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Cardiology > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q

What are the cardiovascular and non-cardiovascular causes of chest pain?

A

Cardiovascular (25%)

  • Myocardial ischaemia
  • Cardiovascular (non-ischaemic)

Non-cardiovascular (75%)

  • Upper gastrointestinal
  • Respiratory
  • Musculoskeletal
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2
Q

What are some causes of myocardial ischaemia?

A

Causes of myocardial ischaemia:

  • Coronary Artery Disease
  • Aortic Stenosis
  • Hypertrophic Cardiomyopathy (HOCM)
  • Tachyarrhythmias
  • Cocaine Use
  • Anaemia
  • Thyrotoxicosis
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3
Q

What are some cardiovascular non-ischaemic causes of chest pain?

A

Cardiovascular non-ischaemic:

  • Aortic Dissection
  • Pericarditis
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4
Q

What are some respiratory causes of chest pain?

A

Respiratory

  • Pulmonary Embolism
  • Pneumothorax
  • Pneumonia
  • Pleurisy
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5
Q

What are some musculoskeletal causes of chest pain?

A

MSK:

  • Costochondritis
  • Herpes Zoster
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6
Q

How do types of pain indicate the cause of chest pain?

A

History:
- SOCRATES of pain

Visceral pain - diffuse, poorly localised
Somatic pain - localised
Sudden onset pain - pulmonary embolism
Pressure/heavy/tight - Acute coronary syndrome, or GORD
Indigestion/belching - ACS or GORD
Severe ripping pain - Aortic dissection
Sharp, stabbing pain - Pleuritic pain (musculoskeletal)

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7
Q

How does the location of pain indicate the cause of chest pain?

A

ACS: left arm, both arms, jaw, neck
Gallstones/cholecystitis: right shoulder
Aortic dissection/GORD/pancreatitis/Peptic ulcer/ACS - intrascapular, back
Pancreatitis/Peptic ulcer/gallstones/ ACS - epigastric pain

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8
Q

How do secondary features of chest pain indicate the cause?

A

ACS/GI - Nausea, vomiting
ACS-PE/Aortic dissection - sweating, clammy
ACS/Resp - shortness of breath
ACS/PE/Aortic stenosis - hypotension, syncope

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9
Q

How does the duration of chest pain indicate its cause?

A

Seconds - MSK or non-cardiac
Minutes - ACS, GORD, MSK
Hours - any
Days - dull, persistent pain - not ACS

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10
Q

How do exacerbating factors of chest pain indicate its cause?

A

Angina - exertion, emotion
ACS/GORD/Peptic ulcer - eating
Pericarditis/GORD/MSK/Pancreatitis - positional

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11
Q

What type of chest pain suggests Aortic Dissection?

A

Severe, ripping pain

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12
Q

What is angina pectoris?

A

Angina:

  • Discomfort in chest and/or adjacent areas (jaw, shoulder, back, arm)
  • Caused by myocardial ischaemia
  • Most commonly due to coronary artery disease
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13
Q

What is typical angina?

A

Typical angina:

  • Constricting discomfort in the front of chest, neck, shoulders, jaw or arms
  • Precipitated by physical exertion
  • Relieved by rest or GTN within 5 minutes

ALL OF THE ABOVE.

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14
Q

What is atypical angina?

A

Atypical angina:

  • Constricting discomfort in the front of chest, neck, shoulders, jaw or arms
  • Precipitated by physical exertion
  • Relieved by rest or GTN within 5 minutes

ONLY TWO OF THE ABOVE

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15
Q

What are the most important risk factors for developing coronary artery disease?

A
  • Age
  • Gender
  • Diabetes
  • Hyperlipidaemia
  • Smoking
  • Hypertension
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16
Q

What other aspects of the history are relevant to a diagnosis of coronary artery disease?

A
  1. Concurrent diagnosis of coronary artery disease (stable angina, previous MI)
  2. Concurrent diagnosis of other atherosclerotic arterial disease (ischaemic stroke, peripheral vascular disease, renovascular disease)
  3. Family history of coronary artery disease or atherosclerotic arterial disease
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17
Q

What ECG changes would be suggestive of coronary artery disease?

A 
1. Pathological Q waves usually indicate current or prior myocardial infarction. Q waves are considered pathological if:
> 40 ms (1 mm) wide
> 2 mm deep
> 25% of depth of QRS complex
Seen in leads V1-3
  1. Left bundle branch block (LBBB). ECG characteristics of LBBB are:
    - Broad QRS (>3small square/0.12sec) and
    - Deep S wave in V1 and
    - No Q wave in V5/V6
  2. ST segment and T wave abnormalities (e.g. ST segment depression or T wave flattening or inversion)
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18
Q

Which patients with chest pain would require admission?

A

Admit patients with features suggesting a serious cause of chest pain:

  • Respiratory rate over 30bpm
  • Tachycardia over 130bpm
  • Systolic BP under 90mmHg
  • Diastolic BP under 60mmHg
  • O2 sats less than 92%, or central cyanosis (of no history of chronic hypoxia
  • Altered level of consciousness
  • High temperature (38.5+)

Also if they have suggested acute coronary syndrome (ACS)

  • Current chest pain
  • Complication signs (pulmonary oedema etc)
  • Are pain free, but have had chest pain in the last 12 hours AND have an abnormal ECG, OR an ECG isn’t available

Consider admission if you suspect ACS if pain has resolved and there are signs of complications

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19
Q

What information should be provided to a patient with stable angina?

A

Clearly explain diagnosis:

  • Factors that can provoke angina (exertion, emotional stress, cold exposure, eating a large meal)
  • Long term course of angina
  • Information of management
  • Implications for daily activities
  • Risk of myocardial infarction
  • Life expectancy
  • Advise medical help if there is sudden worsening in frequency or severity of angina
  • Discuss the reasons, benefits, and side-effects of treatment (flushing, headache, light-headedness)
  • Explore self-management skills regarding stress, anxiety, and depression
  • Advice about driving, flying, work, and physical exertion including sexual activity

Advise patients that the aim of anti-anginal drug treatment is to prevent episodes of angina, and the aim of secondary prevention treatment is prevent further cardiovascular events such as heart attacks or stroke

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20
Q

What drug treatments should be given to patient with stable angina?

A

Drug treatment for symptom relief:
- Prescribe sublingual glyceryl trinitrate (GTN) for rapid relief, and to use before performing activities known to cause angina

If a patient experiences chest pain, they should:

  • Stop what they are doing and rest
  • Use their GTN spray/tablets as instructed
  • Take a second dose after 5 minutes if the pain has not eased
  • Call 999 for an ambulance if this does not help (after second dose) or earlier if pain intensifies or they feel unwell

Prescribe a beta-blocker or calcium-channel blocker as first-line regular treatment

  • reduces symptoms of stable angina, dependent on co-morbidities, contraindications and patient preference
  • If a patient does not tolerate one, switch to the other

If neither beta-blockers or calcium-channel blockers are tolerated, or they are contraindicated, consider monotherapy with one of the following:

  • Long acting nitrate (isosobide mononitrate)
  • Nicorandil
  • Ivabradine
  • Ranolazine

Review response to treatment, including adverse effects, 2-4 weeks after starting or changing drug treatment
- Titrate dose against symptoms up to maximum licensed or tolerated dose

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21
Q

What is the drug treatment for secondary prevention in angina?

A

Consider antiplatelet treatment in all patients with stable angina
(low dose aspirin 75mg daily)
Patients who have had strokes or peripheral artery disease should take clopidogrel, NOT aspirin

Consider use of an ACE inhibitor for patients with stable angina and diabetes mellitus
- Ensure that patients with hypertension, heart failure, chronic kidney disease, or previous MI have been prescribed an ACEi unless contraindicated

  • Offer a statin
  • Offer antihypertensive treatment
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22
Q

What tests and investigations should be done for a patient presenting with chest pain?

A
  • Full history and examination
  • ECG
  • Blood tests - baseline, cardiac troponins
  • Chest x-rays and other radiological imaging
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23
Q

What is the length of time covered by small squares and large squares on an ECG?

A

Small square = 0.04s

Large square = 0.2s

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24
Q

How long should the PR interval be?

A

PR interval = 0.12-0.2s
or
3-5 small squares

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25
Q

How long should the QRS complex be?

A

QRS complex = <0.12s
or
3 small squares

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26
Q

How long should the QT interval be?

A

The QT interval length is inversely proportional with the heart rate:
The faster the HR, the shorter the QT
The slower the HR, the longer the QT

If the HR is 60:
QT interval = 0.35-0.46s
or
9-11 small squares

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27
Q

What signs on an ECG would be suggestive of coronary artery disease (CAD)?

A

Signs of CAD:

1. Pathological Q waves usually indicate current or prior myocardial infarction. Q waves are considered pathological if:
> 40 ms (1 mm) wide
> 2 mm deep
> 25% of depth of QRS complex
- Seen in leads V1-3
  1. Left bundle branch block (LBBB). ECG characteristics of LBBB are:
    - Broad QRS (>3small square/0.12s) and
    - Deep S wave in V1 and
    - No Q wave in V5/V6
  2. ST segment and T wave abnormalities (e.g. ST segment depression or T wave flattening or inversion)
28
Q

What should you initially prescribe for patients with stable angina?

A

Prescribe:
75mg aspirin OD
GTN spray with the following instructions:
If having chest pain -
- Stop what they are doing and rest
- Use GTN spray as instructed
- Take a second dose of GTN after five minutes if the pain has not eased
- Call 999 for an ambulance if the pain has not eased after another five minutes (ie 15 minutes after onset of pain), or earlier if the pain is intensifying or you feel unwell

29
Q

What lifestyle advice should be given to patients with stable angina?

A

NHS choices:

  • Stop smoking
  • Healthy eating
  • Health and fitness
  • Drinking and alcohol
30
Q

Which heart murmurs are systolic?

A

Aortic stenosis

Mitral regurgitation

31
Q

Which heart murmurs are diastolic?

A

Pulmonary stenosis

Tricuspid regurgitation

32
Q

How are S1 and S2 sounds formed?

A

S1 - AV valves closing

S2 - vessel valves closing

33
Q

What kind of murmur is aortic stenosis?

A

Aortic stenosis

  • Ejection systolic murmur
  • Follows slightly after S1 with an ejection click
  • valve does not open fully, causing loud turbulent flow of blood into aorta
  • As the ventricles contract, more blood is pushed through, causing a louder murmur
  • The murmur then becomes quieter as the ventricles relax and blood flow slows down

If stenotic rather than sclerotic, this murmur radiates to the carotids

34
Q

What kind of murmur is mitral regurgitation?

A

Mitral regurgitation:

  • Pansystolic murmur
  • Caused by slight opening of the mitral valve allowing blood flow from the ventricle to the atria
  • The aortic valve also opens allowing for blood flow into the aorta
  • The pressure increases in the atrium, causing dilation of the chamber
  • This means the pressure overall does not increase by much
  • This constant blood flow creates a constant sound that does not change in intensity
  • Stops with S2, closing of the aortic and pulmonary valves

This murmur also radiates to the axilla

35
Q

What further tests are needed to investigate or exclude ACS?

A

Cardiac Troponin testing

  • Test once, then 6 hours later
36
Q

What treatment is given in suspected ACS?

A

Treatment:

- Loading dose of aspirin 300mg

37
Q

How do we monitor patients with suspected ACS?

A

Monitor people with acute chest pain, using clinical judgement to decide how often this should be done, until a firm diagnosis is made
This should include:

  • Exacerbations of pain and/or other symptoms
  • Pulse and blood pressure
  • Heart rhythm
  • Oxygen saturation by pulse oximetry
  • Repeated resting 12-lead ECGs
  • Checking pain relief is effective
38
Q

What would suggest Acute Coronary Syndrome?

A

ACS:

  • Acute chest pain
  • History of stable angina
  • Suspected myocardial infarction
39
Q

What is the initial management for suspected ACS?

A

ACS:

  • ABCDE
  • O2 if needed
  • Aspirin
  • Morphine
  • Nitrates
  • 12 lead ECG
  • Troponin

Remember MONAC

40
Q

What are the treatment options for ACS?

A

ACS treatment:

Unstable angina (no troponin changes):

  • Platelet inhibitors (clopidogrel/ticagrelor)
  • Fondaparinux or LMWH

NSTEMI (troponin changes seen):

  • Platelet inhibitors (clopidogrel/ticagrelor)
  • Fondaparinux or LMWH
  • PCI or thrombolysis
  • Angio/CABG
STEMI:
Depends on length of chest pain
Chest pain LESS than 90 mins:
- Platelet inhibitors (clopidogrel/ticagrelor)
- PCI

Chest pain MORE than 90 mins

  • Platelet inhibitors (clopidogrel/ticagrelor)
  • Fonaparinux or LMWH
  • Thrombolysis
41
Q

How do we treat posterior and inferior myocardial infarctions?

A

Low blood pressure is often seen in right-sided infarcts
Do not give nitrates
The heart becomes dependent on the preload as the right atrium and ventricle aren’t pumping properly

42
Q

Where is t-wave inversion normal?

A

In V1 only

43
Q

WILLIAM MARROW?

A

W - LBBB
M - RBBB
If seen as new - patient is presumed MI
Will see wide QRS complexes, no R wave progression in LBBB

44
Q

What is the pathophysiology of acute coronary syndromes?

A

ACS:

  • Acute thrombosis induced by ruptured atherosclerotic plaque
  • Vasoconstriction
  • Critical reduction on coronary blood flow
  • Clinical sequelae
45
Q

What are the clinical presentations of ACS?

A
  • Prolonged chest pain (over 20 mins) at rest
  • New onset angina pectoris
  • Worsening of existing angina
  • Angina following myocardial infarction
  • Atypical presentations are common over 75 years of age
46
Q

What are some differential diagnoses of ACS?

A
  • Pulmonary embolism
  • Aortic dissection
  • Pericarditis
  • Valvular Heart Disease
  • Pneumothorax
  • Pneumonia
  • Pleural effusion
  • Anaemia
  • Paroxysmal arrythmia
47
Q

How could the ECG be normal in ACS?

A
  • Ischaemia in circumflex territory
  • Isolated RV ischaemia
    (V7-V9 and V3R/V4R leads)
  • Transient episodes of bundle branch block
48
Q

How are troponins used?

A

Troponins:

  • Reflect myocardian cellular damage
  • I and T are the gold standard
  • Troponin levels rise within 2-4 hours
  • Levels may be elevated for 2 weeks
49
Q

What imaging is used in NSTEMI ACS?

A
  • 12 lead ECG
  • Transthoracic (TTE) echocardiography
  • Stress achocardiography
  • Cardiac magnetic resonsance (CMR)
  • Nuclear myocardial perfusion imaging
  • CR coronary angiography
50
Q

How do we calculate ischaemic risk?

A

GRACE score

51
Q

How do we calculate bleeding risk?

A

CRUSADE score

52
Q

How long is dual antiplatelet therapy normally given for after NSTEMI or DES (drug eluting stent) implantation?

A

12 months

53
Q

What are some conditions that can cause a rise in troponin?

A 
• Heart failure- acute and
chronic
• Cardiac contusion,
CABG, pacing, ablation
• Aortic dissection
• Aortic valve disease
• Hypertrophic
cardiomyopathy
• Tachy or
bradyarrhythmias or
heart block
• Apical ballooning
syndrome
• Pulmonary embolism
• Renal Failure
• Acute Neurological
disease (SAH, stroke)
• Critically ill-sepsis,
respiratory failure
• Infiltrative disease,
amyloidosis,
sarcoidosis
• Extreme exertion
54
Q

How does tachycardia affect coronary blood flow?

A

The heart beats more frequently and harder

  • This means diastole is shortened
  • The coronary arteries can only provide blood to the myocardium during diastole (relaxation)
  • This means that myocardial oxygen demand is increased and coronary blood flow is decreased
55
Q

How do troponin levels indicate mortality?

A

The greater the troponin levels, the greater the mortality
There is no increase in troponin in unstable angina
There is a small increase in NSTEMIs, and a larger one in STEMIs

56
Q

What do troponins do?

A

They inhibit contraction by preventing crosslinking between actin and myosin (They are associated with actin)
Troponins are inhibited themselves by the increased intracellular calcium following depolarisation

When cells die from ischaemia, they troponins leak out and become detectable

57
Q

What are causes of ventricular fibrillation and ventricular tachycardia?

A

Scar - disrupts normal electrical conduction:

  • Heart attacks
  • Cardiomyopathy
  • Infection
  • Genetic disorders
  • Years of coronary artery disease

Irritable ventricular cells - overfiring of cells:

  • Coronary artery disease
  • Electrolyte abnormalities

Also consider electrocution!

58
Q

How does ventricular fibrillation present?

A
  • Unconscious
  • Pulseless
  • Pallor
59
Q

How does ventricular tachycardia present?

A
  • Palpitations
  • Shortness of breath
  • Chest pain
  • Lightheadedness
60
Q

How do supraventricular tachycardias present?

A
  • Dizziness
  • Chest pain
  • Anxiety
  • Palpitations
  • Shortness of breath
61
Q

What are causes of atrial fibrillation?

A 
Diseased atrial tissue
- Age
- Inflammation
Enlarged atria
- High blood pressure
- Valve disease
- Lung disease
- Previous afib

Hormonal abnormalities

  • Thyroid
  • Alcohol abuse

INCREASED STROKE RISK - embolism to brain

62
Q

What is cardiac tamponade?

A

When blood gets built up between the heart and pericardium, and makes it more difficult for the heart ot beat effectively

63
Q

What are the consequences of a myocardial infarction?

A
  • Reduced contractility
  • Electrical instability
  • Tissue necrosis
64
Q

What are the consequences of reduced contractility of the heart, following an MI?

A

Reduced contractility:

  • Causes a relative hypotension as blood does not flow around as effectively
  • This means that coronary vessel perfusion is poor
  • This results in further ischaemia
  • This causes cardiogenic shock (the cycle of ischaemia)
65
Q

What are the consequences of electrical instability following an MI?

A

Electrical instability:

  • Arrhythmias
  • Reentral tachycardias - due to circling of impulses around scar tissue
  • Increased risk of emboli and strokes
66
Q

What are the consequences of tissue necrosis following an MI?

A

Tissue necrosis:

  • Pericardial inflammation
  • Necrosis of papillary muscles, causing valve regurgitation
  • Rupture of necrosed tissue (ventricular septum, ventricular rupture)
  • Cardiac tamponade (ventricular rupture)
  • Hypoxaemia and stress in lung vessels (septal rupture)

Cardiology (4 decks)

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