Characteristics of cardiac arrest in cancer patients as a predictor of survival after cardiopulmonary resuscitation.

BACKGROUND: Despite advances in cardiopulmonary resuscitation and the education of its providers, survival remains dismal for cancer patients suffering in-hospital cardiac arrest. In an effort to determine if characteristics of cardiac arrest would represent a useful parameter for prognostication and recommendations regarding the suitability of ongoing resuscitation for various groups, this review was undertaken for patients who experienced in-hospital cardiac arrest. METHODS: A retrospective study of data gathered between January 1993 and December 1997 was undertaken in a 518-bed comprehensive cancer center. The records of 243 inpatients who experienced cardiac arrest and received cardiopulmonary resuscitation were reviewed, and their course observed until hospital discharge or death. RESULTS: Sixteen of 73 patients (22%) who had sudden, unanticipated cardiac arrests survived to be discharged from the hospital; however, none (0 of 171) of the patients who experienced an anticipated cardiac arrest survived (P < 0.001). Logistic regression analysis revealed that anticipated cardiac arrest associated with metabolic derangement was an independent predictor of hospital mortality. CONCLUSIONS: Patients experiencing an anticipated cardiac arrest, the course of which could not be interrupted through aggressive management in an intensive care unit, have an extremely poor prognosis. Ongoing resuscitative measures in these patients need not be routinely provided. The authors suggest an algorithm for resuscitation that evaluates the characteristics of the arrest as a prognostic factor. This algorithm should be implemented once progressive deterioration spirals toward cardiac arrest that cannot be prevented. Such an approach should avoid painful and costly interventions that are futile with the present techniques of cardiopulmonary resuscitation.

Monitoring ventilator weaning--predictors of success.

Improving the prediction of successful ventilator weaning and extubation is a goal that all Intensivists and perioperative physicians strive for. The successful wean and extubation of ventilated patients decreases hospital length of stay and associated costs, but more importantly it also reduces patient morbidity and mortality. This review evaluates traditional and novel indices used in the assessment for ventilatory wean readiness. Novel equipment such as the Bicore pulmonary monitor and the CO2 SMO Plus are now available on the market to assess and monitor ventilator weaning and may offer some value in this process. We also review the non-respiratory factors affecting weaning and the role of the bedside nurse and respiratory therapist. Resolution of the pulmonary compromise and an understanding of respiratory physiology, used in conjunction with monitored indices of weaning parameters in a consistent fashion will continue to improve our success rates of ventilator weaning and extubation.

Management of perioperative arrhythmias.

Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of arrhythmias remains the most important use of this technology today. Several predisposing factors tend to emerge when perioperative arrhythmias are evaluated. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculocardiac reflex, stimulation of the central nervous system, the presence of preexisting heart disease, and the use of intracardiac devices. In the evaluation of cardiac arrhythmias, several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery that may explain the arrhythmia. In addition, it is vital to evaluate the heart rate, the regularity, the number of P waves per QRS, and the configuration of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. Prompt evaluation and management of perioperative arrhythmias reduce anesthetic morbidity and mortality. This article reviews the causes and pharmacological treatment of major abnormalities of atrial and ventricular cardiac arrhythmias occurring in the perioperative period.

Management of perioperative dysrhythmias.

This paper reviews cardiac dysrhythmias occurring in the perioperative period. Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of dysrhythmias remains the most important use of this technology today. While the description of dysrhythmias dates back to the early 1900's, the first large series was reported in 1936. Early descriptions of the kinds seen and the predisposing factors have changed little in the past 50 years. Several factors tend to emerge when one evaluates perioperative dysrhythmias. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculocardiac reflex, stimulation of the central nervous system the presence of pre-existing heart disease, and the use of intracardiac devices. In the evaluation of cardiac dysrhythmias several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery which may explain the dysrhythmia. In addition, one needs to evaluate the heart rate, the regularity, the number of P waves per QRS, and the configurations of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. The two major abnormalities of sinus rhythm are sinus bradycardia and the sinus tachycardia. Sinus bradycardia can be due to hypoxia, vagal stimulation, drug effects, a high sympathetic block or an acute myocardial infarction. Sinus tachycardia can be due pain, light anesthesia, hypovolemia, sepsis, hypoxia, hypercapnia and drug effects. The major atrial dysrhythmias are paroxysmal atrial tachycardia, atrial fibrillation and atrial flutter. Each require treatment if perfusion is impaired or if the heart rate is persistently elevated. The new agents esmolol and adenosine are particularly useful in managing atrial dysrhythmias. The major ventricular dysrhythmias are ventricular premature contractions, ventricular tachycardia and ventricular fibrillation. The later two demand emergency management with DC cardioversion when perfusion is impaired. The major abnormality of conduction is complete heart block which usually requires emergency treatment in the perioperative period. Prompt evaluation and management of perioperative dysrhythmias reduce anesthetic morbidity and mortality.

The anesthesiologist's role in cardiac transplantation.

Cardiac transplantation has become an increasingly common operation and many patients who have transplanted hearts may require anesthetic care at any time. Management of the recipient is similar to managing any patient with severe cardiac failure before the new heart is implanted. Following transplantation the problems are those of the denervated heart and the problems associated with the immunosuppressive agents used for transplantation.

Coagulopathies and the intensive care setting.

The preservation of vascular integrity and blood flow is essential for vital functions. The dynamic equilibrium between bleeding and clotting can be set awry by stimulation of the inflammatory or immune response or by unchecked activation of the coagulation or fibrinolytic systems. It is through greater understanding of the complex interplay between these pathways that we are able to develop agents that can, with increasing specificity, manipulate coagulation and restore hemostasis.

Comparison of the respiratory depressant effects of halothane and isoflurane in routine surgery.

Respiratory depression has been studied in 21 patients anaesthetized with either halothane and nitrous oxide, or isoflurane and nitrous oxide while undergoing routine surgery. Spontaneous ventilation was preserved and the end-tidal concentrations of the two volatile anaesthetics were at approximately equal MAC-multiples. The minute volume of pulmonary ventilation was not significantly different for the two anaesthetics, but tidal volume was significantly greater and frequency significantly lower with isoflurane. Arterial and end-tidal PCO2 were consistently lower in the patients receiving isoflurane, the difference being significant in many of the sub-groups. There was no evidence of a progressive increase in PCO2 with either anaesthetic during surgery lasting up to 225 min. Mean values for PCO2, however, tended to be well above the normal reference range, with mean arterial PCO2 in the range 7.2-8.6 kPa.

The effect of human antiendotoxin monoclonal antibodies on endotoxin-induced lung injury in the rat.

A model of endotoxin-induced lung injury was developed in the rat. We found that 24 h after intravenously administered endotoxin (3 mg/kg) there was increased clearance of the isotope 99mTcDTPA from the lung to blood, increased neutrophils in the lung in bronchoalveolar lavage, and increased levels of products of peroxidation of lipids and nucleic acid in the serum. Using this model, we evaluated the effect of pretreatment of rats with a human monoclonal antibody specific to the core glycolipid that is common to all endotoxins. We found that pretreatment prevented the increased clearance of 99mTcDTPA from the lung, as well as the increase in lipid peroxidation products in the serum. The antibody did not prevent increased neutrophil accumulation in the lung. The findings suggest that the administration of human antiendotoxin monoclonal antibodies prior to endotoxemia may prevent some of the changes in the lung associated with endotoxin.

Cardiovascular effect of intravenous lipid A in rabbits.

The in vivo cardiovascular effect of intravenous administration of monophosphoryl lipid A (mp-lipid A) and diphosphoryl lipid A (dp-lipid A) in awake New Zealand white rabbits was investigated. Observed changes were evaluated in comparison to a control group and an endotoxin-treated group. Rabbits given lipid A showed a significant depression in cardiac index (p less than .025), mean arterial pressure (p less than .025, dp-lipid A only), arterial carbon dioxide tension (p less than .025), and total leukocyte count (p less than .05) compared to controls. Animals receiving lipid A tended to respond overall in a manner closely matching that of the endotoxin group. Dosages of lipid A given were approximately 3.5 times larger than the endotoxin dosages with respect to actual number of molecules administered (1.25-2.0 times larger by mass). These results indicate that lipid A is active in producing the cardiovascular and leukopenic effects characteristic of experimental septic shock.

Leukotriene D4 increases extravascular lung water in the dog.

The peptide leukotrienes have been detected in animals that have received endotoxin injections and also have been associated with patients suffering from the adult respiratory distress syndrome (ARDS). The ability of leukotriene D4 (LTD4) to cause pulmonary capillary permeability changes was investigated in ten anesthetized mongrel dogs. Four dogs were used as controls and six dogs received intravenous LTD4 (0.25 microgram/kg). There was a variable response in that two treated animals showed no apparent effect of LTD4. Analysis of the results from the remaining four treated animals demonstrated a significant increase in extravascular lung water (EVLW) that peaked 3 hr after LTD4 from 5.4 +/- 0.6 to 10.3 +/- 0.5 ml/kg (P less than .01). In these four dogs, EVLW increased before slight, but statistically significant, rises in pulmonary artery wedge pressure (4 +/- 1 to 9 +/- 1 mm Hg, P less than .01) and mean pulmonary artery pressure (13 +/- 1 to 17 +/- 1 mm Hg, P less than .01) occurred. During the same period, cardiac output decreased 56 +/- 7% (P less than .01), but no change in airway resistance was observed. This study is the first in vivo demonstration that LTD4 directly alters pulmonary fluid balance in the dog. We conclude LTD4 can cause increases in EVLW and may be an important mediator of the permeability changes observed in various clinical events that lead to the adult respiratory distress syndrome.

Thermal dye double indicator dilution measurement of lung water in man: comparison with gravimetric measurements.

The thermal dye double indicator dilution technique for estimating lung water was compared with gravimetric analyses in nine human subjects who were organ donors. As observed in animal studies, the thermal dye measurement of extravascular thermal volume (EVTV) consistently overestimated gravimetric extravascular lung water (EVLW), the mean (SEM) difference being 3.43 (0.59) ml/kg. In eight of the nine subjects the EVTV -3.43 ml/kg would yield an estimate of EVLW that would be from 3.23 ml/kg under to 3.37 ml/kg over the actual value EVLW at the 95% confidence limits. Reproducibility, assessed with the standard error of the mean percentage, suggested that a 15% change in EVTV can be reliably detected with repeated measurements. One subject was excluded from analysis because the EVTV measurement grossly underestimated its actual EVLW. This error was associated with regional injury observed on gross examination of the lung. Experimental and clinical evidence suggest that the thermal dye measurement provides a reliable estimate of lung water in diffuse pulmonary oedema states.

The thermal-dye method of lung water measurement is reliable at a low cardiac output.

The measurement of lung water by the thermal-dye double indicator dilution technique was evaluated in dogs with normal and edematous lungs during a state of reduced cardiac output. The technique used cold indocyanine green dye to measure extravascular thermal volume (EVTV) as an estimate of extravascular lung water (EVLW). Anesthesia was maintained with pentobarbital. In 15 of 21 animals, pulmonary edema was first induced with oleic acid (0.75 to 0.18 ml/kg). Cardiac output (CO) was then decreased by a combination of propranolol and slow exsanguination (mean CO reduction to 36% of baseline). Extravascular lung water produced in this model ranged from 1.4 to 30.2 ml/kg. Predetermination measurements of EVTV correlated closely with EVLW as determined by gravimetric analysis (EVTV = 1.1 EVLW + 4.7 ml/kg, n = 21, r = 0.93, P less than 0.001). Thermodilution cardiac output measured in the abdominal aorta (used in the calculation of the EVTV) correlated well with simultaneous measurements of cardiac output by both indocyanine green dye dilution and pulmonary artery thermodilution (r = 0.86 and r = 0.88, respectively, pretermination). The thermal-dye technique appears to provide an accurate reflection of lung water in normal and edematous lungs, even in the presence of a low cardiac output.

Hypothermic preservation of the heart and lungs with Collins solution: effect on cardiorespiratory function following heart-lung allotransplantation in dogs.

The effect of preserving the heart and lungs with hypothermia and Collins solution was studied in 13 mongrel dogs undergoing combined heart-lung transplantation. The five control animals who underwent an immediate transplant following Collins solution perfusion had small increases in extravascular lung water when measured 2.5 hours posttransplant as seen in a previous study. The eight animals who had hypothermic preservation following Collins solution perfusion had significantly higher extravascular lung water than controls (16.3 +/- 1.8 ml/kg in preserved animals; 11.2 +/- 1.7 ml/kg in controls p less than 0.05). The level of lung water reached at 2.5 hours postoperatively was similar to that reached with a previously reported, unacceptable preservation technique. Survival beyond this point was poor due to severe pulmonary edema. We conclude that the use of this solution, given under the experimental conditions which we describe, is not acceptable for hypothermic preservation of the heart and lungs for combined transplantation.