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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
Describe the conservative management of stable angina
Stop smoking Lose weight Exercise
26
How do you treat patients with stable angina when pharmaceutical methods are ineffective?
Percutaneous coronary intervention Coronary Artery Bypass Graft
27
Describe the acute management of ACS
MONA Morphine IV *if severe pain* Oxygen *if sats <94%* Nitrates *if ongoing chest pain/ HTN* Aspirin 300mg
28
What are the eligibility criteria for PCI?
<12h since Sx onset + PCI possible in <120 mins of time when fibrinolysys could be given **>12h** with evidence of ongoing ischaemia
29
Which access if prefered in PCI?
Radial prefered to femoral
30
What drugs must be given prior to PCI?
DAPT: Aspirin + another drug If NOT taking an oral anticoagulant: PRASUGREL If taking an oral anticoagulant: CLOPIDOGREL
31
What drugs should be given during PCI depending on access?
Radial: UFH with bailout GPI Femoral: Bivalirudin with bailout GPI ## Footnote glycoprotein IIb/IIIa inhibitor = GPI
32
What type of stents are used in PCI?
Drug eluting stents Slow release drugs inhibit scar tissue formation + re-stenosis
33
Describe PCI
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
Describe management of STEMI with fibrinolysis
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
What is the mechanism of action of alteplase?
Activates plasminogen to form plasmin Plasmin degrades fibrin leading to clot dissolution + restoration of blood flow (tissue plasminogen activator tPA)
36
List 7 contraindications to thrombolysis
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
Give 3 sides effects of thrombolytics
Haemorrhage Hypotension- more common with streptokinase Allergic reactions may occur with streptokinase
38
What DAPT should be given immediately after fibrinolysis?
Aspirin + Ticagrelor OR Aspirin + Clopidogrel (if high bleeding risk)
39
Detail the immediate management of unstable Angina and NSTEMI
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
What factors are accounted for in GRACE?
Age HR + BP Cardiac (Killip class) + renal function (creatinine) Cardiac arrest on presentation ECG findings Troponin levels
41
What GRACE risk is considered intermediate and what does this indicate?
>3% Coronary angiography with follow-on PCI if necessary within 72h
42
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?
Immediate: if clinically unstable e.g. hypotensive Within 72h: GRACE score >3% Consider if ischaemia experienced after admission
43
If PCI is indicated in an NSTEMI patient, what drugs should they be given prior and during PCI?
Aspirin + Prasugrel/ Ticagrelor OR Clopidogrel (if on oral anticoagulation) During: UFH
44
If a patient has a low risk GRACE score, how are they managed?
Aspirin + ticagrelor OR Aspirin + Clopidogrel/ Aspirin alone for high bleeding risk
45
What management should patients be on post STEMI/ NSTEMI?
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
What drug may be initiated post STEMI if patient has S/S of HF or reduced EF?
Aldosterone antagonist e.g. Eplerenone/ Spironolactone
47
What DAPT should a patient be taking post STEMI/ NSTEMI?
Aspirin 75mg OD lifelong +P2Y12 inhibitor for 12m: Prasugrel 5-10mg OD OR Ticagrelor 90mg BD OR Clopidogrel 75mg OD
48
What is cardiac rehabilitation?
Exercise component Health education: smoking cessation, reduce alcohol, WL, diet changes Stress Mx
49
What are the complications of ACS?
``` DARTH VADER Death Arrhythmias Rupture Tamponade Heart failure Valve disease Aneurysm Dressler's Syndrome Embolism Re-infarction ```
50
List 3 early complications of ACS which are not in DARTH VADER
Heart Block Cardiogenic shock Pericarditis
51
What is used to calculate risk of mortality in patients with unstable angina or NSTEMI?
``` GRACE Score High scores a/w mortality from cardiac events within 6 months ```
52
How do leads localise site of MI?
Inferior: II, III, aVF Anterior: V1-V4 Lateral: I, aVL, V5/6 Posterior: Tall R wave + ST depression in V1-3
53
What are the 4 reciprocal changes on ECG seen in posterior MI?
Changes in V1-3 Horizontal ST depression Tall, broad R wave Upright T waves Dominant R waves in V2
54
Which leads have maximal ST elevation in anterior MI?
SAL Septal (V1-2) Apical (V3-4) Lateral (V5-6)
55
Describe the mortality of ACS
50% deaths occur within 2h onset of Sx
56
What indicates a worse prognosis in ACS?
Elderly LV failure ST changes
57
What system stratifies risk post MI?
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
Which coronary artery supplies the AVN, thus what type of MI is associated with which arrhythmia post MI? How is this treated?
Right coronary artery Inferior MI a/w bradyarrythmia, second/ third degree heart block (usually transient lasting hours- days) Atropine
59
Which structures may rupture acutely (3-5 days) post MI?
Papillary muscles Ventricular septal rupture
60
How does papillary muscle rupture present?
New mitral regurgitation (pan systolic) Pulmonary oedema Hypotension
61
In which type of infarct is papillary muscle rupture more common?
Infero-posterior infarction
62
How are patients with papillary muscle rupture managed?
Vasodilators Often require emergency surgical repair
63
How does ventricular septal rupture present?
Chest pain Biventricular failure (acute HF) Shock New pansystolic murmur
64
What investigations and management are required for ventricular septal rupture?
Echo: diagnostic + r/o MR Mx: urgent surgical correction
65
Which structure can rupture 5 days- 2weeks post MI? How does this present?
Left ventricular free wall Acute HF Tamponade (raised JVP, muffled HS, hypotension)
66
How is left ventricular free wall rupture managed?
Urgent pericardiocentesis + thoracotomy
67
What causes left ventricular wall aneurysm post MI? Why is this dangerous?
Ischaemic damage weakens myocardium resulting in aneurysm formation Blood stagnates here, promoting platelet adherence + thrombus formation
68
How does left ventricular wall aneurysm present?
SOB Persistent ST-elevation No chest pain LV failure: SOB, cough, crackles on auscultation
69
How is left ventricular wall aneurysm managed?
Anticoagulate (high risk of stroke)
70
What is Dressler's syndrome
Late onset post-MI pericarditis 2-6w post-MI AI reaction against antigenic proteins formed as the myocardium recovers
71
Give 4 features of presentation of Dressler's syndrome
Fever Pleuritic pain Pericardial effusion Raised ESR
72
Describe pericarditis post-MI
<48h post-MI Pain worse on lying flat Pericardial rub Pericardial effusion on echo
73
What is the most common cause of death following an MI?
Cardiac arrest Commonly due to developing VF
74
How may cariogenic shock develop post-MI?
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
What arrhythmias can arise post-MI?
Tachyarrhythmias: VF, VT Bradyarrythmias
76
If suspected re-infarct 4-10 days post initial MI what should be measured?
CK-MB (raises for 3-4 days) instead of troponin (raised for 10 days)
77
How should glycemic control in diabetic patients with ACS be managed?
Dose-adjusted insulin infusion with regular blood glucose monitoring (stop other anti-hyperglycaemics)

YR6: CARDIAC (41 decks)

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