Physiology Flashcards
(183 cards)
1
Q
Function of the CVS
A
BULK FLOW SYSTEM:
- O2 and CO2
- Nutrients
- Metabolites,
- Hormones
- Heat
2
Q
Equation for “flow”
A
Flow = change in pressure/ resistance
change in pressure = mean arterial pressure - central venous pressure
3
Q
Resistance in blood vessels
A
Resistance = Radius ^4
controlled by arterioles which act like taps and control flow to each vascular bed
4
Q
Capacitance
A
The ability of a body to store blood
veins and venules = capitance vessels
store lots of blood
5
Q
“in series” arrangement + examples
A
Blood flows through both, one after the other - output must be equal or blood backs up.
E.G.
right heart –> lungs –> left heart
hypothalamus –> anterior pituitary
gut –> liver
6
Q
Reasons for vascular beds in parallel
A
All tissues get oxygenated blood,
Allows regional redirection of blood
7
Q
Elastic arteries + function
A
Pulmonary arteries and aorta.
Maintains a relatively constant (and high) pressure
8
Q
Function of muscular arteries
A
Low resistance
Delivers blood from elastic arteries to resistance vessels
9
Q
Resistance vessels + function
A
Arterioles.
Control resistance and therefore flow,
Allow regional redirection of blood
10
Q
Capacitance vessels + function
A
Veins and venules.
Low resistance,
Reservoir of blood (to be distributed to rest of circulation when needed - fracitonal distribution of blood)
11
Q
The functional syncytium
A
Cardiac muscle cells act as one big cell.
They are joined…
Electrically by gap junctions,
Physically be desmosomes.
12
Q
Intercalated discs
A
alternating desmosomes and gap junctions
13
Q
Permeability of ion channels in different phases of non-pacemaker action potentials
A
RESTING MEMBRANE POTENTIAL:
-High PK+
INITIAL DEPOLARISATION:
-Increase PNa+
PLATEAU:
- Increase PCa2+ (L-type)
- Decrease PK+
REPOLARISATION:
- Decrease PCa2+
- Increase PK+
14
Q
P-wave corresponds to…
A
Atrial depolarisation
15
Q
QRS Complex corresponds to…
A
Ventricular depolarisation
16
Q
T wave corresponds to…
A
Ventricular repolarisation
17
Q
The PR interval corresponds to…
A
Time from atrial depolarisation to ventricular depolarisation
(mainly due to transmission through the AV node)
18
Q
Normal range of the PR interval
A
0.12 - 0.2 seconds
19
Q
Duration of the QRS complex corresponds to…
A
Time for the whole ventricle to depolarise
20
Q
Normal time for duration of the QRS complex
A
0.08 seconds
21
Q
The QT interval corresponds to…
A
Time spent while the ventricles are depolarised
22
Q
Normal time of QT interval
A
~0.42 seconds at 60bpm
varies with heart rate
23
Q
Measuring heart rate from an ECG
A
*Measured from the rhythm strip
Count the R waves in 30 large squares (6 seconds) and multiply by 10
OR count number of small squares between each QRS complex and divide into 300.
e.g 300/5 boxes = 60bpm
24
Q
STEMI
A
ST Elevated Myocardial Infarction.
Elevation of the ST section on an ECG indicates a more severe heart attack (severe muscle damage)
25
Non-STEMI
Non-ST Elevated Myocardial Infarction
26
Normal Sinus Rhythm
Normal rhythm of the heart set by the sinoatrial node
27
Sinus Tachycardia
Fast heart rate because of rapid firing of the sinoatrial node.
>100 bpm
28
Sinus Bradycardia
Slow heart rate because of slow firing of the sinoatrial node.
<60 bpm
29
Exchange vessels
Capillaries
30
Mean arterial pressure (MAP)
The average blood pressure in the arterial circulation over the whole cardiac cycle
31
Central Venous Pressure (CVP)
The blood pressure in the right atrium, measured in the superior vena cava
32
Cardiac Output
The volume of blood pumped through the circulatory system in a minute (L/min)
33
Sinoatrial node
A mass of cardiac muscle cells that act as the pacemakers
34
Function of the atrioventricular node
Receives APs from the sinoatrial node and conducts it to the ventricles.
Delays AP until blood moves from atria to the bundle of His.
35
Function of the Bundle of His
Conducts APs from the AV node to the ventricles
36
Purkinje fibres
Receive APs from the branches of the bundle of His and distribute it to the myocardium of the ventricles, causing them to contract.
37
1st heart sound caused by...
Mitral and tricuspid valves closing
38
2nd heart sound caused by...
Aortic and pulmonary valves closing
39
Valves during Systole
Aortic and pulmonary open
40
Valves during diastole
Mitral and tricuspid open
41
Stroke volume =
End diastolic volume - end systolic volume
42
Ejection fraction =
Stroke volume ÷ end diastolic volume
43
Estimated mean arterial pressure =
Diastolic pressure + (pulse pressure÷3)
44
Pulse pressure =
Systolic pressure - diastolic pressure
45
Systolic pressure (+ normal value)
Maximum pressure in arteries during systole
| 120mmHg
46
Diastolic pressure
| +Normal value
Minimum arterial pressure at the end of diastole
| 80mmHg
47
Normal mean arterial pressure
~93mmHg
48
Normal pulse pressure
~40mmHg
49
End diastolic volume (+normal value)
Volume in ventricle at end of diastole
| ~130ml
50
End systolic volume (+ normal value)
Volume in ventricle at end of systole
| ~60ml
51
a-wave
Slight increase in atrial pressure due to atrial contraction
52
c-wave
Increase in atrial pressure due to ventricle contraction (mitral valve closing).
The mitral valve pushed into the atrium, decreasing volume in atrium.
53
v-wave
Slow increase in atrial pressure throughout systole due to venous return from lungs
54
Isometric contraction period
Period at the start of systole, between mitral valve closing and aortic valve opening.
Ventricular contraction increases pressure but volume remains constant
55
Isometric relaxation period
Period at start of diastole, between aortic valve closing and mitral valve opening.
Ventricular pressure decreases because of ventricle relaxation but volume remains the same.
56
Ejection phases
Once the aortic valve opens during systole, blood is ejected into the aorta.
Start= rapid ejection phase
Then = slower ejection phase
57
Ventricular filling phases
Once the mitral valve opens during diastole, blood flows into the ventricles from the atria.
Start = rapid ventricular filling
Then = slower ventricular filling
58
Formation of the aorticopulmonary septum
Ingrowth of the bulbar ridges in the walls of the truncus arteriosus and bulbus cordosis
59
Early pacemakers
1st - primordial atrium
then - sinus venosus
SA node develops during 5th week
60
Lymphatic system development
6 primary lymph sacs develop around main veins at end of embryonic period (become groups of lymph nodes in early foetal life)
lymphatic vessels connect the sacs layer
61
dextrocardia
Heart tube loops to the left instead of the right so faces right.
62
Atrial Septal Defect (ASD) types
1. foramen secundum defect (enlarged foramen ovale)
2. endocardial cushion defect with foramen primum defect
3. sinus venosus defect (drainage of pulmonary veins into right atrium)
4. common atrium (failure of septal development)
63
Ventricular Septal defect (VSD)
Most common in the membranous septum.
| Many close spontaneously
64
Patent Ductus Arteriosus
The ductus arteriosus fails to close after birth, causes shunt.
Associated with maternal rubella infection.
65
Transposition of great arteries/vessels
Aorta and pulmonary trunk are switched due to:
1. failure of aorticopulmonary septum to spiral
2. defective migration of neural crest cells (menchymal cells) to form aorticopulmonary septum
66
Tetralogy of Fallot
Made up of 4 cardiac defects:
1. Pulmonary valve stenosis
2. VSD
3. Dextroposition of aorta
4. Right ventricular hypertrophy (wall thickening)
CAUSE: Anterior displacement of aorticopulmonary septum = pulmonary stenosis + aorta takes blood from right.
67
Coarctation of the Aorta
Constriction of aorta, usually opposite ductus arteriosus.
Possible cause: muscle tissue of DA incorporated into aorta. when DA contracts after birth, so does aorta.
68
Aberrant subclavian artery
The right subclavian artery has an abnormal origin on the left and must cross behind the trachea and oesophagus and may constrict them.
69
Double aortic arch
A right aortic arch develops in addition to the left one. Forms a vascular ring around the trachea and oesophagus which usually causes dificulty breathing and swallowing.
70
Vitelline Veins
Carry blood from the yolk sac to the sinus venosus
71
Umbilical veins
Carry oxygenated blood from the placenta to the embryo
72
Cardinal veins
Drain the body of the embryo
73
The circulatory system is formed from the...
Lateral plate splanchnic mesoderm
74
The pericardium if formed from the...
intra-embryonic coelom
75
The lateral plate somatic mesoderm forms the...
Parietal serous pericardium and fibrous pericardium
76
The outflow tracts (aorta and pulmonary trunk) are formed by the...
Truncus arteriosus and Bulbus cordis
77
The bulbus cordis forms...
parts of the outflow tracts and the right ventricle
78
The primitive ventricle forms...
the left ventricle
79
The primitive atrium forms
parts of the left and right atria
80
The sinus venosus forms
The right atrium,
SVC,
AV node,
bundle of His
81
The AV node and Bundle of His are formed from...
The sinus venosus and cells of the AV canal
82
Fate of aortic arch 1
Forms maxillary arteries
83
Fate of aortic arch 2
Disappears early
84
Fate of aortic arch 3
Forms:
Common carotid arteries,
1st part of internal carotid arteries
85
Fate of left aortic arch 4
Distal aortic arch
86
Fate of right aortic arch 4
Proximal right subclavian artery
87
Fate of aortic arch 5
Regresses (if it forms at all)
88
Fate of right aortic arch 6
Proximal right pulmonary artery
89
Fate of left aortic arch 6
Left pulmonary artery + ductus arteriosus
90
Proximal umbilical arteries form...
Internal iliac arteries,
| Superior vesicle branches (to bladder)
91
Distal umbilical arteries form...
Medial umbilical ligaments
92
Fate of right umbilical vein
Degenerates completely
93
Fate of left umbilical vein
forms Ligamentes teres
94
Cardinal veins form
SVC and IVC
95
Ductus venosus becomes...
The ligamentum venosum of the liver
96
The oval foramen becomes...
the oval fossa
97
The ductus arteriosus becomes...
The ligamentum arteriosum
98
Function of the ductus venosus
Allows a portion of blood from the umbilical vein to bypass the liver
99
Foramen ovale (definition and function)
An opening between the atria (in the foramen secundum) which allows blood to bypass the lungs.
opened due to increased pressure in the right side of the heart due to hypoxic pulmonary vasoconstriction.
100
Ductus arteriosus
Connects the pulmonary artery to the aorta, allowing blood to bypass the lungs.
101
Formation of the bulboventricular loop
The bulbus cordis and ventricle grow faster than the rest of the primitive heart tube, causing it to loop to the right.
102
Formation of the aortic sac and arches
When the heart tube fuses, the 2 ventral aortae partially fuse to form an aortic sac.
6 aortic branches/arches arise from the sac (not at the same time)
103
Function of the endocardial cushions
Separate the left and right atrioventricular canals,
| Form the cardiac valves
104
Foramen primum
a gap between the septum primum and endocardial cushion
105
Foramen secundum
A gap in the septum primum
106
Sources of tissue for the formation of the membranous interventricular septum
Aorticopulmonary septum
Bulbar ridges
Endocardial cushions
107
Sections of fused primitive heart tube (superior to inferior)
```
Truncus arteriosus,
Bulbus cordis,
Ventricle,
Atrium,
Sinus venosis
```
108
Gradual depolarisation of pacemaker cells in caused by...
Gradual decrease PK+,
Early increase PNa+,
Late increase PCa2+ (T-type)
109
Rapid depolarisation of pacemaker cells caused by...
Increase PCa2+ (L-type)
110
Excitation-contraction in cardiac muscle
Ca2+ is released from the sarcoplasmic reticulum AND outside the cell.
Regulation of Ca2+ release can be used to vary strength of contraction
Ca2+ binds to troponin = contraction
111
Length of cardiac muscle AP (+ consequences)
Long: 250msec (2msec in skeletal)
Because L type Ca2+ ions maintain contraction
= long refractory period
= no tetanus
112
Area of the pressure volume loop
Increases as the heart's work increases.
e.g. due to exercise/ hypertension
113
Ejection fraction
SV/ EDV
114
Dicrotic notch
Increase in aortic pressure when aortic valve shuts
115
Sympathetic effect on heart rate
```
Releases noradrenaline.
(+ circulating adrenaline)
Acts on B1 receptors on sinoatrial node.
Increases slope of pacemaker potential.
= tachycardia
```
116
Parasympathetic effect on heart rate
Vagus nerve releases ACh.
Acts on muscarinic receptors on SA node.
Hyperpolarises cells AND decreases slope of pacemaker potential.
= bradycardia
117
Sympathetic effect on stroke volume
```
Releases noradrenaline.
(+ circulating adrenaline)
Acts on B1 receptors on myocytes.
Increases contractility
= shorter, stronger contraction
```
118
Parasympathetic effect on stroke volume
Little/ no effect.
| Vagus nerve does not innervate ventricular muscle
119
Preload (+ factors it depends on)
The initial (resting) length of muscle fibres.
Controlled by end diastolic volume (EDV), which is controlled by venous return
120
Starling's law
The energy of the contraction is proportional to the initial length of the cardiac muscle fibre.
*Due to the length-tension relationship
121
Effect of preload on stroke volume
Increased preload = increased stroke volume
↑venous return = ↑EDV = ↑SV.
122
Afterload (+ factors it depends on)
The load against which the muscle tries to contract
Controlled by the arterial pressure against which the blood is expelled, which depends on total peripheral resistance (TPR).
123
Effect of afterload on stroke volume
Increased afterload = decreased stroke volume
↑TPR = ↑Arterial pressure = more energy used opening aortic valve = low SV
124
Cardiac output =
Heart rate x Stroke volume
125
significance of shorter contraction with increased contractility
Shortens systolic phase,
More time for ventricular filling
Maintains EDV and therefore preload + SV
126
Korotkoff sounds
Heard with a stethoscope on the brachial artery.
```
CP > SBP = silence
CP < SBP = tapping
CP << SBP = thumping
CP <<< SBP = muffled
CP < DBP = silence
```
*CP = cuff pressure
127
Relationship between blood velocity and total cross-sectional area of vessels
Total flow through all vessels must be equal so vessels with low velocity of blood flow have high total cross-sectional area and vice versa.
flow is fastest in aorta and vena cava, slowest in capillaries
128
Factors affecting pressure and flow in veins
```
Gravity,
Skeletal muscle pump,
Respiratory pump,
Venomotor tone,
Systemic filling pressure
```
129
Effect of gravity on venous pressure
Venous distension (pooling of blood) in legs = less blood in heart = low EDV = low preload = low SV = low MAP/ venous pressure
= decreased baroreceptor firing rate
130
Skeletal muscle pump
Muscle activity from rhythmic exercise promotes venous return
131
Respiratory pump
Inhalation decreases thoracic pressure and draws blood back to the heart
132
Venomotor tone
State of contraction of smooth muscle around veins.
| contracts to increase venous return when more blood is needed - mobilises capacitance
133
Processes of transport between capillaries and tissues
```
Diffusion (across membrane/through channels),
Carrier-mediated transport
Bulk flow (Starling's forces)
```
134
Capillaries in the brain
Completely continuous; no clefts or channels.
This only exists in the brain and is the basis of the blood-brain barrier
135
Blood clotting process
1. formation of a platelet plug
| 2. formation of a fibrin clot
thrombin converts fibrinogen to fibrin
136
Anti-clotting mechanisms of the endothelium
Stops blood contacting collagen (no platelet aggregation).
Produces prostacyclin and NO (inhibit platelet aggregation).
Produces Tissue Factor Pathway Inhibitor (TFPI) (stops thrombin production).
Expresses thrombomodulin and heparin (inactivate thrombin).
Secretes tissue plasminogen activator (t-PA) (activates plasminogen to form plasmin which digests clots)
137
Active (metabolic) hyperaemia
```
INCREASED METABOLIC ACTIVITY:
metabolites accumulate,
Triggers the release of EDRF (NO),
Causes arteriolar dilation,
increases flow.
```
*This matches blood supply to the metabolic needs of that tissue.
138
Pressure (flow) autoregulation
```
DECREASED MAP CAUSES DECREASED FLOW:
metabolites accumulate,
Triggers release of EDRF (NO),
Causes arteriolar dilation,
increases flow.
```
*Ensures a tissue maintains its blood supply despite changes in MAP
139
Reactive hyperaemia
```
OCCLUSION OF BLOOD SUPPLY:
metabolites accumulate,
Triggers release of EDRF (NO),
Causes arteriolar dilation,
increases flow.
```
*occlusion of blood supply causes subsequent increase in blood flow.
140
Injury response
INJURY:
triggers mast cell to release histamine
causes arteriolar dilatation
increased blood flow + permeability
*aids delivery of leukocytes to injured area
141
Sympathetic effect on arteriolar tone
Releases norepinephrine,
Binds to a1 receptors on some smooth muscle (e.g. arterioles supplying skin, kidney),
Causes arteriolar constriction
Binds to b2 receptors on other smooth muscle (e.g. arterioles supplying heart, brain)
Causes arteriolar dilation
142
Parasympathetic effect on arteriolar tone
Usually no effect
143
Hormonal effect of epinephrine on arteriolar tone
SMOOTH MUSCLE:
binds to a1 receptors,
causes arteriolar constriction,
decreases flow
SKELETAL and CARDIAC MUSCLE:
activates b2 receptors,
causes arteriolar dilatation,
increases flow through that tissue
144
Local (intrinsic) controls of arteriolar tone
Active hyperaemia,
Pressure autoregulation,
Reactive hyperaemia,
Injury response.
145
Factors controlling blood flow in coronary circulation
Blood flow interrupted during systole but...
Shows excellent active hyperaemia,
Expresses many b2 receptors (swamp any sympathetic arteriolar constriction)
146
Factors controlling blood flow in cerebral circulation
Shows excellent pressure autoregulation
147
Factors controlling blood flow in pulmonary circulation
Decreased O2 causes arteriolar constriction (opposite to most tissues),
Ensures blood is diverted to the best ventilated parts
148
Factors controlling blood flow in renal circulation
Filtration depends on pressure so shows excellent pressure autoregulation
(pressure independent from MAP)
149
Poiseuille's law meaning
Radius is used to control blood flow
150
Importance of Mean Arterial Pressure (MAP)
MAP is the driving force pushing blood through the circulation
Too low = syncope
Too high = hypertension
151
```
Arterial Baroreceptors
(location and function)
```
Located in the aortic arch and carotid sinuses
Stretch receptors: fire more APs when artery walls are more stretched by high BP.
152
Sensory fibres of the arterial baroreceptor reflex
Aortic arch --> Medullary cardiovascular centres:
Vagus nerve
Carotid sinus --> Medullary cardiovascular centres:
Glossopharyngeal nerve
153
Parasympathetic arterial baroreflex response
Hyperpolarises SA node (decreases slope of pacemaker potential).
Impulse travels in vagus nerve
154
Sympathetic arterial baroreflex response
Noradrenaline acts on b1 receptors to Increase slope of pacemaker potential in SA node,
Noradrenaline acts on b1 receptors on myocytes in the ventricles to increase contractility
Stimulates adrenal medulla to release adrenaline,
Acts on a1 receptors in smooth muscle causing arteriolar constriction and venoconstriction
155
The arterial baroreceptor input
APs travel from arterial baroreceptors to the medullary cardiovascular centres.
More APs = higher BP = parasympathetic response
Less APs = lower BP = sympathetic response
156
Other inputs to cardiovascular medullary centres
| other than arterial baroreceptor input
```
Cardiopulmonary baroreceptors,
Central chemoreceptors,
Chemoreceptors in muscle +
Joint receptors (more blood to exercising areas),
Higher centres
```
157
Cardiopulmonary baroreceptors (low pressure baroreceptors)
Located in large systemic veins and pulmonary vessels.
Respond to blood volume - important in the long-term regulation of blood pressure.
Send sympathetic signals to juxtaglomerular cells when blood volume (=pressure) is low
158
MAP =
CO x TPR
159
Effect on CVS of standing and reflex response
Standing = pooling of blood in veins/ venules of lower limbs
= ↓VR = ↓EDV = ↓preload = ↓SV = ↓CO = ↓MAP
= ↓baroreceptor firing rate
RESPONSE:
↓Vagal tone
↑ sympathetic tone
= ↑MAP
160
High contractility
Shorter, sharper contractions.
Caused by (nor)adrenaline acting on b1 receptors on myocytes
161
Effect of the Valsalva manoeuvre
1. increased thoracic pressure (TP) initially increases MAP
2. Increased TP decreases; VR, EDV, SV, CO, MAP
3. Baroreceptors initiate reflex = increased CO + TPR and therefore MAP
162
Effect of releasing the Valsalva manoeuvre
1. Decreased TP initially decreases MAP
2. VR is restored, increases EDV, SV and therefore MAP
3. MAP decreases to normal
163
Clinical use of the Valsalva manoeuvre
Used to measure strength of baroreceptor reflex
164
Kidney regulation of plasma volume
Modulating Na+ transport out of the collecting duct determines how big the osmotic gradient out of the collecting duct is.
Modulating collecting duct permeability to water determines if water follows it:
Increasing collecting duct permeability = lots of water reabsorption - conserves plasma volume, little urine.
Decreasing collecting duct permeability = little water reabsorption - reduction in plasma volume, lots of urine.
*These processes are modulated by hormone systems.
165
Triggers of renin production
Sympathetic activation to juxtaglomerular cells. (caused by decreased plasma volume sensed by CP baroreceptors, relayed via medullary CV centres)
Decreased distension of afferent arterioles
Decreased delivery of Na+/ Cl- through distal convoluted tubule. detected by Macula densa cells.
(Low Na+ = low filtration pressure/MAP)
166
Juxtaglomerular (granular) cells
Specialised cells around the efferent and afferent arterioles.
Releases renin in response to triggers.
167
Activity of renin
Converts inactive angiotensinogen into angiotensin I
168
Creation of angiotensin II
Angiotensin I in converted to angiotensin II by angiotensin converting enzyme
169
Actions of Angiotensin II
Increases release of ADH from the posterior pituitary gland
Stimulates release of aldosterone from the adrenal cortex
Causes vasoconstriction
170
Triggers of ADH release
Decreased blood volume (sensed by CP baroreceptors, relayed via medullary CV centres)
Increased osmolarity of ISF (sensed by osmoreceptors in the hypothalamus)
Circulating angiotensin II (from the renin-angiotensin-aldosterone system)
171
Effects of ADH
Increases permeability of the collecting duct (decreases diuresis, increases plasma volume)
Increases sense of thirst
Causes vasoconstriction
172
Effects of aldosterone
Increases Na+ reabsorption in the loop of Henle:
- decreses diuresis
- increases plasma volume
173
Diuresis
Urine production
174
Triggers of Atrial Natriuretic Peptide production
Increased MAP
- > distension of atria
- > production of ANP by myocardial cells in atria
175
Triggers of Brain Natriuretic Peptide production
Increased MAP
- > distension of ventricles
- > production of BNP by myocardial cells in ventricles
176
Effects of ANP/BNP
Increased excretion of Na+ (natriuresis)
Inhibits release of renin
Acts of medullary CV centres to reduce MAP
177
Pacemaker action potential
1. Pacemaker potential (pre-potential)
- spontaneous gradual depolarisation
2. Action potential - once threshold is reached
- rapid depolarisation
178
Reason for rapid conduction through bundles of His and purkinje fibres
ventricular cells contract together giving a short, sharp contraction to expel lots of blood
179
Pressure-volume loop x-axis
Left ventricular volume (ml)
180
Pressure-volume loop y-axis
Left ventricular pressure (mmHg)
181
Pressure throughout the vascular tree
Elastic arteries damp down pressure variations from the ventricles
Pressure falls throughout the vascular tree, driving blood forward
182
Systemic filling pressure
The small pressure difference that pushes blood through the veins
183
Function of the blood-brain barrier
Protects the brain from circulating pathogens
