Cardio Flashcards
1
Q
cardiovascular system (CVS)
A
organ system to TRANSPORT molecules and other substances rapidly over long distances between cells, tissues and organs
2
Q
2 heart functions
A
- push blood through vasculature
- irrigate other organs and systems
3
Q
right ventricle function
A
pump blood to lungs to get O2
4
Q
left ventricle function
A
pump blood to body to deliver O2 to working tissue
5
Q
what is vasculature designed to do
A
carry out the blood
6
Q
artery function
A
carry blood away from heart
7
Q
vein function
A
carry blood back to heart
8
Q
conductance definition
A
respond to systolic/diastolic pressure
9
Q
microcirculation
A
exchange between blood and extracellular fluid
10
Q
erythrocytes
A
red blood cells, carry O2
11
Q
leukocytes
A
white blood cells, immunity/inflammation
12
Q
platelets function
A
coagulation
13
Q
3 things CVS brings to cells
A
nutrients, fuel, oxygen
14
Q
what does CVS remove
A
waste products (CO2, urea)
15
Q
2 things that circulate in CVS
A
hormones + antibodies
16
Q
3 things CVS regulates
A
pH, water balance, temperature
17
Q
why do simple organisms not have CVS
A
small enough to operate with only diffusion
18
Q
diffusion definition
A
movement of molecules from high conc area to low conc area
19
Q
5 factors that affect diffusion
A
distance
temp
density/conc of solvent
molecule mass
barrier characteristics
20
Q
how does increasing distance affect diffusion
A
decreases diffusion
21
Q
how does increasing temperature affect diffusion
A
increases diffusion
22
Q
how does increasing solvent conc affect diffusion
A
increases diffusion
23
Q
how does increasing molecular mass affect diffusion
A
decreases diffusion
24
Q
flux of gas equation
A
flux = membrane diffusing capacity x membrane pressure gradient
25
2 things to increase membrane diffusing capacity
area and solubility
26
2 things to decrease to increase membrane diffusing capacity
thickness and size of molecule
27
why does fibrosis decrease O2 diffusion
because thicker membrane
28
comparative physiology
studies and exploits the diversity of functional characteristics of various organisms
29
what is the circulatory fluid in insects
hemolymph
30
does insect circulation transport O2
no because no Hb
31
is insect circulation open or closed
open (from posterior -> anterior)
32
insect dorsal vessel
aorta + thoracic bulbs
33
what is the insect heart
chambers with ostioles
34
how does circulation occur in insects
'heart' pumps hemolymph, valves close w each contraction to allow fluid to move in 2 direction
35
how many chambers do fish have
2 (1 atrium, 1 ventricle)
36
how does circulation occur in fish
ventricle pumps blood through artery -> gill capillaries -> systemic capillaries -> atrium
37
where does blood get oxygenated in fish circulation
gill capillaries
38
how many circulations do amphibs + reptiles have
2 (small/pulmonocutaneous, large/systemic)
39
how many chambers do amphibs + reptiles have
3 (2 atria + 1 ventricle)
40
amphib + reptile small circulation
leaves ventricles towards lungs and skin to get oxygenated, high O2 returns to left atrium, then ventricle
41
amphib + reptile large circulation
high O2 blood in ventricle sent to whole body, low O2 blood returns to right atrium, then ventricle
42
why do high O2 and low O2 blood not mix in amphib and reptile circulation (2)
structure and pressure
43
how many chambers do alligators have
2 atria, 2 ventricles
44
how many aortas do alligators have
2
45
2 alligator circulation pathways
LV -> right aorta -> systemic circ
RV -> left aorta -> systemic circ
46
what valve closes when alligators are underwater and where is it
gear-tooth valve (between RV + pulmonary circulation)
47
what does closing gear-tooth valve do in alligator circulation
causes low O2 blood from right heart to enter left aorta -> enters systemic circ -> left heart valve to aorta also closed therefore tissues receive low O2 blood
48
why are alligators cold-blooded
gas exchange less efficient = no temp control
49
how many chambers for avian and mammalian circulation
4 (2 atria + 2 ventricles)
50
haemodynamics
study of circulation and movement of blood in the body, and the forces involved
51
blood volume
5L
| (75mL/kg avg)
52
blood unit
450 mL
53
stroke volume
70 mL
| (end diastolic (in) volume - end systolic (out) volume)
54
diastole
ventricle opens, blood pours in
55
systole
heart contracts, blood pumps out
56
capacitance system
venous system; compliant and can change accordingly to volume
57
how much blood is in venous system at any one time
61%
58
resistance system
arterial system; ensures enough force for blood flow
59
how much blood is in arterial system at any one time
18%
60
cardiac output
amount of blood heart pumps in 1 min (5L)
61
cardiac output equation
heart rate x stroke volume
62
venous return
blood flow from periphery back to atrium (5L)
63
is distribution to various organs always the same
no, distribution is function-dependent
64
flow equation
flow = V/T AND flow = area x mean velocity (mL/min or L/min)
65
what is area in flow equation
lumen
66
why do we use mean velocity in flow equation
because velocity is not the same at every point in cross-section
67
why does aorta have large diameter
to ensure enough pressure to whole system
68
large artery function
dissipate pressure
69
why do we have many venules
must slow velocity enough for diffusion to occur
70
2 structures for distribution
aorta and large artery
71
2 structures for resistance
small artery and arteriole
72
structure for exchange
capillaries
73
3 structures for capacitance
vena cava, vein, venule
74
4 advantages of branching capillary network
- cells are close to capillary (reduces distance)
- high total area of capillary wall
- low blood flow velocity in capillaries
- high total CSA
75
blood pressure definition
force exerted by blood on blood vessel wall
76
systemic blood pressure
120/80 mmHg
77
central venous pressure
5-15 cmH2O / 6-12 mmHg
78
how does pressure in arteries and arterioles compare to pressure in capillaries, venules and veins?
higher
79
why is pressure higher in arteries and arterioles
because resistance is higher
80
what is the KEY to arteries being resistance vessels
structure!
- changing CSA is important for resistance, and arteries are muscular, allowing for efficient contraction
81
82
how does systemic circ pressure compare to pulmonary circ pressure
higher
83
how do systole pressures compare to diastole pressures and why
higher because need more pressure to pump blood to whole body
84
where are the pressure differences between systole and diastole less significant (2)
arterioles and capillaries
85
where does the pressure difference between systole and diastole disappear (2)
venules and veins
86
perfusion pressure equation
inlet pressure - outlet pressure
delta P = Pin - Pout
87
what is perfusion pressure necessary for
good organ feeding
88
what happens if we have no perfusion pressure
no flow
89
perfusion pressure equation (for an organ)
arterial pressure - venous pressure
delta P = Pa - Pv
90
what is perfusion pressure (delta P) approximately equal to in organs and why
arterial pressure (Pa) because it is typically MUCH higher than venous pressure
91
what is flow proportional to (2)
perfusion pressure, and therefore arterial pressure
92
what type of structure regulates flow and why
arteries because they have more resistance
93
resistance definition
force that opposes movement
94
resistance equation
resistance = perfusion pressure / flow
95
what causes resistance
friction between vessel wall and blood
96
how does resistance change with increase vessel length
increases because increased surface
97
where is resistance greatest and what does this mean for flow
near surface, and therefore slowest flow
98
laminar flow definition
entire fluid flows in same direction
99
viscosity
friction between moving particles
100
what does increased viscosity mean for resistance
increased
101
what does viscosity of blood depend on
hematocrit (more red blood cells = more viscosity)
102
why is viscosity relatively constant
because hematocrit varies very little
103
Poiseuille's law
resistance = 8 x viscosity x (length/radius)
104
why does CSA determine resistance (using Poiseuille's law)
viscosity = constant
length = constant
only radius (aka CSA) changes
105
4 controllers of vessel constriction
- local metabolites
- hormones
- neurotransmitters
- endothelial cells
106
what does increased calcium mean for constriction
increases
107
what does decreased calcium means for constriction
decreases
108
how does vessels in series affect resistance
total resistance is sum of both vessels = inefficient
109
how does vessels in parallel affect resistance
lowers it because radius of vessel at the entrance and exit is bigger than the radius of each vessel in parallel
110
where is most blood found at any one time, and why
veins and venules because high compliance
111
compliance definition
ability of blood vessel to stretch
112
what does compliance depend on
vessel volume gradient (delta V) and transmural pressure gradient (delta P)
113
compliance equation
compliance = delta V / delta P
114
why are veins more compliant
little smooth muscle and few elastic fibres
115
for any given variation in transmural pressure, how does arterial and vein volume change
arterial volume = changes very little because stiff therefore low compliance
vein volume - changes a lot because high compliance
116
how does pressure in peripheral venules compare to pressure in ascending aorta
<10% of pressure in ascending aorta
117
2 mechanisms to maintain blood flow against gravity
valves = ensure 1 way flow
skeletal muscle contraction
118
4 chambers of the heart
right atrium + right ventricle (pulmonary)
left atrium + left ventricle (systemic)
119
superior and inferior vena cava
low O2 blood enters the heart
120
pulmonary trunk
branches into 2 pulmonary arteries
121
right and left pulmonary artery
low O2 blood to right and left lungs
122
left and right pulmonary vein
bring high O2 blood to the heart
123
aorta
sends high O2 blood to body
124
how many organ branches does the aorta have
30-40
125
arteries vs veins (direction and O2 content)
arteries. =take blood away from heart, high O2
veins. =bring blood to heart, low O2
*** opposite O2 levels in pulmonary vessels ***
126
inter-atrial septum
divides left and right atria
127
inter-ventricular septum
divides left and right ventricles (VERY THICK)
128
left ventricular free wall
much thicker for high pressure
129
right ventricular free wall
1/10 as thick as left wall for low pressure system
130
is the heart fed by aorta and vena cava
no
131
where do coronary arteries branch off
just above aortic valve of the aorta
132
where do coronary veins empty deoxygenated blood
right atrium
133
myocaridal infarction
coronary artery block = heart attack
134
tricuspid valve
divides right atrium and right ventricle
135
pulmonary / pulmonic valve
divides right ventricle and pulmonary trunk
136
bicuspid / mitral valve
divides left atrium and left ventricle
137
aortic valve
divides left ventricle and aorta
138
where is the fibrous ring
between atria and ventricles
139
purpose of fibrous ring
electrically isolates atria from ventricles
140
where are the valves of the heart housed
fibrous ring
141
papillary muscles function
contract to prevent valve inversion / prolapse on systole
142
where do papillary muscles attach
cusps of bicuspid and tricuspid valves
143
chordae tendinae
strong fibrous connections between valve leaflets and papillary muscle
144
pericardium / pericardial sac
'bag' that surrounds heart and vessels
145
3 pericardium functions
- prevents overfilling (by not expanding)
- protects heart physically
- provides pericardial fluid
146
pericardial fluid
lubricant to allow heart to freely contract, generated from serous membrane
147
epicardium
outer layer of heart tissue
148
what is epicardium made of
epithelial cells
149
myocardium
muscle! main layer
150
endocardium
inner layer of heart tissue
151
what is endocardium made of
endothelial cells
152
what is the main pacemaker
SA/sinus node
153
what 2 other structures can spontaneously beat if SA node fails
AV node and His-Purkinje cells
154
how often does SA node beat
1 beat/ second
155
how does SA node propagate signal through right atrium toward left atrium
electrically connected to neighbouring cells
156
AV node function
transmits SA node signal to ventricles via bundle branches
157
what is the secondary pacemaker
AV node
158
why does the AV node conduct its signal slowly
to allow the blood to reach ventricles before they contract
159
bundle branches function
propagate signal along septum
160
Purkinje fiber structure
branched tree structure under endocardium
161
order of electrical conduction in the heart (7)
- SA node
- AV node
- Bundle of His
- Bundle branches
- Septum
- Purkinje fibers
- Ventricles
162
why does left bundle branch activate septum but not the right
right bundle branch well insulated by connective tissue, left bundle branch not isolated
163
why do ventricles contract simultaneously
to maximize pressure
164
how does the signal move in the heart
endo -> epi
165
what are gap junctions
connection between cells
166
what do gap junctions contain
wavy intercalated disc
167
voltage of depolarized and resting cell
depolarized = +20mV
resting = -90mV
168
why do positive ions move through gap junction
due to electrical gradient between cells
169
where do Na+ and K+ move in gap junction
K+ = from depolarized to resting (inside cell)
Na+ = from resting to depolarized (outside cell)
170
what does an EKG sense
interstitial local circuit currents
171
local circuit current
form basis of depolarization wave front in working myocardium
172
where are gap junctions concentrated
at the ends of myocytes
173
electrocardiogram (ECG/EKG)
recording of the electrical activity of the heart
174
how is electrocardiogram recorded
electrocardiograph (also referred to as ECG/EKG)
175
4 parts of ECG
patient cable
lead-selector switch
voltmeter
ECG
176
what is the reference lead on ECG
right leg - set to 0, always connected
177
when do extracellular recordings appear on ECG
when there is a potential difference
178
what does 1 cardiac cycle look like on ECG
PQRST waves
179
where do all ECG waves start and end
baseline
180
full cardiac cycle (10)
1. sinus node fires
2. atrial contraction
3. AV node activates
4. His bundle activates
5. left bundle activates
6. septum activates
7. Purkinje fibres activate
8. ventricles contract
9. late activation
10. ventricles repolarize
181
which steps are invisible on ECG (5)
SA node firing
AV node activation
His bundle activation
left bundle activation
Purkinje fiber activation
182
P wave
atrial contraction
183
why don't we see the atra relax on ECG
because bigger currents mask it
184
Q wave
septum activation (1st negative deflection)
185
R wave
ventricle activation
186
S wave
late activation (not always present)
187
T wave
ventricles repolarize
188
what is P-R interval a measure of
AV transit time
189
what does long P-R interval mean
AV block
190
what is P-R segment
time delay between atrial and ventricular activation
191
what is S-T segment
time between ventricular depolarization and repolarization
192
what does an S-T segment above 0V indicate
some tissue have abnormal APs, typical of infarction
193
what is Q-T interval proportional to
AP duration
194
what does long QT indicate, and what can it lead to
repolarization problem - can lead to arrhythmias
195
what does a QRS >100ms mean
slow excitation
196
2 possible causes of long QRS interval
problems with His-Purkinje (bundle branch block)
slow conduction in cardiac muscle (schemia)
197
where do positive and negative ions flow in depolarized vs resting cell (inside vs outside cel)
inside: + ions from depolarized to resting, - ions from resting to depolarized
outside: + ions from resting to depolarized, - ions from depolarized to resting
198
how to measure voltage of depolarizing cell
positive electrode - negative electrode
199
2 situations that lead to positive voltage
depolarization towards positive electrode
repolarization towards negative electrode
200
2 situations thats lead to negative voltage
depolarization towards negative electrode
repolarization towards positive electrode
201
why is T wave positive
because depolarization wave moves opposite to repolarization wave due to difference in AP duration from inside to outside the heart
202
bipolar limb lead
take 2 measurement, subtract 1 from the other
203
3 bipolar limb lead equations
I = Vla - Vra
II = Vll - Vra
III = Vll - Vla
204
why are there 3 bipolar limb leads
to form a triangle across the chest that surrounds the heart, sum total of Voltages = 0
205
unipolar lead = ?
V
206
how many unipolar limb leads are there
9 (aVR, aVL, aVF & V1-V6)
207
why do we need to look at all 12 leads
because not all leads will pick up all the info
208
which 3 leads have special ECGs
V2 = no P wave
V3 = no Q wave
aVR = inverted T wave, no R+S wave
209
how can you tell from the membrane potential graphs that the SA node and His-Purkinje cells have a pacemaking current
they have no resting potential, only a pacemaking potential that drives them to their threshold until depolarization
210
how does ventricular action potential compare to skeletal muscle action potential
longer, and resting potential more hyperpolarized
211
4 stages of ventricular potential
resting potential
upstroke
plateau
repolarization
212
what is happening during ventricular resting potential
poor Na+ and Ca+ conductance, high K+ conductance
213
what is happening during ventricular upstroke
fast inward Na+ current
214
what is happening during ventricular plateau
K+ channels start to close, Ca+ channels open for Ca+ influx
215
what is happening during ventricular repolarization
K+ channels open, Ca+ channels close
216
why is voltage at rest close to K+ value
because Pk much greater than Pca and Pna
217
what generates the upstroke for SA node
Ca+ current
218
what generates Purkinje fibres' upstroke
Na+ current (fast upstroke and fast propagation)
219
why does Purkinje signal move faster than SA node signal
higher upstroke velocity (faster depolarization)
220
which 2 structures have slow APs
SA node and AV node
221
how fast do SA and AV nodes' APs move
0.01-0.05m/sec
222
what is the SA and AV node conduction velocity
1-10 V/sec
223
which 5 structures have fast APs
ventricular muscle
atrial muscle
His bundle
Purkinje fibres
bundle branches
224
how fast do the ventricular muscle, atrial muscle, His bundle, Purkinje fibres and bundle branches AP move
0.5-5 m/sec
225
what is the ventricular muscle, atrial muscle, His bundle, Purkinje fibres and bundle branches conduction velocity
100-1000 V/sec
226
how does atrial cell AP compare to ventricular cell AP
shorter
227
why does ECG only show atrial and ventricular action
because biggest (hides other currents)
228
where and when do local circuit currents occur
on cell level, <1ms before wave propagates from A to B
229
why is V=0 when ventricles are excited?
positive and negative electrodes see same voltage therefore difference = 0
230
when does Ca2+ flow into cytosol
during depolarization plateau
231
where are Ca2+ channels located
in T-tubules
232
when Ca2+ flows into cell, where does it bind
ryanodine receptors on sarcoplasmic reticulum (SR)
233
what does Ca2+ binding to ryanodine receptors of SR do
opens Ca2+ channels intrinsic to these receptors so that Ca2+ flows into cytosol
234
what does increased cytosolic Ca2+ conc do
more troponin binding = more contraction
235
function of calcium pump in cell membrane
bring Ca2+ back up a gradient into SR for next AP
236
what are calcium sensors in membrane sensitive to
voltage
237
why does Ca2+ enter cell with a slight delay (~8ms)
because triggered by AP / voltage
238
where can you observe the delay of Ca2+ entering the cell
calcium transient graph
239
why does mechanical activity always lag electrical activity
because Ca2+ must bind
240
is it possible to have complete dissociation (i.e. no mechanical activity)
yes
241
normal sinus rhythm
70bpm
242
bradycardia
abnormal slow rhythm (<60bpm)
243
tachycardia
abnormal fast rhythm (>100bpm)
244
when are bradycardia and tachycardia physiologic / healthy (3)
- trained athletes can have resting HR of 40 bpm
- during exercise HR can go up to 100bpm
- respiratory sinus arrhythmia
245
respiratory sinus arrhythmia
sinus rate increases as you breathe in and slows as you breathe out (more common when young)
246
pathological sinus tachycardia
resting HR > 100 bpm
247
2:1 AV block
every 2 atrial contractions has 1 ventricular (every other P has no QRST)
248
how does 2:1 AV block affect HR, CO and BP
cuts HR in half
decreased CO
decreased BP
249
where is the system blocked for 2:1 AV block
could be anywhere between AV node and bundle branches
250
solution for 2:1 AV block
electronic pacemaker
251
complete AV block
only P, no QRST
252
why is complete AV block dangerous
no ventricular contraction = no perfusion
253
cause of premature ventricular complexes (PVC)
ectopic pacemaker
254
ectopic pacemaker
excitable group of ventricular cells causes premature heartbeat outside SA node
255
parasystole
constantly firing ectopic pacemaker (benign)
256
are PVC common
yes, can be benign, just uncomfy
257
ventricular tachycardia
parasystole becoming dangerous - leads to fibrillation
258
fibrillation
no more synchronous firing, extremely fast + irregular beats; fatal if not treated in minutes
259
automated external defibrillator (AED)
treatment for fibrillation; resets all cells in heart to beat at once
260
is atrial fibrillation dangerous
no; only quality of life issue
261
what is atrial fibrillation caused by
premature atrial contraction (PAC)
262
what can atrial fibrillation lead to
irregular ventricle activation
263
how to treat atrial fibrillation
pulmonary vein isolation; ensures pulmonary vein waves cannot disturb atria
264
how to map tachycardia
sock array (attach electrodes to heart surface)
265
isochronal map
shows circus movement around an anatomical obstacle (activation propagates in circle around inexcitable scar)
- treatment = remove scar
266
reentrant ventricular tachycardia
dangerously low BP due to inadequate filling
267
what can reentrant ventricular tachycardia transition to
ventricular fibrillation
268
who discovered reentry
George Mines
269
George Mines experiment explanation
found that he could propagate signal in only 1 direction rather than 2 like normal (due to refractory block), but these inactive cells can propagate the single signal later
270
significance of George Mines discovery
possible cause of tachycardia (and it was largely true!)
271
where on the ECG is the refractory period
between QRS and T wave
272
neuron vs myocyte refractory time
neuron = few ms
myocyte = 100-300ms
273
what do colliding waves do to each other in signal propagation
block (cells are refractory to stimulation)
274
how often do the right and left ventricles beat
1/s
275
how does pressure in ventricles compare to pressure in aorta before contraction
lower
276
what causes aortic valve to open
pressure in ventricles becomes higher than pressure in aorta
277
how does aortic pressure compare to ventricular pressure right after aortic valve opens
aortic P tracks ventricular P, then ventricular P drops
278
what happens after ventricular pressure drops
aortic valve closes
279
mean arterial pressure equation
diastolic pressure + 1/3 pulse pressure
280
why do we only add 1/3 pulse pressure to calculate MAP
because pressure wave is wider at the bottom than top
281
for how much of the cycle do ventricles contract to create pressure
1/3
282
Windkessel effect
distension from compliance of vessels maintains pressure for 2/3 of the cycle where ventricles aren't contracting
283
what is the old method of measuring BP (direct)
vertical tube in an artery (liquid height = BP)
284
does liquid height depend on tube area for BP measurement
no
285
palpation
measure pressure in cuff to find BP
286
is palpation direct or indirect measure
indirect
287
2 components of palpation
aneroid sphygmomanometer and aneroid gauge/barometer
288
aneroid sphygmomanometer
cuff w bladder, inflating bulb, needle valve and aneroid gauge
289
how does aneroid gauge pressure compare to bladder pressure
same
290
what did people use before aneroid sphygmomanometer
mercury sphygmomanometer
291
where does palpation measure pulse
radial artery
292
palpation method (3 steps)
- fill cuff until no pressure detected
- release pressure slowly (5mmHg/s)
- when you feel pulse again = systolic BP
293
why does palpation measure systolic BP
the brief period where pulse pressure is higher than cuff pressure allows blood to get through, and this is close to max systolic arterial P
294
auscultation
measure Korotkoff sounds to find BP
295
auscultation equipment
stethoscope: earpiece, bell, diaphragm
296
what can you hear when there is laminar flow in the arteries and the cuff is deflated (auscultation)
nothing
297
auscultation method (3)
1. compress artery
2. place stethoscope bell on uncompressed artery
3. flow expansion from compression to no compression leads to turbulence that can be heard
298
between which two points can you hear Korotkoff sounds
start at systolic P, end at diastolic P
299
oscillometry
machine senses pressure in cuff
300
what is the most common BP measurement method
oscillometry
301
oscillometry method (2)
1. heartbeat creates pressure waves in cuff
2. drop off because cuff loosens therefore don't sense pressure well
302
nominal BP
120/80 mmHg
303
3 reasons BP regulation is important
- adjusts flow according to need e.g. exercise
- keeps flow in organs constant despite fluctuations in pressure ('autoregulation')
- minimize fluctuations in arterial P (neurohormonal control)
304
total peripheral resistance equation
TPR = (MAP - Pa) / CO
TPR = MAP / CO
therefore MAP = HR x SR x TPR
305
mean pulmonary artery pressure and pulmonary vein pressure
15 mmHg
5 mmHg
306
why can we not discount vein pressure in pulmonary perfusion pressure like in MAP
because error would be 30%
307
pulmonary perfusion pressure
10 mmHg
308
how does pulmonary vascular resistance compare to TPR and why do we know this
PVR << TPR because flow to lungs is same as system, therefore must have lower resistance
309
4 stages of cardiac cycle
1. isovolumetric ventricular contraction
2. ventricular ejection
3. isovolumetric ventricular relaxation
4. ventricular filling
310
what is the first step is isovolumetric ventricular contraction
heart contracts = AV valves close
311
how do pressure and volume of ventricles change during isovolumetric ventricular contraction
pressure increases in ventricles, volume stays constant because valves closed
312
what is the state of AV and aortic valves at the end of isovolumetric ventricular contraction
AV = closed, aortic and pulm = closed
313
what happens to ventricular pressure at the start of ventricular ejection
P increases until ventricular P is higher than pulmonary trunk P and aortic P
314
what does the increase in ventricular P at the start of ventricular ejection do
aortic and pulmonary valves open, blood flows out of ventricles
315
what happens to ventricular P during ventricular ejection after valves open
ventricular P peaks then falls
316
what is the state of the valves at the end of ventricular ejection
AV = closed, aortic and pulm = open
317
what happens at the start of isovolumetric ventricular relaxation
ventricular contraction stops, pressure drops
318
what happens as ventricular pressure drops during isovolumetric ventricular relaxation
aortic and pulm valves close, Windkessel effect maintains P in aorta and pulmonary trunk
319
what happens to the ventricles during isovolumetric ventricular relaxation, and how does this affect pressure and volume
ventricles relax, no change in volume therefore pressure drops to 0
320
what has been happening in the atria during isovolumetric ventricular relaxation
they have been filling
321
what is the state of the valves at the end of isovolumetric ventricular relaxation
AV = close, aortic + pulm = closed
322
what happens at the start of ventricular filling
atrial P > ventricular P -> AV valves open to fill ventricles
323
what happens after AV valves open during ventricular filling
SA node fires
324
what happens after SA node fires during ventricular filling
atria contract + atrial kick
325
what is the state of the valves at the end of ventricular filling
AV = open, aortic and pulm = closed
326
Wiggers diagram
shows LV, but parallel events occur in RV with lower pressures
327
how does aortic pressure change on Wickers diagram and why
spikes due to ventricular contraction, falls slowly due to Windkessel effect
328
what does the grey space on Wiggers diagram represent
ventricular filling
329
what are the blue spaces on Wiggers diagram
isovolumetric contraction and isovolumetric relaxation
330
what is the white space on Wiggers diagram
ventricular ejection
331
1st heart sound
lub = mitral/bicuspid valve closing
332
2nd heart sound
dub = aortic valve closing
333
stroke volume equation + values
end-diastolic volume (EDV) - end systolic volume (ESV)
120 - 50 = 70mL
334
ejection fraction equation + values
stroke volume / end diastolic volume
70 / 120 = 0.6
335
cardiac output equation + values
heart rate x stroke volume
70 bpm x 70 mL = 4900mL/min OR 5L/min
336
pulse pressure equation + values
max aorta pressure - min aorta pressure OR systolic - diastolic
120 - 80 = 40
337
purpose of pulse pressure
doesn't do anything because it is the difference in pressure at 2 points in time, not a pressure gradient, but it is used as a diagnostic tool because it can change in disease
338
purpose of aortic pressure
it drives flow through systemic circulation
339
frank starling mechanism
if you stretch a muscle out, it will contract with greater force
340
normal EDV
140 mL
341
what happens when EDV is increased to 210 mL (Frank Starling)
ventricular filling increases, muscle is stretched, increase force of contraction therefore SV goes from 70 to 100 mL
342
what context is Frank Starling important for
exercise
343
preload definition
ventricle wall stretch
344
what is measured as a proxy for preload and why
EDV and pressure in right atria are indices of preload; hard to measure directly
345
autoregulation definition
some critical organs control their own flow
346
experiment that demonstrates autoregulation
attach tubes to coronary arteries so that aorta no longer controls perfusion, then lower coronary perfusion pressure
- coronary flow drops then regulates itself
347
how does coronary flow regulate itself
by dilating arterioles to decrease resistance
348
autoregulatory range
40 - 160 mmHg
pressures in these ranges lead to minor changes in coronary flow; outside range, effect is lost
349
2 situations that lead to autoregulation
decreased perfusion = myogenic autoregulation
increased work = metabolic autoregulation
350
myogenic autoregulation (5 steps)
- drop in local arterial pressure in organ
- decreased blood flow
- drop in O2, increased metabolites, less vessel wall stretch in organ
- arteriolar dilation in organ
- restoration of blood flow toward normal in organ
351
why does a drop in vessel wall stretch lead to arteriolar dilation
less stretch = less calcium = less contraction aka dilation
352
metabolic autoregulation / hyperemia (4 steps)
1. increased metabolic activity of organ
2. less O2, more metabolites in organ interstitial fluid
3. arteriolar dilation in organ
4. more blood flow to organ
353
what kind of feedback systems are autoregulation
negative feedback systems
354
3 things sympathetic system modulates
HR, SV and TPR
355
1 thing parasympathetic system modulates
HR
356
3 ways to increase HR
- increase activity of sympathetic nerves to heart
- increase plasma epinephrine
- decrease activity of parasympathetic nerves to heart
357
how do sympathetic and parasympathetic systems modulate HR
SA node controls HR, systems modulate the rate (but it still beats on its own)
358
where is parasympathetic preganglionic axon
in vagus nerve in brainstem/medulla oblongata
359
what does parasympathetic preganglionic axon go to (and where)
ganglion in cardiac fat pads
360
what does parasympathetic preganglionic axon transmit to ganglion (and what receptors does it bind)
acetylcholine binds to nicotinic receptors in ganglia, causes ganglion to fire
361
what does parasympathetic postganglionic axon release, what does it bind & where
acetylcholine binds to muscarinic receptors in SA
362
how does more parasympathetic neural activity affect HR
decreases it
362
drug to block parasympathetic effects (and mechanism)
atropine binds and blocks muscarinic receptors therefore increases HR
363
where are sympathetic preganglionic neurons located
in spinal cord
364
what do sympathetic preganglionic neurons release onto ganglia
acetylcholine
365
where are sympathetic ganglia located
next to spinal cord
366
what does sympathetic postganglionic axon release (where does it go and what does it bind to)
norepinephrine binds to beta-adrenergic receptors on SA node
367
how does more sympathetic neural activity affect HR
more neural activity = higher HR (fight/flight)
368
beta agonists (HR)
binds and increases HR
369
beta antagonists (HR)
prevents binding therefore decreases HR
370
for SV control, where do the sympathetic ganglia connect
ventricular wall
371
what substance binds to ventricular wall (sympathetic)
norepinephrine
372
why does norepinephrine increase SV
because it increases contractility
373
beta agonist (SV)
binds and increases SV
374
beta antagonist (SV)
prevents binding therefore decreases SV
375
why does increasing contractility increase SV
higher max force, higher force increase rate, decreased duration of contraction (shorter refractory period therefore more APs)
376
how does increasing contractility affect SV curve
shift SV curve upwards
377
is increasing contractility the same as Frank Starling mechanism (2)
no
- same EDV but higher SV
- Frank Starling moves along same SV curve
378
tone
state of contraction of smooth muscle in the walls of the vessel
379
how does sympathetic system control vessel tone
norepinephrine binds to alpha-adrenergic receptors in blood vessels
380
how does increased norepinephrine affect vessel tone
more NE = higher TPR, higher MAP therefore more constriction / tone
381
can sympathetic system control capillary tone
no because no smooth muscle
382
how do sympathetic neurons act, and what does this mean for blood flow
discrete and organ-specific manner therefore blood flow can be regulated independently depending on physiological conditions
383
alpha agonist (TPR and MAP / tone)
activate alpha-adrenergic receptors therefore higher TPR and MAP
384
alpha blocker (TPR and MAP / tone)
bind. to alpha-adrenergic receptors and prevent activation therefore decrease TPR and MAP
385
what is neural control of adrenal glands also known as
global control of vessel tone and HR
386
does neural control of adrenal glands have an associated external ganglion
no
387
what system are adrenal glands a part of
sympathetic nervous system
388
what does adrenal medulla come from
cells of the neural crest
389
what are adrenal glands innervated by
preganglionic axon that releases ACh
390
what are the cells in adrenal gland
modified ganglion cells that don't project out
391
what do cells in adrenal gland synthesize and release into the blood
catecholamines (NE and epinephrine)
392
what are catecholamines and how do they affect HR, SV, TPR and MAP
they are alpha and beta agonists therefore increase HR, SV, TPR and MAP
393
how many blood pressure control systems do we have
MANY
394
3 ways BP control systems differ
- time scales
- strengths/feedback gains
- pressure ranges
395
baroreceptor vs renal time scale
baroreceptor = within seconds (changes HR, TPR, SV)
renal = hours to days
396
baroreceptor vs renal strength/feedback gain
baroreceptor = strong
renal = strongest
397
baroreceptor vs CNS ischemic reflex pressure ranges
baroreceptor = max at healthy normal BP range (120 mmHg)
CNS ischemic reflex = works when BP dangerously low
398
baroreceptor reflex / baroreflex
fast response to BP changes
399
baroreceptors
receptors in carotid arteries that sense pressure (sensory arm of baroreceptor reflex)
400
what do baroreceptors signal then activate (motor arm of baroreceptor reflex)
signal brainstem, then activate autonomic system
401
where are baroreceptors located
aortic arch and carotid sinus
402
4 steps of baroreceptors being mechanosensitive
heartbeat - aorta and carotid sinus stretch - channels in baroreceptors open - signals brain
403
what does the average frequency of baroreceptor firing change with
MAP (higher MAP = more firing)
404
across all MAP levels, where is the highest baroreceptor firing rate
at BP peak
405
how does standing up affect blood flow and BP
400 mL flows from trunk to legs, decreases BP = increase sympathetic and decrease parasympathetic
406
how does decreased baroreceptor firing affect HR, SV, TPR, capacitance vessels and venous return
increase HR, SV, TPR
constrcit capacitance vessels via alpha receptors
increase venous return
407
what kind of system is baroreceptor reflex
negative feedback system (decrease baroreceptor firing = increase sympathetic activation
408
result of cutting 2 nerves from baroreceptors
labile hypertension - same mean BP but more fluctuations "buffer reflex"
409
where are peripheral chemoreceptors located
close to baroreceptors (carotid and aortic body)
410
what 3 things do peripheral chemoreceptors sense
PO2, PCO2 and pH in arterial blood
411
what do peripheral chemoreceptors act on
breathing (increase frequency and tidal volume)
412
how to peripheral chemoreceptors affect HR
increase HR for faster circ (elminiate CO2 and increase O2)
413
how do kidneys control blood volume (2)
urinary loss and RAA system
414
pressure diuresis
increased arterial pressure leads to higher excretion of H2O and Na+
415
kidney function (2)
maintain levels of ions in plasma and remove waste
416
nephrons function (2)
expel H2O and waste, followed by H2O reabsorption
417
what kind of system is kidney control of blood volume
negative feedback system (increased MAP leads to more urine, and when excreted it decreases MAP)
418
what is 60% blood volume
plasma
419
how does decreasing plasma volume affect BV
decreases
420
diuretics
class of drugs used to control BP
421
RAA system (name and function)
renin angiotensin aldosterone system; senses pressure in kidneys
422
what does the RAA system sense changes in filtration rate as
changes in Na+ excretion
423
how does RAA system act on changes in filtration
signals specialized cells to release renin
424
what incdirectly senses pressure in the brain
osmoreceptors in hypothalamic neurons
425
what do baroreceptors pass signals through
vagus nerve
426
what does baroreceptor signaling through vagus nerve lead to
ADH release from hypothalamus neurons
427
what is RAA system 1
renin
428
renin
enzyme released into circulation
429
what leads to increased renin in RAA system 1
decreased MAP (low Na+ in filtrate leads to specialized cells seeing low BP)
430
renin function in RAA system 1
convert angiotensinogen to angiotensin 1
431
where is angiotensinogen made
liver
432
what happens to angiotensin 1 in RAA system 1
ACE converts it to angiotensin 2
433
where is ACE (angiotensin converting enzyme) produced
lungs; produced by pulmonary endothelium
434
what is angiotensin 2
vasocontrictor
435
how does angiotensin 2 affect TPR and MAP, and what is the overall result on RAA system 1
increases TPR and MAP
high MAP lowers renin, therefore decreases MAP
NEGATIVE FEEDBACK SYSTEM
436
RAA system 2
vasopressin / ADH
437
vasopressin / ADH (antidiuretic hormone)
synthesized in hypothalamus, released by pituitary gland into blood
438
how does ADH affect TPR
ADH = vasoconstriction = increase TPR
439
where does ADH act (+ 7 steps)
kidney
- less renal Na+ and H2O excretion
- higher plasma volume
- higher BV
- higher venous return
- higher EDV
- higher SV
- higher CO
440
how is MAP affected by ADH
increased by 2 mechanisms (increasing CO and TPR)
441
what is the overall result of ADH on RAA system 2
ADH increases MAP, which lowers ADH and decreases MAP
NEGATIVE FEEDBACK SYSTEM
442
RAA system 3
aldosterone
443
what does low MAP lead to in RAA system 3
more renin, therefore more angiotensin 2
444
where does angiotensin bind (+ effect) in RAA system 3
binds receptors in adrenal gland to release aldosterone
445
where does aldosterone bind in RAA system 3 (+ effect)
binds receptors in kidney
- causes Na+ and H2O retention
- leads to higher CO and increased MAP
446
what is the overall result of aldosterone on RAA system 3
aldosterone increases MAP, which decreases aldosterone and decreases MAP
NEGATIVE FEEDBACK SYSTEM
447
4 BP (hypertension) drugs
aldosterone receptor antagonists
angiotensin 2 receptor blockers (ARBS)
ACE inhibitors
renin inhibitors
448
aldosterone receptor antagonists
prevent aldosterone binding therefore decrease BP
449
angiotensin 2 receptor blockers (ARBS)
prevent angiotensin 2 biding in brain, arterioles and adrenal glands therefore decrease BP
450
ACE inhibitors
prevent conversion of angiotensin 1 to 2 therefore decrease BP
451
renin inhibitors
prevent conversion of angiotensinogen to angiotensin 1 therefore decrease BP
452
baroreflex in action (standing up) (3 steps)
- BP drops to 75/40 for 10 seconds (without baroreflex it would continue to drop)
- then recovers to approx normal
- systolic overall drops a little, diastolic overall increases a little to give same mean MAP
453
hydrostatic pressure equation
fluid density x gravity x height
P = pgh
454
how do hydrostatic pressure change throughout body
increases from thorax to foot because of gravity
455
why does a small change in hydrostatic pressure in venous compartment lead to large volume change (& what is the result of this)
high compliance
leads to blood pooling in legs
456
central blood volume
blood in thorax, lungs, heart and great vessels
457
how does central blood volume when you stand up
goes from 1.2L to 0.9L
458
how does venous pressure change when standing up
decreases because less blood, therefore smaller venous return
459
how does SV change when standing up (and by how much)
drops by 50% because of low venous return
460
how does CO change when standing up (by how much and why)
drops from 6 to 4.5 (not 50%)
- SV drops by 50%, but HR jumps by 50%, therefore CO = 0.75 of original value
461
how does HR change when standing up
increases by 50% (from 60 to 90)
462
if CO is 75% of what it was, how is MAP preserved
constriction in arterioles leads to increased TPR (baroreflex)
463
2 reasons we faint when standing too long
- blood pooled in leg veins
- loss of plasma volume
464
what does blood pooling in leg veins mean for the body
less central blood volume therefore less venous return
465
how to avoid blood pooling in leg veins
flex calf muscles periodically ('muscle pump' = reduces need for high HR)
466
how do we lose plasma volume when standing for too long (2)
- water moves to interstitial space through capillaries
- higher pressure in legs from standing leads to more plasma volume loss
- leads to lower venous return therefore lower MAP
467
how much plasma volume can we lose by standing for 15 mins
750 mL
468
starling forces
physical forces that determine movement of fluid between capillaries and tissue fluid
469
2 starling forces
hydrostatic pressure and oncotic pressure
470
hydrostatic pressure
force exerted by blood inside capillary / interstitial space
471
oncotic pressure
osmotic pressure generated by large molecules (especially proteins)
472
how much water do we lose a day and how does this compare to plasma volume
lose 4L of water a day, only 3L of plasma
473
how is water returned per day and how
4L returned per day via lymphatic system
474
effect of sympathetic venoconstriction
lower venous capacitance and higher venous return
475
natriuresis
Na+ excretion in the urine by kidnets
476
chronic venous insufficiency
orthostatic hypotension at short time scales
477
2D reentry demo summary
showed why some PVCs lead to tachycardia and then fibrillation
- spiral generated by interaction of ectopic beat (PVC) w normal wave of excitation = tachycardia
- hard to get by chance, which explains why PVCs are often benign
478
different between ventricular tachycardia and ventricular fibrillation
tachycardia = more beats, but overall process. inright order
fibrillation = system out of sync therefore steps not happening in the right order
479
how does HR change with power (exercise) and values
increases linearly (from 60 to 180bpm - 3x increase)
480
why does HR increase with power
due to increased sympathetic tone and decrease in parasympathetic tone
481
how does SV change with power (exercise) and why
increases a little due to increased sympathetic activity, then dips at very high HR because decreased diastolic period = decreased filling time = decreased EDV = decreased SV (frank starling)
482
how does CO change with power (exercise), by how much and why
increases linearly by 3x, mostly depends on HR (from 5 to 15)
483
how does MAP change with power (exercise), by how much and why
increases by approx 20%
- systolic increases from 120-190, diastolic has approx no change
484
cardiac stress test
check to make sure systolic increases to a high level (~200mmHg); measure of the ventricles' ability to generate force - low value may mean damage e.g. scar tissue
485
how does TPR change with power (exercise) and why
drops to 40% of resting value because muscles consume more O2 and generate more waste (metabolic autoregulation)
486
how does O2 consumption change with power (exercise) and why
increases by 9x (up to >2000mL/min) because 3x increase in CO and 3x arteriovenous O2 diff
487
how much does blood flow to muscles, skin, heart and other organs change in exercise
increases 12x in muscles
increases 5x in skin
increases 3.5x to heart
decreases to other organs to keep MAP constant
488
how does the increase in flow compare in trained vs untrained individuals
untrained = 3.5x increase
trained= 7x increase
489
at rest, what determines tone
alpha beta receptor activation balance
490
what overrides the alpha beta receptor activation in exercising muscle
metablolic control
491
what experiences vasoconstriction in arterioles during exercise from neural control
non-exercising muscle
492
does training affect max HR
no
493
why does training increase CO
increases SV (contractility) due to hypertrophy (each cell gets bigger = resting HR falls)
494
who are arrhythmias more common for
trained athletes
