Cardiovascular Flashcards
(203 cards)
1
Q
What are the two phases of blood, what is in each phase and what percentages are involved?
A
Cellular: 45% (99% RBCs, then white blood cells and platelets make up the rest)
Fluid: 55% (plasma)
2
Q
How many litres of blood is normal for a human?
A
5 litres
3
Q
What is haematocrit and what is a normal value?
A
the volume of red blood cells i.e haemoglobin in the blood, normal haematocrit is 0.45
4
Q
What is haemopoiesis? In adults where does this take place?
A
the process of the production of blood cells and platelets which continues throughout life, in adults this is confined to the bone marrow
5
Q
What is the lifetime of RBCs?
A
120 days
6
Q
What is the lifetime of white blood cells?
A
6 hours
7
Q
What is the lifetime of platelets?
A
7-10 days
8
Q
Where are the precursor cells for red blood cells found?
A
The precursor cells of red blood cells are located in the bone marrow:
- In adults this is in the axial skeleton - skull, ribs, spine, pelvis and long bones
- In children this is in all bones
- In utero this is in the yolk sac, then liver and spleen
9
Q
What is precursor cells in the blood an indication of?
A
Leukaemia
10
Q
What do hormonal growth factors do? and what is the specific type for each type of blood cell
A
Hormonal growth factors stimulate precursor stem cells to proliferate and
differentiate:
- Epo/ Erythropoietin (hormone made in kidney) = red blood cells
- G-CSF (granulocyte colony stimulating factor) = white cells
- Tpo = platelets
11
Q
What happens to the oxygen dissociation curve when the pH is decreased or the temperature increases?
A
It will shift to the right
12
Q
What happens to the oxygen dissociaton curve when the pH is increased or the temperature decreases?
A
It will shift to the left
13
Q
Why do red blood cells have such a short lifespan?
A
Simple cells, with no nucleus or mitochondria thus cannot repair itself - why they have such a short lifespan
14
Q
What are young red blood cells called?
A
Reticulocytes
15
Q
What is the role of haemoglobin and what is its structure?
A
Carries oxygen from the lungs to tissues, where it transfers oxygen to myoglobin in muscles
Haemoglobin is formed of 2 alpha and 2 beta chains and 4 haem groups - has an overall quaternary structures - due to the combination of more than two tertiary structures
16
Q
Explain the presence of varying antigen on the surface of blood cells?
A
Some people have the gene that results in the synthesis of the A antigen on the surface of red blood cells, some have the gene that results in the synthesis of the B antigen, some have both genes and some have neither. Those who have neither are said to have O-type erythrocytes. Thus the possible blood types are A(more common than B), B, AB (MOST RARE) & O (MOST COMMON)
17
Q
Which antibodies are in the plasma of a type A individual?
A
anti-B antibodies
18
Q
What is co-dominance and why is it important in blood types? What does this produce?
A
A antigen and B antigen are both codominant. They produce AB. Type AB have neither anti-A or anti-B antibodies in their plasma, has A + B
antigens on surface of red blood cells - UNIVERSAL RECIPIENT
19
Q
What is type O?
A
Type O have both anti-A & anti-B antibodies ( has no A or B antigens) in their plasma [type O is a UNIVERSAL DONOR since don’t have A or B antigens on
surface of red blood cell]. O antigen is RECESSIVE
20
Q
What are these antibodies?
A
They are anti-erythrocyte antibodies and are known as natural antibodies
21
Q
What would happen if a type A patient was transfused with type B blood?
A
1) the anti-B antibodies in the
recipients blood would attack the transfused blood & 2) the anti-A antibodies in the donor blood would attack the recipients blood HOWEVER this is usually of little consequence since the the transfused antibodies become so diluted in the recipients plasma that they are ineffective at inducing a response - it is the
destruction of the TRANSFUSED cells by the recipients antibodies that produces problems
22
Q
What are the Rhesus antigens? What does Rhesus positive mean?
A
C, D, E antigens. D ANTIGEN IS MOST IMPORTANT: Rhesus positive means the D antigen is present. Rhesus negative means the D antigen is not Present
23
Q
What is anaemia?
A
reduction in haemoglobin in the blood
24
Q
What is a normal haemoglobin value?
A
12.5 - 15.5 g/dl
25
What condition causes raised haemoglobin?
Polycythaemia (caused by smoking, lung diseases, inefficient lungs
meaning less O2 is exchanged so more haemoglobin is required etc.)
26
What are the symptoms of anaemia?
Tiredness, lethargy, malaise, reduced exercise tolerance, shortness of breath on exertion and angina
27
What are the signs of anaemia?
Palor, pale mucus membranes and palmar creases (pink hands), glossitis
(sore tongue), angular stomatitis ( cracking at corners of mouth), kylonychia (caused
by the iron deficiency - spoon shaped nails)
28
What are the classifications of anaemia?
Iron deficiency, B12/folate deficiency, anaemia of chronic disorder, haemolysis, bone marrow failure/infiltration
29
What is iron deficiency anaemia? What values would be expected and what are the causes?
Iron is needed for haemoglobin production, lack of
iron results in the reduced production of small red cells
• In iron deficiency anaemia there is a low haemoglobin and MCV < 80 fl
• Causes:
- Bleeding:
• Occult gastrointestinal: can affect anyone, most common cause of iron deficiency
anaemia
• Menorrhagia (heavy periods): Occurs in premenopausal women only or those
who've have repeated child birth
- Dietary:
• Not getting enough iron in diet, in the UK the cause is never diet
• Worldwide the most common cause of iron deficiency anaemia is diet
30
What is MCV?
Red cell size is measure as MCV (mean cell volume), normal = 82 - 96 fl
31
What is B12 folate deficiency anaemia, what values are expected and what are the causes?
MACROCYTIC ANAEMIA - normal red blood cell size = 82-96 fl, in macrocytosis anaemia = > 100 fl (large red blood cells)
- Macrocytosis can occur without anaemia i.e there will be a raised MCV but normal
haemoglobin levels this can be cause by liver disease, alcohol and hypothyroidism
- In macrocytic anaemia, macrocytosis is a sign of it. It occurs due to a vitamin B12
or folate deficiency
- VITAMIN B12 & FOLATE ARE NEEDED FOR DNA SYNTHESIS, thus with a B12 &
folate deficiency red blood cells cannot by made in the bone marrow and thus
less are released = ANAEMIA. This deficiency will affect all dividing cells, but bone
marrow is most active so is affected first
- Causes of B12 deficiency:
• In the terminal ileum B12 absorption occurs, however intrinsic factor PRODUCED
BY THE GASTRIC PARIETAL CELLS IN THE STOMACH is required for absorption to
occur since B12 binds to intrinsic factor and is THEN absorbed. Thus if the
stomach is damaged can result in less parietal cells thus less intrinsic factor thus less
B12 absorbed thus anaemia
• An autoimmune disease called PERNICIOUS ANAEMIA, causes the antibodies to
be made against gastric parietal cells meaning less intrinsic factor can be
produced so there is B12 malabsorption and thus ANAEMIA. However the liver
have a vast store of B12 which can last 4 years, thus pernicious anaemia has a slow
onset
- Causes of folate deficiency:
• Folate is found in vegetables and fruit
• Malabsorption e.g. due to celiac disease
• Dietary e.g. don't eat enough fruit and vegetables
• Increased need e.g. due to haemolysis or anything that results in increased cell
division can cause a folate deficiency
32
What is haemolysis, what values would be expected and what are the causes?
Normal or increased cell production but DECREASED LIFE SPAN < 30 DAYS, red
blood cells are destroyed before their 120 day lifespan
• CONGENITAL (present from birth):
- Membrane issues e.g Spherocytosis (whereby blood cells are spherical, they get stuck in vessels easily). Dominant Condition but variable penetrance
- Enzyme issues e.g Pyruvate Kinase Deficiency - enzyme required to convert phosphoenolpyruvate to pyruvate is deficient, resulting is less ATP production and also a build up of phosphoenolpyruvate, or G6PD DEFICIENCY
- Haemoglobin issues e.g. SICKLE CELL ANAEMIA (defect in beta globin chain in haemoglobin) - whereby red blood cells are sickle shaped thus get trapped in vessels easily, and THALASSAEMIA - mutation in haemoglobin chains, beta is more common
in india + Pakistan whereas alpha is more common in east e.g. Thailand
• ACQUIRED:
- Autoimmune: immune system attacks own red blood cells, can be triggered by a
blood transfusion due to the presence of foreign antibodies
- Mechanical: fragmentation of red blood cells by mechanical heart valve, or intravascular thrombosis in DIC (disseminate intravascular coagulation)
33
What are the issues associated with Rhesus antigens and pregnancy?
HAEMOLYTIC DISEASE OF THE FOETUS & NEWBORN [HDFN]:
• Mother has Rhesus NEGATIVE blood (RhD negative) and baby has Rhesus
POSITIVE blood (RhD positive). When mothers blood is exposed to babies blood in
pregnancy for example, mothers immune system recognises foreign Rhesus positive
blood and begins making antibodies against babies blood - FIRST baby is
unaffected since it takes time for antibodies to be produced, the mother is said to
be SENSITISED to Rhesus positive blood
• However, if mothers second baby also has RhD positive blood, then when mothers
blood is exposed to babies, antibodies are produced IMMEDIATELY and begin
DESTROYING BABIES RED BLOOD CELLS - resulting in HAEMOLYSIS OF
FOETUS/NEWBORN = ANAEMIA AND JAUNDICE. Whilst mother is carrying the
baby, her antibodies can cross to baby via the placenta and begin attacking -
THIS IS KNOWN AS RHESUS DISEASE
34
What are white blood cells?
Normal white blood cells are mature cells that circulate in the blood, they are
produced from immature precursor cells in the bone marrow which are derived
from stem cells. Rate of production is under hormonal control of G-CSF
35
What are neutrophils? What is their lifespan and what is their role?
- Most numerous white cell - lifespan is 10 hours
- Phagocytose & kill bacteria
- Release chemotaxins (signal more white blood cells to come to site) and cytokines -
important in inflammatory response
- Lack of number or function results in recurrent bacterial infections
36
What are lymphocytes?
- B lymphocytes: named after Bone marrow, made in bone marrow - stored in
secondary lymphoid organs, differentiate into plasma cells and produced
immunoglobulins when stimulated by exposure to foreign antigen
- T lymphocytes: made in bone marrow - MATURE in thymus, some are helper
cells (CD4, help B cells in antibody generation, responsible for cellular or cell
mediated immunity), some are cytotoxic cells (CD8)
37
What is acute leukaemia?
Proliferation of primitive precursor cells usually found in bone
marrow, proliferation WITHOUT differentiation, replaces NORMAL BONE
MARROW CELLS - resulting in anaemia (palor and lethargy), neutropenia:
infections (since white cells are not being differentiated) & thrombocytopenia:
excessive bleeding. THE PRESENCE OF PRIMITIVE WHITE PRECURSOR CELLS
IN THE BLOOD IS A SIGN OF acute leukaemia
38
What is the difference between acute myeloblastic leukaemia and acute lymphocytic leukaemia?
AML= Malignant proliferation of the precursor
myeloblasts (unipotent stem cells) in the bone marrow, disease primarily affects adults - 50% survive 5 years
ALL= Malignant proliferation of the lymphoblast
precursor cells in the bone marrow, disease primarily affects children - 80% cured
39
What is high grade lymphoma?
lymphocytes in lymph nodes becoming malignant, very
similar to leukaemia): Classified as Hodgkins disease and Non-Hodgkins lymphoma (NHL), disease usually of the lymph nodes that spreads to the liver,spleen, bone marrow and blood
40
Synthesis of which coagulation proteins is vitamin K essential for?
Factors 10, 9, 7, and 2 (remember 1972)
41
Define Haemostasis and explain its importance?
the arrest of bleeding, involving the physiological processes of blood coagulation and the contraction of damaged blood vessels
Blood is usually fluid inside blood vessels this is because:
• The proteins of the coagulation cascade and the platelets circulate in an inactive
state
• Proteins and platelets are only activated by tissue factor, which is present on every
single cell APART from endothelial cells thus when endothelium is punctured etc.
blood comes into contact with tissue factor and thus starts clotting
- Correct balance is vital to life; if blood clots inside vessel = thrombosis, if blood
fails to clot outside vessels = bleeding disorder
42
What is the coagulation cascade?
series of proteolytic enzymes that circulate in an inactive state being activated (usually by exposure to tissue factor) in a cascade or waterfall sequence - in order to generate the key enzyme THROMBIN which cleaves fibrinogen creating fibrin polymerisation i.e a blood clot
43
What blood cells are responsible for primary haemostasis?
Platelets
44
What is haemophilia A? what is its incidence, causes, symptoms, and treatment?
1 in 10,000 males (rare)
```
not enough clotting factors in blood = slow clotting time or
long PTT (prothrombin time)
Deficiency in CLOTTING FACTOR VIII (8)
```
Bleeding into muscles and joints
Treat with factor VIII
45
What is haemophilia B? What is its incidence, causes, symptoms, and treatment?
1 in 50,000 males (even more rare)
Less common since gene is smaller
Deficiency in clotting factor IX (9)
Bleeding into muscles and joints
Treat with Factor IX
46
What is Von Willebrand Disease? What is its incidence, cause, and symptoms?
Up to 1%
- 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
- Muco-cutaneous bleeding: bleeding in skin & mucous membranes e.g. easy
bruising, prolonged bleeding from cuts, nose bleeds (epistaxis), spontaneous gum
bleeding/GI loss etc.
47
What are acquired bleeding disorders?
Recent onset, not lifelong and no family history
- Most common cause: anti-platelet or anti-coagulation medication
- May be generalised or localised bleeding
48
How can vitamin K deficiency cause bleeding? What is the treatment
VITAMIN K IS NEEDED FOR THE CORRECT SYNTHESIS OF COAGULATION
FACTORS II, VII, XI & X (2, 7, 9 & 10) - 1972
- Vitamin K is a fat soluble vitamin
- Deficiency is caused by malabsorption - especially in obstructive jaundice
- With deficiency coagulation factors are still produced but they do not work
- Newborns are vitamin K deficient, given it at birth
Treat with IV vitamin K
49
How can drugs cause bleeding?
- Aspirin affects platelet function
- Heparin and warfarin (most widely used oral anticoagulant - works by inhibiting
vitamin K) affect coagulation cascade
- Steroids make tissues thin and cause bruising and bleeding
50
What is Disseminated intravascular coagulation (DIC)? How does it cause bleeding, the symptoms and the treatment?
Causes bleeding: Breakdown of haemostatic balance
1) sepsis 2) obstetric (anything that goes wrong with pregnancies e.g. dead
foetus + pre-eclampsia 3) malignancy
Activation of the coagulation cascade inside blood vessels, thrombin is produced,
causing fibrinogen > fibrin, form microvascular thrombosis’(platelet plugs)
everywhere e.g. in organs etc.
- Results in the deficiency of clotting factors & platelets since they've been used up
in the formation of the micro-vascular thrombosis’ - doctors think its a blood
condition causing deficiency but its because of the micro-vascular thrombosis
Symptoms: Simultaneous bleeding & microvascular thrombosis
Treatment: treat underlying cause and stop generations of intravascular
thrombin then transfuse new platelets etc.
51
What is a blood vessel's first response to damage?
its first response is to constrict (due to neural
control + release of endothelin-1 (released by endothelia cells)
This temporarily slows the flow of blood in the affected area. Furthermore, this construction presses opposed endothelial surfaces of the vessel together and
this contact induces a stickiness capable of keeping them ‘glued’ together.
- Permanent closure of the vessel by constriction & contact stickiness only occur
in the very smaller vessels of the microcirculation
52
What is the process of platelet plug formation?
- When a vessel is injured/ruptured, this disrupts the endothelium
- Resulting in the exposure of collagen fibres
- Platelets adhere to the collagen fibres via an intermediary called Von Willebrand
factor (VWF) - the platelet adheres to the factor, which itself is adhered to the
collagen already via a receptor on the platelet membrane called the glycoprotein 1b
Receptor
- This binding of the platelets to the collagen fibre wall, triggers the platelet to release
the contents of their secretory vesicles via exocytosis.
- One of these contents are platelet dense granules, which are also release upon cell
activation, from these granules ADP is released which acts on the P2Y1 and P2Y12
causing platelet amplification
- ATP binds to P2X1 which also causes platelet amplification
- Thrombin binds to PAR1 and PAR4 receptors - inducing platelet activation and
further thrombin release - positive feedback
- These actions result in the platelet changing shape from a smooth discoid
shape to a more spiculated (spiky) with pseudopodia, this increases the
surface area of the platelet - the process of these shape changes occurring is known as PLATELET ACTIVATION
- Platelet activation causes an increase in the expression of glycoprotein IIb/IIIa
(GPIIb/IIIa) receptors on the platelets which binds to FIBRINOGEN (from alpha
granules) enabling new platelets to adhere to the old ones, a positive feedback
mechanism called PLATELET AGGREGATION
- Platelet adhesion rapidly induces them to synthesise THROMBOXANE A2 (causes
vasoconstriction & platelet activation) which is then released into the extracellular
fluid and acts locally to further stimulate platelet aggregation and the release of
there secretory vesicle contents
- All of these actions enable a platelet plug to be rapidly formed, platelet plugs can
completely seal small breaks in vessels. Its effectiveness is further enhanced by
another property of platelets - contraction. Platelets contain a very high
concentration of actin & myosin. This results in compression and strengthening
of the platelet plug
- Whilst platelet activation, aggregation and plug formation is occurring, the vascular
smooth muscle in the damaged vessel is simultaneously being stimulated to
contract - decreasing blood flow to the area & pressure within the damaged vessel.
- This vasoconstriction occurs as a result of platelet activation - due to the
thromboxane A2 released and by the chemicals contained in the platelets secretory
vesicles
53
Why does the platelet plug not expand away from the damaged endothelium in both directions?
• The normal undamaged endothelium either side of the damage begin to synthesise
and release prostacyclin (also known as prostaglandin I2 (vasodilator) )which is a
profound inhibitor of platelet aggregation
• The normal endothelium also release nitric oxide, which is not only a vasodilator but
also an inhibitor of platelet adhesion, activation & aggregation
54
What is blood coagulation?
Blood coagulation or clotting is the transformation of blood into a solid gel called a
clot or thrombus which consists mainly of a protein polymer called fibrin.
- Clotting occurs locally around the platelet plug and is the dominant haemostatic
defence - its function is to support & reinforce the platelet plug and to solidify
blood that remains in the wound channel
55
What are the pathways of the coagulation cascade?
Intrinsic= everything necessary
for it is within the blood
Extrinsic= since a
cellular element outside the blood is needed
56
What is the process of the intrinsic pathway?
The first plasma protein in the intrinsic pathway is called factor XII (12). It is activatedinto factor XIIa when it comes into contact with exposed collagen fibres underlying the damaged endothelium - this is known as contact activation
Factor XIIa then catalyses the activation of factor XI to factor XIa
Factor XIa then catalyses the activation of factor IX to factor IXa
Factor IXa then catalyses the activation of factor X to factor Xa, NOTE; factor VIIIa also is involved in the conversion of factor X into factor Xa, factor VIIIa acts as a cofactor is this conversion with factor IXa to activate factor X (Factor VIII is essential for clotting, in haemophilia A there is a lack of this clotting
factor)
Factor Xa is the enzyme that converts prothrombin to thrombin - thrombin is the enzyme which then goes onto convert the soluble fibrinogen to the insoluble fibrin which can be used to secure the blood clot and build it up
57
What is the process of the extrinsic pathway?
Begins with a protein called tissue factor, which is not a plasma protein. It is located on the outer plasma membrane of various tissue cells, including fibroblasts and other cells in the walls of blood vessels OUTSIDE the endothelium
• Blood is exposed to subendothelial cells when vessel damage disrupts the endothelial lining
Tissue factor then binds a protein called factor VII which becomes activated to factor VIIa - the complex formed, made up of tissue factor and factor VIIa then go on to catalyse the activation of factor X into factor Xa.
Additionally, this complex also catalyses the activation of factor IX, which can then help activate even more factor X by way of the intrinsic pathway
- Thus it can be seen that the clotting cascade can be initiated by either the
activation of factor XII or the generation of the tissue factor - factor VIIa complex
- NOTE: thrombin also contributes to the activation of; 1) factors XI & VIII in the
intrinsic pathway 2) factor V, with factor Va then serving as a cofactor for factor
Xa. Also thrombin also goes on to activate platelets too (mentioned above) - these are its positive feedback mechanisms
58
Thrombin is initially generated by which pathway?
Extrinsic
The amount of thrombin produced in this pathway is too little to produce adequate sustained
coagulation. BUT it is large enough to trigger thrombin’s positive feedback mechanisms on the intrinsic pathway - activation of factors V,VIII & XI and the activation of platelets. This is all that is needed to trigger the intrinsic pathway independently of tissue factor XII. This pathway then generates the large amounts of thrombin required for adequate coagulation.
59
What is the role of the liver in clotting?
the liver plays several important indirect roles in clotting:
- The liver is the site of production for many of the plasma clotting factors
- The liver produces bile salts which are essential for the absorption of the lipid- soluble substance vitamin K. The liver requires vitamin K to produce prothrombin and several other clotting factors
FIBRINOLYTIC SYSTEM: a fibrin clot is not designed to last forever, it is a temporary fix until permanent repair of the vessel occurs:
- Plasminogen is converted by plasminogen activators into plasmin which then goes
on to break fibrin down and thus the entire blood clot
60
What is a normal number of platelets?
140-400 x 109/l (to the power 9 not 109)
61
What are the platelet counts for thrombocytopenia and what are their effects?
< 80 x 109 (10 to power 9)/l= increased bleeding
| <20 x 109 (10 to power 9)/l= spontaneous bleeding
62
What is the effect of high platelet count?
thrombocytosis, can lead to arterial & venous thrombosis, leading to an increased risk of heart attack + stroke
63
Where are platelets made and what are their precursor cells?
Made in bone marrow from cells called megakaryocytes
64
What are the stages of systole and how long does it last?
1. Isovolumetric (iso- equal/unchanging) contraction of the ventricles (increase in pressure but volume remain the same since valves remain closed) - isovolumetric
contraction + relaxation is the only time when all valves of the heart are closed
2. Once the pressure in the ventricles exceeds that in the aorta & pulmonary trunk the aortic & pulmonary valves open and maximal ejection from ventricles into
the arteries occurs - ventricles DO NOT COMPLETELY EMPTY during contraction
It lasts 0.3 seconds
65
What are the stages of diastole and how long does it last?
1. Reduced ejection
2. Ventricles begin to relax and aortic and pulmonary valves close - at this time the atrioventricular valves are closed thus no blood is entering or leaving the
ventricles - ventricular volume is not changing known as isovolumetric ventricular relaxation (decrease in pressure but volume remains the same)
3. Rapid left ventricle filling and ventricle suction - since blood in the atria is slightly pressurised due to the venous return from the superior + inferior vena cava &
pulmonary vein, pressure is enough to open mitral (or bicuspid left) and tricuspid valves (right), also since there is a lower pressure in the ventricles
blood just rushes in down the pressure gradient (effectively sucked in) - this is responsible for 80% of ventricular filling before atrial contraction
4. Slow ventricular filling - since blood keeps flowing into atria from the veins, pressure between the atrium and ventricle are equalising thus slowing filling this
pressure equalisation is known as DIASTASIS - where there is little to no net movement of blood, at this point the AV node is delaying the stimuli from the SAN
to allow full ventricular filling
5. Atrial booster- pressure suddenly increases due to atrial contraction, enables ventricles to be actively filled - squeezing remaining blood from atria into ventricles
It lasts 0.5 seconds
66
For an individual with a typical heart rate of 72 bpm, how long would each cardiac cycle last?
For a normal heart with a typical heart rate of 72 beats/min, each cardiac cycle lasts 0.8 seconds, with 0.3 sec in systole & 0.5 sec in diastole
67
Describe parasympathetic cardiac stimulation and its effects?
* Fibers are transmitted via the vagus nerve (CN10)
* Controlled by acetylcholine which bind to muscarinic receptors
* Decreases heart rate (negatively chronotropic)
* Decreases force of contraction (negatively inotropic)
* Decreases cardiac output (by up to 50%)
* Decreased parasympathetic stimulation will result in an increased heart rate
68
Describe sympathetic cardiac stimulation and its effects?
• Sympathetic postganglionic fibers innervate the entire heart
• Controlled by adrenaline & noradrenaline
• Increases heart rate (positively chronotropic)
• Increases force of contraction (positively inotropic)
• Increases cardiac output (by up to 200%)
• Decreased sympathetic stimulation will result in decreased heart rate & force of
contraction and a decrease in cardiac output by up to 30%
69
Define Stroke Volume?
The volume of blood ejected from each ventricle during systole
70
Define Cardiac Output?
The volume of blood each ventricle pumps as a function of time (liters per minute)
71
Define Total Peripheral Resistance?
The total resistance to flow in systemic blood vessels
| from beginning of aorta to vena cava - arterioles provide the most resistance
72
Define Preload?
the volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction - how much blood is in the ventricles before it pumps (end-diastolic volume). When veins dilate it results in a decrease in preload (since by dilating veins the venous return decreases).
73
Define Afterload?
the pressure the left ventricle must overcome to eject blood during contraction - dilate arteries = decrease in afterload
74
Define contractility?
force of contraction and the change in fibre length - how hard the heart pumps. When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere length
75
Define elasticity?
myocardial ability to recover normal shape after systolic stress
76
Define Diastolic Dispensability?
The pressure required to fill the ventricle to the same diastolic volume
77
Define Compliance?
how easily the heart chamber expands when filled with blood volume
78
Define and Explain Starling's Law?
Force of contrition is proportional to the end diastolic length of cardiac muscle fibre - the more ventricle fills the harder it contracts
• At rest the cardiac muscle is not at optimal length. Below optimal length means the force of contraction is decreased - inefficient
• ↑ venous return = ↑ end diastolic volume = ↑ preload = ↑ sarcomere stretch =
↑ force of contraction thus = ↑ stroke volume and force of contractions
• Standing decreases venous return due to gravity thus, cardiac output decreases, which causes a drop in blood pressure, stimulating baroreceptors to increase
blood pressure
79
Define Intrinsic Autoregulation?
when the arterioles either vasoconstrict or vasodilate in response to changes in resistance seemingly automatically - with the aim of maintaining constant blood flow
80
Define Myogenic Autoregulation?
When blood flow is increased and stretches vascular smooth muscle the muscle automatically constricts until the diameter is normalised or slightly reduced. Furthermore when the smooth muscle isn't getting stretched as much due to low blood pressure, the muscle relaxes and dilates in response
81
Define Hyperaemia?
Increase in blood flow
82
Define Active Hyperaemia?
increase in blood flow when metabolic activity is increased
83
Define Reactive Hyperaemia?
When an organ or tissue has had its blood supply completely occluded a profound transient increase in its blood flow occurs IF blood flow is reestablish - extreme form of autoregulation
84
What is the structure of myosin?
forms majority of thick filament
• Composed of two large polypeptide heavy chains & 4 smaller light chains.
• These polypeptides combines to form a molecule that consists of two globular heads (containing heavy and light chains) and a long tail formed by the two intertwined heavy chains.
• The tail of each myosin molecule lies along the axis of the thick filament and the two globular heads extend out to the sides forming cross-bridges, which make contact with the thin filament and exert force during muscle contraction.
• Each globular head contains two binding sites, one for attaching to the thin filament and one for ATP. Attached to the myosin head is an inorganic phosphate molecule (Pi) and ADP. The ATP binding site also serves as an enzyme - an ATPase that hydrolyses the bound ATP, harnessing its energy for contraction
85
What is the structure of actin?
- Forms majority of thin filament
- The thin filament is composed mainly of actin, but also of troponin & tropomyosin (play important roles in regulating contraction)
- Actin is a globular protein composed of a single polypeptide (a monomer) that polymerises with other actin monomers to form a polymer made up of two INTERTWINED, helical chains. These chains make up the core of the thin filament. Each actin molecule contains a binding site for myosin
86
What is the structure of tropomyosin?
elongated molecule that occupies the grooves between the two actin strands, overlies MYOSIN binding sites on actin
87
What is the structure of troponin?
Protein that changes shape when Ca2+ binds to it, when it does it changes shape in doing so pushes the tropomyosin EXPOSING myosin binding sites on actin enabling contraction to occur
88
What is the A-band?
the region of the sarcomere occupied by thick and a few overlapping thin filaments - overall there are twice as many thin as thick filaments in the region of filament overlap
89
What is the I-Band?
occupied only by thin filaments that extend to the centre of the sarcomere from the Z-lines, two successive Z lines defines the limits of one sarcomere. It also contains tropomyosin and troponin (located on the actin filament)
90
What are Z-lines?
any of the dark thin bands across a striated muscle fiber that mark the junction of actin filaments in adjacent sarcomeres.
91
What is the H-Zone?
contains only thick filaments (myosin)
92
What is the M-Line?
in the centre of the H-zone, comprised entirely of thick filament myosin. Corresponds to proteins that link together the central region of adjacent thick filaments
93
What is Titin?
elastic protein filaments, extend from the Z-line to the M-line, linked to both the M-line proteins and the thick filaments. Both the M-line linkage between the thick filaments and the titin filaments act to maintain the alignment of the thick filaments in the middle of each sarcomere
94
What is a sarcomere and what does it change?
Functional unit of a myocyte and one sarcomere contains 2 half I-bands, 1 A-band, 1 H-zone, 1 M-line & 2 Z-lines
95
What is the sarcoplasmic reticulum?
membrane network that surrounds the contractile proteins. Releases Ca2+ when Ca2+ binds to it ryanodine receptor
96
How is a cardiac resting potential maintained?
```
The resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+ (since K+ channels are open meaning K+ is leaving the cell - RESTING
POTENTIAL IS MAINTAINED BY NA+ & K+ ATPase PUMPS, pumping 3Na+ ions OUT for every 2K+ ions pumped IN) than to Na+ - meaning the resting membrane potential is much closer to the K+ equilibrium potential (-90mV) than to the Na+
equilibrium potential (+60mV)
```
97
What is the first step when an action potential arrives?
When an action potential arrives, Na+ voltage gated ion channels are OPENED, and Na+ entry depolarises the cell, triggering more Na+ channels to open -
positive feedback effect
98
What is step two when an action potential arrives?
When potential in cell is positive (+52mV) then voltage gated Na+ channels CLOSE, at the same time voltage gated K+ channels OPEN - partially REPOLARISING the cell
99
What is step three when an action potential arrives?
At the same time that the Na+ voltage gated ion channels are triggered to OPEN, Ca2+ voltage gated ion channels are ALSO triggered - however these channels open much more slowly than the Na+ channels
100
what is step four when an action potential arrives?
During the partial repolarisation causes by the outflow of K+, the Ca2+ voltage gated channels finally OPEN at T-TUBULES which are part of the sarcolemma
(myocyte membrane), resulting in the INFLOW of Ca2+ into the cell - since these channels remain open for a long duration of time they are often referred to as L-
type Ca2+ channels (L=long lasting), these channels are modified versions of the dihydropyridine (DHP) receptors that function as voltage sensors in excitation-
contraction coupling of skeletal muscles
101
What is step five when an action potential arrives?
The flow of Ca2+ ions into the cell just balances the flow of K+ ions out of the cell and keeps the membrane DEPOLARISED at the PLATEAU VALUE of roughly 0mV.
(NOTE: the membrane also remains depolarised at the plateau value due to the fact that the K+ channels open at the start close as well - maintaining depolarisation)
102
What is step six when an action potential arrives?
Repolarisation eventually occurs due to the eventual closure of the L-type Ca2+ channels, and the reopening of the K+ channels (the ones open at the start) - these are similar to the ones in neurons & skeletal muscle; they open in response to
depolarisation (after a delay) and close once the K+ current has depolarised the membrane back to negative values
103
In Phase 0, what is the change in potential and what is responsible?
Rapid depolorisation, Na+ inflow
104
In Phase 1, what is the change in potential and what is responsible?
Partial repolarisation, K+ outflow and Na+ inflow stops
105
In Phase 2, what is the change in potential and what is responsible?
Plateau, Ca2+ slow inflow
106
In Phase 3, what is the change in potential and what is responsible?
Repolarisation, K+ outflow and inflow of Ca2+ stops
107
In Phase 4, what is the change in potential and what is responsible?
Pacemaker Potential, Na+ inflow and slowing of K+ outflow
108
What is Step 1 of excitation contraction coupling?
When the action potential is generated, there is an influx of Ca2+ via the T-tubules via L-type Ca2+ voltage gated channels
109
What is Step 2 of excitation contraction coupling?
Not only does this Ca2+ influx aid depolarisation but it also causes a small increase in cytosolic Ca2+ concentration
110
What is Step 3 of excitation contraction coupling?
The small amount of Ca2+ ions that influx (too small to be able to initiate muscle contraction)
bind to ryanodine receptors on the sarcoplasmic reticulum - this binding causes the sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell - this initiates cardiac muscle contraction - the start of the CROSS-BRIDGE CYCLE
111
What is Step 4 of excitation contraction coupling?
Ca2+ binds to the Ca2+ binding site on the troponin protein on actin filament- This causes the troponin to change shape and thus displace the tropomyosin protein on the actin filament, exposing the myosin binding sites
112
What is Step 5 of excitation contraction coupling?
The myosin head on the myosin filament then binds to the actin filament via the myosin binding site, the inorganic phosphate is dropped in order for the myosin head to bind to the actin, the ADP still remain attached to the head - this is known as
cross-bridge formation
113
What is Step 6 of excitation contraction coupling?
The myosin head then drops the ADP to contract and pull the actin filament OVER the myosin filament - thereby decreasing the Z lines resulting in muscle
contraction - this is know as the power stroke
114
What is Step 7 of excitation contraction coupling?
ATP then binds to the myosin head, detaching the head from the actin filament, and moving the head to its start position
115
What is Step 8 of excitation contraction coupling?
ATP then binds to the myosin head, detaching the head from the actin filament,and moving the head to its start position
116
What is Step 9 of excitation contraction coupling?
Contraction stops when cytosolic Ca2+ concentration is restored to its original extremely low resting value by primary active Ca2+ - ATPase pumps in the
sarcoplasmic reticulum & sarcolemma AND Na+/Ca2+ counter-transporters in the sarcolemma.
- The amount of Ca2+ returned to the extracellular fluid & sarcoplasmic reticulum
EXACTLY MATCHES the amounts that entered the cytosol during excitation
117
What is the difference between skeletal muscle contraction and cardiac muscle contraction?
Contraction lasts LONGER than in skeletal muscle - up to 15 times longer in duration; this is due to the slow calcium channels
118
What is the refractory period?
The refractory period is the period of time after an action potential where second impulse CANNOT cause a second contraction of cardiac muscle:
• This is to prevent excessive FREQUENT contraction
• To allow adequate filling time
119
What is the equation for Mean Arterial Pressure (MAP)?
MAP= Diastolic Pressure (DP) + 1/3 PP (SP-DP)
120
What is the equation for Cardiac Output (CO)?
CO= Heart Rate (HR) x Stroke Volume (SV) (usually 5L/min)
121
What is the equation for Blood Pressure (BP)?
BP= CO x Total Peripheral Resistance (TPR)
122
What is the equation for Pulse Pressure (PP)?
PP= Systolic- Diastolic Pressure
123
What is the equation for Stroke Volume (SV)?
SV= End Diastolic Volume (EDV)- End Systolic Volume (ESV)
124
What is Poiseuille's Law?
Flow= radius to the power 4
125
What is Ohm's Law?
Flow= pressure gradient/resistance
126
What is the general structure of an artery?
- Contain mainly elastic, collagen & smooth muscle
- The intima is composed of an inner surface lining of endothelial cells & a very small amount of collagen
- The adventitia shows mainly collagenous connective tissue
- There are two elastic laminae, one at the interface of the intima and media and the other on the outer edge of the media
127
What is the general structure of an arteriole?
- May have an obvious media & adventitia
- Smaller arterioles show only a few medial cells with a poorly defined elastic lamina
- A thin adventitia & normal intima also exist
128
What is the general structure of endothelium?
- Single layer or spindle/pavement cells with tight adhesions between adjacent cells
- Little cytoplasm and intra-cellular organelles - but gap/adheren junctions are
prominent
- They may be fenestrated (have pores in them for rapid diffusion) in the liver, kidney
glomeruli & endocrine tissues
- In some areas they may be very thin (lung) to enable rapid fluid & gas transfer
129
What is the general structure of capillaries?
- Tubes of endothelial cells (one cell thick wall - for rapid diffusion) bound to a basement membrane with co-existing pericytes
- Pericytes have muscle fibres and may regulate blood flow
130
What is the general structure of veins and venules?
- Show variable thickness
- Veins generally have collagen and little muscle & elastic with the wall & a single
internal elastic lamina
- Veins contain valves for one way flow to the heart - prevent back flow
- Some veins are surrounded by skeletal muscle which contracts to increase vein
pressure and ensure blood flows back to the heart
131
Describe pulmonary circulation?
Blood leaves the right ventricle via a single large artery, the pulmonary trunk, which divides into the two pulmonary arteries, one supplying the right and one supply the left lung. In the lungs the arteries continue to branch and connect to arterioles, leading to capillaries that unite into venules and then veins. The blood leaves the lungs via four pulmonary veins, which empty into the left atrium
132
Describe Systemic circulation?
Blood leaves the left ventricle via single large artery, the aorta. The arteries of the systemic circulation branch off the aorta, dividing into progressively smaller vessels. The smallest arteries branch into arterioles, which branch into roughly 10 billion very small vessels, the capillaries, which unite to form larger-diameter vessels known as venules. The arterioles, capillaries & venules are collectively referred to as the MICROCIRCULATION. The venules then unite to form larger vessels, veins. The veins from the various peripheral organs and tissues unite to produce two large veins, the inferior and superior vena cava which drain into the right atrium
133
What are gap junctions?
Gap junctions interconnect myocardial cells and allow action potentials to spread from one cell to another. The action potential spreads over cell membranes, the
positive charge from the Na+ affects adjacent cells, resulting in depolarisation, the newly depolarised cells can cause further depolarisation, and the gap junctions
enable ions to travel directly to other cells. The initial excitation of one cardiac cell allows eventually results in the excitation of all cardiac cells
134
What is the role of Sinoatrial Node and what is its usual resting membrane potential?
Normally determines the rate the heart beats at - the number of times the heart contracts per minute
• Resting membrane potential of -55 to -60 mV - this is closer to the threshold of depolarisation thus it depolarises first, it is closer to the depolarisation threshold due to its slow Na+ inflow not found anywhere else in the body
135
What is the pacemaker potential and how is it established?
- The SA node does not have a steady resting potential, instead it undergoes
SLOW DEPOLARISATION - this is known as the pacemaker potential; it brings the
membrane potential to a threshold, at which point an action potential occurs
- Three ion channel mechanisms contribute to the pacemaker potential:
- The first is the progressive reduction in K+ permeability. The K+ channels that opened during the repolarisation phase of the previous action potential gradually close due to the membranes return to negative potentials
- Second, pacemaker cells have a unique set of channels that, unlike most voltage gated channels, open when the membrane potential is at NEGATIVE values - these non- specific cation (positive ions) conductmainly an inward Na+ current, since this is not
normal these channels are referred to as “funny” and are thus called F-type channels
- The third channel is a Ca2+ channel that opens VERY BRIEFLY but contributes to an inward current of Ca2+ which acts as an important final depolarising boost to the pacemaker potential. Since the channel is only opened briefly it can be called transient so these channels are known as T-type Ca2+ channels
136
Why does the SAN initiate action potential and sets the pace for the heart rather than the AVN?
the pacemaker currents in the SA node bring them to threshold more rapidly than the AV node, which explains why the SA node normally initiates action potentials & determines the pace of the heart
137
What is the process of action potential propagation in the myocardium?
Once the pacemaker mechanisms have brought a nodal cell to threshold, an action potential occurs. The depolarising phase is not caused by Na+ but instead by Ca2+ influx through L-type Ca2+ channels. These Ca2+ currents depolarise the membrane more slowly than voltage-gated Na+ channels, and one result of this is that action potential propagate more slowly along nodal cells than in other cardiac cells. This explains the slow transmission of cardiac excitation through the AV node
- Thus the pacemaker potential provides the SA node with automaticity - the ability for
spontaneous, rhythmic self-excitation
The action potential initiated at the SA node spreads through the myocardium,passing from cell to cell by way of gap junctions Depolarisation first spreads through the muscle cells of the atria - with conduction being rapid enough that the right & left atria contract simultaneously
The spread of the action potential to the ventricles involves a different conducting system called the atrioventricular node (AVN) - the action potential is conducted relatively rapidly from the SA node to the AV node through the internodal pathways
After the AV node has been excited, the action potential progresses down the interventricular septum - this pathway of conducting fibres is called the bundle of His
The AV node and the bundle of His constitute the ONLY electrical connection between the atria and ventricles - except from THIS PATHWAY the atria are completely isolated from the ventricles by a layer of nonconducting connective tissue
• Within the interventricular septum, the bundle of His divides into right & left bundle branches, conducting fibers that separate at the bottom (apex) of the heart and enter the walls of both ventricles
These fibers in turn make contact with Purkinje fibers, large-diameter conducting cells that rapidly distribute the impulse throughout much of the ventricles
Finally the Purkinje fibres make contact with ventricular myocardial cells - which spread the action potential through the rest of the ventricles
• The conduction from the AV node to the ventricles is RAPID to enable coordinate ventricular contraction
138
What are the features of the Atrioventricular node?
Located at the base of the right atrium - transmits cardiac impulse from atria to
ventricles
Consists of modified cardiac cells that have lost contractile capability but conduct
action potentials with LOW RESISTANCE
Elongated structure with an important feature; the propagation of action potentials
through the AV node is RELATIVELY SLOW (requiring approximately 0.1 secs) - this is
IMPORTANT since it enables the atria to EMPTY BLOOD into the ventricles, enables
atrial contraction to be completed before ventricular excitation occurs
139
What are the three heart sounds?
* One is a soft, low pitched lub, associated with the closure of the atrioventricular valves
* The second is, a louder dub is associated with the closure of the aortic & pulmonary valves
* The third is the sounds of blood rushing into the left ventricle
140
What is the Electrocardiogram?
NOT a DIRECT RECORD of the changes in membrane potential across individual cardiac muscle cells. But instead it is a measure of the currents generated in the EXTRACELLULAR FLUID by the changes occurring
simultaneously in many cardiac cells
141
What is a P Wave?
Atrial depolarisation - seen in every lead apart from aVR
142
What is the PR Interval?
Time taken for atria to depolarise and electrical activation to get through AV node
143
What is the QRS complex?
Ventricular depolarisation, still called QRS even if Q and/or S are missing depending on what lead you are looking at
144
What is the ST Segment?
Interval between depolarisation & repolarisation
145
What is the T wave?
Ventricular repolarisation
146
What is Tachycardia?
Increased heart rate
147
What is Bradycardia?
Decreased heart rate
148
What is Dextrocardia?
Heart on right side of chest instead of left
149
What happens to the ST segment in an Acute Anterolateral Myocardial Infarction?
ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads
150
What happens to the ST segment in an Acute Inferior Myocardial infarction?
ST segments are raised in inferior (I, III, aVF) leads
151
Why is atrial repolarisation usually not evident on an ECG?
since it occurs at the same time as the QRS complex so is hidden
152
How does the impulse generate the ECG?
Electrical impulses in the heart move in 3 dimensions
• ECG only measure voltage in 1 dimension
• If an impulse is towards the electrode it looks big
• If an impulse is away from the electrode it looks small or even negative
• The impulse from the atria is smaller since the atria are smaller than the ventricles
thus less myocytes
153
What are the 12 leads on a 12 lead ECG?
- Standard limb leads (I, II & III) form a triangle between electrodes on the wrists and left leg (right leg is a ground electrode)- the negative poles are REFERENCE
electrodes and the positive poles are RECORDING electrodes
- Augmented leads (aVR, aVL & aVF) bisect the angles of the triangle by combining two electrodes as reference e.g. for lead aVL, the right wrist & foot are combined as the negative pole, thus creating a reference point along the line between them, pointing
toward the recording electrode on the left wrist
- The precordial leads (V1 - V6) - recording electrodes placed on the chest
154
When reading an ECG, what are the times represented by the small squares and the big squares?
When reading an ECG, the graph shows changes in voltage over time, each small square across represents 40ms & each big square across represents 0.2s
155
Are P waves and T waves positive?
In a normal ECG the p waves are POSITIVE in EVERY LEAD (apart from the aVR)
T waves are POSITIVE in EVERY LEAD (apart from the aVR & sometimes the V1 and V2 depending on trace)
156
Which vessels are the principle site of resistance to vascular flow?
Arterioles
157
What is a basic explanation of the response of arterioles to changes in blood pressure?
Arterioles respond to blood pressure - When the muscle of the arteriole contracts the radius
↓ causing the resistance to flow to ↑ thus causing blood flow to ↓ - and vice versa
158
Describe the response of vasoconstrictors (local factors) and give an example?
* smooth vascular muscle constricts
* Increase in internal blood pressure, resulting in myogenic contraction (when smooth muscle is stretched there will be automatic contraction until diameter is normalised or slightly reduced) due to the blood pressure increase - this is Autoregulation
Example:
Endothelin-1 (ET-1) - released by endothelium cells results in vasoconstriction
[POTENT]
159
Describe the response of vasodilators (local factors) and give examples?
smooth vascular muscle relaxes
* Hypoxia: when O2 supply decreases, there will be an accumulation of vasodilator metabolites which will dilate vessels to increase local blood flow
* Increased CO2
* Decreased pH
* Bradykinin
* Nitric oxide: released by endothelial cells - triggers vasodilation [POTENT]
* Increased K+
* H+
* Tissue breakdown products e.g. lactic acid
* Prostacyclin/ Prostaglandin I2 (PGI2): released by endotheliaal cells - triggers vasodilation [POTENT]
160
Give examples of hormonal vasoconstrictors?
angiotensin II, vasopressin & adrenaline (adrenaline can be both a vasodilator & vasoconstrictor depending on which receptors are present)
161
Give examples of hormonal vasodilators?
Atrial Natriuretic Peptide, adrenaline(adrenaline can be
| both a vasodilator & vasoconstrictor depending on which receptors are present)
162
What is the location and type and effect of stimulus of peripheral chemoreceptors?
In the aortic arch & carotid sinus (base of internal carotid artery - at the division
between the internal and external carotid)
stimulated by a fall in PaO2 & a rise in
PaCO2 & a fall in pH causing blood pressure to increase
163
What is the location, and type and effect of stimulus of arterial baroreceptors?
One found in the aortic arch
Two found where the left and right common carotid divide into two smaller arteries
(internal & external carotid) - this portion of the artery is known as the CAROTID
SINUS (found at the base of the internal carotid)
these are stretch receptors that respond to pressure
aortic arch > vagus > medulla: ↓ sympathetic & ↑
parasympathetic = ↓ in blood pressure
carotid sinus > sinus nerve >
glossopharyngeal > medulla: ↓ sympathetic & ↑ parasympathetic = ↓ in blood
Pressure
- Baroreceptors cause some inhibition of the Renin-angiotensin & aldosterone system,
and are involved in short term blood pressure control
- Cardiopulmonary baroreceptors (in atria, ventricles & pulmonary artery) control
long term blood pressure
164
What is intrinsic regulation of the cardiovascular system, and what are examples?
Results from normal functional characteristics
Examples:
Starling’s law of the heart, Autoregulation
165
What is extrinsic regulation of the cardiovascular system, and what are examples?
Involves neural and hormonal control
Examples:
Parasympathetic stimulation: Supplied by vagus nerve, decreases heart rate, acetylcholine secreted
Sympathetic stimulation: Supplied by cardiac nerves, increases heart rate and force of contraction, epinephrine and norepinephrine released
Higher centers
Reflexes
166
What are the three mechanisms of controlling heart rate?
a) Nervous regulation: Changes in HR by afferent impulses that modify the activity of the cardiac centers in the medulla oblongata.
b) Chemical regulation: Changes in HR due to changes in the chemical composition of blood.
c) Physical regulation: Changes in HR due to changes in body temperature.
167
What is the main goal of the control of circulation?
- The main goal of control of circulation is to maintain mean systemic arterial pressure (MAP) - the average blood pressure in the arteries during the cardiac cycle
168
What is the MAP and what is the equation for it?
- MAP is equal to the diastolic pressure (DP) plus one-third of the pulse pressure
(systolic pressure (SP) - DP)
- MAP = DP + 1/3 (SP-DP)
169
What are the effectors in the regulation of circulation?
blood vessels, heart & kidneys
170
What is the role of the pressor region of the medullary cardiovascular centre, what is its type of response and what is the mechanism?
```
Pressor region (region
responsible for raising blood pressure)
```
Sympathetic
- The pressor region increases blood pressure by ↑ vasoconstriction, ↑ cardiac
output (by ↑ heart rate and stroke volume (more forceful contraction)) and ↑
contractility
- Pressor region > sympathetic route > medulla > spinal cord > synapses at T1-L2> Heart
171
What is the role of the depressor region of the medullary cardiovascular centre, what is its type of response and what is the mechanism?
Depressor Region (region responsible for lowering blood pressure)
Parasympathetic
The depressor region decreases blood pressure by inhibiting the pressor region
- Depressor region > medulla > vagus nerve > heart
172
What is the role of the central chemoreceptors in the medulla?
respond mainly to a decrease in pH (due
| to CO2 diffusing across the blood brain barrier thereby reducing the pH of the CSF
173
What is the location, mechanism, and result of the cardiopulmonary baroreceptors?
Located in the atria, ventricles & pulmonary artery
When stimulated i.e high blood pressure leads to the inhibition of the pressor region/ vasoconstrictor centre in the medulla - leading to a fall in blood pressure
- Also inhibits the Renin-angiotensin & aldosterone system - since angiotensin II stimulates vasoconstriction which will increase blood pressure, also aldosterone stimulates more Na+ and thus H2O reabsorption thereby increasing blood volume and thus pressure
- Also inhibits vasopressin/ADH - since it too stimulates more water reabsorption
Thus when stimulated the cardiopulmonary baroreceptors bring about a decrease in blood pressure by promoting vasodilation & fluid loss
174
In embryology, what is gastrulation?
An early phase in embryonic development that occurs in the 3rd week
• During this phase the embyroblast, develops into a trilaminar (three-layered) structure called the gastrula
175
What is the ectoderm and what structures arise from it?
1. Ectoderm (outer layer):
- Gives rise to structures that are in contact with the outside of the body:
1. Central nervous system
2. Peripheral nervous system
3. Sensory epithelium of nose, ear and eye
4. Epidermis of skin, hair and nails
5. Pituitary, mammary
& sweat glands
6. Enamel of teeth
176
What are the three parts of the mesoderm?
paraxial plate mesoderm, intermediate plate mesoderm, and lateral plate mesoderm
177
What structures arise from the paraxial plate mesoderm?
```
gives rise to somites
- Somites give rise to the supporting tissue of the body:
a. Myotome (muscle tissue)
b. Sclerotome (cartilage and bone)
c. Dermatome (dermis of the
skin)
```
178
What structures arise from the intermediate plate mesoderm?
generates the urogenital system - the kidneys, gonads,
| and their respective duct systems
179
What structures arise from the lateral plate mesoderm?
found at the periphery of the
embryo.
Splits into two layers;
a. Somatic (parietal) layer mesoderm forms:
1. Future body wall
b. Splanchnic (visceral) layer mesoderm forms:
1. Circulatory system
2. Connective tissue for glands
3. Muscle, connective tissue and peritoneal components, of the wall of the gut
180
What is the endoderm and what structures does it give rise to?
It is the bottom layer
It gives rise to the:
a. Epithelial lining of the gastrointestinal tract, respiratory tract and urinary
bladder
b. Parenchyma of the thyroid gland, parathyroid glans, liver and pancreas
c. Epithelial lining of the tympanic cavity and auditory tube
181
Describe foetal circulation and postnatal circulation and discuss the differences?
In foetal circulation:
- Oxygenated blood from the placenta enters the foetus though the umbilical vein
- Most of the newly oxygenated blood bypasses the liver via the ductus venosus and combines with Deoxygenated Blood in the inferior vena cava
- Blood then join deoxygenated blood from the superior vena cava and empires into the right atrium
- Since pressure in the right atrium is larger than the presses in the left atrium, most blood will be shunted through the foramen ovale
- Some blood does travel from the right atrium to the left atrium via the pulmonary trunk but most blood moves directly to the aorta via the Ductus Arteriosus
- Deoxygenated blood returns to the placenta via the Umbilical Arteries originating from the internal iliacs near the bladder
In postnatal circulation:
- With the first breath, increased alveolar O2 pressure causes vasodilation in the
pulmonary vessels
- Obstetrical climbing induces spontaneous constriction and change of theUmbilical Veins to the Ligamentum Teres
- The Umbilical Arteries also change to the Medial Umbilical Ligaments
- Within 10-15 hours after birth, the Ductus Arteriosus constricts to become the Ligamentum Arteriosus
- Increased left atrial pressure and decreased right atrial pressure causes the Foramen Ovale to close and
become the Fossa Ovalis
- The Ductus Venosus also constricts and will become the Ligamentum Venosus
182
What are the stages of the primitive heart tube folding process?
1:
During the third week of development the heart is formed from cells
that form a horseshoe shaped region called the cardiogenic region
2:
By day 19 (third week), two endocardial tubes form. These tubes will fuse to form a single, primitive heart tube
3:
Day 21: As the embryo undergoes lateral folding, the two endocardial tubes have fused to form a single heart tube
4
The heart tube grows and develops bulges
5
By day 22 the heart begins to beat
6
Cardiac Looping:
By day 23 the heart tube begins to fold:
The bulbus cordis moves inferiorly, anteriorly and to the embryo’s right
- The primitive ventricle moves to the embryo’s left side
- The primitive atrium and the sinus venosus move superiorly and posteriorly - resulting in the sinus venosus being posterior to the primitive atrium
183
What are the 5 segements/bulges of the primitive heart tube?
Bulbus Cordis
Primitive/ primordial ventricle
Primitive/ primordial atrium
Sinus Venosus (Right and Left Horns)
Aortic Sac
184
What structures form from the bulbus cordis?
the proximal 1/3rd of the bulbus cordis gives rise to the muscular right ventricle
- the conus cordis (lower part of bulbus cordis) gives rise to smooth outflow portion
of the right and left ventricles
- the truncus cordis (upper part of bulbus cordis) gives rise to the proximal aorta &
pulmonary trunk
185
What structures form from the primitive ventricle?
gives rise to the left ventricle
186
What structures form from the primitive atrium?
gives rise to the anterior part of the right atrium and the entire left atrium and the left and right auricles
187
What structures form from the sinus venosus?
Forms part of the right atrium, vena cava and coronary sinus
188
What structures form from the aortic sac?
Forms the aorta and Pulmonary artery
189
What is the first step in the development of the interatrial septum?
In the developing foetus the lungs (and thus the pulmonary circulation) are not fully functional
- This creates increased vascular resistance in the pulmonary arterial circulation,
and increased pressure in the right side of the heart (which supplies the pulmonary arterial circulation)
- Thus, in the developing foetus, pressure is greater in the right side of the heart than the left side
- As a results, as blood enters the right atrium, much of this blood is shunted to the left atrium - down its pressure gradient
190
What is the 2nd step in the development of the interatrial septum?
At the end of the fourth week, a crescent-shaped tissue called the septum primum starts to grow towards the endocardial cushions
191
What is the 3rd step in the development of the interatrial septum?
The diminishing opening between the septum primum and the endocardial cushion is called the
foramen (ostium) primum. This opening allows blood to be shunted from the right atrium to the left atrium
192
What is the 4th step in the development of the interatrial septum?
Before the foramen primum completely closes, enlarging perforations develop in the wall of the septum primum
- These enlarging perforations form a single opening called the foramen (ostium) secundum
- Thus, a new opening for right-to-left shunting of blood appears before the foramen primum disappears
193
What is the 5th step in the development of the interatrial septum?
As the foramen (ostium) primum disappears, the foramen (ostium) secundum enlarges
194
What is the 6th step in the development of the interatrial septum?
A second crescent-shaped ridge of tissues called the septum secundum grows towards the endocardial cushions. The septum secundum is thick and muscular, compared to the thin, membranous septum primum
- By around the end of the 6th week, the septum secundum finishes growing. The septum secundum contains a permanent opening on its posterior-inferior surface, called the foramen ovale
- Blood will enter from the right atrium go through the foramen ovale and the septum secundum and enter the left atrium
195
What is the 7th step in the development of the interatrial septum?
The foramen secundum enlarges and the upper part of the septum primum gradually degenerates
- The lower part of the septum primum remains and is now called the valve of the foramen ovale. It covers the foramen ovale and forms a flap that moves when blood flows from the right atrium to the left atrium
196
What is the 8th step in the development of the interatrial septum?
At this point the path of blood is as follows; as blood enter the right atrium, it will be shunted from the right side to the left due to the pressure difference between the two sides in the following manner:
1. Blood enters right atrium
2. Blood flows through the foramen ovale
3. Blood pushes the valve of the foramen ovale to the left
4. Blood enters the left atrium
197
What is the 9th step in the development of the interatrial septum?
When the baby is born and takes its first breath, the lungs and pulmonary arterial circulation become fully functional - consequently, the pressure in the right side of the heart drops
- Pressure is now greater in the left side of the heart than the right
- The blood in the left atrium pushes the valve of the foramen ovale against the muscular septum secundum, thereby closing the passageway between the two atria
198
What is the 10th step in the development of the interatrial septum?
The septum secundum and valve of the foramen ovale usually fuse and form a solid interatrial septum about three months after birth
- After the interatrial septum forms, there remains a thinned, oval part of the septum where the foramen ovale used to be. This thinned oval area in the inertial septum is called the fossa ovalis
- The fossa ovalis is a landmark in the adult heart that represent where the valve of the foramen ovale permanently covered the foramen ovale
199
What is the the process of atrioventricular canal division?
Step ONE: Blood first enters the atrium through the superior and inferior vena cava, then it passes through the atrioventricular canal, into the ventricle and then will exit the heart through the truncus arteriosus
Step TWO: Masses of tissue called endocardial cushions grow from the sides of the atrioventricular canal to partition it into two separate openings
- As the endocardial cushions grow together, the atrioventricular canal also is being repositioned to the right side of the heart
Step THREE: The superior & inferior endocardial cushions fuse, forming two separate opening that are now called the right & left atrioventricular canals - these canals will become the right & left atrioventricular openings of the heart
Step FOUR: Now, as blood flows through the heart, it will pass from the atrium, through both atrioventricular openings into the
ventricle, and up though the truncus arteriosus
200
What is the process of the development of the aorta pulmonary trunk, and interventricular septum?
1: Early in heart development blood will flow from the atria, through the left and right atrioventricular canals and into the common ventricle - blood then leaves the heart via the truncus arteriosus - which will eventually be partitioned into an aorta and a pulmonary trunk
2: At the end of the fourth week, a muscular ventricular septum grows superiorly from the floor of the ventricle. This septum divides this area in to left and right ventricles.
3: An opening still remains between the muscular ventricular septum and the fused endocardial cushion. This opening is called the interventricular foramen
4: At the end of the fifth week, two ridges of tissue appear on the sides of the truncus arteriosus. These masses of
tissue are called the conotruncal ridges (truncoconal swellings)
5:These ridges grow towards each other and make a spiral shaped septum, called the aorticopulmonary septum which divided the truncus arteriosus into the aorta and pulmonary trunk
6: As the conotruncal rises grow and fun to form the aorticopulmonary septum, they also grow inferiorly into
the ventricles themselves
7: The aorticopulmonary septum will fuse with the already fused endocardial cushions and the muscular ventricular septum
8: Once the aorticopulmonary septum, endocardial cushions and muscular ventricular septum fuse (by
week 8), they from the membranous ventricular septum - this septum closes off the opening known as the interventricular foramen
9: Now, blood enters the right ventricle through the right atrioventricular opening and leaves via the
newly developed pulmonary trunk
10: Blood enters the left ventricle through the left atrioventricular opening and leaves via the newly developed aorta
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When does aortic vessel development take place?
Occurs from 27 days to 7 weeks old
202
Which aortic arch is notably missing?
5th arch
203
What structures are formed by the aortic arches?
Left 1st arch regresses into part of the maxillary artery
Left 2nd arch regresses into stapedial artery
Left 3rd arch forms Left/right common/internal/external carotid arteries
Left 4th arch forms part of aortic arch
Right 4th arch forms part of right subclavian artery
Left 6th arch forms Left pulmonary artery and ductus arteriosus
Right 6th arch forms Right pulmonary artery
