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MSRA > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Which coronary artery supplies the anterior septum and anterior left ventricular wall?

A

Left anterior descending

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2
Q

Which coronary artery supplies the marginal branches of the left atrium and ventricle?

A

Left circumflex artery

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3
Q

Which coronary artery supplies the right atrium and ventricle?

A

Right coronary artery

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4
Q

Which coronary artery supplies the posterior septum and the posterior right ventricular wall?

A

Right posterior descending

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5
Q

Which coronary artery supplies the sinus and AV nodes?

A

Usually a branch of the RCA but can be left too

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6
Q

How should CHD be investigated?

A
  • Exercise tolerance test
  • Metabolic perfusion scan
  • Stress echo
  • PET
  • Echogardiogram (USS)
  • Cardiac CT
  • Angiography (used to determine management)
  • Nuclear imaging
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7
Q

How is stable angina managed?

A

Antiplatelets - 75mg aspirin daily
Nitrates - GTN spray PRN (can become tolerant)
Either:
- Beta-blockers - atenolol, bisoprolol
- Calcium channel blockers - nifedipine, viramipril (unless used in combo with b-blocker, then give amlodipine or MR nifedipine
Lipid lowering - statins
ACE inhibitors - ramipril

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8
Q

What is ACS?

A
  1. Unstable angina
  2. STEMI
  3. NSTEMI

All 3 involve chest pain at rest or pain not going away - due to atherosclerosis and stenosis of the coronary arteries

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9
Q

Describe how investigations differ in different subtypes of ACS

A

Unstable angina - ECG changes, normal troponin

NSTEMI - ST depression, T wave inversion, raised troponin

STEMI - ST elevation, new LBBB, raised troponin

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10
Q

How should ACS be managed?

A

Morphine ONLY if severe pain (+ antiemetic)
Oxygen (maintain >94%)
Nitrates (GTN spray or IV)
Aspirin (300mg)
Ticagrelor (clopidogrel if high bleed risk or prasugrel if for PCI)
+ Fondaparinux if not having PCI

FOR STEMI or high risk NSTEMI:
- If within 12 hours of symptom onset and PCI can be delivered within 2 hours > PCI (+ prasugrel or clopi if on anticoag).
Give unfractionated heparin with GPI during PCI
Can also consider if after 12h with ongoing ischaemia on ECG

  • If within 12 hours of symptom onset and PCI CANNOT be delivered within 2 hours > fibrinolysis with alteplase (+ ticagrelor). If ECG 90 minutes post fibrinolysis does not show resolution, should be transferred to cardiac centre for PCI
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11
Q

What does PCI involve?

A

Catheter in radial artery is used to place a stent in the coronary arteries in order to open them up.

Uses x-ray to visualise stent.

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12
Q

What is the long term medication for a patient who has had an MI?

A

5 drugs unless contraindicated:
1. Statin
2. ACE inhibitor (BP)
3. B-blocker (cardioprotective)
4. Aspirin (for life!)
5. Ticagrelor/prasugrel/clopidogrel (12 months)

Those with acute MI + LVSF should also start an aldosterone antagonist eg. eplrenone within 3-14 days post MI

Also recommend healthy diet, light exercise
Can have sex 4/52 after uncomplicated MI (no sildenafil until 6 months)

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13
Q

What is the treatment for a patient who has angina which doesn’t respond to treatment, and is not suitable for angioplasty?

A

Coronary artery bypass graft - usually reserved for 3 vessels or more

Uses saphenous and mammary veins.

Less used now as longer recovery time, increased stroke risk despite decreased anginal symptoms

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14
Q

How is a STEMI diagnosed?

A

ECG changes in 2 contiguous leads:

  • 2mm ST elevation in chest leads (1.5mm in women)
  • 1mm ST elevation in limb leads
  • new LBBB
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15
Q

Which leads represent the LAD?

A

V1-4 (chest)

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16
Q

Which leads represent the RCA (inferior MI)

A

II, III, aVf

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17
Q

Which leads represent the LCA (lateral)

A

I, aVL, V5, V6

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18
Q

What can cause ST elevation?

A

LBBB, MI, pericarditis, coronary spasm

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19
Q

What can cause ST depression?

A

Digoxin, myocardial ischaemia, hypokalemia, hypothermia, stroke

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20
Q

Which patients may have an atypical presentation of MI?

A
  • Women

- Diabetics (silent MI)

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21
Q

How is troponin used in MI diagnosis?

A

Take troponin at admission, 6 hours and 24 hours (peak). Levels vary between trusts but are generally above the 99th gentile (>30ng)

Levels decrease to baseline over 5-14 days.

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22
Q

What are the three types of troponin?

A

Troponin C - skeletal muscle
Troponin I - cardiac muscle
Troponin T - cardiac muscle (most sensitive, used in UK)

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23
Q

What can cause a raised troponin?

A

~~~
Cardiac (MI, heart failure)
Trauma
Renal failure
Surgery
Inflammatory states
PE
Sepsis
Burns
Rhadbomyolysis
Drug toxicity

Can also use CK, myoglobin if troponin not helpful

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24
Q

What is prinzmetal angina?

A

Chest pain due to coronary artery spasm, can occur in absence of atherosclerosis.Precipitated by emotional states, cold, drugs, smoking

Pain at rest, shows ST elevation

Give CCBs and GTN (aspirin can aggravate!!)

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25
Q

Which ECG changes occur in acute MI?

A

ST elevation, tall T waves, LBBB

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26
Q

Which ECG changes occur a few days after MI?

A

T wave inversion
Pathological Q wave (think longer and over 25% size of the R wave)

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27
Q

What is a GRACE score?

A

A score system to risk stratify patients with diagnosed ACS to estimate in-hospital admission and 6 month to 3 year mortality - it is also used to decide whether to undergo PCI vs conservative

Looks at:
- age
- HR/BP
- cardiac and renal function
- cardiac arrest on presentation
- ECG findings
- troponin levels

If risk >3% (intermediate), consider PCI within 72h

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28
Q

What are the complications of MI?

A
  • Cardiac arrest
  • Unstable angina
  • Bradycardias/heart block
  • Tachyarrhytmias
  • Heart failure
  • Pericarditis
  • DVT/PE
  • Cardiac tamponade
  • Mitral regurgitation
  • Dresslers syndrome
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29
Q

How do arrhythmias usually present?

A

Palpitation, chest pain, syncope, hypotension, pulmonary oedema

May be asymptomatic

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30
Q

What is long QT syndrome?

A

An inherited condition associated with delayed repolarization of the ventricles which can lead to VT/torsade de pointes. There are 3 types:
LQT1 - associated with exertional syncope eg. swimming
LQT2 - associated with stress related syncope
LQT3 - events occur at night or rest

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31
Q

What causes long QT (>430 in males, >450 in females)?

A

Congenital:
- Jervell-Lange-Nielsen syndrome (includes deafness, due to abnormal K channel)
- Romano-Ward syndrome (no deafness)

Drugs (the usual mechanism of this is by blocking potassium channels):
- Amiodarone, sotalol, class 1a antiarrhythmic drugs
- Antidepressants (TCAs, SSRIs esp citalopram)
- Methadone
- Chloroquine
- Erythromycin
- Haloperidol
- Ondansetron
- Terfenadine (non sedating antihistamine)

Other:
- Electrolytes ( LOW K, Ca, Mg)
- Acute MI
- Myocarditis
- Hypothermia
- SAH

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32
Q

What causes a shortPR?

A

WPW syndrome

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33
Q

What causes U waves?

A

Hypokalemia
Small deflection immediately following the t wave, usually in the same direction

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34
Q

Describe the electrical conduction of the heart

A
  1. Sinoatrial node initiates an electrical impulse causing atrial contraction
  2. Atrial depolarisation (P wave)
  3. Impulse reaches AV node
  4. AV node generates a slow action potential
  5. Activation of the bundle of His and generation of a fast action potential (PR interval)
  6. Impulse conducted to right and left bundle branches
  7. Impulse travels through purkinje fibres causing depolarisation in the ventricles (QRS complex)
  8. Ventricles repolarise and myocardium relaxes (T wave)

NB - atrial repolarisation hidden in QRS complex on ECG

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35
Q

What is heart block?

A

Cardiac electrical disorder defined as impaired conduction from the atria to the ventricles, shown as PR abnormalities and bradycardia on ECG

The severity is described in degrees.

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36
Q

What causes heart block?

A
  • Levs disease (fibrosis/calcification of conduction system)
  • Ischaemic heart disease
  • Cardiomyopathy
  • Myocarditis
  • His Purkinje disease
  • Use of AV nodal blocking agents
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37
Q

What is 1st degree heart block?

A

Electrical impulse moves more slowly through AV node. Common in athletes (increased vagal tone) and caused by certain drugs.

Generally asymptomatic without significant complications.

ECG shows increased PR interval >0.2s

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38
Q

What is 2nd degree heart block - Mobitz I?

A

aka Wenckebachs

PR interval gradually increases until a QRS complex is lost

Due to reversible conduction block at the AV node (athletes, drugs, inferior MI, myocarditis)

Asymptomatic patients dont require treatment - give atropine if symptomatic and stop AV node blocking drugs (ABCD - adensine, beta blockers, CCBs, digoxin)

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39
Q

What is 2nd degree heart block - Mobitz II?

A

Some P waves do not have QRS complexes following them (intermittent non-conducted P waves) without progressive PR prolongation

Due to failure of conductive at the His-Purkinje system (below the AV node), due to drugs, ischaemia, structural damage, hyperkalemia, inflammation

May be symptomatic. More likely to be associated with haemodynamic instability and asystole so need active management with digoxin/pacemaker

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40
Q

What is 3rd degree heart block?

A

No relation between P waves and QRS complexes

Due to complete loss of conduction between atria and ventricles. Perfusing rhythm maintained by a junction or ventricular escape rhythm.

Will be symptomatic (fainting, dizziness, fatigue, SOB, chest pain)

High risk of sudden cardiac death, need urgent monitoring, digoxin, atropine, temporary/permanent pacing

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41
Q

What is a Stokes-Adams attack?

A

Syncopal episode due to a cardiac arrhythmia, most commonly bradycardia/complete heart block

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42
Q

What is bradycardia?

A

Any heart rhythm slower than 60bpm, due to:

  1. Reduced automaticity (sinus node dysfunction) due to increased vagal tone
  2. Conduction block
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43
Q

Why do athletes have bradycardia?

A

Increased vagal tone

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44
Q

How is bradycardia managed?

A

> 40bpm, asymptomatic - no treatment, treat cause (stop drugs, hypothyroidism, sick sinus syndrome)

<40bpm or symptomatic, give atropine up to 6 times > transcutaneous pacing > transvenous pacing or temporary pacing wire if no response

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45
Q

What is sick sinus syndrome?

A

Sinus node dysfunction causing bradycardia and arrest, sinoatrial block or SVT.

Often requires a pacemaker!

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46
Q

What is tachycardia?

A

Any heart rate above 100bpm, due to:

  1. Increased automaticity (exercise, ectopic firing)
  2. Triggered activity (abnormal APs triggered by preceding AP)
  3. Reentry
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47
Q

What causes narrow complex tachycardia (QRS<120)?

A

Narrow complex means that the signal must pass through the AV node

  • Sinus tachycardia
  • Supraventricular tachycardia (p wave absent or inverted)
  • AF (wandering baseline)
  • Atrial flutter (sawtooth)
  • Atrial tachycardia
  • Junctional tachycardia
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48
Q

How are narrow complex tachycardias managed?

A
  1. If patient compromised use DC cardioversion
  2. If not, identify underlying rhythm and treat accordingly
  3. Transient AV block through vagal manoeuvres or IV adenosine
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49
Q

How is SVT managed?

A
  1. Vagal manoeuvres
  2. IV adenosine (6m > 12mg > 18mg UNLESS ASTHMATIC)
  3. IV verapamil (if asthmatic)
  4. DC cardioversion (if treatment refractory or if haemodyamically unstable)

Prevention of future episodes with beta blockers or radiofrequency ablation

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50
Q

How is atrial tachycardia managed?

A
  1. Stop digoxin if this is the cause

2. Maintain potassium levels

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51
Q

What are junctional rhythms?

A

Junctional rhythms occur when the AV node takes over as the main pacemaker of the heart. BUT, AV node can only conduct 40-60 beats
Regular rate, absent p waves, normal QRS

Types of junctional tachycardia:
1. AV nodal re-entry tachycardia
2. AV re-entry tachycardia
3. His bundle tachycardia
OFTEN REQUIRE PACING

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52
Q

How is junctional tachycardia managed?

A
  1. Vagal manoeuvres
  2. IV adenosine
  3. If recurrence, beta blocker or amiodarone
  4. Radiofrequency ablation
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53
Q

What is WPW syndrome (cause, ECG, management?

A

Congenital accessory conduction pathway between the atria and ventricles.

ECG shows short PR interval, wide QRS complex (due to slurred upstroke/delta wave)

Patients present with SVT, AF or atrial flutter.

Refer to cardiologist for electrophysiology and ablation of accessory pathway

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54
Q

What is holiday heart syndrome?

A

Acute arhythmmias due to binge drinking, usually causing SVT and AF

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55
Q

What is atrial fibrillation? What does ECG show?

A

Supraventricular tacchyarrhythmia, characterised by uncoordinated atrial activity. Causes cardiac output to drop as the ventricles aren’t primed reliably by the atria.

ECG shows absent p waves, and irregularly irregular pulse, wandering baseline.

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56
Q

What are the different types of AF?

A

Paroxysmal - episode of AF that terminates spontaneously or with intervention in less than 7 days

Persistent - each episode lasts for longer than 7 days

Permanent - AF that cannot be controlled by medication

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57
Q

What are the symptoms of AF?

A

Palpitations, dyspnoea, angina, dizziness, syncope

May present as stroke, HF

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58
Q

How is acute AF managed (<48h)?

A

Haemodynamically unstable:
- DC cardioversion

Haemodynamically stable:
Offer either rate or rhythm control

RHYTHM
Heparin and either:
- DC cardioversion (this option if haemodynamically unstable)
- Pharmacological cardioversion; IV amiodarone (if structural heart disease) or flecanide

RATE
- Beta blocker/CCB/digoxin

OFFER DOAC IF SINUS RHYTHM NOT ACHIEVED AFTER 48H, HIGH RISK OF RECURRENCE OR HIGH RISK OF STROKE

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59
Q

When should rate control not be offered in non acute AF?

A
  • AF with a reversible causes
  • HF thought to be caused by AF
  • New onset AF
  • Atrial flutter
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60
Q

How is chronic AF managed (>48h)?

A

Offer either rate or rhythm control:

RATE
- Rate control with beta blocker/CCB (verapamil or diltiazem).
- 2nd line - add digoxin
- Consider rhythm if symptoms not controlled on rate control

RHYTHM:
- Amiodarone/dronedarone for 4 weeks then DC cardioversion, then continue amiodarone/dronedarone for 12 weeks after

  • Consider anticoagulation using CHA2DS2VASc score (offer if >=1 in men or >= 2 in women)
  • Lifelong treatment even if reverts to NSR

NB - if cha2ds2vasc 0, needs to have had an echo to exclude valvular heart disease which would be an indication for anticoagulation

61
Q

How is paroxysmal AF managed?

A
  • Pill in the pocket - sotalol or flecainide if no structural heart disease
  • Anticoagulation
  • Consider digoxin mono therapy if very sedentary
62
Q

How do you manageAF, not responding to medical management?

A

Offer left atrial catheter ablation- This is a keyhole technique (surgery performed through a tiny incision), which directs a small, flexible tube (or catheter) to a specific area inside the heart. Once there, it uses heat energy to damage (or ablate) the abnormally active heart muscle.

63
Q

What is the CHA2DS2VASc score and how is it calculated?

A

A score used to determine whether a patient with AF should have long term anticoagulation.

Points scored:
Congestive HF (1)
Hypertension (1)
Age >65 (1)
Diabetes (1)
Stroke/TIA/VTE (2)
Vascular disease (1)
Age >65 (1)
Female (1)

Score 1 or more - consider antiplatelet/anticoagulant

Score 2 or more - start anticoagulant

Note - if pt reverts back to sinus rhythm after 2 episodes, they should stillcontinue anticoagulation

64
Q

Which anticoagulants are used in AF?

A

DOAC- offer if CHADvasc >2, consider if >1

65
Q

What is the ORBIT score?

A

A score calculating bleeding risk whilst on an anticoagulant

Score 1 for:
Age >74
Treatment with antiplatelets
GFR <60

Score 2 for:
Bleeding history
Hb <12 in females, >13 in males

0-2 LOW
3 MODERATE
4-7 HIGH

66
Q

What is atrial flutter? What does ECG show?

A

Tachyarrhythmia in which the atria and ventricles beat at different speeds, usually due to a reentry circuit in the right atrium. Associated with AF!

ECG shows sawtooth appearance, may have 2:1 AV block

nb - AF is when the atria beat irregularly. Flutter is when the atria beat regulalry but at a differet speed to the ventricles

67
Q

How is atrial flutter managed?

A

Haemodynamically unstable:
- DC cardioversion

Stable:
1. B-blocker/CCB/amiodarone
(+ anticaog if appropriate)
2. If unsuccessful, DC cardioversion or ablation (more successful in Afl)

68
Q

What is a broad complex tachycardia?

A

Rate >100 + QRS >120s (3 small sq). This is a tachycardia in which there is dysfunction of the ventricular conduction system (BBB) or a problem with the ventricles themselves.

69
Q

What are the types of broad complex tachycardia?

A
  • VT (most common) - includes torsades de pointes

- VF

70
Q

Which broad complex tachycardias are shockable?

A

VF (looks like bag of worms?)

Pulseless VT

71
Q

How are broad complex tachycardias managed?

A

Regular:
Unstable VT/VF: SHOCK
Stable VT: oxygen, IV amiodarone if monomorphic (load then 24h infusion), IV Mg if polymorphic torsades, consider DC cardioversion
May need ICD long term

Irregular (AF with BBB, AF with ventricular pre-excitation, torsades de pointes):
Seek expert help!

72
Q

What is torsades de points?

A

VT with varying axis (looks like VF) - due to increased QT interval, electrolyte imbalances

73
Q

What are the indications for temporary cardiac pacing?

A
  • Symptomatic bradycardia, unresponsive to atropine
  • After acute MI
  • Suppression of drug-resistant tachyarrhytmias
74
Q

What are the indications for permanent cardiac pacing?

A
  • Complete AV block
  • Mobitz type II
  • Symptomatic bradycardiac
  • Heart failure
75
Q

What is bundle branch block?

A

Cardiac arrhythmia in which one or both bundles of His are delayed or blocked, causing ventricles to beat abnormally

76
Q

What does BBB look like on ECG?

A

RBBB - wide S wave, triphasic QRS (M in V1 and W in V6 MaRRoW) -this can be normal in young healthy patients

LBBB - large R wave, large Q wave (W in V1 and M in v6 WiLLiaM) - this could be a new MI, htn, AS, cardiomyopathy

77
Q

What are systolic and diastolic heart failure?

A

Systolic - inability of ventricle to contract normally causing decreased CO, EF<40%
Caused by IHD, MI, cardiomyopathy

Diastolic - inability of ventricle to relax normally causing increased filling pressures, EF>50%
Caused by constrictive pericarditis, tamponade, restrictive cardiomyopathy, hypertension

These two types usually co-exist?

78
Q

What are left and right heart failure?

A

THINK where does the heart back up to

Left heart failure - causes respiratory symptoms, dyspnoea, poor exercise tolerance, orthopnea, PND, nocturnal cough with pink froth sputum, cardiac asthma

Right heart failure - peripheral oedema, ascites, nausea, pulsation in neck and face

Usually these occur together causing congestive cardiac failure

79
Q

What are acute and chronic heart failure?

A

Acute - new onset or acute decompensation with pulmonary/peripheral oedema, may have signs of hypo perfusion

Chronic - develops slowly with venous congestion

Management is different for both

80
Q

What criteria is used to diagnose congestive cardiac failure?

A

Framingham - CCF requires at least 2 major or 1 major + 2 minor criteria

81
Q

What are the key diagnostic investigations in HF?

A

ECG (may indicate cause) , BNP (>400)- if either abnormal, do ECHO to confirm diagnosis

Caution
- BNP may be falsely high in MI, AF, PE, COPD, liver failure, sepsis, diabetes, renal impairment.
- BNP may be falsely low if the patient is on aldosterone antagonists, ACE inhibitors, ARB, beta blockers or diuretics

82
Q

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

A
  • Cardiomegaly (>50% of the thorax)
  • Kerley B lines
  • Batwing pulmonary oedema
  • Pleural effusions
  • Prominent upper lobe veins
83
Q

What are the signs of heart failure?

A

Cachexia, increased RR and HR, JVP, murmur (if valvular disease), 3rd heart sound, bibasal crops, pitting oedema

84
Q

How is acute heart failure managed?

A

LMNOP

Loop diretics - IV furosemide
Morphine
Nitrates
Oxygen
Positioning

85
Q

How is chronic heart failure managed?

A

1st line:
- ACE-inhibitors - symptomatic and prognostic
- Beta blockers - prognostic
- Loop diuretics - this is symptomatic, not related to mortality

2nd line:
- Spironolactone/eplerenone - add if ongoing symptoms in pts with reduced EF
- SGLT-2 inhibitors, particularly if diabetic

3rd line:
- Ivabradine - if HR >75, EF<35%
- Sacubitril-valsartan - if symptomatic on ACEi/ARB
- Digoxin - if co-existent AF
- Vasodilators (isosorbide, hydralazine) - if intolerant of ACEis/ARB, particularly in Afro-Caribbean patients
- Cardiac resynchronisation therapy (for patients with heart faiure and wide QRS)

86
Q

What is pericarditis?

A

Inflammation of the pericardium causing sharp severe chest pain, worse on inspiration and supine position.

Classically in younger males, after cardiac surgery, viral/bacterial infection or neoplasm, also associated with autoimmune disorders

87
Q

What is the classical clinical triad of pericarditis?

A
  1. Retrosternal chest pain
  2. Pericardial friction rub (high pitched, squeaky rub at left sternal edge with patient leaning forwards at end-expiration)
  3. Serial ECG changes (PR DEPRESSION IS SPECIFIC, widespread saddle ST elevation)

Usualy troponin will be NORMAL, as oppose to myocarditis where it will be high

88
Q

How is pericarditis managed?

A

ALL PATIENTS SHOULD HAVE TTE

If no risk factors - manage as outpatient with NSAIDs/colcihcine and 1 week follow up - continue treating until symptom resolution/normal inflam markers and taper dose

If febrile, high trop or high risk - admit for observation

If purulent - pericardiocentesis and antibiotics

If tamponade - pericardiocentesis

89
Q

What are the complications of pericarditis?

A

Chronic recurrent pericarditis
Constrictive pericarditis
Cardiac tamponade

90
Q

What is constrictive pericarditis?

A

Thickened, fibrotic pericardium limiting cardiac function - due to long term inflammation of the pericardium.

Treat as heart failure

91
Q

What is cardiac tamponade?

A

Accumulation of pericardial fluid, blood, pus or air within the pericardial space.

This increases pressure, restricting cardiac filling and decreasing cardiac output - MEDICAL EMERGENCY

92
Q

What are the signs and symptoms of tamponade?

A

Symptoms - chest pain, syncope

Signs - tachycardia, hypotension (shock), muffled heart sounds, elevated JVP, pulses paradoxus (a fall in BP during inspiration by >10mmHg), positive rub

93
Q

How is tamponade investigated?

A

ECG - electrical alternans (varying height of QRS complex)

ECHO - large effusion, chamber collapse

94
Q

How is tamponade managed?

A

Haemodynamically stable (sBP>110) - anti-inflammatories and observe

Haemodynamically unstable - pericardiocentesis and surgical drainage

95
Q

What is Dresslers syndrome?

A

Perciarditis after MI - will have fever, chest pain, pericarditis

96
Q

What is rheumatic fever?

A

Pharyngeal infection with group A beta-haemolytic streptococci.

Antibody cross reacts with valve tissue and may cause permanent heard damage

97
Q

How do statins work, what are the monitoring requirements and contraindications?

A

Inhibit action of HMG-CoA reductase which is an enzyme involved in cholesterol synthesis

LFTs at baseline, 3 months and 12 months - discontinue treatment if serum transaminases concentrations rise to and persist at 3x the upper limit of the reference range

CI: macrolides, pregnancy

98
Q

Which patients should receive a statin?

  • Established cardiovascular disease (stroke, MI, TIA, IHD, PAD)
  • Q-risk over 10%
  • T1 diabetics >40yo, diagnosed 10y ago or with established neuropathy

Note T2DM should be assess with Q-risk
Use 20mg in primary prevention and 80mg in secondary prevention

A
99
Q

What are the risk factors for infective endocarditis?

A

1st - previous episode of endocarditis
Other - rheumatic valve disease. prosthetic valves, congenital heart defects, IVDU, recent piercings

100
Q

What are the main causative organisms for infective endocarditis?

A
  1. Staph aureus (particularly if acute presentation or IVDU)
  2. Streptococcus viridans (number 1 in developing countries or post dental procedure)
  3. Staph epidermis
  4. Strep bovis (linked with colorectal cancer)
101
Q

What is the main valve affected in infective endocarditis?

A

Mitral valve
Tricuspid valve if IVDU

102
Q

What are the different stages of hypertension?

A

Stage 1: Clinic BP >140/90 and average ABPM/HBPM > 135/85

Stage 2: Clinic BP >160/100 and average ABPM/HBPM >150/95

Severe: Clinic BP >180 or diastolic >120

103
Q

When should stage 1 HTN be treated?

A

Treat if <80yo and any of the following apply:
- Target organ damage
- Established cardiovascular disease
- Renal disease
- Diabetes
- 10y cardiovascular Qrisk >10%

Note if pts <40yo, consider specialist referral to exclude secondary causes

104
Q

How is hypertension treated?

A

Step 1:
If <55 or bg T2DM - ACEi/ARB
If >55, afrocaribbean - CCB or thiazide-LIKE diuretic eg. indapamide (oedema, HF)
If diabetic, regardless of age or ehtnicity - ACEi/ARB

Step 2:
If <55 - add CCB/diuretic
If >55 - add ACEi/ARB/diuretic (note if afrocaribbean, choose ARB over ACEi)

Step 3:
A + C + D

Step 4 (resistant HTN):
Seek specialist advice before adding a fourth drug, consider spironolactone (if K <4.5) /alpha/blocker/beta blocker (if K >4.5)

Remember lifestyle factors!
- Aim <3g/day of salt daily
- Reduce caffeine intake

NB if pt has a history of gout, give CCB instead of thiazide-like diuretic as it may exacerbate his gout

105
Q

What is a hypertensive crisis and how is it managed?

A

Worrying features or acute BP>200 systolic or 120 diastolic

No end-organ damage - oral therapy with CCB/ACe i

Organ damage - admit, closely monitor BP, neuro state, fluid balance, ECG, and give IV labetolol or furosemide (+ hydralazine?)

106
Q

What are the potential complications of MI?

A
  1. Cardiac arrest
  2. Cardiogenic shock
    - if a large part of the myocardium is damaged the EF may decrease causing cardiogenic shock, often need inotropes
  3. Chronic heart failure
  4. Tachyarrhythmias
    - most common is VF
  5. Bradyarrhythmias
    - AV block more common after inferior MIs
  6. Pericarditis
    - common in first 48h following transmural MI
    - may hear a pericardal rub and see an effusion
    - Dresslers is an autoimmune type of pericarditis in which a reaction forms against antigenic proteins formed as the myocardium recovered. Typical to see widespread ST elevation with PR depression, treat with NSAIDs
  7. Left ventricular aneurysm
    - ischaemic damaged from MI weakens the myocardium causing an anuerysm formation
    - this would cause persistent ST elevation and LVF
    - pts should be anticoagulated due to stroke risk
  8. Left ventricular free wall rupture
    - presents as acute HF with features of cardiac tamponade 1-2 weeks post MI
    - urgent pericardiocentesis and thoracotomy are required
  9. Ventricular septal defect
    - presents as acute HF with pansystolic murmur 1 week post MI
    - urgent surgery required
  10. Acute MR
    - common with infero-posterior infarction, due to ischaemia of rupture of papillary muscle
    - presents as acute hypotension and pulmonary oedema with early-to-mid systolic murmur
    - treat with vasodilators, may require surgical repair
107
Q

What are the advantages and disadvantages of bioprosthetic valves?

A
  • Usually bovine or porcine
  • Structurally deteriorate and calcify over time therefore only given to patients over 65/70 yo
  • Advantage is long term anticoagulation not needed (except for warfarin in first 3 months)
  • Pts will be on life long aspirin
108
Q

What are the advantages and disadvantages of mechanical valves?

A
  • Usually bileaflet
  • Low failure rate
  • Major disadvantage is increased thrombosis risk > lifelong warfarin (aim 2.5-3.5 aortic aim 3-4 mitral)
  • Give aspirin if additional indication
109
Q

How are major bleeds on warfarin (regardless of INR) managed?

A

eg. varices, ICH

  • Stop warfarin
  • Give IV vit K 5mg PCC (FFP if not available)
110
Q

How are bleeds on warfarin with INR>8 managed?

A

Major bleeding:
- Stop warfarin
- Give IV vit K1-3mg
- Repeat vit K if INR still high after 24h
- Restart warfarin when INR >5

Minor bleeding:
- Stop warfarin
- Give vit K 1-5mg PO (use IV orally)
- Repeat vit K if INR still high after 24h
- Restart warfarin when INR >5

111
Q

How are bleeds on warfarin with INR 5-8 managed?

A

Minor:
- Stop warfarin
- Give IV vit K 1-3mg
- Restart when INR >5

No bleeding:
- Withhold 1-2 doses of warfarin
- Reduce subsequent maintenance dose

112
Q

What are the clinical features of aortic stenosis?

A
  • Often asymptomatic
  • Mild/moderate AS causes chest pain, dyspnoea, syncope
  • EJECTION SYSTOLIC MURMUR RADIATING TO CAROTIDS (decreased after valsalva)

Severe features:
- Narrow pulse presure
- Slow rising pulse
- Delayed ESM
- Soft or absent S2 or new S4
- Thrills
- LVH or failure

113
Q

What causes aortic stenosis?

A
  • Degenerative calcification (most common in patients >65)
  • Bicuspid aortic valve (most common in patients <65)
  • William’s syndrome (supravalvular aortic stenosis = narrowing of aorta just above the valve)
  • Post-rheumatic disease
  • Subvalvular HCOM
114
Q

How is aortic stenosis managed?

A

Asymptomatic > observe
Asymptomativ with valve gradient >40 with severe features > consider surgery with valve replacement
Symptomatic > valve replacement

Options for AVR:
- Surgical AVR if low risk
- TAVI if high risk
- Balloon valvuloplasty in children without calcification or adults with critical AS

115
Q

What are the clinical features of aortic regurgitation?

A

Can be causes by diseae of aortic valve or by distortion or dilation of the aortic root and ascending aorta

Acute valvular disease:
- Infective endocarditis

Acute aortic root disease:
- Aortic dissection

Chronic valvular disease:
- Rheumatic fever (no 1)
- Calcific valve disease
- Connective tissue disease (RA/SLE)
- Bicuspid aortic valve

Chronic aortic root disease:
- Bicuspid aortic valve
- Spondyloarthropathies
- Hypertension
- Syphilis
- Marfans/ehlers danlos

116
Q

What are the features of aortic regurgitation?

A
  • Early diastolic murmur (intensity increased by handgrip manoeuvr and leaning forward/breathe out and hold)
  • Collapsing pulse
  • Wide pulse pressure
  • Quincke’s sign (nailbed pulse)
  • De Musset’s sign (head bobbing)
  • mid-diastolic Austin-Flint murmur in severe AR
117
Q

How is aortic regurgitation managed?

A
  • Medical management of associated HF
  • Surgery if severe symptomatic or LVEF asymptomatic
118
Q

What are the features of mitral stenosis?

A
  • Obstruction of blood flow across mitral valve leading to increased pressure within the left atrium, pulmonary vasculature and right side of heart
  • Dyspnoea due to PVH
  • Haemoptysis due to pulmonary pressure
  • Mid-late diastolic murmur, best heard when rolling patient to left hand side
  • Loud S1
  • Opening snap (indicates mitral valve leaflets are still mobile)
  • Low volume pulrse
  • Malar flush
  • AF secondary to high atrial pressure and enlargement
119
Q

What are the causes of mitral stenosis?

A
  • Rheumatic fever (main cause)
120
Q

How is mitral stenosis managed?

A

Asymptomatic > regular echos to monitor

Symptomatic > percutaneous mitral balloon valvotomy or mitral valve surgery

Associated AF > anticoagulate with warfarin

121
Q

What are the features of mitral regurgitation?

A
  • Second most common valvular disease after AS
  • Asymptomatic common in healthy patients and doesnt necessarily need treatment
  • Symptoms include fatigue, SOB, oedema due to LVH/arrhythmias/pulmonary hypertension
  • Pansystolic murmur best at apex and radiating to axilla
  • Quiet S1 and split S2
  • Broad p wave on ECG
122
Q

What are the causes of mitral regurgitation?

A
  • Post-MI/coronary artery disease
  • Mitral valve prolapse (trivial)
  • Infective endocarditis (vegetations prevent valve from closing properly)
  • Rheumatic fever
  • Congenital
123
Q

How is mitral regurgitation managed?

A
  • Acutely given nitrates, diuretics, inotropes, balloon pump
  • ACEis/B-blockers for heart failure
  • Surgery if acute and severe > aim to repair rather than replace
124
Q

What causes an ejection systolic murmur?

A

Louder on expiration > AS, HOCM

Louder on inspiration > PS, atrial septal defect

125
Q

What causes a pansystolic murmur?

A
  • Mitral/tricuspid regurgitation
  • Ventricular septal defect
126
Q

What causes a late systolic murmur?

A
  • Mitral valve prolapse
  • Coarctation of the aorta
127
Q

What causes an early diastolic murmur?

A
  • Aortic regurgitation (high pitched and blowing)
  • Pulmonary regurgitation
128
Q

What causes a mid-late diastolic murmur?

A
  • Mitral stenosis (rumbling)
  • Severe aortic regurgitation (asutin flint)
129
Q

What is an S3 and S4 sound?

A

S3:
Caues by the twanging of the chordae tendinae - in young pts this can be normal but in older pts this is likely due to HF as the chordae are weaker

S4:
Always abnormal
Caused by a stiff/hypertrophic ventricle
‘Le lub dub’

130
Q

What is Buerger’s disease?

A

AKA thromboangitis obliterans

  • Small and medium vessel vasculitis that is strongly associated with smoking
  • Symptoms include extremity ischaemia, claudication, ischaemic ulcers, superfical thrombophlebitis and Raynauds
131
Q

What are the side effects of warfarin?

A
  • Haemmorhage
  • Teratogenic (can be used in breastfeeding mothers)
  • Skin necrosis due to reduced protein C (avoid by concurrent heparin)
  • Purple toes
132
Q

What are the features of hypertrophic obstructive cardiomyopathy?

A
  • Autosomal dominent disorder of muscle tissue
  • Mutation in gene encoding B-myosin heavy chaing or myosin-binding protein C
  • Causes LVH > decreased compliance >decreased cardiac output
  • Biopsy shows myofibrillar hypertrophy with chaotic and disorganised fashion myocytes
  • Echo shows MR, SAM ASH - MR, systolic anterior motion, asymmetric hypertrophy
  • Prevalence 1/500
  • Associated with Friedreich’s ataxia and WPW
  • Commonly associated with supraventricular arrhythmias
133
Q

What is the mechanism of sudden death in HOCM?

A

Ventricular tachycardia secondary to ischaemia in the context of extreme exertion

134
Q

How is HOCM managed?

A
  • High dose beta blockers or CCBs (verapamil, diltiazem)
  • Surgical septal myectomy if drug refractory and resting gradient >50 mmHg
  • Dual chamber pacing
  • Alcohol septal ablation (inject alcohol into LAD to cause septal MI which reduces septal hypertrophy)

If sustained or symptomatic VT/VF or high risk for sudden death > offer ICD and/or amiodarone

135
Q

What are the features of dilated cardiomyopathy?

A
  • 90% of cases
  • Causes; idiopathic, IHD, peripartum, HTN, iatrogenic, alcohol/cocaine, inherited, DMD
  • Dilated heart leads to predominantly systolic dysfunction
  • All 4 chambers dilated but left ventricle more so
  • Causes classical findings of HF
  • Balloon appearance on CXR
136
Q

What is restrictive cardiomyopathy?

A
  • Diastolic dysfunction of a non-dilated ventricle
  • Least common of cardiomyopathies
  • Caused by amyloid/sarcoid/genetics
137
Q

What is Takotsubo cardiomyopathy?

A

AKA broken heart syndrome

  • Sudden dysfunction of the left ventricle of heart, symptoms alike MI but in the absence of significant CAD
  • Usually due to severe emotional or physical stress
  • Treat similar to STEMI with antiplatelets, statins, beta blockers, ACE/ARB
138
Q

What are the features of arrhythmogenic right ventricular cardiomyopathy?

A
  • Second most common cause of sudden death after HOCM
  • Autosomal dominant
  • Right ventricular myocardium replaced by fatty and fibrofatty tissue
  • Mutation in gene which encodes desmosome
  • Presents as palpitations/syncope/SCD
  • ECG shows epsilon wave and TWI v1-v3
  • Echo not particularly helpful, MRI shows fibrofatty tissue
139
Q

How is ARVC managed?

A
  • Sotalol
  • Catheter ablation to prevent VT
  • ICD
140
Q

What is Naxos disease?

A
  • Autosomal recessive variant of ARVC
  • Causes triad of ARVC, palmoplantar keratosis and wooly hair
141
Q

What is Brugada syndrome?

A
  • Autosomal dominant disease with mutation in SCN5A gene which encodes the myocardial sodium ion channel protein
  • May present as sudden cardiac death
  • More common in Asians
  • ECG shows convex ST elevation and partial RBBB
  • ECG changes EXACERBATED by fleicanide or ajmaline; this is diagnositc
  • Manage with ICD
142
Q

What are the features of Wolff-Parkinson White syndrome?

A
  • Congenital accessory conducting pathway between atria and ventricles leading to atrioventricular re-entry tachycardia
  • Can degenerate radpidly to VF
  • ECG shows short PR, wide QRS with slurred upstroke (delta wave)
  • Associated with HOCM, mitral valve proplapse, thyrotoxicosis
143
Q

What are the two types of WPW?

A

Type A - left sided pathway, causes RAD and dominant R wave in V1

Type B - right sided pathway, causes LAD and NO dominant R wave

144
Q

How is WPW managed?

A

Definitive - radiofrequency ablation of accessory pathway

Medical - sotalol (provided no AF), amiodarone, flecanide

145
Q

What are the uses and side effects of nicorandil?

A

Use - vasodilatory drug used in angina

SE - headache, flushing, skin/mucosal/eye/GI ulcers

146
Q

What does it mean if someone has 1st degree heart block after an MI?

A

MI has affected inferior leads (right coronary arteries also provide blood supply to the AV node) - II, III, avF will have ST elevation

146
Q

What are the DVLA rules for cardiovascular disorders?

A

Hypertension:
- Can drive unless Group 2 in which you can only drive if <180/100 consistently

Angioplasty:
- 1 week off

CaBG:
- 4 weeks off

ACS (medical treatment):
- 4 weeks off

Pacemaker:
- 1 week off

Angina:
- Cannot drive if symptoms at rest of at the wheel

ICD:
- 1 month if prophylactic insertion
- 6 monhts if implanted for sustained ventricular arrhythmia

Aortic aneurysm:
- If >6cm, notify VLA, they will decide
- If >6.5cm, can’t drive

Heart transplant:
- 6 weeks off, no need to notify DVLA

147
Q

What monitoring is indicated when prescribing ace inibitors?

A
  • Check U&Es before treatment initiation and after increasing dose
  • A change in the creatinine of up to 30% from baseline and potassium up to 5.5 is deemed acceptable
148
Q
A

MSRA (24 decks)

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