1.02

Questions and Answers

What is the primary function of the SA node in the heart?

Distributing blood to the left and right sides of the heart

Controlling the contraction strength of ventricles

Delaying transmission of atrial impulses to the ventricles

Generating impulses to initiate heart contractions (correct)

What effect does the sympathetic nervous system have on heart rate via the SA node?

It decreases heart rate by activating B1 receptors

It has no effect on heart rate

It increases heart rate by activating B1 receptors (correct)

It increases heart rate by activating M2 receptors

Which structure serves as a gateway for impulses from the atrium to the ventricles?

Purkinje Fibers

SA Node

Bundle of His

AV Node (correct)

What is the heart rate at which the Bundle Branches act as pacemakers?

20-40 bpm Signup and view all the answers

Which of the following describes the effect of the AV node on atrial impulses?

It prevents very fast heartbeats by delaying atrial impulses Signup and view all the answers

What is the consequence of a dysfunction in the sinus node?

Subsidiary pacemakers take over, leading to decreased heart rate Signup and view all the answers

What ion primarily causes depolarization during Phase 0 of the SA node action potential?

Ca++ Signup and view all the answers

During which phase of the contractile myocardium action potential does K+ exit the cell?

Phase 3 Signup and view all the answers

Which phase involves a plateau due to the entry of calcium ions in the contractile myocardium action potential?

Phase 2 Signup and view all the answers

What unique ionic movement occurs during Phase 4 of the SA node action potential?

Entry of Na+ via funny current Signup and view all the answers

Which phase is characterized by the simultaneous exit of K+ and entry of Ca++ in the contractile myocardium action potential?

Phase 1 Signup and view all the answers

What is the normal duration range of the PR interval in an ECG reading?

0.12-0.20s Signup and view all the answers

Which formula is used to calculate the heart rate using the RR interval?

60 / RR interval in seconds Signup and view all the answers

What is the duration of the QRS interval in an ECG?

0.10-0.11s Signup and view all the answers

Which phase of the ECG corresponds to the active repolarization of the T wave?

Phase 3 Signup and view all the answers

Which factor is likely less significant when assessing a relatively young patient with no family history of heart disease?

Existence of structural heart disease Signup and view all the answers

When considering the approach to the patient, which aspect is deemed most critical?

Individualized assessments based on patient history Signup and view all the answers

In the context of myocardial infarction, what role does patient history play?

Identifying rapid and serious causes of the MI Signup and view all the answers

For patients without alarming risk factors, which aspect of their history might still warrant further evaluation?

Family history of heart disease Signup and view all the answers

What is the primary use of a Holter Monitor?

To determine the connection between patient symptoms and arrhythmia Signup and view all the answers

Which device is best suited for patients experiencing infrequent episodes of symptoms?

Loop Recorder Signup and view all the answers

What does the Head-Up Tilt Testing primarily evaluate?

Reactions to exaggerated vagal tone in patients with syncope Signup and view all the answers

Which test can induce supraventricular tachycardia (SVT) non-invasively?

Exercise ECG Signup and view all the answers

What is the typical recording duration of implantable loop recorders?

2 years Signup and view all the answers

What is the primary purpose of electrophysiologic testing in relation to cardiac arrhythmias?

To identify arrhythmia mechanisms and guide treatment Signup and view all the answers

Which class of antiarrhythmic drugs is known to block Na+ channels?

Class I Signup and view all the answers

Which of the following is an implication of using Class IV antiarrhythmic drugs?

Impairs impulse propagation in nodal areas Signup and view all the answers

What is a significant benefit of catheter ablation in the treatment of arrhythmias?

It can both diagnose and treat certain types of arrhythmias Signup and view all the answers

Which of the following correctly describes a characteristic of Class III antiarrhythmic drugs?

They prolong the action potential and refractory period Signup and view all the answers

What is the primary indication for a Permanent Pacemaker?

Symptomatic sinus bradycardia Signup and view all the answers

Which device delivers a shock to restore normal rhythm during ventricular tachycardia?

Implantable Cardioverter Defibrillator (ICD) Signup and view all the answers

Which of the following conditions would likely require the use of a Cardioverter Resynchronization Therapy Device?

Heart failure with a low ejection fraction Signup and view all the answers

Which diagnostic tool is most suitable for monitoring infrequent arrhythmia symptoms?

Loop recorder Signup and view all the answers

What age group is most commonly affected by junctional rhythms?

Patients over 50 Signup and view all the answers

What is the typical heart rate associated with sinus bradycardia?

40-60 beats per minute Signup and view all the answers

Which condition is characterized by the malfunction of the heart's natural pacemaker?

Sinus node dysfunction Signup and view all the answers

Which type of arrhythmia is commonly linked to a slower than normal heart rhythm?

Sinus bradycardia Signup and view all the answers

What physiological mechanism primarily causes arrhythmias in the context of sinus node dysfunction?

Inadequate electrical impulse generation Signup and view all the answers

In which scenario would sinus node dysfunction most likely be diagnosed?

Patient experiencing dizziness and fainting spells Signup and view all the answers

What characterizes 1st degree heart block?

Abnormal prolongation of SA conduction time Signup and view all the answers

Which statement is true about Type 2 second-degree heart block?

It shows abrupt absence of one or more P waves. Signup and view all the answers

What differentiates 3rd degree heart block from sinus arrest?

There is an absence of P waves due to impulse failure. Signup and view all the answers

What is a primary symptom of chronotropic incompetence during exercise?

Inability to achieve a maximum heart rate of 100-120 bpm Signup and view all the answers

Which description best fits tachycardia-bradycardia syndrome?

Intermittent tachycardia with brief sinus pauses Signup and view all the answers

Which of the following is a characteristic of the Wenckebach phenomenon seen in Type 1 second-degree heart block?

There is a gradual lengthening of the P-P intervals. Signup and view all the answers

What physiological response can indicate chronotropic incompetence during a stress test?

Fluctuations in heart rate with limited recovery Signup and view all the answers

Which scenario best describes a characteristic of an impulse failing to exit the sinus node?

Sinus impulses alternatively drop with prior prolongation. Signup and view all the answers

What indicates a pause in carotid sinus massage that suggests sinus node dysfunction?

Pause >3 seconds Signup and view all the answers

Which of the following ECG characteristics is associated with first degree AV block?

Fixed PR interval >0.20 seconds Signup and view all the answers

What ECG manifestation is indicative of Type 1 second-degree AV block?

PR interval progressively prolongs before non-conducted P wave Signup and view all the answers

In Type 2 second-degree AV block, what characteristic is typically observed?

Constant PR interval with sudden dropped beat Signup and view all the answers

What could be a possible site of block in second-degree Type 1 AV block?

AV node Signup and view all the answers

Which abnormal response can occur with carotid sinus hypersensitivity?

Syncope or loss of consciousness Signup and view all the answers

What is a common cause of first-degree AV block?

Intra-atrial or inter-atrial conduction delay Signup and view all the answers

Which distinguishing feature is associated with atypical Wenckebach in second-degree AV block?

Progressive changes in RR interval length Signup and view all the answers

What does a 2:1 AV block indicate about the relationship between P waves and QRS complexes?

For every two P waves, there is one conducted beat. Signup and view all the answers

Which characteristic is true about the site of block in a 2:1 AV block?

It occurs at the AV node with prolonged PR intervals. Signup and view all the answers

How does exercise influence the 2:1 AV block as described in the content?

It can reduce the block to a 3:2 ratio. Signup and view all the answers

What defines a high grade AV block in the context of AV conduction?

More than two P waves are dropped for every conducted beat. Signup and view all the answers

In a 2:1 AV block, what can be observed in the ECG manifestation?

Every other beat is nonconducted, creating a regular pattern. Signup and view all the answers

What is a characteristic feature of junctional escape rhythm?

Narrow QRS complexes with no preceding P waves Signup and view all the answers

Which condition is indicated by a pause after a P wave that is a multiple of PP intervals?

Second degree type 2 exit block Signup and view all the answers

What does a pause after QRS complexes that is not a multiple of PP intervals indicate?

Sinus pause or sinus arrest Signup and view all the answers

Which arrhythmia is characterized by having narrow QRS complexes and no preceding P waves?

Junctional escape rhythm Signup and view all the answers

What is suggested by a pause after a P wave followed by a P wave that falls within the expected timing of the next cycle?

First degree AV block Signup and view all the answers

What is the maximum dose of Atropine that can be administered in an acute treatment setting?

3 mg Signup and view all the answers

What is the primary use of Epinephrine IV infusion in acute treatment?

To accelerate heart rate Signup and view all the answers

In the event that atropine does not accelerate the heart rate, what is the next step in management?

Transcutaneous pacing or Epinephrine IV infusion Signup and view all the answers

At what rate should Dopamine IV infusion be titrated during treatment?

5-20 mcg/kg/min Signup and view all the answers

What is the purpose of inserting a wire into the right ventricle during acute treatment?

To pace the heart electrically Signup and view all the answers

For which conditions is long-term management through a pacemaker indicated?

Conditions with no reversible causes Signup and view all the answers

What is the first action to take when assessing an adult with bradycardia?

Maintain patent airway and assist breathing if necessary Signup and view all the answers

Which of the following is NOT a sign that indicates a persistent bradyarrhythmia might be causing issues?

Stable heart rate above 50/min Signup and view all the answers

What should be considered next if atropine is ineffective in treating bradycardia?

Transcutaneous pacing or epinephrine infusion Signup and view all the answers

When monitoring an adult with bradycardia, which of the following should NOT be routinely assessed?

Heart rate below 80/min Signup and view all the answers

Which action is recommended if the bradyarrhythmia is not causing any acute symptoms?

Monitor and observe the patient Signup and view all the answers

Study Notes

SA Node

Located at the junction of right atrium (RA) and superior vena cava (SVC).
Supplies: Right coronary artery (RCA) and left circumflex artery (LCx).
Functions as the primary pacemaker of the heart, initiating synchronous electrical discharge.
Comprised of electrically coupled oscillators that communicate through connexins.
Influenced by both sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) on heart rate (chronotropy).
SNS stimulation via Beta-1 (B1) receptors increases heart rate (+ chronotropy).
PNS stimulation via vagus nerve (CN X) through M2 receptors decreases heart rate (- chronotropy).
Pathway for impulse generation: SA node → atrial tracts via Bachmann's Bundle and internodal pathways → atrioventricular (AV) node.

AV Node

Located in the posterior wall of the right atrium, behind the tricuspid valve, marked by Koch's Triangle.
Supplies: RCA or LCx.
Acts as a delay mechanism for atrial impulse transmission to the ventricles, due to slower depolarization rates in some regions.
Serves as the gateway for impulses from the atria to the ventricles and protects against excessively fast heart rates.

Bundle of His and Bundle Branches

Bundle of His supplies: branches of anterior and posterior descending coronary arteries.
Divides into left bundle branch (LBB) and right bundle branch (RBB), functioning as subsidiary pacemakers with a discharge rate of 20-40 bpm.
Purkinje fibers extend into the inner third of the endocardium, facilitating rapid impulse conduction to ventricles.

Pacemaker Hierarchy

SA node is the primary pacemaker; if its function diminishes, subsidiary nodes like the AV node and bundle branches can take over but at a reduced rate.
A faster impulse from the SA node can inhibit impulses from the AV node and bundle branches.
Dysfunction in the SA node leads to decreased heart rate as subsidiary pacemakers compensate.

SA Node Action Potential

Primarily responsible for initiating heartbeats due to its automaticity.
Phase 4: Depolarization occurs with sodium (Na+) influx, facilitated by funny current channels.
Phase 0: Rapid depolarization ensues with calcium (Ca++) entering the cell, further accelerating depolarization.
Phase 3: Repolarization happens through the efflux of potassium (K+), restoring the cell to its resting membrane potential.
The cycle repeats continuously, ensuring rhythmic heartbeat generation.

Contractile Myocardium Action Potential

Essential for myocardial contraction and effective pumping of blood.
Phase 4: Resting potential maintained by K+ exiting the cell through potassium channels (rectifiers).
Phase 0: Initial depolarization occurs via a rapid influx of sodium (Na+) ions.
Phase 1: Partial repolarization marked by K+ exiting and Ca++ entering, contributing to early repolarization.
Phase 2 (Plateau): Sustained depolarization due to prolonged influx of calcium (Ca++), vital for muscle contraction.
Phase 3: Final repolarization phase where K+ exits, leading the membrane potential back to resting state.
The sequence ensures coordinated contractions of heart muscle during each heartbeat.

Action Potential in SA Node

Phase 4: Slow depolarization occurs due to the influx of sodium ions (Na+) through "funny" currents.
Phase 0: Rapid depolarization results from the influx of calcium ions (Ca++) contributing to a more significant change in membrane potential.
Phase 3: Repolarization is driven by the efflux of potassium ions (K+), returning the membrane potential towards its resting state.
This cycle repeats continuously, allowing for regular cardiac rhythmicity.

Contractile Myocardium Action Potential

Phase 4: Resting phase characterized by the exit of potassium ions (K+) through rectifier channels, stabilizing the resting membrane potential.
Phase 0: Rapid depolarization initiated by the influx of sodium ions (Na+), contrasting with the SA node's reliance on calcium.
Phase 1: Initial repolarization occurs with K+ exiting the cell while calcium ions (Ca++) begin to enter, balancing the charge difference.
Phase 2/Plateau: Sustained depolarization occurs from prolonged entry of calcium ions (Ca++), which is crucial for muscle contraction.
Phase 3: Repolarization is completed with the exit of potassium ions (K+), restoring the membrane potential.
This sequence allows for effective contraction and relaxation of cardiac muscle.

ECG Pattern and Representation

PR Interval: Ranges from 0.12 to 0.20 seconds; represents the time from the onset of depolarization at the sinus node to the ventricles.
Heart Rate Calculation using RR Interval:
- Heart rate can be computed using the formula: 60 / RR interval (in seconds).
- Alternatively, use 300 divided by the number of big squares between RR intervals.
- For RR interval in milliseconds, the formula is 1500 / RR interval.
QRS Interval: Lasts between 0.10 and 0.11 seconds; indicates the duration of ventricular depolarization.
Phases of ECG:
- Phase 0: Corresponds to the onset of the QRS complex.
- Phase 2: Represents the ST segment.
- Phase 3: Related to the active repolarization seen in the T wave.
ST Segment: Serves as the interval between ventricular repolarization and depolarization.

Patient Approach

Individualized approach is essential for effective patient care.
History-taking plays a crucial role in understanding the patient's condition.

Two Key Features

History in Acute Cases:
- In cases like Myocardial Infarction (MI), focus on identifying structural heart disease.
- Family history may provide insights into predisposition to serious conditions.
Contextual Background:
- A healthy and relatively young patient may present different diagnostic considerations.
- Quick assessment of serious potential causes can lead to timely interventions.

Patient Approach Overview

Patient approach is tailored to individual needs, prioritizing uniqueness of each case.

Key Features in Patient Evaluation

History Taking
- Essential for understanding underlying conditions.
- Focused on cases like Myocardial Infarction (MI) for accurate diagnostics.
Assessment of Structural Heart Disease
- Investigate for existing heart conditions to expedite cause determination.
- Consider familial history as a significant factor in risk evaluation.
Young Patients with No Family History
- Healthy patients without familial heart issues may present differently.
- A younger demographic often requires distinct considerations for diagnosis and treatment.

Holter Monitor

Used to connect patient symptoms with potential arrhythmias.
Typically employed for patients experiencing daily or frequent symptoms.

Ambulatory Event Recorders

Designed for patients with less frequent symptoms.
Patient-activated recorders allow users to initiate recordings during symptomatic episodes.

Loop Recorders

Suitable for capturing infrequent episodes of symptoms or monitoring atrial fibrillation.
Implantable loop recorders can continuously monitor for up to two years.

Exercise ECG (Stress Test)

Assesses the presence of myocardial demand ischemia, which can lead to arrhythmias.
Serves as a non-invasive method to provoke supraventricular tachycardias (SVTs).

Cardiac Imaging

Two-dimensional echocardiography (2DED) and cardiac MRI are used for diagnosing arrhythmias.
Relevant for evaluating potential causes or stratification of arrhythmias.

Head-Up Tilt Testing

Assesses patients with loss of consciousness (LOC) or syncope, particularly where exaggerated vagal tone is suspected.
Provides insight into the mechanisms underlying episodes of syncope.

Electrophysiologic Testing

Essential for evaluating and managing cardiac arrhythmias.
Key purposes: defines arrhythmia mechanisms, guides treatment via ablation, and identifies arrhythmia-related symptoms such as syncope or palpitations.

Treatment Approaches

Vaughan Williams Classification of Antiarrhythmic Drugs

Class I: Sodium (Na+) channel blockers.
- Ia: Increases action potential (AP) duration (e.g., quinidine, procainamide, disopyramide).
- Ib: Decreases AP duration (e.g., lignocaine).
- Ic: Has no effect on AP duration (e.g., flecainide).
Class II: Beta-adrenoceptor antagonists.
- Common medications include atenolol and sotalol.
Class III: Potassium (K+) channel blockers.
- Prolongs action potential and refractory periods, useful in suppressing re-entrant rhythms (e.g., amiodarone, sotalol).
Class IV: Calcium channel blockers (CCBs).
- Impairs impulse propagation in nodal tissues and damaged areas (e.g., verapamil).

Catheter Ablation

A key therapeutic strategy for treating arrhythmias, especially tachyarrhythmias.
Functions as both a diagnostic and therapeutic intervention in cardiac arrhythmia management.

Device Therapy

Permanent Pacemaker: Recommended for patients experiencing bradycardia, a condition with an abnormally slow heart rate.
Implantable Cardioverter Defibrillator (ICD):
- Designed for treatment of ventricular tachycardia, which is a leading cause of sudden cardiac death.
- Delivers a shock of approximately 600 volts or 40 Joules when it detects ventricular tachycardia or fibrillation, helping to restore normal heart rhythm.
Cardiac Resynchronization Therapy (CRT) Device:
- Comprises three leads placed in the right atrium (RA), right ventricle (RV), and left ventricle (LV) through the coronary sinus.

Bradyarrhythmias

Sinus Node Dysfunction: Implicates issues with the heart's primary pacemaker.
Atrioventricular (AV) Conduction Abnormalities: Involves disruptions in the electrical signal between the atria and ventricles.
Junctional Rhythms:
- Commonly found in patients older than 50 years.
- Types include symptomatic sinus bradycardia and sinus pauses/arrest, linked to intrinsic sinus node diseases.
- Factors contributing to junctional rhythms can include:
  - Conduction system disease, cardiomyopathy, coronary artery disease (CAD), or heart failure (HF).
  - Autonomic imbalance, such as autonomic neuropathy.
  - History of cardiac surgeries, such as maze or mitral valve surgery.

Diagnostics for Bradyarrhythmias

ECG: Standard tool for visualizing heart rhythm abnormalities.
24-hour Holter Monitor: Records continuous ECG data over a full day to capture infrequent arrhythmias.
Loop Recorders: Useful for monitoring rare symptoms, providing extended data collection.
Electrophysiology (EP) Study: Invasive procedure used to assess and diagnose electrical problems in the heart.

Cardiac Conduction System

SA Node: Located at the junction of right atrium (RA) and superior vena cava (SVC).
Function: Acts as the pacemaker of the heart, generating impulses at 60-100 bpm.
Regulation:
- Sympathetic nervous system (SNS) increases heart rate via beta-1 (B1) receptors.
- Parasympathetic nervous system (PNS) decreases heart rate via vagus nerve (CN X) and M2 receptors.
Impulse Pathway: SA node → atrial tracts through Bachmann's Bundle and internodal pathways → AV node.
AV Node: Located on the posterior wall of RA, behind tricuspid valve (Koch Triangle).
Function: Delays transmission from atria to ventricles, allowing time for ventricular filling; serves as a protective mechanism against rapid heart rates.
Bundle of His: Continuation from AV node, supplied by branches of anterior and posterior descending coronary arteries.
Bundle Branches: Divides into left and right bundles, functioning at 20-40 bpm.
Purkinje Fibers: Extends throughout the ventricles, penetrates the inner third of endocardium.

Action Potential Phases

SA Node:
- Phase 4: Depolarization via influx of Na+ (funny current).
- Phase 0: Rapid depolarization from Ca++ influx.
- Phase 3: Repolarization through K+ efflux.
Contractile Myocardium:
- Phase 4: K+ exits via rectifiers.
- Phase 0: Na+ entry initiates depolarization.
- Phase 1: K+ exits; Ca++ enters.
- Phase 2/Plateau: Ca++ entry continues.
- Phase 3: K+ exits for repolarization.

ECG and Heart Rate Metrics

PR Interval: 0.12-0.20 seconds; measures depolarization duration from SA node to ventricles.
RR Interval: Used to calculate heart rate; formulas include:
- Heart Rate = 60 / RR interval (in seconds).
- Heart Rate = 300 / number of big squares between RR intervals.
- Heart Rate = 1500 / RR interval (in milliseconds).
QRS Interval: 0.10-0.11 seconds; represents ventricular depolarization.

Device Therapy

Permanent Pacemaker: Indicated for bradycardic patients.
Implantable Cardioverter Defibrillator (ICD): For managing ventricular tachycardia; delivers shocks to restore normal rhythm.
Cardiac Resynchronization Therapy: Involves placement of three wires in atrium and both ventricles via coronary sinus.

Bradyarrhythmias

Types:
- Sinus node dysfunction.
- Atrioventricular conduction abnormalities.
- Junctional rhythms, especially in patients over 50, including symptomatic sinus bradycardia and sinus pauses/arrest.
Causes: Intrinsic sinus node disease, conduction system disease, cardiomyopathy, coronary artery disease, heart failure, autonomic imbalance, cardiac surgery.

Patient Approach and Diagnostics

Individualized Assessment: Consider medical history, structural heart disease, and family history in evaluating arrhythmias.
Holter Monitor: Used for daily symptom correlation with arrhythmia.
Exercise ECG (Stress Test): Detects myocardial ischemia that may trigger arrhythmias.
Cardiac Imaging: Utilizes 2D echocardiography and MRI for diagnosing arrhythmias.
Electrophysiologic Testing: Essential for determining arrhythmia mechanisms and providing treatment options like ablation.

Antiarrhythmic Medications

Vaughan Williams Classification:
- Class I: Sodium channel blockers (Ia: quinidine; Ib: lignocaine; Ic: flecainide).
- Class II: Beta-adrenoceptor antagonists (e.g., atenolol, sotalol).
- Class III: Potassium channel blockers (e.g., amiodarone, sotalol).
- Class IV: Calcium channel blockers (e.g., verapamil).
Catheter Ablation: A diagnostic and therapeutic technique used in treating tachyarrhythmias.

Conduction Disorders

1st Degree AV Block: Characterized by abnormal prolongation of sinus node conduction time; typically presents with a fixed delay. Not detectable on surface ECG.
2nd Degree AV Block:
- Type 1 (Wenckebach): Features intermittent failure of sinus impulses with progressive shortening of P-P intervals, resulting in occasional absent or dropped P waves. The pause is less than twice the shortest sinus cycle.
- Type 2: Involves abrupt loss of one or more P waves due to impulse failure from the sinus node without preceding progressive prolongation of conduction time or P-P interval shortening.
3rd Degree AV Block: Exhibits complete absence of P waves due to failure of impulse conduction from the sinus node to the atrium, indistinguishable from sinus arrest on a 12-lead ECG. Sinus arrest results from the failure to generate impulses rather than transmit them.

Syndromes

Tachycardia-Bradycardia Syndrome: Alternating episodes of tachycardia (e.g., paroxysmal Atrial Fibrillation, Atrial Flutter, Atrial Tachycardia) with bradycardia or junctional rhythms. Often ends with a prolonged sinus pause leading to a lower pacemaker escape rhythm.
Chronotropic Incompetence: Defined as the inability to reach 75-80% of age-predicted maximal heart rate during exercise (calculated as 220 minus age). Signs may include early peaking of heart rate and fluctuations during exertion, with insufficient recovery or failure to achieve a sinus rate of 100-120 bpm. Patients often report easy fatigability due to inadequate heart rate response to physical activity.

Carotid Sinus Hypersensitivity

Tight collars can cause loss of consciousness (LOC) or syncope by compressing the carotid arteries.
Carotid sinus massage (CSM) may show abnormal response with a pause exceeding 3 seconds, indicating potential Sinus Node Dysfunction (SND).
SND is more common in elderly patients.
Other physiological responses to CSM can include atrioventricular (AV) block and hypotension.

Atrioventricular Conduction Arrhythmias

First Degree AV Block

Characterized by PR interval longer than 0.20 seconds on ECG.
Every P wave is followed by a QRS complex with a fixed interval.
The most common site of block is at the AV node, particularly with narrow QRS complexes and PR intervals exceeding 0.30 seconds.
Prolonged PR intervals can also occur in the His-Purkinje system, present in 45% of cases.
Caused by intraatrial or interatrial conduction delays, often seen with broad P waves.

Second Degree AV Block

Two types: Type 1 (Wenckebach) and Type 2.

Type 1 (Wenckebach)

Identified by a progressive prolongation of the PR interval leading to a non-conducted P wave.
The RR interval before the dropped beat progressively shortens.
The most common site of block is at the AV node, with atypical Wenckebach occurring in over 50% of these cases.
SA Exit Block Type 1 shows no P wave, while AV Block shows a P wave followed by a dropped beat.

Type 2

Presents with a constant PR interval that may be normal or prolonged, with sudden dropped beats.
Morphology of QRS complexes remains the same before and after the dropped beat.
The site of block is typically the His-Purkinje system and is almost always infranodal.
Infranodal blocks occur in the His bundle around 30% of the time.

2:1 AV Block Overview

Characterized by a dropped beat (P wave) resulting in no QRS complex following it.
For every two P waves, only one QRS complex is conducted, creating a rhythmic pattern of conducted and dropped beats.
The pattern exhibits a sequence: dropped → conducted → dropped → conducted, indicative of a 2:1 AV block.
Cannot distinguish whether it is 2nd degree type 1 or type 2; hence, classified solely as 2:1 AV block.
A higher frequency of dropped beats, such as 3:1 or 4:1, is referred to as high-grade AV block.

ECG Manifestation

Shows that every alternate heartbeat is nonconducted, highlighting the rhythm disruption.

Site of Block

The blockage occurs at the AV node.
In conducted beats, there is a prolonged PR interval with a narrow QRS complex.
Administration of atropine or physical exercise can improve the block, potentially reducing it from 2:1 to 3:2.
This improvement may also reveal any progressive prolongation of the PR interval.

His-Purkinje System

The PR interval remains fixed, despite variations in the RP interval, indicating reliable conduction through this system.

Junctional Escape Rhythm

Characterized by the absence of P waves, indicating the rhythm originates from the junctional area of the heart.
QRS complexes are narrow, measuring less than 0.12 seconds, and appear regular.
P waves do not precede the narrow QRS complexes, distinguishing it from normal sinus rhythms.

Pauses in Cardiac Rhythm

A pause following a P wave suggests the presence of an AV block.
If a pause occurs after a P wave and is consistent with other rhythms, it may indicate:
- First-degree AV block
- Second-degree AV block type 2, if the pause is consistent with PP intervals.
A pause after a P wave characterized by a shorter interval could indicate a second-degree type 1 AV block (Wenckebach).
A pause after a QRS complex that is a multiple of the PP intervals indicates second-degree type 2 exit block.
If the pause after a QRS is not a multiple of the PP intervals, it may represent a sinus pause or sinus arrest.

Bradycardias

Bradycardia refers to a slower-than-normal heart rate, generally considered to be less than 60 beats per minute.
Assessment of heart rate (HR) is essential for diagnosing different types of bradycardias.

Cardiac Conduction System

SA Node: Located at the junction of right atrium (RA) and superior vena cava (SVC), it functions as the heart's primary pacemaker, generating impulses at a rhythm of 60-100 bpm.
AV Node: Situated in the posterior wall of RA, behind the tricuspid valve, and functions to delay atrial impulses to the ventricles at a rate of 40-60 bpm; acts as a gateway and protects against rapid heart rates.
Bundle of His and Bundle Branches: The Bundle of His branches into left and right branches (20-40 bpm), supplying impulses to ventricles.
Purkinje Fibers: Penetrate the inner third of the endocardium, facilitating rapid conduction throughout the ventricular myocardium.

Action Potential Phases

SA Node Action Potential:
- Phase 4: Depolarization initiated by sodium influx (funny current).
- Phase 0: Rapid depolarization due to calcium entry.
- Phase 3: Repolarization through potassium exit.
Contractile Myocardium Action Potential:
- Phase 4: Potassium exit via rectifier channels.
- Phase 0: Sodium influx triggers depolarization.
- Phase 1: Potassium exit equals calcium entry.
- Phase 2: Plateau phase with sustained calcium entry.
- Phase 3: Repolarization occurs via potassium exit.

ECG Insights

PR Interval: Duration of 0.12-0.20 seconds, indicates the time taken for depolarization from the SA node to the ventricles.
QRS Interval: Ranges from 0.10-0.11 seconds, marking ventricular depolarization.
RR Interval: Calculated for heart rate (60 divided by RR interval in seconds or 1500 divided by RR in milliseconds).

Device Therapy

Permanent Pacemaker: Indicated for patients with bradycardia.
Implantable Cardioverter Defibrillator (ICD): Treats ventricular tachycardia and fibrillation, delivering shocks to restore normal rhythm.
Cardiac Resynchronization Therapy: Involves three leads to synchronize heart contractions.

Bradyarrhythmias

Sinus Node Dysfunction: Includes symptomatic sinus bradycardia and sinus pauses.
Atrio-Ventricular Conduction Abnormalities (AV Block):
- First-degree: Prolonged PR interval (>0.20s).
- Second-degree (Type 1): Progressive PR prolongation, followed by a dropped beat (Wenckebach).
- Second-degree (Type 2): Constant PR interval with sudden dropped beats.
- Third-degree: Complete block, P waves not conducted to atria, indistinguishable from sinus arrest on ECG.

Diagnostic Approaches

ECG and Holter Monitoring: For continuous rhythm assessment and correlation of symptoms to arrhythmias.
Ambulatory Event Recorders: Used for infrequent symptoms; patient-activated.
Loop Recorders: Monitors arrhythmias for up to two years.
Exercise ECG and Cardiac Imaging: Identifies ischemia and assesses structural heart issues.

Pharmacological Treatment

Vaughan Williams Classification:
- Class I: Sodium channel blockers; Ia (quinidine), Ib (lignocaine), Ic (flecainide).
- Class II: Beta-blockers (atenolol, sotalol).
- Class III: Potassium channel blockers, prolonging action potential (amiodarone).
- Class IV: Calcium channel blockers impair impulse propagation (verapamil).

Key Syndromes

Tachycardia-Bradycardia Syndrome: Alternating episodes of tachycardia and bradycardia.
Chronotropic Incompetence: Inability to achieve a heart rate of 75-80% of age-predicted maximum during exertion, measured via stress test.

Carotid Sinus Reflex

Carotid Sinus Hypersensitivity: Can cause syncope in patients with tight collars; indicates possible sinus node dysfunction if prolonged pause (>3s) occurs during carotid massage.

Overview of Blocks and Escape Rhythms

First-degree AV Block: Prolonged PR interval; usually unnoticeable on surface ECG.
Second-degree AV Block: Characterized by patterns of dropped beats, seen in Wenckebach (Type 1) and more constant (Type 2).
Junctional Escape Rhythm: Characterized by no P waves; regular narrow QRS complexes.

Pauses

Differentiating block types based on pause patterns following P waves or QRS complexes aids in identifying the type of AV block present.

Acute Treatment

Monitor patients who are asymptomatic and stable without immediate intervention.
Atropine
- Class: Parasympatholytic drug, used to increase heart rate (HR).
- Administration: Initial dose of 1 mg IV bolus; repeat every 3-5 minutes.
- Maximum allowable dose is 3 mg.
- If ineffective, consider transcutaneous pacing or IV Epinephrine infusion.
Epinephrine IV Infusion
- Class: Sympathomimetic agent, utilized to elevate heart rate.
- Dosage: Administer at a rate of 2-10 mcg/min, adjusting based on patient response.
Dopamine IV Infusion
- Dosage: Given at 5-20 mcg/kg/min, while monitoring and titrating according to patient response.
- If no cardiovascular response occurs, proceed with transvenous pacing.
In case of patient non-responsiveness, options include transvenous pacing or temporary pacemaker placement.
Transvenous pacing involves positioning a wire in the right ventricle (RV) to deliver electrical impulses, aiming for a pacing rate of at least 60 beats per minute. Expert consultation is essential.

Pacemakers

Long-Term Management
- Implemented as a definitive management strategy for conditions lacking reversible causes, including myocarditis, infections, and acute heart attacks.

Dosing/Details

Atropine IV Dose
- Initial: 1 mg bolus; permissible repetition every 3-5 minutes.
- Maximum: Not to exceed 3 mg total.
Epinephrine IV Infusion
- Dosage range: 2-10 mcg per minute, tailored to patient response.
Dopamine IV Infusion
- Dosage range: 5-20 mcg/kg per minute, also adjusted according to patient response.

Clinical Assessment of Bradycardia

Bradycardia is defined as a heart rate lower than 50 beats per minute.
Assess for any associated clinical conditions to evaluate severity.

Initial Management Steps

Ensure a patent airway and provide assistance with breathing if necessary.
Utilize cardiac monitoring to identify the heart rhythm accurately.
Administer oxygen to patients exhibiting hypoxemia to improve oxygen saturation levels.
Continuously monitor blood pressure and oximetry for timely interventions.
Establish intravenous access for potential medication administration.
Perform a 12-lead ECG to assess cardiac activity if resources permit.

Signs of Complications

Evaluate for hypotension, which indicates decreased blood flow and pressure.
Look for signs of shock, including altered consciousness or perfusion issues.
Check for acutely altered mental status, which may suggest hypoperfusion to the brain.
Assess for chest discomfort, which could indicate ischemic heart disease.
Identify symptoms of acute heart failure, such as severe shortness of breath or edema.

Intervention for Persistent Bradyarrhythmia

If signs of complications are present, administer Atropine as the first-line treatment.
If Atropine is ineffective, consider advanced interventions:
- Transcutaneous pacing to provide external cardiac stimulation.
- Initiate an Epinephrine infusion to support heart rate and contractility.
- Use Dopamine infusion to improve heart rate and blood pressure.

Additional Considerations

Transvenous pacing may be warranted for sustained management if indicated.
Seek expert consultation if the situation is complex or beyond initial treatment options.

Management in Absence of Complications

If the patient does not exhibit signs of significant distress or complications, monitor and observe their condition closely for any changes.

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Description

Explore the intricate functions of the SA node, the heart's primary pacemaker, located at the junction of the right atrium and superior vena cava. This quiz covers the electrical coupling, effects of the sympathetic and parasympathetic nervous systems on heart rate, and the impulse conduction pathways. Test your knowledge on how these aspects contribute to heart physiology.