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  1. Decrease of Na+: Causes low voltage ECG
  2. Hypothermia → Elevation of the j-point — Osborne wave.
  3. Digitalis toxicity —short QT interval with “scooping” of the ST-T wave comples (i.e. Depression of ST-T segment) Q
  4. Sub arachnoid Hemorrhage “CVAT-wave” pattern à marked QT prolongation with deep wide T-wave inversions Q
  5. Hyper kalemia: Tall peaked T waves. At higher levels, ; Paralysis of atria, prolongation of QRS ventricular arrhythmia. Since the RMP es as ECF K+ es, eventually heart stops in diastole
  6. Hypokalemia:
  7. ST
  8. Prominent U waves
  9. Increase in Ca++ in ECF : Short QT interval , increases myocardial contractility; if too much calcium, there is calcium rigor and the heart stops in systole.
  10. Decrease in Ca++

a. ST segment prolongation

b. QT interval prolongation

HIS Bundle Electrogram (HBE)

1. This is used to study events in the

a. AV node

b. Bundle of His

c. Purkinje system

2. There are 3 waves in HBE:

Wave Denotes
A deflection AV nodal activation
H spike Transmission through bundle of His
V deflection Ventricular depolarization

There are 3 intervals described (marked with the help of HBE and standard (ECG):



From – to


PA (27 ms)

First appearance of atrial depolarization to ‘A’ wave in HBE

Conduction time from SA node to AV node

AH (92 ms)

‘A’ wave to start of ‘H’

AV node conduction time


HV (43 ms)

Start of ‘H’ to start of QRS

Conduction in bundle of His and branches

[Note that PA ++ AH+ HV internal = PR interval]

From the HBE, a distinction can be made between supra ventricular tachycardia (H spike present) and ventricular tachycardia (No H spike)

Cardiac Cycle

Note that mechanical events follow electrical events; atrial systole starts after ‘P’ wave and ventricular systole starts near the end of ‘R’ wave and ends just after ‘T’ wave.



1. Duration of 1 cardiac cycle = 0.8 second


2. Ventricular systole = 0.3 second


3. Ventricular diastole = 0.5 second


4. Atrial systole = 0.1 second


5. Atrial diastole = 0.7 second


Atrial Systole

  1. P wave on the ECG precedes atrial systole, which contributes to ventricular filling that causes the fourth heart sound. duration 0.1 sec.
  2. 30% ventricular filling is due to atrial contraction
  3. Correlates with a- wave in JVP
  4. Ventricular systole : 0.3 sec
    1. Isovolumetric contraction – c wave in JVPb.      
    2. Rapid ejection        x decent in JVP
    3. Slow ejection
    4. the first heart sound (lub) - This sound is generated by the closing of the AV valves (& this occurs because increasing pressure in the ventricles causes the AV valves to close) initially there is no change in ventricular volume (called the period of isovolumetric contraction) because ventricular pressure must build to a certain level before the semilunar valves can be forced open & blood ejected. Once that pressure is achieved, & the semilunar valves open, ventricular ejection occurs in rapid (2/3ed of ejection) and slow ejection.

1. Ventricular diastole: 0.5 sec

  1. Isovolumetric relaxation - v wave in JVP
  2. Rapid filling
  3. Slow filling (diastasis)
  4. the second heart sound (dub)- this sound is generated by the closing of the semilunar valves
  5. Ventricular volume increases rapidly (period of rapid inflow) - this occurs because blood that accumulated in the atria during ventricular systole (when the AV valves were closed) now forces open the AV valves & flows inside. This causes the third heart sound. After this 'rapid inflow', ventricular volume continues to increase, but at a slower rate (the period of diastasis).

2. Waves in JVP

a wave          Venous distention due to right atrial contraction

c wave          Bulging of tricuspid valve into the right atrium during right ventricular isovolumetric                   

                    contraction and by the impact of the carotid artery adjacent to the jugular vein.

x descent      Atrial relaxation and to the downward displacement of the tricuspid valve during

                    ventricular systole.

v wave           Increasing volume of blood in the right atrium during ventricular systole when the tricuspid valve is closed

y descent      Opening of the tricuspid valve and the subsequent rapid inflow of blood into the  

right ventricle.


Some Abnormalities in JVP


1. Giant ‘C’ wave: Seen in tricuspid regurgitation

2. Giant ‘a” wave (common wave) : Seen in complete heart block


Pressures (mmHg)

  1. Pulmonary artery                  25/10
  2. Mean                                   10-15
  3. Aorta                                   120/80
  4. Mean                                   100
  5. Left atrium                           5
  6. Pulmonary capillaries :          8
  7. Left ventricle:                       120/ 0
  8. Right ventricle:                     25/0      


  1. Stroke volume (SV): This is the amount of blood ejected by each ventricle per stroke; it is between 70-90 ml
  2. End- diastolic volume (EDV): This is the amount of blood in the ventricle at the end of diastole; it is around 130ml
  3. End- systolic volume = EDV- SV (it is around 50ml) 
  4. Ejection fraction: ­ the percentage of EDV that is ejected with each stroke and is about 65%
    0-90 x 100 65%  130
  5. The ejection fraction is a valuable index of the ventricular function

a. Cardiac output = S.V. x Heart rate

b. Blood pressure = C.O x peripheral resistance

Heart Sounds

S1:  Closure of A-V valves                                              
S2:  losure of semilunar valves

S3:  Rapid ventricular fillings                                         
S4:  Forceful atrial contraction

Arterial pulse
- this is because of the pressure wave set up in the walls of the vessels. The rate of the pressure wave is

  1. Aorta                 4m/s
  2. Large arteries     8m/s
  3. Small arteries     16m/s

NOTE: the rate of blood flow at the root of the aorta is 40cm/s) With age, the arteries get thickened and the pressure wave, moves faster. The strength of the pulse is determined by the pulse pressure (the difference between systolic and diastolic pressure); it bears no relation to the mean arterial pressure. The dicrotic notch corresponds with the closure of aortic valve.


4. Cardiac output:

Definition: Amount of blood ejected by each ventricle per minute

Value = 5L/ min


Formula= C-O =S.V X H.R


Its value is 3.2 L/Sq.m/min

  1. Fick method
  2. Dye dilution / thermo dilution                         
  3. Doppler plus echocardiograph
  4. FICK’s PRINCIPLE states that blood flow equals the amount of a substance absorbed or excreted by an organ (or whole body) per unit time divided by the arteriovenous difference of that substance across the organ.  This principle can be used to calculate the cardiac output  by measuring the oxygen consumption of body per unit time and A-V difference of oxygen across the lung.
  1. Thermodilution technique
  1. Method - cold saline is injected into the right Atrium. Temperature change in the blood is then recorded in the pulmonary artery.
  2. Principle - The temperature change is inversely proportional to the amount of blood flowing through the pulmonary artery
  3. Facts about estimating CO by thermodilution technique :­
  4. The Indicator dilution (thermo-dilution) method is least reliable when the cardiac out is low and transit of cold bolus through right is delayed.  

Indicator-Dilution techniques

It is based on Stewart – Hamitton Principle

Example : There is severe valvular regurgitation or a low cardiac output state in which the washout of the indicator is prolonged and recirculation begins well before an adequate decline in the indicator curve occurs, determinations are erroneous. Intracardiac shunts may also greatly affect the shape of curve.


Thermo dilution method has several advantages: - it obviates the need for withdrawal of blood from an arterial site- and Less affected by recirculation. However a significant error occurs in patients with severe tricupsid regurgitation. Also, in patients with low outputs (esp < 2.5L/rnin), thermodilution tends to overestimate the cardiac out

Regulation of Cardiac Out Put

Since C-O = HR X SV, it can be regulated by HR and SV
  1. HR: This is influenced by sympathetic and parasympathetic innervation
  2. S.V: This can be changed by

  1. Heterometric regulation: - This is based on Frank Starling Law; more is the initial length of the cardiac muscle preload, as indicated by EDV , more will be the SV (with in physiologic limits).
    Factors that normally increase or decrease the length of ventricular cardiac muscle fibers:


  1. Increase
    1. Stronger atrial contractions
    2. Increased total blood volume
    3. Increased venous tone
    4. Increased pumping action of skeletal muscle
    5. Increased negative intrathoracic pressure
  2. B. Decrease
    1. Standing (Lying to standing in position)
    2. Increased intrapericardiac pressure
    3. Decreased ventricular compliance
  3. Homocentric regulation:- This S.V can also be changed for the same initial length . This is called homometric regulation. For example, positively inotropic agents like catecholamines , xanthines , glucagon and digitalis -  increase the S.V; negatively inotropic states like hypercapnia , hypoxias , acidosis , certain drugs ,(eg barbiturates ,quinidine) heart failure , M.I - decrease the S.V .
  4. To summarise, C.O can be either regulated by heterometric regulation (Frank starling law) with regulation based on a change in initial length or EDV) or by homometric regulation.
  5. Venous return: Venous return is equal to CO, it depends on:
    1. Respiratory pump (negative intrathoracic pressure)
    2. Peripheral Muscle pump
    3. Cardiac pump
    4. Sympathetic tone
    5. Venous Compliance
    6. Gravity (like posture)
    7. Deep fascia
    8. Venous valves
    9. Venous pressure gradient that is VR = Psf – RAF/ RVR in which VR is venous return, Psf is mean systemic filling pressure, PRA is right atrial pressure, and RVR is resistance to venous return. Psf in turn depends on arterial pressure.

Work done / O2 consumption

  1. Work done :- Ventricular work per beat correlates well with O2 consumption
  2. Left ventricular work/ beat = S.V. X M.A.P                in aorta
  3. Right ventricular work/ beat = S.V. X M.A.P in pulmonary artery ( MAP= Means Arterial pressure)
  4. Since aortic pressure is nearly 7 times pulmonary arterial pressure , the left ventricular stroke work is 7 times right ventricular stroke work.
    1. Preload: It is the volume that is present in the ventricles before heart contracts or simply EDV. Can also be said as volume work as more is preload more is the stroke volume (Frank Starling Law).It depends on ventricular compliance, heart rate, venous return etc. It is increased by: ↑ blood vol., ↑ venous return, MR & AR.
    2. Afterload: It is the pressure against which ventricles have to contract. Also called pressure work. It is increased in AS, ↑ MAP or HT, ↑ Resistance to blood flow.
    3. Out of the pressure work and volume work, since work= volume X pressure, the pressure work (Afterload) produces a greater increase in total work done and O2 consumption than volume work (preload).Since work done is asymmetrical there is concentric hypertrophy in AS and Eccentric or dilatational hypertrophy in AR. Secondly chances of MI are more in AS as compared to AI.
O2 consumption by the heart:- The beating heart at rest consumes 9 ml / 100g /min of O2
  1. The arterio – venous O2 difference is maximum in the heart.
  2. The O2 consumption is determined by
    i. Intra myocardial tension                 
    ii. Contractile state of myocardium                  
    iii. Heart rate
  3. Note :- Myocardial O2 usage is most closely related to the tension time index (TTI).
  4. The tension time index is a product of the mean systolic pressure , the duration of systole and the heart rate.
    (The higher the heart rate the greater is the myocardial O2 usage, for any given cardiac output.)
1. The pressure volume (PV) loop analysis depicts the relationship between left ventricular volume and left ventricular pressure during a single cardiac cycle . Opening and closing of the mitral and aortic valves are represented by the inflection points A, B, C, D respectively:
Fig. Normal pressure-volume (PV) loop and valve positions.
AB =     LV filling
BC =     Isovolumetric contraction
CD =     LV ejection
DA =    Isovolumetric relaxation
Point-A = Coincides with MV opening, and represents LV end-systolic volume and early diastolic pressure

Point- B = Coincides with MV closure, and represents LV end diastolic pressure (LV EDP) and volume (LVEDV)

Point-C= Represents opening of Aortic valve and coincides with systemic, aortic diastolic pressure

Point-D= is the closure of the Aortic valve and represents LV end systolic pressure and volume, coinciding with the dicrotic notch in the Aortic pressure tracing

Segment AB => LV compliance is defined by the slope of the filling phase or segment AB ≈ Preload or EDV. The compliance is decreased when the ventricles become stiff or unable to fill properly eg MI, constrictive pericarditis, pericardial effusion etc and the PV loop(baseline shifts up.
Therefore PV loops analysis → gives information about - LV compliance, Preload, contractility. Stroke volume (SV) [SV = EDV - ESV], Ejection Fraction (EF)  and various valvular lesions. Remember: The curve shifts to right side in case of increased preload, Upside in case of increased afterload and to Left & upside in incase of increased myocardial contractility
  • In AS - High LV systolic pressure and an upward and counter clock wise rotation in the end-diastolic pressure volume relationship i.e. AB line shifted to upward. indicative of ↓↓ chamber compliance i.e. ↓ LV compliance.
  1. SV and EF are well preserved
  2. Contractility – ↑↑
  • In Aortic Insufficiency (i.e. AR)

Enlarged LV, minimal change in LVEDP despite the large volume preload (Increase compliance).PV curve shifted to right side.

  • In MS
    PV loop illustrates hypovolemia Since the predominant impact of MS occurs proximal to the left ventricle, the PV loop analysis format is less useful.
  • In MR
    The diastolic PV relationship (line AB) is shifted to the right as it in AI, consistent with a marked increase in compliance (contractility is decreased)

Summary: PV loop (AB line) shifted                                             

  1. To slight right and upwards in AS
  2. To right in MR
  3. To right in AI
  4. In MS à left shift but PV loop analysis is less useful

A = Normal

B = Mitral stenosis

C = Aortic stenosis

D = mitral regurgitation

E = aortic regurgitation


a. Vessels

  1. Wind kessel vessels : show elastic recoil eg aorta, major arteries (2 % in aorta, 8% in rest)
  2. Resistance vessels : innervated, eg arterioles. (max. smooth muscle and wall thickness to    lumen ratio)
  3. Precapillary sphincters : not innervated, affected by local metabolites
  4. Exchange vessels : capillaries, not innervated (5 % of blood vol.)
  5. Capacitance vessels : veins, thin walled, poor innervation (55 % of blood vol. )
  6. Shunt vessels : A-V anastomoses (bypass capillaries), in skin for temp. regulation Cross sectional area : is minimum for aorta and maximum for capillaries

Note:-Cross sectional area: is minimum for aorta and maximum for capillaries


3 types           

  1. Continuous eg. brain, skin
  2. Fenestrated eg. GIT, glomeruli of kidney, endocrine glands, circum ventricular organs
  3. Discontinuous (Sinusoids) eg. liver, bone marrow
  4. The least permeability of capillaries is that is the brain


These are associated with capillaries and post capillary venules. They are similar to the mesangial cells in   the renal glomeruli.

  1. They are contractile
  2. They release vasoactive agents
  3. They synthesize and release constituents of bone marrow and extra cellular matrix.

One of their functions is to regulate the flow through the junction between the endothelia cells, especially during inflammation


c. Distribution of Blood

Systemic veins   54%
Pulmonary circulation                                                                                                                                               18%
Heart cavities                                                                                                                                                              12%
Arteries        8%
Capillaries       5%
Aorta      2%
Arterioles          1%


d. Biophysical principles:-

F=P/R (Where F= flow , P= effective perfusion pressure , R= resistance) or R=P/F If P is expressed in mm Hg and flow is expressed in ml/second, then resistance will be expressed in ‘R’ units

[Or peripheral resistance units (PRU)]

e. Blood Flow Measurement

Direct method    Indirect method
i. Electro magnetic flow meters   
i. Fick method
ii. Doppler flow meter      
ii. Indicator method eg. Kety method for cerebral blood flow using N2O
iii. Plethysmography
  1. While applying the biophysical principles, one must bear in mind that vessels are not rigid tubes and that blood is not a perfect fluid. Thus there can be differences between in vivo and in vitro conditions.
Flow can be laminar (streamline) or turbulent:         
Laminar Turbulent
1. Silent 1. Noisy
2. Paraboloid velocity profile – flow is maximum

in the center of the flow and goes on decreasing towards the wall

2. No such gradient in flow rate from

center of the flow towards the vessel wall exists

3. More efficient (less energy consumption) 3. less efficient
  1. The probability of turbulence in a given flow can be determined by Reynold’s number:
    Re= PDV/ (Where Re = Reynold ‘s number, P = Density of the fluid, D= Diameter of the vessel, V= Velocity of flow and = Viscosity)
  2. More the Reynold’s number, more the chances of turbulence
    If D is measured in cms , V in cm/s, in poises , Then if Re is < 2000 there is usually no turbulence; if Re is > 3000, turbulence almost always there.
f. Average velocity of flow
V= Q/A (Where V= velocity, Q= Quantity / amount of fluid and A= Area) So , if area is more, velocity is less, Therefore the velocity is least in the capillaries (maximum cross- sectional area) and maximum in the aorta (least cross-sectional area). Aorta (Max) > Vena cava > Artery > Arteriole > Capillary
g. Calculation of resistance:
R= 8ηL/ π r 4 (Where R= resistance, η= viscosity, L= length of the vessel and r= radius)
Since     Flow = Pressure/Resistance

  1. The above formula is called the Poiseuille – Hagen formula Viscosity
  2. As seen in the calculation of resistance, one of the factors on which resistance depends is the viscosity of the blood. Viscosity in turn depends mostly on haematocrit. However the change in viscosity with change in haematocrit is much less in vivo than in vitro.
  3. Newtonian and Non- Newtonian fluid: - A Newtonian fluid is a fluid whose viscosity is independent of
  4. the rate of shear eg. Plasma, Saline.
  5. A non-Newtonian fluid is a fluid in which the viscosity changes with the changes in the shear rate.
  6. At very low shear rates, the viscosity is greatly increased; at high rates of flow the fluid behaves almost
  7. as a newtonian fluid. Blood is a non-Newtonian fluid.
  8. Critical closing pressure:- It is the pressure below which flow completely stops; the value of this pressure is not zero but above zero.
  9. Law of Laplace:- This gives the relationship between the distending pressure (P) , the wall tension (T) , the wall thickness (W) and the radius in a hollow viscous organ
Law of Laplace helps to explain as to why Capillaries do not rupture inspite of being thin walled. Dilated hearts have to work more.

Alveoli do not collapse during expiration In thin walled structure, ‘W’ can be ignored. In a spherical structure, P= 2T/r In a cylindrical structure, P= T/r
  1. Pulse Pressure = Systolic B.P. – Diastolic B.P
  2. Mean Pressure = Diastolic B.P. + 1/3 pulse pressure
  • The maximum pressure drop in the vascular circuit is at the level of the arterioles.(as the maximum
  • resistance is at the arterioles)
  • The arterial blood pressure can be measured by
  • Directly using Intraarterial manometer – most accurate, measure end arterial or Total pressure            
  • ( Kinetic + pressure energy)
  • Indirectly using sphygmomanometer auscultatory method – non invasive, measures only the lateral pressure i.e Pressure energy. Since the cuff pressure gets dissipated between the cuff and the artery by the interspersed tissues the blood pressure measured by the sphygmomanometer is always higher than the intraarterial pressure (False High).
    • The cuff pressure at which the sounds are first heard is the systolic pressure.
    • As the cuff pressure is lowered further, the sounds become louder, then dull and muffled. Finally in most individuals, they disappear. The pressure at which they disappear or become muffled is the diastolic pressure.
    • Other points to be noted while measuring BP by sphygmomanometer are:
  • The length of cuff should be 2/3rd of Mid arm circumference
  • The cuff must be always kept at the heart level & mercury scale at eye level.
  • False high BP seen in: Obese, small cuff, Thick sclerotic vessel
  • False low BP seen in: Auscultatory Gap (occurs in very high BP, cause unknown, prevented by palpatory BP first)
  • Effect of gravity on B.P.: Above the heart level , the B.P. falls and below the heart level , the B.P increases The value is 0.77 mm Hg per cm. This is true for arterial as well as for venous pressure.

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