Cardiovascular Physiology

Lectured by Bien Nillos, MD

Hemodynamics

• Arteries – thick walled, extensive

elastic tissue and smooth muscle
• Are under high pressure
• Blood volume contained in the
arteries are called stress volume
• Arterioles – site of highest resistance
in the cardiovascular system
• Arteriolar resistance is regulated by
the autonomic nervous system
• Capillaries – have the largest total
cross-sectional and surface area
• Are the site of exchange of
nutrients , water and gases
• Venules – formed from merged
capillaries
• Veins – thin-walled, under low
pressure, highest proportion of the
blood
• Unstressed volume
Velocity of Blood Flow

• V = Q/A
– Where v = velocity
– Q = blood flow
– A = cross-sectional area

– Blood flow velocity is higher in the aorta

than in the sum of all of the capillaries
Blood Flow
• Q = P/R or
• Cardiac output = mean arterial pressure –
right arterial pressure
Total Peripheral Resistance

Equation of blood flow is analogous to Ohm’s

Law
Blood flows from high pressure to low pressure
Cardiac Electrophysiology
Cardiac Action Potentials
• Resting membrane potential is determined
by the conductance to K and approaches
the K equilibrium potential
• Inward current brings positive charge into
the cell and depolarizes the membrane
potential
• Outward current takes positive charge out
of the cell and hyperpolarizes the
membrane potential
• Phase 0 – upstroke, increase in Na
conductance.
• Phase 1 – initial repolarization, outward
current of K, decrease in Na conductance
• Phase 2 – plateau, transient increase in Ca
conductance, increase in K conductance
• Phase 3 – repolarization, Ca conductance
decreases and K conductance increases
• Phase 4 – resting membrane potential
Excitability
• Ability of cardiac cells to initiate action
potentials in response to inward
depolarizing current
• Absolute refractory Period – begins with the
upstroke and ends after the plateau
• Effective refractory Period – slightly longer
than ARP
• Relative refractory Period – period
immediately after the ARP
• Chronotropic – changes in the heart
rate
• Dromotropic – changes in the
conduction velocity
• Inotropic – contractility of cardiac
muscles
• cardiac output increases or
decreases in response to changes in
heart rate or stroke volume. When a
person stands up, for example,
cardiac output falls because of a fall
in central venous pressure, which
leads to a decrease in stroke volume.
• the ability of the heart to change its
force of contraction and therefore
stroke volume in response to
changes in venous return is called
the Frank-Starling mechanism
• Increased venous return increases the
ventricular filling (end-diastolic volume) and
therefore preload, which is the initial
stretching of the cardiac myocytes prior to
contraction. Myocyte stretching increases the
sarcomere length, which causes an increase
in force generation. This mechanism enables
the heart to eject the additional venous
return, thereby increasing stroke volume.