(Contractility) Properties of cardiac muscle

2026

📘 Cardiac Contractility - Complete Exam Notes

🖇 I. Introduction & Context

📌 Lecture Context

• First time teaching first-year class
• Contractility = final cardiac property topic
• Previously covered: Autorhythmicity and Conductivity
• Concern noted: low student attendance

🖇 II. Basic Cardiac Structure & Synchronization

📌 Cardiac Anatomy Components

• Four chambers: 2 Atria + 2 Ventricles
• Aorta
• Pulmonary Artery
• Valves (separating Atria and Ventricles)
• Four pulmonary veins
• Superior and Inferior Vena Cava

🟣 Syncytium Concept

📌 Heart as Syncytium

• Metaphor: "either we all live, or we all die"
• Means: contract together and relax together
• Does NOT apply to all four chambers simultaneously

🚨 Critical Synchronization Pattern

• Two Atria contract together
• Two Ventricles contract together
• Relaxation follows same pattern

🚨 EXAM POINT:

• Four chambers do NOT contract at same time
• If all four contracted simultaneously = FATAL

📌 Normal Heart Rate

• Average: 70-75 beats per minute
• One beat = One Cardiac Cycle (covered in next lecture)

🖇 III. Autorhythmicity & Electrical Dominance

📌 Primary Pacemaker

• Heart requires Primary Pacemaker = SA Node (Sinoatrial Node)

🚨 Reason SA Node is Pacemaker (Exam Point):

• Generates fastest spontaneous action potential (AP)
• The fastest one dictates the pace

🟣 Electrical Dominance Mechanism

📌 SA Node Control

• When SA Node generates electricity, no other center (e.g., AV Node) can interfere
• When SA Node fires → entire heart enters Depolarization

📌 Depolarization Concept

• Fundamental concept used throughout physiology
• Heart muscle enters Absolute Refractory Period

🚨 Absolute Refractory Period Definition:

• Phase where there is absolutely NO response
• Regardless of strength or magnitude of stimulus
• This dominance allows SA Node to control entire heart

🟣 Automaticity/Autorhythmicity

📌 Definition

• Heart's ability to generate own action potentials rhythmically
• Is MYOGENIC (does not depend on nerve supply)

📌 Nerve Supply Role

• Autonomic nerve supply only modulates the rate:
• • Sympathetic innervation → increases Heart Rate
  • Parasympathetic innervation → decreases Heart Rate

📌 Example

• Heart removed from rabbit will continue to beat on its own

🖇 IV. Cardiac Conductivity

📌 Normal Conduction Pathway SA Node → AV Node → AV Bundle (Bundle of His) → Right and Left Bundle Branches → Purkinje Fibers

📌 Purkinje Fibers Function

• Transmit electrical signal to all parts of heart

🚨 Exam Point:

• Frequently asked exam question every year: Types of action potentials in heart
• • Fast Response
  • Slow Response

🖇 V. Contractility (Inotropism)

🟣 Order of Events (Crucial Concept)

🚨 Sequence Rule:

• Electrical response (action potential) must ALWAYS happen FIRST
• Followed by mechanical response (contraction)
• Contraction CANNOT occur without prior electrical stimulation

🟣 Definitions

📌 Contractility Definition

• The cardiac force generated by muscle to perform shortening

📌 During Contraction

• Muscle shortens AND thickens

🟣 Purpose of Cardiac Contraction (Pumping)

📌 Atrial Contraction

• Atria contract to move blood into Ventricles

📌 Ventricular Contraction

• Ventricles contract to pump blood:
• • Left Ventricle → pumps blood to Aorta
  • Right Ventricle → pumps blood to Pulmonary Artery

🟣 Inotropism Terminology

📌 Scientific Term

• Contractility process = Inotropism

📌 Classifications

• Positive Inotropism = Increased contractility
• Negative Inotropism = Decreased contractility

🖇 VI. Mechanism of Excitation-Contraction Coupling (ECC)

📌 Purpose

• Links electrical excitation to mechanical contraction

🟣 Step-by-Step ECC Process

Step 1: Depolarization & T-Tubule

• Wave of depolarization moves along Sarcolemma (cardiac muscle cell membrane)
• Encounters groove called T-Tubule
• Descends down T-Tubule

Step 2: Receptor Activation

• Descending AP encounters specific receptors:
• • Dihydropyridine receptors
  • Ryanodine receptors
• Located near Sarcoplasmic Reticulum (SR)

Step 3: Initial Calcium Release (SR Source)

• AP stimulates SR (which stores calcium)
• SR releases calcium into cytoplasm
• SR-released calcium = Activator Calcium (Exam Point)

Step 4: Insufficiency Recognition

• Amount of Activator Calcium released is INSUFFICIENT to cause full contraction

Step 5: Secondary Calcium Influx (ECF Source)

• Insufficient calcium level stimulates opening of calcium channels on cell membrane
• Allows calcium to enter from Extracellular Fluid (ECF)
• This incoming calcium = Depolarizing Calcium

🚨 Calcium Sources (Exam Point): Cardiac contraction depends on calcium from TWO sources:

1. Sarcoplasmic Reticulum (Activator Calcium, released first)
2. Extracellular Fluid (Depolarizing Calcium)

Step 6: Contraction Trigger

• Total sufficient calcium binds with Troponin C
• Binding leads to formation of Cross Bridges between Actin and Myosin filaments
• Results in muscle shortening (contraction)

🖇 VII. Mechanism of Relaxation

📌 Fundamental Rule

• "The one who summoned the genie must send him away"
• Goal: Return calcium to its original sources

🟣 Relaxation Steps

Step 1: Removal to SR

• Calcium from Sarcoplasmic Reticulum returned back via Active Re-uptake Process
• Requires ATP

Step 2: Removal to ECF

• Calcium that entered from ECF must be ejected back out

Step 3: Sodium-Calcium Exchanger

• Transport protein called Sodium-Calcium Exchanger
• Removes 1 molecule of Calcium outside cell
• In exchange for 3 molecules of Sodium entering cell

Step 4: Handling Internal Sodium

• Influx of Sodium must be corrected immediately (prevents continuous depolarization)
• Excess Sodium inside cell actively pumped out via Sodium-Potassium Pump (Sodium-Potassium ATPase)
• Exchanges Sodium (out) for Potassium (in)

Step 5: Final Relaxation

• Once calcium removed → Troponin C becomes free
• Cross bridges between Actin and Myosin break
• Muscle relaxes

🖇 VIII. Factors Affecting Contractility

📌 Categories

• Mechanical Factors
• Cardiac Factors
• Extracardiac Factors

🖇 A. MECHANICAL FACTORS: PRELOAD

🚨 Preload (Exam Point)

• Crucial concept
• Appears every year in examination

🟣 Preload Definition & Synonyms

📌 Definition

• The load the muscle encounters when it is about to contract

🚨 Synonyms (Exam Point):

• Preload = Venous Return = End Diastolic Volume (EDV)

📌 EDV Definition

• Volume of blood contained in ventricles at end of diastole (filling phase)
• Just before ejection

🟣 Venous Return Concept

📌 Variability

• Venous return (blood returning from tissues to heart) highly variable
• Depends on activity:
• • Higher during exercise
  • Lower while sleeping

📌 Cardiac Adaptation (Stretch)

• Cardiac muscle can stretch (increase initial length)
• Accommodates higher volumes of venous return
• Example: 10 L during exercise

📌 Stretch Response

• Stretched muscle responds with increased force
• Similar to stretching rubber band

🖇 B. THE FRANK-STARLING LAW

🚨 Frank-Starling Law (Exam Point)

• Defines relationship between stretch and force

🟣 Law Statement

📌 Statement

• Increasing Initial Length of muscle fiber → leads to increase in Force of Contraction

🚨 Crucial Condition (Exam Point):

• This principle applies "WITHIN LIMIT"

📌 Beyond Limit

• If volume exceeds limit (e.g., excessive fluid administration):
• • Heart will fail
  • Contractility will decrease

🟣 Purpose & Mechanism

📌 Purpose

• Starling's Law prepares cardiac muscle to eject all incoming blood
• Ensures no blood left behind (accumulated)

📌 Mechanism (Key Principle)

• Any factor that increases contractility (including preload) ultimately works by increasing entry of Calcium
• Increased stretch (Initial Length) → increased calcium influx → binding with Troponin C → forming more cross bridges

🖇 C. SIGNIFICANCE & APPLICATIONS OF FRANK-STARLING LAW (Exam Point)

🟣 1. In Normal Heart

📌 Mechanism

• When venous return increases → law ensures heart stretches
• Increases contractility
• Maintains balance
• Volume ejected from Right Side = Volume ejected from Left Side

🟣 2. In Denervated Heart (Transplanted Heart)

📌 Clinical Application

• Transplanted heart lacks connections to Sympathetic/Parasympathetic nerves
• Ability to adjust Cardiac Output relies primarily on Starling Mechanism
• Responds to changes in Venous Return

🟣 3. In Chronic Hypertension

🟠 Clinical Note:

Pathophysiology:

• Patient with persistently high blood pressure (increased resistance in Aorta)
• Left Ventricle struggles to pump blood

Sequence of Events:

1. Ventricle may eject some blood but leaves residual blood behind
2. Residual blood + new blood from next beat = increased End Diastolic Volume (Preload)
3. Starling's Law activated:
4. • Heart stretches
   • Increases contraction force
   • Pumps out both old and new accumulated blood

Long-term Consequence:

• If hypertension NOT treated:
• • Chronic overuse of Starling mechanism
  • Muscle eventually fatigues and fails
  • Due to exceeding "within limit" condition

🖇 D. MECHANICAL FACTORS: AFTERLOAD (Introduction)

📌 Definition

• Unexpected resistance encountered by Ventricle during blood ejection

📌 Cardiac Translation

• Encountered as:
• • Increased pressure (e.g., Hypertension)
  • Increased stiffness

🟣 Example: Arteriosclerosis (Aortic Stiffness)

📌 Normal Aorta

• Flexible
• Expands to accommodate ejected blood

📌 Stiffened Aorta

• Loses flexibility
• Presents chronic resistance/load to Ventricle trying to pump blood into it

🖇 IX. Administrative Notes

📌 Key Points

• Significant lecture time dedicated to student attendance discussion
• Coordinator (Dr. Magdy) has strict policy on grading and activity scores
• Activity grades = easily attainable points

🚨 Warning

• Students who don't attend may receive lower activity scores
• Potential loss: up to 20 marks
• Coordinator serious about attendance issue