Adrenal dysfunction in hemodynamically unstable patients in the emergency department.

OBJECTIVE: Adrenal failure, a treatable condition, can have catastrophic consequences if unrecognized in critically ill ED patients. The authors' objective was to prospectively study adrenal function in a case series of hemodynamically unstable (high-risk) patients from a large, urban ED over a 12-month period. METHODS: In a prospective manner, critically ill adult patients presenting to the ED were enrolled when presenting with a mean arterial blood pressure < or =60 mm Hg requiring vasopressor therapy for more than one hour after receiving fluid resuscitation (central venous pressure of 12-15 mm Hg or a minimum of 40 mL/kg of crystalloid). Patients were excluded if presenting with hemorrhage, trauma, or AIDS, or if steroids were used within the previous six months. An adrenocorticotropic hormone (ACTH) stimulation test was performed and serum cortisol was measured. Treatment for adrenal insufficiency was not instituted. RESULTS: A total of 57 consecutive patients were studied. Of these, eight (14%) had baseline serum cortisol concentrations of <20 microg/dL (<552 nmol/L), which was considered adrenal insufficiency (AI). Three additional patients (5%) had subnormal 60-minute post-ACTH-stimulation cortisol responses (<30 microg/dL) and a delta cortisol < or =9 microg/dL, which is the difference between the baseline and 60-minute levels. This is functional hypoadrenalism (FH). There were no laboratory abnormalities that distinguished patients with AI or FH from those with preserved adrenal function (PAF). Rates of survival to discharge did not differ between the AI group (7 of 8) and PAF patients (21 of 46; p = 0.052). CONCLUSIONS: Adrenal dysfunction is common in high-risk ED patients. Overall, it has a frequency of 19% among a homogeneous population of hemodynamically unstable vasopressor-dependent patients. The effect of physiologic glucocorticoid replacement in this setting remains to be determined.

Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation.

OBJECTIVES: To determine the hemodynamic effect of vasopressin on coronary perfusion pressure (CPP) in prolonged human cardiac arrest. METHODS: A prospective, open-label clinical trial of vasopressin during cardiac resuscitation was performed. Ten patients presenting in cardiac arrest initially received resuscitative measures by emergency physicians according to Advanced Cardiac Life Support (ACLS) guidelines. A central venous catheter for fluid and drug administration and a femoral artery catheter for measurement of CPP (aortic minus right atrial relaxation phase pressures) were placed. When each patient was deemed nonsalvageable, 1.0 mg epinephrine was given and CPP was measured for 5 minutes, followed by a dose of vasopressin (1.0 U/kg). CPP measurements were continued for another 5 minutes. RESULTS: The mean duration of cardiac arrest (out-of-hospital interval plus duration of ED ACLS) was 39.6 +/- 16.5 min. There was no improvement in CPP after 1.0 mg of epinephrine. Vasopressin administration resulted in a significant increase of CPP in 4 of the 10 patients. Patients responding to vasopressin had a mean increase in CPP of 28.2 +/- 16.4 mm Hg (range: 10-51.5), with these peak increases occurring at 15 seconds to 4 minutes after administration. The increases in the vasopressin levels after administration did not differ between the responders and nonresponders. CONCLUSIONS: In this human model of prolonged cardiac arrest, 40% of the patients receiving vasopressin had a significant increase in CPP. This pilot study suggests that investigation of earlier use of vasopressin as a therapeutic alternative in the treatment of cardiac arrest is warranted.

Hemodynamic effects of aortic occlusion during hemorrhagic shock and cardiac arrest.

OBJECTIVE: To determine the hemodynamic consequences of aortic occlusion during controlled hemorrhagic arrest. METHODS: Ten anesthetized, hemodynamically monitored swine were subjected to a 40 mL/kg hemorrhage over 10 minutes, followed by a 5-minute period of apnea. At this time (T15), they were randomized into an UP group (n = 5) in which the thoracic aorta was occluded or a DOWN group (n = 5) in which the aorta was not occluded. Simultaneously, volume resuscitation with shed blood plus 20 mL/kg of normal saline was performed over a 10-minute period. Cardiac massage was performed until return of spontaneous circulation (ROSC), which was defined as a sustained systolic blood pressure > 60 mm Hg. After 30 minutes of occlusion (T45), the aortic occlusion was released. Parameters measured include mixed venous and arterial blood gases, serum lactic acid levels, cardiac index, mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), coronary perfusion pressure (CoPP), and left ventricular stroke work index (LVSWI). Oxygen delivery index (DO2I) was measured using a pulmonary artery catheter, and oxygen consumption index (VO2I) was measured by direct calorimetry (Delta Trac metabolic monitor). RESULTS: Four animals in each group achieved ROSC after 3.0 +/- 1.8 and 2.2 +/- 1.8 minutes in the occluded and nonoccluded groups, respectively. During cardiac compressions and volume resuscitation, the CoPP, MAP, and MPAP were greater in the UP group, although the differences did not achieve statistical significance. After volume resuscitation was complete and during the period of aortic occlusion (T25-T45), the UP group had significantly greater MAP (mm Hg), with a difference of 42.5 +/- 20.75 mm Hg at T25 and 44.7 +/- 19 mm Hg at T35 (p < 0.03). Despite no difference in DO2I, VO2I (mL/min/kg) was significantly lower in the UP group than in the DOWN group, 4.28 +/- 0.48 versus 8.33 +/- 0.85 at T25 (p = 0.0002) and 4.62 +/- 0.9 versus 7.09 +/- 0.72 at T35 (p = 0.0005). After release of aortic occlusion at T45, the UP group had significantly lower CoPP (mm Hg) than the DOWN group (20.5 +/- 17.3 versus 66.5 +/- 28.2 at T45, p = 0.03). LVSWI (g/kg) was also lower in the UP than in the DOWN group (18.6 +/- 8.28 versus 36.5 +/- 10.2 at T60 [p = 0.031 and 23.6 +/- 6.48 versus 48.8 +/- 15.3 at T240 [p = 0.021). After release of the occlusion, there were trends toward increased acidosis and lactic acid levels in the UP group. CONCLUSIONS: Aortic occlusion in this controlled hemorrhagic arrest model does not result in improved salvage but is associated with impaired left ventricular function, systemic oxygen utilization, and coronary perfusion pressure in the postresuscitation period.