Exam 1 Flashcards
(169 cards)
1
Q
1 cause of death
A
Cardiovascular disease
2
Q
Name two major cause to cardiac ischemia
A
atherosclerosis and artery spasm
3
Q
white thrombus and red throumbus are also known as what?
A
- white- platelet plug
- red- RBC clot
4
Q
high blood cholesterol is related to ?
A
atherogenesis
5
Q
what characterizes early atherogenesis
A
leukocyte recruitment and expression of proinflammatory cytokines
6
Q
inflammatory pathways promote what?
A
thrombosis
7
Q
Name mechanisms of hemostasis
A
- vascular spasm
- formation of platelet plug
- blood coagulation
- fibrous tissue growth to seal
8
Q
How is vascular constriciton associated with trauma
A
- neural reflexes ( SNS induced from pain)
- local myogenic spasm ( most constriction)
- local humoral factors ( thromboxame A2)
9
Q
the degree of spasm is what to the severity of the trauma
A
parallel
10
Q
platelets contain
A
contractile protiens enzymes calcium ATP Thromboxane A2 serotonin GF
specifically in cell membrane: glycoprotiens (recognize damaged areas), platelet factor 3( (aka thromboplastin) initiates clotting)
11
Q
mechanisms of platelet activation
A
1) swell
2) activate- get spiky
3) contract- releasing granules
4) secrete ADP, Thromboxane A2 ( constriction), serotonin ( constriction)
12
Q
Function of thromboxane A2
A
vasoconstriction and aids in release of granule from platelets
13
Q
platelets important in ______ ruptures
A
minute
14
Q
lack of platelets cause___
A
petekia
15
Q
platelets eliminated by ?
A
macrophage action
16
Q
What is the role of endothelium in homeostasis of blood
A
- prevents platelet aggregation
- produces PGI2( prostacyclin)
- produces factor VIII( clotting)
17
Q
PGI2 functions are?
A
- vasodilator
- –> platelet adenyl cyclase —–I release of granlules
- limits platelet extension
18
Q
Aspririn and Ibuprofen block prostacyclin and thromboxane A2, how?
A
blocks cox enzyme
19
Q
some nsaids inhibit cox enxymes. what happens when cox 1 is inhibited? cox 2?
A
- cox 1 - decreased thomboxane A2
- cox 2- decreased PGI2
20
Q
Anticoagulants vs Lysis of clots
A
- anticoagulants- prevents clots, tye up calcium
- lysis of clots- dissolves existing clots, plasmin
21
Q
precursor for plasmin
A
plasminogen( circulates blood)
22
Q
endogenous activators of plaminogen are found in
A
tissues , plasma urine
23
Q
exogenous activators of plaminogen
A
streptokinase, tpa ( tissue plasminogen activator)
24
Q
How is reperfusion damaging to tissues
A
free radicles
25
whats the role of SNS in collaterization
vasoconstriciton and release of neropeptide Y (NYP)-angiogensis
26
extrinsic mechanism of blood coagulation initiated by?
chemical factors released by damaged tissues
27
intrinsic mechanism of blood coagulation initiated by
components in blood and trauma to blood or exposure of collogen
28
name four Clotting factors
- fibrinogen
- prothombin
- thromboplastin
- clacium
29
What is the livers role in clotting
makes 5 clotting factors( fibrinogen, prothrombin). Needs vit K
30
what does coumarin do
inhibits formation of clotting factors in liver by blocking vit K
31
Hemophilia: AKA, mostly in who
Bleeders, males
32
what factors are affected in hemophilia
factor 8(mc) and 9.
33
what ion is needes for blood coagulation
Ca++
34
Fibrinogen -----?-------> Figrin monomer (soluble)
thrombin
35
factor 13-------?-------> activated factor 13
thrombin
36
fibrin monomer------?-----> fibrin polymer ( insouluble)
activated factor 13
37
what happens in Antiphospholipid antibody syndorme
autoimmune, antibodies attack phopholipids, cause abnormal clots
38
risk factors for heart disease
increasing age, male, heredity, tobacco smoke, high blood pressure, high blood cholesterol, not active, over weight, diabetes mellitus, high blood homocysteine
39
what can homocysteine do?
promote atherosclerosis
oxidize cholesterol into LDL
make blood more likely to clot
40
antigens that are likely to cause reactions in blood transfusion if mismatched
O A B
| Rh
41
A and B surface antigens are known as
Agglutinogens
42
agglutinogens vs agglutinins
aggyltinogens- surgace antigens
agglutinins-soluble antibodies ( anti)
43
which blood type is the best donor?
O
44
which blood type is the best reciver?
AB
45
hemolysis in mismatched transfusion happen immediate and delayed. which is most common
delayed
46
what is the most lethal effect of a transfusion reaction
- kidney failure
| - RBC substances when lysed are toxic, hemoglobin ------blocks renal tubes
47
6 common Rh antigens, which is most common
- D
- Rh+= got the D
- Rh-= dont got the D
48
what happens to a person exposed to Rh+ who is Rh-
they make anti Rh antiboides.
| second exposure will have strong hemolysis reaction
49
what is erthroblastosis fetalis
- agglutination and hemolysis o fetus RBCs by mothers anti Rh agglutinins
- can casue jaundice
50
treatment for erthroblastosis fetalis
replace neonates blood with Rh blood
51
prevention for erthroblastosis fetalis
RhoGAM is given to Mother 28-30 weeks of gestation.it is an anti D antibody
52
heart cells are
striated, 1-2 nuclei
53
define syncytium
many acting as one
54
how can the hear act as an syncytium
intercalated discs
55
excitation-contraction coupling is due to what
Ca++
56
AP from 1st atrial cell (SA node)to last ventricular cell will take how long
.22 secs
57
how does the AV node contribute to the heart contraction
is slows the AP down to allow atria to contract
58
fast channels
na
59
slow channels
na and ca
60
what are the permeability changes
- na- sharp increase at onset of depo
- ca- increased at plateau
- k- increased during resting polarized state
61
the SA nodes uses what channels
slow ca/na
62
tetradotoxin blocks what channels
fast, changes fast response to a slow response
63
during Er( resting membrane potential) what channels are open which are closed
- fast na- closed
- slow ca/na-closed
- K- open
64
what will cause inhibition of the NA/K pump. result?
Digitalis --->increased ca++ = stronger contraction
65
how is ca tied to the NA/ K pump
Ca is pumped out when NA diffuses into the cell
66
what refractory period is unable to re-stimulate cardiac cell and occurs during the platue
absolute refractory period
67
what refractory period requires a supra normal stimulus and occurs during reporlarization
relative
68
in what type of response cardiac muscle cell is the relative refractory period is prolonged.
slow response
69
what protects the ventricles from supra-ventricular arrhythmias
av node and bundle
70
what is the normal pacemaker of the heart?
SA node
71
why is the SA node self exititory
- less negative Er
- leaky membrane to na and ca
- only slow ca/na channels
- no plateau
- spontaneously depolarizes at fastest rate
- contracts feebly
72
does the SA node have a stable Er
NOPE
73
what can change the repolarization rate
```
K eflux (parasympathetic)
-less =short
- more = longer
na /ca permeability (sympathetic)
-more leaky= shorter
-less leaky= longer
```
74
what cells are under overdrive suppression
AV node and purkinje system by the SA node
75
how does the AV node delay depolarization
smaller diameter fibers
76
as HR increases cycle length does what?
decreases
77
at rest is systole greater than or less than diastole
less than
78
what phase(systole or diastole) is effected most when HR is increased
diastole
79
cardiac output (CO) is calculated by what
HR*strove volume
80
T or F pressure is nonproportion to volume and wall tone
false
81
which ventricle is the most variable in pressure
left
82
normal ejection fraction at rest is what
50-60%
83
define EDV and ESV
- End diastolic volume- volume at end of filling(max)
| - End systolic volume- volume in ventricles at end of ejection(min)
84
define preload. what is is proportional too
stretch on wall prior to contraction. proportional to EDV
85
define afterload
changing resistance that the heart has to pump against as blood is ejected
86
Atrial pressure waves are A, C, V what is each associated with?
A- atrial contraction
C- ventricular contraction
V- atrial filling
87
valvular dysfunction can be either stenotic, insufficient, or murmuring. what do these mean
- stenotic- not opening fully
- insufficient- not closing fully
- murmur- vibration noise
88
what heart murmur happen during the pulse ( systolic)
- aortic and pulmonary stenosis
| - mitral and tricuspid insufficiency
89
what heart murmur happen after the pulse ( diastolic)
- aortic and pulmonary insufficiency
| - mitral and tricuspid stenosis
90
what is law of laplace
as radius increases, wall tension increases at a given pressure
wall tension = (pressure * radius)/2
91
chronotropic affects what
HR
92
Dromotropic affects what
conduction velocity
93
Inotropic affects what
strength of contraction
94
what is the frank-starling law of the heart
heart will pump blood that returns to it without allowing excessive damming of blood in veins
95
Venous returen is equal to?
Cardiac out put
96
With mechanisms of Frank straling what is increased when venous return is increased
- cross bridge formation
- calcium influx
- stretch on sa node
97
In homeiometric auto regulation, the ability to increase strength of contraction independent or dependent of a length change
independent
98
how are flow, pressure and rate of the heart affected in homeiometric auto regulation
they are all increased
99
What is treppe related to in homeometric autoregulation
increased heart rate.( increased IPS)
100
what will direct stretch on SA node do?
increase Ca and/or na permability---> increased HR
101
what extrinsic influences will increased HR
- autonomic
- hormonal influences
- Ionic influences
- temperature influences
102
how would SNS effects on the heart be blocked
Propranolol (Beta Blocker)
103
how would Para effects on the heart be blocked
atropine ( muscarinic blocker)
104
Over all what has a dominate inhibitory influence on HR
Parasymp
105
over all what has a dominate stimulatory influence on strength of contraction
SNS
106
SNS directly affects the heart by
Norepinephrine
107
SNS indirectly affects the heart by
circulating catacholamines
108
SNS stimulation of the left stellate ganglion causes what
- decreased ventricular fibrillation threshold ( more likely to go into v fib)
- prolongation of the QT interval
109
SNS stimulation fo the reight stellate ganglion cause what
- increased ventricular fibrillation threshold (protective)
| - increased vagal activity is good
110
how does the cardioacclerator reflex work (AKA brainbridge reflex)
stretch on right atrial wall-----> M.0,------> stimulates SNS out flow of the heart
111
What is neurocardiogenic syncope ( Benzold-Jarishc reflex)
effects hypotenion and bradycardia resulting in fainting..
112
what stimulates the benzold-Jarisch reflex
- occlusion of circumflex artery
| - increase in left ventrical pressure and volume
113
thyroid hormones can affect the heart in what ways
- inotropicly (increase strength of contraction)
- chronotropicly (decrease strength of contraction)
- increase in cardiac output ( from increased BMR)
114
What is the effect of elevated K in ECF
dilation and flaccidity of cardiac muscle (2-3x normal amount)
115
what is the effect of elevated Ca in ECF
spastic concentration
116
What does HR and strenght of contraction do as body temp is increased
increases. ( prolonged temp increase, strength of contraction goes down)
117
The heart is versatile in substrates for energy, which is the most perfered
fatty acids( 70 %)
118
most of the energy the heart uses is converted to what
heat (75%)
119
25% of actual work is done by energy consumption. what work is being done
- pressurization of blood ( 99%)
| - acceleration(1%)
120
If acceleration is more than one percent of work being done. what could cause this
Stenosis
121
What does the EKG mesure
potential difference across surface of myocardium over time
122
on the EKG 1mm = ___sec
.04sec
123
> 100 mm/sec =
tachycardia
124
<50=
bradycardia
125
how long should the PR interval be
.16 sec (4mm)
126
If the PR interval was greater than .2 sec =
1st degree AV block
127
If the PR interval was greater than .10 sec=
inadequate delay / accessory conduction pathway from atria to ventricals
128
P wave=
atrial depolarization
129
QRS complex =
ventriclular depolarization
130
T wave=
ventricluar repolarization
131
where is atrial repolarizaation
buried in QRS complex
132
which are wavey segments or intervals
intervals
133
a wave of deploarization will have a ___ deflection moving twoards a + electrode
positive(high)
134
a wave of reploarization will have a ___ delfection moving twoards a + electrode
negative(low)
135
what will the EKG show if the deflection is perpendicular to lead
nothing
136
how are unipolar limb leads set up
-AvR = right arm (+); left leg and left arm (-)
-AvL = left arm (+); right arm and left leg (-)
-AvF = left leg (+); right arm and left arm (-)
( augmented voltage: R= right leg L=left leg F=foot
137
how are bipolar limb leads set up
- lead I - left arm (+); right arm (-)
- lead II - left leg (+); right arm (-)
- lead III - left leg (+); left arm (-)
138
chest leads are AKA
V leads ( positive electrodes)
139
V1 is located where
4th intercostal space, right sternal border
140
V2 is located where
4th intercostal space, left sternal border
141
V3 is located where
between V2 and V4
142
V4 is located where
5th intercostal spce, mid clavicular line
143
V5 is located where
between V4 and V6
144
V6 is located where
left mid axillary line
145
what is the negative reference for the chest leads
the limb electrodes all hooked together
146
what is looked at with an EKG
- rate
- rhythm and intervals
- axis
- hypertrophy
- infarction
147
what info can an EKG not provide
mechanical performance ( like valve status)
148
PR interval is the time it takes for what to happen
SA node AP to enter the ventricle
149
what can a prolonged QT interval lead too
- increase incidence of sudden cardiac death
| - greater likely hood for ventricular fibrillation
150
longest and shortest RR that vary by greater than .16 sec suggest what
Sinus arrhythmia and heart rate variability
151
what is going on in a 1st degree block
depolarization from atria to ventricle is delayed
152
what is going on in a 2nd degree block
some depolarization waves pass, other blocked
153
what is going on in a 3rd degree block
all depolarization waves from atria to ventricles are blocked
154
prolonged QRS can be associated with what
ventricular hypertrophy or conduction block in purkinje system
155
what direction does the mean electrical axis go
ventricle depolarize fro base to apex and endocardium to epicardium. ADIO
156
normal axis lies between what degrees
-30 and 105
157
a QRS complex greater than .12 can suggest what
hypertrophy
158
what can be concluded if the deflection in V1 is added to the deflection in V5 and is greater than 35mm
left ventricular hypertrophy
159
does contraction of cardiac muscles limit myocardial blood flow?
yes
160
when does left coronary flow peak?
onset of diastole
161
when does right corornary flow peak?
mid systole
162
what is the max extraction rate of O2 the heart can perform at rest?
70%
163
O2 extraction rate system wide is?
25%
164
T of F: first cells to depolarize are the last to repolarize
T
165
T of F: ischemia prolongs depolarization therefore increasing repolarization
F ( decreases repolarization)
166
Inversion of the T wave can allude to what?
cardiac ishcemia
167
can damaged cells repolarize
nope
168
what would an EKG look like with damaged heart cells
elevated ST segment
169
what blood markers are used for cardiac infarction
cardiac troponins T and I ( released with cardiac injury)
