[Aspects of intensive care medicine in emergency medicine]. / Intensivmedizinische Aspekte in der Notfallmedizin.

Emergency medicine and intensive care medicine have many similarities. In this review, we will first discuss the terminology of emergency medicine in a hospital in terms of a uniform designation as a department for emergency medicine or emergency department. Emergency medicine and intensive care medicine are a location-independent concept of patient care in the sense of the recognition, treatment and diagnosis of acute health disorders. Emergency medicine covers the entire range of disease severity, while intensive care medicine focuses on organ replacement and organ preservation, uses highly specialized technology for this purpose and treats only the seriously ill. The treatment of seriously ill patients in the emergency departments requires special intensive care medical knowledge both by the physicians and nursing staff. In the medical field, the curriculum for the European emergency medicine specialist takes into account all aspects necessary for the diagnosis and treatment of critically ill patients. For the nursing sector, Germany has had its own recognized specialty training program in emergency medicine for several years. However, the treatment of critically ill patients in emergency departments also requires that the emergency departments be adequately equipped. In this regard, there is an urgent need for statutory quality criteria that are concrete and structured. We know from the literature that intensive care competence in emergency departments reduces the admission rate to intensive care units and the mortality of all emergency patients. The concept of intensive care units in the emergency department is gaining popularity in the USA and should also be evaluated for implementation in the German-speaking countries.

Troponin T predicts in-hospital and 1-year mortality in patients with pulmonary embolism.

We aimed to determine the prognostic value of troponin T (TNT) for in-hospital and 1-yr mortality in a large sample of patients with pulmonary embolism (PE). Patients presenting at the emergency department of a tertiary care centre from January 1998 to December 2006 with PE were included. A blood sample was taken at the time of presentation. To determine in-hospital and 1-yr mortality, data from the hospital records and the national death register were used. TNT was determined in 563 out of 737 patients with proven PE. TNT was elevated (>0.03 ng x mL(-1)) in 27%. In-hospital survival was 79% in TNT-positive patients compared with 94% in TNT-negative patients (p<0.001). 1-yr survival was 71% in TNT-positive patients compared with 90% in TNT-negative patients (p<0.001). Elevated TNT levels meant a four-times higher risk of in-hospital death and a three-times higher risk of 1-yr mortality, even after adjustment for the other most important risk factors of death in this population. Elevated TNT independently predicts in-hospital and 1-yr mortality in patients with acute PE.

Transport with ongoing cardiopulmonary resuscitation may not be futile.

BACKGROUND: Despite it being generally regarded as futile, patients are regularly brought to the emergency department with ongoing cardiopulmonary resuscitation (CPR). METHODS: Long-term outcome and its predictors in patients who were transported during ongoing CPR were evaluated in an observational study. Adult patients with non-traumatic cardiac arrest admitted to the Department of Emergency Medicine of a tertiary-care facility after transport with ongoing chest compression were retrospectively analysed. Multivariate analysis of epidemiological variables, treatment, blood gas values on admission, cause of arrest, and location of arrest was performed to find factors that were predictive for favourable long-term outcome (6-month survival, best cerebral performance category 1 or 2). RESULTS: Over 15 yr (1991-2006), a total of 2643 patients were treated after cardiac arrest. Of these, 327 patients received chest compressions during transport and were analysed (out-of-hospital cardiac arrest: n=244, in-hospital: n=83; the remaining 2316 patients were either stabilized before transport or suffered their arrest in our department). Return of spontaneous circulation was achieved in 31% of patients (n=102). Of these, 19 (19%) had favourable long-term outcome (6% of total). Independent predictors of good outcome were age, witnessed arrest, amount of epinephrine, and initial shockable rhythm. Among the patients with cardiac origin of arrest, 11 out of 197 patients (6%) survived; pulmonary origin, 4 out of 46 patients (9%); hypothermic arrest, 1 of 10 patients (10%); and intoxications, one out of nine patients (11%). CONCLUSIONS: Post-resuscitation care in patients who receive CPR during transport is not futile. Once restoration of spontaneous circulation is established, one out of five patients will have good long-term outcome.

Compromising bradycardia: management in the emergency department.

AIM OF THE STUDY: Bradycardia may represent a serious emergency. The need for temporary and permanent pacing is unknown. METHODS: We analysed a registry for the incidence, symptoms, presenting rhythm, underlying mechanism, management and outcome of patients presenting with compromising bradycardia to the emergency department of a university hospital retrospectively during a 10-year period. RESULTS: We identified 277 patients, 173 male (62%), median age 68 (IQR 58-78), median ventricular rate 33 min(-1) (IQR 30-40). The leading symptoms were syncope [94 (33%)], dizziness [61 (22%)], collapse [46 (17%)], angina [46 (17%)] and dyspnoea/heart failure [30 (11%)]. The initial ECG showed high grade AV block [134 (48%)], sinus bradycardia/AV block [46 (17%)], sinuatrial arrest [42 (15%)], bradycardic atrial fibrillation [39 (14%)] and pacemaker-failure [16 (6%)]. The underlying mechanisms were primary disturbance of cardiac automaticity and/or conduction [135 (49%)], adverse drug effect [58 (21%)], acute myocardial infarction [40 (14%)], pacemaker failure [16 (6%)], intoxication [16 (6%)] and electrolyte disorder [12 patients (4%)]. In 107 (39%) patients bed rest resolved the symptoms. Intravenous drugs to increase ventricular rate were given to 170 (61%) patients, 54 (20%) required additional temporary transvenous/transcutaneous pacing. Two severely intoxicated patients could be stabilised only by cardiopulmonary bypass. A permanent pacemaker was implanted in 137 patients (50%). Mortality was 5% at 30 days. CONCLUSION: In our cohort, about 20% of the patients presenting with compromising bradycardia required temporary emergency pacing for initial stabilisation, in 50% permanent pacing had to be established.

Platelet function in patients with acute coronary syndrome (ACS) predicts recurrent ACS.

BACKGROUND: Platelet hyperfunction contributes to acute coronary syndromes (ACS). Thus, we hypothesized that platelet function under high shear stress predicts recurrent ACS during long-term follow-up of ACS patients. PATIENTS AND METHODS: Consecutive ACS patients (n = 208) were prospectively followed-up for an average of 28 months. Platelet function was measured with the platelet function analyzer (PFA-100; Dade Behring, Marburg, Germany) at baseline for collagen/adenosine diphosphate closure times (CADP-CT) and for collagen/epinephrine closure times (CEPI-CT) after infusion of a uniform dose of 250 mg aspirin. RESULTS: Of the conventional risk factors, only the prevalence of diabetes was higher in ACS patients with re-events. However, use of clopidogrel and use of beta blockers were also slightly lower in patients with re-events (P < 0.05). The unadjusted risk hazard ratio (HR) for re-events was 3.3 [95% confidence interval (95% CI): 1.4-7.4; P = 0.005] in those patients with the shortest CADP-CT values (lowest quartile). Similarly, the risk was 2.0-fold higher (95% CI: 1.1-3.6; P = 0.02) in ACS patients with CEPI-CT < 300 s as compared with CEPI-CT >or = 300 s. Inclusion of diabetes, clopidogrel and beta blockers in a multivariate Cox regression model enhanced the predictive value of CEPI-CT (HR: 2.7). Inclusion of von Willebrand factor levels did not alter the HR for recurrent ACS (HR: 2.1; 95% CI: 1.1-5.2; P = 0.03) for CEPI-CT < 300 s, but reduced the HR for CADP-CT (HR: 2.8, 95% CI: 0.8-9.8; P = 0.11). CONCLUSION: Shortened CT values reflect biologically relevant platelet hyperfunction in patients with ACS because they predict recurrent ACS.

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.

Pulmonary embolism as a cause of cardiac arrest: presentation and outcome.

BACKGROUND: Pulmonary embolism (PE) is a possible noncardiac cause of cardiac arrest. Mortality is very high, and often diagnosis is established only by autopsy. METHODS: In a retrospective study, we analyzed clinical presentation, diagnosis, therapy, and outcome of patients with cardiac arrest after PE admitted to the emergency department of an urban tertiary care hospital. RESULTS: Within 8 years, PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims. The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Pronounced metabolic acidosis (median pH, 6.95, and lactate level, 16 mmol/L) was found in most patients. In 18 patients (30%), the diagnosis of PE was established only postmortem. In 42 (70%) it was diagnosed clinically, in 24 of them the diagnosis of PE was confirmed by echocardiography. In 21 patients, 100 mg of recombinant tissue-type plasminogen activator was administered as thrombolytic treatment, and 2 (10%) of these patients survived to hospital discharge. Comparison of patients of the thrombolysis group (n = 21) with those of the nonthrombolysis group (n = 21) showed a significantly higher rate of return of spontaneous circulation (81% vs 43%) in the thrombolysis group (P=.03). CONCLUSIONS: Mortality related to cardiac arrest caused by PE is high. Echocardiography is supportive in determining PE as the cause of cardiac arrest. In view of the poor prognosis, thrombolysis should be attempted to achieve return of spontaneous circulation and probably better outcome.

Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome.

BACKGROUND: Moderate elevation of brain temperature, when present during or after ischemia, may markedly worsen the resulting injury. OBJECTIVE: To evaluate the impact of body temperature on neurologic outcome after successful cardiopulmonary resuscitation. METHODS: In patients who experienced a witnessed cardiac arrest of presumed cardiac cause, the temperature was recorded on admission to the emergency department and after 2, 4, 6, 12, 18, 24, 36, and 48 hours. The lowest temperature within 4 hours and the highest temperature during the first 48 hours after restoration of spontaneous circulation were recorded and correlated to the best-achieved cerebral performance categories' score within 6 months. RESULTS: Over 43 months, of 698 patients, 151 were included. The median age was 60 years (interquartile range, 53-69 years); the estimated median no-flow duration was 5 minutes (interquartile range, 0-10 minutes), and the estimated median low-flow duration was 14.5 minutes (interquartile range, 3-25 minutes). Forty-two patients (28%) underwent bystander-administered basic life support. Within 6 months, 74 patients (49%) had a favorable functional neurologic recovery, and a total of 86 patients (57%) survived until 6 months after the event. The temperature on admission showed no statistically significant difference (P =.39). Patients with a favorable neurologic recovery showed a higher lowest temperature within 4 hours (35.8 degrees C [35.0 degrees C-36.1 degrees C] vs 35.2 degrees C [34.5 degrees C-35.7 degrees C]; P =.002) and a lower highest temperature during the first 48 hours after restoration of spontaneous circulation (37.7 degrees C [36.9 degrees C-38.6 degrees C] vs 38.3 degrees C [37.8 degrees C-38.9 degrees C]; P<.001) (data are given as the median [interquartile range]). For each degree Celsius higher than 37 degrees C, the risk of an unfavorable neurologic recovery increases, with an odds ratio of 2.26 (95% confidence interval, 1.24-4.12). CONCLUSION: Hyperthermia is a potential factor for an unfavorable functional neurologic recovery after successful cardiopulmonary resuscitation.

Clinical evaluation of different doses of intravenous enalaprilat in patients with hypertensive crises.

BACKGROUND: The appropriate dose of intravenous enalaprilat to be used in the treatment of hypertensive crisis is controversial. There has been no comparative study of the efficacy and safety of different dosages of enalaprilat in hypertensive patients. METHODS: Sixty-five consecutive patients with hypertensive urgencies (systolic blood pressure > 210 mm Hg and/or diastolic blood pressure > 110 mm Hg) or emergencies (diastolic blood pressure > 100 mm Hg and evidence of end-organ damage, ie, angina pectoris, hypertensive encephalopathy, or congestive heart failure) admitted to an emergency department from January 1, 1994, to September 30, 1994, were identified. The patients were randomized to receive different doses of enalaprilat (0.625, 1.25, 2.5, and 5 mg). Response to treatment was defined as a stable reduction of systolic blood pressure to below 180 mm Hg and diastolic blood pressure to below 95 mm Hg within 45 minutes after the start of treatment and relief of symptoms in patients with hypertensive emergencies. RESULTS: In 41 (63%) of 65 patients, the treatment goal was reached. Twenty-four patients (37%) failed to achieve the goal of treatment within 45 minutes after administration of enalaprilat. The response rates in the 0.625-mg, 1.25-mg, 2.5-mg, and 5-mg groups were 67%, 65%, 59%, and 62%, respectively. The proportion of patients initially randomized who responded to treatment was not different between any of the four groups of enalaprilat doses. There were no significant differences according to enalaprilat dose with respect to changes in systolic, diastolic, and mean arterial blood pressure. No severe side effects were observed. CONCLUSION: Enalaprilat is a safe antihypertensive drug with moderate efficacy in the treatment of hypertensive crisis. As doses above 0.625 mg alter neither response rates nor the magnitude of blood pressure reduction, we recommend 0.625 mg as the initial dose in the treatment of hypertensive crisis.

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.

Acute renal infarction. Clinical characteristics of 17 patients.

We analyzed the medical records of patients with an established diagnosis of acute renal infarction to identify predictive parameters of this rare disease. Seventeen patients (8 male) who were admitted to our emergency department between May 1994 and January 1998 were diagnosed by contrast-enhanced computed tomography (CT) as having acute renal infarction (0.007% of all patients). We screened the records of the 17 patients for a history with increased risk for thromboembolism, clinical symptoms, and urine and blood laboratory results known to be associated with acute renal infarction. A history with increased risk for thromboembolism with 1 or more risk factors was found in 14 of 17 patients (82%); risk factors were atrial fibrillation (n = 11), previous embolism (n = 6), mitral stenosis (n = 6), hypertension (n = 9), and ischemic cardiac disease (n = 7). All patients reported persisting pain predominantly from the flank (n = 11), abdomen (n = 4), and lower back (n = 2). On admission, elevated serum lactate dehydrogenase was found in 16 (94%) patients, and hematuria was found in 12 (71%) of 17 patients. After 24 hours all patients showed an elevated serum lactate dehydrogenase, and 14 (82%) had a positive test for hematuria. Our findings suggest that in all patients presenting with the triad--high risk of a thromboembolic event, persisting flank/abdominal/lower back pain, elevated serum levels of lactate dehydrogenase and/or hematuria within 24 hours after pain onset--contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction.

Energy metabolism in acute and chronic renal failure.

Energy metabolism was measured by indirect calorimetry in 86 patients with various forms of renal failure and in 24 control subjects. In patients with acute renal failure with sepsis, oxygen consumption, carbon dioxide production, and resting energy expenditure were increased (P less than 0.05). In other groups with renal failure (acute renal failure without sepsis, chronic renal failure with conservative treatment or hemodialysis, and severe untreated azotemia) these indices were not different from those of control subjects. Urea nitrogen appearance was decreased in patients with chronic renal failure undergoing conservative treatment, in those with severe untreated azotemia, and in hemodialysis patients (P less than 0.05). We conclude that renal failure has no influence on energy expenditure as long as septicemia is absent. Reduced urea nitrogen appearance rates in chronic renal failure are due to a reduced energy and protein intake. Wasting is a consequence of decreased food intake but not of hypermetabolism in chronic renal failure.

Acute phase reactants in patients with abdominal aortic aneurysm.

BACKGROUND: There is increasing evidence that an inflammatory process is present in abdominal aortic aneurysms (AAAs) to varying degrees. The aim of this study was to compare acute phase reactants in patients with asymptomatic AAA, symptomatic AAA without rupture and ruptured AAA. METHOD: Two hundred and twenty-five consecutive patients treated because of AAA were included in this case-control study. Polynomial logistic regression analysis was applied to compare admission C-reactive protein (CRP) and white blood count (WBC) measured in 111 asymptomatic outpatients, 52 symptomatic patients without rupture and 62 patients with rupture of the aneurysm. We adjusted for the potentially confounding effect of age, sex, haemoglobin levels and aneurysm diameter. RESULTS: Patients with symptomatic AAA and patients with ruptured AAA had significantly elevated CRP (p=0.002) and WBC (p<0.0001) levels compared to asymptomatic patients. There was no statistically significant difference in CRP and WBC between patients with symptomatic AAA and ruptured AAA. Median CRP values of asymptomatic, symptomatic and ruptured AAA were <0.5 (interquartile range (IQR) <0.5-0.85), 1.1(IQR <0.5-4.0) and 2.4 mg/dl (IQR 0.65-8.6), respectively, and median WBC values were 6.5 (IQR 5.5-8.0), 8.7 (IQR 6.8-11.2) and 13.2 (IQR 10.5-17.0), respectively. CONCLUSION: A significant elevation of CRP and WBC could be found in patients who presented with symptoms or rupture of an AAA. These indicators of inflammation were not observed in asymptomatic patients with AAA.

The influence of chronic prearrest health conditions on mortality and functional neurological recovery in cardiac arrest survivors.

PURPOSE: To study the impact of chronic prearrest health conditions on mortality and neurological recovery in patients after witnessed cardiac arrest and primary successful resuscitation. PATIENTS AND METHODS: The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation of adult patients who survived a witnessed cardiac arrest were collected according to an internationally recommended protocol (Utstein-Style). Chronic prearrest health conditions and New York Heart Association (NYHA) functional classes were evaluated. All patients were followed up for 6 months after the event or death. Adverse outcome was defined as death or severe neurological impairment. A forward stepwise logistic regression model was applied to assess the impact of pre-arrest morbidity on unfavorable outcome, expressed as odds ratio (OR) with 95% confidence intervals (CI). RESULTS: Of 411 patients, 269 (66%) had one or more of the following pre-arrest diseases: coronary heart disease (45%), hypertension (26%), congestive heart failure (20%), diabetes mellitus (14%), chronic pulmonary disease (6%), and cerebrovascular disease (5%). In 22% a NYHA class of III or IV was present before cardiac arrest. At 6-month follow-up, 161 (40%) of the patients were alive with favorable neurological recovery; overall mortality was 57% (n = 233). Increasing NYHA classes (OR 1.4 per NYHA class increase; CI 1.1 to 1.7) and increasing age were independent predictors of adverse outcome (OR 1.03 per 10-year increase; CI 1.01 to 1.05), as were durations of cardiac arrest (OR 1.10 per 5-minute increase; CI 1.07 to 1.12) and the presence of ventricular fibrillation or tachycardia (OR 0.3; CI 0.2 to 0.5). The remaining health conditions, as listed above, were not independently associated with outcome. CONCLUSIONS: A large proportion of patients with cardiac arrest had chronic diseases before the event. The presence of impaired functional performance in patients with structural heart disease increased unfavorable outcome within 6 months in primary cardiac arrest survivors. However, the impact of chronic prearrest conditions on outcome seems to be very small, and should not influence decisions whether to withhold or withdraw therapy.

Prevention of upper gastrointestinal bleeding in long-term ventilated patients. Sucralfate versus ranitidine.

Thirty-two long-term ventilated patients were randomly selected for a study of the efficacy of sucralfate (1 g six times per day via gastric tube) versus ranitidine (six 50-mg to six 100-mg doses per day intravenously) for the prevention of upper gastrointestinal bleeding. The patients of the two treatment groups (each 16) were comparable with respect to diseases precipitating acute respiratory failure and risk factors of bleeding, e.g., renal failure, thrombopenia, coagulopathy, and anticoagulant treatment. Mean duration of mechanical ventilation was 7.4 in sucralfate- and 7.7 days in ranitidine-treated patients. During mechanical ventilation, macroscopically visible bleeding developed in three of the sucralfate-treated (18.7 percent) and seven of the ranitidine-treated (43.7 percent) patients. Until the end of the study, only three of the sucralfate-treated but nine of the ranitidine-treated (56.2 percent) patients bled; the difference between the two treatment groups was at all times significant (p less than 0.05). Packed red blood cells had to be administered to the three bleeding patients in the sucralfate group and to seven bleeding in the ranitidine group. Therefore it seems that sucralfate prevented mostly minor bleeding. The high bleeding rate during ranitidine treatment was presumably due to the high number of pH-nonresponders, as almost 30 percent of the gastric aspirates of this group had a pH less than 5. During treatment no difference was found in positive blood culture specimens and bronchial secretions between the two groups. However, nosocomial pneumonia developed in two ranitidine-treated patients, whereas that complication developed in none of the sucralfate-treated patients. In long-term ventilated patients, sucralfate prevented minor upper gastrointestinal bleeding significantly better than ranitidine. However, this does not imply that major upper gastrointestinal bleeding can be prevented by either sucralfate or ranitidine in these patients.

Course of blood pressure within the first 12 h of hypertensive urgencies.

OBJECTIVE: To evaluate the course of blood pressure within 12 h of a hypertensive urgency with or without oral antihypertensive treatment prior to discharge of patients from hospital. DESIGN: A prospective, double-blinded, placebo-controlled and randomized clinical trial. SETTING: Department of Emergency Medicine in a 2000-bed inner city hospital. PATIENTS: Forty patients successfully treated for a hypertensive urgency with intravenous administration of urapidil. INTERVENTIONS: We administered 60 mg urapidil orally or placebo prior to discharge of patients from hospital and evaluated the course of blood pressure within 12 h of the urgency by use of an ambulatory blood pressure measurement unit. MAIN OUTCOME MEASURES: Mean systolic and diastolic blood pressures within the first 12 h of a hypertensive urgency and the number of hypertensive and hypotensive episodes. RESULTS: Mean systolic and diastolic blood pressures were significantly lower in members of the urapidil group than they were in members of the placebo group (132 +/- 14 versus 147 +/- 18 mmHg, P = 0.003; 79 +/- 12 versus 87 +/- 14 mmHg, P = 0.047, respectively). The number of hypotensive episodes was similar for these two groups (three versus one, P = 0.32), whereas the number of hypertensive episodes was significantly lower for the urapidil group (13 versus 34, P = 0.001). CONCLUSIONS: Oral medication with urapidil prior to discharge results in lower overall blood pressure levels and reduces the risk of hypertensive episodes recurring within 12 h of a hypertensive urgency. Therefore, we recommend this therapeutic approach for patients with hypertensive urgencies, who are treated with an intravenous antihypertensive drug.

Increased blood pressure response to the cold pressor test in pregnant women developing pre-eclampsia.

OBJECTIVES: Recent data indicate an increased vascular reactivity due to an overactivity of the sympathetic nervous system in women with pre-eclampsia. We therefore evaluated whether this increased vascular reactivity can be detected prior to the clinical manifestation of preeclampsia by the use of a physiological stimulus. DESIGN: Prospective data collection. SETTING: Clinic of Obstetrics and Gynecology in a 2000 bed tertiary care hospital. PARTICIPANTS: One hundred and twenty-three pregnant women between the 16th to 20th week of gestation. INTERVENTIONS: A cold pressor test was performed by positioning an ice-bag on the forehead of the woman for 3 min. Blood pressure and heart rate were monitored by a continuous, noninvasive blood pressure measurement device during the stimulus and after removal of the icebag. A clinical follow-up was carried out by review of the charts after delivery to identify those women who have developed pre-eclampsia. RESULTS: Ten (8%) out of 123 pregnant women developed pre-eclampsia. During the cold pressor test systolic as well as diastolic blood pressure increased significantly and was more pronounced in women developing pre-eclampsia compared with healthy pregnant women (systolic blood pressure: 14.2 +/- 5.5 versus 8.5 +/- 7.2 mmHg, P= 0.02; diastolic blood pressure: 7.3 +/- 4.9 versus 3.9 +/- 4.7 mmHg, P=0.03). The change in heart rate was similar between both groups (8 +/- 2.6 versus 10.4 +/- 6.4 beats/min, not significant). CONCLUSIONS: An increased vasoconstrictive response to a physiological stimulus is present in women with pre-eclampsia as a sign of an increased vascular reactivity prior to clinical manifestation of the disease. The cold pressor test may be a suitable diagnostic tool to identify women, who will develop pre-eclampsia. However, future studies in larger cohorts are required to establish the final value of this test.

Use of an age-adjusted Doppler E/A ratio in patients with moderate to severe hypertension.

OBJECTIVE: To assess the ratio of early (E) to late atrial (A) mitral Doppler peak flow velocity (Doppler E/A ratio) before and after adjustment for age in patients with moderate to severe hypertension, in whom left ventricular diastolic dysfunction is an early finding. Mitral flow patterns can be used to assess diastolic filling characteristics, and the Doppler E/A ratio is the parameter most commonly used, although it is known to be strongly age dependent. There are no established normal values for this ratio. DESIGN: Retrospective data analysis. SETTING: A 2000-bed tertiary-care teaching hospital. PATIENTS: We studied 190 patients (99 women and 91 men; ages 55 +/- 13 years) with moderate to severe hypertension. INTERVENTIONS: The ratio of early (E) to late atrial (A) mitral Doppler peak flow velocity was measured. As this ratio depends on age, a Z score was calculated to control for this influence. The Z score is the standardized normal deviation of the mean, with a normal value of 0 +/- 2. MAIN OUTCOME MEASURES: Sensitivities and specificities for detecting an age-dependent reduction in Doppler E/A score (Z score less than -2) with a non-age-dependent Doppler E/A ratio (less than 1) were calculated. RESULTS: In 106 of the patients (56%) the Doppler E/A ratio was less than 1.0. Only nine patients (4.7%) had a Z score less than -2. The sensitivity of the Doppler E/A ratio threshold of 1.0 for detecting a Z score less than -2 was 0.89 and the specificity was 0.46. A Z score less than -2 was found only in patients younger than 45 years. CONCLUSIONS: The Doppler E/A ratio was reduced in a large proportion of our patients. However, after correction for age it was decreased in only 4.7% of these patients. The use of a single Doppler E/A ratio threshold value has a weak diagnostic power to detect age-independent changes in mitral flow patterns.

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.

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.