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BSI > Cardio > Flashcards

Cardio Flashcards

1
Q

What is the pericardium?

A

serous membrane that surrounds and protects the heart

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2
Q

What is the function of pericardial fluid?

A

reduces friction between layers

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3
Q

What is another name for the tricuspid valve?

A

atrioventricular valve

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4
Q

what is another name for the pulmonary valve?

A

semilunar valve

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5
Q

what is another name for the bicuspid valve?

A

mitral valve (atrioventricular valve)

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6
Q

what is another name for the aortic valve?

A

semilunar valve

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7
Q

What valves have chordae tendinae and papillary muscle?

A

tricuspid and bicuspid

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8
Q

Where does the blood circulates starting with the right atrium?

A

Right atrium through the tricuspid valve into the right ventricle through the pulmonary valve, into the pulmonary trunk and pulmonary arteries into the pulmonary capillaries, to the pulmonary veins into the left atrium through the bicuspid valve into the left ventricle then through the aortic valve into the aorta and systemic arteries to tissues. Then blood is brought back to the Right atrium by the coronary sinus, inferior vena cava, and the superior vena cava.

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9
Q

Through which vessels does blood enter the right atrium?

A

superior vena cava, inferior vena cava, and the coronary sinus

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10
Q

Through which vessels does blood enter the left atrium?

A

pulmonary veins

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11
Q

Is blood leaving the left ventricle oxygenated or deoxygenated?

A

oxygenated

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12
Q

Is blood leaving the right ventricle oxygenated or deoxygenated?

A

deoxygenated

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13
Q

Is blood entering the right atrium oxygenated or deoxygenated?

A

deoxygenated

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14
Q

What is meant by the term “systemic circulation”?

A

the system of carrying oxygenated blood to tissues and the deoxygenated blood back to the heart.

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15
Q

what vessel does the right and left coronary arteries branch off of?

A

the ascending aorta

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16
Q

What area of the body does the brachiocephalic trunk, left common carotid artery, and the left sub-clavian artery supply blood to?

A

brain

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17
Q

what are of the body do the right and left common iliac arteries supply blood to?

A

organs

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18
Q

where is the SA node located?

A

top of the right atrium

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19
Q

where is the AV node located?

A

bottom right of the right atrium

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20
Q

where is the bundle of His located?

A

behind the AV node

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21
Q

What is the mechanism by which valves open and close?

A

pressure

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22
Q

which valves have papillary muscle and chordae tendinae associated with them?

A

Atrioventricular valves (tricuspid and bicuspid)

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23
Q

What is the function of papillary muscle and chordae tendinae?

A

keep valves from opening backwards

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24
Q

What are the five phases of the cardiac cycle?

A

Atrial contraction, isovolumetric contraction, ejection, isovolumetric relaxation, ventricular filling

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25
Q

What happens to left ventricular volume during each of these phases?

A

Stays the same during isovolumetric contraction and relaxation. Increases during filling and atrial contraction. Decreases during ejection

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26
Q

What happens to left ventricular pressure during each of these phases?

A

Pressure remains constant during ventricular filling and atrial contraction. Pressure increases during isovolumetric contraction, decreases during isovolumetric relaxation. During ejection there is a period where the pressure increases then it will decrease.

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27
Q

Describe when the mitral valve closes during the cardiac cycle?

A

The mitral valve closes when the pressure in the left ventricle is higher than that of the left atrium. It closes during at the beginning of the isovolumetric stage.

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28
Q

Describe when the aortic valve opens during the cardiac cycle.

A

The aortic valve opens when the pressure in the left ventricle is greater than that of the aortic and systemic arteries. This is during the ejection phase and through the isovolumetric relaxation phase.

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29
Q

Describe when the aortic valve closes during the cardiac cycle.

A

The aortic valve closes at the end of the isovolumetric relaxation phase. This is due to the pressure in the left ventricle being lower than the pressure in the aortic artery.

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30
Q

does atrial contraction force the AV valves to open?

A

no

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31
Q

What is the definition of preload?

A

the stretch state before a ventricle contracts

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32
Q

what is the definition of afterload?

A

the pressure the heart has to overcome to eject the blood

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33
Q

what is the definition of contractility?

A

the ability for cardiac muscle to produce tension

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34
Q

how does an increase in venous return affect preload of the left ventricle?

A

the farter the cardiac muscle stretches the greater activation caused

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35
Q

how does aortic pressure affect afterload of the left ventricle?

A

the left ventricle has to pump harder to eject the blood

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36
Q

If preload and contractility both affect strength of contraction, what is the difference between them?

A

pre-load is dependent on sarcomere length

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37
Q

What is the function of the atria?

A

to enhance the amount of blood in ventricles, which enhances ventricular pumping

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38
Q

What is the function of the ventricles?

A

to pump blood through pulmonary circulation and systemic circulation

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39
Q

what can occur with damage to chordae tendinae or papillary muscle?

A

results in backward flow of blood as ventricles contract and could be lethal

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40
Q

What occurs during atrial contraction?

A

AV valve is open; atrium pumps blood into ventricle

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41
Q

what occurs during period of isovolumetric contraction?

A

Ventricle begins to contract-once pressure in ventricle exceeds that of atrium the AV valve will close. This period of contraction while the AV valve and semilunar valve are closed is the isovolumetric contraction phase. Once the pressure in the ventricle exceeds that of the aorta then the semilunar valve will open.

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42
Q

What occurs during the period of ejection phase?

A

as ventricular pressure rises above arterial pressure, semilunar valve opens and blood is ejected out of ventricles

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43
Q

what occurs during the period of isovolumetric relaxation?

A

ventricle begins to relax; pressure begins to drop within ventricles, as pressure drops below arterial pressure, semilunar valve closes. This period of relaxation while both valves are closed is the isovolumetric relaxation phase. ventricle continues to relax and eventually the pressure drops below that of atrium and therefore the AV valve opens.

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44
Q

What occurs during the ventricular filling phase?

A

passive filling of ventricle

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45
Q

what is systolic blood pressure?

A

the pressure in the systemic arteries while the left ventricle is contracting and ejecting blood

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46
Q

what is the diastolic blood pressure?

A

the pressure in the systemic arteries while the left ventricle is relaxing and not ejecting blood

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47
Q

What is end diastolic volume?

A

the amount of blood in the ventricle before it contracts (110ml)

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48
Q

What is End systolic volume?

A

the volume of blood in the ventricle at the end of systole (40ml)

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49
Q

How will an increase in afterload affect ESV?

A

Increase it due to more blood being left behind in the ventricle

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50
Q

How would aortic stenosis affect afterload?

A

increase it

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51
Q

What effect does increased afterload have on SV?

A

Decreases it due to slower volume

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52
Q

What is stroke volume?

A

The volume of blood pumped out of the left ventricle per contraction (70ml)

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53
Q

What is ejection fraction?

A

the fraction of EDV that was pumped out of the left ventricle per contraction (55-70%)

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54
Q

Ejection fraction =?

A

(SV/EDV)*100

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55
Q

What is cardiac output?

A

the amount of blood pumped out of the left ventricle per minute?

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56
Q

CO=?

A

HR * SV

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57
Q

What is venous return?

A

the amount of blood returned to the heart

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58
Q

what is the primary determinant of preload?

A

EDV

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59
Q

what is the primary determinant of afterload?

A

aortic pressure

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60
Q

In order to increase contractility, does there have to be an increase in EDV?

A

No, it is independent of fiber length or stretch

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61
Q

What is cardiac reserve?

A

The work that the heart is able to perform beyond that required of it under basal/resting conditions (300-400%)

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62
Q

Presence of what heart sounds may be an indication of an abnormality?

A

S3: vibrations during rapid phase of ventricular filling.

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63
Q

Where does gas exchange occur?

A

pulmonary capillaries

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64
Q

which of the types of vessels have smooth muscle and thus are capable of constriction and dilation?

A

muscular arteries

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65
Q

are arteries or veins more compliant?

A

veins

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66
Q

define blood pressure?

A

a measure of the force that the blood exerts on the vessel walls

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67
Q

how do you calculate MAP from blood pressure?

A

MAP=DBP + (1/3) (SBP-DBP)

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68
Q

Why does MAP represent the pressure gradient in the systemic circulation?

A

due to the pressure in the right atrium being nearly 0mm Hg

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69
Q

how does an increase in CO affect MAP?

A

increase it

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70
Q

how does an increase in TPR affect MAP?

A

increase it

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71
Q

What is another name for TPR?

A

systemic vasculature resistance

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72
Q

does TPR represent venous resistance or arterial resistance and why?

A

arterial resistance because veins are so compliant

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73
Q

What effect does Ang II directly have on CO and TPR?

A

increases both by increasing arterial pressure

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74
Q

what effect does aldosterone directly have on CO and TPR?

A

no effect directly

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75
Q

what effect does ADH have on CO and TPR?

A

increases vasoconstriction which will increase blood volume

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76
Q

what effect does ANP directly have on CO and TPR?

A

increases vasodilation which will decrease blood volume

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77
Q

what effect does the SNS directly have on CO and TPR?

A

Increases vasoconstriction and increases blood volume

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78
Q

what effect does the PNS directly have on CO?

A

decreases CO through a decrease in heart rate and decrease in stroke volume

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79
Q

Does the PNS directly affect TPR?

A

No, has no affect on vasculature dilation or constriction

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80
Q

What is the baroreceptor reflex?

A

senses pressure change of blood and oxygen, CO2, and H+ levels

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81
Q

What will the baroreceptors do when they notice a decrease in blood pressure?

A

In a decrease of BP the would decrease firing rate which will increase SNS which in turn increases activation of alpha one and beta one receptors to ultimately increase pressure

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82
Q

What is the function of arteries?

A

transport of oxygenated blood

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83
Q

what is the function of arterioles?

A

act as valves for entry into capillaries

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84
Q

what is the function of capillaries?

A

gas and nutrient exchange

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85
Q

what is the function of venules?

A

collects blood from capillaries

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86
Q

what is the function of veins?

A

carry deoxygenated blood back to the heart.

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87
Q

Do capillaries have smooth muscle?

A

No, they are unable to constrict or dilate

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88
Q

Can arterioles and venules constrict or dilate?

A

yes, they have smooth muscle

89
Q

why do veins contain valves?

A

to prevent backflow of blood

90
Q

MAP=?

A

CO * TPR

91
Q

Pulse pressure =?

A

SBP-DBP

92
Q

Greater stroke volume results in ____ pressure rise with each heart beat?

A

greater

93
Q

Lower compliance of artery results in a ____ pressure rise with every beat?

A

greater

94
Q

What is TPR?

A

the resistance to blood flow through all of the vasculature in the body (represents arterial vasculature)

95
Q

What is the venous pump?

A

rhythmic contraction of skeletal muscle helps to push blood in the veins towards the heart; thus it increases venous return

96
Q

What is the respiratory pump?

A

during inspiration, abdominal pressure increases and intrathoracic pressure decreases

97
Q

What is RAAS?

A

Activation of the RAAS system will increase blood pressure

98
Q

What does Ang II cause?

A

vasoconstriction

99
Q

What does ADH do?

A

increases blood pressure through vasocontriction

100
Q

What does the V1a receptor cause?

A

vasocontriction

101
Q

what do the V2 receptors do?

A

mediate antidiuretic effects in the kidney

102
Q

What does ANP do?

A

lowers blood pressure through vasodilation

103
Q

What does the alpha-1 adrenergic receptor do?

A

causes constriction of most vessels of the body

104
Q

Stimulation of beta two receptors causes what?

A

vasodilation

105
Q

generalized activation of the SNS will increase blood pressure and decrease organ perfusion throughout the body except where?

A

in the heart and brain

106
Q

Majority of blood vessels are/are not innervated by PNS?

A

are not

107
Q

what are baroreceptors?

A

stretch receptors located in walls of large arteries

108
Q

What are chemoreceptors?

A

carotid bodies and aortic bodies sense decrease in oxygen and CO2 and H+ content

109
Q

What are atrial and pulmonary stretch receptors?

A

detect changes in pressure in low pressure areas

110
Q

Is blood flow to each organ equal?

A

No

111
Q

At rest, what gets the most blood flow?

A

organs excluding the heart and brain

112
Q

during exercise what gets the most blood flow?

A

skeletal muscle

113
Q

does smooth muscle require an action potential, initiated by the nervous system, to contract?

A

no

114
Q

what types of stimuli can stimulate contraction or relaxation of smooth muscle?

A

nervous signals, hormonal stretch/stimuli, and changes in environment chemically

115
Q

what factors contribute to the increased blood flow to skeletal muscle during exercise?

A

increased O2 demand, arteriovenous O2 difference increases

116
Q

Why does cardiac output increase during excercise

A

activation of the SNS

117
Q

Why does stroke volume plateau with increasing intensity of exercise after an initial increase during exercise?

A

The heart has less time for filling thus will have a lower EDV and a limited SV

118
Q

What is causing the SBP to increase during exercise?

A

The left ventricle is contracting harder to try and get more blood around the body

119
Q

Why does DBP not change during exercise?

A

To increase space for increased blood flow the arteries dilate

120
Q

What is the primary determinant of SBP?

A

CO

121
Q

Why is the RPP (rate-pressure product) increasing during exercise?

A

HR, SPB, and MAP are increased

122
Q

What is the primary determinant of DBP?

A

TPR

123
Q

What determines TPR?

A

the tone of arterial vasculature

124
Q

What can lactate cause?

A

vasodilation

125
Q

What does endothelin do?

A

vasoconstriction

126
Q

what does bradykinin do?

A

arteriole dilation and capillary permeability

127
Q

what do prostaglandins do?

A

arteriole dilation and capillary permeability

128
Q

what does histamine do?

A

arteriole dilation and capillary permeability

129
Q

What is oncotic pressure?

A

pressure determined by protein concentration

130
Q

what is hydrostatic pressure?

A

pressure exerted by a fluid

131
Q

how would an increase in capillary/blood hydrostatic pressure affect the movement of fluid out of the capillary?

A

increase flow out

132
Q

how would an increase in capillary/blood oncotic pressure affect movement of fluid out of the capillary?

A

decrease flow out (increase flow in)

133
Q

At the arterial end of the capillary is net filtration or reabsorption favored?

A

net filtration

134
Q

at the venous end of the capillary is net filtration or reabsorption favored?

A

reabsorption

135
Q

is all of the fluid that was filtered at the arterial end then reabsorbed at the venous end?

A

no

136
Q

what is the role of the lymphatic system in the process of capillary fluid movement?

A

carries away remaining fluid in the interstitial

137
Q

what is edema and how does it develop?

A

rate of fluid that enters the interstitial is greater than what the lymphatic system can remove

138
Q

what is the danger of edema?

A

gas exchange in the capillaries is compromised

139
Q

Why are cells of the SA node autorhythmic?

A

Fibers of SA node are leaky to Na

140
Q

By what mechanism does the SNS increase HR?

A

releases norepinephrine which increases Na permeability

141
Q

By what mechanism does the SNS increase contractility?

A

releases norepinephrine which increases Na permeability

142
Q

By what mechanism does the PNS decrease HR?

A

releases Ach which increases K permeability

143
Q

What is the purpose of the long ARP of the ventricular myocyte action potential?

A

prevents development of a tetanic contraction

144
Q

What does the P wave represent?

A

atrial depolarization

145
Q

What does the QRS complex represent?

A

ventricular depolarization

146
Q

What does the T wave represent?

A

ventricular repolarization

147
Q

What does it mean when the QRS complex comes back to the baseline on the ECG?

A

both atria have fully depolarized

148
Q

Why is the P-Q interval sometimes called the P-R interval instead?

A

There is not always a Q wave

149
Q

What does the X-axis on the ECG represent?

A

Time

150
Q

What does the Y-axis represent?

A

energy (mV)

151
Q

Is a wave of depolarization a wave of positive or negative charges within the muscle cell?

A

positive

152
Q

Is a wave of repolarization a wave of positive or negative charges within the muscle cell?

A

negative

153
Q

A wave of positive charges moving towards a positive electrode would result in an upward or downward deflection on the ECG?

A

upward

154
Q

A wave of positive charges moving towards a negative electrode would result in an upward or downward deflection on the ECG?

A

downward

155
Q

A wave of negative charges moving towards a negative electrode would result in an upward or downward deflection on the ECG?

A

upward

156
Q

What is a lead?

A

angle view of the heard using two different charged electrodes (different does not necessarily mean different charges)

157
Q

Which leads are limb leads?

A

1, 2, 3, AVR, AVL, AVF

158
Q

Which leads are chest leads?

A

V1-V6

159
Q

In lead II of the ECG, the QRS complex should be upward or downward?

A

upward

160
Q

In lead aVR of the ECG, the QRS complex should be upward or downward?

A

downward

161
Q

In lead aVF of the ECG, the QRS complex should be mostly upward or downward?

A

upward

162
Q

Chest leads run horizontal through the chest: True or False?

A

TRUE

163
Q

Why is the transmission through the AV node slower?

A

due to smaller fibers and fewer gap junctions

164
Q

What is the natural pacemaker of the heart?

A

the SA node

165
Q

Fibers of the SA node connect directly to ____ ____ ____ of the atria.

A

regular myocardial fibers

166
Q

How much time does each small box on the EKG show?

A

.04 seconds

167
Q

How much time does each large box on the EKG show?

A

.20 seconds

168
Q

How much voltage does each small box on the EKG show?

A

.10 mV

169
Q

How much voltage does each large box on the EKG show?

A

.50 mV

170
Q

How do you determine HR from an EKG?

A

Find R wave that falls on heavy black line and count off 300, 150, 100, 75, 60, 50 for each consecutive heavy line until you fine the next R wave

171
Q

What is a PAC?

A

premature contraction…originates suddenly in an atrial ectopic focus and produces an abnormal P wave earlier than expected

172
Q

What is a PVC?

A

premature ventricular contraction; QRS is very wide and deep, originates in actopic focus in a ventricle, occurs before a P wave can begin a new cycle

173
Q

What is atrial flutter?

A

p waves occur in rapid succession and each is identical to the next

174
Q

Why will an atrial flutter only occasionally produce a QRS complex?

A

due to the AV node not having enough time to repolarize

175
Q

What is ventricular flutter?

A

ventricular flutter is produced by a single ectopic focus firing at an extremely rapid rate…forms no p or t waves

176
Q

What is atrial fibrillation?

A

caused by many atrial ectopic foci firing at rapid rates causing an exceedingly rapid, erratic atrial rhythm…no true p wave just spikes, will not directly kill but blood may pool

177
Q

what is ventricular fibrillation?

A

caused by a rapid-rate discharge from many foci, only depolarizes a small area and will not have effective pumping…will directly kill you (erratic EKG)

178
Q

What is a sinus block?

A

the SA node stops its pacing activity for at least one cycle, p waves identical but one is missing every so often

179
Q

what is an AV block?

A

delay in transmission, primary has a longer P-R interval, secondary has a progressive P-R prolongation until QRS is dropped, tertiary is a complete block

180
Q

What does an EKG with bundle branch block look like?

A

it has “rabbit ears” as a QRS complex

181
Q

what is ischemia/infarct?

A

inverted symmetrical T waves

182
Q

What do elevated or depressed S-T segments show?

A

sign of acute injury, can return to baseline with time

183
Q

what is significant about very significant Q waves?

A

these are used to make a diagnosis of an MI at some point

184
Q

What is the difference between primary and secondary hypertension?

A

secondary is drug related

185
Q

how would overstimulation of the SNS increase blood pressure?

A

Increase CO and TPR

186
Q

How would increased activation of RAAS increase blood pressure?

A

Not enough excretion out of blood and too much reabsorption

187
Q

What are some contributing mechanisms of how insulin resistance and hyperinsulemia increase blood pressure?

A

higher oncotic pressure

188
Q

Why does an increase in blood volume increase blood pressure?

A

arteries and veins can only hold so much until volume can not change thus pressure will increase

189
Q

How does decreased secretion of bradykinin and nitric oxide contribute to hypertension?

A

decreased vasodilation

190
Q

How does increased secretion of endothelin contribute to hypertension?

A

increased vasoconstriction

191
Q

Where in the body is cholesterol synthesized?

A

Liver

192
Q

What enzyme converts HMG-CoA to mevalonate?

A

HMG-COA reductase

193
Q

What is a lipoprotein?

A

carry cholesterols and triglycerides

194
Q

What role does endothelial injury play in development of atherosclerosis?

A

formation of plaque

195
Q

How does atherosclerosis alter blood flow?

A

increase pressure

196
Q

List three things that can cause endothelial injury.

A

Shear stress, smoking, hypertension

197
Q

How does hypertension contribute to atherosclerosis development?

A

shear stress

198
Q

How does hypercholesterolemia contribute to development of atherosclerosis?

A

LDL can become oxidized and inhibit vessel protection

199
Q

How does hyperglycemia contribute to atherosclerosis?

A

Decrease in Nitric Oxide and increase in cell proliferation

200
Q

What is the mechanism of action of statins and how does this help in reducing risk of atherosclerosis?

A

HMG-CoA reductase inhibitor, less cholesterol in circulation

201
Q

What are chylomicrons?

A

Transports dietary cholesterol and triglycerides to various tissue in body

202
Q

what is VLDL?

A

very low density lipoprotein, transports mostly triglycerides from liver to adipose tissue

203
Q

What is IDL?

A

intermediate density lipoprotein, remnant of VLDL after it delivers triglycerides to tissue, may be cleared from the blood via direct uptake by the liver or remodeled into LDL

204
Q

what is LDL?

A

low density lipoprotein, transports mostly cholesterol from liver to various tissues of body

205
Q

what is HDL?

A

high density lipoprotein, transports cholesterol from peripheral tissues back to liver where it can be excreted via bile

206
Q

What characterizes heart failure?

A

failure to pump adequate blood to satisfy body’s needs

207
Q

what types of conditions can cause heart failure?

A

disorder of coronary arteries, HTN, cardiomyopathy, heart valve disorder, abnormal heart rhythm

208
Q

How can coronary artery disease cause heart failure?

A

decrease in CO and TPR

209
Q

How can hypertension cause heart failure?

A

leads heart to hypertrophy where it will eventually wear itself out

210
Q

What is the difference between systolic and diastolic heart failure?

A

systolic is a pumping problem where diastolic is a filling problem

211
Q

what is the purpose of increased SNS and RAAS activation?

A

to increase blood pressure

212
Q

How can chronic activation of the SNS cause progression of heart failure?

A

causes cardiac cell apoptosis, increase in BP, and increase in O2 uptake by other tissues

213
Q

how can chronic activation of RAAS cause progression of heart failure?

A

arrhythmias, cardiac fibrosis

214
Q

define decompensation

A

loss of cardiac reserve

215
Q

Why does tachycardia occur in heart failure?

A

increased heart rate to try and increase the CO

216
Q

why does a decrease in cardiac reserve occur?

A

weakening of the heart muscles

217
Q

why does SOB occur in heart failure?

A

less oxygen available to tissues

218
Q

Why does edema occur in heart failure?

A

less reabsorption in the pulmonary capillaries

219
Q

How does failure of the left ventricle lead to failure of the right ventricle?

A

Right ventricle has to overcome increased pressure because the left ventricle cannot pump enough blood out, overtime the right ventricle will weaken as well

BSI (7 decks)

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