The experimental development of modern resuscitation.
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This paper provides data about the efficacy of resuscitation before hospital admission of 139 patients with myocardial infarction. Successful resuscitation was effected in 43 (30.9 percent) patients, of whom 29 (20.9 percent) survived and were discharged from hospital. An organizational scheme is given for resuscitation measures before admission, in which the following teams participate: premedical, general first-aid ambulance team and specialized first-aid cardiological team (Mobile Coronary Care Unit, MCCU - definition of World Health Organization). The effectiveness of resuscitation depends upon the patient's age, and the presence and degree of circulatory insufficiency before clinical death. It proved possible to revive successfully patients of advanced age and with proceding mild or moderate acute circulatory insufficiency. Resuscitation was not successful in patients with preceding severe circulatory insufficiency. Blood electrolytes were studied in the post-resuscitation period. There was a statistically significant decline in plasma potassium ion concentration. Potassium salts should be introduced in the form of a polarizing mixture, especially to patients with an irregular cardiac rhythm in the post-resuscitation period. Problems of intracardiac injections of drugs, intubation, and pervenous electric pacing in patients with myocardial infarction during resuscitation are discussed. It has been concluded that the optimum form of resuscitation before admission of patients with myocardial infarction involves rendering maximal aid at the place of occurrence of the infarction.
Recent studies have shown the potential adverse effects of venous volume loading on blood flow during closed chest cardiopulmonary resuscitation (CPR). To examine the effect of arterial and venous infusions, we employed a published computer simulation of the circulation during CPR. This model uses computer simulated electrical networks to model the heart and great vessels. CPR was modeled with compressions at a rate of 80/min and a force of 80 mmHg. Fluid infusions, simulated as current pulses into the abdominal aorta and superior vena cava, were given to measure their effect on myocardial and cranial blood flow. With 600 ml/min infusions into the abdominal aorta, there was a 12% peak increase in myocardial flow and a 3.8% peak increase in cranial flow. Every 100 ml/min increase in infusion from 0 to 900 ml/min produced a 1.4 ml/min linear increase in myocardial flow and a 4.2 ml/min linear increase in cranial flow. In agreement with previous CPR model studies, simulated vasoconstriction of abdominal and lower extremity vessels resulted in increased myocardial and cranial flows. As resistance of these vessels was increased, abdominal aortic infusions resulted in greater flow augmentations. In contrast to arterial results, infusions at 600 ml/min into the vena cava resulted in a 2.2% decrease in myocardial flow and a 0.62% decrease in cranial flow. Rise and fall times for initiation and cessation of flow augmentations were equal to four compression cycles. We conclude that these findings demonstrate the theoretical benefits of rapid arterial infusions during CPR with increases in myocardial and cranial blood flow. This method may provide an early temporary adjunct to myocardial perfusion during CPR.
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Prevalence of bystander CPR and effect on outcome has been evaluated on 3053 out-of-hospital cardiac arrest (CA) events. Bystander CPR was performed in 33% of recorded cases (n = 998) by lay people in 406 cases (family members 178, other lay people 228) and by bystanding health care workers in 592 cases (nurses 86, doctors 506). Family members and lay people mainly applied CPR in younger CA victims at public places, roadside or at the working place. Sudden infant death syndrome (SIDS) and drowning are highly represented. Health care workers performed CPR mainly in older patients, at public places or at the roadside and especially in case of cardiac or respiratory origin. CA caused by trauma/exsanguination and intoxication/metabolic origin received less bystander CPR (23% resp. 22%). Cardiac arrests receiving bystander CPR are more frequently witnessed and have a shorter access time to the emergency medical service (EMS) system and shorter response time of basic life support (BLS). Advanced life support (ALS) response time is significantly longer. In witnessed arrests of cardiac origin receiving bystander CPR a significantly better late survival was observed. In non-witnessed arrests of cardiac origin early and late survival are significantly higher in patients receiving bystander CPR. In CA events where response time of ALS exceeds 8 min, the beneficial effect of bystander CPR is most significant. Furthermore no deleterious effect of bad technique or inefficient bystander CPR can be demonstrated.
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Transoesophageal echocardiography was used to investigate the haemodynamic profile achieved during active compression-decompression cardiopulmonary resuscitation in humans. The mechanism of antegrade blood flow achieved by ACD-CPR is consistent with the cardiac pump theory. Improved right heart compression, antegrade blood flow patterns and left ventricular filling were observed in some patients during ACD-CPR.
The effects of adding active compression-decompression and abdominal binding separately or combined to standard compression CPR was tested in a randomized cross-over design during ventricular fibrillation in eight pigs. The flow and pressure effects of the two techniques appeared to be additive with no interference between the two. Carotid blood flow increased 22% with active compression-decompression, 34% with abdominal binding and 59% with the combination compared to flow with standard compression. Peak antegrade carotid flow occurred in early systole with retrograde flow in early diastole and close to zero in late diastole with no profound alterations induced by active decompression or abdominal binding. Abdominal binding increased the intrathoracic pressure during the compression phase as estimated from the esophageal pressure, while active decompression caused a negative esophageal pressure during the decompression phase. Neither active decompression nor abdominal binding caused any changes in the coronary perfusion pressure, nor in the left ventricular transmural pressure except for a rise in mid-diastolic pressure with active decompression.
OBJECTIVES: This study was designed to test the hypothesis that active compression-decompression cardiopulmonary resuscitation increases transmitral flow and end-decompression left ventricular volume over levels achieved with standard manual cardiopulmonary resuscitation. BACKGROUND: Recently, cardiopulmonary resuscitation incorporating active compression and decompression of the chest has been demonstrated to improve hemodynamic status in a canine model and in humans after cardiac arrest. METHODS: The active compression-decompression device was applied midsternum in five consecutive patients and results compared sequentially (in random order) with those of standard manual cardiopulmonary resuscitation. Both techniques were performed at 80 compressions/min with a 1.5- to 2-in. (3.8 to 5.1 cm) compression depth and a 50% duty cycle. Transesophageal echocardiographic data obtained in each patient included the velocity-time integral of transmitral pulsed Doppler recordings and two-dimensional images of the left ventricle in the long-axis view. Planimetric volume measurements of the left ventricle were obtained at both end-compression and end-decompression. RESULTS: No difference was observed in end-compression volume between the two techniques (p = 0.81). Increased end-decompression volume (active compression-decompression technique 81.3 +/- 12.5 vs. standard technique 69.4 +/- 10.8, p < 0.05), stroke volume (active compression-decompression technique 32.6 +/- 6.8 vs. standard technique 17.6 +/- 5.2, p < 0.05) and velocity-time integral of transmitral flow (active compression-decompression technique 15.8 +/- 4.3 vs. standard technique 7.8 +/- 2.3, p < 0.05) were found in the active compression-decompression group. The transmitral velocity-time integral was highly correlated with left ventricular stroke volume (r = 0.90). CONCLUSIONS: Improved transmitral flow, end-decompression left ventricular volume and stroke volume are seen with active compression-decompression resuscitation, suggesting a biphasic cardiothoracic cycle of flow. Active decompression of the chest appears to be a beneficial adjunct to standard cardiopulmonary resuscitation.
Previous studies have shown that pulmonary edema occurs in half of all pre-hospital cardiac arrest victims who cannot be successfully resuscitated and is a major cause of hypoxemia and poor lung compliance during resuscitation. Pulmonary vascular hypertension and elevation of pulmonary capillary wedge pressure have been observed during cardiac resuscitation in humans. To further define the time course of the pulmonary hemodynamic changes, pulmonary artery diastolic pressure (PAd) was measured on a computerized trend recorder prior to, during, and immediately after arrest in three adult patients. Prior to arrest, PADP was 20.9 +/- 3.1 mm Hg. The PADP rose in all three patients by an average of 30.6% after 5-10 minutes and 71.3% after 10-15 minutes of CPR. Peak PADP reached 35.8 +/- 5.1 mm Hg (difference from pre-arrest level significant, P less than 0.001). In both patients who were resuscitated successfully, the PADP returned to baseline within 5 minutes of effective spontaneous circulation. The finding that such hemodynamic changes occur rapidly during resuscitation and can reverse quickly with resumption of effective spontaneous circulation is consistent with the time course for the early development of pulmonary edema. Development of pulmonary edema many hours following successful resuscitation likely involves other mechanisms.
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There continues to be a debate on the indications for and value of the emergency department thoracotomy, especially with regard to the subject of thoracotomy performed by the emergency physician. The current literature does not deal specifically with thoracotomies performed in the emergency department by an emergency physician on trauma patients. This article describes a technique for emergency department thoracotomy that can be performed by an emergency physician.
Previous research at the Division of Air Medical Services at East Carolina University School of Medicine has demonstrated impairment of chest compression efficacy in the setting of an airborne BO-105 helicopter. This study was undertaken to determine whether in-flight compression efficacy could be improved with utilization of a pressure-sensing monitor providing real-time feedback during cardiopulmonary resuscitation (CPR). Ten flight nurses each performed two minutes of in-flight chest compressions on a mannequin that electronically assessed compression depth and hand placement. The session was then repeated using the pressure-sensing device. The mean proportion of correct compressions (95.7 +/- 3.2%) achieved with utilization of the pressure-sensing monitor was significantly higher (P < .01) than the corresponding proportion for the control group (33.4 +/- 12.1%). This study demonstrated that the difficulties of performing effective in-flight chest compressions are largely overcome with utilization of a pressure-sensing device providing real-time feedback on compression efficacy.
To determine the optimal method of applying abdominal compressions during cardiopulmonary resuscitation (CPR), 3 levels of pressure (25, 50, and 100 torr) were applied to the abdomen a) continuously and b) as 500 msec pulses at 10 different phases during the CPR cycle in 8 anesthetized dogs. Thoracic aortic (Ao) and right atrial (RA) pressures were measured and PAo-PRA was calculated as the coronary perfusion gradient. A pneumatic piston device provided external chest compression (60/min, 120 lbs, for 50% of the cycle) and ventilation (80% O2, 12/min, at 20cm, H2O). Another identical device provided abdominal compression (AC) via an air-filled bladder. High-pressure (100 torr) AC applied for 500 msec commencing 200 msec prior to chest compression demonstrated the best overall profile, raising mean aortic pressure 26 torr (P less than 0.001) and peak coronary perfusion gradient pressure 17 torr (P less than 0.02) from control values during standard CPR of 58 and 41 torr, respectively. We conclude that applying high-pressure, 500-msec pulses of AC 200 msec before chest compressions significantly improves CPR hemodynamics.
The current AHA-ECC guidelines for basic life support focus on the provision of good chest compressions with minimal interruptions for patients with presumed out-of-hospital cardiac arrest. Moreover, international consensus guidelines now support the use of chest compression-only cardiopulmonary resuscitation (CPR) instructions for dispatcher-assisted CPR given over the phone to untrained bystanders. However, evidence that strongly challenge these recommendations have been overlooked. A review of this evidence argues for the need for head rotation (a hands-free method of airway control) and abdominal compressions during bystander CPR.
Survival rates from out-of-hospital cardiac arrest continue to be low despite periodic updates in the Guidelines for Emergency Medical Services and periodic improvements such as the addition of automatic external defibrillators (AEDs). The low incidence of bystander cardiopulmonary resuscitation (CPR), substantial time without chest compressions throughout the resuscitation effort, and a lack of response to initial defibrillation after prolonged ventricular fibrillation contribute to these unacceptably poor results. Resuscitation guidelines are only revised every 5 to 7 years and can be difficult to change because of the lack of randomized controlled trials in humans. Such trials are rare because of a number of logistical difficulties, including the problem of obtaining informed consent. An alternative approach to advancing resuscitation science is for evidence-based demonstration projects in areas that have adequate records, so that one may determine whether the new approach improves survival. This is reasonable because the current guidelines make provisions for deviations under certain local circumstances or as directed by the emergency medical services medical director. A wealth of experimental evidence indicates that interruption of chest compressions for any reason in patients with cardiac arrest is deleterious. Accordingly, a new approach to out-of-hospital cardiac arrest called cardiocerebral resuscitation (CCR) was developed that places more emphasis on chest compressions for witnessed cardiac arrest in adults and de-emphasizes ventilation. There is also emphasis on chest compressions before defibrillation in circulatory phase of cardiac arrest. CCR was initiated in Tucson, Arizona, in November 2003, and in two rural Wisconsin counties in early 2004.