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Pathophysiology > Ch. 17 (TEST #3) > Flashcards

Ch. 17 (TEST #3) Flashcards

1
Q

Is the pulmonary system high pressure?

A

NO

overall it is a lower pressure (less distance and allows more time for gas exchange)

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2
Q

Is the systemic system low pressure?

A

NO

it is under higher pressure (needs to be for the distance the blood has to travel)

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3
Q

What makes up the pulmonary system? (circulatory)

A

The right side of the heart and the pulmonary vessels

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4
Q

What makes up the systemic system? (circulatory)

A

Left side of the heart and the systemic vessels

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5
Q

Is the volume of blood pumped through each side of the heart different?

A

NO

They are actually the same volume, which is surprising considering what each side is pumping to

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6
Q

If a clot forms on the venous side of systemic circulation where will it most likely go?

A

Back to the heart and most likely will get lodged somewhere in the lungs

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7
Q

If a clot dislodges from the left side of our heart or our arterial systemic circulation what might happen?

A

It could get lodged somewhere in out systemic circulation.

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8
Q

Where do the coronary vessels branch from?

A

The AORTIC ARCH

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9
Q

Do the atrias have valves that prevent blood flow from the vena cava (right atrium) or the pulmonary vein (left atria)?

A

NO NO NO

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10
Q

Can the veins store some blood as a compensatory mechanism? What about the liver?

A

YES YES YES (but it can become s problem)

The liver can store up to 2L of blood if it needed to

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11
Q

How much of the blood volume do the arteries generally contain?

A

about 1/6 of TBV

venous side carries the majority

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12
Q

What happens if our blood volume gets too low?

A

Our vessels could collapse

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13
Q

What are two things that create a resistance to fluid flow?

A

Constricting arterioles

Increased hemotocrit

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14
Q

What are the two things that cause the pressure difference of our circulatory system?

A

The heart creating a pressure difference at the ends of the vessel (heart pushes blood through and creates the blood pressure to keep vessels open)

The vessels resistance to blood flow constricting arterioles and increased hematocrit increase this resistance)

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15
Q

Look at the slide she has that shows the pressure differences in each compartment of the heart… (about 13 minutes into her tegrity lecture is where you will find it)

SHE SAID WE DONT HAVE TO MEMORIZE THE NUMBERS, BUT IT IS A GREAT WAY TO UNDERSTAND THE CONCEPT OF DIFFERENCE IN PRESSURE IN THE HEART

A

DO IT NOW!

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16
Q

How does a higher pressure difference affect our flow rate?

A

it increases it

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17
Q

How does the blood flow between pressure differences?

A

It will travel from the area of higher pressure to the area of lower pressure.

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18
Q

What is the main difference in the anatomy between arteries and veins that give them their pressure differences (as well as their abilities to function under high pressure)? What about capillaries?

A

The arteries have a thicker muscular layer (tunica media) while the veins don’t

If the veins get under too high of pressure they will start becoming leaky (edema)

The capillaries have single layer walls that allow for the nutrient, oxygen, and fluid exchange

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19
Q

What cells make up the inner lining of all the blood vessels?

A

endothelial cells

creates a smooth surface and decreases resistance

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20
Q

What is laminar blood flow and where would it be the fastest? The slowest?

A

This is smooth regular blood flow

It will move the fastest in the center

It will move the slowest on the outside

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21
Q

What is turbulent blood flow?

A

This is interrupted forward current flow by crosswise flow

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22
Q

What are some things that can cause turbulent blood flow?

A

Branch points

obstructions

rough surfaces

increased velocity

decreased viscosity

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23
Q

What is one really bad thing that can happen with turbulent blood flow?

A

Platelets can get aggregated and form a clot

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24
Q

What do we look for when we are assessing for turbulent blood flow?

A

Murmurs (the heart)

Bruits

Thrills

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25
Q

Does our body sometimes create a purposeful turbulent flow?

A

YES

for instance, hemostasis

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26
Q

What does the law of LaPlace state?

A

The amount of tension generated in the wall of any vessel depends on the size (this includes the radius of the lumen as well as the thickness of the walls)

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27
Q

Dumb down the law of laplace.

A

Basically there is a pressure that is pushing out on the vessel walls that keep them from collapsing because of the tension that the vessel wall creates (which is dependent on the walls size and the radius)

WALL TENSION IS A PRODUCT OF THE ELASTICITY OF THE VESSEL (INTERNAL RADIUS)

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28
Q

What does the law of Poiseuille state?

A

Movement of blood through the vascular system is opposed by the force of resistance

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29
Q

In relation to poiseuilles law, what is the most important determinant of resistance?

What are a couple of other things that can increase resistance to flow?

A

CHANGE IN DIAMETER

increase in length and increase in viscosity are a couple other things

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30
Q

When you have an increased resistance to flow, what will have to happen?

A

You will need an increase in pressure

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31
Q

How do you calculate the flow rate of a vessel by its radius?

A

Take the radius to the 4th power

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32
Q

In relation to control of blood flow, how does the SNS (sympathetic nervous system) control it?

A

The SNS is the primary controller of blood flow

It mostly affects the arteries (because the veins have little innervation)

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33
Q

In relation to control of blood flow, how does the PSNS (parasympathetic nervous system control it?

A

It is an important regulator of our heart

NOT IMPORTANT TO REGULATION OF PERIPHERAL BLOOD FLOW

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34
Q

Name our great vessels.

A

Vena Cavae (inferior and superior vena cava)

Aorta

Pulmornary artery (deoxygenated)

Pulmonary vein (oxygenated)

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35
Q

What are the mechanical components of the heart?

A

The muscles of the heart and the valves

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36
Q

Name the layers of the heart (from the outside in) as well as their basic function.

A 
Fibrous pericardium (tough outer layer, holds heart in position)
Parietal pericardium (prevents friction)

PERICARDIUM ALSO STOPS HEART FROM BULGING TOO MUCH ON FILLING SO IT CAN BUILD A PRESSURE

Pericardial cavity (has a little bit of fluid to lubricate and prevent friction)

Visceral pericardium (prevents friction)
myocardium (contractions)
endocardium (smooth, prevents clots in heart)
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37
Q

Are you papillary muscles (connected to chordae tendinae) relaxed or contracted when the AV valves are open?

A

They are relaxed

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38
Q

So when the papillary muscles are contracted, the AV valves are closed, how can you make sense of this? (think about where the muscles are attached)

A

These muscles contracted along with the ventricular wall during systole, so it only makes sense that when the ventricles contract we want the AV valves closed so blood doesnt backflow.

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39
Q

What makes our semilunar valves open and shut?

A

Its all about the difference in pressure

When the pressure of the ventricles pushing on the valves exceeds the pressure on the other side of the valve (whether it be the systemic or the pulmonary circulation), it will open up, and it will closed based on the same priciple (pressure on other side of valve exceeds pressure exerted by ventricle)

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40
Q

Can the heart muscle generate its own action potential, is it the only muscle that can?

A

YES YES YES

YES YES YES

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41
Q

Describe the pathway of the impulses through the conduction system of the heart.

A

SA node
…impulse travels thorugh the intranodal pathways and bachmann bundle to the…
AV node

Bundle of his

Bundle branches (left and right)

Purkinje fibers (allow for rapid conduction of all ventricular muscles for almost synchronous contraction)

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42
Q

What is the primary pacemaker of the heart?

A

The SA node

It sets the rate (60-100)

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43
Q

If the SA node goes out and stops generating impulses, the AV node will take over (secondary pacemaker), what rate does the AV node set the heart to?

A

45-50 BPM

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44
Q

Describe a bundle branch block.

A

a delay in the bundle of his that slows transmission of impulse

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45
Q

Resting cardiac muscle cells have some of these channels open, what are they?

A

Calcium channels

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46
Q

The open calcium channels of resting cardiac muscle cells allow for what?

A

Ca2+ to leak into the cells making them more positive

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47
Q

What happens when enough CA2+ leaks into the cell for it to reach its threshold?

A

The NA+ channels will open and the cell will begin to fire

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48
Q

What Ion has a double + charge?

A

Calcium

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49
Q

What are the five phases of the action potential?

A

Phase 0 - As calcium slowly comes into the cells through the open channels it will hit threshold, causing the sodium channels to open and RAPID DEPOLARIZATION will occur

Phase 1 - There is an EARLY REPOLARIZATION where the sodium channels close

Phase 2 - Plateau,the slower calcium channels open allowing for calcium to exit the cell

Phase 3 - RAPID REPOLARIZATION, this is where calcium and sodium stops coming in potassium is pushed out

Phase 4 - RESTING MEMBRANE POTENITAL, the NA/K pumps transport NA out and K back in

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50
Q

Describe the absolute refractory period.

A

This is between phases 0-2 and early phase 3

Basically it is saying the in that time frame there cant be another stimulation (contraction) no matter how big of a stimulus, it has to go down below the threshold potential

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51
Q

Describe relative refractory period.

A

An action potential may be generated between the threshold potential and the Resting membrane potential

WILL TAKE MORE ENERGY THOUGH

52
Q

Why would potassium imbalances effect our resting membrane potential?

A

If you have too much to bring back into the cell then the RMP will be affected in that the cell will reach threshold potential much easier (the cell will be made too positive)

and its the opposite for low potassium (the cell will become too negative and take more energy to become stimulated)

53
Q

What are the two types of action potential generation to cause cell firing (in relation to the heart)?

A

Slow response (Ca/Na channels):

  1. SA node
  2. AV node
Fast response (Na channels)
1. myocardial cells (atria, ventricles, purkinje fibers)

THE POINT OF THIS IS TO SHOW THAT OUR NODES (PREFERRABLY SA NODE) SET THE RATE OF THE HEART. SO IF THOSE GO OUT AND OUR FAST RESPONSE KICKS IN THERE WILL BE CHAOTIC CELL FIRING.

So with A-fib, the cells of the atria are generating the impulses and they are so quick and may not travel far enough that the ventricles only contract every so often.

THE CELLS OF THE FAST RESPONSE DO NOT NORMALLY GENERATE ACTION POTENTIALS, AND IT MAY CAUSE PROBLEMS IF THEY DO

54
Q

What does the P wave signify?

A

Atrial depolarization (contraction)

THE SA NODE GENERATED AN IMPULSE THAT TRAVELS TO THE AV NODE

55
Q

Why is there a delay between the P wave and Q wave of the QRS complex?

A

This allows time for the impulse to travel from the AV node out to the purkinje fibers (allows message to be sent to the whole ventricle at once)

56
Q

What does the QRS complex signify?

A

Venticular depolarization (contraction)

57
Q

What does the T wave signify?

A

Ventricular repolarization

58
Q

Why isnt there a wave to signify atrial repolarization?

A

It is hidden in the QRS complex

59
Q

What is the PR interval and what could an increase in the interval signify?

A

This is the time from the beginning of the P wave to the beginning of the Q wave

If there is a delay there could be a block in the conduction system

60
Q

What if the QRS complex is lengthened in time?

A

there could be a bundle branch block (usually shows rabbit ears on an ECG in the QRS complex)

61
Q

How can the T wave help show us if there is an MI?

A

There could be elevated T waves (after the QRS complex we dont go back to baseline before T wave)

62
Q

Describe systole. (What are the valves doing)

A

The SL valves are open and the AV valves are closed (ejection period)

Both valves are closed during isovolumetric contraction

63
Q

Describe diastole. (What are the valves doing)

A

SL valves close

AV valves open (isovolumetric relaxation)

ventricular filling

64
Q

When does rapid filling occur?

A

In the first 1/3 of diastole

65
Q

Over the first 1/4 of the ejection period, how much of the blood is ejected from the ventricle?

A

over 60% (there is a huge pressure difference in that beginning stage)

66
Q

Describe isovolumetric contraction.

A

This is when all of the valves are closed and the ventricles start to contract to build up intraventricular pressure

67
Q

Describe ventricular ejection.

A

This happens after the pressure builds after isovolumetric contaction

The SL valves open and the blood is ejected

68
Q

Describe isovolumetric relaxation.

A

The SL valves close and the AV close, allowing the atrias to fill up (also the ventricles are relaxing, lowering pressure atria has to push through)

Once the atrias are full the AV valves open causes passive ventricular filling to occur

69
Q

What happens after isovolumetric relaxation and passive ventricular filling?

A

Atrial contraction (maximizes ventricular filling) (this can also be called atrial systole) which is active filling

After this all valves close once more for isovolumetric contraction and the cycle starts over

70
Q

Describe preload.

A

This is the ventricular stretching that occurs at the end of diastole because of the blood volume (can dictate how good of a contraction we have)

THINK FRANK STARLINGS LAW

71
Q

Describe LVEDP (left ventricular end diastolin pressure).

A

This is the volume in the left ventricle that allows the heart to generate pressure

72
Q

How much of the volume in the ventricles does passive ventricular filling account for?

A

70%

So that means that the atrial contraction accounts for 10-30%

73
Q

So if passive filling accounts for most of the ventricular blood volume, how does that relate to A-fib?

A

With A-fib they arent getting a very good atrial contraction, but since most of the blood enters the ventricles through passive filling, there is USUALLY enough volume to put out

74
Q

What is one thing that can affect preload?

A

venous return (dehydrated, bleeding out for example)

75
Q

Describe afterload.

A

This is the resistance (blood pressure) the the ventricles must overcome to eject volume

RV - must overcome pulmonary vascular resistance

LV - must overcome systemic vascular resistance

76
Q

What is stroke volume?

A

The volume of blood ejected with each contraction of the heart

77
Q

What is cardiac output and how do you calculate it?

A

Cardiac output is the liters of blood ejected each minute

CO= SV x HR

78
Q

What is the main thing we are worried about with CO (cardiac output)?

A

Organ perfusion

79
Q

What happens to the AV valves the ventricles contract?

A

Blood is pushed against the AV valves causing them to shut (this is what we hear in S1 or the lub)

80
Q

What happens to the semilunar valves when the ventricles relax?

A

The semilunar valves are slammed shut by the BP of either the pulmonary or systemic circuit (depends on the SL valve)

This is what causes the S2 sound or the dub

81
Q

Does our left ventricle have to overcome our systolic or diastolic BP the eject blood out?

A

DIASTOLIC

82
Q

How would you calculate stroke volume if you didnt have the cardiac output or the HR?

A

End diastolic volume - end systolic volume

83
Q

How would you calculate the ejection fraction? (its a percentage)

A

stroke volume/end diastolic volume (usually want it at least 60%)

84
Q

How do you calculate cardiac output?

A

CO = SV x HR

85
Q

How do we calculate preload?

A

Preload = volume work of the heart = end diastolic volume

86
Q

How is preload related to starlings law?

How does preload and starlings law affect stroke volume?

What affects preload?

A

Preload is that pressure against the ventrical walls that stretches the heart muscle, so it relates to starlings law in that it can create the optimal tension for the best contraction of the heart.

The above statement shows that it can affect stroke volume because if the heart is under-stretched or over-stretched the stroke volume will be decreased.

The thing that affects preload is our venous return.

87
Q

What is afterload again??

A

This is the pressure that the ventricles have to overcome to push blood to the aorta or pulmonary artery.

So people with HTN have a higher afterload.

88
Q

What does inotropic affect?

A

cardiac contractility (independent of starlings law)

89
Q

What does chronotropic affect?

A

TIMING / heart rate

90
Q

What are three things that determine preload?

A

Myocardial compliance (how well the heart can stretch)

Blood volume (is there enough blood volume to create a good preload)

venous return (is the blood making it back to the heart)

91
Q

What does starlings law state?

A

The amount of stretching in the LV at the end of diastole (preload) is directly related to the force of the next contraction.

92
Q

Just to bury this concept into the ground some more, what does the greater the volume create in relation to starlings law?

A

A greater stretch, which makes a stronger contraction to a certain limit

93
Q

What can overstretching of the heart do?

A

decrease the strength of our contractions.

94
Q

How does heart failure relate to all of this talk with starlings law?

A

If we keep overstretching the heart, its going to lose contractile force and have to work even harder to push out its blood volume.

95
Q

What is afterload again?

A

The opposing pressure that resist ventricular ejection.

96
Q

So with afterload the cardiac systole must overcome what pressure?

A

The pulmonary or systemic diastolic pressure

97
Q

What is PVR (pulmonary vascular resistance)?

A

This is the afterload for the right ventricle

98
Q

What is SVR (systemic vascular resistance)?

A

The afterload for the left ventricle.

99
Q

What can a high afterload eventually lead to?

A

Ventricular hypertrophy => heart failure

100
Q

What is the range we like our cardiac output to be at?

A

4-8 liter per minute

101
Q

What determines CO?

What can affect SV?

A

heart rate

stroke volume

  • preload
  • afterload
  • contractility
102
Q

What does an increased workload of the heart demand?

A

An increase in oxygen demand for the heart muscle.

103
Q

In relation to preload and afterload, would we prefer an increase or decrease?

A

With preload we would prefer an increase (to a certain point)

With afterload we would prefer a decrease

104
Q

What does an increase in heart rate do to myocardial oxygen demands?

A

increases it

105
Q

What does a decreased heart rate do to our myocardial perfusion?

A

decreases it => ischemia

106
Q

What does a very rapid heart rate do in relation to ventricular filling?

A

It decreases ventricular filling time, which will decrease our preload, which will decrease our cardiac output.

107
Q

What does contractility do to stroke volume?

A

If its decreased it decreases SV => decreased CO

If its increased it increases SV => increased CO

108
Q

What are some things that can affect heart rate?

A

ANS

temp

ions

epi and norepi (adrenal medulla)

109
Q

What are some things that effect end-systolic volume (and in turn the SV)?

A

preload and afterload => affects force of contraction => ventricular emptying => affects end-systolic volume => affects stroke volume

110
Q

What are some things that affect end-diastolic volume (and in turn the stroke volume)?

A

Venous return and the length of diastole => affects ventricular filling => affects end-diastolic volume => affects stroke volume

111
Q

What can affect the length of diastole?

A

HR

112
Q

What are the pressure differences of the arterial and the venous sides of the systemic circulation?

A

Arterial = higher pressure

venous = lower pressure

113
Q

So if the venous side of the systemic circulation if under lower pressure what does that mean about the right side of the heart?

A

It has to be under lower pressure

114
Q

Are veins more compliant?

A

YES, they dont have to deal with higher pressure so they can stretch with increases of volume (if they stretch too much the hydrostatic pressure will increase too much and may cause edema)

115
Q

How do we create a pressure gradient on the venous side?

A

They have a one way valve system as well as outside muscle pumps

116
Q

What happens if a one way valve of our venous system goes bad?

A

The distance might be too great to build up enough pressure to move the blood properly

117
Q

What can damage the valves?

A

hemorrhoids or dilations of venous system (people that are inactive at greater risk)

118
Q

What does immobility do to venous return?

A

It can cause our blood to stagnate in our veins and we cant build pressure (risk for clots)

ROM HELPS

119
Q

What are some things that control our blood flow (mainly arterial)?

A

autoregulation local control - individual vessels regulate their own arterial resistance (lungs: if one part is damaged those arteries will constrict and another part in healthy area will dilate to redirect for better gas exchange…also with local inflammation (dilation)… muscles during exercise (dilation)… BASED ON OXYGEN NEEDS AND OTHER METABOLIC FACTORS

endothelial control (local) - endothelins and angiotensin II: vasoconstrict and NO (nitric oxide): vasodilator… HEMOSTASIS…

humoral control (systemic) - norepi (vasoconstrict) and epi (constrict or slighty dilate): released by SNS… angiotensin II: vasoconstrict… histamine: vasodilate… serotonin (released by platelets): vasoconstrict… bradykinin: arterial dilation, capillary permeability, venous constriction (more likely to cause edema that just histamine)…. Prostaglandins: constrict or dilate (depends on type)

collateral circulation - more than one artery feeding the same area (mostly in brain) SOMETIMES IN CASES OF CHRONIC HYPOXIC STATE THE AREA WILL GENERATE MORE SMALLER VESSELS (ANGIOGENESIS)

120
Q

describe the autonomic control of cardiac funtion.

A

modifies conduction and contractility

Parasympathetic: vagal stimulation affects HR (decreases)

Sympathetic: Brain stem: increases HR AND CONTRACTILITY (also holds tone in vessels muscle… also other muscles…)

121
Q

What is the CNS ischemic response?

A

This happens when blood flow to the brain is compromised (pulmonary issue, ischemia, ICP WHICH IS RELATED TO CUSHINGS REFLEX)

in the cranial cavity and vessels may collapse, there is a massive vasoconstriction (leads to very high BP, like 220/120 high) to attempt to keep vessels open

122
Q

Describe the cushings reflex.

A

This is seen with high ICP (brain bleed for example)

this is when the ICP gets so high that it starts to compress the blood vessels in brain and lead to ischemia whioch CAUSES THE CNS ISCHEMIC RESPONSE TO KICK IN

123
Q

How would you calculate BP with or without a CO value?

A

BP = CO x peripheral resistance (usually change in diameter)

BP = HR x SV x peripheral resistance

THINK ABOUT WHAT CHANGES IN PR WILL DO TO BP

124
Q

What happens to our skin temp and color with vasoconstriction and vasodilation?

A

constriction - cool and pale

dilation - warm and red

125
Q

What do we assess when we are checking a pulse?

A

rate and quality (1+ 2+ 3+, thready, normal, bounding)

126
Q

What do we assess with respirations?

A

Rate and quality (shallow, normal, deep)

Pathophysiology (13 decks)

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