CARDIAC DYSRHYTHMIAS

Dominic L. Reambonanza, RN

Cardiac Dysrhythmias
Dysrhythmias are disorders of the rhythm of the heart; is an abnormal, disordered, or disturbed rhythm. Arythmias is an irregularity or loss of rhythm of the heartbeat

Cardiac Dysrhythmias results from disturbances in three major mechanisms:

1. Automaticity the normal processes of generating a heart rhythm. This process of automatically initiating an impulse can be altered if the normal pacemaker cells are firing too rapidly, or if an impulse is generated by a cell that normally does not initiate heartbeats, called an ectopic pacemaker. 2. Conduction the impulse travels through the sinus node, AV node, and Purkinje fibers. Latent pacemaker cells can also fire at rates above or below their inherent rate. A rhythm slower than the intrinsic rate is called bradycardia. A rhythm faster than the intrinsic rate is called accelerated or tachycardia.

Cardiac Dysrhythmias results from disturbances in three major mechanisms:

3. Reentry of Impulses - occurs when cardiac tissue is depolarized multiple times by the same impulse, and when two pathways are present: slow and fast pathway. Two pathways can develop from anatomic abnormalities (accessory pathway, fibrosis) or functional defects (ischemia, drug interactions). Reentry can result from myocardial ischemia, the action of antidysrhythmic medications, myocardial fibrosis, existence of an accessory pathway, or bundle-branch block.

Pathophysiology
significance of all dysrhythmias is their effect on cardiac output and therefore cerebral and vascular perfusion During normal sinus rhythm, the atria contract to fill and stretch the ventricles with about 30% more blood, this process called atrial kick, increases the amount of blood (stroke volume) in the ventricles before contractility, thereby increasing cardiac output by 30 % When the impulse originates below the SA node, or more than one area fires in the atria to originate a beat (such as with atrial fibrillation or atrial flutter), the atrial kick is lost and cardiac output falls that 30%.

Clinical Manifestation
reduced cardiac output leads to clinical manifestations of palpitations, dizziness, presyncope or syncope, pallor, diaphoresis, altered mentation, shortness of breath, chest pain orthopnea, paroxysmal nocturnal dyspnea, hypotension, sluggish capillary refill, swelling of the extremities, and decreased urine output develop from either altered impulse formation or altered impulse conduction

Clinical Manifestation
concerns changes in rhythm that are caused by changes in the automaticity of pacemaker cells or by abnormal generation of action potentials by sites other than the SA node (termed ectopic foci) Altered impulse conduction is usually associated with complete or partial block of electrical conduction within the heart. Altered impulse conduction commonly results in reentry, which lead to tachyarrhythmias

Clinical Manifestation
Cardiac Arrhythmias occurs when the heart beats improperly, as a result of incorrect impulse generation, or impulse conduction. Pacemaker cells beat with their own independent rhythm, in synchrony with their neighbours non-pacemaker cells require stimulus to beat, this stimulus comes from the pacemaker cells

Clinical Manifestation
Incorrect impulse generation is the fault of the pacemaker cells, which are beating either too slow, too fast, or not totally in rhythm (asynchrous) Impulse conduction problems are caused because the nervous signal from the pacemaker cells (located primarily at the SA node) fails to reach the non-pacemaker cells correctly a nodal block whereby the signal from the SA node fails to reach the AV node, and a re-entry pathway

Clinical Manifestation
A re-entry pathway occurs when a section of nervous tissue (which conducts the impulse) is damaged in some manner the pathogenesis of arrhythmias falls into one of three basic mechanisms: enhanced or suppressed automaticity, triggered activity, or re-entry Automaticity is a natural property of all myocytes Triggered activity occurs when early after depolarizations and delayed after depolarizations initiate spontaneous multiple depolarizations precipitating ventricular arrhythmias

Clinical Manifestation
Hypercalcemia and hypocalcemia (high and low calcium levels, respectively) may cause heart block and cardiac arrest Hypernatremia (high sodium level) may result in an erratic heart rate as sodium and calcium ions compete with one another to influence the heart Imbalances in potassium and magnesium, however, are the usual culprits of cardiac arrhythmia

Clinical Manifestation
Hyperkalemia initially causes tachycardia and then bradycardia as the heart fatigues in response to the high sustained heart rate and weak cardiac contraction Hypokalemia results in bradycardia and a slow, weak pulse. Hypermagnesemia causes premature ventricular contractions Hypomagnesemia may result in PVCs, atrial fibrillation or ventricular fibrillation

Normal Sinus Rhythm

Rhythm: regular Heart rate: 60 to 100 bpm P waves: rounded, precede each QRS complex, alike PR interval: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds

Normal Sinus Rhythm

Sinus Bradycardia
the same cardiac cycle components as a normal sinus rhythm only difference is a slower heart rate caused by fewer impulses originating from the SA node causes of this are medications, myocardial infarction (MI), and electrolyte imbalances can cause bradycardia

Sinus Bradycardia

Rhythm: regular Heart rate: less than 60 bpm P waves: smoothly rounded, precede each QRS complex alike PR interval: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds

Sinus Bradycardia
rarely produces symptoms unless it is so slow that it reduces cardiac output Oxygen and intravenous (IV) access may be started If bradycardia is due to a heart block dysrhythmia, insertion of a cardiac pacemaker may be required treatment includes atropine sulfate, transcutaneous pacing, and dopamine, epinephrine, or isoproterenol

Sinus Tachycardia
has the same components as a normal sinus rhythm except the heart rate is faster Causes of sinus tachycardia include physical activity; hemorrhage; shock; medications such as epinephrine, atropine, or nitrates; dehydration; fever; MI; electrolyte imbalance; fear; and anxiety

Sinus Tachycardia

Rhythm: regular Heart rate: 101 to 180 bpm P waves: rounded, precede each QRS complex, alike PR interval: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds

Sinus Tachycardia
the patient may experience angina or dyspnea Elderly patients may become symptomatic more rapidly than younger patients Patients with MI may not tolerate a rapid heart rate because it increases cardiac workload treatment goal is to decrease the heart s workload and resolve the cause digoxin, calcium channel blockers (verapamil), or beta blockers (propranolol) Oxygen may prescribed.

Premature Atrial Contraction

When the atria fire an impulse before the SA node fires a premature beat results shortened R-R interval is seen where the premature beat occurs R wave preceding the premature atrial contraction (PAC) and the PAC s R wave are close together Causes of PACs include hypoxia, smoking, stress, myocardial ischemia, enlarged atria in valvular disorders, medications (such as digoxin), electrolyte imbalances, atrial fibrillation onset, and heart failure.

Premature Atrial Contraction

Rhythm: premature beat interrupts underlying rhythm where it occurs Heart rate: depends on the underlying rhythm; if normal sinus rhythm (NSR), 60 to 100 bpm P waves: early beat is abnormally shaped PR interval: usually appears normal, but premature beat could have shortened or prolonged PR interval QRS interval: 0.06 to 0.10 seconds (indicates normal conduction to ventricles)

Premature Atrial Contraction

the patient may report the sensation of palpitations frequent PACs indicate atrial irritability, which may worsen into other atrial dysrhythmias Quinidine or procainamide can be given to a patient having frequent PACs to slow the heart rate.

Atrial Flutter
the atria contract, or flutter, at a rate of 250 to 350 bpm very rapid P waves appear as flutter, or F waves, on ECG and appear in a saw-tooth pattern two to four F waves between QRS complexes Causes of atrial flutter include rheumatic or ischemic heart diseases, congestive heart failure (CHF), hypertension, pericarditis, pulmonary embolism, and postoperative coronary artery bypass surgery. Many medications can also cause this dysrhythmia.

Atrial Flutter

Rhythm: atrial rhythm regular; ventricular rhythm regular or irregular depending on consistency of AV conduction of impulses Heart rate: ventricular rate varies P waves: flutter or F waves with saw-tooth pattern PR interval: none measurable QRS complex: 0.06 to 0.10 seconds

Atrial Flutter
If the ventricular rate is normal, usually no symptoms are present If the rate is rapid, the patient may experience palpitations, angina, or dyspnea. goal is to control the ventricular rate and convert the rhythm rapid ventricular rate or symptoms of decreased cardiac output require cardioversion calcium channel blockers and beta blockers, digoxin

Atrial Fibrillation
the atrial rate is extremely rapid and chaotic 350 to 600 bpm no definable P waves because the atria are fibrillating, or quivering, rather than beating effectively wavy pattern is produced on the ECG Atrial fibrillation can be self-limiting, persistent, or permanent complication of this dysrhythmia is an increased risk of thrombus formation in the atria from blood stasis Causes of atrial fibrillation include aging, rheumatic or ischemic heart diseases, heart failure, hypertension, pericarditis, pulmonary embolism, and postoperative coronary artery bypass surgery

Atrial Fibrillation

Rhythm: grossly or irregularly irregular Heart rate: atrial rate not measurable; ventricular rate under 100 is controlled response; greater than 100 is rapid ventricular response P waves: no identifiable P waves PR interval: none, cant be measured because no P waves are seen QRS complex: 0.06 to 0.10 seconds

Atrial Fibrillation
most patients feel the irregular rhythm If the patient is unstable, cardioversion is done immediately to try to return the heart to normal sinus rhythm If stable, medications to restore and maintain a normal sinus rhythm and control the ventricular rate may be used (digoxin) Dual chamber pacing Implantable Cardioverter Defibrillators If not respond to meds, ablation procedures may be performed

Premature Ventricular Contraction

originate in the ventricles from an ectopic focus (a site other than the SA node) ventricles are irritable and fire prematurely

(A) Unifocal PVCs arise from one area and look the same. (B) Multifocal PVCs arise from different foci and may look different.

Premature Ventricular Contraction

Rhythm: depends on the underlying rhythm; PVC usually interrupts rhythm Heart rate: depends on underlying rhythm P waves: absent before PVC QRS complex PR interval: none for PVC QRS complex: if PVC is greater than 0.11 seconds; T wave is in the opposite direction of QRS complex (i.e., QRS upright, T downward or QRS downward, T upright)

Shape of the PVC is referred to as unifocal (one focus) if all the PVCs look the same because they come from the same irritable ventricular area. Multifocal PVC s do not look the same because they are originating from several irritable areas in the ventricle.

Premature Ventricular Contraction

Several repetitive cycles or patterns of PVCs: Bigeminy is a PVC that occurs every other beat (a normal beat and then a PVC) Trigeminy is a PVC that occurs every third beat (two normal beats and then a PVC). Quadrigeminy is a PVC that occurs every fourth beat (threenormal beats and then a PVC). When two PVCs occur together, they are referred to as acouplet (pair). If three or more PVCs occur in a row, it is referred to as a runof PVCs or ventricular tachycardia.

Premature Ventricular Contraction

Use of caffeine or alcohol, anxiety, hypokalemia, cardiomyopathy, ischemia, and MI are common causes Antidysrhythmic drugs that depress myocardial activity are used to treat PVCs

Ventricular Tachycardia
occurrence of three or more PVCs in a row results from the continuous firing of an ectopic ventricular focus During VT, the ventricles rather than the SA node become the pacemaker of the heart Myocardial irritability, MI, and cardiomyopathy are common causes Respiratory acidosis, hypokalemia, digoxin toxicity, cardiac catheters, and pacing wires

Ventricular Tachycardia

Rhythm: usually regular, may have some irregularity Heart rate: 150 to 250 ventricular bpm; slow VT is below150 bpm P waves: absent PR interval: none QRS complex: greater than 0.11 seconds

Ventricular Tachycardia
Patients are aware of a sudden onset of rapid heart rate and can experience dyspnea, palpitations, and light-headedness severity of symptoms can increase rapidly if the left ventricle fails and complete cardiac arrest results. If the patient is pulseless or not breathing, cardiopulmonary resuscitation (CPR) and immediate defibrillation are required, followed by anti-arrhythmic drugs

Ventricular Fibrillation
occurs when many ectopic ventricular foci fire at the same time Ventricular activity is chaotic with no discernible waves ventricle quivers and is unable to initiate a contraction complete loss of cardiac output If this rhythm is not terminated immediately, death ensues. Hyperkalemia, hypomagnesemia, electrocution, coronary artery disease, and MI are all possible causes of ventricular fibrillation

Ventricular Fibrillation

Rhythm: chaotic and extremely irregular Heart rate: not measurable P waves: none PR interval: none QRS complex: none

Ventricular Fibrillation
Patients experiencing ventricular fibrillation lose consciousness immediately If no heart sounds, peripheral pulses, or blood pressure, these are indicative of circulatory collapse Immediate defibrillation is the very best treatment for terminating ventricular fibrillation CPR is started until the defibrillator is available ACLS protocols and may include epinephrine, vasopressin, amiodarone, lidocaine, magnesium, and procainamide

Asystole
is the absence of electrical activity in the cardiac muscle. It is referred to as cardiac arrest. Ventricular fibrillation and a loss of a majority of functional cardiac muscle due to an MI are common causes of asystole. Hyperkalemia is another cause of asystole.

Asystole
Rhythm: none Heart rate: none P waves: none PR interval: none QRS complex: none

CPR is started immediately. ACLS protocols for asystole are used. Endotracheal intubation to support respirations is performed. Transcutaneous pacing is considered, then epinephrine and atropine are administered.

Diagnostic Procedures
Cardiac Pacemakers

used to override dysrhythmias or to generate an impulse when the heart is beating too slowly Transcutaneous pacemakers are used in emergency situations because they are quick and easy to apply Temporary pacemakers are used for bradycardias or tachycardias that do not respond to medications or cardioversion. pacemaker generator is implanted subcutaneously and attached to one or two leads (insulated conducting wires) that are inserted via a vein into the heart.

Diagnostic Procedures
single-lead pacemaker paces either the right atrium or right ventricle depending on its chamber placement Dual-chamber pacemakers have two leads, with one in the right atrium and the other in the right ventricle Problems that can occur with pacemakers include the following:  Failure to sense the patient s own beat  Failure to pace because of a malfunction of the pulse generator  Failure to capture, which is a lack of depolarization

Diagnostic Procedures
Nursing Care placed on a cardiac monitor and strict bedrest for 12 to 24 hours after insertion apical pulse is monitored frequently to detect changes in the heart rhythm dressing at the pacemaker insertion site is monitored every 2 to 4 hours for signs of bleeding change in heart rhythm, complaints of chest pain, or changes in vital signs must be reported immediately

Diagnostic Procedures
Patients Education: check the incision daily and report evidence of inflammation or infection report if the pulse is slower than the pacemaker s set rate report symptoms of dizziness, fainting, irregular heartbeats, or palpitations understand the importance of wearing medical alert jewelry and carrying a pacemaker information card. should avoid radiation, magnetic fields, high voltage antitheft devices, and large running motors avoid lifting more than 10 pounds

Diagnostic Procedures
Defibrillation lifesaving procedure used for lethal dysrhythmias delivers an electrical shock to reset the heart s rhythm used to terminate pulseless ventricular tachycardia or ventricular fibrillation Self-adhesive pads, conductive jelly, or saline pads are placed on the patients chest

Diagnostic Procedures
For safety, the person defibrillating must announce clear No one should touch the bed or patient during this time to avoid also being shocked If the first shock is unsuccessful, a total of three (3) shocks can be given (200, 300, 360 Joules) After successful defibrillation, the patient is assessed for a pulse and adequate tissue perfusion Emotional support for the patient having experienced cardiac arrest and defibrillation

Diagnostic Procedures
Automatic External Defibrillator (AED) external device that automatically analyzes rhythms and either automatically delivers or prompts operators to deliver an electrical shock if a shockable rhythm is detected patient is connected to the AED with adhesive sternal-apex pads attached to cables coming from the device defibrillation attempts must occur within minutes of cardiac arrest to increase chance of survival

Diagnostic Procedures
Implantable Cardioverter Defibrillator (ICD) surgically placed during a minor procedure into the chest of a patient who experiences life threatening dysrhythmias When an abnormal rhythm is detected that could cause death (ventricular fibrillation), it automatically delivers an electrical shock

Diagnostic Procedures
If the device detects VT, it cardioverts the rhythm using lower energy ICDs also have antitachycardia pacing ability if a tachycardic rhythm is detected ICD Precautions Avoiding MRIs Avoiding metal detectors Avoiding equipment with strong electrical or magneticfields Keeping cell phones 6 inches from the ICD The nurse provides emotional support, answers all questions, and ensures that any misunderstood information is corrected before discharge.

Diagnostic Procedures
Cardioversion used for dysrhythmias such as atrial fibrillation, atrial flutter, and supraventricular tachycardias that are not responsive to drug therapy number of joules delivered with each shock is usually ranges from 25 to 50 joules If the rhythm does not immediately convert, more cardioversion attempts can be made

Diagnostic Procedures
Ablation Intracardiac echocardiography and intracardiac mapping with fluoroscopy are done before ablation Mechanical ablation destroys the involved tissue with cryosurgery or through surgical removal Chemical ablation inserts alcohol or phenol through an angioplasty catheter into the area of the heart producing the unwanted beats Radiofrequency ablation delivers high frequency energy via a catheter to necrose selected conduction pathway areas

Diagnostic Procedures
Electrocardiography (ECG)

measures and records the electrical activity of the heart in exquisite detail Interpretation of these details allows diagnosis of a wide range of heart conditions

Diagnostic Procedures
Holter Monitor a small portable electrocardiogram (ECG) keeps a record of the heart rhythm, typically over a 24-hour period useful for identifying disturbances which are sporadic and which are not readily identified with the usual resting electrocardiogram test