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- Hypo- and Hyperkalemia
- Hypo- and Hypermagnesemia
- Hypo- and Hypocalcemia
Published: March 26, 2023
Last Updated: April 10, 2023
Hypomagnesemia, the medical term for low magnesium levels in the blood, can have disastrous consequences if left untreated. Magnesium is crucial in numerous bodily functions, including nerve and muscle function, heart rhythm, and bone health. Hypomagnesemia can lead to serious complications, such as seizures, cardiac arrhythmias, and even death.
As a nurse, knowing the causes, symptoms, and treatment of hypomagnesemia is essential to provide effective care and improving patient outcomes. This article will provide a comprehensive guide to nursing assessment and treatment of hypomagnesemia, including its causes, clinical manifestations, nursing assessment, treatment, and monitoring.
Magnesium is an electrolyte that is so important for our body’s daily functioning. Magnesium is essential from the cardiovascular system to our muscular system and energy metabolism! When low magnesium levels occur, this can cause issues in these areas! Magnesium functions in the following ways:
Magnesium acts similarly to a calcium channel blocker, helping to regulate the influx of calcium to control the proper timing and duration of electrical impulses in the heart. It also plays a crucial role in stabilizing the cell membrane and maintaining the resting membrane potential. Hypomagnesemia and low magnesium levels can lead to deadly cardiac arrhythmias.
Magnesium is important in the contraction of muscles as well as their relaxation. This helps with the funcitoning of cardiac muscle tissue, the GI system, and skeletal muscle tissue. It also relaxes the smooth muscle in the vessel walls, reducing blood pressure and preventing spasms.
Magnesium is necessary for metabolism as it is a co-factor for many enzymes involved in producing ATP – the body’s primary energy source on a cellular level. It’s also involved in the regulation of glucose metabolism and insulin signaling.
Magnesium is involved in transmitting nerve impulses and coordinating muscle movements, as it helps regulate the release of neurotransmitters and the activation of ion channels.
Magnesium supports the structural integrity of bones and teeth. It is also a co-factor for enzymes that regulate bone metabolism, and low magnesium levels are associated with osteoporosis.
Magnesium, like potassium, is tightly regulated to maintain proper body function and prevent hypomagnesemia and low magnesium levels from occurring. The regulation of magnesium involves a complex interplay of factors, including dietary intake, absorption, excretion, and hormonal mechanisms.
The body regulates its magnesium levels by adjusting how much magnesium it absorbs in the small intestine. When there are low magnesium levels, the absorption increases to prevent hypomagnesemia. The opposite is true as well!
The kidneys play a crucial role in regulating the excretion of magnesium, similar to its role in potassium.
Several hormones can influence magnesium levels. These include the Parathyroid hormone (PTH), which increases GI absorption and decreases kidney excretion. Vitamin D also stimulates magnesium absorption in the small intestines and regulates the activity of PTH.
Similar to hypokalemia, acid-base balance can also influence magnesium levels. Acidosis can cause magnesium to shift out of cells into the bloodstream and extracellular space. Alkalosis causes the opposite, leading to hypomagnesemia.
Normal magnesium levels can range from 1.7 to 2.2 mg/dL. However, only about 1% of the body’s magnesium levels are in the blood. 50-60% of magnesium is stored in the bone, and the rest is located in the muscles, soft tissues, and red blood cells.
Normal Levels: 1.9 – 2.2 mg/dL
Mild Hypomagnesemia: 1.6 – 1.9 mg/dL
Moderate Hypomagnesemia: 1 – 1.5 mg/dL
Severe Hypomagnesemia: <1 mg/dL
Several factors can contribute to hypomagnesemia, including inadequate dietary intake, malabsorption, renal losses, medications, and certain medical conditions. Understanding the underlying causes of low magnesium levels is essential for appropriate treatment and preventing long-term complications for our patients.
Hypomagnesemia can occur with excessive vomiting or diarrhea but occurs more often with diarrhea (it has 15x more magnesium in stool than in vomit).
Certain GI conditions that affect magnesium absorption include irritable bowel disease (IBD – AKA Crohn’s or ulcerative colitis), celiac disease, and pancreatitis.
Medications that increase magnesium loss from the GI system include chronic proton pump inhibitors (PPIs) like Omeprazole may lead to low magnesium levels. Other medications which can do this include H2 blockers, Antacids, and even laxatives.
Conditions that can lead to excessive kidney magnesium loss include renal tubular acidosis, hyperaldosteronism, and even diabetes. Certain medications can also impact this (discussed below).
Medications that can increase the excretion of magnesium in the kidneys include loop diuretics and thiazide diuretics. Other drugs that can cause hypomagnesemia include Aminoglycoside antibiotics, certain chemotherapies, calcineurin inhibitors, and Digoxin.
Chronic alcoholism can impair magnesium absorption in the small intestine and increase excretion in the urine, leading to hypomagnesemia. This magnesium wasting in the urine is reversible after four weeks of sobriety.
Patient’s with an organ transplant are more likely to experience hypomagnesemia, likely from their calcineurin inhibitor medications (like tacrolimus).
High calcium levels can lead to mildly low magnesium levels.
Certain rare genetic conditions can cause decreased magnesium absorption in the small intestine and increased renal magnesium wasting.
Symptoms of hypomagnesemia (low magnesium levels) will depend on the patient and the severity of their hypomagnesemia. As the magnesium levels drop, the symptoms become more pronounced, severe, and potentially life-threatening.
Like low potassium, muscle weakness is common with hypomagnesemia. They may experience fatigue and muscle weakness in their legs which can cause difficulty walking, as well as weakness of any other muscles in their body.
Patients may feel tingling sensations and experience involuntary muscle contractions, particularly in their hands or lower extremities.
As discussed above, magnesium is essential in the conduction as well as the mechanical beating of the heart. If an arrhythmia occurs, patients may experience palpitations, chest pain, shortness of breath, dizziness, or even syncope. Cardiac arrest is possible if they go into a deadly rhythm like VFIB.
Low magnesium levels can cause nausea, vomiting, or abdominal cramping. Additionally, if the patient has diarrhea, that may be a clue on the cause.
Magnesium can cause CNS hyperirritability, leading to confusion, irritability, hyperactive deep tendon reflexes, paresthesias, and seizures.
The physical assessment of a patient with hypomagnesemia will also depend on the severity of the low magnesium levels and other factors.
Overall, while the nursing assessment of hypomagnesemia may not reveal many specific physical findings, monitoring for muscle weakness, irregular heart rhythms, and signs of potential underlying issues such as edema, ascites, and abdominal tenderness is important for identifying the condition and providing appropriate interventions to manage hypomagnesemia and prevent complications.
The treatment for hypomagnesemia depends on the underlying cause, severity, and serum magnesium levels.
When you get your patient’s results back, and they show hypomagnesemia, then follow the following general interventions:
Ensure they don’t have any symptoms and are stable, including recent vital signs.
Make sure your patient is on the cardiac monitor. Obtain an ECG if it still needs to be done. Close cardiac monitoring is essential when infusing electrolytes through the IV as well.
Notify the provider of the potassium levels, your assessment, and their cardiac rhythm. They will order the treatment for hypomagnesemia!
Make sure there is at least one IV site, but place a second line if the hypomagnesemia is severe.
Evaluate if they are on any medications which may lead to hypomagnesemia listed above.
Administer medications that are ordered (discussed below).
Treatment for hypomagnesemia will depend on the severity, as well as any symptoms the patient is having. Severe symptoms that require immediate and likely IV repletion include tetany, arrhythmias, or seizures.
Figuring out why the magnesium is low is essential, but there shouldn’t be any reason to delay replacing the magnesium with Oral or IV options. However, addressing the underlying cause can prevent further loss of magnesium and prevent it from happening again.
PO magnesium is the standard for mild to moderate hypomagnesemia, primarily if there are no or minimal symptoms.
There are many different variations of magnesium pills, such as:
Generally, sustained release options are better because they minimize the renal wasting of the magnesium. Common options include:
If the sustained release is unavailable, magnesium oxide 800-1600mg daily in divided doses may be used, but diarrhea may occur.
IV magnesium is given to patients with severe symptoms or who are NPO for whatever reason.
IV replacement dosing will depend on the severity:
Patients in renal failure should be cautiously replaced with electrolytes like magnesium and potassium, as their ability to excrete those electrolytes is impaired. Therefore, dosing should generally be cut in half, and levels should be closely monitored.
Patients should generally be maintained on magnesium replacement for 1-2 days after the levels have normalized to replete intracellular magnesium. However, if ongoing losses occur, chronic therapy may be needed.
Monitoring patients with hypomagnesemia involves cardiac monitoring and trending the magnesium levels.
Magnesium levels are generally checked at least daily while inpatient until normalization of the magnesium level.
Other electrolytes and monitoring of renal function should also be checked, usually daily, every morning.
Patients with low magnesium are at high risk for cardiac arrhythmias. Additionally, anybody receiving IV replacement with magnesium should be on a cardiac monitor.
Magnesium is an important electrolyte that plays a crucial role in cardiac function, particularly in maintaining normal cardiac rhythm. Hypomagnesemia and low magnesium levels can lead to various cardiac arrhythmias, including:
On ECG, hypomagnesemia can manifest in the following ways:
It is important to note that hypomagnesemia can also exacerbate cardiac arrhythmias caused by other electrolyte imbalances, such as hypokalemia and hypocalcemia.
Nurses should be aware of the potential cardiac complications associated with hypomagnesemia and monitor patients for signs and symptoms of arrhythmias. Timely recognition and treatment of hypomagnesemia can help prevent severe cardiac complications.
Hypomagnesemia is associated with Torsades de Pointes, which is a type of polymorphic ventricular tachycardia that is deadly and will quickly degenerate into Ventricular fibrillation if not treated ASAP. Treatment involves following ACLS protocol, but often IV magnesium is given rapidly if hypomagnesemia is suspected as a cause.
If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
Hypomagnesemia is a condition that nurses should be familiar with, as it can have significant implications for patient health. Magnesium is vital in various bodily functions, including the cardiac, nervous, and gastrointestinal systems.
The body regulates it through dietary intake, absorption, excretion, and hormonal factors. Various factors, such as chronic diarrhea, alcoholism, and certain medications, can cause hypomagnesemia. Treatment often involves magnesium replacement, either orally or intravenously, and addressing any underlying conditions that may contribute to the deficiency.
Nurses are essential in identifying and monitoring hypomagnesemia and low magnesium levels and educating patients on the importance of adequate magnesium intake and potential risk factors. Nurses can provide optimal care and improve patient outcomes by understanding hypomagnesemia’s causes, symptoms, and treatment.
Also check out:
Treatment for Hyperkalemia: A nurse’s comprehensive guide to high potassium levels
Published: July 8, 2022
Last Updated: March 6, 2023
Diabetic Ketoacidosis, or just DKA for short, is a severe complication of diabetes. This occurs when there are high sugars combined with a severe lack of insulin, causing the body to suddenly break down fat stores for energy to use ketone bodies as fuel. This leads to severe acidosis, which can cause the patient to be very sick.
Patients with DKA are usually admitted to the ICU.
In order to understand DKA, we need to have a decent understanding of acid/base balance.
The pH will determine how acidic something is. This scale goes from 0 being the most acidic, to 14 being the most basic (or alkalotic). A pH of 7 is considered completely neutral.
The human body’s normal pH is almost completely in the middle, but slightly basic.
The normal pH of the blood is 7.35 – 7.45, with 7.40 being the sweet spot.
There are two main organ systems that work together to maintain pH balance. These systems are your respiratory system and your renal system, referred to as your “metabolic system” when talking about acidity.
The number of hydrogen ions present in the blood will determine how acidic it is. The more hydrogen ions = the more acidic. The kidneys system will release buffers to lower the pH if it is too high, as well as excrete more hydrogen ions into the urine to decrease the acidity.
At the same time, the respiratory system may increase or decrease the respiratory rate to alter the pH. Breathing out more carbon dioxide out will decrease the overall pH.
Oxygen is breathed into the lungs, transported by the red blood cells, and then delivered to the cells of the body. The cells use the oxygen o create energy through a process called the “Krebs cycle”. A byproduct of this energy creation is carbon dioxide (CO2), which is then breathed out during exhalation.
Whenever the cause of the acidity decreases serum bicarb levels, this is called metabolic acidosis. Whenever the root cause of acidity causes a buildup of carbon dioxide, this is called respiratory acidosis. Metabolic alkalosis and respiratory alkalosis work the same, but with high bicarb and low carbon dioxide, respectively.
(You probably should just check out my ABG article for more info!)
DKA is one of the most common types of metabolic acidosis. This is multifactorial in nature but is characterized by a rapid increase in circulating ketone bodies, which are acidic.
Because there is a complete or severe lack of insulin, glucose is unable to get into the cells to provide energy – since the cells use insulin to help transport glucose across the cell membrane. When this happens, the body starts to freak out. This causes a massive body response by breaking down fat cells to use ketone bodies.
Ketone bodies can passively cross the cell membrane without insulin, so they can provide much-needed energy to cells that are literally starving. The ketone bodies that are created are acetoacetic acid, Beta-hydroxybutyrate, and acetone.
Acetone is actually neutral – it is not acidic. However, its presence likely means there is a presence of other ketone bodies, which ARE acidic. Not every lab will be able to check for beta-hydroxybutyrate.
You will often hear talk about the Anion gap when it comes to DKA and acidosis in general, but what exactly is the Anion Gap?
The anion gap (AGAP or AG), measures the difference between negatively charged and positively charged electrolytes in the blood. Positively charged particles are called cations, and negatively charged particles are called anions.
So essentially, this is the positive electrolyte (Sodium) minus the negative electrolytes (Chloride PLUS Bicarbonate).
Potassium is a cation, but levels are low in comparison to sodium, chloride, and bicarb because most of its content is stored intracellularly, so this doesn’t really impact the anion gap by much. Most calculations now exclude it.
Many type 2 diabetics that have uncontrolled sugars that do not often have DKA. This is probably because they still produce some insulin from their pancreas.
Hyperglycemic Hyperosmolar State (HSS) is another complication that can occur due to high blood sugars, which is more common in older patients with uncontrolled sugars.
Whenever blood glucose is high in the blood, patients can quickly become dehydrated. This is due to a process called osmotic diuresis.
Essentially, the sugar pulls a lot of water with it into the urine which is excreted by the kidneys. This dehydration causes what’s called hyperosmolality of the blood. Basically, the blood and extracellular fluid is super concentrated with sodium, so this pulls water out of cells, leading to cellular dehydration.
Because these patients usually have some level of insulin sensitivity and the presence of insulin, the massive shift of fat breakdown and ketone formation doesn’t occur on the same scale, which means severe acidosis doesn’t occur.
HHS is usually managed with IV fluids and subcutaneous insulin, but sometimes an IV drip is still used.
Patients who are in DKA are often obviously sick.
They often are vomiting, may have abdominal pain, and appear dehydrated and weak. In severe cases, they can also have some altered mental status, especially if they haven’t been able to drink fluids.
70-90% of cases of DKA occur in Type 1 diabetics and are usually due to an underlying cause. These causes include:
Patients who don’t know they are a type 1 diabetic yet
Patients who don’t take insulin as prescribed
If there is an infection, most commonly Pneumonia or UTI
Steroids, high-dose thiazide diuretics, dobutamine, terbutaline, second-generation atypical antipsychotics, or SGLT2 inhibitors
Cocaine use has been associated with recurrent DKA
Symptoms of DKA evolves rapidly over a 24-hour period, whereas HHS is more of a slow worsening of symptoms. Symptoms of DKA include:
May be from delayed gastric emptying and ileus (where a section of the intestinal wall does not perform peristalsis as normal)
Common in DKA, but almost never happens with HHS
Increased urinating is due to the osmotic diuresis described above, and the increased thirst is due to the hyperosmolality of the blood
This is due to water losses, as well as fat losses from the massive lipolysis that occurs
Lethargy, confusion, and/or obtundation can occur. Focal signs are possible as well. AMS tends to be worse in HHS because these patients often have a higher degree of hyperosmolarity.
Increased respiratory rate
This is termed Kussmaul respirations. This is the body trying to breathe off extra CO2 to compensate for the increased acidity caused by the DKA
Dry Mucous Membranes
Looking in their mouth and at their tongue is a great indicator of hydration status. These patients will be dry as a bone.
You may notice a fruity odor coming from the patient’s mouth. This is the acetone that they are breathing out. Years ago, Nurse’s used to taste a patient’s urine as well to check for a sweet glucose taste, but that has fallen out of favor… although i’m not sure why…
Temp: Often normal, but may high if infection
HR: Often tachycardic due to dehydration +/- infection
BP: May be low with severe hypovolemia
SPO2: Usually normal
Respiratory Rate: often >20 rpm (Kussmaul respirations)
Heart: Fast and regular
Lungs: usually clear but frequent and deep
Pulse: Peripheral pulses may feel weak and thready
Abdomen: May have some tenderness but shouldn’t have rebound or guarding
Patients in DKA are prone to severe electrolyte abnormalities such as hypokalemia, which can cause deadly cardiac arrhythmias to occur
Glucose monitors will often read “HI” if above 600 g/dL. However, even “euglycemic” DKA has occurred with near-normal glucose levels.
Any sick patient that may require ICU should have at least 2 IVs placed, preferably at least 20g. These patients will need a large volume of fluid replacement as well as will likely require an insulin drip and IV potassium.
Be sure to draw a gold top for the chemistries, and a lavender top for CBC. If a VBG is ordered, also draw a green top and place it on ice.
These patients are often visibly dehydrated and tachycardic. Hang 1-2L of NS open to gravity (and of course obtain an order to verify).
Ask for and administer medications such as Zofran or pain meds if the patient is nauseous or in severe pain
DKA is diagnosed based on lab work alone. The presence of a high anion gap PLUS a high sugar usually means DKA.
This is the level drawn either with a capillary glucose monitor or within the CMP of the labs. Patients in DKA often have blood sugars between 350-550 mg/dL
A high anion gap acidosis is the hallmark of DKA. The AGAP is usually >20 in DKA. This is usually due to the markedly reduced serum bicarb levels, as well as the accumulation of ketone bodies.
This is always elevated in HHS, but not always elevated in DKA. >295 mOsm/kg is considered hyperosmolar, and in HHS often levels exceed 320. Effective serum osmolality can also be calculated here.
Serum CO2 in the CMP is equivalent to Bicarb in an ABG.
If the CO2 aka Bicarb is lower than 18, this generally indicates metabolic acidosis.
Most patients with DKA are mildly hyponatremic (low sodium), but their levels will often appear even lower. This is because the high blood sugar pulls water out of cells and dilutes the sodium.
For an accurate sodium level, you should add 2 mEq/L for each 100mg increase in glucose above 100 mg/dL. You can also use this calculator.
Most patients with DKA and HHS have a total body deficit of 300-600 mEq of potassium.
This is because a lot of the potassium is urinated out along with water and ketones.
Lab levels usually appear normal and sometimes even elevated – but don’t be fooled!
Due to hyperosmolality and insulin deficiency, intracellular potassium moves out of cells and into the extracellular fluid.
Once insulin is administered, the potassium will be transported back into the cells, and the patient can be left with severely low potassium which can cause arrhythmias and even death.
Kidney function may be elevated from prerenal acute kidney injury from dehydration and hypovolemia. The patient may also have some diabetic nephropathy.
Most patients with DKA will have mild leukocytosis, and this is usually proportional to how many ketones are in the blood. It may also be related to cortisol and stress hormones as well.
A WBC > 25 or bands >10% should raise suspicion of infection.
ABGs are rarely needed in DKA. Remember DKA is metabolic acidosis, and there often is respiratory compensation.
If drawn, this means the pH will be acidic (< 7.35), the HCO3 will be low (<18), and the CO2 will also be low (<35) to compensate.
A VBG is often ordered instead of a full ABG in patients with suspected DKA. We are mainly evaluating the patient’s pH and bicarb levels, which are essentially equivalent to their ABG counterparts.
Serum ketones can be drawn to directly detect ketones within the blood. These do not need to be drawn if the patient has a AGAP acidosis with hyperglycemia, but will depend on the facility and ordering Provider.
Serum acetone or beta-hydroxybutyrate can both be ordered, and different hospitals will have different options.
A urinalysis will often show a decreased specific gravity from the osmotic diuresis. Additionally, it will often show large glucose and often ketones.
Starvation ketosis can occur in diabetics and non-diabetics when they aren’t eating, often accompanied by vomiting. This can lead to ketones in the urine and the blood, but there is no acidosis. This is not treated as DKA and is best treated with IV fluids with dextrose and antiemetics.
Amylase and lipase may be ordered if pancreatitis is suspected, and lipids may also be ordered (but usually with morning labs).
Treatment of DKA aims at reversing the acidosis as well as lower the glucose.
Each hospital and Provider may have their own protocols, but treatment generally involves these two steps:
The first step in treating DKA is to replace IV fluids, usually with Normal Saline, which helps stabilize vital signs, replace fluid losses, increase insulin responsiveness, and reduce stress hormone levels.
Remember that severely high blood sugar causes severe dehydration, so these patients usually need a lot of fluid.
This is usually with 2-4L NS for the first 3-4 hours, infused at 1L per hour.
If the patient has a history of CHF or advanced renal failure, this should be infused slower with careful monitoring for fluid overload.
As long as potassium >3.3, Insulin can be started.
Each hospital will have their own insulin drip protocol. Often a bolus is given first of 10 units (0.1u/kg body weight). Then the infusion is started at 0.1u/kg/hr.
Regular and rapid-acting insulins are equally effective at treating DKA and HHS.
Once the serum glucose reaches between 200-300, dextrose is usually added to the IV fluid until the acidosis resolves.
If >5.3 mEq/L: IV Potassium is held off until levels drop below 5.3. These are checked hourly.
If 3.3 – 5.3 mEq/L: IV potassium is started as long as the patient is making >50ml/hr of urine, indicating appropriate renal function. 20-30mEq is usually added to each liter of IV fluid.
The goal is to maintain the potassium between 4 – 5 mEq/L.
If <3.3 mEq/L: The patient requires 20-40mEq/hr until the potassium is above 3.3. This is often added to NSS or ½ NS.
Insulin therapy should not be started until this level is above 3.3!
Potassium is very irritating to the veins and can lead to pain and phlebitis. Also, rapid infusion of potassium can result in severe hyperkalemia (Rule #1 of nursing: NEVER push IV potassium!).
Potassium shouldn’t exceed 10mEq/hour in a peripheral line, or 20mEq/hour in severe cases.
In a central line, potassium can be infused as fast as 20-40mEq/hr in severe cases.
After the first few hours, IV fluids should be continued at a slower rate. This will be selected by correcting the sodium level for hyperglycemia.
If the sodium level is still low, Normal saline is usually continued.
If the corrected sodium is normal, hypotonic saline is started (i.e. 1/2 NS).
These are usually continued at a rate between 250-300ml/hr.
Potassium is as osmotically active as sodium, so adding potassium to your saline will increase the fluid’s tonicity. To make a relatively “isotonic” solution, 40-60mEq of Potassium is often added to 1/2 NS.
Dextrose is also osmotically active, but the dextrose will be metabolized quickly, ultimately having less of an effect on the tonicity.
While it may seem counterintuitive, IV dextrose is added to the IV fluids once the blood sugar reaches somewhere between 200-300 mg/dL.
This is because insulin is still needed to “close the gap” and reverse the acidosis, but the glucose can still drop too much. If the blood glucose drops below 200-300mg/dL can increase the chance of cerebral edema!
In HHS, its best not to let the glucose drop below 250-300 mg/dL, and in DKA no less than 200 mg/dL.
An example of a fluid would be D5 1/2 NS (likely with potassium added as well).
Check out my article on IV FLUIDS!
Patients with DKA are at high risk for complications, so they should be monitored closely, especially while in the ICU.
Each hospital should have a facility protocol when it comes to insulin drips.
Usually, this requires blood glucose checks every hour.
Once the glucose drops below 250 mg/dL, fluid with dextrose is usually started until the AGAP normalizes, otherwise the patient will become hypoglycemic.
Lowering the glucose too much in these patients can lead to cerebral edema.
As discussed above, this should be monitored frequently.
A BMP is usually checked every 2-4 hours while on an insulin drip.
Monitor for tachycardia, ectopy, or any arrhythmias.
Severe hypokalemia and acidosis can lead to fatal arrhythmias like VFIB, Asystole, and PEA.
Significant acidosis and hypovolemia can cause hypotension.
When the body is acidotic, medications like vasopressors don’t work as well as they should.
Once the AGAP returns to normal, the gap is considered ‘closed” and the patient does not require an IV insulin drip anymore.
They are usually transitioned to subcutaneous insulin at this time.
Hopefully this left you with a good idea of what DKA is, how we recognize it, how we treat it, and what monitoring parameters you need to watch out for as a nurse!
What would you like to learn next? Let me know if the comments below!
Hirsch, I. B., & Emmett, M. (2022). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment
Hirsch, I. B., & Emmett, M. (2022). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-clinical-features-evaluation-and-diagnosis
Hirsch, I. B., & Emmett, M. (2022). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-epidemiology-and-pathogenesis
Melmed, S., Koenig, R., Rosen, C., Auchus, R., & Goldfine, A. (2019). Type 1 Diabetes Mellitus. In Williams textbook of endocrinology (12th ed., pp. 1453 – 1457). Elsevier.
Published: June 14, 2022
Last Updated: March 23, 2023
This ultimate ABGs Blood gas guide is exactly what you’ve been looking for to understand Arterial Blood Gases! ABGs are used frequently in the ER and ICU settings, and many critical patients will need their blood gases monitored frequently.
ABGs, or an Arterial Blood Gas, is a blood sample that is taken from an artery in the wrist. This is different than normal blood work, which is taken from the veins of the arms. The arterial blood sample is obtained by a respiratory therapist or a critical care nurse.
Arterial samples provide better indicators of oxygen and carbon dioxide levels, but ABGs also look at acidity and bicarbonate levels within the blood.
A blood gas is used to look at acid-base disturbances and/or to evaluate the adequacy of oxygenation/ventilation. When an ABG blood gas is ordered, 4 contents of the arterial blood are tested:
Oxygen (O2) and carbon dioxide (CO2) are the main gases within the blood, and these are measured in blood gas. However, ABGs also provide levels of blood pH and Bicarb.
Of all of the measurements, the most important levels to look at are the CO2, the Bicarb, and the pH in determining acid-base balance.
ABGs are very useful in evaluating acid-base disturbances, as well as ventilation/oxygenation disturbances. The patients who are ordered ABGs are often sick – usually ICU bound. The most common patients who might have a blood draw include:
There are some important factors to keep in mind when thinking about ABGs and interpreting them.
Patients can have mixed acid-base disturbances, which can make it confusing. That’s why the interpretation is ultimately best left up to the critical care physicians and other Providers within their care.
Remember the body is always trying to maintain homeostasis. The respiratory system will attempt to compensate for the metabolic system and vice versa.
Always focus on treating the underlying cause.
Okay, so lets dive a little deeper into what each measurement is on the ABG results, and what their levels mean.
pH is the “potential of Hydrogen”, which measures how acidic a solution is. The more hydrogen ions present in a solution, the more acidic it is.
pH may be normal or near-normal in chronic acid-base disturbances from compensation, or the patient can have multiple different acid-base disturbances going on at once.
The PaCO2 is the partial pressure of Carbon Dioxide within the arterial blood. Essentially this is just a measure of the amount of carbon dioxide gas within the blood.
Remember that the lungs breathe in oxygen, deliver the oxygen to the cells, and the cells use that oxygen to create energy. To create energy (ATP), the cells utilize the Kreb’s Cycle, and a byproduct of that cycle is carbon dioxide. That CO2 is then breathed out when you exhale.
CO2 isn’t acidic by itself, but in the blood forms something called carbonic acid, which is acidic. Breathing out less CO2 will cause acidosis, and breathing out too much CO2 can cause alkalosis.
IF THE PaCO2 AND the pH are both high, think RESPIRATORY ACIDOSIS.
When you hold your breath, eventually you need to breathe again because it feels like your blood is boiling. This always helped me remember that when you aren’t breathing enough, the CO2 makes it boil – aka acidosis!
HCO3 on an ABG blood gas is the serum bicarb levels within the arterial blood. Bicarb acts as a buffer to make acidity less acidic. Think of it as the opposite of hydrogen ions. The less bicarb there is, the more acidic the blood is. To get technical, Bicarb reacts with H+ to form carbonic acid, which the body breaks down into CO2 and water – which it breaths out.
PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen blood gas content.
Don’t forget that too much oxygen can be bad too. Oxygen toxicity can produce reactive oxygen species and cause cellular injury, inflammation, and cell death. It can also worsen hypercapnia like in patients with COPD.
The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.
When interpreting ABGs and blood gases, there are 4 general categories we use:
Using these categories, we can better understand what the possible underlying cause of the acid-base disturbance is!
Don’t forget someone can have multiple acid-base disturbances going on at one time, and this makes clinical interpretation difficult – everything is not black and white in medicine, but this should give you a pretty good idea of what may be causing your patient’s acid-base disturbance.
Respiratory acidosis is due to alveolar hypoventilation. The lungs are NOT able to remove enough carbon dioxide quickly enough, so CO2 and Hydrogen build up in the blood.
High CO2 tends to occur late in the lung disease or when respiratory muscles are fatigued – this is usually seen in severe respiratory failure. The acidosis can be acute or chronic.
This classically can happen to patients with COPD because they are less responsive to hypoxia and hypocapnia. There is also increased dead-space ventilation and decreased diaphragmatic function due to fatigue and hyperinflation.
Acute respiratory acidosis could be from multiple different reasons including:
Chronic respiratory acidosis may occur when the PaCO2 is elevated, but the pH remains normal or near-normal because the body adjusts (metabolic compensation). Causes of chronic respiratory acidosis include: be Obesity-Hypoventilation syndrome (Pickwickian syndrome), ALS, interstitial fibrosis, and thoracic skeletal deformities.
When your patient with COPD is on a lot of oxygen, there is always a risk of hypoventilation and CO2 retention. This is the classic patient you should be thinking about with respiratory acidosis.
The treatment for respiratory acidosis is treating the underlying cause (i.e. giving Narcan to someone who overdosed on opioids), but more often than not the treatment is BIPAP or Intubation.
This acid-base disturbance is due to alveolar hyperventilation. The lungs remove too much carbon dioxide too quickly, so hypocapnia (low PaCO2) and alkalosis occur.
It is commonly found in those who are critically ill, but can be found in various other conditions such as:
The settings on the ventilator could be incorrect, and the patient may have a rate that is too fast
Patients experiencing panic attacks, severe anxiety, or psychosis can experience respiratory alkalosis. However, the patient’s with panic attacks almost never have ABGs ordered (it’s unnecessary)
Pneumonia, pneumothorax, pulmonary embolism, asthma, bronchitis. This is more the increased respiratory rate compensating for the disease, but eventually, these issues can cause respiratory acidosis instead
Acute low CO2 levels lead to potassium and phosphorus shifting into the cells and cause calcium to increase its binding to albumin. This can cause temporary symptoms such as numbness/tingling in extremities that many patients may experience with acute panic attacks!
The treatment for respiratory alkalosis is treating the underlying cause, such as adjusting ventilator settings, administering anxiolytics, etc.
A bicarb level <22 mEq/L in addition to a pH <7.35 is metabolic acidosis. This acid-base disturbance is due to increased plasma acidity. Metabolic Acidosis is further broken down into whether or not the Anion Gap is normal or elevated.
Severe HCO3 levels <12 are almost always caused by some degree of metabolic acidosis, instead of just compensation for respiratory alkalosis.
This type of metabolic acidosis usually has high chloride. This is when Bicarbonate is lost within the GI tract or kidneys (is peed or pooped out). This can be caused by:
Diarrhea can cause loss of Bicarb within the stool but tends to save chloride, which does not increase the anion gap.
Typically when GFR is between 20-50ml/min
In RTA, the kidneys do not remove acid from the blood like they should
Replacing large volumes of Normal Saline can cause a modest metabolic acidosis that is termed dilutional acidosis. This can worsen kidney injury. Using Lactated Ringers is a possible benefit to this, as the lactate is used as a buffer.
The anion gap is the difference between the positive ions in the blood (sodium), and the negative ions in the blood (chloride, bicarb, lactic acid, ketones, etc). Common causes of elevated gap metabolic acidosis include:
DKA causes a massive increase of ketone bodies which are acidic, in addition to severe dehydration
Injury to the kidneys can cause a decreased ability to excrete hydrogen ions as well as the ability to increase bicarb levels to help buffer the acidosis
Certain substances are toxic and can cause metabolic acidosis including alcohols, salicylates, cyanide, and carbon monoxide
The treatment of metabolic acidosis is to correct the underlying issue causing the acidosis in the first place. Bicarb drips can be used in severe cases of acidosis (pH < 7.1 or 7.2).
This acid-base disturbance is caused by increased serum bicarb and decreased acidity. Bicarb levels >35 mEq/L are almost always caused by some degree of metabolic alkalosis as opposed to just compensation.
For metabolic alkalosis, the acidity or hydrogen ions (H+) are usually lost in some manner, either through the GI tract or the kidneys:
Gastric secretion has a high content of hydrogen ions, so excessive vomiting can reduce overall acidity within the body
Over time, NG tubes remove a lot of gastric fluid, similar to excessive vomiting, this can cause a decrease in hydrogen ions
Rare, but if you consume massive amounts of milk products or antacids this can cause metabolic alkalosis
The use of certain diuretics or mineralocorticoid excess, and some other rare disorders can cause the kidneys to pee out too many hydrogen ions.
It always helps to have a systematic approach when interpreting ABGs, as blood gasses can be somewhat confusing if you miss a step!
First, see whether or not the patient is acidic (pH <7.35), or alkalotic (pH >7.45). This will tell you if there is an acute acid-base disturbance going on.
See which levels are abnormal. Are they leaning acidic or alkalotic?
See which one (CO2 or HCO3) correlates with pH. For example, if the pH is 7.2 (acidic), which abnormality is also leaning towards acidity? If CO2 was 56 and HCO3 was 30, the CO2 correlates with the pH because both are acidic.
Now check the level that doesn’t correlate with the pH. Is this also abnormal but in the opposite direction? If so this is termed compensation. If the pH is abnormal, it is only partial compensation.
This step is optional and done if there is metabolic acidosis. This will help give you a better idea of which type of acidosis it is. If it is high, think of kidney failure, sepsis, or DKA. If it is low, think severe diarrhea.
Hopefully, this gave a good idea of how to interpret ABGs, as well as the treatment involved with abnormal results.
Emmett, M., & Szerlip, H. (2022). Approach to the adult with metabolic acidosis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/approach-to-the-adult-with-metabolic-acidosis
Emmett, M., & Szerlip, H. (2022). Causes of metabolic alkalosis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/causes-of-metabolic-alkalosis
Hopkins, E., Sanvictores, T., & Sharma, S. (2020, September 14). Physiology, Acid Base Balance. National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK507807/
Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian J Crit Care Med, 14(2), 57-64. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936733/
Theodore, A. C. (2022). Arterial blood gases. In Uptodate. https://www.uptodate.com/contents/arterial-blood-gases
Published: April 13, 2022
Last Updated: March 23, 2023
Atrial Fibrillation (AFIB) and AFIB RVR are common conditions that you’ll see as a nurse within both inpatient and outpatient settings. These patients are often asymptomatic, but may have severe symptoms and even be unstable, especially with AFIB RVR.
Recognizing AFIB on the monitor/EKG and knowing how to treat it is important as the nurse, as you’ll be on the front line with these patients!
Atrial Fibrillation (AF or AFIB) is an “irregularly irregular” arrhythmia that usually occurs in a structurally diseased heart.
AFIB occurs when too many atrial impulses are usually coming from the pulmonary veins, causing rapid fibrillation or “quivering” of both the left and right atria.
Remember, the heart has four chambers: left and right atria on the top and left and right ventricle on the bottom. With AFIB, the top chambers are in a constant state of fibrillation.
During a normal heartbeat, the atria first contract, pushing blood into the ventricles, and the ventricles then pump the blood to the rest of the body. In AFIB, the atria lose this “atrial kick,” leading to ineffective atrial filling and decreased cardiac output, especially at rapid rates.
It is helpful to remember how the cardiac conductions system works to understand what is going on with AFIB.
Remember, the heart has specific electrical conduction tissue, which creates and moves the electrical signal throughout the heart to produce an organized rhythm. This organization lets the heart fill and pump effectively.
The heart’s pacemaker is the sinus node located in the right atrium. This region of cells creates the “normal” impulse and sends it throughout the atria and then through the AV node. This AV node normally slows the conduction to allow for ventricular filling. The PR interval on the EKG denotes this slowing of the conduction.
Once traveling through the AV node, the impulse goes through the Bundle of His. It splits down the left and right bundle branches towards each ventricle, then through the Purkinje fibers and eventually the ventricles, causing a heartbeat.
In AFIB, rapid-firing comes from the atria, usually where the pulmonary veins meet the left atria. This leads to the quivering of both atria and ineffective atrial filling and atrial kick.
While the AV node does slow down conduction, it can only do so much on its own. With such rapid firing from the atria, many of these impulses want to make it down to the ventricles and cause heartbeats.
As you can imagine, this can lead to very fast heart rates – what we call AFIB RVR or rapid ventricular response.
AFIB RVR (Rapid Ventricular Response) occurs due to the frequent electrical impulses from the atria.
The AV node is only able to slow the frequent electrical impulses down so much, so many of the impulses are conducted through to the ventricles, leading to a rapid ventricular response or a fast heart rate >100bpm and often much faster.
Patients with these fast rates are often symptomatic and may become hypotensive. These patients will usually require IV medications to slow down their rate, and possibly even electrical cardioversion (more on that later!).
AFIB usually occurs in predisposed hearts and is often set off by reversible triggers.
Chronic diseases which predispose the heart to AFIB include:
Anything causing atrial enlargement such as CHF, Cardiomyopathy, COPD, OSA, obesity
Rheumatic Fever, aortic stenosis, valve repelacements, etc
Coronary artery disease, past or current myocardial infarctions (heart attacks!)
Usually, some reversible trigger throws the patient into AFIB. These reversible triggers include:
CABG or heart transplants, usually within the first 2 weeks postop
PEs can cause right atrial heart strain and Increased pulmonary vascular resistance
Alcoholics and binge-drinking can cause Holiday Heart syndrome, which can occur in 60% of binge drinkers
Cocaine and amphetamines can increase sympathetic tone and leave the heart predisposed to arrhythmias such as AFIB
Hyperthyroidism (low TSH) can cause increased sympathetic tone and lead to arrhythmias
Low magnesium levels can lead to AFIB, generally levels < 1.5 (check this).
Certain medications can trigger AFIB including Theophylline and adenosine.
Although caffeine is often thought of as contributory to ectopy and AFIB, there is no direct evidence it does trigger AF. However, it is something to consider.
Up to 44% of patients with Afib are asymptomatic. Patients with faster rates are more likely to develop symptoms, and those with CHF are more likely to experience hemodynamic instability and severe symptoms (aka low BP and possible code situation).
Some symptoms of AFIB can include:
Most common complaint
Shortness of breath
Dizziness or lightheadedness
Fluttering or skipping in their chest, or possibly just feeling their heart pounding
Chest pressure, pain, or discomfort
Loss of consciousness
AFIB will NOT have visible P waves. Instead, there will be a fibrillatory baseline. There is no depolarization wave throughout the atria, but rather rapid twitching and many “small” depolarizations, firing at rates 350-600 times per minute.
The QRS complex should be narrow unless an underlying intraventricular conduction delay is present, such as a bundle branch block.
The T waves may be difficult to decipher between the F-wave baseline completely. T wave abnormalities are common, including T wave flattening.
AFIB is irregularly irregular. This means that the R-R interval is continuously changing, and there is no pattern.
AFIB can be at any rate, but faster than 100 is considered AFIB RVR. Without medications to slow it down, rates are usually between 90-170 bpm.
Any patient with cardiac symptoms should get an EKG.
Patients with new AFIB should have a 12-lead EKG to confirm the diagnosis.
If the patient is at significant fast rates, keep them hooked up to grab another one once the rate improves or the patient converts.
Patients with any cardiac symptoms should be placed on the cardiac monitor.
Those patients with a history of AFIB with normal rates does not necessarily need a cardiac monitor.
If the patient is significantly hypoxic or tachypneic, apply 2-4 L/min NC to maintain SPO2 >90%.
Start two peripheral IVs at least 22g, but preferably one at least 20g. If they are in AFIB RVR, they will likely need an IV Cardizem drip and IV heparin in separate lines.
If there is a concern for pulmonary embolism or embolic stroke, make sure to place an 18-20g in the AC.
While drawing blood, make sure to draw a blue top as PT/INR, PTT, and a D-dimer may be ordered.
Remember that any unstable tachyarrhythmia should follow ACLS guidelines. This means the patient may need electrically cardioverted. If they are unstable (Low BP, impending arrest), then place the defibrillation pads on the patient and hook them up to the defibrillator.
The workup will depend if the patient is in new-onset AF or already has chronic AF and if they are in RVR or not.
Patients with a known history of AFIB who have controlled rates don’t need any specific testing. They are usually on chronic medications to control their heart rates and anticoagulants to prevent blood clots.
Patients with new AFIB or AFIB RVR require more extensive testing, and the workup may depend on their symptoms.
General workup for new AFIB includes:
AFIB can be diagnosed with this, as well as to look for any other abnormalities such as a STEMI
CBC, CMP, and magnesium will often be checked
Coag studies such as PT/INR and PTT, BNP if s/s of heart failure, digoxin level if patient is taking, and a D-dimer may be ordered as well
If they have any cardiac or pulmonary complaints this should be obtained
If there is suspicion of a PE. It May also detect atrial thrombi but is not very sensitive
If any altered mental status or stroke-like s/s
So why do we even care about AFIB? Well, there can be disastrous consequences if we do not treat it appropriately.
Patients with AFIB have an inadequate atrial filling of blood, as well a loss of the atrial kick which pushes blood from the atria to the ventricles. This decreases cardiac output. When the ventricles have a rapid response, these insufficiencies worsen and can lead to hemodynamic compromise – hypotension, hypoxemia, and eventually cardiac arrest.
Patients with Left ventricular dysfunction (aka CHF with a low EF) already have a weak heart. This drop in cardiac output will be more significant, often leading to severe symptoms and an unstable patient!
With the atria quivering – stasis of blood occurs. Remember, stasis of blood is one of the 3 factors that can lead to blood clots (Virchow’s triad). This increases the likelihood of thrombus formation.
A thrombus in the right atria can embolize to the lungs and cause a pulmonary embolism, and a left atrial thrombus can embolize to the brain and cause an embolic stroke.
Both of these are very serious conditions which can lead to disability and death, so prevention of this complication is important.
Treatment of AFIB differs and depends on the patient’s symptoms and quality of life. This will involve at least one, but possibly all three of the following:
Which the Provider team and Cardiology will ultimately choose treatment options. We’ll dive a little deeper into each of these treatment options.
Rate-control is achieved via medications to slow down the ventricular response to the AFIB. Common medications include Metoprolol, Diltiazem, Digoxin, Esmolol, Amiodarone, and even magnesium sulfate.
For AFIB RVR, we often give the following medications to control the rate:
Also called Cardizem, this is more commonly given for AFIB RVR. The dose is 0.25mg/kg bolus, which is usually around 20mg. This should be pushed over 2 minutes. A repeat bolus of 0.35mg/kg can be given in 15 minutes if rate control is insufficient, and then a patient should be started on a titratable Cardizem drip.
Also called Lopressor, this is especially helpful if the patient is on a Beta-blocker at home and maybe has missed some doses. The dose is 2.5-5mg IV q5m x 3. Administer the IV push over 2 minutes, and monitor rhythm and blood pressure closely. Use with caution with asthma/COPD exacerbations.
One thing to point out is that those patients with significant left ventricular heart failure and AF RVR may paradoxically improve their blood pressure with rate control, so it still may be wise to administer a low dose of metoprolol or cardizem in these select patients if borderline hypotension is present. Always verify with the Physician/APP.
Rhythm-control is achieved via medications or electrical cardioversion. If the patient is unstable, they will be electrically cardioverted. Otherwise, the cardiologist may choose to start the patient on an antiarrhythmic such as amiodarone, Flecainide, multaq, etc.
Many elderly patients who do not have significant symptoms will not undergo rhythm control. This is ultimately up to the cardiologist.
IV amiodarone can be used, or the cardiologist may choose to start an oral antiarrhythmic such as Amiodarone, Sotalol, Dofetilide, etc
Unstable patients should undergo synchronized cardioversion with the defibrillator
Patients with frequent symptoms (often younger patients) may undergo an ablation to burn off the area of the heart that is triggering AFIB
Anticoagulation is almost always used in patients with AFIB, unless there is acute bleeding or a significant risk of bleeding.
Anticoagulation is used to prevent thrombus formation which can cause PEs and Strokes as explained above. Within the hospital, anticoagulation will include either:
The Provider will order a titratable heparin drip per facility protocol. This usually will have an initial bolus ordered as well. The patient’s PTT will occasionally be checked and the drip will be adjusted accordingly. Heparin drips offer quickly-reversible anticoagulation in case the patient starts bleeding.
SubQ lovenox at a dose of 1mg/kg BID can be given alternatively.
Before being discharged, the patient is then transitioned onto an oral anticoagulant such as coumadin, Eliquis, Xarelto, Pradaxa, or ASA/Plavix.
Coumadin is much less commonly prescribed than it used to be because it requires frequent blood checks of INR, as well as dietary changes and medications, can significantly impact its therapeutic levels
The CHADSVASC score is used to gauge risk for thrombus formation, which factors in age, sex, h/o CHF, HTN, Stroke/TIA/DVT/PE, Vascular disease, or Diabetes. If the patient does not have a high risk of bleeding such as intracranial bleeding, GIB, or frequent falls, then they are usually started on an anticoagulant.
The workup and treatment will depend on the patient’s symptoms and overall clinical picture. With AFIB, there is no one-size-fits-all approach!
Focus on rate control and anticoagulation! Become familiar with IV Cardizem and titrating a Cardizem drip, as well as IV Lopressor!
Patients who are unstable should be electrically cardioverted with a synchronized shock. Remember to press SYNC, and the dose is 50-100J. These patients will require sedation and pain control (i.e. IV fentanyl).
If you want to learn more about cardiac arrhythmias, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.
With this course you will be able to:
I also include some great free bonuses with the course, including:
Check out more about the course here!
Burns, E. (2021). Atrial Fibrillation. In ECG Library. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/
Kumar, K. (2022). Overview of atrial fibrillation. In T. W. Post (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-atrial-fibrillation
Olshansky, B. (2022). The electrocardiogram in atrial fibrillation. In T. W. Post (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/the-electrocardiogram-inatrial-fibrillation
Phang, R., Prutkin, J. M., Ganz, L. I. (2022). Overview of atrial flutter. In T. W. Post (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-atrial-flutter
Prutkins, J. M. (2022). Electrocardiographic and electrophysiologic features of atrial flutter. In T. W. Post (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/electrocardiographic-and-electrophysiologic-features-of-atrial-flutter
Published: March 3, 2022
Last Updated: March 23, 2023
Blood pressure is one of the 5 vital signs, and it is so important to understand what normal and abnormal blood pressures are, and how we manage them (don’t get me started on the “6th” vital sign…).
Within the hospital, vital signs are typically checked every 4 hours, and you will frequently run into both high and low blood pressures.
Low blood pressure is often much more worrisome, and you may want to call an RRT if the BP is significantly low, especially when the patient is altered or has significant symptoms.
High blood pressure is common, but often is not considered a big deal unless VERY high. In these cases, we want to slowly decrease the blood pressure instead of too quickly.
As you probably know, blood pressure is not the pressure of your blood, but rather the pressure within your vascular system.
The vascular system refers to your arteries and veins. When speaking of systemic blood pressure, we are specifically talking about the pressure in the arteries.
This pressure temporarily increases with each heartbeat, and decreases in-between each heartbeat.
The pressure in your arteries when your heart beats or contracts is called the systolic blood pressure. Systolic just means during the heartbeat. Systolic blood pressure can never be below the diastolic pressure.
When the heart is not beating, the pressure “rests” back to its normal baseline pressure. This is called the diastolic blood pressure. The diastolic blood pressure should never be 0.
This pressure is measured in millimeters of mercury (mmHg).
As we said above, systolic is the pressure during contraction of the heart, and diastolic is the pressure in-between beats. When looking at a blood pressure reading, there are two numbers: a numerator and a denominator. The numerator or top number is the systolic blood pressure. The denominator or the bottom number is the diastolic blood pressure.
Normal systolic blood pressures are between 100 – 120 mmHG. Normal diastolic pressures are between 60-80 mm Hg. Traditionally 120/80 mmHg was considered the “gold standard” for blood pressure, but now its recommended to be at most 120/80 mmHg.
A “good pressure” is relative. In the ER, a pressure below 160/90 tends to be considered pretty good and usually won’t require any medications. However, a pressure of 160/90 is considered very high if that is the normal daily blood pressure at home, and should be started on medications.
We check people’s blood pressures in the hospital, in the outpatient office setting, and pretty much every area of patient care. Nowadays, we have machines that do most of it for us. But machines aren’t perfect, and its an essential nursing skill to know how to check blood pressure.
In general, there are 3 main ways to check someone’s blood pressure:
A manual blood pressure is checked using a sphygmomanometer and a stethoscope. The stethoscope if placed over the brachial artery, and the cuff is placed on the patient’s bicep.
The cuff is pumped up to about 160 or 180 (in most people unless BP is very high). Slowly release the cuff pressure while you auscultate the brachial artery.
Systolic blood pressure is identified by the first Korotkoff clicking sound. The diastolic is noted when you can’t hear anything left.
You can palpate the patient’s radial artery when a machine or cuff is pumping up or down. When the radial artery disappears, this is your systolic pressure. There is no way to check diastolic with palpation
An automated blood pressure is checked by a machine, often a portable Dinamap or a bedside monitor. These machines essentially perform a manual BP on their own.
They have a sensor which detects tiny oscillations from your pulse. So when the pulse goes away – this is your systolic pressure. When the pulse reappears, this is your diastolic pressure.
Arterial lines are commonly placed in the ICU for strict BP monitoring. This is the most accurate way to check a blood pressure because it is directly measured by a sensor within the arteries, instead of indirectly like with the methods above. This gives you real-time changes in blood pressure.
If you’ve been working for a bit, or in clinicals, you may hear about the term “MAP”. While systolic blood pressure is often considered the most important part of the blood pressure, the actual important number is the MAP.
The MAP stands for Mean Arterial Pressure. This is the average pressure in the arteries from one cardiac cycle (systolic + diastolic). This is measured by a calculation:
But don’t go busting out your calculators. The bedside monitors should automatically calculate this for you, or possibly your EMR. If you need to calculate it, there are plenty of good online calculators to quickly do it.
MAP is a great indicator of tissue perfusion. If the MAP stays above 65 mmHg, then this should be enough pressure to provide essential tissue perfusion and prevent anoxic injury (injury from a lack of oxygen to the cells!).
Nurses and Providers in the ICU will care much more about MAP than systolic blood pressure, especially when looking at low blood pressures.
Hypertension, also known as high blood pressure, comes in many different forms. While often thought of as “not a big deal”, it really is the silent killer, and can put a lot of strain on the heart, vasculature, and kidneys.
Overtime, this organ damage becomes more pronounced, placing the patient at risk for heart disease, strokes, kidney failure, and more!
Another reason why it’s termed the silent killer is because it often is asymptomatic – meaning there are no symptoms. But just because there aren’t any symptoms doesn’t mean it isn’t dangerous, especially in the long run.
In medicine, we use JNC8 guidelines to classify and manage hypertension.
Blood pressure levels include:
Normal: < 120 / 80 mmHg
Stage 1 HTN: 130 – 140 / 80-89 mmHg
Stage 2 HTN: > 140 / 90 mmHg
Hypertension can be chronic or acute. Its also important to know if the patient is having any symptoms such as chest pain, SOB, headache, etc.
3 main types of hypertension that we’ll talk about include:
Primary hypertension, previously referred to as essential hypertension, is a chronic hypertension that has no clear cause, but is thought to involve genetic, dietary, and lifestyle factors. This is what most people are diagnosed with when they have high blood pressure. Risk factors include:
Hypertensive urgency is a very high blood pressure > 180/110 mmHg. While there is no evidence of organ damage (i.e. lack of symptoms or lab abnormalities), the patient is at risk for organ damage or strokes to occur.
Hypertensive emergency is a very high blood pressure > 180/110 mmHg when there IS evidence of organ damage. The patient should have at least one of the following signs or symptoms:
Treatment of hypertension is often not aggressive, and is often made by slow gradual changes to outpatient medication regimens.
However, if the patient is symptomatic, blood pressure medications should be given.
At home blood pressures should be checked, as patients BPs are often higher in emergency and urgent care settings, and “White coat hypertension” is common.
Some oral medications used to lower BP include:
In hypertensive urgency and when in the hospital, sometimes IV medications may be required including:
In general, blood pressure should never be lowered too fast. In severe cases, the goal should be to lower the MAP by 10-20% within the first hour, then another 5-15% over the next day. In many cases, this is less than 180/120 in the first hour, and less than 160/110 after 24 hours.
Lowering the blood pressure too quickly can actually cause ischemic damage in patients who have had elevated blood pressure for a long time. Basically the body becomes used to that high pressure, and while it is dangerous to have high blood pressure in general, lowering it too quickly can cause damage as well.
When it comes to blood pressure (and even heart rates while we’re at it), its always important to ask the patient if they have any symptoms. Ask about any CP, SOB, dizziness, palpitations, headache, numbness/tingling/ etc.
Hypotension is when the blood pressure is too low. Low blood pressure is defined as any pressure less than 100/60 mmHg. However, this is often not considered true hypotension until below 90/50 mmHg.
Patients who are small in stature and thin may have borderline low blood pressures at baseline.
Worried about the patient’s BP? Trend what their BP has been this hospital visit, as well as previous hospital visits. If their BP is 92/48 but they always run around there and are asymptomatic otherwise – this is reassuring.
Remember if the MAP is less than 65 mmHg, this places the patient at risk for tissue ischemia and organ damage.
Low blood pressure is often a serious sign, especially in the hospital setting. Common causes of hypotension include:
Septic shock is when there is a severe systemic response to infection. These patients will have persistent hypotension despite adequate fluid resuscitation (30ml/kg bolus). They usually require IV vasopressors, a central line, IV antibiotics, and ICU admission.
Anaphylactic shock is a type of distributive shock that occurs with a severe allergy. Release of inflammatory mediators causes massive systemic vasodilation, swelling, and hypotension. This is treated with IV steroids and antihistamines, +/- epinephrine.
When the patient loses enough blood, they will become hypotensive. These patients need STAT blood, usually O negative blood that hasn’t been crossmatched.
Cardiogenic shock occurs when the heart can’t keep up with the body’s demand. This can occur in severe CHF or bradyarrhythmias.
Maintenance medications given for blood pressure can cause low BP, especially if taken in wrong doses or if they become toxic. Some other medications have hypotension as a possible side effect such as amiodarone.
Patients with a history of adrenal insufficiency will often require stress-dosed steroids to maintain their blood pressure.
Dehydration needs to be severe before the patient becomes hypotensive. This can occur in those with DKA or diabetes insipidus, or really anything that causes dehydration.
Treatment of hypotension will involve treating the underlying cause, but generally involves 2 steps:
If fluid boluses do not improve blood pressure, or if the BP drops back again once its done, then the patient may need vasopressors in the ICU.
Depending on the cause, the underlying cause should be addressed, including:
You are going to run into TONS of patients who either have high blood pressure, or low blood pressure. Managing vital signs is a huge part of our jobs as nurses and doctors, and its so important to understand how to manage blood pressure!
Remember these important concepts when it comes to blood pressure:
Double check your blood pressures. If it doesn’t seem right – check a manual BP. The provider may ask you to do this anyway.
If your patients BP is high or low, ask them if they have any symptoms. Focus on any headache, chest pain, shortness of breath, dizziness, lightheadedness, palpitations, syncope, etc.
Remember high blood pressure shouldn’t be corrected too quickly. Look at previous trends. Don’t freak out about blood pressures that are high unless the patient has symptoms. Worry more about low blood pressures!
Basil, J., & Bloch, M. J. (2022). Overview of hypertension in adults. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/evaluation-of-and-initial-approach-to-the-adult-patient-with-undifferentiated-hypotension-and-shock
Calder, S. A. (2012). Shock. In B. B. Hammond & P. G. Zimmerman (Eds.), Sheey’s manual of emergency care (7th ed., pp. 213-221). Elsevier.
Gaieski, D. F., & Mikkelsen, M. E. (2022). Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/overview-of-hypertension-in-adults
Roe, D. M. (2015). Cardiac emergencies. In B. A. Tscheschlog & A. Jauch (Eds.), Emergency nursing made incredibly easy! (2nd ed., pp. 97-197). Lippincott Williams & Wilkins.
Published: February 22, 2022
Last Updated: March 23, 2023
RSI, or Rapid sequence intubation, is the process where we intubate people in the hospital, pre-hospital, and emergency department settings when the patient is awake.
It involves multiple different steps that need to occur to quick succession, to provide first sedation, then paralysis, then insertion of the endotracheal tube into the trachea.
Learn all about RSI intubation, and specifically what the nurse’s role during an intubation is, and which compications and montioring parameters to watch out for!
So when does a person need intubed? Well, this really depends, but emergent intubations often involve severe respiratory distress.
Patients in acute respiratory failure will typically present with:
Increased respiratory rate > 20 rpm
SPO2 < 90%
Increased work of breathing characterized by use of accessory muscles
Presence of abnormal breath sounds including wheezing, crackles, rhonchi, or diminishment
May be present including tachycardia, hypertension, hypotension, fever, or altered mental status
Tripod position is when a patient is sitting over the bed leaning forward, supporting their upper body with their hands on the knees or another surface. This helps accessory muscles breath more easily, but can be an ominous sign to someone who is in respiratory distress. Think COPD!
Indications for Rapid Sequence intubation (RSI intubation) includes:
So what is YOUR responsibility as the nurse? Well don’t worry, you shouldn’t actually be the one to intubate the patient (although there are some exceptions such as NICU nurses and Flight nurses).
The person who placed the Endotracheal (ET) tube is usually a paramedic, physician, and sometimes an advanced practice provider (PA, NP, or CRNA). This is usually:
The nurse’s role is not to physically intubate, but nurses are essential in making sure the intubation goes safely and smoothly. They are also on the front lines to notice and intervene when things go wrong!
The nurse’s role is to prepare the patient and equipment, administer the medications, help manage the airway (although this is usually the job of respiratory therapists), and monitor the patient.
Afterwards, they are required to keep the patient sedated with titratable sedatives.
It is still important for nurses to understand how the RSI intubation process goes, even if they are not the ones placing the ET tube. It takes a team of nurses, respiratory therapists, physicians, and more to have a successful intubation without any complications.
Are there any alternatives to intubation? Yes and no.
There are certainly treatments we can try before jumping to intubation. These include nebulizers, certain IM/SQ meds, a non-rebreather, High-flow nasal cannula, and CPAP or BIPAP.
However, usually when intubation is decided on, it is when the patient is in impending respiratory arrest, or when the other treatments already aren’t enough.
RSI intubation is kind of our last saving measure that we can do to save their life and stabilize their respiratory system.
Before diving into the steps of RSI, we need to review the important medications that are given during RSI.
It is the nurses responsibility to draw these up, reconstitute them, and give them. Any medication that a nurse gives, they should know how the medication works, any side effects, and what to monitor for.
First we’re going to talk about sedatives. A sedative is a medication that acts as a CNS depressant – essentially putting the patient to sleep. Different sedatives work in different ways. Sometimes, it takes multiple different sedatives at the same time to effectively sedate a patient.
Sedatives are also called induction agents – inducing sedation in the patient. They also decrease the sympathetic response, making the body better tolerate the overall intubation experience.
In regards to RSI Intubation, SEDATIVES ARE ALWAYS GIVEN FIRST.
This is because you need to knock the patient out before you paralyze them, as this is a very frightening experience if not. It can also cause tachycardia, hypertension, and increased ICP if you don’t!
Etomidate is the most common sedative that will be ordered for RSI intubation.
Etomidate does not offer any analgesia, so sometimes fentanyl is added to minimize the SNS stimulation for patients with significant cardiovascular disease or increased ICP patients.
Etomidate does not really affect blood pressure, but it can cause some mild increase in airway resistance.
Etomidate can cause myoclonus to occur, which is brief and harmless, but can be mistaken for a seizure.
Etomidate can cause adrenal suppression for 12-24 hours after the injection. This could potentially impact hemodynamic stability (blood pressure), mainly in patients who are at risk such as those with pre-existing adrenal insufficiency or severe sepsis.
Patients with severe sepsis who are intubated with etomidate and become hypotensive despite fluids and a vasopressor should be given a 1x dose of hydrocortisone 100mg IV.
Etomidate doesn’t cause HF, but patients with pre-existing HF may have exacerbated underlying myocardial dysfunction after administration.
Increased respiratory rate > 20 rpm
Versed, also called Midazolam, is the most commonly used Benzodiazepine used for sedation for RSI intubation.
Versed also does not cause analgesia, but is a good choice for patients in status epilepticus because it offers anticonvulsant properties.
However, it can decrease the blood pressure, so this should be avoided in patients who are hemodynamically unstable.
Versed can cause a decrease in Mean Arterial Pressure (MAP) by 10-25%. This means Versed should generally be avoided in hypotensive patients or those at risk for hypotension (severe sepsis, trauma, etc).
Ketamine is a newer sedative used for RSI intubation. It’s structurally similar to PCP, and can cause some interesting side effects. However, it can be a great sedative and analgesic to help with rapid sequence intubation.
The good thing about Ketamine is it preserves the respiratory drive. This makes it excellent choice for minor procedural sedation where intubation is not needed.
However, the increased catecholamine stimulation can cause tachycardia, hypertension, and possibly increased ICP, making it a poor choice for head traumas and hypertensive crises, and also those with cardiac ischemia or aortic dissections.
However, this can be helpful in patients who are hypotensive to increase BP or in severe asthmatics to cause bronchodilation (in theory).
Ketamine increases the risk of laryngospasm, especially in those with history of upper respiratory disease or asthma. This is because ketamine does not suppress pharyngeal and laryngeal reflexes. In this case, it can be helpful to use fentanyl with it
Ketofol is the combination of ketamine and fentanyl. This can cause analgesia, sedation, and amnesia, and can be a good choice for patients with severe bronchospasm.
Ketamine causes increased stimulation of the sympathetic nervous system, releasing catecholamines leading to tachycardia, hypertension, increased myocardial demand, and even possible cardiac arrhythmias.
This can be beneficial in patients who are hypotensive, but dangerous for those with active cardiac disease or aortic dissection.
Ketamine can cause an “emergence phenomenon” primarily when used for procedural sedation. This is when the patient may experience vivid and/or disturbing dreams as they wake up. Hallucinations and frank delirium may occur postoperatively up to 24 hours.
This usually does not happen with patients who are intubated and sedated for over 24 hours.
Propofol is a common sedative, and a frequent agent of choice for maintaining sedation with a slow titratable drip. It has a characteristic appearance of milk.
Propofol is the drug that Michael Jackson was found to have overdosed on. It causes deep sedation and does diminish the patients respiratory drive.
Propofol has the following actions on the body:
Make sure your specific state and facility allow RNs to give IV boluses of propofol, and if so, make sure the provider is always at the bedside. Since propofol causes deep sedation, it may not be within your scope as a nurse to push it. Seems silly, but always protect your license!
Propofol has a blood pressure lowering effect, which can decrease the MAP by 10%, but sometimes even ≥ 30%.
Use caution if the patient has a borderline low pressure or baseline MAP of 60-70 mmHg.
Patients at risk for hypotension include severe sepsis, trauma, severe aortic stenosis, etc.
Propofol can cause bradyarrythmias to occur. This is more common with high doses, prolonged duration, and concurrent medications like beta-blockers, paralytics, and opioids. Patients with a history of cardiac disease are at increased risk.
QT prolongation can predispose your patient to dangerous ventricular arrhythmias like Torsades de Pointes and VFIB. This is more common with:
Anaphylaxis is rare with Propofol but can occur, usually within 5-10 minutes after infusion. Those with a history of soybean or egg allergy are probably fine to take it.
Allergy to soybeans or egg used to be a contraindication for receiving propofol, but newer formulations of the drug rarely produce a reaction and are likely safe
Propofol is a lipophilic fatty solution which contains triglycerides. Infusion can lead to elevations in triglycerides and lipase, which usually occurs 2-4 days after initiation. This can lead to pancreatitis, especially in those who are already at risk.
PRIS stands for Propofol Infusion Syndrome. PRIS is rare but deadly. When occurs, the patient suffers from acute refractory bradycardia which may lead to asystole, and also may have:
This is more common with high doses (>4mg/kg/hr) and long duration of use (>48 hours).
There are some specific scenarios where one sedative may be more appropriate than others. Regardless, it is always the Providers preference and what they’re familiar with.
Propofol or Etomidate
Propofol or Ketamine (+/- fentanyl)
Etomidate +/- Fentanyl
Etomidate 0.15mg/kg or ketamine 1mg/kg
Paralytics, also called neuromuscular blocking agents (NMBAs), are given immediately after the sedative kicks in, which produces a paralyzing effect on the body. This relaxes the patients muscles and makes the intubation easier for the Physician or APP, and minimizes complications.
Succinylcholine or Sux for short, is the classic paralyzing agent for RSI. It is termed a “depolarizing neuromuscular blocker” because they cause the muscle cells to “fire” or depolarize, but then don’t let the muscles repolarize, leading to paralysis.
While used in most scenarios, this is contraindicated in conditions which may cause hyperkalemia or may lead to an exaggerated response. This is because even in normal patients, Sux can increase potassium levels by 0.5-1.0 mEq/L.
These conditions include:
Patients with MG are resistant to Sux, so should be given 2mg/kg
Sux commonly causes fasciculations of the muscles prior to causing full paralysis.
This may increase ICP and stimulate emesis leading to aspiration.
A metabolite of Sux can stimulate muscarinic receptors to release acetylcholine, producing bradycardia of the sinus node. This can be treated with atropine.
Rocuronium or “ROC” for short is a “non-depolarizing” NMBA used for sedation for RSI intubation. This is because it is an acetylcholine antagonist, blocking its effects and leading to paralysis.
ROC is used when Sux is contraindicated as above.
Some conditions which may decrease the efficacy of the paralysis include:
ROC can increase peripheral vascular resistant and cause a temporary increase in BP. It can also cause transient hypotension in some people.
ROC can cause temporary tachycardia for about 5 minutes.
ROC may worsen pulmonary HTN, leading to right-sided heart failure in those who are predisposed.
Other non-depolarizing paralytics include Vecuronium and Pancuronium, but these are not used as often.
Vecuronium, shortened to “VEC”, is not used as frequently, as it has a longer onset of action – around 3 minutes. This can be reduced with a smaller “priming” dose.
To prepare the patient for RSI intubation, make sure they are positioned in the “sniffing” position, supine with their neck flexed. Placing a towel between their head and neck can help.
Make sure the patient is getting hyper-oxygenated at the same time, usually with a Non-rebreather or a Bag-valve mask at 100%.
Respiratory therapists are often in charge of airway along with the Provider.
Place the patient on the monitor including telemetry, continuous pulse ox, and end-tidal CO2 if possible.
Explain the procedure to the patient and ensure informed consent is obtained, either written or verbal. Written is often not able to be obtained due to the emergent nature of many intubations.
If the patient is altered, ensure there is no DNR or DNI order form or POLST.
If using a BVM hooked up to 100% oxygen, make sure you are squeezing the BVM with each spontaneous breath to ensure the valve opens and the oxygen is given to the patient!
Bring the code cart at the bedside. You don’t necessarily need to hook up the defibrillation pads, but always follow facility protocol.
Most of the equipment needed will be found in the Airway drawer, usually one fo the last drawers.
The equipment needed for the actual intubation will be:
Ask the Provider which size ET tube they’ll want, which is often 7.0 for females, and 8.0 for males.
The stylet will need to be placed inside the ET tube, which is usually cuffed. This will be removed once the Provider gets the tube in the right spot.
The Provider will give you a verbal order for which sedative(s) and paralytic they want.
Verbally clarify the name and dose, and begin to draw up the medications. You may need to grab these medications from an “RSI kit” in the Accudose, or they may be located in your code cart.
Usually one of the nurses will assume the “medicine” responsibility while the others are preparing the patient and equipment.
Some medications will require reconstitution. This means you may need to mix saline with powdered medication to make a solution. Verify the final doses/amounts with another nurse.
Make sure to accurately label each, so you don’t mix up the sedative and the paralytic!
Once everyone is ready for the intubation, wait for the Provider’s verbal “ok” to give the medications, and administer the medications as above. Most are given quickly over 5-10 seconds.
First the sedative, then once the patient has decreased LOC and you get the next verbal OK from the Provider, administer the paralytic.
RT should be bagging the patient at this time until the Provider is ready for the intubation. This is usually within 30-60 seconds after administering the paralytic.
Your main job is now done, and now you just watch the intubation procedure and monitor the patient, following any verbal orders that are given.
The Provider will place the ET tube between the vocal cords, typically 21cm deep in women and 23cm in men. This is measured at the teeth.
Immediately after intubation, the tube needs to be verified. This is verified in multiple ways.
First, a CO2 detector may be attached to the ET tube. Observing color change from purple to yellow indicates CO2.
If the patient is hooked up to an ETCO2, with each BVM breath, you should see normal CO2 levels near 35-45 mmHg.
Additionally, someone should listen to all breath sounds listening for equal breath sounds.
Lastly, the patient should have a portable CXR ordered to verify the placement. The radiologist may recommend pulling out or pushing deeper x amount of cm.
Now the patient is successfully intubated. Your main job now is keeping the patient sedated so that the Ventilator can do its job and breath for the patient.
This usually involves a continuous titratable drip, often propofol. The patient may also require additional sedatives, analgesics, and sometimes further paralytics.
Of course, make sure to chart everything and continue to monitor the patient’s vital signs.
If in the ER or Med-Surg, your goal should be to get that patient admitted/transferred ASAP.
Unfortunately, not all RSI intubations go smoothly. These are usually emergent procedures and are not done in a controlled environment.
As the nurse, you are the first one who is going to notice any complications while monitoring your patient. It’s important to know what to look out for and how these complications are managed.
This is when the ET tube is in the esophagus instead of the trachea. This becomes obvious when verifying placement.
When it occurs, the ET tube will be completely removed and the Provider will re-insert the tube with another attempt.
An OG or NG to suction should be placed in all patients after intubation to decompress the stomach to prevent emesis and to decrease intrathoracic pressure.
A foley should also be placed.
If the ET tube is placed slightly too deep, it will often go into the Right Mainstem Bronchus of the right lung. This is because it is more vertical than the left.
If left, the patient may have signs of hypoxemia and worsening respiratory status, and if not fixed can cause barotrauma, pneumothorax, and hemothorax.
Breath sounds should be equal throughout the lobes, but a CXR will need to be done to verify this isn’t the case.
Treatment involves pulling out the ET tube per radiologists recommendations, which the Provider should do.
A traumatic insertion can cause perforation of the esophagus or trachea. This is very rare, but severe.
Signs include presence of subcutaneous emphysema in the mediastinum, and worsening respiratory status.
A CXR may show pneumomediastinum, subcutaneous emphysema, and possible pneumothorax.