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

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

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

Author | Nurse Practitioner

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

IDENTIFYING VTACH

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

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

POLYMORPHIC VTACH

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

IDENTIFYING VFIB

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.

VFIB & VTACH MANAGEMENT

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.

REVERSIBLE Hs & Ts

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!

REFERENCES

Burns, E. (2019). Polymorphic VT and Torsades de Pointes (TdP). In ECG Library. Retrieved from https://https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdp/

Burns, E. (2019). Ventricular Fibrillation (VF). In ECG Library. Retrieved from https://litfl.com/ventricular-fibrillation-vf-ecg-library/

Burns, E. (2020). Ventricular tachycardia – Monomorphic VT. In ECG Library. Retrieved from https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

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 https://www.uptodate.com/contents/sustained-monomorphic-ventricular-tachycardia-clinical-manifestations-diagnosis-and-evaluation

Ganz, L. I., Buxton, A. (2020). Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis. In UpToDate. Retrieved from https://www.uptodate.com/contents/sustained-monomorphic-ventricular-tachycardia-in-patients-with-structural-heart-disease-treatment-and-prognosis

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. https://www.uptodate.com/contents/advanced-cardiac-lifesupport-acls-in-adults

Prutkin, J. M. (2020). ECG tutorial: Ventricular arrhythmias. In UpToDate. Retrieved from https://www.uptodate.com/contents/ecg-tutorial-ventricular-arrhythmias

Zimetbaum, P. J., Wylie, J. V. (2020). Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management. In UpToDate. Retrieved from https://www.uptodate.com/contents/nonsustained-ventricular-tachycardia-clinical-manifestations-evaluation-and-management

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

Oxygen Delivery Devices and Flow Rates

Oxygen Delivery Devices and Flow Rates

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

Author | Nurse Practitioner

Oxygen Delivery Devices and Flow Rates are important concepts to understand as a nurse. Oxygen is a life-saving therapy that nurses and respiratory therapists administer every day in the hospital.

Whether your patient is on chronic oxygen, or whether they are in acute respiratory failure, your patients will commonly have oxygen ordered and it will be up to you as the nurse to administer it. 

Knowing the oxygen delivery devices and flow rates will tremendously help you take care of your patients who requires oxygen.

Oxygen delivery devices and flow rates FB

The Role of Oxygen

Oxygen is used every day in and out of the hospital. In order to understand oxygen delivery devices and flow rates, we need to first understand a few basic principles and definitions.

Oxygen is the most important gas in our atmosphere that allows for humans and animals to live. Our cells use oxygen to create energy (Kreb’s cycle anyone?). Our ability to create energy without oxygen is very limited.

Without oxygen, our cells will die within minutes.

Oxygen occurs naturally in our atmosphere, at a concentration of 21%. Another term for oxygen concentration is FIO2, or fraction of inspired oxygen.

When we breathe in air, the air (including oxygen) enters into our lungs and makes contact with all of the alveoli. Alveoli are small sac-like structures within the lungs.

The oxygen diffuses across these alveoli into the bloodstream, where it attaches to hemoglobin on our red blood cells. Our blood carries this oxygen throughout the body where it is absorbed by the tissue to give life and energy to our cells.

A healthy patient has a respiratory rate of 12-20 respirations per minute (rpm). Lower than 12 is usually from medications like opioids or benzos, and higher is usually from anxiety, asthma, COPD, CHF, a PE, pneumonia, or some other type of respiratory failure.

The tidal volume is the amount of air breathed into the lungs with each breath. The tidal volume will depend on the patient’s physical size of their lungs and their respiratory effort, but is generally around 400-500ml in a healthy adult.

The FIO2 or the fraction of inspired oxygen is the percentage or concentration of oxygen that a person inhales. Remember room air is always at 21% FIO2 on earth.

Oxygen Delivery Devices and Flow Rates

There are different oxygen delivery devices and flow rates to know, with each device allowing for certain flow rates of oxygen (L/min), as well as different concentrations of oxygen (FIO2).

Blow-by Oxygen

Blow-by oxygen is just that – it’s oxygen that blows by. This does not not apply oxygen directly, but rather indirectly by “blowing” on the patient’s face.

This is usually only used in infants and young toddlers who become agitated when masks or tubing is applied.

Less than 30% FIO2 can be provided with this, which is not much greater than room air of 21%.

If used, the oxygen rate should be at least 10 L/min through a simple mask or even a tubing sticking through a styrofoam cup, which infants and toddlers may be less scared of.

Nasal Cannula

Nasal cannula is tubing that runs from the oxygen source to the patient’s bilateral nares or nostrils.

This is the most common use of oxygen within the hospital, especially for non-critical patients and those who need chronic oxygen delivery like with COPD.

Nasal Cannula is typically started at 2L/min and then titrated upwards to as high as 6L/min, although 2-4L/min is ideal. This delivers 25-40% FIO2, depending upon their respiratory rate, tidal volume, and amount of mouth breathing.

The nasal cannula is good for most patient needs with lower levels of oxygen requirements.

Nasal cannula can be very irritating and cause dry nares at rates >2L/min, so the oxygen should be heated and humidified if possible at higher flow rates.

Simple Face Mask

Simple face masks are a mask with tubing that is hooked up directly to an oxygen source. This is similar to Nasal Cannula, except it is delivered in a mask format over the mouth and the nose, instead of just the nose.

Simple face masks allow for flow rates between 6-10L/min, with an FIO2 of 35-50%.

Simple face masks tend to be a temporary solution, used when titrating your oxygen delivery devices and flow rates. 

Ventimask

Ventimask or a Venturi mask is a face mask that is connected to corrugated tubing with a venturi valve on the end.

This piece connects to the oxygen tubing, which mixes oxygen with room air to provide a consistent high flow of oxygen even with irregular respiratory rates or tidal volumes.

Depending on the oxygen flow rate, there are different colored venturi pieces that are used, with FIO2 of 24-60% FIO2 depending on which venturi valve is used. Levels >40% are generally not used and likely don’t offer more benefit.

The oxygen flow rate will be indicated on the specific venturi valve used, but generally is from 3-10L/min.

Some Ventimasks come in an all-in-one rotational setup, where the FIO2 can be adjusted on a single venturi valve.

Ventimasks are usually used with COPD patients when they require high levels of oxygen, but there is concern for CO2 retention. It can also be helpful for asthma exacerbations and general respiratory distress.

This is typically not used long-term.

Non-Rebreather

A Non-rebreather is typically what is initially used when the patient is requiring a high flow of oxygen and nasal cannula’s are not cutting it.

A non-rebreather provides the highest concentration of oxygen that can be provided to a patient who is breathing on their own, up to 95% FIO2, without any additional machines.

However, this is NOT a long-term solution, and unless they can be titrated down, patients will need to be transitioned to a BIPAP, HFNC, or intubation, unless they can be titrated down.

In a non-rebreather, there is a reservoir bag attached to the mask, with a one-way valve separating the two. This prevents exhaled CO2 from entering the reservoir, and only allows oxygen.

There are holes or “exhalation ports” in the sides of the mask that allow expired are out also do not allow room air back in (usually only one of these is “blocked” to prevent suffocation if the oxygen turns off).

Oxygen flow rates of 10-15L/min can deliver FIO2 of up to 95% in these individuals. However, there is a small amount of room air which “gets in” the system, so the FIO2 is invariably lower, more like 80-90%.

Remember over-oxygenation can also be dangerous termed “oxygen toxicity”. This can cause vasoconstriction, worsen outcomes, and even cause seizures.

This means you want to keep the patient’s SPO2 at 94-99%, as a pulse ox does not measure above 100%.

If a patient is still struggling to breathe with SPO2 of 88-94% or lower on a NRB, then they probably need intubated.

High-Flow Nasal Cannula

High-Flow Nasal Cannula (HFNC) is a newer method of delivering a high flow and FIO2 of oxygen in patients who have higher oxygen requirements. COVID patients tend to do well on these devices, but it can be used for all sorts of respiratory distress.

High-flow Nasal cannula consists of a specific machine and tubing used to deliver a very high flow of oxygen that is heated and humidified.

HFNC can be delivered from 8-60L/min (30-60 L/min in adults), and an FIO2 of 100%.

HFNC is more comfortable and studies have shown that using HFNC may be a better alternative than using a face mask.

HFNC also adds PEEP-like pressure equivalent to about 3-4 cm H2O, similar to a CPAP, helping to keep the alveoli open and increase ventilation (gas exchange).

It is also an alternative to BIPAP other than those patients who are hypercarbic (high CO2 levels like in COPD).

Knowing the difference between the oxygen delivery devices and flow rates, HFNC is not a good option for those who are CO2 retainers for very long .

CPAP

CPAP or Continuous Positive Airway Pressure is a method of non-invasive ventilation. This helps open up the alveoli allowing for better gas exchange.

This can be useful in acute pulmonary edema like in CHF, because it reduces intrathoracic pressure and can reduce preload and increase cardiac output, as well as decrease alveolar congestion.

It is also used for obstructive sleep apnea (OSA) to keep the airway open.

Oxygen is not always added (especially if the patient is just using it for OSA). The pressure is set at 5-20 cm H2O, usually beginning at 5-8 cm H2O.

Increased pressures will increase intrathoracic pressures.

Oxygen is added to keep SPO2 >90%.

BIPAP

BIPAP or Bilevel Positive Airway Pressure is the “better” version of CPAP. This can often be used as an alternative to intubation, and is great for hypercapnic respiratory failure (think COPD).

This uses a higher pressure during inspiration and a lower pressure during expiration.

BIPAP uses 3 settings:

  • Rate: The respiratory rate is usually set to a backup or spontaneous rate, as these patients are awake and breathing spontaneously. This is usually 8-12 rpm. Most patients on a BIPAP will be breathing much faster than this.
  • IPAP: The inspiratory positive airway pressure is how much pressure is given during inspiration. This is anywhere from 5-30 cm H2O, but usually started at 8-12 cm H2O. A higher level will increase tidal volume.
  • EPAP: The expiratory positive airway pressure is the pressure during expiration, which is typically 3-5 cm H2O.

Oxygen delivery is then used as well to ensure SPO2 >90%. FIO2 is started at 100% and titrated down.

Clinical Note: Settings are usually given as IPAP/EPAP, Rate, and FIO2. This means you would relay the settings as 10/5, backup rate of 10, and an FIO2 of 30%. The RT should tell you the settings and they should be the ones to titrate the FIO2.

This is used for Acute COPD exacerbations, and acute respiratory failures like in CHF or ARDS. It can work great for reducing CO2 retention in hypercarbia subsequent and respiratory acidosis.

This is not good for those who are nauseous or have thick secretions, as this may be a risk for aspiration. This can be dangerous for those who are altered for the same reason, although is sometimes still used.

Ventilator

Mechanical Ventilation is the best way of controlling a patient’s oxygenation (oxygen delivery) and ventilation (gas exchange).

Mechanical ventilation is used as a last resort when a patient is in severe respiratory distress and cannot tolerate non-invasive ventilation.

These patients are in respiratory failure and may be altered, cannot protect their airways, are throwing up, or just continue to be hypoxic despite alternative oxygenation.

To be put on a ventilator, a patient will need intubated, likely sedated, and hooked up to a ventilator.

Ventilators have various settings which control the respiratory rate, the IPAP, the EPAP, the inspiratory flow rate, and the FIO2%.

If ventilation can be avoided, it should be. Some patients are difficult to wean off the vent (like in severe COPD or ARDS).

And that is an overview of oxygen delivery devices and flow rates. Hopefully you have a solid understanding of each device and when it is appropriate to use each one.

References

Hyzy, R. C., & McSparron, J. I. (2021). Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation. In T. W. Post (Ed.), UpToDate. https://www.uptodate.com/contents/noninvasive-ventilation-in-adults-with-acute-respiratory-failure-practical-aspects-of-initiation

ICU Advantage. (2020, January 13). CPAP vs BiPAP – Non-Invasive Ventilation EXPLAINED [Video]. YouTube. https://www.youtube.com/watch?v=Te0WLR71HwA

Nagler, J. (2021). Continuous oxygen delivery systems for the acute care of infants, children, and adults. In T. W. Post (Ed.), UpToDate. https://www.uptodate.com/contents/continuous-oxygen-delivery-systems-for-the-acute-care-of-infants-children-and-adults

Need to Level Up Your ECG Rhythm Game?

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!

Oxygen delivery devices and flow rates Pin

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

STEMI & NSTEMI

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!

CORONARY ARTERY ANATOMY

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

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)”

ISCHEMIA & INFARCTION (STEMI) ON THE ECG

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

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

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

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.

LBBB OR VENTRICULAR PACED

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”

STEMI PROGRESSION

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.

STEMI LOCATION

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.

ACUTE MANAGEMENT OF STEMI

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!

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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

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.

QRS COMPLEXES

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.

T WAVES

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).

PR INTERVAL

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.

QT INTERVAL

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

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

Vagal Maneuvers: How to Stop your Patient’s SVT

Vagal Maneuvers: How to Stop your Patient’s SVT

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

Author | Nurse Practitioner

Vagal maneuvers are used in the clinical setting to slow down fast heart rates – primarily for supraventricular tachycardia (SVT)  and sometimes rapid atrial fibrillation (AF RVR).

There are numerous physical maneuvers that can slow down the heart rate – and there is an important modified technique which can almost triple your chances of success!

Vagal maneuvers for SVT fbook image

Svt and Vagal Maneuvers

Supraventricular Tachycardia (SVT) is a very rapid regularly arrhythmia caused by a reentrant loop within the heart.

Essentially – the signal goes around and around in a circuit, producing very fast heart rates.

reentrant loop gif

While SVT is an umbrella term for any tachycardia originating above the ventricles of the heart, it usually is used in reference to AV Nodal Reentrant Tachycardia (AVNRT). This arrhythmia is due to a reentrant loop within/near the AV node itself.

Some patients have abnormal conduction tissue in this area, and if a premature beat comes at the wrong time – it can throw them into this very fast heart rhythm.

This condition occurs more often in younger patients, females, and can be secondary to certain triggers like exercise, stimulants, or even alcohol.

Patients will usually be symptomatic and feel palpitations, fatigue, or dizziness. They can also have chest pain, SOB, or syncope.

Remember when the heart is beating this fast, the cardiac chamber’s ability to fill is decreased, and cardiac output can suffer – leading to symptoms.

When a patient comes in with SVT, their heart rate is usually very fast, with rates often between 150-200 bpm.

AVNRT-svt

We want to stop or “break” this rhythm as soon as possible, so the patient does not decompensate.

If we look at the Adult tachycardia ACLS algorithm, we can see that the first thing we do to attempt to stop the SVT in a stable patient is vagal maneuvers.

The Vagus nerve and the Heart

In order to understand vagal maneuvers, you first need to understand how the vagus nerve works.

The vagus nerve is the primary method that the parasympathetic nervous system affects the body.

This is the 10th cranial nerve which travels from your brain throughout the body. This is how the brain controls certain automatic functions.

When the vagus nerve is activated, the following effects on the body occur:

  • Bronchial constriction
  • Pupillary constriction
  • Increased blood flow to the stomach’
  • Increased digestion

Remember – “rest and digest”

Regarding the heart, the vagus nerve also has important physiological effects on the cardiac system. These include:

  • Slowing of the heart rate
  • Slowing of the conduction velocity of the AV node
  • Decreases the strength of contractions

As you can see, stimulation of the vagal nerve can be utilized to slow the conduction and increase the refractory period of the AV node which hopefully breaks the SVT reentrant loop, leading to conversion back to normal sinus rhythm (NSR).

There are various physical maneuvers that can stimulate the vagus nerve – and many you may do without trying. These include:

  • Coughing
  • Vomiting
  • Cold water immersion

Then there are certain physical maneuvers termed “vagal maneuvers” that we can perform in the hospital to intentionally cause vagal response and hopefully slow down a tachyarrhythmia such as with SVT.

These maneuvers include the Valsalva maneuver and the carotid sinus massage.

But did you know that by modifying the Valsalva maneuver – you can almost triple your chances of success?

The Modified Valsalva Maneuver

The Valsalva maneuver is the classic vagal maneuver used to stimulate the vagus nerve and stop SVT.

This is used on patients who are stable (stable vital signs) and can follow commands.

To perform the Valsalva maneuver, the patient intentionally “bears down” or strains for 10-15 seconds.

This has a 17% success rate in converting SVT. However, by modifying the Valsalva maneuver we can almost triple this success rate!

The Modified valsalva or the positional valsalva maneuver has a significantly higher success rate of 43%!

That’s almost half of your patients with SVT who this can convert back to NSR without any additional medications or interventions.

To perform the modified Valsalva maneuver:

  1. Have a Physician or APP at the bedside
  2. Place the patient in a semi-recumbent position (45° Semi-fowlers)
  3. Have the patient take a normal breath in
  4. Have them forcefully exhale with a closed glottis (bearing down) for 15 seconds
  5. Immediately place them supine and raise their legs to 45 degrees for 15 seconds
  6. Return to semi-fowlers position and watch for up to 1 minute for resolution of the SVT

Clinical Tip: If the patient has trouble bearing down, you can place an empty 10-mL syringe in their mouth and have them blow hard enough to see the plunger move.

As you can see, this technique requires a few assistants, but it is clearly the better option when attempting to convert SVT with vagal maneuvers.

The modified valsalva maneuver infographic

The Carotid Sinus Massage

The carotid sinus massage is a vagal maneuver that you can perform on someone who cannot follow commands.

The carotid sinus is an area located just below the internal carotid artery at the level of the thyroid cartilage, near the pulse.

This area is very sensitive to mechanical pressure, and mechanical pressure to this area can stimulate the vagus nerve.

To perform the carotid sinus massage:

  1. Place the patient supine with their neck extended toward the opposite side
  2. Ensure there is no carotid bruit with your stethoscope
  3. Locate the carotid sinus. This is inferior to the angle of the mandible at the level of the thyroid cartilage near the pulse
  4. Apply firm pressure for 5-10 seconds
  5. You can repeat on the other side if needed

The carotid sinus should never be performed in the following circumstances:

  • Without a physician / APP at the bedside
  • On both sides simultaneously
  • In someone with TIA or stroke within the last 3 months
  • In someone with known carotid stenosis or active carotid bruit

Carotid sinus massage infographic

Complications of Vagal Maneuvers

Any side effects from vagal maneuvers are usually short-lived and an “over-exaggeration” of expected effects.

These include sinus pauses, brief asystole, bradycardia, AV blocks and hypotension.

These will usually fix themselves within seconds to minutes.

Strokes are a major concern with the carotid sinus massage and can happen in <1% of patients.

This is why those with potential carotid stenosis or recent history of strokes should not have the carotid sinus massage.

References:

Aehlert, B. J. (2017). ECGs made easy (6th ed.). Elsevier Health Sciences.

Burns, E. (2019). Supraventricular tachycardia. In ECG Library. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Frisch, D. R., Zimetbaum, P. J. (2020). Vagal maneuvers. In UpToDate. Retrieved from https://www.uptodate.com/contents/vagal-maneuvers

Grauer, K., MD. (2014). ECG Pocket Brain: Expanded Version (6th ed., pp. 65-68). Gainesville, FL: KG/EKG Press.

Knight, B. P. (2020). Atrioventricular nodal reentrant tachycardia. In UpToDate. Retrieved from https://www.uptodate.com/contents/atrioventricular-nodal-reentrant-tachycardia

Tintinalli, J. E., Brady, W. J., Laughrey, T. S., & Ghaemmaghami, C. A. (2016). Cardiac Rhythm Disturbances. In Tintinalli’s emergency medicine: A comprehensive study guide (8th ed., pp. 126). McGraw-Hill Education.

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