Circulatory Systems III
Mammals & Birds
Mammals & Birds

Atrioventricular (AV) valves: located
between atrias and ventricles and ensure
one-way flow
◦ Right AV valve = tricuspid valve
◦ Left AV valve = bicuspid valve

Chordate tendinae: anchor valves to the
papillary muscles and prevent them from
opening backwards.
Mammals & Birds
Tricuspid Valve
Bicuspid Valve
Mammals & Birds
Flow of Blood
Flow of Blood
Oxygenated or Deoxygenated?

Systemic Arteries?
◦ Heart to body tissues  oxygenated blood

Systemic Veins?
◦ Body tissues to heart  deoxygenated blood

Pulmonary Arteries?
◦ Heart to lungs  deoxygenated blood

Pulmonary Veins?
◦ Lungs to heart  oxygenated blood
The Cardiac Cycle

Cardiac Cycle:
Rhythmic Pumping of Heart

2 Phases of Cardiac Cycle =
1. Systole – contraction
2. Diastole – relaxation
The Cardiac Cycle

Fish Cardiac Cycle:
◦ Chambers contract in series
The Cardiac Cycle

Mammalian Cardiac Cycle:
◦ Coordinated contraction of atria and ventricles
The Cardiac Cycle
Cardiac Cycle

Mid Ventricular Diastole:
◦ Atria and ventricles are relaxed,
◦ AV valves are open,
◦ Semilunar valves are closed.

Mammals and birds:
◦ Blood returning to heart passes thru the atria and
goes into the ventricles passively.

Fish and some amphibians:
◦ Ventricles fill primarily by contraction of the atrium.
Cardiac Cycle

Atrial Systole:
◦ Atria contract and additional blood gets pushed
into ventricles.

Blood is pumped into the ventricles until
they reach end-diastolic volume (EDV),
the max amount of blood in the ventricle.
Cardiac Cycle

Early Ventricular Systole:
◦ Ventricles contract.
◦  pressure cause AV valves to shut.
◦ Semilunar valves are closed.

Isovolumetric contraction:
◦ Blood is non-compressible, so pressure in the
chamber increases but volume does not.
Cardiac Cycle

Late Ventricular Systole:
◦ Pressure forces semilunar valves open.
◦ Blood flows out of the ventricles into arteries.
◦ Chordae tendinae prevent AV valves from
being forced open; preventing backflow.

Ventricle has reaches its end systolic
volume (ESV) or blood minimum.
Cardiac Cycle

Early Ventricular Diastole:
◦ Ventricles begin to relax, pressure drops.
◦ Pressure in ventricles drops below that of the
arteries
◦ Backpressure forces semilunar valves shut.

Throughout ventricular systole, the atria
have been in diastole filling with blood.

Pressure in filled atria exceeds pressure in
relaxed ventricles and AV valves pop open.
http://www.youtube.com/watch?v=jLTdgrhpDCg
Mammalian Cardiac Cycle

2 ventricles contract simultaneously

Left ventricle contracts much more
forcefully than the right ventricle and
develops a much higher pressure:
◦ Left Ventricle  to body  high resistance
◦ Right ventricle  to lungs  low resistance
Control of Contraction

Cardiomyocytes = myogenic

Produce spontaneous rhythmic
depolarizations that initiate contraction.

Electrically coupled via gap junctions:
◦ depolarization in one spreads to adjacent
cells, triggering coordinated contractions.
Control of Contraction
Control of Contraction
Control of Contraction

Pacemaker cells determine the
contraction rate for the entire heart.

In vertebrates these cells are located in
an area of the right atrium called the
Sinoatrial (SA) Node.
Control of Contraction

Pacemaker cells have unstable resting
potentials (pacemaker potential).

Resting potential drifts from -60mV until
it reaches threshold of -40mV.

At -40mV an action potential is initiated
Control of Contraction

Depolarization initiated in the pacemaker
cells can spread from cell to cell via
electronic current spread.

AP triggered in one cell spreads to
adjacent cells propagating the impulse
throughout the heart.
Control of Contraction

Cardiomyocytes have an extended
depolarization = plateau phase

Corresponds to the refractory period of
the cell in which an action potential
cannot fire.
Control of Contraction
Control of Contraction

Small mammals tend to have HRs and
 plateau phases than larger mammals
whose hearts beat more slowly.
Impulse Conduction in Fish

Impulse conduction via gap junctions is
sufficient to provide coordinated
contraction of the chambers.

Signal travels from sinus venosus to the
atrium and then to the ventricle.

Contraction occurs in a series.
Mammalian Conducting Pathways

Contractile cells of the atrium and
ventricles do no form gap junctions with
each other.

Mammals utilize conduction pathways
Mammalian Conducting Pathways
Mammalian Conducting Pathways

SA node initiates the action potential
◦ Depolarization spreads rapidly via internodal
pathway through the walls of the atria.

Depolarization reaches atrioventricular
(AV) node which communicates signal to
the ventricle.

AV node causes signal delay
◦ allows atrium to finish contracting before
ventricles contract.
Mammalian Conducting Pathways

Signal travels from the AV node through
the bundles of his (“hiss”)

Electrical signal spreads into a network of
conducting pathways - purkinje fibers.

Signal spreads cell to cell via gap junctions
and ventricles contract.
Electrocardiogram (EKG)

Deflections = markers of electrical
activity of the heart
Electrocardiogram (EKG)

P wave = atrial depolarization

QRS complex = ventricular
depolarization and atrial repolarization

T wave = ventricular repolarization
Cardiac Output

Cardiac Output (CO) = the amount of
blood that the heart pumps per unit time.

CO = HR x SV
◦ Heart rate (HR) = beats per minute
◦ Stroke volume (SV) = amount of blood
pumped per beat
Cardiac Output

Animals can modulate CO by regulating
HR, SV, or both.
Decreasing HR = bradycardia
 Increasing HR = tachycardia


Nervous and endocrine systems
modulate force of contraction (SV)
Frank-Starling Effect

When blood enters a ventricle, the
increased volume causes it to stretch.

The more blood that enters the heart at
the end of diastole (EDV), the greater the
degree of stretch.

Frank-Starling Effect = autoregulation

as you stretch a cardiomyocyte the strength
of contraction increases.
Frank-Starling Effect

Allows the heart to automatically
compensate for increases in the amount
of blood returning to the heart.