Chapter 9.2: Cardiac Muscle Continued Flashcards

1
Q

During the creation of a pacemaker potential, what occurs during the FIRST HALF of the SLOW DEPOLARIZATION step?

A

There is a net entry of NA+ through HCN voltage gated Na+ channels.

At the same time, there is a progressive reduction in the passive OUTWARD FLUX of K+ because Cardiac K+ channels that open during the falling phase of the previous action potential SLOWLY CLOSE at negative potentials.

THEREFORE, K+ efflux slowly declines at the same time as the inward leak of Na+ (adds to the drift towards threshold)

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2
Q

When does an HCN channel open up?

A

whent he membrane potenital of the pacemaker cells becomes more negative at the end of repolarization from the previous action potential.

When the previous action potential ends, HCN channels open, causing an inward Na+ current and membrane potential moves closer to threshold potential.

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3
Q

During the creation of a pacemaker action potential, what occurs during the SECOND HALF of the SLOW DEPOLARIZATION step? (before threshold is reached)

A

HCN channels start to close and transient Ca2+ (T-TYPE Ca2+ Channels) channels open.

This causes a brief influx of Ca2+ which further depolarizes the membrane, bringing it to threshold

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4
Q

Why is there K+ efflux during the first half of the slow depolarization of pacemaker potentials?

A

because Cardiac K+ channels that open during the falling phase of the previous action potential SLOWLY CLOSE at negative potentials.

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5
Q

What kind of channel is responsible for finally pushing a pacemaker membrane to threshold? When do these channels close?

A

T-type Ca2+ channels that open after Na+ influx and K+ efflux-slowing has commenced.

These channels close once threshold is reached.

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6
Q

At threshold of a pacemaker potential (self induced action potential), ___-type ___ channels open. What does this cause?

A

L-Type Ca2+ channels open at threshold, producing a large influx of Ca2+ leading to the rapid rising phase of the action potential.

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7
Q

After an action potential is induced in the cardiac pacemaker cells (myogenic cells), what causes the falling phase?

A

falling phase caused by OPENING of voltage gated K+ channels and CLOSURE of the L-type Ca2+ channels.

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8
Q

the HCN channel is also known as the ____ channel

A

funny channel

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9
Q

Main locations of pacemaker cells. (nodes). What side of the heart are they on?

A

1) SA node: small, specialized region in the RIGHT atrial wall (in fish its the sinus venosus)
2) AV node: small bundle of specialized cardiac muscle cells located at the base of the RIGHT atrium near the seotum, just above the junction of the atria and ventricles.

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10
Q

Which node is the main pacemaker? Why?

A

SA node is the main pacemaker of the heart because it exhibits the FASTEST rate of autorhythmicity.

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11
Q

If the AV node also is myogenic, how come it does not depolarize and cause contractions on its own?

A

the AV node does not assume its own slower rate because it is ACTIVATED by action potentials generated from the SA node before it reaches threshold at their own slower rhythym.

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12
Q

why is it important that atrial excitation and contraction is complete before the onset of ventricular contraction?

A

completion of atrial contraction is salient to ensure complete ventricular filling before the ventricle contracts.

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13
Q

What is fibrillation

A

when contraction of the heart becomes random and uncoordinated. Normal spread of excitation ensures that excitation of cardiac muscle fibers is coordinated to ensure that each heart chamber contracts as a unit to accomplish efficient pumping.

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14
Q

Initial depolarization and impulse created by SA node facilitates ____ excitation. Afterwards, the impulse is propagated between the atria and the ventricles through the ____ node. The impulse travels along two tracts, the __ ___ ___ and the ___ ___, to facilitate ventricular excitation.

A

Initial depolarization and impulse created by SA node facilitates ATRIAL excitation.

Afterwards, the impulse is propagated between the atria and the ventricles through the AV node. The impulse travels along two tracts, the BUNDLE OF HIS and the PURKINJE FIBERS, to facilitate ventricular excitation.

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15
Q

What is the AV nodal delay?

A

in the AV ndoe, the impulse from the SA node is delayed momentarily which enables the atria to become completely depolarized and to contract, emptying their contents into the ventricles.

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16
Q

3 steps of the orchestration of the spreading of electrical impulse in the heart

A

1) atrial excitation
2) transmission between teh atria and ventricles (AV nodal delay)
3) ventricular excitation.

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17
Q

Outline the events of the rising phase of an action potential in a cardiac myocyte (contractile cell, no longer a pacemaker cell)

A

when stimulated by the pacemaker cells, voltage gated Na+ channels get activated and membrane potential rapidly climbs to about +20 to +30mV

At peak potential, (+30), permeability to Na+ plummets (like in neurons)

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18
Q

outline the events of the Peak phase of an action potential in a cardiac myocyte.

A

at the peak, a subclass of K+ channels TRANSIENTLY open, causing K+ EFFLUX. This brings a brief and small repolarization as the membrane becomes slightly less positive

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19
Q

outline the events of the Plateau phase of an action potential in a cardiac myocyte

A

plateau phase is the maintenance of a positive potential for several hundred msec.

plateau phase in maintained by two voltage-dependent permeability changes triggered by the sudden voltage change during the rising phase of the action potential.

1) slow L-type Ca2+ channels get ACTIVATED. causes Ca2+ influx
2) Transient AND LEAKY K+ channels close and the cell experiences a DECREASE in K+ permeability (PREVENTS K+ EFFLUX)

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20
Q

purpose of plateau phase

A

prolongs contraction for squeezing the heart chambers.

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21
Q

outline the rapid falling phase of an action potential in a cardiac myocyte

A

(L type) Ca2+ channels become inactivated and the “ordinary” voltage gated K+ channels activate (like in the neuron), causing K+ EFFLUX RAPID

Ca2+ influx stops, K+ efflux occurs, causes membrane potential to FALL. Cell returns to resting potential.

At rest, the voltage gated K+ channels close, but leaky K+ channels remain open

SEE CARDIAC DIAGRAM #3

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22
Q

Where will you find majority of the L-type Ca2+ channels in a cardiac muscle cell?

A

in the T TUBULES! (recall, an AP spreads on the surface of a muscle cell (also seen in skeletal muscle), and can penetrate deeper into the cell through the T Tubules)

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23
Q

Outline the mechanism in which an AP brings about a contraction in cardiac muscle

A

1) L-type Ca2+ channels lie primarily in the T tubules
2) Ca2+ moves into the cytosol from the ECF acros the T tubule membrane (DIFFERNENT THAN IN SKELETAL MUSCLE)
3) entering Ca2+ causes ryanodine Ca2+ release channels in the LATERAL SAC OF THE SR to open
4) a Ca2+ induced Ca2+ release occurs. SR releases Ca2+ into cytosol.
5) the Ca2+ spark turns on the contractile machinery (interacts with toponin and tropomyson, like in skeletal muscle)
6) More Ca2+ means that the contraction can last longer than in skeletal muscle

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24
Q

In cardiac muscle, he extent of cross bridge activity varies with the amount of ___ ____

A

cytosolic Ca2+

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25
Q

where does calcium that triggers myocyte contraction come from?

A

mainly comes from the SR

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26
Q

Why is a long refractory period in cardiac muscle so important

A

to prevent tetanus

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27
Q

Chrief factor responsible for the long refractory period.

A

the inactivation of the Na+ channesl that were activated during the initial Na+ influx of the rising phase.

These Na+ channels get deactivated in the plateau phase.

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28
Q

What is an ECG

A

a complex recording representing the sum of electrical activity spreading throughout all of the heart’s muscle cells during depolarization and repolariziation.

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29
Q

P wave represents

A

atrial depolarization

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30
Q

QRS complex represents

A

ventricular depolarization

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31
Q

T wave represents

A

ventricular repolarization

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32
Q

why is P wave smaller than T wave

A

atria has less mass and thus less electrical activtiy.

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33
Q

Which segment on the ECG is the AV nodal delay?

A

the PR Segment

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34
Q

what segment of the ECG is the plateau phase?

A

the ST segment

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35
Q

what does the TP interval mean?

A

the heart muscle is at rest and the ventricles are re filling.

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36
Q

what does the ECG look like if you have a heart block?

A

a P wave with no subsequent QRST event. Results in a skipped beat even though the SA node is firing, the impulse is not effectively getting to the ventricle.

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37
Q

During Early ventricular diastole, what is happening to ventricular pressure? What is happening to ventricle volume? what point is this on the ECG?

A

Early Ventricular diastole
-there is continuous flow of blood into ATRIUM and causes pressure to be slightly greater than ventricular pressure

  • AV valve opens and blood flow from atrium to ventricle
  • causes ventricle volum eto RISE. rise in ventricular volume causes an increase in ventricular pressure, (but though atrial pressure was higher during early ventricular diastole)

Corresponds to T-P interval on ECG.

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38
Q

What happens in terms of electrical activity during LATE ventricular diastole? What part of the ECG is this? What happens to ventricular pressure?

A

electrical activity: SA node reaches threshold and fires, causing the AP to spread.

You can see this as the P wave.

Atrial contraction is triggered when AP spreads, and this causes more blood to enter the ventricle and ventricular pressure RISES

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39
Q

What is the end diastolic volume?

A

the volume of blood in the ventricles at the ned of the diastole. Occurs after atrial contraction and ventricular filling has been completed (just after the P wave)

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40
Q

When is ventrical excitation and the onset of ventricular systole on the ECG?

What happens to ventricular pressure, and what happens to the AV valves?

A

ventricle excitation and the onset of ventricular systole occurs as the QRS complex on the ECG.

The ventricular pressure curve INCREASES shortly after QRS complex due to ventricular systole (contraction as a result of AP)

As contraction begins, ventricular pressure EXCEEDS artrial pressure, AV valve CLOSES

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41
Q

What occurs during isovolumetric ventricular contraction? where on the ECG does this happen? what happens to the volume and pressure of the ventricle?

A

isovolumetric ventricular contraction is when the volume in the ventricle remains constant because all valves are closed (theres no openings anywhere), but the ventricle is still contracting.

This occurs in between the QRS and the T complex.. Allows ventricular pressure to increase before the AORTIC (if were talknig about the left ventricle) can be opened)

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42
Q

After isovolumetric contraction, Ventricular pressure exceeds ___ pressure, forcing the ____ valve to open.

What happens to aortic pressure at this point?

What happens to ventricular volume?

A

After isovolumetric contraction, Ventricular pressure exceeds AORTIC pressure, forcing the AORTIC valve to open.

This causes the aortic pressure curve to rise as blood is forced into the aorta from the ventricle faster than the blood is draining off intot he smaller vessels at the other end.

Ventricular volume is decreased as blood is pumped out into the aorta.

43
Q

T/F: ventricle empties completely during ejection

A

false. half of the blood is still there.

44
Q

what is the end systolic volume?

A

the amount of blood in the ventricles after ejection into the aorta. half of the blood is still in the ventricle after systole.

45
Q

Stroke volume

A

the amount of blood that is pumped out of each ventricle with each contraction.

46
Q

During ventricular repolarization and onset of the ventricular diastole (T wave), what happens to ventricle pressure? what happens to the aortic valve?

A

no more blood leaves the ventricle after T wave and the ventricle relaxes, the PRESSURE FALLS below AORTIC pressure, BUT ventricle pressure still exceeds the ATRIAL pressure (no blood can enter ventricle from atrium because AV valve is still closed) and the AORTIC VALVE CLOSES

47
Q

Why is there a disturbance on aortic pressure curve during ventricular repolarization and ventricular diastole?

A

because the aortic valve closes

48
Q

at what point are all valves closed? what happens to muscle fiber length and chamber volume? what happens to pressure?

A

occurs during isovolumetric ventricular relaxation (just after T wave).

When aoritc valve closes, AV valve is not yet open because ventricle pressure still exceeds atrial pressure.

thus, all valves are closed

muscle fiber length and chamber volume remain CONSTANT

pressure steadily falls as no blood moves.

49
Q

ventricular diastole includes the periods of both _____ ___ ___ and ventricular ____. How does ventricular filling come about?

A

ventricular diastole includes the periods of both ISOVOLUMETRIC VENTRICULAR RELAXATION and ventricular FILLING.

when ventricular pressure falls because of isovolumetric ventricular diastole/relaxation, it continues to fall below atrial pressure, and AV valves open

blood contrinues to flow from the veings into the atria and atrial pressure rises.

blood rapidly fills ventricles upon opening of AV valve.

as atria empties, atrial pressure decreases and filling of ventricle slows.

During late ventricular diastole, the SA node fires again, and the cardiac cycle starts again.

50
Q

How do you calculate cardiac output? what is it?

A

CO = volume of blood per minute pumped by a heart to the body.

CO (vol/min) = HR x SV

51
Q

Larger animals tend to have SLOWER heart rates and ____ stroke volumes

A

LARGER

52
Q

Heart rate and stroke volume are controlled by ____ control. how?

A

controlled by ANTAGONISTIC CONTROL due to dual innervation of BOTH divisions of the AUTONOMIC NS (para symp and symP)

53
Q

What is the primary parasympathetic nerve that supplies the atrium to help decrease heart rate?

A

the vagus nerve

54
Q

Explain parasympathetic innervation. What Neurotransmitter is invovled? which type of receptor is involved? Activation of these receptors results in what?

A

Ach from vagus nerve binds to muscarinic receptors which opens K+ channels via a G protein.

Ach also binds to another inhibitory G protein which reduces the cAMP pathway.

55
Q

NE from the sympathetic nervous system binds with ____-_ adrenergic receptors that are coupled to a _____ G protein, which accelerates the ____ pathway.

Sympathetic nerves also supply the ___ and ____ to help boost Cardiac OUtput.

A

NE from the sympathetic nervous system binds with BETA 1 adrenergic receptors that are coupled to a STIMULATORY G protein, which accelerates the cAMP pathway.

Sympathetic nerves also supply the ATRIUM and VENTRICLES to help boost Cardiac OUtput.

56
Q

GEnerally, heart rate will decrease or increase when membrane is altered in what region?

A

the SA node

57
Q

3 Main effects of parasympathetic stimulation

A

1) Ach Decreases HR
2) Ach Decreases excitability of the AV node
3) Stimulation of the atrial contractile cell shortens the action potential.

58
Q

How does Ach decrease heart rate?

A

Ach binding onto muscarinic receptors enhances POTASSIUM permeability across SA node and so the inside of the cell is even more negative because K+ exits.

also, Ach inhibits the cAMP pathway and depresses the inward movement of Na+ and Ca2+ through the HCN (funny) and T type channels

Overall, the resting potential is further away from threshold and depolarization is slower so it takes longer to reach threshold. (MORE INFREQUENT ACTION POTENTIAL)

59
Q

How does Ach decrease excitability of the Av node?

A

through changes in AP frequency, the transmission of the APs to the AV node are prolonged so the AV nodal delay is longer than usual. Therefore, there is LONGER TIME BETWEEN ATRIUM AND VENTRICLE CONTRACTIONS.

60
Q

How does Ach cause weaker atrial contraction?

A

there is a reduction in Ca2+ inward movement and results in a SHORTENED Plateau phase of the action potentials. This leads to a shorter action potential and a WEAKER atrial contraction.

61
Q

overall, parasympathetic stimulation of the heart causes the cardiac output to ___

A

LOWER

62
Q

4 main effects of sympathetic stimulation

A

1) NE increases HR
2) NE reduces AV nodal delay
3) NE speeds up the speed of action potential
4) NE increases contractile strength.

63
Q

How does NE increase HR?

A

Ne excites the cAMP pathway and increases influx of Na+ and Ca2+.

means a swifter drift towards threshold and greater frequency of action potentials

64
Q

How does NE reduce the AV nodal delay?

A

conduction velocity is increased by enhancing the typically slow, inward Ca2+ current (because of cAMP pathway activation)

65
Q

How does NE speed up the speed of action potentials?

A

“through the specialized conduction pathway”

66
Q

How does NE increase contractile strength

A

NE prolongs the opening of L-type Ca2+ channels which enhanves the slow Ca2+ influx and intensifies Ca2+ participation in excitation-contraction coupling.

67
Q

control of the heart rate is balanced between the inhibitory effects of the ___ ____ and the stimulatory effects of the cardiac ___ ___

A

control of the heart rate is balanced between the inhibitory effects of the VAGUS NERVE and the stimulatory effects of the cardiac SYMPATHETIC NERVES

68
Q

which part of the brain helps balance sympathetic and parasympathetic input to heart

A

coordinated by the cardiovascular control center located in brain stem

69
Q

Sympathetic input ____ HR and ___ Stroke volume

A

Sympathetic input INCREASES HR and INCREASES Stroke volume

70
Q

2 types of control to increase stroke volume

A

1) intrinsic control: related to the extent of venous return, which increases during activity
2) extrinsic control; from sympathetic stimulation.

71
Q

there is a direct ___ between end diastolic volume and stroke volume

A

direct correlation. As mroe blood is returned to the vertebrate heart, the heart pumps out more blood.

72
Q

Intrinsic control of stroke volume depends on the ___-____ relationship of cardiac muscle

A

length-tension relationship of cardiac muscle

73
Q

for skeletal muscle, maximal contraction occurs at the optimal length, and RESTING LENGTH IS its OPTIMAL LENGTH

For cardiac muscle, what is its resting length relative to optimal?

A

resting length is less than optimal

74
Q

Because resting length is less than optimal, an increase in cardiac muscle fiber length ____ contractile tension following systole

A

INCREASES

75
Q

What happens to cross bridges during greater ventricular filling?

A

as cardiac muscle fiber is stretched from greater ventricular filling, its myofilaments are pulled CLOSER TOGETHER. this reduces the distance between filaments, and MORE CROSS BRIDGE interactions can occur.

76
Q

Draw a frank-starling curve.

A

see cardiac diagram 5. the cardiac muscle fibers length is determine by the EXTENT of VENOUS FILLING.

An increase in end-diastolic volume (INCREASE IN VENOUS RETURN) by moving the cardiac muscle fiber length closer to optimal length increases the contractile tension of the fibers on the next sysole. A stronger contraction squeezes out more blood, therefore, more blood is returned to the heart and the end-diastolic volume increases.

The heart automatically pumps out a correspondingly larger stroke volume.

77
Q

How does increase venous return allow for greater contraction power?

A

an increase in venous return means an increase in end diastolic volume, which indicates greater FILLING OF VENTRICLES.

Filling of ventricles stretches muscle fibers closer to optimal length and thus more tension and great contraction power is generated.

78
Q

Frank-Starling Law of the Heart

A

the greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during diastole.

79
Q

Why is coronary circulation important?

A

the cardiac cells are too thick to obtain any oxygen or nutrients from the blood that is actively being pumped in the heart.

80
Q

What is the coronary circulatory system

A

a circulatory system whose arteries project out of the aorta and supply the heart muscle with

81
Q

How does blood flow in the coronary circulatory system vary?

A

blood flow varies depending on the oxygen demand of the heart. Vasodilation occurs when heart needs more blood.

82
Q

outline the mechanism of coordination of the coronary circulatory system

A

1) reduced oxygen is detected in cardiac myocytes
2) ADP (adenosine) is released

3) ADP triggers vasodilation of coronary vessels
4) vasodilation of coronary vessels causes increased blood flow and O2 delivery to heart.

83
Q

what is the heart’s main fuel source?

A

fatty acids. which is why oxygen is so important because fatty acids cannot be broken down anaerobically.

84
Q

what is the hemodynamic flow law

A

Q= P/R

Q= flow rate
P= change in pressure, pressure at the inflow end of the vessel - Pressure at the outflow
R= resistance of blood vessels.
85
Q

Pressure _____ as blood flows through a vessel. Why?

A

DECREASES.

Blood flows down a pressure gradient and the contraction of the heart increases pressure, so the blood moves through the less pressurized vessels.

There are resistance losses though.

86
Q

the ____ the pressure gradient, the greater the flow rate

A

the greater the pressure gradient, the greater the flow rate.

Note: the CHANGE in pressure determines the rate, not the magnitude of P1 itself.

87
Q

How does gravity help establish the pressure gradient?

A

gravity increases the P2 (Pressure at the end of the vessel).

88
Q

Inorder to maintain a given flow, P1 must be greater than ___

A

GRAVITY. Because gravity increases P2. For humans, P1 needs to be at least 100mmHg.

89
Q

What is laminar flow?

A

when layers of fluid slide smoothly over each other.

90
Q

Key factors of Laminar blood flow

A

1) viscosity of the fluid: friction is developed between proteins and RBCs. There is friction between moving molecules
2) vessel length
3) vessel radium. Large blood vessel means blood comes into contact with LESS of the vessel surface area, so there is less resistance.

91
Q

A small or large vessel would have a higher chance of laminar flow?

A

LARGE. Large blood vessel means blood comes into contact with LESS of the vessel surface area, so there is less resistance.

92
Q

Relationship between resistance and Radius, between flow and radius?

A

Resistance is proportional to 1/R^4

Flow is proportional to R^4

93
Q

2 important STRUCTURAL FEATURES in closed (and usually open) systems:

A

1) closed systems always have initial PARALLEL branching
- means each organ gets newly oxygenized blood
- thus, bloos isn’t passing from one tissue to another.

2) Muscular valves on some of the branching parallel vessels allows flow regulation to SPECIFIC ORGANS.

94
Q

In open systems, a ____ space or sinus bathes hemolymph onto body tissues

A

hemocoel space

95
Q

Explain open circulation in mollusks

A

they have myogenic chamber hearts (they are self-depolarizing).

They do not have capillaries, (still have a hemocoel), but hemolymph flow is not completely random; organs used for burrowing gets more direct flow.

96
Q

Explain the more refined open circulation system in crustacea

A

they have a more well developed circ system than molluscs. They have some highly branched arteries within target tissues. These small arteries open up into small spaces called LACUNAE.

De oxygenated bloos is collected in defined channels (SINUSES), and there are valves to control flow.

97
Q

Outline the flow of hemolymph/blood in a crayfish

A

dorsal heart (pump) to anterior/posterior aortas, to small arteries branching in PARALLEL, to LACUNAE, to SINUSES (where deoxy blood is collected), to gills, to dorsal heart via OSTIA

Usually flows in SERIES, not much parallel flow

98
Q

Outline open circulation in insects. Outline the structure flow.

A

they have a more crude open circulation system beucase they do not require circulation for oxygen.

posterior dorsal heart to dorsal aorta and arterial branches to open spaces throughout the body, to abdoment to dorsal heart VIA OSTIA

Some parallel flow

99
Q

Simple closed circulation loop in water breathing fish

A

ACTUAL (systematic heart) to gills to body organs and sinuses to auxillary hearts (numerous locations) to systematic heart again.

100
Q

Why are gills not suitable for air breathing?

A

gills add a lot of restriction to blood flow that is not necessary when breathing air.

101
Q

Adaptation of air breathing fishes? do they still have gills?

A

they still have gills, and if they are in the water, they will use them. But if they are breathing air, de oxy blood will move to the LUNGS to get oxygenated instead, before moving to the left side of the heart, then body organs, the back to right side of the heart. There is a little mixing of oxy and deoxy blood.

102
Q

Feature of closed circulation in amphibians

A

the have a three chambered heart!

two atrium and a ventricle. Therefore, there is some mixing of oxygenated and deoxygenated blood.

103
Q

In some reptiles, the flow of blood moves from right atria to c. ____ to c. ____ to lungs, to left atria, to c. ____ to c____ to body organs and back to right atria.

A

In some reptiles, the flow of blood moves from right atria to c. VENOSUM to c. PULMONALE to lungs, to left atria, to c. ARTERIOSUM to c. VENOSUM to body organs and back to right atria.

104
Q

Which reptile actually has a complete 4 chambered heart with 2As and 2Vs like humans? What adaptation in their circulation system do they have when diving?

A

Crocodiles. They have a FORAMEN OF PANIZZA, which diverts blood away from lungs when diving.