Cardiovascular Flashcards
1
Q
What are the two main components of the blood?
A
Cellular components (45%) Fluid components (55%)
2
Q
Define Haemopoiesis
A
Formation of blood cells
3
Q
What is the life span of RBC’s, WBC’s and platelets?
A
RBC's = 120 days WBC's = depends on cell type Platelets = 7-10 days
4
Q
Where are blood cells formed in utero?
A
Yolk sac (0-2months) Liver/Spleen (2-7months) Bone marrow (5-9months)
5
Q
Where are blood cells formed in children?
A
All bones
6
Q
Where are blood cells formed in adults?
A
Axial skeleton
7
Q
What are the proper names for RBC’s. WBC’s and platelets?
A
RBC = Erythropoiesis WBC = Myelopoiesis Platelets = Thrombopoiesis
8
Q
Draw a diagram that shows the progression of blood cell formation from the haemocytoblast
A
See diagrams that need to be drawn notes
9
Q
Which hormonal growth factors control the formation of RBC,s WBC’s and platelets?
A
RBC = EPO from kidney WBC = Granulocyte-macrophage colony stimulating factor (GM-CSF) Platelets = thrombopoietin (TPO)
10
Q
Describes the properties of RBC’s
A
No nucleus or mitochondria
Biconcave disc
7.5um diameter
Contains Hb and glycolysis enzymes
11
Q
Describe the structure of adult Haemoglobin
A
4 globin chains each with own Haem molecule
Tetrameric protein (2 alpha/2 beta proteins)
Normal O2 saturation Is 96-98%
12
Q
Describe the structure of foetal haemoglobin
A
2 alpha and 2 gamma proteins
Normal O2 saturation is 0.5-0..8%
13
Q
What is anaemia and what signs and symptoms would you expect?
A
Deficiency of Hb (<130g/L in males and <110g/L in females)
Signs (Pallor, tachycardia)
Symptoms (Tiredness, shortness of breath, angina and claudication
14
Q
Where are RBC’s produced and where are they removed?
A
Made in bone marrow and removed by spleen, bone marrow and by blood loss
15
Q
What diseases result from an RBC production failure?
A
Hypoplastic anaemia (Not enough) Dyshaemopoietic anaemia (Ineffective production)
16
Q
How do you increase RBC removal?
A
Blood loss
Haemolysis
Intrinsic abnormalities (Factors within RBC)
Extrinsic abnormalities (Factos outside RBC)
17
Q
What are the intrinsic RBC abnormalities?
A
Acquired
Hereditary including membrane disorders, enzyme disorders and Hb disorders
18
Q
What are the extrinsic RBC abnormalities?
A
Antibody mediated (AIHA) Mechanical trauma Infections Chemicals Sequestration
19
Q
What are causes of anaemia?
A
Iron deficiency Chronic bleeding Poor diet Malabsorption Hookworm - intestinal parasite
20
Q
Define a reduction mean corpuscular Hb
A
Reduction in the amount of Hb in the cell
21
Q
Define a reduction in mean corpuscular volume
A
Reduction in the size of the cell
22
Q
What are the properties of neutrophils?
A
6-10 hours lifespan Most numerous white blood cell Phagocytose bacteria Release chemotaxis and cytokines as part of inflammatory response Contain a nucleus that has 3-5 lobes
23
Q
What are the properties of monocytes?
A
20-40 hours life span
0.2-0.8 x 10^9 L
Macrophages - phagocytose bacteria
Dendritic cells - present antigens to immune system
24
Q
What are the properties of basophils?
A
Life span of days
0.01-0.1 x 10^9L
Migrate to tissues to become mast cells where they fill with histamine granules, express IgG and play an important role in the allergic response
25
What are the properties of Eosinophils?
Lifespan of days
0.04-0.4 x 10^9L
Role in allergic response and parasite infection protection
26
Construct a table comparing T and B lymphocytes based on origin, blood, receptors, function and markers
See diagrams need to know sheet
27
Define haemostasis
Balance between bleeding (blood failing to clot outside the vessel) and thrombosis (blood clots inside the vessel)
28
Describe the pathway for the formation of platelets
Myloid Stem cell differentiates into megakaryoblast which undergoes endomitosis to megakaryocytic which undergoes membrane blebbing to platelets
29
Describe the properties of platelets
140-400 x10^9L
anucleate cells which circulate in inactive state
Responsible for primary haemostasis
have a life span of 5-10 days
30
How do platelets adhere to damaged blood vessels?
Bind to collagen via glycoprotein Ia (GPIa) and to von willenbrand factor by GPIB and GPIIb
31
How do platelets work? (4 steps)
Bind (Adhere)
Change Shape (Activate)
Release Contents (Degranulate)
Aggregate
32
What two types of granules do platelets contain?
Electron dense granules
| Alpha granules
33
What do platelet electron dense granules contain?
Calcium
ADP and ATP
Serotonin
34
What do platelet alpha granules contain?
Platelet derived growth factor
Fibrinogen
Heparin Antagonist (PF4)
Von Willenbrand Factor
35
What is a normal platelet count?
140-400 x 10^9L
36
What does a reduction in platelet number result in
Increased bleeding - thrombocytopenia
>80 but <140 x 10^9 = increased bleeding
>20 but <80 x 10^9 = spontaneous bleeding
37
What does an increased platelet number cause?
Thrombocytosis
Arterial thrombosis
Venus Thrombosis
38
Describe constituents of plasma
90% water
Salts
Glucose
Proteins (albumin, carrier proteins, coagulation proteins and immunoglobulins)
39
Describe function of albumin and consequences of its absence
Produced in liver and determines oncotic pressure of blood
Albumin carries FA's, steroids and thyroid hormones
Lack can cause oedema, liver disease and nephrotic syndrome
40
Draw a diagram of the coagulation cascade
See diagrams that need to be learnt sheet
41
Describe what coagulation proteins are
Enzymes that circulate in inactive state
Produced in liver
Key enzyme is Thrombin which converts fibrinogen into an insoluble fibrin polymer
42
What do the multiple steps of the coagulation cascade allow for?
Biological amplification of response and regulation
| Not an all or nothing response
43
Draw a diagram to give an overview of clotting
See diagrams I need to know sheet
44
Describe properties and treatment for Haemophilia A
X linked disorder
Severe bleeding into muscle and joints
Deficiency of tissue factor VIII so treat with factor VIII
45
Describe the properties and treatment for haemophilia B
Severe bleeding into muscle and joints
| Deficiency of factor IX so treat with factor IX
46
Describe the properties of von Willebrand disease
Autosomal dominant inheritance
caused by Lack of Von Willebrands Factor (VWF)
- VWF is required for platelets to bind to damaged blood vessels, so lack of VWF =
platelet dysfunction, hence muco-cutaneous bleeding
- Usually a mild bleeding disorder
47
What are the causes of acquired bleeding disorders?
Liver disease
Vit K deficiency
Disseminated intravascular coagulation
anti-platelet/anti-coagulation medicines
48
Why is vitamin K important?
Needed for functional activity of coagulation factors (2, 7, 9 and 10)- remember as 1972
49
What is disseminated intravascular coagulation and what are the causes
Simultaneous bleeding and microvascular thrombosis
| Caused by sepsis, obstetric issues or malignancy
50
What is the result of an decreased platelet count
Thrombocytopenia
<80 = increased bleeding
<20 = spontaneous bleeding
51
What is the result of an increased platelet count?
Thrombocytosis - increased risk of arterial or venous thrombosis
52
Why does the blood remain fluid inside blood vessels?
Because coagulation proteins and platelets circulate in an inactive state
53
When do coagulation factors become activated
When they come into contact with tissue factor which is present in every single cell except endothelial cells thus when endothelium is punctured blood starts clotting
54
Vasoconstriction of a damaged vessel is triggered by the release of what?
Endothelin-1
55
What happens to the shape of the platelet when it becomes activated?
Changes from Smooth discoid to spiniculated with pseudophilia which increases SA and cell to cell interactions
56
Which receptor on platelets does thrombin bind to and what effect does this have?
Binds to PAR1 and PAR4 which induces platelet activation and positively feedback to increase thrombin release
57
Which platelet receptor does ADP bind to and what does It cause?
ADP binds to P2Y1 to cause platelet activation and GPIIb/IIa fibrinogen cross linking
ADP also binds P2Y12 which sustains platelet aggregation and activation but doesn't initiate the process
58
What are the membrane level effects of thrombin binding to PAR-1
Normally in resting platelet, translocase active and scrambalase inactive which aminophospholids kept internal but thrombin binds causing Ca2+ release from internal stores which causes inactivation of translocase and activation of scrambalase. This causes aminophospholipids to move outside cell and form prothrombinase enzyme complex which converts prothrombin to thrombin
59
What is the effect of the release of alpha granules from platelets?
Inflam mediators (P-selectin) from alpha granules interact with WBC's resulting in inflammation in the vessel wall
60
What are the effects of the thromboxane on platelets?
Causes vasoconstriction and platelet activation
61
Why does the platelet plug not extend away from the damaged area?
Undamaged endothelium either side releases prostacyclin which inhibits platelet aggregation and NO which is a vasodilator and inhibits platelet aggregation
62
Describe the pathway by which a fibrin clot is broken down
Fibrinolytic system
Tissue plasminogen activators converts plasminogen to plasmin which catalyses the conversion of fibrin to fibrin degradation products
63
Describe the properties cardiac muscle
Only found in the heart
Striated appearance due to regular sarcomeres consisting of interdigitating thick myosin and thin actin filaments
Each cell contains single nucleus
Cells joined end to end by intercalated discs
64
Describe the structure of myosin chain
Consists of 2 heavy and 4 light polypeptide chains that come together to form a protein with two globular heads that have 2 binding sites for actin and ATP
65
Draw the ultrastructure of a sarcomere
See diagrams I need to learn sheet
66
Describe the structure of actin
Globular protein where two actin monomers become intertwined to form a polymer
67
Describe the location of tropomyosin in actin
Lies in the groove between the two actin molecules and overlies the myosin binding sites on actin
68
Describe the role of troponin in ECC
Troponin molecule changes shape when calcium binds which leads to exposure of myosin binding sites on actin by moving tropomyosin
69
What is the role of titin
elastic filaments that maintain alignment of the sarcomere - extends from Z-line to M-line
70
Define the A band of a sarcomere
Region of sarcomere where there are overlapping thick and thin filaments - twice as many thin as thick
71
Define I Band
Region of sarcomere that contains only thin filaments which extend to centre of sarcomere from Z-line
72
Define H zone
Contains thick filaments only
73
Define the M line
Cetnre of the H-zone comprised entirely of thick filaments
74
Describe the stages of excitation contraction coupling
AP depolarises T-tubule. This causes Ca2+ influx through L-type channels. Cytosolic Ca2+ increases and binds to RYR receptor on sarcoplasmic reticulum - causes calcium induced calcium release (20% comes from outside and 80% from inside). Ca2+ binds to troponin causing change of shape which moves tropomyosin to expose myosin binding sites on actin . Myosin head on myosin binds to actin causing Pi to be dropped = cross bridge formation. Myosin head then drops the ADP group to contract pulling actin over the myosin filament to shorten the z-line and cause muscle to contract = power stroke. ATP binds to the myosin head and causes it to detach from the actin filament and move to starting position.. ATPase in the myosin head hydrolyses ATP to ADP and Pi for next contraction if binding sites remain open
75
How is cytosolic Ca2+ returned to normal after ECC
Primary active Ca2+ATPase pump in SR and sarcolemma and Na+/Ca2+ cotransporters (NCX) or pumped back into the SR by ATP dependent Ca2+ pumps
76
Where do t-tubules invaginate muscle cells?
At the level of the Z-line
77
Define what a sarcomere is?
Functional unit of the contractile apparatus define as the region between a pair of z-lines
78
What are the three troponin subunits and what are their functions?
Troponin C = binds calcium
Troponin I = binds actin
Troponin T = binds tropomyosin
79
Describe the pacemaker potential
Progressive reduction in K+ permeability as K+ channels that opened during repolarisation of previous action potential close. Threshold -60mv reached causes hyperpolarisation cyclic channels (HCN) channels to open which allows inward Na+ current. This causes increases in charge to -40mv at which point T-type Ca2+ channels open causing depolarisation to +20mv. At this point K+ channels open which causes depolarisation and returns negative charge. When hyperpolarisation threshold is reached the cycle begins again
80
What effects does the autonomic nervous system have on pacemaker potential?
Catecholamines speed up HCN channels so threshold reached faster = increase HR
Ach slows HCN channels so threshold takes longer to reach so slows HR
81
What is the main difference between nodal tissue and cardiac myocytes
HCN channels are present in nodal tissue but not in cardiac myocytes
82
What are the differences between the action potential of cardiac myocytes and skeletal muscle?
Cardiac potential has Ca2+ leaving the cell to cause a plateau phase
Cardiac AP is 200-300ms (15x longer) whereas skeletal is shorter
Cardiac muscle has longer refractory period to prevent muscle fatigue and allow for adequate filling time
83
Describe the resting cardiac myocyte membrane potential
Sarcolemma at rest is more permeable to K+ than Na+ so membrane potential is closer to K+ equilibrium potential (-90mv) than Na+ (+60mv)
84
Describe the ionic basis of myocardial AP
AP arrives causing threshold to be breached so Na+ Channels open depolarising membrane to +20mv. At this point K+ channels open and Na+ channels close causing partial repolarisation. at same time as Na+ opened, L-type Ca2+ opened so when Na+ close, Ca2+ are opening at t-tubules causing Ca2+ inflow into cell which balances K+ leaving causing plateau phase at0mv. When L-type close, K+ continues to leave the cell causing repolarisation until resting potential is achieved
85
Describe the role and properties of the SAN
Determines the rate the heart beats (60-100bpm) - resting membrane potential of -55to -60mv related to slow Na+ inflow which is not found anywhere else in the body which is closer to threshold so depolarises first
86
how are cardiac myocytes electrically connected?
by gap junctions
87
Define automaticity
Ability for spontaneous, rhythmic self contraction seen in the SAN due to the SAN potential drifting towards threshold for discharge
88
What is the name of the pathway that connects the SAN and AVN?
Internodal pathway
89
Why is it important that the conduction of AP's through the AVN is slow?
Enables the atria to empty blood into the ventricles enabling atrial contraction to be completed before ventricular excitation occurs
90
What Is the only connection between the atria and the ventricles
AVN and the bundle of His - part from this they are separated by a layer of nonconducting connective tissue
91
What are the effects of sympathetic stimulation on the heart?
Increased HR (up to 180-250bpm (positively chronotropic)
Increased force of conception (Positively inotropic)
Increases Cardiac output (by up to 200%)
92
What are the effects of parasympathetic stimulation of the heart?
Decreased HR (to 30-40bpm)(Negatively chronotropic)
Decreases force of contraction (Negatively inotropic)
Decreases cardiac output (by up to 50%)
93
How does sympathetic stimulation cause increased HR?
Sympathetic postganglionic fibres innervate the entire heart
Adrenaline/Noradrenaline act on type 1 adrenoceptors to increase adenylyl cyclase which increases camp
94
How does parasympathetic stimulation causes decreased HR?
Fibres transmitted by vagus nerve
| Acetylcholine acts on M2 receptors to inhibit adenyl cyclase and reduce camp
95
By what percentage will cardiac output decrease if sympathetic stimulation decreases?
up to 30%
96
Describe the distribution blood volume in the circulatory system?
```
Veins (64%)
Lungs (9%)
Capillaries (5%)
Larger arteries (7%)
Small arteries (8%)
Heart (diastole) (7%)
```
97
What are the three types of capillary?
Continuous
Fenestrated
Discontinuous
98
What is the name of vessels within the walls of larger blood vessels
Vasa Vasorum
99
Describe the properties of veins
Have valves to ensure uni-directional flow of blood to the heart and are surrounded by skeletal muscle which contracts to increase vein pressure ensuring blood returns to the heart
100
Describe the basic plan of circulation
Oxygenated blood is pumped from the left ventricle into the arterial system which carries it to capillaries where it provides oxygen to tissues and then removes waste products of metabolism such as CO2. Deoxygenated blood passes in the venous system returning to the right ventricle where it is pumped in the pulmonary arteries to the lungs. Here it is deoxygenated through proximity of capillary network to alveoli. Oxygenated blood returns to the left ventricle via the pulmonary veinns
101
What are the three layers of blood vessels
```
Tunica intima (endothelial cells)
Tunica media (smooth muscle)
Tunica Adventitia (Fibroblast layer)
```
102
Describe the differences in the structure of arteries and veins
Tunica media in arteries is thicker than veins and veins posse valves to allow blood to only flow in one direction
103
Describe the embryology of vasculature
Lateral mesoderm contains angioblasts which become the first blood vessels. Extraembryonic mesoderm forms blood islands which are haemoblasts surrounded by endothelial cells
104
Describe the process of vasculogenesis
Occurs embryonic days 17-21 - endothelial cells of blood islands spread to form blood vessels around yolk sac, chorionic villus and stalk. By day 18, angioblasts migrate along centre of embryo to form vascular loop for embryonic heart to beat in. Angioblasts know if they will be arteries or veins due to endothelial surface markers. ie. arteries is Ephrin B2 and veins is ephb4
105
Describe the process of angiogenesis in embryology of the circulatory system
Once the primitive vascular loop has formed, endothelial cells will proliferate and migrate to form new blood vessels. process is guided by molecules that attract or repel endothelial cells
106
Name 2 angiogenic growth factors
Vascular endothelial growth factor
| Angiopoietin 1 and 2
107
Name 2 endothelial repulsive signals
Plexin/semaphoring signalling
| Ephrin/Eph interactions
108
Describe what happens to the 1st aortic arch during embryological development
1st arch becomes part of maxillary artery
109
What conditions arise if development of aortic arches falters
Right sided or double sided aorta
| Aortic co-arction
110
Describe what happens to the 2nd aortic arch during development
Becomes the artery to stapedius
111
What happens to the 3rd aortic arch during development
Portion of dorsal aorta between 3rd and 4th disappears
| 3rd becomes common carotid arteries and proximal internal carotid arteries
112
Describe what happens to the left and right 4th aortic arches during development
Right dorsal loses connection to midline aorta and 6th arch but remains attached to right 4th arch - acquires 7th cervical intersegmental artery and grows into right upper limb to become right subclavian artery
Left 4th becomes arch of aorta
113
What happens to the 5th aortic arch during development
There is no 5th aortic arch in humans
114
What happens to the dorsal arch during development
Left dorsal aorta becomes descending aorta
115
What happens to the left and right 6th aortic arches during development
right 6th becomes pulmonary trunk
| Left 6th becomes ductus arteriosus
116
Why do we need to control circulation?
```
Maintain blood flow
maintain arterial pressure
Distribute blood flow
Auto-regulate/homeostasis
Function normally
Prevent catastrophe
Maladapt during disease
```
117
Where is the principal site for resistance to vascular flow?
Arterioles as total arteriolar resistance = total peripheral resistance
118
What is total peripheral resistance
Total resistance to flow in systemic blood vessels determined by arterioles - vascular smooth muscle determines arteriole radius - contraction of VSM decreases radius which increases resistance and decreases flow - relaxation of VSM increases radius, decreases resistance and increases resistance to flow - VSM never completely relaxes due to myogenic tone
119
What is flow rate determined by?
Arteriolar resistance
| Number of open pre-capillary sphincters
120
Why is flow in the lymphatics uni-directional
Smooth muscle in the lymphatic vessels
Skeletal muscle pump
Respiratory pump
121
Where is interstitial fluid returned to the cardiovascular system
Thoracic duct/left subclavian vein
122
Write an equation for cardiac output
CO = SV x HR
123
Write an equation for blood pressure
BP = CO x TPR
124
Write an equation for pulse pressure
Systolic - diastolic
125
Write an equation for mean arterial pressure
diastolic pressure + 1/3PP
126
Write an equation for stroke volume
EDV - ESV
127
Define Poiseuilles law
radius to the power of 4
128
Define Ohms law
Pressure gradient/resistance
129
Define Frank Starling Mechanism
Force of contraction is proportional to EDV - more the ventricle fills the harder it contracts
130
Explain how the Frank Starling mechanism works
VR increases which increases EDV which increases preload which increases sarcomere stretch which increases force of contraction which increases stroke volume
131
Which artery is used to measure blood pressure
Brachial artery
132
What components influence blood flow
```
Autoregulation
Local mediators
Humoral factors
Baroreceptors
Central (neural) control
```
133
Define intrinsic auto regulation
When arterioles vasoconstrict or vasodilate in response to changes in resistance seemingly automatically in order to maintain constant blood flow
134
Define myogenic auto regulation
When blood flow is increased and stretches vascular smooth muscle, the muscle automatically constricts until diameter is normalised or slightly reduced. When smooth muscle isn't stretched as much due to low blood pressure the muscle relaxes and dilates in response
135
Define hyperaemia
Increase in blood flow
136
Define active hyperaemia
increase in blood flow when metabolic activity increases
137
Define reactive hyperaemia
When an organ or tissue has its blood flow completely occluded a profound transient increase in blood flow occurs
138
What are the two types of local humeral factors
Vasoconstrictors
| Vasodilators
139
What molecules are vasoconstrictors
Endothelin-1
| Internal blood pressure (Myogenic contraction)
140
What molecules are vasodilators
Hypoxia, adenosine, bradykinin, NO, K+, CO2, H+, tissue breakdown products
141
What are the three heart sounds
lub = closure of AV valve
dub = close or aortic/pulmonary valves
third sound is blood rushing into left ventricle
142
Define EDV
Volume of blood in the ventricle after contraction
143
Define ESV
Volume of blood in the ventricle before contraction
144
Define afterload
Pressure against which the heart must work to eject blood during systole
145
What does ECG actually measure?
Measure of the currents generated in the extracellular fluid by the changes occurring simultaneously in many cardiac cells
146
What are the 3 bipolar leads in ECG
Right arm
Left arm
Left leg
147
What are the 3 unipolar leads?
aVR - electrical activity towards the right arm
aVL - Electrical activity towards the left arm
aVF - activity from the inferior
148
What are the locations of the 6 unipolar chest leads
```
V1 = 4th intercostal space
V2 = 4th intercostal to the left
V3 = mid clavicular line (5th intercostal)
V4 =
V5 = anterior axillary line
V6= mid axillary line
```
149
How many leads are there on an ECG?
12 in total
150
What does each of the ECG waveforms represent
```
P = atrial depolarisation
QRS = Ventricular depolarisation
T = ventricular repolarisation
```
151
Why is P wave smaller than QRS?
Because the atria have less muscle than the ventricles
152
Are P waves and T waves positive or negative in a normal ECG
P waves are positive in every lead apart from aVR
| T waves are positive in every lead apart from aVR and sometimes V1 and V2 depending on the trace
153
What does the ST segment represent
Interval between ventricular depolarisation and repolarisation
154
What would you see in an ECG of someone with sinus tachycardia
More frequent P waves >100bpm
155
What would you see In an ECG of someone with sinus bradycardia
Less frequent P waves <60bpm
156
What would you see on an ECG of someone with dextrocardia
multiple negative P waves
157
Where can you hear the left ventricle
5th left intercostal space and mid clavicular line responsible for apex beat
158
How long does the cardiac cycle last?
0.8s
159
How long does systole last
0.3s
160
How long does diastole last
0.5s
161
What area of the heart does the right coronary artery supply
Inferior surface of the heart
162
What area of the heart does the left anterior descending supply
Anterior LV wall
163
What area of the heart does the left circumflex supply
Lateral LV wall
164
What is the Normal duration of the PR interval
120-200ms
165
What clinical condition is a short PR interval associated with?
Wolff-Parkinson-White Syndrome- accessory pathway
166
What clinical condition does a long PR interval indicate?
1st degree heart block due to delayed AV conduction
167
Which complex is normally inverted compared to the anterior and inferior leads
Lead aVR
168
Which period is abnormally elevated during acute injury/infarction of a substantial myocardial territory
ST segment
169
What is the normal duration of a QRS complex
Less than 120s
170
What clinical condition is associated with a prolonged QRS (>120s)
Bundle branch block
171
What is the pulmonary pressure during systole?
25mmHg
172
What is pulmonary pressure during diastole
10mmHg
173
What are the three basic events of the cardiac cycle
ventricular contraction
Ventricular relaxation
Ventricular filling
174
Describe the events of ventricular systole (contraction)
left ventricular pressure rises to greater than left atrial pressure causing the mitral valve to close and producing the first heart sound. Isovolumetric contraction occurs where volume in ventricle remains the same but pressure increases. Pressure in ventricle exceeds aortic pressure so aortic and pulmonary valves open and maximal ejection from ventricles and arteries occurs but ventricles don't completely empty
175
Describe the events of ventricular diastole (relaxation)
Left ventricular pressure peaks and then decreases 'phase of reduced ejection' Left ventricular pressure falls below aortic presure so aortic valve closes (2nd heart sound). Both AV and aortic valves closed so isovolumetric relaxation occurs (when pressure decreases but not change in volume).
176
Describe the events of ventricular filling
Ventricular pressure falls below atrial pressure. Atrial pressure due to venous return is enough to open AV valves allowing 80% of ventricular filling to occur. Diastasis occurs where pressure between atria and ventricles equalises so there is little no movement of blood (at this point AV node is delaying stimuli from SAN). Atrial booster causes atrial contraction which increases atrial pressure an enables active ventricular filling
177
Define contractility (Inotropic State)
State of the heart that enables it to increase its contraction velocity to achieve a higher pressure - force of heart contraction that is independent of load
178
Define elasticity
Ability of the myocardium to recover its normal shape after removal of systolic stress
179
Define compliance
Relationship between change in stress and resultant strain - how easily the heart chamber expands when filled with blood volume
180
Define diastolic distensibility
pressure required to fill ventricles to the same diastolic volume
181
Where are the primary (arterial) baroreceptors located?
Carotid sinus and aortic arch
182
Where are secondary baroreceptors located?
In veins, myocardium and pulmonary vessels
183
Afferent feedback from baroreceptors is carried by which nerve
Glossopharyngeal (IX)
184
efferent feedback from baroreceptors is carried by which nerve
Sympathetic ad Vagus (X)
185
What Is the effect of high blood pressure on baroreceptors
High pressure stimulates baroreceptors (increased firing) which leads to inhibition of the pressor/vasoconstrictor centre in the medulla which causes increased PNS and decreased SNS leading to a fall in CO and TPR and a decrease in BP
186
How does the pressor region increase blood pressure?
```
Vasoconstriction
Increase HR
Increase SV
Increases CO
Increase contractility
```
187
How doe cardiopulmonary baroreceptors stimulation reduce blood pressure?
Decrease signals to the vasoconstrictor centre In the medulla leading to fall in BP and decrease the release of angiotensin, aldosterone and vasopressin resulting I fluid loss
188
Which baroreceptors are key in the short term regulation of BP
Arterial baroreceptors
189
Describe the role of central chemoreceptors in BP control
Chemosensitive regions in medulla
190
Outline the short term control of blood pressure
Baroreceptors
Increased blood pressure leads in increased firing leading to increased PNS and decreased SNS which decreases CO and TPR leading to a fall in BP
191
Outline the long term control of BP
Volume of blood
| (Na+ and H2O) - Renin Angiotensin-aldoesterone and ADH
