Causes of Chest Pain Flashcards
1
Q
A
C - left anterior descending artery
2
Q
A
A - aspirin and clopidogrel
this is a typical presentation of a silent heart attack in a diabetic
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
17
Q
What investigations are performed in ACS?
A
- ECG
-
troponin
- elevated troponin suggests myocardial injury - STEMI or NSTEMI
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)*
19
Q
A
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
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
22
Q
What ECG changes are present in an NSTEMI / unstable angina?
A
- ST depression
- T wave inversion
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
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
25
What medications are given immediately to someone presenting with a STEMI?
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)*
26
What medications are given for the long-term management of someone who has had a STEMI?
* **_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
27
What type of occlusion is present in NSTEMI?
How is it managed differently to STEMI?
* 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_**
28
What score is used to determine the risk of someone who has just had an NSTEMI having another CVS event?
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)
29
What mnemonic is used to remember the management of NSTEMI and STEMI?
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
30
What mnemonic can be used to remember the complications of STEMI / NSTEMI?
**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
31
D -Dressler's syndrome
* this is a presentation of **pericarditis** that is occurring **2 - 10 weeks following an MI**
32
D - aspirin + colchicine + NSAIDs
* this is the management for anyone with pericarditis
* aspirin is given as she has a history of MI / heart failure
33
What is the definition of pericarditis?
What can cause this?
* **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**
34
What is Dressler's syndrome?
* 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
35
What are the risk factors for pericarditis?
* male gender
* 20 - 50 years old
* transmural MI
* cardiac surgery
* neoplasm
* uraemia / dialysis
36
What type of pericarditis can occur in heart failure?
What is the result of this on cardiac output?
* **_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_**
37
What are the signs and symptoms associated with pericarditis?
* **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
What is meant by pleuritic chest pain?
* pain that **varies with breathing movements** and is **_worse on inspiration_**
* it is described as **stabbing, knife-like** or **catching**
39
Where is pericardial friction rub best heard?
What does this sound like?
* heard best on the **_lower left sternal edge_**
* it is a **scratching sound** that sounds like 2 pieces of paper rubbing together
40
What is tamponade?
* 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
What triad is present on examination if tamponade is present?
**_Beck's triad_**
* low arterial blood pressure
* muffled heart sounds
* distended neck veins
42
What investigations are performed in pericarditis?
* bloods
* to ensure all electrolytes are balanced
* CXR to check for **pericardial effusion**
* ECG
43
What is a pericardial effusion?
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
What ECG changes are associated with pericarditis?
***widespread saddle shaped ST elevation***
* the ST elevation looks like a "u" shape
45
What is involved in the management of pericarditis?
What if tamponade or uraemic pericarditis is present?
**_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
What are the possible complications of pericarditis?
* pericardial effusion +/- tamponade
* chronic constrictive pericarditis
47
Why are NSAIDs and PPIs given to treat pericarditis?
* 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
In what type of patients does uraemic pericarditis normally occur?
* 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
What is the definition of syncope?
a sudden, temporary, self-terminating loss of consciousness
50
What are the 4 different categories that cause syncope?
What are examples?
***_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
What are the 5 steps involved in differentiating the types of syncope?
* 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
What are the 4 different investigations that are performed to identify what type of syncope is present?
***_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
What are the typical symptoms of seizure that need to be ruled out?
* 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
What is meant by tonic clonic movements and automatisms?
***_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
How long does LOC typically last for during syncope?
* 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
Once established that LOC was not a seizure, then what red flags need to be ruled out?
* 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
How is orthostatic hypotension diagnosed?
* if there is more than a 20 mmHg difference between sitting and standing BP
58
What is the defintion of vasovagal syncope?
What can cause this?
* 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
What are the risk factors associated with vasovagal syncope?
* prior syncope
* emotional stress
* prolonged standing
* heat
* excessive dehydration
60
What are the signs and symptoms of vasovagal syncope?
* nausea
* pallor
* light-headedness
* diminished vision / hearing
* physical injury (pain can lead to LOC)
61
What is involved in the investigations and management of vasovagal syncope?
***_Investigations:_***
* ECG
* bloods (glucose, cortisol, U&Es, FBC, hCG)
***_Management:_***
* patient education on triggers with physical **counter-pressure manoeuvres**
62
What are some of the counter-pressure manoeuvres that are recommended in vasovagal syncope?
* 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
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
What is the definition of atrial fibrillation?
* 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
What are the potential causes of AF?
* idiopathic
* coronary artery disease
* thyroid disorders
* COPD
* electrolyte disturbances
* pneumonia
66
What is the difference between paroxysmal and persistent AF?
* paroxysmal AF terminates within 7 days, either with or without treatment
* persistent AF terminates after 7 days
67
What are the signs and symptoms of AF?
* palpitations
* irregularly irregular pulse rate
* shortness of breath
* chest pain
68
What investigations are performed in AF?
* **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
70
What are the potential complications of AF?
***_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
What must you first establish before deciding how to treat a patient presenting with AF?
* 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
If the AF patient is haemodynamically stable and it has been \< 48 hours then how should they be treated?
* **_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
If the AF patient is haemodynamically stable but it has been \> 48 hours then how should they be treated?
***_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
What is the definition of atrial flutter?
What causes it?
* 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
What does atrial flutter look like on ECG?
saw tooth pattern with loss of isoelectric baseline and p waves
76
What advice is given to patients to stop the symptoms of atrial flutter?
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
What is the definition of heart block?
* a cardiac electrical disorder characterised as **_impaired conduction_** from the **_AV node_**
78
79
What are the causes of heart block?
* **MI / IHD**
* infection - **rheumatic fever**
* drugs - **beta-blockers, CCBs, amiodarone**
* metabolic - **high K+, low T4**
* **sarcoidosis**
80
What are the signs and symptoms of the different types of heart block?
* 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
How can first degree heart block be identified from ECG?
there is a **_prolonged PR interval_** that is **\> 0.2 seconds**
82
How can second degree heart block (type I) be identified on ECG?
* there are **progressive prolonged PR intervals** until a **_QRS complex is dropped_**
* this is also called Wenkebach
83
How can second degree heart block type II be identified on ECG?
* there is **_intermittent loss of a QRS wave_** that might be in a regular pattern (2:1 etc)
84
What does third degree (complete) heart block look like on ECG?
* there is no association between P and QRS waves
85
What investigations are performed for heart block?
* ECG
* troponin
* K+, Ca2+ and pH
* digitalis toxicity
* echo
86
What is involved in the acute and chronic management of heart block?
***_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
What are the potential complications associated with heart block?
* asystole
* heart failure
* cardiac arrest
88
What is the defintion of supraventricular tachycardia?
* 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
What are the signs and symptoms of a supraventricular tachycardia?
* palpitations
* syncope
* shortness of breath
* chest pain
90
What are the 2 different types of SVT?
***_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
What is involved in the management of an SVT once it has been identified on ECG?
* **_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
