Cardiac - Chest pain, arrhythmias, palpitations Flashcards
What makes up ‘Acute Coronary Syndrome’?
- STEMI = complete blockage of an artery
- NSTEMI = partial blockage of an artery
- Unstable angina = chest pain at rest due to narrowing of coronary artery
What is the common underlying pathology shared between the 3 ACS conditions?
Plaque rupture
Thrombosis
Inflammation
What do platelets release that cause vasoconstriction?
Thromboxane A2
Serotonin
What are the main risk factors for ACS?
Smoking Hypertension Hyperlipidaemia Diabetes mellitus Obesity Family history of IHD (MI in first degree relative <55 years) Cocaine use
How does ACS present?
Sudden onset of crushing central chest pain/tightness Pain radiates to back, jaw, left arm Acute dyspnoea Nausea and vomiting Sweating Palpitations
How can you distinguish between ACS and stable angina?
ACS is unresponsive to GTN spray
What would the ECG look like in a STEMI?
Tall tented T waves in hyper-acute
ST elevation OR new-onset LBBB (broad QRS complexes)
Inverted T waves if ECG done days later (shows ischaemia)
Q waves remain for months
How do you differentiate between an MI and unstable angina?
Troponin levels
What ECG changes can be seen in an NSTEMI?
ST depression
T wave inversion
(might be normal)
At what hours post-pain onset do troponin levels rise?
The levels increase 3-12 hours from pain onset
They peak at 24-48 hours
Return to baseline 5-14 days
What does ST elevation in leads II, III, aVF indicate?
Inferior MI in the right coronary artery
What does ST depression in leads V1-4 indicate?
Posterior MI in the posterior descending artery
V1-4 are anterior leads so think of it as an upside down ST elevation in the posterior side of the heart
What does ST elevation in leads V7 to V9 indicate?
Posterior MI in the posterior descending artery
What does a new LBBB indicate?
STEMI
What ECG changes would be seen in a blockage of the circumflex coronary artery?
Acute postero-lateral MI
Posterior infarct
- ST depression in V1-4
- Dominant R waves (= upside down Q waves)
Lateral infarct - ST elevation in V6
What does an anterior STEMI result from?
Occlusion of the LAD (left anterior descending artery)
What ECG changes are seen in an anterior STEMI?
ST segment elevation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
What is troponin?
Protein involved in cardiac and skeletal muscle contraction
When myocardial cells are damaged, troponins are released into the blood
Which troponins are most specific to the heart?
Troponins I and T
Aside from MIs what can cause a rise in troponin?
Other causes of myocardial damage:
- Myocarditis
- Pericarditis
- Ventricular strain
Non-cardiac aetiology:
- Masive PE causing right ventricular strain
- Subarachnoid haemorrhage
- Burns
- Sepsis
- Renal failure
What is the acute management of an MI?
MONAC
Morphine 5-10mg (given with metoclopramide)
Oxygen 15L/min
Nitrates - GTN spray
Aspirin/Clopidogrel 300mg loading dose
If STEMI, refer to cardiologist for PCI
Who should a primary PCI be offered to?
All patients presenting within 12 hours of symptom-onset with a STEMI who either are at or can be transferred to a primary PCI centre within 120min of first medical contact
If PCI is unavailable or it has been >12 hours since symptom-onset, what should be done for patients with a STEMI?
Thrombolysis (-plase) Start fondaparinaux (factor 10a inhibitor) or LMWH
What advice should be given to patients post-MI?
Returning to work - 2-3 months
Driving - do not drive for 1 week if successful angioplasty, or 4 weeks if unsuccessful/no angioplasty, notify insurance
Sex - avoid for few weeks, return when able to walk without discomfort
What are the linings of the aorta?
Intima
Media
Adventitia
What happens in an aortic dissection?
Tear in the intima of the aortic lining, which allows blood to enter the aortic wall
A haematoma forms which separates the intima from the adventitia
A false lumen is created which extends in either direction
As the dissection extends it may damage the aortic valve or prevent circulation to the aortic branch vessels, leading to major ischaemic target organ complications
What are the different types of aortic dissection?
Type A (70%) = ascending aorta
Type B (30%) = descending aorta
What causes death in type A/type B aortic dissection?
Type A - death caused by cardiac tamponade due to sudden severe aortic valve incompetence and interrupted flow to coronary arteries
Type B - death caused by malperfusion of visceral organs or lower limbs
What are the main risk factors for aortic dissection?
Hypertension = most common
Smoking
Hypercholesterolaemia
Bicuspid aortic valve
Inherited conditions:
- Marfan’s
- Ehlers-Danlos
How does aortic dissection present?
Sudden onset of sharp/tearing chest pain
Chest (type A) or back (type B)
Syncope in 10%
What signs might be found on examination of aortic dissection?
Aortic regurgitation murmur
Asymmetrical/absent peripheral pulses
Neurological deficit
Type A - hypotension; type B - hypertension
What provides a definitive diagnosis of aortic dissection?
CT angiogram
What changes would be seen on a CXR in aortic dissection?
Widened mediastinum
‘Double knuckle’ aorta
Tracheal deviation to the right
Separation of wall of a calcified aorta
What is the acute management of an aortic dissection?
Oxygen 15L/min NRBM IV access Cross match for 6-10 units of blood IV beta blockers eg. labetalol (calcium-channel blockers in contraindicated) - aim is to keep systolic BP 100-110 IV morphine + metoclopramide
Escalate to cardiology and ICU
What is the surgical management of a Type A aortic dissection?
- Ascending aorta is reconstructed with a vascular graft
- Arch must be repaired if: primary dissection extends to beyond the aortic arch or if arch is aneurysmal
- Aortic root repair if: aorta is dilated or if aortic valve incompetent
- Coronary artery bypass if coronary circulation is impaired
How are Type B aortic dissections managed?
Medically
Aggressive blood pressure control with nitroprusside and/or beta blocker
Surgery considered if:
- Dissection is compromising blood flow
- Aorta is severely dilated or there is risk of rupture
- Hypertension cannot be controlled with medication
What is Beck’s triad of cardiac tamponade?
Falling BP
Rising JVP
Muffled heart sounds
What are some causes of pericarditis?
MI
Viral - coxsackie, EBV, CMV, rubella, mumps, HIV
Bacterial - TB, pneumonia, rheumatic fever
Metabolic - uraemia, hypothyroidism
How does pericarditis present?
Sharp, central retrosternal chest pain that is worse on lying flat and relieved by sitting forwards
Low grade fever
Dysphagia - if there is large pericardial effusion it can push on the oesophagus
What is heard on auscultation in pericarditis?
Pericardial friction rub that obscures both heart sounds
What is Dressler’s syndrome?
Autoimmune pericarditis (with/without effusion) 2-14 weeks after 3% of MIs
What ECG changes are seen in pericarditis?
Concave (saddle-shaped) ST segment elevation present in all chest leads
PR depression = atrial inflammation
How do you treat pericarditis?
NSAIDs + PPI for 1-2 weeks
Cochicine 500mcg BD for 3 months to reduce risk of recurrence
Definitive treatment depends on cause
What must urgently be done in cardiac tamponade?
Pericardiocentesis - needle drainage under US guidance
What ECG changes are seen in AF?
Absent P waves
Irregularly irregular narrow QRS complexes
What blood tests are appropriate to do in AF?
U&Es (K+)
Cardiac enzymes
TFTs
FBC
What is seen on an ECG in atrial flutter?
Sawtooth pattern
How do you manage acute AF in a patient that is haemodynamically unstable?
If there are signs of shock, syncope, acute heart failure, ischaemia, etc:
Electrical DC cardioversion under sedation
If that is unsuccessful:
IV flecainide 50-150mg or IV amiodarone 300mg then 900mg over 24h
How do you manage AF that started > 48hours a go in a patient that is haemodynamically stable?
Rate control with: IV metoprolol 5mg or a rate-limiting calcium channel blocker (diltiazem/verapamil)
Start LMWH for 3 weeks before rhythm control
What defines a narrow complex tachycardia?
ECG shows a rate >100bpm and QRS complex duration <120ms (3 small squares)
How do you manage a supraventricular tachycardia if the patient is haemodynamically stable?
Vagal manoeuvres:
- Carotid sinus massage for 15 sec
- Valsalva manoeuvre - when patient is supine get them to blow plunger out of syringe
IV adenosine:
- IV adenosine 6mg + saline flush
- If unsuccessful repeat with 12mg then 12mg
What side effects do you need to warn the patient about with adenosine?
Transient chest tightness
Dyspnoea
Headache
Flushing
When is adenosine contraindicated?
Asthma
2nd/3rd degree heart block
Sinoatrial disease e.g. Wolff-Parkinson-White syndrome
What is ventricular tachycardia?
Broad complex tachycardia originating from a ventricular ectopic focus
What drug overdose can cause broad-complex tachycardias?
Tricyclic antidepressant overdose
What electrolyte abnormalities can cause VT?
Low K+
Low Mg2+
Low Ca2+
What is Torsades de Pointes?
A rare form of VT
Associated with hypokalaemia and hypomagnesaemia
Associated with long QT syndrome
How do you treat Torsades to Pointes?
IV magnesium sulphate 2g over 10 minutes
What is the treatment of VT for a haemodynamically unstable patient?
Electrical DC cardioversion under sedation
If that is unsuccessful:
IV flecainide 50-150mg or IV amiodarone 300mg then 900mg over 24h
What is the treatment of VT for a haemodynamically stable patient?
IV amiodarone 300mg over 1hr then 900mg over 23h
What is the most commonly identified arrhythmia in cardiac arrest patients?
Ventricular fibrillation
What conditions is VF most commonly associated with?
Coronary artery disease e.g. acute MI, IHD
What ECG changes are seen in VF?
Rate up to 500bpm
No P, QRS or T waves
How do you manage VF?
Call crash team
Airway
- Head-tilt chin-lift
- Insert airway adjunct
- Insert LMA
Breathing
- Bag valve mask ventilation
Circulation (use ALS algorithm)
- Start CPR 30:2 whilst attaching defibrillator
- Defibrillate - 1 shock
- Immediately resume to CPR for 2 min
- Reassess rhythm
What are the reversible causes of cardiac arrest?
4 Hs:
- Hypoxia
- Hypovolaemia
- Hypothermia
- Hyper/hypokalaemia
4 Ts:
- Tension pneumothorax
- Tamponade (cardiac)
- Toxins
- Thromboembolism
Which arrhythmias are shockable and non-shockable?
Shockable:
- Ventricular fibrillation
- Pulseless ventricular tachycardia
Non-shockable:
- Asystole
- PEA (pulseless electrical activity)
