Arterial blood gases during cardiac arrest: markers of blood flow in a canine model.

Measures of CO2 have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pHa) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 min of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (PetCO2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pHa, PACO2 and PetCO2, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pHa and PaCO2 showed a significant correlation with cardiac output (pHa; R = -0.78, P less than 0.001 and PaCO2; R = 0.87, P less than 0.001) and with coronary perfusion pressure (pHa; R = -0.75, P less than 0.001 and PaCO2; R = 0.75, P less than 0.001). Eventual survivors (n = 15) had an early significant decrease in pHa, base excess and a significant increase in PaCO2 which was not present in non-survivors (n = 9). Neither pHa nor PaCO2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pHa and PaCO2 reflect systemic blood flow and reperfusion washout.     

Arterial carbon dioxide tension and outcome in patients admitted to the intensive care unit after cardiac arrest

Background

Arterial carbon dioxide tension (PaCO₂) affects neuronal function and cerebral blood flow. However, its association with outcome in patients admitted to intensive care unit (ICU) after cardiac arrest (CA) has not been evaluated.

Methods and results

Observational cohort study using data from the Australian New Zealand (ANZ) Intensive Care Society Adult-Patient-Database (ANZICS-APD). Outcomes analyses were adjusted for illness severity, co-morbidities, hypothermia, treatment limitations, age, year of admission, glucose, source of admission, PaO₂ and propensity score.We studied 16,542 consecutive patients admitted to 125 ANZ ICUs after CA between 2000 and 2011. Using the APD-PaCO₂ (obtained within 24 h of ICU admission), 3010 (18.2%) were classified into the hypo- (PaCO₂ < 35 mmHg), 6705 (40.5%) into the normo- (35–45 mmHg) and 6827 (41.3%) into the hypercapnia (>45 mmHg) group. The hypocapnia group, compared with the normocapnia group, had a trend toward higher in-hospital mortality (OR 1.12 [95% CI 1.00–1.24, p = 0.04]), lower rate of discharge home (OR 0.81 [0.70–0.94, p < 0.01]) and higher likelihood of fulfilling composite adverse outcome of death and no discharge home (OR 1.23 [1.10–1.37, p < 0.001]). In contrast, the hypercapnia group had similar in-hospital mortality (OR 1.06 [0.97–1.15, p = 0.19]) but higher rate of discharge home among survivors (OR 1.16 [1.03–1.32, p = 0.01]) and similar likelihood of fulfilling the composite outcome (OR 0.97 [0.89–1.06, p = 0.52]). Cox-proportional hazards modelling supported these findings.

Conclusions

Hypo- and hypercapnia are common after ICU admission post-CA. Compared with normocapnia, hypocapnia was independently associated with worse clinical outcomes and hypercapnia a greater likelihood of discharge home among survivors.     

End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest.

PURPOSE: To evaluate the use of end-tidal carbon dioxide values in predicting survival in cardiopulmonary arrest. BACKGROUND: The decision about when to terminate resuscitative efforts for patients with cardiopulmonary arrest is often subjective. End-tidal carbon dioxide values have been suggested as potential objective criteriafor making this decision. METHODS: This study was a cooperative effort of the St Louis chapter of the American Association of Critical-Care Nurses and its members and involved 6 hospitals and an air evacuation service. All adult patients who had a cardiopulmonary arrest were eligiblefor the study. Once a patient with cardiac arrest was intubated, end-tidal carbon dioxide and cardiac rhythms were measured and recorded every 5 minutes for 20 minutes or until resuscitation efforts were terminated. Patients' survival at the time of the arrest, survival 24 hours after the arrest, and discharge status were followed up. RESULTS: A total of 127 patients were enrolled in the study. All but 1 patient with end-tidal carbon dioxide values less than 10 mm Hg died before discharge. End-tidal carbon dioxide values greater than 10 mm Hg were associated with various degrees of survival. Overall survival to discharge was less than 14%, regardless of the end-tidal carbon dioxide value. CONCLUSION: Measurements of end-tidal carbon dioxide can be used to accurately predict nonsurvival of patients with cardiopulmonary arrest. End-tidal carbon dioxide levels should be monitored during cardiopulmonary arrest and should be considered a useful prognostic value for determining the outcome of resuscitative efforts.     

Arterial pH in out-of-hospital cardiac arrest: response time as a determinant of acidosis

It is unclear why some victims of out-of-hospital cardiac arrest are severely acidotic on arrival to the emergency department (ED), whereas others have a pH within normal limits. To explain the difference among patients, the authors collected data on 119 consecutive out-of-hospital adult nontraumatic cardiac arrest victims brought to the University of Nebraska Medical Center by paramedic rescue squad between December 1982 and January 1984. Patients who experienced restoration of spontaneous circulation (ROSC) in the field had a normal pH (7.40 +/- 0.13) as compared with the pH of patients still receiving cardiopulmonary resuscitation (CPR) on arrival at the ED (7.18 +/- 0.20). A rapid paramedic response time was the best determinant of ROSC and a normal pH on arrival at the ED. Bystander CPR neither significantly increased the number of patients with ROSC in the field nor protected against the development of acidosis, but did improve the neurological outcome of survivors. The presence of acidosis in patients still receiving CPR on arrival in the ED could not be predicted on the basis of paramedic response time, amount of sodium bicarbonate given in the field, whether or not the collapse was witnessed, or whether or not bystander CPR had been performed. Patients who were acidotic had a significantly higher (P less than 0.001) Paco2 (101 +/- 33 mm Hg) and a lower Pao2 (41 +/- 69 mm Hg) than patients with a normal pH (Paco2 37 +/- 10 mm Hg, Pao2 134 +/- 107 mm Hg). Adequacy of ventilation is the principal determinant of acidosis in patients who are still receiving CPR on arrival at the ED.     

Hyperkalemia during cardiac arrest and resuscitation in the canine model

Although recent clinical reports have noted hypokalemia after resuscitation from cardiac arrest, extensive animal work indicates that potassium is released from cells during ischemia. This study was undertaken to define the changes that occur in serum potassium ion during cardiac arrest and resuscitation in a canine model. Fourteen dogs were subjected to 5 min of cardiac arrest followed by 30 min of closed-chest CPR (CCPR). Resuscitation was performed according to a standardized protocol. Serum potassium increased significantly (p less than .001) from baseline, remained elevated 5 min after return of spontaneous circulation (ROSC), but declined to baseline levels at 15 min post-ROSC. Increases in interstitial potassium would be expected to be even greater due to the poor exchange between interstitial and intravascular compartments during CCPR. Interstitial hyperkalemia may play a role in the genesis of wide-complex electromechanical dissociation and may explain the reported success of calcium chloride in treating this problem.     

Application of normothermic cardiac arrest algorithms to hypothermic cardiac arrest in a canine model

BACKGROUND: International guidelines (2000) do not recommend vasopressor and antiarrhythmic medications during ventricular fibrillation (VF) with a core temperature below 30 degrees C. The efficacy of normothermic AHA algorithms using standard doses of epinephrine (EPI) (adrenaline) followed by amiodarone (AMIO) in hypothermic VF is uncertain. OBJECTIVES: To determine the effects of EPI followed by the combination of EPI/AMIO in the treatment of VF in a canine model of severe hypothermia. METHODS: An un-blinded, placebo controlled experiment using 21 mechanically ventilated dogs. Coronary perfusion pressure (CPP), temperature, and electrocardiogram (ECG) were monitored. Animals were cooled to 22 degrees C or the onset of spontaneous VF. VF was induced if necessary. Animals in the treatment group received EPI (0.01 mg/kg IV) and defibrillation. This was followed by EPI (0.01 mg/kg IV), AMIO (10 mg/kg IV) and defibrillation if there was no sustained return of spontaneous circulation (ROSC) for 15 min. RESULTS: Mean CPP in the treatment group increased after the administration of EPI/AMIO (24.7+/-13.3 mmHg to 46.6+/-7.7 mmHg, p<0.004). Cumulatively, the administration of EPI followed by EPI/AMIO achieved ROSC after defibrillation in 10 of 11 animals compared to 3 of 10 in the control group (91% versus 30%, n=21, p=0.0075). CONCLUSIONS: In this model of severe hypothermia, the use of standard 2000 protocols for VF resulted in a significant increase of CPP, and, a higher ROSC rate compared to placebo controls. This study suggests that AHA normothermic algorithms may be beneficial in severe hypothermia.     

Quality control of measurements of pH, carbon dioxide tension, and total carbon dioxide in plasma.

We have measured total carbon dioxide in plasma with a new carbon dioxide analyzer, and compared the results with total carbon dioxide data derived from measurements of carbon dioxide tension and pH. The results agree sufficiently well to demonstrate that the new instrument provides a simple, efficient procedure for monitoring the precision and accuracy of pH, carbon dioxide tension, or total carbon dioxide in plasma.     

Accuracy of mucosal pH and mucosal-arterial carbon dioxide tension for detecting mesenteric hypoperfusion in acute canine endotoxemia

OBJECTIVE: To determine the level of mucosal-arterial Pco2 (Pco2 gap) that is both sensitive and specific for the detection of mesenteric hypoperfusion as defined by either a >50% reduction in portal blood flow or release of lactate by the gut. DESIGN: Animal experiment. SUBJECTS: Seven anesthetized, intubated, mechanically ventilated, and surgically instrumented mongrel dogs. INTERVENTION: Escherichia coli endotoxin (1 mg/kg) given intravenously for 5 mins. MEASUREMENTS AND MAIN RESULTS: Tonometric Pco2, arterial blood gases, arterial and portal venous lactates, and portal and systemic hemodynamic variables were measured. Mucosal pH (pHi) was calculated according to the manufacturers' instructions. From these data, receiver operating characteristics were calculated. Although animals were resuscitated to maintain a constant cardiac output, portal flow decreased from 350+/-101 to 152+/-75 mL/min (p<.01) and the gut released lactate into the portal circulation in all animals. Pco2 gap increased from 13.1+/-3.9 to 40.2+/-39.2 torr (p<.01) and was inversely correlated with portal blood flow (r2 = .20; p<.05). For detection of a >50% reduction in portal blood flow, a Pco2 gap of 20 torr yielded a maximum accuracy of 67% (sensitivity, 55%; specificity, 73%) and was less accurate than a pHi of 7.20, which yielded a maximum accuracy of 76% (sensitivity, 90%; specificity, 70%), although this difference was not significant (p = .24). There was also a correlation between pHi and portal blood flow (r2 = .31; p<.01). For detection of lactate release by the gut, a Pco2 gap of 20 torr was also 67% accurate (sensitivity, 53%; specificity, 78%), whereas a pHi of 7.10 achieved an accuracy of 64% (sensitivity, 40%; specificity, 83%), which was not significantly different. CONCLUSION: Pco2 gap measurements are neither sensitive nor specific for mesenteric hypoperfusion with regard to total gut blood flow reductions of >50% or the release of lactate into the portal circulation.     

Correlations between hemodynamic, oxygenation and tissue perfusion parameters during asphyxial cardiac arrest and resuscitation in a pediatric animal model

Aim

To analyze the correlations between hemodynamic, oxygenation and tissue perfusion values in an infant animal model of asphyctic cardiac arrest (ACA).

Methods

A prospective observational animal study was performed in seventy one, two month-old piglets. CA was induced by removal of mechanical ventilation and was followed by advanced life support after at least 10 min. Correlations between hemodynamic [heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI) and intrathoracic blood index (ITBI) measured by PiCCO method], blood gas values (arterial and central venous saturation), and tissue perfusion values [intramucosal gastric pH (pHi), and tissue oxygenation (cerebral and renal saturation)] were analyzed during asphyxia, resuscitation and after return of spontaneous circulation (ROSC).

Results

Among global hemodynamic parameters, the only moderate significant correlation observed was between CI and ITBI (r = .551). Among tissue oxygenation/perfusion values, a moderate to good significant correlation (r = .460-.763) between arterial oxygen saturation, central venous, renal and cerebral oxygen saturation was observed. Lactic acid, potassium (K) and pHi were correlated (r = .561-.639), but no correlation was found between them and tissue oxygenation parameters. Global hemodynamic parameters (CI, HR, MAP) did not correlate with renal and cerebral saturations and tissue perfusion parameters.

Conclusions

During ACA and after ROSC global hemodynamic parameters do not correlate with oxygenation and tissue perfusion values. Additional studies which assess the potential usefulness of tissue oxygenation/perfusion parameters during cardiac arrest and ROSC are needed.     

Arterial-venous carbon dioxide tension difference during severe hemorrhage and resuscitation.

PURPOSE: To define clinically useful markers for determining the adequacy of resuscitation after hemorrhage. DESIGN: Prospective study of 20 Yorkshire swine, using an established model for hemorrhagic shock in swine. BACKGROUND AND METHODS: Clinically useful markers for assessing the adequacy of resuscitation after hemorrhage do not exist. We assess variables, such as BP and arterial blood pH. However, these variables do not correlate well with restoration of organ perfusion. In this study, 14 anesthetized swine were hemorrhaged to a mean arterial pressure of less than 25 mm Hg. After 30 mins without interventions, each animal was resuscitated with whole blood, hydroxyethyl starch, or normal saline. At baseline and during shock and resuscitation, hemodynamic variables, arterial and mixed venous blood gases, and arterial lactate concentrations were measured to determine which variables correlated most closely with the restoration of blood flow. RESULTS: The correlation between cardiac index and arterial or mixed venous pH and the correlations with arterial lactate values were poor. The correlation between cardiac index and mixed venous hemoglobin saturation also was weak (r2 = .28). Cardiac index correlated best with the arterial-venous PCO2 difference (r2 = .67) and the arterial-venous pH difference (r2 = .38). Using multiple regression, a linear correlation was established between the cardiac index and the arterial-venous pH and PCO2 differences throughout shock and resuscitation (r2 = .91). CONCLUSION: These findings suggest that the adequacy of resuscitation after hemorrhage can be assessed using paired arterial and mixed venous pH and PCO2 values.     

Lack of a neuroprotective effect from N-acetylcysteine after cardiac arrest and resuscitation in a canine model.

Objective: Oxygen free radicals cause brain injury following resuscitation from cardiac arrest. In preclinical trials, some free radical scavenging drugs reduce oxidative neuronal damage after ischemia and reperfusion, but these drugs are generally not yet available for clinical testing or use. N-Acetylcysteine (NAC), a commonly used antidote in acetaminophen poisoning, is also a potent free radical scavenger that can ameliorate oxidative injury following ischemia and reperfusion in neuronal cell culture. We hypothesized that treatment with NAC would improve neurological outcome after cardiac arrest and resuscitation. Methods: In 16 adult female beagles, 10 min of ventricular fibrillation was followed by 3 min of open-chest CPR, and defibrillation. Immediately following return of spontaneous circulation, animals randomly received either 150 mg/kg NAC (3% solution) (n=8) or an equivalent volume of normal saline (n=8). Twenty-three hours later, neurological deficit was scored (0=normal, 100=brain death). Results: All animals were successfully resuscitated, and there were no apparent adverse effects to the administration of NAC in post resuscitative animals. There was, however, no significant difference in neurological deficit in the animals receiving NAC (40±12.9, mean±SD) compared to control animals (44±6.5, P=0.73). Conclusion: No neuroprotective effect was found from the administration of NAC at currently used clinical dosages, to dogs subjected to 10 min of global cerebral ischemia from cardiac arrest and resuscitation.     

Regional carbon dioxide monitoring: a different look at tissue perfusion

Adequate tissue oxygenation is one of the main therapeutic goals for the critically ill patient. Until recently, the perfusion status of the critically ill and injured has been assessed by global indices such as blood pressure, heart rate, and urine output. However, these global parameters are inadequate in that they fail to demonstrate the actual perfusion status of a patient. Research has shown the splanchnic region to be a pivotal organ bed in response to shock. Because this region shows early signs of hypoperfusion and hypoxia, its monitoring provides for more effective and complete resuscitation. To that end, gastric tonometry offers a noninvasive means by which early symptoms of low flow can be determined, allowing for optimization of tissue perfusion and patient outcome. The most proximal segment of the gastrointestinal tract offers promising information regarding tissue perfusion with the use of sublingual capnography.     

End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock

OBJECTIVE: To document the relationships between cardiac index and end-tidal carbon dioxide tension (PetCO2 during diverse low-flow states of circulatory shock. DESIGN: Randomized, prospective, controlled studies on animal models of hemorrhagic, septic, and cardiogenic shock. SETTING: University-affiliated research laboratory. SUBJECTS: Sixteen anesthetized domestic pigs weighing 35-45 kg. INTERVENTIONS: Hemorrhagic shock was induced in five pigs by bleeding followed by reinfusion of shed blood. Septic shock was induced in five pigs by infusion of live Escherichia coli. Cardiogenic shock followed an interval of global myocardial ischemia after inducing and reversing ventricular fibrillation in six pigs. MEASUREMENTS AND MAIN RESULTS: PetCO2 was continuously measured. Cardiac index was measured intermittently by using conventional thermodilution techniques. Cardiac index was correlated with PetCO2 by polynomial regression and Bland-Altman analyses. PetCO2 was highly correlated with cardiac index during hemorrhagic shock (r2 = .69, p < .01), septic shock (r2 = .65, p < .01), and cardiogenic shock (r2 = .81, p < .01). PetCO2 predicted thermodilution cardiac index with bias of -11+/-27 (+/-2 SD) mL/min/kg during hemorrhagic shock, 1.3+/-20.4 (+/- 2 SD) mL/min/kg during septic shock, and -1+/-12 (+/-2 SD) mL/min/kg during cardiogenic shock. CONCLUSIONS: Cardiac output and PetCO2 were highly related in diverse experimental models of circulatory shock in which cardiac output was reduced by >40% of baseline values. Therefore, measurement of PetCO2 is a noninvasive alternative for continuous assessment of cardiac output during low-flow circulatory shock states of diverse causes.     

Transcutaneous carbon dioxide and oxygen tension in newborn infants: Reliability of a combined monitor of oxygen tension and carbon dioxide tension

We evaluated a new combined sensor for monitoring transcutaneous carbon dioxide tension (PtcCO₂) and oxygen tension (PtcO₂) in 20 critically ill newborn infants. Arterial oxygen tension (PaO₂) ranged from 16 to 126 torr and arterial carbon dioxide tension (PaCO₂) from 14 to 72 torr. Linear correlation analysis (100 paired values) of PtcO₂ versus PaO₂ showed anr value of 0.75 with a regression equation of PtcO₂=8.59+0.905 (PaO₂), while PtcCO₂ versus PaCO₂ revealed a correlation coefficient ofr=0.89 with an equation of PtcCO₂=2.53+1.06 (PaCO₂). The bias between PaO₂ and PtcO₂ was –2.8 with a precision of ±16.0 torr (range, –87 to +48 torr). The bias between PaCO₂ and PtcCO₂ was –5.1 with a precision of ±7.3 torr (range, –34 to +8 torr). The transcutaneous sensor detected 83% of hypoxia (PaO₂ <45 torr), 75% of hyperoxia (PaO₂ >90 torr), 45% of hypocapnia (PaCO₂ <35 torr), and 96% of hypercapnia (PaCO₂ >45 torr). We conclude that the reliability of the combined transcutaneousPo ₂ andPCo ₂ monitor in sick neonates is good for detecting hypercapnia, fair for hypoxia and hyperoxia, but poor for hypocapnia. It is an improvement in that it spares available skin surface and requires less handling, but it appears to be slightly less accurate than the single electrodes.