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CR3 > Acute coronary syndrome > Flashcards

Acute coronary syndrome Flashcards

1
Q

Which conditions fall under the term acute coronary syndrome?

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

How is a STEMI classified?

A

ST-segment elevation or new-onset left bundle branch block and raised troponins

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3
Q

How is a NSTEMI classified?

A

Non-specific signs of ischaemia or normal ECG, raised troponins

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4
Q

How is a unstable angina classified?

A

Characteristic clinical features, non-specific signs of ischaemia or normal ECG, normal troponins.

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5
Q

What is a heart attack (MI)?

A

Death of cardiac tissue

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6
Q

What are the requirements for an MI diagnosis?

A

Troponin must show a rise and/or fall with at least one value above the upper limit for normal

Plus at least one of the following:

  • Symptoms of myocardial ischaemia (e.g. chest pain)
  • New or presumed new ECG changes: ST-T wave changes or new LBBB
  • Development of pathological Q waves
  • Imaging evidence of infarction: loss of viable myocardium or new motion abnormality
  • Angiography or autopsy evidence of thrombus
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7
Q

What is angina?

A

chest pain from myocardial ischaemia when there is an increase in the oxygen supply/demand (e.g. on exertion). This quickly improves on rest. Caused by atherosclerosis leads to narrowing of the coronary vessels

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8
Q

What are the modifiable and non modifiable risk factors for atherosclerosis and therefore Ischaemic heart disease?

A

Modifiable risk factors:

​High cholesterol
Hypertension
Smoking
Diabetes
Obesity

Non-modifiable risk factors:

​Age
Family history
Male sex
Premature menopause

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9
Q

List the other potential causes of a myocardial infraction and acute coronary syndrome

A

Other causes of emboli:
​-Valvular disease
- AF

Other causes of coronary occlusion:

  • Vasculitis (e.g. Kawasaki disease)
  • Coronary vasospasm (e.g. spontaneous, cocaine)
  • Coronary dissection

Changes in oxygen demand and / or delivery:
- Anaemia
​- Hyperthyroidism
- Severe sepsis

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10
Q

What are the clinical signs and symptoms of acute coronary syndrome and myocardial ischaemia

A

Signs-

  • Chest pain > 15 minutes: central crushing or pressing pain +/- radiation to neck or arm
  • Shortness of breath
  • Sweating
  • Nausea and vomiting
  • Palpitations

Symptoms

  • Pale
  • Clammy
  • Tachycardia
  • Cardiac failure (e.g.
  • Pulmonary oedema, hypotension)
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11
Q

Which individuals can have an atypical presentation of an MI? What is the main problem with an atypical presentation of an MI?

A

Women
Diabetes patients
Elderly patients
Patients with significant co-morbidities

These types of patients can present with no pain. So they do not call for help on time and are at a higher risk of death

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12
Q

What is the diagnostic wok up of a patient you suspect may be having an acute coronary syndrome?

A
  • ABCDE (if acutely unwell)
  • Take a patient history (symptoms can assist diagnosis)
  • Conduct physical examination

Investigations

  • Conduct a 12 lead ECG (repeat to look for dynamic changes)
  • Cardiac monitoring
  • Blood pressure
  • U and E’s (cardiogenic shock effecting kidneys)
  • LFT’s
  • Lipid profile
  • Coagulation
  • Group and save
  • HbA1c
  • Troponin
  • Blood Glucose
  • Cholesterol
  • FBC

Imaging -

  • Chest X ray (may show signs if heart failure)
  • Echocardiogram (reduced ejection fracture, valvular pathologies, regional wall motion abnormalities)
  • CT pulmonary angiography
  • CT angiography - if aortic dissection suspected or needs to be excluded
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13
Q

Which ECG results may you obtain from someone with an NSTEMI or stable Angina?

A
  • ECG can be normal
  • ST depression
  • T wave inversion
    In region of infarct
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14
Q

Which ECG results may you obtain from someone with an STEMI or someone who has had an STEMI?

A

Regional ST elevation of ≥2 mm in 2 contiguous chest leads or ≥1mm in 2 contiguous limb leads

New left bundle branch block

T wave inversion after days following a STEMI

Pathological Q waves

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15
Q

Describe the 5 classifications of an MI

A

Type 1- Spontaneous AMI, Plaque rupture

Type 2- Ischaemic imbalance, Coronary spasm, embolism, dissection, hypotension etc

Type 3- sudden unexpected Cardiac death, presumed secondary to myocardial ischaemia

Type 4 a - associated with percutaneous coronary intervention - >5 times URL for troponin

Type 4 b- Caused by stent thrombosis - Confirmed at
angiography or autopsy

Type 5 - Related to Coronary Artery Bypass Grafting - >10 times URL for troponin

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16
Q

List 4 other causes of ST elevation

A

Pericarditis
coronary vasospasm
bundle branch block
ventricular aneurysm

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17
Q

List 3 other causes of ST depression

A

electrolyte disturbances, digoxin effect and

bundle branch blocks

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18
Q

Which leads on an ECG correlate to which artery and which region of the heart? Also which leads would show reciprocation? (not posterior MI)

A

Inferior aspect
Leads = II III, AVF
Artery = Right coronary
Reciprocal = I, AVL

Septal aspect
Leads = V1, V2
Artery = LAD
Reciprocal = II, III, AVF

Anterior aspect
Leads = V3, V4
Artery = LAD
Reciprocal = II, III, AVF

Lateral aspect
Leads = V5, V6, I, AVL
Artery = Circumflex
Reciprocal = II, III, AVF

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19
Q

What does the right coronary artery supply?

A

Inferior wall, posterior wall, right ventricle, SA node and AV node

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20
Q

How is a posterior STEMI identified?

A
  • No ST elevation on routine ECG.
  • Dominant high R waves in V1 and V2
  • May see ST elevation by placing posterior leads V7-V9.
  • When posterior leads are placed ST evation will also be seen in V1-V3
  • Reciprocal ST depression on leads V1-V3
  • ST elevation in leads 2, 3 AVF

ST depression in leads 1 and AVL

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21
Q

How does a STEMI change with time?

A 
Minutes to hours: hyperacute T-waves
0-12 hours: ST-elevation
1-12 hours: Q-wave development
Days: T-wave inversion
Weeks: T-wave normalisation and persistent Q-waves
22
Q

Which other conditions can cause a rise in troponin?

A 
Tachyarrythmias
Heart failure
Hypertensive emergencies
Critical illness (e.g. sepsis, burns)
Myocarditis
Cardiomyopathy (e.g. Takotsubo)
Structural heart disease (e.g. aortic stenosis)
Pulmonary embolism
Renal dysfunction
Coronary spasm
Acute neurological event
23
Q

What are the differential diagnosis for chest pain?

A

Cardiac -

  • Angina
  • Acute coronary syndrome
  • Aortic dissection (radiates to the back)
  • Pericarditis (sharp, pleuritic, better leaning forward and sitting up)

Respiratory

  • Pulmonary emboli (pleuritic)
  • Pneumothorax
  • Pneumonia (pleuritic)

Gastrointestinal

  • Oesophagitis
  • Oesophageal spasm
  • Peptic ulcer disease

Other

  • Costochondritis
  • Fib fracture
  • Herpes zoster
  • Depression/ Anxiety
24
Q

How is an acute coronary syndrome immediately managed?

A

ABCDE assessment

MONA
M- Morphine (with ani-emetic)
O- Oxygen (only if SAT is <94 and <88 in those at risk of hypercapnic respiratory failure)
N- Nitrates (subinguinal GNT)
A- Aspirin (loading dose 300mg)
25
Q

How is a STEMI treated?

A

Restore coronary perfusion in those presenting <12h after symptom onset - angiography +/- primary percutaneous coronary intervention (PCI)
should occur within 120 minutes of being diagnosed with ST elevation

Patients should be initiated on aspirin and a second anti-platelet drug prior to PCI. Usually ticagrelor 180 mg loading, following by 90 mg BD as a regular dose. Other options include clopidogrel (600 mg loading), particularly if there is a high bleeding risk, or Prasugrel (60 mg loading).
aspirin and a second anti-platelet agent is referred to as dual anti-platelet therapy (DAPT) and this should be continued for 12 months post-PCI.

Unfractionated heparin or low molecular weight heparin (LWMH). This is usually given at the time of PCI. Additional agents including glycoprotein IIb/IIIa inhibitors (e.g. tirofiban) also given at the time of PCI in the presence of a high thrombus burden

If PCI is unable to be performed within 120 minutes then fibrinolytic agents should be considered (e.g. alteplase) while arranging transfer to a PCI centre. Coronary angiography +/- PCI should be performed in the following 2-24 hours

26
Q

Which scoring systems are used in assessing those with a NSTEMI and Unstable angina?

A

GRACE (Global Registry of Acute Coronary Events): estimates six-month mortality risk in patients with NSTEMI / UA. Divides patients from lowest (≤1.5%) to highest >9.0%).

HEART (History, ECG, Age, Risk factors and Troponin): estimates six-week risk of major cardiac event (AMI, PCI, CABG, death) in patients with NSTEMI / UA.

27
Q

Which drugs are used in the treatment if and STEMI and Unstable angina?

A 
Additional antiplatelet agent (e.g. clopidogrel, ticargrelor) (on top of aspirin)
Antithrombotic agent (e.g. fondaparinux, UFH)
28
Q

How is a high risk NSTEMI and Unstable angina treated?

A

All patients with a GRACE risk stratification score >1.5% should be treated with dual anti-platelet therapy.

In addition, bleeding risk should be assessed and if there are no overt contraindications, patients should be initiated on antithrombotic therapy. - fondaparinux

29
Q

How is a patient with a >1.5% GRACE score treated for NSTEMI and unstable angina treated?

A

Patients deemed low risk can be initiated on aspirin only. Patients should be subsequently initiated on DAPT and fondaparinux if:

Significant delta change in troponin
Worsening/recurrent ischaemic pain
Deterioration (e.g. cardiogenic shock, arrhythmia, dynamic ECG changes)

Coronary angiography can be considered if there is evidence of recurrent pain or deterioration (e.g. heart failure).

In the absence of these, further invasive management should be considered following non-invasive testing for ischaemia. This can include:

Transthoracic echocardiography: assessing for evidence of ischaemia (e.g. RWMAs, LV dysfunction). Also useful to investigate alternative pathologies.

Stress echocardiography: can be considered if negative troponins, normal ECG and chest pain free for several hours.

Cardiac MRI: can assess both perfusion and wall motion abnormalities. Able to detect recent infarction and assess for previous scars.

CT coronary angiography: good at excluding coronary artery disease by visualisation of coronary anatomy.

30
Q

Which type of NSTEMI and stable angina patient is deemed very high risk and how should they be treated?

A

In patients very high risk, coronary angiography would be appropriate immediately and urgent discussions should be had with cardiology. This includes the following patients:

Cardiogenic shock
Pain refractory to medial therapy
Life-threatening arrhythmia or cardiac arrest
Mechanical complication (e.g. valve rupture)
Acute heart failure with refractory angina
Recurrent dynamic ECG changes (esp. brief ST elevation)

31
Q

How are intermediate to high risk patients (>3%) with NSTEMI or angina treated?

A

Coronary angiography within 96 hours of hospital admission.
Within 24 hours if the presence of a high-risk feature (e.g. delta troponin change, dynamic ST-T wave changes, GRACE score >140).

32
Q

What is the grace score?

A

GRACE (Global Registry of Acute Coronary Events) is a scoring system which estimates six-month mortality risk in patients with NSTEMI / UA.

calculated by entering simple clinical risk factors into a web-based model

Factors include:

Age
Heart rate
Systolic BP
Creatinine
Killip class
ST-segment deviation
Cardiac arrest at admission
Abnormal cardiac enzymes
33
Q

What is the longer term management for MI? ( Life style)

A 
Patient advice- 
Smoking cessation
Dietary changes
Exercise
Reduce alcohol consumption

All patients who drive should be advised to check DVLA guidelines on driving. If they are wishing to fly they should seek advice from the UK civil aviation authority. Finally, given no significant complications related to their MI, they can usually resume normal sexual activity within four weeks.

34
Q

What is the longer term management for MI? ( Medical)

A

Dual anti-platelet therapy (e.g. aspirin and clopidogrel): should be continued for one year. Vital if had PCI to prevent in stent thrombosis.

Beta-blockers (e.g. bisoprolol)

High dose statin (e.g. atorvastatin 80 mg)

ACE inhibitor (e.g. ramipril). Angiotensin receptor blocker can be an alternative if side-effects or intolerant to ACE inhibitor)

Consider mineralocorticoid antagonist: reserved for patients with LV dysfunction (i.e. heart failure) following MI. (spironolactone and eplerenone)

35
Q

Which type of Bradyarrhymias complications can be caused by an MI?

A

Intermittent AV node block: Wenckebach (Mobitz 1)

Complete AV node block

Intermittent block of both bundle branches (Mobitz 2)

Complete block of both bundle branches

36
Q

How are Bradyarrhymia complications treated?

A

Intermittent AV node block: Wenckebach (Mobitz 1)

And

Complete AV node block

Treated with -

•Atropine if rate slow
•Pacing rarely needed
•Spontaneous recovery
in <7days
•Prognosis good

Intermittent block of both bundle branches (Mobitz 2)

And

Complete block of both bundle branches

Treated with - 
•Pacing mandatory (cardiac resynchronization therapy)
•No spontaneous
recovery
•Prognosis poor
37
Q

What is the mode of action of Atropine and what are its side effects?

A

Mode of action -

  • Muscarinic antagonist (anticholinergic)
  • Inhibits vagal activity alleviating parasympathetic depression of SA node activity, and as such the heart rate increases
Side Effects - 
Nausea
Blurred vision
Dilated pupils, photophobia
Dry mouth
38
Q

Which Tachyarrhymias

complications can occur due to an MI?

A

Atrial fibrillation
Ventricular tachycardia
Ventricular fibrillation

39
Q

How are Tachyarrhymia complications of MI immediately treated?

A

AF =
Rate control: beta-blocker
DC cardioversion if haemodynamic compromise
If arrhythmia persists needs anticoagulation with later consideration of rate vs rhythm contol

VT, VF
Rhythm control: DC shock (direct current)

40
Q

How does the timing effect the prognosis of ventricular tachycardia and fibrillation?

A 
Ventricular tachyarrhythmias
complicating AMI (VT, VF) usually occur in first 12-24 hours when, if corrected, they have only minor prognostic impact.

But late VT/VF >24 hours after presentation, are a bad prognostic sign and are predictive of sudden death in the first year

41
Q

Where in the blood vessel does atherosclerosis develop?

A

enters subintimal space- below the intima

42
Q

How does Right ventricular failure due to an MI present and how is it treated?

A

Presents with low cardiac output and low JVP

Treatment - Give fluids - avoid avoid vasodilators (eg nitrates) and diuretics

avoid vasodilators (eg nitrates) and diuretics

43
Q

What is the difference between Dressler’s syndrome and post-myocardial infarction pericarditis?

A

Dressler’s syndrome - autoimmune form of acute pericarditis that occurs 2-3 weeks following a myocardial infarction

post-myocardial infarction pericarditis due to direct inflammation from transmural infarction,

44
Q

Pericarditis is usually of viral origin in which case hospital admission is often not required. List the major and minor risk factors associated with pericarditis that would require admission?

A

Major risk factors:

  • Fever > 38º
  • Subacute onset
  • Large pericardial effusion
  • Cardiac tamponade
  • Poor response to 1 week of treatment

Minor risk factors:

  • Myopericarditis
  • Immunosuppression
  • Trauma
  • Oral anticoagulant therapy
45
Q

What are the signs and symptoms of pericarditis?

A
  • Chest pain: sharp, pleuritic (worse on inspiration) -better on leaning forward and sitting up
  • Fever: usually low-grade
  • Breathlessness: may indicate development of complications such as pericardial effusion or myocardial involvement.
  • Cough

Pericardial friction rub: scratchy or squeaking sound heard over the heart

46
Q

What are the signs indicating a cardiac tamponade?

A

Muffled heart sounds,

distended JVP,

pulsus paradoxus (fall in blood pressure > 10 mmHg during inspiration),

hypotension

47
Q

How is acute pericarditis diagnosed?

A

typical history, characteristic ECG findings and exclusion of other causes.

2 of the following 
Typical chest pain
Pericardial friction rub
Characteristic ECG features
New or worsening pericardial effusion
48
Q

What are the characteristic ECG findings associated with an pericarditis?

A

widespread saddle-shaped ST elevation with PR depression.

Reciprocal ST depression sometimes seen in aVR and V1

49
Q

How is pericarditis treated?

A

First-line: ibuprofen (600 mg TDS) or aspirin (600 mg TDS). Ensure no contraindications. Give for 1-2 weeks until pain resolves. Gastric protection (e.g. proton pump inhibitor).

Adjuvant: colchicine (2-3 mg loading then 0.5 mg BD) can be given as an adjunct to NSAID treatment or as primary therapy in patients with contraindications. Typically longer course (i.e. 3 months)

Other: short courses of oral corticosteroids may be required in patients who fail to respond, those with contraindications or development of side-effects.

50
Q

After an MI how long should you wait to resume sexual activity?

A

4 weeks

CR3 (10 decks)

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