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Phase 1 M > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the two main components of the blood?

A 
Cellular components (45%)
Fluid components (55%)
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2
Q

Define Haemopoiesis

A

Formation of blood cells

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3
Q

What is the life span of RBC’s, WBC’s and platelets?

A 
RBC's = 120 days 
WBC's = depends on cell type 
Platelets = 7-10 days
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4
Q

Where are blood cells formed in utero?

A 
Yolk sac (0-2months)
Liver/Spleen (2-7months)
Bone marrow (5-9months)
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5
Q

Where are blood cells formed in children?

A

All bones

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6
Q

Where are blood cells formed in adults?

A

Axial skeleton

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7
Q

What are the proper names for RBC’s. WBC’s and platelets?

A 
RBC = Erythropoiesis 
WBC = Myelopoiesis 
Platelets = Thrombopoiesis
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8
Q

Draw a diagram that shows the progression of blood cell formation from the haemocytoblast

A

See diagrams that need to be drawn notes

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9
Q

Which hormonal growth factors control the formation of RBC,s WBC’s and platelets?

A 
RBC = EPO from kidney 
WBC = Granulocyte-macrophage colony stimulating factor (GM-CSF)
Platelets = thrombopoietin (TPO)
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10
Q

Describes the properties of RBC’s

A

No nucleus or mitochondria
Biconcave disc
7.5um diameter
Contains Hb and glycolysis enzymes

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11
Q

Describe the structure of adult Haemoglobin

A

4 globin chains each with own Haem molecule
Tetrameric protein (2 alpha/2 beta proteins)
Normal O2 saturation Is 96-98%

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12
Q

Describe the structure of foetal haemoglobin

A

2 alpha and 2 gamma proteins

Normal O2 saturation is 0.5-0..8%

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13
Q

What is anaemia and what signs and symptoms would you expect?

A

Deficiency of Hb (<130g/L in males and <110g/L in females)
Signs (Pallor, tachycardia)
Symptoms (Tiredness, shortness of breath, angina and claudication

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14
Q

Where are RBC’s produced and where are they removed?

A

Made in bone marrow and removed by spleen, bone marrow and by blood loss

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15
Q

What diseases result from an RBC production failure?

A 
Hypoplastic anaemia (Not enough)
Dyshaemopoietic anaemia (Ineffective production)
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16
Q

How do you increase RBC removal?

A

Blood loss
Haemolysis
Intrinsic abnormalities (Factors within RBC)
Extrinsic abnormalities (Factos outside RBC)

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17
Q

What are the intrinsic RBC abnormalities?

A

Acquired

Hereditary including membrane disorders, enzyme disorders and Hb disorders

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18
Q

What are the extrinsic RBC abnormalities?

A 
Antibody mediated (AIHA)
Mechanical trauma 
Infections 
Chemicals 
Sequestration
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19
Q

What are causes of anaemia?

A 
Iron deficiency 
Chronic bleeding 
Poor diet 
Malabsorption 
Hookworm - intestinal parasite
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20
Q

Define a reduction mean corpuscular Hb

A

Reduction in the amount of Hb in the cell

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21
Q

Define a reduction in mean corpuscular volume

A

Reduction in the size of the cell

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22
Q

What are the properties of neutrophils?

A 
6-10 hours lifespan 
Most numerous white blood cell 
Phagocytose bacteria
Release chemotaxis and cytokines as part of inflammatory response 
Contain a nucleus that has 3-5 lobes
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23
Q

What are the properties of monocytes?

A

20-40 hours life span
0.2-0.8 x 10^9 L
Macrophages - phagocytose bacteria
Dendritic cells - present antigens to immune system

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24
Q

What are the properties of basophils?

A

Life span of days
0.01-0.1 x 10^9L
Migrate to tissues to become mast cells where they fill with histamine granules, express IgG and play an important role in the allergic response

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25
Q

What are the properties of Eosinophils?

A

Lifespan of days
0.04-0.4 x 10^9L
Role in allergic response and parasite infection protection

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26
Q

Construct a table comparing T and B lymphocytes based on origin, blood, receptors, function and markers

A

See diagrams need to know sheet

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27
Q

Define haemostasis

A

Balance between bleeding (blood failing to clot outside the vessel) and thrombosis (blood clots inside the vessel)

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28
Q

Describe the pathway for the formation of platelets

A

Myloid Stem cell differentiates into megakaryoblast which undergoes endomitosis to megakaryocytic which undergoes membrane blebbing to platelets

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29
Q

Describe the properties of platelets

A

140-400 x10^9L
anucleate cells which circulate in inactive state
Responsible for primary haemostasis
have a life span of 5-10 days

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30
Q

How do platelets adhere to damaged blood vessels?

A

Bind to collagen via glycoprotein Ia (GPIa) and to von willenbrand factor by GPIB and GPIIb

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31
Q

How do platelets work? (4 steps)

A

Bind (Adhere)
Change Shape (Activate)
Release Contents (Degranulate)
Aggregate

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32
Q

What two types of granules do platelets contain?

A

Electron dense granules

Alpha granules

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33
Q

What do platelet electron dense granules contain?

A

Calcium
ADP and ATP
Serotonin

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34
Q

What do platelet alpha granules contain?

A

Platelet derived growth factor
Fibrinogen
Heparin Antagonist (PF4)
Von Willenbrand Factor

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35
Q

What is a normal platelet count?

A

140-400 x 10^9L

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36
Q

What does a reduction in platelet number result in

A

Increased bleeding - thrombocytopenia
>80 but <140 x 10^9 = increased bleeding
>20 but <80 x 10^9 = spontaneous bleeding

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37
Q

What does an increased platelet number cause?

A

Thrombocytosis
Arterial thrombosis
Venus Thrombosis

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38
Q

Describe constituents of plasma

A

90% water
Salts
Glucose
Proteins (albumin, carrier proteins, coagulation proteins and immunoglobulins)

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39
Q

Describe function of albumin and consequences of its absence

A

Produced in liver and determines oncotic pressure of blood
Albumin carries FA’s, steroids and thyroid hormones
Lack can cause oedema, liver disease and nephrotic syndrome

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40
Q

Draw a diagram of the coagulation cascade

A

See diagrams that need to be learnt sheet

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41
Q

Describe what coagulation proteins are

A

Enzymes that circulate in inactive state
Produced in liver
Key enzyme is Thrombin which converts fibrinogen into an insoluble fibrin polymer

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42
Q

What do the multiple steps of the coagulation cascade allow for?

A

Biological amplification of response and regulation

Not an all or nothing response

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43
Q

Draw a diagram to give an overview of clotting

A

See diagrams I need to know sheet

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44
Q

Describe properties and treatment for Haemophilia A

A

X linked disorder
Severe bleeding into muscle and joints
Deficiency of tissue factor VIII so treat with factor VIII

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45
Q

Describe the properties and treatment for haemophilia B

A

Severe bleeding into muscle and joints

Deficiency of factor IX so treat with factor IX

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46
Q

Describe the properties of von Willebrand disease

A

Autosomal dominant inheritance
caused by Lack of Von Willebrands Factor (VWF)
- VWF is required for platelets to bind to damaged blood vessels, so lack of VWF =
platelet dysfunction, hence muco-cutaneous bleeding
- Usually a mild bleeding disorder

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47
Q

What are the causes of acquired bleeding disorders?

A

Liver disease
Vit K deficiency
Disseminated intravascular coagulation
anti-platelet/anti-coagulation medicines

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48
Q

Why is vitamin K important?

A

Needed for functional activity of coagulation factors (2, 7, 9 and 10)- remember as 1972

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49
Q

What is disseminated intravascular coagulation and what are the causes

A

Simultaneous bleeding and microvascular thrombosis

Caused by sepsis, obstetric issues or malignancy

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50
Q

What is the result of an decreased platelet count

A

Thrombocytopenia
<80 = increased bleeding
<20 = spontaneous bleeding

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51
Q

What is the result of an increased platelet count?

A

Thrombocytosis - increased risk of arterial or venous thrombosis

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52
Q

Why does the blood remain fluid inside blood vessels?

A

Because coagulation proteins and platelets circulate in an inactive state

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53
Q

When do coagulation factors become activated

A

When they come into contact with tissue factor which is present in every single cell except endothelial cells thus when endothelium is punctured blood starts clotting

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54
Q

Vasoconstriction of a damaged vessel is triggered by the release of what?

A

Endothelin-1

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55
Q

What happens to the shape of the platelet when it becomes activated?

A

Changes from Smooth discoid to spiniculated with pseudophilia which increases SA and cell to cell interactions

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56
Q

Which receptor on platelets does thrombin bind to and what effect does this have?

A

Binds to PAR1 and PAR4 which induces platelet activation and positively feedback to increase thrombin release

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57
Q

Which platelet receptor does ADP bind to and what does It cause?

A

ADP binds to P2Y1 to cause platelet activation and GPIIb/IIa fibrinogen cross linking
ADP also binds P2Y12 which sustains platelet aggregation and activation but doesn’t initiate the process

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58
Q

What are the membrane level effects of thrombin binding to PAR-1

A

Normally in resting platelet, translocase active and scrambalase inactive which aminophospholids kept internal but thrombin binds causing Ca2+ release from internal stores which causes inactivation of translocase and activation of scrambalase. This causes aminophospholipids to move outside cell and form prothrombinase enzyme complex which converts prothrombin to thrombin

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59
Q

What is the effect of the release of alpha granules from platelets?

A

Inflam mediators (P-selectin) from alpha granules interact with WBC’s resulting in inflammation in the vessel wall

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60
Q

What are the effects of the thromboxane on platelets?

A

Causes vasoconstriction and platelet activation

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61
Q

Why does the platelet plug not extend away from the damaged area?

A

Undamaged endothelium either side releases prostacyclin which inhibits platelet aggregation and NO which is a vasodilator and inhibits platelet aggregation

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62
Q

Describe the pathway by which a fibrin clot is broken down

A

Fibrinolytic system
Tissue plasminogen activators converts plasminogen to plasmin which catalyses the conversion of fibrin to fibrin degradation products

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63
Q

Describe the properties cardiac muscle

A

Only found in the heart
Striated appearance due to regular sarcomeres consisting of interdigitating thick myosin and thin actin filaments
Each cell contains single nucleus
Cells joined end to end by intercalated discs

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64
Q

Describe the structure of myosin chain

A

Consists of 2 heavy and 4 light polypeptide chains that come together to form a protein with two globular heads that have 2 binding sites for actin and ATP

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65
Q

Draw the ultrastructure of a sarcomere

A

See diagrams I need to learn sheet

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66
Q

Describe the structure of actin

A

Globular protein where two actin monomers become intertwined to form a polymer

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67
Q

Describe the location of tropomyosin in actin

A

Lies in the groove between the two actin molecules and overlies the myosin binding sites on actin

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68
Q

Describe the role of troponin in ECC

A

Troponin molecule changes shape when calcium binds which leads to exposure of myosin binding sites on actin by moving tropomyosin

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69
Q

What is the role of titin

A

elastic filaments that maintain alignment of the sarcomere - extends from Z-line to M-line

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70
Q

Define the A band of a sarcomere

A

Region of sarcomere where there are overlapping thick and thin filaments - twice as many thin as thick

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71
Q

Define I Band

A

Region of sarcomere that contains only thin filaments which extend to centre of sarcomere from Z-line

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72
Q

Define H zone

A

Contains thick filaments only

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73
Q

Define the M line

A

Cetnre of the H-zone comprised entirely of thick filaments

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74
Q

Describe the stages of excitation contraction coupling

A

AP depolarises T-tubule. This causes Ca2+ influx through L-type channels. Cytosolic Ca2+ increases and binds to RYR receptor on sarcoplasmic reticulum - causes calcium induced calcium release (20% comes from outside and 80% from inside). Ca2+ binds to troponin causing change of shape which moves tropomyosin to expose myosin binding sites on actin . Myosin head on myosin binds to actin causing Pi to be dropped = cross bridge formation. Myosin head then drops the ADP group to contract pulling actin over the myosin filament to shorten the z-line and cause muscle to contract = power stroke. ATP binds to the myosin head and causes it to detach from the actin filament and move to starting position.. ATPase in the myosin head hydrolyses ATP to ADP and Pi for next contraction if binding sites remain open

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75
Q

How is cytosolic Ca2+ returned to normal after ECC

A

Primary active Ca2+ATPase pump in SR and sarcolemma and Na+/Ca2+ cotransporters (NCX) or pumped back into the SR by ATP dependent Ca2+ pumps

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76
Q

Where do t-tubules invaginate muscle cells?

A

At the level of the Z-line

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77
Q

Define what a sarcomere is?

A

Functional unit of the contractile apparatus define as the region between a pair of z-lines

78
Q

What are the three troponin subunits and what are their functions?

A

Troponin C = binds calcium
Troponin I = binds actin
Troponin T = binds tropomyosin

79
Q

Describe the pacemaker potential

A

Progressive reduction in K+ permeability as K+ channels that opened during repolarisation of previous action potential close. Threshold -60mv reached causes hyperpolarisation cyclic channels (HCN) channels to open which allows inward Na+ current. This causes increases in charge to -40mv at which point T-type Ca2+ channels open causing depolarisation to +20mv. At this point K+ channels open which causes depolarisation and returns negative charge. When hyperpolarisation threshold is reached the cycle begins again

80
Q

What effects does the autonomic nervous system have on pacemaker potential?

A

Catecholamines speed up HCN channels so threshold reached faster = increase HR
Ach slows HCN channels so threshold takes longer to reach so slows HR

81
Q

What is the main difference between nodal tissue and cardiac myocytes

A

HCN channels are present in nodal tissue but not in cardiac myocytes

82
Q

What are the differences between the action potential of cardiac myocytes and skeletal muscle?

A

Cardiac potential has Ca2+ leaving the cell to cause a plateau phase
Cardiac AP is 200-300ms (15x longer) whereas skeletal is shorter
Cardiac muscle has longer refractory period to prevent muscle fatigue and allow for adequate filling time

83
Q

Describe the resting cardiac myocyte membrane potential

A

Sarcolemma at rest is more permeable to K+ than Na+ so membrane potential is closer to K+ equilibrium potential (-90mv) than Na+ (+60mv)

84
Q

Describe the ionic basis of myocardial AP

A

AP arrives causing threshold to be breached so Na+ Channels open depolarising membrane to +20mv. At this point K+ channels open and Na+ channels close causing partial repolarisation. at same time as Na+ opened, L-type Ca2+ opened so when Na+ close, Ca2+ are opening at t-tubules causing Ca2+ inflow into cell which balances K+ leaving causing plateau phase at0mv. When L-type close, K+ continues to leave the cell causing repolarisation until resting potential is achieved

85
Q

Describe the role and properties of the SAN

A

Determines the rate the heart beats (60-100bpm) - resting membrane potential of -55to -60mv related to slow Na+ inflow which is not found anywhere else in the body which is closer to threshold so depolarises first

86
Q

how are cardiac myocytes electrically connected?

A

by gap junctions

87
Q

Define automaticity

A

Ability for spontaneous, rhythmic self contraction seen in the SAN due to the SAN potential drifting towards threshold for discharge

88
Q

What is the name of the pathway that connects the SAN and AVN?

A

Internodal pathway

89
Q

Why is it important that the conduction of AP’s through the AVN is slow?

A

Enables the atria to empty blood into the ventricles enabling atrial contraction to be completed before ventricular excitation occurs

90
Q

What Is the only connection between the atria and the ventricles

A

AVN and the bundle of His - part from this they are separated by a layer of nonconducting connective tissue

91
Q

What are the effects of sympathetic stimulation on the heart?

A

Increased HR (up to 180-250bpm (positively chronotropic)
Increased force of conception (Positively inotropic)
Increases Cardiac output (by up to 200%)

92
Q

What are the effects of parasympathetic stimulation of the heart?

A

Decreased HR (to 30-40bpm)(Negatively chronotropic)
Decreases force of contraction (Negatively inotropic)
Decreases cardiac output (by up to 50%)

93
Q

How does sympathetic stimulation cause increased HR?

A

Sympathetic postganglionic fibres innervate the entire heart
Adrenaline/Noradrenaline act on type 1 adrenoceptors to increase adenylyl cyclase which increases camp

94
Q

How does parasympathetic stimulation causes decreased HR?

A

Fibres transmitted by vagus nerve

Acetylcholine acts on M2 receptors to inhibit adenyl cyclase and reduce camp

95
Q

By what percentage will cardiac output decrease if sympathetic stimulation decreases?

A

up to 30%

96
Q

Describe the distribution blood volume in the circulatory system?

A 
Veins (64%)
Lungs (9%)
Capillaries (5%)
Larger arteries (7%)
Small arteries (8%)
Heart (diastole) (7%)
97
Q

What are the three types of capillary?

A

Continuous
Fenestrated
Discontinuous

98
Q

What is the name of vessels within the walls of larger blood vessels

A

Vasa Vasorum

99
Q

Describe the properties of veins

A

Have valves to ensure uni-directional flow of blood to the heart and are surrounded by skeletal muscle which contracts to increase vein pressure ensuring blood returns to the heart

100
Q

Describe the basic plan of circulation

A

Oxygenated blood is pumped from the left ventricle into the arterial system which carries it to capillaries where it provides oxygen to tissues and then removes waste products of metabolism such as CO2. Deoxygenated blood passes in the venous system returning to the right ventricle where it is pumped in the pulmonary arteries to the lungs. Here it is deoxygenated through proximity of capillary network to alveoli. Oxygenated blood returns to the left ventricle via the pulmonary veinns

101
Q

What are the three layers of blood vessels

A 
Tunica intima (endothelial cells)
Tunica media (smooth muscle)
Tunica Adventitia (Fibroblast layer)
102
Q

Describe the differences in the structure of arteries and veins

A

Tunica media in arteries is thicker than veins and veins posse valves to allow blood to only flow in one direction

103
Q

Describe the embryology of vasculature

A

Lateral mesoderm contains angioblasts which become the first blood vessels. Extraembryonic mesoderm forms blood islands which are haemoblasts surrounded by endothelial cells

104
Q

Describe the process of vasculogenesis

A

Occurs embryonic days 17-21 - endothelial cells of blood islands spread to form blood vessels around yolk sac, chorionic villus and stalk. By day 18, angioblasts migrate along centre of embryo to form vascular loop for embryonic heart to beat in. Angioblasts know if they will be arteries or veins due to endothelial surface markers. ie. arteries is Ephrin B2 and veins is ephb4

105
Q

Describe the process of angiogenesis in embryology of the circulatory system

A

Once the primitive vascular loop has formed, endothelial cells will proliferate and migrate to form new blood vessels. process is guided by molecules that attract or repel endothelial cells

106
Q

Name 2 angiogenic growth factors

A

Vascular endothelial growth factor

Angiopoietin 1 and 2

107
Q

Name 2 endothelial repulsive signals

A

Plexin/semaphoring signalling

Ephrin/Eph interactions

108
Q

Describe what happens to the 1st aortic arch during embryological development

A

1st arch becomes part of maxillary artery

109
Q

What conditions arise if development of aortic arches falters

A

Right sided or double sided aorta

Aortic co-arction

110
Q

Describe what happens to the 2nd aortic arch during development

A

Becomes the artery to stapedius

111
Q

What happens to the 3rd aortic arch during development

A

Portion of dorsal aorta between 3rd and 4th disappears

3rd becomes common carotid arteries and proximal internal carotid arteries

112
Q

Describe what happens to the left and right 4th aortic arches during development

A

Right dorsal loses connection to midline aorta and 6th arch but remains attached to right 4th arch - acquires 7th cervical intersegmental artery and grows into right upper limb to become right subclavian artery
Left 4th becomes arch of aorta

113
Q

What happens to the 5th aortic arch during development

A

There is no 5th aortic arch in humans

114
Q

What happens to the dorsal arch during development

A

Left dorsal aorta becomes descending aorta

115
Q

What happens to the left and right 6th aortic arches during development

A

right 6th becomes pulmonary trunk

Left 6th becomes ductus arteriosus

116
Q

Why do we need to control circulation?

A 
Maintain blood flow 
maintain arterial pressure 
Distribute blood flow 
Auto-regulate/homeostasis 
Function normally 
Prevent catastrophe 
Maladapt during disease
117
Q

Where is the principal site for resistance to vascular flow?

A

Arterioles as total arteriolar resistance = total peripheral resistance

118
Q

What is total peripheral resistance

A

Total resistance to flow in systemic blood vessels determined by arterioles - vascular smooth muscle determines arteriole radius - contraction of VSM decreases radius which increases resistance and decreases flow - relaxation of VSM increases radius, decreases resistance and increases resistance to flow - VSM never completely relaxes due to myogenic tone

119
Q

What is flow rate determined by?

A

Arteriolar resistance

Number of open pre-capillary sphincters

120
Q

Why is flow in the lymphatics uni-directional

A

Smooth muscle in the lymphatic vessels
Skeletal muscle pump
Respiratory pump

121
Q

Where is interstitial fluid returned to the cardiovascular system

A

Thoracic duct/left subclavian vein

122
Q

Write an equation for cardiac output

A

CO = SV x HR

123
Q

Write an equation for blood pressure

A

BP = CO x TPR

124
Q

Write an equation for pulse pressure

A

Systolic - diastolic

125
Q

Write an equation for mean arterial pressure

A

diastolic pressure + 1/3PP

126
Q

Write an equation for stroke volume

A

EDV - ESV

127
Q

Define Poiseuilles law

A

radius to the power of 4

128
Q

Define Ohms law

A

Pressure gradient/resistance

129
Q

Define Frank Starling Mechanism

A

Force of contraction is proportional to EDV - more the ventricle fills the harder it contracts

130
Q

Explain how the Frank Starling mechanism works

A

VR increases which increases EDV which increases preload which increases sarcomere stretch which increases force of contraction which increases stroke volume

131
Q

Which artery is used to measure blood pressure

A

Brachial artery

132
Q

What components influence blood flow

A 
Autoregulation 
Local mediators 
Humoral factors 
Baroreceptors 
Central (neural) control
133
Q

Define intrinsic auto regulation

A

When arterioles vasoconstrict or vasodilate in response to changes in resistance seemingly automatically in order to maintain constant blood flow

134
Q

Define myogenic auto regulation

A

When blood flow is increased and stretches vascular smooth muscle, the muscle automatically constricts until diameter is normalised or slightly reduced. When smooth muscle isn’t stretched as much due to low blood pressure the muscle relaxes and dilates in response

135
Q

Define hyperaemia

A

Increase in blood flow

136
Q

Define active hyperaemia

A

increase in blood flow when metabolic activity increases

137
Q

Define reactive hyperaemia

A

When an organ or tissue has its blood flow completely occluded a profound transient increase in blood flow occurs

138
Q

What are the two types of local humeral factors

A

Vasoconstrictors

Vasodilators

139
Q

What molecules are vasoconstrictors

A

Endothelin-1

Internal blood pressure (Myogenic contraction)

140
Q

What molecules are vasodilators

A

Hypoxia, adenosine, bradykinin, NO, K+, CO2, H+, tissue breakdown products

141
Q

What are the three heart sounds

A

lub = closure of AV valve
dub = close or aortic/pulmonary valves
third sound is blood rushing into left ventricle

142
Q

Define EDV

A

Volume of blood in the ventricle after contraction

143
Q

Define ESV

A

Volume of blood in the ventricle before contraction

144
Q

Define afterload

A

Pressure against which the heart must work to eject blood during systole

145
Q

What does ECG actually measure?

A

Measure of the currents generated in the extracellular fluid by the changes occurring simultaneously in many cardiac cells

146
Q

What are the 3 bipolar leads in ECG

A

Right arm
Left arm
Left leg

147
Q

What are the 3 unipolar leads?

A

aVR - electrical activity towards the right arm
aVL - Electrical activity towards the left arm
aVF - activity from the inferior

148
Q

What are the locations of the 6 unipolar chest leads

A 
V1 = 4th intercostal space 
V2 = 4th intercostal to the left 
V3 = mid clavicular line (5th intercostal)
V4 = 
V5 = anterior axillary line 
V6= mid axillary line
149
Q

How many leads are there on an ECG?

A

12 in total

150
Q

What does each of the ECG waveforms represent

A 
P = atrial depolarisation 
QRS = Ventricular depolarisation 
T = ventricular repolarisation
151
Q

Why is P wave smaller than QRS?

A

Because the atria have less muscle than the ventricles

152
Q

Are P waves and T waves positive or negative in a normal ECG

A

P waves are positive in every lead apart from aVR

T waves are positive in every lead apart from aVR and sometimes V1 and V2 depending on the trace

153
Q

What does the ST segment represent

A

Interval between ventricular depolarisation and repolarisation

154
Q

What would you see in an ECG of someone with sinus tachycardia

A

More frequent P waves >100bpm

155
Q

What would you see In an ECG of someone with sinus bradycardia

A

Less frequent P waves <60bpm

156
Q

What would you see on an ECG of someone with dextrocardia

A

multiple negative P waves

157
Q

Where can you hear the left ventricle

A

5th left intercostal space and mid clavicular line responsible for apex beat

158
Q

How long does the cardiac cycle last?

A

0.8s

159
Q

How long does systole last

A

0.3s

160
Q

How long does diastole last

A

0.5s

161
Q

What area of the heart does the right coronary artery supply

A

Inferior surface of the heart

162
Q

What area of the heart does the left anterior descending supply

A

Anterior LV wall

163
Q

What area of the heart does the left circumflex supply

A

Lateral LV wall

164
Q

What is the Normal duration of the PR interval

A

120-200ms

165
Q

What clinical condition is a short PR interval associated with?

A

Wolff-Parkinson-White Syndrome- accessory pathway

166
Q

What clinical condition does a long PR interval indicate?

A

1st degree heart block due to delayed AV conduction

167
Q

Which complex is normally inverted compared to the anterior and inferior leads

A

Lead aVR

168
Q

Which period is abnormally elevated during acute injury/infarction of a substantial myocardial territory

A

ST segment

169
Q

What is the normal duration of a QRS complex

A

Less than 120s

170
Q

What clinical condition is associated with a prolonged QRS (>120s)

A

Bundle branch block

171
Q

What is the pulmonary pressure during systole?

A

25mmHg

172
Q

What is pulmonary pressure during diastole

A

10mmHg

173
Q

What are the three basic events of the cardiac cycle

A

ventricular contraction
Ventricular relaxation
Ventricular filling

174
Q

Describe the events of ventricular systole (contraction)

A

left ventricular pressure rises to greater than left atrial pressure causing the mitral valve to close and producing the first heart sound. Isovolumetric contraction occurs where volume in ventricle remains the same but pressure increases. Pressure in ventricle exceeds aortic pressure so aortic and pulmonary valves open and maximal ejection from ventricles and arteries occurs but ventricles don’t completely empty

175
Q

Describe the events of ventricular diastole (relaxation)

A

Left ventricular pressure peaks and then decreases ‘phase of reduced ejection’ Left ventricular pressure falls below aortic presure so aortic valve closes (2nd heart sound). Both AV and aortic valves closed so isovolumetric relaxation occurs (when pressure decreases but not change in volume).

176
Q

Describe the events of ventricular filling

A

Ventricular pressure falls below atrial pressure. Atrial pressure due to venous return is enough to open AV valves allowing 80% of ventricular filling to occur. Diastasis occurs where pressure between atria and ventricles equalises so there is little no movement of blood (at this point AV node is delaying stimuli from SAN). Atrial booster causes atrial contraction which increases atrial pressure an enables active ventricular filling

177
Q

Define contractility (Inotropic State)

A

State of the heart that enables it to increase its contraction velocity to achieve a higher pressure - force of heart contraction that is independent of load

178
Q

Define elasticity

A

Ability of the myocardium to recover its normal shape after removal of systolic stress

179
Q

Define compliance

A

Relationship between change in stress and resultant strain - how easily the heart chamber expands when filled with blood volume

180
Q

Define diastolic distensibility

A

pressure required to fill ventricles to the same diastolic volume

181
Q

Where are the primary (arterial) baroreceptors located?

A

Carotid sinus and aortic arch

182
Q

Where are secondary baroreceptors located?

A

In veins, myocardium and pulmonary vessels

183
Q

Afferent feedback from baroreceptors is carried by which nerve

A

Glossopharyngeal (IX)

184
Q

efferent feedback from baroreceptors is carried by which nerve

A

Sympathetic ad Vagus (X)

185
Q

What Is the effect of high blood pressure on baroreceptors

A

High pressure stimulates baroreceptors (increased firing) which leads to inhibition of the pressor/vasoconstrictor centre in the medulla which causes increased PNS and decreased SNS leading to a fall in CO and TPR and a decrease in BP

186
Q

How does the pressor region increase blood pressure?

A 
Vasoconstriction 
Increase HR 
Increase SV
Increases CO 
Increase contractility
187
Q

How doe cardiopulmonary baroreceptors stimulation reduce blood pressure?

A

Decrease signals to the vasoconstrictor centre In the medulla leading to fall in BP and decrease the release of angiotensin, aldosterone and vasopressin resulting I fluid loss

188
Q

Which baroreceptors are key in the short term regulation of BP

A

Arterial baroreceptors

189
Q

Describe the role of central chemoreceptors in BP control

A

Chemosensitive regions in medulla

190
Q

Outline the short term control of blood pressure

A

Baroreceptors
Increased blood pressure leads in increased firing leading to increased PNS and decreased SNS which decreases CO and TPR leading to a fall in BP

191
Q

Outline the long term control of BP

A

Volume of blood

(Na+ and H2O) - Renin Angiotensin-aldoesterone and ADH

Phase 1 M (11 decks)

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