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Y1Systems > Week 2 CVS > Flashcards

Week 2 CVS Flashcards

1
Q

Define atherosclerosis

A

Formation of focal elevated leisons (in intima of large and medium sized arteries)

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2
Q

atheromas

A

In coronary arteries atheromatous plaques narrow lumen leading to ischaemia
Can have serious consequences due to myocardial ischaemia
Complicted by thromboembolism

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3
Q

Ateriosclerosis

A
  • Not Atheromatous
  • Smooth msucle hypertrophy, apparand reduplication of internal elastic laminae, intimal fibrosis decreases vessel diameter
  • Contributes to high frequency of cardiac, cerebral, colonic and renal ischaemia in the elderly.
  • Clinical effects most apparent when CVS further stressed by haemorrhage, minor sugery, infection or shock
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4
Q

What are the 4 different developmental stages of an atheroma?

A

Fatty Streak
Early atheromatous plaque
Fully developed atheromatous plaque
Complicated atheroma

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5
Q

Describe a fatty streak atheroma

A
  • Earliest significant leisons
  • Found in young children
  • Yellow linear elevation of intimal lining
  • Comprises masses of lipid-laden macrophages
  • No clinical significance
  • May disappear
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6
Q

Describe early atheromatous plaques

A
  • Young adults onwards
  • Smooth yellow patches in intima
  • Lipid laden macrophages
  • Progress to established plaques
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7
Q

Describe fully developed atheromatous plaques

A
  • Central lipid core with fibrous tissue cap, covered by arterial endothelium
  • Collagens (produced by smooth muscle cells) in cap provide structural strength
  • Inflammatory cells (macrophages, T-Lymphocytes, mast cells) reside in fibrous cap: recruited from arterial endothelium
  • Central lipid core rich in cellular lipids/debris derived from macrophages (died in plaque)
  • Soft highly thrombogenic, often rim of ‘foamy’ macrophages [foamy due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor]
  • Dystrophic calcification extensive, occurs in late plaque development [marker for atherosclerosis in angiograms/CT]
  • Forms at arterial branching points/bifurcations (turbulent flow)
  • Late stage plaques: Confluent, cover large areas
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8
Q

Describe a complicated atheroma

A
  • Features of established atheromatous plaque (lipid-rich core, fibrous cap) plus
  • Haemorrhage into plaque (calcification)
  • Plaque rupture/fissuring
  • Thrombosis
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9
Q

What are the signs of major hyperlipidaemia

A
  • Familial/primary vs acquired secondary
  • Biochemical evidence: LDL, HDL, total cholesterol, triglycerides
  • Premature corneal arcus
  • Tendon xanthomata (knuckles, achilles)
  • Xanthelasmata
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10
Q

Describe the development of atheromatous plaques

A

Two step process:

  1. Injury to endothelial lining of artery
  2. Chronic inflammation and healing response of vascular wall to agent causing injury
    - Chronic/episodic exposure of arterial wall to these processes -> formation of atheromatous plaques
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11
Q

Describe the pathogenesis of atherosclerosis

A
  1. Endothelial injury and dysfunction
  2. Accumulation of lipoproteins (LDL) in vessel wall
  3. Monocyte adhesion to endothelium → migration into intima and transformation to foamy macrophages
  4. Platelet adhesion
  5. Factor release from activated platelets, macrophages → smooth muscle cell recruitment
  6. Smooth muscle cell proliferation, extracellular matrix production and T-cell recruitment
  7. Lipid accumulation (extracellular and in foamy macrophages)
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12
Q

What are the 2 most common causes of endothelial injury?

A 
Haemodynamic disturbances (turbulent flow)
Hypercholesterolaemia
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13
Q

Describe Describe how hypercholesterolaemia can cause injury to the endothelium

A
  • Chronic hypercholesterolaemia can directly impair endothelial cell function by increasing local production of reactive oxygen species
  • Lipoproteins aggregate in intima and are modified by free radicals produced by inflammatory cells → modified LDL accumulated by macrophages but not completely degraded → foamy macrophages → toxic to endothelial cells plus release of growth factors, cytokines
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14
Q

describe how endothelial cells are functionally altered in atherosclerosis

A
  • enhanced expression of cell adhesion molecules (ICAM-1, E selectin)
  • High permeability for LDL
  • Increased thrombogenicity
  • Inflammatory cells, lipids -> intimal layer -> plaques
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15
Q

Describe advanced plaque formation

A
  • Large numbers macrophages, T-Lymphocytes
  • Lipid-laden macrophages die through apoptosis -> Lipid into lipid core
  • Response to injury = chronic inflammation process
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16
Q

What are the consequences of atheroma

A

Many plaques form over lifetime, many clinically unnoticed

Acute changes in plauqes (complicated atheroma) can have serious consequences

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17
Q

What does stenosis of 50-75% of vessel lumen lead to?

A

Critical reduction of blood flow in distal arterial bed -> reversible tissue ischaemia

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18
Q

What can very severe stenosis lead to?

A

Ischaemia - pain at rest

[unstable angina, eg ileal popliteal artery stenosis -> intermittent claudication]

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19
Q

What can longstanding tissue ischaemia lead to?

A

Atrophy of affected organ eg aterhosclerotic renal artery stenosis -> renal atrophy

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20
Q

What does rupture exposing collagen, lipid and debris to the blood stream do?

A

these are all highly thrombogenic plaque contents. Leads to the actiation of coagulation cascade and thrombotic occlusion in very short time

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21
Q

What does total occlusion of an artery lead to?

A

Irreversible iscahemia

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22
Q

embolisation of the distal arterial bed

A
  • Detachment of small thrombus fragments from thrombosed atheromatous arteries -> embolise distal to ruptured plaque
  • Embolic occlusion of small vessels -> small infarcts in organs
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23
Q

Ruptured atheromatous abdominal aortic aneurysm

A
  • Media beneath atheromatous plaques gradually wakened (lipid-related infammatory activity in plaque)
  • This leads to gradual dilation of vessle
  • Slow but progessive, seen in elderly, often asymptomatic
  • Sudden rupture -> massive retroperitoneal haemorrhage
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24
Q

What diameter does an aneurism become at risk of rupture?

A

5cm

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25
Q

What is a mural thrombuis

A

Emboli to legs

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26
Q

Describe vulnerable atheromatous plaques

A
  • Thin fibrous caps, large lipid core, prominent inflammation
  • Proncounced inflammatory activity -> degradation, weakening fo plaque -? increased risk of plaque rupture
  • Secretion of proteolytic enzymes, cytokines and reactive oxygen species by plaque inflammatory cells
  • Often large fibrocalcific component, little inflammation
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27
Q

What is blood flow?

A

Amount of blood moved per unit time

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28
Q

What is stasis?

A

Stagnation of blood flow

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29
Q

What is turbulence?

A

Forceful, unpredictable flow

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30
Q

What do defects in blood flow cause?

A
  • Thromboembolism
  • Atheroma
  • Hyperviscosity
  • Spasm
  • External compression
  • Vasculitis
  • Vascular steal
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31
Q

What is virchows triad?

A
  • Changes in the blood vessel wall
  • Changges in the blood constituents
  • changes in the pattern of blood flow
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32
Q

Describe the pathogenesis of thrombosis

A
  1. Atheromatous CA
  2. Turbulent blood flow
  3. Loss of intimal cells, denuded plaque
  4. Collagen exposed to which platelets adhere
  5. Fibrin meshwork forms - RBC’s trapped
  6. Alternating bands: Lines of Zahn
  7. Further turbulence and platelet deposition
  8. Propagation
  9. CONSEQUENCES
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33
Q

What do the consequences of thrombosis depend on?

A

Site
Extend
colalteral circ.
Common clinical scenariosL DVT, Ischaemia limb, MI

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34
Q

What is an embolus

A

Detached intravascular soil, liquid or gaseous mass

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35
Q

Where do venous thromboembolus originate from?

A

Originate from deep venous thromboses (lower limbs)

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36
Q

What is the most common thromboembolic disease

A

Venous thromboembolus

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37
Q

What are the types of embolus?

A 
Fat
Gas
Air
Tumour
Trophoblast
Septic material
Amniotic fluid embolism
Bone marrow
Foreign bodies
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38
Q

What is rheumatic fever

A
  • Disease of disordered immunity
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39
Q

Where are some inflammatory changes caused by rheumatic fever

A
  • Heart
  • Joints
  • Sometimes neurological symptoms
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40
Q

What is the presentation of someone with RF

A

Typically present with ‘flitting’ (painful) polyarthritis of large joints (wrists, elbows, knees, ankles) plus skin rashes and fever

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41
Q

What may RF cause in the heart?

A

Pancarditis (inflammation affecting endocardium, myoicadium in acute phase; heart murmers common)

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42
Q

Describe how RF may cause damage to the heart tissue

A

May be combination of antibody mediated and T cell mediated reactions

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43
Q

What is an aschoff body

A

Focus of chronic inflammatory cells, necrosis and activated macrophages.
Seen in heart in acute rheumatic fever

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44
Q

What can pancarditis in acute RF progress to?

A

Chronic Rheumatic heart disease, mainly manifesting as valvular abnormalities

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45
Q

What does inflammation of the endocardium and left sided valves result in?

A

fibrinoid necrosis of the valve cusps/chordea tendineae over which (and long line of closure) form small vegitations

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46
Q

What is rheumatic heart disease characterised by?

A

Principally by deforming fibrotic valvular disease, particularly involving the mitral valve: Typically leaflet thickening commissural fusion and shortening and thickening and fusion of the chordae tendineae

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47
Q

What can RHD cause?

A

Mitral stenosis
Can cause mitral regurg but now most commonly due to ischaemic heart disease
Potentially still causes an aortic regurg/incompetance

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48
Q

What are the 4 types of hypoxia?

A

Hypoxic
Anaemic
Stagnant
Cytotoxic

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49
Q

What is anaemic hypoxia

A

Normal inspired O2 but blood abnormal

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50
Q

What is stagnant hypoxia?

A

Normal inspitred O2 but abnormal delivery

  • Local: occlusion of vessel
  • systemic: Shock
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51
Q

What is cytotoxic hypoxia?

A

Normal inspired O2 but abnormal at tissue level

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52
Q

What is the functional effect of ischaemia

A

Blood O2 supply fails to meet demand due to decreased supply; incrased demand or both

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53
Q

What are the 2 types of necrosis and where are they seen

A

Coagulative necrosis - eg heart, lung

Colliquitive necrosis - brain

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54
Q

Describe the appearance of an infarct after less than 24 hours

A

No change on visual inspection

A few hours to 12 hours post insult, able to see swollen mitochondria on electon microscopy

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55
Q

Describe the appearance of an infarct between 24 and 48 hours

A

Pale infarct seen in myocardium, spleen, kidney and solid tissue
Red infarct seen in the lung and liver
Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features

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56
Q

Describe the appearance of an infarct after approx 72 hours

A

Macroscopically:
pale infarct - yellow/white and red periphery
Red infarct - little change
Microscopically: Chronic inflammtion; macrophages remove debir, granulation tissue, fibrosis

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57
Q

What is the end result of an infarct?

A

Scar replaces area of tissue damage

Shape depends on territory of occluded vessel

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58
Q

Describe the presentation of MI 4-12 hours after the initial occlusion

A

Early coagulation necrosis, oedema, haemorrhage

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59
Q

Describe the presentation of MI 12-24 hours after the initial occlusion

A

Ongoing coagulation necrosis,
myocytes changes
Early neutrophilic infiltrate

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60
Q

Describe the presentation of MI 1-3 days after the initial occlusion

A

Coagulation necrosis
Loss of nuclei and striations
Brisk neutrophilic infiltrate

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61
Q

Describe the presentation of MI 7-10 days after the initial occlusion

A

Well developed phagocytosis

Granulation tissue at margins

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62
Q

Describe the presentation of MI 10-14 days after the initial occlusion

A

Well established granulation tissue with new blood vessels and collagen deposition

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63
Q

Describe the presentation of MI 2-8 weeks after the initial occlusion

A

Increased collagen deposition, decreased cellularity

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64
Q

Describe the presentation of MI >2 months after the initial occlusion

A

Dense collagenous scar

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65
Q

What is a transmural infarction?

A

When the ischaemic necrosis affects the full thickness of the myocardium

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66
Q

What is a subendocardial infarction?

A

When the ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the chart

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67
Q

Describe the histological features of a transmural and subendocardial infarction

A

Histological features are the same - granulation tissue stage followed by fibrosis - in subendocardial infarct possibly slightly shortened compared to transmural infarct

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68
Q

How are acute infarcts classified?

A

According to whether there is elevation of the ST segment on the ECG

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69
Q

What is the classification of a myocardial infarct If there is no ST segment elevation but a significantly elevated serum troponin level

A

Non STEMI or an NSTEMI

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70
Q

What do NSTEMIs tend to correlate with?

A

Subendocardial infarctions

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71
Q

What is angina

A

A discomfort in the chest and or adjacent area associated with myocardial ischaemia but without myocardial necrosis

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72
Q

What is the most common cause of angina?

A

Obstructive coronary atheroma

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73
Q

What features make an angina diagnosis less likely

A

Sharp/Stabbing pain; pleuritic or pericardial
Associated with body movements or respiration
Very localised: pinpoint site
Superficial with/or without tenderness
No pattern to pain, particularly if often occuring at rest
Begins some time AFTER exercise
Lasting for hours

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74
Q

Describe a 1 on the scale of severity of the Canadian classification of angina severity (CCS)

A

Ordinary physical acticity does not cause angina symptoms, only on significant exertion

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75
Q

Describe a 2 on the scale of severity of the Canadian classification of angina severity (CCS)

A

Slight limitation of ordinary activity, symptoms on walking 2 blocks or >1 flight of stairs

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76
Q

Describe a 3 on the scale of severity of the canadian classification of angina severity (CCS)

A

Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs

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77
Q

Describe a 4 on the scale of severity of the canadian classification of angina severity (CCS)

A

Symptoms on any activity, getting washed/dressed causes symptoms

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78
Q

Describe the possible presentation of angina

A 
Obesity
Xanthalasma and corneal arcus (hypercholesterolaemia)
Hypertension
Abdominal aortic aneurism
Arterial bruits
Abscent or reduced peripheral pulses
Diabetic retinopathy
Hypertesive retinopathy
Fundoscopy
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79
Q

What are the signs of exacerbating or associated conditions

A

Pallor anaemia
Tachycardia: Tremor, hyper-reflexia of hyperthyroidism
Ejection systolic murmur of mitral regurg
Signs of HF such as basal crackles, elevated JVP, peripheral oedma

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80
Q

What are the investigations for angina

A

Bloods
CXR
ECG
ETT

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81
Q

What is a diagnostic test for angina

A

ETT

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82
Q

What is seen in an ETT for a positive diagnositc test for angina

A

commonly ST segment depression is seen

-‘ve ETT doesnt exclude significant coronary atheroma but if negative at high workload overall prognosis is good

83
Q

Describe myocardial perfusion imaging

A

Superior to ETT in detection of CAD, localisation of ischaemia
Expensive, invovled radioactivity; depending on availability used where ETT no possible/equivacol
Either exercise or pharmacological stress: Adenosine, dipyridamole or dobutamine
Radionulide tracer injected at peak stress on one occasion obtained and at rest on another
Normal myocardium takes up tracer

84
Q

Describe tracer seen at rest but not after stress

A

= Ischaemia

85
Q

Describe tracer seen seen neither rest or after stress

A

= Infarction

86
Q

What are the indications invasive angiography

A

Early or strongly positive ETT (suggests multi-vessel ds)
angina refractory to medical therapy
Diagnosis not clear after non-invasive tests
Young cardiac patients due to work/life effects
Occupation to lifestyle with risk

87
Q

Where are arterial cannulas inserted into

A

Femoral or radial artery

88
Q

Describe the treatment of angina for influencing disease progression

A

Statins - consider if total cholesterol >3.5 mmol/L
ACEI - if increased CV risk and atheroma
Aspirin 75mg or clipidrogrel if intolerant of aspirin

89
Q

What is the effect of statins in angina

A

Reduce LDL-Cholesterol deposition in atheroma dn aslo stabilise atheroma reducing plaque rupture and ACS

90
Q

What is the effect of ACEI in angina

A

Stabilise endothelium and also reduce plaque rupture

91
Q

What is the effect of aspirin in angina

A

May not directly affect plaque but does protect endothelium and reduces platelet activation/aggregation

92
Q

What are the possible treatments for relief of anginal symptoms

A 
B blockers
Ca Channel Blockers
iK channel blockers
Ca Channel blcokers
Nitrates
K channel blockers
93
Q

What is the effect of B blockers in angina

A

Achieve resint HR < 60bpm

- Reduced myocardial work and have anti-arrhythmic effects

94
Q

What is the effect of Ca channel blockers in angina

A

Achieve resting hr <60bpm

- central acting eg diltiazem/verapamil if beta blockers contraindicated

95
Q

What is the effect of k channel blockers in angina

A

of k channel blockers in angina

Ivabridine is a newer medication which reduced sinus node rate

96
Q

What is the effect of ntirates in angina

A

Produce vasodilation

- Used as short or prolonged acting tablets, patches or as rapidly actin sublingual GTN spray for immediate use

97
Q

Does stenting approve prognosis

98
Q

What is the effect of CABG surgery

A

Good lasting benefit - 80% symptom free 5 years later

99
Q

Describe the patients who derive prognostic benefit from CABG

A

70% of left main stem artery
Significant proximal three vessel coronary artery disease
Two vessel coronary artery disease that includes significant stenosis proximal left anterior descending CA and who have ejection fraction <50%
Patients must continue disease modifying medication and predictable dterioration in vein grafts after 10 years

100
Q

Define hypertension

A

Is that bp at which the benefits of treatment with antihypertensive agnets in reduceing cardiovascular, cerebrovascular and peripheral vascular disease outwight the risks of treatmen

101
Q

Describe Stage 1 hypertension

A

Clinic 140/90 or higher

ABPM daytime average 135/85

102
Q

Describe stage 2 hypertension

A

Clinic 160/100 or higher

ABPM daytime average 150/95

103
Q

Describe Stage 3 hypertension

A

Systolic >180

Diastolic >110

104
Q

When does bp decrease naturally

A

During the night

105
Q

What are the methods of measuring kidney function

A

Renal ultrasound
EGFR
Proteinuria = presence of abnormal proteins in urine which may indicate change to the kidneys

106
Q

What is the treatment for reducing LV mass?

A

ACEI or ARB

107
Q

What is the target BP

108
Q

When do you commence with hypertension treatment?

A

When 10% chance of CVD within 10 years

[treatment reduces MI by 16-30% and cerebrovascular disease 40-50%]

109
Q

Describe the approach to medication for hypertension

A

Stepped approach for treatment of hypertensives

Use low dose of several drugs as this minimises adverse effects and maximises patient compiance

110
Q

Describe renin concentrations over the ages

A

Young people = high renin

Old people = low renin

111
Q

What antihypertensive drugs would you prescribe in a patiennt <55

112
Q

What antihypertensive drugs would you prescribe in a patiennt >55

A

CCB/Thiazide type diuretic

113
Q

Are ACEI teratogenic?

A

YEP - they change the babies, dont change the babies man

114
Q

Whwn would you start treating patients >80-y/o

A 
ABPM 85/135
Established CVD
Diabetes
10 year risk of CVD 20% or greateer
Evidence of target organ damage
Renal disease
115
Q

Anithypertensive drugs are offered to anyone after they are on what stage hypertension?

116
Q

Describe the first step of hypertensive treatment

A

Prescribe a CCB or thiazide type diuretic

[in patients under 55 offere CCB or ACEI]

117
Q

Describe the second step of hypertensive treatment

A

Add thiazide type diretic such as indapamide to CCB or ACEI/ARB

118
Q

Describe the third step of hypertensive treatment

A

Add CCB, ACEI and diuretic together

119
Q

Describe the third step of hypertensive treatment

A
  • Consider compliance issues
  • Consider higher-dose thiazide-like diuretic treatment if the blood K level is higher than 4.5 mmol/l
  • Consider further diuretic therapy with low dose spironolactone (25 mg once daily) if the blood K level is <4.5 mmol/l
    • Caution in people with a reduced EGFR because they have an increased risk of hyperkalaemia
120
Q

Describe the mechanism of thiazide type diuretics

A

Increase Na exretion + urine volume.
Reduction in blood volume
Long term: reduction in the TPR due to suble alterations in the contractile responses of vascular smooth muscle

121
Q

Describe the mechanism of ACE inhibitors and give some examples

A

Rampril + perindopril

  • competitively inhibits actions of angiotensin converting enzyme
  • Has cough as common side effect
122
Q

What are the ACEI contraindications?

A

renal artery stenosis
Renal failure
Hyperkalaemia

123
Q

What are the relevant drug to drug interations concerning ACEI

A

NSAIDS - prepitate acute renal failure
K suppliments = hyperkalaemia
K sparing diruetics = Hyperkalaemia

124
Q

What is Conns syndrome

A

too much aldosterone - renin levels reduced

125
Q

Conns syndrome

A

Hypertension is symptom
Causes are increased size of adrenal glands where aldosterone is produced or adenoma
Uncommon causes: adrenal cancer or familial hyperaldosteronism

126
Q

give examples of ARBS

A

Losartan
Valsartan
Candesartan
Irbesartin

127
Q

What are the 2 types of CCB?

A

Vasodilator or rate limiting

128
Q

Give examples of vasodilating CCBs

A

Amlodipine

Felodipine

129
Q

Give some examples of rate limitng CCBs

A

Verapamil

Diltiazem

130
Q

Describe the mechanism of CCBs

A
  • Block L type ca Channels (voltage type)
  • Selectively between vascular and cardiac L type channels
    Relaxing large + small arteries -> reducing peripheral resistance
131
Q

What are the contraindications for CCBs

A

Acute MI
HF
Bradycardia

132
Q

What are the ADRS for CCBs

A

Flushing
headache
Ankle oedema
Indigestion and reflux oesophagitis

133
Q

What are common side effects for CCBs

A

Bradycardia

Constipation

134
Q

hiazide type diuretics

A

Indapamide
Clortidladone
- Proven benifit in stokre and MI reduction
- ADRs not common but are gout and impotence

135
Q

What are the less commonly used antihypertensive agents?

A

Alpha-adrenorecepor antagonists: doxozosin
Centrally acting agents: Methycdopamonoxnidne
Vasodilators: Hyralazine, monoxidil

136
Q

What is ACS?

A

New onset of a collection of symptoms related to a problem with the coronary arteries

137
Q

What do the CA supply?

A

Myocardial cells

138
Q

What does ACS cause?

A

Myocardial ischaemia

139
Q

What is stable angina caused by?

A

‘Stable’ Coronary leison

140
Q

What are acute coronary syndromes caused by?

A

Unstable coronary leison

141
Q

How do you diagnose ACS?

A

Detection of cardiac cell death (troponin) AND: symptoms of ischaemia

  • New ECG changes
  • Evidence of coronary problem on coronary angiogram or autopsy
  • Evidence of new cardiac damage on another test
142
Q

What is a type 1 MI?

A

Spontaneous MI associated with iscahemia and due to a primary coronary event such as plaque erosion, rupture, fissuring or dissection

143
Q

What is a type 2 MI?

A

Due to imbalance in suppply and demand of oxygen. Result of ischaemia but not ischaemia from thrombosis of CA

144
Q

What is a type 3 MI?

A

Sudden Cardiac death, including cardiac arrest, with symptoms of ischaemia, accompanied by new ST elevation of LBBB. Verified coronary thrombus by angiography or autopsy but death occurring before blood samples could be obtained or before biomarkers appear in the blood

145
Q

What is a type 4a MI?

A

MI associated with PCI. PCI related crease of biomarkers greater than X 99th percentile of the upper reference limit is by convention defined as MI

146
Q

What is a type 4b MI?

A

MI assocaited with verified statment stent thrombosis via angiography or autopsy

147
Q

What is a type 5 MI?

A

MI Assocaiteed with CABG, >5x99th percentile upper reference limit plus new Q waves or LBB or imaging of new loss

148
Q

What does LBBB stand for?

A

Left bundle branch block
[ A cardiac conduction abnormality seen on the ECG. In this condition, activation of the left V of the heart is delayed, which causes the LV to contract later than the RV]

149
Q

What type of MI would be a vasospasm or endothelial dysfunction be?

150
Q

What type of MI would be a fixed atherosclerosis and supply-demand imbalance by?

151
Q

What type of MI would a plaque rupture with a thrombus be?

152
Q

What type of MI would be a supply demand imbalance alone?

153
Q

Describe the typical presentation of a patient with STEMI

A
  • Ischaemic sounding heart pain
  • May radiate to neck/arm
  • Often deny it is a ‘pain’, more of a ‘discomfort, weight or tightening’
  • May be associated with nausea, sweating and breathlesness
154
Q

What does the initial ECG of a person with a complete coronary occlusion show?

A

ST elevation

155
Q

What does the ECG at 3 days show after a complete coronary occlusion

156
Q

What does the initial ECG of a partial coronary occlusion show?

A

ST depression
T wave inversion
May still be normal

157
Q

What does the ECG of a partial coronary occlusion at 3 days show?

A

No Q waves

158
Q

What may show/not be shown on an ECG of a posterior MI

A

As the posterior wall supplied by the let circumflex artery may not see any ST elevation anywhere, even if LCx is completley blocked

159
Q

If a posterior MI is suspected what investigation is reccomended?

A

Put ECG leads on back of chest - will see opposite changes in leads however

160
Q

What is a mechanical reperfusion therapy?

161
Q

What is a pharmacological reperfusion therapy?

A

Thrombolysis

162
Q

When would you not give thrombolysis

A
  • If recent stroke, or ever had a previous intercranial bleed
  • Caution if had recent surgery, on warfarin, or has severe hypertension
163
Q

How do you decide whether to treat with thrombolysis or cath lab

A

If you can get to cath lab within 2 hours, then dont give thrombolysis

164
Q

What are the investigations for a NSTEMI

A 
Serial ECG's
- As to not miss an evolving STEMI or a posterior STEMI
Blood tests
- Troponin
- Cholesterol levels
165
Q

What are the possible treatment options for an ACS with no ST elevation

A 
GTN
Opiates
Antithrombotic drugs with a P2Y12 antagonists
Anticoagulant drugs
B blockers
Statins
ACEI
166
Q

What are the effects of GTN?

A

Vasodilator - opens up CA - wont help if artery is completely blocked

167
Q

How can GTN be given?

A

Sub-lingual or as IV

168
Q

What are the effects of morphine

A

Help relieve anxiety

Helps venodilate which may have haemodynamic effects

169
Q

Describe the procedure of dual anti-platelet therapy for an NSTEMI

A

Aspirin plus one of the P2y12 receptor antagonists:

  • Clopidogrel
  • Tricagrelor
  • Prasugrel
170
Q

Describe the dosing of:

  • Aspirin
  • Clopidogrel
  • Tricagrelor
  • Prasugrel
A

Aspirin: 300mg loading dose, then 75mg
Clopidogrel: 300mg loading dose, then 75mg
Tricagrelor: 180mg loading dose, then 90mg
Prasugrel: 60mg loading dose, then 10mg

171
Q

What procedure is given to those with NSTEMI unless frail/elderly?

A

Coronary angiogram

172
Q

What is the management for someone with an NSTEMI

A
  • Keep attached to cardiac monitor for first 24-48 hours
  • Listen to new murmers and signs of heart failure every day
  • Start ‘secondary prevention’ medication
  • Do an Echo
173
Q

What 2 conditions would be classes as ACS

A

MI (STEMI or NSTEMI)

Unstable angina pectoralis (UAP)

174
Q

What 2 conditions would be classes as stable coronary heart disease

A 
Angina pectoralis (stable)
Silent ischaemia
175
Q

List 8 classes of drugs used to treat stable CAD

A 
B blockers
CCBs
Ivabradine
Nitrates
K Channel activators
Na current inhibitor 
Aspirin/clopidogrel/ticagrelor
Cholesterol lowering agents
176
Q

What is the main action of B blockers

A

Lower HR
Lower force of contraction
Lower systolic wall tension

177
Q

Name 2 examples of B blockers

A

Bisoprolol

Atenolol

178
Q

Describe how B-blockers function?

A

Antagonists of B1 and B2 receptors

i.e block sympathetic system

179
Q

Name 2 rate limiting CCBs

A

Diltiazem

Verapamil

180
Q

Name a vasodilating CCB

181
Q

Describe how CCBs function

A

Prevent Ca influx into myocytes + smooth muscle lining of arteries/arterioles
Via blocking L-type Ca2 channels

182
Q

What is important to remember when prescribing Nifedipine?

A

Never use Nifedipine immediate release (could cause MI/stroke) –> use delayed/sustained release

183
Q

What is the main action of nitrovasodilators/ntirates

A

Vasodilation (arterioles + peripheral)

184
Q

Name 3 vasodilators

A

GTN
Isosorbide mononitrate
Isosorbide dinitrate

185
Q

Describe how nitrovasodilators function

A
  • Relax almost all smoth muscle via NO release
  • This stimulates cGMP production -> smooth muscle relaxation
  • Decreases preload and afterload
  • Thus decreases myocardial O2 consumption
186
Q

What is the main action of potassium channel activators?

A

Coronary vasodilator properties

187
Q

Name a pottasium channel activator

A

Nicorandil

188
Q

Describe how potassium channel activators function

A

Activates ATP sensitive K channels which allow K entry into myoccytes
This inhibits Ca influx
This then induces relaxation of smooth muscle + vasodilatiom

189
Q

What is the main action of a Sinus node inhibitor?

A

Decreases HR and therefore myocardial demand

190
Q

Name a sinus node inhibitor

A

Ivabradine

191
Q

When should ivabradine be used?

A

For symptomatic treatment of chroncic stable angina in adults with normal sinus rhythm + HR >70bpm

192
Q

What is the main action of late Na current inhibitors

A

Decreases heart wall tension causing decreased O2 requirement

193
Q

Name a late Na current inhibitor

A

Ranolazine

194
Q

Describe how late Na current inhibitors function

A
  • Inhibits presistent or late inwardd Na current in heart muscle
  • Leads to decrease in intracellular Ca levels
    Leads to reduced heart wall tension
195
Q

What does NICE reccomend as second line drugs for angina

A

Ranolazine

196
Q

What medications are used for anti-platelet therapy?

A 
Aspirin
P2Y12 inhibitors (eg clopidogrel, icagrelor, prasugrel)
197
Q

Describe how anti-platlet agents function

A

Prevent formation of pletlet aggregates which are important in the pathogenesis of angina

198
Q

how does aspirin inhibit platelet aggregation?

A

Is a potent inhibitor of platelet thromboxane production (thromboxane stimulates platelet aggregation)

199
Q

How do P2Y12 inhibitors work?

A

Block pletlet P2Y receptor, which plays a key role in platelet activation + amplification of arterial thrombus formation

200
Q

When should you use dual anti-platlet therapy

A

In patients with high/moderate risk of ischaemic evetns who do not have a high bleeding risk

201
Q

What is the main action of cholesterol lowering agents?

A

Lower LDL cholesterol level

202
Q

Name 2 cholesterol lowering agents

A

Atorvastatin

Simvastitin

203
Q

How can you identify a cholesterol lowering agent from the name

A

End in statin (as they are statins)

204
Q

Describe how cholesterol lowering agents

A

Are HMG CoA reductase inhibitors

Y1Systems (24 decks)

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