I close my eyes and I’m back to early February 2002. Shortly before I had received a fax from my Dad in which he mentioned he had been experiencing periodic hot flashes and sweats. Based on this, his physician had run a blood test and confidently proclaimed that everything on the test looked good. Of course, it was not unusual that my father would complain of fatigue, various aches, pains and other physical discomforts. After all, he was a 77 year old man who had gone through two coronary bypass operations, was on the usual list of cardiac medications (statins, blood pressure medications, blood thinners, etc.), and was living a lifestyle that was very routine with the exception of an occasional walk on a treadmill and a few of the standard fare CVD supplements that I would recommend. Nevertheless, I was assured by my father and all the medical personnel with whom he routinely consulted that his cardiovascular disease had stabilized. Therefore, he was functioning well and was in no apparent danger of experiencing any major health crises in the near future. However, despite all these assurances, I felt ill-at-ease. For, I kept on looking at the results of a blood chemistry that my father had sent me shortly after blood was drawn in late August of 2001. Certainly it had its fair share of high readings plus others that were a point or two away from being either too high or too low. But again, at the time, my father was assured by his physician that these findings were “normal” for someone at his age and in his condition and, therefore, were of no practical concern. In fact, based on the comments of his physician my father wrote the following note that accompanied this August 2001 blood chemistry:
“I might survive a bit longer.”
Interestingly, despite all the abnormal findings, at that time my level of metabolic knowledge concerning chronic illness led me to the belief that the physician was probably right. Why? As long time readers of this newsletter may recall, most of my writings and lectures on the biochemistry and physiology of chronic illness during the 90s and early 2000s were focused on examinations of the published medical literature with little discussion of practical application. Therefore, in terms of truly understanding how findings on a blood chemistry could be interpreted in terms of health outcomes, both short term and long term, I was still more than a bit naïve.
However, even with my comparative lack of clinical expertise back then, there was one aspect of the blood chemistry that, despite the assurances of the physician, never stopped troubling me. For, even back then I did know the importance of electrolyte balance in helping to maintain optimal cardiac function. But was I being overly cautious by regarding with suspicion a sodium value that was one point above the low cut-off, a chloride that was two points below the high cut-off, and a potassium that was 4.4 – only 0.1 mEq/L below the optimal of 4.5? My knowledge base back then said “Yes”. Nevertheless, my gut said, emphatically “No”.
I close my eyes again and I’m taken back to the night of Saturday, February 16, 2002. Actually it is now about 2 AM on Sunday the 17th and I am being awakened from sleep at a hotel at Georgetown University, where I was scheduled to lecture on Sunday. It is my sister who is frantically telling me that my father is dead, having experiencing a fatal ventricular arrhythmia late Saturday night after coming home from a usual Saturday night dinner out with my mother at a local Italian restaurant. As you can imagine, my life is immediately turned upside down. Somehow, I made it through the lecture on Sunday, came home to Massachusetts on Sunday night, and flew to my home town of Grand Rapids, Michigan on Monday.
Weeks later, when life began the slow process of returning back to normal, I looked at that blood chemistry of August 2001 with a question in mind that kept on playing in a continuous loop:
Why Saturday night, February 16, 2002? Why not a day before – a week before? Why not a day after – a week after? Everybody agreed that his condition had stabilized. Therefore, was there something unusual about that day that acted as “the straw that broke the camel’s back” so to speak that took a bad but manageable situation to a scenario that was unable to sustain any semblance of normal function and, indeed, life itself? I didn’t know why at the time, but I believed, in my heart of hearts, that the crux of the answer to these questions had to do with electrolytes and potassium and magnesium in particular. Of course, as suggested by my father’s blood chemistry, electrolyte imbalances were nothing new. Nevertheless, I felt that something catastrophic occurred with my father’s fluid and electrolyte balance late on that fateful Saturday night that made anything resembling normal ventricular function impossible. Could better knowledge on my part of fluid and electrolyte chemistry and physiology have allowed me to take action that would either have prevented or reduced in magnitude the tragic events of February 16th? No one will ever know. However, I was determined to find out if my suspicion was correct. Even if the time to help my father had passed, perhaps improving my knowledge in this area could help others.
My journey through research on electrolytes and cardiac function with emphasis on potassium and magnesium has now gone on for over twelve years and has led me in directions I thought had no relevance back then. Could fluid and electrolyte balance in relation to catastrophic changes in cardiac function have any connection to a high carbohydrate meal at an Italian restaurant on a Saturday night? Could this type of imbalance relate to hot flashes in someone who, in our typical world of healthcare, should not have hot flashes? As I hope to prove to your satisfaction, an abundance of published research suggests that this electrolyte/carbohydrate/hot flash connection is all too real and vastly under appreciated.
Before continuing, I want to discuss a very unique aspect of the newsletter series that follows. For it will be a significant departure from my customary focus on chronic illness and quality of life considerations. Typically, I shy away from discussions on acute mortality scenarios, leaving these issues to the allopathic crises care experts. In true form, in all the years I have been writing newsletters, I have never touched on any clinical scenario that revolved around unexpected, sudden death. This newsletter series will be different in this aspect. Why write about an area of clinical care that we have typically left to others? While I take great pride in all that we have done over the years as clinical nutritionists and functional medicine practitioners in terms of improving quality of life concerns of chronically ill patients, I feel we now have a unique opportunity in one aspect of acute crisis care that we can no longer ignore from an ethical standpoint. As I hope to prove to you, there exists some vastly under-appreciated aspects of diet and lifestyle that, as I feel may be very likely true in the case of my father’s unexpected, untimely demise, are contributing to the unexpected, untimely demises not only for many more elderly cardiac patients like my father but for all too many young people who make headlines as the result of being cut down far too early due to sudden cardiac death. In short, could we expand our practices from the usual discussions of quality of life to discussions about how to take some simple measures to possibly prevent sudden, tragic, and premature deaths in patients both young and old? I believe the answer is yes. It is my hope that this newsletter series will play a small role in inspiring you to have those discussions that will not only help patients feel better but help them prevent what may be very preventable occurrences of sudden cardiac death.
THE REALITY OF SUDDEN CARDIAC DEATH
As we all know, much progress has been made in both the allopathic and alternative medicine health care worlds in relation to both reducing mortality and improving quality of life in patients experiencing the various manifestations of cardiovascular disease (CVD). However, even with these gains, as pointed out by Kjeldsen in the paper “Hypokalemia and sudden cardiac death” (1) the numbers of people dying from sudden cardiac death are still sobering:
“Worldwide, approximately three million people suffer sudden cardiac death (ie, death from heart disease within 1 h) annually.”
Even more sobering, though, are the statistics on age of death:
“Of these, approximately 0.5 million people are younger than 50 years of age.”
These discouraging numbers led Kjeldsen (1) to state:
“Great progress has been in the treatment of coronary artery disease, heart failure and arrhythmia over the past decades, but a fundamental breakthrough against sudden cardiac death is lacking. Thus, scientists and clinicians in the field of heart disease currently consider fighting sudden cardiac death to be a major challenge.”
Of course, the numbers in a scientific paper really don’t tell the most important aspects of the sudden cardiac death story. The most important aspects of the story are generally described in the obituaries when we read about, most often, men, middle-aged or younger, prematurely leaving behind spouses and children. Or we read about students and athletes losing far too soon beloved teachers and coaches. Or, even more tragically, we read about young athletes, some in their teens, dying, without warning, in the middle of a routine athletic endeavor. Interestingly, when these deaths are more high profile, as is often seen with the death of young athletes, we see an accompanying press release that makes it clear that the cause was either unknown or due to a genetic heart defect.
For most, the detection of a genetic heart defect is enough to “close the book” on the case. However, for those of us in functional medicine, we know that this is not enough. The genetic defect was present since birth. As I suggested above, the presence of this defect, for us, leads to an important question:
What combination of environmental stressors led to the expression of a genetic defect at this time with such tragic consequences? As suggested by the title of the Kjeldsen (1) paper, part of the story may be something so simple and so basic that most “experts” would probably conclude that it can’t be that simple. However, when you read my review of the Kjeldsen (1) paper and so many others on the subject, I hope you will start to conclude, as I have, that at least part of the story is just a simple matter of potassium.
Before continuing, though, I would like to address a thought that may be running through your mind right now. If potassium is an important part of the sudden cardiac death story, why should I bother to continue to read this newsletter series? After all, potassium supplementation is inexpensive and low risk. Why not just give every athlete and middle-aged and older patient who walks in the door potassium supplementation? For, if potassium is part of the problem, isn’t it obvious that some potassium supplements and more potassium in the diet is the complete solution to this part of the sudden cardiac death story? As I hope to convince you with so many papers that follow, the answer is clearly no. Why? As I hope you have seen, one of the themes of Entry Level Clinical Nutrition™ (ELCN) has been that we need to address the reality that nutrients, whether from the diet or supplements, do not automatically go where we want them to go once they are absorbed, particularly in chronically inflamed, chronically ill, acidotic, insulin resistant patients. In fact, as is true for many nutrients and potassium and magnesium in particular, powerful metabolic forces, primarily involving insulin metabolism and chronic inflammation, when misdirected due to lifestyle and environmental imbalances, can create such drastic differences in nutrient content of different tissue compartments, that tragic outcomes are often the result. Therefore, in addition to dietary deficiency, could a plate of pasta at an Italian restaurant after not eating all day or carbohydrate loading before an athletic event without coordination with the rest of the diet also be part of the story? When trying to answer the question “Why now?”, I hope to convince you that it is quite possible that, for a significant amount of those who died, the answer to this question may be “yes”.
SOME BASICS ON POTASSIUM METABOLISM AS THEY RELATE TO RISK OF SUDDEN CARDIAC DEATH
Before reviewing information that directly supports my hypothesis on the involvement of potassium in sudden cardiac death, I would like to present some basics on potassium metabolism as noted in the Kjeldsen (1) paper mentioned above. First, consider the organ systems that are principally involved in potassium homeostasis:
“Long-term (hours and days) potassium homeostasis depends on renal potassium excretion. However, several tissues contribute to transient short-term (seconds to minutes) potassium homeostasis. Here skeletal muscles play an important role primarily because skeletal muscles contain the largest single pool of potassium in the body. Thus, for an adult human subject it can be calculated that the potassium content of the total skeletal muscle pool is approximately 225 times larger than the total potassium content in the plasma. Moreover, due to the large number of Na+/K+-ATPase (also known as Na+/K+ pumps) and K+ channels, the skeletal muscles possess a huge capacity for potassium exchange. Hence, for an adult human subject it can be calculated that if all Na+K+ pumps are activated to maximum capacity for potassium intake, the entire extracellular potassium pool can be cleared in less than 30 s.”
What is the specific impact of this mechanism on blood levels of potassium? Consider the following:
“This mechanism can shift potassium from plasma to stores, causing hypokalemia within seconds to minutes.”
What might cause activation of these pumps, leading to increasing uptake of potassium into muscles at the expense of extracellular tissue compartments such as the blood? Consider the following:
“In cardiovascular patients, hypokalemia is often caused by nonpotassium-sparing diuretics, insufficient potassium intake and a shift of potassium into stores by increased potassium uptake stimulated by catecholamines, beta-adrenoreceptor agonists and insulin.”
Please notice again the last word in the preceding quote. What might lead to significant increases in insulin levels? For my father it could have been his last dinner at the Italian restaurant. For certain athletes, it could have been the carbohydrate loading. Could this scenario, along with the insufficient potassium intake mentioned above, have led to tragic outcomes due to massive, albeit short-term drops in plasma potassium? While I will be answering this question in much more detail later, please consider this quote in the Kjeldsen (1) paper:
“Interestingly, drugs with a proven significant positive effect on mortality and morbidity rates in heart failure patients all increase plasma potassium concentration.”
With this in mind, the author states:
“Thus, it may prove beneficial to pay more attention to hypokalemia and to maintain plasma potassium levels in the upper normal range. The more at risk of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis.”
Before continuing, please notice again the massively important point made in the first sentence of the above quote. Traditionally the range for serum potassium levels has been 3.5 mmol/l to anywhere from 5.3 – 5.5 mol/l. In addition, classic teaching on fluid and electrolyte metabolism has been to only be concerned when serum potassium drops below 3.5 mmol/l. Furthermore, it is not uncommon for even those who are nutritionally aware to regard serum potassium levels from 4.0 – 4.5 mmol/l as part of the optimum range. As Kjeldsen (1) points out as well as other authors whose papers I will be reviewing, when considering the needs of patients at risk for significant heart dysfunction, levels higher than 4.5 mmol/l may be optimal. My father, six months before he died of ventricular arrhythmia, had a level of 4.4 mmol/l. Close…but not close enough. How many of your patients are so close that you feel their potassium levels are of no concern? In reality, there may be a need for significant concern.
Another important point I want to emphasize from the above quotes relates to a continuing theme and a central focus for the Moss Nutrition Select brand for quite some time now. We feel very strongly that under appreciation of optimal muscle mass and function in terms of their impact on chronic illness may be one of the most important considerations today in terms of creating significant improvements in quality of life in chronically ill patients. With this emphasis in mind, please note again that the primary organ system involved in controlling the changes in potassium metabolism discussed above is muscle. In my opinion, this point adds even more weight to the suggestion that we need to make optimization of muscle mass and function a central focus in a very large portion of our chronically ill patients.
INCIDENCE OF HYPOKALEMIA AND POTASSIUM DEPLETION IN PATIENTS EXPERIENCING CARDIOVASCULR DYSFUNCTION
The next quote from the Kjeldsen (1) paper highlights the incidence of suboptimal potassium metabolism in cardiovascular patients:
“It has been known for nearly a century that cardiovascular diseases are associated with hypokalemia and potassium depletion in the heart. Moreover, large-scale studies from recent decades including, in total, more than 13,000 patients have shown that hypokalemia is present in 7% to 17% of patients with hypertension, acute myocardial infarction and heart failure. Also, up to 20% of hospitalized patients and up to 40% of patients on diuretics suffer from hypokalemia.”
What is the impact of these disturbances in potassium metabolism in terms of mortality rates? The author states:
“…in one study, the mortality rate of hospitalized hypokalemic patients was 10-fold higher than that of the general hospitalized population. Moreover, inadequate management of hypokalemia was found in 24% of these cases. In hypertension, diuretic therapy is associated with an increased risk of cardiac arrest and death.”
The next quote has particular meaning for me because it directly refers to potassium and ventricular tachycardia, the immediate cause of death in my father:
“In myocardial infarction, hypokalemia was associated with an increased risk of ventricular tachycardia and ventricular fibrillation. Thus, the incidence of ventricular fibrillation has been found to be fivefold higher in patients with a low serum potassium concentration than in patients with a high serum potassium concentration. Moreover, no episodes of ventricular fibrillation were observed in patients with serum potassium concentrations greater than 4.6 mmol/L.”
Recall that in August of 2001, six months before my father died, his serum potassium was 4.4 mmol/L. The author continues:
“Also, the incidence of ventricular tachycardia has been found to correlate negatively with plasma potassium concentration. Within the range for normal serum potassium concentration, the risk was increased threefold for patients with low serum potassium concentration compared with patients with high serum potassium concentration.”
Again, I cannot emphasize enough the important points made by Kjeldsen (1). For your patients at risk for cardiovascular dysfunction, serum potassium levels at 4.4 mmol/L or lower correlate with an increased risk for an adverse cardiovascular event.
MORE ON THE ROLE OF MUSCLE IN THE REGULATION OF POTASSIUM STORES
The next set of quotes gives more detail on the role of muscle in the control of potassium homeostasis:
“Skeletal muscle acts as a reservoir pool for potassium, maintaining potassium in vital organs such as the heart and brain. The loss of potassium from skeletal muscles seems to be due to a reduced concentration of Na+/K+pumps, decreasing the capacity for potassium uptake. Interestingly, in a study of heart failure patients prescribed nonpotassium-sparing diuretics and potassium supplements, both skeletal muscle potassium and Na+/K+-ATPase concentrations were reduced, even though plasma potassium was maintained in the normal range.”
Why is it important to note this relationship? The author points out:
“This indicates that in the initial phase of potassium depletion, potassium is primarily lost from skeletal muscles, maintaining plasma potassium. Later, potassium is lost from plasma and muscles, and finally, from other compartments, resulting in potassium concentrations so low that life becomes unsustainable. When rats were readministered potassium, plasma and skeletal muscle were almost immediately repleted. However, it took a day before the skeletal muscle Na+/K+ pump concentration was restored.”
Thus, as I hope you can see, by the time serum potassium levels drop into the low fours and high threes, significant losses of potassium have been present in muscle tissue for quite some time. As you can probably imagine, this fact is of serious concern for those patients already at risk for cardiovascular dysfunction.
MORE INFORMATION ON THE SHIFT OF POTASSIUM FROM THE BLOODSTREAM TO TISSUE STORES
Recall from the text above that under certain conditions, particularly from inducement by insulin, potassium can rapidly shift from the blood to tissue stores which are, for the most part, muscle. It is important to note that this effect occurs with no change in total body stores of potassium. Kjeldsen (1) state:
“Because it occurs without any potassium depletion, it is sometimes called pseudohypokalemia to distinguish it from hypokalemia associated with potassium depletion.”
Specifically in relation to insulin, the author states:
“…insulin’s hypokalemic effect is of interest because these patients often have diabetes as a comorbidity.”
As I mentioned before, it is extremely important to understand that all that has been described above in relation to potassium shifts and the impact these shifts can have on serum potassium levels and the risk the for sometimes catastrophic cardiovascular events can happen even with optimal dietary potassium intake. Granted, from a practical standpoint, most of the cardiovascular patients we see will be experiencing both some level of dietary potassium deficiency and dangerous shifts of potassium from the bloodstream to muscle. Nevertheless, because the dogma is so strong that dietary deficiency and absorption are all that matter when considering nutrient metabolism, I simply cannot emphasize enough that even though your dietary and digestive analysis of your cardiovascular patient concerning potassium may suggest no concern whatsoever, other powerful factors concerning potassium metabolism that you have not considered may be creating considerable risk for an unfortunate event.
MORE ON THE EFFECT OF INSULIN ON POTASSIUM METABOLISM
As I have been suggesting throughout this review of the Kjeldsen (1) paper, the impact of insulin on potassium metabolism is of major importance clinically due to the frequency the average patient experiences hyperinsulinemia due to a diet high in refined carbohydrates and, to make matters worse, intake of refined carbohydrates after a prolonged period of minimal to no food ingestion (i.e., skipping meals and then binging on refined carbohydrate snacks foods and liquids). Kjeldsen (1) states:
“…insulin promotes hypokalemia.”
The author continues:
“…an oral glucose load may increase plasma insulin and cause hypokalemia. Hyperinsulinemic clamping in humans resulted in hypokalemia and prolongation of heart repolarization (QTc interval prolongation shown in the electrocardiogram) that were prevented by beta-adrenoreceptor antagonists. Thus, there is speculation that severe hypokalemia is involved in sudden cardiac death of diabetic patients during hypoglycemia. Indeed, many triggers may be involved – insulin, catecholamines, and pre-existing hypokalemia and/or potassium depletion from nonpotassium-sparing diuretic therapy for hypertension or heart failure.”
How does insulin create the hypokalemic state? Kjeldsen (1) reiterates what was stated previously:
“…insulin has been shown to increase skeletal muscle Na+/K+ pump-mediated potassium uptake.”
A BRIEF COMMENT ON TREATMENT AND SOME CONCLUDING THOUGHTS FROM KJELDSEN
While the bulk of the Kjeldsen (1) paper focused on both why potassium is an important consideration with cardiovascular disease and diagnostic considerations about how to determine if any particular patient is at risk, some comments were made concerning potassium supplementation that warrants consideration:
“…another recent re-evaluation of 7788 patients with heart failure indicated that potassium supplements eliminated the increased mortality associated with hypokalemia.”
Lastly, please note this compelling summation provided by Kjeldsen (1) in the conclusion of this excellent paper:
“Recognizing plasma potassium dynamics and that hypokalemia is common and is often inadequately managed, it may be beneficial to pay more attention to hypokalemia and to maintain plasma potassium levels in the upper normal range. This may be of special importance in patients with cardiovascular diseases such as hypertension, coronary artery disease, heart failure and arrhythmia, especially if treated with nonpotassium-sparing diuretics, beta-adrenoreceptor agonists and/or insulin. The more at risk of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis.”
MORE INFORMATION ON OPTIMAL SERUM POTASSIUM LEVELS IN CARDIOVASCULAR PATIENTS
As I hope was made clear by the Kjeldsen (1) paper, probably the biggest clinical misunderstanding that contributes to an under appreciation of the importance of potassium in the occurrence of adverse cardiovascular events is the actual optimal levels of serum potassium in patients suffering from or at risk for CVD. Why does this under appreciation exist? We have generally assumed that, as long as serum levels are within generally accepted normal levels (Anywhere between 3.5 mmol/l and 5.3 mmol/l), which is quite common in CVD patients, potassium metabolism cannot be involved in the creation of an adverse cardiovascular event. As you saw, Kjeldsen (1) makes it very clear that this is not the case. Further evidence of this often tragic misassumption can be seen in the next paper I am about to review, “What is the optimal serum potassium level in cardiovascular patients” by MacDonald et al (2).
The paper begins by discussing one reason why, from an historical standpoint, potassium deficiency is so common:
“Humans evolved ingesting a potassium-rich, sodium-poor diet, and mechanisms developed to retain sodium and excrete potassium. The sodium-rich diet of modern humans produces sodium overload and potassium depletion. Hypokalemia contributes to the pathogenesis of cardiovascular disease, and many cardiovascular disorders and drugs aggravate hypokalemia. Hypokalemia is therefore a common, reversible factor in the natural history of cardiovascular disease.”
The next quote I would like to feature discusses the specific role of potassium in arrhythmia:
“Hypokalemia causes cellular hyperpolarity, increases resting potential, hastens depolarization, and increases automaticity and excitability. Because cardiac repolarization relies on potassium influx, hypokalemia lengthens the action potential and increases QT dispersion (reflecting electrical inhomogeneity). Hypokalemic ventricular ectopy is suppressed by potassium replacement. Thus, hypokalemia increases risk of ventricular arrhythmia and sudden cardiac death.”
By now, I would assume that many of you may be wondering “Why hasn’t Jeff yet mentioned magnesium?” Believe me, before this series is over, you will see reviews of several papers on the subject of magnesium and CVD for several reasons, probably the most important of which is that potassium must be accompanied by magnesium to perform many, if not most, of its most important intracellular functions. Concerning the relationship between potassium and magnesium, and digoxin toxicity, Macdonald et al (2) state the following:
“Hypomagnesemia reduces intracellular potassium by reducing the membrane concentration of the sodium-potassium-ATPase pump and, thus, predisposes to digitoxicity.”
As I mentioned, there will be much more on magnesium in future installments of this series.
The next quote I would like to feature from the Macdonald et al paper (2) provides even more detail than that provided by the Kjeldsen (1) paper as to why potassium is such an important consideration when heart dysfunction becomes a crisis scenario:
“Ischemic myocardium extrudes potassium, causing hypopolarization and reducing the arrhythmic threshold. Ventricular arrhythmia aggravates the hypopolarization and further lowers the arrhythmic threshold.
Adrenaline stimulates the sodium-potassium-ATPase pump via beta2-receptors and shifts potassium intracellularly. The catecholamine surge that accompanies acute myocardial infarction (AMI) causes redistributional hypokalemia and hyperpolarizes non-ischemic myocardium, producing electrical inhomogeneity and ventricular arrhythmias. Potassium repletion abolishes these effects.”
As I hope you can see, the key point made in the above quote is that, no matter what the potassium status is from a dietary standpoint, there is a massive, detrimental change in potassium metabolism in a damaged heart that grossly alters potassium balance between the intracellular and extracellular compartments. Fortunately, the adverse impact of this imbalance can be minimized by potassium repletion.
In the next quote, Macdonald et al (2) affirm the key findings about serum potassium levels and ventricular fibrillation pointed out by Kjeldsen (1):
“Hulting et al. found an inverse relationship between serum potassium and ventricular fibrillation incidence. None occurred when serum potassium was over 4.6 mmol/l.”
The next series of quotes gives more information on correlations between heart dysfunction and various levels of serum potassium. First consider heart failure:
“In class I to III heart failure, a lower serum potassium concentration (4.1 mmol/l vs 4.4 mmol/l is an independent predictor of sudden death.”
The next quote suggests a minimally acceptable serum potassium level with heart failure:
“The evidence is persuasive that serum potassium level should be kept above 4 mmol/l in heart failure.”
The next series of quotes I would like to present concerning serum potassium levels and crisis issues relating to heart health provide a general overview:
“The data linking hypokalemia with arrhythmia and cardiac arrest in acute myocardial infarction (AMI) are fairly strong, but the direct myocardial effect of increased circulating adrenaline is a possible confounder. Despite this, it is sensible to maintain a serum potassium concentration above 4.5 mmol/l during AMI.
In heart failure, there is increasing evidence that the serum potassium level should be maintained above 4.5 mmol/l to minimize the risk of sudden cardiac death.”
How high is too high? Macdonald et al (2) state:
“It would appear wise to avoid potassium levels above 5.5 mmol/l, especially in the community, as these patients often have a degree of renal impairment and are at risk for frank hyperkalemia with dietary changes, dehydration, and intercurrent illness.”
Before concluding this review of the Macdonald et al (2) by presenting more comments on the relationship between potassium and magnesium, I want to make the point that the two papers I have reviewed are not advocating that the entire population be supplemented with potassium to keep serum levels of potassium around 4.5 mmol/l. For there certainly exist populations that appear to be maintaining reasonably good health with serum potassium levels in the high threes and low fours. However, for those patients like my father with indicators of suboptimal cardiovascular function and/or those experiencing high levels of certain types of stress that could compromise cardiovascular function (i.e., athletes), based on the research I have just presented, it may be wise to employ dietary changes and, when necessary, supplementation that will maintain serum potassium levels in the 4.5 mmol/l to 5.0 mmol/l range.
As I mentioned, to conclude my review of the Macdonald et al (2) paper, please consider these important statements about the relationship between magnesium and potassium:
“Hypomagnesemia increases potassium excretion, and hypokalemia is difficult to remedy with concurrent hypomagnesemia because the sodium-potassium-ATPase pump requires the presence of magnesium ions. Hypomagnesemia increases ventricular ectopic activity and is related to prognosis in heart failure. This may be partly due to potassium depletion. Potassium sparing diuretics prevent urinary magnesium wasting.
Hypomagnesemia should be remembered as a cause of refractory hypokalemia”
Before closing, please note the last sentence in the above quote again. If low serum potassium levels are not rising with potassium supplementation, consider concurrent use of magnesium supplementation.
In part II of this series I will review still more research on this interesting, important, and vastly under-appreciated relationship between potassium status and adverse cardiac events.
Moss Nutrition Report #258 – 08/01/2014 – PDF Version
- Kjeldsen K. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 2010;15(4):e96-e9.
- Macdonald JE et al. What is the optimal serum potassium level in cardioavascular patients. J Amer Coll Cardiol. 2004;43(2):155-61.