Types of Dysrhythmias

What is this ECG tracing of?

A, Atrial flutter with a 4 : 1 conduction (four flutter [F] waves to each QRS complex). B, Atrial fibrillation with a controlled ventricular response. Note the chaotic fibrillatory (f) waves (arrows) between the RS complexes. NOTE: Recorded from lead V1.

What is this ECG tracings of?

A. Sinus bradycardia. B. Sinus tachycardia.

Which patient teaching points should the nurse include when providing discharge instructions to a patient with a new permanent pacemaker and the caregiver (select all that apply)? a. Avoid or limit air travel. b. Take and record a daily pulse rate. c. Obtain and wear a Medic Alert ID device at all times. d. Avoid lifting arm on the side of the pacemaker above shoulder. e. Avoid microwave ovens because they interfere with pacemaker function

B, C, and D.

A patient admitted with ACS has continuous ECG monitoring. An examination of the rhythm strip reveals the following characteristics: atrial rate 74 beats/min and regular; ventricular rate 62 beats/min and irregular; P wave normal shape; PR interval lengthens progressively until a P wave is not conducted; QRS normal shape. The priority nursing intervention would be to: a. perform synchronized cardioversion. b. administer epinephrine 1 mg IV push. c. observe for symptoms of hypotension or angina. d. apply transcutaneous pacemaker pads on the patient.

C

The nurse is monitoring the ECG of a patient admitted with ACS. Which ECG characteristics would be most suggestive of myocardial ischemia? a. Sinus rhythm with a pathologic Q wave b. Sinus rhythm with an elevated ST segment c. Sinus rhythm with a depressed ST segment d. Sinus rhythm with premature atrial contractions

C

Important teaching for the patient scheduled for a radiofrequency catheter ablation procedure includes explaining that a. ventricular bradycardia may be induced and treated during the procedure. b. a catheter will be placed in both femoral arteries to allow double-catheter use. c. the procedure will destroy areas of the conduction system that are causing rapid heart rhythms. d. a general anesthetic will be given to prevent the awareness of any "sudden cardiac death" experiences.

C.

Atrial Fibrillation.

Clinical Associations. Associated in a patients with underlying heart disease, such as CAD, valvular heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis. It often develops acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and heart surgery. ECG Characteristics. During atrial fibrillation, the atrial rate may be as high as 350 to 600 beats/minute. P waves are replaced by chaotic, fibrillatory waves. Ventricular rate varies and the rhythm is usually irregular. When the ventricular rate is between 60 and 100 beats/minute, it is atrial fibrillation with a controlled ventricular response. Atrial fibrillation with a ventricular rate greater than 100 beats/minute is atrial fibrillation with a rapid (or uncontrolled) ventricular response. The PR interval is not measurable, and the QRS complex usually has a normal shape and duration. At times, atrial flutter and atrial fibrillation may coexist.1 Clinical Significance. Atrial fibrillation results in a decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response. Thrombi (clots) form in the atria because of blood stasis. An embolized clot may develop and move to the brain, causing a stroke. Atrial fibrillation accounts for as many as 17% of all strokes.9 Treatment. The goals of treatment of atrial fibrillation include a decrease in ventricular response (to less than 100 beats/minute), prevention of stroke, and conversion to sinus rhythm, if possible. Ventricular rate control is a priority for patients with atrial fibrillation. Drugs used for rate control include calcium channel blockers (e.g., diltiazem), β-blockers (e.g., metoprolol), dronedarone, and digoxin (Lanoxin). For some patients, drug or electrical conversion of atrial fibrillation to a normal sinus rhythm may be considered (e.g., reduced exercise tolerance with rate control drugs, contraindications to warfarin). The most common antidysrhythmia drugs used for conversion to and maintenance of sinus rhythm include amiodarone and ibutilide.8 Electrical cardioversion may convert atrial fibrillation to a normal sinus rhythm. If a patient is in atrial fibrillation for longer than 48 hours, anticoagulation therapy with warfarin is needed for 3 to 4 weeks before the cardioversion and for several weeks after successful cardioversion.5 Anticoagulation therapy is necessary because the procedure can cause the clots to dislodge, placing the patient at risk for stroke. A transesophageal echocardiogram may be performed to rule out clots in the atria. If no clots are present, anticoagulation therapy may not be needed before the cardioversion. If drugs or cardioversion does not convert atrial fibrillation to normal sinus rhythm, long-term anticoagulation therapy is needed (Table 35-8). Warfarin is the drug of choice, and patients are monitored for therapeutic levels (e.g., international normalized ratio [INR]). Alternatives to warfarin are available for anticoagulation therapy in patients with nonvalvular atrial fibrillation. Examples include dabigatran (Pradaxa), apixaban (Eliquis), and rivaroxaban (Xarelto). These drugs do not require routine laboratory testing.8

Junctional Dysrhythmias.

Clinical Associations. Associated with CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease. Certain drugs (e.g., digoxin, nicotine, amphetamines, caffeine) can also cause junctional dysrhythmias. ECG Characteristics. In junctional escape rhythm, the HR is 40 to 60 beats/minute. It is 61 to 100 beats/minute in accelerated junctional rhythm and 101 to 180 beats/minute in junctional tachycardia. Rhythm is regular. The P wave is abnormal in shape and inverted, or it may be hidden in the QRS complex (Fig. 35-15). The PR interval is less than 0.12 second when the P wave precedes the QRS complex. The QRS complex is usually normal. Clinical Significance. Junctional escape rhythms serve as a safety mechanism when the SA node has not been effective. Escape rhythms such as this should not be suppressed. Accelerated junctional rhythm is due to sympathetic stimulation to improve CO. Junctional tachycardia indicates a more serious problem. This rhythm may reduce CO, causing the patient to become hemodynamically unstable (e.g., hypotensive). Treatment. Treatment varies according to the type of junctional dysrhythmia. If a patient has symptoms with a junctional escape rhythm, atropine can be used. In accelerated junctional rhythm and junctional tachycardia caused by drug toxicity, the drug is stopped. In the absence of digitalis toxicity, β-blockers, calcium channel blockers, and amiodarone are used for rate control. Cardioversion should not be used.

First-Degree AV Block.

Clinical Associations. Associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (e.g., hypokalemia), vagal stimulation, and drugs such as digoxin, β-blockers, calcium channel blockers, and flecainide. ECG Characteristics. In first-degree AV block, the HR is normal and rhythm is regular. The P wave is normal, the PR interval is prolonged (greater than 0.20 second), and the QRS complex usually has a normal shape and duration. Clinical Significance. First-degree AV block is usually not serious but can be a sign of higher degrees of AV block. Patients with first-degree AV block are asymptomatic. Treatment. There is no treatment for first-degree AV block. Changes to potentially causative situations may be considered. Monitor patients for any new changes in heart rhythm

Ventricular Tachycardia.

Clinical Associations. Associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, long QT syndrome, drug toxicity, and central nervous system disorders. This dysrhythmia can be seen in patients who have no evidence of heart disease. ECG Characteristics. Ventricular rate is 150 to 250 beats/minute. Rhythm may be regular or irregular. AV dissociation may be present, with P waves occurring independently of the QRS complex. The atria may be depolarized by the ventricles in a retrograde fashion. The P wave is usually buried in the QRS complex, and the PR interval is not measurable. The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration). The T wave is in the opposite direction of the QRS complex (Fig. 35-18). Clinical Significance. VT can be stable (patient has a pulse) or unstable (patient is pulseless). Sustained VT causes a severe decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction. This results in hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest. The dysrhythmia must be treated quickly, even if it occurs only briefly and stops abruptly. Episodes may recur if prophylactic treatment is not started. VF may also develop. Treatment. Precipitating causes (e.g., electrolyte imbalances, ischemia) must be identified and treated. If the VT is monomorphic and the patient is clinically stable (i.e., pulse is present) and has preserved left ventricular function, IV procainamide, sotalol, or amiodarone is used. These drugs can also be used if the VT is polymorphic with a normal baseline QT interval. Polymorphic VT with a prolonged baseline QT interval is treated with IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing (discussed later in this chapter). Drugs that prolong the QT interval (e.g., dofetilide [Tikosyn]) should be discontinued. Cardioversion is used if drug therapy is ineffective. VT without a pulse is a life-threatening situation. It is treated in the same manner as VF. Cardiopulmonary resuscitation (CPR) and rapid defibrillation are the first lines of treatment, followed by the administration of vasopressors (e.g., epinephrine) and antidysrhythmics (e.g., amiodarone) if defibrillation is unsuccessful.11 An accelerated idioventricular rhythm (AIVR) can develop when the intrinsic pacemaker rate (SA node or AV node) becomes less than that of a ventricular ectopic pacemaker. The rate is between 40 and 100 beats/minute. It is most commonly associated with acute MI and reperfusion of the myocardium after thrombolytic therapy or percutaneous coronary interventions (e.g., angioplasty). It can be seen with digitalis toxicity. In the setting of acute MI, AIVR is usually self-limiting and well tolerated, and it needs no treatment. If the patient becomes symptomatic (e.g., hypotensive, chest pain), atropine can be considered. Temporary pacing may be required. Drugs that suppress ventricular rhythms (e.g., amiodarone) should not be used, since these can terminate the ventricular rhythm and further reduce the HR.

Paroxysmal Supraventricular Tachycardia.

Clinical Associations. Associated with overexertion, emotional stress, deep inspiration, and stimulants such as caffeine and tobacco. PSVT is also associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale. ECG Characteristics. In PSVT, the HR is 150 to 220 beats/minute and rhythm is regular or slightly irregular. The P wave is often hidden in the preceding T wave. If seen, it may have an abnormal shape. The PR interval may be shortened or normal and the QRS complex is usually normal. Clinical Significance. The clinical significance of PSVT depends on the associated symptoms. A prolonged episode and HR greater than 180 beats/minute will cause decreased CO because of reduced stroke volume. Manifestations include hypotension, palpitations, dyspnea, and angina. Treatment. Treatment for PSVT includes vagal stimulation and drug therapy. Common vagal maneuvers include Valsalva, carotid massage, and coughing. IV adenosine is the drug of choice to convert PSVT to a normal sinus rhythm. This drug has a short half-life (10 seconds) and is well tolerated.5 IV β-blockers and calcium channel blockers (diltiazem and verapamil [Calan]) can also be used. If vagal stimulation and drug therapy are ineffective and the patient becomes hemodynamically unstable, synchronized cardioversion is used

Sinus Tachycardia.

Clinical Associations. 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 drugs such as epinephrine, norepinephrine (Levophed), atropine, caffeine, theophylline, or hydralazine. In addition, many over-the-counter cold remedies have active ingredients (e.g., pseudoephedrine [Sudafed]) that can cause tachycardia. ECG Characteristics. In sinus tachycardia, the HR is 101 to 200 beats/minute and rhythm is regular. The P wave is normal, precedes each QRS complex, and has a normal shape and duration. The PR interval is normal and the QRS complex has a normal shape and duration. Clinical Significance. The clinical significance of sinus tachycardia depends on the patient's tolerance of the increased HR. The patient may have dizziness, dyspnea, and hypotension because of decreased CO. Increased myocardial O2 consumption is associated with an increased HR. Angina or an increase in infarction size may accompany sinus tachycardia in patients with coronary artery disease (CAD) or an acute MI. Treatment. The underlying cause of tachycardia guides the treatment. For example, if the patient is experiencing tachycardia from pain, effective pain management is important to treat the tachycardia. In clinically stable patients, vagal maneuvers can be attempted. In addition, IV β-blockers (e.g., metoprolol [Lopressor]), adenosine (Adenocard), or calcium channel blockers (e.g., diltiazem [Cardizem]) can be given to reduce HR and decrease myocardial O2 consumption. In clinically unstable patients, synchronized cardioversion is used

Second-Degree AV Block, Type II.

Clinical Associations. Associated with rheumatic heart disease, CAD, anterior MI, and drug toxicity. ECG Characteristics. Atrial rate is usually normal. Ventricular rate depends on the degree of AV block. Atrial rhythm is regular, but ventricular rhythm may be irregular. The P wave has a normal shape. The PR interval may be normal or prolonged in duration and remains constant on conducted beats. The QRS complex is usually greater than 0.12 second because of bundle branch block. Clinical Significance. Type II AV block often progresses to third-degree AV block and is associated with a poor prognosis. The reduced HR frequently results in decreased CO with subsequent hypotension and myocardial ischemia. Type II AV block is an indication for therapy with a permanent pacemaker. Treatment. Transcutaneous pacing or the insertion of a temporary pacemaker may be necessary before the insertion of a permanent pacemaker if the patient becomes symptomatic (e.g., hypotension, angina).11 (Temporary pacemakers are discussed on pp. 774 to 775.) Atropine is not an effective drug for this dysrhythmia.

Third-Degree AV Block.

Clinical Associations. Associated with severe heart disease, including CAD, MI, myocarditis, cardiomyopathy, and some systemic diseases such as amyloidosis and progressive systemic sclerosis (scleroderma). Some drugs can also cause third-degree AV block, such as digoxin, β-blockers, and calcium channel blockers. ECG Characteristics. The atrial rate is usually a sinus rate of 60 to 100 beats/minute. The ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to 60 beats/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute. Atrial and ventricular rhythms are regular but unrelated to each other. The P wave has a normal shape. The PR interval is variable, and there is no relationship between the P wave and the QRS complex. The QRS complex is normal if an escape rhythm is initiated at the bundle of His or above. It is widened if an escape rhythm is initiated below the bundle of His. Clinical Significance. Third-degree AV block usually results in reduced CO with subsequent ischemia, HF, and shock. Syncope from third-degree AV block may result from severe bradycardia or even periods of asystole. Treatment. For symptomatic patients, a transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted.7 (Types of temporary pacemakers are discussed on pp. 774-775.) The use of drugs such as dopamine and epinephrine is a temporary measure to increase HR and support BP until temporary pacing is started.11 Patients need a permanent pacemaker as soon as possible. Atropine is not an effective drug for this dysrhythmia.

Premature Ventricular Contractions.

Clinical Associations. Associated with stimulants such as caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin. They are also associated with electrolyte imbalances, hypoxia, fever, exercise, and emotional stress. Disease states associated with PVCs include MI, mitral valve prolapse, HF, cardiomyopathy, and CAD. ECG Characteristics. HR varies according to intrinsic rate and number of PVCs. Rhythm is irregular because of premature beats. The P wave is rarely visible and is usually lost in the QRS complex of the PVC. Retrograde conduction may occur and the P wave may be seen after the ectopic beat. The PR interval is not measurable. The QRS complex is wide and distorted in shape, lasting more than 0.12 second. The T wave is generally large and opposite in direction to the major direction of the QRS complex. Clinical Significance. PVCs are usually not harmful in a patient with a normal heart. In heart disease, PVCs may reduce the CO and lead to angina and HF depending on the frequency. Because PVCs in CAD or acute MI indicate ventricular irritability, assess the patient's physiologic response to PVCs. Obtain the patient's apical-radial pulse rate, since PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit. Treatment. Treatment relates to the cause of the PVCs (e.g., O2 therapy for hypoxia, electrolyte replacement). Assessment of the patient's hemodynamic status is important to determine if treatment with drug therapy is needed. Drug therapy includes β-blockers, procainamide, or amiodarone.

Second-Degree AV Block, Type I.

Clinical Associations. Assosicated from drugs such as digoxin or β-blockers. It may also be associated with CAD and other diseases that can slow AV conduction. ECG Characteristics. Atrial rate is regular, but ventricular rate may be slower because of nonconducted or blocked QRS complexes resulting in bradycardia. Once a ventricular beat is blocked, the cycle repeats itself with progressive lengthening of the PR intervals until another QRS complex is blocked. The rhythm appears on the ECG in a pattern of grouped beats. Ventricular rhythm is irregular. The P wave has a normal shape. The QRS complex has a normal shape and duration. Clinical Significance. Type I AV block is usually a result of myocardial ischemia or inferior MI. It is generally transient and well tolerated. However, in some patients (e.g., acute MI) it may be a warning sign of a more serious AV conduction disturbance (e.g., complete heart block). Treatment. If the patient is symptomatic, atropine is used to increase HR, or a temporary pacemaker may be needed, especially if the patient has had an MI. If the patient is asymptomatic, the rhythm is closely observed with a transcutaneous pacemaker on standby. Bradycardia is more likely to become symptomatic when hypotension, HF, or shock is present.

Ventricular Fibrillation.

Clinical Associations. Asspciated in acute MI and myocardial ischemia and in chronic diseases such as HF and cardiomyopathy. It may occur during cardiac pacing or cardiac catheterization procedures because of catheter stimulation of the ventricle. It may also occur with coronary reperfusion after thrombolytic therapy. Other clinical associations are electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity. ECG Characteristics. HR is not measurable. Rhythm is irregular and chaotic. The P wave is not visible, and the PR interval and the QRS interval are not measurable. Clinical Significance. VF results in an unresponsive, pulseless, and apneic state. If it is not rapidly treated, the patient will not recover. Treatment. Treatment consists of immediate initiation of CPR and advanced cardiovascular life support (ACLS) with the use of defibrillation and definitive drug therapy (e.g., epinephrine, vasopressin). There should be no delay in starting chest compressions and using a defibrillator once available.

Premature Atrial Contraction

Clinical Associations. Can result from emotional stress or physical fatigue or from the use of caffeine, tobacco, or alcohol. A PAC can also result from hypoxia; electrolyte imbalances; and disease states such as hyperthyroidism, chronic obstructive pulmonary disease (COPD), and heart disease, including CAD and valvular disease. ECG Characteristics. HR varies with the underlying rate and frequency of the PAC. The rhythm is irregular. The P wave has a different shape from that of a P wave originating in the SA node, or it may be hidden in the preceding T wave. The PR interval may be shorter or longer than the PR interval coming from the SA node, but it is within normal limits. The QRS complex is usually normal. If the QRS interval is 0.12 second or more, abnormal conduction through the ventricles occurs. Clinical Significance. In persons with healthy hearts, isolated PACs are not significant. Patients may report palpitations or a sense that their hearts "skipped a beat." In persons with heart disease, frequent PACs may indicate enhanced automaticity of the atria or a reentry mechanism. Such PACs may warn of or start more serious dysrhythmias (e.g., supraventricular tachycardia). Treatment. Treatment depends on the patient's symptoms. Withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be needed. β-Blockers may be used to decrease PACs.

Sinus Bradycardia

Clinical Associations. May be a normal sinus rhythm in aerobically trained athletes and in some people during sleep. It also occurs in response to carotid sinus massage, Valsalva maneuver, hypothermia, increased intraocular pressure, vagal stimulation, and certain drugs (e.g., β-blockers, calcium channel blockers). Common disease states associated with sinus bradycardia are hypothyroidism, increased intracranial pressure, and inferior myocardial infarction (MI). ECG Characteristics. In sinus bradycardia, the HR is less than 60 beats/minute and rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration. The PR interval is normal and the QRS complex has a normal shape and duration. Clinical Significance. The clinical significance of sinus bradycardia depends on how the patient tolerates it. Manifestations of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath. Treatment. For the patient with symptoms, treatment consists of giving IV atropine (anticholinergic drug). If atropine is ineffective, transcutaneous pacing or a dopamine or epinephrine (Adrenalin) infusion is considered. Permanent pacemaker therapy may be needed. If bradycardia is due to drugs, these may have to be held, discontinued, or reduced.

Atrial Flutter.

Clinical Associations. Rarely occurs in a healthy heart. It 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. ECG Characteristics. Atrial rate is 200 to 350 beats/minute. The ventricular rate varies based on the conduction ratio. In 2 : 1 conduction, the ventricular rate is typically found to be approximately 150 beats/minute. Atrial rhythm is regular and ventricular rhythm is usually regular. The atrial flutter waves represent atrial depolarization followed by repolarization. The PR interval is variable and not measurable. The QRS complex is usually normal. Because the AV node can delay signals from the atria, there is usually some AV block in a fixed ratio of flutter waves to QRS complexes. Clinical Significance. The high ventricular rates (greater than 100 beats/minute) and loss of the atrial "kick" (atrial contraction reflected by a sinus P wave) that are associated with atrial flutter decrease CO. This can cause serious consequences such as HF, especially in the patient with underlying heart disease. Patients with atrial flutter have an increased risk of stroke because of the risk of thrombus formation in the atria from the stasis of blood. Warfarin (Coumadin) is given to prevent stroke in patients who have atrial flutter.6 Treatment. The primary goal in treatment of atrial flutter is to slow the ventricular response by increasing AV block. Drugs used to control ventricular rate include calcium channel blockers and β-blockers. Electrical cardioversion may be performed to convert the atrial flutter to sinus rhythm in an emergency (i.e., when the patient is clinically unstable) and electively. Antidysrhythmia drugs are used to convert atrial flutter to sinus rhythm (e.g., ibutilide [Corvert]) or to maintain sinus rhythm (e.g., amiodarone, flecainide, dronedarone [Multaq]).5 Radiofrequency catheter ablation is the treatment of choice for atrial flutter.7 The procedure is done in an EPS laboratory and involves placing a catheter in the right atrium. With the use of a low-voltage, high-frequency form of electrical energy, the ectopic foci are ablated (or destroyed), dysrhythmia is ended, and normal sinus rhythm is restored

The ECG monitor of a patient in the cardiac care unit after an MI indicates ventricular bigeminy with a rate of 50 beats/min. The nurse would anticipate a. performing defibrillation. b. treating with IV amiodarone. c. inserting a temporary transvenous pacemaker. d. assessing the patient's response to the dysrhythmia.

D

The nurse prepares a patient for synchronized cardioversion knowing that cardioversion differs from defibrillation in that a. defibrillation requires a lower dose of electrical energy. b. cardioversion is indicated to treat atrial bradydysrhythmias. c. defibrillation is synchronized to deliver a shock during the QRS complex. d. patients should be sedated if cardioversion is done on a nonemergency basis.

D

What is this ECG tracing of?

Heart block. A, First-degree atrioventricular (AV) block with a PR interval of 0.40 sec. B, Second-degree AV block, type I, with progressive lengthening of the PR interval until a QRS complex is blocked. C, Second-degree AV block, type II, with constant PR intervals and variable blocked QRS complexes. D, Third-degree AV block. Note that there is no relationship between P waves and QRS complexes.

What is this ECG tracing of?

Junctional escape rhythm. The p wave is hidden in the RS complex. NOTE: Recorded from lead V1.

What is this ECG tracings of?

Paroxysmal supraventricular tachycardia (PSVT). Arrows indicate beginning and ending of PSVT.

What is this ECG tracings of?

Premature atrial contractions (arrows).

Myocardial Infarction (MI)

The typical ECG change seen during injury is ST segment elevation. ST segment elevation is significant if it is 1 mm or more above the isoelectric line in at least two contiguous leads

Ischemia

Typical ECG changes that are seen in myocardial ischemia include ST segment depression and/or T wave inversion

What is this ECG tracing of?

Various types of premature ventricular contractions (PVCs).

What is this ECG tracing of?

Ventricular fibrillation.

What is this ECG tracing of?

Ventricular tachycardia. A, Monomorphic. B, Torsades de pointes (polymorphic).

Syncope

brief lapse in consciousness accompanied by a loss in postural tone (fainting), is a common diagnosis of patients coming to the emergency department.

Pacemakers

electronic device used to pace the heart when the normal conduction pathway is damaged. The basic pacing circuit consists of a power source (battery-powered pulse generator) with programmable circuitry, one or more pacing leads, and the myocardium. The electrical signal (stimulus) travels from the pulse generator, through the leads, to the wall of the myocardium. The heart muscle is "captured" and stimulated to contrac

Drug Alert: Adenosine (Adenocard)

the injection site should be as close to the heart as possible (antecubital area) give IV dose rapidly (over 1-2 seconds) and follow with a rapid 20 mL normal saline flush monitor patient's ECG continuously. brief period of asystole is common. observe patient for flushing, dizziness, chest pain, or palpitations