Daniel Garner

Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Cardiopulmonary resuscitation (CPR) has been thought to produce blood flow by compression of the heart between the sternum and spine, termed “external cardiac massage,” but there has been-no direct experimental documentation of this proposed mechanism.Micromanometric pressure recordings were synchronized with cineangiograms during mechanical CPR in 17 dogs with induced ventricular fibrillation. Chest compression produced equivalent pressure increases in the aorta (Ao) and right atrium (RA) (Ao 32 + 14 mm Hg, RA 30 ± 14 mm Hg; NS), a linear relationship between aortic and intrapleural pressures (r = 0.87, p < 0.001) over a wide range of induced pressures, cineangiographic blood flow through both left-heart chambers, and a pressure gradient (21 ± 14 mm Hg) between all intrathoracic cardiovascular compartments and the jugular veins that resulted from closure of venous valves at the thoracic inlets. Simultaneous chest compression and lung inflation significantly increased all intrathoracic vascular pressures, the aortojugular venous gradient (42 ± 13 mm Hg, p < 0.05 vs chest compression alone), electromagnetically determined carotid arterial blood flow (1.75 ± 0.81 ml/min/kg vs 0.51 ± 0.27 mI/min/kg during chest compression alone, p < 0.005), and angiographic left-heart flow.We conclude that blood flow during CPR results principally from an increased intrathoracic pressure and that there is selective flow to the brachiocephalic vascular bed because of the arteriovepous gradient produced by venous valves at the thoracic inlets. Greater intrathoracic pressure resulting from simultaneous inflation and compression improves left-heart flow. The left heart is therefore a conduit, not a pump, during CPR.

Endocardial and transcutaneous cardiac pacing, calcium chloride, and epinephrine in postcountershock asystole and bradycardias

Clinically, asystole or a bradyarrhythmia may follow countershock of ventricular fibrillation (VF) in up to 40% of attempts. This study evaluated the effects of artificial cardiac pacing, calcium chloride (CaCl2), and epinephrine in postcountershock asystole/bradycardia. Micromanometer catheters were positioned in the aorta (Ao) and right atrium (RA) of ten dogs and VF induced by right ventricular (RV) stimulation. After 2 min of VF, a 400-J countershock was given. In six animals, asystole or a pulseless bradyarrhythmia followed one countershock. In four animals, up to three countershocks were needed to terminate VF and resulted in asystole or a pulseless bradyarrhythmia. Thirty seconds after termination of VF, cardiac pacing was begun in all animals using conventional RV endocardial pacing (RVEP) or a transcutaneous transthoracic pacing (TTP) technique. RVEP and TTP produced ventricular depolarizations, but electrical capture was never associated with Ao pressure fluctuations. After 2 min of pacing, CaCI2 was given and chest compressions and artificial ventilations (CPR) initiated. CaCl2 had no effect on CPR pressures. After 2 min of CPR, RVEP and TTP were again studied; capture without Ao pressure fluctuations was seen in all animals. Epinephrine was then given and CPR reinstituted. Epinephrine produced a significant increase in CPR Ao systolic pressure (58 ± 13 to 84 ± 24 mm Hg, p < .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 ± 4 to 34 ± 8 mm Hg, p < .001). Within 94 ± 53 sec after epinephrine, spontaneous circulation was restored in eight animals. Of the remaining two animals, one succumbed to a pulseless bradyarrhythmia after one countershock and the other to asystole after multiple countershocks for recurrent VF. Electron microscopic changes in myocardial sections were largely consistent with the duration of ischemia, and there was no intracellular calcium accumulation. Dehiscence of the myocardial intercalated discs was seen in the animal that received multiple countershocks. It is concluded that: (a) pacing in postcountershock asystole/bradycardia may produce electrical capture but not effective cardiac contraction, (b) CaCl2 is of limited value in asystole/bradycardia after countershock and does not facilitate electrical-mechanical coupling during pacing, (c) epinephrine is effective in the management of postcountershock asystole/bradycardia, and (d) asystole after multiple countershocks may be of structural origin and not amenable to therapy.

Monophasic versus biphasic transthoracic countershock after prolonged ventricular fibrillation in a swine model

OBJECTIVE We sought to compare the defibrillation efficacy of a low-energy biphasic truncated exponential (BTE) waveform and a conventional higher-energy monophasic truncated exponential (MTE) waveform after prolonged ventricular fibrillation (VF). BACKGROUND Low energy biphasic countershocks have been shown to be effective after brief episodes of VF (15 to 30 s) and to produce few postshock electrocardiogram abnormalities. METHODS Swine were randomized to MTE (n = 18) or BTE (n = 20) after 5 min of VF. The first MTE shock dose was 200 J, and first BTE dose 150 J. If required, up to two additional shocks were administered (300, 360 J MTE; 150, 150 J BTE). If VF persisted manual cardiopulmonary resuscitation (CPR) was begun, and shocks were administered until VF was terminated. Successful defibrillation was defined as termination of VF regardless of postshock rhythm. If countershock terminated VF but was followed by a nonperfusing rhythm, CPR was performed until a perfusing rhythm developed. Arterial pressure, left ventricular (LV) pressure, first derivative of LV pressure and cardiac output were measured at intervals for 60 min postresuscitation. RESULTS The odds ratio of first-shock success with BTE versus MTE was 0.67 (p = 0.55). The rate of termination of VF with the second or third shocks was similar between groups, as was the incidence of postshock pulseless electrical activity (15/18 MTE, 18/20 BTE) and CPR time for those animals that were resuscitated. Hemodynamic variables were not significantly different between groups at 15, 30 and 60 min after resuscitation. CONCLUSIONS Monophasic and biphasic waveforms were equally effective in terminating prolonged VF with the first shock, and there was no apparent clinical disadvantage of subsequent low-energy biphasic shocks compared with progressive energy monophasic shocks. Lower-energy shocks were not associated with less postresuscitation myocardial dysfunction.

Milrinone Facilitates Resuscitation From Cardiac Arrest and Attenuates Postresuscitation Myocardial Dysfunction

Background—Left ventricular (LV) dysfunction with a low cardiac index after successful CPR contributes to early death attributable to multiorgan failure, and an effective treatment has not been identified. The purpose of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor, as treatment for LV dysfunction after resuscitation. Methods and Results—Ventricular fibrillation (VF) was induced electrically in 32 swine. After 5 minutes of VF, CPR was initiated and animals were randomized to receive either saline (control group, n=16) as a bolus and infusion or milrinone 50 &mgr;g/kg as a bolus and then 0.5 &mgr;g/kg per min for 60 minutes (treatment group, n=16). After 2 minutes of CPR (total VF time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups (24±2 versus 21±4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals (P =0.018). At 30 minutes after restoration of spontaneous circulation, stroke volume (16±3 versus 26±7 mL, P <0.01) and LV dp/dt (793±197 versus 1108±316 mm Hg/s, P <0.02) were higher in the treatment group. Similar differences were observed 60 minutes after restoration of spontaneous circulation. Significant differences in heart rates between groups were not observed, and peripheral vascular resistance was significantly greater in the control group 30 and 60 minutes after resuscitation. Conclusions—Milrinone facilitates resuscitation from prolonged VF and attenuates LV dysfunction after resuscitation without worsening major determinants of myocardial oxygen demand.

Transthoracic monophasic and biphasic defibrillation in a swine model: a comparison of efficacy, ST segment changes, and postshock hemodynamics☆

OBJECTIVE Biphasic waveforms for transthoracic defibrillation (DF) have been tested extensively after brief (15 s) episodes of VF in animal models and in patients undergoing electrophysiologic testing. The purpose of this study was to compare the effects mono- and biphasic waveforms for DF on postdefibrillation ST segments and left ventricular pressure, markers of myocardial injury, after more extended periods of VF (30 and 90 s). METHODS 21 anesthetized and instrumented swine were randomized to truncated exponential monophasic or biphasic waveform DF. VF was induced electrically and 30 s later, DF with the designated waveform was attempted with a shock dose of 200 J. If unsuccessful, 300 J and then 360 J were administered if necessary. Following return to control hemodynamic values and normalization of the surface ECG, VF was again induced and, after 90 s, DF was attempted as in the 30 s VF period. CPR was not performed during VF and each animal was countershocked with only one waveform for both VF episodes. Waveforms were compared for frequency of first shock defibrillation success, surface ECG indicators of myocardial injury (ST segment changes at 10, 20, and 30 s after countershock) and time to return to pre-VF hemodynamics after successful DF, an indicator of postshock ventricular function. RESULTS Successful first shock conversion rates at 30 and 90 s were 60 and 63% for monophasic and 64 and 82% for biphasic (NS). Biphasic DF after 30 s produced ST segment changes (measured 10 s after DF) in 1/10 animals while six of eight animals in the monophasic group showed ST segment changes (P=0.013). After 90 s of VF, ST segment changes were observed in 6/8 in the monophasic group and 2/10 in the biphasic group (P=0.054). Differences in the time to hemodynamic recovery (return to control peak left ventricular pressure) were not observed between biphasic and monophasic waveforms after 30 or 90 s of VF. CONCLUSIONS Monophasic and biphasic transthoracic defibrillation are equally effective in terminating VF of 30 and 90 s duration and restoring a perfusing rhythm. The biphasic waveform produced less ECG evidence of transient myocardial injury. However, there was no difference in the rate of return to control hemodynamics. ST segment changes following countershock of VF of brief duration are transient and of questionable significance.

Functional significance of post-myocardial infarction left ventricular hypertrophy: a beneficial response.

Hypertrophy of noninfarcted myocardium occurs as a chronic response to myocardial infarction, but no previous study has related the changes in wall thickness to serial changes in left ventricular function. Thus the functional significance of postinfarction hypertrophy is unknown. The purpose of this study was to determine the relationship between the development of postinfarction hypertrophy and the resting left ventricular ejection fraction measured by two-dimensional echocardiography. After occlusion of the proximal left anterior descending coronary artery in 11 dogs, the ejection fraction fell acutely (0.63 +/- 0.08 to 0.33 +/- 0.10, p less than 0.001) and rose at 3.5 months to 0.62 +/- 0.12. End-diastolic thickness of the noninfarcted left ventricle increased (11 +/- 1.0 mm to 13 +/- 1.4 mm, p less than 0.01) as did left ventricular mass (101 +/- 18 gm to 134 +/- 21 gm, p less than 0.0001). Restoration of the ejection fraction toward the baseline value correlated with the increases in left ventricular mass (r = 0.79, p = 0.007) and wall thickness (r = 0.71, p = 0.025). Hypertrophy of the noninfarcted myocardium correlated with the magnitude and approximately paralleled the time course of the improvement in the ejection fraction and therefore may have had a beneficial effect on resting left ventricular function as a chronic adaptation to myocardial infarction.

Postcountershock pulseless rhythms: Hemodynamic effects of glucagon in a canine model

Defibillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more.Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.

Predictive value of the ECG in determining cardiac resuscitation outcome in a canine model of postcountershock electromechanical dissociation after prolonged ventricular fibrillation

The purpose of our study was to determine if the surface ECG in postcountershock electromechanical dissociation (EMD) is of value in predicting return of effective myocardial contractile function during CPR. Nine dogs were subjected to five minutes of ventricular fibrillation (VF) without CPR followed by countershock and closed-chest CPR. Intravascular pressures, coronary perfusion pressure, and coronary sinus flow were measured during conventional CPR. After countershock, and before CPR, the frequencies of the following ECG variables were assessed: the presence or absence of P waves, an abnormal QRS duration (greater than 100 ms), a prolonged QTc (greater than 430 ms), and a bradyarrhythmia (QRS rate less than 60/min). Twenty-three episodes of postcountershock EMD were studied. Countershock after prolonged VF without CPR was always followed by EMD. The mean values of ECG variables were not significantly different (P greater than .05) between animals successfully resuscitated and those that were not. The sensitivity, specificity, and predictive values of individual ECG variables in estimating successful cardiac resuscitation exhibited a wide range of values. The QTc had the highest sensitivity (1.00), but the lowest specificity (0.08). The presence or absence of P waves had the highest specificity (0.62), but a sensitivity of only 0.40. QRS rate had the greatest positive predictive value (0.48) but a negative predictive value of 0.46 for successful cardiac resuscitation. The QTc had the greatest negative predictive value (1.00) but a positive predictive value of only 0.45. Multiple regression analysis using the study ECG variables as independent variables demonstrated that ECG variables were not related to outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Technique for the Performance of Repeatable Renal Clearances in the Conscious Male Dog

A preparation for performance of renal clearances in the conscious dog is described. The important aspect of the technique is the use of a Pavlov sling and a specially designed restraining apparatus. Of most importance is the use of a 7 French Swan-Ganz balloon-tipped catheter for urinary bladder catheterization. The use of male dogs obviated the need for an episiotomy. No special training of the animals was required. The animals tolerated long-term and repeated catheterization without any evidence of infection or trauma.

Increased ejection fraction produced by a long-term subhypertensive infusion of norepinephrine in the conscious dog

Five mongrel dogs with chronically implanted catheters in the left atrium, mid-thoracic aorta, and right atrium were continuously infused with subhypertensive doses of norepinephrine for 3 months. Left ventricular cineangiography, determinations of aortic pressure, and cardiac output were performed in the conscious dog. After 3 months of continuous norepinephrine infusion, stroke volume increased from 38 +/- 3.0 to 67 +/- 8.0 ml. (p less than .01), the left ventricular end-diastolic volume increased from 72 +/- 6.4 to 89 +/- 12.9 ml. (p less than .05), and the ejection fraction increased from 52 +/- 3.6 to 76 +/- 3.6% (p less than .005). We postulate that norepinephrine results in an increased myocardial function by producing physiological myocardial hypertrophy.