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PSIO202 > PSIO202 Exam 1 Lectures 1-3 > Flashcards

PSIO202 Exam 1 Lectures 1-3 Flashcards

1
Q

What are the two main branches of the “circulatory tree”?

A

Systemic circulation and pulmonary circulation

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2
Q

Compare and contrast red and blue blood.

A

Red: Arterial blood, oxygen and nutrient rich
Blue: Venous blood, low in oxygen and nutrients

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3
Q

Where does arterial blood enter and leave the heart?

A

Enters the heart from the pulmonary veins into the left atrium (after being oxygenated in the lungs) and leaves the heart through the aorta (left ventricle) to go to the rest of the body.

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4
Q

Where does venous blood enter and leave the heart?

A

Enters right atrium from superior/inferior vena cava + coronary sinus, leaves right ventricle through pulmonary arteries

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5
Q

List the flow of blood through the heart (start with entering through the vena cava)

A

Venous blood enters through inferior/superior vena cava
Right atrium
Tricuspid valve (AV)
Right ventricle
Pulmonary valve (Semilunar)
Pulmonary trunk/arteries
Lungs
Pulmonary veins
Left atrium
Bicuspid/mitral valve
Left ventricle
Aortic valve (semilunar)
Aorta
Body
Repeat

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6
Q

What “side” of the heart is blue/venous and which “side” is red/arterial?

A

Right is blue/venous and left is red/arterial

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7
Q

What do valves in the heart ensure?

A

That blood flows in one direction, from the heart to tissues and back to the heart

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8
Q

What are the two AV valves, and are they pressure dependent or not?

A

The tricuspid and bicuspid/mitral valves, they are not pressure dependent.

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9
Q

What structures control the AV valves, and what does that control look like?

A

The chorda tendinae and pappillary muscles control the AV valves.
Ventricles relaxed = chordae tendonae relaxed, atria contract, shoot blood through valves into ventricle
Ventricles contract = papillary muscles contract, chordae tendonae pull tight to prevent the valves from inverting when the ventricles push blood up through the pulmonary/aortic valve.

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10
Q

Do the chorda tendinae/papillary muscles pull the AV valves open?

A

NO! They just contract to keep the valve from inverting when the ventricle contracts to shoot blood upward (preventing backflow into the atria).

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11
Q

What are the two semilunar valves, and are they pressure dependent or not?

A

The aortic valve and pulmonary valve are pressure dependent.

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12
Q

What does pressure dependent mean, and what is the pressure required for the aortic valve to open?

A

The semilunar valves only open when there is enough pressure in the ventricle to force it open. For the aortic valve, this amount is 100 mmHg. Less than 100 it will not open, more than 100 it will be open.

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13
Q

Which ventricle has a thicker wall? Why?

A

The left ventricle, because it must force blood out to the entire body while the right ventricle only pushes blood out to the lungs.

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14
Q

Where do the right and left coronary arteries originate?

A

The ascending aorta

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15
Q

What does the right coronary supply? What are its two branches? What do they supply?

A

Supplies the right atrium (SA and AV nodes), the ventricles and the interventricular septum
The Marginal Branch: anterior right ventricle
The Posterior Interventricular Branch: posterior both ventricles

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16
Q

What does the left coronary supply? What are the two branches, and what do they supply?

A

Supplies the SA node, left atrium, ventricles and interventricular septum.
The Circumflex Branch: left atrium and posterior left ventricle
The Anterior Interventricular Branch: anterior ventricles

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17
Q

What does the great cardiac vein do?

A

drains the anterior heart

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18
Q

What does the middle cardiac vein do?

A

Drain the posterior heart

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19
Q

Where do the great cardiac vein and middle cardiac vein drain into? (structure and chamber)

A

Coronary sinus in the right atrium

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20
Q

What are the main characteristics of cardiac muscle cells?

A

striated (actin and myosin in myoibrils), 1 central nucleus, branching, intercalated disks and gap juctions, desmosomes, large mitochondria, one T tubule per sarcomere, simple sarcoplasmic reticulum

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21
Q

What are gap junctions? Where are they in a cardiac muscle cell? What is their role regarding electrical impulses and ions?

A

They are channels that allow ionic ionic continuity between the cells (basically, they are a channel for the ions to easily go from one cell to the next). Located at intercalated disks, and they allow electrical impulses to pass from one cell to another.`

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22
Q

Because of gap junctions, does the myocardium contract in a coordinated or uncoordinated fashion? For this reason, it is called a ———- ———–.

A

Coordinated contrcation, Functional syncytium

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23
Q

What are they key differences between cardiac muscle and skeletal muscle?

A

functional syncytium vs multinucleated syncytium, act on the fibrous skeleton of the heart instead of tendons/bones, have much larger mitochondria, and there is only 1 T-tubule instead of 2

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24
Q

What is another name for the cardiac pacemaker?

A

The SA node (sinoatrial node)

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25
Q

Where is the SA node located? What do both nodes do?

A

In the right atrium. They discharge action potentials SPONTANEOUSLY

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26
Q

What is the very first event in the sequence of cardiac muscle excitation?

A

The SA node depolarizes (Na+ moves in)

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27
Q

After the SA node is depolarized, what happens?

A

The action potential travels down the atria causing atrial muscle fiber contraction

28
Q

What structure is located at the AV border? What does it cause? Why is this important?

A

The AV bundle, or Bundle of His, is a band of poorly-conducting tissue with very few gap junctions. It slows the impulse just a little but, which allows the atria to fully empty before the ventricles contract.

29
Q

After the action potential gets through the AV bundle, where does it go next? What occurs?

A

It travels down the bundle branches to the ventricles, and they contract from the bottom up (forcing blood upwards to the semilunar valves)

30
Q

What is the difference between the rate the pacemaker cells discharge action potentials and the resting heart rate?

A

pacemaker cells discharge at 100-120 bpm
resting heart rate is 70 bpm
nervous system (parasympathetic) slows down the heart rate because it knows it doesn’t need to be that fast

31
Q

Because pacemaker cells are auto-rhythmic (spontaneously discharge potentials), are they stable or not?

A

They are unstable.

32
Q

What does the membrane potential graph look like for the pacemaker cells? Draw it.

A

start at -60, slow rise to threshold at -40, jump up to 10, and fall back down to -60

33
Q

What events cause the characteristics of the membrane potential graph for pacemaker cells?

A

1) slow depolarization to threshold - leak current slowly increases permeability to Na+
2) full depolarization - sudden increase of Ca++ permeability when threshold is reached
3) repolarization - permeability to K+ opens and Ca++ stops

34
Q

What does the membrane potential graph for cardiac muscle look like?

A

fast rise from -90 to a peak of 30, slight fall to a plateau around 0, then a steady fall back to resting potential of -90

35
Q

What causes the characteristics of the membrane potential graph for cardiac muscle?

A

fast depolarization to peak - Na+
fall back to resting potential (plateau) - Ca++ in but K+ out
repolarization - Ca++ channels close and K+ stay open

36
Q

What is a refractory period? How long does it last for the muscle cells (time in ms and relation to the action potential)

A

This is the period where the cell will not respond to an additional action potential. It lasts about 250 ms, which is about as long as the action potential.

37
Q

Is the refractory period for cardiac muscle longer or shorter than for skeletal? Can cardiac do summation or tetanus like skeletal muscle?

A

Much longer, and it cannot do summation or tetanus from repeated stimulations (they just wont do anything)

38
Q

What is atrial diastole and ventricular diastole?

A

atrial diastole: when the atria fill passively
ventricular diastole: ventricular muscles are repolarized (relaxed) and drop in pressure resulting in them passively filling

39
Q

What is atrial systole and ventricular systole?

A

Atrial systole: very brief contraction of the atria, actively filling the ventricles
Ventricular systole: pressure in the ventricles rises, the muscle fibers are depolarized and then the ventricles contract

40
Q

During diastole (atrial and ventricular) are the AV valves open or closed?

A

open

41
Q

During systole (atria and ventricles) are the AV valves open or closed?

A

closed

42
Q

What does the P wave of an ECG come from?

A

depolarization of the atria just before they contract (systole) to “top off” the ventricles and make sure everything gets out of the atria

43
Q

What causes the QRS spike on an ECG?

A

ventricular contraction

44
Q

What causes the T wave on an ECG?

A

relaxation of the ventricles (atria are already relaxed) and begin filling everything up again

45
Q

Give an overview of the contraction/relaxations of the chambers in one cycle (start with everything being relaxed)

A

everything is relaxed and filling with blood (running through the atria and into the ventricles)
atria give a little contraction to “top off” the ventricles
Atria relax while the ventricles contract and eject blood out into circulation
everything is relaxed again

46
Q

When does aortic pressure spike? (what time in the contraction/relaxation cycle)

A

When the ventricles contract

47
Q

Which is bigger, the peak pressure for the atrium or ventricles?

A

The ventricular pressure peaks much higher

48
Q

Out of the atria, ventricles, and aorta, which pressure always remains relatively high?

A

the aorta

49
Q

There is a short period where pressure in the ventricles is high but still low in the aorta. What is the term for this? Why does it happen?

A

Isovolumetric contraction. When the ventricles first start to contract they build up pressure but not enough to over come the semilunar valve and open them. Therefore, pressure is increased in the ventricle but not yet the aorta because blood hasn’t been ejected into the aorta yet.

50
Q

What pressure is required for the aortic valve to open?

A

100 mmHg

51
Q

What is the equation for stroke volume?

A

EDV-ESV

52
Q

What is the equation for cardiac output?

A

CO=HRxSV

53
Q

What two main factors affect cardiac output? Draw a flow chart of what affects CO.

A

stroke volume and heart rate

54
Q

What are the determinants of stroke volume?

A

EDV/preload, aortic and pulmonary artery pressure/afterload, and contractility

55
Q

What is afterload?

A

pressure the heart must overcome to eject blood into the aorta/pulmonary artery

56
Q

What is preload/EDV?

A

volume of blood in the ventricles at the end of diastole

57
Q

What factors affect preload/EDV? Why is preload such an important factor in SV?

A

driving pressure, muscle pump, and respiratory pump
The heart can only pump out what it receives, so it needs to receive more blood in each relaxation to be able to pump more out with each contraction.

58
Q

What is driving pressure?

A

heart chambers only fill when the pressure at point 1 is greater than at point 2 (travel down a pressure gradient)

59
Q

How does the respiratory pump impact preload?

A

breathing affects venous return through changes in the right atrial pressure

60
Q

What is passive/Frank-Starling mechanism contractility?

A

Changes in contractilty due to change in the length of cardiac muscle fibers.
When the volume increases, the muscle fibers stretch, and then will produce a more forceful contraction.

61
Q

What is active contractility?

A

Change in contractility due to stimulation of the heart by the sympathetic nervous system

62
Q

With no nervous system input, what will happen to stroke volume if the preload increases?

A

The stroke volume will increase

63
Q

What are chronotropy and inotropy?

A

chronotropy- HR
inotropy- contractility/force

64
Q

How does the nervous system increase contractility?

A

release of norepinepherine increases permeability to Ca++, which causes an increase in cross bridges that increases the strength of contraction

65
Q

After norepinephrine is released by the neurons, how does it increase contractility? (details)

A

binds to B1 adrenergic receptors, opens Ca++ channels, initiates cAMP then PKA which keeps Ca++ open longer, increases the crossbridges and therefore the force of contraction

PSIO202 (27 decks)

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