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Circulatory Systems III

Circulatory Systems III

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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.