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BDS2 BAMS Cardiovascular > 2. Acute Coronary Syndromes > Flashcards

2. Acute Coronary Syndromes Flashcards

1
Q

Processes involved with CVS diseases (2)

A

Ischaemia

Infarction

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2
Q

Definition of ischaemia

A

Blood vessel narrowing

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3
Q

Ischaemia action (3)

A

Inadequate oxygen delivery for tissue needs
‘Cramp’ in affected tissue/muscle
No residual defect at first

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4
Q

Examples of ischaemic diseases (2)

A

Angina pectoris

Peripheral vascular disease (PVD)

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5
Q

Definition of infarction

A

Blood vessel occlusion

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6
Q

Infarction action (3)

A

No oxygen delivery, resulting in tissue death
More severe pain
Loss of tissue funciton

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7
Q

Examples of infarction diseases (2)

A

MI

CVA

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8
Q

Definition of angina pectoris (2)

A

Reversible ischaemia of heart muscles

Involves narrowing of one or more coronary arteries

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9
Q

Aetiology of angina

A

Narrowing and hardening of coronary arteries (atherosclerotic plaques)

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10
Q

Effect of angina (2)

A

Reduces blood supply to heart

Reduces oxygen concentration to heart

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11
Q

Mechanism of angina (3)

A

Reduced oxygen concentration to heart
Myocardial cells switch from aerobic to anaerobic respiration
This progressively impairs metabolic, mechanical and electrical functions

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12
Q

Cause of angina pectoris

A

Chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium (nerve fibres from T1-T4)

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13
Q

Different types of angina (2)

A

Classical

Unstable

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14
Q

Differences between classical and unstable angina (2)

A

Classical - worse with exacerbation/exercise

Unstable - more unpredictable, with symptoms seen at rest with no biomarkers

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15
Q

General angina symptoms (7)

A 
Central, crushing chest pain/discomfort (tight, dully or heavy)
Pain radiates to arm, back, jaw
Breathlessness
Nausea
Feeling unusually tired
Dizziness
Restlessness
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16
Q

Classical angina symptoms (5)

A 
No pain at rest
Pain with certain level of exertion (cold weather)
Pain relieved by rest
Patient lives within limit of tolerance
Gradual deterioration over time
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17
Q

Classical angina signs (2)

A

Often none

Occasionally, when not caused by atherosclerosis alone, hyper dynamic circulation

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18
Q

Components of hyperdynamic circulation

A

Anaemia
Hyperthyroidism
Hypervolaemia

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19
Q

Angina investigations (5)

A 
ECG
Eliminate other diseases (thyroid, anaemia, valve)
Angiography
Echocardiography
Isotope studies (function assessment)
20
Q

ECG results for angina (3)

A

Shows areas of myocardial ischaemia
Angina will appear as an ST segment elevation
AS angina worsens, ST segment will lower, finally showing as an ST segment depression

21
Q

Angina treatment (2)

A

Reducing oxygen demands of the heart

Increase oxygen delivery to tissues

22
Q

Methods to increase oxygen delivery to tissues (2) and descriptions (2)

A

Angioplasty/stenting - dilating blocked/narrowed vessels. Stretch artery back to normal size. Method of percutaneous intervention (PCI)
CABG (coronary artery bypass grafting) - bypass blocked/narrowed vessels

23
Q

Non-drug angina therapies (2)

A 
Explaining illness (learning to live within limitations)
Modifying risk factors
24
Q

Angina drug therapies (4) and example treatments (4)

A

Reduce MI risk - aspirin
Target hypertension - diuretics, Ca-channel blockers, ACE inhibitors, B-blockers
Reduce preload/dilate coronary vessels - nitrates
Emergency treatment - GTN

25
Q

Definition of PVD

A

Angina of tissues, usually lower limbs

26
Q

Cause of PVD

A

Due to atheroma in femoral/popliteal vessels

27
Q

Complications of PVD (4)

A

Claudication in limbs on exercise
Limitation of function
Poor wound healing
May lead to tissue necrosis and gangrene

28
Q

PVD management

A

As with angina

29
Q

Infarction mechanism (3)

A

Atheroma in vessel causes thrombosis on surface which can rapidly enlarge, occluding the vessel
Atheroscerotic plaque detaches from vessel wall, travelling in the blood
Plaque blocks vessel, preventing blood flow

30
Q

Where can infarction occur (3)

A 
Coronary artery (heart)
Femoral/popliteal artery (limb)
Carotid artery (brain)
31
Q

Types of infarction (5_

A 
Spontaneous (primary coronary event)
MI secondary to ischaemia
Sudden death with symptoms of ischaemia and evidence of ST elevation/thrombosis
MI from PCI
MI from CABG
32
Q

Strategy for treating infarctions (2)

A

Reducing tissue loss from necrosis (angioplasty/thrombolysis, CABG)
Prevent further episode (risk factor management, aspirin)

33
Q

Definition of TIA

A

Transcient ischaemic attack - mini stroke of short duration (<24hrs)

34
Q

Effects of TIA

A

Defects variable, usually causes loss of function

35
Q

MI symptoms (5)

A 
Pale
Nausea
Sweaty
Pain radiates from chest/down arm
Patient feels like they're going to die
36
Q

MI investigations (2)

A

Cardiac enzymes - troponin measured as it leaks from dead cardiac muscle

37
Q

MI ECG results

A

ECG - abnormalities vary in position with infarct, but may be normal

38
Q

Primary care MI treatment (4)

A

Get patient to hospital
Administer analgesia and aspirin
Reassure patient
BLS if required

39
Q

Hospital MI treatment (4)

A

Primary PCI (if within 3 hours)
Thrombolysis if indicated (if PCI unavailable)
Drug treatment to reduce tissue damage
Prevent recurrence/complications

40
Q

Hospital care drugs

A

Aspirin

Thrombolysis (streptokinase, TPA)

41
Q

Side effects of TPA

A

TPA will dissolve all clots, not just local clots

42
Q

Thombolysis contraindications (8)

A 
Injury
Surgery
IM injections
Severe hypertension
PUD
Diabetic eye disease
Liver disease
Pregnancy
43
Q

MI complications (6)

A 
Death
Arrhythmias
HF
Ventricular hypo function and thrombosis
DVT and pulmonary embolism
Thrombolysis complications
44
Q

Medical management of MI (2)

A

Prevent next MI

Treat complications

45
Q

Preventing next MI involves (4)

A

Modify risk factors
Aspirin
B-blocker (reduce excitability of heart and reduce arrhythmia effect)
ACE inhibitor
Combo. of aspirin, B-blocker, ACE inhibitor suggests patient is a previous MI sufferer

46
Q

Treating complications include (3)

A

HF
Arrhythmias
Psychological stress

BDS2 BAMS Cardiovascular (7 decks)

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