Cardiovascular Flashcards
1
Q
FUNCTIONS of the Cardiovascular system
A
- Bring nutrients into the body (e.g. from liver to lungs)
- Bringing fuel to cells (e.g. glucose from liver to lungs)
- Bringing O2 to cells from lungs
- Removal of waste products
- Circulation of hormones
- Circulation immune cells and antibodies
- Regulation of pH
- H2O balance
- Thermoregulation
2
Q
What circulation-type in insect circulation?
A
OPEN CIRCULATION with a dorsal vessel
3
Q
How does fluid move in the insect circulation?
A
Fluid pumps out to the head and loathes all the organs and
seeps back in at a very slow rate to re-enter the
cardiovascular system
4
Q
What is the pumped fluid in insect circulation?
A
HAEMOLYMPH
5
Q
What circulation-type in fish/piscine circulation?
A
Blood is always contained in either heart or vessel –> closed circulation
6
Q
What type of circulation is when blood is always contained in either heart or vessel
A
closed circulation
7
Q
How many loops in fish/piscine circulation?
A
Single loop circulation
8
Q
How many chambers in fish/piscine heart?
A
2 chambers
9
Q
Where does gas exchange occur in fish/piscine?
A
Exchange of gas occurs in gill capillaries
10
Q
Where does deoxygenated blood come from?
A
the systemic capillaries
11
Q
How many loops in amphibian/reptile circulation?
A
2
12
Q
How many chambers in amphibian/reptile circulation?
A
3
13
Q
What circulation-type in amphibian/reptile circulation?
A
closed
14
Q
What type of heart do amphibian/reptiles have?
A
Univentricular heart
15
Q
How can amphibian/reptiles breath
A
- Can breathe through skin via diffusion
16
Q
How many loops in avian/mamalian circulation?
A
double-lopped
17
Q
How many chambers in avian/mamalian circulation?
A
4
18
Q
What circulation-type in avian/mamalian circulation?
A
closed
19
Q
How many hearts in avian/mamalian circulation?
A
right and left
20
Q
What seperates the two hearts
A
Interventricular septum
21
Q
What circulation is the right heart
A
pulmonary
22
Q
What circulation is the left heart
A
systemic
23
Q
Cardiac Muscle Cell/Myocyte length and diameter
A
- 100μm long, round, 20μm in diameter
24
Q
Diameter of capillaries
A
~5μm
25
Max distance between capillary and myocyte
~10μm (half of 20μm because of midline)
26
Ratio on average between capillary and cardiac myocyte
- On average 1 capillary/1 cardiac myocyte
27
Flow between capillary and myocyte
Convective flow to inside
28
Wall of capillaries
~5μm
29
How does oxygen come into the capillary?
- Oxygen comes in via bulk flow which is internalized
30
PO2 in alveolus compared to in the RBC in capillary
higher
31
3 Components of the Cardiovascular System
1. Pump = heart 2. Pipes = vessels 3. Fluid = blood
32
Fick’s law states
that flow is directly proportional to:
- diffusion coefficient,
- area,
- concentration difference i.e. gradient
flow is inversely proportional to:
-Thickness of membrane
33
Flux
diameter times the concentration gradient
34
Blood volume value for the standard man
5L
35
Max oxygen/exercise peaks at what age
~25 years of age
36
blood per kg of body weight
~75mL of blood per kg of body weight
37
Match
- VENOUS SYSTEM
- ARTERIAL SYSTEM
> Resistance system
> Capacitance system
VENOUS SYSTEM --> CAPACITANCE SYSTEM
| ARTERIAL SYSTEM --> RESISTANCE SYSTEM
38
right and left ventricles volumes and pressures
Both right and left ventricles are pumping out the same volumes
just with different pressures
39
the left heart pumps out a flow of blood which
splits and divides among all the organs
40
Where does the flow leave and enter? what side?
leaving the left heart
| entering the right heart
41
Lungs connection/flow with the heart
lungs are in series with the left heart therefore they have the same flow
42
organs connection/flow with the heart
the organs are in parallel with the heart therefore they have
different flows
43
Cardiac Output =
Venous Return = 5L/min
44
The flow or flow rate through a vessel depends on 2 factors:
Velocity of flow
| Cross-sectional area of the lumen
45
DISTIBUTION VESSELS
bring blood from the heart to the organ
46
The velocity of blood at all points in a cross-section
The velocity of blood is not the same at all points in a cross section since the blood close to the walls is
slower and blood close to the middle is faster and therefore, we must take the mean velocity when calculating flow
47
distribution vessels examples
```
Aorta and other large vessels are called distribution vessels
function to bring blood from the heart to the organ
```
48
vessel that drains the bottom 1⁄2 of the body
Lower vena cava
49
vessel that drains the upper 1⁄2 of the body
Superior vena cava
50
Almost all of resistance to flow lies in the
small arteries and arterioles; the anatomical sites that
| generate the resistance to flow
51
What occurs in the capillaries
exchange of oxygen and carbon dioxide and sugars (wall = 1 cell thick --> small
diffusion barrier)
52
Why is the aorta thick?
§ The aorta is thick because it needs to withstand a high pressure
53
Number of each of the vesels, most and least
capillaries, then venules, arterioles, veins, arteries, vena cava, aorta
54
From the vena cava’s blood, where does the blood go?
it goes to the right atrium
55
Arterial tree is created by
draining all the blood from a subject and injecting a rubber material a.k.a arterial cast
56
Vessel place with the most area
capillaries
57
Vessel place with the greates vecloity of blood
capillaries
58
Every cell in the kidney is close to a small vessel why?
so diffusion is able to create a large flux
59
The summed cross-sectional area gets higher from
the aorta to the
| capillaries
60
§ The advantages of a branching network
Any cell is very close to a capillary
A high total area of the walls and capillaries
A low blood flow velocity in capillaries
A high total cross-sectional area
61
The practical unit of pressure
cm H2O; mmHg
62
Blood pressure values
120/80 mmHg
63
Central Venous Pressure
5-10 cm H2O
64
Intravenous infusion
squeeze bag to increase pressure
65
The average mean pressure of the aorta
100mmHg
66
Veins mean pressure
~ 5mmHg
67
Resistance vessels
arterioles and small arteries
68
Pressure in systemic circulation
120/80 mmHg
69
Size and pressure of left ventricle vs right
The left ventricle is bigger. generates a high pressure to
the systemic circulation and the right ventricle to the pulmonary circulation is a lot smaller and therefore generates a smaller pressure
70
How long is the aortic value open for? what does this do?
Aortic valve opens for ~1/3 of the cardiac cycle which will increase the pressure due to the dumping of stroke volume into the aorta and then the valve will close and stay closed for 2/3 of the cardiac cycle and during that time the blood in the aorta will close and stay closed for 2/3 of the cardiac cycle and during that time the blood in the aorta and the vessels will leak out which decreases the pressure
71
The waveform of very strong pulse in the arterial system
PULSALTILE WAVEFORM
72
Max pressure vs min pressure on pulse waveform
Systolic Pressure = Max
| Diastolic Pressure = Min
73
What happens to oscillations as they reach the veins
As you move through the vascular tree, these oscillations get damped out and by the time you get to the veins they are basically gone
74
Pressure in the venous system
almost CONSTANT
75
SYSTEMIC PRESSURE vs PULMONARY PRESSURE
SYSTEMIC PRESSURE > PULMONARY PRESSURE
76
Hydrostatic Pressure
Pressure due to standing water
The pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of
gravity
77
Why does hydrostatic pressure arise
Hydrostatic pressure is due to the fact that we are
| sitting in a gravitational force field
78
Mercury Sphygmomanometer
Manometer measures pressure in liquid or gas
It is the measure of arterial blood pressure
Mercury is a neurotoxin
As you pump air into a bag the pressure will rise because the pressure at the bottom rises
79
CVP or RAP is
5-10 cmH2O
80
Perfusion Pressure =
inlet pressure (arterial pressure) – outlet pressure (venous pressure)
81
Normally Perfusion Pressure is
Normally the arterial pressure is much bigger than the venous pressure (100 mmHg vs 5 mmHg) so: ∆pressure is ≈ 95 mmHg ≈ arterial pressure
82
what drives blood flow through the tube
Perfusion pressure
83
Flow =
Perfusion pressure/ resistance
84
Can resistance be directly measured
You cannot make direct measurements of resistance
85
Laminar or Parabolic Flow
Blood close to the walls moves the slowest and blood close to the midline moves the fastest
There are infinitely thin layers of blood
sliding over each other therefore, there is friction which produces viscosity and generates heat which results in a loss of pressure
-Viscosity is due to internal friction between layers
-It’s a parabolic velocity profile
86
Why does pressure drop?
§ Pressure drops because of internal friction
87
Poiseulles Law formula
R= 8vL/pi r^4
88
If you double the radius, how the resistance change
get a 16-fold fall in resistance
89
When is Poiseulles Law valid?
§ Poiseuille’s Law is only valid for Laminar Flow
90
How do Frictional losses in a viscous fluid affect pressure and heat
generate heat which causes
| a fall in pressure down the vessel
91
§ The body controls vessel resistance by:
o Perfusion Pressure
o Length of Vessel
o Viscosity of Blood
o Radius of Vessel (vasoconstriction and vasodilation)
92
Vessel Resistance happens at the level of
resistance vessels (small arteries and arteries
93
what acts on the smooth muscle to make it relax ? why
Local metabolites are what act on the smooth muscle to make it relax which causes a decrease in
resistance which increases flow
94
All arterioles and smooth muscle in the body are innervated by
ANS
95
Restistance vs radius
R= 1/r^4
96
When you put things in series the overall resistance
increases, combined resistance is ALWAYS higher than either one of the 2 component’s resistance
97
When you put things in parallel the overall resistance
decreases, combined resistance is ALWAYS lower than either one of the 2 component’s resistance
98
Compliance
how stretchy something is
99
capacitance vessels
Most of the blood is stored in veins and venules which are
capacitance vessels
o Pretty compliant
100
Compliance in veins
the total pressure is low and the volume is higher so the slope is low
which means it has a high compliance
101
Compliance in arteries
the total pressure is
| higher than the veins and the total volume is lower, therefore the slope is higher and thus the compliance is lower
102
Why is the complaince of arteries less than veins?
The external diameter of the arteries and the veins are the same but
the lumen is much smaller in arteries because they have a much
thicker vessel wall due to more layers of smooth muscle and
therefore the blood flows through a smaller diameter when passing through
As the fluid increases the pressure increase, once again the veins are much more compliant than the arterie
103
How many chambers in human heart
4
104
Where is deoxygenated blood in the heart
right atrium + ventricle
105
Where is oxygenated blood in the heart
left atrium and ventricle
106
when the right ventricle contracts what happens
the valve opens to go into the pulmonary trunk
107
Flow in the Right Heart
```
Superior vena cava
right atrium
right ventricle
pulmonary trunk
bifurcation to the left and right pulmonary arteries
right/left lung
```
108
Flow in the Left Heart
```
2 left + 2 right pulmonary veins bring in blood from the lungs
left atrium
crosses valve
left ventricle
aorta
```
109
the right and left atria are separated by
The inter-atrial septum
110
the right and left ventricles are separated by
the inter- ventricular septum
111
Size of ventricular free wall
the left ventricular free wall is much bigger than the right ventricular free wall
the thickness of the muscle is much thicker in the left ventricle
o generates 10x greater pressure
112
valves in heart
2 atrioventricular valves, 2 semilunar valves (outlet of the ventricle)
113
The right atrioventricular valve
tricuspid valve
114
The left atrioventricular valve
mitral/bicuspid valve
115
The right semilunar valve
pulmonary valve
116
The left semilunar valve
aortic valve
117
All 4 of the valves lie in the
fibrous ring of the connective tissue
118
Is the right semilunar valve open or closed? why
As the right ventricle contracts the valve is closed but as the pressure builds it pushes the valve open
119
What is attached to the top of the papillary muscles
| ?
Chordae tendinae
120
When the ventricles contract, what happens to the pressure and flow?
there is a high pressure in the ventricle and a low pressure in the atrium
so the flow goes to the ventricle
121
When the ventricles contract, what happens to the papillary muscles
Papillary muscles contract at the same time as the ventricles, anchored to the end by the free wall
122
EVERTED
When the leaflet of the valve moves out
| You want to avoid eversion or prolapse of the valve
123
endocardium/endothelium
The connective tissue that lines the inside of the heart
124
epicardium
The connective tissue that lines the outside of the myocardium
Epicardium (inner), pericardial fluid/space, pericardium (fibrous sac)
125
If the papillary muscle ruptures, what happens?
you get
| mitral regurgitation and thus need a mitral valve replacement
126
What is the electrical/mechanical device in cardio?
heart
127
What causes causes depolarization
| and an action potential of the heart muscle cell
ACh binds to receptors on the muscle cell
128
What does the action potential of the heart muscle cell trigger
an influx of calcium ions into the cell
| which generates the force of contraction
129
If there is no action potential then there is
no mechanical contraction
130
What makes up 99% of the heart
Cardiac muscle cells
131
Sinus node is made of
specialized cardiac cells that drive the beat
| of the heart
132
The heart beats because
the cells in the SA (sinoatrial) node are
| spontaneously active
133
Where does the depolartization spead to?
The wave of depolarization/activation spreads across the 2 atria but
can’t go further because of the fibrous ring
134
Where does the AV node travel?
```
The AV (atrioventricular) node travels down the bundle of His which
branches into the left and right bundle branches
```
135
Purkinje fibers
are cardiac cells and are NOT nerves
2 different action potentials are travelling down and end
up in this branching structure
which are
embedded in the myocardium on the endocardial side of the muscle
136
The activation moves from
Purkinje cell to cardiac cell
137
The simultaneous activation of all the cells in the ventricle creates
a very
| powerful contraction
138
Cardiac cells meet at
the intercalated disks and the membranes are
| stuck together by gap junctions
139
Gap junctional channels
are hemichannels which means that there is half
| in each cell
140
as action potential propagation what is the direction of K+ and Na+
K+ moves in the same direction as action potential propagation and Na+ moves in the opposite
direction (the local current)
141
What follows the depolarization
| wave
A Repolarization wave
142
Electrocardiogram
Recording of the electrical activity of the heart from the surface of the body
143
ECG
extracellular recording
144
This lead is essential as it is the reference lead
The right leg lead is essential as it is the reference lead and always needs to be attached to the patient
145
The amplitude of an action potential vs ECG
The amplitude of an action potential is ~100mV (intracellular) whereas the amplitude for an ECG is 1mV (extracellular)
146
Action potential vs ECG
Action potential- intracellular
| ECG - extracellular
147
Where does Atrial excitation start and end
Atrial excitation starts at the SA node and ends at the AV node (P-wave)
148
P wave
end of Atrial excitation at the AV node
149
How does Ventricular excitation begin
after atrial relaxation (Q-wave)
150
How does Ventricular excitation end
```
completes with the contraction of the
Purkinje fibers (R, S waves)
```
151
Do you see anything with the activation of the SA node
you can see nothing with the activation of the
SA node, only start to see something when the
atrium contracts
152
T-wave
Ventricles Relax (T-wave) --> repolarization
153
Leads
Electrode itself: e.g. RA lead
| Combination of electrodes taken to the voltmeter: e.g. lead 1
154
Bipolar Limb Leads
2 leads from the voltmeter are put on the surface of the body
right leg not involved
155
Unipolar chest leads
V1-V6 (left to right)
156
Number of unipolar leads
12 unipolar leads (maybe 9)
157
ischemia
An inverted T-wave
158
Unipolar limb leads
aVR, aVL, aVF
159
How do Action potentials spread through the heart
Action potentials spread from left to right and from top to bottom through the septum
160
2 steps to ventricular activation
Septum
| Ventricular walls
161
The duration of action potentials in cardiac muscle vs nerve or skeletal muscle
The duration of action potentials in cardiac muscle is longer
than in nerve or skeletal muscle
162
Resting potential in cardiac vs neurons
Resting potential more hyperpolarized than in neurons (more
| negative)
163
Resting potential cardiac cell
-90mV
164
Upstroke of the resting potential
local current circuits
| activate
165
calcium channels
2 CaL (long-lasting)
166
Nernst Potential:
quation that relates the reduction
potential of an electrochemical reaction to the standard electrode potential, temperature, and activities of the chemical species undergoing reduction and oxidation
167
Membrane with K+ channels
equilibrium potential
-100mV which is why the Nernst potential sits at -
90mV because it’s basically all K+
168
sodium channels at rest
Very few sodium channels are open at rest but it rises
| and falls very quickly (~ 1ms)
169
At rest compare the following
| Pk, P Na P Ca
Pk >> P Na P Ca
170
What is the upstroke
the fast inward Na+ current
171
What is the plateau
inward motion of sodium
172
How many potassium channels
many
173
Do sinus node cells have a resting potential
no,
Sinus node cells are NEVER at rest therefore, they don’t have a resting potential
instead they have a pacemaker potential or a spontaneous diastolic depolarization
174
Slow depolarization is the cause of
a spontaneous diastolic depolarization
175
diastole
The muscle is relaxing
176
Sinus node vs ventricle action potential
The upstroke is much slower because there are no
sodium channels or current
No INa in the sinus node cells, instead they rely on ICaL to
generate the upstroke
177
Rate of Rise of Upstroke in slow vs fast
§ Slow: 1-10 V/sec
| § Fast: 100-1000 V/sec
178
Conduction velocity in slow vs fast
§ Slow: 0.01-0.05 m/sec
| § Fast: 0.5-5 m/sec
179
Examples of slow action potentials
SA node
| AV node
180
Examples of fast action potentials
```
ventricular muscle
atrial muscle
bundle of his
bundle branches
purkinje fibres
```
181
The ECG is related to the
atrial and ventricular AP
182
On the ECG, Atrial AP occurs at the
P wave: depolarization of right and left atrium
183
On the ECG, 1st cell in the ventricle to activate
happens at the start of the Q wave
184
Premature Ventricular Contraction (PVC)
Pain in chest, angina pectoris which means he has myocardial ischemia (aka not getting enough blood flow to the cardiac muscle)
185
ectopic beat
comes from an unusual place that it shouldn’t be in the ventricles and is a direct consequence of the fact that the individual is suffering from significant myocardial ischemia;
186
What does a PVC progress to?
to a regular ventricular tachycardia (VT) before progressing to ventricular fibrillation (irregular)
187
Ventricular Tachycardia
| time?
A tachycardia is when the heart rate is too fast due to the PVC
the time between ventricular complexes is 0.2 seconds
188
Ventricular Tachycardia origin
the origin is in the ventricles themselves
| - ventricular tachycardia
189
What can PVC and ventricular tachycardia result in
not enough blood can enter in a short amount of time so the stroke volume and cardiac output will fall
PVC to ventricular tachycardia to ventricular fibrillation (3rd arrythmia)
190
cardiac output during ventricular fibrillation
none
191
During VT what is happening to the action potentials
when the AP is whipping around, a part of the wave front will block the actual
productions which will stop propagation, by the time you are in VFib there are multiple AP circulating in the heart that come out of nowhere
192
treatment for VFib
defibrillation whereby you inject a pulse of current into the ventricles
193
arterial pulse in VFib
As soon as you go into VFib there is no more
| arterial pulse
194
AED
Automated External Defibrillator (external
| because the current is applied from the outside of the body)
195
Mapping of Cardiac Electrical Activity
Computer constructs an activation map
| Base of ventricle at top (rings go from the apex to the base)
196
Heart attack
myocardial infarction, death of muscle in the ventricle
197
circus movement re-entry cure
To cure this arrythmia they must remove the scar tissue
198
The transition from VT to VF
involves the breakup of a single wave with VT into multiple AP in a
circulating, random, chaotic way
199
RE-ENTRANT VENTRICULAR TACHYCARDIA involves
cardiac muscle that is inhomogeneous which means that is doesn’t have exactly the same
refractory period everywhere
200
AFib
atrial activation (premature) which triggers AFib (PAC)
201
The origin of most PSE
is inside the veins (where the ectopic beat comes from)
202
Excitation-Contraction Coupling
Process by which the AP sweeps through the atrial and ventricular muscle
203
As the AP arrives, what happens to the channels?
As the AP arrives the Ca channels being to open and calcium
floods into the cell and diffuses through the cytoplasm where it
binds to a receptor
204
What does calcium bind to/
to a receptoràRyanodine Receptor aka Ca Channel
205
When calcium binds to the receptor it opens, what happens?
The Sacroplasmic Receptors is full of
calcium so if the cannel opens the concentration outside is low
and the calcium leaves to make its way into the cytoplasm
206
the initiation of the whole series of contraction with myosin
and actin
Ca bind to troponin complex
207
Calcium channels cluster at the
base of the T-tubules
208
As the calcium concentration increases in the cytoplasm there will be
more binding of the calcium to
| the troponin
209
calcium concentration and contraction time compared to AP
Both the calcium concentration and contraction are delayed
with respect to the AP
The calcium current comes in a bit later than the action
potential because it takes time for both the binding and
diffusion
210
Does Activation = contraction
No Activation ≠ contraction
211
Electro-mechanical dissociation
an example of pulseless
| electrical activity
212
Can AP propagate if the heart is dead
AP can still propagate through the heart even if dead; this would be an example of when the electrics
are working but the mechanics are not
213
When does systole start
Systole starts with the contraction of ventricles
214
for
| valves to open/close, what does the pressure in the ventricles have to do?
Pressure in the ventricles only goes up a few mmHg for
| valves to open/close
215
When the aortic valve closes the ventricular pressure
falls
extremely quickly and will dip to be lower than the
pressure in the atrium
216
Does the mitral valve close or open until the next beat
stays open
217
At resting heart rate diastole takes how much of the cardiac cycle
~2/3
218
If the pressure in the atrium is higher than the ventricles, what happens
AV valve opens
219
P-wave
atrial activation, extra pump of blood due to the atrial contraction
220
The QRS complex starts after the
invasion of the ventricular muscle by the AP of strokes where you get the influx of calcium and a rise in ventricular pressure due to the opening of the aortic wave and the closing of the mitral valve
221
T-wave occurs
during the fall of ventricular pressure as the levels of free calcium in the cytoplasm fall for the strength of contraction
222
At the end of the diastolic period, wat is the volume in the ventricle? name?
At the end of the diastolic period, you have the maximal
| amount of volume in the ventricle and that’s called the END DIASTOLIC VOLUME
223
minimum volume in the ventricle
The minimum volume is called the END SYSTOLIC VOLUME
224
First heart sound is known as
LUB
225
Second heart sound is known as
DUB
226
What makes the LUB sound
When the mitral/AV valves simultaneously close you get the 1st sound (LUB)
227
What makes the DUB sound
When the aortic/pulmonary valves simultaneously close you get the 2nd sound (DUB)
228
What produces the sounds
When the valves snap shut it creates vibrations in the blood/valves which produces the sounds
229
What side of the heart is the wiggers diagram for ?
left
230
2 phases in systole
isovolumeric ventricular contraction
| ventricular ejection
231
2 phases in diastole
isovolumeric ventricular relaxation
| ventricular filling
232
first sound occurs during what phase
isovolumeric ventricular contraction
233
second sound occurs during what phase
isovolumeric ventricular relaxation
234
Stroke volume
END DIASTOLIC VOLUME - END SYSTOLIC VOLUME
235
Stroke volume amount
70
236
END DIASTOLIC VOLUME
120
237
END SYSTOLIC VOLUME
50
238
EJECTION FRACTION
STROKE VOLUME/END DIASTOLIC VOLUME
239
EJECTION FRACTION VALUE
70/120 = 0.6 or 60%
240
CARDIAC OUTPUT
HR x stroke volume
241
CARDIAC OUTPUT VALUE
5 L/min
242
major difference between the left and right heart
he pressure is much lower in the right heart
243
the peak pressure in the left heart
110mmHg
244
the peak pressure in the right heart
25mmHg
245
How does increased End-Diastolic Volume (EDV) affect Stroke Volume (SV)
increased End-Diastolic Volume (EDV) produces increased Stroke Volume (SV)
246
the more you fill the ventricles, how does the force of contraction change?
the more you fill the ventricles, the larger the force of contraction
247
If the pressure in the right atrium increases and the AV valve is open
the ventricle will fill more causing
the EDV to increase and thus the stretch in the walls of the ventricles will increase so the force of contraction and thus the stroke volume will also increase
248
What is the Systemic Arterial Blood Pressure (BP) measuring
the pressure on the arterial side of circulation NOT venous side
249
Systolic BP
maximum pressure (120 mmHg in standard man)
250
Diastolic BP
minimum pressure 80 mmHg in standard man)
251
BP
[systolic BP / diastolic BP] (120/80)
252
Mean/Average BP (MAP)
≈ diastolic pressure + 1/3 pulse pressure = 100 mmHg
253
Windkessel Effect
Air decompresses to push air out of the nozzle
254
What happens as you increase stretch
contraction is greater because of frank sterling mechanism
255
Windkessel Effect in the heart
• For 2/3 of the cycle the ventricles aren’t contributing to the pressure because they are closed
• The stroke volume dumps blood into the aorta which causes it to stretch out
• The aortic valve then closes so the pressure will be available during the diastolic
period to drive blood out of the systemàduring that period the heart is NOT
pumping
• Results in a waveform where the pressure stays high for a long time
• Converting your cyclic pump (where you go up to 120mmHg for 1/3 of the
cycle and then come back down to 0) into a steady pressure that lasts xthroughout the cardiac cycle
• Flow is constant
• There is electrical resistance, capacitance is compliance
256
How to measure BP
```
direct
indirect
- palpation
- ausultation
- oscillometry
```
257
Method of Palpation
Feel pulse in the radial artery
| Artery gets squeezed--> completely occluded
258
When you feel pulse in palpation what are you getting
SYSTOLIC BP
259
Why is there no sound during flow
• Flow in this artery is laminar -
260
Why do you begin to hear a noise in palpation
You begin to hear a noise because the blood is squeezing through to get blood expansion which creates turbulent flow
• The turbulent flow is what shakes the walls of the arteries and creates noise called Korotkoff sounds or BP sounds
• You hear the sounds all the way down until you hit the diastolic pressure because there the artery is partially occluded
261
Method of Auscultation
• Most frequently used
• Automated method
• Pressure transducer in the cuff is what makes the measurements
• Computer looks at the shape of the waveforms to make the measurements
of BP
262
Auscultation sounds
Systole starts at the start of the 1st heart soundàthe moment the AV valves
close and ends when the diastole starts which is when the aortic valve closes
263
Why is Blood Pressure Important?
Perfusion pressure is essentially perfusion pressure divided by resistance to flow
• Organs adjust flow according to their need via the change in resistance
• The body is trying to keep arterial pressure (flow) constant, despite fluctuation is P (autoregulation)
• Minimize fluctuations in P-arterial (neuro-hormonal control)
264
Total Peripheral Resistance (Systemic Vascular Resistance)
The resistance that the left ventricle has to pump against, combined with the resistance of all the organs on the systemic side of circulation
265
Total Peripheral Resistance (Systemic Vascular Resistance) formula
• [MAP- Pressure in Right Atrium ]/flow of aorta (cardiac output)
* Mean pulmonary artery pressure = 15mmHg
* Pulmonary vein pressure = 5 mmHg
* Pulmonary Perfusion Pressure = 10 mmHg
266
The mean arterial BP is determined by 3 things
o Heart Rate
o Stroke Volume
o TPR
267
PVR vs TPR
• PVR << TPR (~1/10)
268
Autoregulation (Flow) occurs in
Brain, heart, kidneys
269
What is Autoregulation (Flow)? why?
• Vital organs like the brain, heart, kidney have a lot of order and thus regulation (other organs it doesn’t
matter)
• Brain/heart are aerobic so they need oxygenated blood
270
Steady state effect
Flow is being regulated to be more or less independent of the
perfusion pressure
• Perfusion pressure = 0 --> flow = 0
271
2 Mechanisms of Auto-Regulation
Local Metabolic Control
| Myogenic Mechanism
272
Local Metabolic Control
o Primary is change of metabolic activity of the organ, which then changes the blood flow
o The supply of the blood flow matched the requirement of the tissue
o Autoregulation; the stimulus is a change in BP and the reflex is to bring flow back to normal
273
Hyperemia
; e.g. seizure
274
Local Metabolic Control muscle cells
skeletal muscle, cardiac muscle
275
Myogenic Mechanism muscle cells
Arteriolar smooth muscle
276
Myogenic Mechanism
* Origin of the myo-reflex is in the walls of the smooth muscle vessels
* Both metabolic and myogenic mechanisms are occurring simultaneously
* An increase in arterial blood pressure simply flips all the arrows
* This is very important for vital organs
277
Where is the cell body in the autonomic innervation of the sinoatrial node?
The cell body of the neuron sits in the brainstem
278
A drug given frequently to INCREASE HEART RATE is
ATROPINE
279
What does ATROPINE do
Binds to the muscarinic receptor (PNS ANTAGONIST) or blocker
| Increases the heart rate which increases the cardiac output which increases the blood pressure
280
Sympathetic neuro transmitter
pre ganglion ACH
| post ganglion NE
281
Parasympathetic neuro transmitter
pre ganglion ACh
| post ganglion ACh
282
Parasympathetic receptors
pre ganglion nicotinic receptor
| post ganglion muscarinic recptor
283
sympathetic receptors
pre ganglion nicotinic receptor
| post ganglion ß-receptor
284
Binding of NE to ß-receptor affect on heart
results in speeding up
| of the heart rate
285
ß-antagonists
Slow heart rate
286
ß-agonist
activates the receptors therefore the heart rate, cardiac output, and MAP increase
287
What happens to the axons that interact with ventricular muscle
NE binds to the same ß-adrenergic receptor which goes through a whole cascade of intracellular events to eventually result with an increase in calcium inside the cell so the force of contraction increases which causes the contractility of the muscle to increase
288
Autonomic Control of Heart Rate
this increase the activity of the nerves to the heart rate through activation of the ß-adrenergic receptor which also activates the adrenal glands which causes an increase in the concentrations of epinephrine and norepinephrine in the blood that eventually makes its way to the ß-adrenergic receptors on the SA node
289
Baroreceptor Reflex
Baroreceptors are never terminals that lie in 2 places in your body:
o Arch of the Aorta
o Carotid Sinus
290
The carotid artery
bifurcates into an internal carotid artery that
supplies your brain and an external carotid artery that supplies your jaw, face, scalp
Right where it bifurcates you have a swelling which is a sinus (carotid sinus)
o The nerve terminals are embedded in the carotid sinus and the arch of the aorta
o They send information to the brain to communicate the state of the blood pressure (MAP)
291
As the rate of MAP increases, affect on rate of firing
As the rate of MAP increases, the rate of firing also increases and
vice versa
292
• When the BP falls, the reflexes tries to do 4 things:
o Increase Heart Rate
o Increase Contractility of Ventricular Muscles
o Effect of Vasoconstriction
o Effect of Baroreceptor
293
If the stroke volume is cut in 1⁄2 then the cardiac output should? why does it not?
also be cut in half but it only goes to 3⁄4 the original volume which means that the heart rate increased
-The heart rate increases in the 1st cycle that you stand up due to the action of the baroreceptor reflex
294
orthostasis/static
miantenane of an upright stnading posture
295
What would happen if the baroreceptor reflex wasn't working when going from sitting to standing?
Arterial BP would continue to fall
296
baroreceptor reflex
negative feedback to one of the body's homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels.
297
when going from sitting to standing, what happens to arterial blood pressure?
no change
298
when going from sitting to standing, what happens to right atrial mean pressure?
drops from 6 to 0
299
when going from sitting to standing, what happens to cardiac output?
drops by 0.75
300
when going from sitting to standing, what happens to stoke volume?
drops by 0.5
301
when going from sitting to standing, what happens to heart rate?
increases by 1.5
302
when going from sitting to standing, what happens to forearm blood flow?
decreases
303
when going from sitting to standing, what happens to renal blood flow?
decreases
304
How does the body maintain arterial blood pressure?
contractility
venoconstricture
heart rate
arteriolar constriction
305
when going from standing to calve contractions, what happens to arterial blood pressure?
no change (slight increase)
306
when going from standing to calve contractions, what happens to right arterial mean pressure?
increases back to resting level
307
when going from standing to calve contractions, what happens to cardiac output?
increases back to resting level
308
when going from standing to calve contractions, what happens to stroke volume?
increases back to resting level
309
when going from standing to calve contractions, what happens to heart rate?
decreases back to resting level
310
when going from standing to calve contractions, what happens to forearm blood flow/renal?
increases back to resting level
311
When you stand, what is the hydrostatic pressure as you go lower
When you stand, there is a big hydrostatic pressure and the lower down you go the more the pressure
increases
312
Muscle Pump in Orthostasis
When you constrict the calf muscles, it increases the pressure in the veins which will push open the one valve while closing another
• This is the muscle pump and the volume of the blood in there is reduced so the pressure will fall
• By simply constricting your leg muscle, you bring the pressure in the veins down to a low level,
otherwise it’s at a very high level
313
Starling forces
a pressure that is driving fluid or water out
| of vessels
314
Filtration
pushing fluid out
315
Absorption
pulling fluid in
316
Max Heart Rate =
220 – age (years)
317
Max Heart Rate is proportional to
Power
318
As you increase the intensity of exercise, you are increasing
the activity of the SNS which acts on the
sinus node to increase the heart rate
o You also have inhibition of parasympathetic tone
319
Heart Rate vs Power
increases linearly
320
Stroke Volume vs Power
increases until very high HR
321
Epinephrine affect on HR and CO
• Epinephrine will help to increase HR and CO; they increase during exercise
322
TPR vs Power
• Big change in TPR falls to about 40% of what it was
decreases
323
At very high HR, what happens to stroke volume
might fall
324
Cardiac output vs power
increases 3X
325
Arterial pressure
systolic increases slightly
mean flat
diastolic flat
326
oxygen consumption vs power
increases 9X
327
arteriovenous oxygen difference
oxygen used in ateriovenous exchange increases 3X
328
Blood flows in excercise
Heart increases 3.5 x
skeletal muscle increases 12 x
kidneys, abdominal, other, decrease
329
Fick’s Principle:
oxygen consumption is the flow x the difference in the content of the blood VO2=COxa–vO2 diff
330
Why does the SNS constrict muscles in the abdomen during exercise?
Decrease in flow of the blood to the abdominal organs because the SNS is constricting the muscles, to
keep the TPR up so the BP doesn’t fall
331
What happens to HR, cardiac output, stroke volume if you are a trained athlete?
HR decreases at rest
increase your SV
higher cardiac output
By training you make your heart stronger --> hypertrophy
332
Where are norepinepherine and epinephrine made
Adrenal medulla
333
NE AND E affect on blood vessel
Vasoconstriction and binding to alpha receptors
