What associated symptoms might you get in an MI and why do you get them?
- Breathlessness - HF or arrythmias
- Nausea / sweating - associated with cardiac disease (vagal afferent)
What are the investigations that you could do for chest pain (not some of these branch out to give further tests)? Give CVS tests only not resp, and start with the first most appropriate test usually
- ECG - STEMI / NSTEMI?
- Troponin
- +ve → do coronary angiography (to check for MI)
- -ve → suggests it is not an MI and may be angina → so do an exercise tolerance test
- Echocardiogram
- To see any regional wall motion abnormality or ventricular dysfunction (due to arrhythmias, vavular dysfunction etc)
- Blockage of one of the coronaries in MI for example - RWMA (regional wall motion abnormality) in that territory
Give a DDx of chest pain and some key things that can help differentiate between them (i.e. what might tip you off that it is this diagnosis) where possible
1) CVS
2) GI - no key things for this one
3) Resp
4) MSK
5) Other
1)
- IHD
- Angina pectoris (stable or unstable) -
- ACS (MI) - crushing chest pain radiating to left arm and jaw
- Aortic dissection
- Sudden onset chest pain radiating to back,
- BP differential across arms and early diastolic murmur (aortic regurgitation)
- Thoracic aortic aneurysm
- Pericarditis
- Pleuritic chest pain (worse on inspiration and improved by leaning forward
- Preceding flu-like illness
- Cocaine induced coronary spasm
2)
- Oesophageal spasm
- Oesophagitis
- Gastritis
- Peptic ulcer disease
- Acute pancreatitis
- Cholecystitis
- Boerhave’s perforation
3)
- Pulmonary Embolism
- Pleuritic chest pain
- Acute onset SOB
- Swollen leg (DVT?)
- Haemoptysis
- Pneumonia
- Fever
- Cough
- Sputum
- Pneumothorax
- Pleuritic chest pain
- Acute onset
4)
- MSK INFLAMMATION (note this is THE most likely diagnosis - most common). Caused by…..
- ….Costochondritis (Tietze’s syndrome)
- MSK tenderness
5)
- Anxiety
On an ECG which leads are the…
1) Anterior leads
2) Lateral leads
3) Inferior leads
1)
- V1-V4
2)
- V5, V6, I, aVL
3)
- II, III, aVF
1) Describe the coronary artery supply to the heart
2) Now map which would be affected in an anterior MI, lateral MI and inferior MI
3) Now put it all together and say for the anterior MI, lateral MI and inferior MI which coronary artery will be affected, and in which leads you may see changes (ST elevation)
1)
- Left main stem gives rise to the circumflex and LAD arteries. The circumflex artery then travels to the side and back of the heart while the LAD continues straight down on the LHS
- The RCA supplies the right hand side of the heart and runs along the bottom of the heart towards the apex
2)
- Anterior MI - LAD
- Lateral MI - Circumflex artery
- Inferior MI - RCA
3)
- Anterior MI - LAD - V1-V4
- Lateral MI - Circumflex artery - V5, V6, I, aVL
- Inferior MI - RCA - II, III, aVF
Why is it important to measure serial troponin (serial measurements) when measuring troponin?
- To get a whole picture - is it rising or falling?
What would suggest from the history (in terms of presenting complaint) before, during and after the collapse episode, that the cause of collapse is cardiovascular or that the collapse is neurological in origin?
BEFORE
- Aura - neurological cause
- No warning of the collapse beforehand (no aura)
DURING
- Tongue biting - associated with seizure (neurological)
- No tongue biting - evidence for CVS cause
AFTER
- Confused - post-ictal confusion after seizure (neurological)
- Not confused - evidence for CVS cause
What are the 5 differential diagnoses for collapse, sorting by the category of the cause?
- Vasovagal
CVS
- Outflow obstruction - aortic stenosis or pulmonary embolism
- Arrythmias - tachycardia or bradycardia
- Postural hypotension
Neurological
- Seizure
- Hypoglycaemia
What investigations should you carry out in the case of arrythmias?
- ECG (long QT can predispose to VT)
- Cardiac monitor
- 24 hour tape
Whatssigns might there be and what investigation might you carry out for assessment if there is an outlfow obstruction causing the collapse episode?
- Low volume / slow-rising pulse
- Ejection systolic murmur
- Echocardiogram
What investigation might you carry out for suspected postural hypotension?
- Lying and standing blood pressure - siginificant when there is a drop in 20mmHg
What signs / history might you get from seizure as a cause of collapse?
- Aura
- Stereotypical movements
- Biting tongue
- Incontinence
- Post-ictal confusion
What investigation might you carry out for suspected hypoglycaemia as a cause of collapse?
- Capillary blood glucose (CBG)
1) What is long QT syndrome and what does it predispose to?
2) What are the 2 types of causes and describe these further?
3) How to identify long QT on an ECG?
1) Abnormal ventricular repolarisation - predisposes to ventricular tachycardia
2)
Congenital:
- Long QT syndrome - mutations in K+ channels
Acquired:
- Low K+ / Mg2+
- Drugs
3)
- Normal QT - T-wave should finish before halfway point between RR interval - if extended beyond this = long QT
What effect can IVDU have on the heart?
- IVDU → infective endocarditis → affects right heart → tricuspid regurgitation
What heart murmur do you hear in
1) Mitral regurgitation?
2) Tricuspid regurgitation?
1)
- Pansystolic murmur
- S1 + S2 + PSM
2)
- Pansystolic murmur
- S1 + S2 + PSM
- (SAME)
Why may you get hepatomegaly in tricuspid regurgitation?
- Tricuspid regurgitation → back pressure causes hepatocongestion → hepatomegaly
Give the DDx for raised JVP, including sub-causes
- Right heart failure
- Secondary to left heart failure (=congestive heart failure)
- Secondary to Pulmonary HTN which is secondary to PE or COPD (COPD → chronic hypoxia → chronic vasoconstriction → pulmonary HTN
- Tricuspid regurgitation
- Damage to valve leaflets (infective endocarditis)
- Right ventricle dilatation of the valve ring (valve root enlarges)
- Constrictive pericarditis (thickening / calcification of pericarditis)
- Infection e.g. TB
- Inflammation e.g. connective tissue disease: lupus, sarcoid
- Malignancy
Give the ddx for systolic murmurs - 4 cause and then say for each of them how to differentiate them by
1) Where they are loudest
2) When they are loudest
3) Where they radiate to
4) What they are associated with - i.e. what other sign etc
- Aortic stenosis
- Loudest over aortic area
- Loudest during expiration
- Radiates to carotids
- Associated witth slow-rising pulse (thrill under thumb, soft S2 at carotids)
- Mitral regurgitation
- Loudest over mitral area
- Loudest during inspiration
- Radiate to axilla
- Associated with displaced apex beat
- Tricuspid regurgitation
- Loudest over tricuspid area - LLSE (lower left sternal edge)
- Loudest during inspiration
- Doesn’t really radiate anywhere
- Assocated with pulsatile liver, raised JVP
- Ventricular septal defect
- Loudest at left sternal border
- …
- Doesn’t really radiate
- Associated with parasternal thrill
What’s a good way of differentiating between the causes of a pan-systolic murmur in a rough way in terms of which side of the heart is causing it? Note that there are better ways of differentiating between them
- Right heart murmurs - louder on inspiration so tricuspid or pulmonary therefore if tricuspid regurgitation is causing the pan-systolic murmur, then it will be lounder on inspiration
- Left heart murmurs - louder on expiration so mitral or aortic therefore if mitral regurgitation is causing the pan-systolic murmur, then it will be louder on expiration
What is meant by sinus tachycardia, how does it look on an ECG, and what are the causes of sinus tachycardia?
- Sinus tachycardia = normal rhythm but fast HR
- All waveforms are as normal
- Causes:
- Sepsis
- Hypovolaemia
- Endocrine (thyrotoxicosis, phaechromocytoma)
What is the cause behind SVT, and what are the 2 types of SVT?
- Re-entry circuits
- AVNRT - AV nodal re-entry tachycardia
- AVRT - AV re-entry tachycardia
1) What is AVNRT, what is the mechanism causing AVNRT
2) What are the characteristic findings on an ECG of AVNRT?
3) Treatment?
1)
- AVNRT = AV nodal re-entry tachycardia - a form of SVT (supra-ventricular tachycardia)
- Re-entry circuits about the AV node - 2 circuits in the right atrium - one slow and one fast
2)
- Characteristic ECG findings:
- Fast (tachcardia)
- Regular (important! differentiates from AF)
- Narrow QRS (rapid depolarisation due to re-entrant circuit)
- No p-wave as the depolarisation is coming purely from the re-entrant circuit about the AVN and there is no SAN input (which normally gives the p-wave)
- Delta-wave (slurred upstroke before QRS wave)
3)
- If haemodynamically unstable → DC cardioversion
- If haemodynamically stable →
- Valsalva manouevre
- Adenosine
1) What is AVRT, what is the mechanism causing AVRT?
2) What are the characteristic findings on an ECG of AVRT?
3) Treatment?
1)
- Type of SVT
- Re-entrant circuit
2)
- Fast (tachycardia)
- Regular
- P-waves still present
- Short PR interval
- Delta wave (slurred upstroke before QRS wave) - when not tachycardic
3)
- Radiofrequency catheter ablation +….
- If haemodynamically unstable → DC cardioversion
- If haemodynamically stable →
- Valsalva manouevre
- Adenosine
