Pulseless Ventricular Tachycardia Risk Factors
Published on: October 26, 2024
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Sofia Donnabelle Mananghaya Olivera

Master of Science - MSc in Bioinformatics, <a href="https://www.ed.ac.uk/" rel="nofollow">University of Edinburgh, Scotland</a>

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Nimra Khan

BSc Honours, Biomedical Science, University of Westminster

Overview

Pulseless Ventricular Tachycardia (ta·kuh·kaa·dee·uh) or PVT is a condition where the electrical system that is used to keep the heart in rhythm becomes disorganised, so much so that the pulse becomes undetectable. Blood is therefore unable to be transported to important organs or to other parts of the body which can result in organ failure, and ultimately death.

As such, it is treated as a medical emergency, and those undergoing PVT require defibrillation (electrical shocks to restart the heart).1 To prevent PVT from occurring, it is important to acknowledge its risk factors. Below we will explore what PVT is, the signs and symptoms, the relevant risk factors, and preventative measures. 

The heart

The heart is an important organ; it is a muscle responsible for transporting deoxygenated and oxygenated blood to the lungs and the rest of the body, respectively. Oxygenated blood is the backbone of body functionality, as organs and tissues use oxygen to make energy. Without proper transport of oxygenated blood (or oxygen in general), such as in the event of a heart attack, the brain can face negative effects. Examples include:

  • Personality changes
  • Brain injury
  • Dizziness 
  • Speech and language problems

The heart’s structure

The heart is split into specific chambers known as the right and left atria (plural: atria; singular: atrium), and right and left ventricles. Regarding blood flow, the superior and inferior vena cava carry deoxygenated blood into the right atrium, from either the upper or lower portion of the body. The deoxygenated blood then moves from the right atrium to the right ventricle.

The blood is then transported to the lungs for oxygenation through the pulmonary arteries. After being oxygenated, the pulmonary veins bring the blood back to the left atrium. The oxygenated blood is then pumped to the left ventricle. A diagram of the heart is shown below:

Figure 1: Overview of the heart’s structure. The “right” side of the heart sits on the left side of the diagram, as this orientation shows how the heart is structured when facing a person. Diagram created with Biorender

What is the ‘heart’s electricity’?

Throughout medical history, researchers have found that the contraction of the heart when it beats is mostly myogenic.2 This means that the signal responsible for the heart beating comes from the heart itself, not the brain. To pump blood correctly, the heart has its own particular electrical system (also known as the cardiac conduction system) that causes contractions. 

The sinoatrial (SA) node is responsible for the start of the electrical system; it sends an electrical signal causing both atria to contract, a process known as atrial depolarisation. The electrical signal continues to another node, known as the atrioventricular (AV) node that slightly delays the electrical signal. This allows blood to fully enter the ventricles. The electrical current continues through the Bundle of His, a segment of the system that splits into right and left branches, and eventually to the Purkinje fibres that cause the ventricles to contract (ventricular depolarisation). The cycle repeats (repolarisation), and the heart cells relax to prepare for the next contraction. 

Generally, the SA node will signal to create 60–100 contractions (beats per minute [bpm]). However, due to the myogenic nature of the heart, if the SA node somehow fails, the AV node can continue contractions at 40–60 bpm.3 If the AV node also fails, then the Purkinje fibres have their contractions, generally around 40 bpm.4 Below is a diagram focusing on the electrical system in the heart.

Figure 2: Overview of the heart’s electrical conduction system. The “right” side of the heart sits on the left side of the diagram, as this orientation shows how the heart is structured when facing a person. Diagram created with Biorender.

The biology of heart contractions

All parts of the body are composed of cells, and human cells contain a membrane that has ‘potential.’5 The cell membrane potential is a term used to describe the difference of charge between the inside and outside of the cell. Inside and outside the cells, there are ions (molecules with positive or negative charges) that move between these environments.6,7

When an electrical signal is sent out, channels controlled by voltage containing calcium ions (positively charged) open and release into cells. When the calcium binds to specific binding sites on the heart muscle, structural changes occur leading to muscle contraction (in this case, a heartbeat).7 

PVT and diagnosis

PVT is diagnosed using an ECG or EKG (electrocardiograph) machine,2 by placing electrodes on the skin.8 These machines can measure and graph a heart's contraction (i.e., depolarisation and repolarisation) through the skin via the electrical activity caused by the depolarisation that occurs when the heart contracts. When measuring these contractions, the ECG is said to have a particular pattern which is labelled as follows:2

P wave

The P wave represents the depolarisation of the atria.

PR Interval

A segment that represents the time between the P wave and the QRS wave.

QRS wave (complex)

Three waves (Q, R and S) that represent ventricular depolarization.

  • Q: Smaller waves that represent the depolarisation of the tissue that contracts in between the left and right ventricles (interventricular septum)
  • R: The largest wave, signalling the main portion of the ventricles to contract
  • S: Depolarisation of the lower portion of the ventricles, a smaller wave

In normal adults, this process takes 80-120 milliseconds.

ST segment

A segment that represents the time between the QRS wave and the T wave. This segment is neither in depolarisation nor repolarisation.

T wave

The T wave represents the repolarisation of the ventricles. Repolarisation of the atria is not detected due to the QRS wave being large. 

What is ventricular tachycardia (VT)?

Ventricular tachycardia (VT) is a condition where the heartbeats are more than 100 bpm. It can either be pulsed or pulseless and is caused by the ventricles contracting irregularly.9 In terms of wave measurement, VT is when the QRS wave exceeds 120 milliseconds. This is also known as having a prolonged QRS complex.10 VT can be further divided into nonsustained or sustained VT.

Nonsustained VT lasts 30 seconds or less whereas sustained VT lasts more than 30 seconds.10 Sustained VT includes the use of procedures such as defibrillation or drugs (cardioversion) to restore the heart to normal (even if the event lasted less than 30 seconds).10 Using an ECG machine, the waves of the QRS complex can present either as a uniform wave (monomorphic) or different each contraction (polymorphic).10 

What is the difference between VT and PVT?

Unlike PVT, VT is not necessarily a medical emergency (although it still has the potential to become one). PVT is classified as a medical emergency since the ventricles are unable to contract properly/weakly, making it pulseless and unable to deliver blood properly.10 Therefore, those with PVT will typically be unconscious.2

Lack of blood flow means a lack of oxygen to important body parts and organs, which may eventually lead to death within minutes.2 It is therefore important to immediately treat PVT to prevent further damage.2 

Risk factors of pulseless ventricular tachycardia

Risk factors are conditions that lead to increased chances of a disease and/or death occurring. These can be genetic (inherited, cannot be controlled), or lifestyle-related (food and exercise). VTs (including PVT) can be caused by many risk factors. Most causes of VT (including PVT) are associated with heart disease. Several risk factors are listed below showing the other risk factors involved with PVT.2 

Some medicines which cause delays between the electrical signals can also increase PVT, which include:

  • Clarithromycin
  • Erythromycin
  • Metoclopramide
  • Haloperidol
  • Methadone
  • Droperidol
  • Fluoroquinolone antibiotics
  • Antiemetics 
  • Antiarrhythmics 

Syndromes that cause prolonging between signals are also risk factors which include:

Other risk factors include:

Reducing your risk

Since VTs generally stem from heart diseases, patients with those diseases should strive to have healthier lifestyle changes.2 Examples include eating healthier diets (lower cholesterol) and exercising more regularly. Cholesterol is a type of fat that can build up (plaque) in the blood and lead to blockages in the vessels leading to or in the heart.

This build-up makes the heart need to beat harder and can disrupt the electrical system leading to issues such as PVT. Similarly, smoking can cause swelling of the blood vessels from inflammation. Consequently, smoking can also lead to a build-up of plaque in the vessels and therefore conditions such as PVT. 

Signs and symptoms

Before PVT occurs, patients will typically feel:2

During PVT, patients will be unconscious and unresponsive without a pulse.

Treatment and post-resuscitation therapies

PVT is mainly treated by defibrillation. The process involves the use of electricity to restart the heart in hopes that the heart will restart in proper rhythm. Even a slight delay in defibrillation can lead to a decrease in survival rate (two-minute delay: 22.2% vs immediate: 39.3%).2,11 Cardiopulmonary resuscitation, more widely known as CPR, should also be done in between shocks from the defibrillator. In a hospital setting, medicines that can decrease irregular rhythms (arrhythmia) can be injected into the bloodstream intravenously (IV).2,12

Following the PVT event, patients should contact a cardiologist for further checks on any possible issues that may have occurred, and to check if any other medical interventions must be used.12 If PVT was caused by medicine, the cardiologist may look into other medicines that could be used instead.2,12

Summary

Pulseless ventricular tachycardia (PVT) is a condition that is considered a medical emergency. PVT is predominantly caused by heart diseases, and therefore healthy diets and exercise are recommended to prevent the condition. High-cholesterol diets can lead to a disruption in the heart’s electrical system, which prevents the proper contraction of the heart to pump blood to the rest of the body.

In PVT, the ventricles contract too rapidly and ineffectively, leading to the heart being ‘pulseless.’ Medical intervention should be immediate and include defibrillation, CPR, and drugs that reduce arrhythmia. Patients who have had a PVT event are highly encouraged to talk to their cardiologist about further preventative measures. 

References

  1. Foglesong A, Mathew D. Pulseless Ventricular Tachycardia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Mar 22]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK554467/.
  2. Silverman ME, Grove D, Upshaw CB. Why does the heart beat? The discovery of the electrical system of the heart. Circulation. 2006; 113(23):2775–81. Available from: https://pubmed.ncbi.nlm.nih.gov/16769927/ 
  3. Wang Y, Hill JA. Electrophysiological Remodeling in Heart Failure. J Mol Cell Cardiol [Internet]. 2010 [cited 2024 Mar 22]; 48(4):619–32. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879059/.
  4. Brooker G. Chapter Fourteen - Pacemakers. In: Segil J, editor. Handbook of Biomechatronics [Internet]. Academic Press; 2019 [cited 2024 Mar 22]; p. 567–89. Available from: https://www.sciencedirect.com/science/article/pii/B9780128125397000143.
  5. Strathmann H, editor. Chapter 2 - Electrochemical and Thermodynamic Fundamentals. In: Membrane Science and Technology [Internet]. Elsevier; 2004 [cited 2024 Mar 22]; bk. 9, p. 23–88. Available from: https://www.sciencedirect.com/science/article/pii/S0927519304800330.
  6. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Ion Channels and the Electrical Properties of Membranes. In: Molecular Biology of the Cell. 4th edition [Internet]. Garland Science; 2002 [cited 2024 Mar 22]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26910/.
  7. Calderón JC, Bolaños P, Caputo C. The excitation–contraction coupling mechanism in skeletal muscle. Biophys Rev [Internet]. 2014 [cited 2024 Mar 22]; 6(1):133–60. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5425715/.
  8. Ashley EA, Niebauer J. Conquering the ECG. In: Cardiology Explained [Internet]. Remedica; 2004 [cited 2024 Mar 22]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK2214/.
  9. Foth C, Gangwani MK, Ahmed I, Alvey H. Ventricular Tachycardia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Mar 22]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK532954/.
  10. Mortimore RR Gerri. Pulsed ventricular tachycardia: a case study. British Journal of Nursing [Internet]. 2023 [cited 2024 Mar 22]. Available from: https://www.britishjournalofnursing.com/content/professional/pulsed-ventricular-tachycardia-a-case-study/.
  11. Chan PS, Krumholz HM, Nichol G, Nallamothu BK, American Heart Association National Registry of Cardiopulmonary Resuscitation Investigators. Delayed time to defibrillation after in-hospital cardiac arrest. N Engl J Med. 2008; 358(1):9–17. Available from: https://pubmed.ncbi.nlm.nih.gov/18172170/ 
  12. Neumar RW, Shuster M, Callaway CW, Gent LM, Atkins DL, Bhanji F, et al. Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015; 132(18 Suppl 2):S315-367. Available from: https://pubmed.ncbi.nlm.nih.gov/26472989/ 

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Sofia Donnabelle Mananghaya Olivera

Master of Science - MSc in Bioinformatics, University of Edinburgh, Scotland

Sofia, a recent international graduate hailing from the Philippines, is driven by her passion to make knowledge more accessible. After graduating with an undergraduate degree in genetics and microbiology, she pursued a master’s in bioinformatics where she delved deeper into data analysis and coding techniques. During her placement year at Roche as a Clinical Pharmacology student, Sofia gained invaluable experience in analysing data and drug development. Currently, she uses her expertise as a freelance copy editor for open-access journals, striving to make research accessible to all.

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