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NURS 287
Rick Nilson

DYSRHYTHMIAS  Sinus bradycardia has a normal sinus rhythm, but the SA node fires at a rate less than 60 beats/minute and is referred to as absolute bradycardia. o Clinical associations. Sinus bradycardia may be a normal sinus rhythm (e.g., in aerobically trained athletes), and it may occur in response to carotid sinus massage, Valsalva maneuver, hypothermia, and administration of parasympathomimetic drugs. o Disease states associated with sinus bradycardia are hypothyroidism, increased intracranial pressure, obstructive jaundice, and inferior wall myocardial infarction (MI). o Treatment consists of administration of atropine (an anticholinergic drug) for the patient with symptoms. Pacemaker therapy may be required.  Sinus tachycardia has a normal sinus rhythm, but the SA node fires at a rate greater than 100 beats/minute as a result of vagal inhibition or sympathetic stimulation. o Clinical associations. Sinus tachycardia is associated with physiologic and psychologic stressors such as exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. It can also be an effect of certain drugs. o Angina may result from sinus tachycardia due to the increased myocardial oxygen consumption that is associated with an increased HR. o Treatment is based on the underlying cause. For example, if a patient is experiencing tachycardia from pain, tachycardia should resolve with effective pain management.  Premature atrial contraction (PAC) is a contraction originating from an ectopic focus in the atrium in a location other than the sinus node. A PAC may be stopped (nonconducted PAC), delayed (lengthened PR interval), or conducted normally through the AV node. o Clinical associations. PACs can result from emotional stress or physical fatigue; from the use of caffeine, tobacco, or alcohol; from hypoxia or electrolyte imbalances; and from disease states such as hyperthyroidism, chronic obstructive pulmonary disease (COPD), and heart disease including coronary artery disease (CAD) and valvular disease. o In healthy persons, isolated PACs are not significant. In persons with heart disease, frequent PACs may indicate enhanced automaticity of the atria or a reentry mechanism and may warn of or initiate more serious dysrhythmias. o Treatment depends on the patient’s symptoms. For example, withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be warranted.  Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His. o PSVT occurs because of a reentrant phenomenon (reexcitation of the atria when there is a one-way block) and is usually triggered by a PAC. o In the normal heart, PSVT is associated with overexertion, emotional stress, deep inspiration, and stimulants such as caffeine and tobacco. It is also associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale. o Prolonged PSVT with HR greater than 180 beats/minute may precipitate a decreased CO, resulting in hypotension, dyspnea, and angina. o Treatment for PSVT includes vagal stimulation and drug therapy (i.e., IV adenosine).  Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth- shaped flutter waves that originate from a single ectopic focus in the right atrium. o Atrial flutter is associated with CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism, and the use of drugs such as digoxin, quinidine, and epinephrine. o High ventricular rates (over 100/minute) and the loss of the atrial “kick” (atrial contraction reflected by a sinus P wave) can decrease CO and cause serious consequences such as chest pain and HF. o Patients with atrial flutter are at increased risk of stroke because of the risk of thrombus formation in the atria from the stasis of blood. o The primary goal in treatment of atrial flutter is to slow the ventricular response by increasing AV block.  Atrial fibrillation is characterized by a total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction. o Atrial fibrillation usually occurs in the patient with underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis. It can be caused by thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery. o Atrial fibrillation can often result in a decrease in CO, and thrombi may form in the atria as a result of blood stasis. An embolized clot may develop and pass to the brain, causing a stroke. o The goals of treatment include a decrease in ventricular response and prevention of cerebral embolic events.  Junctional dysrhythmias refer to dysrhythmias that originate in the area of the AV node, primarily because the SA node has failed to fire or the signal has been blocked. In this situation, the AV node becomes the pacemaker of the heart. o Junctional premature beats are treated in a manner similar to that for PACs. o Other junctional dysrhythmias include junctional escape rhythm, accelerated junctional rhythm, and junctional tachycardia. These dysrhythmias are treated according to the patient’s tolerance of the rhythm and the patient’s clinical condition. o Junctional dysrhythmias are often associated with CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease. Certain drugs (e.g., digoxin, amphetamines, caffeine, nicotine) can also cause junctional dysrhythmias. o Treatment varies according to the type of junctional dysrhythmia.  First-degree AV block is a type of AV block in which every impulse is conducted to the ventricles but the duration of AV conduction is
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