Conduction Abnormalities Notes

CONDUCTION ABNORMALITIES

BASIC PRINCIPLES

• Graphical Representation: Used specially ruled paper to represent the heart's electrical impulses when documenting cardiac activity. The graphical representation allows for the precise measurement of electrical activity over time, aiding in diagnoses.

• Myocardium Functions:

  • Typical Myocytes (cells/myocytes): These cells respond to electrical stimuli, allowing them to contract and pump blood effectively throughout the body. Myocytes play a crucial role in maintaining cardiac output during physical activities and at rest.

  • Nodal Cells: These cells, found in the sinoatrial (SA) and atrioventricular (AV) nodes, have a high rhythmicity rate, generating electrical impulses to initiate heartbeats. However, they have slow conduction rates, which is critical for the timing of atrial contraction before ventricular contraction.

  • Transitional Cells: Located between the nodal and Purkinje cells, these cells conduct electrical impulses twice as fast as nodal cells, facilitating a more rapid spread of electrical signals through the heart muscle.

  • Purkinje Fibers: These fibers have a low rhythmicity rate but a high conduction rate, allowing the electrical impulse to be rapidly distributed throughout the ventricles, enabling coordinated contraction during systole.

ELECTRICAL STIMULATION

• Ion Permeability: Electrical stimulation leads to increased permeability of the cell membrane to ion flow. Changes in permeability are crucial for the propagation of action potentials in myocardial cells.

• Resting State: Characterized by potassium ions moving into the cell while sodium ions move out (PISO), maintaining a negative resting membrane potential. This resting state is essential for the myocardial cells to be ready for the next electrical stimulus.

  • Depolarization: When the cardiac muscle is stimulated, sodium ions flow inward through fast sodium channels, while potassium ions flow outward slowly. This results in a positive charge inside the cell, leading to muscle contraction and effectively pumping blood.

  • Repolarization: Following contraction, sodium exits the cell while potassium re-enters, returning the membrane potential to a negative state. This phase is crucial for muscle relaxation and preparing the heart for the next contraction.

• Electrocardiogram (ECG): An ECG records the wave of depolarization toward a positive electrode placed on the skin, providing valuable insight into the heart's electrical activity over time.

CARDIAC MUSCLE PROPERTIES

• Automaticity: Myocardial cells have the ability to independently generate electrical impulses, allowing the heart to maintain a regular rhythm without external stimulation.

• Rhythmicity: This refers to the regular pacemaking activity of the SA node, which sets the pace for the heart's rhythm.

• Conductivity: Myocardial cells can rapidly spread electrical impulses to adjoining cells, ensuring synchronized contraction across the heart muscle.

• Autonomic Nervous System Influences:

  • Sympathetic: This branch of the autonomic nervous system has an excitatory effect, increasing heart rate (HR), contractility, and conduction velocity through the release of norepinephrine, thereby preparing the body for physical exertion.

  • Parasympathetic: In contrast, this branch is inhibitory, reducing heart rate and automaticity while slowing conduction velocity through acetylcholine released via the vagus nerve. This influence is significant during rest and digestion, promoting relaxation of the heart.

CONDUCTION SYSTEM

• Pathway of Electrical Activity: The sequence of activation for electrical impulses in the heart follows this pathway:

  1. SA Node (Right Atrium) - initiates each heartbeat.

  2. LA via Bachmann Bundle (Internodal Tract) - connects to the left atrium, ensuring time for atrial contraction.

  3. AV Node (Junctional Node) - delays the impulse to allow for ventricular filling.

  4. His Bundle - transmits the impulse from the AV node to the ventricles.

  5. Bundle Branches (Right & Left) - divide the conduction path for rapid ventricular activation.

  6. Purkinje Fibers - spread the impulse throughout the ventricles for synchronized contraction.

• Waveforms in ECG:

  • P Wave: Represents atrial depolarization (contraction), typically seen before each QRS complex.

  • PR Interval: Indicates the time between atrial contraction and ventricular contraction. Normal is 0.12 - 0.20 sec.

  • QRS Complex: Indicates ventricular depolarization (contraction), with a duration of 0.06 - 0.10 sec.

  • ST Segment: Marks the beginning of repolarization after ventricular contraction, important for identifying ischemic events.

  • T Wave: Represents the completion of ventricular repolarization, indicating recovery of the myocardial cells.

ECG RECORDING

• Graph Paper Specs: Electrocardiograms are recorded on graph paper where each 1 mm division (square) denotes electrical activity. The paper is specifically scaled to measure voltage and time effectively. This precision is critical in diagnosing cardiac conditions.

  • Height/Depth = 0.1 mV/mm.

  • Time: Small squares = 0.04 sec; Large squares = 0.2 sec; Speed = 25 mm/sec.

• Standard 12 Lead ECG: A comprehensive assessment of cardiac activity is achieved through a standard 12-lead ECG, which includes:

  • Limb Leads: I, II, III, aVR, aVL, aVF (representing the frontal plane of the heart).

  • Chest Leads: V1 to V6 (representing the horizontal plane of the heart). V1 and V2 assess the right heart, V5 and V6 assess the left heart, while V3 and V4 focus on the ventricular septum.

• Key Elements to Assess:

  • Heart rate, heart rhythm, signs of hypertrophy, and indicators of ischemia/infarction, all of which are essential for evaluating overall cardiac health.

HEART RATE MEASUREMENT

• 6-Second Tracing Method: Count the number of specific R waves in a 6-second segment and multiply by 10 to estimate heart rate (HR/min). This method is useful for quick assessments.

• Large Box Method: Count the number of large boxes between successive R waves, with the formula 300 divided by the number of large boxes equating to heart rate per minute. This is another quick calculation method used in clinical settings.

NORMAL WAVE FORMS

• P Wave Characteristics: Normal P waves are rounded, symmetric, and upright, with each P wave preceding every QRS complex. This represents proper atrial activation.

• PR Interval: A normal PR interval ranges from 0.12 to 0.20 sec, reflecting appropriate conduction from the atria to the ventricles.

• QRS Complexes: Should be identical in appearance, with normal duration between 0.06 and 0.10 sec, indicative of efficient ventricular depolarization.

• QT Interval: Normal duration ranges between 0.32 and 0.40 sec and encompasses both depolarization and repolarization of the ventricles.

• Heart Rate: Defined normal range is 60-100 beats per minute (bpm), essential for assessing cardiac function.

ABNORMAL ECG PATTERNS

SINUS BRADYCARDIA

• Characterized by a heart rate <60 bpm and may be normal in trained athletes due to increased vagal tone. It is usually asymptomatic but can be associated with fatigue or dizziness in others, sometimes requiring no treatment or addressing the underlying cause.

SINUS TACHYCARDIA

• Defined by a rate >100 bpm, commonly benign and often a response to sympathetic nervous stimulation (stress, exercise). Management focuses on identifying and treating underlying causes, such as dehydration or anxiety.

PREMATURE ATRIAL COMPLEXES (PACs)

• These are early beats originating from ectopic foci in either atria, marked by a distinct early P wave. Management is typically based on hemodynamic stability, as isolated PACs may require no treatment, whereas frequent PACs may indicate underlying issues.

ATRIAL TACHYCARDIA

• Identified by 3 or more PACs at a heart rate of 100-200 bpm; this rhythm can be benign or symptomatic, warranting evaluation. Management often involves addressing the underlying cause and possibly rate control through medications.

ATRIAL FLUTTER

• Rapid atrial depolarization occurring at rates of 250-350 bpm, with P waves appearing as flutter waves. Management usually includes rate control through medications, such as digoxin or beta-blockers, and consideration for rhythm restoration.

ATRIAL FIBRILLATION

• Marked by erratic quivering from multiple ectopic foci, resulting in absence of detectable P waves and an irregular rhythm. It indicates a risk of emboli; treatment strategies typically include anticoagulation therapy and controlling heart rate or rhythm through various medications or procedural interventions.

AV BLOCKS

• 1st Degree AV Block: Identified by a prolonged PR interval (>0.20 sec), usually benign without symptoms.

• 2nd Degree Type I (Wenckebach): Characterized by progressive PR interval lengthening leading to a dropped QRS complex, often benign but requires monitoring.

• 2nd Degree Type II (MOBITZ II): Demonstrates non-conducive impulses with a consistent PR interval, which may necessitate the implantation of a pacemaker.

• 3rd Degree AV Block: Represents complete block where there is no impulse transmission from the atria to the ventricles; this condition requires immediate medical attention or pacing intervention.

VENTRICULAR ARRHYTHMIAS

• Premature Ventricular Complexes (PVCs): Characterized by wide, bizarre QRS complexes without a preceding P wave, often felt as palpitations, and require further evaluation depending on frequency and symptoms.

• Ventricular Tachycardia (Vtach): Defined by 3 or more PVCs occurring in succession; the condition can be sustained (emergency) or nonsustained (less severe). Treatment generally includes antiarrhythmic medication, with sustained Vtach requiring urgent intervention.

• Ventricular Fibrillation (Vfib): This erratic pattern results in loss of mechanical contractility, requiring immediate defibrillation to restore normal rhythm, as it can lead to sudden cardiac death.

• Torsades de Pointes: Recognized by rapidly twisting QRS complexes, this is a medical emergency often triggered by electrolyte imbalances (e.g., hypomagnesemia) necessitating cardioversion and addressing underlying causes.

MYOCARDIAL INFARCTION INDICATORS

• Zone of Infarction: Pathological Q waves can be observed, indicating past myocardial damage.

• Zone of Injury: A depressed ST segment on the ECG reflects myocardial injury due to ischemia, indicating an acute process that may require further intervention.

• Zone of Ischemia: T-wave inversions can suggest areas of decreased blood flow, and prompt assessment and treatment to prevent further cardiac injury are necessary.