CPR in children

CPR has not been well studied in children and little is known about factors predictive of outcome. We conducted a study with three goals: longitudinal determination of demographic and laboratory data characterizing pediatric arrest victims; identification of factor(s) predictive of outcome; and determination of the prevalence of ionized hypocalcemia in pediatric arrest victims. All resuscitation efforts were documented during a one-year period in a 240-bed tertiary care children's hospital. Patients were classified into two groups--respiratory arrest (RA, requiring only assisted ventilation), and cardiac arrest (CA, absence of palpable cardiac activity requiring closed-chest CPR). Collected data and laboratory tests were analyzed using a step-wise discriminant analysis to determine which factors were predictive of outcome. There were 113 arrests in 93 children; 53 were CA victims and 40 were RA victims. CA had a high in-hospital mortality (90.6%) compared to RA (32.5%). The population was young (55% less than 1 year old) and 87% had at least one chronic underlying disease. No laboratory or demographic value was significantly associated with eventual outcome. The number of doses of epinephrine in CA victims, or bicarbonate in RA victims, was associated with eventual outcome. None of 31 CA victims receiving more than two doses of epinephrine survived to discharge. Low ionized calcium concentrations (less than 3.5 mg/dL) were identified in ten patients; septic shock was present in seven, and chronic renal failure in two.(ABSTRACT TRUNCATED AT 250 WORDS)     

Selective venous hypercarbia during human CPR: implications regarding blood flow

Thirty-five patients presenting to the emergency department in cardiopulmonary arrest had simultaneous measurement of central venous (cv) and arterial (a) blood gases during CPR with a pneumatic chest compressor and ventilator. The mean cv, arterial pH, and PCO2 values were markedly different (P less than .001). The mean pH gradient (pHa - pHcv) was .31 +/- .10 units and the mean PCO2 gradient (PcvCO2 - PaCO2) was 60.5 +/- 23.6 torr. This selective venous hypercarbia is probably due to a cardiac output that is inadequate to eliminate the CO2 produced from both residual aerobic metabolism and the buffering of anaerobically produced lactic acid. Central venous blood gases are probably a better reflection of actual tissue environment during prolonged cardiac arrest than are arterial blood gases.     

Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis

Hepatic venous catheterization is widely used to assess portal pressure. However, it remains unclear whether wedged hepatic venous pressure is a close indicator of portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. To address this issue, we analyzed the data from our previous published studies. Forty patients with nonalcoholic cirrhosis (HBV infection in five, HCV infection in 28, and cryptogenic in seven) were available in this analysis. A vasoconstrictor (N=14), vasodilator (N=10), or combination (N=16) was administered. The agreement of the changes between portal and wedged hepatic venous pressures during pharmacological manipulation was assessed by an intraclass correlation coefficient. The intraclass correlation coefficient in each subgroup was more than 0.60 (0.62 in vasoconstrictor group, 0.87 in vasodilator group, and 0.73 in combination group). When the analysis was performed according to the cause of liver disease, the values were 0.67 in HBV infection, 0.73 in HCV infection, and 0.74 in cryptogenic cirrhosis. These results suggest that wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in patients with nonalcoholic cirrhosis.     

A comparison of serum ionized calcium in arterial and mixed venous blood during CPR

Changes in the actual ionized calcium level (aCa2+) of serum in arterial and mixed venous blood during CPR were investigated in 22 patients with intrinsic cardiopulmonary arrest. Measurements were carried out at an average of 5.4 +/- 0.6 minutes (group 1) and 30 minutes (group 2) after the beginning of CPR, using simultaneously taken blood samples. The aCa2+ of groups 1 and 2 revealed no difference between arterial and mixed venous bloods. As CPR proceeded, the aCa2+ of both bloods diminished, and group 2 had a significantly lower value than did group 1 (arterial blood: 2.36 +/- 0.04 mEq/L vs 2.09 +/- 0.09 mEq/L, P less than .01; mixed venous blood: 2.37 +/- 0.05 mEq/L vs 2.13 +/- 0.06 mEq/L, P less than .001). Conversely, pH values were significantly higher for arterial blood rather than for mixed venous blood, but there was no significant change in pH between groups 1 and 2 (arterial blood, 7.11 +/- 0.05 vs 7.14 +/- 0.04; mixed venous blood, 6.93 +/- 0.04 vs 6.98 +/- 0.03). Furthermore, an analysis of the aCa2+ serum level measurements was carried out in relation to survivors and nonsurvivors and to the presence or absence of a witness at the time of the cardiac arrest. In all groups, there was no difference in aCa2+ between arterial and mixed venous blood. As CPR proceeded, however, the aCa2+ showed a significant decrease in all groups. This decrease was accompanied by a pH increase in arterial blood of patients with a witnessed cardiac arrest and in mixed venous and arterial blood of survivors.     

The clinical implications of continuous central venous oxygen saturation during human CPR.

STUDY OBJECTIVE: The purpose of this study was to observe, measure, and describe the changes in central venous oxygen saturation during CPR and immediately after return of spontaneous circulation. It also was to examine the clinical utility of continuous central venous oxygen saturation monitoring as a indicator of return of spontaneous circulation during CPR in human beings. DESIGN AND SETTING: Eight-month, prospective, non-outcome, observational, nonrandomized case series in the ED of a large urban hospital. TYPES OF PATIENTS: Adult normothermic, nontraumatic, out-of-hospital cardiopulmonary arrests. INTERVENTIONS: All patients were managed according to advanced cardiac life support guidelines. A proximal aortic and double-lumen central venous catheter was placed. Central venous oxygen saturation was measured continuously spectrophotometrically with a fiberoptic catheter in the central venous location. MEASUREMENTS: Aortic blood pressure and central venous oxygen saturation were simultaneously measured throughout each resuscitation. Return of spontaneous circulation was defined as a systolic blood pressure of more than 60 mm Hg for more than five minutes. RESULTS: One hundred patients who experienced 68 episodes of cardiac arrest were studied. Patients with return of spontaneous circulation had a higher initial and statistically higher mean and maximal central venous oxygen saturation than those without return of spontaneous circulation (P = .23, .0001, and .0001, respectively; P less than .05 is significant). No patient attained return of spontaneous circulation without reaching a central venous oxygen saturation of at least 30%. Only one of 68 episodes of return of spontaneous circulation was attained without reaching a central venous oxygen saturation of at least 40%. A central venous oxygen saturation of greater than 72% was 100% predictive of return of spontaneous circulation. CONCLUSION: Continuous central venous oxygen saturation monitoring can serve as a reliable indicator of return of spontaneous circulation during CPR in human beings.     

Hemodynamic determinants of subdiaphragmatic venous return during closed-chest CPR in a canine cardiac arrest model

OBJECTIVE: To assess the hemodynamic determinates of peripheral subdiaphragmatic venous-to-right-heart return during closed-chest CPR. MODEL: Seven anesthetized dogs subjected to electrically induced ventricular fibrillation for five minutes. INTERVENTIONS: Conventional closed-chest CPR and closed-chest CPR with continuous abdominal binding at a chest compression rate of 60 per minute, a compression-to-relaxation ratio of 50:50, and a ventilation-to-compression ratio of 1:5. METHODS: Solid-state catheters were positioned in the ascending aorta, right atrium (RA), and inferior vena cava (IVC). Cannulating electromagnetic flow probes were inserted into the IVC and a carotid artery. Analog-to-digital conversion was performed electronically. Five minutes after ventricular fibrillation was induced, interventions were performed in an alternating sequence. Systolic, diastolic, and mean pressures and flows were measured and compared. STATISTICAL METHODS: Two-tailed, unpaired t test applied to equal sample size, linear regression analysis, and multiple regression analysis. RESULTS: Abdominal binding during CPR significantly increased (P less than .05) all measured systolic and diastolic CPR intravascular pressures compared with CPR without abdominal binding but did not affect IVC-to-right-heart venous return. During conventional CPR without abdominal binding, venous return was dependent on the diastolic IVC pressure (r = .86, P = .014), mean IVC pressure (r = .80, P = .03), and carotid blood flow (r = .99, P = .001) but not on the IVC-to-RA pressure gradient. With abdominal binding, venous return was not correlated with any study hemodynamic variable, including the peripheral venous-to-RA pressure gradient. CONCLUSION: Venous return from the subdiaphragmatic venous bed during CPR is dependent on venous pressure, not on the peripheral venous-to-right-heart pressure gradient. Abdominal binding during CPR does not affect venous return. Venous return during CPR diastole is highly dependent on central venous capacitance (left heart outflow during CPR systole).     

Central venous and bladder pressure reflect transdiaphragmatic pressure during pressure support ventilation

STUDY OBJECTIVES: To determine whether the change in bladder pressure (Pblad) and central venous pressure (Pcvp) may reflect the changes in esophageal pressure (Pes) and gastric pressure (Pgas) when inspiratory pressure support (IPS) is altered. DESIGN: Prospective clinical study. SETTING: The ICUs of a teaching hospital. PATIENTS: Ten patients currently receiving IPS ventilation via a tracheostomy or an endotracheal tube who already had bladder and central venous catheters in situ. MEASUREMENTS AND RESULTS: Airway pressure, Pes, Pgas, Pcvp, Pblad, and flow were measured at the original IPS setting. IPS then was reduced by 5-cm H(2)O increments until IPS was zero or was at the minimum pressure that could be tolerated by each patient. At each level of IPS, pressures and flow were measured at steady-state breathing. The maximum pressure difference for each pressure during inspiration was calculated. We found that the Delta Pblad correlated closely with the Delta Pgas (r = 0.904) and that the Delta Pes correlated with the Delta Pcvp (r = 0.951). When the Delta Pcvp - Delta Pblad was compared with the transdiaphragmatic pressure for each patient as the IPS was altered, the correlation coefficients varied from 0.952 to 0.999. CONCLUSION: Although absolute values for the Delta Pcvp during mechanical ventilation do not always reflect the Delta Pes, useful information can be obtained from this route. In individual patients, the two sites of measurement followed each other when IPS was changed, enabling a bedside assessment of the response to reducing respiratory support.     

Selective perfusion of ischemic myocardium during coronary venous retroinjection: a study of the causative role of venoarterial and venoventricular pressure gradients

Coronary venous retroinjection is often associated with preferential distribution of flow to ischemic myocardium. The purpose of this study was to define the mechanism of such retrodistribution of flow. In 24 anesthetized open chest dogs, Monastral blue dye (10 ml) was injected by way of a balloon catheter in the distal great cardiac vein as a marker for retrograde flow distribution. The injection rate (0.6 to 2.4 ml/s) was adjusted such that systolic pressure in the anterior interventricular vein ranged between 60 and 85 mm Hg. In 11 dogs with no ischemia and normal myocardial perfusion pressure (96 +/- 8 mm Hg), no myocardial staining occurred despite retrograde filling of epicardial veins. One minute after occlusion of the left anterior descending coronary artery, dye injections caused selective staining of the cyanotic area in 15 of 18 episodes, sparing the normal myocardium within the zone of retroperfused veins. In five dogs, with the arterial pressure less than 55 mm Hg, retroinjection resulted in homogeneous staining of all the myocardium drained by the retroperfused veins. Selective staining of the ischemic myocardium caused by retroinjection was associated with the following pressure gradients: during systole from the anterior interventricular vein to the occluded coronary artery, 31 to 58 mm Hg, and during diastole from the retroperfused veins to the left ventricular chamber, 9 to 28 mm Hg. There was no diastolic venoarterial gradient in the ischemic myocardium. In normal myocardium, retroinjection did not reverse the arteriovenous pressure gradient. In conclusion, retrograde flow is primarily directed to myocardium with low anterograde perfusion pressure. Selective retrograde penetration of acutely ischemic myocardium can thus be achieved by a mechanism consistent with the development of venoarterial and venoventricular pressure gradients.     

Comparison of central venous and arterial pH and PCO2 during open-chest CPR in the canine model

Arterial blood gases are difficult to obtain during cardiopulmonary resuscitation (CPR) in human beings, and the possibility of venous sampling is raised frequently. The reliability of central venous gases as a substitute for arterial blood gases in assessing acid base status, however, has not been investigated adequately under conditions of CPR. Therefore, femoral arterial and central venous catheters were placed in 24 mongrel dogs, and ventricular fibrillation was electrically induced. After varying predetermined downtimes from five to 60 minutes, open-chest CPR was begun, and arterial and central venous blood gases were simultaneously drawn every five minutes during a 30-minute period. Arterial pH (pHa) was consistently higher than central venous pH (pHcv) by an average of .048 units. A significant correlation existed between the pHa and pHcv at all times during CPR, with an overall r = .9771 (P less than .0001). The difference between central venous PCO2 (PcvCO2) and arterial PCO2 (PaCO2) was 5.17 mm Hg prior to cardiac arrest, but it increased 300% to a mean of 15.51 mm Hg during CPR. Correction of pHcv using conventional methods to account for this respiratory component decreased the correlation between pHa and pHcv to r = .6905. The ability of pHcv to substitute for pHa was assessed, and showed a sensitivity of 100% when pHa of 7.2 was used as a criterion for treatment. In this model, pHcv is a sensitive indicator of pHa and it may be used to guide bicarbonate therapy. The increased PcvCO2 during CPR probably results from the marked tissue lactic acid production and subsequent shift of the bicarbonate buffer into free carbon dioxide.     

Value and limitations of pulsed Doppler echocardiography in the determination of pressure gradients in children

The aim of this study was to evaluate the results of pulsed Doppler echocardiography in assessing pressure gradients in children despite the theoretical limitations of this technique in the measurement of high velocity blood flow (due mainly to the phenomenon of "aliasing"). 20 patients with an average age of 6.7 years (range 3 months to 19 years) were studied by 2D echocardiography and pulsed Doppler within 48 hours of cardiac catheterisation. Valvular stenosis was present in 14 cases (aortic, 7, pulmonary, 7). There were 3 cases of infundibular obstruction and 2 vascular stenosis (coarctation of the aorta and stenosis of a branch of the pulmonary artery). One patient had stenosis at the origin of a prosthetic tube graft. The gradient was estimated from the Doppler flow curves using simplified Bernoulli formula (P = 4 X maximal jet velocity). In 17 patients (gradients of 20 to 90 mmHg) an excellent correlation was observed between the pulsed Doppler and haemodynamic results (r = 0.90). In 3 cases with gradients over 80 mmHg it was not possible to quantify the gradient but pulsed Doppler fixed an inferior limit of 80 mmHg. Therefore, using a 3 or 2.25 MHz probe at the low depths of investigation encountered in childhood, pulsed Doppler gave a reliable indication of pressure gradients less than or equal to 80 mmHg. These results and the non-invasive nature of the method make pulsed Doppler a particularly interesting complementary examination in children or babies with stenotic cardiac lesions.