Cardiopulmonary resuscitation for clinicians.
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Cardiopulmonary Resuscitation↗
Biomedical subjects
M Müllner
Publications and source records attributed to M Müllner.
The influence of chest compressions and external defibrillation on the release of creatine kinase-MB and cardiac troponin T in patients resuscitated from out-of-hospital cardiac arrest.
OBJECTIVES: This study sought to determine the influence of resuscitative procedures, such as chest compressions and external defibrillation, on the release of creatine kinase (CK)-MB and cardiac troponin T (cTnT). METHODS: In 87 patients with out-of-hospital cardiac arrest and successful cardiopulmonary resuscitation (CPR), the initial ECG rhythm, the duration of cardiac arrest and CPR, and the number of defibrillations were assessed on arrival in the hospital. The serum CK-MB and cTnT were measured 12 h after the event. We also assessed whether the patient developed cardiogenic shock within 12 h, and if the patient had acute myocardial infarction (AMI), which was confirmed or eliminated by of typical ECG findings, thallium-201 myocardial scintigraphy, or autopsy within the hospital stay. A backward stepwise linear regression model was applied to assess the association between the markers of myocardial injury (CK-MB and cTnT) and the above clinical variables. RESULTS: CK-MB concentrations were independently associated with the presence of AMI [B 68.5 (SE 28.5, P = 0.018)], the duration of CPR (as a measure of trauma to the chest by means of chest compressions) [B 2.07 (SE 1.01, P = 0.045)] and cardiogenic shock [B 52.3 (SE 23.4, P = 0.03)]. The remaining clinical variables listed were excluded by the model. Cardiac troponin T concentrations were only associated with the presence of AMI [B 4.86 (SE 1.34, P = 0.0005)]. There was a non-significant association between increasing serum cTnT concentrations and the presence of cardiogenic shock [B 2.51 (SE 1.46, P = 0.09)]. The remaining clinical variables were excluded by the model. CONCLUSION: The release of CK-MB appears to be influenced by the duration of resuscitation and the presence of cardiogenic shock. This has to be considered when interpreting serum CK-MB concentrations after CPR. The release of cTnT seems to be only associated with acute myocardial infarction, but not with the duration of chest compressions, or with the number of defibrillations administered.
Aged↗
Poor diagnostic value of colonic CD44v6 expression and serum concentrations of its soluble form in the differentiation of ulcerative colitis from Crohn's disease.
BACKGROUND: Increased expression of CD44v6 on colonic crypt epithelial cells in ulcerative colitis has been suggested as a diagnostic tool to distinguish ulcerative colitis from colonic Crohn's disease. AIMS: To investigate colonic CD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6) in patients with ulcerative colitis and Crohn's disease. METHODS: Colonic biopsy samples were obtained from 16 patients with ulcerative colitis, 13 with ileocolonic Crohn's disease, and 10 undergoing polypectomy. Serum samples were obtained from 15 patients with active ulcerative colitis, 20 with active Crohn's disease, and 20 healthy donors. Colonic CD44v6 expression was evaluated immunohistochemically by monoclonal antibody 2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6 concentrations were measured by ELISA. RESULTS: 2F10 stained colonic epithelium of inflamed ulcerative colitis and Crohn's disease samples in 80% and 40% of cases, respectively, and VFF18 in 95% and 87%, respectively. Both monoclonal antibodies displayed a sensitivity and specificity of 60% and 87% to differentiate ulcerative colitis from colonic Crohn's disease. Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis (median 153 ng/ml; interquartile range (IQR) 122-211) compared with Crohn's disease (219; IQR 180-243) and healthy donors (221; IQR 197-241 (p = 0.002)). Its sensitivity and specificity to discriminate ulcerative colitis from Crohn's disease was 75% and 71%, respectively. CONCLUSION: Colonic CD44v6 and serum sCD44v6 concentrations do not facilitate reliable differential diagnosis between ulcerative colitis and Crohn's disease.
Acute Disease↗
Attenuation of thrombolysis-induced increase of plasminogen activator inhibitor-1 by intravenous enalaprilat.
We examined the effect of intravenous enalaprilat on the course of PAI-1 plasma levels in 23 patients with acute myocardial infarction undergoing thrombolytic therapy. All patients received 100 mg aspirin, 1000 IU/h heparin, thrombolysis with 100 mg rt-PA within 90 min, and betablockers. Eleven out of 23 patients received 5 mg enalaprilat intravenously prior to thrombolysis. Blood samples for determination of PAI-1 plasma levels were collected on admission, 2, 4, 6, 12, and 24 h after thrombolysis. PAI-1 plasma levels in patients receiving enalaprilat were similar to those of the control patients before thrombolysis (5 ng/ml, 95% confidence interval: 2-10 vs. 7 ng/ml, 95% confidence interval: 2-10; p = 0.5). The PAI-1AUC was 9 ng/ml/h (95% confidence interval: 5-10) in the enalaprilat group and 19 ng/ml/h (95% confidence interval: 13-26) in the control group (p = 0.0006). The maximum difference was observed 6 h after thrombolysis (enalaprilat: 13 ng/ml, 95% confidence interval: 5-25, control: 42 ng/ml, 95% confidence interval: 18-55; p = 0.003). Our study clearly demonstrates that application of intravenous enalaprilat prior to thrombolysis attenuates the thrombolysis-related increase of PAI-1. This finding may suggest a possible therapeutic approach to influence the fibrinolytic system in patients with acute myocardial infarction after thrombolysis.
Adult↗
[Experiences with inhalative nitric oxide in internal medicine intensive care patients with adult respiratory distress syndrome].
Inhalative nitric oxide (NO) has recently been included in the therapeutic armament for the treatment of ARDS. We evaluated the effect of inhalative NO on hemodynamic and oxygen transport parameters in 30 internal intensive care patients suffering from ARDS. All patients received a pulmonary artery catheter. Hemodynamics were assessed prior to NO therapy and after 1, 6, 12, and 24 h. 80% (n = 24) of the patients were classified as therapy responders. The median NO dose was 15 ppm (range 5 to 40 ppm). The PaO2/FiO2--ratio increased significantly after initiation of NO (p = 0.0002) while the pulmonary shunt fraction (Qs/Qt) decreased significantly (p = 0.0019). All other measured or calculated parameters including arterial and pulmonary arterial blood pressure remained unchanged. No negative effects of the therapy could be observed. Inhalative NO improves oxygenation in most intensive care patients with ARDS and thus offers the possibility to reduce invasiveness of mechanical ventilation.
Administration, Inhalation↗
[A protocol for the assessment of patients with coma of unknown origin].
OBJECTIVE: Evaluation of the applicability of a protocol designed for the quick and efficient management of patients with coma of unknown origin (CUO). METHODS: Every patient admitted to our Emergency Department with the diagnosis of CUO was evaluated with our diagnostic protocol. The first diagnostic steps included evaluation of the hemodynamic and respiratory situation, Glasgow Coma Scale, basic neurologic and clinical examination, as well as blood withdrawal, for analysis of metabolic and toxicologic parameters. If indicated, cranial computer tomography (CCT) and/or lumbar puncture were performed. RESULTS: Within the study period from 1. 1. 1995 until 30. 9. 1996, 122 patients (65 males, median age 50 years, 25 and 75 percentile: 33; 69) were included. Blood analysis and the toxicological screening were diagnostic effective in 66 patients, clinical examination and body temperature in one case each, CCT in 50 patients and lumbar puncture in 2 patients. By the use of this diagnostic protocol 51 neurologic, 38 toxicologic, 28 metabolic and 2 infectious causes of coma were diagnosed (98%). Etiology of 2 of the comas remained unclear. CONCLUSION: By using our protocol, 98% of the causes of CUO were clarified. The main causes of coma were of neurological, toxicological and metabolic origin. CCT and the blood analysis were the most important procedures leading to a final diagnosis.
Adult↗
Safety and efficacy of urapidil and sodium nitroprusside in the treatment of hypertensive emergencies.
OBJECTIVE: To assess the safety and efficacy of urapidil compared to sodium nitroprusside in the treatment of hypertensive emergencies. DESIGN: Randomized, prospective clinical study. SETTING: Emergency department in a 2000-bed inner city hospital. PATIENTS: Eighty-one patients with hypertensive emergencies defined as elevation of systolic blood pressure above 200 mmHg and/or diastolic blood pressure above 110 mmHg plus evidence of end-organ damage were included in the study protocol. The efficacy of therapy was defined as 1) blood pressure reduction below 180/95 mmHg within 90 min and 2) no re-elevation of blood pressure during a 4-h follow-up period in primary responders. The safety of both drugs was defined as the number of minor and major side effects during treatment. INTERVENTIONS: Patients received either sodium nitroprusside (n = 35; continuous intravenous administration with a starting dose of 0.5 microgram/kg per min; increase in increments of 0.5 microgram/kg per min every 15 min until response to treatment or a maximum of 3 micrograms/kg per min) or urapidil (n = 46; intravenous bolus; starting dose: 12.5 mg; repetitive administration of 12.5 mg every 15 min until response or a maximum dose of 75 mg). MEASUREMENTS AND RESULTS: Blood pressure was measured every 2.5 min by using a non-invasive oscillometric blood pressure measurement unit. Response to treatment within 90 min was observed in 75 (93%) patients (urapidil: n = 41 [89%]; nitroprusside: n = 34 [97%]; p = 0.18). During the follow-up period 8/34 (24%) patients in the nitroprusside group and 1/41 (2%) patients in the urapidil group exhibited blood pressure re-elevation. Major side effects were observed in seven patients receiving nitroprusside and two patients in the urapidil group (p = 0.04). CONCLUSION: Urapidil is equally effective, compared to sodium nitroprusside, in the treatment of hypertensive emergencies. Due to a smaller number of adverse events, urapidil is a reasonable alternative to nitroprusside in the treatment of hypertensive emergencies.
Adult↗
The association between blood lactate concentration on admission, duration of cardiac arrest, and functional neurological recovery in patients resuscitated from ventricular fibrillation.
OBJECTIVE: To assess the association between arterial lactate concentration on admission and the duration of human ventricular fibrillation cardiac arrest, and to what degree the arterial lactate concentration on admission is an early predictor of functional neurological recovery in human cardiac arrest survivors. DESIGN: Cohort study. Arterial lactate concentrations and out-of-hospital data concerning cardiac arrest and cardiopulmonary resuscitation were collected retrospectively according to a standardized protocol. Functional neurological recovery was assessed prospectively at regular intervals for 6 months. SETTING: Emergency department of an urban tertiary care hospital. PATIENTS: A total of 167 primary survivors of witnessed out-of-hospital ventricular fibrillation cardiac arrest. MEASUREMENTS: The association between arterial lactate concentration on admission, the duration of cardiac arrest, and functional neurological recovery was assessed. Further, we assessed whether admission concentrations of arterial lactate and duration of cardiac arrest can predict unfavorable functional neurological recovery. Functional neurological recovery was measured in cerebral performance categories (CPC). No or minimal functional impairment (CPC 1 and 2) was defined as favorable outcome; the remaining categories (CPC 3, 4 and 5) were defined as unfavorable functional neurological recovery. RESULTS: In 167 patients, a weak association between total duration of cardiac arrest and admission levels of lactate (r = 0.49, P < 0.001) could be shown. With increasing admission concentrations of arterial lactate functional neurological recovery was more likely to be unfavorable (OR 1.15 per mmol/l increase, 95% CI 1.04-1.27). Nevertheless, only at very high levels of lactate (16.3 mmol/l) could unfavorable neurological recovery be detected with 100% specificity, yielding a very low sensitivity of 16%. CONCLUSIONS: The arterial admission lactate concentration after out-of-hospital ventricular fibrillation cardiac arrest is a weak measure of the duration of ischemia. High admission lactate levels are associated with severe neurological impairment. However, this parameter has poor prognostic value for individual estimation of the severity of subsequent functional neurological impairment.
Aged↗
Blood glucose concentration after cardiopulmonary resuscitation influences functional neurological recovery in human cardiac arrest survivors.
Experimental data suggest that postischemic blood glucose concentration plays an important role in modulating both ischemic cerebral infarction and selective neuronal necrosis. This study investigated the association between functional neurological recovery and blood glucose concentrations in human cardiac arrest survivors. A group of 145 nondiabetic patients were evaluated after witnessed ventricular fibrillation cardiac arrest. Data regarding cardiac arrest were collected according to an internationally accepted protocol immediately after arrival. Blood glucose was measured on admission and 6, 12, and 24 h thereafter. To control for duration of cardiac arrest and cardiogenic shock, both known to influence outcome as well as blood glucose, levels, Spearman rank partial correlation was used. In this multivariate analysis, a high admission blood glucose level tended to be associated with poor neurological outcome (rs = -0.16, n = 142, p = 0.06). The association between high median blood glucose levels over 24 h and poor neurological outcome was strong and statistically significant (rs = -0.2, n = 145, p = 0.015). High blood glucose concentrations occurring over the first 24 h after cardiac arrest have deleterious effects on functional neurological recovery. Whether cardiac arrest survivors might benefit from reduction of blood glucose levels needs further investigation.
Adult↗
The emergency department in a 2000-bed teaching hospital: saving open ward and intensive care facilities.
Providing emergency medicine at the entrance to the hospital proves to be a sufficient link between pre- and inhospital medical care. The aim of our study is to investigate how many open ward and intensive care facilities can be saved within the hospital by the emergency department. Therefore, the data of our emergency department within a 2000-bed teaching hospital are retrospectively analysed. Unstable life-threatening emergencies for acute care, stable for immediate care and non-life-threatening emergencies are defined. Patients were discharged, admitted to an open ward, intensive care unit, the operation theatre or died. According to the level of care needed in the emergency department the continuing medical management is investigated. Over a 2-year period, 102,411 patients entered our emergency department. Overall 1498 (1%) needed acute care, 3652 (4%) immediate care and 97,261 (95%) delayed care. Of the acute care patients, 29 (2%) were discharged, 573 (38%) were admitted to an open ward, 551 (37%) to an intensive care unit, 67 (4%) needed surgery and 278 (19%) died. Of the immediate care patients, 1611 (44%) were discharged, 1755 (48%) were admitted to an open ward, 551 (37%) to an intensive care unit, and 286 (8%) needed surgery. Of the delayed care patients, 93061 (96%) were discharged and 4200 (4%) were admitted to an open ward. Of 5150 patients with life-threatening diseases, 551 (11%) needed an intensive care unit and 2328 (45%) an open ward. Providing acute and immediate care in our emergency department saves both intensive care and open ward facilities of the hospital.
Adult↗
Creatine kinase-mb fraction and cardiac troponin T to diagnose acute myocardial infarction after cardiopulmonary resuscitation.
OBJECTIVES: This study sought to evaluate the diagnostic value of the biochemical markers creatine kinase (CK), creatine kinase-MB fraction (CK-MB) and cardiac troponin T (cTNT) to diagnose acute myocardial infarction (AMI) after cardiopulmonary resuscitation (CPR). BACKGROUND: Elevations of CK and CK-MB after CPR are a frequent finding and might be associated with ischemic myocardial injury, as well as physical trauma to the chest. METHODS: Patients who had cardiac arrest and primary successful resuscitation were included in the study. The diagnosis of AMI was confirmed or ruled out by means of typical electrocardiographic findings, thallium-201 myocardial scintigraphy or autopsy, if death occurred during the hospital period, in 39 primary survivors of sudden cardiac death. In 24 patients (62%) the diagnosis of AMI was established. Serum cTNT, CK and CK-MB were measured, and the CK-MB/CK ratio was calculated on admission and after 12 h. RESULTS: On admission all markers of myocardial injury proved to be weak methods for the diagnosis of AMI. After 12 h cTNT as well as CK-MB exhibited a similar diagnostic performance; CK and the CK-MB/CK ratio proved to be worthless. Sensitivity and specificity for a cTNT cutoff value of 0.6 ng/ml, 12 h after cardiac arrest, were 96% and 80%, respectively. For a CK-MB cutoff value of 26 U/liter, sensitivity was 96% and specificity was 73%. CONCLUSIONS: Cardiac TNT and CK-MB are valuable tools in detecting AMI as the cause of sudden cardiac death. However, there is a considerable lack of sensitivity and specificity. Cardiac injury is probably caused not only by AMI, but also by myocardial damage related to CPR efforts.
Animals↗
Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest.
The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6, 12, and 24 hours) in 107 adult patients surviving a witnessed cardiac arrest for 24 hours. CK and CK-MB were elevated in >75% of the patients within 24 hours. Release of CK and CK-MB was mainly associated with electrocardiographic evidence of acute myocardial infarction (AMI) cumulative energy administered during defibrillation, and duration of chest trauma by compression. The CK-MB/CK ratio was elevated in 32% of the patients. Of patients with electrocardiographic evidence of AMI, only 49% had an elevated CK-MB/CK ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a frequent finding, and is associated with ischemic myocardial injury, as well as physical trauma to the chest. This should be considered when interpreting the course of CK and CK-MB fraction for the diagnosis of AMI.
Adult↗
Analysing calls by lay persons reporting cardiac arrest.
Prior to establishing a protocol for pre-arrival instructions for cardio-pulmonary resuscitation in the Vienna emergency medical system dispatch centre, a study was performed to determine whether any problems exist which may compromise guidance for basic life-support on the telephone. To evaluate the feasibility of prearrival instructions, a retrospective analysis of cardiac arrest calls was performed. We reviewed the Vienna emergency medical services dispatch centre tape recordings, ambulance run sheets and the hospital charts of 114 patients suffering from atraumatic cardiac arrest. Analysis showed that in 59 cases the arrest occurred in the victim's home. The telephone and the patient were either in the same or in adjoining rooms in 55% of the calls. We did not experience any technical or language difficulties. The caller and victim were related in 51 cases. The callers were completely calm in 77% and fairly calm in an additional 15%. Not one caller was distraught. Our data show that most objections to the feasibility of pre-arrival instructions can be refuted. We conclude that in Vienna the setting and location of arrest will impose few problems on the performance of bystander-cardio-pulmonary resuscitation using pre-arrival instructions given by dispatchers.
Austria↗
Possibilities of brain protection with tirilazad after cardiac arrest.
Cardiac arrest and resuscitation often create a cerebral insult caused by the initial cessation of blood flow, followed by the incomplete ischemia of cardiopulmonary resuscitation (low flow), and, following the return of spontaneous circulation, by the post-resuscitation syndrome. A cascade of physiologic, vascular, and biochemical events is set in motion, including changes in neuropeptides, electrolytes such as calcium and magnesium, excitatory neurotransmitters such as glutamate and acetylcholine, lymphokines such as interleukin-1, and arachidonic acid metabolites such as prostaglandins and leukotrienes; and formation of oxygen free radicals and lactic acid. Oxygen free radical-induced lipid peroxidation appears to increase tissue injury during and after brain ischemia. The 21-aminosteroid U74006F (tirilazad mesylate) is a novel inhibitor of lipid membrane peroxidation induced by oxygen free radicals, which has been shown, in animal models of subarachnoid hemorrhage, central nervous system trauma, and cerebral ischemia, to limit the extent of secondary tissue damage, thus improving functional recovery. Since tirilazad appears to have little or no behavioral or physiologic side effects, it appears to be an ideal agent for widespread brain ischemia prophylaxis. Tirilazad mesylate studies in out-of-hospital cardiac arrest are currently being planned.
Antioxidants↗
Mild resuscitative hypothermia and outcome after cardiopulmonary resuscitation.
Recovery without residual neurological damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional, and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no-flow cardiovascular states has been well documented both clinically and experimentally since the 1950s. Most studies have used moderate (28-33 degrees C) to deep (20-28 degrees C) hypothermia to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia, and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the postresuscitation syndrome and improves neurologic function and reduces histologic brain damage. More importantly, such benefits can be demonstrated with mild (34-36 degrees C) hypothermia, thus minimizing complications and requiring less time for induction of hypothermia. Ice water nasal lavage, direct carotid infusion of cold fluids, use of a cooling helmet, and peritoneal cooling are promising techniques for clinical cerebral cooling. External auditory canal temperature (e.g., tympanic membrane temperature changes) could provide an approximation to brain temperatures. For accurate temperature monitoring, however, a central pulmonary artery thermistor probe should be inserted. Temperature monitoring is needed to avoid temperature < 30 degrees C. Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia; it may also prove to be a useful method of cerebral resuscitation after global ischemic states, thereby promoting the prevention of neuromental diseases.
Austria↗
Systemic and cerebral oxygen extraction after human cardiac arrest.
The aim of this study was to observe cerebral and systemic oxygen extraction after human cardiac arrest with return of spontaneous circulation. Eight adult patients after non-traumatic, cardiac arrest were included. Cerebral and systemic oxygen extraction ratios were measured together with haemodynamic variables beginning 2 hours after cardiac arrest and every 4 hours thereafter until 24 hours. Between 2 and 12 hours after cardiac arrest cerebral oxygen extraction values ranged from very low over normal to very high. In the further course these values were reduced until 24 hours in six patients. Two patients who were still alive after 6 months, both severely mentally disabled, had a higher cerebral oxygen extraction ratios in comparison with non-survivors. Systemic oxygen extraction seemed to vary more than the cerebral oxygen extraction. The two long-term survivors had normal to supranormal values from 8 to 24 hours. In conclusion cerebral oxygen extraction was higher in long-term cardiac arrest survivors than in non-survivors between 12 and 24 hours after the event. Further, a better quality of neurological recovery was associated with higher cerebral oxygen extraction. Systemic oxygen extraction was also impaired, but to a lesser extent, especially in long-term survivors.
Aged↗
Arterial blood pressure after human cardiac arrest and neurological recovery.
BACKGROUND AND PURPOSE: In animal cardiac arrest studies, outcome has been improved by inducing arterial hypertension early after return of spontaneous circulation. The aim of our study was to evaluate whether arterial blood pressure within the first minutes and hours after return of spontaneous circulation influences neurological recovery in human cardiac arrest survivors. METHODS: Of 136 retrospectively evaluated patients after sudden cardiac death, two groups were defined: group 1, mean arterial blood pressure (MABP) within 5 minutes after return of spontaneous circulation above 100 mm Hg; group 2, MABP of 100 mm Hg or less. Thereafter MABP was measured every 5 minutes until 2 hours after return of spontaneous circulation. The groups were compared in regard to age, sex, in/out of hospital, witnessed/not witnessed, first electrocardiographic rhythm, time from cardiac arrest to beginning of life support and to return of spontaneous circulation, cumulative epinephrine dose administered, and best neurological outcome within 6 months. RESULTS: In group 1 (n = 54) good neurological recovery was observed in 63% and in group 2 (n = 82) in 55% (chi 2 = 0.87, P = NS). Both groups exhibited comparable baseline values except that time intervals from beginning of life support to return of spontaneous circulation were shorter in group 1. After we controlled for this difference with Spearman's partial rank correlation (rs), there was no association between MABP measured within the first 5 minutes and outcome (rs = -.023; P = NS). Good neurological recovery was independently and directly related to MABP measured during 2 hours after return of spontaneous circulation (rs = .26; P < .01). CONCLUSIONS: In human cardiac arrest survivors, good functional neurological recovery was independently and positively associated with arterial blood pressure during the first 2 hours after human cardiac arrest but not with hypertensive reperfusion within the first minutes after return of spontaneous circulation.
Aged↗
Efficacy of different antihypertensive drugs in the emergency department.
Hypertensive crises are a commonly observed problem in an emergency department. The aim of the study was to evaluate the efficacy and safety of different antihypertensive agents in the treatment of patients with hypertensive crises. 168 patients (mean age: 52 +/- 12 years) admitted to the emergency department with a hypertensive urgency (systolic (SBP) blood pressure > 210 mm Hg and/or diastolic (DBP) blood pressure > 110 mm Hg) or a hypertensive emergency (DBP > 100 mm Hg and evidence of end-organ damage) were included into the study protocol. Blood pressure (BP) was measured every 5 min automatically using a noninvasive BP measurement unit. After a resting period of 30 min the patients received the following drugs: 5 mg enalaprilat intravenous (n = 43) or 25 mg urapidil intravenous (n = 48) or 10 mg nifedipine-capsule sublingual (n = 47) or 2 x 5 mg nifedipine-spray sublingual (n = 30). The aim of treatment was to reduce SBP below 180 mm Hg and DBP below 95 mm Hg within 45 min after start of treatment. When evaluating the response rates the highest rate was observed in the urapidil group (96%). The response rate of enalaprilat and both preparations of nifedipine were similar (70-72%). The rate of major side effects was higher in the urapidil compared to the other drugs (4% vs 2% in the nifedipine-group or 0% in the enalaprilat-group). All four drugs are suitable in the treatment of patients with hypertensive crisis in the emergency department. Urapidil should be used as a first choice drug in critically ill patients with hypertensive crisis due to its higher response rate.
Adult↗