Paroxysmal Supraventricular Tachycardia (Nursing)

Yamama Hafeez; Bryan Quintanilla Rodriguez; Intisar Ahmed; Shamai Grossman

Paroxysmal Supraventricular Tachycardia (Nursing)

Learning Outcome

Recognize reportable critical abnormalities in rhythm
Recognize paroxysmal supraventricular tachycardia
Distinguish paroxysmal supraventricular tachycardia from other abnormal rhythms
Summarize basic medical and nursing therapy
Understand and be able to explain the importance of rapidly reducing the heart rate to the patient and family
Understand the need for cardioversion and nursing responsibilities

Introduction

The atrioventricular node (AV) measures approximately 1 by 3 by 5 millimeters and sits within an anatomic region bordered anteriorly by septal tricuspid valve annulus, superiorly by the tendon of Todaro and posteriorly by the coronary sinus ostium. This anatomic region is also commonly referred to as the triangle of Koch. The AV node is a subendocardial structure located in the inferior-posterior right atrium. The blood supply to the AV node is from the AV nodal branch of the right coronary artery (90%) or the left circumflex artery (10%) depending on right or left dominant blood supply to the heart. The first septal perforator of the left anterior descending artery also supplies blood to the AV node.[1][2][3][4][5]

Paroxysmal supraventricular tachycardia (PSVT) accounts for intermittent episodes of supraventricular tachycardia with sudden onset and termination. PSVT is part of the narrow QRS complex tachycardias with a regular ventricular response in contrast to multifocal atrial tachycardia, atrial fibrillation, and atrial flutter. SVTs are classified based on the origin of the rhythm and whether the rhythm is regular or irregular.[6][7][8][9][10][11]

Atrial in Origin and Regular Rhythm

Sinus tachycardia
Inappropriate sinus tachycardia
Sinoatrial nodal reentrant tachycardia
Atrial flutter
Atrial fibrillation

Atrial in Origin and Irregular Rhythm

Multifocal atrial tachycardia
Atrial flutter with variable block
Atrial fibrillation

AV Node in Origin and Regular Rhythm

Junctional tachycardia
Atrioventricular nodal reentrant tachycardia
Atrioventricular reentrant tachycardia

AV Node in Origin and Irregular Rhythm

None

SVT is known to occur in individuals of all ages, but treatment is often difficult. The clinical presentation of SVT is variable- ranging from asymptomatic to severe palpitation. Electrophysiologic studies are usually necessary to determine the pathophysiology of impulse formation and pathways of conduction.

Nursing Diagnosis

Anxiety-related to altered health state
Decreased cardiac output related to inadequate ventricular filling with rapid tachycardia
Ineffective tissue perfusion related to decreased cardiac output

Causes

Numerous conditions and medications can lead to PSVT in patients. [6][12][13][14]

Some of these conditions and medications are listed below:

Hyperthyroidism
Caffeinated beverages
Nicotine
Hydralazine
Atropine
Adenosine
Verapamil
Salbutamol
Ecstasy
Cocaine
Amphetamines
Alcohol
Digoxin toxicity
Myocardial infarction
Structural heart disease
Ebstein anomaly
Pericarditis
Myocarditis
Cardiomyopathy
Pulmonary embolism
Rheumatic heart disease
Mitral valve prolapse
Pneumonia
Chronic lung disease
Chest wall trauma
Anxiety
Hypovolemia
Hypoxia

Risk Factors

In the United States, the prevalence of PSVT is approximately 0.2%, and it has an incidence of one to three cases every thousand patients. The most common of the PSVT is atrial fibrillation with a prevalence rate of approximately 0.4% to 1% occurring in men and women equally, it is projected to affect as many as 7.5 million patients by 2050. The risk of developing PSVT was found to be twice in women as compared to men in a population-based study, with the prevalence of the PSVT higher with age. Atrioventricular nodal reentrant tachycardia is found more commonly in patients who are middle-aged or older. Whereas PSVT with an accessory pathway is most common in adolescents, and their occurrence decreases with age.[15][16][17]

Besides occurring in healthy people. PSVT can also occur after a myocardial infarction (MI), rheumatic heart disease, mitral valve prolapse, pneumonia, chronic lung disease, and pericarditis. Digoxin toxicity is often associated with PSVT.

Assessment

The severity of symptoms in patients with PSVT depends on any underlying structural heart disease, the frequency of PSVT episodes, and the patient's hemodynamic reserve. Usually, patients with PSVT present with symptoms of dizziness, syncope, nausea, shortness of breath, intermittent palpitations, pain or discomfort in the neck, pain or discomfort in the chest, anxiety, fatigue, diaphoresis, and polyuria secondary atrial natriuretic factor secreted mainly by the heart's atria in response to atrial stretch. The most common symptoms are dizziness and palpitations. Patients with PSVT and a known history of coronary artery disease may present with a myocardial infarction secondary to the stress on the heart. Patients with PSVT and a known history of heart failure may come in with acute exacerbation. Frequent PSVTs in a patient can result in new-onset of heart failure secondary to tachycardia-induced cardiomyopathy.[18]

A detailed history of the patient with PSVT should include past medical and cardiac history, time of symptom onset, prior episodes, and treatments. The patients' current medication list must be obtained. Investigations of involvement in physical activities such as exercise or outdoor sports should be made, as patients who have symptomatic PSVT's avoid such hobbies. Patients presenting with PSVTs should get a thorough physical exam, including vital signs (respiratory rate, blood pressure, temperature, and heart rate) to help assess their hemodynamic stability.[19]

Evaluation

A significant component of evaluation for a patient who presents with signs and symptoms of PSVT is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate), review of the patient's medication list, and a 12-lead electrocardiogram. During an evaluation, a health care provider should establish if the patient is hemodynamically stable and whether they have any underlying ischemic heart disease or heart failure. Digoxin toxicity should be ruled out.

Healthcare providers should consider thyroid function testing, pulmonary function testing, including routine blood work, and echocardiography as part of their initial evaluation of patients presenting with symptomatic PSVTs.[20][21]

ECG features:

Sinus tachycardia with a heart rate more than 100 bpm with normal P waves
Atrial tachycardia with a heart rate between 120-150 bpm. The P wave morphology may be different from normal sinus rhythm
Multifocal atrial tachycardia with heart rates from 120-200 bpm with 3 or more different P wave morphologies
Atrial flutter with a heart rate of 200-300 bpm
Atrial fibrillation with irregularly irregular rhythm and no visible P waves
AVNRT with a heart rate of 150-250 bpm, P waves before or within the QRS complex, short PR interval
AVRT with a heart rate between 150-250 bpm, narrow QRS complex in orthodromic conduction and wide QRS complex in antidromic conduction

Medical Management

Treatment of PSVT in a patient is dependent on the type of rhythm present on the electrocardiogram and the patient's hemodynamic stability. Patients presenting with hypotension, shortness of breath, chest pain, shock, or altered mental status are considered hemodynamically unstable, and their electrocardiogram evaluation must be done to determine if they are in sinus rhythm or not. If they are not in sinus rhythm, these patients should undergo urgent cardioversion. If they are determined to be in appropriate sinus tachycardia, then their underlying etiology must be treated. For any manifestations of cardiac ischemia, intravenous beta-blockers should be considered. If they have inappropriate sinus tachycardia on the electrocardiogram and are determined to be hemodynamically unstable, treatment with intravenous beta-blockers may be appropriate.[22][23][24]

If on the initial evaluation, a patient is to found to be hemodynamically stable, then the treatment of the patient depends on the specific PSVT present on the electrocardiogram. If the 12-lead electrocardiogram shows that the rhythm is irregular and P waves are absent, then the patient should be appropriately treated for atrial fibrillation. If the rhythm on the electrocardiogram is irregular and flutter waves are present, then the patient should be treated for atrial flutter. If the rhythm on the electrocardiogram is irregular and multiple P wave morphologies are present, then the patient should be treated for multifocal atrial tachycardia.[25]

In patients who are hemodynamically stable and showing a regular rhythm with visible P waves on the electrocardiogram, then an assessment of the atrial rate, the relationship between the atrial and ventricular pacing, P-wave morphology and the P-wave position in the rhythm cycle is required. Type of PSVT present (atrial tachycardia, multifocal atrial tachycardia, atrial flutter, atrial flutter with a variable block, intra-atrial reentrant tachycardia, sinus tachycardia, sinoatrial node reentrant tachycardia, atrioventricular nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, junctional ectopic tachycardia, and nonparoxysmal junctional tachycardia) determines the treatment.[26][27]

In patients who are hemodynamically stable and have an electrocardiogram that shows a regular rhythm with undetectable P waves, Valsalva maneuvers, carotid sinus massage, or intravenous adenosine might be used to slow the ventricular rate or convert the rhythm into sinus rhythm and thus aid in the diagnosis. In some instances, increasing the electrocardiogram paper speed from 25 mm per second to 50 mm per second might help as well. If intravenous adenosine does not work, then intravenous or oral calcium channel blockers or beta-blockers should be used. Patients with PSVTs must also undergo evaluation for any underlying pre-excitation syndrome, and patients who fail medical treatment or those who might need radiofrequency catheter ablation need cardiology consultation.[28][29][30]

Nursing Management

Obtain an order for oxygen per nasal cannula adjusted to oxygen saturation
Monitor ECG for rate, rhythm, and conduction
Assess vital signs and ECG and report abnormal changes to the clinician
Explain the importance of rapidly reducing the heart rate to the patient and family
Cardioversion
- If necessary, explain the cardioversion procedure and answer questions
- Encourage verbalization of fears and concerns
- Administer intravenous medications such as diazepam as ordered before cardioversion
- Document pretreatment vital signs, level of consciousness, and peripheral pulses
- Place emergency crash cart with drugs and airway management supplies near the patient's room
- Assist with cardioversion
- Assess vital signs and the level of consciousness, level of sedation, capillary refill, cardiovascular, and respiratory status following cardioversion
- Document procedure, post cardioversion rhythm, and response to intervention

When To Seek Help

Unstable vital signs
Changes in vital signs
Sudden increases in the rate
Abnormal rhythm

Outcome Identification

Maintain adequate cardiac output and tissue perfusion
Demonstrate a ventricular rate within normal limits
Return to stable vital signs
Verbalize reduced anxiety
Verbalize an understanding of the rationale for the treatment measures

Coordination of Care

Treatment of PSVT can involve an interprofessional team, including emergency department physicians and nurses, cardiologists and cardiology nurses, primary care providers, and pharmacists. Emergency medical technicians are often the first to encounter patients and provide treatment. The team should evaluate, as outlined above. Nurses, pharmacists, and physicians can provide education. Pharmacists should educate patients about medication side effects and compliance, as well as checking for drug interactions. [Level 5]

Health Teaching and Health Promotion

Educating patients at risk for this rhythm and making a closed-loop communication between them and their providers can help further improve the management of these rhythms. If available, patient education should be provided using resources familiar to the patient including online resources and pamphlets.

Pearls and Other issues

Frequent PSVT can result in tachycardia-induced cardiomyopathy, a study on pregnant females found that PSVT in the first to second gestational month increase the chances of the child developing ostium secundum atrial septal defect.

(Click Image to Enlarge)

<p>Narrow Complex Tachycardia With Incomplete Right Bundle Branch

Narrow Complex Tachycardia With Incomplete Right Bundle Branch. A 12-lead ECG shows a narrow complex tachycardia (with incomplete right bundle branch). The P waves are not distinctly visible. However, a negative deflection at the end of the QRS complex in lead II could be a retrograde P wave, creating the impression of "pseudo S" wave.