The ppt give us knowledge about introduction of cardiovascular systen

3.  The cardiovascular system, also known as
circulatory system or the vascular system, is
an organic system that permits blood to
circulate and transport nutrients ( such as
amino acids and electrolytes) , oxygen ,
carbon dioxide, hormones , and blood cells
to provide nourishment and help in fighting
diseases, stabilize temperature and pH , and
maintain homeostasis.
 Cardiovascular system consist of the blood ,
the heart , and blood vessels

4.  The blood must be constantly pumped
through the body’s blood vessel so that it
can reach body cells & exchange materials
with them.
 In normal adult, human heart beats about
1,00,000 times every day, 35 million beats in
a year.
 The heart rests on the diaphragm, near the
midline of thoracic cavity , it lies in the
mediastinum , a mass of tissue that extend
from sternum to vertebral column b/w the
lungs.

5.  To measure the function of heart we have to
measure cardiac output.
CARDIAC OUTPUT:
It is the amount of blood that heart eject per
min
It depends on heart rate and stroke volume.
Contraction of heart per min is known as heart
rate
Volume of blood eject at each contraction is
known as stroke volume .

6.  Cardiac output = Heart rate x stroke volume
 Heart rate is controlled by Autonomic
nervous system(ANS) and hormones.
ANS
Sympathetic Parasympathetic

7.  Sympathetic :
 It release adrenaline which which get bind to
beta (ß) 2 receptor which is present on SA
node , which lead to increase heart rate.
 Parasympathetic :
 It release the acetylcholine which bind to SA
node and decrease the Na+ and Ca+ and
increase K+ ions movement in heart , which
lead to decrease the heart rate.

8.  Stroke volume (SV):
 Amount of blood pumped by venticle during
each heart beat.
 Calculation:
SV = EDV – ESV
EDV = End diastolic volume
ESV = End systolic volume
EDV ; the volume of blood in heart before
contraction
ESV; the volume of blood left in heart after
contraction.

9.  Factor affecting stroke volumn:
• PRELOADA
• FORCE OF
CONTRACTIONB
• AFTERLOADC

10.  Amount of blood / venous return reqiure to fill
the ventricle is known as preload.
Stroke volume increase
Amount of streching also increase and preload
increase
If their is increase amount of blood in ventricles

11.  The more the stretch on the wall of ventricles
the stronger contraction of ventricle to push
the excess of fluid out of the system.

12.  Resistance or pressure by blood during
ejection of blood through ventricles.
 Pressure against which the ventricles eject
their blood.
 Increase afterload lead to decrease SV.
 Decrease afterload lead to increase SV.
 If we want to decrease afterload we have to
give vasodilator to the patient to dilate the
vessels and SV will increase(hypertension).

13.  Ability of ventricle to contract and eject the
blood out.
 Increase contractility lead to increase stroke
volume ( sympathetic stimulation, positive
ionotropic drugs).
 Decrease contractility lead to decrease
stroke volume( negetive ionotropic drugs).

14. ACTION POTENTIALS AND IMPULSE
CONDUCTION
ACTION POTENTIAL: electrial stimulation
created by a sequence of ion fluxes through
specialized channels in the membrane (
sarcolemma) of cardiomyocytes that leads to
cardiac contraction

15.  It is composed of 5 phase (0-4), beginning
and ending with phase 4.
 PHASE 4: THE RESTING PHASE:
 The resting potential is a cardiomyocyte is -
90 mV due to a constant outward leak of K+
through inward rectifier channels.
 Na+ and Ca+ channels are closed at resting
transmembrane potential.

16.  An action potential triggered in a neighbouring
cardiomyocyte or pacemaker cell causes the TMP(
transmembrane potential is the diff of electrical
potential b/w the inside and the outside of the cell)
to rise above -90mV
 Fast Na+ channel start to open one by one and
Na+ leaks into the cell, further raising the TMP.
 TMP approaches -70mV, the threshold potential in
cardiomyocytes , i.e. The point at which enough
fast Na+ channels have opened to generate a self –
sustaining inward Na+ current.

17.  The large Na+ current rapidly depolarizes
the TMP to 0 mV and slightly above 0 mV for
a transient period of time called the
overshoot; fast Na+ channels close ( recall
that fast Na+ channels are time- dependent).
 L- type(“long- opening “) Ca+ channels open
when the TMP is greater than -40mV and
cause a small but steady influx of Ca2+
down its concentration gradient.

19.  TMP is now slightly positive.
 Some K+ channels open briefly and an
outward flow of K+ returns the TMP to
approximately 0 mV.

20.  L-type Ca2+ channels are still open and there is
a small, constant inward current of Ca2+. This
becomes significant in the excitation-contraction
coupling process described below.
 K+ leaks out down its concentration gradient
through delayed rectifier K+ channels.
 These two counter currents are electrically
balanced, and the TMP is maintained at
a plateau just below 0 mV throughout phase 2.

21.  L-type Ca2+ channels are still open and there is
a small, constant inward current of Ca2+. This
becomes significant in the excitation-contraction
coupling process described below.
 K+ leaks out down its concentration gradient
through delayed rectifier K+ channels.
 These two countercurrents are electrically
balanced, and the TMP is maintained at
a plateau just below 0 mV throughout phase 2.

22.  Automaticity: unlike other cardiomyocytes,
pacemaker cells do not require external
stimulation to initiate their action potential;
they are capable of self-initiated
depolarization in a rhythmic fashion. This
property is known as automaticity, whereby
the cells undergo spontaneous
depolarization and an action potential is
triggered when threshold voltage is reached.

23.  Unstable membrane potential: Pacemaker cells
have an unstable membrane potential and their
action potential is not usually divided into
defined phases.
 No rapid depolarization phase: Pacemaker cells
have fewer inward rectifier K+ channels than do
other cardiomyocytes, so their TMP is never
lower than −60 mV. As fast Na+ channels need
a TMP of −90 mV to reconfigure into an active
state, they are permanently inactivated in
pacemaker cells so there is no rapid
depolarization phase.

26.  The sequence of events for pacemaker action
potential:
 Spontaneous flow of ions mainly through slow
Na+ channels slowly depolarizes TMP above −60
mV. This is called the funny current (also known
as pacemaker current); it is active at TMPs of less
than −55 mV.
 At TMP −55 mV, T-type Ca2+ channels open and
continue slow depolarization.
 TMP −40 mV is the threshold potential for
pacemaker cells. L-type Ca2+ channels open and
depolarize cell to 0 mV, then overshoot to +40 mV.
 Delayed rectifier K+ channels counteract the L-type
Ca2+ channels for a brief plateau phase and then
return the TMP back to −60 mV as Ca2+ channels
close.

27.  Synchronous contraction: all cardiomyocytes
(including pacemaker cells) are electrically
coupled through gap junctions. An action
potential in one cell will cause all neighbouring
cells to depolarize, allowing the heart chambers
to act as a unit.
 Dominance: the cell with the highest inherent
rate of pacemaker activity will therefore also set
the heart rate, as all other pacemaker cells will
be depolarized and rendered inactive by this
stimulus.

28.  Defined as the time from phase 0 until the next
possible depolarization of a myocyte, i.e. once
enough fast Na+ channels have recovered (as TMP
decreases below −50 mV).
 Cardiomyocytes have a longer refractory period
than other muscle cells given the long plateau from
slow Ca2+ channels (phase 2). This is a
physiological mechanism allowing sufficient time for
the ventricles to empty and refill prior to the next
contraction.
 Different degrees of refractoriness are encountered
during an action potential, reflecting the number of
fast Na+ channels that have recovered from their
inactive state and are capable of reopening.

29.  Absolute refractory period (ARP): the cell is
completely unexcitable to a new stimulus.
 Effective refractory period (ERP): ARP +
short segment of phase 3 during which a
stimulus may cause the cell to depolarize
minimally but will not result in a propagated
action potential (i.e. neighbouring cells will
not depolarize).

30. › Relative refractory period (RRP): a greater
than normal stimulus will depolarize the
cell and cause an action potential.
› Supranormal period:
a hyperexcitable period during which a
weaker than normal stimulus will depolarize
the cells and cause an action potential. Cells
in this phase are particularly susceptible to
arrhythmias when exposed to an
inappropriately timed stimulus, which is why
one must synchronize the electrical stimulus
during cardioversion to prevent inducing
ventricular fibrillation.

31.  The SA node normally initiates electrical activation.
 The impulse propagates through atrial tissue to
the AV node. There is no direct electrical
connection between the atrial and ventricular
chambers other than through the AV node, as
fibrous tissue surrounds the tricuspid and mitral
valves. AV node allows a very short delay in
conduction (approximately 0.1 second) because it
is composed of slower conducting fibers. This
pause has two important purposes:

32.  Allows the atria time to contract and fully
empty prior to ventricular stimulation.
 Allows the AV node to act as a gatekeeper,
limiting the transmission of ventricular
stimulation during abnormally rapid atrial
rhythms.
 After crossing the AV node, the impulse
spreads into the rapidly conducting bundle of
His and through the bundle branches to
thePurkinje fibers. The electrical impulse is
distributed throughout the bulk of the
ventricular myocyte for precisely timed
stimulation and contraction of the ventricles.

33.  Their are several disease that occurs in
cardiac vascular system like ;
 Hypertension
 Arrhythmia
 Ischemia
 Heart Failure
 Hyperlipidemia
 Stroke

34.  Hypertension (HTN or HT), also known
as high blood pressure (HBP), is a long-
term medical condition in which the blood
pressure in the arteriesis persistently
elevated.[10] High blood pressure usually
does not cause symptoms.[1] Long-term high
blood pressure, however, is a major risk
factor for several disease like heart failure .
Stroke etc.

35.  Heart arrhythmia (also known
as arrhythmia, dysrhythmia, or irregular
heartbeat) is a group of conditions in which
the heartbeat is irregular, too fast, or too
slow.[2] A heart rate that is too fast – above
100 beats per minute in adults – is
called tachycardia and a heart rate that is too
slow – below 60 beats per minute – is
called bradycardia

36.  Ischemia or ischaemia is a restriction
in blood supply to tissues, causing a shortage
of oxygen that is needed for cellular metabolism (to
keep tissue alive).
[3]
 Ischemia is generally caused by problems
with blood vessels, with resultant damage to or
dysfunction of tissue. It also means local anemia in
a given part of a body.
 Ischemia comprises not only insufficiency of
oxygen, but also reduced availability
of nutrients and inadequate removal of metabolic
wastes. Ischemia can be partial (poor perfusion) or
total.

37.  Heart failure (HF), often referred to
as congestive heart failure (CHF), is when
the heart is unable to pump sufficiently to
maintain blood flow to meet the body's
needs.
 Signs and symptoms commonly
include shortness of breath, excessive
tiredness, and leg swelling.

39.  Hyperlipidemia, or high cholesterol, refers to
high levels of fat proteins in the blood.
 The condition can affect one fat protein or
several. Most people will have no symptoms,
but having hyperlipidemia increases the risk
of developing heart disease.

40.  A stroke is a medical condition in which
poor blood flow to the brain results in cell
death.
 There are two main types of
stroke: ischemic, due to lack of blood flow,
and hemorrhagic, due to bleeding.
 They result in part of the brain not
functioning properly.Signs and symptoms of
a stroke may include an inability to move or
feel on one side of the body, problems
understanding or speaking