Physiology
Medical physiology for MBBS: cell and body fluids, blood, nerve and muscle, and the cardiovascular, respiratory, gastrointestinal, renal, endocrine, reproductive and nervous systems, special senses and integrative physiology.
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Definition
The cardiac cycle is the sequence of events in one heartbeat, made of systole (contraction) and diastole (relaxation); duration ~0.8 s at 72 beats/min.
Phases
- Atrial systole — atria contract, top up ventricles
- Isovolumetric contraction — all valves closed
- Ventricular ejection — semilunar valves open
- Isovolumetric relaxation — all valves closed
- Ventricular filling — AV valves open
Key Events
- AV valves close → S1; semilunar valves close → S2
- Stroke volume ~70 mL
- End-diastolic volume ~120 mL; end-systolic ~50 mL
One beat: fill → contract (valves shut) → eject → relax → fill again. Phase Duration Valves Atrial systole 0.1 s AV open Isovol. contraction 0.05 s All closed Ejection 0.3 s Semilunar open Isovol. relaxation 0.08 s All closed Filling 0.5 s AV open Applied
- Basis of heart sounds and murmurs
- Pressure–volume loop
- Valve disease alters the phases
🔑KEY POINTS TO REMEMBER- Cardiac cycle = systole + diastole (~0.8 s).
- S1 = AV valves close (start systole); S2 = semilunar close (start diastole).
- EDV ~120, ESV ~50, stroke volume ~70 mL.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Cardiac output (CO) is the blood pumped by each ventricle per minute; CO = heart rate × stroke volume (~5 L/min at rest).
Determinants
- Heart rate — autonomic nerves, adrenaline
- Stroke volume — preload, contractility, afterload
Stroke Volume Factors
- Preload — venous return (Frank–Starling)
- Contractility — sympathetic, adrenaline
- Afterload — arterial resistance (↑ afterload → ↓ SV)
Regulation
- Intrinsic — Frank–Starling law
- Extrinsic — autonomic nerves, hormones
- ↑ in exercise (up to 20–25 L/min)
Output rises by increasing rate or stroke volume. Factor Effect on CO ↑ Heart rate ↑ CO ↑ Preload ↑ SV → ↑ CO ↑ Contractility ↑ CO ↑ Afterload ↓ SV Applied
- Cardiac index = CO / body surface area
- ↓ CO in heart failure and shock
- Ejection fraction ~60%
🔑KEY POINTS TO REMEMBER- CO = HR × SV (~5 L/min).
- SV set by preload, contractility, afterload.
- Regulated intrinsically (Frank–Starling) & extrinsically (autonomic).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The electrocardiogram (ECG) is a graphic record of the electrical activity of the heart recorded from the body surface.
Waves & Meaning
- P wave — atrial depolarisation
- QRS complex — ventricular depolarisation
- T wave — ventricular repolarisation
Intervals
- PR interval (0.12–0.2 s) — AV conduction
- QRS (<0.12 s) — ventricular activation
- QT interval — total ventricular activity
The ECG maps the electrical journey: P (atria), QRS (ventricles), T (recovery). Wave/Interval Represents Duration P Atrial depolarisation 0.1 s PR AV conduction 0.12–0.2 s QRS Ventricular depol. <0.12 s T Ventricular repol. 0.2 s Applied (Uses)
- Arrhythmias and heart block
- Myocardial infarction (ST/T changes)
- Chamber enlargement; electrolyte effects (K⁺)
🔑KEY POINTS TO REMEMBER- ECG = electrical record of the heart.
- P = atrial depol; QRS = ventricular depol; T = ventricular repol.
- PR 0.12–0.2 s; QRS <0.12 s.
- Used for arrhythmia, MI, block.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Blood pressure (BP) is the lateral pressure of blood on the arterial wall (~120/80 mmHg). BP = cardiac output × peripheral resistance.
Determinants
- Cardiac output
- Peripheral resistance
- Blood volume, viscosity, vessel elasticity
Short-term Regulation (nervous)
- Baroreceptor reflex — rapid, via medulla
- Chemoreceptors
- Acts within seconds
Long-term Regulation (renal/hormonal)
- Kidney — salt and water balance
- RAAS (renin–angiotensin–aldosterone)
- ADH, ANP
- Acts over hours to days
A fast neural system and a slow renal/hormonal system keep BP steady. Type Mechanism Time Short-term Baroreceptor reflex Seconds Intermediate RAAS, capillary shift Minutes–hours Long-term Renal Na/water Hours–days Applied
- Hypertension → stroke, IHD, renal failure
- Antihypertensive drugs target these mechanisms
🔑KEY POINTS TO REMEMBER- BP = CO × peripheral resistance (~120/80).
- Short-term: baroreceptor reflex (seconds).
- Long-term: kidney & RAAS (hours–days).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The conduction system generates and conducts impulses so the heart beats rhythmically without external stimulation (autorhythmicity).
Components (in order)
- SA node — pacemaker (right atrium)
- AV node — delays the impulse
- Bundle of His → right & left bundle branches
- Purkinje fibres → ventricular muscle
Pacemaker Hierarchy
- SA node ~70–80/min (dominant)
- AV node ~40–60/min
- Purkinje ~20–40/min (escape)
Properties of Cardiac Muscle
- Rhythmicity (autorhythmic)
- Excitability, conductivity, contractility
- Long refractory period (cannot be tetanised)
- Functional syncytium (all-or-none)
Impulse: SA → atria → AV (delay) → His → Purkinje → ventricles. Pacemaker Rate/min SA node 70–80 AV node 40–60 Purkinje 20–40 Applied
- SA node failure → AV node takes over
- Heart block → may need a pacemaker
- Long refractory period prevents tetanus
🔑KEY POINTS TO REMEMBER- Conduction: SA → AV (delay) → His → bundle branches → Purkinje.
- SA node is the pacemaker (fastest); overdrive-suppresses others.
- Cardiac muscle: autorhythmic, long refractory, functional syncytium.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Heart sounds are produced during the cardiac cycle by closure of the heart valves, heard as ‘lub-dub’.
The Sounds
- S1 (‘lub’) — AV valves close; start of systole
- S2 (‘dub’) — semilunar valves close; start of diastole
- S3 — rapid ventricular filling (may be normal in children)
- S4 — atrial contraction (usually abnormal)
S1 marks the start of systole, S2 the start of diastole. Sound Cause Timing S1 AV valves close Start systole S2 Semilunar close Start diastole S3 Rapid filling Early diastole S4 Atrial contraction Late diastole Applied
- Murmurs → valve stenosis or regurgitation
- Each valve has a specific auscultation area
🔑KEY POINTS TO REMEMBER- S1 = AV valves close (systole); S2 = semilunar close (diastole).
- S3/S4 = filling/atrial contraction (often abnormal).
- Murmurs indicate valve disease.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The Frank–Starling law states that the greater the stretch of cardiac muscle (preload), the stronger its contraction — the more the heart fills, the more it pumps.
Mechanism
- ↑ Venous return → ↑ end-diastolic volume
- → greater stretch of cardiac fibres
- → better actin–myosin overlap
- → stronger contraction → ↑ stroke volume
A fuller heart contracts harder — automatically matching venous return. Significance
- Matches output of the two ventricles
- Adjusts to venous return automatically (no nerves)
- Basis of the ventricular function curve
Applied
- Fails in heart failure (over-stretched heart)
- Explains the response to exercise
Condition Effect ↑ Venous return ↑ stretch → ↑ stroke volume ↓ Venous return ↓ stroke volume Heart failure Mechanism exhausted 🔑KEY POINTS TO REMEMBER- Frank–Starling: ↑ preload → stronger contraction → ↑ SV.
- Balances the two ventricles automatically.
- Exhausted in heart failure.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The baroreceptor reflex is a rapid negative-feedback mechanism that buffers short-term blood-pressure changes via stretch receptors in the carotid sinus and aortic arch.
Pathway
- Baroreceptors sense BP (carotid sinus, aortic arch)
- Afferents → vasomotor centre (medulla)
- ↑ BP → ↑ vagal, ↓ sympathetic → ↓ HR, vasodilation
- ↓ BP → the opposite
Baroreceptors let the medulla correct blood pressure within seconds. BP change Reflex response ↑ BP ↓ HR, vasodilation → BP falls ↓ BP ↑ HR, vasoconstriction → BP rises Applied
- Prevents fainting on standing (postural change)
- Impaired in the elderly → postural hypotension
🔑KEY POINTS TO REMEMBER- Baroreceptor reflex = fast negative feedback for BP.
- Sensors in carotid sinus & aortic arch → medulla.
- ↑ BP → ↓ HR + vasodilation (and vice versa).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The coronary circulation supplies the heart muscle via the right and left coronary arteries arising from the aorta.
Features
- Coronary arteries arise from the aortic sinuses
- Left coronary → LAD + circumflex
- Right coronary → SA/AV node (usually)
- Flow occurs mainly in diastole
- High oxygen extraction (~70%)
Why Flow Is Diastolic
- Systole compresses the coronary vessels
- So most flow occurs during diastole
- Tachycardia (short diastole) → ↓ coronary flow
The heart is perfused mainly in diastole; blockage starves the muscle. Applied
- Atherosclerosis → angina
- Complete block → myocardial infarction
- Coronary end-arteries → poor collateral supply
Artery Supplies Left (LAD) Anterior LV, septum Circumflex Lateral LV Right coronary RV, SA/AV node 🔑KEY POINTS TO REMEMBER- Coronary supply: right & left coronary arteries from aorta.
- Flow mainly in diastole; ~70% O₂ extraction.
- Block → angina (partial) or MI (complete).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The sinoatrial (SA) node is the natural pacemaker of the heart, in the upper right atrium, setting the heart rate (~70–80/min).
Pacemaker Activity
- Unstable resting potential (‘prepotential’)
- Slow Na⁺ (funny) current drifts to threshold
- Ca²⁺ influx → depolarisation
- Fires automatically and rhythmically
Why the SA Node Leads
- Fastest intrinsic rate
- Overdrive-suppresses slower pacemakers
- Sets the pace for the whole heart
The SA node depolarises spontaneously and fastest, so it drives the heart. Autonomic Control
- Sympathetic → ↑ rate (tachycardia)
- Vagus → ↓ rate (bradycardia)
Stimulus Effect on SA node Sympathetic ↑ rate (tachycardia) Vagus ↓ rate (bradycardia) Adrenaline ↑ rate 🔑KEY POINTS TO REMEMBER- SA node = pacemaker (right atrium, ~70–80/min).
- Unstable prepotential → spontaneous firing.
- Sympathetic ↑ rate, vagus ↓ rate.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Pulse pressure = systolic − diastolic (~40 mmHg). Mean arterial pressure (MAP) is the average pressure driving blood through the circulation.
Formulae
- Pulse pressure = SBP − DBP (120 − 80 = 40)
- MAP = DBP + 1/3 × pulse pressure ≈ 93 mmHg
- MAP = CO × systemic vascular resistance
Significance
- MAP weighted toward diastole (which lasts longer)
- MAP = true perfusion pressure of organs
- Must stay > ~60 mmHg to perfuse brain and kidney
MAP is weighted toward diastole and is the real perfusion pressure. Parameter Value Systolic 120 mmHg Diastolic 80 mmHg Pulse pressure 40 mmHg MAP ~93 mmHg Applied
- ↑ Pulse pressure — aortic stiffening, aortic regurgitation
- ↓ MAP → shock, poor organ perfusion
🔑KEY POINTS TO REMEMBER- Pulse pressure = SBP − DBP (~40 mmHg).
- MAP = DBP + 1/3 PP ≈ 93 mmHg = perfusion pressure.
- MAP must stay >60 mmHg for organ perfusion.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Capillary fluid exchange is governed by Starling forces — the balance of hydrostatic and oncotic pressures across the capillary wall.
The Forces
- Capillary hydrostatic pressure — pushes fluid OUT
- Plasma oncotic pressure — pulls fluid IN
- Interstitial hydrostatic & oncotic pressures (minor)
Net Effect
- Arterial end — hydrostatic > oncotic → filtration (out)
- Venous end — oncotic > hydrostatic → reabsorption (in)
- Excess fluid drained by lymphatics
Fluid leaves at the arterial end and mostly returns at the venous end. End Dominant force Fluid movement Arterial Hydrostatic Out (filtration) Venous Oncotic In (reabsorption) Applied (Oedema)
- ↑ Hydrostatic — heart failure
- ↓ Oncotic — low albumin (liver/kidney)
- Lymphatic block — filariasis
🔑KEY POINTS TO REMEMBER- Starling forces: hydrostatic (out) vs oncotic (in).
- Filtration at arterial end, reabsorption at venous end.
- Imbalance → oedema (↑ hydrostatic, ↓ oncotic, lymph block).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).