Most cited article - PubMed ID 23688243
Mild therapeutic hypothermia is superior to controlled normothermia for the maintenance of blood pressure and cerebral oxygenation, prevention of organ damage and suppression of oxidative stress after cardiac arrest in a porcine model
Extracorporeal life support is a treatment modality that provides prolonged blood circulation, gas exchange and can substitute functions of heart and lungs to provide urgent cardio-respiratory stabilization in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Generally, the therapy targets blood pressure, volume status, and end-organs perfusion. As there are significant differences in hemodynamic efficacy among different percutaneous circulatory support systems, it should be carefully considered when selecting the most appropriate circulatory support for specific medical conditions in individual patients. Despite severe metabolic and hemodynamic deterioration during prolonged cardiac arrest, venoarterial extracorporeal membrane oxygenation (VA ECMO) can rapidly revert otherwise fatal prognosis, thus carrying a potential for improvement in survival rate, which can be even improved by introduction of mild therapeutic hypothermia. In order to allow a rapid transfer of knowledge to clinical medicine two porcine models were developed for studying efficiency of the VA ECMO in treatments of acute cardiogenic shock and progressive chronic heart failure. These models allowed also an intensive research of adverse events accompanying a clinical use of VA ECMO and their possible compensations. The results indicated that in order to weaken the negative effects of increased afterload on the left ventricular function the optimal VA ECMO flow in cardiogenic shock should be as low as possible to allow adequate tissue perfusion. The left ventricle can be also unloaded by an ECG-synchronized pulsatile flow if using a novel pulsatile ECMO system. Thus, pulsatility of VA ECMO flow may improve coronary perfusion even under conditions of high ECMO blood flows. And last but not least, also the percutaneous balloon atrial septostomy is a very perspective method how to passively decompress overloaded left heart.
INTRODUCTION: Mild therapeutic hypothermia (MTH) is being used after cardiac arrest for its expected improvement in neurological outcome. Safety of MTH concerning inducibility of malignant arrhythmias has not been satisfactorily demonstrated. This study compares inducibility of ventricular fibrillation (VF) before and after induction of MTH in a whole body swine model and evaluates possible interaction with changing potassium plasma levels. METHODS: The extracorporeal cooling was introduced in fully anesthetized swine (n = 6) to provide MTH. Inducibility of VF was studied by programmed ventricular stimulation three times in each animal under the following: during normothermia (NT), after reaching the core temperature of 32°C (HT) and after another 60 minutes of stable hypothermia (HT60). Inducibility of VF, effective refractory period of the ventricles (ERP), QTc interval and potassium plasma levels were measured. RESULTS: Starting at normothermia of 38.7 (IQR 38.2; 39.8)°C, HT was achieved within 54 (39; 59) minutes and the core temperature was further maintained constant. Overall, the inducibility of VF was 100% (18/18 attempts) at NT, 83% (15/18) after reaching HT (P = 0.23) and 39% (7/18) at HT60 (P = 0.0001) using the same protocol. Similarly, ERP prolonged from 140 (130; 150) ms at NT to 206 (190; 220) ms when reaching HT (P < 0.001) and remained 206 (193; 220) ms at HT60. QTc interval was inversely proportional to the core temperature and extended from 376 (362; 395) at NT to 570 (545; 599) ms at HT. Potassium plasma level changed spontaneously: decreased during cooling from 4.1 (3.9; 4.8) to 3.7 (3.4; 4.1) mmol/L at HT (P < 0.01), then began to increase and returned to baseline level at HT60 (4.6 (4.4; 5.0) mmol/L, P = NS). CONCLUSIONS: According to our swine model, MTH does not increase the risk of VF induction by ventricular pacing in healthy hearts. Moreover, when combined with normokalemia, MTH exerts an antiarrhythmic effect despite prolonged QTc interval.
- MeSH
- Time Factors MeSH
- Potassium blood MeSH
- Electrophysiological Phenomena * MeSH
- Ventricular Fibrillation blood etiology physiopathology MeSH
- Linear Models MeSH
- Extracorporeal Membrane Oxygenation MeSH
- Disease Models, Animal MeSH
- Sus scrofa MeSH
- Body Temperature MeSH
- Hypothermia, Induced adverse effects MeSH
- Animals MeSH
- Check Tag
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Potassium MeSH
