Cardiac Activity and Ventricular Tachycardia (VT) Waveform

Cardiac Activity and Ventricular Tachycardia (VT) Waveform Lachlan Donnet-Jones Sudden cardiac death (SCD) is one of the leading causes of mortality in Australia. One of the primary causes of SCD is cardiac dysrhythmias, such as, Ventricular Tachycardia (VT). The most effective treatment for life-threatening cardiac dysrhythmias is defibrillation. This essay will examine the relationship between cardiac activity and the Ventricular Tachycardia (VT) waveform, and discuss how defibrillation may terminate this dysrhythmia, allowing the heart to return to a normal rhythm. The typical healthy adult heart will have a resting heart rate of between 60 and 100 beats per minute (Saladin, 2011). When the heart beats abnormally fast, it pumps less effectively, which decreases the level of perfusion to the tissue of the body, including the heart itself. This rapid heart rate increases the hearts muscle tissues (myocardium) demand for oxygen, and without intervention, can lead to the death of myocardial cells, which is known as a Myocardial Infarction (MI) (Huazers, 20). Each year in Australia approximately 55,000 people suffer a heart attack, or an Acute Myocardial Infarction (AMI). This is equal to 150 heart attacks per day or one in every 10 minutes (Heart Foundation). The Australian Bureau of Statistics reported that over 350,000 Australians will suffer an AMI at some point in their lives (ABS, health survey). In Trappes’ 2012 research article, Trappe notes that there is no single factor that causes an AMI, it is a multifactorial problem, however, approximately ninety percent of AMI’s are caused by tachyarrhythmia’s (Trappe, 2012). Before one can gain a thorough understanding of dysthymias, it is necessary to develop a fundamental grasp of the heart’s electrical conduction system and the associated physiology and pathophysiology. The primary function of the electrical conduction system is to transmit electrical impulses from the sinoatrial node (SA node) (normal site of conception) down to the atria and ventricles, triggering a contraction of heart muscle (myocardium) and controlling the heart rate. In a normal sinus rhythm, originating from the SA node, there are three phases; atrial depolarisation, ventricular depolarisation and atrial and ventricular repolarisation. The SA node is found within the wall of the right atrium proximal to the entrance of the superior vena cava. Similar to all electrical nodes within the heart, the SA node is composed of pacemaker cells which generate automatic and regular electrical impulses. These electrical impulses travel through the walls of the right atrium, causing contraction of the heart muscle (myocardium), to the atrioventricular node (AV node) via internodal conduction tracts (anterior, middle, and posterior). A final SA node conduction pathway, known as Bachmann’s bundle (interatrial conduction tract), transmits electrical impulses across the heart to the left atrium. On an electrocardiogram (ECG) this atrial depolarisation is represented by the P wave. The fibrous annulus is a non-conductive layer of tissue which prevents the electrical impulse from travelling outside the perimeter of the atrium. The primary function of the AV node is to process the electrical impulses from the atria to the bundle of His in a way that slows the impulses arrival at the ventricles by approximately 0.12 seconds. This delay allows for the atria to empty and the ventricles to fill before the next contraction. After the bundle of His, the electrical impulse will travel down the right bundle branch and the left common bundle branch. These bundle branches continue to subdivide into smaller branches, the smallest of which connect to the Purkinje network, an elaborate mesh of minute Purkinje fibres which spread throughout the ventricles. In a normal functioning heart it will take an electrical impulse approximately 0.2 seconds to travel from the SA node to the Purkinje network in the ventricles. On an ECG, this is shown as the P-R interval. At this point the impulse causes the ventricles to contract, pumping the blood out of the ventricles and into the systemic circulation. This depolarisation of the ventricles is represented by the QRS complex. Immediately following a QRS complex, is a period of time in which there is no electrical activity in the myocardium. This is known as the S-T segment and is normally represented as a flat line, level with the isoelectric line of an ECG. The proceeding T wave represents the repolarisation of the ventricles to their resting state. If at any point in this process the electrical impulse is disturbed, it can create a cardiac dysrhythmia, such as if the SA node were to produce rapid electrical impulses, resulting in tachycardia (fast heart beat). Ventricular Tachycardia (VT) is a type of tachycardia that originates within the inferior chambers of the heart, called the ventricles. The ventricles are the primary pumps of the heart, therefore, when they are compromised it can quickly deteriorate into a life-threatening dysrhythmia, such as, ventricular fibrillation (VF) or asystole (Chou, 2008). The diagnosis of VT is made by examining the rhythm seen on a 12-lead electrocardiogram (ECG). Although numerous diagnostic criteria have been developed, such as the ‘Brugada Criteria’ (Brugada, 1991), the following are the most commonly accepted (Riley, 2008). The rate of VT is above 100 per minute, typically 150 to 200, with a regular rhythm. The R-S complex is absent in precordial leads, and there are three or more consecutive Premature Ventricular Contractions (PVCs) present (AV dissociation). The ectopic pacemaker is below the Atrioventricular node (AV node), therefore, the PR interval is irrelevant. In addition, different ambulance services will have their own specific diagnostic criteria for VT, for example, Ambulance Tasmania (AT) Clinical Practice Guidelines (CPG’s) state that the rhythm must present with QRS complexes of over 0.12 seconds, and be sustained for a period of over 30 seconds (sustained VT). VT can be classified using three methods; morphology, episode duration, and symptoms. In regards to morphology, there are two primary categories of VT; monomorphic and polymorphic. Monomorphic VT has numerous causes, but is determined by consistent appearance across all leads of an ECG. A common reason that the beats from each lead appear the same, is because the impulse is being generated from an increased rate of automaticity in a single point from the left or right ventricles. This means that the pacemaker cells, such as the Purkinje fibres in the left and right ventricles, that are able to reach an action potential on their own accord (automaticity), have increased the rate at which they fire impulses (intrinsic rate). Another reason for monomorphic VT is due to the presence of a re-entry circuit within the ventricle. A re-entry circuit occurs when an electrical impulse constantly travels in a constricted circle within the heart, as opposed to moving from one end of the heart to the other, like a normal electrical impulse circuit. Although monomorphic VT has many causes and contributing factors, the most common cause is scarring of the myocardial tissue from a previous MI episode. The scarred tissue left behind does not conduct electrical impulses, and therefore, the potential for a circuit around the scar can result in tachycardia. This is similar to the aforementioned re-entrant circuit, and is a common cause of other dysrhythmias, such as, atrial flutter (Af) and supraventricular tachycardia (SVT). Scar-related monomorphic VT is predominantly prevalent in patients who have a previously survived a MI, particularly in those who have damaged myocardium as a result (John, reference). Unlike the cons istent rhythm seen is monomorphic VT, polymorphic VT is an irregular rhythm that has constant variations in its morphology. A second method to define VT is studying the duration of the episode. Three or more consistent contractions on an ECG, originating from within a ventricle at over 100 beats per minute, is determined as VT. If the tachycardia rhythm terminates itself in under 30 seconds, it is considered non-sustained VT. If the rhythm continues beyond 30 seconds, it is considered sustained VT. The final method to classify VT is reviewing symptoms. When a patient is in VT, the loss of co-ordinated atrial contraction and high heart rate can impair cardiac output (CO), and therefore, they will not have a palpable pulse. This is known as Pulseless VT. Pulseless VT is concomitant with an absence of cardiac output (CO), and therefore, according to AT clinical practice guidelines, is to be treated as worst case scenario, which is ventricular fibrillation (VF), a shockable rhythm (CPG Reference). In a report from the American College of Cardiology, Zipes et. al note that VT can occasionally be accompanied by reasonable cardiac output and may even present as asymptomatic, however, the heart will not tolerate this rhythm for a sustained period of time, and will eventually deteriorate to pulseless VT or VF. Supraventricular Tachycardia (SVT) with a bundle branch block (BBB) or Wolff-Parkinson-White syndrome is commonly misdiagnosed as VT (Trappe). This is due to the similar diagnostic characteristics, such as, wide QRS complexes and high heart rates, which are mutual in all wide complex tachycardia (litfl). It is important to differentiate the two because certain medications used to treat SVT could potentially worsen the patient’s condition. As Trappe notes in his research article ‘Treating critical supraventricular and ventricular arrhythmias’, it is always beneficial to treat for the worst case scenario, in this case, VT (Trappe, 2010). This opinion is mutual in regards to Ambulance Tasmania CPG’s, where it recommends treating for worst case scenario. Once a shockable dysrhythmia has been recognised, it is necessary to intervene with an external source of electrical activity to correct the hearts rhythm. Defibrillation is the standard and most effective treatment for cardiac dysrhythmias, such as VT and VF (Reference). Defibrillation is the process of using a device called a defibrillator to deliver a therapeutic measure or ‘shock’ of electrical current through the heart. The current delivered, aims to depolarise a critical mass (Critical mass theory**) of the heart muscle (myocardium), interrupting the dysrhythmia and allowing the heart’s natural pacemaker, the SA node, to return to a normal sinus rhythm. Defibrillators are becoming widely available in the form of transvenous, implanted (implantable cardioverter-defibrillator), or external (automated external defibrillators) devices. Despite the different forms a defibrillation device may present in, they all operate on the same principle. There are two different methods of delivering an electrical shock from a defibrillation device; monophasic and biphasic waveforms. Monophasic is the ‘old’ method in which the electrical current travelled in one direction through a patient’s chest. The second method is using a biphasic waveform, meaning the current is delivered to the heart in two vectors (two directions). Due to the use of two vectors, the peak electrical current needed to revert a dysrhythmia is decreased to 200 joules, as opposed to 360 joules of a monophasic waveform. Due to the high voltage (360 joules) used in monophasic waveform it can cause superficial burns to the patients skin. Additionally, _____ found the use of a biphasic waveform to be more effective at returning the heart to a sinus rhythm and resulted in less damage to myocardium, leading to better patient outcomes (Reference) . ____ notes that for the aforementioned reasons, monophasic waveform defibrillation is quickly being replaced with biphasic (Reference). Page 1 of 5