In intact chronically instrumented dogs, left ventricular dynamics were studied during cardiopulmonary resuscitation (CPR). Electromagnetic flow probes measured cardiac output and coronary blood flow, ultrasonic transducers measured cardiac dimensions, and micromanometers measured left ventricular, right ventricular, aortic, and intrathoracic pressures. The dogs were anesthetized with morphine, intubated, and fibrillated by rapid ventricular pacing. Data were obtained during manual external massage with dogs in the lateral and supine positions. Force of compression was varied from a peak intrathoracic pressure of 10 to 30 mm Hg, and compression rate was varied from 60 to 150/ min. Increasing force of compression increased stroke volume up to a peak intrathoracic pressure of approximately 20 mm Hg, beyond which stroke volume remained constant or declined. Stroke volume appeared to result primarily from direct transmission of manual compression force to the heart rather than from positive intrathoracic pressure because peak cardiac or vascular pressures or the change in these pressures were consistently two to four times greater than the corresponding intrathoracic pressures during manual compression. With increasing compression rate, stroke volume remained relatively constant, and total cardiac output increased significantly: 425 + 92 ml/min at 60/min, 643 130 ml/min at 100/min, and 975 ± 219 ml/min at 150/min (p < .05). Left ventricular dimensions decreased minimally at higher manual compression rates. In four patients undergoing CPR, systolic and diastolic arterial blood pressure increased with faster compression rates, correlating well with data obtained in the dog. Dynamic coronary blood flow in canine experiments decreased to zero or negative values during compression. Antegrade coronary flow occurred primarily during noncompression periods and seemed to be related to diastolic aortic perfusion pressure; coronary flow at a compression rate of 150/min averaged 75% of control. Therefore stroke volume and coronary blood flow in this canine preparation were maximized with manual chest compression performed with moderate force and brief duration. Increasing rate of compression increased total cardiac output while coronary blood flow was well maintained. Direct cardiac compression appeared to be the major determinant of stroke volume during manual external cardiac massage.

SUMMARY. In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r > 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P < 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar enddiastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function. (Circ Res 52: 85 -104, 1983)

The influence of chest compression rate on initial resuscitation success and 24 hr survival after prolonged manual cardiopulmonary resuscitation (CPR) was investigated in 26 morphine-anesthetized dogs (17 to 30 kg). After placement of aortic and right atrial micromanometers and induction of ventricular fibrillation, manual CPR was commenced immediately and continued for 30 min. One group of 13 dogs underwent manual CPR at a compression rate of 60/min, and the other group at a rate of 120/min. The compression durations in the two groups were not significantly different (51.7 + 1.8% at 60/min vs 51.6 + 1.9% at 120/min). No drugs other than sodium bicarbonate were administered during CPR. A maximum of three attempts was permitted to defibrillate the heart. Successfully defibrillated animals were followed for 24 hr, during which time no treatment, other than naloxone, was given to reverse the effects of morphine. Arterial blood pH, Pco2, and Po2 were not significantly different in the two groups throughout the CPR period. When compared with the compression rate of 60/min, the compression rate of 120/min produced more successfully defibrillated animals (12/13 at 120/min vs 2/13 at 60/min, p < .002) and more 24 hr survivors (8/13 at 120/min vs 2/13 at 60/min, p < .03). All 24 hr survivors were conscious and able to sit, stand, and drink normally. One 24 hr survivor in each group had difficulty walking. Improved survival with the high-rate compression technique was consistent with the significantly higher mean aortic (systolic and diastolic) and coronary perfusion pressures attained with high-rate compressions (all p < .002). Although the clinical applicability of these findings has yet to be demonstrated, they provide empirical support for the recent decision to increase the chest compression rate for manual CPR recommended by the American Heart Association, and indicate that the hemodynamic and survival benefits of faster compression rates in this experimental preparation were not dependent on covariant alterations in compression duration.

Extreme heat is the leading weather-related killer in the United States. Vulnerability to extreme heat has previously been identified and mapped in urban areas to improve heat morbidity and mortality prevention efforts. However, only limited work has examined vulnerability outside of urban locations. This study seeks to broaden the geographic context of earlier work and compute heat vulnerability across the state of Georgia, which offers diverse landscapes and populations with varying sociodemographic characteristics. Here, a modified heat vulnerability index (HVI) developed by Reid et al. is used to characterize vulnerability by county. About half of counties with the greatest heat vulnerability index scores contain the larger cities in the state (i.e., Athens, Atlanta, Augusta, Columbus, Macon, and Savannah), while the other half of high-vulnerability counties are located in more rural counties clustered in southwestern and east-central Georgia. The source of vulnerability varied between the more urban and rural high-vulnerability counties, with poverty and population of nonwhite residents driving vulnerability in the more urban counties and social isolation/population of elderly/poor health the dominant factor in the more rural counties. Additionally, the effectiveness of the HVI in identifying vulnerable populations was investigated by examining the effect of modification of the vulnerability index score with mortality during extreme heat. Except for the least vulnerable categories, the relative risk of mortality increases with increasing vulnerability. For the highest-vulnerability counties, oppressively hot days lead to a 7.7% increase in mortality.