Case 1 Flashcards
What are the determinants of myocardial oxygen supply?
A major concern in the anesthetic management of patients with coronary artery disease (CAD) is maintaining a favorable balance between myocardial oxygen supply and demand (Figure 1-1). Myocardial oxygen supply is tenuous in patients with CAD because blockages in coronary arteries by atherosclerotic plaques, thrombi, and emboli disrupt the f low of oxygen-rich blood to heart muscle distal to the obstruction. Coronary perfusion is preserved by maintaining both coronary perfusion pressure and length of the diastolic interval. The left coronary artery is perfused during diastole. The right coronary artery is perfused during both diastole and systole. It is important to prevent shortening of the diastolic interval by preventing increases in heart rate. Coronary perfusion pressure is maintained by ensuring normal to high diastolic arterial pressure and normal to low left ventricular end-diastolic pressure (LVEDP).
Explain the determinants of myocardial oxygen consumption (demand).
Heart rate is probably the most important parameter regulating myocardial oxygen supplydemand balance. Decreasing heart rate increases oxygen supply by prolonging diastole (allowing for more subendocardial perfusion) and decreases oxygen demand. The association between tachycardia and myocardial ichemia is well documented. Severe bradycardia should be avoided because it causes decreased diastolic arterial pressure and increased LVEDP. b-Adrenergic blocking drugs are commonly used to maintain mild bradycardia in patients with CAD.
2. Myocardial contractility refers to the ability of the heart to generate force at a given preload. - Myocardial contractility is very difficult to measure and is poorly described by cardiac output or even left ventricular ejection fraction.
- Determination of loading conditions and measurement of velocity, force, and extent of muscle shortening facilitate description of myocardial contractility.
- Decreased myocardial contractility is associated with decreased myocardial oxygen demand, and decreasing myocardial contractility may be beneficial in patients with CAD.
- Specifically, agents that depress myocardial contractility but are not potent vasodilators may be beneficial as long as coronary perfusion pressure is maintained. Examples of such agents include midazolam and etomidate.
All volatile anesthetic agents decrease systemic blood pressure by decreasing vascular resistance in a dosedependent fashion. Although isoflurane is the most widely studied volatile anesthetic for its effect on coronary artery dilation and coronary artery steal, sevoflurane and desflurane show similar mild vaodilating effects. Intravenous anesthetic agents such as propofol, midazolam, etomidate, and ketamine have shown slight negative inotropic effects, but thiopental may have strong negative inotropic effects, which could explain the hypotension associated with its use. Dexmedetomidine is associated with decreases in heart rate and cardiac output in a dose-dependent manner but usually offers excellent hemodynamic stability. “Myocardial depressants” could be useful for patients with CAD as long as coronary perfusion pressure is maintained because they theoretically decrease myocardial oxygen demand. Myocardial oxygen supply and demand are kept in balance by properly managing left ventricular preload, afterload, heart rate, and contractility. Major increases in preload (left ventricular end-diastolic volume) add to the volume work of the heart (increased demand) and decrease coronary perfusion pressure because of the associated increase in LVEDP (decreased supply). Nitroglycerin assists in maintaining a normal to low preload (see later). Excessive increases in afterload result in increased pressure work of the heart (wall tension) during systole (increased demand) despite the increase in coronary perfusion pressure. At the other end of the spectrum, extreme vasodilation (decreased afterload) decreases the diastolic arterial pressure and decreases myocardial oxygen supply (Table 1-1). A decline in the blood flow supply-demand ratio can lead to myocardial ischemia, or impaired myocardial function. Ischemia results from reduced perfusion that leads to oxygen deprivation and inadequate removal of metabolites.
What are the pharmacologic alternatives for treating myocardial ischemia in this patient?
The goals of medical therapy should be to optimize coronary artery perfusion pressure (systemic diastolic pressure minus LVEDP) and control heart rate
If the patient is receiving light anesthesia, it may be beneficial to increase the depth of anesthesia to treat tachycardia and hypertension. Based on the patient’s hemodynamic prof ile, one or more of the following therapies should be used to achieve the above-described goals. Nitroglycerin and other nitrates exert antianginal effects by dilating epicardial coronary arteries and decreasing left ventricular preload and wall tension. This is accomplished by systemic venodilation. Nitrates also cause mild arterial vasodilation and consequently may decrease the pressure work of the myocardium. The limiting factor of nitrate therapy is hypotension, which would decrease myocardial oxygen supply and possibly cause reflex tachycardia. b-Adrenergic blocking drugs slow the heart rate, which has two beneficial effects on myocardial ischemia. First, the duration of diastole increases and improves coronary perfusion. Second, myocardial oxygen consumption is decreased. b-Adrenergic blockers also decrease myocardial contractility, which decreases myocardial oxygen consumption. Finally, treatment of hypertension may decrease afterload, which decreases work. Metoprolol has been used for many years to achieve intraoperative b-adrenergic blockade. Esmolol, a shortacting intravenous b-adrenergic blocker, has become increasingly popular among anesthesiologists because of its relative cardiac (b1 receptor) selectivity and favorable pharmacokinetics.
Describe the considerations for performing surgery on patients with drug-eluting coronary stents.
Current American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend delaying elective surgery for 12 months after implantation of a DES. In patients who cannot wait that long for their surgery, such as patients undergoing cancer operations, careful assessment of the risks and benefits of withdrawing thienopyridine therapy must be undertaken. A cardiologist should be consulted to assess the degree of myocardium at risk, and the possibility of continuing antiplatelet therapy through the perioperative period should be considered. Many surgeons agree to operate with continued aspirin therapy, but few agree to continue thienopyridine. Additionally, there is no current evidence that “bridging therapy” with lowmolecular-weight heparin or short-acting antiplatelet therapy is beneficial. Increased vigilance for acute perioperative myocardial infarction is required for all patients undergoing surgery within the first 12 months (and possibly longer) after DES placement.
Is perioperative b-adrenergic blockade indicated for this patient?
b-Adrenergic blockers are part of routine care for patients with unstable angina and recent myocardial infarction. b-Adrenergic blocker therapy should be initiated within the first 24 hours for ST-segment elevation myocardial infarction in patients who do not have signs of heart failure, evidence of low cardiac output, increased risk for cardiogenic shock, or other relative contraindications (i.e., P–R interval .0.24 seconds, second-degree or third-degree heart block, asthma, or reactive airway disease).
The 2009 ACC/AHA focused update on perioperative b blockade recommends the following: • In patients undergoing surgery, b-adrenergic blockers should be continued for patients already receiving them. • In patients who have CAD, have evidence of cardiac ischemia, or are at high cardiac risk, b-adrenergic blockers should probably be initiated preoperatively and considered intraoperatively to titrate heart rate and blood pressure during vascular or intermediaterisk surgery. • b-Adrenergic blockers should not be given to patients undergoing surgery who have an absolute contraindication to receiving them. • In patients undergoing noncardiac surgery, it is not advisable to give high doses of b blockers to patients not currently taking them. Continuation of preoperative b-adrenergic blockade during the 48-hour perioperative period is a current Surgical Care Improvement Program quality measure.
How should this patient be monitored intraoperatively?
○ The most important modality for monitoring this patient intraoperatively is a multiple-lead ECG system.
- Of the ECG changes of myocardial ischemia that are present on a standard 12-lead ECG, 89% can be detected by a V5 precordial ECG lead alone.
- Since the late 1970s, the recommendation has been to follow limb lead II and precordial lead V5 simultaneously for detection of intraoperative myocardial ischemia. This combination reflects the distribution of both the right and the left coronary arteries and should enable .90% of ischemic episodes to be detected.
- Current operating room ECG systems are usually capable of continuous ST-segment monitoring.
- Generally, this monitoring determines the relationship of the ST segment 60–80 msec after the J-point (junction between the QRS complex and the ST segment) to the baseline (during the PQ interval).
- Ischemia may be defined as .0.1 mV of horizontal or downsloping STsegment depression or .0.2 mV of ST-segment elevation.
- These systems are rendered less effective by left ventricular hypertrophy and frequent electrocautery and are not useful in left bundle-branch block or ventricular pacing.
○ Transesophageal echocardiography (TEE), if available, is an extremely sensitive method of detecting myocardial ischemia. - TEE is performed by continuously imaging the transgastric short-axis view of the left ventricle.
- The images represent distributions of the three major coronary vessels.
- The attention of busy practitioners is frequently diverted from continuous TEE observation by other important tasks.
- Changes in regional wall motion are not specific for myocardial ischemia, even if they are highly sensitive.
- Additionally, equipment cost and need for specialized training limit the use of TEE.
