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Here are your comprehensive, exam-oriented CVS Physiology notes for MBBS 1st Year β€” short-answer format with diagrams described.

πŸ«€ Cardiovascular System Physiology

MBBS 1st Year β€” Exam-Oriented Notes

(Source: Costanzo Physiology 7e, Guyton & Hall, Ganong's)

1. CARDIAC ACTION POTENTIAL

Q. Describe the phases of ventricular action potential with ionic basis.

The ventricular (and atrial/Purkinje) action potential has 5 phases (0–4):
PhaseNameIon MovementCurrent
0Upstroke (rapid depolarization)Na⁺ rushes inFast inward INa
1Initial repolarizationNa⁺ inactivates; K⁺ flows outIto (transient outward K⁺)
2PlateauCa²⁺ flows in (L-type channels) balances K⁺ outflowICa (slow inward)
3Rapid repolarizationK⁺ flows out rapidly; Ca²⁺ channels closeIK (delayed rectifier K⁺)
4Resting membrane potentialStable at –85 to –90 mV (K⁺ equilibrium)IK1 (inward rectifier)
Key points:
  • Resting membrane potential is maintained by K⁺ (high gK at rest)
  • Na⁺-K⁺ ATPase maintains concentration gradients but has minor direct effect
  • Long plateau β†’ long refractory period β†’ prevents tetany (crucial for pumping)
  • Action potential duration: Atrium = 150 ms, Ventricle = 250 ms, Purkinje = 300 ms

Q. Compare ventricular and SA nodal action potentials.

FeatureVentricular APSA Nodal AP
Resting potential–85 to –90 mV (stable)–55 to –60 mV (unstable)
UpstrokeFast (Na⁺)Slow (Ca²⁺)
PlateauPresent (Ca²⁺)Absent
Phase 4Flat (no spontaneous depol.)Spontaneous depolarization (If = "funny" Na⁺ current)
dV/dTHigh (~300 V/s)Low (~10 V/s)
Diagram: Three action potential waveforms side-by-side (ventricle, atrium, SA node). Ventricle shows sharp upstroke + broad plateau. SA node shows slow upstroke with a sloping phase 4 (pacemaker potential). Atrium is intermediate β€” sharp upstroke, shorter plateau than ventricle. (Fig. 4.12, Costanzo)

Q. What is the pacemaker potential? Explain automaticity of SA node.

  • Phase 4 of SA node is not flat β€” it spontaneously depolarizes toward threshold
  • This is driven by the If (funny) current β€” inward Na⁺ current activated by hyperpolarization
  • Once threshold (~–40 mV) is reached, L-type Ca²⁺ channels open β†’ upstroke
  • SA node fires at 60–100/min β†’ normal sinus rhythm
  • Automaticity hierarchy: SA node (60–100) > AV node (40–60) > Purkinje (20–40)
  • SA node is dominant because it fires fastest and resets all lower pacemakers

2. CONDUCTION SYSTEM OF THE HEART

Q. Describe the conduction pathway and velocities in the heart.

Pathway: SA node β†’ atrial muscle β†’ AV node β†’ Bundle of His β†’ Left & Right bundle branches β†’ Purkinje fibres β†’ ventricular muscle
StructureConduction VelocitySignificance
SA Node0.05 m/sPacemaker
Atrial muscle0.3–1.0 m/sFast spread across atria
AV Node0.01–0.05 m/s (slowest)AV delay (100 ms) β€” allows atria to empty before ventricles contract
Bundle of His1–4 m/sFast
Purkinje fibres2–4 m/s (fastest)Rapid, simultaneous ventricular activation for efficient ejection
Diagram: Heart schematic showing SA node (right atrium), conduction to AV node, His bundle, then branching into left and right bundle branches down the interventricular septum, ending in Purkinje fibre network spreading to subendocardium of both ventricles. Numbers in milliseconds (0 at SA node, 30 ms at AV node entry, 130 ms at AV node exit, 220 ms at farthest Purkinje branches) show total activation time. (Fig. 4.14, Costanzo)
AV delay function: Ensures complete atrial emptying into ventricles before ventricular contraction begins.

3. THE CARDIAC CYCLE

Q. Describe the events of the cardiac cycle. (Most asked question)

The cardiac cycle has 7 phases, best correlated with ECG, pressure-volume changes, valve movements, and heart sounds simultaneously.
PhaseEventsECGValvesHeart Sound
A Atrial SystoleAtria contract; final ventricular filling; LV pressure shows small rise ("a" wave in venous pulse)P waveMV openS4 (not normal)
B Isovolumetric Ventricular ContractionVentricles contract; all valves closed; LV pressure rises sharply; no change in volumeQRSMV closesS1 ("lub")
C Rapid Ventricular EjectionLV pressure peaks; blood ejected fast; aortic pressure rises to maxST segmentAortic valve opensβ€”
D Reduced Ventricular EjectionSlower ejection; LV volume reaches minimum (ESV)T waveβ€”β€”
E Isovolumetric Ventricular RelaxationVentricles relax; all valves closed; LV pressure falls; no change in volumeβ€”Aortic valve closesS2 ("dub")
F Rapid Ventricular FillingVentricles fill passively; LV volume rises; low LV pressureβ€”MV opensS3 (not normal)
G Reduced Ventricular Filling (Diastasis)Slow filling; cycle awaits next P waveβ€”β€”β€”
Diagram (Wiggers Diagram): Multi-panel graph with shared time axis. Top panel: ECG (P, QRS, T). Second panel: Pressure curves β€” Aortic pressure (highest, 80–120 mmHg), Left ventricular pressure (rises sharply in systole, falls in diastole), Left atrial pressure (low, shows a, c, v waves). Third panel: Left ventricular volume curve (rises in diastole from ~70 mL ESV to ~140 mL EDV, then falls during ejection). Fourth panel: Heart sounds (S1 at isovolumetric contraction, S2 at isovolumetric relaxation). Vertical lines separate the 7 phases A–G. (Table 4.5, Costanzo β€” the single most important CVS diagram for exams)
Key values to remember:
  • EDV = 140 mL, ESV = 70 mL, Stroke Volume = 70 mL
  • Ejection Fraction = SV/EDV = 70/140 = 0.5 (50%) β€” normal >55%

4. HEART SOUNDS

Q. What are the causes of heart sounds S1, S2, S3, S4?

SoundTimingCauseHeard best atClinical note
S1 "lub"Start of systole (isovolumetric contraction)Closure of mitral + tricuspid (AV) valves; vibration of taut valves, chordae, and ventricular wallsApexLoud in MS with mobile valve; soft in MS with calcified valve
S2 "dub"End of systole (isovolumetric relaxation)Closure of aortic + pulmonary (semilunar) valvesAortic/pulmonary areaPhysiological splitting on inspiration (A2 before P2)
S3Early diastole (rapid filling)Rapid deceleration of blood hitting ventricular wall during fast fillingApexNormal in children/young adults; Pathological = dilated cardiomyopathy, HF (ventricular gallop)
S4Late diastole (atrial systole)Atrial contraction pushing blood into stiff, non-compliant ventricleApexAlways pathological; seen in LVH, hypertension, hypertrophic cardiomyopathy (atrial gallop)
S2 Splitting: On inspiration β†’ increased venous return to RV β†’ RV takes longer to eject β†’ P2 delayed β†’ A2 and P2 are heard separately ("split S2"). On expiration they merge.

5. CARDIAC OUTPUT

Q. Define cardiac output. Explain factors determining it.

Cardiac Output (CO) = Volume of blood ejected by each ventricle per minute
$$\text{CO} = \text{Stroke Volume (SV)} \times \text{Heart Rate (HR)}$$
  • Normal CO = 70 mL Γ— 72 beats/min β‰ˆ 5 L/min (at rest)
  • Cardiac Index = CO / BSA = ~3.2 L/min/mΒ²
Stroke Volume is determined by 3 factors:
FactorDefinitionEffect on SV
PreloadEnd-diastolic volume (EDV); amount of ventricular stretch before contraction↑ Preload β†’ ↑ SV (Frank-Starling)
AfterloadResistance the ventricle must overcome to eject blood (= aortic pressure / TPR)↑ Afterload β†’ ↓ SV
ContractilityIntrinsic force of contraction at a given preload (inotropy)↑ Contractility β†’ ↑ SV

Q. State and explain the Frank-Starling Law of the Heart.

Law: The stroke volume ejected by the ventricle is directly proportional to the end-diastolic volume (venous return).
Mechanism:
  • ↑ Venous return β†’ ↑ EDV β†’ ↑ stretch of ventricular muscle fibres
  • Greater stretch β†’ better overlap of actin-myosin β†’ more crossbridges formed β†’ stronger contraction β†’ ↑ SV
  • This ensures cardiac output = venous return in steady state (right and left sides are balanced)
Diagram (Frank-Starling curve): X-axis = EDV or right atrial pressure (preload). Y-axis = Stroke volume or CO. Curve rises steeply then plateaus. A second curve shifted upward = increased contractility (e.g., sympathetic stimulation, positive inotropes). A curve shifted downward = decreased contractility (e.g., heart failure).
Clinically: Heart failure = depressed Frank-Starling curve. Inotropes (digoxin, dobutamine) shift curve upward.

6. REGULATION OF ARTERIAL BLOOD PRESSURE

Q. What is mean arterial pressure? How is it regulated?

$$\text{MAP} = \text{CO} \times \text{TPR}$$ $$\text{MAP} \approx \text{Diastolic BP} + \frac{1}{3}(\text{Pulse Pressure})$$
Normal MAP = 70–105 mmHg (approximately 93 mmHg)
Regulation mechanisms:
  1. Short-term (seconds): Baroreceptor reflex (most important)
  2. Medium-term (hours): Renin-Angiotensin-Aldosterone System (RAAS), chemoreceptors
  3. Long-term (days): Renal fluid control (Guyton pressure-natriuresis)

Q. Describe the baroreceptor reflex. (Frequently asked)

Baroreceptors: Stretch-sensitive mechanoreceptors located in:
  • Carotid sinus (where common carotid bifurcates) β€” sensitive to both ↑ and ↓ BP
  • Aortic arch β€” sensitive mainly to ↑ BP
Afferent pathway:
  • Carotid sinus β†’ Carotid sinus nerve β†’ Glossopharyngeal nerve (CN IX) β†’ Nucleus Tractus Solitarius (NTS), medulla
  • Aortic arch β†’ Vagus nerve (CN X) β†’ NTS, medulla
Response to ↑ Blood Pressure:
↑ BP β†’ ↑ Baroreceptor stretch β†’ ↑ Firing rate in CN IX/X
β†’ Medulla: ↓ Sympathetic output + ↑ Parasympathetic (vagal) output
β†’ ↓ HR (vagus on SA node) + ↓ Contractility + Vasodilation (↓ TPR)
β†’ BP falls back to normal
Response to ↓ Blood Pressure (e.g., haemorrhage):
  • ↓ Baroreceptor firing β†’ ↑ Sympathetic + ↓ Parasympathetic
  • β†’ ↑ HR, ↑ Contractility, Vasoconstriction β†’ restores BP
Diagram: Reflex arc diagram showing: Carotid sinus/aortic arch β†’ CN IX/X β†’ NTS in medulla β†’ vasomotor centre β†’ sympathetic chain (efferent) to heart (SA node, AV node, ventricles) and blood vessels. Separate vagal efferent to SA node. Arrows showing response to ↑ BP (inhibitory pathway dashed lines). (Fig. 4.31, Costanzo)
Important: Baroreceptors respond most strongly to rapid changes in BP. In chronic hypertension, baroreceptors are reset to a higher set point β†’ they fail to correct hypertension.

7. JUGULAR VENOUS PULSE (JVP)

Q. Describe the waves of JVP and their significance.

JVP reflects right atrial pressure changes and is visible in the internal jugular vein.
WaveCauseCorresponds to
a waveAtrial contractionP wave on ECG
c waveTricuspid valve closure; slight backward bulgeEnd of QRS
x descentAtrial relaxation + downward displacement of tricuspid annulus during ventricular systoleAfter c wave
v waveVenous filling of atrium while tricuspid is closed (during ventricular systole)T wave on ECG
y descentOpening of tricuspid valve β†’ blood flows from RA to RVAfter v wave
Pathological changes:
  • Absent a wave β†’ Atrial fibrillation
  • Giant a wave β†’ Tricuspid stenosis, pulmonary hypertension (atrium contracts against resistance)
  • Cannon a waves (irregular giant a) β†’ Complete heart block (atria contract against closed tricuspid)
  • Giant v wave β†’ Tricuspid regurgitation
  • Absent x descent β†’ Tricuspid regurgitation
  • Absent y descent β†’ Cardiac tamponade, constrictive pericarditis

8. PRESSURE-VOLUME LOOP

Q. Draw and describe the ventricular pressure-volume loop.

Diagram description: Plot of LV pressure (y-axis, 0–120 mmHg) vs LV volume (x-axis, 50–150 mL). The loop is traced anti-clockwise:
  • Bottom right corner (EDV ~140 mL, low pressure ~10 mmHg) = End of diastole / MV closes β†’ start of isovolumetric contraction (vertical line going up)
  • Top right corner β†’ Aortic valve opens β†’ ejection phase (pressure peaks at ~120 mmHg, volume falls to ESV ~70 mL)
  • Top left corner (ESV ~70 mL, ~80 mmHg) = Aortic valve closes β†’ isovolumetric relaxation (vertical line going down)
  • Bottom left corner β†’ MV opens β†’ filling phase (volume rises from ESV back to EDV at low pressure)
  • Width of loop = Stroke volume; Area of loop = Stroke work
Changes in loop:
  • ↑ Preload β†’ loop shifts right (wider)
  • ↑ Afterload β†’ loop taller, narrower (less SV)
  • ↑ Contractility β†’ loop shifts left + taller (more efficient ejection)

9. QUICK-RECALL TABLES

Normal CVS Values (Must Memorize)

ParameterValue
HR60–100 beats/min
SV70 mL
CO~5 L/min
EDV120–140 mL
ESV50–70 mL
EF55–75% (normal >55%)
MAP70–105 mmHg
Systolic BP120 mmHg
Diastolic BP80 mmHg
Pulse Pressure40 mmHg

Drugs and CVS Effects

DrugHRContractilityNotes
Adrenaline↑↑β1 + Ξ²2 + Ξ±
NoradrenalineReflex ↓ (vagal)↑α dominant, ↑ TPR
Atropine↑—Blocks vagus (M2 blocker)
Digoxin↓↑Na/K ATPase inhibitor; +ive inotrope
Ξ²-blockers↓↓Blocks Ξ²1

10. HIGH-YIELD EXAM POINTS

TopicKey Fact
Isovolumetric phasesAll 4 valves closed; volume doesn't change
S1MV + TV closure = start of systole
S2Aortic + Pulmonary closure = end of systole
S3 (pathological)HF, dilated CM β€” "ventricular gallop"
S4 (always pathological)Stiff ventricle β€” "atrial gallop"
AV delaySlowest conduction (AV node, 0.01–0.05 m/s); 100 ms; allows ventricular filling
Purkinje fibersFastest conduction (2–4 m/s); simultaneous ventricular activation
SA node upstrokeCa²⁺ (not Na⁺)
Plateau (phase 2)Ca²⁺ in = K⁺ out; prevents tetany
Frank-Starling↑ EDV β†’ ↑ SV; ensures CO = venous return
Baroreceptor afferentCN IX (carotid sinus), CN X (aortic arch)
Baroreceptor resetIn chronic HTN β†’ fails to correct elevated BP
EF normal>55%; in HF with reduced EF = <40%
Sources: Costanzo Physiology 7th Edition | Guyton & Hall Textbook of Medical Physiology | Ganong's Review of Medical Physiology 26th Ed.
These notes cover the highest-yield CVS topics for MBBS 1st year university exams. Let me know if you want me to expand any section, add MCQs, or cover additional topics like microcirculation, coronary circulation, or fetal circulation.
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