Physiology of The Cardiovascular

System

Cardiovascular System
Cardiac muscles are involuntary and striated muscles

Autorhythmicity

Hearts ability to trigger its own contraction

Ventricle
single chamber at the bottom of the heart
Atria
thin-walled chambers located above the ventricle

Cardiovascular System

Sinoatrial (SA) node

Formed from the sinus venosus
consists of a cluster of cells that are situated in the upper part of the wall
of the right atrium
Pacemaker of the human heart
Transmit electrical signals to make the heart contract in a rhythmic
manner
modified conductive muscle cells that compose the bundle of His
embedded in the septum separating the two atria
electrical signal from the SA node reaches the atrioventricular node (AV
node),
cluster of cells situated in the center of the heart between the atria
and ventricles
serves as a gate that slows the electrical current before the signal is
permitted to pass down through to the ventricles
the delay ensures that the atria have a chance to fully contract
before the ventricles are stimulated

Cardiovascular System
Membrane polarization in cardiac action
potential
phase 0,1,2,3,4
depolarization-repolarization mechanism

Sphygomanometer
instrument for measuring blood pressure
typically consisting of an inflatable rubber cuff that is
applied to the arm and connected to a column of
mercury next to a graduated scale, enabling the
determination of systolic and diastolic blood pressure
by increasing and gradually releasing the pressure in
the cuff.

Cardiac Cycle
Diastolic phase
phase of the heartbeat when the heart muscle relaxes (not
contracting) and allows the chambers to fill with blood
blood is passively flowing from the LA and RA into the LV
and RV, respectively
The blood flows through atrioventricular valves (mitral and
tricuspid) that separate the atria from the ventricles
The RA receives venous blood from the body through the
superior vena cava and inferior vena cava
The LA receives oxygenated blood from lungs through four
pulmonary veins
At the end of diastole, both atria contract, which propels
an additional amount of blood into the ventricles

Cardiac Cycle
Systolic phase
time during which the left and right ventricles
contract and eject blood into the aorta and pulmonary
artery, respectively
aortic and pulmonic valves open to permit ejection
into the aorta and pulmonary artery
The atrioventricular valves are closed during systole
therefore no blood is entering the ventricles; however, blood
continues to enter the atria though the vena cava and
pulmonary veins

Electrocardiogram
a machine that can be used to record and display
the electrical activity of the heart
Different peaks shown corresponds to voltage
changes in specific regions of the heart
P wave

atrial depolarization

QRS complex

atrial repolarization and ventricular depolarization

T wave

ventricular repolarization

Electrocardiogram

Kymograph
an instrument for recording variations in
pressure
in sound waves or in blood within blood vessels,
by the trace of a stylus on a rotating cylinder

Drugs affecting heart rate

Acetylcholine
Released by the parasympathetic nervous system

Epinephrine (adrenaline)
Released by postganglionic sympathetic nerves
Norepinephrine (noradrenaline)

Pilocarpine
Stimulates muscarinic acetylcholine receptors

Atropine
A plant alkaloid that blocks acetylcholine receptors of the heart

Nicotine
Other drugs
Digitalis

Starlings Law
Stroke volume
Blood ejected by the heart (EDV ESV)

EDV/SDV
Volume in the ventricle before and after cardiac contraction

Starlings law of the heart

Preload/Afterload
Degree to which ventricles are stretched by the EDV; back pressure
generated by the blood in the aorta and pulmonary trunk

Contractility
Strength of cardiac muscle contraction (ventricle)

Length tension-relationship
Cardiac Output
Amount of blood the heart can pump in a minute

Objectives
Show how to use the kymograph in explaining
cardiovascular system physiology
Determine the effect of temperature
Determine the effect of drugs
Define the Starlings law of the heart

Materials & Methods

Kymograph Experiments
A frog was
double-pithed
and secured
ventral side up
on a dissecting
board

A bent pin was

inserted through
the tip of the
ventricle and the
thread was
fastened to a
heart lever

A longitudinal
incision from the
thorax was to the
abdomen was
made, and the
skin was peeled
to expose the
sternum and ribs

The sternum was

cut to expose the
thoracic cavity
then the
pericardial sac of
the heart was
also cut

The kymograph
drum was set to
medium to fast
speed and a one
second interval
was marked off
at the start of the
cycle

The normal cycle

was recorded for
1 min. and the
systolic and
diastolic phases
were marked

The apex of the

heart was
attached to the
kymograph lever
using a small
hook

Materials & Methods

Kymograph Experiments: Recording baseline
heart rate and ECG
The heartbeat
was recorded for
30 seconds

Materials & Methods

Kymograph Experiments: Effect of
temperature
Room
temperature and
baseline data for
30 seconds was
recorded

The heart was

bathed warm
(40C) Frog
Ringers solution

The heart was

bathed cold
(10C) Frog
Ringers solution

The apex of the

heart was
attached to the
kymograph lever
using a small
hook

Materials & Methods

Kymograph Experiments: Starlings law of the
heart
10 seconds of
baseline data
was recorded

While recording,
the tension on
the heart was
increased slowly
by raising the
lever

Immediately, the
lever was
returned to its
original position
to reduce the
tension

Materials & Methods

Kymograph Experiments: Effects of drugs on
the heart
30 seconds of
baseline data
was recorded

The drug was

applied using a
syringe and the
data was
recorded for 2
minutes

2-3 drops of
acetylcholine (0.1
mg/mL)

2-3 drops of
epinephrine (1
mg/mL)
2-3 drops of
pilocarpine (0.2
mg/mL)

2-3 drops of atropine (1

mg/mL) then after 30
seconds, 2-3 drops of
acetylcholine (0.1
mg/mL)

Basal heart rate

Basal heart rate and ECG

60 100 bpm in humans
40 50 bpm in frogs
No. of beats in
selection

Time differential between first

and last beat (sec)

Calculated heart rate

18

26

42

Basal heart rate and ECG

The baseline heart rate or resting heart rate is the
number of contractions of the heart that occur in a
single minute while the body is at complete rest
Amplitude and frequency of the heart beat varies
according to the size of the animal, the bigger the
animal the lesser the frequency
Changes in the general metabolism induces bradycardia, or
decreasing of the heart rate
Shortage of oxygen supply or an excess carbon dioxide also
induces bradycardia
Exposure to nitrogen may cause an immediate tachycardia, or
increasing heart rate

Basal heart rate and ECG

The baseline heart rate or resting heart rate
is the number of contractions of the heart that
occur in a single minute while the body is at
complete rest
Amplitude and frequency of the heart beat
varies according to the size of the animal, the
bigger the animal the lesser the frequency
Temperature influences the heart rate of frogs
Frogs are poikilotherms, animals that change internal
body temperature depending on the external
environment

ECG
P wave
Represents atrial depolarization or atrial systole
A heart beat begins with an action potential signal
from the SA node
The signal spreads to both atria causing the
muscles of the atrium to depolarize and contract
Slow cell-to-cell atrial conduction spreads the
depolarization slower and gives the P wave a
rounded deflection

ECG
QRS complex
Represents the depolarization of the ventricles and
consequently ventricular systole
The sharp deflection of the complex is due to the fast
electrical impulse conduction done by ventricular
conducting fibers, namely the bundle of His, bundle
branches, and the Purkinje fibers; and, the ventricular
muscle mass is greater than that of the atria
Q wave: is the downward deflection following the P wave
R wave: is the first upward deflection following the P wave
S wave: is the first downward deflection following the R
wave

ECG
T wave
Represents the ventricular repolarization, and
consequently, ventricular diastole
Ventricular muscles recover from the influx of ions
and are returning to their resting state
At this point, more blood enters the ventricle in
preparation for its circulation into the arteries

Basal heart rate and ECG

An arrhythmia, also called dysrhythmia, is an
irregular or abnormal heartbeat
Tachycardia: a fast heart rhythm
Bradycardia: a slow heart rhythm
Supraventricular arrhythmias: arrhythmias that
begin above the ventricles or in the atria
Ventricular arrhythmias: arrhythmias that begin in
the ventricles
Bradyarrhythmias: slow heart rhythms that may be
caused by disease in the hearts conduction system,
such as the SA node, atrioventricular AV node or
HIS-Purkinje network

Guide Question
First sound heard as pressure is being released
from the cuff slowly
The first sound heard is the systolic pressure. This
pressure indicates the pressure of the blood that
is pumped out by the heart where the blood starts
flowing again in the blood vessel after the flow
has been disrupted by the pressure applied on the
sphygmomanometer cuff.

Guide Question
Basis for the delay between the atrial and ventricular
contractions
The delay between the atrial and ventricular contractions
will allow the atria to completely empty their contents into
the ventricles. Simultaneous contraction would cause
inefficient filling and backflow. If the atria and ventricles
contract simultaneously, atria cannot give any help in filling
the ventricles, which is needed, especially in those with
stiff ventricles as in the elderly. The delay is programmed
in the body by a delay at the atrioventricular node (AV
node), through which the signals conduct from the
pacemaker (SA node) conduct to the ventricle. This
ensures the completion of atrial contraction at the end of
ventricular diastole, just before the ventricular contraction.

Effect of Temperature
Homeotherms
Animals that maintain internal body temperature
between 35.8 38.2 C

Poikilotherms
Hypothermia/Hyperthermia

Guide Question
Effect of temperature on heart rate
Consequence of being a poikilotherm
Warmer temperatures cause the heart to beat faster and place
considerable strain on the body. When it is hot, the body must
move more blood to the skin to cool it while also maintaining
blood flow to the muscles. The only way to do both of these
things is to increase the overall blood flow, which means that
the heart must beat faster. Poikilotherm, which is an organism
whose body temperature adjusts to its environment can
sometimes face consequences. For a large fluctuation in water
temperature in an aquatic environment can cause the organisms
to be stressed or can effectively kill them. Organisms will tend to
have a difficult time in adjusting and coping from an
environment that varies temperature from time to time. Many
factors could be affected like for example its metabolism.

Effect of Temperature
Increase
increase in temperature would render the cardiac muscle to
increase the pumping action, therefore an increase in the heart
rate of the frog
increase of temperature allows the movement of other ions
inside the cardiac membrane of cardiac muscles therefore a
greater metabolic rate

Decrease
the decrease in temperature would render the heart rate of the
frog to decrease due to its thermal response
Decrease in temperature lessens the concentration of calcium
ions in the cell fluids, and in turn, the contraction force of the
heart is reduced. The slowed down heartbeat may be due to the
decrease in metabolic activities of the heart

Guide Question
Starlings Law of the Heart
The law states that the greater the volume of
blood entering the heart during diastole, the
greater the volume of blood ejected during
systole.

Starlings Law
Effect of tension on heart beat amplitude
As the ventricle was further stretched, the tension
force also increases directly
Contraction strength of the cardiac muscles increases
in proportion with the preload tension or the stroke
volume
Greater stretch would render greater contractile force
which is also known as Starlings law
The stretching of ventricles enables an increase of
blood that enters through the atria and this would
lead to greater heart contraction as well as greater
heart beat

Effects of drugs / chemical modifiers

Cholinergic / Adrenergic
Chemical modifiers that inhibit/mimic/enhance
acetycholine; epinephrine

Agonist / Antagonist
Chemical modifiers that works in the same fashion as the
neurotransmitter; in opposition to the neurotransmitter

Chronotropic / Inotropic
Chemical modifiers that affect heart rate; affect force of
contraction

Acetylcholine

Acetylcholine
Acetylcholine
Neurotransmitter that promotes skeletal muscles
contraction but decreases the contraction of cardiac
muscles
Rapid decrease of heart rate
Induced when the potassium channels are activated
and potassium ions can easily pass through the
membrane
Continuous diastolic depolarization will be slower in
the SA node cells
Impulses on AV node travels longer towards the
ventricle

Pilocarpine

Pilocarpine
Pilocarpine
Impulses on AV node travels longer towards the
ventricle
Slower heart rate and cardiac muscle contraction

Atropine

Atropine & Acetylcholine

Anticholinergic, muscarinic receptor
antagonist
Competes to the acetylcholine at the binding
site of its receptor
Increases the activity of the SA node and
conduction through the AV node
Increase of the heart rate and contraction of
the heart

Guide Question
Mechanism of the drugs
Acetylcholine
Acetylcholine (Ach) is a neurotransmitter that binds to
muscarinic cholinergic receptors which in turn activates
G proteins that results to hyperpolarization. Then,
hyperpolarization allows the passage of K ions by
opening K channels and thereby closing Na and Ca
channels. The closing of the Na and Ca channels
decreases the heart rate significantly.

Guide Question
Mechanism of the drugs
Epinephrine
Epinephrine is an adrenergic agonist which binds to
adrenergic receptors such as B1 and B2, or Alpha 1,
thus increasing the heart beat. In addition, it behaves in
the same manner as norepinephrine. It increase the
heart rate through its effect on cAMP, which increases
the influx the Na+ and Ca2+. It also reduced the AV
nodal delay at the AV node by increasing the
conduction velocity.

Guide Question
Mechanism of the drugs
Atropine followed by Acetylcholine
Atropine is a cholinergic antagonist which blocks the
acetylcholine receptor causing increased sympathetic
tone increasing the heart rate. ACh is neurotransmitter:
works on ganglion and muscarinic receptors and
nicotinic receptors which binds to these receptors
causing increasing parasympathetic tone, thus,
decreasing the heart rate. Adding both together, will
result in a weak action of ACh that tails off as all the
mAChRs become blocked by Atropine.

Nicotine

Nicotine
Triggers the release of catecholamines,
adrenaline and noradrenaline
Causes rapid increase in the heart rate and
heart contraction
Causes the constriction of the arteries

Conclusion

References