Ventricular Dysrhythmias

Ventricular Dysrhythmias

DRG Category:309
Mean LOS:3.5 days
Description:MEDICAL: Cardiac Arrhythmia and Conduction Disorders With CC

A ventricular dysrhythmia is a disturbance in the normal rhythm of the electrical activity of the heart that arises in the ventricles (Fig. 1). Types of ventricular dysrhythmias include premature ventricular contractions (PVCs), which can have one focus or can arise from multiple foci; ventricular tachycardia (VT), which can lead to ventricular fibrillation or sudden cardiac death; ventricular fibrillation (VF), which results in death if not treated immediately; and ventricular asystole (cardiac standstill), in which no cardiac output occurs and full cardiopulmonary arrest results (Table 1).

Types of Ventricular Dysrhythmias
Table 1. Types of Ventricular Dysrhythmias
TYPEDESCRIPTIONCAUSE
  • PVCs
  • Early ectopic beats that arise from the ventricles
  • Atrial rate: Regular
  • Ventricular rate: Irregular
  • QRS complex; wide and distorted, usually longer than 0.14 sec
  • Occurrence: Singly, in pairs, or alternating with regular sinus beats
  • Heart failure
  • Myocardial infarction
  • Cardiac trauma
  • Myocardial irritation from pacemaker or pulmonary artery catheter insertion
  • Hypercapnia, hypokalemia, or hypocalcemia
  • Medication toxicity (digitalis, aminophylline, tricyclic antidepressants, beta-adrenergic stimulants)
  • Caffeine, tobacco, or alcohol use; physiological and psychological stress
  • VT
  • Three or more premature ventricular contractions in a row dissociated from the atrial contraction
  • P waves: In sustained VT, none are identifiable; usually buried within aberrant, bizarre ventricular contractions
  • Ventricular rate: Usually 100–220 beats per min
  • Ventricular rhythm: May start and stop suddenly
  • Myocardial ischemia
  • Myocardial infarction
  • Rheumatic heart disease
  • Mitral valve prolapse
  • Heart failure
  • Cardiomyopathy
  • Electrolyte imbalances such as hypokalemia, hypomagnesemia, and hypercalcemia
  • Medication toxicities: Digitalis, procainamide, epinephrine, or quinidine
  • Ventricular fibrillation (VF)
  • Disorganized, ineffective contraction of the ventricle
  • P waves: None
  • QRS complex: None
  • Ventricular rhythm: Chaotic rhythm with a wavy baseline
  • Medication toxicities: Digitalis, procainamide, epinephrine, or quinidine
  • Ventricular asystole (cardiac standstill)
  • Atrial rhythm: None
  • P, QRS, T waves: None
  • Ventricular rhythm: None
  • Myocardial ischemia
  • Myocardial infarction
  • Valvular disease
  • Severe heart failure pH and electrolyte imbalances (severe acidosis, hypokalemia, or hyperkalemia in particular)
  • Electric shock
  • Pulmonary embolism
  • Cardiac rupture
  • Cardiac tamponade
  • Cocaine overdose

Causes

Conditions associated with cardiac dysrhythmias include myocardial ischemia, myocardial infarction, electrolyte imbalance, drug toxicity, and degeneration of the conduction system by necrosis. A dysrhythmia can be the result of a disturbance in the ability of the myocardial cell to conduct an impulse (conductivity), a disturbance in the ability to initiate and maintain an inherent rhythm spontaneously (automaticity), or a combination of both.

Genetic considerations

Mutations in a variety of genes have been associated with the production of familial ventricular dysrhythmias (LQT1, CMD1A, MVP). The long QT syndrome (caused by mutations in potassium, sodium channels, and an anchoring protein) can result in a polymorphic VT called torsades de pointes. Long QT can be passed as an autosomal dominant (Romano-Ward) or recessive (Jervell and Lange-Nielsen) trait. Brugada syndrome is caused by a sodium channel mutation and results in episodes of VF and sudden cardiac death. Catecholaminergic polymorphic VT results from defects in calcium or potassium channel genes.

Gender, ethnic/racial, and life span considerations

Although these rhythms can occur at any point in the life span and in both sexes, they are more common in the elderly population because of the increased incidence of cardiac diseases, atherosclerosis, and degenerative hypertrophy of the left ventricle. Intrinsic degeneration of the conduction system and a higher propensity toward drug toxicity because of altered metabolism and excretion are contributing factors as patient’s age. In addition, many of the medications that aging people take to manage heart failure (digitalis and diuretics in particular) place them at risk for drug toxicities and electrolyte imbalances. Men are more likely than women to have VT, which is also unusual in children. African American males have the highest incidence of sudden cardiac death from VF.

Global health considerations

While people around the world have ventricular dysrhythmias, no data are available on prevalence. VT and VF are common throughout most of the developed world but are less common in developing countries. VF is prevalent worldwide, and the largest number of people with VF live in the northern hemisphere.

Assessment

History

If the patient is unable to provide a history of the life-threatening event, obtain it from a witness. Many patients with suspected cardiac dysrhythmias describe a history of symptoms indicating periods of decreased cardiac output. Although occasional PVCs do not usually produce symptoms, some patients report a history of dizziness, fatigue, activity intolerance, a “fluttering” in their chest, shortness of breath, and chest pain. In particular, question the patient about the onset, duration, and characteristics of the symptoms and the events that precipitated them. Obtain a complete history of all illnesses, dietary and fluid restrictions, activity restrictions, and a current medication history.

Physical examination

Lethal dysrhythmias such as VF may lead to a full cardiopulmonary arrest. If the patient does not have adequate airway, breathing, or circulation (ABCs), initiate cardiopulmonary resuscitation (CPR) as needed. If the patient is stable, complete a general head-to-toe physical examination. Pay particular attention to the cardiovascular system by inspecting the skin for changes in color or the presence of edema. Auscultate the heart rate and rhythm and note the first and second heart sounds and also any adventitious sounds. Auscultate the blood pressure. Perform a full respiratory assessment and note any adventitious breath sounds or labored breathing.

Psychosocial

Ventricular dysrhythmias may cause a life-threatening event and a great deal of anxiety and fear because of the potential alterations to current lifestyle and functioning. Assess the ability of the patient and significant others to cope. If the dysrhythmia requires a pacemaker insertion or an automatic implantable cardioverter defibrillator (ICD), determine the patient’s response.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
12-lead electrocardiogram (ECG)Regular sinus rhythmVaries with dysrhythmias (Table 1)Detects specific conduction defects; monitors the patient’s cardiac response to electrolyte imbalances, drug effects, and toxicities

Other Tests: Resting and exercise ECG, Holter monitoring, electrophysiologic studies, chest x-ray

Primary nursing diagnosis

Diagnosis

Altered tissue perfusion (cardiopulmonary, cerebral, renal, peripheral) related to rapid heart rates or the loss of the atrial kick

Outcomes

Circulation status; Cardiac pump effectiveness; Tissue perfusion: Cardiopulmonary, Cerebral, Renal, Peripheral; Vital sign status

Interventions

Circulatory care; Dysrhythmia management; Emergency care; Vital signs monitoring; Cardiac care; Cardiac precautions; Oxygen therapy; Fluid/electrolyte management; Fluid monitoring; Shock management: Volume; Medication administration; Resuscitation; Surveillance

Planning and implementation

Collaborative

The first step of treatment is to maintain ABCs. Low-flow oxygen by nasal cannula or mask may decrease the rate of PVCs. Higher flow rates are usually needed for the patient with VT, and if pulseless VT or VF occurs, the patient needs immediate endotracheal intubation, support of breathing with a manual resuscitator bag, and closed chest compressions (CPR). The most important intervention for a patient with pulseless VT or VF is rapid defibrillation (electrical countershock). If a defibrillator is not available, give a sharp blow to the precordium (precordial thump or thumpversion) to try to convert VT or VF into a regular sinus rhythm. Maintain CPR between all other interventions for patients without adequate breathing and circulation.

The drugs of choice to manage PVCs or VT with a pulse depends on the morphology of the ventricular beats and include amiodarone, lidocaine, or procainamide. If the patient has pulseless VT or VF, the treatment of choice is to defibrillate the patient as discussed previously, intubate the patient, administer epinephrine, and then administer amiodarone. If the patient has electrolyte imbalances, or they are suspected, supplemental potassium, calcium, and/or magnesium is administered intravenously (IV).

In stable patients, trials of various medications or combinations of medications may be used to control the dysrhythmia. Antidysrhythmics, such as bretylium and procainamide, may be used if lidocaine or amiodarone are not successful. Other drugs such as quinidine, propranolol, metoprolol, and verapamil may be used depending on the cause and nature of the dysrhythmia. Other alternatives include surgical implantation of either a pacemaker or an ICD and surgical ablation of aberrant electrical conduction sites.

The patient with ventricular asystole is managed with CPR. Initiate CPR, intubate the patient immediately, provide oxygenated breathing with a manual resuscitator bag, and obtain IV access. Confirm the ventricular asystole in a second lead to make sure the patient is not experiencing VF, which would indicate the need to defibrillate. If the rhythm still appears as ventricular asystole, administer epinephrine and then atropine in an attempt to have the patient regain an effective cardiac rhythm. The physician may consider a transcutaneous or transvenous pacemaker, but if efforts do not convert the cardiac rhythm, the physician may terminate resuscitation efforts.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
Epinephrine1 mg IV or intraosseous (IO) 1:10,000 solution; repeat every 3–5 minCatecholamineCardiac stimulant
AmiodaroneVF and pulseless VT: 300 mg IV or IO after dose of epinephrine if no initial response to defibrillation; repeat 150 mg IV in 3–5 min; Wide complex QRS: 150 mg IV with calcium chloride 1 gm IVAntidysrhythmic agentFor VF and pulseless VT; prolongs action potential and repolarization
Lidocaine1–1.5 mg/kg of body weight IVAntidysrhythmic agentManages PVCs or VT with a pulse; inhibits conduction of nerve impulses
Bretylium5 mg/kg undiluted by rapid IV injectionAntidysrhythmic agentManages PVCs or VT; directly affects myocardial cell membrane; initially releases norepinephrine, then inhibits release
Procainamide17 mg/kg up to 50 mg/min in divided doses IV injectionAntidysrhythmic agentManages PVCs or VT; prolongs refractory period by direct effect, decreasing myocardial excitability and conduction velocity

Other Drugs: Vasopressors/sympathomimetics (epinephrine, vasopressin, dopamine, norepinephrine), atropine, sodium bicarbonate, propranolol, electrolytes (magnesium sulfate, calcium chloride)

Independent

As with all potentially serious conditions, the first priority is to maintain the patient’s ABCs. If the patient is not having a cardiopulmonary arrest, maximize the amount of oxygen available to the heart muscle. During periods of abnormal ventricular conduction, encourage the patient to rest in bed until the symptoms are treated and subside. Remain with the patient to ensure rest and to allay anxiety.

For some patients with PVCs, strategies to reduce stress help limit the incidence of the dysrhythmia. A referral to a support group or counselor skilled at stress reduction techniques is sometimes helpful. Teach the patient to reduce the amount of caffeine intake in the diet. Explain the need to read the ingredients of over-the-counter medications to limit caffeine intake. If appropriate, encourage the patient to become involved in an exercise program or a smoking-cessation group.

Patients who experience dysrhythmias are often facing alterations in their lifestyle and job functions. Provide information about the dysrhythmia, the precipitating factors, and mechanisms to limit the dysrhythmia. If the patient is placed on medications, teach the patient and significant others the dosage, route, action, and side effects. If the patient is at risk for electrolyte imbalance, teach the patient any dietary considerations to prevent electrolyte depletion of vital substances.

The most devastating outcome of a ventricular dysrhythmia is sudden cardiac death. If the patient survives the episode, provide an honest accounting of the incident and support the patient’s emotional response to the event. If the patient does not survive, remain with the family and significant others, support their expression of grief without being judgmental if it varies from your own ways to express grief, and notify a chaplain or clinical nurse specialist if appropriate to provide additional support.

Evidence-Based Practice and Health Policy

Habibovic, M., Pedersen, S.S., van den Broek, K.C., Theuns, D.A., Jordaens, L., van der Voort, P.H., …Denollet, J. (2013). Anxiety and risk of ventricular arrhythmias or mortality in patients with an implantable cardioverter defibrillator. Psychosomatic Medicine, 75(1), 36–41.

  • In a prospective study among 1,012 patients newly implanted with a cardioverter defibrillator, 19% experienced a ventricular dysrhythmia during the year-long follow-up period. The 1-year mortality rate was 4%.
  • Anxiety was associated with a 1.017 times increased risk of ventricular dysrhythmia (95% CI, 1.005 to 1.028; p = 0.005) and a 1.038 times increased risk of mortality (95% CI, 1.014 to 1.063; p = 0.002).
  • Patients in the highest third of anxiety scores were 1.9 times more likely to experience a ventricular dysrhythmia compared to patients in the lowest third (95% CI, 1.329 to 2.753; p = 0.001). The mean anxiety score among patients in this sample was 38.9 (range, 20 to 80).

Documentation guidelines

  • Cardiopulmonary assessment: Heart and lung sounds, cardiac rate and rhythm on the cardiac monitor, blood pressure, quality of the peripheral pulses, capillary refill, respiratory rate and rhythm
  • Activity tolerance and ability to perform self-care
  • Complications: Dizziness, syncope, hypotension, electrolyte imbalance, loss of consciousness, uncorrected cardiac dysrhythmias, ineffective patient or family coping

Discharge and home healthcare guidelines

Explain to the patient the importance of taking all medications. If the patient needs periodic laboratory work to monitor the effects of the medications (e.g., serum electrolytes or drug levels), discuss with the patient the frequency of these laboratory visits and where to have the tests drawn. Explain the actions, the route, the side effects, the dosage, and the frequency of the medication. Discuss methods for the patient to remember to take the medications, such as numbered medication boxes or linking the medications with other activities such as meals or sleep. Teach the patient how to take the pulse and recognize an irregular rhythm. Explain that the patient needs to notify the healthcare provider when symptoms such as irregular pulse, chest pain, shortness of breath, and dizziness occur.

Stress the importance of stress reduction and smoking cessation. If the patient has a pacemaker or an ICD, provide teaching about the settings, signs of pacemaker failure (dizziness, syncope, palpitations, fast or slow pulse rate), and when to notify the physician. Explain any environmental hazards based on the manufacturer’s recommendations, such as heavy machinery and airport security checkpoints. Make sure the patient understands the schedule for the next physician’s checkup. If the patient has an ICD, encourage the patient to keep a diary of the number of times the device discharges. Most physicians want to be notified the first time the ICD discharges after implantation.

References in periodicals archive ?
Other electrocardiographic manifestations of hypothermia include PR-, QRS- and QT-interval prolongation, as well as atrial and ventricular dysrhythmias.
Bronchoconstriction with neostigmine and atracurium Quinidine Prolongs the effects of neuromuscular blockers (NMB) Procainamide, Antagonizes neostigmine, Ventricular dysrhythmias when combined with phenotiazides Calcium channel Bradycardia and myocardial depression with blocker, halogenated agents and dantrolene, potentiates NMB.
Patients with ventricular dysrhythmias unrelated to heart failure and AV block should not be prescribed digoxin.
The risks of atrial fibrillation, ventricular dysrhythmias (including sudden death) and heart block all increase.
Chronic cocaine abusers are at an increased risk of cardiac events, especially coronary ischemia and ventricular dysrhythmias, in the perianesthetic period.
If enough of the gas is absorbed, it can lead to ventricular dysrhythmias, pulmonary edema, cardiac arrest, and sudden death.
After discharge, the authors contacted subjects within at least 30 days and inquired about ventricular dysrhythmias, nonfatal MI, recurrent chest pain, and recurrent cocaine use.
Once reserved to treat life-threatening ventricular dysrhythmias, amiodarone is increasingly used for atrial tachyarrhythmias.
However, treatment is obviously necessary in patients with symptomatic and/or life-threatening atrial and ventricular dysrhythmias.
Eight patients developed serious ventricular dysrhythmias (sustained ventricular tachycardia and ventricular fibrillation) after admission; all responded to routine measures.
Clinical factors such as acute myocardial infarction and cardiomyopathy that contribute to ventricular remodeling and dilatation increase the frequency of ventricular dysrhythmias (Effat, 1995).