Hypocalcemia Guide for Nurses: Nursing Assessment and Management

Hypocalcemia Guide for Nurses: Nursing Assessment and Management

Published: April 10, 2023

Last Updated: April 10, 2023

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

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An image of IV magnesium sulfate with Magnesium in a ball with low levels with surrounding foods that are high in magnesium

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.

Learn about the causes, nursing assessment, and treatment for hyperkalemia in this comprehensive guide for nurses and medical professionals.

Why is Calcium Important in the Body?

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.

A normal human cell

Bones and Teeth

Calcium provides the structural support for strong and healthy bones and teeth.

A depiction of a neuron

Nerve Transmission

Calcium helps regulate the transmission of nerve impulses, which is critical for communication between the brain and other body parts.

An image of a muscle

Muscle Contraction

Calcium helps with muscle contraction and relaxation, including the muscles involved in breathing and the heart beating.

a desaturated heart and yellow cardiac conductive tissue showing the SA node, AV node, and ventricles

Cardiac Conduction

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.

A bundle of red blood cells that are clotted together

Blood Clotting

Calcium is necessary to form blood clots, which help stop bleeding after an injury.

An enzyme and two substrates

Enyzme Activity

Calcium activates and regulates a wide range of enzymes, which are essential for the body to function as it’s supposed to!

How is Calcium Regulated in the Body?

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:

A generic hormone depiction

Parathyroid Hormone (PTH)

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.

A yellow sun with vitamin D in the middle

Vitamin D

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.

A generic hormone depiction

Calcitonin

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 & Hypocalcemia

Normal calcium levels can range from 8.5 – 10.5 mg/dL

Calcium Levels

  • Normal Levels: 8.5 – 10.5 mg/dL
  • Hypocalcemia: <8.5 mg/dL
  • Critical Hypocalcemia: <4.4 mg/dL

What are Ionized Calcium levels?

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. 

Ionized Calcium Levels

  • Normal Levels: 4.4 – 5.4 mg/dL
  • Hypocalcemia: <4.4 mg/dL
  • Critical Hypocalcemia: <3.0 mg/dL

Albumin and Calcium

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. 

Causes Of Hypocalcemia:

There are multiple causes of hypocalcemia, including:

An image of the thyroid and parathyroid glands

Hypoparathyroidism

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.

Vitamin D in a softgel

Vitamin D Deficiency

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, with the left one transected so you can see the inside

Chronic Kidney Disease

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.

Milk overflowing

Hyperphosphatemia

High phosphate levels lead to depositing calcium outside the blood, such as in skeletal muscle or bones.

Milk overflowing

Abnormal Magnesium Levels

Hypomagnesemia can cause parathyroid hormone resistance or decrease PTH secretion in severe cases.

Severe hypermagnesemia can also induce hypocalcemia.

An image of an inflamed appendix

Acute Pancreatitis

Acute pancreatitis can lead to calcium deposition in the pancreatic tissue, leading to decreased calcium levels in the blood.

A bottle of medications that are prescription

Medications

Certain medications can cause low calcium levels, including:

  • Bisphosphonates
  • Colchicine
  • Chemos (cisplatin)
  • Immunomodulators
  • Anticonvulsants (Dilantin, Phenobarbital)
A bag of Type A blood

Other Conditions

There are various other causes of low calcium levels, including:

  • Certain genetic conditions
  • Sepsis or severe illness
  • Post-surgical state
  • Massive blood transfusions (from citrate in the blood)

Hyperventilation

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. 

Nursing Assessment Of Hypocalcemia

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:

Lips with blue tingling numbness around it

Peri-oral numbness

Numbness and/or tingling around the mouth and lips.

A muscle with red electric bolts indicating pain

Muscle Cramps and spasms

Hypocalcemia can cause muscle cramps, carpopedal spasms, and even laryngospasms which can cause hypoxia and respiratory distress.

A hand with blue electric bolts indicating tingling

Paresthesias

The patient may have numbness or tingling of their hands or their feet.

Other generalized symptoms of hypocalcemia include:

A fatigued muscle with a sad tired expression

Muscle Weakness

Low calcium can cause generalized weakness and fatigue.

A silhouette of a head with red and orange markings above the head, indicating anxiety

Mental Health

Hypocalcemia can lead to anxiety, irritability, and even depression.

A blue brain with yellow lightning bolts depicting a seizure

Seizures

Severe hypocalcemia can cause focal or generalized seizures.

PHYSICAL Assessment

When performing a physical exam for a patient suspected of having hypocalcemia, the nurse should assess for the following:

Vital Signs

  • HR: May be irregular (indicating an arrhythmia)
  • BP: May be decreased
A face with the facial nerve present, which is causing Chvostek sign

Chvostek's Sign

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.

  • Sensitivity: 10-64%
  • Specificity: 69-92%

This means that it is not always present in hypocalcemia, but if it is present, then hypocalcemia is a good possibility. 

 

An image of carpopedal spasms occurring with a blood pressure cuff inflated on the upper arm

Trousseau's sign

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.

  • Sensitivity: 30-94%
  • Specificity: 29-63%

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”

Treatment for Hypocalcemia

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:

Assess the Patient

Ensure they don’t have any symptoms and are stable, including recent vital signs.

Cardiac Monitor

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

Notify the provider of the calcium levels, your assessment, and their cardiac rhythm (and if any QT prolongation is present).

Ensure IV access

Make sure there is at least one IV site, but place a second line if the hypocalcemia is severe.

Administer Treatment

Administer medications that are ordered (discussed below).

Treatment for hypocalcemia:

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.

Bag of IV magnesium sulfate

IV Calcium

IV calcium is given for patients with severe symptomatic hypocalcemia. This includes patients with:

  • Carpopedal spasms
  • Laryngospasms
  • Bronchospasms
  • Seizures
  • Prolonged QT interval on ECG
  • Levels < 7.5 mg/dL who are at higher risk for serious complications

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).

Calcium

Oral Calcium Supplementation

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:

  • Calcium carbonate 1250mg, Take 1 tablet PO TID
  • Calcium citrate 950mg, Take 2 tablets PO BID

 

Vitamin D softgels

Vitamin D Supplementation

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).

  • Ergocalciferol (D2) 50,000 iU PO weekly x 6-8 weeks
  • Cholecalciferol (D3) 50,000 iU PO weekly x 6-8 weeks

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.

  • Calcitriol 0.25mcg PO BID

 

Bag of IV magnesium sulfate

Magnesium Replacement

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.

Monitoring of Hypocalcemia

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:

A Gold top blood vial filled with blood

Calcium Levels

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.

A Gold top blood vial filled with blood

Other Electrolytes

Other electrolytes and monitoring of renal function should also be checked, usually daily, every morning. Important related electrolytes include:

 

A Gold top blood vial filled with blood

Other Labs

Other important tests that may be ordered with a patient with hypocalcemia includes:

  • PTH levels
  • Vitamin D levels

 

A Gold top blood vial filled with blood

Cardiac Monitoring

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.

A round calcium ion Ca++

Foods High in Calcium

  1. Cheese
  2. Yogurt
  3. Milk
  4. Sardines
  5. Tofu
  6. Fortified soy, almond, and/or oat milk
  7. Fortified orange juice
  8. broccoli
  9. Kale
  10. Almonds

Hypocalcemia and Cardiac Arrhythmias

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:

  • Torsades de Pointes: Torsades de Pointes is a type of ventricular tachycardia characterized by twisting the QRS complex around the isoelectric line.
  • Atrial fibrillation: Hypocalcemia can increase the risk of atrial fibrillation, due to impaired atrial and AV nodal conduction.
  • Ventricular Tachycardia: Hypocalcemia-induced VTACH can occur due to increased automaticity of the ventricular myocardium.
  • Premature ventricular contractions (PVCs): Hypocalcemia can increase the risk of PVCs, which are abnormal contractions that originate from the ventricles rather than the atria.
  • Atrioventricular (AV) blocks: Hypocalcemia can cause AV blocks, which occur when there is impaired conduction between the atria and ventricles.

On ECG, hypocalcemia can manifest in the following ways:

  • QT interval: Hypocalcemia can prolong the QT interval on ECG, increasing the risk of arrhythmias such as torsades de pointes.
  • ST-Segment: Hypocalcemia can also prolong the ST-segment. This is because low calcium levels can delay the repolarization of the heart muscle, leading to a prolonged ST segment.
QT interval prolongation and ST-segment prolongation with hypocalcemia
Torsades De Pointes is a polymorphic VTACH that occurs due to QT prolongation

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. 

Want to learn more?

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:

  • Identify all cardiac rhythms inside and out
  • Understand the pathophysiology of why and how arrhythmias occur
  • Learn how to manage arrhythmias like an expert nurse
  • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

I also include some great free bonuses with the course, including:

  • ECG Rhythm Guide eBook (190 pages!)
  • Code Cart Med Guide (code cart medication guide)
  • Code STEMI (recognizing STEMI on an EKG)

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. 

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Download this Article!

If you’d like to download this article in PDF form, click here!

References

UpToDate & Other Database Sources:

Textbooks

Other:

  • The diagnostic accuracy of clinical diagnostic tests in assessing patients with potential calcium disorders: A systematic review and meta-analysis. (European Journal of Internal Medicine)

    Hypermagnesemia causes, nursing assessment, and treatment

    Hypermagnesemia causes, nursing assessment, and treatment

    Published: April 2, 2023

    Last Updated: April 10, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    An image of IV magnesium sulfate with Magnesium in a ball with low levels with surrounding foods that are high in magnesium

    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.

    Learn about the causes, nursing assessment, and treatment for hyperkalemia in this comprehensive guide for nurses and medical professionals.

    Normal Magnesium Levels & Hypermagnesemia

    Normal magnesium levels can range from 1.9 to 2.2 mg/dL.

    Magnesium Levels

    • 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

    Causes Of Hypermagnesemia:

    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, with the left one transected so you can see the inside

    Kidney Dysfunction

    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.

    pills of magox

    Excessive magnesium intake

    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.

    Bag of IV magnesium sulfate

    IV Magnesium Sulfate Drip

    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.

    Milk overflowing

    Magnesium Enema

    Epsom salt enemas are not recommended as they can raise the serum magnesium to dangerous levels,  even as high as 6-16 mEq/L!!

    A depiction of the parathyroid gland

    Other conditions

    Mild hypermagnesemia (and asymptomatic) can occur in a variety of other medical conditions and scenarios including:

    • Primary hyperparathyroidism
    • DKA
    • Tumor lysis syndrome
    • Lithium
    • Milk-alkali syndrome
    • Adrenal insufficiency (Addison’s disease)

    Nursing Assessment Of Hypermagnesemia

    Symptoms

    Symptoms of hypermagnesemia are directly correlated with the level of the magnesium in the blood.  

    A fatigued muscle with a sad tired expression

    Magnesium 4 – 6 mEq/L:

    • Nausea and vomiting
    • Flushing
    • Drowsiness or lethargy
    • Decreased deep tendon reflexes
    A muscle with red electric bolts indicating pain

    Magnesium 6 – 10 mEq/L

    • Somnolence
    • Hypocalcemia
    • Absent Deep tendon reflexes
    • Hypotension
    • Bradycardia
    • ECG changes (discussed below)
    A muscle with red electric bolts indicating pain

    Magnesium over 10 mEq/L

    • Muscle paralysis (flaccid quadriplegia)
    • Apnea and respiratory failure
    • Complete heart block
    • Cardiac arrest

    NOTE

    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.

    PHYSICAL Assessment

    The physical assessment of a patient with hypermagnesemia will also depend on the severity of the magnesium levels and other factors.

    Vital Signs

    • Temp: Normal
    • HR: May be low in severe cases
    • BP: May be Lower
    • SPO2: Usually normal unless respiratory failure
    • Respirations: usually normal

    Inspection

    • May appear lethargic, drowsy, or weak
    • May have facial flushing

    Auscultation

    • Heart rate and rhythm (any signs of arrhythmia/irregularity)
    • Signs of respiratory distress, such as decreased breath sounds or respiratory rate
    a gloved hand palpating unspecified skin

    Palpation

    • Warmth of the skin (indicating vasodilation)
    • Decreased grip strength
    • Assess for any neuromuscular irritability (twitching, cramping, tetany)
    • Abdominal tenderness (SBO or ileus from smooth muscle relaxation)
    • Radial pulses (can be weak/thready if BP low)

    How to Check Deep Tendon reflexes

    1. Position the patient: Ask the patient to relax and sit or lie in a comfortable position. Have the patient place their legs hanging over the edge of the bed.
    2. Locate the tendon: Identify the tendon you want to test. Commonly tested tendons include the patellar tendon (knee jerk), Achilles tendon (ankle jerk), and biceps tendon (elbow jerk). We are going to be talking about the patellar tendon since that is the easiest and most common.
    3. Strike the tendon: Use a reflex hammer or your stethoscope to strike the tendon directly and briskly. Be sure to hit the tendon, not the muscle belly, as this can produce an inaccurate response.
    4. Observe the response: Observe the limb’s movement and the magnitude and duration of the reflex response. Normal reflexes are typically brief and mild, with a quick contraction and relaxation of the muscle.
    5. Interpret the response: Interpret the response based on the degree of reflex contraction.
    6. Repeat on the other side: Repeat the test on the opposite side for comparison.

    Treatment for Hypermagnesemia

    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:

    Assess the Patient

    Ensure they don’t have any symptoms and are stable, including recent vital signs.

    Stop Magnesium

    Stop any magnesium infusions or medications if the patient is currently getting them.

    Cardiac Monitor

    Make sure your patient is on the cardiac monitor. Obtain an ECG if not already done.

    Notify the Provider

    Notify the provider of the magnesium levels, your assessment, and their cardiac rhythm.

    Ensure IV access

    Make sure the patient has good access with at least one good IV.

    Administer Treatment

    Administer medications that are ordered (discussed below).

    Treatment for Hypermagnesemia

    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:

    The kidneys, with the left one transected so you can see the inside

    Stop Magnesium

    Stopping magnesium intake will typically bring levels back down to normal pretty quickly in the absence of renal failure.

    pills of magox

    Diuretics

    Diuretics like Loop diuretics (Lasix) or thiazide diuretics can also be used to lower magnesium levels pretty safely

    Bag of IV magnesium sulfate

    Isotonic FLuids

    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).

    Bag of IV magnesium sulfate

    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.

    A 10-ml vial of calcium gluconse 10% with 10mL drawn up into a syringe

    IV Calcium Gluconate

    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 of Hypermagnesemia

    Monitoring patients with hypermagnesemia involves cardiac monitoring and trending the magnesium levels.

    A Gold top blood vial filled with blood

    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.

    A Gold top blood vial filled with blood

    Other Electrolytes

    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.

    A Gold top blood vial filled with blood

    Kidney function

    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).

    A Gold top blood vial filled with blood

    Cardiac Monitoring

    Patients with hypermagnesemia should be closely monitored for signs of cardiac arrhythmias, particularly those caused by prolonged QT intervals (see ECG changes below).

    A Gold top blood vial filled with blood

    Respiratory Status

    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.

    graphic of a brain

    Neuro status

    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!

    Hypermagnesemia on the ECG

    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:

    • Bradycardia: Excessive magnesium can cause a slowing of the heart rate, which can manifest as bradycardia on ECG.
    • Heart block: Hypermagnesemia can interfere with the normal conduction of electrical impulses in the heart, leading to heart block, manifesting as a widened QRS complex on ECG.
    • Cardiac arrest: In severe cases of hypermagnesemia (levels > 15 mg/dL), the excessive accumulation of magnesium can cause complete cardiac arrest.

    On ECG, hypermagnesemia can manifest in the following ways:

    • P waves: Flattened
    • PR interval: Prolonged (> 200ms)
    • QRS complex: Widened (>120ms)
    • QT Interval: Prolonged (>500ms)
    • T waves: Peaked

    It is important to note that hypermagnesemia can also exacerbate cardiac arrhythmias caused by other electrolyte imbalances, such as hyperkalemia, hypokalemia, or hypocalcemia.

    A graph of a PQRST complex with changes associated with Hypomagnesemia, including QRS widening, QT prolongation, and flattened or inverted T waves

    Want to learn more?

    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:

    • Identify all cardiac rhythms inside and out
    • Understand the pathophysiology of why and how arrhythmias occur
    • Learn how to manage arrhythmias like an expert nurse
    • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

    I also include some great free bonuses with the course, including:

    • ECG Rhythm Guide eBook (190 pages!)
    • Code Cart Med Guide (code cart medication guide)
    • Code STEMI (recognizing STEMI on an EKG)

    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.

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    Download this Article!

    If you’d like to download this article in PDF form, click here!

    Managing hypomagnesemia: A complete guide to nursing assessment and treatment of low magnesium levels

    Managing hypomagnesemia: A complete guide to nursing assessment and treatment of low magnesium levels

    Published: March 26, 2023

    Last Updated: April 10, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    An image of IV magnesium sulfate with Magnesium in a ball with low levels with surrounding foods that are high in magnesium

    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.

    Learn about the causes, nursing assessment, and treatment for hyperkalemia in this comprehensive guide for nurses and medical professionals.

    Why is Magnesium So Important in the Body?

    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:

    An illustration of the heart with the pulmonary and aortic vessels

    Cardiac Function

    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.

    An image of a muscle

    Muscle Function

    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.

    An image depicting ATP

    Energy Metabolism

    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.

    A depiction of a neuron

    Nerve Transmission

    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.

    A normal human cell

    Bone Health

    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.

    How is Magnesium Regulated in the Body?

    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.

    A depiction of the small bowel, which is largely responsible for absorption of magnesium

    Intake & Absorption

    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!

    A muscle with red electric bolts indicating pain

    The Kidneys

    The kidneys play a crucial role in regulating the excretion of magnesium, similar to its role in potassium.

    A depiction of the parathyroid gland

    Hormones

    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.

    A liquid drop with "H+" indicating acid or acidity or hydrogen ions

    Acid-base Balance

    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 & 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.

    Magnesium Levels

    • 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

    Causes Of Hypomagnesemia:

    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.

    The colon with liquid diarrhea dripping out

    GI Losses

    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.

     

    A purple and gray pill, depicting omeprazole, which can lead to hypomagnesemia and low magnesium levels

    Medications

    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.

    The kidneys, with the left one transected so you can see the inside

    Renal Losses

    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).

    A bottle of medications that are prescription

    Medications

    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.

    Alcohol whiskey bottle and glass with ice

    Alcohol

    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.

    A donation box of ice with a kidney in it

    Post-transplant

    Patient’s with an organ transplant are more likely to experience hypomagnesemia, likely from their calcineurin inhibitor medications (like tacrolimus).

    Milk overflowing

    Hypercalcemia

    High calcium levels can lead to mildly low magnesium levels.

    A strand of DNA

    Genetic Causes

    Certain rare genetic conditions can cause decreased magnesium absorption in the small intestine and increased renal magnesium wasting.

    Nursing Assessment Of Hypomagnesemia

    Symptoms

    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.

    A fatigued muscle with a sad tired expression

    Muscle Weakness

    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.

    A muscle with red electric bolts indicating pain

    Muscle Cramps & Twitching

    Patients may feel tingling sensations and experience involuntary muscle contractions, particularly in their hands or lower extremities.

    A cardiac monitor showing ventricular tachycardia

    Cardiac Arrhythmias

    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.

    The colon with liquid diarrhea dripping out

    GI Symptoms

    Low magnesium levels can cause nausea, vomiting, or abdominal cramping. Additionally, if the patient has diarrhea, that may be a clue on the cause.

    A brain with yellow connecting lights which indicate the central nervous sytem

    Neuro Symptoms

    Magnesium can cause CNS hyperirritability, leading to confusion, irritability, hyperactive deep tendon reflexes, paresthesias, and seizures.

    PHYSICAL Assessment

    The physical assessment of a patient with hypomagnesemia will also depend on the severity of the low magnesium levels and other factors. 

    Vital Signs

    • HR: May be fast or slow, depending on any arrhythmias.
    • BP: May be increased
    • Respirations: usually normal
    • SPO2: Usually normal
    • Temp: Normal

    Inspection

    • Muscle weakness or trouble walking or moving
    • May appear fatigued or lethargic

    Auscultation

    • Auscultate for an Irregular heartbeat
    a gloved hand palpating unspecified skin

    Palpation

    • May have tender muscles
    • Edema or ascites may indicate underlying kidney or liver failure
    • Abdominal tenderness may be present, especially with any GI symptoms

    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.

    Treatment for Hypomagnesemia

    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:

    Assess the Patient

    Ensure they don’t have any symptoms and are stable, including recent vital signs.

    Cardiac Monitor

    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

    Notify the provider of the potassium levels, your assessment, and their cardiac rhythm. They will order the treatment for hypomagnesemia!

    Ensure IV access

    Make sure there is at least one IV site, but place a second line if the hypomagnesemia is severe.

    Evaluate Medications

    Evaluate if they are on any medications which may lead to hypomagnesemia listed above.

    Administer Treatment

    Administer medications that are ordered (discussed below).

    Treatment for Hypomagnesemia (medications):

    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.

    The kidneys, with the left one transected so you can see the inside

    Address Underlying Causes

    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.

    pills of magox

    Oral Magnesium Supplementation

    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:

    • Magnesium Oxide: Most common and inexpensive, but it has a low absorption rate and may cause diarrhea.
    • Magnesium Chloride: Has better absorption and higher bioavailability than magnesium oxide. Also less likely to cause GI side effects and may be better for skin health and wound healing.
    • Magnesium Carbonate: Good for heartburn, but not the best absorption.
    • Magnesium L-lactate: Less likely to cause GI symptoms like diarrhea.
    • Magnesium Glycinate: Highly absorbable and less likely to cause diarrhea. It may have a calming effect on the body.
    • Magnesium Citrate: Good absorption rate but also a laxative and will cause diarrhea and cramping. They are not typically used for magnesium replacement.

    Generally, sustained release options are better because they minimize the renal wasting of the magnesium. Common options include:

    • Magnesium Chloride 64-71.5mg elemental magnesium, 6-8 tabs in divided doses
    • Magnesium L-lactate with 84mg elemental magnesium, 6-8 tabs in divided doses

    If the sustained release is unavailable, magnesium oxide 800-1600mg daily in divided doses may be used, but diarrhea may occur.

    Bag of IV magnesium sulfate

    IV Magnesium Sulfate

    IV magnesium is given to patients with severe symptoms or who are NPO for whatever reason.

    IV replacement dosing will depend on the severity:

     

    • Mild (1.6 – 1.9 mEq/L): 1-2 grams of mag sulfate over 1 – 2 hours
    • Moderate (1.0 – 1.5 mEq/L): 2 – 4 grams of mag sulfate over 4 – 12 hours
    • Severe (< 1.0 mEq/L): 4 – 8 grams of mag sulfate over 12 – 24 hours

    Kidney Failure

    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 of Hypomagnesemia

    Monitoring patients with hypomagnesemia involves cardiac monitoring and trending the magnesium levels.

    A Gold top blood vial filled with blood

    Magnesium Levels

    Magnesium levels are generally checked at least daily while inpatient until normalization of the magnesium level.

    A Gold top blood vial filled with blood

    Other Electrolytes

    Other electrolytes and monitoring of renal function should also be checked, usually daily, every morning.

    A Gold top blood vial filled with blood

    Cardiac Monitoring

    Patients with low magnesium are at high risk for cardiac arrhythmias. Additionally, anybody receiving IV replacement with magnesium should be on a cardiac monitor.

    Foods High in Magnesium

    1. Seeds & Nuts (Pumpkin seeds, chia seeds, almonds, Cashews, peanuts)
    2. Spinach
    3. Dark Chocoloate
    4. Black Beans
    5. Avocados
    6. Salmon
    7. Quinoa
    8. Soymilk

    Hypomagnesemia and Cardiac Arrhythmias

    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:

    • Torsades de Pointes: Torsades de Pointes is a type of ventricular tachycardia characterized by twisting the QRS complex around the isoelectric line. It can occur in patients with hypomagnesemia and prolongation of the QT interval and is classic with hypomagnesemia.
    • Atrial fibrillation: Hypomagnesemia can increase the risk of atrial fibrillation due to magnesium’s effect on atrial muscle cells.
    • PVCs: Low magnesium leads to impaired ion channels, leading to excitable cardiac conduction, which can trigger PVCs or VTACH.

    On ECG, hypomagnesemia can manifest in the following ways:

    • Prolonged QT interval: Hypomagnesemia can prolong the QT interval, leading to an increased risk of Torsades de Pointes.
    • Widened QRS complex: Hypomagnesemia can cause a widened QRS complex, which can be seen on ECG.
    • ST segment and T wave changes: Hypomagnesemia can cause ST segment depression and flattening or inversion of T waves on ECG.

    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.

    A graph of a PQRST complex with changes associated with Hypomagnesemia, including QRS widening, QT prolongation, and flattened or inverted T waves
    Torsades De Pointes is a polymorphic VTACH that occurs due to QT prolongation

    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.

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    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.

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    • Identify all cardiac rhythms inside and out
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    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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    Treatment for Hyperkalemia: A nurse’s comprehensive guide to high potassium levels

    Treatment for Hyperkalemia: A nurse’s comprehensive guide to high potassium levels

    Published: March 19, 2023

    Last Updated: March 23, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    Treatment for hyperkalemia including IV Calcium gluconate, IV insulin, and IV dextrose 50%

    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!

    Learn about the causes, nursing assessment, and treatment for hyperkalemia in this comprehensive guide for nurses and medical professionals.

    Hyperkalemia And Normal Potassium Levels

    Potassium Levels

    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

     

    • Normal = 3.5 – 5.0 mEq/L
    • Mild Hyperkalemia: 5.1 – 5.9 mEq/L
    • Moderate Hyperkalemia: 6.0 – 6.9 mEq/L
    • Severe Hyperkalemia: > 7.0 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.

    Causes Of 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:

    Renal Failure

    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.

    A bottle of medications that are prescription

    Medications

    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).

    A liquid drop with "H+" indicating acid or acidity or hydrogen ions

    Metabolic Acidosis

    Acidosis, when a buildup of hydrogen ions in the blood, causes a potassium shift from inside to outside the cells, leading to hyperkalemia.

    What about Respiratory acidosis?

    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.

    An organic chemistry representation of aldosterone the hormone

    Hormones

    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!

    A red cell that is bursting open, releasing its contents into the extracellular space

    Hemolysis & Tissue Injury

    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.

    A bottle of medications that are prescription

    Medications that Can Cause Hyperkalemia

    • ACEI/ARBs: Lisinopril, ramipril, and losartan can all cause increased potassium levels by reducing/blocking aldosterone.
    • Potassium-Sparing Diuretics: Potassium-sparing diuretics like Aldactone, Spironolactone, and amiloride block the action of aldosterone in the kidneys, leading to decreased potassium excretion.
    • NSAIDs: NSAIDs, such as Ibuprofen or Toradol, interfere with the production of prostaglandins, which regulate potassium levels in the kidneys.
    • Beta-Blockers: While this is usually a mild effect, non-selective beta-blockers (like propranolol or atenolol) decrease potassium uptake into cells, which can lead to a mild increase in potassium.
    • Digoxin: Digoxin can interfere with the sodium-potassium pump and increase blood potassium levels.

      Part of the treatment for hyperkalemia is avoiding these medications!

      A strand of DNA

      Risk Factors for Hyperkalemia

      • CKD: Chronic kidney disease can lead to the inability to regulate potassium levels efficiently
      • Diabetes: Especially with uncontrolled type 1 diabetes, the absolute lack of insulin can lead to elevated potassium levels.
      • Older age: Older patients have less efficient kidneys, as well as often have comorbid conditions.
      • Trauma or Burn patients: As stated above, trauma and burns can cause rapid release of potassium into the blood from damaged tissue.
      • Addison’s Disease: These patients are at increased risk of hyperkalemia due to a lack of aldosterone.

      What is PseudoHyperkalemia?

      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:

      Red blood cells bursting open, indicating hemolysis

      Hemolysis of the blood sample

      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.

      An animal cell with arrows pointing in and out of the cell membrane, indicating redistribution of potassium across the cell membrane

      Potassium Shifts

      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.

      A half-eaten banana, indicating low potassium levels

      Leukocytosis or Thrombocytosis

      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.

      A strand of DNA

      Genetic Condition

      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.

      Nursing Assessment Of Hyperkalemia

      Symptoms

      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:

      A weak arm with no muscle, indicating muscle weakness

      Muscle Weakness

      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.

      A cardiac monitor showing ventricular tachycardia

      Cardiac Arrhythmias

      Symptoms of cardiac arrhythmias may occur if the patient is experiencing an arrhythmia, such as palpitations, chest pain, Shortness of breath, dizziness, or syncope.

      The colon with liquid diarrhea dripping out

      GI Symptoms

      High potassium levels can affect the smooth muscles of the GI tract, leading to nausea, vomiting, and possibly abdominal pain/cramping or diarrhea.

      A hand with blue electric bolts indicating tingling

      Paresthesias

      Like with hypokalemia, hyperkalemia can also cause numbness or tingling, typically in the extremities or the face.

      A kidney with low fluid levels

      Shortness of breath

      This is usually only in severe cases with severe muscle fatigue of the respiratory muscles, and the patient may even need to be intubated.

      A silhouette of a head with red and orange markings above the head, indicating anxiety

      Anxiety & Irritability

      High potassium levels can also agitate the central nervous system, leading to anxiety or restlessness.

      PHYSICAL EXAM

      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.

      Vital Signs

      • HR: May be fast or slow, depending on any arrhythmias. It may also be abnormal.
      • BP: Severe hyperkalemia can cause hypotension.
      • Respirations: usually normal, but may be increased or decreased if respiratory failure is present
      • SPO2: Usually normal
      • Temp: Normal

      Inspection

      • Abdominal distention or bloating
      • Bradycardia or arrhythmias on the monitor
      • Respiratory distress in severe cases
      • Patient may appear anxious or irritable, restless, or even confused

      Auscultation

      • Listen for slow or irregular heart rhythm, which may be caused by ectopy or arrhythmia from the hyperkalemia. May also have diminished or absent S3 and S4 heart sounds.
      a gloved hand palpating unspecified skin

      Palpation

      • Muscle weakness in the lower or upper extremities, particularly in the legs. These muscles may be tender to palpation.
      • Weak or thready pulses in the extremities (radial pulse)
      • Abdominal tenderness or discomfort

      Treatment for Hyperkalemia

      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:

      Assess the Patient

      Ensure they don’t have any symptoms and are stable, including recent vital signs.

      Cardiac Monitor

      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

      Notify the provider of the potassium levels, your assessment, and their cardiac rhythm. The treatment for hyperkalemia will be ordered by them!

      Ensure IV access

      Make sure there is at least one IV site, but place a second line if the hyperkalemia is severe.

      Evaluate Medications

      Evaluate if they are on any medications which may lead to hyperkalemia listed above.

      Administer Treatment For Hyperkalemia

      Administer medications that are ordered (discussed below).

      Treatment for Hyperkalemia

      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:

      The kidneys, with the left one transected so you can see the inside

      Address Underlying Causes

      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.

      A bottle of potassium supplements

      Avoid More Potassium

      Avoid potassium supplements or foods rich in potassium until the potassium has normalized. All medications which can worsen hyperkalemia should be stopped.

      A 10-ml vial of calcium gluconse 10% with 10mL drawn up into a syringe

      IV Calcium

      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.

      What about Calcium Chloride?

      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 inuslin bottle with insulin syringe drawn up to 10 units

      IV Insulin

      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.

      A code cart box of dextrose 50% with the auto-injector ready to inject

      IV Dextrose

      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.

      A person with a nebulizer on their face

      Beta-2 Adrenergic Agonist

      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.

      A code cart box of sodium bicarb with the auto-injector ready to inject

      IV Sodium Bicarb

      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.

      A bottle of kayexalate

      Remove Potassium from the Body

      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.

      1. Through the Urine: Giving loop diuretics, like Lasix, to patients who do not have severe kidney failure can help excrete excess potassium in the urine. This is often given in addition to IV fluids to maintain fluid balance (unless they are hypervolemic to begin with).
      2. Through the Stool: The administration of potassium-binders is standard to remove excess potassium. Traditionally this was usually Kayexalate (sodium polystyrene sulfonate), and is still often used. HOWEVER, there is newer cation exchangers that are preferred with less complications – namely Patiromer (Veltassa) or Sodium Zirocinum Cyclosilicate (SZC). Veltassa is preferred since it has a more rapid onset and is less likely to cause bowel necrosis (a rare complication from Kayexlate).If the patient is NPO for whatever reason, these can also be given as an enema.
      3. Through a Machine: Hemodialysis should be done in patients with severe kidney function impairment and is usually the best option for severe hyperkalemia, especially if the patient already has dialysis access or is newly diagnosed with severe renal failure.

      Monitoring after Treatment for Hyperkalemia:

      Patients with hyperkalemia need good monitoring, especially if they have moderate to severe hyperkalemia.

      A Gold top blood vial filled with blood

      Potassium Levels

      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.

      A Gold top blood vial filled with blood

      Glucose Levels

      If insulin is given, glucose levels must be checked hourly for 4-6 hours, as hypoglycemia is common (even if you administer dextrose).

      A Gold top blood vial filled with blood

      Other Labs

      Closely monitor the patient’s renal function (BUN & Creatinine), other electrolytes, and acid-base balance (CO2).

      A Gold top blood vial filled with blood

      Cardiac Monitoring

      As discussed, high potassium levels can lead to bradycardia and arrhythmias. Continuous cardiac monitoring should be maintained, and intermittent ECGs may also be warranted.

      A Gold top blood vial filled with blood

      Respiratory Function

      Severe hyperkalemia can cause respiratory failure, so monitoring their breathing, lung sounds, respiratory rate, and pulse ox is important.

      A Gold top blood vial filled with blood

      Vital Signs

      Vital signs should be checked per facility protocol.

      A graduated cylinder with urine in it

      Urine Output

      Monitoring urine output is important, especially in patients where loop diuretics are given, and potassium is being wasted through the kidneys.

      Hyperkalemia and Cardiac Arrhythmias

      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:

      • P Waves: Decreased amplitude of P waves is common
      • PR interval: The PR interval is prolonged and delayed, indicating slower transit of the electrical impulse from the SA node through the AV node.
      • QRS: The QRS often widens with hyperkalemia
      • T waves: Tall peaked “tented Ts” are common with hyperkalemia.

      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.

      The ECG changes seen on the PQRST with hyperkalemia, which includes P wave flattening, PR prolongation, QRS widening, and Tented or peaked T waves

      Want to learn more?

      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:

      • Identify all cardiac rhythms inside and out
      • Understand the pathophysiology of why and how arrhythmias occur
      • Learn how to manage arrhythmias like an expert nurse
      • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

      I also include some great free bonuses with the course, including:

      • ECG Rhythm Guide eBook (190 pages!)
      • Code Cart Med Guide (code cart medication guide)
      • Code STEMI (recognizing STEMI on an EKG)

      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!

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      If you’d like to download this article in PDF form, click here!

      Nursing Interventions for Hypokalemia: A Comprehensive Guide for Nurses

      Nursing Interventions for Hypokalemia: A Comprehensive Guide for Nurses

      Published: March 12, 2023

      Last Updated: March 22, 2023

      William Kelly, MSN, FNP-C

      Author | Nurse Practitioner

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      A picture of a half-eaten banana and an IV bag of potassium chloride

      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.

      WHY IS POTASSIUM SO IMPORTANT IN THE BODY

      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:

      A muscle with red electric bolts indicating pain

      Muscle Function

      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!

      A kidney with low fluid levels

      Fluid Balance

      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.

      An emoji of the heart

      Cardiac System

      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!

      A glucometer which reads "HIGH" indicating hyperglycemia

      Blood Sugar Control

      Studies show that high-potassium diets can help improve insulin sensitivity and reduce the risk of type 2 diabetes.

      A brain with yellow connecting lights which indicate the central nervous sytem

      Nervous System

      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.

      A normal human cell

      Cellular Function

      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!

      How Is Potassium Regulated In The Body?

      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, with the left one transected so you can see the inside

      The kidneys

      The kidneys play a crucial role in regulating potassium levels. These filter out excess potassium and retain more potassium when levels are low.

      A vial of insulin

      Hormones

      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.

      A liquid drop with "H+" indicating acid or acidity or hydrogen ions

      Acidity

      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.

      A normal banana unopened

      Diet

      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. 

      Potassium levels and Acidotic States

      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!

      Hypokalemia And Normal Potassium Levels

      Normal Potassium Levels

      • Normal = 3.5 – 5.0 mEq/L
      • Mild Hypokalemia: 3.0 – 3.5 mEq/L
      • Moderate Hypokalemia: 2.5 – 3.0 mEq/L
      • Severe Hypokalemia: < 2.5 mEq/L

      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.

      Causes Of Hypokalemia:

      As we’ve discussed, many factors impact how the body regulates potassium levels, and similarly, there are various causes of hypokalemia. These include:

      An animal cell with arrows pointing in and out of the cell membrane, indicating redistribution of potassium across the cell membrane

      Redistribution

      Certain medications and conditions can shift potassium into the cells, which can cause low potassium levels. This includes Insulin, inhalers like albuterol, and alkalosis.

      The colon with liquid diarrhea dripping out

      GI Losses

      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.

      Renal Losses

      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.).

      A half-eaten banana, indicating low potassium levels

      Decreased Intake

      Often, this is not the only cause, as the body is pretty good about compensating for inadequate dietary intake.

      Nursing Assessment Of Hypokalemia

      Symptoms

      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:

      A weak arm with no muscle, indicating muscle weakness

      Muscle Weakness

      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.

      A muscle with red electric bolts indicating pain

      Muscle Cramps & Rhabdo

      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 battery symbol which is low

      Fatigue

      A generally non-specific symptom, but patients with low potassium often experience fatigue.

      The colon with liquid diarrhea dripping out

      GI Symptoms

      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.

      A hand with blue electric bolts indicating tingling

      Paresthesias

      Hypokalemia can cause numbness and tingling in the hands or feet.

      A bladder full of urine

      Polyuria

      Low potassium can cause the kidneys to produce more urine, leading to increased urination.

      Shortness of Breath

      This is usually only in severe cases with severe muscle fatigue of the respiratory muscles, and the patient may even need to be intubated.

      A vector of a heart with a ventricular fibrillation arrhythmia with three "!" indicating seriousness

      Cardiac Arrhythmias

      Abnormalities such as premature beats (PAC, PVC), Afib, sinus bradycardia, or even VTACH or VFIB or asystole/PEA.

      Risk Factors for Hypokalemia

      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:

      • CKD: Chronic kidney disease can lead to the inability to regulate potassium levels efficiently
      • Diabetes: Especially with hyperglycemia, osmotic diuresis can occur, which also causes potassium losses.
      • GI disorders: Certain GI disorders like chronic diarrhea or vomiting can lead to potassium losses
      • Alcoholism: Excessive alcohol intake can lead to decreased potassium intake and increased urinary losses
      • Patients on Diuretics: Patients on Diuretics, such as those with hypertension or CHF, are at increased risk of developing hypokalemia.

       

      A bottle of medications that are prescription

      Medications that Can Cause Hypokalemia

      • Diuretics: These increase urinary output and lead to potassium loss in the urine (Furosemide, hydrochlorothiazide, Metalozone, etc.)
      • Corticosteroids: These also cause urinary potassium loss and decrease potassium absorption
      • Beta-agonists: This shifts potassium into the cells, leading to lower levels outside the cells. It tends to be temporary.
      • Insulin: Also shifts potassium into the cells as discussed above.

      PHYSICAL EXAM

      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. 

      Vital Signs

      • HR: May be fast or low depending on cardiac arrhythmias present
      • BP: Largely unaffected, but hypokalemia can increase the risk of hypertension
      • Respirations: usually normal, but may be decreased in severe cases that cause paralysis
      • SPO2: Usually normal unless respiratory failure
      • Temp: Normal

      Inspection

      • Signs of muscle weakness, such as difficulty walking or moving
      • Signs of fatigue or lethargy

      Auscultation

      • Listen for irregular heart rhythm, which may be caused by ectopy or arrhythmia from the hypokalemia
      a gloved hand palpating unspecified skin

      Palpation

      • Muscle tenderness may be from hypokalemia.
      • Edema or ascites, which may indicate underlying kidney or liver failure that can cause hypokalemia
      • Abdominal tenderness, which can indicate GI issues that may be leading to hypokalemia

      Treatment of Hypokalemia

      Treatment of hypokalemia depends on the severity of the hypokalemia and any symptoms or complications present.

      Nursing Interventions:

      When you get your patient’s results back, and they show hypokalemia, especially < 3.0 mEq/L, then follow the following general interventions:

      Assess the Patient

      Make sure they don’t have any symptoms and are stable, including a recent set of vital signs.

      Cardiac Monitor

      Make sure your patient is on the cardiac monitor. Obtain an ECG if it still hasn’t been done.

      Notify the Provider

      Notify the provider of the potassium levels, your assessment, and their cardiac rhythm.

      Ensure IV access

      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 Medications

      Evaluate if they are on any medications which may lead to hypokalemia, listed above.

      Administer Replacement

      Administer treatment as ordered: Administer PO or IV potassium as ordered.

      Treatment for Hypokalemia

      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:

      A kidney with low fluid levels

      Address Underlying Causes

      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.

      Magnesium with low fluid levels with surround foods that are high in magnesium

      Correct Hypomagnesemia

      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).

      Potassium PO pills (K-dur) potassium chloride

      Oral Potassium (PO)

      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.

      • Mild to moderate hypokalemia = 10-20mEq of potassium given 2-4x/day
      • severe hypokalemia or severe symptoms = Doses up to 40mEq 3-4x/day in ADDITION to IV potassium
      An IV bag of KCL

      IV Potassium (IV)

      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.

      • Mild to Moderate hypokalemia: typically not needed, and PO is fine, but if the patient is NPO, then IV can be given. Through a peripheral line, 10mEq “K-riders” are usually ordered, and you can expect the potassium to increase by ~0.1 mEq per K-rider.
      • Severe hypokalemia: In extreme cases, can give 20mEq every 2-3 hours

      IV Potassium Infusion Rates

      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.

      Monitoring for Hypokalemia

      Patients with hypokalemia need good monitoring, especially if they have moderate to severe hypokalemia.

      A Gold top blood vial filled with blood

      Potassium Levels

      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).

      Cardiac Rhythm

      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.

      Respiratory Function

      Severe hypokalemia can cause respiratory failure, so monitoring their breathing, lung sounds, respiratory rate, and pulse ox is essential.

      A picture of an IV that is dressed in the forearm

      IV Site

      Monitoring for phlebitis and thrombophlebitis at the insertion site is essential, as IV potassium often burns.

      IV KCL 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!

      Hypokalemia and Cardiac Arrhythmias

      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:

      • Premature Ventricular contractions (or ventricular premature beats VPBs)
      • Ventricular tachycardia (VTACH or VT). 

      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:

      • ST segment: Often can cause some ST depression
      • T wave: T wave flattening is common
      • U waves: U waves become more prominent and visible in hypokalemia. Remember, these are seen best in V4-V6.
      • QT Interval: Is prolonged with hypokalemia.

      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.

      Want to learn more?

      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:

      • Identify all cardiac rhythms inside and out
      • Understand the pathophysiology of why and how arrhythmias occur
      • Learn how to manage arrhythmias like an expert nurse
      • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

      I also include some great free bonuses with the course, including:

      • ECG Rhythm Guide eBook (190 pages!)
      • Code Cart Med Guide (code cart medication guide)
      • Code STEMI (recognizing STEMI on an EKG)

      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!

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      If you’d like to download this article in PDF form, click here!

      Sepsis and Severe Infections: A Primer for Nurses

      Sepsis and Severe Infections: A Primer for Nurses

      Published: December 19, 2022

      Last Updated: February 24, 2023

      William Kelly, MSN, FNP-C

      Author | Nurse Practitioner

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      Sepsis is a potentially life-threatening condition that occurs when the body has a systemic response to an infection. It is not caused by a specific type of bacteria but can be triggered by any type of infection, including bacterial, viral, or fungal. Most cases of sepsis in the hospital will be caused by severe bacterial infections. 

      According to the CDC, sepsis is a leading cause of death in the United States. It is estimated that more than 1.7 million cases of sepsis occur each year, and kills about 270,000 people each year. The mortality rate for sepsis varies, but it can be as high as 50% in severe cases. This mortality rate is highest in patients who are over 75 and have multiple comorbidites.

      It is important for nurses to be aware of the signs and symptoms of sepsis and to know how to recognize and manage it.

      What is sepsis?

      Sepsis is a common clinical syndrome that represents the body’s response to severe bacterial infection. Within the hospital, you will take care of patients with sepsis in any department, but especially in the ER and ICU.

      Sepsis is a severe condition with a poor prognosis

      Early sepsis– while not clearly defined – is the presence of infection and bacteremia (bacteria in the blood) – which can and likely will progress to sepsis without intervention. Recognizing and intervening early when the sepsis is still early can significantly improve patient outcomes. 

      An enlarged prostate and urinary retention

      The definition of sepsis changed in 2016

      Sepsis is now is defined as life-threatening organ dysfunction in response to infection. Organ dysfunction, usually from hypoperfusion, can be evidenced by hypotension, altered mental status, tachypnea, or increased sofa score by 2 points. 

      What is SIRS?

      Sepsis used to be identified using SIRS criteriaSystemic Inflammatory Response syndrome. This is somewhat outdated and no longer used, but you still may often hear about this in your hospital. 

      SIRS was a term that was used to describe the early stages of sepsis. It was defined as the presence of two or more of the following criteria:

      • Body temperature above 100.4°F or below 96.8°F
      • Heart rate above 90 beats per minute
      • Respiratory rate above 20 breaths per minute or PaCO2 below 32 mm Hg
      • White blood cell count above 12,000/mm3, below 4,000/mm3, or more than 10% immature neutrophils (bands)

      The idea behind using the SIRS criteria to diagnose sepsis was that it could help identify patients who were at risk of developing sepsis and who may need early intervention. However, over time, it became clear that the SIRS criteria were not sensitive or specific enough to accurately diagnose sepsis. 

      As a result, the SIRS criteria are no longer used to diagnose sepsis. Instead, the more recent Sepsis-3 criteria is recommended. 

      SEPSIS-3 Criteria

      The Sepsis-3 criteria is now used to help clinicians detect and diagnose sepsis, which includes the following 3 criteria:

      1. A suspected or confirmed infection
      2. An elevated lactic acid (>2 mmol/L)
      3. At least one of the following:
        • Hypotension requiring vasopressors to maintain a mean arterial pressure (MAP) of 65 mm Hg or higher
        • A serum lactate level greater than 2 mmol/L after adequate fluid resuscitation
        • An acute increase in the serum lactate level by at least 2 mmol/L within 24 hours

      These criteria are designed to be more sensitive and specific than the SIRS criteria. It’s also more specific to identifying patients who are at high risk of dying from sepsis and are more likely to need aggressive intervention.

      SEPSIS-3 CRITERIA

      CriteriaDescription
      1Suspected or confirmed infectionThe presence of a suspected or confirmed infection, such as pneumonia, urinary tract infection, or septicemia
      2Serum lactate level above normalA serum lactate level above the upper limits of normal, indicating tissue hypoperfusion and cellular injury
      3aHypotension requiring vasopressorsHypotension that requires the use of vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher
      3bSerum lactate level greater than 2A serum lactate level greater than 2 mmol/L after adequate fluid resuscitation
      3cAcute increase in lactate levelAn acute increase in the serum lactate level by at least 2 mmol/L within 24 hours
      Only need one of the last 3 items (3a, 3b, and/or 3c)

      What is Septic Shock?

      Septic shock is a type of distributive shock and occurs when the body is under severe distress and releases a lot of mediators and toxins which can cause vasodilation, decrease circulating blood volume, and tank the blood pressure. Septic shock is generally diagnosed when the patient has a MAP <65 mmHg and a lactic >2.0 mmol/L, often after their initial fluid bolus. These patients require vasopressors and should be monitored in the ICU.

      Septic shock is a medical emergency and requires immediate treatment. If not treated promptly, it can lead to multiple organ failure and death.

      Causes of Sepsis and Septic Shock

      Sepsis can be caused by any infection that is left untreated or resistant to antibiotics that eventually causes systemic infection and reaction. While severe viral or fungal infections can cause sepsis, this is less common. Common bacterial infections that are more likely to cause sepsis include:

      A bunch of E coli bacteria swimming around

      Urinary Tract Infection (UTI)

      Urinary Tract Infections (UTIs) are common causes of sepsis in elderly individuals. When a Cystitis (inflammation/infection of the bladder) can also travel up the ureters to the kidneys and cause pyelonephritis (infection of the kidney), which is more likely to cause sepsis as well. When a UTI becomes sepsis, this is called Urosepsis.

      A bunch of E coli bacteria swimming around

      Pneumonia

      Pneumonia is a bacterial infection of the lungs. Left untreated, this commonly causes sepsis. In fact, severe sepsis can occur in almost half of patients admitted to the hospital with pneumonia.

      Skin rashes - cellulitis

      Cellulitis

      Cellulitis is infection of the skin and surrounding tissue. Patient’s with severe cellulitis often have other risk factors, like obesity, diabetes, and other comorbid conditions which increase their liklihood of becomign septic.

      Assessment of sepsis

      Symptoms

      Since sepsis isn’t only caused by one thing, the symptoms are going to depend on the underlying infection. However, there are some common symptoms that all sepsis usually share. These include:

      A bunch of E coli bacteria swimming around

      Fever & Chills

      Fevers and chills are classic for infection. A true fever is greater than 100.4° F or 38° C. Sepsis often presents with even higher fevers of 102°, 103°, or 104° F

      Chills are subjective, and many patients will report them (even for minor infections). However, patients with sepsis often have signifiacnt chills and tremors.

      A bunch of E coli bacteria swimming around

      Weakness & Fatigue

      Whenever the body is fighting infection, it takes a toll on energy levels. With sepsis it also does this, but to an even larger degree as this is a systemic response.

      graphic of a brain

      Altered Mental Status

      Altered Mental Status (AMS) commonly occurs with sepsis. This is due to decreased perfusion of the brain, as well as their body’s systemic reaction. Older and sicker patients are more likely to experience this. This is often exacerbated by dehydration. This can manifest as:

      • Drowsiness
      • Lethargy
      • Confusion

      Other symptoms of sepsis will depend on the underlying cause of the infection. Some examples include:

      • Pneumonia: productive cough, shortness of breath
      • UTI: Dysuria, urinary frequency, pain (flank, back, or suprapubic region)
      • Cellulitis: Redness, swelling, and swelling of skin (often the legs)
      • Abdominal Abscess: Abdominal pain
      • Diverticulitis: Abdominal pain, diarrhea, bloody BMs

      The patient should be asked about symptoms that may indiciate a cause for the infection.

      Physical Exam

      The physical exam is essential in patients with sepsis, as these patients are often very sick or on their way to becoming very sick. 

      It is important to note that not all people with sepsis will have the same physical findings, and some may not have any physical findings at all. This is why it is important for healthcare providers to perform a thorough and complete assessment to identify any signs or symptoms of sepsis.

      A bunch of E coli bacteria swimming around

      Vital signs

      • Temp: A fever above100.4°F (38°C)
        • Could be hypothermic in severe sepsis
      • BP: Often low, hypotensive < 90/60 mmHg or MAP < 65 is worrisome
      • Pulse/HR: Tachycardic, may be between 90-140 bpm
      • Respirations: Normal but often somewhat increased (above 20 rpm)
      • Pulse Ox: May be normal or low, especially with respiratory infections
      A bunch of E coli bacteria swimming around

      Inspection

      • NEURO: Altered mental status (AMS)
      • HEENT: Dry mucous membranes
      • RESPIRATORY: Fast breathing, respiratory distress
      • SKIN:  pale or flushed, may have rashes, redness, or swelling
      Skin rashes - cellulitis

      Auscultation

      • Heart: Often rapid and regular
      • Lungs: May have crackles and/or Rhonchi if a respiratory infection is present
      Skin rashes - cellulitis

      Palpation

      • CARDIOVASCULAR: Peripheral pulses may be faint, cap refill often delayed, distal extremities may be warm
      • ABDOMEN: Usually non-tender;
      • BACK: Mid-line spinal tenderness with should prompt evaluation for spinal abscess

      Nursing Interventions for Sepsis

      When you suspect sepsis, there are multiple things you should do as the patient’s nurse. Timing is so important, and that’s why so many departments have quality metrics and procedures in place for septic patients to get things done quickly. The faster we act, the better the chances of the patient surviving. 

      Bedside Monitor

      Hook up the patient to the bedside monitor to monitor their vitals frequently, especially their heart rhythm and their blood pressure. Set the machine to check BP every 15 minutes. 

      NOTIFY PROVIDER

      Be sure to notify the provider ASAP, as these patients are very sick and need orders STAT.

      Place the IV

      Place at least two IVs, 18-20g, and draw blood. This is for fluid and medication administration such as antibiotics and maybe even vasopressors until a central line can be placed. 

      Drawing blood

      Once placing the IV, you can grab labs off of the IV site. You will want to grab a basic rainbow (Blue top, Mint or gold top, and a lavender top), as well as blood cultures and a lactic (if your facility protocol allows 1 blood culture from the IV site). 

      Prime your Fluids

      Prime fluids to be given once ordered – probably at least 2 liters. Septic patients need at least 30ml/kg bolus of isotonic fluids to improve their symptoms, stabilize their vitals, improve their lactic acidosis, and improve their survival rates!

      An enlarged prostate and urinary retention

      CHF or ESRD?

      Should your patient with ESRD or CHF get the same amount of fluids? Keep reading below to find out!

      Workup of sepsis

      Since sepsis is a clinical syndrome, there’s not exactly a lab test that will definitely tell you whether the patient is in sepsis or not. However, there are common labs and imaging that may be ordered.

      Blood Work

      CBC

      Usually have WBC counts above 12,000/mm3, although severe sepsis can also present with leukopenia of < 4,000/mm3. Bands over 10% are consistent with sepsis. 

      An enlarged prostate and urinary retention

      Bands & "Left Shift"

      Bands are a type of immature white blood cells that when present in higher numbers indicate severe infection and sepsis. Bands are normally 0-5%, and bands >10% are worrisome. 

      A “left-shift” is an ill-defined term that refers to an increased number of bands in the absolute neutrophil count.

      CMP

      A complete metabolic panel is drawn to see evidence of anything else going on, any possible source of infection, or of any organ damage that the sepsis may have already occurred. This will look at:

      • Kidney function (creatinine, BUN)
      • Liver function (AST/ALT, Alk Phos, Bili, etc)
      • Acid-base (Agap, CO2)
      • Glucose & Electrolytes
      An enlarged prostate and urinary retention

      CO2 = Bicarb

      Look at the CO2 in the CMP. This is equivalent to the Bicarb in a venous blood gas sample. If it is < 18, they are likely acidotic, probably from lactic acidosis

      A specific cup half filled with yellow urine

      Coags

      Coag studies (PT/INR, PTT) are ordered in septic patients to detect clotting abnormalities. Severe sepsis can activate the clotting cascade, cause organ dysfunction, and ultimately lead to DIC.

      A specific cup half filled with yellow urine

      blood cultures

      Aerobic and anaerobic blood cultures should be obtained from two different sites. This will be used for a gram stain and will be cultured to see if any bacteria grows, as well as to perform sensitivity reports to various antibiotics.

      A specific cup half filled with yellow urine

      Procalcitonin

      Procalcitonin is a non-specific inflammation marker (kind of like ESR and CRP). This isn’t always ordered for Sepsis, but it can help show clinical response to antibiotics, especially from bacterial respiratory infections. This can help guide the Provider to know when to switch to oral antibiotics or stop the antibiotics altogether.

      A specific cup half filled with yellow urine

      Lactic acid (lactate)

      If the lactic acid, or lactate, is greater than 2 mmol/L, this indicates lactic acidosis. High lactate levels indicate decreased tissue perfusion of the organs, which is classic in Sepsis.

      This will often be repeated every 4-6 hours until the level becomes normal.

      Remember that Lactic acid is checked with a gray top (sometimes dark green), and should be transported ON ICE!

      An enlarged prostate and urinary retention

      Lactate from where?

      Remember in cell biology learning about how cells make energy or ATP? They do this primarily with oxygen using the Krebs cycle. When oxygen isn’t as available, it switches to a backup method of creating energy called glycolysis, which a byproduct of that is lactic acid. 

      Other Labs

      A specific cup half filled with yellow urine

      Urinalysis

      Checking a urine sample is a MUST for anybody with sepsis, as urinary tract infections are a super common cause of sepsis. The presence of leukocyte esterase and WBCs, nitrites, and bacteria supports a UTI diagnosis. Check out the full article on how to interpret a UA!

      A specific cup half filled with yellow urine

      Other Collections

      Other labs that might be ordered depending on the symptoms of the patient includes:

      • Anaerobic and Aerobic culture swabs of open wounds
      • Sputum culture if productive cough
      • Stool culture, ova/parasite, C-diff

      Imaging

      A specific cup half filled with yellow urine

      A Chest X-ray

      A CXR is always ordered in patients with sepsis to see if there is any pneumonia or to detect any other possible abnormalities. 

      A specific cup half filled with yellow urine

      CT abdomen/pelvis w/ Contrast

      Sometimes an abdominal CT may be ordered if the patient has abdominal signs/symptoms, or significantly elevated liver enzymes. Contrast is preferred as this will better visualize any abscesses or fluid collections present, assuming their kidney function isn’t too bad. 

      A specific cup half filled with yellow urine

      CT thorax w/o contrast

      A CT of the thorax without contrast is sometimes recommended but the radiologist after a chest x-ray is obtained. A chest-xray only has a sensitivity for pneumonia of about 43%.  aren’t perfect and could miss pneumonia or other findings that the CT will have much better sensitivity for picking up infection. 

      An enlarged prostate and urinary retention

      "PAN scan"

      Sometimes a CT chest, abdomen, and pelvis is ordered when there is no known source for infection – this can be especially helpful when there is little history to go off of, and the patient is unable to express their symptoms. 

      treatment of sepsis

      Remember that sepsis is a systemic response to infection. Our first priority is to stabilize their vital signs and provide support. Our second priority is to give antibiotics to kill the bacteria. Because sepsis has such a high mortality rate, these should be done quickly!

      Supportive Care

      IV Fluids

      All septic patients should get a bolus of crystalloid fluids (Normal saline or Lactated Ringers). It’s recommended that septic patients get 30ml/kg bolus – so a 70kg patient would get 2,100 mL of roughly 2 liters.

      This should be run wide open, and if the patient is hypotensive, you should use pressure bags. 

      This bolus should be finished infusing within the first 3 hours after the patient presents to the ER. 

      antipyretics

      Patients who are septic in the hospital often have fevers. Administering antipyretics can help reduce their fluid losses and improve their symptoms overall. Options include:

      • Tylenol 650mg every 4-6 hours (or 1000mg every 8 hours)
      • Ibuprofen 600-800mg every 4-6 hours (or other NSAIDs)
      An enlarged prostate and urinary retention

      What about CHF?

      Even patients with CHF or renal failure need fluids during sepsis, although may require less. The nurse and Provider should continuously assess for signs of pulmonary edema, such as increased SOB, tachypnea, hypoxemia, and/or pulmonary crackles/rales. If this develops – stop the fluids, notify the provider, and expect to give diuretics and/or intubate the patient

      Medical therapies

      A vector graphic of a bed

      antibiotics

      Antibiotics are crucial in treating sepsis, as we need to fight the underlying bacteria that are trying to kill our patients. These should be given within the FIRST hour after the patient gets to the ER.

      The choice of antibiotics should depend on multiple factors including the patient’s history, risk factors, as well as the suspected source of infection. In practice, you will commonly see an agent that covers MRSA (Vanco), plus a broad-spectrum antibiotic. Common regimens include:

      • Vancomycin + Zosyn
      • Vanco + Cefepime
      • Vanco + Imipenem
      An enlarged prostate and urinary retention

      What about Fungus?

      Sometimes fungal infections can cause severe sepsis, and should be considered in some cases. If the patient is neutropenic or has risk factors for a severe fungal infection, the provider may order antifungal medications. This is likely best decided by Infectious Disease.

      A vector graphic of a bed

      Vasopressors

      Vasopressors or “pressors” are medications that increase blood pressure through various means, usually by causing vasoconstriction of the blood vessels. This improves perfusion to important organs like the brain and the heart. However, these are also high-risk medications and only ordered when absolutely necessary.

      In sepsis, the vasopressor of choice is often Norepinphephrine (also known as Levophed).

      Vasopressors can usually be started peripherally in a pinch but eventually will require a central line to be placed. This is primarily because vasopressors can damage tissue if there is extravasation.

      All vasopressors need to be closely titrated by a critical care nurse, and the goal is usually related to the MAP, not the systolic blood pressure.

      An enlarged prostate and urinary retention

      The MAP

      The MAP stands for Mean Arterial Pressure. This is the average pressure in the arteries from one cardiac cycle (systolic + diastolic). This gives a better idea of the perfusion of the organs. To read more about this, check out here.

      Norepinephrine (Levophed)

      Vasopressor


      Mechanism of Action

      Stimulates Beta-1 and alpha-adrenergic receptors to increase the strength of contractions, the heart rate, and causes vasoconstriction – all of which increases systemic BP and coronary blood flow.

      Sepsis DOSING

      0.05 – 0.15 mcg/kg/min; titrate to MAP ≥ 65 mmHg.
      * Always follow facility protocol and orders*

      Max Dose

      1 – 3.3 mcg/kg/min

      SIDE EFFECTS

      Hypertension, tachycardia, palpitations, headache,
      nausea/vomiting, peripheral vasoconstriction

      Glucocorticoids

      In general, steroids like Solu-Medrol are not recommended during sepsis. However, it may sometimes be ordered by the critical care physician if the patient does not respond well to fluids and vasopressors. 

      Monitoring & Complications of Sepsis

      Lactic Acid

      The lactic acid should be trended if it is elevated from the start. This is generally checked every 4-6 hours until it falls below 2 mmol/L

      WBC & BAnds

      WBCs should be trended as well, at least daily until resolution. This will usually immediately decrease with fluids and antibiotic administration.

      A specific cup half filled with yellow urine

      Urine output

      A foley is often placed to track this closely, and it a strong indicator of kidney perfusion. The goal is often to have a urine output ≥0.5 mL/kg per hour.

      Cardiac Monitor

      Septic patients are usually tachycardic, and they are at increased risk for arrhythmias as well as myocardial infarctions. Close monitoring per department protocol is warranted.

      Blood cultures & Sensitivities

      Gram staining will be performed of the blood cultures usually within 24 hours, and cultures will grow bacteria if present in about 48-72 hours. This will depend on your hospital’s lab. The antibiotics may be changed depending on sensitivities. 

      Hemodynamics

      Blood pressure and MAP should be monitored for hypotension and improvement with interventions like fluids and vasopressors.  Goal is usually a MAP ≥65 mmHg

      Assessment

      The patient will need to be assessed per department protocol. You should be assessing for signs of worsening perfusion such as:

      • Pallor and sweating
      • Confusion
      • Worsening vital signs
      A specific cup half filled with yellow urine

      IV & extremities

      Assess the IV sites and/or central line sites per protocol. Remember vasopressors can cause vasoconstriction of the extremities, so monitor for signs of decreased circulation such as:

      • Delayed capillary refill
      • Distal pallor or cyanosis
      • Necrosis of the fingertips

      S/S of fluid overload

      Patients who are septic are receiving plenty of fluids and are under a lot of stress overall. This can put a lot of strain on the heart, especially when the patient has a history of cardiac disease. Watch for s/s of fluid overload including:

      • Increased shortness of breath
      • Increased JVD
      • Respiratory Crackles/rales

      If the patient is on vasopressors, make sure you are assessing their extremities pulses and capillary refill. Vasopressors can cause necrosis of the extremities like fingers or toes if they are clamping down too much.

      Early recognition and treatment of sepsis are crucial for improving patient outcomes. The mortality rate for sepsis can be high, but quick action by nurses and doctors can make a significant difference in the patient’s outcome. It is important for nurses to be aware of the signs and symptoms of sepsis and to know how to recognize and manage it. By recognizing and treating sepsis early, nurses can help improve patient outcomes and save lives.

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