VTACH & VFIB: A Nurse's Guide to Ventricular Arrhythmias

Cardiac ECG Emergency (ER) Critical Care

Updated June 2026 · Medically reviewed for nurses

11 min read

A nurse's guide to ventricular arrhythmias: VFIB and VTACH

Ventricular arrhythmias like VTACH and VFIB occur in and out of the hospital — the difference is that outside it, no one is on the monitor, so instead of catching the arrhythmia you find the patient unresponsive.

VTACH and VFIB are huge deals, and these rhythms are deadly. Knowing how to recognize them is essential for any nurse in the inpatient or ER setting.

In This Guide

What Is a Ventricular Arrhythmia?
What Causes Them?
Identifying VTACH
Monomorphic VTACH
Polymorphic VTACH & Torsades
QT Prolongation
Identifying VFIB
VFIB & VTACH Management
Reversible Hs & Ts
References

What Is a Ventricular Arrhythmia?

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

When we talk about them, we're primarily talking about VTACH (ventricular tachycardia) or VFIB (ventricular fibrillation). Ventricular escape rhythm is a backup rhythm for very slow heart rates and isn't covered here.

VTACH

A fast rhythm originating in the ventricles. May or may not perfuse — the patient may have a pulse, or may be pulseless and in cardiac arrest.

VFIB

Chaotic, disorganized firing of all the ventricular cells. Never perfuses — it is always a CODE BLUE and degenerates into asystole unless reversed.

What Causes Ventricular Arrhythmias?

Ventricular arrhythmias are usually caused by coronary artery disease (CAD). Any lack of blood flow (i.e. a heart attack) deprives ventricular cells 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.

Coronary artery disease / MI — the most common cause; hypoxic myocytes become irritable.

Severe electrolyte abnormalities — especially low magnesium, potassium, or calcium.

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 — meaning the patient may not have a pulse.

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

Chest Pain

From the strain of the very fast, poorly perfusing rhythm.

Shortness of Breath

Reduced cardiac output from impaired ventricular filling.

Dizziness

Lightheadedness from falling cardiac output.

Syncope

Loss of consciousness if perfusion drops far enough.

If VTACH is pulseless, the patient will go unresponsive and be a CODE BLUE. VTACH is essentially a "run" of PVCs that just doesn't stop. There are different types based on morphology (how it looks): Monomorphic and Polymorphic VTACH.

Monomorphic VTACH

EKG rhythm strip showing monomorphic ventricular tachycardia — Monomorphic VTACH — a regular, wide-complex tachycardia.

Monomorphic VTACH originates from the same ventricular focus. The same cells act as the pacemaker, and the rest of the heart follows their lead.

Regular R-R interval.

HR 100–330 bpm (often near 200).

Wide QRS (>140 ms, or 3.5 small boxes).

AV dissociation: P waves are absent in about 40% of cases, but in the rest you may see them with no relation to the QRS — superimposed P waves marching through the VTACH.

AV dissociation in monomorphic VTACH with superimposed P waves, fusion, and capture beats — AV dissociation with visible superimposed P waves, plus occasional fusion and capture beats.

The morphology of monomorphic VTACH looks different depending on whether it arises from the left or the right ventricle. Knowing which doesn't change management, so just be aware that there can be more than one general "look."

Different morphologies of monomorphic VTACH depending on the ventricle of origin — Monomorphic VTACH morphology varies with the ventricle of origin.

Polymorphic VTACH & Torsades de Pointes

Polymorphic VTACH originates from multiple different ventricular foci. Different regions of cells fire impulses, leading to an irregular, deadly rhythm.

Irregular rhythm.

Wide but differing QRS morphologies.

No distinguishable P waves.

The most common polymorphic VTACH is Torsades de Pointes — literally "twisting of the points." It creates a ribbon-like effect that looks like it's twisting in on itself, usually caused by a prolonged QT interval from electrolyte abnormalities or medications. Torsades is unstable and often degenerates into VFIB.

QT Prolongation

The QT interval measured on an EKG — Measuring the QT interval.

QT prolongation is the main driver of Torsades, defined as a QT interval >440 ms in men and >460 ms in women. Dangerous ventricular arrhythmias are unlikely until >500 ms. It's caused by:

Electrolyte Abnormalities

Hypomagnesemia, hypokalemia, and hypocalcemia.

Medications

Antipsychotics, certain antibiotics, and antiemetics.

Ischemia

Reduced coronary blood flow.

Congenital / Acquired

Inherited long-QT syndromes and other acquired disorders.

Identifying VFIB

VFIB is similar to polymorphic VTACH but on a much wider scale. Essentially all of the ventricular cells are irritable, producing a disorganized, chaotic arrhythmia that does not perfuse the body and is a CODE BLUE. It will degenerate into asystole unless rapidly reversed.

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

Irregular — completely chaotic.

No organized pattern. Either coarse (>3 mm amplitude) or fine (<3 mm amplitude) fibrillation.

EKG rhythm strip showing ventricular fibrillation — VFIB — chaotic, disorganized, no identifiable complexes.

VFIB & VTACH Management

Now that we can identify these rhythms — what do we actually do? First, know that you will not be dealing with this alone. These are true emergencies: a Code Blue or RRT should be called, and other nurses and providers will arrive to help. Management is covered extensively in ACLS, which should always be followed. Here are the 5 basic steps in the hospital setting.

Check for a Pulse / Breathing

If you see a ventricular arrhythmia on the monitor, assess your patient first — go (preferably run) to the room and check responsiveness. If unresponsive, immediately check a carotid pulse and breathing at the same time. In true VFIB the patient is always unresponsive and pulseless. VTACH is hit or miss; if pulseless, it's treated just like VFIB.

Call an RRT or Code Blue

If the patient is pulseless, call for help and call a Code Blue. If they have a pulse but are in VTACH, call an RRT — it's still emergent and they can go down at any minute. This is the in-hospital equivalent of activating the emergency response system in BLS.

Start CPR If Needed

If the patient is pulseless, immediately start compressions as you call for help. Per ACLS, compress at a rate of 100–120 bpm, at least 2 inches or ⅓ the depth of the chest, at 30 compressions for every 2 breaths until the patient is intubated, then continuously.

Give Life-Saving Treatment

Defibrillation is the goal with unstable or pulseless ventricular arrhythmias because it can restore a perfusing rhythm — and each minute of delay drops the chance of success. Epinephrine 1 mg IV every 3–5 minutes is given in pulseless codes. Antiarrhythmics like amiodarone (sometimes lidocaine) can chemically convert the rhythm.

Reverse Any Known Causes (Hs & Ts)

ACLS teaches the Hs and Ts — an acronym to brainstorm reversible causes of these arrhythmias (as well as asystole or PEA). Once a potential cause is found, it should actively be reversed. See the full list below.

Pulseless = Defibrillate

Time is muscle — and brain. For pulseless VTACH and VFIB, high-quality CPR plus early defibrillation is what restores a perfusing rhythm. Don't wait.

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Reversible Hs & Ts

Use this acronym to brainstorm and reverse the causes of cardiac arrest:

Hypovolemia

From hemorrhage or shock, though it must be severe to cause arrest.

Hypoxia

From pulmonary embolism or respiratory failure.

Hydrogen Ions (Acidosis)

From severe DKA or respiratory failure.

Hyperkalemia

Usually secondary to severe ESRD or AKI.

Hypokalemia

From severe GI losses, diuretics, or decreased intake.

Hypothermia

From environmental exposure, hypoglycemia, or severe sepsis.

Tension Pneumothorax

Usually from penetrating trauma or spontaneous.

Tamponade (Cardiac)

From chest trauma, MI, or pericarditis.

Toxins

Overdoses of opioids, benzos, TCAs, beta-blockers, or CCBs.

Thrombosis

Large pulmonary embolism or myocardial thrombosis / infarction.

Clinical Pearls

Assess the patient, not the monitor. Any ventricular arrhythmia on the screen means going to the bedside and checking a pulse and breathing first.

Pulseless VTACH is treated like VFIB. CPR plus early defibrillation is the priority.

Torsades means think QT. A twisting polymorphic VTACH points to a prolonged QT — check magnesium, potassium, and the med list.

Always work the Hs & Ts. Reversing the underlying cause is often what brings the patient back for good.

References

Clinical Databases & Guidelines

Pozner CN, Post TW. Advanced cardiac life support (ACLS) in adults. UpToDate.
Prutkin JM. ECG tutorial: Ventricular arrhythmias. UpToDate.
Ganz LI, Buxton A. Sustained monomorphic ventricular tachycardia: clinical manifestations, diagnosis, and evaluation. UpToDate.
Burns E. Polymorphic VT and Torsades de Pointes (TdP). LITFL ECG Library.
Burns E. Ventricular Fibrillation (VF). LITFL ECG Library.

Textbooks

Dubin D. Rapid Interpretation of EKG's (6th ed.). Cover Pub. Co.
Grauer K. ECG Pocket Brain: Expanded Version (6th ed.). KG/EKG Press.

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