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14. Cardiac arrhythmias
Cardiac arrhythmias are disruptions in the regular rate and rhythm of the heart, caused by issues in the heart's electrical conduction system. These arrhythmias can arise from conditions intrinsic to the heart or external physiological factors.
Causes of Arrhythmias:
Cardiogenic causes include ischemic heart disease, which is the most frequent cause, alongside others such as valve diseases, cardiomyopathies, congenital heart defects, effects of heart surgeries, and disorders related to ion channels like the long QT syndrome.
Non-cardiogenic causes involve factors such as increased sympathetic nervous system activity, disturbances in electrolytes like potassium and calcium, acid-base imbalances, thyroid dysfunction, reduced oxygen levels (hypoxemia), and the impact of certain medications including antiarrhythmics and beta-blockers.
Pathophysiological Mechanisms:
Accelerated Automaticity: This is caused by an increased rate of diastolic depolarization and changes in the threshold potential, often due to alterations in calcium and potassium levels. Factors contributing to this include enhanced sympathetic tone, reduced parasympathetic activity, thyroid conditions, and medications like digoxin, which also impairs the sodium/potassium pump affecting the resting membrane potential.
Triggered Activity (After-depolarizations):
Early After-depolarizations: Occur during the relative refractory period and can extend the repolarization phase. This can be triggered by electrolyte imbalances, use of potassium channel blockers, and conditions such as long QT syndrome.
Late After-depolarizations: Happen during the resting phase, often due to an overload of intracellular calcium from excessive catecholamines or digoxin, increasing both inotropic (force of contraction) and chronotropic (rate of contractions) activity.
Re-entry: This occurs when an electrical impulse circulates around a structural obstacle within the heart, creating a loop of electrical activity. This loop divides into two pathways: one fast-conducting with a long refractory period and another slow-conducting with a shorter refractory period. When these pathways reconverge, the mismatch in timing can cause the heart to generate additional beats. Structural changes like scarring, tissue degeneration, or chamber dilation can predispose to this mechanism.
Basic Types of Arrythmias
Bradyarrhythmias: These involve issues with signal generation or conduction, leading to a slower heart rate (under 60 beats per minute). Symptoms may include exertional dyspnea (shortness of breath during physical activity) and syncope (fainting).
Tachyarrhythmias: These occur when a specific area in the heart generates impulses at a faster rate, or when impulses circulate within a re-entry loop, causing a heart rate over 100 beats per minute. Symptoms can include palpitations, fatigue, dizziness, syncope, and in severe cases, sudden cardiac death.
Supraventricular arrhythmias: These originate in the atria (upper chambers of the heart) and typically show a narrow QRS complex on an ECG because the signal travels quickly through the normal conduction pathway.
Ventricular arrhythmias: These originate in the ventricles (lower chambers of the heart). The QRS complex is wider on an ECG because the signal travels more slowly through the ventricular muscle rather than the normal conduction pathway.
Types of Atrial Origin Bradyarrythmias
Respiratory sinus arrhythmia: A physiological variation where the heart rate increases with inhalation and decreases with exhalation, often more pronounced in younger individuals.
Sinus bradycardia: Common in athletes or those on certain heart medications such as beta-blockers or calcium channel blockers, characterized by a normal ECG but a heart rate less than 60 bpm.
Sinus arrest: A condition where the sinoatrial node (SA node) fails to produce an impulse, visible on an ECG as an absence of the P-wave, sometimes followed by an escape rhythm if the pause is prolonged.
Tachycardia-bradycardia syndrome: Characterized by alternating fast and slow heart rates, often a manifestation of sick sinus syndrome, where the heart's natural pacemaker (SA node) malfunctions.
Sick Sinus Syndrome SSS
Sick sinus syndrome (SSS) is a condition where the sinoatrial (SA) node, which is responsible for setting the pace of the heart, malfunctions. This results in a variety of arrhythmias, including sinus bradycardia, SA pause or block, and arrest, as well as episodes of supraventricular tachycardia. Here’s a breakdown of the key aspects of sick sinus syndrome:
Causes:
Primary cause: Degeneration and fibrosis of the SA node and surrounding myocardium, which is most common in the elderly.
Medication-induced: Certain medications such as beta-blockers, digoxin, and non-dihydropyridine calcium channel blockers can exacerbate or precipitate the symptoms of SSS.
Common Presentations:
Bradycardia symptoms: Patients may experience dizziness, syncope (fainting spells), and an inability to increase heart rate during physical exertion. An Adams-Stokes attack, which is a type of syncope due to heart rhythm abnormalities, may also occur.
Tachycardia-bradycardia syndrome: This manifests as alternating fast and slow heart rates, leading to palpitations, shortness of breath (dyspnea), and chest pain (angina pectoris).
Diagnostics of sick sinus syndrome:
Electrocardiogram (ECG): An ECG can show various arrhythmias indicative of SSS.
Exercise stress test: May reveal an inadequate increase in heart rate in response to exercise.
Treatment of sick sinus syndrome:
Medication review and adjustment: If symptoms are medication-induced, adjusting the dosages or discontinuing the offending drugs may be necessary.
Pacemaker placement: For patients with significant symptoms, especially those involving bradyarrhythmias, a pacemaker may be necessary to maintain a stable and appropriate heart rate.
Selective beta-blockers: For cases involving tachyarrhythmias, low-dose, cardioselective beta-blockers like metoprolol or bisoprolol might be used, though care must be taken as they can also exacerbate bradycardia.
AV BLOCKS
AV (atrioventricular) blocks are types of heart block that affect the electrical conduction between the atria and ventricles of the heart. These can range from mild to severe and are caused by various factors including increased vagal tone, fibrosis of the conduction system, ischemic heart disease, cardiomyopathies, infections like Lyme disease, medication effects, or following cardiac procedures. Here's a detailed look at the types of AV blocks:
First-Degree AV Block
Description: Prolonged conduction time through the AV node, but all impulses eventually reach the ventricles.
Causes: Increased vagal tone, use of beta-blockers or calcium channel blockers.
Symptoms: Often asymptomatic and discovered incidentally on an ECG.
ECG Findings: PR interval exceeds 200 milliseconds.
Management: Generally requires no treatment unless symptomatic or part of broader cardiac issues.
Second-Degree AV Block
Type I (Wenckebach or Mobitz I) Second-Degree AV Block:
Mechanism: Progressive prolongation of AV conduction until an impulse fails to be conducted.
Causes: Increased vagal tone or degenerative changes in the AV node.
Symptoms: Often asymptomatic, possible episodes of syncope.
ECG: Increasing PR interval followed by a non-conducted P-wave.
Management: Usually only observation unless symptoms develop.
Type II (Mobitz II) Second-Degree AV Block:
Mechanism: Sudden failure of AV conduction without preceding PR interval prolongation.
Causes: More likely due to disease within the conduction system.
Symptoms: Higher risk of progressing to complete heart block, symptoms of bradycardia such as fatigue, dyspnea, chest pain, and syncope.
ECG: Fixed PR intervals with intermittent non-conducted P-waves.
Management: Pacemaker implantation is often required due to the risk of progression to third-degree block.
Third-Degree AV Block (Complete Heart Block)
Description: No atrial impulses are conducted to the ventricles; atria and ventricles beat independently.
Causes: Severe damage to the electrical conduction system.
Symptoms: Variable, can include syncope, heart failure symptoms, Adams-Stokes attacks (sudden fainting due to asystole or severe bradycardia), and potential cardiac arrest.
ECG Findings of third degree AV block: Complete dissociation between P waves and QRS complexes.
Junctional rhythm: Occurs if the escape rhythm originates above the bundle of His; typically presents with a narrow QRS complex and a rate of 40-60 bpm.
Idioventricular rhythm: Occurs if the escape rhythm originates below the bundle of His; presents with a broad QRS complex and a rate of 20-40 bpm.
Management of third degree AV block: Immediate pacemaker placement is indicated due to the risk of life-threatening arrhythmias and sudden cardiac death.
Bundle branch blocks (BBB)
Bundle branch blocks (BBB) are disruptions in the normal pattern of electrical conduction in the heart's ventricles. They occur when the pathway that transmits electrical impulses to the heart muscle (the bundle branches) is delayed or blocked.
Right Bundle Branch Block (RBBB)
Mechanism: Delay in the conduction of electrical impulses to the right ventricle, which results in the left ventricle contracting a fraction of a second before the right ventricle.
Causes: Right ventricular hypertrophy, myocardial infarction (MI) of the lateral wall, pulmonary embolism, chronic lung disease.
ECG Characteristics of Right Bundle Branch Block (RBBB) :
Axis deviation between +90 to +180 degrees.
Negative deflections in lead I, positive deflections in leads II and III.
QRS duration greater than 120 milliseconds.
RSR' pattern in leads V1-V2, resembling a 'rabbit ear' appearance.
Wide S-waves in lead I.
T-wave inversions and ST-segment depression in leads V1-V3, indicating right ventricular repolarization disturbances.
Left Bundle Branch Block (LBBB)
Mechanism: Delay in the conduction of impulses to the left ventricle, causing the right ventricle to contract slightly before the left.
Causes: Aging, left ventricular hypertrophy, myocardial infarction of the inferior wall.
ECG Characteristics of Left Bundle Branch Block:
Axis deviation between -30 to -90 degrees.
Positive deflections in lead I, negative deflections in leads II and III.
QRS duration greater than 120 milliseconds.
Broad monophasic R-waves in leads V5-V6, resembling an 'M' shape.
Absence of Q-waves, with RSR' patterns in V5-V6.
Deep S-waves in leads V1-V2.
Left Anterior Hemiblock (LAH)
Mechanism: Conduction block in the anterior fascicle of the left bundle branch, resulting in a delay of impulses to the upper front part of the left ventricle.
ECG Characteristics:
Left axis deviation (-30 to -90 degrees).
Narrow QRS complex, as the block does not affect the overall QRS width.
Left Posterior Hemiblock (LPH)
Mechanism: Conduction block in the posterior fascicle of the left bundle branch, affecting the electrical activity directed to the lower back part of the left ventricle.
ECG Characteristics:
Right axis deviation (+90 to +180 degrees).
Narrow QRS complex.
Appearance of the QRS complex on an electrocardiogram (ECG)
The table you uploaded outlines how the electrical axis and certain conditions can alter the appearance of the QRS complex on an electrocardiogram (ECG) across three standard leads: I, II, and III. The axis and additional conditions affect the direction (upright, down, or biphasic) of the QRS complexes in these leads. Here's a breakdown of each row:
Normal Axis (-30 to 90 degrees)
Lead I: Upright QRS complex
Lead II: Upright QRS complex
Lead III: Upright QRS complex
Additional: This is the standard QRS orientation indicating normal heart electrical activity.
Physiologic Left Axis (-40 to 0 degrees)
Lead I: Upright QRS complex
Lead II: Upright or Biphasic QRS complex
Lead III: Down QRS complex
Additional: Often normal, especially in tall, thin individuals.
Pathologic Left Axis (-40 to -90 degrees)
Lead I: Upright QRS complex
Lead II: Down QRS complex
Lead III: Down QRS complex
Additional: Anterior Hemiblock, suggesting a block in the anterior superior branch of the left bundle branch.
Right Axis (90 to 180 degrees)
Lead I: Down QRS complex
Lead II: Upright or Biphasic QRS complex
Lead III: Upright QRS complex
Additional: Posterior Hemiblock, which can occur in cases of hypertrophy or other structural changes in the heart.
Extreme Right Axis (180 to -90 degrees)
Lead I: Down QRS complex
Lead II: Down QRS complex
Lead III: Down QRS complex
Additional: Ventricular origin, indicating a problem in ventricular conduction that overrides normal atrial origin of the heartbeat.
Treatment of Bradyarrhythmias:
Stop Triggering Medication: Medications like beta-blockers and calcium channel blockers can induce or worsen bradyarrhythmias. Stopping or adjusting these medications is a primary step in treatment.
Implantation of Pacemaker: For significant symptomatic bradyarrhythmias or those with a high risk of complications (like syncope or heart failure), a pacemaker may be implanted to maintain adequate heart rates and rhythm.
Atrial-Origin Tachyarrhythmias:
Sinus Tachycardia:
Caused by sympathetic activation and decreased vagal tone.
ECG shows a regular rhythm with P-waves preceding each narrow QRS complex, indicating normal atrial origin but increased rate.
Atrial Tachycardia:
Atrial rates between 140-220 bpm.
ECG can show a very short PQ-segment; P-waves may appear negative if the electrical signals are originating from lower in the atria, sending impulses retrograde to the SA node.
Atrial Flutter:
Atrial rate of 250-350 bpm but fewer ventricular responses due to the refractory period of the AV node.
ECG typically displays sharp, triangular P-waves known as F-waves, especially noticeable in leads II, III, and aVF. The QRS complexes are regular but may be preceded by multiple F-waves. T-waves are often obscured by the atrial activity.
Carries a risk of thrombus formation due to rapid atrial rates.
Atrial Fibrillation:
Very high atrial rate (>350 bpm) with a resultant ventricular rate typically <200 bpm.
The atria generate chaotic electrical impulses that sporadically penetrate the AV node, leading to irregularly irregular QRS timings (variable RR intervals).
ECG shows an absence of distinct P-waves; instead, irregular and rapid fibrillation waves (f-waves) are seen.
There's a high risk of atrial thrombus formation due to the turbulent and stagnant blood flow in the fibrillating atria.
AV Node Tachycardia
AV node tachycardia encompasses several types of arrhythmias related to and involving the atrioventricular (AV) node. These are primarily seen as types of supraventricular tachycardia (SVT), where the arrhythmia involves structures above the ventricles. Here's a breakdown of the three main types mentioned:
1. Atrioventricular Re-Entry Tachycardia (AVRT)
Pathophysiology of Atrioventricular Re-Entry Tachycardia (AVRT): Involves an accessory pathway that bypasses the normal AV node conduction system, which can lead to a re-entry circuit. This is often seen in Wolff-Parkinson-White (WPW) syndrome where the presence of a delta wave is notable.
ECG Characteristics of Atrioventricular Re-Entry Tachycardia (AVRT):
Regular rhythm with a rate of 150-250 bpm.
P-waves may be inverted in leads II, III, and aVF.
QRS complex may be narrow or wide, often with a delta wave indicating pre-excitation.
Clinical Presentation of Atrioventricular Re-Entry Tachycardia (AVRT): Paroxysmal supraventricular tachycardia (PSVT), possible progression to atrial fibrillation.
Treatment of Atrioventricular Re-Entry Tachycardia (AVRT): Catheter ablation of the accessory pathway is often curative.
2. Atrioventricular Nodal Re-Entry Tachycardia (AVNRT)
Pathophysiology of Atrioventricular Nodal Re-Entry Tachycardia (AVNRT): Involves dual AV nodal pathways (fast and slow), allowing for a re-entry mechanism that triggers and sustains tachycardia.
ECG Characteristics Atrioventricular Nodal Re-Entry Tachycardia (AVNRT):
Regular rhythm with a rate of 150-250 bpm.
Narrow QRS complex, usually obscuring the P-waves which may appear just at the end of or merged with the QRS complex.
Clinical Presentation Atrioventricular Nodal Re-Entry Tachycardia (AVNRT): Presents as episodes of sudden-onset, rapid heart rate (PSVT).
Treatment Atrioventricular Nodal Re-Entry Tachycardia (AVNRT): Initial management with vagal maneuvers or adenosine to temporarily block AV node conduction and terminate the tachycardia. Chronic cases may require catheter ablation.
3. Junctional Tachycardia
Pathophysiology of Junctional Tachycardia: The AV node or adjacent tissues take over as the primary pacemaker of the heart, often associated with enhanced automaticity or triggered activity.
ECG Characteristics of Junctional Tachycardia:
Regular rhythm with a rate of 100-130 bpm.
P-waves may appear before, during, or after the QRS complex and can be inverted if the activation is retrograde.
Narrow QRS complex due to origin near or at the AV node.
Clinical Presentation of Junctional Tachycardia: Often occurs in the setting of digoxin toxicity, myocarditis, or after a myocardial infarction.
Treatment of Junctional Tachycardia: Depends on the underlying cause but may involve managing the immediate effects of the tachycardia, correcting electrolyte imbalances, and potentially using antiarrhythmic drugs.
PREMATURE BEATS
Premature beats are early heartbeats that interrupt the normal, regular rhythm of the heart. They can originate from the atria (supraventricular) or the ventricles. Here's an explanation of the types mentioned:
1. Supraventricular Extrasystole
Origin: These premature beats arise from the atria above the ventricles.
ECG Characteristics:
P-wave is usually present and precedes a normal QRS complex.
Incomplete compensatory pause: the interval after the premature beat is shorter than twice the normal RR interval because the extrabeat resets the SA node.
Causes of Supraventricular Extrasystole: Can occur in healthy individuals (physiological) or be associated with electrolyte imbalances, stress, caffeine, alcohol, or underlying heart disease.
Clinical Significance of Supraventricular Extrasystole: Generally benign but can be uncomfortable for the patient; may indicate underlying pathology if persistent.
2. Ventricular Extrasystole
Origin: These beats originate within the ventricles.
ECG Characteristics:
Absence of a preceding P-wave.
Wide and premature QRS complex (>120 ms) due to the ectopic signal originating in the ventricles and not following the usual conduction pathway.
Complete compensatory pause: the interval following the premature beat is exactly twice the normal RR interval because the ectopic beat does not affect the next normal beat generated by the SA node.
Causes of Ventricular Extrasystole: Can be linked to heart disease, electrolyte imbalances, hypoxia, or changes associated with aging.
Clinical Significance of Ventricular Extrasystole: While often benign, frequent ventricular extrasystoles may need further evaluation, especially in patients with known heart disease, as they can sometimes precede more serious arrhythmias.
Patterns of Extrasystoles
Bigeminy: Every normal beat is followed by a premature beat.
Trigeminy: Every two normal beats are followed by a premature beat.
Monotopic: Premature beats look the same on ECG, indicating they are coming from the same location in the heart.
Polytopic: Premature beats look different on ECG, suggesting multiple origins within the heart, which might indicate a more extensive underlying cardiac issue.
Ventricular Tacharrythmias
Ventricular tachyarrhythmias are severe cardiac rhythm disturbances originating from the ventricles, and they are critical conditions that can lead to significant morbidity or sudden cardiac death if not treated promptly. Here's a breakdown of the types mentioned:
1. Ventricular Tachycardia (VT)
Definition of Ventricular Tachycardia (VT): A run of three or more consecutive premature ventricular beats.
ECG Characteristics of Ventricular Tachycardia (VT): Shows a wide QRS complex that is typically greater than 120 ms because the electrical impulse does not follow the normal conduction pathway through the AV node but instead originates and spreads through the ventricles abnormally.
Causes of Ventricular Tachycardia (VT): Most commonly associated with coronary artery disease, previous myocardial infarction (MI), or structural heart diseases such as cardiomyopathies.
Clinical Significance of Ventricular Tachycardia (VT): VT can be stable (patient is conscious) or unstable (patient is symptomatic with low blood pressure), and it requires immediate medical intervention to prevent progression to more severe forms of arrhythmias.
2. Torsades de Pointes
Type: A specific form of polymorphic ventricular tachycardia characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line on an ECG.
Causes: Often triggered by a prolonged QT interval, which can be due to congenital ion channel defects (long QT syndrome), certain medications that prolong the QT interval, or electrolyte imbalances (notably hypokalemia).
Clinical Significance: Torsades de Pointes can rapidly deteriorate into ventricular fibrillation if not treated promptly, posing a high risk of cardiac arrest.
3. Ventricular Fibrillation (VF)
Characteristics of Ventricular Fibrillation (VF): Characterized by rapid, erratic electrical impulses from the ventricles, leading to ineffective quivering instead of coordinated contractions.
ECG Appearance of Ventricular Fibrillation (VF): Shows extremely irregular and varying waveforms without a discernible pattern, no P waves, and a very high rate exceeding 300 beats per minute.
Causes of Ventricular Fibrillation (VF): Most commonly occurs in the context of acute myocardial infarction, severe myocardial ischemia, or underlying structural heart disease.
Outcome of Ventricular Fibrillation (VF): VF results in the cessation of effective blood circulation, leading to sudden cardiac death if not immediately reversed by defibrillation.
Treatment of Ventricular Tachyarrhythmias
Immediate Management: The primary treatment for VT and VF is prompt electrical defibrillation. Additional measures include administering antiarrhythmic drugs (e.g., amiodarone, lidocaine) and correcting any reversible causes such as electrolyte imbalances.
Long-term Management: May include the use of implantable cardioverter-defibrillators (ICDs) in patients at high risk of recurrent VT or VF, especially in those with significant structural heart disease or previous cardiac arrest.
The Clinical Classification of Tachyarrhythmias
The clinical classification of tachyarrhythmias is primarily based on the appearance of the QRS complex on an electrocardiogram (ECG), which helps in identifying the origin of the arrhythmia:
Narrow QRS Complex: Indicates supraventricular tachyarrhythmia, where the arrhythmia originates above the ventricles, typically in the atria. The QRS complex remains narrow (<120 ms) because the ventricles are activated normally through the intact ventricular conduction system.
Wide QRS Complex: Suggests a ventricular origin of the arrhythmia, or a supraventricular arrhythmia that is conducted abnormally through the ventricles either due to a pre-existing bundle branch block or an accessory pathway that bypasses the normal conduction system (e.g., antidromic atrioventricular re-entrant tachycardia (AVRT) often seen in Wolff-Parkinson-White (WPW) syndrome).
Treatment of Tachyarrhythmias:
The treatment of tachyarrhythmias varies based on the type and severity of the arrhythmia, as well as the underlying cause and the patient's overall health:
Antiarrhythmic Drugs:
Class I: Fast sodium channel blockers (e.g., propafenone, flecainide) that slow conduction across the heart, which can be effective in controlling arrhythmic episodes.
Class II: Beta-blockers (e.g., metoprolol, esmolol, carvedilol) reduce the effects of adrenaline on the heart, slowing the heart rate and reducing the force of contraction.
Class III: Potassium channel blockers (e.g., amiodarone, sotalol) prolong repolarization and increase the duration of the action potential and the QT interval.
Class IV: Calcium channel blockers (e.g., verapamil, diltiazem) affect the heart and blood vessels, making it harder for the calcium to enter the heart's cells, thus reducing the heart's pumping strength and relaxing blood vessels.
Class V: Other drugs like adenosine, which can quickly interrupt supraventricular tachycardia by hyperpolarizing the heart cells, and digoxin, which decreases heart rate while increasing contractility through its action on the cardiac Na/K ATPase pump.
Catheter Ablation:
Used especially in cases where tachyarrhythmias recur despite medication or when an accessory pathway (like in WPW syndrome) is present. This procedure involves destroying the small area of heart tissue that is causing the irregular heartbeats.
Implantable Cardioverter Defibrillator (ICD):
Recommended for patients at high risk of life-threatening arrhythmias. The ICD constantly monitors the heart rhythm and delivers electric shocks when a dangerous tachyarrhythmia is detected to restore a normal heart rhythm.