Gerard B. Martin

Continuous central venous oximetry and shock index in the emergency department: Use in the evaluation of clinical shock

Initial therapy of shock in the emergency department (ED) emphasizes the normalization of physiologic variables such as heart rate (HR), mean arterial pressure (MAP), and central venous pressure (CVP) rather than restoration of adequate tissue oxygenation. After hemodynamic stabilization of MAP, CVP, and HR, the authors examined tissue oxygenation as indicated by continuous central venous oximetry (SCVO2), lactic acid concentration, and shock index (SI). Sixteen consecutive nonrandomized patients presenting to the ED of a large urban hospital in shock (MAP < 60 mm Hg, HR > 120 beats/min, and altered sensorium) were initially resuscitated with fluid, blood, inotropes, and/or vasoactive drug therapy to normalize MAP, CVP, and HR. In addition, SCVO2, arterial lactate concentration, and SI were measured after completion of resuscitation in the ED. Eight patients (group no. 1) had inadequate tissue oxygenation reflected by low SCVO2 (less than 65%). Four patients in group no. 1 had elevated arterial lactic acid concentration. All group no. 1 patients had an elevated SI (> 0.7) suggesting persistent impairment of left ventricular stroke work. Eight patients (group no. 2) had normal or elevated SCVO2 (> 65%). In group no. 2, arterial lactic acid concentration was elevated in six and SI in seven patients. Normalization of hemodynamic variables does not adequately reflect the optimal endpoint of initial therapy in shock in the ED. Most (94%) of these patients continue to have significant global ischemia and cardiac dysfunction as indicated by reduced SCVO2 and elevated lactic acid concentration and SI. Systemic tissue oxygenation should be monitored and optimized in the ED in these critically ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms.

Pressure gradients across and between the head and chest were studied during mechanical cardiopulmonary resuscitation (CPR) in 22 humans. Patients in medical cardiac arrest, managed by ACLS guidelines, underwent placement of aortic arch (Ao), jugular venous bulb (JVB), and right atrial (RA) catheters. Simultaneous pressures were measured, and intercatheter gradients were calculated. The JVB to RA pressure difference is the gradient between the cervical and central venous circulations. It was negative when averaged throughout the CPR cycle and was more negative during compression than relaxation, -19 +/- 12 and -2 +/- 6 mm Hg, respectively. This indicates that the intrathoracic pressure rise was not transmitted to the jugular venous system, supporting the concept of a competent jugular valve mechanism during CPR. It is consistent with the thoracic pump model of cerebral perfusion. JVB to RA was positive only during early relaxation, allowing blood return from the head. The Ao to JVB gradient, although not equal to cerebral perfusion pressure, is the maximum potential pressure gradient for blood flow across the cerebral vasculature. It was positive throughout CPR, 25 +/- 17 during compression, and 9 +/- 10 mm Hg during relaxation. The Ao to RA gradient during the relaxation phase is CPR coronary perfusion pressure. In most patients, it was minimally positive in both phases of the CPR cycle: 7 +/- 14 in compression and 7 +/- 9 mm Hg during relaxation. This appears to be inadequate in providing sufficient blood flow to meet the metabolic needs of the myocardium. Four patients had larger gradients during compression suggestive of cardiac compression.(ABSTRACT TRUNCATED AT 250 WORDS)

A characterization of hypothalamic-pituitary-adrenal axis function during and after human cardiac arrest

ObjectiveThis study characterizes hypothalamic-pituitary-adrenal axis function during cardiopulmonary arrest and after return of spontaneous circulation. DesingProspective case series. SettingA large urban emergency department and intensive care unit over an 8-month period. PatientsTwo hundred five adult patients presenting in cardiopulmonary arrest to an urban emergency department. Three patients known to be taking corticosteroids were excluded from the study. Measurements and Main ResultsCortisol concentrations were measured before and after advanced cardiac life support and for five consecutive hours after return of spontaneous circulation. Adrenocorticotropic hormone (ACTH) concentrations were measured before advanced cardiac life support and when the cosyntropin stimulation tests were performed 6 and 24 hrs after the return of spontaneous circulation.The mean initial serum cortisol concentration was 32.0 ± 33.1 μg/dL (882.9 ± 913.2 nmol/L). Fifty-three percent of patients had cortisol concentrations of<20 μg/dL (< 552 nmol/L) at the end of cardiac arrest. Among 44 patients who achieved return of spontaneous circulation, 98% had initial cortisol concentrations of >10 μg/dL (>276 nmol/L) and 73% of patients had initial cortisol concentrations of >20 μg/dL (>552 nmol/L). Mean serum cortisol concentrations increased significantly (p = .0001) from 1 to 6 hrs after return of spontaneous circulation and decreased dignificantly (p = .03) from 6 to 24 hrs. A serum cortisol concentration of<30 μg/dL (< 828 nmol/L) was associated with a 96% and 100% mortality rate at 6 and 24 hrs, respectively. Mean ACTH concentrations were increased without a significant difference between the initial and 6-hr concentrations. Mean ACTH concentrations decreased between 6 and 24 hrs (p = .06). There were no significant responses to the cosyntropin stimulation at 6 and 24 hrs. ConclusionsCortisol concentrations after out-of-hospital cardiac arrest are lower than those concentrations reported in other stress states. There is an association between cortisol concentrations and short-term survival after cardiac arrest. Survivors have a significantly greater increase in serum cortisol concentrations than nonsurvivors during the first 24 hrs. Lower than expected cortisol concentrations for the extreme stress of cardiac arrest may have pathologic significance in the hemodynamic instability seen after return of spontaneous circulation. The etiology of the low cortisol concentrations may be primary adrenal dysfunction. (Crit Care Med 1993;21:1339–1347)

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 Conclusion: Continuous central venous oxygen saturation monitoring can serve as a reliable indicator of return of spontaneous circulation during CPR in human beings.

Effect of epinephrine on end-tidal carbon dioxide monitoring during CPR

End-tidal carbon dioxide (ETCO2) has been shown to correlate with coronary perfusion pressure (CPP) during CPR and has been proposed as a useful noninvasive monitor of CPR efficacy. The effects of therapeutic epinephrine dosing on ETCO2 and CPP in six dogs were examined. Ventricular fibrillation was induced and left untreated for five minutes before CPR was initiated. After five minutes of CPR, epinephrine 0.045 mg/kg IV was administered. CPP and ETCO2 were compared immediately before and two minutes after epinephrine administration. There was a significant increase in CPP from 12.2 +/- 9.6 to 26.8 +/- 7.1 mm Hg (P = .006) after epinephrine. This was accompanied by a significant decrease in ETCO2 from 8.2 +/- 2.9 to 3.8 +/- 2.0 mm Hg (P = .01). These data indicate that after epinephrine administration, caution must be exercised in using ETCO2 as an indicator of CPP.

Aortic and right atrial pressures during standard and simultaneous compression and ventilation cpr in human beings

Coronary perfusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient, has been shown to correlate well with coronary blood flow during standard external CPR (SE-CPR) and is an important determinant of successful cardiac resuscitation. Few studies have documented such Ao-RA gradients in human beings, however. Twenty patients sustaining out-of-hospital cardiopulmonary arrests and basic cardiac life support were instrumented with thoracic aortic and right atrial catheters on arrival in the emergency department. The mean time from arrival in the ED to catheter placement was 16.5 +/- 6.0 minutes. With SE-CPR, peak systolic aortic and right atrial pressures were 73.7 +/- 20.2 mm Hg and 69.6 +/- 18.3 mm Hg, respectively. End diastolic aortic and right atrial pressures were 27.9 +/- 7.3 mm Hg and 20.3 +/- 7.2 mm Hg, respectively, with an end diastolic gradient of 7.9 +/- 9.1 mm Hg. Three patients had systolic Ao-RA gradients of more than 25 mm Hg, which is consistent with some cardiac compression as a mechanism of flow. Five patients also had one-minute trials of simultaneous compression and ventilation CPR (SCV-CPR). Ao-RA end diastolic gradients decreased in four of the five during SCV-CPR. No patient in this study was resuscitated successfully. We conclude that ED SE-CPR provides little coronary perfusion for victims of prehospital cardiac arrest. Although SCV-CPR has been shown to improve carotid blood flow in human beings, it appears to have an adverse effect on the already minimal myocardial perfusion provided by SE-CPR.

Cardiopulmonary bypass vs CPR as treatment for prolonged canine cardiopulmonary arrest

Although in vitro studies have demonstrated functional recovery of neurons after prolonged ischemia, in vivo experience with patients resuscitated from cardiopulmonary arrest demonstrates much less cerebral resistance to global ischemia. The purpose of our investigation was to compare the effectiveness of femoro-femoral veno-arterial cardiopulmonary bypass (CPB) to standard cardiopulmonary resuscitation in the treatment of prolonged cardiopulmonary arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without any therapy for 12 minutes. Subsequently, either CPB (n = 5) or CPR (n = 5) was initiated and resuscitation attempted according to a standardized protocol that included administration of the calcium channel blocker lidoflazine in an effort to optimize cerebral and myocardial recovery. If there was return of spontaneous circulation, the animal was managed in an intensive care setting with invasive hemodynamic monitoring and ventilatory support for up to nine hours. Neurologic function was graded using a standardized neurologic deficit scoring (NDS) system at 12 hours after insult and daily for one week or until death. Prearrest hemodynamic and metabolic parameters were comparable in both groups (P greater than .05). All CPB animals were resuscitated successfully and alive at 24 hours after insult as opposed to none in the CPR group (P less than .005). In addition, three of the CPB animals were neurologically normal at final grading with NDS scores of zero. The other two CPB animals had persistent severe neurologic impairment and a mean NDS score of 51%. Thus CPB is more effective than CPR in the treatment of prolonged cardiopulmonary arrest. The improved outcome probably results primarily from improvement in blood flow with CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of open chest cardiopulmonary resuscitation after failure of standard closed chest CPR: illustrative cases

Compared to standard closed chest CPR, open chest cardiac massage improves vital organ perfusion and survival in animal models of medical cardiac arrest. Yet its use is essentially limited to the treatment of traumatic arrest. Three cases of medical cardiac arrest are presented in which open chest compression was used after failure of external chest compression. These cases illustrate the range of potential outcomes and how this therapy can be optimally applied. Approaches we have used to prevent application of futile intensive therapy in patients unlikely to be neurologically intact survivors are described. Replacement of open chest CPR by closed chest CPR as the standard of care for the in-hospital cardiac arrest was not justified by experimental data. The circumstances of refractory cardiac arrest make it unlikely that well controlled human studies will be able to demonstrate the superiority of open chest CPR in selected patients. The decision to use this therapy will likely remain within the art of medicine.

Effects of arterial and venous volume infusion on coronary perfusion pressures during canine CPR

Intraarterial (IA) volume infusion has been reported to be more effective than intravenous (IV) infusion in treating cardiac arrest due to exsanguination. A rapid IA infusion was felt to raise intraaortic pressure and improve coronary perfusion pressure (CPP). The purpose of this study was to determine if IA or IV volume infusion could augment the effect of epinephrine on CPP during CPR in the canine model. Nineteen mongrel dogs with a mean weight of 26.3 +/- 4.2 kg were anesthetized and mechanically ventilated. Thoracic aortic (Ao), right atrial (RA) and pulmonary artery catheters were placed for hemodynamic monitoring. Additional Ao and central venous catheters were placed for volume infusion. Ventricular fibrillation was induced and Thumper CPR was begun after 5 min (t = 5). At t = 10, all dogs received 45 micrograms/kg IV epinephrine. Six animals received epinephrine alone (EPI). Five dogs received EPI plus a 500 cc bolus of normal saline over 3 min intravenously (EPI/IV). Another group (n = 8) received EPI plus the same fluid bolus through the aortic catheter (EPI/IA). Resuscitation was attempted at t = 18 using a standard protocol. There was a significant increase in CPP over baseline in all groups. The changes in CPP from baseline induced by EPI, EPI/IV and EPI/IA were 20.6 +/- 3.7, 22.8 +/- 4.2 and 22.2 +/- 2.4 mmHg, respectively. Volume loading did not augment the effect of therapeutic EPI dosing. By increasing both preload and afterload, volume administration may in fact be detrimental during CPR.

Nuclear magnetic resonance spectroscopy study of human brain after cardiac resuscitation.

We used 31P nuclear magnetic resonance spectroscopy to study the cerebral metabolic function of eight patients with severe postischemic anoxic encephalopathy secondary to cardiac arrest. Spectroscopy was performed at 18 +/- 13 and 64 +/- 20 hours after resuscitation. Glasgow Coma Scale scores at the time of initial and repeat spectroscopy were 3.6 +/- 1.2 and 3.5 +/- 1.2, respectively. In those patients whose spectra were of adequate quality to monitor pH, all demonstrated tissue alkalosis in at least one brain region. The mean brain pH at initial spectroscopy was 7.14 +/- 0.09 and was significantly alkalotic when compared with age- and sex-matched normal controls (pH = 6.98 +/- 0.04, p less than 0.0001). Five of the eight patients showed at least one region of persistent alkalosis at repeat spectroscopy, whereas one patient demonstrated severe acidosis with a pH of 6.42. Spectra demonstrated marked metabolic heterogeneity, ranging from normal in appearance to complete obliteration of all high-energy phosphates with only inorganic phosphate remaining.