Current Review-

Care of the Adult Cardiac Surgery Patient

PART I

Pezzella AT, Ferraris VA, Lancey RA,
Care Of The Adult Cardiac Surgery Patient:
Part I Current Problems In Surgery Volume 41, Number 5, May 2004

 

PART I

INTRODUCTION
RISK ASSESSMENT / SEVERITY SCORES / OUTCOMES ASSESSMENT
RISK AFTER ARRIVAL IN THE INTENSIVE CARE UNIT
LONG TERM RESULTS
COST
EVIDENCE BASED MEDICINE (EMB) / GUIDELINES / META-ANALYSIS

CLINICAL ASPECTS

ANESTHESIA
‘FAST TRACK’ PROGRESSION OF PATIENT RECOVERY
MONITORING
   
Temperature
    Hemodynamics
        Arterial pressure
        CO/CI – mixed venous O2 saturation
        Pulmonary Artery Catheter
        Transesophageal Echocardiography
        Left atrial pressure lines and drug administration
        Gastric tonometry
   
Respiratory monitoring
    Neurologic monitoring
    Critical Care Charting

CARDIOPULMONARY BYPASS
MYOCARDIAL PROTECTION
CRITICAL CARE UNIT COMPOSITION
POINT OF CARE (POC) TESTING
DIAGNOSTIC ADVANCES
 

SUBSYSTEM APPROACH
    HEMODYNAMIC
   
    Low Cardiac Output
        Pharmacological Support
            Mechanical Circulatory Support
            Intra-aortic balloon counter-pulsation (IAB)
            Mechanical Assist
       
Vasodilation with Normal/High Cardiac Output
        Arrhythmias
            Atrial Fibrillation
            Ventricular Arrhythmias
            Heart Block
       
Bleeding/Cardiac Tamponade
        Perioperative Myocardial Ischemia/Infarction
        Systemic Hypertension
        Pulmonary Hypertension / RV Failure
        Cardiac Resuscitation/ Chest Re-Opening

PART II- SUBSYSTEM APPROACH (continued)

    RESPIRATORY
       
Pulmonary embolism
    RENAL
    HEMATOLOGICAL
    FLUIDS AND ELECTROLYTES
       
Calcium
        Potassium
        Magnesium
        Sodium
        Acid-Base Disorders
NEUROLOGICAL
       
CNS
        Phrenic Nerve Injury (PNI)
        Peripheral Nerve Injury / Brachial Plexus Injury
        Neuromuscular / Myopathy
INFECTIOUS
       
Fever
        Sepsis / Septic Shock
METABOLIC / ENDOCRINE
       
Diabetes Mellitus
        Thyroid Function
        Adrenal Function
        Oxidative Stress Response
        Natriuretic Peptides
GASTROINTESTINAL
VASCULAR
WOUNDS
       
Delayed Sternal Closure/ Sternal Infection
NUTRITION


In Brief

Cardiac surgery had its beginning at the dawn of the 20th century. Ludwig Rehn was the first to successfully suture a penetrating wound of the heart in 1896(1). Subsequently, closed cardiac procedures evolved in the first half of the 20th century, notably PDA ligation, Blalock Taussig shunts, removal of foreign bodies from the heart, and closed approaches to the mitral valve (2). Cardiac surgery utilizing cardiopulmonary bypass (CPB) dominated the second half of the 20th century, after a brief period of clinical series utilizing systemic hypothermia (3), and cross circulation approaches (4). The number of operations utilizing CPB has grown to a present annual rate of almost 800,000 cases in the USA with the majority being coronary artery bypass grafting (CABG) (Figure one)(5). The major goals of cardiac surgery are to improve clinical outcomes by correcting or palliating an existing or acquired cardiac condition.

Increased knowledge and experience, coupled with improved clinical processes, and technical advances, have made open-heart surgery safer and more readily available, with decreased morbidity, mortality and lower costs. The raw operative mortality for cardiac surgery in the USA is under 5% with isolated CABG under 3%(6). Representative institutional experiences are summarized in (figure 2 a, b)(7). Morbidity, however, is noted in 25-40% of patients following cardiac surgery with individual incidences of specific complications in the 2-4% range (figure three)(a, b)(6) (7). This has remained stable despite changing demographics (age, sex, and body surface area), complex cardiac pathology with decreased Left Ventricular (LV) function, and increasing associated comorbidities (Table 1)(8-11). Pre-operative selection and preparation, sophisticated operative approaches and technique, and advances in the intensive care unit (ICU) have contributed to this continued success. The ICU has emerged as the dominant area where the fragile transition from the operating room to sophisticated care occurs.

The evolution from the first dedicated ICU at Johns Hopkins Hospital in 1923 through the establishment of a specialized coronary care unit in 1962 to the present multi-specialized and sub-specialized units of today has been nothing short of dramatic (12). The care in the cardiac surgery intensive care unit in many medical centers has become a cooperative and collaborative effort involving the cardiac surgery team, the cardiac anesthesiologists, the critical care team, a sophisticated group of medical consultants, and allied health personnel, particularly critical care nurses and respiratory therapists. Diagnostic support, increasing electronic interface, bedside computerized nursing, and point of care testing have become integral components of the critical care pathway. The present review gives an overview of the care of the adult cardiac surgical patient with particular emphasis on the early postoperative phase in the ICU utilizing a subsystem approach.


Introduction

Cardiac Surgery has made significant advances over the past fifty years. Despite increasing age and comorbidity the results continue to improve. This is due principally to the specific areas of improvement and experience in pre-operative selection and preparation; database and risk analysis; operative advances, especially in monitoring, anesthesia, surgical techniques, perfusion; and postoperative care, particularly in the intensive care unit. A two-part review is presented to give a review of the care of the adult cardiac surgery patient. Part one will focus on the general clinical area and the subsystem approach to perioperative care. Part two will continue this subsystem approach to critical care.

RISK ASSESSMENT/SEVERITY SCORES/OUTCOMES

Open-heart surgery has become increasingly important in terms of access, cost and results, particularly in the setting of a more sophisticated public which desires more information regarding both surgeon specific and institutional outcomes which is now readily available on the internet (Table 2). A number of scoring systems utilizing univariate and multivariate regression models have emerged to help the cardiologist and cardiac surgeon better counsel the patient and family regarding surgical risk (13). They are essential tools for risk assessment, cost analysis, and to study the benefit of surgery for the patient. Operative mortality is recorded as both raw, unadjusted mortality and expected mortality, and may be defined as less than 30 days, or ‘in-hospital’ mortality, (i.e., the patient does not survive to discharge.). The major determinants of perioperative morbidity and mortality remain demographics (age, sex, body surface area), acuity of the operation (elective, urgent, emergency), associated co-morbidities (especially smoking, diabetes, obesity, renal dysfunction, hypertension, stroke, chronic obstructive pulmonary disease, and peripheral vascular disease); and the degree of cardiac dysfunction.

(Table 3). Univariate analysis is used to correlate a particular risk factor with a specific outcome, which is the methodology utilized in the Society of Thoracic Surgeons (STS) database. This calculation is difficult to assess when multiple factors are involved. In multivariate regression analysis, only those variables found significant in univariate analysis are used to assess the independent association of these variables with specific outcome or results. Several multivariate risk models allow for bedside calculation of operative risk. The Cleveland Clinic (CCF in Table 3) severity scoring system is practical in that the score is directly correlated with predicted mortality. (Figure 4 a-b) (22) The risk of advanced age will become even more important and relevant in terms of access to care, cost, and outcome. At present, three percent of Americans are octogenarians, and by 2010 there is projected to be an increase to 4.3%, representing 12 million people (28). Between 1987 and 1990 there was a 67% increase in cardiac surgery in octogenarians (29). Mortality and quality of life are the prime indicators of success in all age groups. Operative mortalities between 7.9% and 13.5% have been reported in octogenarians, with one study reporting a 5-year median survival of 55%, compared to 69% in age group 70-79 years, and 81% for age group 60-69 years (29). Utilizing Standard Form 36 Health questionnaire (SF-36 form) and the Seattle Angina Questionnaire, 83.7% of surgical octogenarian patients were living at home with 74.8% enjoying good or excellent health (30) . Females remain at higher risk for myocardial revascularization. Two recent studies show a two-to three-fold increase in mortality for women versus men (31, 32).

Interestingly none of the risk scores for myocardial revascularization include either hospital or surgeon-specific volumes as specific risks for mortality or adverse outcome. At least 10 large studies have addressed the notion that hospitals performing small numbers of CABG operations have higher operative mortality. Seven of these 10 studies found increased operative mortality in low volume providers (33-39). In three other large studies there was no such association (40-42). Interestingly, in the three studies done more recently (since 1996) there was no clear relationship between outcome and volume. The Institute of Medicine summarized the relationship between higher-volume and better outcome (http:// www.nap.edu/catalog/1005.html) and concluded that procedure or patient volume is an imprecise indicator of quality even though a majority of the studies reviewed showed some association of higher-volume and better outcome (43). The dilemma is that some low volume providers have excellent outcomes while some high-volume providers have poor outcomes. These observations on operator volume and outcome prompted some authorities to suggest ‘regionalization’ to refer nonemergent CABG patients to large volume centers (38,44,45). A role for ‘selective regionalization’ was advocated by Nallamothu et al (42), since they found that low risk patients did equally well in high volume or low volume hospitals. They suggest regional referral for elective high-risk patients to high volume institutions. Crawford et al (46) pointed out that a policy of regionalized referrals for CABG might have several adverse effects on health care including increased cost, decreased patient satisfaction, and reduced availability of surgical services in remote or rural locations.

RISK AFTER ARRIVAL IN THE INTENSIVE CARE UNIT

Risk is stratified for the overall cardiac surgery experience, including early outcomes for the operative procedure based on pre-operative risk factors. The APACHE III score (Acute Physiologic And Chronic Health Evaluation) is commonly used for non-cardiac surgery patients based on clinical presentation upon arrival in the ICU. Since application of the Apache III to cardiac surgery is difficult (with many variables changing rapidly due to the manipulation that occurs early), a refined APACH E III was developed for patients undergoing CABG. Independent predictors of survival were acute physiology score, age, emergency operation, reoperation, number of grafts performed, and gender (47). Higgins, at the Cleveland Clinic, (48) reported an ICU admission score for predicting morbidity and mortality (Figure 5). This allowed sequential assessment of prognosis, and improved stratification because of a continuously updated data. For example, the use of intra-aortic balloon counter-pulsation (IABP) signified a worsening prognosis likely due to significant intracardiac event related to degree of pathology, myocardial protection, and technical events. This applied to extended cardiopulmonary bypass (CPB) times as well.

 

Long term results

Outcomes after hospitalization have become increasingly important in terms of quality of life. The SF-36 form is a short questionnaire with eight multi-item variables (49). Lindsay (50) reported on 214 patients undergoing CABG in whom SF-36 was used before and after operation. At a mean of 16.4 months post-operatively, the SF-36 score showed high levels of social support were associated with improved health status and quality of life. Simchen (51), in a study from Israel, reported on 1270 patients 1 year following CABG. One-third reported their quality of life as not good, particularly females and those of lower socioeconomic status. Rehabilitation programs were targeted as a means of improvement. Quality of life measures following CABG will undoubtedly become more important as the population ages.

COST

The number of Medicare patients has risen to over 40 million. At the same time, the number of uninsured in the USA is also rising. Access to care and rising costs continue to challenge health care providers. The Health Care Financing Administration [HCFA: now called Centers for Medicare and Medicaid Services (CMS)] budget has risen from 21.5 billion in 1977 to 214.6 billion in 1997 (52), with treatment for coronary artery disease accounting for more than 80 billion of that cost in 1997, yet continuing to be the leading cause of death and morbidity in the USA. At the same time, expensive medical technology continues to grow and develop. With the escalating costs of cardiac surgery, attempts have been made to find effective ways to reduce these costs while maintaining good outcomes. Beginning in the last decade, individual cardiac surgeon and institutional results in New York State were made available to the media and public, causing outcries both within the medical establishment and the general public (53). HCFA has mandated progressively lowered reimbursements, utilizing DRG’s for cardiac surgical procedures, in a further attempt to control the continuing growth of operations and cost. The reimbursement for cardiothoracic surgery from Medicare decreased 9.3% from 1991 to 1997 (52). With a rising population and the influx of the baby boomers into the patient mix, financial issues will become even more important.

The specific cost of CABG has been studied extensively, with particular attention given to pre-operative risk factors and complications, which increase LOS. Taylor (54) prospectively studied 500 patients undergoing CABG, and found a charge of $11,900 ± 12,700. No preoperative clinical features were significant predictors of cost, whereas post-operative sternal wound infection, respiratory failure, and LV failure were. Ferraris and co-workers (55) studied hospital charges in 938 patients undergoing CABG. They found that risk factors for postoperative morbidity are different than those for postoperative mortality. Their findings suggested that older patients with preoperative anemia and low blood volume who also have other co-morbidities (CHF, stroke, COPD or hypertension) are an increased risk for postoperative complications and increased hospital costs. The most costly outcome in their study was perioperative death. Cohen (56) et al, analyzed hospital cost, (not charges) for 89 elective CABG patients with an average postoperative LOS of 9.3 days, and found the total costs were from $17,420, $19,153, and $21, 828 for the 25th, 50th, and 75th percentiles, respectively. Williams et al (57), found increased cost to be correlated with higher average risk (utilizing the Parsonnet equation) and increased LOS in 2,589 CABG patients. Shahian et al (58), however, showed no correlation between hospital size, volume of surgery, and cost.

Strategies to decrease cost include operating on lower-risk patients, more expedient surgery (i.e. on the same admission as diagnostic catheterization), same-day admissions, decreasing ICU and restrictive hospital stay, improved home care, and greater use of chronic care facilities and rehabilitation centers). Shorter LOS in the acute care hospital, however, has led to increased readmission rates, and more frequent discharges to chronic facilities, along with increasing utilization of home health services. Lazar et al (59), demonstrated a distinct change from 1990 to 1998, with discharge-to-home-with-services increasing from 14.75 to 46.7%, and transfer to rehabilitation units increasing from 2.9% to 13.7%. Readmission rates following cardiac surgery range from 5.3% to 20.9% (59-63). Preoperative risk factors associated with increased readmission rates include female sex, diabetes, chronic lung disease, and pre-operative atrial fibrillation (62-63). Common readmission diagnoses include atrial fibrillation, angina, congestive heart failure, ventricular tachycardia, wound problems, pneumonia, and gastrointestinal complaints (60).

Evidence Based Medicine (EBM)

Simply put evidence is the link between what we know and what we do in medicine. EBM is designed to achieve optimal management of clinical problems or challenges. From this, practice management guidelines, paradigms, and algorithms can be developed. The ultimate goal of risk stratification and outcome assessment is to account for differences in patient risk factors so that patient outcomes can be used as an indicator of quality of care. A major problem arises in attaining this goal because uniform definitions of quality of care are not available. This is particularly true of cardiovascular disease. For example, there are substantial geographic differences in the rates at which patients with cardiovascular disease undergo diagnostic procedures and, incidentally, there is little, if any, evidence that these variations are related to survival or improved outcome (64-67). In one study, coronary angiography was performed in 45% of patients after acute myocardial infarction for patients in Texas compared to 30% for patients in New York State (p<0.001 for comparison between states) (65). In these patient populations the rate of coronary revascularization was similar, and the survival in these patients was not related to the type of treatment of diagnostic procedures. Regional variations of this sort suggest that a rigorous definition of the "correct" treatment of acute myocardial infarction, as in other cardiovascular disease states, is elusive and the definition of quality of care for such patients in imperfect. Similar imperfections exist for nearly all outcomes in patients with cardiothoracic disorders. Risk adjustment methodologies can isolate patient risk factors that are associated with poor outcome, but what to do about these risk factors and how to improve outcomes based on risk stratification is uncertain. More work is required to define optimal outcomes and treatment standards based on risk profile.

Recognizing the difficulties in defining ‘best practices’ for a given illness, professional organizations have opted to promote practice guidelines or ‘suggested therapy’ for given disease (68,69) (Figure 8,9). These guidelines or recommendations represent a compilation of available published evidence, including randomized trials and risk-adjusted observational studies, as well as consensus among panels of experts proficient at treating the given disease (69). For example, the practice guideline for coronary artery bypass grafting is available on the internet (http://www.acc.org/clinical/guidelines/bypass/

ExecIndex.htm) for both practitioners and the lay public. These guidelines were developed using a summation of available randomized controlled trials, risk-adjusted observational studies, and expert consensus. They are meant to provide clinicians with accepted standards of care that most would agree upon, with an ultimate goal of limiting deviations from accepted standards. Guideline development represents a work in progress. The methodology for developing guidelines for disease treatment is evolving. Many published guidelines do not adhere to accepted standards for developing guidelines (70). The area where greatest improvement is needed is in the identification, evaluation, and synthesis of the scientific evidence.

In summarizing available medical evidence on a given subject, information retrieval is king. Nowhere is this more evident than in the Cochrane Collection of Available randomized trials on various medical subjects. For example, a recent Cochrane review (http://www.update-software.com/abstracts/ab002138.htm) found 17 trials that evaluated postoperative neurological deficit in having hypothermic CPB compared to normothermic CPB (71). This compares to a recently published meta-analysis on a similar topic that only fund 11 trials on which to perform a similar analysis (72). To date little EBM recommendations are available related to perioperative care of the cardiac surgery patient. It is difficult to assess evidence in critical care. As an example, Scheinkestel et al (73), points out that multiple interventions in a cohort of patients without informed consent are difficult to study in a randomized prospective way. Such issues as the use of pulmonary artery catheters, colloid fluid resuscitation, target hemoglobin level, choice of inotropic agents, and the degree and route of nutritional support remain unsettled and controversial.

Clinical Aspects

Anesthesia

Advances in cardiac anesthesiology techniques have been attributed to increased experience, safer and improved pharmacology, predictable and proven anesthetic techniques, and technological advances in hemodynamic monitoring. The anesthesiologist, nurse anesthetist (CRNA), and anesthesia technician continue to play expanding roles in the preoperative, operative, and postoperative phases of cardiac surgery, particularly with the increasing population of OPCAB (off pump coronary artery bypass) procedures.

Advances in preoperative anesthetic assessment for non-cardiac surgery have included implementation of the AHA/ACC guidelines in addition to the traditional ASA risk classification (Figure 7,8) (74,75). With over 28 million patients in the USA per year undergoing surgery, anesthesia has assumed an increasing role in the pre-operative medical evaluation, preparation, and clearance of patients for surgery (76). This experience in non-cardiac operations has been extended to cardiac surgery as well.

Intraoperative advances include sophisticated monitoring, anesthesia protocols, and improved hemodynamic drug regimens for weaning from CPB. Tuman et al (77) reviewed five anesthetic techniques in 1094 CABG patients. These included high dose fentanyl (> 50 ug/kg); moderate dose fentanyl (< 50 ug/kg); sufentanil (3-8 ug/kg); diazepam (0.4–1 mg/kg) with Ketamine (3-6 mg/kg) or halothane (0.5-2.5% inspired concentration after thiopental induction). Multivariate analysis did not suggest any difference in terms of incidence of myocardial infarction (MI), low cardiac output state, or mortality between the various anesthetic agents. Anesthesia during CPB is unique as the lungs are eliminated as a means to administer drugs and the depth of anesthesia is difficult to monitor. During CPB inhaled and intra-arterial drugs are usually given through the oxygenator and perfusion circuit. The most challenging role has been the expanded involvement of anesthesia with OPCAB procedures. This involves a more interactive role between the anesthesiologist and surgeon in order to maintain hemodynamic stability (78). The major intraoperative anesthetic considerations are maintenance of hemodynamic stability, normothermia, and adequate anticoagulation. The intraoperative anesthetic techniques have a significant effect on perioperative mechanical ventilator weaning strategies. Postoperative concerns are focused on earlier extubation and pain control. An interesting technique, thoracic epidural anesthesia for CABG, shows initial gratifying results (79, 80). Advantages include excellent analgesia, early extubation, and sympathetic blockade. There is evidence to show improvement in the myocardial endocardial to epicardial blood flow ratio, with a subsequent decrease in ischemic events. Concerns, however, have been raised regarding hemodynamic instability, related to sympathetic blockade, and the risk of epidural hematoma in the anticoagulated patient.

Aggressive weaning from mechanical ventilation has been applied to even high-risk patients. Anesthesiologists play a major role in this effort especially in regards to balancing intraoperative inhalation and intravenous anesthetic agents. In the previous era of high dose intravenous narcotic anesthesia and overnight ventilation, pain control was not a major problem. With ‘fast track’ extubation protocols a balance must now be reached between sedation, amnesia, pain control, and respiratory suppression.

‘FAST TRACK’ Progression of Patient Recovery

‘Fast track’ is a term coined by Dr. Richard Engleman in 1994 (81), and refers to earlier extubation of post-operative cardiac surgery patients. This is not a new concept. Klineberg et al (82) reported a series of 72 patients in 1977 with 62.5% being extubated within 5 hours of arrival in the critical care unit. Gall et al (83), showed that early extubation with spontaneous respiration resulted in decreased intrapleural pressure and significant increases in left ventricular end-diastolic diameter, ejection diameter shortening, stroke work, and cardiac output. Krohn et al (84) reported on 240 patients undergoing early extubations, with a subsequent postoperative length of stay (LOS) median of 4 days. Engleman et al (81), utilized a comprehensive approach that involved, in addition to early extubation, a complete spectrum of interventions to shorten hospital stay. This included short acting anesthetic agents, early mobilization, prophylactic drug intervention to minimize postoperative atrial fibrillation, and aggressive preoperative counseling regarding postoperative expectations. Retrospective studies of 562 patients in two groups were evaluated. The initial results showed a shortened ICU stay (2.4 vs. 1.9) and postoperative LOS (8.3 vs. 6.8). Both hospital charges and costs were reduced. Cheng et al (85) reported on a prospective randomized group of 120 patients undergoing elective CABG. Extubation time was 4.1 hours in the fast track group vs. 18.9 hours in the conventional group. There was no increase in morbidity, but both ICU and LOS were decreased in the fast track group. It is still unclear as to the ideal time for extubation. In general, within 3-6 hours after arrival in the critical care unit, the majority of eligible candidates are hemodynamically stable with no evidence of ischemia, or mediastinal bleeding. At this point most patients are awake with no neurological deficit, acceptable blood gases, and adequate respiratory mechanics. Given adequate parameters, these patients are extubated (c.f. Respiratory Subsystem).

MONITORING (86,87,88)

Monitoring in the critical care unit has advanced well beyond the traditional parameters of temperature, heart rate, blood pressure, respiratory rate, patient weight, fluid intake/output, and clinical evaluation. Understanding and tracking the physiological response to surgery and the subsequent interpretation and treatment of pathophysiologic variations has been enhanced with more sophisticated, yet user-friendly, monitoring devices and regimens, along with appropriate alarm devices. Continuous cardiac output and mixed venous oxygen saturation, ventilatory mechanics, urologic function, and neurologic function, can all be monitored in most units. Additional monitoring will be highlighted in the subsystem approach to postoperative care. The basic cardiac surgery perioperative monitoring capability includes the electrocardiogram, i.e. telemetry via five lead electrodes including leads II and V, often with ST segment analysis, and arrhythmia tracking. The combination of leads II and V5 gives a sensitivity of over 80% for detecting myocardial ischemia. Hemodynamic assessment includes cuff blood pressure, direct arterial pressure (usually radial or femoral) and central venous pressure. Respiratory function is assessed with continuous pulse oximetry and end tidal CO2 monitoring. Pulmonary artery (PA) catheters may be used for recording or calculating pulmonary artery pressures, cardiac output, systemic vascular resistance (SVR), and mixed venous oxygen saturation (SVO2), although their use is not mandatory. Volume status is assessed with urinary output, chest tube drainage, and nasogastric decompression tubes. Intermittent assessment of neurologic function, especially level of consciousness, completes the usual monitoring routine.

Temperature

Body temperature parameters are important to track. Bladder, rectal, nasopharyngeal, tympanic membrane temperatures, and central venous temperatures from the pulmonary artery catheters have been employed, with the pulmonary artery core temperature being most reflective of core body temperature (89). Axillary temperatures are not reliable in the critical care environment.

Hemodynamic Monitoring (90)

Assessment of adequate vital organ perfusion begins with the clinical assessment. Mental status, the presence of peripheral pulses, skin color, and temperature, capillary filling (<3 seconds), and urine output are non-invasive methods of assessment.

Arterial pressure

The radial artery (usually right side for aortic surgery) is the most common access site for determining systemic arterial pressure (SAP). Technical considerations, along with spasm in this muscular artery, accentuated by hypothermia, may make this unreliable at times. The common femoral artery is often a more accurate access site, assuming no major aortoiliac pathology. By either method, the mean arterial pressure (MAP) is more constant and reliable than SAP. As an independent variable SAP is not totally reflective of cardiac function.

Cardiac Output/Index/ (CO/CI) Mixed Venous Oxygen Saturation) SVO2

The routine use of continuous or intermittent measurement of calculated hemodynamic indices is not necessary for routine low risk patients undergoing CABG (91). To abandon this modality necessitates a broad based re-education of those who have become dependent on this information, including nurses, residents, fellows, and surgeons. In addition to the hemodynamic data measured with PA catheters (92,93), new technology requiring less invasive techniques has emerged. Esophageal Doppler monitor (EDM) is able to determine cardiac output, as well as assessments of pre-load, afterload, and contractility based on waveform analysis (CO = P D 2/4 x Vm x 60 where Vm is mean velocity and D is diameter of aorta) (94,95). Another method, the non-invasive partial rebreathing method (NICO) calculates CO by combining end-tidal CO2 monitoring with arriving mechanics and a special inline circuit (96). Still evolving, a bioimpedence method utilizing skin leads was developed by Wang and has been studied primarily in non-cardiac surgical patients (97).

Measurement of RV ejection fraction is now possible utilizing thermodilution technique (98, 99). There are many constraints to its use, particularly in the presence of tricuspid regurgitation or atrial fibrillation, as the computer requires a discenerable R-wave, which may be distorted by atrial fibrillation.

Pulmonary Artery Catheterization (PAC)

Lewis Dexter in 1945, was the first to perform PA catheterization, making the diagnosis of congenital heart problems possible (100). In 1947 he used the PA wedge pressure and determined this to be reflective of left-sided filling pressure. Swan introduced the present day catheter in 1970 (101). A landmark study by Gore and associates in 1987 (102) raised concerns of the merits of routine PA catheter use in patients with myocardial infarction and congestive heart failure (CHF). Other reports supporting the dangers and advantages of PA catheterization have been well documented (103, 104). Complications of PAC must be recognized and appreciated (105). Catheter-induced pulmonary artery ruptures or operations, especially in the anticoagulated patient, can be lethal. Sirivella (106) reported an incidence of 0.1% in a series of 850 patients, undergoing cardiac surgery with CPB. The overall mortality in that group was 42%. They present a practical algorithm outlining recognition and management. Retained catheters require cooperation of the interventional cardiologist for extraction. Occasionally surgery is required for safe removal, especially if trapped in trabeculated RV muscle or wrapped around a tricuspid papillary muscle.

Transesophageal Echocardiography

Transesophageal echocardiography (TEE) has had increased use both intraoperatively and post-operatively. There are separate TEE certification programs for anesthesiologists (107). Intraoperative TEE is used for both routine and complex cardiac cases, (108) and is a rapid and valuable diagnostic modality with a low complication rate (0.18-0.50%), primarily esophageal. Intraoperatively, its primary value is the assessment of global systolic LV function and ejection fraction (EF); valve function following replacement or repair; assessment of intracardiac air; and ascending/arch aortic scanning, looking particularly for dissection and atheromatous plaques. Post-operatively, it is helpful with assessment of pericardial effusions, presence of intra cardiac shunts, valve insufficiency, especially aortic insufficiency in patients with intra-aortic balloons (IAB), and evaluation of cardiac recovery in patients with mechanical assist devices. The routine use of TEE to assess cardiac output has not been thoroughly validated in the perioperative setting (108, 109). To assess atherosclerotic plaques in the ascending aorta, the use of intraoperative epiaortic scanning has been advocated (110, 111). It is more advantageous than TEE, particularly in the middle and distal ascending aorta segments. Recently the emergence of hand held portable echocardiography units offers some advantages in terms of ease of use and rapid screening (112). However, TEE probes for these compact units are not yet available. Also they are, as yet, not equipped with pulsed or continuous Doppler.

Left Atrial Pressure Lines and Drug Administration (113, 114)

Prior to the use of multi-port pulmonary artery catheters, both right and left atrial catheters were routine practice. The dangers of air or particulate emboli along with fracture and retained lines remain a hazard. However, left atrial pressure determinations may be helpful. More importantly, left sided infusion of vasoconstricitve drugs, particularly epinephrine and norepinephrine, has certain advantages, as right-sided infusion may suffer from a dilutional effect as well as pulmonary elimination. Further, pulmonary vasoconstriction may trigger an increase in pulmonary pressures and resistance.

Gastric Tonometry (115, 116)

This modality allows monitoring of splanchnic perfusion. Tissue perfusion may be addressed on a regional rather than systemic basic. Gastrointestinal ischemia is an early manifestation of this impaired tissue perfusion. Systemic oxygen delivery and re-uptake is the sum of re-uptake in individual organs and does not account for regional perfusion, and more importantly malperfusion. Unfortunately the technology is cumbersome, and this modality has not gained widespread use.

Respiratory Monitoring

Modern mechanical ventilators offer a variety of mechanisms to monitor adequate ventilation (117). Additional alarms warn of mechanical malfunction. Blood gas analysis provides data regarding ventilation, gas exchange, and acid/base status. Capnography is the graphic display of CO2 concentration. The end-tidal CO2 (PET CO2) is measured in the exhaled ventilation. This correlates well with the pa CO2. Transcutaneous pulse oximetry gives on estimation of arterial hemoglobin oxygen saturation. With predictable accuracy, this determination has added significantly in weaning FIO2 concentrations and decreasing the number of blood gas determinations (118, 119). Following extubation, pulse oximetry improves patient safety with detection of desaturation episodes that are sometimes not apparent clinically.

 

 

Neurological Monitoring

Neurological monitoring begins in the operating room. Intraoperative electroencephalography (EEG) can be used during CPB. The detection of CNS ischemia, effect of drugs, adequacy of non-pulsatile perfusion, depth of anesthesia, and brain function especially during hypothermic circulatory arrest (HCA) can be monitored (120). The Bispectral Index (BIS) is a processed EEG variable that quantifies and records high-frequency activity (within the 70-110 HZ frequency range) (121). Intraoperative transcranial Doppler ultrasonography is utilized to assess cerebral blood flow and embolic phenomenon (usually air or debris), as evidenced by high intensity transient signals (HITS) in the cerebral circulation (mostly middle cerebral artery) (122, 123). Transcranial near-infrared spectroscopy (NIRS) provides continuous non-invasive transcutaneous measurement of oxygenated and hemoglobin in the frontal cortical area. This is calculated as cerebral oxygen saturation (ScO2) (124). This correlates well with jugular venous bulb oxygen saturation.

Critical Care Charting

Nursing charting and notes are an integral part of monitoring patient care. The majority of critical care units continue to use the labor-intensive manual charting systems. It has become increasingly difficult to record and access the increasing amount of data necessary and available. The critical care nurse is sometimes overwhelmed with the task of recording and charting. Additionally the transfer of information between shifts varies between verbal or dictated reports. A number of computerized systems are available and are becoming increasingly popular in major critical care units. Hewlett Packard pioneered the Care Vue â system. Improved systems are available that create a network to bring laboratory results and diagnostic tests into the bedside computer (Caremaster TM Plus, Spacelabs Intesys, Redmond WA.).

As already mentioned, accurate patient data is essential in order to apply the principles of risk stratification and quality improvement outlined above. Therefore, risk assessment methodology has placed greater reliance on data extracted from the medical record. The American College of Surgeons was among the earliest advocates of the utility of medical records for quality review (125). In the 1960’s, Weed advocated standardization and computerization of medical records (126-128). Little substantive progress had been made as far as the computerization of medical records until the need arose for management of large amounts of data of the sort required for risk adjustment and outcomes assessment. Medical records are an invaluable source of information about patient risk factors and outcomes. With these facts in mind, more and more pilot studies are being undertaken to computerize and standardize the medical record in a variety of clinical situations (129-130). The Veterans Administration has been among the leaders in the use and implementation of the electronic medical record, yet suggests that they may not adequately reflect the importance of chronic disability and decreased functional status (131). Nevertheless, it is apparent that the need for data about large groups of patients with enormous amounts of information exists, especially for managed care and capitation initiatives.

CARDIOPULMONARY BYPASS (CPB)

The evolution of CPB over the past 50 years has been dramatic, especially during the past decade. Notable advances include use of centrifugal pumps, improved anticoagulation strategies, pH management, heparin bonded circuits, and ultra filtration, especially in the pediatric group. The clinical perfusionist has become an integral member of the cardiac surgery team and their duties range from being responsible for supervising and conducting CPB, to cell saver, intra-aortic balloon (IAB), and mechanical devices. CPB, though important and strategic to provide a bloodless, dry, and quiet surgical field to allow routine and complex cardiac procedures, does cause a multi-system insult to the host. It evokes a pathophysiological state because it is non-pulsatile, requires total body heparinization, and exposes blood to a variety of non-organic contact surfaces. The exposure of this blood to biomaterial in the oxygenator and perfusion circuit and non-endothelial cells in open surgical wounds changes the entire hemostatic mechanism (132). As a result, cardiopulmonary bypass induces an inflammatory reaction, referred to as the systemic inflammatory response syndrome (SIRS). This is a complex activation of complement and plasma contact systems and also involves stimulation of leukocytes with liberation of proteolytic enzymes, oxygen free radicals, and vasoactive amines, as well as the production of proinflammatory cytokines (133). Taylor, in 1999 (134, 135) summarized this leukocyte response:

" Whereas the usual inflammatory response is a local response, the SIRS affects all tissues and organs. Free flowing leukocytes in the bloodstream roll along the vascular endothelium. Adhesion molecules called selections mediate this. The next phase is attachment to the endothelium, mediated by integrins. Ultimately these activated leukocytes transmigrate into the extravascular tissue."

All the major subsystems discussed are affected, especially hematologic. Thrombocytopenia occurs commonly, but usually reverses by the 3rd postoperative day. Dilutional thrombocytopenia is accentuated by the deposition of platelets on the membrane oxygenator and circuit. This quantitative effect is worsened by significant qualitative changes. On arrival in the critical care unit it must be appreciated that the patient has been in this non-pulsatile state with rapid shifts in temperature, major fluctuations of the fluid spaces with anywhere from 5-10 kg total body weight gain, and in a hemodiluted state with hematocrits ranging from 25%-28%.

Advances in oxygenators have seen the membrane as the predominant device now used (136). Bubble oxygenators affect gas transfer by direct transfer of dispersed gas (100% O2) into returning desaturated venous blood. Membrane oxygenators eliminate direct gas transfer. This decreases or eliminates gaseous microemboli and blood changes, especially platelet destruction and dysfunction, damage to block cells, and depletion of clotting factors. Mechanical aspects of CPB include the use of the positive displacement pump (PDP) or the centrifugal pump (CP). PDP operates by occluding tubing between a stationary raceway and a rotating roller or occluder (137). The CP propels the fluid by creating kinetic energy, which is transmitted to the fluid through the forced rotation of an impellar or cone (137). This will not generate excessive pressure and hence there is less risk of tubing separation with any obstructions in the system. There is an associated decrease in the potential for air embolism, as well as platelet trauma with CPB. Recent data supports decreased neurological events with centrifugal pumps (138).

Acid/base balance during CPB is maintained by one of two methods, alpha stat and pH stat. With hypothermia CO2 goes into solution with a resultant increased pCO2 and increased pH. With alpha stat method no changes are made, whereas with pH stat method, CO2 is added to the oxygenator to maintain pH at the same levels that were present at normothermia (134).

Ultrafiltration is the removal of water and solutes from blood across a semi permeable membrane. This modality has been incorporated into CPB systems to help with removal of excess water and solutes, especially during extended pump runs, and as an adjunct to limit hemodilution, and decrease blood and blood product usage (139). There is recent data to suggest that modified versions of ultrafiltration may decrease cytokines and decrease the incidence of SIRS (140). Another device, the cell saver has become cost effective in terms of salvaging blood and decreasing blood usage (see Hematological subsystem).

CPB is not possible without heparin, heparin substitutes, or heparin-coated circuits. There is a considerable literature related to the pharmacology, dosing, monitoring, and reversal of heparin during cardiac surgery. Heparin resistance or the need for increased dosing includes ATIII deficiency, thrombocytosis (platelet > 700,000 ul), and ongoing heparin therapy. Heparin induced thrombocytopenia with or without thrombosis (HIT/HITT) is a recent difficult problem (see Hematological subsystem).

ACT monitoring of unfractionated heparin dosing is the most common method utilized. The presence of heparin allergy, protamine allergy, or HIT/HITT requires alternative approaches. In these instances, fractionated low molecular weight heparins have been utilized. Other agents including heparinoids or glycosaminoglycons, defibrinogenating agents like pit viper venom (ancrod), or hirudin have also been used as alternatives to unfractionated heparin (141). Heparin resistance is usually treated with increasing heparin, fresh frozen plasma (FFP)(FFP is a source of AT III), or recombinant AT III. Recently, Antithrombin (AT III) concentrate has shown good results in obtaining therapeutic ACT’s in heparin resistant patients (i.e. ACT < 480 seconds after > 450 IU/kg heparin) (142). Heparin neutralization with protamine is usually done in a fixed dose regimen (1.0-1.3 mg protamine / 100 units of heparin). Other methods of heparin reversal with protamine include obtaining dose response curves measuring, heparin levels, and protamine titration (143). Protamine related hypotension is common with heparin reversal. The rare dramatic protamine reaction with catastrophic hemodynamic collapse may be fatal. Putative risk factors include diabetics using protamine containing insulin, prior protamine exposure, fish allergy, vasectomy, and a history of non-protamine medication allergies (144).

Heparin-bonded circuits (HBC) attenuate the activation of neutrophils, platelets, and complement during CPB. The mechanism is presumed to be alteration of the blood-surface interface (145). The results have been debated, yet there is a suggestion that in high-risk patients there is less blood usage, and improved respiratory and renal function (145,146). A recent comparison of the two HBC technologies shows no differences in routine CABG operations. (Carmeda Bio Active Surface, Medtronic Inc., Minneapolis, Minnesota; Duraflo II, Boston Healthcare Corporation, Irvine, California)(147).

Embolic phenomena remain a challenge for CPB. The types of emboli include blood borne, foreign material, and gaseous. Blood borne emboli are cellular elements or aggregates of platelets. Gaseous micro-bubbles are seen less frequently with membrane oxygenators and particle filters (148). The use of intraoperative echocardiography has been of value in detecting and assessing air bubbles, particularly with valve operations.

A recent innovation in CPB has been surface-modifying additives (SMA) circuits. Two copolymers are added to the resin polymer structure of the CPB circuit (149). This reduces fibrinogen absorption and subsequent platelet activation. In a small series of patients a decrease in complement (C4a) generation has been noted (150).

The entire subject of CPB is beyond the scope of this discussion. Exciting areas of development have occurred in left heart bypass, hypothermic circulatory arrest (HCA), retrograde and antegrade cerebral perfusion, and non-cardiac applications of CPB, including extracorporeal membrane oxygenation (ECMO). (See further reading)

MYOCARDIAL PROTECTION

In order to provide a quiet bloodless field to perform a technically satisfactory operation on the heart, the aorta is usually cross-clamped thus interrupting coronary artery perfusion and risking hypoxic/anoxic myocardial damage. Melrose introduced potassium citrate cardioplegia in 1955 in order to provide diastolic arrest and protect the myocardium (151). This high dose potassium regimen was abandoned in the late 50’s in favor of systemic and local hypothermia techniques, intermittent ischemic arrest, cold fibrillatory arrest, and direct coronary artery perfusion. Modified potassium regimens with lower concentrations were reintroduced by Gay and Ebert in 1973 (152). Since that time an immense literature, especially with the work of Gerald Buckberg, has been generated relative to the ideal cardioplegia composition and the methods of administration (151)(153). At the present time an antegrade cold 4:1 blood cardioplegia regimen is the most common technique employed. Blood provides oxygen and natural buffers as well as preserving high-energy phosphate stores. Local hypothermia decreases myocardial energy demand as well as increasing its buffering capacity. The cardioplegia constituents may include varying doses of dextrose, potassium, magnesium, sodium, bicarbonate, and mannitol. Topical cold saline furthers protection. Intermittent or continuous retrograde coronary sinus delivery systems as well as varying local myocardial temperatures from cold to tepid to warm have been championed (154).

More recent developments offer new insight into myocardial protection. The depolarized arrest mechanism of hyperkalemic cardioplegia is not perfect. Untoward effects include contractile dysfunction, conduction disturbances, abnormal transmembrane fluxes, and cellular swelling. Potassium channel openers arrest the myocardium at hyperpolarized potentials (155). This is close to the natural resting state of the cell membrane. Another advance is the concept of ischemic preconditioning, which is believed to be an adenosine-mediated phenomenon (156).

CRITICAL CARE UNIT COMPOSITION

Intensive care units account for only 5% of all hospital beds in the USA yet accrue 20% – 28% of total hospital costs (157). The requirements for medical staff organization, unit organization, staff availability, and service needs are well outlined by the Society of Critical Care Medicine (158). Savino et al (159), outlines the practical administration of a CT intensive care unit. The cardiac surgery patient is transferred to the recovery room, designated cardiac surgery unit or a general intensive care unit. An organized transfer with monitoring enroute is vital, as is a coordinated transfer from the anesthesiologist to the critical team. Immediate transfer of monitoring devices, along with establishment of mechanical ventilation, and coordination of infusing devices and suction for drainage tubes are all important components of the transfer. A detailed description of the operation including procedure, type of anesthesia administered, drugs and volume given, and laboratory results are provided. The first 30 minutes is a critical period adjusting the patient to this new environment. One-to-one nursing is customary. The majority of stable patients are transferred to step down units or telemetry wards after 24 hours or less. The Toronto General Hospital has developed an innovative concept of keeping patients in the critical care unit and only changing the nurse ratio to 1:2 or 1:3 on subsequent days, while changing single rooms to double rooms with alteration in glass partitioning (160). Craft (161) presents exciting information regarding the future of intensive care with particular emphasis on computer technology.

 

POINT OF CARE TESTING

This exciting advance in critical care has enhanced the capability of obtaining accurate and essentially on-line laboratory data in the operating room and the critical care unit, reducing the turn around times from 30-60 minutes to 5-10 minutes. Moving from the central laboratory to the "stat" laboratory, and finally to the bedside ultimately saves both time and money (162, 163) . The technology responsible for this testing includes whole-blood biosensors, ion-selective electrodes, substrate-specific electrodes, polarography, and potentiometry (164). Microprocessing techniques have made the devices smaller and more efficient (165). Over 80% of hospitals have adopted some type or variety of point-of-care testing with well over 85% of the testing being performed by nurses or allied health care personal (165). Recent technology even provides simultaneous entry into bedside nursing computers. The average amount blood required from routine testing is considerably less. Without POC testing, the average loss of blood per patient in the ICU is 25 to 125 cc/day. The results of cost saving have been mixed with some programs showing a savings of $150,000 to $400,000 /year (166). It is important that standards be kept. Strict guidelines for standards and quality assurance have been established by CLIA (Clinical Laboratory Improvement Amendment of 1988) along with CAP (College of American Pathologists) and JCAHO (Joint Commission on Accreditation of Healthcare Organizations) (167). Intraoperative POC testing includes ACT, electrolytes, glucose, and blood gases and is also available at the bedside in the critical care unit. Hand held machines are readily available to nursing and respiratory technicians. Despotis et al (168), showed the advantage of POC assessment of platelet count and PT/APTT. There was a 25% change in initial therapy of coagulation changes. This resulted in decreased blood and blood product usage, as well as decreased mediastinal chest tube drainage.

DIAGNOSTIC ADVANCES

As with POC testing, sophisticated diagnostic techniques are available at the bedside. Echocardiography, ultrasonography, fluoroscopy, radiography, and perfusion scans are portable and practical. Doppler ultrasonography is particularly helpful with vascular evaluation and access. Recently, surgeons have become more experienced and facile with bedside ultrasound (US) (169). Applications in the critical care setting continue to evolve. The evaluation of maxillary sinuses, localization of central veins, arteries, pleural-based processes, intraabdominal fluid/abscess, and screening for deep venous thrombosis are but a few of the uses.

CT scanning may be particularly useful in the assessment of intrathoracic processes in the critical care patient (170). These include subtle pneumothoraces, the presence and location of effusions, and defining lung or mediastinal processes. Subsequent CT or ultrasound guided needle biopsies or catheter drainage techniques are more precise and accurate (171). Routine chest roentgenography on admission to the critical care unit following cardiac surgery has been challenged as unnecessary (172). Yet, in most centers, an immediate postoperative chest roentgenogram is performed to check position of the endotracheal tube, Swan Ganz catheter, nasogastric tube, chest tubes, baseline evaluation of the cardiac silhouette, and presence of pleural fluid, atelectasis, or pneumothorax. Done in the supine position a pneumothorax will usually appear laterally or medially.

 

SUBSYSTEM APPROACH

The traditional approach of the post-operative surgical patient includes a review of the temperature, vital signs, input/output, clinical examination, review of diagnostic data, present treatment, formulation of a problem list, and a plan for the day. Although useful for the majority of uncomplicated patients this approach is not suitable in the critical care unit. The Weed subsystem approach initiated in the late 60’s attempted to collate the problems (126, 127, 128). The SOAP (subjective, objective, assessment, plan) history, physical, progress note serves well in the chronic medical patient care area but not in the critical care area where problems change acutely and constantly (173). The subsystem approach, pioneered by Kirklin better serves this acute multi system problem patient (174). This is particularly applicable to the postoperative cardiac surgery patient and has been adopted by most cardiac surgery centers. It allows a very quick and organized approach to an otherwise complicated critically ill patient. The overall advantage of a subsystem approach is that it can be applied to all patients, whereas the problem list approach is unique to that particular patient. It allows control of the variables rather than becoming a slave to an unorganized database. It provides a system where the data is interpreted in an organized and analytical fashion. With a subsystem approach there is an anticipation of accepted complications of cardiac surgery, including bleeding trends, transient or fixed neurological defect, renal dysfunction, and respiratory failure.

Hemodynamics

The hemodynamic subsystem is a major disturbed subsystem and the most important determinant of the ultimate successful outcome from cardiac surgery. Cardiac surgery results in significant physiological stress. The patient may arrive in the operating room in any one of a variety of unstable conditions, including cardiogenic shock following acute myocardial infarction or failed PTCA stent; evolving myocardial infarction persistent unstable angina or ST changes; valvular insufficiency with congestive heart failure; or hypertension/hypotension in the setting of acute type A aortic dissection. Intraoperative hemodynamic instability is ameliorated or accentuated by the technical aspects of the operation, myocardial protection, and the stress of comorbidities. On arrival in the critical care unit the patient is either stable, marginally stable, or unstable. No matter the scenario the goal of postoperative care is to restore a normal homeostatic state and allow an uncomplicated convalescence. Kirklin, in 1981 (175), emphasized the need to achieve a normal convalescence with minimal intervention. The cornerstone of this convalescence is the maintenance of a cardiac index of 2.0 to 2.5 l/min/m2. A mixed venous oxygen saturation (SVO2) > 60 is also consistent with a normal convalescence. A recent trial of goal-orientated hemodynamic therapy in critically ill patients tested the hypothesis of supranormal cardiac index and oxygen delivery. In a series of 10,726 patients there was no survival advantage in achieving supranormal cardiac index or SVO2 (176).

With this in mind, the goal for the hemodynamic subsystem is to maintain appropriate oxygen delivery to the vital organs. Maintenance of adequate hemoglobin with arterial oxygen saturation (SaO2) and a cardiac index in the range of 2.5 L/min/m2 is the target goal. A hematocrit of 23% with hemoglobin of 8gm/dl or more in the hemodiluted patient is generally adequate. A pO2 > 60cm Hg with a TcO2 by pulse oximetry > 92 % are adequate to maintain hemoglobin oxygen carrying capacity. Manipulation of the cardiac output is aimed at maximizing the pumping capability of the cardiovascular system. An appreciation of pre-load or volume status, afterload (i.e. systemic and pulmonary vascular resistance), heart rate/arrhythmias, and myocardial contractility is necessary (Figure 9) (177). An overall assessment of an integrated cardiovascular performance is summarized in Figure 10.

Low Cardiac Output

Myocardial pump failure following cardiac surgery is a morbid event and a principal cause of perioperative mortality. This remains the seminal perioperative event in cardiac surgery. Unfortunately, the literature is confusing in terms of definition, treatment strategies, and outcome. The cardiac output must be correlated with other derived hemodynamic data and the clinical state of the patient. For example, a low cardiac output or cardiac index in a cold, hypertensive patient with normal arterial pH and with a high SVR, may have an entirely different meaning than a low cardiac output in a patient with, high PA and low systemic pressures, arterial acidosis, and oliguria.

An appreciation of the data is essential to the initiation of further diagnostic pursuits and therapeutic interventions. The major interventions include temperature control, sedation, volume administration, use of cardiotonic drugs, mechanical assistance (IAB), and/or return to the operating room for exploration, further surgery, or more complex mechanical support systems. A rapid logical etiological evaluation is summarized in (Figure 11).

Kirklin divided the cardiovascular system into normal and abnormal convalescence (175). With normal convalescence major changes in preload, afterload, contractily, heart rate, arrhythmias, blood hemoglobin and oxygen consumption do not have to be made. Initial stability during the first hour of CPB is followed by a 4-5 hour period of decreased LV function with return to pre-operative levels by 24 hours. Maintenance of preload and afterload are the two variables that usually warrant adjustment. With sinus bradycardia or nodal rhythm, atrial or A-V sequential pacing is of benefit. The abnormal or suboptimal state requires attention to poor myocardial contractility. Surgical correction, drugs, IAB, and mechanical assist are used in a logical and planned manner. The etiology of decreased contractility may include underlying pre-operative systolic and/or diastolic dysfunction; intraoperative inadequate myocardial protection; technical problems; perioperative myocardial ischemia or infarction; a mechanical myocardial process e.g. mitral regurgitation; residual aortic outflow obstruction or regurgitation; or cardiac tamponade. Recent attention regarding treatment of poor contractility stresses the role of right ventricular (RV) contractility as well as left ventricular (LV) contractility. Pre-operative risk factors for low cardiac output have been analyzed by the Toronto group (178). The risk factors include LV EF < 20%; redo operation; emergency operation; female gender; diabetes; age > 70; left main CAD; recent MI; and extensive three vessel CAD. The overall incidence of low output was 9.1% with an overall mortality of 16.9%. The development of lactate release during reperfusion may be a significant predictor or low cardiac output (179). Following rapid etiological assessment interventions must be made (Figure 12). Gorman et al (180) summarizes nicely the evaluation and management of the low output state, emphasizing shock as the common denominator. Shock occurs when oxygen demand is not met. Oxygen delivery requires cardiac oxygen, adequate hemoglobin concentration and arterial oxygen saturation.

Pharmacological Support

Hemodynamic drug support that alters preload, afterload, myocardial contractility, or combinations are among the initial interventions, with volume loading considered a component of drug treatment (181, 182). The benefits of crystalloid versus colloid resuscitation are unresolved (see Fluid Electrolyte Subsystem). Caution should be exercised in acute volume loading in the immediate post-operative period, especially in the presence of RV dysfunction (183). Pharmacological support includes venodilation, arterial dilation, inotropes, and vasoconstrictors’ (Figure 13). Inotropic drugs are classified as to their effect on intracellular cAMP (184). The cAMP dependent drugs include the adrenergic agonists epinephrine, isoproterenol, and the dopaminergic drugs dobutamine and dopamine. The cyclic nucleotide phosphodiesterase inhibitors (i.e. milrinone) are also in this class. A selective inhibitor of phosphodiesterase activity, milrinone has become a mainstay of inotropic support perioperatively (185). Recent data also shows a suppression of cytokine production through an elevation of cyclic adenosine monophasphate (186). This may have a positive effect on limiting the systemic inflammatory response (187). Pre-operative beta blockade is usually continued through the perioperative phase. There is debate about whether perioperative beta blockade is harmful because of negative inotroprism or beneficial because of decreased myocardial oxygen consumption (188). A rationale approach is to use beta blockade cautiously in patients with decreased LV function. Glucose- Insulin – Potassium (GIK) infusion has gained increased use for LV dysfunction (189). The usual approach is infusion of GIK started at anesthetic induction and continued 8 – 12 hours post-operatively. The use of angiotensin- converting enzyme (ACE) inhibitors perioperatively in patients with LV dysfunction may be useful but should be started with caution in the early postoperative period (190). Sirivella et al (191) in a randomized study showed a decrease of IAB use (86 hours versus 169) and mortality (14.5% versus 31%) with use of ACE inhibitors in selected patients. The use of thyroid hormone has also been advocated (see Endocrine/metabolic subsystem).

Intra-aortic balloon counterpulsation (IAB)

The IAB remains the first mechanical line of defense for perioperative LV dysfunction. IAB decreases cardiac work (MVO2) by deflating during systole, thus reducing afterload, and augmenting coronary perfusion with inflation during diastole. Torchiana et al, (192) reviewed the Massachusetts General Hospital experience of 4,756 IAB patients from 1968 to 1995. In their series the use of IAB intraoperatively or postoperatively was associated with 35.7% and 35.9% mortality respectively, along with a trend towards increased preoperative use. Ghali et al, (193) examined the use of IAB in 12 Massachusetts hospitals. There was a 13.4% use in CABG cases. Many reports show an increase in IAB placement preoperatively in patients with decreased LV function (194, 195). This does not include failed PTCA/stenting, post-infarction refractory angina, or cardiogenic shock patients undergoing urgent or emergency placement. The Alabama group, (196) did not show a survival advantage with preoperative IAB but did show improved convalescence and decreased hospital LOS. The overall use of IAB has been reviewed by the Benchmark Counterpulsation Outcomes Registry (197). Between June 1996 and August 2000, 203 hospitals worldwide (90% USA) examined 16,909 patient case records. The indications for IAB use included: support during or after cardiac catheterization (20.6%), cardiogenic shock (18.8%), weaning from CPB (16.1%), preoperative placement in high risk cardiac surgery (13.0%), and refractory unstable angina (12.3%). When the traditional common femoral artery percutaneous or open approach is not possible, or the ABI is <0.9 aortic arch placement of the IAB is considered. This requires reoperation for removal and is associated with a higher incidence of postoperative neurological events (198). Complications related to femoral IAB placement is in the 8 – 25% range (197)(199) Aortic perforation, aortoilial dissection, retroperitoneal hematoma, limb ischemia, local nerve root compression, AV fistulas, pseudoanerysms, and wound hematomas have all been reported (199). Females, older patients, and peripheral vascular disease (PVD) are independent risk factors for morbidity (197).

Mechanical Assist

The goal of mechanical circulatory support is to allow the failing or stunned myocardium time to recover by providing multisystem support. As many as 3-6% of open-heart operations may require some type of circulatory support, including IAB, but this type of mechanical assistance is not used in all centers that perform cardiac surgery. A variety of mechanical devices are available to support the failing heart and circulation. The intra-aortic balloon pump (IAB) is the first in the armamentarium, with the recent generation of the artificial heart as the ultimate line of defense. Whether used as a temporary measure or a bridge to transplantation in a selected group, implementation of these devices requires judgment experience and technical expertise. Mechanical devices can provide LV support (LVAD), RV support (RVAD) or both (BVAD). The IAB may or may not be used in combination with this mechanical support. McGovern’s group, and others (200, 201) pioneered the use of the centrifugal pump for ventricular assist. Noon et al, (202) reviewed a series of 129 patients who received Bio-Medicus centrifugal pump support. Weaning was achieved in 56.3%; and 21.0% were discharged from the hospital. The need for post cardiotomy mechanical support ranges from <1% to 3-6% if an IAB is already in place. The ultimate goal is to provide a period of time for the injured or stunned myocardium to recover. The etiology of myocardial dysfunction is sometimes difficult to ascertain. The usual causes include pre-operative myocardial dysfunction, myocardial ischmia 2o to technical problems, or inadequate myocardial protection. The recent 5th International Conference on circulatory support devices for severe cardiac failure summarizes nicely the recent advances in mechanical support (203). They divide the symposium into acute heart failure; bridging to transplant and alternatives to transplant; implantable non-pulsatile devices; and implantable pulsatile devices.

Vasodilatation with Normal/High Cardiac Output

This phenomenon has been seen increasingly in recent years. As the patient warms, prior to emerging from anesthesia, the cardiac output rises with hyperthermia, decreased SVR, decreased filling pressures, and systemic hypotension. This usually resolves with volume, reducing body temperature, and disappearance of anesthetic agents with subsequent recovery of normal patient reflexes. This has been termed the "low systemic vascular resistance syndrome" or "vasodilatory shock". The Columbia group (204) noted an association of lower EF (<35%) and the use of angiotensin – converting enzyme (ACE) inhibitors as predisposing variables. Intravenous heparin and vancomycin have also been implicated (205, 206). Short-term arginine vasopressin, a potent vasoconstrictor has been used with initially gratifying results (207).

Arrhythmias

The most common arrhythmias and conduction disturbances following cardiac surgery are atrial fibrillation; atrial flutter; sinus tachycardia; sinus bradycardia; ventricular arrhythmias (ectopy; ventricular tachycardia; ventricular fibrillation); and heart block (junctional (nodal) rhythm; 1st, 2nd, 3rd degree block).

Many centers employ routine temporary atrial and/or ventricular epicardial pacing wire electrodes. Transesophageal pacing, surface electrode transthoracic pacing, and endocardial pacing wires and Swan-Ganz pacing catheters are also available. Recent success has also been found with temporary atrial patch electrodes that allow low-energy defibrillation of atrial fibrillation (208). This require placement of wires on both atria, as opposed to the usual 2-wire placement on the right atrium. The presence of atrial wires provides a means of atrial or AV sequential pacing as well as an atrial ECG tracing to help differentiate supraventricular and ventricular arrhythmias. The complication rate of temporary epicardial pacing is < 0.5%. Complications include failure of ventricular sensing with resultant VT/VF; failure to capture; bleeding from wire sites; RV lacerations; injury to vein grafts; and injury to the superior epigastric artery (209). Capture and threshold are usually determined in the operating room prior to closure. Most surgeons remove the wires on the 3rd or 4th postoperative day. Occasionally wires are cut below the skin line if they are difficult to remove, or in the presence of high INR values.

Atrial Fibrillation

Atrial fibrillation (AF) is the most common post-operative arrhythmia with an incidence ranging from 5% to 40% in CABG patients and up to 50% in valve operations (210, 211). The prevention remains elusive and the incidence rises with the age of the patient. It is the single most common variable for prolonging hospital stay (2-4 days), increasing hospital cost and increasing the readmission rate following open-heart surgery. It usually occurs on the 2nd to 4th postoperative day. The stroke rate rises from 1.4 to 3.3% in the presence of AF. There is no standardized treatment and no prophylactic regimen to date has proven totally efficacious. Direct cardioversion is warranted in the presence of hemodynamic instability. The primary goals of pharmacotherapy are to control heart rate and restore normal sinus rhythm (NSR). If NSR is not restored between 24-48o anti-coagulation is usually advised. Unfortunately, the true pathogenesis remains unknown. Several therapeutic strategies have evolved.

Two meta-analysis studies by Andrews (212) and Kowry (213) have shown a reduction in the incidence of atrial tachy arrhythmias with prophylactic beta blockade. Other membrane active agents have not been proven efficacious in prevention (214). Gomes et al (215) reported that oral d, l sotalol reduced postoperative AF 38% to 12.5%. The authors suggested avoiding this drug in patients with heart failure or LV dysfunction. Haan and Geraci (216) summarized nicely 7 recent amiodarone trials (Figure 14). The use of magnesium sulfate has also been advocated (224). Yet Solomon et al (225), in a randomized study of 167 CABG patients showed no difference in propanolol versus propanolol-magnesium treated groups (19.5% versus 22.4%). Two recent reviews offer a practical overview of incidence and treatment strategies, with both prophylactic and perioperative algorithms (226, 227). The ACC/AHR consensus recommendations are summarized in (Figure 15) (228).

Ventricular Arrhythmias

Ventricular arrhythmias are very worrisome following cardiac surgery. Unifocal and multifocal PVC’s, ventricular tachycardia, and ventricular fibrillation are the common arrhythmias. Myocardial ischemia, hypoxia, electrolytes imbalance, (particularly hypokalemia and hypomagnesimia), decreased LV function, ventricular scar, and occasional irritability from pulmonary catheters are the frequent causes. Interventional Electrophysiology (EPS) has assumed an increasing role in the evaluation and treatment of disturbing or recalcitrant perioperative ventricular arrhythmias. Myocardial revascularization reduces the risk of ventricular arrhythmias but the results are unpredictable. Pre-operative VT/VF and ¯ LV function (EF<30%) remain incremental risk factors for perioperative VT/VF (229). The approach to postoperative ventricular irritability involves assessment and treatment of hypoxia, hypovolemia, electrolyte imbalance, and myocardial ischemia. Frequent PVC’s, multifocal PVC’s, PVC’s occurring on the T-wave, bigemeny, trigeminy, and runs of VT warrant aggressive treatment (230). Lidocaine remains the first line drug, but prophylactic lidocaine is not useful for prophylaxis of ventricular ectopy in postoperative cardiac surgical patients (231). Beta blockade is useful for controlling heart rate and decreasing ectopic foci. The aggressive approach to recalcitrant life-threatening ventricular arrhythmias includes earlier use of intravenous amiodarone and EPS testing to assess the inducibility and suppression of malignant ventricular rhythms, especially in patients with recent infarction, and LV dysfunction (232,233).

 

Heart Block

In the presence of sinus bradycardia, nodal rhythms, and varying degrees of heart block, atrial or AV sequential pacing has been shown to increase heart rate and recruit atrial contraction to augment cardiac output (234). Heart block is usually transient in most coronary revascularization procedures. The need for permanent cardiac pacemaker implantation is 0.4 to 1.1% for CABG and rises to 3.0-6.0% for valvular procedures, especially following aortic valve replacement (AVR) for calcific aortic stenosis (235).

Bleeding/Cardiac Tamponade

Some degree of pericardial effusion occurs in most patients following cardiac surgery. Progressive effusions can occur dramatically or insidiously. Extrinsic compression of the heart, particularly the right atrium and anterior right ventricle can dramatically or progressively decrease venous return and subsequent pump function. Following cardiac surgery the pericardium is left open in the majority of cases. There are advocates for routine pericardial closure to decrease re-entry problems in subsequent open-heart surgery (236). Blood can fill the open anterior mediastinal space. If the left pleural space has been opened, usually for IMA harvest, blood may initially fill the left chest space. Progressive or sudden bleeding into the pericardium with subsequent tamponade is a fatal complication unless recognized and treated aggressively, with reoperation and drainage. The etiology is surgical bleeding and/or diffuse coagulopathy. The major advance beyond clinical and hemodynamic parameters in the recognition of tamponade has been transthoracic (TTE) or transesophageal (TEE) 2D echocardiography. TTE or TEE is helpful to assess RV diastolic collapse in the setting of a large pericardial effusion and particularly in the situation of unexplained hemodynamic stability (237). Subtle localized left-sided or lateral effusions may impair LV function in the absence of RV diastolic collapse. The usual methods of monitoring the clinical course, equalization of diastolic pressures, chest tube drainage, serial widening of chest x-ray with increasing left sided effusion, and decreasing hemoglobin levels still remain important. The accepted approaches include redo sternotomy, subxyphoid drainage, and radiological percutaneous catheter drainage. This last approach usually applies to delayed tamponade or chronic effusions. Delayed or late tamponade occurred in 43 of 9,612 patients over a seven-year period following cardiac surgery at Massachusetts General Hospital (238). The presentation occurred at an average of 18 days after operation with successful pericardiocentesis and catheter placement in 97% of the patients.

Perioperative Myocardial Ischemia/Infarction

The incidence and criteria of new perioperative myocardial damage has been difficult to document. The STS database reports an incidence of <2% following CABG operations (http://www.ctsnet.org/doc/2988), but this incidence is unreliable because of differences in reporting between participating centers and because of lack of standard definitions for the diagnosis of perioperative MI. The short and long term effects of a perioperative infarction are inconclusive. The major causes of perioperative infarction include preoperative evolving myocardial ischemia or infarction, technical problems, myocardial protection, and perioperative spasm. The consequences of a perioperative infarction range from clinically insignificant, to hemodynamic compromise, requiring temporary support and even re-operation to correct revascularization sites and possibly identify other coronary targets. The diagnosis of perioperative myocardial infarction includes interpretation of ECG changes, biochemical markers, echocardiography, and nuclear scans. Some degree of transient myocardial ischemia occurs in over 40% of patients undergoing CABG. This is usually seen in the first 4-6 hours following CPB. The incidence of perioperative myocardial infarction ranges from 7%-15% (239). The Brigham and Women’s experience of 499 consecutive patients revealed an incidence of 5% definite MI and probable MI in 2%. Definite MI criteria were total peak creatinine phospho-kinase (CK) > 7000 u/L, creatine kinase MB (CK-MB) > 30 ng/ml, and new Q waves on ECG. Probable MI included CK>700 u/L, CK-MB> 30 ng/ml, and a new wall motion abnormality on 2D ECHO or LV angiogram (240). Recently, Troponin I (CTNI) and T have been used as markers for myocardial injury following cardiac surgery (241- 244). Early graft failure or suspicion of failure warrants an aggressive approach. Angiographic evaluation better assesses the need for surgical reintervention (245, 246). The Guardian trial, (247) found that high-risk CABG patients with CK-MB ratio elevation are at higher risk for six-month mortality and highlights the potential harmful effects of perioperative myocardial damage.

Systemic Hypertension

Transient periods of systemic hypertension following cardiac surgery are common (30 – 50% in CABG patients) (248). In the presence of adequate LV function and absence of underlying primary idiopathic hypertension or secondary hypertension (e.g. renal artery stenosis), the usual cause is increased systemic vascular resistance (>1200 dynes/sec/cm-5) secondary to hypothermia and increased circulating levels of catecholomines, renin, and angiotensin II. The goal of treatment is to maintain the mean arterial pressure in the 70-90 mmHg range. Systemic re-warming, relief of pain, sedation, avoidance of shivering, and maintaining of adequate urine output is important. Treatment should be individualized to varying circumstances (e.g. a higher mean pressure for known hypertensives, and a lower mean arterial pressure control for tenuous aortic suture lines.) A variety of agents are currently available (Figure 16). Intravenous nitroglycerin is widely used as a primary venodilator and to increase intercoronary collateral blood flow (249). Sodium nitroprusside though used by many, may cause a coronary steal phenomenon.

Pulmonary Hypertension/RV Failure

Pulmonary hypertension or increased pulmonary vascular resistance (PVR) is difficult to treat. The usual clinical problem in cardiac surgery is pulmonary hypertension secondary to left sided cardiac disease and subsequent RV dysfunction. Primary drugs to reduce PVR include nitroprusside, nitroglycerin, tolazoline (PGI2), hydralazine, and milrinone (250). A more contemporary approach includes nitroglycerin, prostacyclin, adenosine, and inhaled nitric oxide. Prostaglandin E1 (PEG1) is a vasodilator that may be of value in the setting of pulmonary hypertension usually following transplantation, severe mitral valve disease, or isolated RV failure (251, 252). Adenosine, a nucleoside, activates membrane receptors on the pulmonary vascular smooth muscle cells. Fullerton et al (253), utilized adenosine in ten cardiac patients with pulmonary hypertension and found a significant reduction in PAP (36 to 28 mm Hq) and PVR (560 to 260 dynes.s.cm-5). In another group of 15 valve patients and 25 CABG patients they used inhaled nitric oxide (NO) (254). Results showed a 24% decrease in PAP and PVR with CABG patients but no response with the valve group. Another rare problem complicating RV failure is intra cardiac right to left shunt at the atrial level through a patent foramen ovale, causing refractory hypoxemia (255).

Cardiac Resuscitation/Chest Re-Opening

Closed cardiac resuscitation for cardiac arrest in the post-operative cardiac surgery patient is a rare event. The standard ACLS protocol is utilized (256, 257), but open resuscitation necessitating re-sternotomy should be considered at an earlier time period during full resuscitation. Reopening of the sternal incision early after operation occurred 0.6% of the time in the Toronto series (258). The most common indications for chest reopening is tamponade secondary to post-operative bleeding. Mackey et al (259) did a prospective audit over a six-year period of open resuscitation of post-operative cardiac surgery patients. The overall survival till discharge was 25% (20/79). Favorable factors included arrest in the ICU, arrest within 24 hours of surgery, and reopening within 10 minutes of the arrest. Survival was better in surgical problems (bleeding, tamponade, graft problems) than poor cardiac function.

References

  1. Shumaker, HB. The Evolution of Cardiac Surgery.
    Indiana University Press, Bloomington, 1992 Ch 2 p. 11-17

  2. Harken DE. The emergence of cardiac surgery I. Personal Recollections of the 1940s and 1950s. J Thorac Cardiovasc Surg 1989; 98:805-813

  3. Bigelow WG, Callaghan JC, Hopps JA. General hypothermia for experimental intracardiac surgery. Ann Surg 1950; 32:531-539

  4. Lillehei CW, Varco RL, Cohen M, Warden HE, Patton C, Moller JH. The first open-heart repairs of Ventricular Septal defect, and Atrioventricular Communis, and Tetralogy of Fallot using Extracobporeal circulation by cross-circulation: A 30 year follow up. Ann Thorac Surg 1986; 41:4-21

  5. Popovic JR, Hall MJ. 1999 National Hospital Discharge Survey, Advance Data number 319, Center for Disease Control and prevention April 24, 2001 p. 1-20

  6. http://www.sts.org/database/dataananlysis/2000

  7. Cheng DC, David TE. Perioperative care in cardiac anesthesia  and surgery. Landes Bioscience Georgetown, TX, 1999, p2

  8. Lahey SJ, et al., Preoperative risk factors that predict hospital length of stay in coronary artery bypass patients > 60 years old. Circulation, 1992; 8: II1 81-85

  9. (9) Ferraris VA, Ferraris SP. Risk factors for postoperative morbidity. Journal of Thoracic and Cardiovascular Surgery, 1996; 11: 731-38; discussion 738-741

  10. Hammermeister KE., et al. Identification of patients at greatest risk for developing major complications at cardiac surgery. Circulation, 1990; 82: IV380-389
  11. Tu JV, Jaglal SB, Naylor CD. Multicenter validation of a risk index for mortality, intensive care unit stay, and overall hospital length of stay after cardiac surgery. Steering Committee of the Provincial Adult Cardiac Care Network of Ontario. Circulation, 1995; 91: 677-684
  12. Morris DC, St. Claire D. Management of Patients after Cardiac Surgery. Curr. Probl Cardiology April 1999 p. 172-173
  13. Bojar RM. Manual of Perioperative Care in Cardiac Surgery.
    Third Edition Malden MA, Blackwell Science, 1999; 4:79-92
  14. Grunkemeier GL, Zerr KJ, Jin R. cardiac surgery report cards: making the grade. Ann Thorac Surg, 2001; 72:1845-1848
  15. Hannan EL., et al., Improving the outcomes of coronary artery bypass surgery in New York State. JAMA, 1994; 271: 761-766
  16. Ghali WA, Quan H, Brant R. Coronary artery bypass grafting in Canada: national and provincial mortality trends, 1992-1995. Cmaj, 1998; 159: 25-31
  17. Ghali WA, et al. Statewide quality improvement initiatives and mortality after cardiac surgery. Jama, 1997; 277: 379-382
  18. Weintrub WS, et al., Changing clinical characteristics of coronary surgery patients. Differences between men and women. Circulation, 1993; 88: II79-86
  19. Grover FL., et al., Factors predictive of operative mortality among coronary artery bypass subsets. Annals of Thoracic Surgery, 1993; 56: 1296-1306; discussion 1306-7
  20. Iyer VS, et al., Mortality and myocardial infarction after coronary artery surgery. A review of 12,003 patients. Medical Journal of Australia, 1993; 159: 166-170
  21. Ivanov J, Tu JV, Naylor CD. Ready-made, recalibrated, or Remodeled? Issues in the use of risk indexes for assessing mortality after coronary artery bypass graft surgery. Circulation, 1999; 99: 2098-2104
  22. Higgins TL, et al. ICU admission score for predicting morbidity and mortality risk after coronary artery bypass grafting. Annals of Thoracic Surgery, 1997; 64: 1050-1058
  23. Mozes B., et al. A national study of postoperative mortality associated with coronary artery bypass grafting in Israel. ISCAB Consortium. Israel Coronary Artery Bypass Study. Annals of Thoracic Surgery, 1998; 66: 1254-1262; discussion 1263
  24. DeLong ER, et al. Comparing risk-adjustment methods for provider profiling. Statistics in Medicine, 1997; 16: 2645-2664
  25. O Connor GT, et al. Multivariate prediction of in-hospital mortality associated with coronary artery bypass graft surgery. Northern New England Cardiovascular Disease Study Group. Circulation, 1992; 85: 2110-2118
  26. Reich DL, et al. Intraoperative hemodynamics predictors of mortality, stroke, and myocardial infarction after coronary artery bypass surgery. Anesthesia and Analgesia, 1999; 89: 814-822
  27. Bernstein AD. And Parsonnet V. Beside estimation of risk as an aid for decision-making in cardiac surgery. Annals of Thoracic Surgery 2000; 69: 823-828
  28. Pifarre R. Open Heart Operations in the Elderly: Changing Risk Parameters. Ann Thorac Surg 1993; 56:S71-73
  29. Craver JM, Puskas JD, Weintraub WW, et al. 601 Octogenarians Undergoing Cardiac Surgery: Outcome and Comparison With Younger Age Groups. Ann Thorac Surg 1999; 67:1104-1110
  30. Fruitman DS, MacDougall CE, Ross DB. Cardiac Surgery in Octogenarians: Can Elderly Patients Benefit? Quality of Life After Cardiac Surgery. Ann Thorac Surg 1999; 68:2129-2135
  31. Abramov D, Tamariz MG, Sever JY, Christakis GT, et al. The Influence of Gender on the Outcome of Coronary Artery Bypass Surgery. Ann Thorac Surg 2000; 70:800-806
  32. O’Rourke DJ, Malenka DJ, Olmstead EM, et al. Improved In-Hospital Mortality in Women Undergoing Coronary Artery Bypass Grafting. Ann Thorac Surg 2001; 71:507-511
  33. Riley G, Lubitz J. Outcomes of surgery among the Medicare aged: surgical volume and mortality. Health Care Financing Review. 1985:71: 37-47
  34. Showstack JA., et al. Association of volume with outcome of coronary artery bypass graft surgery. Scheduled vs nonscheduled operations. JAMA, 1987; 257: 785-789
  35. Hannan EL., et al. Investigation of the relationship between volume and mortality for surgical procedures performed in New York State hospitals. JAMA 1989; 262: 503-510
  36. Hannan EL., et al. Coronary-Artery Bypass-Surgery- the Relationship between In-hospital Mortality-Rate and Surgical Volume after Controlling for Clinical risk factors. Medical Care, 1991; 29: 1094-1107
  37. Farley DE, Ozminkowski RJ. Volume-outcome relationships and in-hospital mortality: the effect of changes in volume over time. Medical care 1992; 30: 77-9
  38. Grumbach K, et al. Regionalization of Cardiac-Surgery in the United-states and Canada – Geographic Access, choice, and Outcomes. Jama-journal of the American Medical Association, 1995; 274: 1282-1288
  39. Hannan EL, et al. The decline in coronary artery bypass graft surgery mortality in New York State. The role of surgeon volume. Jama 1995; 273: 209-213
  40. Shroyer ALW, et al. No continuous relationship between Veterans Affairs hospital coronary artery bypass grafting surgical volume and operative mortality. Annals of Thoracic Surgery, 1996; 61: 17-20
  41. Sollano JA, et al. Volume-outcome relationships in cardiovascular operations: New York State, 1990-1995. Journal of Thoracic and cardiovascular Surgery 1999; 117: 419-430
  42. Nallamothu BK, et al. The role of hospital volume in coronary artery bypass grafting: Is more always better? Journal of the American College of Cardiology, 2001; 38: 1923-1930
  43. Hewitt M, and f.t.C.o.Q.o.o.H.C.I.A.a.t.N.C.P. Board, Interpreting the Volume-Outcome Relationship in the Context of Health Care Quality: workshop Summary. 2000, Washington, D.C.: Institute of Medicine. I-viii, 1-128
  44. Luft HS, Bunker JP, Enthoven AC. Should operations be regionalized? The empirical relation between surgical volume and mortality. New England Journal of Medicine 1979; 301: 1364-1369
  45. Tu JV, Naylor CD. Coronary artery bypass mortality rates in Ontario. A Canadian approach to quality assurance in cardiac surgery. Steering Committee of the Provincial Adult Cardiac Care Network of Ontario. Circulation, 1996; 94: 2429-2433
  46. Crawford FA, et al. Volume requirements for cardiac surgery credentialing: a critical examination. The Ad Hoc Committee on Cardiac Surgery Credentialing of the Society of Thoracic Surgeons. Annals of Thoracic Surgery. 1996; 61: 12-16
  47. Higgins TL. Quantifying Risk and assessing outcome in Cardiac Surgery. J Cardiothorac Vasc Anes 1998; 12:330-340
  48. Higgins TL, Estatanous FG, Loop FD, et al. ICU admission score for predicting morbidity and mortality risk after coronary artery bypass grafting. Ann Thorac Surg 1997; 64:1050-1058
  49. Jenkinson C, Coulter A, Wright L. Short form 36 (SF 36) health survey questionnaire: normative data for adults of working age. British Med J 1993; 306:1437-1440
  50. Lindsay GM, Harlon P, Smith LN, Wheatley DJ. Assessment of changes in general health status using the short-term 36 questionnaire 1 year following coronary artery bypass grafting. European J Cardio-thorac Surg 2000; 18:557-564
  51. Simchen E, Galai N, Braun O, Zitser-Gurevich Y, Shabtai E, Naveh I. Sociodemographic and clinical factors associated with low quality of life one year after coronary bypass operations: The Israeli Coronary Artery Bypass Study (ISCAB). J Thorac Cardiovasc Surg 2001; 121:909-919
  52. Iglehart JK. The American Health Care System. Medicare. NEJM 1999; 340:327-332
  53. Harlan BJ. Statewide Reporting of Coronary artery surgery results: A view from California. J Thorac Cardiovasc Surg 2001; 121:409-417
  54. Taylor GJ, Mikell FL, Moses HW, et al. Determinant of Hospital Charges for Coronary Artery Bypass Surgery: The Economic Consequences of Postoperative Complications. Am J Cardiol 1990; 65:309-313
  55. Ferraris VA, Ferraris SP, Singh A. Operative outcome and hospital cost. Journal of Thoracic and Cardiovascular Surgery 1998; 115: 593-602; discussion 602-603
  56. Cohen, DJ, Breall JA, Ho KKL, et al. Economics of Elective Coronary Revascularization. Comparison of Costs and Charges for Conventional Angioplasty, Directional Atherectomy, Stenting and Bypass surgery. J Am Coll Cardiol 1993; 22:1052-1059
  57. Williams Jr TE, Fanning WJ, Benton WC, et al. What Is the Marginal Cost for Marginal Risk Cardiac Surgery? Ann Thorac Surg 1998; 66:1969-1971
  58. Shahian DM, Heatley GJ, Westcott GA. Relationship of hospital size, case volume, and cost for coronary artery bypass surgery: Analysis of 12,774 patients operated on in Massachusetts during fiscal years 1995 and 1996. J Thorac Cardiovasc Surg 2001; 122:53-64
  59. Lazar HL, Fitzgerald CA. Ahmad T, et al. Early discharge after coronary artery bypass graft surgery: Are patients really going home earlier? J Thorac Cardiovasc Surg 2001; 121:943-950
  60. Lahey SJ, Campos CT, Jennings B, Pawlow P, Stokes T, Levitsky S. Hospital Readmission After Cardiac Surgery. Does "Fast Track" Cardiac Surgery Result in Cost Saving or Cost Shifting? Circulation. 1998;98:II -35-II-40.
  61. D’Agostino RS, Jacobson J, Clarkson M, Svensson LG, Williamson C, Shahian DM. Readmission After Cardiac Operations: Prevalence, Patterns, And Predisposing Factors. J Thorac Cardiovasc Surg 1999; 118:823-832
  62. Stewart RD, Campos CT, Jennings B, Lollis SS, Levitsky S, Lahey SJ. Predictors of 30-Day Hospital Readmission After Coronary Artery Bypass. Ann Thorac Surg 2000; 70:169-174
  63. Ferraris VA, Ferraris SP, Harmon RC, Evans BD. Risk factors for early hospital readmission after cardiac operations. J Thorac Cardiovasc Surg 2001; 122:278-286
  64. Gatsonis CA., et al. Variations in the utilization of coronary angiography for elderly patients with an acute myocardial infarction. An analysis using hierarchical logistic regression. Medical Care, 1995; 33: 625-642
  65. Guadagnoli E., et al. Variation in the use of cardiac procedures after acute myocardial infarction. New England Journal of Medicine 1995; 333: 573-578
  66. Mark DB., et al. Use of medical resources and quality of life after acute myocardial infarction in Canada and the United States. New England Journal of Medicine 1994; 331: 1130-1135
  67. Anderson GM., et al. Use of coronary artery bypass surgery in the United States and Canada. Influence of age and income. Jama 1993; 269: 1661-1666
  68. Yusuf S, Cairns JA, Camm AJ, Fallen EL, Gersh BJ. Evidence based Cardiology. 1998 BMJ Books, London p. 3-23
  69. Eagle KA, et al. ACC/AHA Guidelines for coronary Artery Bypass graft Surgery: A report of the American College of cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1991 Guidelines for Coronary Artery Bypass Graft Surgery). American College of Cardiology/American Heart Association. Journal of the American College of Cardiology 1999; 34: 1262-1347
  70. Shaneyfelt TM, Mayo-Smith MF, Rothwangl J. Are guidelines following guidelines? The methodological quality of clinical practice guidelines in the peer-reviewed medical literature. Jama 1999; 281: 1900-1905
  71. Rees K., et al. Hypothermia to reduce neurological damage following coronary artery bypass surgery (Cochrane Review). 2001; CD002138
  72. Bartels C, Gerdes A, Babin-Ebell J, et al. Cardiopulmonary bypass – ‘evidence- or experienced-based’. Journal of Thoracic and Cardiovascular Surgery 2002; 124: 20-27
  73. Scheinkestel CD, Davies AR, Bristow PJ. Evidence-based medicine in intensive care. Med J Aust 2001 May 21; 174(10): 526-527
  74. Eagle KA, Brundage BH, Chaitman BR, et al. ACC/AHA Guidelines for Perioperative Cardiovascular Evaluation Guidelines. Circulation 1996; 93: 1280- 1317/Guideline Update Circulation 2002; 105: 1257-1267
  75. Dripps RD, Lamon A, Eckenhoff JE. The role of anesthesia in surgical mortality.
    JAMA 1961; 178:261
  76. Wiklund RA, Rosenbaum SH. Medical Progress: Anesthesiology, First of Two Parts. NEJM 1997; 337: 1132-1141
  77. Tuman KJ, McCarthy RJ, Spiess BD, Da Valle M, Dabir R, Ivankovich AD. Does choice anesthetic agent significantly affect outcome after coronary artery surgery? Anesthesiology 1989; 70: 189-198
  78. Kaur S. Anesthetic Considerations in Minimally Invasive Cardiac Surgery. Progress in Anesthesiology. 1998; 12:431-441
  79. Liem TH, Williams JP, Hensens AG, Singh SK. Minimally Invasive Direct Coronary Artery Bypass Procedure Using a High Thoracic Epidural Plus General Anesthetic Technique. J Cardiothoracic Vasc Anes 1998; 12: 668-672
  80. Sanchez R, Nygard E. Epidural Anesthesia in Cardiac Surgery: Is There an Increased Risk? Journal of Cardiothoracic and Vascular Anesthesia 1998; 12: 170 –173
  81. Engelman RM, Rousou JA, Flack III JE, et al. Fast-track Recovery of the Coronary Bypass Patient. Ann Thorac Surg 1994; 58: 1742-1746
  82. Klineberg PL, Greer RT, Hirsh RA, Aukburg SJ. Early extubation after coronary artery bypass graft surgery. Crit Care Med 1977; 5: 272-274
  83. Gall SA, Olsen CO, Reves JG, et al. Beneficial effects of endotracheal extubation on ventricular performance. J Thorac Cardiovasc Surg 1988; 95: 819-827
  84. Krohn BG, Kay JH, Mendes MA, Zubiate P, Kay GL. Rapid sustained recovery after cardiac operations. J Thorac Cardiovasc Surg 1990; 100: 194-197
  85. Cheng DCH, Karski J, Peniston C, et al. Morbidity Outcome In Early Versus Conventional Tracheal Extubation After Coronary Artery Bypass Grafting: A Prospective Randomized Controlled Trial. J Thorac Cardiovasc Surg 1996; 112: 755-764
  86. Hessel II EA. What’s new in monitoring the coronary surgery patient? Perfusion 192; 7: 161-194
  87. Varon AJ, Civetta JM. Physiologic Monitoring of the Surgical Patient. In: Principles of Surgery. Sixth Edition. New York: McGraw-Hill, Inc. 1994; 489-512
  88. Barie PS. Advances in Critical Care Monitoring. Arch Surg. 1997; 132: 734-739
  89. Erickson RS, Kirklin SK. Comparison of ear-based, bladder, oral, and axillary methods for core temperature measurement. Critical Care Medicine 1993; 21: 1528-1534
  90. Augoustides, Weiss SJ, Pochettino A. Hemodynamic Monitoring of the Postoperative Adult Cardiac Surgical Patient. Seminars in Thorac Cardiovasc Surg 2000; 12: 309-315
  91. Stewart RD, Psyhojos T, Lahey SJ, Levitsky S, Campos CT. Central Venous Catheter Use in Low-Risk Coronary Artery Bypass Grafting. Ann Thorac Surg 1998; 66: 1306-1311
  92. Edwards JD. Continuous thermodilution cardiac output: A significant step forward in hemodynamic monitoring. Crit Care Med 1997; 25: 381-382
  93. Zollner C, Polasek J, Kilger E. et al. Evaluation of a new continuous thermodilution cardiac output monitor in cardiac surgical patients: A prospective criterion standard study. Crit Care Med 1999; 27: 293- 298
  94. Madan AK, UyBarreta VV, Aliabadi-Wahle S, Jesperson R, Hartz RS, Flint LM, Steinberg SM. Esophageal Doppler Ultrasound Monitor versus Pulmonary Artery Catheter in the Hemodynamic Management of Critically Ill Surgical Patients. The Journal of Trauma: 1999; 46: 607-612
  95. DiCorte CJ, Latham P, Greilich PE, Cooley MV, Grayburn PA, Jessen ME. Esophageal Doppler Monitor Determinations of Cardiac Output and Preload During Cardiac Operations. Ann Thorac Surg 2000; 69: 1782-1786
  96. Guzzi L, Jaffe MB, Orr JA. Clinical Evaluation of a New Non-Invasive Method of Cardiac Output Measurement: Preliminary Results in CABG Patients. Anesthesiology 1998; 89: A543
  97. Shoemaker WC, Wo CCJ, Bishop MH, et al. Noninvasive Physiologic Monitoring of High-Risk Surgical Patients. Arch Surg 1996; 131: 732-737
  98. Rafferty T, Durkin M, Hines R, Elefteriades J, Harris SN, O’Connor TZ. Thermodilution right ventricular ejection fraction measurement reproducibility- A study in patients undergoing coronary artery bypass graft surgery. Crit Care Med 1992; 20: 1524-1528
  99. Dorman BH, Spinale FG, Kratz JM, Alpert CC, Ford M. Use of a combined right ventricular ejection fraction oximetry catheter system for coronary bypass surgery. Crit Care Med 1992; 20: 1650-1656
  100. Dalen JE, Bone RC. Is It Time to Pull the Pulmonary Artery Catheter? JAMA 1996; 276: 916-918
  101. Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D. Catheterization of the Heart in Man with use of a flow-directed balloon-tipped catheter. N Eng J Med 1970; 283: 447-451
  102. Gore JM, Goldberg RJ, Spodick DH, Alpert JS, Dalen JE. A community-widespread assessment of the use pulmonary artery catheters in patients with acute myocardial infarction. Chest 1987; 92: 721-727
  103. Vender JS. Resolved: A pulmonary Artery Catheter Should Be Used in the Management of the Critically Ill Patient. Pro. J Cardiothorac Vasc Anes 1998; 12: 9-12
  104. Becker Jr K. Resolved: A Pulmonary Artery Catheter Should Be Used in the Management of the Critically Ill Patient. Con. J Cardiothorac Vasc Anes 1998; 12: 13-16
  105. Shah KB, Raw TLK, Laughlin S, El-Etr AA. A Review of Pulmonary Artery Catheterization in 6,245 Patients. Anes 1984; 61: 271-275
  106. Sirivella S, Gielchinsky I, Parsonnet V. Management of Catheter-Induced pulmonary artery perforation: A rare complication in cardiovascular operations. Ann Thorac Surg 2001; 72: 2056-2059
  107. Shanewise JS, Cheung AT, Aronson S, Stewart WJ, Weiss RL, Mark JB, et al. ASE/SCA Guidelines for Performing a Comprehensive Intraoperative Multiplane Transesophageal Echocardiography Examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. Anesth Analg. 1999; 89: 870-884
  108. Joffe II, Jacobs LE, Lampert C, Owen AA, Iola AW, Kotler MN. Role of echocardiography in perioperative management of patients undergoing open-heart surgery. Am Heart J 1996; 131: 162-176
  109. Izzat MB, Regragui IA, Wilde P, Angelini GD, Bryan AJ. Transesophageal Echocardiographic Measurements of Cardiac Output in Cardiac Surgical Patients. Ann Thorac Surg 1994; 58: 1486-1489
  110. Wareing TH, Davila-Roman VG, Barzilai B, Murphy SF, Kouchoukos NT. Management of the severely atherosclerotic ascending aorta during cardiac operations. J Thorac Cardiovasc Surg 1992; 103: 453-461
  111. Wilson MJ, Boyd SYN, Lisagor PG, Rubal BJ, Cohen DJ. Ascending Aortic Atheroma Assessed Intraoperatively by Epiaortic and Transesophageal Echocardiography. Ann Thorac Surg 2000; 70: 25-30
  112. Goodkin GM, Spevack DM, Tunick PA, Kronzon I. How Useful Is Hand-Carried Bedside Echocardiography in Critically Ill Patients? J Am Coll Cardiol 2001; 37; 2019-2022
  113. Aral A, Oguz M, Ozberrak H, et al. Hemodynamic Advantages of Left Atrial Epinephrine Administration in Open Heart Operations. Ann Thorac Surg 1997; 64:1046-9
  114. Santini F, Gatti G, Borghetti V, Oppido G, Mazzucco A. Routine left atrial catheterization for the post-operative management of cardiac surgical patients: is the risk justified? European Journal of Cardio-thoracic Surgery 1999; 16: 218-221
  115. Gutierrez G, Khan AU. Gastric tonometry monitoring. Current Opinion in Critical Care 1996; 2:193-198
  116. Hamilton MA, Mythen MG. Gastric tonometry: where do we stand? Curr Opin Crit Care 2001; 7: 122-127
  117. Pilbeam SP. Noninvasive Monitoring of Mechanically Ventilated Patients. In: Russell J, ed. Mechanical Ventilation-Physiological and Clinical Applications. St. Louis, MO: Mosby, 1998:94-115
  118. Nickerson BG, Sarkisian C, Tremper K. Bias and Precision of Pulse Oximeters and Arterial Oximeters. Chest 1988; 93: 515-517
  119. Bierman MI, Stein KL, Snyder JV. Pulse Oximetry in the Postoperative Care of Cardiac Surgical Patients. Chest 1992; 102:1367-1370
  120. Sebel PS. Central Nervous System Monitoring During Open Heart Surgery: An Update. Journal of Cardiothoracic and Vascular Anesthesia 1998; 12:3-8
  121. Sebel PS, Lang E, Rampil IJ, et al. A Multicenter Study of Bispectral Electroencephalogram Analysis for Monitoring Anesthetic Effect. Anesth Analg 1997; 84:891-899
  122. van der Linden J, Wesslen O, Ekroth D, Tyden H, von Ahn H. Transcranial Doppler-estimated versus thermodilution-estimated cerebral blood flow during cardiac operations. J Thorac Cardiovasc Surg 1991; 102: 95 - 102
  123. Kofidis T, Fischer S, Leyh , et al. Clinical relevance of intracranial high intensity transient signals in patients following prosthetic aortic valve replacement. European J. Cardiothorac Surg 2002; 21: 22-26
  124. Reents W, Muellges W, Franke D, Babin-Ebell J, Elert O. Cerebral oxygen saturation assessed by Near Infrared Spectroscopy during coronary artery bypass grafting and early postoperative cognitive function. Ann Thorac Surg 2002; 74: 109-114
  125. Anonymous, American College of Surgeons: Standard of efficiency for the first hospital survey by the College. Bulletin of the American College of Surgeons, 1918; 3: 1-4
  126. Weed LL. Medical records that guide and teach. New England Journal of Medicine, 1968; 278: 593-600
  127. Weed LL. Medical records that guide and teach. New England Journal of Medicine. 1968; 278: 652-657 conclusion
  128. Weed LL. What physicians worry about: how to organize care of multiple-problem patients. Modern Hospital, 1968; 110: 90-94
  129. Tierney WM. Improving clinical decisions and outcomes with information: a review. International Journal of Medical Informatics, 2001; 62: 1-9
  130. Tierney WM, et al. Physician inpatient order writing on microcomputer workstations. Effects on resource utilization. JAMA 1993; 269: 379-383
  131. Iezzoni L. Measuring the severity of illness and case mix, in Providing Quality Care: The Challenge to Clinicians, N.D. Goldfield N, Editor. 1989, American College of Physicians: Philadelphia. P 70-105
  132. Edmunds Jr LH, Stenach N. Blood-Surface Interface. In: Gravlee GP, Davis RF, Kurusz M, Utley JR. Cardiopulmonary Bypass. Principles and Practice. Philadelphia: Lippincott Williams & Wilkins, 2000:149-166
  133. Edmunds Jr LH. Inflammatory Response to Cardiopulmonary Bypass. Ann Thorac Surg 1998; 66:S12-S16
  134. Taylor KM. Honored Guest’s Address. A Practical Affair. J Thorac Cardiovasc Surg 1999; 118:394-403
  135. Hornick P, Taylor KM. Immune and Inflammatory Responses After Cardiopulmonary Bypass. In: Gravlee GP, Davis RF, Kurusz M, Utley JR. Cardiopulmonary Bypass. Principles and Practice. Philadelphia: Lippincott Williams & Wilkins, 2000:303-319
  136. Pearson DT. Gas Exchange: Bubble and Membrane Oxygenators. In: Loop FD, Taylor KM. Seminar In Thoracic and Cardiovascular Surgery, 1990; 2:313-319
  137. Stammers AH. Trends in Extracorporeal Circulation for the 1990s: Renewed Interest and Advancing Technologies. J Cardiothorac Vasc Anes 1992; 6:226-237
  138. Parolari A, Alamanni F, Naliato M, et al. Adult cardiac surgery outcomes: role of the pump type. European Journal of Cardio-thoracic Surgery 2000; 18:575-582
  139. Magilligan DJ. Indications for Ultrafiltration in the cardiac surgical patient. J Thorac Cardiovasc Surg 1985; 89:183-189
  140. Kiziltepe U, Uysalel A, Corapcioglu T, Dalva K, Akan H, Akalin H. Effects of Combined Conventional and Modified Ultrafiltration in Adult Patients. Ann Thorac Surg 2001; 71:684-693
  141. Lesserson-Shore L, Gravlee GP. Anticoagulation For Cardiopulmonary Bypass. In: Cardiopulmonary Bypass. Principles and Practice. Gravlee GP, Davis RF, Kurusz M, Utley JR. Philadelphia: Lippincott Williams & Wilkins, 2000:437-472
  142. Williams MR, D’Ambra AB, Beck JR, et al. A Randomized Trial of Antithrombin Concentrate for Treatment of Heparin Resistance. Ann Thorac Surg 2000; 70:873-877
  143. Patla V, Comunale ME, Lowenstein E. Heparin Neutralization. In: Cardiopulmonary Bypass. Philadelphia: Lippincott Williams & Wilkins, 2000:473-491
  144. Kimmel SE, Sekeres MA, Berlin JA, Ellison N, DiSesa VJ, Strom BL. Risk Factors for Clinically Important Adverse Events After Protamine Administration Following Cardiopulmonary Bypass. J Am Coll Cardiol 1998; 32:1916-1922
  145. Aldea GS, Lilly K, Gaudiani JM, et al. Heparin-bonded Circuits Improve Clinical Outcomes in Emergency Coronary Artery Bypass Grafting. J Card Surg 1997; 12:389-397
  146. Ranucci M, Mazzucco A, Pessotto R, et al. Heparin-Coated Circuits for High-Risk Patients: A Multicenter, Prospective, Randomized Trial. Ann Thorac Surg 1999; 67:994-1000
  147. Ovrum E, Tangen G, Oystese R, Ringdal MAL, Istad R. Comparison Of Two Heparin-Coated Extracorporeal Circuits With Reduced Systemic Anticoagulation In Routine Coronary Artery Bypass Operations. J Thorac Cardiovasc Surg 2001; 121:324-330
  148. Butler BD, Kurusz M. Embolic Events. In: Cardiopulmonary Bypass. Philadelphia: Lippincott Williams & Wilkins, 2000:320-341
  149. Defraigne JO, Pincemail J, Dekoster G, et al. SMA Circuits Reduce Platelet Consumption and Platelet Factor Release During Cardiac Surgery. Ann Thorac Surg 2000; 70: 2075-2081
  150. Gu YJ, Boonstra PW, Rijnsburger AA, Haan J, van Oeveren W. Cardiopulmonary Bypass Circuit Treated With Surface-Modifying Additives: A Clinical Evaluation of Blood compatibility. Ann Thorac Surg 1998; 65:1342-1347
  151. Shiroishi MS. Myocardial Protection. The Rebirth of Potassium-Based Cardioplegia. Tex Heart Inst J 1999; 26:71-86
  152. Gay WA, Ebert PA. Functional, metabolic, and morphologic effects of potassium-induced cardioplegia. Surgery 1973; 74: 284-290
  153. Johansen-Vinten J, Ronson RS, Thourani VH, Wechsler AS. Surgical Myocardial Protection. In: Gravlee GP, Davis RF, Kurusz M, Utley JR. Philadelphia: Lippincott Williams & Wilkins, 2000:215-264
  154. Caputo M, Ascione R, Angelini GD, Suleiman MS, Bryan AJ. The end of the cold era: from intermittent cold to intermittent warm blood cardioplegia. European Journal of Cardio-thoracic Surgery 1998; 14:467-475
  155. Ducko CT, Stephenson ER, Jayawant AM, Vigilance DW, Damiano RJ. Potassium Channel Openers: Are They Effective as Pretreatment of Additives to Cardioplegia? Ann Thorac Surg 2000; 69:1363-1368
  156. Belhomme D, Peynet J, Florens E, Tibourtine O, Kotakaze M, Menasche P. Is Adenosine Preconditioning Truly Cardioprotective in Coronary Artery Bypass Surgery? Ann Thorac Surg 2000; 70:590-594
  157. Calvin JE, Habet K, Parrillo JE. Critical Care In The United States. Who Are We and How Did We Get Here? Critical Care Clinics 1997; 13:363-376
  158. Haupt MT, Bekes CE, Bayly RW, et al. Critical care services and personnel: Recommendations based on a system of categorization into two levels of care. Crit Care Med 1999; 27:422-426
  159. Savino JS, Hanson III CW, Gardner TJ. Cardiothoracic Intensive Care: Operation and Administration. Seminars in Thoracic and Cardiovasc Surg 2000; 12:362-370
  160. Vegas A, Cheng DCH. Routine CVICU Care: Early Extubation to Discharge. In: Perioperative Care in Cardiac Anesthesia and Surgery. Texas: Landes Bioscience, 1999:176-183
  161. Craft RL. Trends in technology and the future intensive care unit. Crit Care Med 2001; 29: 151-158
  162. Statland BE, Brzys K. Evaluating STAT Testing Alternatives by Calculating Annual Laboratory Costs. Chest 1990; 97:198S-203S
  163. Salem M, Chernow B, Burke R, Stacey J, Slogoff M, Sood S. Bedside Diagnostic Blood Testing. Its Accuracy, Rapidity, and Utility in Blood Conservation. JAMA 1991; 266:382-389
  164. Kost GJ, Hague C. The Current and Future Status of Critical Care Testing and Patient Monitoring. Am J Clin Pathol 1995; 104(suppl I): S2-S17
  165. Harvey MA, Point-of-Care Laboratory Testing in Critical Care. Am J Crit Care 1999; 8: 72 - 83
  166. Woo J, Henry JB. The Advance Of Technology As A Prelude To The Laboratory Of The Twenty-First Century. Clinics In Laboratory Medicine 1994; 14:459-470
  167. Ehrmeyer SS, Laessig RH. Regulatory Requirements (CLIA ’88, JCAHO, CAP) for Decentralized Testing. Am J Clin Pathol 1995; 104(Suppl I): S40-S49
  168. Despotis GJ, Santoro SA, Spitnagel E, et al. Prospective evaluation and clinical utility of on-site monitoring of coagulation in patients undergoing cardiac operation. J Thorac Cardiovasc Surg 1994; 107:271-279
  169. Rozycki GS. Surgeon-Performed Ultrasound. Its Use in Clinical Practice. Annals Surgery 1998; 228:16-28
  170. Snow N, Bergin KT, Horringan TP. Thoracic CT Scanning in Critically Ill Patients. Information Obtained Frequently Alter Management. Chest 1990; 97:1467-1470
  171. Walser E, Savage C, Zwischenberger JB. Thoracic imaging in the ICU: Intervential Radiology. Chest Surg. Clin N. Am 2002; 12: 209-226
  172. O’Brien W, Karski JM, Cheng D, Carroll-Munro J, Peniston C, Sandler A.
  173. Routine Chest Roentgenography On Admission To Intensive Care Unit After Heart operations: Is it of any value. J. Thorac Cardiovasc Surg. 1997; 113: 130-133
  174. Katz NM, Ottinger LW. System-Structured Management of Acutely Ill surgical Patients. Arch Surg 1976; 111:239-242
  175. Kirklin JW, Archie JP. The Cardiovascular Subsystem In Surgical Patients. Surgery, Gynecology & Obstetrics 1974; 139:17-23
  176. Kirklin JK, Kirklin JW. Management of the Cardiovascular Subsystem after Cardiac Surgery. Ann Thorac Surg. 1981; 32:311-319
  177. Gattinoni L, Brazzi L, Pelosi P, et al. A Trial Of Goal-Oriented Hemodynamic Therapy in Critically Ill Patients. N Engl J Med 1995; 333:1025-1032
  178. Augoustides J, Weiss SJ, Pochettine A. Hemodynamic Monitoring of the Postoperative Adult Cardiac Surgical Patient. Seminars in Thoracic and Cardiovascular Surgery. 2000; 12:309-315
  179. Rao V, Ivanov J, Weisel RD, Ikonomidis JS, Christakis GT, David TE. Surgery For Acquired Heart Disease. Predictors Of Low Cardiac Output Syndrome After Coronary Artery Bypass. J Thorac Cardiovasc Surg 1996; 112:38-51
  180. Demers P, Elkouri S, Martineau R, Couturier A, Cartier R. Outcome With High Blood Lactate Levels During Cardiopulmonary Bypass in Adult Cardiac Operation. Ann Thorac Surg 2000; 70:2082-2086
  181. Gorman JH, Gorman RC, Milas BL, Acker MA. Circulatory Management of the Unstable Cardiac Patient. Seminars in Thoracic and Cardiovascular Surgery. 2000; 12:316-325
  182. DiSesa VJ. Pharmacologic Support for Postoprative Low Cardiac Output. Seminars in Thoracic and Cardiovascular Surgery 1991; 3:13-23
  183. Marchetti A, Weschler AS. Pharmacologic Intervention for Acute Low Cardiac Output. Advances in Cardiac Surgery 1996; 7:31-64
  184. Boldt J, Kling D, Moosdorf R, Hempelmann G. Influence of acute volume loading on right ventricular function after cardiopulmonary bypass. Crit Care Med 1989; 17:518-522
  185. Doyle AR, Dhir AK, Moors AH, Latimer RD. Treatment of Perioperative Low Cardiac Output Syndrome. Ann Thorac Surg 1995; 59: S3-S11
  186. Doolan LA, Jones EF, Kalman J, Buxton BF, Tonkin AM. A Placebo-Controlled Trial Verifying the Efficacy of Milrinone in Weaning High-Risk Patients From Cardiopulmonary Bypass. Journal of Cardiothoracic and Vascular Anesthesia, 1997; 11: 37-41
  187. Hayashida N, Tomoeda H, Oda T. et al. Inhibitory Effect of Milrinone on Cytokine Production After Cardiopulmonary Bypass. Ann Thorac Surg 1999; 68:1661-1667
  188. Takeuchi K, del Nido PJ, Ibrahim AE. et al. Vesnarinone and Amrinone Reduce the systemic inflammatory response syndrome. J Thorac Cardiovasc Surg 1999; 117:375-382
  189. Wesslen O, Hallhagen S, Ekroth, et al. High-dose intravenous B1-blockade in patients early after cardiac operations. J Thorac Cardiovasc Surg 1992; 104:1672-1678
  190. Lazar HL, Chipkin S, Philippides G, Bao Y, Apstein C. Glucose-Insulin-Potassium Solutions Improve Outcomes in Diabetics Who Have Coronary Artery Operations. Ann Thorac Surg 2000; 70:145-150
  191. Manche A, Galea J, Busuttil W. Tolerance to ACE inhibitors after cardiac surgery. Eur J of Cardio-thoracic Surg 1999; 15:55-60
  192. Sirivella S, Gielchinsky I, Parsonnet V. Angiotensin Converting Enzyme Inhibitor Therapy in Severe Postcardiotomy Dysfunction: A Prospective Randomized Study. J Card Surg 1998; 12:11-17
  193. Torchiana DF, Hirsch G, Buckley MJ. et al. Intraaortic Balloon Pumping For Cardiac Support: Trends In Practice And Outcome, 1968 to 1995. J Thorac Cardiovasc Surg 1997; 113:758-769
  194. Ghali WA, Ash AS, Hall RE, Moskowitz MA. Variation in Hospital Rates of Intraaortic Balloon Pump Use in Coronary Artery Bypass Operations. Ann Thorac Surg 1999; 67:441-445
  195. (194) Christenson JT, Simonet F, Badel P, Schmuziger M. Optimal Timing of Preoperative Intraaortic Balloon Pump Support in High-Risk Coronary Patients. Ann Thorac Surg 1999; 68:934-939
  196. Kang N, Edwards M, Larbalestier R. Preoperative Intraaortic Balloon Pumps in High-Risk Patients Undergoing Open Heart Surgery. Ann Thorac Surg 2001; 72:54-57
  197. Holman WL, Li Q, Kiefe CL. et al. Prophylactic Value of Preincision Intra-Aortic Balloon Pump: Analysis of a Statewide Experience. J Thorac Cardiovasc Surg 2000; 120:1112-1119
  198. Ferguson JT, Cohen M, Freedman RJ, et al. The current practice of Intra-aortic balloon counterpulsation: Results from the Benchmark Registry. J Am Coll Cardiol 2001; 38: 1456-1462
  199. Mueller DK, Stout M, Blakeman BM. Morbidity and Mortality of Intra-aortic Balloon Pumps Placed Through the Aortic Arch. CHEST 1998; 114:85-88
  200. Arafa OE, Pederson TH, Svennevig JL, Fosse E, Geiran OR. Vascular Complications of the Intraaortic Balloon Pump in Patients Undergoing Open Heart Operations: 15-Year Experience. Ann Thorac Surg 1999; 67:645-651
  201. Park SB, Liebler GA, Burkholder JA. et al. Mechanical Support of the Failing Heart. Ann Thorac Surg 1986; 42:627-631
  202. Katz, NM. Left and Right Ventricular Assist With the Bio-Medicus Centrifugal Pump. Operative Techniques in Thoracic and Cardiovascular Surgery. 1999; 4:268-276
  203. Noon, GP, Ball JW, Short HD. Bio Medicus Centrifugal Ventricular Support for Postcardiotomy cardiac failure: A review of 129 cases. Ann Thorac Surg 1996; 61: 291 - 295
  204. Magovern GJ, Naka Y, Oz MC, Pennington DG, Guest editors. Supplement to The Annals Of Thoracic Surgery. 2001; Vol 71, No 3
  205. Argenziano M, Chen JM, Choudhri AF et al. Management Of Vasodilatory Shock After Cardiac Surgery: Identification Of Predisposing Factors And Use Of A Novel Pressor Agent. J Thorac Surg 1998; 116:973-980
  206. Mekontso-Dessap A, Houel R, Soustelle C, Kirsch M, Thebert D, Loisance D. Risk Factors for Post-Cardiopulmonary Bypass Vasoplegia in Patients With Preserved Left Ventricular Function. Ann Thorac Surg 2001; 71:1428-1432
  207. Romaneli VA, Howie MB, Myerowitz PD. et al. Intraoperative and postoperative effects of vancomycin administration in cardiac surgery patients: A prospective, double-blind, randomized trial. Crit care Med 1993; 21: 1124-1131
  208. Morales DLS, Gregg D, Helman DN. et al. Arginine Vasopressin in the Treatment of 50 Patients With Postcardiotomy Vasodilatory Shock. Ann Thorac Surg 2000; 69:102-106
  209. Kleine P, Blommaert D, van Nooten G. et al. Multicenter results of TADpole heart wire system used to treat postoperative atrial fibrillation. Euro J Cardio Thorac Surg 1999; 15:525-527
  210. Del Nido P, Goldman BS. Temporary Epicardial Pacing after Open Heart Surgery: Complications and Prevention. J Cardiac Surg 1989; 4: 99 -103
  211. Pires LA, Wagshal AB, Lancey R, Huang SKS. Arrhythmias and conduction disturbances after coronary artery bypass graft surgery: Epidemiology, management, and prognosis. Am Heart J 1995; 129:799-808
  212. Sloan SB, Weitz HH. Postoperative Arrhythmias And Conduction Disorders. Med Clin of N. America 2001; 85:1171-1189
  213. Andrews TC, Reimold SC, Berlin JA, Antman EM. Prevention of Supraventricular arrhythmias after randomized control trials. Circulation 1991; 84 Suppl III: III 236- III 243
  214. Kowey PR, Taylor JE, Rials SJ, Marinchak RA. Meta-analysis of the effectiveness of prophylactic drug therapy in preventing supraventricular arrhythmias early after coronary artery bypass grafting. Am J Cardiol 1992; 36: 963-965
  215. Ommen SR, Odell JA, Stanton M. Atrial Arrhythmias After Cardiothoracic Surgery. New England J of Med 1997; 336:1429-1434
  216. Gomes JA, Ip J, Santoni-Rugiu F. et al. Oral d,l Sotalol reduces the Incidence of Postoperative Atrial Fibrillation in Coronary Artery Bypass Surgery Patients: A Randomized, Double-Blind, Placebo-Controlled Study. J Am Coll Cardiol 1999; 34:334-339
  217. Haan CK, Geraci SA. Role of Amiodarone in Reducing Atrial Fibrillation After Cardiac Surgery in Adults. Ann Thorac Surg 2002; 73: 1665-1669
  218. Lee SH, Chang CM, Lu MJ, et al. Intravenous amiodarone for prevention of atrial fibrillation after coronary artery bypass grafting. Ann Thorac Surg 2000; 70: 157-161
  219. Dorge H, Schoendube FA, Schoberer M, Stellbrink C, Voss M, Messmer BJ. Intraoperative amiodarone as prophylaxis against atrial fibrillation after coronary operations. Ann Thorac Surg. 2000; 69: 1358-1362
  220. Butler J, Harris DR, Sinclair M, Westaby S. Amiodarone prophylaxis for tachycardias after coronary artery surgery: a randomized, double blind, placebo-controlled trial. Br Heart J 1993; 70: 56-60
  221. Guarnieri T, Nolan S, Gottlieb SO, Dudek A, Lowry DR. Intravenous Amiodarone for the Prevention of atrial Fibrillation After Open Heart Surgery: The Amiodarone reduction in Coronary Heart (ARCH) Trial. J Am Coll Cardiol 1999; 34:343-347
  222. Hohnloser SH, Meinertz T, Dammbacher T, et al. Electrocardiographic and antiarrhythmics effects of intravenous amiodarone: results of a prospective, placebo-controlled study. Am Heart U 1991; 121: 89-95
  223. Daoud EG, Strickberger SA, Man KC, Goyal R. et al. Preoperative Amiodarone As Prophylaxis Against Atrial Fibrillation After Heart Surgery. The New England J of Medicine 1997; 337:1785-1792
  224. Redle JD, Khurana S, Marzan R, et al. Prophylactic oral amiodarone compared with placebo for prevention of atrial fibrillation after coronary artery bypass surgery. Am Heart J 1999; 138-144-150
  225. Toraman F, Karabulut EH, Alhan HC, Dagdelen S, Tarcan S. Magnesium Infusion Dramatically Decreases the Incidence of Atrial Fibrillation After Coronary Artery Bypass Grafting. Ann Thorac Surg 2001; 72:1256-1262
  226. Solomon AJ, Berger AK, Trivedi KK, Hannan RL, Katz NM. The Combination of Propranolol and Magnesium Does Not prevent Postoperative Atrial Fibrillation. Ann Thorac Surg 2000; 69:126 -129
  227. Borzak S, Silverman NA. Treatment of Postoperative Atrial Fibrillation. Seminars in Thorac and Cardiovasc Surg 1999; 11:314-319
  228. Hogue Jr CW, Hyder Ml. Atrial Fibrillation After Cardiac Operation: Risk, Mechanisms, and Treatment. Ann Thorac Surg 2000; 69:300-306
  229. Fuster V, Ryden LE, Asinger RW. Et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary: A report of the American College of Cardiology/American Heart Association task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2001; 38:1231-1265
  230. Kaul TK, Fields BL, Riggins LS, Wyatt DA, Jones CR. Ventricular arrhythmia following successful myocardial revascularization: incidence, predictors and prevention. Euro J of Cardio-Thoracic Surg 1998; 13:629-636
  231. Freeley TW. Management of Perioperative Arrhythmias. J of Cardiothoracic and Vasc Anest 1997; 11:10-15
  232. Johnson RG, Goldberger AL, Thurer RL, Schwartz M, Sirois C, Weintraub RM. Lidocaine Prophylaxis in Coronary Revascularization Patients: A Randomized, Prospective Trial. Ann Thorac Surg 1993; 55:1180-1184
  233. Scheinman MM, Levine JH, Cannom DS, et al. Dose-Ranging Study of Intravenous Amiodarone in Patients With Life-Threatening Ventricular Tachyarrhythmias. Circulation 1995; 92: 3264-3272
  234. Kowey PR, Levine JH, Herre JM, et al. Randomized, Double-Blind Comparison of Intravenous Amiodarone and Bretylium in the Treatment of Patients With Recurrent, Hemodynamically Destabilizing Ventricular Tachycardia or Fibrillation. Circulation 1995; 92: 3255-3263
  235. Hartzler GO, Maloney JD, Curtis JJ, Barnhorst. Hemodynamic Benefits of Atrioventricular Sequential Pacing After Cardiac Surgery. The Am J of Cardio 1977; 40:232-236
  236. Gordon RS, Ivanov J, Cohen G, Ralph-Edwards AL.Permanent Cardiac Pacing After a Cardiac Operation: Predicting the Use of Permanent Pacemakers. Ann Thorac Surg 1998; 66: 1698 -1704
  237. Rao V, Komeda M, Weisel RD, Cohen G, Borger M, David TE. Should the Pericardium Be Closed Routinely After Heart Operations? Ann Thorac Surg 1999; 67: 484 -488
  238. Chuttani K, Tischler MD, Pandian NG, Lee RT, Mohanty PK. Diagnosis of cardiac tamponade after cardiac surgery: Relative value of clinical, Echocardiographic, and hemodynamic signs. Am Heart J 1994; 127: 913 -918
  239. Mangi AA, Palacios IF, Torchiana DF. Catheter Pericardiocentesis for delayed tamponade after cardiac valve operation. Ann Thorac Surg 2002; 73: 1479-1483
  240. Newman MF. Troponin I in cardiac surgery: Making the future. Am Heart J 2001; 141: 325 -326
  241. Greaves SC, Rutherford JD, Aranki SF. et al Current incidence and determinants of perioperative myocardial infarction in coronary artery surgery. Am Heart J 1996; 132: 572-578
  242. Greenson N, Macoviak J, Krishnaswamy P. et al. Usefulness of cardiac troponin I in patients undergoing open-heart surgery. Am Heart J 2001; 141:447-455
  243. Vermes E, Mesquich M, Houel R. et al. Cardiac Troponin I Release After Open Heart Surgery: A Marker of Myocardial Protection? Ann Thorac Surg 2000; 70:2087-2090
  244. Carrier M, Pellerin M, Perrault LP, Solymoss BC, Pelletier LC. Troponin Levels in Patients With Myocardial Infarction After Coronary Artery Bypass Grafting. Ann Thorac Surg 2000; 69:435-440
  245. Eigel P, van Ingen G, Wagenpfeil S. Predictive value of perioperative cardiac Troponin I for adverse outcome in coronary artery bypass surgery. Euro J Cardio-thorac Surg 2001; 20:544-549
  246. Rasmussen C, Thiis JJ, Clemmensen P. et al. Significance and management of early graft failure after coronary artery bypass grafting. Feasibility and results of acute angiography and re-re-vascularization. Euro J Cardio-thorac Surg 1997; 12:847-852
  247. Fabricius AM, Gerber W, Hanke M, Garbade J, Autschbach R, Mohr F. Early angiographic control of perioperative ischemia after coronary artery bypass grafting. Euro J Cardio-thorac Surg 2001; 19:853-858
  248. Klatte K, Chaitman BR, Theroux P. et al. Increased Mortality After Coronary Artery Bypass Graft Surgery Is Associated With Increased Levels of Postoperative Creatine Kinase-Myocardial Band Isoenzyme Release. J Am Coll Cardiol 2001; 38:1070-1077
  249. Wallach R, Karp RB, Reves JG, Oparil S, Smith LR, James TN. Pathogenesis of Paroxysmal Hypertension Developing During and After Coronary Bypass Surgery: A Study of Hemodynamic and Humoral Factors. The American Journal of Cardiology 1980; 46:559-565
  250. Flaherty JT, Magee PA, Gardner TL, Potter A, MacAllister NP. Comparison of Intravenous Nitroglycerin and Sodium Nitroprusside for Treatment of Acute Hypertension Developing after Coronary Artery Bypass Surgery. Circulation 1982; 65:1072-1077
  251. Lunn RJ. Inhaled Nitric Oxide therapy. Mayo Clin Proc 1995; 70:247-255
  252. D’Ambra MN, LaRaia PJ, Philbin DM, Watkins WD, Hilgenberg AD, Buckley MJ. Prostaglandin E1. A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 1985; 89:567-572
  253. Heerdt PM, Weiss CI. Prostaglandin E1 and Intrapulmonary Shunt in Cardiac Surgical Patients With Pulmonary Hypertension. Ann Thorac Surg 1990; 49:463-465
  254. Fullerton DA, Jones SD, Grover FL, McIntyre RC. Adenosine Effectively Controls Pulmonary Hypertension After Cardiac Operations. Ann Thorac Surg 1996; 61:1118-1124
  255. Fullerton DA, Jaggers J, Wollmering MM, Piedalue F, Grover FL, McIntyre RC. Variable Response to Inhaled Nitric Oxide After Cardiac Surgery. Ann Thorac Surg 1997; 63:1251-1256
  256. Sharif H, Pezzella AT, Farah HH, Baljepally R, Maki D. Intracardiac Right-To-Left Shunt Complicating Right Ventricular Failure. Asian Cardiovasc Thorac 1999; 7:287-291
  257. Eisenberg MS, Mengert TJ. Cardiac Resuscitation. N Engl J Med 2001; 344: 1304-1313
  258. Bojar RM. Manual of Perioperative Care in Cardiac Surgery. Third Edition Malden Ma, Blackwell Science 1999; 10:259-263
  259. Cheng DCH, David TE. Perioperative Care in Cardiac Anesthesia and Surgery. Georgetown, TX Landes Bioscience 1999; 7:201-206
  260. Mackay JH, Powell SJ, Osgathorp J, Rozario CJ. Six-year prospective audit of chest reopening after cardiac arrest. Eur J Cardiothorac Surg 2002; 22: 421-425

Table One

Risk Factors Associated with Either Increased Length of Stay (L) or Increased Incidence of Organ failure

Morbidity (M) or Both (L/M) Following coronary Revascularization.

Risk factor Boston (8) Albany (9) VA(10) Canada (11)
Demographics        
Advanced age

L

 

M

L

Increased ratio of age/red blood cell volume  

L/M

   
Female gender      

L

Disease specific diagnoses        
CHF or cardiomegaly

L

L/M

M

 
Concomitant valve disease    

M

L

Reoperation    

M

L

LV dysfunction (ejection fraction)      

L

Surgical priority    

M

L

IABP pre-op

L

     
Active endocarditis    

M

 
Comorbid conditions        
Obesity

L

     
Renal dysfunction

L

L

M

 
Peripheral vascular disease  

L

M

 
Chronic obstructive lung disease  

L

   
Cerebrovascular disease  

L/M

   
Hypertension  

L/M

   

Abbreviations: CHF= congestive heart failure; LV = left ventricular; IABP = intraaortic balloon counterpulsation

 

Table Two

Partial listing of publicly available information sources related to Thoracic Surgery

Source

Targeted audience

Communication media

Information available

American college of Cardiology/

American Heart Association

Patients needing CABG (nationwide) Internet

(http://www.acc.org/clinical/guidelines/bypass/bypass7.htm)

Literature-based indications for CABG
Agency for Health Care Research & Quality Broad base of health care consumers and providers Internet (http://www.ahcpr.gov/) Large knowledge base focusing on empowering consumers to judge health care quality.
California Office of Statewide Health Planning and Development Patients who purchase healthcare insurance in California Internet

(http://www.oshpd.cahnet.gov/hpp/ccmrp/ccmrp summary.pdf

In-hospital CABG mortality data from 1998
Canadian Health Care System Provide consumers with hospital outcomes for various procedures that might indicate quality at a given hospital Internet (http://www.hcsc.gc.ca/ohihbsi/available/conference/presentations/guerriere e.pdf) Risk-adjusted hospital mortality rates for Canadian hospitals.
Cochrane Collaboration

 

 

All interested consumers Internet (http://www.cochraneconsumer.com/) Summarizes available published evidence about a wide variety of healthcare interventions including cardiac surgery.
Dartmouth University

 

 

Use large healthcare databases to inform the public of nationwide trends in health care delivery Internet (http://www.dartmouthatlas.org/99US/chap 5 sec 12.php) CABG mortality rates across the U.S. based primarily on claims databases
Health Care Choices New York not-for-profit corporation dedicated to educating the public about the nation’s health care system Internet

http://www.healthcarechoices.org/cardiacsurgery.htm

Select state CABG mortality rates, Primitive attempt to collate all publicly available data about physicians. Not nearly complete enough but evolving
HealthFinder NIH Government sponsored information web site about a wide variety of medical problems. Internet (http://www.healthfinder.gov/healthcare/) General information in fairly specific detail about cardiac procedures (with drawings and diagrams).
Healthoutcomes.com Patients requiring operation or catheter-based intervention nationwide Internet www.healthoutcomes.com In-hospital outcome for medicare patients having selected procedures (e.g. CABG)
The Leapfrog Group (Consortium of Fortune 500 companies and health care insurers Provide consumers with list of hospitals that employ Leapfrog defined quality measures Internet (http://www.leapfroggroup.org/index.html) List of hospitals that use quality measures. Hospitals that use these quality measures will be financially rewarded by Leapfrog Group.
Medscape Inc. Consumer information source for all types of medical conditions and for preventive medicine Internet (http://www.medscape.com/px/urlinfo Comprehensive, searchable website with multiple links to external sites capable of finding comprehensive information about details of cardiac surgery.
New Jersey State Department of Health Patients having cardiac procedures in New York State Internet (http://www.health.state.ny.us/nysdoh/consumer/heart/1996-98cabg.pdg) Surgeon-specific and hospital in-hospital mortality rates for CABG.
Pennsylvania Health Care Cost Containment Council Patients who require CABG in the state of Pennsylvania Internet (http://www.phc4.org/reports/cardiaccare.htm) Hospital-and surgeon-specific CABG mortality rates.
Rand Corporation Provide the public with summary data about health care outcomes for cardiac surgery Internet (http://www.rand.org/publications/MR/MR1255/MR1255.app4.pdf) Summary of publicly available CABG mortality rates with critical appraisal of methods and some estimation of appropriateness of care.
Society of Thoracic Surgeons Provide the public with results of cardiac surgery over as broad of a population as possible (including VA, Northern New England Consortium, and Great Britain) Internet (http://www.ctsnet.org/section/outcomes/) Mortality and other outcomes data for a variety of thoracic procedures. Some of the data is presented as raw mortality data without risk adjustment. One of the only databases that includes non-cardiac surgery.
Washington Post Medical Website Provider of medical information reports to consumers in North America Internet (http://www.medifocus.com/) General information about cardiac disease.
WebMd Inc. Provide information to consumers and physicians about a broad spectrum of health care issues. Internet (http://my.webmd.com/content/dmk/dmk article 53203) Information about CABG and expected outcomes.
Women’s Heart Foundation Provide health-related information for women Internet (http://www.womensheartfoundation.org/content/HeartSurgery/state report cards on ohs.asp) Links to internet-available report cards on cardiac surgery.

 

Table Three

Risk Models for Operative Mortality for CABG (14) *

Risk model

NYS (15)

Canada

(16)

Mass (17)

Emory (18)

VA (19)

Australia (20)

Toronto (21)

CCF (22)

Israeli (23)

Alabama (24)

NNE (25)

NYC (26)

Parsonnet (27)

Sum

No. of patients 174,210 57,187 50,357 17,128 13,368 12,712 12,003 7,491 4,918 4,835 3,654 3,055 2,152  
No. of risk factors 29 16 13 7 6 9 5 9 7 9 9 10 8  
Age X X   X X X X X X X X X X 12
Gender X X X X X   X X   X   X   9
Urgency X   X   X X   X   X X X   8
EF X X     X   X X   X X X   8
Renal

dysfunction

X X X X           X X   X 7
Previous CABG X   X X       X     X X   6
NYHA class X X X X   X       X       6
Left main CAD X X           X   X X X   6
# diseased vessels X X     X     X   X   X   6
PVD X   X     X   X X         5
Diabetes X X     X         X     X 5
Prior Stroke X   X X   X               4
Intraop/postop variables     X       X X       X 4
Prior MI X X X X                   4
Body Size X X                   X   3
Preop IABP X X       X               3
Shock X X                 X     3
COPD X X                       2
Prior PTCA X   X                     2
Angina   X         X             2
IV NTG X         X               2
Arrhythmias X               X         2
Hx of heart operation   X       X               2
Hemodynamic instability X                       X 2
Charison comorbidity                     X X   2
Dialysis dependence X X                       2
Pulmonary hypertension X                       X 2
Diuretics X         X               2
HTCVD               X           1
Serum albumin                 X         1
Race X                         1
Previous CHF                     X     1
MI timing X                         1
Cardiac index                 X         1
LVEDP                       X   1
CVA timing X                         1
Liver disease     X                     1
Neoplasia     X                     1
Ventricular aneurysm     X                     1
Steroids X                         1
Digitalis X                         1
Thrombolytic therapy                         X 1
Arterial bicarbonate                 X         1
Calcified aorta                         X 1

* Reprinted with permission: Grunkemeier GL, Zerr KJ. Cardiac Surgery Report Cards. Ann Thorac. Surg. 2001; 72: 1845-1848

 

Abbreviations: NYS = New York State; Mass – Massachusetts; VA = Veteran’s Administration; CCF = Cleveland Clinic Foundation; NNE = Northern New England; NYC= New York City; EF = ejection fraction; NYHA = New York Heart Association; CAD = coronary artery disease; PVD = peripheral vascular disease; MI = myocardial infarction; IABP – intra-aortic balloon pump; COPD = chronic obstructive pulmonary disease; PTCA = percutaneous transluminal coronary angioplasty ± stent; NTG = nitroglycerin; Hx = history; HTCVD = hypertensive cardiovascular disease; LVEDP = left ventricular end-diastolic pressure; CVA = cerebrovascular accident

*Reprinted with permission

Figure One

Open Heart Operations

USA, 1997*

Coronary Artery Bypass graft (CABG) 553,000
Valve replacement or Repair 89,000
Other open-heart operations 92,000
  734,000

*(http://www.americanheart.org)

 

Figure Two (a)

Toronto General Hospital Experience (7) *
Operations performed from 1993-1997

  Number Meaning age Timing mortality
    (mean +/-S.D.) Urgent Emergent rate
           
           

 

 

Coronary 7,371 62 ± 10 44% 3% 2.3%

Artery bypass

Aortic valve surgery 1,070 63 ± 15 32% 2% 2.5%

Mitral valve surgery 704 59 ± 14 27 % 6% 4.3%

Double/triple 381 57 ± 16 23% 3% 9.0%

valve surgery

Ascending aorta ± arch 475 57 ± 16 26% 16% 6.6%

± aortic valve surgery

Congenital heart 473 42 ± 15 11% 1% 3.2%

surgery in adults

Miscellaneous 638 57 ± 14 33% 23% 10.2%

______________________________________________________________________________________________________

*Left ventricular aneurysms (254), heart transplantation (99), myectomy (94), mapping +ablation (44), post infarction rupture of the septum (37), atrial myxoma (29), others (82).

Figure Two (b) *

Cleveland Clinic

1998

Mortality

CABG 1%

CABG (redo) 2%

Aortic Valve Surgery 2.8%

Mitral Valve Surgery 1.5%

Great Vessel Surgery 6%

 

 

 

 

 

 

 

 

 

_______

 

*Cleveland Clinic Department of Thoracic and Cardiovascular Surgery, 1998

Department Review

 

Figure Three (a)

Toronto General Hospital Experience (7) *

Complications rates from 1993-1997

CABG Valves AA/A CHD Miscellaneous

Re-exploration for bleeding 1.5% 4.0% 6.5% 4.2% 4.2%

Perioperative stroke 1.4% 2.5% 6.6% 0.0% 2.2%

Perioperative myocardial 2.4% 1.3% 1.7% 0.6% 1.6%

Infarction

Deep sternal infection 0.8% 0.7% 1.1% 0.6% 0.2%

Superficial wound infection 1.7% 0.8% 1.7% 1.9% 1.4%

Sternal dehiscence 0.3% 0.1% 0.6% 0.0% 0.2%

Renal failure 0.3% 0.3% 0.6% 0.0% 1.6%

Mean ICU stay (days) 1.9 2.5 3.3 2.4 3.4

Abbreviations CABG = coronary artery bypass graft; AA/A = ascending aorta + / - arch; CHD = congenital heart disease

* Reprinted with permission- Cheng DC, David TE. Perioperative care in cardiac anesthesia and surgery. Landes Bioscience Georgetown, TX 1999, p2

Figure Three (b)

STS NATIONAL DATABASE *

1997 CABG (161,018 patients)

Complications

Infection – sternum – deep 0.63%

Infection – Leg 1.26%

Infection – UTI 1.52%

CVA – transient 0.74%

Delirium 2.62%

- Pulmonary embolism 0.33%

- Pulmonary Edema 2.12%

- ARDS 0.87%

- Pneumonia 2.45%

With dialysis 0.87%

- Heart Block requiring pacemaker 0.81%

- Tamponade 0.39%

- Atrial fibrillation 19.37%

- Cardiac arrest 1.46%

 

 

 

______________

* http://www.sts.org

 

 

 

Figure Four (a)

Cleveland Clinic Clinical

Severity Scoring System (22)

Preoperative Factor Factor

Emergency case 6

Creatinine > 1.6-1.8 1

Creatinine > 1.9 4

Severe LV dysfunction 3

Reoperation 3

Mitral regurgitation 3

Age 65-74 1

Age >75 2

Prior vascular surgery 2

COPD 2

Hematocrit <34% 2

Aortic stenosis 1

Weight < 65 kg 1

Diabetes 1

Cerebrovascular disease 1

 

 

 

 

 

 

Figure Four (b)

 

 

 

 

 

 

Figure Five

Intensive Care Unit Risk Stratification Score (48)

Variable Value

Preoperative Factors

Small body size (BSA < 1.72 m2) 1

Prior hear operation

One 1

Two or more 2

History of operation or angioplasty 3

for peripheral vascular disease

Age > 70 years 3

Preoperative creatinine > 1.9 mg/dL 4

Preoperative albumin < 3.5 mg/dL 5

Intraoperative factors

CPB time > 160 minutes 3

Use of IABP after CPB 7

ICU admission physiology

A-a O2 gradient > 250 mm Hg 2

Heart rate > 100 beats/min 3

Cardiac index < 2.1 L. min-1. m-2 3

CVP > 17 mm Hg 4

Arterial bicarbonate < 21 mmol/L 4

A-a = alveolar-arterial; BSA = body surface area; CPB = Cardio-pulmonary bypass; CVP = central venous pressure; IABP = intraaortic balloon pump; ICU = intensive care unit

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure Six

ACC/AHA Classification for Guidelines Series (69)

The ACC/AHA classifications I, II, and III are used to summarize indications as follows:

Class I: Conditions for which there is evidence and/or general agreement that a given

procedure or treatment is useful and effective.

Class II: Conditions for which there is conflicting evidence and/or a divergence of

opinion about the usefulness/or efficacy of a procedure.

Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.

Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful.

 

 

Figure Seven

Cardiac Risk* Stratification for Noncardiac Surgical Procedures (74) ◊

High (Reported cardiac risk often >5%)

Intermediate (Reported cardiac risk generally <5%)

Low¦ (Reported cardiac risk generally <1%)

*Combined incidence of cardiac death and nonfatal myocardial infarction.

¦ Do not generally require further preoperative cardiac testing.

 

◊ From: Eagle KA, Brundage BH, Chaitman BR, et al. ACC/AHA Guidelines for Perioperative Cardiovascular Evaluation Guidelines. Circulation 1996; 93: 1280- 1317/Guideline Update Circulation 2002; 105: 1257-1267

Reproduced with permission

 

 

 

 

 

 

 

Figure Eight

Physical status classification of the American Society of Anesthesiologists (75)

Class Patient characteristics

I No organic, physiologic, biochemical, or psychiatric disturbance; localized pathologic process for which operation is to be performed; no systemic disturbance

II Mild-to-moderate systemic disturbance caused by the condition to be treated surgically or by other pathophysiologic processes

III Severe systemic disturbance or disease from whatever cause, with the potential for perioperative complications

IV Severe systemic disorders that are already life-threatening, not always correctable by operation

V Moribund with little chance of survival

E Emergency operation (the letter E is placed beside the numeric classification to indicate increased risk and poorer physical condition associated with emergency procedure)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure Nine

Clinical Measures Of Left Ventricular Performance *

Preload

Pulmonary capillary wedge pressure

Left ventricular end-diastolic volume

Afterload

Arterial systolic pressure

Vascular resistance

Contractility

Left ventricular ejection fraction (normal afterload)

Left ventricular dP/dtmax (at constant LVEDV)

Left ventricular end-systolic volume or dimension

Systolic function

Left ventricular ejection fraction

Stroke work

Diastolic function

Pulmonary capillary wedge pressure

Mitral valve flow velocity

Other echo-Doppler parameters (e.g., isovolumic relaxation time, peak early

diastolic annular myocardial velocity, propagation velocity)

Integrated cardiopulmonary function

Mixed venous oxygen saturation

Exercise performance

 


 

*From Braunwald E, Zipes DP, Libby P. Clinical Measures of Left Ventricular Performance. In: Heart Disease: A Textbook of Cardiovascular Medicine 6th ed. W. B. Saunders Company, Philadelphia, 2001

Reproduced with permission

 

 

 

Figure Ten*

________________________________________________________________________

Hemodynamic Evaluation Based on the Pulmonary Artery Catheter (PAC) Hemodynamic Profile (177)

Hemodynamic Central Cardiac Systemic

Profile Pressures Output Vascular Tone

________________________________________________________________________

Hypovolemia Low Low Normal-High

Pump failure High Low Normal-High

Low SVR Normal-low Normal-High Low

High PVR High Low High

_______________________________________________________________________

 

 

 

The Diagnostic Approach to Mixed Venous Oxygen Saturation (SvO2)

Equation Variable Clinical Scenario

That Affects SvO2 That Decreases SvO2

Cardiac output Pump failure

Arterial saturation Hypoxia

Hemoglobin level Hemorrhage

Oxygen consumption Patient shivering

 

 

 

______

* From Augoustides J, Weiss SJ, Pochettine A. Hemodynamic Monitoring of the Postoperative Adult Cardiac Surgical Patient. Seminars in Thoracic and Cardiovascular Surgery. 2000; 12: 309-315

Reproduced with permission

Figure Eleven

Initial hemodynamic Instability: Etiological Considerations

- Hypovolemia - ¯ SVR; non-cardiac bleeding – chest/abdomen/thigh

 

 

 

 

 

 

Figure Twelve

Treatment of Low Cardiac Output *

  1. Think of surgical complications, including coronary graft occlusion, valve malfunction, tamponade, bleeding, and coronary spasm.
  2. Optimize heart rate and rhythm.
  3. Increase rate to 90-100.

    Atrial placing if no heart block

    A-V pacing if heart block

  4. Low blood pressure (systolic < 100 or MAP < 75)
  5. If PA < 15 mmHg:

    Give Ringer’s lactate or hetastarch if Hct > 25%.

    Give PRBC if Hct < 25%.

    If PAD > 15 mmHg

    Give dopamine (start at 3-5 mg/kg/min, maximum

    rate 15 ug/kg/min) or other inotrope.

    When bp > 100, begin nitroglycerin (0.3-0.6 ug/kg/min)

  6. Normal or high blood pressure (systolic > 100, MAP > 75)
  7. If PAD < 15 mmHg:

    Give Ringer’s lactate or hetastarch if Hct > 25%.

    Give PRBC if Hct < 25%.

    Continue stepwise treatment with volume and vasodilators.

    Until CI adequate (> 2.5), do not allow PAD to remain > 15 mmHg

    or BP to remain < 100.

  8. If BP and CO still low, insert IABP.

 

 

 

________

* Adapted from Vander Salm T.J., Stahl R.E. Chapter 12 Early Postoperative Care, p. 342. In: Edmunds L.H., ed. Cardiac Surgery in the Adult. McGraw-Hill, New York, 1997.

Reproduced with permission

 

 

 

 

 

 

Figure Thirteen

Hemodynamic Drugs*

HR MAP PAP CVP SVR CO

Vasodilating Agents

Nitroglycerin ­ ¯ ¯ O/¯ ¯ ­

Nitroprusside ­ ¯ ¯ O/¯ ¯ ­

Vasopressor Agents

Phenyleprine O/¯ ­ ­ ­ ­ ­ /¯

Mixed Activity Agents

Epinephrine ­ ­ ­ ­ ­ ­

Norepinephrine O/­ ­ ­ ­ ­ ­ /¯

Dopamine O/­ O/­ O/­ O/­ O/­ ­

Inotropic Agents

Dobutamine O/­ O/­ O O/­ O/¯ ¯

Milrinone O/­ ¯ ¯ O/¯ ¯ ­

Digoxin ¯ O O/¯ O/¯ ­ ­

Key: O: little or not change, ­ : Increase, ¯ : decrease

CO: cardiac output, CVP: central venous pressure, HR: heart rate, MAP: mean arterial pressure, PAP: pulmonary artery pressure, SVR: systemic vascular resistance

 

______

* Adapted from Cada DJ, Covington TR, Hussar DA, et al. Drug Facts and Comparison Wolters Kluwer, St. Louis, Missouri 2002

Reproduced with permission

Figure Fourteen

Amiodarone Trial Results (216)*

Percent Incidence in AF

Author Ref No. Baseline Medications a Amiodarone Dosing Rate

Lee et al 217 Digoxin, Calcium-channel 150mg load, 0.4mg/kg/h 3 12% versus 34%

blockers , ß-blockers: all days pre-op to 5 days post-op (p<0.01b)

NS between groups

Dorge et al 218 None noted; exclusion for 300mg load→20mg/kg/d 24% and 285, versus

Digoxin use for 3 days; 150mg load→ 34% (p=NS)

10mg.kg.d for 3 days

 

Butler et al 219 None noted 24-hour infusion at 15 17% versus 20% by

mg/kg, then 200mg 3 Holter (p=NS),

times a day for 5 days clinically 8% versus 20%

(p= 0.07)

Guarnieri et Digoxin, Calcium-channel 1 g/day for 2 days 35% versus 47% (p=0.01*)

al 220 blockers, ß-blockers: all

NS between groups

Hohnloser Digoxin, Calcium-channel 300 mg load→1,200 5% versus 21% (p<0.05*)

et al 221 blockers, ß-blockers: all mg/day for 2 days, 900

NS between groups mg/day for 2 days

Daoud et Digoxin, Calcium-channel 600 mg/day for 7 days, 25% versus 53%

al 222 blockers, ß-blockers: all then 200mg/day until (p= 0.003*)

NS between groups discharge

Redle et Calcium-channel 2 g pre-op (over 1-4 24.7% versus

al 223 blockers, ß-blockers; all days), then 4mg/day for 32.8% (p=0.30)

NS between groups 7 days

AF= atrial fibrillation; NS= not significant; post-op = postoperatively; pre-op=preoperatively.

a For both study groups

b Statistical significance at p < 0.05

* From Haan CK, Geraci SA. Role of Amiodarone in Reducing Atrial Fibrillation After

Cardiac Surgery in Adults. Ann Thorac Surg 2002; 73: 1665-1669

Reproduced with permission

Figure Fifteen

RECOMMENDATIONS FOR PREVENTION AND MANAGEMENT OF POSTOPERATIVE AF (228)*

 

Class I

    1. Treat patients undergoing cardiac surgery with an oral beta-blocker to prevent postoperative AF, unless contraindicated. (Level of evidence; A)
    2. In patients who develop postoperative AF, achieve rate control by administration of AV nodal blocking agents. (Level of Evidence: B)

 

Class IIa

    1. Administer sotalol or amiodarone prophylactically to patients at increase risk of developing postoperative AF. (Level of Evidence: B)
    2. Restore sinus rhythm in patients who develop postoperative AF by pharmacological cardioversion with ibutilide or direct-current cardioversion, as recommended for nonsurgical patients. (Level of Evidence: B)
    3. In patients with recurrent or refractory postoperative AF, attempt maintenance of sinus rhythm by administration of antiarrhythmics medications, as recommended for patients with CAD who develop AF. (Level of Evidence: B)
    4. Administer antithrombotic medication in patients who develop postoperative AF, as recommended for nonsurgical patients. (Level of Evidence: B)

__________

 

* From Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC/ Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary: A report of the American College of Cardiology/American Heart Association task force on Practice Guidelines and the European Society of Cardiology (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2001; 38:1231-1265

Reproduced with permission

Figure Sixteen

COMMON PARENTERAL DRUGS FOR TREATMENT OF SEVERE HYPERTENSION*

Drug Class Route and Dose Onset Duration Comments

Diazoxide – Arteriolar IV: 1-3 mg/kg (max 1-5 min 6-12 hrs May cause reflex

(Hyperstat, and vasodilator 150 mg) q5-15 min tachycardia; not

Others) for patients with

angina pectoris,

myocardial

infarction,

dissecting

aneurysm or

pulmonary edema

Enalaprilat – Angiotensin IV: 1.25-5 mg q6h 15 min 6-12 hrs Variable,

(Vasotec IV) converting sometimes

enzyme excessive

Inhibitor response

Fenoldopam – Dopamine- 1 IV infusion pump 4-5 min <10 min May cause reflex

(Corlopam) receptor 0.1-1.6 ug/kg/min tachycardia; may

increase

intraocular

pressure

Labetalol – Alpha-and beta IV: 20 mg initially 5 min 3-6 hrs Not for patients

(Trandate, adrenergic then 40-80 mg q10 min or less with

Normodyne) blocker (300 mg max) brochospasm, congestive

heart failure, >1st degree heart

block,

cardiogenic

shock or severe

bradycardia

Nicardipine – Calcium IV: 5 mg/hr, 1-5 min 3-6 hrs May cause reflex

(Cardene IV) channel blocker increased by 2.5 tachycardia

mg/hr q 15 min up

to 15 mg/hr

Nitroglycerin – Venous >> IV infusion pump 2-5 min 5-10 min Headache,

(Nitro-bid IV) arteriolar 5 to 100 ug/min tachycardia can

vasodilator occur; tolerance

may develop with

prolonged use

Sodium Arteriolar and IV infusion pump seconds 3-5 min Thiocyanate or

(Nitroprusside) venous 0.3-10 ug/kg/min cyanide toxicity

vasodilator with prolonged or

too rapid infusion

* Adapted from The Medical Letter 1998; 40: p. 57

Reproduced with permission

Legends -Part I

Figure One Open Heart Operations

Figure Two (a) Toronto General Hospital Experience

Figure Two (b) Cleveland Clinic

Figure Three (a) Toronto General Hospital Experience

Figure Three (b) STS National Database

Figure Four (a)) Cleveland Clinic Clinical Severity Scoring System

Figure Four (b) Clinical Severity Score

Figure Five Intensive Care Unit Risk Stratification Score

Figure Six ACC/AHA Classification for Guidelines Series

Figure Seven Cardiac Risk Stratification for non-cardiac surgical

procedures

Figure Eight Physical status classification of the American Society of

Anesthesiologists

Figure Nine Clinical Measures of Left Ventricular performance

Figure Ten Hemodynamic Evaluation based on the Pulmonary Artery

Catheter (PAC) Hemodynamic Profile

Figure Eleven Initial Hemodynamic Instability: Etiological Considerations

Figure Twelve Treatment of Low Cardiac Output

Figure Thirteen Hemodynamic Drugs

Figure Fourteen Amiodarone Trial Results

 

 

 

 

 

Figure Fifteen Recommendation for Prevention and Management of

Postoperative AF

Figure Sixteen Common Parenteral Drugs for Treatment of Severe

Hypertension


Table One Risk Factors

Table Two Partial listing of publicly available information sources

Table Three Risk Models