Cardioplegia
| Cardioplegia | |
|---|---|
| Intervention | |
| ICD-9-CM | 39.63 |
Cardioplegia is intentional and temporary cessation of cardiac activity, primarily for cardiac surgery.
The word cardioplegia combines the Greek cardio meaning the "heart", and plegia "paralysis". Technically, this means arresting or stopping the heart so that surgical procedures can be done in a still and bloodless field. Most commonly, however, the word cardioplegia refers to the solution used to bring about asystole of the heart, or heart paralysis.
The main goals of hypothermic cardioplegia are:
The most common procedure for accomplishing asystole is infusing cold cardioplegic solution into the coronary circulation. This process protects the myocardium, or heart muscle, from damage during the period of ischemia.
To achieve this, the patient is first placed on cardiopulmonary bypass. This device, otherwise known as the heart-lung machine, takes over the functions of gas exchange by the lung and blood circulation by the heart. Subsequently, the heart is isolated from the rest of the blood circulation by means of an occlusive cross-clamp placed on the ascending aorta proximal to the innominate artery. During this period of heart isolation, the heart is not receiving any blood flow, thus no oxygen for metabolism. As the cardioplegia solution distributes to the entire myocardium, the ECG will change and eventually asystole will ensue. Cardioplegia lowers the metabolic rate of the heart muscle, thereby preventing cell death during the ischemic period of time.
Cardioplegic solution is the means by which the ischemic myocardium is protected from cell death. This is achieved by reducing myocardial metabolism through a reduction in cardiac work load and by the use of hypothermia.
Chemically, the high potassium concentration present in most cardioplegic solutions decreases the membrane resting potential of cardiac cells. The normal resting potential of ventricular myocytes is about -90 mV. When extracellular cardioplegia displaces blood surrounding myocytes, the membrane voltage becomes less negative and the cell depolarizes more readily. The depolarization causes contraction, intracellular calcium is sequestered by the sarcoplasmic reticulum via ATP-dependent Ca2+ pumps, and the cell relaxes (diastole). However, the high potassium concentration of the cardioplegia extracellular prevents repolarization. The resting potential on ventricular myocardium is about −84 mV at an extracellular K+ concentration of 5.4 mmol/l. Raising the K+ concentration to 16.2 mmol/l raises the resting potential to −60 mV, a level at which muscle fibers are inexcitable to ordinary stimuli. When the resting potential approaches −50 mV, sodium channels are inactivated, resulting in a diastolic arrest of cardiac activity. Membrane inactivation gates, or h Na+ gates, are voltage dependent. The less negative the membrane voltage, the more h gates that tend to close. If partial depolarization is produced by a gradual process such as elevating the level of extracellular K+, then the gates have ample time to close and thereby inactivate some of the Na+ channels. When the cell is partially depolarized, many of the Na+ channels are already inactivated, and only a fraction of these channels is available to conduct the inward Na+ current during phase 0 depolarization.
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