Biomedical subjects

A Pernat

Publications and source records attributed to A Pernat.

8 recordsLinked to original sources

PubMed2004

Two cases of complications of the thrombolysis of right heart free-floating thrombi with pulmonary embolism: important role of echocardiographically based management.

We present two cases where successful thrombolysis of right heart thrombi and pulmonary embolism was accompanied by serious adverse events. In patient 1 with massive pulmonary thromboembolism, transesophageal ultrasound revealed large right atrial thrombus entrapped in a patent foramen ovale. Initial treatment with heparin was substituted with thrombolysis, which resulted in clinical improvement and dissolution of right heart thrombus but was followed by fatal intracerebral haemorrhage. In patient 2, thrombolysis caused mobilisation of thrombotic mass as evidenced by disappearance of thrombus on ultrasound. Massive pulmonary thromboembolism resulted in circulatory collapse. Short cardiopulmonary resuscitation restored spontaneous circulation and the patient recovered completely.

Adult↗

PubMed2001

Optimizing timing of ventricular defibrillation.

OBJECTIVE: Our intent was to evolve a prognosticator that would predict the likelihood that an electrical shock would restore a perfusing rhythm. Such a prognosticator was to be based on conventional electrocardiographic signals but without constraints caused by artifacts resulting from precordial compression. The adverse effects of "hands off" intervals for rhythm analyses would therefore be minimized. Such a prognosticator was further intended to reduce the number of electrical shocks and the total energy delivered and thereby minimize postresuscitation myocardial dysfunction. DESIGN: Observational study. SUBJECTS: Medical research laboratory of a university-affiliated research and educational institute. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation was induced in an established porcine model of cardiac arrest. Recordings of scalar lead 2 over the frequency range of 4-48 Hz were utilized. The area under the curve representing the amplitude and frequency was defined as the amplitude spectrum area (AMSA). MEASUREMENTS AND MAIN RESULTS: A derivation group of 55 animals yielded a threshold value of AMSA that uniformly predicted successful resuscitation. A separate group of 10 animals, a validation group, confirmed that an AMSA value of 21 mV.Hz predicted restoration of perfusing rhythm after 7 of 8 electrical shocks and failure of electrical conversion in 21 of 23 electrical shocks, yielding sensitivity and specificity of about 90%. The negative predictive value of AMSA was 95% and statistically equivalent to that of coronary perfusion pressure, mean amplitude, and median frequency. The positive predictive value that would prompt continuation of cardiopulmonary resuscitation without interruption for an unsuccessful defibrillation attempt was greatly improved with AMSA (78%) as compared with coronary perfusion pressure (42%), mean amplitude (32%), and median frequency (29%). CONCLUSION: AMSA has the potential for guiding more optimal timing of defibrillation without adverse interruption of cardiopulmonary resuscitation or the delivery of unsuccessful high energy electrical shocks that contribute to postresuscitation myocardial injury.

Algorithms↗

PubMed2000

End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock.

OBJECTIVE: To document the relationships between cardiac index and end-tidal carbon dioxide tension (PetCO2 during diverse low-flow states of circulatory shock. DESIGN: Randomized, prospective, controlled studies on animal models of hemorrhagic, septic, and cardiogenic shock. SETTING: University-affiliated research laboratory. SUBJECTS: Sixteen anesthetized domestic pigs weighing 35-45 kg. INTERVENTIONS: Hemorrhagic shock was induced in five pigs by bleeding followed by reinfusion of shed blood. Septic shock was induced in five pigs by infusion of live Escherichia coli. Cardiogenic shock followed an interval of global myocardial ischemia after inducing and reversing ventricular fibrillation in six pigs. MEASUREMENTS AND MAIN RESULTS: PetCO2 was continuously measured. Cardiac index was measured intermittently by using conventional thermodilution techniques. Cardiac index was correlated with PetCO2 by polynomial regression and Bland-Altman analyses. PetCO2 was highly correlated with cardiac index during hemorrhagic shock (r2 = .69, p < .01), septic shock (r2 = .65, p < .01), and cardiogenic shock (r2 = .81, p < .01). PetCO2 predicted thermodilution cardiac index with bias of -11+/-27 (+/-2 SD) mL/min/kg during hemorrhagic shock, 1.3+/-20.4 (+/- 2 SD) mL/min/kg during septic shock, and -1+/-12 (+/-2 SD) mL/min/kg during cardiogenic shock. CONCLUSIONS: Cardiac output and PetCO2 were highly related in diverse experimental models of circulatory shock in which cardiac output was reduced by >40% of baseline values. Therefore, measurement of PetCO2 is a noninvasive alternative for continuous assessment of cardiac output during low-flow circulatory shock states of diverse causes.

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↗

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

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↗

PubMed1997

Heart conduction disturbances and cardiovascular collapse after disopyramide and low-dose metoprolol in a patient with hypertrophic obstructive cardiomyopathy.

Disopyramide as an antiarrhythmic can be prescribed to patients with atrial fibrillation and, owing to its negative inotropic effect, to patients with hypertrophic obstructive cardiomyopathy. It is known that in patients with cardiac conduction disturbances and heart failure, disopyramide can adversely affect heart rhythm and conduction and induce cardiovascular collapse. A patient with hypertrophic obstructive cardiomyopathy and paroxysms of atrial fibrillation is described who was treated with disopyramide and also, during the 5 days before admission, with metoprolol. In spite of normal cardiac conduction and function before disopyramide, this treatment was followed by hypotension, bradycardia, and cardiac conduction disturbances. Our case shows the potential for disopyramide, especially when combined with metoprolol, to induce grave adverse effects even in patients with normal cardiac conduction and ventricular function.

Anti-Arrhythmia Agents↗