20 Dysrhythmias and conduction disturbances
Overview/pathophysiology
Dysrhythmias are abnormal rhythms of the heart’s electrical system. They can originate in any part of the conduction system, such as the sinus node, atrium, atrioventricular (A-V) node, His-Purkinje system, bundle branches, and ventricular tissue. Although a variety of diseases may cause dysrhythmias, the most common are coronary artery disease (CAD) and myocardial infarction (MI). Other causes may include electrolyte imbalance, changes in oxygenation, and drug toxicity. Cardiac dysrhythmias may result from the following mechanisms:
Disturbances in automaticity:
May involve an increase or decrease in automaticity in the sinus node (e.g., sinus tachycardia or sinus bradycardia). Premature beats may arise from the atria, junction, or ventricles. Abnormal rhythms, such as atrial or ventricular tachycardia, also may occur.
Disturbances in conductivity:
Conduction may be too rapid, as in conditions caused by an accessory pathway (e.g., Wolff-Parkinson-White syndrome), or too slow (e.g., A-V block). Reentry is a situation in which a stimulus reexcites a conduction pathway through which it already has passed. Once started, this impulse may circulate repeatedly. For reentry to occur, there must be two different pathways for conduction: one with slowed conduction and one with unidirectional block.
Assessment
Signs and symptoms:
Can vary on a continuum from absence of symptoms to complete cardiopulmonary collapse. General indicators include alterations in level of consciousness (LOC), vertigo, syncope, seizures, weakness, fatigue, activity intolerance, shortness of breath, dyspnea on exertion, chest pain, palpitations, sensation of “skipped beats,” anxiety, and restlessness.
Physical assessment:
Increases or decreases in heart rate (HR), blood pressure (BP), and respiration rate (RR); dusky color or pallor; crackles (rales); cool skin; decreased urine output; weakened and paradoxical pulse and abnormal heart sounds (e.g., paradoxical splitting of S1 and S2).
Electrocardiogram (ECG) results:
Some findings seen with various dysrhythmias include abnormalities in rate such as sinus bradycardia or sinus tachycardia, irregular rhythm such as atrial fibrillation, extra beats such as premature atrial contractions (PACs) and premature junctional contractions (PJCs), wide and bizarre-looking beats such as premature ventricular contractions (PVCs) and ventricular tachycardia (VT), a fibrillating baseline such as ventricular fibrillation (VF), and a straight line as with asystole.
Diagnostic tests
Serum electrolyte levels:
To identify electrolyte abnormalities that can precipitate dysrhythmias. The most common are potassium and magnesium abnormalities.
Drug levels:
To identify toxicities (e.g., of digoxin, quinidine, procainamide, aminophylline) that can precipitate dysrhythmias, or to determine substance abuse that can affect heart rate and rhythm, such as cocaine.
Ambulatory monitoring (e.g., holter monitor or cardiac event recorder):
To identify subtle dysrhythmias, associate abnormal rhythms by means of patient’s symptoms, and assess response to exercise.
Electrophysiologic study:
Invasive test in which two to three catheters are placed into the heart, giving it a pacing stimulus at varying sites and of varying voltages. The test determines origin of dysrhythmia, inducibility, and effectiveness of drug therapy in dysrhythmia suppression.
Exercise stress testing:
Used in conjunction with Holter monitoring to detect advanced grades of PVCs (those caused by ischemia) and to guide therapy. During the test, ECG and BP readings are taken while patient walks on a treadmill or pedals a stationary bicycle; response to a constant or increasing workload is observed. The test continues until patient reaches target heart rate or symptoms such as chest pain, severe fatigue, dysrhythmias, or abnormal BP occur.
Oximetry or ABG values:
To document trend of hypoxemia.
Nursing diagnosis:
Decreased cardiac output
related to altered rate, rhythm, or conduction or to negative inotropic changes
Desired Outcome: Within 1 hr of treatment/intervention, patient has improved cardiac output as evidenced by BP 90/60 mm Hg or higher, HR 60-100 bpm, and normal sinus rhythm on ECG.
| ASSESSMENT/INTERVENTIONS | RATIONALES |
|---|---|
| Assess patient’s heart rhythm continuously on a monitor. | This assessment will reveal whether dysrhythmias occur or increase in occurrence. |
| Assess BP and symptoms when dysrhythmias occur. | Signs of decreased cardiac output include decreased BP and symptoms such as unrelieved and prolonged palpitations, chest pain, shortness of breath, weakened and rapid pulse (more than 150 bpm), sensation of skipped beats, dizziness, and syncope. |
| Report significant findings to health care provider. | Decreased cardiac output should be reported promptly for timely intervention, because it may be life threatening. |
| If symptoms of decreased cardiac output occur, prepare to transfer patient to CCU. | Transfer to CCU for specialized and intensive care and monitoring is essential. |
| Document dysrhythmias with rhythm strip, using a 12-lead ECG as necessary. | This assessment will identify dysrhythmias and their general trend. |
| Monitor patient’s laboratory data, particularly electrolyte and digoxin levels. | Serum potassium levels less than 3.5 mEq/L or more than 5.0 mEq/L can cause dysrhythmias. Digoxin toxicity may cause heart block or dysrhythmias. |
| Administer antidysrhythmic agents as prescribed; note patient’s response to therapy based on action of the following classifications: | |
| Class IA: sodium channel blockers; quinidine, procainamide, disopyramide | Decreases depolarization moderately and prolongs repolarization. |
| Class IB: sodium channel blockers; phenytoin, mexiletine, tocainide | Decreases depolarization and shortens repolarization. |
| Class IC: sodium channel blockers; encainide, flecainide, propafenone | Significantly decreases depolarization with minimal effect on repolarization. |
| Class II: beta-blockers; propranolol, metoprolol, atenolol, acebutolol | Slows sinus automaticity, slows conduction via A-V node, controls ventricular response to supraventricular tachycardias, and shortens the action potential of Purkinje fibers. |
| Class III: potassium channel blockers; bretylium, amiodarone, sotalol, Ibutilide, dofetilide | Increases the action potential and refractory period of Purkinje fibers, increases ventricular fibrillation threshold, restores injured myocardial cell electrophysiology toward normal, and suppresses reentrant dysrhythmias. |
| Class IV: calcium channel blockers; verapamil, diltiazem, nifedipine | Depresses automaticity in the sino-atrial (S-A) and A-V nodes, blocks the slow calcium current in the A-V junctional tissue, reduces conduction via the A-V node, and is useful in treating tachydysrhythmias because of A-V junction reentry. This class of drugs also vasodilates. |
| Monitor corrected QT interval (QTc) when initiating drugs known to cause QT prolongation (e.g., sotalol, propafenone, dofetilide, flecainide). | When QTc is prolonged, it can increase risk of dysrhythmias. QTc equals QT (in seconds) divided by the square root of the R to R interval (in seconds). |
| Provide O2 as prescribed. | O2 may be beneficial if dysrhythmias are related to ischemia, or are causing hypoxia. |
| Deliver O2 with humidity. | Humidity helps prevent oxygen’s drying effects on oral and nasal mucosa. |
| Maintain a quiet environment, and administer pain medications promptly. | Both stress and pain can increase sympathetic tone and cause dysrhythmias. |
| If life-threatening dysrhythmias occur, initiate emergency procedures and cardiopulmonary resuscitation (as indicated by advanced cardiac life support [ACLS] protocol). | This action provides circulation to vital organs and restores heart to normal or viable rhythm. |
| When dysrhythmias occur, stay with patient; provide support and reassurance while performing assessments and administering treatment. | This action reduces stress and provides comfort, which optimally will decrease dysrhythmias. |
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