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
ETIOLOGY
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
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
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
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
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
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
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.
