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Y3 - DPD > Interactive cases 1 > Flashcards

Interactive cases 1 Flashcards

1
Q

What associated symptoms might you get in an MI and why do you get them?

A
  • Breathlessness - HF or arrythmias
  • Nausea / sweating - associated with cardiac disease (vagal afferent)
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2
Q

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

A
  • 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
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3
Q

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

A

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
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4
Q

On an ECG which leads are the…

1) Anterior leads
2) Lateral leads
3) Inferior leads

A

1)

  • V1-V4

2)

  • V5, V6, I, aVL

3)

  • II, III, aVF
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5
Q

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)

A

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
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6
Q

Why is it important to measure serial troponin (serial measurements) when measuring troponin?

A
  • To get a whole picture - is it rising or falling?
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7
Q

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?

A

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
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8
Q

What are the 5 differential diagnoses for collapse, sorting by the category of the cause?

A
  1. Vasovagal

CVS

  1. Outflow obstruction - aortic stenosis or pulmonary embolism
  2. Arrythmias - tachycardia or bradycardia
  3. Postural hypotension

Neurological

  1. Seizure
  2. Hypoglycaemia
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9
Q

What investigations should you carry out in the case of arrythmias?

A
  • ECG (long QT can predispose to VT)
  • Cardiac monitor
  • 24 hour tape
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10
Q

Whatssigns might there be and what investigation might you carry out for assessment if there is an outlfow obstruction causing the collapse episode?

A
  • Low volume / slow-rising pulse
  • Ejection systolic murmur
  • Echocardiogram
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11
Q

What investigation might you carry out for suspected postural hypotension?

A
  • Lying and standing blood pressure - siginificant when there is a drop in 20mmHg
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12
Q

What signs / history might you get from seizure as a cause of collapse?

A
  • Aura
  • Stereotypical movements
  • Biting tongue
  • Incontinence
  • Post-ictal confusion
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13
Q

What investigation might you carry out for suspected hypoglycaemia as a cause of collapse?

A
  • Capillary blood glucose (CBG)
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14
Q

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?

A

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
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15
Q

What effect can IVDU have on the heart?

A
  • IVDU → infective endocarditis → affects right heart → tricuspid regurgitation
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16
Q

What heart murmur do you hear in

1) Mitral regurgitation?
2) Tricuspid regurgitation?

A

1)

  • Pansystolic murmur
  • S1 + S2 + PSM

2)

  • Pansystolic murmur
  • S1 + S2 + PSM
  • (SAME)
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17
Q

Why may you get hepatomegaly in tricuspid regurgitation?

A
  • Tricuspid regurgitation → back pressure causes hepatocongestion → hepatomegaly
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18
Q

Give the DDx for raised JVP, including sub-causes

A
  1. 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
  1. Tricuspid regurgitation
  • Damage to valve leaflets (infective endocarditis)
  • Right ventricle dilatation of the valve ring (valve root enlarges)
  1. Constrictive pericarditis (thickening / calcification of pericarditis)
  • Infection e.g. TB
  • Inflammation e.g. connective tissue disease: lupus, sarcoid
  • Malignancy
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19
Q

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

A
  1. Aortic stenosis
  • Loudest over aortic area
  • Loudest during expiration
  • Radiates to carotids
  • Associated witth slow-rising pulse (thrill under thumb, soft S2 at carotids)
  1. Mitral regurgitation
  • Loudest over mitral area
  • Loudest during inspiration
  • Radiate to axilla
  • Associated with displaced apex beat
  1. 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
  1. Ventricular septal defect
  • Loudest at left sternal border
  • …
  • Doesn’t really radiate
  • Associated with parasternal thrill
20
Q

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

A
  • 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
21
Q

What is meant by sinus tachycardia, how does it look on an ECG, and what are the causes of sinus tachycardia?

A
  • Sinus tachycardia = normal rhythm but fast HR
  • All waveforms are as normal
  • Causes:
    • Sepsis
    • Hypovolaemia
    • Endocrine (thyrotoxicosis, phaechromocytoma)
22
Q

What is the cause behind SVT, and what are the 2 types of SVT?

A
  • Re-entry circuits
  • AVNRT - AV nodal re-entry tachycardia
  • AVRT - AV re-entry tachycardia
23
Q

1) What is AVNRT, what is the mechanism causing AVNRT
2) What are the characteristic findings on an ECG of AVNRT?
3) Treatment?

A

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
24
Q

1) What is AVRT, what is the mechanism causing AVRT?
2) What are the characteristic findings on an ECG of AVRT?
3) Treatment?

A

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
25
Q

1) What are the characteristic features of atrial fibrillation on an ECG?
2) What feature is it that makes it distinct from SVT?

A

1)

  • Fast
  • Irregularly irregular
  • No p-waves
  • Narrow QRS

2)

  • Irregular whereas there is a regular rhythm in SVT
26
Q

What are the causes of atrial fibrillation?

A
  • Thyrotoxicosis
  • Alcohol
  • Heart:
    • Muscle (IHD, HTN)
    • Valve (Rheumatic heart disease)
    • Pericardium (Pericarditis)
  • Lungs:
    • Pneumonia
    • PE
    • Cancer
    • Other lung pathology
27
Q

What is thought to be the pathogenesis of atrial fibrillation?

A
  • AF originates in RA near the pulmonary vasculature
  • Changes in oxygen, CO2 or pressure on these cells → AF
28
Q

What are the characteristic ECG features of atrial flutter?

A
  • No p-waves
  • Narrow QRS
  • Saw-tooth baseline
29
Q

What is the management of acute fast AF?

A
  • If haemodynamically stable → DC Cardioversion
  • If haemodynamically unstable →
    • Anticoagulation to reduce risk of stroke
    • Rate control - beta-blocker, digoxin (note this is used less in pneumonia patients)
    • Rhythm control - if onset >48 hours, anticoagulate for 3-4 weeks before cardioversion (to reduce risk of stroke)
    • Think of underlying cause - treat sepsis and penumonia if these are causing it
    • Think of complications (anticoagulation) → CHADVASC score
  • Warfarin / rivaroxaban / apixiban
30
Q

What are the characteristic findings of ventricular tachycardia on an ECG?

A
  • Broad complex tachycardia (so tachycardia but the QRS complexes are broader than expected)
  • Fast (tachycardia)
  • Regular
31
Q

Give 3 causes of ventricular tachycardia

A
  1. Ischaemia
  2. Electrolyte abnormality (K+, Mg2+)
  3. Long QT (look at old ECGs)
32
Q

What is the management for VT?

A
  • If pulseless VT → defibrillate
  • If no haemodynamic compromise (hypotension)
    • IV amiodarone (anti-arrythmic)
    • Treat underlying cause - ischaemia, electrolyte imbalance, long QT
    • If recurrent, consider an implantable cardiac defibrillator (ICD)
33
Q

What are the causes of left ventricular hypertrophy?

A

Think about it, it makes sense. Its whatever makes the left side of the heart work harder

  1. HTN
  2. Aortic stenosis
34
Q

How is left ventricular hypertrophy diagnosed?

A
  • ECG (S in V1 + R in V6 should add up to equal to or more than 7 large squares. Remember S1R6 (deep S in V1/2 and Tall R in V5/6)
  • Echocardiogram (gold standard)
35
Q

1) Where does 1st degree heart block occur?
2) What is the characteristic ECG feature in 1st degree heart block?

A

1)

  • Occurs between SAN and AVN

2)

  • Prolonged PR interval (>200ms)
36
Q

1) What are the 2 types of 2nd degree heart block - where do they occur?
2) What are the characteristic ECG features of both of these?

A

1)

  • Mobitz type 1 (Wenkebach) - occurs in AVN
  • Mobitz type 2 - occurs after AVN in bundle of His or Purkinje fibres

2)

  • Mobitz type 1 (Wenkebach) - slowly increasing PR interval then dropped QRS complex
  • Mobitz type 2 - fixed PR interval and dropped beats
37
Q

1) What is 3rd degree heart block and where does it occur?
2) What are the characteristic features on an ECG of 3rd degree heart block?

A

1)

  • Occurs anywhere from the AVN down, causing complete blockage of conduction

2)

  • Complete dissociation between p-waves (atrial rate) and QRS waves (ventricular activity)
  • Broad QRS complexes (due to generation from ventricles)
38
Q

What is the management for VF and what is an exception to this management plan, and what would you do instead

A
  • This is a shockable rhythm - so shock
  • CPR throughout
  • Adrenaline every 3-5 mins (after 3rd shock too)
  • Amiodarone 300mg after 3 shocks
  • Unless the patient is hypothermic - affecting drug metabolism (therefore cardiotoxic) and shock will not work so just do CPR
39
Q

What are the shockable rhythms?

A
  • VF
  • Pulseless VT
40
Q

What are the non-shockable rhythms?

How do you manage these?

A
  • PEA (pulseless electrical activity)
  • Asystole

2)

  • CPR
  • Adrenaline every 3-5 mins
  • Correct reversible causes
41
Q

What are the 8 reversible causes of cardiac arrest?

A

4Hs:

  1. Hypoxia
  2. Hypothermia
  3. Hypo- / hyperkalaemia
  4. Hypovolaemia

4Ts:

  1. Thrombosis
  2. Tamponade
  3. Toxins
  4. Tension pneumothorax
42
Q

What heart murmur does pericarditis give?

A
  • S1 + S2 + S3
  • 1….2…3
  • This is not actually due to any blood flow reason at all unlike in other murmurs such as in valve disorders such as mitral and tricuspid regurgitation
  • It is instead due to ‘pericardial friction rub’ - rubbing together of 2 layers of pericardial sac
43
Q

What is the management of pericarditis?

A
  • Analgaesics and reassurance initially
  • Diuretics after
  • Pericardiectomy last
44
Q

Give the ddx for pleuritic chest pain - 6 causes

A
  1. Pericarditis
  2. PE
  3. Pneumonia
  4. Pneumothorax
  5. Pleural pathology
  6. (Sub-diaphragmatic pathology) - e.g. hepatic abscess
45
Q

What heart murmurs do you hear in heart failure and why?

A
  • S3 gallop - S1…S2…S3 - kentucky - due to rapid ventricular filling
  • Note: this is best heard using the bell rather than the diaphragm
  • S4 gallop - S4…..S1…S2 - tennnessee - due to ventricular hypertrophy
46
Q

What is the management of heart failure?

A
  • Sit up
  • High FiO2 therapy - 60-100% O2
  • GTN infusion (venodilator → ↓ preload)
  • Diamorphine (venodilator → ↓ preload)
  • Furosemide (IV)
    • Given IV because if they have gut oedema with pulmonary oedema they will not absorb the drug orally
  • Treat underlying cause (e.g. MI)
47
Q

What is the prescription formula?

A
  • Medication name
  • Dose
  • Route
  • Frequency

Y3 - DPD (4 decks)

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