the added time constraint, especially after a sudden collapse, to establish mechanical support or initiation of extracorporeal circulation before hypoxic cerebral injury occurs.
An elevated level of postoperative care is necessary in cardiac patients who have undergone emergency abdominal surgery, and intensive care unit (ICU) admission should be considered for these patients for prompt recognition and management of complications. In the immediate postoperative period, there is usually relative hypovolemia from third spacing with associated increased myocardial work. During this phase, resuscitation fluids should be administered cautiously guided by invasive hemodynamic monitoring and circulatory support in the form of vasopressor/inotrope, to prevent precipitation of heart failure. Over the ensuing postoperative days, a state of equilibrium develops when active sequestration stops, followed by a phase of diuresis during which the patient mobilizes fluid and recovers. These fluid shifts are associated with intracellular movement of ions. Hypophosphatemia, hypomagnesemia, and, in particular, hypokalemia are usually evident, requiring regular serum chemistry monitoring. During the equilibrium phase, administration of IV fluid is balanced on whether the current aim is to augment intravascular volume to ensure adequate organ perfusion or to prevent further tissue edema. During the diuretic phase, the main goals are to allow the patient to return to baseline body weight and to aggressively replete electrolytes. Due to the risk of postoperative sepsis, respiratory, and cardiac events being the most common causes of death after discharge from the ICU, patients should be continued to be watched carefully on the floor.
In the United States, the number of patients aged 65 years and older is expected to rise from 46 million currently, to 82 million by 2040, and exceeding 98 million individuals by 2060 (which will constitute nearly one-quarter of the U.S. population). Trauma victims are typically represented by a younger demographic. However, older trauma patients have higher rates of established cardiac disease compared with younger patients; hence, older patients are more susceptible to the effects and vicissitudes of trauma. A second high-risk population that may be encountered in the trauma arena are adults with uncorrected or corrected congenital heart disease (CHD). By 2015, more than 80% of all children with CHD had survived to adulthood and after trauma may present to a hospital without prior experience with CHD. Adult trauma victims with CHD are similar to the older adult trauma patient in that they present unique clinical and care challenges.
The central pathophysiology involved in most trauma involves hemorrhage and resultant hypovolemia. Hemorrhage may be distant from structures most germane to cardiac patients (great vessels, heart, lungs) or may be caused by their direct injury. Uncontrolled hemorrhage progresses to hypovolemic shock, which results in a constellation of physiologic and end-organ–related perturbations. Hypovolemic shock is associated with metabolic acidosis, which leads to regulatory cell enzyme dysfunction, resulting in cellular swelling, phospholipid membrane disruption, and ultimately cell death. Many of the normal compensatory mechanisms that counter the aforementioned shock cascade are impaired in cardiac patients. In the following section, caring for stereotypical older trauma patients with cardiac disease, as well as younger trauma patients with corrected CHD, will be addressed.
Trauma victims frequently arrive to the receiving hospital emergency department (ED) unconscious, intubated, or unable to provide a history. History from emergency medical workers or family may reveal the details of the trauma patient's cardiac history. However, this often may not be readily available. For a trauma patient brought emergently to the OR when a brief history is unattainable, various signs may indicate the presence of prior or current cardiac disease.
A cursory physical examination revealing a midline sternotomy scar is likely associated with prior cardiac surgery. In an older patient, evidence of a prior sternotomy should alert the physician to either prior coronary bypass grafting surgery and history of CAD or potentially prior valve surgery. Clinicians should consider the presence of congenital correction in a younger trauma patient with a sternotomy scar. Other evidence of cardiac disease includes the presence of an implanted cardiac electronic device (i.e., implanted pacemaker or defibrillator) or the battery pack and driveline of a VAD.
Additionally, rapidly identified physical examination clues of current cardiac disease may include clubbing of digits indicating uncorrected cyanotic heart disease, a heave on chest palpation indicating an enlarged cardiac chamber, an audible or palpable thrill demonstrative of severe valvular abnormality, or the auscultation of the click associated with mechanical prosthetic valves. The electrocardiogram (ECG) may reveal pacer spikes in a pacer-dependent patient.
Consideration should also be given to the potential concomitant use of outpatient anticoagulation and antiplatelet medications in trauma patients with possible prosthetic heart valves, CAD, or other implanted devices (e.g., VADs). Plans should be made for immediate coagulation testing and possible massive blood product administration in this context.
Finally, in older trauma patients without obvious signs or symptoms of cardiac disease, the clinician should presume that at least mild diastolic dysfunction exists, and consideration should be made for rational fluid management and resuscitation with appropriate monitoring.
Trauma patients with cardiac disease require careful planning and preparation. This planning should include a review, time permitting, of the patient's prior medical and surgical history, a review of the current trauma presentation (including mechanism, issues with transport, field or ED resuscitative efforts), preoperative imaging, and any recent studies (cardiac catheterization, echocardiography, device interrogation). When time is limited and patients present directly to the OR, as much history as possible should be obtained before induction, as well as a limited physical examination focusing on signs of heart failure, previous cardiac surgery, and the presence of existing implanted devices (pacemakers, defibrillators, VADs, medication pumps).
During this preparatory period, consideration should be given to induction agents, circulatory access, and monitoring needs ( Table 16.2 ).
Induction Drug Issues | Venous Access Issues | Monitoring Issues |
---|---|---|
Propofol: myocardial depressant and vasodilator | Peripheral IV catheter: based on Hagen-Poiseuille law: short- or large-bore IV will have highest flow rate | Invasive arterial blood pressure: mandatory in significant trauma or significant coexisting cardiac disease |
Etomidate: minimal cardiac effects, but concern for postoperative adrenal suppression | Central IV catheter: better suited than peripheral IV if vasoactive drug administration needed; requires increased time and access to neck, chest, or groin, which may not be feasible depending on trauma location | CVP: may be helpful in guiding resuscitative efforts, although there is robust literature demonstrating no correlation between CVP and volume status |
Ketamine: usually minimal cardiovascular effects | Intraosseous line: less familiarity for some clinicians; less commonly used; limited flow rate | TEE: may be helpful in guiding resuscitation as well as monitoring or diagnosing preexisting or new cardiac issues; requires expertise; may be contraindicated in penetrating abdominal or chest trauma |
Midazolam: minimal cardiac effects but may be significantly sympatholytic if combined with fentanyl or other induction agents | Pulse-pressure wave analysis (i.e., FloTrac): provides real-time cardiac output from invasive arterial catheter; requires specialized equipment; may be invalid in certain surgical procedures, arrhythmias, or with certain vasoactive drug use |
In addition to the preparation of appropriate induction drugs and anesthetic maintenance agents, clinicians should also prepare basic cardiac vasoactive drugs for the purposes of optimizing intraoperative hemodynamics. In a time-limited emergency scenario, preparation of three basic vasoactive drugs (nitroglycerin, epinephrine, norepinephrine) enables the rapid management of most hemodynamic issues for the majority of cardiac patients. Nitroglycerin (starting dosage of 0.5–1.0 µg/kg per minute) provides varying degrees of venous, coronary, and arterial dilation; epinephrine (starting dose of 0.01–0.05 µg/kg per minute) provides arterial vasoconstriction and inotropic support, and norepinephrine (starting dose of 0.01–0.05 µg/kg per minute) provides primarily arterial vasoconstriction with a small degree of inotropic support.
Numerous cardiac structural and functional changes accompany aging ( Table 16.3 ). In addition to age-related cardiac changes, cardiac-related medications, such as antihypertensive drugs, may also affect the care of older trauma patients. β-Blockers and calcium channel blockers have both negative chronotropic and inotropic effects, which attenuate the normal trauma-induced adrenergic response. Hence, intrinsic compensatory responses to injury may be blunted, and there may be diagnostic challenges because of the lack of an expected HR increase in response to hypovolemia. In addition, there may be issues in the inadequate physiologic response with relation to implanted cardiac devices, which include VADs and implanted electronic devices (defibrillators, pacemakers).
Changes | Impact on Cardiac Function |
---|---|
Expected | |
Myocyte number decreases; replaced with noncontractile matrix | Diminished ventricular compliance; increase in diastolic dysfunction |
Sinoatrial node and conduction fiber dysfunction | Conduction defects, increased risk for brady- and tachyarrhythmias |
Decrease in aortic and pulmonary artery compliance | Contributor to diastolic dysfunction |
Decrease in cardiac adrenergic receptors | Diminished effects of exogenous catecholamines |
Pathologic | |
Atherosclerosis or coronary artery disease | Myocardial oxygen supply–demand mismatch leading to possible myocardial ischemia |
Valvular disease (mitral regurgitation and aortic regurgitation less common than aortic stenosis) | Increased risk for development of acute heart failure, especially with aortic stenosis |
Right heart dysfunction secondary to left heart or pulmonary disease | Increased risk of right heart failure, especially with trauma-associated hypoxia or acidosis |
Determination of the severity and degree of hypovolemia in cardiac trauma in older adults may be difficult because of the aforementioned reasons. It is well established that the expected baroreceptor reflex findings of tachycardia and hypotension may be minimal or absent in older adults. Therefore older patients may be significantly hypovolemic but not demonstrate tachycardia or hypotension until extremes of blood loss have occurred.
Management of trauma patients with concomitant CAD poses multiple challenges. The hemodynamic goals in this context are similar to those in nontrauma patients with CAD: to optimize the ratio of myocardial oxygen supply to demand. Trauma and the loss of oxygen-carrying hemoglobin, a high sympathetic tone situation, and hypotension may all contribute to exacerbating existing coronary disease or unmasking occult disease. Table 16.4 displays the factors governing oxygen supply and demand. Of note, HR is the most important determinant of oxygen demand. Therefore appropriate attention to the rapid reinstitution of hemodynamic stability and oxygen-carrying capacity is paramount to limit the impact on patients with CAD.
Patients with valvular disease additionally may not tolerate the high sympathetic tone seen with hypotension. In particular, those with stenotic lesions (i.e., aortic or mitral stenosis) do not tolerate significant tachycardia without leading to impaired ventricular filling, further exacerbated by the hypovolemic state. Appropriate resuscitation and hemodynamic control are essential. Intraoperative monitoring with TEE can serve as both a diagnostic modality for patients with unknown valvular disease and as a monitor to guide resuscitation in such patients.
The use of antifibrinolytics (aminocaproic acid, tranexamic acid) in major trauma is becoming increasingly frequent. Moreover, other procoagulants (e.g., prothrombin complex concentrates, recombinant factor VIIa) are also used on occasion in the context of trauma-related coagulopathy. Clearly, there is an indication for the use of these agents when hemorrhage or coagulopathy is overwhelming and hindering an adequate resuscitation. However, in patients with flow limitation in their native coronary arteries, stented arteries, or grafted arteries, these agents may lead to intraarterial thrombosis and precipitate significant myocardial ischemia. Careful consideration should be given to the use of procoagulant agents in these patients. Any patient with a recently implanted coronary stent or graft (or any vascular stent or graft) should be considered at risk for stent or graft occlusion and these procoagulant agents should be administered with extreme caution and only when they are deemed lifesaving. Similar considerations should apply to patients with cardiac prostheses such as mechanical prosthetic valves or LV assist devices.
There are a wide variety of corrected CHD defects that may exist into adulthood and therefore may potentially present in trauma patients, including defects ranging from simple atrial and ventricular septal defects to complex repairs of single ventricles or truncus arteriosus. As of 2017, there were approximately 1.4 million adults with corrected CHD. CHD that is considered complex and of higher risk includes prior Fontan procedures, severe pulmonary arterial hypertension, cyanotic CHD, complex CHD with malignant arrhythmias, and any pregnant patient with CHD ( Table 16.5 ). Although there are recommendations that adults with CHD be cared for in specialized centers, there is always the potential that a trauma victim may be brought to any given hospital at any given time.
Congenital Heart Disease Type | Common or Major Coexisting Problems | Intraoperative Issues | Key Hemodynamic Issues | Intraoperative Variables to Avoid |
---|---|---|---|---|
Fontan population | Supraventricular arrhythmias Heart failure Pulmonary AVF Liver cirrhosis |
Positive pressure induced hemodynamic instability caused by passive lung perfusion | Impaired systolic function Preload dependence Impaired chronotropy |
Tachycardia Bradycardia Hypovolemia Positive-pressure ventilation |
Cyanotic heart disease with shunt repairs (intracardiac, vascular, complex): all are usually left to right | Shunt reversal or cyanosis possible if PVR↑, SVR↓, RVOTO | Maintain SVR Minimize PVR |
Acidosis Hypercarbia Hypoxia Hypothermia Systemic hypotension |
Three groups of CHD patients who may present as trauma victims may be generalized: those with uncorrected CHD, those who have received palliative surgery, and those with corrected CHD. Even with the same structural cardiac lesion, each of these three CHD patients may differ greatly from each other from an anatomy or physiology standpoint. For example, multiple variants of tetralogy of Fallot exist with a range of pulmonary stenosis, leading to a spectrum of “pink” to severely cyanotic patients. Hence, any and all preoperative history and physical examination findings should be obtained to help guide planning and intraoperative management.
Ideally, the following four parameters should be determined preoperatively, time permitting:
The patient's anatomic disease and the clinical status: What exactly is the anatomic or structural and physiologic nature of the CHD? That is, what shunts exist, and what is the nature of the blood flow in these shunts? Is the patient fully compensated, or is there coexistent heart failure? It should be noted that heart failure is the leading cause of death in the adult CHD population, and the presence of compensated heart failure should be strongly considered in adults with complex CHD. Are there coexisting arrhythmias or conduction disturbances? Malignant arrhythmias are the second leading cause of morbidity and mortality in the CHD population, with supraventricular tachyarrhythmias being most common. Is there residual PH, and is it fixed or reversible? Last, a large number of patients with CHD receive chronic antiplatelet and anticoagulation therapy, which should be factored into the preoperative planning.
The patient's prior cardiac interventions: What has the patient's CHD course been? What surgeries or interventions have been undertaken to date? Is the patient palliated or considered corrected?
The patient's additional comorbidities: What are other comorbidities (renal, hepatic, hematologic, neurologic, infectious, endocrine) associated with the patient's CHD?
The currently planned traumatic surgery: What is the planned procedure in relation to cardiac anatomy? (For example, emergent exploratory laparotomy has fewer potential anatomic implications than emergency thoracotomy.)
In many regards, the anesthetic considerations for the intraoperative management of the trauma patient with CHD are analogous to considerations in older cardiac patients. First, consideration should be given to the need for GA. Regional anesthesia lends itself to potentially fewer hemodynamic fluctuations along with obviating the need for mechanical ventilation. It is important to note that local anesthetic–induced methemoglobinemia (e.g., use of prilocaine) may be fatal in the context of cyanotic CHD. Nonetheless, most abdominal, chest, or neurotrauma demands GA. Although GA using a balanced technique is common in nonemergent surgery in the CHD population, it is similarly recommended in trauma patients. The most important principle is an understanding of the resultant anesthesia-induced hemodynamic changes in the context of the given CHD. The effects of anesthesia, volume status, and sympathetic state on CHD will depend on whether the CHD issue relates to intracardiac shunting, pressure overload, or volume overload of the systemic or pulmonary ventricle. See Chapter 8 for further discussion on specific CHD pathologies.
Similar to older trauma patients requiring GA, invasive blood pressure monitoring is mandatory, and adjunctive monitors should be considered (e.g., TEE, central venous pressure [CVP] monitoring). In preparation of venous lines and hemodynamic drips, attention to removing air bubbles is essential because CHD patients may have residual cardiac shunting.
Neurosurgical emergencies that require immediate surgery and care by an anesthesiologist are mostly caused by head or spinal cord trauma, rupture of cerebral aneurysms or arteriovenous malformations, hematomas, acute hydrocephalus, and intracranial tumors with possible brain herniation. Intracranial hematomas may arise epidurally, subdurally, or intracerebrally and can expand rapidly or slowly. Emergencies affecting the spinal cord include tumors or hematomas causing compression of the spinal cord, which can cause acute spinal cord injuries (SCI).
Patients with severe traumatic brain injury (TBI) or SCI also tend to have other injuries. In addition, if these patients also have significant cardiac disease, management is complex and requires a multidisciplinary approach. Surgery and anesthesia can also subject the injured brain to other secondary injuries as a result of hypotension or hypertension, hypoxemia, hypocarbia or hypercarbia, hypoglycemia or hyperglycemia, fever, or increased intracranial pressure (ICP) that can cause further adverse outcomes.
Preanesthesia evaluation should be as complete as possible but is frequently limited by the emergency of the clinical situation. The preanesthetic considerations for patients with cardiac disease involve assessing cardiac and overall health risk, identifying factors that may cause significant perioperative issues, working with cardiology to help optimize cardiac issues if time permits, assessing the risk for a perioperative cardiac event, and developing an anesthetic plan to avoid cardiovascular complications. Patients with coexisting cardiac disease who require urgent or emergent surgical procedures are at increased risk for cardiovascular complications, regardless of the severity of the disease and baseline risk ( Box 16.1 ).
Airway (cervical spine)
Breathing: ventilation and oxygenation
Circulatory status
Associated injuries
Neurologic status (Glasgow Coma Scale)
Preexisting chronic illness
Circumstances of the injury
Time of injury
Duration of unconsciousness
Associated alcohol or drug use
The preanesthetic assessment includes:
Airway assessment and management plan ( Fig. 16.1 )
Severity and chronicity of the cardiac lesion
Effects of the surgical procedure and anesthetic technique on the preexisting condition and cardiac function
Plan regarding the use of invasive monitoring and risks and benefits of planned invasive monitors
Plan regarding the selection and use of vasoactive agents
Use of surface echocardiography for quick assessment of cardiac status and use of TEE based on hemodynamics
When these patients are brought to the OR emergently, there is usually minimal time for a complete preoperative assessment. In these situations, obtaining any significant cardiac history can be extremely difficult, either because of a lack of reliable source of history or the patient being unable to communicate because of mental status changes. The anesthesiologist may have to depend on physical signs and symptoms to look for signs of heart disease or dysfunction. The presence of chest scars may indicate possible prior heart surgery. Physical examination of the chest and listening to the heart sounds may also provide valuable clues to the presence of heart disease. Signs and symptoms of CHF should be carefully assessed. They include rales, wheezing, hepatomegaly, jugular venous distention, ascites, and edema. Physical deconditioning may also be present in patients with significant preexisting cardiac disease. Close monitoring of vital signs as the patient is brought in to the operating suite is vitally important.
Patients who have had a recent myocardial infarction (MI) within the past 4 weeks and require emergent surgery are at extremely high risk for a perioperative cardiac event. For emergent surgery, the goals should be to prevent, detect, and treat ischemia. Consultation should be obtained from a cardiologist if needed and feasible for risk stratification and further management.
Patients with recent cardiac percutaneous coronary intervention (PCI) are also at increased risk if noncardiac surgery is performed within 6 weeks of stenting. This is closely associated with the cessation of antiplatelet therapy in the setting of a surgery-induced prothrombotic state. In patients requiring emergent surgery, the risk of surgical bleeding by continuing antiplatelet drugs has to be balanced against the risk of adverse cardiac events. This can be particularly problematic in patients requiring emergent neurologic surgery because bleeding into the brain can be devastating. Patients in this scenario usually require platelet transfusions in the perioperative period.
Rapid neurologic assessment is performed using the Glasgow Coma Scale (GCS) to stratify the severity of the TBI. A key priority in the management of patients with neurosurgical emergencies is a rapid and accurate diagnosis with computed tomography (CT) to evaluate an expanding lesion that requires immediate surgical intervention. Lesions such as epidural hematomas, subdural hematomas, intracerebral hematomas, and contusions should be evacuated as soon as possible.
The primary goal in neurologic emergencies is the prevention of secondary neurologic injury. In the past few decades, the understanding of the causes and the early treatment of secondary brain injury have led to a decrease in the mortality rate of patients with acute neurologic injury. The outcomes of acute neurologic injury are determined by the presence or absence of secondary brain injury. The main contributors to secondary injuries include hypoxia, hypotension, hypercapnia, intracranial hypertension, and brainstem herniation. These factors can also significantly impact the cardiac status of patients with significant cardiac disease ( Table 16.6 ). The duration of systemic hypotension, hypoxia, and pyrexia have all been found to be strongly associated with death. High-dose steroids do not reduce ICP in head trauma and have not been shown to affect outcome. They are not routinely used in the management of these patients. Steroids may be useful in reducing edema in patients with a brain tumor, however.
Secondary Insults | Number of Patients | Outcome (% of Patients) | ||
---|---|---|---|---|
Good or Moderate | Severe or Vegetative | Dead | ||
Total number of cases | 699 | 43 | 21 | 37 |
Neither insult | 456 | 51 | 22 | 27 |
Hypoxia (Pa o 2 <60 mm Hg) | 78 | 45 | 22 | 33 |
Hypotension (systemic blood pressure <90 mm Hg) | 113 | 26 | 14 | 60 |
Both | 52 | 6 | 19 | 75 |
Some of the key points to be considered while managing these patients include ( Box 16.2 ):
Maintain cerebral perfusion pressure and treat increased ICP.
Avoid secondary injuries such as hypotension, hypoxia, hypercarbia and hypocarbia, hypoglycemia and hyperglycemia, and coagulation abnormalities.
Provide adequate anesthesia and analgesia.
Prevention of hypoxemia: maintain Pa o 2 >60 mm Hg or Sa o 2 >90%:
Increase inspired oxygen tension.
Treat pulmonary pathologic condition.
Consider positive end-expiratory pressure (≤10 cm H 2 O).
Maintenance of blood pressure:
Prevent hypotension—maintain systolic blood pressure >90 mm Hg:
Avoid glucose-containing solutions.
Maintain intravascular volume status; aim for euvolemia.
Treat hypertension:
Sympathetic nervous system overactivity
Increased intracranial pressure
Light anesthesia
Reduction in intracranial pressure:
Head position
Brief periods of hyperventilation
Hyperosmolar therapy
Sedation
Hypothermia
Surgical procedures: drainage of cerebrospinal fluid and evacuation of hematoma
Aggressive attempts at the treatment of hypoxia are essential in head injury patients because hypoxemia is associated with the development of secondary brain injury, worsening neurologic outcomes, and increased mortality rate, and these are worse when associated with systemic hypotension ( Table 16.6 ). The goal should be to maintain an oxygen saturation of 90% or higher or a PaO 2 greater than 60 mm Hg. Many patients with significant brain injury require intubation to maintain these goals. There is concern that positive end-expiratory pressure (PEEP) may cause an increase in ICP in patients with neurologic injury because it may decrease cerebral venous outflow and thus increase cerebral venous volume.
Any episode of hypotension, defined as systolic blood pressure less than 90 mm Hg, has been correlated with higher morbidity and mortality rates in patients with neurologic injury. These episodes of hypotension can also be significantly detrimental to patients with cardiac disease. The common causes of hemodynamic instability in patients with neurologic injury are hypovolemia caused by blood loss and diuresis caused by mannitol use.
The injured brain does not tolerate hypotension well, and adequate resuscitation is required to restore intravascular volume. Hypotension may become severely exacerbated when the brain is decompressed. Patients with ischemic heart disease and aortic stenosis also poorly tolerate hypotension.
In some situations, after trauma when there is an isolated neurologic injury, stress-induced activation of the sympathetic nervous system may lead to a release of catecholamines generating systemic hypertension. Because neuroautoregulation is usually impaired after head injury, hypertension can cause hyperemia and lead to increases in ICP. Before pharmacologically treating hypertension, causes such as increased ICP and light anesthesia should be addressed. Patients with neurologic injury may also need to be treated with β-blockade to reduce tachycardia, ST and T-wave changes, and myocardial necrosis that may be associated with severe neurologic injury. This is particularly important in patients with preexisting cardiovascular disease ( Table 16.7 ).
Cerebrovascular Disease (%) | Abdominal Aortic Disease (%) | Peripheral Artery Disease (%) | |
---|---|---|---|
Coronary artery disease | 8–40 | 30–40 | 4–40 |
Cerebrovascular disease | — | 9–13 | 17–50 |
Abdominal aortic disease | — | — | 7–12 |
a Significant overlap exists in risk factors for coronary, cerebrovascular, aortic, and peripheral arterial disease. As many as 50% of patients with atherosclerotic disease in one vascular bed will have concomitant disease present in at least one other vascular distribution.
Stress-induced hyperglycemia is common in neurologically injured patients, and this has been associated with increased morbidity and mortality rates after head trauma and cardiac arrest. Multiple mechanisms (mitochondrial damage, intracellular acidosis, endothelial damage, and inflammation) have been described for the hyperglycemia-related increased neurologic damage, but the exact cause is still unclear. The exact level about which injury occurs is not known but appears to be less than 200 mg/dL. On the other hand, tight glycemic control is also detrimental because of the high incidence of hypoglycemia and thus worsening of outcome. Solutions that contain glucose should not be administered to patients with neurologic injury. Part of the difficult management comes from determining the safe level of blood glucose.
A core temperature greater than 38°C is strongly associated with worse neurologic outcomes and increased mortality rates in patients with neurologic injury. It can also lead to detrimental effects in patients with cardiac disease because it can increase oxygen consumption and lead to demand ischemia. Infusion of warm IV fluids, in the setting of hypovolemia, should be performed cautiously, with the risk of hyperthermia in mind.
The different modalities to decrease temperature in patients with acute neurologic injuries include antipyretic drugs, external devices such as cooling blankets, and internal cooling such as infusion of cold saline and endo-cooling devices.
Reducing ICP is a major goal in the acute management of patients with brain injury. It can be achieved with changes in head position, hyperventilation, hyperosmolar fluids or diuretics, barbiturates, and sometimes surgical intervention.
Head-up position or reverse Trendelenburg (up to 30 degrees) position with the neck being neutral promotes cerebral venous drainage and can potentially decrease ICP, assuming the venous pathways are still patent. Tight endotracheal tube ties around the neck should be avoided because they can potentially restrict venous drainage and increase the ICP.
Hypocapnia from hyperventilation is a useful therapeutic tool in the management of increased ICP. Although this can lower ICP, it has to be used with caution because it can also increase cerebral ischemia.
Hyperosmolar therapy using mannitol decreases brain water content and ICP mainly by increasing the plasma osmolality and hence creating an osmotic gradient across the blood-brain barrier. Transient hypotension may occur after rapid administration of mannitol, which may be problematic in patients with significant cardiac disease. After the transient blood pressure drop, mannitol then increases blood volume and cardiac index. These hemodynamic changes should be closely watched because they can be poorly tolerated in patients with significant cardiac disease.
Diuretics, such as furosemide, can lower ICP when used in larger doses, up to 1 mg/kg, or in smaller doses when combined with mannitol. Using furosemide may be advantageous in patients with a coexisting cardiac disease because it does not increase blood volume. Still, it has to be used with caution because it can acutely decrease blood pressure, which can be detrimental to patients with significant cardiovascular disease.
Barbiturates and other sedatives can also be used to reduce cerebral metabolism and ICP. Barbiturates work well in the acute control of ICP, but as a class of drugs, barbiturates are myocardial depressants, which may restrict their use in patients with preexisting cardiac disease. Propofol, also a myocardial depressant, can also be used with care in similar situations. Other options include midazolam with or without opioids.
Similar to patients with head injury, one of the primary goals in the management of SCI is the prevention of secondary cord injury. A key way to do this is to immobilize the spine, and subsequent treatment has involved anatomic realignment and stabilization with or without surgery.
Secondary neurologic injury is further prevented by maintaining spinal cord perfusion and correcting hypoxia. Autoregulation can be impaired for several hours after injury. Hence, vasopressors, mainly norepinephrine, should be used to maintain mean arterial pressures (MAPs) of at least 65 mm Hg to improve spinal cord perfusion pressure. This may also be required in patients with CAD to maintain cardiac perfusion. Hypertension is also not helpful because it can cause hemorrhage and increase spinal cord edema.
Hyperglycemia should also be avoided after SCI. Blood glucose levels above 177 mg/dL have been associated with worsening neurologic outcomes. Glucose-containing solutions should be avoided in the first 24 hours, and hyperglycemia should be carefully treated.
Large doses of steroids, especially methylprednisolone, have been reported to improve outcomes in patients with spinal injuries in some studies but not confirmed in others. Currently, the administration of steroids remains an institutional or physician preference.
Cerebral aneurysm surgery may be emergent in situations when patients present with a subarachnoid hemorrhage. Preoperative evaluation includes assessment of the patient's neurologic condition and grading of the subarachnoid hemorrhage, assessment of the intracranial pathology with review of CT scans and angiograms, monitoring of ICPs, and evaluation of other systemic issues, including cardiac issues.
Careful management of blood pressure during anesthesia induction is particularly important in these patients. Aneurysm rupture or rebleeding during induction of anesthesia may be precipitated by sudden increases in blood pressure during intubation and is associated with a high mortality rate. The risk of ischemia from a reduction in cerebral perfusion pressure has to be balanced with the benefit of reduced chance of aneurysmal rupture, taking into consideration the clinical Hunt-Hess grade. Patients with lower grades usually have normal ICP, but patients with higher grades tend to have higher ICPs, and these patients tolerate hypotension poorly. This has also to be balanced against the risk of myocardial ischemia in patients with CAD or critical aortic stenosis. The use of high dose narcotics during induction is common to prevent the rise in blood pressure with intubation. Although succinylcholine has been reported to cause an increase in ICP, it has been successfully used in many aneurysm patients with no known sequelae. Many anesthesiologists tend to use nondepolarizing agents. In patients with a full stomach, the risk of aspiration must be balanced against the risk of aneurysm rupture.
In addition to standard GA monitors, monitoring should also include an arterial catheter, preferably placed before induction. Careful blood pressure management is needed during head pinning because this can also increase the blood pressure and potentially cause aneurysm rupture. A central venous catheter (CVC) is usually placed to manage the large fluid shifts and potential need for resuscitation. Placement of a CVC in the internal jugular vein should be discussed with the neurosurgeon because of the potential for venous obstruction to cerebral venous outflow. Placement of a PAC in patients with significant cardiac disease should also be considered. Other less frequently used monitors include jugular bulb oxygen saturation and transcranial Doppler.
The main goals during maintenance of anesthesia are to provide a “relaxed” brain, maintenance of cerebral perfusion, reduction in transmural pressure during final clipping of an aneurysm if necessary, and to allow early neurologic assessment if possible at the end of surgery. Sometimes the neurosurgeon requests cardiac standstill to facilitate clipping of a large aneurysm, and this can be achieved with a bolus of adenosine. This has to be done with extreme caution and is frequently contraindicated in patients with significant cardiac disease. Some large aneurysms may also require circulatory arrest with cardiopulmonary bypass.
Electrophysiology monitoring with electroencephalography, somatosensory and motor evoked potentials (SSEPs and MEPs) are sometimes used as additional monitoring tools. They may allow an intraoperative detection of cerebral ischemia.
The incidence of intraoperative rupture varies with the size and location of the aneurysm. Management of rupture during surgery depends on the ability to maintain blood pressure. If the leak is small, sometimes the surgeon is able to gain control with suction and permanent clipping. At other times, temporary clipping is needed to gain control. Communication between the surgeon and anesthesiologist regarding optimal management of emergence and postoperative management is essential (e.g., early extubation to assess neurologic status versus airway protection for patients who come in for emergent surgery).
Interventional neuroradiology is the discipline that uses endovascular methods to treat vascular conditions of the central nervous system (CNS). Common goals in the anesthetic management of patients in interventional neuroradiology include maintaining immobility during the procedure, rapid recovery to assess neurologic function, managing anticoagulation, treating and managing unexpected procedure-related complications, and medical management of transportation. Although some of the procedures done in interventional neuroradiology tend to be of an elective nature, two common emergencies are intracranial aneurysm ablation and thrombolysis or thrombectomy of acute stroke.
The two basic approaches are occlusion of the proximal parent artery and obliteration of the aneurysmal sac. Patients with aneurysmal subarachnoid hemorrhage often have increased ICP or decreased compliance, usually caused by the subarachnoid hemorrhage, hydrocephalus, or parenchymal injury.
The management of these cases involves being prepared for aneurysmal rupture and a new acute subarachnoid hemorrhage at all times. This can happen from spontaneous rupture of a leaky sac, injury from vascular manipulation, or arterial occlusion. The morbidity and mortality rates are high for an intraprocedural rupture. If a rupture does occur, anticoagulation must be quickly reversed, and cerebral perfusion pressure must be maintained at adequate levels. Most patients develop a Cushing response, with hypertension and bradycardia. Emergency placement of an external ventricular drain by the surgeon must be considered, and emergency imaging should be obtained to assess extent of damage and to plan further management.
In an acute thromboembolic stroke, attempts are made to recanalize the occluded vessel by highly selective intraarterial thrombolytic therapy using agents that are delivered in high concentration through a microcatheter that is navigated close to the clot. Neurologic deficits may be reversed if treatment is completed within several hours of onset of ischemia in the carotid territory and somewhat longer if ischemia is in the vertebrobasilar territory. Another new method is to remove the thromboembolic material from the vessels using retrieval devices.
Both tissue plasminogen activator administration and retrieval with a device have the risk of promoting hemorrhage. Anesthetic challenges involved in the acute care of these patients are that they are generally older, and commonly little is known about their comorbidities. These types of cases can be done under GA or sedation. The options have to be carefully considered, weighing the ability to monitor neurologic status and the risk of patient agitation and movement. Most of these patients also have vasculopathy and systemic hypertension. This can complicate the management because frequently there is the need to maintain MAPs at higher levels because of inadequate collateral circulation, and balancing the risk of vessel rupture or clot propagation.
When patients with ischemic heart disease present for emergency neurologic surgery, in addition to the above-mentioned goals, close attention must be given to prevention, detection, and treatment of myocardial ischemia.
Low to normal HR should be maintained while maintaining blood pressure. Tachycardia compromises oxygen supply and demand. Tachycardia shortens the duration of diastole, the primary interval for coronary artery blood flow. The relationship between HR and diastolic time is not linear. Oxygen consumption in the myocardium more than doubles when the HR doubles. Treatment of tachycardia has to be prompt, initially by deepening the anesthetic or adding an opioid. A β-blocker, such as esmolol, may be added when these measures are not effective.
Every attempt should be made to maintain the blood pressure within 20% of the baseline, but with an increased ICP and the associated reflex hypertension, this may be untenable. Diastolic blood pressure should be maintained because of the role it plays in coronary perfusion. Prompt treatment of hypotension is needed to prevent ischemia, but this should be done with caution because hypertension may precipitate demand ischemia by increasing ventricular wall stress. Treatment of hypertension can be done by deepening the anesthetic or adding an opioid. Sometimes the addition of a vasodilating agent may be required. For hypertensive patients who develop persistent myocardial ischemia, an IV infusion of nitroglycerin, starting at 0.1 to 4 µg/kg per minute, may need to be titrated to control the blood pressure. Nitroglycerin causes dilatation of the coronary arteries and decreases the LV preload because of venodilation.
Fluid status should be managed carefully to avoid volume overload or overt heart failure, especially in patients with diastolic heart disease. CVP can sometimes be used as a surrogate but has multiple limitations as a volume status surrogate. Patients can also be hypotensive because of being vasoplegic due to prior administration of angiotensin-converting enzyme (ACE) inhibitors or from being in septic shock. These patients may require vasopressin boluses or infusion (usually at 0.04 U/min).
Hemoglobin levels must be adequate (> 8 gm/dL), to attempt to maximize the amount of oxygen in coronary arterial blood. Patients with known ischemic heart disease may need to be transfused to keep their hemoglobin levels closer to 10 g/dL for optimal oxygen delivery.
Hyperthermia is associated with worsening neurologic injury. Although hypothermia is sometimes used for neuroprotection, it is associated with shivering, which can increase myocardial oxygen demand and can lead to ischemia.
The above factors have to be closely considered throughout the entire perioperative period because myocardial ischemia can continue to occur in the recovery room or the ICU.
Severe aortic stenosis leads to obstruction of LV outflow, LV pressure overload, and concentric hypertrophy over time. Hemodynamic management includes carefully monitoring the following key factors.
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