FUCK!!! Flashcards
(224 cards)
1
Q
the AV valves between atria and ventricles
A
tricuspid and mitral valves
2
Q
chronotropy
A
rate of depolarization; heart rate
3
Q
ionotropy
A
aka contractility; Ca2+ binds troponin
4
Q
preload
A
ventricular filling ~ end diastolic volume
5
Q
blood flows from
A
high to low pressure
6
Q
how much of ventricular filling is passive
A
80%
7
Q
s3 and s4 heart sounds
A
s3 can be healthy or pathologic
s4 is pathologic; atria force blood into non compliant ventricle
8
Q
which ventricle has the higher pressure
A
Left Ventricle
9
Q
Aorta is 120/80mmHg so its
A
the blood pressure value
10
Q
more force; atria or ventricles
A
ventricles
11
Q
ACXVY for at the atria
A
A wave: atrial contraction (atrial systole)
C wave: tricuspid buldge
X-descent: atrial relax (atrial diastole)
V wave: passive filling (ventricular systol)
y-descent: atria empty into ventricles with open AV valves
12
Q
dicrotic notch
A
division between 2 waves in aortic valves; when valve closes (elastic recoil)
13
Q
Stroke volume
A
volume ejected with each heart beat
14
Q
SV=
A
SV= EDV-ESV
15
Q
cardiac output
A
volume ejected each systole x heart rate
–> give o2 and nutrients to tissues
–> equal in left and right ventricles
16
Q
CO=
A
CO = SV x HR
17
Q
ejection fraction
A
proportion of EDV ejected with each heart beat
–>estimated heart function in heart failure
18
Q
EF=
A
EF= SV/ EDV
EF= (EDV-ESV)/ EDV
19
Q
preload of 1 ventricle depends on ____ of other ventricle
A
cardiac ouput
20
Q
treppe effect
A
accumulate Ca2+ in SR as HR increases (not enough time to remove calcium)
21
Q
skeletal myocyte excitation- contraction coupling
A
Ach (nicotinic receptor) –> depolarize –> Na+ VGC open –> Ca2+ VGC open –> t tubules get AP deeper –> Ca2+ binds troponin and open the myosin binding site on actin by moving tropomyosin out of the way –> cross bridge formation
22
Q
where does most of the calcium come from in skeletal muscle contraction
A
little bit from Ca2+ VGC
but the main action of Ca2+ VGC is to open ryanodine receptor in SR and the SR is where most of the Ca2+ is from
23
Q
cardiac myocytes differences from skeletal myocytes
A
-no tetany bc long refractory period
-synctium; intercalated disks (gap junctions and desmosomes) = coordinated heart contraction
-t tubules less important; rely more on L-type Ca2+ channels
-1 nucleus, lots of mitochondria; ATP, oxidative metabolism with fats
24
Q
automatic cells 4 phases
A
phase 4: unstable, funny current (Na+ and K+)
phase 0: depolarize by L-type Ca2+ channels (NOT Na+ VGC)
-no phase 1 or phase 2 plateau
-phase 3: repolarize; K+ efflux
25
where is there a delay in heart conduction
AV node; give atria time to eject blood to ventricles and time for ventricles to fill
26
bundle of His (AV bundle) purpose
carry AP along septum to ventricle
27
purkinje fibers carry AP to...
apex then base = ventricular contraction
28
fibrous skeleton so
atria and ventricles can only communicate through AV node
29
Bachman's bundle
right and left atrium contract simultaneously
30
4 major types of APs in the heart
1. myocyte APs (ventricular and atrial)
2. purkinje cell APs (almost same as ventricular but unstable 4 like automatic cell)
3. automatic cell APs
31
automatic cells
-SA and AV node
-depolarize without external stimuli
32
what cell takes over in complete heart block
purkinje cells give AP because cant go from atria to ventricles with AV node and SA
33
SA node is
pacemaker; HR = 60-100bpm
34
4 typical phases of myocyte APs
phase 4- resting membrane potential, leaky K+, Nernst = -84mv
phase 0- rapid depolarization, Na+ VGC open; influx
phase 1- initial repolarization, close Na+ VGC, K+ VGC open= efflux
phase 2- plateau- open L-type Ca2+, influx (Ca2+ and K+ balance out)
phase 3- slow repolarization; close Ca2+, open slow K+ VGCs
35
calcium spark
1 Ca2+ VGC opens and elicits small Ca2+ release from neighbouring ryanodine receptor on SR --> summation = increase in Ca2+ in cytosol (some contribution from ECF)
36
3 things remove Ca2+ from cytosol
-SERCA
-Na+ Ca2+ exchanger; 3 Na in, 1 Ca out
-sarcolemma calcium ATPase; Ca out
37
what is SERCA regulated by
phospholambdin phosphorylation
38
beta 1 receptors (SNS)
beta 1 --> cAMP --> phospholambdan --> phosphorylate troponin --> L-type Ca2+ VGC --> Ca2+ influx --> enhance contractility and quicker Ca2+ reuptake into SR
39
ECG measures? what is a little box?
electrical activity
-little box is 0.1mV high and 0.04 seconds wide
40
P wave
atrial depolarization via SA node
41
PR interval
impulse from SA node through atria and AV node to ventricles (AV node delay for ventricular filling)
AP from SA --> AV node
42
QRS complex
ventricular depolarization (via bundle of His and Purkinje)
43
ST segment
ventricles fully depolarized, before they depolarize
44
T wave
ventricular repolarization
45
QRS interval
AP from end of AV node to throughout ventricles
46
QT interval
ventricle depolarize and repolarize
47
3 layers of blood vessels
tunica intima
tunica media
tunica externa/adventitia
48
tunica intimia is made of
simple squamous endothelium
49
tunica media is made of
muscle cells
50
which layer is thickest in arteries
tunica media
51
which layer is thickest in veins
tunica externa/adventitia
52
tunica externa/adventitia components
vasa vosaorum (blood vessels), fibroelastic CT
53
4 types of arteries
elastic arteries/conducting
muscular arteries/distributing
arterioles
metaarterioles
54
elastic arterioles/ conducting
i.e. aorta, pulmonary trunk
elastic fibers for high pressure near heart, major pressure reservoirs
55
muscular arteries/ distributing
i.e. brachial and femoral arteries
smooth muscle, most abundant in body
56
most common artery in body
muscular arteries/ distributing
57
arterioles
constrict and dilate, control systemic BP
58
metaarterioles
regulate flow into capillaries via pre capillary sphincters
59
3 types of capillaries
continuous capillaries
fenestrate capillaries
sinusoidal capillaires
60
which are the majority of capillary in the body
continuous capillaries
61
what is least permeable and most permeable capillary
least- continuous capillary
most- sinusoidal capillary
62
continuous capillaries
least permeable, majority, intercellular junctions for water soluble substances to pass
exception: BBB, BtestesB --> tight junctions (Claudius and occluding)
caveolae (caves): endocytosis of macromolecules
intracellular cleft; for small (albumin cant go through)
coalesces and make vesicular channels --> pinocytosis and endocytose ECF --> increase in inflammation to transport antibodies and nutrients
63
3 types of veins
large
medium
small (venules)
64
large veins
vena cava, portal vein, pulmonary veins
thick tunica advanetitia with dense CT, collagen, elastic fibers, vasa vasorum
65
medium veins
femoral, renal and brachial veins
valves to prevent back flow to limbs
66
small veins (venules)
post capillary and collecting venules
collect blood from capillaries
67
valves formed via
reflection of tunica intima
68
lumen bigger in vein or artery
vein
69
2/3 blood in
systemic vein
70
veins can somewhat constrict via
catecholamines
71
poiselles law vs Reynolds #
poiselles; laminar flow
Reynolds; turbulent flow (i.e. atherosclerosis, hypotension)
--> likely if increased blood velocity, decreased or irregular diameter and decreased viscosity (faster)
72
pressure and velocity in arteries, capillaries and veins
arteries- high pressure, fast velocity
capillaries- low pressure, slow velocity
veins- low pressure, moderate velocity
73
basement membrane of capillaries
type IV collagen
74
series circulation vs parallel circulation
series- higher resistance
parallel- majority, reduce resistance even though small radius i.e. capillaries
75
lower resistance in parallel or series circulation
parallel
76
compliance
amount of pressure need to change volume
77
high compliance
small amount of pressure= large change in volume
78
what are more complaint; veins or arteries
veins; blood resevoir
arteries have low compliance to maintain high BP
79
mean arterial pressure MAP
MAP= DP + 1/3 (SP-DP)
1/3 of cardiac cycle in systole
80
edema
too much movement across capillary walls
albumin keeps H2O in capillary
glycosaminoglycans absorb H2O and reduce edema
81
what reduces edema
albumin and glycosaminoglycans
82
2 ways capillary blood flow is regulated
1. autoregulation
2.myogenic regulation
83
autoregulation of capillaries
capillary bed regulates flow via local tissue factors
h2o, o2, co2, [lactate, K+, adenosine= exercise] all vasodilate
84
myogenic regulation of capillaries
constant flow despite changes in MAP because if pressure drops then dilate and if pressure increases then constrict
Increased Blood Pressure (Stretch):
When blood pressure increases, it causes the walls of arterioles (the small arteries leading to capillaries) to stretch.
The smooth muscle cells in the walls of these arterioles respond to this stretch by contracting (a phenomenon known as the myogenic response). This constriction reduces the diameter of the arteriole, thereby decreasing the flow of blood into the capillaries.
This is a protective mechanism to prevent overdistention of the capillaries and potential damage to delicate capillary walls.
Decreased Blood Pressure (Reduced Stretch):
When blood pressure decreases, the walls of the arterioles are less stretched. In response, the smooth muscle cells in the arteriole walls relax, causing the arterioles to dilate.
This dilation helps maintain blood flow through the capillary network by preventing the pressure in the capillaries from becoming too low, ensuring adequate perfusion to tissues.
85
NO effect and pathway
vasodilate via shear stress
NO --> guanylyl cyclase --> cGMP --> PKG --> dephosphorylate myosin and relax
86
vasodialtors of capillaries
histamine
bradykinin
prostaglandin E2 and I2
NE, E via beta 2 receptors
87
vasoconstriction of capillaries
NE, E alpha 1 receptors
serotonin
ADH
AT II
thromboxane A2 and prostaglandin F
88
NE and E 2 receptors
beta 2= vasodilate
alpha 1= vasoconstrict
89
cerebral blood flow is regulated by
ph and adenosine
90
cushing reflex in the cerebrum
increased intracranial pressure will decrease perfusion
91
pulmonary capillaries are unique- low oxygen causes
vasoconstriction; for efficient gas exhange
92
skin receptors
SNS alpha 1, body temperature
93
coronary capillaries regulated by
oxygen and adenosine
94
causes of edema
increased hydrostatic pressure (from increased arterial pressure i.e. malignant hypertension, decrease venous drainage)
decreased oncotic pressure (albumin, i.e. nephrotic syndrome and hepatic filature)
increased vascular permeability
blocked lymph (malignancies, surgeries)
increase Na+ and H20 retention via ADH and aldosterone
damaged endothelium
95
transudate vs exudate in edema
transudate- low protein and cell content from pressure imbalances
exudate- high protein and cell content from inflammation and vessel damage
96
arterial and venous; is hydrostatic or oncotic pressure greater
arterial: H > O
venous: O > H
97
anasarca and angioedema
anasarca- generalized edema in body
angioedema- in deep layers of face
98
what is most severe edema
pulmonary and brain
99
hyperemia and congestion are both from
local increase in blood volume
100
hyperemia
arteriol dilation increases blood flow; erythema i.e. blood flow when warmed up after being in cold outside
causes local increase in blood flow
101
congestion
passive hyperemia; decreased blood outflow from a tissue; cyanosis because of red blood cell stasis
can be systemic or local
RBC breakdown and get hemosiderin= hemoglobin degrade in macrophage
local increase in blood volume
102
long standing congestion
hypoxia, apoptosis, fibrosis, hemosderin laden macrophages
103
pulmonary vs hepatic congestion causes
pulmonary- left heart failure
hepatic- right heart failure
104
nutmeg liver from
hepatic congestion
105
infarct
tissue death from ischemia
106
white vs red infarct
white= organs with single blood supply (kidney or spleen)
red= dual blood supply (lung, intestine, testis)
107
arterial or venous occlusion for white and red infarcts
white infarct= arterial occlusion (cause white appearance; abrupt and severe damage since cut off only blood supply)
red infarct= venous occlusion (blood pools and causes red/blue colour, slow process because dual blood supply)
108
shock
inadequate blood flow to organs
109
types of shock
cardiogenic- MI, myocarditis, cardiac tamponande, pulmonary embolus
hypovolemic- hemorrhage, diarrhea, dehydration
septic- infection
distributive (too much dilation; not enough pressure= anaphylactic and neurogenic)
anaphylactic; type 1 hypersensitivity
neurogenic- brain damage or spinal cord injury
110
in shock the myocardial pump fails causing
decreased blood volume, vasodilation, increased vascular permeability
(inadequate blood flow to organs)
111
stage 1 (compensated) vs stage 2 (decompensated) shock
compensated= tachycardia with normal BP
decompensated= tachycardia and hypotension
112
symptoms in ischemic heart disease
asymptomatic or chest pain, dyspnea, fatigue, palpitations
113
what is the mechanism in ischemic heart disease
blood flow to the myocardium is inadequate
114
main cause of ischemic heart disease (90%)
atherosclerosis
115
what makes ischemic heart disease worse
things that increase heart metabolic demands; HR, Ca2+ contractility, wall tension
116
stable angina
IHD symptoms during activity, 50-75% of lumen decreases, Bette with rest and worse with exercise, fixed with nitrgoclycerine
117
unstable angina
IHD symptoms at rest, 80-90% of lumen decreased, not better with rest or nitroglycerine
thrombus breaks down
118
acute coronary syndrome
unstable angina + MI
119
acute IHD
-stable or unstable angina
-MI
-sudden cardiac death (dysrhythmia)
120
chronic IHD can lead to
heart failure
121
IHD diagnosis
ECG
cardiac enzymes; CK-MB, troponin T and I
angiogram
echocardiogram
122
IHD treatment
ASA antiplatelet agent (decrease thrombus)
antihypertensive
beta blocker
nitroglycerine (decrease preload and afterload; vasodilate)
Ca2+ channel blocker (decrease contractility)
123
IHD complications
MI
124
chronic IHD can lead to
congestive heart failure
125
pritizmetal angina (vasospastic or variant angina) cause
coronary artery spasm
126
pritizmetal angina (vasospastic or variant angina) symptoms
at rest in the morning
respond to Ca2+ blockers and nitroglycerine
127
adaptations in chronic ischemia of the heart
hypertrophy and collateral circualtion
128
MI symptoms
pain could be in scapula, heart burn, dyspnea, fatigue- not typical presentation always
129
cells in MI
cells and mitochondria swell and lose glycogen
130
what opens in MI
MPTP (mitoahcondria pore) opens from an increase in Ca2+ --> please H+, no ATP, more Ca2+ in cytosol
131
time frame in MI
30-60 min: irreversible, coagulative necrosis (Ca2+ accumulate, ROS, decrease ATP, open MPTP)
2-3 days: neutrophils in necrotic tissue, edema, hemorrhage
5-7 days: scar tissue, replace neutrophils with macrophages, myofibroblasts deposit collagen
132
reperfusion injury after MI
damage cardiomyocytes if restore blood to quick after ischemia
contraction band necrosis
133
transmural infarcts/ STEMI
blocked coronary artery
use clot busting drugs
134
non-transmural infarct/ NSTEMI
partially blocked coronary artery; transient occlusion
135
what to do in STEMI and NSTEMI
revascularize- angiopalsty or stent
136
MI most common vessel effected
anterior descending branch of left coronary artery (50%)
137
diagnose heart failure
ECG
BNP
HFrEF, decreased ejection fraction <40%
HFpEF, EF >50%, left ventricle hypertrophy
138
2 most common cause of heart failure
1. chronic IHD (HFrEF)
2. hypertension (concentric LV hypertrophy)
139
mechanisms of heart failure
-increased afterload --> hypertrophic ventricles
-chronic ischemia from low oxygen
-decreased compliance (cant relax)
-cardiomyopathy- damaged myocardium impairs compliance and contractility
140
2 types of heart failure
systolic dysfunction/ HFrEF
diastolic dysfunction/ HFpEF
141
HFrEF (heart failure with reduced ejection fraction)/ systolic dysfunction
impaired contraction, rely on increased preload
142
HFpEF (heart failure with preserved ejection fraction)/ diastolic dysfunction
impaired EDV (compliance), elevated diastolic pressure, but contraction OK
143
forward flow vs backward flow problem in heart failure
forward= impaired cardiac output
backward= congestion
144
what is first to fail in heart failure
left ventricle because greatest afterload
145
what is it called when the right ventricle fails first in heart failure
cor pulmonale (COPD, OSA, pulmonary hypertension)
146
pulmonary microcircualtion
constrict if low O2
147
concentric vs eccentric hypertrophy usually happens 1st
concentric
148
concentric hypertrophy
ventricular wall thickens, no increase in chamber size
149
eccentric hypertrophy
myocytes increase length and the chamber enlarges
150
ventricular remodelling in heart failure via
increased TGF b
151
2 main pathways in CHF
RAAS and SNS
152
angiotensin II in CHF
AT II increases when cardiac output to kidneys decrease
causes vasoconstriction, edema, increased BP
153
SNS in CHF
beta adrenergic
154
endothelin 1 in CHF
vasoconstriction
155
JNK and MAPK in CHF
inflammation and apoptosis
156
Ca2+ in CHF
less released for contraction, inhibited uptake (increased in diastole and decreased in systole)
157
IGF1 and PI3K in CHF
hypertrophy
158
ANP and BNP in CHF
become resistant to them and no longer lead to Na+ and H2O loss
159
signs in CHF
pitting edema
increased JVP
s3,s4
crackle, wheeze
hepatosplenomegaly
160
3 causes/ mechanisms in atherosclerosis
-diabetes (AGEs)
-dislipidemia (LDL)
-Lp(a)- increased endothelial damage via immune cells and plaque formation also inhibits clot breakdown
161
lp(a) mechanism
increased endothelial damage via immune cells and plaque formation also inhibits clot breakdown
162
medications for CHF and angina
-beta blocker (SNS- NE)
-cardiac glycosides (digoxin): inhibit Na/K+ pump which decreases Na+ Ca2+ exchangers = increased Ca2+ in systole
-diuretics: increase water and sodium loss
163
angina medications
-Ca2+ channel blockers
--> dihydropyridine: vasodilate
--> nondihydropyrine: slow AV conduction (HR) and contractility
-nitrates (NO): vasodilate
164
medications for dyslipidemia
-HMG CoA reductase inhibitors (statins); decrease hepatocyte cholesterol production
-PCSK9 inhibitors: block the degradation of LDL receptors
-ezetimibe: decrease cholesterol absorption
-niacin B3: inhibit lipolysis
165
valve pathologies
stenosis (narrow)
regurgitation (backflow)
--> incompetence: valve doesnt close
--> prolapse: valve into proximal chamber
166
aortic stenosis/sclerosis
very common, >65yrs
from congenital bicuspid aortic valves
calcific aortic stenosis: myofibroblast become osteoblast like --> valve calcifies which increases afterload and causes concentric hypertrophy
167
aortic regurgitation
related to aortic stenosis, ankylosing spondylitis, rheumatic heart disease, infective endocarditis
can cause shock
168
most common valve pathology
mitral valve prolapse
169
mitral valve prolpase
go back into left atrium
enlarged annulus and chord tendinae, myxomatous CT, proteoglycans, redundant leaflets
cadherin deficit, CT problem
170
mitral valve regurgitation
from chronic mitral valve prolapse
papillary or chordae tendinae rupture
171
rheumatic fever cause
autoimmune from group A strep (strep thoat or strep skin)
M protein
172
rheumatic heart disease (group A strep)
affect all cardiac layers (Endo, myo, peri)
2-3 weeks after infection
inflammation --> valvular stenosis
= mitral (chordae tendinae)
=aortic stenosis (bicuspid)
most common
173
most common valve pathologies from rheumatic heart disease
= mitral (chordae tendinae)
=aortic stenosis (bicuspid)
174
3 types of cardiomyopathies
1. dilated cardiomyopathy
2. hypertrophic cardiomyopathy
3. restrictive cardiomyopathy
175
most common cardiomyopathy
dilated
176
HF_EF in the cardiomyopathies
dilated= HFrEF
hypertrophic= HFpEF (can delve into HFrEF)
restrictive= HFpEF
177
dilated cardiomyopathy causes
genetic sarcomere, infection, inflammation, toxic (alcohol, catecholamines, sarcoidosis, x linked)
178
what happens in dilated cardiomyopathy
heart muscle enlarges and weakens; LV enlarges most- mitral regurgitation
179
what valve issue in dilated cardiomyopathy
mitral regurgitation (LV enlarged most)
180
symptoms of dilated cardiomyopathy
hypertrophy and fibrosis of cells
asymptomatic --> heart failure (fatigue, dyspnea), palpitate, syncope
181
hypertrophic cardiomyopathy cause
-genetic deficit in sarcomere (gain of function)
182
mechanism in hypertrophic cardiomyopathy
overgrown septum; obstruct outflow of LV to aorta
183
symptoms in hypertrophic cardiomyopathy
asymptomatic, syncope (lose consciousness bc cerebral hypoperfusion)
184
least common cardiomyopathy
restrictive cardiomyopathy
185
causes of restrictive cardiomyopathy
deposits of ECM, amyloidosis (accumulate protein), hemochromatosis (iron), sarcoidosis (granuloma infiltrate), autosomal dominant
186
mechanism in restrictive cardiomyopathy
restricted ventricular filling, decreased diastolic volume, normal systole
187
where is Lp(a) made and in response to
made in liver bc increased IL6, cytokines (inflammation)
188
what is a key feature in lp(a)
kringel units
189
what does lp(a) look like
LDL - both contain apo(b)
190
what is the pathogenic factor of lp(a)
transports oxidized phospholipids
191
unstable plaques
what degrades collagen and makes the cap weaker
-rupture and release pro-coagulant molecules
weaker cap: macrophages make metalloproteinases to degrade collagen
192
more stable cap
increase collagen via growth factors
193
hallucination
sensory perception
formed (voice commands), unformed (non specific sounds)
with insight (aware) or without insight (think is real)
194
schizophrenia DSM5
>2 symptoms for 6 months or 1 month active symptoms (1-4), need 1 of the 1st 3
1. delusion
2. hallucination
3. disorganized speech
4. disorganized or catatonic behaviour
5. negative symptoms
195
cause of schizophrenia
dysregulated dopaminergic system- hyperactive tonic firing and reduced GABA in hippocampus
196
2 things that back up schizophrenia and dopamine hypothesis
1. antipsychotics block D2 receptors
2. drugs that increase dopamine (l-dopa, amphetamines) increase psychosis
197
GABA interneurons
inhibit dopamine in schizo- develop last and are damaged by ROS
198
monoamines in the dopaminergic system
NE, serotonin, dopamine
199
what part of the brain releases dopamine
midbrain- VTA and substantial nigra
200
reward/motivation for dopamine
VTA --> nucleus accumbens and ventral striatum
201
motor for dopamine
substantia nigra --> striatum
202
executive function in dopamine
VTA and substantia nigra --> many cortical areas
203
tonic firing for dopamine
slow, at rest, pacemaker via ventral palladium
slower by GABA
204
phasic firing in dopamine system
RAS: glutamate release onto dopamine --> AP
in response to stimuli
205
phasic firing changes
stronger via hippocampus if new stimuli
weaker phasic and tonic firing via amygdala in chronic stress
206
schziophrenia and inflammation
-kyurenic acid blocks NMDA receptor= psychosis
activate microglial cells - prune synapses
207
what causes pain in migraine
trdigemiocervical complex (TCC) --> thalamus --> cortex
208
things that cause pain in migraine
serotonin and CGRP (vasodilate)
209
medication for migraine
5HT-1 receptors for serotonin are blocked by "-triptans"
block CGRP (vasodilate)
210
cause of migraine
spreading depression wave (excitability) through cortex and activate TCC
211
central sensitization in migraine
central sensitization: cytokines --> release nerve growth factor from mast cells --> BDNF in C fibers --> pro pain
c fibers release CGRP and substance P
212
c fibers release (in migraines)
c fibers release CGRP (vasodilate) and substance P (edema, vasodilate, mast cell degranulation)
213
stomach microbiome and migraines
-h pylori triggers CGRP release
IBS increase serotonin
gut permeability --> LPS --> infalmmatory cytokines
214
POTS (Postural orthostatic tachycardia syndrome)
lying to standing; HR increases > 30bpm with no hypotension or drop in blood pressure
or HR >120bpm
215
if from lying to standing and HR increases and BP drops what is it
orthostatic hypotension
216
symptoms of POTS
light headed, blurry vision, weak, nausea, palpitations
217
who does POTS effect more
women > men
218
test for POTS
tilt table test
219
3 types of POTS
neuropathic POTS
hypovolemic POTS
hyperadrenergic POTS
220
neuropathic POTS
lower limb blood pool because of less NE in the limbs
221
hypovolemic POTS
decrease blood volume
-elevated renin and AT II
-inadequate aldosterone
-deconditioning
222
hyperadrenergic POTS
increase NE
beta 1 and 2 autoantibodies
223
4 heart sounds in order from right to left top to bottom
APTM
224
location of SA, AV and purkinje
SA node: superior right atrium- sends signal to both atria
AV node: inferior RA- connect atria and ventricles
AV bundle of HIS sends signal to ventricles
Purkinje in ventricles
