Ventricular Dysrhythmias


DRG Category: 309

Mean LOS: 2.9 days

Description MEDICAL Cardiac Arrhythmia and Conduction Disorders With Complication or Comorbidity


A ventricular dysrhythmia is a disturbance in the normal rhythm of the electrical activity of the heart that arises in the ventricles (Fig. 1). Experts estimate that sudden cardiac death occurs in approximately 300,000 cases each year in the United States, and up to one-third are attributable to ventricular fibrillation (VF) (Fig. 3). People who have survived a major cardiac event, such as myocardial infarction or cardiac arrest, are at increased risk for VF up to 2 years after the event. Types of ventricular dysrhythmias include premature ventricular contractions (PVCs), which can have one focus or can arise from multiple foci; ventricular tachycardia (VT) (Fig. 2), which can lead to VF or sudden cardiac death; VF, which results in death if not treated immediately; and ventricular asystole (cardiac standstill) (Fig. 4), in which no cardiac output occurs and full cardiopulmonary arrest results (Table 1).

Table 1 Types of Ventricular Dysrhythmias

  • PVC
  • 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 or hypocalcemia
  • Medication toxicities: Digitalis, procainamide, epinephrine, or quinidine
  • VF
  • Disorganized, ineffective contraction of the ventricle
  • P waves: None
  • QRS complex: None
  • Ventricular rhythm: Chaotic rhythm with a wavy baseline
  • Coronary heart disease, myocardial infarction, myocardial ischemia, cardiomyopathy, heart failure, low ejection fraction
  • 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

Most sudden deaths are caused by either VT or VF. Many patients have nonfatal VT, and it is often associated with chronic heart failure, cardiomyopathy, and ischemic heart disease. VF causes approximately 50% of deaths that occur from coronary heart disease (CHD). The highest incidence of VF occurs in people with chronic heart failure with low ejection fractions, and people who are recovering after a cardiac arrest or a myocardial infarction. Typically, VF occurs in the first 24 months after these events. Complications include syncope, brain injury, seizures, myocardial infarction, acute renal insufficiency, or sudden death.


Conditions associated with cardiac dysrhythmias include myocardial ischemia, myocardial infarction, structural heart disease such as cardiomyopathy, inherited conduction disturbances, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), 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. Risk factors include CHD, use of recreational drugs such as cocaine, smoking, electrolyte abnormalities, family history of rhythm disorders, and toxicities from medications such as digitalis, procainamide, epinephrine, aminophylline, tricyclic antidepressants, beta-adrenergic stimulants, or quinidine.

Genetic Considerations

Mutations in a variety of genes have been associated with the production of familial ventricular dysrhythmias (LQT1, LMNA, 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 (SCN5A) and results in episodes of VF and sudden cardiac death. Catecholaminergic polymorphic VT results from defects in calcium or potassium channel genes.

Sex Life Span Considerations

Although these rhythms can occur at any point in the life span and in both sexes, they are more common in older adults 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 patients 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 three times more likely than women to have VF, and slightly more men than women have VT. VT and VF are unusual in children. Women are less likely to receive placement of resynchronization therapy devices with defibrillator as compared to men, creating health disparities for women.

Health Disparities Sexual/Gender Minority Health

The Centers for Disease Control and Prevention report that 11.5% of White persons, 9.5% of Black persons, 7.4% of Hispanic persons, and 6.0% of Asian persons have heart disease. Black persons have higher morbidity and mortality rates of CHD and sudden cardiac death; the burden for Black persons is higher than for White persons because of the prevalence of hypertension, obesity, metabolic syndrome, and Black, Indigenous, and other people of color are known to receive care less often guided by standard cardiac care guidelines than White persons. Unless patients have health insurance, White patients are more likely to receive coronary angiograms and other coronary interventions than Black and Hispanic patients. Black and Hispanic persons are also less likely to be referred to cardiologists and cardiac surgeons than White persons (Batchelor et al., 2019). In the United States, Asian Indian persons have a higher prevalence of CHD than White persons.

Transgender is a term used to describe persons whose gender identity is different from their sex assigned at birth. Approximately 1% of the U.S. population identify themselves as transgender. Sexual and gender minority persons have higher odds for multiple chronic conditions, cancer, and poor quality of life and are more apt to have disabilities than cisgender males and females. (Cisgender is a term used to describe persons whose gender identity and gender expression are aligned with their assigned sex listed on their birth certificate.) Gender-affirming hormone therapy is the use of hormone therapy for gender transition or gender affirmation and can be masculinizing or feminizing. It may also affect cardiovascular health in transgender females. Several case reports suggest that feminizing hormone therapy may place transgender women at risk for dysrhythmias. In a large sample, researchers have found that transgender men and women are more likely to be overweight than cisgender women. Compared to cisgender women, transgender women reported higher rates of diabetes, ischemic stroke, angina/coronary disease, and myocardial infarction. Gender-nonconforming men and women reported higher odds of myocardial infarction than cisgender women. Transgender women also had higher rates of any cardiovascular disease than cisgender men (Cacerese, Jackman, et al., 2020; Connelly et al., 2019). While large-scale studies are not available, these factors may place some sexual and gender minority persons at risk for ventricular dysrhythmias.

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; this prevalence is likely due to nutritional, occupational, and lifestyle factors as well as heredity.



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. They may report dizziness, syncope, fatigue, dyspnea, palpitations, diaphoresis, chest pain, and activity intolerance. Question patients to determine if they have seen a medical provider recently; many patients who experience VT or VF have seen their physician recently for vague complaints such as fatigue, palpitations, or shortness of breath. In particular, question the patient or family about the onset, duration, and characteristics of the symptoms and the events that precipitated them. Determine if the patient has experienced a previous myocardial infarction, syncope, cardiomyopathy, or valvular disease. Obtain a complete history of all illnesses, dietary and fluid restrictions, activity restrictions, and a current medication history.

Physical Examination

Patients with VT may be awake and symptomatic. Common symptoms are dizziness, fatigue, activity intolerance, a “fluttering” in their chest, shortness of breath, and chest pain. They may have syncope from decreased perfusion to the brain, pallor, diaphoresis, hypotension, and dyspnea from diminished perfusion to the lungs. Changes in cerebral perfusion may be manifested by anxiety, agitation, lethargy, or coma. Lethal dysrhythmias such as VF and ventricular asystole usually 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, presence of peripheral pulses, or 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. Perform a neurological examination to determine level of responsiveness and presence of reflexes.


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, serum electrolytes, serum calcium, ionized calcium, serum magnesium, cardiac enzymes, creatine kinase, complete blood count, arterial blood gases, toxic screen, thyroid-stimulating hormone, B-type natriuretic peptide, electrophysiological studies, echocardiogram, chest x-ray, nuclear imaging to assess myocardial damage

Primary Nursing Diagnosis

Diagnosis: Risk for decreased cardiac and ineffective cerebral tissue perfusion as evidenced by dizziness, decreased level of consciousness, chest pain, shortness of breath, pulselessness, apnea, shock, and/or cardiopulmonary arrest

Outcomes: Respiratory status; Circulation status; Cardiac pump effectiveness; Cardiopulmonary status; Tissue perfusion: Cardiac, Pulmonary, Cerebral, Peripheral; Vital signs, Neurological status

Interventions: Airway management; Dysrhythmia management; Emergency care; Vital signs monitoring; Cardiac care; Oxygen therapy; Fluid/electrolyte management; Fluid monitoring; Shock management: Cardiac; Medication administration; Resuscitation

Planning and Implementation


It is important to follow the most current Advanced Cardiac Life Support algorithms, which are updated regularly based on scientific evidence and best practices. In out-of-hospital resuscitations, the American Heart Association recommends chest-compression-only CPR, also known as cardiocerebral resuscitation. If the patient is in full arrest, use current CPR guidelines. CPR for patients in the hospital is performed with a compression-to-ventilation ratio of 30:2 until the defibrillator arrives. If the patient is not in full arrest, 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, and support of breathing with a manual resuscitator bag. The most important intervention for a patient with pulseless VT or VF is rapid defibrillation (electrical countershock). If a defibrillator is not available, and the arrest was witnessed, begin chest compressions and, as soon as possible, 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 depend on the morphology of the ventricular beats and include amiodarone, lidocaine, or depending on the morphology of the electrocardiogram, magnesium sulfate. 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 or lidocaine. If the patient has electrolyte imbalances, or they are suspected, supplemental potassium, calcium, and/or magnesium is administered IV. Procainamide may be given to treat sustained ventricular tachycardia or recurrent VF if other interventions have not been successful. Long-term management may be done by ICDs.

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 every 3 to 5 minutes in an attempt to have the patient regain an effective cardiac rhythm. Depending on setting and expertise, practitioners 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

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


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 asymptomatic short runs of 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 Health Policy

Long, B., Brady, W., Bridwell, R., Ramzy, M., Montrief, T., Singh, M., & Gottlieb, M. (2021). Electrocardiographic manifestations of COVID-19. American Journal of Emergency Medicine, 41, 96-103.  [PMID:33412365]

  • The authors note that although COVID-19 is a lower respiratory condition, the disease can also impact the cardiovascular system and lead to abnormal electrocardiographic findings. Up to 90% of patients who are critically ill with COVID-19 have cardiac dysrhythmias. There are a number of causes, such as cytokine storm, hypoxic injury, electrolyte imbalances, microthrombi, or direct endothelial injury.
  • Although sinus tachycardia is the most common dysrhythmia during COVID-19, ventricular dysrhythmias such as ventricular tachycardia and fibrillation often occur. Rhythm presentations that are associated with poor outcomes include atrial fibrillation, ST segment and T wave changes, ventricular tachycardia, and ventricular fibrillation.

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.


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Figure 1 Electrical Conduction System of the Heart

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Figure 2 Ventricular Tachycardia

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Figure 3 Ventricular Fibrillation

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Figure 4 Asystole