Cardiovascular Physiology Flashcards
1
Q
function of the heart
A
to pump oxygen and glucose around the body
2
Q
properties of an effective heart
A
- Regular contractions at an appropriate rate for metabolism
- Guaranteed time for ventricular filling after atrial and ventricular contractions
- Contraction duration long enough for physical movement of fluid
- Contractile strength sufficient to generate appropriate pressures
- Ventricular pressure directed towards exit valves
- Co-ordination of left and right, and atrial and ventricular contractions
- Matched volumes of emptying anf filling
3
Q
where is the heart located
A
- The heart is located centrally in the thoracic cavity above the diaphragm
- Contained within mediastinum
- 2/3 offset to the left of the midline of the sternum
4
Q
1
A
superior vena cava
5
Q
2
r
A
right pulmonary artery
6
Q
3
A
right pulmonary veins
7
Q
4
A
pulmonary semilunar valve
8
Q
5
A
right atrium
9
Q
6
A
tricuspid valve
10
Q
7
A
right ventricle
11
Q
8
A
inferior vena cava
12
Q
9
A
aorta
13
Q
10
A
left pulmonary artery
14
Q
11
A
pulmonary trunk
15
Q
12
A
left pulmonary veins
16
Q
13
A
left atrium
17
Q
14
A
aortic semilunar valve
18
Q
15
A
bicuspid valve
19
Q
16
A
chorda tendinae
20
Q
17
A
interventricular septum
21
Q
18
A
papillary muscle
22
Q
19
A
left ventricle
23
Q
20
A
apex of heart
24
Q
21
A
descending aorta
25
where does the superior vena cava come from
upper body
26
what kind of blood is in superior vena cava
deoxygenated
27
where does the right pulmonary artery go to
right lung
28
what kind of blood is in the right pulmonary artery
deoxygenated
29
where do the right pulmonary veins come from
right lung
30
what kind of blood is in the right pulmonary veins
oxygenated
31
where does the inferior vena cava come from
lower body
32
what kind of blood is in the inferior vena cava
deoxygenated
33
where does the aorta go
systemic organs
34
what kind of blood is in the aorta
oxygenated
35
where does the left pulmonary artery go
to the left lung
36
what kind of blood is in the left pulmonary artery
deoxygenated
37
where do the left pulmonary veins come from
left lung
38
what kind of blood is in the left pulmonary veins
oxygenated
39
wheredoes the descending aorta go
lower body
40
what kind of blood is in the descending aorta
oxygenated
41
what seperates the atria from the ventricles
septum
42
septum function
prevents blood mixing across the hear
43
approximately how much does the heart weigh
250-350 grams
44
why is ventricular muscel thicker than atrial muscle
ventricles pump blood further than the atria, so they work harder
45
why is the left ventricular muscle thicker than the right
enables left ventricle to develop greater pressure as it pumps blood to all the organs not just the lungs like the right
46
what is the pericardium
tough double-layered membranous sac which attaches heart to surrounding tissues
47
two layers of pericardium
- 1 visceral layer - attached to heart surface
- 1 parietal layer - outer pericardial layer
48
what is pericardial fluid and what is its function
Lubricating fluid between layers reduces friction during movement of the heart’s surface with contraction
49
what is pericarditis
Inflammation of the pericardium which causes pain due to friction as the heart beats
50
when do pericardiac seizures occur
- when there is too much fluid in the pericardium
- Causes: covid, cancer, circulation issues, TB
51
1
myocardium
52
2
endocardium
53
3
parietal pericardium
54
4
visceral pericardium
55
5
pericardial cavity
56
three layers of the heart's wall
- Epicardium: - outer layer of connective tissue
- Myocardium - middle layer of cardiac muscle
- Endothelium - inner layer of epithelial cells
57
describe cardiac muscle
- Striated appearance
- Ordered sarcomere arrangement
- Irregular shaped cells
- Single centralised nuclei
- Intercalated disks:
58
intercalated discs
gap junctions that link adjacent cardiac muscles so that electrical impulses can travel between cells and causes to contract almost simultaneously
59
why does the myocardium not require external neural input
myocardial cells can self-generate eclectrical activity
60
name the two pacemaker areas
- Sinoatrial node (SA node)
- Atrioventricular node (AV node)
61
what is activity of the myocardium controlled by
the autonomic nervous system
62
what is hypertrophy of the heart
changes to the heart's structure
63
two physiological causes of heart hypertrophy and their outcomes
pregnancy & exercise
- eccentric muscular remodelling
- enhanced function
- improved metabolism
64
three pathological causes of hypertrophy
- hypertension
- infarction
- diabetes
65
effects of hypertention
| heart hypertrophy
- concentric remodelling
- fibrotic lesions
66
effects of infarction
| heart hypertrophy
- eccentric dilation
- fibrotic lesions
- impaired EF
67
effects of diabetes
| heart hypertrophy
- fatty and fibrotic lesions
- increased ventricular mass
- diastolic dysfunction
68
fibrous skeleton
layer of fibrous connective tissue separating the atrial myocardium from the ventricular myocardium
69
how are valves adhered to the myocardium
by papillary muscles and chorda tendineae
70
valves function
to prevent blood from flowing backwards
71
when do the AV valves open
when atrial pressure is higher than ventricular pressure
72
when do AV valves close
when ventricular pressure is higher than atrial pressure
73
another name for the bicuspid valve
mitral valve
74
what is valve prolapse
- Occurs when ventricular pressure is so great one or more valve cusps is pushed into the atria
- The edges of the cusps can no longer meet properly when the valve closes, and the valve cannot seal completely
75
where is the aortic valve found
between the left ventricle and the aorta
76
where is the pulmonary valve located
between the right ventricle and the pulmonary trunk
77
when do the semilunar valves open
hen ventricular pressure is greater than arterial pressure (when the ventricles contract)
78
when do the semilunar valves close
When the ventricles relax and ventricular pressure becomes lower than arterial pressure
79
1
right AV valve (tricuspid)
80
2
aortic valve
81
3
left AV valve (bicuspid)
82
4
pulmonary semilunary valve
83
what word describes the contractile activity of the heart
myogenic
84
what does myogenic mean
contractions are triggered by signals originating from within the muscle, not the CNS
85
Autorhythmicity
the ability of the heart to generate signals that trigger its contractions on a periodic basis ie to generate its own rhythm
86
two types of autorhythmic cells
- pacemaker cells
- conduction fibres
87
pacemaker cells function
initiate action potentials and establish the heart rhythm
88
conduction fibres function
transmit action potentials through the heart
89
what are contractile cells
cells that generate the contractile force
90
what is the SA node
Cardiac pacemaker
91
where is the SA node located
within right atrial wall at junction with superior vena cava
92
intrinsic rate of SA node
80-100 A.P. per min
93
conduction speed of SA node
0.05m/sec
94
where is the AV node located
above cardiac septum at the junction of atria and ventricles
95
intrinsic rate of AV node
40-60 A.P. per min
96
conduction speed of AV node
0.05m/sec
97
where is the bundle of his located
left and right Branches run down ventricular septum to apex of the heart
98
instrinsic rate of bundle of his
20-40 A.P. per min
99
conduction speed od bundle of his
1m/sec
100
where are purkinje fibres located
throughout ventricular myocardium from apex to base
101
intrinsic rate of purkinje fibres
15-40 A.P. per min
102
conduction speed of purkinje fibres
4m/sec
103
electrical pathway of heart (simple)
SA node → atria and AV node → bundle of His → purkinje fibres → ventricles
104
1
interatrial pathway
105
2
SA node
106
3
right atrium
107
4
internodal pathway
108
5
right ventricle
109
6
right branch of bundle of his
110
7
AV node
111
8
left atrium
112
9
left branch of bundle of his
113
10
left ventricle
114
11
purkinje fibres
115
why is the SA node the pacemaker of the heart
Pacemaker cells in the SA node have a faster inherent rate of spontaneous depolarization and the SA node and AV node are connected by conduction fibers the SA node drives the depolarization of the cells in the AV node and throughout the heart
116
how does excitation spread through the heart
- action potential initiated in pacemaker cells → wave of excitation moves through the atria → atria depolarise → atria contract → wave of excitation moves through ventricles → ventricles depolarise → ventricles contract
- Rapid transmission of action potentials is possible because all cardiac muscle cells are connected by gap junctions, which permit electrical current to pass in the form of ions from one cell to another.
117
electrical activity during heartbeat (detailed)
1. Action potential initiated in the SA node and travels to the AV node by internodal pathways, and to atrial muscle by interatrial pathways
2. The AV node transmits action potentials slower than other cells of the conduction system (called the AV nodal delay) to stop the atria and ventricles contracting simultaneously
3. From the AV node, the impulse travels through the bundle of His. The AV node and bundle of His are the only electrical connection between the atria and the ventricles.
4. The signal splits into left and right bundle branches; which conduct impulses to the left and right ventricles
5. From the bundle branches, impulses travel through Purkinje fibers which spread through the ventricular myocardium from the apex upward toward the valves. From these fibers, impulses travel through the rest of the myocardial cells
118
cardiac action potential explanation
- A cardiac contractile cell fires an action potential when it is depolarized to threshold by a stimulus
- Normally, this stimulus is a circulating electrical current originating in neighboring cells
- This current enters the cell through gap junctions that connect it with its neighbors.
- The current then exits the cell by passing through the plasma membrane, and in doing so it triggers depolarization.
119
pacemaker (SA node) action potential
Slow depolarisation after action potential → causes potassium channels to open → potassium leaves the cell → cell becomes hyperpolarised → funny channels open → sodium enters cell → cell depolarised → funny channels close → T-type calcium channel opens temporarily → causes more depolarisation to fire the action potential → L-type calcium channel opens → lots of calcium enters cell → L-type calcium channels close → postassium channels open → reset membrane potential
120
ventricular action potential
resting membrane potential → action potential arrives from Bundle of His → initiates ventricular action potential → increase in Ca2+ entry to cell → depolarisation occurs → fast sodium channels open → Na+ ions enter and cause rapid depolarisation → L-type Ca2+ channels open → Ca2+ enters cell → contraction is initiated → Ca2+ and Na+ channels close → K+ channels open → K+ hyperpolarises cell → membrane potential returns to resting level
121
what occurs during P wave of ECG
atrial depolarisation
122
how long does P wave of ECG last
80-100ms
123
what occurs during QRS complex of ECG
ventricular depolarisation and atrial repolarisation
124
how long does QRS complex of ECG last
80-100ms
125
what occurs during ST segment of ECG
time during which ventricles are contracting and emptying
126
how long does ST segment of ECG last
70-80ms
127
what occurs during T wave of ECG
ventricular repolarisation
128
how long does T wave ECG last
200ms
129
what occurs during the TP interval of an ECG
ventricles are relaxing and filling
130
functions of an ECG
- Assessment of orientation of the heart
- Localisation of areas that do not conduct electrical activity normally
- Assessment of myocardial hypertrophy or atrophy
- Accurate measurement of heart rate
131
systole
period of cardiac contraction
132
diastole
period of cardiac relaxation
133
5 mechanical phases of the cardiac cycle
1. late diastole
2. atrial systole
3. isovolumic ventricular contraction
4. ventricular ejection
5. isovolumic ventricular relaxation
134
what occurs during the late diastole phase of the cardiac cycle
both sets of chambers are relaxed and ventricles fill passively
135
what occurs during the atrial systole phase of the cardiac cycle
atrial contraction forces a small amount of additional blood into the ventricles
136
what occurs during the isovolumic ventricular contraction phase of the cardiac cycle
first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
137
what occurs during the ventricular ejection phase of the cardiac cycle
as ventricular pressure rises and exceeds arterial pressure, the semilunar valves open and blood is ejected
138
what occurs during the isovolumic ventricular relaxation phase of the cardiac cycle
as ventricles relax, pressure in ventricles falls, blood flows back onto the cusps of the semilunar valves, closing them
139
what does one pressure volume loop represent
one cardiac cycle
140
when does diastole begin
| PV loop
at the end of isovolumic relaxation
141
what happens to LV volume during diastole
| PV loop
it increases
142
what happens to LV volume at end-diastole
it is maximal
143
what happens when end-diastole is reached
| PV loop
isovolumic contraction begins
144
what happens at the peak of isovolumic contraction and what is it called
LV pressure exceeds aortic pressure and blood begins to eject from the LV into the aorta - this is the systolic ejection phase
145
what does ESVP stand for
| pressure volume loop
end-systolic pressure-volume point
146
what happens during systolic ejection phase and what is it called
LV volume decreases until aortic pressure exceeds LV pressure and the aortic valve closes, which the ESPV
147
what is stroke volume represented as
| pressure volume loop
by the width of the PV loop as the volume difference between end-systolic and end-diastolic volumes
148
what does the area within the loop represent
| pressure volume loop
stroke work
149
what is load-independent LV contractility also known as
Emax
150
what is load-independent LV contractility or Emax
the maximal slope of the ESPV point under various loading conditions, known as the ESPV relationship
151
what does ESPVR stand for
ESPV relationship
152
what is effective arterial elastance (Ea)
a component of LV afterload and is defined as the ratio of end-systolic pressure and stroke volume
153
what is the ratio of Ea:Emax at under steady conditions (at optimal LV pump efficiency)
| pressure volume loop
it is approaching 1
154
what does the loop of a cardiac cycle in acute myocardial infarction (heart attack) look like
- LV contractility (Emax) is reduced
- LV pressure, SV, and LV stroke work may be unchanged or reduced
- LVEDP is increased
155
what does a loop representing a cardiac cycle in cadiogenic shock (acute heart failure) look like
| pressure volume loop
- Emax is severely reduced
- LVEDV and LVEDP are increased
- SV is reduced
156
cardiac output
volume of blood ejected by each ventricle each minute
157
do systemic and pulmonary systems recieve similar amounts of blood from the heart
yes
158
venous return
volume of blood returning to atrium each minute, it must be equivalent to cardiac output
159
three factos that influence cardiac outout
- metabolism
- age
- body size (body surface area BSA)
160
explain how BSA influences cardaiac input
- Cardiac output increases approximately in proportion to BSA
- Gives rise to the Cardiac Index (cardiac output per square metre of BSA)
161
two components which control cardiac output
- heart rate
- stroke volume
162
what is the autonomic nervous system
- Involuntary branch of PNS
- Sympathetic and parasaympathetic branches (often have opposing effects)
163
central output of the autonomic nervous system
- Parasympathetic nervous system (vagus) via nucleus ambiguous
- Sympathetic nervous system via rostral ventrolateral medulla
- Sympathetic chain
164
what does EDV stand for
end diastolic volume
165
what is end diastolic volume (EDV)
volume of blood in ventricle at end of diastole
166
what does ESV stand for
end systolic volume
167
what is end systolic volume (ESV)
volume of blood in ventricle at end of systole
168
what is ejection fraction
| stroke volume
% EDV ejected with each stroke (ranges 50-75%) A good index of ventricular function
169
what is the approximate SV at rest
70ml (EDV = 40ml; ESV = 70ml)
170
three factors controlling stroke volume
- preload
- contractility
- afterload
171
what is starling's law
*The more the heart chambers fill, the stronger the ventricular contraction and therefore the greater the stroke volume*
- Frank-Starling Law is the relationship between EDV, contraction strength, and SV
172
what is the frank starling mechanism
- The Frank-Starling Mechanism is a Length Tension Relationship due to the varying degree of stretching of the myocardium by the EDV
- As EDV increases the myocardium is increasingly
stretched and contracts more forcefully
- Therefore increased preload (EDV), increases contractility,
which then increases stroke volume
173
is preload intrinsic or extrinsic
intrinsic mechanism
174
explain preload
- Preload is the wall stress S (force applied to unit cross-sectional area) in resting myocardium
- The preload (diastolic wall stress) depends on the end diastolic pressure P, chamber radius r and wall thickness (w)
- Laplace’s Law: *S=Pr/2w*
175
what is laplace's law
* States that for a hollow sphere, the internal pressure (P) is proportional to the wall tension (T) and inversely proportional to the internal radius (r)
* Tension is a force euqal to wall stress (S) times wall thickness (W)
* Increasing the radius reduces the curvature, and therefore the inward component of the wall stress so pressure falls
176
how to find internal pressure with wall tension
| laplace's law
177
how to find internal pressure with wall stress and wall thickness
178
what is contractility
the force of contraction achieved from a given initial fibre length
179
is contractility an intrinsic or extrinsic mechanism
has both intrinsic and extrinsic influences
180
how can contractility force be measured
either by increased contractility and/or by increasing the resting fibre length through end-diastolic stretch (Frank-Starling Mechanism)
181
what are psitive inotropic agents
factors that increase
contractility
182
name some positive inotropic agents
sympathetic neurotransmitters noradrenaline, circulating adrenaline, Beta agonists, digoxin and reduced beat interval
183
what are negative inotropic agents
factors which reduce contractility
184
name some negative inotropic agents
ischemia, acidosis, heart failure, anaesthetics, parasympathetic fibre activity, Beta anatagonists and calcium channel blockers
185
what is afterload
he force per unit cross-sectional area (stress) that opposes the shortening of an isotonically contracting muscle.
186
is afterload an intrinsic or extrinsic mechanism
extrinsic
187
what does afterload depend on
arterial pressure, chamber radius and wall thickness
188
percentage of people under 65 with heart failure
1%
189
percentage of people between 25 and 84 who have heart failure
7%
190
percentage of people over 85 with heart failure
15%
191
what happens to stroke volume in systolic heart failure
a smaller than normal SV is ejected (the heart’s contractility is weakened)
192
what can help in early stages of systolic heart failure
sympathetic stimulation helps to compensate (augmented by expanded blood
volume, controlled by kidneys)
193
is the circulatory system open or closed
closed
194
what is pressure
| circulatory system
the force exerted by blood against vessel walls
195
how does flow occur
| circulatory system
Flow occurs from high pressure to low pressure
196
what does the heart do
| flow
creates a pressure gradient for the bulk flow of blood
197
flow equation
198
how is blood flow calculated
as flow per unit time
Flow = Volume/Time (volume flow rate)
199
what is flow dictated by
- pressure gradients in the vasculature
- resistance in the vasculature
200
what is the pressure gradient across the pulmonary circuit
he pressure in pulmonary arteries take away the pressure in pulmonary veins
- Pulmonary arterial pressure is 15 mm Hg
- Pulmonary venous pressure is 0 mm Hg
- Pressure gradient = 15 - 0 = 15 mm Hg
201
what is the pressure gradient across the systematic system
the pressure in the aorta minus teh pressure in the vena cave just before it empties into the right atrium
202
what is the pressure in the aorta
he mean arterieal pressure (MAP) = 85mm Hg
203
what is the pressure in the vena cava
the central venous pressure = 0mm Hg
204
pressure gradient equation
| systemic circuit
Pressure gradient = MAP - CVP = 85 - 0 = 0 mm Hg
205
pulse pressure equation
Pulse pressure = systolic - diastolic = 110 - 70 = 40
206
MAP equation
- MAP = diastolic + 1/3 pulse = 70 + (40/3) = 70 = 13.3 = 83.3 mm Hg
- MAP = 2/3 diastolic + 1/3 systolic
207
poiseuille's law
208
factors affecting resistance to flow
- Length of vessel
- Viscosity of fluid
- Radius of the vessel
209
which of the factors affecting resistance to flow is most important
Radius of the vessel
210
example of how vessel radius is critical in pathological conditions
atherosclerosis - the deposition of fats into the arterial wall
211
how does vasoconstriction affect arteriole radius
Decrease radius by contracting smooth muscle → increase resistance → decrease blood flow
212
how does vasodilation affect arteriole radius
Increase radius by relaxing smooth muscle → decrease resistance → increase blood flow
213
what is arteriole radius dependent on
the contraction state of smooth muscle in arteriole wall
214
what is the state of smooth muscle contraction in an arteriole wall while at rest
arteriolar tone (partially contracted) - this maintains some resistance and pressure becuase if there is no pressure at all upstream haemodynamics are impacted causing a vicious cycle
215
what are extrinsic factors
factors which are neuronal and hormonal
216
two examples of extrinsic factors influencing vasodilation and vasoconstriction
- Autonomic nervous system (sympathetic nervous system causes constriction)
- Hormones - eg. adrenaline causes constriction
217
what are intrinsic factors
those which are conrolled locally
218
examples of intrinsic factors influencing vasoconstriction and vasodilation
- metabolism
- changes in blood flow
- stretch of arteriolar smooth muscle
- locally secreted chemical messengers
219
explain how metabolism influences vasoconstriction and vasodilation
increases in metabolism decreases O2, and causes vasodilation (active hyperemia)
220
explain how changes in blood flow influence vasoconstriction and vasodilation
reduction in blood flow causes vasodilation: (reactive hyperemia)
221
explain how stretch of arteriolar smooth muscle influences vasoconstriction and vasodilation
when perfusion pressure is high it causes vasoconstriction: (myogenic response) the purpose of this is to keep blood flow constant (autoregulate)
222
name fur vasodilators
nitric oxide, prostacyclin, adenosine, bradykinin
223
name a vasoconstrictor
endothelin-1
224
what does TPR stand for
total peripheral resistance
225
what is total peripheral resistance or TPR
the amount of force exerted on circulating blood by the vasculature of the body
226
two factors which influence TPR
- arteriolar radius
- blood viscosity
227
name intrinsic factors which influence arteriolar radius
- response to stress - compensates for changes in longitudinal force of floq
- myogenic responses to stretch - minor role in acve and reactive hyperemia
- heat and cold
- histamine release - involved in injuries and allergic responses
- local metaboli changes in O2 and other metabolites - important in matching blood flow with metabolic needs
228
extrinsic factors influencing arteriolar radius
- vasopressin - hormone important for fluid balance - vasoconstrictor effect
- angiotensin II - hormone important for fluid balance - vasoconstrictor effect
- epinephrine and norepinephrine - hormones which reinforce sympathetic nervous system
- sympathetic activity - exterts generallised vasoconstrictor effect
229
what does blood viscosity depend on
number of red blood cells
230
what does CVP stand for
central venous pressure
231
what is CVP
- the pressure in the large veins of the thoracic cavity that lead into the heart
- Pressure gradient between central veins and atria drives blood back into the heart
- Venous pressure – atrial pressure = 5 - 10 mm Hg
232
what does a decrease in venous pressure cause for venous return
A decrease in venous pressure decreases driving force for venous return
233
what effect does a decrease in venous return have on blood flow to an organ
Decrease in venous return → decreases end-diastolic volume → decreases stroke volume → decreases cardiac output → decreases blood flow to organ
234
factors affecting CVP and venous return
- skeletal muscle pump
- respiratory pump
- Blood volume: decreased blood volume decreases CVP (bleeding, dehydration…)
- Venomotor tone (sympathetic nerves constrict veins) favors venous return
235
how does inspiration increase blood flow to heart
thoracic pressure decreases → abdominal pressure raises → increases blood flow to the heart
236
how does expiration increase blood flow to the heart
thoracic pressure increases → abdominal
pressure falls, valves prevent backward flow, so, blood driven towards the heart
237
three determinants of mean arterial pressure
- Heart rate
- Stroke volume
- Total peripheral resistance - combined resistance of all blood vessels
238
Effects of Cardiac Output on Mean Arterial Pressure
increase of MAP when TPR stays the same
239
Effects of Total Peripheral Resistance on Mean Arterial Pressure
increase of MAP when CO remains the same
240
what happens when MAP is less than normal
- Hypotension
- Inadequate blood flow to tissues
241
what happens when MAP is greater than normal
- Hypertension
- Stress on heart and walls of blood vessels
242
normal blood pressure
less than 120 systolic and less than 80 diastolic
243
elevated blood pressure
120-129 systolic and less than 80 diastolic
244
hypertension stage 1
130-139 systolic or 80-89 diastolic
245
hypertension stage 2
greater than 139 systolic or greater than 90 diastolic
246
when does systolic pressure occur
with ventricular contraction
247
when does diastolic pressure occur
with ventricular refilling
248
what is pulse pressure at rest
40 mm Hg
249
what can high pulse pressures at rest indicate
vascular disease
250
how is blood pressure measured (auscultation)
- Recorded at heart level via brachial artery
- Korotkoff sounds via turbulent flow, upon cuff pressure release
- Inflate cuff above expected systolic pressure.
- Slowly deflate cuff: blood flows when blood pressure is greater than cuff pressure
- Clear tapping audible via stethoscope indicates Systolic Pressure
- Diastolic pressure indicated at disappearance of muffled sound
251
what does short term refer to in regulation of MAP
seconds to minutes
252
what is short term regulation of MAP
regulation of cardiac output and total peripheral resistance
253
what structures does short term regulation of MAP involve
heart and blood vessels
254
what type of control is short term regulation of MAP
Primarily neural control
255
what does long term refer to in regulation of MAP
minutes to days
256
what is long term regulation of MAP
regulation of blood volume
257
what structures are involved in long-term regulation of MAP
kidneys
258
what type of control is used in long term regulation of MAP
primarily hormonal control
259
explain the renin-angiotensin-aldosterone system
- Decreased NaCl/decreased ECF volume/decreased arterial blood pressure → increased production of renin by kidney → combines with already circulating angiotensinogen (produced by liver) → forms angiotensin I → combines with angiotensin-converting enzyme produced by lungs → forms angiotenstin II
- stimulates adrenal cortex to produce aldosterone → travels to kidney → makes kidney increase Na+ reabsorption by kidney tubules (increased Cl- reabsorption follows passively → Na+ (and Cl- conserved) → Na+ (and Cl-) osmotically hold more H2O in ECF → H2O is conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
- increases vasopressin → increases H2O reabsorption by kidney tubules → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
- increases thirst → increases fluid intake → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
- increases arteriolar vasoconstriction → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
260
neural control of MAP
- Negative feedback loops
- The detectors are called baroreceptors
- The integration centre are the cardiovascular centres in the brainstem
- The controllers are the autonomic nervous system
- The effectors are the heart and blood vessels
261
what are baroreceptors
- Baroreceptors are stretch receptors - specialised nerve endings that respond to stretch of vessel wall
- They have an indirect response to changes in blood pressure
262
what are arterial baroreceptors
- high pressure baroreceptors
- sinoaortic baroreceptors
263
where are arterial baroreceptors found
in the carotid sinus and the aortic arch
264
explain type A baroreceptors
- Myelinated
- Low pressure (30-90 mmHg)
- Important at rest
265
explain type A baroreceptors
- Myelinated
- Low pressure (30-90 mmHg)
- Important at rest
266
explain type C baroreceptors
- Unmyelinated
- High pressure (70-140 mmHg)
- Increasingly active at higher pressures
267
where are cardiac and venous baroreceptors found
in walls of large systemic veins and walls of the atria
268
what are cardiac and venous baroreceptors
Low pressure baroreceptors and are volume receptors
269
explain the parasympathetic input to the cardiovascular system
input to:
- SA node (which decreases heart rate)
- AV node
270
explain sympathetic input to cardiovascular system
input to:
- SA node (increase heart rate)
- AV node
- Ventricular myocardium (increase contractions)
- Arterioles (increase resistance)
- Veins (increase venomotor tone)
271
explain the baroreceptor reflex with an example
- A person who had been lying down stands up quickly
- Gravity causes venous pooling in the legs → causes a decrease in VR → a decrease in CO → a decrease in blood pressure
- Baroreceptors sense the decrease and the reflex occurs
- The reflex causes increased sympathetic and decreased parasympathetic activity
- CO and TPR are increased
- Blood pressure is increased back to normal.
272
explain the bainbrdge reflex
- Vena cava stretch receptors → neural mediated increase in heart rate
- Avoids venous congestion
273
explan how artrial stretch receptors are an input to the cardiovascular system
- Myelinated vagal afferents sensitive to blood volume
- Located at junction of great veins and atria
- Influence endocrine regulation of blood volume via:
- Hypothalamic ADH → renal water retention
- Renin-Angiotensin-aldosterone system (RAS) → renal salt & water retention
- Atrial Natriuretic Peptide → renal salt & water excretion
274
where in the brain receives input from baroreceptors
nuceleus tractus solidaruis in medulla
275
where does the NTS send outputs to
- Parasympathetic NS (vagus)
- via nucleus ambiguus
- cardiac control (limits heart rate)
- Sympathetic NS
- via rostral ventrolateral medulla
- cardiac and blood vessel control (increased contractile strength/tone)
- Hypothalamus & amygdala
- Allows these areas to override the baroreceptor reflex during stress
- Allows a stress-associated increase in BP to occur
276
what does parasympathetic stimulation to the heart cause
decreased heart rate → decreased cardiac output → decreased blood presssure
277
what does sympathetic simulation to the heart cause
- → contractile strength of heart → increase stroke volume → cardiac input → increase blood pressure
278
what does sympathetic stimulation to the arterioles cause
increase vasoconstriction → increase in total peripheral resistance → increase in blood pressure
279
what does sympathetic stimulation to the veins cause
increase in vasoconstriction → increase in venous return → increase in stroke volume → increase in cardiac output → increase in blood pressure
280
what does haemorrhage cause
- Baroreceptor reflex
- Increase in sympathetic activity
- Decrease in parasympathetic activity
281
how does haemorrhage effect the GI tract
- Increased resistance
- Decreased blood flow
282
how does haemorrhage effect the brain
- Vasculature not subject of extrinsic control
- No change in resistance
- Blood diverted from GI tract to brain
283
three hormones that control MAP
- epinephrine
- vasopressin
- angiotensin II
284
how does epinephrine control MAP
- Released by adrenal medulla in response to sympathetic activity
- Increases mean arterial pressure
- Acts on heart
- Increases heart rate
- Increases stroke volume
- Acts on smooth muscle of arterioles
- Increases TPR
- Acts on smooth muscle of veins
- Increases venomotor tone
285
how does epinephrine control MAP
- Released by adrenal medulla in response to sympathetic activity
- Increases mean arterial pressure
- Acts on heart
- Increases heart rate
- Increases stroke volume
- Acts on smooth muscle of arterioles
- Increases TPR
- Acts on smooth muscle of veins
- Increases venomotor tone
286
how do vasopressin and angiotensin II control MAP
- Vasoconstrictors
- Increase TPR
- Increase MAP
