|Mean LOS:||3.5 days|
|Description:||MEDICAL: Cardiac Arrhythmia and Conduction Disorders with CC|
A cardiac dysrhythmia is any disturbance in the normal rhythm of the electrical excitation of the heart. It can be the result of a primary cardiac disorder, a response to a systemic condition, or the result of an electrolyte imbalance or a drug toxicity. The severity of a dysrhythmia, depending on its hemodynamic effect on the cardiac output, varies based on the cause of the dysrhythmia and the myocardium’s ability to adapt. An atrial dysrhythmia arises in the atria of the heart. If the dysrhythmia causes the patient to lose the “atrial kick” (the blood that is ejected into the ventricle during atrial systole), the patient may have more symptoms. The atrial kick provides approximately 35% of the total end-diastolic volume, which is an essential contribution to ventricular filling in individuals with heart disease. Atrial dysrhythmias that cause the loss of the atrial kick include atrial flutter and atrial fibrillation. Figure 1 illustrates types of atrial dysrhythmias in Lead II.
Sinus bradycardia, a heart rate less than 60 beats per minute, has a rhythm that is regular, with the electrical impulse originating in the sinoatrial (SA) node. There is a 1:1 ratio of P waves to QRS complexes, and the P wave and QRS complexes are of normal configuration. Sinus bradycardia is primarily caused by an excessive parasympathetic response. It can be a normal, asymptomatic occurrence in healthy individuals such as athletes or a desired medication effect with drugs such as digoxin and verapamil. Abnormal conditions such as pain, anxiety, increased intracranial pressure, or myocardial infarction can also cause sinus bradycardia. Because of its effects on cardiac output, sinus bradycardia can cause symptoms of dizziness, fatigue, palpitations, chest pain, and congestive heart failure.
Sinus tachycardia, a heart rate greater than 100 beats but rarely more than 160 beats per minute, is a regular rhythm whose electrical impulse originates in the SA node. There is a 1:1 ratio of P waves to QRS complexes, and the P wave and QRS complexes are of normal configuration. Sinus tachycardia is generally the result of increased stimulation of the sympathetic nervous system and the resulting release of catecholamines. It can also be a normal response to an increased demand for oxygenation, as in exercise or fever, or in response to a decreased cardiac output, as in congestive heart failure or shock syndromes. It can also occur in response to stress; anxiety; or an intake of caffeine, nicotine, or anticholinergic medications.
Sinus arrhythmia, defined as a variable rate of impulse discharge from the SA node, occurs when the rhythm is irregular and usually corresponds to the respiratory pattern. The rhythm increases with inspiration and slows with expiration. There is a 1:1 ratio of P waves to QRS complexes, and the P wave and QRS complex are of normal configuration. Sinus arrhythmia can be a normal variation in children. The vagal effect of some medications and of SA nodal disease and conditions that affect vagal tone can also be a cause.
Atrial fibrillation, a rapid and disorganized atrial dysrhythmia, occurs at atrial rates of 400 to 600 beats per minute. There are no clearly discernible P waves, but rather irregular fibrillatory waves. The QRS complex appears normal, but there is a variable, irregular ventricular response because of the atrioventricular (AV) node’s ability to respond only partially to this rapid rate. Although atrial fibrillation can occur in healthy individuals, it is generally found in patients with underlying cardiovascular diseases such as ischemic heart disease, mitral valve disease, congestive heart failure, and pericarditis.
Atrial flutter, defined as an abnormally fast, regular atrial rhythm that originates from an ectopic atrial focus, is usually in the range of 250 to 400 beats per minute. It is characterized by regular flutter or sawtooth-appearing waves. The QRS complex appears normal in configuration, and there is not a 1:1 ratio of the P to QRS complex because the ventricle cannot respond to the fast atrial rate. Atrial flutter is seldom seen in a healthy individual. Most frequently, atrial flutter is associated with ischemic myocardial disease, acute myocardial infarction, and rheumatic heart disease. The patient is usually asymptomatic because of a controlled ventricular response.
Premature atrial contractions (PACs), cardiac contractions initiated in the atria, occur earlier than expected. The underlying rhythm is regular, with the early beat producing a slight irregularity. There is usually a 1:1 ratio of P wave to QRS complex unless the P wave is blocked because of the refractory period of the AV node. The P wave of the premature beat may exhibit a slightly different configuration because it does not originate in the SA node but from another area of the atrium. There may be a short “compensatory” pause after the ectopic (electrical stimulation of a cardiac contraction beginning at a point other than the SA node) beat. PACs can be a normal occurrence in all age groups or they can be the result of ischemic heart disease, rheumatic heart disease, stimulant ingestion, or digitalis toxicity.
Paroxysmal supraventricular tachycardia (PSVT), the sudden onset of a rapid atrial and ventricular rate of 160 to 250 beats per minute, occurs with a regular but aberrant P wave. The P waves are difficult to discern from the preceding T wave, but a P wave precedes each QRS. PSVT occurs when there is an intrinsic abnormality of the AV conduction or in conditions associated with stress, hypoxia, hypokalemia, hypertension, heart disease, or hyperthyroidism. It is also associated with digitalis toxicity, caffeine ingestion, and the use of central nervous system stimulants.
Each type of atrial dysrhythmia has specific causes, as listed previously.
A number of atrial arrhythmias have been found to run in families. Potassium channel gene mutations can cause familial atrial fibrillation. Sick sinus syndrome can be caused by a sodium channel mutation (SCN5A), via recessive inheritance, or through mutations in the cardiac pacemaker channel gene HCN4 via dominant inheritance. Wolff-Parkinson-White syndrome can be seen in both autosomal and mitochondrial disease.
Gender, ethnic/racial, and life span considerations
The normal aging process is associated with an increase in atrial tachydysrythmias and bradydysrythmias. They occur in both males and females; increasing incidence of cardiac diseases, atherosclerosis, and degenerative hypertrophy of the left ventricle that occurs with aging are all contributing factors. Ethnicity and race have no known effect on the risk of appendicitis.
Global health considerations
No data are available.
Many patients with suspected cardiac dysrhythmias describe a history of symptoms, indicating periods of decreased cardiac output. Although many atrial dysrhythmias are asymptomatic, 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 restrictions, and activity restrictions and a current medication history.
Inspect the patient’s skin for changes in color or the presence of edema. Auscultate the patient’s heart rate and rhythm and note the first and second heart sounds and any adventitious sounds. Auscultate the patient’s blood pressure. Perform a full respiratory assessment and note any adventitious breath sounds or labored breathing.
Although not usually life-threatening, any change in heart rhythm can provoke a great deal of anxiety and fear. Assess the ability of the patient and significant others to cope with this potential alteration.
|Test||Normal Result||Abnormality With Condition||Explanation|
|12-lead electrocardiogram (ECG)||Regular sinus rhythm||See Figure 1, Types of Atrial Dysrhythmias||To detect specific conduction defects and to monitor the patient’s cardiac response to electrolyte imbalances, drug effects, and toxicities|
Other Tests: Pulse oximetry, echocardiography, continuous ambulatory monitoring to provide a 12- to 24-hour continuous recording of myocardial electrical activity as the patient performs normal daily activities; event recorders for ECG monitoring as long as a month; exercise ECG; electrophysiology study; thyroid function tests; digoxin level
Primary nursing diagnosis
DiagnosisAltered tissue perfusion (cardiopulmonary, cerebral, renal, peripheral) related to rapid heart rates or the loss of the atrial kick
OutcomesCirculation status; Cardiac pump effectiveness; Tissue perfusion: Cardiopulmonary, Cerebral, Renal, Peripheral; Vital sign status
InterventionsCirculatory 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
The dysrhythmia needs to be identified and appropriate treatment started (Table 1). Trials of various medications or combinations of medications may be used to control the dysrhythmia if the patient is symptomatic. Low-flow oxygen by nasal cannula or mask is often prescribed for patients during tachycardic rhythms. Some patients may require cardioversion, a synchronized countershock for atrial dysrhythmias that are resistant to medical therapy.
|Paroxysmal supraventricular tachycardia|
|Medication or Drug Class||Dosage||Description||Rationale|
|Calcium channel blockers||Varies by drug||Inhibits influx of calcium through the slow channels into the cells of the myocardial and arterial smooth muscles||Decreases nodal conduction leading to an antiarrhythmic effect|
|Beta-adrenergic antagonists||Varies by drug||Blocks beta-adrenergic receptors||May be used to slow the rate in sinus tachycardia if the patient has myocardial ischemia; may also be used to control a rapid ventricular response in atrial fibrillation|
Maintain the patient’s airway, breathing, and circulation. To maximize oxygen available to the myocardium, 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. Discuss any potential precipitating factors with the patient. For some patients, strategies to reduce stress or lifestyle changes help to limit the incidence of dysrhythmias. Teach the patient to reduce the amount of caffeine intake in the diet. If appropriate, encourage the patient to become involved in an exercise program or a smoking-cessation group. Provide emotional support and information about the dysrhythmia, the precipitating factors, and mechanisms to limit the dysrhythmia. If the patient is at risk for electrolyte imbalance, teach the patient any dietary considerations to prevent electrolyte depletion.
Evidence-Based Practice and Health Policy
Ammash, N.M., Phillips, S.D., Hodge, D.O., Connolly, H.M., Grogan, M.A., Friedman, P.A., …Asirvatham, S.J. (2012). Outcome of direct current cardioversion for atrial arrhythmias in adults with congenital heart disease. International Journal of Cardiology, 154(3), 270–274.
- Cardioversion is considered an effective treatment for atrial dysrhythmias that are resistant to medical therapy.
- In one study among 63 adults with atrial dysrhythmias secondary to congenital heart disease, direct current cardioversion (DCCV) was successful in 94% of the attempts. However, 52% of patients in whom DCCV was initially successful had a recurrent atrial dysrhythmia.
- In this sample, 46% of patients had atrial fibrillation, 46% had atrial flutter, and 8% had supraventricular tachycardia. Atrial fibrillation was most common among the patients in which DCCV initially failed or dysrhythmia reoccurred (p = 0.009).
- Complications of DCCV, including bradycardia and minor skin burns, occurred in 7.5% of patients.
- 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, ability to perform self-care
- Complications: Dizziness, syncope, hypotension, electrolyte imbalance, uncorrected cardiac dysrhythmias, ineffective patient or family coping