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Hyperkalemia and Hypocalcemia - Literature Review Modalidades De Parada Cardíaca Induzida: Hipercalemia E Hipocalcemia - Revisão De Literatura

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Hyperkalemia and Hypocalcemia - Literature Review Modalidades De Parada Cardíaca Induzida: Hipercalemia E Hipocalcemia - Revisão De Literatura Oliveira MAB,SPECIAL et al. - Modes ARTICLE of induced cardiac arrest: hyperkalemia and Rev Bras Cir Cardiovasc 2014;29(3):432-6 hypocalcemia - Literature review Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - Literature review Modalidades de parada cardíaca induzida: hipercalemia e hipocalcemia - revisão de literatura Marcos Aurélio Barboza de Oliveira1, MD, MsC; Antônio Carlos Brandi2, MD; Carlos Alberto dos Santos2, MD; Paulo Henrique Husseini Botelho2, MD; José Luis Lasso Cortez3, MD; Domingo Marcolino Braile4, MsC, PhD DOI: 10.5935/1678-9741.20140074 RBCCV 44205-1572 Abstract Resumo The entry of sodium and calcium play a key effect on myocyte A entrada de sódio e cálcio desempenham efeito chave no miócito subjected to cardiac arrest by hyperkalemia. They cause cell submetido à parada cardíaca por hiperpotassemia. Eles provocam swelling, acidosis, consumption of adenosine triphosphate and edema celular, acidose, consumo de trifosfato de adenosina e desen- trigger programmed cell death. Cardiac arrest caused by hypo- cadeiam processo de morte celular programada. A parada cardíaca calcemia maintains intracellular adenosine triphosphate levels, provocada por hipocalcemia mantém os níveis intracelulares de improves diastolic performance and reduces oxygen consumption, trifosfato de adenosina, melhora o rendimento diastólico e reduz o which can be translated into better protection to myocyte injury consumo de oxigênio, o que pode ser traduzido em melhor proteção induced by cardiac arrest. do miócito às lesões provocadas pela parada cardíaca induzida. Descriptors: Heart Arrest, Induced. Myocardial Ischemia. Descritores: Parada Cardíaca Induzida. Isquemia Miocárdi- Hyperkalemia. Hypocalcemia. ca. Hiperpotassemia. Hipocalcemia. INTRODUCTION to approach intracardiac diseases[3] by using substances that trigger controlled cardiac arrest, commonly known as cardio- The first cardiac surgeries were performed on a beating plegic agents [4]. heart, being limited to the correction of minor illnesses, such Although several myocardial protection methods produce as suturing of cardiac wounds, pericardial drainage, and clos- satisfactory results, none can be considered ideal. The perfect ing of the arterial channel. At that time, complications were cardioplegic agent must meet the following requirements [5]: related to myocardial depression [1,2]. In 1953, John Gibbon 1. Cardiac arrest: fast and efficient induction, with re- performed the first open heart surgery, making it possible laxed myocardium and minimum ATP consumption; 1 São José do Rio Preto Medical School (FAMERP), São José do Rio Preto, Correspondence address: SP, Brazil; Centro Universitário de Votuporanga (UNIFEV), Santa Casa Vo- Marcos Aurélio Barboza de Oliveira tuporanga, Votuporanga, SP, Brazil. Avenida República do Líbano, 2700, casa 80 2São José do Rio Preto Base Hospital. São José do Rio Preto, SP, Brazil. São José do Rio Preto, SP,Brazil 3Santa Casa Votuporanga, Votuporanga, SP, Brazil. Zip code: 15092-440 4 São José do Rio Preto Medical School (FAMERP), São José do Rio Preto, E-mail: [email protected] SP, Brazil. Work carried out at São José do Rio Preto Medical School (FAMERP), São José do Rio Preto, SP, Brazil. Article received on December 15th, 2013 No financial support. Article accepted on May 26th, 2014 432 Rev Bras Cir Cardiovasc | Braz J Cardiovasc Surg Oliveira MAB, et al. - Modes of induced cardiac arrest: hyperkalemia and Rev Bras Cir Cardiovasc 2014;29(3):432-6 hypocalcemia - Literature review In addition, the L-type calcium channel (dihydropyri- Abbreviations, acronyms & symbols dine), which is activated when Em is between -20mV and ATP Adenosine triphosphate -30mV, allows calcium to enter the cytosol[13], a phenomenon CPB Cardiopulmonary bypass [5] + + known as calcium window . The Na /Ca2 exchanger is then HTK Histidine-tryptophan-ketoglutarate activated on reverse mode, removing intracellular sodium Em Resting potential + + CPK Creatine phosphokinase and allowing Ca2 influx. H ions (resulting from ischemia) leave the cell via Na+/H+ antiporter, contributing to even higher sodium influx (Figure 1)[5,10]. The Na+/K+ pump is inhibited by the increased concen- 2. Myocardial protection: protective effects to delay irre- tration of extracellular potassium, acidosis, and hypother- versible cell injury caused by global ischemia as well as to mia, allowing intracellular Na levels to continue elevated + + limit the extent of the reperfusion injury; and, consequently, the Na /Ca2 exchanger to continue 3. Reversibility: immediate reversal of cardiac arrest with working on reverse mode. The elevated intracellular cal- heart rate and force of contraction, allowing for early wean- cium causes myocyte contraction, without action potential ing from cardiopulmonary bypass (CPB); being triggered and with energy consumption. Elevated 4. Low toxicity: short half-life without toxic effects to sodium levels lead to cellular edema and cytolysis during other systems after termination of CPB; reperfusion[5]. Thus, hyperkalemic cardioplegia can neither 5. Allowing good visualization of the operative field. inhibit calcium influx in myocardial cells nor avoid its neg- In this context, the aim of this study is to discuss a few ative effects (Figure 1)[12,13]. biochemical and physiological considerations related to hy- perkalemic and hypocalcemic cardioplegia. Hyperkalemic Cardioplegia In 1955, Melrose et al.[6] introduced myocardial perfusion using hypothermic crystalloid solution containing 2.5% po- tassium citrate, but soon gave up employing this technique due to myocardial necrosis and death of several patients. Gay & Ebert[7] reintroduced this technique with lower concentra- tions of potassium and they were able to provide metabolic and functional benefits to the myocardium without any ap- parent structural change. Based on these results, the use of potassium-rich, hypothermic crystalloid solution for myocar- dial protection became widespread. In 1975, Hearse et al.[8] introduced the St. Thomas solution, containing 10-30 mM potassium chloride. With these solutions, stone heart was Fig. 1 - Schematic of the metabolic pathways of hyperkalemic no longer a problem and solutions containing adequate con- cardioplegia harmful to myocytes centrations of potassium to induce cardiac arrest became the gold standard in myocardial protection [9,10]. However, Cohen et al.[11] later found a correlation between the use of these solutions and postoperative myocardial dys- function due to failure to fully protect the myocardium from Calcium physiology in cardiac fibers ischemia and reperfusion injury, which led to the search for Calcium functions as an effector in cardiac fibers, con- safer alternatives for patients. necting the ventricular contraction phase to the excitation phase through action potential. Such mechanism is known Metabolic pathways of hyperkalemic cardioplegia as excitation-contraction coupling[14] and it is also present in Elevated extracellular potassium concentration (10- skeletal striated muscle cells; however, there are a few dif- 40mM) alters resting potential (Em) for myocyte, from ferences in cardiac fibers with important implications to their -85mV to between -65mV and -40mV, leading to fast sodi- contraction[15]. um channels inactivation. The new Em blocks conduction of Similar to skeletal muscle, when action potential travels myocardial action potential, thereby inducing depolarized through the myocardial membrane, it also propagates to the arrest. However, slow sodium channels are not fully inacti- interior of cardiac muscle fibers along the t-tubule mem- vated (sodium window), causing a slow increase in its intra- branes. Action potential in t-tubules, in turn, cause the in- cellular concentration (Figure 1)[5,10,12]. stant release of calcium ions from the sarcoplasmic reticulum 433 Rev Bras Cir Cardiovasc | Braz J Cardiovasc Surg Oliveira MAB, et al. - Modes of induced cardiac arrest: hyperkalemia and Rev Bras Cir Cardiovasc 2014;29(3):432-6 hypocalcemia - Literature review into the sarcoplasm. Then, in a few thousandths of a second, Baker et al.[17], when comparing the effects of several calcium ions diffuse into myofibrils and catalyze chemical concentrations of calcium in St. Thomas solution in imma- reactions that promote sliding of actin and myosin filaments, ture rabbit hearts, found that the lower the concentration of which in turn produces muscle contraction. So far, the exci- calcium, the lower the concentration of creatine phosphoki- tation-contraction coupling mechanism is the same as that of nase (CPK). However, they also found that recovery of aortic skeletal muscle; however, from this point on, a fundamental flow did not follow the same distribution. It showed para- difference starts to emerge. Besides the calcium ions released bolic behavior with its zenith at 0.3 mmol/L, when the heart into the sarcoplasm from the sarcoplasmic reticulum, great obtained the highest aortic flow values. quantities of calcium are also diffused into the sarcoplasm Comparing hypocalcemic and normocalcemic solutions during t-tubule action potential[15]. in blood cardioplegia in immature pig hearts, with or without In fact, without the extra calcium in the t-tubules, car- ischemia, under CPB, Bolling et al. [18] observed that the non- diac muscle contraction strength would be considerably ischemic group benefited from both types of cardioplegia. On reduced since cardiac muscle cisternae are less developed the other hand, in the ischemic group,
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