DYSRHYTHMIAS = ARRHYTHMIA

• Dysrhythmias: disorders of the formation or conduction (or both) of the electrical impulses in the heart.
• These disorders can cause disturbances of:
  • Rate
  • Rhythm
  • Both rate and rhythm
• Potentially can alter blood flow & cause hemodynamic changes
• Diagnosed by analysis of ECG waveform

SA NODE DYSRHYTHMIAS

• The SA Node can:
  • Fire Too Slow - Sinus Bradycardia
  • Fire Too Fast - Sinus Tachycardia
  • Normal rate but irregular - Sinus Arrhythmia

SINUS BRADYCARDIA

• Sinus bradycardia occurs when the SA node creates an impulse at a slower-than-normal rate.
• Deviation from NSR
  • Rate = < 60 bpm
  • Other's = NORMAL    

ETIOLOGY

• SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

CAUSES INCLUDE

• Lower metabolic needs (sleep, athletic training, hypothyroidism),
• Vagal stimulation (from vomiting, suctioning, severe pain, extreme emotions),
• Medications (calcium channel blockers, amiodarone, beta-blockers),
• Idiopathic sinus node dysfunction,
• Increased intracranial pressure (ICP), and
• Myocardial infarction (MI), especially of the inferior wall
• Other possible contributing factors in clinically significant bradycardia include following. These are referred to as the H's and the T's.
  • H's - Hypovolemia, Hypoxia, Hydrogen Ion (Acidosis), Hypokalemia or Hyperkalemia, Hypoglycemia, And Hypothermia;
  • T's - Toxins, Tamponade (cardiac), Tension Pneumothorax, Thrombosis (Coronary Or Pulmonary), And Trauma (Hypovolemia, Increased ICP)

(American Heart Association [AHA], 2005)

MANAGEMENT

• Treatment of choice of sinus bradycardia is Atropine, 0.5 mg given rapidly as an intravenous (IV) bolus every 3 to 5 minutes to a maximum total dose of 3 mg, is the medication of choice in treating symptomatic sinus bradycardia. It blocks vagal stimulation, thus allowing a normal rate to occur.

SINUS TACHYCARDIA

• Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rate.
• Deviation from NSR
  • Rate = >100 bpm
  • Other's = NORMAL    

ETIOLOGY

• SA node is depolarizing faster than normal, impulse is conducted normally.
• Causes may include the following:
  • Physiologic or psychological stress (eg, acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise, anxiety)
  • Medications that stimulate the sympathetic response (eg, catecholamines, aminophylline, atropine), stimulants (eg, caffeine, alcohol, nicotine), and illicit drugs (eg, amphetamines, cocaine, Ecstasy)
  • Enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced parasympathetic tone, a condition called inappropriate sinus tachycardia.
  • Autonomic dysfunction, which results in a type of sinus tachycardia called postural orthostatic tachycardia syndrome (POTS). Patients with POTS have tachycardia without hypotension within 5 to 10 minutes of standing.
• Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

MANAGEMENT

• Treatment of sinus tachycardia is usually determined by the severity of symptoms and directed at identifying and abolishing its cause.
• Beta-blockers and calcium channel blockers, although rarely used, may be administered to reduce the heart rate quickly.

SINUS ARRHYTHMIA

• Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; the rate usually increases with inspiration and decreases with expiration.
• Sinus arrhythmia does not cause significant hemodynamic effect and usually it is not treated.
• Deviation from NSR
  • Regularity = Irregular
  • Other's = NORMAL
  • Rate Usually normal (60–100 bpm); may be <60 bpm

ATRIAL DYSRHYTHMIAS

• Atrial cells can:
  • Fire occasionally from a focus - Premature Atrial Contractions / Complex (PACs)
  • Fire continuously due to a looping re-entrant circuit - Atrial Flutter
  • Fire continuously from multiple foci or fire continuously due to multiple micro re-entrant "wavelets" - Atrial Fibrillation

PREMATURE ATRIAL CONTRACTIONS

• Premature atrial complex (PAC) is a single ECG complex that occurs when an ectopic electrical impulse originate in the atrium before the next normal impulse of the sinus node., therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.

ETIOLOGY

• The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (eg, as in hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states (eg, with pregnancy), or atrial ischemia, injury, or infarction. PACs are often seen with sinus tachycardia.

CHARACTERISTICS

• Ventricular and atrial rate: Depends on the underlying rhythm
• P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent.
• PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds.
• QRS shape and duration: usually normal, but it may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC).
• P:QRS ratio: usually 1:1
• PACs are common in normal hearts. The patient may say, "My heart skipped a beat." A pulse deficit (a difference between the apical and radial pulse rate) may exist.

MANAGEMENT

• If PACs are infrequent, no treatment is necessary.
• If they are frequent (more than six per minute), this may herald a worsening disease state or the onset of more serious dysrhythmias, such as atrial fibrillation.
• Treatment is directed toward the cause.

ATRIAL FLUTTER

• Atrial flutter occurs because of a premature electrical impulse arising in the atria due to that Instead of P waves a rapid, regular atrial flutter waves ("sawtooth" in pattern) are formed that causes rate, usually between 250 and 400 times per minute.
• The atrial rate is faster than the AV node can conduction. so, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node.

ETIOLOGY

• Atrial flutter often occurs in patients with chronic obstructive pulmonary disease, valvular disease, and thyrotoxicosis, as well as following open heart surgery and repair of congenital cardiac defects
• Atrial flutter can cause serious signs and symptoms, such as chest pain, shortness of breath, and low blood pressure.

CHARACTERISTICS

• Rate: Atrial rate - between 250 to 400; ventricular rate - between 75 to 150
• Rhythm: atrial rhythm - regular; ventricular rhythm - usually regular but may be irregular because of a change in the AV conduction
• P wave: Saw-toothed shape; these waves are referred to as F waves
• PR interval: Multiple F waves may make it difficult to determine the PR interval
• QRS shape and duration: Usually normal, but may be abnormal or absent
• P:QRS ratio: 2:1, 3:1, or 4:1

MANAGEMENT

• The urgency of treatment depends on the ventricular response rate and resultant symptoms. Too rapid or slow a rate will decrease CO.
• A calcium channel blocker, (diltiazem), may be used to slow AV nodal conduction. Use with caution in the patient with heart failure, hypotension, or concomitant beta-adrenergic blocker therapy.
• Digoxin may be used.
• If drug therapy is unsuccessful, atrial flutter will typically respond to Electrical cardioversion (50 to 100 joules) with anticoagulation therapy are usually successful.

ATRIAL FIBRILLATION

• Atrial fibrillation is an uncoordinated atrial electrical activation that causes a rapid, disorganized, and uncoordinated twitching of atrial musculature. No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node).

ETIOLOGY

• Usually occurs in people of advanced age with structural heart disease, such as VHD (AV Valve), inflammatory or infiltrative disease, CAD, HTN, CHD (especially ASD), and heart failure (diastolic or systolic).
• Also may be found in people with diabetes, obesity, hyperthyroidism, pheochromocytoma, pulmonary hypertension and embolism, obstructive sleep apnea, and acute moderate to heavy ingestion of alcohol ("holiday heart" syndrome), as well as following pulmonary or open heart surgery.
• Sometimes it occurs with no underlying pathophysiology called lone atrial fibrillation).

CHARACTERISTICS

• Rate: Atrial rate - between 300 to 600; ventricular rate - between 120 to 200.
• Rhythm: atrial & ventricular rhythm - highly irregular
• P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen and are referred to as fibrillatory or F waves
• PR interval: Cannot be measured
• QRS shape and duration: Usually normal, but may be abnormal
• P:QRS ratio - Many:1

MANAGEMENT

• Treatment of atrial fibrillation depends on the cause, pattern, and duration of the dysrhythmia; the ventricular response rate; and the patient's symptoms, age, and comorbidities.
• In many patients, atrial fibrillation converts to sinus rhythm within 24 hours and without treatment.
• Atrial Fibrillation management include -
  • Electrical cardioversion -
  • Pharmacological management for control the heart rate in persistent atrial fibrillation, an IV beta-blocker or a nondihydropyridine calcium channel blocker (diltiazem and verapamil) is recommended
  • Antithrombotic therapy is indicated for all patients with atrial fibrillation.

JUNCTIONAL DYSRHYTHMIAS

• Junctional Dysrhythmias include -
  • Premature Junctional Complex
  • Junctional Rhythm
  • Atrio-ventricular Nodal Reentry Tachycardia

PREMATURE JUNCTIONAL COMPLEX

• A premature Junctional complex is an impulse that starts in the AV nodal area before the next normal sinus impulse reaches the AV node.
• Premature junctional complexes are less common than PACs.
• Causes include digitalis toxicity, heart failure, and coronary artery disease.

CHARACTERISTICS

• Ventricular and atrial rate: Depends on the underlying rhythm
• P wave: Absent, inverted, buried, or retrograde in the PJC
• PR interval: None or short ; but less than 0.12 seconds.
• QRS shape and duration: usually normal, but it may be abnormal.
• P:QRS ratio: usually 1:1

MANAGEMENT

• Treatment for frequent premature junctional complexes is the same as for frequent PACs.
• If infrequent, no treatment is necessary.
• If frequent (more than six per minute), this may herald a worsening disease state or the onset of more serious dysrhythmias, such as atrial fibrillation.
• Treatment is directed toward the cause.

JUNCTIONAL RHYTHM

• Junctional or idionodal rhythm occurs when the AV node, instead of the sinus node, becomes the pacemaker of the heart. When the sinus node slows (eg, from increased vagal tone) or when the impulse cannot be conducted through the AV node (eg, because of complete heart block), the AV node automatically discharges an impulse.

CHARACTERISTICS

• Rate: 40–60 bpm
• Rhythm: Regular
• P Waves: May be absent, inverted, after the QRS complex, or before the QRS; may be inverted, especially in lead II
• PR Interval: None, short, or retrograde; If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds
• QRS shape and duration: usually normal, but it may be abnormal
• P:QRS ratio: 1:1 or 0:1

MANAGEMENT

• Junctional rhythm may produce signs and symptoms of reduced cardiac output.
• The treatment is the same as for sinus bradycardia. Atropine, 0.5 mg given rapidly as an intravenous (IV) bolus every 3 to 5 minutes to a maximum total dose of 3 mg.
• Emergency pacing may be needed.

ATRIOVENTRICULAR NODAL REENTRY TACHYCARDIA

• AVNRT is a common dysrhythmia that occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate. Each time the impulse is conducted through this area, it is also conducted down into the ventricles, causing a fast ventricular rate.

CHARACTERISTICS

• Rate: Atrial - usually 150 to 250; ventricular - usually 120 to 200
• Rhythm: Regular; sudden onset and termination of the tachycardia
• P wave: Usually very difficult to discern
• PR interval: If the P wave is in front of the QRS, the PR interval is < 0.12s
• QRS shape and duration: Usually normal, but may be abnormal
• P:QRS ratio - 1:1or 2:1
• The clinical symptoms vary with the rate and duration of the tachycardia and the patient's underlying condition. The tachycardia usually is of short duration, resulting only in palpitations.
• Fast rate may also reduce cardiac output, resulting in significant signs and symptoms such as restlessness, chest pain, shortness of breath, pallor, hypotension, and loss of consciousness.

MANAGEMENT

• The aim of therapy is to break the reentry of the impulse.
• Vagal maneuvers, such as carotid sinus massage, gagging, breath holding, and immersing the face in ice water, may be used to interrupt AVNRT. These techniques increase parasympathetic stimulation, causing slower conduction through the AV node and blocking the reentry of the rerouted impulse.
• If the vagal maneuvers are ineffective, the patient may then receive a bolus of adenosine to correct the rhythm; this is nearly 100% effective in terminating AVNRT.
• If the patient is unstable or does not respond to the medications, cardioversion is the treatment of choice.
• Treatment for recurrent sustained AVNRT,
  • calcium channel blockers such as verapamil and diltiazem,
  • class 1a antiarrhythmic agents such as procainamide and disopyramide,
  • class 1c antiarrhythmics such as flecainide and propafenone, and
  • class 3 agents such as sotalol and amiodarone .

VENTRICULAR ARRHYTHMIAS

• Premature Ventricular Complex
• Ventricular Tachycardia
• Ventricular Fibrillation
• Idioventricular Rhythm
• Ventricular Asystole

PREMATURE VENTRICULAR COMPLEX

• Premature ventricular complex (PVC) is an impulse that starts in a ventricle and is conducted through the ventricles before the next normal sinus impulse.
• PVCs may be uniform (same form) or multiform (different forms).

ETIOLOGY

• PVCs can occur in healthy people, especially with intake of caffeine, nicotine, or alcohol.
• PVCs may be caused by cardiac ischemia or infarction, increased workload on the heart (eg, heart failure, and tachycardia), digitalis toxicity, hypoxia, acidosis, or electrolyte imbalances, especially hypokalemia.

CHARACTERISTICS

• Rate: Depends on the underlying rhythm (sinus rhythm)
• Rhythm: Irregular whenever a PVC occurs
• P wave: Usually normal; None associated with the PVC
• PR interval: Usually normal; None associated with the PVC
• QRS shape and duration: Usually normal, but wide and bizarre appearance with the PVC
• P:QRS ratio - 1:1or 0:1with the PVC

MANAGEMENT

• Initial treatment is aimed at correcting the cause.
• In the absence of disease, PVCs usually are not serious.
• PVCs that are frequent and persistent may be treated with amiodarone or sotalol.
• Long-term pharmacotherapy for only PVCs is not indicated.
• In patients with acute MI, PVCs may warrant more aggressive therapy. Lidocaine (Xylocaine) may be used in the patient with acute MI.
• Patients with acute MI who did not receive thrombolytics and had more than 10 PVCs per hour and those who did receive thrombolytics and had more than 25 PVCS per hour were found to be at the greatest risk for sudden cardiac death.

VENTRICULAR TACHYCARDIA

• VT is defined as three or more PVCs in a row, occurring at a rate exceeding 100 bpm. Impulse is originating in the ventricles (no P waves, wide QRS).

ETIOLOGY

• The causes are similar to those of PVC.
• VT is usually associated with CAD and patients with larger MI's and lower ejection fractions are at higher risk of lethal ventricular tachycardia.
• VT is an emergency because the patient is usually (although not always) unresponsive and pulseless.

CHARACTERISTICS

• Rate: Atrial - depends on sinus rhythm; ventricular - between 100 to 200.
• Rhythm: atrial & ventricular rhythm - Usually regular
• P wave: Very difficult to detect, so atrial rate and rhythm may be indeterminable
• PR interval: Cannot be measured; if P waves are seen, Very irregular
• QRS shape and duration: 0.12 seconds or more; bizarre, abnormal shape
• P:QRS ratio - Difficult to determine, if P waves are apparent, usually 1:Many

MANAGEMENT

• If the patient is stable, continuing the assessment, especially obtaining a 12-lead ECG, may be the only action necessary. However, the patient may need antiarrhythmic medications, antitachycardia pacing, or direct cardioversion.
• Antiarrhythmic medication of choice
  • IV procainamide - for a patient with stable acute MI with VT, whereas
  • IV amiodarone - for a patient with unstable VT or impaired cardiac function.
• lidocaine has been the medication most commonly used for immediate, short-term therapy, especially for patients with impaired cardiac function.
• Cardioversion is the treatment of choice for monophasic VT in a symptomatic patient. Defibrillation is the treatment of choice for pulseless VT.
• Any type of VT in a patient who is unconscious and without a pulse is treated in the same manner as ventricular fibrillation: immediate defibrillation is the action of choice.
• For long-term management
  • Patients with an ejection fraction less than 35% should be considered for an implantable cardioverter defibrillator.
  • Those with an ejection fraction greater than 35% may be managed with amiodarone.

VENTRICULAR FIBRILLATION

• The most common dysrhythmia in patients with cardiac arrest is ventricular fibrillation, which is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles.
• No atrial activity is seen on the ECG.

ETIOLOGY

• The ventricular cells are excitable and depolarizing randomly. Rapid drop in cardiac output and death occurs if not quickly reversed.
• The most common cause of ventricular fibrillation is coronary artery disease and resulting acute MI. Other causes include untreated or unsuccessfully treated VT, cardiomyopathy, valvular heart disease, several proarrhythmic medications, acid-base and electrolyte abnormalities, and electrical shock.
• Another cause is Brugada syndrome, in which the patient (frequently of Asian descent) has a structurally normal heart, few or no risk factors for coronary artery disease, and a family history of sudden cardiac death.

CHARACTERISTICS

• Ventricular rate: Greater than 300 per minute
• Ventricular rhythm: Extremely irregular, without a specific pattern
• QRS shape and duration: Irregular, undulating waves without recognizable QRS complexes

MANAGEMENT

• Ventricular fibrillation is always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations.
• Because there is no coordinated cardiac activity, cardiac arrest and death are imminent if the dysrhythmia is not corrected.
• Early defibrillation is critical to survival, with administration of immediate bystander cardiopulmonary resuscitation (CPR) until defibrillation is available.
• The chance of survival decreases by 7% to 10% for every minute in delay of defibrillation.

IDIOVENTRICULAR RHYTHM

• Idioventricular rhythm, also called ventricular escape rhythm, occurs when the impulse starts in the conduction system below the AV node. When the sinus node fails to create an impulse (eg, from increased vagal tone) or when the impulse is created but cannot be conducted through the AV node (eg, due to complete AV block), the Purkinje fibers automatically discharge an impulse.

CHARACTERISTICS

• Ventricular rate: 20 and 40; if the rate exceeds 40, the rhythm is known as accelerated idioventricular rhythm (AIVR)
• Ventricular rhythm: Regular
• QRS shape and duration: Bizarre, abnormal shape; duration is 0.12 seconds or more
• Idioventricular rhythm commonly causes the patient to lose consciousness and experience other signs and symptoms of reduced cardiac output.

MANAGEMENT

• The treatment is the same as for asystole and pulseless electrical activity (PEA).
• Interventions include
  • Identifying the underlying cause;
  • Administering IV epinephrine,
  • Atropine,
  • Vasopressor medications; and
  • Initiating emergency transcutaneous pacing
• In some time it may cause no symptoms of reduced cardiac output. but, bed rest is prescribed so as not to increase the cardiac workload.

VENTRICULAR ASYSTOLE

• Commonly called flat line, ventricular asystole is characterized by absent QRS complexes confirmed in two different leads, although P waves may be apparent for a short duration. There is no heartbeat, no palpable pulse, and no respiration. Without immediate treatment, ventricular asystole is fatal.
• Ventricular asystole is treated the same as PEA, focusing on high-quality CPR with advanced cardiovascular life support (ACLS).
• The key to successful treatment is rapid assessment to identify a possible cause, which may be hypoxia, acidosis, severe electrolyte imbalance, drug overdose, hypovolemia, cardiac tamponade, tension pneumothorax, coronary or pulmonary thrombosis, trauma, or hypothermia.