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Biomedical subjects

M H Weil

Publications and source records attributed to M H Weil.

At least 37 records · Page 2Linked to original sources
PubMed2000

Low-energy biphasic waveform defibrillation reduces the severity of postresuscitation myocardial dysfunction.

Both clinical and experimental studies have demonstrated substantial impairment of ventricular function after resuscitation from cardiac arrest. Indeed, postresuscitation myocardial dysfunction has been implicated as a potentially important mechanism, accounting for fatal outcomes after successful resuscitation in 70% of victims within the first 72 hrs. Recent experimental studies implicated the total electrical energy delivered during defibrillation as an important correlate with the severity of postresuscitation myocardial dysfunction and postresuscitation survival. This prompted us to investigate the option of using lower electrical energy biphasic waveform defibrillation. We compared the effects of low-energy biphasic waveform defibrillation with conventional monophasic waveform defibrillation after a short (4 mins), intermediate (7 mins), or prolonged (10 mins) interval of untreated ventricular fibrillation. Biphasic waveform defibrillation with a fixed energy of 150 joules proved to be as effective as conventional monophasic damped sine waveform defibrillation for restoration of spontaneous circulation, with significantly lower delivered energy. This was associated with significantly less severity of postresuscitation myocardial dysfunction. The low-energy biphasic waveform defibrillation is, therefore, likely to be the future direction of transthoracic defibrillation in settings of cardiopulmonary resuscitation.

Animals↗
PubMed2000

K(ATP) channel activation reduces the severity of postresuscitation myocardial dysfunction.

Postresuscitation myocardial dysfunction has been recognized as a leading cause of the high postresuscitation mortality rate. We investigated the effects of ischemic preconditioning and activation of ATP-sensitive K(+) (K(ATP)) channels on postresuscitation myocardial function. Ventricular fibrillation (VF) was induced in 25 Sprague-Dawley rats. Cardiopulmonary resuscitation (CPR), including mechanical ventilation and precordial compression, was initiated after 4 min of untreated VF. Defibrillation was attempted after 6 min of CPR. The animals were randomized to five groups treated with 1) ischemic preconditioning, 2) K(ATP) channel opener, 3) ischemic preconditioning with K(ATP) channel blocker administered 1 min after VF, 4) K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning, and 5) placebo. Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mmHg, the rate of left ventricular decline, cardiac index, and duration of survival, was significantly improved in both preconditioned and K(ATP) channel opener-treated animals. K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning completely abolished the myocardial protective effects of preconditioning. We conclude that ischemic preconditioning significantly improved post-CPR myocardial function and survival. These results also provide evidence that the myocardial protective effects of ischemic preconditioning are mediated by K(ATP) channel activation.

Adenosine Triphosphate↗
PubMed2000

Atrial function during cardiac arrest caused by ventricular fibrillation.

OBJECTIVES: To report observations on preserved regular atrial electrical and mechanical systole during ventricular fibrillation (VF) and to quantitate blood flow generated by atrial contractions in this setting. METHODS: In 10 rats, right atrial pressure pulses were continuously recorded before and for an interval of 8 min after inducing VF. In 3 isolated, perfused rat hearts, epicardial right atrial electrograms were recorded after inducing VF. In 15 pigs, transesophageal echo-Doppler measurements were obtained with pulsed and color-Doppler visualization of flow across the mitral valve after onset of VF. RESULTS: In each rat, regular right atrial pressure pulses were documented during VF. These persisted over an average interval of 7.5 min. In isolated, perfused hearts, right atrial contractions were accompanied by regular atrial depolarizations. In pigs, regular atrial contractions generated atrial stroke volumes of approximately 12 mL, or 25% of prearrest values during the first minute after onset of VF, but those declined to approximately 6 mL after 10 min of untreated cardiac arrest. Blood flow from the left atrium into the left ventricle failed to advance significantly into the systemic circuit. During atrial diastole, we observed reversal of flow into the left atrium. CONCLUSIONS: Atrial contractions are preserved during the initial 8 min or more after cardiac arrest due to VF. Substantial forward flow into the left ventricle failed to advance through the outflow tract but regurgitated into the atrium during atrial diastole.

Animals↗
PubMed2000

Comparisons between sublingual and gastric tonometry during hemorrhagic shock.

STUDY OBJECTIVES: To compare sublingual tissue PCO(2), a disarmingly simple and noninvasive measurement of the severity of perfusion failure, with gastric tonometric PCO(2) during hemorrhagic shock in five male domestic pigs weighing between 35 and 40 kg. DESIGN: Prospective animal study. SETTING: Animal laboratory in a research institution. PARTICIPANTS: Domestic pigs. INTERVENTIONS: Hemorrhagic shock was induced by a modification of the Wigger's method. BP was maintained at 50 mm Hg for 120 min followed by reinfusion of shed blood at a rate of 100 mL/min with the aid of an infusion pump. MEASUREMENTS AND RESULTS: During bleeding, the mean arterial pressure decreased from an average of 127 to 42 mm Hg, and cardiac output decreased from 7.7 to 2.4 L/min. Arterial blood lactate concentration concurrently increased from 1.2 to 13.9 mmol/L. Sublingual PCO(2) (PslCO(2)) increased from 59 to 105 mm Hg, and gastric PCO(2) increased from 61 to 111 mm Hg. The correlation between time-coincident sublingual and gastric measurements of PCO(2) was r = 0.91 (p<0.0001). Bland-Altman analyses demonstrated a close correspondence between the two measurements. The reinfusion of shed blood promptly reversed the hemodynamic abnormalities and reestablished gastric and PslCO(2) to near baseline values. This contrasted with a delayed reversal of lactic acidosis. CONCLUSIONS: Under experimental conditions of hemorrhagic shock, sublingual capnometry yielded measurements that were interchangeable with those of gastric tonometry.

Animals↗
PubMed2000

Sublingual PCO2.

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Animals↗
PubMed1999

The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function.

OBJECTIVES: The purpose of this study was to compare the effects of biphasic defibrillation waveforms and conventional monophasic defibrillation waveforms on the success of initial defibrillation, postresuscitation myocardial function and duration of survival after prolonged ventricular fibrillation (VF). BACKGROUND: We have recently demonstrated that the severity of postresuscitation myocardial dysfunction was closely related to the magnitude of the electrical energy of the delivered defibrillation shock. In the present study, the effects of fixed 150-J low-energy biphasic waveform shocks were compared with conventional monophasic waveform shocks after prolonged VF. METHODS: Twenty anesthetized, mechanically ventilated domestic pigs were investigated. VF was induced with an AC current delivered to the right ventricular endocardium. After either 4 or 7 min of untreated ventricular fibrillation (VF), the animals were randomized for attempted defibrillation with up to three 150-J biphasic waveform shocks or conventional sequence of 200-, 300- or 360-J monophasic waveform shocks. If VF was not reversed, a 1-min interval of precordial compression preceded a second sequence of up to three shocks. The protocol was repeated until spontaneous circulation was restored or for a total of 15 min. RESULTS: Monophasic waveform defibrillation after 4 or 7 min of untreated VF resuscitated eight of 10 pigs. All 10 pigs treated with biphasic waveform defibrillation were successfully resuscitated. Transesophageal echo-Doppler, arterial pressure and heart rate measurements demonstrated significantly less impairment of cardiovascular function after biphasic defibrillation. CONCLUSIONS: Lower-energy biphasic waveform shocks were as effective as conventional higher energy monophasic waveform shocks for restoration of spontaneous circulation after 4 and 7 min of untreated VF. Significantly better postresuscitation myocardial function was observed after biphasic waveform defibrillation.

Analysis of Variance↗
PubMed1999

Electrocardiographic prediction of the success of cardiac resuscitation.

OBJECTIVES: To identify a method for predicting the success or failure of a defibrillatory shock such as to avoid potentially detrimental interruptions of cardiopulmonary resuscitation (CPR). Such a method would also guide more optimal programming of automated external defibrillators. DESIGN: Prospective, observational animal study. SETTING: Medical research laboratory in a university-affiliated research and educational foundation. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation (VF) was electrically induced in 66 domestic pigs. After an interval of between 3 and 5 mins of untreated VF, precordial compression was begun. Electrocardiographic lead 2 was monitored and artifacts produced during precordial compression were removed by digital filtering. MEASUREMENTS AND MAIN RESULTS: In the derivation study, electrical defibrillation restored spontaneous circulation in 30 of the 66 animals. Successfully resuscitated animals had significantly greater coronary perfusion pressure, maximum VF amplitude, mean VF amplitude, and dominant VF frequency. No animals were resuscitated if the coronary perfusion pressure was <8 mm Hg, maximum amplitude was <0.48 mV, mean amplitude was <0.25 mV, or dominant frequency <9.9 Hz independently of the duration of untreated VF. When mean amplitude and dominant frequency were combined, the predictability was further improved. In an additional validation study of 14 animals, consecutive defibrillations were uniformly unsuccessful if the combination of mean amplitude and dominant frequency did not exceed the threshold values obtained in derivation study. CONCLUSION: Mean VF amplitude alone or in combination with dominant frequency of VF was expressed as a numerical score. It served as an objective noninvasive measurement on a par with that of coronary perfusion pressure for predicting the success of defibrillation. As such, it minimizes the detriment of repetitively interrupting mechanical interventions during CPR for electrical defibrillation when an electrical shock predictably fails to restore an effective rhythm.

Animals↗
PubMed1999

Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock.

OBJECTIVE: To investigate the feasibility and predictive value of sublingual Pco2 (P(SL)CO2) measurements as a noninvasive and early indicator of systemic perfusion failure. DESIGN: A prospective, criterion study. SETTING: Emergency department and medical and surgical intensive care units of an urban community medical center. PARTICIPANTS AND PATIENTS: Five normal human volunteers and 46 patients with acutely life-threatening illness or injuries. INTERVENTIONS: Intra-arterial or automated cuff blood pressure and arterial blood lactate (LAC) were measured concurrently with P(SL)CO2. RESULTS: P(SL)CO2 in five healthy volunteers was 45.2 +/- 0.7 mm Hg (mean +/- sD). Twenty-six patients with physical signs of circulatory shock and LAC >2.5 mmol/L had a P(SL)CO2 of 81 +/- 24 mm Hg. This contrasted with patients admitted without clinical signs of shock and LAC of <2.5 mmol/L who had a P(SL)CO2 of 53 +/- 8 mm Hg (p < .001). The initial P(SL)CO2 of 12 patients who died before recovery from shock was 93 +/- 27 mm Hg, and this contrasted with 58 +/- 11 mm Hg (p < .001) in hospital survivors. Increases in P(SL)CO2 were correlated with increases in LAC (r2 = .84; p < .001). When P(SL)CO2 exceeded a threshold of 70 mm Hg, its positive predictive value for the presence of physical signs of circulatory shock was 1.00. When it was <70 mm Hg, it predicted survival with a predictive value of 0.93. CONCLUSION: P(SL)CO2 may serve as a technically simple and noninvasive clinical measurement for the diagnosis and estimation of the severity of circulatory shock states.

Adolescent↗
PubMed1999

Effects of hyper- and hypoventilation on gastric and sublingual PCO(2).

We investigated the effects of hyper- and hypoventilation on gastric (Pg(CO(2))) and sublingual (Psl(CO(2))) tissue PCO(2) before, during, and after reversal of hemorrhagic shock. Pg(CO(2)) was measured with ion-sensitive field-effect transistor sensor and Psl(CO(2)) with a CO(2) microelectrode. Under physiological conditions and during hemorrhagic shock, decreases in arterial (Pa(CO(2))) and end-tidal (PET(CO(2))) PCO(2) induced by hyperventilation produced corresponding decreases in Pg(CO(2)) and Psl(CO(2)). Hypoventilation produced corresponding increases in Pa(CO(2)), PET(CO(2)), Pg(CO(2)), and Psl(CO(2)). Accordingly, acute decreases and increases in Pa(CO(2)) and PET(CO(2)) produced statistically similar decreases and increases in Pg(CO(2)) and Psl(CO(2)). No significant changes in the tissue PCO(2)-Pa(CO(2)) gradients were observed during hemorrhagic shock in the absence or in the presence of hyper- or hypoventilation. Acute changes in Pg(CO(2)) and Psl(CO(2)) should, therefore, be interpreted in relationship with concurrent changes in Pa(CO(2)) and/or PET(CO(2)).

Animals↗
PubMed1999

Combined effects of buffer and adrenergic agents on postresuscitation myocardial function.

Although buffer agents alone have failed to improve the success of resuscitation, we now examine the widely held concept that it is the combined effect of alkaline buffer and adrenergic agents that improves outcomes of cardiopulmonary resuscitation. In the present report, the effects of both CO(2)-consuming and CO(2)-generating buffer agents in combination with adrenergic vasopressor drugs were investigated. Ventricular fibrillation was electrically induced in Sprague-Dawley rats weighing between 450 and 550 g. Precordial compression and mechanical ventilation were initiated after 8 min of untreated ventricular fibrillation. Animals were then randomized to receive bolus injections of either inorganic sodium bicarbonate buffer, organic tromethamine buffer, or saline placebo. The beta(1) adrenergic effects of epinephrine were blocked with esmolol. The vasopressor amine was injected 2 min after injection of the buffer agent. Electrical defibrillation was attempted at the end of 8 min of precordial compression. In 15 additional animals, the sequence of administration of the adrenergic vasopressor and buffer agents was reversed such that the adrenergic vasopressor was injected before the buffer agents. All animals were restored to spontaneous circulation. Both bicarbonate and tromethamine significantly decreased coronary perfusion pressure from 26 to 15 mm Hg and reduced the magnitude of the vasopressor effect of the adrenergic vasopressor. When the vasopressor preceded the buffer, declines in coronary perfusion pressure after administration of buffer agents were prevented. In each instance, however, greater impairment of postresuscitation myocardial function and decreased postresuscitation survival were observed after treatment with buffer agents.

Adrenergic beta-Agonists↗
PubMed1998

Decreases in organ blood flows associated with increases in sublingual PCO2 during hemorrhagic shock.

Earlier studies demonstrated that not only the stomach but also the esophageal wall served as an appropriate site for estimating the severity of circulatory shock by using tonometric methods. We then conceived of the option of sublingual tonometry. In the present study, we tested the hypothesis that the changes in sublingual PCO2 serve as indicators of decreases in blood flow to sublingual and visceral tissue. In Sprague-Dawley rats, sublingual PCO2 increased from 50 to 127 Torr and arterial blood lactate increased from 0.9 to 11.2 mmol/l during bleeding. Sublingual blood flow simultaneously decreased to approximately 32% of preshock values. After reinfusion of shed blood, organ blood flows and sublingual PCO2 were promptly restored to near-baseline values. There were corresponding decreases in blood flows in the tongue, stomach, jejunum, colon, and kidneys during hemorrhagic shock. Increases in sublingual PCO2 were highly correlated with decreases in sublingual blood flow (r = 0.80), tongue blood flow (r = 0.81), gastric blood flow (r = 0.74), jejunal blood flow (r = 0.65), colon blood flow (r = 0.80), and renal blood flow (r = 0.75). Unbled control animals demonstrated no significant changes. Therefore, we anticipate that sublingual tonometry will provide a useful, noninvasive alternative for monitoring visceral PCO2.

Animals↗
PubMed1998

Sublingual capnometry for diagnosis and quantitation of circulatory shock.

We investigated sublingual tissue PCO2 during hemorrhagic and septic shock. Hemorrhagic shock was induced in 10 rats. Sublingual PCO2 increased from 45 to 125 mm Hg and arterial pressure declined from 138 to 49 mm Hg, end-tidal PCO2 decreased from 35 to 13 mm Hg, and cardiac index fell from 290 to 77 ml/min/kg. Arterial blood lactate increased from 0.9 to 15.8 mmol/L. Gastric PCO2 was measured in five animals and it increased from 46 to 87 mm Hg. No significant changes were observed in eight "sham" bled animals including the five animals in which gastric PCO2 was measured. Highly significant linear correlations (p < 0.001) between sublingual PCO2 and gastric PCO2 (r = 0.71), cardiac index (r = -0.74), and arterial lactate (r = 0.59) were documented. We subsequently investigated sublingual PCO2 in five animals in which sepsis was induced by intravenous infusion of live Staphylococcus aureus. Like hemorrhagic shock, highly significant linear correlations were observed between end-tidal PCO2 and cardiac index and between sublingual PCO2 and arterial blood lactate. Sublingual PCO2 promises to serve as a technically simple, noninvasive, and rapid response quantitator of severity of circulatory shock states.

Animals↗
PubMed1998

Tissue hypercarbic acidosis as a marker of acute circulatory failure (shock).

Measurement of pH of the stomach wall (gastric intramural pH) by the tonometric method has been utilized both experimentally and clinically as an indicator of the capability of the stomach to extract and utilize oxygen. As such, it serves as a metabolic marker of acute perfusion failure (circulatory shock). More recently, researchers have found that increases in the PCO2 accounted for the decline in pH; this was documented in tissues other than the stomach wall, including the esophageal and sublingual mucosa. In this review, tissue PCO2 is identified as a universal indicator of impaired perfusion and contrasted with conventional hemodynamic and metabolic markers of perfusion failure.

Acidosis↗