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Cardiac and Respiratory Care.doc

  2. 2. Introduction Cardiac and respiratory complications are the two most frequent and most lethal groups of complications that occur after general surgery operations. Using modern understandings of cardiac and pulmonary pathophysiology, surgeons can now prevent or manage these events with frequent patient salvage and full recovery. This issue of Selected Readings in General Surgery (SRGS) reviews current information pertinent to the successful management of cardiac and respiratory diseases and complications in general surgery patients. Perioperative cardiac complications Evidence of atherosclerotic cardiovascular disease is found at autopsy on nearly all patients dying after the age of 40 years. Symptoms of atherosclerotic cardiovascular disease have become increasingly common as the population of the United States ages and cardiovascular disease is the leading cause of death among older adults in North America. Increasingly, older patients with moderate-to-severe comorbid cardiovascular diseases are presenting for surgical care. Current data estimate that 60%-80% of postoperative deaths after elective operation are traceable to cardiovascular complications of surgical procedures. In the first section of the overview for this issue of SRGS, we review pertinent data on the topic of perioperative cardiac complications. Important issues relevant to risk recognition, risk modification, and prevention are discussed. Data pertinent to the diagnosis and management of myocardial infarction, cardiac failure, arrhythmias, and cardiac arrest will be reviewed. Fundamental aspects of the diagnosis and management of cardiac conduction system disorders and management of pacemakers and implantable defibrillators are included. Risk factors for postoperative cardiac complications Effective prevention of perioperative cardiac complications is possible only if patients at risk can be identified. Identification of high-risk patients can lead to development and use of preventive strategies. These approaches obviously will be most useful for patients who are scheduled to undergo elective operations. In this patient group, there is time for a detailed history and physical examination, laboratory studies, electrocardiogram, and imaging. The articles reviewed in this section of the overview detail the fundamental features of perioperative cardiac risk assessment and risk modification. The first article reviewed is by Davenport and coauthors1 entitled, “Multivariable predictors of postoperative cardiac adverse events after general and vascular surgery: results from the patient safety in surgery study.” This article is supplied as a full-text reprint with this issue of SRGS. The authors begin noting that cardiac complications 2 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  3. 3. occur after 1%-5% of surgical procedures. Given an annual number of operations currently exceeding 30 million, this estimate would result in as many as 1.5 million adverse cardiac events annually. The estimated mortality for adverse cardiac events exceeds 50%. Thus, as many as 750,000 deaths could be expected annually. The authors cite data that have identified age > 75years, diabetes mellitus, hypertension, and baseline electrocardiographic findings indicative of ischemia as risk factors for perioperative adverse cardiac events. The current means of estimating the risk of perioperative cardiac events are summarized in three available scoring systems focusing on factors pertinent to the operation (elective versus emergency; simple versus complex), and on cardiac-specific risk factors such as a history of hypertension, symptomatic ischemic heart disease, diabetes, and cardiac failure. The authors stress that popular risk scoring systems, introduced in the late 1980s, award one point for each of several risk factors; clinical reviews of these systems have noted increased risk of adverse cardiac events with increasing risk scores. Nonetheless, there remains controversy over the ability of the available scoring systems to identify accurately patients for whom the procedure should be delayed in order to conduct further evaluation. Furthermore, assigning a specific risk to an individual patient is difficult using existing scoring systems. In an attempt to clarify and improve cardiac risk scoring for surgical patients, Davenport and coauthors used the Patient Safety in Surgery database that contains a standard dataset for patients from 128 Veterans Administration hospitals and from 14 academic medical centers. This database contains multiple demographic, preoperative, perioperative, and outcomes variables obtained from medical record reviews conducted in a standard fashion by experienced nurse reviewers using standardized definitions. Data on more than 180,000 patients were subjected to multivariate logistic regression analysis. Adverse cardiac events were defined as cardiac arrest or acute myocardial infarction within 30 days of operation. Adverse cardiac events were recorded in 2362 patients and the mortality rate for these events was 60%. The authors tested a predictive model on a sample of patients drawn from the database after logistic regression modelling of risk factors from the entire database. Prediction of adverse events was accurate using a model that included ASA score, operation complexity (as reflected in procedure relative value work units), age, and type of operation. Interestingly, none of the conventional cardiac specific risk factors such as hypertension, prior history of myocardial infarction, or prior history of a cardiac surgical procedure was valuable as a predictor of perioperative adverse cardiac events. When the subgroup of patients from non-VA medical facilities was considered, the authors found that these patients, as a group, were younger and contained more women than the VA cohort. The frequency of adverse cardiac events was less in this 3 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  4. 4. subgroup but cardiac-specific risk factors failed to predict outcomes in this subgroup also. The authors provide a table of risk point assignments for the factors they identified as most influential in determining outcomes. A graph in their report indicates that significant cardiac risk (>1% risk of adverse event) is recognized beginning with a total risk score of 12-15 points. Davenport and colleagues emphasize the diminished predictive power of conventional cardiac specific risk factors and report that these factors become less predictive when considered together with more global risk indicators such as ASA score. They also note that, in the current era, patients with known conventional risk factors are often treated preoperatively with medications and, occasionally, interventions that serve to reduce risk. This would also work to reduce the influence of cardiac-specific risk factors. They further emphasize the lethality of adverse cardiac events. The mortality risk for patients who sustain these events is large, and recognition of this serves as a stimulus to improve perioperative management. Use of measures such as avoiding emergency operation, preoperative stabilization of cardiac failure and rhythm disturbances, optimization of intraoperative monitoring, use of regional anesthesia, and use of drugs to control heart rate and stabilize atherosclerotic plaque, are potentially useful measures. These are discussed in more detail in the following sections of the overview. If emergency operation can be avoided, preoperative approaches to optimize coagulation, renal function, and nutrition might assist in minimizing the risk of cardiac adverse events. The authors conclude that their approach to outcomes prediction is well suited for inclusion in efforts to identify high and low performing hospitals as is done in the National Surgical Quality Improvement Program (NSQIP) sponsored by the American College of Surgeons. Furthermore, their risk scoring system is designed for easy incorporation into electronic medical records. The risk prediction model could be made available at the bedside on a hand-held computer. Risk assessment Additional detailed data relevant to cardiac risk assessment is in an article by Poldermans and coauthors2 in the Journal of the American College of Cardiology, 2008. These authors report European experience with adverse cardiac events in the perioperative period. An annual rate of 400,000 perioperative cardiac events has been recorded in the European Union. One hundred thirty-three thousand deaths occurred because of these complications. They agree with Davenport and colleagues that the type of operation is a major driver of risk. They cite data showing that patients older than 40 years of age have a 2.5% risk of adverse cardiac events after operation. The risk rises to more than 6% in patients undergoing vascular surgical procedures. They stress that the incidence of perioperative cardiac events varies because of the means used to make the 4 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  5. 5. diagnosis. When the diagnosis was made with Troponin T or I assays, the frequency of events rose to 25% in high-risk patients. They further agree that advancing age is a driver of cardiac risk. Postoperative myocardial infarction is the most important adverse cardiac event. The pathophysiology of this complication is complex. Patients whose preoperative images show discrete areas of impaired myocardial perfusion are thought to be at increased risk for perioperative myocardial infarction. It is now clear, however, that "culprit" coronary lesions are not the predominant cause of perioperative myocardial infarction. Plaque rupture and thrombosis in coronary arteries at sites of noncritical coronary artery stenosis are frequent causes of perioperative myocardial infarction. This understanding helps to explain the lack of benefit of preoperative myocardial revascularization of culprit lesions. Emphasis has shifted away from identification of culprit coronary lesions and toward global pharmacologic measures for reducing cardiac risk. The topic of preoperative interventions is discussed in a later section of the overview. Poldermans and associates note that features of the metabolic response to operation contribute to imbalances in myocardial oxygen demand and availability. The increased secretion of catecholamines results in tachycardia, which can create unfavorable myocardial oxygen demand/supply situations. This topic is addressed in more detail in a report by Sander and coauthors3 in Critical Care Medicine, 2005. These authors identified 69 patients deemed at high risk for adverse cardiac events. In a subgroup of 39 patients with sustained (>12 hours) tachycardia (heart rate > 95 bpm), the risk of a major adverse cardiac event was 49%. In the 30 high-risk patients who did not have tachycardia, the risk of an adverse cardiac event was 13%. The majority of the tachycardic rhythms were sinus tachycardia, although there were 16 patients with new- onset atrial fibrillation. The authors cite data that document an association of tachycardia with prolonged ST-segment depression, a finding known to predict perioperative myocardial infarction. Poldermans and coauthors2 agree, noting that prolonged ST-segment depression is a known precursor of perioperative myocardial infarction in patients undergoing vascular surgical procedures. In Sander’s report, tachycardia occurred during the 24- hour period in which the myocardial infarction occurred in 90% of patients. Sander and associates conclude with the observation that the subgroup of their patients where no tachycardia occurred were more likely to be receiving β-blocking drugs and epidural analgesia. They suggest that these factors might be protective against tachycardia and the adverse cardiac events that accompany this change in cardiac rhythm. 5 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 1 2
  6. 6. Poldermans and colleagues point out that the inflammatory response that sometimes follows major surgery procedures creates an environment that contributes to hypercoagulability because of activation of the coagulation mechanism and reduced fibrinolytic activity. As noted in the discussion of atherosclerotic vascular disease in a previous three-issue series of SRGS (Volume 35, Numbers 1-3), inflammatory cytokines are potent forces that produce plaque instability and rupture. Inflammation might also contribute to the onset of postoperative tachyarrhythmias. This topic is discussed in an article by Anselmi and coauthors4 in Annals of Thoracic Surgery, 2009, focusing on causes of new-onset atrial fibrillation after cardiac operations. These authors note that cardiopulmonary bypass is a potent stimulus of the inflammatory response. Inflammation, as evidenced by elevated levels of C-reactive protein, is associated with increased risk of atrial fibrillation in surgery and nonsurgery patients. Lower C-reactive protein levels have also been associated with improved responses to cardioversion for new-onset atrial fibrillation. They cite one study where reduction of risk for recurrent atrial fibrillation occurred with specific anti- inflammatory therapy with the antioxidant Vitamin C. Anselmi and associates point out that reductions of perioperative inflammation observed with off-pump coronary artery bypass, use of perioperative corticosteroids, and use of preoperative statin drugs are all associated with lowered risk of atrial fibrillation. These observations support an association between perioperative inflammation and perioperative atrial fibrillation. Because new-onset atrial fibrillation is associated with perioperative cardiac events, as noted by Sander and associates3 , efforts to control the inflammatory response seem warranted. Available pharmacologic therapies that reduce inflammation such as β- blockers and statins are discussed in a subsequent section of the overview. Poldermans and coauthors2 go on to note that existing cardiac risk scoring systems are imprecise. Improved risk assessment would result with the inclusion of global risk factors such as age and operation characteristics. This assertion is in agreement with the findings of Davenport and coauthors1 , noted above. The difficulty encountered by clinicians attempting to quantify cardiac risk preoperatively using the available scoring systems has stimulated researchers to investigate alternative means of assessing risk for perioperative cardiac events. Two of these approaches are discussed here. Normal cardiac function depends, in large measure, on an appropriate balance between the influences of the sympathetic and parasympathetic nervous systems. This balance is assessable clinically by use of special ambulatory electrocardiographic monitoring with assessment of heart rate variability. Heart rate variability is a sign of healthy cardiac function, while loss of variability signals an imbalance in the relative influences of the sympathetic and parasympathetic nervous systems on the heart. Loss 6 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  7. 7. of heart rate variability has been associated with an increased risk of sudden cardiac death, an increased risk of death in multiple trauma patients, and adrenal insufficiency in the critically ill surgical patient. The fundamental physiology of heart rate variability and the potential application of this assessment to the preoperative evaluation are discussed in an article by Laitio and coauthors5 in Anesthesia and Analgesia in 2007. These authors begin by noting that heart rate variability is an indicator of the integrated function of the parasympathetic nervous system (especially vagus nerve activity), the sympathetic nervous system, and the baroreceptor system. They describe the various measures used in analyses of heart rate variability, including time domain analyses that express variability in terms of instantaneous heart rate and intervals between normal QRS complexes. Frequency domain analyses commonly express variability in terms of “power-law” spectral analyses of RR-interval variability. These methods of assessing heart rate variability are time-tested and accepted but they do not adequately describe the complex, fractal system that is heart rate variability. Because of this, dynamic assessments of heart rate variability have been developed to analyze correlations of multiple time series of RR intervals. These analyses can be graphed and patterns typical of normal patients, patients with heart failure, and patients prone to ischemic events can be displayed. Similar graphic displays are obtained using Poincare plots. These show typical compact “comet shaped” patterns in normal patients and patients analyzed after myocardial revascularization. These graphs show diurnal variation. Heart rate variability changes during ischemic episodes are characterized by irregular widely spread graphic patterns with loss of diurnal variation. The actions of anesthetic drugs to down-regulate vagal activity result in changes in heart rate variability. Changes in heart rate variability accurately predict hypotensive episodes after induction of spinal anesthesia especially when the block reaches the thoracic spinal levels. Loss of heart rate variability in elderly patients and in diabetic patients with dysfunction of the autonomic nervous system accurately predicts episodes of hemodynamic instability. The authors cite several studies that have related loss of heart rate variability to short- and long-term operative mortality from myocardial ischemia and prolonged ICU stays. The presence of heart rate variability abnormalities improves the predictive capability of the available cardiac risk scales, especially for predicting long-term cardiac mortality. In the cited studies, the combination of abnormal heart rate variability and high-risk scores accurately predicted perioperative cardiac morbidity for patients undergoing cardiac and noncardiac procedures. Laitio and colleagues speculate that 7 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  8. 8. loss of heart rate variability indicates unopposed sympathetic influence on the heart that might increase myocardial oxygen demand by augmenting ventricular contractility. This situation favors the development of ischemia in susceptible patients. The need for 24-hour electrocardiographic monitoring and manual assessment of the tracings are significant disincentives that have reduced the utility of heart rate variability measurements for preoperative patients. With improved, computer-assisted methodologies, these disadvantages might be overcome. Additional data on the use of heart rate variability assessments as a means of predicting perioperative cardiac morbidity risk are found in an article by Hanss and coauthors6 in Anaesthesia, 2008. These authors report an initial analysis of 50 patients who underwent heart rate variability analysis preoperatively and, during the postoperative period, had 24-hour electrocardiographic monitoring and sequential measurements of creatine kinase MB band in blood samples. Cardiac events were detected by a combination of electrocardiographic changes and elevations of the CPK- MB level. Seventeen of the initial patients had cardiac events and the authors established that a heart rate variability power value <400 ms2 Hz-1 was a useful cut-off value for prediction of cardiac events. This cut-off value was then assessed prospectively in 50 additional patients. Cardiac events and hospital length of stay were both increased in the 26 patients with low power scores in the prospective group. The authors conclude that heart rate variability power analysis is a useful predictor of postoperative cardiac events and the additional information might improve the predictive power of cardiac risk scoring systems. Additional predictive power can be obtained using serum markers that reflect vulnerability of the myocardium to ischemia. Two of these, B-type natriuretic peptide (BNP) and N-terminal pro-brain natriuretic peptide (NT-proBNP), are discussed. The first of these is by Cuthbertson and coauthors7 in the British Journal of Anaesthesia, 2007, who analyzed outcomes data on 204 patients undergoing major noncardiac surgery procedures. Preoperative BNP levels were obtained in each patient. Perioperative cardiac events were defined as an elevation of the troponin level or death within three days of operation. The authors found that a preoperative elevation of BNP >40 pg/mL was predictive of perioperative cardiac events. They performed rigorous multivariate statistical analysis and found that the preoperative BNP level was more accurate for risk prediction than findings on history, physical examination, or electrocardiogram. BNP was more predictive than the revised cardiac risk score. Nonetheless, five patients with significant postoperative cardiac events were not identified by the preoperative BNP elevation. This observation suggests that BNP cannot be used alone to establish risk for perioperative adverse cardiac events. 8 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  9. 9. An article analyzing the potential usefulness of NT-proBNP levels assessed preoperatively and with a single postoperative sample by Mahla and coauthors8 appeared in Anesthesiology, 2007. These authors analyzed results in 218 patients who underwent major vascular reconstructive procedures. Patients were followed for 30 months postoperatively. Twenty percent sustained a significant cardiac event during the followup interval. The authors found that a preoperative value for NT-proBNP equal to 280 pg/mL coupled with a postoperative increase to 557 pg/mL accurately predicted short- and long-term cardiac morbidity. The authors state that NT-proBNP is released from cardiac myocytes in response to ischemia and stretch and, therefore, this hormone might be a good candidate for prediction of perioperative myocardial ischemia. The accuracy of the preoperative and postoperative levels combined was good, with an area under the receiver-operating-characteristic curve of 0.8 that is as good as or better than all available risk-scoring systems. The authors conclude that this test might offer improved prediction of cardiac events in high-risk patients undergoing major vascular operations. Preoperative evaluation for coronary artery disease and preoperative interventions Once a high-risk patient is identified, the next decision concerns the need for additional preoperative cardiac testing. Exercise testing, dobutamine stress echocardiography, and myocardial scintigraphy with vasodilator stress are tests commonly contemplated. Recommendations by the American Heart Association state that testing is indicated in patients who have symptoms suggesting unstable cardiac syndromes (decompensated cardiac failure or unstable angina), patients who have poor functional capacity where a high-risk operation is contemplated (major vascular reconstruction), and patients with known valvular heart disease. Poldermans and colleagues stress the lack of a positive contribution of preoperative cardiac testing in cardiac stable patients, especially those who are already using β-blocking drugs and statins with good control of heart rate. They further emphasize that coronary artery bypass in cardiac stable patients has not resulted in improved surgical outcomes and the intervention delays the planned noncardiac procedure. Percutaneous coronary interventions similarly delay the planned procedure because the risk of stent thrombosis is substantial in the first weeks following stent placement when multiple drug antiplatelet therapy is used. With drug-eluting stents, this interval might be as long as one year. Additional data on the use of extensive preoperative cardiac testing and preoperative cardiac interventions to prevent perioperative adverse cardiac events are reported by Jaroszewski and coauthors9 in the Journal of Thoracic and Cardiovascular Surgery, 2008, who performed a retrospective review of 294 patients who underwent thoracotomy for a noncardiac operation in a single institution. One hundred eighty-four patients underwent extensive preoperative assessment including, in addition to history 9 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 1 2
  10. 10. and physical examination with 12-lead electrocardiogram, stress testing, stress echocardiography, and/or myocardial scintigraphy. Based on preoperative test findings, 40 patients were selected to undergo coronary angiography and four of these had preoperative coronary revascularization by either operation or stenting. There was no difference in the frequency of perioperative myocardial infarction in patients who had testing and intervention compared with those who did not have testing. In fact, of the four patients who underwent revascularization, two had perioperative myocardial infarction. One of these was from perioperative coronary stent thrombosis. These authors concluded that there was no benefit to testing and intervention in cardiac stable patients. Medications for reducing cardiac risk Poldermans and coauthors2 stress the importance of general medical approaches to cardiac risk modification in patients undergoing major elective operations. These approaches have generally consisted of careful risk stratification, and use of pharmacologic approaches designed to alter, favorably, myocardial oxygen consumption/oxygen demand relationships as well as stabilize plaque through control of perioperative inflammatory responses. The authors note that the high catecholamine release states created by the stress of operation alter both myocardial energetics and inflammation. Initial approaches to balancing myocardial energetics included the use of β-blocking drugs. Initially, drugs used were combined β-1 and β-2 agents, such as propranolol. As additional human trial data have become available, important lessons have been learned. Poldermans and associates describe these progressive steps. For example, they stress the observation that trials of beta blockade have generally shown reductions in the frequency of perioperative cardiac events but some trials have disclosed risks of hypotension and stroke, especially in older patients not judged at high risk for cardiac events. Two prospective, randomized trials cited by these authors (references 40 and 45 in their bibliography) showed effective reduction in cardiac events but at the cost of a significantly increased risk of stroke and overall mortality. These trials disclosed the potential danger of pharmacologically lowering blood pressure to 100 mmHg or lower in elderly patients. The type of beta-blocking drug used, timing of drug therapy, and dosing are also important features of approaches that achieve maximum success. Drugs that are β-1 selective agents (such as bisoprolol) are more effective than drugs that target both the β-1 and β-2 receptors. Blockade of both receptor types results in a state of predominant α receptor stimulation that results in hypertension and increased myocardial stress. Prospective, randomized trials have shown no impact of beta blockade on the risk of perioperative cardiac events if the drug is started on the day before or the day of the 10 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  11. 11. operation. This finding implies that maximum stabilization of cardiac energetics and plaque requires time. In fact, the DECREASE trial (reference 37 in Poldermans’ bibliography) started treatment, on average, 37 days before operation and with incremental adjustment of the dose upward based on blood pressure and heart rate. This study disclosed a 10-fold reduction in the risk of perioperative cardiac events and death. All of the data cited by Poldermans and associates support the use of β-1 selective drugs with a long half-life. The drug should be started at least one month before operation and adjusted to obtain optimum heart rate (current American Heart Association recommendations are resting heart rates in the 60-66 bpm range) without episodes of hypotension. Patients at low risk for cardiac events should not take beta- blocking drugs unless they are using these drugs chronically. Moderate risk patients undergoing major vascular operations are acceptable candidates for beta-blocking therapy and high-risk patients undergoing any type of major operation are excellent candidates for this approach. Drugs should not be withdrawn in the perioperative period because benefit has been shown for protection against both short-term and long-term cardiac morbidity. Downsides of beta-blocking drug usage include a range of contraindications (asthma, for example) and consistent observations that up to 25% of patients have episodes of tachycardia in the perioperative period despite seemingly adequate beta blockade. Further analysis of the use of beta blockade for prevention of perioperative cardiac events comes from a review by Chopra and coauthors10 entitled “Perioperative beta- blockers for major noncardiac surgery: Primum non nocere.” This article appeared in The American Journal of Medicine in 2009 and a full-text reprint of the article is provided with this issue of SRGS. These authors review the actions of beta-blocking drugs. They note that there are three subtypes of beta-receptors and these receptors are presented on the cell surface of many types of human tissue. Beta one receptors are found in the myocardium, the kidney, and the eye. Beta two receptors are found in adipose tissue, liver, pancreas, smooth muscle, and skeletal muscle. Beta three receptors are primarily involved with metabolic regulation and lipolytic pathways. The receptors are G-coupled proteins that activate intracellular adenyl cyclase and produce intracellular effects via adenosine monophosphate production and opening of excitatory channels. Chopra and associates confirm the observations of Poldermans and coauthors2 and suggest that beta blockade use be targeted toward patients at high risk for perioperative cardiac events. Beta-blocking drug therapy should be started at least one month before operation, and tight heart rate control should be sought with maximum protection against hypotensive events. Drug therapy should be continued during the postoperative period, and that use of statins and/or aspirin should be considered. 11 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 1 2
  12. 12. Supporting data on the value of tight heart rate control is in a meta-analysis authored by Beattie and coauthors11 in Anesthesia and Analgesia, 2008. These authors provide an analysis that specifically focuses on reasons for inadequate heart rate control in trials of beta-blocking drugs. They emphasize that early implementation of beta blockade with progressive upward adjustment of dose to obtain consistent resting heart rates in the 60-65 bpm range is associated with maximum reductions of risk of perioperative cardiac events. Several recent trials have shown that fixed dose approaches do not produce maximum protection against perioperative cardiac events. They stress that the available trial data strongly indicate that variation in achieving optimum heart rate control accounts for 60% of the variability in trial results. They also document that the type of drug used and the concomitant use of calcium channel blockers might alter the heart rate response. Based on their analysis they recommend that beta-blocking drugs other than metoprolol be chosen, especially in patients concomitantly using calcium channel blockers. Most of the available trials disclose failure to achieve heart rate goals in 20%- 35% of patients. Suboptimum heart rate control might be the result, according to Beattie and colleagues, of the presence of the AA variant of the beta-receptor resistant to the beta-blocking drugs. In the setting where optimum heart rate is not achieved, combination therapy with calcium channel blockers might be necessary. Beattie and colleagues point out that available data does not adequately address the risk of exacerbation of congestive heart failure from tight heart rate control with beta- blockers. Nor does the data adequately evaluate the use of other approaches to stabilization of myocardial energetics such as the use of regional anesthesia/analgesia and α-2 receptor agonists, which have both been shown to reduce the frequency of perioperative cardiac events. The authors recommend therapy to obtain optimum heart rate control but caution that the best approach to achieve this goal might not be available yet. An alternative approach to achieving optimum balance between control of heart rate and maintenance of cardiac output is described in an article by Suttner and coauthors12 in the British Journal of Anesthesia, 2009. These authors note that concerns about the effect of beta-blocking drugs on blood pressure and cardiac output have led to reluctance on the part of some clinicians to use beta blockade for high-risk patients, especially those who might need urgent or emergent intervention. In the current study, an analysis is presented of results in 75 high-risk (as defined by three or more risk factors) vascular surgery patients randomized to receive continuous perioperative beta blockade with intravenous esmolol alone, esmolol plus enoximone (a phosphodiesterase type III inhibitor), and standard therapy. 12 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  13. 13. Perioperative cardiac events were documented by elevations of troponin or BNP. The authors explain that phosphodiesterase inhibitors such as enoximone and milrinone have the potential to maintain cardiac contractile function when catecholamine pathways are pharmacologically blocked. In this study, they noted no abnormalities of troponin in either group receiving esmolol. BNP was lowest in the esmolol + enoximone group and this group had the best maintenance of cardiac index. They suggest that enoximone support of cardiac index occurred because of its action that promotes influx of calcium into myocytes, thereby favoring increased contractility. In vascular smooth muscle, enoximone promotes calcium efflux, favoring vasodilation. These authors rightly caution that dosing of esmolol and enoximone should be managed carefully because higher doses might predispose to new-onset arrhythmias. While these salutary effects were obtained in high-risk vascular surgery patients, the numbers of patients are small. Furthermore, even though these patients were said to be at high risk for perioperative cardiac events, fewer than 20% of each group received preoperative beta-blocker and/or statin therapy. The results of this study suggest, but do not prove, that an approach such as described might have protective effects in high- risk patients who are not using beta-blocking drugs and who require urgent or emergent operation. Additional plaque stability effects accrue to patients from the use of drugs such as statins and aspirin. Several trials have shown protection against perioperative cardiac events, and both short- and long-term mortality with the use of statins. Sustained release preparations are preferred because intravenous statin preparations are not available. As with beta-blocking drugs, therapy should not be withdrawn postoperatively, and patients who are chronically using statins should have these continued in the postoperative period. Low-dose aspirin has also been shown to be protective against both short- and long-term cardiac events and death. Because of data suggesting benefit in terms of reduction of perioperative cardiac events for high-risk patients from statins and from beta-blocking drugs, it is useful to determine whether using the drugs in combination would be helpful. This issue is addressed in a study by Dunkelgrun and coauthors13 in Annals of Surgery, 2009. This article concerns a randomized prospective trial of beta blockade using bisoprolol compared with the use of a statin drug (fluvastatin) alone, a combination of the two drugs, or neither drug. The patients were deemed intermediate risk (cardiac event risk of up to 6%). The authors noted that cardiac event rates were significantly reduced in patients receiving beta blockade with or without the statin drug. A lesser reduction (nonsignificant) was seen with the statin drug alone. Although this study does not support the addition of statin drugs to beta blockade as a means of gaining additional 13 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  14. 14. control of cardiac event risk, the study is limited because of the small number of enrolled patients. From the perspective of the editor, there is convincing evidence to support careful preoperative cardiac risk assessment. Furthermore, it is expected that an increasing number of patients will present for operation already taking beta-blocking drugs, statins, or both. In this case, drug therapy with both drugs should be continued during and after the perioperative period with dose and type of drug adjusted to make certain that full effects of both drugs are maintained. For intermediate-risk patients undergoing high-risk operations (abdominal or thoracic vascular procedures) and for high-risk patients, beta-blocking drug therapy, at least, should be implemented and dosage adjusted progressively during the preoperative interval to obtain a resting heart rate in the 55-65 bpm range. Therapy should continue into the postoperative recovery period. Other adjuncts, such as regional anesthesia/analgesia, aspirin therapy, and statin therapy might be useful. Perioperative myocardial infarction In the foregoing discussion, emphasis was placed on the vulnerability of coronary artery plaque and the hazard of plaque rupture with thrombosis of the coronary artery as the proximate cause of perioperative myocardial infarction. The significant, and increasing, prevalence of coronary artery disease in surgery patients is a reminder to surgeons that this problem is a continuing challenge. Increased resource consumption from postoperative myocardial infarction is significant. In a 2006 report by Mackey and coauthors,14 results from a prospective analysis of 236 patients deemed at high risk showed significant incremental increases in both hospital and ICU lengths of stay when vascular surgery patients developed a perioperative myocardial infarction. Perioperative myocardial infarction was a marker for long-term use of healthcare resources as well. Nearly one-quarter of the study patients discharged alive returned to the emergency department for care during the year after discharge. Frequently, postoperative myocardial infarction occurs without chest pain. Nonspecific signs such as hypotension, dyspnea, arrhythmia, onset of new cardiac murmur, and alterations in the level of consciousness might be the only clinical symptoms. Electrocardiographic diagnosis and laboratory diagnosis using serum markers such as troponin might yield nonspecific results. The typical electrocardiographic findings of spontaneous myocardial infarction include the appearance of Q waves, ST-segment elevation, and T-wave inversion. In contrast, postoperative myocardial infarction is associated with intervals, occasionally prolonged, of ST-segment depression indicating subendocardial ischemia. Increasingly, echocardiographic cardiac imaging is used to obtain diagnostic information. Features of 14 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  15. 15. the pathophysiology, diagnosis, and management of perioperative myocardial infarction will be discussed. Pathophysiology of myocardial infarction The first article discussed is by Burke and Virmani15 entitled “Pathophysiology of myocardial infarction.” The review appeared in Medical Clinics of North America in 2007. The authors begin by noting that 80% of spontaneous myocardial infarctions are caused by thrombosis of coronary arteries critically narrowed by atherosclerotic plaque. Unusual causes of myocardial infarction are coronary embolization, coronary spasm, and thromboses of nondiseased coronary arteries. Concentric subendocardial necrosis that might result from prolonged global ischemia from cardiac arrest can also lead to coronary artery thrombosis. Myocardial ischemia results in acute pallor of the myocardium, visible grossly within 12 hours of the onset of ischemia. Tetrazolium salt staining of the myocardium can detect myocardial necrosis within 2-3 hours of the onset of ischemia. After 5-7 days, the infarcted area is soft with a hyperemic border. If reperfusion occurs, the infarcted area might be reddened from trapped red blood cells. Healing of a myocardial infarction takes from 4 weeks to 3 months and the lesion evolves into a white scar, which might be the source of rhythm disturbances. Histologic findings begin with the development of tissue eosinophilia followed by typical inflammatory changes, followed by fibrosis and scarring. Infarctions that involve more than 50% of the myocardial wall thickness are termed transmural and these produce Q- wave changes in the electrocardiogram. In humans, reperfusion of ischemic myocardium within 4-6 hours of the onset of ischemia results in myocardial salvage. In this circumstance, the ischemic area remains subendocardial and transmural extension does not occur. Myocardial energy metabolism depends upon the oxidation of free fatty acids to produce ATP. Ischemia causes an immediate shift to anaerobic glycolysis. Exhaustion of ATP supply leads to inhibition of Na/K ATPase with breakdown of cell membrane defenses and influx of sodium and chloride into the myocardial cell. Increases in cytosolic calcium and cellular acidosis lead to myocyte contractile dysfunction. Cell death can result from necrosis, oncosis, apoptosis, or autophagy. Because apoptosis is an energy consuming function, this occurs in perfused myocardium surrounding the necrotic area. Autophagic cell death also requires energy and occurs in a manner that is independent of the caspase-mediated pathway leading to apoptosis. Infarct size is determined by the extent and efficiency of coronary collateral circulation. Well-developed coronary collaterals are present in approximately 40% of adult men and these individuals are resistant to the development of transmural infarctions. Rather, coronary atherosclerosis in these patients produces anginal pain. In 15 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  16. 16. patients with well-developed collateral circulation, another means of myocardial protection is ischemic preconditioning. Ischemic preconditioning is the term applied to the phenomenon of preservation of myocyte energy-producing capability after an ischemic event preceded by a short interval (10 minutes) of ischemia followed by reperfusion. Potassium-ATP channels play a central role in ischemic preconditioning. Blockage of these channels prevents the protective effect of ischemic preconditioning. Interestingly, cardiac myocyte protection can be induced by ischemic events in distant tissue sites. This phenomenon is known as remote ischemic preconditioning. A review of the potential for remote ischemic preconditioning to produce cardiac myocyte protection comes from an article by Walsh and coauthors16 in the Journal of Vascular Surgery, 2009. These authors report that myocyte protection has been produced after the production of ischemia to kidney, intestine, and skeletal muscle. Preoperative tourniquet ischemia of an upper extremity was associated with reduced risk for postoperative cardiac events in patients undergoing coronary artery bypass grafting. These authors report results of ischemic preconditioning in randomized analysis involving 82 patients undergoing open abdominal aortic aneurysm repair. Ten minutes of ischemia to each leg was produced by clamping the iliac arteries individually. Thirteen of the 42 control patients developed clinically significant perioperative myocardial ischemia. Only two of the 40 patients who had ischemic preconditioning developed myocardial ischemic events. Because this study was conducted in patients who had undergone maximum preoperative preparation with beta-blocking drugs, the results suggest there might be incremental protection because of ischemic preconditioning; this technique should be further evaluated. Burke and Virmani15 assert that plaque instability universally preceded coronary thrombosis. Seventy-five percent of coronary thromboses are the result of plaque rupture and the remaining 25% result from plaque erosion. The left anterior descending coronary artery is the most frequent site of thrombosis, followed by the right coronary artery and the left circumflex coronary artery. Arrhythmias and contractile dysfunction in myocardium distal to a thrombosis might be aggravated by post-thrombosis microembolization. Complications of myocardial infarction include cardiac rupture, ventricular aneurysm, mural thrombus with embolization, mitral valve insufficiency from papillary muscle rupture, and pericardial effusion. Additional information on complications of myocardial infarction is in a review by Wilansky and coauthors17 in Critical Care Medicine in 2007. These authors provide short descriptions of clinical characteristics of the most important complications of myocardial infarction. Left ventricular free wall rupture, a frequently lethal complication of myocardial infarction, traditionally has afflicted up to 6% of patients sustaining myocardial infarction. With the onset of rapid reperfusion protocols and 16 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  17. 17. angioplasty, the frequency of this complication has dropped to 1%. Nonetheless, up to 17% of the deaths from myocardial infarction result from ventricular free wall rupture. This complication occurs within the first week after infarction with nearly half occurring during the first 24 hours. Older age, male gender, first infarction, single vessel disease, lack of ventricular hypertrophy, transmural infarction and anterior location of the infarction are all risk factors for left ventricular free wall rupture. This condition can result in acute hemopericardium and pericardial tamponade. Approximately one-third of patients with free wall rupture present with a more subacute clinical picture characterized by persistent chest pain, right heart failure, and hemodynamic deterioration. Electrocardiogram findings are nonspecific. Echocardiography might show pericardial effusion. As noted in the article by Burke and Vimani,15 approximately 25% of myocardial infarction patients will have nonspecific pericardial effusion, and this will make diagnosis of cardiac rupture difficult. Doppler imaging or contrast echocardiography might be needed to show pericardial blood clot or the rupture site. Surgical repair of the rupture will be required. Some patients might be amenable to stabilization with fluids, pressors, and/or intraaortic balloon pump. A variant of cardiac rupture is ventricular septal rupture. Older age, female gender, hypertension, absence of a smoking history, and anterior infarction location are risk factors for septal rupture. Clinically, this complication presents with hemodynamic collapse in the presence of a new systolic murmur. Diagnosis is established with echocardiography. Surgical revascularization and septal repair are therapies of choice. Left ventricular outflow tract obstruction from severe systolic anterior motion of the mitral valve is an unusual complication of myocardial infarction. The clinical presentation is one of a new systolic murmur and refractory hypotension in the setting of an apical infarction. Echocardiography can confirm the diagnosis. Therapy includes volume expansion, beta-blocking drugs to reduce hyperdynamic contraction of the heart, and alpha agonists to support blood pressure. Mitral regurgitation might complicate myocardial infarction because of ischemia of the valve or from papillary muscle rupture. Ischemic mitral regurgitation might be clinically silent and evidenced only by the presence of a cardiac murmur. Transesophageal echocardiography is the mainstay of diagnosis. Management varies according to the clinical status of the patient and the hemodynamic effects of the valvular dysfunction. Papillary muscle rupture is a critical care emergency with acute pulmonary edema and cardiogenic shock commonly present. A loud systolic murmur is present. Immediate management includes support of cardiac function with afterload reduction and the use of an intraaortic balloon pump. Transesophageal echocardiography provides accurate delineation of the valvular anatomy and the extent 17 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  18. 18. of dysfunction. Surgical management of the mitral regurgitation and critical coronary stenoses is associated with significant operative mortality (25%-40%), but survivors have good quality of life in long-term followup. Diagnosis and management of postoperative myocardial infarction Traditionally, the diagnosis of myocardial infarction is made based on the presence of typical chest pain, electrocardiographic evidence of ischemia (ST-segment elevation, presence of Q waves), and elevation of biomarkers such as troponin. As noted previously, perioperative myocardial infarction might be clinically silent. Chest pain might be absent because patients are receiving analgesics, are sedated for mechanical ventilation, or are emerging from general anesthesia. Troponin levels might be elevated in surgery patients in the absence of myocardial infarction, but persistent elevations of troponin > 3, especially combined with ST segment depression intervals of > 60 min on electrocardiographic monitoring, predict an increased risk of myocardial infarction and mortality. An article evaluating diagnostic accuracy of the electrocardiogram in critically ill patients by Lim and coauthors appeared 18 in Critical Care Medicine, 2006. These authors determined intra- and inter-rater reliability for electrocardiogram interpretation in patients at high risk for myocardial infarction in a single ICU. The authors reaffirm the difficulties in detecting clinical symptoms of myocardial ischemia. Interpreting troponin levels in patients recovering from noncardiac operations and in patients who are critically ill is also challenging. Lim and colleagues state that the lack of reliability of troponin measurements has led to increased emphasis on electrocardiographic changes as a means of confirming the diagnosis of myocardial infarction. This study was an analysis by two observers of all electrocardiograms obtained on patients at risk for myocardial infarction in a single ICU during two months. The changes sought as evidence of myocardial infarction were those recommended by the European Society of Cardiology/American College of Cardiology diagnostic criteria. The findings included pathologic Q waves, ST-segment elevation in at least two contiguous leads, ST-segment depression in at least two contiguous leads, symmetric inversion of T-waves (> 1mm) in at least two contiguous leads, T-wave flattening, and new onset left bundle branch block. The last criterion was chosen because left bundle branch block could obscure ST-segment elevation. The analysis of rater performance indicated that intra-rater and inter-rater reliability was poor when the raters had no knowledge of the serum troponin level. The raters were more likely to diagnose accurately electrocardiographic signs of myocardial infarction if they knew that there was a significant elevation of the serum troponin level. Electrocardiographic abnormalities most often identified accurately were T-wave inversion, Q-waves, and left bundle branch block. These authors conclude that accurate diagnosis of myocardial 18 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  19. 19. infarction in critically ill patients (who have physiologic similarities to postoperative patients) are facilitated using a synthesis of clinical information that includes the electrocardiogram, troponin levels, and, possibly, echocardiographic imaging. In an editorial by Engel19 that accompanies Lim’s article, the difficulty in arriving at an accurate diagnosis of myocardial infarction is reemphasized. Engel agrees that use of the electrocardiogram as the principle means of diagnosis of myocardial infarction in postoperative or critically ill patients is hazardous. Furthermore, choosing interventional therapy in this patient subgroup is challenging because thrombolysis, coronary angiography, and percutaneous coronary interventions requiring antiplatelet therapy might not be safe. Management of the patient who has had a perioperative myocardial infarction is based on providing support for the patient’s heart function while planning for appropriate means of revascularization. Support from cardiologists and cardiothoracic surgeons will be needed to facilitate these decisions. Cardiogenic shock is the most common lethal complication of perioperative myocardial infarction. Management of this condition is discussed in detail in the next issue of SRGS. Perioperative cardiac arrhythmia In an earlier portion of this overview, we noted the association of postoperative inflammation, postoperative tachycardia, and postoperative atrial fibrillation with cardiac morbidity. In patients at high risk for perioperative cardiac events, control of heart rate and rapid diagnosis and therapy for treatable tachycardias are important for prevention of cardiac complications. The most common treatable tachycardias encountered in postoperative patients are supraventricular tachycardias and atrial flutter/fibrillation. In this section of the overview, we review pertinent features of the diagnosis and management of these cardiac rhythm disorders. Management of supraventricular tachycardia and atrial fibrillation Supraventricular tachycardia is the subject of a review by Fox and coauthors20 in Mayo Clinic Proceedings, 2008. A full-text reprint of this article is included with this issue of SRGS. The authors provide a working definition of supraventricular tachycardia that includes all tachycardias arising cephalad to the bifurcation of the His bundle and all tachycardias dependent on the His bundle for impulse transmission. These tachycardias usually have rates exceeding 100 bpm (unless atrioventricular conduction block is present), and QRS morphology is usually normal. In the presence of bundle branch block, however, QRS complexes might be widened or otherwise abnormal in shape. Data from long-term ambulatory electrocardiographic monitoring have permitted estimates of the incidence of supraventricular tachycardia. The authors cite data that disclose an incidence of 76% in a group of elderly patients with a 20% 19 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  20. 20. incidence of symptomatic coronary artery disease. In studies of asymptomatic healthy patients aged 18-65 years, the incidence ranged from 12-18%. Supraventricular tachycardia is usually of sudden onset and might spontaneously terminate. The patient might complain of chest pain, and syncope occasionally occurs (usually in very rapid tachycardias associated with reductions in cardiac output). Although no clear association between chest pain during a tachycardia episode and coronary artery disease has been established, the diagnosis might be suspected in elderly patients with tachycardia and chest pain. Patients usually complain of palpitations; patients with chronic heart failure might not sense the palpitations but, instead, present with cardiac decompensation. The catecholamine response stimulated by tachycardia and hypotension serves to perpetuate the rhythm disturbance. These authors note that atrioventricular nodal re-entry, atypical atrioventricular nodal re-entry, or atrial tachycardias are the usual mechanisms of these rhythm disturbances. Atrioventricular node dependent tachycardias are usually terminated by inducing atrioventricular nodal block with a vagal stimulating maneuver (Valsalva, carotid sinus massage, or immersion of the face in cold water), or pharmacologically. Atrioventricular node independent rhythms include atrial flutter and atrial fibrillation. Diagnosis of tachycardia is usually possible using a 12 lead electrocardiogram, which is preferred over a rhythm strip. QRS morphology is usually normal with QRS duration of 90 milliseconds or less. QRS complexes might be abnormal if there is intermittent or permanent bundle branch block. Other factors to be considered in interpreting the electrocardiogram are the heart rate, mode of onset and termination of the tachycardia, relative position of the P-wave within the RR interval, and morphology of the P wave. The tachycardia rate is usually higher than 100 bpm and can be variable. A steady rate of 150 bpm suggests atrial flutter with a 2:1 atrioventricular block, according to Fox and associates. Another means of determining the type of tachycardia is by examining the relationship of the P wave to the preceding and subsequent R wave. When the distance between the R wave and the next P wave is longer than the subsequent PR interval, the tachycardia is a “long RP” rhythm. If the distance between the R wave and the subsequent P wave is shorter than the subsequent PR interval, the rhythm is termed “short RP.” Long RP tachycardias are atrial and might progress to flutter or fibrillation. Supraventricular tachycardias, according to these authors, are mainly short RP rhythms. At very rapid heart rates, RP and PR intervals become very short and might be difficult to interpret. Management of supraventricular tachycardia is usually straightforward because the patients are usually hemodynamically stable. If there is instability, the patient is 20 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  21. 21. managed according to the typical ABC approach emphasizing airway, breathing, and circulation. Vagal maneuvers such as carotid sinus massage might terminate the rhythm promptly and these maneuvers are ineffective in atrial flutter/fibrillation. Carotid sinus massage should not be done if there is a carotid bruit present. Pharmacologic management of supraventricular tachycardia is accomplished using adenosine, calcium channel blockers, or β-blocking drugs. Adenosine is the first-line drug and is given in 6 mg or 12 mg boluses. Smaller doses are used in patients taking dipyridamole. Broadening of the QRS complex might occur in supraventricular tachycardia if there is bundle branch block. Fox and colleagues caution that if the patient is older than 70 years or there is a history of symptomatic coronary artery disease, a broad QRS tachycardia should be considered a ventricular tachycardia until proved otherwise. An article discussing the use of response to adenosine bolus therapy as a means of differentiating supraventricular from ventricular tachycardia when wide QRS tachycardia comes from Critical Care Medicine, 2009, by Marill and coauthors.21 The authors note that differentiation of atrial from ventricular tachycardia when the heart rate is steady and the QRS complex is widened is important, but current algorithms are neither sensitive nor specific in identifying the type of rhythm present. Drug therapy using procainamide or amiodarone might effectively treat the rhythm but side effects such as hypotension limit the usefulness of these agents. Electrical cardioversion is effective but is painful, does not protect against recurrence of the rhythm, and offers little diagnostic information. These authors hypothesize that adenosine will safely terminate most supraventricular tachycardias, will slow heart rate enough to allow detection of atrial flutter or fibrillation, and will be not predictably alter ventricular tachycardia. In a 15- year interval, these authors treated 197 patients with steady-rate wide QRS complex tachycardia with a 12 mg bolus of adenosine. Patients determined to have ventricular tachycardia were older, more often had a history of myocardial infarction and prior episodes of ventricular tachycardia. Two of 81 patients with ventricular tachycardia responded to adenosine while 104 of 116 patients with nonventricular tachycardia responded to adenosine. There were no serious adverse events (defined as emergent drug therapy or electrical shock) observed in either subgroup. These authors concluded that nonresponse to adenosine was the only factor that diagnosed ventricular tachycardia with a high sensitivity and specificity. The nondihydropyridine group of calcium channel blockers (verapamil and diltiazem) are alternative drugs used to terminate supraventricular tachycardia. A summary of the data supporting these drugs in comparison to adenosine, by Anugwom and coauthors22 appeared in American Family Physician, 2007. These authors reviewed data from eight studies involving nearly 600 patients. The data disclose that adenosine 21 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  22. 22. and calcium channel blockers are equivalently effective in terminating paroxysmal supraventricular tachycardias. Transient, minor side effects such as flushing, nausea, and headache are common with adenosine. Severe side effects (cardiac arrest and hypotension) were observed only in patients treated with calcium channel blockers. These authors note that the American Heart Association guidelines recommend adenosine as first-line therapy for paroxysmal supraventricular tachycardia because of the low risk of severe side effects, the rapid onset of action, and the short half-life of the drug. The advanced cardiac life support course also recommends adenosine for the management of supraventricular tachycardia. Of the atrial arrhythmias, atrial fibrillation is the most commonly encountered. A discussion of the management of acute atrial fibrillation is in an article by Siu and coauthors23 in Critical Care Medicine, 2009. These authors report a randomized, nonblinded trial comparing the effectiveness of diltiazem, digoxin, and amiodarone for rate control and symptom improvement in patients presenting acutely with symptomatic, new-onset atrial fibrillation. The authors note that atrial fibrillation is a common arrhythmia and the frequency of this condition is increasing. Traditionally, two approaches have been used to manage atrial fibrillation, rhythm control and rate control. Rhythm control approaches use direct current cardioversion; this modality might not be available on a 24/7 basis. Guidelines published from the American Heart Association recommend emergency direct current cardioversion only for patients with acute atrial fibrillation who are hemodynamically unstable. Direct current cardioversion might require that the patient be anticoagulated, especially if there is atrial enlargement. This fact limits application of this modality to postoperative patients. The authors analyzed results in 166 patients. Patients were excluded from the study if they were unstable, had evidence of symptomatic coronary artery disease, were hypotensive, had an implanted defibrillator, had a history of recent myocardial infarction, had a history of heart failure, or had angina pectoris. Drug therapies used were diltiazem, digoxin, and amiodarone. The endpoints examined were control of heart rate (heart rate < 90 bpm, sustained, at 24 hours after initiation of therapy) and improvement of symptoms. In this study, rate control and symptom improvement was best achieved with diltiazem. There was only one adverse event recorded, an episode of phlebitis at the injection site, in one of the patients receiving amiodarone. In an editorial by Karth24 that accompanies Siu’s article, the editorialist stresses that these data, though valuable and convincing, were obtained in relatively healthy patients and, because of this, the data might not be directly applicable to typical postoperative patients since surgical patients are increasingly presenting with significant comorbid conditions. Nonetheless, there is sufficient reason, based on the data reported by Siu, to 22 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  23. 23. consider diltiazem as initial therapy in patients with acute, new-onset atrial fibrillation when rhythm control strategies are not appropriate. In surgery patients, prevention of postoperative atrial fibrillation would be desirable if risk for the development of this arrhythmia could be quantified, and if safe, pharmacologic prevention strategies were available. A prevention strategy is discussed in a report by Zebis and coauthors25 in Annals of Thoracic Surgery, 2007. These authors report a randomized, placebo controlled, double blind trial comparing amiodarone with placebo in a group of patients undergoing coronary artery bypass (a known high-risk group for the development of postoperative atrial fibrillation). These authors noted a 14% absolute risk reduction for patients treated prophylactically with amiodarone. Of the patients in the placebo group who developed atrial fibrillation, more than 80% were symptomatic; just over 40% of the patients in the amiodarone group who developed atrial fibrillation were symptomatic. While these data have limited application to typical general surgery patients, a preventive strategy might be considered in patients who have previously undergone cardioversion for atrial fibrillation if antiarrhythmia drugs are not already being used. Management of surgical patients with disorders of the cardiac conduction system A single review article is discussed in this section of the overview by Allen26 from Anaesthesia in 2006. The article is entitled “Pacemakers and implantable cardioverter defibrillators” and a full-text reprint of this article is provided with this issue of SRGS. The author opens the discussion noting that pacemaker implantation is increasing with increasing age of the surgery patient population. Likewise, the number of implanted cardioverter defibrillators is increasing. Patients who have these devices are elderly with histories of significant symptomatic heart disease. The author notes that modern pacemakers work by delivering, via an intracardiac electrode, a low-voltage impulse to cardiac muscle. Devices in current use are capable of detecting the intrinsic electrical signals within the heart so that the devices deliver pacing impulses only when they are needed. Improvement in pacing lead design has led to “active fixation” leads that ensure optimum contact with the endocardial surface of the heart. These leads also are designed to elute steroid medications to minimize inflammation at the contact site. Battery life has improved so that battery replacement is only necessary once in each 10-year interval. Furthermore, the titanium casing of modern pacemakers is light and protects the device from outside electromagnetic interference so that patients can safely use microwave ovens, electric shavers, and mobile telephones. In addition, modern devices carry electromagnetic interference detection software that offers additional protection. For patients who undergo surgical procedures, the most common 23 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  24. 24. form of electromagnetic interference comes from use of electrical coagulation devices. Bipolar diathermy is preferred when the patient has an implanted cardiac device. If monopolar diathermy use is unavoidable, the contact plate should be placed as far away from the pacemaker as possible. Advice from the clinician who implanted the pacemaker can be sought to reprogram the device if necessary. Reprogramming ideally occurs just before beginning the procedure. Ideally, the physician who inserted the pacemaker would remain in the area until the procedure is completed. While earlier devices paced the ventricle alone, current devices offer dual-channel pacing which improves cardiac output by taking advantage of atrial systolic contraction. Allen emphasizes data that have documented reductions in risk for mitral and tricuspid regurgitation and reductions in frequency of heart failure and chronic atrial fibrillation with dual-chamber pacing. Allen goes on to provide information on the various pacing modes of current pacemaker devices. More than three-quarters of currently used pacemakers are rate- sensing so that pacing current is supplied only when heart rates fall below a preselected level. More than half of currently implanted devices are dual-chamber pacing devices. Currently, rate-sensing pacemakers adjust current output based on surrogates for increased physical activity such as body movement and respiratory excursion. Ideally, rate-sensing devices would assess catecholamine levels or autonomic activity. Such sensors are under development but, as of 2006, were not available. Pacemaker rate sensors can sometimes interpret signals from intraoperative monitoring devices (such as respiratory rate monitors that determine thoracic impedance) as body movement. This results in rapid pacing. In patients with chronic heart failure, multiple sites within the cardiac chambers are paced; this is termed cardiac resynchronization therapy. In these devices, impulse delivery to both ventricles in multiple sites can be timed to maximize cardiac output. Implanted cardioverter defibrillators are equipped with complex algorithm software that tailors a response to a detected dangerous ventricular rhythm. Rate, beat-to-beat variation, atrial activity, and QRS morphology can be detected by the software and electrical shocks are delivered based on the rhythm detected. All implantable cardiac convertor defibrillators have pacemaker capability. These devices are not generally sensitive to external electromagnetic interference, but it will be wise to obtain advice from the clinician who implanted the device about any precautions anticipated during anesthesia and surgery. Cardiac failure in the surgical patient Cardiac failure is an extremely common medical problem. More than 1 million hospitalizations annually in the United States are for cardiac failure; there is a 50% 24 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  25. 25. likelihood of death or recurrence of cardiac failure during the six months subsequent to a hospital admission. Cardiac failure will develop in up to one-third of patients with symptomatic ischemic cardiac disease; this condition will develop in 15% of diabetics and 10% of patients with hypertension. While it is unlikely that surgeons will be involved in the first-line management of patients with acutely decompensated cardiac failure, surgeons will be called to assist in the care of patients with heart failure who develop conditions requiring elective or urgent surgical conditions. It is important that surgeons understand the fundamentals of disordered cardiac function characteristic of the various forms of heart failure, and the pharmacology and side effects of the various therapies employed in these patients. This set of topics is reviewed in this section of the overview. Systolic cardiac failure The first article reviewed by Chatterjee and Rame27 appears in Critical Care Medicine, 2008, entitled “Systolic heart failure: chronic and acute syndromes.” The authors define systolic cardiac failure as inadequate function of the heart as a pump manifest by reduced ejection fraction. The condition most often emerges in patients with diabetes, hypertension, or ischemic heart disease. Systolic heart failure might also be encountered in patients with dilated cardiomyopathy from other conditions such as myocarditis. Systolic cardiac failure results from a process termed “ventricular remodelling.” The ventricles take on a more globular shape and chamber size increases. Although ventricular muscle mass increases, chamber size increases results in an increased chamber/ventricular wall ratio. The alteration in the chamber/ventricular wall ratio results in increased ventricular wall stress; the result of these changes is an increase in end diastolic and end systolic chamber volumes, resulting in diminished ejection fraction. Chatterjee and Rame emphasize the importance or neurohumoral activation as the process required for progression of systolic cardiac failure. Adrenergic, renin- angiotensin, and aldosterone systems are all activated and the degree of activation is linearly related to severity of symptoms and outcome. In the cardiac myocyte, results of neurohumoral activation are hypertrophy, apoptosis, necrosis, and fibrosis. There is evidence of increased oxidative stress that produces additional cytotoxicity. Increases in peripheral vascular resistance, ventricular filling pressures, and arterial stiffness are also results of neurohumoral activation, and these features contribute to cardiac failure progression. Additional insight into the complex metabolic processes that influence the severity and progression of heart failure is from an article by Ashrafian and coauthors28 in Circulation, 2007. These authors open their discussion with a description of myocardial energy metabolism and the balances necessary for efficient energy use. They point out 25 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  26. 26. that daily myocardial ATP turnover is much greater than the myocardial ATP pool, and normal myocardial energy metabolism extracts only 25% of available substrate. Because of these facts, subtle changes in the efficiency of myocardial energy metabolism have far-reaching implications for cellular energy levels. One of the most important areas of study has been altered myocardial carbohydrate metabolism and the related state of myocardial insulin resistance. At the cellular level, as insulin concentrations vary, an attenuated glucose response results. These authors cite research data that demonstrate a steadily increasing risk of heart failure with age in diabetic patients. There is also an increasing risk of heart failure as hemoglobin A1c levels increase. Persistent hyperglycemia predicts increased risk for the development of heart failure and for heart-failure-related hospitalizations. They refer to additional evidence supporting a linkage between myocardial insulin resistance and the subsequent development of cardiac failure. Neurohumoral disorders characteristic of cardiac failure also facilitate the development of hyperglycemia. Persistent inflammation, demonstrable in patients with cardiac failure, contributes to hyperglycemia and myocardial insulin resistance. The aggregate result of the metabolic dysfunctions noted in cardiac failure is a heart that is energy deficient. Because the heart must produce ATP in amounts many times the weight of the heart, energy deficiency becomes a major factor in the onset and progression of heart failure. In addition, heart failure is associated with major reductions (approximating 70%) in phosphocreatine, the “energy reserve” of the heart. Implications for management of cardiac failure emphasize control of the neurohumoral dysfunction concurrently with optimization of glucose levels as a means of combating insulin resistance. Ashrafian and associates discuss several new pharmacologic agents that have the potential to improve myocardial energetics in cardiac failure patients. Patients with Type 2 diabetes and the metabolic syndrome are at increased risk for the development of cardiac failure. Management of this patient group is challenging because the two mainstays of diabetic therapy for Type 2 diabetes, the biguanides (metformin) and the thiazolidinediones (rosiglitazone) are currently contraindicated in patients with clinical evidence of cardiac failure. Several classes of diabetic drugs are available as adjuncts to conventional neurohumoral modulating agents in this patient group. This topic is reviewed in detail in an article by Masoudi and Inzucchi.29 Interested readers are encouraged to review this article. Anemia is an additional condition frequently observed in patients with cardiac failure. A discussion of this topic comes from an article by Mitchell30 in the American Journal of Cardiology, 2007. The author notes that anemia is present, overall, in 33% of 26 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  27. 27. heart failure patients and the proportion of patients who are judged to be anemic (hemoglobin level < 12 gm/dL) increases with increasing severity of heart failure. New York Heart Association Class IV patients have a 76% prevalence of anemia. The causes of anemia are complex, with contributions from impaired erythropoietin synthesis and utilization, hemodilution, impaired iron and vitamin B12 absorption, and persistent gastrointestinal bleeding in patients who take aspirin. Anemia, like other disease features, is associated with increased levels of proinflammatory mediators and oxidative stress factors. Anemia is known to be an independent driver for increased rates of heart failure hospitalization and death. Mitchell cites several confirming data sources. Mortality risk is particularly high when anemia and renal insufficiency coexist. Because ischemic cardiac disease is an important precursor of cardiac failure, assessment of this patient group for anemia has been carried out by several investigators cited by Mitchell. Data disclose an association of anemia with the onset and progression of ischemic cardiac disease. Anemia might lead to increased cardiac output that contributes to imbalances of myocardial energy availability/utilization that contribute to progression of cardiac failure. Mitchell notes that elevation of hemoglobin levels is associated with improved left ventricular ejection fraction and improved quality of life indices. Elevation of hemoglobin levels with erythropoietin analogues and iron is desirable. Red blood cell transfusion has lowered short-term mortality in a small group of elderly patients but it is not clear, according to this author, whether the benefit of transfusion outweighs the risks. Additional information on this topic is in an article by Gerber31 in Critical Care Medicine, 2008. The focus of this article is the use of transfusion in patients with ischemic cardiac disease. It is likely, however, that many of the basic findings pertinent to the ischemic cardiac disease patient will also be appropriately applied to patients with cardiac failure. The author begins by reviewing the complications of transfusion with acute complications such as transfusion reaction and transfusion-related lung injury (this topic is discussed in more detail later in the overview), and the medium term complication of blood-borne disease transmission. Because there are significant risks to transfusion, the decision to use transfusion must depend on an assessment of the extent to which oxygen availability to cells will be increased by raising the number of red blood cells with transfused cells and documentation of improved outcomes in anemic heart disease patients who receive transfusions. Gerber notes that the average storage age of transfused red blood cells is 17 days. Currently, stored red cells have lost 2,3 diphosphoglycerate and the p50 of the cells has changed so that cellular affinity for oxygen is increased and the ability to offload oxygen from transfused red cells to tissue is reduced. Structural changes in red cells have also occurred and the cells have become 27 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 1 2
  28. 28. stiff so that passage into and through the microcirculation is impaired. Although measured oxygen content of blood might increase following transfusion of stored red cells, increased cellular oxygen availability is by no means assured. Data from studies of septic patients and patients in septic shock, cited by Gerber, suggest that cellular oxygen delivery is not increased by red blood cell transfusion. Gerber then reviews several studies where outcomes have been analyzed in anemic heart disease patients who have been transfused. Only one study has shown improved outcomes, and the improvement was observed only in elderly patients with admission hematocrits < 33%. In all the other studies there was no improvement, with several studies suggesting worse outcomes in transfused patients. He concludes by stressing that there is no convincing evidence to support the routine use of transfusion to improve outcomes in anemic patients with cardiac disease. Diastolic cardiac failure Approximately 50% of patients with acute symptoms of cardiac failure, manifest as dyspnea with radiologic signs of pulmonary edema, have preserved left ventricular ejection fraction, according to data presented in an article by Kumar and coauthors32 in Critical Care Medicine, 2008. Patients with this form of cardiac failure are often elderly, female, and less likely to be African American than are patients with other forms of cardiac failure. The clinical presentation in many patients consists of signs of acute pulmonary edema associated with elevated systolic blood pressure. Because echocardiographic imaging that documents maintenance of left ventricular ejection fraction is performed, in many patients, after treatment for heart failure has begun, the suggestion has been made that ejection fractions were depressed at the time of symptom onset and improved with treatment. Kumar and associates cite a report of echocardiographic analyses performed in patients acutely and after 24 hours of treatment. There was maintenance of left ventricular ejection fraction at both time points, suggesting that heart failure occurred in the presence of normal left ventricular ejection fraction. These authors note that diastolic cardiac failure and pulmonary edema are likely caused when venous return to the right ventricle acutely increases and an increased volume of blood is delivered to the pulmonary circulation. Left ventricular dysfunction creates a situation in which the left ventricle cannot accept the increased blood flow without elevating left atrial pressure. In the setting of elevated left ventricular pressure (especially with a peak late in systole), left ventricular relaxation is impaired. Pulmonary blood volume increases and this overcomes the ability of the pulmonary lymphatics to remove fluid from the pulmonary interstitium. Pulmonary edema is the result. 28 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  29. 29. Additional data on diastolic cardiac function are found in an article entitled “Left ventricular diastolic function” by Hoit33 in Critical Care Medicine, 2007. Hoit notes that cardiac diastole is the result of processes whereby the heart loses ability to generate contractile force produced by myocyte shortening. The heart returns to a precontractile state in preparation for filling and the subsequent systole. Responsible for this series of events are myocardial relaxation and the pressure/volume properties of the ventricle. Relaxation is an energy-consuming process. Calcium is released from troponin C and actin-myosin cross bridges detach. Calcium is sequestered in the sarcoplasmic reticulum and, simultaneously, calcium is extruded from myocyte cytoplasm by active sodium-calcium exchange. Multiple factors influence the left ventricular end diastolic pressure-volume relationship including left ventricular physical properties (stiffness), the efficiency of relaxation, and extrinsic factors such as pericardial restraint and intrapleural pressure. Echocardiography is a valuable means for quantifying left ventricular diastolic function. Ventricular compliance and left atrial volume can be assessed with echocardiographic imaging. Using Doppler imaging, flow velocities across the mitral valve and in the pulmonary veins can be measured and the relaxation dynamics of the left ventricle can be determined. Acute echocardiographic imaging is emerging as an important tool permitting quantification of cardiac function and intravascular volume status in patients with suspected myocardial infarction, hypovolemia, or cardiac failure. Features of acute echocardiographic evaluation are reviewed in detail in an article by Glassberg and coauthors34 in Critical Care Medicine, 2008. These authors describe the use of Doppler echocardiographic imaging to assess preload and afterload. They note that recent data disclose an increased rate of cardiac adverse events in patients with acute cardiac decompensation monitored using pulmonary artery catheters. They further note that Doppler echocardiography has the capability of providing accurate estimates of cardiac output, right atrial pressure, pulmonary artery mean, systolic, and diastolic pressures as well as left ventricular filling pressure. Echocardiographic imaging might produce clinical information that is equivalent to the information gained from the pulmonary artery catheter without the risk of central venous catheterization. They conclude that acute echocardiographic imaging is an important component of the evaluation of patients with acute hemodynamic instability where cardiac failure is an important part of the differential diagnosis. Management of heart failure in the surgical patient Where systolic or diastolic cardiac failure is suspected, the history, physical examination, and acute echocardiographic imaging are used to establish a diagnosis. Laboratory studies, including serum assays of brain natriuretic peptide (BNP) or N- terminal pro-brain natriuretic peptide (NT-proBNP) might be helpful in providing additional diagnostic information. The use of these serum markers is discussed in an 29 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 1 2
  30. 30. article by Omland35 in Critical Care Medicine, 2008. Omland stresses the value of diagnostic information that can be gained from serum levels of BNP or NT-proBNP obtained in the emergency department or in the ICU when patients present with acute dyspnea. Abnormal BNP or NT-proBNP was 84%-90% accurate diagnosing diastolic cardiac failure as the cause of acute dyspnea in several studies cited by this author. Omland stresses that BNP levels are frequently normal in patients with chronic heart failure. Furthermore, BNP and NT-proBNP levels were not consistently useful as means of assessing progression or improvement of cardiac failure. Data discussed earlier describe the limitations of serum tests in postoperative patients. Therapy for systolic cardiac failure depends on the clinical presentation. The presence of echocardiographic evidence of increased filling pressures suggests the use of loop diuretics (furosemide) to improve pulmonary congestion, dyspnea, and hypoxia. Significant low cardiac output states in patients with systolic cardiac failure can be treated with afterload reduction using vasodilators. Sublingual nitroglycerin is the first- line approach in this regard. With very low cardiac output, short duration inotropic therapy can be considered. The use of inotropic drugs for systolic cardiac failure is the topic of an article by Petersen and Felker36 in Critical Care Medicine, 2008. These authors emphasize data, which they review in this article, indicating a lack of clinical value of inotropic drugs in patients without clearly documented end-organ hypoperfusion. They further report the clinical challenges in documenting end-organ hypoperfusion. Traditionally, this diagnosis has been made by documenting worsening renal function. Petersen and Felker note that increases in serum creatinine after the institution of loop diuretic therapy might indicate presence of cardiorenal syndrome and not end-organ hypoperfusion. These authors note that some patients with very low cardiac output states will maintain normal levels of serum creatinine. These patients will frequently have nonspecific symptoms such as abdominal pain, nausea, fatigue, and diminished cognitive function. Documentation of low cardiac output with echocardiography or pulmonary artery catheter monitoring will likely provide confirmatory evidence. The authors note that documented low cardiac output in patients with systolic heart failure is a marker for increased short-term mortality. If inotropic therapy is contemplated, dobutamine and milrinone are the first-line drugs. Both drugs produce improvements in cardiac output via augmentation of cellular cyclic AMP. Milrinone has greater vasodilating function than dobutamine and might have lower risk of inciting arrhythmias. Devices useful for supporting cardiac function include the intraaortic balloon pump, left ventricular assist devices, and ultrafiltration devices. These devices reliably support cardiac function until definitive therapies using 30 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  31. 31. revascularization or transplantation can be organized and implemented. These devices are discussed in a review by Kale and Fang37 in Critical Care Medicine, 2008. According to Kumar and coauthors,32 treatment of acute pulmonary edema, the main clinical manifestation of diastolic cardiac failure, focuses on improving oxygenation and relieving patient symptoms. Noninvasive ventilation with continuous positive airway pressure is valuable for reversing hypoxia. Early administration of a loop diuretic along with intravenous β-blocking drugs will improve pulmonary congestion, lower blood pressure and heart rate, and relieve patient symptoms. These authors stress that diuretic-naïve patients might have a very brisk diuresis and, therefore, lower diuretic doses initially might provide a greater margin of safety. Morphine is helpful for relieving symptoms also. Afterload reduction with sublingual nitrate drugs is frequently helpful. Perioperative management of diastolic cardiac failure is discussed in a review by Pirrachio and coauthors38 in the British Journal of Anesthesia, 2007, who stress that the focus of perioperative management is to choose an anesthetic strategy that will not decrease left ventricular function. Intravenous agents such as propofol and most muscle relaxants do not affect left ventricular function. Volatile anesthetics such as sevoflurane and desflurane also do not change left ventricular function. These authors stress the importance of aggressively controlling the catecholamine response that accompanies operation and they recommend preoperative beta blockade supplemented by intravenous short-acting agents such as esmolol for management of hypertension and tachycardia. Cardiopulmonary resuscitation Data on the frequency of out-of-hospital and in-hospital cardiac arrest appear in articles by Ramsay and Maxwell,39 Ali and Zafari,40 and Ehlenbach and coauthors.41 The articles by Ramsay and Maxwell and Ali and Zarari are supplied as full-text reprints with this issue of SRGS. These articles confirm that there are more than 400,000 sudden deaths annually ascribed to cardiac disease resulting in cardiac arrest. Ramsay and Maxwell cite data indicating that there are 165,000 witnessed episodes of out-of- hospital cardiac arrest in the United States each year. In-hospital cardiac arrest occurs at a rate of nearly three events/1000 admissions, according to data cited by Ehlenbach and coauthors. Cardiac arrest is the cause of 5.6% of all deaths annually in the United States, according to data cited in the article by Ali and Zafari. Despite the availability of effective methods of cardiopulmonary resuscitation, mortality for witnessed out-of- hospital and in-hospital cardiac arrest exceeds 80%. All the authors cited note the disappointing statistics indicating that nearly three-quarters of the patients who sustain witnessed cardiac arrest have no attempt at resuscitation made. In this section of the 31 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  32. 32. overview, we review several topics pertinent to effective management of witnessed out- of-hospital cardiac arrest and in-hospital cardiac arrest. History of cardiopulmonary resuscitation Ramsay and Maxwell describe a short history of cardiopulmonary resuscitation in their article from The American Surgeon in 2009. The authors note that descriptions of mouth-to-mouth rescue breathing appear in the Old Testament. In the 14th century, rescue breaths were administered using bellows devices placed intranasally or through a reed inserted into the trachea via an anterior neck incision. During the 18th and 19th centuries, “humane societies” were formed in several European countries to foster the use of artificial respiration techniques for drowning victims. In studies on animals, John Hunter noted that cessation of breathing led to cardiac standstill and immediate resumption of breathing led to restoration of cardiac action. The use of electricity for defibrillation was championed by Wiggers who also supported the use of open cardiac massage. Open massage was used for resuscitation of intraoperative cardiac arrest by Beck of Johns Hopkins Medical School, and this method of resuscitation was the focus of his research from 1920–1937. Closed chest massage was developed at Johns Hopkins and described in a 1960 publication in the Journal of the American Medical Association by Kouwenhoven, Knickerbocker, and surgeon James Jude. Training in techniques of cardiopulmonary resuscitation for emergency medical services personnel and citizen responders was made simpler and more effective by the development of life-like mannequins for intubation and resuscitation by Safar and Laerdal. Currently, national standards for citizen, emergency medical services, and in- hospital cardiopulmonary resuscitation are promulgated by courses sponsored by the American Heart Association (Basic Cardiac Life Support and Advanced Cardiac Life Support). Current practice and outcomes for cardiopulmonary resuscitation Ali and Zafari40 note that sudden cardiac arrest is, in the main, caused by coronary artery disease. They cite data from autopsy studies indicating that more than 80% of nonsurvivors of cardiac arrest have severe coronary artery disease confirmed by post- mortem examination. Other causes of cardiac arrest are aortic stenosis, Wolf- Parkinson-White syndrome, cardiomyopathy, and congenital cardiac disease. The presence of a “shockable” (ventricular tachycardia or ventricular fibrillation) rhythm is associated with better outcomes of cardiopulmonary resuscitation. These authors note that these rhythms are being documented less often during cardiopulmonary resuscitation events. Fewer than one-third of patients have a shockable rhythm on initial electrocardiographic tracing. Asystole and pulseless electrical activity rhythms are being recorded with increasing frequency. 32 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2
  33. 33. These authors describe a “four phase” classification of a cardiac arrest event. The “electrical phase” extends from time 0–4 minutes after arrest. The “circulatory phase” extends from 4-10 minutes post arrest. The “metabolic phase” begins at 10 minutes post arrest. During the electrical phase, defibrillation is the most effective therapy if a shockable rhythm is noted. During the circulatory phase, qood-quality cardiac compression is critical. In the metabolic phase, resuscitative efforts focus on reversing the effects of global ischemia. The importance of defibrillation during the electrical phase supports the distribution of automatic defibrillators and the use of these devices by trained citizen rescuers since it is unlikely that trained emergency medical services personnel will arrive on the scene before the late circulatory or metabolic phase of resuscitation. Data cited in Table 2 of the article by Ali and Zafari confirm the value of early defibrillation if a shockable rhythm is discovered within the first five minutes following the arrest event. Adequate cardiac compressions (optimum rate with optimum excursion) given before defibrillation shock are associated with improved outcomes, according to data cited by Ali and Zafari. They also note that optimum cardiac compressions provide coronary perfusion that serves to minimize the depleting affect of ventricular fibrillation on cardiomyocyte energy stores. Rescue breaths (two breaths administered by mouth-to-mouth or mouth-to-airway respiration before instituting cardiac compression) are currently recommended by the American Heart Association, but this is controversial and subject to change. Ramsay and Maxwell39 note that current recommendations urge rescuers to perform chest compressions with two hands in adults at a rate of 100 compressions/minute with a compression excursion of 4 cm. For patients who have an airway placed, the ratio of compressions/breaths is recommended at 30:2. Mouth-to- mouth and mouth-to-airway “rescue breaths” previously recommended to precede chest compressions are now eliminated in many regional protocols recognizing that encouragement to administer mouth-to-mouth breaths is a strong disincentive to provision of any sort of rescue resuscitation. As noted above, in current studies, no resuscitation attempt is made in the majority of witnessed out-of-hospital cardiac arrests. Recent data cited by Ramsay and Maxwell (reference 9 in their bibliography) indicate that chest compressions without rescue breaths result in improved outcomes for cardiopulmonary resuscitation in witnessed out-of-hospital cardiac arrest events. A more favorable neurologic outcome, more frequent occurrence of shockable cardiac rhythm on initial electrocardiogram, and improved overall survival when resuscitation was begun within four minutes of cardiac arrest were all confirmed in the 33 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 1 2