QJM Advance Access originally published online on March 10, 2005
QJM 2005 98(4):305-316; doi:10.1093/qjmed/hci046
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Masterclasses in medicine |
An approach to the patient with severe hypokalaemia: the potassium quiz
From the 1Department of Nephrology, Leiden University Medical Center, The Netherlands, 2Renal division, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan (ROC), 3Nephrology Unit and Department of Internal Medicine, Stellenbosch University, Cape Town, South Africa, and 4Division of Nephrology, St. Michael's Hospital, University of Toronto, Toronto, Canada
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Summary |
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 Top Summary IntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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The objective of this teaching session with Professor McCance is to develop an approach to the management of patients with a very low plasma potassium (K+) concentration (PK). The session begins with a quiz based on six recent medical consultations for a PK < 2 mmol/l. Professor McCance outlined how he would proceed with his diagnosis and therapy, using the synopsis that described each patient. This approach was then applied to a new patient, a 69-year-old woman who had a large volume of dependant oedema and developed a severe degree of weakness and hypokalaemia during more aggressive diuretic therapy that included a K+-sparing diuretic. The initial challenge for Professor McCance was to deduce why the K+-sparing diuretic was not effective in this patient. He also needed to explain why the PK was so low on admission.
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Introduction |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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In this clinical teaching exercise, the central figure is Professor McCance, an imaginary consultant who practiced medicine
70 years ago. The overall objective is to demonstrate how applying principles of integrative physiology at the bedside can be extremely helpful in revealing the pathophysiology of disease, making more accurate clinical diagnoses, and to plan optimal therapy. |
The consultation |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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When the medical registrar received the first referral of the day, she was surprised that it was another request to evaluate a patient who had a very low plasma potassium (K+) concentration (PK). ‘There seems to be an epidemic of hypokalaemia’, she mused, because their team had seen six patients with a similar reason for a medical consult that year.
In the present consultation, the patient is a 69-year-old woman with a medical history of Parkinson's disease, hypertension and a large volume of dependent oedema. She had normal plasma electrolyte concentrations before her diuretic therapy was doubled to thiazide 50 mg/day and triamterene 25 mg/day. With this change, she developed severe hypokalaemia. None of her other medications was likely to influence her PK. In the first two weeks after this increase in diuretic therapy, there was a marked decrease of oedema fluid, but she felt very weak and had a decrease in appetite. On examination in the emergency department, her blood pressure was only 110/60 mmHg, and she had obvious muscle wasting. Laboratory testing revealed hypokalaemia (PK 1.7 mmol/l), metabolic alkalosis (pH 7.54, plasma bicarbonate (
) concentration (PHCO3) 43 mmol/l), and an urine K+ concentration (UK) of 36 mmol/l (Table 1).
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Knowing that they would meet Professor McCance on rounds the next morning, the registrar asked one of the interns to prepare a synopsis of the six recent cases with severe hypokalaemia and present it to their Professor as a diagnostic challenge. In their minds, he was the ultimate ‘clinical detective’ and would no doubt relish the opportunity to grapple with these interesting cases. As to their current case, they had one major question for their Professor, ‘Why might renal K+ excretion be so high while on a K+-sparing diuretic?’
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On rounds the next day with professor McCance |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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The medical team was eager to discuss the present consultation as well as learn how their Professor would respond to the ‘K+-quiz’ (Table 2). ‘Would he have any difficulty matching the case vignettes with their list of possible diagnoses?’ they wondered. They would soon discover that generic approaches, while useful as a guide, could not replace a deductive and thorough interpretation based on integrative physiology for each individual case.
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Professor McCance stood at the blackboard with chalk in hand—the focus was on the K+-quiz. Because he loved problem-solving, he immediately accepted the challenge. He knew that while simply matching the cases with the diagnoses might be entertaining, it would be of little benefit to his younger colleagues, and he was never one to miss a good teaching opportunity. Rather, illustrating a physiology-based approach would be a better way to proceed. Changing the rules of the game somewhat, he announced that he would solve the puzzle while developing a diagnostic algorithm, and invited them to assist in this task.
The initial difficulty in designing a flow chart is to define a rational starting point. The first question should address potential emergencies for the patient, said Professor McCance (Flow Chart 1). Accordingly, he began by asking, ‘What are the major dangers faced by a patient with an extremely low PK?’
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Question 1. What are the major dangers faced by a patient with an extremely low PK?
Physiology principle 1. There are two factors that can influence the movement of K+ across cell membranes, the driving force which is the electrical voltage across cell membranes, and the presence of open K+ channels.1 The ratio of K+ concentrations in the ICF and ECF compartments reflects this electrical driving force.
Return to the bedside. The major problem for a patient with an abnormal trans-membrane voltage is when it affects the heart because life-threatening cardiac arrhythmias can develop. This possible threat is best evaluated by examining the EKG. A second issue for an extreme degree of hypokalaemia is weakness of the respiratory muscles, especially if there is a need for increased ventilation (e.g. metabolic acidosis).
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A. Patients with a low rate of excretion of K+ |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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At this point, the intern stated that there was no emergency demanding urgent therapy in any of their cases because only ‘U’ waves were seen on the EKG, there was no apparent respiratory muscle weakness, and the arterial PCO2 was not unduly high. Therefore Professor McCance proceeded with diagnostic issues, because this would reveal the goals for therapy. For example, if a shift of K+ into cells were the most important cause for hypokalaemia, the goal of therapy would be to reverse this shift without causing a large negative balance for K+. In contrast, if the low PK were due primarily to a large total body deficit of K+, the major goals for therapy would be to decrease K+ loss and to replace the deficit of K+, typically with a large input of potassium chloride (KCl). Because the PK is so low, he asked, ‘Which patients are more likely to have a major shift of K+ into cells?’
Question 2. Which patients are more likely to have a major shift of K+ into cells?
Physiology principle 1, restated. The driving force to cause a K+ shift into cells is a more negative voltage in cells; this is created by the net export of positively charged ions (Figure 1). If a more negative intracellular fluid (ICF) voltage were the only defect, one should have hypokalaemia with few other biochemical abnormalities.
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The nephrology consultant explained that the Na-K-ATPase pumps positive voltage out of cells; it extrudes three sodium ions (Na+) for every two K+ ions that enter cells2,3 (Figure 1). The main hormones that increase the activity of this Na-K-ATPase are ß2-adrenergic agonists and thyroid hormone.4 There is a second way to pump more Na+ out of cells without activating the Na-K-ATPase per se: increase in the concentration of Na+ in cells. The mechanism begins when Na+ ions enter cells in an electroneutral fashion; this is achieved by activating the Na+/H+ exchanger (NHE) in cell membranes, a transporter that is normally inactive in cell membranes unless insulin levels rise appreciably (Figure 1).5 This helps to prevent hyperkalaemia when K+ is ingested in food that also contains sugar.
With that important background information, the team had no problems responding to McCance's next question: ‘What features on clinical presentation suggest that the sole basis for a very low PK might be a shift of K+ into cells?'
Question 3. What features on clinical presentation suggest that the sole basis for a very low PK might be a shift of K+ into cells?
Physiology principle 2. There is a very large quantity of K+ in cells (50 mmol/kg body weight), and the rate of K+ excretion can decline to 0.2 mmol/kg/day when the PK begins to fall. Therefore it will usually take many months of poor K+ intake to be the sole cause of a very low PK. In addition, if the PK falls in a much shorter time, look for a cause other than just a low K+ intake.
Return to the bedside. While not always reliable, the first clue to suggest that the basis for a severe degree of hypokalaemia is a shift of K+ into cells is its timing—did it occur in a matter of hours, rather than days, weeks or months? If the answer is yes, suspect that there is an important component of K+ shift into cells. This impression could be supported if the patient was also suffering from acute paralysis.
When acute hypokalaemic periodic paralysis (HPP) is suspected, there are a number of other supporting facts to help in this regard.6 It is common to find provoking factors such as a high carbohydrate meal (high insulin levels activate NHE and the Na-K-ATPase) and vigorous exercise (ß-adrenergic agonists activate Na-K-ATPase). It is particularly important to look for clinical evidence of hyperthyroidism, including a wide pulse pressure and tachycardia. The helpful laboratory data suggestive of HPP are a low rate of excretion of K+ and the absence of an acid-base disorder.6 More detailed information is provided in Table 3.
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Because a low rate of excretion of K+ is so important in this differential diagnosis and it is readily obtained from simple laboratory tests, the initial step McCance used to construct Flow Chart 2 was to divide patients into two major pathophysiological groups, based on their current rate of excretion of K+. It is not necessary or desirable to wait for a timed urine collection for this purpose; the same information can be obtained by comparing the UK to the concentration of another urinary constituent that is excreted at a constant rate, such as creatinine (UCreatinine).7 ‘The index I use to assess the K+ excretion rate is the UK/UCreatinine ratio’, said Professor McCance. ‘Patients with a very low K+ excretion rate (
10–15 mmol/day8) and a creatinine excretion rate of 10–15 mmol/day should have a UK/UCreatinine that is <1.5 in mmol terms, or 15 in UK /g UCreatinine for those who use decadent units for creatinine’, he said with a smile. There is a caveat when using this UK /UCreatinine ratio: because creatinine is derived from skeletal muscle, one must make an adjustment in patients who have a very low or very high muscle mass.9 Before leaving this topic, a member of the medical team asked, ‘Might a patient develop a very low PK without having a shift of K+ into cells or a high UK /UCreatinine?’
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Question 4. Might a patient develop a very low PK without having a shift of K+ into cells or a high current UK /UCreatinine?
Physiology principle 3. Be certain that the data you examine represent steady state values, so that they can be interpreted correctly in a chronic condition.
Return to the bedside. ‘If I do not have to consider a shift of K+ into cells, let me turn my attention to settings where the excretion of K+ may be intermittent and driven at times by non-physiological stimuli,’ said Professor McCance. If a patient were to take a drug that augmented the excretion of K+, this rate of excretion would be high when the drug acted and low when the drug was not being used. The best example of a ‘former K+ excretion’ would be the use of diuretics in the past, but not currently. Now the UK/UCreatinine should be low because the patient did not take a diuretic recently.
Return to the K+-quiz. Using the above principles, Professor McCance deduced that patient 1 had thyrotoxic periodic paralysis (TPP), whereas patient 2 had familial periodic paralysis (FPP) or spontaneous periodic paralysis (SPP).
One of the registrars pointed out that it is important to make a diagnosis of TPP because there is now a specific and effective therapy for this type of HPP. Administering a large dose of a non-specific ß-adrenergic receptor blocker (propranalol 3 mg/kg) quickly reverses both the paralysis and the hypokalaemia.10
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B. Patients with a high rate of excretion of K+ |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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All the remaining cases in Table 2 had a high UK/UCreatinine and an acid-base disorder. Professor McCance therefore turned to Flow Chart 3 and asked: ‘How should we subdivide the patients with a very low PK and a high UK /UCreatinine?'
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Question 5. What should the initial step be to subdivide the patients with a very low PK and a high UK /UCreatinine?
Physiology principle 4. The rate of excretion of K+ is dependent on two factors: the flow rate and the K+ concentration in the nephron segment that controls the secretion of K+, the cortical collecting duct ([K+]CCD, equation 1).11 The flow rate is dependent on the osmole delivery rate12 and the [K+]CCD is largely determined by the negative voltage in the lumen of the terminal CCD. This voltage is reflected by the transtubular K+ concentration ratio (TTKG).13
 | (1) |
In-depth look at the K+ secretory process in the CCD. To have a high rate of K+ excretion, one usually needs a high [K+]CCD. This occurs when a lumen-negative voltage is generated by reabsorbing Na+ ions at a faster rate than Cl– ions (Figure 2, top left side). This can occur if there is delivery of Na+ with an anion other than Cl– to the CCD, together with a stimulus to reabsorb Na+ (high aldosterone level), in conditions where ENaC is active due to a molecular lesion, or in situations where cortisol acts like a mineralocorticoid. Measuring the activity of renin and the level of aldosterone in plasma can help in this differential diagnosis (Figure 3).
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can slow the reabsorption of Cl–. ENaC, epithelial Na channel.
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The nephrology consultant added one more observation. The presence of
ions in the lumen of the CCD can cause a faster rate of Na+ than Cl– ion reabsorption, because ions may slow the rate of Cl– ion reabsorption in the CCD (Figure 2, bottom right). Professor McCance now applied this physiology of K+ excretion to the patients with an acid-base disorder: first those patients with metabolic acidosis and then those with metabolic alkalosis.
(i) Group with metabolic acidosis:
Physiology principle 5. Patients with hyperchloraemic metabolic acidosis and a high UK/UCreatinine can be separated into two groups based on their rate of ammonium (
) excretion. Those with a high rate of excretion have a non-renal, direct loss of NaHCO3 (e.g. diarrhoea14) or an indirect loss of NaHCO3 where there is production of an acid such as hippuric acid, followed by the excretion of some hippurate anions with Na+ or K+ instead of 
, Figure 4). 15 The group of patients with a low rate of excretion of has a renal defect that leads to a low rate of excretion of (called distal renal tubular acidosis or RTA).16 Professor McCance added one more clinical pearl. in the urine can be detected by its charge (urine net charge17) or as a urinary particle (urine osmolal gap18).
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Returning to the K+ quiz, Professor McCance pointed out that patient 3 had a UK/UCreatinine >1.5, and a urine that appeared to have a low
concentration, as judged from the urine electrolyte concentrations (Na+ + K+ > Cl–). Because Uosm was not appreciably higher than 2(UNa + UK) + urine urea (not shown, but inferred), her urine flow rate was not high, so the excretion rate should not be appropriately elevated.
The nephrology consultant added that the two lesions to suspect are distal RTA due to impaired H+ secretion in the distal nephron,19 or the secretion of in this nephron segment as occurs in certain patients with an abnormal Cl–/HCO3 anion exchanger.20 None of the patients had evidence suggesting a high rate of excretion (e.g. patients with diarrhoea or others who sniff glue producing hippuric acid15).
(ii) Group with metabolic alkalosis
The first question asked by Professor McCance concerned the blood pressure of these patients. His rationale was that a high blood pressure along with a high UK/UCreatinine and TTKG would suggest that its basis was faster reabsorption of Na+ via ENaC in the CCD if the patient was not receiving diuretics.
The nephrology consultant added the following comments. The list of causes include: an inborn error of metabolism that results in higher ENaC levels in the CCD; higher aldosterone levels; or settings where compounds other than aldosterone activate the mineralocorticoid receptor in principal cells of the CCD. Measuring the plasma levels of aldosterone, the activity of renin, and cortisol levels in plasma can help subdivide these patients (Figure 3). Patient 6 could have any of these lesions. The medical team supplied additional information at this point. Because this patient was elderly (age 78), had absent aldosterone and normal cortisol levels in plasma and admitted to using a large amount of liquorice to sweeten his tea, the diagnosis was liquorice abuse.21
The final diagnostic category with metabolic alkalosis is the group with a very low PK, a high K excretion rate, and the absence of hypertension. The major subgroups include the use of diuretics, vomiting or conditions that lead to a slower reabsorption of Na+ and Cl– in the loop of Henle or the distal convoluted tubule (DCT) and thereby an enhanced delivery of Na+ and Cl– to the CCD while aldosterone levels are high (lower right portion of Figure 2). In all the patients reported in Table 2, the urine was negative for diuretics when the UNa and UCl were high. In addition, vomiting, diarrhoea and laxative abuse were not present.
A word of caution is necessary at this point, warned the nephrology consultant. ‘Patients who take diuretics or those who have conditions that mimic diuretic actions such as inborn errors that compromise Na+ and Cl– reabsorption in the loop of Henle or the DCT (like Bartter's or Gitelman's syndromes) rarely have such low PK values. When present, suspect that there are other factors that either cause a low K + intake, a shift of K+ into cells and/or K+ loss by renal or non-renal routes’. He then provided a few pointers to aid in identifying the defective nephron segment.
Loop of Henle: Because this nephron segment is responsible for concentrating the urine and it is an important site for Ca2+ reabsorption, expect a low maximum Uosm and a Ca excretion rate that is not low.
Distal convoluted tubule: Disorders affecting Na+ and Cl– in this nephron segment have intact concentrating ability (unless there is a second lesion) and a low rate of excretion of Ca.9 This nephron segment is the last one that regulates the excretion of magnesium (Mg) and hypokalaemia is often accompanied by hypomagnesemia, especially later in the disease.
Based on the above, patient 5 with a modestly high Uosm (not tested after dDAVP), a low UCa/Ucreatinine, and a low PMg fits a DCT lesion.9 Patient 4 would best fit a loop of Henle lesion, if the Uosm failed to rise after dDAVP was administered. Given the age of the patient, the most likely lesion in the loop of Henle is an acquired problem such as the presence of a cation that occupies the calcium-sensing receptor (Ca-SR) on the basolateral membrane of the medullary thick ascending limb of the loop of Henle.22 Ligands that may bind to this receptor include Ca2+ (hypercalcaemia), cationic drugs such as aminoglycosides, and cationic proteins (globulins) as might be present in multiple myeloma.
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Current consultation |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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The team now turned their attention to the current consultation. Following the steps outlined in Flow Chart 1, there were no medical emergencies as judged from her clinical picture, EKG and her PaCO2. ‘There were no urine data available in the time when the PK fell, so I cannot comment on the UK/Ucreatinine’, said Professor McCance. ‘Notwithstanding, given the patient's age and therapy, I will presume that renal K+ loss was an important component of the very low PK’. Therefore I will turn to the question posed by the medical team that cared for this patient.
Why might the renal excretion of K+ so high while on a K+-sparing diuretic?
‘For a K+-sparing diuretic to be taken but not act, its effect on the kidney must be ‘amputated’’, pronounced Professor McCance. I was told that this class of diuretics should prevent the generation of a lumen-negative voltage in the CCD and thereby diminish the secretion of K+. Although there are several possibilities to do this (Figure 2), I would guess that blocking Na+ reabsorption rather than accelerating Cl– reabsorption in the CCD would be the most likely mechanism, because this class of drugs promotes the excretion of Na+ (they are diuretics). The nephrology consultant confirmed that Na+ reabsorption in the CCD occurs via a specific ion channel, ENaC and that this class of K+-sparing diuretics acts by blocking the ENaC in the luminal membrane of the principal cells of the CCD.
To block this Na+ ion channel in the luminal membrane in the CCD, it is likely that K+-sparing diuretics will resemble Na+ in some way. Compounds with an amine group have the potential of bearing a positive charge when they bind H+ (equation 2). One must also examine the pK of these compounds, suggested McCance. The nephrology consultant informed the group that because the pK of triamterene or amiloride is much higher than the luminal fluid pH in the CCD in vivo, they would always bear a positive charge and therefore compete with Na+ for entry into ENaC. In contrast, trimethoprim has a pK 7.2, so the luminal fluid pH can affect its ability to be cationic (luminal pH in the high 6–8 range). Thus, making the luminal fluid pH more alkaline by giving NaHCO3 can amputate the ability of trimethoprim to block ENaC, but not so for the other K+-sparing diuretics.23 Professor McCance therefore had to find another mechanism to ‘amputate’ the renal actions of triamterene. ‘How can one lower its concentration of in the lumen of the CCD?’ he asked.
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Question 6. How can one lower the concentration of triamterene in the lumen of the CCD?
Physiology principle 6. Concentration terms have numerators and denominators.
Return to the bedside. If the drug entered the tubular lumen as expected, one can lower its concentration by having a very large flow rate in the CCD. Hence the next question is, ‘How can the flow rate in the CCD be raised?’
Question 7. How can the flow rate in the CCD be raised?
Physiology principle 7. The CCD is permeable to water when vasopressin acts. Therefore the osmolality in its luminal fluid will equal that of the interstitial fluid in the cortex (or the plasma osmolality, Posm). Hence the number of osmoles delivered to the CCD will determine the volume in the lumen of the CCD (equation 3) (Figure 5).24
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Return to the bedside. The major osmoles delivered to the CCD are urea and electrolytes. The other factor that permits a high rate of secretion of K+ in the CCD is aldosterone, because it causes the ENaC to be open. The low effective circulating volume will provide this signal to release aldosterone, because it activates the renin-angiotensin system. In this patient, the higher dose of thiazides led to a larger delivery of Na+ and Cl– to the CCD. Because there was such a large excess of Na+ and Cl– in her body (the oedema fluid), she was able to have a large enough volume in her CCD to dilute the concentration of triamterene and minimize its renal effect.
‘If you want to ensure a K+-sparing effect, perhaps one should use drugs that block aldosterone action at a site other than ENaC, such as the mineralocorticoid receptor in principal cells,’ volunteered a final year student. ‘An excellent suggestion and one I will keep in mind when next I have a similar case,’ agreed the nephrology consultant.
Not wishing to omit anything, Professor McCance also considered factors that could cause K+ to shift into cells in this patient. Following the rationale of physiology principle 1, the major factors that cause K+ to shift into cells are hormones, metabolic alkalosis and cell growth. While Professor McCance could rule out cell growth with confidence in this patient, he could see a possible role for hormones and metabolic alkalosis.
Hormones: Because of the actions of the diuretics, her effective circulating volume was low. The latter could invoke an adrenergic response. If the 
-adrenergic effect dominated, there would be an inhibited release of insulin from ß-cells (25) and a tendency for the PK to rise. On the other hand, if the ß-adrenergic effect was dominant, this could activate the Na-K-ATPase, make the ICF voltage become more negative, and thereby shift K+ into cells (Figure 1).
Metabolic alkalosis: The patient had a severe degree of metabolic alkalosis so this could be an important factor that caused K+ to shift into cells. Before Professor McCance could continue, the razor-sharp student raised his hand and asked: ‘Without vomiting and HCl loss, the presence of little dietary intake of alkali, and poor renal function (adjusting her PCreatinine for muscle mass), how could this patient have such a high PHCO3? ’
Question 8. Why might this patient have such a high PHCO3?
Physiology principle 8. The PHCO3 can rise because of an addition of or a fall in the ECF volume.
Return to the bedside. While there is little evidence for a gain of , there was a marked reduction in her ECF volume (loss of oedema fluid). It would not be surprising for this to almost double her PHCO3 by halving her ECF volume.14 This is a contraction form of metabolic alkalosis.26 In fact, this should be the most common setting for contraction alkalosis, the administration of diuretics to a person with a reasonable GFR and a large volume of retained oedema fluid.
Professor McCance nodded in agreement, but he had not finished his analysis of the basis for the patients’ low PK. There are two factors I can identify, he said. First, for the same amount of K+ loss, the presence of a low K+ intake would lead to larger K+ deficit and thereby, a lower PK. While this was one factor the medical team had considered, they were unable to describe a second one that could have caused such a severe degree of hypokalaemia. Therefore Professor McCance asked his question in a more direct fashion. ‘What could cause the PK to be lower in one of two patients, if both patients had the same total body K + deficit and identical factors influencing the distribution of K + across cell membranes? ’
Question 9. What could cause the PK to be lower in one of two patients given the same K+ deficit and identical factors influencing the distribution of K+ across cell membranes?
Physiology principle 9. For the same ratio of K+ concentrations in the ICF to ECF compartments, the smaller the ICF compartment, the lower the PK for a given total K+ deficit.
Return to the bedside. Since the vast majority of the ICF volume is in skeletal muscle and the patient has muscle wasting due to Parkinson's disease, her total ICF K+ content should be very low. Therefore this could contribute to the severity of the degree of hypokalaemia.
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Concluding remarks |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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Professor McCance said that he enjoyed participating in the K-quiz. What he found even more rewarding was the opportunity to introduce his younger colleagues to the application of principles of integrative physiology (Table 4), to permit them to deduce answers that may be correct. He also emphasized the importance of a quantitative analysis. After considerable thought, he developed Flow Charts 1–3
to illustrate an approach to accurate diagnosis and therefore logical therapy for patients with a severe degree of hypokalaemia.
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Regarding the new consultation, his message was that more than one mechanism is likely to be involved to produce such a severe abnormality. Adding to this diuretic-induced K+ loss, were a low intake of K, a shift of K into cells (hormone actions and metabolic alkalosis), and an ability to ‘amputate’ the renal effects of a K+-sparing diuretic. The latter could be explained when he considered both the numerator and denominator of the concentration of this drug in the lumen of the CCD. Finally, he added that one must consider the magnitude of the K+ deficit and the size of the total body K+ store (mainly muscle mass) to determine how a modest deficit of K might produce such a severe degree of hypokalaemia. The basis for this low K+ store capacity was muscle wasting.
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Footnotes |
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Address correspondence to Professor M.L. Halperin, University of Toronto, St Michael's Hospital Annex, Lab #1, Research Wing, 38 Shuter Street, Toronto, Ontario, M5B 1A6, Canada. email: mitchell.halperin{at}utoronto.ca
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References |
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TopSummaryIntroductionThe consultationOn rounds the next...A. Patients with a...B. Patients with a...Current consultationConcluding remarksReferences |
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