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1. CARDIAC CYCLE
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
Phases:
Atrial systole - 0.1 sec
Atrial diastole- 0.7 sec
Ventricular systole – 0.3 sec
Ventricular diastole – 0.5 sec
ATRIAL SYSTOLE
Contraction of atria & expulsion of blood into ventricles
Contributes 25% of the ventricular filling
Last phase of ventricular diastole
Produces fourth heart sound
ATRIAL DIASTOLE
Gradual filling of atria by blood brought by veins
VENTRICULAR SYSTOLE
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
VENTRICULAR DIASTOLE
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
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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
Diastasis
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
HEART SOUNDS
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
HEMODYNAMIC CHANGES
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
contraction
‘v’ wave – due to filling of atria after the closure of AV valves
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Wiggers Chart
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2. CARDIAC OUTPUT
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%
METHODS TO DETERMINE CARDIAC OUTPUT
Direct method
Indirect method
Fick principle
Dilution principle (Dye. Isotope & Thermo dilution)
Ballistocardiography
Pulse pressure contour
X – ray cardiometry
FICK PRINCIPLE
The cardiac output is calculated by the following formula
X
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
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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
e.g
- 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
contractility
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
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d) Drugs:
β – blockers: e.g Propanaolol – block the β – receptors and decreases the myocardial
contractility
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
Increase in BP
↓
Stimulation of baroreceptors
(Carotid sinus and aortic arch)
↓
Stimulation of NTS (Nucleus of Tractus Solitarius) in medulla
↓
Inhibition of SNS
(Sympathetic Nervous Stimulation of vagus
System)
Heart
Blood vessel Adrenal medulla
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 SNS
(Sympathetic Nervous Inhibition of vagus
System)
Heart
Blood vessel Adrenal medulla
Net effect:
Increased Peripheral resistance
& Increase in BP
Increase in cardiac output
Stimulation of SNS
(Sympathetic Nervous
System)
Increased sympathetic
tone
Blood vessel
Vasoconstriction
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
Stimulation of VMC
(Vasomotor center)
Stimulation of SNS
(Sympathetic Nervous
System)
Increased sympathetic
tone
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Blood vessel
Vasoconstriction
Increase in BP Decrease in BP
Hormones:
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
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Decrease in BP
Increase in BP
(Restoration of BP)
(Restoration of BP)
Decrease in GFR
Angiotensinogen Angiotensin I
Angiotensin II
&
Angiotensin III
reabsorption of reabsorption of
Na+ & Cl- water