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N Bircher

Publications and source records attributed to N Bircher.

17 recordsLinked to original sources
PubMed1996

Future directions for resuscitation research. II. External cardiopulmonary resuscitation basic life support.

In sudden cardiac deaths outside hospitals, the present performance of external cardiopulmonary resuscitation-basic life support (CPR-BLS), as a bridge to advanced life support (ALS) attempts for restoration of spontaneous circulation (ROSC), still yields suboptimal results. Therefore, future education research should develop more effective, simpler and quicker ways to enable everyone to acquire the necessary BLS skills. Individualized self-training by lay persons is being revived. Although airway control and direct mouth-to-mouth ventilation skills are difficult to acquire, they must continue to be taught to the lay public and health professionals, primarily for use on relatives and friends where infection risk is not a problem. In children and trauma victims, steps A and B alone may be lifesavers. The best way to ventilate and oxygenate during the initiation of brief external CPR-BLS should be re-evaluated. There is a great difference between animals and humans in the behavior of the airway and thorax during coma, and thus in the need for added positive pressure ventilation. During chest compressions in humans, steps A and B are needed. Details deserve re-evaluation. The low perfusion pressures (borderline blood flows) produced by standard external CPR remain the most serious limitation of this method. In spite of extensive efforts so far, novel laboratory research to remedy this limitation is important for the development of more effective emergency artificial circulation. The results of such studies are greatly influenced by different details in animal models. Active compression-decompression (ACD) external CPR, also called 'push-pull' CPR, with a plunger-type device used by hand or a machine, and intermittent abdominal compression (IAC) external CPR are both promising modifications of standard external CPR. Both need further experimental and clinical clarification. For BLS, developing a more effective purely manual CPR-BLS method for help in rapid ROSC should be given high priority. Portable external CPR machines need improvements. They will serve for bridging ROSC-resistant cases through transport and ALS attempts, primarily by freeing the hands of health professionals for more effective sophisticated ALS measures.

Cardiopulmonary Resuscitation↗
PubMed1996

Future directions for resuscitation research. III. External cardiopulmonary resuscitation advanced life support.

This discussion about advanced cardiac life support (ACLS) reflects disappointment with the over 50% of out-of-hospital cardiopulmonary resuscitation (CPR) attempts that fail to achieve restoration of spontaneous circulation (ROSC). Hospital discharge rates are equally poor for in-hospital CPR attempts outside special care units. Early bystander CPR and early defibrillation (manual, semi-automatic or automatic) are the most effective methods for achieving ROSC from ventricular fibrillation (VF). Automated external defibrillation (AED), which is effective in the hands of first responders in the out-of-hospital setting, should also be used and evaluated in hospitals, inside and outside of special care units. The first countershock is most important. Biphasic waveforms seem to have advantages over monophasic ones. Tracheal intubation has obvious efficacy when the airway is threatened. Scientific documentation of specific types, doses, and timing of drug treatments (epinephrine, bicarbonate, lidocaine, bretylium) are weak. Clinical trials have failed so far to document anything statistically but a breakthrough effect. Interactions between catecholamines and buffers need further exploration. A major cause of unsuccessful attempts at ROSC is the underlying disease, which present ACLS guidelines do not consider adequately. Early thrombolysis and early coronary revascularization procedures should also be considered for selected victims of sudden cardiac death. Emergency cardiopulmonary bypass (CPB) could be a breakthrough measure, but cannot be initiated rapidly enough in the field due to technical limitations. Open-chest CPR by ambulance physicians deserves further trials. In searches for causes of VF, neurocardiology gives clues for new directions. Fibrillation and defibrillation thresholds are influenced by the peripheral sympathetic and parasympathetic nervous systems and impulses from the frontal cerebral cortex. CPR for cardiac arrest of the mother in advanced pregnancy requires modifications and outcome data. Until more recognizable critical factors for ROSC are identified, titrated sequencing of ACLS measures, based on physiologic rationale and sound judgement, rather than rigid standards, gives the best chance for achieving survival with good cerebral function.

Animals↗
PubMed1996

Future directions for resuscitation research. IV. Innovative advanced life support pharmacology.

The topics discussed in this session include a partial review of laboratory and clinical studies examining the effects of adrenergic agonists on restoration of spontaneous circulation after cardiac arrest, the effects of varying doses of epinephrine, and the effects of novel vasopressors, buffer agents (NaHCO3, THAM, 'Carbicarb') and anti-arrhythmics (lidocaine, bretylium, amiodarone) in refractory ventricular fibrillation. Novel therapeutic approaches include titrating electric countershocks against electrocardiographic power spectra and of preceding the first countershocks with single or multiple drug treatments. These approaches need to be investigated further in controlled animal and patient studies. Epidemiologic data from randomized clinical outcome studies can give clues, but cannot document pharmacologic mechanisms in the dynamically changing events during attempts to achieve restoration of spontaneous circulation from prolonged cardiac arrest. Also, rapid drug administration by the intraosseous route was compared with intratracheal and intravenous (i.v.) drug administration. Many studies on the above treatments have yielded conflicting results because of differences between healthy hearts of animals and sick hearts of patients, differences in arrest (no-flow) times and cardiopulmonary resuscitation (CPR) (low-flow) times, different pharmacokinetics, different dose/response requirements, and different timing of drug administration during low-flow CPR versus during spontaneous circulation. The need to stabilize normotension and prevent rearrest by titrated novel drug administration, once spontaneous circulation has been restored, requires research. Most of the above topics require some re-evaluation in clinically realistic animal models and in cardiac arrest patients, especially by titration of old and new drug treatments against variables that can be monitored continuously during resuscitation.

Adrenergic Agonists↗
PubMed1996

Sodium bicarbonate in cardiac arrest: a reappraisal.

The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.

Acid-Base Equilibrium↗
PubMed1996

Improved cerebral resuscitation from cardiac arrest in dogs with mild hypothermia plus blood flow promotion.

BACKGROUND AND PURPOSE: In past studies, cerebral outcome after normothermic cardiac arrest of 10 or 12.5 minutes in dogs was improved but not normalized by resuscitative (postarrest) treatment with either mild hypothermia or hypertension plus hemodilution. We hypothesized that a multifaceted combination treatment would achieve complete cerebral recovery. METHODS: With our established dog outcome model, normothermic ventricular fibrillation of 11 minutes (without blood flow) was followed by controlled reperfusion (with brief normothermic cardiopulmonary bypass simulating low flow and low PaO2 of external cardiopulmonary resuscitation) and defibrillation at < 2 minutes. Controlled ventilation was provided to 20 hours and intensive care to 96 hours. Control group 1 (n = 8) was kept normothermic (37.5 degrees C), normotensive, and hypocapnic throughout. Experimental group 2 (n = 8) received mild resuscitative hypothermia (34 degrees C) from about 10 minutes to 12 hours (by external and peritoneal cooling) plus cerebral blood flow promotion with induced moderate hypertension, mild hemodilution, and normocapnia. RESULTS: All 16 dogs in the protocol survived. At 96 hours, all 8 dogs in control group 1 achieved overall performance categories 3 (severe disability) or 4 (coma). In group 2, 6 of 8 dogs achieved overall performance category 1 (normal); 1 dog achieved category 2 (moderate disability), and 1 dog achieved category 3 (P < .001). Final neurological deficit scores (0% [normal] to 100% [brain death]) at 96 hours were 38 +/- 10% (22% to 45%) in group 1 versus 8 +/- 9% (0% to 27%) in group 2 (P < .001). Total brain histopathologic damage scores were 138 +/- 22 (110 to 176) in group 1 versus 43 +/- 9 (32 to 56) in group 2 (P < .001). Regional scores showed similar group differences. CONCLUSIONS: After normothermic cardiac arrest of 11 minutes in dogs, resuscitative mild hypothermia plus cerebral blood flow promotion can achieve functional recovery with the least histological brain damage yet observed with the same model and comparable insults.

Animals↗
PubMed1985

Cerebral preservation during cardiopulmonary resuscitation.

Thirty-two dogs subjected to 4 min of ventricular fibrillation were equally divided into four treatment groups: (a) immediate defibrillation (control); or 30 min of (b) standard CPR (SCPR), (c) simultaneous ventilation-compression CPR (SVC-CPR), or (d) open-chest CPR (OCCPR). After 30 min of CPR, restoration of spontaneous circulation was attempted using drug therapy and countershocks and the animals maintained for 24 h or until refractory hypotension occurred. During CPR, OCCPR yielded higher mean arterial and lower central venous pressures than either external method. Circulation was restored in all control dogs, and by 24 h they had nearly normal neurologic deficit scores. In the SCPR group, the heart was restarted in six dogs. Five of these dogs had severe neurologic damage and did not survive 24 h. The animal that survived 24 h, however, was nearly normal neurologically. Although circulation was restored in five SVC-CPR dogs, all were brain-dead and none survived 24 h. In the OCCPR group, seven animals survived 24 h and their neurologic deficit scores were not significantly different from control values. We conclude that OCCPR is greatly superior to SCPR and SVC-CPR with respect to preservation of the brain during resuscitation.

Animals↗
PubMed1984

Manual open-chest cardiopulmonary resuscitation.

Although the mechanistic differences between standard external cardiopulmonary resuscitation (SCPR) and open-chest CPR (OCCPR) are clear, it remains unclear when OCCPR offers a benefit over SCPR for nontraumatic cardiac arrest. Experimentally OCCPR has been shown to generate much higher arterial and much lower venous pressures, resulting in increased perfusion pressures across both heart and brain. Most studies have shown increased blood flow with OCCPR. Mechanical OCCPR has been shown to sustain electroencephalographic activity for up to one hour after up to four minutes of arrest. It has been shown in several studies that cardiac resuscitability is greater with OCCPR than with SCPR. Cerebral blood flow approaches normal with OCCPR; the best reported for SCPR is 50% of normal. After four minutes of cardiac arrest, OCCPR for 30 minutes does not yield a neurological deficit significantly different from immediate defibrillation; all animals studied returned to nearly normal by 24 hours postresuscitation. After the same arrest time, nearly all animals receiving either SCPR or simultaneous ventilation-compression CPR for 30 minutes were dead by 24 hours. Clinically early series reported up to 28% survivorship (patients discharged home) after OCCPR. Survivors after up to 2.5 hours of OCCPR and after successful restoration of spontaneous circulation by OCCPR after failure of SCPR for 75 minutes have been reported. Reported incidences of wound infection and iatrogenic cardiac injury range from 0 to 9.1% and 0 to 1.4%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Cerebral and hemodynamic variables during cough-induced CPR in dogs.

To assess the potential of self administered, cough-induced cardiopulmonary resuscitation (CICPR) to sustain cerebral function during sudden onset ventricular fibrillation (VF), the authors studied four groups of six dogs each. Cough was simulated by: spontaneous gasping (group 1); cough elicited by bilateral electrical stimulation of the vagi (group 2); gasping with artificial glottic closure (group 3); and as a control, apnea under paralysis (group 4). Sudden onset of VF during apnea (group 4) resulted in cessation of arterial blood flow in 11 +/- 3 sec (mean +/- SD) and an isoelectric EEG in 26 +/- 5 sec. Spontaneous gasping (group 1) and cough resulting from vagal stimulation (group 2) resulted in minimal systemic and cerebral perfusion pressures and common carotid artery blood flows (CCABF). CCABF became 0 in group 1 at 31 +/- 12 sec, and in group 2 at 33 +/- 16 sec after the onset of VF. EEG silence occurred at 57 +/- 9 sec and 54 +/- 19 sec in groups 1 and 2, respectively. The decay of vital parameters was delayed further when spontaneous gasping via tracheal tube was against artificial glottic closure, which augments airway pressure fluctuations (group 3); pulselessness occurred at 52 +/- 28 sec and EEG silence at 66 +/- 27 sec. Self-induced fluctuations of intrathoracic pressure generated sufficient blood flow to briefly but statistically significantly (p less than 0.001) prolong EEG activity compared to apneic controls. In this dog preparation, gasping with artificial glottic closure sustained cerebral electrical activity for a maximum of 112 sec. CICPR may offer a means of briefly sustaining consciousness after the sudden onset of VF and, thus, constitutes self-administered CPR.

Animals↗
PubMed1980

A comparison of standard, "MAST"-augmented, and open-chest CPR in dogs. A preliminary investigation.

Hemodynamic, respiratory, and cerebral variables during 2 h of standard external CPR were studied in 5 dogs. In an additional 12 dogs, possible augmentation of these variables by Military Anti-Shock Trousers (MAST) was evaluated. In 9 dogs, external and internal cardiac massage were compared. During ventricular fibrillation (VF) and after 2 min of circulatory arrest, standard CPR basic life support (without drug support) could sustain only borderline values: systolic arterial pressure (SAP) remained at 70--80 mm Hg and mean arterial pressure (MAP) at 35--45 mm Hg. Sternal compressions increased central venous pressure (CVP) to near SAP, and also increased intracranial pressure (ICP), but less than CVP. Thus, systemic perfusion pressures (SPP, i.e., MAP-mean CVP) control value 130 mm Hg) were only 11--15 mm Hg; and cerebral perfusion pressures (CPP, i.e., MAP-ICP) were 20--32 mm Hg during CPR. Common carotid arterial blood flow (CCABF) remained at an average of 8--20% of control values. Normalization of aerobic metabolism proved impossible (final pHa of 7.1). During external CPR, MAST inflation moderately increased MAP, SAP, SPP, and CPP; and significantly increased CCABF from 6.8 to 13.2% of prearrest control. The MAST failed to improve cerebral venous PO2, pupil signs, and EEG activity. With fixed pressure IPPV/100% O2, the MAST decreased tidal volumes and PaO2 (increased shunting); and increased PaCO2 and acidemia. Epinephrine 1 mg iv improved arterial pressures but not flows. A switch to open-chest (internal) cardiac massage (OCCM) after 2 h of external CPR significantly increased arterial and perfusion pressures (decreased venous pressures) and more than doubled CCABF; and resulted in a return of EEG activity and pupillary constriction. Prolonged standard CPR, and to a lesser extent MAST-augmented CPR, seem unlikely to maintain adequate oxygen transport for vital organ systems viability, particularly the brain. OCCM might better sustain viability.

Animals↗