AFIB RVR on EKG: Management of Atrial Fibrillation

AFIB RVR on EKG: Management of Atrial Fibrillation

Published: April 13, 2022

Last Updated: March 23, 2023

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

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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

    Published: March 3, 2022

    Last Updated: March 23, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    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: Nurse’s Reference Guide

    Published: February 10, 2022

    Last Updated: March 23, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    A graphic illustraction of a pulmonary embolism lodged in a pulmonary artery, depicting the lung vasculature and teh heart

    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

    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!

    VTACH + VFIB | A Nurse’s Guide to Ventricular Arrhythmias

    VTACH + VFIB | A Nurse’s Guide to Ventricular Arrhythmias

    Published: August 19, 2021

    Last Updated: February 24, 2023

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

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    Ventricular arrhythmias like VTACH and VFIB occur in and out of the hospital. The only difference is, people aren’t hooked up to the monitors. So instead of catching the arrhythmia, the patient goes unresponsive.

    VTACH and VFIB are HUGE deals, and these ventricular arrhythmias are deadly! Knowing how to recognize VFIB and VTACH is essential for any nurse in the inpatient or ER setting.

    Check out this nurse's guide to ventricular arrhythmias (VFIB + VTACH)

    What is a Ventricular Arrhythmia (VTACH or VFIB)?

    Ventricular arrhythmias are those originating from the ventricles. Since the ventricles are responsible for pumping blood to the lungs and throughout the body, ventricular arrhythmias are often deadly.

    When talking about ventricular arrhythmias, we are primarily talking about VTACH (ventricular tachycardia), or VFIB (ventricular fibrillation). Ventricular escape rhythm is a backup rhythm for very slow heart rates, but that rhythm won’t be discussed in this article.

    What Causes Ventricular Arrhythmias?

    Ventricular arrhythmias are usually caused by coronary artery disease (CAD). Any lack of blood flow (i.e. a heart attack) will cause ventricular cells to be deprived of oxygen. When the cardiac myocytes become hypoxic, they become irritable and prone to firing when they shouldn’t, which leads to PVCs, VTACH, and even VFIB.

    Other causes of ventricular arrhythmias include:

    • Severe electrolyte abnormalities
    • QT prolongation from medications
    • Aortic stenosis or dissection
    • Blunt chest trauma
    • Genetic or inherited syndromes


    VTACH is a tachycardic rhythm originating within the ventricles. This produces very fast heart rates which may or may not be perfusing.

    AKA they might not have a pulse. 

    If they do have a pulse, the patient may be asymptomatic. More likely they will experience:

    • Chest pain
    • Shortness of breath
    • Dizziness
    • Syncope.

    If VTACH is pulseless, the patient will go unresponsive and be a CODE BLUE.

    VTACH essentially is a “run” of PVCs that just doesn’t stop, or takes some time to spontaneously stop.

    There are different types of VTACH based on its morphology or how it looks. These include Monomorphic VTACH and Polymorphic VTACH.


    Monomorphic VTACH originates from the same ventricular focus. This means that the same ventricular cells or region of cells are functioning as the pacemaker for this rhythm.

    They create the impulse, and the rest of the heart follows the lead.

    Monomorphic VTACH will have the following features:

    • Regular (R-R interval)
    • HR 100-330bpm (often near 200)
    • Wide QRS (>140ms or 3.5 small boxes)

    P waves are absent in 40% of cases, but sometimes can be seen in no relation to the QRS complex (termed AV dissociation).

    This means you may be able to see superimposed P waves throughout the VTACH.

    AV Dissociation is found in 60% of monomoprhic VTACH, with visible p waves superimposed on the rhythm, as well as occasional fusion and capture beats

    The morphology of Monomorphic VTACH will look different depending on which ventricle it originates from – the left or the right.

    Knowing the difference between these doesn’t exactly matter because the management is exactly same. Just be aware that there can be more than one general “look” to Monomorphic VTACH.

    Torsades De Pointes is a polymorphic VTACH that occurs due to QT prolongation


    Torsades De Pointes is a polymorphic VTACH that occurs due to QT prolongation

    Polymorphic VTACH originates from multiple different ventricular foci.

    This means that different ventricular cells or regions of cells are sending electrical impulses picked up by the rest of the heart. This leads to an irregular deadly rhythm.

    Polymorphic VTACH has the following features:

    • Irregular
    • Wide but differing QRS morphologies
    • No distinguishable P waves

    Torsades creates a ribbon-like effect, where it looks like it’s twisting in on itself.

    The most common polymorphic VTACH is called Torsades De Pointes which literally means twisting of the points. This is usually caused by a prolonged QT interval, often from electrolyte abnormalities or medications.

    Torsades de Pointes is an unstable rhythm and often will degenerate into VFIB.

    QT Prolongation

    QT prolongation is the main cause of Torsades and is defined when the QT interval is >440ms in men and >460ms in women.

    However, dangerous ventricular arrhythmais are unlikely to occur until >500ms.

    QT prolongation is caused by:

    • Electrolyte abnormalities: Hypomagnesemia, hypokalemia, hypocalcemia
    • Medications (Antipsychotics, certain antibiotics, antiemetics)
    • Ischemia
    • Congenital or acquired disorders


    VFIB is similar to polymorphic VTACH, but on a much wider scale. Essentially, all of the ventricular cells are irritable and it produces a disorganized chaotic arrhythmia that does not perfuse the body and is a CODE BLUE.

    This will degenerate into asystole unless rapidly reversed.

    VFIB is usually caused by CAD, with active or previous myocardial infarction being a primary cause. The other causes of ventricular arrhythmias like severe electrolyte abnormalities, hypoxia, or trauma (See Hs & Ts below).

    VFIB has the following features:

    • Irregular
    • No organized pattern

    There is either coarse (>3mm amplitude), or fine (<3mm amplitude) fibrillation.


    Okay – so now we know how to identify these rhythms, but what do we actually need to do about them?

    Well first off – know that you will NOT be dealing with this alone.

    These situations are true emergencies, and a Code Blue or RRT should be called, and various other nurses and Providers should show up to manage the arrhythmia.

    Secondly, the management of these emergent arrhythmias is extensively overviewed in ACLS, which hopefully your unit will enroll you in.

    ACLS guidelines should always be followed, and you can review those here. But I do want to briefly outline 5 basic steps when dealing with a dangerous ventricular arrhythmia within the hospital setting.

    1. Check for a Pulse / Breathing

      If you see a ventricular arrhythmia on the monitor, you should immediately assess your patient first. This involves going to their room (preferably running), and seeing if they’re responsive and awake.

      Check carotid pulse and check for breathing when finding your patient unresponsiveIf they are not responsive, immediately assess for a carotid pulse and check for breathing at the same time. This is the first step in BLS and ACLS.

      In true VFIB, the patient will always be unresponsive and pulseless. Sometimes if they take their lead wires off then artifact can look like asystole or VFIB.

      VTACH is hit or miss. Sometimes the patient will be completely asymptomatic and “fine”, but this isn’t a sustainable rhythm and can degenerate quickly into VFIB.

      If VTACH is pulseless, it’s treated just like VFIB.

    2. Call an RRT or Code Blue

      Code cart for RRT or Code BluesIf the patient is pulseless, call for help and call a CODE BLUE.

      If the patient has a pulse but in VTACH, an RRT should be called as this is still an emergent rhythm and the patient can go down at any minute.

      Calling these codes within the hospital is the equivalent of “activating the emergency response system” in BLS.

      This will get everyone who needs to be there ASAP. Hopefully an ICU attending as well as nurses will come to help the Code or RRT.

    3. Start CPR if Needed

      High-quality CPR is essentialIf the patient is pulseless, when you scream out for help, immediately start compressions.

      High-quality compressions are super important in bringing the patient back to a perfusing rhythm.

      As taught in ACLS, compressions should be at a rate of 100-120bpm, at least 2 inches or ⅓ depth of the chest.

      30 compressions for every 2 breaths until the patient is intubated, and then continuously.

    4. Give Life-Saving Treatment

      Which medications and treatments given will depend on whether we are dealing with VTACH with a pulse, or pulseless VTACH or VFIB.

      Defibrillation is the ultimate goal with unstable or pulseless ventricular arrhythmias because defibrillation can restore a perfusing rhythm.

      Each minute you wait, the chances of restoring a perfusing rhythm drop dramatically.

      Epinephrine is always given in pulseless codes as well, 1mg IV every 3-5 minutes.

      Antiarrhythmics are important during ventricular arrhythmias that can also chemically convert the patient’s heart rhythm. Amiodarone is most often recommended, but sometimes lidocaine or others can be given.

    5. Reverse any known causes (Hs & Ts)

      In ACLS you are taught all about Hs and Ts.

      Basically, this is an acronym to help you brainstorm potential causes for these deadly arrhythmias (as well as asystole or PEA).

      You can read more about the Hs & Ts below.

      Once potential causes are found, these should actively try to be reversed.


    Hypovolemia from hemorrhage or shock can cause cardiac arrest, although must be severe

    Hypoxia from pulmonary embolisms or respiratory failure

    Hydrogen Ions aka acidosis from severe DKA or respiratory failure

    Hyperkalemia, usually secondary to severe ESRD or AKI

    Hypokalemia, usually from severe GI losses, diuretics, and decreased Intake

    Hypothermia, usually from environmental exposures, hypoglycemia, or severe sepsis

    Tension Pneumothorax usually from penetrating trauma or spontaneous

    Tamponade (cardiac), usually from chest trauma, MI, or pericarditis

    Toxins such as overdoses from opioids, benzos, TCAs, BB, or CCB

    Thrombosis such as large pulmonary embolisms or myocardial thrombosis / infarction

    Hopefully this gave you a solid understanding of V TACH and VFIB, and your role as the nurse to help manage these deadly ventricular arrhythmias.

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

    With this course you will be able to:

    • 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. (2019). Polymorphic VT and Torsades de Pointes (TdP). In ECG Library. Retrieved from https://

    Burns, E. (2019). Ventricular Fibrillation (VF). In ECG Library. Retrieved from

    Burns, E. (2020). Ventricular tachycardia – Monomorphic VT. In ECG Library. Retrieved from

    Dubin, D. (2000). Rapid Interpretation of EKG’s: An interactive course (Sixth edition., pp. 154157). Tampa, Fla.: Cover Pub. Co.

    Ganz, L. I., Buxton, A. (2020). Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation. In UpToDate. Retrieved from

    Ganz, L. I., Buxton, A. (2020). Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis. In UpToDate. Retrieved from

    Grauer, K., MD. (2014). ECG Pocket Brain: Expanded Version (6th ed., pp. 73-74). Gainesville, FL: KG/EKG Press.

    Pozner, C. N., & Post, T. W. (2021). Advanced cardiac life support (ACLS) in adults. In UpToDate. UpToDate.

    Prutkin, J. M. (2020). ECG tutorial: Ventricular arrhythmias. In UpToDate. Retrieved from

    Zimetbaum, P. J., Wylie, J. V. (2020). Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management. In UpToDate. Retrieved from

    Check out this nurse's guide to ventricular arrhythmias (VFIB + VTACH)

    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!

    You may also like:

    How to read an EKG Rhythm Strip - Pin Share

    How to Read an EKG Rhythm Strip

    How to Read an EKG Rhythm Strip

    This post may contain affiliate links, which means I get a commission if you decide to purchase through my links, at no cost to you. Please read affiliate disclosure for more information

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

    Author | Nurse Practitioner

    Learning how to read an EKG rhythm strip is an essential skill for nurses!

    This skill becomes especially handy for nurses on Med-Surg, Telemetry, the Emergency Department, or Critical Care units.

    If reading an EKG rhythm strip is new to you – this is the perfect place to start!

    How to read an EKG Rhythm Strip - FB Share

    What is a Rhythm Strip?

    An EKG or ECG stands for Electrocardiography, which is the electrical activity of the heart traced on paper (or a monitor).

    A rhythm strip is at least a 6-second tracing printed out on graph paper which shows activity from one or two leads.

    Leads are “views” of the heart. There are 12 leads that are traditionally obtained with a 12-lead EKG, but most portable and bedside monitors only monitor 3-5 leads at a time.

    Luckily – interpreting a single rhythm strip is much easier than a 12-lead EKG. Most rhythm strips are interpreted from Lead II as this gives a great view of the heart.

    The goal of reading an EKG rhythm strip is to determine the rate and rhythm of the patient. This is great for identifying baseline cardiac rhythm as well as any arrhythmias or ectopy that may occur (like a premature beat).

    A 12-lead EKG also looks at the rate and rhythm, but additionally gives nearly a complete 360° view of the heart.

    This means it can be used to assess for things like cardiac ischemia or infarction, conduction delays, and even enlarged chamber size.

    The ECG Rhythm Strip Tracing

    As I said earlier – an ECG Rhythm tracing is the electrical activity of the heart recorded on paper or a monitor.

    This is traditionally printed out on a 6-second strip. This can make it easy to determine the rate of an irregular rhythm if it is not given to you (count the complexes and multiply by 10).

    Thick black lines are printed every 3 seconds, so the distance between 3 black lines is equal to 6 seconds.

    As you can see, a printed ECG rhythm strip is comprised of boxes – both small boxes and large boxes. 5 small boxes make up one large box.

    Each small box is 1mm wide, signifying 0.04 seconds or 40 milliseconds (ms).

    Each large box is 5 small boxes, signifying 0.20 seconds or 200ms.

    This becomes important to remember when determining the rate of regular rhythms. The boxes and lines are also important in recognizing whether a rhythm is regular or irregular.

    The PQRST

    Okay so that covers the paper, but what about the actual tracings? That’s where the alphabet comes into play. By alphabet – I mean PQRST.

    An electrical tracing of the heart is made up of waves, lines, complexes, and intervals, and each of these represents specific conduction within the heart. This is the key to interpreting a rhythm strip.


    P waves represent atrial depolarization. This means that the electrical signal that starts in the SA node (the normal pacemaker of the heart) is traveling through both atria (top chambers of the heart) during the P wave.

    A P wave should look smooth and upright in most leads including lead II.

    The 3 things you’ll want to specifically look for in P waves in a rhythm strip are:

    • Are there P waves before each QRS complex?
    • Are there any P waves that do not have a QRS complex that follows?
    • Do all the P waves look the same / have the same shape?

    Keeping these 3 questions in mind will help you determine where the rhythm originates from (i.e. the sinus node), if there are any potential extra beats, or if there could be certain heart blocks present.

    An inverted P wave means there is anterograde conduction to the atria (backwards direction). This means the electrical impulse originates from near, at, or below the AV node. Examples of this include Junctional rhythm, certain PACs, and PJCs.


    The QRS complex represents ventricular depolarization. This means that the electrical signal is traveling through both ventricles (the bottom chambers of the heart). In a healthy heart – this should correlate with the pulse.

    The QRS complex is actually made up of 1-3 waves, the Q wave, the R wave, and the S wave. Depending on which lead you look at and the specific heart, any combination of these waves may be present.

    In lead II, usually all three waves are present. This includes an initial downward deflection (Q wave), an upward deflection (R wave), followed by a downward deflection (S wave).

    The presence of a QRS complex indicates that the ventricles are receiving the electrical signal. These should follow shortly after a P wave in a sinus rhythm.

    The main abnormality that can occur is a wide QRS complex. This either means that there is aberrant conduction (like a bundle branch block), or that the electrical signal starts in either the left or right ventricle (i.e. a PVC or Ventricular Tachycardia).

    A bundle branch block just means there is a delay in the conduction tissue transmitting the signal to either the right or left ventricle. If the widened QRS is preceded by a P wave, it is probably a sinus rhythm with a BBB.

    If there is no preceding P wave, you may have a PVC or even VTACH if it is sustained.


    The T wave represents ventricular repolarization. This means that the myocardial cells within the ventricles are recovering and “getting ready for the next beat”.

    This should be smooth and upright in most leads, including lead II.

    Sometimes, the T wave can be inverted or flipped. This is nonspecific but can indicate cardiac ischemia or infarction, especially if it is in at least 2 contiguous leads (pertaining to the same anatomical area of the heart).

    People may have flipped waves in certain leads at baseline after a heart attack, with a bundle branch block, or with a PVC, VTACH, or ventricular paced rhythms.

    Tall or tented T waves are those that are > 1 large box in lead II and may be particularly pointed. This could be normal for the patient, but can also indicate hyperkalemia (high potassium).


    The PR interval is from the beginning of the P wave to the beginning of the QRS complex. This represents the time it takes for the electrical signal to reach the ventricles from the SA node.

    This should be 3-5 small boxes or 120-200ms. If longer, this is considered a first degree AV block.

    A short PR interval could be from a a PAC, a junctional rhythm (associated with an inverted P wave), or Wolff-Parkinson-White syndrome.


    The QT interval is the time between the start of the QRS complex to the end of the T wave. This will change depending on the heart rate, so a QTc (QT corrected) is calculated.

    This should be 350-440ms in men, and 350-460ms in women. A QT interval >500ms predisposes the patient to deadly ventricular arrhythmias such as Torsades de Pointes.

    QT prolongation can be caused by ischemia, electrolyte abnormalities, or from medications such as psych medications, Zofran, Azithromycin, Cipro, etc.

    While you can calculate the QT interval from a single strip, a 12-lead EKG should be obtained and it will be listed on the EKG for you. Otherwise, there are online calculators which can be used to determine the corrected QT interval for the heart rate.

    Arrhythmias on the ECG Rhythm Strip

    An arrhythmia is any abnormal rhythm other than normal sinus rhythm – the baseline rhythm of the heart. This can be a benign variant (like sinus arrhythmia), or it could be deadly (like ventricular fibrillation).

    In order to know how to read an EKG rhythm strip, you need to first be able to understand what normal sinus rhythm (NSR) looks like.

    You should be comparing every rhythm strip to NSR. Recognizing where the rhythm differs from NSR will help you identify the rhythm.

    Normal Sinus Rhythm (NSR)

    Normal sinus rhythm is the gold standard. This is what a normal functioning heart beat should look like.

    The “sinus” in the name indicates that the electrical signal is coming from the Sinoatrial node (SA node), the “normal” pacemaker of the heart.

    The presence of sinus rhythm means the cardiac conduction system is functioning appropriately (although certain blocks may still be present).

    The rate of NSR is 60-100 bpm.  Slower is sinus bradycardia, and faster is sinus tachycardia. This just means that the heart is functioning at altered rates, possibly due to sleep, medications, infection, exercise, etc.

    All sinus rhythms should be regular, meaning each of the QRS complexes are mapping out.

    You can do this by measuring the R-R interval between any two beats, and then making sure the R-R interval stays constant throughout the strip. Some people use calipers, but I recommend a good old-fashioned alcohol pad or piece of paper and a pen.

    Additionally, a P wave should precede each QRS complex.

    The QRS complex should be narrow unless there is a bundle branch block present.

    The ECG Rhythm Strip Interpretation

    To read an EKG rhythm strip, you should do so in a systematic way, so that you don’t miss anything.

    1. Is the rhythm regular? Is every R-R interval equal?
    2. What’s the rate? This is usually printed for you
    3. P wave: Are there P waves before every QRS?
    4. PR interval: Is it wide >200ms?
    5. QRS: Is the QRS narrow or wide (>100-120ms)?
    6. T waves: Are the T waves upright and normal-appearing?

    Using this systematic approach should help you interpret what each rhythm is. But you need to be familiar with most of the arrhythmias out there.

    Systematic approach to reading a rhythm strip

    Other Sinus Rhythms

    Other sinus rhythms are rhythms that may still “normal”. I include paced rhythms in this section as this replaces NSR once a pacemaker is placed.

    Sinus Bradycardia (SB)

    Sinus bradycardia is the same as NSR, but the HR is <60bpm.

    This can be normal for well-conditioned individuals like athletes, can be normal if the patient is on a beta-blocker or similar medication, and can also be normal while sleeping.

    The most important thing when the patient has SB is

    1. Is it new or severe (<40bpm or so)
    2. Are they symptomatic? (dizziness, lightheadedness, syncope, SOB, chest pain, etc)

    Since this is often a normal variant – if the patient is asymptomatic there’s usually nothing that needs to be done.

    Make sure a slow HR is actually SB and not a heart block!

    Sinus Tachycardia (ST)

    Sinus tachycardia is the same as NSR, but the HR is >100bpm and usually <150bpm, at least while at rest.

    This can often be seen with exercise, but ST at rest often indicates anxiety, certain drugs, sepsis, dehydration, or volume loss. ST is usually a response to an underlying cause within the body.

    You never treat the ST, but rather treat the underlying issue (i.e. give fluids with volume depletion).

    Paced Rhythm

    Paced rhythms will look different depending on the location of the leads. If the lead is in the right atria, the rhythm will appear like NSR but with a pacer spike before the P wave.

    If the lead is in the right ventricle, it will look like a slow VTACH with a pacer spike before the QRS. There can also be both of these at the same time.

    Some monitors only show the pacer spike if you turn that function on – if you see a very slow VT – ask the patient if they have a pacemaker and adjust the monitors appropriately.

    Other Cardiac Arrhythmias

    Heart Blocks

    Heart blocks are when there is significant delay or blockage in transmitting the signal from the atria to the ventricles. This is usually associated with a junctional or ventricular escape rhythm.

    First degree AV block is generally “no big deal” and common in older age and with beta-blockers. The PR interval is consistently >200ms.

    Second degree type 1 AV block or Wenckebach, is when there is a progressive lengthening of the PR interval which eventually leads to a dropped QRS complex.

    Second degree type 2 AV block or Mobitz II is when there is a consistent PR interval but QRS complexes are randomly dropped.

    Third degree AV block or complete heart block is when there is complete dissociation of the atria and the ventricles.

    Atrial Fibrillation (AF)

    Atrial Fibrillation is a very common type of arrhythmia that you will definitely run into in the hospital. AF could be new-onset, RVR (rapid ventricular response), could be intermittent (paroxysmal), or chronic/persistent.

    AF is an irregularly irregular rhythm, meaning that there is no rhyme or reason for the regularity of each QRS complex.

    This is usually from a structurally diseased heart where both atria are quivering rapidly, termed fibrillation. This leads to fast ventricular rates (AF RVR), as well as poor blood flow through the atria – predisposing the patient to blood clots.

    This is why these patients are started on rate-control medications such as metoprolol or Cardizem, and usually anticoagulants like heparin, Eliquis, etc.

    AF will not have p waves but instead, have a fibrillatory baseline. The QRS complexes will usually be narrow, and will not map out with each other in any way.

    Rates >100bpm are considered AF RVR.

    Atrial Flutter

    Atrial Flutter (Aflutter) is similar to Atrial fibrillation and is treated largely the same.

    This is when the atria aren’t fibrillating but rather “fluttering”. This is usually from a reentrant loop near the AV node.

    This will usually lead to a conduction ratio of 2:1, and a HR around 150bpm. Conduction ratios can be 3:1 (100bpm), 4:1 (75bpm) and variable as well.

    You will see saw-tooth P waves termed “f waves”. Depending on the conduction ratio, you will see 2 (3 or 4) F waves per QRS complex. Aflutter is usually regular.

    Supraventricular Tachycardia (SVT)

    Supraventricular Tachycardia is an umbrella term referring to any fast tachycardia that originates above the ventricles. However, in clinical terms, this usually refers to AV Nodal Reentrant Tachycardia (AVNRT).

    This occurs when there is an abnormal pathway of conduction tissue near/within the AV node, termed a “reentrant loop”.

    If a PAC or PVC comes at the wrong time, this can send the electrical signal around and around this loop of conduction tissue, leading to very fast heart rates.

    SVT can be as “slow” as 140bpm to as fast as 220bpm. The faster the heart rate, the more symptomatic the patient usually is.

    In SVT, P waves are usually not present, there is usually ST depression, and the rhythm is regular with narrow QRS complexes.

    Treatment for this involves vagal maneuvers and often adenosine or Cardizem.

    Ventricular Tachycardia (VTACH or VT)

    Ventricular Tachycardia is a fast tachyarrhythmia originating within the ventricles. This leads to very fast heart rates with or without a perfusing rhythm.

    This means the patient may not have a pulse and may be a code blue. Either way, VT is a very serious arrhythmia.

    VT is usually caused by Coronary heart disease, like a previous or current MI.

    The rhythm is regular, and the rate is anywhere from 100-330bpm, and the QRS complex is wide (>140ms).

    P waves are usually absent or undetectable, but 60% of cases can have AV dissociation present.

    If there is no pulse, you use ACLS cardiac arrest algorithm.

    If there is a pulse, you utilize the ACLS Adult tachycardia with a pulse algorithm.

    Ventricular Fibrillation (VF or VFIB)

    Ventricular Fibrillation is a deadly ventricular arrhythmia. There will not be a pulse, and the patient will be coding.

    VF is a similar concept as AF, except the ventricles are the ones fibrillating. Coronary artery disease is again one of the main causes of VF. Severe electrolyte abnormalities can also cause VF.

    VF is irregular and has no pattern. There is either coarse or fine fibrillation, eventually degenerating into asystole if not shocked back into a normal rhythm.

    These patients need fast defibrillation, high-quality CPR, Epinephrine, antiarrhythmics, etc (Code blue algorithm).


    Asystole is the absence of cardiac activity. This is essentially a straight wavy line but may have occasional p waves initially. The patient is dead. Follow ACLS algorithms as above.

    Pulseless Electrical Activity (PEA)

    PEA appears like a normal rhythm (Usually NSR or SB), but there is no actual mechanical contraction (no pulse). The patient will be unresponsive, pulseless, and this is a code blue as well (follow ACLS).

    Want to learn more?

    Hopefully this gave you a good idea about how to read an EKG rhythm strip. Unfortunately, I couldn’t include every single arrhythmia or detail, but this definitely should give you a good understanding of the basics!

    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!

    You may also like:

    Heart Blocks EKG Rhythm Infographic
    How to read an EKG Rhythm Strip - Pin Share