L17: Chest pain and acute coronary syndrome Flashcards

1
Q

What steps need to be done in order to diagnose chest pain?

A

History needs taking
Clinical examination
Investigations –> ECG, Blood test (troponin, FBC etc)

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2
Q

How is a history taken for examining pain?

A

SQITARS
S- site- location of the pain, if it radiates
Q- quality- how the pain feels (shape, dull, stabbing etc)
I- intensity- on a scale of 1-10 how bad is the pain
T- time/timing- when did it start, sudden or gradual
A- aggravating factors- what makes the pain worse
R- relieving factors- what makes the pain better
S- secondary symptoms- other symptoms

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3
Q

What are the different causes of chest pain?

A

Repiratory causes
Cardiac causes
MSK causes
Gastrointestinal causes

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4
Q

What are the respiratory causes?

A
Pneumonia 
Pulmonary embolism 
Pain usually caused by problems with parietal pleura
Other questions to ask:
-Fever (pneumonia)
-Coughing up sputum--> green/yellow (pneumonia)
-Previous swelling in legs (PE)
-SoB (pneumonia and PE)
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5
Q

What are the cardiac causes?

A

Myocardial infarction (STEMI and Non-STEMI)
Stable/unstable angina
Pericarditis (present with more pleuritic symptoms)

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6
Q

What are the MSK causes?

A

Broken rib
Costochondritis–> infection of the costal cartilage
Spasm of intercostal muscle

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7
Q

What are the gastrointestinal causes?

A

Gastro-oesophageal reflux

  • -> Burning up the middle of the chest
  • -> Usually after eating
  • -> Worse when lying down
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8
Q

What is the difference between cardiac and pleuritic pain?

A

Cardiac–> Visceral pain

  • -> Dull, poorly localised pain
  • -> worsens with exertion

Pleuritic–> somatic

  • -> Sharp, well localised pain
  • -> Worsens with inspiration, coughing or positional movement
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9
Q

What is pericarditis? What do patients present with? How can it be diagnosed?

A

Inflammation of the pericardium
More common in men
S- Retrosternal chest pain
Q- Sharp, localised to front of chest
(I/T-N/A)
A- Aggravated by inspiration, coughing or lying flat
R- Relieved by sitting and leaning forward
S- Pericardial rub–> ‘Lub’ ‘Dub’ followed by rustling
(Usually present after viral infection)

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10
Q

What does a ECG of pericarditis look like?

A

Widespread ST elevation
Across all chest leads
Saddle shaped

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11
Q

What is cardiac (ischaemic) chest pain?

A

Pain secondary to pathology involving the heart

Potentially life threatening

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12
Q

Define ischeamic heart disease?

A

Disease of the coronary arteries

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13
Q

What is atherosclerosis?

A

Narrowing of the artery due to build up of a plaque (atheroma)
Atheroma–> Lipid rich core with fibrous cap

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14
Q

What are the risk factors for IHD?

A
Split into modifiable and non modifiable 
Modifiable:
- Smoking
- Hypertension 
- Dyslipidaemia
- Diabetes
- Obesity
- Sedentary lifestyle 

Non-modifiable:

  • Age
  • Gender (males more likely)
  • Family history
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15
Q

What is stable angina?

A

Ischaemia only occurs when the metabolic demand of cardiac muscle is greater than what can be delivered by coronary arteries e.g. on exertion

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16
Q

What is unstable angina?

A

Ischaemia and pain on rest due to narrowing of artery preventing sufficient amount of blood passing
Pain maybe more intense
Pain may last longer
Risk of deteriorating into MI

17
Q

What are the different forms of acute coronary syndrome?

A

Unstable angina, MI (non-STEMI and STEMI)

18
Q

What are acute coronary syndromes?

A
Acute myocardial ischaemia caused by atherosclerotic coronary artery disease 
Sudden onset (plaque rupture, thrombus formation...)
Spectrum of occlusion from a common pathophysiological mechanism
19
Q

What usually causes the acute coronary syndromes?

A

Atheromatous plaque rupture with thrombus formation
Causes acute increased occlusion (already partially occluded)
Leading to ischaemia… potential infarction

20
Q

What is ischaemia?

A

Restricted blood supply to a tissue

21
Q

What is the difference between the different types of acute coronary syndromes?

A

Unstable angina–> plaque ruptured, small thrombus formation, ischaemia to heart tissue but not infarction
–> no enzymes releaded

NSTEMI–> plaque ruptures, thrombus formation, partial occlusion (more than unstable angina), injury and infarct to subendocardial myocardium
–> cardiac enzymes released

STEMI–> plaque ruptures, complete occlusion of artery, infarction to myocardium
–> cardiac enzymes released

22
Q

What are the features of unstable angina?

A

Pain on rest
Pain maybe more intense
Pain may last longer
ST depression, T wave inversion or maybe normal
Blood test–> troponin negative (not myocardial damage)

23
Q

What are the features of MI?

A

Chest pain at rest
Severe pain
Radiates to jaw and shoulder/arm
Autonomic input–> sweaty, nausea, pallor
ECG–>
NSTEMI–> ST depression, T wave inversion
Troponin positive
STEMI–> ST elevation, T wave inversion
Troponin positive (not normally done)–> STEMI well detected on ECG

24
Q

How does the ECG for STEMI change?

A

Mins-hours–> ST elevation, potentially hyperacute T waves
Hours-1 day–> ST elevation, T inversion, Q wave
1 week–> ST elevation, T inversion, Q wave
Months–> T wave normal, Q wave still present

25
Q

How does the ECG change in NSTEMI and unstable angina?

A

ST depression

T wave inversion or flattening

26
Q

Which types of chest pain cause troponin levels to increase?

A

Myocardial infarction

STEMI and NSTEMI

27
Q

Why do patients get pain down their arm and into their jaw during MI?

A

Referred pain
Viscera not set up to sense pain where as skin is
ANS in viscera can have afferent pathway back to CNS when inflammed, in pain etc…
Brain interprets these signals as coming in from the skin as it doesn’t expect them from the heart so it feels pain in the skin.
Heart has T1-4 spinal cord innervation so pain is felt in T1-T4 dermatome
Phrenic nerve C3, 4, 5 sensory innervation to pericardium
Therefore sensory information form pericardium goes back into CNS
Brian not expecting information for pericardium (other point of innervation)
Therefore interprets it as from the C3, 4 and 5 dermatome jaw, neck, shoulder region