Electrolyte disturbances: Pathology review

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Case Study0:00–0:47

Two people came to the Emergency Department during your shift. One of them is 75-year-old Karen who has palpitations and muscle weakness.
Karen also has heart failure and one of the medications she’s currently on is digitalis. The other one is 25-year-old Carmen who has tetany.
On the clinical examination, Carmen has a positive Chvostek sign. In both these individuals, an ECG was done and levels of electrolytes were taken.
Karen’s ECG showed a wide QRS complex with peaked T waves and high levels of potassium, while Carmen’s ECG showed prolonged QT and low levels of calcium.
Okay, now let’s start talking about electrolytes and what happens when their levels are either too high or too low. Let’s begin with potassium, which is a cation that’s mostly in the intracellular fluid, or ICF for short.

Hyperkalemia0:47–5:54

It’s essential for the normal functioning of excitable tissues, such as nerves and muscles, including the cardiac muscle, and also maintains the resting membrane potential.So, with hyperkalemia, there’s too much potassium in the extracellular fluid or ECF.
And in order for there to be hyperkalemia, there are two possibilities. The first is an external balance shift, like when there’s decreased potassium excretion by the kidneys, leading to increased serum potassium.
There’s also internal balance shift where potassium moves out of cells, and into the interstitium and blood. One potential cause is hyperosmolarity.
Osmolarity reflects the number of solute particles per liter of solvent, and normally, the osmolarity of the ICF equals the osmolarity of the ECF, even though the exact composition of solutes differs.
So when there’s hyperosmolarity, this means that there’s something in the ECF that creates an osmotic force capable of dragging water from inside the cells, like glucose, for example.
As water leaves the cells, the intracellular potassium concentration increases and this creates a driving force for potassium to leave the cell, leading to a rise in extracellular potassium and hyperkalemia.Next, acid-base disturbances also play a role in this.
pH reflects the concentration of hydrogen ions and normal blood pH is about 7.4. To maintain pH balance, hydrogen moves in and out of the cells.
In order for hydrogen to move across the cell membrane, it must be accompanied by an anion, meaning an ion with a negative charge, or it must be exchanged for another cation, like potassium.
When there’s an increase in the hydrogen ion concentration in the blood, this is called metabolic acidosis. As a coping mechanism, hydrogen must enter the cells in exchange for potassium, which leaves the cells.
And this leads to hyperkalemia. Another important mechanism is the sodium-potassium ATPase, which normally transports sodium out of the cell and potassium in.
Commonly tested medications like digitalis and beta blockers block the sodium-potassium ATPase, so more potassium is left outside the cell, leading to hyperkalemia.
Another medication that causes internal potassium balance shift is succinylcholine. Succinylcholine combines with nicotinic receptors to inhibit neuromuscular transmission and produce skeletal muscle depolarization, which leads to relaxation.
With depolarization, some of the potassium gets out of the cell which in turn can cause hyperkalemia. Finally, there’s cell lysis or cell damage.
When cells are destroyed, they release all their potassium into the ECF which naturally, leads to hyperkalemia. Some examples of cell lysis include crush injuries, like when a piano falls on someone’s legs, or tumor lysis syndrome, which occurs when cancer treatment causes lots of tumor cells to die all at once, or rhabdomyolysis, which is the rapid destruction of skeletal muscle cells.
Alright, on to external potassium balance shifts resulting in hyperkalemia, which has to do with potassium intake and excretion.
That said, simply taking in too much potassium can lead to hyperkalemia, but this would typically arise from rapid, excessive infusion of potassium into the bloodstream, like in individuals receiving intravenous fluids.
Most other cases, have to do with the kidneys and their ability to regulate what stays in the blood and what gets excreted into the urine.
Now, an important hormone that helps regulate potassium reabsorption or secretion in the kidneys is aldosterone. Aldosterone promotes potassium secretion by the principal cells of the distal tubule and collecting duct of the nephron.
So, in situations where somebody’s unable to produce enough aldosterone, which is called hypoaldosteronism, there’s less potassium secretion by the principal cells, and therefore more potassium is retained, leading to hyperkalemia.
Along the same lines, medications that reduce the effect of aldosterone can also cause hyperkalemia, and these include renin inhibitors, ACE inhibitors, angiotensin II receptor antagonists, selective aldosterone blockers, and potassium-sparing diuretics.Acute and chronic kidney injury can also cause hyperkalemia because both can impair potassium excretion.
Some associated clues include oliguria or anuria, which means decreased or no urine excretion, volume overload and in advanced stages, uremia, which refers to the accumulation of uremic toxins, including urea itself.
Moving on to causes of hypokalemia, which is when there’s too little potassium in the ECF, there are, similarly, two possibilities.

Hypokalemia5:54–10:21

The first is an external balance shift most often caused by an increase in potassium excretion in the kidneys, and the second is an internal balance shift where potassium moves into the cells, from the interstitium and blood.
One high-yield cause of internal potassium shift is hyposmolality, meaning there are too little osmotic substances, like when there’s hyponatremia, for example, then water goes back into the cells and can sometimes even drag potassium along with it, leading to hypokalemia.
However, bear in mind that alternatively, in some cases of hyperosmolarity, like in hyperglycemic hyperosmolar state, or HHS, which is a complication of diabetes mellitus, osmolarity can get so high that it leads to osmotic diuresis.
Osmotic diuresis can also drag that potassium into the urine. And this may lead to total body potassium loss and hypokalemia.
Now, with acid-base disturbances, when there’s a primary decrease in the hydrogen concentration in the blood, this is called metabolic alkalosis.
As a coping mechanism, hydrogen must leave the cells in exchange for potassium. More potassium gets inside the cells and this leads to hypokalemia.
Next, there are things that affect the sodium-potassium ATPase. Specifically, beta agonists promote the activity of the sodium-potassium ATPase, leading to hypokalemia.
Next, there’s insulin which normally stimulates the sodium-potassium ATPase. When there’s insulin deficiency, like with diabetes mellitus, there can also be hyperkalemia and when there’s too much insulin, there can be hypokalemia.
Moving on to external potassium balance shifts resulting in hypokalemia, these have to do with potassium intake or excretion.
Low potassium intake is rare since potassium is abundant in most foods. So it typically happens in cases of anorexia, prolonged fasting, or specific types of diets.
Excess potassium excretion from the kidneys is a lot more common. In situations where somebody produces too much aldosterone, like primary hyperaldosteronism, called Conn syndrome, there’s more potassium secretion by the principal cells, meaning more gets excreted in the urine.
Other pathological conditions that cause increased aldosterone levels include compensated heart failure and cirrhosis. For your exams, it’s important to know that loop diuretics and thiazide diuretics also increase potassium excretion in the urine.Alternatively, potassium can be lost through increased gastrointestinal secretions, typically due to vomiting and diarrhea, like from infections, inflammatory bowel diseases, as well as laxative abuse.
Finally, a very small amount of potassium is also lost in sweat, which could come up in your test as an individual who exercises a lot in a hot climate.Now, once a person has hypo- or hyperkalemia, the first thing to do is an ECG.
That’s because the resting membrane potential of the cardiomyocytes depends on potassium balance. With hyperkalemia, the main changes are wide QRS complexes and peaked T waves which put a person at risk for heart arrhythmias.
This happens because initially, the rise in potassium in the ECF makes the cell membrane less electronegative and this increases the membrane excitability, so the cardiac muscle contracts more easily, but it can’t repolarize effectively to allow another contraction.
For your tests, remember that another symptom of hyperkalemia is muscle weakness. With hypokalemia, the main changes are flattened T waves and the appearance of U waves, which are thought to represent the repolarization of Purkinje fibers of the heart.
This happens because hypokalemia increases both the resting membrane potential and the duration of the refractory period, but has a greater effect on the refractory period, meaning it takes longer for the heart to recharge.
It also decreases conductivity, which can further lead to heart arrhythmias. Other symptoms of hypokalemia include muscle weakness, muscle cramps, or spasms.
Let’s move on and talk about sodium, which is a cation that’s mostly in the ECF and is essential for maintaining water balance, as well as a nerve impulse conduction and muscle contraction.

Hypernatremia10:21–12:22

So with hypernatremia, there is too much sodium in the extracellular fluid. This can happen because a person has gained more sodium than water, or has lost more water than sodium.
Either way this increases the sodium concentration in the extracellular fluid, draws water out of the cells. Sodium gain happens most commonly when someone in the hospital is given too much sodium intravenously too quickly.
The other possibility is salt poisoning, which is a rare scenario, but if it is seen, it’s typically in infants and young children who have been abused.
Water losses, on the other hand, is much more common, and can result in hypernatremia if the lost water is not replaced.
There are 3 possible sources: skin, gastrointestinal, and urinary losses. Increased skin losses can occur in individuals with extensive burns, fever, exercise, and exposure to high temperatures.
Then we have the gastrointestinal losses, like vomiting, or diarrhea. Finally, too much water can be lost through the kidneys because of osmotic diuresis.
This occurs when the osmolarity of the fluid in the renal tubules are too high and it sucks more water into the tubules which is then lost as urine.
A high yield example of this is diabetes mellitus where there’s too much glucose being filtered into the pre-urine. Other examples include acute kidney failure, when urea builds up; or during treatment with mannitol, which is an osmotic diuretic.When there’s hypernatremia, water will move from the ICF to the ECF until both compartments become isotonic.
This means that the cells will lose water and become dehydrated. When neurons are affected, it can lead to symptoms such as irritability, stupor, which is when a person becomes almost unconscious and even coma.
On the other hand, true hyponatremia or low concentration of sodium in the extracellular fluid, can be caused by either losing more sodium than water, or gaining more water than sodium.

Hyponatremia12:22–15:08

This shouldn’t be confused with false hyponatremia or pseudohyponatremia. This is where the body water and sodium levels are normal, but there’s an excessive amount of lipids, like in hypertriglyceridemia, or proteins, like in multiple myeloma.
High levels of lipids and proteins affect the laboratory instruments that measure the sodium concentration, making the instruments say the sodium concentration is too low.Broadly speaking, true hyponatremia can be divided into three categories based on water volume status.
The first is hypervolemic hyponatremia, where there’s an enormous increase in total body water with a less significant increase in total body sodium.
Typically, this is seen in conditions like congestive heart failure, cirrhosis, or nephrotic syndrome, which all present with edema, especially in the ankles.
The second category is hypovolemic hyponatremia where there’s a small decrease in total body water with a large decrease in total body sodium.
This can occur in conditions like diarrhea or vomiting, or in response to certain medications like diuretics. Another more nuanced condition is cerebral salt wasting which is when an intracranial injury like meningitis disrupts the normal sympathetic nervous system stimulation of the kidneys leading to disproportionate loss of sodium and, along with it, water.
A third category is euvolemic hyponatremia, or normal volume hypovolemia, which is where there’s normal body sodium with an increase in total body water.
Ηowever, we call it “euvolemic” because there’s no edema. Euvolemic hyponatremia can be split into cases with dilute urine and concentrated urine.
Conditions that cause dilute urine include drinking too much water called polydipsia. The main condition that causes concentrated urine is the syndrome of inappropriate antidiuretic hormone secretion, or SIADH for short.
Certain neurological disorder can increase the secretion of ADH and this includes strokes, hemorrhages or trauma, while certain medications like mood stabilizers and antiepileptics can also increase its secretion.
It could also be excreted ectopically by tumors, and small cell lung carcinoma is the most commonly tested.When there’s hyponatremia, water will move from the ECF in the ICF, so the cells will swell up.
When neurons are affected, it causes symptoms like nausea, malaise, stupor, coma and even seizures. Okay, moving to calcium, which is a cation that’s mostly located in the bones and is essential for muscle contraction, enzyme activity and blood coagulation.

Hypercalcemia15:08–18:31

It also helps with releasing neurotransmitters from neurons, as well as releasing hormones from the endocrine glands. About 1 percent of calcium is in the ECF.
Now hypercalcemia, or too much calcium in the ECF, is most commonly caused by excess parathyroid hormone secretion by the parathyroid glands, and is known as PTH-mediated hypercalcemia.
This results in increased osteoclastic bone resorption, and this is where osteoclasts break down the bone and release calcium into the blood.
Hypercalcemia can also be parathyroid hormone-related protein, or PTHrP-mediated. PTHrP is a hormone that mimics the effect of parathyroid hormone, so it stimulates the osteoclasts.
It can be secreted by various malignancies, but for your exams, remember squamous cell carcinomas of the lung. Other malignancies like multiple myeloma, breast and lung cancer can also cause hypercalcemia, but without secreting PTHrP.
Instead, they spread to the bones, overstimulating osteoclasts, and creating lytic lesions.Another cause of hypercalcemia is excess vitamin D either through the diet or through supplements, which can cause too much calcium to be absorbed in the gut.
There are also some medications like thiazide diuretics that increase calcium reabsorption in the distal tubule of the kidney which contributes to hypercalcemia.Finally, hypercalcemia can be caused by familial hypocalciuric hypercalcemia.
This is a genetic disorder caused by defective calcium-sensing receptor in the parathyroids and the kidney. These receptors are less sensitive to calcium levels in the blood so the parathyroids might overproduce PTH.
When the kidneys can’t sense calcium levels, they will increase calcium reabsorption, leading to hypocalcemia and hypercalcemia.
Now, you can remember symptoms of hypercalcemia with the mnemonic “Stones, bones, groans, thrones, and psychiatric overtones”.
For “stones”, it’s important to know that the kidneys try to dump all that excess calcium into the urine, causing hypercalciuria.
Hypercalcemia can also cause some form of resistance to the antidiuretic hormone or ADH. This means that not enough water will be retained and in turn, this leads to frequent urination which can cause dehydration.
Now, for your tests, remember that the combination of hypercalciuria and dehydration can lead to calcium oxalate kidney stones.
For “bones”, in the case where there’s bone resorption, we might also have bone pain. For “thrones”, voltage-gated sodium channels are less likely to open up, which makes it harder to reach depolarization, and makes the neuron less excitable.
The sluggish firing of neurons also leads to slower muscle contraction, which causes constipation which in turn can cause abdominal pain.
Finally, for “psychiatric overtones”, in the central nervous system, hypercalcemia can cause anxiety and altered mental status, since calcium also helps with releasing neurotransmitters from neurons.
Alright, now in hypocalcemia, there’s too little calcium in the ECF. This can be caused either by less calcium entering the blood or by too much calcium leaving the blood.

Hypocalcemia18:31–21:45

For your exams, remember that less calcium entering the blood is the most common cause of hypocalcemia, and this can be due to hypoparathyroidism, which means lower levels or lower activity of parathyroid hormone.
Hypoparathyroidism can be caused by surgical removal or autoimmune destruction of the parathyroid gland, by congenital problems involving the parathyroid gland, like DiGeorge syndrome, or by magnesium deficiency, since magnesium is needed for parathyroid hormone production.
Low levels of vitamin D can also lead to hypocalcemia, and these can be caused by a deficient diet, malabsorption, cirrhosis, lack of sunlight, or chronic renal failure, among other causes.Then, there’s too much calcium leaving the blood.
For example, in kidney failure, the nephron doesn’t effectively reabsorb calcium, which means that calcium is excreted into the urine.
Another cause of calcium leaving the blood is tissue injury, like burns, rhabdomyolysis, and tumor lysis syndrome, where large numbers of cells die and release intracellular phosphate into the blood.
This phosphate binds to the ionized calcium and form calcium phosphate, making the calcium insoluble and effectively decreasing the total amount of calcium in the blood.
Other inflammatory processes can also cause too much calcium to leave the blood. For example, note that in acute pancreatitis, lipase that leaks out breaks down fat in the body.
The free fatty acids end up binding to ionized calcium, making it insoluble and precipitating out as a soap-like substance.Finally, calcium levels can fall as a result of having too many blood transfusions.
This is because additives to the blood, like citrate and ethylenediaminetetraacetic acid, or EDTA, can chelate or bind to calcium, forming calcium complexes, which is an inactive molecule.
With hypocalcemia, voltage-gated sodium channels are less stable and more likely to open up, which allows the cell to depolarize more easily, and makes the neuron more excitable.
This can trigger tetany or the involuntary contraction of muscles, a classic symptom of hypocalcemia. The spontaneous firing of neurons also leads Chvostek's sign, which is when facial muscles twitch after the facial nerve is lightly finger tapped 1 cm below the zygomatic process.
It also can cause Trousseau's sign, which is where a blood pressure cuff putting pressure on the nerve is enough to make it fire, which results in a muscle spasm that makes the wrist and metacarpophalangeal joints flex.
Now, calcium is also important for cardiac muscle contraction. The action potential in the cardiac muscle has 4 phases.
In phase 2, the cardiac muscle tries to repolarize and get ready for another contraction by letting more calcium in the cardiac cells.
Well, in hypocalcemia it will take longer for the cardiac muscle to repolarize. Now, we can see this on the ECG as a prolonged QT interval, since QT interval accounts for both ventricular depolarization and repolarization.
Moving on to magnesium, which is another cation that acts as a cofactor in many enzymatic reactions and also helps to maintain good nerve and muscle function, including the cardiac muscle.

Hypermagnesemia21:45–25:32

Magnesium also helps with strengthening the bones. In hypermagnesemia, there’s too much magnesium in the ECF.
This most commonly occurs when the kidneys cannot excrete magnesium properly, which can happen in renal failure. Another cause of hypermagnesemia is ingesting more magnesium than the kidneys can excrete.
Sometimes this can be due to an intravenous infusion of magnesium that isn’t prepared correctly. Other times it can be due to a magnesium-containing medication like magnesium hydroxide which can be used to treat symptoms like constipation and heartburn.
With hypermagnesemia, there can be some serious complications. At the neuromuscular junction, there are voltage-gated calcium channels on presynaptic neurons that need to open and let calcium in to cause the neuron to release neurotransmitters and cause muscle contraction.
Under normal circumstances, magnesium seems to inhibit calcium influx a little bit, which actually helps stabilize the axon.
But with too much magnesium floating around, it tends to inhibit calcium influx even more, which interferes with neurotransmitter release and ultimately slows muscle contraction.
So with hypermagnesemia, for your tests, remember that with hypermagnesemia, deep tendon reflexes might be decreased and lethargy can occur.
Also, normally, PTH usually stimulates calcium release into the blood. Hypermagnesemia seems to inhibit the release of parathyroid hormone from the parathyroid gland, which causes calcium levels to fall, leading to hypocalcemia, which is usually transient and asymptomatic.
Really high levels of magnesium also alter the electrical potential across the cardiac cell membrane, which can lead to bradycardia and even cardiac arrest.
Now, with hypomagnesemia, there’s too little magnesium in the ECF. This can be due to prolonged malnutrition, where not enough magnesium is consumed.
Alternatively, enough magnesium might be consumed, but it might not be absorbed in the gastrointestinal tract. This could happen because of interference from medications like proton pump inhibitors or from a bout of diarrhea.
Another scenario that can lead to this is when the nephron fails to reabsorb the magnesium that’s filtered out of the blood.
This is commonly due to diuretics, particularly loop and thiazide diuretics, but it can also result from Gitelman syndrome, where there’s a mutation in the gene coding for the Na-Cl cotransporters in the distal tubule.
This could change the electrochemical gradient and cause more magnesium to stick around in the lumen and then be peed out.The last commonly tested cause of hypomagnesemia is hungry bone syndrome, which is when the thyroid or parathyroid glands are surgically removed, leading to increased bone formation.
In this case, the osteoblasts, or bone-forming cells, are literally hungry for ions to make more mineralized matrix, and they consume all the magnesium in the blood.Now symptoms of hypomagnesemia are often neuromuscular.
This happens because, under normal circumstances, at the neuromuscular junction, without magnesium floating around, calcium can enter neurons easily.
This makes the muscles and nerves more excitable, meaning that a person can present with tetany. Severe hypomagnesemia can even lead to convulsions or seizures, as well as abnormal heart rhythms.
On the ECG, with hypomagnesemia, a form of ventricular tachycardia called torsades de pointes can occur. Additionally, hypomagnesemia is commonly associated with hypokalemia, partly because a lot of the conditions that cause hypomagnesemia, like diarrhea and diuretic therapy, are also responsible for hypokalemia.

Hypomagnesemia25:32–25:57

It’s also thought that normally magnesium in the cells of the nephron tend compete with potassium for potassium channels, so with less magnesium, more potassium is excreted in the urine.Finally, there’s phosphate which is an anion that’s mostly located in the bone.

Hyperphosphatemia25:57–28:28

Phosphate is also a component of nucleotides that make up the DNA and RNA, high-energy molecules, like adenosine tri-phosphate and metabolic intermediates.
Phosphate also acts as a buffer for hydrogen. With hyperphosphatemia, there’s too much phosphate in the ECF and that can happen in a few different ways.
The first possibility is as a result of acute or chronic kidney disease, where the kidneys cannot excrete phosphate properly.
All right, so because parathyroid hormone causes excretion of phosphate and reabsorption of calcium, another cause of hyperphosphatemia is hypoparathyroidism, where the parathyroid glands don’t produce enough parathyroid hormone in the first place, resulting in increased reabsorption of phosphate and decreased reabsorption of calcium.
This can happen following a thyroid gland removal surgery when the parathyroids are accidentally taken out too or after radiation treatment for cancer of the head or neck.
Also, people with the genetic disease DiGeorge syndrome are often born with parathyroid glands that are too small and can’t produce enough parathyroid hormone.
Related to this is pseudohypoparathyroidism, which is where the kidneys don’t respond to parathyroid hormone because of a genetic defect in the parathyroid hormone receptor.
Alternatively, phosphate levels can rapidly increase in the blood from excessive intake of a phosphate-based laxative and absorption through the gastrointestinal tract or through the bloodstream via intravenous fluids.
A final cause of hyperphosphatemia relates to the fact that most phosphate in the body is within the cells. Any time a lot of cells die, that phosphate is spilled into the bloodstream, causing hyperphosphatemia.
This cause includes things like crush injuries, tumor lysis syndrome, or rhabdomyolysis. Remember that this is classically accompanied by hyperkalemia.With hyperphosphatemia, the excess phosphate can stick to calcium which forms bone-like crystals containing calcium and phosphate in places that they shouldn’t be, like just beneath the skin, in the walls of blood vessels, in the joints.
For your tests, remember that these are called metastatic calcifications. When calcium-phosphate reach the kidneys, they can form kidney stones.
Remember that since the phosphate binds to calcium in the ECF, another complication is hypocalcemia. Now, with hypophosphatemia, there’s too little phosphate in the ECF.

Hypophosphatemia 28:28–30:44

This can arise from excessive loss of phosphate, such as in conditions like primary hyperparathyroidism, where there’s too much parathyroid hormone, leading to more phosphate being excreted in the urine.
Another example of this kind of condition is Fanconi syndrome, which is where the proximal convoluted tubule essentially loses its capacity to reabsorb a variety of solutes, including phosphate, which once again means that it’s excreted in the urine.
Another thing that can lead to hypophosphatemia is not absorbing enough phosphate through the gastrointestinal tract. Some substances like alcohol can impair phosphate absorption.
Also, medications including antacids that contain aluminum, calcium, or magnesium, all of which are positive ions, can bind with the negatively charged phosphate and prevent absorption.
Alternatively, a person might not get enough phosphate in their diet, although this is unusual because it’s found in nearly all foods.
The exception is someone who’s starving and severely malnourished, or someone who is actively depriving themselves of food, like in anorexia nervosa.
Now, there’s also something called refeeding syndrome. When a person is starved, blood glucose levels are low, and, as a result, cellular metabolism slows down considerably.
When an individual in this state starts to suddenly eat healthy meals again, like in a hospital setting, they suddenly have a bunch of glucose in their blood, and insulin usually skyrockets in response to this in order to push that newfound glucose into the cells.
This causes a demand for phosphate in cells because the first step in glucose metabolism is to have the enzyme hexokinase attach phosphate to the glucose.
Also, the production of ATP molecules themselves requires a lot of phosphate. The increase in metabolism also increases the uptake of other ions, so we also get hypokalemia and hypomagnesemia.Now, consequences of hyperphosphatemia include weak bones, osteomalacia in adults and rickets in children, as well as bone loss.
This happens over time due to prolonged hypophosphatemia, because phosphate is an important component of the bone and when there’s not enough phosphate in the body, bone mineralization is decreased.
Okay, as a quick recap! Hyperkalemia presents with muscle weakness and palpitations and the ECG shows wide QRS complexes and peaked T waves.

Review30:44–32:10

Hypokalemia presents with muscle weakness, cramps and spasms, as well as palpitations and the ECG shows flattened T waves and U waves.
Hypernatremia can present with irritability, stupor and coma, while hyponatremia presents with nausea, malaise, seizures and stupor and coma.
Hypercalcemia can lead to kidney stones, abdominal pain, bone pain, as well as increased urinary frequency, anxiety and altered mental status.
Hypocalcemia presents with tetany, positive Chvostek and Trousseau signs and the ECG shows prolonged QT. Hypermagnesemia presents with lethargy, decreased deep tendon reflexes, hypotension, hypocalcemia, bradycardia and even cardiac arrest, while hypomagnesemia presents with tetany, hypocalcemia, hypokalemia and torsades de pointes.
Finally, hyperphosphatemia can lead to hypocalcemia, kidney stones and metastatic calcifications, while hypophosphatemia can lead to bone loss, osteomalacia in adults and rickets in children.Back to our cases.
Lab tests and the ECG show that Karen has hyperkalemia that was probably due to digitalis. Her symptoms included muscle weakness and palpitations.

Summary32:10–32:33

Remember the key findings on ECG are a wide QRS and peaked T waves. while Carmen has hypocalcemia which is causing the tetany.
She also had a positive Chvostek sign on the clinical examination. Key findings on ECG was the prolonged QT.
on the ECG with a prolonged