Normal physiology Flashcards
1
Q
What is autorhythmicity?
A
The heart is capable of beating rhythmically in the absence of external stimuli
2
Q
Where does excitation normally originate from?
A
Pacemaker cells in the SA node
3
Q
Where is the SA node located?
A
Upper right atrium close to where the SVC enters
4
Q
What is sinus rhythm?
A
Where the beating of the heart is controlled by the SA node. On ECG, where every P wave is followed by a QRS complex.
5
Q
Which cells exhibit spontaneous pacemaker potential and what is it?
A
Pacemaker cells in the SA node
Spontaneous pacemaker potential means the cells do not have a stable resting potential and the spontaneous pacemaker potential increases the membrane potential to the threshold to generate an AP in the SA node
6
Q
What causes the pacemaker potential?
A
1) Decrease in K+ efflux
2) The funny current (Na+ and K+ influx)
3) Transient Ca++ influx through T type Ca++ channels
7
Q
What is the threshold value in pacemaker cells?
A
-40mV
8
Q
What causes the upstroke of the action potential in pacemaker cells?
A
Activation of L type calcium channels which open for a long time => Ca++ influx and depolarisation
9
Q
What causes repolarisation in pacemaker cells?
A
Inactivation of L type Ca++ channels
Activation of K+ channels => K+ efflux
10
Q
What is the sequence of cardiac conductance from SA node to ventricular myocytes?
A
SA node => Cell to cell conductance => AV node => Bundle of His => Purkinje Fibres => ventricular myocytes
11
Q
How many branches of the bundle of His and what is the function of purkinje fibres?
A
2 = Right and Left
Purkinje fibres are a fast track conduction so all the ventricles contract at the same time
12
Q
How does cell to cell conduction take place?
A
Gap junctions
13
Q
What is the AV node and where is it found?
A
Small bundle of specialised cardiac cells with slow conduction velocity at the base of the right atrium. Only point of electrical contact between the atria and the ventricles
14
Q
Atrial and ventricular myocytes normally have a stable resting potential. True or false?
A
True
15
Q
What is the resting potential of atrial and ventricular myocytes?
A
-90mV
16
Q
What is phase 0 of the atrial and ventricular AP and what is it caused by?
A
Depolarisation
Causes by rapid Na+ influx (faster than pacemaker cells)
This rapidly reverses membrane potential to +20mV
17
Q
What is phase 1 of the atrial and ventricular AP and what is it caused by?
A
Start of plateau phase
Caused by the closure of Na+ channels and transient K+ efflux
18
Q
What is phase 2 of the atrial and ventricular AP and what is it caused by?
A
Maintenance of the plateau phase
Caused by Ca++ influx through L type calcium channels (slow opening)
19
Q
How long is the plateau phase of the atrial and ventricular AP?
A
150-200ms
20
Q
What is phase 3 of the atrial and ventricular AP and what is it caused by?
A
Repolarisation
Caused by inactivation of L type Ca++ channels and activation of K+ channels => K+ efflux
21
Q
What is phase 4 of the atrial and ventricular AP and what is it caused by?
A
Resting membrane potential maintained by the Na+/K+ pump
22
Q
What changes the heart rate normally?
A
Autonomic nervous system
1) Sympathetic stimulation will speed up the heart
2) Parasympathetic stimulation will slow down the heart
23
Q
What is vagal tone?
A
Where the parasympathetic stimulation to the heart dominates as the vagus nerve exerts an continuous influence of the SA node at rest.
It lowers the intrinsic heart rate form 100bpm to 70bpm
24
Q
What is defined as:
1) normal heart rate
2) Bradycardia
3) Tachycardia
A
1) Normal heart rate =60-100bpm
2) Tachycardia = >100bpm
3) Bradycardia = <60bpm
25
The parasympathetic nervous system via the vagus nerve supplies both the SA and AV node. True or flase?
True therefore vagal stimulation slows the heart rate and increases AV nodal delay
26
What is the neurotransmitter and receptor used by the vagus nerve at the heart?
```
Neurotransmitter = ACh
Receptor = Muscarinic M2 receptor (GPCR)
```
27
What drug is a competitive inhibitor of ACh and can be used to speed up the heart in bradycardia?
Atropine
28
How does vagal stimulation produce a negative chronotrophic effect?
1) Causes hyperpolarisation
2) Decreasing the slope of the pacemaker potential
=> takes longer to reach threshold
29
Which parts of the heart are supplied by the sympathetic nervous system?
SA node
AV node
Myocardium
30
What are the effects of sympathetic stimulation on the heart?
Increased heart rate and decreased AV nodal delay
| Increases the force of contraction of the heart via the Frank Starling mechanism
31
What is the neurotransmitter and receptor used by the sympathetic nervous system on the heart?
```
Neurotransmitter = Noradrenaline
Receptor = Beta 1 adrenoceptor
```
32
How does sympathetic stimulation increase the heart rate?
Increases the slope of the pacemaker potential
33
What is an ECG?
Record of depolarisation and repolarisation cycle of the cardiac muscle as obtained from the skin surface
34
How does the heart generate force?
Branched striated muscle due to arrangements of actin and myosin filaments.
The cardiac myocytes are electrically coupled by Gap junctions.
Desmosomes within inter collated discs provide the mechanical adhesion between adjacent cells. They endure the tension from one cell is transmitted to the next
35
What are gap junctions?
Protein channels which form low resistance electrical communication pathways between adject myocytes
36
What is the functional unit of a muscle cell?
Sarcomeres- arrangements of actin and myosin within each myofibril
37
How does myosin bind to actin to form a cross bridge?
1) Energy is stored within the myosin head but Ca++ must be present for for the muscle to contract and myosin cross bridges to form
2) When the muscle is relaxed, the myosin binding sites on actin are covered by the regulatory proteins in the troponin/tropomyosin complex
3) When Ca++ is present it binds to troponin, producing a conformational change ad the troponin tropomyosin complex is moved to expose the myosin binding site => cross bridge formation
38
How does excitation-contraction coupling work?
1) Ca++ is released from the SR which is divided into segments by T tubulee. The release of Ca++ form the SR is dependent on presence of extra cellular Ca++.
2) When Ca++ enters the cardiac myocytes suring the plateau phase, this causes the release of more Ca++ from the SR (CICR)
3) When the action potential has passed Ca++ influx ceases and Ca++ is resequestered in the SR by Ca++ ATPase => relaxation of the heart muscle
39
What is a refractory period and how is this generated?
A refractory period is the period floowing and action potential in which its impossible to generate another action potential
Generated because during plateau phase the Na+ channel are in the inactivated state and cannot be opened and during the repolaristion phase the K+ channels are open and K+ is leaving the cell
40
Why does the heart have a long refractory period?
This prevents tetanic contraction which would result in arrest
41
What is the stroke volume?
The volume of blood ejected by each ventricle per heart beat
42
How can stroke volume be calculated?
End diastolic volume- end systolic volume
43
What are the intrinsic mechanisms of control f stroke volume?
Changes in diastolic length of myocardial fibres. This is determined by the EDV which can stretch the myocardial fibres
44
What is cardiac preload?
How much the heart is loaded with blood before it contracts- regulated by EDV
45
What determines the EDV?
Venous return to the heart
46
What is the Frank Starling mechanism?
Description of the relationship between Venous return, end diastolic volume and stroke volume.
The greater the EDV the greater the SV.
47
What are the benefits of stretching the heart muscle with a greater EDV?
Moving the muscle towards its optimum length and cross bridge formation.
Stretch also increase the affinity of troponin to Ca++ => increase stroke volume.
48
How can the Frank Starling mechanism partially compensate for a decreased stroke volume caused by a decreased after load?
When the afterload increases initially the heart is unable to eject a fill strke volume => increase EDV
The heart muscle is stretched and the force of contraction rises via the frank starling mechanism
49
What is the afterload?
The resistance into which the heart is pumping.
50
If the afterload remains high, eg untreaed hypertension, how will the heart overcome the resistance?
Increase left ventricular muscle mass
51
What are the extrinsic controls fro stroke volume?
Nerves and hormones
| The ventricular muscle is is innervated by the sympathetic nerves
52
How does the release of noradrenaline lead to a positive ionotrophic effect on the heart
1) Activation of Ca++ channels => increased Ca++ influx mediated by cAMP
2) Peak ventricular pressure rises and the rate of pressure change during systole rises which reduces the duration of systole giving adequate time for the ventricle to refill
3) The rate of ventricular relaxation increases due to increased rate of Ca++ pumping to remove it from the cell which reduces the duration of diastole
53
Parasympathetic nerves innervate the ventricle and have an effect on stroke volume. True or false?
False
54
Which hormones have an effect on stroke volume?
Adrenaline and noradrenaline released from the adrenal medulla have a positive ionotrophic and chronotrophic effect
55
What is cardiac output?
The volume of blood pumped by each ventricle per minute
56
How is cardiac output calculated and what is the normal cardiac output?
```
CO = HR x SV
Normal = 5L/minute
```
57
What are the 5 stages to the cardiac cycle?
1) Passive Filling
2) Atrial contraction
3) Isovolumetric ventricular contraction
4) Ventricular ejection
5) Isovolumetric ventricular relaxation
58
What occurs during passive filling?
1) Pressures in the artia and ventricles are close to zero but pressure in atria is greater than pressure in the ventricles
2) AV valve open so venous return flows into the ventricles- ventricles become 80% full by passive filling
3) The semi lunar valves are shut
59
What occurs during atrial contraction?
1) The P wave on the ECG signals atrial depolarisation
2) The atria contract between the P wave and QRS complex
3) Atrial contraction completes the EDV (~130ml at rest)
60
What occurs during isovolumetric ventricular contraction?
1) Ventricular contraction occurs in the ST segment of the ECG => increased ventricular pressure
2) When ventricular pressure > artial pressure the AV valves close creating a lub sound (S1)
3) The tension rises around a closed volume so ventricular pressure rises steeply
61
What occurs during ventricular ejection?
1) When ventricular pressure > aortic/pulmonary pressure the semi lunar valves open
2) Stroke volume is ejected by each ventricle, leaving behind end systolic volume
3) SV = EDV - ESV = 135ml - 65ml = 70ml
4) Aortic pressure rises
5) T wave signals ventricular repolarisation so the ventricles relax and ventricular pressure falls
6) When ventricular pressure< aortic/pulmonary pressure, the semi lunar valves shut creating a dub sound (S2)
62
What produces the dicrotic north in the aortic pressure curve?
Valve vibration of the closing of the semi lunar valve
63
What occurs during isovolumetric ventricular relaxation?
1) Closure of the semi lunar valves signals the start of this period. The volume in the ventricles remains constant as the tension falls around a closed volume
2) When ventricular pressure < atrial pressure the AV valves open and the heart begins a new cycle
64
What is S1?
Closure of the AV valves and marks the start of systole
65
What is S2?
Closure of the semi lunar valves and the start of diastole
66
What is S3?
An early systolic sound- "Kentucky"
67
What is S4?
A late diastolic sound- "Tennessee"
68
Why does arterial pressure not fall to zero during diastole?
Elastic fibres produce an elastic reciol which maintains the blood pressure as arteries are streched during systole
69
When does the JVP occur and what is it an estimate of?
Just after right atrial pressure waves and is an indirect measurement of central venous pressure. It is a wavy pulse
70
In the JVP, what does the a,c and v wave represent?
```
a = atrial contraction
c = bulging of the tricuspid valve into the atrium during ventricular contraction
v = Rise of atrial pressure during atrial filling and the decent is when the AV valves open
```
71
The internal jugular vein connects the right atrium without any intervening valves. True or Flase?
True
72
Where do you listen for the mitral valve and palpate the apex beat?
5th intercostal space, mid clavicular line
73
Where do you listen for the tricuspid valve?
4th intercostal space at the parasternal edge (left side)
74
Where do you listen for the aortic valve?
2nd intercostal space, right parasternal edge
75
Where do you listen for the pulmonary valve?
2nd intercostal space, left sternal edge
76
How much does a normal heart weigh and what is the size in an adult?
200-400g
| 9cm x 12cm
77
4 reasons why its important to know the position of the heart?
1) Directs you to the apex beat
2) Indicates listening areas for the heart sounds
3) Helps you to know where to place the electrodes for the ECG
4) Helps you to know where to do CPR
78
What is contained in the coronary sulcus?
Right coronary artery
79
How many pulmonary veins drain blood into the left atrium?
4
80
What is contained within the posterior interventricular sulcus?
Right posterior descending artery
81
What are the main branches of the right coronary artery?
Right coronary artery
Right marginal artery
Right posterior descending artery
82
What are the main branches of the left coronary artery?
Left coronary artery branches into
Left anterior descending and Circumflex artery
Left marginal artery (branch of the circumflex)
Left diagonal arteries (branch off the LAD)
83
Where do the right and left coronary arteries arise from?
Aorta- coronary astia- just above the aortic valve
84
How many cusps do the semi lunar valves have?
3
85
How many leaflets do the mitral and tricuspid valves have?
Mitral = 2
| Tricuspid =3
86
What is the cerebral ischemic response?
When cerebral perfusion is restricted there is potent sympathetic peripheral vasoconstriction and cardiac stimulation which increases arterial blood pressure and restores blood flow to vital organs
87
How is MAP controlled in the long term?
Control of extracellular fluid volume
88
What makes up the extracellular fluid?
Plasma Volume + interstitial volume
89
What 2 main factors effect extracellular fluid volume?
Water excess or deficit
| Na+ excess or deficit
90
What does RAAS stand for?
Renin Angiotensin-Aldosterone System
91
Where is renin produced and released from?
Juxtaglomerular apparatus in the kidney
92
The formation of angiotensin 1 is stimulated by what?
Renin release from the kidney
93
What is the precursor to angiotenisin 1 and where is it produced?
Angiotensinogen produced by the liver
94
Which enzyme converts angiotensin 1 to angiotensin 2?
Agiotensin converting enzyme- ACE
95
Where is ACE produced?
The pulmonary vascular endothelium
96
What are the 3 functions of angiotensin 2?
1) Stimulate the release of aldosterone from the adrenal cortex
2) Casuses sympathetic vasoconstriction which increases SVR
3) Stimulates thirst and ADH release
97
What is aldosterone, where is it release from and where does it target?
steroid hormone released from the adrenal cortex and acts on the kidneys
98
What is the function of aldosterone?
To act on the kidneys to increase Na+ reabsorption and water retention to increase the plasma volume
99
What type of cells are in the Juxtaglomerular appaatus in the kidney?
Macula densa, extra-glomerular mesangial cells and granular cells (these release renin)
100
What stimulates renin release?
1) Renal artery hypotention- caused by systemic hypotention
2) Stimulation of renal sympathetic nerves
3) Decrease Na+ in renal tubular fluid (sensed by macula densa
101
What are natiuretic peptides?
peptide hormones synthesised by the heart (also brain and other organs)
102
When are naturitic peptides released?
Released in response to cardiac distention or neurohormonal stimuli
103
What is the function of natiuretic peptides?
Cause excretion of salt and water in the kidneys to reduce blood volume and pressure.
1) Decrease renin release
2) Act as vasodilators to decrease SVR and MAP
104
What are the 2 main types of Natiuretic peptides released by the heart?
Atrial Natiuretic Peptides- ANPs
| Brain Natiuretic Peptides- BNPs
105
What is Atrial Natiuretic Peptide, where is it stored and when is it released?
28 amino acid peptide synthesised and stored in atrial myocytes.
Released in response to atrial distention
106
What is Brain Natiuretic Peptide, where is it stored and when is it released?
32 amino acid peptide systhesised by the ventricles, brain and other organs and released in response to ventricular distention.
107
Explain how BNP is cleaved from preproBNP to BNP?
prepro BNP is cleaved to pro BNP (108 amino acids) and then cleaved to BNP which is 32 amino acids
108
What type of natiuretic peptide would be measured in a patient with suspected heart failure?
Serum BNP and NT-Pro-BNP. These would be raised in heart failure. Only used in borderline cases or for prognosis.
109
What is ADH and where is it synthesised and stored?
Antidiuretic hormone
| Synthesised from a prehormone precursor in the hypothalamus and stored in the posterior pituitary gland
110
What stimulates ADH secretion?
1) Reduced extracellular fluid volume
| 2) Increased ECF osmorality
111
What monitors plasma osmorality?
Osmoreceptors in the brain, close to the hypothalamus
112
How does ADH act?
1) ADH acts on the kidney tubules to increase the reabsorption of water producing more concentrated urine (antidiuresis) which increases ECF volume and plasma volume => increased CO and MAP
2) Also acts on blood vessels causing vasoconstriction (small effect but important in hypovolaemic shock)
113
What is the effect of alcohol on ADH release?
Alcohol will inhibit ADH release => dehydration
114
Resistance to blood flow is directly proportional to what?
Blood viscosity and length of blood vessel
115
Resistance to blood flow is inversley proportional to what?
The radius of the vessel to the power 4
116
How is resistance to blood flow mainly controlled?
Vascular smooth muscle changing the radius of arterioles
117
Vascular smooth muscle is innervated by the sympathetic nervous system. What is the neurotrasmitter and what is the receptor?
```
Neurotransmitter = Noradrenaline
Receptor = alpha 1 adrenoceptors
```
118
How does an increase in sympathetic discharge affect the vasomotor tone?
Increases vasomotor tone => vasoconstriction
119
How does an decrease in sympathetic discharge affect the vasomotor tone?
Decreases vasomotor tone => vasodilation
120
There is no significant parasymathetic innervation of arterial smooth muscle except where?
clitoris and penis
121
Where is adrenaline released from and what causes its release?
Released from the adrenal medulla due to sympathetic stimulation
122
What is the effect of adrenaline on alpha 1 adrenoceptors and where are these receptors found?
Vasoconstriction
| Skin, gut and kidney arterioles
123
What is the effect of adrenaline on beta 1 adrenoceptors and where are these receptors found?
Vasodilation
| Cardiac and skeletal muscle arterioles
124
How is blood flow to specific tissues matched to the metabolic needs of that tissue?
Intrinsic chemical and physical control factors. This can override extrinsic control
125
Which local metabolites can cause relaxation of arteriole smooth muscle => vasodilation and metabolic hyperaemia?
```
Decreased local oxygen
Decreased local pH
Increased local carbon dioxide
Increased extracellular K+
Increased osmorality of ECF
Increased adenosine release from ATP hydrolysis
```
126
Which local humoral agents can be released causing dilation of local arterioles?
Histamine
Bradykinin
Nitric oxide
127
Where and how is nitric oxide produced?
continuously produced by vascular endothilium from the amino acid L-arganine through the enzymatic action of Nitric Oxide Synthase- NOS
128
What is the function of nitric oxide?
Potent vasodilator with a half life of seconds
Important in regulation of blood flow and maintaining vascular health.
NO diffuses from the endothilium into the smooth muscle where it activates cGMP which is the second messenger signalling smooth muscle relaxation.
129
Why is NO released?
Increased blood flow causes sheer stress on vascular endothilial cells which causes the release of Ca++ into the endothilial cells which activates NOS => production of NO.
Chemical stimuli can also induce NO formation
130
What local humoral agents can be released causing local vasoconstriction?
Serotonin, Thromboxane A2, Leukotrienes and Endothelin
131
What is endothelin?
Potent vasoconstricter released from endothelial cells which is important in the maintenance of vascular health .
It is pro thrombotic, proinflamatory and prooxidant
132
WHat physical factors can affect local vascular resistance?
Temperature- warmth => vasodilation, cold => vasoconstriction
Myogenic response to stretch (important in the brain and kidneys. If MAP increases the vessels constrict to reduce flow
Shear stress- dilation of arterioles causes shear stress in arteries up stream to make them dilate. This increases flow to metabolically active tissues
133
The brain does not participate in the barroreceptor response. What controls blood flow to the brain?
Myogenic response
| Blood flow to the brain is kept cnstant between a MAP of 60-160mmHg
134
Where do the coronary arteries come from?
Ascending aorta just above the aortic valve at the coronary ostia
135
Where does coronary venous blood drain to?
Coronary sinus into the right artium
136
What are the adaptations of the coronary circulation to supply a high oxygen demand?
High capillary density
High basal blood flow
High oxygen extraction (75% compared to a body average of 25%). This means extra oxygen when required cannot be obtained by increasing extraction and can only be supplied by increasing coronary blood flow by extrinsic and intrinsic mechanisms
137
How is coronary blood flow increased by intrinsic mechanisms?
Low oxygen causes vasodilation of coronary artorioles
Metabolic hyperaemia matches flow to demand
Adensosine from ATP hydroysis is a potent vasodilator
138
How is coronary blood flow controlled by extrinsic mechanisms (nerves)? What is this called?
Coronary arteries are supplied by sympathetic vasoconstrictor nerves BUT...
This is overridden by metabolic hyperaemia as a result of increased heart rate and stroke volume
=> Sympathetic stimulation of the heart results in coronary vasodilation despite the direct vasconstrictor effect.
Functional sympatholysis
139
How is coronary blood flow controlled by extrinsic mechanisms (hormones)?
Circulating adrenaline (caused by sympathetic stimulation) activates beta 2 adrenoceptors which cause vasodilation
140
When is the left ventricle muscle perfused?
During diastole because during systole, contraction of the left ventricle causes constriction of the left coronary arterie
141
Why can tachycardia cause chest pain?
Increase in HR shortens dyastole and the blood flow to the left side of the heart is reduced => chest pain even though the patient does not have ischemic heart disease
142
When is the right ventricle perfused?
During systole and diastole (peaks in systole) because the pressure in the right ventricle is not as high.
NB: Overall most coronary blood flow and cardiac perfusion occurs during diastole
143
Which blood vessels supply the brain?
Internal carotid arteries and vertebral arteries. The two vertebral arteries form the basilar artery.
The basilar artery and internal carotid arteries anastamose to form the circle of Willis.
All major cerebral arteries arise from the circle of Willis
144
Grey matter is very sensitive to hypoxia. Why is the circle of Willis beneficial?
Cerebral perfusion should be maintained even if ine carotid artery gets obstructed due to the collateral circulation. But an obstruction to a smaller artery would deprive a region of the brain of its blood supply => Stroke
145
What are the 2 types of stroke?
Ischemiac and haemorrhagic
146
How is cerebral blood flow regulated?
Autoregulation maintains cerebral blood flow when MAP is between 60- 160mmHg.
- If systemic MAP falls, cerebral arterioles dilate to maintain flow
- If systemic MAP rises, cerebral arterioles constrict to restrict flow
NB: direct sympathetic stimulation has little effect on cerebral blood flow
147
When does auto regulation fail?
If MAP falls below 60mmHg or rises above 160mmHg.
| MAP below 50mmHg results in confusion, fainting and brain damage
148
What other factors can affect cerebral blood flow?
Increased PCO2 causes cerebral vasodilation
| Decreased PCO2 causes cerebral vasoconstriction
149
Why can hyperventilation lead to fainting?
Decreased PCO2 => cerebral vasoconstriction=> decreased cerebral blood flow
150
How does blood flow increase to parts of the brain that are active?
Regional hyperaemia- mechanism unknown. May be due to increased K+ in arterioles due to K+ efflux from active neurones
151
What is normal intracranial pressure?
8-13mmHg
152
What is contained in the skull?
80% brain
12% blood
8% CSF
153
What can cause an increase intracranial pressure?
Trauma, inflammation, bleeding, tumour. This can cause a reduction in cerebral perfusion pressure. It can also lead to failure of autoregulation of cerebral blood flow
154
What is the cerebral perfusion pressure?
MAP- ICP
155
What forms the blood brain barrier?
Cerebral capillaries have tight intercellular junctions
156
What is the BBB permeable and impermeable to?
Permeable to CO2, oxygen and glucose
Impermeable to Hydrophillic substances such as ions catacholamines and proteins (H+) This helps to protect the brain from fluctuting levels of ions in the blood
157
How are the metabolic needs of the airways met?
Systemic bronchial arteries and veins
158
What is pulmonary resistance and pulmonary artery BP?
Resistance is 10% of the systemic circulation
| BP is 20-25/6-12mmHg
159
What is pulmonary and systemic capillary pressure?
```
Systemic = 17-25mmHg
Pulmonary = 8-11mmHg
```
160
What protects against pulmonary oedema?
Low pulmonary capillary pressure meaning absorptive forces are greater than filtration forces.
161
What effect does hypoxia have on pulmonary arterioles?
Vasoconstriction which helps to divert blood from poorly ventilated areas to well ventilated areas where arterioles will dilate
162
What is the resting blood flow to skeletal muscles?
Low because of sympathetic vasoconstrictor tone
163
What happens during exercise to skeletal muscle flow?
Increases because local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
Circulating adrenaline also causes vasodilation via beta 2 adrenoceptors
SV, HR and CO all increase during exercise which increases blood flow to skeletal muscle.
164
Why can diastolic BP decrease during exercise?
Circulating adrenaline causes vasodilation via Beta 2 adrenoceptors
165
What is the skeletal muscle pump?
Large veins in limbs lie between musceles so contraction of these muscles aids venous return
One way venous valves allow blood to move towards the heart.
166
Skeletal muscle pump helps to prevent postural hypotention and fainting. T or F?
True
167
Blood pools in lower limbs if venous valves become incompetent => varicose veins. Why does this usually not lead to a reduction in CO?
There is a chronic compensatory increase in blood volume
