Cardiovascular 1 - cardiac emergencies Flashcards
What makes up ‘Acute Coronary Syndrome’? Describe the difference in their pathophysiology.
Unstable angina
- Partial occlusion of coronary vessel -> decreased blood supply -> ischaemic symptoms
NSTEMI
- Partial occlusion of a coronary artery
- Affects the inner layer of the heart (subendocardial infarction)
STEMI
- Complete occlusion of a coronary artery
- Affects full thickness of the myocardium (transmural infarction)
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 an MI typically 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 features are seen on an ECG of a STEMI?
- Tall tented T waves in hyper-acute
- ST elevation OR new-onset LBBB (broad QRS complexes)
- ST elevation must be seen in two contiguous leads with reciprocal ST depressions
- 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 so always compare to previous ECGs)
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 is a LBBB and what does a new LBBB on an ECG indicate? What are the ECG signs of a LBBB?
Indicates a STEMI
LBBB = Cardiac conduction alteration in which there is delay or obstruction of impulses sent through the left bundle branch pathway, leading to delayed left ventricle contraction
ECG signs include:
- QRS duration ≥ 120 ms
- a rS or QS complex in lead V1
- a notched (M-shaped) R wave in V6
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:
- Massive PE causing right ventricular strain
- Subarachnoid haemorrhage
- Burns
- Sepsis
- Renal failure
What is the pharmacological management of an MI?
MONAT
Morphine 5-10mg (given with metoclopramide)
Oxygen 15L/min
Nitrates - GTN spray 2 sprays
Aspirin 300mg PO - then taken 75mg OD lifelong
Ticagrelor 180mg PO - then taken 90mg BD for 12 months
LMWH for NSTEMI or STEMI that is not candidate for primary 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 + arch of 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 Cocaine/amphetamine use Inherited conditions: - Marfan's - Ehlers-Danlos
How does aortic dissection present?
Sudden onset of sharp/tearing chest pain
- Chest (type A)
- Back between scapulas (type B)
Depending on how far the dissection extends:
- Syncope in 10%
- Bowel/limb ischaemia
- Renal failure
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 may 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 initial 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 Cardiac monitoring
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 labetolol
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
Rheumatic disease - SLE, RA, sarcoidosis
Metabolic - uraemia due to renal failure, 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 defines a narrow complex tachycardia? What tachycardias are classed as narrow complex?
ECG shows a rate >100bpm and QRS complex duration <120ms (3 small squares)
Examples:
- SVT
- AF
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 lying down get them to blow the 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 causes a broad complex tachycardia?
Ventricular tachycardia
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? What is it associated with?
A rare form of VT
Associated with hypokalaemia and hypomagnesaemia
Associated with long QT syndrome
How do you treat Torsades de Pointes?
IV magnesium sulphate 2g over 10 minutes
What is the treatment of VT for a haemodynamically stable patient?
Amiodarone 300mg IV over 20-60 min
Then amiodarone 900mg IV over 24 hours
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)
What can be given in a cardiac arrest whilst CPR is being done and when is it given?
- Give adrenaline 1:10,000 1ml every 3-5minutes
- Give amiodarone after 3 shocks
Who is most likely to suffer a silent MI?
Diabetics - polyneuropathy
What is seen on an ECG in first degree heart block?
PR interval > 200ms (this indicates prolonged conduction of electrical activity through the AV node)
Does first degree heart block require management?
No, it is benign and does not need treating
What is seen on an ECG in Mobitz Type 1 heart block?
Progressive lengthening of the PR interval, which results in a P wave that fails to conduct a QRS
What can cause heart block?
Myocardial infarction - especially inferior or anterior
Drugs: calcium-channel blockers, beta-blockers, digoxin, amiodarone
High vagal tone e.g. in athletes
Cardiac surgery
Inflammatory conditions - Myocarditis, SLE, rheumatic heart disease
What is seen on an ECG in Mobitz Type 2 heart block?
There are intermittent non-conducted P waves caused by a conduction system failure, especially at the His-Purkinje system
PR interval remains constant
How does complete heart block present?
Syncope
What is seen on an ECG in complete heart block?
Severe bradycardia
Dissociation between the P waves and the QRS complexes
What is the definitive management for both Mobitz Type II and complete heart block?
Permanent pacemaker
What are the different classifications of AF?
- Acute - <48 hours
- Paroxysmal - < 7 days and is intermittent
- Persistent - >7 days but is amenable to cardioversion
- Permanent - >7 days and is not amenable to cardioversion
What constitutes fast AF?
HR > 100bpm
What are some non-cardiac causes of AF?
- Dehydration
- Endocrine causes - hyperthyrodism
- Infective causes - sepsis
- Pulmonary causes - pneumonia, PE
- Environmental toxins - alcohol abuse
- Electrolyte disturbances - hypokalaemia, hypomagnesaemia
What are signs that a patient with a tachycardia is unstable?
Shock - end organ hypoperfusion
Syncope - brain hypoperfusion
Chest pain - myocardial ischaemia
Pulmonary oedema - heart failure
(2 S, 2H - shock, syncope, heart attack, heart failure)
What is the management of an unstable patient with tachycardia?
Synchronised DC shock (with sedation if conscious) for up to 3 attempts
If that fails, seek expert help and:
- Amiodarone 300mg IV over 10-20 min
- Repeat shock
- Then amiodarone 900mg over 24 hours
What is the rate/rhythm treatment for AF if no reversible causes are found?
Rate control
- Beta-blocker - bisoprolol
- Non-dihydropyridine calcium-channel blocker - diltiazem or verapamil
- Digoxin – especially for patients who are hypotensive or have co-existent heart failure; avoid in young patients as in increases cardiac mortality
Rhythm control
- Only used in young patients or those with disabling symptoms
- Flecainide - Na+ channel blocker
- Amiodarone (only given to older, sedentary patients)
- Sotalol - beta-blocker with additional K+ channel blocker action
What must be considered before starting a patient on anticoagulation?
Thromboembolic risk
Bleeding risk
How do you calculate thromboembolic risk?
CHADS2VASc2 Score • Congestive cardiac failure - 1 • Hypertension - 1 • Age > 75 - 2 • Diabetes - 1 • Stroke or TIA - 2 • Vascular disease - 1 • Age 65-74 - 1 • Female - 1 Males who score 1+ points or females who score 2+ points should be anticoagulated
How do you calculate bleeding risk?
HASBLED Score • Hypertension - 1 • Abnormal renal or liver function - 2 if both present • Stroke - 1 • Major bleed (previous) - 1 • Labile INR - 1 • Elderly > 65 - 1 • Drugs/alcohol use - 2 if both
What options are available for anticoagulation in AF? What are the pros and cons
DOACs - apixaban, rivaroxaban, dabigatran
- Do not require monitoring
- Less bleeding risks than warfarin
- 12 hour half-life so if patient misses dose, they are not covered
Warfarin
- Requires cover with LMWH for 5 days when initiating treatment because warfarin is initially pro-thrombotic
- Requires regular INR monitoring and it can be affected by many drugs/food
- 40 hour half-life so anticoagulant effect lasts days
LMWH
- Daily treatment dose injections
- Rare option in those who cannot tolerate oral treatment
What treatment can be offered for patients with AF who do not have uncontrolled symptoms and have an identifiable locus in their left atrium?
Atrial ablation
What effect does digoxin have on the heart?
It inhibits the sodium potassium adenosine triphosphatase ([Na+/K+ ATPase) ion pump in the myocardium and also has parasympathetic effects on the AV node
It is thereforenegatively chronotropic and positively ionotropic(i.e. slows heart rate but increases contractility).
What is the immediate management of bradycardia in a patient with adverse features (i.e. shock, syncope, heart failure, MI)?
- Atropine 500mcg IV
- If unsatisfactory response:
- Atropine 500mcg IV again
OR
- Transcutaneous pacing
OR
- Adrenaline 2-10mcg/min IV - Arrange transvenous pacing
What is the delta change in troponin levels?
Delta troponin is the percent difference between two troponin results taken in the same patient within a 3 - 8 hour time period
If it is greater than 20%, this is consistent with an MI
What investigations should be done in all post-ACS patients?
Echocardiogram - check LV function
Lipid profile
HbA1c
What are the DVLA regulations regarding ACS?
Stop driving for 4 weeks if no PCI/unsuccessful PCI
OR
Stop driving for 1 week if successful PCI
In both cases, the DVLA does not need to be informed
HGV drivers must inform the DVLA and stop driving for 6 weeks then meet with doctor to see if fit
What are the 5 types of MI?
- Spontaneous MI due to plaque rupture
- Low oxygen/hypoperfusion due to increased oxygen demand (fibrillation/tachycardia) or decreased supply (septic shock, anaemia)
- Sudden unexpected cardiac death
- Associated with PCI or stent thrombosis
- Associated with cardiac surgery
What is the long-term management after a STEMI?
Aspirin Clopidogrel/ticagrelor Beta-blockers ACE inhibitor Statins
