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


    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!


    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

    Blood Pressure Crash Course for nurses

    Blood Pressure

    Crash course for nurses

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    Blood pressure is one of the 5 vital signs, and it is so important to understand what normal and abnormal blood pressures are, and how we manage them (don’t get me started on the “6th” vital sign…).

    Within the hospital, vital signs are typically checked every 4 hours, and you will frequently run into both high and low blood pressures.

    Low blood pressure is often much more worrisome, and you may want to call an RRT if the BP is significantly low, especially when the patient is altered or has significant symptoms.

    High blood pressure is common, but often is not considered a big deal unless VERY high. In these cases, we want to slowly decrease the blood pressure instead of too quickly.

    What is Blood Pressure?

    As you probably know, blood pressure is not the pressure of your blood, but rather the pressure within your vascular system.

    The vascular system refers to your arteries and veins. When speaking of systemic blood pressure, we are specifically talking about the pressure in the arteries. 

    This pressure temporarily increases with each heartbeat, and decreases in-between each heartbeat. 

    The pressure in your arteries when your heart beats or contracts is called the systolic blood pressure. Systolic just means during the heartbeat. Systolic blood pressure can never be below the diastolic pressure.

    When the heart is not beating, the pressure “rests” back to its normal baseline pressure. This is called the diastolic blood pressure. The diastolic blood pressure should never be 0. 

    This pressure is measured in millimeters of mercury (mmHg).

    “Normal” Blood Pressure

    As we said above, systolic is the pressure during contraction of the heart, and diastolic is the pressure in-between beats. When looking at a blood pressure reading, there are two numbers: a numerator and a denominator. The numerator or top number is the systolic blood pressure. The denominator or the bottom number is the diastolic blood pressure.

    Normal systolic blood pressures are between 100 – 120 mmHG. Normal diastolic pressures are between 60-80 mm Hg. Traditionally 120/80 mmHg was considered the “gold standard” for blood pressure, but now its recommended to be at most 120/80 mmHg. 

    A "Good" Pressure

    A “good pressure” is relative. In the ER, a pressure below 160/90 tends to be considered pretty good and usually won’t require any medications. However, a pressure of 160/90 is considered very high if that is the normal daily blood pressure at home, and should be started on medications.

    How to Measure Blood Pressure

    We check people’s blood pressures in the hospital, in the outpatient office setting, and pretty much every area of patient care. Nowadays, we have machines that do most of it for us. But machines aren’t perfect, and its an essential nursing skill to know how to check blood pressure.

    In general, there are 3 main ways to check someone’s blood pressure:

    Manual Blood Pressure

    A manual blood pressure is checked using a sphygmomanometer and a stethoscope. The stethoscope if placed over the brachial artery, and the cuff is placed on the patient’s bicep.

    The cuff is pumped up to about 160 or 180 (in most people unless BP is very high). Slowly release the cuff pressure while you auscultate the brachial artery. 

    Systolic blood pressure is identified by the first Korotkoff clicking sound. The diastolic is noted when you can’t hear anything left.

    Palpating BP?

    You can palpate the patient’s radial artery when a machine or cuff is pumping up or down. When the radial artery disappears, this is your systolic pressure. There is no way to check diastolic with palpation

    Automated Blood Pressure

    An automated blood pressure is checked by a machine, often a portable Dinamap or a bedside monitor. These machines essentially perform a manual BP on their own.

    They have a sensor which detects tiny oscillations from your pulse. So when the pulse goes away – this is your systolic pressure. When the pulse reappears, this is your diastolic pressure.

    A-Line Blood Pressure

    Arterial lines are commonly placed in the ICU for strict BP monitoring. This is the most accurate way to check a blood pressure because it is directly measured by a sensor within the arteries, instead of indirectly like with the methods above. This gives you real-time changes in blood pressure.

    What’s the deal with the “MAP”?

    If you’ve been working for a bit, or in clinicals, you may hear about the term “MAP”. While systolic blood pressure is often considered the most important part of the blood pressure, the actual important number is the MAP. 

    The MAP stands for Mean Arterial Pressure. This is the average pressure in the arteries from one cardiac cycle (systolic + diastolic). This is measured by a calculation:

    But don’t go busting out your calculators. The bedside monitors should automatically calculate this for you, or possibly your EMR. If you need to calculate it, there are plenty of good online calculators to quickly do it. 

    MAP is a great indicator of tissue perfusion. If the MAP stays above 65 mmHg, then this should be enough pressure to provide essential tissue perfusion and prevent anoxic injury (injury from a lack of oxygen to the cells!).

    Nurses and Providers in the ICU will care much more about MAP than systolic blood pressure, especially when looking at low blood pressures.


    Hypertension, also known as high blood pressure, comes in many different forms. While often thought of as “not a big deal”, it really is the silent killer, and can put a lot of strain on the heart, vasculature, and kidneys.

    Overtime, this organ damage becomes more pronounced, placing the patient at risk for heart disease, strokes, kidney failure, and more!

    Another reason why it’s termed the silent killer is because it often is asymptomatic – meaning there are no symptoms. But just because there aren’t any symptoms doesn’t mean it isn’t dangerous, especially in the long run. 

    In medicine, we use JNC8 guidelines to classify and manage hypertension. 

    Blood pressure levels include:

    Normal: < 120 / 80 mmHg
    Stage 1 HTN: 130 – 140 / 80-89 mmHg
    Stage 2 HTN: > 140 / 90 mmHg

    Normal Blood Pressure Levels

    Hypertension can be chronic or acute. Its also important to know if the patient is having any symptoms such as chest pain, SOB, headache, etc.

    3 main types of hypertension that we’ll talk about include:

    Primary Hypertension

    Primary hypertension, previously referred to as essential hypertension, is a chronic hypertension that has no clear cause, but is thought to involve genetic, dietary, and lifestyle factors. This is what most people are diagnosed with when they have high blood pressure. Risk factors include:

    • Increased age
    • Obesity
    • Family History of HTN
    • Black race
    • High sodium diet
    • Excessive ETOH
    • Sedentary lifestyle

    Hypertensive Urgency

    Hypertensive urgency is a very high blood pressure > 180/110 mmHg. While there is no evidence of organ damage (i.e. lack of symptoms or lab abnormalities), the patient is at risk for organ damage or strokes to occur.

    Hypertensive Emergency

    Hypertensive emergency is a very high blood pressure > 180/110 mmHg when there IS evidence of organ damage. The patient should have at least one of the following signs or symptoms:

    • Chest Pain or SOB
    • Pulmonary Edema
    • Severe headache, Seizures, or confusion
    • Elevated Troponin
    • Acute Kidney Injury (elevation in creatinine levels)

    Treatment of Hypertension:

    Treatment of hypertension is often not aggressive, and is often made by slow gradual changes to outpatient medication regimens.

    However, if the patient is symptomatic, blood pressure medications should be given. 

    At home blood pressures should be checked, as patients BPs are often higher in emergency and urgent care settings, and “White coat hypertension” is common. 

    Some oral medications used to lower BP include:

    • ACE Inhibitors like Lisinopril
    • ARBs like Losartan
    • Calcium channel blockers like Amlodipine
    • Beta-blockers like Labetalol
    • Diuretics like Hydrochlorothiazide
    • Alpha blockers like Clonidine

    In hypertensive urgency and when in the hospital, sometimes IV medications may be required including:

    • IV Hydralazine
    • IV Cardizem or Nicardipine
    • IV Labetalol
    • IV Lopressor (metoprolol)

    In general, blood pressure should never be lowered too fast. In severe cases, the goal should be to lower the MAP by 10-20% within the first hour, then another 5-15% over the next day. In many cases, this is less than 180/120 in the first hour, and less than 160/110 after 24 hours. 

    Lowering the blood pressure too quickly can actually cause ischemic damage in patients who have had elevated blood pressure for a long time. Basically the body becomes used to that high pressure, and while it is dangerous to have high blood pressure in general, lowering it too quickly can cause damage as well.

    BP & Symptoms

    When it comes to blood pressure (and even heart rates while we’re at it), its always important to ask the patient if they have any symptoms. Ask about any CP, SOB, dizziness, palpitations, headache, numbness/tingling/ etc.


    Hypotension is when the blood pressure is too low. Low blood pressure is defined as any pressure less than 100/60 mmHg. However, this is often not considered true hypotension until below 90/50 mmHg.

    Patients who are small in stature and thin may have borderline low blood pressures at baseline.

    Trend Alert

    Worried about the patient’s BP? Trend what their BP has been this hospital visit, as well as previous hospital visits. If their BP is 92/48 but they always run around there and are asymptomatic otherwise – this is reassuring.

    Remember if the MAP is less than 65 mmHg, this places the patient at risk for tissue ischemia and organ damage. 

    Low blood pressure is often a serious sign, especially in the hospital setting. Common causes of hypotension include:


    Septic shock is when there is a severe systemic response to infection. These patients will have persistent hypotension despite adequate fluid resuscitation (30ml/kg bolus). They usually require IV vasopressors, a central line, IV antibiotics, and ICU admission.


    Anaphylactic shock is a type of distributive shock that occurs with a severe allergy. Release of inflammatory mediators causes massive systemic vasodilation, swelling, and hypotension. This is treated with IV steroids and antihistamines, +/- epinephrine.


    When the patient loses enough blood, they will become hypotensive. These patients need STAT blood, usually O negative blood that hasn’t been crossmatched. 

    Cardiogenic Shock

    Cardiogenic shock occurs when the heart can’t keep up with the body’s demand. This can occur in severe CHF or bradyarrhythmias.

    Drugs / Medications

    Maintenance medications given for blood pressure can cause low BP, especially if taken in wrong doses or if they become toxic. Some other medications have hypotension as a possible side effect such as amiodarone. 

    Adrenal insufficiency

    Patients with a history of adrenal insufficiency will often require stress-dosed steroids to maintain their blood pressure. 

    Severe dehydration

    Dehydration needs to be severe before the patient becomes hypotensive. This can occur in those with DKA or diabetes insipidus, or really anything that causes dehydration.

    Treatment of Hypotension:

    Treatment of hypotension will involve treating the underlying cause, but generally involves 2 steps:

    • IV Fluid boluses: to increase the volume of the blood
    • Vasopressors: To cause constriction of the blood vessels

    If fluid boluses do not improve blood pressure, or if the BP drops back again once its done, then the patient may need vasopressors in the ICU.

    Depending on the cause, the underlying cause should be addressed, including:

    • Blood for blood loss
    • Antibiotics and fluids for sepsis
    • Steroids for adrenal crisis
    • Steroids & Antihistamines for Anaphylaxis

    Wrapping Up

    You are going to run into TONS of patients who either have high blood pressure, or low blood pressure. Managing vital signs is a huge part of our jobs as nurses and doctors, and its so important to understand how to manage blood pressure!

    Remember these important concepts when it comes to blood pressure:

    Double Check the Pressure

    Double check your blood pressures. If it doesn’t seem right – check a manual BP. The provider may ask you to do this anyway.

    Always ask about Symptoms

    If your patients BP is high or low, ask them if they have any symptoms. Focus on any headache, chest pain, shortness of breath, dizziness, lightheadedness, palpitations, syncope, etc.

    Trend the Pressures

    Remember high blood pressure shouldn’t be corrected too quickly. Look at previous trends. Don’t freak out about blood pressures that are high unless the patient has symptoms. Worry more about low blood pressures!


    Basil, J., & Bloch, M. J. (2022). Overview of hypertension in adults. In T. W. Post (Ed.), Uptodate.

    Calder, S. A. (2012). Shock. In B. B. Hammond & P. G. Zimmerman (Eds.), Sheey’s manual of emergency care (7th ed., pp. 213-221). Elsevier.

    Gaieski, D. F., & Mikkelsen, M. E. (2022). Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. In T. W. Post (Ed.), Uptodate

    Roe, D. M. (2015). Cardiac emergencies. In B. A. Tscheschlog & A. Jauch (Eds.), Emergency nursing made incredibly easy! (2nd ed., pp. 97-197). Lippincott Williams & Wilkins.

    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


    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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    Blood Transfusion Reactions: A Comprehensive Nursing Guide

    Blood Transfusion Reactions: A Comprehensive Nursing Guide

    William J. Kelly, MSN, FNP-C
    William J. Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    Blood transfusion reactions are common within the hospital setting because so many blood products are given. Transfusing blood products that are lacking or actively being lost (i.e. GI bleed) is literally life-saving treatment.

    In this article, we will talk about the different blood products, why they are given, and then dive into each type of blood transfusion reaction, what causes them, their signs and symptoms, and how to manage them as the nurse.

    Acute Hemolytic Transfusion Reaction

    What are blood products?

    There are multiple different blood products that are transfused within the hospital, and each one can have adverse reactions called blood transfusion reactions.

    Packed Red Blood Cells (PRBCs)

    Packed Red Blood Cells or PRBCs are given to patients when their hemoglobin levels are low. This is called anemia. Some common causes of anemia that may need a transfusion include:

    • Acute and chronic blood loss (i.e. GI Bleed)
    • Untreated ongoing Anemia (Iron-deficiency anemia)
    • Destruction of blood cells
    • Decreased production of red blood cells (i.e. Chemotherapy, aplastic anemia)

    PRBCs are usually ordered when hemoglobin levels drop below 7g/dL, but it depends on the nature of the patient’s anemia as well as their medical history and their hemodynamic stability (are their vital signs normal?)

    1 to 2 units will be ordered of PRBCs depending on how low the patient’s hemoglobin level is, as well as if there is active blood loss. Each unit of PRBCs should increase the hemoglobin by about 1g/dL.

    Before blood products are given, a type and screen is done to verify the patient’s blood type and screen for any antibodies that may require special blood. The exception is if the patient has significant ongoing hemorrhage and the patient needs emergent blood. In this case, O Negative blood is given as they are the universal donor.

    Each unit of blood will take about 2 hours to transfuse, but the maximum amount of time is 4 hours when the blood will expire. In emergencies, blood can be run as fast as needed, often with pressure bags.

    Fresh Frozen Plasma (FFP)

    Fresh Frozen Plasma or just Plasma is the portion of whole blood that doesn’t include the red blood cells, which contains clotting factors.

    Some reasons FFP may be ordered for your patient include:

    • Massive blood transfusions
    • Severe liver disease or DIC
    • Coumadin with bleeding or surgery (in addition to Vitamin KL when Kcentra not available)
    • Factor deficiency with bleeding or surgery

    In massive transfusions, you replace 1 unit of FFP for every unit of PRBCs replaced (along with 1 unit of platelets).


    Platelets are a blood product that help the body form blood clots and prevent bleeding.

    These can often become low from various autoimmune disorders, cancers and chemotherapies, medication reactions, and liver disease.

    Platelets are replaced when platelet levels are low, termed thrombocytopenia. Platelets are usually ordered for:

    • Active bleeding with platelet count <50,000/microL
    • Thrombocytopenia in need of invasive procedure or surgery
    • To prevent spontaneous bleeding, usually when platelet levels <10,000/microL

    Most platelets that are given are obtained by “apheresis”. One apheresis unit is equal to 4-6 “pooled random donor units”. 1 unit of platelets by apheresis should increase the platelets by about 30K.

    Why are Blood products Given?

    Blood products are given whenever the blood levels are too low, or when there is acute bleeding. While this will depend on each specific patient and clinician, blood products are generally given when:

    • PRBCs are given when hemoglobin is below 7 or there is ongoing blood loss with hemodynamic compromise
    • Platelets are given when active bleeding with levels <50K, or when <10K.
    • FFP is given with massive blood transfusions, severe liver disease or DIC, or as a coumadin reversal option.

    Blood Transfusion Reactions

    As with any medication or fluid, there are possible adverse reactions that can occur and that you need to monitor for.

    Because we are infusing blood products from a donor, this adds an increased risk of adverse reactions to occur.

    Because of this, nurses must monitor their patients very closely during blood product transfusions. The nurse must stay with the patient the first 15 minutes of a blood transfusion (may change depending on specific facility protocol), and frequently check vital signs.

    There are common blood reactions, and then there are more rare and severe reactions that can occur.

    Acute Hemolytic Transfusion Reaction

    An acute hemolytic transfusion reaction is a rare life-threatening blood transfusion reaction to receiving blood, specifically PRBCs.

    This happens when incompatible blood is accidentally infused with the patient. This is why the patient’s blood type is checked in the first place so that an appropriate donor can be given.

    Compatible blood is outlined below:

    Acute Hemolytic Transfusion Reaction

    When having a true acute hemolytic reaction, the patient will quickly experience:

    • Fever and/or chills
    • Severe flank pain or back pain
    • Signs of DIC (like oozing form IV site)
    • Hypotension
    • Urine turning red or brown (hemoglobinuria)

    This is a severe reaction as the patient’s own immune system and the donor’s immune system attack each other, destroying blood products and causing damage in the process. The patient may experience hemodynamic instability including life-threatening hypotension.

    If this reaction occurs, the nurse should:

    Acute Hemolytic Reaction: Nursing Steps

    If an acute hemolytic reaction is suspected, the nurse should:

    1. Stop the blood immediately and check vitals
    2. Hang NS through a patent IV line. Pt should be ordered least 100-200ml/hr to prevent oliguria/renal failure, or boluses if hypotensive
    3. Notify the MD/APP and blood bank, or call an RRT if unstable
    4. Recheck identifying tags and numbers on blood
    5. Administer diuresis as ordered in those at risk for volume overload
    6. Additional testing may include DIC testing and additional blood compatibility and screenings.
    7. Transfer the patient if required

    The Provider should guide treatment, but these are serious reactions and would likely need monitoring in the ICU.

    Your facility should have a specific protocol in the event of significant blood transfusion reactions, which often involves re-testing the patient as well as re-testing the blood unit itself.

    Acute Hemolytic Blood Transfusion Reaction

    Anaphylactic Transfusion Reaction

    An anaphylactic transfusion reaction is a severe allergic reaction to something within the blood product. These are rare, with an estimated 1 in 20-50K transfusions.

    This reaction occurs seconds to minutes after starting the transfusion.

    The recipient is severely allergic to something within the donor blood, which they may have antibodies against, specifically those who are IgA deficient or haptoglobin deficient.

    Signs of an anaphylatic reaction include:

    • Urticaria
    • Wheezing and/or Respiratory Distress
    • Angioedema (facial swelling)
    • Hypotension with/without Shock

    Treatment involves immediately stopping the transfusion, and then treatment with standard anaphylactic medications. These medications include:

    • Solumedrol 125mg IV STAT
    • Benadryl 50mg IV STAT
    • PEPCID 20mg IV STAT
    • IV Fluids

    More significant interventions may be needed, including:

    • Epinephrine .3mg IM STAT +/- IV epinephrine drip with severe bronchospasm or airway edema
    • Vasopressors for hypotension
    • Oxygen and Intubation

    The blood cannot be restarted, and additional testing will need to be performed, and blood from another donor will have to be given.

    Anaphylactic Blood Transfusion Reaction

    Urticarial Transfusion Reaction

    An urticarial transfusion reaction is a less severe allergic reaction to a component within the blood products, but much more common, occurring in 1-3% of blood transfusions. This is an antigen-antibody interaction, usually with donor serum proteins.

    Patients with this blood transfusion reaction will develop urticaria (hives) with no other allergic signs/symptoms such as wheezing, angioedema, or hypotension.

    When an urticarial transfusion reaction occurs:

    1. Immediately stop the transfusion
    2. Check Vital signs and ask the patient for other symptoms (like trouble breathing or facial/throat swelling, dizziness, chest pain, etc)
    3. Notify the Provider
    4. Give IV antihistmine as ordered
    5. Restart blood if hives resolve and no other signs of allergic reaction develop

    When an urticarial transfusion reaction is diagnosed, stop the blood for 15-30 minutes, give IV antihistamine like Benadryl, and then restart the infusion once hives resolve but slowly and cautiously. Check your specific facility’s protocol.

    Urticarial Blood Transfusion Reaction

    Febrile Non-Hemolytic Transfusion Reaction (FNHTR)

    A febrile non-hemolytic transfusion reaction is exactly what it sounds like – the patient develops a fever after/during a transfusion, but they are not experiencing other signs of a hemolytic reaction.

    This is usually due to a systemic response to cytokines which developed during the process of storing the blood.

    These are very common, occurring in .1-1% of all transfusions.

    This fever will occur 1-6 hours after the transfusion begins.

    Signs/symptoms include:

    • Fever (38-39*+ C)
    • Chills
    • Severe Rigors
    • Mild dyspnea

    If the temperature is more than 39°C or 102.2°F, consider a hemolytic transfusion reaction.

    Whenever there is a fever present, the main thing to consider is if this could be the first sign of a more serious transfusion reaction such as a hemolytic reaction, TRALI (see below), or Sepsis.

    If there is just a fever and no other significant reaction is suspected, antipyretics should be be given, usually Acetaminophen 650-975mg PO. The transfusion can usually be continued but monitored closely.

    Future transfusions should be “leukocyte reduced”, which is a process that removes most of the white blood cells within the blood.

    Febrile Non-Hemolytic Blood Transfusion reaction

    Transfusion-Associated Acute Lung Injury (TRALI)

    Transfusion-Associated Acute Lung Injury, known as TRALI, is a rare but one of the severe blood transfusion reactions that can occur after transfusion of a blood product.

    This is when the transfused product activates the recipient’s neutrophils, causing acute lung damage.

    Patients at risk for TRALI include patients with:

    • Liver transplants
    • Chronic ETOH abuse
    • Smokers
    • Volume overload
    • Shock

    The patient will experience sudden and severe respiratory failure during or shortly after a transfusion, but up to 6 hours after the transfusion. This is often associated with:

    • Hypoxia
    • Fever
    • Hypotension
    • Cyanosis

    New bilateral infiltrates on CXR are often seen.

    TRALI: Nursing Actions

    When TRALI is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and ask patient their symptoms
    3. Call an Rapid Response if the patient is in respiratory distress and/or hypoxic/hypotensive (or notify Provider in ED/ICU).
    4. Support oxygen status (oxygen, intubation if needed)
    5. Support blood pressure (fluid boluses, vasopressors if needed)
    6. Notify the Blood Bank
    7. Obtain a Stat portable CXR
    8. Follow any additional orders / administer any additional medications

    Sometimes steroids are given, although evidence is not great.

    These patients may need to be intubated and will likely need to be transferred to the ICU and closely monitored.

    They do not seem to be at increased risk for TRALI to occur again with a different transfusion in the future, however, donors who are implicated are banned from donating ever again.


    Transfusion-Associated Sepsis

    Transfusion-Associated Sepsis is a life-threatening blood transfusion reaction that can occur with the administration of contaminated blood products which are infected with bacteria.

    The patient will start developing signs or symptoms within 5 hours after the infusion, but usually around 30 minutes.

    Signs/Symptoms of transfusion-associated sepsis includes:

    • Fever >39ºC or 102.2ºF, sometimes hypothermia
    • Rigors
    • Tachycardia >120bpm or >40bpm above baseline
    • Rise or fall of systolic BP 30mmHg
    • Abdominal pain or back pain
    • Nausea and vomiting

    Remember that Transfusion-associated Sepsis, Acute Transfusion Hemolytic Reaction, and TRALI can all have similar symptoms.

    SEPSIS: Nursing Actions

    If transfusion-associated sepsis is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and quickly assess the patient
    3. Notify the Provider (Call an RRT if patient unstable)
    4. Support oxygen and hemodynamic status with oxygen, fluids, etc
    5. Obtain blood work from opposite arm (blood cultures, Coombs test, plastma-free hgb, and repeat crossmatch
    6. Administer ordered antibiotics ASAP (Usually Vanco/Zosyn)
    7. Notify the Blood Bank
    8. Follow any additional orders / administer any additional medications
    Transfusion Associated Sepsis

    Transfusion-Associated Circulatory Overload (TACO)

    Transfusion-Associated circulatory overload, also known as TACO, is when the patient develops acute volume overload after administration of blood products.

    This blood transfusion reaction is fairly common, occurring in up to 1% or more of transfusions. This can occur up to 12 hours after the transfusion is given, and risk factors include patients with:

    • CHF
    • End-Stage Renal Failure (i.e. on dialysis)
    • Extremes of age
    • Small stature & low body weight

    The more units transfused and the quicker transfused, the higher risk of TACO (just like with IV fluids).

    Patients will develop symptoms of respiratory distress which include:

    • Dyspnea
    • Tachypnea
    • Hypoxia
    • Orthopnea

    The patient will also usually develop hypertension.

    Remember TRALI can have similar symptoms, as well as a pulmonary embolism.

    TACO: Nursing Actions

    When TACO is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and quickly assess the patient (pay attention to respiratory status and breath sounds)
    3. Notify the Provider (Call an RRT if patient unstable)
    4. Support oxygen status with supplementary oxygen, BIPAP, or intubation if needed
    5. Make sure a STAT portable CXR is ordered/performed
    6. Administer diuretics as ordered (i.e. 40mg IV Lasix)
    7. Follow any additional orders / administer any additional medications

    In milder cases, the patient may just require diuretics and supplemental oxygen. More severe cases may require Bipap or intubation.


    It is a smart idea for the Provider to order 20mg IV Lasix in-between units when multiple units of blood are ordered in someone with a history of CHF or who is very old. If it is not ordered and you feel it may benefit the patient, offer this suggestion to the Provider as it can prevent TACO from occurring.

    “Hey this is Jan calling from Med-surg, I just wanted to make sure you didn’t want any Lasix in-between blood units for Mark Smith in 147-2, as they have a history of CHF?”

    TACO blood transfusion Reaction

    Primary Hypotensive Reactions

    Primary hypotensive reactions are very rare, but occur when there is a sudden drop in systolic blood pressure >30 mmHg within minutes of starting a transfusion.

    The blood pressure normalizes once the transfusion is stopped. While rare, other severe blood transfusion reactions can also have hypotension, so the patient will need to be evaluated to rule those out as well.

    Patients who take an ACE inhibitor like lisinopril are at increased risk for this to occur.

    This is also more common with platelet administration.

    And those are the acute blood transfusion reactions that can occur when administering blood in the hospital.

    Keep in mind that there can also be transmission of infections such as HIV and hepatitis, although very rare and will not present itself during the transfusion or shortly after.


    Kleinman, S., & Kor, D. (2022). Transfusion-related acute lung injury (TRALI). In UpToDate. UpToDate. Retrieved from

    Silvergleid, A. (2022). Approach to the patient with a suspected acute transfusion reaction. In UpToDate. UpToDate. Retrieved from

    Silvergleid, A. (2022). Immunologic transfusion reactions. In UpToDate. UpToDate. Retrieved from

    Silvergleid, A. (2022). Transfusion-associated circulatory overload (TACO). In UpToDate. UpToDate. Retrieved from

    Spelman, D., & MacLaren,G. (2022). Transfusion-transmitted bacterial infection. In UpToDate. UpToDate. Retrieved from

    10 Tips for a New Charge Nurse

    10 Tips for a New Charge Nurse

    A charge nurse is so important in keeping a hospital department running smoothly. Whether in the ER, ICU, or inpatient floor settings – the charge nurse is essential to the team.

    Many times being a charge nurse comes with years of experience, but sometimes it comes with less than 1 year! (believe me – I was one of them!) Many units may have high turnover, and you can find yourself being a charge nurse with a year or less experience.

    While this is nerve-wracking, it is possible to do a good job as a charge nurse, even with not-so-ideal nursing experience.

    Here are some charge nurse tips to help you on your way to becoming an amazing charge nurse to serve as a resource to your team.

    Oxygen delivery devices and flow rates FB

    What Is the Role of a Charge Nurse?

    A charge nurse is the “nurse in charge” on the unit. They are the leader of the team (at least for the shift). They are often the nurses on the floor during the shift that has the most experience and knowledge.

    Their job will differ depending on which unit they work in, but usually involves:

    • Keeping the floor moving (admissions and discharges)
    • “Floating” and helping the nurses
    • Being used as a resource (aka answer questions)
    • Sometimes taking their own patients as well

    In the emergency department, a major role of the charge nurse is throughput. That means keeping the department moving: getting patients who are admitted, discharged, or transferred out of the department, and making space for new patients coming in.

    They may even need to take some of their own patients on a busy day/night, and may need to function as a triage nurse after certain times during night shift or when short-staffed (which let’s be real – is basically the norm).


    Tip #1: Know The Policies

    A major job of a charge nurse is to know the policies inside and out. This is basically the rules of flow of the specific department, aka “how it all works”. 

    This includes policies related to the admission, discharge, and transfer process; medication administration policies, transfusion policies, and more.

    These policies will be specific to each facility and department, and a nurse will naturally learn these over time with experience on the floor.

    However, each facility should have some sort of intranet (online database) or printed resource with policies, which you can look up, print, and save as needed.

    Tip #2: Know Your Backup

    While it’s ideal to have a charge nurse who has years of experience on the floor, this is just not always possible. Nursing turnover is real, and many departments struggle with nurse retention, especially on night shift.

    You may find yourself becoming a charge nurse on night shift with as little as one year of experience or less.

    As a nurse with a year of experience or less, you simply cannot be expected to know everything, including all of the policies and how to troubleshoot any situation that arises.

    While this can be terrifying, there are resources that are available to you if you just don’t know the answer.

    Even though you are the charge nurse of the floor, there should be a “higher-up” that you have access to.

    During dayshift, you may have access to the department director or nursing managers. They can often be contacted by telephone if needed even after they end their workday.

    During night shift, there is usually a nursing supervisor of the hospital as who can answer questions.

    You can also call other charge nurses on other departments to ask for advice during a situation.

    If there is an in-house hospitalist team, they can also be used as a resource for medical concerns, or you can call the attending.


    I moonlight as a night shift hospitalist, and had a charge nurse on a med-surg unit with less than 1 year experience reach out to me as she was concerned with a patient’s HR going in the 30s during sleep. This patient was asymptomatic and had been bradycardic in the 50s while awake. She was concerned because she had never seen a HR consistently that low, even during sleep. I reassured her that this was okay and even expected in this specific patient, and if he developed any symptoms or abnormal rhythm to notify us immediately.

    Tip #3: Good at Throughput

    A charge nurse’s primary responsibility is to keep the department moving. This is super important in the emergency department but is important on any nursing floor.

    Patients come into the ER and often need IVs started, labs drawn, transported to imaging and back, medications administered, call bells answered, and discharge instructions given. Patients who are admitted need report called and need to be transported to the floors.

    Delays in throughput are common, especially within the ER, and may be due to:

    • The nurse being backed up due to too many patients (all too common) or a critical or needy patient
    • The Provider being too busy to discharge or admit their patients immediately
    • Lab or radiology delays
    • Admission delays (i.e. floor nurse too busy to take report)
    • Admission holds (not enough beds upstairs)
    • COVID test results
    • Delays in transportation

    A charge nurse can help minimize many of these delays and keep the department moving by being proactive.

    They can discuss transport patients, clean stretchers, make phone calls, help out their nurses, and remind the Provider to reevaluate and disposition their patients! These are all ways the charge nurse can help become an expert at throughput.

    Tip #4: Help Out

    The nurses in the department are busy and overworked. You can say that again!

    Being chronically understaffed is all too common. This means nurses are often behind in their assessments, procedures, medication administration, and charting. This can seriously impact throughput as well as patient satisfaction and worst of all, patient outcomes.

    As the charge nurse, you will need to find time to help out your nurses wherever they need it. You may need to place IVs, transport patients to or from radiology or the floors, obtain EKGs, triage patients, and give medications that are ordered.

    Not only does this make you a good team player, it helps the whole department run smoothly.

    There’s nothing worse than a charge nurse who seems to sit there and do nothing the whole shift… DON’T BE THAT CHARGE NURSE!

    Tip #5: Charge Nurse by Example

    As a charge nurse, it is your job to lead by example. You may not have a formal manager position, but your selection as a charge nurse for a shift means that you are the team leader, at least for the shift.

    Don’t do one thing and expect another from your nurses. Constantly help out when you can, maintain good rapport with the patients, providers, and ancillary staff, and conduct yourself with professionalism and integrity.

    Tip #6: Stay Calm in Crisis

    It is so important to stay calm during emergencies and crises as a nurse, but especially a charge nurse.

    It will be your job to put out fires left and right, as well as make sure the nurses on your unit handle emergency situations appropriately.

    Emergency situations happen in the hospital all the time – it’s the name of the game. But it’s not just life and death that will test you.

    Families may be yelling at you because they’re angry or frustrated, and patients will literally be trying to die on you.

    Staying calm is easier said than done, but one thing that helps you stay calm is KNOWING YOUR STUFF.

    If you know what the policies are, and what to do in specific emergency situations like cardiac arrhythmias or codes, then you will be more prepared. This should give you a sense of calm, especially when these emergencies inevitably arise. 

    There is nothing more stressful than uncertainty.

    Tip #7: Good Team Player

    Being a good team player is important for any nurse, but especially a charge nurse. There are many ways to be a good team player.

    Be a hard worker and willing to help out other nurses. Don’t expect them to return the favor later, but if they are a good team player they eventually will.

    As a person who is in “charge”, it’s important to not play favorites. The nurses will resent you, and you need to be as fair to them as possible. This means don’t give your “besties” easier assignments or fewer admissions.

    Always have your teams back. Understand situations from their point of view and give them the benefit of the doubt. Nurses aren’t perfect and do make mistakes, but be sure to support them however you can. Don’t immediately throw them under the bus.

    These traits are important for not only charge nurses but any leadership position.

    Tip #8: Stay Organized

    Staying organized is so important for nurses. Charge nurses have an even bigger need to stay organized, because they aren’t just managing their own patients. They are managing the entire department or floor!

    Knowing who has what assignment, which patients they have, and what needs to be done is important. In stressful environments, it can be easy to know you have so much to do, but not even know where to get started.

    Staying organized is key. Get there early if you need to, make lists and prioritize what needs to be done. Chart in real-time to avoid the backlog of charting weighing you down and making you more stressed.

    Also check out: How to Stay Organized as a New Nurse

    Tip #9: Good at IVs and Procedures

    As the charge nurse, you will be used as a resource. Your nurses will come to you if they have difficulty placing an IV or other procedure, or if they have never done the procedure before.

    It is a great idea for the charge nurse to be great at IVs – because this is a common need on any department, but especially within the ER.

    Placing lines and drawing blood work is essential for throughput and good patient care, and excelling at this procedure is a great skill set for the charge nurse to have in their scrub pocket.

    Practice, practice, practice. Make sure you know all the IV tips and tricks as well.

    Related content:

    Tip #10: Good at Rhythms and Codes

    Probably the most stressful part of being a charge nurse is having the pressure of knowing what to do during emergency situations. These are usually intubations, code blues, or other emergent cardiac arrhythmias.

    Knowing your cardiac ECG rhythms is so important for every nurse, but many nurses struggle with this. As the charge nurse – you need to be an expert at this as your nurses will be coming to you for advice or interpretation.

    You should know all about each drawer of the code cart, the code cart meds, and how to reconstitute them, and definitely know how to use the defibrillator!

    This includes knowing:

    • Cardiac defibrillation
    • Synchronized cardioversion
    • Transcutaneous Pacing

    You should also be familiar with the basics of how to recognize a STEMI

    If you feel like your ECG rhythm interpretation and cardiac arrhythmia procedure knowledge can use some work, I have a digital course that I think you’ll find super helpful!

    If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.

    With this course you will be able to:

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

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

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

    Check out more about the course here!

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    STEMI & NSTEMI: A Nurse’s Comprehensive Guide


    A Nurse’s Comprehensive Guide

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    A STEMI is an ST-Segment Elevation Myocardial Infarction – the worst type of heart attack. This type of heart attack shows up on the 12-lead EKG.

    An NSTEMI (or Non-STEMI) does not have any ST elevation on the ECG, but may have ST/T wave changes in contiguous leads.

    Patients with STEMI usually present with acute chest pain and need to be sent to the cath lab immediately for reperfusion therapy – usually in the form of a cardiac cath with angiography +/- stent(s).

    Ruling out a STEMI is the main reason 12-lead ECGs are obtained, and it is critical that you learn to identify them – even as nurses.

    While Physicians/APPs should be laying their eyes on ECGs relatively quickly, this isn’t always the case. The sooner a STEMI is identified, the better the chance for survival for the cardiac tissue as well as for your patient!


    The coronary arteries lie on the surface of the heart (the epicardium).

    These arteries deliver vital blood flow and oxygen to the myocardial tissue to keep the heart perfused and beating.

    The three main coronary arteries are the left anterior descending artery (LAD), the circumflex artery (Cx), and the right coronary artery (RCA).

    The Right Coronary Artery (RCA)

    The RCA travels down the right side of the heart in the groove between the right atrium and right ventricle. The RCA supplies blood to

    • Right atria
    • Right ventricle
    • Inferior and posterior surface of the left ventricle (85% of people)
    • SA node (60% of people)
    • AV bundle (85-90% of people)

    The Left Coronary Artery

    The Left coronary artery begins thicker and is called the left main coronary artery. This branches off into the LAD and the Cx.

    The Left Anterior Descending Artery

    The LAD lies on the surface of the heart between the right and left ventricles. It often extends to the inferior surface of the left ventricle in most patients. The LAD supplies blood to:

    • Anterior surface and part of the lateral surface of the left ventricle
    • The anterior 2/3 of the intraventricular septum

    The Circumflex Artery

    The Cx wraps around the left side of the heart in the groove between the left atrium and left ventricle in the back (the coronary sulcus). The Cx supplies blood to:

    • The left atrium
    • The other part of the lateral surface of the left ventricle
    • Rarely the inferior and/or posterior portions of the LV
    • SA node (40%)
    • AV bundle (10-15%)

    The Posterior Descending Artery

    The posterior descending artery usually branches off from the RCA, although less commonly from the Cx. Whichever one does form the posterior descending artery is considered the “dominant coronary artery”.


    Acute coronary syndrome (ACS) is an umbrella term referring to any condition which causes decreased blood flow to the heart – also known as ischemia. Prolonged ischemia can lead to infarction – which is cell death of the heart tissue.

    This cell death causes the release of troponin into the bloodstream, an enzyme that is not usually found in the systemic circulation.

    Cardiac ischemia is usually secondary to atherosclerosis which is a buildup of plaque within the coronary arteries. This is usually caused by unhealthy eating habits, obesity, sedentary lifestyle, hyperlipidemia, smoking, and genetics.

    This plaque can rupture, releasing contents into the bloodstream which causes a local inflammatory reaction as well as begins a coagulation cascade.

    This blood clot can completely occlude an artery – leading to infarction.

    A Non-ST segment elevation myocardial infarction (NSTEMI) refers to a complete occlusion of a coronary artery that does not cause ST-segment elevation on the ECG.

    While some heart tissue dies, this is usually less extensive than a STEMI. The infarction is usually limited to the inner layer of the myocardial wall.

    NSTEMIs will often have nonspecific changes on the EKG. These changes include T wave inversion or ST-segment depression with or without T wave inversion in anatomically contiguous leads. However, NSTEMIs could also present with a completely normal ECG.

    Troponin levels will be elevated indicating myocardial cell death. However, the ECG does not have ST-segment elevation.

    An ST-segment Elevation Myocardial Infarction (STEMI) refers to a complete occlusion of a coronary artery that causes more significant infarction that extends the entire thickness of the myocardium (termed transmural).

    A STEMI will have ST-segment elevation in at least 2 contiguous leads on the ECG.

    Where this elevation occurs will indicate which heart wall is infarcting, as well as within which coronary artery.

    You may also like: “Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)”


    The ST-segment is the segment on the ECG right after the QRS segment and before the T wave. This represents the initial phase of ventricular repolarization and should be at the isoelectric line.

    The TP-segment should be used as the isoelectric baseline, but you can use the PR segment if the TP is difficult to see.

    The J-point is the point on the ECG where the QRS complex meets the ST segment. This is important for recognizing ST segment elevation.


    ST-segment depression most commonly identifies cardiac ischemia, as well as reciprocal changes in an acute MI.

    It can also indicate heart strain, digitalis effect, hypokalemia, hypomagnesemia, or even be rate related. However, these changes are usually more diffuse as opposed to localized to at least 2 contiguous leads.

    ST-segment depression is defined as ≥0.5 mm depression (1/2 small box) below the isoelectric line 80 ms after the J-point (2 small boxes).

    Horizontal and Down-sloping ST-segment depression are more specific to cardiac ischemia, whereas up-sloping tends to be less serious although still could indicate ischemia.

    De Winter T waves can be seen in 2% of acute LAD occlusions without significant ST-segment elevation. Instead, there will be ST-segment depression at the J-point with upsloping and tall, symmetric T waves in the precordial leads (V1-V6).


    ST-segment elevation usually indicates myocardial infarction when appearing in at least 2 contiguous leads.

    Other possible causes of ST-segment elevation include coronary vasospasm, pericarditis, benign repolarization, left BBB, LV hypertrophy, ventricular aneurysm, Brugada syndrome, ventricular pacemaker, increased ICP, blunt chest trauma, and hypothermia.

    ST-segment elevation is defined as ≥1 mm elevation (1 small box) above the isoelectric line at the J-point. However, in leads V2 and V3, it needs to be > 1.5mm in women, > 2mm in men >40, and > 2.5mm in men < 40.

    Concave ST elevation is considered less ominous and sometimes can indicate benign variant called early repolarization, especially when diffuse.

    Convex upward ST elevation is almost always indicative of a large MI. This is termed “tombstoning”.


    Q waves are the initial positive deflection of the QRS complex indicating septal depolarization. These are normal in all leads except V1-V3.

    Pathologic Q waves are abnormal Q waves that indicate underlying pathology – usually a current or previous MI.

    Pathologic Q waves are defined as >40ms wide (1 small box) and >2 mm deep (2 small boxes).

    Any Q waves seen in V1-V3 are always pathologic.

    Pathologic Q wave

    Q waves can begin hours to days after an infarction begins, and can last for years, even forever.


    Recognizing ST-segment elevation or depression can be difficult in the case of a left bundle branch block (LBBB) or ventricular paced rhythm. This is because there is normally some associated ST-elevation and discordant T waves with these conduction abnormalities.

    To determine possible ischemia or infarction in a patient with these conduction abnormalities, one of the following should be present:

    • ST-segment Elevation > 1mm in a lead with a positive QRS complex (concordant ST elevation)
    • ST-segment depression >1mm in V1, V2, or V3

    These are not always present, but if they are – you should highly suspect ACS in a patient with a pre-existing LBBB morphology.

    This is why a new LBBB and acute chest pain or SOB is concerning for acute MI.

    You may also like: “How to Read a Rhythm Strip”


    STEMIs typically have a normal progression that will be seen on the ECG.

    Hyperacute T waves are first seen, which are tall, peaked, and symmetric in at least 2 contiguous leads. These usually last only minutes to an hour max.

    Then, ST-segment elevation occurs in at least 2 contiguous leads at the J-point, initially concave, and then becomes convex or rounded upwards.

    The ST-segment eventually merges with the T wave and the ST/T wave becomes indistinguishable. This is a “tombstone” pattern.

    Reciprocal ST depression may be seen in opposite leads.

    The ST segment then returns to baseline after a week or so.

    Q waves eventually develop within hours to days, followed by T wave inversion which could be temporary. Over time, the Q wave deepens.


    STEMIs are classified based on where they are located anatomically – so which leads are they are affecting on the ECG.

    Contiguous leads simply means leads that are pertaining to the same anatomical region of the heart.

    The following leads pertain to each region of the heart:

    • Anteroseptal: V1, V2
    • Anteroapical: V3, V4
    • Anterolateral: V5, V6
    • Lateral: I, aVL
    • Inferior: II, III, aVF

    The precordial and lateral leads are often affected together as the area of infarction is not always exact. 

    As an example, the EKG below is an inferior wall STEMI:

    Inferior wall MI with ST elevation in leads II, III, and aVF, with reciprocal changes in the lateral leads.


    STEMIs are true medical emergencies.

    The patient is at a high risk of significant conduction disturbances and arrhythmias including cardiac arrest.

    The longer you wait – the more heart cells will die, leading to worse cardiac outcomes as well as increasing the possibility of patient death.

    A 12-lead ECG should be obtained within 10 minutes of any patient with significant cardiac symptoms including chest pain or SOB.

    Women, older adults, and diabetics may have atypical presentations including a “silent” MI, where they don’t even have chest pain.

    There are many actions that need to be taken in a short amount of time, and many medications that will need to be administered before the cath team gets there.

    A code STEMI should be activated (or whatever your facility’s version of it is), so the interventional cardiologist and the cath team can be alerted ASAP.

    The patient should be hooked up to the monitor, vital signs obtained, IV access x 2 should be established (preferably an 18g), labs drawn and sent including troponin and PT/PTT, and the defibrillation pads should be applied.

    Any abnormal vital signs should be addressed, and any arrhythmias should be managed via ACLS guidelines.

    STEMI medications

    Oxygen should be administered to maintain O2 >90%.

    Aspirin 324mg should be chewed and swallowed. A rectal suppository of 300mg can be given if the patient cannot tolerate PO for some reason.

    Antiplatelet therapy with P2y12 receptor blockers such as Plavix or Brilinta should be given in addition to the aspirin.

    Nitroglycerin should be administered 0.4mg SL x 3 q5min if the patient has persistent chest discomfort, HTN, or signs of heart failure.

    However, do not give if they have used phosphodiesterase inhibitors like Viagra or Cialis within the last 24h.

    Don’t give Nitro if they have a low blood pressure, if they have severe aortic stenosis, or if there is a possibility of a right ventricular infarct (sometimes presents with inferior wall MIs). Nitro can cause severe hypotension in these patients.

    For persistent symptoms, an IV nitro drip can be used.

    Anticoagulants like an unfractionated heparin drip should be given. Other options include Lovenox.

    If the patient has signs of left heart failure, treat with nitro as above, loop diuretic like Lasix, +/- Bipap.

    Morphine 2-4mg slow IVP q5-15min can be given for persistent severe chest pain or anxiety. However, there is research indicating an increased risk of death when morphine is given in STEMI.

    It is possible that morphine may interfere with the antiplatelet effect of P2y 12 receptor blockers. So morphine should be avoided unless absolutely required for pain control.

    Atorvastatin 80mg PO should be given ASAP, preferably before PCI in those who are not already on a statin. If the patient on it already, their dose should be increased to 80mg.

    Primary percutaneous coronary intervention (PCI) is the preferred reperfusion method and should happen ASAP.

    This is when the interventional cardiologist will take the patient to the cardiac cath lab and perform angiography and stent placement to open up the occluded vessel.

    Fibrinolytics can alternatively be given, specifically if there is no access to a cath lab within a reasonable time frame (120 min), as long as symptoms < 12 hours and no contraindications (i.e. risk of bleeding).

    Beta-blockers are initiated within 24 hours, unless they are contraindicated such as with bradycardia, HF, or severe reactive airway disease. This can be started after PCI.

    You may also like: “Adverse Drug Reactions Nurses Need to Know”

    Non-ST Segment Elevation Myocardial Infarction (STEMI)

    As the name suggests, an NSTEMI does not have ST elevation seen on the ECG, but it is still a heart attack.

    An elevated and rising troponin level is associated with an NSTEMI.

    The ECG can be completely normal, or it can have nonspecific T wave changes or even ST depression in contiguous leads.

    Management of an NSTEMI is similar to a STEMI in terms of medications. However, they are not given fibrinolytic and are not emergently brought to the cath lab. They may or may not get a cardiac cath during their hospital stay.

    Instead, medication therapy is maximized like the ones described above. The patient is continued to be monitored, and troponin levels are trended usually every 6-8 hours.

    STEMIs and NSTEMIs are critical emergent events that nurses need to know well! You will be running into this at some point in your nursing career, and you want to know exactly what you’re doing when it happens! Being able to recognize a STEMI on the ECG is the first step!

    Want to learn more?

    If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.

    With this course you will be able to:

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

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

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

    You can use the code “SPRING2021” for a limited time 15% discount, exclusive to my readers!

    Check out more about the course here!

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    How to read an EKG Rhythm Strip - Pin Share