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Ischemic spinal cord damage from cardiac arrest is rare. A 48-year-old man underwent a straightforward retroperitoneal aortofemoral bypass operation. The following day, he developed cardiac arrest and was resuscitated successfully, but permanent paraplegia was observed soon afterwards.
OBJECTIVE: To evaluate the frequency, presentation and outcome of non-traumatic aortic dissection/rupture as a cause of cardiac arrest. DESIGN: Retrospective analysis of a cardiac arrest registry in a tertiary care hospital emergency department. RESULTS: Over 11.5 years, aortic dissection/rupture was identified as the immediate cause of cardiac arrest in 46 (2,3%) out of 1990 patients with sudden cardiac arrest, primarily affecting the abdominal aorta in 25 and the thoracic aorta in 21 cases. The characteristics of the 46 patients were as follows: male gender (74%), median age 71 years (IQR 59-76), high co-morbidity (89%), previously known aortic aneurysm (33%), pulseless electric activity (70%) as initial cardiac rhythm. When performed, bedside abdominal sonography or echocardiography was almost always diagnostic. Patients with abdominal aortic dissection/rupture had abdominal (52%) and/or flank pain (32%). Patients with thoracic aortic dissection/rupture complained of chest pain (48%) or dyspnoea (19%). Return of spontaneous circulation occurred in 12 (26%) of 46 patients, emergency surgery was performed in eight of these patients, 2 (4%) survived to discharge in good neurological condition. CONCLUSIONS: Cardiac arrest caused by aortic dissection/rupture is rare, and mortality remains very high, even when circulation can be restored initially. Common features such as previously known aortic aneurysm, old age, male gender and pulseless electrical activity as initial cardiac rhythm should increase suspicion of the condition.
OBJECTIVE: Methylene blue (MB), a free-radical scavenger inhibiting the production and actions of nitric oxide, may counteract excessive vasodilatation induced by nitric oxide during cardiac arrest. Effects of MB in cardiac arrest and cardiopulmonary resuscitation were investigated. DESIGN: Randomized, prospective, laboratory animal study. SETTING: University animal research laboratory. SUBJECTS: A total of 63 piglets of both sexes. INTERVENTIONS: A pig model of extended cardiac arrest (12 mins of untreated cardiac arrest and 8 mins of cardiopulmonary resuscitation) was employed to assess the addition or no addition of MB to a hypertonic saline-dextran solution. These two groups (MB and hypertonic saline-dextran group [MB group] and hypertonic saline-dextran-only group) of 21 animals were each compared with a group receiving isotonic saline (n = 21). MEASUREMENTS AND MAIN RESULTS: Although the groups were similar in baseline values, 4-hr survival in the MB group was increased (p = .02) in comparison with the isotonic saline group. Hemodynamic variables were somewhat improved at 15 mins after restoration of spontaneous circulation in the MB group compared with the other two groups. The jugular bulb levels of 8-isoprostane-prostaglandin F2alpha and 15-keto-dihydro-prostaglandin F2alpha (indicators of peroxidation and inflammation) were significantly decreased in the MB group compared with the isotonic saline group. Significant differences were recorded between the three groups in levels of protein S-100beta (indicator of neurologic injury), with lower levels in the MB group compared with the isotonic saline and hypertonic saline-dextran-only groups. Troponin I and myocardial muscle creatine kinase isoenzyme arterial concentrations (indicators of myocardial damage) were also significantly lower in the MB group. CONCLUSIONS: MB co-administered with a hypertonic-hyperoncotic solution increased 4-hr survival vs. saline in an experimental porcine model of cardiac arrest and reduced oxidative, inflammatory, myocardial, and neurologic injury.
Emergency percutaneous cardiopulmonary bypass support was instituted in 11 patients in cardiac arrest refractory to conventional resuscitation measures. Emergency percutaneous cardiopulmonary bypass support was used in five patients in whom cardiac arrest occurred as a result of a complication in the cardiac catheterization laboratory (group 1) and in six other patients in cardiac arrest (group II). A 21F cannula and a 17F cannula were percutaneously inserted into the femoral vein and artery. Flow rates of 3 to 5 L/min were achieved with restoration of mean arterial pressure to 70 mm Hg (range 50 to 75). The status of all 11 patients was improved initially both clinically and hemodynamically with percutaneous cardiopulmonary bypass. Of the group II patients, three had anatomy unsuitable for percutaneous transluminal coronary angioplasty or coronary bypass grafting, could not be weaned from cardiopulmonary support, and died; three of these patients had coronary artery bypass grafting and two survived. All five group I patients underwent successful coronary bypass grafting and survived. Of the seven patients with anatomically correctable disease, all seven were discharged from the hospital. With conventional management nearly all seven of these patients would have died. Nine of 11 patients underwent a cardiac operation and seven of the nine survived. The operative mortality rate was 22% and the overall survival rate was 64%. At follow-up (mean 7 months), all seven patients are alive and six have resumed a normal and active life-style. In conclusion, emergency percutaneous cardiopulmonary bypass support is a powerful resuscitative tool that may stabilize the condition of patients in cardiogenic shock and cardiac arrest to allow for definitive intervention.
The aim of this study was to observe cerebral and systemic oxygen extraction after human cardiac arrest with return of spontaneous circulation. Eight adult patients after non-traumatic, cardiac arrest were included. Cerebral and systemic oxygen extraction ratios were measured together with haemodynamic variables beginning 2 hours after cardiac arrest and every 4 hours thereafter until 24 hours. Between 2 and 12 hours after cardiac arrest cerebral oxygen extraction values ranged from very low over normal to very high. In the further course these values were reduced until 24 hours in six patients. Two patients who were still alive after 6 months, both severely mentally disabled, had a higher cerebral oxygen extraction ratios in comparison with non-survivors. Systemic oxygen extraction seemed to vary more than the cerebral oxygen extraction. The two long-term survivors had normal to supranormal values from 8 to 24 hours. In conclusion cerebral oxygen extraction was higher in long-term cardiac arrest survivors than in non-survivors between 12 and 24 hours after the event. Further, a better quality of neurological recovery was associated with higher cerebral oxygen extraction. Systemic oxygen extraction was also impaired, but to a lesser extent, especially in long-term survivors.
OBJECTIVES: Implantable cardioverter defibrillators (ICDs) are highly effective at preventing cardiac arrest, but their availability is limited by high cost. Automated external defibrillators (AEDs) are likely to be less effective, but also less expensive. We used decision analysis to evaluate the clinical and economic trade-offs of AEDs, ICDs, and emergency medical services equipped with defibrillators (EMS-D) for reducing cardiac arrest mortality. METHODS: A Markov model was developed to compare the cost-effectiveness of three strategies in adults meeting entry criteria for the MADIT II Trial: strategy 1, individuals experiencing cardiac arrest are treated by EMS-D; strategy 2, individuals experiencing cardiac arrest are treated with an in-home AED; and strategy 3, individuals receive a prophylactic ICD. The model was then used to quantify the aggregate societal benefit of these three strategies under the conditions of a constrained federal budget. RESULTS: Compared with EMS-D, in-home AEDs produced a gain of 0.05 quality-adjusted life-years (QALYs) at an incremental cost of $5225 ($104,500 per QALY), while ICDs produced a gain of 0.90 QALYs at a cost of $114,660 ($127,400 per QALY). For every $1 million spent on defibrillators, 1.7 additional QALYs are produced by purchasing AEDs (9.6 QALYs/$million) instead of ICDs (7.9 QALYs/$million). Results were most sensitive to defibrillator complication rates and effectiveness, defibrillator cost, and adults' risk of cardiac arrest. CONCLUSIONS: Both AEDs and ICDs reduce cardiac arrest mortality, but AEDs are significantly less expensive and less effective. If financial constraints were to lead to rationing of defibrillators, it might be preferable to provide more people with a less effective and less expensive intervention (in-home AEDs) instead of providing fewer people with a more effective and more costly intervention (ICDs).
INTRODUCTION: Cardiac arrest due to chest wall blows (commotio cordis) has been reported with increasing frequency in children, and only about 15% of victims survive. Automated external defibrillators (AEDs) have been shown to be life saving in adults with cardiac arrest, but data on their use in children are limited. In a swine model of commotio cordis designed to be most relevant to young children, we assessed the efficacy of a commercially available AED for recognition and termination of ventricular fibrillation. METHODS AND RESULTS: Ventricular fibrillation was produced in anesthetized juvenile swine by precordial impact from a baseball under controlled conditions. Animals were randomized to defibrillation after 1, 2, 4, or 6 minutes of ventricular fibrillation. Twenty-six swine underwent 50 ventricular fibrillation inductions. Sensitivity of the AED for recognition of ventricular fibrillation was 98%, and specificity for nonshockable episodes was 100%. All episodes of ventricular fibrillation were successfully terminated by the AED. CONCLUSION: In this experimental model of commotio cordis, the AED proved to be highly sensitive and specific for recognition of ventricular fibrillation and effective in terminating the arrhythmia and restoring sinus rhythm. These findings suggest that early defibrillation with the AED could save young lives on the athletic field.
OBJECTIVE: To compare the prognostic ability of sensory evoked potentials in cardiac arrest survivors with the outcome predicted by a panel of experienced emergency physicians based on detailed prehospital, clinical, and laboratory data. DESIGN: Inception cohort study. SETTING: Medical intensive care unit and department of emergency medicine at a university hospital. PATIENTS: A total of 162 unconscious, mechanically ventilated patients who survived > or =24 hrs after resuscitation from cardiac arrest. INTERVENTIONS: Recording of sensory evoked potentials and outcome prediction after review of detailed clinical and laboratory data by emergency physicians within 24 hrs after cardiac arrest. MEASUREMENTS AND MAIN RESULTS: At 6 months, the outcome of 36 patients was classified as favorable and 126 patients were rated as poor. After review of prehospital data, emergency physicians predicted favorable vs. poor outcome with a sensitivity of 70% and a specificity of 65%. After additional assessment of data 1 hr after cardiac arrest, the sensitivity of emergency physician predictions increased to 80%, whereas the specificity decreased to 48%. Outcome prediction by emergency physicians was most accurate after obtaining detailed patient data 24 hrs after cardiac arrest (sensitivity, 81%; specificity, 58%). In 35 of 36 patients with favorable outcomes, the cortical evoked potential N70 peak was detected between 72 and 128 msec. Of 113 patients with an N70 peak latency >130 msec or an absent N70 peak, all except one had a poor outcome. By using a cutoff of 130 msec, the N70 peak latency alone had a sensitivity of 94% and a specificity of 97%. The predictive accuracy of the N70 peak latency was significantly higher than the clinical assessment 24 hrs after cardiac arrest (91% vs. 76%, p = .0003). CONCLUSION: In unconscious cardiac arrest survivors, a recording of long-latency sensory evoked potentials is more accurate in predicting individual outcome than an emergency physician review of clinical data.
Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy.
We hypothesize that brain injury from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. We conducted a study to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron in low-molecular-weight species (LMWS iron) used the o-phenanthroline test on an ultrafiltered (molecular weight less than 30,000) tissue sample; malondialdehyde (MDA), a product of lipid peroxidation, in brain tissue was assayed by the thiobarbituric acid test (TBA). Samples of the parietal cortex from 11 nonischemic control dogs (Group 1) had LMWS iron levels of 9.6 +/- 4.9 nmol/100 mg tissue and MDA levels of 7.7 +/- 2.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 15 minutes of cardiac arrest (Group 2) had LMWS iron levels of 9.3 +/- 3.1 nmol/100 mg tissue and MDA levels of 6.1 +/- 1.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 45 minutes of cardiac arrest (Group 3) had LMWS iron levels of 6.7 +/- 3.3 nmol/100 mg tissue and MDA levels of 5.6 +/- 0.4 nmol/100 mg tissue. There was no significant difference among the three groups for either LMWS iron or MDA. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 4). Following resuscitation the chest was closed and the dogs were given intensive care for two hours.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Heart disease is the primary cause of mortality in Canada and survival to hospital discharge from out-of-hospital cardiac arrest is low. OBJECTIVE: To provide an overview of the outcomes for out-of-hospital cardiac arrest in Canada. METHODS: A national, descriptive, Utstein-style analysis of cardiac arrest care and emergency medical services was conducted. Data were compiled from five sources: the City of Edmonton Emergency Response Department, the British Columbia Ambulance Service, the Nova Scotia Emergency Health Services, the Urgences-santé corporation of the Montreal Metropolitan region and the Ontario Prehospital Advanced Life Support (OPALS) Study database. RESULTS: There were 5288 cardiac arrests from a range of small communities to large provincial cardiac arrest registries in 2002. They were men (62.6% to 70.1%) in their sixties and seventies, witnessed (35.2% to 55.0%), rarely receiving bystander cardiopulmonary resuscitation (CPR) (14.7% to 46.0%), often in asystole (35.7% to 51.3%), arresting at home (56.1%) and rarely surviving to hospital discharge (4.3% to 9.0%). Bystander CPR and early first responder defibrillation were significantly associated with increased survival. Cardiac arrest incidence rates per 100,000 varied between 53 and 59 among provinces and followed a downward trend. CONCLUSIONS: The results of this study could be an important first step toward a national cardiac arrest registry comparing the impact of regional differences in patient and system characteristics. Many communities do not have accurate data on their performance with regards to the chain of survival, or need to significantly improve their capacity for providing citizen bystander CPR and rapid first responder defibrillation.
Experimental data suggest that postischemic blood glucose concentration plays an important role in modulating both ischemic cerebral infarction and selective neuronal necrosis. This study investigated the association between functional neurological recovery and blood glucose concentrations in human cardiac arrest survivors. A group of 145 nondiabetic patients were evaluated after witnessed ventricular fibrillation cardiac arrest. Data regarding cardiac arrest were collected according to an internationally accepted protocol immediately after arrival. Blood glucose was measured on admission and 6, 12, and 24 h thereafter. To control for duration of cardiac arrest and cardiogenic shock, both known to influence outcome as well as blood glucose, levels, Spearman rank partial correlation was used. In this multivariate analysis, a high admission blood glucose level tended to be associated with poor neurological outcome (rs = -0.16, n = 142, p = 0.06). The association between high median blood glucose levels over 24 h and poor neurological outcome was strong and statistically significant (rs = -0.2, n = 145, p = 0.015). High blood glucose concentrations occurring over the first 24 h after cardiac arrest have deleterious effects on functional neurological recovery. Whether cardiac arrest survivors might benefit from reduction of blood glucose levels needs further investigation.
Sixty sudden and unexpected lethal cardiac arrests, with entirely negative findings on autopsy, were reported among 50,314 morbidly obese patients in the care of surgeons performing operations to achieve weight loss. This represented an extrapolated overall annual mortality rate of 65 deaths per 100,000 patients, about 40 times higher than the rate of unexplained cardiac arrests in a matched nonobese population. Eight sudden deaths occurred while waiting for obesity surgery and 22 had cardiac arrest within 10 days after the operation. Late postoperative deaths (more than 4 weeks postoperatively) occurred in 30 instances. A possible marker of a predisposition for sudden, unexpected cardiac arrest was an electrocardiographic abnormality; namely, a Q-Tc interval prolonged to greater than 0.43 seconds. This feature, present in 29 of 38 tracings, denoted increased susceptibility to malignant ventricular arrhythmias. The perioperative clustering of arrests implicated nonspecific stresses incident to otherwise uneventful operations as triggers of lethal dysrhythmias in the absence of organic cardiac disease. Anoxemia after abdominal surgery is an added hazard. Length of postoperative survival among the late deaths was found to be unrelated to degree of initial obesity or to magnitude of weight loss. Patients who died in the late postoperative phase were still grossly obese (mean weight 114.2 kg). Cardiac weights in patients who died within 10 postoperative days (12 patients) or after an average of 103 days (20 patients) were the same (464 and 469 g, respectively), indicating that myocardial mass had remained intact. The data do not suggest nutritional depletion or lean tissue loss as plausible explanations for the cardiac arrests. Screening and postoperative monitoring for Q-T interval prolongation is indicated. Prophylactic beta-blockade in this vulnerable subset of the morbidly obese population may be instituted in anticipation of obesity surgery. The attendant physiologic stresses should be minimized by appropriate measures.
BACKGROUND: Pulmonary embolism (PE) is a possible noncardiac cause of cardiac arrest. Mortality is very high, and often diagnosis is established only by autopsy. METHODS: In a retrospective study, we analyzed clinical presentation, diagnosis, therapy, and outcome of patients with cardiac arrest after PE admitted to the emergency department of an urban tertiary care hospital. RESULTS: Within 8 years, PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims. The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Pronounced metabolic acidosis (median pH, 6.95, and lactate level, 16 mmol/L) was found in most patients. In 18 patients (30%), the diagnosis of PE was established only postmortem. In 42 (70%) it was diagnosed clinically, in 24 of them the diagnosis of PE was confirmed by echocardiography. In 21 patients, 100 mg of recombinant tissue-type plasminogen activator was administered as thrombolytic treatment, and 2 (10%) of these patients survived to hospital discharge. Comparison of patients of the thrombolysis group (n = 21) with those of the nonthrombolysis group (n = 21) showed a significantly higher rate of return of spontaneous circulation (81% vs 43%) in the thrombolysis group (P=.03). CONCLUSIONS: Mortality related to cardiac arrest caused by PE is high. Echocardiography is supportive in determining PE as the cause of cardiac arrest. In view of the poor prognosis, thrombolysis should be attempted to achieve return of spontaneous circulation and probably better outcome.
OBJECTIVE: To determine the relative efficacy of high- vs standard-dose catecholamines in initial treatment of prehospital cardiac arrest. DESIGN: Randomized, prospective, double-blind clinical trial. SETTING: Prehospital emergency medical system of a major US city. PATIENTS: All adults in nontraumatic cardiac arrest, treated by paramedics, who would receive epinephrine according to American Heart Association advanced cardiac life support guidelines. INTERVENTIONS: High-dose epinephrine (HDE, 15 mg), high-dose norepinephrine bitartrate (NE, 11 mg), or standard-dose epinephrine (SDE, 1 mg) was blindly substituted for advanced cardiac life support doses of epinephrine. MAIN OUTCOME MEASURES: Restoration of spontaneous circulation in the field, admission to hospital, hospital discharge, and Cerebral Performance Category score. RESULTS: Of 2694 patients with cardiac arrests during the study period, resuscitation was attempted on 1062 patients. Of this total, 816 patients met study criteria and were enrolled. In the entire cardiac arrest population, 63% of the survivors were among the 11% of patients who were defibrillated by first responders. The three drug treatment groups were similar for all independent variables. Thirteen percent of patients receiving HDE regained a pulse in the field vs 8% of those receiving SDE (P = .01), and 18% of HDE patients were admitted to the hospital vs 10% of SDE patients who were admitted to the hospital (P = .02). Similar trends for NE were not significant. There were 18 survivors; 1.7% of HDE patients and 2.6% of NE patients were discharged from the hospital compared with 1.2% of SDE patients, but this was not significant (P = .37; beta = .38). There was a nonsignificant trend for Cerebral Performance Category scores to be worse for HDE (3.2) and NE patients (3.7) than for SDE patients (2.3) (P = .10; beta = .31). No significant complications were identified. High-dose epinephrine did not produce longer hospital or critical care unit stays. CONCLUSIONS: High-dose epinephrine significantly improves the rate of return of spontaneous circulation and hospital admission in patients who are in prehospital cardiac arrest without increasing complications. However, the increase in hospital discharge rate is not statistically significant, and no significant trend could be determined for neurological outcome. No benefit of NE compared with HDE was identified. Further study is needed to determine the optimal role of epinephrine in prehospital cardiac arrest.
The use of a high reliability cardiac arrest alarm utilising the continuously monitored values of patient heart rate and mean arterial blood pressure is described, based on a sample of 167 patients monitored for a total of 5116 h. The analogue heart rate and mean blood pressure signals are sampled at 1 s intervals, and a smoothing algorithm is applied to each of the resulting series which rejects artefacts, and identifies slope and step changes in each. Certain combinations of events in the 2 series, occurring within a preset time window, determine whether a cardiac arrest alarm or warning signal should be activated by the system. A total of 30 acute events occurring in 14 patients during the course of the study were each identified within 10 s. No cardiac arrest event was misdiagnosed by the algorithm during the period of the study. The algorithm also generates warnings which may have predictive value, and which will be the subject of further research. A final false alarm rate of about 1/200 h of monitoring was observed in adults (1/50 h in children), with evidence that these rates could be substantially improved.
BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.
Organ malfunction often occurs following cardiac arrest and resuscitation. Renal function, inulin clearance (Cln), was examined in 27 dogs before and after (days 2, 4, and 6) cardiac arrest and resuscitation. Group A (n = 7) had no ventricular fibrillation (VF), but cardiopulmonary support was applied for 20 min, and three transthoracic countershocks were delivered. In groups B (n = 7), C (n = 7), and D (n = 6) VF was induced for 2.5, 5.0, and 7.5 min, respectively, followed by cardiopulmonary support for 20, 20, and 15 min, respectively. When necessary, epinephrine and sodium bicarbonate were given during resuscitation. Countershock was applied for defibrillation. Kidneys were examined histologically in groups C and D. Following cardiac arrest, Cln was significantly less in the arrested groups compared to the nonarrested group. Within group C, which received the most epinephrine, Cln correlated negatively with epinephrine administration, and with the energy applied for defibrillation. Histologically, group C showed the highest incidence of cortical tubular cytoplasmic vacuolization, regeneration, inflammation, and tubular casts. Groups C and D showed outer medullary tubular cytoplasmic vacuolization, renal vascular changes, and calcification. In conclusion, cardiac arrest and resuscitation may precipitate acute renal hypofunction as well as reversible and irreversible morphological changes in normal functioning canine kidneys. The confounding effect of pre-existing renal disease remains to be examined experimentally.