(Autorhythmicity) Properties of cardiac muscle

السلام عليكم ورحمة الله وبركاته

كيف حالكم يا دكاترة

دي الاسئله المهمه اللي دكتور مجدي قال عليها في المحاضره دي

1- Enumerate cause of base maker potential

2-Explain The mechanism of base maker potential

السؤالين دول اجابتهم واحده بس صيغة السؤال مختلفة

3-Define base maker potential

4- Define Auto rhythmicity

5-Enumerate factors affect Auto rhythmicity

الدكتور قال مش مهمه اوي بس نقرأها عشان وارد انها تيجي

6-Explain the effect sympathetic on the Auto rhythmicity

وممكن يجي السؤال بصيغه تانيه اللي هيا

Explain the mechanism by which sympathetic increase the Auto rhythmicity

في ملحوظه مهمه اوي لازم نعرفها

ان الاشاره اللي طالعه من القلب بتكون Myogenic وليست Neurogenic

بيجي عليها سؤال مهم

Why Cardiac muscle contract without innervation?

Because signal for contraction is Myogenic not Neurogenic

والسلام عليكم ورحمة الله وبركاته

2026

📘 Cardiac Automaticity and Conduction - Complete Exam Notes

🖇 I. Cardiac Conduction System Structure

📌 Components & Function

• Responsible for generating and transmitting electrical signals (impulses)
• Specialized tissue that cannot contract
• Two sole functions:
• • Automaticity: generating the impulse
  • Conductivity: transmitting the impulse
• Impulse transmitted to surrounding muscle dendrites

📌 Anatomical Components

• SA Node (S-node/Sinus Node)
• AV Node (AV-node)
• Bundle of His (Hiss bundle)
• Purkinje System

📌 Signal Pathway

• Originates in S-node
• Travels down to right and left branches
• Descends to the ventricles
• Branches out through Purkinje system
• Each terminal branch innervates a single muscle fiber

🖇 II. Myogenicity of Cardiac Impulse

🚨 Nature of Impulse

• Cardiac impulse is MYOGENIC (muscle-originated) (Exam Point)
• NOT neurogenic (nerve-originated)

📌 Proof of Myogenicity

Experimental Evidence:

• Heart isolated from body and placed in suitable nutrient solution
• All cardiac nerves severed (sympathetic and parasympathetic)
• Heart continues to contract for a period

🟠 Clinical Evidence:

• Heart transplant patients receive denervated hearts (transplanted without nerves)
• Transplanted heart continues to function and beat normally (Exam Point)
• Signal generation ability originates from specialized muscle cells themselves

🖇 III. Pacemaker Centers & Automaticity Rates

📌 Pacemaker Definition

• Anatomical locations that generate cardiac signals
• Arabic term: صانع الخطوة (Maker of the Step)

🚨 Fundamental Principle

• Heart follows the FASTEST center (Exam Point)
• The center with highest inherent impulse generation rate dictates heart rate

📌 Intrinsic Rates (Exam Point)

Pacemaker CenterIntrinsic Rate

SA Node (Sinus Node)

100-110 impulses/minute

AV Node

45-60 impulses/minute

Purkinje System (Ventricles)

25-40 impulses/minute

🖇 IV. Classification of Pacemakers

📌 Hierarchical Classification

Primary Pacemaker:

• SA Node = Normal Pacemaker of the heart (Exam Point)
• Fastest inherent rate (100-110/min)

Secondary Pacemaker:

• AV Node
• Takes over if primary pacemaker fails
• Rate: 45-60/min

Tertiary Pacemaker:

• Purkinje System/Bundle of His (Idioventricular Rhythm)
• Protected backup system
• Rate: 25-40/min
• Main ventricular function is contraction; Purkinje system given inherent pacing ability for protection

🖇 V. Vagal Influence & Ventricular Protection

📌 Vagal Effects

• Vagus (Parasympathetic) nerve decreases heart rate
• Vagal stimulation primarily affects SA and AV nodes (located in atrium)
• Can stop SA/AV nodes from working

🚨 Critical Protection Mechanism

• Ventricle is NOT supplied by vagus (Exam Point)
• Under intense vagal stimulation:
• • SA/AV nodes may stop
  • Tertiary Pacemaker (ventricle) automatically maintains rhythm
  • Slow rate: 30-40 bpm

🟠 Clinical Importance

• Slow ventricular rhythm insufficient for long, active life
• Serves as vital safeguard
• Allows patient survival until medical intervention (e.g., pacemaker implantation)

🖇 VI. Ectopic Foci

📌 Definition & Mechanism

• Pathological area of muscle tissue (atrium or ventricle)
• Causes: smoking, cardiac sclerosis
• Acquires automaticity and generates signals at high rate (e.g., 200/min)
• Abnormal, centralized focus = Ectopic Focus (Exam Point)

🚨 Clinical Consequence

• Heart follows ectopic focus because it fires faster than normal pacemakers
• Overrides normal pacemaker hierarchy

🖇 VII. Role of Cardiac Nerves & Vagal Tone

📌 Nerve Function

• Cardiac nerves (sympathetic and parasympathetic) are NOT responsible for impulse generation (Exam Point)
• Function: Strictly MODIFICATION (تعديل) of existing rate (Exam Point)
• Can accelerate or decelerate impulse rate

📌 Examples

• Strong physical blow (vagal stimulation) → slows or stops heart
• Emotional arousal (sympathetic stimulation) → increases heart rate

🟣 Vagal Tone (Exam Point)

📌 Concept Explanation

• SA Node intrinsic rate: 100-110 bpm
• Normal resting heart rate: approximately 70-75 bpm
• Difference explained by Vagal Tone

📌 Mechanism

• At rest: parasympathetic (vagal) system dominant over sympathetic
• Vagal tone actively reduces SA Node's inherent firing rate
• Example: from 105 bpm down to 70 bpm

🚨 Physiological Significance

• Creates physiological reserve (احتياطي)
• During physical activity or stress:
• • Removing vagal suppression allows heart rate to increase easily and quickly
  • Meets increased demands

🖇 VIII. Mechanism of Automaticity: The Pacemaker Potential

📌 Pacemaker Cell Characteristics

• Pacemaker cells (P-cells) = specialized smooth muscle cells
• Resting Membrane Potential (RMP): -55 mV to -60 mV

🚨 Unique Property

• RMP of pacemaker cells is inherently UNSTEADY (Exam Point)
• Unlike typical nerve/muscle cells that remain quiescent after repolarization
• Automatically change potential toward positive direction without external stimulation

🟣 Pacemaker Potential Definition

📌 Terminology (Exam Point)

• Gradual, spontaneous depolarization during resting phase = Pacemaker Potential
• Also called:
• • Pre-potential
  • Diastolic Potential (occurs during diastole - relaxation and filling phase)
• Type: Graded Potential

📌 Characteristics

• Spontaneously rises from -60 mV toward firing level of -45 mV

🟣 Ionic Mechanism of Pacemaker Potential (Exam Point)

📌 Four Key Ionic Events:

1. Early Part (-60 mV to approximately -50 mV):

🔹 Funny (If) Sodium Channels Opening:

• Also called H-channels
• NOT voltage-gated or chemically-gated (lack gates or operate unusually = "funny")
• Open spontaneously when membrane potential approaches -60 mV
• Allow Sodium (Na+) to flow inward
• Initiates depolarization

🔹 Decreased Potassium Permeability:

• Potassium (K+) permeability decreases progressively as potential nears -60 mV
• K+ efflux (outward flow) reduced
• Positive charge retention inside cell contributes to depolarization

2. Late Part (-50 mV to -45 mV):

🔹 Transient (T-type) Calcium Channels Opening:

• Allow Calcium (Ca²⁺) to flow inward (from outside cell)
• Reduces potential further toward firing level

🟣 Action Potential Phases

📌 When Firing Level (-45 mV) Reached:

Phase 0 - Depolarization:

• Long-lasting (L-type) Calcium Channels open (Exam Point)
• Massive influx of Calcium from outside cell
• Causes rapid depolarization
• Peak potential: approximately +10 mV
• Action potential in SA/AV nodes = Slow Action Potential

Phase 3 - Repolarization:

• L-type Calcium channels close
• Potassium Channels open
• K+ efflux occurs
• Repolarization back toward resting potential of -60 mV

📌 Phase Mapping

• Phase 4 = Pacemaker potential
• Phase 0 = Depolarization
• Phase 3 = Repolarization

🖇 IX. Factors Affecting Automaticity (Chronotropy)

📌 Definitions

• Factors affecting heart rate = Chronotropic Factors
• Positive Chronotropic = increases rate
• Negative Chronotropic = decreases rate

🟣 1. Neural Factors (Exam Point)

FactorEffectNeurotransmitter/ReceptorMechanism

Sympathetic Stimulation

Positive Chronotropic (increases HR)

Norepinephrine / Beta-1 (β₁) Receptors

1. Activates T-type Calcium Channels<br>2. Inhibits (Closes) Potassium Channels<br>Result: Increases slope of pacemaker potential, shortening time to reach firing level

Parasympathetic/Vagal Stimulation

Negative Chronotropic (decreases HR)

Acetylcholine / Muscarinic (M₂) Receptors

1. Inactivates Calcium Channels<br>2. Opens Potassium Channels for longer duration<br>Result: Hyperpolarization (potential drops below -60 mV), flattening slope of pacemaker potential, requiring more time to reach firing level

🟣 2. Thermal Factors

📌 Temperature Effect

• Temperature = positive chronotropic factor

🚨 Rule:

• Increase of 1°C in body temperature = increase of 10-20 beats/minute in heart rate

📌 Mechanism

• Increased temperature increases metabolism of SA Node cells
• Makes SA Node activity faster
• Increases heart rate
• Reverse true for decreased temperature

🟣 3. Mechanical Factors (Distension)

📌 Trigger

• Rapid intravenous fluid infusion
• Causes distension (stretching) of Right Atrium
• Distension increases heart rate

📌 Proposed Mechanisms:

1. Bainbridge Reflex (Reflexive):

• Distension stimulates atrial stretch receptors in Right Atrium
• Receptors send signals via afferent fibers to CNS (Vaso-motor center in brain)
• CNS sends efferent signals to increase heart rate

2. Stretching Effect (Mechanical):

• Distension directly stretches SA Node tissue
• Stretching increases rate of impulse generation

🟣 4. Chemical Factors (Ions & Hormones)

📌 Hormones

Adrenaline/Noradrenaline:

• Increase heart rate
• Work directly on β₁ receptors

Thyroxine (Thyroid Hormone):

• Increases heart rate by direct effects
• Increases SA Node activity

📌 Electrolytes (Exam Point)

Hyperkalaemia (High K+) & Hypercalcaemia (High Ca²⁺):

• Both cause activation of Potassium Channels
• Increased K+ efflux
• Leads to Hyperpolarization
• Negative Chronotropic effect

Hypokalaemia (Low K+) & Hypocalcaemia (Low Ca²⁺):

• Both cause inactivation (closing) of Potassium Channels
• Decreased K+ efflux
• Leads to Depolarization
• Positive Chronotropic effect

Hypernatraemia (High Na+) or Hyponatraemia (Low Na+):

• Both decrease automaticity
• Mechanism for this specific effect is unknown

📌 pH Changes

Acidosis:

• Decreases automaticity
• Mechanism: Acidosis causes Hypercalcaemia (increasing available Ca²⁺) → K+ channel activation → hyperpolarization

Alkalosis:

• Increases automaticity
• Mechanism: Alkalosis causes Hypocalcaemia (decreasing available Ca²⁺) → K+ channel inactivation → depolarization

🟣 5. Drug Factors

📌 Digitalis (Digoxin) (Exam Point)

Clinical Use:

• Treats heart patients with weakened contraction

🟠 Clinical Goal:

• Achieve strong, slower contraction

📌 Two Effects:

1. Direct depressive effect on Pacemaker cells
2. Vagal effect (potentiating vagus nerve) on pacemaker tissue

📌 Result:

• Heart rate decreases (e.g., from 80-90 bpm to 60 bpm)
• Improves ventricular filling
• Improves cardiac efficiency

📌 Propranolol

• Used for patients with rapid heart rates (tachycardia)
• Anti-arrhythmic drug

📌 Diphtheria

• Exception among febrile diseases
• Most febrile diseases cause tachycardia
• Diphtheria toxins depress SA Node
• Causes bradycardia (slow heart rate) despite high fever

📌 Hypothyroidism & Jaundice (Icterus)

• Both associated with slow heart rate

📝 Summary Table: Chronotropic Factors

FactorEffect on HRClassification

Sympathetic stimulation

Increases

Positive Chronotropic

Parasympathetic/Vagal stimulation

Decreases

Negative Chronotropic

Increased temperature

Increases

Positive Chronotropic

Adrenaline/Noradrenaline

Increases

Positive Chronotropic

Thyroxine

Increases

Positive Chronotropic

Hypokalaemia/Hypocalcaemia

Increases

Positive Chronotropic

Alkalosis

Increases

Positive Chronotropic

Hyperkalaemia/Hypercalcaemia

Decreases

Negative Chronotropic

Acidosis

Decreases

Negative Chronotropic

Hypernatraemia/Hyponatraemia

Decreases

Negative Chronotropic

Digitalis

Decreases

Negative Chronotropic

Diphtheria toxins

Decreases

Negative Chronotropic

Hypothyroidism/Jaundice

Decreases

Negative Chronotropic