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YR6: CARDIAC > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

Define IHD

A

decreased blood supply to heart muscle resulting in chest pain (angina pectoris).
May present as stable angina or acute coronary syndrome.

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2
Q

How can ACS be subdivided?

A

Unstable angina: rest pain due to ischaemia, without cardiac injury
NSTEMI: ST depression, subendocardial injury
STEMI: ST elevation with transmural infarction

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3
Q

Define Myocardial Infarction

A

cardiac muscle necrosis resulting from ischaemia

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4
Q

Describe the epidemiology of ischaemic heart disease

A

COMMON
5/1000 PA
Prevalence: > 2 %
M > F

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5
Q

Describe the aetiology of Angina Pectoris

A

Myocardial O2 demand exceeds supply
Often due to atherosclerosis
Rarer causes: coronary artery spasm (e.g. cocaine), arteritis + emboli

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6
Q

List 9 risk factors for IHD

A 
Male
Age
FH
DM
HTN 
Hyperlipidaemia  
Smoking
Diet + exercise
Alcohol
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7
Q

Describe the pain that characterise ACS

A

Acute-onset chest pain
Central, heavy, tight, crushing
Radiates to L arm, neck, jaw or epigastrium
Occurs at rest
More severe + frequent pain than previously occurring stable angina

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8
Q

What are 3 associated symptoms of ACS?

A

Dyspnoea
Sweating
N+V

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9
Q

What may occur in elderly or diabetic patients with ACS?

A

Silent infarcts

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10
Q

Describe the presenting symptoms of stable angina

A

Constricting discomfort in the chest, neck, shoulders, jaw + arms on exertion
Relieved by GTN/ rest within 5 mins

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11
Q

What are 8 signs of ACS?

A 
May be NO CLINICAL SIGNS 
Pale  
Sweating  
Restless 
Low-grade pyrexia  
Check both radial pulses to r/o aortic dissection 
Arrhythmias/ New heart murmurs  
Disturbances of BP  
Signs of complications (e.g. acute HF, cardiogenic shock)
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12
Q

What are the appropriate bloods to take for suspected ACS?

A 
FBC
U+E's (electrolyte imbalance, renal function)
Glucose
Lipid profile
Amylase  (pancreatitis could mimic MI) 
CRP
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13
Q

Which cardiac enzymes rise in ACS and when?

A

CK-MB (within 6h)
Troponin I + T (3-6h after infarction, peak at 12-24h, remain raised for up to 14 days)

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14
Q

Describe ECG findings for NSTEMI

A

ST depression or T wave inversion

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15
Q

Describe ECG findings for STEMI

A

Hyperacute tall T waves
ST elevation (> 1mm in limb leads, > 2 mm in chest leads)
New-onset LBBB
Later: T wave inversion, Pathological Q waves

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16
Q

What may a CXR in ACS show?

A

Complications of ischaemia eg, pulmonary oedema
Cardiomegaly
Enlarged mediastinum

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17
Q

What is the medical management strategy of stable angina?

A

Symptomatic (GTN)
Anti-anginals (BBs/CCBs)
RF reduction (statin + aspirin)

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18
Q

List 4 side effects of nitrates

A

Hypotension (vasodilation)
Tachycardia (reflex)
Headaches (dilation of cerebral vessels)
Flushing

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19
Q

Which CCB’s can be used as monotherapy in angina?

A

Rate limiting:
Verapamil
Diltiazem

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20
Q

Which b-blockers are used in angina?

A

Metoprolol
Timolol
Bisoprolol
Carvedilol

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21
Q

What is the further management of angina not controlled with monotherapy?

A
  1. Increase to max. tolerated dose
  2. Add other class (CCB/ BB)
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22
Q

Which calcium channel blockers can be used in conjunction with beta blockers?

A

Long acting dihydropyridines:
Amlodipine
Modified release Nifedipine
Modified release Felodipine

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23
Q

If addition of a CCB or BB is not tolerated in a symptomatic patient with angina, what drugs can be used third line?

A

Long acting nitrate
Ivabradine
Nicorandil
Ranolazine

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24
Q

If a patient is taking both a BB and CCB but is still symptomatic, how can they be managed?

A

Refer to cardiologist for angiography
Only add a 3rd drug whilst awaiting assessment for PCI or CABG

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25
Q

Describe the conservative management of stable angina

A

Stop smoking
Lose weight
Exercise

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26
Q

How do you treat patients with stable angina when pharmaceutical methods are ineffective?

A

Percutaneous coronary intervention
Coronary Artery Bypass Graft

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27
Q

Describe the acute management of ACS

A

MONA
Morphine IV if severe pain
Oxygen if sats <94%
Nitrates if ongoing chest pain/ HTN
Aspirin 300mg

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28
Q

What are the eligibility criteria for PCI?

A

<12h since Sx onset + PCI possible in <120 mins of time when fibrinolysys could be given

>12h with evidence of ongoing ischaemia

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29
Q

Which access if prefered in PCI?

A

Radial prefered to femoral

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30
Q

What drugs must be given prior to PCI?

A

DAPT: Aspirin + another drug
If NOT taking an oral anticoagulant: PRASUGREL
If taking an oral anticoagulant: CLOPIDOGREL

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31
Q

What drugs should be given during PCI depending on access?

A

Radial: UFH with bailout GPI

Femoral: Bivalirudin with bailout GPI

glycoprotein IIb/IIIa inhibitor = GPI

32
Q

What type of stents are used in PCI?

A

Drug eluting stents
Slow release drugs inhibit scar tissue formation + re-stenosis

33
Q

Describe PCI

A
  1. Catheterise radial/ femoral artery
  2. Feed guidewire to coronary arteries under XR guidance
  3. Inject contrast to identify occlusion
  4. Open occlusion with balloon + place stent to maintain patency
34
Q

Describe management of STEMI with fibrinolysis

A

Fibrinolytic: Tenecteplase or Alteplase
+
Anticoagulate at same time: Enoxaparin
+
Start DAPT immediately after
+
Repeat ECG at 60-90 mins, if persistent myocardial ischaemia consider PCI

35
Q

What is the mechanism of action of alteplase?

A

Activates plasminogen to form plasmin
Plasmin degrades fibrin leading to clot dissolution + restoration of blood flow
(tissue plasminogen activator tPA)

36
Q

List 7 contraindications to thrombolysis

A

Active internal bleeding
Recent haemorrhage, trauma or surgery (inc. dental extraction)
Coagulation + bleeding disorders
Intracranial neoplasm
Stroke < 3 months
Aortic dissection
Recent head injury
Severe HTN

37
Q

Give 3 sides effects of thrombolytics

A

Haemorrhage
Hypotension- more common with streptokinase
Allergic reactions may occur with streptokinase

38
Q

What DAPT should be given immediately after fibrinolysis?

A

Aspirin + Ticagrelor
OR
Aspirin + Clopidogrel (if high bleeding risk)

39
Q

Detail the immediate management of unstable Angina and NSTEMI

A

300mg Aspirin
+
Fondaparinux
if low bleeding risk + no immediate PCI planned
OR
UFH if coronary angiogram planned or creatinine >265
+
Risk assess using GRACE (6 month mortality)

40
Q

What factors are accounted for in GRACE?

A

Age
HR + BP
Cardiac (Killip class) + renal function (creatinine)
Cardiac arrest on presentation
ECG findings
Troponin levels

41
Q

What GRACE risk is considered intermediate and what does this indicate?

A

> 3%
Coronary angiography with follow-on PCI if necessary within 72h

42
Q

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?

A

Immediate: if clinically unstable e.g. hypotensive

Within 72h: GRACE score >3%

Consider if ischaemia experienced after admission

43
Q

If PCI is indicated in an NSTEMI patient, what drugs should they be given prior and during PCI?

A

Aspirin
+
Prasugrel/ Ticagrelor
OR
Clopidogrel (if on oral anticoagulation)

During: UFH

44
Q

If a patient has a low risk GRACE score, how are they managed?

A

Aspirin + ticagrelor
OR
Aspirin + Clopidogrel/ Aspirin alone for high bleeding risk

45
Q

What management should patients be on post STEMI/ NSTEMI?

A
  1. DAPT
  2. BB e.g. Bisoprolol (or CCB if CI e.g. Verapamil)
  3. ACEi: Enalapril/ Ramipril (or ARB e.g. Valsartan)
  4. Statin
  5. Cardiac rehab
46
Q

What drug may be initiated post STEMI if patient has S/S of HF or reduced EF?

A

Aldosterone antagonist e.g. Eplerenone/ Spironolactone

47
Q

What DAPT should a patient be taking post STEMI/ NSTEMI?

A

Aspirin 75mg OD lifelong
+P2Y12 inhibitor for 12m:
Prasugrel 5-10mg OD
OR
Ticagrelor 90mg BD
OR
Clopidogrel 75mg OD

48
Q

What is cardiac rehabilitation?

A

Exercise component
Health education: smoking cessation, reduce alcohol, WL, diet changes
Stress Mx

49
Q

What are the complications of ACS?

A 
DARTH VADER
Death
Arrhythmias
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler's Syndrome
Embolism
Re-infarction
50
Q

List 3 early complications of ACS which are not in DARTH VADER

A

Heart Block
Cardiogenic shock
Pericarditis

51
Q

What is used to calculate risk of mortality in patients with unstable angina or NSTEMI?

A 
GRACE Score 
High scores a/w mortality from cardiac events within 6 months
52
Q

How do leads localise site of MI?

A

Inferior: II, III, aVF
Anterior: V1-V4
Lateral: I, aVL, V5/6
Posterior: Tall R wave + ST depression in V1-3

53
Q

What are the 4 reciprocal changes on ECG seen in posterior MI?

A

Changes in V1-3
Horizontal ST depression
Tall, broad R wave
Upright T waves
Dominant R waves in V2

54
Q

Which leads have maximal ST elevation in anterior MI?

A

SAL
Septal (V1-2)
Apical (V3-4)
Lateral (V5-6)

55
Q

Describe the mortality of ACS

A

50% deaths occur within 2h onset of Sx

56
Q

What indicates a worse prognosis in ACS?

A

Elderly
LV failure
ST changes

57
Q

What system stratifies risk post MI?

A

Killip class (30 day mortality)
I: no clinical signs of HF
II: lung crackles, S3
III: frank pulmonary oedema 38%
IV: cardiogenic shock 83%

58
Q

Which coronary artery supplies the AVN, thus what type of MI is associated with which arrhythmia post MI? How is this treated?

A

Right coronary artery
Inferior MI a/w bradyarrythmia, second/ third degree heart block (usually transient lasting hours- days)
Atropine

59
Q

Which structures may rupture acutely (3-5 days) post MI?

A

Papillary muscles
Ventricular septal rupture

60
Q

How does papillary muscle rupture present?

A

New mitral regurgitation (pan systolic)
Pulmonary oedema
Hypotension

61
Q

In which type of infarct is papillary muscle rupture more common?

A

Infero-posterior infarction

62
Q

How are patients with papillary muscle rupture managed?

A

Vasodilators
Often require emergency surgical repair

63
Q

How does ventricular septal rupture present?

A

Chest pain
Biventricular failure (acute HF)
Shock
New pansystolic murmur

64
Q

What investigations and management are required for ventricular septal rupture?

A

Echo: diagnostic + r/o MR
Mx: urgent surgical correction

65
Q

Which structure can rupture 5 days- 2weeks post MI? How does this present?

A

Left ventricular free wall
Acute HF
Tamponade (raised JVP, muffled HS, hypotension)

66
Q

How is left ventricular free wall rupture managed?

A

Urgent pericardiocentesis + thoracotomy

67
Q

What causes left ventricular wall aneurysm post MI? Why is this dangerous?

A

Ischaemic damage weakens myocardium resulting in aneurysm formation

Blood stagnates here, promoting platelet adherence + thrombus formation

68
Q

How does left ventricular wall aneurysm present?

A

SOB
Persistent ST-elevation
No chest pain
LV failure: SOB, cough, crackles on auscultation

69
Q

How is left ventricular wall aneurysm managed?

A

Anticoagulate (high risk of stroke)

70
Q

What is Dressler’s syndrome

A

Late onset post-MI pericarditis
2-6w post-MI
AI reaction against antigenic proteins formed as the myocardium recovers

71
Q

Give 4 features of presentation of Dressler’s syndrome

A

Fever
Pleuritic pain
Pericardial effusion
Raised ESR

72
Q

Describe pericarditis post-MI

A

<48h post-MI
Pain worse on lying flat
Pericardial rub
Pericardial effusion on echo

73
Q

What is the most common cause of death following an MI?

A

Cardiac arrest
Commonly due to developing VF

74
Q

How may cariogenic shock develop post-MI?

A

If large part of ventricular myocardium is damaged in infarction the EF may decrease to the point of cariogenic shock
OR
mechanical complications e.g. LVFW rupture

75
Q

What arrhythmias can arise post-MI?

A

Tachyarrhythmias: VF, VT
Bradyarrythmias

76
Q

If suspected re-infarct 4-10 days post initial MI what should be measured?

A

CK-MB (raises for 3-4 days) instead of troponin (raised for 10 days)

77
Q

How should glycemic control in diabetic patients with ACS be managed?

A

Dose-adjusted insulin infusion with regular blood glucose monitoring
(stop other anti-hyperglycaemics)

YR6: CARDIAC (41 decks)

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