Mansoura National University · Physiology Department
General Physiology

بسم الله الرحمن الرحيم
مذكرة شاملة لمادة GENERAL PHYSIOLOGY
إعداد متكامل يغطي كامل مقرر الامتحان.

✨ كل محاضرة فيها 5 أقسام
📖
الشرح
🧠
مايند ماب
🫒
الزتونة
أهم النقاط
MCQ
كود التفعيل
4.0 GPA
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مذكرةGeneral Physiology🎯
السعر
100 جنيه
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📚 محتوى المذكرة — 6 محاضرات
Lecture 1 · Blood — Lecture 2 · Respiration 1 — Lecture 3 · Respiration 2 — Lecture 4 · Respiration 3 — Lecture 5 · CVS 1 — Lecture 6 · CVS 2
✨ كل محاضرة فيها 5 أقسام
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❓ MCQ — اختبار تفاعلي 30 سؤال لكل محاضرة
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مذكرة احترافية · FullMark Study Guide

General Physiology

شرح · مايند ماب · الزتونة · أهم النقاط · 30 MCQ لكل محاضرة

6محاضرات
180سؤال MCQ
6مايند ماب
6زتونة
Lecture 1 · Blood
Blood Revision
Composition · Plasma Proteins · RBCs · WBCs · Hemostasis · Blood Transfusion
🩸 Blood — General
Volume
~5 litres
Composition
Plasma 55% + Blood cells 45%
  • Transport: O₂ & CO₂ (RBCs), nutrients, waste, hormones
  • Homeostatic: maintains constant internal environment
  • Hemostatic: platelets prevent blood loss
  • Defense: gamma globulins (antibodies) + WBCs phagocytosis
🧪 Plasma
Water
90%
Solids
Organic 9% + Inorganic 1%
Total Protein
6–8 gm/dL
Albumin
3.5–5 gm/dL — main osmotic pressure
  • Albumin & Globulin: carrier functions + CO₂ transport
  • Fibrinogen & Prothrombin: blood coagulation + viscosity
  • γ-Globulin (antibodies): made by lymphatic tissue
  • Liver: forms all plasma proteins except γ-globulins
🔴 RBCs (Red Blood Corpuscles)
  • Not true cells — no nucleus, no mitochondria
  • Hb = 34% of weight | Chief cation: K⁺
  • Energy from anaerobic glycolysis
  • Contains carbonic anhydrase enzyme (CO₂ transport)
  • Main function: transport O₂ (at Hb) & CO₂
Erythropoiesis sites: Red bone marrow. Infants → all bones. Adults (>20y) → membranous bones (vertebrae, sternum, ribs).
Most important factor: Tissue oxygenation — hypoxia → ↑ erythropoietin (90% kidney, 10% liver)
⚪ WBCs
Normal Count
4000–11,000 /mm³
Type%Function
Neutrophils60–70%1st defense vs bacterial infection
EosinophilsDefense vs parasitic infection
BasophilsRelease heparin & histamine
Lymphocytes20–30%T-cell (cellular immunity), B-cell (antibodies)
MonocytesPhagocytosis of bacteria & old cells
🛑 Hemostasis & Clotting
  • Platelets count: 150,000–400,000/mm³ | Life span: 8–12 days
  • Steps: 1) Vascular spasm → 2) Platelet plug → 3) Blood clot
  • Clot mechanism: Prothrombin activator → Prothrombin → Thrombin → Fibrinogen → Fibrin
HeparinWarfarin
RouteIV injectionOral
MechanismFacilitates antithrombin IIIInhibits Vit K (competitive)
OnsetRapid (minutes)Slow (1–2 days)
AntidoteProtamineVitamin K
💉 Blood Transfusion
  • Dangers: Incompatibility (shock, hyperkalemia, jaundice) | Allergic reactions | Disease transmission (AIDS, hepatitis, malaria)
  • Indications: restore whole blood (hemorrhage), RBCs (anemia), WBCs (leucopenia), platelets (purpura), clotting factors (hemophilia)
🩸 Blood
Composition
Plasma 55% (water 90% + proteins)
Blood cells 45%
RBCs · WBCs · Platelets
Plasma Proteins
Total: 6–8 gm/dL
Albumin → osmotic pressure
γ-Globulin → antibodies
Fibrinogen → coagulation
Liver makes all except γ
RBCs
No nucleus, no mitochondria
Hb = 34% of weight
Anaerobic glycolysis (energy)
Erythropoiesis: red bone marrow
Hypoxia → erythropoietin ↑
WBCs
4000–11,000 /mm³
Neutrophils (60–70%) → bacteria
Lymphocytes (20–30%) → immunity
Basophils → heparin + histamine
Hemostasis
Vascular spasm → Platelet plug → Clot
Heparin: rapid, IV, antidote = protamine
Warfarin: slow, oral, antidote = Vit K
🫒
الزتونة — Blood
سكيمات الامتحان — لو لقيت كذا، اختار كذا
💡
لو سألك عن الـ osmotic pressure أو سبب الـ edema في نقص البروتين
Albumin — it's responsible for maintaining plasma oncotic pressure
نقص الـ albumin → ↓ oncotic pressure → fluid leaks to tissues → edema
💡
لو سألك أي خلية تتأثر أول في حالة hypoxia أو high altitude
Kidney releases erythropoietin (90%) → stimulates RBC production
الترتيب: Hypoxia → Kidney → Erythropoietin → Bone marrow → ↑ RBCs
💡
لو سألك عن الـ antidote بتاع Heparin أو Warfarin
Heparin → Protamine | Warfarin → Vitamin K
Warfarin = inhibits Vit K → antidote = Vit K | Heparin = antithrombin III facilitator → antidote = protamine
💡
لو سألك عن مصدر طاقة الـ RBCs أو سبب عدم وجود mitochondria
RBCs use anaerobic glycolysis — no mitochondria, no nucleus → called corpuscles not cells
💡
لو سألك عن complications of blood transfusion
Incompatibility → Circulatory shock (↓ ABP) + Hyperkalemia (cardiac arrhythmia) + Jaundice
كمان: allergic reactions + disease transmission (AIDS, hepatitis, malaria)
💡
لو سألك مين بيعمل γ-globulins (antibodies)
Lymphatic tissue (plasma cells) — NOT the liver
الكبد بيعمل كل البروتينات ما عدا الـ γ-globulins
1
Plasma

Total plasma proteins = 6–8 gm/dL. Albumin = 3.5–5 gm/dL. Main function of albumin = osmotic pressure.

2
RBCs

No nucleus → called corpuscles. Energy from anaerobic glycolysis. Hb = 34% of weight.

3
Erythropoiesis

Most important factor = tissue oxygenation. Hypoxia → erythropoietin (kidney 90%, liver 10%).

4
WBCs

Neutrophils = 1st line defense. Basophils = heparin + histamine. Lymphocytes = T-cell + B-cell immunity.

5
Anticoagulants

Heparin: IV, rapid, antidote = protamine. Warfarin: oral, slow (1-2 days), antidote = Vitamin K.

6
Clotting

Prothrombin activator → Prothrombin → Thrombin → Fibrinogen → Fibrin clot.

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Lecture 2 · Respiration 1
Physiology of Respiration — Ventilation
Divisions · Anatomy · Pulmonary Ventilation · Pressures · Surfactant · Compliance
🫁 Divisions of Respiration
  • External respiration: pulmonary ventilation + gas exchange at alveoli
  • Respiratory function of blood: carriage of O₂ & CO₂
  • Internal respiration: oxidation of food → energy at cellular level
🌬️ Pulmonary Ventilation
  • Normal rate: 16 breaths/min at rest
  • Inspiration = ACTIVE (diaphragm + external intercostal muscles contract)
  • Expiration = PASSIVE (relaxation → recoil)
  • Diaphragm descends 1.5–7 cm → ↑ vertical diameter
📊 Pressures
PressureNormal Values
Intrapulmonary (alveolar)0 at rest | −2 mmHg inspiration | +2 mmHg expiration
Intrapleural−3 mmHg (end expiration) | −6 mmHg (end inspiration) | −30 mmHg (forced insp.) | +40 mmHg (forced exp. closed glottis)
Importance of negative IPP: helps lung expansion + venous return + lymph flow + pulmonary blood flow
🧴 Surfactant
  • Lipoprotein secreted from Type II alveolar cells
  • ↓ surface tension between air & fluid lining alveoli
  • Functions: ↓ muscular effort + prevent lung collapse + antibacterial
  • Decreases in: premature babies (RDS) | cigarette smoking | cardiac surgery | premature C-section
📏 Compliance
  • Ability of lung & chest to expand per unit ↑ in pressure
  • Normal value: 130 ml/cmH₂O
  • Affected by: elasticity, surfactant, condition of bones & muscles
🔧 Factors Affecting Ventilation
  • 1) Airway resistance (bronchodilation ↓ resistance, bronchoconstriction ↑ resistance)
  • Sympathetic → bronchodilation | Parasympathetic → bronchoconstriction
  • 2) Pressures in thoracic cavity
  • 3) Surfactant
  • 4) Compliance
🫁 Respiration 1 — Ventilation
Divisions
External: ventilation + gas exchange
Blood: O₂ & CO₂ carriage
Internal: cellular oxidation
Breathing Mechanics
Inspiration = ACTIVE (diaphragm + ext. intercostal)
Expiration = PASSIVE (recoil)
Rate = 16/min at rest
Pressures
Intrapulmonary: ±2 mmHg
Intrapleural: always negative
−3 (exp) to −6 (insp)
Surfactant
Type II alveolar cells
↓ surface tension
Prevents collapse
↓ in premature babies, smoking
Autonomic Control
Sympathetic → bronchodilation
Parasympathetic → bronchoconstriction
🫒
الزتونة — Resp 1
سكيمات الامتحان
💡
لو سألك inspiration active ولا passive
Inspiration = ACTIVE (diaphragm + external intercostal muscles contract) | Expiration = PASSIVE
💡
لو سألك عن surfactant مكانه أو وظيفته الأهم
Made by Type II alveolar cells | Most important function = prevent lung collapse
💡
لو سألك bronchial asthma ليه بتضيق الـ airways
↑ Parasympathetic activity → bronchoconstriction → ↑ resistance to airflow
💡
لو سألك intrapleural pressure ليه negative
1) No air in pleural cavity 2) Continuous lung traction against rigid chest wall
💡
لو سألك compliance ومين اللي يأثر عليه
Normal = 130 ml/cmH₂O | Affected by: elasticity + surfactant + bones & muscles condition
1
Active/Passive

Inspiration = Active (muscles contract). Expiration = Passive (muscles relax, recoil).

2
Surfactant

From Type II alveolar cells. ↓ surface tension. Prevents alveolar collapse. ↓ in prematurity & smoking.

3
IPP Values

Intrapleural: −3 (end exp) | −6 (end insp) | −30 (forced insp) | +40 (forced exp closed glottis).

4
Autonomic

Sympathetic → bronchodilation (↓ resistance). Parasympathetic → bronchoconstriction (↑ resistance).

5
Compliance

Normal = 130 ml/cmH₂O. Ability of lung + chest to expand per unit pressure change.

6
IPP Importance

Negative IPP → helps lung expansion + venous return + lymph flow + pulmonary circulation.

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Lecture 3 · Respiration 2
Gas Exchange & Gas Transport
Respiratory Membrane · O₂ Dissociation Curve · O₂ & CO₂ Transport · Hypoxia
🔬 Respiratory Membrane
  • 6 layers: fluid lining → alveolar epithelium → epithelial BM → interstitial space → capillary BM → capillary endothelium
  • Thickness: 0.6 μm | diffusion rate ∝ 1/thickness
  • Surface area: 50–100 m² | diffusion rate ∝ surface area
  • ↓ surface area in: pneumonectomy (half) | emphysema (alveolar wall loss)
🌬️ Gas Properties & V/P Ratio
ParameterPO₂ (mmHg)PCO₂ (mmHg)
Alveolar air10040
Arterial blood10040
Venous blood4046
CO₂ diffuses 20× faster than O₂ (high lipid solubility despite high MW)
V/P ratio = 0.8 (ventilation 4L/min ÷ perfusion 5L/min)
🩸 O₂ Transport
O₂ in physical solution
0.3 ml/100ml (arterial) | 0.13 ml/100ml (venous)
O₂ capacity
20 ml/100ml (15g Hb × 1.33)
O₂ content (arterial)
19.5 ml/100ml
O₂ utilization coefficient
25% at rest | 75% during exercise
O₂ Dissociation Curve shifts RIGHT (Hb gives MORE O₂): ↑PCO₂ | acidosis | ↑temp | ↑2,3-DPG
Shifts LEFT (Hb gives LESS O₂): alkalosis | ↓PCO₂ | ↓temp | CO poisoning
💨 CO₂ Transport
FormArterial CO₂ %Tidal CO₂ %
Physical solution5%10%
Carbamino compounds6%20%
Bicarbonate (HCO₃⁻)89%70%
Arterial CO₂ = 48–52 ml/100ml | Tidal CO₂ = 5ml/100ml added by tissues
⚠️ Hypoxia Types
TypeCauseCyanosis?
HypoxicDefective external resp (high altitude, asthma)Central cyanosis
Anemic↓ Hb amount or functionNo cyanosis
Stagnant↓ tissue blood flow (heart failure, shock)Central or peripheral
HistotoxicEnzyme blockage (cyanide, alcohol poisoning)No cyanosis
🫁 Resp 2 — Gas Exchange & Transport
Resp Membrane
6 layers | thickness 0.6 μm
Surface area 50–100 m²
↓ in emphysema & pneumonectomy
O₂ Transport
98% in chemical combination with Hb
O₂ capacity = 20 ml/100ml
Utilization = 25% rest, 75% exercise
O₂ Curve Shift
Right: ↑CO₂, acidosis, ↑temp, ↑2,3-DPG
Left: alkalosis, ↓CO₂, ↓temp, CO poisoning
CO₂ Transport
89% as bicarbonate (arterial)
70% as bicarbonate (tidal)
CO₂ diffuses 20× faster than O₂
Hypoxia
Hypoxic: external resp defect
Anemic: ↓ Hb (no cyanosis)
Stagnant: ↓ blood flow
Histotoxic: cyanide (no cyanosis)
🫒
الزتونة — Resp 2
سكيمات الامتحان
💡
لو سألك ليه CO₂ بيـdiffuse أسرع من O₂
CO₂ lipid solubility is 24× greater than O₂ → net result: CO₂ diffuses 20× faster
رغم أن MW بتاع CO₂ أكبر بس الـ lipid solubility بتغلب
💡
لو سألك O₂ dissociation curve بتتحرك إيه في muscular exercise
Shifts RIGHT — exercising muscle is acidic + hot + high PCO₂ → Hb releases more O₂
💡
لو سألك CO poisoning — cyanosis بتحصل ولا لأ
No cyanosis — carboxyHb is cherry red in color
💡
لو سألك anemia cyanosis بتحصل ولا لأ
No cyanosis — threshold = 5 gm% reduced Hb, but in anemia total Hb is decreased so can't reach threshold
💡
لو سألك main form of CO₂ transport
Bicarbonate (HCO₃⁻) — 89% of arterial CO₂ | 70% of tidal CO₂
1
CO₂ vs O₂

CO₂ diffuses 20× faster than O₂ (high lipid solubility despite high MW).

2
O₂ Capacity

20 ml/100ml blood. O₂ content: 19.5 arterial | 14.5 venous. Utilization: 25% rest.

3
Curve Shift

Right shift = ↑CO₂, acidosis, ↑temp (exercise). Left shift = CO poisoning, alkalosis.

4
CO₂ Forms

Bicarbonate = 89% (arterial) main form. Physical = 5%. Carbamino = 6%.

5
Cyanosis Rule

No cyanosis in: anemia + histotoxic + CO poisoning (cherry red). Cyanosis in: hypoxic + stagnant.

6
V/P Ratio

Normal = 0.8 (ventilation 4L/min ÷ perfusion 5L/min). Zone I (apex) = 3.3, Zone III (base) = 0.6.

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Lecture 4 · Respiration 3
Regulation of Respiration & Hypoxia
Respiratory Centers · Nervous & Chemical Regulation · Cyanosis
🧠 Respiratory Centers
  • Located bilaterally in the brainstem
  • Medullary: DRG (inspiratory) + VRG (expiratory)
  • Pontine: Apneustic (lower pons) + Pneumotaxic (upper pons)
CenterLocationAction
DRG (inspiratory)Dorsal medullaIntrinsic periodic firing → basic rhythm
VRG (expiratory)Ventral medullaInactive in normal exp. (passive) | active in forced exp.
ApneusticLower 1/3 ponsContinuous excitatory impulses to DRG = pacemaker
PneumotaxicUpper 1/3 ponsInhibitory impulses to apneustic + insp. center
🔄 Generation of Rhythmic Respiration
  • Apneustic → continuous stimulation to DRG
  • Pneumotaxic → inhibits apneustic → stops inspiration
  • DRG sends signals via phrenic nerve (C3,4,5) to diaphragm + intercostal nerves (T1-10)
🧪 Chemical Regulation (MAIN mechanism)
  • ↑CO₂ = most important stimulus for respiration
  • ↑H⁺ (acidosis) → ↑ respiratory rate
  • Hypoxia → stimulates peripheral chemoreceptors
🫀 Nervous Regulation — Reflexes
  • Hering-Breuer reflex: stretch receptors → negative feedback (stops over-inflation)
  • Bainbridge reflex: ↑ venous return → ↑ HR
  • Marey's law: ↑ ABP → ↓ HR (via baroreceptors)
  • Respiratory sinus arrhythmia: inspiration ↑ HR | expiration ↓ HR
🔵 Cyanosis
  • Threshold: 5 gm% reduced Hb in superficial capillaries
  • Cyanosis occurs in: Hypoxic (central) + Stagnant (central or peripheral)
  • NO cyanosis in: histotoxic | anemic | CO poisoning (cherry red carboxyHb)
🧠 Resp 3 — Regulation
Medullary Centers
DRG = inspiratory (basic rhythm)
VRG = expiratory (forced exp only)
Pontine Centers
Apneustic (lower) = pacemaker → excites DRG
Pneumotaxic (upper) = inhibits apneustic
Chemical Regulation
↑CO₂ = MOST IMPORTANT
↑H⁺ (acidosis) → ↑ RR
Hypoxia → peripheral chemoreceptors
Cyanosis
Threshold = 5 gm% reduced Hb
Present: hypoxic + stagnant
Absent: anemic, histotoxic, CO poisoning
🫒
الزتونة — Resp 3
سكيمات الامتحان
💡
لو سألك most important stimulus for respiration
↑CO₂ (hypercapnia) — more important than hypoxia
💡
لو سألك apneustic center لو اتحذف يحصل إيه
Loss of pacemaker → irregular breathing (apneustic breathing = prolonged inspiration)
💡
لو سألك respiratory sinus arrhythmia
Inspiration → ↑ HR | Expiration → ↓ HR
💡
لو سألك VRG (expiratory center) امتى بيتفعّل
Only in forced expiration (active process) — inactive in normal (passive) expiration
💡
لو سألك Hering-Breuer reflex وظيفته
Negative feedback — stretch receptors in lung → stop over-inflation → limit tidal volume
1
Main Stimulus

↑CO₂ = most important respiratory stimulus. Then H⁺, then hypoxia.

2
DRG vs VRG

DRG = basic rhythm (always active). VRG = only in forced expiration.

3
Pontine

Apneustic (lower pons) = pacemaker. Pneumotaxic (upper pons) = inhibits apneustic.

4
Cyanosis

Threshold = 5 gm% reduced Hb. NOT in anemia, histotoxic, CO poisoning.

5
Phrenic Nerve

DRG → phrenic nerve C3,4,5 → diaphragm | intercostal nerves T1–10.

6
Sinus Arrhythmia

Inspiration → ↑ HR | Expiration → ↓ HR (respiratory sinus arrhythmia).

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Lecture 5 · CVS 1
Cardiovascular System & Cardiac Properties
Heart Structure · Conducting System · Cardiac Properties · Action Potential
🫀 CVS Overview
Arteries
Elastic vessels — transport blood to tissues
Arterioles
Resistance vessels
Capillaries
Exchange vessels — very thin walls
Veins
Capacitance vessels — blood to heart
Systemic (General)Pulmonary (Lesser)
Begins atLt ventricle → aortaRt ventricle → pulmonary artery
Ends atSVC/IVC → Rt atriumPulmonary veins → Lt atrium
FunctionRemove waste from tissuesOxygenate the blood
🏗️ Heart Wall & Muscle Fibers
  • 3 layers: Endocardium · Myocardium · Epicardium
  • 3 types of cardiac muscle fibers: Nodal · Conducting · Contractile
Node/StructureLocationRole
SANPosterior wall, Rt atrium (near SVC)Pacemaker — impulse origin (110/min)
AVNRt side of interatrial septumConducts to Bundle of His (90/min)
Bundle of HisAV fibrous ringOnly muscular connection between atria & ventricles
Purkinje fibersTerminal branchesFastest conduction 4 m/sec (35/min rhythm)
⚡ 4 Properties of Cardiac Muscle
Rhythmicity
Regular beating — myogenic (not neurogenic)
Excitability
Ability to respond to stimuli
Conductivity
Spread excitation wave throughout heart
Contractility
Convert energy → mechanical work
⚡ Action Potential Phases
  • Phase 0 (Rapid depol.): fast Na⁺ channels open → rapid Na⁺ influx
  • Phase 1 (Early repol.): Cl⁻ influx + limited K⁺ efflux
  • Phase 2 (Plateau): slow Ca²⁺ channels open → Ca²⁺ influx (unique to cardiac!)
  • Phase 3 (Rapid repol.): K⁺ channels open → rapid K⁺ efflux
  • Phase 4 (Complete repol.): Na-K pump restores resting level
🔀 Conduction Velocities
PathVelocity
Atrial muscle (SAN → AVN)1 m/sec
AV node (delay!)0.1 m/sec (slowest)
Purkinje fibers4 m/sec (fastest)
Ventricular muscle0.4 m/sec
AV node delay allows atria to complete filling ventricles before ventricles contract
🫀 CVS 1 — Heart Structure & Properties
Heart Structure
3 layers: endo/myo/epicardium
3 fiber types: nodal, conducting, contractile
Conducting System
SAN → pacemaker (110/min)
AVN → 90/min | delay 0.1 m/sec
Purkinje → fastest 4 m/sec
4 Properties
Rhythmicity (myogenic)
Excitability
Conductivity
Contractility
Action Potential
Phase 0: Na⁺ in (rapid depol)
Phase 2: Ca²⁺ in (PLATEAU)
Phase 3: K⁺ out (repol)
Vessels
Arterioles = resistance
Capillaries = exchange
Veins = capacitance
🫒
الزتونة — CVS 1
سكيمات الامتحان
💡
لو سألك ليه SAN هو pacemaker
Because it has the highest automaticity (110/min) — it fires before any other tissue
الترتيب: SAN 110 → AVN 90 → Bundle 45 → Purkinje 35 → Ventricles 25
💡
لو Purkinje بقى pacemaker — heart rate هتبقى كام
35/min (its intrinsic rhythm)
💡
لو سألك الـ plateau phase بيحصل ليه — إيه المميز في cardiac
Phase 2: slow Ca²⁺ channels open → Ca²⁺ influx — unique to cardiac muscle (not skeletal)
💡
لو سألك AV node delay ليه مهم
Allows atria to finish contracting and fill ventricles before ventricular contraction starts
💡
لو سألك rhythmicity بتاعت الـ heart — myogenic ولا neurogenic
Myogenic (inherent) — heart beats even if all nerves cut
1
SAN

Normal pacemaker. Highest rhythm = 110/min. Located: posterior wall Rt atrium near SVC.

2
Conduction Speed

Slowest: AVN = 0.1 m/sec. Fastest: Purkinje = 4 m/sec. Atrial muscle = 1 m/sec.

3
Phase 2 (Plateau)

Unique to cardiac muscle — slow Ca²⁺ channels open → prolonged depolarization → prevents tetany.

4
Rhythmicity

Myogenic origin (inherent) — not neurogenic. Heart beats even without neural input.

5
Bundle of His

Only muscular connection between atria and ventricles through the AV fibrous ring.

6
Vessel Types

Arterioles = resistance | Capillaries = exchange | Veins = capacitance.

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Lecture 6 · CVS 2
Cardiac Cycle · Heart Rate · Cardiac Output
Phases of Cardiac Cycle · Nervous & Chemical Regulation of HR · Factors Affecting COP
🔄 Cardiac Cycle
Total duration
0.8 sec
Atrial systole
0.1 sec
Ventricular systole
0.3 sec
Ventricular diastole
0.4 sec
  • Ventricular systole: pressure rises from 0 → 80 mmHg (Lt) or 0 → 10 mmHg (Rt) → opens semilunar valves
  • Ventricular diastole: relaxation → semilunar valves close → AV valves open → ventricular filling
  • Atrial systole pumps 30% of venous return into ventricles
💓 Heart Rate Regulation
Normal HR
70 beats/min in adult male at rest
CenterAction on HR
CAC (Cardioacceleratory)↑ HR via sympathetic
CIC (Cardioinhibitory)↓ HR via parasympathetic
  • Bainbridge reflex: ↑ venous return → ↑ HR (atrial baroreceptors)
  • Marey's law: ↑ ABP → ↓ HR (arterial baroreceptors)
  • Respiratory sinus arrhythmia: Inspiration → ↑ HR | Expiration → ↓ HR
  • Oculocardiac reflex: pressure on eyeball → ↓ HR (vagal)
💊 Chemical & Physical Regulation of HR
↑ HR↓ HR
Atropine (blocks ACh)Bile salts (inhibit SAN directly)
Histamine (↓ ABP → reflex tach.)Morphine (stimulates CIC)
SympathomimeticsParasympathomimetics
Thyroxine (stimulates SAN)↑ blood temperature → +10/min per 1°C (then plateau)
↑ Blood temperature 1°C → ↑ HR by 10 beats/min
📊 Cardiac Output (COP)
COP (normal)
5 litres/min at rest
EDV
110–130 ml (end diastolic)
ESV
40–60 ml (end systolic)
Stroke Volume
SV = EDV − ESV = 70 ml
  • COP = HR × SV
  • ↑ Venous return → ↑ EDV → ↑ stretch → ↑ force → ↑ SV → ↑ COP (Starling's law)
  • Moderate ↑HR → SV ↓ but COP stays constant
  • Extreme ↑HR or extreme ↓HR → ↓ COP
  • ABP: within limits → no change in COP
🫀 CVS 2 — Cardiac Cycle & Output
Cardiac Cycle
Total = 0.8 sec
Atrial systole = 0.1 sec
Ventricular systole = 0.3 sec
Ventricular diastole = 0.4 sec
Heart Rate
Normal = 70/min
Bainbridge: ↑VR → ↑HR
Marey's law: ↑ABP → ↓HR
↑Temp 1°C → ↑10 beats
Cardiac Output
COP = 5 L/min at rest
SV = EDV − ESV = 70 ml
EDV = 110–130 ml
ESV = 40–60 ml
Factors ↑ COP
↑ Venous return (Starling)
Moderate ↑ HR
↑ Contractility
Chemicals Affecting HR
↑HR: Atropine, thyroxine
↓HR: Bile salts, morphine
🫒
الزتونة — CVS 2
سكيمات الامتحان
💡
لو سألك Stroke Volume يتحسب إزاي
SV = EDV − ESV = 130 − 60 = 70 ml
COP = HR × SV = 70 × 70 ≈ 5000 ml = 5 L/min
💡
لو سألك Bainbridge reflex أو لو venous return زاد
↑VR → ↑EDV → stretch → ↑contraction force → ↑SV → ↑COP (Starling's law)
💡
لو سألك bile salts تأثيرها على الـ HR
↓ HR — directly inhibit SAN (not via nerve)
💡
لو سألك adrenaline تأثيرها على HR في الحيوان الحي (in vivo)
Adrenaline → ↑ABP → reflex bradycardia (Marey's law) — in vivo only
In isolated heart: direct ↑ HR
💡
لو سألك ventricular systole — الـ pressure بيوصل لكام
Lt ventricle: 0 → 80 mmHg | Rt ventricle: 0 → 10 mmHg
💡
لو سألك COP ÷ HR = إيه
Stroke Volume (SV)
1
Cardiac Cycle

Total = 0.8 sec. Atrial systole 0.1 | Ventricular systole 0.3 | Ventricular diastole 0.4.

2
COP

Normal = 5 L/min. SV = EDV(130) − ESV(60) = 70 ml. COP = HR × SV.

3
Bainbridge

↑ Venous return → ↑ HR (atrial stretch receptors). Opposite to Marey's law (↑ABP → ↓HR).

4
Temperature

↑ 1°C blood temp → ↑ 10 beats/min HR. Opposite for ↓ temperature.

5
Starling's Law

↑ EDV → ↑ stretch → ↑ force of contraction → ↑ SV → ↑ COP.

6
Ventricular Pressure

Lt ventricle systole: 0 → 80 mmHg. Rt ventricle: 0 → 10 mmHg.

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