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This chapter discusses ventricular arrhythmias, which occur due to abnormal electrical activity in the heart. The three main types covered are premature ventricular contractions (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF). PVCs are extra beats from the ventricles, often occurring in older people with heart disease. VT is a rapid ventricular rhythm that can lead to sudden cardiac death. VF is the most lethal arrhythmia, causing uncoordinated contractions of the ventricles. Treatment options include medications, cardioversion, and implantable cardioverter defibrillators (ICDs). Chapter 4 Ventricular Cardiac Arrhythmias There are a variety of ventricular arrhythmias which are the topic of this chapter. They occur when there is an abnormality in the electrical activity of the heart, which may result in a fast heartbeat, the absence of a perfusable heartbeat, or an irregularity of the heartbeat. A ventricular arrhythmia can cause a sudden decrease in cardiac output and complications including sudden cardiac death. The three main ventricular arrhythmias covered in this chapter include premature ventricular contractions, or PVCs, ventricular tachycardia, and ventricular fibrillation. Premature Ventricular Contractions Premature ventricular contractions, or PVCs, are the most common irregular heart rhythm, especially in older people who have known heart disease. Normally the SA node is the pacemaker of the heart. With PVCs, extra beats from the ventricles replace the normal SA node electrical signal. They happen before SA node impulses and are followed by a brief pause and finally a stronger heartbeat. The heart has extra blood in it from the pause, so there is a more forceful beat after the PVC. PVCs can be random or occur at specific intervals. PVCs are extremely common. Among healthy young individuals, the incidence of PVCs is about 0.5% in people under 20 years of age and about 2% in people over the age of 50 years. People with a family history of irregular heartbeats will have a greater incidence of PVCs. Anyone with a history of heart disease has an increased risk of PVCs. PVCs can occur at any age and most cases are idiopathic. However, the incidence is higher among people with heart disease. Electrolyte abnormalities can cause PVCs as well as certain medications, high stress levels, caffeine, alcohol, exercise, and illicit drug use. Most patients with PVCs do not need treatment unless they are frequent and symptomatic. Reducing triggers like tobacco use and caffeine use can decrease the incidence of PVCs. The main medication for PVCs is a beta blocker, although amiodarone and calcium channel blockers have been used. Radiofrequency ablation of the ectopic site is used when medications fail to control the frequent beats. Ventricular tachycardia Ventricular tachycardia is the second most common cause of sudden cardiac death after ventricular fibrillation, causing about 300,000 deaths in the U.S. alone per year. V-tach, or VT, is any rapid ventricular rhythm with at least three ventricular beats originating at or distal to the bundle of his. The rate is at least 100 beats per minute. Refer to Figure 1 for an ECG rhythm strip of ventricular tachycardia. The incidence of VT is approximately the same rate as sudden cardiac death incidence, which accounts for half of all cardiac-related deaths. About 50 people out of 100,000 will have sudden cardiac death. This doesn't include patients who have non-fatal ventricular tachycardia, and is somewhat inaccurate because some patients will have sudden cardiac death from ventricular fibrillation. VT can be classified according to the appearance of the ECG. If each QRS complex is identical to all the others, the patient is said to have monomorphic VT. If the QRS changes from beat to beat, the VT is said to be polymorphic. Most cases of VT stem from an ischemic heart disease where there is a myocardial scar that leads to a reentrant beat. Other causes of VT include hypertrophic cardiomyopathy, the most common genetic cause of VT, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia, Chagas disease, and previous ventricular surgery. Of the electrolyte disturbances, the most common finding in ventricular tachycardia is hypokalemia, followed by hypomagnesmia. Less commonly, hyperkalemia can cause VT. Prolongation of the QT interval, genetic or acquired, can predispose a person to having VT. Congenital long QT syndrome can also lead to VT. Long QT syndrome can lead to Torsades de Pointe. Hypertrophic cardiomyopathy is the most common genetic cause of VT in young people. Miscellaneous causes of ventricular tachycardia include electrolyte disturbances, rheumatoid arthritis, lupus, hemochromatosis, methamphetamine or cocaine use, digoxin toxicity, drugs resulting in a long QT interval, and drugs that slow the conduction rate in the heart. Inherited channelopathies can also cause VT, such as short QT syndrome, long QT syndrome, catecholaminergic polymorphic VT, and Brugada syndrome. The typical signs and symptoms of VT include the onset of lightheadedness, syncope, palpitations, chest pain, and anxiety. On examination, the patient may present with hypotension, elevated venous jugular pressure, diaphoresis, pallor, and tachypnea. Severe cases can result in sudden cardiac death. The ECG will show characteristically a rapid rate and a wide ventricular beat. Patients should have their serum electrolytes checked if time permits, as hypocalcemia, hypomagnesmia, and hypokalemia can predispose a person to ventricular tachycardia. Other tests that should be drawn include a digoxin level, toxicology tests for illicit drugs, and serum troponin 1 levels if an MI is suspected. After cardioversion, an ECG should be repeated and labs should be drawn if they haven't been already. An echocardiogram and coronary angiogram may be necessary after conversion to look for heart disease as a cause of the VT, as this is the number one cause of ventricular tachycardia. The ECG must show a wide complex QRS with a rate faster than the atrial rate and no P waves found or dissociation of the P waves from the QRS complex. There are usually fusion beats present and capture beats may be found. According to ACLS protocol, a patient who is unstable with monomorphic VT should have synchronized cardioversion starting at 100 joules. Patients with unstable polymorphic ventricular tachycardia should have unsynchronized defibrillation. An unstable patient with ventricular tachycardia will have evidence of underperfusion, such as an altered level of consciousness, hypotension, shortness of breath or chest pain. The unstable patient with monomorphic VT needs synchronized cardioversion, while the unstable patient with polymorphic VT needs defibrillation. Stable patients can be treated medically. Lidocaine or amiodarone are preferred if there is dysfunction of the left ventricle. Lidocaine is probably the best choice for stable ventricular tachycardia because it works faster than amiodarone. If medications don't work, synchronized cardioversion at 50 to 200 joules with sedation is recommended. Polymorphic but stable ventricular tachycardia usually resolves spontaneously. Medications given after restoration of normal sinus rhythm should be IV sotolol or IV procainamide with IV lidocaine effective in peri-infarct VT. Patients found to have torsades de pointes should receive magnesium sulfate. Long-term treatment involves any of the class III antiarrhythmic drugs like sotolol or amiodarone. Patients with heart failure should receive a beta blocker plus an aldosterone agonist or an ACE inhibitor. Patients with pulseless VT are treated similarly to ventricular fibrillation with defibrillation at 150 to 200 joules initially followed by defibrillation at about 300 joules. A maximum of 360 joules is recommended. This should involve chest compressions and oxygenation between defibrillations. IV access should be obtained ASAP in order to provide medical therapy. If the patient is resistant to shocking, IV amiodarone is the drug of choice. Lidocaine can also be given. Some patients require an implantable cardioverter defibrillator or ICD. This is useful in patients at risk for sudden cardiac death due to sustained ventricular tachycardia or ventricular fibrillation. They will prevent this rhythm from being sustained and will restart the heart with a more normal rhythm. The ICD is implanted under the skin with electrodes that are attached to the heart. The device detects a serious rhythm disturbance and sends an electrical signal to interrupt the disturbance, restoring normal rhythm. Candidates for an ICD include those who have had previous near-sudden-death experience, unexplained syncope with cardiomyopathy, coronary artery disease with recurrent stable sustained ventricular tachycardia, or known genetic sudden-death syndrome. Radiofrequency ablation, or RFA, is done with a catheter directed at the origin of the ectopy in patients with cardiomyopathy, a bundle branch re-entry problem, LV dysfunction after an MI, or idiopathic ventricular tachycardia. Slow ventricular tachycardia, or the finding of an accelerated idioventricular rhythm, is considered a variant of ventricular tachycardia with a rate that is between 60 and 120 beats per minute. It can be seen in patients with heart disease and will not generally cause a cardiovascular collapse or hypotension. It only needs treatment if there is cardiovascular or hemodynamic compromise with antiarrhythmic drugs as the treatment of choice. Patients with known CAD and recurrent ventricular tachycardia will have a sudden-death incidence over two years of about 30%. Patients with idiopathic ventricular tachycardia have a much better prognosis, but can be injured during recurrent syncopal spells. Treatment with beta-blockers can reduce the risk of sudden cardiac death from ventricular tachycardia, and ICDs can reduce the death rate. Ventricular fibrillation. Ventricular fibrillation, or VF, is the most lethal cardiac arrhythmia. There is an uncoordinated rhythm on ECG and an uncoordinated contraction of the ventricles with severe pump failure. About 65 to 85% of patients with cardiac arrest are found to be in VF at the time they are evaluated by EMS personnel. VF often results in death within a few minutes. Refer to Figure 2 for an example of ventricular fibrillation on ECG. Up to a third of sudden cardiac death cases are secondary to ventricular fibrillation, giving VF an incidence of about 0.08 to 0.16% per year in adults, and about 100,000 deaths in the U.S. per year. Ventricular fibrillation is often the first sign that a person has coronary artery disease and accounts for half of all cases of cardiac death. Ventricular fibrillation tends to occur within an hour of an acute myocardial infarction. Up to a third of all survivors of ventricular fibrillation will have a recurrent cardiac arrest in the first year after the initial arrest. The main cause of VF is coronary artery disease, usually in the setting of an acute MI or from scar tissue from an old MI. Ventricular tachycardia can degenerate into ventricular fibrillation if not treated. The ECG will look like a chaotic, irregular pattern in all leads. The QRS complex can gradually flatten out, increasing the chances of developing ventricular fibrillation. Patients who survive ventricular fibrillation have up to an 80% chance of having severe coronary artery disease. There is no single blockage that is associated with ventricular fibrillation over any other blockage. About 20% of all sudden cardiac deaths from slow ventricular fibrillation show evidence of a new MI. About 40% to 70% of cases will show a healed myocardial infarction. The most common precursor rhythm to ventricular fibrillation is ventricular tachycardia. Up to 15% of young people under 40 years of age can have ventricular fibrillation without any predisposing structural heart problems. The second most common cause of ventricular fibrillation is non-ischemic cardiomyopathy, which accounts for about 10% of all ventricular fibrillation situations. This can include dilated cardiomyopathy, accounting for about 7 out of 100,000 people. These people have a poor prognosis with a one-year mortality rate of 10% to 50%. Dilated cardiomyopathy can be secondary to alcohol use, genetics, viral infections, autoimmune diseases, and idiopathic causes. Genetic dilated cardiomyopathy is an autosomal dominant disease affecting proteins that normally code for cardiac sarcomeres. There is an X-linked cardiomyopathy linked to also having Duchenne muscular dystrophy. Rarely, an autosomal recessive case of dilated cardiomyopathy can happen, involving a mutation in the troponin 1 muscle protein. Hypertrophic cardiomyopathy is inherited in an autosomal dominant, incompletely penetrant genetic condition stemming from a mutation of one of up to 45 different genes that encode normal cardiac sarcomere. The four most common mutations occur in the MYH7 gene, the TNNT2 gene, the MYBPC3 gene, and the cardiac troponin 1 gene. The incidence of ventricular fibrillation in these patients is about 4 to 6 percent per year in adolescents and 2 to 4 percent per year in adults with the mutation. This makes this the most common cause of ventricular fibrillation in people under the age of 30 years. There are eight different types of genes linked to most causes of ARBC, forward slash D, or arrhythmogenic right ventricular cardiomyopathy or dysplasia. The right ventricular wall gets replaced with fibrofatty tissue, as well as having left ventricular involvement. The genetic problem is related to abnormalities of the desmosomes that bind cardiac muscle cells together. The patient will present with sustained monomorphic ventricular tachycardia with left bundle branch block on ECG. There is a 2 percent risk of ventricular fibrillation per year in these people. MRI can diagnose this disorder. In children, ventricular fibrillation is generally due to congenital heart disease. Typical congenital heart disease leading to ventricular fibrillation include transposition of the great vessels, tetralogy of Fallot, Marfan syndrome, aortic stenosis, Ebstein anomaly, congenital heart block, Eisenmenger syndrome, and aortic stenosis. Some acquired diseases in children can cause ventricular fibrillation such as dilated cardiomyopathy, myocarditis, and Kawasaki syndrome. Other causes of ventricular fibrillation and sudden cardiac death include pulmonary embolism, which can come from recent orthopedic surgery, hypercoagulable states, cancer, and deep venous thromboembolism. Aortic dissection can lead to sudden cardiac death in patients who have Ehlers-Danlos syndrome, Marfan syndrome, or aortic cystic medial necrosis. Rare causes of ventricular fibrillation that aren't related to structural heart disease include catecholamine polymorphic ventricular tachycardia, Wolff-Parkinson-White syndrome, Long QT syndrome, pulmonary hypertension, Brugada syndrome, or commotio cortis, which is trauma to the chest leading to ventricular fibrillation or ventricular tachycardia. Patients can rarely develop catecholaminergic polymorphic ventricular tachycardia that degrades into ventricular fibrillation. It is secondary to exercise or severe emotional stress. Wolff-Parkinson-White syndrome is rare and involves having multiple accessory pathways. It can be inherited in an autosomal dominant fashion. Brugada syndrome was first identified in 1992 as a condition that can lead to sudden cardiac death. It is a type of channelopathy, meaning that it affects the ion channels in the heart. It is about 10 times more common in males and is inherited in an autosomal dominant fashion. Patients will have a right bundle branch block and ST segment elevation in V1 and V2 with no known structural heart problem. The main gene identified as being abnormal in Brugada syndrome is the SCN5A gene, although others have been identified. The treatment of choice in ventricular fibrillation from Brugada syndrome is ibuprocanamide, although these patients have a good chance of survival with an ICD, making this the treatment of choice in preventing ventricular fibrillation in these patients. Key takeaways. The major ventricular arrhythmias include frequent PVCs, ventricular tachycardia, and ventricular fibrillation. The outcome of ventricular arrhythmias is often a sudden cardiac death. The most common underlying problem in ventricular arrhythmias is coronary artery disease. There are a number of genetic diseases that can lead to either ventricular tachycardia or ventricular fibrillation. Quiz. Number one. Which arrhythmia is considered the most lethal arrhythmia to have? A. Ventricular fibrillation. B. Ventricular tachycardia. C. Superventricular tachycardia. D. Bradycardia. Answer. A. Ventricular fibrillation involves a lack of perfusable rhythm and a lack of contractility of either the ventricles or the atria. It is easily the most lethal arrhythmia for a person to have. Question two. You are evaluating a 65-year-old male with a previous MI and an irregular cardiac rhythm. What is the most common cause of an irregular cardiac rhythm in this setting? A. Atrial flutter. B. Premature ventricular contractions. C. Ventricular tachycardia. D. Wolf-Parkinson-White syndrome. Answer. B. The most common cause of an irregular rhythm in this setting would be frequent premature ventricular contractions. Question three. What is the approximate incidence of PVCs in a population older than 50 years of age? A. 0.5%. B. 1%. C. 2%. D. 5%. Answer. C. The approximate incidence of PVCs in people older than 50 years of age is about 2%. Question four. What should the cardioverter be set to for a patient with monomorphic ventricular tachycardia as in the first setting? A. 50 joules. B. 100 joules. C. 200 joules. D. 300 joules. Answer. B. The patient should have the synchronized cardioverter set to 100 joules in unstable monomorphic ventricular tachycardia. Question five. What is the medication of choice for patients who have Torsad Zipwant? A. Lidocaine. B. Amiodarone. C. Sotalol. D. Magnesium sulfate. Answer. D. The most effective treatment for Torsad Zipwant is magnesium sulfate. Question six. What is considered a good long-term treatment for the prevention of recurrent ventricular tachycardia? A. Amiodarone. B. Ace inhibitor. C. Lidocaine. D. Digoxin. Answer. A. Any of the class III antiarrhythmic drugs can be a good long-term treatment for recurrent ventricular tachycardia. Question seven. What is the mortality rate from sudden cardiac death over a two-year period of time in patients with CAD and recurrent ventricular tachycardia? A. 10%. B. 30%. C. 60%. D. 80%. Answer. B. The mortality rate in coronary artery disease patients with ventricular tachycardia is about 30% over two years. Question eight. What is the drug of choice to treat stable ventricular tachycardia? A. Amiodarone. B. Procainamide. C. Lidocaine. D. Procranolol. Answer. C. Lidocaine is the treatment of choice for stable ventricular tachycardia with amiodarone being a second-line agent. Question nine. What is the most common cause of ventricular fibrillation? A. Hypokalemia. B. Digoxin toxicity. C. Hypertrophic cardiomyopathy. D. Coronary artery disease. Answer. D. The most common cause of ventricular fibrillation, accounting for 80% of cases, is coronary artery disease. Question ten. In a patient with Brugada syndrome at risk for ventricular fibrillation, what is the treatment of choice in order to prolong survival? A. Procainamide. B. Amiodarone. C. Beta-blocker therapy. D. Implantable cardiac defibrillator, or ICD. Answer. D. The treatment of choice for patients with Brugada syndrome is to have an ICD placed to prevent sustained ventricular tachycardia or ventricular fibrillation.
