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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 very best treatment for life-threatening cardiac dysrhythmias is defibrillation. This article will examine the partnership 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 center will have a relaxing heartrate of between 60 and 100 beats each and every minute (Saladin, 2011). If the heart is better than abnormally fast, it pumps less effectively, which reduces the level of perfusion to the structure of your body, including the center itself. This immediate heart rate escalates the hearts muscle tissues (myocardium) demand for oxygen, and without intervention, can lead to the loss of life of myocardial skin cells, which is actually a Myocardial Infarction (MI) (Huazers, 20??).

Each time in Australia approximately 55, 000 people undergo a coronary attack, or an Severe Myocardial Infarction (AMI). This is add up to 150 heart episodes per day or one atlanta divorce attorneys 10 minutes (Heart Foundation). The Australian Bureau of Figures reported that over 350, 000 Australians are affected an AMI at some point in their lives (Washboard abs, health study). In Trappes' 2012 research article, Trappe records that there surely is no single factor that triggers an AMI, this can be a multifactorial problem, however, about ninety percent of AMI's are induced by tachyarrhythmia's (Trappe, 2012).

Before you can gain a thorough knowledge of dysthymias, it is necessary to develop a fundamental knowledge of the heart's electric powered conduction system and the associated physiology and pathophysiology. The primary function of the electrical conduction system is to transmit electric powered impulses from the sinoatrial node (SA node) (normal site of conception) down to the atria and ventricles, triggering a contraction of heart and soul muscle (myocardium) and handling 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 structure of the right atrium proximal to the access of the superior vena cava. Similar to all electric powered nodes within the heart and soul, the SA node is composed of pacemaker cells which generate computerized and regular electric powered impulses.

These electrical impulses travel through the walls of the right atrium, triggering contraction of the center muscle (myocardium), to the atrioventricular node (AV node) via internodal conduction tracts (anterior, middle, and posterior). Your final SA node conduction pathway, known as Bachmann's bundle (interatrial conduction tract), transmits electric impulses over the heart left atrium. With an electrocardiogram (ECG) this atrial depolarisation is represented by the P influx. The fibrous annulus is a non-conductive layer of structure which inhibits the electro-mechanical impulse from travelling beyond your perimeter of the atrium.

The major function of the AV node is to process the electrical impulses from the atria to the pack of His in a way that slows the impulses entrance at the ventricles by about 0. 12 seconds. This delay allows for the atria to clear and the ventricles to fill up prior to the next contraction. After the pack of His, the electronic impulse will travel down the right bundle branch and the kept common bundle branch. These package branches continue steadily to subdivide into smaller branches, the tiniest of which hook up to the Purkinje network, an elaborate mesh of minute Purkinje fibres which spread throughout the ventricles. In a normal functioning heart it will require an electrical impulse roughly 0. 2 seconds to visit from the SA node to the Purkinje network in the ventricles. By using an ECG, this is shown as the P-R period.

At this point the impulse causes the ventricles to long term contract, pumping the blood from the ventricles and into the systemic blood flow. This depolarisation of the ventricles is represented by the QRS organic. Immediately following a QRS complex, is a time frame in which there is absolutely no electric powered activity in the myocardium. That is known as the S-T segment and is normally represented as a set line, level with the isoelectric line of an ECG. The proceeding T influx represents the repolarisation of the ventricles with their resting state. If at any point in this process the electronic impulse is disturbed, it can create a cardiac dysrhythmia, such as if the SA node were to produce rapid electric powered impulses, leading to tachycardia (fast pulse).

Ventricular Tachycardia (VT) is a type of tachycardia that originates within the poor chambers of the center, called the ventricles. The ventricles will be the most important pumps of the heart and soul, therefore, when they are affected it can easily deteriorate into a life-threatening dysrhythmia, such as, ventricular fibrillation (VF) or asystole (Chou, 2008). The medical diagnosis of VT is manufactured by evaluating the rhythm seen on the 12-lead electrocardiogram (ECG).

Although numerous diagnostic requirements have been developed, including the 'Brugada Standards' (Brugada, 1991), the following are the most commonly accepted (Riley, 2008). The speed of VT is above 100 per minute, typically 150 to 200, with a normal rhythm. The R-S organic is absent in precordial leads, and there are three or even 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. Furthermore, different ambulance services will have their own specific diagnostic requirements for VT, for example, Ambulance Tasmania (AT) Clinical Practice Recommendations (CPG's) declare that the rhythm must present with QRS complexes of over 0. 12 seconds, and become sustained for a period of over 30 seconds (sustained VT).

VT can be labeled using three methods; morphology, show period, and symptoms.

In relation to morphology, there are two primary types of VT; monomorphic and polymorphic. Monomorphic VT has numerous causes, but is determined by consistent appearance across all leads of any ECG. A common reason that the beats from each lead seem the same, is basically because the impulse is being generated from an elevated rate of automaticity in a single point from the kept or right ventricles. Which means that the pacemaker cells, like the Purkinje fibres in the kept and right ventricles, that are able to reach an action potential on their own accord (automaticity), have increased the pace of which they fire impulses (intrinsic rate).

Another reason behind 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 group within the center, instead of moving from one end of the center to the other, like a normal electronic impulse circuit. Although monomorphic VT has many causes and contributing factors, the most common cause is scarring of the myocardial tissue from a prior MI episode. The scarred muscle left behind will not conduct electric powered impulses, and for that reason, the potential for a circuit throughout the scar can result in tachycardia. This is like the above mentioned re-entrant circuit, and it is a common reason behind other dysrhythmias, such as, atrial flutter (Af) and supraventricular tachycardia (SVT). Scar-related monomorphic VT is mainly widespread in patients who've a previously survived a MI, specifically in those who have damaged myocardium therefore (John, reference point). Unlike the steady rhythm seen is monomorphic VT, polymorphic VT can be an irregular tempo that has frequent variations in its morphology.

A second solution to explain VT is studying the period of the instance. Three or more consistent contractions on an ECG, from inside a ventricle at over 100 beats per minute, is determined as VT. In case the tachycardia tempo terminates itself within 30 seconds, it is known as non-sustained VT. If the rhythm proceeds beyond 30 seconds, it is considered sustained VT.

The final solution to classify VT is looking at symptoms. When a patient is within VT, the loss of co-ordinated atrial contraction and high heart rate can impair cardiac end result (CO), and for that reason, they will not have a palpable pulse. That is known as Pulseless VT. Pulseless VT is concomitant with an lack of cardiac result (CO), and therefore, regarding to AT scientific practice guidelines, is to be treated as most detrimental case scenario, which is ventricular fibrillation (VF), a shockable tempo (CPG Guide). In a written report from the North american School of Cardiology, Zipes et. al remember that VT can occasionally be combined with reasonable cardiac result and may even present as asymptomatic, however, the center will not tolerate this rhythm for a continual time frame, and can eventually deteriorate to pulseless VT or VF.

Supraventricular Tachycardia (SVT) with a lot of money branch stop (BBB) or Wolff-Parkinson-White symptoms is often misdiagnosed as VT (Trappe). This is because of the similar diagnostic characteristics, such as, large QRS complexes and high heart and soul rates, which are mutual in every wide intricate tachycardia (litfl). It's important to differentiate the two because certain medications used to take care of SVT may potentially aggravate 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 most detrimental case scenario, in cases like this, VT (Trappe, 2010). This opinion is mutual when it comes to Ambulance Tasmania CPG's, where it advises treating for most severe case situation.

Once a shockable dysrhythmia has been accepted, it's important to intervene with an external way to obtain electrical activity to improve the hearts tempo. Defibrillation is the standard and most effective treatment for cardiac dysrhythmias, such as VT and VF (Reference point). Defibrillation is the procedure of using a device called a defibrillator to provide a therapeutic solution or 'shock' of electric current through the center. The current sent, aspires to depolarise a crucial mass (Critical mass theory**) of the heart and soul muscle (myocardium), interrupting the dysrhythmia and allowing the heart's natural pacemaker, the SA node, to return to a standard sinus tempo. Defibrillators are becoming widely available in the form of transvenous, implanted (implantable cardioverter-defibrillator), or external (automated external defibrillators) devices.

Despite different forms a defibrillation device may within, they all are powered by the same basic principle. You can find two different ways of delivering a power distress from a defibrillation device; monophasic and biphasic waveforms. Monophasic is the 'old' method in which the electronic current travelled in a single direction via a patient's chest. The second method is using a biphasic waveform, signifying the current is sent to the heart and soul in two vectors (two directions). Due to the use of two vectors, the optimum electrical current needed to revert a dysrhythmia is lowered to 200 joules, as opposed to 360 joules of your monophasic waveform. Due to the high voltage (360 joules) found in monophasic waveform it can cause superficial burns to the patients epidermis. On top of that, _____ found the use of the biphasic waveform to be more effective at returning the heart and soul to a sinus tempo and led to less harm to myocardium, resulting in better patient outcomes (Research). ____ notes that for the aforementioned reasons, monophasic waveform defibrillation is quickly being replaced with biphasic (Reference).

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