High-risk Cardiac Patients Research Articles

Target-controlled infusion or manually controlled infusion of propofol in high-risk patients with severely reduced left ventricular function

Objective: To compare hemodynamics, time to extubation, and costs of target-controlled infusion (TCI) with manually controlled infusion (MCI) of propofol in high-risk cardiac surgery patients. Design: Prospective, randomized. Setting: Major community university-affiliated hospital. Participants: Twenty patients undergoing first-time implantation of a cardioverter-defibrillator with severely reduced left ventricular function (left ventricular ejection fraction <30%). Interventions: Anesthesia was performed using remifentanil, 0.2 to 0.3 μg/kg/min, and propofol. Propofol was used as TCI (plasma target concentration, 2 to 3 μg.mL; n = 10) or MCI (2.5 to 3.5 mg/kg/hr; n = 10). Measurements and Main Results: Hemodynamics were measured at 6 data points: T1, before anesthesia; T2, after intubation; T3, after skin incision; T4, after first defibrillation; T5, after third defibrillation; and T6, after extubation. There were no significant hemodynamic differences between the 2 groups. Dobutamine was required to maintain cardiac index >2 L/min/m2 in significantly more patients of the TCI group than of the MCI group. Mean dose of propofol was higher in the TCI patients (6.0 ± 1.0 mg/kg/hr) than in the MCI patients (3.0 ± 0.4 mg/kg/hr) (p < 0.05), whereas doses of remifentanil did not differ. Time to extubation was significantly shorter in the MCI (11.9 ± 2.4 min) versus the TCI group (15.6 ± 6.8 min). Costs were significantly lower in MCI patients ($34.73) than in TCI patients ($44.76). Conclusions: In patients with severely reduced left ventricular function, TCI and MCI of propofol in combination with remifentanil showed similar hemodynamics. TCI patients needed inotropic support more often than MCI-treated patients. Although extubation time was longer in TCI patients and costs were higher, both anesthesia techniques can be recommended for early extubation after implantation of a cardioverter-defibrillator. Copyright © 2001 by W.B. Saunders Company

The management of heart failure--an overview.

National and international societies have issued guidelines on the management of heart failure: The European Society of Cardiology, WHO, ACC/AHA Task Force Report, US Department of Health and Human Services, German Society of Cardiology. The therapeutic approaches to heart failure have undergone considerable changes during the last few years. The guidelines have to be updated almost yearly due to new results from prospective randomized studies. Although an agreement could be reached with respect to general measures and drug treatment, no agreement on mechanical devices, pacemakers and surgical interventions has been reached. The basis for medical treatment of chronic heart failure depends on diuretics, digitalis, ACE inhibitors, and beta-blockers. Calcium antagonists and other positive inotropic drugs, other than digitalis, should be avoided as far as possible. Thiazides, loop diuretics and aldosterone antagonists are needed for acute and chronic treatment of heart failure, alone or in combination (diuretic resistant heart failure!). Digitalis glycosides are needed in patients with atrial fibrillation with a fast ventricular rate or atrial flutter and in patients with systolic dysfunction, large hearts and symptomatic failure class NYHA III and IV. However, digitalis does not convert atrial fibrillation to sinus rhythm. Today there is no question that ACE inhibitors improve the prognosis of all patients with heart failure in all stages, if ejection fraction is reduced. Therefore, most patients after myocardial infarction or after having experienced pump failure due to myocarditis or cardiomyopathy are treated with ACE inhibitors and diuretics. The beneficial effects of ACE inhibitors seem to be most pronounced the worse the situation is. Relative risk reductions (mortality!) between 10% and 40% have been published depending on the severity of symptomatic left ventricular dysfunction. Those patients with high absolute risk have more to gain than those with low risk for any given "risk reduction", of course. Recent studies also indicate that most high risk cardiac patients profit from ACE inhibitors even if pump function is normal (i.e., patients with coronary heart disease, diabetes mellitus, cerebral vascular disease, hypertension) (15). AT1 antagonists can substitute for ACE inhibitors, if the latter are not tolerated due to cough. Up to now, beta-blocking agents apart from diuretics seem to be the best investigated drugs in heart failure. Large controlled studies with bisoprolol, carvedilol and metoprolol in addition to diuretics, digitalis and ACE inhibitors convincingly yielded positive results in chronic left ventricular failure patients. Reduction of mortality by 35% and even of sudden cardiac deaths by 40% have been proven beyond doubt. Thus, heart failure patients today should also receive beta-blocking agents in all stages of the disease. In the era of controlled prospective studies (evidence-based medicine), physicians are well advised to use only drugs that have been proven beneficial in large controlled studies.

Part 12: From Science to Survival

Part 12: From Science to Survival

Preoperative Cardiac Evaluation and Interventions Before Aortic Surgery: Are They Justified?

The role of cardiac risk assessment and preoperative cardiac intervention prior to elective vascular surgery remains controversial. In high cardiac risk patients (severe or unstable angina, recent myocardial infarction, decompensated congestive heart failure [CHF]), the risk of an adverse cardiac event is so great that most would agree that these patients should undergo a preoperative cardiac work-up. In most instances strong consideration in these patients should be given to proceeding directly to coronary arteriography In patients with low cardiac risk (those with no active cardiac symptoms, and no Eagle risk factors [angina, age >70 years, history of CHF, Q-wave on EKG, diabetes, ventricular ectopy requiring medication]), the adverse cardiac event rate is so low that one can proceed safely to vascular surgery without any additional cardiac testing. The moderate risk group (patients with one or more Eagle risk factors but without severe or recent cardiac symptoms) may potentially benefit from aggressive...

The role of vitamin E in the prevention of heart disease.

Data from the 1970s first suggested that vitamin E may be effective in decreasing mortality from cardiovascular disease. As the understanding of the antioxidant effect of this vitamin evolved, researchers began to further study the biologic effects of vitamin E. In vitro studies have shown vitamin E to have several potentially cardioprotective effects, including antagonizing the oxidation of low-density lipoproteins, inhibiting platelet aggregation and adhesion, preventing smooth muscle proliferation, and preserving normal coronary dilation. Several prospective studies, including the US Nurses' Health Study and the US Health Professionals' Follow-up Study, found a 34% and 39% reduction, respectively, in the risk of having a cardiac event for those taking vitamin E supplements. The Iowa Women's Health Study found a 47% reduction in cardiac mortality. Results of randomized, controlled clinical trials have not found consistent benefit, however. The best known of these trials, the Cambridge Heart Antioxidant Study, found a 47% reduction in fatal and nonfatal myocardial infarction in patients with proven coronary atherosclerosis who were given 400 or 800 IU of vitamin E daily. There was, however, no effect on mortality. While emerging and promising data suggest the potential benefit of vitamin E for high-risk cardiac patients, physicians should be alert to the results of randomized, controlled clinical trials already in progress.

Recomendaciones sobre el uso de la monitorización ambulatoria de presión arterial.: Documento de consenso de la Sociedad Chilena de Hipertensión

Continuous ambulatory blood pressure monitoring is a diagnostic technique devised as a consequence of the great variations in blood pressure measurements. It allows multiple daily measurements, nocturnal monitoring, avoids the stress of blood pressure measurements, gives a picture of pressure behavior during 24 hours and reduces observer related errors. The equipment used must be accurate and validated using international protocols. Accepted indications for continuous ambulatory blood pressure monitoring are white coat hypertension, episodic hypertension, resistance to medications and assessment of symptoms or autonomic dysfunction. Other indications with less clear cut usefulness, are high risk cardiac, renal or pregnant patients and an accurate blood pressure control. We describe equipment calibration, elements that must be considered in the reports, result interpretation and conclusions. Normal blood pressure ranges for children and pregnant women are also reported.

The Role of the Myocardial Sodium‐Hydrogen Exchanger in Mediating Ischemic and Reperfusion Injury: From Amiloride to Cariporidea

There is convincing evidence that the Na-H exchanger (NHE) plays a pivotal role in mediating tissue injury during ischemia and reperfusion. Extensive studies with NHE inhibitors have consistently shown protective effects against ischemic and reperfusion injury in a large variety of experimental models and animal species, particularly in terms of attenuating contractile dysfunction. These protective effects of NHE inhibition appear to be superior to other strategies, including ischemic preconditioning. Such studies have contributed greatly to the overwhelming evidence that NHE activation mediates ischemic and reperfusion injury. The NHE inhibitor HOE 642 (cariporide) is currently undergoing clinical evaluation in high-risk cardiac patients. Moreover, there is now emerging evidence that NHE may be involved in mediating cardiotoxicity directly produced by various ischemic metabolites such as lipid amphiphiles or reactive oxygen species. NHE inhibition also attenuates apoptosis in the ischemic myocardium, a process that may be of importance in the subsequent development of postinfarction heart failure. In conclusion, NHE represents an important adaptive process in response to intracellular acidosis that results in a paradoxical contribution to cardiac tissue injury.

Anesthetic management of high-risk cardiac patients undergoing noncardiac surgery under the support of intraaortic balloon pump

Patients with severely impaired left ventricular function, an uncorrectable coronary artery disease, and a recent myocardial infarction are at high risk of cardiac complications after major noncardiac surgery. We present two patients with extensive three-vessel coronary artery disease who underwent intraperitoneal surgery under the support of intraaortic balloon pump (IABP). In one patient, the IABP was inserted urgently because of the development of chest pain with significant ST depression on arrival in the operating room, and the other patient was managed with prophylactic IABP. There were no intraoperative or postoperative cardiac events in either patient. Thus, IABP should be considered in the perioperative management of patients with severe cardiac diseases.

Total intravenous anesthesia with remifentanil and propofol for implantation of cardioverter-defibrillators in patients with severely reduced left ventricular function

Objective: To determine the cardiocirculatory effects of total intravenous anesthesia (TIVA) using remifentanil and propofol in high-risk cardiac surgical patients. Design: Prospective study of 20 patients undergoing first-time implantation of a cardioverter-defibrillator (ICD). Setting: Major, community, university-affiliated hospital. Participants and Interventions: In 20 patients with severely reduced left ventricular function (left ventricular ejection fraction <30%) undergoing first-time implantation of an ICD, TIVA using remifentanil and propofol was performed. Measurements and Main Results: Extensive hemodynamic monitoring using a pulmonary artery catheter was performed: (T1) before induction of anesthesia, (T2) after intubation, (T3) after skin incision, (T4) after first defibrillation, and (T5) 10 minutes after extubation. Propofol, 3.0 ± 0.6 mg/kg/h (range, 1.9 to 4.4 mg/kg/h), and remifentanil, 0.30 ± 0.05 μg/kg/min (range, 0.21 to 0.40 μg/kg/min), were used. Total costs added up to US $44.60 per patient. Patients could be extubated within 12.5 ± 4.2 minutes after stopping anesthesia. There were significant decreases in heart rate (HR; from 77 ± 12 to 57 ± 10 beats/min [T3]), mean arterial blood pressure (MAP; from 98 ± 14 to 70 ± 12 mmHg [T2]), and systemic vascular resistance (from 1,551 ± 309 to 1,233 ± 274 dyne · s · cm −5 [T2]). Cardiac index (CI) slightly decreased only at T3 (from 2.46 ± 0.42 to 1.92 ± 0.29 L/min/m 2; p = 0.04). The decrease in MAP could easily be treated by volume infusion in most patients (17 patients). Sixty-five percent of the patients needed dobutamine to increase CI to greater than 2.0 L/min/m 2 (mean dose, 2.2 ± 1.8 μg/kg/min). Dobutamine could be stopped before extubation in all patients. No patient needed sustained inotropic or ventilatory support and intensive care therapy could be avoided. Conclusion: TIVA using remifentanil and propofol in patients with severely reduced left ventricular function is safe, well-controllable, and allows early extubation after implantation of an ICD. Because patients without complications did not need a postoperative intensive care stay, costs may be considerably reduced.

Perioperative cardiovascular morbidity in patients with coronary artery disease undergoing vascular surgery after percutaneous transluminal coronary angioplasty

Objective: Patients with coronary artery disease (CAD) who undergo noncardiac surgery are at increased risk for perioperative myocardial infarction (PMI). Undergoing successful coronary artery bypass grafting (CABG) before such surgery has been shown to decrease perioperative cardiac morbidity and mortality. Percutaneous transluminal coronary angioplasty (PTCA) is an alternative treatment for these patients. Perioperative cardiac morbidity in patients with CAD who underwent PTCA before their vascular surgery was reviewed. Setting: A tertiary care referral center for patients with cardiovascular heart disease. Participants: Review of vascular surgery database for patients who underwent vascular surgery preceded by PTCA between 1984 and 1995. Patients were excluded if they had a history of CABG within 2 years of surgery, had PTCA more than 18 months before surgery, or had incomplete data. Measurements: Data were collected concerning cardiac history, left ventricular (LV) function, perioperative cardiac morbidity (angina, MI, congestive heart failure [CHF], and arrhythmias). Main Results: Of 194 patients who underwent aortic abdominal surgery, carotid endarterectomy (CEA), or peripheral vascular surgery preceded by PTCA, 104 (54%) had a previous MI. Twenty-six patients (13.4%) had perioperative cardiac morbidity. Only one patient had an MI (0.5%; 95% confidence interval [CI], 0.0 to 2.8), whereas one patient died of CHF followed by multisystem organ failure (0.5%). The median interval between PTCA and surgery was 11 days (interquartile range, [IQR] 3 to 49 days). Patients who developed perioperative cardiac morbidity were older than those who did not ( p = 0.02). Patients who had a history of CABG (before PTCA) had a higher incidence of postoperative angina ( p = 0.04). The degree of preoperative LV dysfunction was linearly related to the incidence of new postoperative CHF ( p = 0.01). Arrhythmias were more common in patients undergoing abdominal vascular surgery (17.9%) than in those undergoing CEA (2.5%; p = 0.03) or peripheral vascular surgery (5.2%; p = 0.02). Conclusion: High-risk cardiac patients undergoing vascular surgery who have had PTCA performed up to 18 months preoperatively have a low incidence of perioperative cardiac morbidity. Prophylactic PTCA may be beneficial in patients with CAD who are at high risk for perioperative cardiac complications.

The Critically Ill Cardiac Patient

The Critically Ill Cardiac Patient

Advances in myocardial protection.

The success of cardiac surgery is due in large part to the myocardial protection techniques employed to maintain cardiac viability during the period of induced ischemic arrest. As the number of older, high-risk cardiac surgical patients increases, advances in myocardial protection have become necessary to achieve a quiet, bloodless operative field without the production of irreversible intraoperative myocardial damage. Current efforts to provide optimal myocardial protection have focused on the effects of cardioplegic perfusate temperature, distribution of cardioplegia flow, and components of the arresting solution. Minimally invasive techniques have expanded surgical options and have led to the development of new methods to protect the myocardium.

Pressure-dependent Collateral Perfusion during Cerebral Ischemia in Pigs on Bypass

Patients with coexisting cerebrovascular disease have an increased risk of neurologic injury during cardiopulmonary bypass (CPB) [1,2]. However, the optimal perfusion pressure to maintain during CPB in high-risk cardiac surgical patients remains controversial, with studies of more than 6,000 patients resulting in no consensus. Using a porcine model of cerebral ischemia during CPB, we examined whether pressure-dependent collateral cerebral perfusion exists during nonpulsatile CPB. Methods. In an approved study, 20 anesthetized pigs were placed on normothermic CPB. Global cerebral ischemia was produced by ligating the innominate and left subclavian arteries. Collateral cerebral blood flow was measured by radioactive microspheres injected through the aortic cannula. Distal arterial occlusion pressure was measured downstream from the site of cerebral vessel occlusion by a transducer-tipped catheter inserted through the right internal mammary artery. Mean aortic blood pressure during CPB was maintained at 50 mm Hg (n=10) or 80 mm Hg (n=10) by adjusting pump flow. Data are expressed as mean +/- SEM. Results. During cerebral ischemia, distal arterial occlusion pressure was greater at 80 mm Hg aortic pressure (12.2 +/- 1.2 mm Hg) than at 50 mm Hg (4.0 +/- 0.7 mm Hg; p < 0.01). Similarly, collateral cerebral perfusion at 80 mm Hg (8.2 +/- 1.7 ml/min/100g) exceeded that at 50 mm Hg (3.2 +/- 0.5 ml/min/100g; p< 0.05). Overall, collateral cerebral perfusion varied directly with distal arterial occlusion pressure where collateral flow = (0.6) (distal pressure) + 0.8 ml/ min/ 100g (r=0.69; p<0.005; Figure 1).Figure 1Discussion. Pressure-dependent collateral cerebral perfusion exists during non-pulsatile CPB over a clinically applicable range of aortic pressures, supporting the concept of maintaining elevated aortic pressures during CPB in high-risk patients. In this study, perfusion pressure was augmented by increasing pump flow; perfusion pressure could be elevated by infusing a vasoconstrictor although at the potential risk of splanchnic hypoperfusion [3].

Thoracoabdominal aortic aneurysm repair in high risk cardiac patients: A modified grafting technique

Thoracoabdominal aortic aneurysm repair in high risk cardiac patients: A modified grafting technique

The myocardial sodium-hydrogen exchanger (NHE) and its role in mediating ischemic and reperfusion injury.

A major mechanism by which the heart adapts to intracellular acidosis during ischemia and recovers from the acidosis after reperfusion is through the sodium-hydrogen exchanger (NHE). There are at least 5 NHE isoforms thus-far identified with the NHE-1 subtype representing the major one found in the mammalian myocardium. This 110 kDa glycoprotein extrudes protons concomitantly with Na influx in a 1:1 stoichiometric relationship rendering the process electroneutral. Although NHE is critical for the maintenance of intracellular pH during acid loading conditions such as ischemia, there is convincing evidence that it also plays a pivotal role in mediating tissue injury during ischemia and reperfusion. The mechanism for this paradoxical deleterious role of NHE reflects the fact that under conditions of tissue stress, including ischemia, Na-K adenosine triphosphate (ATP)ase is inhibited thereby limiting Na extrusion resulting in an elevation in intracellular Na concentrations. The latter effect, in turn, will increase intracellular Ca concentrations via Na-Ca exchange. In addition, NHE-1 expression in the diseased myocardium is increased suggesting that elevated production of the antiporter represents a long-term adaptive process in an attempt by the cardiac cell to regulate intracellular pH which, paradoxically, contributes to cardiac pathology. Extensive studies using NHE inhibitors such as amiloride or its analogs, or more specific compounds including 3-methylsulphonyl-4-piperidinoloenzoyl-guanidine methanesulphonate (HOE 694) or 4-isopropyl-3-methylsulphonylbenzcyl-guanidine methane sulphonate (HOE 642) have consistently shown protective effects against ischemic and reperfusion injury in a large variety of experimental models and animal species particularly in terms of attenuating contractile dysfunction. Such studies have contributed greatly to the overwhelming evidence that NHE activation mediates ischemic and reperfusion injury. Indeed, HOE 642 (Cariporide) is currently undergoing clinical evaluation in high risk cardiac patients. Moreover, there is now emerging evidence that NHE may be involved in mediating cardiotoxicity directly produced by various ischemic metabolites such as lipid amphiphiles or reactive oxygen species. In this regard, we have demonstrated that NHE inhibitors can effectively attenuate the cardiac injury produced by lysophosphatidylcholine and hydrogen peroxide. In addition, it now appears that NHE inhibition reduces apoptosis in the ischemic myocardium, a process which may be of importance in the subsequent development of postinfarction heart failure. In conclusion, NHE represents an important adaptive process in response to intracellular acidosis resulting in a paradoxical contribution to cardiac tissue injury.

Pathophysiological and clinical aspects of the CO2 pneumoperitoneum (CO2-PP).

Experimental studies demonstrated a severe cardiac load of the CO2 pneumoperitoneum caused by an accelerated after- and a decreased preload. Patients displaying cardiovascular risks are therefore often rejected from laparoscopic surgery. Hence, the pathophysiological changes and the intraoperative risk of the CO2 pneumoperitoneum in high-risk cardiopulmonary patients (NYHA II-III, n = 15) undergoing laparoscopic cholecystectomy are described. The changes in cardiac after- and preload seem to be due to the elevated intraabdominal pressure rather than transperitoneally resorbed CO2 and are reversible by desufflation. In one patient conversion to open operation had to be performed because of a severe drop in cardiac output and right ventricle ejection fraction. Mixed oxygen saturation was predicting intraoperative worsening in this case. The described pathophysiological changes may seem to be well tolerated even in high-risk cardiac patients. Monitoring of hemodynamics should include an arterial catheter line and blood gas analyses. Pharmacologic interventions or pressureless laparoscopic procedures might not be necessary as long as laparoscopic cholecystectomy is performed.

Rationale and specifications for an automatic cardiac arrest-driven alarm and 911 caller ID (ACADA/911)

The rationale and specifications for a permanent non-invasive cardiac monitoring device are described, including both an alarm and a device-initiated call (giving patient residence identification) to the emergency services number 911, if cardiac arrest is detected. This device may be useful for high-risk cardiac patients, who incur an unwitnessed cardiac arrest, by providing a prompt call and alarm for early initiation of bystander CPR, cardiac defibrillation (if necessary), advanced cardiac life-support, and early transfer of resuscitated patients to a hospital cardiac care unit. Unwitnessed cardiac arrest patients otherwise have a dismal prognosis because of prolonged circulatory arrest times and late initiation of defibrillation attempts. With out-of-home unwitnessed cardiac arrest, ACADA-911 specifications also include a cardiac arrest-triggered determination of the patient's location through a commercially inexpensive global positioning system device, whose output is transmitted to EMS via an attached cellular phone/priority call network. A randomized controlled study evaluation of the device is proposed.

Clinical Transesophageal Echocardiography

Assistant Professor, Section on Cardiac Anesthesia, Bowman Gray School of Medicine of Wake Forest University, Medical Center Boulevard, Winston-Salem, North Carolina 27157.James C. Eisenach, M.D., EditorClinical Transesophageal Echocardiography: A Problem-Oriented Approach, by Yaso Oka and Stephen N. Konstadt. Philadelphia, New York, Lippincott-Raven Publishers, 1996. Pages: 382. Price: $149.00.Clinical Transesophageal Echocardiography is a first-edition hard-bound text designed to highlight the many useful applications of transesophageal echocardiography in the care of high-risk cardiac and general surgical patients. The book is intended as an educational tool for the intermediate and advanced level echocardiographer and provides specific examples of how to use transesophageal echocardiography in the care of complex surgical patients.The book is organized in two major sections, with the first section covering applications of transesophageal echocardiography in the cardiac surgery patient and the second discussing applications in the noncardiac surgical patient. An impressive variety of applications of transesophageal echocardiography are covered in each section, including key chapters on evaluation of rheumatic and ischemic mitral valve disease, evaluation of aortic plaque and dissection, and use of transesophageal echocardiography in the hypotensive patient. Additional, less frequently considered, uses for transesophageal echocardiography are well covered, including such applications as liver transplantation and resection and lung transplantation. Each chapter is organized in a problem-oriented approach, with a background discussion of the lesion, its pathophysiology and surgical treatment, and a case example focusing on the echocardiographic evaluation of the lesion. In each case example, the echocardiographic findings and their importance to the care of the patient are well described.The book contains many excellent echocardiographic images and diagrams that serve as a helpful guide to the reader in increasing understanding. The chapter on hypertrophic obstructive cardiomyopathy is particularly well illustrated, with excellent echocardiographic images and diagrams of the surgical treatment. Each chapter is well referenced, and the book contains a useful bibliography.Although each chapter describes the mechanics of performing the various echocardiographic evaluations, this text is not suited for the beginning echocardiographer, and assumes the reader has some baseline knowledge of the transesophageal echocardiograpic examination.Overall, Clinical Transesophageal Echocardiography: A Problem Oriented Approach, is a well organized and well written text, which highlights, using a case example format, many important uses of transesophageal echocardiography in the care of surgical patients. This text is a useful companion to Dr. Oka's previous textbook, entitled Transesophageal Echocardiography, which nicely demonstrates the basic aspects of the transesophageal echocardiography examination. Echocardiographers at the intermediate level and beyond will find this a useful tool to further their skills in the application and interpretation of echocardiograms in a wide variety of surgical patients.Robert Brooker, M.D., Assistant Professor, Section on Cardiac Anesthesia, Bowman Gray School of Medicine of Wake Forest University, Medical Center Boulevard, Winston-Salem, North Carolina 27157.

Temporary axillofemoral bypass: Its use in high risk cardiac patients requiring urgent abdominal aneurysm repair: A.G. Lossing and E.M. Hatswell. Welksley Hospital, Toronto, Ontario, Canada. Can J Cardiol 1996;12:467–8

The creation of a temporary axillofemoral bypass in a patient undergoing surgery for an 8.1 cm symptomatic infrarenal aortic aneurysm is described. This adjunctive procedure, rarely used in abdominal aortic surgery, may have contributed to minimizing variations in afterload in a patient with a 20% ejection fraction and severe mitral regurgitation.

Application of chaos theory to a model biological system: evidence of self-organization in the intrinsic cardiac nervous system.

The neutral organization that determines the specific beat-to-beat pattern of cardiac behavior is expected to be demonstrated in the independent regulation of the RR intervals (chronotropy) and the corresponding QT subintervals (inotropy), as the former defines the rate of contraction and the latter has a linear negative correlation with the peak pressure inside the contracting ventricular muscles. The neurons of the isolated cardiac nervous system, many of which are located in the fat-pads of the heart, exhibit the same types of mechanical and chemical receptors and the same types of cholinergic and noradrenergic effectors as those found in the neural superstructure. In the surgically isolated and perfused rabbit heart we studied the responses of the QT and RR intervals evoked by block of coronary blood flow. We found that if we separated each RR cycle into QT and RR-QT components, then the dynamics of variation for each subinterval series often had the same fractional number of degrees of freedom (i.e., chaotic dimensions), a finding which suggests they are both regulated by the same underlying system. The ischemia/anoxia evoked transient dimensional increases and separations between the two subinterval series that, after the temporary divergence, reconverged to having the same lower value. The dimensional fluctuations occurred repeatedly and preceded or coincided with alterations in the magnitude and sign of the slope of QT vs RR-QT. We interpret the dimensional fluctuations of the two subinterval series as correlates of adaptation-dependent self-organization and reorganization in the underlying intrinsic cardiac nervous system during accumulating ischemia/anoxia. Such attempts at functional reorganization in this simple neurocardiac system may explain the transient dimensional changes in the RR intervals that precedes by 24 hrs the occurrences of fatal ventricular fibrillation in high-risk cardiac patients.