Cardiac Activity and Ventricular Tachycardia (VT) Waveform

Cardiac Activity and Ventricular Tachycardia (VT) beat formLachlan Donnet-J wizardsSudden cardiac demolition (SCD) is bingle of the leading causes of mortality in Australia. One of the special causes of SCD is cardiac dysrhythmias, such as, Ventricular Tachycardia (VT). The close to efficacious ploughment for life-threatening cardiac dysrhythmias is defibrillation. This essay will control the relationship between cardiac application and the Ventricular Tachycardia (VT) wave form, and discuss how defibrillation whitethorn terminate this dysrhythmia, allowing the fancy to return to a normal rhythm.The typical estimable adult embrace will have a resting titty identify of between 60 and 100 crush per minute (Saladin, 2011). When the gist beats abnormally fast, it pumps less effectively, which decreases the level of perfusion to the tissue of the body, including the tender unionedness itself. This rapid softheartedness rate increases the hearts muscle tissues (myocardi um) demand for oxygen, and without intervention, shtup lead to the death of myocardial cells, which is know as a Myocardial Infarction (MI) (Huazers, 20). individually 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 look for article, Trappe notes that thither is no single factor that causes an AMI, it is a multifactorial problem, however, approximately 90 percent of AMIs atomic number 18 caused by tachyarrhythmias (Trappe, 2012).Before one hindquarters gain a thorough understanding of dysthymias, it is necessary to expatiate a fundamental grasp of the hearts electric parcel outivity system and the associated physiology and pathophysiology. The primary function of the galvanic conduction system is to stockpile electric pulse rates from the sinoatrial knob (SA thickener) (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 fistula rhythm, originating from the SA node, there argon three phases atrial depolarization, ventricular depolarisation and atrial and ventricular repolarisation. The SA node is found at bottom the wall of the right atrium proximal to the entrance of the superior vena cava. Similar to all electric 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 lowest SA node conduction pathway, known as Bachmanns bundle (inte ratrial 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 stage 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 h gaga up 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 discriminate and the left jet bundle branch. These bundle branches continue to subdivide into little branches, the smallest of which connect to the Purkinje nedeucerk, 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 ne 2rk 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 originat es within the inferior chambers of the heart, called the ventricles. The ventricles atomic number 18 the primary pumps of the heart, therefore, when they atomic number 18 compromised it can quickly throw 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 in a higher place 100 per minute, typically 150 to 200, with a regular rhythm. The R-S complex is preoccupied in precordial leads, and there are three or more consecutive Premature Ventricular Contractions (PVCs) present (AV dissociation). The ectopic pacemaker is infra the Atrioventricular node (AV node), therefore, the PR interval is irrelevant. In addition, different ambulance function will have thei r own specific diagnostic criteria for VT, for example, Ambulance Tasmania (AT) Clinical do Guidelines (CPGs) state that the rhythm must present with QRS complexes of over 0.12 seconds, and be prolong for a period of over 30 seconds (sustained VT).VT can be classified ad using three manners 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 self-consistent display across all leads of an ECG. A common movement that the beats from from each one 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 nitty-gritty 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 lot (automaticity), have increased the rate at which they fire impulses (intrins ic rate).Another reason for monomorphic VT is due to the presence of a re-entry roofy within the ventricle. A re-entry circuit occurs when an electrical impulse constantly travels in a constricted wad 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 add factors, the most common cause is scarring of the myocardial tissue from a antecedent 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 customary in patients who have a previously survived a MI, particularly in those who have damaged myocardium as a result (John, reference). Unlike the c onsistent 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 siding (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 lather solecism scenario, which is ventricular fibrillation (VF), a shockable rhy thm (CPG Reference). In a report from the American College of Cardiology, Zipes et. al note that VT can once in a while be accompanied by reasonable cardiac output and may even present as asymptomatic, however, the heart will not resist 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, long-cut 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 patients 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 opinio n is mutual in regards to Ambulance Tasmania CPGs, where it recommends treating for worst case scenario.Once a shockable dysrhythmia has been recognised, it is necessary to intervene with an external man-made lake 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 hearts 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 defibrill ation 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 patients 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 postulate 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 interrupt patient outcomes (Reference). ____ notes that for the aforementioned reasons, mono phasic waveform defibrillation is quickly being replaced with biphasic (Reference).Page 1 of 5