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Circulatory System — Overview
Components of Circulatory System
- Circulating fluid — Blood / Lymph
- Blood vessels — Arteries, Veins, Capillaries, Lymph capillaries
- Pumping device — Heart
Types of Circulatory System
- Open Circulatory System — Blood pumped into open body cavities called sinuses (haemocoel); blood not always in vessels; e.g. Arthropods (insects, prawns), Molluscs
- Closed Circulatory System — Blood always circulated through closed network of blood vessels; e.g. Annelids (earthworm), Vertebrates including humans
Heart Chambers in Different Animals
| Animal | Heart Chambers | Circulation | Blood Type |
| Fish | 2-chambered (1A + 1V) | Single circulation | Only deoxygenated blood in heart |
| Amphibians (Frog) | 3-chambered (2A + 1V) | Double circulation | Mixed blood in ventricle |
| Reptiles (except Crocodile) | 3-chambered (2A + 1V incompletely divided) | Double circulation | Mixed blood |
| Crocodile | 4-chambered (2A + 2V) | Double circulation | Oxygenated & deoxygenated separated |
| Birds & Mammals | 4-chambered (2A + 2V) | Double circulation | Complete separation |
Q. Which animals have 3-chambered heart with double circulation but mixed blood?
✅ Answer: Amphibians (frogs, toads) and most Reptiles (except crocodile)
Explanation
Both amphibians and most reptiles have 3-chambered hearts with 2 atria and 1 ventricle. Even though they have double circulation (blood goes to lungs AND to body), the single undivided ventricle causes mixing of oxygenated and deoxygenated blood. Crocodile is the exception among reptiles — it has a 4-chambered heart like birds and mammals, allowing complete separation of blood. Birds and mammals have the most efficient double circulation with complete separation.
Basic Facts About Human Heart
- Origin: Mesodermal
- Weight: 250–300 grams
- Position: Between the lungs, in mediastinum, tilted slightly left; enclosed in pericardial cavity
- Covered by: Pericardium (double-walled membranous sac) — outer Fibrous Pericardium (collagen) + inner Serous Pericardium (Parietal + Visceral layers)
- Pericardial fluid fills the space — reduces friction during beating
- Base of heart is at top, apex points left downward
Wall of Heart (Outside → Inside)
- Epicardium — outer layer (simple squamous epithelium)
- Myocardium — thick middle layer of cardiac muscle — responsible for pumping
- Endocardium — inner layer lining all chambers (simple squamous endothelium)
- Left ventricle wall is thicker than right — pumps blood against higher pressure to whole body
Valves of the Heart
| Valve | Location | Function |
| Tricuspid Valve (3 flaps) | Between Right Atrium and Right Ventricle | Prevents backflow from RV to RA during ventricular contraction |
| Bicuspid (Mitral) Valve (2 flaps) | Between Left Atrium and Left Ventricle | Prevents backflow from LV to LA during ventricular contraction |
| Pulmonary Semilunar Valve | Base of Pulmonary trunk (exit of RV) | Prevents backflow from pulmonary artery to RV during diastole |
| Aortic Semilunar Valve | Base of Aorta (exit of LV) | Prevents backflow from aorta to LV during diastole |
Chordae Tendineae & Papillary Muscles
Chordae Tendineae — tendon-like cords of collagen fibres that connect AV valve flaps to papillary muscles in the ventricular wall. They prevent the valve cusps from inverting into the atria during ventricular systole (like parachute strings). Present only in ventricles.
Also note: Eustachian valve — guards the opening of inferior vena cava in right atrium.
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Conduction System of Heart
Nodal Tissue — Autorhythmicity of Heart
The heart is myogenic — it generates its own impulse without external nervous stimulation. This is due to specialized nodal tissue with automatic rhythmic depolarization.
| Node / Structure | Location | Impulse Rate | Role |
| SA Node (Sinoatrial Node) — Pacemaker | Upper right corner of Right Atrium | 70–75 impulses/min (intrinsic = 100/min, but inhibited by Vagus to 70–75) | Initiates each heartbeat; sets the rhythm for the whole heart |
| AV Node (Atrioventricular Node) | Lower left corner of Right Atrium | 40–60 impulses/min | Receives impulse from SA node; delays it slightly (0.1 sec) to allow atria to empty before ventricles contract |
| Bundle of His (AV Bundle) | Interventricular septum | 40–45 impulses/min | Conducts impulse from AV node into ventricular walls |
| Purkinje Fibres | Walls of ventricles | 25 impulses/min | Rapidly spread impulse throughout ventricular myocardium → simultaneous contraction |
Regulation of Heart Beat Rate
- Vagus nerve (Cranial nerve X) — Parasympathetic — decreases heart rate (negative chronotropic)
- Sympathetic nerves + Adrenal medulla (epinephrine/norepinephrine) — increases heart rate (positive chronotropic)
- Ca²⁺ — increases heart rate
- K⁺ — decreases heart rate
- If SA node is non-functional → Artificial Pacemaker is implanted
Q. Why is SA node called the pacemaker of the heart?
✅ Answer: SA node generates impulses at the highest rate (70–75/min) and sets the rhythm for the entire heart
Explanation
The SA node has the highest rate of spontaneous depolarization among all nodal tissues. Its intrinsic rate is about 100 impulses/min, but the inhibitory effect of the Vagus nerve (parasympathetic) brings it down to 70–75/min — the normal resting heart rate. Since it fires first and fastest, it drives all other cardiac tissue. Every heartbeat is initiated by the SA node, making it the natural pacemaker. If SA node fails, AV node takes over at its slower rate (40–60/min), causing bradycardia.
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Cardiac Cycle & Heart Sounds
Cardiac Cycle — Duration 0.8 seconds (75 beats/min)
- Atrial systole — 0.15 sec → atria contract → fill remaining 1/3 (30%) blood into ventricles
- Ventricular systole — 0.30 sec → ventricles contract → blood pumped to aorta & pulmonary trunk
- Joint diastole — 0.35 sec → both atria and ventricles relax → 2/3 (70%) of ventricular filling happens passively
At end of diastole — 70% filling happens passively; remaining 30% by atrial systole
Stroke Volume, EDV, ESV & Cardiac Output
- EDV (End Diastolic Volume) = 120 ml — blood in ventricle at end of diastole
- ESV (End Systolic Volume) = 50 ml — blood remaining in ventricle after systole
- Stroke Volume (SV) = EDV − ESV = 120 − 50 = 70 ml per beat
- Cardiac Output (CO) = Heart Rate × Stroke Volume = 72 × 70 = 5040 ≈ 5 L/min
Heart Sounds
- 1st Sound "LUBB" — Caused by closing of AV valves (Tricuspid + Bicuspid) at beginning of ventricular systole; long, low-pitched
- 2nd Sound "DUBB" — Caused by closing of Semilunar valves (Aortic + Pulmonary) at beginning of ventricular diastole; short, high-pitched
Q. What is Cardiac Output and how is it calculated?
✅ Answer: CO = Heart Rate × Stroke Volume = 72 × 70 = ~5000 ml/min (5 L/min)
Explanation
Cardiac Output is the total volume of blood pumped by each ventricle per minute. It equals heart rate (beats/min) multiplied by stroke volume (ml/beat). Normal resting values: Heart rate = 72 beats/min, Stroke Volume = 70 ml/beat → CO = 72 × 70 = 5040 ml/min ≈ 5 L/min. This means the entire blood volume (~5 L) circulates once every minute. During exercise, CO can increase up to 20–25 L/min due to increased heart rate and stroke volume.
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ECG — Electrocardiograph
What is ECG?
ECG is a graphical representation of the electrical activity of the heart during a cardiac cycle. Obtained using an Electrocardiograph machine (invented by Einthoven). Electrodes placed on both wrists and left ankle.
| Wave | Represents | Duration |
| P Wave | Depolarisation of atria → leads to atrial contraction (atrial systole) | ~0.08 sec |
| QRS Complex | Depolarisation of ventricles → leads to ventricular contraction (ventricular systole begins) | ~0.08 sec |
| T Wave | Repolarisation of ventricles → ventricular relaxation (ventricular diastole); atrial repolarization hidden within QRS | ~0.16 sec |
Abnormalities Detected by ECG
- Enlarged P wave → enlarged atria
- Increased R wave amplitude → ventricular hypertrophy (enlarged ventricle)
- Elevated ST interval → myocardial ischaemia (lack of O₂ to heart muscle)
- Flat T wave / ST deviation → cardiac arrest / ischaemia
Q. What does the QRS complex in an ECG represent?
✅ Answer: Depolarisation of ventricles, which initiates ventricular systole (contraction)
Explanation
In the ECG, the QRS complex represents the wave of electrical depolarization spreading through the ventricular myocardium via Bundle of His and Purkinje fibres. This depolarization causes both ventricles to contract simultaneously (ventricular systole). The QRS complex follows the P wave (atrial depolarization) with a small delay — this delay is the AV nodal delay that ensures atria finish contracting before ventricles start. Heart rate can be calculated by counting the number of QRS complexes per minute.
Basic Facts About Blood
- Blood is a fluid connective tissue — Origin: Mesodermal (Haematopoietic tissue)
- Study of blood = Haematology
- Volume: Male = 5–6 L (8% body weight); Female = 4–4.5 L (7% body weight)
- pH: 7.35–7.45 (slightly alkaline) — maintained by NaHCO₃ buffer; pH in vein slightly lower than artery
- Composition: Plasma (55%) + Formed elements (45%)
Blood Plasma — Composition
Plasma (55% of blood)
- Water — 90–92% of plasma
- Proteins (6–8%):
- Albumin — most abundant, smallest; made in liver; maintains osmotic pressure of blood
- Globulins — α-globulin, β-globulin (transport), γ-globulin (Immunoglobulins/Antibodies) — made by plasma cells (activated B-lymphocytes)
- Fibrinogen — made in liver; essential for blood clotting (converted to Fibrin)
- Prothrombin — clotting factor, made in liver
- Inorganic ions: Na⁺ > Ca²⁺ > Mg²⁺ > K⁺ (order of abundance); NaHCO₃ acts as buffer
- Serum = Plasma without fibrinogen (clotting factors removed)
- Normal blood glucose = 80–120 mg/dL; hyperglycaemia if >120
- Normal cholesterol: HDL (High Density Lipoprotein = good); LDL (Low Density Lipoprotein = bad, causes heart disease)
- Normal urea = 20–40 mg/dL; ↑ urea = Uraemia
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Formed Elements — RBC, WBC, Platelets
Erythrocytes — RBC
Key Facts — RBC
- Count: 5–5.5 million/mm³ (male slightly higher)
- Size: 7.5 μm diameter × 2 μm thick
- Shape: Biconcave disc — increases surface area for gas exchange
- No nucleus, no mitochondria, no other organelles — only in mature RBC; enucleation conserves space for more Hb and reduces O₂ consumption by RBC itself
- Respiration type: Anaerobic (glycolysis only — no Krebs cycle); so RBC doesn't use the O₂ it carries
- Life span: 120 days → destroyed in Spleen (Graveyard of RBC) and liver
- Haemoglobin (Hb): 12–16 g/dL blood; each RBC has ~280 million Hb molecules
- Hb = Globin protein + Haem; Haem = Porphyrin ring + Fe²⁺; 4 subunits (2α + 2β in adults)
- After RBC breakdown → Hb → Bilirubin + Biliverdin (yellow/green bile pigments) → responsible for jaundice if excess
RBC Production — Erythropoiesis
- In embryo: first in Yolk sac → then Liver → then Spleen
- After birth: Red Bone Marrow (skull, ribs, sternum, vertebrae, long bone ends)
- Stimulated by hormone Erythropoietin (released by kidney in response to low O₂)
- Raw materials needed: Iron, Vitamin B₁₂, Folic acid, proteins
- Stem cell → Proerythroblast → Erythroblast → Reticulocyte → Mature RBC (loses nucleus in process)
Q. Why do RBCs have no nucleus and no mitochondria?
✅ Answer: To maximize space for haemoglobin and to prevent the RBC from consuming the oxygen it carries
Explanation
RBCs are highly specialized for their single function — transporting oxygen. Losing the nucleus frees up space for more haemoglobin molecules (~280 million per RBC). Losing mitochondria means RBCs cannot perform aerobic respiration — they only do glycolysis (anaerobic). This is a critical advantage: if RBCs had mitochondria, they would consume the O₂ they are supposed to deliver to tissues. So the absence of organelles is an adaptation for maximum O₂ transport efficiency.
Leucocytes — WBC
Key Facts — WBC
- Count: 6000–8000/mm³
- RBC:WBC ratio = 600:1
- Leucocytosis = increase in WBC count (during infection, inflammation, cancer)
- Leukaemia = cancer of blood — uncontrolled increase in WBC
- Diapedesis = movement of WBCs through capillary walls to reach infection site
- Life span: variable — Neutrophils few days; Monocytes months; Lymphocytes years
| WBC Type | % | Size | Nucleus Shape | Function |
| Neutrophils (PMNL) | 60–65% | 10–12 μm | Multi-lobed (4–7 lobes) | Phagocytosis; first responders to bacterial infection |
| Lymphocytes | 20–25% | 8–10 μm | Large round, fills cell | Immune response — T cells (CMI) and B cells (Humoral/Antibody) |
| Monocytes | 6–8% | 18 μm (largest WBC) | Kidney-shaped | Phagocytosis; become macrophages in tissues |
| Eosinophils | 2–3% | 10–12 μm | Bilobed | Antiparasitic; lysis of parasite wall; involved in allergies |
| Basophils | <1% | 10 μm | Bilobed (S-shaped) | Release Heparin (anticoagulant), Serotonin, Histamine; involved in inflammation and allergy |
T-Lymphocyte Sub-types
- TH cells (Helper T) — control both Cell-Mediated and Humoral immunity
- TC cells (Cytotoxic T / Killer T) — kill cancer cells and virus-infected cells
- TS cells (Suppressor T) — suppress immune response after infection is cleared
- T-memory cells — remember antigen for faster response on re-exposure
Thrombocytes — Platelets
Key Facts — Platelets
- Not present in all mammals (absent in non-mammalian vertebrates — they have nucleated thrombocytes)
- Count: 1,50,000–3,50,000/mm³
- Life span: One week (7–10 days)
- Shape: Round/oval, no nucleus
- Formed by fragmentation of Megakaryocytes (large cells in red bone marrow)
- Function: Blood clotting — release Thromboplastin (Factor III) to initiate clotting cascade
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Blood Clotting (Coagulation)
Clotting Cascade — Step by Step
- Injury → Platelets release Thromboplastin (Factor III)
- Thromboplastin + Ca²⁺ → activates clotting cascade
- Prothrombin (inactive) → Thrombin (active) — conversion requires Ca²⁺
- Fibrinogen (soluble, inactive) → Fibrin (insoluble, active) — catalyzed by Thrombin
- Fibrin forms a mesh → traps RBCs → Soft clot forms
- Soft clot contracts → Hard clot (Scab) forms
- Remaining liquid = Serum (plasma without fibrinogen)
13 clotting factors involved; each product of one step acts as catalyst for next (cascade)
Anticoagulants
- Heparin — naturally present in blood (released by basophils & mast cells); prevents clotting inside vessels
- Warfarin — isolated from plants; used as anticoagulant drug (rat poison in high doses)
- EDTA (Ethylenediaminetetraacetic acid) — chelates Ca²⁺ → prevents clotting (used in blood collection tubes)
- Sodium citrate / Sodium oxalate — calcium binders; used in blood banks for storage
Q. What is the role of Ca²⁺ in blood clotting?
✅ Answer: Ca²⁺ is essential for the conversion of Prothrombin to Thrombin — a key step in the coagulation cascade
Explanation
Calcium ions (Ca²⁺) act as a cofactor at multiple steps in the blood clotting cascade (Factor IV). The most critical role is in activating Prothrombin activator, which then converts Prothrombin → Thrombin. Thrombin then converts soluble Fibrinogen → insoluble Fibrin threads that form the clot mesh. This is why EDTA (which chelates/binds Ca²⁺) and sodium citrate/oxalate (calcium binders) prevent clotting — they remove free Ca²⁺ from blood. Blood banks use sodium citrate to keep donated blood from clotting.
ABO Blood Group System
Based on presence or absence of antigens A and B on RBC surface, and corresponding antibodies (anti-A, anti-B) in plasma.
| Blood Group | Antigen on RBC | Antibody in Plasma | Can Donate To | Can Receive From |
| A | A | Anti-B | A, AB | A, O |
| B | B | Anti-A | B, AB | B, O |
| AB | A and B | None (nil) | AB only | A, B, AB, O — Universal Recipient |
| O | None (nil) | Anti-A and Anti-B | A, B, AB, O — Universal Donor | O only |
Rh Blood Group System (Antigen D)
- Rh antigen (also called Antigen D) — similar to antigen found in Rhesus monkeys
- Rh positive (Rh⁺) — Rh antigen present on RBC surface (80% humans)
- Rh negative (Rh⁻) — Rh antigen absent (20% humans)
- Unlike ABO, natural Rh antibodies are NOT present — anti-Rh antibodies are produced only after exposure to Rh⁺ blood
Erythroblastosis Foetalis — Rh Incompatibility in Pregnancy
- Condition: Rh⁻ mother + Rh⁺ foetus
- First pregnancy: Rh⁺ foetal RBCs enter mother's blood during delivery → mother produces anti-Rh antibodies + memory B cells → first baby is usually unaffected
- Second pregnancy (Rh⁺ foetus): Memory cells → rapid large-scale anti-Rh antibody production → antibodies cross placenta → destroy foetal RBCs → Erythroblastosis Foetalis
- Symptoms in baby: severe anaemia, jaundice, oedema (hydrops)
- Prevention: Inject anti-Rh antibodies (RhoGAM) into Rh⁻ mother within 72 hrs of first delivery → destroys foetal RBCs before mother forms memory cells
Q. Why is O blood group called Universal Donor?
✅ Answer: O group has NO antigens (A or B) on RBC surface, so it does not trigger antibody-antigen reaction in any recipient
Explanation
In blood transfusion, the problem arises when donor's RBC antigens meet recipient's plasma antibodies — this causes agglutination (clumping) and haemolysis. O blood group has no A or B antigens on its RBCs, so it cannot be attacked by anti-A or anti-B antibodies in any recipient's plasma. Therefore O can donate to A, B, AB, and O groups — making it the universal donor. However, O group people can only receive from O, because their plasma contains both anti-A and anti-B antibodies. In practice, cross-matching is always done before transfusion.
| Feature | Artery | Vein | Capillary |
| Direction | Away from heart | Towards heart | Connects arterioles to venules |
| Blood type | Oxygenated (except pulmonary & umbilical) | Deoxygenated (except pulmonary & umbilical) | Exchange of gases, nutrients, wastes |
| Wall | Thick, muscular, elastic | Thin, less elastic | Single layer endothelium only |
| Blood pressure | High | Low | Very low |
| Valves | Absent (except at base) | Present (semilunar valves) | Absent |
| Lumen diameter | Smaller relative to wall | Larger relative to wall | Extremely small |
Wall Layers of Blood Vessels (3 Tunicas)
- Tunica externa (outer) — collagen fibres; provides strength
- Tunica media (middle) — smooth muscle + elastic fibres; controls diameter; thicker in arteries
- Tunica interna (inner) — endothelium (simple squamous epithelium); smooth surface prevents clotting
Portal Veins — Special Veins (Blood flows from one capillary bed to another)
- Hepatic Portal Vein — stomach → liver (carries nutrients absorbed from gut to liver)
- Hypophyseal Portal Vein — hypothalamus → anterior pituitary (carries releasing hormones)
- Renal Portal Vein — absent in humans (present in fish, amphibians)
Highest BP — Aorta; Lowest BP — Venacava; Tachycardia — increased HR; Bradycardia — decreased HR
Normal BP = 120/80 mmHg; Hypertension = ≥140/90 mmHg; Pulse pressure = Systolic − Diastolic = 120 − 80 = 40 mmHg
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Lymph & Lymphatic System
Formation of Lymph
Lymph is derived from blood plasma that leaks out of capillaries into the tissue spaces (becomes interstitial/tissue fluid). This fluid is then collected by blind-ended lymph capillaries → lymphatic vessels → Left Lymphatic (Thoracic) Duct → empties into subclavian vein (blood).
Lymph acts as a middleman between blood and tissue cells — transports nutrients, waste, fat (from gut as chylomicrons), and immune cells.
| Feature | Blood | Lymph |
| Colour | Red (due to Hb) | Colourless (no Hb) |
| RBC | Present | Absent |
| Platelets | Present | Absent |
| WBC | Present | Present (mainly lymphocytes) |
| Proteins | Albumin, Globulin, Fibrinogen | Less protein (mainly Albumin) |
| Flow direction | Heart → arteries → capillaries → veins → Heart (circular) | One direction only — tissue → lymph capillary → blood |
| Pressure | High (pumped by heart) | Low (moves by muscle compression, valves) |
Lymphoid Organs
- Primary lymphoid organs — sites of lymphocyte maturation: Thymus (T-cell maturation), Bone marrow (B-cell maturation)
- Secondary lymphoid organs — sites of immune response & interaction with pathogen: Spleen, Lymph nodes, Tonsils, Peyer's patches (intestine), MALT (Mucosa-Associated Lymphoid Tissue), Appendix
- Lymph nodes — filter lymph; contain macrophages that destroy pathogens
- Spleen — filters blood, destroys old RBCs, stores blood, immune response
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Disorders of Circulatory System
| Disorder | Cause | Key Features |
| Hypertension | Blood pressure consistently ≥140/90 mmHg; linked to stress, obesity, diet, genetics | Damages blood vessels; leads to heart disease, stroke, kidney failure |
| Coronary Artery Disease (CAD) | Atherosclerosis — deposition of calcium, fat, cholesterol, fibrous tissue in coronary artery walls → narrows lumen → reduced blood flow to heart muscle | Most common heart disease; reduced O₂ supply to myocardium |
| Angina Pectoris | Myocardial ischaemia — insufficient O₂ reaching heart muscle during exertion | Chest pain/pressure radiating to left arm; warning sign of CAD; not a heart attack itself |
| Myocardial Infarction (Heart Attack) | Complete blockage of a coronary artery (by clot/thrombus) → death of heart muscle tissue | Severe chest pain, sweating, breathlessness; emergency — permanent muscle damage if not treated fast |
| Heart Failure | Heart cannot pump blood effectively to meet body's needs; also called Congestive Heart Failure | Fluid accumulation in lungs/limbs, breathlessness, fatigue |
| Cardiac Arrest | Sudden cessation of heart pumping — often due to blockage of main coronary artery | No pulse, unconsciousness; medical emergency — brain damage within 4–6 min |
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Quick Revision — Must-Know Points
Pacemaker → SA Node
Largest WBC → Monocyte (18 μm)
Graveyard of RBC → Spleen
Universal donor → Blood group O
Universal recipient → Blood group AB
RBC lifespan → 120 days
Platelet lifespan → 1 week (7–10 days)
Stroke volume → 70 ml
Cardiac output → ~5 L/min
Normal BP → 120/80 mmHg
P wave → Atrial depolarization
QRS complex → Ventricular depolarization
T wave → Ventricular repolarization
Heparin released by → Basophils
Antibodies (γ-globulin) made by → Plasma cells (B-lymphocytes)
Heart origin → Mesodermal
Serum = Plasma − Fibrinogen
Cardiac cycle duration → 0.8 sec