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Block 2; Week 1 > The Heart...LeBlanc Wk1 & Physio reading. > Flashcards

The Heart...LeBlanc Wk1 & Physio reading. Flashcards

1
Q

What is cardiac output?

A

The amount of blood that is pumped out of either ventricle.

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2
Q

What is venous return?

A

The amount of blood that is returned to either atrium.

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3
Q

What’s the deal w/ cardiac output & ventricles & venous return & atria @ steady state?

A

Cardiac output is equal in either ventricle at steady state. Venous return is equal in either atrium at steady state. Cardiac output=venous return at steady state.

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4
Q

Describe the arterioles’ innervation from the nervous system. note: this is the site of highest resistance in the cardiovascular system.

A

Alpha 1 adrenergic: causes vasoconstriction higher affinity for NE than
Beta 2 adrenergic: causes vasodilation

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5
Q

T/F All capillaries are always perfused with at least some blood.

A

No. False. Selective Perfusion of Capillaries b/c of autonomic stimulation.

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6
Q

Why can veins contain so much blood? How can you change that?

A

B/c unlike arteries…they don’t have a lot of elastic tissue.
Can change this thru alpha 1 adrenergic stimulation…which causes contraction & reduces their capacitance.

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7
Q

What is the significance of this equation: v=Q/A

A

velocity = blood flow/ cross sectional Area.
Explains why the important slow velocity that allows for exchange in capillaries exists…they have a large cross sectional area.

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8
Q

What is the significance of this equation:

R=8nl/pir^4?

A

n(nu) is the viscosity of the blood.
l is the length of the blood vessel
r is the radius of the blood vessel
R is resistance to flow.

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9
Q

If you increased your hematocrit…what would happen to your resistance to blood flow?

A

This would increase the viscosity of the blood. This would increase the resistance.

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10
Q

What would happen to resistance to blood flow if you shortened the length of the blood vessel?

A

this would decrease the resistance of the blood flow.

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11
Q

What would happen if you decreased the radius of a blood vessel by 1/2?

A

It would increase resistance by a factor of 16!

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12
Q

What is the significance of Reynold’s number as signified by this equation: Nr=pdv/n?

A

The higher Nr the more likely the blood vessel will experience turbulent flow (and not laminar flow) which is bad. this means that the higher the velocity of the blood & the lower the viscosity of the blood…the more likely you’re gonna get turbulent flow. When diameter gets smaller, the velocity gets larger–>more turbulent flow.

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13
Q

In Reynold’s number what wins out in terms of effect…diameter or velocity?

A

Velocity! When you see changes in diameter…just think the smaller the diameter the faster the velocity & think about the effect of that.

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14
Q

Anemia causes turbulent flow. Why?

A

Low hematocrit…lower viscosity…higher Nr.

High cardiac output…higher velocity…higher Nr.

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15
Q

Thrombi cause turbulent flow. Why?

A

This decreases the diameter of the blood vessel lumen. This increases velocity & therefore Nr.

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16
Q

Total Volume of Blood=Unstressed Volume + Stressed Volume + Volume of blood in the heart. What does this mean?

A

Unstressed Volume=volume of blood in the veins. At low pressure (low stress)
Stressed Volume=volume of blood in the arteries. At high pressure

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17
Q

How does the equation for capacitance: C=V/P relate to veins & arteries?

A

Veins have a high capacitance or compliance. They can hold a lot of blood at a given pressure. Their pressure is typically very low.
Arteries have a lower capacitance or compliance. They don’t hold as much blood at a given pressure. Their pressure is typically very high.

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18
Q

In terms of the concept of compliance…why do older people typically have higher blood pressure?

A

Their arteries are stiffer (less compliant) so C decreases. And in order to hold the same V volume of blood…they need to also increase their pressure.

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19
Q

Where is the greatest drop in arterial pressure? Why? What is the pressure of the vena cava & of the RA?

A

At the level of the arterioles b/c they have the highest resistance & deltaP=Q X R. Blood flow is constant, so if there is a higher resistance there must be a higher drop in pressure. Also…vena cava BP is about 4mmHg & RA is about 0mmHg.

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20
Q

The pulsatile flow of blood near the aorta reflects what?

A

The cardiac cycle w/ each pulse. : ) Highest pressure shows ejection during systole (systolic pressure) & lowest pressure shows relaxation during diastole (diastolic pressure). Difference b/w Systolic & Diastolic is the pulse pressure…reflects stroke volume.

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21
Q

What is the dicrotic notch?

A

It is the little dip in the arterial pressure that signifies the closure of the aortic valve. Here a little blood flows back & momentarily decreases arterial pressure.

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22
Q

Note: pulsation in larger arteries is larger than in the aorta.

A

It’s weird. Just accept it.

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23
Q

What is the equation for mean arterial pressure? Explain why.

A

Mean Arterial pressure=Diastolic Pressure + 1/3 pulse pressure.
More emphasis is given to the diastolic pressure b/c more time is spent in diastole.

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24
Q

What can change mean arterial pressure?

A

Mainly changes in pulse pressure. This can be changed by changes in stroke volume or compliance of the vessel.

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25
Q

What happens to pressure w/ arteriosclerosis?

A

Plaque buildup makes the arteries less compliant. By the equation C=V/P…this requires an increase in systolic & mean & pulse pressure.

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26
Q

What happens to pressure w/ aortic stenosis?

A

C=V/P. The narrowing of the aortic valve will cause a decrease in stroke volume. This will cause a decrease in mean arterial, pulse, systolic pressure.

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27
Q

How can you have the same cardiac output in both circulations (pulmonary & systemic) when the pressure in the pulmonary circuit is so much lower?

A

Q=P/R. The blood flow must be constant in both circulations.
So b/c the pressure in the pulmonary circuit is lower…the resistance must also be lower than in the systemic circulation.

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28
Q

What is the difference b/w contractile cells & conducting cells?

A

Contractile Cells–in atrial & ventricular tissues; working cells of the heart; AP here leads to contraction
Conducting Cells–SA, atrial internodal, AV, Bundle of His, Purkinje. Can spontaneously generate AP. They are muscle cells but don’t create force. They transmit AP to contractile cells.

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29
Q

What do the atrial internodal tracts do?

A

They are conducting cells that spread the AP from the right atrium @ the SA node to both atria & to the AV node.

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30
Q

Why is slow conduction thru the AV node so important?

A

This delay helps give the ventricles time to fill sufficiently. If the AV node conduction were faster then the ventricle wouldn’t fully fill.

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31
Q

Is the conduction thru Bundle of His & Purkinjes slow or fast?

A

It is fast. It goes to the ventricular muscle cells.

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32
Q

What are the requirements for a normal sinus rhythm?

A

AP originates @ the SA node.
SA impulses @ a rate of 60-100 bpm.
Activation of the myocardium must occur in the proper order.

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33
Q

Which ion primarily determines the resting membrane potential in cardiac cells?

A

Potassium.

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34
Q

How much of a contribution does the sodium potassium pump make to the membrane potential?

A

Very little. It does keep the conc’n gradients of sodium & potassium proper.

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35
Q

What will happen to membrane potential when the conc’n of potassium outside of the cell is decreased?

A

There will be a larger conc’n gradient & desire for potassium to get outside the cell. The membrane potential will then be closer to that of potassium (more negative).

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36
Q

In ventricular cells, there is low permeability to ______ions except during________.

A

Sodium.

Except during the upstroke of the AP.

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37
Q

What are the characteristics that define the atrial, ventricular, & Purkinje system cells?

A

Long duration w/ a plateau. Longer refractory period.

Stable resting membrane potential–they don’t really spontaneously depolarize.

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38
Q

What are the different phases of the atrial, ventricular, Purkinje cells’ APs?

A

Phase 0: rapid depolarization…caused by transient sodium conductance.
Phase 1: initial repolarization
Phase 2: plateau @ about 20 mV
Phase 3: repolarization
Phase 4: resting membrane potential again…

39
Q

What causes the plateau in atrial, ventricular & purkinje system cells?

A

Inward movement of calcium thru voltage-gated calcium channels & outward movement of potassium by the electrochemical gradient. They are equal & create the plateau.

40
Q

What is a side effect of calcium plateau?

A

CICR.

41
Q

What are the characteristics of the SA node?

A

automaticity, unstable membrane potential, no sustained plateau, short refractory period

42
Q

What are the phases experienced by the SA node AP?

A

Phase 0: rapid depolarization BY Calcium!!
Phase 3: Repolarization mainly by potassium
Phase 4: higher membrane potential that helps it to be automatic…Slow depolarization thru this phase b/c of Ifunny…a sodium current.
Change in Heart rate affects the rate of phase 4.

43
Q

What are the latent pacemakers of the cell?

A

AV node, Bundle of His, Purkinje Fibers

44
Q

What determines the heart rate of the heart?

A

The SA node. Whichever thing depolarizes the fastest. SA node has the shortest refractory period.

45
Q

Where in the heart is the conduction velocity the slowest & where is it the fastest?

A

Slowest conduction velocity: AV node

Fastest Conduction Velocity: Purkinje fibers

46
Q

Why is there such fast conduction thru the myocardium?

A

The gap junctions allow for low resistance.

47
Q

What are chronotropic effects?

A

Changes in heart rate.
Sympathetic: Beta 1; increases If @ the SA node.
Parasympathetic: Muscarinic 2: decreases If @ the SA node.

48
Q

What are dromotropic effects?

A

Symp: increase in conduction velocity.
Parasymp: decrease in conduction velocity.

49
Q

What does the P wave represent on the ECG?

A

Atrial Depolarization

Longer wave if slower conduction velocity.

50
Q

What does the PR segment correspond to?

A

AV node conduction.

Decrease in conduction velocity thru the AV node corresponds to a longer PR segment.

51
Q

What does the QRS complex correspond to?

A

Ventricular depolarization.

Very fast even tho ventricles large b/c of how fast the His & Purkinje cells are…

52
Q

What does the T wave represent?

A

Ventricular Repolarization

53
Q

What does the QT interval correspond to?

A

The beginning of ventricular depolarization to the last of the ventricular repolarization. This includes the ST segment.

54
Q

What does the ST segment correspond to?

A

The plateau of the ventricular action potential.

55
Q

How do you determine heart rate?

A

HR=1/cycle length (R-R interval)

56
Q

What are thick & thin filaments made up of in cardiac muscle sarcomeres?

A

Thick: myosin
Thin: actin, tropomyosin (binds myosin), troponin (3 subunits–C when bound to calcium…releases tropomysoin & binding can happen).

57
Q

What are T tubules?

A

Invagination of the sarcolemma of cardiac muscle…AP gets here & calcium released into cell & SR are very close to it & releases calcium.

58
Q

The tension of contraction in myocardial cells is proportional to what?

A

The calcium…more calcium you have the stronger the contraction.

59
Q

What causes the relaxation of the cardiac muscle?

A

Getting a lower intracellular calcium conc’n.
this happens w/ Ca++ ATPase in the SR.
& the calcium/sodium exchanger in the sarcolemma.

60
Q

What are inotropic effects?

A

Positive: increased rate of contraction & strength of contraction
Negative: decreased rate of contraction & strength of contraction

61
Q

If there is beta 1 adrenergic stimulation to increase contractility…what are the mechanisms that would take place?

A

phosphorylation of sarcolemmal Ca++ channels allows more calcium to enter the cell…
phosphorylation of phospholamban (on the SR Ca++ATPase)…this increase the activity of the ATPase allowing for faster relaxation so that there can be faster restimulation & more storing of calcium in the SR.

62
Q

How does an increase in heart rate cause an increase in contractility?

A

Faster HR you get a buildup of the calcium that increases contractility.

63
Q

What do glycosides do & what are they used to treat?

A

Glycosides inhibit the Na+/K+ ATPase…this causes an accumulation of sodium inside the cell which stops the sodium/calcium exchanger. This causes an accumulation of calcium inside the cell which increases the strength of the contraction.
Glycosides are used to treat congestive heart failure which usu includes low contractility.

64
Q

What is preload & afterload?

A

Preload: ventricular end diastolic volume.
Afterload: the pressure the ventricle has to overcome to eject the blood. If LV: aortic pressure.

65
Q

What is stroke volume?

A

volume of blood ejected by the ventricle with each beat.

SV=End diastolic volume-End systolic volume

66
Q

What is ejection fraction?

A

Fraction of end diastolic volume that is ejected in one stroke volume….a measure of contractility.
Normal: 55%
Ejection Fraction=SV/EDV

67
Q

What is cardiac output?

A

volume of blood ejected by the ventricle per unit time.

CO=SV X HR

68
Q

What is the Frank Starling Mechanism?

A

The more the wall of the heart is stretched, the more forcefully it will contract.
Therefore, the stroke volume (how much blood is ejected from the heart) is dependent on how much blood is put in there! (the end diastolic volume).

69
Q

If you are looking at a PV loop…with A (L) B (R) C (roof) & D (floor)…and B pushed more toward the right…what could cause this change?

A

An increase in preload or venous return. This increases end diastolic volume. increases stroke volume.

70
Q

If you are looking at a PV loop…with A (L) B (R) C (roof) & D (floor)…and C is pushed up and A moves to the right…what could cause this change?

A

increased afterload. Increased aortic pressure.
You need a stronger isovolumic contraction to reach that demand (high C). Then it’s hard to stay at that pressure for a long time, so the stroke volume decreases (end systolic volume increases). This explains why A is farther right.

71
Q

If you are looking at a PV loop…with A (L) B (R) C (roof) & D (floor)…and C isn’t pushed but it arcs a little higher & A is farther left. What could cause this change?

A

Increased contractility. Stroke volume increases & end systolic volume decreases.

72
Q

What does the S4 heart sound correspond to?

A

Atrial contraction.

73
Q

Why does the 2nd heart sound split?

A

B/c the aortic valve closes slightly before the pulmonic valve.

74
Q

What happens to the AP of a cardiac muscle cell if you increase its contractility?

A

It has a more positive plateau.

75
Q

What is the resting membrane potential of a cardiac muscle cell?

A

-90mV

76
Q

What are 3 things that can alter conduction velocity?

A

A larger diameter means a lower resistivity & a faster conduction velocity.
Larger AP…domino effect & faster conduction velocity.
More membrane depolarization fewer active Na+ channels & slow conduction velocity.

77
Q

What do high potassium conditions do to a cell?

A

Inactivate some sodium channels.

78
Q

What is the advantage that sympathetic innervation of the heart has over parasympathetic innervation?

A

Symp innervate everything that parasymp does + the ventricular cells.

79
Q

What are the effects of hypokalemia & hyperkalemia on pacemaker cells?

A

Hypokalemia: accelerates automaticity of pacemaker cells when you have less potassium in the serum surrounding the cell.
Hyperkalemia: depresses automaticity of pacemaker cells when you have more potassium in the serum surrounding the cell.

80
Q

What is the basic idea of the EKG?

A

There are currents in the heart that reach to the skin (enhanced by gel) and there are electrical potentials b/w them that can be read.

81
Q

What’s the deal with the dipole of the EKG?

A

Create a pos & neg point & a dipole. If you are in line with this you will get the largest magnitude read. If you are at a 90 degree angle to it you will read 0.

82
Q

If both regions that you are studying are depolarized…what reading will you get?

A

A reading of no potential difference. Can’t tell if both depolarized or both resting.

83
Q

When the first part that you are studying has depolarized and the second hasn’t what reading do you get?

A

An inverted waveform.

84
Q

Why is the ST segment straight?

A

B/c all cells are depolarized. No potential difference.

85
Q

Where is atrial repolarization in the EKG?

A

Buried in the QRS complex.

86
Q

What is required in order to get a deflection on an EKG?

A

It is required that you have a difference in potentials.

87
Q

Why don’t we see the Bundle of His on the EKG?

A

Not enough mass to cause a deflection.

88
Q

What does a lengthened PR interval tell us?

A

Delayed AV conduction.

89
Q

What does a widened QRS complex tell us?

A

Delayed conduction thru the ventricles.

90
Q

What does ST segment elevation or depression tell us?

A

Can be something like MI or ischemia.

91
Q

Where are the leads placed in a normal EKG?

A 
Electrode @ left foot (+)
Electrode @ right arm (-) 
Electrode @ left arm (+ or -)
Lead 1: b/w left & right arm
Lead 2: b/w right arm & left foot
Lead 3: b/w left arm & left foot
92
Q

In which leads is it normal to have inverted waves? Where is there the most positive R wave?

A

Inverted normal in aVR & aVL.

Most positive R wave @ lead II.

93
Q

Of the chest leads, which will show the highest R wave?

A

V4 & V5

Block 2; Week 1 (9 decks)

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