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Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?

Dobson GP, Faggian G, Onorati F, Vinten-Johansen J - Front Physiol (2013)

Bottom Line: Today's cardiac surgery patient is older, has a "sicker" heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago.The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon.We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the "cath lab" may not be the place where the new wave of high-risk morbid patients are best served.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Heart and Trauma Research Laboratory, James Cook University Townsville, QLD, Australia.

ABSTRACT
Despite surgical proficiency and innovation driving low mortality rates in cardiac surgery, the disease severity, comorbidity rate, and operative procedural difficulty have increased. Today's cardiac surgery patient is older, has a "sicker" heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago. The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon. A confounding factor that may influence clinical outcome is high K(+) cardioplegia. For over 40 years, potassium depolarization has been linked to transmembrane ionic imbalances, arrhythmias and conduction disturbances, vasoconstriction, coronary spasm, contractile stunning, and low output syndrome. Other than inducing rapid electrochemical arrest, high K(+) cardioplegia offers little or no inherent protection to adult or pediatric patients. This review provides a brief history of high K(+) cardioplegia, five areas of increasing concern with prolonged membrane K(+) depolarization, and the basic science and clinical data underpinning a new normokalemic, "polarizing" cardioplegia comprising adenosine and lidocaine (AL) with magnesium (Mg(2+)) (ALM™). We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the "cath lab" may not be the place where the new wave of high-risk morbid patients are best served.

No MeSH data available.


Related in: MedlinePlus

A schematic of the effect of hyperkalemia and prolonged myocardial membrane depolarization on Na+ entry through the “window current” and the net influx of Ca2+ into the myocardial cell via the reversal of the Na+/Ca2+ exchanger [3Na+ ions are extruded in exchange for 1 Ca2+ entry (Bers and Despa, 2009) at a membrane potential of −50 mV (Baczko et al., 2003)]. Global or regional ischemia and metabolic acidosis impact further on Ca2+ loading, with increases in intracellular H+ further activating the Na+/H+ exchanger (Avkiran, 2001) resulting in 1Na+ ion being exchange for 1 H+ ion. The diagram was adapted from Bers and colleagues (Bers et al., 2003; Bers and Despa, 2006).
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Figure 4: A schematic of the effect of hyperkalemia and prolonged myocardial membrane depolarization on Na+ entry through the “window current” and the net influx of Ca2+ into the myocardial cell via the reversal of the Na+/Ca2+ exchanger [3Na+ ions are extruded in exchange for 1 Ca2+ entry (Bers and Despa, 2009) at a membrane potential of −50 mV (Baczko et al., 2003)]. Global or regional ischemia and metabolic acidosis impact further on Ca2+ loading, with increases in intracellular H+ further activating the Na+/H+ exchanger (Avkiran, 2001) resulting in 1Na+ ion being exchange for 1 H+ ion. The diagram was adapted from Bers and colleagues (Bers et al., 2003; Bers and Despa, 2006).

Mentions: The clinical problems associated with prolonged membrane depolarization include Ca2+ loading of the myocyte and IR injury (arrhythmias, stunning, inflammation, necrosis, and apoptosis) (Suleiman et al., 2001). Depolarization-induced Ca2+ loading occurs first from Na+ entry through the voltage-dependent Na+ fast channels. At −50 mV (16 mM K+), despite ~3.5% availability of Na+ channels and only 0.1% of maximal Na+ conductance compared to −80 mV, the high sodium driving force (ΔGNa+out/in = −15 KJmol−1) leads to Na+ entry via the small Na+ “window” current that remains open at these depolarized states (Bers et al., 2003). A rise in cell Na+ leads to a reversal of the voltage-dependent Na+/Ca2+ exchanger (3 Na+out: 1 Ca2+ in), with a resulting rise in intracellular Ca2+ (see Figure 4).


Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?

Dobson GP, Faggian G, Onorati F, Vinten-Johansen J - Front Physiol (2013)

A schematic of the effect of hyperkalemia and prolonged myocardial membrane depolarization on Na+ entry through the “window current” and the net influx of Ca2+ into the myocardial cell via the reversal of the Na+/Ca2+ exchanger [3Na+ ions are extruded in exchange for 1 Ca2+ entry (Bers and Despa, 2009) at a membrane potential of −50 mV (Baczko et al., 2003)]. Global or regional ischemia and metabolic acidosis impact further on Ca2+ loading, with increases in intracellular H+ further activating the Na+/H+ exchanger (Avkiran, 2001) resulting in 1Na+ ion being exchange for 1 H+ ion. The diagram was adapted from Bers and colleagues (Bers et al., 2003; Bers and Despa, 2006).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3755226&req=5

Figure 4: A schematic of the effect of hyperkalemia and prolonged myocardial membrane depolarization on Na+ entry through the “window current” and the net influx of Ca2+ into the myocardial cell via the reversal of the Na+/Ca2+ exchanger [3Na+ ions are extruded in exchange for 1 Ca2+ entry (Bers and Despa, 2009) at a membrane potential of −50 mV (Baczko et al., 2003)]. Global or regional ischemia and metabolic acidosis impact further on Ca2+ loading, with increases in intracellular H+ further activating the Na+/H+ exchanger (Avkiran, 2001) resulting in 1Na+ ion being exchange for 1 H+ ion. The diagram was adapted from Bers and colleagues (Bers et al., 2003; Bers and Despa, 2006).
Mentions: The clinical problems associated with prolonged membrane depolarization include Ca2+ loading of the myocyte and IR injury (arrhythmias, stunning, inflammation, necrosis, and apoptosis) (Suleiman et al., 2001). Depolarization-induced Ca2+ loading occurs first from Na+ entry through the voltage-dependent Na+ fast channels. At −50 mV (16 mM K+), despite ~3.5% availability of Na+ channels and only 0.1% of maximal Na+ conductance compared to −80 mV, the high sodium driving force (ΔGNa+out/in = −15 KJmol−1) leads to Na+ entry via the small Na+ “window” current that remains open at these depolarized states (Bers et al., 2003). A rise in cell Na+ leads to a reversal of the voltage-dependent Na+/Ca2+ exchanger (3 Na+out: 1 Ca2+ in), with a resulting rise in intracellular Ca2+ (see Figure 4).

Bottom Line: Today's cardiac surgery patient is older, has a "sicker" heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago.The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon.We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the "cath lab" may not be the place where the new wave of high-risk morbid patients are best served.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Heart and Trauma Research Laboratory, James Cook University Townsville, QLD, Australia.

ABSTRACT
Despite surgical proficiency and innovation driving low mortality rates in cardiac surgery, the disease severity, comorbidity rate, and operative procedural difficulty have increased. Today's cardiac surgery patient is older, has a "sicker" heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago. The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon. A confounding factor that may influence clinical outcome is high K(+) cardioplegia. For over 40 years, potassium depolarization has been linked to transmembrane ionic imbalances, arrhythmias and conduction disturbances, vasoconstriction, coronary spasm, contractile stunning, and low output syndrome. Other than inducing rapid electrochemical arrest, high K(+) cardioplegia offers little or no inherent protection to adult or pediatric patients. This review provides a brief history of high K(+) cardioplegia, five areas of increasing concern with prolonged membrane K(+) depolarization, and the basic science and clinical data underpinning a new normokalemic, "polarizing" cardioplegia comprising adenosine and lidocaine (AL) with magnesium (Mg(2+)) (ALM™). We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the "cath lab" may not be the place where the new wave of high-risk morbid patients are best served.

No MeSH data available.


Related in: MedlinePlus