Physiology Flashcards
1
Q
what is the name for the mechanism of the heart beating rhythmically in the absence of external stimuli?
A
autorhythmicity
2
Q
where does excitation of the heart normally originate?
A
pacemaker cells in the sino-atrial node
3
Q
where is the SA node located?
A
upper right atrium
close to where the SVC enters the RA
4
Q
what is it called when a heart is controlled by the sino-atrial node?
A
sinus rhythm
5
Q
why do cells within the SA node have spontaneous pacemaker potential?
A
they do not have a stable resting membrane potential so the drift through depolarisation spontaneously
6
Q
what is the name of the slow depolarisation of membrane potential, that takes the potential to a threshold for the AP to occur?
A
pacemaker potential
7
Q
what is the pacemaker potential (ie the slow depolaristation to a threshold) due to?
A
decreasing in K+ efflux
slow Na + influx
(resulting in an increasingly positive membrane potential)
8
Q
what happens in a pacemaker cell once the threshold has been reached?
(the rising phase of action potential)
A
activation of voltage-gated Ca++ channels causing an Ca++ influx
9
Q
what is the falling phase of the pacemaker action potential caused by?
A
activation of K+ channels
resulting in K+ efflux
10
Q
why is there a short pause of the electrical impulse at the AV node?
A
to allow time for both atria to contract in order for co-ordination of systole
11
Q
from SA node to the atria what is the process of excitation spread?
A
cell-to-cell spread of excitation via gap junctions
12
Q
what are gap junctions?
A
low resistance protein channels
13
Q
within the ventricles, what is the process of excitation spread?
A
cell-to-cell spread of excitation via gap junctions
14
Q
where is the AV node located?
A
at the base of the right atrium
just above the junction of atria and ventricles
15
Q
what should be the only point of electrical contact between atria and ventricles?
A
AV node
16
Q
how do the cells within the AV node facilitate the pause that allows co-ordination of systole?
A
slow conduction velocity between them
17
Q
what are the pathways by which the electrical impulse is spread from the SA node to the AV node?
A
internodal pathways
cell-to-cell spread (gap junctions)
18
Q
what is the function of the bundle of his and the purkinje fibres?
A
allow rapid spread of action potential to the ventricles
19
Q
what is the resting potential of ventricular muscle action potentials?
A
-90mV (until cell is excited)
20
Q
what causes the rising phase of action potential within the ventricular muscle cell?
A
fast Na+ influx
21
Q
what does the fast influx of sodium reverse the ventricular muscle action potential to?
A
+30mV
from -90mV
22
Q
what phase is the rising phase of action potential within the ventricular muscle cell?
A
phase 0
23
Q
what causes phase 1 of the ventricular muscle action potential?
A
closure of Na+ channels and transient K+ efflux
24
Q
what phase is the plateau phase of the ventricular muscle action potential?
A
phase 2
25
what causes phase 2 (plateau phase) of the ventricular muscle action potential?
opening of Ca++ voltage gated channels and Ca++ influx
| with background K+ efflux causing it to balance out
26
what causes phase 3 of the ventricular muscle action potential?
closure of voltage gated Ca++ channels and K+ efflux
27
what is phase 4 of the ventricular muscle action potnential?
membrane rests at resting membrane potential
| -90mV
28
what is the unique characteristic of contractile cardiac muscle cell's action potential?
the plateau phase
29
what part of the nervous system influences the heart rate?
autonomic nervous system
30
what does sympathetic stimulation do to the heart rate?
increases heart rate
31
what does parasympathetic stimulation do to the heart rate?
decreases the heart rate
32
what nerve supplies parasympathetic innervation to the heart?
vagus nerve
33
under normal resting condition what autonomous tone dominates in control to the heart?
vagal tone
34
what is the intrinsic heart rate? (ie without vagal tone)
100bpm
35
what is the name for a resting heart rate below 60bpm?
bradycardia
36
what is the name for a resting heart rate more than 100bpm?
tachycardia
37
what areas of the heart does the vagus nerve supply?
SA and AV node
38
what does vagal stimulation of the AV node cause?
increases AV nodal delay
39
what muscarinic receptors in the heart are acted on by the parasympathetic system?
M2 muscarinic receptors
| ACh
40
why is atropine used in extreme bradycardia to speed up the heart?
atropine is a competitive inhibitor of acetylcholine so blocks the slowing down effect of the parasympathetic system
41
what is a negative chronotropic effect?
decreases the heart rate
42
what is a positive chronotrophic effect?
increases the heart rate
43
what does vagal stimulation do to the slope of the pacemaker potential?
decreases slope of pacemaker potential
| and so frequency of AP decreases
44
what does sympathetic stimulation do to the slope of the pacemaker potential?
increases slope of pacemaker potential
| and so frequency of AP increases
45
explain effect of parasympathetic system and sympathetic system on heart rate in terms of chronotropic effect?
sympathetic- positive chronotropic effect
parasympathetic- negative chronotropic effect
46
what areas of the heart do sympathetic nerves supply?
SA node
AV node
myocardium
47
what effect does the sympathetic system have on the myocardium?
increases force of contraction
| positive inotropic effect
48
what receptors in the heart does the sympathetic system act through?
B1 adrenoceptors
49
what does the sympathetic system do to the rate of K+ efflux during pacemaker potential?
decreases the rate of K+ efflux
| allowing membrane potential to depolarise and reach threshold faster
50
what does the parasympathetic system do to the rate of K+ efflux during pacemaker potential?
increases the rate of K+ efflux
| causing membrane potential to take more time to depolarise and reach threshold
51
what does the sympathetic system do to the rate of Na+ influx during pacemaker potential?
increases the rate of Na+ influx
| allowing membrane potential to depolarise and reach threshold faster
52
what does the parasympathetic system do to the rate of Na+ influx during pacemaker potential?
decreases rate of Na+ influx
| causing membrane potential to take more time to depolarise and reach threshold
53
what does the parasympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?
decreases the rate of Ca++ influx
| slowing the impulse down
54
what does the sympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?
increases the rate of Ca++ influx
| speeding the impulse up
55
what are the wires that make up Lead I in an ECG?
RA- LA
56
what are the wires that make up Lead II in an ECG?
RA- LL
57
what are the wires that make up Lead III in an ECG?
LA- LL
58
what does the p wave on an ECG correspond to?
atrial depolarisation
59
what does the QRS complex on an ECG correspond to?
ventricular depolarisation
60
what does the T wave on an ECG correspond to?
ventricular repolarisation
61
what makes up most of the PR interval of an ECG?
AV node delay
62
what occurs in the ST segment of an ECG?
ventricular systole
63
what occurs in the TP interval of an ECG?
diastole
64
what type of muscle is the cardiac muscle?
smooth and striated
65
how are the cardiac myocytes electircally coupled?
gap junctions which allow APs to spread from one cell to the next
66
whats the difference between skeletal muscle and cardiac muscle in terms of nerve supply?
each skeletal muscle cell needs a nerve supply so contain neuromuscular junctions
cardiac myocytes dont
67
what are desmosomes?
mechanical adhesions between adjacent cells that ensure the tension developed by one is transmitted to the next
68
myofibrils contain alternating segments of thick and thin protein filaments, what are the names of the filaments?
myosin: thick filaments- causes the darker appearance
actin: thin filaments- causes the lighter appearance
69
what is the name of the band of muscle fibre that is arranged of actin and myosin?
sarcomere (the functional unit of the muscle)
70
how is muscle tension produced?
by sliding of actin filaments on myocin filaments
71
within a muscle cell cycle what is ATP used for?
contraction and relaxation
72
what happens to an energized myosin filament if no calcium is present?
it goes into the resting phase
73
what happens to an energized muscle filament if calcium is present?
binding of the myosin filament to the actin filament
74
once a myosin filament as binded to an actin filament what occurs?
bending (the power stroke where myosin and actin overlap)
| -energy is released
75
once bending has occured, what happens to the myosin and actin if there is fresh ATP available?
detachment
76
once bending has occured, what happens to the myosin and actin if there is no ATP available?
forms a rigor complex
| which can no longer be used
77
what does the detached myosin do with the ATP'?
becomes energised, now it can either go onto resting phase, or it can go onto binding phase and then contraction again
78
within a muscle cell cycle what is ATP used for?
contraction (energy released) and relaxation (ATP itself attached to myosin)
[same ATP molecule, different actions required for contraction and relaxation]
79
why in the absence of calcium does an energised myosin go into the resting phase?
because cross-bridge binding sites are covered by troponin-tropomyosin complex
so myosin cross bridge cannot bind to actin binding sites
80
why in the presence of calcium does an energised myosin go into the binding phase? (to move onto contraction)
calcium binds to the troponin and movex the troponin-tropomyosin complex out the way thus exposing the cross-bridge binding sites.
myosin cross bridge can now bind to the actin binding sites
81
what is needed to switch on cross bridge formation?
Calcium
82
in a cardiac muscle cell, what is the release of Ca from SR dependent on?
the presence of extra-cellular Ca
83
what is needed to switch off the cross bridge formation and cause relaxation?
removal of calcium (either back into SR or out of cell)
84
when the muscle fibre is relaxed why is there no cross-bridge binding?
because the cross bridge binding site on actin is physically covered by the troponin-tropomyosin complex
85
what is the refractory period?
the amount of time it takes for an excitable membrane to be ready for a second stimuli following an exictation
86
what is a tetanic contraction?
continuous contraction
87
what does the refractory period prevent?
a tetanic contraction
88
what is the stroke volume?
the volume of blood ejected by each ventricle per heart beat
89
SV =
EDV- ESV
| end diastolic volume - end systolic volume
90
what is the intrinsic mechanism regulating the stroke volume?
frank-starling mechanism
91
what is the extrinsic mechanism regulating the stroke volume?
nervous and hormonal control
92
what is the diastolic length of myocardial fibres determined by? (the stretch)
the end diastolic volume
| eg preload
93
what is the end diastolic volume?
the volume of blood within each ventricle at the end of diastole
94
what is the end diastolic volume determined by?
venous return to the heart
95
as venous return increases what happens to the stroke volume?
as venous return increase
EDV increases
stretch increases
stroked volume increases (to a max force)
96
the max force of contraction by the myocytes is when the muscle fibres are at what length?
optimal length
97
what does stretch do to the affinity of troponin for calcium?
increases it
98
what is the difference between skeletal muscle and cardiac muscle in terms of optimal fibre length?
skeletal muscle: optimal fibre length is resting muscle length
cardiac muscle: optimal length is achieved by stretching the muscle
99
what does starlings law do to the stroke volumes of RV and LV?
matches them
100
what is the afterload?
the resistance into which heart is pumping
101
at first, what partially compensated for the increased afterload?
frank starling mechanism
incresed afterload causes decreased stroke volume causing increased EDV causing increased contractile force cause stroke volume to return to normal
102
if increased afterload persists (eg untreated hypertension) what happens to the ventricle?
ventricular hypertrophy in order to overcome the resistance (and provide a constant higher contractile force)
103
what are the intrinsic factors of SV?
preload/venous return
afterload (determined by resistance)
contractility of the muscle itself
104
what does an inotropic effect (such as sympathetic nerve stimulation) do to the frank-starling curve?
shift it to the left
105
CO =
SV x HR
106
what is the cardiac output?
the volume of bloof pumped by each ventricle per minute
107
what is the normal CO in a resting adult?
5L
108
at a heart rate of 75, what is the average time taken for diastole?
0.5s
109
at a heart rate of 75, what is the average time taken for systole?
0.3s
110
what are the 5 main events during the cardiac cycle?
1. passive filling
2. atrial contraction
3. isovolumetric ventricular contraction
4. ventricular ejection
5. isovolumetric ventricular relaxation
111
how does passive filling of the ventricles come about?
the pressure gradient allows passive filling of ventricles from high pressure atria to lower pressured ventricles
112
how much of the ventricles become full by passive filling?
80%
113
when do the AV valves shut?
when the ventricular pressure exceeds the atrial pressure
114
what produced the first heart sound? (lub)
AV valves shutting
115
what is isometric contraction of the ventricles?
the period of the cardiac cycle where both valves are closed creating a closed volume, but the pressure is increasing due to the contraction of the ventricles
116
when do the AV valves open?
when the atrial pressure (which is filling with blood) exceeds the ventricular pressure (which is rapidly falling due to relaxation)
117
what produces the first heart sound? (lub)
AV valves shutting
118
when do the aortic/pulmonary valves open?
when the pressure the pressure within the ventricles exceeds aorta/pulmonary artery pressure
119
when do the aortic/pulmonary valves close?
when the ventricular pressure falls below aortic pressure
| remember ventricles are relaxing now
120
what produces the second heart sound? (dub)
the closing of the aortic/pulmonary valves
121
what does the vibration of the valve closure cause in the aortic pressure curve?
dicrotic notch
122
what is isometric relaxation of the ventricles?
the valves are both closed causing a closed volume, and the pressure is decreasing due to the relaxation of the ventricles
123
what are the 4 areas that must be auscultated in a cardiac exam?
aortic
pulmonary
tricuspid
mitral
124
why do arterial pressures not fall to zero during diastole?
due to the arterial stretch and recoil
125
what does the a wave of the right atrial pressure/JVP correspond to?
atrial contraction
126
what does the c wave of the right atrial pressure/JVP correspond to?
bulging of tricuspid valve into atrium during ventricular contraction
127
what does the 'v' wave of the right atrial pressure/JVP correspond to?
the rise of atrial pressure during atrial filling
128
when do the JVP waves occur in releation to the right atrial pressure waves?
JVP occurs AFTER right atrial pressure waves
129
how does blood flow through the arteries under normal circumstances?
laminar fashion
130
when is sound audible through a stethoscope?
when there is turbulent flow and not laminar flow
131
how is turbulent flow in the arteries produced?
occluding an artery but not fully blocking it
132
what is Kortkoff sound 1?
| BP measuring
first sound heard
| occurs at peak systolic pressure
133
what are Kortkoffs sounds 2 and 3?
| BP measuring
intermittent sounds heard due to turbulent spurts of flow cyclically exceeds cuff preeure
134
what is Kortoff sound 4?
| BP measuring
the last sound heard
occurs at minimum diastolic pressure
(very muffled)
135
what is Kortfoff sound 5?
| BP measuring
point where sound disappears due to uninterrupted smooth laminar flow
136
when is diastolic pressure recorded?
at 5th Kortkoff sound
137
what drives blood around the systemic circulation?
a pressure gradient between the aorta and the right atrium:
MAP - CVP
(RA pressure is close to 0 so main driving force for blood flow is MAP)
138
what is Mean Arterial Blood Pressure?
the average arterial blood pressure during a single cardiac cycle
139
MAP =
| in terms of diastolic and systolic pressure
[2xDBP + SBP] /3
140
what is the normal range of MAP?
70-105mmHg
141
what is the minimum MAP needed to perfuse the coronary arteries, brain and kidneys?
60mmHg
142
MAP =
| in terms of cardiac output and peripheral resistance
CO x TPR
| HR x SV x TPR
143
what is total peripheral resistance?
the sum of resistance of all the peripheral vasculature in the systemic circulation
144
what are the main resistance vessels?
arterioles
145
what reflex is in control of the short-term regularion of mean arterial blood pressure?
the baroreceptor reflex
146
what type of feedback mechanism is the baroreceptor reflex?
negative feedback
147
where are the 2 group of baroreceptors?
aortic arch
| carotid sinus
148
what cranial nerve do the carotid baroreceptors signal to the medulla via?
glossopharyngeal (IX)
149
what cranial nerve do the aortic baroreceptors signal to the meduall via?
vagus (X)
150
what reflex is important in the prevention of postural blood pressure changes?
baroreceptor reflex
151
what happens to the systolic blood pressure when healthy people stand from lying position?
no change
| baroreceptors notice a transient change and reflex arc causes increased heart rate and TPR
152
what happens to the diastolic blood pressure when healthy people stand from lying position?
slight increase due to the increased TPR (baroreflex)
153
what is the name for the failure of baroreceptor reponses to gravitational shifts in blood when moving from horizontal to vertical position?
postural hypotention
154
what happens if high blood pressure is sustained?
baroreceptors firing decreases and they will re-set to a higher steady state level
155
what 2 types of body fluids make up the total body fluid?
```
intracellular fluid (2/3rds)
extracellular fluid (1/3rd)
```
156
what 2 types of fluid make up the extracellular fluid?
plasma volume and interstitial fluid
157
what is the interstitial fluid?
the fluid the bathes the cells and acts as a go between the blood and the body cells
158
how would you dexcribe the relationship between the plasma and he interstitial fluid?
equilibrium with each other
159
what are the 2 main factors which affect extracellular fluid volume?
water excess or deficit
| Na+ ecess or deficit
160
what 3 hormones/hormone systems regulate the extracellular fluid volume?
1. Renin-Angiotensin-Aldosterone System (RAAS)
2. Atrial Natriuretic Peptide (ANP)
2. Antidiuretic Hormone ADH
161
where is renin released from?
kidneys
162
where is angiotensinogen produced?
liver
163
what is the function of renin?
stimulates the formation of angiotensinogen to angiotensin I
164
what enzyme converts angiotensin I to angiotensin II?
ACE
| angiotensin converting enzyme
165
what 3 functions does angiotensin II have?
1. stimulates the release of aldosterone from the adrenal cortex
2. causes systemic vasoconstriction (increases TPR + BP)
[3. stimulates thirst and ADH release to increase plasma volume slightly and therfore BP]
166
where is ACE produced?
pulmonary vascular endothelium
167
what is the function of aldosterone?
acts on the kidneys to increase sodium (and therefore water) retention to greatly increase plasma volume and therefore BP
168
what is Renin usually secreted in response to?
1. hypotension
2. stimulation of renal sympathetic nerves
3. decreased [Na+] in renal tubular fluid
169
what is the rate limiting step for RAAS?
the renin secretion rate
170
where is atrial natriuretic peptide (ANP) synthesised and stored?
atrial myocytes
171
what is atrial natriuretic peptide (ANP) released in response to?
atrial distension
| hypervolaemic state
172
what are the 4 main function of atrial natriuretic peptide (ANP)?
1. excretion of salt and water in the kidneys (reduced blood volume and BP)
2. vasodilator (decreases BP)
3. decreases renin release (decreases BP)
4. acts as a counter-regulatory mechanism for the Renin-Angiotensin-Aldosterone System
173
where is ADH synthesised and stored?
derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary
174
what is ADH secreted in response to?
1. reduced extracellular fluid
| 2. increased extracellular fluid osmolarity
175
what is plasma osmolarity monitored by?
osmoreceptors mainly in the brain close to the hypothalamus
176
what does ADH do?
1. act in the kidney tubules to increase the reabsorption of water and concentrate urine (antidiuresis)
[increases BP]
2. vasoconstriction [increases BP]
177
when is the effect of ADH important?
in hypovolaemic shock (eg haemorrhage)
178
explain the relationship between resistance to blood flow, blood viscosity, length of blood vessel and radius of blood vessel?
resistance to blood flow is directly proportional to the blood viscosity and the length of the blood vessels
resistance to blood flow is inversely proportional to the radius of the blood vessels to the power of 4
179
what is the name for the way the vascular smooth muscle is partially constricted at rest?
vasomotor tone
180
what receptor does noradrenaline act on to constrict the blood vessels?
alpha 1 adrenoreceptors
181
what receptor does adrenaline act on to constrict the blood vessels?
alpha adrenoceptors
182
what receptors does adrenaline act on to dilate the blood vessels?
beta adrenoceptors
183
where are alpha adrenoceptors mainly found in the circulation?
skin, gut, kidney arterioles
184
where are beta adrenoceptors mainly found in the circulation?
cardiac and skeletal muscle arterioles
185
what 6 local metabolic factors cause vasodilation of systemic circulation?
```
decreased local PO2
increased local PCO2
increased local [H+]
increased extra-cellular [K+]
increased osmolarity of ECF
adenosine release
```
[all are factors of metabolically active tissues]
186
what 4 local humoral agents cause vasodilation of systemic circulation?
histamine
prostaglandins
bradykinin
nitric oxide
187
where is nitric oxide produced?
vascular endothelium
188
what enzyme catalyses the production of nitric oxide from L-argine (amino acid)?
nitric oxides synthase (NOS)
189
describe the half life of nitric oxide?
very short
190
what are the 2 functions of nitric oxide?
the regulation of blood flow
| maintenance of vascular health
191
what is angiotensin II's effect on vascular smooth muscle?
vasoconstriction
| through endothelin production
192
what is ADH's effect on vascular smooth muscle?
vasoconstriction
| through endothelin production
193
what is flow dependent Nitric Oxide formation?
shear stress on vascular endothelium (due to increased blood flow) causes release of calcium in vascular endothelial cells and the subsequent activation of NOS
194
what is receptor stimulated Nitric Oxide formation?
vasoactive substances act through stimulation of NO formation and act as a chemical stimuli to induce NO formation
195
once released from the vascular endothelium, where does nitric oxide diffuse into?
adjacent smooth muscle cells
196
in smooth muscle cells, what does nitric oxide do?
activates the formation of cGMP (timulates smooth muscle relaxation)
197
what 4 local humoral agents cause vasoconstriction?
serotonin
thromboxane A2
leukotrienes
endothelin
198
what is the production of endothelin stimulated by?
angiotensin II
| vasopressin (ADH)
199
what is thromboxane A2 released from?
platelets
200
what is endothelin released from?
endothelial cells
201
what is the local effect of cold temperature on vasculature? and why?
vasoconstriction
| to conserve heat at peripheries
202
what is the local effect of warm temperature on vasculature?
vasodilation
| to provide blood supply to metabolically active tissues
203
where is the myogenic response to stretch important?
brain and kidneys
204
if MAP rises what happens to the vasculature in organs with a myogenic response?
constrict to limit flow
205
if MAP falls what happens to the vasculature in organs with a myogenic response?
dilate to increase flow
206
what are the 4 factors increasing venous return?
venomotor tone
skeletal muscle pump
respiratory pump
blood volume
207
what 3 factors does venomotor tone effect?
venous return
stroke volume
MAP
208
what 2 factors does vasomotor tone effect?
TPR
| MAP
209
during exercise what autonomic system dominates?
sympathetic nervous system
210
during exercise what happens to the vasculature that provides blood to kidneys and gut?
vasoconstrction to reduce flow
211
during exercise what happens to the vasculature that provides blood to the skeletal and cardiac muscle?
vasodilation to increase flow
| due to local metabolic factors and adrenalines effect on b adrenoceptors
212
during exercise what happens to the SBP, DBP and pulse pressure?
SBP increases
DBP decreases
pulse pressure increases
213
what are 6 chronic CVS responses to exercise?
1. reduction in sympathetic tone and noradrenaline levels
2. increased parasympathetic tone to the heart
3. cardiac remodeling
4. reduction in plasma renin levels
5. improved endothelial function (ie increased vasodilators and decreased vasoconstrictors)
6. reduced arterial stiffening
214
what are the 4 different types of shock?
hypovolaemic
cardiogenic
obstructive
distributive
215
what is shock?
an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation
216
what are the steps from shock to cellular failure?
1. shock
2. inadequate tissue perfusion
3. inadequate tissue oxygenation
4. anaerobic metabolism
5. accumulation of metabolic waste products
6. cellular failure
217
what are the steps from hypovolaemic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)
1. loss of blood volume
2. decreased blood volume
3. decreased venous return
4. decreased end diastolic volume
5. decreased stroke volume
6. decreased cardiac output and decreased blood pressure
7. inadequate tissue perfusion
218
what is cardiogenic shock?
sustained hypotenstion caused by decreased cardiac contractibility
219
what are the steps from cardiogenic shock to inadequate tissue perfusion?
(from here it carries on to cellular failure)
1. decreased cardiac contractility
2. decreased stroke volume
3. decreased cardiac output and decreased blood pressure
4. inadequate tissue perfustion
220
what does cardiac failure do to the frank starling curve?
shifts it to the right
221
what does exercise do to the frank starling curve?
shifts it to the left
222
what type of shock would a tension pneumothorax fall under?
obstructive shock
223
what are the steps from obstructive shock to inadequate tissue perfusion?
1. increased intrathoracic pressure
2. decreased venous return (due to reduced gradient)
3. decreased end diastolic volume
4. decreased stroke volume
5. decreased cardiac output and decreased blood pressure
6. inadequate tissure perfusion
224
what are the steps from neurogenic shock to inadequate tissue perfusion?
1. loss of sympathetic tone
2. massive venous and arterial vasodilation
3. decreased venous return and decreased TPR
4. decreased cardiac output and decreased blood pressure
5. inadequate tissue perfusion
225
what type of shock is sepsis?
distributive shock
226
what are the steps from distributive (vasoactive) shock to inadequate tissue perfusion?
1. release of vasoactive mediators
2. massive venous and arterial vasodilation + increased capillary pemeability
3. decreased venous return and decreased TPR
4. decreased cardiac output and decreased blood pressure
5. inadequate tissue perfusion
227
what are the 4 steps for the treatment of shock?
1. ABCDE approach
2. high flow oxygen
3. volume replacement
4 shock specific treatment
228
after ABCDE, high flow oxygen and volume replacement, what is the next step for cardiogenic shock?
give inotropes
229
after ABCDE, high flow oxygen and volume replacement, what is the next step for a pneumothorax? (obstructive shock)
immediate chest drain for tension pneumothorax
230
after ABCDE, high flow oxygen and volume replacement, what is the next step for anaphylactic shock? (distributive shock)
adrenaline
231
after ABCDE, high flow oxygen and volume replacement, what is the next step for septic shock? (distributive shock)
vasopressors
232
what are the 2 types of hypovolaemic shock?
haemorrhagic
| non-haemorrhagic
233
what are 3 causes of non-haemorrhagic shock?
vomitting , diarrhoea, excessive sweating
| causing reduced extracellular fluid volume
234
how much blood loss can compensatory mechanisms work to maintain blood pressure?
until 30% blood loss
235
what compensatory mechanisms work to maintain blood pressure during blood loss? (up to 30%)
baroreceptor reflex
| chemoreceptors
236
what does the ALTS classification quantify?
the level of haemorrhagic shock
237
where do right and left coronary arteries arise from?
base of the aorta
238
where do cardiac veins drain into?
right atrium via coronary sinus
239
what is the oxygen extraction of the coronary circulation compared to the rest of the body?
75% compared to 25% body average
240
what is the only way extra O2 can be supplied to the cardiac muscle?
increasing coronary blood flow
| cant be achieved through increasing O2 extraction since it is so high already
241
what does local hypoxaemia of the myocardium cause?
vasodilation of the coronary arteries
242
what does local production of adenosine from the myocardium cause?
vasodilation of the coronary arteries
243
how is adenosine made?
ATP-ADP-AMP-adenosine
244
what does sympathetic stimulation of the heart result in? (in respect to the blood supply) and why?
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coronary vasodilation
(due to metabolic hyperaemia overriding sympathetic vasoconstriction)
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245
what is circulating adrenalines effect on the coronary arteries B2 adrenoceptors?
vasodilation
246
when does the majority of the blood flow through the coronary arteries occur?
diastole
247
in the brain what do the 2 vertebral arteries join to make?
basilar artery
248
what do the 2 internal carotid arteries join the basilar artery to make?
circle of Willis
249
where do cerebral arteries arise from?
circle of Willis
250
what does the circle of Willis allow?
cerebral perdusion to staty mainained even if one caroid artery gets obstructed
251
what are the 2 types of stroke?
haemorrhagic
| ischaemic
252
what do stroked cause?
interruption of blood supply to a region of the brain
253
what causes a haemorrhagic stroke?
rupture of a damaged artery
254
what causes a ischaemic stroke?
obstruction due to emboli or atherothrombosis
255
for what range of MAP can the brain guard against changes in cerebral flow? (myogenic effect- autoregulation)
60 -160mmHg
256
what happens out with 60-160mmHg to the cerberal flow?
autoregulation fails
257
what do high levels of carbon dioxide in cerebral tissues cause on local vasculature?
vasodilation
258
what do low levels of carbon dioxide in cerebral tissues cause on local vaculature?
vasoconstriction
259
why can hyperventilation lead to fainting?
low CO2, leads to vasoconstriction of cerebral blood flow, brain doesnt get enough oxygen
260
cerebral perfusion pressure (CPP) =
MAP -ICP (intercranial pressure)
261
what happens to CPP and cerebral blood flow if there is increased ICP?
decreased CPP and so decreased cerebral blood flow
262
what makes up the blood brain barrier?
tight intercellular junctions int he cerebral capillaries
263
how does glucose cross the blood brain barrier?
facilitated diffusion using specific carrier molecules
264
how does the pulmonary circulation protect against pulmonary oedema considering it is such a low pressure system?
absorptive forces exceed filtration forces
265
what is the local effect of hypoxia on the pulmonary arterioles?
vasoconstriction
| opposite to systemic arterioles
266
what is the purpose of the vasoconstrictive effects of hypoxia on pulmonary arterioles?
diverts blood away from poorly ventilated areas of the lungs
267
what happens during exercise to ensure the skeletal muscle get enough blood supply?
metabolic hyperaemia (and circulating adrenaline) overcomes sympathetic vasoconstrictor activity
268
what are varicose veins?
when blood pools in lower limbs because of incompetent valves
269
why do varicose veins not lead to a reduction in cardiac output?
chronic compensatory increase in blood volume
270
why is blood flow through the capillary bed slow?
to allow adequate exchange time
271
what regulates the regional blood flow to capillary beds in most tissues?
terminal arterioles
| occasionally there are precapillary sphincters
272
how do exchangeable proteins move across the vascular bed into the interstitial fluid?
vesicular transport
273
how do lipid soluble substances get from the capillary bed to the interstitial fluid?
through endothelial cells
274
how do water soluble substances get from the capillary bed to the interstitial fluid?
through the water filled pores
275
what are the forces favouring filtration in the transcapillary fluid flow?
capillary hydrostatic pressure (Pc)
| interstitial fluid osmotoic pressure (pieI)
276
what are the forces opposing filtration?
capillary osmotic pressure (pieC)
| interstitial fluid hydrostatic pressure (Pi)
277
Net filtration pressure =
(PC + pieI) - (pieC + Pi)
278
at the arteriolar end of the capillary bed what force wins? (filtration or reabsorption)
filtration forces
279
at the venular end of the capillary bed what force wins? (filtrative or reabsorptive)
reabsorptive forces
280
how is excess fluid in the interstitial fluid returned to the circulation?
via the lymphatic as lymph
281
what is oedema?
accumulation of fluid in the interstitial space
282
why is gas exchange compromised in pulmonary oedema?
diffusion distance increases
283
what are the 4 causes of oedema?
1. raised capillary pressure
2. reduced plasma osmotic pressure
3. lymphatic insufficiency
4. increased capillary permeability
284
what are the 2 reasons for raised capillary pressure resulting in oedema?
arteriolar dilation
| raised venous pressure
285
in left ventricular failure, where is the oedema and why?
pulmonary oedema due to back pressure causing raised pulmonary venous pressure
286
in right ventricular failure, where is the oedema and why?
peripheral oedema due to back pressure causing raised systemic venous pressure
287
what are the 3 reasons for reduced plasma osmotic pressure?
malnutrition
protein malabsorption
excessive renal excretion of protein
288
what type of oedema is caused by heart failure?
pitting oedema
