NCLEX Questions for Cardiac Dysrhythmias

Hypotension and dizziness The client with uncontrolled atrial fibrillation with a ventricular rate more than 150 beats a minute is at risk for low cardiac output because of loss of atrial kick. The nurse assesses the client for palpitations, chest pain or discomfort, hypotension, pulse deficit, fatigue, weakness, dizziness, syncope, shortness of breath, and distended neck veins.

Atrial fibrillation Atrial fibrillation is characterized by a loss of P waves; an undulating, wavy baseline; QRS duration that is often within normal limits; and an irregular ventricular rate, which can range from 60 to 100 beats per minute (when controlled with medications) to 100 to 160 beats per minute (when uncontrolled).

Tightly secured cable connections. Motion artifact, or “noise,” can be caused by frequent client movement, electrode placement on limbs, and insufficient adhesion to the skin, such as placing electrodes over hairy areas of the skin. Electrode placement over bony prominence's also should be avoided. Signal interference can also occur with electrode removal and cable disconnection.

Notify the physician promptly PVCs are often a precursor of life-threatening dysrhythmias, including ventricular tachycardia and ventricular fibrillation. An occasional PVC is not considered dangerous, but if PVCs occur at a rate greater than 5 or 6 per minute in the post MI client, the physician should be notified immediately. More than 6 PVCs per minute is considered serious and usually calls for decreasing ventricular irritability by administering medications such as lidocaine. Increasing the IV infusion rate would not decrease the number of PVCs. Increasing the oxygen concentration should not be the nurse’s first course of action; rather, the nurse should notify the physician promptly. Administering a prescribed analgesic would not decrease ventricular irritability.

Vagus nerve to slow the heart rate Carotid sinus massage is one of the maneuvers used for vagal stimulation to decrease a rapid heart rate and possibly terminate a tachydysrhythmia. The others include inducing the gag reflex and asking the client to strain or bear down. Medication therapy often is needed as an adjunct to keep the rate down or maintain the normal rhythm.

Blood pressure and peripheral perfusion Premature ventricular contractions can cause hemodynamic compromise. The shortened ventricular filling time with the ectopic beats leads to decreased stroke volume and, if frequent enough, to decreased cardiac output. The client may be asymptomatic or may feel palpations. PVCs can be caused by cardiac disorders or by any number of physiological stressors, such as infection, illness, surgery, or trauma, and by the intake of caffeine, alcohol, or nicotine.

Ventricular tachycardia Ventricular tachycardia is characterized by the absence of P waves, wide QRS complexes (usually greater than 0.14 second), and a rate between 100 and 250 impulses per minute. The rhythm is usually regular.

The RR intervals are relatively consistent | One P wave precedes each QRS complex The consistency of the RR interval indicates regular rhythm. A normal P wave before each complex indicates the impulse originated in the SA node. The number of complexes in a 6 second strip is multiplied by 10 to approximate the heart rate; normal sinus rhythm is 60 to 100. Elevation of the ST segment is a sign of cardiac ischemia and is unrelated to the rhythm. The QRS duration should be less than 0.12 second; the PR interval should be 0.12 to 0.20 second.

Administer amiodarone (Cordarone) intravenously First-line treatment of ventricular tachycardia in a client who is hemodynamically stable is the use of anti-dysrhythmics such as amiodarone (Cordarone), lidocaine (Xylocaine), and procainamide (Pronestyl). Cardioversion also may be needed to correct the rhythm (cardioversion is recommended for stable ventricular tachycardia). Defibrillation is used with pulseless ventricular tachycardia. Epinephrine would stimulate and already excitable ventricle and is contraindicated.

Inhale deeply and cough forcefully every 1 to 3 seconds. Cough cardiopulmonary resuscitation (CPR) sometimes is used in the client with unstable ventricular tachycardia. The nurse tells the client to use cough CPR, if prescribed, by inhaling deeply and coughing forcefully every 1 to 3 seconds. Cough CPR may terminate the dysrhythmia or sustain the cerebral and coronary circulation for a short time until other measures can be implemented.

Syncope and low ventricular rate In complete atrioventricular block, the ventricles take over the pacemaker function in the heart but at a much slower rate than that of the SA node. As a result there is decreased cerebral circulation, causing syncope.

Defibrillate the client Ventricular fibrillation is a death-producing dysrhythmia and, once identified, must be terminated immediately by precordial shock (defibrillation). This is usually a standing physician’s order in a CCU.

Widening of QRS complexes to 0.12 second or greater. Bundle branch block interferes with the conduction of impulses from the AV node to the ventricle supplied by the affected bundle. Conduction through the ventricles is delayed, as evidenced by a widened QRS complex.

Ventricular fibrillation Ventricular fibrillation is characterized by irregular, chaotic undulations of varying amplitudes. Ventricular fibrillation has no measurable rate and no visible P waves or QRS complexes and results from electrical chaos in the ventricles.

Normal sinus rhythm. Measurements are normal, measuring 0.12 to 0.20 second and 0.4 to 0.10 second, respectively.’