Questions Flashcards
1
Q
What is the number 1 cause of death?
A
cardiovascular disease
2
Q
What is the major underlying cause of cardiovascular disease?
A
ischemia due to atherosclerosis, white thrombus, red thrombus or artery spasm
3
Q
What is the link to atherogenesis?
A
high blood cholesterol and inflammatory mechanisms
4
Q
What characterizes early atherogenesis?
A
leukocyte recruitment and expression of proinflammatory cytokines
5
Q
What promotes inflammatory pathways and is responsible for most MIs and strokes?
A
thrombosis
6
Q
What can modulate inflammation?
A
nervous system
7
Q
Define hemostasis.
A
prevention of blood loss
8
Q
What are the mechanisms of hemostasis?
A
vascular spasm, formation of a platelet plug, blood coagulation, fibrous tissue growth to seal
9
Q
What is vascular constriction associated with?
A
trauma
10
Q
What can cause vascular constriction?
A
neural reflexes, local myogenic spasm, local humoral factors
11
Q
What is responsible for most vascular constriction?
A
local myogenic spasm
12
Q
What are local humoral factors?
A
thromboxane A2 from platelets
13
Q
What type of vascular constriction is important for small blood vessels?
A
local humoral factors
14
Q
How does neural reflex work for vascular constriction?
A
the sympathetic nervous system induces constriction because of pain
15
Q
True or false: platelets function as whole cells, including being able to divide
A
False
16
Q
What do platelets contain?
A
contractile proteins (actin and myosin), enzymes, calcium, ADP, ATP, thromboxane A2, serotonin and growth factors
17
Q
What do platelet cell membranes contain?
A
glycoproteins and phospholipids containing platelet factor 3
18
Q
What is thromboplastin?
A
a phospholipid containing platelet factor 3 that initates blood coagulation
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
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
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
22
Q
What is the half life of platelets?
A
8-12 days
23
Q
How are platelets eliminated?
A
mostly by macrophage action
24
Q
What does the endothelial wall produce and prevent?
A
prevents platelet aggregation
produces prostacyclin (PG12) and factor VIII
25
What does prostacyclin do?
it is a vasodilator, stimulates platelet adenylcyclase and inhibits platelet degranulation
26
When platelet adenyl cyclase is activated, what does it do?
supresses release of granules
27
What is the pathway to create thromboxane A2?
phospholipid --lipase--> ARA --FA cyclooxygenase--> PGG PHG --thromboxane synthetase--> Thromboxane A2
28
What is the pathway to create prostacyclin?
phospholipid --lipase--> ARA --FA cyclooxygenase--> PGG PHG --prostacyclin synthetase--> prostacyclin
29
What do aspirin and ibprofen do?
block thromboxane A2 and prostacyclin prodution by blocking FA cyclooxygenase which in turn converts ARA to PGG and PGH (intermediates
30
Why take aspirin to prevent heart attacks?
to block platelet function
31
What do anticoagulants do?
prevent clots from forming
32
How do anticoagulants prevent clots from forming?
they use chelators (tie up calcium), heparin (complexes with antithrombin IIII) and dicumarol (inhibits vitamin K dependent factors
33
What are the factors that are synthesized by hepatocytes?
II, VII, IX and X
34
Where are endogenous activators found?
tissues, plasma and urine
35
What are the exogenous activators of plasminogen?
streptokinase and tissue plasminogen activator
36
What is reperfusion injury associated with?
formation of highly reactive oxygen species with unpaired electrons
37
When are free radicals generated?
when pressure on tissues is relieved and again perfused with blood
38
What is collateralization?
the ability to open up alternate routes of blood flow to compensate for a blocked vessel
39
What are the types of collateralization?
angiogenesis and vasodilation
40
What is the role of the sympathetic nervous system on collateralization?
may impede via vasoconstriction, may augment via release of neuropepetide Y
41
What is the extrinsic mechanism for thrombosis?
initiated by chemical factors released by damaged tissues
42
What is the intrinsic mechanism for thrombosis?
requires only components in blood and trauma to blood or exposure to collagen
43
What are the names of the clotting factors we need to know?
fibrinogen, prothrombin, thromboplastin, calcium
44
What organ is key in clotting?
liver
45
What are the 5 clotting factors that are synthesized in the liver?
fibrinogen, prothrombin, SPCA, AHF B, stuart factor
46
What does coumarin do?
depresses liverformation of II, VII, IX and X by blocking action of vitamin K
47
What is hemophilia?
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)
48
Which steps of blood coagulation have calcium?
all but the first two steps
49
When the extrinsic and intrinsic factors merge, what happens?
it activates factor V and X and prothrombin to thrombin
50
What is needed to activate factors IX and X?
calcium
51
What are the final commonsteps of fibrin (polymer)?
fibrinogen + thrombin --> fibrin (monomer) + activated factor XIII
52
What breaks down the mesh (fibrinogen)?
plasmin
53
What is antiphospholipid antibody syndrome?
an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes which cause abnormal clots to form
54
What are some risk factors for heart disease?
```
increasing age
male gender
heredity (race included)
tobacco smoker
high cholesterol
high blood pressure
physical inactivity
obesity/overweight
diabetes mellitus
high blood homocysteine
```
55
What is homocysteine?
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
56
What are the agglutinogens (surface markers) that are found on each of the blood types?
O- none
A- A
B- B
AB- A and B
57
What are the agglutins (soluble antibodies) that are found on each of the blood types?
O- anti A and B
A- Anti B
B- Anti A
AB- none
58
When are agglutinins produced?
after birth, arising spontaneously
59
When are antibody titers peak?
around 10 years old
60
Which blood types have anti A sera?
A, AB
61
Which blood types have anti B sera?
B, AB
62
Which blood type has neither seras?
O
63
How does the body lyse RBC when the wrong blood type is given?
antibodies (primarily IgM) cause kysis of RBCs by activating the compliment system which releases proetolytic enzymes rupturing cells membrane
64
What is the most lethal effect of a transfusion reaction?
kidney failure
65
Why is kidney failure associated with a transfusion reaction?
toxic substances are released from hemolysed RBCs, which causes circulatory shock, the hemoglobin from lysed RBCs preceipitates and blocks renal tubules
66
What are the 6 common Rh antigens?
C, D, E, c, d, e
67
Can a person with D Rh factor have d as well?
no
68
Which Rh factor is the most common?
D
69
Whathappens when Rh+ RBCs are infused into a person who has Rh-?
it stimulates the production of anti-Rh antibodies which develop slowly and reach maximum concentrations 2-4 months later
70
What is Heolytic disease of the newborn?
agglutination and hemolysis of the fetus' RBCs by the mother's anti Rh agglutinins, which can cause jaundice in the fetus
71
How does hemolytic disease of the newborn occur?
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.
72
When do we usually see hemolytic disease of the newborn?
Usually during the second or third pregnancy
73
What is erythroblastosis fetalis?
when the mother's agglutinins circulate in the fetus after birth and destroy RBCs, causing anemia
74
What are some side effects of erythroblastosis fetalis?
bilirubin might precipitate in neurons of the brain causing mental impairment (kernicterus)
this causes enlargement of the liver and spleen of the baby
75
What is the treatment of erythroblastosis fetalis?
replace the neonate's blood with rh- blood
76
How can one prevent erythroblastosis fetalis?
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
77
What do cardiac muscle cells look like?
long, striated and grouped in irregular anastomosing columns with 1-2 centrally located nuclei
78
What are SA node, AV node and Purkinje fibers generally?
specialized excitatory and conductive muscle fibers
79
Define syncytium
many acting as one
80
Why is there a syncytial nature of cardiac muscle?
because of the presence of intercalated discs
this makes low resistance pathways connecting cardiac cells end to end
there are also gap junctions
81
What is the duration of a cardiac action potential (AP)?
.2-.3 seconds
82
What are the channels that allow AP in cardiac muscle?
fast Na+
slow Ca2+/Na+
K+
83
Describe the permeability changes of sodium, calcium and potassium in the cardiac muscle.
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
84
When is the conductance for potassium greatest?
during the resting polarized state
85
What kind of channels does the SA node have? Why?
only slow CA2+/na+ to increase the depolarization time
86
What kind of channels does the typical cardiac cell have?
both fast Na+ and slowCa2+/Na+ channels
87
What does tetradotoxin do?
blocks fast Na+ channels selectively changing a fast response into a slow response
88
What must we also consider when the channels are open?
the concentration gradient, electrical gradient and the membrane permeability
89
What will ions seek if the ion channels are open?
Nernst equilibrium potential
90
What is the Nernst equilibrium potential?
when the concentration gradient favoring ion movement in one direction is offset by the electrical gradient
91
What happens during the resting membrane potential?
fast Na+ and slow Ca2+/Na+ channels are closed and K+ channels are open. Therefore, K+ ions are free to move
92
When is a stable Er maintained?
when K+ reaches the Nernst equilibrium potential
93
Is the Na+/K+ pump energy dependent?
yes
94
Why is the ratio of Na+ and K+ 3:2, respctively?
there is a net loss of one + charge from the interior each cycle, which helps the interior of the cell remain negative
95
what does the protein pump utilize?
energy from ATP
96
What binds to and inhibits the Na+/K+ pump?
digitalis
97
What happens to the cardiac cell membrane protein when the Na+/K+ pump is inhibited?
the function of the exchange protein is reduced and more Ca2+ is allowerd to accumulate in the cardiac cell increases contractile strength
98
Describe the absolute refractory period.
it is unable to re-stimulate the cardiac cell and occurs during the plateau of the AP
99
Describe the relative refractory period.
requires a supra-normal stimulus and occurs during repolarization of the AP
100
Can you stimulate a cardiac cell during absolute refractory period?
no
101
How would you describe the relative refractory period in a slow response?
the relative refractory period is prolonged and the refractory period is about 25% longer
102
What is the function of the the AV node and bundle?
to protect the ventricles from supra-ventricular arrhythmias
103
How do SA nodes have a self excitatory nature?
```
less negative Er
leaky membrane to Na+/Ca2+
only slow Ca2+/Na+ channels operational
spontaneously depolarizes at fastest rate
contracts feebly
```
104
What is different about the AP for an SA node compared to a cardiac cell AP?
the SA node has no stable resting polarized state
105
What is overdrive suppression?
when you drive a self-excitatory cell at a rate faster than its own inherent rate
106
What is the mechanism behind overdrive suppression?
increased activity of the Na+/K+ pump creating a more negative Er
107
What is an example of overdrive suppression normally found in the heart?
the AV node and purkinje system are under overdrive suppression by the SA node
108
What is the function of the AV node?
delays the wave of depolarization from entering the ventricle, which allows the atria to contract slightly before the ventricles
109
What can act as an SA node if the SA node isn't present?
the AV node, but it is slower than the SA node would be
110
As the heart rate ____, cycle length ____
increases, decreases
111
Which is higher at resting heart rate: systole or diastole?
diastole
112
What happens to the duration of systole and diastole as the heart rate increases?
both get shorter, but diastole shortens to a greater extent
113
When is left coronary artery pressure peaked?
at the beginning of diastole
114
When is right coronary artery pressure peaked?
in the middle of systole
115
What happens when there an increase in potassium efflux?
increased heart rate
116
What happens when there is a decrease in potassium efflux?
decreased heart rate
117
What happens when there is a decreased influx of Na/Ca?
decreased heart rate
118
What happens when there is an increased influx of Na/Ca?
heart rate increases
119
When there is an increase in potassium efflux and an increase in Na/Ca influx, what happens?
there isno net change in the AP
120
What happens during systole?
isovolumic contraction of the ventricle and ejection of blood
121
What happens during diastole?
isovolumic relaxation of theventricle, rapid inflow (70-75%), diastasis, and atrial systole (25-30%)
122
What is end diastolic volume (EDV)?
volume in ventricles at the end of filling
123
What is end systolic volume (ESV)?
volume in ventricles at the end of ejection
124
What is stroke volume (SV)?
volume ejected by ventricles
125
What is the ejection fraction?
% of EDV ejected (SV/EDV X 100%)
| normal is 50-60%
126
If someone had an EDV of 300 and an ESV of 150, what is their ejection fraction? Is this normal?
300 - 150 = 150
150/300 = 50%
Yes, this is a normal ejection fraction
127
Define preload.
stretch on the wall prior to contraction (proportional to the EDV)
128
Define afterload.
the changing resistance (impedance) that the heart has to pump against as blood is ejected
129
What is an A wave?
it is a wave associated with atrial contraction
130
What is a C wave?
it is a wave associated with ventricular contraction, specifically bulging of AV valves and tugging on atrial muscle)
131
What is a V wave?
a wave associated with atrial filling
132
Draw the atrial pressure wave graph created in class and label all of the important points on the graph.
Try to understand exactly what that graph is saying.
133
What is the function of the valves?
to open with a forward pressure gradient and close with a backward pressure gradient
134
Give an example of a forward pressure gradient (draw the schematic if necessary).
when the left ventricular pressure is greater than the aortic pressure, the aortic valve is open
135
Give an example of a backward pressure gradient (draw the schematic if necessary).
when the aortic pressure is greater than the left ventricular pressure, the aortic valve is closed
136
What is a forward pressure gradient also known as?
systole
137
What is a backward pressure gradient also known as?
diastole
138
What is it called when both the aortic and mitral valve are closed and the left ventricular pressure is rising?
isovolumic contraction
139
What is it called when both aortic and mitral valve are closed and the left ventricular pressure is decreasing?
isovolumic relaxation
140
What is a jugular pulse?
right atrial pressure release
141
Describe the mitral and tricuspid valve.
thin and filmy, have corda tendinae that act as check lines to prevent prolapse, have papillary muscles to increase tension on chorda tendinae
142
Describe the pulmonic and aortic valves.
stronger construction
143
Define stenosis.
when the valve doesn't open fully
144
Define insufficiency when related to valves.
when the valve doesn't fully close
145
What is the vibrational noise created by either a stenosis or insufficiency?
murmur
146
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?
mitral stenosis, aortic insufficiency
147
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?
tricuspid stenosis, pulmonary insufficiency
148
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?
mitral insufficiency, aortic stenosis
149
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?
tricuspid insufficiency, pulmonary stenosis
150
At a given operating pressure, as ventricular radius increases, developed wall tension ____?
increases
151
What happens to the force of the ventricular contraction when the tension is increased?
the force also increases
152
How does the law of laplace explain how capillaries can withstand high intravascular pressure?
the small radius makes it easier on the vessels so there's not so much wall tension
153
Define cronotropic.
anything that affects heart rate
154
What are some examples of something that could be +cronotropic?
caffeine, NE
155
Define dromotropic
anything that affects conduction velocity
156
What are some examples of something that could be + dromotropic?
NE
157
Define inotropic.
anything that affects the strength of contraction
158
What is an example of something that could be +inotropic?
caffeine, NE
159
What is the Frank-Starling Law of the Heart?
within physiologic limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in the veins
160
What is the mechanism behind the Frank-Starling Law of the Heart?
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
When cardiac fibers are stretched beyond their limit, what happens?
the cross bridges become smaller, the less the cross bridge, the less calcium that can influx
162
What is homeometric autoregulation?
the ability to increase strength of contraction independent of a length change
163
During homeometric autoregulation, when is flow induced?
when the increased stroke volume is maintained even as the EDV decreases back to its initial levels (ESV also decreases)
164
During homeometric autoregulation, when is pressure induced?
when an increase in aortic BP will increase the force of the left ventricular contraction
165
During homeometric autoregulation, when is rate induced?
when increased heart rate (decreased cycle length) increases force "treppe"
166
Why can ESV also decrease when flow is induced?
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
What happens when there is direct stretch on the SA node?
increases calcium and/or sodium permeability which will increase heart rate
168
What are some extrinsic influcences on the heart?
autonomic nervous system, hormonal influences, ionic influences, temperature influences
169
When sympathetics control the heart, what is true?
+ cronotropic
+inotropic
+ dronotropic
170
When parasympathetics control the heart, what is true?
- cronotropic
- inotropic
- dronotropic
171
How is the SNS blocked from the heart?
with propranolol (a beta blocker) which blocks beta receptors
172
How is the PSNS blocked from the heart?
with atropine which blocks muscarinic receptors, which with increase heart rate, butdecrease strength of contraction
173
Parasympathetic NS exerts a _______ _______ influence on heart rate while sympathetic NS exerts a ______ ______ influence.
dominant inhibitory
| dominant stimulatory
174
What accounts for most of the SNS effect on the heart?
direct innervation
175
What causes indirect effects of the SNS on the heart?
catecholamines (epinephrine, NE) from the adrenal medulla in the blood
176
When you stimulate the left stellate ganglion of the SNS, what happens to the heart?
decrease in ventricular fibrillation threshold
| prolonged QT interval
177
When you stimulate the right stellate ganglion of the SNS, what happens to the heart?
increased ventricular fibrillation threshold
178
What is the cardioaccelerator reflex?
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
What is the purpose of the cardioaccelerator reflex?
to prevent damming of blood in the heart and central veins
180
What is the benzold-Jarisch reflex?
stimulation of the sensory endings mainly in the ventricles that reflex via CN X to the CNS
181
What is the Benzold-Jarisch reflex stimulated by?
occlusion of the circumflex artery
| increase in left ventricular pressure and left ventricular volume (like in aortic stenosis)
182
What do thyroid hormones do to the heart?
+ inotropic
+ chronotropic
causes an increase in CO by increasing basal metabolic rate
183
What is the effect of increased potassium on the heart?
dilation and flaccidity of the cardiac muscle at concentrations 2-3X normal
decreases resting membrane potential
184
What is the effect of increased calcium on the heart?
spastic contraction
185
What does the Benzold-Jarisch reflex result in?
hypotension and bradycardia (which would eventually cause you to pass out)
186
Norepinephrine has an affinity for what?
alpha and beta receptors
187
Epinephrine has an affinity for what?
beta receptors
188
What happens when the body has a fever?
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
What happens when the body's temperature is decreased?
the heart rate and strength decrease
190
What is the preferred energy substrate for the heart?
FA
191
What are the other energy sources the heart can use?
glucose, glycerol, lactate, pyruvate, amino acids
192
How much energy the heart uses is turned into heat?
75%
193
What is the other 25% of the energy used for?
pressurization of the blood (99%), acceleration of blood (1%)
194
What kind of energy is pressurization of the blood?
potential energy
195
What is pressurization of the blood?
moving blood from low pressure to high pressure
196
What kind of energy is acceleration to the blood's ejection velocity?
kinetic
197
What does an EKG measure?
potential difference across the surface of the myocardium with respect to time
198
What is the lead?
a pair of electrodes
199
What is the axis of the lead?
line of connecting leads
200
What is the transition line?
line perpendicular to the axis of the lead
201
Where can leads be placed on the body?
right arm, left arm
right arm, left leg
left arm, left leg
202
Which lead is always negative? Positive? Both?
```
negative= Right arm
positive= left leg
both= left arm
```
203
What does the P stand for in an EKG?
SA and atrial node depolarization
204
What does the QRS stand for in an EKG?
ventricular depolarization (atrial repolarization is covered up by this)
205
What does the T stand for in an EKG?
ventricular repolarization
206
What is PR in an EKG?
the start of atrial and ventricular depolarization
| the AV node causes the atrial and ventricular contractions to happen separately
207
1 mm on an EKG is equal to how much time?
0.04 seconds
208
What is the time frame for a healthy PR interval?
0.16 seconds
209
What if the PR interval is greater than 0.20 seconds?
there is a first degree AV block
210
What is the PR inteval is less than 0.10 seconds?
there is an inadequate delay possible from the accessory conduction pathway from atria to ventricle
211
What makes an electrode positive or negative?
the deflection is based on what the active electrode sees relative to the reference electrode
212
In a bipolar limb lead, the leads are connected to which body parts in lead I, II, and III?
I- left arm, right arm
II- left leg, right arm
III- left leg, left arm
213
The wave of depolarization is moving toward the positive electrode. What happens to the deflection?
increased deflection
214
The wave of repolarization is moving toward the negative electrode. What happens to the deflection?
increased deflection
215
The wave of depolarization is moving toward the negative electrode. What happens to the deflection?
decreased deflection
216
The wave of repolarization is moving toward the positive electrode. What happens to the deflection?
decreased deflection
217
With a unipolar limb lead, what is positive and what is negative in an AvR?
+ right arm, - left arm and left leg
218
With a unipolar limb lead, what is positive and what is negative with an AvL?
+ left arm, - right arm and left leg
219
With a unipolar limb lead, what is positive and what is negative with an AvF?
+ left leg, -left arm and right arm
220
Where do we place positive electrodes specifically?
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
Where is the negative electrode?
all limb electrodes hooked together
222
What do we analyze in an EKG?
rate, rhythm and intervals, axis, hypertrophy, infarction
223
Draw out the chart that we learned in class for heart rate
MM 5 10 15 20 25 30
sec .2 .4 .6 .8 1.0 1.2
HR 300 150 100 75 60 50
224
What is the PR inteval?
time from SA node to entering the ventricle and includes AV nodal delay
225
What can happen with a prolonged QT interval?
increased incidence of sudden caridac death
| high propensity to develop ventricular fibrillation
226
Describe a sinus arrhythmia
longest and shortest RR vary by .16 sec
| heart rate variability
227
What is a 1st degree AV block?
depolarization wave from atria to ventircle is delayed excessively (PR interval > 2 seconds
228
What is a second degree AV block?
some depolarization waves pass, others blocked
| dropped beat- P wave with no associated QRS complex
229
What is a thrid AV block?
all depolarization waves from atria to ventricles are blocked
no relationship between P waves and QRS waves
230
How long should a normal QRS complex last?
between .06 and .08 seconds
| a prolonged one would be greater than .12 seconds
231
What is a prolonged QRS wave associated with?
ventricularhypertrophy or conduction block in purkinje system
232
What is the mean electrical axis??
the average of ventircular depolarization
233
How does the ventricle depolarize?
from base to apex and from endocardium to epicardium ADIO
234
What is the range for a normal axis?
-30 to 105 degrees
235
What does it mean when there is an axis deviation?
conduction block and hypertrophy shift axis to the side of the problem (ex: left bundle branch block creating a left axis deviation
236
What can cause hypertrophy of a ventricle?
anything that creates an abnormally high work load on that chamber
237
What blood vessels is the myocardium supplied by?
coronary arteries and their branches
238
Where else can cells of the heart receive blood?
chamber blood (endocardial cells only)
239
When does the myocardium take the max oxygen out of the perfusing coronary flow?
resting HR (70% extraction rate
240
Any ___ demand must be met by ___ coronary flow
increase, increase
241
What can ischemia do to the depolarization and repolarization of the heart?
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
What do damaged cells lose the ability to do?
repolarize
243
When does damage to heart muscle occur and what is it associated with ?
damage occurs upon reperfusion and is associated with free radical damage
244
How do you determine if MEA is normal?
If the QRS of lead I and AvF is positive
245
What limits myocardial blood flow, especially in the left ventricle?
Contraction of cardiac muscle
