Facts and fears regarding blood transfusions in decision making for thrombolytic therapy.
Explore the source record for details and available documents.
Acquired Immunodeficiency Syndrome↗
Biomedical subjects
A D Guerci
Publications and source records attributed to A D Guerci.
Sternal force-displacement relationship during cardiopulmonary resuscitation.
A viscoelastic model is presented to describe the dynamic response of the human chest to cyclic loading during manual cardiopulmonary resuscitation (CPR). Sternal force and displacement were measured during 16 clinical resuscitation attempts and during compressions on five CPR training manikins. The model was developed to describe the clinical data and consists of the parallel combination of a spring and dashpot. The human chests' elastic and damping properties were both augmented with increasing displacement. The manikins' elastic properties were stiffer and both elastic and damping properties were less dependent on displacement than the humans'.
Biomechanical Phenomena↗
The potential utility of a rapid CK-MB assay in evaluating emergency department patients with possible myocardial infarction.
STUDY OBJECTIVES: To determine the sensitivity, specificity, and predictive values of a new rapid creatine kinase-MB (R-CK-MB) assay compared with a standard CK-MB (S-CK-MB) assay and to determine its potential use in the evaluation of emergency department patients with possible myocardial infarction. DESIGN: Retrospective patient identification with subsequent testing of excess sera for CK-MB and total CK using an identity-unlinked procedure. SETTING: Large, urban, teaching hospital ED. PARTICIPANTS: All adult patients with excess sera and one of several defined presentations chosen to identify those with possible myocardial ischemia or infarction. Patients with clearly documented noncardiac etiologies of their symptoms or signs were excluded. MAIN RESULTS: The sensitivity, specificity, and positive and negative predictive values of 271 patient specimens for the R-CK-MB assay compared with the S-CK-MB assay were 100%, 96.8%, 75.0%, and 100%, respectively. The R-CK-MB assay was positive for 32 patients (11.8%). Of these, eight (25.0%) were admitted to unmonitored beds, and five (15.6%) were discharged home. All of these 13 patients had initial ECGs without evidence of ischemia or infarction. On follow-up, at least eight of the 13 had evidence of infarction. CONCLUSION: The R-CK-MB assay demonstrated high sensitivity and specificity compared with the S-CK-MB assay. When used for patients in whom a cardiac care unit admission is not considered, the rapid assay may identify some patients with unsuspected myocardial infarction and prevent inadvertent discharge or admission to unmonitored beds.
Adult↗
Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation.
Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.
Animals↗
Vital organ perfusion during assisted circulation by manipulation of intrathoracic pressure.
BACKGROUND: We have previously shown, in dogs with severe cardiac depression, that modest cyclic increases in intrathoracic pressure, starting synchronously with left ventricular isovolumic contraction, significantly increase aortic flow and pressure. However, little is known of changes in vital organ perfusion during this technique of assisted circulation. METHODS AND RESULTS: We studied regional organ flow using radioactive labeled microspheres in 13 20-25-kg mongrel dogs. In the control group, after chemical induction of cardiac depression with verapamil and propranolol, coronary flow fell from 129.1 +/- 14.4 to 51.6 +/- 11.3 ml/100 g/min (p less than 0.005) and continued to decline over a 14-minute time period (flow was 32.2 +/- 11.5 ml/100 g/min at 7 minutes and 20.7 +/- 9.5 ml/100 g/min at 14 minutes [n = 6]; all p less than 0.05). In the intervention group, regional blood flow was evaluated before and after the induction of cardiac depression and also during assisted circulation using 400-msec, 20-25-mm Hg intrathoracic pressure increases delivered by a circumthoracic pneumatic vest, starting synchronously with left ventricular isovolumic contraction. In the intervention group, coronary flow fell from 119 +/- 26.7 to 47.9 +/- 13.1 ml/100 g/min 1 minute after the induction of cardiac depression (p less than 0.005). With the initiation of assisted circulation, coronary flow increased to 55.8 +/- 19.2 ml/100 g/min at 7 minutes and fell to 23.1 +/- 15.9 ml/100 g/min on termination of assisted circulation at 14 minutes (p less than 0.05 and p = NS versus control group flows at 1 and 14 minutes, respectively). During assisted circulation, cerebral, renal, and small intestinal flows also increased (all p less than 0.05 versus flows during myocardial depression). No significant increase in hepatic flow was observed. CONCLUSIONS: In the canine model, manipulation of intrathoracic pressure appears to be an effective, short-term, noninvasive means of not only increasing aortic pressure but also increasing vital organ perfusion during cardiogenic shock. Further studies are needed to assess the usefulness of this technique of assisted circulation in humans.
Animals↗
Thrombolytic therapy: state of the art.
Explore the source record for details and available documents.
Aged↗
Preservation of ventricular function by treatment of ventricular fibrillation with phenylephrine.
Epinephrine promotes resuscitation from ventricular fibrillation because of its peripheral vasoconstrictive effects. However, the beta-adrenergic effects of epinephrine may be detrimental because of the stimulation of myocardial oxygen demand. To test whether functional recovery from fibrillation in hearts treated with a selective alpha-adrenergic agent is greater than in hearts treated with epinephrine, ventricular fibrillation was induced in eight isolated dog hearts while coronary perfusion pressure was maintained at 30 mm Hg. In random order, epinephrine (5 micrograms/min), phenylephrine (50 micrograms/min) or no drug was infused for 5 min. The heart was then defibrillated, the drug infusion stopped and coronary perfusion pressure increased to 100 mm Hg. Coronary blood flow (ml/min per 100 g), arteriovenous oxygen difference (ml O2/dl) and myocardial oxygen consumption (ml O2/min per 100 g) measured after 4 min of ventricular fibrillation were greater with epinephrine (mean +/- SD 30.9 +/- 11.7, 17.5 +/- 1.6 and 5.4 +/- 1.9, respectively) than with phenylephrine (24.4 +/- 6.0, 15.7 +/- 2.6 and 3.8 +/- 1.1, respectively) or no drug (19.8 +/- 5.2, 12.8 +/- 1.8 and 2.6 +/- 0.7, respectively) (p less than 0.05, p less than 0.05 and p less than 0.05, respectively). The slope of the end-systolic pressure-volume relation 10 min after defibrillation and restoration of normal coronary perfusion pressure was depressed (percent of prefibrillation value) most by epinephrine infusion (72 +/- 17%, n = 6), less by no drug infusion (82 +/- 12%, n = 4) and was increased after phenylephrine infusion (143 +/- 17%, n = 6) (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Observations of hemodynamics during human cardiopulmonary resuscitation.
To evaluate hemodynamics during human CPR, 32 patients with witnessed cardiac arrest were studied during manual and mechanical conventional CPR. In eight patients during manual conventional CPR, peak systolic radial artery, right atrial (RAP), and pulmonary artery pressures were found to be similar (59.8 +/- 4.3, 70.8 +/- 4.7, 71.2 +/- 8.2 mm Hg) and higher than external jugular venous pressure (33.8 +/- 1.9 mm Hg, p less than .0001). The diastolic radial artery to RAP gradient was found to be only 10.7 +/- 2.1 mm Hg. In four patients, maneuvers that avoid chest compression and thus obviate cardiac compression, i.e., rhythmic compression of the abdomen, yielded arterial pressures comparable to those generated by conventional CPR (48 +/- 6.4 vs. 52.8 +/- 3.4 mm Hg, NS). In 13 other patients during mechanical conventional CPR at constant chest compression force, radial artery pressure was higher during the first compression after ventilation as compared with subsequent chest compressions (67.5 +/- 5.0 vs. 61.9 +/- 4.8 mm Hg, p less than .007). These hemodynamic observations are similar to those reported in large dogs during CPR and support the generation of vascular pressures during CPR by an increase in intrathoracic pressure. They also suggest that despite anatomic differences, the similarity of hemodynamics in dogs and humans justifies the use of large dogs as a human model during acute resuscitation studies.
Arm↗
Manipulation of external pressure as a method to assist the failing heart.
The development and state of the art in circulatory assistance using external pressure variations is reviewed. All of these techniques use the principle that by cyclic external pressure waves properly timed to the cardiac cycle, hemodynamic energy can be noninvasively transmitted to assist the circulation. Cyclic pressure waves to the lower body require that the high pressure phase occurs in diastole in order to augment cardiac output or coronary flow. In contrast, pressure waves to the chest would optimally augment cardiac output if they begin at the onset of ventricular systole. Manipulation of lung pressure by synchronized ventilation may be also utilized to augment cardiac output. The above methods are discussed in detail in the manuscript with special emphasis on the pathophysiology and mechanisms of cardiac assistance.
Animals↗
Identification of dynamic mechanical parameters of the human chest during manual cardiopulmonary resuscitation.
Survival from cardiac arrest is dependent on timely cardiopulmonary resuscitation (CPR). Since CPR is often unsuccessful, the outcome may be improved by a better understanding of the relationship between force applied to the sternum and the resulting hemodynamic effects. The first step in this complex chain of interactions is the mechanical response of the chest wall to cyclical compression. We formulated a dynamic mechanical model of the chest response and developed a method of identification of the model parameters based on force, displacement, and acceleration data acquired during cyclical compressions. The elasticity, damping, and equivalent mass of the human chest were estimated with a constrained nonlinear least-mean-square identification technique. The method was validated on data acquired from a test apparatus built for this purpose. The model fit was measured with the normalized chi-square statistic on residuals obtained between recorded force and force predicted by the model. In the analysis of one human chest, the elasticity was found to be nonlinear and statistically different during compression and release. A considerable amount of damping was found, with no significant difference between compression and release. The equivalent mass was too small to be determined accurately. This method can be used to obtain the dynamic mechanical parameters of the human chest and may lead to a better understanding of CPR.
Biomechanical Phenomena↗
Vasoconstrictors during CPR. Are they used optimally?
Explore the source record for details and available documents.
Epinephrine↗
Thrombolytic therapy for myocardial infarction.
Thrombolytic therapy has provided a practical means of reducing infarct size and infarct-related mortality. Clinicians must weigh the apparent risks and benefits of thrombolytic therapy: if the ischemic region is large, if treatment can be applied early enough to salvage ischemic myocardium, and if there is no obvious risk of life-threatening hemorrhage, it is likely the patient will benefit from thrombolytic therapy.
Aged↗
Clinical management of acute myocardial infarction.
There is increasing evidence that angiography and revascularization soon after thrombolytic therapy offer no benefit over expectant medical therapy. Rather, intervention should be held in reserve for those patients in whom ischemia recurs. The hospital management of acute myocardial infarction, beginning when the patient is admitted to the coronary care unit, is discussed.
Angioplasty, Balloon↗
TIMI II and the role of angioplasty in acute myocardial infarction.
Explore the source record for details and available documents.
Angioplasty, Balloon↗
Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs.
Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.
Animals↗
Comparison of prehospital conventional and simultaneous compression-ventilation cardiopulmonary resuscitation.
Nine hundred ninety-four patients were enrolled in a field trial in which ambulance crews were randomly assigned to use simultaneous compression-ventilation (SC-V) CPR or conventional CPR procedures in the prehospital setting. Survival to hospital admission and to discharge was superior in the conventional CPR group vs. the experimental group (p less than .01). In a subset of adult cases whose causes of arrest were nontraumatic, survivor rates still favored the conventional CPR group: 33.5% of 337 vs. 22.5% of 365 (p less than .001). In limited cases where cardiac arrest was due to other heart disease, was vascular in origin or secondary to other natural diseases or from hypertensive cardiovascular disease, or when ECG on arrival was an agonal rhythm, survival was better (but not statistically significantly) in the experimental group. There were no statistically significant differences in the Glasgow coma scores between surviving patients in either group at 24 h post-hospital admission or discharge. It is concluded that survival in the SC-V CPR group was lower, likely reflecting a deleterious effect of the experimental technique of resuscitation. Also noted was that 14% of the control patients and 6% of the experimental patients survived with manual CPR alone.
Adolescent↗
Circulatory assistance by intrathoracic pressure variations: optimization and mechanisms studied by a mathematical model in relation to experimental data.
The hemodynamic effects of phasic variations in intrathoracic pressure (ITP) timed to the cardiac cycle were predicted by a mathematical model and were compared with data from canine experimental studies. The model was used to predict the hemodynamic effects of changing the onset of the ITP rise relative to the start of cardiac systole, as well as the hemodynamic effects of changes in the duration and amplitude of the ITP rise. The predictions of the model were compared with hemodynamic data from seven anesthetized dogs. Cardiac function was depressed with large doses of verapamil and propranolol, and the hearts were atrioventricular sequentially paced at a rate of 72 beats/min. Phasic ITP variations were generated by a perithoracic vest and were electronically timed to the cardiac cycle. The model predicted, and the experimental data confirmed, that phasic intrathoracic pressure variations generated by vest inflation, timed to the cardiac cycle, can augment both peak and mean aortic flow. The following predictions of the model were also confirmed by the experimental data: 1) Maximum flow augmentation occurs when the onset of the ITP rise is simultaneous with the onset of left ventricular isovolumic contraction, and the ITP rise has a duration of 400 msec. 2) The magnitude of the flow augmentation is a function of the amplitude of the ITP rise. The experimental data showed that there was little further flow augmentation when the ITP rise was greater than 30-40 mm Hg. 3) The magnitude of flow augmentation was inversely proportional to the peak left ventricular elastance (Emax). The best fit between the measured and predicted flow augmentations was obtained for an assumed Emax of 0.5 mm Hg/ml, while Emax measurements in three dogs, using a volume conductance catheter and transient vena caval occlusion, yielded values of 0.4-1.6 mm Hg/ml. Thus, both the mathematical model and canine experiments showed that relatively low-amplitude ITP variations, rising synchronously with the onset of cardiac systole and having an optimal duration, assist the failing heart by augmentation of aortic flow. The degree of cardiac assistance decreases if the ITP variations do not rise synchronously with the onset of systole, or if their duration is not optimal. Thus, properly applied ITP variations may be used as an efficient, noninvasive method to temporarily assist the failing heart.
Animals↗