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Phase 1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the lifespan of erythrocytes?

A

100-120 days

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2
Q

What is the average size of erythrocytes?

A

-6.2-8.2um length
-2-2.5um wide

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3
Q

Where are erythrocytes found?

A

-Blood
-Bone marrow

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4
Q

What is the hormone that regulates the formation of erythrocytes?

A

-Erythropoietin
-Can use recombinant erythropoietin to boost RBC production

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5
Q

Why can erythrocytes not repair themselves?

A

-They are simple cells
-Anucleate and have no mitochondria

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6
Q

What is a young red blood cell known as?

A

Reticulocyte

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7
Q

What does a red blood cell consist of?

A

-Membrane enclosing
-Enzymes of glycolysis
-Haemoglobin

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8
Q

Why can haemoglobin not be allowed to travel in the blood by itself?

A

It would clog up the kidneys

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9
Q

What makes up haemoglobin?

A

-2 alpha chains
-2 beta chains
-4 haem groups
-Overall quaternary structure

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10
Q

What does haemoglobin do?
What does it transfer to in muscles?

A

Carries oxygen from the lungs to tissues where it transfers oxygen to myoglobin in muscles

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11
Q

What does oxygen bind to in haemoglobin?

A

Oxygen binds to Fe2+ in haem reversibly

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12
Q

What are the 4 major blood types?

A

-A
-B
-AB
-O

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13
Q

How many red blood cells are produced each minute and where?

A

2-3 million produced and released from the marrow every second

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14
Q

What is the shape of erythrocytes?

A

Biconcave

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15
Q

Approximately how many antigens do red blood cells have on their surface and how many are blood group antigens?

A

-Millions of antigens on their surface
-Several hundred are blood group antigens

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16
Q

Why is the ABO system so potently antigenic?

A

The ABO system is so potently antigenic because the corresponding antibodies to each antigen occur naturally

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17
Q

In what type of inheritance pattern are ABO antigens inherited?

A

Mendelian pattern

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18
Q

Name 3 facts about the inheritance of the ABO blood group:

A

-Each group has 25% chance of production from alleles
-Genes code for enzymes rather than for the sugar itself
-Another gene also codes for the sugar base the ‘A’ or the ‘B’

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19
Q

What makes up the H antigen?

A

-Glucose
-Galactose
-N-acetylglucosamine
-Galactose
-Fucose

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20
Q

How are the blood groups made from the H antigen and what are they called?

A

-A or B antigen is added onto the H antigen
-O blood group just has a H antigen
-“h” antigen has no H antigen
-Above called bombay

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21
Q

What is the approximate number of ABO antibodies at what ages?

A

-Infants <3 months will produce little to no antibodies (maternal prior to this)
-First true antibodies will be >3 months
-Maximal titre at 5-10 years
-Titre decreases with age

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22
Q

What are ABO antibodies a mixture of?

A

-IgM
-IgG

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23
Q

Which type of antibody are mainly for groups A and B?

A

IgM

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24
Q

Why are ABO antibodies able to react at 37 degrees?

A

They have a wide thermal range

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25
Q

For each blood group, name:
-Red blood cell type
-Antibodies in plasma
-Antigens on red blood cells

A
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26
Q

How many different rhesus (Rh) antigens are there?

A

Over 45 different Rh antigens

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27
Q

Where is the genetic locus of rhesus antigen?

A

Chromosome 1

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28
Q

Name 4 things about rhesus antigens genes:

A

-Co-dominant
-2 genes
-RHD for RhD
-RHCE for RhC and RhE

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29
Q

Are rhesus antigens immunogenic and why?

A

-Highly immunogenic
-High proportion of D neg people will form anti-D if exposed to D pos blood

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30
Q

What two reactions can RhD antigens cause?

A

-Haemolytic transfusion reactions
-Haemolytic disease of the fetus and newborn (HDFN)

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31
Q

What is HDFN?

A

-Haemolytic disease of foetus/newborn
-Rh D sensitisation most common cause
-Development of antibodies from sensitising event

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32
Q

What can HDFN cause?

A

Hydrops fetalis

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33
Q

How can you prevent HDFN?

A

-Detect mothers at risk
-Maternal-fetal free DNA
-Anti D prophylaxis

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34
Q

What is forward blood typing?

A

-Patient’s RBC
-Separate testing with anti-A and anti-B regent
-Testing with anti-D reagent

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35
Q

What is reverse blood typing?

A

-Patient’s plasma
-Test with A or B RBC
-Indirect Coomb’s test

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36
Q

What is an indirect anti-globulin test?

A

Testing donor RBC with recipient plasma to see if there will be a transfusion reaction

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37
Q

What is a direct Antiglobulin Test?

A

Detecting autoantibodies on the surface of RBC

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38
Q

What two types of blood can be given to a patient?

A

-Exact blood type
-Compatible blood type

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39
Q

When is DAT used?

A

-Patient with possible autoimmune haemolysis
-Transfusion reactions
-Detecting haemolysis due to fetal/maternal group incompatibility
-Can be positive for many other reasons - many not clinically significant

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40
Q

What blood type is this?

A

BD-

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41
Q

What blood type is this?

A

OD+

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42
Q

What ages of people can be first time donors?

A

17-65 year olds

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43
Q

Where are donors screened?

A

Donation centers

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44
Q

What factors are asked of donors on a pre-donor questionnaire and why?

A

-Highlight those at risk of infectious or transmissible disease
-Health, lifestyle, travel, medical history, medications

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45
Q

Whats the minimum body weight to donate blood?

A

Minimum 50kg

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46
Q

What is tested in selected donor bloods?

A

Test for anaemia in selected patients

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47
Q

What are exclusion criteria for donating blood?

A

-Temporary:
-Travel
-Tattoos
-Lifestyle
-Permanent:
-Certain infectious diseases
-Received a blood transfusion or organ-tissue transplant since 1980
-notified risk of vCJD

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48
Q

What are the two types of blood donation?

A

-Whole blood
-Apheresis - Blood is removed and separated externally and then the components not needed are returned

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49
Q

What are the mandatory tests for donated blood?

A

-Hep B
-HIV
-Hep C
-Syphylis
-Human T cell lymphotropic virus
-Groups and antibodies

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50
Q

What tests are done on some donated blood?

A

-CMV
-Malaria
-West nile virus
-Trypanosoma

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51
Q

What are the first 2 things done to donated blood?

A

-Whole blood donated into closed-system bags
-Blood spun to separate down to packed red cells/ buffy coat and plasma

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52
Q

What donors is plasma only kept from?

A

Male donors

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53
Q

What can plasma be frozen to make?

A

-FFP (fresh frozen plasma)
-Further processed to make cryoprecipitate

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54
Q

How are RBC processed?

A

-Red cells kept at ambient temperature for a short time
-Passed through a leucodepletion filter and resuspended in additive

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55
Q

What happens to buffy coats from donated blood?

A

Buffy coats pooled with donations of matching ABO and D type and then leucodepleted to make platelets

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56
Q

How are RBC stored and for how long?

A

-Stored at 4oC
-35 day shelf life
-Some units are irradiated to eliminate risk of transfusion-associated graft (lymphocyte in bone marrow) vs host disease)

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57
Q

What is an indication of RBC transfusion?

A

Severe anaemia (not purely iron deficiency)

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58
Q

What is the transfusion threshold for RBC?

A

-Haemoglobin <70g/dL or <80g/dL if symptomatic
-Transfuse 1 unit and re-check FBC (unless massive transfusion required)

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59
Q

What type of blood are available in certain areas of hospital (A&E, maternity)?

A

Emergency stocks of OD-

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60
Q

How many donations are most platelet units pooled from?

A

4 donations

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61
Q

How are platelets stored and for how long?

A

-Stored at 22oC
-Continuous agitation
-7 day shelf life if they are monitored for bacterial contamination

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62
Q

What are the indications for platelet transfusion?

A

-Thrombocytopenia and bleeding
-Severe thrombocytopenia <10 due to marrow failure (normal plt 150-450)

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63
Q

What is the platelet transfusion threshold?

A

-<10 x 109 if not bleeding and asymptomatic
-<30 x 109 if minor bleeding
-<50 x 109 if significant bleeding
-<100 x 109 if critical site bleeding (brain/eye)
-Part of a massive transfusion protocol
-ABO type still important as antibodies present in plasma still able to cause recipient red cell haemolysis

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64
Q

What is FFP derived from?

A

-Whole blood donations or apheresis
-From male donors only

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65
Q

What are exclusion criteria for FFP donation?

A

-Only patients born >1996
-Can only receive plasma from low vCJD risk (not UK plasma)

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66
Q

What is the different between single donor packs and pooled donor packs for FFP?

A

-Single donor have a variable amount of clotting factor
-Pooled versions can be more standardised

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67
Q

What are indications for FFP?

A

-Multiple clotting factor deficiencies and bleeding (DIC)
-Some single clotting factor iron deficiencies where a concentrate isn’t available

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68
Q

How is cryoprecipitate made?

A

-Thawing FFP to 4oC and skimming off fibrinogen rich layer

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69
Q

What is the dose and use for cryoprecipitate transfusion?

A

-Therapeutic dose is 2 packs each pooled from 5 donations of plasma
-Used in DIC with bleeding and massive transfusion

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70
Q

What is made from large pools of donor plasma?

A

Immunoglobulin (IVIg)

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71
Q

What is normal IVIg used for?

A

-Contains Ab to viruses common in the population
-Used predominantly in immune conditions such as ITP

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72
Q

What is specific IVIg used for?

A

-Chosen for selected patients
-Contains known high Ab levels to particular infections/conditions
-Anti-D immunoglobulins used in pregnancy
-VZV immunoglobulin in severe infection

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73
Q

When are granulocytes transfused?

A

-Very rarely as effectiveness is controversial
-Severely neutropenic patients with life-threatening bacterial infections
-Must be irradiated

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74
Q

Where do blood factor transfusions come from?

A

-Recombinant versions from the lab concentrated
-Reduces risk of viral or prion transmission

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75
Q

What are some examples of blood factor concentrates that are transfused?

A

-Factor VIII for severe haemophilia A
-Factor I (fibrinogen)
-Prothrombin complex concentrate
-Multiple factors
-Rapid reversal of warfarin

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76
Q

What 4 things ensure the safe delivery of blood?

A

-Patient identification checked
-2 sample rule (2 people take 2 samples at 2 different times)
-Hand-written patient details
-Blood selected and serologically cross-matched

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77
Q

What mistakes occur in blood transfusion?

A

-Most common is patient identification errors
-Wrong blood in wrong tube
-Less commonly - lob errors
-Blood transfusions delayed
-Too much blood transfused

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78
Q

How can blood transfusion be avoided?

A

-Optimise patients with planned surgical procedures pre-op
-Use of erythropoietin-stimulating drugs
-Renal failure and cancers
-Intra-operatively
-Cell salvage
-IV iron for severe iron deficiency
-Some patients may tolerate lower Hbs and if well not require transfusions at all

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79
Q

How safe are blood transfusion and why?

A

-Very safe
-Heavily regulated and monitored (SHOT,MHRA)

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80
Q

What are the potential risks of viral infections from blood transfusion of Hep B, Hep C and HIV?

A

-Hep B <1 in 1.2 million
-Hep C <1 in 7 million
-HIV <1 in 28 million

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81
Q

How is the risk of tranfusion-related GvHD reduced?

A

Risk reduced by leucodepletion and then even further by irradiation

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82
Q

Where are problems with blood transfusion most likely to occur?

A

After the blood leaves the lab - patient misidentification, over/under transfusion

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83
Q

What is the most serious haemolytic reaction?

A

-ABO incompatibility
-Rapid intravascular haemolysis
-Cytokine release
-Acute renal failure and shock
-Disseminated intravascular coagulation
-Can be rapidly fatal
-Can be acute or delayed (=>24 hours after transfusion)

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84
Q

What is the treatment for ABO incompatibility?

A

-Stop transfusion immediately
-Fluid resuscitate - A,B,C

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85
Q

What do haemolytic reactions need to be reported to?

A

SHOT

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86
Q

What type of contamination occurs most often with platelet transfusions?

A

Bacterial contamination

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87
Q

Symptoms of bacterial contamination of platelet transfusion:

A

-Occurs very soon after starting transfusion
-Fevers and rigors
-Hypotension
-Shock
-Inspection of the unit may show abnormal colouration/ cloudiness

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88
Q

What is TRALI?

A

-Transfusion-related acute lung injury

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89
Q

What causes TRALI?

A

-Ab in donor blood reacting with recipient pulmonary endothelium/neutrophils
-Inflammatory cells cause plasma to leak into alveolar spaces

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90
Q

What are symptoms of TRALI?

A

-SOB
-Cough productive of frothy sputum
-Hypotension
-Fevers

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91
Q

What is the treatment of TRALI?

A

Supportive treatment

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92
Q

What is TACO?

A

Transfusion-associated circulatory overload
-Acute or worsening pulmonary oedema within 6 hours of transfusion
-One of most common adverse events related to transfusion

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93
Q

Who is more at risk of TACO?

A

Older patients

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94
Q

What are symptoms of TACO?

A

-Respiratory distress
-Evidence of positive fluid balance
-Raised blood pressure

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95
Q

What is treatment of TACO?

A

-Careful assessment of transfusion need
-Limiting amount can help to avoid

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96
Q

Where are the erythropoietin gene and receptor?

A

-Chromosome 7
-EPOR - chromosome 19

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97
Q

What problems arise with RBC?

A

Anaemia causing hypoxia

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98
Q

What are the 2 types of anaemia?

A

-Hypo-regenerative - Bone marrow can’t produce enough RBC
-Hyper-regenerative - Increased destruction of RBC

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99
Q

What are the two groups of problems with RBC?

A

-Corpuscular - Inside RBC
-Extra-corpuscular - Outside RBC

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100
Q

What is polycythemia and what does it cause?

A

-Too many RBC
-Thrombosis
-Primary and secondary (caused by other things)

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101
Q

What corpuscular problems can occur with RBC?

A

-Membrane (spherocytosis, PNH)
-Haemoglobin (haemoglobinopathy)
-Enzymes (G6PD, PK)

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102
Q

What are extra-corpuscular problems with RBC?

A

-Reduced production
-B12
-Folate deficiency
-Increased destruction/loss
-Bleeding
-Haemolysis
-Auto or alloimmune
-Redistribution (hypersplenism)

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103
Q

What does this show?

A

Hb destruction product in urine

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104
Q

What can SCD cause and why?

A

-Rigid RBC
-Vaso-occlusion event
-Ischaemia
-Haemolysis
-Decreased NO

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105
Q

What can SCD cause in children?

A

Dactylitis

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106
Q

What chest condition can SCD cause?

A

-Acute chest disease
-Clinical or radiological evidence of consolidation

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107
Q

What are the symptoms of acute chest disease?

A

-Chest pain
-Fever
-Dyspnoea
-Cough

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108
Q

What is crizanlizumab?

A

-Binds to P-selectin
-Blocks its interaction with PSGL-1 on neutrophils and monocytes
-Prevents platelet aggregation, maintaining blood flow
-Minimize sickle-cell related pain crisis

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109
Q

What is the size of white blood cells?

A

-7-30um

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110
Q

What is the lifespan of WBC?

A

Hours/days/years

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111
Q

Where are WBC found?

A

-Thymus
-Bone marrow
-Blood
-Lymphatic organs

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112
Q

What cells make up the innate (non-specific immunity)?

A

-Neutrophil
-Eosinophil
-Basophil
-Macrophage
-Mast cell

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113
Q

What cells make up the adaptive (specific) immunity?

A

-CD4 T-helper cells
-CD8 T-cells
-B-cells
-DCa

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114
Q

What are humoral and cell-mediated immunity?

A
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115
Q

What is the lymphoid journey?

A
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116
Q

What are some WBC abnormalities?

A

-Neutrophil leukocytosis/ neutropenia
-Eosinophilia/ eosinopenia
-Basophilia
-Monocytosis/ monocytopenia
-Lymphocytosis/ lymphopenia
-Myeloid malignancies
-Lymphoid/plasma cell malignancies

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117
Q

When is cellular therapy/ CAR-T used?

A

When a patient would not respond to chemotherapy (failed 2 lines)

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118
Q

What is cellular therapy/ CAR-T?

A

-Take out patient’s T cells
-Genetically engineered molecule added to T-cells
-Genetically modified T-cells put back into patient which attack cancer

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119
Q

What is an allogenic bone graft?

A

-Chemotherapy destroys recipient’s bone marrow
-Graft from donor replaces stem cells
-Recipient immune system supressed

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120
Q

What tissues can an allogenic bone graft attack?

A

-Gut
-Skin
-Liver
-Lung
-(Acute or chronic)
-Can attack remaining malignant cells (+ve)

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121
Q

What can be given in addition to allogenic bone graft?

A

-Lymphocyte infusion from donor
-Kill donor haemopoiesis

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122
Q

What is BITE?

A

-Modify immune cells
-Link patient immune system to cancer

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123
Q

What is the term for the proportion of red blood cells in the blood?

A

-Haematocrit
-Normal is 0.45

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124
Q

What are the two phases of blood and their proportions?

A

-Cellular 45%
-fluid 55%

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125
Q

What proportion of the cellular component of blood is RBC?

A

RBC - 99%

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126
Q

What term describes the continous production of blood cells and platelets throughout life?

A

Haemopoiesis

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127
Q

In adults where does haemopoiesis occur?

A

Bone marrow

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128
Q

Where are reticulocytes found?

A

Bone marrow
-Adults - Axial skeleton
-Children - All bones

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129
Q

What is the normal haemoglobin level?

A

-12.5-15.5 g/dl
-Lower = anaemia (reduction in haemoglobin in blood)

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130
Q

How big are platelets?

A

2-5um

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131
Q

What is the average lifespan of a platelet?

A

7-10 days

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132
Q

What cells do platelets arise from and by what process?

A

-Megakaryocytes
-Exocytosis

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133
Q

where can you find platelets?

A

-Bone marrow
-Blood

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134
Q

What is the cytokine of platelets?

A

Thrombopoietin

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135
Q

What makes up a platelet?

A

-Plasma membrane
-Cytoskeleton
-Dense tubular system
-Secretory granules:
-Alpha (VWF, PF4, plasminogen)
-Dense (serotonine)
-Lysosome
-Prexisome

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136
Q

What are the 2 big groups of bleeding (clotting problems)?

A

-Platelet type (thrombocytopenia/thrombocytopathy)
-Haemophilia type

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137
Q

What are traits of PLT type bleeding?

A

-Hx of skin & mucosal bleeding (GI,GU)
-Early post-procedural bleeding
-Petechial rash
-VW disease, ITP, congenital thrombocytopathy
-Medication, liver disease, renal failure

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138
Q

What are traits of haemophilia bleeding?

A

-Hx of muscle/ joint bleeding, late post-procedural bleeding
-Large suffusions, haemotomas
-Haemophilia A,B,C
-Non-functioning coagulation cascade, platelet unaffected

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139
Q

What kind of rash do you see for PLT disorders and what do you watch for?

A

-Non-blanching petechial rash
-Watch signs of malignancy, liver disease, splenomegaly

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140
Q

What kind of rash do you see with haemophilia bleeding?

A

-Large suffusions
-Haematoma
-Likely haemophilia

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141
Q

What is the pathogenic classification of thrombocytopenia?

A

-Reduced production (reduced megakaryocytes)
-Congenital
-Acquired
-Increased destruction
-Immune (auto/allo)
-Increased megakaryocytes
-Altered redistribution
-Pseudothrombocytopenia

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142
Q

What is thrombocytopenia?

A

Low platelet count in the blood

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143
Q

What are congenital and acquired methods of thrombocytopenias?

A

Congenital:
-Adhesion - Bernard-Soulier (GPIb-IX-V), PLT type vWF(GPIb)
-Aggregation - Glanzman (GPIIb-IIIa)
-Secretion - Gray platelet (alpha granule), storage pool disease (dense granule)
-procoagulant activity

Acquired:
-Medication related
-Underlying disease

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144
Q

For risky procedures, what needs to be checked?

A

Platelet counts prior to procedure to see risk of internal bleeding

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145
Q

What are problems to tackle with some patients in terms of plasma?

A

-Liver cirrhosis patients are anticoagulating themselves - prone to bleed
-Procedures and anticoagulation are not safe in liver cirrhosis patients

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146
Q

What happens in normal haemostasis?

A

-Primary haemostasis
-Normal PLT count & function
-Coagulation cascade
-Normal procoagulants (PT, APTT) and anticoagulants
-(PC, PS, AT), normal FBG level and structure
-Termination
-Fibrinolysis
-Normal pro and antifibrinolytics

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147
Q

What happens in liver cirrhosis haemostasis?

A

-Primary haemostasis
-Low PLT count but vWF high
-ADAMTS13 very low, increased PLT activation to rebalance the low activation of platelets
-Coagulation cascade
-Low procoagulants (prolonged PT, APTT - except FVIII) and anticoagulants
-Low fibrinogen but prothrombotic FBG
-Termination
-Fibrinolysis
-Low pro and antifibrinolytics to rebalance the low procoagulants

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148
Q

Do liver cirrhosis patients bleed more?

A

-No
-They develop different systems to balance
-Most patients even with acute liver failure has normal haemostasis

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149
Q

What is under-used in liver cirrhosis patients?

A

-Thromboprophylaxis and anti-thrombotic treatment is underused which increases the risk of thrombosis

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150
Q

What is thrombocytosis?

A

High platelet count

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151
Q

What are the two type of thrombocytosis?

A

-Clonal
-Reactive

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152
Q

What are 4 causes of reactive thrombocytosis and some treatments?

A

-Bleeding/iron deficiency
-Infection/inflammation
-Hyposplenism
-Trauma surgery/haemolysis
-TREAT UNDERLYING CONDITION

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153
Q

What can cause clonal thrombocytosis and some treatments?

A

-MPN
-MDS
(JAK-2, CALR, MPL, BCR-ABL, 5q-)
-Increased risk of arterial or venous thrombosis
-TREATMENT: ANTIPLATELET, ANTICOAGULANTS, CYTOREDUCTION, VENESECTION, APHERESIS

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154
Q

What is blood plasma?

A

-Liquid component of blood that holds the cellular components of blood
-55% of blood volume

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155
Q

What is the composition of blood plasma?

A

-95% water
-6-8% proteins (fibrinogen, albumin, globulin)
-Glucose
-Coagulation factors
-Electrolytes (Na, Ca, Mg,HCO, CL)
-Hormones
-Carbon dioxide and oxygen

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156
Q

What is blood serum?

A

Blood plasma with clotting factors taken out

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157
Q

What are some plasma-derived blood products and their uses?

A

-FFP
-Human albumin
-Cryoprecipitate
-Fibrinogen
-Coagulation factor
-IVIG

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158
Q

What are some uses of plasma-derived blood products?

A

-Volume
-Massive transfusion packs
-Bleeding disorders
-Passive immunisation
-PEX
-Albumin replacement

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159
Q

What are the 4 main groups of bleeding disorders?

A

-Coagulation cascade
-PLT
-Vascular
-Inherited/acquired

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160
Q

When you asses someone for a procedure what clotting tests are used as standard?

A

-Prothrombin time (PT)
-Activated partial thromboplastin time (APTT)
(POOR TESTS)

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161
Q

In an ECG trace, what is the time value of:
-1 small square
-5 small squares
-1 big square
-5 big squares

A

-0.04s
-0.2s
-0.2s
-1s

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162
Q

What are the typical setting for an ECG trace?

A

-25mm/sec (speed)
-10mm/mV (voltage)

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163
Q

In an ECG trace, what is the voltage value of 1 big square?

A

0.5mV

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164
Q

What is a rhythm strip?

A

A copy of one of the leads for better examination

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165
Q

How can you calculate heart rate from an ECG?

A

-300/no. large squares in between each cycle
-Number of cycles every 10s x 6

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166
Q

What is normal resting heart rate and what are the names for high and low heart rate?

A

-60-100bpm
- <60 = bradycardia
- >100 tachycardia

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167
Q

What makes the ECG trace?

A

The summation of all of the action potentials across the heart

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168
Q

What do positive and negative deflections show in an ECG?

A

-Positive = current flowing towards the lead
-Negative= current flowing away from the lead
-0 = isoelectric point (no current)

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169
Q

What is the trigger point of the cardia cycle?

A

SAN

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170
Q

What is the fastest depolarising part of the heart?

A

-SAN
-Sets the pace of the heart

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171
Q

What conducts electricity from the atria to the ventricles and what is its function?

A

-AVN
-Has an in-built delay to allow the atria to fully empty their blood into the ventricles during their contraction

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172
Q

Where does electrical stimulation pass through after the AVN?

A

-3 bundles of His
-1 right
-2 left

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173
Q

What do purkinje fibres do

A

Spread the electrical activity throughout the ventricles

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174
Q

What is the P wave on the ECG?

A

-1st step
-SAN depolarises and spreads across atria
-Atrial depolarisation followed by atrial contraction

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175
Q

What phase of the cardia cycle don’t you see a wave for?

A

Atrial repolarisation

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176
Q

What does the isoelectric phase after the P wave show?

A

-Delay
-Current flows through the AVN

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177
Q

What does the QRS complex on an ECG show?

A

Ventricular depolarisation

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178
Q

What does the T wave on an ECG show?

A

Ventricular repolarisation

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179
Q

What is normal, regular PQRS complex referred as?

A

Sinus rhythm

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180
Q

What is it called when there is no P wave, can show as erratic?

A

-Atrial fibrillation
-Random atrial activity
-Random ventricular capture
-Irregularly irregular rhythm

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181
Q

What is it called when there if fluttering of atria (short circuit)?

A

-Atrial fluttering
-Organised atrial activity (300/min)
-Ventricular capture at ratio to atrial rate (2:1)
-Usually regular
-Can be irregular is ratios vary

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182
Q

What is the normal PR time interval and why?

A

-120-200ms
-(3 to 5 small squares)
-Small delay between atrial and ventricular contractions)

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183
Q

What can cause a long PR interval?

A

-Degeneration of conduction system
-1st heart block
-Delayed AV conduction
-Can lead to total heart block (stop)

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184
Q

What is the normal QRS time period?

A

-Less than 120ms
-(3 small squares)

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185
Q

What are the most common causes of prolonged QRS?

A

-Bundle branch block
-One of bundle of His working slowly
-Widening of the QRS due to different times of depolarisation of right and left ventricle

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186
Q

What is the normal QT time interval and why is it important?

A

-Men - 350-440ms
-Women - 250-460ms
-Measure of time of ventricular repolarisation
-Time from onset of QRS to end of T

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187
Q

What can prolong the QT interval?

A

-Congenital
-Drugs
-Predisposed to arrhythmia

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188
Q

How many leads are there on an ECG?

A

-12 lead
-Rhythm strip

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189
Q

What 3 leads are used on a 3 lead ECG?

A

I, II, III

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190
Q

What is the different between an electrode and a lead?

A

-Electrode:
-Physical connection to patients in order to measure potential at that point
-10 electrodes to record a 12 lead ECG
-Lead:
-Graphical representation of electrical activity at a particular vector
-Calculated by machine
-12 leads
-I-III, aVL, aVF, aVR, V1-6

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191
Q

When doing an ECG, where are the limb electrodes placed?

A

Arms and legs

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192
Q

What are the two types of ECG lead?

A

-Bipolar lead:
-Measures pd between two electrodes
-One electrode designated +ve and other -ve
-Unipolar lead:
-Measures pd between an electrode (+ve) and a combined reference electrode (-ve)
-Known as augmented leads

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193
Q

Which limb electrode is a neutral electrode?

A

-Right leg
-Not directly involved in ECG measurement

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194
Q

Describe lead I:

A

-RA = NEG
-LA = POS
-RA -> LA = POS deflection

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195
Q

Describe lead II:

A

-RA = NEG
-LL = POS
-RA -> LL = POS deflection

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196
Q

Describe lead III:

A

-LA = NEG
-LL = POS
-LA -> LL = POS deflection

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197
Q

Describe the triangle of leads I, II and III:

A
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198
Q

What angles are leads I-III?

A

-I = 0
-II = +60
-III = +120

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199
Q

At what angle should maximal degree of current flow in the heart?

A

-60 degrees
-Heart is offset at roughly this angle

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200
Q

What is the normal cardiac axis of conduction?

A

–30 - +90 in reference to lead I
-Away from this is axis deviation

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201
Q

What are the 3 unipolar limb leads and where are they?

A

-aVR
-aVL
-aVF

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202
Q

What are the angles of the 3 unipolar limb leads?

A

-aVR = -150
-aVL = -30
-aVF = +90

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203
Q

What is normal axis?

A

Lead I and II are both +ve

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204
Q

What does it show if lead I is +ve and lead II is -ve?

A

Left axis deviation

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205
Q

What does it show if II is +ve and I is -ve?

A

Right axis deviation

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206
Q

In what planes do leads I, II, III, aVR, aVF and aVL show?

A

Coronal (frontal) plane

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207
Q

In what plane do leads V1-6 show?

A

Transverse (horizontal) plane

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208
Q

What do the chest leads look at and which parts?

A

-Left ventricle
-V1+2 = Septal
-V3+4 = Anterior
-V5+6 = Lateral

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209
Q

What can problems in different chest leads tell us?

A

Which vessels of the heart are likely to be blocked that supply the corresponding part of the heart to that chest lead

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210
Q

What can an ST elevation signify?

A

Acute myocardial ischaemia

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211
Q

What do each sections that the leads represent correspond to in terms of vessels?

A

-Lateral - Circumflex artery
-Anterior - Left anterior descending artery
-Inferior - Right coronary artery

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212
Q

What portion of the heart do the three bipolar limb leads represent?

A

-I = lateral
-II = Inferior
-III = Inferior

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213
Q

What portion of the heart do the three unipolar limb leads correspond to?

A

-aVR = None
-aVL = lateral
-aVF = Inferior

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214
Q

What is the membrane of the heart muscle cell normally only permeable to?

A

K+

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215
Q

What is the membrane potential of a heart muscle cell usually determined by?

A

Ions that can cross the membrane

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216
Q

How is a negative membrane potential maintained in a heart muscle cell?

A

-K+ ions diffuse outwards (high to low concentration)
-Anions cannot follow
-Excess of anions inside the cell
-Generates negative potential inside the cell

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217
Q

What are the relative extra/intracellular concentrations of Na+, K+, Ca2+ and Cl-

A
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218
Q

How do myocyte membrane pumps maintain negative resting potential?

A

-K+ pumped IN cells
-Na+ and Ca2+ pumped OUT of cells
-Pumped against their concentration gradients
-This requires ATP for energy for active transport

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219
Q

How does this table show which ions will diffuse IN or OUT of the cell and which require active transport?

A

-Sodium and calcium have to be actively transported out of the myocyte
-Potassium would passively diffuse out of the myocyte

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220
Q

What does the graph of cardiac action potential look like?

A
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221
Q

What are the four stages of the cardiac action potential?

A

-4 = polarised (resting potential)
-0 = action potential/depolarisation
-1 = initial repolarisation
-2 = gradual repolarisation (plateau)
-3 = quick repolarisation
-4 repeats again (maintenance of resting potential)

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222
Q

What stage of the cardiac action potential is this?

A

Stage 4 - resting potential

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223
Q

What are the missing values and what does it represent?

A

-Stage 4
-Resting potential

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224
Q

What are the two protein transporters covered and what stage are they?

A

-Stage 4 (resting potential)

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225
Q

What stage of the cycle does this represent and what proteins are involved?

A

-Stage 0 (depolarisation)

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226
Q

What stage of the cycle does this represent?

A

-Stage 1 (initial repolarisation)

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227
Q

What stage of the cycle is happening here and what protein is involved?

A
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228
Q

What stage of the cycle does this represent?

A

-Stage 2 (plateau)

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229
Q

What is going on in this diagram and what protein is involved?

A

-Stage 2 (plateau)

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230
Q

What stage of the cycle does this represent?

A

-Stage 3 (repolarisation)

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231
Q

What is going on in this diagram and what protein is involved?

A
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232
Q
A
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233
Q
A
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234
Q
A
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235
Q
A
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236
Q
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237
Q
A
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238
Q

How does an ECG trace line up with the potential of myocytes?

A

QRS complex lines up with depolarisation

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239
Q

What is the wave of depolarisation of an action potential?

A

-Local depolarisation activates nearby Na+ channels (voltage gated)
-This causes a further influx of sodium ions
-This causes adjacent voltage gated sodium ions to open, causing further sodium influx

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240
Q

What does a wave of depolarisation cause?

A

The action potential to spread across the membrane

241
Q

What allows cell-to-cell conduction and propagation across the whole myocardium?

A

Gap junctions

242
Q

What does the influx of each ion look like for each part of the cardiac action potential?

243
Q

Why is the action potential of a myocyte different?

A

Contraction of the heart muscle requires appropriately timed delivery of Ca2+ into the cytoplasm

244
Q

Explain the first step of excitation-contraction coupling in terms of calcium and what stage of the polarisation cycle is corresponds to:

A

-Depolarisation of membrane
-Calcium influx through surface ion channels
-2

245
Q

Explain the second step of excitation-contraction coupling in terms of calcium:

A

-Amplification of calcium ions with NaCa transporter

246
Q

Explain the third step of excitation-contraction coupling in terms of calcium:

A

-Calcium ions induce the sarcoplasmic reticulum to release more calcium ions
-Concentration of calcium ions in the sarcoplasm is now high

247
Q

Briefly describe how Troponin-Tropomyosin-Actin complex induces muscles contraction:

A

-Calcium ions bind to troponin
-Conformational change of tropomyosin reveals myosin binding sites
-Myosin head cross-links with actin
-Myosin head pivots causing muscle contraction

248
Q

What is the difference between contraction of skeletal muscle and cardiac muscle?

A

-Cardiac muscle contraction lasts longer than skeletal muscle
-Up to 15 times longer
-Due to slow calcium channels
-Decreased permeability of membrane to potassium after action potential

249
Q

What are the 3 specialist conduction tissues in the heart?

A

-SAN
-AVN
-His/Purkinje system

250
Q

What are some specific points about the SAN action potential?

A

-Upsloping phase 4
-Less rapid phase 0
-No discernable phase 1/2

251
Q

What is the pattern of depolarisation at the SAN?

A

-Gradual depolarisation
-Until a threshold of roughly 35mV
-Then rapid depolarisation via calcium ion influx

252
Q

Place each of these on the diagram and what they stand for:
-If
-ICa,T
-ICa,L

A

-Funny current
-Transient calcium current
-Long lasting calcium current

253
Q

What 5 things affect the phase 4 slope?

A

-Autonomic tone
-Drugs
-Hypoxia
-Electrolytes
-Age

254
Q

What does the SAN phase 4 do?

A

-Drifts towards the threshold
-Steeper the drift, the faster the pacemaker

255
Q

What innervation affects the gradient of phase 4 drifting?

A

-Higher sympathetic innervation = Higher gradient
-Higher vagal = lower gradient

256
Q

What does increased sympathetic stimulation of the heart result in?
Specific terms?

A

-Increase heart rate (+ve chronotropic) (up to 180-250bpm)
-Increase force of contraction (+ve inotropic)
-Increase cardiac output (large, by up to 200%)

257
Q

What does parasympathetic stimulation of the heart result in?

A

-Decrease heart rate (-ve chronotropic)
-Decrease force of contraction (-ve inotropic)
-Decrease cardiac output

258
Q

What neurotransmitters control the heart rate and how do they work?

A

-Andrenaline and noradrenaline
-Type 1 beta adrenoreceptors
-Increases adenyl cyclase -> increases cAMP

259
Q

What does a decrease in sympathetic stimulation result in?

A

-Decreased heart rate
-Decreased force of contraction
-Decreased cardiac output (by up to 30%)

260
Q

What is parasympathetic stimulation of the heart controlled by (transmitters) and how does it work?

A

-Acetylcholine
-M2 receptors
-Inhibit adenyl cyclase -> reduced cAMP

261
Q

What does increased parasympathetic stimulation to the heart result in?

A

-Decreased heart rate (temporary pause or as low as 30-40bpm)
-Decreased force of contraction
-Decreased cardiac output (up to 50%)

262
Q

What does decreased parasympathetic stimulation to the heart result in?

A

increased heart rate

263
Q

What does the AVN do?

A

-Transmits cardia impulse between atria and ventricles
-Delays impulse
-Limits dangerous tachycardias

264
Q

How is the delayed impulse through the AVN achieved and why?

A

-Fewer gap junctions
-AV fibres are smaller than atrial fibres
-Allows atria to empty blood into ventricles
-Limits dangerous tachycardias

265
Q

Where is the fastest speed of transmission of impulse in the heart?

A

-Faster in specialised fibres
-Purkinje fibres - 4m/s

266
Q

What is the speed of impusle transmission in atrial and ventricular muscle and purkinje fibres?

A

-Atrial and ventricular muscle - 0.3 to 0.5m/s
-Purkinje fibres - 4m/s

267
Q

What is the purpose of the His-Purkinje system?

A

-Transmit impulse from AVN to ventricles
-Rapid conduction

268
Q

What is the purpose of rapid conduction in the His-Purkinje system and how is it achieved?

A

-Allow coordinated ventricular contraction
-Very large fibres
-High permeability at gap junctions

269
Q

How does the automacity of heart tissues change in the heart?

A

-Spontaneous discharge rate of heart muscle cells decrease down the heart
-SAN usually the fastest
-Ventricular myocardium the slowest
-This relates to the speed of repolarisation (3)

270
Q

What does hyperpolarisation mean and what is it part of?

A

-Forms the refractory period in between channel proteins being open and being closed but activatable
-Channel proteins are closed and in activatable

271
Q

What is the time period for the normal refractory period of a ventricle and is it greater or smaller for atria?

A

-Approx 0.25s
-Less for atria than ventricles

272
Q

What is the point of the refractory period in the heart muscle?

A

-Prevents excessively frequent contraction
-Allows adequate time for heart to fill

273
Q

What is the ARP and RRP?

A

-Absolute refractory period - No depolarisation can take place
-Relative refractory period - Some strong stimuli can cause action potentials
-Some sodium channels still inactivated
-Potassium channels still open
-Affected by heart rate

274
Q

What heart condition does a rise in extracellular potassium cause?

A

-Tachyarrhythmia
-Myocytes are less polarised
-Less polarised myocytes are more easily activated

275
Q

What will all new drugs undergo modelling for in terms of the heart?

A

-How they might interact with cardiac ion channels
-Will they affect QT interval?

276
Q

What do calcium channel blocker drugs do?

A

Prolong the refractory period of cardiac tissues

277
Q

What are some classes of drugs that can affect the cardiac action potential?

A

-Calcium channel blockers
-Potassium channel blockers
-Beta-blockers
-Sodium channel blockers

278
Q

What is long QT syndrome and what causes it?

A

-Abnormality of K+ channel causes loss of function
-Slower outward K+ current delays repolarisation
-This increases risk of Early Afterdepolarisations (EAD)
-Risk of syncope/ sudden cardiac arrest

279
Q

What are the 4 main components of myocardium?

A

-Contractile tissue
-Connective tissue
-Fibrous frame
-Specialised conductive system

280
Q

What does the pumping action of the heart depend on?

A

Interactions between contractile proteins in its muscular wall

281
Q

What do the interactions between contractile proteins in the heart muscle wall do?

A

-Transform chemical energy derived from ATP into mechanical work
-This moves blood under pressure from the great veins into the pulmonary artery, and from the pulmonary veins into the aorta

282
Q

What activates contractile proteins in the heart muscle wall?

A

Signalling process called excitation-contraction coupling

283
Q

When does excitation-contraction coupling begin and end?

A

-Begins when action potential depolarises the cell
-Ends when Ca2+ in the cytosol binds to the Ca2+ receptor of the contractile apparatus

284
Q

How does Ca2+ move into the cytosol?

A

-Passive movement
-Mediated by Ca2+ channels

285
Q

What happens chemically to cause the heart to relax?

A

Ion exchangers and pumps transport Ca2+ out of the cytosol against a concentration gradient

286
Q

What is plasma membrane’s role in mycoardium?

A

-Regulates excitation-contraction coupling and relaxation
-Separates the cytosol from extra-cellular space and sarcoplasmic reticulum

287
Q

What is a myocardial cell full of?

A

Cross-striated myofibrils

288
Q

What does myocardial metabolism rely on and why?

A

-Free fatty acids during aerobic respiration
-Efficient energy production

289
Q

What happens to myocardium during hypoxic conditions and why?

A

-No FFA metabolism
-Anaerobic metabolism of glucose ensues
-Produced energy sufficient to maintain survival of affected muscle without contraction

290
Q

What are myofibrils?

A

Contractile proteins arranged in a regular array of thick and thin filaments (organelle)

291
Q

What is the A band?

A

Region of the sarcomere occupied by the thick filament

292
Q

What is the I band?

A

-Area occupied only by thin filaments that extend towards the centre of the sarcomere from the Z lines
-Contains tropomyosin and troponins

293
Q

What is the Z line?

A

Bisects each I band

294
Q

What is a sarcomere?

A

Functional unit of the contractile apparatus

295
Q

What defines each sarcomere?

A

The region between a pair of Z lines

296
Q

What is inside the sarcomere?

A

-Two half I bands
-One A band

297
Q

What is the sarcoplasmic reticulum?

A

-Membrane network that surrounds the contractile proteins
-Sarcotubular networks at the centre of the sarcomere
-Subsarcolemmal cisternae - abut the T-tubules and the sarcolemma

298
Q

What are the T-tubules?

A

-Transverse tubular system
-Lined by a membrane continuous with the sarcolemma
-Lumen of the T-tubules carries extracellular space towards the centre of the myocardial cell

299
Q

What happens in the sarcolemma during contraction and what does it require?

A

-Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule
-Heads form cross-bridges that interact with actin

300
Q

When can myosin heads form cross-bridge interactions with actin?

A

-After linkage between calcium and TnC
-Deactivation of tropomyosin and TnI

301
Q

Describe myosin:

A

-2 heavy chains - also responsible for the dual heads
-4 light chains
-Heads perpendicular on thick filament at rest, bend towards centre of sarcomere during contraction
-Alpha and Beta myosin

302
Q

Describe actin:

A

-Globular protein
-Double stranded macromolecular helix (G)
-Both form the F actin

303
Q

Describe tropomyosin:

A

-Elongated molecule made of two helical peptide chains
-Occupies each longitudinal groove between the two actin strands
-regulates the interaction between the other three

304
Q

Describe troponin:

A

-I - With tropomyosin, inhibits actin and myosin interaction
-T - binds troponin complex to tropomyosin
-C - High affinity calcium binding sites, signalling contraction

305
Q

What happens when Ca2+ binds to troponin C?

A

Drives TnI away from actin, allowing its interaction with myosin

306
Q

How does the myosin head move during contraction?

A

Bends towards the M line (centre of sarcomere)

307
Q

What 3 things control the contractile cycle?

A

-Calcium ions
-Troponin phosphorylation
-Myosin ATPase

308
Q

Give the locations and salient properties of each protein in the contraction cycle:

309
Q

Why do we need control of the circulation (5)?

A

-Maintain blood flow
-Maintain arterial pressure
-Distribute blood flow
-Auto-regulate/homeostasis
-Function normally

310
Q

What are the 5 main components of circulation?

A

-Anatomy
-Blood
-Pressure
-Volume
-Flow

311
Q

What 4 organs/ structures take the most blood flow and in what proportion?

A

-Liver - 27%
-Kidneys - 22%
-Muscle = 155
-Brain - 14%

312
Q

What proportion of total blood flow does skin, bone and heart take?

A

-Skin - 6%
-Bone - 5%
-Heart - 4%

313
Q

What is the split of blood volume in the circulation?

314
Q

Describe arteries:

A

-Low resistance conduits
-Elastic
-Cushion systole
-Maintain blood flow to organs during diastole

315
Q

What are arterioles important in providing?

A

-Principal site of resistance to vascular flow
-TPR = total arteriolar resistance
-MAJOR role in determining arterial pressure
-Major role in distribution flow to organs/tissues

316
Q

What factors affect arteriole resistance?

A

-Local
-Neural
-Hormonal

317
Q

What determines radius of arterioles and how does it change?

A

-Vascular smooth muscle (VSM)
-VSM contract = lower radius = higher resistance = lower flow
-VSM relaxes = increase radius = lower resistance = higher flow
-(Vasoconstriction/vasodilation)

318
Q

What is myogenic tone?

A

The vascular smooth muscle is never completely relaxed

319
Q

Do capillaries have fast or slow flow and why?

A

-40,000km length
-Large area

320
Q

Why do capillaries have slow flow?

A

Allows time for nutrient/waste exchange

321
Q

What is flow in capillaries dependant on?

A

-Plasma or interstitial fluid flow determines the distribution of ECF between compartments
-Arteriolar resistance
-No. of open pre-capillary sphincters

322
Q

Describe veins:

A

-Compliant
-Low resistance conduits
-Capacitance vessels
-Valves aid venous return (VR) against gravity

323
Q

How much blood volume is in the veins and at what pressure?

A

-70% of blood volume
-10mmHg

324
Q

What aids return of blood through the venous vessels?

A

-Valves
-Skeletal muscle/ respiratory pump
-SNS mediated vasoconstriction maintains VR/VP

325
Q

Describe lymphatics:

A

-Fluid/protein excess filtered from capillaries
-Return of this interstitial fluid to CV system
-Thoracic duct, left SC vein

326
Q

What is the flow in lymphatics and what is it aided by?

A

-Uni-directional flow
-Aided by:
-Smooth muscle in lymphatic vessels
-Skeletal muscle pump
-Respiratory pump

327
Q

What is the equation for cardiac output (CO)?

A

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

328
Q

What is the equation for blood pressure (BP)?
Not systolic or diastolic pressures

A

Blood Pressure (BP) = CO x Total Peripheral Resistance (TPR)

329
Q

What is the equation for Pulse Pressure (PP)?

A

Pulse Pressure (PP) = Systolic pressure - Diastolic pressure

330
Q

What is the equation for Mean Arterial Pressure (MAP)?

A

Mean Arterial Pressure (MAP) = Diastolic pressure + 1/3PP

331
Q

What two equations govern flow?

A

-Ohm’s Law
-Poiseuille’s equation

332
Q

What is Ohm’s law for blood flow?

333
Q

What is poiseuille’s equation for blood flow?

A

-P = pressure
-u = viscosity
-L = length
-Q = flow rate
-R = radius

334
Q

What is the Frank-Starling mechanism?

A

-SV increases as EDV increases
-Due to length-tension relationship of muscle
-Higher EDV = more stretch = higher force of contraction
-Cardiac muscle at rest is NOT at optimum length

335
Q

Describe the Frank-Starling graph:

336
Q

How does venous return affect cardiac output and why?

A

-Frank-Starling relationship
-Higher venous return = higher EDV = higher SV = higher CO
-(Even if HR constant)

337
Q

What does the pressure/volume loop of LV function look like?

338
Q

What is important about venous return?

A

-Important beat to beat (FS mechanism)
-Blood volume is an important long term moderator

339
Q

What things can affect blood volume (4)?

A

-Na+, H2O
-Renin-Angiotensin-Aldosterone system
-ADH
-Adrenals and kidneys

340
Q

How do you calculate MAP from CO?

A

MAP = CO x TPR

341
Q

What is the main goal of circulation control and what does it rely on? Equation

A

-Maintain blood flow
-Needs pressure to push blood through peripheral resistance
-MAP = CO x TPR

342
Q

What is blood pressure?

A

Pressure of blood within and against arteries

343
Q

What are systolic and diastolic blood pressure?

A

-Systolic - Highest, when ventricles contract (100-150mmHg)
-Diastolic - Lowest, when ventricles relax (NOT 0 due to aortic valves and aortic elasticity, 60-90mmHg)

344
Q

What measures blood pressure and where?

A

-Sphygmomanometer
-Brachial artery
-Convenient. to compress
-Level of heart

345
Q

Where can you hear sounds when measuring blood pressure?

346
Q

What 5 things are involved in BP control?

A

-Autoregulation
-Local mediators
-Humural factors
-Baroreceptors
-Central (neural control)

347
Q

What is myogenic autoregulation?

A

-Stretch of vascular smooth muscle
-Contraction until diameter is normalised or slightly reduced

348
Q

What is autoregulation?

A

-Intrinsic ability of an organ
-Constant flow despite perfusion pressure changes

349
Q

Which vessels have better autoregulation properties?

A

-Renal/cerebral/coronary = Excellent
-Skeletal muscle/splanchnic = Moderate
-Cutaneous = Poor

350
Q

Does intrinsic or extrinsic control dominate brain and heart and why?

A

-Intrinsic control
-Maintain BF to vital organs

351
Q

Is intrinsic or extrinsic control more important to skin?

A

-Extrinsic
-BF is important in general vasocontrictor response and also responses ti temperature via extrinsic via hypothalamus

352
Q

What dominates control of skeletal muscle blood flow, intrinsic or extrinsic?

A

-BOTH
-At rest, vasoconstrictor is dominant (extrinsic)
-Upon exercise, intrinsic mechanisms predominate

353
Q

What are 2 local humoral factors that lead to vasoconstriction?

A

-Endothelin-1
-internal blood pressure (myogenic autoregulation)

354
Q

What are 5 things/groups that are local humoral factors that lead to vasodilation?

A

-Hypoxia
-Adenosine
-Bradykinin
-Small molecules (NO, K+, CO2, H+)
-Tissue breakdown products

355
Q

What is the main function of the endothelium?

A

-Control functions

356
Q

What are 3 substances that are produced by endothelium and what are their effects?

A

-Nitric Oxide (NO) = potent vasodilator
-Prostacyclin = potent vasodilator
-Endothelin = potent vasoconstrictor

357
Q

What is Furchgott’s experiment and what did it show?

A

-Two vessels, one without endothelium
-Expose to Acetyl choline
-One with endothelium dilates, other constricts
-Endothelium produces NO

358
Q

What are 3 circulating hormonal factors that produce vasoconstriction?

A

-Epinephrine (skin)
-Angiotensin II
-Vasopressin (ADH)

359
Q

What 2 circulating hormonal factors cause vasodilation?

A

-Epinephrine (muscle)
-Atrial natriuretic peptide

360
Q

What are baroreceptors?

A

Pressure sensing receptors

361
Q

Where are primary and secondary baroreceptors?

A

-Primary (Arterial) = carotid sinus & aortic arch
-Secondary = veins, myocardium, pulmonary vessels

362
Q

What are the afferent and efferent nerves for baroreceptors to and from the CNS to effectors?

A

-Afferent = Glossopharyngeal (IX)
-Efferents = Sympathetic and vagus (X)

363
Q

What is the firing rate of baroreceptors proportional to?

A

-MAP
-PP
-integrated in the medulla

364
Q

How does an increase in BP affect baroreceptors and what is the response?

A

Increased BP = increased firing = Increased PNS / Decreased SNS = decreased CO/TPR = Decreased BP

365
Q

what do arterial baroreceptors play a key role in?

A

-Short-term regulation of BP
-minute to minute control
-response to exercise
-haemorrhage

366
Q

What happens to arterial baroreceptors if arterial pressure deviates for norm for more than a few days?

A

-They adapt/reset to new baseline pressure
-e.g. in hypertension
-Major factor in long-term BP control is blood volume (H2O, Na+

367
Q

Where are cardiopulmonary baroreceptors?

A

-Atria
-Ventricles
-PA stretch

368
Q

What do cardiopulmonary barorecepetors release?

A

Atrial natriuretic hormone (ANP)

369
Q

What effects does ANP have (specific)?

A

-Lower activity of vasoconstrictor centre in medulla
-Lower BP
-Lower release of angiotensin, aldosterone and vasopressin (ADH), fluid loss
-Blood volume regulation

370
Q

What is the central neural control loop?

371
Q

What are the main 6 neural influences on medulla?

A

-Baroreceptors
-Chemoreceptors
-Hypothalamus
-Cerebral cortex
-Skin
-Changes in blood O2 and CO2

372
Q

How does the autonomic nervous system affect each organ via sympathetic and parasympathetic pathways?

373
Q

What do CV reflexes require? CNS

A

Hypothalamus and pons

374
Q

What does stimulation of anterior hypothalamus cause?

A

-Decreased Bp and HR
-Reverse happens with posterolateral hypothalamus

375
Q

What other organ is the hypothalamus important in regulating?

A

Regulation of skin blood flow in response to temperature

376
Q

What can the cerebral cortex affect in terms of cardiology?

A

-Blood flow and pressure
-Stimulation usually = increased vasoconstriction
-Emotion can increase vasodilation and depressor responses e.g. blushing, fainting
-Effects mediated by medulla but some directly

377
Q

Where are central chemoreceptors?

A

Chemosensitive regions in the medulla

378
Q

What do central chemoreceptors detect?

A

-High and low PaCO2
-High and low pH

379
Q

What does an increase or decrease in PaCO2 and pH detected by central chemoreceptors cause?

A

-Increase = Vasoconstriction = Increase in peripheral resistance = Increase in BP
-Decrease = Decrease medullary tonic activity = Decrease in BP
-pH reverse (more peripheral)

380
Q

What are the effects of PaO2 changes more detected by?

A

-Peripheral chemoreceptors
-In central chemoreceptors:
-Moderate decrease = vasoconstriction
-Severe decrease - general depression

381
Q

Show on the diagram how chemoreceptors play an important role in controlling respiration:

382
Q

What is short term BP control determined by?

A

-Baroreceptors
-Increase BP = Increase firing = Increased PNS/Decreased SNS = Lower CO/TPR = Lower BP

383
Q

What is long term BP control determined by?

A

-Volume of blood
-Na+, H2O, RAAS and ADH

384
Q

Where are the key central effectors of blood pressure?

A

-Peripheral
-Blood vessels (vasoconstriction & vasodilation - affects TPR)
-Heart (rate & contractility: CO = HR x SV)
-Kidney (fluid balance - longer term control)

385
Q

Desribe fainting:

386
Q

Describe blood loss:

387
Q

Describe Orthostatic hypotension:

388
Q

Describe POTS:

389
Q

Describe Heart failure:

390
Q

Describe the minute by minute homeostatic feedback loop:

391
Q

What are the basic 3 events of the cardiac cycle?

A

-LV contraction
-LV relaxation
-LV filling

392
Q

What are the two phases of LV contraction?

A

-Isovolumetric contraction (b)
-Maximal ejection (c)

393
Q

What are the 5 phases of LV relaxation?

A

-Start of relaxation and reduced ejection (d)
-Isovolumetric relaxation (e)
-Rapid LV filling and LV suction (f)
-Slow LV filling (diastasis) (g)
-Atrial booster (a)

394
Q

Name the 7 steps of ventricular systole:

A

-Wave of depolarisation arrives
-opens the L-calcium tubule (R peak on ECG)
-Ca2+ arrive at contractile proteins
-LVp rises > LAp
-MV closes - M1 of 1st HS
-LVp rises (isovolumetric contraction) >Aop
-AoV opens and ejection starts

395
Q

Name the 6 steps of ventricular diastole:

A

-LVp peaks then decreases
-Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR
-“phase of reduced ejection”
-Ao flow is maintained by aortic distensibility
-LVp < Aop, Ao valve shuts, A2 of the 2nd HS
-“isovolumetric relaxation”, then MV opens

396
Q

What is distensibility?

A

-A measure of elasticity
-How well something (vessel) can stretch under pressure

397
Q

Name the 4 steps of ventricular filling:

A

-LVp < LAp, MV opens, Rapid filling starts (E)
-Ventricular suction (active diastolic relaxation), may also contribute to E filling
-Diastasis (seperation): LVp = LAp, filling temporarily stops
-Filling is renewed when A contraction (booster) raises LAp creating a pressure gradient

398
Q

What is the physiological vs cardiological systole?

A

-Physiological:
-Isovolumetric contraction
-Maximal ejection
-Cardiological:
-From M1 to A2
-Only part of isovolumteric contraction (includes maximal and reduced ejection phases)

399
Q

What is the physiological vs cardiological diastole?

A

-Physiological:
-Reduced ejection
-Isovolumetric relaxation
-Filling phase
-Cardiological:
-A2 to M1 interval (filling phases included)

400
Q

What is preload?

A

The load present before LV contraction has started

401
Q

What is afterload?

A

The resistance the left ventricle must overcome to circulate blood

402
Q

What is Starling’s Law of 1918?

A

Within physiological limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction

403
Q

What is left ventricular filling pressure?

A

-Difference between the LAp and LV diastolic pressure
-The relationship reaches a plateau

404
Q

What is the force-length interaction that relates to Starling’s Law?

A

-Force produced by the skeletal muscle declines when the sarcomere is less than the optimal length (Actin’s projection from Z disc “1um” X 2)
-In the cardiac sarcomere, at 80% of the optimal length, only 10% of maximal force is produced

405
Q

At what length must the cardiac sarcomere operate at?

A

-Must function near the upper limit of their maximal length
-Lmax = 2.2um

406
Q

What affects the physiological LV changes?

A

When the sarcomere lengthens from 85% of Lmax to Lmax

407
Q

What kind of relationship does length-dependant activation have?

A

Steep relationship

408
Q

What is it called when the heart increases the pressure even when volume is fixed?

A

Isovolumetric contraction

409
Q

What does increased diastolic heart volume cause and through what system?

A

-Increased velocity and force of contraction
-Isovolumetric contraction + Frank-Starling
-Large force
-+ve inotropic effect

410
Q

What is contractility?

A

-Inotropic state
-State of the heart which enables it to increase its contraction velocity
-Higher contractility = higher pressure achieved (independent of load)

411
Q

What is elasticity?

A

Myocardial ability to recover its normal shape after removal of systolic stress

412
Q

What is compliance?

A

The relationship between the change in stress and the resultant strain - dP/dV

413
Q

What is diastolic distensibility?

A

Pressure required to fill the ventricles to the same diastolic volume

414
Q

What reflects the contractility?

A

Pressure-volume loop in the end-systolic pressure volume relationship

415
Q

What reflects compliance?

A

End diastolic pressure volume relationship

416
Q

What are the effects of pressure vs volume work on the LV?

417
Q

When are isometric conditions found in the heart?

A

Isovolumetric contraction

418
Q

When would you find isotonic contraction in the heart?

A

-NEVER
-Isotonic contraction is totally impossible in the heart

419
Q

Describe the phases of the cardiac cycle hidden in this diagram:

420
Q

Describe the ECG hidden in this diagram:

421
Q

Describe the heart sounds hidden in this diagram:

422
Q

Describe the pressures hidden in this diagram:

423
Q

Be able to recall all of these labels:

424
Q

What is gastrulation?

A

Mass movement and invagination of the blastula to form three layers: ectoderm, mesoderm (middle) and endoderm

425
Q

What comes from the ectoderm (outside)?

A

-Skin
-Nervous system
-Neural crest (contributes to cardiac outflow, coronary arteries)

426
Q

What comes from the mesoderm (middle)?

A

-All types of muscle
-Most system
-Kidneys
-Blood
-Bone

427
Q

What comes from the endoderm?

A

-GI tract (inc liver, pancreas, but not smooth muscle)
-Endocrine organs

428
Q

What developmental region does most of the cardiovascular system derive from?

A

-Cells which were situated in the mesoderm
-Blood, heart, smooth muscle, endothelium

429
Q

Where does a small proportion of the cardiovascular system derive from developmentally?

A

Cardiac neural crest cells from the ectoderm

430
Q

What 3 cardiac milestones are significant in cardiovascular developmental biology?

A

-Basic tube
-Single loop
-Double loop septated heart

431
Q

What is an example of a condition related to what developmental region the cardiovascular system arises from?

A

-Heart and blood vessels sometimes try to turn into bone
-Both derived from the mesoderm

432
Q

Which colours represent the first heart field and second heart field and what day does it form?

A

-First heart field = Red
-Second heart field = Yellow
-Day 15

433
Q

What is the function of the first heart field?

A

Generates a scaffold which is added to by the second heart field and cardiac neural crest

434
Q

What do the First heart field and Second heart field go on to form?

A

-FHF = Future left ventricle
-SHF = Outflow tract, future right ventricle, atria

435
Q

What happens by day 21 of heart development?

A

-Single ventricle
-Inflow tract into 2 structures that will become right and left atria
-Conus trunk (truncus arteriosus)

436
Q

What day of development is this?
Label it:

437
Q

What happens by day 28?

A

-More looped structure
-R atrium + Left atrium
-R ventricle + L ventricle
-Conus trunk (truncus arteriosus)

438
Q

What day of heart development is this?
label it:

439
Q

What happens by day 50 of heart development?

A

-Fully developed heart

440
Q

What day of heart development is this?

441
Q

What is a gene?

A

DNA which when expressed is transcribed into RNA which is translated into protein with a function

442
Q

What is a transcription factor?

A

A type of protein which when expressed “turns on/off” many other gene(s) expression: master regulators of complex processes

443
Q

What are some examples of cardiac transcription factors?

A

-NKx2.5
-GATA
-Hand
-Tbx
MEF2
-Pitx2
Fog-1

444
Q

How are transcription factors expressed?

A

They are expressed in a tissue-specific manner

445
Q

What process accounts for increasing complexity of development through evolution?

A

-As organisms evolve, gene duplication occurs sporadically (from single gene to entire genome)
-Each copy of each gene can evolve separately into different (but related) genes

446
Q

What are the 3 main stages of cardiac formation?

A

-Formation of the primitive heart tube
-Cardiac looping
-Cardiac septation

447
Q

Describe the first step of the formation of the primitive heart tube:

A

-Formed from cells that form a horseshoe shape called the cardiogenc region

448
Q

Describe the second step of the formation of the primitive heart tube:

A

-Day 19
-Two endocardial tubes form
-Two tubes will fuse to form a single, primitive heart tube

449
Q

What is the third step of the formation of the primitive heart tube?

A

-Day 21
-Embryo undergoes lateral folding
-Two endocardial tubes have fused to form. a single heart tube

450
Q

Label each part of the primitive heart tube and what they form:

451
Q

What does the Bulbis Cordis form?

A

-Most of the right ventricle
-Parts of. the outflow tract for aorta and pulmonary trunk

452
Q

What does the primitive ventricle form?

A

Most of the left ventricle

453
Q

What does the primitive atrium form?

A

Anterior parts of the right and left atria

454
Q

What does the sinus venosus form?

A

-Superior vena cava
-Part of the right atrium
-Splits between right and left horn

455
Q

What does overexpression of Nkx2.5 cause?

A

Increases heart size
(Fish heart)

456
Q

What does preventing GATA4 transcription cause?

A

-Induces cardia bifida
-Failure of the endocardial tubes to fuse
(Chick heart)

457
Q

Describe the first part of cardiac looping:

A

-Tubus cordis moves inferiorly, anteriorly and to the embryos right

458
Q

By what day of embryo development does the heart start to beat?

459
Q

Describe the second stage. of cardiac looping:

A

The primitive ventricle moves to the embryo’s left side simultaneous to the movement of the bulbis cordis

460
Q

Describe the third stage of cardiac looping:

A

Primitive atrium and sinus venosus move superiorly and posteriorly
-Sinus venosus is posterior ti the primitive atrium

461
Q

Describe the general altogether movement during cardiac looping:

462
Q

What must all vertebrae hearts have?

A

Leftward ventricle

463
Q

What are many mutations associated with in terms of heart positioning?

A

-Improper left-right positioning
-Kartagener’s syndrome

464
Q

What is involved in determining left and right sides of the heart?

A

-The node secretes nodal, which circulates to the left due to ciliary movement
-A cascade of transcription factors transduce looping

465
Q

What is present in the heart at the end of cardiac looping?

A

-One common atrium
-One common ventricle
-Joined by the atrioventricular canal
-Future superior vena cava

466
Q

How does blood move through the primitive heart?

467
Q

What is the first part of cardiac septation?

A

-Masses of tissue called endocardial cushions grow from the sides of the atrioventricular canal
-Position the canal into two separate openings as they fuse
-Push the atrioventricular canal to the right
-Now the right and left atrioventricular canals

468
Q

Where do the 2 endocardial cushions grow?

469
Q

What will the right and left atrioventricular canals go on to form?

A

Right and left atrioventricular openings of the heart

470
Q

How will blood move through the heart after cardiac septation?

A

-Through primative atrium
-Through both atrioventricular canals
-Through primitive ventricle
-Through trunucs arteriosus

471
Q

What is the importance of platelets in disease?

A

-Thrombosis
-Formation of a clot (thrombus) inside a blood vessel
-Platelets have central role in arterial thombosis
-Heart attack
-Stroke
-Sudden death

472
Q

What kind of medication can be lifesaving in terms of thrombus?

A

Antiplatelet medication

473
Q

Label this diagram:

474
Q

What are atherogenesis and atherothrombosis?

A

-Build up of fatty plaque
-Eventual damage to endothelial wall and occlusive thrombus forming

475
Q

Label this diagram and name the processes:

A

Atherogenesis and atherothrombosis

476
Q

What does activation of platelets cause and why?

A

-Shape change
-Smooth discoid to spiculated + pseudopodia
-Increased surface area
-increased possibility of cell-to-cell interactions

477
Q

Where are glycoprotein IIb/IIIa receptors and what causes a change?

A

-Surface of platelet
-50,000-100,000 on resting platelet
-Platelet activation:
-Increases number of receptors
-Increases receptor affinity for fibrinogen

478
Q

What causes platelets to aggregate?

A

Fibrinogen links glycoprotein IIb/IIIa receptors, binding platelets together

479
Q

What happens after atherosclerotic plaque rupture?

A

Platelets adhere to damaged vessel wall

480
Q

How do platelets adhere to damaged vessel walls and what happens?

A

-Collagen receptors on platelets bind to subendothelial collagen which is exposed
-GPIIb/IIIa also binds von Willebrand factor (VWF) which is attached to collagen
-Soluble agonists are also released and activate platelets

481
Q

What is the first stage of platelet plugging?

A

Endothelial damage

482
Q

What is the second step of platelet plug formation?

A

Initial adhesion vis GPIB/VWF

483
Q

What is the third step of platelet plug formation?

A

-Rolling GPIb/VWF
-alpha2beta1/collagen adhesion
-Platelets are activated

484
Q

What is the fourth step of platelet plug formation

A

-Stable adhesion
-Activation/aggregation
-GPVI GPIIb/IIIa

485
Q

Binding of what platelet receptor to what causes platelet activation?

A

GPVI to collagen

486
Q

What does platelet adhesion look like?

A

Due to all receptors adhering to collagen

487
Q

What agonists can cause activation of platelets?

A

-ADP -> P2Y1
-Collagen -> GPVI
-Thromboxane A2 -> TPalpha
-Thrombin -> PAR1 + PAR 4

488
Q

Label the diagram:

489
Q

What does platelet activation lead to (3)?

A

-Shape change
-Cross-linking of GPIIb/IIIa
-Platelet aggregation

490
Q

What inhibits an activation pathway of platelets and how?

A

-Aspirin
-Prevents production and release of Thromboxane A2 when collagen binds to GPVI

491
Q

Where is the apex beat?

A

-Left 5th intercostal space
-Mid-clavicular line

492
Q

What defines the right heart border?

A

-SVC
-Right atrium

493
Q

What defines the left heart border?

A

-Aortic knuckle
-Left pulmonary artery
-Left atrial appendage
-Left ventricle

494
Q

What defines the anterior border of the heart?

A

Mainly right ventricle

495
Q

What defines the posterior border of the heart?

A

Mainly left atrium and pulmonary veins

496
Q

What is the mediastinum?

A

The area in between the right and left pleura

497
Q

How is the mediastinum divided?

A

-Plane between sternal angle and T4/5 divides superior and inferior mediastinum
-Pericardium divides anterior, middle and posterior mediastinum

498
Q

What does the pericardium consist of?

A

-Fibrous (parietal) layer
-Visceral layer

499
Q

What is inbetween the two pericardial layers?

A

-Pericardial space
-Potential space

500
Q

What’s it called when there is a rapid collection of pericardial fluid and what does it cause?

A

-Cardiac tamponade
-Restricts and impairs filling

501
Q

What allows drainage of pericardial fluid and to where?

A

-Pleural reflection
-From the left of the xiphisternum

502
Q

What valves are intrinsic to the ventricles?

A

-Atrioventricular valves
-Tricuspid and mitral

503
Q

What do disorders of the ventricle often affect?

A

Disorders of the ventricle often affect function of the relevant atrioventricular valve

504
Q

What connect to the atrioventricular valves and by what?

A

-Papillary muscles
-Connect via chordae tendinae

505
Q

What valves are an intrinsic part of the great vessels?

A

-Semilunar valves
-Aortic and pulmonary

506
Q

What do disorders of the aorta or pulmonary artery often affect?

A

Function of their respective valve

507
Q

Does arterial blood always leave the heart fully oxygenated?

508
Q

What is blood leaving the heart called?

A

-Arterial blood
-Not always fully oxygenated

509
Q

What is blood returning to the heart called?

A

-Venous blood
-Not always deoxygenated

510
Q

What artery carries deoxygenated blood from the heart?

A

Pulmonary artery

511
Q

What veins carry oxygenated blood back to the heart?

A

Pulmonary veins

512
Q

What are COX enzymes?

A

Cyclooxygenase 1 and 2

513
Q

What processes do COX-1 and COX-2 catalyse as enzymes and where?

A

-Arachidonic Acid -> Prostaglandin H2
-In both platelets (COX-1) and endothelial cells (COX-1 and COX-2)

514
Q

What is prostaglandin H2 converted into and in what cells?

A

-In platelets:
-Prostaglandin H2 -> Thromboxane A2
-In endothelial cells:
-Prostaglandin H2 -> Prostacylcin

515
Q

What is the effect of Thromboxane A2 and Prostacylin production?

A

-Thromboxane A2 amplifies:
-Platelet aggregation
-Vasoconstriction
-Prostacyclin inhibits above two processes

516
Q

Label this diagram:
What does it show?

A

Thromboxane A2 amplification pathway

517
Q

How does low and high dose aspirin work?

A

-Low dose - inhibits COX-1
-High dose - inhibits COX-1 & COX-2
-Preferential effect on platelets as not much reaches endothelial cells
-Inhibits platelets activation

518
Q

What proteins are linked to P2Y1 and P2Y12 receptors?

A

-P2Y1 - Gq protein
-P2Y12 - Gi protein

519
Q

What role does ATP have outside the cell?

A

Signalling molecule

520
Q

What is the first receptor that ADP binds to on the platelet and what amplification does it cause?

A

-Binds to P2Y1
-Activates it
-Amplifies Phospholipase C pathway
-Triggers release of Ca2+ from intracellular stores
-Activates protein kinase C

521
Q

What does activation of Protein kinase C and release of intracellular Ca2+ cause?

A

-Initiation of aggregation
-Shape change (spiculated)

522
Q

Label this diagram:
What does it show?

A

ADP amplification pathway P2Y1

523
Q

What is the second type of receptor that ADP binds to on the platelet and what does it cause?

A

-P2Y12 protein
-Activates it
-Inhibits Adenylate cyclase
-Inhibits formation of Cyclic AMP (cAMP) from adenylate cyclase
-Activates PI3 kinase

524
Q

What do inhibition of adenylate cyclase and amplification of PI3 kinase cause?

A

-Amplification of:
-Platelet activation
-Aggregation
-Granule release

525
Q

Label this diagram:
What does it show?

A

ADP amplification pathway P2Y12

526
Q

Explain ADP-induced platelet aggregation:

A

-ADP binds to P2Y1 and activates it
-This induces platelet activation
-This activates GPIIb/IIIa
-Fibrinogen can bind to GPIIb/IIIa and cause cross-linking platelet aggregation

527
Q

Explain ADP activation amplification:

A

-ADP binds to P2Y12
-This amplifies the activation of platelets through P2Y1
-Sustains platelet activation and aggregation

528
Q

Where does most of the ADP involved in platelet activation and amplification come from?

A

-Dense granules
-Released from the cell surface to bind to P2Y receptors

529
Q

How does GPIIb/IIIa affect platelet activation?

A

Amplifies the platelet activation response

530
Q

What receptor does thrombin bind to and how is it generated?

A

-Thrombin is generated through the coagulation cascade
-Binds to PAR-1 receptor
-Can bind to PAR-4

531
Q

What does thrombin binding to PAR-1 cause?

A

-Release of ADP through dense granules
-ADP binding to P2Y1 activating platelets
-ADP binding to P2Y12 further amplifying activation

532
Q

What is platelet procoagulant activity?

A

Platelets provide a surface for proteins involved in coagulation to assimilate on

533
Q

What is the resting state of platelet procoagulant activity?

A

-Aminophospholipids only on inner surface of bi-layer
-Maintained by protein called translocase

534
Q

What does activation of PAR-1 cause?

A

-Thrombin activates PAR-1
-Amplification of Ca2+ release from intracellular stores

535
Q

What is the effect of an increase of intracellular Ca2+ in a platelet?

A

-Negative inhibition of translocase
-Positive amplification of scramblase
-Scramblase causes aminophospholipids to move to the extra-cellular side of membrane

536
Q

What happens when aminophospholipids are expressed on the extracellular side of the platelet membrane?

A

-Allows assembly of proteins of the coagulation cascade
-Va and Xa can bind together to form prothrombinase
-This complex can then convert prothrombin into thrombin

537
Q

What does thrombin amplify the production of?

A

Amplifies its own production

538
Q

What forms as a result of the relationship between platelets and the coagulation cascade?

A

-Platelet-fibrin clots
-Fibrin at the centre of this relationship

539
Q

What is released by the endothelium in the first step in the fibrinolytic system and what does it cause?

A

-tPA - tissue plasminogen activator
-Converts plasminogen into plasmin

540
Q

What does plasmin do in the fibrinolytic system?

A

Converts fibrin into fibrin degradation products

541
Q

What inhibitor acts on tPA?

542
Q

What inhibitor acts on plasmin?

A

Antiplasmin (plasmin, antiplasmin complex)

543
Q

What do alpha granules contain?

A

-Coagulation factors
-Inflammatory mediators

544
Q

What relationship do platelets have with leuokocytes?

A

-Pro-inflammatory and prothrombotic interactions with leukocytes
-Release inflammatory mediators from alpha granules
-Through P-selectin

545
Q

What is P-selectin and what does it do?

A

-Contained in alpha granules
-When released, expressed on platelet surface
-Leukocytes have counter-receptor called PSGL-1
-Binding of two receptors
-Increases inflammatory response

546
Q

Describe the thickness of each heart chamber:

A

-Left ventricle
-Systemic ventricle
-Right ventricle has a thin muscular wall
-Atria are thin walled

547
Q

How many pulmonary veins are there and where do they drain into?

A

-Four pulmonary veins (usually)
-Drain into the left atrium

548
Q

What drains blood from the heart muscle and where into?

A

-Coronary sinus
-Right atrium

549
Q

What are the two sections of the right atrium?

A

-Smooth (from sinus venosus)
-Trabeculated (from original atrium)

550
Q

What separates the smooth and trabeculated portions of the right atrium?

A

Crista terminalis

551
Q

What is the fossa ovalis a remnant of?

A

Remains of the foramen ovale which was present in foetal life

552
Q

How do cardiac muscle cells join?

A

-Cross-link
-Join at intercalated discs

553
Q

Where do coronary arteries stem from and what do they supply?

A

-Arise from the aortic root sinuses
-Supply the heart itself

554
Q

Are coronary arteries accessible by surgeons and why?

A

-Yes (bypass surgery)
-They are epicardial

555
Q

What are the names of the main coronary arteries?

A

Left and right main coronary arteries

556
Q

What kind of arteries are coronary arteries?

A

-Functional end arteries
-Only one area of tissue is supplied by the artery (do not connect)
-Unless collateral supply has developed

557
Q

What does the left main coronary artery branch into?

A

-Left anterior descending (LAD)
-Circumflex (Cx)

558
Q

Where does the LAD run?

A

Runs in the anterior interventricular groove

559
Q

What branches does the LAD give off?

A

-Septal branches - Septum
-Diagonal branches - Left ventricular myocardium

560
Q

Where does the Cx run?

A

Runs in the left atrioventricular groove

561
Q

What branches does the Cx give off?

A

Obtuse marginal branches to the posterolateral LV wall

562
Q

In what % of the population does the Cx give off the posterior descending artery?

563
Q

Where does the right coronary artery run?

A

Right atrioventricular groove

564
Q

What does the right coronary artery normally supply?

A

-SAN
-AV node
-Branches to the anterior RV wall

565
Q

What do distal RCA branches branch into?

A

-Posterolateral arteries
-Posterior descending artery (70%)

566
Q

In what % of the population does the RCA branch into the posterior descending artery?

567
Q

Where does the posterior descending artery run and what does it supply?

A

-Posterior interventricular groove
-Supplies inferior septum and LV

568
Q

What does dominance refer to in terms of coronary arteries?

A

-Refers to the artery which supplies the posterior descending artery
-RCA or Cx

569
Q

What are the proportions of coronary artery dominance in the heart?

A

-10% left dominant - Cx
-20% co-dominant - Cx + RCA
-70% right dominant - RCA

570
Q

Why do we need circulation?

A

-Every cell in body need bathed in fluid and 2mm from oxygenation
-Reproduces extracellular primitive uni and multi-cellular organisms in primeval ocean

571
Q

Label this diagram:

572
Q

Describe the arterial system:

A

-Conduits of blood
-Physical properties:
-Elastic arteries - increase efficiency
-Muscular arteries - regulatory control of distribution

573
Q

Describe the elastic arteries:

A

-Major distribution vessels
-Aorta, brachiocephalic, carotids, subclavian, pulmonary
-Biggest

574
Q

Describe muscular arteries:

A

-Mains distributing arteries
-Smaller than elastic, bigger than arterioles

575
Q

Describe arterioles:

A

-Terminal branches
-Smaller than muscular and elastic arteries
- <300 um diameter

576
Q

Describe capillaries:

A

-Functional part of circulation
-Blood flow regulated by precapillarry sphincters
-Between 3-40 microns in diameter
-Three types:
-Continuous (most common)
-Fenestrated
-Discontinuous (liver sinusoids)

577
Q

Describe the venous system:

A

-Return blood to heart
-System of valves allows “muscular pumping”
-Some peristaltic movement

578
Q

Label this diagram:

579
Q

What is this?
When is it present?

580
Q

What are the consequences of circulatory embryology abnormalities?

A

-Abberrant embryology accounts for many congenital abnormalities in fetal death
-Many processes which pattern blood vessels in embryo are also used in post-natal physiological and pathalogical processes

581
Q

What day starts formation of blood vessels?
-Describe it:

582
Q

What is the second stage of blood vessel formation?
Describe it:

583
Q

What happens of day 18 in terms of vessel formation?

A

Axial vessel formation

584
Q

Describe what happens in day 18 in terms of vessel formation?

585
Q

What happens on day 18 onwards in terms on blood vessel formation?

586
Q

What happens during blood vessel formation after this stage?

A

Other mesodermal cells are recruited

587
Q

What drives embryonic vessel development?

A

-Angiogenic growth factors (vascular endothelial growth factor, angiopentin 1 and 2)
-Repulsive signals
-Attractive signals (VEGF)

588
Q

What is the difference between arteries and veins?

A

-Structure
-Flow conditions
-Specific features
-Specific embryonic proteins in arteries and veins (gene activation)

589
Q

What does this show and at what stage of embryonic development is it?

A

-Aortic arches
-7 weeks

590
Q

Label arches 1, 2 and 3:

591
Q

Label arches 4 and 6:

592
Q

Label 7th seg and dorsal aorta:

593
Q

What do 1st and 2nd aortic arches form?

594
Q

What do 3rd aortic arches form?

595
Q

What does right 4th aortic arch and right dorsal aorta form?

596
Q

What does left 4th aortic arch and left dorsal aorta form?

597
Q

What do the 5th aortic arches form?

598
Q

What do the 6th aortic arches form?

Phase 1 (23 decks)

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