Optimizing standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve.

OBJECTIVES: This study was designed to assess whether intermittent impedance of inspiratory gas exchange improves the efficiency of standard cardiopulmonary resuscitation (CPR). BACKGROUND: Standard CPR relies on the natural elastic recoil of the chest to transiently decrease intrathoracic pressures and thereby promote venous blood return to the heart. To further enhance the negative intrathoracic pressures during the "relaxation" phase of CPR, we tested the hypothesis that intermittent impedance to inspiratory gases during standard CPR increases coronary perfusion pressures and vital organ perfusion. METHODS: CPR was performed with a pneumatically driven automated device in a porcine model of ventricular fibrillation. Eight pigs were randomized to initially receive standard CPR alone, while seven pigs initially received standard CPR plus intermittent impedance to inspiratory gas exchange with a threshold valve set to -40 cm H2O. The compression:ventilation ratio was 5:1 and the compression rate was 80/min. At 7-min intervals the impedance threshold valve (ITV) was either added or removed from the ventilation circuit such that during the 28 min of CPR, each animal received two 7-min periods of CPR with the ITV and two 7-min periods without the valve. RESULTS: Vital organ blood flow was significantly higher during CPR performed with the ITV than during CPR performed without the valve. Total left ventricular blood flow (mean+/-SEM) (mL/min/g) was 0.32+/-0.04 vs 0.23+/-0.03 without the ITV (p<0.05). Cerebral blood flow (mL/min/g) was 20% higher with the ITV (+ITV, 0.23+/-0.02; -ITV, 0.19+/-0.02; p<0.05). Each time the ITV was removed, there was a statistically significant decrease in the vital organ blood flow and coronary perfusion pressure. CONCLUSIONS: Intermittent impedance to inspiratory flow of respiratory gases during standard CPR significantly improves CPR efficiency during ventricular fibrillation. These studies underscore the importance of lowering intrathoracic pressures during the relaxation phase of CPR.

Synergistic effects of vasopressin plus epinephrine during cardiopulmonary resuscitation.

Both epinephrine (Epi) and vasopressin (VP) increase coronary perfusion pressure (CPP) when administered during cardiac arrest. Given their different mechanisms of action we tested the hypothesis that during cardiopulmonary resuscitation (CPR) a combination of VP plus Epi would be superior to either agent alone. Epi(40 microg/kg), VP(0.3 U/kg) and the combination of both agents were assessed in a porcine model of ventricular fibrillation (VF). Maximum CPP (diastolic aortic-right atrial pressures) during CPR was similar among the groups but the time course of action was different in each group: with Epi + VP the increase in CPP was significantly more rapid than with VP alone whereas the CPP remained significantly higher for a longer periods of time with VP or VP + Epi versus Epi alone. Left ventricular blood flow (ml/min per g) determined during CPR two min after drug administration was similar between groups: Epi 1.06 +/- 0.16; VP 0.82 +/- 0.26; Epi + VP 0.83 +/- 0.14 (P = N.S.). Post drug administration. 2 min, cerebral blood flow (ml/min per g) in the VP group (0.76 +/- 0.15) was more than two times higher compared with Epi alone (Epi:0.30 +/- 0.08, P < 0.01 versus VP) and Epi plus VP (Epi + VP:0.23 +/- 0.03, P < 0.01 versus VP). We conclude that combination of VP + Epi during cardiac arrest results in a more rapid rise in CPP when compared with VP alone and a more sustained elevation in CPP than observed with Epi alone. Thus, the synergistic effects of these two potent vasopressor agents may be of benefit during CPR.

Improving active compression-decompression cardiopulmonary resuscitation with an inspiratory impedance valve.

BACKGROUND: Active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) has recently been demonstrated to provide significantly more blood flow to vital organs during cardiac arrest. To further enhance the effectiveness of this technique, we tested the hypothesis that intermittent impedance to inspiratory gas exchange during the decompression phase of ACD CPR enhances vital organ blood flow. METHODS AND RESULTS: ACD CPR was performed with a pneumatically driven automated compression-decompression device in a porcine model of ventricular fibrillation (VF). Nine pigs were randomized to receive ACD CPR alone, while 8 pigs received ACD CPR plus intermittent impedance to inspiratory gas exchange with a threshold valve set to 40 cm H2O. Results comparing 2 minutes of ACD CPR alone versus ACD CPR with the inspiratory impedance threshold valve (ITV) revealed significantly higher mean (+/- SEM) coronary perfusion pressures (diastolic aortic minus diastolic right atrial pressures) in the ITV (31.0 +/- 2.3 mm Hg) group versus with ACD CPR alone (21 +/- 3.6 mm Hg) (P < .05). Total left ventricular and cerebral blood flows, determined by radiolabeled microspheres, were 0.77 +/- 0.095 and 0.47 +/- 0.06 mL/min per gram, respectively, with ACD CPR plus the ITV versus 0.45 +/- 0.1 and 0.32 +/- 0.016 mL/min per gram, respectively, with ACD CPR alone (P < .05). Similar improvements in the ITV group were observed after 7 minutes of ACD CPR. After 16 minutes of VF and 13 minutes of ACD CPR, 6 of 8 pigs in the ITV group were successfully resuscitated with less than three successive 150-J shocks, whereas only 2 of 9 pigs with ACD CPR alone were resuscitated with equivalent energy levels (P < .02). With up to three additional and successive 200-J shocks, all pigs in the ITV group and 7 of 9 pigs with ACD CPR alone were resuscitated (P = .18). CONCLUSIONS: Intermittent impedance to inspiratory flow of respiratory gases during ACD CPR significantly improves coronary perfusion pressures and vital organ blood flow and lowers defibrillation energy requirements in a porcine model of VF.

Evaluation of standard and active compression-decompression CPR in an acute human model of ventricular fibrillation.

BACKGROUND: The mechanisms that underlie cardiopulmonary resuscitation (CPR) in humans remain controversial and difficult to study. This report describes a new human model to evaluate CPR during the first 1 to 2 minutes after the onset of ventricular fibrillation (VF). With this model, standard CPR was compared with active compression-decompression (ACD) CPR, a method that uses a handheld suction device to actively compress and actively decompress the chest. METHODS AND RESULTS: During routine inductions of VF as part of a transvenous lead cardioverter/defibrillator implantation procedure, CPR was performed in 21 patients if the first defibrillation shock failed and until a successful rescue shock was delivered. Compressions during CPR were performed according to American Heart Association guidelines. For ACD CPR, decompression was performed with up to -30 lbs. Radial arterial and right atrial pressures were measured in all patients. Esophageal pressures, intratracheal pressures, or minute ventilation was measured in the last 13 patients. Application of both CPR techniques increased arterial and right atrial pressures. The mean coronary perfusion pressure was increased throughout the entire CPR cycle with ACD CPR (compression, 21.5 +/- 9.0 mm Hg; decompression, 21.9 +/- 8.7 mm Hg) compared with standard CPR (compression, 17.9 +/- 8.2 mm Hg; decompression, 18.5 +/- 6.9 mm Hg; P < .02 and P < .02, respectively). Ventilation per compression-decompression cycle was 97.3 +/- 65.6 mL with standard CPR and 168.4 +/- 68.6 mL with ACD CPR (n = 7, P < .001). Negative inspiratory pressure was -0.8 +/- 4.8 mm Hg with standard CPR and -11.4 +/- 6.3 mm Hg with ACD CPR (n = 6, P < .04). CONCLUSIONS: Patients undergoing multiple inductions of VF during cardioverter/defibrillator implantation with transvenous leads provide a well-controlled and reproducible model to study the mechanisms of CPR. Using this model, ACD CPR significantly increased arterial blood pressure, coronary perfusion pressure, minute ventilation, and negative inspiratory pressure compared with standard CPR.

Cellular electrophysiologic effects of dexamethasone sodium phosphate: implications for cardiac stimulation with steroid-eluting electrodes.

Impregnation of implantable cardiac pacemaker electrodes with dexamethasone sodium phosphate dexamethasone) has been associated with reduced energy requirements for both atrial and ventricular stimulation. To determine whether cardiac cellular electrophysiologic effects of dexamethasone could in part account for lower stimulation thresholds, conventional microelectrode recording and stimulation techniques were used to assess both the immediate (acute) effects of dexamethasone (10(-6) and 10(-4) M) in superfused isolated rabbit right atrial and right ventricular preparations, and chronic effects in rabbit right ventricular tissue following 2 weeks of either daily parenteral dexamethasone (5 mg/kg, plasma concentration approximately 1 to 5 x 10(-5) M) or saline placebo injections. In acute superfusion studies, dexamethasone resulted in a concentration dependent prolongation of spontaneous right atrial cycle length, but did not significantly affect right atrial transmembrane action potential characteristics or refractoriness. However, acute dexamethasone superfusion tended to increase right ventricular resting membrane potential and diminish stimulation threshold. On the other hand, compared to findings in saline-injected control rabbits, chronic dexamethasone injection had little effect on right ventricular stimulation threshold transmembrane action potential characteristics, or right ventricular refractoriness. Thus, the acute direct electrophysiologic effects of high-dose dexamethasone are compatible with the early reduction of cardiac stimulation thresholds associated with dexamethasone impregnated pacing electrodes. On the other hand, electrophysiologic findings in the presence of chronic dexamethasone exposure do not fully account for long-term reduction of stimulation energy requirements.

Electrophysiological effects of transient aortic occlusion in intact canine heart.

This study utilized sonomicrometers transmural multipolar electrodes and cardiac electrical stimulation techniques to examine the effect on myocardial electrophysiological characteristics of altering ventricular systolic mechanical properties by transient aortic occlusion. Nine anesthetized open-chest dogs were atrially paced, and timed extrastimuli were inserted during alternate drive-train sequences at right or left ventricular (RV, LV) epicardial sites to measure ventricular effective refractory period (ERP). Sonomicrometer measurements of LV systolic mechanical parameters and both RV and LV electrophysiological findings were determined prior to and during periods of transient aortic occlusion. Aortic occlusion was applied just prior to the last beat of each eight-beat atrial drive train and released immediately following the programmed ventricular extrastimulus. Aortic occlusion increased LV systolic pressure (+42 +/- 26.6 mmHg, P less than 0.01) and diminished segmental stroke shortening (0.100 +/- 0.059 mm, P less than 0.02), shortening fraction (0.086 +/- 0.048, P less than 0.001), mean velocity of stroke shortening (0.444 +/- 0.186 mm/s, P less than 0.001), and stroke work (P less than 0.001). LV epicardial and endocardial ERP were prolonged as a result of aortic occlusion (5 +/- 7.2 and 6 +/- 6.5 ms, respectively, P less than 0.05), whereas RV ERP was unchanged. Latency of premature beats at equivalent coupling intervals was unaltered. ERP prolongation correlated most strongly with reductions of segmental stroke shortening (r = 0.928, P less than 0.001), shortening fraction (r = 0.901, P less than 0.001), and mean shortening velocity (r = 0.819, P less than 0.01). Thus transient aortic occlusion prolonged LV refractoriness, and electrophysiological changes closely paralleled the severity of systolic mechanical disturbance.

Bromocriptine treatment of digitalis-induced ventricular tachyarrhythmias: studies in a canine model.

Ventricular tachyarrhythmias associated with digitalis toxicity are believed to be due, in part, to cardiac glycoside-mediated increased central sympathetic neural activity. Because dopaminergic receptor agonists reduce sympathetic outflow, this study assessed effectiveness of the available dopaminergic agonist, bromocriptine, in slowing or terminating ouabain-induced ventricular tachycardia in anesthetized dogs. In all experiments, ouabain was administered intravenously (20 micrograms/kg body weight bolus injection, followed by 2.5 micrograms/kg per min infusion) until the onset of stable ventricular tachycardia. Of seven untreated dogs (Group 1), ouabain-induced ventricular tachyarrhythmias resulted in ventricular fibrillation in three, while in four dogs tachycardia persisted without significant change in rate until the study was terminated. Fourteen dogs (Group 2) received bromocriptine, either 30 micrograms/kg (Group 2A) or 50 micrograms/kg (Group 2B), after the onset of ventricular tachycardia. Tachycardia slowed in all 14 dogs and terminated with resumption of sinus rhythm in 8 of the 14. In all six dogs pretreated with the peripheral dopaminergic antagonist domperidone (Group 3), bromocriptine, 50 micrograms/kg, slowed ventricular tachycardia and in three of the six, tachycardia terminated. In contrast, of five dogs pretreated with haloperidol, a central and peripheral dopaminergic receptor antagonist (Group 4), bromocriptine, 50 micrograms/kg, failed to slow ventricular tachycardia in three, and two of the three developed ventricular fibrillation. In summary, the dopaminergic receptor agonist, bromocriptine, presumably acting at central dopaminergic receptor sites, consistently slowed and in most cases reversed ouabain-induced ventricular tachycardia in a canine model.

Cellular electrophysiological changes in "round heart disease" of turkeys: a potential basis for dysrhythmias in myopathic ventricles.

Arrhythmias are commonly recorded in "round heart disease", a presumed viral, congestive cardiomyopathy of turkeys. To assess whether cellular electrophysiological changes may be associated with arrhythmia susceptibility, we compared transmembrane action potential characteristics in left and right ventricular endocardial muscle fibres from 19 inbred myopathic turkeys with findings in 13 normal control turkeys (age 1 to 74 days). In left ventricular tissue, as a group, action potential duration at 50% repolarisation (APD50) was reduced in myopathic hearts (201+/-6(SEM) vs 228+/-9 ms in controls. P less than 0.01), while the maximum rate of phase 0 (dV/dtmax) action potential amplitude, diastolic resting membrane potential and action potential duration at 90% repolarisation (APD90) did not differ from control turkeys. By contrast, in myopathic right ventricular tissue, as a group, both APD50 (186+/-5 vs 206+/-4 ms in controls) and APD90 (208+/-4 vs 228+/-3 ms in controls) were shorter (P less than 0.01). The plateau potential in both right and left ventricular tissue was significantly higher in inbred turkeys. Since a spectrum of cardiac dilatation and hypertrophy is present in myopathic turkeys, we examined the effect of hypertrophy on action potential characteristics. In "round heart disease" turkeys, left ventricular hypertrophy was characterised by reduced dV/dtmax (98+/- vs 274+/-26 V.s-1, P less than 0.01) and right ventricular hypertrophy by further shortening of both APD50 (174+/-7 vs 202+/-6 ms, P less than 0.01) and APD90 (193+/- vs 224+/-5 ms, P less than 0.01), but no change in dV/dtmax (105+/-13 vs 120+/-9 V.s-1, P = NS). These results indicate that certain electrophysiological differences (eg reduced action potential duration), may, in part, contribute to dysrhythmia susceptibility in this presumed viral cardiomyopathy model.