Paid by Perezimor Etifa from University of Hertfordshire

University of Hertfordshire, Hatfield, Hertfordshire
p.etifa@herts.ac.uk

07568 791975

Ventricular tachycardia – General overview

Ventricular tachycardia is an arrhythmia originating from the lower chambers of the heart. It is characterized by an abnormally rapid heartbeat. It is described as a wide complex tachyarrhythmia with QRS (ventricular electrical impulse) duration greater than 120 milliseconds and with a heart rate that exceeds 100 beats per minute, that is, three or more irregular heartbeats in continuous succession. It is also known as VT or V-tach (Mayo Clinic, 2018). It occurs when the electricals signals that coordinate the heartbeat are disrupted, or malfunction and the impulse are sent too quickly. It can last for a few seconds, and if it occurs in a healthy heart for a short time, it may not cause a severe medical issue. In such cases, it occurs asymptomatically. However, if it lasts for a longer time, especially in a weak or compromised heart, it could be severe (Cedars-Sinai, 2020). It can also graduate to a much more serious condition known as ventricular fibrillation. These arrhythmias may also be so severe that they cause the heart to stop working suddenly. Most of the deaths in the United States from sudden cardiac arrest are as a result of ventricular fibrillation and VT. They result in high morbidity rates, and mortality rate estimates are up to 300,000 annual deaths. Prevalence peaks at infancy and old age (above 75 years) (Johns Hopkins Medicine, 2020; Krause, 2016)

The normal heartbeat and heart rate physiology

The heart’s electrical system, together with involuntary (autonomic) nervous and endocrine systems, controls the rhythm of one’s heartbeat and heart rate. The cardiac conduction system coordinates the pumping action of the heart’s chambers to pump blood in from and out to the rest of the body. The sympathetic and parasympathetic nervous systems control and determine the heart rate (BIOE 3340, 2020). The SNS triggers the release of catecholamine hormones to increase heart rate and myocardial contractions while the PNS slows it down via the release of acetylcholine. The sinoatrial node or the sinus node is a small area of specialized tissue in the heart’s upper right chamber (atrium), that spontaneously depolarize to fire a regular electrical signal. This cluster of cells has an intrinsic rhythm and is the heart’s natural pacemaker  (Johns Hopkins Medicine, 2020).

Under normal resting conditions in a healthy heart, the stimuli occur 60-100 times in a minute, which causes the normal heart rate. It is also known as the normal sinus rhythm. Continuous input from the PNS sets this pace, which averages at 75 beats per minute. The signal activates the upper chambers, spreading electrical activity through them and causing them to contract for a short period. The impulses travel from the sinoatrial node through an internodal pathway to the atrioventricular node. This bundle of cells located between the atria and ventricles acts as a gateway to allow passage of the electrical stimuli to the lower chambers. It has its own intrinsic pace at 50 beats per minute. The AV node gate momentarily reduces the speed of the impulse to give the atria a chance to contract and empty the blood into the ventricles (Cleveland Clinic, 2020; BIOE 3340, 2020).The conduction pathway gives way to the HIS-Purkinje network in the ventricles. The signal continues through the bundle of His. The pathway leads to the right and left ventricles, where the bundle of His divides into bundle branches and Purkinje fibers that enervate the ventricular myocardium (BIOE 3340, 2020). The signal follows this division to trigger ventricular contraction, which represents a heartbeat. The heart’s chambers can pump blood out of the heart. When the SA node generates another signal, another heartbeat occurs (Johns Hopkins Medicine, 2020).

For the normal sinus rhythm, electrical signaling from the sinus node follows the anatomically defined conduction pathway through planar or rectilinear excitation waves, eventually resulting in synchronized ventricular myocardial excitation and subsequent contraction (Qu & Weiss, 2015). The situation can be described as the autowave process (Moskalenko, 2014).The action potentials that generate the electrical impulses are consequent to the successive opening and closing of ion channel proteins in the plasma membrane of individual myocardial cells. Electrical coupling between these cells mediated by gap junctions conducts the impulses. The different ionic channel properties result in the action potential waves (rectilinear excitation waves). Depolarization, opening, and closing of voltage-gated ion channels to allow for diffusion of ions, repolarization of membrane potential, and such kind of activity throughout the cells in the pathway make up the cardiac action potential process in the human heart. The unique feature that differentiates pacemaker myocytes like SA-node cells from others is their automaticity or autorhythmicity (BIOE 3340, 2020). This property causes spontaneous depolarization, which activates and maintains the rising slope of the membrane potential eliciting spontaneous action potentials).

Abnormal heartbeat- underlying mechanisms

Cardiac arrhythmias constitute abnormal heartbeats where the rhythm becomes irregular, too slow or too fast, for instance, in V-tach. They arise from mechanisms divided into two major categories. One arrhythmogenic mechanism is by conduction disturbances in the autowave process. The other is a focal activity, which is either by abnormal impulse formation or abnormal automaticity (Moskalenko, 2014; Antzelevitch & Burashnikov, 2011). Altered automaticity can result from triggered activity (by early or delayed after depolarization- EADs, DADs). After depolarizations activate cardiac tissues prematurely. They are a second subthreshold depolarization triggered by one or more preceding action potentials (Tse, 2016). They take place either during (EADs) or after repolarization (DADs) of the action potential.

An abnormal impulse can occur from abnormal automatic mechanisms, that is, induced/ abnormal automaticity. This mechanism happens when non-pacemaker myocardial cells in the ventricles and atria exhibit spontaneous diastolic depolarization and, thus, automaticity. Conditions that reduce resting membrane potential and drive maximum diastolic potential towards threshold potential can trigger automaticity. They can result from injury. Another source is a shift in the impulse initiation site (normal automaticity altered by specific influences). Tachycardia may result from pharmacological substances and some metabolic abnormalities that influence the ANS and concern hormones, for instance, during exercise or fever. Bradycardia may come about if the automaticity of the SA node is suppressed and the other latent (slower) pacemakers take over (Gaztanaga, Marchlinski, & Betensky, 2012). Reduced automaticity causes bradycardia, while tachycardia results when it is enhanced.

The other category stems from the autowave or impulse conduction process. They are also divided into various forms. One is a conduction delay or conduction block whereby the propagating impulse fails to conduct. Membrane properties determine the success of conduction. Conditions, including degenerative processes and drugs like beta-blockers, may affect these properties. Reentry, which is divided into various types, is a significant cause of arrhythmias and differs in mechanism from automaticity or triggered activity. The two main groups are anatomical and functional reentry. In the latter, the circuit does not have anatomic boundaries, while in the former, anatomical structures determine the circuit. Examples of anatomic reentrant are spiral wave and ring model reentry. Functional reentrant includes fibrillation, multiple and autowave reverberators (Moskalenko, 2014; Antzelevitch & Burashnikov, 2011). Reentry can also be classified based on obstacles which are either anatomical or functional. The presence of obstacles creates circus-type reentry. An action potential travels in a circular pathway around an inexcitable anatomical or functional obstacle, then the wavefront reenters and reexites the site of origin. Often this kind of reentry is anatomical (Tse, 2016)

Figure 1: Normal sinus rhythm VS. ventricular tachycardia

Figure 2: Mechanisms of cardiac arrhythmias (Gaztanaga, Marchlinski, & Betensky, 2012; Antzelevitch & Burashnikov, 2011)

Causes and underlying mechanisms of ventricular tachycardia

VT can occur from most of the mechanisms explained above, except those that suppress the SA node and reduce automaticity. They are often associated with venticulo-atrial dissociation, whereby the atrial rhythm is at a slower rate. Reentry, triggered activity, and abnormal automaticity are the main underlying mechanisms responsible for most VT. Reentry is the most frequent (Gaztanaga, Marchlinski, & Betensky, 2012). Various disease conditions can produce VT. Acute myocardial infarction and ischemic heart disease are the most common. Others include heart attack, heart valve disease, adult and congenital structural heart disease, myocarditis, channelopathies, and cardiomyopathy. It can also occur due to inherited arrhythmia like Brugada, catecholaminergic polymorphic ventricular tachycardia, long QT syndrome, or arrhythmogenic right ventricular dysplasia. It can be idiopathic and occur in a healthy, structurally normal heart due to some irritable force. In such cases, it may not be serious and is easy to address and can stop by itself. Other cases result from electrolyte imbalances (hypocalcemia), medication, digitalis toxicity, and illicit drugs (cocaine). Intense exercise, emotional states, and excessive alcohol or caffeine consumption may also cause VT (Cedars-Sinai, 2020)

Examples of specific mechanisms that result in ventricular tachycardia include DAD- induced triggered activity. A delayed- after depolarization may cause catecholaminergic polymorphic ventricular tachycardia (CPVT). The mechanism involved is that the DAD increases intracellular calcium ions due to extremely high levels of catecholamines. catecholamine stimulation aggravates a mutation in the type 2 ryanodine receptor (RyR2), causing it to be leaky (Antzelevitch & Burashnikov, 2011). Triggered activity and automatic mechanisms are responsible for VT in the absence of structural heart diseases. The reentry mechanism, however, underlies VT (monomorphic VT) stemming from heart injury such as ischemic cardiomyopathy. The injury results in a scar that, for instance, disrupts cell coupling or gap junctions. The scar is an obstacle or anatomic substrate which can block, delay, or discontinue conduction through the tissue, causing the development of reentrant VT (Gaztanaga, Marchlinski, & Betensky, 2012).

Classification, signs and symptoms, risk factors and diagnosis

VT exhibit different behaviors and characteristics. They are very heterogeneous in terms of mechanism, rhythm, and fatality. Their classification is based on QRS morphology (heartbeat pattern), further divided into polymorphic and monomorphic. It is also classified according to the duration of the episode, and the effect on the heart’s ability to pump (hemodynamic effect). This classification is further divided into non-sustained VT and sustained VT (Foth, Gangwani, & Alvey, 2020; Krause, 2016). Signs and symptoms include rapid palpitations causing a fluttering (racing) sensation in the chest. It also affects normal blood pressure and can result in symptoms like syncope (fainting) and dizziness. Other effects include angina (chest pains), sweating, and shortness of breath. The most serious sign or consequence is cardiac arrest causing sudden death. Sometimes VT is asymptomatic. Complications accompanying the condition include frequent fainting spells and heart failure. VT may graduate into more serious conditions like ventricular fibrillation and cardiac arrest. The main risk factor is structural and functional heart damage and all conditions that can result in the same. These have been cited among the causes above. VT may also occur as a result of medication side effects, illicit stimulant drugs, and severe electrolyte imbalance. Trauma and genetic diseases such as hypertrophic cardiomyopathy, sarcoidosis, and long QT syndrome, among others also cause VT (Cedars-Sinai, 2020; Johns Hopkins Medicine, 2020).

VT diagnosis requires an electrocardiogram (ECG) to record the heart rhythm. A Holter monitor or event recorder can be used to monitor the heart’s activity for a longer period. ECG monitoring can extend through various applications to smartwatches, smartphones, and other personal devices. An electrophysiological test, a stress test, and a tilt table test can reveal VT. Each has its purpose. For instance, the electrophysiological test confirms the diagnosis. The stress test checks the heart under conditions like medication and physical activity, and the tilt table test is used to check the link between VT and fainting (Mayo Clinic, 2018). The telemetry method and the transtelephonic monitor constantly check the heart rhythm. The transtelephonic monitor must be worn continuously. For a very extended period, where VT is suspected, a small implantable electronic device called a loop recorder is injected into the skin area covering the heart. It can record the heart rhythm for up to 3 years (Cedars-Sinai, 2020).

It is important to differentiate ventricular tachycardia from other variants like supraventricular tachycardia because the treatment strategies are different. Some factors indicate or favor the diagnosis of VT. These include AV dissociation, ventricular fusion beats, and the Brugada’s sign, which is a response shock (RS) interval of more than 100 milliseconds in a precordial lead. The QRS complex indicates VT when it has a width greater than 0.16 seconds with the left bundle branch block pattern or one more than 0.14 seconds with the right bundle branch block pattern. QRS with negative concordance in the precordial leads is another factor favoring VT diagnosis  (Foth, Gangwani, & Alvey, 2020). Cardiac imaging methods like MRIs, CT scans, X-rays, coronary angiograms, and ECGs can be used to determine the underlying anatomic heart problems to confirm VT diagnosis.

Biomedical treatment- General overview

Biomedical treatment options are often used for serious cases of VT. They include defibrillation and cardioversion, which involve the use of electric currents. Devices such as pacemakers, implantable cardiac defibrillators, or automated external defibrillators (AED) deliver these electric jolts aimed at restoring a normal heartbeat. Implantable cardiac defibrillators are, for instance, used for patients who survive sudden cardiac arrest. Cardioversion involves the use of chest electrode patches or AEDs and a heart-monitoring machine in hospital settings. It is suitable for patients with myocardial infarction. Internal cardioversion involves the use of chest electrode patches and catheters inserted through a vein in the groin. Therapies that prevent and manage VT episodes include catheter ablation, used when there is an extra, discrete electrical pathway causing the tachycardia. It involves the insertion of catheters into the heart through blood vessels in the arms, neck, or groin. There are electrodes at the tips of the catheter that use radiofrequency or extreme cold to destroy that extra pathway, thus preventing it from the electrical transmission. Cardiac resynchronization therapy through a biventricular pacemaker also regulates the heartbeat and is used in VT management (Cedars-Sinai, 2020)

The defibrillator system uses and underlying mechanisms  

Defibrillation is the non-synchronized administration of electric shock at random during a cardiac cycle.  The electricity from an electrical device known as a defibrillator depolarizes the myocardium in an attempt to prevent or convert a dysrhythmia (non-perfusing rhythm) and allow or restore coordinated contractions. It is applied in conditions such as life-threatening V-tach, ventricular fibrillation, and cardiac arrest  (Cedars-Sinai, 2020). It is quite effective when used correctly for the appropriate type of VT. There are different types of defibrillators, including automated and semi-automated external defibrillators (AEDs),  wearable cardioverter-defibrillators and implantable cardiac defibrillators (ICDs) like the transvenous ICD and the subcutaneous implantable cardioverter-defibrillator (Ong, Lim, & Venkataraman, 2015).

External defibrillation is used in sudden cardiac arrest, life-threatening arrhythmias, and other cardiac emergencies to restore a normal heartbeat. It is performed as soon as such a situation is identified through unresponsiveness, lack of pulse, or from an ECG. A semi-automated external defibrillator has an ECG display, manual override, and can pace, unlike an automated ED. These external defibrillation devices have a battery that stores a large amount of energy at low energy levels when not in use. Its capacitor (comprising metal plate conductors that can store energy at very high levels) delivers the defibrillation current when the energy is released from the battery during a circuit. The AED prompts instruct a user to correctly use the machine for instance to patient and check that no one is inadvertently in contact with the patient. It assesses the heart’s electrical output, to establish whether the patient requires a shock and delivers it if necessary. There are two defibrillator systems. In monophasic systems (generating monophasic waveforms), current travels unidirectionally from the cathode to the anode. In biphasic systems, it moves from one electrode to another and goes back with polarity reversal several times. Biphasic waveforms are preferred to the monophasic shocks because they are safer and more efficient (Nichol, Sayre , Guerra , & Poole, 2017)

ICD wires are connected to the heart and work by monitoring the heart rhythm continuously. These devices have two parts, the battery-powered pulse generator monitors the heartbeat and is connected to the heart with a wire or wires (lead) that sends signals back and forth (familydoctor.org, 2019). ICDs are used for sustained or life-threatening VT caused by underlying heart conditions that predispose patients to recurrent episodes. Viable candidates include patients with stable sustained or hemodynamically unstable VT, those that survive out-of-hospital sudden cardiac death (SCD), or with a moderate risk of SCD and those with ischemic heart disease. ICDs are especially recommended if the VT has no reversible trigger. Another condition for qualification is if the patient’s estimated meaningful survival time is more than a year. When these devices detect an arrhythmia that meets the preprogrammed detection rates and arrhythmia duration, they overdrive or stop the pace of the VT or deliver the electric shock therapy to restore normalcy (Cedars-Sinai, 2020; Foth, Gangwani, & Alvey, 2020). The wearable cardioverter-defibrillator is an AED-ICD in-between and is used when an ICD is deferred, becomes unnecessary, or the risk of implantation is too high. It is a temporary protection against cardiac arrest.

The underlying cellular mechanism of action depends on the cellular characteristics that propagate electrical excitation in cardiac cells and muscles. The cell requires a sufficiently strong electrical stimulus for excitation and downstream development of action potentials, which the SA node can naturally provide. External signals in defibrillation come from electrodes. The strength of the shock should be enough to raise the cellular transmembrane potential to its activation threshold. Aside from the strength of the electrical stimulus, the state of the cell also determines its response to electric shock. The timing of the shock can, therefore, alter the response depending on whether the cell was at rest, in a refractory state, or a partially refractory state. A combination of the two factors determines the type of and response to the electrical field generated in the cell. Various responses include change or lack thereof in the duration of an existing action potential, the ability to trigger or prevent a new one, or terminate it prematurely or no effect to the action potential. Since cardiac cells do not respond independently, surroundings involved in electrical excitation such as extracellular space, gap junctions, fiber curvature, and tissue orientation, among others, influence the response to the electric field (Dosdall, Fast, & Ideker, 2014). With all these factors to consider, defibrillators are programmed in such a way that the shock harmoniously depolarizes the myocardium to either prevent or convert a dysrhythmia. The device monitors the heart’s rhythms, using it to decide on the timing and strength of the shock.

Reentrant VT terminated automatically by an ICD (Compton S. J., 2017)

Results, indications contraindications and risks

Although the survival rates for patients experiencing an out-of-hospital cardiac arrest are low (less than 10%), V-tach interventions such as early recognition, immediate CPR, and public access defibrillation raise these rates. In-hospital and after treatment survival rates are better than out-of-hospital, but the early recognition is crucial (Foth, Gangwani, & Alvey, 2020). Defibrillation as a therapy for life-threatening ventricular arrhythmias is often effective within the first five minutes. It prevents damage to the brain, further damage to the heart, and death by restoring a regular heart rate capable of producing a pulse  (Al-Khatib et al., 2017). The fact that defibrillators are both diagnostic and therapeutic means that they can preempt V-tach via diagnosis and intervene in the different ways presented depending on severity, for instance, pacing signals, cardioversion, and defibrillation for mild and strong shocks (familydoctor.org, 2019). Other therapies are used alongside defibrillation depending on the conditions and underlying diseases.

The primary indication for defibrillations is the presence of shockable rhythms as in unconscious VT, ventricular fibrillation, or cardiac conditions leading to the absence of a pulse. One, therefore, has to check the patient, the rhythm, and cardiac electrical activity to ensure that the shock is necessary. If inappropriately delivered, defibrillation may increase morbidity and mortality and worsen instead of improving the condition. It may trigger, rather than mediate, VT and cause physiological and mechanical damage to the cardiac system. Automation and implantable devices solve some of these issues. However, it is crucial to determine whether defibrillation is the correct treatment for the condition. One should check that no one else is inadvertently in contact with the patient during defibrillation and that they are in a safe, dry, non-conducting area. Defibrillation contraindications are the reverse of the indications. For instance, when the patient has non-shockable rhythms like bradycardias, conscious VT, asystole, supraventricular tachycardia, among others or a do not resuscitate order. Defibrillation presents risks such as skin burns from the defibrillator paddles, ICD shocks due to device malfunctions, electromagnetic interference, supraventricular arrhythmias, and ventricular arrhythmias that do not necessitate shocks. Irregular and abnormal heart rhythms, or further damage to the heart muscle and blood clots may also develop (AbdelWahab & Sapp, 2017; Ong, Lim, & Venkataraman, 2015).

Conclusion

Pulse rate one is of the vital signs medical practitioners use to determine a person’s wellbeing. Ventricular tachycardia occurs when the electrical impulses coordinating the heartbeat are not working as they should, resulting in a faster than usual pulse rate. It can range from mild and asymptomatic to life-threatening, depending on the causes and underlying mechanisms. There are various ways to treat VT aimed at restoring regular heart rate, controlling the tachycardia, or preventing future episodes. They depend on the cause, the type of VT, the level of severity, and symptoms. Defibrillation is a biomedical form of therapy that treats this condition. It has specific indications, and though it presents with some risk, it is very efficient when properly used.

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