Visceral, hematologic and bacteriologic changes and neurologic outcome after cardiac arrest in dogs. The visceral post-resuscitation syndrome.

We studied the post-resuscitation syndrome in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (< or = 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We reported previously, in the same dogs, no difference in resuscitability, mortality, or neurologic outcome between the three insult groups. There was no pulmonary dysfunction, but post-arrest cardiovascular failure, of greater severity in the 12.5 min arrest group. This report concerns renal, hematologic, hepatic and bacteriologic changes. Renal function recovered within 1 h after arrest, without permanent dysfunction. Clotting derangements at 1-24 h postarrest reflect transient disseminated intravascular coagulation with hypocoagulability, more severe after longer arrests, which resolved by 24 h after arrest. Hepatic dysfunction was transient but more severe in the animals that did not recover consciousness and correlated with neurologic dysfunction, but not with brain histologic damage. Bacteremia was present in all animals postarrest. We conclude that in the previously healthy organism after cardiac arrest of 7.5-12.5 min no flow, visceral and hematologic changes, although transient, can retard neurologic recovery.

Cardiovascular function and neurologic outcome after cardiac arrest in dogs. The cardiovascular post-resuscitation syndrome.

We studied cardiovascular changes and neurologic outcome at 72 h in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (< or = 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We found no difference in resuscitability, mortality, neurologic deficit scores, or overall performance categories between the three insult groups. There was no major pulmonary dysfunction. During controlled normotension post-CPR, all dogs presented a transient reduction in cardiac output. In the 12.5-min cardiac arrest group the decrease in cardiac output persisted beyond 12 h post-CPR (P < 0.01) and was associated with more severe arrhythmias (P < 0.05) and worse morphologic myocardial damage (P < 0.01). Both cardiac and neurologic malfunction at 72 h correlated with arrest time. Only cardiac malfunction correlated with CPR time. Neurologic recovery correlated with mild (inadvertent) pre-arrest hypothermia, diastolic arterial pressure during CPR and absence of cardiovascular impairment at 12 h post-CPR. We conclude that prolonged cardiac arrest in previously healthy dogs is followed by persistent cardiovascular derangements that correlate with impaired neurologic recovery.

Effects of combined superoxide dismutase and deferoxamine on recovery of brainstem auditory evoked potentials and EEG after asphyxial cardiac arrest in dogs.

In a randomized study in 23 dogs, we tested the following anti-free radical combination therapy, administered at the beginning of CPR, following apnea-induced cardiac arrest of 7 min: a) ventilation with 100% nitrogen for 30 s to allow the delivery of therapy before oxygen; b) superoxide dismutase (10 mg/kg i.a. followed by 10 mg/kg i.v. over 1 h) to scavenge the superoxide anion radical; and c) deferoxamine (20 mg/kg i.v. over 1 h) to prevent membrane lipid peroxidation. We evaluated the effects of this treatment on the recovery of cardiovascular and cerebral variables short term (6 h) after resuscitation. We reported previously that this treatment mitigated the post-arrest cerebral blood flow changes and enhanced the recovery of somatosensory evoked potentials. This is a secondary report from the same study concerning the effects of this treatment on the recovery of brainstem auditory evoked potentials (BAEPs) and EEG. Compared to control (n = 10), the experimental treatment (n = 10) did not exert a clearcut, significant effect on the recovery of BAEP which normalized in both groups at 1 h post-arrest and enhanced the post-arrest recovery of EEG spectra total power by reducing the post-arrest increase in slow frequency bands. However, the relative distribution of EEG frequencies never recovered the pre-arrest pattern in either group, during the 6 h post-arrest observation period. We conclude that the combination treatment tested enhances the recovery but does not normalize cerebral function post-arrest, suggesting that other treatments should also be entertained or that, indeed, such an insult may not be completely ameliorated by any such treatments.

Protective effects of combined superoxide dismutase and deferoxamine on recovery of cerebral blood flow and function after cardiac arrest in dogs.

Oxygen free radicals generated during reoxygenation after cardiac arrest may impair recovery of cerebral blood flow and function. In a randomized study in vivo, we tested the following anti-free radical combination therapy administered at the beginning of cardiopulmonary resuscitation after apnea-induced cardiac arrest of 7 minutes: 1) ventilation with 100% nitrogen for 30 seconds to allow the delivery of therapy before oxygen, 2) 10 mg/kg i.a. superoxide dismutase followed by 10 mg/kg i.v. over 1 hour to scavenge the superoxide anion radical, and 3) 20 mg/kg i.v. deferoxamine over 1 hour to prevent membrane lipid peroxidation. We evaluated the effects of this combined treatment on the recovery of cardiovascular variables, cerebral blood flow and oxygen consumption, and somatosensory evoked potentials in 20 dogs 6 hours after resuscitation. Compared with standard treatment (n = 10), the combined treatment (n = 10) did not affect cardiovascular variables, significantly mitigated cerebral blood flow changes after cardiac arrest, and enhanced recovery of somatosensory evoked potentials. We conclude that oxygen free radicals play a role in the pathogenesis of the arrest-related derangements of cerebral blood flow and function that are effectively reduced by this combined treatment; we recommend evaluation of its components in outcome studies.

Reliability of the vestibulo-ocular reflex as an index of the effects of hypnotic drugs on the central nervous system.

The vestibulo-ocular reflex was tested after the administration of step doses of thiopentone or propanidid in 171 unpremedicated patients. The dose of thiopentone (3 mg kg-1) required to induce loss of nystagmus also abolished the response to verbal command. The dose required to inhibit the reflex in 95% of patients was 7.22 mg kg-1 and prevented adrenergic responses to nociceptive stimulation. The dose of propanidid required to induce loss of nystagmus was greater than that necessary to abolish response to verbal command. The reflex inhibition rate increased proportionally to the dose up to 8 mg kg-1; larger doses exerted a facilitatory effect and reduced the reflex inhibition rate. The vestibulo-ocular reflex is a reliable and sensitive means of demonstrating the different effects exerted by step doses of hypnotic drugs.

Analogue chromatic continuous scale (ACCS): a new method for pain assessment.

A new pain rating scale, Analogue Chromatic Continuous Scale (ACCS), has been developed. The ACCS was tested in fifty consecutive patients suffering from pain of different origins, and compared with a simple descriptive scale (SDS) and a traditional 100 mm visual analogue scale (VAS). VAS and ACCS values showed a highly significant, positive correlation (r = 0.947, P less than 0.001). The means of the VAS and ACCS values, either considered as a whole or stratified according to SDS scores, did not differ significantly. The ACCS proved to be more sensitive than VAS (P less than 0.05), allowing a greater discrimination of grades of pain. Furthermore, the ACCS is very easy to use.

The treatment of hydrogen sulfide intoxication: oxygen versus nitrites.

A case of severe H2S intoxication, treated with oxygen, respiratory support and thiopental cerebral protection, is presented. The usual antidotal treatments using nitrites or oxygen are discussed, examining the risks of nitrite use and the efficacy of oxygen. The successful outcome of the case presented suggests that H2S poisoning be treated with oxygen and vigorous organ supportive care.