(Stroke. 1996;27:59-62.)
© 1996 American Heart Association, Inc.
Articles |
Arterial Blood Pressure After Human Cardiac Arrest and Neurological Recovery
From the Departments of Emergency Medicine (M.M., F.S., G.M., H.H., A.N.L.), Dermatology (M.B.), and Anesthesiology (K.H.), Vienna General Hospital, University of Vienna Medical School (Austria).
Correspondence to Fritz Sterz, MD, Department of Emergency Medicine, Vienna General Hospital, University of Vienna, Medical School, Waehringer Guertel 18-20/6D, 1090 Vienna, Austria. E-mail fritz.sterz@akh-wien.ac.at.
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Abstract |
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 Top Abstract IntroductionSubjects and Methods Results Discussion References |
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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%
(
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.
Key Words: heart arrest • hypertension • outcome • resuscitation
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Introduction |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Prolonged cardiac arrest is frequently followed by functional cerebral failure. Neurological recovery is influenced by delayed and suboptimal cardiopulmonary resuscitation and preexisting disease.1 2 Another factor influencing neuronal damage is post-ischemic-anoxic encephalopathy, also called cerebral postresuscitation disease,3 4 caused by multifactorial disturbances such as cerebral blood flow,5 6 7 cerebral oxygen metabolism,8 and blood glucose levels.9 Novel therapies of cerebral resuscitation aim for amelioration of postresuscitation syndrome and require multifaceted therapies. In animal models, cerebral blood flow6 10 and neurological outcome were improved by induced hypertension after successful resuscitation.11 12 It has been suggested that human cardiac arrest survivors might benefit from hypertensive reperfusion early after cardiac arrest and controlled normotension thereafter.3 However, until now only a few reports support this theory in human cardiac arrest.13 14
The aim of our study was to evaluate whether the BP level within the first few minutes and during an extended period of 2 hours after cardiac arrest has an influence on functional neurological recovery.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Subjects
Patients for this study were selected from the population served by the Department of Emergency Medicine at Vienna General Hospital, a tertiary care university hospital. The study period ranged from August 1, 1991, through December 29, 1994. Patients older than 18 years who had cardiopulmonary arrest in or outside the hospital with return of spontaneous circulation were eligible for inclusion in the study. Cardiopulmonary arrest was defined as the absence of both spontaneous respiration and palpable pulse. Patients whose cardiopulmonary arrest was associated with trauma, hypothermia, drowning, drug overdose, or a primary respiratory arrest were excluded from the study. Treatment was in accordance with the American Heart Association guidelines for basic and advanced cardiac life support and for postresuscitation care.1 All patients received standard intensive care treatment such as controlled mechanical ventilation, sedoanalgesia with midazolam (0.2 mg/kg per hour), fentanyl (0.004 mg/kg per hour), and low-dose dopamine (1.5 µg/kg per minute). According to our protocol, epinephrine was given to maintain MABP above 70 mm Hg. Other medications were left to the discretion of the attending physician.
Study Design and Data Collection
The study was performed
retrospectively. Data acquisition was
performed according to Utstein style, the recommended guidelines for
uniform reporting of data from out-of-hospital cardiac
arrest,2 on the arrival of each patient. Evaluated data
included location of cardiac arrest (in and out of hospital), witnessed
or not, time of cardiac arrest, duration of the interval from time of
cardiac arrest to beginning of basic life support, duration of the
interval from beginning of basic and/or advanced life support until
return of spontaneous circulation, preclinical medication, first ECG
rhythm, and patient history, particularly concerning the cause of
cardiac arrest. The time of recognition of collapse until time of
calling the emergency medical system was evaluated by one of the
investigators personally interviewing one or more witnesses. The time
of cardiac arrest was estimated from time of calling the emergency
medical system and time of recognition of collapse. For the time
interval from cardiac arrest to beginning of basic and/or advanced life
support, we presumed no sufficient systemic blood flow (ie, time of
duration of no blood flow).15 The time interval from
beginning of life support until return of spontaneous circulation was
presumed to be representative of the duration of low
systemic blood flow. Return of spontaneous circulation was defined as
electrical activity in ECG and palpable pulses.
BP was measured by emergency physicians by means of sphygmomanometry and auscultation of Korotkoff sounds on the left or right arm.16 The highest BP reading within 5 minutes after return of spontaneous circulation was recorded and used for analysis. BP was measured every 5 minutes until the patient's arrival in the Department of Emergency Medicine. To avoid artifacts, results were only recorded when the environmental conditions allowed reliable results. In the Emergency Department BP was measured and recorded in 5-minute increments by means of the oscillometric method (noninvasive BP module HPM1008A, Hewlett-Packard) until an intra-arterial catheter was inserted. Thereafter, BP was measured continuously and recorded in 5-minute increments until 2 hours after return of spontaneous circulation.
MABP was calculated according to a standard formula: diastolic BP+(systolic-diastolic BP)/3.17 Adequate systemic perfusion pressure was presumed for the range of 75 to 100 mm Hg.18
Assignment to Groups
If MABP exceeded 100 mm Hg within the
first 5 minutes after
return of spontaneous circulation, patients were considered
hypertensive and assigned to group 1; they were assigned to group 2 if
MABP was 100 mm Hg or less. The groups were compared for differences in
baseline data.
Outcome Measures
Cerebral function was assessed on arrival
and at regular
intervals within 6 months after return of spontaneous circulation,
expressed in terms of CPC.2 Definitions are as follows:
CPC 1, conscious and alert with normal function or only slight
disability; CPC 2, conscious and alert with moderate disability; CPC 3,
conscious with severe disability; CPC 4, comatose or in a persistent
vegetative state; and CPC 5, brain death. A CPC score of 1 or 2 was
considered good neurological outcome, and a CPC score of 3, 4, or 5 was
considered poor neurological outcome.
Statistical Analysis
Data are expressed as median and IQR.
Percentages were
determined for dichotomous variables. To analyze serial BP
measurements, the AUC was calculated for each patient with the use of
the trapezium rule.19 To achieve more familiar figures,
the resulting AUCs were divided by the elapsed time interval and named
MABPAUC. All data were computed with SPSS for
Windows. The Mann-Whitney U test was used to compare groups
of continuous data. To assess the influence of BP within the
postresuscitation period (after 5 minutes and MABPAUC for 2
hours after return of spontaneous circulation) on neurological
recovery, we used Spearman's partial rank correlation
(rs)19 20 to control for
durations
of no and low systemic blood flow. The absence or reduction of systemic
blood flow might influence outcome as well as BP in the
postresuscitation period.20 21 The 2
test was used for the comparison of dichotomous variables, and the
odds ratio and its 95% confidence interval were calculated. A value of
P<.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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In an observational period of 41 months, a total of 506 patients were admitted to the Department of Emergency Medicine because of cardiac arrest.
Study Group
A total of 136 patients fulfilled inclusion
criteria and were
enrolled in the study. The median age was 62 years (IQR, 53 to 72
years); 96 patients (71%) were male. Cardiac arrest occurred in 84
cases (62%) out of hospital and was witnessed in 129 cases (95%). The
first ECG rhythm on presentation was
ventricular fibrillation in 63% (n=86),
ventricular tachycardia in 10% (n=14),
pulseless electrical activity in 17% (n=23), and asystole in 10%
(n=13). The median time interval from collapse to beginning of life
support therapy (presumed no systemic blood flow) was 2 minutes (IQR, 0
to 4 minutes), and the median time interval from beginning of life
support therapy until return of spontaneous circulation was 7 minutes
(IQR, 3 to 19 minutes).
Subgroups
In 54 patients MABP was above 100 mm Hg (group 1)
within the first
5 minutes after return of spontaneous circulation, and in 82 patients
MABP was 100 mm Hg or lower (group 2). Thirty-four patients in
group 1 (63%) had good neurological outcome within 6 months. In group
2 good neurological outcome was observed in 45 patients (55%). This
difference was not statistically significant
(2=0.87; P=NS; odds ratio, 0.72; 95%
confidence interval, 0.36 to 1.44). Patients in group 1 exhibited
shorter durations of low blood flow (P=.04)
(Table
). After we controlled for durations of no and low
systemic blood flow by Spearman's partial rank correlation, there was
still no association between neurological recovery and MABP within 5
minutes after return of spontaneous circulation
(rs=-.023; n=129;
P=NS). In the
further course of 2 hours, MABPAUC was lower in group 2 (76
mm Hg; IQR, 61 to 82 mm Hg) than in group 1 (87 mm Hg; IQR, 77 to 101
mm Hg) (P<.0001). Spearman's partial rank correlation
revealed an independent, positive association between good neurological
recovery and MABPAUC during the first 2 hours after return
of spontaneous circulation (rs=.26; n=129;
P<.01).
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Discussion |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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The finding of this study is that cardiac arrest patients with arterial hypertension within the first 5 minutes after successful resuscitation had a nonsignificant tendency toward better neurological outcome within 6 months after cardiac arrest. Patients with higher initial BPs also had shorter cardiac arrest durations. When we controlled for this difference, there was no association between neurological recovery and BP measured within the first 5 minutes after return of spontaneous circulation. However, BP averaged during the first 2 hours after return of spontaneous circulation was independently and positively associated with good functional neurological recovery.
Neuronal damage after cardiac arrest with return of spontaneous circulation is not the only sequela of initial complete global brain ischemia. Other important sequelae are secondary derangements during and after reperfusion and reoxygenation, the cerebral postresuscitation disease3 4 that leads to further destruction of neurons. Global and regional cerebral blood flow disturbances in the post-cardiopulmonary resuscitation period5 6 7 10 22 due to vasospasm, edema, and blood cell aggregates23 24 lead to cerebral oxygen delivery/uptake mismatch. A possible approach to open highly resistant areas of the cerebral microcirculation and thus to overcome regional and global perfusion disturbances is hypertensive reperfusion.3
In a canine cardiac arrest model, Sterz et al11 showed that hypertension (MABP 150 mm Hg within 5 minutes after the start of reperfusion) was associated with lower neurological deficit scores as well as lower histopathologic damage scores. Hypertension also led to increased cerebral blood flow values.6 10 11 Martin et al13 defined a subgroup from a study of out-of-hospital cardiac arrest patients receiving standard or high doses of epinephrine during cardiopulmonary resuscitation.25 In these patients an association between initial high BP and good neurological outcome was shown. However, the sample size was very small, and baseline variables with potential impact on outcome were not reported.
In our patient population, arterial BP within the first minutes after return of spontaneous circulation was not associated with neurological recovery. Baseline values of both groups were similar with the exception of the duration of low blood flow. It is known that myocardial and cerebral perfusion during cardiopulmonary resuscitation are reduced to less than 5% and 30% of control values, respectively.26 27 28 Thus, prolonged no and low systemic blood flow durations might lead directly to neuronal and/or myocardial damage, causing reduced cardiac output, which would make it impossible for the cardiovascular system to achieve high BPs early after the return of spontaneous circulation. After we controlled for these variables, no association between outcome and initial MABP was observed.
Mean arterial BP values early after cardiac arrest in our patients were lower than the MABP readings in the canine cardiac arrest model by Sterz et al11 and Leonov et al,12 probably because hypertension in our study was spontaneous, or as a result of epinephrine administration before the return of spontaneous circulation. Cerebrovascular autoregulation after cardiac arrest is known to be impaired but not completely abolished.29 Thus, the BP in our patients was probably not high enough to overcome residual cerebrovascular autoregulatory function, which might explain the differences in neurological recovery compared with the canine cardiac arrest model. Noteworthy is that five of six patients with MABP greater than 150 mm Hg had good neurological outcome.
Systemic perfusion pressure measured during an extended period of 2 hours in our study population proved to be more important for functional neurological recovery than initial hypertensive reperfusion or initial BP. In a study in which the calcium entry blocker lidoflazine was used to ameliorate brain damage after cardiac arrest, the authors discussed that hypotension, which occurred more frequently in the lidoflazine group, may have offset a beneficial effect of the experimental drug.30 One study that reanalyzed the data of the Brain Resuscitation Clinical Trial II30 showed that patients who were hypotensive within 1 hour after cardiac arrest had a lower neurological recovery rate.14 However, in that study no baseline variables were given.
Both groups in our study received a similar dose of epinephrine during cardiopulmonary resuscitation. In the further course of 2 hours, epinephrine was administered to keep MABP between 75 and 100 mm Hg. Even though we did not perform quality control of the treatment, we assumed that hypotension occurred despite vasopressor treatment. Probably the dose administered could have been increased at some points without fear of causing heart failure or worsening cerebral vasogenic edema.31 However, until now there have been no data concerning the use of vasopressors in the early postresuscitation period and their impact on outcome.
One limitation of the study is the retrospective design. Difficulties in conducting clinical studies in cardiac arrest patients, particularly in acquiring comparable groups, are numerous and well recognized.2 By using an internationally recognized protocol,2 we eliminated some of the flaws of retrospective studies.
Imprecisions surrounding the exact time of collapse were minimized by tracing back from the accurate time of the activation of emergency medical service to the time of recognition of collapse by one investigator personally interviewing the witnesses.
Another limitation is the BP measurement by means of sphygmomanometry and auscultation in the prehospital arena. The problems and limitations of this method are well recognized.14 However, BP had always been measured by an experienced emergency physician according to a standardized protocol, which minimized related problems. Nevertheless, as long as there are no better facilities for noninvasive BP measurement in the preclinical field or at the bedside in a regular ward, sphygmomanometry will remain the accepted standard in clinical practice.
Conclusion
According to our data, there is no convincing
evidence for a
beneficial effect of hypertensive reperfusion within the first minutes
after return of spontaneous circulation of a cardiac arrest survivor.
Systemic blood flow promotion over an extended period seems to play an
important role in functional neurological recovery.
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Selected Abbreviations and Acronyms |
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Received July 24, 1995; revision received September 25, 1995; accepted October 12, 1995.
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References |
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