Plant Growth and Development

COMPREHENSIVE CHAPTER NOTES: BODY FLUIDS AND CIRCULATION

BLOOD: COMPOSITION AND FUNCTIONS

**Blood** is a specialised connective tissue consisting of a fluid matrix (plasma) and formed elements. It serves as the transport medium for nutrients, oxygen, waste products, and hormones throughout the body.

Plasma Composition and Functions

**Plasma** constitutes approximately **55% of blood volume** and is a straw-coloured, viscous fluid with the following composition:

**Water content**: 90-92% — serves as the solvent medium

**Proteins**: 6-8% of plasma (major proteins include):

**Fibrinogen** — essential for blood coagulation/clotting; inactive form present in plasma

**Globulins** — involved in immune defence mechanisms; antibodies are globulins

**Albumins** — maintain osmotic balance and regulate blood pressure

**Ions/Minerals**: Small amounts including Na⁺, Ca²⁺, Mg²⁺, HCO₃⁻, Cl⁻; crucial for nerve impulse conduction and muscle contraction

**Organic compounds in transit**: Glucose (energy substrate), amino acids (protein synthesis), lipids (energy and hormone precursors)

**Clotting factors**: Present in inactive form; activated during coagulation cascade

**Hormones and enzymes**: Transported through plasma for metabolic regulation

**Serum** is defined as plasma without clotting factors (fibrinogen and other coagulation factors removed).

FORMED ELEMENTS OF BLOOD

Formed elements constitute approximately **45% of blood volume** and include erythrocytes (RBCs), leucocytes (WBCs), and platelets.

Erythrocytes (Red Blood Cells)

**Normal count**: 5.0-5.5 million cells/mm³ of blood

**Key characteristics**:

**Most abundant** blood cells

**Biconcave disc shape** — increases surface area for gas exchange

**Nucleus absent** in mammals (present in amphibians, birds, and reptiles)

**Origin**: Red bone marrow in adults (myeloid tissue)

**Colour**: Red due to iron-containing protein **haemoglobin**

**Haemoglobin**:

Complex iron-containing (Fe²⁺) protein

**Normal concentration**: 12-16 gms/100 mL blood (varies: males 13.5-18 g/dL, females 12-16 g/dL)

Each haemoglobin molecule binds **4 oxygen molecules** reversibly

Functions in oxygen transport from lungs to tissues and CO₂ transport (some CO₂ binds to globin chains)

Forms **oxyhaemoglobin** in lungs (bright red); **deoxyhaemoglobin** in tissues (dark red)

**Life span and fate**:

**Average lifespan**: 120 days

**Destruction site**: Spleen (referred to as "graveyard of RBCs")

Destroyed RBCs release bilirubin (converted to bile in liver) and iron (recycled by bone marrow)

Leucocytes (White Blood Cells)

**Normal count**: 6,000-8,000 cells/mm³ of blood

**Characteristics**:

**Nucleated** (possess nucleus unlike RBCs)

**Colourless** — lack haemoglobin

**Short-lived** — lifespan ranges from hours to years depending on type

**Functions**: Defence against pathogens, immune responses, inflammation control

**Classification and types**:

**1. Granulocytes** (possess granules in cytoplasm):

**Neutrophils** (60-65% of total WBCs)

Most abundant WBC

**Phagocytic function** — engulf and destroy bacteria and foreign particles

Lifespan: 1-2 days; released from bone marrow in response to infection

**Eosinophils** (2-3% of total WBCs)

**Functions**: Resist parasitic infections; associated with allergic reactions

Increase in number during parasitic infections or allergy

**Basophils** (0.5-1% of total WBCs)

Least abundant WBCs

**Secretory function**: Release histamine, serotonin, heparin

**Role**: Involved in inflammatory and allergic reactions; heparin is anticoagulant

**2. Agranulocytes** (absence of granules):

**Lymphocytes** (20-25% of total WBCs)

**Two major types**:

**T-lymphocytes** — cell-mediated immunity; attack infected/cancerous cells

**B-lymphocytes** — humoral immunity; produce antibodies (immunoglobulins)

Both involved in **specific immune responses**

**Memory cells** formed after antigen exposure provide long-term immunity

**Monocytes** (6-8% of total WBCs)

**Largest WBC**

**Phagocytic function** — engulf pathogens and cell debris

Develop into **macrophages** in tissues for enhanced phagocytosis

Platelets (Thrombocytes)

**Normal count**: 1.5-3.5 lakh cells/mm³ (150,000-350,000/μL) of blood

**Characteristics**:

**Cell fragments** derived from megakaryocytes (multinucleated cells in bone marrow)

**Nucleus absent**

**Life span**: 7-10 days

**Appearance**: Small, disc-shaped, colourless

**Functions**:

**Haemostasis** — arrest blood flow after injury through:

Adhesion to damaged blood vessel walls

Aggregation to form platelet plug

Release of coagulation factors

**Coagulation** — release various substances involved in clot formation:

Platelet factor III (thromboplastin)

ADP (adenosine diphosphate) — platelet aggregator

5-HT (serotonin) — vasoconstrictor

Fibrinogen (stabilises clot)

**Clinical significance**:

**Thrombocytopenia** (reduced platelets) → excessive bleeding/haemorrhage

**Thrombocytosis** (increased platelets) → increased clotting risk

BLOOD GROUPS: ABO AND RH CLASSIFICATION

Blood typing is essential for safe transfusions. Two major grouping systems determine blood compatibility:

ABO Grouping System

**Basis**: Presence or absence of **surface antigens A and B** on RBC membrane and corresponding **natural antibodies in plasma**.

**Antigens**: Proteins/polysaccharides on RBC surface that trigger immune response

**Antibodies**: Proteins in plasma (naturally occurring) that react against foreign antigens

**Blood group classification**:

| Blood Group | Antigens on RBCs | Antibodies in Plasma | Universal Donor For | Can Receive From |

|---|---|---|---|---|

| **A** | A | Anti-B | A, AB | A, O |

| **B** | B | Anti-A | B, AB | B, O |

| **AB** | A, B | Nil (None) | AB only | AB, A, B, O (all groups) |

| **O** | Nil (None) | Anti-A, Anti-B | A, B, AB, O (all groups) | O only |

**Key concepts**:

**Universal donor** — **O group** (no antigens; transfusion does not trigger agglutination in recipient regardless of group)

**Universal recipient** — **AB group** (no antibodies; can accept RBCs from any group without agglutination)

**Agglutination** — clumping of RBCs when incompatible blood groups mix; donor antigen reacts with recipient antibodies causing RBC destruction, leading to shock and kidney failure

**Mechanism of transfusion reaction**:

Incompatible blood → antigen-antibody complex formation → RBC aggregation and lysis → haemoglobin release → kidney damage, fever, jaundice

Rh Grouping System

**Basis**: Presence or absence of **Rh antigen** (similar to antigen in Rhesus monkeys) on RBC surface

**Classification**:

**Rh positive (Rh⁺ve)** — possess Rh antigen; approximately **80% of human population**

**Rh negative (Rh⁻ve)** — lack Rh antigen; approximately **20% of human population**

**Key characteristic**: Unlike ABO, **natural antibodies against Rh antigen are NOT present**. Rh⁻ve individuals develop anti-Rh antibodies **only after exposure** to Rh⁺ve blood.

**Clinical significance — Erythroblastosis Foetalis (Haemolytic Disease of Newborn)**:

**Scenario**:

Mother: Rh⁻ve (Rh negative)

Foetus: Rh⁺ve (Rh positive)

**Pathophysiology**:

**First pregnancy**:

Placenta acts as **impermeable barrier** — separates maternal and foetal blood circulation

No mixing occurs during pregnancy

**During delivery**: Placental barrier ruptures → foetal Rh⁺ve blood enters maternal circulation (fetomaternal haemorrhage)

Mother's immune system recognises Rh antigen as foreign → produces **anti-Rh IgG antibodies** (sensitisation)

These antibodies take time to develop; first child usually unaffected

**Subsequent pregnancies** (with Rh⁺ve foetus):

Mother already has **circulating anti-Rh IgG antibodies** from previous pregnancy

IgG antibodies are small, cross placental barrier → enter foetal circulation

Antibodies attack foetal RBCs → **haemolysis** (destruction)

**Consequences**:

Severe anaemia in foetus

Increased bilirubin from destroyed RBCs → **jaundice** (hyperbilirubinaemia)

**Hydrops foetalis** — foetal oedema, ascites, cardiac failure (fatal if untreated)

**Prevention**:

Administer **anti-Rh antibodies (RhoGAM)** to Rh⁻ve mother **within 72 hours of delivery of first child**

Anti-Rh antibodies neutralise/destroy foetal RBCs before mother develops her own antibodies

Prevents sensitisation; protects subsequent pregnancies

BLOOD COAGULATION (CLOTTING)

**Purpose**: Haemostasis — arrest bleeding and prevent excessive blood loss following injury

**Observation**: Dark reddish-brown scab/clot forms at wound site after injury

**Clot composition**: Network of **fibrin threads** (protein fibres) trapping dead/damaged blood cells and platelets

Coagulation Cascade (Intrinsic and Extrinsic Pathways)

**Key enzyme conversions**:

1. **Prothrombin → Thrombin** (catalysed by **thrombokinase/Factor X**)

Prothrombin: inactive precursor present in plasma

Thrombin: active serine protease enzyme essential for clot formation

2. **Fibrinogen → Fibrin** (catalysed by **thrombin**)

Fibrinogen: soluble protein in plasma

Fibrin: insoluble protein forming mesh framework of clot

**Cofactors and initiators**:

**Calcium ions (Ca²⁺)** — **absolutely essential** for all coagulation reactions; cofactor for enzyme complexes

**Thrombokinase/Factor X** — enzyme complex formed by cascade of enzymic reactions

**Tissue factors (TF)** — released from damaged tissue cells; initiates extrinsic pathway

**Platelet factors** — released from activated platelets; accelerates coagulation

**Triggers of coagulation**:

**Trauma/injury** — disrupts blood vessels and activates platelets

**Tissue damage** — releases tissue factor (TF)

**Platelet activation** — releases phospholipids and clotting factors

**Cascade process**: Linked enzymic reactions where product of one reaction serves as reactant for next (amplification system)

**Anticoagulants**:

**Heparin** — secreted by basophils; prevents thrombin formation

**EDTA (ethylenediaminetetraacetic acid)** — lab use; chelates calcium, preventing coagulation

**Citrate** — lab use; binds calcium

LYMPH (TISSUE FLUID/INTERSTITIAL FLUID)

Formation and Composition

**Origin**: Fluid that leaks out of blood capillaries into tissue spaces

**Mechanism of formation**:

As blood circulates through capillaries, **hydrostatic pressure forces** water and small solutes out of capillary lumen

**Large proteins and formed elements remain** in blood due to colloidal osmotic pressure (oncotic pressure) exerted by proteins

Resulting fluid is **interstitial fluid (tissue fluid)**

**Composition**:

**Mineral distribution** — identical to plasma

**Proteins** — much lower concentration than plasma (lacks fibrinogen and most globulins)

**Lymphocytes** — specialised white blood cells responsible for immune responses

**Nutrients** — glucose, amino acids transported to cells

**Hormones** — transported to target cells

**Waste products** — metabolic wastes collected from cells

**Colour**: **Colourless** (unlike blood)

Lymphatic System and Circulation

**Components**:

**Lymph vessels/capillaries** — blind-ended tubes in tissues collecting interstitial fluid

**Lymph ducts** — larger vessels (right lymphatic duct, thoracic duct) draining into venous system

**Lymph nodes** — filtering stations along lymph vessels; contain lymphocytes for immune response

**Lymphoid organs** — spleen, thymus, tonsils

**Functions**:

1. **Drainage** — collects tissue fluid and returns it to blood circulation (prevents oedema)

2. **Transport** — carries **fats absorbed in intestines** through **lacteals** (lymph capillaries in intestinal villi) to bloodstream

3. **Immunity** — lymphocytes in lymph provide immune defence against pathogens

4. **Hormone/nutrient transport** — distributes these molecules to tissues

**Return to circulation**:

Right lymphatic duct → drains **upper right body** → empties into right subclavian vein

Thoracic duct → drains **lower body and left side** → empties into left subclavian vein

**Note**: Lymph moves in **one direction only** (toward heart) due to valves in lymph vessels and body movements

CIRCULATORY PATHWAYS: COMPARATIVE ANATOMY

Open vs. Closed Circulatory Systems

**Open Circulatory System**:

Found in: **Arthropods, molluscs**

Blood pumped by heart flows through **large vessels into open body cavities** called **sinuses**

Blood directly bathes tissues

Disadvantage: Slow, inefficient; pressure cannot be regulated precisely

**Closed Circulatory System**:

Found in: **Annelids, all chordates/vertebrates**

Blood always contained within **closed network of blood vessels** (arteries, capillaries, veins)

Advantage: **Precise regulation** of blood flow; rapid, efficient oxygen delivery; maintained pressure supports high metabolic rates

**More advantageous** for higher organisms with complex physiology

Vertebrate Heart Chambers and Circulatory Types

**2-chambered heart**:

Found in: **Fishes**

Structure: 1 atrium + 1 ventricle

Blood flow: Deoxygenated → ventricle → gills (oxygenation) → body → deoxygenated → atrium

**Single circulation** — blood passes through heart once per complete circuit

Limitation: Lower blood pressure; slow circulation

**3-chambered heart**:

Found in: **Amphibians, most reptiles** (except crocodiles)

Structure: 2 atria + 1 ventricle

Blood mixing: Oxygenated blood from lungs + deoxygenated blood from body mix in single ventricle

**Incomplete double circulation** — mixed blood pumped to lungs and body

Consequence: Lower oxygen content reaching tissues; supports moderate metabolic rate

**4-chambered heart**:

Found in: **Crocodiles, birds, mammals (including humans)**

Structure: 2 atria + 2 ventricles (right and left)

**Complete separation** of oxygenated and deoxygenated blood pathways

**Double circulation** — two separate circuits:

1. Pulmonary circulation (heart → lungs)

2. Systemic circulation (heart → body)

Advantage: **Maximum oxygenation** of tissues; supports high metabolic rates required for endothermy

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HUMAN CIRCULATORY SYSTEM

Heart: Structure and Location

**Position**:

Located in **thoracic cavity** between two lungs

**Slightly tilted to the left**

Protected by **double-walled serous membrane** called **pericardium**

**Pericardial fluid** — lubricates heart movement, reduces friction

**Size**: Approximately size of **closed fist** (~250-350 grams)

**Derivation**: **Mesodermal origin**

Internal Structure of Heart

**Four chambers**:

1. **Right atrium** — receives deoxygenated blood from:

**Superior vena cava** — from upper body

**Inferior vena cava** — from lower body

**Coronary sinus** — from heart muscle

2. **Right ventricle** — pumps deoxygenated blood to lungs via **pulmonary artery**

3. **Left atrium** — receives oxygenated blood from **four pulmonary veins** (two from each lung)

4. **Left ventricle** — pumps oxygenated blood to body via **aorta** (largest artery)

Septa (Walls) Separating Chambers

**Inter-atrial septum** — thin muscular wall separating right and left atria

**Inter-ventricular septum** — **thick muscular wall** separating right and left ventricles; strength ensures complete separation of blood

**Atrio-ventricular septum** — separates atria from ventricles

**Openings/connections**:

Each septum has opening(s) connecting adjacent chambers, guarded by valves

Heart Valves: Structure and Function

**Valve function**: Ensure **unidirectional blood flow** (prevent backflow)

**1. Atrio-ventricular (AV) valves** — between atria and ventricles:

**Tricuspid valve** (right side)

**Three muscular flaps (cusps)**

Located between right atrium and right ventricle

Attached to **chordae tendinae** (connective tissue cords) anchoring to ventricular walls

Prevents backflow during ventricular contraction

**Bicuspid (Mitral) valve** (left side)

**Two muscular cusps**

Located between left atrium and left ventricle

Also anchored by chordae tendinae

Prevents backflow during ventricular contraction

**2. Semilunar (SL) valves** — between ventricles and arteries:

**Pulmonary valve** — guards opening of right ventricle into pulmonary artery

**Aortic valve** — guards opening of left ventricle into aorta

Both have **3 cusps** shaped like half-moon (semilunar)

Prevent backflow of blood from arteries into ventricles during ventricular relaxation

**Valve closure produces heart sounds**:

**Lub sound** (first heart sound) — closure of tricuspid and mitral valves (start of ventricular systole)

**Dub sound** (second heart sound) — closure of semilunar valves (end of ventricular systole)

Heart sounds audible with **stethoscope**; diagnostic value

Cardiac Muscle and Nodal Tissue

**Cardiac muscle**:

Forms complete wall of heart (myocardium)

**Characteristics**: Striated, branched, uninucleate cells; intercalated discs provide rapid conduction

**Wall thickness**: Ventricular walls much thicker than atrial walls (ventricles pump against higher resistance)

Left ventricular wall thicker than right (systemic circulation requires higher pressure than pulmonary)

**Nodal tissue (Conduction System)**:

Specialised cardiac muscle capable of **generating action potentials without external stimuli** (autoexcitable/automaticity)

**Components**:

1. **Sino-atrial node (SAN)**

Location: **Right upper corner (posterior) of right atrium** near superior vena cava opening

**Function**: Primary pacemaker of heart

**Autorhythmicity**: Generates maximum action potentials — **70-75 per minute**

**Initiates and maintains** rhythmic contractions of heart

Responsible for **normal heart rate** (average 72 beats/min)

2. **Atrio-ventricular node (AVN)**

Location: **Lower left corner of right atrium** near atrio-ventricular septum

**Function**: Conducts action potentials from atria to ventricles

**Delay zone**: Slows conduction velocity (0.02-0.05 m/s) allowing atrial contraction to complete before ventricular contraction

Generates 40-60 action potentials/min (slower than SAN)

3. **Atrio-ventricular bundle (AV bundle/Bundle of His)**

Continuation from AVN through atrio-ventricular septum

Divides into **right and left bundle branches** on inter-ventricular septum

Rapid conduction of action potentials (1-4 m/s)

4. **Purkinje fibres (Terminal branches)**

Minute fibres distributed throughout ventricular myocardium

Rapid conduction velocity (2-4 m/s)

Ensure **simultaneous ventricular contraction** for effective pumping

**Action potential conduction pathway**:

SAN → atrial muscle → AVN → AV bundle → bundle branches → Purkinje fibres → ventricular muscle

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CARDIAC CYCLE

**Definition**: Sequence of events occurring during one complete heartbeat (contraction and relaxation of all four chambers); cyclically repeated

**Duration**:

At heart rate of 72 beats/min: **Cardiac cycle duration = 60 sec ÷ 72 = 0.8 seconds** (0.8 sec per beat)

**Atrial systole**: 0.1 second

**Ventricular systole**: 0.3 second

**Joint diastole**: 0.4 second

Phases of Cardiac Cycle

**Phase 1: Joint Diastole (Ventricular Filling)**

All four chambers **relaxed**

**Tricuspid and bicuspid (AV) valves OPEN** — blood flows passively from atria into ventricles

**Semilunar valves CLOSED**

Pulmonary veins deliver oxygenated blood to left atrium

Superior and inferior vena cava deliver deoxygenated blood to right atrium

**Ventricular filling**: ~70% passive during diastole

**Phase 2: Atrial Systole (Atrial Contraction)**

**SAN generates action potential**

Action potential spreads across both atria via internodal pathways

Both atria **contract simultaneously**

**Atrial pressure increases** → forces remaining blood into ventricles

**Increases ventricular filling by ~30%** (atrial kick)

Duration: ~0.1 second

**AV valves remain OPEN**

**Semilunar valves remain CLOSED**

Atrial systole followed immediately by atrial diastole

**Phase 3: Ventricular Systole (Ventricular Contraction)**

AVN receives action potential from atria

**Conduction delayed at AVN** (0.1 second) — allows complete atrial emptying before ventricular contraction

Action potential transmitted via AV bundle and Purkinje fibres

Ventricular myocardium **contracts simultaneously** (coordinated contraction)

**Ventricular pressure increases sharply**

**Sub-phase 3a: Isovolumetric Contraction** (early systole)

Duration: ~0.05 second

Ventricular walls contract but volume remains constant (both AV and SL valves closed)

Pressure increases rapidly without ejection

Atria begin relaxation (diastole)

**Sub-phase 3b: Ventricular Ejection** (mid-to-late systole)

As ventricular pressure exceeds atrial pressure → **AV valves (tricuspid and mitral) SNAP CLOSED** due to attempt of blood backflow

Closure prevents backflow into atria

As ventricular pressure continues rising and exceeds pressures in pulmonary artery and aorta → **semilunar valves FORCED OPEN**

Right ventricle ejects deoxygenated blood into pulmonary artery (to lungs)

Left ventricle ejects oxygenated blood into aorta (to body)

**Stroke volume** ejected: ~70 mL per ventricle per beat

Duration: ~0.25 second

**Phase 4: Ventricular Diastole (Ventricular Relaxation)**

Ventricular muscles relax

Ventricular pressure declines sharply below pressures in pulmonary artery and aorta

**Semilunar valves SNAP CLOSED** — prevents backflow (produces "dub" sound)

Closure also marks end of systole/ventricular ejection

Blood pressure in ventricles falls further

**Isovolumetric Relaxation** (early diastole)

Ventricular pressure continues falling while volume constant (both valve sets closed)

Duration: ~0.07 second

**Ventricular Filling** (continued)

Ventricular pressure falls below atrial pressure

**AV valves PUSH OPEN** by atrial pressure

Blood freely flows from atria into ventricles

Cycle returns to joint diastole, repeats

Heart Sounds and Phonocardiography

**First heart sound (S1 - "Lub")**

**Caused by**: Closure of tricuspid and mitral (AV) valves

**Timing**: Marks onset of ventricular systole (isovolumetric contraction phase)

**Characteristics**: Louder, longer duration, lower pitch

**Clinical significance**: Prolonged S1 suggests valve disease; splits suggest bundle branch block

**Second heart sound (S2 - "Dub")**

**Caused by**: Closure of aortic and pulmonary (semilunar) valves

**Timing**: Marks end of ventricular systole and beginning of diastole

**Characteristics**: Higher pitch, shorter duration

**Physiological split**: Aortic valve closes slightly before pulmonary (normal in young adults during inspiration)

**Clinical significance**: Fixed split S2 suggests atrial septal defect

**Normal heart rhythm**: Lub-dub, Lub-dub, Lub-dub... (70-75 times per minute)

Cardiac Output and Stroke Volume

**Stroke volume (SV)**:

**Definition**: Volume of blood ejected by each ventricle per contraction

**Normal value**: ~70 mL per beat

**Influenced by**:

**Preload** — end-diastolic ventricular volume (stretching of cardiac myocytes)

**Afterload** — resistance against which heart pumps (arterial pressure)

**Contractility** — force of ventricular contraction

**Cardiac output (CO)**:

**Definition**: Volume of blood pumped out by each ventricle **per minute**

**Formula**: **CO = Stroke Volume (SV) × Heart Rate (HR)**

**Normal resting value**: 5 litres/minute (5,000 mL/min) in healthy adult

Calculation: 70 mL × 72 beats/min = 5,040 mL/min ≈ 5 L/min

**Range**: 4-8 litres/minute (varies with fitness, body size, metabolic demands)

**Factors affecting cardiac output**:

1. **Increased heart rate** (exercise, stress, fever, caffeine) → increased CO

2. **Increased stroke volume** → increased CO

3. **Sympathetic stimulation** (epinephrine, norepinephrine) → increased HR and contractility → increased CO

4. **Parasympathetic stimulation** (acetylcholine, vagal tone) → decreased HR, contractility → decreased CO

5. **Fitness level**: Athletes have higher CO due to increased SV and lower resting HR

**Athletes vs. sedentary individuals**:

**Athletes**: Lower resting HR (50-60 bpm) but higher SV → similar or higher CO

**Sedentary**: Higher resting HR (75-80 bpm) but lower SV → lower CO

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ELECTROCARDIOGRAM (ECG/EKG)

**Definition**: Graphical representation of **electrical activity of heart** during cardiac cycle

**Principle**: Electrical currents generated during heart depolarisation (excitation) and repolarisation are detected and recorded

ECG Recording Procedure

**Equipment**: Electrocardiograph machine

**Lead placement** (standard ECG):

**3 limb leads**:

1 electrode on each **wrist** (right and left)

1 electrode on **left ankle**

**Additional leads**: Multiple chest leads (V1-V6) for detailed evaluation

Leads continuously monitor heart's electrical activity from different angles

**Mechanism**: Electrodes detect voltage differences between regions → amplified and displayed as trace on paper/screen

Normal ECG Waves and Complexes

**Each complete ECG shows cyclical pattern with characteristic waves/complexes**:

**P-wave**:

**Represents**: Atrial depolarisation (electrical excitation of atria)

**Cause**: Action potential generated by SAN spreads across both atria

**Result**: Triggers atrial contraction (atrial systole)

**Timing**: Precedes AV valve closure

**Characteristics**: Small, rounded, positive wave

**Duration**: ~0.1 second

**PR interval**:

**Definition**: Time from start of P-wave to start of QRS complex

**Represents**: Conduction time from atria through AVN to ventricles

**Normal duration**: 0.12-0.2 seconds (120-200 ms)

**Clinical significance**:

Prolonged PR interval (>0.2 sec) suggests **first-degree AV block** (delayed conduction)

Varies with heart rate (shorter in tachycardia, longer in bradycardia)

**QRS complex**:

**Represents**: Ventricular depolarisation (electrical excitation spreading through ventricles)

**Cause**: Action potential from AV bundle and Purkinje fibres depolarises ventricular muscle

**Result**: Triggers ventricular contraction (ventricular systole)

**Timing**: Marks beginning of systole

**Composed of three deflections**:

**Q wave** — initial downward deflection (not always present)

**R wave** — upward deflection; tallest component

**S wave** — downward deflection after R (not always present)

**Normal duration**: 0.06-0.1 seconds (60-100 ms)

**Characteristics**: Large amplitude (5-20 mm); most prominent feature of ECG

**Clinical significance**:

Abnormal QRS duration suggests bundle branch block

Abnormal morphology suggests chamber enlargement or ischaemia

**ST segment**:

**Definition**: Flat line from end of S wave to start of T wave

**Represents**: Plateau phase of ventricular action potential (all ventricles fully depolarised)

**Duration**: ~0.2 second

**Clinical significance**:

**ST elevation** — suggests **myocardial infarction** (MI/heart attack)

**ST depression** — suggests myocardial ischaemia (reduced blood flow)

**T-wave**:

**Represents**: Ventricular repolarisation (return of ventricles from excited to resting state)

**Cause**: Ventricular myocytes recover electrical polarity

**Timing**: Marks end of ventricular systole

**Characteristics**: Rounded, positive deflection (opposite of QRS)

**Duration**: ~0