The Diagnosis and Treatment of Arrhythmia

Arrhythmias cause irregular hearts beats in ways that can be life-threatening but there are a number of different types of arrhythmias that require different interventions. To determine the facts, this paper reviews the relevant literature to provide the etiology and pathogenesis, prevalence, clinical signs and symptoms, diagnostic pathways and optimal therapeutic approaches for paroxysmal atrial tachycardia, ventricular fibrillation and Brady arrhythmias, followed by a summary of the research and important findings concerning these three disease states in the conclusion.

Paroxysmal Atrial Tachycardia

Etiology & Pathogenesis. This type of arrhythmia can occur in individuals who have normal hearts as well as in people who have structurally abnormal hearts including those with congenital heart disease, especially following surgical repair of valvular or congenital heart disease (Budzikowski & Rottman 2015).

Common causes of the arrhythmia, risk factors, definition of rhythm via EKG findings. Paroxysmal Atrial Tachycardia (PAT) is caused by irregular firing of the electrical signals in the heart's upper chambers which then affects the electrical signals transmitted from the heart's natural pacemaker, the sinoatrial node (Overview of Paroxysmal Atrial Tachycardia 2016). As a result, the heart rate is accelerated which adversely affects the normal blood-pumping processes of the heart and the normal flow of oxygen and blood (Overview of Paroxysmal Atrial Tachycardia 2016).

Prevalence/Incidence. In the United States, there are approximately 89,000 new cases of PAT each year and about 570,000 individuals suffer from the condition (Orejarena & Vidailletpersons 1998). This population is comprised of two subgroups: (a) those with PAT as well as (b) those who also suffer from other cardiovascular disease conditions (Orejarena & Vidailletpersons 1998).

Clinical Signs & Symptoms. The majority of PAT sufferers do not experience any discernible clinical signs or symptoms; however, in some cases, PAT sufferers may experience any of the follows:

Lightheadedness;

Dizziness;

Heart palpitations;

Angina; and,

Breathlessness (Overview of Paroxysmal Atrial Tachycardia 2016).

In addition, but more rarely, PAT can also cause unconsciousness and/or cardiac arrest (Overview of Paroxysmal Atrial Tachycardia 2016).

Diagnostic Pathways. In most cases, an electrocardiogram (ECG) test is used to diagnose PAT (Overview of Paroxysmal Atrial Tachycardia 2016).

Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. Although the majority of individuals who experience a PAT will not require any medicinal or interventional therapy, for those who suffer from frequently recurring or severe episodes may require such treatments (Overview of Paroxysmal Atrial Tachycardia 2016). In some cases, vagal maneuvers are prescribed to slow the heart rate; if these methods are inadequate to resolve the condition, pharmacological interventions may be prescribed, including .

flecainide (Tambocor) or propafenone (Rythmol) to slow the heart rate (Overview of Paroxysmal Atrial Tachycardia 2016). In extreme cases, a catheter ablation may be required (Overview of Paroxysmal Atrial Tachycardia 2016). In addition, Burke and Laramie (2000) report that beta blockers can also be used to control the heartbeat rate in a majority of episodic paroxysmal atrial tachycardia events.

Ventricular fibrillation

Etiology & Pathogenesis. This is the most common arrhythmia type and left untreated can be life-threatening within minutes of onset (Gialama & Prezerakos 2014). Ventricular fibrillation (VF) is caused by the erratic firing of electrical impulses from the heart ventricles, limiting the heart's ability to pump sufficient amounts of blood and oxygen (Gialama & Prezerakos 2014). A number of risk factors exist for this condition, including the following:

Previous myocardial infarction (MI);

Coronary artery disease (CAD);

Left ventricular ejection fraction (LVEF) of less than 40% combined with ventricular tachycardia (VT);

Prior episode of sudden cardiac arrest (SCA);

Family history of SCA or sudden cardiac death (SCD);

Personal or family history of certain abnormal heart rhythms such as long QT syndrome (LQTS); Wolff-Parkinson-White syndrome; extremely low heart rates or heart block;

VT or VF after a myocardial infarction (MI);

Blood vessel abnormalities;

History of syncope (fainting episodes of unknown cause);

Heart failure (HF);

Dilated cardiomyopathy (DCM);

Hypertrophic cardiomyopathy (HCM);

Significant changes in blood levels of potassium and magnesium (from using certain drugs);

Obesity;

Diabetes mellitus;

Recreational drug abuse;

Genetic factors; and,

Molecular and other structural heart defects (Gialama & Prezerakos 2014)

Prevalence. Although precise numbers are unavailable because a number of VF episodes are not recorded, current estimates indicate that up to 33% of the approximately 300,000 new cases of SCD each year are caused by VF (Goyal & Rottman 2016). This rate equals an incidence of between 0.08-0.016% per year in the adult population of the United States, but even this seemingly modest incidence means that VF accounts for more deaths each year than from lung cancer, breast cancer, or acquired immunodeficiency syndrome (Goyal & Rottman 2016). By contrast, the pediatric and adolescent age groups are estimated to have an annual incidence of 1.3-8.5 cases of VF per 100,000 persons annually, representing about 5% of all deaths in these age groups (Goyal & Rottman 2016).

Clinical Signs & Symptoms. The clinical signs and symptoms of VF include the following:

Chest pain;

Rapid heartbeat (tachycardia);

Dizziness;

Nausea;

Shortness of breath; and,

Loss of consciousness (Symptoms of ventricular fibrillation 2016).

Diagnostic Pathways. Ventricular fibrillation can be diagnosed using the following methods:

Heart monitoring;

Electrocardiogram;

Blood tests;

Chest x-ray;

Echocardiogram;

Angiogram; and,

Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI) (Tests and diagnosis for ventricular fibrillation 2016).

Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. According to Gialama and Prezerakos (2014), beta blockers, angiotensin-converting enzyme (ACE) inhibitors, statins and calcium channel blockers can all be used to manage VF. In addition, potassium channel blockers and amiodarone have been shown to be efficacious in the long-term management of ventricular arrhythmias (Gialama & Prezerakos 2014). In some cases, implantable cardioverter defibrillators (ICDs) may be required to moderate the heart beat (Gialama & Prezerakos 2014).

Brady Arrhythmias

Etiology & Pathogenesis. This type of arrhythmias occurs when the heart fails to beat at least 60 times per minute (Brady arrhythmias 2016). This can be caused by sick sinus syndrome or heart block (Brady arrhythmias 2016). Interventions, though, are not typically required until the heart beat is reduced to fewer than 40 beats per minute (Brady arrhythmias 2016). There are several different types of brady arrhythmias, including (a) sinus bradycardia and (b) atrioventricular electrical impulse conduction delays (these include first-degree atrial-ventricular block; second-degree atrial-ventricular block (Mobitz I and II); and third-degree, or complete heart block (Waldstein & Elias 2001).