Cardiovascular Disease

Chapter 22 Cardiovascular Disease




Coronary artery disease




1. What percent of adult patients undergoing surgery are estimated to have, or be at risk for, coronary artery disease?


2. What are some components of a routine preoperative cardiac evaluation? What are some more specialized methods of cardiac evaluation? What is the ultimate purpose of a preoperative cardiac evaluation?


3. What are some important aspects of the preoperative history taken from patients with coronary artery disease with respect to their cardiac status?


4. What are some coexisting noncardiac diseases that are frequently present in patients with coronary artery disease?


5. By what percent can a major coronary artery be stenosed in an asymptomatic patient?


6. What is the best indicator for a patient’s cardiac reserve?


7. When is angina pectoris considered “stable”?


8. When is angina pectoris considered “unstable”? What is the clinical implication of unstable angina?


9. What is it likely an indication of when dyspnea follows the onset of angina pectoris?


10. How does angina pectoris due to spasm of the coronary arteries differ from classic angina pectoris?


11. What is silent myocardial ischemia?


12. What is the most common symptom of angina in men and women?


13. Approximately what percent of myocardial ischemic episodes are not associated with angina pectoris? Approximately what percent of myocardial infarctions are not associated with angina pectoris?


14. Is hypertension or tachycardia more likely to result in myocardial ischemia in the patient with coronary artery disease? What is the physiologic explanation for this?


15. What is the basis for the common recommendation that elective surgery be delayed until 6 months or more after a prior myocardial infarction?


16. What is the approximate incidence of perioperative myocardial infarction 6 months after a myocardial infarction? What is the approximate incidence of perioperative myocardial infarction in patients who have not had a prior myocardial infarction?


17. What time period after surgery do most perioperative myocardial infarctions occur?


18. What are some cardiac medications that patients with coronary artery disease are likely to be taking? What is the recommendation regarding the patient’s preoperative medicine regimen with regard to their regular cardiac medicines?


19. What information can be gained from a preoperative electrocardiogram?


20. How might myocardial ischemia appear on the electrocardiogram?


21. Complete the following table:




















Electrocardiogram Lead Coronary Artery Responsible for Myocardial Ischemia Area of Myocardium That May Be Involved
II, III, Avf    
V3-V5    
I, aVL    

 


22. Name some determinants of myocardial oxygen requirements and delivery.


23. What are some intraoperative goals for the anesthesiologist in an attempt to decrease the risk of myocardial ischemia in patients at risk?


24. What is the difference between risk stratification and risk reduction?


25. What are the risks of recent percutaneous coronary angioplasty in surgical patients and how do they differ with bare metal versus drug eluting stents?


26. What are two potential benefits of administering premedication preoperatively to patients with coronary artery disease?


27. How should anesthesia be induced in patients at risk for myocardial ischemia?


28. Why is there an increased risk of myocardial ischemia during direct laryngoscopy? What are some things the anesthesiologist may do during this time to minimize this risk?


29. What are some methods of maintenance of anesthesia that may be employed by the anesthesiologist for the patient with coronary artery disease?


30. What is coronary artery steal syndrome? What is its clinical significance?


31. What is a concern regarding the administration of a regional anesthetic to patients with coronary artery disease?


32. What are some considerations an anesthesiologist should take when selecting a neuromuscular blocking drug for patients with coronary artery disease? What is unique about pancuronium in this situation?


33. How should neuromuscular blockade be reversed in patients with coronary artery disease?


34. What are some factors that influence the intensity of intraoperative monitoring by the anesthesiologist?


35. When might an intraoperative pulmonary artery catheter be useful? What information does it provide?


36. What is some information that may be provided by an intraoperative transesophageal echocardiogram?


37. What are some treatment options when myocardial ischemia is detected intraoperatively?


38. What is the problem with decreases in body temperature that may occur intraoperatively in patients with coronary artery disease?


39. Why is it important to monitor heart rate in the patient with coronary artery disease?



Valvular heart disease




40. What information can be gained from Doppler echocardiography in patients with valvular heart disease?


41. How should anesthetic drugs and neuromuscular blocking drugs be selected for the patient with valvular heart disease?


42. When is it important to administer antibiotics to patients with known valvular heart disease?


43. What is mitral stenosis? How does it affect left atrial and pulmonary venous pressures? At what chronic left atrial pressure is an increase in pulmonary vascular resistance likely to be seen?


44. What is the most common cause of mitral stenosis? How does it present?


45. Why are patients with mitral stenosis at an increased risk of atrial fibrillation?


46. Why are patients with mitral stenosis at an increased risk of thrombus formation in the left atrium?


47. What are some anesthetic considerations for patients with mitral stenosis?


48. How can the maintenance of anesthesia be achieved in patients with mitral stenosis?


49. How might the adequacy of intravascular fluid replacement be monitored in patients with mitral stenosis? Why is this important?


50. Why might the mechanical support of ventilation be required postoperatively in patients with mitral stenosis?


51. What is mitral regurgitation? How is mitral regurgitation reflected on the recording of pulmonary artery occlusion pressure tracings?


52. What is the most common cause of mitral regurgitation? What other pathologic process is often present under these circumstances? What are some other causes of mitral regurgitation?


53. What are some anesthetic considerations for patients with mitral regurgitation?


54. How can the maintenance of anesthesia be achieved in patients with mitral regurgitation?


55. What is aortic stenosis? How is the severity of aortic stenosis estimated? What is considered to be hemodynamically significant aortic stenosis?


56. Name at least two causes of aortic stenosis. What is the natural course of aortic stenosis?


57. Why might patients with aortic stenosis have angina pectoris despite the absence of coronary artery disease?


58. How is aortic stenosis diagnosed on cardiac auscultation? Why is it important for the anesthesiologist to rule out aortic stenosis by auscultation preoperatively?


59. What are some anesthetic considerations for the patient with aortic stenosis?


60. What would result from tachycardia, bradycardia, or decreases in systemic vascular resistance in the patient with aortic stenosis?


61. How can the maintenance of anesthesia be achieved in patients with aortic stenosis?


62. How should the intravascular fluid status be managed intraoperatively in patients with aortic stenosis?


63. In patients with chronic aortic stenosis, why might the pulmonary artery occlusion pressure not be reflective of the left ventricular end-diastolic volume?


64. How effective are external cardiac compressions in patients with aortic stenosis during cardiopulmonary arrest?


65. What is aortic regurgitation? What is the effect of chronic aortic regurgitation on the left ventricle?


66. What is acute aortic regurgitation most likely due to? What is chronic aortic regurgitation most likely due to?


67. Why might a patient with aortic regurgitation have angina pectoris despite the absence of coronary artery disease?


68. What are the goals for the anesthetic management of aortic regurgitation? The anesthetic management of aortic regurgitation resembles the anesthetic management for which other valvular disease?


69. What is mitral valve prolapse? What percent of the adult population is estimated to have mitral valve prolapse?


70. What are some other conditions associated with mitral valve prolapse?


71. What symptoms do most patients with mitral valve prolapse have?


72. What are some potential complications of mitral valve prolapse?


73. What is the goal of the maintenance of anesthesia in patients with mitral valve prolapse? How should the intravascular fluid volume status be managed in patients with mitral valve prolapse?


74. What is the potential problem with regional anesthesia in patients with mitral valve prolapse?



Disturbances of cardiac conduction and rhythm




75. What are some tools available to the clinician for the diagnosis of disturbances in cardiac conduction and rhythm?


76. What are some types of conduction defects? Are conduction defects above or below the atrioventricular node usually permanent?


77. Is the placement of a prophylactic artificial cardiac pacemaker before surgery indicated in a patient with a bifascicular block? Why or why not? What is the theoretical concern?


78. How is third-degree atrioventricular heart block treated? What are the various methods by which this can be accomplished? How can third-degree heart block be treated pharmacologically?


79. What is sick sinus syndrome? How does it present? How is it treated?


80. What are ventricular premature beats? What are the hallmark features of a ventricular premature beat on an electrocardiogram?


81. When do premature ventricular beats warrant treatment? How are they treated under these circumstances?


82. What may be some causes of ventricular premature beats?


83. When is ventricular tachycardia diagnosed? How can it be treated?


84. What are preexcitation syndromes?


85. What is Wolff-Parkinson-White (WPW) syndrome? What is the incidence of WPW syndrome in the general population? How is it characterized on the electrocardiogram?


86. What is the most common cardiac dysrhythmia associated with WPW syndrome? How can it be treated?


87. What is the goal of the anesthetic management of a patient with WPW syndrome?


88. What are the various methods by which paroxysmal atrial tachycardia or fibrillation may be treated in the perioperative period in patients with WPW syndrome?


89. What is prolonged QT interval syndrome? What adverse events are associated with a prolonged QT interval? How can they be treated pharmacologically?


90. What is a congenital cause of prolonged QT interval syndrome? How is a stellate ganglion block thought to work for this?


91. What is the goal of the anesthetic management of a patient with a chronically prolonged QT interval?




Essential hypertension




99. What is the definition of essential hypertension? What is the benefit of the long-term treatment of patients with essential hypertension?


100. What should be included in the preoperative evaluation of a patient with essential hypertension?


101. How should blood pressure medications be managed in the perioperative period in the patient with essential hypertension?


102. What other medical problems are frequently seen in patients with essential hypertension? Approximately what percent of patients with peripheral vascular disease can be assumed to have 50% or greater stenosis of one or more coronary arteries even in the absence of symptoms?


103. How is the curve for the autoregulation of cerebral blood flow altered in patients with essential hypertension?


104. What is the value of treating essential hypertension in patients before an elective procedure?


105. How do patients with essential hypertension frequently respond physiologically to the induction of anesthesia with intravenous medications? Why is this thought to occur?


106. How do patients with essential hypertension frequently respond physiologically to direct laryngoscopy? What are these patients at risk of during this time? How can this response be attenuated?


107. What is the goal for the anesthetic management of patients with essential hypertension?


108. How can the maintenance of anesthesia in patients with essential hypertension be achieved?


109. How might intraoperative hypotension be managed by the anesthesiologist in patients with essential hypertension?


110. What is the potential problem with regional anesthesia in patients with essential hypertension?


111. How frequently does hypertension occur in the early postoperative period in patients with essential hypertension? How can it be managed?








Cardiopulmonary bypass




145. How is blood drained from the venae cavae during cardiopulmonary bypass?


146. What are two different types of pumps that are used to return blood to the arterial system during cardiopulmonary bypass? Which results in less trauma to blood?


147. How is blood kept from entering the heart from the superior and inferior venae cavae during cardiopulmonary bypass for mitral valve or intracardiac surgery?


148. Under what conditions does the aorta need to be cross-clamped distal to the aortic valve and proximal to the inflow cannula during cardiopulmonary bypass?


149. How can venous drainage from the inferior and superior venae cavae during cardiopulmonary bypass be facilitated?


150. What is the required cardiac index delivered by the roller pump on the cardiopulmonary bypass machine dependent upon? What approximate cardiac index is usually sufficient?


151. What is the advantage of low flows during cardiopulmonary bypass?


152. What are two different types of oxygenators that are used to oxygenate blood that is returning to the arterial system during cardiopulmonary bypass?


153. What is the advantage of a bubble oxygenator? What is the disadvantage of a bubble oxygenator?


154. What is the advantage of a membrane oxygenator? What is the disadvantage of a membrane oxygenator?


155. How can the patient’s body be heated or cooled by the cardiopulmonary bypass machine?


156. How is blood loss from the field recirculated to the patient during cardiopulmonary bypass?


157. What is a problem with the cardiotomy suction used during cardiopulmonary bypass?


158. Why might the left ventricle need a vent during cardiopulmonary bypass? How might this be achieved?


159. How are systemic emboli from cellular debris prevented from occurring during cardiopulmonary bypass?


160. What does priming of the cardiopulmonary bypass system refer to? What is the cardiopulmonary bypass system primed with?


161. What is the patient’s hematocrit maintained at during cardiopulmonary bypass? Why is it important to hemodilute the patient’s blood during cardiopulmonary bypass?


162. Why is it important to remove all air from the cardiopulmonary bypass system during cardiopulmonary bypass?


163. Why is heparin-induced anticoagulation of the patient’s blood necessary during cardiopulmonary bypass? What dose of heparin is usually administered? How is the adequacy of anticoagulation confirmed?


164. What are some explanations for the low mean arterial pressure often seen after the institution of cardiopulmonary bypass? What blood pressure is typically considered acceptable?


165. Why does blood pressure slowly rise spontaneously after some time on cardiopulmonary bypass?


166. What are the dangers of hypertension while on cardiopulmonary bypass? How can hypertension under these circumstances be treated?


167. What are some methods by which the adequacy of tissue perfusion during cardiopulmonary bypass can be evaluated?


168. Why is diuresis induced during cardiopulmonary bypass?


169. What may be the cause of an increasing central venous pressure with or without facial edema while on cardiopulmonary bypass? How can this be confirmed?


170. What may be the cause of increasing abdominal distention while on cardiopulmonary bypass?


171. What are some complications of extracorporeal circulatory support or cardiopulmonary bypass?


172. How should ventilation of the lungs be managed during cardiopulmonary bypass?


173. What is the goal of myocardial preservation during cardiopulmonary bypass? What are some methods by which this can be achieved?


174. What is the oxygen consumption of a normally contracting heart at 30° C? What is the oxygen consumption of a fibrillating heart at 22° C? What is the oxygen consumption of an electromechanically quiet heart at 22° C?


175. How is the effectiveness of cold cardioplegia of the heart measured?


176. What are two potential negative effects of intramyocardial hyperkalemia due to cold cardioplegia after cardiopulmonary bypass? How can they be treated?


177. What are two potential sources for systemic hyperkalemia during cardiopulmonary bypass? How can the hyperkalemia be treated if it were to persist at the conclusion of cardiopulmonary bypass?


178. Why might supplemental intravenous anesthetics be administered during cardiopulmonary bypass?


179. Why might supplemental neuromuscular blocking drugs be administered during cardiopulmonary bypass?


180. Is supplemental anesthesia routinely required during rewarming after the conclusion of cardiopulmonary bypass?


181. What conditions in the patient must be present for cardiopulmonary bypass to be discontinued?


182. When are the aortic and vena cava cannulae removed after cardiopulmonary bypass?


183. What are some potential problems associated with persistent hypothermia after cardiopulmonary bypass?


184. What special precautions must be taken before discontinuing cardiopulmonary bypass in patients who have had the left side of the heart opened, as during valve replacement surgery? What is the potential risk?


185. For each of the following situations, please complete the diagnosis and appropriate therapy:



 


186. Why might a patient have posterior papillary muscle dysfunction after cardiopulmonary bypass? How would this be manifest on the pulmonary artery occlusion pressure tracing?


187. What is a mechanical addition to the pharmacologic support of cardiac output in patients with a poor cardiac output after cardiopulmonary bypass? How does it work? What physiologic alterations may interfere with its efficacy?


188. When is protamine administered after cardiopulmonary bypass? Why?


189. What are some possible side effects of protamine administration?


190. What does the perfusionist do with blood and fluid that remains in the cardiopulmonary bypass circuit after cardiopulmonary bypass?


191. Why might there be a gradient between central aortic and radial artery blood pressures in the early period after cardiopulmonary bypass? How long can this effect persist?




Answers*



Coronary artery disease




1. It is estimated that 40% of adult patients undergoing surgery have, or are at risk for, coronary artery disease. (384)


2. Components of a routine preoperative cardiac evaluation include the history and physical examination, evaluation of the patient’s electrocardiogram, and reviewing or ordering more specialized procedures. Specialized methods of cardiac evaluation include a Holter monitor, exercise electrocardiogram, echocardiogram, radioisotope imaging, cardiac catheterization, and angiography. The ultimate purpose of a preoperative cardiac evaluation is to assess the patient’s risk of an adverse perioperative cardiac event, to determine whether the patient is in optimal medical condition for surgery, and to reduce operative risk. (384)


3. Important aspects of the preoperative history taken from patients with coronary artery disease with respect to their cardiac status include their exercise tolerance, characteristics of their angina, and the presence of a previous myocardial infarction. It is also important to learn what cardiac medicines the patient may be taking and what the potential interactions of these are with anesthetics that may be administered for surgery. (384)


4. Noncardiac diseases that are frequently present in patients with coronary artery disease include peripheral vascular disease, chronic obstructive pulmonary disease, renal dysfunction, chronic hypertension, and diabetes mellitus. (384)


5. A major coronary artery can be stenosed by as much as 50% to 70% in an asymptomatic patient. (384)


6. The best indicator for a patient’s cardiac reserve is by evaluation of their exercise tolerance. A limited exercise tolerance in the absence of significant pulmonary disease gives evidence of a decrease in a patient’s cardiac reserve. Alternatively, the cardiac reserve of a patient who is able to climb up two to three flights of stairs without stopping is probably adequate. (384)


7. Angina pectoris is considered “stable” when there has been no change in the patient’s anginal symptoms for at least 60 days. Factors related to the angina that should be evaluated include the precipitating factors, frequency, and duration. (384)


8. Angina pectoris is considered “unstable” when there has been a change in the patient’s anginal symptoms. Changes that should be evaluated include the degree of activity a patient can do before the onset of angina and the duration of each anginal episode. Another symptom of unstable angina is chest pain occurring at rest. The clinical implication of unstable angina is that the patient may be at risk of an impending myocardial infarction. (384)


9. Dyspnea after the onset of angina pectoris is likely an indication of acute left ventricular dysfunction due to myocardial ischemia and acute, transient cardiac failure. (384)


10. Angina pectoris due to spasm of the coronary arteries differs from classic angina pectoris in that the pain may occur at rest but may not occur during periods of exertion. Angina of this type is associated with ST segment changes on the electrocardiogram. This type of angina is referred to as Prinzmetal’s or variant angina. (384)


11. Silent myocardial ischemia is myocardial ischemia that occurs in the absence of angina. This type of angina is more common in patients with diabetes mellitus and carries the same prognosis as myocardial ischemia associated with angina. (384)


12. The most common symptom of angina in men is dyspnea on exertion. Shortness of breath with climbing stairs is very common. Walking on a flat surface does not seem to be sufficient to elicit shortness of breath until the symptoms are severe. Waking from sleep with angina is also a symptom of severe angina. Women most commonly complain of nonspecific fatigue, making identification of angina more difficult. (384)


13. Approximately 70% of myocardial ischemic episodes are not associated with angina pectoris, and myocardial infarctions are not associated with angina pectoris approximately 15% of the time. (384)


14. Tachycardia is more likely than hypertension to result in myocardial ischemia in the patient with coronary artery disease secondary to an increased oxygen consumption with a decreased duration for coronary blood flow to the left ventricle. Tachycardia results in an increased myocardial oxygen requirement as oxygen consumption is per beat combined with a decreased myocardial perfusion time. Myocardial perfusion to the left ventricle, and thus myocardial oxygen supply, occurs during diastole. Hypertension, on the other hand, leads to an increased myocardial oxygen requirement, but it is also a simultaneous increase in myocardial perfusion. (384)


15. The basis for the common recommendation that elective surgery be delayed until 6 months after a prior myocardial infarction is based on numerous epidemiologic studies. These studies have shown that there is a 5% to 86% reinfarction rate in the perioperative period if previous myocardial infarction preceded the surgical procedure by less than 6 months. This rate of myocardial infarction is 1.5 to 10 times higher than if more than 6 months separated the previous myocardial infarction and the surgical procedure. (385)


16. The approximate incidence of perioperative myocardial infarction 6 months or more after a myocardial infarction is 5% to 6%, whereas the approximate incidence of perioperative myocardial infarction in patients who have not had a prior myocardial infarction is 0.13%. (385, Table 25-1)


17. Most perioperative myocardial infarctions occur in the first 48 to 72 hours postoperatively. (385)


18. Cardiac medications that patients with coronary artery disease are likely to be taking include β antagonists, nitrates, calcium channel blockers, antihypertensives, and diuretics. The recommendation is that patients continue taking their regular cardiac medicines throughout the perioperative period. (385)


19. Preoperative electrocardiograms may provide evidence of myocardial ischemia, prior myocardial infarction, cardiac hypertrophy, abnormal cardiac rhythm or conduction disturbances, and electrolyte abnormalities. (386)


20. Myocardial ischemia may appear as ST segment changes or T wave changes on an electrocardiogram. (386)


21. (386, Table 25-2)


Table 25-2



















Electrocardiogram Lead Coronary Artery Responsible for Myocardial Ischemia Area of Myocardium That May Be Involved
II, III, aVF Right coronary artery Right atrium, atrioventricular node, right ventricle
V3-V5 Left anterior descending coronary artery Anterolateral portion of left ventricle
I, aVL Circumflex coronary artery Lateral aspects of the left ventricle

 


22. Determinants of myocardial oxygen requirements and delivery are related to factors that affect myocardial oxygen supply or myocardial oxygen demand. Myocardial oxygen supply is decreased by tachycardia, hypotension, increased preload, hypocapnia, coronary artery spasm, anemia, and hypoxemia. Myocardial oxygen demand is increased by tachycardia, increased wall tension, and increased myocardial contractility. A goal of the anesthetic management of patients with coronary artery disease is maintenance of the balance between myocardial oxygen supply and demand to minimize the risk of myocardial ischemia. (389, Table 25-4)


23. In an attempt to decrease the risk of a perioperative myocardial infarction in patients at risk, the anesthesiologist should attempt to maintain stable patient hemodynamics. In general, the desired hemodynamics to minimize the risk of intraoperative ischemia include slower heart rates, lower filling pressures, and normal systolic blood pressures. A common recommendation for patients at risk of myocardial ischemia is that heart rate and blood pressure be maintained within 20% of awake values intraoperatively. Even so, approximately 50% of all new perioperative myocardial ischemic episodes are not preceded by or associated with changes in heart rate or blood pressure. Nevertheless, the anesthesiologist may choose to closely monitor the patient’s more limited hemodynamic status using invasive monitors to achieve these goals. He or she should also be prepared to intervene quickly with pharmacologic interventions should they become necessary. (389)


24. Risk stratification is the identification of risk factors in patients that lead to the determination of preoperative risk. Risk stratification does not actually decrease risk, it simply identifies it. Risk reduction requires changing the care provided to the patient either through medications such as the administration of perioperative blockade, or through an alteration in the anesthetic or surgical plan. (386-388, Table 25-2)


25. Patients with recent intracoronary stents have an increased risk of myocardial infarction and death if platelet inhibitors are withdrawn for surgery. Patients with bare metal stents likely require 3 or more months of antiplatelet therapy and those with drug eluting stents may require a year or more before risk is acceptable to discontinue platelet inhibitors for surgery. Many patients who have had percutaneous intervention should be operated on while on aspirin if surgical conditions allow. (388)


26. Two benefits of administering premedication preoperatively to patients with coronary artery disease are the decrease in the secretion of potentially harmful catecholamines and the potential to prevent the increase in myocardial oxygen requirements that may occur with tachycardia and hypertension related to anxiety. (390)


27. The induction of anesthesia in patients at risk for myocardial ischemia is typically achieved with great care. The patient’s standard daily medications should be reviewed and administered if there are no specific contraindications. Patients on β-blockers should receive them. A preinduction intraarterial line may help recognize hemodynamic perturbations reducing risk. Infusions of phenylephrine are helpful to reduce hypotension on induction. Careful administration of intravenous induction agents, narcotics, and inhaled agents, combined with monitoring and careful vasoconstrictor use, are essential. It is important to avoid tachycardia with consummate increases in myocardial oxygen requirements. (390)


28. Direct laryngoscopy is associated with an increased risk of myocardial ischemia because it often produces intense sympathetic nervous system stimulation leading to tachycardia and hypertension. To minimize this risk, there must be adequate levels of anesthesia to suppress sympathetic nervous system stimulation. Volatile anesthetics, intravenous anesthetics other than ketamine, opioids, and lidocaine may all be used to blunt the response to direct laryngoscopy. β antagonists may be administered before induction to attenuate the increase in heart rate and blood pressure that can occur. (390)


29. The maintenance of anesthesia for the patient with coronary artery disease may be achieved through the administration of volatile anesthetics, propofol, dexmedetomidine, and opioids, with or without nitrous oxide. (391)


30. Coronary artery steal syndrome is a theoretical risk in which administration of a coronary artery vasodilator to a patient with coronary artery disease could result in diversion of blood flow from the ischemic areas, in which stenotic coronary arteries are maximally dilated, to areas in which the coronary arteries are patent and able to vasodilate. Isoflurane, of all the volatile anesthetics, is the most potent coronary vasodilator. It was once thought that isoflurane is the volatile anesthetic that is most likely to result in this syndrome. Clinically, however, the administration of isoflurane to patients with coronary artery disease has not been shown to increase the risk of myocardial ischemia through the coronary artery steal syndrome. (391)


31. The administration of a regional anesthetic to patients with coronary artery disease can result in hypotension, which may in turn lead to decreased blood flow through pressure-dependent stenosed coronary arteries. For this reason it is important for the anesthesiologist to be prepared to treat decreases in blood pressure with induction of any anesthetic. An advantage of regional anesthesia for patients with coronary artery disease is that the anesthesiologist may continue to monitor the patient for symptoms of angina and treat them accordingly. (391)

May 31, 2016 | Posted by in ANESTHESIA | Comments Off on Cardiovascular Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access