CARDIOVASCULAR

PHYSIOLOGY
CARDIOVASCULAR SYSTEM ORGANIZATION
HEART
Chambers: Two atria receive blood. Two ventricles pump blood.

Valves: Atrioventricular (AV) valves prevent backflow. Semilunar valves guard major arteries.

BLOOD VESSELS:
Arteries: Thick-walled vessels. Carry oxygenated blood away from the heart.

Veins: Thinner walls, larger lumens. Return deoxygenated blood to the heart.

Capillaries: Microscopic vessels. Allow nutrient and gas exchange in tissues.

BASIC CIRCULATORY PRINCIPLES

HEARTBEAT: A rhythmic cycle of contraction and relaxation. Atrial systole precedes ventricular
systole.

CIRCULATORY PATH

Pulmonary Circuit: The right side of the heart pumps blood to the lungs. Oxygen is gained, and
carbon dioxide is expelled.
Systemic Circuit: The left side of the heart pumps oxygenated blood to the body. Nutrients are
delivered, and waste is collected.

OXYGEN TRANSPORT

Arterial Blood: Oxygen-rich blood pumped into systemic circulation.

Venous Blood: Deoxygenated blood returns to the heart.

NUTRIENT EXCHANGE

Capillary Beds: Networks where oxygen and nutrients move into tissues. Waste products exit for
removal.

BLOOD PRESSURE

Maintained: Adequate pressure ensures continuous flow.

Regulated: Nervous and hormonal control for balance.

CLOSED-LOOP SYSTEM

Continuous Circulation: Blood never leaves vessels during circulation. Essential for sustaining
metabolic processes.

Aspect Pulmonary Circulation Systemic Circulation

Function Sends blood to the lungs for Distributes oxygenated blood to the
oxygenation body
Starting Point The right ventricle of the heart left ventricle of the heart
Ending Point Returns oxygenated blood to the left Returns deoxygenated blood to the
atrium right atrium
Blood Oxygenation Oxygen-poor blood becomes oxygen- Oxygen-rich blood delivers oxygen to
rich tissues
Major vessels Involved Pulmonary arteries and veins Aorta, arteries, and veins throughout
the body
Gas Exchange Location Lungs-alveoli facilitate oxygen Systemic capillaries in various body
exchange tissues
Blood Pressure Lower pressure compared to the Higher pressure to distribute blood
systemic circulation widely
Purpose Eliminate carbon dioxide, gains oxygen Supplies oxygen, nutrients, and
removes waste
Pathway Shorter pathway – heart to lungs and Longer pathway – heart to body and
back back
 Circulatory Blood Volume Cross-Sectional Blood Velocity Blood Pressure
Component (Approx.) Area
Heart 5 liters N/A Varies during Highest in left
cardiac cycle ventricle
Arteries  12% of total blood Smaller than veins Rapid during Highest in large
volume systole, slower in arteries
diastole
Arterioles  7% of total blood Smaller than Decreases as it Drops significantly
volume arteries approaches
capillaries
Capillaries  5-7% of total Extensive networks Slowest due to Reduced to
blood volume increased total facilitate exchange
cross-sectional
area
Venules  5% of total blood Similar to arterioles Increases Rises slightly
volume compared to
capillaries
Veins  64% of total blood Larger than arteries Increases Lowest in large
volume compared to veins
arteries
Vena Cava/Right N/A N/A Blood flows Lowest in right
Atrium continuously atrium
CARDIAC ACTION POTENTIALS
SA NODE ACTION POTENTIAL
The sinoatrial (SA) node is a specialized group of cells in the heart that serves as the natural
pacemaker. The SA nodal action potential involves distinct phases, reflecting its role in initiating the
cardiac cycle.

PHASE 4 (DIASTOLIC DEPOLARIZATION)

The SA node maintains a gradual, spontaneous depolarization during diastole. The influx of sodium
and calcium ions, mainly through funny channels (If), contributes to the slow depolarization.
Potassium channels are also active during this phase.

THRESHOLD (INITIATION OF ACTION POTENTIAL)

The diastolic depolarization reaches a threshold, typically around -40 mV. Voltage-gated calcium
channels open, causing a rapid influx of calcium ions.

UPSTROKE (PHASE 0)

Rapid depolarization due to the influx of calcium ions. Sodium channels may also contribute to the
upstroke.

EARLY REPOLARIZATION (PHASE 1)

Transient outward potassium current causes a brief repolarization.

PLATEAU (PHASE 2)

L-type calcium channels contribute to the plateau phase, maintaining depolarization. Potassium
efflux is countered by calcium influx, balancing membrane potential.

FINAL REPOLARIZATION (PHASE 3)

Potassium channels fully open, leading to repolarization. Calcium channels begin to close, allowing
for the return to the resting membrane potential.
EFFECTS OF AUTONOMIC NERVOUS SYSTEM
The autonomic nervous system (ANS) exerts control over the sinoatrial (SA) node action potential,
influencing heart rate through the modulation of ion channels, particularly the “funny currents” (If).

SYMPATHETIC NERVOUS SYSTEM (SNS) EFFECTS

Increased Heart Rate (Chronotropy): Norepinephrine released by sympathetic nerves binds to beta-
adrenergic receptors on SA nodal cells. Activation of the cyclic AMP (cAMP) pathway enhances funny
current (If) and accelerates diastolic depolarization. This results in a quicker threshold reached, faster
upstroke, and an overall increase in heart rate.

Enhanced Conduction Velocity: Sympathetic stimulation increases calcium current, leading to faster
conduction of action potentials through the heart.

PARASYMPATHETIC NERVOUS SYSTEM (PNS) EFFECTS

Decreased Heart Rate (Chronotropy): Acetylcholine released by parasympathetic nerves binds to

muscarinic receptors on SA nodal cells. Activation of the acetylcholine-activated potassium current
and inhibition of cAMP reduces the funny current (If). Slowed diastolic depolarization, increased
threshold, and a slower heart rate result.

Reduced Conduction Velocity: Parasympathetic activation decreases calcium current, slowing the
conduction of action potentials.
FUNNY CURRENT
The “funny current,” denoted as If, refers to a mixed sodium and potassium inward current that plays
a pivotal role in the spontaneous depolarization of the sinoatrial (SA) node cells in the heart.

It is primarily found in the SA node, the heart’s natural pacemaker. It contributes to the diastolic
depolarization phase, the gradual increase in membrane potential during the resting state. It helps to
bring the membrane potential closer to the threshold, facilitating the initiation of the action
potential.

Composition: It is a mixed sodium-potassium current, meaning it involves the movement of both

sodium (Na+) and potassium (K+) ions.

Ivabradine:Funny current channel blocker(decrease HR)

Ventricular Action Potential

The ventricular action potential refers to the series of electrical events that occur in the cells of the
ventricles during the contraction and relaxation of the heart.

PHASE 0 (DEPOLARIZATION)
Rapid depolarization is initiated by the opening of fast voltage-gated sodium channels. Sodium influx
leads to a sharp upstroke of the action potential.

PHASE 1 (EARLY REPOLARIZATION)

Transient outward potassium current contributes to a brief repolarization. It marks the initial part of
the repolarization process.

PHASE 2 (PLATEAU)

Balanced inflow of calcium ions through L-type calcium channels and outflow of potassium ions.
Maintains a prolonged depolarized state, crucial for the sustained contraction of the myocardium.

PHASE 3 (REPOLARIZATION)

Potassium efflux dominates, leading to rapid repolarization. Voltage-gated potassium channels open,
allowing the outflow of potassium ions.

PHASE 4 (RESTING STATE)

Resting membrane potential is re-established, and ion concentrations return to baseline. Sodium and
potassium channels are closed, maintaining the resting state until the next cycle.

Aspect Ventricular Action Potential SA Node Action Potential

Location
Initiation
Phase 4 (Resting)
Phase 0 (Depolarization)
Phase 1 (Early Repolarization)
Phase 2 (Plateau)
Phase 3 (Repolarization)
Phase 4 (Resting)
Ventricles
External signals (from atria)
Stable resting membrane potential
Rapid depolarization due to Na+
influx
Brief Repolarization due to K+
efflux
Prolonged depolarization due to
Ca2+ influx
Rapid Repolarization due to K+
efflux
Resting membrane potential re-
established
Sinoatrial (SA) Node
Intrinsic automaticity
Spontaneous diastolic
depolarization
Gradual depolarization due to If
(funny current) and Ca2+ influx
Transient outward K+ current
Plateau phase less pronounced,
Ca2+ influx
Repolarization, mainly K+ efflux
Spontaneous diastolic
depolarization continues

THE CONDUCTION SYSTEM OF THE HEART

The conduction system of the heart is a specialized network of cells responsible for generating and
transmitting electrical impulses, ensuring the coordinated contraction of the heart muscle.

SINOATRIAL (SA) NODE

Location: In the right atrium near the superior vena cava.

Function: Initiates electrical impulses, serving as the natural pacemaker.

Action Potential: Characterized by spontaneous diastolic depolarization, driven by “funny currents”

(If). It reaches the threshold, leading to an action potential.

ATRIA

The electrical impulse generated by the SA node spreads across both atria through specialized
pathways (internodal pathways). Atrial muscle cells depolarize, leading to atrial contraction (atrial
systole).

ATRIOVENTRICULAR (AV) NODE

Location: Near the interatrial septum.

Function: Delays the electrical impulse, allowing time for the atria to contract and fill the ventricles.

Action Potential: Slower conduction compared to the atria, essential for proper coordination
between atrial and ventricular contractions.

BUNDLE OF HIS:

Location: In the interventricular septum.

Function: Divides into the left and right bundle branches, conducting the electrical impulse toward
the apex of the heart.

Action Potential: Rapid conduction through specialized conducting fibers.

PURKINJE FIBERS
Location: Spread throughout the ventricles.

Function: Transmit the electrical impulse to the ventricular muscle cells, ensuring synchronous
contraction.

Action Potential: Fast conduction, ensuring rapid and coordinated ventricular depolarization.

VENTRICLES

The electrical impulse reaches the ventricular muscle cells, leading to depolarization and subsequent
contraction (ventricular systole). After contraction, repolarization occurs, resetting the cells for the
next cardiac cycle.

Clinical Correlation!

ARRHYTHMIAS

Abnormalities in conduction pathways can lead to arrhythmias, such as atrial fibrillation (AF), atrial flutter,
ventricular tachycardia, or heart block.

Antiarrhythmic medications like beta-blockers, calcium channel blockers, and anti-arrhythmic drugs are used
to control and manage irregular heart rhythms.

ATRIOVENTRICULAR (AV) BLOCK

Dysfunction in the AV node or bundle of His can result in AV blocks (first, second, or third degree).

Depending on the severity, medications such as atropine or pacemakers may be used to manage AV blocks.

WOLFF-PARKINSON-WHITE (WPW) SYNDROME

Extra electrical pathways (accessory pathways) between the atria and ventricles can cause abnormal
conduction, leading to supraventricular tachycardias.

Medications like antiarrhythmics or catheter ablation may be used to manage symptoms.

BRADYCARDIA

Slow heart rate can result from issues in the SA node or AV node.
 THE NORMAL
ELECTROCARDIOGRAM
ECG INTRODUCTION
Electrocardiography (ECG or EKG) is a non-invasive diagnostic tool that records the electrical activity
of the heart over time. The resulting ECG graph represents the depolarization and repolarization of
the heart’s chambers during each cardiac cycle. Electrodes are placed on the skin to detect electrical
impulses, and the recorded data is visualized as a series of waves and intervals.

EINTHOVEN TRIANGLE

The Einthoven Triangle is a conceptual triangle formed by three limb leads in the standard ECG
placement. It was introduced by Willem Einthoven, a Dutch physiologist, and it serves as a
fundamental aspect of ECG interpretation.

Lead I: Connects the right arm (RA) electrode to the left arm (LA) electrode.

Lead II: Connects the right arm (RA) electrode to the left leg (LL) electrode.

Lead III: Connects the left arm (LA) electrode to the left leg (LL) electrode.

The Einthoven Triangle helps in visualizing the electrical forces in the frontal plane of the body and
aids in understanding the direction and magnitude of electrical impulses during different phases of
the cardiac cycle.
AUGMENTED LEADS
In addition to the Einthoven Triangle, there are three augmented leads (aVR, aVL, aVF), which are
unipolar limb leads that provide additional perspectives on the heart’s electrical activity.

aVR (Augmented Vector Right): The positive electrode is placed on the right arm, and it “looks”
toward the left arm and left leg.

aVL (Augmented Vector Left): The positive electrode is placed on the left arm, and it “looks” toward
the right arm and left leg.

aVF (Augmented Vector Foot): The positive electrode is placed on the left leg, and it “looks” toward
the right arm and left arm.

Augmented Leads:

Lead Positive Electrode Placement Looks Toward

aVR Right Arm Left Arm and Left Leg
aVL Left Arm Right Arm and Left Leg
aVF Left Leg Right Arm and Left Arm

Standard Limb Leads:

Lead Electrodes Direction Placement

I RA (-) to LA (+) Left to Right Right Arm to Left Arm
II RA (-) to LL (+) Lower Left to Upper Right Right Arm to Left Leg
III LA (-) to LL (+) Lower Left to Upper Left Left Arm to Left Leg
Precordial (Chest) Leads:

Lead Electrodes Placement

V1 Right 4th ICS, Parasternal Right side of the sternum
V2 Left 4th ICS, Parasternal Left side of the sternum
V3 Midway between V2 and V4 Anteriorly between V2 and V4
V4 Left 5th ICS, Midclavicular Left midclavicular line
V5 Left 5th ICS, Anterior Axillary Left anterior axillary line
V6 Left 5th ICS, Midaxillary Left midacillary line

CORONARY CIRCULATION

The heart receives its blood supply through the coronary circulation, which ensures the delivery of
oxygen and nutrients essential for its function.

CORONARY ARTERIES

The coronary arteries originate from the base of the aorta. The main coronary arteries are the Left
Coronary Artery (LCA) and the Right Coronary Artery (RCA).

Left Coronary Artery (LCA)

Branches into the Left Anterior Descending (LAD) Artery and the Left Circumflex (LCx) Artery.

The LAD supplies the anterior interventricular septum and most of the anterior left ventricle.

The LCx supplies the lateral and posterior left ventricles.

Right Coronary Artery (RCA)

Supplies the right atrium, right ventricle, and part of the posterior left ventricle. In many individuals,
the RCA also provides blood to the AV (atrioventricular) node.
CORONARY VEINS

Coronary veins collect deoxygenated blood from the heart muscle. The major coronary vein is the
Great Cardiac Vein, which runs alongside the LAD artery.

CORONARY SINUS

The coronary sinus is a large vein that collects blood from the coronary veins and delivers it to the
right atrium.

Clinical Correlation!

ISCHEMIA AND INFARCTION

Reduced blood flow (ischemia) or a complete blockage (infarction) of coronary arteries can lead to myocardial
damage. Myocardial Infarction (heart attack) occurs when a coronary artery is blocked, causing irreversible
damage to the heart muscle.
Coronary artery bypass grafting (CABG) and angioplasty are common interventions to restore blood flow in
diseased coronary arteries. Medications such as antiplatelets and statins are prescribed to manage coronary
artery disease.

ECG LEADS AND SURFACES OF THE CORONARY ARTERY SUPPLY

Lead Heart Surface/Part Coronary Artery Supply
I Left lateral wall of the left ventricle Left Circumflex Artery (LCx)
II Inferior wall of the left ventricle Right Coronary Artery (RCA)
III Inferior wall of the left ventricle Right Coronary Artery (RCA)
aVR Right atrium Right Coronary Artery (RCA)
 aVL Left lateral wall of the left ventricle Left Circumflex Artery (LCx)
aVF Inferior wall of the left ventricle Right Coronary Artery (RCA)
V1 Septal wall of the right ventricle Right Coronary Artery (RCA)
V2 Septal wall of the right ventricle Right Coronary Artery (RCA)
V3 Anterior wall of the left ventricle Left Anterior Descending Artery (LAD)
V4 Anterior wall of the left ventricle Left Anterior Descending Artery (LAD)
V5 Lateral wall of the left ventricle Left Circumflex Artery (LCx)
V6 Lateral wall of the left ventricle Left Circumflex Artery (LCx)

ECG PAPER
SMALL SQUARE

Horizontal (Time): Each small square represents 0.04 seconds (s) horizontally.

Vertical (Voltage): Each small square represents 0.1 millivolts (mV) vertically.

LARGE SQUARE

Consists of a 5 x 5 grid of small squares.

Horizontal (Time): Each large square represents 0.2 seconds (s).

Vertical (Voltage): Each large square represents 0.5 millivolts (mV).

INTERPRETATION

1. Heart Rate Calculation: Count the number of R waves (QRS complexes) in a standard 6-second
strip (30 large squares) and multiply by 10 for beats per minute (BPM).

2. Duration of Intervals: Measure the duration of intervals using small squares

PR Interval: 3 to 5 small squares (120-200 ms).

QRS Complex: 2 to 3 small squares (80-120 ms).

QT Interval: Varies with heart rate, often measured and corrected (QTc).

3. Voltage Amplitudes: Assess voltage amplitudes using vertical squares.

P-wave: Usually < 2.5 mm in height.

QRS Complex: Usually < 5 mm in height.

T-wave: Varies, but typically < 5 mm in height.

4. Regularity and Rhythm: Analyse the regularity of R-R intervals for regular or irregular rhythms.

Assess P-P intervals for regularity in atrial rhythms.

5. ST Segment and T-wave Analysis: Examine the ST segment for elevation or depression.

Evaluate T-wave morphology, looking for symmetry and abnormalities.

THE ECG WAVES

 1) ECG Waves:

Wave Description Duration Significance

P-wave Atrial depolarization 80-120 ms (2-3 small Initiates atrial contraction
squares)
QRS Complex Ventricular 80-120 ms (2-3 small Indicates ventricular
depolarization squares) contraction
T-wave Ventricular Varies, typically < 200 Represents recovery
Repolarization ms phase of ventricles
U-wave Not always present; may Varies Associated with
follow T-wave Repolarization of
papillary muscles or
Purkinje fibers

2) Segments in ECG:

Segment Description Significance

PR Segment Flat segment after P-wave and Represents delay at the AV node;
before QRS complex Should be isoelectric
ST Segment Time between QRS complex and T- Represents early ventricular
wave Repolarization; Should be
isoelectric
TP Segment Time between T-wave and next P- Should be isoelectric; Represents
wave end of cardiac cycle

3) Intervals in ECG:

Interval Description Duration Significance

PR Interval From start of P-wave to
start of QRS Complex
QRS Interval Time taken for ventricular
depolarization
QT Interval From start of QRS complex
to end of T-wave
120-200 ms (3-5 small Represents atrial
squares) depolarization and AV
nodal delay
80-120 ms (2-3 small Indicates ventricular
squares) contraction
Varies with heart rate, Represents total time
corrected QT (QTc) for ventricular
often used depolarization and
repolarization

DIRECTION OF DEPOLARISATION AND REPOLARISATION

DEPOLARIZATION

Atrial Depolarization: Originates at the sinoatrial (SA) node. Travels through the atria, causing the P-
wave on the ECG.Typically moves from the right atrium to the left atrium and from the top to the
bottom. Always starts in the septum to the endocardium to the epicardium.

Ventricular Depolarization: Initiated at the atrioventricular (AV) node after a brief delay. Travels
down the interventricular septum through the bundle of His and Purkinje Fibers. Depolarization
spreads from the septum outward, generally from left to right and bottom to top in the ventricles.
Always starts in the epicardium to the endocardium to the septum.

REPOLARIZATION

Atrial Repolarization: Usually not visible on the surface ECG. Occurs during ventricular
depolarization.

Ventricular Repolarization: Begins shortly after the QRS complex. Typically moves from the apex
(bottom) to the base (top) of the heart. Reflected in the T-wave on the ECG.

CARDIAC AXIS
MEAN ELECTRICAL AXIS (MEA)
Calculated by assessing the net direction of electrical forces during ventricular depolarization.
Normal MEA is approximately -30 to +90 degrees.

DETERMINING AXIS DEVIATIONS

Left Axis Deviation (LAD): If the QRS complex is mainly positive in lead I and negative in lead aVF.
Right Axis Deviation (RAD):If the QRS complex is mainly positive in lead aVF and negative in lead I.

Changes in the axis may indicate heart conditions such as hypertrophy, conduction abnormalities, or
structural issues.

CLINICAL ASPECTS OF ECG (BASICS)

Common ECG Findings:

Finding Description
Sinus Rhythm Normal heart rhythm originating from the SA node
Atrial Fibrillation Chaotic atrial activity, no distinct P-waves
Atrial Flutter Regular atrial activity, “sawtooth” pattern
Ventricular Tachycardia Three or more consecutive ventricular beats at a rapid rate
Ventricular Fibrillation Chaotic, rapid ventricular activity, life-threatening emergency
ST Elevation Indicates myocardial infarction (heart attack)
ST Depression May indicate ischemia or coronary artery disease
T-wave Inversion Can be a sign of myocardial ischemia or other cardiac conditions

Examples of ECG
ATRIAL FIBRILLATION
ATRIAL FLUTTER

VENTRICULAR TACHYCARDIA

VENTRICULAR FIBRILLATION
ST ELEVATION AND ST DEPRESSION

THE JUGULAR VENOUS PRESSURE (JVP)

The Jugular Venous Pressure (JVP) is an essential clinical sign that provides information about the
right atrial pressure and indirectly reflects the central venous pressure. It is commonly assessed by
examining the pulsations of the internal jugular vein.

ASSESSMENT TECHNIQUE:

The patient is positioned at a 45-degree angle, usually in a semi-recumbent position. The examiner
stands on the patient’s right side to assess the right internal jugular vein.

NORMAL JUGULAR VENOUS PULSE WAVEFORM:

The JVP waveform consists of multiple positive and negative waves.

The three upward waves are labelled ‘a,’ ‘c,’ and ‘v,’ and the two downward waves are ‘x’ and ‘y.’

‘a’ Wave: Due to atrial contraction. It is prominent in conditions with increased resistance to right
atrial emptying (e.g., tricuspid stenosis).

‘c’ Wave: Reflects right ventricular contraction and bulging of the tricuspid valve into the right atrium
during ventricular contraction.

‘v’ Wave: Represents venous return to the right atrium, especially during atrial filling.

‘x’ Descent: Corresponds to atrial relaxation and downward displacement of the tricuspid valve.

‘y’ Descent: Represents rapid filling of the right ventricle after tricuspid valve opening.

JVP Component Description Clinical Significance

‘a’ Wave Atrial contraction Prominent in tricuspid stenosis
‘c’ Wave Right Ventricular contraction Elevated in conditions with
tricuspid regurgitation
‘v’ Wave Venous return to the right atrium Increased in conditions with
tricuspid regurgitation
‘x’ Descent Atrial relaxation and tricuspid valve Absent ‘x’ descent may occur in
descent tricuspid regurgitation
‘y’ Descent Rapid filling of the right ventricle after Absent ‘y’ descent may occur in
tricuspid valve opening tricuspid stenosis
 Clinical Correlation!
Increased JVP: Indicates elevated right atrial pressure, often seen in heart failure, constrictive pericarditis, or
tricuspid regurgitation.

Pulsatile JVP: Suggestive of tricuspid regurgitation.

Absent ‘a’ Wave: This may indicate atrial fibrillation.

Heart Failure: Impaired emptying of the right ventricle.

Constrictive Pericarditis: Restriction of cardiac filling.

Tricuspid Regurgitation: Backflow of blood into the right atrium during ventricular systole.

CARDIAC CYCLE
The cardiac cycle consists of several distinct phases, encompassing both the systole (contraction) and
diastole (relaxation) of the heart chambers. Here are the key phases of the cardiac cycle:

ATRIAL CONTRACTION (ATRIAL SYSTOLE): Initiated by the depolarization of the atria (P-wave on the
ECG). Atria contract, pushing blood into the ventricles. Represents the final phase of ventricular
filling.

ISOVOLUMETRIC CONTRACTION (VENTRICULAR SYSTOLE - FIRST PHASE): Ventricles begin to

contract. AV valves close to prevent blood backflow into the atria. Ventricular volume remains
constant (isovolumetric) until pressure exceeds atrial pressure.

EJECTION PHASE (VENTRICULAR SYSTOLE - SECOND PHASE): Ventricular pressure surpasses arterial
pressure. Semilunar valves open, allowing blood to be ejected into the pulmonary artery and aorta.
Represents the active ejection of blood from the ventricles.

ISOVOLUMETRIC RELAXATION (VENTRICULAR DIASTOLE - FIRST PHASE): Ventricles relax, and

pressure drops. Semilunar valves close to prevent blood backflow into the ventricles. Ventricular
volume remains constant (isovolumetric) until atrial pressure exceeds ventricular pressure.

RAPID FILLING (VENTRICULAR DIASTOLE - SECOND PHASE): AV valves open. Blood from the atria
rapidly fills the ventricles. Represents the passive filling of the ventricles.

ATRIAL DIASTOLE: Atria remains in diastole, receiving blood from the veins. Represents the period
between the end of an atrial contraction and the beginning of the next atrial contraction.
SUMMARY
PHASES OF CARDIAC CYCLE

Phase Description
Atrial Contraction (Atrial Systole) Initiated by atrial depolarization atria contract,
pushing blood into the ventricles
Isovolumetric Contraction (Ventricular Systole – Ventricles begin to contract; AV valves close;
First Phase) ventricular volume remains constant
Ejection Phase (Ventricular Systole – Second Ventricular pressure surpasses arterial pressure;
Phase) semilunar valves open, ejecting blood
Isovolumetric Relaxation (Ventricular Diastole – Ventricles relax; semilunar valves close;
First Phase) ventricular volume remains constant
Rapid Filling (Ventricular Diastole – Second AV valves open; blood from atria rapidly fills
Phase) ventricles
Atrial Diastole Atria remains in diastole; and receive blood from
veins.
KEY CARDIAC EVENTS AND ASSOCIATED ECG

Cardiac Event Associated ECG Wave

Atrial Contraction (Atrial Systole) P-Wave (atrial depolarization)
Isovolumetric Contraction (Ventricular Systole – QRS Complex (ventricular depolarization)
First Phase)
Ejection Phase (Ventricular Systole – Second QRS Complex (continuation of ventricular
Phase) depolarization)
Isovolumetric Relaxation (Ventricular Diastole – T-wave (ventricular Repolarization)
First Phase)
Rapid Filling (Ventricular Diastole – Second -
Phase)
Atrial Diastole -

HEART SOUNDS
Heart Timing Associated Sound Component Location Clinical
Sound Event Characteristic s Significance
s
S1 (Lub) Closure of Beginning of “Lub” sound M1 (mitral Loudest at -
AV valves ventricular and T1 the apex
systole (tricuspid)
S2 (Dub) Closure of Beginning of “Dub” sound A2 (aortic) Loudest at -
semilunar ventricular and P2 the base
valves diastole (pulmonic)
S3 Early Rapid filling of Low – - Heard best Normal in young
diastole the ventricles frequency at apex abnormal in
sound adults (heart
failure)
S4 Late Atrial Low – - Heard best Associated with
diastole contraction frequency at apex conditions like
sound hyper-trophic
 cardiomyopathy

Clinical Correlation!

MURMURS
Murmurs can be either innocent (benign) or pathological. Innocent murmurs are often heard in healthy
individuals, particularly during periods of rapid growth, and are not associated with any structural heart
abnormalities. Pathological murmurs, on the other hand, may indicate heart valve disorders, structural
abnormalities, or other cardiac conditions.

Pathological murmurs can result from conditions such as valvular stenosis (narrowing), valvular regurgitation
(leakage), septal defects, or abnormal blood flow patterns within the heart chambers.

Murmurs can occur during specific phases of the cardiac cycle. Systolic murmurs occur between the first heart
sound (S1) and the second heart sound (S2), while diastolic murmurs occur between S2 and the next S1. Some
murmurs, known as continuous murmurs, span both systole and diastole.

PRESSURE-VOLUME GRAPH
A pressure-volume (PV) loop graph is a valuable tool in understanding the changes in pressure and
volume within the heart during one cardiac cycle. This loop helps visualize various phases of the
cardiac cycle and provides insights into cardiac function.
COMPONENTS OF A PRESSURE-VOLUME LOOP

1. ISOVOLUMETRIC CONTRACTION: The initial phase where ventricles contract and the volume
remain constant (isovolumetric). Pressure in the ventricles rises rapidly.

2. RAPID EJECTION: Following isovolumetric contraction, the aortic valve opens, and blood is
ejected into the aorta. Ventricular volume decreases, and pressure in the ventricles decreases
slightly.

3. REDUCED EJECTION: AS ejection continues, the rate of blood leaving the ventricle slows.
Ventricular pressure decreases further.

4. ISOVOLUMETRIC RELAXATION: The aortic valve closes, marking the beginning of

isovolumetric relaxation. Ventricular volume remains constant as the pressure decreases.

5. RAPID FILLING: The mitral valve opens, and blood rapidly fills the ventricle. Ventricular
volume increases, and pressure in the ventricles remains low.
6. REDUCED FILLING: AS ventricular volume increases, the rate of filling decreases. The
ventricles reach their maximum diastolic volume.

Interpretation of the Loop:

The loop travels counterclockwise during systole and diastole. The area enclosed by the loop
represents stroke work, indicating the work done by the heart to pump blood during one cardiac
cycle. Changes in the shape and size of the loop can indicate alterations in cardiac contractility,
afterload, or preload.

DERIVATIONS FROM PRESSURE VOLUME GRAPH

From a pressure-volume (PV) loop graph, several important parameters and indices can be derived to
assess cardiac function and performance.

1. STROKE VOLUME (SV): SV is the difference between end-diastolic volume (EDV) and end-
systolic volume (ESV).

Equation: SV = EDV - ESV

Clinical Significance: SV represents the volume of blood ejected by the ventricle in one cardiac cycle.

2. EJECTION FRACTION (EF): EF is the ratio of stroke volume to end-diastolic volume.

Equation: EF = SV/EDV X 100

Clinical Significance: EF is a crucial indicator of ventricular function, commonly used in assessing

heart failure.

3. PRELOAD: Preload is approximated by the end-diastolic volume (EDV).

Clinical Significance: Preload represents the initial stretching of the cardiac muscle fibers before
contraction.

4. AFTERLOAD: Afterload can be estimated by the systolic pressure during ejection.

Clinical Significance: Afterload is the resistance against which the heart must pump blood, often
associated with aortic pressure.

5. CARDIAC OUTPUT (CO): CO is the product of heart rate (HR) and stroke volume (SV).

Equation: CO= HR X SV

Clinical Significance: CO represents the total volume of blood pumped by the heart per minute.

6. END-DIASTOLIC PRESSURE (EDP) AND END-SYSTOLIC PRESSURE (ESP): EDP is the pressure in
the ventricle at the end of diastole, and ESP is the pressure at the end of systole.

Clinical Significance: These pressures provide insights into ventricular function and contractility.
CLINICAL IMPORTANCE OF PRESSURE-VOLUME GRAPH
The pressure-volume (PV) loop graph is clinically important in understanding and managing various
cardiac conditions, including mitral stenosis, aortic stenosis, aortic regurgitation, and mitral
regurgitation.

1. MITRAL STENOSIS

Reduced stroke volume due to impaired filling of the left ventricle during diastole. Elevated left atrial
pressure, representing increased resistance to blood flow through the narrowed mitral valve.

Clinical Implications:

The PV loop helps quantify the degree of obstruction in mitral stenosis and guides decisions
regarding intervention (e.g., mitral valve replacement or balloon valvuloplasty).

2. AORTIC STENOSIS:

Increased afterload as the ventricle works against a narrowed aortic valve. Concentric hypertrophy of
the left ventricle due to the increased workload.

Clinical Implications:

PV loop analysis aids in evaluating the severity of aortic stenosis and helps determine the
appropriate timing for intervention (e.g., aortic valve replacement).
3. AORTIC REGURGITATION:

Elevated end-diastolic volume due to regurgitation of blood back into the left ventricle during
diastole. Increased stroke volume as the ventricle compensates for the regurgitant volume.

Clinical Implications:

PV loop assessment assists in quantifying the severity of aortic regurgitation and guiding decisions
regarding surgery or other interventions.

4. MITRAL REGURGITATION:

Increased end-diastolic volume due to the backflow of blood into the left atrium during systole.
Increased stroke volume as the ventricle accommodates the regurgitant volume.

Clinical Implications:

PV loop analysis helps evaluate the impact of mitral regurgitation on ventricular function and guides
decisions regarding surgical repair or replacement of the mitral valve.
WIGGER DIAGRAM
The Wiggers diagram, developed by Carl J. Wiggers, is a visual representation of the cardiac cycle,
illustrating the dynamic changes in various cardiovascular parameters over time. This diagram serves
as a fundamental tool in comprehending the complex interplay between electrical and mechanical
events within the heart during one complete cycle.
KEY COMPONENTS OF THE WIGGERS DIAGRAM:

X-Axis (Time): Represents the progression of time, moving from left to right.

Y-Axis (Pressure): Reflects changes in pressure within specific regions of the heart and major vessels.

CARDIAC CYCLE PHASES

Atrial Contraction (P-Wave): Depicts the electrical activity and pressure changes during atrial
contraction, leading to ventricular filling.
Isovolumetric Contraction (QRS Complex): Illustrates ventricular contraction with closed
atrioventricular (AV) valves, marking the beginning of systole.

Ejection Phase (ST Segment to T-Wave): Demonstrates the ejection of blood from the ventricles into
the aorta and pulmonary artery.

Isovolumetric Relaxation (T-Wave): Depicts ventricular relaxation with closed semilunar valves,
marking the end of systole.

Rapid Filling (Late T-Wave to P-Wave): This represents the passive filling of the ventricles as blood
flows from the atria.

ECG WAVEFORMS

Superimposed on the diagram to show the electrical activity of the heart, correlating with different
phases of the cardiac cycle.

ARTERIAL BLOOD PRESSURE

Reflects changes in aortic pressure, providing insights into the hemodynamic aspects of the cardiac
cycle. Clinicians use the Wiggers diagram to explain and interpret cardiovascular abnormalities and
diseases.

CARDIAC OUTPUT AND

VENOUS RETURN
CARDIAC OUTPUT (CO)
Cardiac Output (CO) is the volume of blood pumped by the heart per unit of time, typically measured
in Liters per minute (L/min). It is a crucial parameter reflecting the heart’s ability to meet the body’s
circulatory demands.

CO = HR X SV

where:

HR is the heart rate (beats per minute)

SV is the stroke volume (volume of blood ejected by the heart in one contraction)

STROKE VOLUME (SV)

Stroke Volume is the amount of blood ejected from the left ventricle during each heartbeat.

SV = EDV – ESV

SV of a 70 Kg old male

Normally EDV = 120ml

ESV = 50 ml

SV = 120 - 50 = 70ml

FACTORS INFLUENCING STROKE VOLUME

1. Preload: Preload is the initial stretching of the heart muscle fibers before contraction. Adequate
preload enhances ventricular filling, leading to increased stroke volume
2. Afterload: Afterload is the resistance the heart must overcome to eject blood. Increased
afterload can reduce stroke volume.
3. Contractility: Contractility is the force generated by the heart during contraction. Positive
inotropic agents increase contractility, enhancing stroke volume.

HEART RATE (HR): Heart Rate is the number of heartbeats per minute.
FACTORS INFLUENCING HEART RATE

1. Nervous System: Sympathetic stimulation increases heart rate, while parasympathetic

stimulation decreases it.
2. Autonomic Hormones: Hormones like epinephrine can increase heart rate.

BLOOD PRESSURE
Blood Pressure is the force exerted by the blood against the walls of the arteries.
Formula: BP= CO X SVR

Where SVR is the Systemic Vascular Resistance.

SYSTEMIC VASCULAR RESISTANCE (SVR)

Systemic Vascular Resistance is the resistance the heart must overcome to pump blood into the
systemic circulation.

Formula: SVR = MAP/ CO

Where MAP is the Mean Arterial Pressure.

AFTERLOAD

Afterload refers to the resistance the heart encounters when ejecting blood into the systemic
circulation during systole.

Influencing Factors

Determined by arterial resistance, vascular tone, blood viscosity, and aortic pressure. Increased
afterload hinders the ejection of blood from the heart.

Clinical Significance:

Elevated afterload can reduce stroke volume, impacting cardiac output. Commonly increased in
hypertension, contributing to left ventricular hypertrophy.

Higher afterload requires increased cardiac work, potentially elevating myocardial oxygen demand.
Vasodilators are used to reduce afterload, and managing conditions like heart failure and
hypertension.

Parameters to assess factors regulating Stroke volume

Factor Parameter
Preload End diastolic volume (EDV)
Afterload Aortic pressure/total peripheral resistance
Contractility (Inotropy) Ejection fraction (EF).
In heart failure, EF decreases. To increase EF,
positive inotropic agents like Digitalis or
Dobutamine are given.

CARDIAC INDEX
Cardiac index (CI) is a measure of cardiac output (CO) normalized to body surface area (BSA). It
provides a more accurate assessment of cardiac function by considering individual variations in body
size.

CALCULATION

The cardiac index (CI) is calculated by dividing the cardiac output (CO) by the body surface area
(BSA).
 CI = CO / BSA

The units of cardiac index are typically expressed in Liters per minute per square meter (L/min/m^2).

Clinical Significance:

Cardiac index helps to assess cardiac performance relative to an individual’s body size, allowing for
better comparison between individuals.

It’s used in the diagnosis, management, and monitoring of various cardiac conditions, particularly
those affecting cardiac function and output.

Cardiac index values outside the normal range may indicate cardiac dysfunction, such as heart
failure, cardiogenic shock, or other circulatory disturbances.

The normal range for cardiac index can vary depending on factors such as age, gender, and overall
health.

Generally, the normal range is considered to be between 2.5 and 4.2 Liters per minute per square
meter (L/min/m^2) in adults.

CONTROL OF CARDIAC OUTPUT BY VENOUS RETURN

The control of cardiac output by venous return is a fundamental concept in cardiovascular physiology
known as the Frank-Starling mechanism. Here are detailed notes on this mechanism:

FRANK-STARLING MECHANISM
The Frank-Starling mechanism describes the intrinsic ability of the heart to adjust its stroke volume
(SV) in response to changes in venous return, which is the volume of blood returning to the heart
from systemic circulation.

According to the Frank-Starling mechanism, an increase in venous return stretches the myocardial
fibers of the ventricles, leading to an increased force of contraction and subsequently increasing
stroke volume. Conversely, a decrease in venous return results in decreased myocardial fiber stretch,
leading to decreased stroke volume.

Mechanism

Increased venous return increases the preload, which is the degree of stretch of the myocardial
fibers at the end of diastole. Increased preload stretches the sarcomeres within the myocardial
fibers, leading to an optimal overlap of actin and myosin filaments, thus enhancing the force of
contraction during systole. The increased force of contraction results in increased ejection of blood
from the ventricles, leading to a higher stroke volume.
FACTORS THAT CAUSE HYPEREFFECTIVE HEART

1. NERVOUS STIMULATION

Sympathetic Nervous System Activation: Increased sympathetic nervous system activity, such as
during stress or exercise, can stimulate the heart to beat faster and with more force, leading to
increased cardiac output.

Release of Catecholamines: The sympathetic nervous system releases catecholamines (e.g.,

adrenaline, noradrenaline), which bind to beta-adrenergic receptors on cardiac muscle cells,
enhancing contractility and increasing heart rate.

2. HYPERTROPHY OF THE HEART MUSCLE

Physiological Hypertrophy: Regular aerobic exercise can lead to physiological hypertrophy of the
heart muscle, where the heart adapts to increased workload by increasing muscle mass and
contractility.

Pathological Hypertrophy: Chronic conditions such as hypertension, aortic stenosis, or

hypertrophic cardiomyopathy can lead to pathological hypertrophy of the heart muscle, where the
heart muscle thickens abnormally in response to increased pressure or volume overload.

FACTORS THAT CAUSES HYPOEFFECTIVE HEART

 1. HEART FAILURE: Heart failure can result from various underlying conditions such as coronary
artery disease, hypertension, or myocardial infarction, leading to impaired cardiac function and
reduced cardiac output.

2. CARDIOMYOPATHY: Structural abnormalities or damage to the heart muscle can impair its
ability to contract effectively, resulting in decreased cardiac output.

3. MYOCARDIAL INFARCTION: Acute blockage of coronary arteries leading to myocardial

ischemia or infarction can result in impaired cardiac function.

4. CARDIAC TAMPONADE: Compression of the heart by fluid or blood in the pericardial sac can
impair cardiac filling and lead to decreased cardiac output.

5. SEVERE HYPOVOLEMIA: Significant loss of blood volume, such as in haemorrhage or severe

dehydration, can lead to reduced preload and decreased cardiac output.

NORMAL VENOUS RETURN CURVE

The venous return curve represents the relationship between right atrial pressure (RAP) and cardiac
output (CO) or venous return (VR). Here are the key features of a normal venous return curve:

SHAPE: The curve is typically upward-sloping from right to left, indicating that increasing right atrial
pressure leads to increased venous return.

LINEAR PORTION: low right atrial pressures, the curve is relatively flat or linear, suggesting that
venous return is relatively insensitive to changes in right atrial pressure. This reflects the capacity of
the venous system to accommodate blood volume changes without significant changes in venous
return.
PLATEAU: As right atrial pressure increases, the curve reaches a plateau where further increases in
right atrial pressure have minimal effect on venous return. This plateau represents the point at which
venous return is maximized, typically corresponding to the maximum capacity of the venous system
to return blood to the heart.

FACTORS AFFECTING THE CURVE

1. Venous Tone: Changes in venous tone can shift the entire curve up or down. Increased venous
tone (vasoconstriction) shifts the curve upward, leading to increased venous return at any given right
atrial pressure, while decreased venous tone (vasodilation) shifts the curve downward.

2. Blood Volume: Changes in blood volume can alter the position of the entire curve along the x-axis
(right atrial pressure axis). An increase in blood volume shifts the curve to the right, reflecting
increased venous return at any given right atrial pressure, while a decrease in blood volume shifts
the curve to the left.

CLINICAL SIGNIFICANCE

The venous return curve provides insights into the relationship between venous return and right
atrial pressure under various physiological and pathological conditions.

It is an essential concept in understanding the regulation of cardiac output and hemodynamic

responses during changes in preload, such as during exercise, haemorrhage, or volume resuscitation.

DISTRIBUTION OF CARDIAC OUTPUT

Region Blood flow Arterio- O2 consumption Percentage of total
venous
Oxygen
difference
(ml/L) O2
extraction
ml/ ml/100g/ ml/min ml/100g/ Cardia O2
min min min c consumptio
output n
Liver 1500 57.7 34 51 2.0 27.8 20.4
Kidney 1260 420 14 18 6.0 23.3 7.2
Brain 750 54 62 46 3.3 13.9 18.4
Skin 462 12.8 25 12 0.3 8.6 4.8
Skeleta 840 2.7 60 50 0.3 15.6 20
l
Heart 250 84 114 29 9.7 4.7 11.6

MEASUREMENT OF CARDIAC OUTPUT USING THE OXYGEN FICK PRINCIPLE

The Oxygen Fick Principle is a method used to measure cardiac output (CO) based on the principle of
oxygen consumption and the oxygen content of blood.

Principle:
The Oxygen Fick Principle is based on the law of conservation of mass, which states that the amount
of a substance entering a system must equal the amount leaving the system.

In the context of cardiac output measurement, it states that the amount of oxygen taken up by the
tissues (oxygen consumption, VO2) must equal the amount of oxygen delivered by the blood (oxygen
delivery, DO2) to maintain tissue oxygenation.

Equation:

The equation used to calculate cardiac output (CO) using the Oxygen Fick Principle is:

Total O2 consumption
❑

Measure Oxygen Consumption (VO2): Oxygen consumption can be measured using various
techniques, such as indirect calorimetry, which estimates VO2 based on the rate of oxygen
consumption and carbon dioxide production.

Determine the Oxygen Content of Blood:

Arterial Oxygen Content (CaO2): Arterial blood is sampled to measure the partial pressure of oxygen
(PaO2) and oxygen saturation (SaO2). The oxygen content of arterial blood is calculated using the
oxygen-haemoglobin dissociation curve.

Venous Oxygen Content (CvO2): Venous blood is sampled, typically from the pulmonary artery or
central venous catheter, to measure the partial pressure of oxygen (PvO2) and oxygen saturation
(SvO2). CvO2 is calculated similarly to CaO2.

Calculate Cardiac Output: Using the measured values of VO2, CaO2, and CvO2, cardiac output can be
calculated using the Oxygen Fick Principle equation mentioned above.

Clinical Applications:
The Oxygen Fick Principle is commonly used in clinical settings, particularly in cases where direct
measurement of cardiac output using invasive methods (e.g., thermodilution, pulmonary artery
catheterization) is not feasible or desired.

It’s often used in conjunction with other hemodynamic monitoring techniques to assess cardiac
function and oxygen delivery to tissues in critically ill patients, especially those with shock, heart
failure, or respiratory failure.

CONTROL OF THE HEART BY SYMPATHETIC AND

PARASYMPATHETIC NERVES
The heart is innervated by both the sympathetic and parasympathetic branches of the autonomic
nervous system, which play crucial roles in regulating heart rate, contractility, and cardiac output.

SYMPATHETIC NERVOUS SYSTEM

Sympathetic nerves originate from the thoracic and upper lumbar segments of the spinal cord.

The primary neurotransmitter released by sympathetic nerves is norepinephrine (also called

noradrenaline).

EFFECTS ON THE HEART

Increases heart rate (positive chronotropic effect): Sympathetic stimulation accelerates the firing
rate of the sinoatrial (SA) node, the heart’s natural pacemaker, leading to a faster heart rate.

Increases contractility (positive inotropic effect): Sympathetic activation enhances the strength of
cardiac muscle contraction, resulting in increased stroke volume and cardiac output.

Increases conduction velocity:(Positive Dromotropic effect): Sympathetic stimulation speeds up the

conduction of electrical impulses through the atrioventricular (AV) node and Purkinje fibers,
facilitating rapid transmission of impulses within the heart.

PARASYMPATHETIC NERVOUS SYSTEM

Parasympathetic nerves originate from the medulla oblongata and the Vagus nerve (cranial nerve X).
The primary neurotransmitter released by parasympathetic nerves is acetylcholine.

EFFECTS ON THE HEART

Decreases heart rate (negative chronotropic effect): Parasympathetic stimulation slows down the
firing rate of the SA node, resulting in a slower heart rate.

Decreases contractility (negative inotropic effect): Parasympathetic activation reduces the strength
of cardiac muscle contraction, leading to decreased stroke volume and cardiac output.

Slows conduction velocity (negative dromotropic effect): Parasympathetic stimulation decreases the
conductivity of the AV node, prolonging the time it takes for electrical impulses to pass from the atria
to the ventricles.

BALANCE BETWEEN SYMPATHETIC AND PARASYMPATHETIC CONTROL

The heart is under continuous influence from both sympathetic and parasympathetic nerves, which
work together to maintain appropriate heart rate and cardiac output in response to changing
physiological demands.

The balance between sympathetic and parasympathetic activity is dynamically regulated by higher
centers in the central nervous system and reflex mechanisms to ensure optimal cardiac function
under various conditions, such as rest, exercise, stress, and sleep.

REGULATION OF CORONARY BLOOD FLOW

Coronary blood flow regulation ensures that the heart receives adequate oxygen and nutrients to
meet its metabolic demands.

1. METABOLIC REGULATION

Metabolic factors such as oxygen demand, adenosine levels, and pH play a significant role in
coronary blood flow regulation.

During increased myocardial activity (e.g., during exercise), there is an increased demand for oxygen
and nutrients. This leads to the release of metabolic byproducts such as adenosine, which dilates
coronary arteries to increase blood flow to meet the increased demand.

Similarly, during reduced myocardial activity (e.g., during rest), metabolic factors such as adenosine
levels decrease, resulting in vasoconstriction of coronary arteries to match blood flow with metabolic
demand.

2. NEURAL REGULATION

Sympathetic and parasympathetic nerves innervate the coronary vasculature and modulate coronary
blood flow.

Sympathetic stimulation leads to coronary artery vasoconstriction, which can occur during stress or
exercise to redistribute blood flow to areas of greater demand.
Parasympathetic stimulation causes coronary artery vasodilation, although its role in basal coronary
blood flow regulation is less significant compared to metabolic factors.

3. ENDOTHELIAL REGULATION

Endothelial cells lining the coronary arteries produce vasodilator and vasoconstrictor substances that
influence coronary blood flow.

Nitric oxide (NO) is a potent vasodilator released by endothelial cells in response to shear stress and
various stimuli. It relaxes vascular smooth muscle, leading to coronary artery dilation.

Endothelin-1 is a vasoconstrictor peptide released by endothelial cells in response to various stimuli

such as hypoxia, inflammation, and endothelial dysfunction. It contributes to coronary artery
constriction.

4. MYOGENIC REGULATION

The myogenic response refers to the ability of vascular smooth muscle cells to contract or relax in
response to changes in intravascular pressure.

When coronary artery pressure increases (e.g., during systole), vascular smooth muscle cells
contract, leading to vasoconstriction and regulation of coronary blood flow.

Conversely, when coronary artery pressure decreases (e.g., during diastole), vascular smooth muscle
cells relax, leading to vasodilation and maintenance of coronary blood flow.

5. HORMONAL REGULATION

Various hormones such as adrenaline (epinephrine), angiotensin II, and vasopressin influence
coronary blood flow.

Adrenaline released during stress or exercise stimulates β-adrenergic receptors on coronary smooth
muscle cells, leading to vasodilation and increased coronary blood flow.

Angiotensin II and vasopressin can cause vasoconstriction of coronary arteries, particularly in

response to low blood pressure or hypovolemia.
 SHOCK
Shock is a state of critical illness where the body's organs and tissues are not receiving enough
oxygen and nutrients due to inadequate blood flow. Shock can be caused by various factors that
disrupt the normal circulation of blood, including:

1. HYPOVOLEMIC SHOCK

Hypovolemic shock occurs due to a significant decrease in blood volume, leading to inadequate
perfusion of tissues.

Causes include haemorrhage (e.g., trauma, gastrointestinal bleeding), severe dehydration (e.g.,
vomiting, diarrhoea), and fluid loss from burns.

2. CARDIOGENIC SHOCK

Cardiogenic shock results from the inability of the heart to pump blood effectively, leading to
decreased cardiac output and tissue perfusion.

Causes include myocardial infarction, severe heart failure, myocarditis, and arrhythmias.

3. DISTRIBUTIVE SHOCK

Distributive shock is characterized by widespread vasodilation and impaired vascular tone, leading to
inadequate blood flow distribution despite normal or increased cardiac output.

Types of distributive shock include

Septic Shock: Caused by a systemic inflammatory response to infection, leading to vasodilation,

increased vascular permeability, and tissue hypoperfusion.

Anaphylactic Shock: Caused by a severe allergic reaction, leading to systemic vasodilation, increased
vascular permeability, and bronchoconstriction.

Neurogenic Shock: Caused by disruption of sympathetic nervous system control, leading to

widespread vasodilation and decreased vascular tone (e.g., spinal cord injury).

4. OBSTRUCTIVE SHOCK

Obstructive shock occurs when physical obstruction hinders blood flow through the circulatory
system, leading to inadequate tissue perfusion.

Causes include pulmonary embolism, tension pneumothorax, cardiac tamponade, and severe aortic
stenosis.

5. MIXED SHOCK

In some cases, shock may involve a combination of mechanisms, such as hypovolemia with
distributive features (e.g., septic shock with concurrent haemorrhage), making it challenging to
categorize into a single type.
STAGES OF HYPOVOLEMIC SHOCK
Hypovolemic shock is a life-threatening condition resulting from a significant decrease in blood
volume, leading to inadequate tissue perfusion and oxygen delivery. It typically progresses through
several stages as the severity of hypovolemia worsens. Here are the stages of hypovolemic shock.

1. INITIAL STAGE (COMPENSATED SHOCK)

In the initial stage, the body’s compensatory mechanisms are activated to maintain blood pressure
and tissue perfusion.

Symptoms may include anxiety, restlessness, increased heart rate (tachycardia), increased respiratory
rate (tachypnoea), and peripheral vasoconstriction.

Compensatory mechanisms such as increased heart rate, vasoconstriction, and the release of
catecholamines help maintain blood pressure and cardiac output despite reduced blood volume.

2. NON-PROGRESSIVE STAGE (DECOMPENSATED SHOCK)

As hypovolemia worsens, compensatory mechanisms become overwhelmed, and tissue perfusion

begins to deteriorate.

Symptoms become more pronounced and may include worsening tachycardia, hypotension (low
blood pressure), decreased urine output (oliguria), cool and clammy skin, and altered mental status.

The body’s ability to compensate for reduced blood volume becomes inadequate, leading to
progressive tissue hypoperfusion and the onset of organ dysfunction.

3. PROGRESSIVE STAGE (IRREVERSIBLE SHOCK)

In the progressive stage, tissue hypoperfusion becomes severe and irreversible organ damage occurs.

Symptoms include profound hypotension, marked tachycardia, altered mental status (confusion,
lethargy, coma), profound metabolic acidosis, and multiple organ failure.

Despite aggressive resuscitative efforts, the body is unable to restore adequate tissue perfusion and
oxygen delivery, leading to irreversible organ damage and death if left untreated.
NEUROGENIC SHOCK
Neurogenic shock is a type of distributive shock characterized by widespread vasodilation and
reduced vascular tone resulting from disruption of sympathetic nervous system control. It typically
occurs following spinal cord injury or severe central nervous system trauma.

CAUSES

Spinal Cord Injury: Traumatic injury to the spinal cord, particularly in the cervical or upper thoracic
regions, disrupts sympathetic nervous system control over vascular tone.

Severe Central Nervous System Trauma: Traumatic brain injury or other severe brain lesions can also
result in neurogenic shock due to disruption of autonomic nervous system function.

MECHANISM

Disruption of Sympathetic Tone: Damage to the spinal cord or brain interferes with sympathetic
nervous system signals that regulate vascular tone.

Loss of Vascular Tone: Without sympathetic stimulation, blood vessels throughout the body undergo
vasodilation, leading to a decrease in systemic vascular resistance (SVR) and blood pressure.

Redistribution of Blood: The vasodilation redistributes blood from central (core) circulation to
peripheral (limb) circulation, further decreasing blood pressure and impairing tissue perfusion.

CLINICAL FEATURES

Hypotension: Neurogenic shock typically presents with hypotension, which may be profound and
refractory to fluid resuscitation.

Bradycardia: Due to loss of sympathetic tone, neurogenic shock often manifests with bradycardia or
relative bradycardia (a less pronounced increase in heart rate in response to hypotension).
Warm and Dry Skin: Unlike other types of shock, neurogenic shock may present with warm and dry
skin due to peripheral vasodilation.

Hypothermia: Peripheral vasodilation can lead to heat loss and hypothermia in neurogenic shock
patients.

Altered Mental Status: Severe cases of neurogenic shock may be associated with altered mental
status, reflecting impaired cerebral perfusion.

Table: Types of Shock

Type of Shock Description Primary Causes Key Features
Hypovolemic Shock Resulting from a Hemorrhage, severe Hypotension,
significant loss of dehydration, burns, tachycardia, cool
blood volume or fluid. trauma clammy skin,
decreased urine
output
Cardiogenic Shock Caused by impaired Myocardial infarction, Hypotension,
heart function leading heart failure, pulmonary
to inadequate cardiac cardiomyopathy congestion, signs of
output. heart failure
Distributive Shock Characterized by Septic shock, Warm, flushed skin;
excessive vasodilation anaphylactic shock, wide pulse pressure;
leading to decreased neurogenic shock altered mental status
systemic vascular
resistance.
Obstructive Shock Results from Pulmonary embolism, Signs specific to the
mechanical tension underlying cause; e.g.,
obstruction of blood pneumothorax, dyspnea in pulmonary
flow. cardiac tamponade embolism
Septic Shock A subset of Bacterial, viral, or Hypotension
distributive shock fungal infections refractory to fluid
resulting from a resuscitation, fever,
systemic inflammatory altered mental status
response to infection.