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Year 3 > Cardiology Block > Flashcards

Cardiology Block Flashcards

1
Q

What drugs are used to increase HR in an ECHO when exercise isn’t possible?

A

Atropine + Dobutamine

300ug or 600ug if vasovagal episode

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2
Q

What is the treatment following an NSTEMI?

A

Aspirin + Ticagrelor for 1y (Aspirin then continued for life)

ACE inhibitor
B-blocker
Statin

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3
Q

What is R-wave progression in ECG?

A

R wave gets bigger from V1-V6

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4
Q

What is the normal diameter of the RV and LV?

A 
RV = 5mm
LV = 15mm
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5
Q

What are possible causes of decreased R wave progression? Increased R wave progression?

A

Decreased R wave progression:

  1. Myocardial infarct (scar tissue)
  2. Dilated cardiomyopathy (larger LV to maintain SV + thinning of muscle = decreased electrical activity)
  3. Pericardial effusion
  4. Infiltrative cardiac disease

Increased R wave progression:
1. RVH (pulmonary HTN/cor pulmonale)

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6
Q

What is 1 small square equivalent to on ECG? 1 large square?

A

1 small square = 0.04s

1 large square = 0.2s

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7
Q

What is the definition of a broad QRS complex?

A

> 3 small squares (> 0.12s)

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8
Q

What is the normal axis on ECG?

A

-30º to + 90º

Note: VT can cause extreme axis deviation (not common)

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9
Q

What is the physiology of RBBB?

A

Fast depolarization through the LV and slowly depolarizes RV

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10
Q

What is bifasicular block?

A

Left axis deviation + RBBB

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11
Q

What do the V1/V2 leads represent? V3/V4 leads?

A 
V1/V2 = RV leads -> big voltage here = RVH (pulmonary HTN)
V3/V4 = Septal
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12
Q

What is atrial flutter?

A

Circuit in the SA node @ 300bpm and conducts @ 2:1 = 150bpm (not dependent on AV node)
- AV node slows down electrical activity

Adenosine stops AV conduction -> asystole and can be used to distinguish Atrial Flutter from SVT

Tx: DC cardio version; rate slowing drugs (same for AF)

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13
Q

What is SVT?

A

Dependent on AV node thus with adenosine SVT will be cured

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14
Q

What is coarse AF?

A

Little “rotas” forming within the atria (looks like flutter in some leads of ECG)

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15
Q

When are broad complex tachycardias seen?

A
  1. Ventricular origin
  2. SVT with BBB
  3. Accessory pathways (i.e. Wolff-Parkinson White syndrome)
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16
Q

What are the different kinds of heart block?

A

Type 1: Long PR

Type 2 (Mobitz 1/Wekenbach): PR gets longer and longer then dropped QRS

Type 2 (Mobitz 2): Regularly dropped QRS (2:1, 3:1 conduction)

Type 3: No relation between atria and ventricles

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17
Q

What are the possible characters of chest pain?

A

Constricting = angina, esophageal spasm, anxiety

Sharp = from pleura, pericardium, chest wall

Prolonged (>1/2h), dull, central crushing pain/pressure = MI

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18
Q

Where does chest pain radiate to?

A

To shoulder, either or both arms, neck/jaw = cardiac ischemia

Instantaneous, tearing, interscapular, retrosternal = aortic dissection

Epigastric pain may be cardiac

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19
Q

What are the precipitants of chest pain?

A

Pain associated with cold, exercise, palpitations, or emotion = cardiac pain/anxiety

Brought on by food, lying flat, hot drinks, alcohol = esophageal spasm/disease (meals can also cause angina)

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20
Q

What are the relieving factors of chest pain?

A

Relieved within minutes by rest/GTN = angina

Antacids help = GI cause

Pericardiac pain improves on leaning forward

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21
Q

What are associated symptoms to chest pain?

A

Dyspnea (with cardiac pain, PE, pleurisy, anxiety)
N/V, sweating (with MI)

Angina -> coronary artery disease + aortic stenosis, hypertrophic cardiomyopathy, paroxysmal supraventricular tachycardia -> exacerbated by anemia

Chest pain with tenderness = Tietze’s syndrome

Odd neurological symptoms + atypical chest pain = aortic dissection

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22
Q

What is pleuritic pain?

A

Pain exacerbated by inspiration. Implies inflammation of the pleura from pulmonary infection, inflammation or infarction

It causes us to “catch our breath”

Differentials:

  1. Musculoskeletal pain
  2. Fractured rib (exacerbated by gentle pressure on sternum)
  3. Subdiaphragmatic pathology (i.e. gallstones)
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23
Q

What would you do for a patient complaining of chest pain + who is acutely unwell?

A
  • Admit
  • Check pulse, BP in both arms, JVP, heart sounds
  • Examine legs for DVT
  • Give O2
  • IV line
  • Relieve pain (5-10mg IV morphine)
  • Cardiac monitor
  • 12-lead ECG
  • CXR
  • ABG
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24
Q

What are causes of dyspnea?

A
  1. LVF
  2. PE
  3. Any respiratory cause (i.e. pneumonia, pneumothorax)
  4. Anemia
  5. Pain
  6. Anxiety
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25
Q

What are specific symptoms associated with heart failure?

A
  1. Paroxysmal nocturnal dyspnea (waking up in the middle of the night gasping for air)
  2. Orthopnea (no. of pillows used to sleep)
  3. Peripheral oedema
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26
Q

What are causes of palpitations?

A
  1. Ectopics
  2. Sinus tachycardia
  3. AF
  4. SVT
  5. VT
  6. Thyrotoxicosis
  7. Anxiety
  8. Pheochromocytoma (rarely)
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27
Q

What should you ask when discussing heart palpitations?

A
  1. Previous episodes
  2. Precipitating/relieving factors
  3. Duration of symptoms
  4. Associated chest pain
  5. Dyspnea
  6. Dizziness
  7. Collapse
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28
Q

What questions should you ask about syncope?

A
  1. Prodromal symptoms:
    - Chest pain, palpitations, dyspnea = arrhythmia
    - Aura, headache, dysarthria, limb weakness = CNS cause
  2. During the episode:
    - Pulse?
    - Limb jerking, tongue biting, urinary incontinence?
    * Hypoxia from lack of cerebral perfusion may cause seizures
  3. Recovery:
    - Rapid = arrhythmia
    - Prolonged, with drowsiness = seizure
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29
Q

How do you calculate the rate on an ECG if it’s regular? Irregular?

A

Regular = 300/(# of big squares between RR intervals)

Irregular = # of R waves x 6

Normal rate = 60-100bpm

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30
Q

How do you calculate rhythm on an ECG?

A

If cycles are not clearly equal, use the “card method”.

If not equal check if:
1. there is slight but regular lengthening + then shortening (with respiration) = sinus arrhythmia (normal in young people)

  1. There are different rates which are multiples of each other - varying block
  2. It is 100% irregular - AF or VF
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31
Q

What is the appearance of AF on an ECG?

A

AF has no discernible P waves + QRS complexes are irregularly irregular

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32
Q

What is the appearance of atrial flutter on ECG?

A

A sawtooth baseline of atrial depolarization (~300bpm) and regular QRS complexes

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33
Q

How would a ventricular-originating rhythm present on ECG?

A

QRS complexes > 0.12s (broad complex) with P waves following them or absent

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34
Q

What does the axis on an ECG represent?

A

The overall direction of depolarization across the patient’s anterior chest. This is the sum of all the ventricular electrical forces during ventricular depolarization.

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35
Q

What are some causes of left axis deviation?

A
  1. Left anterior hemiblock
  2. Inferior MI
  3. VT from a left ventricular focus
  4. Wolff-Parkinson White Syndrome
  5. LVH
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36
Q

What are some causes of right axis deviation?

A
  1. RVH
  2. PE
  3. Anterolateral MI
  4. Wolff-Parkinson White Syndrome
  5. Left posterior hemiblock
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37
Q

In which leads are P waves upright? Inverted?

A

Upright: II, III, aVF
Inverted: aVR

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38
Q

In which conditions is the P wave absent?

A
  1. AF

2. P hidden due to junctional or ventricular rhythm

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39
Q

What is P mitrale? P pulmonale?

A

Bifid P waves
Signifies L atrial hypertrophy

Peaked P waves
Signifies R atrial hypertrophy

Pseudo-P-pulmonale seen in hyperK+

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40
Q

What is the PR interval? How long is it? What does it indicate if its prolonged/shortened?

A

Measure from the start of the P wave to the start of the QRS complex

Normal range = 0.12-0.2s (3-5 small squares)

Prolonged = delayed AV conduction (1st degree heart block)

Shortened = Unusually fast AV conduction down an accessory pathway (i.e. WPW)

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41
Q

Define the components of a QRS complex

A 
Q = First negative deflection from the isoelectric line
R = Any positive deflection
S = Any negative deflection after an R wave
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42
Q

What is the QRS complex? How long is it? What does it indicate if its prolonged/shortened?

A

Normal duration < 0.12s (less than 3 small squares)

Broad (> 0.12s):

  • Ventricular conduction defects (bundle branch block)
  • Metabolic disturbance
  • Ventricular origin (i.e. ventricular ectopic)

High-amplitude QRS (normal Q waves < 0.04s wide + < 2mm deep):
- Ventricular hypertrophy

Often sen in leads I, aVL, V5-V6 and reflect normal septal depolarization

Pathological Q waves (wide + deep) = within a few hours following an acute MI

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43
Q

What is the QT interval?

A

Measure from start of QRS to end of T wave. It varies with rate.

The corrected QT interval (QTc) = QT/(RR)^0.5

Normal QTc = 0.38-0.42s

Long QT can lead to VT + sudden death

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44
Q

What is the ST segment?

A

Usually isoelectric.

Planar elevation > 1mm or depression >0.5mm implies infarction or ischemia respectively

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45
Q

What is the T wave?

A

Normally inverted in aVR, V1, occasionally V2
Normal if inverted in isolation in lead III

Abnormal if inverted in I, II, V4-V6

Peaked in hyperkalemia and flattened in hypokalemia

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46
Q

What is a J wave?

A

The J point is where the S wave finishes and ST segment starts

J wave is a notch seen at this point -> in hypothermia, SAH, hypercalcemia

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47
Q

What abnormalities can be seen in an ECG?

A
  1. Sinus Tachycardia: Rate > 100bpm
  2. Sinus bradycardia: Rate < 60bpm
    - Physical fitness
    - vasovagal attacks
    - sick sinus syndrome
    - drugs (b-blockers, digoxin, amiodarone)
    - hypothyroidism
    - hypothermia
    - increased intracranial pressure
    - cholestasis
  3. AF
    - IHD
    - Thyrotoxicosis
    - Hypertension
    - Obesity
    - Heart failure
    - Alcohol
  4. Heart Block: Disrupted passage of electrical impulse through AV node
    - 1st degree HB: PR interval is prolonged + unchanging; no missed beats
  • 2nd degree HB (Mobitz I): PR interval becomes longer + longer until a QRS complex is missed, the pattern then resets. This is Wenckebach phenomenon.
  • 2nd degree HB (Mobitz II): QRS are regularly missed (i.e. P QRS P P QRS P - 2:1 block). This is a dangerous rhythm as it may progress to complete HB
  • 3rd degree HB: No impulses passed from atria to ventricles so P waves and QRS appear independently of each other. As tissue distal to the AVN paces slowly, the patient becomes very bradycardic, and may develop hemodynamic compromise. Urgent treatment required.
  • IHD (inferior MI)
  • Idiopathic (fibrosis)
  • Congenital
  • Aortic valve calcifications
  • Cardiac surgery/trauma
  • Digoxin toxicity
  • Infiltration (abscesses, granulomas, tumours, parasites)
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48
Q

What conditions cause ST elevation? ST depression?

A

ST elevation:

  • Normal variant (high take-off)
  • Acute MI (STEMI)
  • Prinzmetal’s angina
  • Acute pericarditis (saddle-shaped - across all leads)
  • L ventricular aneurysm

ST depression:

  • Normal variant (upward sloping)
  • Digoxin toxicity (downward sloping)
  • Ischemic (horizontal): angina, NSTEMI, acute posterior MI (ST depression in V1-V3)
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49
Q

When do you get T inversion on an ECG?

A

In V1-V3:

  • Normal (black patients + children)
  • RBBB
  • RV strain (2º to PE)

In V2-V5:

  • Anterior ischemia
  • Hypertrophic cardiomyopathy
  • Subarachnoid hemorrhage
  • Lithium

In V4-V6 + aVL:

  • Lateral ischemia
  • LVH
  • LBBB

In II, III, avF:
- Inferior ischemia

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50
Q

What is the presentation of MI on ECG?

A
  1. Within hours: T wave may become peaked + ST segments begin to rise
  2. Within 24h: T wave inverts. ST elevation rarely persists, unless a left ventricular aneurysm develops. T wave inversion may/may not persist.
  3. Within a few days: Pathological Q waves begin to form. Q waves usually persist but may resolve in 10% of patients.
  4. The location of these changes indicates the ischemic area location
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51
Q

What are considered pathological Q waves?

A

Q waves are considered pathological if:

  1. > 1mm (1 small square) wide
  2. > 2 mm (2 small squares) deep
  3. > 25% of depth of QRS complex
  4. Seen in leads V1-3
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52
Q

What ECG changes occur in PE?

A
  1. Sinus tachycardia (commonest)
  2. RBBB
  3. RV strain pattern (R axis deviation, dominant R wave + T wave inversion/ST depression in V1 + V2)

Rarely S1Q3T3 pattern occurs:

  • Deep S waves in I
  • Pathological Q waves in III
  • Inverted T waves in III
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53
Q

What ECG changes are seen in digoxin toxicity?

A
  1. Down-sloping ST depression
  2. Inverted T wave in V5-V6 (“reversed tick”)

Any arrhythmia may occur (ventricular ectopics + nodal bradycardia are common)

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54
Q

What ECG changes are seen in hyperkalemia?

A
  1. Tall, tented T waves
  2. Widened QRS
  3. Absent P waves
  4. “sine wave” appearance
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55
Q

What ECG changes are seen in hypokalemia?

A
  1. Small T waves
  2. Prominent U waves
  3. Peaked P waves
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56
Q

What ECG changes are seen in hypercalcemia?

A
  1. Short QT interval
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57
Q

What ECG changes are seen in hypocalcemia?

A
  1. Long QT interval

2. Small T waves

58
Q

What can cause a R wave taller than the S is deep (R dominance) if seen in V1 + V2?

A

R ventricular strain or Posterior MI

59
Q

What are the ECG territories? Which heart territory and coronary artery do they coincide to?

A

I, aVL, V4-V6 = lateral -> circumflex artery

V1 - V3 = anterioseptal -> LAD artery

II, III, aVF = inferior -> RCA in 80%; circumflex in 20% (L dominant)

V7 - V9 = posterior -> Circumflex

60
Q

What pattern is seen in RBBB on ECG?

A

QRS > 0.12s

MARROW (M shape in V1, W shape in V6)

  1. RSR pattern in V1 (dominant R in V1)
  2. Inverted T waves in V1-V3 or V4
  3. Wide, slurred S wave in V6

Causes:

  • Normal variant (isolated RBBB)
  • Pulmonary embolism
  • Cor pulmonale (pulmonary HTN)
61
Q

What is the pattern of LBBB on ECG?

A

QRS > 0.12s

WILLIAM (W shape in V1, M shape in V5/6)

  1. Dominant M pattern in V5
  2. Inverted T waves in I, aVL, V5-V6
  3. Dominant S wave in V1

Causes:

  • IHD
  • HTN
  • Cardiomyopathy
  • Idiopathic fibrosis
    • If there is LBBB, no comment can be made on ST elevation or T wave inversion!
    • New LBBB = STEMI
62
Q

What is bifascicular block?

A

The combination of RBBB + Left bundle hemiblock, manifest as an axis deviation (i.e. Left axis deviation in the case of left anterior hemiblock)

63
Q

What is trifascicular block?

A

Bifascicular block + 1st degree HB -> may need pacing

Suspect LVH if:

  1. R wave in V6 > 25mm (5 large squares)
  2. Sum of the S wave in V1 + R wave in V6 > 35mm (7 large squares)

Suspect RVH if:

  1. Dominant R wave in V1
  2. T wave inversion in V1-V3 or V4
  3. Deep S wave in V6
  4. Right axis deviation

Other causes of dominant R wave in V1:

  • RBBB
  • Posterior MI
  • Type A WPW syndrome
64
Q

What are causes of low-voltage QRS complex?

A

QRS < 5mm (1 large square) in all limb leads

  1. Hypothyroidism
  2. COPD
  3. Increased hematocrit
  4. Changes in chest wall impedance
  5. PE
  6. BBB
  7. Carcinoid heart disease
  8. Myocarditis
  9. Cardiac amyloid
  10. Doxorubicin cardiotoxicity
  11. Heart muscle diseases
  12. Pericardial effusion
  13. Pericarditis
65
Q

What are the 5 modalities of cardiac imaging?

A
  1. Chest x-ray
    - Cardiomegaly = Congestive heart failure
    - Pulmonary oedema = Decompensated heart failure
    - Globular heart = Pericardial effusion
    - Metal wires + valves = previous cardiothoracic surgery
    - Dextrocardia
    - Rib notching = clue in coarctation of the aorta
  2. Echocardiography
    - Transthoracic or transesophageal
    - At rest, during exercise, or after infusion of a pharmacological stressor (dobutamine, atropine)
  3. Cardiac CT
    - Info on cardiac structure + function
    - CT angiography = imaging of coronary arteries (to diagnose stenosis of the arteries)
    - Medications often given to slow heart down
    - less invasive than routine trans catheter coronary angiography
  4. Cardiac MR
    - First-choice of imaging to look at diseases that directly affect the myocardium
  5. Nuclear Imaging
    - Assessing whether myocardium distal to the blockage is able + so whether stenting or CABG will be of value
    - Perfusion assessed at rest + with exercise/pharmacologically-induced stress
66
Q

What is an indication for transesophageal ultrasound?

A

Diagnosing aortic dissections

67
Q

What are the uses of cardiac ECHO?

A
  1. Quantification of global LV function
  2. Estimating R heart hemodynamics (i.e. pulmonary artery flow)
  3. Valve disease
  4. Congenital heart disease
  5. Endocarditis
  6. Pericardial effusion: fluid may first accumulate between the posterior pericardium + L ventricle, then anterior to both ventricles, and anterior/lateral to R atrium
  7. HCM (hypertrophic cardiomyopathy)
68
Q

What is cardiac catheterization?

A

Insertion of a catheter into the heart via the femoral or radial artery or into the venous system, and manipulating it within the heart + great vessels to, for example, perform angioplasty, valvuloplasty (TAVI)

69
Q

Name 3 antiplatelet drugs and their uses

A
  1. Aspirin -> secondary prevention following MI, TIA/stroke, angina, peripheral vascular disease
  2. Clopidogrel/Ticagrelor -> with aspirin after coronary stent insertion, in ACS
  3. Tirofiban -> unstable angina/MI
70
Q

Which anticoagulants are used in ACS?

A
  1. LMWH
  2. Fondaparinux
  3. Bivalirudin
71
Q

When are B-blockers used? What are their contraindications? What are their side effects?

A

Used in:

  1. Angina
  2. HTN
  3. Antidysrhythmic
  4. Post MI (decreased mortality)
  5. Heart failure (with caution)

Contraindicated in:

  1. COPD/Asthma
  2. Heart block

Side Effects:

  1. Lethargy
  2. Erectile dysfunction
  3. Headache
72
Q

What blood result should be monitored when a patient is on ACE inhibitors?

A

U&E (kidney function)

  • Creatinine rise of > 20% is concerning
  • Check 1-2 weeks after starting an ACE inhibitor

** If renal function deteriorates rapidly, investigate for renal artery stenosis

SE:

  • Dry cough
  • Urticaria (rash)
73
Q

Name the 3 classes of diuretics, their uses, and their side effects

A
  1. Loop diuretics (i.e. furosemide)
    - Used in heart failure
    - Inhibit the Na/2Cl/K co-transporter
    - SE: dehydration, low Na/K/Cl, ototoxic
  2. Thiazides (i.e. indapamide, metolazone)
    - Used in HTN + heart failure
    - SE: Low K/Mg, High Ca, Gout/urate, impotence
  3. Potassium-sparing diuretics (i.e. spironolactone, eplerenone)
74
Q

What 2 drugs have an effect on the heart and should NOT be given together?

A

Ca2+ channel blockers + B-blockers
(i.e. Verapamil + bisoprolol)

  • Can cause severe bradycardia + LVF
75
Q

List 12 cardiovascular drug classes

A
  1. Antiplatelets
  2. Anticoagulants
  3. ACE inhibitors
  4. B-blockers
  5. Diuretics
  6. Calcium channel blockers
  7. Vasodilators
  8. Digoxin
  9. Sodium channel blockers
  10. Amiodarone
  11. Ivabradine
  12. Statins
76
Q

What are the side effects of taking digoxin?

A
  1. Any arrhythmia (SVT with AV block)
  2. Yellow vision
  3. Confusion
  4. Gynecomastia
77
Q

What are the side effects of amiodarone? What kind of drug is it and how often does it need monitoring?

A

SE:

  1. Thyroid disease
  2. Liver disease
  3. Pulmonary fibrosis
  4. Peripheral neuropathy

Monitor TFTs and LFTs every 6mo

78
Q

What drug blocks the pacemaker “funny current”?

A

Ivabradine

- Used in angina and heart failure

79
Q

Name 3 drugs that slow conduction through the AV node

A
  1. Digoxin
  2. Adenosine
  3. Verapamil

**Do not use in patients with accessory pathways (ie. WPW)

80
Q

What is angina and what are its features?

A

Angina is symptomatic reversible myocardial ischemia

Features:

  1. Constricting/heavy discomfort to the chest, jaw, neck, shoulders or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5mins by rest or GTN spray

All 3 features = typical angina
2 features = atypical angina
0-1 features = non-anginas chest pain

81
Q

What are the causes of angina?

A

Atheroma

Rarely:

  • Anemia
  • Coronary artery spasm
  • Aortic stenosis
  • Tachyarrhythmias
  • Hypertrophic cardiomyopathy
  • Arteritis/small vessel disease (microvascular angina/cardiac syndrome X)
82
Q

Describe the 4 different causes of angina

A

Stable Angina:

  • Induced by effort, relieved by rest
  • Good prognosis

Unstable Angina:

  • Angina of increasing frequency or severity
  • Occurs on minimal exertion or at rest
  • Associated with increased risk of MI

Decubitus Angina:
- Precipitated by lying flat

Variant (Prinzmetal) Angina:
- Caused by coronary artery spasm (rare: may coexist with fixed stenoses)

83
Q

What tests are used to diagnose angina?

A
  1. ECG
    - Usually normal but may show ST depression
    - Flat/inverted T waves
    - Signs of past MI
  2. Blood Tests
    - FBC
    - U+E
    - TFTs
    - Lipids
    - HbA1c
  3. ECHO
  4. Chest X-ray
84
Q

what is the management of angina?

A
  1. Address exacerbating factors: anemia, tachycardia (fast AF), thyrotoxicosis
  2. Secondary prevention of cardiovascular disease
    - Stop smoking, exercise, optimize HTN + diabetes control
    - 75mg aspirin daily
    - Address hyperlipidemia
    - Consider ACE inhibitors (if diabetic)
  3. PRN symptom relief
    - GTN spray/sublingual tablets
    - Repeat dose if pain not gone after 5min and to call ambulance if pain still present 5min after 2nd dose
    - SE: headache, low BP (sit while taking)
  4. Anti-Anginal medication
    - First line = B-blockers OR Ca2+ channel blockers (not combined)
    - i.e. Atenolol 50mg BD; Bisoprolol 5-10mg OD
    - i.e. Amlodipine 5mg OD; Diltiazem
  • Then isosorbide mononitrate, ivabradine, ranolazine, nicorandil
  1. Revascularization
    - When optimal medical therapy proves inadequate
    - PCI: balloon inflated inside stenosed vessel, opening the lumen
    - Dual antiplatelet therapy (aspirin + clopidogrel) recommended for at least 12mo following procedure
    - CABG: Less likely to need repeat revascularization compared to PCI patients, but recovery is slower and patient is left with 2 large wounds (sternal + vein harvesting)
85
Q

What are the investigations for ischemic heart disease?

A
  1. Exercise ECG - assess for ischemic ECG changes
  2. Angiography - either using cardiac CT with contrast, or trasncatheter angiography
  3. Functional imaging: myocardial perfusion scintigraphy, stress echo (echo whilst undergoing exercise or receiving dobutamine), cardiac MRI
86
Q

What are risks/triggers for variant (Prinzmetal) angina? What is the treatment?

A
  • Smoking increases risk, but HTN and hypercholesteremia do not
  • Triggers = cocaine, amphetamines, marijuana, low magnesium, artery instrumentation (during angiography)

Treatment:

  • Avoid triggers
  • Correct low magnesium
  • Stop smoking
  • PRN GTN
  • Calcium channel blockers ± long-acting nitrate (isosorbide mononitrate)
  • Avoid non-selective B-blockers, aspirin, and triptans (can cause more spasms!)
87
Q

What is ACS?

A
  • ACS includes unstable angina + MIs
  • These share a common underlying pathology - plaque rupture, thrombosis, and inflammation

Myocardial Infarction:
- Myocardial cell death, releasing troponin

Ischemia:

  • Lack of blood supply ± cell death
  • MIs have troponin rises, unstable angina does NOT
88
Q

How can an MI present on ECG?

A

STEMI
- ST elevation or new onset LBBB

NSTEMI

  • Trop + ACS without ST segment elevation
  • ECG may show ST depression, T wave inversion, non-specific changes, or be normal
89
Q

What are the symptoms and signs of ACS?

A

Symptoms:

  • Acute central chest pain, lasting > 20min, often associated with nausea, sweatiness, dyspnea, palpitations
  • ACS without chest pain = silent -> mostly in elderly + diabetics
  • Silent MIs present with syncope, pulmonary oedema, epigastric pain, vomiting, post-operative hypotension or oliguria, acute confusional state, stroke, diabetic hyperglycaemic states

Signs:

  • Distress, anxiety, pallor, sweatiness, pulse changes, BP changes, 4th heart sound
  • Signs of heart failure (increased JVP, 3rd heart sounds, bibasal crepitations)
  • Pansystolic murmur (papillary muscle dysfunction/rupture, VSD)
  • Low grade fever
  • Pericardial friction rub/peripheral oedema (may later develop)
90
Q

What tests are done to diagnose ACS?

A
  1. ECG
    - STEMI = classically tall T waves, ST elevation, new LBBB within hours; T wave inversion + pathological Q waves follow over hours to days
    - NSTEMI: ST depression, inverted T waves, non-specific changes, normal ECG
  2. Chest x-ray
    - Cardiomegaly
    - Pulmonary oedema
    - Widened mediastinum
  3. Bloods
    - FBC, U&Es, Glucose, Lipids, Cardiac enzymes
  4. Cardiac Enzymes
    - Troponin levels (T + I most sensitive/specific)
  5. ECHO
    - Regional wall abnormalities
91
Q

What are possible differentials for ACS type symptoms/signs?

A
  1. Stable angina
  2. Pericarditis
  3. Myocarditis
  4. Takotsubo cardiomyopathy
  5. Aortic dissection
  6. PE
  7. Esophageal reflux/spasm
  8. Pneumothorax
  9. Musculoskeletal pain
  10. Pancreatitis
92
Q

What other conditions, outside of MI, can cause a rise in troponin levels?

A
  1. Massive PE (causing RV strain)
  2. Subarachnoid hemorrhage
  3. Burns
  4. Sepsis
  5. Renal failure (consistently elevated troponin!!)

** Normal level < 14ng/L

93
Q

What is the management of ACS?

A
  1. Symptom control
    - GTN spray
    - Opiates
  2. Modify risk factors
    - Stop smoking
    - Treat HTN, diabetes, hyperlipidemia
    - Advise diet high in oily fish, fruit, veggies, fibre, low in saturated fats
    - Encourage daily exercise
  3. Optimize cardioprotective medications
    - Antiplatelets: 75mg aspirin, clopidogrel for 12mo; consider PPI for gastric protection (lansoprazole)
    - Anticoagulate: fondaparinux until discharge
    - B-blocker: reduces heart oxygen demand; slowly increase monitoring pulse + BP (if contraindicated consider diltiazem/verapamil)
    - ACE-inhibitor: in patients with LV dysfunction, HTN, diabetes (monitor renal function)
    - High-dose statin: atorvastatin 80mg
    - Echo to assess LV function. Eplerenone (K+ sparing diuretic) improves outcomes in MI patients with heart failure (LVEF<40%)
  4. Revascularisation
    - STEMI = immediate angiography ± PCI
    - NSTEMI with Grace score > 140 = angiography within 24h
    - NSTEMI with score 109-140 = angiography within 3D
    - NSTEMI low-risk = non-invasive testing
    - Multivessel disease = CABG instead of PCI
94
Q

What are some complications of MI?

A
  1. Cardiac arrest
  2. Cardiogenic shock
  3. LVF
  4. Bradyarrhythmias
  5. Tachyarrhythmias
  6. RVF/infarction
  7. Pericarditis
  8. Systemic embolism
  9. Cardiac tamponade
  10. Mitral regurgitation
  11. Ventricular septal defect
  12. Late malignant ventricular arrhythmias
  13. Dressler’s syndrome
  14. LV aneurysm
95
Q

What is the presentation of Dressler’s syndrome?

A
  • Occurs 1-3weeks post MI
  • Recurrent pericarditis, pleural effusions, fever, anemia, and increased ESR
  • Treatment: NSAIDs, steroids if severe
96
Q

List the adverse effects of amiodarone

A
  1. thyroid dysfunction: both hypothyroidism and hyper-thyroidism
  2. corneal deposits
  3. pulmonary fibrosis/pneumonitis
  4. liver fibrosis/hepatitis
  5. peripheral neuropathy, myopathy
  6. photosensitivity
  7. ‘slate-grey’ appearance
  8. thrombophlebitis and injection site reactions
  9. bradycardia
  10. lengths QT interval
97
Q

What are cardiac and non-cardiac causes of arrhythmias?

A

Cardiac:

  • Ischemic heart disease
  • Structural changes (L atrial dilatation 2º to mitral regurgitation, cardiomyopathy, myocarditis, pericarditis, aberrant conduction pathways)

Non-Cardiac:

  • Caffeine
  • Smoking
  • Alcohol
  • Pneumonia
  • Drugs (B2 agonists, digoxin, L-dopa, tricyclics, doxorubicin)
  • Metabolic imbalance (K+, Ca2+, Mg2+, hypoxia, hypercapnia, metabolic acidosis, thyroid disease)
  • Phaeochromocytoma
98
Q

What is the typical presentation of someone with an arrhythmia?

A
  1. Palpitations
  2. Chest pain
  3. Presyncope/syncope
  4. Hypotension
  5. Pulmonary oedema
99
Q

What investigations would you perform for someone with suspected arrhythmias?

A
  • Bloods (FBC, U&E, Ca2+, Mg2+, TSH)
  • ECG (IHD, AF, short PR interval - WPW syndrome, long QT - metabolic imbalance, drugs, congenital, U waves - hypokalemia)
  • 24h ECG monitoring
  • ECHO looking for structural heart disease, eg. mitral stenosis, HCM
  • Provocation tests: exercise ECG, cardiac catheterization ± electrophysiological studies
100
Q

What is the management of arrhythmias?

A
  1. Conservative
  2. Medical management
  3. Interventional management (i.e. pacemakers, ablation, implantable cardioverter defibrillators)
101
Q

What is sick sinus syndrome?

A

Sick sinus syndrome = usually caused by sinus node fibrosis, typically in older patients.

The sinus node becomes dysfunctional slowing to the point of sinus bradycardia or sinus pauses and in others causing AF or atrial tachycardia.

Symptoms: syncope + pre-syncope, light-headedness, palpitations, breathlessness

Management:

  • Thromboembolism prophylaxis
  • Permanent pacemaker
102
Q

What is the treatment for narrow complex tachycardia?

A

These include AF and atrial flutter

  • DC cardioversion
  • If AVRT/AVNRT suspected try blocking AVN (via adenosine or vagal manoeuvres: carotid sinus massage, valsava manoeuvre)
103
Q

Name 3 broad complex tachycardias

A
  1. Ventricular fibrillation
  2. Ventricular tachycardia
  3. Torsades de pointes
104
Q

How do you manage chronic AF?

A
  • Anticoagulation (heparin)
  • Rate control: B-blocker or Ca2+ channel blocker (first line). If this fails add amiodarone.
  • Rhythm control: Elective DC cardio version. Give amiodarone 4wks before + 12mo after.
105
Q

What are the indications for a pacemaker?

A
  • Complete AV block
  • Mobitz type II AV block
  • Persistent AV block after anterior MI
  • Symptomatic bradycardias (sick sinus syndrome)
  • Heart failure (cardiac resynchronization therapy - if LVEF < 35% and QRS > 0.12s)
  • Drug-resistant tachyarrhythmias
106
Q

What is the treatment of a patient with WPW and AF?

A

Flecainide

- Avoid Diltiazem, verapamil, and digoxin!

107
Q

What is the definition of heart failure?

A

Cardiac output is inadequate for the body’s requirement

  • Systolic Failure: Inability of ventricles to contract normally, resulting in decreased cardiac output. EF < 40%. Causes: IHD, MI, Cardiomyopathy
  • Diastolic Failure: Inability of the ventricle to relax and fill normally, causing increased filling pressures. Typically EF > 50%. Causes: Ventricular hypertrophy, Constrictive pericarditis, Tamponade, Restrictive cardiomyopathy, Obesity
  • Often the two above co-exist
108
Q

What are the symptoms of LVF and RVF?

A

LVF:

  • Dyspnea
  • Poor exercise tolerance
  • Fatigue
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Nocturnal cough (± pink frothy sputum)
  • Cardiac wheeze
  • Nocturia
  • Cold peripheries
  • Weight loss

RVF:

  • LVF
  • Pulmonary stenosis
  • Lung disease (cor pulmonale)
  • Peripheral oedema (up to thighs, sacrum, abdominal wall)
  • Ascites
  • Nausea
  • Anorexia
  • Facial engorgement (peri-orbital oedema)
  • Epistaxis
109
Q

What is the acute + chronic treatment of ACS?

A

Acute:

  • Morphine
  • Oxygen
  • Nitrates (GTN spray or IV)
  • Antiplatelets (aspirin + Ticagrelor) + fondaparinux

Chronic:

  • Aspirin (lifelong) + Ticagrelor (12mo)
  • Atorvastatin
  • Bisoprolol
  • Ramipril
110
Q

What are the investigations for heart failure?

A
  • ECG
  • BNP
  • ECHO
  • FBC, U&E
  • CHEST XRAY
111
Q

What is the New York Classification of Heart Failure?

A 
I = heart disease present, but no undue dyspnea from ordinary activity
II = comfortable at rest, dyspnea during ordinary activities
III = less than ordinary activity causes dyspnea, which is limiting
IV = Dyspnea present at rest, all activity causes discomfort
112
Q

What are the findings of heart failure on x-ray?

A

ABCDE:

  • Alveolar oedema (“bat’s wings”)
  • Kerley B lines (interstitial oedema)
  • Cardiomegaly
  • Dilated prominent upper lobe vessels
  • Pleural Effusion
113
Q

What is the treatment for chronic heart failure?

A
  1. Diuretics (furosemide/bumetanide; thiazide - metalazone)
  2. ACE-inhibitors (ramipril)
  3. B-blockers (Carvedilol)
  4. Mineralocorticoid receptor antagonists (spironolactone)
  5. Digoxin
  6. Vasodilators (hydralazine + isosorbide dinitrate - if intolerant to ACE/ARBs)
114
Q

What conditions cause an elevated BNP?

A
  1. Heart failure
  2. Tachycardia
  3. Cardiac ischemia
  4. COPD
  5. PE
  6. Renal disease
  7. Sepsis
  8. Hepatic cirrhosis
  9. Diabetes
  10. Old age
115
Q

How is hypertensive retinopathy graded?

A
  1. Tortuous arteries with thick shiny walls (silver or copper wiring)
  2. AV nipping (narrowing where arteries cross veins)
  3. Flame hemorrhages + cotton-wool spots
  4. Papilloedema
116
Q

What valvular diseases are affected by infective endocarditis?

A

Mitral regurgitation + aortic regurgitation

117
Q

What is the commonest cause of aortic stenosis?

A

Senile calcification

118
Q

What is the classical presentation triad in aortic stenosis?

A
  1. Angina
  2. Syncope
  3. Heart failure
119
Q

Which heart murmur classically displays bifid p waves (cor mitrale) on ECG?

A

Mitral stenosis

120
Q

What are the extra-cardiac signs of aortic regurgitation?

A
  1. Corrigan’s Sign: carotid pulsation
  2. De Musset’s Sign: head nodding with each heart beat
  3. Quincke’s Sign: capillary pulsations in nail beds
  4. Duroziez’s Sign: in the groin, a finger compressing the femoral artery 2cm proximal to the stethoscope gives systolic murmur; 2cm distal = diastolic murmur
  5. Traube’s Sign: “pistol shot” sound over femoral arteries

Austin Flint murmur = severe aortic regurgitation

121
Q

What are the signs of R heart valve disease (tricuspid regurgitation)?

A
  • Prominent JVP
  • RV heave
  • Pansystolic murmur, heard best at lower sternal edge in inspiration
  • Pulsatile hepatomegaly
  • Jaundice
  • Ascites
122
Q

What cardiac abnormalities are the following patients more likely to have:

  • Hemochromatosis
  • Hypothyroidism
  • Marfan’s Syndrome
  • Rheumatoid arthritis
A

Hemochromatosis = AF, cardiomyopathy

Hypothyroidism = Sinus bradychardia; low pulse pressure; pericardial effusion; coronary artery disease; low-voltage ECG

Marfan’s = Mitral valve prolapse; AR; Aortic dissection

RA = Conduction defects; pericarditis; LV dysfunction; aortic regurgitation; coronary arteritis.

123
Q

What are the symptoms that lead you to a diagnosis of endocarditis until proven otherwise?

A

Fever + new murmur

124
Q

What is the commonest organism for acute infective endocarditis?

A

Staph aureus

125
Q

What are the signs and symptoms of acute myocarditis?

A
  • ACS-like symptoms
  • heart failure symptoms
  • palpitations
  • tachycardia
  • soft S1, S4 gallop
126
Q

What conditions are associated with dilated cardiomyopathy?

A
  • alcohol
  • increased BP
  • chemotherapeutic
  • hemochromatosis
  • thyrotoxicosis
  • viral infection
  • autoimmune
  • Peru/postpartum
  • congenital (x-linked)
127
Q

What are the signs of dilated cardiomyopathy?

A 
Increased pulse
Low BP
Increased JVP
Displaced &amp; diffuse apex beat
S3 gallop
Mitral/tricuspid regurgitation
Pleural effusion
Oedema
Jaundice
Hepatomegaly
Ascites
128
Q

What are the causes of restricted cardiomyopathy?

A 
Idiopathic
Amyloidosis
Hemochromatosis
Sarcoidosis
Scleroderma
Loffler’s eosinophilic endocarditis
Endomyocardial fibrosis
129
Q

What are the causes of acute pericarditis?

A
  1. Idiopathic
  2. Bacteria: TB, Lyme disease, Q fever, pneumonia, rheumatic fever
  3. Viruses: coxsackie, echovirus, EBV, CMV, adenovirus, mumps, varicella, HIV
  4. Fungi/parasitic
  5. Autoimmune: SLE, RA, Vasculitides
  6. Drugs: procainamide, penicillin, isoniazid, hydralazine, chemotherapy
130
Q

What are the symptoms of acute pericarditis?

A

Central chest pain worse on inspiration/lying flat and relieved by sitting forward.

Pericardial friction rub.

Look for evidence of pericardial effusion or cardio tamponade.

Fever may occur.

131
Q

What ECG findings would you see in acute pericarditis?

A

Concave (saddle-shaped) ST elevation + PR depression

132
Q

What are the causes of pericardial effusion?

A

Accumulation of fluid in the pericardial sac (10-50ml)

  • Pericarditis
  • Myocardial rupture
  • Aortic dissection
  • Pericardium filling with pus
  • Malignancy
133
Q

What are the clinical features of pericardial effusion?

A
  • Dyspnea
  • Chest pain
  • Signs of local structures being compressed
  • Muffled heart sounds
  • Look for signs of cardiac tamponade
134
Q

What is the most common cause of constrictive pericarditis outside of the UK?

A

TB

135
Q

What are the clinical features of constrictive pericarditis?

A
  • RHF
  • Increased JVP
  • Kussmaul’s sign (JVP rising paradoxically with inspiration)
  • Soft, diffuse apex beat
  • Quiet heart sounds
  • S3
  • Diastolic pericardial knock
  • Hepatosplenomegaly
  • Ascites
  • Oedema
136
Q

What is cardiac tamponade?

A

A pericardial effusion that raises intrapericardial pressure, reducing ventricular filling and thus dropping cardiac output

Can lead rapidly to cardiac arrest

137
Q

What are signs of cardiac tamponade?

A 
Increased pulse
Decreased BP
Pulsus paradoxus
Increased JVP
Kussmaul's sign
Muffled S1 + S2
138
Q

What is coarctation of the aorta?

A

Congenital narrowing of the descending aorta.

Usually occurs just distal to the origin of the L subclavian artery.

More common in boys.

Associations:

  • Bicuspid aortic valve
  • Turner’s syndrome
139
Q

What are the signs of coarctation of the aorta?

A
  • Radiofemoral delay
  • Weak femoral pulse
  • Increased BP
  • Scapular bruit
  • Systolic murmur (best heard over L scapula)
  • Cold feet
140
Q

What would be visible on chest X-ray in someone with coarctation of the aorta?

A

Rib notching

141
Q

What is Tetralogy of Fallot?

A

Most common cyanotic congenital heart disorder.

Believed to be due to abnormalities in separation of the trunks arterioles into the aorta and pulmonary arteries early in gestation.

Features are:

  1. Ventricular septal defect
  2. Pulmonary stenosis
  3. R ventricular hypertrophy
  4. Aorta overrides the VSD, accepting right heart blood
    (5. ASD)
142
Q

What does Fallot’s Tetralogy look like on ECG? X-ray?

A

ECG:

  • RV hypertrophy
  • RBBB

X-ray:
- Classic boot-shaped heart

Year 3 (7 decks)

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