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Pathophysiology > Cardio Diseases > Flashcards

Cardio Diseases Flashcards

1
Q

What does the functional model of the cardio system show?

A

the heart and blood vessels as a single closed loop

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2
Q

The elastic systemic arteries are a _______ reservoir that maintains blood flow during ventricular relaxation

A

pressure

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3
Q

The arterioles have “adjustable screws” that alter their diameter. This is the site of _________ ________

A

variable resistance

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4
Q

Exchange between the blood and cells takes place only at the….

A

capillaries

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5
Q

Systemic veins serve as an _______ ________ reservoir

A

expandable volume

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6
Q

Each side of the heart functions as what?

A

an independent pump

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7
Q

Define hemodynamics

A

principles of physics that regulate blood flow

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8
Q

Define flow rate

A

volume of blood moving per unit time

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9
Q

Velocity (V) = ?

hint: its an eq

A

V= flow rate (Q) / cross sectional area (A)

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10
Q

T/F:

We have the same flow rate through entire system

A

TRUE

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11
Q

Define velocity (in the context of blood vessels)

A

distance blood is flowing per unit time

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12
Q

The ________ the vessel, the faster the velocity of flow

A

narrower

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13
Q

What is cross sectional area represented by?

A

pi r^2

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14
Q

When talking about the area of blood vessels what does this mean?

A

cross sectional area of the vessel TYPE

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15
Q

Velocity of fluid varies ______ w/ cross sectional area. Velocity increases/faster in small area than big area

A

inversely

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16
Q

Blood is slower in capillaries than the aorta. Why?

A

bc capillaries are the exchange vessels

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17
Q

The flow rate (CO) is the same throughout the vessel and entire system. Why?

A

bc blood moves slower in larger area and faster in smaller area

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18
Q

Blood flow depends on what?

A

the pressure difference or pressure gradient between the vessels or 2 ends of a vessel

it also depends on resistance

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19
Q

Q= delta P / R

What does this equation mean?

A

blood flow is directly proportional to pressure gradient and blood flows from high to low pressure

blood flow inversely proportional to resistance

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20
Q

What does Q stand for?

A

flow or flow rate

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21
Q

What does delta P stand for?

A

difference in pressure, or pressure gradient

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22
Q

What does R stand for?

A

resistance

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23
Q

Blood flow _____ go down a pressure gradient, and will be ______ by resistance

A

must, inhibited

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24
Q

Fluid flow through a tube depends on what?

A

pressure gradient

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25
Q

What does TPR stand for?

A

total peripheral resistance

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26
Q

What does SVR stand for?

A

systemic vascular resistance

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27
Q

What are the 2 blood vessels that are bringing blood to the R atrium called?

A

SVC and IVC

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28
Q

Is pressure higher, lower or equal at the SVC and IVC than the R atrium?

A

the pressure is slightly higher than in the R atrium

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29
Q

What are the 2 blood circulations in the body?

A

systemic and pulmonary circulation

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30
Q

Which circulation has the greatest resistance in the body? What is this resistance called?

A

systemic circulation has the greatest resistance = TPR (total peripheral resistance)

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31
Q

Resistance to blood flow depends on 3 things. What are they?

A

1) the radius of vessel
2) vessel length
3) viscosity of blood

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32
Q

What does n stand for?

A

viscosity of blood

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33
Q

What does l stand for?

A

length of blood vessel

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34
Q

What does r^4 stand for?

A

radius of blood vessel to the 4th power

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35
Q

What is the Poiseuille eq?

A

R= 8Ln/ pi r^4

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36
Q

In the Poiseuille eq, resistance is _______ proportional to the viscosity of blood

A

directly

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37
Q

What blood cells are responsible for the blood viscosity? Why?

A

RBCs bc hematocrit is the percentage of RBCs within whole/all blood

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38
Q

What is the hematocrit average?

A

originally, we were told 40-45%

now, Roop tells us it is 45-48%

so 40-48%

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39
Q

Increase in RBCs = ________ in blood viscosity

A

increase

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40
Q

In the Poiseuille eq, resistance is ______ proportional to the length of blood vessel

A

directly

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41
Q

In the Poiseuille eq, resistance increases with what?

A

vessel length

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42
Q

Is adipose vascular or avascular?

A

VASCULAR

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43
Q

Increased fat results in what?

A

increased blood supply AND increased resistance

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44
Q

Obesity is related to what blood/heart problem?

A

hypertension

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45
Q

In the Poiseuille eq, resistance is ________ proportional to radius of blood vessels to the 4th power

A

inversely

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46
Q

As the radius of blood vessels becomes smaller, what happens to resistance?

A

it increases

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47
Q

T/F:

As the radius of a tube decreases, the resistance to flow also decreases

A

FALSE- resistance to flow increases

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48
Q

The smaller the radius, the _____ the resistance to the 4th power

hint: less or greater

A

greater

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49
Q

What are the smallest blood vessels?

A

Capillaries

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50
Q

Capillaries have low resistance. Why?

A

bc its offset by the number of capillaries (remember that were looking at the blood vessel TYPE)

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51
Q

What is atherosclerosis and how does it affect the blood?

A

fatty plaque will decrease the radius of blood vessels, which will increase resistance and increase turbulent flow

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52
Q

Vessels that carry well-oxygenated blood are _____; those with less well-oxygenated blood are _____

A

red, blue

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53
Q

Define distensibility

A

the ease with which a vessel dilates/stretches when filling pressure increases or pressure is applied

basically, ability to expand

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54
Q

veins are _____ compliant bc they can expand more

A

more

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55
Q

What are the blood reservoirs of the body?

A

veins

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56
Q

Veins distend more than arteries. So, the venous system has a higher what?

A

compliance of competence than arterial system

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57
Q

Veins are the blood reservoirs and contain the ________ volume

A

unstressed

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58
Q

Arteries have _______ volume because they have higher pressure (than veins)

A

stressed

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59
Q

Every time the L ventricle contracts, or sends blood out to what structure? What is this blood called?

A

aorta

this blood is called stroke volume (SV) per beat

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60
Q

What is stroke volume?

A

how much blood you are ejecting per heartbeat

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61
Q

What is cardiac output?

A

blood ejecting per unit time

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62
Q

What is systole and diastole in simplest terms? What is it in this- 110/60?

A

systole = contraction
diastole = relaxation

110/60
S/D

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63
Q

As blood is being ejected out, the aorta expands to hold ____ stroke volume

A

1

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64
Q

As blood is being ejected out, the aorta expands to hold 1 SV. The aorta, however, cannot get all the blood to capillaries during systole. It gets all the blood over during diastole. What is this known as?

A

diastolic runoff

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65
Q

Large arteries _____ during systole for a full SV, but transmit it to the capillary beds during diastole, which is diastolic runoff

A

expand

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66
Q

The aorta has enough pressure to move blood during ____. Why?

A

diastole

bc blood has to move down a pressure gradient even if the heart is “relaxed”

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67
Q

What is the largest elastic artery?

A

aorta

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68
Q

The energy for flow in diastole is stored where?

A

elastic tissues of the arteries during systole

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69
Q

The energy for flow in diastole is stored in the elastic tissues of the arteries during systole. What does this result in/what is it called?

A

storage and runoff effect = windkessel

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70
Q

If a pt has atherosclerosis and fatty plaque in the aorta, how will the body compensate?

A

increased:
-hr
-force of contraction (to try to eject same volume of blood)

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71
Q

If a pt has atherosclerosis and fatty plaque in the aorta, but no medical intervention, what happens?

A

the heart workload will increase and hypertrophy

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72
Q

What happens to the cardio system, when a pt has arteriosclerosis?

A

-vessels become less compliant w/ old age
-arterial walls become stiff/thick
-happens when blood vessels lay down more collagen w/ age
-hypertension develops (high bp)

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73
Q

T/F:

Pressure is equal in cardiovascular system

A

FALSE- its unequal

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74
Q

Where is the highest pressure in the cardio system?

A

aorta

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75
Q

Where is the lowest pressure in the cardio system?

A

vena cava

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76
Q

Why does the aorta have the highest pressure in cardio system, and vena cava have the lowest pressure?

A

because it’s how blood moves systemically through body

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77
Q

Does systolic pressure or diastolic pressure have a higher pressure?

A

systolic pressure is higher

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78
Q

Diastolic pressure is lower pressure than systolic. Can it still move blood in relaxation phase? Why/why not?

A

yes, even though the heart is relaxing not contracting, it still has enough pressure to move blood through gradient

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79
Q

Blood moves from the:
-left ventricle
-arteries
-arterioles
-capillaries
-venules/veins
-right atrium

As you go down the list is pressure increasing or decreasing?

A

PRESSURE IS DECREASING

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80
Q

The closer you are to the heart, the pressure is ______

A

pulsatile

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81
Q

Pulsations in arteries coincide with what?

A

the beating of the heart

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82
Q

1 pulse = ____ cardiac cycle = _____ heart beat

A

1:1:1 ratio!

1 pulse, 1 cardiac cycle, 1 heart beat

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83
Q

What is the eq for pulse pressure?

A

pulse pressure (PP) = systolic pressure - diastolic pressure

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84
Q

What is the eq for mean arterial pressure?

A

mean arterial pressure (MAP)= diastolic pressure + 1/3 (pulse pressure)

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85
Q

Is pulse pressure related to stroke volume?

A

yes, bc pulse pressure is dependent on stroke volume (volume of blood ejected from the heart w/ each beat)

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86
Q

What is mean arterial pressure (MAP)?

A

measure of the force of blood moving through system

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87
Q

If pulse pressure is an indicator of stroke volume, then….

A

pathologic conditions that affect one will affect the other

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88
Q

What happens to SV and pulse pressure when a pt has a severe hemorrhage?

A

SV and PP decrease (has less blood moving through system)

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89
Q

What happens to the cardio system with congestive heart failure (CHF)? How does this affect SV and PP?

A

blood is not moving from heart/heart is not a good enough pump anymore

SV and pulse pressure decrease (decreased blood movement through system)

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90
Q

What happens to the cardio system with atherosclerosis patients?

A

-plaque on artery walls
-decreased diameter in vessels
-less compliant vessels
-decreased SV, pulse pressure, and blood circulation

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91
Q

What happens to the cardio system with arteriosclerosis?

A

-decreased diameter in vessels
-less compliant vessels
-decreased SV, PP, and blood circulation

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92
Q

Is pulmonary circulation a long or short circuit?

A

short circulation

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93
Q

Does pulmonary circulation have high or low pressure?

A

low pressure

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94
Q

CO of the R side of the heart must _____ the CO of L side of heart

A

equal

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95
Q

CO = VR on ______ person

A

healthy

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96
Q

The heart has 2 different types of cardiac muscle cells. What are they?

A

contractile cells and conducting cells

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97
Q

____ of heart cells are contractile fibers, and ____ are conducting fibers

A

99%, 1%

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98
Q

conducting fibers in the heart are the ones that can’t do what?

A

cannot contract anymore (can no longer generate pressure)

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99
Q

What do conducting fibers do?

A

generate spontaneous APs

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100
Q

Every other organ in the body depends on the NS, whereas the heart depends on….

A

itself for heart rate and APs

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101
Q

Does the autonomic NS still have a role with the heart even though it doesn’t fully control HR and APs of heart?

A

yes!!!

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102
Q

Autorhythmic cells do what?

A

generate APs and send APs to contractile fibers which is what causes heart to beat

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103
Q

Where are autorhythmic cells found?

A

-SA node
-AV node
-bundle of His
-bundle branches
-internodal pathway
-Purkinje fibers

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104
Q

What are the 5 textbook steps to electrical conduction pathway of heart?

A

1) SA node depolarizes

2) electrical activity goes rapidly to AV node via internodal pathways

3) depolarization spreads more slowly across atria and conduction slows through AV node

4) depolarization moves rapidly through ventricular conducting system to the apex of the heart

5) depolarization wave spreads from the apex

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105
Q

What does “SA” in SA node stand for?

A

sinoatrial node

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106
Q

Where is the SA node located within the heart?

A

lays within R atrium and at the entrance of the SVC

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107
Q

What is the pacemaker of the heart?

A

SA node

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108
Q

What are the functions of the SA node?

A

set the pace of the heart

generate APs that will spread between both atria (atrial internodal pathway)

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109
Q

What is the SA node linked to?

A

linked to both atria by gap junctions

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110
Q

The electrical signal moves through both ______ and gets to the AV node

A

atria

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111
Q

What does “AV” stand for in AV node?

A

atrioventricular

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112
Q

Where is the AV node located?

A

R atrium of heart

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113
Q

What happens at the AV node?

A

conduction velocity/signal slow down here

this is bc of extra layer of fibrotic CT and plate of cartilage

it acts an electrical insulator

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114
Q

Why does the conduction velocity/signal slow down at the AV node?

A

because it has an extra layer of fibrotic CT and plate of cartilage

acts as an electrical insulator

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115
Q

electrical activity ______ mechanical activity

A

precedes

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116
Q

What mechanical activity is the AV node waiting for the heart to catch up with?

A

waiting for atria to contract and fill w// blood before electrical pathway continues

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117
Q

If the heart doesn’t slow down at the AV node, what happens?

A

ventricular filling decreases, which also decreases SV and CO

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118
Q

From the AV node, the ventricles must be stimulated to contract from _____ to the superior aspect of the ventricles

A

apex

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119
Q

The heart contracts from the ______ to _____. Why?

A

apex to base

this is bc this is how blood is ejected out of heart

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120
Q

Once the signal leaves the AV node, it goes really fast. Where is its next “stop”?

A

goes to bundle of His (superior part of the AV septum)

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121
Q

Bundle of His splits into R+L ________ _______ and runs along the AV septum and Purkinje fibers

A

bundle branches

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122
Q

Purkinje fibers are electrically connected to what and by what? Additionally, what will this allow?

A

connected to ventricular cardiac muscles by gap junctions

will allow contractile fibers to take over at this point

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123
Q

What are the 5 phases of cardiac muscle APs?

A

0= Na+ channels open (depolarization)
1= Na+ channels close
2= Ca+2 channels open, fast K+ channels close
3= Ca+2 channels close, slow K+ channels open (repolarization)
4= (stable) resting potential

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124
Q

Cardiac muscles have ____ phases to a fast AP

A

5

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125
Q

All cardiac muscle cells on the sarcolemma have what?

A

voltage-gated ion channels

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126
Q

All cardiac muscle cells on their sarcolemma have voltage-gated ion channels. Once they get their signal from the 1% of conducting fibers, what happens?

A

sodium channels open!

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127
Q

Sodium channels are ______ channels going from -90 to 20 mV

A

FAST

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128
Q

Get signal, open, and sodium rushes in. This is called…..

A

depolarization, or stage 0

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129
Q

Phase 0 of AP, what happens?

A

upstroke, or rapid depolarization caused by opening of sodium channels

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130
Q

While sodium channels were opening really fast during AP, what other channels were also opening? What is the difference?

A

K+ channels were also opening, but K+ channels are slow channels (unlike sodium which is fast)

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131
Q

Phase 1 of AP, what happens?

A

Na+ inactivation and gates close, and there is a fast efflux of K+

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132
Q

Phase 2 of AP, what happens?

A

a plateau, it’s a long phase of stable, depolarized membrane potential

plateau is maintained by a Ca+2 influx through L-type channels

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133
Q

When K+ ions are equal to Ca+2 (K+ out, Ca+2 in), or inward current = outward current, then there is a…..

A

flat plateau

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134
Q

What are the 2 examples of calcium channel blocker medications we learned in class?

A

1) nifedipine (procardia)
2) diltiazem (cardizem)

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135
Q

What are calcium channel blocker meds used for?

A

to treat heart failure and hypertension

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136
Q

What ion is needed for muscle contraction to happen?

A

calcium

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137
Q

Phase 2 of APs, has 10 steps. What are they?

She didn’t go over this in depth but there is chart in pp, so just read over it a few times just in case

A

1) action potential enters from adjacent cell
2) voltage gated calcium channels open, calcium enters cell
3) calcium induced calcium release through ryanodine receptor channels (RyR)
4) local release causes calcium spark
5) summed calcium sparks create a calcium signal
6) calcium binds to troponin to initiate contraction
7) relaxation occurs when calcium unbinds from troponin
8) calcium is pumped back into the sarcoplasmic reticulum (SR) for storage
9) calcium is exchanged with sodium by the NCX antiporter
10) sodium gradient is maintained by the sodium/potassium ATPase

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138
Q

Calcium moves in through L-type calcium channels and causes more calcium to be released from sarcoplasmic reticulum (SR). This is known as…..

A

CICR (calcium induced calcium release)

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139
Q

Influx of calcium causes release of intracellular calcium for ________ ________ _________

A

excitation-contraction coupling

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140
Q

What are antihypertensive drugs used for? How do they work?

A

decreases contraction, and blocks L-type channels

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141
Q

Phase 3 of AP, what happens?

A

repolarization

a slow K+ channel opens as Ca+2 channels begin to close

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142
Q

Phase 4 of AP, what happens?

A

resting membrane potential or also known as electrical diastole

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143
Q

T/F:

Phase 4 of AP is a baseline to be able to repeat process over and over

A

true

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144
Q

What are chronotropic effects?

A

effects of ANS on HR

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145
Q

sympathetic NS ________ HR

A

increases

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146
Q

parasympathetic NS _________ HR

A

decreases

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147
Q

CO is dependent on what?

A

HR

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148
Q

CO= HR x SV

What does this mean in terms of chronotropic effects?

A

SA node (pacemaker of heart) is heavily regulated by autonomic NS

can change the rate if it needs to in order to maintain CO

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149
Q

Sympathetic NS regulates what cells?

A

autorhythmic cells on SA node

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150
Q

Where do autorhythmic cells of the sympathetic NS bind to?

A

B1 receptors

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151
Q

B1 receptors are what type of receptor?

A

GPCRs

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152
Q

Sympathetic NS regulates autorhythmic cells on SA node and these cells bind to B1 receptors. What does this cause?

A

an increase in adenylyl cyclase and in cAMP

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153
Q

What is an example of a second messenger?

A

cAMP

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154
Q

Sympathetic NS regulates autorhythmic cells on SA node and these cells bind to B1 receptors. This causes an increase in adenylyl cyclase and cAMP. What happens now?

A

increase in sodium and calcium

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155
Q

Sympathetic NS regulates autorhythmic cells on SA node and these cells bind to B1 receptors. This causes an increase in adenylyl cyclase and cAMP. This causes an increase in sodium and calcium. What happens as a result?

A

increased rate of depolarization and increased heart rate

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156
Q

Sympathetic neurons release ______ on B1 receptors of the nodal cells. Receptors are coupled to ______ _______ by a G protein.

A

NE

adenylyl cyclase

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157
Q

Parasympathetic NS releases what? What will this react with?

A

releases Ach

this will react to muscarinic receptors

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158
Q

Parasympathetic NS releases Ach which will react to muscarinic receptors. What does this cause?

A

decrease in adenylyl cyclase and cAMP

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159
Q

Parasympathetic NS releases Ach which will react to muscarinic receptors. This causes a decrease in adenylyl cyclase and cAMP. What happens next?

A

decrease in calcium and sodium influx and INCREASE in potassium EFFLUX

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160
Q

Parasympathetic NS releases Ach which will react to muscarinic receptors. This causes a decrease in adenylyl cyclase and cAMP. This allows calcium and sodium influx to decrease, and potassium efflux ro increase. What happens as a result?

A

decrease in calcium and sodium influx= decreased rate of depolarization and decreased HR

increase in potassium efflux= cell hyperpolarizes and HR decreases even more

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161
Q

Parasympathetic neurons release ____ onto nodal cells. This binds to muscarinic type 2 receptors which are also ______, but they inhibit adenylyl cyclase activity

A

ACh, GPCRs

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162
Q

Parasympathetic neurons release Ach onto nodal cells. This binds to muscarinic type 2 receptors which are also GPCRs, but they inhibit adenylyl cyclase activity. But, this G protein also increases the conductance of a _____ channel known as the _____ channel.

A

K+

K+/Ach channel

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163
Q

Parasympathetic neurons release Ach onto nodal cells. This binds to muscarinic type 2 receptors which are also GPCRs, but they inhibit adenylyl cyclase activity. But, this G protein also increases the conductance of a K+ channel known as the K+/Ach channel. The K= efflux results in what?

A

hyperpolarization

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164
Q

Chronotropic effects are of the ________ NS

A

autonomic

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165
Q

Dromotropic effects of the autonomic NS includes…..

A

conduction/velocity of the AV node

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166
Q

If contractions are sped up through AV node, it means what?

A

decrease in ventricular filling

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167
Q

Sympathetic NS has a _________ dromotropic effect

A

positive

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168
Q

Sympathetic NS has a positive dromotropic effect. What does this mean?

A

increase conduction velocity of the AV node

increasing APs from the atria to ventricles by increased inward calcium current

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169
Q

Parasympathetic NS has a _________ dromotropic effect

A

negative

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170
Q

Parasympathetic NS has a negative dromotropic effect. What does this mean?

A

decrease conduction velocity of AV node

decreasing APs = heart block

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171
Q

The only connection between atria and ventricles is the……

A

AV node

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172
Q

What are the 2 types of heart blocks?

A

mild= few APs coming through
severe= minimal/none APs coming through, pt will need pacemaker

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173
Q

Contractility is also regulated by autonomic NS. This is known as….

A

inotropism

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174
Q

What does a positive inotropic effect mean?

A

increased contractility

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175
Q

What does a negative inotropic effect mean?

A

decreased contractility

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176
Q

What ion is in charge of contractility (aka also inotropism)?

A

calcium

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177
Q

Beta- blockers block what receptors on heart? What does this do?

A

B1 receptors

this decreases rate and force of contraction

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178
Q

Beta-blockers like propranolol block _____ and ______

A

Epi and NE

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179
Q

What are 2 examples of cardiac glycosides?

A

digoxin and ouabain

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180
Q

Digoxin, a cardiac glycoside, is most often used when?

A

in extreme cases of heart failure

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181
Q

What is the purpose of cardiac glycosides? What is it used for?

A

used as positive inotropic agents

inhibits Na+/K+ ATPase (which increases calcium + contractility)

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182
Q

_______ disease is major problem in North America

A

heart

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183
Q

List some preventative measures of heart disease

A

1) diet (decrease cholesterol and salty diets because they cause hypertension)
2) dont smoke (nicotine is a vasoconstrictor and also causes platelet adhesion, which causes clots)
3) don’t drink alcohol
4) control weight
5) exercise (keeps heart healthy)
6) medications

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184
Q

What are some medications for heart disease?

A

1) nitroglycerin
2) cholesterol lowering drugs “statins”
3) Beta-blockers
4) anticoagulants or blood thinners
5) calcium channel blockers
6) diuretics
7) cardiac glycoside
8) ACE inhibitors

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185
Q

Nitroglycerin is used for heart disease. Why?

A

-increases vasodilation
-increases oxygen supply to organs

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186
Q

What is an example of a cholesterol lowering drug “statin”?

A

simvastatin (zocat)

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187
Q

What is the purpose of cholesterol lowering drugs “statins”?

A

the liver makes good cholesterol, we don’t need anymore “bad cholesterol” from our diets

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188
Q

What is an example for Beta- blockers besides propranolol?

A

lopressor (metoprolol)

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189
Q

Beta blockers, such as propranolol or metoprolol, do what?

A

decreases HR and contractility

block the B1 adrenergic receptors of heart

190
Q

What are 2 examples of anticoagulants or blood thinners?

A

low dose aspirin or warfarin (coumadin)

191
Q

What are calcium channel blockers usually used for?

A

hypertension

192
Q

What do calcium channel blockers do?

A

decrease contractility

193
Q

What is an example of a calcium channel blocker?

A

cardizem (diltiazem)

194
Q

What is diuresis?

A

production of increased/excess urine

195
Q

What are diuretics used for?

A

kidneys will excrete more sodium (and water always follows)

196
Q

What is the most common drug prescribed in US for hypertension?

A

lasix (furosemide)

it’s a diuretic

197
Q

What is a cardiac glycoside that is “old” and only used in extreme cases?

A

lanoxin (digoxin)

198
Q

What does ACE stand for?

A

angiotensin-converting enzyme

199
Q

What are ACE inhibitors commonly used for?

A

hypertension

200
Q

ACE inhibitors convert _____ to ____

A

Ang I to Ang II

201
Q

What is the most potent vasoconstrictor in our body?

A

Ang II

202
Q

ACE inhibitors decrease….

A

vasoconstriction and hypertension

203
Q

What is an example of an ACE inhibitor?

A

captopril

204
Q

What does CAD stand for?

A

coronary artery disease

205
Q

What does CAD include?

A

angina pectoris and MI

206
Q

Describe pain in CAD

A

pain is dull and can radiate to arm, neck, or jaw for both angina and MI

207
Q

T/F:

For patients with CAD, pain will get worse upon breathing

A

FALSE

breathing does not affect patients with CAD

208
Q

What are the 3 types of angina?

A

1) stable angina
2) unstable angina
3) prinzmetal angina

209
Q

What is stable angina?

A

patient will be able to do activity, but will progressively develop pain throughout exertion

pain will go away upon rest

210
Q

What is unstable angina?

A

pain is random and can happen at any point with or w/o exertion

211
Q

What is prinzmetal angina?

A

pain happens primarily in women in their 30s at night/ rest

pain is caused by vasospasms

THIS DOES NOT HAPPEN DURING SLEEP

212
Q

What is MI?

A

heart attack, damage to heart muscle that is irreversible

pain does NOT stop w/ rest

pain will be uninterrupted until heart tissue is dead

213
Q

What are the 4 causes of CAD?

A

1) atherosclerosis
2) spasm
3) emboli
4) congenital

214
Q

What is the most common cause of CAD?

A

atherosclerosis

215
Q

What are the risk factors for atherosclerosis?

A

1) hypertension
2) hypercholesterolemia
3) DM
4) smoking
5) genetics

216
Q

coronary artery vasospasm (one of causes of CAD) can occur in which population?

A

any population, but most prevalent in Japanese

217
Q

Vasoconstriction appears to be mediated by what?
Hint: 4 things

A

1) histamine
2) serotonin
3) catecholamines
4) endothelium-derived factors

218
Q

Because spasm can occur at any time, the chest pain is often not _______ related

A

exertion

219
Q

What is the rarest cause of CAD?

A

emboli

220
Q

When can an embolism occur (in regards to CAD)?

A

from vegetations in patients with endocarditis

221
Q

Congenital coronary artery abnormalities are present in 1-2% of the population. However, only a small fraction of these abnormalities cause ________ ________

A

symptomatic ischemia

222
Q

What is the leading cause of death in men/women in the US?

A

CAD

223
Q

T/F:

More men have CAD, but women tend to have more complications

A

TRUE

224
Q

What is a general term for changes in small arteries/arterioles that occur with age?

A

arteriosclerosis

225
Q

Atherosclerosis occurs where?

A

in medium/large arteries

226
Q

What is the good cholesterol?

A

HDL

227
Q

What is the bad cholesterol?

A

LDL

228
Q

Lipids move through circulation bound to ______

A

proteins

229
Q

HDL transports cholesterol from cells to _______, and liver will convert it and excrete it as a part of ________

A

liver, bile

230
Q

LDL transports _________ to cells

A

cholesterol

231
Q

LDL damages _________ of blood vessel walls, especially at areas of branching

A

endothelium

232
Q

With atherosclerosis, the body reacts with lots of inflammation. What happens here?

A

will bring in macrophages, complement proteins, and C reactive proteins

macrophages have scavenger receptors and will recognize LDL

233
Q

Injury to vessel and changes like oxidation of LDLs will result in what?

A

inflammation, which will bring in macrophages, complement, and c-reactive protein

234
Q

macrophages phagocytize LDLS and form ______ cells with fatty streaks

A

foam

235
Q

After vascular injury, __________ bind to the endothelium, then cross it to the subendothelial space, and become activated tissue _________.

A

monocytes, macrophages

236
Q

After vascular injury, monocytes bind to the endothelium, then cross it to the subendothelial space, and become activated tissue marchpages. The macrophages take up oxidized low-density lipoproteins (______), becoming foam cells.

A

LDLs

237
Q

After vascular injury, monocytes bind to the endothelium, then cross it to the subendothelial space, and become activated tissue marchpages. The macrophages take up oxidized low-density lipoproteins (LDLs), becoming foam cells. T cells release _______, which also activate ________.

A

cytokines, macrophages

238
Q

After vascular injury, monocytes bind to the endothelium, then cross over to the subendothelial space, and become activated tissue macrophages. The macrophages take up oxidized low-density lipoproteins (LDLs), becoming foam cells. T cells release cytokines, which also activate macrophages. In addition, the ________ cause smooth muscle cells to proliferate.

A

cytokines

239
Q

Under the influence of _______ _______, the smooth muscle cells then move to the subendothelial space, where they produce collagen and take up LDL, adding to the population of foam cells

A

growth factors

240
Q

T cells produce cytokines to recruit more macrophages and stimulate smooth muscle cells in ______ ______to proliferate and phagocytize

A

tunica media

241
Q

T cells release cytokines which will _______ inflammatory response

A

increase

242
Q

Platelets see all of the fat tissue and stick to it, which develops an _______ (fatty plaque). This causes 3 things. What are they?

A

atheroma

1) creates turbulent flow
2) can cause embolism
3) can cause an aneurysm

all 3 of these is because of increased inflammation

243
Q

An atheroma partially blocking the coronary arteries would cause what?

A

angina pectoris (Ischemic heart disease)

244
Q

An atheroma with total occlusion of coronary arteries would cause what?

A

MI

245
Q

Partial occlusion to the carotid or cerebral arteries would cause what?

A

TIA

246
Q

Total occlusion to the carotid or cerebral arteries would cause what?

A

CVA

247
Q

Total occlusion to the peripheral arteries or aorta causes what?

A

aneurysm

248
Q

Atheroma to the legs, specifically, the iliac arteries would cause what?

A

PVD (gangrene and amputation)

249
Q

What is a multifactorial disease we discussed during cardio lecture?

A

atherosclerosis

250
Q

List some conditions that accelerate the progression of atherosclerosis

A

1) males (or females after menopause)
2) family hx of ischemic heart disease or stroke
3) primary/secondary hyperlipidemia
4) cigs smoking
5) hypertension
6) DM 1 and 2
7) Obesity (abdominal obesity)
8) nephrotic syndrome
9) hypothyroidism
10) high lipoprotein
11) elevated plasma homocysteine

251
Q

Angina is chest pain, and is due to what?

A

lack of oxygen because of lack of blood supply

252
Q

In normal circumstances, what is it called when the body can help regulate itself?

A

autoregulation

253
Q

T/F:

With arteriosclerosis and atherosclerosis, there is no autoregulation

A

TRUE

254
Q

Why is there no autoregulation with atherosclerosis and arteriosclerosis?

A

bc they cannot vasodilate enough in order to get oxygen to meet the demands

255
Q

What is chest pain/angina usually due to?

A

sudden exertion and increased need for oxygen

256
Q

Where does chest pain/angina usually start?

A

center chest

257
Q

Where does chest pain/angina typically radiate to?

A

extend down to L arm, can extend to neck or jaw

258
Q

How long does angina last for?

A

few sec- min of dull pain

259
Q

What are the treatment options for angina?

A

-rest in upright position
-nitroglycerin pills

260
Q

What are nitroglycerin pills taken for and how? What happens once metabolized?

A

-taken for angina
-taken sublingually to reach bloodstream quickly
-once metabolized, it becomes nitric oxide (NO- which is a vasodilator)

261
Q

MI is caused by the blockage of one of the _______ arteries or its branches

A

coronary

262
Q

If a pt has a MI, what are they increased risk for?

A

-second MI
-stroke
-CHF

263
Q

MI results in ______, _______, and _______

A

ischemia, necrosis, and infarction

264
Q

What are the major branches from the L coronary artery?

A

L anterior descending artery (LAD) and circumflex artery

265
Q

What are the major branches from the R coronary artery?

A

marginal artery and posterior interventricular artery

266
Q

LAD used to be known as what?

A

widowmaker

bc if there was a blockage in it, the patient’s wife will become a widow

267
Q

What is the most commonly blocked coronary branch?

A

LAD (L anterior descending artery), also known as anterior interventricular artery because it runs in anterior interventricular groove

268
Q

Most infarctions are _______. What does this mean?

A

transdermal

will go through all layers of heart and all 3 layers of heart will be damaged

269
Q

Can cardiac tissue regenerate? What happens as a result?

A

no, scar tissue/ fibrotic CT will replace it and decrease function of heart

270
Q

With MI, oxygen will decrease. What happens as a result?

A

inflammation and myocardium releases enzymes

271
Q

With MI, if oxygen continues to decrease, what happens?

A

decreased conduction and contractility

272
Q

For MI pts, if blood flow can be restored by _______ circulation or by ______ within 20-30min, damage can be reversed

A

collateral, thrombolytics

273
Q

What are the S&S of MI?

A

-severe steady pain
-men: chest pain radiated to L arm, neck, and/or jaw
-women: acid reflux/indigestion
-low-grade fever
-pallor
-dyspnea
-diaphoresis (excess sweat)
-hypotension
-anxiety
-shock

274
Q

What are the diagnostic tests for MI?

A

-EKG
-blood tests for inflammatory enzymes of biomarkers released from necrotic tissue (LDH1 and CPK-MB, myosin and cardiac troponin T levels, leukocytosis, ESR, CPK, CRP)

275
Q

What are the 2 most common biomarkers to be elevated after MI? When can you see this in blood work?

A

LDH1 and CPK-MB

within 4-6 hrs after MI, and peak at 24 hrs

276
Q

What are 2 other biomarkers commonly seen in blood work besides LDH1 and CPK-MB? When will it be seen?

A

myosin and cardiac troponin T levels

elevated 2-6 hrs after MI, and peaks 12-26 hrs

277
Q

Which biomarker in blood work indicates MI damage?

A

troponin (higher levels= the worse the damage)

278
Q

Blood work is used as a diagnostic tool for MI to look for inflammation. What are some of the inflammatory signs or proteins to look out for?

A

-leukocytosis
-ESR
-CPK
-C-reactive protein

279
Q

For MI, 25% of patients will not make it and die from some kind of _____. This is because conducting fibers of the heart have been damaged

A

arrhythmia

280
Q

If function of L ventricle is compromised, then this is….

A

CHF

281
Q

What are the treatment options for MI?

A

-analgesic (morphine)
-oxygen
-if pt makes it to hospital within 20-30 min= streptokinase (a thrombolytic)
-defib
-cardiac cath
-bypass

282
Q

If pt survives MI, what is the protocol and following risks?

A

-cardiac rehab and diet/lifestyle changes
-high risk for second MI

283
Q

What is A?

A

P wave (atrial depolarization)

284
Q

What is B?

A

QRS complex (ventricular depolarization)

285
Q

What is C?

A

T wave (atrial depolarization)

286
Q

If a normal sinus rhythm has an atrial depolarization, ventricular depolarization, and ventricular repolarization visible, then where is atrial repolarization?

A

its hidden by QRS complex

287
Q

Are arrhythmias and dysrhythmias the same thing?

A

yes, they both mean irregular heart beat

288
Q

What are some causes for arrhythmias?

A

-electrolyte imbalances (especially potassium)
-stress
-MI
-inflammatory disease

289
Q

T/F:

Arrhythmias are not usually constant

A

true!

290
Q

What is a diagnostic tool for arrhythmias?

A

holter monitor, it monitors ECG for an extended period (according to Roop it’s about a week)

291
Q

If a pt has an arrhythmia, what is it impacting?

A

CO

292
Q

What is bradycardia?

A

heart beat less than 60 bpm

293
Q

What is this showing?

A

Rhythm strip showing bradycardia resulting from sinus node pause

the black arrows are showing atrial activity suddenly ceasing and after approx 3sec a junctional escape beat is observed (J)

294
Q

What is an ectopic pacemaker?

A

abnormal pacemaker

SA node is no longer acting as pacemaker and something else takes over

295
Q

Bradycardia can result from…..

A

AV block (heart block, will need pacemaker bc impulses are not getting to the ventricles)

296
Q

What does NSR stand for?

A

normal sinus rhythm

297
Q

What does PAT stand for and what is it?

A

paroxysmal (sudden) tachycardia

rhythm pattern remains the same, even with the rapid heart rate

298
Q

What is tachycardia?

A

heartbeat is more than 100 bpm

previously she said 90+ in pds

299
Q

What can tachycardia be caused from?

A

exercise, stress, etc.

300
Q

With tachycardia, the heart is ________ compensating for something in body. What is it most commonly compensating for?

A

ALWAYS

usually compensating for low blood volume

301
Q

With tachycardia, if QRS complex is narrow, what does this mean?

A

supraventricular tachycardia (ventricles are depolarizing and tachycardia is happening at AV node or above AV node)

302
Q

With tachycardia, if QRS complex is wide, what does this mean?

A

ventricular tachycardia (tachycardia is originating in the ventricles)

303
Q

What is sick sinus syndrome?

A

alternating bradycardia and tachycardia (pacemaker is def needed)

304
Q

What is the most common type of arrhythmia?

A

atrial conduction abnormalities

305
Q

What is an example of a type of atrial conduction abnormality?

A

PAC (premature (paroxysmal) atrial contraction)

306
Q

What happens in a PAC (premature (paroxysmal) atrial contraction)?

A

-there is an early P wave that differs from the normal P wave (an extra heartbeat)

307
Q

What is a fibrillation or palaption? What can it be due to?

A

heart racing

due to:
-stress
-caffeine
-smoking

308
Q

What is an atrial fibrillation (A-fib)?

A

-rapid P waves and irregular QRS complexes
-more than 300 bpm
-blood is regurgitating into atria/pooling

309
Q

A-fib pts are high risk for……

A

heart failure

310
Q

A-fib is a type of ________ _________

A

supraventricular tachycardia

311
Q

What is atrial flutter?

A

-160-300 bpm
-problem w/ ventricular filling, SV, and CO

312
Q

What is a bundle branch block?

A

-R or L bundle branch is blocked
-delayed conduction in 1 of the branches
-wide QRS on EKG
-doesn’t really have effect on pt bc its only 1 bundle branch affected

313
Q

What is ventricular fibrillation (V-fib)?

A

-complete disruption of a normal rhythm
-no CO

314
Q

Pts w/ V-fib are prone to getting what?

A

heart attack

315
Q

What is PVC (premature ventricular contraction)?

A

-most people will get this at least once in lifetime
-doesn’t happen often/doesn’t really have an affect
-ectopic beats in ventricles
-If it continues long term, then it can eventually convert to v-fib (problematic)

316
Q

Find the cause and treat the cause for any _______

A

arrhythmia

317
Q

What is asystole (cardiac arrest)?

A

-no conduction of impulses (heart stops beating)
-respiration stops
-brain is losing oxygen fast

318
Q

What should you do if you see a flatline on EKG?

A

call 911, AED, and CPR (in that order)

319
Q

T/F:

CHF is an end result of something else

A

true

320
Q

What is CHF?

A

heart cannot pump enough blood to maintain the system (heart is weak)

321
Q

____ million people in the US are affected with CHF

A

3

322
Q

There are ________ new cases of CHF every year in US

A

400,000

323
Q

What are the causes of CHF?

A

-heart problems (ex: past MI)
-valvular problems
-HTN
-lung disease
-decreased ventricular filling or contractility (not enough CO)

324
Q

T/F:

With CHF, regardless of cause, both sides of the heart will fail at same time

A

false!!!!!

one side of heart will fail before the other

325
Q

Compensations for the heart are also _________

A

complications!

326
Q

Describe how the body is compensating with CHF

Dont hate me, this is long, but hey its “all logical” ;)

A

-body recognizes it is not getting enough blood from the heart
-ANS will step in and kidneys will activate RAAS (renin-angiotensin-aldosterone system)
-CO is decreased and so is BP
-ANS will have sympathetic NS vasoconstrict to try to increase BP
-kidneys will reabsorb more sodium, and water will (of course) always follow
-this will result in increased blood volume and bp
-this will increase the “afterload” which is pressure L ventricle has to overcome in order to open valve so blood can move
-this will increase overall heart workload when its already not working properly

327
Q

If there is systolic dysfunction with CHF, what is affected?

A

CO

328
Q

If there is a diastolic dysfunction w/ CHF, what is affected?

A

there will be a ventricular filling problem

329
Q

What is the primary cause of CHF?

A

CAD (angina + MI)

330
Q

What are some causes of L ventricular failure?

A

-volume overload (ex: regurgitant valves such as mitral or aortic valve, anemia, or hyperthyroidism)

-pressure overload (ex: systemic HTN, aortic stenosis)

-loss of muscle (ex: MI from CAD or connective tissue disease such as systemic lupus erythematosus)

-loss of contractility (ex: poisons such as alcohol, cobalt, or doxorubicin, bacterial or viral infections, and genetic mutations)

-restricted filling (ex: mitral stenosis, pericardial disease)

331
Q

What are some pathophysiological changes associated with heart failure?

A

-hemodynamic changes (decreased output or filling)
-neurohormonal changes (RAAS)
-cellular changes (fibrosis, apoptosis, etc.)

332
Q

What is the pathway with L-sided congestive heart failure?

A

1) L ventricle weakens and cannot empty
2) decreased CO
3) decreased renal blood flow stimulates RAAS
4) backup of blood into pulmonary vein
5) high pressure in pulmonary capillaries leads to pulmonary congestion or edema

333
Q

L sided CHF can be a result of what?

A

MI in L ventricle or HTN

334
Q

What happens to heart/body with left-sided CHF?

A

increased:
-pressure
-afterload

overtime, L ventricle will hypertrophy

CO will decrease

blood will regurg and cause increased hydrostatic pressure, which will result in pulmonary congestion

fluid will go into alveoli, dilute surfactant, and alveoli will collapse = no gas exchange

335
Q

What is another name for CHF?

A

hypertensive heart disease

336
Q

What are the S&S of L-sided CHF?

A

-dyspnea
-orthopnea (decreased breathing laying down)
-paroxysmal nocturnal dyspnea
-cough or hemoptysis
-rale breath sounds
-subject to infections

337
Q

What is the pathway with R-sided congestive heart failure?

A

1) right ventricle weakens and cannot empty
2) decreased CO
3) decreased renal blood flow stimulates RAAS
4) backup of blood into systemic circulation (IVC + SVC)
5) increased venous pressure results in edema in legs and liver and abdominal organs
6) very high venous pressure causes distended neck vein and cerebral edema

338
Q

R- sided CHF can be the result of what?

A

something wrong with pulmonary semilunar valves (such as stenosis) or pulmonary disease that damages blood vessels

339
Q

What happens to heart/body with R-sided CHF?

A

increased resistance and workload on R ventricle will result in muscle hypertrophy

this also results in systemic congestion

340
Q

What is a common symptom seen with R-sided CHF when there is an issue with semilunar valve?

A

edema of legs, ankles, and feet

341
Q

If there is R sided CHF due to pulmonary disease, what is this called?

A

Cor pulmonale

342
Q

What are the S&S of R-sided CHF, specifically cor pulmonale?

A

-edema of legs/feet
-ascites (accumulation of fluid in peritoneal cavity), which will result on abdominal edema, hepatomegaly, and/or splenomegaly

343
Q

If a pt has cor pulmonale and does not receive medical intervention what happens?

A

-once IVC is full, blood will go through SVC
-pts will have distended neck, may be delirious, or have seizures

344
Q

What are the general S&S of both L AND R sided CHF?

A

-fatigue
-dyspnea
-exercise intolerance

345
Q

What are the secondary compensations for both L AND R sided CHF?

A

-tachycardia
-polycythemia (increased EPO/RBCs)
-decreased daytime oliguria (urine output)

346
Q

What does CHD stand for?

A

congenital heart defect

347
Q

When can a CHD occur?

A

as early as 8 weeks in embryonic stage

348
Q

Every year ~40K babies in US are born with some kind of ______ _______. Surgery has decreased mortality rate in US

A

heart defect

349
Q

CHD is a problem with what?

A

valve or septum of heart

350
Q

What is the first sign of CHD?

A

dr will detect heart murmur

351
Q

Any kind of heart defect usually means…..

A

decreased oxygen (minor or major) systemically

352
Q

Most cases of CHD are _________ but genetics play a big role

A

multifactorial

353
Q

What are some causes for CHD?

A

-multifactorial
-infection during pregnancy will impact baby such as Rubella (German measles)
-alcoholic pregnant mama
-smoking pregnant mama

354
Q

How will the body try to compensate with CHD?

A

Sympathetic NS will try to compensate by increasing HR/contractility

heart will work over time and can hypertrophy

355
Q

Babies w/ CHD will suffer from hypoxia, this can develop into….

A

secondary polycythemia (increased EPO)

356
Q

Most minor defects are _______ and are discovered by dr during check-ups. Can patient live with it?

A

asymptomatic

yes, pt can live with it and sometimes it corrects on its own as pt gets older

357
Q

If a baby is born with CHD and it’s a major problem, what is usually required?

A

surgical intervention

358
Q

What are the S&S of major CHD?

A

-pallor or cyanotic
-developmental delay
-tachycardia
-tachypnea
-exercise intolerance

359
Q

All CHD patients should be given _______ ________ before any kind of medical procedure

A

prophylactic antibiotics

360
Q

Ventricular septal defect has blood flow through defect usually from ______ to _______

A

left to right

361
Q

What is wrong with a ventricular septal defect?

A

something is wrong with the septum between the 2 ventricles

362
Q

What is the most common type of congenital abnormality/heart defect?

A

Ventricular septal defect

363
Q

What is an atrial septal defect?

A

foramen ovale does not close properly at birth

364
Q

In basic terms what is ventricular or atrial septal defect?

A

hole in heart

365
Q

Ventricular septal defect is sometimes called a _____ to ____ shunt. Why?

A

L to R shunt

bc of pressure gradient

366
Q

What happens when ventricular septal defect is severe?

A

blood will regurg and convert to R to L shunt

367
Q

Where are valvular defects usually found?

A

in semilunar valves (aortic and pulmonary valves)

whack bc roop also said that one of the most common valvular defects is a mitral valve stenosis

368
Q

What is a stenosis in the heart?

A

valvular defect, very narrow opening

heart has to work harder to push same amount of CO though opening

369
Q

What is an incompetent valve?

A

does not close properly = backflow

370
Q

What is the most common type of incompetent valve? What happens here?

A

mitral valve prolapse

mitral valve flaps are enlarged and cannot close properly

371
Q

All valvular defects will cause…..

A

decreased SV = heart will work harder = hypertrophy

372
Q

What is the treatment for valvular defects?

A

valve replacement

373
Q

How does a porcine or mechanical heart valve differ from a normal heart valve?

A

porcine/mechanical heart valve:
-lasts decades
-thrombus can develop around valve
-pts are usually put on low-dose aspirin to prevent thrombus

374
Q

Tetralogy of Fallot includes ____ defects

A

4

375
Q

Babies with tetralogy of fallot are born _______, this is why they are called “ _____ babies”

A

cyanotic, blue

376
Q

What is the first defect of Tetralogy of Fallot?

A

pulmonary valve stenosis

heart is trying to pump full SV through a valve that will not open properly

377
Q

What is the 2nd defect of Tetralogy of Fallot?

A

R ventricular hypertrophy

378
Q

What is the 3rd defect of Tetralogy of Fallot?

A

ventricular septal defect (VSD)

this increases pressure in RV

379
Q

What is the 4th defect of Tetralogy of Fallot?

A

overriding aorta

aorta is over both ventricles and VSD

this means that both ventricles will have bad blood flow

380
Q

What is the treatment for Tetralogy of Fallot?

A

babies will have surgery approx 1 month after birth, or sometimes 1 year after

1st surgery is to try to open pulmonary valve and close VSD

will need additional surgeries later, especially for overriding aorta

381
Q

What are the 4 causes of mitral stenosis?

A

1) rheumatic
2) calcific (usually causes mitral regurg but can cause mitral stenosis in some cases)
3) congenital
4) collagen-vascular disease (systemic lupus erythematosus and rheumatoid arthritis, but extremely rare)

382
Q

What is the most common cause of mitral stenosis?

A

rheumatic fever

narrowing results from fusion and thickening of the commissures, cusps, and chordae tendineae

symptoms usually develop 20 years after acute rheumatic fever

383
Q

One of the causes of mitral stenosis is rheumatic fever. When does rheumatic fever usually occur?

A

children 5-15 yrs old

384
Q

One of the causes of mitral stenosis is rheumatic fever. How does infection begin? How does it develop

sorry its kinda long

A

-strains of Group A beta hemolytic streptococcus
-some people react with abnormal immune response (inflammation affecting skin, joints, and heart)
-starts as URT infection or strep throat
-most people will recover, those who don’t recover will have Abs and those Abs will react with/bind to CT in skin, joints, brain and heart, leading to inflammation
-heart will have scar tissue and develop to rheumatic heart disease

385
Q

Rheumatic fever affects large joints in body and results in….

A

synovitis

386
Q

Rheumatic fever affects small joints in body and results in….

A

subcutaneous nodules in wrists and ankles

387
Q

5% of population with rheumatic fever will have skin affected with non-pruritic rash called….

A

erythema marginatum

388
Q

20-30% of people w/ rheumatic fever will have basal nuclei in brain affected. What is this called and what does it result in? Whats recovery time?

A

sydenham’s chorea or St. vitus dance

uncontrolled rapid jerking movements of arms, legs, and/or face

pts will spontaneously recover within 2 months- 2 years

389
Q

What is the major problem with rheumatic fever?

A

inflammation of heart, can affect all 3 layers

390
Q

If rheumatic fever affects the pericardium, what is this called and what happens?

A

pericarditis

effusion= fluid collecting around the heart

heart will be unable to pump how it should

391
Q

If rheumatic fever affects the myocardium, what is this called and what happens?

A

myocarditis

nodules appearing in myocardium (made up of lymphocytes, macrophages, and fibrotic CT), this is called Ashoff-Geipel bodies

this can cause arrhythmias because the myocardium is so damaged

392
Q

If rheumatic fever affects the endocardium, what is this called and what happens?

A

endocarditis

will damage valves bc heart valves are made up of endothelium

393
Q

What is the most common heart layer to be affected with rheumatic fever?

A

endocardium, leading to endocarditis

394
Q

What is the diagnosis process for rheumatic heart disease?

A

test serum for Abs and perform ECG

395
Q

What is the treatment for rheumatic heart disease?

A

-antibiotics such as PCM (penicillin)
-antiinflammatories such as prednisone

396
Q

Rheumatic heart disease is when there is thicken flaps of _____ valve and ______ ______. This results in mitral stenosis.

A

mitral, chordae tendineae

397
Q

What are the 2 types of HTN?

A

primary (essential) and secondary HTN

398
Q

What are some causes of secondary HTN?

A

-renal HTN
-endocrine-metabolic HTN
-Drug-induced or drug-related

399
Q

Vascular disorders include….

A

the heart and blood vessels

400
Q

HTN is an ______ vascular disorder

A

arterial

401
Q

Which disorder is said to be the silent killer?

A

HTN

402
Q

____ adults in US have hypertension

A

1/3

403
Q

HTN is more common in _____ than women until ________, then women take over with higher number

A

men, menopause

404
Q

The majority of HTN is…..

A

essential/primary HTN and is idiopathic

405
Q

~10% of all HTN is _________ HTN. What is it usually due to?

A

secondary, usually due to some kind of renal disease or endocrine disorder

406
Q

endocrine disorder = high risk for what vascular problem?

A

HTN

407
Q

What is normal BP? Hypertensive?

A

normal = 120/80
hypertensive = 140/90 or higher on 3 consecutive dr visits

408
Q

Systolic number ________ increases w/ age

A

ALWAYS

409
Q

What is the most common cause of HTN?

A

increased resistance

410
Q

MAP = CO x TPR

What does this mean?

A

increase CO = increase MAP
increase R = increase MAP

basically increased MAP causes HTN

411
Q

As you increase ______usually due to vasoconstriction, vasoconstriction will also occur in the kidneys and decrease _____ ______. Once they detect that they are getting less blood, then they will trigger RAAS and cause further vasoconstriction. This will cause damage to blood vessels and increase ______

A

resistance

blood flow

BP

412
Q

overtime, hypertensive arteries can become hard and cause an ________

A

aneurysm

413
Q

HTN can result in 3 things. What are they?

A

1) renal HTN (kidneys fail)
2) hypertensive encephalopathy
3) hypertensive retinopathy

414
Q

What is hypertensive encephalopathy affecting? What are the symptoms?

A

brain

seizures, confusion, cerebral edema

415
Q

What is hypertensive retinopathy?

A

-blood vessels in eyes become infected
-blood vessels can rupture and cause retinal hemorrhages
-pts can go blind

416
Q

What are the risks of primary HTN?

A

-bad diet (increased salt, cholesterol)
-smoking

417
Q

lots of pts with HTN will be ______ and won’t know till they go to dr that they have HTN

A

asymptomatic

418
Q

What is PVD?

A

peripheral vascular disease

anything abnormal in arteries or veins far away from heart (in periphery)

419
Q

What is PVD primarily caused by?

A

plaques or atheroma

420
Q

A partial occlusion in PVD would result in what?

A

pts will have problems w/ muscle function in legs

may lose sensory function in legs

421
Q

A complete occlusion in PVD would result in what?

A

ischemia, necrosis, ulcers, and gangrene

422
Q

Most commonly affected blood vessels with PVD are the……

A

abdominal aorta, femoral artery, and iliac arteries

423
Q

What are the S&S for PVD?

A

-intermittent claudication
-increased fatigue
-weakness
-paresthesias
-decreased or absent pulses distal to occlusion
-pallor when legs are elevated (or cyanotic), and dependent erythema when legs are released

424
Q

If a pt tells you they have intermittent claudication, automatically assume what?

A

they have PVD

425
Q

what are the treatment options for PVD?

A

-lifestyle changes (diet with decreased cholesterol, exercise, etc)
-vasodilator meds
-anticoagulants
-surgery (bypass)

426
Q

What is an aortic aneurysm?

A

weakness in wall, usually turbulent flow causes this (typically because of some type of atheroma)

427
Q

What are the 3 types of aortic aneurysms?

A

1) fusiform
2) saccular
3) dissecting

428
Q

What is a fusiform aortic aneurysm?

A

dilation all around the vessel

429
Q

What is a saccular aortic aneurysm?

A

dilation on one side of the vessel

430
Q

What is a dissecting aortic aneurysm?

A

tear in the tunica intima allowing blood to flow between the layers

431
Q

If aortic aneurysms are not treated, what can happen?

A

they can rupture

432
Q

What is the worst type of aortic aneurysm?

A

dissecting

433
Q

aortic aneurysms result from problem with….

A

tunica media or in thoracic/abdominal aorta

434
Q

w/ aortic aneurysm, overtime the dilation increases or ______ forms

A

thrombus

435
Q

aortic aneurysms can be asymptomatic. If this is the case, dr will find a bruit. What does this mean and for what type of aortic aneurysms?

A

turbulent blood flow for fusiform or saccular aortic aneurysms, typically in abdomen, and may have mild pain

436
Q

If a pt complains of severe, sharp pain and you suspect they have an aortic aneurysm, what type of aneurysm is this?

A

dissecting

437
Q

What are the diagnostic tests for aortic aneurysms?

A

CT scan and/or US

438
Q

aortic aneurysms are considered _______ emergencies, and a graft will need to be done

A

surgical

439
Q

What is the most common venous disorder?

A

varicose veins

440
Q

What are varicose veins?

A

torturous, dilated vessels in legs (superficial or deep veins of legs, can also occur in rectum or esophagus)

441
Q

Superficial veins don’t have a lot of mechanical support from muscles. This is why superficial veins are the most common ones to be affected with …..

A

varicose veins

442
Q

Varicose veins have _____ hydrostatic pressure bc of ______ ______

A

increase, incompetent valves

443
Q

Varicose veins are common in who?

A

pregnant women or people who stand for long periods of time

444
Q

As valves fail, blood regurges and pools in periphery veins. What is this?

A

varicose veins

445
Q

What are pts told to do if they have been diagnosed with varicose veins?

A

to elevate legs whenever sitting and to wear compression stocking to help blood move up

446
Q

What are the treatment options for severe cases of varicose veins?

A

vein stripping (bypass surgery) or sclerotherapy (saline injected into veins and will collapse them)

447
Q

What is thrombophlebitis?

A

inflammation + thrombus in veins

448
Q

What is phlebothrombosis?

A

thrombus w/o inflammation in veins

449
Q

Venous blood has to go ________ gravity

A

against

450
Q

venous disorders develop bc of….

A

-sluggish blood flow
-endothelial damage/injury
-increased coagulability (such as through polycythemia)

451
Q

What are the S&S of venous disorders?

A

-erythematous
-warm legs
-edema
- positive homan sign (dorsiflex foot and its extremely painful in calves)

452
Q

What are the treatment options for thrombophlebitis or phlebothrombosis?

A

anticoagulant therapy or in severe cases= surgery

453
Q

What are the 4 different types of shock?

A

1) hypovolemic shock (decreased blood volume)
2) distributive shock (also called vasogenic or low-resistance shock, marked vasodilation)
3) cardiogenic shock (inadequate output by disease heart)
4) obstructive shock (obstruction of blood flow)

454
Q

What are some causes of hypovolemic shock?

A

-hemorrhage
-trauma
-surgery
-burns
-fluid loss associated with vomiting or diarrhea

455
Q

Distributive shock is system-wide _______

A

vasodilation

456
Q

What are some causes of distributive shock?

A

-fainting (neurogenic shock)
-anaphylaxis
-sepsis (also causes hypovolemia due to increased capillary permeability with loss of fluid into tissues)

457
Q

What are some causes of cardiogenic shock?

A

-MI
-Heart failure
-arrhythmias

458
Q

cardiogenic shock is where the heart is _______ as a pump

A

failing

459
Q

What are some causes of obstructive shock?

A

-tension pneumothorax
-pulmonary embolism
-cardiac tumor
-pericardial tamponade

460
Q

Shock is any abnormality in the _____________ system

A

circulatory

461
Q

Shock will _____ CO, _____ tissue perfusion, and cause hypoxia

A

decrease, decrease

462
Q

Shock will _____ BP

A

decrease

463
Q

What are the S&S of shock?

A

-restless
-thirsty (osmoreceptors will be activated w/ low blood volume)
-vasoconstriction will cause cold/pale skin
-tachycardia
-oliguria

464
Q

Septic shock is caused by some kind of ______

A

pathogen

465
Q

With septic shock, the skin will look ______ and feel ____ to touch

A

erythematous, warm

466
Q

Septic shock decreases BP, which will make pt feel….

A

weak and dizzy

467
Q

CO is low in septic shock. What does this mean?

A

oxygen is also low, which means CO2 is high

this is metabolic acidosis

468
Q

Metabolic acidosis will increase with septic shock and affect what?

A

CNS and renal system as glomerular-filtration rate (GRF) decreases

469
Q

Metabolic acidosis will make pt breath faster or slower during septic shock?

A

faster

470
Q

What is the treatment option for shock?

A

call 911, keep them warm, treat cause

Pathophysiology (6 decks)

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