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Cardioplegia is intentional and temporary cessation of cardiac activity, primarily for cardiac surgery.

Overview

The word cardioplegia combines the roots cardio- meaning the heart, and plegia- paralysis.^[1] 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 four main goals of hypothermic cardioplegia are:

Immediate and sustained electromechanical quiescence
Rapid and sustained homogenous myocardial cooling
Maintenance of therapeutic additives in effective concentrations
Periodic washout of metabolic inhibitors^[2]

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.^[3]

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, and 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.

History

Physiology

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 approximately -90mV.^[4] 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 -84mV at an extracellular K⁺ concentration of 5.4 mmol/l. Raising the K⁺ concentration to 16.2 mmol/l raises the resting potential to -60mV, a level at which muscle fibers are inexcitable to ordinary stimuli. When the resting potential approaches -50mV, sodium channels are inactivated resulting in a diastolic arrest of cardiac activity.^[5] 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 are available to conduct the inward Na⁺ current during phase 0 depolarization.^[6]

Interestingly, the use of two other cations, Na⁺ and Ca²⁺, also can be used to arrest the heart. By removing extracellular Na⁺ from perfusate the heart will not beat because the action potential is dependent upon extracellular Na⁺ ions. However the removal of Na⁺ does not alter the resting membrane potential of the cell. Likewise removal of extracellular Ca²⁺ results in a decreased contractile force, and eventual arrest in diastole. An example of a low [K⁺] low [Na⁺] solution is HTK (Histidine-tryptophan-ketoglutarate). Conversely, increasing extracellular Ca²⁺ concentration enhances contractile force. Elevating Ca²⁺ concentration to a high enough level results in cardiac arrest in systole. This unfortunate irreversible event is referred to as "stone-heart" or rigor.

Hypothermia is the other key component of most cardioplegic strategies. It is employed as another means to further lower myocardial metabolism during periods of ischemia. The Van 't Hoff equation allow calculation that oxygen consumption will drop by 50% for every 10 °C reduction in temperature. This Q₁₀ effect combined with a chemical cardiac arrest can reduce myocardial oxygen consumption (MV02) by 97%.^[7]

Cold cardioplegia is given into the heart through the aortic root. Blood supply to the heart arises from the aorta root through coronary arteries. Cardioplegia in diastole ensures that the heart does not use up the valuable energy stores (ATP- adenosine triphosphate) . Blood is commonly added to this solution in varying amounts from 0-100%. Blood acts a buffer and also supplies nutrients to the heart during ischemia.

Once the procedure on the heart vessels (CABG- coronary artery bypass grafting) or inside the heart like valve replacement or correction of congenital heart defect etc. is over the cross-clamp is removed and the isolation of the heart is terminated so that normal blood supply to the heart is restored and the heart starts beating again.

The cold fluid (usually at 4 °C) ensures that the heart cools down to an approximate temperature of around 15–20 °C thus slowing down the metabolism of the heart and thereby preventing damage to the heart muscle. This is further augmented by the cardioplegia component which is high in potassium

When solution is introduced into the aortic root (with an aortic cross-clamp on the distal aorta to limit systemic circulation), this is called antegrade cardioplegia. When introduced into the coronary sinus it is called retrograde cardioplegia.^[8]

Ingredients

St. Thomas' Solution
Bretschneider Solution
University of Wisconsin Solution
Custodiol HTK
Celsior

There are many cardioplegic solutions of varying additives. The only vital additive in most solutions is potassium chloride in a 20-30 mmol/L concentration range. Other additives such as mannitol, sodium bicarbonate, procaine, et cetera, are of secondary importance. Below are several generic crystalloid cardioplegia solutions.

Induction

Sodium Bicarbonate 8.4% 31.25 mEq
Potassium Chloride 35 mEq
Mannitol 25% 3.75 g
Isolyte-S pH 7.4 133 mL

Add prior to use with induction:
Lidocaine 2% 62.5 mg
Nitroglycerin 500 mcg
Albumin 25% 12.5 g

Reperfusate

Mannitol 20% 37.5 mL
Isolyte-S pH 7.4 291.75 mL
CPD 30 mL
MSA/MSG 0.92M 70 mL

Add prior to use:
Sodium bicarbonate 62.5 mEq (62.5 mL)
Lidocaine 2% 125 mg (6.2 mL)
Nitroglycerin 1000 mcg (0.2 mL)

Ringers

Ringer’s Solution 1000 mL
Potassium Chloride 20 mEq
Magnesium Chloride 32 mEq
Mannitol 20% 10 g
Sodium Bicarbonate 8.4% 6.5 mEq

Add prior to use:
Procaine 10% 2.73 mL

Maintenance

Sodium Bicarbonate 8.4% 125 mEq
Potassium Chloride 25 mEq
Mannitol 25% 15 g
Isolyte-S pH 7.4 802 mL

References

^ http://cancerweb.ncl.ac.uk/cgi-bin/omd?action=Search+OMD&query=cardioplegia
^ Kaplan J Cardiac Anesthesia. 3rd Edition. W.B Saunders Company. 1993
^ "Cold Crystalloid Cardioplegia" Hans J. Geissler* and Uwe Mehlhorn, Department of Cardiothoracic Surgery, University of Cologne
^ http://www.cvphysiology.com/Arrhythmias/A007.htm
^ Hensley F, Martin D. A Practical Approach to Cardiac Anesthesia. 2nd Edition. Little, Brown and Company. 1995
^ Berne R, Levy M. Physiology. 3rd Edition. Mosby St. Louis 1993.
^ Gravlee G, Davis R, Utley J. Cardiopulonary Bypass Principles and Practice. Williams & Williams Baltimore 1993.
^ "Cardioplegia Delivery Systems" hosted on Washington University, St. Louis, web site

UpToDate Contents

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Changes in cardiac arrest patients' temperature management after the 2013 "TTM" trial: results from an international survey.

Deye N1, Vincent F2, Michel P3, Ehrmann S4, da Silva D5, Piagnerelli M6, Kimmoun A7, Hamzaoui O8, Lacherade JC9, de Jonghe B10, Brouard F11, Audoin C12, Monnet X13, Laterre PF14; SRLF Trial Group.
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