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Block 2 > Week 4: CTB > Flashcards

Week 4: CTB Flashcards

1
Q

Define Haemorrhage

A

Extravasation of blood into the extravascular space

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2
Q

Define Ischaemia

A

Inadequate flow of blood to a part of the body resulting in lack of oxygen and nutrient delivery and build up of toxins

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3
Q

Infarction

A

Tissue death due to inadequate blood supply (ischaemic necrosis)

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4
Q

Define Thrombus

A

Solid mass of blood products in a vessel lumen

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5
Q

Define Embolus

A

A detached intravascular sold, liquid or gas that is carried by the blood to a site distant from its point of origin

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6
Q

List the Features of Virchow’s Triad

A
  • Represents group of factors that predispose to thrombosis:
  • Endothelial injury
  • Abnormal blood flow (turbulence or stasis)
  • Hypercoagulability
  • Can act independently or interact - Endothelial integrity is the single most important factor
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7
Q

Describe Venous Thrombi

A
  • Commonly associated with stasis of blood flow
  • Hypercoagulability can also be an important precipitating factor
  • Venous thromboembolism (VTE) includes
    o Deep vein thrombosis – DVT
    o Pulmonary embolism – PE
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8
Q

Describe Arterial Thrombi

A
  • Associated with endothelial injury and/or abnormal flow
  • Most common cause of arterial thrombosis is atherosclerosis
    o Causes endothelial injury and turbulent blood flow around the plaque
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9
Q

Describe Mural Thrombi

A
  • Thrombi that are attached to the wall of a blood vessel (commonly aorta) or a cardiac chamber
    o Aortic mural thrombi – Due to Ulcerated atherosclerotic plaques or aneurysmal (abnormal) dilations
    o Cardiac mural thrombi – Due to
     abnormal Myocardial contraction E.g. Following a myocardial infarction
     Endomyocardial injury (e.g. Catheter trauma)
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10
Q

What changes occur as a result of endothelial dysfunction in vascular pathologies

A

Procoagulant + Anti-fibrinolytic

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11
Q

Why is laminar flow important in preventing thrombosis?

A
  • Laminar flow means platelets + other cellular components of blood are confined to the centre of the flow and separated from endothelium by slower of slower moving acellular plasma
  • Reduces chance of unwanted platelet-endothelial interactions and binding
  • Also ensures dilation and removal of clotting factors near endothelial cells, reducing chance of unwanted coagulation and clot formation
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12
Q

What are the consequences of Stasis in Abnormal Blood flow

A
  • Results in endothelial dysfunction - Flow-induced changes in endothelial gene expression
  • loss of laminar flow - Contact of platelets with endothelium, limits dilution and washout of activated clotting factors
  • Contributing factor in venous thrombosis
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13
Q

What are the consequences of Turbulence in Abnormal Blood Flow

A
  • Direct endothelial injury and endothelial dysfunction, secondary to chaotic blood flow
  • Formation of pockets of stasis
  • Allows platelets to come into contact w/endothelium
  • Limits diffusion and washout of activated clotting factors, limited inflow of clotting factor inhibitors.
  • Occurs in arterial vessels - Contribute to arterial thrombosis
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14
Q

What Pathologies can result in Abnormal Venous Blood Flow

A
  • Venous Compression (stasis and venous thromboembolism)
  • Varicose Veins
  • Increased blood viscosity e.g. dehydration
  • Immobilisation (e.g. bedridden - stasis and venous thromboembolism)
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15
Q

What Pathologies can result in Abnormal Venous Blood Flow

A
  • Aneurysm
  • Atrial Fibrillation (Stasis of blood in left atrium and thrombosis and embolism)
  • Myocardial infarction and non-contractile wall segment (result in local blood stasis, predisposing to mural thrombi)
  • Atherosclerotic stenosis or plaque ulceration
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16
Q

What is the result of Hypercoagulability in Vascular Pathologies

A
  • Increased Increased tendency for the blood to clot, usually due to alteration in coagulation factors
    o Important contributing factor in venous thrombosis
    o Hypercoagulability states can be due to:
     Primary (inherited) disorder
     Secondary (acquired) disorder
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17
Q

Why do fibrinolytic agents need to be administered within the first few hours of an acute thrombotic event?

A
  • Fibrinolytic dissolution is most effective in newly formed thrombi before extensive fibrin polymerisation has occurred which makes plasmin-mediated breakdown less effective
  • Fibrinolytic agents generally not effective unless administered within a few hours of thrombus formaiton
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18
Q

what is an embolus?

A
  • An embolus is a detached intravascular solid, liquid, or gas that is carried by the blood to a site distant from its point of origin
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19
Q

What is the term used to describe an embolism arising form a thrombus?

A

Thromboembolism

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20
Q

What causes Fat Embolisms

A
  • Caused by fractures, orthopaedic procedures, massive soft tissue injury or severe burns
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21
Q

What is Fat Embolism Syndrome

A
  • Mechanical obstruction, platelet platelet activation and aggregation, and toxic endothelial injury
  • Results in Pulmonary insufficiency, neurologic symptoms, anaemia, thrombocytopaenia, and diffuse petechial rash, (10% cases) death
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22
Q

What is Deep Vein Thrombosis

A

Venous thrombus forming in the major deep vein in the leg, thigh, pelvis, or abdomen

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23
Q

What components from Virchow’s Triad are related to DVT?

A
  • Stasis and Hypercoagulability

- Endothelial injury - May also be related, resulting in endothelial dysfunction

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24
Q

Why is Bed rest/Immobilisation a RF for DVT?

A
  • Reduced muscle action and slow venous return - Stasis
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25
Q

What are Potential Signs and Symptoms of DVT?

A
  • Swelling
  • Pain
  • Tenderness
  • Erythema
  • Increased temperature
  • 50% cases asymptomatic
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26
Q

Why can a patient present with a swollen leg in DVT?

A
  • Venous thrombi can cause congestion and oedema distal to the obstruction
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27
Q

What is Well’s score for DVT?

A
  • Often used for non-hospitalised patients to assess risk for DVT
  • Uses measures including: Active cancer, bedridden recently, calf swelling >3cm, collateral superficial veins present, entire leg swollen, tenderness, pitting oedema, paralysis , previous DVT
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28
Q

In some patients with suspected DVT a D-dimer is performed. What is a D-dimer and how can it be useful in the diagnosis of DVT?

A
  • D-dimer is a fibrin degradation product and is formed after a clot has formed and is in the process of being broken down
  • Negative D-dimer test can be helpful in excluding a DVT in pt who are lower risk of DVT according to Well’s score
  • High risk pt should have imaging
  • D-dimer is non-specific and low positive predictive value
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29
Q

Where would an embolus from a deep vein thrombosis embolise to?

A
  • Pulmonary circulation
  • Right side of heart
  • = Pulmonary embolism (PE)
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30
Q

What is a Paradoxical Embolism?

A

Presence of an atrial septal defect allows the embolus to lodge in the systemic arterial circulation

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31
Q

What is Pulmonary Embolism?

A
  • A life-threatening condition resulting from dislodged thrombi occluding the pulmonary vasculature
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32
Q

What is a saddle embolus?

A
  • Pulmonary embolism which lodges and occludes major pulmonary arteries at a point of bifurcation
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33
Q

What are Clinical Features of PE?

A
  • Dyspnoea
  • Pleuritic chest pain (Pain on inspiration)
  • Cough and Haemoptysis
  • Tachycardia
  • Tachypnoea
  • Hypoxia
  • Hypotension, Syncope, Cardiogenic shock
  • Signs and Symptoms of DVT
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34
Q

What is syncope?

A

Temporary loss of consciousness caused by a fall in blood pressure

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35
Q

A common symptom of PE is pleuritic chest pain. What is pleuritic chest pain and why does it occur?

A

A sharp localised pain on deep breathing. Caused by irritation or inflammation of the parietal pleura

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36
Q

Pulmonary infarction is a potential complication of PE. However, it does not always occur. Why might pulmonary infarction not occur in the context of a pulmonary embolus?

A
  • Lungs supplied by two vascular systems with many anastomoses
  • Pulmonary vascular system + Bronchial Vascular system
  • So Emboli affecting Pulmonary vascular system, lungs will use alternative blood supply
  • Has ability to increase flow + tissue receives oxygen directly from inspired air
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37
Q

How can PE lead to local Pulmonary capillary haemorrhage?

A
  • Due to higher pressure of the bronchial arteries (alternative lung blood supply)
  • Locally increased vascular permeability, and capillary endothelial injury
  • Usually resolves as tissue regenerates
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38
Q

What components of Virchow’s Triad are involved in Thrombosis in patient with AF?

A
  • Stasis - Due to AF blood flow, atrial dilation and loss of coordinated systole
  • Hypercoagulability
  • Endothelial dysfunction
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39
Q

Cardiac mural thrombi are prone to embolisation. What are the consequences of an embolism in the systemic arterial circulation? What factors do you think will affect the significance of those consequences?

A
  • Embolisation in systemic arterial circulation results in Ischaemia and Infarction of Downstream Tissues
  • Consequences depend on the side of the occluded vessel, the collateral supply and vulnerability of the affected tissue to anoxia
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40
Q

What is the mechanism of action of LMWH?

A

Low molecular weight heparin binds and activates antithrombin III by inducing a conformational change that ‘opens up’ antithrombin III. Heparin-activated antithrombin III binds FXa directly via the ‘open’ active site and this inactivates FXa

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41
Q

What are the three components of Virchow’s triad?

A
  • Hypercoagulability
  • Abnormal blood flow
  • Endothelial injury
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42
Q

List three stimuli or exposures that can lead to endothelial dysfunction?

A
  • Inflammation
  • Bacterial endotoxins
  • Toxins from cigarette smoke
  • Hypercholesterolaemia
  • Chronic Hyperglycaemia
  • Abnormal blood flow
  • Hypertension
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43
Q

What type of embolism is associated with decompression sickness?

A
  • Air embolism

- Due to formation of bubbles of nitrogen gas in the blood and tissues

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44
Q

What term is used to describe both DVT and PE?

A
  • Venous Thromboembolism (VTE)
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45
Q

What is the most common condition underlying thrombosis in arteries?

A

Atherosclerosis

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46
Q

What is the term used to describe thrombi that develop on heart valves?

A

Vegetations

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47
Q

Define ARTERIOSCLEROSIS

A
  • General term: Hardening or loss of elasticity of the arteries of any cause
  • Three patterns of Arteriosclerosis:
  • Atherosclerosis
  • Arteriolosclerosis
  • Mönckeberg medial calcific sclerosis
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48
Q

Define ATHEROSCLEROSIS

A
  • Progressive arteriosclerosis of medium/large arteries due to atheroma formation
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49
Q

Define Arteriosclerosis

A
  • Thickening of small artery and arteriole vessel walls and reduction in vessel lumen size.
  • Associated with systemic hypertension and DM.
  • Particularly affects vessels in kidney, pancreas, gallbladder, small intestine, adrenals, and retina.
  • May result in distal ischaemia
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50
Q

Define Mönckeberg medial calcific sclerosis

A

Calcific deposits in muscular arteries in older individuals. Do not reduce the size of the vessel lumen

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51
Q

Describe Atherosclerosis

A
  • Progressive disease affecting large-medium arteries
  • Focal accumulation of lipid-rich material in tunica intima and development of atheromas (atheromatous plaques)
  • Areas of turbulent flow particularly vulnerable - Branch points
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52
Q

What can Atherosclerosis lead to? (diseases)

A
  • Leading cause of morbidity and mortality in western world
  • Underlies pathogenesis of:
  • Coronary artery disease (angina, MI)
  • Cerebral vascular disease
  • Aortic Aneurysm
  • Peripheral arterial disease
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53
Q

specifically hypercholesterolaemia – Major risk factor for development of atherosclerosis
Which is the main cholesterol component associated with increased risk of atherosclerosis?

A

LDL Cholesterol - Delivers cholesterol to peripheral tissues

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54
Q

What are Risk Factors for Atherosclerosis

A
  • Male gender
  • Genetic - familial hypercholesterolaemia
  • Age
  • Family hx
  • Inflammation
  • Hyperlipidaemia
  • Cigarette smoking
  • Hypertension
  • Diabetes
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55
Q

What is Atherogenesis

A

Development of an atherosclerotic plaque

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56
Q

Describe the Response-to-Injury Hypothesis

A
  • Atherosclerosis is a chronic inflammatory response of arterial wall to chronic endothelial injury
  • Chronic endothelial injury/Turbulent blood flow
  • Leads to endothelial dysfunction/activation = Upregulation of inflammatory adhesion molecules –> Promotes monocyte, T cell, and platelet adhesion + Increased permeability to lipids + LDL –> Accumulates in tunica intima
  • Fatty Streak Formation = Monocytes migrate into intima –> Macrophages, take up LDL oxidised by ROS, T lymphocytes inflammation, Smooth muscle cells recruited and migrate into intima. Lipid filled macrophages = Form fatty streaks
  • Atherosclerotic plaque formation = lipid-rich core and fibrous cap
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57
Q

Outline the Progression of Atherosclerosis

A
  • Fatty streak - Intracellular lipid accumulation
  • Intermediate lesion - Beginning of extracellular lipid accumulation
  • Atheroma - Obvious extracellular lipid accumulation
  • Advanced plaque - Multiple extracellular lipid with fibrosis and calcification
  • Complicated plaque - Thrombosis, haemorrhage, surface defects
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58
Q

What are the 3 Principle Components of atherosclerotic plaques

A
  • Cells - Smooth muscle cells, T cells, Macrophages
  • Extracellular matrix
  • Intracellular and Extracellular lipid
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59
Q

Explain Clinical Consequences of Atheroma Formation

A
  • Mural thrombosis, Embolisation, Wall weakening -> Aneurysm and Rupture
  • Plaque rupture, erosion, haemorrhage, Mural thrombosis, embolisation -> Occlusion by thrombosis
  • Progressive plaque growth -> Critical stenosis
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60
Q

Explain Pathological Consequences of Atheroma Formation

A
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61
Q

What is an Aneurysm

A

Abnormal dilation of a blood vessel

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62
Q

what is intermittent claudication?

A

Leg pain on exercise and walking due to atherosclerosis and critical stenosis in lower limb arteries (peripheral arterial disease)

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63
Q

What is stable angina

A

chest pain on exertion due to atherosclerosis and critical stenosis in coronary arteries

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64
Q

What is the consequence of thrombosis on plaques?

A
  • Partial / Total vessel occlusion -> Ischaemia +/- Infarction
  • Non-occlusive thrombi can result in healing and remodelling -> Enlargement of atherosclerotic plaque
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65
Q

What components of Virchow’s triad are involved in thrombus formation associated with rupture of an atherosclerotic plaque?

A
  • Endothelial Injury - Atherosclerotic plaque ulcerates and ruptures exposes subendothelial matrix and thrombogenic contents of plaque, leading to platelet adherence, activation and formation of thrombus
  • Turbulence - Ulcerated plaques
  • Hypercoagulability - Pt will have predisposing factors e.g hypercholesterolaemia, smoking etc. Unlikely to be major factor
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66
Q

What are potential consequences of atherosclerotic plaque rupture?

A
  • Aneurysm
  • Thrombus formation
  • Haemorrhage
  • Microemboli of plaque debris = Cholesterol embolus/atheroembolus
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67
Q

What term is used to describe the deposition of calcium in the tunica media of medium and small muscular arteries in older adults, and which is not associated with luminal narrowing?

A

Mönckeberg medial calcific sclerosis

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68
Q

What is meant by the term ‘critical stenosis’ in the context of atherosclerotic plaque growth?

A

Point at which blood flow is limited to a degree that demand exceeds supply, and ischaemia occurs

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69
Q

What features are associated with a vulnerable/unstable atherosclerotic plaque?

A
  • Thin fibrous cap
  • Large numbers of foam cells
  • Large amount of extracellular lipid
  • Dense inflammatory lipid
  • Stability depends on strength and thickness of fibrous cap, dependent on balance between inflammation (driven by leukocytes) and repair (driven by smooth muscle cells)
  • If inflammation predominates then cap may become thinner and less stable - more likely to rupture
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70
Q

How do the P wave and the QRS complex relate to phases of the cardiac cycle?

A
  • P wave - Represents atrial depolarisation, appears right before atrial systole
  • QRS complex - Represents ventricular depolarisation and occurs right before and during isoventricular contraction
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71
Q

What causes the 1st and 2nd heart sounds?

A
  • 1st atrioventricular valves shutting

- 2nd Semilunar valves shutting

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72
Q

What happens during Isovolumetric Relaxation?

A

(Diastole)

  • Atrioventricular valves closed
  • Semilunar valves closed
  • Ventricular pressure Rapid Fall
  • Ventricular volume Constant
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73
Q

Define stroke volume

A
  • Volume of blood that is ejected from each ventricle during one ventricular contraction
  • SV = EDV - ESV
  • Usually referring to left ventriclev
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74
Q

What does a raised JVP indicate?

A

An increase in pressure in the right side of the heart. One of most common causes is heart failure

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75
Q

During which two phases of the cardiac cycle is the ventricle a close chamber with no change in volume?

A
  • During Isovolumetric Relaxation - After aortic valve closes until bicuspid valve opens during ventricular diastole
  • During Isovolumetric Contraction - After bicuspid valve closes until aortic valve opens during ventricular systole
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76
Q

What causes the mitral valve to close and at what point does this happen in the cardiac cycle?

A
  • Closes as the ventricles contract and the pressure within the ventricles exceeds that of the atria
  • Happens at beginning of isovolumetric contraction
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77
Q

Why does the ventricular pressure fall initially during ventricular filling?

A
  • Initially ventricles still relaxing so ventricular pressure falls despite filling and increase in ventricular volume
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78
Q

Which component of the JVP waveform corresponds to atrial systole?

A

a wave - Contraction of right atrium causes transient backpressure into vena cava and internal jugular vein

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79
Q

Describe the JVP waveform

A
  • A wave - Atrial systole - Transient back pressure into vena cava + IJP
  • C wave - Bulging of tricuspid valve - Into atrium during isovolumetric contraction
  • X descent - Atria relax –> Pressure reduced during ventricular systole
  • V wave - Atrial filling during ventricular systole against closed tricuspid valve
  • Y descent - Passive ventricular filling during diastole as tricuspid opens
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80
Q

Define End-Diastolic Volume (EDV)

A

The volume of blood in the ventricle at the end of diastole i.e. just before contraction

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81
Q

Define End-Systolic Volume (ESV)

A

The volume of blood in the ventricle after contraction

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82
Q

What is ejection fraction?

A
  • The proportion of end-diastolic volume that is ejected during systole
  • EF (%) = SV /EDV x100
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83
Q

What is preload?

A
  • The degree of ventricular cardiomyocyte stretch at the end of diastole (i.e. just before contraction)
  • Determined by End-diastolic volume - The greater the EDV the greater the preload
84
Q

Explain the Length-Tension Relationship in relation to cardiomyocytes

A
  • Increasing length increases active tension development by:
  • Increasing number of possible cross-bridges that can form
  • Increases calcium sensitivity of troponin c
  • Increases calcium release from sarcoplasmic reticulum
  • To a maximal point
85
Q

Explain the physiology underlying Starling’s law

A
  • Energy released during contraction depends upon initial fibre length, greater the cardiomyocytes are stretched (preload) the greater energy released by contraction (force of contraction) up until a point
  • Volume of blood ejected by ventricle depends on volume of blood in ventricle at end of diastole
  • Stroke volume - Depends on End-diastolic volume
  • Matched to venous return
  • Ensures two ventricle outputs are matched
86
Q

Define Afterload

A
  • The force or stress on cardiomyocytes during systole i.e. the ‘load’ that the heart must eject against
  • Afterload in LV - Aortic Pressure
  • Afterload in RV - Pulmonary artery Pressure
  • Related to radius of ventricular chamber and Wall thickness
87
Q

What does Positive Inotropy effect mean?

A
  • Increases contractility of the heart
88
Q

Define Myocardial Contractility (Inotropy)

A
  • Force of contraction for a given fibre length
89
Q

which branch of the autonomic system acts to increase contractility?

A

Sympathetic nervous system

90
Q

Patient has echocardiogram which measures his end-diastolic volume as 140ml and end-systolic volume as 50ml

a) what is his stroke volume in mls
b) What is his ejection fraction

A

a) 140-50 = 90mls

b) EF = SV/EDV x 100 = 90/140 x 100 = 64.3% (>50% is normal)

91
Q

What is preload and how is it related to end-diastolic volume?

A
  • Preload is the degree of cardiomyocyte stretch at the end of diastole and is determined by the end-diastolic volume
92
Q

What two mechanisms can alter force of contraction of the heart and how?

A
  • Changes in end-diastolic volume (preload) via length-dependent mechanisms
  • Changes in contractility via length-independent mechanisms
93
Q

What is the main determinate of afterload in the left ventricle?

A

Aortic Pressure is the main determinant

94
Q

Outline the factors which determine afterload

A
  • Main - Aortic/Pulmonary artery pressure
  • Ventricular inside radius
  • Ventricular wall thickness
95
Q

Describe the effect of increasing afterload on ventricular function

A
  • Heart has to eject against a greater pressure
  • Heart has to generate greater ventricular pressure during isovolumetric contraction and ejection to overcome this
  • Stroke volume is reduced (less energy left for ejection)
  • End-systolic volume increased (more blood left in ventricle)
  • Ejection fraction decreased (less blood ejected)
96
Q

What effect will changing afterload have on the Starling curve?

A
  • Decreasing afterload - Increases stroke volume at given end-diastolic volume - Curve shifts upwards
  • Increasing afterload - Decreased stroke volume at given end-diastolic volume - Curve shifts downwards
97
Q

What is the Starling curve?

A
  • Measures stroke volume (SV) (Y-axis)

- Against End-diastolic volume (EDV) or End-diastolic Pressure (EDP)

98
Q

Describe the effects of increasing contractility (inotropy) on ventricular function

A
  • Increasing contractility increases stroke volume by increasing force of contraction at a given preload and afterload
  • Increases SV, Decreases ESV, Increases Ejection fraction
99
Q

What effect will changing contractility have on the Starling curve

A
  • Increasing contractility e.g exercise - Starling curve shifted upwards and to the left - For any given end diastolic volume, stroke volume is greater
  • Decreasing contractility e.g. heart failure - Starling curve shifted downwards and to the right - For any given end diastolic volume, stroke volume is reduced
100
Q

What factors Increase contractility of the heart (Positive Inotropy)

A
  • Sympathetic (SNS) Activation via noradrenaline and beta-adrenoreceptors
  • High levels of Circulating catecholamines (in exercise/anxiety) (e.g. noradrenaline, adrenaline) can augment effects of SNS
  • Parasympathetic inhibition in atria
  • Increasing heart rate - Bowditch effect
  • Increasing afterload - Partially compensates for increased ESV and Reduced SV - Anrep Effect
101
Q

What factors Increase Preload

A
  • Increased ventricular compliance - Determines EDV
102
Q

what impact can the following conditions have on preload:

a) Aortic stenosis
b) Atrial fibrillation
c) Haemorrhage

A

a) Increase preload + Afterload - Narrowing of aortic valve
b) Reduce preload - Will impair atrial contraction
c) Decrease preload - Reduced total blood volume, reduced venous pressure

103
Q

Describe the Interdependent relationships of preload, afterload and contractility

A
  • Increasing contractility
  • Increases SV
  • Decreased End-systolic volume - Secondary change: Decreased ESV and preload
  • Also Secondary change Increasing afterload; Increases ESV and secondarily EDV
  • Results in Steady state: Smaller increase in SV, reduction in ESV and smaller reduction in EDV
104
Q

Define Cardiac Output

A
  • Volume of blood ejected by each ventricle per minute

- Cardiac output (ml/min / L/min) = Heart rate X Stroke volume (ml/min)

105
Q

Outline factors affecting cardiac output

A
  • Heart rate - ANS + Circulating catecholamines
  • Stroke Volume - ANS + Circulating catecholamines + Renin-Angiotensin-Aldosterone system + Antidiuretic hormone –> Changes in preload, contractility and afterload –> EDV-ESV = SV
  • CO = HR x SV
106
Q

What effect does afterload have on stroke volume, end-systolic volume and (secondarily) on end-diastolic volume

A
  • Increasing afterload decreases stroke volume and increases end-systolic volume
  • Secondarily slightly increasing End-diastolic volume as left over blood from ESV
107
Q

What effect would reduced ventricular compliance (e.g. ventricular hypertrophy) have on end-diastolic volume at a given end-diastolic pressure?

A
  • Reduced end-diastolic volume as heart unable to expand and take more in for a given pressure. Would need higher pressure.
108
Q

What factors can influence central venous pressure and how does that relate to changes in preload?

A
  • Venous pressure influenced by venous compliance and venous blood volume - Determined by total blood volume and rate of venous return to thoracic compartment
  • Increases in central venous pressure increase filling pressure, right ventricular end-diastolic volume and preload
109
Q

A patient has a heart rate of 72 beats per minute and stroke volume of 70mls. What is their cardiac output in L/min?

A

72X70 = 5040 = 5 L/min

110
Q

How does Coronary Artery Disease result in Myocardial Ischaemia?

A
  • Fixed obstruction - Vessel stenosis due to atherosclerotic plaques
  • Variable obstruction - Thrombosis or Vasospasm
111
Q

How is Coronary Artery Disease Classified clinically?

A
  • Stable angina
  • Acute coronary syndrome - Unstable angina, non-ST-elevation Myocardial infarction, and ST-elevation myocardial infarction
112
Q

Define Critical Stenosis

A
  • Reduction in luminal cross-sectional area of 70%

- Or 50% in left main coronary artery

113
Q

Outline Factors which intensify ischaemia

A
  • Reduced oxygen delivery
  • Increased oxygen demand
  • Large mass of ischaemic myocardium distal to occlusion
  • Longer length lesions
114
Q

Outline factors which reduce Ischaemia

A
  • Well-developed collateral supply

- Distally located lesion meaning that a smaller mass of tissue if affected

115
Q

Define Myocardial Ischaemia

A
  • Myocardial ischaemia occurs when there is an imbalance between cardiac blood supply (coronary perfusion) and myocardial oxygen and nutritional requirements
116
Q

List Risk Factors for Coronary artery disease

A
  • Age, Positive Family hx, Male

- DM, Elevated CRP, Hyperlipidaemia, Cigarette smoking, Hypertension, Obesity, Heavy alcohol consumption, Certain drugs

117
Q

What is Angina Pectoris

A

Used to describe intermittent chest pain due to transient, reversible myocardial ischaemia

118
Q

What are typical features of Stable angina?

A
  • Constricting discomfort in the front of the chest, or in the neck, shoulder, jaw or arms
  • Precipitated by physical exertion
  • Relieved by rest of GTN within about 5 minutes
119
Q

What is meant by primary prevention in the context of cardiovascular disease?

A

Prevention of the atherosclerotic disease process

120
Q

What is meant by secondary prevention in the context of cardiovascular disease?

A

Treatment of the atherosclerotic disease process (i.e. treatment of the disease or its complications)

121
Q

What risk factors would be important to address in a patient with stable angina?

A
  • Smoking
  • Hypertension
  • Diabetes
  • Hypercholesterolaemia
  • Management involves both lifestyle changes and medications
122
Q

Lipid modification therapy is an important aspect of primary and secondary prevention of cardiovascular disease. In some patients, medications are indicated. Which class of medications would be used?

A

HMG-CoA reductase inhibitor (Statin)

123
Q

Which antiplatelet drug is indicated first-line as part of secondary prevention in patients with stable angina?

A
  • Aspirin

- Reduces platelet aggregation, and aims to lower the risk of future myocardial infarction and death

124
Q

Which medication administered sublingual (under the tongue) can be used to relieve acute ischaemic chest pain in stable angina?

A
  • Glyceryl trinitrate (GTN)
  • A nitrate which relaxes vascular smooth muscle in coronary arteries, leading to vasodilation and improved coronary blood supply
  • Helps relieve ischaemic chest pain in stable angina
125
Q

What is Acute Coronary Syndrome (ACS)

A
  • Acute disruption of an atherosclerotic plaque and thrombus formation resulting in acute myocardial ischaemia +/- infarction
  • Umbrella term including
  • Unstable angina
  • Non-ST-elevation Myocardial Infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
126
Q

How are the Clinical Categories of ACS differentiated between?

A

ECG changes and measurement of biomarkers

127
Q

Explain the pathophysiology of Unstable Angina - ACS

A
  • Coronary artery occlusion is incomplete or short-lived -> Myocardial ischaemia but no myocardial damage
128
Q

Explain the pathophysiology of Myocardial Infarctions

A
  • Death of cardiomyocytes due to ischaemia
  • Area most at risk = Subendocardial regions (furthest distance from epicardial vessels + high intramural pressure which impedes blood flow)
  • Can have Subendocardial infarcts (infarct in inner third of myocardium)
  • Transmural infarcts (Infarct of full thickness of wall)
129
Q

Describe Subendocardial Infarcts

A
  • Regional infarct: Partial/transient occlusion of coronary vessel//Good collateral supply around occluded vessel//Small artery/branch affected
  • Circumferential infarct: Severe coronary artery atherosclerosis combined with transient decrease in oxygen delivery (e.g. hypotension) or prolonged increased demand (hypertension) - Tend to present as NSTEMI
130
Q

Describe Transmural Infarcts

A
  • Affects complete thickness of wall
  • Due to permanent occlusion of an epicardial vessel
  • Tend to present as STEMI
131
Q

Outline the factors affecting infarction

A
  • Factors which influence the location, size, and consequences of a myocardial infarction include:
  • Size and distribution of vessel involved
  • Rate of development and duration of occlusion
  • Metabolic demands of the myocardium
  • Extent of collateral blood supply
132
Q

Outline the Stages of Myocardial Infarction

A
  • Coagulative necrosis
  • Acute inflammation
  • Chronic inflammation
  • Fibrosis and scarring
133
Q

What is infarction?

A

An area of ischaemic necrosis in a tissue or organ due to reduced or absent blood supply

134
Q

Explain differences between unstable angina, NSTEMI and STEMI

A
  • Unstable Angina
    o Ischaemia without necrosis  No elevation of cardiac biomarkers
    o ECG: May show ST-depression, T wave inversion or may be normal
  • NSTEMI
    o Cardiomyocyte necrosis -> elevation of cardiac biomarkers
    o ECG: may show ST-depression, T-wave inversion, non-specific changes, or may be normal
  • STEMI
    o Significant myocardial necrosis -> elevation of cardiac biomarkers
    o ECG: ST-elevation or new left bundle branch block
135
Q

What are Cardiac Biomarkers?

A
  • Cardiac troponins (Troponin I and T)
  • Released by damaged cardiomyocytes and indicate presence of infarction and necrosis
  • Levels usually begin to rise around 2-3 hours after onset of myocardial ischaemia
136
Q

What is the best myocardial biomarkers to use to confirm the diagnosis of a MI?

A
  • Cardiac Troponin (TnT or Tnl)

- More specific than CK-MB or Myoglobin

137
Q

Where is the ST segment and what does it represent?

A
  • ST segment is flat, isoelectric section of ECG between end of S wave and beginning of T wave.
  • Represents interval between ventricular depolarisation and repolarisation
138
Q

The ST segment should be flat and isoelectric. What does isoelectric mean in this context?

A
  • Isoelectric means that it should be at the same level as the baseline of the record between the end of the T wave and the next P wave
139
Q

Describe the Leads in terms of the territories of the heart they visualise

A
  • V1-V4 = Anterior
  • V1-V2 = Septal
  • I, aVL, V5-6 = Lateral
  • II, III, aVF = Inferior
  • V7-V9 = Posterior
140
Q

What does the T wave represent in a normal ECG?

A

Ventricular repolarisation

141
Q

What does a positive T wave indicate about the overall direction of repolarisation relative to the recording electrode?

A
  • Repolarisation is moving away from the electrode
  • Causes positive deflection if it is moving away from the electrode and negative deflection if it is moving toward the electrode
  • Opposite to depolarisation
142
Q

In which leads is the T wave normally inverted?

A
  • Inverted in leads aVR and V1
  • T wave inversion in lead III is a normal variant, but new T wave inversion compared with previous ECGs is always abnormal
143
Q

What is a Q wave?

A

A negative deflection preceding the R wave

144
Q

Small Q waves can represent normal left-to-right depolarisation the interventricular septum. In which leads is it normal to see these Q waves and why?

A
  • Small Q waves typically seen in left sided leads
  • Leads I, aVL, V5, V6
  • Direction of depolarisation of the septum (left to right) is moving away from these leads, and so is seen as a small negative deflection
  • Deeper Q waves (>2mm) may be seen in leads III and aVR as normal variants
  • Q waves should not normally be seen in right-sided leads (V1-V3)
145
Q

What Clinical Examination findings may be associated with Cardiogenic shock?

A
  • Hypotension
  • Confusion
  • Pallor
  • Reduced capillary refill time
146
Q

What Clinical Examination findings may be associated with Left Ventricular Failure?

A
  • Displaced apex beat
  • 3rd or 4th heart sounds
  • Bibasal crackles
147
Q

What Clinical Examination findings may be associated with Right Ventricular Failure?

A
  • Elevated JVP

- Peripheral Oedema

148
Q

What is the aim of initial treatment for people with myocardial infarctions?

A
  • Pain relief, limitation of myocardial damage, and treatment of complications.
  • If unstable angina and NSTEMIs - Aim to prevent thrombus extension and antiplatelet drugs important in this
  • If STEMI - Urgent reperfusion therapy with primary PCI or fibrinolysis important in limiting size of infarct
149
Q

What is PCI?

A
  • Primary Percutaneous Coronary Intervention
  • Endovascular procedure used to treat the narrowed coronary arteries.
  • Involves widening of artery with a balloon and insertion of a stent
150
Q

Symptoms of stable angina usually occur when the luminal cross-sectional area of a coronary vessel has been decreased by how much?

A

70% or more

151
Q

What pattern of necrosis is characteristic of myocardial infarction?

A

Coagulative

152
Q

What type of valve dysfunction can occur as a result of dysfunction or rupture of the papillary muscles?

A
  • Regurgitation

- Most commonly mitral valve regurgitation

153
Q

Describe the cellular and molecular components of blood

A
  • Blood plasma (~55%) - Water, Small organic compounds & electrolytes, proteins (albumin, globulins (alpha, beta, gamma), Fibrinogen
  • Cells (~45%) - RBCs (44%), White blood cells and platelets (1%)
154
Q

What is Plasma vs Serum

A
  • Plasma - Liquid component of blood once cells have been removed. EDTA anticoagulant added to stop clotting in the tube
  • Serum - Fluid that is left when blood is allowed to clot naturally - Does not contain clotting factors
155
Q

Plasma vs Serum - Which do you want for FBC?

A
  • Plasma - Purple tube

- Less clotting factors etc in the way

156
Q

What is Haematopoeisis

A
  • The process by which blood cells are made
157
Q

What is Erythropoiesis

A

Making RBC

158
Q

What is Thrombopoiesis

A

Making platelets

159
Q

What is Myelopoiesis/Lymphopoiesis

A

Making WBC

160
Q

Where is the predominant site of Haematopoiesis in adults?

A
  • Bone marrow - E.g. Pelvis, Sternum, Ribs, Proximal ends of large bones
  • Within the HSC niche
161
Q

Describe the different types of stem cell

A
  • Totipotent cells - Can differentiate into any cell type, embryonic and extra-embryonic
  • Pluripotent cells - Any cell type of the embryo
  • Multipotent cells - Into several different but related cell types - Haematopoietic stem cells
  • Oligopotent cells - Into small number of very closely related cell types
  • Unipotent cells - Cells of identical cell type
  • All have self-renewal ability
162
Q

List the differentiated cells produced via haematopoiesis and their functions

A
  • Multipotential Haematopoietic stem cell (Haemocytoblast) –> Common Myeloid Progenitor –> Cells
  • Megakaryocyte - Large cell off which platelets bud - Clotting and Haemostasis
  • Erythrocyte (reticulocyte progenitor) - RBC carry Hb with oxygen to cells
  • Mast cell - Found in tissues, allergic reaction
  • Myeloblast progenitor for Basophils (Hypersensitivity response), Eosinophil (Immediate hypersensitivity response and allergic response, and parasitic response), Neutrophil (Bacterial invasion and inflammation, chemotaxis, phagocytosis and respiratory burst), Monocytes (blood)–> Macrophages (tissues) ingest small pathogens via phagocytosis
163
Q

What Growth Factors are important in Haematopoiesis?

A
  • Erythropoietin - Made in kidney - Increased Red Blood Cell production
  • Thrombopoietin - Made in liver - Increase Platelet formation
  • Work via negative feedback loops
  • Also Interleukins, and GCSF (Granulocyte Colony Stimulating Factor) - Increase Granulocytes (WBCs)
164
Q

What is the mechanism by which the Kidneys increase RBC production?

A
  • Interstitial cell within the kidney is put into Hypoxic environment - Maybe due to patient anaemic
  • Hypoxia Response Element (HRE) becomes stable under hypoxic conditions
  • HRE attaches to EPO gene
  • Increases production of EPO mRNA (Transcription)
  • Increased Erythropoietin protein travels to bone marrow to act on erythropoiesis –> Increase proliferation and reduce apoptosis of RBC progenitor.
  • Thus increases RBC production
165
Q

Why may a patient with Chronic Renal Disease suffer with anaemia?

A
  • Kidney makes Erythropoietin which controls RBC production
  • Kidney dysfunction reduced ability to produce EPO
  • Thus patient may become anaemic (reduced RBC)
166
Q

Explain the consequences of iron insufficiencies for normal haematopoiesis

A
  • Iron-deficiency Anaemia

- RBC become small and pale –> Microcytic Hypchromic Anaemia

167
Q

Describe causes of Iron deficiency anaemia

A
  • Insufficient intake
  • Insufficient/Faulty Absorption - Coeliac disease
  • Increased requirements - Pregnancy
  • Loss of blood - Most important cause - GU (menorrhagia) / GI (gastric ulcer, cancer, haemorrhoids, any other blood loss
168
Q

Define Systolic Blood Pressure

A
  • Maximal pressure in the aorta following left ventricle ejection of blood
169
Q

Define Diastolic Blood Pressure

A
  • The lowest pressure in the aorta just before left ventricle ejects blood again/contracts
170
Q

Define Pulse Pressure

A
  • Difference between systolic blood pressure (SBP) and Diastolic Blood pressure (DBP)
  • Pulse pressure (PP) = SBP - DBP
171
Q

Define Mean Arterial Blood Pressure

A
  • Average arterial pressure throughout one cardiac cycle which drives blood flow in the systemic circulation from an area of higher pressure to lower pressure
  • MAP = 1/3 SBP + 2/3 DBP
172
Q

What is the Formula for calculating Mean Arterial Blood Pressure (MAP)

A

1/3 SBP + 2/3 DBP

173
Q

What does Increasing Heart rate do to Mean arterial blood pressure?

A
  • Shortens diastole more than systole

- MAP is closer (higher) to the mathematical average of SBP and DBP

174
Q

If cardiac output suddenly falls on standing, which variable will be primarily altered in order to maintain mean arterial pressure?

A
  • Systemic Vascular Resistance will be Increased
175
Q

What is the Physiological Equation for MAP (mean arterial pressure)

A
  • MAP = (HR x SV) x SVR x CVP (usually 0)

- So MAP = Cardiac Output x Systemic Vascular Resistance

176
Q

What are the factors which affect Resistance? What is the formula?

A
  • Radius
  • Length of tube
  • Viscosity
  • R = 8nl/pi(r^4)
177
Q

Define Systemic Vascular Resistance (SVR)

A
  • AKA Total peripheral resistance TPR
  • Resistance to blood flow from all systemic vasculature, excluding pulmonary vasculature
  • Vasoconstriction and Vasodilation via smooth muscles can alter SVR (radius affects resistance)
178
Q

Describe and explain the pressure changes across the vascular tree

A
  • Aorta to Large arteries - Slight increase in pressure due to relative low resistance relative to flow
  • To small arteries and arterioles - High resistance relative to flow results in large pressure drop across small arteries and arterioles (70% SVR)
  • Capillaries, Venules, Small + Large veins, Vena Cava - Pressure falls further to almost 0
  • Pulmonary vascular resistance is much lower, so although pressure is lower, flow is the same
178
Q

Pressure gradient = Flow x Resistance

A
179
Q

What is Vascular Tone?

A
  • Degree of constriction relative to its maximal dilated state
  • Determined by balance of constrictor influences and dilator influences which can be extrinsic (neurohormonal e.g. ANS/hormones - alter SVR to regulate arterial blood pressure) or intrinsic (local blood flow regulation)
180
Q

Explain the functions of the veins

A
  • Venules
  • Site of exchange - Large macromolecules and fluid
  • Venular tone - Altered by SNS, contributes to capillary hydrostatic pressure
  • Veins
  • Capacitance vessels - 70-80% blood volume reservoir
  • Helps regulate cardiac output
  • Valves prevent backflow and ensure blood flow is towards heart, aided by skeletal muscle
181
Q

How would peripheral venoconstriction affect cardiac output and what are the underlying mechanisms?

A
  • Venoconstriction decreased venous compliance, resulting in a decrease in venous blood volume and an increase in venous pressure
  • Causes blood to be translocated from peripheral veins into thoracic compartment, and increases Central Venous Pressure
  • Increases end-diastolic volume and preload
  • Increases Stroke volume via Starlings Law of the Heart,
  • Increasing cardiac output
182
Q

Explain the functions of the lymphatics system in the cardiovascular system

A
  • Return fluid and large molecules e.g. proteins, fats from GI tract from interstitial fluid to systemic circulation
  • Flow enabled by intrinsic intermittent contraction of lymphatic walls and external compression - skeletal muscles
  • Interstitial fluid pressure also influences lymph formation and flow
  • Valves ensure one way flow
  • Drain into thoracic and right lymphatic ducts - into right and left subclavian veins
183
Q

A person has a blood pressure of 110 / 68 mmHg

a) What is the mean arterial blood pressure?
b) What is the pulse pressure?

A

a) (1/3 x 110) + (2/3 x 68) = 82 mm Hg - MAP

b) 110-68 = 42 mmHg

184
Q

What is the primary mechanism by which systemic vascular resistance is altered?

A
  • Vasoconstriction/ Vasodilation of Small arteries/arterioles
185
Q

Patient involved in a large road traffic accident has a blood pressure of 102/88. Their normal BP is 118/76 mmHg. What do you notice about their systolic, diastolic and pulse pressure and can you explain the underlying physiological response?

A
  • Systolic BP reduced secondary to reduced total blood volume, reduced preload, reduced stroke volume
  • Diastolic BP increased secondary to increased systemic vascular resistance (due to vasoconstriction to try maintain MAP)
  • Pulse pressure has decreased from 42 to 14 - Narrowing - A sign that patient may be very unwell
186
Q

What are the roles of local perfusion? (6)

A
  • Delivery of O2
  • Delivery of nutrients
  • Removal of CO2
  • Removal of H2
  • Maintenance of Conc of ions in tissues
  • Transport of hormones
187
Q

Describe the Mechanisms of Control of Local blood perfusion (Microcirculation)

A
  • Metabolic Mechanisms
  • Autoregulation
  • Local vasoconstrictive hormones and signalling molecules
187
Q

Describe the Mechanisms of Control of Local blood perfusion (Microcirculation)

A
  • Metabolic Mechanisms
  • Autoregulation
  • Local vasoconstrictive hormones and signalling molecules
187
Q

Describe the Mechanisms of Control of Local blood perfusion (Microcirculation)

A
  • Metabolic Mechanisms
  • Autoregulation
  • Local vasoconstrictive hormones and signalling molecules
188
Q

Describe when Autoregulation of Local blood flow is not possible

A
  • When proximal stenosis of e.g. coronary a
  • Perfusion pressure may be reduced below the autoregulatory range and distal vessels will be maximally dilated and flow will be reduced
  • Means when they need to increase flow, due to increased demands, vessel cannot accommodate this and ischaemia can occur
189
Q

Explain Metabolic Mechanisms for control of blood pressure and tissue perfusion at local level

A
  • Alters tissue blood flow in response to changes in tissue metabolism or oxygen availability
  • Theories:
  • Vasodilator theory - Related to increased amounts of vasodilator substances, metabolite products - E.g. adenosine, CO2, K+, H+
  • Oxygen demand theory - Reduced ppO2 –> Hypoxia-induced vasodilation - Could be reduced supply/demand
190
Q

Explain the Active Hyperaemia Mechanism for control of blood pressure and tissue perfusion at local level

A
  • Increased blood flow associated with increased metabolism in highly active tissues
  • Result reduced nutrients. used up + release of large quantities of vasodilator substances
  • e.g. muscles during exercise
191
Q

Explain the Reactive Hyperaemia Mechanism for control of blood pressure and tissue perfusion at local level

A
  • Transient increase in blood flow following temporary interruption to the blood supply to a tissue
  • Resulting hypoxia + lack of nutrients delivered to tissue –> ischaemia
  • Accumulation of metabolic vasodilators
  • When blood flow restored vasodilation occurs + blood flow is increased immediately
192
Q

What situations cause Reactive Hyperaemia?

A
  • Raynaud’s phenomenon
193
Q

Explain the Autoregulatory Mechanism for control of blood pressure and tissue perfusion at local level

A
  • Maintains constant blood flow despite changes in perfusion pressure, Involves vasodilation + vasoconstriction - Only possible to a certain degree/range
  • Theories:
  • Metabolic - Changes in O2 supply and levels of vasodilator substances e.g. when arterial pressure increases, perfusion increases, too much O2 and washes out vasodilators = Vasoconstriction
  • Myogenic - Mechanosensitive ion channels on vascular smooth muscle cells respond to stretch
194
Q

Within what microcirculations is the Autoregulatory mechanism of local blood flow control particularly relevant in?

A
  • Cerebral
  • Coronary
  • Renal
195
Q

Explain the Local Vasoactive Hormonal + Signalling Mechanism for control of blood pressure and tissue perfusion at local level

A
  • Released typically by endothelial tissue
  • Nitric oxide - Vasodilation of small arteries and arterioles upstream to microvasculature in response to increased flow/binding of vasoactive substances
  • Endothelin (Haemostasis) - Vasoconstriction to prevent excessive bleeding
  • Others - Prostaglandins (Prostacyclin, Leukotrienes, Thromboxanes), Histamine, Bradykinin, Serotonin, Platelet activating factor
196
Q

How is NO used pharmacologically?

A
  • To treat Angina attack

- Vasodilation of coronary vessels

197
Q

Explain the Chronic mechanisms involved in the control of blood pressure and tissue perfusion at local level.

A
  • Increased vascularity - Increase in number and size of blood vessels - E.g. long-term exercise training
  • Collateral circulation e.g. vessel obstruction
198
Q

How does local vascular response to hypoxia differ between the systemic and pulmonary circulation?

A
199
Q

What is the difference between active and reactive hyperaemia?

A
200
Q

What is the purpose of autoregulation?

A
  • To maintain local blood pressure and tissue perfusion despite changes in perfusion pressure
201
Q

What is the role of NO?

A
  • Vasodilation of small arteries and arterioles upstream to area of microcirculation
  • Affects smooth muscle cells by diffusing in
202
Q

Outline the mechanisms involved in the control of blood pressure and tissue perfusion at systemic level

A
  • BP regulated within narrow range
  • Mean arterial pressure - Modulated by changes to venous return, heart rate, myocardial contractility, and systemic vascular resistance
  • Neural mechanisms - Short term regulation
  • Hormonal Mechanisms - Longer term regulation
203
Q

What are the clinical signs and symptoms of heart failure?

A
  • Signs - Elevated JVP, Pulmonary crackles, displaced apex beat
  • Symptoms - Breathlessness, Ankle swelling, fatigue
204
Q

What is the Pathophysiological definition of Heart Failure?

A
  • An abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolising tissues

Block 2 (15 decks)

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