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.

The role of Chlamydia pneumoniae in human aortic disease-a hypothesis revisited.

BACKGROUND: The role of Chlamydia pneumoniae in the pathogenesis of aortic aneurysm is controversial. We investigated the presence of C. pneumoniae in tissue samples excised from patients and controls. METHODS: Aortic wall specimens were obtained from 17 patients with acute Stanford type A aortic dissection, 25 patients with thoracic aortic aneurysms (TAA) and 23 patients with abdominal aortic aneurysms (AAA). Eighty-three tissue samples of 73 control patients free of aortic disease were obtained either at surgery or autopsy. The presence of Chlamydia subspecies DNA (sequences specific for all known Chlamydiaceae) and DNA of C. pneumoniae, C. trachomatis and C. psittaci were assessed by a validated highly sensitive and specific real time polymerase chain reaction (PCR) analysis. Atherosclerotic risk factors were assessed in all patients. RESULTS: We failed to detect C. pneumoniae and C. psittaci-DNA in any of the 148 vessel specimens. C. trachomatis-DNA was detected in 1/65 patients and in none of 83 controls (P=0.43). Chlamydia subspecies DNA was found in samples of eight cases and in one control (P=0.01), however, no significant differences were found between the subgroups aortic dissection (P=0.09), TAA (P=0.99) and AAA (P=0.15) and respective controls. CONCLUSIONS: C. pneumoniae does not play a clinically relevant role in acute and chronic aortic disease. The impact of other organisms of the family Chlamydiaceae needs further evaluation.

Acute type A aortic dissection: the prognostic impact of preoperative cardiac tamponade.

OBJECTIVE: Acute type A aortic dissection requires emergency surgery and is associated with considerable mortality. The aim of the study was to evaluate whether occurrence of preoperative cardiac tamponade with or without palpable pulses in these patients is associated with higher incidence of multiple organ failure (MOF) and in-hospital mortality. METHODS: A retrospective cohort study included 87 patients with acute type A aortic dissection, who were admitted via an emergency department between December 1991 and December 1999 for emergency surgery. Impending cardiac tamponade (with palpable pulses) and severe cardiac tamponade (without palpable pulses) were recorded and patients were followed for occurrence of MOF and/or in-hospital mortality. RESULTS: Impending cardiac tamponade with palpable pulses was diagnosed in 33 patients (38%), signs of severe cardiac tamponade without palpable pulses were found in seven patients (8%). MOF occurred in 41 patients (47%); 32 patients (37%) died during the present stay, all of them had MOF. Preoperative severe cardiac tamponade without palpable pulses was associated with a significantly increased risk for poor outcome (odds ratio (OR)=16.1, 70% confidence interval (CI) 4.8-71.7, P=0.04), particularly preoperative death (n=6 of 7). Impending cardiac tamponade with palpable pulses (OR=1.6, 70% CI 0.8-3.3, P=0.2) was not associated with the occurrence of MOF/death. Hemodynamic shock (OR=6.5, 70% CI 3.0-13.9, P=0.01) was also associated with poor outcome. CONCLUSION: Patients with acute type A aortic dissection and signs of preoperative cardiac tamponade without palpable pulses had a 16-fold increased risk for poor outcome, particularly preoperative death. In contrast, cardiac tamponade with palpable pulses was not associated with increased frequency of MOF/in-hospital mortality.

Admission for syncope: evaluation, cost and prognosis.

BACKGROUND: Despite extensive in-hospital evaluation the cause of syncope remains unexplained in up to 40% of patients. AIMS: To determine the application and cost of diagnostic tests, cost of hospital stay, success of evaluation and prognosis of patients admitted via the emergency department after syncope. METHODS: A retrospective cohort study including all consecutive patients admitted via the emergency department for evaluation of syncope between 1 January 1994 and 31 December 1998. The findings obtained from clinical history, physical examination and diagnostic tests were reviewed systematically. The costs of specific tests and hospital stay were analysed. Patients were followed until 31 December 1998. RESULTS: 127 patients underwent a median of 4 diagnostic tests (interquartile range, 3 to 6) over 12 days (IQR 8 to 17). The overall median cost of syncope evaluation was 106,728 ATS/7,756 EUR (IQR 70,860 to 143,583 ATS) per patient; the cost of diagnostic tests per patient was 6,863 ATS/499 EUR (IQR 3,345 to 11,969 ATS); hospital maintenance and in-hospital care accounted for the major part of these costs [median 97,680 ATS/7,099 EUR (IQR 65,120 to 138,380 ATS)]. At the time of hospital discharge, syncope remained unexplained in 48 patients (38%). The strength of agreement between the emergency department diagnosis and the discharge diagnosis was moderate (kappa = 0.49, 95% confidence interval 0.36 to 0.61). None of the patients had recurrent syncope or died during the hospital stay. Within the first 30 days after the index event 2 patients (2%) died due to known pre-existing diseases. CONCLUSION: The emergency department diagnosis markedly influenced the work-up of syncope, but not the cost of evaluation. The moderate diagnostic yield, high cost of in-hospital evaluation and good short term prognosis indicate the need for alternative strategies of in-hospital evaluation.

G-protein beta3 subunit gene (GNB3) polymorphism 825C-->T in patients with hypertensive crisis.

OBJECTIVE: The polymorphism 825C-->T in exon 10 of the gene GNB3 encoding the beta3 subunit of heterotrimeric guanine nucleotide binding regulatory proteins (G-proteins) results in a splicing variant (GNB3-s) in which the nucleotides 498-620 of exon 9 are deleted. The T allele has been shown to be overrepresented in patients with essential hypertension. Because GNB3-s may support the development of severe elevation of blood pressure, we hypothesized that GNB3 825C-->T may be present more frequently in patients with hypertensive crisis. DESIGN: Case control study. SETTING: Department of Emergency Medicine at the University Hospital of Vienna, Vienna, Austria. PATIENTS: A total of 174 patients admitted to an emergency department for treatment of hypertensive crisis diagnosed as suffering from essential hypertension. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients were genotyped for the 825C-->T transition in GNB3. An equal number of age- and gender-matched normotensive, healthy individuals served as the control population. The allele frequency of 825C-->T in the GNB3 gene was 0.310 in patients with hypertensive crisis and 0.342 in the control group. There was no difference in genotype distribution and allele frequency between the patients and the age- and gender-matched control group or between the observed prevalence and the occurrence rate expected from the Hardy-Weinberg principle within each group. CONCLUSIONS: GNB3 825C-->T is not associated with the phenotype of hypertensive crisis in patients suffering from essential hypertension. Furthermore, our data do not support the concept that the 825C-->T transition in the GNB3 gene is associated with essential hypertension.

Heroin and opiate emergencies in Vienna: analysis at the municipal ambulance service.

Vienna suffered an epidemic of heroin abuse in recent years, with drug-deaths due to opioids increasing from 62 in 1991 to 143 in 1993. The aim of this study was to make observations about illicit opioid-use with the ambulance service as a data source. From June 1994 to August 1995, the structured run records of the ambulance service were reviewed. Those with a presumptive diagnosis of "heroin or opiate" overdose were collected, characteristics of emergencies and patients were analyzed. The run records demonstrated a large number of non-fatal emergencies due to opioids, involving 528 men and 179 women in 1087 emergencies. These emergencies were on the average 6.8 times as prevalent as drug-fatalities. A group of 189 persons could be identified, who caused 52.2% of all emergencies and showed a threefold mortality rate during the observation period. In Vienna, the records of the municipal ambulance service provided valuable insights on opioid-abuse. We suggest local analysis of non-fatal emergencies due to opioids, as this might lead to a new source of information on illicit abuse of these drugs.

[Edrophonium chloride (Tensilon) test: a safe method in diagnosing myasthenia gravis]. / Der Edrophonium-Chlorid (Tensilon)-Test: Ein sichere Methode in der Diagnostik der Myasthenia gravis.

OBJECTIVE: To evaluate the safety of edrophonium chloride in the course of the Tensilon test by measurement of hemodynamic and ECG parameters and the observation of adverse events. METHODS: 25 patients with known or suspected myasthenia gravis were included in an open, prospective study concerning the performance of the Tensilon test. Blood pressure, heart rate, continuous ECG and adverse events were recorded 10 minutes following intravenous application of Tensilon. RESULTS: Blood pressure and heart rate did not change significantly during the observation period. One patient on beta-blockers developed a grade I AV block. Self-limiting adverse events of short duration were observed in 11 patients. Serious adverse events such as syncope or hemodynamic deterioration did not occur. CONCLUSION: The Tensilon test appears to be a safe procedure. A detailed clinical cardiac history, the history of medication and twelve lead ECG recordings should be documented in all patients undergoing the Tensilon test. Patients with a history of dysrhythmia receiving digitalis, beta-blocking agents or Ca antagonist therapy should be managed with special care, as Tensilon enhances vagal effects.

The association between C-reactive protein on admission and mortality in patients with acute myocardial infarction.

OBJECTIVE: In patients presenting with acute myocardial infarction the pathophysiologic and prognostic value of serum C-reactive protein is not well defined. This study assessed the association between serum C-reactive protein levels on admission and mortality in patients admitted because of acute myocardial infarction. DESIGN: Retrospective cohort study. SETTING: Tertiary care centre. PATIENTS: A total of 729 patients with acute myocardial infarction admitted within a period of 3 years. MAIN OUTCOME MEASURES: C-reactive protein levels on admission, cardiovascular risk factors and survival within the observational period. RESULTS: Within the 3-year observational period, 118 patients died of a cardiovascular cause. With increasing serum C-reactive protein levels (<0.5, 0.5 to <2, 2 to <5, 5-10 and >10 mg dL-1) mortality also increased (14%, 19%, 20%, 39% and 28%, respectively). When controlling for the confounding effect of age, thrombolytic treatment, the time interval between onset of pain and admission, smoking, diabetes mellitus, hypercholesterolemia, hypertension, and elevated creatine kinase on admission in a multivariate Cox regression model, there was only a weak and nonsignificant association between increased serum C-reactive protein and the risk of death. CONCLUSIONS: Patients with elevated concentrations of serum C-reactive protein admitted to the hospital because of acute myocardial infarction are at an increased risk of dying. This association is however, largely explained by other baseline variables, in particular by an estimate of the duration of myocardial ischaemia. If C-reactive protein measured by means of an ultra-sensitive assay is more suitable for risk stratification of unselected patients with acute myocardial infarction, needs further study.

Causes and outcome of syncope.

BACKGROUND: Little is known about the frequency of patients presenting to the emergency department with syncope. Regarding mortality and predictors of outcome the literature remains inconclusive. AIMS: The aims of the study were to determine the frequency of patients presenting with syncope to an emergency department, to assess mortality among these patients and to determine potential predictors of poor outcome. METHODS: Data of all consecutive patients who were treated at our emergency department between January 1st 1994 and September 1st 1997 following syncope were collected retrospectively. The presumptive causes of syncope were classified into six categories (cardiogenic, neurogenic, autonomic dysfunction, psychiatric, toxic/alcoholic, idiopathic/unexplained). Patients were followed until December 31st, 1997. RESULTS: 701 patients (0.35% of all emergency department visits) were treated for this reason. 507 patients were eligible for the study. During follow-up 8% (n = 38) of the patients died. Three patients died within the first 28 days, all with a known severe underlying disease (congestive heart failure, malignancy, ischemic cerebral infarction). Non-survivors more frequently had a cardiogenic (34%) or neurogenic (13%) cause of syncope (p < 0.01). Age > 60 years, syncope due to neurogenic cause and abnormal ECG findings were independent predictors of increased mortality. CONCLUSIONS: Patients with syncope only comprise a small proportion of those seen at the emergency department. Mortality among these patients is 8%. Clinical history and ECG findings are major determinants of risk stratification: Age > 60 years, syncope due to neurogenic causes and abnormal ECG are independent predictors of poor outcome.

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.

Assessment of myocardial injury by serum tumour necrosis factor alpha measurements in acute myocardial infarction.

Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor alpha. Therefore, an attempt was made to correlate changes in serum tumour necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acute myocardial infarction, blood samples for evaluation of tumour necrosis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collected every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhythm disturbances, by enzymatic methods such as cumulative release of alpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late resting single photon emission tomography--201 thallium scintigraphy--using an extent score and by echocardiography using a wall motion index. The maximum change in serum tumour necrosis factor alpha after infarction (delta TNF) was calculated by subtracting tumour necrosis factor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha level was observed 84 h after admission (median: 12 pg.ml-1). Between the 72nd and the 96th h no significant changes in tumour necrosis factor alpha values were observed. Analysis of the data showed that larger delta (TNF) values were found to be associated significantly with signs of heart failure (P = 0.003), the presence of rhythm disturbances (P = 0.001), increased enzymatic infarct extent indicated by cumulative release of alpha-hydroxybutyrate-dehydrogenase (r = 0.74; P < 0.001), large myocardial perfusion defects measured with 201 thallium scintigraphy (r = 0.80; P < 0.001), and a considerable number of left ventricular wall motion abnormalities (r = 0.57; P < 0.001). In conclusion, delta (TNF) is a reliable method of assessing damage severity in the myocardium after acute myocardial infarction. As only two blood samples are necessary within 84 h, the method may be one of the more convenient for the assessment of infarct size in clinical practice.

Conservative management of foreign bodies in the gastrointestinal tract.

There are at present no clear guidelines whether foreign body ingestion in the gastrointestinal tract should be managed conservatively, endoscopically or surgically. Retrospectively we have, therefore, analyzed 78 foreign body ingestion's in 42 patients (age 15-72 years) admitted to the Emergency Department of the University Hospital in Vienna. Our intention was to assess the value of a conservative management, defined as daily follow-up visits until the foreign body spontaneously appeared in the feces and to find criteria when endoscopic or surgical management is required. Of 78 foreign bodies, 67 (86%) passed the gastrointestinal tract spontaneously without complications, 9 (11%) were removed endoscopically, and only 2 (3%) required surgery. There were no gastrointestinal perforations. Even foreign bodies with a maximal length of 13.5 cm appeared in the feces spontaneously within a few days. Our data suggests that more than 80% of adults with foreign body ingestion can be managed safely as outpatients by means of conservative treatment. Endoscopic or surgical removal is only indicated in very rare circumstances.

Factitious hyperthyroidism causing acute myocardial infarction.

Myocardial ischemia is a rare but severe and possibly life threatening manifestation of hyperthyroidism, but does not usually result in persistent ischemia. We report on a 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years ago. Since then, she had been maintained on oral levothyroxine replacement therapy at a dose of 0.15 mg alternating with 0.2 mg daily. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg a day. Three weeks later, the patient suffered from an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still revealed a persistent perfusion defect. Since it is known that thyroid hormones increase oxygen demand, the rapid elevation of oxygen utilization caused by thyrotoxicosis factitia is likely to be responsible for this patient's myocardial infarction. The case illustrates that a sudden increase in levothyroxine replacement dose should be avoided.

Poor ventilatory response to mild hypoxia may inhibit acclimatization at moderate altitude in elderly patients after carotid surgery.

Peripheral chemoreceptors (carotid bodies) are the main sensing organs for hypoxaemia. During carotid surgery, the carotic body in the bifurcation of the common carotid artery is often involved and damaged or destroyed. Animals lose their ability to adapt to high altitude after experimental denervation of the carotid bodies. The objective of our study was to evaluate the ability of human patients to adapt to moderate altitude after single side carotid surgery. Blood gas analysis at rest at 171 m and after car and cable car transport to 1600 m before and after carotid surgery was performed. Mean(s.d.) paO2 decreased insignificantly from 74.8(3.56) at 171 m altitude to 71.6(2.07) at 1600 m (P = n.s.), means(s.d.) paCO2 decreased significantly from 36.2(2.86) to 31.4(2.7) mmHg (P < 0.05) before carotid surgery. Months after surgery, a significant drop in paO2 occurred after identical passive exposure to moderate altitude: mean(s.d.) paCO2 at 171 m 74.4(3.65) mmHg, at 1600 m 65.8(3.70) mmHg (P < 0.01), paCO2 did not change significantly. Mean(s.d.) paCO2 at 171 m: 36.0(2.35), at 1600 m 36.2(2.86) mmHg (P = n.s.). Although the sample investigated was small, after single side carotid surgery patients seem to lose their ability for satisfactory ventilatory response to acute exposure to moderate altitude. This is of possible alpine medical importance.

Action of ATP on ventricular automaticity.

ATP is an effective treatment of supraventricular tachycardia when the atrioventricular (AV) node is part of the reentrant circuit. However, the lower a pace-maker in the pacemaker hierarchy, the more sensitive it is to adenosine. Therefore, we investigated the effects of ATP on ventricular automaticity in in vivo and in vitro conditions. Wide and narrow QRS complex tachycardia in 46 patients was treated with 6, 12, and 18 mg ATP as sequential intravenous (i.v.) bolus. ATP terminated tachycardias in 67%. Bolus infusion ATP caused < or = 6.4-s asystole that was self-limited. Perfusion of isolated spontaneously beating guinea pig heart with 100 microM ATP completely suppressed ventricular automaticity. After ATP-infusion was discontinued, the first ventricular beat was evident after 3.1 +/- 0.9 s and sinus node activity recovered with a time constant of 3.0 +/- 1.1 s. Because sinus node and ventricular automaticity recovered within seconds after ATP infusion was discontinued in vitro, recovery in vivo is also likely to be determined by the short half-life (+1/2) of ATP.

Adenosine for the management of patients with tachycardias--a new protocol.

We developed a new protocol for diagnosis and treatment of patients with sustained tachycardias (heart rate > 150 beats.min-1). The patients first underwent vagal manoeuvres; if those remained unsuccessful, i.v. adenosine in increasing doses of 6, 12, and 18 mg was administered until sinus rhythm (SR) or transient atrioventricular (AV) block, unmasking the underlying rhythm, was recorded. In the latter and in the non-responding cases other antiarrhythmics were applied. Ninety-three episodes of tachycardia in 46 patients were treated according to this protocol. Six episodes (6%) were terminated by carotid massage, 64 of the remaining 87 episodes (74%) responded to adenosine with return to SR. Conversion to SR occurred more often in episodes with narrow- than in wide-complex tachycardia (81 vs. 59%, P < 0.05). To achieve SR, the mean adenosine dose was lower in narrow- than in wide-complex tachycardia (13 +/- 8 vs 21 +/- 10 mg; P < 0.01). The duration of asystole after adenosine did not differ between these two groups, whereas the duration of arrhythmia after adenosine differed significantly (8.5 +/- 5.8 vs 18.6 +/- 22.9 s; P < 0.05). Side effects of adenosine such as flush, dyspnoea, and chest pain did not seem to be dose dependent and occurred in about 20%. According to our protocol, in more than 75% SR was achieved in patients with sustained tachycardias after vagal manoeuvres and adenosine.

Energy metabolism in patients with acute and chronic liver disease.

Energy expenditure and substrate oxidation rate for fat, glucose and protein were evaluated by indirect calorimetry in 20 normal individuals, 35 patients with acute hepatitis and 22 patients with biopsy-proven alcoholic cirrhosis in the postabsorptive state. Measurements were done in the resting state after an overnight fast (10 to 12 hr). Oxygen consumption (ml/min/1.73 m2) in normal subjects, in patients with acute hepatitis and in patients with cirrhosis was 206.5 +/- 4.0 (mean +/- S.E.M.), 216.4 +/- 4.7 and 228.8 +/- 7.1 (p less than 0.05 vs. controls), respectively. When related to body surface area (kcal/min/1.73 m2), resting energy expenditure did not differ between normal subjects (0.98 +/- 0.02), patients with acute hepatitis (1.03 +/- 0.02) and cirrhotic patients (1.06 +/- 0.03). However, when related to 24-hr urinary creatinine excretion as an estimate of lean body mass, energy expenditure was increased in cirrhosis (p less than 0.0001). In cirrhosis an inverse association between the severity of liver disease according to Pugh and oxygen consumption and resting energy expenditure was found. In cirrhotic patients the percentages of total calories derived from fat (86% +/- 5%), carbohydrate (2% +/- 4%) and protein (12% +/- 1%) were different from those of normal controls who metabolized 45% +/- 4%, 38% +/- 4%, 17% +/- 1%, respectively. In acute hepatitis no alterations in metabolism could be found apart from a decreased protein oxidation rate. In conclusion no appreciable changes in energy metabolism exist in acute hepatitis. The pattern of fuel use in cirrhosis resembles that in starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Weaning using continuous-flow CPAP: hemodynamics and gas exchange]. / Weaning mit continuous-flow CPAP: Hämodynamik und Gasaustausch.

The present study was designed to investigate hemodynamics and gas exchange during weaning from mechanical ventilation (assist/control mode) to spontaneous breathing with continuous high flow (chf)-CPAP, and to study the predictive value of these parameters in respect of longterm success or failure of weaning. Hemodynamic and gas exchange parameters were obtained in 10 patients without severe pulmonary and cerebral dysfunction at -240, -60, -30, and -15 min before, and at +15, +30, +45, +60, +120, +180, +240 min after chf-CPAP. During chf-CPAP significant increases in heart rate/min (92 +/- 17 to 103 +/- 20), cardiac index (3.9 +/- 0.7 to 4.4 +/- 1.0 1/min.m2), respiratory rate/min (15 +/- 1 to 28 +/- 7), PaCO2 (36.7 +/- 3.0 to 41.2 +/- 5.9 torr) and oxygen delivery (12.2 +/- 2.7 to 13.9 +/- 2.3 ml/min.kg) were found. Arterial and pulmonary artery pressures rose only briefly within the first hour. All other parameters changed non-significantly. In the 4 patients who required mechanical ventilation 12 to 34 hours after the end of the study we found a significantly more pronounced increase in heart rate than in those who where weaned successfully (114 +/- 19 vs 89 +/- 9). Increases in heart rate, respiratory rate, cardiac index, PaCO2 and oxygen delivery can therefore be expected during weaning from mechanical ventilation to spontaneous breathing with CPAP. A pronounced increase in heart rate may suggest a weaning failure.