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Fritz Sterz

Publications and source records attributed to Fritz Sterz.

40 records · Page 3Linked to original sources

Survivors of ventricular tachyarrhythmias due to a transient or reversible disorder have a high recurrence rate of lethal cardiac events.

OBJECTIVES: The recurrence rate of lethal cardiac events after the survival of a primary cardiac arrest in patients not having received an implantable cardioverter defibrillator (ICD) is investigated. BACKGROUND: According to current guidelines, only a small percentage of patients after successful cardiopulmonary resuscitation due to an underlying cardiac problem are eligible for the implantation of an ICD. METHODS: For retrospective analysis, we used a data registry of patients admitted to an emergency department after cardiac arrest. Patients who had a primary cardiac cause for their cardiac arrest and who did not die within the first month after successful restoration of spontaneous circulation were selected. RESULTS: From 1246 patients, 360 met the inclusion criteria. A second lethal cardiac event occurred in 94 (26%). Of those 94 patients, 57 (61%) had good neurological function before their second cardiac arrest. Of the survivors with good neurological function, 47 (82%) did not have an ICD or a cardiac transplant. Another cardiac arrest due to a primary cardiac event occurred in 34 (72%) of these patients. CONCLUSIONS: Cardiac arrest survivors without an apparent indication for an ICD have a high risk of suffering from a re-arrest of cardiac origin.

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Endothelin-1 elevates regional cerebral perfusion during prolonged ventricular fibrillation cardiac arrest in pigs.

Since adrenaline (epinephrine) also has negative effects during and after cardiopulmonary resuscitation (CPR) a non-adrenergic vasoconstrictor like endothelin might be an alternative to increase vital organ blood flow. We studied the effect of different doses of endothelin-1 compared with adrenaline on the ability to resuscitate, cerebral and myocardial blood flow (MBF) in a closed chest cardiac arrest pig model. After 5 min of ventricular fibrillation, CPR with a ventilator and a mechanical compression device was started. At 10 min, 31 pigs were randomized to receive a single dose of endothelin-1 50, 100 or 200 microg or repeated doses of adrenaline 0.04 mg kg(-1) or saline every 3 min. After 25 min, the pigs were defibrillated to achieve restoration of spontaneous circulation. Blood flow was measured with the fluorescent microsphere method. In animals receiving endothelin-1 50, 100 and 200 microg the cerebral blood flow (CBF) increased from median 28 (25th; 75th quartile: 16; 40), 32 (15; 48) and 17 (4; 65) to 36 (31; 54), 47 (39; 57) and 63 (35; 83) ml min(-1) per 100 g, respectively, 6 min after drug administration (P<0.05 endothelin-1 50 microg vs. Control, P<0.01 endothelin-1 100 and 200 microg vs. Control). At the same time CBF decreased in the control and adrenaline group from 36 (21; 41) and 39 (15; 50) to 12 (2; 25) and 24 (15; 26) ml min(-1) per 100 g, respectively, (P<0.05 adrenaline vs. endothelin-1 200 microg). There was no difference in MBF between the treatment groups despite a higher coronary perfusion pressure (CoPP) in the endothelin-1 groups. Restoration of spontaneous circulation could be only achieved in the endothelin-1 50 microg (3 of 7; 43%) and 100 microg (5 of 7; 71%) group. This study suggests that endothelin-1 enhances CBF during CPR better than adrenaline and increases resuscitation success.

Animals↗

Cerebral resuscitation potentials for cardiac arrest.

Permanent brain damage after cardiac arrest and resuscitation is determined by many factors, predominantly arrest (no-flow) time, cardiopulmonary resuscitation (low-flow) time, and temperature. Research since around 1970 into cardiopulmonary-cerebral resuscitation has attempted to mitigate the postischemic-anoxic encephalopathy. These efforts' results have recently shown outcome benefits as documented in clinically relevant outcome models in dogs and in clinical trials. Pharmacologic strategies have so far yielded relatively disappointing results. In a recent exploration of 14 drugs in dogs, only the antioxidant tempol administered at the start of prolonged cardiac arrest improved functional outcome in dogs. Cerebral blood flow promotion by hypertensive reperfusion and hemodilution has resulted in improved outcome in dogs, and brief hypertension after restoration of spontaneous circulation is associated with improved outcome in patients. Postarrest hypercoagulability of blood seems to yield to therapeutic thrombolysis, which is associated with improved cerebral outcome in animals and patients. In a clinically relevant dog outcome model, mild postarrest cerebral hypothermia (34 degrees C), initiated with reperfusion and continued for 12 hrs, combined with cerebral blood-flow promotion increased from 5 to >10 mins the previously longest normothermic no-flow time that could be reversed to complete cerebral recovery. Mild hypothermia by surface cooling after prolonged cardiac arrest in patients has been found effective in recent clinical studies in Australia and Europe. Preliminary data on the recent randomized study in Europe have been reported. For presently unresuscitable cardiac arrests, research since the 1980s in dog outcome models of prolonged exsanguination cardiac arrest has culminated in brain and organism preservation during cardiac arrest (no-flow) durations of up to 90 mins, perhaps 120 mins, at a tympanic temperature of 10 degrees C and complete recovery of function and normal histology. This "suspended animation for delayed resuscitation" strategy includes use of an aortic flush of cold saline (or preservation solution) within the first 5 mins of no flow. This strategy should also be explored for the larger number of patients with unresuscitable out-of-hospital cardiac arrests. Suspended animation for prolonged preservation of viability could buy time for transport and repair during hypothermic no flow followed by resuscitation, or it could serve as a bridge to prolonged cardiopulmonary bypass.

Animals↗

Deterministic nonlinearity in ventricular fibrillation.

We provide numerical evidence that the electrocardiogram data collected from pigs during induced ventricular fibrillation cannot be described by a monotonic nonlinear transformation of linearly filtered noise. To establish this we use surrogate techniques and apply two test statistics: (1) the Takens' maximum likelihood estimator of the Grassberger-Procaccia correlation dimension and (2) an improved correlation dimension estimation routine. The improved dimension estimates provide evidence that the correlation dimension of the underlying dynamics during the episode of VF in the first 30 s is slightly less than 6. This result is consistent and reproducible among subjects. (c) 2000 American Institute of Physics.

Journal Article↗