Week 4 - Conduction Disorders - Chapter 22

Patho review of how the blood flows^

Blood enters heart from:

• superior vena cava & inferior vena cava

Electrical conduction of the heart^

• Sinoatrial Node (SA node)

  • is the yellow bulb like gland on the left side of the picture above

• when atrials contract they contract together

• when ventricles contract, they contract together

• depolarization = atrias have contracted (squeezed together) —> they are ejecting blood into ventricles

• Bundle of his branches into Purkinje fibers in right & left ventricles, which ensures a synchronized contraction of the ventricles, allowing for effective pumping of blood to the lungs and the rest of the body.

• SA node → AV node → bundle of his → Purkinje Fibers (in left & right ventricles) → ventricles contract (depolarization) → repolarization of ventricles

The Electrocardiogram:

• Electrocardiography (ECG or EKG)

  • Records the electrical impulse that travels through the heart known as electrocardiogram (ECG)

  • putting leads/wires on patient chest to track electrical conductions of the heart

• Each phase of the cardiac cycle is represented by specific waveforms

  • P wave

  • QRS Complex

  • T wave

• These waveforms can be visualized via:

  • A cardiac monitor screen

  • A strip of ECG graph paper

ECG Monitoring Systems:

• Electrodes are attached to cable wires connected to one of the following devices:

• Standard 12-Lead ECG Machine

  • Placed at the patient’s bedside for an immediate recording

• Hardwire Cardiac Monitor

  • Provides continuous monitoring at the bedside

• Telemetry Monitor

  • Small portable transmitter, sends ECG data by radio waves to a central monitoring station

• Continuous ECG Monitoring (Holter or Patch Monitor)

  • Small wearable device that records ECG continuously

• Intermittent Monitoring (Loop Recorder)

  • Small implanted or external device that records ECG activity when the patient experiences symptoms

^This is the best patient position for the best ECG/EKG reading

• 5 blue squares make 1 big green square (as shown in picture above)

• you will receive 30 square strips (6 second long strips)

• know how to count calculate P waves, QRS waves, T waves

• know how to count the boxes

• the amount of PQRST waves is the heart rate, which can be determined by analyzing the waveform patterns from the ECG strips.

• WILL BE ON QUIZ^

Normal Sinus Rhythm (NSR):

• Electrical conduction begins in the SA node, generating a sinus rhythm

  • Characteristics of NSR

    • Rate (Atrial & Ventricular): 60–100 bpm (adult)

      • IF NOT 60-100 IT IS NOT NORMAL SINUS RHYTHM (NSR)

    • Rhythm: Regular

    • QRS Complex: Usually normal shape and duration

    • P Wave: Normal, consistent shape; precedes each QRS

      • P wave MUST come before QRS or else = non sinus rhythm

    • P:QRS Ratio: 1:1

• Clinical Significance

  • Indicates good cardiovascular health

• Rise in resting heart rate ≥10 bpm increases risk of:

  • Sudden cardiac death

  • Atrial fibrillation

  • Heart failure

  • Coronary artery disease

  • Stroke

  • Cardiovascular disease

Electrocardiogram:

• P wave

  • Electrical impulse from SA Node

  • Atrial depolarization

  • 0.11 seconds or less

• P-R interval

  • Time needed from SA node stimulation → period before ventricular depolarization (contraction)

  • 0.12 – 0.2 seconds

• QRS Complex

  • Ventricular depolarization

  • 0.12 seconds

• ST Segment

  • Ventricular repolarization

• T wave

  • Ventricular repolarization

• QT Interval

  • Measures total time for ventricular depolarization and repolarization

  • 0.32 seconds – 0.40 seconds

• each peak is a cycle so you see 6 QRS complex (peaks) which means 6 cycles

• 6 beats within 6 seconds

• 6 seconds x 10 = 60 seconds

• 6 beats x 10 = 60 beats

• MEANING: 60 beats per minute (60 bpm)

Sinus Bradycardia:

• Bradycardia

  • Slowed heart rhythm < 60 bpm

  • Originates from the SA node

  • All other sinus rhythm features are normal

• ECG Features:

  • Rate: < 60 bpm

  • Rhythm: Regular

  • P wave: Normal, before every QRS

  • PR interval: 0.12–0.20 sec

  • QRS: Usually normal

• Causes:

  • Low metabolic needs: sleep, athletic training, hypothyroidism

  • Vagal stimulation: vomiting, suctioning, severe pain

  • Medications: beta-blockers, calcium channel blockers, amiodarone

  • Cardiac: coronary artery disease, inferior MI, sinus node dysfunction

  • Other: increased ICP, hypoxemia, acute heart failure, delirium

REGULAR PATTERN, same consistent pattern but going slow^

Management of Sinus Bradycardia:

• Management:

  • Dependent on cause

    • Asymptomatic: monitor & treat underlying cause

    • Symptomatic/unstable:

      • Alteration in mental status, chest discomfort, hypotension

      • Treatment: Atropine, pacemaker, address underlying cause

  • Avoid vagal stimulation and medications that slow HR

Sinus Tachycardia:

• Sinus tachycardia occurs when the SA node fires faster than normal, leading to a heart rate >100 bpm in adults (usually <120 bpm).

  • It is essentially normal sinus rhythm but faster, and it is nonparoxysmal (does not start or stop suddenly)

• Common Causes

  • Physiologic or psychological stress

    • Examples: blood loss, anemia, shock, heart failure, pain, fever, exercise, anxiety

    • Any condition increasing sympathetic activity or metabolic demand

  • Medications and stimulants

    • Sympathomimetic drugs: catecholamines, aminophylline, atropine

    • Stimulants: caffeine, nicotine

    • Illicit drugs: amphetamines, cocaine, ecstasy

  • Enhanced SA node automaticity or excessive sympathetic tone

    • Called inappropriate sinus tachycardia (heart rate high without clear physiologic need)

  • Autonomic dysfunction

    • Example: Postural Orthostatic Tachycardia Syndrome (POTS)

    • Characterized by: rapid heart rate without hypotension, palpitations, lightheadedness, weakness, blurred vision upon standing

Management of Sinus Tachycardia:

Goal: Identify and treat underlying cause; relieve symptoms.

• 1. Vagal Maneuvers / Non-Drug Interventions

  • Carotid sinus massage

    • massage someone carotid artery

    • IF NOT IN SINUS RHYTHM they will pass out

  • Gagging

  • Bearing down against a closed glottis (Valsalva maneuver)

  • Forceful, sustained coughing

  • Cold stimulus to the face (ice-cold wet towel)

  • Adenosine IV to interrupt tachycardia

• 2. Hemodynamically Unstable Patients

  • Signs: altered mental status, chest discomfort, hypotension

  • Synchronized cardioversion (electrical current timed with QRS)

    • if patient is unstable do cardioversion (the charge & clear defibrillators)

    • stable patients give some medications

  • Used if vagal maneuvers or adenosine fail

• 3. Hemodynamically Stable Patients

  • IV Beta-blockers (Class II antiarrhythmic)

  • IV Calcium channel blockers (Class IV antiarrhythmic)

  • Cardioversion if medications fail or are contraindicated

• 4. Persistent / Inappropriate Sinus Tachycardia

  • SA node catheter ablation if unresponsive to other treatments

  • means none of the medications or treatments are working so, ablation of SA node

• 5. POTS (Postural Orthostatic Tachycardia Syndrome)

  • Tachycardia without hypotension; presyncopal symptoms on standing

  • Treatment targets underlying cause:

    • Hypovolemia → increase fluids and sodium, or use salt tablets

    • Combination of approaches as needed

Summary: Stepwise management → Vagal maneuvers → Medications → Cardioversion → Ablation

Atrial Fibrillation:

• Atrial Fibrillation (AFib)

  • Prevalence & Public Health Impact

  • 2.7–6.1 million Americans have AFib (CDC, 2017)

  • Strongly associated with aging, making it a growing concern in older adults

• Pathophysiology

  • Abnormal impulse formation in atrial tissue → rapid, disorganized, uncoordinated atrial twitching

  • Structural or electrophysiologic changes in atria trigger arrhythmia

    • structural issues or ions are off (electrophysiologic)

  • Central nervous system (brain & spinal cord) and Cardiac Autonomic Nervous System (CANS) both contribute

  • CANS: network of autonomic ganglia within epicardium, atrial myocardium, and pulmonary veins

    • Hyperactive ganglia → impulses from pulmonary veins → AV node

  • Ventricular response depends on:

    • AV node conduction

    • Accessory pathways

    • Medications

Atrial Fibrillation: Classification of AFib

• Paroxysmal: sudden onset, terminates spontaneously

  • have patient have a heart monitor for 24-48 hrs; ask what symptoms they experienced

• Persistent: sustained, requires intervention to terminate

  • will not resolve spontaneously; patient will need something done to fix this such as medication adjustment, electrical cardioversion, or in some cases, catheter ablation or repair the valve (like incase there is a leaky valve)

• Permanent: continuous, resistant to intervention

  • not going anywhere, heart constantly in A-fib

  • heart may be resistance to treatments (pts live with chronic A-fib)

• Nonvalvular: absence of moderate-severe mitral stenosis, absence of mechanical valve

Complications:

• blood stasis:

  • ineffective atrial contraction causes blood to pool

  • stagnant blood eventually forms clots (thrombi)

• risk of emboli

  • if a clot dislodges, it can travel through blood stream and cause a stroke such as pulmonary emboli, emboli in other organs

• AFib is a common arrhythmia in adults, especially the elderly

• Results in ineffective atrial contraction → risk of stroke, heart failure, and other complications

• Ventricular rate and symptoms vary depending on AV conduction and treatment

A-fib & Coagulation:

• Atrial quivering:

  • Atria twitch or fibrillate instead of contracting efficiently

  • Blood stasis:

    • Ineffective atrial contraction causes blood to pool

    • Stagnant blood eventually forms clots (thrombi)

    • not good filling into heart so blood is stagnant and leading to possible clots

      • take blood thinners (aka anticoagulants) to combat blood clots (THIS IS THE MED YOU USE TO TREAT A-FIB)

        • LIFE-LONG TREATMENT

  • Risk of embolism:

    • If a clot dislodges, it can travel through the bloodstream →

    • Leading to stroke (most common), pulmonary emboli, emboli in other organs

    • Treatment: Patients often take anticoagulants (e.g., warfarin, apixaban) to prevent clot formation

Atrial Fibrillation – EKG Characteristics:

• Rate

  • Atrial rate: 300–600 bpm

  • Ventricular rate: 120–200 bpm

• Rhythm

  • Highly irregular

• QRS Complex

  • Typically normal

  • May be abnormal if conduction changes are present

• P Wave

  • Absent

  • Replaced by fibrillatory (f) waves

  • Irregular, varying in amplitude and shape

• PR Interval

  • Cannot be measured

• P:QRS Ratio

  • Many atrial impulses per ventricular response, not 1:1

• the 1st to 2nd box on strip is known as F wave, which represents the atrial activity and is a key indicator in diagnosing conduction disorders. It demonstrates the presence of multiple atrial impulses failing to conduct through the ventricular system.

Fibrillatory “f wave” pattern

▪ “p waves” are indistinguishable, atrial rate is indeterminate

▪ There are 10 “R” peaks x 10 = 100 Ventricular Rate

Medical Management of Atrial Fibrillation (AFib):

• Goal:

  • Prevent embolic events (e.g., stroke)

  • Control ventricular rate

  • Restore sinus rhythm when appropriate

• 1. Factors Influencing Treatment

  • Cause, pattern, and duration of AFib

  • Ventricular response rate

    • what’re the ventricles doing

  • Presence of structural or valvular heart disease

  • Coexisting cardiac conditions (e.g., coronary artery disease, heart failure)

  • Patient-provider shared decision-making

• 2. Management Approaches

  • Rate control: Use antiarrhythmic medications to control ventricular response

  • Rhythm control: Attempt to convert to sinus rhythm (cardioversion)

  • Observation: Some AFib converts spontaneously within 24–48 hours

  • Permanent AFib: When patient and provider decide not to attempt sinus rhythm restoration

• 3. Pharmacologic Therapy

  • A. Antithrombotic Medications

    • Reduce risk of stroke and embolic events

    • Include anticoagulants and antiplatelet drugs

      • difference is they work on different clotting factors

    • Indicated for most patients with nonvalvular AFib

    • Risk assessment: Use CHA₂DS₂-VASc score to guide therapy

  • B. Antiarrhythmic Agents

    • Control ventricular rate

    • Facilitate conversion to sinus rhythm if appropriate

      • can cardiovert a patient and be on antiarrhythmics

• 4. Catheter Ablation

  • destruction of specific cells that are causing the tachyarrhythmia (fibrillation)

• 5. Electrical Cardioversion

  • medical treatments that uses quick, low energy shocks to restore a regular heart rhythm

  • indications

    • hemodynamically unstable AF patients

      • ex: acute mental status changes, chest discomfort, hypotension

    • medication-refractory Afib

      • meds used to work for Afib but are no longer working

  • Antiarrhythmic drugs may be given before cardioversion to increase the success rate and maintain sinus rhythm

    • most common antiarrhythmics:

      • flecainide

      • propafenone

      • amiodarone

      • dofetilide

      • sotalol

______________________________________________________________

Electrical Cardioversion for Atrial Fibrillation:

• Indications:

  • Hemodynamically unstable AF patients

  • Examples: acute mental status changes, chest discomfort, hypotension

  • Most effective when combined with antiarrhythmic therapy if appropriate

  • Medication-refractory Afib

• Pre-treatment (Optional):

  • Antiarrhythmic drugs may be given before cardioversion to:

  • Increase the success rate

  • Maintain sinus rhythm

• Common Antiarrhythmics Used:

  • Flecainide, Propafenone, Amiodarone, Dofetilide, Sotalol

Atrial Flutter:

• Atrial Flutter

  • Caused by a conduction defect in the atrium

  • Rapid, regular atrial impulses at 250–400 bpm

  • AV node can blocks some impulses to prevent ventricular rates from reaching atrial rates

    • Protects against life-threatening ventricular fibrillation

Atrial Flutter – ECG Characteristics:

Rate

• Atrial rate: 250–400 bpm

• Ventricular rate: Usually 75–150 bpm

Rhythm

▪ Atrial rhythm: Regular

▪ Ventricular rhythm: Usually regular, may be irregular if AV conduction varies

QRS Complex

• Usually normal

• May be abnormal or absent

P Wave

• Saw-toothed shape, called F waves PR Interval

• Difficult to measure due to multiple F waves

P:QRS Ratio

• Commonly 2:1, 3:1, or 4:1

Look for the atrial “saw-tooth” pattern

▪ There are 27 “p waves” x 10 = 270 Atrial Rate

▪ There are 7 “R” peaks x 10 = 70 Ventricular Rate

Medical Management of Atrial Flutter:

Symptoms:

• Chest pain

• Shortness of breath

• Hypotension

Acute Management:

• Vagal maneuvers

  • increase parasympathetic activity to slow AV node conduction

  • massage the patients carotid or have patient bear down

• Adenosine (IV):

  • Slows AV node conduction → may terminate tachycardia or reveal flutter waves for diagnosis

  • Rapid IV push followed by 20 mL saline flush

  • Elevate arm to promote rapid circulation

Ongoing Management:

• Antithrombotic therapy

• Rate control - beta-blockers, calcium channel blockers

• Rhythm control - antiarrhythmics

• Electrical Cardioversion:

  • Often successful in converting atrial flutter to sinus rhythm

Vagal maneuvers:

• Physical actions that stimulate the vagus nerve

  • Goal: temporarily slows conduction through the atrioventricular (AV) node in conditions such sinus tachycardia, atrial flutter, or AV nodal reentrant tachycardia (AVNRT)

carotid massage is only on one side to prevent potential complications such as carotid artery dissection or ischemic stroke.