chpt 9: heart tings Flashcards

1
Q

what type of Ca2+ is found in the heart tings

A

cytosolic Ca2+

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2
Q

what is a prolapsed valve

A
  • backward valve
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3
Q

function of chordea tendinae

A

prevent everted valves

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4
Q

when do valves open

A

when the pressure is greater behind the valve

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5
Q

what happens when the pressure is greater in front of the valve

A

valve closed

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6
Q

what is the inflammation of the pericardial sac

A

pericarditis

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7
Q

what happens when one has pericarditis

A
  • painful friction rub b/w pericardial layers

- viral or bacterial infection

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8
Q

what is the innermost and thinnest wall of the heart that comes in contact with blood

A

endocardium/ endothelium

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9
Q

what is endocarditis

A

infection in the endocardium

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10
Q

what happens when one has endocarditis

A
  • sudden heart attack and then death
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11
Q

which heart wall layer has cardiac muscle

A

myocardium

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12
Q

which layer has intercalated discs

A

myocardium

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13
Q

desmosomes and gap junctions make up

A

intercalated discs

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14
Q

function of gap junctions

A
  • signals pass through fast
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15
Q

what type of junction is an adhering junction

A

desmosomes

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16
Q

function of desmosomes

A
  • hold cells together
  • handle mechanical stress
  • transfer signals fast without heart rupturing
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17
Q

epicardium is the

A

thin outer layer of the heart

- surrounded by pericardal sac

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18
Q

function of secretory lining of pericardial sac

A

lubricates heart

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19
Q

what allows the heart to remain properly positioned

A

tough, fibrous covering of pericardial sac

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20
Q

name of heart contracting itself

A

autorythmicity

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21
Q

which cells are 99% of cardiac muscle cells

A

contractile cells

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22
Q

do contractile cells initiate ap

A

no

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23
Q

function contractile cells

A
  • mechanical work/ pumping
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24
Q

which cardiac cells make up less than 1% of the cells and set the electrical activity/ pace of heart

A

autorythmic cells

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25
Q

do autorythmic cells contract

A

no

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26
Q

location of sinoatrial node

A

r.a, near superior vena cava

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27
Q

which node is the pacemaker of the heart than triggers contractile cells

A

SA node

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28
Q

SA node beats/ min is

A

70-80

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29
Q

which node is located at the base of R.A near septum

A

AV node

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30
Q

slient / latent pacemakers are

A

AV nodes and bundles of his and Purkinje fibers

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31
Q

what node sets the beat for 40-60 beats / min

A

AV node

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32
Q

Bundles of His location

A

originate from AV node and enter interventricular spetum

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33
Q

beats / min of Bundles of His and purkinje fibers

A

2-40

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34
Q

where does the 100 msec delay occur in the internodal pathway of excitation and why

A

AV node, to allow ventricles to fill in

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35
Q

function of interatrial spread of excitation

A
  • ensures both atria become depolarized simultaneously
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36
Q

when does a 30-sec delay occur

A
  • sa node to av node (internodal)
  • sa node to sa node (interatrail)
  • av node to bundle of his (internodal)
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37
Q

complete heart block is

A

when conducting tissue b/w atria and ventricle is damaged

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38
Q

what is dysfunctioning in complete heart block

A

SA node

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39
Q

50b/ min occur during

A

complete heart bock

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40
Q

how does one feel during complete heart block

A

long-lasting fatigue

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41
Q

when does AV node take over

A

complete heart block

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42
Q

abnormally excited area, initiates a premature ap that spreads through the heart occurs when

A

all nodes except of pf are working

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43
Q

what are the beats/ min of Pf during ectopic focus

A

140b/ min

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44
Q

when does the ventricle contract before the atria

A

ectopic focus

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45
Q

what is the resting membrane potential for pacemaker cells

A
  • 60 mV
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46
Q

slow depolarization =

A

pacemaker potential

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47
Q

when does slow depolarization b/f depolarize

A

pacemaker activity

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48
Q

what channel is activated during slight hyperpolarization

A

If (current, funny)

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49
Q

function of If

A
  • increases Na and K permeability
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50
Q

why is If also considered HCN (Hyperpolirzation- activated Cyclic Nucleotide)

A
  • cuz it is activated upon hyperpolarization
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51
Q

what causes slow depolarization

A

Ca2+ transient channels, Na and K influx, and slow closing K channels

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52
Q

what is the Ca2+ transient channels are also known as

A

t- type ca2+ channels

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53
Q

when do t- type ca2+ channels open

A
  • open at lower membrane potential

-

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54
Q

what helps cause more depolarization and helps it reach the threshold

A

Ca2+

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55
Q
  • 40mV is ___ for pacemaker activity
A

threshold

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56
Q

what is peak for pacemaker activity

A

0mV

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57
Q

function of L-type Ca2+

A
  • causes the rising phase in pacemaker activity

- bring in more Ca2+

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58
Q

what channel is slower than Na+ channeled cells

A

L-type Ca2+

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59
Q

function of K+ in pacemaker activity

A

causes repolarization

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60
Q

when is there a prolonged refractory period like ap

A
  • electrical activity in contractile cells
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61
Q

is there summation in contractile cells

A

no

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62
Q

-80 mV is the resting potential for

A

contractile cells

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63
Q

what causes the rising phase in contractile cells

A

I Na, current Na

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64
Q

+30 mV is ___ for contractile cells

A

peak

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65
Q

what causes peak/ rising phase in contractile cells

A

Na increase

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66
Q

I Ca 2+ L function in contractile cells

A

plateau, long lasting

- balance of ions in and out

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67
Q

what is the delayed rectifier

A

its the current K increase

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68
Q

what does the current K/ delayed rectifier do

A

falling phase / increase K+ efflux

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69
Q

how long is the plateau/ refractory period + function

A

250 sec, allows blood to fill in

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70
Q

Electrocargiogram function

A
  • see how the heart is behaving
  • shows entire cardiac cycle
  • record of electric activity that reaches the surface of body cuz of depolarization and repolarization
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71
Q

where are leads of ECG placed

A
  • R arm, L Arm, L leg
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72
Q

P wave is responsible for

A

atrial depolarization

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73
Q

what does p wave determine

A

rthym, rate, block

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74
Q

what refers to the AV nodal delay of 100 msec

A

PR segment

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75
Q

significance of QRS complex

A
ventricle depolarization (pump blood out) 
- mask atrial repolarization
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76
Q

what is it called when the ventricles are contracting and relaxing?

A

ST segment

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77
Q

what is a section called when contractile cells are in plateau and ventricles have completely depolarized

A

ST segment

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78
Q

T wave is

A

ventricle repolarization

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79
Q

when are ventricles relaxing and filling with blood

A

during the TP interval

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80
Q

analyzing rate is

A

determined from distance b/w 2 consquetives ORS

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81
Q

tachycardia is

A

high heart rate of more than 100 beats/ min

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82
Q

which segment is looked at to determine tachycardia

A

P to P

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83
Q

top of QRS to the next R determines

A

bradycardia

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84
Q

what is it called when the heart rate is less than 60b/ min

A

bradycardia

85
Q

what node determines the heart rate

A

SA node, cuz it has a fast rate of depolarization to threshold

86
Q

rhythm is the

A

regulating or spacing of ECG waves

87
Q

variation for normal rhythm and sequence of excitation of the heart is known as

A

arrhythmia

88
Q

heart rate for atrial flutter

A

200-380b/ min

89
Q

atrial flutter is

A

the rapid but regular sequence of atrial depolarization

90
Q

when is there no distinct P wave and ORS occurs sporadically

A

atrial fib

91
Q

what is a rapid, controlled and irregular beating/ depolarization of atria known as

A

atrial fib

92
Q

what happens to the ventricles and atrial fib

A

irregular rhythms

93
Q

why is contraction weaker in atrial fib

A

less filling occurs so contraction is weaker

94
Q

when does pulse deficit occur/ what is it

A

the difference in heart rate + pulse rate in atrial fib

95
Q

what does the ECG look like during ventricular fib

A

saw-edged

96
Q

what arrhythmia is more serious

A

Ventricular fib

97
Q

what triggers the SA node to restart and multiple impulses all over the place

A

Ventricular fib

98
Q

what happens to vital organs in ventricular fib

A

possible failure

99
Q

a block is

A

defects in cardiac conducting system where the ventricle sometimes fail

100
Q

what sequences of P: QRS does block occur in

A

2:1 or 3:1

101
Q

what does the number in P mean in heart block

A

how often impulses pass to ventricles

102
Q

what is complete heart block

A
  • complete disassociation b/w atrial and ventricular activity
103
Q

when do ventricles govern own rate at lower rate

A

complete heart block

104
Q

cardiac myopathies is

A

damage of heart muscles

105
Q

what is it called when there is an inadequate delivery of O2 blood to heart tissue

A

myocardial ischemia

106
Q

necrosis is

A

death of heart muscle cells

107
Q

what happens when a bv supplying the heart is blocked or ruptured

A

acute myocardial infraction aka heart attack

108
Q

TP is interval is ___ event of the cardiac cycle

A

diastole

109
Q

when are AV valves open and SL valves closed

A

diastole

110
Q

how much blood enters the ventricles during diastole

A

80%

111
Q

what marks the end of diastole

A

end diastole volume

112
Q

what happens to the SA node during late ventricular diastole

A
  • sa node reaches threshold and fires (P wave)
113
Q

when does 20% enter the ventricle

A

late ventricular diastole

114
Q

end of diastole / end diastolic volume does ___ to ventricle

A
  • increase pressure
115
Q

what marks the closure of AV valves

A

end of diastole / end diastolic volume

116
Q

what is end diastolic volume

A

135ml of blood in the ventricle at the end of diastole

117
Q

what is the max amount of blood that the ventricle can contain during a cycle

A

~135mL

118
Q

when does isovolumetric contraction occurs

A

after end of diastole

119
Q

when are all valves closed but the pressure in ventricles continues to increase

A

isovolumetric contraction

120
Q

how long before atrial contraction occur before ventricular contraction

A

160 msec

121
Q

at which event of the cardiac cycle is the QRS formed

A

ventricle systole

122
Q

what happens during ventricle systole

A
  • ejection of blood begins
  • ventricles empty
  • SL valves are open, AV valves are closed
123
Q

how much blood is left behind during isovolumetric ventricular relaxation

A

65mL

124
Q

when does the heart go back to normal

A

isovolumetric ventricular relaxation

125
Q

ESV/ end systolic volume is

A

65mL of blood left in the heart

126
Q

how is heart health measured

A

by cardiac output

127
Q

what is cardiac output

A

volume of blood pumped by each ventricle / min / whats happening in the heart

128
Q

how do you calculate cardiac output

A

(EVD-ESV) x heart rate

129
Q

what does it mean when 5L/ min of blood is pumped

A

normal cardiac output

130
Q

amount of blood pumped out per contraction is referred to as

A

stroke volume

131
Q

what determines stroke volume

A
  • venous system

- sympathetic activty

132
Q

what is the first heart sound thats heard at the closure of AV vlaves

A

Lub

133
Q

lub marks the

A

begning to ventricular systole

134
Q

what does lub sound like

A

longer, soft, dull

135
Q

dup is the

A
  • second heart sound
  • marks ventricular diastole
  • heart is filling w blood
136
Q

closing of ___ valves determines shart, short sound of dup

A

SL valves

137
Q

valve disfunction causes/ is known as

A

heart murmurs

138
Q

types of murmurs

A
  • stenotic
  • infufficent
  • diastolic (timing)
  • systolic (timing)
139
Q

when does a stenotic murmur occur

A
  • stiff narrowed valve due to disease
140
Q

what type of murmur creates a whistling sound

A

stenotic

141
Q

what happens to the AV valves when in stenotic murmur

A
  • blood doesnt flow forward

- valve doesnt open properly

142
Q

lub-dup- whistle is an example of

A

diastolic, stenotic flow

143
Q

when is the valve leaky, incomplete, and doesnt close properly

A
  • insufficient murmur
144
Q

what kind of sound is made during an insufficient murmur

A

swish

145
Q

lub-swish-dup is an example of

A
  • insufficient, leaky AV
146
Q

when do systolic murmurs occur

A
  • lub- murmur- dup
147
Q

lub-dup-whistle happens during

A

stenotic, av, diastolic murmurs

148
Q

an insuffienct, leaking SL valve with a diastolic murmur sounds like

A

lub-dub- swish

149
Q

stenotic, SL valve doesnt open with a systolic murumur sounds like

A

lub-whistle-dup

150
Q

what disease can causes murmurs

A

rheumatic fever

151
Q

what causes rheumatic fever

A
  • strep throat bacteria
152
Q

how does one fix a dysfunctional valve

A
  • valve replacement or death
153
Q

what happens when strep throat goes untreated

A

rheumatic fever = valves disfunction = heart attack or heart failure

154
Q

what does the para sym system secerte / vagus nerve

A

ACh

155
Q

what do muscarinic receptors receive/ respond to

A

ACh

156
Q

funcation of parasym innervation in heart

A
  • slow heart down

- decrease rhythm of SA node

157
Q

what CN supplies the para sym function of the heart

A

Vagus (CN 10)

158
Q

location of vagus nerve in parasym

A

atria and AV node

159
Q

what allows heart rate to vary activity of cAMP

A

parasym and sym

160
Q

what secretes NE or E which binds with B receptors

A

sympathetic sys

161
Q

atria and ventricles are innervated by

A

nerves from the sympathetic sys

162
Q

function of sympathetic sys in heart

A

increase:

  • stroke volume
  • heart rate
  • rythm of SA node
  • contraction of heart
  • EDV
163
Q

what brings NE or E into the heart to do work

A

increased EDV

164
Q

extrinsic factors that influence the heart are

A
  • sympathetic sys stimulation

- increased E that contracts heart

165
Q

intrinsic factors that influence the heart are

A

increase Sv by increasing contraction of heart

- increased EDV which bring in NE or E

166
Q

what does the frank starling law of heart state

A
  • increasing diastolic filling = increasing EDV and the heart is then more stretched = increased SV
167
Q

heart failure is

A

inability of CO to keep pace with bodys demand of supplies and waste removal

168
Q

what does the frank straking curve look like in a prime defect

A

shift right and downwards

169
Q

decreased cardiac contractility and less SV being pumped occurs during

A

prime defect

170
Q

how does one compensate for heart failure

A
  • sympathetic system increases activity for a limited time

- kidneys retain extra salt and water

171
Q

why do kidneys retain extra salt and water to compensate for heart failure

A
  • expand bv
  • increase EDV to stretch cardiac muscles
  • to increase SV
172
Q

what is forward failure

A

heart fails to pump an adequate amount of blood forward

173
Q

why does forward failure occur

A

cuz SV is small

174
Q

what is it called when blood and enters and is pumped out and the venous sys dams up

A

backward/ congestive heart failure

175
Q

which side of the heart will it worse to get any kind of heart problems

A

left side

176
Q

how much O2 does the heart use at rest

A

65% available

177
Q

when is most of the O2 received

A

during diastole

178
Q

why is most of the blood received during diastole

A
  • the heart is compressed during systole

- aortic valve partially blocks entrance of coronary valve

179
Q

function of adenosine in the heart

A

helps move blood, causes vasodilation of vv

180
Q

what kinda of chemical messanger system does adenosine use

A

paracrine signals

181
Q

what causes coronary artery disease

A

changes within the ca that prevent blood from getting through coronary vessels

182
Q

myocardial ischemia and heart attacks are the results of

A

coronary artery disease

183
Q

how does coronary artery disease occur

A
  • profound vascular spasm of ca
  • formation of atherosclerotic plaque
  • thromboemolidm
184
Q

how does one fix cornonary artery disease

A
  • digitalis
  • verampil
  • nitroglycerin
185
Q

how common are heart attacks in canada

A

32p of pop die fromthem

186
Q

function verapamil

A
  • Ca2+ channel blocking agent
187
Q

function of digitalis

A

increase cardiac contractility by inducing accumulation of cytosolic ca

188
Q

function of nitroglycerin

A
  • allows coronary dilation

- relaxes vascular smooth muscles

189
Q

what is the first indicator of coronary artery disease

A

profound vascular spasm of ca

190
Q

how is profound vascular spasm of ca reversible

A
  • diet and exercise
191
Q

what causes when one has profound vascular spasm of ca

A

decreased O2 which leads to platelet activary factor (spasms)

192
Q

what is the first stage of the formation of atherosclerotic plaque

A
  • inflammatory response and oxidized LDL
193
Q

waht is formation of atherosclerotic plaque

A

plaque forming in chain rxns

194
Q

what else causes plaque forming in chain rxns

A
  • BP

- free radical bacteria and virsues

195
Q

what does oxidized LDL attract

A

phagocyte and monoctyes

196
Q

what becomes large macrophages that consume oxidized LDL

A

monocytes

197
Q

whats triggers the inflammatory response and what does it set up

A
  • injury to bv that sets up formation of plaque

-

198
Q

eating of LDL forms

A

foam cells and fatty strands that smooth muscles gather around

199
Q

smooth muscles gathering around form

A

Benin tumor or atheromas which forms plaque

200
Q

how does plaque block blood flow

A

unit with Ca+ and it hardens

201
Q

what is Angina Pectoris

A

chest pain felt on the left side (arm and shoulder)

202
Q

what cuases Angina Pectoris

A

reduced blood flow and O2

203
Q

drugs (glycerin) and rest can reverse

A

Angina Pectoris

204
Q

what happens when plaque breaks away

A

it forms a clot (thrombosis) which moves around and blocks vessels (embolism)

205
Q

why is it so dangerous for an embolism to be a bit above the left coronary artery

A

85p of blood comes there from the heart

206
Q

what is immediate death

A
  • acute cardiac failure
207
Q

what causes immediate death

A

the heart is too weak to pump effectively to support body tissues

208
Q
  • fatal rupture of death caused by degenerating area of heart is known as
  • slowly progressive
A

delayed death from complications

209
Q

fatal ventricular fibrillation brought by oxygen deprived heart causes

A

immediate death