Cardiovascular Flashcards
What are the two phases of blood, what is in each phase and what percentages are involved?
Cellular: 45% (99% RBCs, then white blood cells and platelets make up the rest)
Fluid: 55% (plasma)
How many litres of blood is normal for a human?
5 litres
What is haematocrit and what is a normal value?
the volume of red blood cells i.e haemoglobin in the blood, normal haematocrit is 0.45
What is haemopoiesis? In adults where does this take place?
the process of the production of blood cells and platelets which continues throughout life, in adults this is confined to the bone marrow
What is the lifetime of RBCs?
120 days
What is the lifetime of white blood cells?
6 hours
What is the lifetime of platelets?
7-10 days
Where are the precursor cells for red blood cells found?
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
What is precursor cells in the blood an indication of?
Leukaemia
What do hormonal growth factors do? and what is the specific type for each type of blood cell
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
What happens to the oxygen dissociation curve when the pH is decreased or the temperature increases?
It will shift to the right
What happens to the oxygen dissociaton curve when the pH is increased or the temperature decreases?
It will shift to the left
Why do red blood cells have such a short lifespan?
Simple cells, with no nucleus or mitochondria thus cannot repair itself - why they have such a short lifespan
What are young red blood cells called?
Reticulocytes
What is the role of haemoglobin and what is its structure?
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
Explain the presence of varying antigen on the surface of blood cells?
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)
Which antibodies are in the plasma of a type A individual?
anti-B antibodies
What is co-dominance and why is it important in blood types? What does this produce?
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
What is type O?
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
What are these antibodies?
They are anti-erythrocyte antibodies and are known as natural antibodies
What would happen if a type A patient was transfused with type B blood?
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
What are the Rhesus antigens? What does Rhesus positive mean?
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
What is anaemia?
reduction in haemoglobin in the blood
What is a normal haemoglobin value?
12.5 - 15.5 g/dl
What condition causes raised haemoglobin?
Polycythaemia (caused by smoking, lung diseases, inefficient lungs
meaning less O2 is exchanged so more haemoglobin is required etc.)
What are the symptoms of anaemia?
Tiredness, lethargy, malaise, reduced exercise tolerance, shortness of breath on exertion and angina
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)
What are the classifications of anaemia?
Iron deficiency, B12/folate deficiency, anaemia of chronic disorder, haemolysis, bone marrow failure/infiltration
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
What is MCV?
Red cell size is measure as MCV (mean cell volume), normal = 82 - 96 fl
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
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)
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
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
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
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)
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
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
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
Synthesis of which coagulation proteins is vitamin K essential for?
Factors 10, 9, 7, and 2 (remember 1972)
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
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
What blood cells are responsible for primary haemostasis?
Platelets
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
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
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.
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
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
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
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.
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
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
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
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
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
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
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
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.
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
What is a normal number of platelets?
140-400 x 109/l (to the power 9 not 109)
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
What is the effect of high platelet count?
thrombocytosis, can lead to arterial & venous thrombosis, leading to an increased risk of heart attack + stroke
Where are platelets made and what are their precursor cells?
Made in bone marrow from cells called megakaryocytes
What are the stages of systole and how long does it last?
- 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 - 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
What are the stages of diastole and how long does it last?
- Reduced ejection
- 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) - 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 - 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 - 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
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
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
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%
Define Stroke Volume?
The volume of blood ejected from each ventricle during systole
Define Cardiac Output?
The volume of blood each ventricle pumps as a function of time (liters per minute)
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
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).
Define Afterload?
the pressure the left ventricle must overcome to eject blood during contraction - dilate arteries = decrease in afterload
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
Define elasticity?
myocardial ability to recover normal shape after systolic stress
Define Diastolic Dispensability?
The pressure required to fill the ventricle to the same diastolic volume
Define Compliance?
how easily the heart chamber expands when filled with blood volume
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
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
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
Define Hyperaemia?
Increase in blood flow
