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My MRCP > Ischaemic Heart Disease including ACS > Flashcards

Ischaemic Heart Disease including ACS Flashcards

1
Q

Define Stable Angina [3]

A

Discomfort in the chest and/or adjacent areas
Associated with myocardial ischemia
But without myocardial necrosis

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2
Q

Name 6 causes of Stable Angina
Think in terms of things that cause:
reduced coronary blood flow, reduced oxygen transport, increased myocardial demand

A 
Obstructive Coronary Atheroma
Coronary artery spasm
Coronary artery inflammation
Anaemia
LVH
Thyrotoxicosis
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3
Q

What are the risk factors for SIHD? [10]

A

Old - Race - Male - FH - Smoker
- Low exercise - Poor Diet-
Diabetes - Hypertension - Hypercholesterolaemia

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4
Q

Describe the site, character and radiation of Ischaemic heart pain? [3]

A

Retrosternal (Centre)
Tight band/pressure or heaviness
Radiates to neck, jaw and medial arms

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5
Q

What triggers [4] and relieves [2] symptoms of SIHD?

A

Triggered by Stress, exertion, cold weather and large meals

Relieved by rest & GTN spray

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6
Q

What could you see on an examination of a SIHD patient?
6 signs
4 findings of exacerbating/associated conditions

A

Tar Staining - smoker
Obesity
Tachycardia
Xanthalasma/Corneal Arcus - Hypercholesterolaemia
Hypertensive retinopathy - DM/HTN
Pansystolic murmur at mitral - Mitral Regurgitation
Ejection systolic murmur @ Aortic area - Aortic Stenosis

Associated conditions:
Pallor- Anaemia
Elevated JVP, basal crackles & peripheral oedema - Heart Failure
Hyperreflexia - thyrotoxicosis
Reduced peripheral pulses + abdominal bruit - AAA

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7
Q

How would you investigate suspected SIHD? [5]

What 6 blood tests will u request?

A 
Bloods - FBC, lipid profile, Glc, U&Es , LFTs & thyroid function
CXR
ECG
Exercise Tolerance Test (ETT)
Myocardial Perfusion Imaging
Coronary Angiography
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8
Q

What would an ECG show in a SIHD patient? [3]

A

Pathological Q waves indicative of a past MI [1]

High voltages [1], ST depression [1] - Strain pattern indicates LVH

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9
Q

Whats the use of an ETT in a SIHD patient? [1]

What will a positive test show [1]

A

Can confirm the diagnosis but unsuitable in those that cannot walk for 9 mins
A +ve test shows ST depression

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10
Q

Treatment approach to stable angina

A

Rx: symptom relief (lower HR + vasodilation) [1] AND influence disease progression [1]

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11
Q

What meds treat the symptoms of angina? [7]

A 
Lower HR:
\+ B-blockers, CCBs
Vasodilation:
\+ Isosorbide Mononitrate 
\+ Long acting nitrate
Influence disease progression:
\+ Statins, ACEi, aspirin 75mg
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12
Q

What type of PCI is used in coronary revascularization?

A

Percutaneous Transluminal Coronary Angioplasty

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13
Q

What are the advantages of CABG over PCI? [2]

A

CABG is better in multi vessel disease [1]

Unlike PCI it can help prognostically [1] as well as the symptoms.

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14
Q

In what unusual way can SIHD present? [3]

What demographic is this atypical presentation most common? [2]

A

Without pain but with SOB on exertion, Excessive Fatigue OE and Near Syncope OE.
Usually in people with reduced pain sensation e.g. elderly & diabetics

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15
Q

What is the classification of angina stages? [4]

A

Canadian Cardiovascular Society scale of Angina Severity (CCS scale):
1 - Asymptomatic unless strenous acitvity
2 - Slight limitation e.g. walking >2 blocks or mu;tiple flights of stairs
3 - Marked Limitation e.g. i flight of stairs
4 - Cant really dress or wash etc

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16
Q

Which long acting nitrates are used? [3]

How are GTN sprays used? [4]

A

IVABRADINE, NICORANDIL or RANZOLAZINE monotherapy

GTN to prevent and treat angina episodes

  • taken before planned exercise and on symptoms
  • repeat dose after 5 mins if not resolved
  • call ambulance if not resolved 5 mins after taking second dose
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17
Q

Define an ACS? [2]

A

Any sudden cardiac event [1] suspected to be related to occlusion of the coronary arteries [1]

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18
Q

What is an atypical ACS presentation? [3]

A

In people with reduced pain sensation such as the elderly, diabetics and women, ACS can present as: SOB

Signs of heart failure (i.e. pulmonary oedema, raised JVP etc)

Nausea/vomiting

But without the classic chest pain

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19
Q

What causes an ACS? [2]

A

Rupture of thin fibrous cap with exposed necrotic core, highly inflammatory and prothrombotic
Triggers (sub)occlusive thrombus

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20
Q

ACS investigations for diagnosis [2] What is needed for diagnosis of MI [4]

A
  1. ECG
  2. Cardiac biomarkers detect cardiac cell death

Positive cardiac biomarkers + ONE OF:

  • Sx of ischemia >20 mins
  • New ECG changes in 2 or more contiguous leads
  • Evidence of coronary problem on coronary angiogram
  • Evidence of new cardiac damage on another test
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21
Q

Initial management for STEMI

A

ASPIRIN 300 MG loading dose

    • PCI +/- stenting, if within 12h of symptom onset and PCI available 120 mins of admission
  • Thrombolysis if PCI not available in next 120 mins
  • If still ST elevation after thrombolysis, then transfer for PCI if possible
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22
Q

Why cant streptokinase be used more than once? What will be used instead

A

Its bacterial so the patient will grow immune and may even have an allergic reaction to a 2nd dose. If treatment is needed for a 2nd MI then it will be rtPA.

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23
Q

If theres no ST elevation how do we distinguish between NSTEMI & UAP (unstable angina pectoris?

A

Blood Tests for biomarkers of myocardial necrosis- cardiac troponin (cTn), specifically type I & T (type C is present in blood anyway)

If present it indicates an NSTEMI & if absent its UAP.

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24
Q

How do we treat NSTEMI/UAP?

Think of the acronym - give egs for each [5]

Specialist things to prescribe [1]

A
  • MONA - aspirin 300mg
  • GRACE score estimates 6 month mortality
  • Give fondaparinux if no immediate PCI
  • Low risk <3% - conservative management: give ticagrelor
  • High risk >3% offer PCI, give prasugrel or ticagrelor, give uH.
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25
Q

What is involved in secondary prevention of ACS?

4 lifestyle mods

Rx [6]

A

Lifestyle modification: - Smoking Cessation - Healthy limits for alcohol consumption - Daily Exercise & healthier diet (with weight loss if applicable)

Medication: -

  • Aspirin 75mg + Clopidogrel for 1 year (dual anti-platelet therapy) then aspirin alone indefinitely
  • Beta-blockers to reduce average O2 demand of heart (e.g. Metopolol/Atenolol)
  • Statins to lower cholesterol & so reduce risk of atheroma
  • ACEI/ARB to control BP (e.g. Ramipril/Losarten respectively)
  • Mineralocorticoid receptor antagonist (EPLERENONE): if EF<40% and clinical signs HF or DM (assess with echo before discharge)
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26
Q

Why would thrombolytics be contraindicated? Name 5 instances

A

When theres any chance of bleeding due to injury elsewhere in the body as thrombolytics could impair clotting

Intercranial Haemorrhage - Malignant Intercranial Neoplasm - Ischaemic Stroke - Aortic Dissectoin - Bleeding diathesis (Coagulopathy)

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27
Q

How do GP2b3a receptor blockers work? [2]

A

The GP2a3b complex is a receptor found on platelets that activates in the presence of fibrinogen. By blocking the receptor platelets arn’t activated and so clotting doesn’t occur.

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28
Q

What do we give following PCI?

A

Anti-platelets e.g. Aspirin and Clopidogrel for min 12 months
Unfractionated heparin

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29
Q

Troponin is not specific to MI, what are other causes of a rise in troponin [4]

How long before you’d expect a rise in MI?

A
  1. Pulmonary embolism
  2. Sepsis
  3. Renal failure
  4. Sub-arachnoid hemorrhage

Elevated in MI within 3-12h after onset of chest pain

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30
Q

5 Types of MI

Describe the difference between Type 1 and 2

A

Type 1: Spontaneous MI

  • Associated with ischemia and due to primary coronary event
  • eg plaque erosion, rupture, fissuring or dissection

Type 2

  • Due to imbalance in supply and demand of oxygen
  • Result of ischemia but not ischemia from thrombosis of coronary artery
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31
Q

5 Types of MI

Describe the 2 classifications of Type 3 MI [2]

Describe the similarities of Type 4 and Type 5 MI [2]

A

SCD

Verified coronary thrombus by angiography or autopsy

Type 4 and 5 are iatrogenic

  • Type 4 - MI associated with PCI
  • Type 5- MI associated with CABG
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32
Q

Causes of Type 1 MI

Whats the usual or main cause [1]

Name 5 other causes

A

Usually - atherosclerosis

Other causes

  • Coronary vasospasm eg cocaine, triptans, 5-FU
  • Cocaine, triptans, 5-FU (chemotherapy)
  • Coronary dissection
  • Embolism of material downstream from coronary artery eg from AF
  • Inflammation of coronary arteries (vasculitis)
  • Radiotherapy to chest can cause fibrosis and stenosis of coronary arteries
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33
Q

NSTEMI VS STEMI - what does it mean in terms of damage to heart muscle?

A

NSTEMI = partial thickness damage of heart muscle

STEMI full thickness damage

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34
Q

Acute management of ACS [5]

Investigations [1]

Blood tests [4]

A
  • Morphine 5-10mg IV + antiemetic metoclopromide
  • Give O2 non-rebreathe (if SpO2 <94%)
  • GTN Sub-lingual or IV (ROA)
  • Aspirin 300mg

Investigations

  • Serial ECGs

Blood tests

  • Check not anaemic
  • Kidney function
  • Cholesterol
  • Thyroid
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35
Q

Follow up care post ACS

Review [2]

A

Review: 5w to review symptoms (SOB, angina, palpitations) and 3m to check lipids

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36
Q

Anti-anginal drugs - Contraindications

Nitrates
Beta blockers
Ivabradine
Ranolazine

A

Nitrates - HOCM
BB- 2nd degree HB, asthma, severe COPD, severe PVD
Ivabradine - severe liver disease
Ranolazine - severe liver disease

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37
Q

Name 2 contraindications to trimetazidine (anti-anginal)

A

Parkinsons disease & other movement disorders, including tremor
Renal disease

38
Q

Contraindications to
CCB - heart rate slowing
CCB - dyhydropyridine

A
  • CCB - heart rate slowing - contraindicated in CHF
  • CCB - dyhydropyridine- contraindicated in severe aortic stenosis, HCM
39
Q

Which two anti-anginals are contraindicated in congestive heart failure

A
  • CCB- HR slowing
  • Nicorandil
40
Q

When would you consider isosorbide mononitrate in patients with angina

A
  • many patients who take nitrates develop tolerance and experience reduced efficacy
    NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
    this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate
41
Q

What is defined as significant features of ischaemia on an ECG?

A
  • 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years,
  • or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
    1.5 mm ST elevation in V2-3 in women
    1 mm ST elevation in other leads
  • new LBBB (LBBB should be considered new unless there is evidence otherwise)
42
Q

STEMI initial management

PCI
Name 3 medications need to be given

A
  • Prarugrel
  • Radial access - give UH + glycoprotein 11b/111a inhibitor
  • Drug-eluting stents
43
Q

STEMI initial management

Fibrinolysis

A

Give antithrombin at same time like fondaparinux
Following fibrinolysis, give ticagrelor
If ongoing myocardial ischaemia, consider PCI

44
Q

STEMI initial management

  • What if patient is showing signs of cardiogenic shock?
  • What if patient is high bleeding risk?
  • What if patient is on oral anticoagulants?
A
  • Cardiogenic shock > PCI
  • High bleeding risk - swap prasugrel for ticagrelor
  • Oral anticoagulants - swap prarugrel for clopidogrel
45
Q

NSTEMI conservative management
Low grace score ie >3%

A

Ticagrelor for 1 year
Aspirin 75mg lifelong
Fondaparinux

46
Q

Drug eluting stents vs bare-metal stents

A
  • stent coated with paclitaxel or rapamycin which inhibit local tissue growth.
  • Whilst this reduces restenosis rates, the stent thrombosis rates are increased as the process of stent endothelisation is slowed
47
Q

Why aspirin lifelong and the length of second anti-platelet is often 1 year?

A

Following insertion, the most important factor in preventing stent thrombosis is antiplatelet therapy. Aspirin should be continued indefinitely. The length of clopidogrel treatment depends on the type of stent, reason for insertion and consultant preference. Antiplatelets should only be stopped following discussion with the cardiology team (e.g. if the patient is due to have surgery) due to the risk of stent thrombosis.

48
Q

Percutaneous Coronary Intervention

Peri-procedural complications

A
  • minor bleeding/hematoma at site of vascular access
  • retroperitoneal haematoma
  • femoral pseudoaneurysm
  • Cholesterol embolisation
49
Q

PCI

Describe presentation of retroperitoneal hematoma

A

may occur if the puncture site occurs proximal to the inguinal ligament
may be asymptomatic or present with flank pain/hypotension

50
Q

PCI

Describe presentation of femoral pseudoaneurysm [3]

A

pulsatile mass, femoral bruit and compromised distal pulses

51
Q

PCI

Describe presentation of cholesterol embolisation [4]

A
  • occurs due to embolisation of cholesterol released from atherosclerotic plaques
  • purpura, livedo reticularis
  • renal impairment
  • blue toes
52
Q

DAPT post-PCI

A

post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months

53
Q

Timing of starting eplerenone after an acute MI

A

should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy - indicated for HF and LVSD.

54
Q

What are the complications of MI [10]

A 
Papillary muscle rupture, Mitral regurgitation 
VSD
Heart failure 
Ventricular free wall rupture 
Pericarditis
Cardiac tamponade 
LV Aneurysm
Embolization 
Organ failure 
AF, VT, VF: Arrhythmia 
Decreased contractility and CO
- Cardiac arrest - usually due to VT / VF
- Cardiogenic shock
HF - R+L
- Angina
55
Q

What does stasis after MI cause? [2] What is the management of this complication [2]

A

Systemic embolism: from left mural thrombus after large anterior MI; mx is WARFARIN for 3m

56
Q

What is ventricular free wall rupture?

What area is common and what happens

A 
FATAL 
Common in LAD area 
Necrosis decreases strength and blood haemorrhages out of ventricle 
Cardiac tamponade 
False aneurysm if contained
57
Q

Pathophysiology pericarditis post-MI [2]

A
  • Necrotic tissue irritates pericardium

- If fluid accumulates = cardiac tamponade which puts pressure on heart and reduces ventricle filling

58
Q

What are the signs of papillary muscle rupture [6]

A

Mitral regurgitation - harsh systolic - pan systolic
SOB - pulmonary edema
Sympathetic activation - tachycardia, N+V, sweating
Chest pain
Shock
Raised JVP

59
Q

How do you treat papillary muscle rupture [4]

A

IV nitrates
Inotropes
IABP - intra-aortic balloon pump
Surgery

60
Q

How do you differentiate between papillary muscle rupture and VSD

A

Cath lab - angio

ECHO

61
Q

What are the signs of cardiac tamponade [5]

A 
3 D's 
- Distended JVP - increased 
- Decreased BP 
- Distant / muffled HS 
SOB
Renal failure
62
Q

When does free wall rupture occur

A

1-2 weeks after MI

63
Q

How does rupture present? [5]

A 
Acute HF secondary to tamponade
Raised JVP
Pulsus paradoxus
Diminished HS
New murmur
64
Q

What do you do for rupture / tamponade

A

URGENT pericardiocentesis

ECHO

65
Q

Who is more at risk of rupture (free wall or septal) [4]

A

Elderly
Female
High BP
Anterior MI - LAD

66
Q

What does septal wall rupture cause?

A 
Same as tamponade / free wall 
Pansystolic murmur
Raised JVP
Acute HF secondary to tamponade
Pulsus paradoxus
Diminshed HS 
Anterior MI
67
Q

What are signs of mitral regurgitation [4]

A

New murmur
Worsening SOB
Increased JVP
Low BP

68
Q

What will MR lead to [2]

A

Cardiogenic shock

Heart failure

69
Q

How do you treat MR [2]

A

Treat LVF e.g. with vasodilators

Valve replacement is required

70
Q

What does pericarditis present like [3]

Ix [2]

A 
Central chest pain 
Better forward
Often 1st 24 hours 
ECG changes
ECHO - look for effusion
71
Q

How do you treat pericarditis [2]

A

NSAID

Colchicine

72
Q

What is Dresslers syndrome
Dx [3]
Rx [2]

A 
Autoimmune pericarditis - 1-3 week post MI
Recurretn effusion
Fever
Pericardial rub 
Anaemia
Dx:
- ECG shows global ST elevation and T inversion
- ECHO
- raised inflammatory markers
Rx = NSAID and steroid
73
Q

What else can you get 1-3 week post MI and how do you manage? [2]

A

Late malignant ventricular arrhythmia

  • Avoid hypokalaemia
  • 24hr ECG monitoring prior to discharge for large MI
74
Q

Left Ventricular aneurysm
Onset
Clinical features [3]
Rx [2]

A

1 month post MI

  • Left ventricular failure
  • ST elevation in anterior leads
  • Angina
  • Recurrent VT/systemic embolism

Mx: warfarin +/- excision

75
Q

PE
Origin of thrombus
How to prevent?

A

Due to mural thrombus

Consider anti-coagulation for 3 months post MI

76
Q

What is cardiogenic shock

A

Inadequate tissue perfusion to meet demands

77
Q

What causes cardiogenic shock [8]

A 
Post MI
Arrhythmia
PE
Tension pneumothorax 
Cardiac tamponade
Myocarditis
Endocarditis
Dissection
78
Q

How do you Dx cardiogenic shock [4]

A

ECG
U+E, troponin, ABG
CXR
ECHO

79
Q

How do you Rx shock [6]

A 
Treat MI / reversible cause 
Admit to CCU
Oxygen
Diamorphine - pain + anxiety
Plasma expander if hypo-perfused
Inotropes if overfilled - dobutamine
80
Q

How do you measure CO / monitor [7]

A 
BP + pulse
MAP 
CVP 
ABG 
ECG - every hour until Dx made
Urine output
81
Q

What is sudden cardiac death

A

Death due to cardiac cause <6 hours from symptom onset

82
Q

What causes sudden cardiac death [7]

A 
STEMI
CAD
CABG
Embolism
HCM
Long QT
Valvular disease
83
Q

What is the prognosis of SCD?

A

Only 2% survive

Most survivors in VT or VF and can be shocked

84
Q

What are reversible causes of cardiac arrest:
5 H’s
4 T’s

A 
Hypoxia
Hypovolaemia
Hyperkalaemia
Hypoglycaemia
Hypocalcaemia

Thrombosis
Tension pneumothorax
Tamponade
Toxin

85
Q

What rhythm will they be in after SCD? [3]

A

VT / VF
Asystole
Pulseless electrical activity

86
Q

How do you treat SCD [2]

What do you do if witnessed on cardiac monitor?

What do you do if not witnessed?

A

CPR
Defib

Adrenaline if VF / VT after 3rd shock and every 5 minutes if witnessed on cardiac monitor

1 shock + adrenaline if not witnessed on cardiac monitor

87
Q

Mnemonic for complications

A 
DREAD
Death
Rupture septum or papillary
Oedema / new onset HF
Arrhythmia / aneurysm
Dresslers'
88
Q

Indications for temporary pacemaker

A

symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block
trifascicular block prior to surgery

89
Q

Indications for temporary pacemaker: would it be indicated in post-inferior MI?

A

post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable

90
Q
A

My MRCP (43 decks)

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