No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
Current practice and problems in resuscitation
Abstract
Cardiopulmonary resuscitation Is the progressive management of sudden cardiac arrest with the goal of restoring spontaneous circulation and preserve vital organ functions. Sudden cardiac death occurlng out of hospital Is still one of the major causes of death among otherwise healthy and young population however, approppriate management certainly Including resuscitation as the first step - might provide a reasonably good quality of life. Long term outcome of resuscitation is mainly determined by the links of the Chain of Survival, eg. early access, early CPR, early defibrillation and early advanced care. The aim of this review Is to present the up-to-date concepts for the best management of these survival links.
ResearchGate has not been able to resolve any citations for this publication.
Echocardiographic studies were conducted during CPR to establish whether blood flow through the heart was passive or whether cardiac compression accounted for forward blood flow. M-mode and two-dimensional echocardiographic studies were performed on anesthetized minipigs during external CPR and open-chest cardiac massage. With external compression, mitral valve closure was observed during compression systole and valve opening during compression diastole. The aortic valve opened during compression systole and closed during compression diastole. Identical observations were made during open-chest cardiac compression. Left ventricular area was computed during compression systole. A 24% reduction in the area of the left ventricle during precordial compression confirmed left ventricular ejection of blood. Saline tracer was injected into the right and left ventricles. Echocardiographic observation of the tracer demonstrated forward blood flow across the pulmonic and aortic outflow tracts during compression. There was minimal valvular regurgitation. These findings support the concept of cardiac compression as a mechanism for forward blood flow during open- and closed-chest CPR.
There has been controversy over whether forward blood flow during closed-chest cardiopulmonary resuscitation (CPR) is generated by a general increase in intrathoracic pressure (chest-pump theory) or by creating atrioventricular gradients that close the mitral valve and open the aortic valve during thoracic compression (cardiac pump theory). The crucial issue is the position of the mitral valve during the downstroke of chest movement. Questions remain over the actual mechanics of mitral and aortic valve function. This report describes an intraoperative cardiac arrest followed by CPR during which routinely instituted two-dimensional transoesophageal Doppler echocardiography enabled study of the motion of the valves of the left heart and the transmitral blood flow.
As exemplified in this discussion of ACLS antiarrhythmic drugs, the evidence-based evaluation process has created a high standard for the acceptance and ranking of therapies for cardiac arrest. This process also has identified critical areas needing further investigation, fostered a healthy sense of discomfort with the adequacy of our present interventions for cardiac arrest, and hopefully will continue to spur the science while sifting the dogma out of CPR.
To quantitate stroke volumes generated by precordial compression during cardiopulmonary resuscitation and to determine their relationship to coronary perfusion pressure and the success of resuscitation.
Prospective, observational animal study.
Medical research laboratory in a university-affiliated research and educational foundation.
Domestic pigs.
Ventricular fibrillation was electrically induced in 25 anesthetized male domestic pigs. After an interval of 7 mins, electrical defibrillation was attempted. Failing to reverse ventricular fibrillation in each instance, precordial compression was begun coincident with mechanical ventilation.
Stroke volumes were computed from differences between diastolic and systolic areas of the left ventricle by utilizing transesophageal echocardiography. Both stroke volumes and coronary perfusion pressure were consistently greater in successfully resuscitated animals. Progressive decreases in stroke volumes during precordial compression were predictive of unsuccessful resuscitation. A linear correlation between stroke volume and coronary perfusion pressure (r =.70) was documented.
These observations support the concept that stroke volumes generated by precordial compression are quantitatively related to the coronary perfusion pressure and to the success of cardiopulmonary resuscitation.
Shock-resistant ventricular fibrillation is defined as ventricular fibrillation persisting after three defibrillation attempts. In approximately 10 to 25% of all cardiac arrests, shock-resistant ventricular fibrillation develops, and 87 to 98% of these patients die.
In the treatment of shock-resistant ventricular fibrillation, defibrillation using biphasic waveforms is considered as an intervention of choice. Intravenous amiodarone is also acceptable, safe, and useful, based on evidence from two randomized clinical trials. Intravenous vasopressin is acceptable and probably safe and useful, but the evidence supporting this recommendation is coming from a small, randomized clinical trial. Procainamide is acceptable but not recommended. In the presence of acute myocardial infarction and recurrent ventricular fibrillation, if all other therapies fail, beta-blockers can be considered. Magnesium, lidocaine, and bretylium are not recommended in the treatment of shock-resistant ventricular fibrillation.
Biphasic defibrillation and intravenous amiodarone are useful in shock-resistant ventricular fibrillation.
In dogs, isotonic saline at 0-4 degrees C, flushed into the aorta at a rate of 1-2 L/min, with drainage of the vena cava, can achieve deep to profound hypothermia of vital organs at a cooling rate of up to 3 degrees C per minute. This achieves preservation of viability of the organism during predictable durations of no flow: cardiac arrest of 15-20 mins at Tty of 30-35 degrees C, cardiac arrest of 30 mins at Tty of 25 degrees C, cardiac arrest of 60 mins at Tty of 15 degrees C, and cardiac arrest of 90 mins at Tty of 10 degrees C. So far, pharmacologic approaches have not resulted in any breakthrough effect on outcome above that achieved with hypothermia, except perhaps the antioxidant tempol. Additional studies of novel drugs and, perhaps, combination therapies remain warranted. The optimal fluids to have in the circulation during circulatory arrest and reperfusions need to be determined. As laboratory studies to optimize suspended animation proceed, clinical trials should be initiated. In addition, devices should be developed to facilitate induction of suspended animation, eventually in the field.