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M Noc

Publications and source records attributed to M Noc.

26 records · Page 2Linked to original sources
PubMed1994

Spontaneous gasping during cardiopulmonary resuscitation without mechanical ventilation.

Spontaneous gasping is frequently observed during cardiac arrest, especially when mechanical ventilation is withheld during precordial compression. We related spontaneous gasping to pulmonary gas exchange and cardiac resuscitability in a rodent model of cardiac arrest. Ventricular fibrillation was electrically induced in 15 Sprague-Dawley rats. After 4 min untreated ventricular fibrillation, precordial compression was initiated. Coronary perfusion pressure was maintained between 25 and 30 mm Hg. Oxygen was supplied at the tracheal tube port coincident with start of precordial compression in 10 animals. Five additional control animals were identically treated except they were mechanically ventilated coincident with start of precordial compression. After 6 min precordial compression, defibrillation was attempted and five of 10 nonventilated animals, and all control animals, were resuscitated by direct current countershock. In the successfully resuscitated, nonventilated animals, the frequency of spontaneous gasping during precordial compression progressively increased to an average of 19 gasps/min but it was < 6 gasps/min in nonresuscitated animals. More frequent gasping was associated with correspondingly greater arterial PO2 (110 versus 51 mm Hg, p < 0.01) and lesser PCO2 (55 versus 91 mm Hg, p < 0.01). In control animals, no spontaneous gasping was observed during precordial compression. Arterial PO2 and PCO2 of mechanically ventilated animals was more like that of spontaneously gasping rats. According, the frequency of spontaneous gasping in absence of mechanical ventilation is predictive of cardiac resuscitation success and associated with improved arterial oxygenation and CO2 removal.

Analysis of Variance↗
PubMed1994

Ventricular fibrillation voltage as a monitor of the effectiveness of cardiopulmonary resuscitation.

Ventricular fibrillation (VF) voltage was previously identified as a predictor of the success of cardiopulmonary resuscitation. In the present study we investigated the mechanism by which VF voltage predicts the success of cardiac resuscitation in a well-established rodent model of cardiac arrest. After 4 minutes of untreated VF, precordial compression was initiated and maintained for 6 minutes. Increases in coronary perfusion pressure during precordial compression were associated with concomitant increases in VF voltage (r = 0.61, p = 0.013). Significantly greater coronary perfusion pressure (24 vs 17 mm Hg) and VF voltage (0.17 vs 0.12 mV) were observed in resuscitated animals. To obviate electrical artifacts produced by precordial compression, boluses of oxygenated blood were injected into the ascending aorta in another 5 animals as an alternative method of cardiac resuscitation. This restored myocardial perfusion before defibrillation. Increases in VF voltage from 0.04 mV to 0.47 mV during aortic infusions were again correlated with coronary perfusion pressure (r = 0.62, p < 0.01) and predicted the success of cardiac resuscitation. Greater VF voltages after initiation of cardiac resuscitation were associated with increases in myocardial creatine phosphate, from 0.23 to 0.70 mmol/kg wet weight, and significant decreases in lactate content, from 22.8 to 13.9 mmol/kg wet weight. Increases in creatine phosphate were highly correlated with increases in VF voltage (r = 0.99, p < 0.01). Accordingly, increases in VF voltage during cardiac resuscitation reflect increases in myocardial perfusion and favorable changes in myocardial energy metabolism. As such, VF voltage, like coronary perfusion pressure, serves as a quantitative predictor of the success of cardiopulmonary resuscitation.

Action Potentials↗
PubMed1993

Correlation between QTc interval duration and left ventricular systolic dysfunction in patients with acute myocardial infarction.

QTc interval and left ventricular regional wall motion abnormality score (WMS) were assessed in 61 consecutive patients with 4-day-old acute myocardial infarction (AMI). There were 45 men and 16 women, aged 60.6 +/- 8.7 years; 24 had anterior wall AMI and 37 had inferior wall AMI. Twenty-nine patients received thrombolytic treatment, which was presumably successful in 19. The longest QTc interval from a standard 12-lead electrocardiogram, corrected by Bazett's formula, was considered for the study. The WMS was evaluated echocardiographically. The authors found a statistically significant correlation between WMS and QTc interval duration; the correlation was stronger in patients with anterior AMI (r = .9, P < .001) than in those with inferior AMI (r = .66, P < .001). The WMS and QTc values were significantly lower in patients with successful thrombolytic treatment compared to those with unsuccessful thrombolysis (P < .003 and P < .002, respectively). The authors could demonstrate no significant correlation between serum potassium concentration and the QTc interval. In patients with anterior AMI, QTc interval duration might represent an additional marker of left ventricular systolic dysfunction. It could also be used as an additional noninvasive criterion of coronary artery reperfusion in patients with AMI.

Echocardiography↗
PubMed1993

Augmented efficacy of external CPR by intermittent occlusion of the ascending aorta.

BACKGROUND: After prolonged cardiac arrest, conventional methods of closed-chest cardiac compression are ineffective. This is primarily because of failure to generate minimal threshold levels of coronary perfusion pressure for cardiac resuscitation. This report introduces a new option for cardiac resuscitation by use of a combination of intermittent ascending aortic balloon occlusion, aortic infusion, and precordial compression to increase the pressure gradient for coronary perfusion. METHODS AND RESULTS: Twenty anesthetized, mechanically ventilated, normovolemic domestic pigs were investigated. A 10F balloon catheter was advanced from the left femoral artery into the ascending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. Precordial compression was initiated after 7 minutes of untreated ventricular fibrillation. The animals were randomized to one of four groups: (1) balloon occlusion with proximal infusion of oxygenated saline, (2) balloon occlusion alone, (3) proximal aortic infusion together with epinephrine without balloon occlusion, and (4) injection of epinephrine without balloon occlusion or proximal infusion. For balloon occlusion, the balloon was inflated for 30 seconds during each minute of cardiopulmonary resuscitation. In the subsets of animals that received infusions, oxygenated saline (30 mL) was injected into the proximal aorta immediately after balloon occlusion. Epinephrine was used in two subsets: It was injected as a bolus in amounts of 30 micrograms/kg into the right atrium at 30 seconds after start of precordial compression and repeated as required to maintain coronary perfusion pressure within the range of 25 to 30 mm Hg. Defibrillation was attempted at 1 minute after start of precordial compression and at 1-minute intervals thereafter. Resuscitation attempts were continued until there was return of spontaneous circulation or for a total of 30 minutes after start of precordial compression. Coronary perfusion pressure generated by precordial compression was significantly increased after balloon occlusion. Each of 10 animals was successfully resuscitated and survived for 48 hours after balloon occlusion whether or not it was combined with infusion. Three of five animals were resuscitated by a combination of infusion and epinephrine in the absence of aortic occlusion, but none survived for 48 hours (P = .02). Only one epinephrine-treated animal was successfully resuscitated and survived for 48 hours in the absence of balloon occlusion or infusion (P < .05). CONCLUSIONS: Ascending aortic balloon occlusion with or without proximal aortic infusion strikingly increased resuscitability and 48-hour survival after cardiac arrest under conditions when conventional methods failed.

Animals↗
PubMed1993

Comparison of gastric luminal and gastric wall PCO2 during hemorrhagic shock.

Measurement of gastric wall PCO2 has emerged as a promising monitor of perfusion deficits during low-flow states of circulatory shock. In the present study, gastric luminal PCO2 measured with the gastric tonometer was compared with the PCO2, measured directly in the wall of the stomach during hemorrhagic shock in two groups of five Sprague-Dawley rats. One group was pretreated with the H2 blocker, ranitidine. During a 120-min interval of hemorrhage, tonometer PCO2 increased from 60 +/- 7 mmHg to 90 +/- 10 mmHg, and time-coincident gastric wall PCO2 from 52 +/- 5 mmHg to 131 +/- 14 mmHg. Following reinfusion of shed blood, tonometer PCO2 remained elevated for an interval exceeding 60 min, but gastric wall PCO2 returned to control levels within approximately 10 min. Ranitidine pretreatment did not alter the relationships between gastric wall PCO2 and tonometer PCO2. These observations indicate that gastric luminal PCO2 underestimates relatively rapid increases in gastric wall PCO2 during profound hemorrhagic shock in rats.

Animals↗