Spontaneous gasping produces carotid blood flow during untreated cardiac arrest

We have shown previously that arginine vasopressin (AVP) given during sinus rhythm increases mean arterial blood pressure (MAP) and left anterior descending (LAD) coronary artery cross sectional area. AVP was assumed to result in vasodilatation via activation of the endothelial nitric oxide system. The purpose of the present study was to assess the effects of AVP before and after NO-inhibition. Nine domestic pigs were instrumented for measurement of haemodynamic variables using micromanometer-tipped catheters, and measurement of LAD coronary artery cross sectional area employing intravascular ultrasound (IVUS). Haemodynamic variables, LAD coronary artery cross sectional area and cardiac output were measured at baseline, 90 s and 5, 15, and 30 min after AVP (0.4 U kg (-1) IV) before and after blockade of nitric oxide synthase with N(G)-nitro L-arginine methyl ester (L-NAME). Compared with baseline, AVP significantly increased MAP after 90 s (89+/-4 versus 160+/-5 mm Hg), increased LAD coronary artery cross sectional area (11.3+/-1 versus 11.8+/-1 mm(2)) and decreased cardiac index (138+/-6 versus 53+/-6 mL/min kg(-1)). After blockade of nitric oxide synthase, AVP significantly increased MAP after 90 s (135+/-4 versus 151+/-3 mm Hg), increased LAD coronary artery cross sectional area (8.7+/-1 versus 8.9+/-1 mm(2)), and significantly decreased cardiac index (95+/-6 versus 29+/-4 mL/min kg (-1)). IMPLICATIONS: During sinus rhythm, AVP increased MAP and LAD coronary artery cross sectional area, but decreased cardiac index.     

Incidence and significance of gasping or agonal respirations in cardiac arrest patients

PURPOSE OF REVIEW: This review examines the clinical significance of agonal respirations associated with cardiac arrest. RECENT FINDINGS: Observational data indicate that agonal respirations are frequent (55% of witnessed cardiac arrests and probably higher) and that they are associated with successful resuscitation. They also are found more commonly in ventricular fibrillation compared with other rhythms. Agonal respirations pose the greatest challenge to bystanders at the scene and to emergency dispatchers. Bystanders are often lulled into thinking the person is still breathing thus identification of cardiac arrest may be missed by the dispatcher. In a study from King County, Washington, cardiopulmonary resuscitation instructions were not provided by emergency dispatchers in 20% of cardiac arrest cases because the caller reported signs of life - typically abnormal breathing. SUMMARY: Agonal respirations occur frequently in cardiac arrest. Emergency dispatchers and the general public must be more aware of their presence and significance.     

Dye circulation times during cardiac arrest

Dye dilution curves have been used to calculate cardiac output under conditions of normal circulation. Unfortunately, these curves cannot be integrated easily to determine cardiac output under the low flow states of CPR. The time to initial dye appearance (circulation time), may be useful in judging relative changes in flow when studying experimental resuscitation techniques. The purpose of this study was to investigate the relationship between dye circulation times and other hemodynamic measures during CPR. Repeated measurements of coronary perfusion pressure, dye circulation times, blood gases, and end-tidal CO2 (ETCO2) were made in dogs undergoing CPR. Dye circulation time was significantly associated with the systolic, diastolic, and coronary perfusion pressures. The correlation between circulation time and ETCO2 was -0.70 (P less than 0.0001). There was no correlation with the arterial-venous PO2 gradient. There were significant correlations between the circulation time and both the A-V PCO2 and the A-V pH gradients. We conclude that dye circulation times may be used to gauge relative changes in blood flow during CPR, particularly in laboratory investigations involving repeated measurements.     

Spontaneous variability of cardiac output in ventilated critically ill patients

OBJECTIVE: To define the magnitude of spontaneous cardiac output variability over time in sedated medical intensive care unit patients attached to a continuous cardiac output monitor, and to determine whether high level positive end-expiratory pressure or inverse inspiratory-to-expiratory (I:E) ratio ventilation resulted in greater variability over time than low positive end-expiratory pressure with conventional I:E ratio ventilation. DESIGN: Prospective study. SETTING: Medical intensive care unit in a tertiary medical center. PATIENTS: A total of 22 hemodynamically stable acute respiratory failure patients with a pulmonary artery catheter inserted for hemodynamic monitoring INTERVENTIONS: After being sedated, patients were randomized ultimately to receive pressure control ventilation first at setting A (high positive end-expiratory pressure [15 cm H2O] with conventional I:E ratio [1:2]) and then at setting B (low positive end-expiratory pressure [5 cm H2O] with inverse I:E ratio [2:1]), or vice versa, and then at setting C (low positive end-expiratory pressure [5 cm H2O] with conventional I:E ratio [1:2]). Each ventilation setting period lasted 1 hr. MEASUREMENTS AND MAIN RESULTS: Cardiac output (CO) was measured continuously. The continuous CO value displayed was updated every 30-60 secs. The updated value reflected an average of the previous 3-6 mins. The coefficient of variation (CV) of CO for each setting in each patient was calculated to represent the spontaneous variability. The mean CO+/-SD and CV of each setting was 5.7+/-1.8 L/min and 4.4% for setting A, 5.6+/-1.5 L/min and 4.6% for setting B, and 5.9+/-1.7 L/min and 4.8% for setting C. Analysis of variance revealed no significant differences between the CVs of the three settings. The 95% confidence interval for the COs for each setting was approximately the mean CO+/-0.1 x mean CO measured. CONCLUSIONS: In critically ill sedated medical intensive care unit patients with stable hemodynamics, the spontaneous variability of cardiac output over time was not significant. High positive end-expiratory pressure (15 cm H2O) and inverse ratio ventilation (2:1) did not contribute to increased spontaneous variability of cardiac output.     

Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest.

OBJECTIVE: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest. DESIGN: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features. RESULTS: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome. CONCLUSIONS: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.     

Hemodynamic-directed cardiopulmonary resuscitation during in-hospital cardiac arrest

Cardiopulmonary resuscitation (CPR) guidelines assume that cardiac arrest victims can be treated with a uniform chest compression (CC) depth and a standardized interval administration of vasopressor drugs. This non-personalized approach does not incorporate a patient's individualized response into ongoing resuscitative efforts. In previously reported porcine models of hypoxic and normoxic ventricular fibrillation (VF), a hemodynamic-directed resuscitation improved short-term survival compared to current practice guidelines. Skilled in-hospital rescuers should be trained to tailor resuscitation efforts to the individual patient's physiology. Such a strategy would be a major paradigm shift in the treatment of in-hospital cardiac arrest victims.     

Cerebral function and preservation during cardiac arrest

Neurologic impairment remains a serious consequence of cardiac arrest. While current investigations are difficult to compare due to their lack of standardization, our understanding of the pathophysiology of CNS ischemia has been greatly increased. Ion fluxes, especially K and Ca, may contribute to injury by initiating a cascade of events culminating in free fatty acid, prostaglandin, and free radical formation, with their related pathogenetic potential. Treatment measures currently consist of CPR (although disagreement exists as to which form of CPR), standard supportive measures, and attention to intracranial pressure control. There is some experimental evidence to support the use of calcium channel-blockers, phenytoin, prostaglandin inhibitors, and free-radical scavengers or inhibitors; however, no human trials have been performed. Steroids and barbiturates have been investigated in human trials and do not appear to be efficacious in ameliorating CNS injury after cardiac arrest.