Cardiovascular Physiology
Gian Carlo Delante, PhB PTRP RPT
Anatomy Review: The Heart
The Intrinsic Conduction
System
Important things to
remember
The intrinsic conduction system of
the heart initiates depolarization
impulses
Action potentials spread throughout
the heart, causing a coordinated
heart contraction
An ECG wave tracing records the
electrical activity of the heart
Myocardial Cells
Contractile cells
Have features similar to skeletal
muscles
Nodal/Conducting cells
Have features similar to nerves
Contractile Cells
Considered to be the real muscle cells of the
heart
Contain the same contractile proteins actin &
myosin arranged in bundles of myofibrils
surrounded by a SR
Difference: only one nucleus & far more
mitochondria
Extremely efficient at extracting O2 from blood
(about 2x more than other cells)
Branched and joined together by intercalated
discs
Tight Junctions & Gap
Junctions
Intercalated Discs contain tight
junctions and gap junctions
TIGHT JUNCTIONS: bind cells together
GAP JUNCTIONS: allow for the
movement of ions and ion currents
between myocardial cells; allows the
conduction of action potentials from
cell to cell without the need for
nerves
Nodal/Conducting Cells
Special cells able to spontaneously generate
action potentials without the help of nervous
system input
Properties: Self-Excitability, Conducting
Rhythmicity - chronotropy
Excitability - bathmotropy
Contractility - inotropy
Conductivity dromotropy
Relaxation - lusitropy
Origin of Self-Excitability
General site of origin: SINOATRIAL
NODE or SA NODE
The first area to spontaneously
depolarize hence the pacemaker of
the heart
Spontaneous depolarization of the SA
node: Pacemaker potential
Location: upper posterior wall of the
right atrium
The Cardiac Cycle
Two primary phases
Systole
Diastole
Five Steps of the Cardiac
Cycle
Step 1 Atrial systole. This first
phase of the cycle begins with the
depolarization of the atria (in the
ECG). The atria contract. Atrial
pressure (P wave) is greater than
ventricular pressure. The AV (mitral)
valve opens and blood flows into the
ventricle. Ventricular volume
increases slightly (this is the end
diastolic volume).
Step 2 Isovolumetric ventricular
contraction (also called early
ventricular systole).This begins with
the ventricles depolarizing (QRS
complex) then contracting.
Ventricular pressure increases rapidly
(above atrial but below aortic
pressures). The mitral valve closes.
No change in ventricular volume.
Step 3 Ventricular systole (also
called ejection period). The
ventricles are still contracting, but
now ventricular pressure is above
aortic. The aortic valve opens. Blood
flows into the aorta, and ventricular
volume decreases.
Step 4 Early ventricular diastole
(also called isovolumetric
relaxation phase). Ventricular
pressure falls below aortic pressure,
and the aortic valve closes. Some
blood remains in the ventricles (end
systolic volume). Ventricular pressure
continues to fall. No change in
ventricular volume.
Step 5 Late ventricular diastole.
Ventricular pressure drops below
atrial pressure. The mitral valve
opens, and blood flows into the
ventricle. Ventricular volume
increases. P wave begins, and the
cycle repeats.
Period of Ejection
For blood to be ejected from the
heart:
Ventricular pressure < / > / = aortic
pressure?
Aortic pressure = 80 mmHg
Ventricular pressure: reaches up to __
mmHg
Heart Sounds
Opening of heart valves
Slowly developing process
Produces no sound
Closing of heart valves
There are sudden pressure differences
Produces sound that resonate around the chest
LUB (first heart sound)
Closure of AV valves
Low pitched and of relatively longer duration
DUP (second heart sound)
Closure of semilunar valves
High pitched and of relatively shorter duration
Cardiac Output
Volume of blood that the heart can
pump out in one minute
At rest = 5 liters
During vigorous exercise
Normal individual = 20 liters
Trained athlete = up to 40 liters
Cardiac Output
Control of Heart Rate
Control of Heart Rate
Without ANS influence over the
heart, it will beat at an intrinsic rate
of 100bpm via the autorhythmic SA
node
Constant influence by the PNS at rest
explains why normal HR is usually
around 70bpm
AKA: vagal tone
ANS and Neurotransmitters
PNS: Acetylcholine
SNS: Epinephrine and Norepinephrine
Stroke Volume
Factors Affecting Stroke
Volume
Input from the ANS either PNS or
SNS
EDV and preload
ESV
Control of Stroke Volume through
ANS Input
How will the ANS control SV (or
EDV/ESV)
Calcium ion influx control
Acetylcholine
SNS or PNS? Increase or decrease Ca influx
Epinephrine/Norepinephrine
SNS or PNS? Increase or decrease Ca influx
Control of Stroke Volume through
Changing EDV and Preload
Preload is directly related to end
diastolic volume (EDV)
Greater EDV means also a greater
Preload
So how can SV be affected by EVD
and preload?
Frank-Starling Law
A muscle, including heart muscle,
responds to increased stretching at
rest by an increased force of
contraction when stimulated
In other words, an increase in end
diastolic volume (EDV) will result to
an increase in stroke volume (SV)
So how then can we increase
EDV/preload?
Increasing EDV/Preload
SNS
Constriction of veins
Exercise
Muscle pump
