Cardiovascular Physiology
Download
Report
Transcript Cardiovascular Physiology
Cardiovascular
Physiology
Blood Pressure
=force
exerted by the blood against
the walls of the blood vessel;
Changes throughout cardiac cycle
– Systolic Blood pressure=maximal
pressure achieved by ventricular
contraction
– Diastolic Blood pressure=lowest
pressure remaining in blood vessels
after ventricle contracts
Blood Pressure
Blood flow - amount of blood flowing at
any given time. Dependent on Cardiac
output (CO).
Blood pressure - force per unit area
exerted on wall of blood vessel
Autonomic
Nervous System
– Sympathetic – causes
vasoconstriction of arterioles
Increases
blood pressure
– Parasympathetic – causes
vasodilation
Decreases
blood pressure
Blood Pressure
Systolic
pressure
Diastolic pressure
Pulse pressure = systolic - diastolic
MAP = Diastolic + (Pulse pressure/3)
Hypotension - Low blood pressure
(Nutritional, anesthesia)
Hypertension - High blood pressure
(increased peripheral resistance,
high blood viscosity)
Pressure
Systemic
circulation-high hydraulic
pressure required to overcome
gravitational forces and resistance
Arteriole-vessels with high resistance
to reduce pressure before reaching
capillary beds
Pulmonary Circulation-low pressure,
due to low resistance to blood flow
Effects of High Blood Pressure
Abnormally
high blood pressure
within veins-can cause leaking of
fluid from blood vessels
– Result-edema
– Congestive heart failure
Right
cava
heart failure-leaking of fluid from vena
– Pleural effusion
Left
heart failure-leaking of fluid within
lungs
– Pulmonary edema
Distribution of Blood Flow
Pulmonary
Circulation – 15%
Systemic Circulation – 80%
– 65% in veins
– 10% in arteries and arterioles
– 5% in capillary beds
Heart
– 5%
Functions of the CV System
Maintain
blood pressure within the
arteries
Maintain blood flow to the tissues
Maintain normal blood pressures
within the capillaries and veins
=Perfusion
Perfusion
Allows
delivery of oxygen and
nutrients (i.e. glucose)
Removal of waste products
– Carbon dioxide
Transport
of hormonal messages
from one part of the body to another
Forces
Heart
must adjust contractility
(inotropic state) based on forces
working on the heart.
– Preload
– Afterload
Afterload
=Sum
of forces the ventricles must
contract against to make blood flow
forward
Increased systemic blood pressure
– Increases or Decreases Afterload????
– Chronic blood pressure-increases the
work of the heart-heart enlarges!
Preload
=Amount
of blood in the heart just
prior to contraction of the ventricle
=Venous Return or amount of blood
returning to the heart
– Leaky valves-regurgitate blood back
into the atrium
Increases
or Decreases Preload??
Inotropic State
Adjustments
in contractility based on
Calcium and contractile protein
interactions
– Sympathetic tone (norepinephrineneurotransmitter)
– Increases heart rate and contractility by
increasing Calcium availability
– Starling’s law-increased contractility
with stretching of sarcomere
The Cardiac Cycle
“Pacemakers”
of the heart-send
electrical signal through heart
– Systole-ventricular contraction
– Diastole-Heart is relaxed allowing filling
of the heart
**Based on Ventricle, although atria also
contract and relax
The Cardiac Cycle
End
of Diastole-maximal ventricular
filling
Electrical signal-triggers ventricular
contraction.
Pressure in Ventricle > Atria = closes
AV valves; semilunar valves not
open yet
The Cardiac Cycle
First Heart Sound =closure of AV valves
Semilunar Valves open once pressure in
ventricle is greater than aorta or
pulmonary artery
Stroke Volume = amount of blood ejected
(end diastolic volume-end systolic volume)
Second Heart Sound= Closure of the
Semilunar valves
The Cardiac Cycle
Semilunar Valve-open
AV valves-closed
Ventricle Relaxes
Once pressure in the ventricle is less than
the atrium-AV valves open allowing filling
of ventricle
Third heart sound =passive filling of the
ventricle
– Normal to hear in horses and ruminants-not
carnivores
Ventricular Filling
Initial,
rapid filling phase-passive
Slow-filling phase-atrial contraction
Fourth
heart sound =atrial
contraction
– Normal in ruminants and equine, not in
carnivores
Cardiac Muscle
Striated
muscle
Impulse from cell to cell
Automaticity-cells can become selfexcitable
– Small portion of the muscle cells
Activation of cell
Depolarization=Opening
of fast
sodium channels
Wave of depolarizations travels down
myocardium-Ca++ channels open in
sarcoplasmic reticulum
– Crosslink of myocardium
Refractory
Period-resting between
depolarization, unable to contract
Cardiac Impulse Propagation
Automatic
Tissues-generate action
potentials
Sequence of activation
– Sinoatrial (SA) node-fastest rate!
Atrial
Contraction
– AV node
– Bundle of His
– Rt. And Lt. Bundle Branch to v. apex
– Purkinje fibers to myocardium
Conduction Propagation
Action Potential
THE WHOLE PICTURE
Na + influx creates (+) internal
charge
1
+
CHARGE
INSIDE 0
CELL
-
2
Repolarization
3
0 Depolarization
K+ leaves cell
and cell
returns to it’s
resting or
repolarized
4
state
Resting cell
TIME
**Purple numbers indicate phase numbers
Action Potential
0-Sodium enters cell
via fast channels
1-fast sodium
channels close
2-Ca and Na enter cell
via slow channels
3-K exits cells
4- Na and K
equilibrium
Intrinsic Rate
SA
node-fastest
AV note-40-60 bpm
Sympathetic and Parasympathetic
Nervous System-alter the intrinsic
rate
– SNS-increase rate of depolarization
– PNS-decrease rate of depolarization
Heart Rate Regulation
Baroreceptors-in
heart chamber
blood vessels and
– If blood pressure decreases
Brain>>Increased
Sympathetic nervous
system
Increases Heart rate and vasoconstricts to
increase blood pressure
– If blood pressure increases?
Excitation-Contraction Coupling
See
muscle physiology!!
Ca++ influx
Myofibrils couple via
troponin/tropomysin complex
The Electrocardiogram (ECG)
Recording
of electrical activity of the
heart
Waves-positive vs. negative
depending on the direction the
impulse is traveling
ECG
P
wave-
– Atrial depolarization
QRS
complex
– Ventricular
depolarization
T
wave-ventricular
repolarization
Conduction
This workforce solution was funded by a grant awarded under the Workforce Innovation
in Regional Development (WIRED) as implemented by the U.S. Department of Labor’s
Employment and Training Administration working in partnership with the Colorado
Department of Labor and Employment, the Metro Denver Economic Development
Corporation, and the City and County of Denver's Office of Economic
Development. The solution was created by the grantee and does not necessarily reflect
the official position of the U.S. Department of Labor. The Department of Labor makes
no guarantees, warranties, or assurances of any kind, express or implied, with respect
to such information, including any information on linked sites and including, but not
limited to, accuracy of the information or its completeness, timeliness, usefulness,
adequacy, continued availability, or ownership. This solution is copyrighted by the
institution that created it. Internal use by an organization and/or personal use by an
individual for non-commercial purposes is permissible. All other uses require the prior
authorization of the copyright owner.