Monomorphic Ventricular Tachycardia
Cardiac arrhythmias often require immediate medical care that may include resuscitation (Ray, 2004). The diagnosis of cardiac arrhythmias can be challenging particularly in situations whereby the patient is asymptomatic and ECG findings are normal between symptomatic episodes (Cruickshank, 2008). Distinguishing between supraventricular and ventricular tachycardia is also a challenge (Australian Resuscitation Council, 2008). Cardiac arrhythmia should be suspected in patients with a history of syncope, near syncope, palpitations, and/or chest pain (Cruickshank, 2008). This paper will justify why monomophic ventricular tachycardia is the most likely diagnosis of a male patient who collapsed abruptly and has hypotension (BP 63/38), tachycardia (135 beats/min), tachypnea (RR 28), Spo2 of 91%. His skin is also cool and clammy. The paper will further describe the pre-hospital management of the patient as well as the initial 24 hours management of the patient in hospital settings.
Pathophysiology and Etiology
At the cell level, ventricular tachycardia occurs due to abnormal automaticity or electrical reentry. The possibility of electrical reentrant circuits is increased in the presence of myocardial scarring. The electrical reentrant circuits largely involve a zone in which normal conduction of electrical signals is slowed by a scar. The origin of sustained monomorphic ventricular tachycardia in most cases is usually a ventricular scar formed during a prior myocardial infarction. Ventricular tachycardia in a heart that is essentially normal structurally results from mechanisms like enhanced automaticity and triggered activity. Cardiac output during ventricular tachycardia is decreased as a result of reduced ventricular filling from one, rapid heart rate and two, inappropriately timed and poorly coordinated atrial contraction. Mitral inadequacy and ischemia can additionally contribute to reduced ventricular stroke output as well as hemodynamic intolerance. Very rapid heart rates and an underlying dysfunction of the left ventricle increase the probability of hemodynamic collapse during ventricular tachycardia. Reduced cardiac output leads to reduced myocardial perfusion. This worsens the inotropic response and can degenerate to ventricular fibrillation and sudden cardiac death. However, ventricular tachycardia can also elicit congestive heart failure and consequently, hemodynamic compromise in the absence of an underlying structural heart disease (Tung, Boyle, and Shivkumar, 2010).
As already described, ventricular tachycardia can occur in the presence or absence of structural heart disease. Conditions that result in the creation of myocardial scar tissue, the substrate for electrical reentry, include ischemic heart disease, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia (Marcus et al., 2010), hypertrophic cardiomyopathy, surgical incisions of the ventricle, and chagas disease (Compton, 2015). Ventricular tachycardia that occurs in the absence of structural heart conditions can be due to enhanced automaticity. Enhanced automaticity frequently originates from the right ventricular outflow tract or bundle of fibers of the heart’s conduction system. Bundle-branch reentrant ventricular tachycardia occurs in those patients with disease of the conduction system that are distal to the His bundle. Functional reentrant ventricular tachycardia occurs in patients who have inherited channelopathies but otherwise structurally normal hearts. Ventricular tachycardia can also be caused by electrolyte deficiencies, systemic diseases affecting the myocardium, digitalis toxicity, sympathomimetic agents, and drugs that lengthen the QT interval or those that slow the velocity of conduction (Brugada, Brugada, and Brugada, 2007).
Signs and Symptoms
The patient with ventricular tachycardia presents with palpitations, syncope, anxiety, chest pain, and dyspnea. Patients with very rapid heart rates or impairments of the left ventricle often present with signs of hemodynamic compromise. Physical examination for patients experiencing ventricular tachycardia can reveal signs of decreased perfusion such as reduced level of consciousness, diaphoresis, and pallor. It can also reveal hypotension, high jugular venous pressure, and variations in the intensity of the first heart sound (Sanders, McKenna, Lewis, and Quick, 2012). The patient in this case has a rapid heart rate of 135 and hence can be said to have ventricular tachycardia. Ventricular tachycardia is defined as a rhythm more than 100 and in some cases 120 beats per minute with 3 or more consecutive irregular heartbeats. Notably though, no information is provided on the regularity of the patient’s pulse rate. The patient in this case also has signs of decreased cerebral perfusion, fluctuating levels of consciousness and reduced peripheral perfusion that are cool, clammy extremities. The patient is also hypotensive with a BP of 63/38 and also has tachypnea with a breathing rate of 28. The patient’s family history of sudden premature death (paternal grandfather’s abrupt death at 38 years of age) is also suggestive of an underlying structural heart disease. The patient’s past medical history is not available hence the possibility of a condition that can cause myocardial scarring cannot be ruled out.
Diagnosis of Ventricular Tachycardia
The diagnosis of ventricular tachycardia in a patient who is unconscious or hemodynamically unstable like the patient in this case is based on physical examination findings and 12-lead ECG findings (American Heart Association, 2005). The ECG attributes of ventricular tachycardia are wide QRS complexes, pulse rate >100, regular rhythm although there may be some level of beat-to-beat variation, and constancy of the QRS complex (Levis, 2011). Ventricular tachycardia can either be polymorphic or monomorphic. Polymorphic ventricular tachycardia occurs when the QRS complex differs from beat to beat. It indicates variations in electrical activation sequence. Monomorphic ventricular tachycardia refers to a situation whereby the ECG pattern remains constant. It denotes constancy in the ventricular activation sequence and is often seen in patients with an underlying structural heart defect. Ventricular tachycardia should be differentiated from supraventricular tachycardia. This is because inappropriate treatment of ventricular tachycardia with medications used for the treatment of supraventricular tachycardia can have adverse consequences such as severe hemodynamic deterioration, ventricular fibrillation, and cardiac arrest (Levis, 2011). In cases where the patient is unstable and differentiation of ventricular tachycardia from supraventricular tachycardia is uncertain, the presenting rhythm should be managed as ventricular tachycardia (Australian Resuscitation Council, 2009). Physical examinations findings in the patient with ventricular tachycardia are likely to reflect hemodynamic instability but do not indicate the mechanism of tachycardia. Wide-complex regular tachydysrhythmias that fail to exhibit regular sinus activity should be managed as ventricular tachycardia. Atrioventricular dissociation, when present, is diagnostic of ventricular tachycardia (Alzand and Crijins, 2010). Atrioventricular dissociation is, however, difficult to detect on a 12-lead ECG (Levis, 2011).
Pre-Hospital Management of Ventricular Tachycardia
The Australian Resuscitation Council 2009 Guideline 11.9 on management of acute dysrhythmias recommends that in peri-arrest settings, broad-complex tachycardia should be assumed to be of ventricular origin. This recommendation is informed by the fact that management of supraventricular tachycardia as if it was ventricular tachycardia is less likely to lead to more deterioration of the patient than treatment of ventricular tachycardia as supraventricular tachycardia. Although the patient in this case has a pulse, he is unstable and has worsening of adverse features. Therefore, he should be managed using advanced life support guidelines (Australian Resuscitation Council, 2009). The pre-hospital management of this patient will thus involve assessment of ABCDE, administration of oxygen, 12-lead ECG, establishment of intravenous access, cardiopulmonary resuscitation, direct current electrical cardioversion (Zipes et al., 2006), administration of amiodarone, transportation of the patient to a hospital for definitive care, and continuous cardiac monitoring of the patient en-route to the hospital. 300mg of amiodarone should be administered intravenously slowly over 10-20 minutes if electrical cardioversion is unsuccessful (Australian Resuscitation Council, 2016). Electrical cardioversion should then be repeated.
Initial 24-hour management of Ventricular Tachycardia
The initial hospital management of the patient will follow advanced cardiac life support protocols (Australian Resuscitation Council, 2009). The patient is admitted in a monitored bed. After the initial dose of amiodarone, an infusion of the drug (900 mg) should be given over 24 hours (Cruickshank, 2008). If a sinus rhythm will have been restored and the patient stabilized by the time he reaches the hospital, history taking and laboratory tests can be performed. A 12-lead ECG is repeated (Editore, 2014). Laboratory studies that can be performed include assessment of electrolyte levels to include serum calcium, potassium, magnesium, and phosphate levels. Serum levels of therapeutic agents like digoxin and toxicology screens need also to be evaluated (Compton, 2015). Assays of markers of myocardial ischemia or infarction are also indicated. Echocardiography and cardiac imaging studies like MRIs are also indicated. Reversible causes of ventricular tachycardia are then addressed depending on the findings of the laborotary studies. The patient is also started on antiarrhythmic medications (Tung, Boyle, and Shivkumar, 2010).
Conclusion
In summary, this paper has diagnosed a patient with a history of sudden collapse and hemodynamic compromise as having monomorphic ventricular tachycardia. Ventricular tachycardia is most often caused by structural anomalies of the heart although it can be triggered by other causes such as electrolyte imbalances. On 12-lead ECG, monomorphic ventricular tachycardia presents as wide-complex but regular QRS waves. Presenting symptoms of ventricular tachycardia include reduced levels of consciousness, dyspnea, and hypotension amongst others signs present in this patient. The pre-hospital management of this patient includes history taking, assessment according to the ABCDE algorithm, 12-lead ECG, and immediate electrical cardioversion. The initial 24 hour hospital management will incorporate admission into a monitored bed, history taking, 12-lead ECG, antiarrhythmic medications, and diagnostic tests.
References
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