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Results obtained during animal investigations cannot be directly applied to patients because of the anatomical and physiological differences present. Experience has shown that cases of sudden cardiac arrest can only be effectively helped if cardiac massage and artificial ventilation are carried out as soon as possible, and that no sodium bicarbonate need be given when resuscitation measures are begun immediately, or very soon after arrest. In this situation it is better to use adrenaline only, in order to improve organ perfusion. The examples presented show that giving bicarbonate can alter potassium kinetics. Very low serum potassium concentrations are often measured during and following successful resuscitation, and giving too large an amount of buffer solution can worsen this hypokalaemia and lead to a further arrest. The infusion of sodium bicarbonate and the rapid increase in blood sugar levels during resuscitation can lead to a marked rise in serum osmolality which in turn can jeopardize the return of cerebral function. Because in the presence of reduced cerebral perfusion, high blood glucose levels increase the degree of cerebral lactacidosis blood glucose levels should be measured and corrected as necessary.

Previous reports have advocated the use of mixed venous blood gases to estimate arterial pH and as a reflection of tissue acid-based balance. However, true mixed venous samples are difficult to obtain during cardiac arrest as they require a pulmonary artery catheter. The purpose of this study was to determine whether central or femoral venous samples could be used in place of pulmonary artery samples. Blood gases from these sites were drawn at intervals during experimental cardiac arrest in dogs. The PO2, PCO2, and pH from the pulmonary artery samples were strongly correlated with those from the central venous (r = .93, .99, and .99, respectively) and from the femoral venous samples (r = .73, .93, and .97, respectively). There were no significant differences in the pulmonary artery, central, or femoral venous gases. This animal model suggests that femoral and central venous samples mirror true mixed venous blood gases from the pulmonary artery and could be used in their place.

Blood ionized and total calcium levels, and pH values were obtained in 12 patients who were being ventilated and given external cardiac massage after having had an out-of-hospital cardiac arrest. On admission they had marked ionized hypocalcemia, with mean ionized calcium levels of 0.67 +/- 0.22 mmol/L, (range, 0.26 to 0.89), but normal total calcium levels. There was a positive correlation between pH and ionized calcium levels (r = 0.71). Of the six patients who were successfully resuscitated, four were discharged and two died; the other six could not be resuscitated and died. By comparison, ionized and total calcium levels obtained within 3 minutes of cardiac arrest were normal in 9 patients who had cardiac arrests in the intensive care unit or during surgery. All were discharged. These data are the first to document the occurrence of severe ionized hypocalcemia after out-of-hospital cardiac arrest. Hypocalcemia appears to be time-dependent and due essentially to extracellular complexing of calcium. Further work is needed to determine whether patients who have out-of-hospital cardiac arrests can benefit from calcium administration.

Multivariate analysis was performed to evaluate significant differences between electrolytes, serum magnesium, and successful resuscitation in cardiac arrest victims in a prospective controlled study. Twenty-two cardiac arrest victims having ventricular fibrillation or tachycardia, electromechanical dissociation, or asystole were compared with 19 matched controls with no ventricular arrhythmias. Of the control group, one was hypermagnesemic (5%), 17 normomagnesemic (90%), and one hypomagnesemic (5%). In the arrest group, eight were hypermagnesemic (36%), nine normomagnesemic (41%), and five hypomagnesemic (23%). Thirteen of 22 cardiac arrest victims (59%) had an abnormal serum magnesium level. All hypermagnesemic and hypomagnesemic patients expired (100%). In the normomagnesemic group, four out of nine (44%) were successfully resuscitated. A positive correlation was identified between normomagnesemia and successful resuscitation (P less than .01). There was no correlation between other electrolytes and successful resuscitation (P greater than .05).

Symptoms of hyperphosphatemia usually relate to the associated hypocalcemia. In a 33-year-old patient accidental infusion of a bolus of potassium phosphate (5 ml intravenously) was immediately followed by cardiac arrest. During CPR, clinically important hypocalcemia or hyperkalemia was not detected, but serum phosphorus was significantly increased. Because acute phosphate load can precipitate life-threatening cardiac arrhythmias, familiarity with doses and rate of infusion of phosphate is extremely important.

Simultaneous arterial (aortic), mixed venous (pulmonary artery), and myocardial venous (great cardiac vein) blood gas and lactate concentrations were obtained in 12 dogs before and during cardiac arrest and CPR. We observed marked mixed venous and myocardial venous acidosis and increased PaCO2 but normal pHa and reduced PaCO2. Furthermore, the pH was significantly lower and the PCO2 significantly higher at the myocardial venous site compared to the mixed venous site, and marked myocardial lactate production occurred during CPR. Calculated bicarbonate and CO2 content (CCO2) did not increase during CPR from any site compared to control values and actually decreased significantly in arterial and myocardial venous samples. Changes in hydrogen ion concentration in both mixed venous and myocardial venous blood correlated with changes in lactate concentration but not total CCO2. Our results during CPR demonstrate a) a significant discrepancy between arterial and mixed venous blood gases but also a large and significant discrepancy between mixed venous and myocardial venous blood gases, b) significant anaerobic systemic and myocardial metabolism, and c) that mixed venous and myocardial venous acidosis is possibly a result of lactic acidosis.

In 22 digitalized (of a total of 39) patients studied at random by radioimmunoassay during cardiac arrest, the mean serum digoxin concentration was 2.6 (+/- 1.86, range 0.6-8.2) ng/ml, significantly higher (P less than 0.001) than the "eudigitalized" concentration (1.3 +/- 0.52, range 0.5-2.3 ng/ml) determined under carefully standardized conditions in a non-toxic population. Half of the arrest patients had serum digoxin levels in the toxic range (2.4 ng/ml or above), mainly due to significant renal failure (mean serum creatinine concentration 2.9 +/- 2.66 v. 1 +/- 0.26 mg/dl for non-toxic subjects, P less than 0.001), partly due to a higher mean daily digoxin dose (0.40 v 0.31 mg/day, P less than 0.05) and frequently associated with potent diuretic therapy (73 v 54%). A smaller fraction of digitalized patients survived, both short- (27%) and long-term (14%), than did non-digitalized subjects (35% and 26%, respectively). The mean myocardial digoxin concentration was 150 (+/- 63.3, range 52-252) ng/g with an average myocardial/serum ratio of 62.5 (range 38-91). There were significant positive correlations between the serum digoxin and left-ventricular myocardial digoxin concentration (r=0.8107, P less than 0.01) or serum creatinine concentration (r=0.4637, P less than 0.001).

To assess arteriovenous differences in acid-base status, we measured the pH and partial pressure of carbon dioxide (PCO2) in blood drawn simultaneously from the arterial and central venous circulations in 26 patients with normal cardiac output, 36 patients with moderate and 5 patients with severe circulatory failure, and 38 patients with cardiac or cardiorespiratory arrest. The patients with normal cardiac output had the expected arteriovenous differences: venous pH was lower by 0.03 unit, and venous PCO2 was higher by 0.8 kPa (5.7 mm Hg). These differences widened only slightly in those with moderate cardiac failure. Additional simultaneous determinations in mixed venous blood from pulmonary arterial catheters were nearly identical to those in central venous blood. In the five hypotensive patients with severe circulatory failure there were substantial differences between the mean arterial and central venous pH (7.31 vs. 7.21) and PCO2 (5.8 vs. 9.0 kPa [44 vs. 68 mm Hg]). Large arteriovenous differences were present during cardiac arrest in patients whose ventilation was mechanically sustained, whether sodium bicarbonate had been administered (pH, 7.27 vs. 7.07; PCO2, 5.8 vs. 8.6 kPa [44 vs. 65 mm Hg]) or not (pH, 7.36 vs. 7.01; PCO2, 3.7 vs. 10.2 kPa [28 vs. 76 mm Hg]). By contrast, in patients with cardiorespiratory arrest, large arteriovenous differences were noted only when sodium bicarbonate had been given (pH, 7.24 vs. 7.01; PCO2, 9.5 vs. 16.9 kPa [71 vs. 127 mm Hg]). We conclude that both arterial and central venous blood samples are needed to assess acid-base status in patients with critical hemodynamic compromise. Although information about arterial blood gases is needed to assess pulmonary gas exchange, in the presence of severe hypoperfusion, the hypercapnia and acidemia at the level of the tissues are detected better in central venous blood.

Lymphocytosis in older adults is unusual and frequently indicates chronic lymphocytic leukemia or other lymphoproliferative disorder. This report describes 73 patients, aged 43 to 93 years, who presented with emergency medical conditions and who had absolute lymphocytosis, with absolute lymphocyte counts ranging from 4.1 to 12.9 X 10(9)/L (4100 to 12,900/mm3). The lymphocytosis was characterized morphologically by atypical lymphocytes and was transient, followed, in most instances, by a neutrophilia. Most of the patients presented with serious cardiac conditions; the remaining presented with other critical disorders including status epilepticus and traumatic injuries. The mortality rate was high (50%). The lymphocytosis in some patients was probably secondary to the administration of epinephrine. The lymphocytosis in those not receiving epinephrine may have represented a physiologic reaction to severe stress.

EEG activity and regional cerebral blood flow were monitored during 5 hour survival following cardiac arrest in 32 pentobarbital anesthetized mongrel dogs. The animals were mechanically ventilated and blood gases were maintained at physiologic levels. Regional cerebral blood flow and cardiac output were measured using 15 mu microspheres. EEG was recorded from 6 epidural electrodes using bipolar techniques. The animals were divided into 3 groups. The animals in Group I had an arrest of 8-11 minutes and those in Group II and III had an arrest of 12-16 minutes. Group II animals received no treatment. Group III animals were given 1 g/kg of dextran 40 at a concentration of 10% in normal saline following the arrest and maintained with 10 mg/kg/min during the 5 hours of recovery. In Groups I and III there was shorter duration of a flat EEG and 5 hours after the arrest the EEG activity was closer to normal than in Group II. After 5 hours the EEG scores of Group III were significantly greater than Group II (p less than 0.03). The cortical grey matter and hippocampus had the greatest reduction of blood flow following cardiac arrest. The mean cortical grey matter blood flow in Group II was less than in Groups I and III at 3 hours. After 5 hours the grey matter blood flow was greater in Group III than in Group II (p less than 0.09). The findings of this study are consistent with the hypothesis that after cardiac arrest perfusion abnormalities persist or develop after return of blood pressure and that these can be corrected or prevented with improved functional survival by treatment with dextran 40 after the arrest.

Studies have shown that over 50% of cardiovascular deaths occur before hospitalization. A major factor associated with survival in cases of out-of-hospital cardiac arrest is the time from cardiovascular collapse to the initiation of cardiopulmonary resuscitation (CPR) or "downtime." The purpose of this study was to determine whether blood lactate levels could be used to predict downtime in the canine cardiac arrest model. Femoral arterial and Swan-Ganz catheters were placed in 22 mongrel dogs, and ventricular fibrillation was electrically induced. The dogs remained in ventricular fibrillation without ventilation for 5, 10, 15, 30, or 60 minutes. After the predetermined fibrillation time, a left anterolateral thoracotomy was performed, and open-chest cardiac massage was begun. Arterial and mixed venous lactate levels were determined for every 5 minutes during 30 minutes of cardiopulmonary resuscitation. The correlation coefficient between the mixed venous and arterial lactate levels was 0.96 or greater during all stages of resuscitation. Peak serum lactate level increased linearly in relation to downtime. The increase in lactate level was not evident until after CPR was begun, and it remained at peak levels or decreased insignificantly, despite optimal open-chest CPR. Linear regression analysis revealed that 84% of the variability in serum lactate levels could be explained by downtime differences. In this model, blood lactate level is a reliable and objective measure of downtime and may be a useful indicator of the adequacy of CPR if levels decrease or remain stable. The clinical implications of this study lie with the use of blood lactate levels in the emergency department to guide the aggressiveness of resuscitative efforts.

An association between high glycemia on admission after resuscitation from an out-of-hospital cardiac arrest and poor neurological recovery has been reported. It remains controversial whether the high glycemia on admission causes the poor outcome or is just an epiphenomenon. The Cerebral Resuscitation Study Group therefore registered the glycemia on admission in 417 patients resuscitated after an out-of-hospital cardiac arrest. Our data confirm that a high glycemia on admission is related to a poor outcome. There is no relationship between the glycemia on admission and the duration of cardiopulmonary resuscitation (CPR). However, there is a positive but weak correlation between the dose of adrenaline administered during CPR and the glycemia on admission. This indicates that the higher glycemia on admission in patients with a poor outcome may, at least in part, be due to CPR parameters, such as the amount of adrenaline used, that are linked with a bad prognosis. However, it cannot be excluded that a high glycemia contributes to the brain damage after cardiac arrest.

The usefulness of peripheral venous sampling in determining acid-base status in acutely ill patients was studied. A total of 171 nonarrest patients and 12 patients in cardiac arrest had paired samples of arterial and venous blood compared for correlation of blood gas results. Linear equations relating arterial and venous values of pH, PCO2, and bicarbonate were developed in both groups of patients; however, the accuracy of predicting arterial values from venous values was limited. Severe acid-base disturbances were essentially ruled out by normal or nearly normal venous blood gases. Extremely abnormal venous levels reliably reflected comparable arterial abnormalities. The results suggest that immediate intravenous bicarbonate therapy should be considered for patients with pH less than or equal to 7.05 and PCO2 less than or equal to 40 torr despite the possibility of inadvertent venous sampling. A larger series is needed to verify these results in the setting of cardiac arrest.

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.

Investigation into the cause of extreme systemic acidosis during cardiac arrest led to the discovery that a major contributing factor was Abbott 1:10,000 single-dose epinephrine, which contained a large unsuspected acid level. Analysis of this product, both in vivo and in vitro, demonstrated that it contained 8.2 times the acid content of a presumably identical product from Bristol Laboratories and also of a presumably identical product from Bristol Laboratories and also 1,850 times the acid content of an identical epinephrine dose made from a Parke-Davis preparation. Abbott epinephrine injected into the central circulation or directly into the heart causes extreme acidemia, which may be potentially lethal by itself when superimposed on pre-existing acidosis as in cardiac arrest.

The American Heart Association's current standards for CPR indicate that acid-base therapy should be guided by measurements of arterial blood gases. However, we have discovered a striking discrepancy between arterial and venous blood gases during CPR: severe venous hypercarbia and acidosis may coexist with simultaneous arterial alkalosis. Arterial blood gases during CPR, therefore, may not accurately reflect the acid-base status of mixed venous blood and thus may fail to indicate systemic acid-base status.

To further investigate the incidence and etiology of hypokalemia during cardiac arrest, the authors compared data on 74 adult nontrauma cardiac arrest patients (44 men, 30 women, age 65 +/- 13 years) who had a serum potassium (K+) level documented during or immediately following resuscitation with data on 53 adult controls with life-threatening medical emergencies presenting to the emergency department who did not experience arrest. Hypokalemia (serum K+ less than 3.6 mEq/l) occurred in 25 arrest patients (34%) compared with nine controls (17%). Serum K+ was not significantly different shortly before (3.7 +/- 0.4) versus immediately after arrest (3.6 +/- 0.8) in a small subgroup of patients, making intracellular shifting of K+ because of metabolic events during resuscitation an unlikely etiology. Hypokalemia was associated with a 2.5-fold increase in relative risk for cardiac arrest. Patients who were receiving diuretics without K+ supplementation had the highest risk of arrest (4.4-fold increase). Supplementation of K+ appeared to be protective in patients on diuretics. The authors confirm the association between hypokalemia and cardiac arrest and suggest that this metabolic abnormality may be an important risk factor for cardiac arrest.

The acid-base and electrolyte conditions which favor survival were examined in 105 patients during and after CPR. There was a sharp decrease in survival when arterial pH exceeded 7.55 during the initial 10 min after initiation of CPR. Measurements made one hour after successful resuscitation also demonstrated an increase in mortality when pH exceeded 7.55. Arterial blood lactate also served as a sensitive quantitative indicator of prognosis, both during and one hour after successful CPR. The adverse effects of alkalemia were largely explained by increases in whole-blood bicarbonate, plasma sodium, and plasma osmolality after administration of sodium bicarbonate.