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Physiology 3 > Unit 1 Cardiac physiology > Flashcards

Unit 1 Cardiac physiology Flashcards

1
Q

What is the number one cause of death

A

Cardiovascular disease

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2
Q

What are the major underlying cause of ischemia

A

Atherosclerosis
White Thrombus
Red Thrombus
Artery spasm

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3
Q

What pathway promotes thrombosis

A

Inflammatory pathways

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4
Q

What is thrombosis responsible for

A

Myocardial infarction

Strokes

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5
Q

What leads to atherogenesis

A

Blood cholesterol

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6
Q

What body system can modulate inflammation

A

The nervous system

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7
Q

What are the mechanisms in Hemostasis

A

Vascular spasm
Formation of platelet plug
Blood coagulation
Fibrous tissue growth

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8
Q

What causes Vascular constriction associated with traums

A

Neural reflexes
Local myogenic spasm
Local Humoral factors

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9
Q

What is responsible for the majority of the vascular constriction

A

Myogenic spasm

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10
Q

What type of vascular constriction is important in smaller vessels

A

Humoral factors (Thromboxane A2 from platelets)

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11
Q

What is released from platelets that causes vascular constriction

A

Thromboxane A2

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12
Q

What is found in the platelet cell membrane that initiates clotting

A

Thromboplastin

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13
Q

What happens when platelets contact a damaged area

A

1) Swell
2) move to surface
3) Granules release
4) Secrete ADP, Thromboxane A2

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14
Q

What is Thromboxane A2

A

Vasoconstrictor

Potentiates but not essential for granule release

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15
Q

What is the half life of platelets

A

8-12 days

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16
Q

What prevents platelet aggregation

A

Endothelium

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17
Q

What does the endothelium produce

A 
PGI2 (procyclin)
Factor VIII (Clotting)
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18
Q

What is Procyclin

A

Vasodilator
suppresses release platelet granules
Limits platelet extension

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19
Q

How does Aspirin and Ibuprofen work in the clotting cascade

A

Prevent the production of Thromboxane A2 and Prostacylin by blocking fatty acid cyclooxygenase

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20
Q

What do anticoagulants do

A

Prevents clots from forming

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21
Q

What causes lysis of clots

A

Plasmin (from plasminogen)

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22
Q

What are exogenous activators of plaminogen

A

Streptokinase

tPA

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23
Q

What is the reason tissues are damaged in an infarction

A

Reperfusion

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24
Q

What causes the damage in reperfusion

A

free radicals are generated when pressure on tissues are relieved and perused with blood

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25
Q

What is Collateralization

A

The ability to open up alternative routes of blood flow to compensate for a blocked vessel

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26
Q

What is the extrinsic mechanism in blood coagulation

A

Chemical factors released by damaged tissues

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27
Q

What is the intrinsic mechanism in blood coagulation

A

components in blood and trauma to blood or exposure to collagen

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28
Q

What chromosme is the hemophilia gene on

A

X

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29
Q

What clotting factor defect is most common in hemophilia cases

A 
Factor VIII (85%)
Factor IX (15%)
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30
Q

What clotting factors are made in the liver

A 
I
II
VII
IX
X
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31
Q

What prevents the liver from making clotting factors

A

Warfarin

Cumadin

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32
Q

How does Warfarin and Cumadin prevent the liver from making clotting factors

A

By blocking action of Vitamin K

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33
Q

What is the key step in clotting

A

Conversion of Firbinogen to firbin

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34
Q

What is required to convert Fibrinogen to fibrin

A

Thrombin

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35
Q

What is Antiphospholipid antibody syndrome

A

An autoimmune disorder where the body makes antibodies against phospholipids in cell membranes (causes abnormal clotting)

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36
Q

What does Homocysteine do

A

Can irritate blood vessels –>Atherosclerosis
turn cholesterol into Oxidized LDL
Make blood more likely to clot

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37
Q

How can you reduce the amount of Homocysteine in blood

A

Increasing the intake of Folic Acid

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38
Q

What age are agglutinins produced

A

2-8 months

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39
Q

when do antibody titers in blood peak

A

age 10

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40
Q

What is the universal donor

A

O-

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41
Q

What is the universal acceptor

A

AB+

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42
Q

How can hemolysis cause kidney failure

A

Hemoglobin precipitates and blocks renal tubules

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43
Q

how many antigens are there in the Rh blood typing system

A

6
C D E
c d e

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44
Q

What is the most common and most antigenic antigen with respect to Rh+ blood

A

D antigen

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45
Q

What happens if someone is lacking the D antigen

A

they are Rh-

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46
Q

If you put Rh+ blood in a person with Rh- blood, how long does it take for the Rh antibodies to develop and cause Hemolysis

A

2-4 months

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47
Q

What is Erythroblastosis Fetalis

A

agglutination and hemolysis of the fetus’ RBC by the mothers anti Rh agglutinins

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48
Q

what do macrophages convert hemoglobin into

A

Bilirubin (Jaundice in Erythroblastosis Fetalis)

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49
Q

What is the most common cause of Erythroblastosis Fetalis

A 
Mom = Rh-
Dad = Rh+
Fetus = Rh+
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50
Q

When do symptoms of Erythroblastosis Fetalis occur

A

2nd (3%) and 3rd (10%) trimester of the pregnancy

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51
Q

After a child is born with Erythroblastosis Fetalis how long does it take for anemia to set in

A

1-2 months

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52
Q

What is caused when bilirubin precipitates into the brain during Erythroblastosis Fetalis

A

Mental impairment (Kernicterus)

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53
Q

What is the treatment for Erythroblastosis Fetalis

A

Replace neonates blood with Rh- blood

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54
Q

How can Erythroblastosis Fetalis be prevented

A

Rh immunoglobulin globulin administer to mother at 28 weeks gestation

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55
Q

what does Rh immunoglobulin globulin do

A

Suppress immune response to D antigen in fetal RBC’s that may cross placenta or enter moms circulation

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56
Q

What is another name for Erythroblastosis Fetalis

A

Hemolytic disease of the Newborn

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57
Q

How are heart muscles arragned

A

Striated, irregular columns with 1-2 centrally nuclei

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58
Q

What is the word used to describe the nature of heart muscles

A

Syncytium, they work together

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59
Q

How to heart muscles work together

A

Intercalated discs provide low resistance pathways

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60
Q

How long is the average action potential

A

.2 - .3 seconds

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61
Q

What happens to the ions during an action potential

A

Na+ increase during depol
Ca++ increase during plateau
K+ increase during repol

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62
Q

What happens to Na+ during cardiac action potential (depol + repol)

A

Depolarization: Increase
Repolarization: decrease

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63
Q

What happens to Ca++ during cardiac action potential (depol + repol)

A

Depolarization: Increase
Repolarization: Decrease

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64
Q

What happens to K+ during cardiac action potential (depol + repol)

A

Depolarization: Decrease
Repolarization: Increase

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65
Q

What are the fast channels in cardiac muscle

A

Na+

66
Q

What are the slow channels in cardiac muscle

A

Ca++/Na+

67
Q

What cardiac channels are operational during depolarization due to the SA node

A

Ca++/Na+ (slow channels)

68
Q

What is the result of only having the slow channels (Ca++/Na+) open during depolarization

A

Depolarization time is increased

69
Q

What causes passive ion movement across cells

A

Concentration gradient
Electrical gradient
Membrane permeability

70
Q

When cardiac muscles are at rest what channels are open and what ones are closed

A

Closed: Na+ and Ca++/Na+
Open: K+

71
Q

What happens to the contractile strength of cardiac muscle is the Na+/K+ pump is inhibited (Ca++ increases in cell)

A

Contraction strength increases

72
Q

What is the ratio of Na+ to K+ that is pumped from the Na+/K+ pump

A

3 Na+ out

2 K+ in

73
Q

Can cardiac muscle be stimulated during the absolute refractory period

A

no

74
Q

Can cardiac muscle be stimulated during the Relative refractory period

A

Yes, it requires a supra-normal stimuls

75
Q

When does the absolute refractory period occur

A

During plateau

76
Q

When does the relative refractory period occur

A

During repolarization

77
Q

What protects ventricles from supra-ventricular arrhythmias

A

Av node and Bundle

78
Q

What is the pacemaker of the heart

A

the SA node

79
Q

What channels does the SA node open

A

Slow (Ca++/Na+)

80
Q

What is overdrive suppression

A

Drive a self-excitatory cell at a rate faster than its own inherent rate, suppressing its automaticity

81
Q

What is it called when cells is excited faster than its inherent rate, suppressing its automaticity

A

Overdrive suppression

82
Q

What happens to cycle length as heart rate increase

A

Cycle length decreases as HR increases

83
Q

What is Systole

A

Isovolumetric Contraction

84
Q

What is Distole

A

Isovolumetric Relaxation

85
Q

at resting heart rate what is greater (in time) Systole or Distole

A

Distole

86
Q

As HR increases what happens to Systole and Distole

A

Both shorten, Distole shortens more than Systole

87
Q

What is EDV

A

End Diastolic volume (volume in ventricles at end of filling)

88
Q

What is ESV

A

End Systolc volume (volume in ventricles at the end of ejection)

89
Q

What is EDV-ESV

A

Stroke Volume (Volume ejected by ventricles)

90
Q

What is the Ejection fraction

A

% of EDV ejected

91
Q

What is a normal ejection fraction

A

50-60%

92
Q

What are the different Artial Pressure waves

A

A wave
C wave
V wave

93
Q

What is the A wave

A

Atrial contraction

94
Q

What is the C wave

A

Ventricular contraction

95
Q

What is the V wave

A

Atrial filling

96
Q

How do valves function

A

Open with fwd pressure

Close with Bwd pressure

97
Q

What are the two AV valves

A

Mitral

Tricuspid

98
Q

What are the two semilunar valves

A

Aortic

Pulmonic

99
Q

What valves have a strong construction

A

Semilunar valves

100
Q

What is it called when a valve does not open fully

A

Stenotic

101
Q

What is it called when a valve does not close fuly

A

Insufficient/leaky

102
Q

What is it called when a valve makes vibrational noise

A

Murmurs

103
Q

What is going on when there is a heart murmur during systolic phase

A

Aortic+pulmonry stenosis
or
Mirtral + Tricuspid insufficiency

104
Q

What is going on when there is a heart murmur during diastoic phase

A

Aortic + pulmonary Insufficiency
or
Mirtal + tricuspid stenosis

105
Q

What is the Law of Laplace

A

As ventricular radius increases, wall tension increases

106
Q

What happens to the force of ventricular contraction when tension on ventricular walls increases

A

Contraction Force increases

107
Q

If left ventricle is larger than the right, which ventricle will need to generate more tension to match the other

A

The left ventricle because it is larger and needs to fill more to generate the same tension

108
Q

What is the problem with having large ventricles

A

The heart will need to consume more energy and oxygen in order to have a strong contraction

109
Q

What does Chronotropic mean

A

Anything that affects heart rate

110
Q

What is Dromotropic

A

Anything that affects conduction velocity

111
Q

What in Inotropic

A

Anything that affects strength of contraction

112
Q

What is Frank-Starlings law of the heart

A

The heart will pump all the blood that returns to it without allowing excessive damming of blood in veins

113
Q

An increase in venous return causes an increase in what

A

Stretch of cardiac muscle fibers (increase Contraction force, and HR)

114
Q

Stretching of the SA node will cause what

A

An increase of Ca++ and or Na+ permeability, thus increasing HR

115
Q

What are some extrinsic influences on Cardiac muscle

A

Autonomic nervous system
Hormonal influences
Ionic influences
Temperature influences

116
Q

What does the sympathetic NS do to the heart

A

Increase HR
Increase contraction str
Increase conduction velocity

117
Q

What does the parasympathetic NS do the the heart

A

Decrease HR
Decrease contraction Str
Decrease conduction velocity

118
Q

What is used to block SNS effects on the heart

A

Propranolol (Beta blocker)

119
Q

What is used to block parasymp NS effects on the heart

A

Atrpoine (blocks muscarinic receptors)

120
Q

What happens when the Parasym NS is blocked by Atrpoine

A

HR increase

Decreased contraction Str

121
Q

Parasympathetic NS exerts what type of effect on the heart

A

Dominate inhibitory influence on HR

122
Q

Sympathetic NS exerts what type of effect on the heart

A

Dominate stimulatory influence on contraction Str

123
Q

Direct SNS influence on the heart uses what hormone. What percent of SNS influence is direct

A

Norepinephrine

85%

124
Q

Indirect SNS influence on the heart used what hormone. What percent of SNS influence is indirect

A

Epinephrine and Norepinephrine from adrenal medulla

15%

125
Q

If the SNS stimulates the left stellate ganglion, what is the result

A

Decreased Ventricular fibrillation threshold

Prolongation of QT interval

126
Q

is the SNS stimulates the right stellate ganglion what is the result

A

Increased ventricular firbeilation threshold

127
Q

What is the brainbridge reflex

A

Stretch on atrial wall + stretch receotors send signals to Medulla and increase SNS outflow

128
Q

What is the Benzold-Jarisch reflex

A

Barroreceptors in LV send info to CNS via CN X due to occlusion of artery. Increase in LVP and LV volume

129
Q

What do thyroid hormones do to the heart

A

Increase Inotropic
Increase Chronotropic
Increase COs by increasing BMR

130
Q

What happens if K+ is elevated (2-3x normal)

A

Dilation and flaccidity of cardiac muscle

Decrease resting membrane potential

131
Q

What happens if Ca++ is elevated

A

Spastic contrations

132
Q

How are HR and body temp related

A

HR increases ~10 beats per 1 degree F in body temp

133
Q

What happens to the contractile str when body temp increases

A

It will increase temporarily, but prolonged fever can decrease contractile str (exhaustion)

134
Q

What happens to HR when body temp drops

A

Decreased HR and contraction STR

135
Q

How much energy the heart utilizes is converted into heat

A

75%

136
Q

if 75% of the energy the heart uses why is the rest of the energy used for

A

99% of the 25% is for pressurization of blood

1% of the 25% is for acceleration of blood

137
Q

What does an EKG measure

A

Potential difference across the surface of the myocardium with respect to time

138
Q

What is a normal HR

A

between 60-80

139
Q

What is a Tachycardia

A

High HR (over 100)

140
Q

What is a Bradycardia

A

Low HR (under 50)

141
Q

What are the different intervals in a EKG

A

PR interval
P wave
QRS
T wave

142
Q

What is the PR interval

A

the AV node Delay

143
Q

What is the P wave on a EKG

A

Atrial depolarization

144
Q

What is the QRS complex on a EKG

A

Ventricular depolarization

145
Q

What is the T wave on a EKG

A

Ventricular depolarization

146
Q

Where is atrial repolarization in an EKG

A

It is hidden in the QRS complex

147
Q

On an EKG what node is the active electrode and what one is the reference

A

+ is Active

- is reference

148
Q

What is a first degree AV block

A

Depolarization wave from atria to ventricle is delayed

149
Q

What is a second degree AV block

A

Some depolarization wave pass other blocked (Dropped P wave with no QRS)

150
Q

What is a third degree AV block

A

All depolarization waves from atria are blocked, no relation between P and QRS

151
Q

How can you tell if there is hypertrophy in an EKG

A

Prolonged QRS
Axis deviation to side of problem
increased voltage in QRS

152
Q

What happens to the myocardial blood flow during contraction

A

Blood flow become limited

153
Q

During a contraction what heart chamber has the most impaired myocardial blood flow

A

Left ventrical

154
Q

What does left coronary flow peak

A

at the onset of diastole

155
Q

How much oxygen is taken from the blood by the myocardium at rest

A

70%

156
Q

What direction are depolarization and repolarization in relation to eachother

A

Opposite

157
Q

What does ischemia do to depolarization and repolarization

A

Prolongs Depolarization

Delays repolarization

158
Q

What does the T wave look like in a EKG of someone who has ischemia

A

The T wave inverts from normal (opposite to direction of the ventricular depolarization)

159
Q

What happens to cells in an infarction

A

Cell are no longer able to repolarize

160
Q

What happens to the EKG when a patient has an infarction

A

Depressed baseline which appears an an elevated ST segment

161
Q

What a preferred blood markers for myocardial injury

A

Troponins T and I

162
Q

what is troponin

A

a contractile protein not found in serum

Physiology 3 (4 decks)

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