The ECG is a diagnostic tool that measures electrical currents in the heart during the cardiac cycle using electrodes placed on the body. It provides information about heart rate and rhythm, as well as signs of conditions like myocardial infarction, chamber enlargement, and conduction delays or blocks. Key aspects of the ECG include the P wave, QRS complex, T wave, and intervals between them like the PR interval. Abnormal rhythms and conduction patterns seen on ECG can help diagnose conditions affecting the heart's electrical system.

1. THE
ELECTROCARDIOGRA
M (ECG)

2. Introduction
• ECG is a crucial diagnostic tool in clinical practice
• Useful in diagnosing rhythm disturbances, changes in electrical
conduction, and myocardial muscle condition
• Electrical currents are measured by an array of electrodes placed
at specific locations on the body surface
• The repeating waves of the ECG represent the sequence of
depolarization and repolarization of the atria and ventricles

3. • ECG does not measure absolute voltages, but voltage changes from a
baseline (isoelectric) voltage.
• ECG are generally recorded on paper at a speed of 25 mm/sec and
with a vertical calibration of 1 mV/cm.
• Light lines describe small squares each of 1 x 1 mm size.
• Dark lines describe large squares each of 5 x 5 mm size.
• X axis denotes time – 1 small square = 0.04 seconds.
• Y axis denotes the amplitude of the wave produced – 1 small square =
0.1 mV.

5. Methods for Recording
Electrocardiograms
• The electrical currents generated by the cardiac muscle during each
beat of the heart change electrical potentials and polarities on the
respective sides of the heart in less than 0.01 second
• Apparatus for recording electrocardiograms be capable of responding
rapidly to these changes in potentials
• Measures the flow of electric current around the heart during the
cardiac cycle
• Flow of electrical currents in the chest around the heart

7. ECG Leads: Placement of Recording
Electrodes
• on each arm and leg, and six electrodes are placed at defined locations
on the chest
• three types of leads – standard Limb leads, augmented and precordial
(chest) leads
• Each leads views the heart at a unique angle enhancing its sensitivity
to a particular region of the heart.
• are connected to a device that measures potential differences between
selected electrodes to produce the characteristic ECG tracings.

8. Electrocardiographic Leads
• Three Bipolar Limb Leads
• Bipolar means that the electrocardiogram is recorded from two
electrodes located on different sides of the heart
• “lead” is not a single wire connecting from the body but a
combination of two wires and their electrodes to make a complete
circuit between the body and the electrocardiograph.
• unipolar leads because they have a single positive electrode with
the other electrodes coupled together electrically to serve as a
common negative electrode augmented leads and chest leads

9. ECG Limb Leads
• Lead I = has the +VE electrode on the LA and –VE RA
therefore measuring the potential difference across the chest
between the two arms. electrode on the right leg is a reference
electrode for recording purposes
• the lead II configuration, the positive electrode is on the left leg
and the negative electrode is on the right arm.
• Lead III has the positive electrode on the left leg and the
negative electrode on the left arm.
• Form Equilateral triangle

10. Einthoven’s Law
• is drawn around the area of the heart
• Einthoven’s law states that if the electric potentials of any two of
the three bipolar limb electrocardiographic leads are known at any
given instant, the third one can be determined mathematically by
simply summing the first two.

12. • The augmented limb leads are,
• AVR – (-50 degrees): Right arm is +ve and other limbs are –ve.
• AVL – (-30 degrees): Left arm +ve and other limbs are –ve.
• AVF – (90 degrees): Legs are +ve and other limbs are –ve.
• Note these augmented are so named as they amplify the tracings
to get an adequate recording.

13. Precordial leads
• view the electrical forces moving anteriorly and posteriorly
• These are,
• V1: Placed in the 4th intercostal space right to the sternum.
• V2: Placed in the 4th intercostal space left to the sternum.
• V3: Placed between leads V2 and V4.
• V4: Placed in the 5th intercostal space in the mid clavicular line.
• V5: Placed between the leads V4 and V6.
• V6: Placed in the 5th intercostal space in the mid axillary line.

14. • leads V1 and V2, the QRS recordings of the normal heart are mainly
negative because nearer to the base of the heart than to the apex,
• QRS complexes in leads V4, V5, and V6 are mainly positive because
the chest electrode in these leads is nearer the heart apex, which is the
direction of electropositivity during most of depolarization

17. wave of the ECG
• P wave. It represents the wave of depolarization that spreads from the
SA node throughout the atria; it is usually 0.08 to 0.1 seconds
• a small, rounded, upward (positive) deflection
• the P-R interval The period of time from the onset of the P wave to
the beginning of the QRS complex, 0.12 to 0.20
• Represents the time between the onset of atrial depolarization and the
onset of ventricular depolarization

18. • QRS complex and is caused by depolarization of the ventricles
• normally 0.06 to 0.1 seconds, indicating that ventricular depolarization
occurs rapidly
• ST segment: The isoelectric period (following the QRS is the period
at which the entire ventricle is depolarized and roughly corresponds to
the plateau phase of the ventricular Action potential
• Important to diagnosis of Ventricular ischemia
• Can become either depressed or elevated indicating non uniform
membrane potentials in ventricular cells.

19. • T wave represents ventricular repolarization (phase 3 of the action
potential) and lasts longer than depolarization.
• Q-T interval, both ventricular depolarization and repolarization occur
• roughly estimates the duration of ventricular action potentials.
• The Q-T interval can range from 0.2 to 0.4 seconds depending on heart
rate.

20. Cardiac Electrical Activity

21. Sequence and procedure of ECG analysis
Determination of the excitation source.
Evaluation of correctness of heart rate – based on duration comparing
of R-R-intervals. Normally observed an insignificant difference of
duration within 0,1 sec
Determination of heart rate. With normal heart rate you should divide
60 seconds by the duration of R-R-interval in seconds
Determination of the electrical axis direction
Analysis of ECG elements

25. Interpretation of ECG
1. cardiac rhythm, by recording a rhythm strip
•a consistent, one-to-one correspondence exists between P waves
and the QRS complex
•P wave is followed by a QRS complex (ventricular depolarization
is being triggered by atrial depolarization) →sinus rhythm

26. • SINUS RYTHM
• Normal rhythm of heart
• Cardiac impulse originated in SA
node, atria depolarize
• Represented by P wave
• Travel down to AV node
• AV nodal delay
• Represented by PR interval
•Impulse travel down to purkinje
fibers
•Ventricles depolarize
•Represented by QRS complex
•Then repolarize
•Represented by T wave
• Again SA node send another
impulse and cycle repeats
•Sinus node discharge these impulse
at a pace of 60-100/min

27. • Rhythm that originated by SA
node
• on ECG, P wave followed by
QRS complex
• QRS complex followed by P
wave
• @ 60-100 impulses per min

28. • SINUS BRADYCARDIA
• Sinus rhythm
• Originated in SA node
• P wave followed by QRS
complex
• Rate < 60BPM

29. • SINUS TACHYCARDIA
• Sinus rhythm
• Originated in SA node
• P wave followed by QRS
complex
• Rate more than 100/min

30. • SINUS ARRHYTHMIA
• Normal physiological mechanism
• Minimal variation in pace of SA node
with respiration
• Minimal increase in heart rate with
inspiration
• Inspiration- activated sympathetic
stimulation of SA node
• Minimal decrease in heart rate with
expiration
• Expiration –activated
parasympathetic stimulation of SA
node

31. Detects abnormalities related to rhythm
• Abnormal rhythmicity of the pacemaker.
• Shift of the pacemaker from the sinus node to another place in the
heart.
• Blocks at different points in the spread of the impulse through the
heart.
• Abnormal pathways of impulse transmission through the heart.
• Spontaneous generation of spurious impulses in almost any part of the
heart

32. Sinoatrial Block
• Atrioventricular Block
• Incomplete Atrioventricular
Heart Block
• Prolonged P-R (or P-Q) Interval
First-Degree Block.
• a delay of conduction from the
atria to the ventricles but not
actual blockage of conduction.

33. Second-Degree Block
• conduction through the A-V
bundle is slowed enough to
increase the P-R interval to 0.25
to 0.45 second
• there will be an atrial P wave but
no QRS-T wave, and it is said
that there are “dropped beats”

34. Complete A-V Block (Third-Degree
Block).
• complete block of the impulse
from the atria into the ventricles
occurs
• the P waves become dissociated
from the QRS-T complexes
• the ventricles have “escaped”
from control by the atria

35. Left Bundle Branch Block.
• Block of the left bundle or both
fasicles of the left bundle.
• Electrical potential must travel
down RBB.
• Depolarisation from right to left
via cell transmission.
• Cell transmission longer due to
LV mass.

36. Left Bundle Branch Block (LBBB).

37. ECG Criteria for LBBB.
• QRS Duration >0.12secs.
• Broad, mono-morphic R wave leads I and V6.
• Broad mono-morphic S waves in V1 (can also have small 'r' wave).

38. LBBB consequence.
• Mostly abnormal ECG finding - indicates heart disease.
• Coronary artery disease (indication for thrombolysis - if associated with chest
pain and raised Troponin).
• Valvular heart disease.
• Hypertension.
• Cardiomegaly.
• Heart failure.
• Impacts on prognosis - QRS duration.
• Use of Bi-Ventricular Pacemakers.

39. Right Bundle Branch Block.
• Impulse transmitted normally by
left bundle.
• Blocked right bundle results in
cell depolarisation to spread
impulse (slower).
• Impulse to IV septum and RV
delayed.
• Results in an additional vector.

40. Right Bundle Branch Block (RBBB).

41. ECG Criteria RBBB.
• QRS duration >0.12 secs.
• Slurred 'S' wave in leads I and
V6.
• RSR' pattern in V1 - bunny ears!!

42. • Premature Contractions is a contraction of the heart before the time
that normal contraction would have been expected.
• This condition is also called extra systole, premature beat, or ectopic
beat →result from ectopic foci in the heart
• Possible causes of ectopic foci are
1. local areas of ischemia
2. small calcified plaques at different points in the heart
3. toxic irritation
Premature Atrial Contractions & Premature Ventricular
Contractions

43. • Paroxysmal Tachycardia abnormalities in different portions of the
heart, including the atria, the Purkinje system, or the ventricles, can
occasionally cause rapid rhythmical discharge of impulses that spread
in all directions throughout the heart.
• Atrial Paroxysmal Tachycardia
• Ventricular Paroxysmal Tachycardia

44. Ventricular Fibrillation
• most serious of all cardiac arrhythmias
• cardiac impulses that have gone berserk within the ventricular muscle
mass, stimulating first one portion of the ventricular muscle, then
another portion,
• never a coordinate contraction of all the ventricular muscle at once,
which is required for a pumping cycle of the heart

45. 2. Detects mean electrical axis
•the preponderant direction of the vectors of the ventricles during
depolarization is mainly toward the apex of the heart
•this axis can swing even in the normal
•heart from about 30 degrees to about 100 degrees.

50. • When one ventricle greatly hypertrophies, the axis of the heart
shifts toward the hypertrophied ventricle for two reasons.
1. Greater quantity of muscle exists → allows generation of greater
electrical potential on that side.
2. More time is required for the depolarization wave to travel than
normal

51. • LVH
• mean electrical axis pointing in
the −15-degree direction
• hypertension
• Pregenancy
• Obesity
• Infract right ventricles

52. • RVH
• intense right axis deviation, to an
electrical axis of 170 degrees
• congenital pulmonary valve
stenosis.
• tetralogy of Fallot and
interventricular septal defect
• Infarct in left ventricle.

53. ECG changes seen in electrolyte
imbalances
• Hyperkalemia
• Tall peaked T waves across the
entire 12 lead ECG.
• PR interval is prolonged and
gradually it flattens or disappears
• QRS complexes widens and
merges with the T waves
• Ventricular fibrillation
• Hypokalemia
• ST segment depression.
• Flattening of the T wave.
• Appearance of U wave
• Hypo/Hyper calcemia
• Hypo with prolonged QT
interval
• hyper is associated with short QT
interval

54. Heart sounds:
• The mechanical activities of the heart during each cardiac
cycle, cause the production of some sounds, which are called
heart sounds.
Factors involved in the production of heart sounds
are:
• The movement of blood through chambers of the heart.
• The movement of cardiac muscle.
• The movement of valves of the heart.

55. First heart sound:
• It is produced during isometric
contraction and earlier part of
ejection period.
• It resembles spoken word ‘LUBB’.
Characteristics:
• It is long, soft, low pitched sound.
• Duration of this sound is 0.10 – 0.17
sec
Causes:
• It mainly occurs due to sudden
closure of atrioventricular valves.
First heart sound and ECG:
• It coincides with peak of ‘R’ wave of
ECG

56. Second heart sound:
• It produces during the onset of diastole.
• It resembles the spoken word ‘DUBB’
Characteristics:
• It is short, sharp and high pitched sound.
• Duration of this sound is 0.10 – 0.14 seconds.
Causes:
• It mainly produces during sudden closure of the semilunar
valves.
Second heart sound and ECG:
• It coincides with the ‘T’ wave of ECG.

57. Third heart sound:
• It is produced during rapid filling period of the cardiac cycle.
Characteristics:
• It is short and low pitched sound.
• Duration of this sound is 0.07 – 0.10 seconds.
Causes:
• It is produced due to the vibrations which set up in
ventricular wall, due to rushing of blood in to ventricles
during rapid filling phase.
Third heart sound and ECG:
• It appears between ‘T’ and ‘P’ waves of ECG.

58. Fourth heart sound:
• It is produced during atrial systole
and considered as physiologic heart
sound.
Characteristics:
• It is short and low pitched sound.
• Duration of the sound is 0.02 – 0.04
seconds.
Causes:
• It occurs due to vibrations which set
up in atrial musculature during atrial
systole.
Fourth heart sound and ECG:
• It coincides with interval between
end of ‘P’ wave and onset of ‘Q’
wave in ECG.

59. Triple heart sound:
• In some conditions like myocardial
infarction and severe hypertension,
the intensity of third and fourth heart
sounds increases and they could be
heard as a single sound along with
the first and second heart sound. This
is known as triple heart sound.
Importance of the heart
sounds:
• Heart sound generally alters during
cardiac diseases involving the valves
of the heart. That’s why heart sounds
are having important diagnostic
value.

60. 62
Murmurs:
• Intensity: see grading scale
• Quality: Blowing, harsh, grating, rumble.
• Pitch: High vs low pitched
• Timing: Early/mid/late systolic vs. holosystolic. Early/mid diastolic.
• Configuration: Crescendo-decrescendo, decrescendo, plateau, others.

61. 67
Characteristic Systolic Murmurs
• Innocent or functional murmurs: arise from pulmonic or aortic outflow tracts in
the presence of normal pulmonic/aortic valves. Common in young, healthy
individuals. Usually Grade I or II, get louder with squatting and very soft or
absent with standing/valsalva. Mid-systolic, short.
• Aortic stenosis: harsh, often loud, best heard base/aortic area, C/D
(crescendo/decrescendo), radiate to neck/carotids. Length of murmur correlates
with severity of obstruction. Best heard with diaphragm.

62. 68
Characteristic Systolic Murmurs
• Mitral regurgitation: high pitched, blowing, best heard at apex, holosystolic (if
not acute), radiates to axilla. Best heard with diaphragm.
• MV prolapse with MR: high pitched, blowing, best heard at apex, mid to late
systolic and often preceded by valve click. Best heard with diaphragm.
• Pulmonic stenosis (congenital defect): harsh, best heard at base/pulmonic area,
radiates down. Louder in inspiration.

63. 69
Characteristic Diastolic Murmurs
• Aortic regurgitation/insufficiency: high pitched, blowing, best heard,
2nd
/3rd
ICS, begins with S2, radiates down. Best heard with diaphragm.
• Mitral stenosis: low pitched, rumbling, best heard at apex, mid
diastolic. Best heard with bell- easily missed with diaphragm.

64. Methods to study heart sounds:
• There are three methods to study heart sounds:
1. By using stethoscope
2. By using microphone
3. By using phonocardiogram
Stethoscope:
• The chest piece of the stethoscope is placed over 4 areas
of the chest, which are called auscultatory areas. The
auscultatory areas are as follow:
1. Mitral area or bicuspid area:
• Situated in the left V intercostal space about 3 inches
from midline. This is the area of apex beat. Mitral valve
sound best heart near this region.
2. Tricuspid area:
• Present over xiphoid process . Tricuspid valve sound best
heart near this region.
3. Pulmonary area:
• Present over the left II intercostal space close to the
sternum. Semilunar valve sound best heart near this
region.
4. Aortic area:
• Situated over right II intercostal space near to the
sternum. Semilunar valve sounds are best heard near this
region.
 First heart sound is best heard in mitral and tricuspid area
where second heart sound is best heard in pulmonary
and aortic areas.

65. Cardiac cycle

66. • The cardiac cycle is a period from the beginning of one heart beat to
the beginning of the next one.
• The cardiac cycle describes pressure, volume and flow phenomena in
the ventricles as a function of time.
• Similar for both LV and RV except for the timing, levels of pressure.
• Ventricular contraction called systole.
• Ventricular relaxation called diastole
• Each part of the cardiac cycle consists of several phases
characterized by either a strong pressure change with constant
volume or a volume change with a relatively small change in pressure

67. Systole includes:
•Isovolumic contraction.
•Ejection.
•Diastole includes:
•Isovolumic relaxation.
•Rapid ventricular filling.
•Slow ventricular filling (diastasis).
•Atrial contraction

68. • The duration of the cardiac cycle is inversely proportional to the
heart rate
• At a normal heart rate, one cardiac cycle lasts 0.8 second.
• Under resting conditions, systole occupies ⅓ and diastole ⅔ of the
cardiac cycle duration

69. • Mechanical events in the heart
• Pressure and volume changes in both the atria and the ventricles.
• The pressure changes in the right atrium are seen in the recording of
the venous pulse.
• Pressure changes in the arteries – arterial pulse.
• Electrical activity of the heart – electrocardiogram (ECG)
• Heart sounds or phonocardiogram

70. 1. Isovolumic Contraction
1.1. Heart
•the pressure inside the ventricles rapidly increases due to the
ventricular depolarization → ventricles contract → after a ventricular
contraction begins, the pressure in the ventricles exceeds the pressure
in the atria
•the atrioventricular valves shut → semilunar valves are closed because
the ventricular pressure is lower than that in the aorta

71. 1.2. Pressure and volume changes
Ventricles ventricles contract and all valves are closed, so no blood can
be ejected
ventricular pressure rises considerably without any change in the
ventricular blood volume – isovolumic contraction
blood volume in the ventricles equals to the end-diastolic volume
(≈130 ml).

72. • Atria
• The atrioventricular valves are bulged backward into the atria
because of increasing pressure in the ventricles. This event causes the
c wave in the venous pulse
• Arteries
• Pressures in arteries of both systemic and pulmonary circulations
decrease constantly

74. 1.3. Electrocardiogram
• depolarization spreads from the
atrioventricular node to the
septum and the walls of both
ventricles through the bundle of
His and Purkyne fibres
• The ventricular depolarization
causes the QRS complex in the
ECG

75. 1.4. Heart sounds
• the first heart sound appears
• caused by vibrations of the
atrioventricular valves
• due to the closure of the
atrioventricular valves

76. 2. Ejection
• 2.1. Heart
• ventricular contraction continues Both left and right ventricular
pressure > the pressure in the aorta and in the pulmonary artery
respectively → the semilunar valves open.
• blood is ejected from the left and the right ventricles to the aorta and
the pulmonary artery

77. 2.2. Pressure and volume changes
• Ventricles
• rapid ejection: first part of the ejection, the ventricular pressure rises
and blood is intensively ejected to the arteries
• decreased or slow ejection: the blood volume in the ventricles ↓, the
ventricular pressure starts to decline
• maximum ventricular pressure at the top of the ejection reaches 120
mmHg and 25 mmHg in the left and right ventricles, respectively
• systolic pressure.

78. • about 70 ml of blood is ejected from each ventricle during ejection;
this volume is called the stroke or systolic volume
• 60 ml of blood remains in each ventricle at the end of systole – the
end-systolic volume
• ratio of the stroke volume and the end-diastolic one is called the
ejection fraction.
• It is the fraction of the ventricular blood which is ejected during
systole. Its physiological value is about 60 %.

79. • Atria
• As the ventricles contract they also shorten. The shortening ventricles
elongate the atria and the big veins, lowering their pressure.
• This pressure decrease is represented by the x wave in the venous
pulse

80. Ejection - pressure and volume changes
Red line - pressure in the left ventricle, black - the aortic pressure, dark
blue - the pressure in the right atrium, light blue - the ventricular volume.

81. 2.3. Electrocardiogram
• ventricles are completely
depolarized at the beginning of
the ejection – segment ST in the
ECG.
• The T wave appears due to the
ventricular repolarization in the
second half of this phase

82. 3. Isovolumic Relaxation
• 3.1. Heart
• At the end of systole, the ventricles relax and the ventricular pressure
decreases rapidly
• the elevated pressures in the aorta and the pulmonary artery push
the blood back toward the ventricles to close the semilunar valves.
• atrioventricular valves are closed because the pressure in the atria is
lower than the ventricular pressure

84. • 3.2. Pressure and volume changes
• Ventricles :ventricles relax without changing blood volume in
ventricles
• ventricular relaxation leads to a significant pressure decrease→ is
close to zero in both ventricles
• Atria : Blood flows from the veins to the atria while the AV valves are
closed
• Arteries : dicrotic notch that is seen in the aortic pulse.

86. Electrocardiogram
• ventricular repolarization is
being completed and the end of
the T wave

87. Heart sounds
• the second heart sound appears
• due to the closure of the
semilunar valves

88. 4. Rapid Ventricular Filling
4.1. Heart
•the ventricular pressure falls
bellow the atrial pressure,
•the atrioventricular valves open.
Blood flows rapidly from the atria
to the ventricles.
• The semilunar valves are closed

89. 4.2. Pressure and volume changes
Ventricles
ventricles are rapidly filled with
the blood cumulated in the atria
ventricular volume increases, the
ventricular pressure is not
changed significantly due to the
ventricular relaxation

90. • Atria
• the blood will be evacuated from the atria to the ventricles →
negative y wave in the venous pulse
• Arteries
• diastolic pressure is about 80 mmHg and 8 mmHg in the systemic and
the pulmonary circulations, respectively
• After the semilunar valves close, the arterial pressure slowly
decreases, the pressure in the large arteries never falls to zero due to
their elastic property

91. Rapid ventricular filling - pressure and volume changes
Red line - pressure in the left ventricle, black - the aortic pressure, dark blue - the
pressure in the right atrium, light blue - the ventricular volume

92. 4.3. Electrocardiogram
• No electrical activity is produced
by cardiac cells thus the
isoelectric line is present in the
ECG

93. 4.4. Heart sounds
• The third heart sound, which
occurs rarely, is probably caused
by the rapid blood flow

94. 5. Slow Ventricular Filling
5.1. Heart : The atrioventricular valves remain open while the
semilunar valves are closed
5.2. Pressure and volume changes: the middle part of a diastole a
small volume of blood flows into the ventricles.
the blood flowing from veins and passing the atria to fill the ventricles.
Since the pressure in both ventricles is close to zero
Arteries
•The pressures in arteries of both systemic and pulmonary circulations
decrease constantly

96. 5.3. Electrocardiogram
• the end of slow ventricular
filling, depolarization spreads
from sino-atrial node in all
directions over the atria to
produce the P wave in ECG

97. 6. Atrial Systole
• 6.1. Heart
• the last phase of a diastole
during which the ventricular
filling is completed.
• The atrioventricular valves are
open; the semilunar valves are
closed
• The atria contract to eject blood
into the ventricles

98. 6.2. Pressure and volume changes
• Ventricles
• 25 % of the ventricular filling
volume is ejected from the
atrium to the ventricle
• ventricular myocardium is
relaxed, the ventricular pressure
does not change significantly
• the end of the atrial systole each
ventricle contains 130 ml of
blood; end-diastolic volume

99. 6.3. Electrocardiogram
• atrial depolarization is
completed and the end of the P
wave appears at the beginning
of the atrial systole.
• the PR segment is visible in the
ECG

100. 6.4. Heart sounds
• fourth heart sound is a soft
sound due to an increase in the
ventricular pressure following an
atrial systole
• rarely occurs in a healthy
person

102. The cardiac cycle of the LV can be divided into four basic phases : .
• Isovolumetric contraction phase.
• Ejection phase.
• Isovolumetric relaxation phase.
• Ventricular filling phase

103. Pressure-Volume loop
Point 1 on the PV loop is the
pressure and volume at the end
of ventricular filling (diastole),
and therefore represents the
end-diastolic pressure and end-
diastolic volume (EDV) for the
ventricle.

104. Pressure-Volume loop
As the ventricle begins to
contract isovolumetrically
(phase b), the LVP increases
but the LV volume remains the
same, therefore resulting in a
vertical line (all valves are
closed).
Once LVP exceeds aortic
diastolic pressure, the aortic
valve opens (point 2) and
ejection (phase c) begins.

105. Pressure-Volume loop
During this phase the LV volume
decreases as LVP increases to a peak
value (peak systolic pressure) and
then decreases as the ventricle begins
to relax.
When the aortic valve closes (point
3), ejection ceases and the ventricle
relaxes isovolumetrically - that is,
the LVP falls but the LV volume
remains unchanged, therefore the
line is vertical (all valves are closed).

106. Pressure-Volume loop
The LV volume at this time is the end-
systolic volume (ESV).
When the LVP falls below left atrial
pressure, the mitral valve opens (point
4) and the ventricle begins to fill.
Initially, the LVP continues to fall as
the ventricle fills because the ventricle
is still relaxing.
However, once the ventricle is fully
relaxed, the LVP gradually increases as
the LV volume increases.

109. Cardiac Output and Venous Return
•Cardiac output is the quantity of blood
pumped into the aorta each minute.
Cardiac output = stroke volume x heart rate
•Venous return is the quantity of blood flowing
from the veins to the right atrium.
•Except for temporary moments, the cardiac
output should equal the venous return

110. Normal Cardiac Output
•Normal resting cardiac output:
- Stroke volume of 70 ml
- Heart rate of 72 beats/minute
- Cardiac output ~ 5 litres/minute
•During exercise, cardiac output may increase
to > 20 liters/minutes

111. Cardiac Output
• Stroke Volume = the vol of blood pumped by either the right
or left ventricle during 1 ventricular contraction.
SV = EDV – ESV
CO = SV x HR
5,250 = 70 ml/beat x 75 beats/min
CO = 5.25 L/min

112. Cardiac Output
• Regulation of Stroke volume
• Preload: Degree of stretch of heart muscle (Frank-Starling) –
greatest factor influencing stretch is venous return (see Below)
• Contractility – Strength of contraction
Increased Ca2+
is the result of sympathetic nervous system

113. A Simple Model of Stroke Volume

114. Cardiac Output
• Other chemicals can affect contractility:
- Positive inotropic agents: glucagon, epinephrine,
thyroxine, digitalis.
- Negative inotropic agents: acidoses, rising K+
, Ca2+
channel blockers.
Afterload: Back pressure exerted by arterial blood.
Regulation of Heart Rate
• Autonomic nervous system
• Chemical Regulation: Hormones (e.g., epinephrine, thyroxine)
and ions.

115. Regulation of Cardiac Output
• Frank-Starling Mechanism -- Cardiac output‐
changes in response to changes in venous
return.
• Autonomic control -- Control of heart rate and‐
strength of heart pumping by the autonomic
nervous system.

116. Chemical Regulation of the Heart
• The hormones epinephrine and thyroxine increase
heart rate
• Intra- and extracellular ion concentrations must be
maintained for normal heart function

117. Regulation of Stroke Volume
• SV: volume of blood pumped by a ventricle per beat
SV= end diastolic volume (EDV) minus end systolic volume
(ESV); SV = EDV - ESV
• EDV = end diastolic volume
• amount of blood in a ventricle at end of diastole
• ESV = end systolic volume
• amount of blood remaining in a ventricle after contraction
• Ejection Fraction - % of EDV that is pumped by the
ventricle; important clinical parameter
• Ejection fraction should be about 55-60% or higher

118. Factors Affecting Stroke Volume
• EDV - affected by
• Venous return - vol. of blood returning to heart
• Preload – amount ventricles are stretched by blood
(=EDV)
• ESV - affected by
• Contractility – myocardial contractile force due to
factors other than EDV
• Afterload – back pressure exerted by blood in the
large arteries leaving the heart

120. Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac muscle cells before
they contract is the critical factor controlling stroke volume;
↑EDV leads to ↑stretch of myocardium.
• ↑preload → ↑stretch of muscle → ↑force of contraction → ↑SV
• Unlike skeletal fibers, cardiac fibers contract MORE FORCEFULLY when
stretched thus ejecting MORE BLOOD (↑SV)
• If SV is increased, then ESV is decreased!!
• Slow heartbeat and exercise increase venous return (VR) to
the heart, increasing SV.
• VR changes in response to blood volume, skeletal muscle activity,
alterations in cardiac output
• ↑VR → ↑EDV and ↓in VR → ↓ in EDV
• Any ↓ in EDV → ↓ in SV
• Blood loss and extremely rapid heartbeat decrease SV.

121. Frank-Starling Law of the Heart
• Relationship between EDV, contraction
strength, and SV.
• Intrinsic mechanism:
• As EDV increases:
• Myocardium is increasingly
stretched.
• Contracts more forcefully.
• As ventricles fill, the myocardium
stretches:
• Increases the number of interactions
between actin and myosin.
• Allows more force to develop.
• Explains how the heart can adjust to rise
in TPR.
Figure 14.3

122. Extrinsic Control of Contractility
• Contractility:
• Strength of contraction at
any given fiber length.
• Sympathoadrenal system:
• NE and Epi produce an
increase in contractile
strength.
• + inotropic effect:
• More Ca2+
available
to sarcomeres.
• Parasympathetic
stimulation:
• Does not directly
influence contraction
strength.
Figure 14.2

123. Frank-Starling Mechanism
The force of cardiac muscle contraction
increases as the muscle stretches,
within limits.
Due to more optimal overlap of actin
and myosin filaments during stretch -
same in skeletal muscle
So, with increase venous return and
increased stretching, the force of
contraction increases and the stroke
volume increases.
Moreover, stretching of the SA node
increasing the firing rate of the pacemaker
(increasing heart rate).

124. Frank---Starling
Summary: within physiological limits, the heart
pumps all the blood that returns to it from the
veins.
Venous return increases when there is an
increase in the blood flow through peripheral
organs. So, peripheral blood flow is a major
determinant of cardiac output

125. Factors Affecting Stroke Volume

126. Extrinsic Factors Influencing Stroke
Volume
• Contractility is the increase in contractile strength, independent of stretch and EDV
• Referred to as extrinsic since the influencing factor is from some external source
• Increase in contractility comes from:
• Increased sympathetic stimuli
• Certain hormones
• Ca2+
and some drugs
• Agents/factors that decrease contractility include:
• Acidosis
• Increased extracellular K+
• Calcium channel blockers

127. • Sympathetic stimulation
• Release norepinephrine from symp. postganglionic fiber
• Also, EP and NE from adrenal medulla
• Have positive ionotropic effect
• Ventricles contract more forcefully, increasing SV, increasing
ejection fraction and decreasing ESV
• Parasympathetic stimulation via Vagus Nerve -CNX
• Releases ACh
• Has a negative inotropic effect
• Hyperpolarization and inhibition
• Force of contractions is reduced, ejection fraction decreased
Effects of Autonomic Activity on
Contractility

128. Contractility and Norepinephrine
• Sympathetic
stimulation releases
norepinephrine and
initiates a cyclic
AMP 2nd-messenger
system
Figure 18.22

129. Autonomic
Nervous System

130. Preload and Afterload
Figure 18.21

131. Effects of Hormones on
Contractility
• Epi, NE, and Thyroxine all have positive ionotropic
effects and thus ↑contractility
• Digitalis elevates intracellular Ca++
concentrations by
interfering with its removal from sarcoplasm of cardiac
cells
• Beta-blockers (propanolol, timolol) block beta-
receptors and prevent sympathetic stimulation of heart
(neg. chronotropic effect)

132. Autonomic Control of Cardiac Output
Sympathetic increases cardiac output
‡Can increase heart rate 70 to 180-200 BPM
‡Can double force of contraction
Sympathetic nerves release norepinephrine
‡Believed to increase permeability of Ca2+ and
Na+.
Parasympathetic (vagal) decreases cardiac
output
‡Can decrease heart rate to 20-40 BPM
‡Can decrease force of contraction by 20-30%
Parasympathetic nerves release acetylcholine
‡Increases permeability to K+

133. Cardiac Output and Peripheral
Resistance
Increasing the peripheral resistance
decreases cardiac output.
cardiac output =
arterial pressure
total peripheral resistance

135. Other Factors Affecting Cardiac Output
• Age
• Gender
• Exercise/body temperature

137. Blood Vessels

138. Blood Vessels: Overview
• Structure of blood vessel wall
• Tunica externa – outer covering mostly collagen
• Tunica media – elastin & encircling smooth muscle
• Tunica interna – endothelium
• Lumen – the channel
• Vasa Vasorum – in large vessels, supplies blood to the
outer layers of the vessel wall
Figure 19.1b

139. Types of Blood Vessels
• Arteries – carry cardiac outflow.
• Thicker walled & more muscular.
• Repeated bifurcation (divisions): elastic arteries 
muscular arteries  arterioles  then to:
• Capillaries – wall has single cell thickness. Repeated
anastomosis (merging) yield:
• Venules which then anastomose to form:
• Veins – thin wall, less muscle, more expansible, large lumen,
carry venous return to heart
Figure 19.1b

140. Arteries: Types
• Elastic arteries – expand & contract passively to
accommodate blood volume. Smoothes out pulsatile
flow
• Muscular arteries – distribution arteries. Deliver
blood to organs. Less elastic / more muscle
(vasoconstriction)
• Arterioles – smallest; endothelium & a single layer of
smooth muscle – regulate flow to capillary beds
Figure 19.1b

141. Capillaries: Types
• Continuous: Endothelium with
occasional intercellular clefts

142. Capillaries: Types
• Fenestrated: Endothelial cells full of pores. Very
permeable. Absorption / filtration

143. Capillaries: Types
• Sinusoids: large irregular lumen, fenestrations &
intercellular clefts. Allow movement of large
molecules / plasma between circulatory system
& extracellular space

144. Capillary Beds
• True capillaries are exchange vessels
• Precapillary sphincter: smooth muscle that controls blood flow
between metarteriole & true capillary
• Vascular Shunt: arteriole  metarteriole  venule
• Pericytes: spaced along capillaries to anchor & stabilize Figure 19.4a,b

145. Veins
• Venules: small caliber, porous; allow fluid & WBC movement
out of circulation
• Veins: capacitance vessels which hold 65% of blood supply.
Pressure is low.
• Venous valves: one way valves that inhibit retrograde flow
• Small amount of smooth muscle or elastin
• Venous sinuses – thin walled flattened veins supported by
surrounding tissue (coronary sinuses, dural sinuses)
Figure 19.1b

146. Anastomoses
• Anastomoses: collaterals, bypasses & shunts
• Arterial
• Arteriovenous
• Venous

147. Physiology of Circulation
• Introduction to hemodynamics:
• Blood flow (F)
• Blood pressure (BP) &
• Resistance (R)

148. Blood flow
• Blood flow = volume of blood flowing through a structure;
ml/min
• Total blood flow = Cardiac Output
• Individual structure blood flow varies
• example: skin (hot vs. cold); gut (digestion)

149. Blood pressure
• Blood pressure: force of blood against vessel walls (i.e. 120
mmHg systolic)
• Pressure gradient keeps blood moving

150. ARTERIAL BLOOD PRESSURE
• Systolic pressure
• Pressure peak after
ventricular systole. Ave
= 120 mm Hg.
• Diastolic Pressure
• Pressure drop during
ventricular diastole.
Ave = 80 mm Hg.
BP = 120/80 mm Hg

151. Resistance
• Resistance: opposition to flow; friction of blood moving
through vessels
• Blood viscosity = blood’s internal resistance to flow
• Laminar flow: blood at the wall moves slower than blood
in center

152. Resistance
• Blood vessel length:
• increased length = increased resistance
• Blood vessel diameter:
• decreased diameter = increased resistance

153. Resistance
• Resistance varies inversely to the radius4
(i.e. 1/r4
)
• Doubling the radius:
• Decreases resistance to R/16
• Halving the radius
• Increases resistance to 16R

154. Relationships: Flow, Pressure &
Resistance
• F = rP
R
• rP = Phigh - Plow
• Increased rP yields:
• Increased Flow
• Decreased rP yields:
• Decreased Flow

155. Relationships: Flow, Pressure &
Resistance
• F = rP
R
• Increased R yields:
• Decreased Flow
• Decreased R yields:
• Increased Flow
• Resistance has a greater influence than change in
Pressure on Flow

156. Systemic Blood Pressure
• Systemic BP
• Arterial BP: depends upon distensibility of the great vessels
& the volume of blood pumped into them (pulsatile)
• Ventricular contraction  blood flow  to aorta  aortic
stretch  pressure:

157. Systemic Blood Pressure
• Systolic Pressure: peak pressure with aortic filling increases
to ~120 mmHg.
• Blood run off begins & flows down the pressure gradient into
the systemic circulation.
• Diastolic pressure: lowest pressure. As aorta recoils, pressure
decreases to ~80 mmHg.

158. Systemic Blood Pressure
• Pulse pressure -
Difference between
systolic & diastolic
pressures. Felt as a pulse
during systole.
PP = 120 - 80 = 40 mm Hg

159. Systemic Blood Pressure
• Pulse pressure = systolic - diastolic
• Mean Arterial Pressure = average pressure throughout the cycle
• MAP = diastolic + pulse pressure
3
• MAP = ~90 mmHg

160. Capillary BP
• Capillary BP
• ~40 mmHg at the start of the capillary bed
• ~20 mmHg at the end
• Higher pressure would destroy capillaries
• Capillary permeability is high enough that exchange process occurs at
low pressure

161. Venous BP / Venous Return
• Venous BP (non pulsatile)
• Respiratory pump: pressure changes
in the thorax & abdomen b/c of
breathing
• Muscular pump: skeletal muscle
activity

162. Maintaining BP
• Maintaining BP: CO = P
R
• P = CO x R
• Alteration of BP depends on CO & R
• CO = HR x SV; a function of venous return; under neural &
hormonal influences
• P = (HR x SV) x R

163. Neural Effectors
of CO

164. Resistance: Short Term Control
• Short term control by neural & chemical factors
• Alters blood distribution
• Maintains MAP by changes in vessel diameter
• Operate via baroreceptors & chemoreceptors

165. Short Term: Neural Control
• Vasomotor center (medulla): exerts vasomotor tone via vasomotor
fibers that innervate smooth muscle of vessels
• SNS activity  generalized vasoconstriction
• Input from baroreceptors & chemoreceptors to vasomotor center
modifies vasomotor output

166. Short Term: Neural Control
• Baroreceptors:
• Carotid sinuses (monitor blood flow to brain)
• Aortic (monitor blood flow to periphery)
• Detect changes in MAP
• Chemoreceptors: detect [O2], [CO2] & pH (carotid & aortic bodies)

168. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Epinephrine and Norepinephrine -
• Enhances the sympathetic nervous system.
Epi increases cardiac output; NE is a
vasoconstrictor.

169. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Atrial Natriuretic Peptide (ANP) -
• Antagonist of aldosterone. Causes
excretion of Na+
and H2O from body
• Reduces blood volume and blood pressure

170. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Antidiuretic Hormone (ADH) -
• Released at high amounts when MAP drops
to low levels; it acts as a vasoconstrictor (its
other name is vasopressin).
It also conserves water,
but this is not an important
short-term mechanism.

171. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Angiotensin II - A potent vasoconstrictor
produced within the blood.
ACE
Angiotensinogen
Angiotensin I

172. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Nitric Oxide (NO) -
• Promotes vasodilation, lowering MAP.
• Secreted by endothelial cells in response
to high flow rate

173. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Inflammatory chemicals - Histamine and
other chemicals released during inflammation are
vasodilators.

174. MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical
•Alcohol -
• Antagonist of ADH (lowers blood volume and blood
pressure)
• Promotes vasodilation (thereby reducing resistance and
blood pressure).

175. Long term control: Renal
• Direct renal
• Increased renal flow & BP  increased filtrate from
kidney which results in decreases in volume & in pressure
• Decreased renal flow & BP  decreased filtrate;
conservation of volume & increases in BP
• Indirect renal
• Decreased BP results in renin release
•   Angiotensin II (vasoconstrictor) which stimulates:
• Aldosterone & ADH release which conserve Na & water

176. MAINTAINING BLOOD PRESSURE
Long Term
Mechanisms:
Renal

177. Alterations in BP
• Hypotension (low BP): systolic <100 mmHg
• Hypertension (high BP) systolic >140/90
• Primary HTN – no specific cause; lifestyle &
heredity
• Secondary HTN – identifiable cause; increased
renin, arteriosclerosis, endocrine disorders

178. Alterations in BP
• Autoregulation; local changes in blood flow
• Intrinsic: modifying diameter of local arterioles
• Metabolic: endothelial response (NO, etc)
• Myogenic: smooth muscle responds to increased stretch
with increased tone

179. Blood Flow Through
Capillaries
• Fluid exchange:
• Hydrostatic pressure vs. colloid osmotic pressure
• Hydrostatic Pressure pushes fluid out down pressure gradient (HPc)
• Interstitial Hydrostatic Pressure (HPif) pushes fluid into capillaries
• Colloid Osmotic Pressure: large molecules pull H2O toward themselves.
Interstitial (OPif) & Capillary (OPc)
• NFP = (HPc – HPif) – (OPc – OPif)
Figure 19.16

180. Net Filtration Pressure of
Capillaries
• Net Filtration Pressure of capillaries
• NFP = (HPc – HPif) – (OPc – OPif)
• NFP at arterial end of capillary bed = 10 mmHg
• Hydrostatic
• NFP at venous end of capillary bed = -8 mmHg
• Oncotic
Figure 19.16

181. Circulatory Shock
• Circulatory Shock: marked decrease in blood
flow
• Symptoms: increased HR, thready pulse,
marked vasoconstriction;
• Marked fall in BP is a late symptom

182. Circulatory Shock: Causes
• Hypovolemic: inadequate volume (hemorrhage,
dehydration, burns)
• Vascular: normal volume but global vasodilation
• Anaphylaxis: allergies (histamine)
• Neurogenic: failure of autonomic nervous
system
• Septic: bacteria (bacterial toxins are
vasodilators)
• Cardiogenic pump failure