Vasopressor-resistant Hypotension Research Articles

VASOPRESSOR-RESISTANT HYPOTENSION, COMBINATION VASOPRESSOR THERAPY, AND SHOCK PHENOTYPES IN CRITICALLY ILL ADULTS WITH VASODILATORY SHOCK.

ABSTRACTObjective: To examine the risk factors, resource utilization, and 1-year mortality associated with vasopressor-resistant hypotension (VRH) compared with vasopressor-sensitive hypotension (VSH) among critically ill adults with vasodilatory shock. We also examined whether combination vasopressor therapy and patient phenotype were associated with mortality. Design: Retrospective cohort study. Setting: Eight medical-surgical intensive care units at the University of Pittsburgh Medical Center, Pittsburgh, PA. Patients: Critically ill patients with vasodilatory shock admitted between July 2000 and October 2008. Interventions: None. Measurements and Main Results: Vasopressor-resistant hypotension was defined as those requiring greater than 0.2 μg/kg per minute of norepinephrine equivalent dose of vasopressor consecutively for more than 6 h, and VSH was defined as patients requiring ≤0.2 μg/kg per minute to maintain MAP between 55 and 70 mm Hg after adequate fluid resuscitation. Of 5,313 patients with vasodilatory shock, 1,291 patients (24.3%) developed VRH. Compared with VSH, VRH was associated with increased risk of acute kidney injury (72.7% vs. 65.0%; P < 0.001), use of kidney replacement therapy (26.0% vs. 11.0%; P < 0.001), longer median (interquartile range [IQR]) intensive care unit length of stay (10 [IQR, 4.0–20.0] vs. 6 [IQR, 3.0–13.0] days; P < 0.001), and increased 1-year mortality (64.7% vs. 34.8%; P < 0.001). Vasopressor-resistant hypotension was associated with increased odds of risk-adjusted mortality (adjusted odds ratio [aOR], 2.93; 95% confidence interval [CI], 2.52–3.40; P < 0.001). When compared with monotherapy, combination vasopressor therapy with two (aOR, 0.91; 95% CI, 0.78–1.06) and three or more vasopressors was not associated with lower mortality (aOR, 0.93; 95% CI, 0.68–1.27). Using a finite mixture model, we identified four unique phenotypes of patient clusters that differed with respect to demographics, severity of illness, processes of care, vasopressor use, and outcomes. Conclusions: Among critically ill patients with vasodilatory shock, VRH compared with VSH is associated with increased resource utilization and long-term risk of death. However, combination vasopressor therapy was not associated with lower risk of death. We identified four unique phenotypes of patient clusters that require further validation.

Life-Threatening Amlodipine Over Dose Requiring ECMO Support Treated by High-Cut-Off Dialysis and Cytosorb

Calcium Channel Blockers (CCBs) may cause profound vasopressor resistant hypotension in case of intoxication. Recently, the EXTRIP workgroup recommended against the use of Extra Corporeal Treatment Modalities (ECTM) for the elimination of amlodipine. Anecdotal evidence suggests that Veno-Arterial Extra Corporeal Membrane Oxygenation (VA-ECMO) may be beneficial in patients with severe shock due to amlodipine intoxication. We report a case of severe amlodipine poisoning (total amlodipine intake 625 mg), in which we used awake-VA- ECMO support for hemodynamic stabilization. A combination of a HCO dialyzer and the Cytosorb® adsorber was used to eliminate amlodipine in two consecutive treatment sessions. Amlodipine dialyzer clearance and Cytosorb® adsorber clearance were 13.8 (-2,3–20.4) mL/min and 17.5 (9.6–25.6) mL/min, respectively. Clearance levels varied depending on drug plasma levels. During this treatment, initial amlodipine levels fell by 48% and 15% with a total eliminated amount of 242 and 352 μg of amlodipine, respectively, in the dialysate. EXTRIP criteria for dialyzability could not be met by the investigated modalities. ECMO therapy was discontinued after three days and the patient fully recovered. In conclusion, VA-ECMO support can be used for hemodynamic stabilization of patients with severe amlodipine poisoning, while the extracorporeal elimination techniques used in this setting were unable to remove a meaningful amount of drug.

Abstract 16542: Hypotension and Pericardial Effusion Associated With High Frequency Jet Ventilation

Introduction: High frequency jet ventilation (HFJV) is used to increase catheter stability and improve outcomes during pulmonary vein isolation (PVI) [1,2,4]. In studies, hemodynamic intolerance of HFJV was rare. [1,3]. Hypothesis: HFJV during PVI is well tolerated and vasopressor-resistant hypotension requiring return to conventional ventilation is rare. Methods: Retrospective observational analysis of hemodynamic, blood gas, and echocardiographic data of PVIs performed with HFJV by 2 operators (PT, JW) at our institution between February 2019 and June 2020. Results: Among 193 PVIs, 8 cases (4%) of rapid onset hypotension associated with HFJV were found (Table). In 7 of 8 cases, persistent hypotension and abnormal gas exchange required conversion to conventional ventilation and a new, small pericardial effusion without tamponade was noted just after HFJV initiation. In these cases, initiation of HFJV was associated with a decrease in systolic function. Both the hemodynamic changes and effusion resolved completely within minutes of stopping HFJV. Four of 8 patients were rechallenged with HFJV, and had recurrent hypotension and effusion which resolved immediately after return to conventional ventilation. Conclusions: HFJV-associated rapid onset hypotension, often accompanied by transient pericardial effusion, is more common than previously reported, and resolves with cessation of HFJV. The mechanism of these changes may occur via CO2 levels and warrants further study.

Adrenal insufficiency in coronavirus disease 2019: a case report

BackgroundNovel coronavirus disease 2019 presents with fever, dry cough, fatigue, and shortness of breath in most cases; however, some rare manifestations in other organs have also been reported so far.Case presentationHere, the case of a 69-year-old Iranian man with coronavirus disease 2019 is presented who suffered from frequent episodes of vasopressor-resistant hypotension during intensive care unit admission, which was finally attributed to the occurrence of acute adrenal insufficiency.ConclusionsAs this is a rare complication, adrenal insufficiency might be easily overlooked. However, early detection of this disease among critically ill patients infected with coronavirus disease 2019 could be lifesaving, especially among those unresponsive to vasopressor agents.

Arterial Stiffness Predicts General Anesthesia–Induced Vasopressor-Resistant Hypotension in Patients Taking Angiotensin-Converting Enzyme Inhibitors

Patients chronically treated with angiotensin-converting enzyme inhibitors (ACEIs) may develop hypotension after induction of general anesthesia. A fraction of these patients are resistant to therapeutic doses of vasopressors, which poses serious concerns for hemodynamic management. The authors hypothesized that the patients who develop refractory hypotension, compared with those who do not, show lower central arterial stiffness due to the profound effect of ACEIs. Prospective observational study. Single tertiary center. Fifty surgical patients chronically treated with ACEIs were enrolled. Prior to surgery, all the patients had central arterial stiffness assessment measured by carotid-femoral pulse-wave velocity. Patients were categorized into 2 groups according to the systolic blood pressure response during the first 10 minutes after induction of general anesthesia: a vasopressor-resistant hypotension group requiring more than 200 µg phenylephrine, or a control group requiring no more than 200 µg of phenylephrine to maintain systolic blood pressure above 90 mmHg during the study period. Carotid-femoral pulse-wave velocity was significantly lower in the vasopressor-resistant hypotension group compared to the control group (7.6 [7.2-8.3] m/s v 9.9 [8.7-12.0] m/s, p = 0.001 [Hodges-Lehman median difference 2.2, 95% confidence interval = 1.1-4.4]). These findings suggested that preoperative measurement of carotid-femoral pulse-wave velocity in patients chronically treated with ACEIs could help identify patients at increased risk of developing hypotension refractory to vasopressors after induction of general anesthesia.

Acute Infectious Purpura Fulminans Complicated with Multiple Erosions

An 80-year-old man was extremely skinny and developed a left leg phlegmon. He was admitted and underwent an infusion of cefazolin. On the third day, he suddenly collapsed, and advanced cardiac life support resulted in a return of his circulation. He showed vasopressor-resistant hypotension and therefore received an infusion of steroids and multiple supportive therapies. A blood culture later showed Pseudomonas aeruginosa. While his blood pressure increased, he showed peripheral and labile cyanotic changes, even though his peripheral arteries were palpable. On the third day after the collapse, he showed blisters at purpura sites and labile, resulting in the formation of erosions. On the fourth day, massive effusion was drained from the erosive lesions. He temporarily showed a return of consciousness, but his extremities became necrotic, and he ultimately died due to a secondary infection at the erosive lesions. The present fatal case of acute infectious purpura fulminans might have been induced by a P. aeruginosa infection due to complications with multiple blisters, similar to Stevens-Johnson syndrome/toxic epidermal necrolysis. Early aggressive surgical amputation or debridement might be required to obtain a survival outcome when encountering such cases.

Cortisol precursors in neonates with vasopressor-resistant hypotension in relationship to demographic characteristics

Objective: To correlate between cortisol precursors in neonates with vasopressor resistant hypotension and demographic characteristics. Methods: We investigated 48 neonates with vasopressor-resistant hypotension. Gestation at birth ranged from 34 to 42 weeks and postnatal age from 4 to 14 days. Cortisol and precursor steroids were measured soon after the onset of volume expansion and inotropes for treatment of shock. Their concentrations were determined using liquid chromatography/mass spectrometry. Results: In neonates with vasopressor-resistant hypotension, the serum levels of cortisol were within normal nonstress range. There was a strong negative linear association between postnatal age and dehydroepiandrosterone level (r = −0.50, p < .01), which decreased with neonatal age. In addition, there was a significant positive association between gestational age at birth and 17-hydroxy-pregnenolone (r = 0.33, p = .02). No further significant associations were evident between the neonatal weight, duration of gestation or gender and of the levels of cortisol or the other steroids (p > .05). The cause of therapy-resistant hypotension did not appear to influence the steroid levels. Conclusions: Cortisol stress response is absent in these severely ill late preterm and term infants. This may be due to inhibition of the distal pathway of cortisol synthesis.

Hyperdehydroepiandrosterone in neonates with hypoxic ischemic encephalopathy and circulatory collapse

Circulatory collapse is a very common complication of the critical illnesses in neonates including neonates with hypoxic ischemic encephalopathy; it can be the end result and cause of death of several conditions. Often, despite treatment with fluid resuscitation and vasopressor agents, circulatory collapse persist, and blood pressure can remain critically low, compromising adequate blood flow to vital organs and brain. Low blood pressure has been associated with increased mortality. To investigate adrenal function in newborn infants who suffer from circulatory collapse during hypoxic ischemic encephalopathy. A total of 30 infants were analyzed in the study: 15 neonates in group A (neonates had hypoxic ischemic encephalopathy with vasopressor resistant hypotension) and 15 neonates in group B (neonates with hypoxic ischemic encephalopathy without vasopressor resistant hypotension). All the studied patients were subjected to history, examinations and laboratory investigation including serum cortisol concentrations and cortisol precursor's levels. The cortisol concentrations did not differ significantly between the two groups: (12.9±4.3) μg/dL and (12.1±2.4) μg/dL in group A and group B, respectively. There are highly significant differences between groups A and B regarding Dehydroepiandrosterone (342.1±101.3) μg/dL, (33.4±16.5) μg/dL, respectively. In this study, we noticed that cortisol concentrations did not differ between both groups in contrast to the expectation that neonates with critical illnesses should have higher cortisol concentrations than normal neonates. However, the marked increase in dehydroepiandrosterone DHEA may cause decrease cortisol function, so those neonates having accumulation of dehydroepiandrosterone may suffer from manifestation of adrenal insufficiency and vasopressor resistant hypotension in spite of normal cortisol level.

Inotrope and Vasopressor Support in Neonates

Hemodynamic instability is a common problem in neonates and has important implications for long-term outcomes. Inotropes and vasopressors are commonly used to treat low blood pressure or poor perfusion in neonatal intensive care, despite limited evidence to guide optimal management in specific clinical situations. Dopamine is the most commonly used agent in clinical practice, increasing blood pressure with limited adverse effects compared with epinephrine. Dobutamine is less commonly used but may be the optimal agent for premature neonates with poor perfusion due to immature myocardial contractility. New evidence is emerging to guide the treatment of hypotension in the setting of sepsis and persistent pulmonary hypertension. Norepinephrine and vasopressin may have utility in the setting of refractory hypotension due to sepsis. Increasing evidence supports use of norepinephrine, milrinone, and vasopressin in the setting of persistent pulmonary hypertension. Hydrocortisone should be reserved for vasopressor-resistant hypotension in preterm neonates; however, this agent may also prove useful in the treatment of persistent pulmonary hypertension in term neonates. Further clinical trials are necessary to determine the optimal treatment algorithm for neonates with hemodynamic instability. Future trials should include physiologically relevant end points and long-term follow-up. However, one approach may not be efficacious for all neonates even with a similar diagnosis. Therefore, bedside assessment techniques should continue to be explored to allow tailored therapy based on real-time assessment of underlying physiology.

Population Pharmacokinetics of Unbound Hydrocortisone in Critically Ill Neonates and Infants With Vasopressor-Resistant Hypotension

To determine the population pharmacokinetics of unbound hydrocortisone in critically ill neonates and infants receiving IV hydrocortisone for treatment of vasopressor-resistant hypotension and to identify patient-specific sources of pharmacokinetic variability. Prospective observational cohort study. Level 3 neonatal ICU. Sixty-two critically ill neonates and infants receiving IV hydrocortisone as part of standard of care for the treatment of vasopressor-resistant hypotension: median gestational age 28 weeks (range, 23-41), median weight 1.2 kg (range, 0.5-4.4), and 29 females. None. Unbound baseline cortisol and postdose hydrocortisone concentrations measured from blood samples being drawn for routine laboratory tests. A one-compartment model best described the data. Allometric weight and postmenstrual age were significant covariates on unbound hydrocortisone clearance and volume of distribution. Final population estimates for clearance, volume of distribution, and baseline cortisol concentration were 20.2 L/hr, 244 L, and 1.37 ng/mL, respectively. Using the median weight and postmenstrual age of our subjects (i.e., 1.2 kg and 28 wk) in the final model, the typical unbound hydrocortisone clearance and volume of distribution were 1.0 L/hr and 4.2 L, respectively. The typical half-life for unbound hydrocortisone was 2.9 hours. A sharp and continuous increase in unbound hydrocortisone clearance was observed at 35 weeks postmenstrual age. We report the first pharmacokinetic data for unbound hydrocortisone, the pharmacologically active moiety, in critically ill neonates and infants with vasopressor-resistant hypotension. Unbound hydrocortisone clearance increased with body weight and was faster in children with an older postmenstrual age. Unbound hydrocortisone clearance increased sharply at 35 weeks postmenstrual age and continued to mature thereafter. This study lays the groundwork for evaluating unbound hydrocortisone exposure-response relationships and drawing definitive conclusions about the dosing of IV hydrocortisone in critically ill neonates and infants with vasopressor-resistant hypotension.

Adrenal and thyroid function in the fetus and preterm infant.

Adrenal and thyroid hormones are essential for the regulation of intrauterine homeostasis, and for the timely differentiation and maturation of fetal organs. These hormones play complex roles during fetal life, and are believed to underlie the cellular communication that coordinates maternal-fetal interactions. They serve to modulate the functional adaptation for extrauterine life during the perinatal period. The pathophysiology of systemic vasopressor-resistant hypotension is associated with low levels of circulating cortisol, a result of immaturity of hypothalamic-pituitary-adrenal axis in preterm infants under stress. Over the past few decades, studies in preterm infants have shown abnormal clinical findings that suggest adrenal or thyroid dysfunction, yet the criteria used to diagnose adrenal insufficiency in preterm infants continue to be arbitrary. In addition, although hypothyroidism is frequently observed in extremely low gestational age infants, the benefits of thyroid hormone replacement therapy remain controversial. Screening methods for congenital hypothyroidism or congenital adrenal hyperplasia in the preterm neonate are inconclusive. Thus, further understanding of fetal and perinatal adrenal and thyroid function will provide an insight into the management of adrenal and thyroid function in the preterm infant.

Steroids and Vasopressor-Resistant Hypotension in Preterm Infants

Despite our inability to appropriately define the gestational- and postnatal-age dependent normative values of blood pressure, hypotension is often been diagnosed and treated in preterm neonates especially during the transitional period. Although the perceived normal blood pressure values can be restored in the majority of preterm neonates by administration of volume and vasopressor-inotropes, some patients will not respond even to higher doses of vasoactive medications. In these neonates with so-called “vasopressor-resistant hypotension”, steroid administration is usually effective in increasing the blood pressure to the perceived normal range and decreasing vasopressor requirement. The etiology of vasopressor-resistant hypotension is thought to be a combination of transient adrenocortical insufficiency of prematurity and downregulation of the cardiovascular adrenergic receptors. In the clinical practice, hydrocortisone is used most frequently for the management of vasopressor-resistance. Importantly, low-dose hydrocortisone appears to improve blood pressure without compromising cardiac function or systemic perfusion in these patients. However, caution must be exercised when hydrocortisone is administered during the first postnatal week as significant side effects including gastrointestinal perforation may occur especially in infants co-exposed to indomethacin. In addition, although the available data on the lack of a documented impact of early low-dose hydrocortisone administration on brain development are encouraging, more and appropriately powered studies are needed to put this concern to rest. Keywords: Vasopressor-resistant hypotension, preterm neonate, hydrocortisone, relative adrenal insufficiency of prematurity, adrenergic receptor downregulation

Steroids and Vasopressor-Resistant Hypotension in Preterm Infants

Steroids and Vasopressor-Resistant Hypotension in Preterm Infants

Is refractory hypotension in preterm infants a manifestation of early ductal shunting?

Clinicians frequently use hydrocortisone (HC) to treat vasopressor-resistant hypotension even before establishing its cause. To identify the etiologic factors leading to development of refractory hypotension, and to assess if patent ductus arteriosus (PDA) is associated with refractory hypotension during the first week of life. The medical records of 290 consecutively born infants <or=30 weeks' gestational age (GA) were reviewed to identify the escalating need for vasopressors to maintain mean arterial blood pressure (MABP) at or above a level equal to the GA in completed weeks. Refractory hypotension was defined as MABP unresponsive to fluid boluses and high-dose vasopressors (dopamine and dobutamine at doses 20 microg/kg/min each and/or epinephrine) prompting the use of HC. Eighty-nine (30.7%) of 290 infants had refractory hypotension between postnatal days 2 and 7. Infants with refractory hypotension were more likely to have a lower birth weight and GA (P<0.001), been treated with surfactant (P=0.004) and received indomethacin for a symptomatic PDA (P<0.001). To identify the etiologic factors, a univariate analysis revealed that the use of high-frequency oscillatory ventilation, presence of air leaks, PDA, sepsis, hyperkalemia and intraventricular hemorrhage (IVH) were significantly associated with refractory hypotension. However, multivariate analysis confirmed the independent association of only PDA (odds ratio (OR) 7.6, 95% confidence interval (CI) 3.3-17.7, P=0.000), severe IVH (OR 2.6, 95% CI 1.1-6.4, P=0.03) and GA (OR 0.7, 95% CI 0.6-0.8, P=0.001). Evaluation for early ductal shunting and closure of the ductus, if patent, should be attempted before HC is considered in hypotensive infants with escalating needs for vasopressors.

Arginine-vasopressin in neonates with vasodilatory shock after cardiopulmonary bypass

Successful therapy of vasodilatory shock in adults and children with arginine-vasopressin (AVP) has been reported previously. Data on the use of vasopressin in neonates is limited. This retrospective study reports the effects of AVP-treatment in neonates with catecholamine-resistant systemic vasodilatation after cardiopulmonary bypass. From March 2003 through December 2005, 172 neonates underwent open-heart surgery, 17 developed vasopressor-resistant hypotension and were treated with AVP. Thirteen patients had a stage I palliation of single ventricle, two had a Ross-operation and two had an arterial switch operation. All patients received multiple traditional inotropes and vasopressors prior to administration of AVP. AVP was started at median 0.0001 U x kg(-1) x min(-1) (range 0.00005-0.0002) and titrated up to a maximum of median 0.0003 U x kg(-1) x min(-1) (range 0.0001-0.001). AVP led to a significant increase in blood pressure (from 49+/-8 mmHg to 69+/-7 mmHg) and the requirement of traditional vasopressors decreased significantly. No peripheral vasoconstriction or ischemia was observed. Four of 13 patients, all with single ventricle palliation, died. In two patients death occurred due to additional complications 6 days after AVP was discontinued. One patient, who was still on AVP, died 42 hours postoperatively after prolonged hypoxemia not responding to inhaled nitric oxide. One patient arrested on the third postoperative day when AVP was almost weaned. In neonates with vasodilatory shock after cardiopulmonary bypass AVP is a potent agent to increase blood pressure when traditional vasopressors are failing.

Hydrocortisone is effective in treatment of vasopressor-resistant hypotension in very low birth weight neonates

Ng PC, Lee CH, Bnur FL, Chan IHS, Lee AWY, Wong E, et al. A double-blind, randomized, controlled study of a “stress dose” of hydrocortisone for rescue treatment of refractory hypotension in preterm infants. Pediatrics 2006;117:367-75.

Management of hypotension and low systemic blood flow in the very low birth weight neonate during the first postnatal week

Systemic hypotension during the first postnatal week is associated with increased mortality and morbidity in the very low birth weight (VLBW) neonate. Hypotension is generally defined as blood pressure below the fifth percentile of the gestational- and postnatal-age dependent blood pressure norms. Recent studies indicate that in most VLBW neonates, cerebral blood flow autoregulation is indeed lost when blood pressure reaches the fifth percentile. Treatment of the circulatory compromise should address the primary pathogenic factor(s) of the condition (hypovolemia, myocardial compromise, failure of vasoregulation or a combination of factors). Recent findings also suggest that vasopressor resistance can be treated with a brief course of low-dose hydrocortisone. However, due to the short- and potential long-term side effects of early hydrocortisone treatment, its use should be restricted to neonates with vasopressor-resistant hypotension. Finally, concomitant administration of hydrocortisone with indomethacin should be avoided due to the increased incidence of gastrointestinal perforations.

Hydrocortisone and Vasopressor-Resistant Shock in Preterm Neonates

Because systemic hypotension and significant fluctuations in blood pressure in the immediate postnatal period are associated with increased mortality and major adverse outcomes in preterm neonates, most neonatologists attempt to maintain blood pressure in the perceived gestational- and postnatal-age–dependent “normal” range. Many very low birth weight (VLBW) neonates respond to medium-to-high doses of dopamine, epinephrine, and/or dobutamine and are able to wean off the medications within a few days. However, more than half of them become dependent on medium-to-high–dose vasopressor/inotrope support beyond the first few postnatal days or do not respond at all. Findings of a few observational and retrospective studies have suggested that these neonates respond to relatively low doses of hydrocortisone, with normalization of their cardiovascular status and decreasing vasopressor/inotrope requirement.1–3 Despite the limited information provided by these publications on safety and efficacy and despite the lack of appropriately designed prospective clinical trials, hydrocortisone has now become the choice of treatment of preterm neonates with vasopressor-resistant hypotension. The study by Ng et al,4 published in this issue of Pediatrics , is indeed the first prospective randomized clinical trial that assessed the effectiveness of relatively low doses of hydrocortisone in the treatment of refractory hypotension of VLBW neonates during the immediate postnatal period. The findings of this prospective, double-blind, randomized, controlled trial indicate that a 5-day course of 3 mg/kg per day of hydrocortisone started on the first postnatal day decreases the cumulative doses of vasopressors/inotropes and volume expanders as well as the number of patients who require vasopressor/inotrope support by 72 hours of the drug administration. In addition, mean arterial blood pressure was significantly and consistently higher in the hydrocortisone-treated group. These beneficial cardiovascular effects were not accompanied by apparent adverse effects such as an increased incidence of hyperglycemia, systemic infections, or intestinal perforation. … Address correspondence to Istvan Seri, MD, PhD, Childrens Hospital Los Angeles, 4650 Sunset Blvd, MS 31, Los Angeles, CA 90027. E-mail: iseri{at}chla.usc.edu

Prevalence of Low Cortisol Values in Term and Near-Term Infants with Vasopressor-Resistant Hypotension

To determine the prevalence of low cortisol values and to evaluate clinical responses to hydrocortisone in ill term and near-term newborns. Retrospective cohort study including infants >or=35 weeks gestational age who were mechanically ventilated, received vasopressor therapy, and had a cortisol concentration obtained for evaluation of vasopressor-resistant hypotension. In those infants treated with hydrocortisone, physiologic responses were evaluated and correlated with cortisol values (<15 vs >or=15 microg/dl). A total of 32 infants had cortisol values obtained; 18 (56%) were <15 microg/dl. In all, 21 infants were treated with hydrocortisone of whom 13 had cortisol values <15 microg/dl. These 13 infants showed decreased heart rate, dopamine support and fluid bolus requirements after treatment, compared to infants with values >or=15 microg/dl (n=8). A significant number of hypotensive, mechanically ventilated infants have evidence of inadequate adrenal function. Hydrocortisone therapy resulted in hemodynamic stabilization in this population.