Cardiac – Physiology · FCPS Part 1

One Liners

Superficial Cardiac Plexus supplied by - Left Vagus Nerve
Deep Cardiac Plexus supplied by - Left and Right Vagus nerve
Pulmonary Valve opens when pressure in RV exceeds - 8 mmHg

Stroke volume, cardiac output and ejection fraction

Parameter	Formula	Typical resting value
Stroke volume (SV)	EDV − ESV	Approximately 70 mL/beat
Cardiac output (CO)	Heart rate × SV	Approximately 5 L/min
Ejection fraction (EF)	SV ÷ EDV × 100	Approximately 55–60%
End-diastolic volume (EDV)	Volume in ventricle at end of filling	Approximately 110–120 mL
End-systolic volume (ESV)	Volume remaining after ejection	Approximately 40–50 mL

Cardiac cycle

The cardiac cycle describes the sequence of filling, contraction, ejection and relaxation during one heartbeat.

Phase	Valve status	Main event
1. Atrial systole	AV valves open; semilunar valves closed	Atrial contraction completes ventricular filling
2. Isovolumetric contraction	All valves closed	Ventricular pressure rises; volume remains constant
3. Rapid ejection	Semilunar valves open; AV valves closed	Blood is rapidly ejected into the aorta and pulmonary artery
4. Reduced ejection	Semilunar valves remain open until ventricular pressure falls below arterial pressure	Ejection slows
5. Isovolumetric relaxation	All valves closed	Ventricular pressure falls; volume remains constant
6. Rapid filling	AV valves open; semilunar valves closed	Blood flows rapidly into ventricles
7. Reduced filling (diastasis)	AV valves open; semilunar valves closed	Passive filling slows before the next atrial systole

Valve	Location	Main function
Tricuspid	Right atrium → right ventricle	Prevents regurgitation into right atrium during systole
Mitral (bicuspid)	Left atrium → left ventricle	Prevents regurgitation into left atrium during systole
Pulmonary	Right ventricle → pulmonary artery	Prevents backflow into right ventricle during diastole
Aortic	Left ventricle → aorta	Prevents backflow into left ventricle during diastole

Chordae tendineae and papillary muscles stabilise the AV valves during ventricular systole and prevent valve prolapse. They do not actively close the valves; pressure differences drive valve movement.

Ventricular filling, preload and afterload

Term	Definition	Main influence
Preload	Initial myocardial stretch before contraction; often approximated by EDV or end-diastolic pressure	Venous return and ventricular filling
Afterload	Load the ventricle must overcome to eject blood	Arterial pressure and ventricular wall stress
Contractility	Intrinsic force-generating ability at a given initial muscle length	Ca²⁺ handling and sympathetic stimulation
Stroke volume	Volume ejected per beat	Preload, afterload and contractility

HB Dissociation Curve

1. The Sigmoidal (S-shaped) Curve
Unlike many simple chemical bindings, the curve is sigmoidal (S-shaped) due to a phenomenon called cooperative binding:
• The first step is the hardest: When hemoglobin has no oxygen bound to it, its affinity for the first O2 molecule is relatively low.
• The domino effect: Once the first O2 binds, it induces a conformational change (from the tense "T" state to the relaxed "R" state) that makes it much easier for the second, third, and fourth O2 molecules to bind.
• The plateau: At very high PO2 (like in the lungs), hemoglobin becomes almost fully saturated (approx 97-100%), so the curve flattens out.

Factor	Right Shift ➡️ (Unloads O2 easily)	Left Shift ⬅️ (Holds O2 tightly)
pH	Decreased (Acidic)	Increased (Alkaline)
PCO_2	Increased	Decreased
Temperature	Increased	Decreased
2,3-DPG	Increased	Decreased
P50 value	Increased	Decreased

Heart Sounds

S1 ("Lubb"): Caused by the closure of the mitral and tricuspid (AV) valves at the beginning of systole.
S2 ("Dupp"): Caused by the closure of the aortic and pulmonary (semilunar) valves at the end of systole (start of diastole).
S3: Caused by rapid ventricular filling in early diastole.
S4: Caused by atrial contraction ("atrial kick") pushing blood into a stiff, non-compliant ventricle in late diastole (associated with ventricular hypertrophy or active ischemia).

Comparison Table of Cardiac Phases

Cardiac Cycle Phase	Aortic Pressure	Ventricular Volume	Status of Valves
Isovolumic contraction	Moderate / Rising	Highest (End-Diastolic Volume)	All valves closed
Rapid ejection phase	Highest (Dynamic Peak)	Decreasing Rapidly	Aortic/Pulmonary open; AV closed
Isovolumic relaxation	High (Post-ejection load)	Lowest (End-Systolic Volume)	All valves closed
Rapid filling phase	Decreasing	Increasing Rapidly	AV open; Aortic/Pulmonary closed
Slow filling phase	Lowest (Baseline decay)	Increasing Slowly	AV open; Aortic/Pulmonary closed

The Cushing reflex (or Cushing triad)

is a life-saving, last-resort nervous system response to dangerously high intracranial pressure (ICP), such as from a brain bleed, tumor, or trauma.
1. The Squeeze: When ICP rises above your mean arterial blood pressure, it physically compresses the blood vessels inside the brain, cutting off normal blood flow.
2. Brain Ischemia: This lack of blood flow causes local ischemia (oxygen deprivation) and a massive buildup of CO_2 right inside the brain's vasomotor center (medulla).
3. The Sympathetic Surge: In a desperate attempt to force blood back into the brain, the sympathetic nervous system goes into overdrive. It causes intense, widespread systemic vasoconstriction.
4. Massive Hypertension: This vasoconstriction spikes your systemic blood pressure higher than the intracranial pressure, so blood can physically penetrate the skull again.

Conduction Pathway

Tissue	Main function	Conduction characteristic
SA node	Initiates normal heartbeat	Spontaneous pacemaker activity
AV node	Delays conduction before ventricular activation	Slowest conduction
Bundle of His	Conducts impulses into ventricles	Connects atrial and ventricular conduction systems
Bundle branches	Carry impulses down the interventricular septum	Rapid conduction
Purkinje fibres	Distribute impulses throughout ventricular myocardium	Fastest conduction

Why is AV nodal delay important? It allows atrial contraction to contribute to ventricular filling before ventricular systole begins.

ECG

ECG Feature	Start Point	End Point	What it Clinically Represents
PR segment	End of P wave	Start of QRS complex	Conduction delay through the AV node (isoelectric line).
PR interval	Start of P wave	Start of QRS complex	Time for electrical impulse to travel from atria to ventricles.
ST segment	End of QRS complex (J-point)	Start of T wave	Ventricles are completely depolarized (plateau phase of action potential).
QT interval	Start of QRS complex (End of atrial events)	End of T wave	Total ventricular electrical activity (Depolarization + Repolarization).

Autonomic effects on ECG

Stimulation	Effect on AV node	Typical ECG effect
Sympathetic stimulation	Increases conduction velocity	PR interval may shorten
Vagal stimulation	Decreases conduction velocity	PR interval may lengthen

Electrolyte disturbances and ECG

Disturbance	Typical ECG changes	Main concern
Hyperkalaemia	Tall peaked T waves; later PR prolongation, P-wave flattening or loss, QRS widening	Potentially fatal conduction abnormalities
Hypokalaemia	Flattened T waves, ST depression and prominent U waves	Increased arrhythmia risk
Hypercalcaemia	Shortened QT interval	Altered ventricular repolarisation
Hypocalcaemia	Prolonged QT interval	Increased risk of ventricular arrhythmias

Exam pearl: Hyperkalaemia can progress from peaked T waves to loss of P waves and widening of the QRS complex. The sequence varies, and severe cases may not show every classic stage.

Cardiac action potentials

There are two major action-potential patterns to distinguish:

Fast-response action potentials: Working atrial muscle, ventricular muscle and Purkinje fibres.
Slow-response action potentials: SA and AV nodal cells.

Conduction velocity and refractory periods

Conduction velocity

Tissue	Relative conduction speed	Physiological importance
AV node	Slowest	Allows time for ventricular filling
Atrial myocardium	Intermediate	Spreads excitation through the atria
Ventricular myocardium	Intermediate	Coordinates ventricular activation
Purkinje fibres	Fastest	Produces rapid, coordinated ventricular activation

Refractory periods

Period	Definition	Importance
Absolute refractory period (ARP)	No second action potential can be generated	Prevents immediate re-excitation
Effective refractory period (ERP)	A stimulus cannot produce a normally propagated response	Limits premature impulse propagation
Relative refractory period (RRP)	A stronger-than-normal stimulus may generate an action potential	Occurs during later repolarisation

FCPS pearl: The prolonged refractory period of cardiac muscle prevents summation and tetanus, allowing the heart to relax and refill between contractions.

Resting Membrane Potential

Phase	Common MCQ Name	Dominant Ion Channel / Movement	Membrane Potential Trend
Phase 0	Rapid Depolarization	Fast Na+ Influx	Spikes to positive (approx +20 mV)
Phase 1	Initial Repolarization	Transient outward K+ Outflux	Drops slightly toward 0 mV
Phase 2	Plateau Phase	Ca2+ Influx balances K+ Outflux	Stays flat near 0mV
Phase 3	Rapid Repolarization	Massive K+ Outflux	Drops sharply back to negative
Phase 4	Resting Potential / Diastole	High K+ permeability (K1 channel)	Stable at -90 mV

Quick Review of the Mechanical Matchups:

Phases 0, 1, and 2 align with systole (the contraction and ejection phase of the heart).
Phase 3 represents the transition as the muscle begins to rapidly reseting.
Phase 4 is strictly diastole (the relaxation and filling phase).

Blood Circulation

Functional differences between blood vessels

Vessel	Main function	High-yield feature
Arteries	Carry blood away from the heart	Thick walls; withstand high pressure
Arterioles	Regulate organ blood flow	Main resistance vessels
Capillaries	Exchange gases, nutrients and fluid	Largest total cross-sectional area
Venules	Collect blood from capillaries	Drain into veins
Veins	Return blood to the heart	High compliance; major blood-volume reservoir

Left vs right cardiac output

Left ventricular output supplies the systemic circulation.
Right ventricular output supplies the pulmonary circulation.
At steady state, right and left cardiac outputs must be equal.
Persistent imbalance leads to blood accumulation in the pulmonary or systemic venous circulation.

Blood Hemodynamics

Poiseuille's law — classic FCPS calculation

Resistance is inversely proportional to the fourth power of vessel radius.

Change in radius	Change in resistance
Radius decreases to ½	Increases 16-fold
Radius decreases to ¼	Increases 256-fold
Radius doubles	Falls to 1/16
Radius increases fourfold	Falls to 1/256

Pressure and velocity through the circulation

Feature	Highest / greatest	Lowest / least
Blood pressure	Aorta and large arteries	Venae cavae
Pressure drop	Across arterioles is steepest	—
Blood velocity	Aorta, under typical resting conditions	Capillaries
Total cross-sectional area	Capillaries	Aorta

Resistance, compliance and blood-volume distribution

Concept	Arteries	Arterioles	Veins
Main role	Pressure distribution	Resistance regulation	Blood storage and return
Compliance	Lower than veins	Relatively low	High
Effect of constriction	Increases vascular tone	Raises TPR	Mobilises stored blood
Important clinical association	Arterial stiffening increases pulse pressure	Controls tissue perfusion	Venoconstriction increases venous return

Frank–Starling mechanism

Autonomic regulation of the cardiovascular system

Site	Receptor	Main effect
SA node	β₁ adrenergic	Increased heart rate
SA node	M₂ muscarinic	Decreased heart rate
AV node	β₁ adrenergic	Faster conduction
AV node	M₂ muscarinic	Slower conduction and longer PR interval
Ventricles	β₁ adrenergic	Increased contractility
Skin, splanchnic and renal arterioles	α₁ adrenergic	Vasoconstriction; increased TPR
Skeletal muscle arterioles	α₁ and β₂ effects	Constriction or dilation depending on neural and circulating influences

Sympathetic vs parasympathetic effects

Effect	Sympathetic	Parasympathetic
Heart rate	Increases	Decreases
AV conduction	Increases	Decreases
Ventricular contractility	Increases	Relatively little direct effect
Venous tone	Increases	Limited direct effect
Arteriolar resistance	Generally increases through α₁ stimulation; regional exceptions occur	Limited direct control in most systemic vascular beds

Sympathetic activation can raise both cardiac output and vascular resistance, supporting arterial pressure.

Cardiovascular reflexes

Reflex	Sensor location	Stimulus	Response
Baroreceptor reflex	Carotid sinus and aortic arch	Change in arterial stretch	Rapid adjustment of sympathetic and parasympathetic outflow
Chemoreceptor reflex	Carotid and aortic bodies	Low PO2 ,high PCO2, increased H⁺	Increased ventilation and cardiovascular responses
Bainbridge reflex	Atria and great veins	Increased venous return and atrial stretch	Tends to increase heart rate
CNS ischaemic response	Medullary vasomotor centres	Severe reduction in brainstem perfusion	Powerful sympathetic pressor response

Baroreceptor reflex: standing up

Standing causes blood to pool in the compliant veins of the lower limbs.
Venous return and stroke volume decrease.
Arterial pressure tends to fall.
Baroreceptor firing decreases.
Sympathetic activity increases and vagal activity decreases.
Heart rate, contractility, venous tone and arteriolar resistance increase to help restore pressure.

FCPS pearl: The baroreceptor reflex is a rapid, short-term controller of blood pressure, not the main long-term regulator of blood volume.

Local control of blood flow

Mechanism	Principle	Example
Myogenic	Vascular smooth muscle contracts when stretched by increased pressure	Helps stabilise organ blood flow
Metabolic	Local metabolites accumulate during increased activity or reduced oxygen availability, promoting vasodilation	Active skeletal muscle and coronary circulation
Endothelial	Endothelial mediators modify vascular tone	Nitric oxide promotes vasodilation

Important local vasodilators include CO₂, H⁺, K⁺, lactate, adenosine and nitric oxide. Their effects depend on the vascular bed and physiological conditions.

Special features of regional circulations

Circulation	High-yield feature	FCPS pearl
Coronary	Very high resting oxygen extraction, approximately 75%	Flow is greatest during diastole, especially in the left ventricle
Cerebral	Autoregulation maintains flow across a range of perfusion pressures	CO₂ is a powerful regulator of cerebral vascular tone
Skeletal muscle	Local metabolic vasodilation increases flow during exercise	Local metabolites can override sympathetic α₁-mediated constriction
Skin	Blood flow is regulated for thermoregulation	Sympathetic control and arteriovenous anastomoses are important
Renal	Afferent and efferent arterioles form two resistance beds in series	Angiotensin II preferentially constricts the efferent arteriole at lower levels

Coronary circulation

The myocardium extracts a large fraction of delivered oxygen at rest.
During increased cardiac work, oxygen demand is met mainly by increasing coronary blood flow.
Left ventricular contraction compresses intramyocardial vessels, reducing flow during systole.
Adenosine is an important local metabolic vasodilator.

Cerebral circulation

Cerebral blood flow is autoregulated over a range of mean arterial pressures.
Your notes give an approximate range of 60–150 mmHg; this is not a fixed limit for every patient.
Increased arterial CO₂ generally causes cerebral vasodilation; decreased CO₂ causes vasoconstriction.

Renal circulation

Angiotensin II preferentially constricts the efferent arteriole at appropriate concentrations, helping maintain glomerular capillary pressure and GFR when renal perfusion falls. Strong or sustained activation can nevertheless reduce renal blood flow and eventually lower GFR.

Microcirculation and Starling forces

Starling forces determine fluid movement between capillaries and the interstitial space.

Which forces favour filtration or absorption?

Force	Effect on fluid movement
Increased capillary hydrostatic pressure P_c	Favours filtration out of capillaries
Increased interstitial hydrostatic pressure P_i	Opposes filtration
Increased plasma oncotic pressure pi_c	Favours fluid retention within capillaries
Increased interstitial oncotic pressure pi_i	Favours filtration into interstitium

Hormonal and renal control of blood pressure

Renin–angiotensin–aldosterone system (RAAS)

RAAS components and actions

Component	Main action
Renin	Initiates angiotensin formation
Angiotensin II	Potent vasoconstriction; stimulates aldosterone, thirst and ADH
Aldosterone	Increases renal Na⁺ reabsorption and promotes K⁺ secretion, especially in the distal nephron
ACE	Converts angiotensin I to angiotensin II
Angiotensin II in proximal tubule	Stimulates Na⁺/H⁺ exchange, supporting Na⁺ reabsorption

ADH vs ANP

Feature	ADH (vasopressin)	Atrial natriuretic peptide (ANP)
Release / trigger	Released from posterior pituitary in response to increased osmolality or reduced effective circulating volume	Released by atrial myocytes in response to stretch
Renal effect	Increases water reabsorption through V₂ receptors in collecting ducts	Promotes natriuresis and diuresis
Vascular effect	V₁ receptors cause vasoconstriction at higher concentrations	Promotes vasodilation
RAAS effect	Supports volume and pressure maintenance	Suppresses renin and aldosterone
Overall tendency	Conserves water and supports pressure	Reduces volume and pressure