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Phys III Exam 1 > Questions > Flashcards

Questions Flashcards

1
Q

What is the number 1 cause of death?

A

cardiovascular disease

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2
Q

What is the major underlying cause of cardiovascular disease?

A

ischemia due to atherosclerosis, white thrombus, red thrombus or artery spasm

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3
Q

What is the link to atherogenesis?

A

high blood cholesterol and inflammatory mechanisms

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4
Q

What characterizes early atherogenesis?

A

leukocyte recruitment and expression of proinflammatory cytokines

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5
Q

What promotes inflammatory pathways and is responsible for most MIs and strokes?

A

thrombosis

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6
Q

What can modulate inflammation?

A

nervous system

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7
Q

Define hemostasis.

A

prevention of blood loss

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8
Q

What are the mechanisms of hemostasis?

A

vascular spasm, formation of a platelet plug, blood coagulation, fibrous tissue growth to seal

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9
Q

What is vascular constriction associated with?

A

trauma

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10
Q

What can cause vascular constriction?

A

neural reflexes, local myogenic spasm, local humoral factors

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11
Q

What is responsible for most vascular constriction?

A

local myogenic spasm

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12
Q

What are local humoral factors?

A

thromboxane A2 from platelets

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13
Q

What type of vascular constriction is important for small blood vessels?

A

local humoral factors

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14
Q

How does neural reflex work for vascular constriction?

A

the sympathetic nervous system induces constriction because of pain

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15
Q

True or false: platelets function as whole cells, including being able to divide

A

False

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16
Q

What do platelets contain?

A

contractile proteins (actin and myosin), enzymes, calcium, ADP, ATP, thromboxane A2, serotonin and growth factors

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17
Q

What do platelet cell membranes contain?

A

glycoproteins and phospholipids containing platelet factor 3

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18
Q

What is thromboplastin?

A

a phospholipid containing platelet factor 3 that initates blood coagulation

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19
Q

What is the mechanism of Platelet Activation when platelets contact damaged area?

A

1) swell
2) irregular form with irradiating processes protruding from the surface
3) contractile proteins contract causing granule release
4) secrete ADP, Thromboxane A2 and serotonin

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20
Q

What is thromboxane A2?

A

it is a vasoconstrictor and stimulates platelet degranulation

it also accelerates platelet activation, it is NOT needed to activate

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21
Q

What happens when there aren’t enough platelets in the blood?

A

are associated with small hemorrhagic areas under the skin and throughout internal tissues

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22
Q

What is the half life of platelets?

A

8-12 days

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23
Q

How are platelets eliminated?

A

mostly by macrophage action

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24
Q

What does the endothelial wall produce and prevent?

A

prevents platelet aggregation

produces prostacyclin (PG12) and factor VIII

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25
Q

What does prostacyclin do?

A

it is a vasodilator, stimulates platelet adenylcyclase and inhibits platelet degranulation

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26
Q

When platelet adenyl cyclase is activated, what does it do?

A

supresses release of granules

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27
Q

What is the pathway to create thromboxane A2?

A

phospholipid –lipase–> ARA –FA cyclooxygenase–> PGG PHG –thromboxane synthetase–> Thromboxane A2

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28
Q

What is the pathway to create prostacyclin?

A

phospholipid –lipase–> ARA –FA cyclooxygenase–> PGG PHG –prostacyclin synthetase–> prostacyclin

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29
Q

What do aspirin and ibprofen do?

A

block thromboxane A2 and prostacyclin prodution by blocking FA cyclooxygenase which in turn converts ARA to PGG and PGH (intermediates

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30
Q

Why take aspirin to prevent heart attacks?

A

to block platelet function

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31
Q

What do anticoagulants do?

A

prevent clots from forming

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32
Q

How do anticoagulants prevent clots from forming?

A

they use chelators (tie up calcium), heparin (complexes with antithrombin IIII) and dicumarol (inhibits vitamin K dependent factors

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33
Q

What are the factors that are synthesized by hepatocytes?

A

II, VII, IX and X

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34
Q

Where are endogenous activators found?

A

tissues, plasma and urine

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35
Q

What are the exogenous activators of plasminogen?

A

streptokinase and tissue plasminogen activator

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36
Q

What is reperfusion injury associated with?

A

formation of highly reactive oxygen species with unpaired electrons

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37
Q

When are free radicals generated?

A

when pressure on tissues is relieved and again perfused with blood

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38
Q

What is collateralization?

A

the ability to open up alternate routes of blood flow to compensate for a blocked vessel

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39
Q

What are the types of collateralization?

A

angiogenesis and vasodilation

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40
Q

What is the role of the sympathetic nervous system on collateralization?

A

may impede via vasoconstriction, may augment via release of neuropepetide Y

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41
Q

What is the extrinsic mechanism for thrombosis?

A

initiated by chemical factors released by damaged tissues

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42
Q

What is the intrinsic mechanism for thrombosis?

A

requires only components in blood and trauma to blood or exposure to collagen

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43
Q

What are the names of the clotting factors we need to know?

A

fibrinogen, prothrombin, thromboplastin, calcium

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44
Q

What organ is key in clotting?

A

liver

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45
Q

What are the 5 clotting factors that are synthesized in the liver?

A

fibrinogen, prothrombin, SPCA, AHF B, stuart factor

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46
Q

What does coumarin do?

A

depresses liverformation of II, VII, IX and X by blocking action of vitamin K

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47
Q

What is hemophilia?

A

a sex linked disease that almost exclusively in males

85% of cases have a defect in factor VIII (antihemophilic factor A

15% of cases defect in factor IX (antihemophilic factor B)

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48
Q

Which steps of blood coagulation have calcium?

A

all but the first two steps

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49
Q

When the extrinsic and intrinsic factors merge, what happens?

A

it activates factor V and X and prothrombin to thrombin

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50
Q

What is needed to activate factors IX and X?

A

calcium

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51
Q

What are the final commonsteps of fibrin (polymer)?

A

fibrinogen + thrombin –> fibrin (monomer) + activated factor XIII

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52
Q

What breaks down the mesh (fibrinogen)?

A

plasmin

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53
Q

What is antiphospholipid antibody syndrome?

A

an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes which cause abnormal clots to form

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54
Q

What are some risk factors for heart disease?

A 
increasing age
male gender
heredity (race included)
tobacco smoker
high cholesterol
high blood pressure
physical inactivity
obesity/overweight
diabetes mellitus
high blood homocysteine
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55
Q

What is homocysteine?

A

an amino acid in the blood that may irritate blood vesels promoting atherosclerosis
it can also cause cholesterol to change into oxidized LDL
itcan make blood mroe likely to clot
high levels of homocystein in the blood can be reduced by increasing folic acid, B6 and B12 in the blood

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56
Q

What are the agglutinogens (surface markers) that are found on each of the blood types?

A

O- none
A- A
B- B
AB- A and B

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57
Q

What are the agglutins (soluble antibodies) that are found on each of the blood types?

A

O- anti A and B
A- Anti B
B- Anti A
AB- none

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58
Q

When are agglutinins produced?

A

after birth, arising spontaneously

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59
Q

When are antibody titers peak?

A

around 10 years old

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60
Q

Which blood types have anti A sera?

A

A, AB

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61
Q

Which blood types have anti B sera?

A

B, AB

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62
Q

Which blood type has neither seras?

A

O

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63
Q

How does the body lyse RBC when the wrong blood type is given?

A

antibodies (primarily IgM) cause kysis of RBCs by activating the compliment system which releases proetolytic enzymes rupturing cells membrane

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64
Q

What is the most lethal effect of a transfusion reaction?

A

kidney failure

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65
Q

Why is kidney failure associated with a transfusion reaction?

A

toxic substances are released from hemolysed RBCs, which causes circulatory shock, the hemoglobin from lysed RBCs preceipitates and blocks renal tubules

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66
Q

What are the 6 common Rh antigens?

A

C, D, E, c, d, e

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67
Q

Can a person with D Rh factor have d as well?

A

no

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68
Q

Which Rh factor is the most common?

A

D

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69
Q

Whathappens when Rh+ RBCs are infused into a person who has Rh-?

A

it stimulates the production of anti-Rh antibodies which develop slowly and reach maximum concentrations 2-4 months later

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70
Q

What is Heolytic disease of the newborn?

A

agglutination and hemolysis of the fetus’ RBCs by the mother’s anti Rh agglutinins, which can cause jaundice in the fetus

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71
Q

How does hemolytic disease of the newborn occur?

A

the fetus inherits Rh+ from the father and the mother is Rh-

the mother will develop anti Rh agglutinins from exposure to the fetus’ Rh factor.

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72
Q

When do we usually see hemolytic disease of the newborn?

A

Usually during the second or third pregnancy

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73
Q

What is erythroblastosis fetalis?

A

when the mother’s agglutinins circulate in the fetus after birth and destroy RBCs, causing anemia

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74
Q

What are some side effects of erythroblastosis fetalis?

A

bilirubin might precipitate in neurons of the brain causing mental impairment (kernicterus)
this causes enlargement of the liver and spleen of the baby

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75
Q

What is the treatment of erythroblastosis fetalis?

A

replace the neonate’s blood with rh- blood

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76
Q

How can one prevent erythroblastosis fetalis?

A

give an Rh immunoglobulin globulin (an anti-D antibody) to the mother at 28-30 weeks of gestation, whcih interferes with the immune response to the D antigen in the fetal RBCs that may cross the placenta and enter mother’s circuation

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77
Q

What do cardiac muscle cells look like?

A

long, striated and grouped in irregular anastomosing columns with 1-2 centrally located nuclei

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78
Q

What are SA node, AV node and Purkinje fibers generally?

A

specialized excitatory and conductive muscle fibers

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79
Q

Define syncytium

A

many acting as one

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80
Q

Why is there a syncytial nature of cardiac muscle?

A

because of the presence of intercalated discs
this makes low resistance pathways connecting cardiac cells end to end
there are also gap junctions

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81
Q

What is the duration of a cardiac action potential (AP)?

A

.2-.3 seconds

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82
Q

What are the channels that allow AP in cardiac muscle?

A

fast Na+
slow Ca2+/Na+
K+

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83
Q

Describe the permeability changes of sodium, calcium and potassium in the cardiac muscle.

A

Na+ sharp increase at the onset of depolarization, decrease during repolarization
Ca2+ increased during the plateau of the AP, decrease during repolarization
K+ increased during the resting polarized state, decreased at depolarization

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84
Q

When is the conductance for potassium greatest?

A

during the resting polarized state

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85
Q

What kind of channels does the SA node have? Why?

A

only slow CA2+/na+ to increase the depolarization time

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86
Q

What kind of channels does the typical cardiac cell have?

A

both fast Na+ and slowCa2+/Na+ channels

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87
Q

What does tetradotoxin do?

A

blocks fast Na+ channels selectively changing a fast response into a slow response

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88
Q

What must we also consider when the channels are open?

A

the concentration gradient, electrical gradient and the membrane permeability

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89
Q

What will ions seek if the ion channels are open?

A

Nernst equilibrium potential

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90
Q

What is the Nernst equilibrium potential?

A

when the concentration gradient favoring ion movement in one direction is offset by the electrical gradient

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91
Q

What happens during the resting membrane potential?

A

fast Na+ and slow Ca2+/Na+ channels are closed and K+ channels are open. Therefore, K+ ions are free to move

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92
Q

When is a stable Er maintained?

A

when K+ reaches the Nernst equilibrium potential

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93
Q

Is the Na+/K+ pump energy dependent?

A

yes

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94
Q

Why is the ratio of Na+ and K+ 3:2, respctively?

A

there is a net loss of one + charge from the interior each cycle, which helps the interior of the cell remain negative

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95
Q

what does the protein pump utilize?

A

energy from ATP

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96
Q

What binds to and inhibits the Na+/K+ pump?

A

digitalis

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97
Q

What happens to the cardiac cell membrane protein when the Na+/K+ pump is inhibited?

A

the function of the exchange protein is reduced and more Ca2+ is allowerd to accumulate in the cardiac cell increases contractile strength

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98
Q

Describe the absolute refractory period.

A

it is unable to re-stimulate the cardiac cell and occurs during the plateau of the AP

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99
Q

Describe the relative refractory period.

A

requires a supra-normal stimulus and occurs during repolarization of the AP

100
Q

Can you stimulate a cardiac cell during absolute refractory period?

A

no

101
Q

How would you describe the relative refractory period in a slow response?

A

the relative refractory period is prolonged and the refractory period is about 25% longer

102
Q

What is the function of the the AV node and bundle?

A

to protect the ventricles from supra-ventricular arrhythmias

103
Q

How do SA nodes have a self excitatory nature?

A 
less negative Er
leaky membrane to Na+/Ca2+
only slow Ca2+/Na+ channels operational
spontaneously depolarizes at fastest rate
contracts feebly
104
Q

What is different about the AP for an SA node compared to a cardiac cell AP?

A

the SA node has no stable resting polarized state

105
Q

What is overdrive suppression?

A

when you drive a self-excitatory cell at a rate faster than its own inherent rate

106
Q

What is the mechanism behind overdrive suppression?

A

increased activity of the Na+/K+ pump creating a more negative Er

107
Q

What is an example of overdrive suppression normally found in the heart?

A

the AV node and purkinje system are under overdrive suppression by the SA node

108
Q

What is the function of the AV node?

A

delays the wave of depolarization from entering the ventricle, which allows the atria to contract slightly before the ventricles

109
Q

What can act as an SA node if the SA node isn’t present?

A

the AV node, but it is slower than the SA node would be

110
Q

As the heart rate ____, cycle length ____

A

increases, decreases

111
Q

Which is higher at resting heart rate: systole or diastole?

A

diastole

112
Q

What happens to the duration of systole and diastole as the heart rate increases?

A

both get shorter, but diastole shortens to a greater extent

113
Q

When is left coronary artery pressure peaked?

A

at the beginning of diastole

114
Q

When is right coronary artery pressure peaked?

A

in the middle of systole

115
Q

What happens when there an increase in potassium efflux?

A

increased heart rate

116
Q

What happens when there is a decrease in potassium efflux?

A

decreased heart rate

117
Q

What happens when there is a decreased influx of Na/Ca?

A

decreased heart rate

118
Q

What happens when there is an increased influx of Na/Ca?

A

heart rate increases

119
Q

When there is an increase in potassium efflux and an increase in Na/Ca influx, what happens?

A

there isno net change in the AP

120
Q

What happens during systole?

A

isovolumic contraction of the ventricle and ejection of blood

121
Q

What happens during diastole?

A

isovolumic relaxation of theventricle, rapid inflow (70-75%), diastasis, and atrial systole (25-30%)

122
Q

What is end diastolic volume (EDV)?

A

volume in ventricles at the end of filling

123
Q

What is end systolic volume (ESV)?

A

volume in ventricles at the end of ejection

124
Q

What is stroke volume (SV)?

A

volume ejected by ventricles

125
Q

What is the ejection fraction?

A

% of EDV ejected (SV/EDV X 100%)

normal is 50-60%

126
Q

If someone had an EDV of 300 and an ESV of 150, what is their ejection fraction? Is this normal?

A

300 - 150 = 150

150/300 = 50%

Yes, this is a normal ejection fraction

127
Q

Define preload.

A

stretch on the wall prior to contraction (proportional to the EDV)

128
Q

Define afterload.

A

the changing resistance (impedance) that the heart has to pump against as blood is ejected

129
Q

What is an A wave?

A

it is a wave associated with atrial contraction

130
Q

What is a C wave?

A

it is a wave associated with ventricular contraction, specifically bulging of AV valves and tugging on atrial muscle)

131
Q

What is a V wave?

A

a wave associated with atrial filling

132
Q

Draw the atrial pressure wave graph created in class and label all of the important points on the graph.

A

Try to understand exactly what that graph is saying.

133
Q

What is the function of the valves?

A

to open with a forward pressure gradient and close with a backward pressure gradient

134
Q

Give an example of a forward pressure gradient (draw the schematic if necessary).

A

when the left ventricular pressure is greater than the aortic pressure, the aortic valve is open

135
Q

Give an example of a backward pressure gradient (draw the schematic if necessary).

A

when the aortic pressure is greater than the left ventricular pressure, the aortic valve is closed

136
Q

What is a forward pressure gradient also known as?

A

systole

137
Q

What is a backward pressure gradient also known as?

A

diastole

138
Q

What is it called when both the aortic and mitral valve are closed and the left ventricular pressure is rising?

A

isovolumic contraction

139
Q

What is it called when both aortic and mitral valve are closed and the left ventricular pressure is decreasing?

A

isovolumic relaxation

140
Q

What is a jugular pulse?

A

right atrial pressure release

141
Q

Describe the mitral and tricuspid valve.

A

thin and filmy, have corda tendinae that act as check lines to prevent prolapse, have papillary muscles to increase tension on chorda tendinae

142
Q

Describe the pulmonic and aortic valves.

A

stronger construction

143
Q

Define stenosis.

A

when the valve doesn’t open fully

144
Q

Define insufficiency when related to valves.

A

when the valve doesn’t fully close

145
Q

What is the vibrational noise created by either a stenosis or insufficiency?

A

murmur

146
Q

When listening to a patient’s heart, you hear a murmur during diastole. What pathology could they have if there was a problem on the left side of the heart?

A

mitral stenosis, aortic insufficiency

147
Q

When listening to a patient’s heart, you hear a murmur duing diastole. What pathology could they have if there was a problem on the right side of the heart?

A

tricuspid stenosis, pulmonary insufficiency

148
Q

When listening to a patient’s heart, you hear a murmur during systole. What pathology could they have if there was a problem on the left side of the heart?

A

mitral insufficiency, aortic stenosis

149
Q

When listening to a patient’s heart, you hear a murmur during systole. What pathology could they have if there was a problem on the right side of the heart?

A

tricuspid insufficiency, pulmonary stenosis

150
Q

At a given operating pressure, as ventricular radius increases, developed wall tension ____?

A

increases

151
Q

What happens to the force of the ventricular contraction when the tension is increased?

A

the force also increases

152
Q

How does the law of laplace explain how capillaries can withstand high intravascular pressure?

A

the small radius makes it easier on the vessels so there’s not so much wall tension

153
Q

Define cronotropic.

A

anything that affects heart rate

154
Q

What are some examples of something that could be +cronotropic?

A

caffeine, NE

155
Q

Define dromotropic

A

anything that affects conduction velocity

156
Q

What are some examples of something that could be + dromotropic?

A

NE

157
Q

Define inotropic.

A

anything that affects the strength of contraction

158
Q

What is an example of something that could be +inotropic?

A

caffeine, NE

159
Q

What is the Frank-Starling Law of the Heart?

A

within physiologic limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in the veins

160
Q

What is the mechanism behind the Frank-Starling Law of the Heart?

A

increased venous return causes increased stretch of cardiac muscle fibers, which increases cross-bridge formation and increased calcium influx (which both increase the force of the contraction). It also increases the streth on the SA node which increases heart rate

161
Q

When cardiac fibers are stretched beyond their limit, what happens?

A

the cross bridges become smaller, the less the cross bridge, the less calcium that can influx

162
Q

What is homeometric autoregulation?

A

the ability to increase strength of contraction independent of a length change

163
Q

During homeometric autoregulation, when is flow induced?

A

when the increased stroke volume is maintained even as the EDV decreases back to its initial levels (ESV also decreases)

164
Q

During homeometric autoregulation, when is pressure induced?

A

when an increase in aortic BP will increase the force of the left ventricular contraction

165
Q

During homeometric autoregulation, when is rate induced?

A

when increased heart rate (decreased cycle length) increases force “treppe”

166
Q

Why can ESV also decrease when flow is induced?

A

because there is a little blood left over after a contraction, so the ESV can go lower, there will just be less leftover blood

167
Q

What happens when there is direct stretch on the SA node?

A

increases calcium and/or sodium permeability which will increase heart rate

168
Q

What are some extrinsic influcences on the heart?

A

autonomic nervous system, hormonal influences, ionic influences, temperature influences

169
Q

When sympathetics control the heart, what is true?

A

+ cronotropic
+inotropic
+ dronotropic

170
Q

When parasympathetics control the heart, what is true?

A
  • cronotropic
  • inotropic
  • dronotropic
171
Q

How is the SNS blocked from the heart?

A

with propranolol (a beta blocker) which blocks beta receptors

172
Q

How is the PSNS blocked from the heart?

A

with atropine which blocks muscarinic receptors, which with increase heart rate, butdecrease strength of contraction

173
Q

Parasympathetic NS exerts a _______ _______ influence on heart rate while sympathetic NS exerts a ______ ______ influence.

A

dominant inhibitory

dominant stimulatory

174
Q

What accounts for most of the SNS effect on the heart?

A

direct innervation

175
Q

What causes indirect effects of the SNS on the heart?

A

catecholamines (epinephrine, NE) from the adrenal medulla in the blood

176
Q

When you stimulate the left stellate ganglion of the SNS, what happens to the heart?

A

decrease in ventricular fibrillation threshold

prolonged QT interval

177
Q

When you stimulate the right stellate ganglion of the SNS, what happens to the heart?

A

increased ventricular fibrillation threshold

178
Q

What is the cardioaccelerator reflex?

A

when there is stretch on the right atrial wall that increases stretch receptors which in turn send signals to the MO and increase SNS outflow to the heart

179
Q

What is the purpose of the cardioaccelerator reflex?

A

to prevent damming of blood in the heart and central veins

180
Q

What is the benzold-Jarisch reflex?

A

stimulation of the sensory endings mainly in the ventricles that reflex via CN X to the CNS

181
Q

What is the Benzold-Jarisch reflex stimulated by?

A

occlusion of the circumflex artery

increase in left ventricular pressure and left ventricular volume (like in aortic stenosis)

182
Q

What do thyroid hormones do to the heart?

A

+ inotropic
+ chronotropic
causes an increase in CO by increasing basal metabolic rate

183
Q

What is the effect of increased potassium on the heart?

A

dilation and flaccidity of the cardiac muscle at concentrations 2-3X normal
decreases resting membrane potential

184
Q

What is the effect of increased calcium on the heart?

A

spastic contraction

185
Q

What does the Benzold-Jarisch reflex result in?

A

hypotension and bradycardia (which would eventually cause you to pass out)

186
Q

Norepinephrine has an affinity for what?

A

alpha and beta receptors

187
Q

Epinephrine has an affinity for what?

A

beta receptors

188
Q

What happens when the body has a fever?

A

heart rate increases about 10 beats for every degree F elevation in body temperature
the contractile strength will increase temporarily but prolonged fever can decrease contractile strength dueto exhaustion of metabolic systems

189
Q

What happens when the body’s temperature is decreased?

A

the heart rate and strength decrease

190
Q

What is the preferred energy substrate for the heart?

A

FA

191
Q

What are the other energy sources the heart can use?

A

glucose, glycerol, lactate, pyruvate, amino acids

192
Q

How much energy the heart uses is turned into heat?

A

75%

193
Q

What is the other 25% of the energy used for?

A

pressurization of the blood (99%), acceleration of blood (1%)

194
Q

What kind of energy is pressurization of the blood?

A

potential energy

195
Q

What is pressurization of the blood?

A

moving blood from low pressure to high pressure

196
Q

What kind of energy is acceleration to the blood’s ejection velocity?

A

kinetic

197
Q

What does an EKG measure?

A

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

198
Q

What is the lead?

A

a pair of electrodes

199
Q

What is the axis of the lead?

A

line of connecting leads

200
Q

What is the transition line?

A

line perpendicular to the axis of the lead

201
Q

Where can leads be placed on the body?

A

right arm, left arm
right arm, left leg
left arm, left leg

202
Q

Which lead is always negative? Positive? Both?

A 
negative= Right arm
positive= left leg
both= left arm
203
Q

What does the P stand for in an EKG?

A

SA and atrial node depolarization

204
Q

What does the QRS stand for in an EKG?

A

ventricular depolarization (atrial repolarization is covered up by this)

205
Q

What does the T stand for in an EKG?

A

ventricular repolarization

206
Q

What is PR in an EKG?

A

the start of atrial and ventricular depolarization

the AV node causes the atrial and ventricular contractions to happen separately

207
Q

1 mm on an EKG is equal to how much time?

A

0.04 seconds

208
Q

What is the time frame for a healthy PR interval?

A

0.16 seconds

209
Q

What if the PR interval is greater than 0.20 seconds?

A

there is a first degree AV block

210
Q

What is the PR inteval is less than 0.10 seconds?

A

there is an inadequate delay possible from the accessory conduction pathway from atria to ventricle

211
Q

What makes an electrode positive or negative?

A

the deflection is based on what the active electrode sees relative to the reference electrode

212
Q

In a bipolar limb lead, the leads are connected to which body parts in lead I, II, and III?

A

I- left arm, right arm
II- left leg, right arm
III- left leg, left arm

213
Q

The wave of depolarization is moving toward the positive electrode. What happens to the deflection?

A

increased deflection

214
Q

The wave of repolarization is moving toward the negative electrode. What happens to the deflection?

A

increased deflection

215
Q

The wave of depolarization is moving toward the negative electrode. What happens to the deflection?

A

decreased deflection

216
Q

The wave of repolarization is moving toward the positive electrode. What happens to the deflection?

A

decreased deflection

217
Q

With a unipolar limb lead, what is positive and what is negative in an AvR?

A

+ right arm, - left arm and left leg

218
Q

With a unipolar limb lead, what is positive and what is negative with an AvL?

A

+ left arm, - right arm and left leg

219
Q

With a unipolar limb lead, what is positive and what is negative with an AvF?

A

+ left leg, -left arm and right arm

220
Q

Where do we place positive electrodes specifically?

A

V1- intercostal space, right sternal border
V2- 4th intercostal space, left sternal border
V3 equidistant between V2 and V4
V4 5th intercostal space, mid clavicular line
V5 equidistant between V4 and V6
V6 left midaxillary line

221
Q

Where is the negative electrode?

A

all limb electrodes hooked together

222
Q

What do we analyze in an EKG?

A

rate, rhythm and intervals, axis, hypertrophy, infarction

223
Q

Draw out the chart that we learned in class for heart rate

A

MM 5 10 15 20 25 30
sec .2 .4 .6 .8 1.0 1.2
HR 300 150 100 75 60 50

224
Q

What is the PR inteval?

A

time from SA node to entering the ventricle and includes AV nodal delay

225
Q

What can happen with a prolonged QT interval?

A

increased incidence of sudden caridac death

high propensity to develop ventricular fibrillation

226
Q

Describe a sinus arrhythmia

A

longest and shortest RR vary by .16 sec

heart rate variability

227
Q

What is a 1st degree AV block?

A

depolarization wave from atria to ventircle is delayed excessively (PR interval > 2 seconds

228
Q

What is a second degree AV block?

A

some depolarization waves pass, others blocked

dropped beat- P wave with no associated QRS complex

229
Q

What is a thrid AV block?

A

all depolarization waves from atria to ventricles are blocked
no relationship between P waves and QRS waves

230
Q

How long should a normal QRS complex last?

A

between .06 and .08 seconds

a prolonged one would be greater than .12 seconds

231
Q

What is a prolonged QRS wave associated with?

A

ventricularhypertrophy or conduction block in purkinje system

232
Q

What is the mean electrical axis??

A

the average of ventircular depolarization

233
Q

How does the ventricle depolarize?

A

from base to apex and from endocardium to epicardium ADIO

234
Q

What is the range for a normal axis?

A

-30 to 105 degrees

235
Q

What does it mean when there is an axis deviation?

A

conduction block and hypertrophy shift axis to the side of the problem (ex: left bundle branch block creating a left axis deviation

236
Q

What can cause hypertrophy of a ventricle?

A

anything that creates an abnormally high work load on that chamber

237
Q

What blood vessels is the myocardium supplied by?

A

coronary arteries and their branches

238
Q

Where else can cells of the heart receive blood?

A

chamber blood (endocardial cells only)

239
Q

When does the myocardium take the max oxygen out of the perfusing coronary flow?

A

resting HR (70% extraction rate

240
Q

Any ___ demand must be met by ___ coronary flow

A

increase, increase

241
Q

What can ischemia do to the depolarization and repolarization of the heart?

A

prolong depolarization and therefore delay repolarization, which can cause the waves to go in the same direction, which causes an inversion of the T wave

242
Q

What do damaged cells lose the ability to do?

A

repolarize

243
Q

When does damage to heart muscle occur and what is it associated with ?

A

damage occurs upon reperfusion and is associated with free radical damage

244
Q

How do you determine if MEA is normal?

A

If the QRS of lead I and AvF is positive

245
Q

What limits myocardial blood flow, especially in the left ventricle?

A

Contraction of cardiac muscle

Phys III Exam 1 (2 decks)

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