Some Thoughts on Sudden Cardiac Death – Part III

In parts I and II of this series I presented the large body of research that definitively demonstrates the intimate relationship between less than optimal potassium status and cardiac dysfunction, with particular emphasis on sudden cardiac death.  Then, in part II I presented the disturbing research that makes it clear that many prescription diuretics, the use of which is growing significantly in our society, can make a major contribution to low serum potassium levels (hypokalemia).  However, even though diuretic usage is high, can diuretic use alone explain the significant incidence of potassium depletion and its potential adverse impact on cardiac health?  I would guess no.  Why?  Of course, as nutritionists, our first and most logical answer to this question would be poor dietary intake.  Given that potassium is primarily found in fresh, whole foods and green, leafy foods in particular, it cannot be denied that this suggestion has merit in a society that has a massive rate of refined food intake.

Could use of certain diuretics and chronically low potassium intake alone create a crisis such as sudden cardiac death?  As I have suggested in previous installments, I feel the answer is no.  For, I am of the opinion that something else has to also happen to take someone from low grade, chronic, long-term illness that might be caused by factors such as diuretic use and poor diet to a life-threatening crisis situation.  In this installment I would like to discuss several studies that make it clear that many factors that are commonplace in today’s modern life could, unbeknownst to many, in literally, “a blink of an eye,” create this “something else” that transforms a chronically low potassium scenario that leads to long-term but survivable ill-health to a low potassium mortality crisis.

Before delving into those studies, though, I feel it is important to discuss again a key point made in part I of this series about exactly how this “something else” works to create a potassium crisis.  In “Hypokalemia and sudden cardiac death” by Kjeldsen (1) the following is stated:

“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.”

In this quote, that “something else” I mentioned above is described very precisely in the last four lines.  What this means, in simpler terms, is that when catecholamine or insulin production is enhanced, or when catecholamine receptors are stimulated, potassium stores are shifted from the plasma and other extracellular compartments to intracellular stores.  While our first response might be to think that this is good based on an assumption that the higher the intracellular content the better, in the case of key electrolytes this assumption is tragically flawed.  For, in the case of fluid and electrolytes, balance between the extra- and intracellular compartments is crucial.  Therefore, in contrast, as suggested by Kjeldsen (1), any sudden shift of potassium that leads to lower plasma levels and increased intracellular levels can lead to sometimes life-threatening outcomes.  Furthermore, as I reported in the first installment, MacDonald et al (2) strongly suggest that for some higher risk individuals even serum potassium levels below 4.5 mmol/l, which is way above the generally accepted low cut-off point of 3.5 mmol/l for serum potassium, can create considerable cardiac risk.

As we all know, there exists a whole host of substances in the diet of the average American that can either increase insulin or catecholamine production or stimulate catecholamine receptors.  Of course, when we typically think of these substances, we tend to associate them in terms of issues such as obesity, fatigue, anxiety, sleeplessness, etc.  What I am suggesting now is that we need to expand our concern about these substances from the classic chronic illness situations mentioned above to include risk of crisis scenarios caused by relatively sudden changes in extracellular/intracellular potassium ratios.


Before discussing the common dietary substances that can lead to extracellular/intracellular potassium imbalances, I would like to address a common misconception.  Many in the allopathic community and even the nutritional community are of the opinion that electrolyte imbalances that pose a significant threat to health or life are relatively rare and are seen almost exclusively in hospitalized, acute care situations.  As pointed out by Liamis et al (3) in “Electrolyte disorders in community subjects: Prevalence and risk factors” this assumption is incorrect:

“In hospitalized patients, electrolyte disorders are often acute and severe, which may explain poorer outcomes.  In recent years, however, it has become clear that chronic and mild electrolyte disorders also are associated with adverse outcomes, including in the general population.”

The authors go on to point out the following in their examination of the prevalence of hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia:

“The principal results indicate that electrolyte disorders are common in community-dwelling subjects aged 55 years or more, with approximately 1 in 6 subjects having at least 1 electrolyte disorder.”

Furthermore, Liamis et al (3) emphasize that even if the electrolyte disorders are not severe, health consequences can still occur:

“…a number of recent studies suggest that even mild electrolyte disorders can have adverse outcomes in the long term.”

With this evidence in mind, it would serve all of us well as health care professionals to take electrolyte imbalances more seriously than we have in the past.  In turn, I would now like to discuss what I consider to be a major cause of hypokalemia and other electrolyte imbalances that is not only incredibly relevant to a society that has experienced a massive increase in refined carbohydrate intake in the last 10-20 years but has been incredibly under-appreciated: refeeding syndrome.


Before presenting a series of quotes from papers describing the refeeding syndrome, I would like to present a very brief overview of what it is, its history, and its pathogenesis.

What is it?

It is a series of adverse health outcomes, which can include cardiac dysfunction, that occur when feeding an individual, who has not eaten for several hours or longer, a meal, particularly a meal that is high carbohydrate.

In whom does it occur?

The refeeding syndrome was first discovered during World War II when Allied troops started giving food to prisoners of war who had been experiencing starvation for a prolonged period of time.  It was noticed very often upon feeding that these prisoners would become violently ill.  Subsequently, similar outcomes were seen in other populations experiencing a very low calorie intake.  The period of low caloric intake can be just a few hours as might occur in a trauma/critical care patient who has been unconscious or a prolonged period of time as might occur with anorexia, fad diets, and the elderly.


After a period of very low or non-existent caloric intake, energy production shifts to non-insulin-mediated forms of energy production such as gluconeogenesis and production of lactate (The Cori cycle).  After food ingestion, energy production shifts to insulin-mediated forms of energy production.  Of course, in healthy individuals experiencing regular cycles of eating at meals and not eating between meals, there exists an optimal balance between insulin production levels, insulin-mediated energy production, and non-insulin mediated energy production.  However, when ingesting a meal, particularly a meal high in carbohydrate after a period of several hours or longer when little or no food has been ingested and non-insulin mediated energy production is predominant, rapid increases in insulin production (hyperinsulinemia) can occur.

As we all know, hyperinsulinemia promotes glucose uptake into the cell.  What is less well known is that insulin promotes intracellular uptake of many other factors such as protein, fat and, most importantly in the context of this discussion, electrolytes.  The key electrolytes involved in this massive and rapid insulin-mediated shift to inside the cell are magnesium, phosphate and, as you might expect, potassium.  In turn, plasma levels experience an equally massive decrease with the resultant extracellular/intracellular imbalance potentially leading to a whole host of health issues including possibly lethal cardiac events.


With the above overview in mind, please consider the following review of three papers that discuss details about the exact nature of refeeding syndrome and its clinical significance.  The first paper, for me, is the most important because it helps to dispel one of the greatest misconceptions about refeeding syndrome that is largely responsible for keeping this incredibly important clinical phenomenon mired in obscurity.  What is this misconception?  Because refeeding syndrome was initially discovered in very sick individuals such as prisoners of war and crisis care hospitalized patients, it has been assumed that it is not a concern for the outpatient population we see in our practices.

As suggested by the title by Obeid et al (4), “Refeeding and metabolic syndromes: two sides of the same coin,” by virtue of the fact it is very similar to the metabolic syndrome, it is actually quite common, albeit in a less severe form, in the general population.  The first quote I would like to present from this paper states the classic definition of refeeding syndrome:

“Refeeding syndrome represents a group of metabolic and clinical changes that occur in severely malnourished patients undergoing aggressive nutritional support.  Metabolic changes include: hypophosphatemia, hypokalemia, hypomagnesemia, sodium retention and hyperglycemia.”

The next quote presents in great detail the pathophysiology of refeeding syndrome that I summarized above:

“The pathophysiology of refeeding syndrome is related to the fact that under conditions of starvation, the body shifts from carbohydrate to fat and protein utilization (state of catabolism) to produce glucose and energy.  Therefore, malnutrition, which usually exists in different disease states including cancer, Marasmus/Kwashiorkor, neurological problems, respiratory diseases, gastrointestinal and liver diseases, and so on, is the major risk factor for refeeding syndrome.  Upon refeeding, especially with carbohydrate, the body shifts back instantaneously to carbohydrate metabolism (state of anabolism).  Concomitantly, insulin secretion is increased leading to an increase in the cellular uptake of glucose and macrominerals (in particular phosphorus, potassium and magnesium) mainly occurring in the liver and muscles, and thus resulting in hypophosphatemia, hypomagnesaemia and hypokalemia.  Simultaneously, insulin resistance prevails as indicated by the coexistence of hyperglycemia and hyperinsulinemia, which reduces sodium clearance leading to sodium retention and thus resulting in fluid retention and expansion of the extracellular fluid volume.  Thus, the clinical manifestations of these macromineral abnormalities have serious deleterious effects, some of which are hypotension, bradycardia, weakness, heart failure and arrhythmias.  In brief, refeeding syndrome is the consequence of the ingestion of a high carbohydrate-low macrominerals diet following prolonged fasting.”

In particular, I want to emphasize the last sentence of the above quote because it crystallizes the idea that refeeding syndrome is so much more than an obscure phenomenon seen only in hospitals and refugee camps.  How many patients do we encounter everyday who ingest meals high in carbohydrate and low in macrominerals such as potassium and magnesium after skipping meals for several hours during a busy, hyperactive day?  In addition, how often do we hear from these patients that they experience a whole variety of symptoms after a period of binging on carbs after skipping meals?  While the symptoms they typically experience have been classified under many descriptors that include terms such as “reactive hypoglycemia,” in fact they were experiencing refeeding syndrome to varying degrees.  Therefore, even though the term “refeeding syndrome” might not be familiar to you, there is little doubt that you have encountered it, often in minor forms, when dealing with patients who skip meals and engage in a diet high in refined carbohydrates.

The next quote I would like to feature from the Obeid et al (4) paper provides more detail on how macromineral physiology is affected by meal timing and macromineral content:

“In normal subjects and under normal conditions, energy metabolism is known to fluctuate diurnally, as meal ingestion causes a shift to carbohydrate metabolism and an increase in both energy expenditure and carbohydrate oxidation.  Meal ingestion ensues an increase in cellular uptake and utilization of glucose and macrominerals (predominantly phosphorus, potassium and magnesium), as a result of increased insulin secretion and demand for metabolic processes (for example, phosphorylation and so on).  Therefore, plasma status of these macrominerals depends on insulin secretion (that is highly dependent on carbohydrate intake) and their meal content of macrominerals.  Ingestion of pure glucose is known to be associated with a reduction in plasma concentration of these macrominerals and their inclusion in a meal was reported to improve their status.”

As you can see, the above quote makes it clear that intracellular and extracellular ebbs and flows of key minerals such as potassium is heavily dependent on meal timing and the meal content not only of the minerals but carbohydrate.  With this concept in mind, refeeding syndrome is not an isolated, pathologic entity but a scenario where normal macronutrient/macromineral physiology has been pushed to an unacceptable metabolic extreme generally due to a combination of poor diet and poor eating behaviors.

With this interpretation of refeeding syndrome in mind, the authors state:

“Thus it is reasonable to postulate that under normal conditions the postprandial metabolic changes following ingestion of high carbohydrate-low macrominerals diet resemble those of the refeeding syndrome but to a lower extent.”

The last quote I would like to present from the Obeid et al (4) paper brings up an interesting twist on what has been discussed above.  As was mentioned, diet induced insulin imbalances can have a major adverse impact on potassium metabolism.  Could the reverse be true where potassium deficiency create disturbances in insulin metabolism?  According to the following quote, the answer is yes:

“…potassium depletion resulting from a low potassium diet impairs insulin secretion, which in turn induces glucose intolerance.  Similarly, another study by Dluhy et al. found that the potassium ion is involved in regulating or augmenting the secretion of insulin in humans.  Resnick et al. further confirmed that potassium deficiency is a common feature involved in essential hypertension as well as in type 2 diabetes.”


Virtually all the literature on refeeding syndrome refers to the electrolyte imbalances created by sudden refeeding in terms of what was discussed above – increases in intracellular concentrations and decreases in extracellular concentrations.  In terms of creating ill health, though, is refeeding the sole inducer of the problem or is it making a bad situation worse, i.e., “the straw that breaks the camel’s back?”  Of course, a portion of this question has already been answered in that refeeding syndrome follows a period of suboptimal diet where key electrolytes are deficient.  However, could the biochemistry and physiology created by long term ingestion of a low calorie, low macro- and micronutrient diet actively lead to whole body depletion of potassium and other key electrolytes that exacerbates the problems caused by suboptimal intake?  According to two papers on the refeeding syndrome, this is exactly what happens.  In “Hypokalemia during the early phase of refeeding in patients with cancer” by Grasso et al (5) the following is stated:

“…it is well known that glucose levels decline with starvation or under conditions of carbohydrate restriction.  Consequently, non-carbohydrate sources (muscle proteins) are metabolized into glucose.  In addition, in the hepatocytes, fatty acid oxidation can generate ketone bodies via the Krebs cycle.  Under this condition, there is significant depletion of potassium, phosphate and magnesium, as well as losses of body fat and protein mass.”

In agreement, the following is stated by Viana et al (6) in “Refeeding syndrome: Clinical and nutritional relevance”:

“It has been established that, in fasting, insulin secretion is reduced and glucagon concentrations are increased.  Fat and protein stores are mobilized to be transformed into energy via gluconeogenesis.  Adipose tissue provides large amounts of fatty acids and glycerol as the muscular tissue degrades to provide amino acids.  In these circumstances ketone bodies and free fatty acids replace glucose as the major energy source.  This mobilization of energy results in loss of body mass and loss of intracellular electrolytes, particularly phosphate buffer…despite normal plasma concentrations.”

Therefore, as I hope you can see, in your patients who ingest a meal high in carbohydrate after a significant period of eating little or no food, or in those patients whose long term diet consists of skipping meals and then ingesting large amounts of carbohydrate laden foods, a “perfect storm” of sorts is created.  In this “perfect storm,” the electrolyte imbalances created by not eating combine with the electrolyte imbalances created by sudden eating.  This, in turn, can potentially lead to the creation of health issues that can range from the subtle changes seen with “reactive hypoglycemia” all the way to a cataclysmic cardiac event.


Beyond issues of suboptimal electrolyte metabolism, there exist other important clinical considerations in terms of recognition and management of these patients.

Patient demographics

While refeeding syndrome can be seen in almost anyone who ingests high carbohydrate meals after skipping meals for a significant period of time, there are certain groups of patients who tend to experience it more often, as noted in the quote below from the paper “The importance of the refeeding syndrome” by Crook et al (7):

“The total incidence of the refeeding syndrome has been put at as high as about 25% in cancer patients who are nutritionally supported.  That study also reported that the syndrome was more common in those fed enterally than parenterally and tended to manifest in the first few days after commencement of feeding.  Further, it is more common in the elderly, although mortality figures per se are difficult to establish accurately because patients often have other underlying disease states.”

In particular, please notice again in the above quote that refeeding syndrome can occur in cancer patients who are being nutritionally supported.  As we all know, sometimes well-meaning practitioners, family and friends of cancer patients can sometimes be quite aggressive in their dietary recommendations, particularly for those cancer patients who are fatigued and have experienced significant weight loss.  Therefore, if you see a cancer patient who starts to experience any of the symptoms mentioned below after following aggressive dietary recommendations, you may want to advise the patient to switch to the less aggressive dietary regimen to be discussed in the section that follows on management of refeeding syndrome. 

Typical symptoms

Since laboratory measurements of electrolytes are not always readily available in outpatient clinical practices such as ours, what are the typical symptoms seen in a patient experiencing refeeding syndrome?  Unfortunately for us, most papers on the subject only discuss the extreme symptomatology seen with hospitalized patients in surgical or trauma situations or experiencing gross starvation.  However, the quote below from “Refeeding syndrome: A literature review” by Khan et al (8) discusses the wide range of presentations based on refeeding syndrome severity:

“Symptoms of refeeding syndrome (RFS) are variable, and may occur late.  Symptoms occur because changes in serum electrolytes affect the cell membrane potential impairing function in nerve, cardiac, and skeletal muscle cells.  The variable clinical picture in RFS reflects the type and severity of biochemical abnormality present.  With mild derangements in these electrolytes, there may be no symptoms.  More often, the spectrum of presentation ranges from simple nausea, vomiting, and lethargy to respiratory insufficiency, cardiac failure, hypotension, arrhythmias, delirium, coma, and death.  Clinical deterioration may occur rapidly if the cause is not established and appropriate measures not instituted”

Most likely, in the low-grade refeeding syndrome we tend to see in our practices, the most common symptoms after ingesting a high carbohydrate meal after several hours of not eating will be GI disturbances such as indigestion or nausea, fatigue, rapid heartbeat and/or heart palpitations, and behavioral disturbances that many include anxiety or depression.

Other nutrient deficiencies seen with refeeding syndrome

Just as important as recognizing the electrolyte deficiencies and imbalances that are induced by refeeding syndrome is the recognition of other micronutrients that are adversely affected.  In particular, ingesting high carbohydrate meals after a period of not eating as seen with refeeding syndrome has a very disturbing impact on thiamin status.  However, before discussing the thiamin situation specifically, please note the following quote from the paper “Refeeding syndrome: Treatment considerations based on collective analysis of literature case reports” by Boateng et al (9) that provides a general overview of the impact of refeeding syndrome on micronutrient status:

Vitamin deficiency results from the rapid depletion of vitamins after onset of refeeding due to their role in various biochemical functions.  For example, thiamine is necessary for glucose metabolism but its stores are depleted during starvation.  Sudden introduction of glucose drives already depleted thiamine stores to a nadir, precipitating Wernicke’s encephalopathy and lactic acidosis.

Trace element deficiency also results from increased enzymatic activity during the anabolic process.  For example, the importance of trace elements such as zinc and selenium as functional components of many enzymes involved in DNA/RNA metabolism and oxidative-reduction processes is well known.”

As I mentioned above, rarely will we encounter patients experiencing gross starvation, making the chances of seeing Wernicke’s encephalopathy in our patients highly unlikely.  However, as I also mentioned above, it is very likely that our many patients who skip meals and then ingest high carbohydrate snacks and meals will experience a low-grade form of refeeding syndrome that occurs in combination with a long-term pre-existing micronutrient deficiency due to poor diet in general.  This potent mix makes thiamine and trace element deficiency a real possibility in this population.

What can be stated about thiamine and refeeding syndrome specifically?  Please note the following from Boateng et al (9):

“Thiamine is a component of several enzymes of the tricarboxylic acid cycle in glucose metabolism in man.  Deficiency in thiamine also causes a buildup of pyruvic and lactic acids and can lead to fatal metabolic acidosis, making monitoring thiamine levels an essential role in the management of RFS.”

Of course, as I have been suggesting, it is unlikely that our patient population will encounter potentially fatal thiamine deficiencies.  Therefore, ongoing monitoring of thiamine levels, given the cost and inconvenience, is not necessary.  However, in my opinion, it would be wise, due to the low cost and low risk of adverse effects, to recommend a B complex supplement to any patient you feel may be at risk for experiencing any level of a refeeding syndrome scenario.


As you might expect, since refeeding syndrome is brought on by rapid refeeding of primarily carbohydrate-based foods, the key factor in prevention and treatment of refeeding syndrome is slow increases in caloric content of a high quality, balanced, whole food diet with, as you will see in the following quote, emphasis on optimal intake of protein.  As you will also see, this quote from the paper by Crook et al (7) makes it very clear that increases in caloric intake should be much slower than we might intuitively suspect:

“The calorie repletion should be slow at approximately 20 kcal/kg per day or, on average, 1000 kcal/d initially.  However, this rate may not meet patients’ fluid, sodium, potassium, or vitamin requirements unless these are specifically addressed.  The usual protein requirement is about 1.2 to 1.5 g/kg or about 0.17 g of nitrogen/kg per day.  Gradual introduction of calories, particularly over the first week of refeeding, may be prudent until the patient is metabolically stable.”

Khan et al (8) suggest, after 2-4 days from the onset of therapy, to increase caloric intake by 5 kcal/kg/day.  Then, after 5-7 days from the onset of therapy, increase caloric intake to 20-30 kcal/kg/day.  Finally, at days 8-10 it will probably be safe to increase caloric intake to usual optimum levels.  Concerning micronutrient supplementation, Khan et al (8) recommend a B complex supplement 30 minutes before meals and potassium and magnesium supplementation.


Next I would like to present a published case report on the type of patient we might see in our practices who would be likely to present with refeeding syndrome, in this case an elderly patient who has just completed chemotherapy.  While, as you will see from the lab values, she is sicker than the usual patient we might typically encounter, her case gives you some idea how refeeding syndrome might present to you.  The case report comes in the form of a letter to the editor entitled “Hydroelectrolytic disorders secondary to refeeding syndrome” by Macias-Toro et al (10).  The first quote I would like to present describes how the patient initially presented:

“We report the case of a 70-year-old female with high blood pressure and endometrial adenocarcinoma diagnosed in 2010, who was treated with hysterectomy, chemotherapy and pelvic radiation therapy.  About a month after completing chemotherapy, she was admitted with febrile neutropenia, ileal enteritis and E. colibacteraemia.  Tests highlighted severe leukopenia (0.22×109/l, 0 neutrophils), creatinine 70.2 mmol/l, sodium 139 mmol/l, potassium 3.74 mmol/l, serum calcium 2.45 mmol/l, serum phosphate 1.2 mmol/l, metabolic acidosis (pH 7.27, pCO2 45 mm Hg, bicarbonates 20.7 mmol/l) and hypoalbuminaemia (32 mg/l).”

Initial treatment included bowel rest, IV fluid therapy, antibiotics, and granulocyte colony-stimulating factor.  On the third day parenteral feeding was introduced of 1500 kcal/day.  Twenty-four hours later the following was noted:

“After 24 hours, she presented neurological symptoms with generalized tremors, hyperreflexia, Chvostek and Trousseau signs, peripheral oedema and QTc prolongation on electrocardiogram.  Tests highlighted hypocalemia (1.6 mmol/l-1.76 albumin-corrected), hypomagnesaemia (0.45 mmol/l), hypophosphataemia (0.68 mmol/l), hypokalaemia (2.59 mmol/l), normal renal function and acid-base balance with pH 7.41, pCO2 31 mmHg, pO2 48 mmHg and bicarbonate 19.6 mmol/l.  Given the temporal relationship with the start of parenteral nutrition, refeeding syndrome was suggested as the clinical profile.”

Before continuing, please notice again how much the serum potassium dropped in just 24 hours (From 3.74 mmol/l to 2.59 mmol/l).

The next two quotes provide the authors’ interpretation of how refeeding syndrome expressed in this patient and how it was resolved:

“After refeeding, nutrient availability generated increased levels of insulin with the subsequent introduction of phosphorus, potassium, magnesium and thiamine intracellularly, used to reactivate the glycolysis process.  These components decreased rapidly in plasma, which added to metabolic and water overload in a depressed baseline myocardium, producing serious clinical consequences.”

Macias-Toro et al (10) continue:

“Our case dealt with a patient with multiple comorbidities, cancer, with a high risk of suffering RFS, who started parenteral nutrition with standard caloric intake, which resulted in hypophosphataemia, hypokalaemia, hypomagnesaemia (secondary hypocalcaemia) and hypervolaemia, with neurological consequences and electrocardiography repercussions.  Caloric intake decreased to 1000 kcal per day (but did not stop) as well as the volume of intravenous fluid therapy.  Corrective treatment of the electrolyte imbalances was started and thiamine supplements were administered, with improvement of neurological symptoms, peripheral oedema and correction of electrolyte imbalances.”


While the next case report I am going to review is not a classic refeeding syndrome presentation, it does show how an extreme diet used to promote weight loss can create potassium depletion with resultant fatal cardiac dysfunction.  The case report is entitled “Sudden cardiac death of an adolescent during dieting” by Stevens et al (11).  The first quote describes the initial patient presentation:

“Emergency teams were summoned to a local high school to care for a 16-year-old girl who had suddenly collapsed.  She was 5 feet 8 inches tall and weighted approximately 80 to 85 kg (176-187 lb).  The patient had been in good health with no known history of medical problems.  She had started a low-carbohydrate/high-protein diet 1 or 2 weeks earlier in an effort to lose weight.  She had learned about the diet from video tapes, purchased from an advertisement on television.  Her mother had been on the same diet.  She had complied with the dietary regimen, eating meat, cheese, and salads without fasting.  When the paramedics arrived, the girl was pulseless and apneic.  The electrocardiogram revealed ventricular fibrillation.  The patient’s trachea was intubated and cardiopulmonary resuscitation was initiated.  Resuscitative measures, including defibrillation, were without effect.  On arrival in the emergency department, the patient remained pulseless, with no evidence of cardiac activity.  Arterial blood gas analysis revealed a pH of 6.89, with a base deficit of -19.8.  Other laboratory values were serum sodium 142 mEq/L, ionized calcium 1.12 mEq/L, and serum potassium 3.8 mEq/L.  Further resuscitative efforts were without effect.  Postmortem and toxicologic examinations revealed no apparent cause for the death.  Subsequent cardiologic evaluation of the patient’s 12-year-old sibling including echocardiography and electrocardiography was within normal limits.”

Unfortunately, as we all well know, we have heard about way too many cases during the last few years of teenagers suddenly dying from a heart attack with no reason given.  Is this just another case that fits this pattern?  According to the authors, no.  They feel that the diet could have induced low serum potassium and cardiac arrest, as noted in the following quote:

“The potential role of the dietary regimen as a contributing factor to the hypokalemia and subsequent cardiac arrest are discussed.”

How severe was the hypokalemia?  Stevens et al (11) state:

“During resuscitation, with a pH of 6.89, the serum potassium level was 3.8 mEq/L, suggesting profound hypokalemia if corrected for the pH.”

In addition, the authors feel that low serum magnesium, which is often seen with low serum potassium, may have also led to cardiac arrest:

“Because potassium and magnesium undergo similar handling mechanisms in the renal tubules, hypomagnesemia is another potential cause of our patient’s cardiorespiratory arrest.”

With the above in mind, Stevens et al (11) suggest:

“When considering the potential causes of these electrolyte disturbances in an otherwise healthy female adolescent, questions arise regarding the potential role of the low-carbohydrate/high-protein diet compounded by a period of inadequate caloric intake and the resultant catabolic state.”


As I hope you can see, serious health consequences induced by suboptimal potassium status are not just seen in the acute, intensive care settings of hospitals.  Rather, they can very well occur in your patients and loved ones, sometimes due to lifestyle and dietary imbalances that, all too often, we do not take seriously enough.  While I am not saying everyone you see who binges on carbs after a period of no food or employs the Atkins diet is going to suffer a life-threatening heart attack, I do feel that we need to start giving lifestyle and diet-induced alterations in potassium status a much higher priority, both diagnostically and therapeutically, then we traditionally have in the past.

In part IV of this series, I will present still more research suggesting that common illnesses and lifestyle indiscretions that we sometimes take for granted can have serious implications in terms of both potassium status and overall health.          

Moss Nutrition Report #262 – 04/01/2015 – PDF Version


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