Flashcards
Cardiovascular
Flashcards do conjunto (200)
- 1Describe the constituents of the blood?Cellular component: (45%) red cells, white cells and platelets
Fluid component: (55%) Plasma - 2How much blood does the average persons have?5 Litres
- 3Define: Haematocrit?The volume of red blood cells i.e. the haemoglobin in the blood, normal haemocrit is 0.45
- 4Define: Haemopoiesis?The process of the productions of blood cells and platelets which continues throughout life
- 5Where does haemopoiesis occur in adults?In adults it is confined to the bone marrow
- 6What are the lifetimes of the different cell types?Red blood cells: 120 days
Platelets: 7 to 10 days - 7Which of these cells have nuclei? RBC? Platelet? WBC?RBC: anucleate
Platelet: anucleate
WBC: lobed nuclei - 8Where is bone marrow found in adults?The axial skeleton:
- Skull
- Ribs
- Spine
- Pelvis
- Long bones - 9Where is bone marrow found in children?All bones
- 10Where is bone marrow found in utero?Yolk sac, then liver and spleen
- 11What happens if precursor cells to RBCs are found in the blood?This is a sign of leukaemia
- 12What stimulates the proliferation of precursor stem cells?Hormonal growth factors stimulate precursor stem cells to proliferate and differentiate
Erythropoietin (Epo) made in kidney = RBCs
G-CSF (Granulocyte Colony Stimulating Factor) = White cells
Tpo = Platelets - 13What happens when to the oxygen dissociate curve when: - temperature is increased - pH is decreasedOxygen dissociation curve shifts right
- 14What would cause the oxygen dissociation curve to shift to the left?pH is increased
Temperature is decreased - 15What is a young red blood cell known as?Reticulocyte
- 16Why do RBCs have such a short lifespan?They are simple cells with no nucleus or mitochondria and therefore cannot repair themselves
- 17What do RBCs consist of?A membrane to enclose haemoglobin
Enzymes of glycolysis
Haemoglobin - 18Describe the function and properties of Haemoglobin?- Carries oxygen from the lung tissues where it transfers oxygen to myoglobin in the muscles
- Consists of the protein haemoglobin, oxygen binds to the Fe2+ reversibly
- Haemoglobin is formed of 2 alpha and 2 beta chains with 4 haem groups - 19What is the same as the blood group, The antibody in the serum The antigen present on the RBCThe antigen present on the RBC
- 20What blood group is the universal donor and why?O (O-) Because it has no antigens on its surface
- 21What blood group is the universal receiver and why?AB (AB+) Because it has no antibodies in its serum
- 22—
- 23Describe the ABO antigensA and B: Co dominant
O: Recessive - 24What are the anti-erythrocyte antibodies known as?Natural antibodies
- 25What are the Rhesus blood groups?C, D and E
D antigen is the most important
D+ means the D antigen is present
D- means that the D antigen is not present - 26Define: Anaemia?A reduction in the haemoglobin in the blood
Symptoms: Tiredness, lethargy, malaise, reduced exercise tolerance, shortness of breath on exertion and angina
Signs: Palor, pale mucous membranes, glossitis, angular stomatitis (cracking at corners of mouth) kylonychia (spoon shaped nails) - 27W12.5-15.5 g/dl
- 28What haemoglobin that is too high referred to as?Polycthaemia
Caused by smoking, lung diseases, inefficient lungs meaning less O2 is exchanged so more haemoglobin is required - 29What is iron deficiency anaemia?Iron is needed for haemoglobin production
Lack of iron results in the reduced production of small red cells
MCV <80fl - 30What are the classifications of anaemia?Iron deficiency
B12/Folate deficiency
Anaemia of chronic disorder
Haemolysis
Bone marrow failure/infiltration - 31What is the normal MCV (mean cell volume) of RBCs?MCV 82 - 96 fl
- 32What causes iron deficiency anaemia?- Bleeding
- Occult gastrointestinal
- Menorrhagia
- Dietary (uncommon in UK) - 33Define: Macrocytic anaemia?MCV > 100 fl
Macrocytosis can occur without anaemia i.e. there will be a raised MCV but normal haemoglobin levels, this can be caused by a liver disease, alcohol and hypothyroidism
In macrocytic anaemia, macrocytosis is a sign of it and it occurs due to a B12 or folate deficiency - 34What are the causes of B12 deficiency?- In the terminal ileum B12 absorption occurs, however intrinsic factors by the gastric parietal cells in the stomach is required for absorption to occur since the B12 binds to intrinsic factors and THEN is absorbed
- An auto immune disease called pernicious anaemia - 35Describe pernicious anaemia?It causes antibodies to be made against gastric parietal cells meaning that less intrinsic factor can be produced so there is B12 malabsorption and thus anaemia
The liver has a vast store of B12 (4 years) so pernicious anaemia has a slow onset - 36What causes folate deficiency?- Malabsorption of folate due to coeliac disease
- Dont eat enough fruit and veg
- Increase need due to haemolysis or anything that results in increase cell division - 37Define: Haemolysis?Normal or increased cell production but decreased life span <30 days
Red blood cells destroyed before their 120 day lifespan
Can be congenital or acquired - 38Describe the features of congenital haemolysis?- Spherocytosis: Whereby blood cells are spherical and they get stuck in blood vessels easily. Dominant condition but variable penetrance
- Pyruvate kinase deficiency: Enzyme require to convert phosphoenolpyruvate to pyruvate is deficient resulting in less ATP production and a build up of phophoenolpyruvate
- Sickle cell anaemia
- Thalassaemia - 39Describe the features of acquired haemolysis?- Autoimmune: immune system attaches own RBCs can be triggered by blood transfusion due to presence of foreign antibodies
- Mechanical: Fragmentation of RBCs by mechanical heart valve
- Pregnancy: Mother has RhD NEG and baby has RhD POS. First baby is unaffected as antibodies take time, second baby RBCs immediately destroyed - 40Describe normal white blood cells?They are mature cells that circulate in the blood, they are produced from immature precursor cells in the bone marrow which are derived from immature precursor cells in the bone marrow
Rate of production is under hormonal control of G-CSF - 41Describe neutrophils?- Most numerous white cell
- Lifespan 10 hours
- Phagocytose and kill bacteria
- Release chemotaxins and cytokines
- Lack of number or function results in recurrent bacterial infections - 42Describe lymphocytes?B and T cells
- Vital to immunity
- Generate antibodies against specific foreign antigens
- Immunological memory which generates immunity and allows vaccination - 43Describe B Lymphocytes?- Named after Bone marrow, as they are made in the bone marrow and stored in the secondary lymphoid organs
- The differentiate int plasma cells and produce immunoglobulins when they are stimulated by exposure to a foreign antigen - 44Describe T Lymphocytes?- Made in the bone marrow and MATURE in the thymus
- Some are helper cells (CD4 help B cells in antibody production) and some are cytotoxic cells (CD8) - 45Describe acute leukaemia?Proliferation of primitive precursor cells usually found in bone marrow
Proliferation without differentiation replaces normal bone marrow cells resulting in anaemia, neutropenia, thrombocytopenia - 46Describe acute myeloblastic leukaemia?Malignant proliferation of the precursor myeloblasts (unipotent stem cells) in the bone marrow
Primary affects adults and 50% survive 5 years - 47Describe acute lymphocytic leukaemia?Malignant proliferation of the lymphoblast precursor cells in the bone marrow, disease primarily affects children and 80% area cured
- 48Describe high grade lymphoma?Lymphocytes becoming very malignant
Classified as either Hodgkins disease and non Hodgkins lymphoma
Disease of lymph nodes that spreads to the liver, spleen, bone marrow and blood - 49Describe platlets?- Small cytoplasmic anucleate cells that block up holes in blood vessels
- Made in bone marrow from cells called megakaryocytes
- Spherical and cannot self repair
- Lifespan of 5 to 10 days
- Normal number: 140-400 X 10^9 /l - 50What does decreased platelets lead to?Thrombocytopenia
<80 = Increase bleeding
<20 = Spontaneous bleeding - 51What does increased platelets lead to?Thrombocytosis
Can lead to arterial and venous thrombosis leading to an increased risk of heart attack and stroke - 52What are the proteins in the blood?- Coagulation proteins: produced in liver, key enzyme thrombin, vit K essential for coagulation factors II, VII, XI and X, (1972) they circulate in inactive form and convert fibrinogen to fibrin
- Plasma proteins: soluble in plasma component
- Albumin: produced in liver and maintains oncotic pressure, lack of results in oedema and it carries carry acids steroids and thyroid hormones
- Carrier proteins: nutrients and hormones
- Immunoglobulins: antibodies from plasma cells, IgG IgM, IgA, IgE - 53Define: Haemostasis?The arrest of bleeding, involving the physiological process of blood coagulation and the contraction of damaged blood vessels
- 54Why is blood usually fluid inside vessels?- The proteins of coagulation cascade and platelets circulate in an inactive form
- Proteins and platelets are only activated by tissue factor which is present on every cell apart from endothelial therefore when endothelial is punctured blood comes into contact and clots - 55What happens if blood clots inside vessel?Thrombosis
- 56Describe haemophilia?Severe bleeding disorder, bleeding into muscles and joints
Not enough clotting factors in the blood so there is a long PTT
Mostly affects males as it is recessive X linked - 57Describe haemophilia A vs BHaemophilia A:
1 in 10,000
Deficient in clotting factor VIII
Haemophilia B.:
1 in 50,000
Deficient in clotting factor XI - 58Describe Von Willebrands disease?Autosomal dominant inheritance
Lack of Von Willebrands Factor
VWF is required for platelets to bind to damaged blood vessels so lack of VWF = platelet dysfunction hence the muco-cutaneous bleeding
Usually mild, often unrecognised and undiagnosed, up to 1% incidence - 59Define: Muco-cutaneous bleeding?Bleeding in the skin and mucous membranes
Easy bruising, prolonged bleeding from cuts, nose bleeds, spontaneous gum bleeding - 60Describe acquired bleeding disorders?- Recent onset, not lifelong and no family history
- May be generalised or localised bleeding
- Most common cause: anti-platelet or anti-coagulation medication
- Other causes include liver disease, Vit K deficiency and drugs - 61How can vitamin K disease affect bleeding?- vit K is needed for the correct synthesis of coagulation factors II VII XI and X
- It is a fat soluble vitamin
- Caused by malabsorption and manifests as PTT
- Newborns given vit K at birth - 62What drugs affect bleeding?- Aspirin: affects platelet function
- Heparin and warfarin: both affect coagulation cascade
- Steroids: make tissues thin - 63Describe disseminated intravascular coagulation?- Breakdown of haemostatic balance
- Simultaneous bleeding and microvascular thrombosis
- Lifethreatening
- Activation of the coagulation cascade inside vessels, thrombin produced therefore platelet plugs
- Deficiency of clotting factors as they've been used up in microvascular thrombosis - 64Causes of disseminated intravascular coagulation?- Causes:
1. Sepsis
2. Obstetric
3. Malignancy
Treatment is to rest underlying vascular thrombosis - 65Describe a platelet plug and coagulation cascade?- When a blood vessel is damaged, its first response is to constrict
- This temporarily slows the slow of blood in the affected area, furthermore the constriction presses opposed endothelial surfaces together and the stickiness keeps them glued together
- Permanent closure of the vessel by constriction and contact stickiness only occurs in microcirculatory vessels
- The stopping of bleeding depends on two interdependent processes that occur in rapid succession
1) Platelet plug
2) Blood coagulation - 66Describe the formation of the platelet plug?1. When a vessel is injured/disrupted, resulting in exposure of collagen fibres
2. Platelets adhere to the collagen fibres via an intermediary called Von Willebrand Factors
3. The. binding of the platelets to the collagen fibre wall triggers platelets to release the contents of the secretory vesicle via exocytosis, incl. platelet dense granules releasing ADP which acts on P2Y1 and P2Y12
4. ATP binds to P2X1 causing platelet amplification
5. Thrombin binds to PAR 1 and PAR4 receptors causing positive feed back of thrombin
6. Platelets change shape from smooth disc to spiculated with pseudopodia increase surface area
7. Platelet activation causes an increase in the expression of GPllb/llla receptors binding fibrinogen (platelet aggregation)
8. Thromboxane A2 causing vasoconstriction and platelet activation is synthesised and released due to platelet adhesion - 67What do platelet plugs allow?- They can rapidly seal small breaks in vessels
- Effectiveness is enhanced by another property of platelets - contraction
- Platelets have a very high concentration of actin and myosin and this results in the compression and strengthening of the platelet plug - 68Why doesn't the platelet plug expand away from the damaged endothelium?- Normal undamaged endothelium either side of the damage begin to release prostacyclin which is an inhibitor of platelet aggregation
- Normal endothelium also releases nitric oxide which is not only a vasodilator but also an inhibitor of platelet adhesion, activation and aggregation - 69What is the coagulation cascade?Blood coagulation is the transformation of blood into a solid gel called a clot or thrombus which consists mainly of a protein polymer called fibrin
- 70Where does clotting occur?Clotting occurs locally around the platelet plug and is the dominant haemostatic defence - its function is to support and reinforce the platelet plug and solid the blood that remains in the would channel
- 71How can the coagulation cascade be divided?Extrinsic pathway: Since a cellular element outside the blood is needed
Intrinsic pathway: Everything that is necessary inside the blood - 72Describe the intrinsic coagulation pathway?- The first plasma protein in the intrinsic pathway is called factor XII and it is activated to factor XIIa when it comes into contact with exposed collagen fibres (contact activation)
- Factor XIIa catalyses XI to XIa
- XIa catalyses IX to IXa
- IXa catalyses X to Xa using VIIIa as a cofactor
- VIIIa is lacking in haemophilia
- Xa converts prothrombin to thrombin
- Thrombin converts soluble fibrinogen to insoluble fibrin - 73Describe the extrinsic coagulation pathway?- Begins with a protein called tissue factor (not a plasma protein)
- Blood is exposed to subendothelial cells
- Tissue factor binds to a protein called factor VII activated VIIa (also catalysed X to Xa)
- VIIa also catalyses activation of IX further activating X
- It can be seen that the clotting cascade can be activated via activation - 74What is the usual pathway of clotting in the blood?The extrinsic pathway is the usual way with factor XII playing little if any role
Thus thrombin is initially generated only to be the extrinsic pathway however to amount is too small for sustained coagulation
It is a large enough amount however to trigger thrombin's positive feedback mechanisms on the intrinsic pathway which generates large amounts of thrombin - 75What are the indirect roles of the liver 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 vit K which the liver requires to produce prothrombin - 76What is the 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 covered by plasminogen activators into plasm which then goes on to break down fibrin and thus the entire clot - 77Describe cardiac muscle?- Found only in the heart
- Combines the properties of both skeletal and smooth muscle
- Has a striated appearance due to regularly repeating sarcomeres composed of myosin containing thick filaments interdigitating with thin filaments containing actin
-Individual cardiac muscle cells are relatively small and contain a single nucleus
- Adjacent cells are joined end to end at structures called intercalated discs within which are desmosomes holding the cells together to which the myofibrils area attached
- Also found intercalated discs are gap junctions
- Cardiac muscle cells are arranged in layers around the blood filled chambers of the heart - 78What are myofibrils?They are contractile proteins: actin and myosin
Arranged in a regular array of thick (myosin)
And thin (actin) filaments - 79Define: Myosin?Forms majority of the thick filament
Composed of two large polypeptide chains and four smaller light chains
These polypeptides combination to form a molecule that consists of two globular heads (heavy and light) and a long tail formed by the two intertwined heavy chains - 80How does the myosin head work?- Each chain of the 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 during contraction
- Each globular head contains two binding sites, one for attaching to the thin filament and one for ATP
- Attached to the myosin is an inorganic phosphate and ADP
- The ATP binding site also serves as an ATPase that hydrolyses the bound ATP harnessing its energy for contraction - 81Describe the thin filament?Mostly formed of actin
Also composed of troponin and tropomyosin
Actin is a globular portion composed of a single polypeptide that polymerises with other actin monomers to form a polymer made of two intertwined helical chains making the core
- Each actin molecule contains a binding site for myosin - 82dAn elongated molecule that occupies the grooves between the two actin strands
Overlies the myosin binding sides on the actin - 83Describe troponin?Protein that changes shape when Ca2+ binds to it, when it does it changes shape in doing so pushes the tropomyosin exposing the myosin bind sites on the actin enabling contraction to occur
- 84What 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 - 85What is the I band?Occupied only by thin filaments and it extends to the centre of the sarcomere from the Z lines
- 86What defines the limits of one sarcomere?The space inbetween 2 Z lines
- 87What is the H zone?Contains thick filaments only
- 88What is the M line?In the centre of the H zone, comprised entirely of the thick filament myosin
Corresponds to the proteins that link together the central region of adjacent thick filaments - 89What is titin?Elastic protein filaments that extend from the Z line to the M line
Linked to both the M line and the thick filaments
Both the M line linkage between thick filaments and the titin filaments act to maintain the alignment of the thick filaments in the middle of each sarcomere - 90What does one sarcomere consist of?2 Half I bands
1 A band
1 H zone
1 M line
2 Z lines - 91What is the sarcoplasmic reticulum?A membrane network that surrounds the contractile proteins
Releases Ca2+ which Ca2+ binds to its ryanodine receptor - 92How is the resting potential of the cardiac muscle maintained?- The sarcolemma is much more permeable to K+ since K+ channels are open K+ is leaving the cell
- The resting potential is maintained by Na+ and K+ ATPase pumps pumping 3 Na+ out for every 2K+ pumped in - 93Describe the effectors of an action potential arriving on the sarcolemma?1. Na+ voltage gated channels open, Na+ entry depolarises the cell triggering more Na+ to open because of positive feedback
2. When the cell potential is positive (+52mV) the voltage gated Na+ close and voltage gated K+ channels open partially repolarising the cell
3. At the same time that the Na+ open Ca2+ channels are also triggered but they open much slower
4. During the partial repolarisation causes the outflow of K+. the voltage gated Ca2+ channels open at the T tubules which are part of the sarcolemma and they remain ope n for a long duration which is why they are referred to as L type T tubules
These channels are modified versions of the dihydropyridine receptors that function as voltage sensors in skeletal muscles)
5. The flow of Ca2+ ions into the cells just balances the flow of K+ ions out of the cell and keeps the membrane depolarised at the plateau value of roughly 0mV
6. Repolarisation eventually occurs due to closure of L type Ca2+ channels and the reopening of K+ channels - 94—
- 95Describe excitation contraction coupling in cardiac muscle?- When the action potential is generated, there is an influx of Ca2+ via the T-tubules via L type Ca2+ voltage gated channels
- Not only does this influx aid depolarisation by it also causes a small increase in cytosolic Ca2+ contraction
- The small amount of Ca2+ influx is not enough to initiate muscle contraction bt they bind to ryanodine receptors on the sarcoplasmic reticulum
- This releases many Ca2+ ions into the cell initiated cardiac muscle contraction and its the start of the cross bridge cycle - 96Describe the cross bridge cycle?1. The Ca2+ binds to the troponin protein on the actin filament
2. This causes the troponin to change shape and thus displace the tropomyosin protein on the actin filament
3. The myosin head on the myosin filament then binds to the actin filament via the myosin binding site, Pi is dropped in order for the myosin head to bind to actin and ADP remains attached - CROSS BRIDGE FORMATION
4. The myosin head then drops the ADP to contract and pull the actin filament over the myosin filament thereby decreasing Z lines resulting in muscle contraction - this is known as the power stroke
5. ATP then binds to the myosin head detaching from the actin filament moving the head to its start position
6. The ATPase in the myosin head hydrolyses the ATP into ADP and Pi ready for the next contraction if the myosin binding sites remain open - 97Describe the power stroke?The myosin head drops ADP to contract and pull the actin filament over the myosin filament decreasing the Z lines resulting in muscle contraction
- 98Why are skeletal muscles stiff in rigour mortis?Because ATP is required for the myosin head to detach from the actin, there is no ATP when a person has died therefore the myosin doesn't detach resulting in stiffness
- 99When does contraction stop?Contraction stops when cytosolic Ca2+ concentration is restored to its extremely low resting value by primary active Ca2+ ATPase pumps in the sarcoplasmic reticulum and the Na+ / Ca2+ counter transporters in the sarcolemma
- 100Compare cardiac muscular contraction to skeletal muscular contraction?- Contraction lasts longer in skeletal muscles - up to 15 times longer in duration and this is due to slow calcium channels
- The refractory period is the period of time after an action potential where a second impulse cannot cause a second contraction:
This is much longer in the heart and it is to prevent excessive frequent contraction to allow filling time - 101Describe the blood supply of the myocardial cells?Supplied by the coronary arteries
Coronary arteries exit from behind the aortic valve cusps in the very first part of the aorta
Most of the coronary arteries drain into a single vein called the coronary sinus which empties into the right action - 102What coordinates the heartbeat?- Approx 1% of cardiac cells do not function in contraction but have specialised features essential for normal head excitation
- These cells constitute a network called the conducting system of the heart and are in electrical contact with the cardiac myocytes via GAP JUNCTIONS
- The conducting system initiates the heartbeat and helps spread the action potential rapidly through the heart
- Gap junctions interconnect and allow action potentials to spread from one cell to another
- The action potential spreads over cell membranes and the positive charge results in depolarisation, the newly depolarised cells can cause further depolarisation and the GJ allow ions to travel directly to other cells
- The excitation of one cardiac cell eventually results in the excitation of all the cardiac cells - 103Describe the propagation of an action potential?The initial depolarisation normally arises from a small group of conducting system cells called the sinoatrial node
Located in the right atrium near the entrance of the superior vena cava the action potential spread from the SAN through atria, to the AVN and then throughout the ventricle - 104What ion channels are involved in the SAN?SA node does not have a steady resting potential, instead it undergoes SLOW DEPOLARISATION known as pacemaker potential and it brings the membrane potential to a threshold at which potent and action potential occurs
Three ion channels mechanisms contribute to the pacemaker potential
The first is the progressive reduction in K+ permeability: K+ channels that opened during the repolarisation phase of previous AP close due to membranes returning to negative potentials
The second are unique channels (funny channels) that open at NEGATIVE values and these non specific cation conduct mainly an inward Na+ current referred to as F-type channels
The third is a Ca2+ channel that opens very briefly but contributes to an inward current of Ca2+ which acts as a final depolarising boost: as they're only opened briefly it can be called transient so these channels are known as T-type Ca2+ channels - 105Why does the SA node initiate action potentials and determine the pace of heart?Because although they are similar in shape. the pacemaker currents in the SA node bring them to a threshold more rapidly than the AV node
- 106Why is there a slow transmission of cardiac excitation through the AV node?- One the pacemaker cells 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 membrane more slowly than voltage gated Na+ channels and one result is that the action potential propagates more slowly along nodal cells than other cardiac cells - 107What does the pacemaker potential provide the SA node with?Automaticity
The ability for spontaneous, rhythmic, self-exciatatiom - 108How does the action potential spread through the myocardium?By 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 and left atria contract simultaneously
The speed of the action potential to the ventricles involves a different conduction system the AVN
The action potential is conducted relatively rapidly from the SA node to the AV node through internodal pathways - 109Describe the atrioventricular node?- Located at the base of the right atrium
- Transmits cardiac impulses from the atria to the ventricles
- Consists of modified cardiac cells that have lost contractile capability but conduct action potentials with a low resistance
- Elongated structure with an important feature: propagation of AV node is relatively slow (0.1s) and is important as it allows the atria to empty blood into ventricles, so atrial conduction is completed BEFORE ventricular excitation occurs - 110Describe the conduction of the AV node?After the AV node has been excited the action potential progresses down the inter ventricular septum through 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 non conducting connective tissue
Within the inter ventricular septum the bundle of His divides into the left and right bundle branches that separate at the apex and enter the walls of both ventricles
These fibres make contact with the Purkinje fibres - large diameter conducting cells that rapidly distribute the impulse throughout much of the ventricles
Finally the Purkinje fibres make contact with the ventricular myocardial calls that spread through the rest of the ventricles - 111Describe the parasympathetic innervation of the heart?Fibers transmitted via the vagus nerve CN10
Controlled by acetylcholine that bind to the muscarinic receptors
- Decreases heart rate (negatively chronotropic)
- Decreases force of contraction (negatively inotropic)
- Decreases cardiac output by up to 50%
- Decreased parasympathetic stimulation will increase heart rate - 112Describe the sympathetic innervation of the heart?Sympathetic postganglionic fibres innervate the entire heart
Controlled by adrenaline and 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 a decrease HR and force of contraction and a decrease in cardiac output by up to 30% - 113What does the ECG record?It is a measure of the currents generated in the extra cellular fluid by the changes occurring simultaneously in many cardiac cells
It is NOT a DIRECT RECORD of the changes in membrane potential across individual cardiac muscle cells - 114What are the phases of a myocyte action potential?Phase 0: rapid depolarisation of Na+
Phase 1: Partial depolarisation inward Na+ current deactivated and outflow of K+
Phase 2: Plateau, slow inward Ca2+ current
Phase 3: Repolarisation, K+ outflow, Ca2+ current deactivated
Phase 4: Pacemaker potential, slow Na+ inflow, slowing of K+ outflow
- 115Decribe: P wave?Atrial depolarisation - seen in every lead apart from aVR
- 116Describe: PR interval time?Time taken for atria to depolarise and electrical activation to get through AV node and electrical activation to get through AV node
- 117Describe: QRS complex?Ventricular depolarisation
Still called QRS even if Q and/or R are missing depending on what you are looking at - 118Describe: ST segment?Interval between depolarisation and repolarisation
- 119Where is: - PR interval - PR segment - QRS - ST segment - QT interval
- 120Define: Tachycardia?Increased heart rate
- 121Define: Bradycardia?Decreased heart rate
- 122Define: Dextrocardia?Heart on the right side of instead of the left?
- 123Describe: acute anterolateral myocardial infarction?ST segments are raised in anterior (V3 and V4) and lateral (V5 and V6) leads
- 124Describe: Acute inferior MI?ST segments are raised in inferior (II, III and aVF)
- 125Why is atrial repolarisation usually not evident on an ECG?Because it occurs at the same time as the QRS complex so is hidden
- 126Describe the measurement of electrical impulses via ECG?Electrical impulses in the heart move in three directions
ECG only measures voltage in 1 direction
In an impulse moves towards the electrode it looks small or even negative
The impulse for the atria is smaller since the atria are smaller that the ventricles thus less myocytes - 127What are the standards limb leads?I, II and III
The standard limb leads form a triangle between the electron on the wrists and the LEFT leg
The negative poles are REFERENCE and the positive poles are RECORDING electrodes
The right leg is a ground electrode - 128What are the augmented leads?aVR, aVL and aVF
These bisect the angles of the triangle by combining tow electrodes as a reference thus creating. a reference point along the line between them pointing towards the recording electrode on the left wrist - 129Where are the leads on a person?
- 130What are the precordial leads?V1 to V6
The recording electrodes placed on the chest
- 131What does each square represent on the ECG?Each small square represents 40ms and each big square represents 0.2s
- 132What does an ECG show?Changes in voltage over time
- 133What are the P waves like in a normal ECG?The P waves are positive in every lead apart from aVR
- 134What are the T waves like in a normal ECG?They are positive in every lead apart from aVR and sometimes the V1 and V2 depending on the trace
- 135Describe: systole?Ventricular contraction and blood ejection - 0.3s
- 136Describe: diastole?Ventricular relation and blood filling 0.5s
- 137What are the stages of the cardiac cycle?1. Isovolumetric contraction
2. Maximal ejection
3. Start of relaxation and reduced ejection
4. Isovolumetric relation
5. Rapid left ventricle filling and suction
6. Slow left ventricle filling - diastasis
7. Atrial booster - 138Describe: Isovolumetric contraction?- Aortic valve opens and aortic pressure rises
- Atrial pressure initially dips due to crossover and then starts to rise
- First heart sound is the mitral valve closing - 139Describe: maximal ejection?- This is when you feel your pulse and aortic pressure peaks
- 25% of blood is still left in the ventricle after maximal ejection - 140Describe: the start of relaxing and reduced ejection?Aortic valve closes and this is the second heart sound
- 141Describe: isovolumetric relaxation?The high pressure in the atria causes the mitral valve to open
- 142Describe: rapid left ventricle filling and suction?The pressure difference between the filled atria and the empty ventricle causes rapid filling of the ventricle
80% of ventricular filling is passive due to the pressure difference - 143Describe: slow left ventricle filling?Diastasis
When the pressure in the atria and the ventricles is the same so not much filling - 144Describe: atrial booster?There is an electrical impulse which causes the contraction of the atria, they actively squeeze blood from the atria into the ventricles
- 145What is the first heart sound?Atrioventricular valves closing
Low pitched Lub - 146What is the second heart sound?Aortic and pulmonary valves closing
Louder dub - 147What is the third heart sound?The jitter of the ventricle recieving blood from the atria
Only physiological in under 25s
If you can hear over 25 suggests heart failure - 148What is the fourth heart sound?Atrial fibrillation
- 149Wigger and Lewis diagram?
- 150Define: Left ventricle?Palpated in the 5th, left, intercostal space and mid clavicular line
Responsible for the apex beat - 151Define: stroke volume?The volume of blood ejected from each ventricle during systole
- 152Define: Cardiac output?Total volume of blood each ventricle pumps as a function of time (litres per minute_
- 153Define: Total peripheral resistance?The total resistance to flow in systemic blood vessels from the beginning of the aorta to the vena cava
Arterioles provide most of this resistance - 154Define: 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 the veins dilate it results in a decrease in preload since by dilating veins venous return decreases - 155Define: Afterload?The pressure the left ventricle must overcome to eject blood during contraction
dilate arteries = decrease in after load - 156Define: Contractility?The force of contraction and change in fibre length
How hard the heart pumps
When muscle contracts the myofibrils stay the same length but the sarcomere shortens - the force of heart contraction is independent of sarcomere length - 157Define: Elasticity?Myocardial ability to recover normal shape after systolic stress
- 158Define: Diastolic dispensability?The pressure required to fill the ventricle to the same diastolic volume
- 159Define: Compliance?How easily the heart chamber expands when filled with blood volume
- 160Define: Starlings Law?The force of contraction is proportional to the end diastolic length of cardiac muscle fibre - the more the ventricle fills the harder it contracts
- 161What does increased venous return mean?Increased end diastolic volume = Increased preload =
Increased sarcomere stretch =
Increased force of contraction thus =
Increased stroke volume and force of contractions - 162What does standing up result in?Standing decreases venous return due to gravity thus cardiac output decreases, which causes a drop in blood pressure, stimulating baroreceptors to increase blood pressure
- 163Define: Intrinsic auto regulation?When the arterioles either vasoconstrict or vasodilator in response to changes in resistance seemingly automatically with the aim of maintaining constant blood flow
- 164Define: 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 - 165Define: Hyperemia?Increase in blood flow
- 166Define: Active hyperemia?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 reestablished
An extreme form of autoregulation - 167What is the central control of circulation?A key component is central neural control
The main goal is to maintain mean systemic arterial pressure (MAP)
The average blood pressure in the arteries during the cardiac cycle - 168What is the Mean systemic Arterial Pressure equal to?MAP is equal to diastolic pressure (DP) plus one third of the pulse pressure (SP-DP)
MAP = DP + 1/3 (SP-DP) - 169What are the effectors of blood pressure?Blood vessels
Heart
Kidneys - 170Describe the pressor region?Located in the medullary cardiovascular region, within this there is a region called the pressor region (region responsible for raising BP)
It is sympathetic
The pressor region increases blood pressure by vasoconstriction, increasing cardiac output (by inc. HR and SV for more forceful contraction) and increasing contractility - 171Describe the route from the pressor region to the heart?Pressor region>sympathetic route> medulla>spinal cord>synapses at T1 - L2 > heart
- 172Describe the depressor region?Also located in the medulla within the medullary cardiovascular region is a region called the depressor region
It is parasympathetic
The depressor region decreases blood pressure by inhibiting the pressor region - 173Describe the route from the depressor region to the heart?Depressor region> medulla> vagus nerve> heart
- 174Describe 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
- 175Describe cardiopulmonary baroreceptors?- Located in the atria, ventricles and pulmonary artery
- When stimulated (i.e high BP) leads to the inhibition of the pressor region / vasoconstrictor in the medulla - leading to a fall in blood pressure
- Also inhibits the Renin-angiotensin and aldosterone system sing angiotensin II stimulates vasoconstriction which will increase blood pressure, also aldosterone stimulate more Na+ and thus H2O absorption thereby increased blood volume and thus pressure
- Also inhibits vasopressin/ADH since it also stimulates water reabsorption - 176What happens when cardiopulmonary baroreceptors are stimulated?It brings about a decrease in blood pressure by promoting vasodilation and fluid loss
- 177Why is the total peripheral resistance mainly dependent on arteriole resistance?Because arterioles are the principle site of resistance to vascular flow
- 178What happens when smooth muscle contracts in the arteriole?Radius decreases
Resistance to flow increases
Blood pressure increases - 179What does endothelin-1 result in?Released by the endothelium cells it results in vasoconstriction
- 180What is autoregulation?An increase in internal blood pressure resulting in myogenic contraction (when smooth muscle is stretched there will be an automatic contraction until diameter is normalised) due to the blood pressure increase
- 181What causes vasodilation?- Increased CO2
- Decreased pH
- Bradykinin
- Nitric oxide
- Increased K+
- H+
- Tissue breakdown products e.g. lattice acid - 182What hormones cause vasoconstriction?Angiotensin II
Vasopressin
Adrenaline - 183What hormones cause vasodilation?Atrial Natriuretic Peptide
Adrenaline - 184Is adrenaline (also sometimes referred to as epinephrine) a vasodilator or vasoconstrictor?It is BOTH a vasoconstrictor and dilator depending on what receptors are present
- 185Where are the peripheral chemoreceptors?In the aortic arch and carotid sinus (base of the internal carotid artery and the division of internal and external carotid)
Stimulated by a fall in PaO2 and a rise in PaCO2 and a fall in pH causing blood pressure to increase - 186What are the arterial baroreceptors and where are they found?These are stretch receptors that respond to pressure
One found in the aortic arch and two in the carotid sinus - 187Do baroreceptors affect the Renin-angiotensin and aldosterone system?They cause some inhibition and are involved in short term blood pressure control
- 188Which receptors affect long term BP?Atria, Ventricles and Pulmonary artery
The cardiopulmonary baroreceptors - 189Cardiac output =Heart rate x Stroke volume
Typically 5L / Min - 190Blood pressure =Cardiac output x Tetal peripheral resistance
- 191Pulse pressure =Systolic - Diastolic pressure
- 192Mean arterial pressure =Diastolic pressire X 1/3(pulse pressure)
- 193Stroke volume =End diastolic volume - end systolic volume
- 194Pouiseuille's equation =Radius to the power of 4
- 195Ohms law =Pressure gradient / resistance
- 196Describe and structure arteries?- Contain mainly elastic, collagen and smooth muscle
1. Lumen and centre of vessels
2. Surrounded by endothelium
3. Surrounded by basement membrane
4. Intima: surrounded by loose connective tissue
5. Internal elastic lamina
6. Media: smooth muscle, fibroblasts, collagen and elastic fibres
7. External elastic lamina
8. Adventitia: loose connective tissue
- 197What are elastic arteries?Arteries found by the heart e.g. the aorta and the pulmonary arteries
Media contains concentric sheets of elastin seen as red lines - 198What are the muscular arteries?Most arteries are muscular arteries
Media compromises of layers of smooth muscle
Little elastin is still found in the media
e.g. radial and splenic artery - 199Describe arterioles?Arterioles are resistance vessels
- Arbitrarily defined as having 3 or fewer muscle layers in the media
- Elastic laminae are poorly defined - 200Describe capillaries?Endothelium and basement membrane
Pericytes can constrict capillaries
Discontinuous in small capillaries and continuous in larger capillaries
Informações
- Descrição
- PHASE 1 MED (Cardiovascular and Respiratory ) FlashCards sobre Cardiovascular , criado por Erin Dunn em 08-01-2019.
- Criado por
- Erin Dunn
- Visualizações
- 3
- Avaliação