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Both RPP and TI are used to measure myocardial oxygen demand. Angina threshold depends on the severity of coronary artery occlusion. Angina threshold of RPP usually ranges from 15,000 to 20,000 mm Hg per minute. A high RPP or TI indicates a potential danger of myocardial ischemia, but a normal or low RPP and TI do not rule out ischemia. Patients with tachycardia and hypotension may have a normal RPP, but both tachycardia (increasing oxygen demand, decreasing oxygen supply) and hypotension (decreasing oxygen supply) may cause myocardial ischemia. Precordial lead V5 ECG and angina (awake patients) are more important monitors for ischemia. Most important is to keep all three factors (i.e., SBP, HR, PCWP) as close as possible to their normal values. It is usually recommended to keep RPP less than 12,000 and TI less than 150,000.
The RPP has been shown to be a useful measure of myocardial oxygen demand in awake patients, but direct comparisons of myocardial oxygen demand in anesthetized patients have shown an unreliable correlation.
B.5. What factors determine myocardial oxygen supply?
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Coronary blood flow depends on the following:
- Aortic diastolic pressure
- LVEDP
- Patency of coronary arteries
- Coronary vascular tone
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B.6. Would you discontinue digoxin? Why? What is its half-life?
To prevent digitalis intoxication after cardiopulmonary bypass (CPB), digitalis preparations are usually discontinued one half-life (1.5 to 1.7 days for digoxin, 5 to 7 days for digitoxin) before surgery. Digitalis intoxication is quite possible, particularly after CPB when acid–base and electrolyte levels are abnormal. If the patient is in congestive heart failure (CHF) and digitalis dependent, digitalis is continued until the night before surgery. However, the predisposing factors to digitalis intoxication, especially hypopotassemia and hypercalcemia, have to be prevented.
B.7. Would you discontinue propranolol? Why? What is its half-life? What is the role of the β-adrenergic blockers in treating congestive heart failure?
Propranolol should be continued not only until surgery, but probably throughout the perioperative period. Propranolol is generally continued until the time of surgery. In patients with unstable angina, sudden withdrawal of propranolol may produce an exacerbation of symptoms and may precipitate acute myocardial infarction. The dose of propranolol need not be reduced before surgery to avoid bradycardia, hypotension, or difficulty in weaning from CPB. The half-life of oral propranolol is 3.4 to 6 hours. Propranolol disappears from the plasma and atria within 24 to 48 hours after discontinuing doses of 30 to 240 mg per day. It has been shown that with a 0.5-mg dose of propranolol intravenously, blood levels as high as 50 ng/mL are obtained but rapidly decrease to unmeasurable levels within 5 to 10 minutes. There has been no myocardial depression seen with these small intravenous doses.
Reductions in HR with propranolol occur at lower serum levels than depression of myocardial contractility. Accordingly, as drug levels decrease after discontinuation of therapy, reductions in chronotropic response last longer than reductions in inotropy. This is an important concept in treating tachycardias in patients with significant ventricular dysfunction and CHF.
Numerous studies have confirmed improvements in cardiac function, exercise capacity, and long-term survival in patients with heart failure resulting from myocardial infarction, hypertrophic cardiomyopathy, or idiopathic dilated cardiomyopathy with β-antagonists. β-Antagonists may also be of benefit in patients with diastolic dysfunction secondary to hypertension.
Potential benefits of β-adrenergic blockade in heart failure include decreased HR and normalization of β-receptor function. Diastolic function by increasing diastolic filling time, myocardial perfusion, and myocardial oxygen consumption are all improved by slower HRs. β-Adrenergic receptors are downregulated in heart failure, but their response is normalized by long-term beta-blockade. Partial β-agonists may provide baseline sympathetic drive but act as antagonists against excessive sympathetic stimulation.
B.8. If the patient who is on propranolol develops hypotension intraoperatively, how would you manage it?
The specific antagonists for propranolol are not the first choice. The more common causes of intraoperative hypotension, such as hypovolemia, deep anesthesia, and surgical manipulation, should be corrected first. In rare instances, it is necessary to administer atropine for bradycardia or epinephrine, isoproterenol, glucagon, calcium, or digitalis to counteract the beta-blockade. Cardiogenic hypotension is usually associated with high PCWP and low blood pressure (BP).
B.9. What is nifedipine? How does it work?
Nifedipine is a calcium channel blocker. The commonly used calcium channel blockers in the United States are nifedipine, verapamil, and diltiazem hydrochloride. The calcium channel blockers that have been approved for clinical use in the United States have diverse chemical structures. Five classes of compounds have been examined: phenylalkylamines, dihydropyridines, benzodiazepines, diphenylpiperazines, and a diarylaminopropylamine. At present, verapamil (a phenylalkylamine); diltiazem (a benzodiazepine); nicardipine, nifedipine, isradipine, amlodipine, felodipine, and nimodipine (dihydropyridines); and bepridil (a diarylaminopropylamine ether) are approved for clinical use in the United States. They inhibit excitation–contraction coupling of myocardial and smooth muscle by blocking calcium influx at cellular membranes. This results in decreased myocardial contractility and in vasodilation. Therefore, myocardial oxygen consumption is decreased. Calcium channel blockers are effective for the treatment of variant angina (Prinzmetal angina), angina pectoris, and possibly acute myocardial infarction. (See Chapter 18, section A.11.)
Although nitrates and β-adrenergic blockers are effective for angina, the calcium channel blockers are longer acting and may be used in the presence of chronic obstructive pulmonary disease and asthma. Calcium also plays a key role in cardiac electrical activity. The electrical activity of the sinuatrial (SA) and atrioventricular (AV) nodal cells are especially dependent on the calcium or "slow" current, whereas the rest of the specialized conduction system is more dependent on the sodium or "fast" current. Verapamil has a more profound influence on the calcium current of the SA node (SAN) and the AV node (AVN). This drug has been most useful in the treatment of supraventricular tachyarrhythmias, which are often caused by reentry through the AVN. In contrast, nifedipine has less influence on the SAN and no effect on AV conduction time. Therefore, nifedipine might be used where further suppression of AV conduction is undesirable. The relative cardiovascular effects of calcium channel blockers are shown in Table 7.1. Verapamil was found to profoundly depress the cardiovascular system during high concentrations of halothane, enflurane, or isoflurane anesthesia. However, because of a tendency for increased incidence of sinus arrest and bradycardia and more hemodynamic depression during enflurane anesthesia, Rogers and colleagues concluded that intravenous verapamil is better tolerated during low-dose isoflurane and halothane anesthesia than during comparable concentrations of enflurane anesthesia.
B.10. How would you premedicate the patient? Why?
The patient should be well sedated to prevent anxiety, which may precipitate angina. I usually give diazepam, 5 to 10 mg orally, or lorazepam, 1 to 2 mg orally, 1 hour before surgery. Two inches of nitroglycerin paste (Nitropaste) are applied prophylactically to the chest wall.
Even though atropine or scopolamine is not contraindicated, atropine is not given at the New York Presbyterian Hospital–Cornell Medical Center because of the possibility of tachycardia, which will increase oxygen demand.
All antianginal and antihypertensive drugs are continued until the time of surgery.
作者: xyz-cn99 时间: 2009-8-21 18:36
C. Intraoperative Management
C.I. Before Cardiopulmonary Bypass
C.I-1. How do you monitor the patient?
- ECG: simultaneous leads V5 and II, multiple-lead ST-segment analysis if available
- Arterial line for BP and arterial blood gas analyses
- Swan–Ganz catheter: PCWP, pulmonary artery diastolic pressure (PAD), hemodynamic study
- Central venous pressure (CVP) line: if the patient has good left ventricular function and no problems are expected
- Urine output
- Temperature: esophageal or pulmonary artery (PA), rectal or bladder, and tympanic or nasopharyngeal
- Laboratory: arterial blood gases, electrolytes, hematocrit, activated coagulation time (ACT), and PVO2
- Oxygen analyzer for inspired gas mixture
- End-tidal carbon dioxide analyzer
- Pulse oximeter for arterial oxygenation
- Transesophageal echocardiography (TEE) if not contraindicated (esophageal or stomach pathology)
- Cerebral oximeter, particularly for patients with high risks of postoperative neurologic outcomes
The Allen test is used to detect collateral ulnar circulation. The radial and ulnar arteries are occluded by the examiner's hands. The patient is then asked to make a tight fist to empty blood from the hand. The hand is held above the heart level to help venous drainage. If the patient is under anesthesia, the blood in the hand may be drained by a third person squeezing the hand. Then the hand is opened slowly and put down to the heart level. Only the ulnar compression is released. The flush of the hand is watched.
- Normal: less than 7 seconds
- Borderline: 7 to 15 seconds
- Abnormal: more than 15 seconds
C.I-3. Why do you need both esophageal and rectal temperatures?
In many medical centers, measurement of two or more temperatures is common practice. During cooling and rewarming, there is uneven distribution of body temperature. Esophageal, nasopharyngeal, or tympanic temperature represents core temperature; rectal temperature represents peripheral temperature. During cooling and rewarming using the pump oxygenator, esophageal temperature changes rapidly and the rectal temperature changes slowly. During surface cooling or warming, the rectal temperature changes quickly and the esophageal temperature changes slowly. To estimate the average temperature and to achieve even distribution of body temperature, it is necessary to record both esophageal and rectal temperatures. However, bladder temperature monitoring through a Foley catheter is quite convenient and popular; it reflects the body temperature between esophageal and rectal temperature.
Temperatures are measured during cooling to ensure that the organs believed most vulnerable to potential hypoperfusion actually receive the protective effect of the desired hypothermia. In this regard, the brain is usually the target. Nasopharyngeal, tympanic membrane, and esophageal temperatures are the usually accepted best estimates of brain temperature, even though they at times overestimate or underestimate the actual brain temperature. During rewarming, cerebral hyperthermia is often detected and should be avoided and corrected immediately because hyperthermia increases brain oxygen consumption and may exacerbate postoperative neuropsychologic dysfunction.
C.I-4. How would you know whether the Swan–Ganz catheter is in the right ventricle or the pulmonary artery?
There are three main differences in the pressure tracings, as shown in Fig. 7.2
Figure 7.2. Pressure tracings of right atrium (RA), right ventricle (RV), pulmonary artery (PA), and pulmonary capillary wedge pressure (PCWP).
Copyright © 2003 by Lippincott Williams and Wilkins
Diastolic Pressure Is Higher in the Pulmonary Artery than in the Right Ventricle
- PA pressure: 20 to 25/5 to 10 mm Hg
- RV pressure: 20 to 25/0 to 5 mm Hg
- PA pressure tracing has diacritic notch from closure of pulmonary valve.
- RV pressure tracing has plateau and sharp drop in early diastole.
- In the late diastolic phase, PA pressure is going down while the right ventricular pressure is going up because of ventricular filling.
- Normal: 4 to 12 mm Hg
- Borderline: 13 to 17 mm Hg
- Heart failure: more than 18 mm Hg
C.I-6. Is it necessary to monitor pulmonary artery pressure for coronary artery operations?
The indication to monitor PA pressure depends on left ventricular function. Patients may be divided into two categories on the basis of left ventricular function. For patients who have good left ventricular function (EF > 0.5 and good ventricular wall motion), the CVP correlates well with the PCWP; therefore, pulmonary pressure monitoring may not be necessary for this group of patients. On the other hand, for patients with poor left ventricular function (EF < 0.4 or ventricular dyssynergy), the CVP does not correlate with the PCWP; therefore, pulmonary pressure monitoring is indicated. Other indications for monitoring PA pressure include the presence of pulmonary hypertension, combined coronary stenosis and valvular disease, and complex cardiac lesions.
However, recently in an observational study of critically ill patients, after adjustment for treatment selection bias, monitoring PA pressure was associated with increased mortality and increased use of resources. The cause of this apparent lack of benefit is unclear. The result of this analysis should be confirmed in other studies. These findings justify reconsideration of a randomized controlled trial of right heart catheterization and may guide patient selection for such a study.
C.I-7. What are the complications of Swan–Ganz catheterization?
From Venipunctured Sites (as for Central Venous Pressure)
Common complications include the following:
- Infection: sepsis
- Hematoma
- Air embolism
- Thrombosis
- Catheter shearing and embolization
Subclavian approach:
- Pneumothorax
- Hemothorax
- Hydrothorax
Internal jugular approach:
- Pneumothorax
- Neck hematoma from puncture of carotid artery
- Possible vagus nerve injury and brachial plexus injury
- Thoracic duct perforation from the left-side approach
The basilar or cephalic vein approach has fewer complications, but the failure rate is higher.
From Swan–Ganz Catheter
Arrhythmias 1.5% to 11%, complete heart block, thromboemboli, pulmonary infarction from continuous wedging, massive hemorrhage from perforation of PA or right atrium, failure to wedge, hemoptysis, intracardiac knotting, balloon rupture, endocardial thrombi, and tricuspid valve injury
C.I-8. What are the hemodynamic consequences of myocardial ischemia? How can you detect myocardial ischemia? Is pulmonary capillary wedge pressure a sensitive indicator of myocardial ischemia?
For four decades after the classic observation of Tennant and Wiggers on the effects of coronary occlusion on myocardial contraction, it was believed that transient severe ischemia caused either irreversible cardiac injury—that is, infarction—or prompt recovery. However, in the 1970s it became clear that after a brief episode of severe ischemia, prolonged myocardial dysfunction with gradual return of contractile activity occurred, a condition termed myocardial stunning. Alternatively, severe chronic ischemia can result in diminished contractile performance such as chronic regional wall motion abnormalities (RWMAs) (hibernation).
Acute myocardial ischemia affects systolic and diastolic pump function. Systolic dysfunction is usually manifested before alterations in diastolic function. The immediate impact on ventricular compliance is related to the etiology of the ischemic event. Decreased myocardial oxygen supply is initially accompanied by an increase in compliance. In contrast, increased myocardial oxygen demand is associated with an immediate loss of ventricular compliance (i.e., the ventricle becomes stiffer). Thus, the ventricle requires a higher filling pressure (end-diastolic pressure [EDP]) to maintain a given stroke volume. A cascade of events occur that may include wall motion abnormalities, dysrhythmias, and conduction block. An 80% reduction of coronary blood flow causes akinesis, and a 95% decrease causes dyskinesis. If the ischemia becomes severe, the rise in EDP will lead to pulmonary edema (Fig. 7.3).
Figure 7.3. Hemodynamic consequences of myocardial ischemia. Ischemia occurs when demand exceeds supply. (LVEDP, left ventricular end-diastolic pressure; LVEDV, left ventricular end-diastolic volume; EF, ejection fraction; ST, ST-segment changes; CHF, congestive heart failure.) (From Barash PG. Monitoring myocardial oxygen balance: physiologic basis and clinical application. ASA Refresher Courses in Anesthesiology 1985;13:24, with permission.)
Although a number of sensitive techniques are available for detection of ischemia, such as magnetic resonance spectroscopy, radiolabeled lactate determinations, or direct measurement of EDP, they are impractical. The most popular and accepted sign of ischemia is ECG ST-segment changes. The ECG criteria for ischemia are horizontal or down-sloping ST-segment depression at least 0.1 mV at 0.06 second from J point, up-sloping ST-segment depression at least 0.2 mV at 0.08 second from J point, and ST-segment elevation at least 0.15 mV (1 mV = 10 mm). Other ECG signs of ischemia include inverted T waves and a new onset of arrhythmias or conduction abnormalities.
RWMAs, detected with two-dimensional (2D) echocardiography, have been shown to be the earliest and most sensitive sign of myocardial ischemia. A 25% decrease in coronary blood flow produced an RWMA without ECG changes, and a 50% decrease was required to cause ECG signs of ischemia. In patients with CAD, during exercise, an RWMA occurred after 30 seconds, and ECG changes did not occur until after 90 seconds. Smith and colleagues found that an RWMA was four times more sensitive than an ST-segment change on the ECG in detecting intraoperative ischemia. Moreover, ST-segment changes cannot be analyzed when the patient has conduction disturbance such as bundle–branch block or ventricularly paced rhythms. They found that patients experiencing persistent RWMAs were more likely to have myocardial infarction than those having only transient changes. No patient without a new wall motion abnormality had myocardial infarction. Hopefully, a smaller and more affordable echocardiography machine will be available in the future. Although TEE is the most sensitive monitor for myocardial ischemia, a recent study by Eisenberg and colleagues concludes that routine monitoring for myocardial ischemia with TEE or 12-lead ECG during noncardiac surgery appears to have little incremental clinical value over preoperative clinical data and two-lead ECG monitoring in identifying patients at high risk of perioperative ischemic outcome.
Measurement of PCWP has been suggested as an early and sensitive indicator of ischemia, to be used when the ECG is nondiagnostic. Although acute increases in PCWP or development of V waves may reflect ischemia, the absence of a change in PCWP does not ensure the absence of ischemia. Haggmark and colleagues reported that the sensitivity, specificity, and predictive value (positive and negative) of PCWP abnormalities for ischemia ranged between 40% and 60%. In patients undergoing CABG surgery, Lieberman and colleagues also found a low positive predictive value (24%) but a higher negative predictive value (85%); however, the PCWP was no better than CVP measurement, except in patients with moderate to severe preoperative ventricular dysfunction. Leung and colleagues found that 61% of TEE wall motion abnormalities in patients undergoing CABG surgery occurred without significant changes (>20% of control) in HR, systolic arterial pressure, or PA pressure. Only 10% of episodes were accompanied by 5 mm Hg or greater changes in PA pressure. Roizen and colleagues found that 11 of 12 patients developed TEE wall motion abnormalities when the aorta was cross-clamped above the supraceliac artery, but that PCWP remained normal (12 mm Hg) in 10 of 12 patients, with only 2 of the 12 patients having transient increases. Therefore, these studies question the value of PA catheterization and monitoring for detection of intraoperative ischemia.
C.I-9. How would you monitor electrocardiograms? Why V5? If you do not have precordial leads in your electrocardiography machine, how can you monitor the left ventricle?
Multiple-lead ECG monitoring provides the best clinically available method of detecting perioperative ischemia. Based primarily on results obtained from exercise treadmill testing, combined ECG leads II and V5, which can detect 96% of ischemic events, are suggested optimal leads for detecting intraoperative myocardial ischemia. However, London and colleagues recently found that the standard combination of leads II and V5 was only 80% sensitive, whereas combining leads V4 and V5 increased sensitivity to 90% in patients with known or suspected CAD undergoing noncardiac surgery with general anesthesia. The sensitivity increased to 96% by combining leads II, V4, and V5. If only one lead can be displayed, V5 should be used because lead V5 has the greatest sensitivity, 75% intraoperatively and 89% during exercise treadmill testing. (See Chapter 18, section C.3.)
C.I-10. Discuss the principles and clinical applications of intraoperative transesophageal two-dimensional echocardiography.
TEE is a well-established technique to visualize cardiac anatomy and function. Echocardiography is based on fundamental ultrasonic principles. Ultrasound is defined as sound above the upper threshold of human hearing (20,000 Hz). The ultrasound waves (1 to 7 MHz) are created by striking an appropriate piezoelectric crystal with an alternating electric current of 500 to 1,500 pulses per second. A short burst or pulse of high-frequency, low-intensity sound is then emitted and directed through the human body to detect boundaries between structures of different acoustic impedance. The ultrasound wave is partially reflected at the boundary of different acoustic impedance, a property that is primarily determined by the slight difference in density between different tissues. This technique is termed pulse-reflected ultrasound. The transmission of pulse-reflected ultrasound through the heart, with detection of the returning echoes detailing the position and movement of cardiac acoustic interfaces, is termed cardiac ultrasound or echocardiography. The difference between the M-mode and 2D techniques is that the M-mode ultrasonic beam is aimed in one direction and therefore depicts only one dimension of the target structure in an image that does not resemble cardiac structure, whereas the 2D beam sweeps in an arc to give a panoramic view of the heart that results in cross-sectional images that are anatomically recognizable. (See Chapter 8, section B.6.)
Doppler echocardiography provides an alternative method for imaging blood flow by applying Doppler frequency shift analysis to echoes reflected by the moving red blood cells. The Doppler principle states that the frequency of ultrasound reflected by a moving target (red blood cells) is different from the frequency of the emitted ultrasound. The shift in frequency is proportional to the speed of the moving target (red blood cells). Color-coded Doppler flow imaging (color Doppler) simultaneously presents real-time images of intracardiac flow and structure in two dimensions: continuous color maps of flow superimposed on monochromatic cross-sectional echocardiograms. Color Doppler greatly improves the evaluation of valvular function and intracardiac shunts.
The clinical applications of intraoperative echocardiography are listed in the following sections.
Monitoring Left Ventricular Filling and Ejection
When the left ventricular short-axis cross section is monitored at the midpapillary muscle, TEE provides the anesthesiologist with a direct quantitative method to assess left ventricular preload and ejection in real time to guide the administration of fluids and inotropes.
Ischemic Heart Disease
RWMAs, such as hypokinesia, akinesia, and dyskinesia, are the earliest signs of myocardial ischemia, as discussed in section C.I-8. Measurements of systolic wall thickening, another excellent sign of myocardial ischemia, are not reproducible because of a difficulty in delineating the epicardial border accurately in 2D echocardiography.
Valvular Heart Disease: Air Embolism
In the left atrium, left ventricle, and aorta, air embolism can be detected by TEE during open-heart surgery. Therefore, TEE can be used to help the surgeon more extensively evacuate air bubbles from the left heart before the heart ejects blood and air into the systemic circulation.
Valvular Regurgitation
Valvular regurgitation can be determined intraoperatively by color Doppler echocardiography immediately after conservative valve repair, annuloplasty, commissurotomy, or valve replacement.
Congenital Heart Disease
TEE technique will allow a more aggressive approach to complex cardiac reconstructions because the surgeon will have the ability to visualize the heart and evaluate adequacy of the surgical repair immediately after the operative procedure.
Thoracic Aorta
TEE can accurately diagnose thoracic aortic aneurysms, dissection, disruption, and atheromatosis. At the New York Presbyterian Hospital–Cornell Medical Center, TEE is routinely used for all patients to screen severe atheromatosis of aortic arch and descending aorta. Epiaortic echocardiography is performed to identify ascending aorta and arch if severe atheromatosis is found in the descending aorta or arch. Severe atheromatosis of the thoracic aorta is an independent predictor of postoperative neurologic outcome. The atheroma is graded as follows: grade I, normal to mild intimal thickening; grade II, severe intimal thickening; grade III, atheroma protruding more than 5 mm into the lumen; grade IV, atheroma protruding more than 5 mm; and grade V, atheroma with a mobile component.
Cardiac Tumors
Atrial myxoma can be easily diagnosed by TEE. Preoperative and postoperative TEE with contrast can assess the presence and severity of mitral regurgitation secondary to valve damage from the ball-valve effect of the myxoma.
Other Cardiac Lesions
Hypertrophic obstructive cardiomyopathy (HOCM) (idiopathic hypertrophic subaortic stenosis) can be identified with the development of systolic anterior motion (SAM) of the mitral valve. Cardiac tamponade by pericardial effusion or hematoma can be detected for preoperative differential diagnosis.
Neurosurgery
TEE was found to be the most sensitive monitor to detect venous air embolism during neurosurgery in the sitting position. Patent foramen ovale and paradoxical air embolism can be detected by TEE.
作者: xyz-cn99 时间: 2009-8-21 18:50
C.I-11. How would you induce anesthesia?
Midazolam, 1 to 2 mg, is given before insertion of an arterial line under local anesthesia. A smooth induction is essential to prevent hypotension, hypertension, and tachycardia. Different techniques may be used to achieve a smooth induction. For patients with good left ventricular function, anesthesia is induced with fentanyl, 5 to 10 μg/kg, and thiopental, 2 to 4 mg/kg. The patient is ventilated by mask with 100% oxygen. After administration of succinylcholine, 1 mg/kg, or pancuronium, 0.1 mg/kg, the patient is intubated. Alternatively, anesthesia is induced with thiopental, 4 mg/kg, and deepened with fentanyl, 5 to 10 μg/kg, and 2.0% isoflurane for 3 to 5 minutes. When adequately anesthetized, the patient is given a muscle relaxant and intubated. If the patient has a history of hypertension or the initial BP is more than 150 mm Hg systolically, fentanyl, 10 μg/kg, is usually required to blunt hypertension and tachycardia from intubation. For patients with poor left ventricular function, potent inhalation agents such as enflurane, isoflurane, and halothane are avoided during induction and maintenance of anesthesia. More midazolam, 2 to 5 mg, and less thiopental, 1 to 2 mg/kg, will be given for induction. Alternatively, etomidate, 0.2 mg, may be administered for induction. (See Chapter 14, section C.6, for other measures to prevent tachycardia and hypertension at the time of intubation.)
C.I-12. How would you maintain anesthesia?
Again, smooth anesthesia is essential to achieve a balance between myocardial oxygen demand and supply. Different agents and techniques may be used to accomplish the same goal. A combination of fentanyl and isoflurane is a popular choice. Alternatively, a neuroleptic technique with a moderate dose of the combination of fentanyl/droperidol/nitrous oxide/oxygen for maintenance of anesthesia may be used safely. After the patient is intubated, a mixture of 60% nitrous oxide and 40% oxygen is administered to keep the patient unconscious.
The depth of anesthesia must be titrated to meet the requirements of the varying intensities of surgical stimulation. Skin incision and sternal splitting are very painful. But the strongest stimulation is usually from sternal retraction with the self-retaining retractor. Fentanyl, 5 μg/kg, is given right before the skin incision. Droperidol, 0.1 mL/kg, is titrated in after the skin incision to keep SBP around 100 to 120 mm Hg. Another dose of fentanyl, 5 μg/kg, is given before sternotomy. Then fentanyl, 5 μg/kg, is given every 30 to 60 minutes to maintain anesthesia. Very high doses of fentanyl or sufentanil, with or without droperidol, and oxygen without nitrous oxide, have been successfully used for cardiac anesthesia. Diazepam or midazolam is administered to achieve unconsciousness and amnesia if droperidol is not used. I prefer droperidol because of its α-blocking effects, which can easily control hypertension when combined with a moderate dose of fentanyl. Meanwhile, at my institution, we believe mild cardiac depression from nitrous oxide may decrease the cardiac oxygen demand in a way similar to the effect of propranolol. The possibility of oxygen toxicity from the use of 100% oxygen should also be kept in mind. Nitrous oxide is not used after CPB, because it will increase potential air embolism in the bypass grafts, coronary circulation, and systemic circulation.
C.I-13. What is the better anesthetic agent for this operation: an inhalation or intravenous agent?
The choice of anesthetic agents is still debatable. Both inhalation and intravenous and combined agents have been used successfully. They both have advantages and disadvantages. Understanding the cardiovascular effects of each anesthetic agent and careful titration of each drug will improve the balance between myocardial oxygen demand and supply. Early detection and appropriate control of the major determinants of myocardial oxygen consumption (i.e., BP, HR, and PCWP) are mandatory if myocardial ischemia is to be avoided. Another consideration is the desirability of early extubation. High-dose narcotic and large doses of sedatives and muscle relaxants should be avoided if early extubation is planned.
Three large-scale outcome studies of patients undergoing CABG surgery reported that anesthetic choice did not affect incidence of perioperative morbidity and mortality.
C.I-14. What are the cardiovascular effects of halothane, enflurane, isoflurane, desflurane, sevoflurane, morphine, and fentanyl?
In general, halothane, enflurane, isoflurane, desflurane, and sevoflurane produce a dose-related depression in ventricular function and vascular tonus. Halothane sensitizes the heart to catecholamine much more than enflurane, isoflurane, desflurane, and sevoflurane. Isoflurane and desflurane depress cardiac output to a lesser degree than halothane or enflurane secondary to their greater vasodilating capacity. The HR changes least with halothane and increases most with desflurane. Isoflurane may cause tachycardia; the mechanism is unclear. Most studies suggest that halothane, enflurane, and isoflurane decrease coronary vascular resistance. Of these, isoflurane is the most potent coronary vasodilator.
All of the potent drugs decrease arterial pressure in a dose-related manner. The mechanism of the decrease in BP includes vasodilation, decreased cardiac output resulting from myocardial depression, and decreased sympathetic nervous system tone. With halothane, decreased cardiac output is the predominant cause. Halothane also increases venous compliance, and in patients who have high sympathetic tone, such as those with heart failure, halothane decreases systemic vascular resistance. Enflurane causes both vasodilation and decreased myocardial contractility. With isoflurane and desflurane a low peripheral resistance is the major cause of hypotension. Evidence of the relatively greater myocardial depression with halothane and enflurane is the greater increase in right atrial pressure seen with these drugs than with isoflurane.
Narcotics such as morphine and fentanyl at their clinical dose have minimal cardiovascular effects. Both may cause bradycardia. Neither sensitizes the heart to catecholamine or depresses myocardial function. The cardiovascular effects of morphine depend on the dose used. Large doses of morphine sulfate have reportedly caused myocardial lactate production and reduction in coronary blood flow in animals. Sethna and colleagues found that morphine sulfate, 0.25 mg/kg intravenously, did not produce a global myocardial ischemia in patients with CAD. High doses of morphine, 1 mg/kg, produce a significant decrease in arterial BP and systemic vascular resistance accompanied by an average 750% increase in plasma histamine. On the other hand, high doses of fentanyl, 50 file:///H:/images/special/mulower.gifg/kg, do not produce any significant changes in BP, vascular resistance, and plasma histamine levels.
C.I-15. Is isoflurane dangerous for the patient with coronary artery disease?
In patients with CAD, the use of isoflurane is still controversial. Reiz and colleagues reported that 1% isoflurane induced coronary vasodilation that was not related to normal autoregulation and that both decreased coronary perfusion pressure (systemic hypotension) and redistribution of myocardial blood flow (coronary steal) may contribute to the development of regional myocardial ischemia. Another study by Reiz and Ostman, using 1.5 minimum anesthetic concentration (MAC) isoflurane/nitrous oxide anesthesia, concluded that isoflurane may cause coronary steal with myocardial ischemia in patients with CAD. However, Smith and colleagues reported that the substitution of 0.5% to 1.12% isoflurane for 85 μg/kg of fentanyl did not result in an increased incidence of myocardial ischemia, as seen by ST-segment or segmental wall motion changes in patients with CAD. Moreover, Tarnow, Markschies-Hornung, and Schulte-Sasseu demonstrated that 0.5% isoflurane with 50% nitrous oxide improved the tolerance to pacing-induced myocardial ischemia in patients with significant CAD. Two large-scale prospective outcome studies by Slogoff and colleagues and Turman and colleagues could find no evidence that the incidence of ischemia was increased by isoflurane in patients with CAD undergoing CABG surgery. Furthermore, this finding held true even for patients with steal-prone coronary anatomy in the studies by Slogoff and colleagues, Pulley and colleagues, and Leung and colleagues.
Several animal studies further confused this issue. Priebe proved that isoflurane was a myocardial depressant and a potent coronary vasodilator in the dog. Sill and colleagues demonstrated that high concentrations of isoflurane (1.5% and 2.5%) dilated intramyocardial arterioles rather than epicardial coronary arteries in the intact dog. Buffington and colleagues reported that isoflurane (1.2% to 1.5%) produced a decrease in collateral flow and a decrement in collateral zone contraction while enhancing flow in the normally perfused zone. They concluded that isoflurane was an arteriolar vasodilator and hence produced coronary steal in dogs with chronic coronary occlusion. On the contrary, Cason and colleagues found that in the dog, isoflurane or halothane at 0.5% MAC and 1.5 MAC had little effect on coronary vascular resistance, and ischemia was precipitated by tachycardia or hypotension rather than by coronary steal. Moreover, Davis and Frank demonstrated that isoflurane decreased myocardial infarct size after left anterior descending coronary artery occlusion in dogs. In addition, Gilbert and colleagues reported greater coronary reserve in swine anesthetized with isoflurane versus halothane at 0.5 to 2.0 MAC. Recently, Hartman and colleagues demonstrated that adenosine but not isoflurane redistributed blood flow away from collateral-dependent myocardium in the presence of a coronary steal-prone anatomy in the chronically instrumented dog. They further found that reductions in myocardial perfusion during isoflurane anesthesia depend on systemic arterial pressure and that isoflurane did not produce coronary steal in this model of multivessel CAD. Furthermore, Cheng and colleagues found that neither isoflurane nor halothane as the sole anesthetic in clinical concentrations caused significant coronary vasodilation or coronary steal from 55 to 30 mm Hg coronary perfusion pressure in a swine model of chronic coronary occlusion with collateral development.
On the basis of recent animal and clinical studies, we can conclude that isoflurane in clinical concentrations may be used safely in patients with CAD provided that hypotension and tachycardia are avoided.
C.I-16. What is the cardiovascular effect of nitrous oxide?
Nitrous oxide is a weak central nervous system depressant. It has been generally considered to have minimal effects on other organ systems. Nitrous oxide has significant cardiovascular effects that may be depressant or stimulatory depending on the anesthetics with which it is used. When high-dose fentanyl is used during coronary surgery, the effects of nitrous oxide depend on the patient's cardiac function. After the administration of 50% nitrous oxide, there are no significant changes in any of the hemodynamic parameters in patients with normal left ventricular function (LVEDP < 15 mm Hg). On the contrary, there is a significant decrease in cardiac index and stroke volume index in patients with left ventricular dysfunction (LVEDP > 15 mm Hg). When added to other inhalational anesthetics, nitrous oxide increases arterial pressure and systemic vascular resistance, suggesting that it has a vasoconstrictive action. Nitrous oxide increases pulmonary vascular resistance in patients with mitral stenosis and pulmonary hypertension.
The pulmonary vascular effects of nitrous oxide are also variable. Patients with elevated PA pressure may have further increases when nitrous oxide is added. Konstadt and colleagues did not corroborate these findings in patients with mitral valvular disease. A study in infants failed to show further increases of pulmonary vascular resistance with the addition of nitrous oxide. It is of interest that the decrease in pulmonary vascular resistance with isoflurane is less than the decrease in systemic vascular resistance.
The contribution of nitrous oxide to myocardial ischemia is controversial. Philbin and colleagues suggested that addition of nitrous oxide to anesthesia with high-dose fentanyl, 100 μg/kg followed by 1 μg/kg per minute, or sufentanil, 30 μg/kg followed by 0.3 μg/kg per minute, can produce clinically inapparent regional myocardial ischemia in the areas supplied by stenotic coronary arteries of dogs. However, using 2D TEE, nitrous oxide added to low-dose fentanyl, 15 μg/kg followed by 0.2 μg/kg per minute, or high-dose sufentanil, 20 μg/kg, did not cause myocardial ischemia in patients with CAD.
Clinically, nitrous oxide may be used before CPB if high-dose narcotics are not used and hypotension does not occur. However, after CPB, nitrous oxide should be avoided because of the possibility of expanding air bubbles in the coronary and cerebral circulation.
C.I-17. What kind of muscle relaxant would you use? Why?
We usually use pancuronium. When full paralyzing doses are given in a bolus, D-tubocurarine tends to produce bradycardia and hypotension from ganglionic blockade and histamine release, whereas pancuronium and gallamine generally produce tachycardia and hypertension caused by vagolytic effect and norepinephrine released from cardiac sympathetic nerves. D-Tubocurarine may be given in increments of 6 mg every 5 to 10 minutes until patients are fully paralyzed (0.3 mg/kg). BP and HR are usually not changed by this small dose and slow injection rate. Pancuronium is a better choice if hypotension (BP < 80 mm Hg systolically) and bradycardia (HR < 50 beats per minute) are present. Theoretically, pancuronium may increase myocardial oxygen consumption caused by tachycardia and hypertension. However, pancuronium is the most commonly used muscle relaxant for CABG. In practice, most patients with CAD take file:///H:/images/special/betalower.gif-adrenergic blocking agents, which can decrease the vagolytic effect of pancuronium. Also, the bradycardia associated with the popular narcotic anesthetic techniques can attenuate the tachycardia induced by pancuronium. Vecuronium and cisatracurium have no major cardiovascular effects, but their intermediate duration of action necessitates frequent administration of the relaxant. Pipecuronium and doxacurium are two new long-acting, nondepolarizing muscle relaxants. They seem to have no hemodynamic side effects associated with neuromuscular blockade. They can be used in large bolus doses.
C.I-18. If ST-segment depression is seen during surgery, how would you treat it? What is the relationship between perioperative myocardial ischemia and postoperative myocardial infarction?
ST-segment depression indicates myocardial ischemia, either from increased oxygen demand or decreased oxygen supply. The treatment includes the following:
Gerson, Hickey, and Bainton (in experimental dogs) found that elevation of ST segments induced by occlusion of the coronary artery was more limited with halothane than with a combination of nitroprusside and propranolol. The more favorable effect of halothane was explained by its effects on coronary vascular reserve and the known effect of nitroprusside to reduce myocardial blood flow to ischemic myocardium.
If there are no obvious changes in BP, HR, and pulmonary wedge pressure, nitroglycerin is indicated for coronary spasm. Nitroglycerin may be given by intravenous drip. Sublingual nifedipine or intravenous nicardipine or diltiazem may be given to relieve coronary spasm.
In 1985, Slogoff and Keats reported that perioperative myocardial ischemia occurred in 37% of all patients undergoing CABG. They proved that perioperative myocardial infarction was almost three times as frequent in patients with ischemia (6.9%) compared with patients without ischemia (2.5%). Intraoperative tachycardia was associated with a higher incidence of myocardial ischemia and infarction. However, Knight and colleagues demonstrated that 42% of patients undergoing CABG had preoperative episodes of myocardial ischemia, 87% of which were clinically silent. They further found that anesthesia and surgery did not worsen the preoperative ischemic pattern. Furthermore, in another study in 1989, Slogoff and Keats postulated that approximately 90% of new myocardial ischemia observed during anesthesia was the manifestation of silent ischemia observed in the patient before the operation and only 10% was related to anesthetic management. Therefore, the relationship between intraoperative ischemia and postoperative outcome is still unsolved.
C.I-19. Would you use prophylactic nitroglycerin during coronary artery bypass grafting to prevent intraoperative myocardial ischemia or perioperative myocardial infarction?
No. It has been reported that prophylactic administration of nitroglycerin, 0.5 or 1.0 mg/kg per minute, during fentanyl anesthesia in patients undergoing CABG did not prevent myocardial ischemia or reduce the incidence of perioperative myocardial infarction.
C.I-20. How would you correct hypertension?
BP=blood flow/resistance
Hypertension is usually due to inadequate depth of anesthesia. Occasionally, it is due to fluid overloading. The treatment of hypertension includes the following:
C.I-21. How would you treat hypotension?
Hypotension is usually caused by hypovolemia, deep anesthesia, bradycardia, or CHF. The treatments are as follows:
C.I-22. What are the indications for intravenous propranolol or esmolol during surgery? How much would you give? What are the relative contraindications?
Indications
Dosages
Propranolol, 0.25-mg increments every 1 to 2 minutes, total dose 2 to 3 mg
Esmolol, 10-mg increments up to 0.5 mg/kg followed by 50- to 300-μg/kg per minute intravenous drip
C.I-23. How would you correct increased pulmonary capillary wedge pressure?
It is important to treat the patient as a whole. All monitors must be considered together, not only one single parameter. Increased PCWP is usually due to a light level of anesthesia or CHF. Combining the readings of PCWP and BP will produce a differential diagnosis. Occasionally, an increased PCWP with hypotension and low cardiac output is caused by HOCM. HOCM can be diagnosed by TEE, which demonstrates SAM of mitral valve, mitral regurgitation, and usually good left ventricular contractility.
Inadequate Anesthesia: Increased PCWP with Hypertension
C.I-24. During sternal splitting, would you do something?
Stop ventilation and deflate the lungs to prevent lung injury from the electric saw.
C.I-25. Would you monitor pulmonary capillary wedge pressure continuously? Why?
No, if the Swan–Ganz catheter balloon is inflated continuously, pulmonary infarction distal to the occlusion may ensue. Usually PA diastolic pressure (PADP) is monitored continuously because PADP is very close to PCWP.
C.I-26. Discuss autologous transfusion and blood conservation for cardiac surgery.
Autologous transfusion is the collection and reinfusion of the patient's own blood or blood components. The realization that homologous blood is responsible for transmission of acquired immune deficiency syndrome (AIDS), hepatitis, transfusion reaction, and autosensitization has led to increased interest in autologous transfusion and blood conservation. There are several options for autologous transfusion: preoperative autologous blood donation, preoperative use of erythropoietin, intraoperative normovolemic hemodilution, intraoperative plasmapheresis, pharmacologic treatment, and perioperative blood salvage.
Preoperative Autologous Blood Donation
Donations are appropriate for properly selected patients with stable CAD, stable valvular disease, and congenital heart disease. The risk of blood donation may be higher for patients with unstable angina or severe aortic stenosis; these patients are usually not considered good candidates for autologous blood donation. The patient should have a hemoglobin level of more than 11 g/dL to donate blood.
The optimal donation period begins 4 to 6 weeks before surgery, and the last donation is usually collected no later than 72 hours before surgery.
Preoperative Use of Erythropoietin
This is an established and efficacious but relatively expensive therapy to reduce blood transfusions. To optimize the hemoglobin response, oral or intravenous iron supplementation is recommended.
Intraoperative Normovolemic Hemodilution
This is the removal of blood through an arterial or venous catheter immediately after induction of anesthesia, before CPB or the administration of heparin. Depending on the patient's size and hematocrit level, 500 to 1,000 mL of blood is collected into blood bags containing CPDA-1 anticoagulant and is kept at room temperature.
This blood is spared the rigors of CPB, including hemolysis, platelet destruction, and clotting factor degradation. The autologous blood is transfused after reversal of the heparin with protamine. It has been demonstrated that the effect of 1 unit of fresh whole blood on platelet aggregation after CPB is at least equal, if not superior, to the effect of 8 to 10 stored platelet units. However, if the patient's hematocrit level is less than 33% or the hemoglobin level is less than 11 g/dL, normovolemic hemodilution is not recommended because further decreasing the oxygen-carrying capacity may worsen myocardial ischemia. In addition, hemodilution during CPB will further decrease the hematocrit to levels that require homologous blood transfusion. Normovolemic hemodilution should be performed cautiously in patients with critical left main coronary stenosis and aortic stenosis because sudden cardiac arrest has been observed during the procedure.
Intraoperative Plasmapheresis
Coagulopathy associated with hypothermia, shock, CPB, multiple transfusions, and the blood salvage technique, which removes clotting factors and platelets, often necessitates use of fresh frozen plasma and platelet packs to control postoperative bleeding and clotting problems. Recently a plasma-collection system has been developed to salvage up to 1,000 mL of platelet-rich plasma before CPB. This technique does not cause hemodilution, so it can be used in all patients, including those with anemia. The platelet-rich plasma can be stored at room temperature until transfused, usually after protamine reversal of the heparin. It is recommended that the collected product be placed on a rocker until infusion and that the pH level be held constant.
Pharmacologic Treatment
The prophylactic use of aprotinin, ε-aminocaproic acid (EACA) and tranexamic acid reduces blood transfusions in cardiac surgery. Aprotinin inhibits a host of proteases, including trypsin, plasmin, kallikrein, and factor XIIa activation of complement. The adult dose is 2 million kallikrein-inhibition units (KIU) for the patient and bypass pump, followed by 500,000 KIU per hour for 4 hours. The synthetic antifibrinolytics, EACA and tranexamic acid, bind to plasminogen and plasmin, thus inhibiting binding of plasminogen at the lysine residues of fibrinogen. Effective antifibrinolysis requires a loading dose of 100 to 150 mg/kg for EACA or 10 mg/kg for tranexamic acid and a constant infusion for each at one tenth the loading dose each hour.
Perioperative Blood Salvage
This is the collection and reinfusion of blood lost during and immediately after surgery. The posttransfusion survival of perioperatively salvaged red blood cells has been shown to be comparable to that of allogeneic red blood cells. At the conclusion of CPB, all blood remaining in the oxygenator and bypass circuits should be salvaged and if needed infused. Blood salvaged intraoperatively may be transfused directly (unwashed) or processed (washed) before infusion. Commercially available equipment exists for each option. Blood collected by intraoperative salvage represents an excellent source of red blood cell support. However, salvaged blood is deficient in coagulation factors and platelets.
Postoperative blood salvage is another technique of autologous blood transfusion using blood lost after surgery. Blood salvaged after cardiac surgery is generally collected from mediastinal and chest drains and transfused without washing. Because it is usually defibrinated, it does not require anticoagulation before transfusion. Though dilute, the blood is sterile and contains viable red cells.
作者: 老骥伏枥 时间: 2009-10-6 21:36
本帖最后由 老骥伏枥 于 2009-10-19 19:43 编辑
问题导向的麻醉管理
一个57岁老人，有三支冠脉病变，拟行CABG，7个月前有心肌梗死病史。现正服用硝酸甘油，地高辛，普萘洛尔，异硝酸山梨醇（消心痛），硝苯地平。血压120\80mmHg,心率60bpm。
A内科疾病和鉴别诊断。1，什么是三支冠脉疾病？说出这几支冠脉血管的名字。2，CABG的适应症是什么？3，什么是经皮冠状动脉球囊扩张术？说出其适应症，禁忌症和并发症。4，CABG的并发症？
B，围术期评估和准备？1，你会指定哪些术前检查？如何评估患者的左室功能？2，决定心肌耗氧的三大主要因素是什么？临床上它们如何测量？3，4，决定心肌氧供的因素是什么？5，你会停用地高辛吗？它的半衰期与多长？6，你会停用普萘洛尔吗？其半衰期？肾上腺素能阻断剂在治疗充血性心力衰竭时所起到的作用是什么？7,如果正在服用普萘洛尔的患者术中出现了低血压，你如何处理？8，硝苯地平是什么？它的作用原理？9，如何投以术前用药？为什么？
C1，CPB术中管理：1，需要哪些监护？什么是Allen试验？2，你需要测量食道和直肠温度吗？3，你如何判断S-G导管是在右室还是肺动脉？4，什么是肺小动脉楔压？5，对于冠状动脉手术有必要监测肺动脉压吗？6，放置S-G导管的并发症？7，心肌缺血的血流动力学变化如何？你怎样发现心肌缺血？PCWP是心肌缺血的灵敏指标吗？8，你如何监测ECG？V5导联的使用？（为什么是V5？）9，如果你没有胸前导联，如何监测左室？10，说出经食道二维超声的原理及应用？11，怎样减浅麻醉，怎样维持麻醉？12，对于该手术较好的麻醉药是什么？吸入或静脉药？13，什么是氟烷，异氟醚，恩氟醚，七氟醚，地氟醚，吗啡，芬太尼的心血管效应？14，对于伴有冠状动脉疾病的患者，异氟醚比较危险吗？15，笑气的心血管效应？15，你会选择哪种肌松药，为什么？16，如果术中S-T段一直压低，你如何对待？术中心肌缺血与术后心肌梗塞的联系？17，CABG你会预防性使用硝甘来预防心肌缺血与围术期心梗吗？18，你会如何纠正高血压？18，你如何纠正低血压？19，术中应用普萘洛尔和艾洛的指征？你会给多少？其相关禁忌症是什么？20，你怎样调节升高的PCWP？21，撑开胸骨时你会做什么？22，你会持续监测PCWP吗？为什么？23，讨论心脏手术的自体输血和血液保护。
C2，1，CPB期间。CPB之前你会给什么抗凝剂？给多少？其作用机理是什么？
2，肝素的半衰期？它如何消除？如何监测肝素的量？什么是ACT？
3，什么是全心肺分流？什么是部分心肺分流？
4，左室减压的意义？
5，氧合器有几种类型？各自的优缺点？
6，你会使用哪种预充液？量？用不用血预充？为什么？
7，血液稀释的优缺点？
8，你用哪种泵？是搏动性的吗？
9，期间你会观察患者吗？
10，在CPB期间血压会维持多少？为何？
11，CPB期间的低血压如何处理？
12，CPB期间的高血压如何处理？（MAP>100mmHg）
13，你怎样准备硝甘和硝普钠的静脉输入？常用剂量？你会选择哪种？
14，CPB期间用哪种泵维持？
15，低温时如何调节泵流量？
16，低温的优势？低温能否提供神经保护？
17，在低温和血压稀释时血粘度如何改变？
18，意外低温与死亡相关的主要原因？
19，CPB中你会给麻醉药吗？为什么？
20，CPB期间你会给肌松药吗？为什么？CPB对肌松药的活性有什么样的影响？
21，你怎么知道CPB期间病人得到了良好灌注？
22，你使用的人工肺气体流量是多少？你用的哪种气体？为什么？
23，CPB期间低PaCO2的不利之处是什么？
24，CPB期间动脉血气与电解质结果如下：pH, 7.36; PaCO 2, 42 mm Hg; PaO 2, 449 mm Hg; CO2 content, 24 mEq/L; Na, 128 mEq/L; K, 5.8 mEq/L; and HcT, 20%. 病人的体温是27°C. 血气是在温度多少时测量的? 如何根据患者的体温更正血气结果? 你在监测血气是否异常的时候是以37摄氏度还是病人现在的温度为标准？
1，如果氧合器的液面降低，你会用什么补充？血液？平衡盐？
2，你如何知道CPB期间的液体平衡？
3，CPB期间的心肌保护？
4，什么是心脏停跳液？用量？
5，主动脉可以被阻断多长时间？
6，为什么CPB2个小时后尿液会变成粉色？什么是血浆蛋白的肾阈？
7，病人可以脱离心肺旁路的温度？
8，为什么用心肺机给病人复温的时间比降温的时间要长？
9，为什么脱机时常常要投以氯化钙？
10, 如果心率40bpm，你会如何处理？
11,CPB中血糖如何变化？为什么？高血糖会增加CPB期间神经系统并发症吗？
12,CPB对血小板和凝血因子有什么影响？
13, 你会为停机做哪些准备？
14, 你如何判断是否需要变力支持？
C2你会如何中和肝素？用多少鱼精蛋白？，
1，鱼精蛋白的作用机制？
2，鱼精蛋白过多的并发症？
3，为什么有点而患者给鱼精蛋白后会出现肺动脉高压？你会如何处理？如何预防之？
4，IABP的适应症？
5，IABP的原理？
6，IABP的并发症？
7，CABG后PAWP能否反映LVEDP？
D1，术后的并发症有哪些？
2， 你会拮抗肌松药吗？为什么？何时脱离呼吸机？
3，脱离呼吸机的标准？
A1,三支冠脉疾病通常包括：右冠脉，左前降支，左回旋支。冠脉的分支如图7.1所示。人群中50%——60%窦房结是由右冠脉供血的，其余40%——50%由左回旋支供血。对于85%——90%的人群来说房室结有右冠脉供血，另10%——15%是由左回旋支供血。所以，对于85%——90%的人群来说右主干占支配地位。最常见的CABG手术针对的是左前降支，钝缘支，后降支。
A2，CABG的指征，是出于改善生活质量的需要。对于药物无法控制的心绞痛，不能耐受药物副作用的病人都应考虑血管重建。如今，PTCA已经成为上述缺血性心脏病患者的第一选择。自PTCA1978年引进以来，它已经将进行血管成形术的患者进行了分类：那些有近心端散在的冠状动脉狭窄者应作PTCA，不适合行PTCA者应作CABG。而适合做CABG者通常是那些有更严重缺血性心脏病和左室功能下降的老年病人。CABG的指征：1，不稳定心绞痛和持久的心肌缺血发作。2，投以最佳药物，心绞痛治疗仍不满意。3，心梗后反复发作的心肌缺血。4，有冠状动脉阻塞的变异型心绞痛。5，左冠脉主干高度闭塞，三支或双支阻塞，左前降支近心端阻塞。6，急性心梗，心源性休克，难以控制的室性心律失常。7，干扰正常生活的稳定性心绞痛。
A3，自从PTCA1977年引进以后便得到了快速发展。对于一些特定的心绞痛病人来说是可以接受的。该技术是用一个3F的小导管进入相应的冠状动脉，随着导管的气囊部分通过狭窄，充气的的气囊使狭窄扩张。内膜腔的增宽是由可控制的损伤造成的（包括斑块压缩，内膜龟裂，中层拉伸）来实现的。PTCA的指征最近有所更改。随着技术的进步，PTCA已经可用于尽管最好的药物治疗仍不能控制的缺血症状者，以及无论什么原因引起的局灶性阻塞性冠脉疾病者。PTCA的指征如下：1，孤立，散在的近端血管病变。2，近端双支病变。3，CABG术后新的狭窄形成或吻合口的远端狭窄。4，PTCA术后再狭窄。5，存在CABG的禁忌症。6，心脏移植后的冠脉狭窄。7，6个月以内的血管狭窄，且狭窄<15mm。8，以血管重建为目的的链激酶治疗术后。
PTCA的适应症：1，左主干病变且远端血管尚未形成代偿。2，伴有严重的主动脉粥样硬化的多支病变。3，无严重的阻塞性病变。4，不能实施合法的心外手术的机构。PTCA的结果如下：最初成功率是90%，治疗后6个月内再狭窄的几率是30%，再次实施球囊扩张的概率是90%，二次处理后动脉倾向于保持开放。随着支架的引入，冠状动脉再狭窄的几率降低了。A4，冠脉旁路手术的结果：Kuan, Bernstein, and Ellestad报道围术期心肌梗死率是4%——6%，大型医学中心CABG总的死亡率是1%，而再次手术死亡率是2%——3%，Rahimtoola和同事们研究了因不稳定心绞痛而十年前曾行CABG者的生存状态。第一个月的死亡率是1.8%，五年生存率是92%，十年生存率是83%，每年会有1%——2%的曾行CABG者会再次手术。81%曾行CABG者完全没有或仅有轻微的心绞痛。Loop和同事们发现接受乳内动脉移植者与静脉移植者十年生存率相比，单支病变93.4%与88%，双支90%与79.5%，三支病变82.6%与71%。Zai CABG术后的第一个年末，乳内动脉未闭率约85%——95%，而大隐静脉未闭率为38%——45%。7个随机试验大体展示了1972——1984年间冠脉旁路手术与药物治疗在2649名患者中的比较。曾行CABG者与接收药物治疗者在第5，7，10年相比有明显的低死亡率。但到了第十年，药物治疗族的41%将接受CABG。CABG延长了如下病人的生存期限：严重左主干病变者（无论症状如何），多支血管病变者，左室功能损害者，以及包括左前降支病变在内的三支病变。（不论左室功能如何）。外科治疗已被证明可以延长双支血管病变以及左室功能障碍者的生存期，特别是那些有左前降支严重狭窄者。虽然没有文献报道单支病变者通过外科治疗可获得生存率的改善，但已有证据证明有严重左室功能损害者长期生存率极低。有心绞痛和或心肌缺血的证据能胜任轻到中度的运动者，特别是那些有左前降支阻塞者，可以从再血管化手术中（血管成形术或旁路手术）中获益。
B1,1，通过心绞痛与心肌缺血的病史。2，左心衰的症状与体征：呼吸困难，夜间端坐呼吸，凹陷性水肿。3，心导管检查：冠脉造影，超声心动图。4，射血分数。5，左室舒张末期压与毛细血管楔压（正常6——15mmHg）！6，左室壁运动：不运动，运动减退，反常运动。7，心指数（正常3L\min\m2）。8，与压力容积环相关的收缩末期压力——容积关系。B3 决定心肌氧耗的三大主要因素是室壁张力，收缩力，心率。可通过下列手段测量：室壁张力：1，前负荷，LVEDP，LVEDV，PCWP。2，后负荷：无主动脉狭窄时的收缩压以及收缩期室内压。收缩力：侵入性的检查，如最大收缩速度，心室压力——时间描记图或者左室收缩末期压力——容积比。非侵入性的检查：射学前期时间\射血时间。超声心动图所示的室壁运动情况。心率：ECG。
作者: roseseana 时间: 2011-9-26 18:10
triple index 我怎么第一次知道 好无知。。。
Although a number of sensitive techniques are available for detection of ischemia, such as magnetic resonance spectroscopy, radiolabeled lactate determinations, or direct measurement of EDP, they are impractical. The most popular and accepted sign of ischemia is ECG ST-segment changes. The ECG criteria for ischemia are horizontal or down-sloping ST-segment depression at least 0.1 mV at 0.06 second from J point, up-sloping ST-segment depression at least 0.2 mV at 0.08 second from J point, and ST-segment elevation at least 0.15 mV (1 mV = 10 mm). Other ECG signs of ischemia include inverted T waves and a new onset of arrhythmias or conduction abnormalities.
RWMAs, detected with two-dimensional (2D) echocardiography, have been shown to be the earliest and most sensitive sign of myocardial ischemia. A 25% decrease in coronary blood flow produced an RWMA without ECG changes, and a 50% decrease was required to cause ECG signs of ischemia. In patients with CAD, during exercise, an RWMA occurred after 30 seconds, and ECG changes did not occur until after 90 seconds. Smith and colleagues found that an RWMA was four times more sensitive than an ST-segment change on the ECG in detecting intraoperative ischemia. Moreover, ST-segment changes cannot be analyzed when the patient has conduction disturbance such as bundle–branch block or ventricularly paced rhythms. They found that patients experiencing persistent RWMAs were more likely to have myocardial infarction than those having only transient changes. No patient without a new wall motion abnormality had myocardial infarction. Hopefully, a smaller and more affordable echocardiography machine will be available in the future. Although TEE is the most sensitive monitor for myocardial ischemia, a recent study by Eisenberg and colleagues concludes that routine monitoring for myocardial ischemia with TEE or 12-lead ECG during noncardiac surgery appears to have little incremental clinical value over preoperative clinical data and two-lead ECG monitoring in identifying patients at high risk of perioperative ischemic outcome.
Measurement of PCWP has been suggested as an early and sensitive indicator of ischemia, to be used when the ECG is nondiagnostic. Although acute increases in PCWP or development of V waves may reflect ischemia, the absence of a change in PCWP does not ensure the absence of ischemia. Haggmark and colleagues reported that the sensitivity, specificity, and predictive value (positive and negative) of PCWP abnormalities for ischemia ranged between 40% and 60%. In patients undergoing CABG surgery, Lieberman and colleagues also found a low positive predictive value (24%) but a higher negative predictive value (85%); however, the PCWP was no better than CVP measurement, except in patients with moderate to severe preoperative ventricular dysfunction. Leung and colleagues found that 61% of TEE wall motion abnormalities in patients undergoing CABG surgery occurred without significant changes (>20% of control) in HR, systolic arterial pressure, or PA pressure. Only 10% of episodes were accompanied by 5 mm Hg or greater changes in PA pressure. Roizen and colleagues found that 11 of 12 patients developed TEE wall motion abnormalities when the aorta was cross-clamped above the supraceliac artery, but that PCWP remained normal (12 mm Hg) in 10 of 12 patients, with only 2 of the 12 patients having transient increases. Therefore, these studies question the value of PA catheterization and monitoring for detection of intraoperative ischemia.
C.I-9. How would you monitor electrocardiograms? Why V5? If you do not have precordial leads in your electrocardiography machine, how can you monitor the left ventricle?
Multiple-lead ECG monitoring provides the best clinically available method of detecting perioperative ischemia. Based primarily on results obtained from exercise treadmill testing, combined ECG leads II and V5, which can detect 96% of ischemic events, are suggested optimal leads for detecting intraoperative myocardial ischemia. However, London and colleagues recently found that the standard combination of leads II and V5 was only 80% sensitive, whereas combining leads V4 and V5 increased sensitivity to 90% in patients with known or suspected CAD undergoing noncardiac surgery with general anesthesia. The sensitivity increased to 96% by combining leads II, V4, and V5. If only one lead can be displayed, V5 should be used because lead V5 has the greatest sensitivity, 75% intraoperatively and 89% during exercise treadmill testing. (See Chapter 18, section C.3.)
C.I-10. Discuss the principles and clinical applications of intraoperative transesophageal two-dimensional echocardiography.
TEE is a well-established technique to visualize cardiac anatomy and function. Echocardiography is based on fundamental ultrasonic principles. Ultrasound is defined as sound above the upper threshold of human hearing (20,000 Hz). The ultrasound waves (1 to 7 MHz) are created by striking an appropriate piezoelectric crystal with an alternating electric current of 500 to 1,500 pulses per second. A short burst or pulse of high-frequency, low-intensity sound is then emitted and directed through the human body to detect boundaries between structures of different acoustic impedance. The ultrasound wave is partially reflected at the boundary of different acoustic impedance, a property that is primarily determined by the slight difference in density between different tissues. This technique is termed pulse-reflected ultrasound. The transmission of pulse-reflected ultrasound through the heart, with detection of the returning echoes detailing the position and movement of cardiac acoustic interfaces, is termed cardiac ultrasound or echocardiography. The difference between the M-mode and 2D techniques is that the M-mode ultrasonic beam is aimed in one direction and therefore depicts only one dimension of the target structure in an image that does not resemble cardiac structure, whereas the 2D beam sweeps in an arc to give a panoramic view of the heart that results in cross-sectional images that are anatomically recognizable. (See Chapter 8, section B.6.)
Doppler echocardiography provides an alternative method for imaging blood flow by applying Doppler frequency shift analysis to echoes reflected by the moving red blood cells. The Doppler principle states that the frequency of ultrasound reflected by a moving target (red blood cells) is different from the frequency of the emitted ultrasound. The shift in frequency is proportional to the speed of the moving target (red blood cells). Color-coded Doppler flow imaging (color Doppler) simultaneously presents real-time images of intracardiac flow and structure in two dimensions: continuous color maps of flow superimposed on monochromatic cross-sectional echocardiograms. Color Doppler greatly improves the evaluation of valvular function and intracardiac shunts.
The clinical applications of intraoperative echocardiography are listed in the following sections.
Monitoring Left Ventricular Filling and Ejection
When the left ventricular short-axis cross section is monitored at the midpapillary muscle, TEE provides the anesthesiologist with a direct quantitative method to assess left ventricular preload and ejection in real time to guide the administration of fluids and inotropes.
Ischemic Heart Disease
RWMAs, such as hypokinesia, akinesia, and dyskinesia, are the earliest signs of myocardial ischemia, as discussed in section C.I-8. Measurements of systolic wall thickening, another excellent sign of myocardial ischemia, are not reproducible because of a difficulty in delineating the epicardial border accurately in 2D echocardiography.
Valvular Heart Disease: Air Embolism
In the left atrium, left ventricle, and aorta, air embolism can be detected by TEE during open-heart surgery. Therefore, TEE can be used to help the surgeon more extensively evacuate air bubbles from the left heart before the heart ejects blood and air into the systemic circulation.
Valvular Regurgitation
Valvular regurgitation can be determined intraoperatively by color Doppler echocardiography immediately after conservative valve repair, annuloplasty, commissurotomy, or valve replacement.
Congenital Heart Disease
TEE technique will allow a more aggressive approach to complex cardiac reconstructions because the surgeon will have the ability to visualize the heart and evaluate adequacy of the surgical repair immediately after the operative procedure.
Thoracic Aorta
TEE can accurately diagnose thoracic aortic aneurysms, dissection, disruption, and atheromatosis. At the New York Presbyterian Hospital–Cornell Medical Center, TEE is routinely used for all patients to screen severe atheromatosis of aortic arch and descending aorta. Epiaortic echocardiography is performed to identify ascending aorta and arch if severe atheromatosis is found in the descending aorta or arch. Severe atheromatosis of the thoracic aorta is an independent predictor of postoperative neurologic outcome. The atheroma is graded as follows: grade I, normal to mild intimal thickening; grade II, severe intimal thickening; grade III, atheroma protruding more than 5 mm into the lumen; grade IV, atheroma protruding more than 5 mm; and grade V, atheroma with a mobile component.
Cardiac Tumors
Atrial myxoma can be easily diagnosed by TEE. Preoperative and postoperative TEE with contrast can assess the presence and severity of mitral regurgitation secondary to valve damage from the ball-valve effect of the myxoma.
Other Cardiac Lesions
Hypertrophic obstructive cardiomyopathy (HOCM) (idiopathic hypertrophic subaortic stenosis) can be identified with the development of systolic anterior motion (SAM) of the mitral valve. Cardiac tamponade by pericardial effusion or hematoma can be detected for preoperative differential diagnosis.
Neurosurgery
TEE was found to be the most sensitive monitor to detect venous air embolism during neurosurgery in the sitting position. Patent foramen ovale and paradoxical air embolism can be detected by TEE.
作者: xyz-cn99 时间: 2009-8-21 18:50
C.I-11. How would you induce anesthesia?
Midazolam, 1 to 2 mg, is given before insertion of an arterial line under local anesthesia. A smooth induction is essential to prevent hypotension, hypertension, and tachycardia. Different techniques may be used to achieve a smooth induction. For patients with good left ventricular function, anesthesia is induced with fentanyl, 5 to 10 μg/kg, and thiopental, 2 to 4 mg/kg. The patient is ventilated by mask with 100% oxygen. After administration of succinylcholine, 1 mg/kg, or pancuronium, 0.1 mg/kg, the patient is intubated. Alternatively, anesthesia is induced with thiopental, 4 mg/kg, and deepened with fentanyl, 5 to 10 μg/kg, and 2.0% isoflurane for 3 to 5 minutes. When adequately anesthetized, the patient is given a muscle relaxant and intubated. If the patient has a history of hypertension or the initial BP is more than 150 mm Hg systolically, fentanyl, 10 μg/kg, is usually required to blunt hypertension and tachycardia from intubation. For patients with poor left ventricular function, potent inhalation agents such as enflurane, isoflurane, and halothane are avoided during induction and maintenance of anesthesia. More midazolam, 2 to 5 mg, and less thiopental, 1 to 2 mg/kg, will be given for induction. Alternatively, etomidate, 0.2 mg, may be administered for induction. (See Chapter 14, section C.6, for other measures to prevent tachycardia and hypertension at the time of intubation.)
C.I-12. How would you maintain anesthesia?
Again, smooth anesthesia is essential to achieve a balance between myocardial oxygen demand and supply. Different agents and techniques may be used to accomplish the same goal. A combination of fentanyl and isoflurane is a popular choice. Alternatively, a neuroleptic technique with a moderate dose of the combination of fentanyl/droperidol/nitrous oxide/oxygen for maintenance of anesthesia may be used safely. After the patient is intubated, a mixture of 60% nitrous oxide and 40% oxygen is administered to keep the patient unconscious.
The depth of anesthesia must be titrated to meet the requirements of the varying intensities of surgical stimulation. Skin incision and sternal splitting are very painful. But the strongest stimulation is usually from sternal retraction with the self-retaining retractor. Fentanyl, 5 μg/kg, is given right before the skin incision. Droperidol, 0.1 mL/kg, is titrated in after the skin incision to keep SBP around 100 to 120 mm Hg. Another dose of fentanyl, 5 μg/kg, is given before sternotomy. Then fentanyl, 5 μg/kg, is given every 30 to 60 minutes to maintain anesthesia. Very high doses of fentanyl or sufentanil, with or without droperidol, and oxygen without nitrous oxide, have been successfully used for cardiac anesthesia. Diazepam or midazolam is administered to achieve unconsciousness and amnesia if droperidol is not used. I prefer droperidol because of its α-blocking effects, which can easily control hypertension when combined with a moderate dose of fentanyl. Meanwhile, at my institution, we believe mild cardiac depression from nitrous oxide may decrease the cardiac oxygen demand in a way similar to the effect of propranolol. The possibility of oxygen toxicity from the use of 100% oxygen should also be kept in mind. Nitrous oxide is not used after CPB, because it will increase potential air embolism in the bypass grafts, coronary circulation, and systemic circulation.
C.I-13. What is the better anesthetic agent for this operation: an inhalation or intravenous agent?
The choice of anesthetic agents is still debatable. Both inhalation and intravenous and combined agents have been used successfully. They both have advantages and disadvantages. Understanding the cardiovascular effects of each anesthetic agent and careful titration of each drug will improve the balance between myocardial oxygen demand and supply. Early detection and appropriate control of the major determinants of myocardial oxygen consumption (i.e., BP, HR, and PCWP) are mandatory if myocardial ischemia is to be avoided. Another consideration is the desirability of early extubation. High-dose narcotic and large doses of sedatives and muscle relaxants should be avoided if early extubation is planned.
Three large-scale outcome studies of patients undergoing CABG surgery reported that anesthetic choice did not affect incidence of perioperative morbidity and mortality.
C.I-14. What are the cardiovascular effects of halothane, enflurane, isoflurane, desflurane, sevoflurane, morphine, and fentanyl?
In general, halothane, enflurane, isoflurane, desflurane, and sevoflurane produce a dose-related depression in ventricular function and vascular tonus. Halothane sensitizes the heart to catecholamine much more than enflurane, isoflurane, desflurane, and sevoflurane. Isoflurane and desflurane depress cardiac output to a lesser degree than halothane or enflurane secondary to their greater vasodilating capacity. The HR changes least with halothane and increases most with desflurane. Isoflurane may cause tachycardia; the mechanism is unclear. Most studies suggest that halothane, enflurane, and isoflurane decrease coronary vascular resistance. Of these, isoflurane is the most potent coronary vasodilator.
All of the potent drugs decrease arterial pressure in a dose-related manner. The mechanism of the decrease in BP includes vasodilation, decreased cardiac output resulting from myocardial depression, and decreased sympathetic nervous system tone. With halothane, decreased cardiac output is the predominant cause. Halothane also increases venous compliance, and in patients who have high sympathetic tone, such as those with heart failure, halothane decreases systemic vascular resistance. Enflurane causes both vasodilation and decreased myocardial contractility. With isoflurane and desflurane a low peripheral resistance is the major cause of hypotension. Evidence of the relatively greater myocardial depression with halothane and enflurane is the greater increase in right atrial pressure seen with these drugs than with isoflurane.
Narcotics such as morphine and fentanyl at their clinical dose have minimal cardiovascular effects. Both may cause bradycardia. Neither sensitizes the heart to catecholamine or depresses myocardial function. The cardiovascular effects of morphine depend on the dose used. Large doses of morphine sulfate have reportedly caused myocardial lactate production and reduction in coronary blood flow in animals. Sethna and colleagues found that morphine sulfate, 0.25 mg/kg intravenously, did not produce a global myocardial ischemia in patients with CAD. High doses of morphine, 1 mg/kg, produce a significant decrease in arterial BP and systemic vascular resistance accompanied by an average 750% increase in plasma histamine. On the other hand, high doses of fentanyl, 50 file:///H:/images/special/mulower.gifg/kg, do not produce any significant changes in BP, vascular resistance, and plasma histamine levels.
C.I-15. Is isoflurane dangerous for the patient with coronary artery disease?
In patients with CAD, the use of isoflurane is still controversial. Reiz and colleagues reported that 1% isoflurane induced coronary vasodilation that was not related to normal autoregulation and that both decreased coronary perfusion pressure (systemic hypotension) and redistribution of myocardial blood flow (coronary steal) may contribute to the development of regional myocardial ischemia. Another study by Reiz and Ostman, using 1.5 minimum anesthetic concentration (MAC) isoflurane/nitrous oxide anesthesia, concluded that isoflurane may cause coronary steal with myocardial ischemia in patients with CAD. However, Smith and colleagues reported that the substitution of 0.5% to 1.12% isoflurane for 85 μg/kg of fentanyl did not result in an increased incidence of myocardial ischemia, as seen by ST-segment or segmental wall motion changes in patients with CAD. Moreover, Tarnow, Markschies-Hornung, and Schulte-Sasseu demonstrated that 0.5% isoflurane with 50% nitrous oxide improved the tolerance to pacing-induced myocardial ischemia in patients with significant CAD. Two large-scale prospective outcome studies by Slogoff and colleagues and Turman and colleagues could find no evidence that the incidence of ischemia was increased by isoflurane in patients with CAD undergoing CABG surgery. Furthermore, this finding held true even for patients with steal-prone coronary anatomy in the studies by Slogoff and colleagues, Pulley and colleagues, and Leung and colleagues.
Several animal studies further confused this issue. Priebe proved that isoflurane was a myocardial depressant and a potent coronary vasodilator in the dog. Sill and colleagues demonstrated that high concentrations of isoflurane (1.5% and 2.5%) dilated intramyocardial arterioles rather than epicardial coronary arteries in the intact dog. Buffington and colleagues reported that isoflurane (1.2% to 1.5%) produced a decrease in collateral flow and a decrement in collateral zone contraction while enhancing flow in the normally perfused zone. They concluded that isoflurane was an arteriolar vasodilator and hence produced coronary steal in dogs with chronic coronary occlusion. On the contrary, Cason and colleagues found that in the dog, isoflurane or halothane at 0.5% MAC and 1.5 MAC had little effect on coronary vascular resistance, and ischemia was precipitated by tachycardia or hypotension rather than by coronary steal. Moreover, Davis and Frank demonstrated that isoflurane decreased myocardial infarct size after left anterior descending coronary artery occlusion in dogs. In addition, Gilbert and colleagues reported greater coronary reserve in swine anesthetized with isoflurane versus halothane at 0.5 to 2.0 MAC. Recently, Hartman and colleagues demonstrated that adenosine but not isoflurane redistributed blood flow away from collateral-dependent myocardium in the presence of a coronary steal-prone anatomy in the chronically instrumented dog. They further found that reductions in myocardial perfusion during isoflurane anesthesia depend on systemic arterial pressure and that isoflurane did not produce coronary steal in this model of multivessel CAD. Furthermore, Cheng and colleagues found that neither isoflurane nor halothane as the sole anesthetic in clinical concentrations caused significant coronary vasodilation or coronary steal from 55 to 30 mm Hg coronary perfusion pressure in a swine model of chronic coronary occlusion with collateral development.
On the basis of recent animal and clinical studies, we can conclude that isoflurane in clinical concentrations may be used safely in patients with CAD provided that hypotension and tachycardia are avoided.
C.I-16. What is the cardiovascular effect of nitrous oxide?
Nitrous oxide is a weak central nervous system depressant. It has been generally considered to have minimal effects on other organ systems. Nitrous oxide has significant cardiovascular effects that may be depressant or stimulatory depending on the anesthetics with which it is used. When high-dose fentanyl is used during coronary surgery, the effects of nitrous oxide depend on the patient's cardiac function. After the administration of 50% nitrous oxide, there are no significant changes in any of the hemodynamic parameters in patients with normal left ventricular function (LVEDP < 15 mm Hg). On the contrary, there is a significant decrease in cardiac index and stroke volume index in patients with left ventricular dysfunction (LVEDP > 15 mm Hg). When added to other inhalational anesthetics, nitrous oxide increases arterial pressure and systemic vascular resistance, suggesting that it has a vasoconstrictive action. Nitrous oxide increases pulmonary vascular resistance in patients with mitral stenosis and pulmonary hypertension.
The pulmonary vascular effects of nitrous oxide are also variable. Patients with elevated PA pressure may have further increases when nitrous oxide is added. Konstadt and colleagues did not corroborate these findings in patients with mitral valvular disease. A study in infants failed to show further increases of pulmonary vascular resistance with the addition of nitrous oxide. It is of interest that the decrease in pulmonary vascular resistance with isoflurane is less than the decrease in systemic vascular resistance.
The contribution of nitrous oxide to myocardial ischemia is controversial. Philbin and colleagues suggested that addition of nitrous oxide to anesthesia with high-dose fentanyl, 100 μg/kg followed by 1 μg/kg per minute, or sufentanil, 30 μg/kg followed by 0.3 μg/kg per minute, can produce clinically inapparent regional myocardial ischemia in the areas supplied by stenotic coronary arteries of dogs. However, using 2D TEE, nitrous oxide added to low-dose fentanyl, 15 μg/kg followed by 0.2 μg/kg per minute, or high-dose sufentanil, 20 μg/kg, did not cause myocardial ischemia in patients with CAD.
Clinically, nitrous oxide may be used before CPB if high-dose narcotics are not used and hypotension does not occur. However, after CPB, nitrous oxide should be avoided because of the possibility of expanding air bubbles in the coronary and cerebral circulation.
C.I-17. What kind of muscle relaxant would you use? Why?
We usually use pancuronium. When full paralyzing doses are given in a bolus, D-tubocurarine tends to produce bradycardia and hypotension from ganglionic blockade and histamine release, whereas pancuronium and gallamine generally produce tachycardia and hypertension caused by vagolytic effect and norepinephrine released from cardiac sympathetic nerves. D-Tubocurarine may be given in increments of 6 mg every 5 to 10 minutes until patients are fully paralyzed (0.3 mg/kg). BP and HR are usually not changed by this small dose and slow injection rate. Pancuronium is a better choice if hypotension (BP < 80 mm Hg systolically) and bradycardia (HR < 50 beats per minute) are present. Theoretically, pancuronium may increase myocardial oxygen consumption caused by tachycardia and hypertension. However, pancuronium is the most commonly used muscle relaxant for CABG. In practice, most patients with CAD take file:///H:/images/special/betalower.gif-adrenergic blocking agents, which can decrease the vagolytic effect of pancuronium. Also, the bradycardia associated with the popular narcotic anesthetic techniques can attenuate the tachycardia induced by pancuronium. Vecuronium and cisatracurium have no major cardiovascular effects, but their intermediate duration of action necessitates frequent administration of the relaxant. Pipecuronium and doxacurium are two new long-acting, nondepolarizing muscle relaxants. They seem to have no hemodynamic side effects associated with neuromuscular blockade. They can be used in large bolus doses.
C.I-18. If ST-segment depression is seen during surgery, how would you treat it? What is the relationship between perioperative myocardial ischemia and postoperative myocardial infarction?
ST-segment depression indicates myocardial ischemia, either from increased oxygen demand or decreased oxygen supply. The treatment includes the following:
- Increase oxygen supply: Correct hypotension and hypoxemia.
- Decrease oxygen demand: Correct hypertension, tachycardia, and increased PCWP or CVP by deepening anesthesia or by using vasodilators and propranolol. All the major determinants must be considered and corrected to their normal levels.
Gerson, Hickey, and Bainton (in experimental dogs) found that elevation of ST segments induced by occlusion of the coronary artery was more limited with halothane than with a combination of nitroprusside and propranolol. The more favorable effect of halothane was explained by its effects on coronary vascular reserve and the known effect of nitroprusside to reduce myocardial blood flow to ischemic myocardium.
If there are no obvious changes in BP, HR, and pulmonary wedge pressure, nitroglycerin is indicated for coronary spasm. Nitroglycerin may be given by intravenous drip. Sublingual nifedipine or intravenous nicardipine or diltiazem may be given to relieve coronary spasm.
In 1985, Slogoff and Keats reported that perioperative myocardial ischemia occurred in 37% of all patients undergoing CABG. They proved that perioperative myocardial infarction was almost three times as frequent in patients with ischemia (6.9%) compared with patients without ischemia (2.5%). Intraoperative tachycardia was associated with a higher incidence of myocardial ischemia and infarction. However, Knight and colleagues demonstrated that 42% of patients undergoing CABG had preoperative episodes of myocardial ischemia, 87% of which were clinically silent. They further found that anesthesia and surgery did not worsen the preoperative ischemic pattern. Furthermore, in another study in 1989, Slogoff and Keats postulated that approximately 90% of new myocardial ischemia observed during anesthesia was the manifestation of silent ischemia observed in the patient before the operation and only 10% was related to anesthetic management. Therefore, the relationship between intraoperative ischemia and postoperative outcome is still unsolved.
C.I-19. Would you use prophylactic nitroglycerin during coronary artery bypass grafting to prevent intraoperative myocardial ischemia or perioperative myocardial infarction?
No. It has been reported that prophylactic administration of nitroglycerin, 0.5 or 1.0 mg/kg per minute, during fentanyl anesthesia in patients undergoing CABG did not prevent myocardial ischemia or reduce the incidence of perioperative myocardial infarction.
C.I-20. How would you correct hypertension?
BP=blood flow/resistance
Hypertension is usually due to inadequate depth of anesthesia. Occasionally, it is due to fluid overloading. The treatment of hypertension includes the following:
- Deepen the anesthesia. Inhalation agents, such as halothane, enflurane, and isoflurane are more effective than narcotics because of their vasodilator effect.
- Sodium nitroprusside produces more arteriolar dilation than venodilation. Dose: 10- to 100-μg per minute intravenous drip titration.
- Nitroglycerin produces more venodilation than arteriolar dilation. Dose: 20- to 200-μg per minute intravenous drip titration, or bolus in 20-μg increments.
C.I-21. How would you treat hypotension?
Hypotension is usually caused by hypovolemia, deep anesthesia, bradycardia, or CHF. The treatments are as follows:
- Increase fluid infusion and put the patient in a head-down position when CVP or PCWP is low.
- Lighten the level of anesthesia or use a vasoconstrictor: phenylephrine, 0.1-mg intravenous increments, to correct vasodilation produced by anesthesia.
- Atropine, 0.2 to 2.0 mg, for bradycardia, or isoproterenol, 1 mg/100 mL of 5% dextrose intravenous drip titration, rarely indicated.
- Treat CHF when PCWP is high and TEE shows hypokinesia:
- Lighten the level of anesthesia.
- Restrict fluids.
- Diuretics: furosemide (Lasix) 20 to 40 mg intravenously
- Inotropic agents
- CaCl2 (0.5 to 1.0 g)
- Epinephrine: 2 to 8 μg per minute intravenous drip
- Dobutamine or dopamine: 5 to 20 μg/kg per minute intravenous drip
- Amrinone, 0.75 to 1.5 mg/kg, then 5 to 10 μg/kg per minute intravenous drip, or
- Milrinone, 0.05 mg/kg, then 0.5 to 0.7 μg/kg per minute intravenous drip
- Norepinephrine if peripheral vascular resistance is low
- Intraaortic balloon pump (IABP)
C.I-22. What are the indications for intravenous propranolol or esmolol during surgery? How much would you give? What are the relative contraindications?
Indications
- ST-segment depression associated with tachycardia; no response to deepening the level of anesthesia
- Supraventricular tachycardia more than 120 per minute
- Recurrent ventricular arrhythmias
- CHF
- Asthma, chronic obstructive pulmonary disease
Dosages
Propranolol, 0.25-mg increments every 1 to 2 minutes, total dose 2 to 3 mg
Esmolol, 10-mg increments up to 0.5 mg/kg followed by 50- to 300-μg/kg per minute intravenous drip
C.I-23. How would you correct increased pulmonary capillary wedge pressure?
It is important to treat the patient as a whole. All monitors must be considered together, not only one single parameter. Increased PCWP is usually due to a light level of anesthesia or CHF. Combining the readings of PCWP and BP will produce a differential diagnosis. Occasionally, an increased PCWP with hypotension and low cardiac output is caused by HOCM. HOCM can be diagnosed by TEE, which demonstrates SAM of mitral valve, mitral regurgitation, and usually good left ventricular contractility.
Inadequate Anesthesia: Increased PCWP with Hypertension
- Deepen the level of anesthesia with inhalation agents, such as isoflurane, halothane, or enflurane, which also have a vasodilator effect.
- Give a vasodilator. Nitroglycerin is a better venodilator than nitroprusside.
- Lighten the level of anesthesia.
- Restrict fluids.
- Use vasodilators.
- Give diuretics.
- Use inotropic agents.
- β-Blocker to decrease HR and contractility
- Fluid loading to keep left ventricle full and decrease left ventricular outflow tract obstruction
- Increase afterload to keep left ventricle full
C.I-24. During sternal splitting, would you do something?
Stop ventilation and deflate the lungs to prevent lung injury from the electric saw.
C.I-25. Would you monitor pulmonary capillary wedge pressure continuously? Why?
No, if the Swan–Ganz catheter balloon is inflated continuously, pulmonary infarction distal to the occlusion may ensue. Usually PA diastolic pressure (PADP) is monitored continuously because PADP is very close to PCWP.
C.I-26. Discuss autologous transfusion and blood conservation for cardiac surgery.
Autologous transfusion is the collection and reinfusion of the patient's own blood or blood components. The realization that homologous blood is responsible for transmission of acquired immune deficiency syndrome (AIDS), hepatitis, transfusion reaction, and autosensitization has led to increased interest in autologous transfusion and blood conservation. There are several options for autologous transfusion: preoperative autologous blood donation, preoperative use of erythropoietin, intraoperative normovolemic hemodilution, intraoperative plasmapheresis, pharmacologic treatment, and perioperative blood salvage.
Preoperative Autologous Blood Donation
Donations are appropriate for properly selected patients with stable CAD, stable valvular disease, and congenital heart disease. The risk of blood donation may be higher for patients with unstable angina or severe aortic stenosis; these patients are usually not considered good candidates for autologous blood donation. The patient should have a hemoglobin level of more than 11 g/dL to donate blood.
The optimal donation period begins 4 to 6 weeks before surgery, and the last donation is usually collected no later than 72 hours before surgery.
Preoperative Use of Erythropoietin
This is an established and efficacious but relatively expensive therapy to reduce blood transfusions. To optimize the hemoglobin response, oral or intravenous iron supplementation is recommended.
Intraoperative Normovolemic Hemodilution
This is the removal of blood through an arterial or venous catheter immediately after induction of anesthesia, before CPB or the administration of heparin. Depending on the patient's size and hematocrit level, 500 to 1,000 mL of blood is collected into blood bags containing CPDA-1 anticoagulant and is kept at room temperature.
This blood is spared the rigors of CPB, including hemolysis, platelet destruction, and clotting factor degradation. The autologous blood is transfused after reversal of the heparin with protamine. It has been demonstrated that the effect of 1 unit of fresh whole blood on platelet aggregation after CPB is at least equal, if not superior, to the effect of 8 to 10 stored platelet units. However, if the patient's hematocrit level is less than 33% or the hemoglobin level is less than 11 g/dL, normovolemic hemodilution is not recommended because further decreasing the oxygen-carrying capacity may worsen myocardial ischemia. In addition, hemodilution during CPB will further decrease the hematocrit to levels that require homologous blood transfusion. Normovolemic hemodilution should be performed cautiously in patients with critical left main coronary stenosis and aortic stenosis because sudden cardiac arrest has been observed during the procedure.
Intraoperative Plasmapheresis
Coagulopathy associated with hypothermia, shock, CPB, multiple transfusions, and the blood salvage technique, which removes clotting factors and platelets, often necessitates use of fresh frozen plasma and platelet packs to control postoperative bleeding and clotting problems. Recently a plasma-collection system has been developed to salvage up to 1,000 mL of platelet-rich plasma before CPB. This technique does not cause hemodilution, so it can be used in all patients, including those with anemia. The platelet-rich plasma can be stored at room temperature until transfused, usually after protamine reversal of the heparin. It is recommended that the collected product be placed on a rocker until infusion and that the pH level be held constant.
Pharmacologic Treatment
The prophylactic use of aprotinin, ε-aminocaproic acid (EACA) and tranexamic acid reduces blood transfusions in cardiac surgery. Aprotinin inhibits a host of proteases, including trypsin, plasmin, kallikrein, and factor XIIa activation of complement. The adult dose is 2 million kallikrein-inhibition units (KIU) for the patient and bypass pump, followed by 500,000 KIU per hour for 4 hours. The synthetic antifibrinolytics, EACA and tranexamic acid, bind to plasminogen and plasmin, thus inhibiting binding of plasminogen at the lysine residues of fibrinogen. Effective antifibrinolysis requires a loading dose of 100 to 150 mg/kg for EACA or 10 mg/kg for tranexamic acid and a constant infusion for each at one tenth the loading dose each hour.
Perioperative Blood Salvage
This is the collection and reinfusion of blood lost during and immediately after surgery. The posttransfusion survival of perioperatively salvaged red blood cells has been shown to be comparable to that of allogeneic red blood cells. At the conclusion of CPB, all blood remaining in the oxygenator and bypass circuits should be salvaged and if needed infused. Blood salvaged intraoperatively may be transfused directly (unwashed) or processed (washed) before infusion. Commercially available equipment exists for each option. Blood collected by intraoperative salvage represents an excellent source of red blood cell support. However, salvaged blood is deficient in coagulation factors and platelets.
Postoperative blood salvage is another technique of autologous blood transfusion using blood lost after surgery. Blood salvaged after cardiac surgery is generally collected from mediastinal and chest drains and transfused without washing. Because it is usually defibrinated, it does not require anticoagulation before transfusion. Though dilute, the blood is sterile and contains viable red cells.
作者: 老骥伏枥 时间: 2009-10-6 21:36
本帖最后由 老骥伏枥 于 2009-10-19 19:43 编辑
问题导向的麻醉管理
一个57岁老人，有三支冠脉病变，拟行CABG，7个月前有心肌梗死病史。现正服用硝酸甘油，地高辛，普萘洛尔，异硝酸山梨醇（消心痛），硝苯地平。血压120\80mmHg,心率60bpm。
A内科疾病和鉴别诊断。1，什么是三支冠脉疾病？说出这几支冠脉血管的名字。2，CABG的适应症是什么？3，什么是经皮冠状动脉球囊扩张术？说出其适应症，禁忌症和并发症。4，CABG的并发症？
B，围术期评估和准备？1，你会指定哪些术前检查？如何评估患者的左室功能？2，决定心肌耗氧的三大主要因素是什么？临床上它们如何测量？3，4，决定心肌氧供的因素是什么？5，你会停用地高辛吗？它的半衰期与多长？6，你会停用普萘洛尔吗？其半衰期？肾上腺素能阻断剂在治疗充血性心力衰竭时所起到的作用是什么？7,如果正在服用普萘洛尔的患者术中出现了低血压，你如何处理？8，硝苯地平是什么？它的作用原理？9，如何投以术前用药？为什么？
C1，CPB术中管理：1，需要哪些监护？什么是Allen试验？2，你需要测量食道和直肠温度吗？3，你如何判断S-G导管是在右室还是肺动脉？4，什么是肺小动脉楔压？5，对于冠状动脉手术有必要监测肺动脉压吗？6，放置S-G导管的并发症？7，心肌缺血的血流动力学变化如何？你怎样发现心肌缺血？PCWP是心肌缺血的灵敏指标吗？8，你如何监测ECG？V5导联的使用？（为什么是V5？）9，如果你没有胸前导联，如何监测左室？10，说出经食道二维超声的原理及应用？11，怎样减浅麻醉，怎样维持麻醉？12，对于该手术较好的麻醉药是什么？吸入或静脉药？13，什么是氟烷，异氟醚，恩氟醚，七氟醚，地氟醚，吗啡，芬太尼的心血管效应？14，对于伴有冠状动脉疾病的患者，异氟醚比较危险吗？15，笑气的心血管效应？15，你会选择哪种肌松药，为什么？16，如果术中S-T段一直压低，你如何对待？术中心肌缺血与术后心肌梗塞的联系？17，CABG你会预防性使用硝甘来预防心肌缺血与围术期心梗吗？18，你会如何纠正高血压？18，你如何纠正低血压？19，术中应用普萘洛尔和艾洛的指征？你会给多少？其相关禁忌症是什么？20，你怎样调节升高的PCWP？21，撑开胸骨时你会做什么？22，你会持续监测PCWP吗？为什么？23，讨论心脏手术的自体输血和血液保护。
C2，1，CPB期间。CPB之前你会给什么抗凝剂？给多少？其作用机理是什么？
2，肝素的半衰期？它如何消除？如何监测肝素的量？什么是ACT？
3，什么是全心肺分流？什么是部分心肺分流？
4，左室减压的意义？
5，氧合器有几种类型？各自的优缺点？
6，你会使用哪种预充液？量？用不用血预充？为什么？
7，血液稀释的优缺点？
8，你用哪种泵？是搏动性的吗？
9，期间你会观察患者吗？
10，在CPB期间血压会维持多少？为何？
11，CPB期间的低血压如何处理？
12，CPB期间的高血压如何处理？（MAP>100mmHg）
13，你怎样准备硝甘和硝普钠的静脉输入？常用剂量？你会选择哪种？
14，CPB期间用哪种泵维持？
15，低温时如何调节泵流量？
16，低温的优势？低温能否提供神经保护？
17，在低温和血压稀释时血粘度如何改变？
18，意外低温与死亡相关的主要原因？
19，CPB中你会给麻醉药吗？为什么？
20，CPB期间你会给肌松药吗？为什么？CPB对肌松药的活性有什么样的影响？
21，你怎么知道CPB期间病人得到了良好灌注？
22，你使用的人工肺气体流量是多少？你用的哪种气体？为什么？
23，CPB期间低PaCO2的不利之处是什么？
24，CPB期间动脉血气与电解质结果如下：pH, 7.36; PaCO 2, 42 mm Hg; PaO 2, 449 mm Hg; CO2 content, 24 mEq/L; Na, 128 mEq/L; K, 5.8 mEq/L; and HcT, 20%. 病人的体温是27°C. 血气是在温度多少时测量的? 如何根据患者的体温更正血气结果? 你在监测血气是否异常的时候是以37摄氏度还是病人现在的温度为标准？
1，如果氧合器的液面降低，你会用什么补充？血液？平衡盐？
2，你如何知道CPB期间的液体平衡？
3，CPB期间的心肌保护？
4，什么是心脏停跳液？用量？
5，主动脉可以被阻断多长时间？
6，为什么CPB2个小时后尿液会变成粉色？什么是血浆蛋白的肾阈？
7，病人可以脱离心肺旁路的温度？
8，为什么用心肺机给病人复温的时间比降温的时间要长？
9，为什么脱机时常常要投以氯化钙？
10, 如果心率40bpm，你会如何处理？
11,CPB中血糖如何变化？为什么？高血糖会增加CPB期间神经系统并发症吗？
12,CPB对血小板和凝血因子有什么影响？
13, 你会为停机做哪些准备？
14, 你如何判断是否需要变力支持？
C2你会如何中和肝素？用多少鱼精蛋白？，
1，鱼精蛋白的作用机制？
2，鱼精蛋白过多的并发症？
3，为什么有点而患者给鱼精蛋白后会出现肺动脉高压？你会如何处理？如何预防之？
4，IABP的适应症？
5，IABP的原理？
6，IABP的并发症？
7，CABG后PAWP能否反映LVEDP？
D1，术后的并发症有哪些？
2， 你会拮抗肌松药吗？为什么？何时脱离呼吸机？
3，脱离呼吸机的标准？
A1,三支冠脉疾病通常包括：右冠脉，左前降支，左回旋支。冠脉的分支如图7.1所示。人群中50%——60%窦房结是由右冠脉供血的，其余40%——50%由左回旋支供血。对于85%——90%的人群来说房室结有右冠脉供血，另10%——15%是由左回旋支供血。所以，对于85%——90%的人群来说右主干占支配地位。最常见的CABG手术针对的是左前降支，钝缘支，后降支。
A2，CABG的指征，是出于改善生活质量的需要。对于药物无法控制的心绞痛，不能耐受药物副作用的病人都应考虑血管重建。如今，PTCA已经成为上述缺血性心脏病患者的第一选择。自PTCA1978年引进以来，它已经将进行血管成形术的患者进行了分类：那些有近心端散在的冠状动脉狭窄者应作PTCA，不适合行PTCA者应作CABG。而适合做CABG者通常是那些有更严重缺血性心脏病和左室功能下降的老年病人。CABG的指征：1，不稳定心绞痛和持久的心肌缺血发作。2，投以最佳药物，心绞痛治疗仍不满意。3，心梗后反复发作的心肌缺血。4，有冠状动脉阻塞的变异型心绞痛。5，左冠脉主干高度闭塞，三支或双支阻塞，左前降支近心端阻塞。6，急性心梗，心源性休克，难以控制的室性心律失常。7，干扰正常生活的稳定性心绞痛。
A3，自从PTCA1977年引进以后便得到了快速发展。对于一些特定的心绞痛病人来说是可以接受的。该技术是用一个3F的小导管进入相应的冠状动脉，随着导管的气囊部分通过狭窄，充气的的气囊使狭窄扩张。内膜腔的增宽是由可控制的损伤造成的（包括斑块压缩，内膜龟裂，中层拉伸）来实现的。PTCA的指征最近有所更改。随着技术的进步，PTCA已经可用于尽管最好的药物治疗仍不能控制的缺血症状者，以及无论什么原因引起的局灶性阻塞性冠脉疾病者。PTCA的指征如下：1，孤立，散在的近端血管病变。2，近端双支病变。3，CABG术后新的狭窄形成或吻合口的远端狭窄。4，PTCA术后再狭窄。5，存在CABG的禁忌症。6，心脏移植后的冠脉狭窄。7，6个月以内的血管狭窄，且狭窄<15mm。8，以血管重建为目的的链激酶治疗术后。
PTCA的适应症：1，左主干病变且远端血管尚未形成代偿。2，伴有严重的主动脉粥样硬化的多支病变。3，无严重的阻塞性病变。4，不能实施合法的心外手术的机构。PTCA的结果如下：最初成功率是90%，治疗后6个月内再狭窄的几率是30%，再次实施球囊扩张的概率是90%，二次处理后动脉倾向于保持开放。随着支架的引入，冠状动脉再狭窄的几率降低了。A4，冠脉旁路手术的结果：Kuan, Bernstein, and Ellestad报道围术期心肌梗死率是4%——6%，大型医学中心CABG总的死亡率是1%，而再次手术死亡率是2%——3%，Rahimtoola和同事们研究了因不稳定心绞痛而十年前曾行CABG者的生存状态。第一个月的死亡率是1.8%，五年生存率是92%，十年生存率是83%，每年会有1%——2%的曾行CABG者会再次手术。81%曾行CABG者完全没有或仅有轻微的心绞痛。Loop和同事们发现接受乳内动脉移植者与静脉移植者十年生存率相比，单支病变93.4%与88%，双支90%与79.5%，三支病变82.6%与71%。Zai CABG术后的第一个年末，乳内动脉未闭率约85%——95%，而大隐静脉未闭率为38%——45%。7个随机试验大体展示了1972——1984年间冠脉旁路手术与药物治疗在2649名患者中的比较。曾行CABG者与接收药物治疗者在第5，7，10年相比有明显的低死亡率。但到了第十年，药物治疗族的41%将接受CABG。CABG延长了如下病人的生存期限：严重左主干病变者（无论症状如何），多支血管病变者，左室功能损害者，以及包括左前降支病变在内的三支病变。（不论左室功能如何）。外科治疗已被证明可以延长双支血管病变以及左室功能障碍者的生存期，特别是那些有左前降支严重狭窄者。虽然没有文献报道单支病变者通过外科治疗可获得生存率的改善，但已有证据证明有严重左室功能损害者长期生存率极低。有心绞痛和或心肌缺血的证据能胜任轻到中度的运动者，特别是那些有左前降支阻塞者，可以从再血管化手术中（血管成形术或旁路手术）中获益。
B1,1，通过心绞痛与心肌缺血的病史。2，左心衰的症状与体征：呼吸困难，夜间端坐呼吸，凹陷性水肿。3，心导管检查：冠脉造影，超声心动图。4，射血分数。5，左室舒张末期压与毛细血管楔压（正常6——15mmHg）！6，左室壁运动：不运动，运动减退，反常运动。7，心指数（正常3L\min\m2）。8，与压力容积环相关的收缩末期压力——容积关系。B3 决定心肌氧耗的三大主要因素是室壁张力，收缩力，心率。可通过下列手段测量：室壁张力：1，前负荷，LVEDP，LVEDV，PCWP。2，后负荷：无主动脉狭窄时的收缩压以及收缩期室内压。收缩力：侵入性的检查，如最大收缩速度，心室压力——时间描记图或者左室收缩末期压力——容积比。非侵入性的检查：射学前期时间\射血时间。超声心动图所示的室壁运动情况。心率：ECG。
作者: roseseana 时间: 2011-9-26 18:10
triple index 我怎么第一次知道 好无知。。。
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