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cardiology core conditions > Myocardial infarction/acute coronary syndrome > Flashcards

Myocardial infarction/acute coronary syndrome Flashcards

1
Q

What are the three conditions under acute coronary syndrome?

A
  1. ST-elevation myocardial infarction (STEMI)
  2. Non-ST-elevation myocardial infarction (NSTEMI)
  3. Unstable angina
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2
Q

What is a myocardial infarction (MI)?

A

MI is defined as the death of cardiac myocytes due to prolonged myocardial ischaemia.

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3
Q

How do you differentiate between unstable angina and NSTEMI?

A

NSTEMI: occluding thrombus => myocardial necrosis and a rise in serum troponin I & T and creatinine kinase-MB.

Unstable angina: ruptured plaque with non-occlusive thrombus + no rise in troponin

No ST elevation in both

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4
Q

What are the 5 different types of MI?

A

Type 1: Spontaneous MI with ischaemia (due to primary coronary event i.e. plaque eruption/rupture, fissuring or dissection

Type 2: MI 2nd to ischaemia (due to increased O2 demand or decreased supply i.e. coronary spasm or embolism, anaemia, arrhythmias and hyper/hypotension)

Type 3: MI in sudden cardiac arrest

Type 4a: MI related PCI

Type 4b: MI related to stent thrombosis

Type 5: MI related to CABG

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5
Q

What is the underlying pathophysiology of acute coronary syndromes?

A

Rupture of the fibrous cap of a coronary artery plaque.

This leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction & distal thrombus embolisation.

Presence of a rich lipid core and think fibrous cap = increased risk of rupture.

Thrombus formation and vasoconstriction produced by platelet release of serotonin and thromboxane-A2 => myocardial ischaemia due to reduction in coronary blood flow.

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6
Q

What are the risk factors?

A

Non-modifiable:
Age
Male
Family Hx of ischaemic heart disease (MI in 1st degree relative <55years)

Modifiable:
Smoking
Hypertension
Diabetes
Hyperlipidaemia 
Obesity
Sedentary lifestyle
Cocaine use

Controversial risk factor:
Stress
Type A personality
Left ventricular hypertrophy

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7
Q

What are the symptoms of acute coronary syndrome (ACS)?

A

New onset acute central chest pain (at rest or deterioration of angina) lasting >20 mins

Assoc. w/ nausea, sweatiness, dyspnoea, palpitations

Atypical features = indigestion, pleuritic chest pain or dyspnoea

ACS w/o chest pain = silent (mostly seen in elderly & diabetic patients)

Silent MI’s present with syncope, pulmonary oedema, epigastric pain and vomiting

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8
Q

Which investigations are carried out to confirm ACS?

A
  1. ECG
  2. Chest X-ray
  3. Bloods: FBC, U&E, glucose, cholesterol/lipids, cardiac enzymes
  4. Cardiac enzymes: Troponin I & T (most sensitive & specific markers of myocardial necrosis)
  5. Echo
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9
Q

Describe the changes seen in an ECG in the event of an ACS (STEMI / NSTEMI)?

A

12-lead ECG : ST elevation & T-wave inversion highly suggestive of an ACS, esp assoc. with anginas chest pain.

ECG should be repeated when patient is in pain and monitor continuous ST segment.

STEMI : hyperacute, tall T waves, persistent ST elevation or new left bundle branch block occur within hours (due to complete occlusion of coronary vessel).
T-wave inversion and pathological Q waves follow over hours to days.

NSTEMI/unstable angina : ST depression, T wave inversion, non-specific changes or normal

*In 20% MI, ECG normal initially

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10
Q

Troponin is the most specific and sensitive biochemical marker in ACS.

What are troponins and what is the function of Troponin I, Troponin T and Troponin C?

A

Troponin are proteins involved in skeletal and cardiac muscle contraction.

Troponin I, T and C are on the thin-acting filament alongside tropomyosin to form the cardiac myofilament.

Troponin T attaches the complex to tropomyosin.

Troponin C binds calcium during excitation-contraction coupling.

Troponin I inhibits the myosin binding site on actin.

*High troponin levels = high mortality risk in ACS

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11
Q

What happens to troponin on myocardial death?

A

Troponins are released and enter the blood stream within hours of the result.

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12
Q

Which troponins are the most specific to the heart?

A

Troponin I and T

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13
Q

Which other cardiac conditions result in a raised troponin?

A

Myocarditis
Pericarditis
Ventricular strain (ie. 2nd to PE)

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14
Q

What are some non-cardiac causes of raised troponin?

Causes that are/have:

  • Indirectly related to heart
  • No cardiac relation
  • Iatrogenically
  • Consistently raised troponin
A

Indirectly related to heart:
Massive PE causing right ventricular strain

No cardiac relation:
Subarachnoid haemorrhage
Burns
Sepsis

Common cause of consistency raised troponin = renal failure

Iatrogenically:
CPR
DC cardioversion
Ablation therapy

Tachyarrhythmias = rise in troponin similar to ACS

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15
Q

Which two main scoring system is used to stratify ACS risk score?

A
  1. Thrombolysis in myocardial infarction (TIMI) score
  2. Global Registry of Acute Coronary Events (GRACE) score

The GRACE score is based on age, heart rate, systolic blood pressure, serum creatinine and the Killip score.

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16
Q

What is the acute management for chest pain and ACS without ST elevation?

A

M - Morphine 5-10mg IV + metoclopramide 10mg IV

O - Oxygen if SaO2 <90% or breathless, low flow O2

N - Nitrates ; GTN spray or sublingual tablet

A - Aspirin 300mg loading dose then 75mg once daily

T - Tricagrelor or clopidogrel (2nd anti-platelet agent in confirmed ACS)

17
Q 
After acute management of chest pain using MONA in ACS without ST elevation, how do you manage a high risk patient whose troponin is rising, dynamic ST or T wave changes and the patient has either 
diabetes, 
CKD, 
left ventricular ejection fraction <40, 
early angina post MI, 
recent PCI, 
previous CABG or 
intermediate to high risk GRACE score.
A
  1. Anti-thrombin drugs : Fondaparinux, enoxaparin (both = factor Xa inhibitor)
  2. 2nd anti-platelet agent (if not already added) : ticagrelor (or clopidogrel in lower risk patients)
  3. IV nitrate if pain continues, titrate to pain and maintain systolic BP >100mmHg
  4. Oral B-blocker : Bisoprolol 2.5mg OD
  5. ACE-inhibitor + monitor renal function
  6. Lipid management : Atorvastatin 80mg OD
  7. Cardiologist review for angiography urgent if:

Ongoing angina (<120min after presentation) and evolving ST changes, signs of cardiogenic shock or life threatening arrhythmias

Early (<24h) if GRACE score >140 and high risk patient

Within 72h if lower risk patient

18
Q

When may beta-blockers be contraindicated?

What alternative may be used?

A

Cardiogenic shock
Heart failure
Asthma/COPD
Heart block

Rate limiting calcium antagonist i.e. verapamil / diltiazem

19
Q

What is the prognosis for ACS without ST elevation (unstable angine and NSTEMI)?

Which risk factors increase the risk of death?

A

Risk of death 1-2% ; 15% for refractory angina

Risk stratification (GRACE score) to predict and manage better.

Risk factors:
Hx of unstable angina
ST depression or widespread T-wave inversion
Raised troponin
Age >70yrs
Comorbidity (previous MI, diabetes, poor left ventricle function)

20
Q

What other interventions may be needed for a high risk NSTEMI patient (GRACE score >140) with
persistent chest pain not responding to medical therapy,
clinical signs of heart failure,
haemodynamically unstable,
cardiogenic shock or
life-threatening arrhythmias (ventricular fib/tachycardia)?

A

Very high risk = Urgent angiography within 2h

High risk (GRACE score >140) = Coronary angiography ± PCI within 24h

Intermediate risk (GRACE score 109-140) = Angiography within 72h

Patients with multi-vessel disease = consider CABG not PCI

21
Q

How do you manage a low risk ACS patient without ST elevation after acute management of chest pain?

After acute management of chest pain using MONA in ACS without ST elevation, how do you manage a low risk patient who has 
No recurrent chest pain
No signs of heart failure
Normal ECG
No rise in troponin
A

Conservative management
Medical therapy
Outpatient investigations e.g. stress test

22
Q

What is the underlying pathophysiology of a STEMI?

A

Rupture of a coronary artery plaque => prolonged occlusion of a coronary artery => myocardial necrosis within 15-30 minutes.

Initially, subendocardial myocardium is affected but with continued ischaemia, the infarct zone extends through to the subepicardial myocardium => producing a transmural Q wave MI.

23
Q

Which factors increased the risk of death?

A 
Age >65 ; >75 
Hx of angina ; hypertension ; diabetes
Systolic BP <100mmHg
Heart rate >100bpm
Killip score II=IV
Weight >67kg
Anterior MI or LBBB
Delay to treatment >4h
24
Q

What are the typical + atypical signs and symptoms of a STEMI?

A
  1. Severe chest pain lasting more than 20mins

Pain does not respond to sublingual GTN & opiate is required for analgesia

Pain may radiate to left arm, neck, jaw.

  1. In elderly/diabetic patients symptoms are atypical:
    Dyspnoea
    Fatigue
    Pre-syncope / syncope
  2. Autonomic symptoms are common:
    Pale & clammy
    Marked sweating
  3. Signs:
    Pulse thready with sig. hypotension, bradycardia or tachycardia.
25
Q

Which investigations are carried out in a STEMI?

A

ECG - if baseline ECG normal then continue monitoring every 15 mins if in continuous pain.

Continuous cardiac monitoring required in case of significant cardiac arrhythmias.

Blood tests: Cardiac troponin I & T ; FBC ; serum electrolyte ; glucose ; lipid profile ; U&E

Transthoracic echocardiography (TTE)

26
Q

Which ECG leads exhibit ST elevations anterior MI?

A
  1. 2mV or more at J point in leads V1-V4

0. 1mV or more in other leads

27
Q

Which ECG leads exhibit changes in lateral MI?

A

Leads I, AVL and V5/V6

28
Q

Which ECG leads exhibit changes posterior MI?

A

ST depression in V1-V3 with dominant R wave,

ST elevation in lead V5/V6

29
Q

Initial management for STEMI is the same as above using MONA to stabilise chest pain. STEMI patients are then referred to PCI centre be managed via reperfusion therapy.

Explain Primary percutaneous coronary intervention (PCI).

Which medications are required alongside PCI?

A

PCI is the preferred reperfusion therapy for STEMI + should be offered to all patients within 12h of symptom onset with a STEMI.
=> Radial access = preferred route as reduces complications.

Dual anti-platelet therapy: aspirin and ADP receptor blocker i.e. tricagrelor or prasugrel.

Anti-coagulant : Enoxaparin, anti-fractionated heparin

30
Q

Initial management for STEMI is the same as above using MONA to stabilise chest pain. If primary PCI centre not available within 120 mins then STEMI patients are first managed by thrombolysis.

Explain thrombolysis mechanism of action.

Which drug is used in thrombolysis therapy?

When should you thrombolyse?

When should you not thromboses?

Which medications are required alongside thrombolysis?

If fibrinolysis unsuccessful then transfer patient to primary PCI centre for rescue PCI or for angiography.

A

Thrombolytic agents enhance the break down of the thrombus occluding the vessel by activating plasmin from plasminogen.

Thrombolysis is appropriate if PCI not available within 120 mins of STEMI diagnosis.

Thrombolysis best achieved with tissue plasminogen activator (TPA) i.e tenecteplase as a single IV bolus

Do not thrombolyse ST depression alone, T-wave alone, or normal ECG.

Dual anti-platelet therapy: aspirin and ADP receptor blocker i.e. tricagrelor or prasugrel.

Anti-coagulant : Enoxaparin, anti-fractionated heparin

31
Q

What are the absolute and relative contraindications of thrombolysis?

A

Absolute:
1. Haemorrhagic stoke / stroke of unknown origin

  1. Ischaemic stroke <6months
  2. CVS damage
  3. Recent trauma/surgery/head injury
  4. GI bleeding within last month
  5. Bleeding disorder
  6. Aortic dissection

Relative:
1. Anticoagulant therapy

  1. Pregnancy or 1 week postpartum
  2. Refractory hypertension
  3. TIA <6months
  4. Infective endocarditis
  5. Active peptic ulcer
  6. Prolonged /traumatic resus
  7. Advanced liver disease
32
Q

What is coronary artery bypass surgery (CABG)?

A

CABG diverts blood from occluded coronary arteries to improve blood flow and oxygen supply to the heart.

CABG reserved for complications of MI i.e ventricular septal defect or mitral regurgitation.

33
Q

What are the complications of MI?

A
  1. Heart failure : post MI = poor prognosis
    * Killip classification assesses patients with heart failure post MI
  2. Myocardial rupture and aneurysm dilation
  3. Ventricular septal defect
  4. Mitral regurgitation
  5. Cardiac arrhythmias : Ventricular tachycardia and fibrillation / bradyarrhythmias
  6. Conduction disturbances
  7. Dressler syndrome (immune response after injury => pericarditis)
  8. Cardiac tamponade
34
Q

What are post ACS lifestyle modifications?

A

Cardiac rehab program: education and information on lifestyle

Exercise rehab part of program

Dietary control: calorie control of obesity, increase fruit & vegetables, reduce trans & saturated fat, reduce salt intake (patients with hypertension)

Alcohol within safe limits (<14 units per week), no binge drinking

Physically active (30 mins of moderate aerobic exercise 5x a week)

Stop smoking

BP reduced to systolic <140mmHg

Diabetes maintained 53mmol/mol

35
Q

What are post ACS drug therapy and assessment?

A
  1. Aspirin 75mg
  2. ADP receptor blocker ie tricagrelor, clopidogrel
  3. Oral beta-blocker to maintain heart rate <60bpm
  4. PPI (for patients high risk of bleeding while on dual anti-platelet therapy)
  5. ACE inhibitor or ARB (angiotensin receptor blocker) esp if LVEF <40%
  6. Statin (cholesterol <1.8mmol/L)

cardiology core conditions (8 decks)

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