dysrhythmias

electrical route of heart

A normal cardiac impulse begins in the sinoatrial node (SA) in the upper right atrium. it spreads over the atrial myocardium via interatrial and intermodal pathways, causing atrial contraction. the impulse then travels to the atrioventricular (AV) node, through the bundle of His, down the left and right bundle branches. it ends in the Purkinje fibers, which transmit the impulse to the ventricles.

on an ECG each small square equals

.04 seconds.

Ventricular Tachycardia

A run of THREE OR MORE PVCs defines ventricular tachycardia (VT). It occurs when an ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker. Different forms of VT exist, depending on QRS configuration. Monomorphic VT has QRS complexes that are the same in shape, size, and direction. Polymorphic VT occurs when the QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats.

Indications for Permanent Pacemakers

Acquired AV block • Second-degree AV block • Third-degree AV block • Atrial fibrillation with a slow ventricular response • Bundle branch block • Cardiomyopathy • Dilated • Hypertrophic • Heart failure • SA node dysfunction • Tachydysrhythmias (e.g., ventricular tachycardia

Prodysrhythmia

Antidysrhythmia drugs can cause lifethreatening dysrhythmias similar to those for which they are given. The patient who has severe left ventricular dysfunction is the most susceptible to prodysrhythmias. Digoxin and class IA, IC, and III antidysrhythmia drugs can cause a prodysrhythmic response. The first several days of drug therapy are the vulnerable period for developing prodysrhythmias. For this reason, many oral antidysrhythmia drug regimens are started in a monitored hospital setting.

clinical significance of A Fib

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.

ECG characteristics of AFlutter

Atrial rate is 200 to 350 bpm. The ventricular rate varies based on the conduction ratio. In 2:1 conduction, the ventricular rate is typically found to be approximately 150 bpm. 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.

Treatment of Pulseless Electrical Activity

CPR followed by drug therapy, such as epi, and intubation. correcting underlying cause is critical.

treatement of asystole

CPR with initiation of ACLS measures. Drug therapy with epi or vassopresin, and intubation.

treatment of A Fib continued

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. Anticoagulation therapy is necessary because the procedure can cause the clots to dislodge, placing the patient at risk for stroke.

V tach without pulse

Emergency!! Treated in the same manner as Venticular Fibrilation (VF) (CPR) and rapid defibrillation are the first lines of treatment, followed by the administration of vasopressors (epinephrine) & antidysrhythmics (amiodarone) if defibrillation is unsuccessful.

Maze procedure

For patients with drug-refractory atrial fibrillation or those who do not respond to electrical conversion, radiofrequency catheter ablation. The Maze procedure is a surgical intervention that stops atrial fibrillation by interrupting the ectopic electrical signals that are responsible for the dysrhythmia. Incisions are made in both atria, and cryoablation is used to stop the formation and conduction of these signals, and restore normal sinus rhythm.

ECG characteristics

HR is 101 to 200 beats/minute and the 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.

ECG Characteristics of Paroxysmal Superventricular Tachycardia (PSVT)

HR is 150 to 220 beats/minute, and the 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.

ECG characteristics of Vfib

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.

ECG characteristics of bradycardia

HR less than 60 bpm, regular rhythm.

ECG characteristics of PVC's

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.

ECG characteristics of Premature Atrial Contraction (PAC)

HR varies with the underlying rate and frequency of the PAC, and 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.

A secondary pacemaker from another site may fire in two ways... The first way...

If the SA node fires more slowly than a secondary pacemaker, the electrical signals from the secondary pacemaker may "escape." The secondary pacemaker will then fire automatically at its intrinsic rate. These secondary pacemakers may start from the AV node at a rate of 40 to 60 times per minute or the His-Purkinje system at a rate of 20 to 40 times per minute.

treatment of V fib

Immediate initiation of CPR and advanced cardiac life support (ACLS). With the use of defibrillation and definitive drug therapy (epi, vasopressin.) there should be no delay in using a defibrillator once available.

clinical significance of Premature Atrial Contraction (PAC)

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).

clinical associations of Paroxysmal Superventricular Tachycardia (PSVT)

In the normal heart, PSVT is 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.

clinical associations of bradycardia

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 administration of certain drugs (β-adrenergic blockers, calcium channel blockers). Common disease states like hypothyroidism, increased intracranial pressure, hypoglycemia, and inferior myocardial infarction (MI).

Multifocal PVC's

PVCs that arise from different foci appear different in shape from each other

Unifocal PVC's

PVCs that have the same shape

treatment of v-tach

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.

Radiofrequency in treatment of AFlutter

Radiofrequency catheter ablation is the treatment of choice for atrial flutter. The procedure is done in the EPS laboratory and involves placing a catheter in the right atrium. With use of a low-voltage, high-frequency form of electrical energy, the tissue is ablated (or destroyed), the dysrhythmia is ended, and normal sinus rhythm is restored.

A secondary pacemaker from another site may fire in two ways... The second way...

Secondary pacemakers can start is when they fire more rapidly than the normal pacemaker of the SA node. Triggered beats (early or late) may come from an ectopic focus or accessory pathway (area outside the normal conduction pathway) in the atria, AV node, or ventricles. This results in a dysrhythmia, which replaces the normal sinus rhythm.

Pacemaker

The artificial cardiac pacemaker is an electronic device used to pace the heart when the normal conduction pathway is damaged. The electrical signal (stimulus) travels from the pulse generator, through the leads to the wall of the myocardium. The myocardium is "captured" and stimulated to contract.

clinical significance of tachycardia

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 oxygen 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.

automaticity

The heart has specialized cells in the SA node, atria, AV node, and bundle of His and Purkinje fibers (His-Purkinje system), which can fire (discharge) spontaneously.

clinical significance of AFlutter

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 pts who have atrial flutter.

implantable Cardioverter-Defibrilator

The implantable cardioverter-defibrillator (ICD) is an important technology for patients who (1) have survived SCD, (2) have spontaneous sustained VT, (3) have syncope with inducible VT or VF during EPS, or (4) are at high risk for future life-threatening dysrhythmias (have cardiomyopathy).

Excitability

The impulse started by the SA node or an ectopic focus must be conducted to the entire heart. The property of myocardial tissue that allows it to be depolarized by a stimulus is called excitability. The level of excitability isdetermined by the length of time after depolarization that the tissues can be restimulated.

treatment of tachycardia

The underlying cause of tachycardia guides the treatment. In clinically stable patients, vagal maneuvers can be attempted. In addition, IV β-adrenergic blockers (metoprolol [Lopressor]), adenosine (Adenocard), or calcium channel blockers (e.g., diltiazem [Cardizem]) can be given to reduce HR and decrease myocardial oxygen consumption. In clinically unstable patients, synchronized cardioversion is used.

The nurse is reviewing the monitored rhythms of several patient in the cardiac step down unit. The patient with which cardiac arrhythmia has the greatest need of attention by the nurse?

Torsades de pointes

Treatment of Premature Atrial Contraction (PAC's)

Treatment depends on the patient's symptoms. Withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be needed. β-Adrenergic blockers may be used to decrease PACs.

treatment of PVC's

Treatment relates to the cause of the PVCs( oxygen 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-adrenergic blockers, procainamide (Pronestyl), or amiodarone.

The automatic external defibrillator electrodes are placed on the patient who is unconscious and pulseless. The nurse prepares to immediately defibrillate if the monitor show which cardiac rhythm?

V-fib

treatment of Paroxysmal Superventricular Tachycardia (PSVT)

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. IV β-adrenergic blockers, calcium channel blockers, and amiodarone (Cordarone) can also be used. If vagal stimulation and drug therapy are ineffective and the patient becomes hemodynamically unstable, synchronized cardioversion is used.

ECG characteristics of Vtach

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.

Ventricular Bigeminy

When every other beat is a PVC

stimulation of vagus nerve causes...

a decreased rate of firing of the SA node and slowed impulse conduction of the AV node.

Bigeminy pattern of premature atrial contractions

a pattern of premature atrial contractions occurring every other beat

Normal sinus rhythm

a rhythm that starts in the SA node at a rate of 60-100 bpm and follows the normal conduction pathway.

Treatment of Bradycardia

administration of atropine (an anticholinergic drug). If atropine (AtroPen) is ineffective, transcutaneous pacing, or a dopamine (Intropin) or epinephrine (Adrenalin) infusion iS considered. Permanent pacemaker therapy may be needed. If bradycardia is due to drugs, these may need to be held, discontinued, or given in reduced dosages.

Clinical Associations of Asystole

advanced cardiac disease, severe cardiac conduction system disturbance, or end stage HF.

clinical associations of vtach

associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, drug toxicity, and central nervous system disorders. This dysrhythmia can be seen in patients who have no evidence of cardiac disease.

ECG Characteristics of A Fib

atrial rate may be as high as 350 to 600 bpm. 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 bpm, it is atrial fibrillation with a controlled ventricular response. Atrial fibrillation with a ventricular rate greater than 100 bpm 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.

Atrial Flutter

atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium or, less commonly, the left atrium

Nervous control of the heart

autonomic nervous system controls impulse formation, speed of conduction, and strength of cardiac contraction. Vagus nerve fibers of parasympathetic nervous system and nerve fibers of sympathetic nervous system.

An electrophysiologic study (EPS)

can identify the causes of heart blocks, tachydysrhythmias (dysrhythmias with rates greater than 100 beats/minute), bradydysrhythmias (dysrhythmias with rates less than 60 beats/minute), and syncope. An EPS study can also locate accessory pathways and determine the effectiveness of antidysrhythmia drugs.

Supraventricular tachycardia

characterized by rapid atrial depolarization with a rate of 350-350 beats per minute

Atrial flutter

classically the p waves occur in a sawtooth pattern

how to prepare patient for ECG

clip excessive chest hair, rub skin with dry gauze until slightly pink. if skin is oily, wipe with alcohol first. if sweaty, apply skin protectant before electrode.

Sinus tachycardia

conduction pathway is the same in sinus tachycardia as that in normal sinus rhythm. The discharge rate from the sinus node increases because of vagal inhibition or sympathetic stimulation. The sinus rate is 101 to 200 beats/minute.

The Holter monitor

continuously records the ECG while the patient is ambulatory and performing daily activities. The patient keeps a diary and records activities and any symptoms. Events in the diary are correlated with any dysrhythmias seenon the ECG.

Premature Ventricular contractions

contraction coming from an ectopic focus in the ventricles. It is the premature (early) occurrence of a QRS complex. A PVC is wide and distorted in shape compared with a QRS complex coming down the normal conduction pathway

how do you calculate HR on ECG

count the number of QRS complexes in one minute OR count the number of R-R intervals in 6 seconds and multiply that number by 10.

clinical significance of sinus brady

depends on how pt tolerates it. S&S of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath.

Dysrhythmias result from...

disorders of impulse formation, conduction of impulses, or both.

Paroxysmal Superventricular Tachycardia (PSVT)

dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His. PSVT occurs because of a reentrant phenomenon (reexcitation of the atria when there is a one-way block). Usually a PAC triggers a run of repeated premature beats. Paroxysmal refers to an abrupt onset and ending. Termination is sometimes followed by a brief period of asystole (absence of all cardiac electrical activity). Some degree of AV block may be present.

ventricular trigeminy

every third beat is a PVC

Atrial fibrillation

fine fibrillatory waves associated with increased risk of clot formation in the atria

treatment of A Fib

goals of treatment 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 pts with atrial fibrillation. Drugs used for rate control include calcium channel blockers (diltiazem), β-adrenergic blockers (metoprolol), dronedarone, and digoxin (Lanoxin). most common antidysrhythmia drugs used for conversion to and maintenance of sinus rhythm include amiodarone and ibutilide.

Clincial Significance of PVC's

health; not harmful. With disease, reduce CO and lead to angina and HF depending on frequency. 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.

Causes of Pulseless Electrical activity (PEA)

hypovolemia, hypoxia, metabolic acidosis, hyperkalemia, hypokalemia, hypoglycemia, hypothermia, toxins (e.g., drug overdose), cardiac tamponade, thrombosis (e.g., MI, pulmonary embolus), tension pneumothorax, and trauma.

Clinical Associations with Premature Atrial Contraction (PAC)

in a normal heart, can result from emotional stress or physical fatigue or from the use of caffeine, tobacco, or alcohol. can also be a result of hypoxia, electrolyte imbalnaces, and diseases such as hyperthyroidism, COPD, and CAD.

stimulation of sympathetic nerves...

increases SA node firing, AV node impulse conduction, and cardiac contractility.

Premature Atrial Contraction (PAC)

is a contraction starting from an ectopic focus in the atrium (i.e., a location other than the SA node) and coming sooner than the next expected sinus beat. The ectopic signal starts in the left or right atrium and travels across the atria by an abnormal pathway. This creates a distorted P wave. At the AV node, it may be stopped (nonconducted PAC), delayed (lengthened PR interval), or conducted normally. If the signal moves through the AV node, in most cases it is conducted normally through the ventricles.

SA node

is the pacemaker of the heart. It spontaneously fires 60 to 100 times per minute

recovery period after stimulation

is the refractory phase or period. The absolute refractory phase or period occurs when excitability is zero and the heart cannot be stimulated.

If drugs or cardioversion does not convert atrial fibrillation to normal sinus rhythm...

long-term anticoagulation therapy is required. Warfarin is the drug of choice, and patients are monitored for therapeutic levels.

how long does v-tach last?

may be sustained, longer than 30 seconds, or nonsustained, less than 30 seconds. The development of v-tach is an ominous sign. life threatening because decreased CO and possibility of development of VF, which is lethal.

Clinical Associations of VFib

occurs 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.

relative refractory period

occurs slightly later in the cycle, and excitability is more likely. In states of full excitability, the heart is completely recovered.

Ventricular tachycardia

occurs when there are three or more consecutive PVC's. (wide or broad shape QRS complex)

Clinical Significance of Paroxysmal Superventricular Tachycardia (PSVT)

prolonged episode and HR greater than 180 beats/minute will cause decreased CO because of reduced stroke volume. Symptoms often include hypotension, palpitations, dyspnea, and angina.

clinical significance of asystole

pt usually has end stage heart disease or has a prolonged arrest and cannot be resuscitated.

Ventricular fibrillation

rapidly fatal if not corrected in 3-5 minutes

clinical associations with AFlutter

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.

symptomatic bradycardia

refers to an HR that is less than 60 beats/minute and is inadequate for the patient's condition, causing the patient to experience symptoms (e.g., chest pain, syncope).

Sudden Cardiac Death

refers to death from a cardiac cause. Most SCDs result from ventricular dysrhythmias, specifically VT or Venticular Fibrilation (VF)

clinical significance of V Fib

results in unresponsive, pulseless, and apneic state. If it is not rapidly treated, the pt will not recover.

Venticular Fibrilation (VF)

severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude. This represents the firing of multiple ectopic foci in the ventricle. Mechanically the ventricle is simply "quivering," with no effective contraction, and consequently no CO occurs. Venticular Fibrilation (VF) is a lethal dysrhythmia.

Pulseless Electrical Activity

situation in which organized electrical activity is seen on the ECG, but there is no mechanical activity of the ventricles and the patient has no pulse. It is the most common dysrhythmia seen after defibrillation. Prognosis is poor unless the underlying cause is quickly identified and treated

treatment of AFlutter

slow ventricular response . Drugs used to control ventricular rate include calcium channel blockers and β-adrenergic blockers. Electrical cardioversion may be performed to convert the atrial flutter to sinus rhythm in an emergency (when the patient is clinically unstable) and electively. Antidysrhythmia drugs are used to convert atrial flutter to sinus rhythm (ibutilide [Corvert]) or to maintain sinus rhythm (amiodarone, flecainide [Tambocor], dronedarone [Multaq]).

clinical associations of PVC's

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, and CAD.

clinical associations of tachycardia

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 (Theo-Dur), or hydralazine (Apresoline).

Sinus Bradycardia

the conduction pathway is the same as that in sinus rhythm but the SA node fires at a rate less than 60 beats/minute.

Sinus arrhythmia

the rhythm fluctuations occur with an increase in the rate on inspiration and a decrease in the rate on expiration

Asystole

total absence of ventricular electrical activity. Occasionally, P waves are seen. No ventricular contraction occurs because depolarization does not occur. Patients are unresponsive, pulseless, and apneic. Asystole is a lethal dysrhythmia that requires immediate treatment. Venticular Fibrilation (VF) may masquerade as asystole. Always assess the rhythm in more than one lead. The prognosis of a patient with asystole is extremely poor.

Atrial Fibrillation

total disorganization of atrial electrical activity because of multiple ectopic foci, resulting in loss of effective atrial contraction. The dysrhythmia may be paroxysmal (beginning and ending spontaneously) or persistent (lasting more than 7 days). Atrial fibrillation is the most common, clinically significant dysrhythmia with respect to morbidity and mortality rates and economic impact.

treatment of polymorphic VT with prolonged baseline QT interval

treated with IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing. Drugs that prolong the QT interval (dofetilide [Tikosyn]) should be discontinued. Cardioversion is used if drug therapy is ineffective.

defibrillation

treatment of choice to end VF and pulseless VT. It is most effective when the myocardial cells are not anoxic or acidotic. Rapid defibrillation (within 2 minutes) is critical to a successful patient outcome. Defibrillation involves the passage of an electric shock through the heart to depolarize the cells of the myocardium. The goal is that the following repolarization of myocardial cells will allow the SA node to resume the role of pacemaker.

couplet

two consecutive PVC's

clinical associations with AFib

usually occurs in the patient 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 cardiac surgery.

artifact

will see artifact on monitor when leads and elcetrodes are not secure, or when there is muscle activity or electrical interference. Artifact is a distortion of the baseline and waveforms seen on the ECG.