Electrocardiogram (ECG) and

Cardiac cycle

1
 Electrocardiogram (ECG or EKG)
• The ECG is a composite record of AP produced by heart
muscle fibers during each heart beat.
– Recording of voltage of beating heart at the surface of body.
– Measurement of vector ( have both force and direction).

• The instrument used to record the changes is

Electrocardiograph.
– ECG of heart is recorded from specific sites of body in graphic form
relating voltage (vertical axis) with time (horizontal axis).
– Waves – Produced due to fluctuation of needle during ECG
recording.
2
 Application of ECG
• The Electrocardiograph used for
– 1. Detect the abnormality in conducting pathway.
– 2. Detect the enlargement and damaged regions of heart.
– 3. Detect the cause of chest pain.

• By analyzing electric potential fluctuations, physician can get

some insight into
– Determination of Heart rate,
– Relative size of heart chambers,
– A variety of disturbances of rhythm, conduction arrhythmia and
conduction block,
– Location and progress of ischemic damage (myocardial infarction) 3
Heart Excitation Related to ECG

4
5
Direction of depolarization

4
1
4
5 2

4
3
4

6
Vectorial Analysis
Summary

7
ECG Machine

Assignment
How Many leads and electrodes are There in
12 – lead ECG?
What is the d/ce b/n lead and electrode8in
Electrocardiographic Leads

• Three types of
electrocardiographic leads.

• 1. Standard bipolar limb

leads.

• 2. Augmented unipolar
limb leads.
– aVR, aVL and aVF.

• 3. Precordial chest leads.

– V1, V2, V3, V4, V5 and V6.
9
 Electrocardiographic Leads
• Standard bipolar limb leads.

• Two electrodes located on

different sides of heart, in this
case on limbs.

• The “lead” is not a single wire

connecting from body but
combination of two wires and
their electrodes to make a
complete circuit between
body and electrocardiograph.10
With respect to average potential in body
 Standard bipolar limb leads

• Recorded from two electrodes located on different sides of heart, in

this case, on limbs.
– Record voltage between 2 electrodes (leads) placed on wrists and legs.
• Lead I.
– Negative terminal of ECG connected to RA and positive terminal to LA.
• Electric potential difference b/n Left arm & Right arm.
• Lead II.
– Negative terminal of ECG connected to RA and positive terminal to LF.
• Electric potential difference b/n Left leg & Right arm.
• Lead III.
– Negative terminal of ECG is connected to LA and positive terminal to LF.
• Electric potential difference b/n Left arm & Left leg.

11
 Chest Leads (Precordial Leads)

• This electrode is connected to positive terminal of ECG and

negative electrode called indifferent electrode, is connected
through equal electrical resistances to RA, LA and LF at same time.
– The different recordings of leads V1, V2, V3, V4, V5, and V6.

• Heart surfaces are close to chest wall, records electrical potential

of cardiac musculature beneath electrode.

– Relatively minute abnormalities in ventricles in anterior ventricular wall,

cause marked changes in ECG.

12
13
Chest Leads (Precordial Leads)

• QRS in V1, V2, are negative

because chest electrodes are
nearer the base of the heart
(direction of electronegativity).

• V3 is in between
electronegative and
electropositive – biphasic.

• QRS of leads v4-v6 are positive

because they are nearer the apex
(direction of electropositivity).
14
Voltage and Time Calibration of ECG
• Horizontal calibration lines are
arranged 10 of small line divisions
upward or downward in standard
electrocardiogram is 1 mV.
• 1 inch in vertical direction is 1
second and each inch is divided into
5 dark vertical lines.
– Intervals between these dark lines
represent 0.20 second.
– The 0.20 second intervals are again
divided into 5 smaller intervals by thin
lines by 0.04 second.
– Paper speed
• 25mm/sec or 300 big sq/min.
15
 Electrocardiograph
Atria Ventricles – Cardiac AP arise from SA node, at
0.04 sec P wave appears in ECG.
Ventricular
Depolarization • P wave for Atrial / SA node
Ventricular depolarization.
Atrial Repolarization
Depolarization – Spreads from SA node through
contractile fibers in both atria.
– Speed is moderate velocity.
– About 0.2 sec after onset of P
wave, AP enter into AV bundle

• Atrial repolarization record is

masked by larger QRS
complex. 16
 Electrocardiograph
• QRS complex for rapid Ventricular depolarization. (3 steps)
– The AP spreads through ventricular contractile fibers.
• 1. Ventricular septal depolarization.
• 2. Major ventricular depolarization towards apex.
• 3. Basal ventricular depolarization.
– After 0.2 sec onset of P wave, Depolarization of ventricle produce QRS
complex.

• T wave indicates ventricular repolarization (recover from

depolarization). (0.4 sec after onset of P wave)
– Repolarization of ventricular contractile fibers begins at apex and spreads
throughout the ventricular myocardium.
– By 0.6 sec, ventricular repolarization is complete and ventricular contractile
fibers are relaxed.
17
 Interval and segments
• P-Q interval
– Time required for AP to travel through atria, AV node
and remaining fibers of conduction system (upto
Apex).
• P-R segment (End of P wave and when Q wave
absent)
– Duration of current is held in AV node.
• P-R interval (starting from P wave)
– Atrial depolarization and AV nodal delay (0.16 sec).
– Longer P-R interval is AV node block.
• Normal R-R interval is 0.83 sec HR = 60/R-R
interval.
• S-T segment,
– Ventricular fibers completely depolarized during
plateau phase of AP.
• Q-T interval.
– Beginning of ventricular depolarization to end of
ventricular repolarisation.
• U wave 18
 Interpretation of ECG
• Larger P waves - Enlargement of an atrium (mitral stenosis) .
• Inverted P wave – slow HR (60 b/min).

• Enlarged Q wave - Myocardial infarction.

• Enlarged R wave - Enlarged ventricles.
• S-T segment is elevated - Acute myocardial infarction.
• S-T segment is depressed- Heart receive insufficient O2

– T wave flattened - myocardial ischemia

• (heart muscle is receiving insufficient O2)
– T wave inverted - ventricular myocardial infarction
– T wave peaked - Hyperkalemia.
• Q-T interval lengthened - 19
 Cardiac cycle
• Events that occur in one complete heart beat.
– One complete sequence of contraction and relaxation of
all four chambers of heart.
– Each cycle is initiated by AP of Sinus node.
– When heart beats, 2 atria contract together, 2 ventricles
contract together and both relaxed.

– Systole is contraction phase of cardiac cycle.

• Contraction of atria and ventricles.
– Diastole is relaxation phase of cardiac cycle.
• Muscle fiber lengthening and filling of atria and ventricles.
• Coronary perfusion occurs. 20
 Events of Cardiac Cycle
• Electrical events of summated
ECG voltage changes:
– P wave,
– QRS complex,
– T waves.
• Mechanical events of :
– Myocardial systole and diastole .
– Opening and closing of cardiac
valves.
– Pressure changes.
– Volume changes .
– Heart sounds . 21
 AV valve open

All valves are

closed 5

SL valve closed
Dubb AV valve closed
80
Lubb
120

All valves are

8 - 25
120 closed
SL valve open

22
 Cardiac cycle of left ventricular function

RPVF SPVF
A.C

SEP
Left Ventricular
pressure REP

Mitral Mitral
close open

Left atrial
pressure

Time scale
S3: Audible in children and in adults during exercise (During rapid filling). 23
S4:Caused by rapid ventricular filling during atrial systole (hypertropied heart). (Very rarely audible)
 Atria as Primer Pumps
• Atrial diastole
– R. Atria receives blood from SVC & IVC.
– L. Atria receives blood from Pulmonary veins.
• Atrial systole
– 80% of blood flow from veins directly reach ventricles through atria.
– Atrial contraction causes an additional 20% filling of ventricles.
• However heart can work without 20% of filling, because it has
capacity of pumping 300 to 400 % more blood than is required
by the resting body.
– The atria fail to function only at the time of exercise or physically
active. (shortness of breath)
• That’s why persons with atrial fibrillation survive for many
24
years without any circulatory problem.
 Pressure Changes in the Atria
• Three minor pressure curve for atria.
• a wave – when atria contracted.
– RA pressure increases to 4-6 mm Hg and LA pressure increases to 7-8 mm Hg.
• c wave – When ventricles starts contracted.
– Slight backflow of blood into atria at onset of ventricular contraction but mainly
by bulging of A-V valves.
• v wave – Occurs at end of ventricular contraction.
– Slow flow of blood into atria from veins while A-V valves are closed during
ventricular contraction.
• A cardiac AP arises in SA node.
– During atrial depolarization, P wave appears in ECG.
– After P wave begins, the atria contract (0.1 sec).
• End of atrial systole is the end of ventricular diastole (relaxation).
• End of ventricular diastole each ventricle contains 110 - 120 ml of blood
25
called end-diastolic volume (EDV).
 Atrial systole

After 0.16 sec

Starting of Atrial contraction Atrial contraction Starting of ventricle contraction

Isovolumetric Contraction
26
 Ventricular systole and diastole
• Ventricular systole.
• 1. Isovolumetric Contraction Period (IVC).
• 2. Ventricular Ejection.
– Maximum ejection period (REP).
– Reduced ejection period (SEP).

• Ventricular diastole.
• 1. Isovolumetric relaxation (IVR).
• 2. Filling phase

27
 Isovolumetric contraction
– Atrial systole fills ventricles.
• Contraction of ventricular contractile fibers begins shortly
after QRS complex appears and continues during S-T
segment.
– Ventricular depolarization causes ventricular systole.
– 0.05 sec both SL valves and AV valves closed.
– Closure of A.V Valves produce 1st heart sound (Lubb).
• During this period, tension is increasing in muscle but
little or no shortening of muscle fibers is occurring.
– but no emptying only Intraventricular pressure rises.
– This is the period of isovolumetric contraction. 28
 Ventricular Ejection
• Continued contraction of ventricles causes pressure inside the
chambers to rise sharply.
• L. ventricular pressure raise above 80 mmHg upto 120 mmHg.
•
– The SL valves are open is ventricular ejection last for 0.25 sec.
• Immediate opening of SL valves cause Maximum ejection of blood (70%).
• It is called as Maximum ejection period or Period of Rapid ejection.
• Period of slow ejection (30%).
• When some blood is moved out, the rate of ejection becomes slower.
• Hence it is called as Reduced ejection period or Period of slow ejection.
•
• R. ventricular pressure slightly above 8 mm Hg -25 mmHg.
• Ejection of blood causes increase pressure in aorta and pulmonary
artery.
– Decrease Intraventricular Pressure.
29
– Closure of SL valves produce 2nd heart sound (Dubb).
 Ventricular- end systolic volume
• Left and R. ventricle ejects 70 mL of blood into aorta
and pulmonary artery.
– The volume remaining in each ventricle at end of systole,
about 50 ml, is end- systolic volume (ESV).
• Stroke volume.
– The volume ejected per beat from each ventricle.
– Equals end-diastolic volume minus end systolic volume.
• SV = EDV - ESV. 120 ml - 50 ml = 70 ml (SV).
– T- wave marks onset of ventricular repolarization.
30
 Isovolumetric relaxation
• Atria and the ventricles are both relaxed.
– Ventricular repolarization causes ventricular diastole.
– Ventricles relax - pressure decreases – blood from aorta and
pulmonary trunk cause back flow, which close SL valves.
– SL valves close, ventricular blood volume does not change
because all four valves are closed
• This period is called isovolumetric relaxation.
• When ventricular pressure drops below atrial pressure,
the AV valves open and ventricular filling begins.

31
 Relaxation period

Ventricular ejection Ventricular Repolarization Ventricular filling

Isovolumetric relaxation
32
 Ventricular Diastole
• A-V valves closed, blood accumulate in R and L atria.
• After atria filled by blood, push A-V valve open allow blood to flow rapidly
into ventricles.
– Cause rise of left ventricular volume curve.

• Period of filling of ventricles divided into three parts.

• Period of rapid filling. (Rapid Passive Ventricular Filling)
– Pressure gradient blood rushes rapidly from atria into ventricles.
– About 75 % filling occurs due to pressure gradient only.
• small amount of blood normally flows into ventricles. (Slow P V F)
– It is other wise called as Diastasis – (from veins to ventricles) No flow phase.
• atria contract give additional thrust to inflow of blood into ventricles.
– 20 % of the filling of ventricles during each heart cycle.
33
– Next cardiac cycle begins with P wave.
Summary of cardiac cycle

34
 Ventricular volumes
• Ventricular end diastolic volume (VEDV).
– Volume of blood in ventricle at the end of ventricular diastole
(relaxation phase)
• EDV = 110 - 120 ml.
• Ventricular end systolic volume (VESV).
– Volume of blood that remains in ventricle at the end of ventricular
systole (contraction phase).
• ESV = 40 - 50 ml.
• Stroke volume output (SV).
– Volume of blood ejected from ventricle during ventricular systole.
– (stroke volume) SV = EDV – ESV = 70 ml.
• Ejection fraction: Fraction of end-diastolic volume that is
ejected EF = SV/EDV = 60% .
35
 Heart Valves and Heart Sounds

• Closing of valves causes audible sounds but opening of valves not

produce any sound .

– “Lub” is associated with closure of A-V valves at beginning of V. systole. (1st

sound)
• The first sound about 0.14 second.
– “Dub” is associated with closure of SL (aortic and pulmonary) valves at the end
of V. systole. (2nd sound).
• SL valves are more rigid than AV valves. The second about 0.11 second.
• Greater elastic coefficient of tight arterial walls provide principal vibrating chambers
sound.

• Sound due to
– When AV valves close, Vibration of taut valves immediately after closure, along
with vibration of adjacent walls of heart and major vessels around heart.
– When SL valves close, they bulge backward toward ventricles and their elastic
36
 Location of valves and
auscultation sites for heart sounds.

37
Listening to sounds of body, usually with aid of a stethoscope, is called
Valves of Heart

A valve in which leaflets adhere to one

another so extensively that blood
cannot flow through it normally is said
to be stenosed.

when the valve edges are destroyed by

scar tissue, they cannot close as the
ventricles contract, Regurgitation.

Hemolytic streptococcal infection .

38
 Murmurs (bruits)

• Abnormal sounds heard in various parts of vascular

system.
– May be caused by turbulent blood flow that is speeding
up when an artery or a heart valve is narrowed.
• Turbulence →vibrations in chest wall felt with flat
hand →palpable murmur (thrill).
• Examples of vascular sounds outside the heart:
– Bruit heard over large vascular goitre.
– Bruit heard over a carotid artery.
39
 Phonocardiograms
Normal and murmurs

• Systolic Murmur of Aortic Stenosis.

– Blood is ejected from left ventricle through
only a small fibrous opening of aortic valve.
– Sound heard in upper chest and lower neck
called “Thrill”
• Systolic Murmur of Mitral Regurgitation.
– Blood flows backward through the mitral
valve into L. atrium during systole.
• Diastolic Murmur of Aortic Regurgitation.
– No abnormal sound is heard during systole,
but during diastole.
• Diastolic Murmur of Mitral Stenosis.
– Blood passes with difficulty through the
stenosed mitral valve from L. atrium into the
L. ventricle.
40
 Work Output of Heart

• Two types of work output of heart

– The stroke work output.
• Amount of energy that heart converts to work during each heartbeat.
– The Minute work output.
• Total amount of energy converted to work in 1 minute.
• This is equal to stroke work output times the heart rate per minute.
• Two forms of work out put
– Volume-pressure work or external work.
• Major proportion is used to move blood from low-pressure veins to high-pressure
arteries.
– Kinetic energy of blood flow
• Minor proportion of energy used to accelerate blood to its velocity of ejection through
aortic and pulmonary valves.
• R. ventricular work output is 1/6th work output of L. ventricle because
of 6 fold difference in systolic pressures. 41
 Analysis of Ventricular Pumping

• Diastolic pressure curve

is determined by filling
heart with greater
volumes of blood.
• Systolic pressure curve
is determined by
recording systolic
pressure achieved
during ventricular
5 mm Hg contraction at each
volume of filling.
– R. Ventricle Systole
Pressure is 60- 80 mm42
Volume-pressure curves.
 volume-pressure diagram of the cardiac
cycle
• Phase I – Period of filling.
– Ventricular volume is 45ml (ESV) and diastolic pressure is 0 mm Hg.
– Ventricular volume increase to 115 ml (EDV).
– Diastolic pressure increase to 5 mm Hg.
• Phase II – Period of isovolumic contraction.
– No change in ventricular volume (All valves closed).
– Pressure inside the ventricle increases to pressure in aorta (80 mm Hg).
• Phase III – Period of ejection.
– Systolic pressure rises higher due to more contraction of ventricle (120 mm Hg).
– Volume of ventricle decreases because aortic valve has opened and blood flows out
of ventricle into aorta.
• Phase IV – Period of isovolumic relaxation.
– At the end of period of ejection, aortic valve closes and ventricular pressure falls
back to diastolic pressure level.
– The ventricle returns to its starting point, with about 50ml of blood left in ventricle
43
and at an atrial pressure near 0 mmHg.
 Cardiac Output (CO)
• CO is volume of blood pumped by each ventricle in 1 min to
pulmonary and systemic circulation.
• CO is product of heart rate (HR) and stroke volume (SV).

– CO = Stroke volume X Heart rate

– SV is amount of blood pumped out by ventricle each beat. (70
ml/beat).
– HR is number of heart beats per minute. (75 beats / minute).
– CO = 70 X 75 ml / min = 5250 ml/ min = 5.25 L / min.

– CO always equals the venous return. 44

 Stroke volume
• Stroke volume (SV) = EDV – ESV.
• To increase stroke volume
• Increase EDV
– Increase venous return
• Increase blood flow by decrease resistance (F = ∆P/ R).
– Increase ventricular compliance
• Decrease ESV
– Increase contractility
– Decrease after load.

• Three factors regulate the stroke volume.

– 1. Preload/ VR/ EDV (effect of stretching).
– 2. Myocardial Contractility. 45
–
 Effect of preload
• Preload (based on Frank – Starling law).
• Length tension relationship of cardiac muscle.
• Stretched muscle contracts more forcefully than outstretched
muscle.
– Volume of blood reach the ventricle at the end of diastole (EDV).
After passive (80%) and active filling (20%).
– VR increased – EDV increased– more forceful the next contraction.
– Increase SV leads to increase in CO.
– Pressure during filling of ventricle.

– Change in EDV – Change in myocardial stretch – change in myocardial

contractility – change in strove volume (Ejection fraction).
– Heart rate is inversely proportional with EDV. 46
 Frank-Starling Law of the Heart
• Intrinsic ability of heart to adapt to increasing volumes of inflowing blood.
• Diastolic filling of heart is directly proportional with displacement of heart
muscle.

– Greater the heart muscle is stretched during filling →↑force of contraction

→↑blood pumped to aorta.
– More the heart fills, greater the force of contraction.
– Preload or degree of stretch, of cardiac muscle cells before they contract is the
critical factor controlling stroke volume.

• Depends on EDV.
– Exercise increases venous return to the heart, increasing EDV→↑ SV.
– Blood loss and extremely rapid heartbeat (decreases ventricular filling time and
decreasing EDV) →↓SV.
47
Frank-Starling Law

48
 Contractility
– Effect the contractile force of ventricular
myocardium.
• Positive ionotropic agent (Increase SV).
• Increase Heart rate. Increase AP.
– More Ca2+ enter the AP.
• Sympathetic stimulation – Norepinephrine –
stimulate B1 receptors.
– Increase the activity of Ca2+ pump.
– Concentration of intracellular Ca2+ in SR.
• Cardiac glycosides (digitalis).
– Inhibit Na+ - K+ ATP ase – increase intracellular
Ca2+ .
• Negative ionotropic agent (decrease SV)
• Increased K+ level in interstitial fluid.
• Parasympathetic stimulation
49
– Decrease intracellular Ca2+
Effect of contractility in
Frank starling law

50
 Effect of After load
• Afterload - (increase Total Peripheral resistance)
• Pressure in ventricles causes blood to push SL valves open.
• The pressure that must be overcome before a SL valve can
open is termed afterload.
• Arterial pressure against which the ventricle contract .
– Pressure exerted by blood in large arteries leaving the
heart.
• Increase afterload due to increase hypertension or
atherosclerosis.
• Afterload inversely proportional with cardiac output.

51
Preload and After load

52
 Effect in volume pressure curve.

Preload increase EDV, increase SV , increase pressure volume curve.

After load decrease stroke volume, decrease pressure volume curve and increase ESV.
Contractility increase stroke volume leads to decrease end systolic volume. 53
O2 consumption Vs CO

54
 Heart failure
• Weak heart leads to decrease CO

• Two types of heart failure.

• L. Ventricle fails – Decrease systemic CO.
• R. Ventricle fails – Decrease pulmonary CO.

• Atherosclerosis – hypertension – work load of

ventricle – stroke volume – CO.
55
 Heart Rate
• HR is the number of cardiac cycles per minute
– Normal HR: 60 to 100 beats/minute.
– Resting person HR is 75 b/min.
• < 60 beats/minute, bradycardia but normal in athletes.
• > 100 beats/minute, tachycardia. (upto 250 b/ min).
• HR varies with the following factors
– Age: Higher in newborn infants (120 b/min) gradually with childhood.
– Sex: Higher in females (85 b/min).
– Time of the day: ↓morning, ↑evening.
– Resting and sleep: Decreased.
– Physical training: low in athletes (45-60 b/min).
– Body position: ↑standing, ↓supine positions.
– Temperature : Temperature ↑ HR ↑ (During fever).
• How to count HR
– Counting arterial pulsation, heart sound and ECG cycles.
56
 Heart regulation
– Adjustment in HR important in short term control of CO and BP.
• Tissues require different volumes of blood flow under different conditions.
• During exercise, hemorrhage, decrease SV in myocardial damage.

• There are 3 primary properties regulated within heart.

– All properties have both positive and negative effects.
– They can increase HR to 4 - 5 times.

• 1. Chronotropic properties (Refers to heart rate).

• 2. Dromotropic properties (Refers - speed of conduction).
• 3. Inonotropic properties (Refers – force of contraction).
57
 Heart Regulation
• Intrinsic regulation
– Increase Venous blood return to R. Atrium.
– Cause SA node to stretch, leads to SA node depolarized faster
– Increase blood to R. Atrium cause increase HR.
• This is called as bainbridge reflux.

• Extrinsic regulation (ANS)

– Parasympathetic nervous system signals via vagus nerves –
decreased HR and force of contraction.
• Affect both chronotropic and ionotropic properties.

– Sympathetic nervous system signals via T1- T5 in spine, effect

chronotropic and dromotropic properties of heart. 58
Bainbridge reflex
40 to 60 %
15% by nerves • Increase in atrial pressure leads
to increase HR (upto 75%).
– Increased atrial volume stretch
SA node increase 15% HR.
– Additional 40 to 60 % increase in
rate is caused by nervous reflex
called Bainbridge reflex.
• Stimulation of sympathetic
nerves to increase HR and
strength of heart contraction.
– This reflex helps prevent
damming of blood in veins,
atria and pulmonary circulation.

59
 Effect of sympathetic nervous system
• Sympathetic (HR 250 > 100 b/ min).
• Release more Norepinephrine (NE) than Epinephrine (E).
• NE binds to beta-1 receptors on cardiac muscle fibers cause two effects.
– 1. In SA and AV node fibers, NE speeds the rate of spontaneous
depolarization. Which fire impulses more rapidly and HR increases.
– 2. In contractile fibers, atria and ventricles, NE enhances Ca 2+ entry through
voltage-gated slow Ca2+ channels, thereby increasing Contractility. (greater
ejection during systole)

• When stimulated
– Increasing volume of blood pumped and increasing ejection pressure.
Increase the maximum cardiac output.
• When depressed
60
– Decreases both HR and strength of ventricular muscle contraction.
 Effect of parasympathetic
nervous system
• Parasympathetic Nerves (Vagus) (HR < 20 b/ min).
– Vagal axons terminate in SA node, AV node and atrial myocardium.
– Released Ach cause hyperpolarization of SA node.
– Decreases HR by slowing the rate of spontaneous depolarization in
autorhythmic fibers.
– Negative chronotropic Na+ during depolarization.
– Negative dromotropic effect due to Ca2+ and K+

• Has no or little effect in contractility of ventricles.

– When parasympathetic stimulation continues it leads to heart
beat at the rate of 20 to 40 b/ minute.
– Decrease strength of heart muscle contraction by 20 to 30 %. 61
Cardiac ANS

62
 Regulation by cardiovascular center
• Cardiovascular center receive information from
– 1. Proprioceptors
• Monitoring the position of limbs and muscles send nerve
impulses at an increased frequency to the cardiovascular center.
– 2. Chemoreceptors
• Monitor chemical changes in the blood, ↓PO 2, ↑PCO2, ↑H+.
– 3. Baroreceptors (Arch of aorta and in carotid arteries).
– Monitor the stretching of major arteries and veins caused
by pressure.
• Arch of aorta sent signal to medulla by vagus nerve and carotid
sinus by glossopharyngeal nerves.
63
• Stimulate or inhibit parasympathetic nerves.
 Nervous system control of heart.
Medulla oblongata

Thoracic region

Release Adrenaline

Enhances Ca2+ entry through voltage-

gated slow Ca2+ channels
64
 Chemical Regulation of Heart Rate

• Hypoxia, Acidosis (low pH) and Alkalosis (high pH) all depress
cardiac activity.
• 1. Hormones. Epinephrine, Nor epinephrine and Thyroid.
• Enhance cardiac contractility and increase HR.
• 2. Cations
– Elevated blood K+ decrease HR and contractility.
• Excess Na + blocks Ca2 + inflow during cardiac AP, force of contraction.
– whereas excess K+ blocks generation of AP.
• Dilation of heart, flaccid and slow the heart rate.
• Cause weakness of heart and abnormal rhythm leads to death.
– Moderate interstitial Ca2+ level speeds HR and strengthens HB.
– Excess calcium ions. - Spastic contraction of heart muscles.
– Deficiency of calcium leads to
65
• Cardiac flaccidity – similar to the effect of high K + ions.
 Role of SA node in Regulating HR
• HR is determined by the rate of discharge of
impulse from SA-node.
• Following factors affect SA node directly or
indirectly.
– Factors that directly stimulate SA-node.
• ↑Body temperature = ↑HR.
• R-atrial distension, by ↑blood volume = ↑HR
– R-atrial distension →Stretch receptors → medullary CV-center →
sympathetic stimulation → ↑HR
• Catecholamine: AD, NAD = ↑HR (+ve chronotropic effect).
66
The End

67