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Definition: The cyclical changes that take place in the heart during each beat (one systole and
one diastole)
Duration for one cycle = 0.8 sec
 Atrial systole - 0.1 sec
 Atrial diastole- 0.7 sec
 Ventricular systole – 0.3 sec
 Ventricular diastole – 0.5 sec
 Contraction of atria & expulsion of blood into ventricles
 Contributes 25% of the ventricular filling
 Last phase of ventricular diastole
 Produces fourth heart sound
 Gradual filling of atria by blood brought by veins
 Contraction of ventricles & expulsion of blood into respective blood vessels
 Includes three phases
Isovolumetric contraction-0.05sec
Maximal ejection – 0.1 sec
Reduced ejection – 0.15 sec
Isovolumetric contraction
 Period between closure of AV valves & opening of semilunar valves
 Ventricles contract as closed chambers
 No change in the volume of blood in the ventricles
 Intraventricular pressure increases
Maximal Ejection phase
 Increase in intraventricular pressure
 Semilunar valves are forced to open
 Due to High Pressure gradient, blood is rapidly ejected out of ventricles
 About 2/3rd of stroke volume is ejected
Reduced ejection
 Due to decreased pressure gradient, the rate of ejection of blood is reduced
 About 1/3rd of stroke volume is ejected
 Filling of ventricles by the blood flowing from atria
 Includes five phases
Protodiastolic period – 0.04 Sec
Isovolumetric relaxation – 0.08 Sec
Rapid inflow – 0.11
Diastasis – 0.19
Atrial systole – 0.11

Protodiastolic phase
 Ventricle relaxes
 Intraventricular pressure in less than the pressure in the aorta/Pulmonary Arteries
 Semilunar valves close to prevent the back flow of blood from arteries into ventricles
 Closure of SLV produces second heart sound
Isovolumetric relaxation
 Period between closure of semilunar valves & opening of AV valves
 SLV and AV valves are closed
 Ventricle relaxes as closed chamber
 No change in the volume of blood in the ventricles
 Intraventricular pressure decreases
Rapid inflow phase
 Intraventricular pressure less than intra atrial pressure
 Hence AV valves open
 Blood flows from atria to ventricle at a faster rate
 Turbulence due to rapid flow produces third heart sound
 Increase in intraventricular pressure
 Blood flow from atria to ventricle at low rate or static
Atrial systole
 Last phase of ventricular diastole
 Contributes additional 25% of ventricular filling
4 recordable heart sounds (Phonocardiogram)
 First heart sound-S1 – Caused by closure of AV valves. Occurs at the beginning of
ventricular systole
 Second heart sound S2- Caused by closure of Semi Lunar Valves. Occurs at the end
of ventricular systole
 Third heart sound- Due to rapid ventricular filling
 Fourth heart sound- Caused by atrial systole
Pressure and volume changes in the atria & ventricle during cardiac cycle
 Intra atrial pressure curve
 Intraventricular pressure curve
 Aortic pressure curve
 Ventricular volume curve
Intra-atrial pressure curve
3 Positive waves – a, c & v (caused by increase in intraatrial pressure)
2 Negative waves - x & y (caused by decrease in intraatrial pressure)
 ‘a’ wave - due to atrial systole
 ‘c’ wave – due to bulging of AV valve into the ventricles during isovolumetric
 ‘v’ wave – due to filling of atria after the closure of AV valves

Intraventricular pressure curve: (Left ventricular pressure)

 During isovolumetric contraction phase – Pressure rises steeply due to a rise in
 Maximum ejection phase – Maximum pressure (120 mmHg) develops as the ventricle
is contracting with a maximum force
 Reduced ejection phase – Pressure is less during this phase
Aortic pressure Curve:
 During diastole of heart, the aortic pressure is maintained at 80 mmHg
 During systole of the heart, it rises to 120 mmHg
Ventricular volume curve:
 End diastolic volume – During diastole, ventricular volume increases. The maximum
volume of blood in the ventricle at the end of diastole is called End Diastolic
volume. It is normally 130 ml.
 Stroke Volume: Volume of blood ejected out from ventricle during systole. It is 80 ml
 End Systolic Volume: The minimal volume of blood remaining in the heart at the end
of systole
“P” wave = is due to atrial depolarization which occurs before atrial systole
“QRS” complex = is due to ventricular depolarization which occurs before ventricular
“T” wave is due to ventricular repolarization which occurs before ventricular diastole

Wiggers Chart

A) Definition:
Cardiac output (CO) – Volume of blood ejected by each ventricle / minute
Stroke volume (SV) – Volume of blood ejected by each ventricle / beat
Cardiac Index (CI) – Cardiac output / square meter of the body surface Area
End Diastolic Volume (EDV) – Volume of the blood in the ventricle at the end of diastole
Ejection Fraction (EF) – Fraction of the end diastolic volume that is ejected
Peripheral Resistance (PR) – The resistance offered to the blood flow in the peripheral
blood vessels
B) Normal values:
Cardiac output – 5 lts / min
Stroke volume – 70 ml/ beat
Cardiac index – 3 lts/ min/square metre of body surface area
End diastolic volume – 120 ml
Ejection Fraction -- 65%
Direct method
Indirect method
 Fick principle
 Dilution principle (Dye. Isotope & Thermo dilution)
 Ballistocardiography
 Pulse pressure contour
 X – ray cardiometry
The cardiac output is calculated by the following formula
Q = ----------
A – V difference
Q – Blood flow
X – Amount of substance taken up by an organ
A -- V difference = Arterio venous difference in the concentration of a substance
As pulmonary blood flow is equal to cardiac output, pulmonary blood flow determined
by Fick principle is taken as cardiac output.
Pulmonary blood flow = amount of O2 taken by the lungs/minute
Arterio venous difference of O2
For example
Amount of oxygen taken by lungs / minute = 250 ml
(Determined by spirometer)
Arterial oxygen content = 20 ml / 100 ml of blood
(Estimated from any peripheral artery)
Venous oxygen content = 15 ml / 100 ml of blood
(Estimated from right atrium)
Pulmonary blood flow = 250
--------- X 100 = 5000 ml 0r 5 lts
20 - 15

As pulmonary blood flow = cardiac output, CO = 5 lts

A known amount of dye is injected into the peripheral vein and blood samples are
collected from the peripheral artery and the concentration of the dye in each sample is
Cardiac output can be calculated by using the following formula:
Amount of the dye injected
Mean concentration of the dye over a period of 1 minute
The commonly used dye is EVAN”S BLUE (T—1824)
C) Regulation of Cardiac output:
Cardiac output = Stroke volume x Heart rate
Peripheral resistance

Stroke volume = Myocardial contractility X End Diastolic Volume (EDV)

Heart rate End Diastolic Volume

(chronotropic) Cardiac Output (Pre load)

Myocardial Peripheral resistance

Contractility (After load)

Cardiac Output Regulation

Heterometric regulation Homometric regulation

(Factors which cause an increase in the initial (Factors which do not cause any change
length of cardiac muscle before contraction) in the initial length of cardiac muscle
before contraction)
Heterometric regulation of cardiac output
I. Intrinsic factors regulating myocardial contractility
Frank – Starling Phenomenon:
The force of contraction is directly proportional to the initial length of the
cardiac muscle. The initial length of the muscle depends on the end diastolic
volume. Any increase in the EDV stretches the ventricular myocardium,
increasing the length of the muscle fiber
– helps to match the stroke volume of the ventricles
– helps to maintain the minute output
– prevents venous engorgement

Force Frequency relation:

Any increase in the frequency of heart beat increases myocardial contractility
within physiological limits. The increase in contractility is due to accumulation of
intracellular calcium ions
II. End Diastolic volume:
End Diastolic Volume (EDV) is the volume of blood in the ventricles
at the end of diastole. Any increase in the EDV increases the cardiac output by
increasing the stroke volume.
Mechanism: Increase in EDV  stretching of ventricular muscle fibres 
Increase in the length of fibres  stronger muscle contraction
Increase in cardiac output (Frank Starling’s law)
Factors influencing EDV:
i) Venous return
ii) Ventricular compliance
iii) Diastolic pause
iv) Atrial systole
Venous return: The volume of blood that returns to the atria through the veins in
one minute. This increases EDV & there by increases cardiac
Factors influencing venous return:
1. Cardiac pump: The pumping action of ventricles increases
venous return by 2 forces:
 Vis – a – tergo (propelling force from behind):
- Left ventricular contraction during systole and
elastic recoiling of arteries during diastole push
the blood from aorta towards the right atrium
 Vis – a –fronte (suction force from front) – Right
atrial pressure:
- Less pressure in right atrium during diastole helps
in suction of blood from the great veins into the
right atrium
2. Capacity of venous reservoir: This factor is inversely
proportional to venous return .
Venoconstriction  decrease in venous capacity  increase
in venous return
3. Blood Volume: Directly proportional to venous return.
e.g., hemorrhage  decrease in blood volume  decrease in
venous return
4. Respiratory pump: Venous return increases during inspiration
Inspiration  negative intrathoracic pressure  suction of
blood into thoracic big veins  increased venous return
5. Muscle pump: Intermittent contractions of skeletal muscle
particularly leg muscle  squeeze the veins  increases the
flow of venous blood towards the heart  increase in venous

6. Abdominal pump: Contractions of abdominal muscles 

compresses the great veins, pushing venous blood towards the

Right atrial pressure

Blood volume Respiratory pump

Cardiac pump Venous return Vascular capacity

Abdominal pump Muscle pump

Ventricular compliance:
- refers to the stretchability of ventricular myocardium
- any increase in the compliance reduces EDV and thereby stroke volume
e.g constrictive pericarditis & pericardial effusion
Diastolic pause:
- refers to the duration of diastole of ventricles
- this influences the ventricular filling
- this factor is directly related to EDV within physiological limits
Atrial systole:
- contributes 20% of ventricular filling at rest
- influences EDV directly
- increase in atrial systole during exercise  increase in EDV
- in atrial flutter & fibrillation, the contribution of atrial systole in ventricular
filling is reduced
Homometric Regulation of Cardiac Output
I . Extrinsic Factors Regulating Myocardial Contractility
a) Neural factors:
Sympathetic stimulation: Releases nor-epinephrine  binds to β1 receptors  increases
cAMP  increase in intracellular calcium  increase in myocardial contractility
Parasympathetic stimulation: Releases acetylcholine  binds to muscarinic receptors
(M2)  hyperpolarization of SA nodal and myocardial cells  decrease in myocardial
b) Hormones:
Epinephrine & Nor-epinephrine: Bind to β1 receptors increase in cAMP  increase in
intracellular calcium  increase in myocardial contractility
Glucagon: Increases myocardial contractility by increasing intracellular calcium without
binding to β1 receptors
Thyroxine: Increases the myocardial contractility by increasing the metabolic rate.
c) Ions:
Sodium & Potassium – decreases the myocardial contractility
Calcium – increases the myocardial contractility

d) Drugs:
β – blockers: e.g Propanaolol – block the β – receptors and decreases the myocardial
Calcium-channel blocker: e.g Verapramill – block the calcium channel  decrease in
intracellular calcium  decrease in myocardial contractility
Digitalis: Blocks Na+ - K+ ATPase  decrease in Na+ gradient across the membrane 
calcium accumulation inside the cell  increase in myocardial contractility
e) Coronary blood flow:
Decrease in coronary blood flow

Hypoxia, hypercapnia & acidosis

Decrease in myocardial contractility

Intrinsic Factors Extrinsic Factors

Frank-Starling phenomenon O Neural
C Parasympathetic
R Catecholamines
D Hormonal Glucagon
I Thyroxine
Force – Frequency relation A
L Ions (Na+, K+ & Ca2+)
C β-blockers
Drugs Calcium channel blockers
T Digitalis
A Coronary blood flow

Influence of heart rate on cardiac output

- Direct relationship between heart rate and cardiac output
Increase in HR

Increase in intracellular calcium

Increase in force of contraction

- This happens by two ways:

1. As a multiplying factor
2. Staircase phenomenon
(This relation is linear upto 180 BPM. Beyond this level, venous return falls 
decrease in cardiac output)
Influence of peripheral resistance on cardiac output:
- Initially, the variation in peripheral resistance tends to influence cardiac output
- But the indirect effects maintain the cardiac output
Blood Pressure : The lateral pressure exerted by the moving column of blood on the walls
of the arteries
Systolic BP : The maximum BP in the arteries during systole of the heart.
Diastolic BP : The minimum BP in the arteries during diastole of the heart.
Pulse pressure : The difference between systolic and diastolic pressure
Mean Arterial BP : The average BP in the arteries. This is calculated as Diastolic BP + 1/3 of
pulse pressure
Normal Values:
Blood Pressure : 120/80 mm Hg
Systolic BP : 90 – 140 mm Hg
Diastolic BP : 60 – 90 mm Hg
Pulse pressure : 40 mm Hg
Mean Arterial BP : 95 mm Hg

Regulation Of Arterial Blood Presssure:

Short – Term or Rapid Acting Mechanisms

1. Baroreceptor reflex
2. Chemoreceptor reflex
3. Cushing reflex
4. Stress relaxation & inverse stress relaxation
5. Capillary fluid shift
6. Hormones
Baroreceptor reflex:
- Also called as “Marey’s reflex” or “Sino-Aortic reflex”
- Initiated by increase in blood pressure
- Receptors are mechanoreceptors which respond to stretch in blood vessel wall
- Receptors are called “Baroreceptors”. They are present in the carotid sinus and
aortic arch
- This mechanism can correct 2/3rd of fall in BP
- The working range of BP is 60-200 mm Hg

Increase in BP

Stimulation of baroreceptors
(Carotid sinus and aortic arch)

Stimulation of NTS (Nucleus of Tractus Solitarius) in medulla

Inhibition of VMC Stimulation of CVC

(Vasomotor center) (Cardiovascular center-
Nucleus Ambiguus)

Inhibition of SNS
(Sympathetic Nervous Stimulation of vagus

Decreased Increased vagal tone

sympathetic tone

Blood vessel Adrenal medulla

Vasodilatation Decreased catecholamine Bradycardia

Venodilatation secretion

Net effect:
Decreased Peripheral resistance
&  Decrease in BP
Decrease in cardiac output

Decrease in BP

Inhibition of baroreceptors
(Carotid sinus and aortic arch)

NTS is not stimulated

stimulation of VMC Inhibition of CVC

(Vasomotor center) (Cardiovascular center-
Nucleus Ambiguus)

Stimulation of SNS
(Sympathetic Nervous Inhibition of vagus

Increased sympathetic Decreased vagal tone


Blood vessel Adrenal medulla

Vasoconstriction Increased catecholamine Tachycardia

Venoconstriction secretion

Net effect:
Increased Peripheral resistance
&  Increase in BP
Increase in cardiac output

CNS ischemic response:

- This mechanism occurs due to ischaemia of brain
- This may result due to severe fall in BP below 40 mmHg
- If this response is specifically due to increase in intracranial pressure, it is called
as “Cushing reflex”
- The response is called “last ditch effort” as it tries to prevent the death of a
- The working range for this mechanism is 15-50 mm Hg
- It can correct 90% of the fall in BP
Decrease in BP (below 40 mm hg)

Decreased blood flow to the brain

Ischemia of brain

Stimulation of VMC
(Vasomotor center)

Stimulation of SNS
(Sympathetic Nervous

Increased sympathetic

Blood vessel


Increase in BP

Chemoreceptor Reflex:
- Receptors respond to chemicals. So called as chemoreceptors
- Two types of receptors – peripheral & central chemoreceptors
- Peripheral chemoreceptors - Carotid bodies & Aortic bodies
- Stimuli for receptors : Hypoxia, Hypercapnia & Acidosis

Decrease in BP (<40 mm Hg)

Cerebral hypoxia, hypercapnia & acidosis

Stimulation of VMC
(Vasomotor center)

Stimulation of SNS
(Sympathetic Nervous

Increased sympathetic

Blood vessel


Stress relaxation and reverse stress relaxation mechanism:

Increase in BP  Stretching of blood vessels  Stress relaxation  Loss of
vasomotor tone  increased capacity of vascular bed  Pooling of blood 
Decrease in circulating blood volume  Decrease in BP

Decrease in BP Blood vessels are not stretchedIncrease in vasomotor tone 

decreased capacity of vascular bed Increase in circulating blood volume Increase
in BP
Capillary Fluid Shift Mechanism:

Increase in BP Decrease in BP

Increase in capillary Decrease in capillary

Hydrostatic pressure Hydrostatic pressure

Fluid Decrease in BP Fluid Increase in BP

Interstitial space Interstitial space

1. Catecholamines: Fall in BP  release of catecholamines (epinephrine &
norepinephrine) from adrenal medulla  Vasoconstriction & increase in cardiac output
 increase in BP
2. ADH: In large amounts ADH causes vasoconstriction  increase in BP
3. Glucocorticoids: Cortisol and corticosterone sensitize the vascular smooth muscle to the
action of catecholamines (permissive role)
4. Nitric oxide (Endothelium Derived Relaxing factor) :released by endothelium and acts
locally causing vasodilatation
Long Term Regulation of Blood Pressure
1. Renal body fluid mechanism
2. Renin-Angiotensin mechanism
3. Hormones – Aldosterone & ADH

Renal body fluid mechanism:

Increase in BP Decrease in BP

Increase in renal blood flow Decrease in renal blood flow

Increase in GFR Decrease in GFR

Increase in urine formation Decrease in urine formation

Decrease in ECF volume Increase in ECF volume

Decrease in BP
Increase in BP
(Restoration of BP)
(Restoration of BP)

Renin – Angiotensin Mechanism:

Decrease in BP

Decrease in renal blood flow

Decrease in GFR

Renal ischemia or decreased

Na+ & Cl- at macula densa

Release of renin from

juxtaglomerular cells of

Angiotensinogen Angiotensin I

Angiotensin II
Angiotensin III

Angiotensin II & Angiotensin III

Vasoconstriction reabsorption of Aldosterone ADH secretion

Na+ & Cl- secretion
(direct effect on kidney)

reabsorption of reabsorption of
Na+ & Cl- water

Increase in ECF volume

Increase in blood volume

Increase in blood pressure

Hormones Regulating Blood Pressure:

Aldosterone: Secreted from adrenal cortex in response to decrease in ECF volume.
Increases the reabsorption of Na+ & Cl- in kidney tubules. This causes
increase in ECF volume and blood pressure
ADH: Secreted from posterior pituitary. Increases water reabsorption from kidney 
increase in ECF volume and blood pressure
ANP: Secreted from atrial myocardium in response to increase in ECF volume facilitates
Na+, Cl-& H2O excretion into urine  decrease in ECF volume & blood pressure