Sepsis and Severe Infections: A Primer for Nurses

Sepsis and Severe Infections: A Primer for Nurses

Published: December 19, 2022

Last Updated: December 28, 2022

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 This is somewhat outdated and no longer used, but you still may often hear about this in your hospital.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.


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 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 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


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


  • 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


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


  • 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. 


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


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


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.


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


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 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


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


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. 


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 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 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 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)


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.


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


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


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. 


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


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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How to care for DKA: An Expert Nurse’s Guide to Diabetic Ketoacidosis

How to Care for DKA

An expert nurse’s guide to Diabetic ketoacidosis

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

What is Diabetic Ketoacidosis (DKA)?

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. 

What causes dka?

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 (O2) to carbon Dioxide (CO2)

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.

What is the “Anion Gap”?

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). 

What about Potassium?

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.

DKA vs Hyperglycemic Hyperosmolar State (HHS)

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.

Nursing Assessment

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:

New Onset Type 1 DM

Patients who don’t know they are a type 1 diabetic yet

Noncompliance with insulin therapy

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:

Nausea or vomiting

May be from delayed gastric emptying and ileus (where a section of the intestinal wall does not perform peristalsis as normal)

Abdominal Pain

Common in DKA, but almost never happens with HHS

Polyuria & Polydipsia

Increased urinating is due to the osmotic diuresis described above, and the increased thirst is due to the hyperosmolality of the blood

Weight Loss

This is due to water losses, as well as fat losses from the massive lipolysis that occurs

Altered Mental Status

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.

The Physical Exam


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.

Your Other Senses?

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…

Vital Signs

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

Nursing intervention

Cardiac Monitoring

Patients in DKA are prone to severe electrolyte abnormalities such as hypokalemia, which can cause deadly cardiac arrhythmias to occur

Blood Glucose

Glucose monitors will often read “HI” if above 600 g/dL. However, even “euglycemic” DKA has occurred with near-normal glucose levels.

Place IV

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.

Draw Labs

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.

Hang Fluids

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 WOrkup & Diagnosis

DKA is diagnosed based on lab work alone. The presence of a high anion gap PLUS a high sugar usually means DKA.

Blood Glucose

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

Anion Gap

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.

Plasma osmolality

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

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

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.

Other Labs

Amylase and lipase may be ordered if pancreatitis is suspected, and lipids may also be ordered (but usually with morning labs).

DKA Treatment

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:

IV Isotonic fluids

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.

IV Insulin Drip

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.

IV Potassium

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!

IV Potassium Rate

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.

More IV Fluids

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!

Patient Monitoring

Patients with DKA are at high risk for complications, so they should be monitored closely, especially while in the ICU. 

Blood Glucose

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.

Serum Potassium

As discussed above, this should be monitored frequently.

A BMP is usually checked every 2-4 hours while on an insulin drip.

Cardiac Monitor / EKG

Monitor for tachycardia, ectopy, or any arrhythmias.

Severe hypokalemia and acidosis can lead to fatal arrhythmias like VFIB, Asystole, and PEA.

Blood Pressure

Significant acidosis and hypovolemia can cause hypotension.

When the body is acidotic, medications like vasopressors don’t work as well as they should.

Anion Gap

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.

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.

Hirsch, I. B., & Emmett, M. (2022). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis. In T. W. Post (Ed.), Uptodate.

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.

The Ultimate ABGs Blood Gas Guide you Need to Calm Your Nerves

The Ultimate ABGs Blood Gas Guide you Need to Calm Your Nerves

Published: June 14, 2022

Last Updated: December 24, 2022

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

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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.

Featured Image for ABGs blood gas interpretation guide for nurses

What Are ABGs or a Blood Gas?

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 Levels: This measures PaO2 as well as SaO2
  • Carbon Dioxide levels: PaCO2 levels
  • pH: the acidity of the blood
  • Bicarbonate: The amount of bicarb, which is a buffer

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.

When are ABGs ordered?

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:

Things to keep in Mind with ABGs

There are some important factors to keep in mind when thinking about ABGs and interpreting them.

Things Aren't Always Simple

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.

Underlying Cause

Always focus on treating the underlying cause.

THE ABGs: Blood Gas Measurements

Okay, so lets dive a little deeper into what each measurement is on the ABG results, and what their levels mean.

The pH

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. 

  • Normal pH of blood: 7.35-7.45
  • Low pH (<7.35): Indicates acidosis, and is termed acidemia
  • High pH (>7.45): Indicates alkalosis (metabolic or respiratory), and is termed alkalemia

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

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.

  • Normal: 35-45 mmHg
  • Elevated: >45 mmHg, termed hypercapnia
  • Decreased: <35 mmHg, termed hypocapnia

My Blood is BOILING

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!

The HCO3 (Bicarb)

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.

  • Normal: Between 22-26 mEq/L
  • Elevated: >26 mEq/L, associated with metabolic alkalosis
  • Decreased: <22 mEq/L (associated with metabolic acidosis)

The PaO2

PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen blood gas content.

  • Normal: > 80 mmHg
  • Elevated: > 100 mmHg, usually due to over-oxygenation
  • Decreased: <80 mmHg, associated with respiratory failure, although could be from severe anemia as well

Oxygen Toxicity

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

The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.

  • Normal: Above 94-96%
  • Decreased: <90-92%


When interpreting ABGs and blood gases, there are 4 general categories we use:

  • Respiratory Acidosis
  • Respiratory Alkalosis
  • Metabolic Acidosis
  • Metabolic Alkalosis

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

Acute respiratory acidosis could be from multiple different reasons including:

  • Respiratory Failure & Airway Obstruction: Severe asthma, COPD, CHF
  • CNS disease: Stroke, Traumatic brain injury
  • Drug-induced: Opioid or benzodiazepine overdose
  • Neuromuscular Disease: Myasthenia Gravis, ALS, Guillan Barre

Chronic Respiratory Acidosis

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.

  • COPD with Chronic CO2 retention
  • Obesity-hypoventilation Syndrome: Also called Pickwickian syndrome
  • Others: ALS, Interstitial fibrosis, thoracic skeletal deformities

COPD & Oxygen

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:

Ventilated Patients

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)

Early-Intermediate Lung Disease

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

Numbness & Tingling with Hyperventilation

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. 

Metabolic Acidosis

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.

Normal Gap Metabolic Acidosis

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.

Chronic Renal Failure

Typically when GFR is between 20-50ml/min

Renal Tubular Acidosis

In RTA, the kidneys do not remove acid from the blood like they should

Large-Volume Fluid Replacement

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.

Elevated Gap Metabolic Acidosis

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:

    Diabetic Ketoacidosis

    DKA causes a massive increase of ketone bodies which are acidic, in addition to severe dehydration

    Lactic Acidosis

    Lactic acidosis, especially in setting of sepsis, can cause metabolic acidosis

    Acute Kidney Injury

    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

    Ingestion of certain Poisons

    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:

    Excessive Vomiting

    Gastric secretion has a high content of hydrogen ions, so excessive vomiting can reduce overall acidity within the body

    NG Tube

    Over time, NG tubes remove a lot of gastric fluid, similar to excessive vomiting, this can cause a decrease in hydrogen ions

    Alkalotic overdose

    Rare, but if you consume massive amounts of milk products or antacids this can cause metabolic alkalosis

    Renal Losses

    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!

    Determine the pH

    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.

    PCO2 + HCO3 Abnormalities

    See which levels are abnormal. Are they leaning acidic or alkalotic?  

    Correlate with pH

    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.

    Determine Compensation

    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. 

    Check the Anion Gap

    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.

    Emmett, M., & Szerlip, H. (2022). Causes of metabolic alkalosis. In T. W. Post (Ed.), Uptodate.

    Hopkins, E., Sanvictores, T., & Sharma, S. (2020, September 14). Physiology, Acid Base Balance. National Library of Medicine.

    Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian J Crit Care Med, 14(2), 57-64.

    Theodore, A. C. (2022). Arterial blood gases. In Uptodate.

    AFIB RVR on EKG: Management of Atrial Fibrillation


    Management of Atrial fibrillation

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    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!

    AFIB RVR Atrial Fibrillation Featured Image-min

    What is Atrial Fibrillation (AFIB)?

    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.

    Cardiac Conduction Review

    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.

    Cardiac Conduction System: AFIB RVRThe 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.

    What is AFIB RVR?

    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!).

    What causes AFIB?

    AFIB usually occurs in predisposed hearts and is often set off by reversible triggers.

    Chronic diseases which predispose the heart to AFIB include:

    Atrial Enlargement

    Anything causing atrial enlargement such as CHF, Cardiomyopathy, COPD, OSA, obesity

    Valvular Heart Disease

    Rheumatic Fever, aortic stenosis, valve repelacements, etc

    Ischemic Heart Disease

    Coronary artery disease, past or current myocardial infarctions (heart attacks!)

    Usually, some reversible trigger throws the patient into AFIB. These reversible triggers include:

    Surgical Procedures

    CABG or heart transplants, usually within the first 2 weeks postop

    Pulmonary Emblolisms

    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.

    Nursing Assessment of AFIB RVR

    Symptoms of AFIB

    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 Pain

    Chest pressure, pain, or discomfort


    Loss of consciousness

    The Physical Exam


    • Pallor or flushed
    • Diaphoresis
      • May appear tachypneic

      Vital Signs

      • BP: May be low at fast rates and with poor cardiac output
      • Pulse/HR: Often >100 (RVR)
      • Respirations: Normal or increased
      • SPO2: Usually normal


      • Lungs
        • Usually Normal
        • May have crackles if CHF
      • Heart
        • Rapid and irregular rate

      Identifying AFIB RVR on the ECG

      Atrial fibrillation (AFIB RVR)

      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.

      AFIB: Atrial Fibrillation Notes

      Initial Nursing Interventions

      STAT EKG

      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.

      Cardiac Monitoring

      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.

      Oxygen Support

      If the patient is significantly hypoxic or tachypneic, apply 2-4 L/min NC to maintain SPO2 >90%.

      IV Access

      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.

      Unstable Tachyarrhythmia

      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.

      Workup for AFIB RVR

      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:

      12-lead ECG

      AFIB can be diagnosed with this, as well as to look for any other abnormalities such as a STEMI

      Basic Labs

      CBC, CMP, and magnesium will often be checked

      Additional Labs

      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

      CT head

      If any altered mental status or stroke-like s/s

      Complications of AFIB

      So why do we even care about AFIB? Well, there can be disastrous consequences if we do not treat it appropriately.

      Unstable Symptoms

      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.

      Worsened CHF

      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!

      Blood Clots

      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 RVR

      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:

      • Rate control: Control the heart rate with AFIB (preventing RVR)
      • Rhythm Control: Convert and maintain the patient in a normal sinus rhythm
      • Anticoagulation: Giving blood thinners to prevent blood clot formation within the atria

      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

      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:

      IV Diltiazem

      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.

      IV Metoprolol

      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.

      Low BP & RVR

      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

      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.

      Chemical Cardioversion

      IV amiodarone can be used, or the cardiologist may choose to start an oral antiarrhythmic such as Amiodarone, Sotalol, Dofetilide, etc

      Electrical Cardioversion

      Unstable patients should undergo synchronized cardioversion with the defibrillator

      Radiofrequency Ablation

      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:

      Heparin Drip

      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

      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.

      Clinical Pearls

      Patient Specific

      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!

      AFIB RVR

      Focus on rate control and anticoagulation! Become familiar with IV Cardizem and titrating a Cardizem drip, as well as IV Lopressor!

      Unstable = Shock

      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).

      Want to learn more?

      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:

      • 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!


      Burns, E. (2021). Atrial Fibrillation. In ECG Library. Retrieved from

      Kumar, K. (2022). Overview of atrial fibrillation. In T. W. Post (Ed.), UpToDate. Retrieved from

      Olshansky, B. (2022). The electrocardiogram in atrial fibrillation. In T. W. Post (Ed.), UpToDate. Retrieved from

      Phang, R., Prutkin, J. M., Ganz, L. I. (2022). Overview of atrial flutter. In T. W. Post (Ed.), UpToDate. Retrieved from

      Prutkins, J. M. (2022). Electrocardiographic and electrophysiologic features of atrial flutter. In T. W. Post (Ed.), UpToDate. Retrieved from

      RSI Intubation for Nurses: Rapid Sequence Intubation

      RSI Intubation for nurses

      Rapid Sequence Intubation

      William Kelly, MSN, FNP-C

      Author | Nurse Practitioner

      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!

      RSI intubation: rapid sequence intubation for nurses Featured Image

      Indications for RSI Intubation?

      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 WOB

        Increased work of breathing characterized by use of accessory muscles

        Adventitious Breath Sounds

        Presence of abnormal breath sounds including wheezing, crackles, rhonchi, or diminishment

        Other Abnormal Vital signs

        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:

        • Acute Respiratory Failure (from pneumonia, COPD, CHF, Covid, etc)
        • Anaphylactic reaction or Angioedema
        • When the patient cannot protect their airway (severe alcohol intoxication, drugs, etc.)
        • For surgery

        The Nurses Role during RSI

        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:

        • EM Physician but sometimes APP
        • IM Physician
        • Anesthesia

        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.

        Alternatives to RSI intubation

        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. 

        RSI Medications

        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.

        Side Effects & Monitoring


        Etomidate can cause myoclonus to occur, which is brief and harmless, but can be mistaken for a seizure.

        Adrenal Suppression

        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.

        Heart Failure Exacerbation

        Etomidate doesn’t cause HF, but patients with pre-existing HF may have exacerbated underlying myocardial dysfunction after administration.


        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.

        Side Effects & Monitoring


        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). 

        Side Effects & Monitoring


        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.

        Increased Cardiac Activity

        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.

        Emergence Reactions

        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:

        • Decreases airway resistance: Good for bronchospasm
        • Neuro-Inhibition: Good for intracranial pathology
        • Suppresses SNS: Good for hypertension, bad for hypotension & conditions which decrease cerebral perfusion

        Propofol IV Push?

        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!

        Side Effects & Monitoring


        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

        QT prolongation can predispose your patient to dangerous ventricular arrhythmias like Torsades de Pointes and VFIB. This is more common with:

        • High propofol doses
        • Elderly patients
        • Structural heart disease
        • Congenital Long QT
        • QT prolonging medications
        • Electrolyte Disturbances


        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.

        Soybean Allergy

        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

        Elevated Triglycerides & Lipase

        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:

        • severe metabolic acidosis,
        • cardiovascular collapse,
        • rhabdomyolysis
        • hyperlipidemia
        • renal failure
        • hepatomegaly

        This is more common with high doses (>4mg/kg/hr) and long duration of use (>48 hours).

        Choosing the Right Sedative

        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. 

        Head Injury or Stroke


        Status Epilepticus

        Propofol or Etomidate

        Severe Bronchospasm

        Propofol or Ketamine (+/- fentanyl)

        Cardiovascular Disease

        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:

        • Malignant hyperthermia (personal or family history)
        • Neuromuscular disease with denervation (i.e. MS)
        • Muscular dystrophy
        • Stroke > 72h old (especially with significant motor denervation)
        • Rhabdho
        • Significant burn(s) over 72h old
        • Significant Hyperkalemia

        Myesthenia Gravis

        Patients with MG are resistant to Sux, so should be given 2mg/kg

        Side Effects & Monitoring


        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:

        • Respiratory alkalosis
        • Hypercalcemia
        • Demyelinating lesions (MS)
        • Peripheral neuropathies
        • Muscle trauma

        Side Effects & Monitoring


        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.

        Right-sided HF

        ROC may worsen pulmonary HTN, leading to right-sided heart failure in those who are predisposed.

        Other Paralytics

        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.


        Prepare the Patient

        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. 

        Using a BVM

        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!

        Prepare the Equipment

        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:

        • Laryngoscope
        • ET tube
        • Stylet
        • 10cc syringe
        • Suction Tubing & Yankauer
        • ETCO2 or CO2 detector
        • Stethoscope
        • Bag-valve mask

        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.

        Administer Medications

        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.

        The Intubation

        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.

        Verify Placement

        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.

        Maintain Vent + Sedation

        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.

        RSI Intubation Complications

        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.

        Esophageal Intubation

        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.

        Gastric Tube

        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.

        Right Mainstem Intubation

        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.

        Pulmonary Embolism: Nurse’s Reference Guide

        Pulmonary embolism


        William Kelly, MSN, FNP-C

        Author | Nurse Practitioner

        A pulmonary embolism, frequently abbreviated as a PE, is a blood clot that lodges into the pulmonary vasculature of the lungs. Sometimes this can be asymptomatic, often there are mild-moderate symptoms, and other times patients can go into cardiac or respiratory arrest.

        No matter the symptoms, pulmonary embolisms can be deadly, and it is important for nurses to understand this disease and how to treat and monitor your patients with pulmonary embolisms.

        This article is part of a new series where we outline various medical conditions and the nursing assessment and management involved with each condition.

        What is a Pulmonary Embolism?

        A pulmonary embolism is a blood clot that lodges within the lungs. These are more commonly abbreviated to PEs. These can be very large or very small; only one, or many at the same time.

        The larger and more PEs that there are, the more dangerous this can be on the body. This can put significant strain on the heart, and can even cause cardiac arrest.

        Remember that a Thombus is one of the Hs and Ts to think about when a patient is coding!

        Pulmonary embolism‘s are highly associated with Deep Vein Thrombosis (DVT). You might hear the term VTE, which is an umbrella term for any blood clot within the body including DVTs and PEs.

        Pulmonary Embolism

        Causes of a PE

        There are many different causes that can cause a PE to develop, but it all goes back to Virchow’s Triad.

        Virchow’s Triad

        Virchow states that in order for blood clots to form within the body, there needs to be at least one of three things:

        Stasis of Blood

        Anything that causes blood to “sit still”

        Endothelial Injury

        Damage to the vascular system (arteries & veins)

        Hypercoagulable State

        Something that increases likelihood for clotting

        The more they have – the higher their risk of a blood clot from forming. However, a small percentage of patients won’t have any of these risk factors and still get a blood clot.

        Breaking down Virchow’s Triad, common risk factors for blood clot formation includes:

        Stasis of Blood

        • Immobility
        • Hospitalization
        • Varicose Veins
        • Atrial Fibrillation
        • Heart Failure
        • Elderly Age (>65)

        Endothelial Injury

        • Recent Surgery (especially orthopedic surgeries)
        • Trauma
        • Chemotherapies
        • Implanted devices
        • Central Lines
        • Inflammation
        • Sepsis

        Hypercoagulable State

        • Malignancy
        • Estrogen use (i.e. birth control)
        • Pregnancy
        • Inherited genetic predisposition (i.e. Factor V Leidin mutation)
        • Severe liver disease
        • Smoking
        • Obesity
        Pulmonary Embolism

        Nursing Assessment

        Patients with pulmonary embolisms usually present to the hospital or emergency department with shortness of breath.

        This is because an area of their lungs are not able to exchange gas normally. They are able to breathe in adequate oxygen, however they are unable to exchange that oxygen with carbon dioxide wherever the PE is, leading to a ventilation perfusion mismatch.

        Symptoms of a PE

        Common symptoms of a PE include:


        Also referred to as shortness of breath, and may be with exertion or at rest

        Chest Pain

        Usually pleuritic, aka worse with deep breaths or coughing


        Usually not productive, but may have pinky frothy or bloody sputum


        Syncope with chest pain and SOB is suspicious for PE

        Signs of DVT

        • Extremity Erythema
        • Extremity Edema
        • Extremity Pain
        Many patients may be asymptomatic or have mild nonspecific symptoms as well, or they could go right into cardiac arrest, especially with very large PEs.

        Quick Note

        Hemoptysis is not nearly as common of a symptom in a PE as your nursing textbook may have led you to think!

        The Physical Exam


        • Respiratory Distress
          • Tachypnea
          • Increased work of breathing
          • Use of accessory muscles
        • Cough
        • Pallor
        • Diaphoresis

        Vital Signs

        • Temp: May have low grade temps
        • BP: Normal, increased, or decreased (severe)
        • Pulse/HR: Tachycardic
        • Respirations: Increased
        • SPO2: May be normal or low


        • Lungs
          • Usually Normal
          • May be diminished
          • May have crackles if pulmonary infarct or acute CHF
          • Pleural friction rub
        • Heart
          • Tachycardia

        Quick Tip

        If a patient has CP/SOB and just recently had surgery or is pregnant, always think PE!

        The first thing you’ll usually notice is an increased rate of respirations, also called tachypnea. Patients with PEs are often in some visible respiratory distress.

        Patients with PEs often have pleuritic chest pain as well, so they’re unable to take full breaths without significant pain. This can increase the respiratory rate as they compensate by taking more frequent, shallow breaths.

        Patient’s pulse ox will often be normal unless there is significant respiratory distress. Patients may have a low-grade fever as well.

        Patience with PEs will often have tachycardia – which is a heart rate greater than 100 bpm.

        Blood pressure is often normal, but may be high secondary to pain. However very large PEs can put significant strain on the heart, causing significant hemodynamic compromise including hypotension and shock.

        When auscultating the lungs, a lot of times you aren’t really going to hear any specific bad breath sounds. You may hear some diminishment in the lung with the PE. Sometimes you may hear crackles and rarely wheezing.

        Nursing Interventions

        Cardiac Monitoring

        Place all patients with chest pain or SOB on a cardiac monitor to detect any arrhythmia that may occur and monitor heart rate.

        Patients with PEs will often have sinus tachycardia that does not completely improve with fluid administration.

        Patients with PEs can have all sorts of arrhythmias including:

        • Atrial fibrillation
        • bradycardia
        • RBBB
        • PVCs
        • VTACH/VFIB

        STAT EKG

        All patients presenting with chest pain and/or SOB should have an EKG obtained within 10 minutes of arrival.

        This is primarily to rule out any STEMI or ischemia. However, large PEs can cause significant righ theart strain.

        While they occur in < 10% of patients, signs of right heart strain on an EKG include:

        • Right heart strain pattern
        • S1Q3T3
        S1Q3T3 teaser

        Oxygen Support

        If the patient is significantly hypoxic or tachypneic, apply 2-4 L/min NC. If this is not enough to titrate SPO2 > 90%, apply a non-rebreather.

        In these cases, BIPAP or Intubation may be needed.

        IV Access

        Start a peripheral IV at least 18-20g in an AC line, as there is a high likelihood that these patients will be needing a CTA. These large bore IVs are needed to inject high-pressure dye.

        While drawing blood, make sure to draw a blue top as D-dimer may be ordered, as well as a PT/INR.

        Diagnosis of a PE

        To diagnose a PE, you will usually need advanced lung imaging, but lab work is part of the workup as well.

        Well's Criteria

        The Wells’ Criteria for PE is a clinical tool that is able to be used to determine the risk of a PE.

        This assigns points to each of the following:

        • Signs of DVT: 3 points
        • PE #1 likely dx: 3 points
        • HR > 100 bpm: 1.5 points
        • Immobiilization x 3 days: 1.5 points
        • Surgery within 4 weeks: 1.5 points
        • Previous PE/DVT dx: 1.5 pnts
        • Hemoptysis: 1 point
        • Malignancy w/ tx in last 6mo or palliative: 1 point

        Once you calculate their score, you can stratify their risk into one of the following:

        • Low risk: 0-1 point
        • Moderate: 2-6 points
        • High risk: >6 points

        Scores of 4 or less with a negative D-dimer can effectively rule out a PE.


        Blue Top blood work - DdimerOne way to minimize radiation is to obtain a D-Dimer in a patient with low to moderate suspicion of a PE.

        A D-dimer is a byproduct of fibrin which is increased in the blood whenever there is a blood clot.

        While this is a great test to see if there is a possibility of blood clots within the body, it is not very specific. This means that a negative D dimer (less than the threshold) is a pretty good way to tell if someone doesn’t have a blood clot. However, a positive D-dimer doesn’t necessarily mean there IS a blood clot in the body.

        Any bruise or minor injury can cause elevations in D-dimer, as well as pregnancy, heart disease, infections, and more.

        This means that if a D-dimer is above the threshold (around 230 but depends on your lab), then the Provider is pretty much forced to get a CTA to see if their truly is a PE.

        If a D-dimer is less than the threshold, then a PE can usually be ruled out. However, this is only the case is clinical suspicion is low to moderate.

        In patients who have a high liklihood of a PE, a D-dimer can miss a PE up to 15% of the time!

        Other Lab Work

        A troponin should be ordered in patients with chest pain and/or SOB. This can sometimes be mildly elevated in PEs, or significantly elevated if a PE causes a STEMI or NSTEMI.

        A BNP may be ordered if there are s/s of heart failure.

        Renal function should be checked before a CTA can be done, to make sure their kidneys can handle the dye. A GFR > 30 is usually adequate to obtain a CTA.

        Coagulation studies may be performed inpatient to see if there are any genetic mutations predisposing the patient to forming thrombi.


        An ABG may be obtained if the patient is in significant respiratory distress or has altered mental status.

        With a PE causing significant distress, you’ll typically see the following results on an ABG:

        • PaO2: Low (<80 mmHG)
        • PCO2: Low (<35 mmHG)
        • pH: Alkalotic (> 7.45)
        • HCO3: May be low (<22 mEq)


        A chest x-ray (CXR) will almost always be ordered on patients who are suspected of having a PE, because these can rule out some other causes of chest pain and SOB such as a pneumothorax or pneumonia.

        However, a CXR is not going to pick up a pulmonary embolism. A CXR may show nonspecific signs including atelectasis or effusions, but often will be completely normal.

        In order to actually see the pulmonary embolism, a CT pulmonary angiography (CTPA or just CTA) is required.


        Angiography is when a radiopaque dye is injected into the patient’s vein in order to get a good look at the patient’s vasculature during a CT scan. This can be timed to look at specific areas of the heart.

        CT Pulmonary Angiography is when this is done to look at the pulmonary arteries and veins. This means the radiologist can directly visualize pulmonary embolisms.

        If the patient’s GFR is <30, we generally avoid contrast dye. However, this may be completely facility dependent.

        If a patient cannot be given the dye (GFR < 30 or anaphylactic reaction), the alternative test is to obtain a V/Q Scan.

        Pulmonary Embolism

        V/Q Scan

        A VQ scan is a nuclear medicine test where they use radioisotopes in conjunction with X-rays to see if there are any ventilation/perfusion mismatches. Well this is not as definitive as a CTA, it does give probabilities of their being a PE, such as a “very low probability”.

        Quick Note

        The patients CXR really should be a clear study, otherwise the VQ scan will be poor quality. So if the patient has significant consolidation or pleural effusions, the VQ scan is unlikely to be very sensitive to finding a PE.

        Treatment of PE

        Treatment of a patient with a PE who is hemodynamically stable will generally consist of admission to the hospital, parenteral anticoagulation, and then transition onto an oral anticoagulant.

        Patients who have significant hemodynamic compromise may require reperfusion therapy.

        Parenteral Anticoagulation

        Treatment for pulmonary embolisms primarily involve anticoagulation.

        In the hospital setting this is usually IV unfractionated heparin. This Heparin is given as a Heparin drip, which is titratable depending on PTT levels. Each facility should have their own heparin drip protocol.

        In general, a bolus dose is given IV (can push fast), and then a slow drip is started. The PTT levels are usually checked every 6 hours but will depend on the protocol.

        SQ Lovenox is an alternative to IV heparin, and is given in a dose of 1mg/kg BID.

        But how does anticoagulants really help if the blood clot is already there? The role of the anticoagulants are to prevent further clots from forming, as well as to stabilize the clot from moving. This can be especially helpful if there is a DVT or an atrial thrombus within the heart. These can embolize and cause further PEs or even strokes.

        Quick Note

        I’ve found that usually IV heparin is ordered because this is more easily titrated and can be stopped quicker in case there is any bleeding or procedure that need done while inpatient.

        Oral Anticoagulation

        Sometimes the patient can be started directly on an oral anticoagulant and discharged home if they are otherwise stable, but this will depend on the Provider and the facility standards.

        Eliquis for PEOnce the patient is stable enough for discharge, they are started on long-term oral anticoagulation, such as Eliquis or coumadin.

        Patients with very recent surgery, hemorrhagic stroke, or active bleeding are not started on anticoagulation.

        Patients will often need to stay on the anticoagulation for at least 3 months, but sometimes longer. The blood clot should be reabsorbed by the body in about 6 weeks, but will depend on the size of the thrombus.

        Some patients will require life-time anticoagulation if they are found to have any genetic predispositions to blood clots. This is also true for patients with atrial fibrillation.

        IVC Filter

        IVC Filter for PEAn inferior vena cava filter, commonly referred to as an IVC filter, is a device that is sometimes placed to “catch” clots before they enter the right atria.

        This is usually placed in for patients who cannot be on anticoagulation, or those who have gotten repeat PEs despite anticoagulation therapy.

        They can be temporary and need removed eventually, but some that are placed are permanent.


        In patients who are hemodynamically unstable from their PE, thrombolytic therapy can be given to dissolve the clot. This is like TPA in a stroke, but given for a PE.

        However, there are many contraindications to thrombolytic therapy, and there is a risk of bleeding.

        Procedural Removal

        An Embolectomy can be performed if needed and if the facility is capable of doing so, particularly when thrombolytic therapy is unsuccessful or cannot be used due to contraindications.

        There are additional procedures that can be done to retrieve / break up the clot including:

        • Ultrasound-assisted thrombolysis
        • Rheolytic embolectomy
        • Rotational embolectomy
        • Suction embolectomy
        • Thrombus fragmentation
        • Surgical embolectomy

        Many facilities will not have these capabilities, but most should have thrombolytics.

        Saddle PE

        A Saddle pulmonary embolus is a very large PE located at the bifurcation of the main pulmonary artery. These PEs are rare but likely to cause significant hemodynamic compromise and cardiopulmonary respiratory arrest!

        Patient monitoring

        Monitoring the patient will mainly consist of monitoring their vital signs and supporting them however you can.

        Oxygen Support

        Monitor their oxygen status by respirations and pulse oximetry. Stable patients may only need q4h vitals.

        oxygen delivery devices and flow rates - simple maskIf their oxygen is low or if there is significant respiratory distress, titrate up their oxygen levels.

        A BIPAP or Intubation may be needed in severe cases.

        Blood Pressure Support

        Monitor their blood pressure per department protocol.

        If hypertensive, treat with analgesics and antihypertensives.

        If hypotensive, treat with fluid boluses, paying careful attention to respiratory and cardiac status. 

        Vasopressors may be required in severe cases.

        Cardiac Monitoring

        These patients should have telemetry ordered. 

        Monitor their cardiac rhythm per department protocol, and notify any changes to the Provider.

        Bleeding / Falls

        These patients are usually placed on anticoagulation as above. Be sure to place the patient on fall precautions, and monitor for any bleeding.

        Titrate the heparin drip according to protocol, and a high PTT may require that you stop the heparin drip for some time.

        Clinical Deterioration

        If the patient begins to deteriorate, be sure to notify the physician or APP and/or call an RRT.

        Remember that PEs put strain on the heart, so patients can go into flash pulmonary edema. Those with pre-existing CAD may have heart attacks.

        Overall Pulmonary Embolisms are a serious medical condition that can be deadly, so it is important to know how to treat these patients at the bedside.

        Do you have any crazy PE stories? Let us know in the comments below!


        Haag, A., et al (2022). Pulmonary embolism. In R. I. Donaldson (Ed.), WikEM, The Global Emergency Medicine Wiki

        Sharma, R. (2022). Pulmonary embolism | Radiology reference article. Retrieved February 8, 2022, from

        Tapson, V. F., & Weinberg, A. S. (2022). Treatment, prognosis, and follow-up of acute pulmonary embolism in adults. In T. W. Post (Ed.), Uptodate

        Thompson, B. T., Kabrhel, C., & Pena, C. (2022). Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In T. W. Post (Ed.), Uptodate

        Thompson, B. T., & Kabrhel, C. (2022). Overview of acute pulmonary embolism in adults. In T. W. Post (Ed.), Uptodate

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