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- Hypo- and Hyperkalemia
- Hypo- and Hypermagnesemia
- Hypo- and Hypocalcemia
Published: May 7, 2023
Last Updated: May 14, 2023
Hypercalcemia is when the blood has high calcium levels, which can lead to deadly hypercalcemia complications. These complications can be severe and potentially life-threatening if not identified and managed promptly.
As healthcare professionals who may have to care for patients with hypercalcemia, nurses need to be aware of the potential complications associated with this condition.
In this article, we will discuss levels of hypercalcemia, causes, treatment, complications, and monitoring parameters that nurses need to know about.
Normal calcium levels can range from 8.5 – 10.5 mg/dL.
There are multiple causes of hypercalcemia, including:
Primary hyperparathyroidism is the most common cause of hypercalcemia, accounting for about 80% of cases. It occurs when the parathyroid glands produce too much parathyroid hormone (PTH), increasing calcium levels in the blood.
The most common cause of this is a benign tumor called a parathyroid adenoma, which develops in one of the parathyroid glands. Other less common causes of primary hyperparathyroidism include parathyroid hyperplasia, parathyroid cancer, and inherited genetic disorders.
Some types of cancer, such as multiple myeloma, lung cancer, breast cancer, and kidney cancer, can cause hypercalcemia by releasing substances that increase calcium levels in the blood.
Taking too much vitamin D supplements or having a disease that increases vitamin D levels in the body, such as sarcoidosis, can lead to hypercalcemia.
Prolonged immobilization, such as when a patient is bed-bound, can cause hypercalcemia by increasing bone resorption and calcium release.
Certain medications can cause high calcium levels, including:
Other generic and acquired positions can lead to hypercalcemia complications, including hyperthyroidism, acromegaly, pheochromocytoma, adrenal insufficiency, and TPN.
Hypercalcemia can cause a wide range of symptoms, most nonspecific. The severity and type of symptoms depend on the calcium level in the blood, the underlying cause of hypercalcemia, and how quickly the levels change.
Common symptoms of hypercalcemia include:
Hypercalcemia can cause anorexia, constipation, nausea, and vomiting.
Patients with hypercalcemia often feel tired and weak, just like with many other electrolyte abnormalities.
High calcium levels lead to decreased concentration ability of the kidneys and subsequent urinary frequency/dehydration.
Chronic high calcium levels in the urine can lead to nephrolithiasis (kidney stones).
Hypercalcemia can affect the central nervous system, leading to cognitive impairment and even confusion, stupor, or coma.
Hypercalcemia can affect the heart’s electrical conductivity, leading to arrhythmias, which may cause palpitations, chest pain, shortness of breath, dizziness, or syncope. This is generally not as common with hypercalcemia as with other electrolyte abnormalities.
Chronic hypercalcemia can lead to the deposition of calcium in heart valves, coronary arteries, and the heart muscle itself. This can also lead to hypertension and heart failure.
Bone pain can be a symptom of high calcium due to malignancy or primary hyperparathyroidism.
When performing a physical exam for a patient suspected of having hypercalcemia, the nurse should assess for the following:
The treatment of hypercalcemia depends on the severity of the condition and the underlying cause.
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still needs to be done.
Notify the provider of the calcium levels, your assessment, and their cardiac rhythm.
Make sure there is at least one IV site, but place a second line if the hypercalcemia is severe.
Administer medications and fluids that are ordered (discussed below).
Mild hypercalcemia often does not require any specific calcium-lowering therapies, but instead can usually be managed by:
Patients who have moderate to severe hypercalcemia often are volume depleted. This helps to correct the hypovolemia and increase calciume excretion in the urine.
NS or LR given at 200-300ml/hr and then adjusted to a urine output of 100-150ml/hr is recommended for 24-48 hours until the volume depletion is corrected.
Loop diuretics aren’t traditionally recommended, however, patients with heart or kidney failure may benefit/require loop diuretics in addition to fluid.
Calcitonin is a hormone that can lower calcium levels in the blood by decreasing bone resorption. This is usually reserved for severe hypercalcemia with neurologic symptoms like decreased mental status.
The recommended dose is 4 units/kg SQ or IM every 12 hours for 24-48 hours.
These medications can reduce bone resorption and lower calcium levels in the blood. Bisphosphonates are used for longer-term control of hypercalcemia, especially when related to malignancy.
If given IV for severe hypercalcemia in the hospital, Zalendronic acid is recommended 4mg IV over 15 minutes. This can be repeated in 7 days if needed.
Denosumab is a monoclonal antibody that is sometimes used if Bisphosphonates are not effective or not able to be used. There is a higher risk of hypocalcemia occurring with this medication, so it is avoided when possible.
This is primarily only given if the hypercalcemia is caused by lymphoma, sarcoidosis, or other granulomatous disease that increases calcitriol production and subsequently increases calcium absorption.
In severe cases, dialysis may be needed to remove excess calcium from the blood, especially if they also have heart failure or severe renal failure.
Underlying conditions, such as cancer, may need to be treated to improve calcium levels.
As a nurse, it is essential to monitor patients with hypercalcemia closely to identify and manage any potential complications. The following parameters should be observed:
Serum calcium levels should be monitored regularly to assess treatment response and to identify potential complications such as hypocalcemia.
Measuring parathyroid hormone helps determine the etiology of the high calcium levels. If PTH is elevated, this points to primary hyperparathyroidism. If it is low, is is likely not from hyperparathyroidism.
The nurse should monitor laboratory values such as serum calcium, magnesium, and phosphate levels and liver and kidney function tests to assess for complications and monitor treatment progress.
Possible hypercalcemia complications include arrhythmias, so continuous telemetry monitoring, as well as occasional 12-lead ECGs are indicated.
Patients with severe hypercalcemia that warrants significant calcium-reducing therapies should have a nephrology consult on board!
Hypercalcemia can cause a variety of ECG changes, including:
Arrhythmias are less common with hypercalcemia than with other electrolyte abnormalities but still can cause them including:
These ECG changes are thought to be due to altered myocardial repolarization caused by hypercalcemia.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
In conclusion, hypercalcemia is a potentially serious condition that requires prompt diagnosis and treatment to prevent complications.
As a nurse, it is important to be aware of the causes, symptoms, and ECG changes associated with hypercalcemia, as well as the monitoring and treatment options available. By taking a proactive approach to monitoring and managing patients with hypercalcemia, nurses can help improve outcomes and prevent serious complications.
If you’d like to download this article in PDF form, click here!
Published: April 10, 2023
Last Updated: April 10, 2023
Hypocalcemia is when there are low levels of calcium in the blood. Calcium is an electrolyte that plays a vital role in many bodily functions, including muscle contraction, nerve transmission, and bone formation.
Various factors, including nutritional deficiencies, medications, and underlying medical conditions, can all lead to low calcium levels. As a nurse, it is essential to be familiar with the signs, symptoms, and treatment options for hypocalcemia to provide adequate and timely care to patients.
This article will discuss the importance of calcium in the body, the causes of hypocalcemia, nursing assessment and interventions, treatment options, and monitoring parameters for hypocalcemia.
Calcium is an essential electrolyte that plays a critical role in maintaining the structure and function of our bones and teeth. It is also necessary for proper nerve function, muscle contraction (including the heart), blood clotting, and enzyme activity. In addition, calcium regulates the release of hormones and other chemicals in the body.
Calcium provides the structural support for strong and healthy bones and teeth.
Calcium helps regulate the transmission of nerve impulses, which is critical for communication between the brain and other body parts.
Calcium helps with muscle contraction and relaxation, including the muscles involved in breathing and the heart beating.
Calcium ions are necessary for the contraction of the heart muscles, but they also play a critical role in the generation and transmission of electrical impulses that coordinate the heart’s rhythm. These electrical impulses regulate the heart rate and ensure that the heart muscles contract in a coordinated manner. Without sufficient calcium, the heart may experience arrhythmias or other electrical disturbances.
Calcium is necessary to form blood clots, which help stop bleeding after an injury.
Calcium activates and regulates a wide range of enzymes, which are essential for the body to function as it’s supposed to!
Calcium levels in the body are tightly regulated through a complex system involving hormones and their effects on the bones, intestines, and kidneys.
The regulation of calcium involves several hormones, including:
The parathyroid glands releases parathyroid hormone (PTH) in response to low calcium levels in the blood. It stimulates the release of calcium from bones and increases the reabsorption of calcium by the kidneys.
Vitamin D has similar effects to PTH, including increasing calcium absorption in the intestines and decreasing kidney excretion. It can also mobilize calcium from bones, but to a lesser extent than PTH.
The C-cells of the thyroid gland release calcitonin in response to high calcium levels in the blood. It inhibits calcium release from bones and promotes calcium excretion by the kidneys. This essentially has the opposite effect of PTH.
When calcium levels fall too low, PTH is released, which causes calcium to be released from bones and increases the reabsorption of calcium by the kidneys. In addition, PTH stimulates the production of vitamin D, which helps increase calcium absorption from the intestines. These actions work together to increase calcium levels in the blood.
When calcium levels are too high, calcitonin is released, inhibiting the release of calcium from bones and promoting the kidneys’ excretion of calcium. This helps reduce calcium levels in the blood.
Overall, regulating calcium in the body is a complex process involving multiple hormones and organs. Disrupting this process can lead to hypocalcemia or hypercalcemia, which can have serious consequences.
Normal calcium levels can range from 8.5 – 10.5 mg/dL.
When a patient has low calcium, you may have heard that an ionized calcium level is specifically checked.
Ionized calcium is ordered because it represents the blood’s physiologically active form of calcium.
Total calcium (checked on a BMP or CMP), includes both ionized and protein-bound calcium. Total calcium levels can be influenced by pH and albumin levels.
Ionized calcium is considered a more accurate reflection of the body’s calcium status.
Albumin is a protein in the blood that binds to calcium and other ions, reducing the amount of ionized calcium available for cellular processes.
As a result, total calcium levels may be affected by changes in albumin levels.
Ionized calcium levels are unaffected by changes in albumin levels and are considered a more accurate reflection of the body’s calcium status. This means if the calcium is low but the albumin level is also low, ionized calcium should definitely be checked. There is a correction calculator, but this isn’t always accurate so it’s best to check an ionized calcium level to verify.
There are multiple causes of hypocalcemia, including:
Hypoparathyroidism is when the parathyroid glands produce insufficient amounts of PTH, leading to decreased calcium levels in the blood. This is usually caused by surgery or radiation.
As stated above, vitamin D is essential for calcium absorption from the intestines. This means a lack of vitamin D can lead to hypocalcemia.
The kidneys play a critical role in regulating calcium levels in the blood. Chronic kidney disease can cause decreased vitamin D production, as well as too much calcium excretion.
High phosphate levels lead to depositing calcium outside the blood, such as in skeletal muscle or bones.
Hypomagnesemia can cause parathyroid hormone resistance or decrease PTH secretion in severe cases.
Severe hypermagnesemia can also induce hypocalcemia.
Acute pancreatitis can lead to calcium deposition in the pancreatic tissue, leading to decreased calcium levels in the blood.
Certain medications can cause low calcium levels, including:
There are various other causes of low calcium levels, including:
Anxiety and hyperventilation can lead to a decrease CO2 in the blood, which can result in respiratory alkalosis.
Alkalosis can cause calcium ions to bind more readily to proteins like albumin, resulting in decreased levels of ionized calcium in the blood. This is often why patient’s having panic attacks experience numbness, tingling, and even muscle spasms.
Having the patient breathe into a non-rebreather not hooked up to oxygen (or a good ole paper bag) can help them retain more CO2 and decrease symptoms.
Hypocalcemia can cause many symptoms, with tetany being the most common and hallmark sign.
Tetany is when there is hyper-irritability of the peripheral neurons and their control over muscles. This can range from mild symptoms to more severe symptoms. This is unlikely to occur until calcium levels below 7-7.5 mg/dL.
Symptoms of tetany include:
Numbness and/or tingling around the mouth and lips.
Hypocalcemia can cause muscle cramps, carpopedal spasms, and even laryngospasms which can cause hypoxia and respiratory distress.
The patient may have numbness or tingling of their hands or their feet.
Other generalized symptoms of hypocalcemia include:
Low calcium can cause generalized weakness and fatigue.
Hypocalcemia can lead to anxiety, irritability, and even depression.
Severe hypocalcemia can cause focal or generalized seizures.
When performing a physical exam for a patient suspected of having hypocalcemia, the nurse should assess for the following:
Chvostek’s sign is positive when tapping the facial nerve in front of the ear causing twitching of the facial muscles on that side in patients with hypocalcemia.
This means that it is not always present in hypocalcemia, but if it is present, then hypocalcemia is a good possibility.
Trousseau’s sign is positive when spasms of the hand and wrist occur after inflating a blood pressure cuff above the patient’s systolic BP for 3-5 minutes.
This means it is likely more commonly present in hypocalcemia than Chvostek’s sign, but its presence doesn’t necessarily mean it is from hypocalcemia.
There are no other specific physical findings for low calcium, but you should observe for weakness, irregular heart rhythms, and possibly painful muscles to palpation.
Also check out: “The Cranial Nerve Assessment for Nurses”
The treatment of hypocalcemia depends on the severity of the condition and the underlying cause. When you get a low calcium level back on the blood work of your patient, as the nurse you should:
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still needs to be done. Close cardiac monitoring is essential when infusing electrolytes through the IV as well.
Notify the provider of the calcium levels, your assessment, and their cardiac rhythm (and if any QT prolongation is present).
Make sure there is at least one IV site, but place a second line if the hypocalcemia is severe.
Administer medications that are ordered (discussed below).
Treatment for hypocalcemia will depend on the severity, as well as any symptoms the patient is having. Severe symptoms that require immediate and likely IV repletion include tetany, arrhythmias, or seizures.
IV calcium is given for patients with severe symptomatic hypocalcemia. This includes patients with:
Calcium Gluconate 1-2g (90 – 180mg elemental calcium) in 50mL of 5% dextrose or NS infused over 10-20 minutes. This can be repeated after 10-60 minutes if needed. This is expected to raise serum calcium levels for only 2-3 hours.
After the bolus is given, a solution of 10% calcium gluconate can be used for a continuous infusion, started at 50ml/hr (11g calcium gluconate diluted in 1000ml of NS or D5W).
Oral calcium supplementation is started with mild symptoms or levels above 7.5 – 8.0 mg/dL, or for chronic hypocalcemia.
Patients should be given 1-2g of elemental calcium in divided doses.
Example Dosing:
Vitamin D should be started if the patient has low vitamin D levels. This is because low vitamin D levels can decrease calcium absorption in the intestines (as discussed above).
Calcitriol is a vitamin D metabolite that is preferred in patients with severe hypocalcemia, or in those with chronic kidney or liver disease. This effectively skips the need for the kidney and/or liver to process the vitamin D, leading to more rapid correction.
Hypomagnesemia is a common cause of hypocalcemia, as this can cause a decrease in PTH and its efficacy.
You can read all about magnesium replacement here.
As a nurse, it is essential to monitor patients with hypocalcemia closely to identify and manage any potential complications. The following parameters should be observed:
Serum calcium levels should be monitored regularly to assess treatment response and to identify potential complications such as hypercalcemia. This may include ionized calcium for a more accurate reflection of calcium status. Initially may need to be checked every 4-6 hours.
Other important tests that may be ordered with a patient with hypocalcemia includes:
Patients with low calcium are at higher risk for QT prolongation and cardiac arrhythmias. They should be on a continuous cardiac monitor and have an ECG checked.
Hypocalcemia is important in the conduction and beating of the heart. Very low levels can cause ECG abnormalities and arrhythmias. Some of these arrhythmias include:
On ECG, hypocalcemia can manifest in the following ways:
Hypocalcemia can also cause Torsades de Pointes, a type of polymorphic ventricular tachycardia that is deadly and quickly degenerates into Ventricular fibrillation if not treated ASAP. This does not happen as commonly as with hypomagnesemia.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
Hypocalcemia is an important electrolyte abnormality that must be recognized and treated quickly in the inpatient and ER settings. This is often caused by hypoparathyroidism, vitamin D deficiency, chronic kidney disease, or certain medications. It can cause symptoms such as tetany, evidenced sometimes by positive Chvostek or Trusseau signs.
Treatment involves oral or IV calcium and supplementation of Vitamin D and/or magnesium if applicable. Monitoring involves checking electrolytes, labs like PTH and Vitamin D, and montioring the ECG and continuous cardiac monitor.
If you’d like to download this article in PDF form, click here!
Published: April 2, 2023
Last Updated: April 10, 2023
Hypermagnesemia is a serious electrolyte imbalance that can lead to various complications, including cardiac and neuromuscular disturbances. Nurses are critical in recognizing and managing hypermagnesemia by performing a comprehensive nursing assessment, monitoring electrolyte levels and cardiac function, and initiating appropriate treatment interventions. Early recognition and treatment of hypermagnesemia can help prevent severe complications and improve patient outcomes.
Normal magnesium levels can range from 1.9 to 2.2 mg/dL.
Normal Levels: 1.9 – 2.2 mg/dL
Mild Hypermagnesemia: 2.5– 3.0 mg/dL
Moderate Hypermagnesemia: 3.0 – 5.0 mg/dL
Severe Hypermagnesemia: >5 mg/dL
Like with most electrolytes, the kidneys play a crucial role in regulating magnesium levels in the blood. You can read more about how the body regulates magnesium here. Hypermagnesemia is not too common of an electrolyte abnormality and is pretty limited on what actually can cause this. This includes:
The kidneys are responsible for filtering magnesium from the blood and excreting it through the urine. When the kidneys are not functioning properly, magnesium levels can build up in the blood, leading to hypermagnesemia. This can occur in patients with chronic kidney disease or acute kidney injury.
Antacids or laxatives with magnesium in them should be avoided in patients with End-stage Renal disease (ESRD) as it can cause a significant buildup of magnesium in the blood.
One of the most common causes of hypermagnesemia is the excessive intake of magnesium-containing supplements or medications. This can occur when patients take high doses of magnesium supplements to treat conditions like constipation or migraines, or when they are administered magnesium-containing medications in hospital settings. This is usually combined with Kidney failure unless a massive quantity is taken in a person with normal kidney function.
Pregnant women with pre-eclampsia are often placed on an IV magnesium sulfate drip to prevent seizures. This can increase their magnesium levels between 5-7 mEq/L.
Epsom salt enemas are not recommended as they can raise the serum magnesium to dangerous levels, even as high as 6-16 mEq/L!!
Mild hypermagnesemia (and asymptomatic) can occur in a variety of other medical conditions and scenarios including:
Symptoms of hypermagnesemia are directly correlated with the level of the magnesium in the blood.
High magnesium levels tells the parathyroid gland to stop secreting as much parathyroid hormone, which can lead to low calcium levels (hypocalcemia) which can also cause ECG changes.
The physical assessment of a patient with hypermagnesemia will also depend on the severity of the magnesium levels and other factors.
Treatment for hypermagnesemia aims to reduce serum magnesium levels and address any underlying causes. Treatment is going to depend on what their kidney function is. Common treatment strategies include:
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Stop any magnesium infusions or medications if the patient is currently getting them.
Make sure your patient is on the cardiac monitor. Obtain an ECG if not already done.
Notify the provider of the magnesium levels, your assessment, and their cardiac rhythm.
Make sure the patient has good access with at least one good IV.
Administer medications that are ordered (discussed below).
Treatment for hypermagnesemia aims to reduce serum magnesium levels and address any underlying causes. Treatment is going to depend on what their kidney function is. Common treatment strategies include:
Stopping magnesium intake will typically bring levels back down to normal pretty quickly in the absence of renal failure.
Diuretics like Loop diuretics (Lasix) or thiazide diuretics can also be used to lower magnesium levels pretty safely
IV isotonic fluids like Normal saline should be given in moderate cases of kidney failure to help restore kidney perfusion/function. Should not be given if the patient is anuric (and on dialysis).
May be required if the patient is already on dialysis or if the above measures fail. This can lower magnesium to non-toxic ranges within 2-4 hours.
Like hyperkalemia, giving IV calcium can help reverse hypermagnesemia’s neuromuscular and cardiac effects. However, this is given in a lower dose and over a longer period, with a recommended 100-200mg of elemental calcium over 5-10 minutes.
For a 10% calcium gluconate infusion, that would be 1-2mL (as opposed to 10mL given for Hyperkalemia).
Monitoring patients with hypermagnesemia involves cardiac monitoring and trending the magnesium levels.
Serum magnesium levels should be monitored frequently in patients with hypermagnesemia to assess the effectiveness of treatment and adjust interventions as needed. This is particularly important for patients with impaired kidney function or those receiving magnesium-containing medications, as they may be at increased risk for hypermagnesemia.
Besides magnesium levels, nurses should monitor other electrolyte levels, including calcium, potassium, and sodium, which may be affected by hypermagnesemia or its treatment. Hypocalcemia, in particular, can be a serious complication of hypermagnesemia and should be closely monitored and treated as needed.
Patients with hypermagnesemia should be monitored for signs of kidney dysfunction, particularly those with pre-existing kidney disease or impaired renal function. Creatinine and BUN should be monitored regularly (at least daily while in the hospital).
Patients with hypermagnesemia should be closely monitored for signs of cardiac arrhythmias, particularly those caused by prolonged QT intervals (see ECG changes below).
Monitor for signs of respiratory depression, particularly those with severe hypermagnesemia or impaired respiratory function. Patients may require intubation, mechanical ventilation, or other interventions to maintain adequate oxygenation and ventilation.
Patients with hypermagnesemia may experience neuromuscular irritability or depression, which can manifest as muscle twitching, cramping, or weakness. These patients are fall risks and should not be getting up without assistance!
Magnesium is a critical electrolyte that is crucial in regulating cardiac function, particularly in maintaining normal cardiac rhythm. However, hypermagnesemia can disrupt cardiac conduction and lead to various cardiac arrhythmias, including:
On ECG, hypermagnesemia can manifest in the following ways:
It is important to note that hypermagnesemia can also exacerbate cardiac arrhythmias caused by other electrolyte imbalances, such as hyperkalemia, hypokalemia, or hypocalcemia.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
Hypermagnesemia is a complex condition that can have serious consequences for patients, particularly those with impaired renal function or those taking magnesium-containing medications or supplements.
Nurses play a critical role in recognizing the signs and symptoms of hypermagnesemia, monitoring electrolyte levels and cardiac function, and initiating appropriate treatment interventions.
With proper nursing assessment and timely treatment, hypermagnesemia can be effectively managed to prevent severe complications such as cardiac arrhythmias, respiratory depression, and neuromuscular irritability or depression. By staying vigilant and proactive in their care, nurses can help promote optimal patient outcomes and improve the overall quality of care for patients with hypermagnesemia.
If you’d like to download this article in PDF form, click here!
ELECTROLYTE DISORDERS AND ARRHYTHMOGENESIS (JOURNAL OF INNOVATIONS IN CARDIAC RHYTHM MANAGEMENT)
Published: March 26, 2023
Last Updated: April 10, 2023
Hypomagnesemia, the medical term for low magnesium levels in the blood, can have disastrous consequences if left untreated. Magnesium is crucial in numerous bodily functions, including nerve and muscle function, heart rhythm, and bone health. Hypomagnesemia can lead to serious complications, such as seizures, cardiac arrhythmias, and even death.
As a nurse, knowing the causes, symptoms, and treatment of hypomagnesemia is essential to provide effective care and improving patient outcomes. This article will provide a comprehensive guide to nursing assessment and treatment of hypomagnesemia, including its causes, clinical manifestations, nursing assessment, treatment, and monitoring.
Magnesium is an electrolyte that is so important for our body’s daily functioning. Magnesium is essential from the cardiovascular system to our muscular system and energy metabolism! When low magnesium levels occur, this can cause issues in these areas! Magnesium functions in the following ways:
Magnesium acts similarly to a calcium channel blocker, helping to regulate the influx of calcium to control the proper timing and duration of electrical impulses in the heart. It also plays a crucial role in stabilizing the cell membrane and maintaining the resting membrane potential. Hypomagnesemia and low magnesium levels can lead to deadly cardiac arrhythmias.
Magnesium is important in the contraction of muscles as well as their relaxation. This helps with the funcitoning of cardiac muscle tissue, the GI system, and skeletal muscle tissue. It also relaxes the smooth muscle in the vessel walls, reducing blood pressure and preventing spasms.
Magnesium is necessary for metabolism as it is a co-factor for many enzymes involved in producing ATP – the body’s primary energy source on a cellular level. It’s also involved in the regulation of glucose metabolism and insulin signaling.
Magnesium is involved in transmitting nerve impulses and coordinating muscle movements, as it helps regulate the release of neurotransmitters and the activation of ion channels.
Magnesium supports the structural integrity of bones and teeth. It is also a co-factor for enzymes that regulate bone metabolism, and low magnesium levels are associated with osteoporosis.
Magnesium, like potassium, is tightly regulated to maintain proper body function and prevent hypomagnesemia and low magnesium levels from occurring. The regulation of magnesium involves a complex interplay of factors, including dietary intake, absorption, excretion, and hormonal mechanisms.
The body regulates its magnesium levels by adjusting how much magnesium it absorbs in the small intestine. When there are low magnesium levels, the absorption increases to prevent hypomagnesemia. The opposite is true as well!
The kidneys play a crucial role in regulating the excretion of magnesium, similar to its role in potassium.
Several hormones can influence magnesium levels. These include the Parathyroid hormone (PTH), which increases GI absorption and decreases kidney excretion. Vitamin D also stimulates magnesium absorption in the small intestines and regulates the activity of PTH.
Similar to hypokalemia, acid-base balance can also influence magnesium levels. Acidosis can cause magnesium to shift out of cells into the bloodstream and extracellular space. Alkalosis causes the opposite, leading to hypomagnesemia.
Normal magnesium levels can range from 1.7 to 2.2 mg/dL. However, only about 1% of the body’s magnesium levels are in the blood. 50-60% of magnesium is stored in the bone, and the rest is located in the muscles, soft tissues, and red blood cells.
Normal Levels: 1.9 – 2.2 mg/dL
Mild Hypomagnesemia: 1.6 – 1.9 mg/dL
Moderate Hypomagnesemia: 1 – 1.5 mg/dL
Severe Hypomagnesemia: <1 mg/dL
Several factors can contribute to hypomagnesemia, including inadequate dietary intake, malabsorption, renal losses, medications, and certain medical conditions. Understanding the underlying causes of low magnesium levels is essential for appropriate treatment and preventing long-term complications for our patients.
Hypomagnesemia can occur with excessive vomiting or diarrhea but occurs more often with diarrhea (it has 15x more magnesium in stool than in vomit).
Certain GI conditions that affect magnesium absorption include irritable bowel disease (IBD – AKA Crohn’s or ulcerative colitis), celiac disease, and pancreatitis.
Medications that increase magnesium loss from the GI system include chronic proton pump inhibitors (PPIs) like Omeprazole may lead to low magnesium levels. Other medications which can do this include H2 blockers, Antacids, and even laxatives.
Conditions that can lead to excessive kidney magnesium loss include renal tubular acidosis, hyperaldosteronism, and even diabetes. Certain medications can also impact this (discussed below).
Medications that can increase the excretion of magnesium in the kidneys include loop diuretics and thiazide diuretics. Other drugs that can cause hypomagnesemia include Aminoglycoside antibiotics, certain chemotherapies, calcineurin inhibitors, and Digoxin.
Chronic alcoholism can impair magnesium absorption in the small intestine and increase excretion in the urine, leading to hypomagnesemia. This magnesium wasting in the urine is reversible after four weeks of sobriety.
Patient’s with an organ transplant are more likely to experience hypomagnesemia, likely from their calcineurin inhibitor medications (like tacrolimus).
High calcium levels can lead to mildly low magnesium levels.
Certain rare genetic conditions can cause decreased magnesium absorption in the small intestine and increased renal magnesium wasting.
Symptoms of hypomagnesemia (low magnesium levels) will depend on the patient and the severity of their hypomagnesemia. As the magnesium levels drop, the symptoms become more pronounced, severe, and potentially life-threatening.
Like low potassium, muscle weakness is common with hypomagnesemia. They may experience fatigue and muscle weakness in their legs which can cause difficulty walking, as well as weakness of any other muscles in their body.
Patients may feel tingling sensations and experience involuntary muscle contractions, particularly in their hands or lower extremities.
As discussed above, magnesium is essential in the conduction as well as the mechanical beating of the heart. If an arrhythmia occurs, patients may experience palpitations, chest pain, shortness of breath, dizziness, or even syncope. Cardiac arrest is possible if they go into a deadly rhythm like VFIB.
Low magnesium levels can cause nausea, vomiting, or abdominal cramping. Additionally, if the patient has diarrhea, that may be a clue on the cause.
Magnesium can cause CNS hyperirritability, leading to confusion, irritability, hyperactive deep tendon reflexes, paresthesias, and seizures.
The physical assessment of a patient with hypomagnesemia will also depend on the severity of the low magnesium levels and other factors.
Overall, while the nursing assessment of hypomagnesemia may not reveal many specific physical findings, monitoring for muscle weakness, irregular heart rhythms, and signs of potential underlying issues such as edema, ascites, and abdominal tenderness is important for identifying the condition and providing appropriate interventions to manage hypomagnesemia and prevent complications.
The treatment for hypomagnesemia depends on the underlying cause, severity, and serum magnesium levels.
When you get your patient’s results back, and they show hypomagnesemia, then follow the following general interventions:
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still needs to be done. Close cardiac monitoring is essential when infusing electrolytes through the IV as well.
Notify the provider of the potassium levels, your assessment, and their cardiac rhythm. They will order the treatment for hypomagnesemia!
Make sure there is at least one IV site, but place a second line if the hypomagnesemia is severe.
Evaluate if they are on any medications which may lead to hypomagnesemia listed above.
Administer medications that are ordered (discussed below).
Treatment for hypomagnesemia will depend on the severity, as well as any symptoms the patient is having. Severe symptoms that require immediate and likely IV repletion include tetany, arrhythmias, or seizures.
Figuring out why the magnesium is low is essential, but there shouldn’t be any reason to delay replacing the magnesium with Oral or IV options. However, addressing the underlying cause can prevent further loss of magnesium and prevent it from happening again.
PO magnesium is the standard for mild to moderate hypomagnesemia, primarily if there are no or minimal symptoms.
There are many different variations of magnesium pills, such as:
Generally, sustained release options are better because they minimize the renal wasting of the magnesium. Common options include:
If the sustained release is unavailable, magnesium oxide 800-1600mg daily in divided doses may be used, but diarrhea may occur.
IV magnesium is given to patients with severe symptoms or who are NPO for whatever reason.
IV replacement dosing will depend on the severity:
Patients in renal failure should be cautiously replaced with electrolytes like magnesium and potassium, as their ability to excrete those electrolytes is impaired. Therefore, dosing should generally be cut in half, and levels should be closely monitored.
Patients should generally be maintained on magnesium replacement for 1-2 days after the levels have normalized to replete intracellular magnesium. However, if ongoing losses occur, chronic therapy may be needed.
Monitoring patients with hypomagnesemia involves cardiac monitoring and trending the magnesium levels.
Magnesium levels are generally checked at least daily while inpatient until normalization of the magnesium level.
Other electrolytes and monitoring of renal function should also be checked, usually daily, every morning.
Patients with low magnesium are at high risk for cardiac arrhythmias. Additionally, anybody receiving IV replacement with magnesium should be on a cardiac monitor.
Magnesium is an important electrolyte that plays a crucial role in cardiac function, particularly in maintaining normal cardiac rhythm. Hypomagnesemia and low magnesium levels can lead to various cardiac arrhythmias, including:
On ECG, hypomagnesemia can manifest in the following ways:
It is important to note that hypomagnesemia can also exacerbate cardiac arrhythmias caused by other electrolyte imbalances, such as hypokalemia and hypocalcemia.
Nurses should be aware of the potential cardiac complications associated with hypomagnesemia and monitor patients for signs and symptoms of arrhythmias. Timely recognition and treatment of hypomagnesemia can help prevent severe cardiac complications.
Hypomagnesemia is associated with Torsades de Pointes, which is a type of polymorphic ventricular tachycardia that is deadly and will quickly degenerate into Ventricular fibrillation if not treated ASAP. Treatment involves following ACLS protocol, but often IV magnesium is given rapidly if hypomagnesemia is suspected as a cause.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
Hypomagnesemia is a condition that nurses should be familiar with, as it can have significant implications for patient health. Magnesium is vital in various bodily functions, including the cardiac, nervous, and gastrointestinal systems.
The body regulates it through dietary intake, absorption, excretion, and hormonal factors. Various factors, such as chronic diarrhea, alcoholism, and certain medications, can cause hypomagnesemia. Treatment often involves magnesium replacement, either orally or intravenously, and addressing any underlying conditions that may contribute to the deficiency.
Nurses are essential in identifying and monitoring hypomagnesemia and low magnesium levels and educating patients on the importance of adequate magnesium intake and potential risk factors. Nurses can provide optimal care and improve patient outcomes by understanding hypomagnesemia’s causes, symptoms, and treatment.
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Published: March 19, 2023
Last Updated: March 23, 2023
Treatment for Hyperkalemia is essential in the hospital and acute care settings, as it can be deadly!
Hyperkalemia is when a patient’s serum potassium level rises above 5.0 mEq/L. This potentially life-threatening medical condition is one that nurses must be familiar with, as this can lead to cardiac arrhythmias and cardiac arrest.
Nurses are crucial in preventing, detecting, and managing hyperkalemia through various nursing interventions and treatment options. This article will discuss the causes of hyperkalemia, nursing interventions, and treatment of hyperkalemia, providing nurses with the knowledge and tools necessary to identify and manage this deadly condition.
If you haven’t read the article on Hypokalemia, be sure to read that post first as it has some great background information about how the body regulates potassium in the body!
The normal range for potassium levels within the body is 3.5-5.0 mEq/L. Hyperkalemia is any level that is higher than 5.0 mEq/L
The higher the level, the more likely your patient will experience side effects or complications from hyperkalemia.
Remember that this is the level of potassium that is OUTSIDE the cells of the body. The actual amount (3.5-5mEq/L) is very low. However, the inside of the cell usually has 120-150mEq/L… That’s 30 times the level from the outside! This is why conditions that cause lysis of cells on a large scale can cause large increases in hyperkalemia.
We discussed in the previous article about how potassium regulates the body and understanding how potassium works and then also what causes high potassium levels is important to understand before diving into the treatment for hyperkalemia.
There are various causes of hyperkalemia, including:
The kidneys are the main way the body regulates potassium levels. When potassium levels are too high, the kidneys will excrete excess potassium. When the kidneys don’t work like they should and can’t filter out the excess potassium like usual, this is really the primary reason you’ll see potassium levels rise significantly in the blood. This can be from acute or chronic kidney disease.
Certain medications can cause an increase in serum potassium levels, such as lisinopril, potassium-sparing diuretics (like Spironolactone), and even NSAIDs. These impact how the kidneys normally excrete potassium. Beta-blockers even can increase potassium levels, but to a lesser degree (usually < 0.5 mEq/L elevation).
Acidosis, when a buildup of hydrogen ions in the blood, causes a potassium shift from inside to outside the cells, leading to hyperkalemia.
Respiratory acidosis is largely caused by an excess buildup of CO2 in the blood. Since CO2 is a small, uncharged molecule, it can easily diffuse across the cell membrane and does not directly affect potassium levels within cells. Therefore, in respiratory acidosis, potassium levels in the blood are generally not significantly affected.
Insulin and aldosterone both impact potassium levels.
A deficiency in insulin (such as with DKA) leads to potassium accumulation outside the cell.
In hypoaldosteronism (Addison’s disease), there is not enough aldosterone. Aldosterone normally promotes potassium excretion in the kidney. So not having enough leads to higher potassium levels.
You’ll see later that we can utilize one of these hormones in the actual treatment for hyperkalemia!
When a cell lyses or splits open, its contents are released into the extracellular space. As we discussed, potassium concentration is much higher in the cells.
Whenever a condition or injury leads to massive destruction and lysis of cells, this can lead to hyperkalemia.
These conditions include major trauma, crush injuries, tumor-lysis syndrome, rhabdomyolysis, major burns, and hemolytic anemia.
Part of the treatment for hyperkalemia is avoiding these medications!
Pseudohyperkalemia is essentially a “false positive” elevation of potassium. This occurs during the blood draw or after the blood has been drawn. It’s important to recognize cases of “fake” high potassium before implementing treatment for hyperkalemia, as this can lead to hypokalemia!
Possible causes of pseudohyperkalemia include:
Blood sample hemolysis usually occurs when drawing blood draw from mechanical trauma. This often occurs if the catheter is against the vein wall and causes red blood cell lysis during the draw. This blood can have a red tint due to released hemoglobin.
Repeated fist-clenching can cause potassium to shift out of the muscles temporarily. This can lead to elevations by more than 1-2 mEq/L in that forearm.
Significant elevations in platelet levels and very high WBCs (in the setting of chronic lymphocytic leukemia) can cause false potassium elevations, since the white blood cells are very fragile and break after the draw.
Certain forms of hereditary pseudohyperkalemia exist due to potassium shifting out of red blood cells.
Whenever a high potassium level comes back and the clinical picture doesn’t make sense (such as normal renal function, no symptoms, and no other findings), then suspect pseudo-hyperkalemia.
Symptoms of hyperkalemia will vary depending on the patient and how severe the hyperkalemia is. The higher the potassium level, the more likely the patient will exhibit symptoms, and the worse they often are, the more quickly treatment for hyperkalemia will need to be initiated!
Some possible symptoms of hyperkalemia or high potassium include:
Muscle weakness can also be a sign of hyperkalemia, just as it can be a sign of hypokalemia. As potassium levels rise, there can initially be increased contractions and cause spasms and twitches.
However, as the potassium level continues to rise, skeletal muscle excitability decreases, resulting in muscle weakness and even paralysis.
Symptoms of cardiac arrhythmias may occur if the patient is experiencing an arrhythmia, such as palpitations, chest pain, Shortness of breath, dizziness, or syncope.
High potassium levels can affect the smooth muscles of the GI tract, leading to nausea, vomiting, and possibly abdominal pain/cramping or diarrhea.
Like with hypokalemia, hyperkalemia can also cause numbness or tingling, typically in the extremities or the face.
This is usually only in severe cases with severe muscle fatigue of the respiratory muscles, and the patient may even need to be intubated.
High potassium levels can also agitate the central nervous system, leading to anxiety or restlessness.
The physical assessment of a patient with hyperkalemia will also depend on the severity of the potassium and other factors, but most patients will have no specific physical findings.
The treatment for hyperkalemia depends on the underlying cause, severity, and serum potassium level.
When you get your patient’s results back, and they show hyperkalemia, especially >5.5 mEq/L, then follow the following general interventions:
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still needs to be done. Close cardiac monitoring is essential when infusing electrolytes through the IV as well, as some electrolytes like calcium are essential in the treatment for hyperkalemia!
Notify the provider of the potassium levels, your assessment, and their cardiac rhythm. The treatment for hyperkalemia will be ordered by them!
Make sure there is at least one IV site, but place a second line if the hyperkalemia is severe.
Evaluate if they are on any medications which may lead to hyperkalemia listed above.
Administer medications that are ordered (discussed below).
The treatment of hyperkalemia will depend on how severe the level is and any symptoms or cardiac arrhythmias the patient is currently experiencing. The patient’s Provider team will order this. Treatment generally includes:
Identifying and addressing the underlying causes of hyperkalemia. The first thing would be to look at their renal function on their labs – if it is elevated, the high potassium level is likely true. Ensure it is true hyperkalemia instead of pseudohyperkalemia as above.
Avoid potassium supplements or foods rich in potassium until the potassium has normalized. All medications which can worsen hyperkalemia should be stopped.
Calcium is a very important part of the treatment for hyperkalemia. When given, it stabilizes cardiac conduction and decreases the risk of arrhythmias such as Vfib or VTACH.
Calcium gluconate is preferred, with the dose being 1,000mg (10mL of 10% solution) infused over 2-3 minutes. This dose can be repeated if ECG changes persist.
As with any electrolyte, your patient should be on the cardiac monitor during this infusion.
Calcium chloride (from the code cart) can also be given in a similar dose (500-1000mg). This does actually deliver 3-times the concentration of elemental calcium. However, it does irritate the vein and can cause tissue necrosis if extravasation occurs.
IV insulin is given to all patients (not just patients with diabetes) with moderate to severe hyperkalemia when dialysis is not readily available/indicated, since insulin drives potassium into the cells. This is a temporary fix but will decrease potassium levels by about 1 mEq/L pretty quickly, lasting for about 4-6 hours. The dose may need to be repeated at that time.
Please note this should be given with dextrose so it doesn’t cause hypoglycemia. Patients who’s glucose is > 250 can receive the insulin alone.
Glucose monitoring should be monitored every hour for 5-6 hours.
Dextrose is given with insulin to prevent hypoglycemia but can also lead to endogenous insulin secretion, which further enhances the potassium-reducing effect.
The dosage is typically 25gm, or 1 full amp (the total amount in the code cart). This is pushed slowly and is very thick and sticky.
Even with one amp given, hypoglycemia still occurs in many patients. It’s recommended to start a 10% dextrose infusion at 50-75ml/hr until 5-6 hours after administering the insulin.
Beta-agonists, such as albuterol, are sometimes used as a treatment for hyperkalemia to cause a shift of potassium into the cells (similar to the effect of insulin). This is not always ordered but should be considered in patients with significant symptoms or ECG changes despite the above treatment.
Beta-agonists can reduce potassium levels by 0.5 – 1.5 mEq/L, and is usually given in an hour-long treatment. SubQ Terbutaline is an alternative to albuterol.
This will also increase heart rate, and patients with heart disease and at risk for cardiac complications may be better off not getting a beta-agonist.
Sodium bicarbonate can reduce potassium levels in patients with metabolic acidosis. 1 amp (50 mEq) can be given in 50ml, or alternatively 150mEq can be given in 1 L of 5% Dextrose over 2-4 hours.
This treatment for hyperkalemia should be limited to patients with metabolic acidosis, and multiple doses can lead to hypernatremia.
Shifting the potassium into the cells is a great short-term solution to prevent complications from hyperkalemia. Still, the true treatment for hyperkalemia is removing excess potassium from the body.
Removing potassium from the body is done in 3 main ways.
Patients with hyperkalemia need good monitoring, especially if they have moderate to severe hyperkalemia.
Potassium levels will be redrawn and assessed depending on the severity and what type of treatment for hyperkalemia was ordered.
Mild to moderate levels can be rechecked in 4-6 hours, but severe hyperkalemia may need to be checked more frequently.
If insulin is given, glucose levels must be checked hourly for 4-6 hours, as hypoglycemia is common (even if you administer dextrose).
Closely monitor the patient’s renal function (BUN & Creatinine), other electrolytes, and acid-base balance (CO2).
As discussed, high potassium levels can lead to bradycardia and arrhythmias. Continuous cardiac monitoring should be maintained, and intermittent ECGs may also be warranted.
Severe hyperkalemia can cause respiratory failure, so monitoring their breathing, lung sounds, respiratory rate, and pulse ox is important.
Vital signs should be checked per facility protocol.
Monitoring urine output is important, especially in patients where loop diuretics are given, and potassium is being wasted through the kidneys.
Potassium is very important in the heart’s conductive system and for each heartbeat. The higher the potassium level, the more likely ECG changes may be seen, and the higher chance that an arrhythmia may occur.
The more common arrhythmias associated with hyperkalemia are sinus bradycardia, AV blocks, VTACH, Vfib, and asystole.
On the ECG, hyperkalemia can manifest in a few ways, including:
Whenever there are ECG changes, the treatment for hyperkalemia becomes even more essential, as patients with ECG changes are more likely to experience deadly arrhythmias.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
In conclusion, nurses should have an essential understanding of electrolyte abnormalities and the treatment for hyperkalemia.
Through medications that protect the patient from cardiac arrhythmias (like calcium), medications that shift potassium into cells temporarily (like insulin, albuterol, or sodium bicarb), and treatments for hyperkalemia that remove potassium from the body (like Lasix, Kayexalate, or dialysis), we can successfully reduce our patient’s potassium and save their lives!
Also check out:
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Published: March 12, 2023
Last Updated: March 22, 2023
Hypokalemia is when the body has low potassium levels outside the cell (in the bloodstream). Potassium is an electrolyte that plays a vital role in many bodily functions, particularly in the heart and cardiovascular system. Therefore, it is essential for the proper functioning of the body, and when potassium levels are high or low, this can cause our patients to be very sick and can even cause death.
As a nurse, it’s essential to be aware of the signs and symptoms of hypokalemia and the nursing interventions and low-potassium treatments that can be used to manage this condition. In this article, we’ll explore the symptoms of hypokalemia, nursing interventions that can be used to address low potassium levels, and effective treatment options for patients with this condition.
Electrolytes help our bodies perform daily functions and survive. Without potassium or our other electrolytes, we literally couldn’t survive.
Electrolytes are ions with a positive or negative charge, and these help cells create energy, conduct impulses, and do what they need to do. Potassium is positively charged. Some of the functions that potassium helps regulate in the body include:
Potassium is essential for proper muscle function, including both skeletal and smooth muscle. It helps the muscles contract and relaxes, impacting movement, digestion, and much more!
Potassium is essential in regulating fluid balance within the body. Potassium has the same tonicity as sodium, drawing water with it wherever it goes. Potassium is essential in the movement of fluid across cell membranes.
Probably one of potassium’s most essential functions, it helps the cardiac system function! The heart uses conductive tissue, which uses potassium to help transmit its signal for every heartbeat – just like it uses calcium, magnesium, and sodium as well!
Studies show that high-potassium diets can help improve insulin sensitivity and reduce the risk of type 2 diabetes.
Just like our heart, the nervous system is ALL about conducting electricity and “action potentials,” but on a much more complex level. Potassium helps our nerve cells communicate with each other.
This is a catch-all, but the sodium-potassium pump is essential for the proper function of almost every cell in our body. That’s how vital potassium is and how hypokalemia can affect our patient’s health!
The body regulates potassium in many ways to maintain it at the appropriate level to help it maintain homeostasis and function at its optimal capacity. Nurses should be aware of these mechanisms and take proper steps to monitor and maintain healthy potassium levels in their patients, particularly those with conditions that may affect potassium balance, such as kidney disease or heart disease.
Some of the ways the body regulates potassium and prevents hypokalemia include:
The kidneys play a crucial role in regulating potassium levels. These filter out excess potassium and retain more potassium when levels are low.
Several hormones impact potassium levels, primarily Aldosterone and Insulin.
Aldosterone, produced by the adrenal glands, is a signal that tells the kidneys to retain more sodium and potassium.
Insulin, which is produced by the pancreas, helps to promote the uptake of potassium into the cells.
The body’s acidity can also affect potassium levels, with acidosis causing potassium to move out of the cells into the bloodstream and interstitial spaces.
Dietary potassium intake is essential in helping the body maintain adequate potassium levels; however not as important as you might think since the body is good at keeping extra potassium if dietary intake is inadequate.
Remember that severely acidotic states, like that in DKA, leave the body with significant decreases in potassium. There is a LACK of insulin, which normally moves potassium into cells, and then there is also acidosis which further shifts potassium out of cells. That’s why it is SO important to replace potassium FIRST before insulin (if low). Read more about DKA here!
The lower the potassium level, the more likely your patient will experience side effects or complications from hypokalemia.
Remember that this is the level of potassium that is OUTSIDE the cells of the body. The actual amount of potassium that is outside the cell normally is very low. The inside of the cell as approximately 120-150mEq/L… That’s 30 times the level from the outside!
This is why conditions that dramatically shift the potassium outside the cells (like DKA) can lead to a massive depletion of potassium. This is also why replacing potassium is SO important in these instances before fixing the acidosis and the hyperglycemia.
As we’ve discussed, many factors impact how the body regulates potassium levels, and similarly, there are various causes of hypokalemia. These include:
Certain medications and conditions can shift potassium into the cells, which can cause low potassium levels. This includes Insulin, inhalers like albuterol, and alkalosis.
A common cause of hypokalemia is when it is lost from the GI system. This is usually from either excessive vomiting, diarrhea, or tube drainage.
There isn’t a ton of potassium in the emesis, but excessive vomiting leads to increased potassium wasting in the urine.
This is when potassium is lost in the urine and is often caused by diuretics like LOOP diuretics (Lasix) or increased mineralocorticoid activity (like hyperaldosteronism, crushing’s syndrome, etc.).
Often, this is not the only cause, as the body is pretty good about compensating for inadequate dietary intake.
Symptoms of hypokalemia will vary depending on the patient and how severe the hypokalemia is. Still, the lower it is, the more likely the patient will exhibit symptoms, and the worse they often are.
Some possible symptoms of hypokalemia or low potassium include:
Muscle weakness is one of the most common symptoms of hypokalemia, which can affect the legs, arms, chest muscles, or any muscle in the body. The patient may have trouble walking, taking the stairs, or lifting objects. This usually only occurs if levels drop below 2.5 mEq/L.
Severe hypokalemia can lead to muscle cramps and even a buildup of myoglobin, leading to rhabdomyolysis. This can be damaging to the kidneys. Hypokalemia also leads to decreased perfusion of the muscles during exercise, which can worsen rhabdo.
A generally non-specific symptom, but patients with low potassium often experience fatigue.
Hypokalemia can cause ileus and constipation and lead to abdominal distention, nausea, and vomiting. The patient may have diarrhea which may contribute to the hypokalemia, but can also have constipation from hypokalemia.
Hypokalemia can cause numbness and tingling in the hands or feet.
Low potassium can cause the kidneys to produce more urine, leading to increased urination.
This is usually only in severe cases with severe muscle fatigue of the respiratory muscles, and the patient may even need to be intubated.
Abnormalities such as premature beats (PAC, PVC), Afib, sinus bradycardia, or even VTACH or VFIB or asystole/PEA.
Even still, most patients with low potassium on blood work will not have any specific symptoms. Certain patients have an increased risk for potassium issues. This includes:
The physical assessment of a patient with hypokalemia will depend on the severity of the potassium and other factors as well, but most patients will have no specific physical findings.
Treatment of hypokalemia depends on the severity of the hypokalemia and any symptoms or complications present.
When you get your patient’s results back, and they show hypokalemia, especially < 3.0 mEq/L, then follow the following general interventions:
Make sure they don’t have any symptoms and are stable, including a recent set of vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still hasn’t been done.
Notify the provider of the potassium levels, your assessment, and their cardiac rhythm.
Make sure there is at least one IV site that is working well. If the level is severely low, it is best to place a second line as well.
Evaluate if they are on any medications which may lead to hypokalemia, listed above.
Administer treatment as ordered: Administer PO or IV potassium as ordered.
The treatment of hypokalemia will depend on how severe the level is low and if the patient has any significant symptoms. This will be ordered by the patient’s Provider team. Treatment generally includes:
Identifying and addressing the underlying causes of hypokalemia is critical before correcting the potassium. The potassium may not be low but has shifted into the cells from something like alkalosis, hypothermia, and certain medications.
Low magnesium can cause potassium wasting in the kidneys. This means the magnesium level should be evaluated in all patients with hypokalemia and replaced first (assuming the patient is stable).
We need to replace potassium, and a large amount of potassium can be absorbed by the GI system. How much is ordered will depend on the severity of the hypokalemia.
You are limited in how fast you can infuse potassium through the IV to prevent arrhythmias and IV site irritation. Rates can be faster in a central line and slower in a peripheral IV line.
Where your potassium is infusing will change how fast you can infuse. While this may vary based on your specific facility protocol, generally, you can infuse in a peripheral line up to 10 mEq/L over 1 hour and in a central line 20 mEq/L over 1 hour.
However, rates of up to 40 mEq/L can be appropriate in critical and code situations. Again, this should be infused into a central line or multiple peripheral IVs.
Patients with hypokalemia need good monitoring, especially if they have moderate to severe hypokalemia.
Potassium levels will be redrawn and assessed depending on the severity and what the Provider orders. Generally, mild hypokalemia is often only rechecked on the next lab draw (usually by the following day). Severe hypokalemia being replaced is recommended to be checked every 2-4 hours (usually in the ICU).
As we’ve discussed, low potassium levels can impact cardiac rhythms, and whenever a patient’s getting IV replacement of potassium or magnesium, they should be on a cardiac monitor to monitor for cardiac ectopy or arrhythmias.
Severe hypokalemia can cause respiratory failure, so monitoring their breathing, lung sounds, respiratory rate, and pulse ox is essential.
Monitoring for phlebitis and thrombophlebitis at the insertion site is essential, as IV potassium often burns.
If you are running IV potassium alone through an IV, this will often burn the patient. Applying ice packs can help, but your best bet is running fluids slowly and piggybacking the IV potassium into the Y site above, diluting the potassium. And, of course, you should have an order for these IV fluids!
Potassium is super important in the proper conduction of cardiac tissue. Remember that each heartbeat involves rapid depolarization (firing) and repolarization of cardiac conductive cells.
Potassium plays a crucial role in maintaining the resting membrane potential and regulating the overall electrical activity of the heart.
The more common arrhythmias associated with hypokalemia include:
These are induced by early afterdepolarizations and triggered activity, which can be caused by hypokalemia.
Hypokalemia can cause other arrhythmias include PACs, PJCs, AV blocks, and even Afib.
On the ECG, hypokalemia can manifest in a few ways, including:
The risk of hypokalemic-induced arrhythmias is highest in elderly patients, those with heart disease, and patients on digoxin or antiarrhythmic drugs who are already predisposed to arrhythmias.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
In conclusion, potassium is an essential electrolyte that plays a vital role in many bodily functions, including muscle function, fluid balance, cardiac and nervous systems, blood sugar control, and cellular function.
Nurses must be aware of the signs and symptoms of hypokalemia and the nursing interventions and low-potassium treatments that can be used to manage this condition.
Patients with hypokalemia require careful monitoring, especially with moderate-to-severe hypokalemia, with careful attention to their cardiac rhythm and respiratory function!
If you’d like to download this article in PDF form, click here!