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Core Conditions - Cardiovascular > Causes of Chest Pain > Flashcards

Causes of Chest Pain Flashcards

1
Q
A

C - left anterior descending artery

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2
Q
A

A - aspirin and clopidogrel

this is a typical presentation of a silent heart attack in a diabetic

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3
Q

What is the definition of ischaemic heart disease?

A
  • decreased blood supply to the myocardium which results in chest pain (angina pectoris)
  • it is primarily due to atherosclerosis of the coronary arteries
  • this results in a mismatch between the oxygen supply to the heart and oxygen demand
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4
Q

What are the different types of ischaemic heart disease?

A
  • IHD is an umbrella term
  • it can be divided into atherosclerotic and vasospastic causes
  • atherosclerotic causes can be further divided into stable angina and ACS
  • ACS is an umbrella term that covers:
    • unstable angina
    • non ST-elevation MI
    • ST-elevation MI
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5
Q

What is Prinzmetal angina?

A
  • a condition characterised by angina-type chest pain at rest
  • it occurs due to abnormal coronary artery spasm
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6
Q

What are the risk factors for ischaemic heart disease?

A
  • hypertension
  • diabetes
  • smoking
  • family history of IHD
  • hyperlipidaemia and hypercholesterolaemia
    • this can be due to diet or familial hypercholesterolaemia
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7
Q

What are some signs of hyperlipidaemia that may be picked up on examination?

A
  • xanthelasma
    • this describes yellow coloured deposits of cholesterol around the eyes
  • xanthomata
    • this describes yellow cholesterol-rich deposits that can appear anywhere in the body
  • corneal arcus
    • a cholesterol-rich deposit that forms a ring within the cornea
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8
Q

What is the definition of stable angina?

A
  • chest pain brought on during exertion and relieved by rest
  • the pain occurs due to myocardial ischaemia, most commonly due to atherosclerotic plaques reducing blood flow to the heart
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9
Q

What signs might be seen on examination of someone with stable angina?

What investigations should be performed?

A
  • examination is normal in chronic stable angina
    • unless there is an underlying heart condition (e.g. HF)
  • bloods should be performed:
    • ​FBC
    • lipids - to check for hyperlipidaemia
    • glucose - to check for diabetes
  • ECG should be performed to make sure more sinister causes aren’t missed (e.g. silent MI)
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10
Q

What is involved in the conservative managment of stable angina?

A
  • management aims to reduce risk factors
  • weight loss
  • improving diet
  • smoking cessation
  • if conservative measures are ineffective, then medical management is considered
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11
Q

What is involved in the medical management of stable angina?

A
  • ACE inhibitors
  • antiplatelets - usually aspirin
  • statins
  • anti-anginals
    • beta-blocker or calcium channel blocker
  • GTN spray
    • ​this should be used when anginal pain is felt to relieve it
    • if the pain is not relieved by GTN, patient needs to go to hospital as they could be having an MI
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12
Q

Why does anginal pain actually occur in stable angina?

A
  • there is increased oxygen demand by the body (and heart) during exercise
  • vessels containing stable atherosclerotic plaques are unable to dilate enough to allow adequate blood flow to meet the myocardial demand
  • this leads to myocardial ischaemia (lack of oxygen), which causes the pain
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13
Q

What is the definition of acute coronary syndrome?

A
  • a range of conditions due to a sudden reduction in blood flow to the heart
  • this is usually due to atherosclerotic plaques within the coronary arteries
  • these plaques may cause complete or substantial occlusion of the artery
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14
Q

What investigations can be performed to identify which type of ACS is present?

A
  • first an ECG is performed to look for any visible changes
    • if there is ST elevation - it is a STEMI
  • if there are no ECG changes then look at troponin
    • troponin is released when myocardial cells infarct
  • in an NSTEMI there is cell infarction so troponin is raised
    • ​it would also be raised in STEMI
  • there is no infarction in unstable angina, so troponin is not raised
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15
Q

What is unstable angina?

A
  • chest pain at rest due to ischaemia but without cardiac injury
  • it occurs when an atherosclerotic plaque ruptures and a thrombus forms around the ruptured plaque
  • this causes partial occlusion of the coronary artery, which leads to angina-type pain
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16
Q

What are the signs and symptoms associated with ACS?

Which groups do special attention need to be paid to?

A
  • acute central chest pain that is gripping / heavy
    • pain may radiate to the neck, arm and/or jaw
  • sweating
  • pallor
    • ​reduced CO might lead to patient becoming hypotensive
  • +/- shortness of breath
  • can be silent in the elderly and diabetics
    • ​often there is no central chest pain
    • they may be nauseous or have a different type of pain
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17
Q

What investigations are performed in ACS?

A
  • ECG
  • troponin
    • elevated troponin suggests myocardial injury - STEMI or NSTEMI
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18
Q

What ECG changes can be seen in ACS?

A
  • ST segment elevation
  • ST segment depression
  • T wave inversion
  • (look at the difference between the baseline and where the ST segment starts to see if there is elevation / depression)*
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19
Q
A
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20
Q

What ECG changes are seen in a STEMI?

A
  • hyperacute T waves
  • ST elevation
  • new LBBB
  • there may also be T wave inversion
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21
Q

What is shown in these images?

A

they all show ST elevation

there are many different forms of ST elevation

the ST segment must just be raised from the baseline

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22
Q

What ECG changes are present in an NSTEMI / unstable angina?

A
  • ST depression
  • T wave inversion
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23
Q

What ECG change is associated with an old infarct?

A

pathological Q waves

these indicate that the patient has had some form of myocardial ischaemia in the past

the Q wave appears deeper

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24
Q

How much of the artery is occluded in a STEMI?

What are the different treatments available depending on the time since symptom onset?

A
  • in a STEMI, there is complete occlusion of a coronary artery
  • if < 12 hr since symptom onset AND PCI available in 120 mins then PCI is performed
    • this involves placing a stent or balloon into the artery to open it up
  • if < 12 hr since symptom onset and PCI NOT available in 120 mins then thrombolysis is performed
    • this aims to dissolve the clots and open up the arteries
  • if > 12 hr since symptom onset, there are too many risks with invasive procedures

angiography is performed, then possibly followed by PCI

  • this involves inserting a needle in the femoral / radial artery and a catheter into the heart to visualise the perfusion of the heart
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25
Q

What medications are given immediately to someone presenting with a STEMI?

A

remember MONAC - these drugs are all given immediately:

  • M - morphine
  • O - oxygen (if sats < 90%)
  • N - nitrates
  • A - aspirin
  • C - clopidogrel
  • (aspirin & clopidogrel oral tablets - 300mg of each*
  • then obtain IV access to give 2.5mg diamorphine*
  • nitrates are not always given - they help with the pain and open up the arteries to prevent further damage)*
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26
Q

What medications are given for the long-term management of someone who has had a STEMI?

A
  • beta-blocker
    • do not give in acute heart failure
  • ACE-inhibitor
    • this will help with BP and should be given within 24 hours of presentation
  • statin
    • this will reduce the cholesterol
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27
Q

What type of occlusion is present in NSTEMI?

How is it managed differently to STEMI?

A
  • in an NSTEMI there is a near complete occlusion of a coronary artery
  • management is the SAME as the STEMI drugs but with LMWH
  • this is usually in the form of fondaparinux or enoxaparin
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28
Q

What score is used to determine the risk of someone who has just had an NSTEMI having another CVS event?

A

the GRACE score is used

  • low risk patients have outpatient angiography
  • moderate / high risk patients have inpatient angiography with possible PCI
    • also given GpIIb/IIa inhibitors (abciximab)
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29
Q

What mnemonic is used to remember the management of NSTEMI and STEMI?

A

MONAC BAS

  • M - morphine
  • O - oxygen
  • N - nitrates
  • A - aspirin
  • C - clopidogrel
  • B - beta blocker
  • A - ACE inhibitor
  • S - statin
  • MONAC are given immediately at presentation
  • BAS are part of long term management
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30
Q

What mnemonic can be used to remember the complications of STEMI / NSTEMI?

A

DARTH VADER

  • D - death
  • A - arrhythmia
  • R - rupture
  • T - tamponade
  • H - heart failure
  • V - valve disease
  • A - aneurysm
  • D - Dressler’s syndrome
  • E - embolism
  • R - reinfarction
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31
Q
A

D -Dressler’s syndrome

  • this is a presentation of pericarditis that is occurring 2 - 10 weeks following an MI
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32
Q
A

D - aspirin + colchicine + NSAIDs

  • this is the management for anyone with pericarditis
  • aspirin is given as she has a history of MI / heart failure
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33
Q

What is the definition of pericarditis?

What can cause this?

A
  • inflammation of the pericardium

Causes:

  • idiopathic
  • viral - Coxsackie A9, mumps, EBV
  • bacterial - pneumococcus, staph, strep
  • connective tissue disorders - sarcoidosis
  • system autoimmune disorders - SLE, rheumatoid arthritis
  • Dressler syndrome (2 - 10 weeks post-MI)
  • malignancy
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34
Q

What is Dressler’s syndrome?

A
  • this is a form of pericarditis that occurs 2 to 10 weeks following an MI
  • it is thought to be antibody-related after damage to the pericardium
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35
Q

What are the risk factors for pericarditis?

A
  • male gender
  • 20 - 50 years old
  • transmural MI
  • cardiac surgery
  • neoplasm
  • uraemia / dialysis
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36
Q

What type of pericarditis can occur in heart failure?

What is the result of this on cardiac output?

A
  • constrictive pericarditis can occur
  • the pericardium becomes thicker as part of a chronic process
  • a thicker pericardium does not allow for as much movement of the heart, so both ventricular filling and CO are reduced
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37
Q

What are the signs and symptoms associated with pericarditis?

A
  • sharp, stabbing pleuritic chest pain that is relieved on sitting forwards
    • this may radiate to the trapezius ridge
  • corysal symptoms if it is of viral origin
    • ​e.g. runny nose, viral / flu-like symptoms
  • pericardial friction rub on examination
  • tamponade
    • ​Beck’s triad is present on examination if this is present
38
Q

What is meant by pleuritic chest pain?

A
  • pain that varies with breathing movements and is worse on inspiration
  • it is described as stabbing, knife-like or catching
39
Q

Where is pericardial friction rub best heard?

What does this sound like?

A
  • heard best on the lower left sternal edge
  • it is a scratching sound that sounds like 2 pieces of paper rubbing together
40
Q

What is tamponade?

A
  • this occurs when the pericardial sac is filled with blood
  • this is life-threatening as the blood filling the pericardium compresses the heart, meaning it cannot beat properly
  • there is not enough blood being ejected to the body / brain
41
Q

What triad is present on examination if tamponade is present?

A

Beck’s triad

  • low arterial blood pressure
  • muffled heart sounds
  • distended neck veins
42
Q

What investigations are performed in pericarditis?

A
  • bloods
    • to ensure all electrolytes are balanced
  • CXR to check for pericardial effusion
  • ECG
43
Q

What is a pericardial effusion?

A

this occurs when there is fluid in the pericardium

there is not as much fluid present in the pericardium as there would be in tamponade

44
Q

What ECG changes are associated with pericarditis?

A

widespread saddle shaped ST elevation

  • the ST elevation looks like a “u” shape
45
Q

What is involved in the management of pericarditis?

What if tamponade or uraemic pericarditis is present?

A

NSAID + PPI + colchicine

  • exercise restriction is recommended (if viral)
  • if tamponade is present or it is purulent, pericardiocentesis is performed in addition and antibiotics are given
  • in uraemic pericarditis, dialysis is given
46
Q

What are the possible complications of pericarditis?

A
  • pericardial effusion +/- tamponade
  • chronic constrictive pericarditis
47
Q

Why are NSAIDs and PPIs given to treat pericarditis?

A
  • NSAIDs are given to relieve the pain
  • PPI is given to protect against NSAID related stomach ulcers
  • colchicine is a treatment for acute gout that has been shown to prevent recurrence of pericarditis
48
Q

In what type of patients does uraemic pericarditis normally occur?

A
  • there is a build up of uric acid in the body
  • this usually occurs in patients with chronic kidney disease
  • it is treated with dialysis
49
Q

What is the definition of syncope?

A

a sudden, temporary, self-terminating loss of consciousness

50
Q

What are the 4 different categories that cause syncope?

What are examples?

A

Arrhythmia-related:

  • due to CO compromise from arrhythmia
    • e.g. ventricular tachycardia, heart block

Cardiac:

  • structural heart disease - most notably LV outflow obstruction
    • ​e.g. HOCM, severe AS, PE, aortic dissection

Orthostatic:

  • failure to maintain BP when standing

Reflex:

  • reflex vasodilation / bradycardia due to a trigger
    • ​vasovagal or carotid sinus syncope
51
Q

What are the 5 steps involved in differentiating the types of syncope?

A
  • establish there was a definite loss of consciousness with no/few features of seizure
  • determine if there were any cardiac red flag symptoms
  • carry out investigations
  • if there are negative investigations with typical precipitant/prodrome in history - this is vasovagal syncope
  • if diagnosis is uncertain then risk stratify
52
Q

What are the 4 different investigations that are performed to identify what type of syncope is present?

A

ECG:

  • if arrhythmia is identified, then this is arrhythmic syncope

Imaging - if suspicion of PE / aortic dissection:

  • performed to confirm diagnosis

Echo:

  • this can confirm cardiac structural abnormalities that cause cardiac syncope

Sitting / standing BP:

  • used to identify orthostatic syncope
53
Q

What are the typical symptoms of seizure that need to be ruled out?

A
  • typically there is an aura beforehand
    • patient describes seeing / smelling something strange before passing out
  • then a witness account of:
    • tonic-clonic movement
    • automatisms
    • bitten tongue
    • confusion post-LOC
    • drowsy
54
Q

What is meant by tonic clonic movements and automatisms?

A

Tonic clonic:

  • during the “tonic” phase, the person loses consciousness, their body goes stiff and they fall to the floor
  • during the “clonic” phase, the limbs jerk about, the patient bites their tongue / cheek and may have trouble breathing
    • there may also be loss of control of the bladder / bowel

Automatisms:

  • absent seizures where people start fiddling with their hair, absent-mindedly moving their fingers etc. and don’t realise what they are doing
55
Q

How long does LOC typically last for during syncope?

A
  • LOC should be transient and typically lasts around 30 seconds
  • if it lasts for more than 5 minutes, think that this could be a seizure
56
Q

Once established that LOC was not a seizure, then what red flags need to be ruled out?

A
  • need to determine whether there are any cardiac red flag symptoms
  • LOC during exertion
    • this is typical of aortic stenosis
  • severe valvular disease
  • previous arrhythmia
  • concerning ECG features
    • e.g. features that suggest LVH
57
Q

How is orthostatic hypotension diagnosed?

A
  • if there is more than a 20 mmHg difference between sitting and standing BP
58
Q

What is the defintion of vasovagal syncope?

What can cause this?

A
  • it is a sudden, temporary, self-terminating loss of consciousness often triggered by an emotional upset
  • caused by a temporary reduction in cerebral flow as a response to a stressful trigger
    • increase in the vagal nerve discharge causes low BP and HR
    • this results in reduction of CO
59
Q

What are the risk factors associated with vasovagal syncope?

A
  • prior syncope
  • emotional stress
  • prolonged standing
  • heat
  • excessive dehydration
60
Q

What are the signs and symptoms of vasovagal syncope?

A
  • nausea
  • pallor
  • light-headedness
  • diminished vision / hearing
  • physical injury (pain can lead to LOC)
61
Q

What is involved in the investigations and management of vasovagal syncope?

A

Investigations:

  • ECG
  • bloods (glucose, cortisol, U&Es, FBC, hCG)

Management:

  • patient education on triggers with physical counter-pressure manoeuvres
62
Q

What are some of the counter-pressure manoeuvres that are recommended in vasovagal syncope?

A
  • leg crossing + buttock and thigh muscle tensing
    • this is a skeletal muscle pump that squeezes veins to try and push blood back up
  • isometric forearm grip
  • squatting
    • ​getting lower to the ground means it is less effort for the heart to pump blood around the body
63
Q
A

D - reflexive vasodilation

  • this is due to vasovagal syncope
  • the trigger is having blood taken, which leads to a drop in HR and BP
64
Q

What is the definition of atrial fibrillation?

A
  • a form of supraventricular tachycardia with uncoordinated atrial electrical activation causing ineffective atrial contraction
  • the atria are not contracting together in a coordinated way
  • this means that reduced amounts of blood are entering the ventricles
65
Q

What are the potential causes of AF?

A
  • idiopathic
  • coronary artery disease
  • thyroid disorders
  • COPD
  • electrolyte disturbances
  • pneumonia
66
Q

What is the difference between paroxysmal and persistent AF?

A
  • paroxysmal AF terminates within 7 days, either with or without treatment
  • persistent AF terminates after 7 days
67
Q

What are the signs and symptoms of AF?

A
  • palpitations
  • irregularly irregular pulse rate
  • shortness of breath
  • chest pain
68
Q

What investigations are performed in AF?

A
  • ECG
  • bloods - FBC, clotting, U&Es, TSH
    • to ensure there is no underlying thyroid condition or electrolyte disturbances
  • CXR
    • ​to check the size of the heart and ensure there is no HF occurring
  • TEE (Echo) pre-cardiovert
    • ​do this before cardioverting the patient to check the structural integrity of the heart
69
Q
A
70
Q

What are the potential complications of AF?

A

Thromboembolism:

  • uncoordinated atrial contractions means that blood stays in the atria longer than it should
  • the chances of clotting increases when blood is static
  • if a thrombus forms in the atria, it can get pumped into the ventricles and around the body

Worsened heart failure

71
Q

What must you first establish before deciding how to treat a patient presenting with AF?

A
  • need to determine whether they are haemodynamically stable
    • i.e. BP is > 90/60 and there are no other signs of shock
  • if they are NOT stable, then DC cardioversion is performed
    • ​this prevents them from entering cardiogenic shock, which is life threatening
72
Q

If the AF patient is haemodynamically stable and it has been < 48 hours then how should they be treated?

A
  • rhythm control is performed to try and get the patient back into sinus rhythm
    • the chance of a clot forming within 48 hours is very small
  • this can be performed through DC cardioversion
  • or through chemical cardioversion with flecanide or amiodarone
    • ​flecanide is contraindicated in IHD
  • if this fails, then rate control is performed
73
Q

If the AF patient is haemodynamically stable but it has been > 48 hours then how should they be treated?

A

Anticoagulation:

  • this involves LMWH (fondaparinux) + warfarin loading
    • the chance of a clot happening > 48 hours is much higher
  • they are then DC cardioverted 4-6 weeks later and given a rate control drug in the meantime

Rate control:

  • bisoprolol
  • verapamil
  • diltiazem
  • digoxin
74
Q

What is the definition of atrial flutter?

What causes it?

A
  • large re-entry circuit in right atrium causes a saw-tooth pattern due to ineffective atrial contraction
  • it is caused by underlying heart conditions
  • it has very similar signs/symptoms, investigations and management to AF
75
Q

What does atrial flutter look like on ECG?

A

saw tooth pattern with loss of isoelectric baseline and p waves

76
Q

What advice is given to patients to stop the symptoms of atrial flutter?

A

to stop palpitations, take a massive deep breath in and hold it

this causes compression on the heart which can help it get back into a normal rhythm

77
Q

What is the definition of heart block?

A
  • a cardiac electrical disorder characterised as impaired conduction from the AV node
78
Q
A
79
Q

What are the causes of heart block?

A
  • MI / IHD
  • infection - rheumatic fever
  • drugs - beta-blockers, CCBs, amiodarone
  • metabolic - high K+, low T4
  • sarcoidosis
80
Q

What are the signs and symptoms of the different types of heart block?

A
  • first degree heart block is asymptomatic
  • second degree type I is asymptomatic
  • second degree type II or third degree presents with dizziness, palpitations, chest pain & heart failure
81
Q

How can first degree heart block be identified from ECG?

A

there is a prolonged PR interval that is > 0.2 seconds

82
Q

How can second degree heart block (type I) be identified on ECG?

A
  • there are progressive prolonged PR intervals until a QRS complex is dropped
  • this is also called Wenkebach
83
Q

How can second degree heart block type II be identified on ECG?

A
  • there is intermittent loss of a QRS wave that might be in a regular pattern (2:1 etc)
84
Q

What does third degree (complete) heart block look like on ECG?

A
  • there is no association between P and QRS waves
85
Q

What investigations are performed for heart block?

A
  • ECG
  • troponin
  • K+, Ca2+ and pH
  • digitalis toxicity
  • echo
86
Q

What is involved in the acute and chronic management of heart block?

A

Chronic:

  • permanent pacemaker for Mobitz II or 3rd degree

Acute - occurring 2o to MI:

  • IV atropine and temporary external pacing
  • these patients often become bradycardic so need to raise the heart rate with atropine and then pace this rhythm
87
Q

What are the potential complications associated with heart block?

A
  • asystole
  • heart failure
  • cardiac arrest
88
Q

What is the defintion of supraventricular tachycardia?

A
  • a dysarrhytmia originating at or above the AVN with a regular, narrow complex tachycardia (QRS < 120 mm) at >100 bpm with no p waves
89
Q

What are the signs and symptoms of a supraventricular tachycardia?

A
  • palpitations
  • syncope
  • shortness of breath
  • chest pain
90
Q

What are the 2 different types of SVT?

A

Atrioventricular re-entry tachycardia (AVRT):

  • accessory pathway exists from the ventricles back up to the atria

Atrioventricular nodal re-entry tachycardia (AVNRT):

  • accessory pathway exists from the AV node to the atria
    • this is the Bundle of Kent in WPW
91
Q

What is involved in the management of an SVT once it has been identified on ECG?

A
  • vasovagal manoeuvres (Valsalva)
    • these stimulate the vagal nerve to decrease the HR
  • if this does not work then give 6mg adenosine IV
    • verapamil 2.5-5mg used in asthma
    • ​repeat this step if ineffective
  • if still ineffective, then give 12mg adenosine IV
  • if still ineffective then give IV amiodarone and refer to specialist

Core Conditions - Cardiovascular (6 decks)

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