Emergency department cardiopulmonary bypass in the treatment of human cardiac arrest.

OBJECTIVE: To study the use of emergency department (ED) femoro-femoral cardiopulmonary bypass (CPB) in the resuscitation of medical cardiac arrest patients. DESIGN: Prospective, uncontrolled trial. SETTING: Urban academic ED staffed with board-certified emergency physicians (EPs). PARTICIPANTS: Ten patients with medical cardiac arrest unresponsive to standard therapy. INTERVENTIONS: Femoro-femoral CPB instituted by EPs. RESULTS: The time of cardiac arrest prior to CPB (mean+/-SD) was 32.0+/-13.6 min. The cardiac output while on CPB was 4.09+/-1.03 L/min with an average of 229+/-111 min on bypass. All 10 patients had resumption of spontaneous cardiac activity while on CPB. Seven of these were weaned from CPB with intrinsic spontaneous circulation. Of these, six patients were transferred from the ED to the operating room for cannula removal and vessel repair while the other patient died in the ED soon after discontinuing CPB. Mean survival was 47.8+/-44.7 h in the six patients leaving the ED. Although these patients had successful hemodynamic resuscitation, there were no long-term survivors. CONCLUSION: CPB instituted by EPs is feasible and effective for the hemodynamic resuscitation of cardiac arrest patients unresponsive to advanced cardiac life support therapy. Future efforts need to focus on improving long-term outcome.

Progress in pediatric cardiopulmonary resuscitation.

The success rate for cardiopulmonary resuscitation (CPR) in children is dismal. This review discusses the physiology of CPR, the basis for pharmacologic therapy, and the rationale for advanced interventions. It focuses attention on those areas in which research indicates hope for improved outcomes.

Mastering pediatric cardiopulmonary resuscitation.

Premature and unexpected death, especially in children, is tragic and very unacceptable. Effective treatments for sudden death of pediatric patients continue to emerge. Modern cardiopulmonary resuscitation function began with the widespread introduction of closed-chest cardiac massage in 1960; however, despite 35 years of research and refinement, more than 90% of children who receive cardiopulmonary resuscitation do not survive. This article summarizes and expands on current treatment concepts for pediatric sudden death. Emphasis is placed on procedures and techniques that likely are accessible in most medical centers caring for critically ill and injured children.

High atrial natriuretic peptide concentrations blunt the pressor response during cardiopulmonary resuscitation in humans.

OBJECTIVE: To determine the relationship of circulating atrial natriuretic peptide concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. DESIGN: Prospective study. PATIENTS: Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. INTERVENTION: Patients received high-dose epinephrine (0.2 mg/kg) i.v. when standard advanced cardiac life support (including multiple 1-mg dosages of epinephrine) failed to result in return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were termed the "low atrial natriuretic peptide" and "high atrial natriuretic peptide" groups, respectively. Their aortic pressure response to high-dose (0.02 mg/kg) epinephrine was compared. The proportion with positive assays was compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide group was 151 +/- 82 pg/mL. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) (p = .002). The maximal increase in the aortic relaxation-phase pressures after high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic peptide group (p = .03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic peptide group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic peptide group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients in the high atrial natriuretic peptide group. CONCLUSIONS: Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may improve outcomes in patients suffering cardiac arrest.

Simultaneous radial, femoral, and aortic arterial pressures during human cardiopulmonary resuscitation.

OBJECTIVE: To examine the validity of interchanging arterial sites and their responses to graded doses of epinephrine during human cardiopulmonary resuscitation (CPR). DESIGN: Consecutive case series. SETTING: Large, urban Emergency Department. PATIENTS: Adult, normothermic, nonhemorrhagic cardiac arrest patients. INTERVENTIONS: While receiving advanced cardiac life support, patients received right atrial (n = 40), aortic (n = 40), radial (n = 40), and femoral (n = 17) artery catheters. Pressures were measured simultaneously at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine. MEASUREMENTS AND MAIN RESULTS: The mean aortic compression-phase pressure was 9.3 +/- 10 (SD), 8.1 +/- 11, and 4.4 +/- 9.5 mm Hg higher than radial artery pressure at baseline, after 0.01 mg/kg, and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the mean aortic compression-phase pressure was also 3.0 +/- 6.8, 1.9 +/- 8, and 0.6 +/- 7.7 mm Hg higher, respectively (none statistically significant). The aortic relaxation-phase pressure was 1.3 +/- 3.6, 1.1 +/- 3.8, and 1.6 +/- 2.5 mm Hg lower than the radial artery at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the aortic relaxation-phase pressure was 0.6 +/- 2.0, 0.3 +/- 3.3, and 0.3 +/- 2.4 mm Hg lower, respectively (none statistically significant). CONCLUSIONS: Radial artery relaxation-phase pressure, although statistically higher, correlated with aortic relaxation-phase pressure. Femoral artery relaxation-phase pressure was not statistically different from aortic relaxation-phase pressure. Aortic pressure was statistically higher and had a lower correlation with radial artery pressures during compression phase. The aortic to radial artery and aortic to femoral artery compression-phase gradients abated with increasing doses of epinephrine therapy. Caution must be used when substituting compression-phase pressure obtained at radial or femoral artery sites for aortic pressure during human CPR. Coronary artery perfusion pressures obtained with radial and femoral arteries correlate with aortic pressure when measuring the response to vasopressor therapy during CPR when an interpretable waveform exists.

Functional responses to extremely high plasma epinephrine concentrations in cardiac arrest.

OBJECTIVE: To evaluate the action of high-dose epinephrine by measuring simultaneously its vasopressor and norepinephrine releasing effects in humans during cardiac arrest. DESIGN: A prospective study on consecutive patients admitted with cardiac arrest. SETTING: Emergency Department in a large, urban hospital. PATIENTS: Eighteen patients with out-of-hospital cardiac arrest undergoing cardiopulmonary resuscitation (CPR). INTERVENTIONS: Catheterization of both the aorta and right atrium for the recording of pressure and collection of blood samples. Throughout the study period (12.5 mins), 18 patients received epinephrine at both the standard dose (1 mg, approximately 0.015 mg/kg) and high dose (0.2 mg/kg). Blood samples were drawn five times, every 2.5 mins. MEASUREMENTS AND MAIN RESULTS: Plasma epinephrine and norepinephrine concentrations; aorta, right atrial, and coronary perfusion pressures. Epinephrine concentrations (normal at rest = 160 +/- 10 [SEM] pmol/L) were increased at the time of the first sample (2.5 mins) by approximately 3,000-fold (to approximately 0.5 mumol/L), and, increased further to 12,000-fold (approximately 2.0 mumol/L) during the study. Aortic pressure increased from 20 +/- 3 to 28 +/- 3 mm Hg (p < .001), and coronary perfusion pressure increased from 4 +/- 3 to 10 +/- 3 mm Hg (p < .001). Simultaneous plasma norepinephrine concentrations were 30-fold higher than the normal resting value of 1.30 +/- 0.04 nmol/L, and increased by 90-fold during the study (p < .001). The spectral distributions of the individual correlations between plasma epinephrine and norepinephrine concentrations were segregated into high correlations (r > .83) in 12 of 18 patients and low r values (r = .29 to .79) in the remaining six patients. The distribution of the correlations was nonuniform by the Kolmogorov-Smirnov goodness-of-fit test with p < .001; this profile suggests that norepinephrine responsiveness to epinephrine can separate two populations, one of which (r > .83) would have preserved viability of the corresponding epinephrine receptors. The correlations between plasma epinephrine concentrations and coronary perfusion pressures were distributed more evenly, also in a nonuniform pattern (p < .02 by Kolmogorov-Smirnov goodness-of-fit test) and the relationship between the two sets of correlations was not significant. CONCLUSIONS: Despite the very high prevailing plasma epinephrine concentrations during cardiac arrest, further epinephrine increases still elicit biological responses. The present work provides physiologic support for the use of large doses of epinephrine during the course of CPR.

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.

Cerebral oxygen extraction during severe viral encephalitis.

Viral encephalitis can cause devastating neurologic injury. Little is known about cerebral hemodynamics and metabolism in this condition. We report two patients with severe encephalitis, one proven and the other suspected to be due to herpes simplex, in whom the global cerebral oxygen extraction ratio (OER) and carbon dioxide (CO2) responsiveness was assessed. OER was low in both patients throughout the acute period. CO2 responsiveness was present initially in both and disappeared later in the more severely affected child. These cases demonstrate that cerebral hyperemia occurs in severe viral encephalitis and that hyperventilation can effectively reduce the intracranial pressure.

Aortic pressure during human cardiac arrest. Identification of pseudo-electromechanical dissociation.

We measured aortic pressure during clinically apparent cardiac electromechanical dissociation (EMD). Patients with pulse pressures were designated as having pseudo-EMD; those without, as having true EMD. Of the 200 patients studied, 54 presented with EMD, and 40 others developed it during resuscitation. Of the 94 with EMD, 39 were found to have pseudo-EMD. We compared the two types of EMD for electrocardiographic duration, return of palpable pulses, and response to standard- and high-dose epinephrine. The mean resting aortic pressure was 18 +/- 11 mm Hg in patients with true EMD and 28 +/- 11 mm Hg in those with pseudo-EMD. The mean pulse pressure in patients with pseudo-EMD was 6.3 +/- 3.5 mm Hg. Patients with pseudo-EMD had a higher proportion of witnessed arrests, higher PaO2, and lower PaCO2 than patients with true EMD. Patients with pseudo-EMD had shorter QR and QRS durations than patients with true EMD. They had a better response to standard- and high-dose epinephrine than patients with true EMD. Many patients diagnosed clinically to be in EMD have mechanical cardiac activity; this should be considered when interpreting the results of cardiac arrest research.

Aortic-carotid artery pressure differences and cephalic perfusion pressure during cardiopulmonary resuscitation in humans.

OBJECTIVE: Animal studies have shown an aortic-carotid artery pressure difference during cardiopulmonary resuscitation (CPR), which compromises cerebral perfusion. This pressure difference is most marked with prolonged CPR and can be abolished with administration of high doses of epinephrine. To better understand the mechanism of cerebral blood flow during CPR in humans, we determined the aortic-carotid artery pressure difference, the cephalic perfusion pressure (the carotid artery-jugular vein pressure difference), and thoracic inlet venous "valving" (the central venous-jugular vein pressure difference), while administering standard doses of epinephrine. DESIGN: Prospective study with randomization as to which side the carotid artery was catheterized. SETTING: The resuscitation room of a large urban hospital's emergency department. PATIENTS: Fifteen adults in normothermic, nontraumatic prehospital cardiac arrest treated according to Advanced Cardiac Life Support guidelines, including administration of 1 mg epinephrine iv every 5 mins. INTERVENTIONS: The descending aorta, cervical common carotid artery, internal jugular vein, and central venous system were catheterized. Pressures were recorded during standard CPR for 5 mins after administration of 1 mg epinephrine iv. MEASUREMENTS AND MAIN RESULTS: Most patients received CPR for greater than 20 mins before the first epinephrine dose and for greater than 45 mins before pressure recording as described above. There was no significant difference between aortic and carotid artery compression and relaxation phase pressures. The mean +/- SD compression central venous-jugular vein pressure difference was 22.1 +/- 15.0 mm Hg, and the mean cephalic perfusion pressure was 20.8 +/- 19.5 mm Hg. CONCLUSIONS: There is no clinically important aortic-carotid artery pressure difference during human CPR using the standard dose of epinephrine, even with prolonged CPR. Despite carotid artery patency and thoracic inlet venous valving, the cephalic perfusion pressure is low during CPR in humans.

Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans.

Regional cerebrovascular oxygen saturation, a quantitative measure of hemoglobin saturation in the combined arterial, venous, and microcirculatory compartments of the brain, can be measured noninvasively with near infrared spectroscopy. We assessed the sensitivity of this aggregate saturation to cerebral hypoxia during transient cerebral hypoxic hypoxia in seven human subjects. Regional cerebrovascular oxygen saturation measured over the middle frontal gyrus and analog electroencephalogram were recorded. We compared the time to achieve two end points: the earliest paroxysmal burst of theta-delta background slowing and a cerebrovascular oxygen saturation of less than 55%. Saturation fell below 55% prior to the electroencephalographic change (p less than 0.05). In a related effort, we also compared spectroscopically measured regional cerebrovascular oxygen saturation with an estimate of this value calculated from arterial and cerebral mixed venous saturation in nine patients. A positive linear relation (n = 68, R2 = 0.55, s = 4.2) was noted.

Treatment of acute hypoxemic respiratory failure caused by chlorine exposure.

Chlorine inhalation may rapidly cause pulmonary edema, leading to acute hypoxemic respiratory failure. We report a 12 year old with acute respiratory failure from inhalation injury after he accidentally dropped chlorine tablets into a swimming pool. Supplemental oxygen alone failed to provide adequate arterial oxygenation. We administered positive end expiratory pressure (PEEP) in the emergency department, resulting in markedly improved oxygenation. Early institution of PEEP should be considered in patients with chlorine poisoning when supplemental oxygen alone is insufficient.

The effect of standard- and high-dose epinephrine on coronary perfusion pressure during prolonged cardiopulmonary resuscitation.

We studied the effect of standard and high doses of epinephrine on coronary perfusion pressure during cardiopulmonary resuscitation in 32 patients whose cardiac arrest was refractory to advanced cardiac life support. Simultaneous aortic and right atrial pressures were measured and plasma epinephrine levels were sampled. Patients remaining in cardiac arrest after multiple 1-mg doses of epinephrine received a high dose of 0.2 mg/kg. The increase in the coronary perfusion pressures was 3.7 +/- 5.0 mm Hg following a standard dose, not a statistically significant change. The increase after a high dose was 11.3 +/- 10.0 mm Hg; this was both statistically different than before administration and larger than after a standard dose. High-dose epinephrine was more likely to raise the coronary perfusion pressure above the previously demonstrated critical value of 15 mm Hg. The highest arterial plasma epinephrine level after a standard dose was 152 +/- 162 ng/mL, and after a high dose, 393 +/- 289 ng/mL. Because coronary perfusion pressure is a good predictor of outcome in cardiac arrest, the increase after high-dose epinephrine may improve rates of return of spontaneous circulation.

High-dose epinephrine improves outcome from pediatric cardiac arrest.

STUDY OBJECTIVE: Animal studies suggest that the standard dose of epinephrine (SDE) for treatment of cardiac arrest in human beings may be too low. We compared the outcome after SDE with that after high-dose epinephrine (HDE) in children with refractory cardiac arrest. DESIGN: Prospective intervention versus historic control groups. TYPE OF PARTICIPANTS: Two similar groups of 20 consecutive patients each (median ages, 2.5 and 3 years) with witnessed cardiac arrest who remained in arrest after at least two SDEs (0.01 mg/kg). INTERVENTIONS: Treatment with an additional SDE versus HDE (0.2 mg/kg). MEASUREMENTS AND MAIN RESULTS: The rates of return of spontaneous circulation and long-term survival were compared. Fourteen of the HDE group (70%) had return of spontaneous circulation, whereas none of the SDE group did (P less than .001). Eight children survived to discharge after HDE, and three were neurologically intact at follow-up. No significant toxicity from HDE was observed. CONCLUSION: HDE provided a higher return of spontaneous circulation rate and a better long-term outcome than SDE in our series of pediatric cardiac arrest. HDE may warrant incorporation into standard resuscitation protocols at an early enough point to prevent irreversible brain injury.

Right atrial-jugular venous pressure gradients during CPR in children.

OBJECTIVE: This study measured the internal jugular vein and right atrium pressures during pediatric CPR to detect and quantify venous pressure gradients across the thoracic inlet. DESIGN: Ten children from 2 months to 15 years old who underwent CPR had simultaneous pressure measurements recorded from the right atrium and jugular vein. RESULTS: The right atrium-jugular vein peak compression-phase gradient was 18.3 +/- 4.7 mm Hg (mean +/- SD), and the end-relaxation gradient was 0.7 +/- 0.6. Jugular vein pressure exceeded the right atrium only in the early-relaxation phase (right atrium-jugular vein = -2.1 +/- 1.2). Thoracic inlet venous valving persisted throughout the duration of CPR. CONCLUSION: There is a large venous gradient across the thoracic inlet during chest compressions in children, facilitating cerebral blood flow. This gradient reversed only in the early-relaxation phase. The data suggest that jugular venous return occurs only in the early-relaxation phase, whereas cerebral venous drainage persists throughout the CPR cycle.

Systemic atropine administration during cardiac arrest does not cause fixed and dilated pupils.

OBJECTIVES: Systemic administration of atropine during CPR may postpone brain death determination because of its reputed ability to produce fixed and dilated pupils. We studied the effect of atropine administered in the usual doses as an adjunct to endotracheal intubation and for cardiac arrest to determine if it would interfere with neurological assessment. DESIGN: Two groups of children were studied. Group 1 consisted of 28 patients who received atropine (0.03 +/- 0.003 mg/kg) prior to endotracheal intubation. Group 2 consisted of 21 patients previously without evidence of brainstem disease who suffered a witnessed arrest and had prompt return of spontaneous circulation and received an atropine dose of 0.03 +/- 0.01 mg/kg. RESULTS: In group 1, pupillary size averaged 4.02 +/- 0.78 mm before and 4.75 mm +/- .84 mm after atropine (P less than .001). In group 2, the pupillary examination was conducted 30 minutes after return of spontaneous circulation. The pupillary diameter was 4.80 +/- 0.91 mm. All pupils were reactive to light in both groups. CONCLUSION: Atropine administration in conventional dose causes slight pupillary dilation but does not abolish pupillary light reactivity.

Jugular bulb catheterization does not increase intracranial pressure.

Cerebral venous monitoring through jugular bulb catheterization (JBC) allows assessment of global oxygen delivery adequacy. Because of concern that venous obstruction by catheterization may cause or exacerbate intracranial hypertension, physicians are reluctant to puncture this vessel in brain-injured patients. We evaluated the impact of JBC on intracranial pressure (ICP). 37 consecutive pediatric patients with jugular bulb catheters and ICP monitoring were studied. ICP was monitored in 28 patients during JBC. Also immediately after JBC and daily thereafter the contralateral, ipsilateral, and bilateral jugular veins were compressed in all 37 patients to assess patency of these vessels. Change in ICP was noted. If ICP increased more than 5 torr, compression was stopped. Preinsertion ICP was 17.3 +/- 5.1 and postinsertion 17.2 +/- 5.1 torr. The maximum rise in ICP was 2 torr in a single patient while 6 others had a decrease in ICP. 120 compression tests were performed. Compression ipsilateral to the catheter caused the ICP to rise from 16.0 +/- 4.3 to 18.4 +/- 4.4 torr, and in contralateral compression 15.9 +/- 4.2 to 17.0 +/- 4.4. Neither the duration of catheterization nor the precompression ICP correlated with the rise in ICP. These data revealed no evidence of jugular venous obstruction in the catheterized vessel. We conclude that JBC can be performed in patients without aggravating an elevated ICP.