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Cardiovascular > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

What are the clinical classifications for unstable angina?

A

Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina – angina out of the blue – somethings happened to the coronary artery

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2
Q

What is a diagnosis of angina based on?

A

history
ECG
troponin (no significant rise in unstable angina)

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3
Q

When can an ST elevated MI be diagnosed? (STEMI)

A

can usually be diagnosed on ECG at presentation

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4
Q

What is a non- ST- elevation MI?

A

retrospective diagnosis made after troponin results and sometimes other investigation results are available

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5
Q

Where is the ST segment?

A

ST segment between QRS complex and T wave is elevevated

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6
Q

How can a Q-wave MI or non-Q wave MI be defined?

A

basis of whether new pathological Q waves develop on the ECG as a result of MI

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7
Q

What are ST elevation MI and MI assosciated with LBBB related to?

A

larger infarcts
unless effectively treated more likely to lead to pathological Q wave formation, heart failure or death

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8
Q

R wave and MI

A

R wave generated by electrically viable myocardium under ECG lead – if we replace this with scar tissue lose R wave and you get pathological R wave

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9
Q

NON-Q wave MI?

A

Poor R wave progression - not much R wave, generate small amount
ST elevation - residual
Biphasic T wave

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10
Q

Q wave MI?

A

Complete loss of R wave

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11
Q

Cardiac chest pain in MI?

A

unremitting
usually severe but may be mild or absent
occurs at rest
associated with sweating, breathlessness, nausea and/or vomiting
one third occur in bed at night
Caused by occlusion of arteries

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12
Q

What does MI do?

A

Usually causes permanent heart muscle damage although this may not be detectable in small MIs

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13
Q

Risk factors for MI?

A

higher age
diabetes
renal failure
left ventricular systolic dysfunction
elevated NT
proBNP level
Elevated Troponin

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14
Q

What is the initial management for acute coronary syndrome?

A

Get in to hospital quickly – 999 call
Need defibrillator

Paramedics – if ST elevation, contact primary PCI centre for transfer

Take aspirin 300mg immediately

Pain relief

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15
Q

What is the hospital management for MI?

A

Make diagnosis
Bed rest
Oxygen therapy if hypoxic
Pain relief – opiates/ nitrates
Aspirin +/- platelet P2Y12 inhibitor
Consider beta-blocker
Consider other antianginal therapy
Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy

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16
Q

Main cause of acute coronary syndrome?

A

Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases

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17
Q

Some uncommon causes of acute coronary syndrome?

A

Stress-induced cardiomyopathy
coronary vasospasm without plaque rupture
drug abuse (amphetamines, cocaine)
dissection of the coronary artery related to defects of the vessel connective tissue
thoracic aortic dissection

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18
Q

What is troponin?

A

Troponin C Troponin I and Troponin T
Protein complex regulates actin:myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for acute coronary syndrome
May not represent permanent muscle damage

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19
Q

Positive troponin is found in?

A

gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs

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20
Q

Elevated troponin indicates what in patients suspected with ACS?

A

Higher risk

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21
Q

What are the agonists for platelet activation?

A

Thrombin > Coagulation
Thromboxane A2
Collagen
5HT
ADP
ATP
Fibrinogen > Fibrin

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22
Q

What is the effect of aspirin?

A

Irreversible inactivation of cyclo-oxygenase 1
Stops conversion of collagen to Thromboxane A2

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23
Q

What does Thrombin do?

A

activates platelets – final factor in coagulation cascade as it cleaves fibrin from fibrinogen

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24
Q

What is the fibrinolytic system?

A

Endothelium releases tissue plasminogen activator (TPA)
TPA > Plasminogen > plasmin > Fibrin to fibrin degradation products

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25
Q

What is P2Y12?

A

important amplification process in platelet activation
Makes response of platelets much more aggressive

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26
Q

What are some P2Y12 antagonists/ inhibitors?

A

Clopidogrel
Prasugrel
Ticagrelor

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27
Q

What do P2Y12 inhibtors do?

A

Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’
Increase risk of bleeding so need to exclude serious bleeding prior to administration

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28
Q

What are some GPIIb/IIIa antagonists?

A

Abciximab
Tirofiban Eptifibatide

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29
Q

What do GPIIb/IIIa antagonists do?

A

Only intravenous drugs available

Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

Increase risk of major bleeding so used selectively

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30
Q

What do anticoagulants do?

A

Used in addition to antiplatelet drugs

Target formation and activity of thrombin

Inhibit both fibrin formation and platelet activation

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31
Q

What does fondaparinux (anticoagulant) do?

A

used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used

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32
Q

When do you use full dose anticoagulation?

A

used during PCI: options are
heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin)
direct thrombin inhibitor bivalirudin (expensive, not used in Sheffield)

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33
Q

When is high dose heparin used?

A

cardiopulmonary bypass for CABG surgery

34
Q

When is a coronary angiography usually performed?

A

for patients with troponin elevation or unstable angina after medical therapy

35
Q

What is the most used revascularisation procedure?

A

PCI

36
Q

What are the factors affecting response to clopidogrel?

A

Dose
Age
Weight
Disease states such as diabetes mellitus
Drug-drug interactions e.g. omeprazole and strong CYP3A inhibitors
Genetic variants: CYP2C19 loss-of-function alleles

37
Q

What are adverse effects of P2Y12?

A

Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance

38
Q

What are the adverse effects of ticagrelor?

A

Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel (which are not associated with the same adverse effect but do not have the same evidence for longterm mortality reduction)

Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment

39
Q

Risk factors for CHD?

A

Clinical risk factors (hypertension, lipids, diabetes)

Lifestyle risk factors (smoking, diet, physical inactivity)

Environmental risk factors (air pollution, chemicals)

Demographic risk factors (age, sex, ethnicity, genetic)

Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)

40
Q

What are the coronary arteries?

A

LCA - LAD, circumflex, diagnonal branch, left marginal of circumflex

RCA- Right marginal artery, posterior descending artery

41
Q

What is angina?

A

The onset of chest pain

Mismatch of oxygen demand and supply

42
Q

What is stable angina?

A

From exertion and physical activity
Usually relieved by GTN spray
Also calcium channel blockers and beta blockers for long term
Dont use beta blockers for severe asthma
For someone who has heart failure before use non rate limiting CCBs and beta blockers
Non - rate limiting CCB - amlodopine

43
Q

First line for angina

A

GTN spray

44
Q

Second line angina

A

CCB or Beta blockers

45
Q

3rd line (contraindications)

A

CCB and Beta blockers and anti anginal eg ivabradine
Also long lasting nitrate effects

46
Q

What is the commonest reason for angina?

A

IHD

47
Q

Risk factors for IHD?

A

Age
Cigarette smoking
Family history
Diabetes mellitus
Hyperlipidemia
Hypertension
Kidney disease
Obesity
Physical inactivity
Stress
Male

48
Q

What are the exacerbating factors for angina? (Supply)

A

Anemia - not enough blood to carry oxygen - causes angina
Hypoxemia

Rarer -
Polycythemia
Hypothermia
Hypovolaemia
Hypervolaemia

49
Q

What are the exacerbating factors for angina? (Demand)

A

Hypertension
Tachyarrhythmia
Valvular heart disease
Hyperthyroidism
Hypertrophic cardiomyopathy – muscle of heart has excessive growth

50
Q

What are the environmental causes of angina?

A

Exercise
cold weather
heavy meals
emotional stress

51
Q

What is the physiology of myocardial ischemia?

A

Myocardial ischemia occurs when there is an imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:

  1. Impairment of blood flow by proximal arterial stenosis, narrowed coronary artery
  2. Increased distal resistance eg left ventricular hypertrophy
  3. Reduced oxygen-carrying capacity of blood eg anemia
52
Q

What are some types of angina?

A

Crescendo angina
Unstable angina
(both due to CHD)

Prinzmetal’s angina (coronary spasm) – very rare – vessesles become narrow with coronary spasm
Microvascular angina (Syndrome X) ‘ANOCA’

53
Q

Epidemiology of angina

A

More prevalent in men than women

54
Q

What is the history we need to check for IHD?

A

Personal details (demographics, identifiers)
Presenting complaint
History of PC + risk factors
Past medical history
Drug history, allergies
Family history
Social history
Systematic enquiry

55
Q

What are the cardiac symptoms of IHD?

A

Chest pain (tightness/ discomfort)
Breathlessness
No fluid retention (unlike heart failure)
Palpitation (not usually)
Syncope or pre-syncope (very rare)

56
Q

What are the factors pointing towards ischaemic cardiac pain?

A

Character
Location
Provoking factors
Relieving factors
Associated symptoms
Associated risk factors

57
Q

What are the differential diagnoses of chest pains?

A

Myocardial ischemia
Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Gastro-oesophageal (reflux, spasm, ulceration)

58
Q

What are the treatment options for IHD?

A

Reassure
smoking
Weight
Exercise
diet
Advice for emergency
Medication
Revascularisation

59
Q

Why is the CT coronary angiogram used and what is it used for?

A

Good ‘rule-out’ test and at spotting severe disease
Not so good at moderate disease
Anatomical, not functional
Do it on a single breath hold

60
Q

What is excercise testing used for?

A

Good functional test
But relies upon patient’s ability
To walk on a treadmill
(useless for elderly, obese,
arthritic etc)

61
Q

What are myoview scans used for?

A

Uses pharmacological stressor (regadenoson) to
Increase HR and CO
Fuzzy pictures: imperfect sensitivity and specificity

62
Q

What are stress echos used for?

A

Pharmacological stressor
Highly skilled operative required
Seeks regional wall abnormality
Not often used

63
Q

What is the best of the non invasive tests?

A

Perfusion MRI

64
Q

What are the effects of beta blockers on the heart?

A

decreased HR (-ve chronotropic )
decreased Left ventricle contractility (-ve inotropic)
Both of these lead to:
decreased cardiac output > decreased O2 demand

65
Q

Beta blocker side effects

A

Tiredness
Nightmares
Erectile dysfunction
Bradycardia
Cold hands and feet

66
Q

What are contrainidicators of beta blockers?

A

Never give beta blockers to someone with asthma – blocks beta blockers – bronchoconstrictor

67
Q

What are the effects of nitrates (venodilators)

A

Ischaemia occurs
arterioles dilate
Decreased BP
Decreased afterload
Decreased venous return
Decreased preload
coronary arteries dilate
Main effect is on venous return – expands venous capacity – reduces pre load on heart – small affect on arterioles
Dilates coronary arteries

68
Q

What do Calcium channel blockers do?

A

Decrease HR >
Decreased LV contraction and decreased work >
Arteries dilate >
Decreased BP >
Decreased Afterload >
Decreased O2 demand >
Coronary arteries dilate

69
Q

What are the side effects of calcium channel blockers?

A

Flushing
Postural hypotension
Swollen ankles

70
Q

Aspirin

A

Cyclo-oxygenase inhibitor
↓ prostaglandin synthesis, incl. thromboxane
↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic
Gastric ulceration

71
Q

Statins

A

HMG CoA Reductase inhibitors
Reduce manafucture of LDL cholesterol
Used in CVD

72
Q

RAAS System

A

Angiotensinogen from liver (Renin from JG apparatus)>
Angiotensin 1 (ACE from lung)> Angiotensin 2 Causes vasoconstriction
Angiotensin 2 > Alodsterone from adrenal cortex > Na+ pump activated (distal renal tubule) > Na+ +H20 retention (kidney) ascending renal tubule

73
Q

Example of ACE inhibitors

A

Ramipril

74
Q

Example of ARBs

A

LOSARTAN

75
Q

Who are ACE inhibitors given to?

A

Given to patients
With IHD and
HBP or DM

76
Q

Treatment summary for angina

A

Immediately GTN Spray
Long term calcium channel blockers and beta blockers
Secondary prevention aspirin, ACE inhibtor, beta blockers clopidogrel

77
Q

What is PCI?

A

Percutaneous coronary intervention
Coronary angioplasty/ stenting

78
Q

What is a CABG?

A

cORONARY ANGIOgram bypass graft

79
Q

Pros of PCI

A

Less invasive
Convenient
Repeatable
Acceptable

80
Q

Cons of PCI

A

Risk stent thrombosis
Risk restenosis
Can’t deal with complex disease
Dual antiplatelet therapy

81
Q

Pros of CABG

A

Prognosis
Deals with complex disease

82
Q

Cons of CABG

A

Invasive
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay
Time for recovery

Cardiovascular (14 decks)

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