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Core Conditions - Cardiovascular > Myocardial Infarction & Acute Coronary Syndromes > Flashcards

Myocardial Infarction & Acute Coronary Syndromes Flashcards

1
Q

What is “acute coronary syndrome”?

A

a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart

this results in ischaemia (and sometimes infarction) of the myocardium

it is a medical emergency and requires immediate hospital admission

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2
Q

What are the 3 different types of ACS?

A
  • STEMI - ST elevation MI
  • NSTEMI - non-ST elevation MI
  • unstable angina - ischaemia, without infarction
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3
Q

What is the difference in the way that STEMIs and NSTEMIs are usually diagnosed?

A
  • STEMI is diagnosable on the basis of classical ECG changes
  • NSTEMI is usually diagnosed on the basis of a suggestive history with positive biochemical markers
    • e.g. positive / raised troponin
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4
Q

How is unstable angina usually diagnosed?

Why is it significant to identify?

A
  • there are no obvious ECG changes
  • biochemical markers (troponin) are negative
  • history is suggestive of ACS
  • unstable angina is significant as there is a high risk (50%) of MI in the subsequent 30 days
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5
Q

Why are NSTEMI, STEMI and unstable angina all grouped together?

A

they all share a common mechanism

this is rupture or erosion of the fibrous cap of a coronary artery plaque

they can be thought of as a spectrum with unstable angina being the least severe and STEMI being the most severe

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6
Q

What is the “textbook presentation” of ACS?

A

STEMI, NSTEMI and unstable angina can all have a similar clinical presentation

  • acute onset of central or left-sided chest pain
  • the pain often comes at rest, in the morning, and gradually increases in intensity over a period of minutes
  • pain radiates down the left arm
  • pain is associated with diaphoresis (sweating), pre-syncopal or syncopal symptoms
  • 30% of patients present without pain
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7
Q

What is the difference in how much the coronary arteries are occluded in the different types of acute coronary syndromes?

A
  • STEMI is associated with complete or almost complete occlusion of one or more of the coronary arteries
  • NSTEMI and unstable angina are associated with partial occlusions
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8
Q

What % of cases of MI are fatal?

How many deaths occur within 2 hours of symptom onset?

A

15% of cases of MI are fatal

50% of deaths occur within 2 hours of onset of symptoms

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9
Q

What is the incidence of coronary heart disease?

A

300,000 cases per year

coronary artery disease accounts for 3% of admission to UK hospitals each year

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10
Q

What are the non-modifiable risk factors for ACS?

A
  • advancing age
  • male gender
  • family history of IHD
    • only significant if symptoms presented before the age of 55 in the relative
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11
Q

What are the modifiable risk factors for ACS?

A
  • smoking
  • hypertension
  • diabetes
  • obesity
  • hyperlipidaemia
  • sedentary lifestyle
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12
Q

What are the controversial risk factors for ACS?

A
  • stress
  • having a Type A personality
  • left ventricular hypertrophy (LVH)
  • cocaine use
  • increased fibrinogen
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13
Q

How can cocaine use increase the risk of ACS?

A
  • acutely it can cause coronary vasospasm which causes MI
  • chronically it increases the risk of MI from a traditional atherosclerotic disease process
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14
Q

What are the symptoms of ACS?

A
  • chest pain
  • diaphoresis (sweating)
  • breathlessness
    • in many cases this may be the only symptom
  • syncope (fainting)
  • tachycardia
  • vomiting and sinus bradycardia
  • distress (also sometimes a “feeling of impending doom”)
  • sudden death

infarction can occur in the absence of any physical signs

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15
Q

Where does the chest pain radiate to in ACS?

Where does it radiate to if it is more predictive of MI?

A
  • radiates down the inside of the left arm and into the neck and jaw
  • can also radiate to the epigastrium and the back
  • it is more predictive of MI if it radiates to the RIGHT arm or BOTH arms
    • contrary to the classical textbook definition of radiating down the left arm
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16
Q

What type of pain is present in ACS?

How long does it last and how severe is it?

A
  • it is a “crescendo pain” that increases in severity over a period of minutes after onset
  • pain typically lasts up to a couple of hours
  • typically a “mid-range” pain - i.e. 5-7/10
17
Q

Why might syncope occur in ACS?

A

syncope occurs as a result of severe hypotension or severe arrhythmia

18
Q

Why might vomiting and sinus bradycardia occur in ACS?

What might make this worse?

A

occurs as a result of excessive vagal stimulation, which is most common in inferior MI

nausea and vomiting can be aggravated by opiates given for pain relief

19
Q

Why can sudden death occur in ACS?

When do most of these deaths occur?

A

sudden death is usually the result of ventricular fibrillation or asystole

most deaths occur within the first hour

20
Q

Why is it important to get help as soon as possible for patients with ACS?

A

if the patient survives the first hour, the likelihood of severe arrhythmias still remains, but diminishes with each subsequent hour

cardiac failure is the major cause of death in those that survive the first few hours

whether or not this develops depends on the extent of myocardial damage

21
Q

Why are MIs and strokes more common in the morning?

A
  • the blood pressure lowers overnight
  • BP then rises again when the person wakes up
  • the higher BP is thought to dislodge any thrombus that has formed overnight
22
Q

What factors are particularly significant for the likelihood of ACS compared to other causes of chest pain?

A
  • pain lasting for > 15 minutes
  • pain that radiates to the arms or jaw
  • diaphoresis
  • vomiting
  • exertional chest pain
23
Q

What features suggest non-ACS chest pain?

A
  • reproducible chest pain
    • e.g. tender chest wall or positional pain
  • pleuritic chest pain
24
Q

What features of chest pain are NOT useful to predict the likelihood of ACS?

A
  • the severity of the pain
  • response to GTN spray
  • response to PPIs or antacids
25
Q

What is a silent MI?

What % of MIs are this kind?

A

a silent MI is an MI that presents WITHOUT chest pain

30% of MIs are silent

26
Q

In which groups is it particularly important to look out for an atypical presentation of MI?

i.e. silent MI

A
  • women
  • the elderly
  • individuals with diabetes
27
Q

In women, the elderly and people with diabetes, what are particularly significant historical features suggestive of silent MI?

A
  • shortness of breath - especially if present on exertion (SOBOE)
  • generalised weakness
  • dizziness
28
Q

What are other symptoms associated with a silent MI?

A
  • syncope
  • pulmonary oedema
  • epigastric pain
  • vomiting
  • acute confusional state
  • stroke
  • diabetic hyperglycaemia
29
Q

What can be heard on examination that suggests impaired myocardial function?

A
  • hearing 3rd / 4th heart sounds
  • pan-systolic murmur
  • pericardial rub
  • crepitations in the lungs if pulmonary oedema is present
  • quiet first heart sound
30
Q

What other clinical signs are suggestive of impaired myocardial function?

A
  • hypotension
  • narrow pulse pressure (difference of <40 mmHg)
  • raised JVP
31
Q

What are the 3 clinical signs of sympathetic activation?

A
  • pallor (looking pasty)
    • can be localised or generalised - only significant if generalised
    • most evident on the palms and the face
  • sweating
  • tachycardia
32
Q

What are the cardiac differentials for ACS?

A
  • angina
  • pericarditis
  • myocarditis
  • aortic dissection
33
Q

What are the pulmonary differentials for ACS?

A
  • pulmonary embolism
  • pneumothorax
  • anything that causes pleuritic chest pain
34
Q

What are the oesophageal differentials for ACS?

A
  • oesophageal reflux
  • oesophageal spasm
  • tumour
  • oesophagitis
35
Q

What usually always causes MI?

How does the pain relate to angina pain?

A

usually always due to occlusive thrombus formation at the site of rupture or erosion of an atheromatous plaque

pain experienced is the same as angina, but lasts longer and may be more severe

36
Q

When should a patient call an ambulance after experiencing “angina-type pain”?

A

they should call an ambulance if they experience “angina type pain”, which after using GTN spray, does not subside within 15 minutes

37
Q

What are the 2 different mechanisms by which MI can occur?

A
  • the fibrous cap of the plaque gets a superficial injury and a thrombus forms on it
  • in more advanced, unstable plaques, the fibrous cap completely ruptures

not only can some of the contents escape, but blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque

38
Q

After fibrous cap rupture and thrombus formation, how does ischaemic injury result?

A
  • platelets release serotonin and thromboxane A2
  • this causes vasoconstriction in the area
  • this results in reduced blood flow to the myocardium and ischaemic injury
39
Q

What is the difference between a transmural MI and a nontransmural MI?

A

Transmural MI:

  • an infarct that causes necrosis of tissue through the full thickness of the myocardium

Nontransmural MI:

  • an MI that does NOT cause necrosis through the full thickness of the myocardium

Core Conditions - Cardiovascular (6 decks)

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