RU2432186C1 - Method of deliberate cardiac arrest before aortic compression in cardiac surgeries employing extracorporeal circulation in patients with aortic valve incompetence - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention refers to medicine, namely to cardiosurgery, and can be used in cardiac surgeries employing extracorporeal circulation in patients with aortic valve incompetence. For this purpose, at the stage of parallel extracorporeal circulation ATP 100 mg and lidocaine 2 mg/kg are introduced in a contour of an apparatus. Then, the aorta is clamped, and an aortic root opening is exposed. A cannula is inserted in a coronary artery mouth, and a cardioplegic fluid is infused wit underlying drug-induced asystole.

EFFECT: method enables effective myocardium adaptation to ischemia ensured by drug-induced asystole before aortic compression, with escaping stages of global ischemia and preventing aortotomy hemorrhage.

1 ex

Description

The invention relates to medicine, namely to cardiac surgery, and can be used to prevent intraoperative ischemic damage to the myocardium during heart surgery.

In heart surgery under cardiopulmonary bypass (IR), cardiac arrest is achieved by compressing the aorta with a clamp and infusion into the coronary bed of a cardioplegic solution.

For this, after cannulation of the great vessels in the region of the aortic root, a “cardioplegic” cannula is installed and fixed with a purse string suture. After the onset of IR in hypothermic mode and a decrease in the patient’s body temperature to 25-27 degrees in the esophagus with the appearance of heart fibrillation, the ascending part of the aorta is squeezed with a transverse clamp above the cardioplegic cannula, and immediately the cardioplegic solution is infused into the aortic root [Cardiovascular surgery. Leadership. Edited by V.I. Burakovsky and L.A. Bokeria. - M .: Medicine, 1989, p.24, 527].

In case of aortic valve insufficiency, infusion of cardioplegic fluid is carried out selectively, directly to the mouth of the coronary arteries. Moreover, after clamping the aorta below the (proximal) aortic clamp, an aortotomy is performed. The edges of the aortotomic wound are diluted and special cannulas are placed in the mouths of the coronary arteries (in turn or simultaneously), and the cardioplegic solution is immediately infused [Cardiovascular surgery. Leadership. Edited by V.I. Burakovsky and L.A. Bokeria. - M .: Medicine, 1989, p.24].

With any embodiment of cardioplegia, from the moment the clamp is applied to the aorta until the heart stops completely, global ischemia of the contracting or fibrillating myocardium occurs. The duration of global ischemia is more significant in patients with aortic valve insufficiency, associated with the need to perform aortotomy and infusion of cardioplegic fluid in the mouth of the coronary arteries. The aggravation of myocardial ischemia from the moment of clamping the aorta to the achievement of cardioplegic cardiac arrest is facilitated by the absence of coronary blood flow, continued contractions of the left ventricle and the outflow of blood from the aortotomy incision.

According to a number of experimental studies, the effect of increasing resistance by “mechanical” preconditioning, based on the use of repeated short episodes of regional ischemia for a subsequent longer episode of ischemia, can be used to adapt myocardium to ischemia (Murry CE, Jenings RB, Reimer RA Preconditioning with ischemia: a delay of letal cell injury in ischemic myocardium. Circulation 1986; 74: 1124-1136). However, this technique does not provide spontaneous cardiac arrest, but involves mechanical compression of the heart vessel before clamping on the aorta and cannot be used to prevent ischemic damage to the myocardium in clinical practice.

It is known pharmacological preconditioning of the myocardium in an experiment on an isolated heart by adding thymogen at a concentration of 0.1-1 μM / L in cardioplegic solution [application RU 94022332, published on 08/10/1996]. This technique cannot be used to intentionally stop cardiac activity before clamping the aorta, it is aimed only at potentiating the effect of cardioplegia.

The prototype of the invention is a method for myocardial preconditioning, which consists in the prophylactic intravenous infusion of A1 agonists of adenosine receptors before an episode of in vivo ischemia on the hearts of rabbits and dogs. The authors concluded that adenosine stimulates A1 cardiac receptors during occlusion, which protects the heart from a heart attack even after adenosine has been removed [Liu G.S., Thronton J., VanWinkle D.M. et al. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart. Circulation. 1991; 84: 350-356). Precondensation can be mediated by activation of ATP-sensitive potassium channels (Grover GJ, Sleph PG, Dzwonczyk S. Role of myocardial ATP-sensitive potassium channels in mediating preconditioning in the dog heart and their possible interaction with adenosine A1-receptors. Circulation. 1992; 86; 1310-1316).

The disadvantages of this method are the limited possibilities of application only within the framework of the experiment, the absence of clamping of the aorta.

The objective of the invention was the development of a method of deliberate cardiac arrest for the period from clamping to the aorta until cardioplegic cardiac arrest is achieved in patients with aortic valve insufficiency, which allows achieving pharmacological asystole before clamping the aorta, bypassing the stage of global ischemia caused by aortic compression on a working heart.

The technical result when using the invention is to prevent the stage of global myocardial ischemia and blood loss from the aortotomy incision.

The proposed method is as follows. For heart operations under IR conditions after cannulation of the great vessels and the start of perfusion, ATP solutions (Sol. Acidi adenosintriphosphorici 1% - 10 ml (100 mg)) are introduced into the circuit of the IR apparatus before squeezing the aorta to achieve asystole. (M.D. Mashkovsky. Medicines: in 2 hours. Part 2. - Мn .: Belarus, 1987. - С.124-126) and lidocaine (Sol. Lidocaini hydrochloridi 2%, based on 2 mg / kg, depending on the patient’s body weight) ( MD Mashkovsky. Medicines: in 2 hours. Part 1. - Mn .: Belarus, 1987. - P.289-290). After 30-40 seconds, asystole occurs, after which a clamp is placed on the aorta, the aortic root is opened, a cannula is placed in the mouth of the coronary artery (usually the left one) and cardioplegic fluid is infused against the background of drug asystole. At the same time, the heart is covered with ice crumbs.

A relaxed myocardium allows for an earlier and more effective cardioplegic response when performing cardioplegia on an irreducible heart. ATP and lidocaine cause not only a suppression of the contractile activity of the myocardium, but also its preconditioning before prolonged ischemia.

The proposed method is based on the following properties of ATP and lidocaine:

1. With intravenous administration, ATP causes temporary blockage of the heart in the atrioventricular node. This effect is transmitted through receptor A1, which inhibits adenylate cyclase and reduces the concentration of cAMP, thus causing hyperpolarization of cells through an increase in the flux of K + ions from the outside. It also causes endothelial-dependent relaxation of the smooth muscles located inside the walls of the arteries. The consequence of this is the expansion of the "normal" segments of the arteries in which the endothelium is not separated from the tunica media by atherosclerotic plaques.

ATP, as a potential trigger of A1 adenosine receptors, pharmacologically preconditions the heart for the effects of a subsequent episode of ischemia (Liu GS, Thronton J., VanWinkle DM et al. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart. Circulation. 1991; 84: 350-356), (Grover GJ, Sleph PG, Dzwonczyk S. Role of myocardial ATP-sensitive potassium channels in mediating preconditioning in the dog heart and their possible interaction with adenosine A1-receptors. Circulation. 1992; 86: 1310- 1316), (Takano H., Bolli R., Black RG et al. A1 or A3 adenosine receptors inducelate preconditioning against infarction in conscious rabbits by differentmechanisms. Circ Res. 2001; 88: 520-528).

2. Lidocaine is an antiarrhythmic agent of class I B. It has membrane stabilizing activity. It causes blockade of sodium channels of excitable membranes of neurons and membranes of cardiomyocytes. Reduces the duration of the action potential and effective refractory period in Purkinje fibers, suppresses their automatism. At the same time, lidocaine suppresses the electrical activity of depolarized, arrhythmogenic regions, but minimally affects the electrical activity of normal tissues. It has a vasodilating effect.

The invention is illustrated by the following example.

Patient B., 63 years old, was operated on for insufficiency of the aortic valve complicated by cardiomegaly (6.8 cm CRD), calcification of the aortic valve 3 tbsp., Chronic atrial fibrillation. FC IV.

The patient underwent aortic valve replacement.

In operations after sternotomy, the main vessels (aorta, vena cava) are cannulated for cardiopulmonary bypass. After the beginning of parallel IR, against the background of the readiness to clamp the aorta, Sol was introduced into the circuit of the heart-lung machine: Sol. Acidi adenosintriphosphorici 1% - 10 ml (100 mg) and Sol. Lidocaini hydrochloridi 2%, based on 2 mg / kg. After 33 seconds, pharmacological asystole occurred. A clamp was placed on the aorta, immediately a transverse section revealed the lumen of the aortic root, and a cannula was installed at the mouth of the left coronary artery, and an infusion of cardioplegic fluid was started. Infusion of a cardioplegic solution according to standard methods, in the calculated dosage, under the control of pressure in the aortic root. At the same time, the heart is covered with ice crumbs. The onset of persistent cardioplegia is controlled by an ECG (lack of electrical activity). After completion of the infusion of cardioplegic fluid, a valve-replacing heart operation was performed. The perfusion parameters are spontaneous cooling to 33.2 ° C, PI = 2.6 l / min / sq.m. After removing the clamp from the aorta, cardiac activity recovered spontaneously, sinus rhythm. Aortic occlusion was 74 minutes, total IR time 91 minutes. In the early postoperative period, drug stimulation of cardiac activity was not required. Negative dynamics from the ST-segment was not observed. On the second day, the patient was transferred from the intensive care unit to the cardiac surgery department. In dynamics, the ejection fraction increased from 46% initially to 56% after surgery. On the 9th day after the operation was discharged from the hospital.

Claims (1)

A method of myocardial preconditioning during heart surgery, characterized in that at the stage of parallel cardiopulmonary bypass, 100 mg of ATP and lidocaine are administered at a dose of 2 mg / kg, after which a clamp is placed on the aorta, the aortic root is opened, a cannula is placed in the mouth of the coronary artery and performed cardioplegic fluid infusion on the background of medical asystole.