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Medical Physiology > Lecture 5: Cardio > Flashcards

Lecture 5: Cardio Flashcards

1
Q

What does the right heart pump to?

A

Pumps blood through the lungs

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2
Q

What does the left heart pump to?

A

Pump blood through the body

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3
Q

What are some key characteristics of cardiac myocytes/conductive muscle.

A

Contracts very much like skeletal muscle except the duration of the contraction is much longer.

There are specialized excitatory and conductive fibers.

contract only feebly and contain few contractile fibers.

Exhibit automatic rhythmical electrical discharge in the form of action potentials (SA node).

Or conducts action potentials through the heart

controls the rhythmical beating of the heart.

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4
Q

What is the SA node’s intrinsic heart rate?

A

60-100 bpm, but generally higher without ANS modulation.

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5
Q

What are the key anatomical differences in cardiac myocytes vs skeletal muscle?

A

Latticework (fibers randomly divide and join other fibers and then recombine and spread again)

Functional syncytium made from intercalated discs.

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6
Q

what are intercalated discs

A

form permeable “communicating junctions” gap junctions that allow rapid diffusion of ions.

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7
Q

What is a syncytium?

A

A combined cytoplasm, usually made by intercalated discs.

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8
Q

Where are the two syncytia of the heart?

A

Atrial and ventricular.

Note:
They are separated by an insulated fibrous layer in their AV valves to the signal does not pass through them. Signal goes via interventricular septum.

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9
Q

What are the two action potential related differences between skeletal and cardiac muscle?

A

Cardiac has two channels, fast sodium + calcium-sodium.

fast sodium is very fast to close. (skeletal muscle has these)

Calcium-sodium is slower to open and remains open for much longer (several tenths of a second). (skeletal muscle doesnt have these)

Calcium for the muscle AP comes from the sarcoplasmic reticulum AND the T tubules.

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10
Q

What does the strength of contraction of a cardiac muscle fiber depend on?

A

ECF concentration of calcium.

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11
Q

What does calcium channel blockers do to the heart

A

they clock the calcium channels which means the calcium channels do not open which mean slower repolarization of the cardiac cells. aka decreased heart rate

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12
Q

What does beta-adrenergic stimulation of the heart do?

A

Increase cardiac contractility and acceleration.

Note:
Think of dobutamine, the beta-1 agonist we learned in pharm.

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13
Q

What does DHP stand for?

A

Dihydropyridine.

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14
Q

Fill in the blanks

A

yayyyyy

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15
Q

What class antiarrhythmic is amiodarone?

A

Class III, because it works on phase 3 of the cardiac AP.
This is the part of the phase that is dependent on potassium, so amiodarone affects potassium channels.

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16
Q

What part of the cardiac action potential does a calcium channel blocker (CCB) affect?

A

It is class IV, a non-DHP CCB.

It affects phase 2 of the cardiac AP, which is the plateau phase of the cardiac action potential. It slows electrical conductivity, extending the phase.

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17
Q

The SA node action potential gives us a consistent rate that is controlled by the ANS by a …….

A

spontaneous cyclic depolarization of primary pacemaker cells in the SAN. (establishes intrinsic HR)

(as a result of a unique time dependent characteristic of a variety of depolarizing and hyperpolarizing currents. )

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18
Q
A
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19
Q

What is the slow depolarization of the SA node action potential known as?

A

Pacemaker potential

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20
Q

Explain the process of the SA node’s AP. (at what mV do certain channels open and close in the heart.)

A

At -60 mV, K+ channels close, slow Na+ channels open.

Slow increase to -40. -60 to -40 is the pacemaker potential.

-40 is when Ca channels open , which goes to +5.

At the peak, Ca channels close and K+ channels open, reducing the membrane potential. As it repolarizes, the Ca permeability decreases at -10 and the K+ permeability increases at -30.

Note:
Above -40 is the AP, below -40 is the pacemaker potential.

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21
Q

What 3 things does parasympathetic innervation do to the SA node’s AP?

A

Reduces rate of depolarization.
Increase in action potential hyperpolarization.
Upward shift in AP threshold potential.

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22
Q

What does S1 represent?

A

AV valve closure/ventricular contraction

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23
Q

What does S2 represent?

A

Semilunar valve closure.

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24
Q

When does isovolumic contraction occur between?

A

AV valve closure and semilunar valve opening.

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25
Q

When does isovolumic relaxation occur between?

A

Semilunar valve closure and AV valve opening.

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26
Q

What are EDV and ESV?

A

End diastolic volume = the volume at the end of diastole (when ventricle are filled)
End systolic volume = the volume at the end of systole. (the amount left when ventricles empty)

EDV - ESV = SV, or stroke volume.

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27
Q

Where does the cardiac cycle begin? (where is the location of the beginning of the electrical potential that passes through the heart)

A

SA node, located in the superolateral wall of the R atrium near the opening of the SVC.

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28
Q

what initiates heart contraction

A

action potential of SA node

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29
Q

where is the SA node located

A

the superior lateral wall of the right atrium near the opening of the superior vena cava.

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30
Q

What is diastole?

A

A period of relaxation when the heart is filling with blood.

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31
Q

What is systole?

A

A period of contraction.

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32
Q

How does blood flow into the ventricles during diastole?

A

Mainly gravity, with a minor amount of atrial contraction contributing.

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33
Q

What are the AV valves specifically designed to prevent?

A

Backflow of the blood from the ventricles to the atria

(bicuspid and ticuspid)

Note:
Think of their shape.

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34
Q

Which AV valve is right and which is left

A

Right = Tricuspid
Left = bicuspid = mitral

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35
Q

What are the Semilunar valves specifically designed to prevent?

A

Backflow of the blood from the aorta and pulmonary trunk to the ventricles

(semilunar = aortic and pulmonary valves)

Note:
Think of their shape

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36
Q

When do papillary muscles contract

A

when the ventricular wall contracts

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37
Q

What does contraction of the chordae tendineae do?

A

Prevents the valves from bulging. It is NOT to help the valves close.

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38
Q

describe filling of the ventricles during diastole

A

as soon as systole is over and the ventricle pressure begins to fall again to the low diastolic values.

moderately increased pressure has developed in the atria during ventricular systole immediately pushes the AV valves open.

this allows blood to rapidly flow into the ventricles.

thus a rise of the LV volume curve.

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39
Q

What is the increase of LV volume also known as?

A

Period of rapid filling of the ventricles.

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40
Q

describe the process of emptying of the ventricles during systole (period of isovolumetric/isometric contraction)

A

immediatly after Ventricular contraction begins, ventricular pressure rises abruptly

AV valves close

then an additional .02-.03 seconds is required for the ventricle to build up sufficient pressure to push the semilunar valves open against the pressures in the aorta and pulmonary artery.

no emptying.

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41
Q

Why does isovolumic contraction occur?

A

The AV valves close and volume stays identical, hence isovolumic. However, it takes .02-.03 secs to build up pressure to open the semilunar valves.

(iso = equal, therefore there is no emptying)

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42
Q

What is the pressure of the LV during systole?

A

Slightly above 80mm Hg.

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43
Q

deescribe the pressure of the left and right ventricle during the period of ejection

A

left V pressure rises slightly above 80mmHG
right V pressure is slightly above 8mmHG

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44
Q

what valves open during the period of ejection

A

the semilunar valves.
blood begins to pour out of the ventricles.

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45
Q

What are the two parts of ejection?

A

Period of rapid ejection and slow ejection.
Rapid = 70%, during the first 1/3 of ejection.
Slow = 30%, during the 2nd 2/3 of ejection.

46
Q

describe the period of isovolumetric relaxation

A

at the end of systole when ventricular relaxation begins suddenly

both the R and L intraventricular pressures decrease rapidly

aortic and pulm valves close

this relaxation of the ventricles continues for .03-.06 seconds.

47
Q

Why does isovolumic relaxation occur?

A

The ventricle begins relaxing, reducing pressure and closing the valves. Even with the valves shut, the ventricles are still relaxing back to normal.

48
Q

What is ejection fraction?

A

The amount of blood the left ventricle ejects per stroke relative to its end diastolic volume.

Essentially, its how much of the blood in the left ventricle during contraction gets ejected out.

EF is therefore (SV/EDV) x 100.

49
Q

what does valves opening sound like

A

slow process/no sound

50
Q

what is the sound created when the valves close

A
  • vanes of valves
  • vibrating fluid sounds in response to sudden pressure change
51
Q

What does S1 sound like?

A

Low in pitch, relatively long-lasting.
first heart sound - occurs when ventricles contract/AV valves close

52
Q

What does S2 sound like?

A

Rapid snap, with vibration after.
at end of systole when SL valves close

53
Q

What does aortic stenosis look like on a phonogram?

A

It appears between S1 and S2 as a big constant vibration. This is because the narrow valve means all the blood goes through it in intervals.

54
Q

What does mitral regurgitation look like on a phonogram?

A

Small vibrations between S1 and S2. This is because blood flowing back will stop the valves from closing fully.

55
Q

What does aortic regurgitation look like on a phonogram?

A

Small vibrations after S2 all the way to S1. This is because blood flowing back will stop the valves from closing fully in the aorta.

56
Q

What does a patent ductus arteriosus sound like?

A

Constant vibrations the whole time, no distinct S1 and S2.

57
Q

When is LV pressure greatest?

A

During systole, aka when the ventricle is contracting and is therefore at its highest volume. It will peak a little before it ejects the last 1/3 of its SV.

58
Q

When is LV pressure lowest?

A

During diastole, aka when the ventricles are filling and relaxed.

59
Q

What is the usual ESV? EDV?

A

ESV:50 mL
EDV: 120 mL

60
Q

Explain the volume pressure curve for the left ventricle, beginning at the start of diastole.

A

Phase 1 - period of filling:
LV volume & pressure are at minimum. Volume will increase as the mitral valve stays open, so blood from the atrium pours into the ventricle.

Phase 2 - period of isovolumic contraction:
Once the ventricle is filled, its volume is maxed and the mitral valve closes. It begins to contract, increasing pressure without a volume change (Isovolumic contraction).

Phase 3 - period of ejection:
Once pressure exceeds the threshold, the aortic valve opens, and volume will rapidly decrease as the ventricle squeezes it into the aorta.

Phase 4 - Period of isovolumetric relaxation
Once the squeeze is done, pressure is reduced and the aortic valve closes. The ventricle begins relaxing but volume does not change (isovolumic relaxation)

The cycle begins anew.

61
Q

What is rate pressure product? Why is it significant?

A

RPP is used as a measure of myocardial work.

Of note, the heart consumes 70% of the oxygen from coronary arteries, which is 3x more than skeletal muscle. It can also increase its coronary blood flow up to 4x.

Note:
RPP increased for patients being trained before angina petoris and ST depression occurred in pts with heart disease.

62
Q

How do I calculate RPP? Typical values?

A

RPP = HR X SBP (systolic blood pressure)

A regular HR of around 50 bpm and SBP of 120mmHg means work is around 6000 at rest.

A HR of around 200 bpm and a SBP of 200 mm Hg means work is around 40,000 at maximum exercise for example.

63
Q

what are significant correlations of RPP and heart disease

A
  • correlation between RPP and onset of angina pectoris and ST depressions
  • RPP increases by 11.5% before ischemic symptoms appear during graded exercise testing
64
Q

How is the stroke volume adjusted in the heart?

A

Intrinsic regulation by venous return and ANS modulation.

65
Q

Describe Frank Starling’s mechanism.

A

Venous return is directly proportional to SV.

The greater the heart muscle is stretched while filling (diastole), the greater the force of contraction (systole)

AKA the more blood our veins send to our RA, the more we can eject from our LV.

66
Q

Describe why more stretch causes more contraction.

A

The greater the stretch, the better the orientation between actin and myosin, which causes greater crossbridge action = more force.

67
Q

What is preload? What affects it?

A

Preload, aka end diastolic filling volume.

It is affected by muscle pump (aka muscle contraction increases venous return)

Respiratory pump (reduced intrathoracic pressure causes blood to rise up from the lower body)

Venoconstriction by the SNS

Dynamic work (aka a runner constantly moving)

68
Q

What is afterload? What affects it?

A

Afterload is blood exiting the heart.

SBP
Aortic stenosis
Arteriosclerosis
Static work (aka a weight lifter lifting a weight slowly)

69
Q

What can SNS and PNS do to the volume of blood we pump?

A

Sympathetic can increase HR to 180-200 in a young adult.
Force of contraction increases by 2x.
Increased SV
Increased ejection pressure.

therefore sympathetic stimulation can often increase the max cardiac output by as much as 2-3x in addition to the increased output caused by the Frank-Starling mechanism.

70
Q

Where are SNS and PNS nerve fibers found on the heart?

A

PNS: (the vagi)
distributed mainly by the SA and AV nodes. A few to the atria, very little to ventricles via vagus nerves.

SNS:
All parts of the heart, but mainly ventricular muscle.

71
Q

If I depress the SNS, what usually happens to the heart?

A

Heart rate (chronotropic) and strength of ventricular contraction (Inotropic) decrease by around 30%, since the SNS is always sending a slow, continuous signal.

72
Q

If I increase the PNS, what can happen to the heart?

A

It can stop for a few seconds.

but then the heart usually “escapes” and beats at a rate of 20-40 beats per minute as long as the PS continues.

Decreases heart contraction (inotropic) by up to 30%, but because the fibers don’t really go much to ventricles, HR is affected since its mainly atria affected, so the overall effect is HR reduction (chronotropic).

73
Q

What is the Fick Equation? What is it used for?

A

VO2 = CO * a-VO2 diff, which is used to determine the rate at which oxygen is being used during physical activity

74
Q

What is the formula for cardiac output

A

CO = HR * SV

75
Q

What increases mainly in an athlete?

A

Stroke volume. HR also increases SLOWER but has the SAME MAX.
a-VO2 difference also increases much SLOWER in an athlete, as their max oxygen consumption is far greater.

76
Q

What determines local blood flow control?

A

Tissues!

The amount of oxygen a tissue wants dictates how much blood flow it gets.

note to self: Acute local blood flow control refers to intrinsic regulation, or control, of arterial vascular tone at a local level, meaning within a certain tissue type, organ, or organ system.

77
Q

What 3 organs require most of our blood flow?

A

Liver: 27
Kidneys: 22
Brain: 14

78
Q

How much can blood flow increase to muscles? How?

A

20x increase.
More capillaries
Bigger capillaries

79
Q

What is acute blood control achieved by?

A

Arteriole, metaarteriole, and pre-capillary sphincters.

Occurs within seconds to minutes.

note to self: Acute local blood flow control refers to intrinsic regulation, or control, of arterial vascular tone at a local level, meaning within a certain tissue type, organ, or organ system.

80
Q

What is long-term blood control achieved by?

A

Increases/decreases in capillaries.
Increases/decreases in capillary size.

Slow, controlled changes.

81
Q

What substances vasodilate?

A

Hydrogen ions, Adenosine phosphate compounds, Histamine, Potassium ions, Adenosine, CO2,

HAH PAC

82
Q

What is the oxygen lack theory ?

A

Vessels need oxygen to make energy for vessels to constrict, so in the absence of oxygen, vessels will dilate.

83
Q

What are the two structures in the kidney that affect acute blood flow?

A

Macula densa
Juxtaglomerular apparatus

84
Q

What other molecules affect brain blood flow?

A

CO2 and H+, causing cerebral vessel dilation.

The brain’s level of excitability is highly dependent on CO2 and H+, so it needs to get rid of excess.

85
Q

How is blood flow affected by the skin?

A

Cutaneous and subcutaneous blood flow regulates blood flow, since blood carries heat. It is controlled mainly by sympathetic nerves.

86
Q

Where does Nitric Oxide come from?

A

Endothelium, from the synthesis of arginine and oxygen by nitrix oxide synthase. It has a half-life of 6s and acts locally.

87
Q

When is NO released and what is its effect?

A

When enodthelial cells experience shear stress, they get contorted and NO is released. This relaxes the blood vessel, dilating it.

It can also come from angiotensin II, which releases it to prevent excessive vasoconstriction, since angiotensin II is a vasoconstrictor.

88
Q

What is the term we use for a tissue increasing its blood flow over time by getting bigger and more vessels?

A

Angiogenesis.

89
Q

What does a hyper oxygenated environment cause?

A

angiogenesis in the eyes

For babies, it can stop vascular growth, specifically in the retina. Leaving the environment can cause explosive growth, leading to blindness since the tissue suddenly grows super fast.

Retrolental fibroplasia

90
Q

What is BP a measure of?

A

BP = CO * TPR or SVR

TPR = total peripheral resistance
SVR = systemic vascular resistance
Both are interchangeable.

91
Q

What is MAP?

A

Mean arterial pressure.
MAP = DBP + 1/3(SBP -DBP)

92
Q

What is pressure a calculation of?

A

Pressure = flow * resistance.

Flow = CO

Resistance = TPR or SVR.

Pressure is therefore proportional to flow and resistance.

93
Q

What is Ohm’s law?

A

It is the flow through a vessel.

Flow = Pressure difference divided by resistance.

Pressure difference is the change in pressure from one point in the vessel to another point. Resistance is the friction as the blood flows along the endothelium of a vessel.

94
Q

What is laminar flow? Where does it occur?

A

It is smooth and steady flow, found at the center of a vessel.

95
Q

What is turbulent flow? Where does it occur?

A

It is flow that mixes and flows in multiple directions, occurring when:
rate of blood flow is too great for vessel size
sharp turn
rough surface
vessel obstruction/occlusion

96
Q

What is flow most affected by?

A

Vessel diameter.

97
Q

What is pouiselle’s equation for?

A

AKA more viscous fluids flow slower (like honey/syrup)
Bigger vessels have higher flow
Longer vessels have slower flow

98
Q

Which BP changes the most during exercise?

A

SBP. Diastolic decreases barely, but SBP sharply increases and then increases steadily.

99
Q

What happens if I see a SBP drop during exercise?

A

Indicative of possible heart failure.
The heart has been stressed to the point where it cannot keep up with the work required by the exercise.

100
Q

Describe the SAnode
(what does it look like, how wide is it, how long is it)

A

small, flattened, ellipsoid strip of specialized cardiac tissue
3mm wide
15mm long

101
Q

what special characteristic of the SA node allows it to control the rate of beating of the entire heart

A

self-excitation

102
Q

what special characteristic of the SA node allows it to control the rate of beating of the entire heart

A

self-excitation

103
Q

What is the resting membrane potential of a ventricular fiber

A

~70mV

104
Q

What is the resting membrane potential of a ventricular fiber

A

~70mV

105
Q

what happens once the SA node fires

A

the action potential spreads through the entire atrial muscle mass and then to the AV node

106
Q

how fast does conduction in the heart muscle travel from the SA node to the AV node

A

.3m/s

107
Q

how fast does conduction in the heart muscle travel from the SA node to the small bands of the atrial fibers

A

1m/sec

108
Q

what small band of the atrial fibers passes through the anterior walls of the atria to the left atrium

A

anterior interatrial band

109
Q

where is the AV node located

A

in the posterior wall of the right atrium immediatly behind the tricuspid valve

110
Q

kay look at the second to last slide of the rhythmical excitation of the heart because my brain simply wont process it

A

sounds great thanks

Medical Physiology (14 decks)

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