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MSRA Content > Cardiovascular - Level 2 > Flashcards

Cardiovascular - Level 2 Flashcards

1
Q

Description of pathology of stable angina?

A
  • Pain (discomfort) arising from the heart due to myocardial ischaemia
  • Coronary artery disease – atherosclerotic plaques cause progressive narrowing of the arteries (coronary), decreasing blood supply and thus oxygen/nutrients to myocardium
  • Symptoms occur when blood flow does not provide adequate oxygen in times of high demand (exercise)
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2
Q

Epidemiology of stable angina?

A
  • More than 1.5 million in UK

- CVD accounts for 25% of deaths – CHD 45% of CVD deaths

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3
Q

Risk factors of stable angina?

A
  • Older age, male gender, ethnicity
  • Hyperlipidaemia, hypertension, DM, obesity
  • Smoker, FHx, lack of exercise, high fat diet, stress, alcohol
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4
Q

Symptoms of stable angina?

A

Central, crushing, retrosternal chest pain
o Comes on exertion, relieved by rest, exacerbated by cold weather, anger and excitement
o Radiates to arms, shoulders, jaw and neck

Provoked by physical exertion, especially after meals, anger and in cold weather

Pain fades within minutes with rest

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5
Q

Symptoms of decubitus angina?

A

o Angina lying down, associated with LV dysfunction due to CAD

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6
Q

Symptoms of nocturnal angina?

A

o Occurs at night and may wake patient, provoked by vivid dreams
o Usually in critical CAD and may be vasospasm

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7
Q

Symptoms of variant (prinzmetal) angina?

A

o Without provocation, usually at rest due to coronary artery spasm
o Often women, ST elevation during pain/spasm

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8
Q

Symptoms of unstable angina?

A

o Classed as ACS

o Increasing rapidly in severity, occurs at rest with <1 month onset

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9
Q

Who to refer in stable angina?

A
  • Refer all people with typical or atypical angina to specialist chest pain clinic
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10
Q

Management of stable angina whilst awaiting diagnosis?

A

o Sublingual GTN spray used to relieve symptoms
 If they experience chest pain, stop and rest, use GTN as instructed
 Take 2nd dose after 5 mins, if pain still present call 999

o Aspirin (75mg) if likely to be stable angina

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11
Q

Initial tests in specialist chest pain service of stable angina??

A

 Bloods
• FBC (anaemia), TFTs, HbA1c, Lipids

 ECG
• May show ST depression, T wave flattening/inversion, pathological Q waves, LBBB

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12
Q

Diagnostic imaging in specialist chest pain service of stable angina??

A

 1st line - CT coronary angiography
 2nd line - Non-invasive functional imaging, offer when CT angiogram has shown CAD of uncertain functional significance or non-diagnostic
• Myocardial perfusion scintigraphy with SPECT
• Stress Echo
• Contrast MRI
 3rd line – Invasive coronary angiography, if results inconclusive

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13
Q

Investigations if known CAD in stable angina? Criteria for this?

A

o If known CAD (previous MI, revascularisation, previous angiograpy)
 Exercise testing ECG – ST depression <6 mins

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14
Q

Diagnosis of angina confirmed when?

A
  • Significant CAD during invasive or 64-slice CT angiography or,
  • Reversible myocardial ischaemia during non-invasive functional imaging
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15
Q

General advice given in management of stable angina?

A

o Lose weight, regular exercise, control DM
o Stop smoking, limit alcohol consumption
o Impact of stress on angina
o Take GTN before sex if needed
o Inform DVLA

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16
Q

Drug treatments given in stable angina?

A

o Sublingual GTN spray (sublingual tablets) used to relieve symptoms
 If they experience chest pain, stop and rest, use GTN as instructed
 Take 2nd dose after 5 mins, if pain still present call 999

o Beta-blocker/CCB (N-DHP) (1st line regular)
 Use both if symptoms persist (BB & DHP CCB)
 Alternatives if cannot tolerate BB/CCB or both CI: Isosorbide mononitrate, nicorandil, ivabradine, ranolazine

o Monitor 2-4 weeks after starting or changing dose

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17
Q

Secondary prevention of CVD in stable angina?

A

o Aspirin 75mg OD
o Atorvastatin 80mg OD
o ACEi (if hypertensive/diabetic)

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18
Q

Follow up in stable angina?

A

o Review every 6-12 months depending on severity

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19
Q

When to refer to cardiologist and for what in stable angina?

A
  • Referral to cardiologist for angiography (and possible revascularisation) if:
    o Extensive ischaemia on ECG
    o On optimal drug treatment given (2 drugs max doses)
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20
Q

Definitive management for patient of stable angina - for people adequately controlled on medical therapy?

A

 Consider further functional or anatomical testing (if not already available) to assess whether benefit from surgery

 Coronary angiogram – if functional testing indicates extensive ischaemia or likely left main stem or proximal three-vessel disease

 Coronary Artery Bypass Graft (CABG) if left main stem disease or proximal three-vessel disease

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21
Q

Definitive management for patient of stable angina - for people not adequately controlled on medical therapy?

A

 Revascularisation (CABG/PCI)

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22
Q

Management if remain symptomatic despite reperfusion interventions?

A

o Offer Myocardial perfusion scintigraphy using SPECT

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23
Q

Complications of stable angina?

A
  • Stroke, MI, Unstable angina
  • Sudden Cardiac death
  • Reduced QoL and anxiety
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24
Q

Prognosis of stable angina?

A
  • Indicators of prognosis – extent and severity of CAD, LV function, exercise tolerance and comorbidities
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25
Q

Description of AF?

A
  • Atrial activity chaotic and ineffective, rapidly firing cells cause conduction through atria but only proportion activate AV node
  • Irregular ventricular RR intervals and often >160bpm – atrial rhythm 300-600bpm
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26
Q

Definition of paroxysmal AF?

A

2 or more episodes >30 seconds but <7days and self-terminating/recur
rent

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27
Q

Definition of persistent AF?

A

o Episodes >7 days

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28
Q

Definition of permanent AF?

A

o AF fails to terminate using cardioversion or > 1 year where cardioversion is not indicated

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29
Q

Definition of atrial flutter?

A

o Abnormal, rapid heart rhythm

o Macro-reentrant tachycardia

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30
Q

Types of atrial flutter?

A

 Typical – origin in right atrium at level of tricuspid valve
 Atypical – Origin elsewhere in right or left atrium

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31
Q

How common is AF?

A
  • Most common sustained arrhythmia – 10% of patients >65 years
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32
Q

Causes of AF?

A
  • IHD
  • Hypertension
  • Valvular heart disease
  • Hyperthyroidism
  • Rheumatic heart disease
  • Sick sinus syndrome
  • Heart failure
  • Cardiomyopathy
  • Thyroxine, bronchodilators
  • Acute infection
  • PE
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33
Q

Risk Factors for AF?

A
  • Caffeine
  • Alcohol intake
  • Obesity
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34
Q

Symptoms of AF?

A 
o	Asymptomatic
o	Chest pain
o	Palpitations
o	SOB
o	Syncope
o	Reduced exercise tolerance
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35
Q

Signs of AF?

A

o Irregularly irregular pulse
o Tachycardia
o 1st HS variable intensity
o Signs of reduced LVF

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36
Q

Investigations to perform if suspected AF?

A
  • Pulse – irregularly irregular
  • ECG
    o No P waves, chaotic baseline, irregularly irregular rate
    o Tachycardia
    o Atrial flutter- sawtooth baseline prominent in AVF, II, III and V1
  • Bloods
    o FBC, Ca, Mg, glucose, TFTs, U&Es, Cardiac enzymes
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37
Q

Investigations to perform if paroxysmal AF suspected?

A

o 24-hour ambulatory ECG monitor/7-day Holter monitor

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38
Q

Management of acute AF (<48 hours) - investigations?

A

Investigations
o Bloods – FBC, VBG, TFT, LFT, U&E
o CXR

Are there signs of haemodynamic instability?
o BP<100
o Tachycardia
o LoC or dizziness

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39
Q

Management of acute AF (<48 hours) - if no life-threatening signs of haemodynamic instability?

A

Offer rate or rhythm control if <48 hours
 BB or CCB – target HR<110bpm
Consider cardioversion
 Electrical DC cardioversion
 Pharmacological
• IV amiodarone (preferred in structural heart disease) or IV flecainide

Offer rate control if >48 hours

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40
Q

Management of acute AF (<48 hours) - if haemodynamically unstable?

A 
o	O2
o	Emergency electrical DC cardioversion 
o	Treat cause
o	Verapamil/Bisoprolol
o	LMWH
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41
Q

Management of chronic AF - rate control?

A

 Monotherapy Beta-blocker/CCB (bisoprolol/diltiazem)
 Add on other drug if not controlled with monotherapy
 Digoxin if needed/sedentary

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42
Q

Management of chronic AF - rhythm control?

A

o Refer to cardiologist for consideration of rhythm-control

o Rhythm Control (if symptoms continue after HR control or not successful)

 DC cardioversion
• DC if <48 hours
• If >48 hours, need 3 weeks anticoagulation and 4 weeks after
• Amiodarone for >4 weeks before and 12 months after

 Pharmacological cardioversion
• Flecainide
• Amiodarone (if structural heart disease)

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43
Q

Management of chronic AF - rhythm control if drug measures fail?

A
  • Catheter ablation of left atrium or AV node or pulmonary veins
  • Pacing?
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44
Q

Management of chronic AF - paroxysmal specifically?

A

 PRN flecainide – Pill in the pocket

• If no LVHF, valvular disease, IHD, have BP >100 and HR >70

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45
Q

Management of chronic AF - anticoagulation?

A

o Use CHA2DS2-VASc stroke-risk score and HASBLED major-bleed score to assess risk – IN NON-VALVULAR DISEASE (valvular disease ALWAYS ANTICOAGULATE – mitral regurgitation or prosthetic valve)

o Offer anticoagulation when CHADVASc score of 2 or above/1 or above in men
 DOACs (Apixaban/dabigatran) or warfarin (if DOACs not tolerated)
 Calculate TTR at each visit (Rosendaal method)
 Review annually

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46
Q

When to review anticoagulation in AF?

A

o Review at aged 65 if not taking anticoagulant or when they develop diabetes, HF, PAD, CHD, CVA

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47
Q

Management of chronic AF - general advice?

A

o Harmful alcohol consumption
o Inform DVLA
o Flying OK

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48
Q

Management of chronic AF - Follow up?

A

o 1 week of starting rate-control treatment

o After starting anticoagulation treatment
 Warfarin
• Calculate time in therapeutic range (TTR) and INR
• Poor control need correction of compliance, medications, lifestyle factors such as diet and alcohol
 Dabigatran/Apixaban
• Calculate time in therapeutic range (TTR)
• At least annually

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49
Q

Complications of AF?

A
  • Stroke and thromboembolism
  • Heart Failure
  • Tachycardia-induced cardiomyopathy
  • Reduced QoL
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50
Q

Prognosis of AF?

A
  • 2x more likely to die prematurely
  • Associated with CVD
  • 5x more likely for stroke
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51
Q

Description of SVT?

A
  • Supraventricular tachycardia is narrow complex tachycardia

- Rate>100bpm, QRS<120ms

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52
Q

Pathology of SVT?

A

o Reentry circuit forming next to, or within, the AV node

o The circuit most often involves two tiny pathways one faster than the other

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53
Q

Types of narrow complex tachycardias?

A 
o	Sinus tachycardia
o	SVT
o	AF
o	Atrial flutter
o	Atrial tachycardia
o	Junctional tachycardia
o	WPW
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54
Q

Symptoms and signs of SVT?

A
  • Palpitations
  • Chest pain
  • Presyncope/Syncope
  • Hypotension or pulmonary oedema
  • SOB
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55
Q

ECG findings in SVT?

A

o Regular rhythm
o High HR
o P waves absent or inverted after QRS (merged in T wave)
o Normal QRS

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56
Q

Initial management of tachyarrhythmias?

A

o Monitor O2, give oxygen if hypoxic
o Monitor ECG and BP and record 12-lead ECG
o Obtain IV Access
o Identify and treat any electrolyte abnormalities (K, Mg, Ca)
 Bloods – U&Es, cardiac enzymes, Ca, Mg, K
 VBG
 ABG (if pulmonary oedema, sepsis)

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57
Q

Management of tachyarrhythmias - assessing for adverse features? What are they? Management of yes or no?

A 
o	Shock (sBP<90, pallor, sweating, cold, clammy, confusion)
o	Syncope (transient LoC)
o	Myocardial ischaemia (typical chest pain and/or MI on ECG)
o	Heart failure (pulmonary oedema and/or raised JVP)

 If yes, Synchronised DC cardioversion – up to 3 attempts
• Then Amiodarone 300mg IV over 10-20 mins and repeat shock then 900mg over 24 hours
• Correct K and Mg
• Further cardioversion if needed
• Consider flecainide, lidocaine

 If no, move down
• Correct K and Mg

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58
Q

Management of tachyarrhythmias - assessing QRS complexes?

A

o If >0.12s – broad complex tachycardia treatment

o If <0.12s – narrow complex tachycardia – move below

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59
Q

Management of tachyarrhythmias - assessing rhythm - if irregular narrow complex?

A

o Irregular – Treat as AF
 Rate control with B-Blockers or digoxin
 If <48h – cardioversion with either amiodarone 300mg IVI over 20-60 mins then 900mg over 24h or DC shock
 Anticoagulation

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60
Q

Management of tachyarrhythmias - assessing rhythm - if regular narrow complex tachycardia?

A

o Regular Narrow complex tachycardia
 Vagal manoeuvres (carotid sinus massage, Valsalva manoeuvre)
 Adenosine 6mg IV bolus
• 2nd 12 mg and then 3rd 12mg if needed
• CI in 2o and 3o heart block, WPW and asthmatics
 Continuous ECG trace
 If adenosine fails, Verapamil 5mg IV over 2-3 mins (not if on BB)
• 2nd 5mg if <60

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61
Q

What happens if management of regular narrow complex tachycardia does not resolve with initial management?

A

 If resolves, probable re-entrant paroxysmal SVT

 If still not resolved – expert help

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62
Q

Description of VT?

A 
-	Broad complex tachycardias
o	ECG shows rate >100bpm with QRS >120ms
-	Ventricular tachycardia defined as >3 ventricular complexes at rate of >100
-	If >30s – sustained
-	Can be monomorphic or polymorphic
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63
Q

Pathology of VT?

A

o The electrical signals causing this rapid beating originate in the ventricles
o May lead to life threatening conditions such as ventricular fibrillation, asystole and sudden death

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64
Q

Predisposing condition to VT?

A 
o	Brugada syndrome
o	WPW
o	Prolonged QT (Macrolides, metoclopramide, TCA, haloperidol, methadone)
o	Abnormal K, low Mg, low Ca
o	Structural heart disease
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65
Q

Symptoms and signs of VT?

A
  • Palpitations
  • Chest pain
  • Presyncope/Syncope
  • Hypotension or pulmonary oedema
  • SOB
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66
Q

What is Torsades de pointes?

A

o Polymorphic VT associated with low Mg, K, long QT)
o QRS undulate in amplitude and may degenerate VF
o Rx with magnesium sulphate

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67
Q

ECG findings in VT?

A

o Regular, tachycardia
o Broad QRS, often bizarre
o Positive QRS concordance in chest leads
o Marked left axis deviation
o AV dissociation or AV block
o Fusion beats (normal beat fuses with VT complex)
o Capture beats (normal QRS between abnormal beats

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68
Q

Initial management of tachyarrhythmias?

A

o ABCDE Approach
o Monitor O2, give oxygen if hypoxic
o Monitor ECG and BP and record 12-lead ECG
o Obtain IV Access
o Identify and treat any electrolyte abnormalities (K, Mg, Ca)
 Bloods – U&Es, cardiac enzymes, Ca, Mg, K
 VBG
 ABG (if pulmonary oedema, sepsis)

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69
Q

Management of tachyarrhythmias - adverse features?

A 
o	Shock (sBP<90, pallor, sweating, cold, clammy, confusion)
o	Syncope (transient LoC)
o	Myocardial ischaemia (typical chest pain and/or MI on ECG)
o	Heart failure (pulmonary oedema and/or raised JVP)

 If yes, Synchronised DC cardioversion – up to 3 attempts
• Then Amiodarone 300mg IV over 10-20 mins and repeat shock then 900mg over 24 hours
• Correct K and Mg
• Further cardioversion if needed
• Consider flecainide, lidocaine
 If no, move down
• Correct K and Mg

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70
Q

Management of tachyarrhythmias - assessing QRS complex and assessing rhythm?

A
  • Assess QRS complex
    o If >0.12s – broad complex tachycardia – see below
  • Assess rhythm
    o Irregular – Seek expert help
     Possible AF with BBB, pre-excited AF or polymorphic VT
    o Regular – move on
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71
Q

Management of regular broad complex tachycardias?

A

o Amiodarone 300mg IV over 20-60 mins via central line
o Then Amiodarone 900mg over 24 hours
o May need cardioversion

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72
Q

Description of mitral stenosis?

A
  • Fusion, thickening and immobility of valves leaflets reduces orifice area and leads to obstruction from LA to LV
  • Atrial pressure elevates and leads to pulmonary hypertension and RVF
  • Normal mitral valve orifice area is 4-6cm2 but severe stenosis is <1cm2
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73
Q

Epidemiology of mitral stenosis?

A
  • 50% had rheumatic fever and 90% had rheumatic heart disease
  • Women > Men
  • Usually in 4th and 5th decades
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74
Q

Causes of mitral stenosis?

A 
o	Rheumatic heart disease following rheumatic fever
	Group A beta-haemolytic streptococci
	RF: overcrowding, poor hygiene
	Symptoms: sore throat (3 weeks prior), arthritis, carditis, chorea, subcutaneous nodules, fever, ESR/CRP raised
	Ix: antibody titres, throat swab, ECG
	Rx: Penicillin, aspirin 
o	Congenital
o	Carcinoid tumours
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75
Q

Symptoms of mitral stenosis?

A 
o	Exertional dyspnoea (worsening)
o	Orthopnoea
o	Productive blood-tinged cough
o	Palpitations (AF)
o	Chest pain
o	Fatigue
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76
Q

Signs of mitral stenosis?

A 
o	Malar flush
o	Low volume pulse
o	AF
o	Tapping apex beat
o	Loud S1
o	Rumbling mid-diastolic murmur (worse on expiration, left side)
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77
Q

Investigations of mitral stenosis?

A
  • ECG
    o Progressive RAD, AF, LA hypertrophy (bifid P wave), RVH
  • CXR
    o Left atrial enlargement, pulmonary oedema, calcifications
  • Transthoracic Echo
    o Diagnostic – hockey stick-shaped mitral deformity
    o Used to measure mitral orifice area and assess pulmonary artery pressure
  • Cardiac Catheterisation
    o If surgical correction planned, severe
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78
Q

Management of mitral stenosis - if asymptomatic?

A

o No treatment

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79
Q

Management of mitral stenosis - if symptomatic?

A

o Diuretics (furosemide 40mg)
o Surgery
 Percutaneous balloon valvotomy
 Mitral valve repair/replacement

  • Follow Up
    o Annual
80
Q

Complications of mitral stenosis?

A 
o	AF
o	Pulmonary hypertension
o	Emboli
o	Hoarseness
o	Dysphagia
o	Infective endocarditis (rare)
81
Q

Description of mitral regurgitation?

A
  • Mitral valve consists of anterior and posterior leaflets, chordae tendineae, anterolateral and posteromedial papillary muscles and mitral annulus
  • Mitral valve regurgitation may result from defects in any part of valve
82
Q

Pathology of mitral regurgitation?

A

o Longstanding regurgitation produces increase in atrial pressure and dilatation
o Increase can cause pulmonary hypertension and oedema – LV dilatation

83
Q

How common is mitral regurgitation?

A
  • 2nd most prevalent valve disease after aortic stenosis
84
Q

Aetiology of mitral regurgitation?

A 
o	Functional (LV dilatation)
o	Annular calcification
o	Rheumatic heart disease
o	Mitral valve prolapse
o	Infective Endocarditis
o	Ruptured chordae tendineae
o	Papillary muscle rupture
o	Hypertrophic Cardiomyopathy
o	Ehlers Danlos Syndrome
85
Q

Symptoms of mitral regurgitation?

A 
o	SOB (exertional)
o	Fatigue
o	Lethargy
o	Palpitations
o	Oedema
86
Q

Signs of mitral regurgitation?

A 
o	Heart failure
o	Apex beat laterally displaced
o	RV heave
o	Soft S1
o	S3 in early diastole 
o	Pansysytolic murmur
	Loudest at apex, radiates axilla
87
Q

Investigations of mitral regurgitation?

A
  • ECG
    o AF, P-mitrale, LVH
  • CXR
    o Dilated LA/LV, calcification, pulmonary oedema
  • Transthoracic or oesophageal Echo
    o Assess severity and function
  • Doppler
    o Assess severity of regurgitation, LV dimensions and size and function of RV
  • Catheterisation
    o Exclude other valve disease, assess CAD
88
Q

Management of severe, acute mitral regurgitation?

A 
o	Annuloplasty or mechanical valve
o	Diuretics (furosemide)
89
Q

Management of chronic mitral regurgitation - asymptomatic?

A

 If LVEF >60%
• ACE inhibitors (captopril/enalapril/lisinopril)
• Beta-blockers (metaprolol/atenolol)

 If LVEF <60%
• Valvuloplasty/annuloplasty/mechanical/prosthetic valve replacement

90
Q

Management of chronic mitral regurgitation - symptomatic?

A

 LVEF >30%
• Valvuloplasty/ annuloplasty/ mechanical/ prosthetic valve replacement
• ACE inhibitor (captopril/enalapril/lisinopril)
• Beta-blocker (metaprolol/atenolol)
• Diuretic (furosemide)

 LVEF <30%
• ACE inhibitor (captopril/enalapril/lisinopril)
• Beta-blocker (metaprolol/atenolol)
• Diuretic (furosemide)
• Intra-aortic balloon counterpulsation (reduces afterload)

91
Q

Follow up of chronic mitral regurgitation?

A

o Regular follow up and echocardiogram

92
Q

Complications of chronic mitral regurgitation?

A 
o	Prosthesis stenosis
o	AF
o	Pulmonary Hypertension
o	Post-operative stroke
o	Heart Failure
93
Q

Prognosis of chronic mitral regurgitation?

A

o Progression variable

o May remain asymptomatic for many years

94
Q

Description of aortic stenosis?

A
  • Degeneration and calcification of aortic valve
    o Endocardium of valve damaged and inflamed, leading to deposition of calcium on valve – limits aortic leaflet mobility and stenosis
    o Occurs slowly and pressure overload leads to LVH (increased afterload)
    o Increased myocardial oxygen demand, relative ischaemia
95
Q

Epidemiology of aortic stenosis?

A
  • Most common valvular disease
  • 2nd most common cause for cardiac surgery
  • Incidence highest in over 70s
  • Bicuspid valve and William’s syndrome present earlier
96
Q

Risk factors of aortic stenosis?

A

o Advanced age
o Congenital bicuspid valve
o Rheumatic fever
o CKD

97
Q

Aetiology of aortic stenosis?

A

o Senile degeneration
o Congenital (bicuspid valve, Turner’s syndrome, William’s syndrome)
o Rheumatic heart disease

98
Q

Symptoms of aortic stenosis?

A
  • Usually asymptomatic until <1/3 normal size
-	Symptoms
o	Exertional SOB
o	Angina
o	Exertional syncope
o	Dizziness
99
Q

Signs of aortic stenosis?

A 
o	Congestive heart failure
o	Slow rising pulse
o	Narrow pulse pressure
o	Heaving, non-displaced apex
o	LV heave, aortic thrill
o	Ejection systolic murmur
	Heard best at right sternal edge, radiates to carotid
o	Ejection click (or S4)
100
Q

Investigations and their findings in aortic stenosis?

A
  • ECG
    o P-mitrale
    o LVH with strain pattern (T-wave inversion, ST depression)
    o LBBB or complete block
  • Transthoracic Echo & doppler
    o Diagnostic – elevated aortic pressure gradient, measures valve area and LVEF
  • CXR
    o LVH, calcified aortic valve, post-stenotic dilatation of ascending aorta
  • Cardiac Catheterisation
    o Used if echo inconclusive
    o Assess function and CAD but risks emboli
101
Q

Management of aortic stenosis - asymptomatic?

A

follow up and echo

102
Q

Management of aortic stenosis - symptomatic?

A

o Surgery
 Aortic valve replacement
 TAVI

o Anticoagulation
 Vitamin K antagonist (warfarin)
• If prosthetic mechanical valve

103
Q

Management of aortic stenosis - general management?

A

o Good oral hygiene

104
Q

Complications of aortic stenosis?

A

o Congestive heart failure
o Infective endocarditis
o Systemic emboli

105
Q

Definition of aortic regurgitation?

A
  • Diastolic leakage of blood from aorta into left ventricle
  • Due to inadequate coaptation of valve leaflets
  • Leads to LV hypertrophy and dilatation
  • Stroke volume increases and pulse pressure rises
106
Q

Acute risk factors of aortic regurgitation?

A

 Infective Endocarditis
 Ascending aortic dissection
 Chest trauma

107
Q

Chronic risk factors of aortic regurgitation?

A 
	Congenital – bicuspid aortic valve
	Connective tissue disorders (Marfans, Ehlers-Danlos)
	Rheumatic fever
	Takayasu arteritis
	RA
	SLE
	Hypertension
	Syphilis
108
Q

Symptoms of aortic regurgitation?

A 
o	Exertional SOB, orthopnoea, PND
o	Palpitations (pounding)
o	Angina
o	Syncope
o	Congestive heart failure
109
Q

Signs of aortic regurgitation?

A

o Collapsing (Waterhammer pulse)
o Wide pulse pressure
o Displaced laterally-thrusting apex beat
o High-pitched early diastolic murmur
 Heard best in aortic area on expiration, with patient sitting forwards

110
Q

Investigations of aortic regurgitation?

A 
Investigations	-	ECG
o	LVH (strain pattern -  T-wave inversion, ST depression)
  • Echocardiogram & Doppler
    o Diagnostic
  • CXR
    o Cardiomegaly, dilatation of ascending aorta, pulmonary oedema
  • Cardiac Catheterisation
111
Q

Management of aortic regurgitation - asymptomatic?

A

Asymptomatic patients (LVEF>50%):
o Regular 6-12 month follow up and echo
o ACE inhibitors – if hypertensive

112
Q

Management of aortic regurgitation - symptomatic?

A
  • Symptomatic patients, enlarging heart, ECG changes, LVEF <50%:
    o Aortic valve replacement
    o TAVI
113
Q

Management of acute, severe aortic regurgitation?

A

o Inotropes and vasopressors

o Urgent aortic valve replacement

114
Q

Definition of infective endocarditis?

A
  • Infection of endocardium of heart valve
  • Mass of fibrin, platelets and infectious organisms form vegetations along edges of valves
  • Virulent organisms destroy valve and produce regurgitation
115
Q

Risk factors of infective endocarditis?

A 
Cardiac disease
	Valvular heart disease (stenosis or regurgitation)
	Hypertrophic cardiomyopathy
	Previous IE
	Structural congenital heart disease
	Valve replacement
Dermatitis
IVDU
Renal failure
Organ transplant
DM
116
Q

Organisms of infective endocarditis?

A

o Staph Aureus (indwelling catheters, IVDU, DM, cellulitis)
o Streptococcal viridans (oral disease/procedures)
o Enterococci (GU disease, hospitalisation)
o Streptococcal bovis (bowel malignancy)
o HACEK organisms
 Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens, Kingella kingae
o Culture negative (prior Abx, Coxiella, chlamydia, legionella)
o SLE
o Malignancy

117
Q

Most common valves of infective endocarditis?

A

o Mitral valve
o Aortic valve
o Combined aortic and mitral
o Tricuspid valve

118
Q

Symptoms of infective endocarditis?

A

o Fever + new murmur (endocarditis until proven otherwise)

o Fatigue, flu-like illness, arthralgia, weight loss

119
Q

Signs of infective endocarditis - systemic?

A

 Fever, Rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing

120
Q

Signs of infective endocarditis - cardiac?

A

 New murmur
 Regurgitation
 Aortic root vegetation may prolong PR interval – heart block

121
Q

Signs of infective endocarditis - immune complex?

A

 Vasculitis
 Microscopic haematuria
 Acute glomerulonephritis

122
Q

Signs of infective endocarditis - FROMJASE?

A

 Fever
 Roth spots (boat-shaped retinal haemorrhage with pale centre)
 Oslers nodes (painful pulp infarcts in fingers and toes)
 Murmur
 Janeway Lesions (painless, red haemorrhagic spots on palms/soles)
 Anaemia
 Splinter Haemorrhages
 Emboli

123
Q

Investigations performed in infective endocarditis?

A

Blood Cultures
o Before antibiotics, 3 sets over 24 hours from different peripheral sites

Bloods
o	FBC (normochromic normocytic anaemia, neutrophilia), CRP (raised), ESR (raised), LFT, U&amp;Es

Urinalysis
o Microscopic haematuria

CXR

ECG

Echocardiogram <24 hours (TTE then TOE)

Cardiac CT scan can be used

124
Q

Diagnostic criteria of infective endocarditis?

A

o Duke Criteria for IE

125
Q

What are major diagnostic criteria in infective endocarditis?

A
  • Positive blood culture (typical organism in 2 separate cultures or persistently positive in 3)
  • Endocardium involved (positive echo or new valvular regurgitation)
126
Q

What are minor diagnostic criteria in infective endocarditis?

A
  • Predisposition (heart problems, IVDU)
  • Fever >38
  • Vascular signs (arterial emboli, septic pulmonary infarcts, infectious aneurysms, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions)
  • Immunological phenomenon (glomerulonephritis, Oslers nodes, Roths spots, RF)
  • Positive blood culture or positive echo that does not meet criteria
127
Q

Criteria for diagnosis of infective endocarditis?

A

2 major or 1 major and 3 minor or all 5 minor

128
Q

Management of infective endocarditis - empirical?

A

o 4-6-week IV course of antibiotics

 Native – Amoxicillin +/- gentamicin
• Pen allergic: use vancomycin +/- gentamicin

 Prosthetic – Vancomycin + Gentamicin + Rifampicin

129
Q

Specific management of infective endocarditis - staphylococcus? Native and prosthetic?

A

 Native – Flucloxacillin (4 weeks, at least 6 weeks if secondary lung abscess or osteomyelitis)
• If pen allergic or MRSA – vancomycin + rifampicin

 Prosthetic – Flucloxacillin + rifampicin + gentamicin (6 weeks, review need for gentamicin at 2 weeks)
• If pen allergic – vancomycin + rifampicin + gentamicin

130
Q

Specific management of infective endocarditis - streptococcus?

A

 Benzylpenicillin +/- gentamicin (4-6 weeks, 6 weeks prosthetic valve)
• If pen allergic – vancomycin + gentamicin

131
Q

Specific management of infective endocarditis - enterococci?

A

 Amoxicillin + gentamicin (4-6 weeks, 6 weeks for prosthetic valve, after 2 weeks review need for gentamicin)
• If pen allergic – vancomycin + gentamicin
• If gentamicin resistant – Amoxicillin + streptomycin

132
Q

Specific management of infective endocarditis - HACEK microorganisms?

A

 Amoxicillin + gentamicin (4 weeks, 6 weeks for prosthetic valve, stop gentamicin after 2 weeks)
• If amoxicillin resistant – ceftriaxone + gentamicin

133
Q

Surgical management of infective endocarditis? When is it indicated?

A

o Total removal of infected tissues and reconstruction of cardiac morphology or valve replacement

Indications:
o severe valvular incompetence
o aortic abscess (often indicated by a lengthening PR interval)
o infections resistant to antibiotics/fungal infections
o cardiac failure refractory to standard medical treatment
o recurrent emboli after antibiotic therapy

134
Q

Complications of infective endocarditis?

A 
o	MI, pericarditis, arrhythmias
o	CHF
o	Valvular insufficiency
o	Aortic root or myocardial abscesses
o	Emboli
o	Glomerulonephritis
135
Q

Prognosis of infective endocarditis?

A

o 1-year mortality at 30%

136
Q

Definition of PE?

A
  • DVT embolised into pulmonary circulation
137
Q

Pathology of PE?

A

o Embolism obstructs outflow tract and causes acute right sided failure
o Lung tissue ventilated but not perfused so no gas exchange

138
Q

Risk factors of PE?

A 
o	Surgery (pelvic/abdominal)
o	Thrombophilia
o	Leg fracture
o	Bed rest/Reduced mobility
o	Malignancy
o	Pregnancy
o	OCP/HRT
139
Q

Causes of PE?

A 
o	Embolism of DVT
o	RV thrombosis (post-MI)
o	Right endocarditis
o	Fat, air or amniotic fluid
o	Neoplastic cells
140
Q

Symptoms of PE?

A 
o	Acute dyspnoea
o	Pleuritic chest pain
o	Cough and Haemoptysis
o	Syncope
o	Symptoms of DVT
141
Q

Signs of PE?

A 
o	Tachycardia
o	Tachypnoea
o	Hypotension
o	Pyrexia with lung infarction
o	Pleural rub
o	Cyanosis
o	Gallop rhythm
o	Increased JVP
o	RV heave
142
Q

Assessment of patient with suspected PE? What is PE rule out criteria?

A 
o	ECG
o	CXR
o	Pulmonary Embolism Rule-Out Criteria
	Rule out PE if none of 8 criteria are present with low Wells Score (<2)
•	age < 50 years
•	pulse < 100 beats min
•	SaO2 ≥ 95%
•	No haemoptysis
•	No oestrogen use
•	No surgery/trauma requiring hospitalization within 4 weeks
•	No prior VTE
•	No unilateral leg swelling
143
Q

Initial management of PE?

A

o Full history and examination of respiratory and CV systems
o Examine legs for signs of DVT
o CXR
 Often normal – wedge shaped area of infarction, decreased vascular markings, small pleural effusion
 Excludes pneumonia and pneumothorax
o PE Wells Score

144
Q

What is the PE Well’s score?

A

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3

An alternative diagnosis is less likely than PE
3

Heart rate > 100 beats per minute 1.5

Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5

Previous DVT/PE 1.5

Haemoptysis 1

Malignancy (on treatment, treated in the last 6 months, or palliative) 1

145
Q

Interpretation of PE Well’s Score?

A

 Score of more than 4 – PE likely

 Score of 4 or less – PE unlikely

146
Q

Management of PE Well’s score more than 4? When is PE diagnosed?

A

• Immediate CTPA
o If CTPA cannot be carried out immediately – interim LMWH anticoagulation and hospital admission
o IF CTPA negative and DVT suspected – proximal leg US
o V/Q Scan
 If allergy to contrast or renal impairment (eGFR<30) or pregnant or woman <40

  • Diagnosed PE with positive CTPA or V/Q scan
  • Consider alternative diagnosis if negative CTPA and no suspected DVT
147
Q

Management of PE Well’s score 4 or less? When is PE excluded?

A

• D-Dimer
o If positive, then CTPA
 If CTPA cannot be carried out immediately – interim LMWH anticoagulation and hospital admission
 V/Q Scan
• If allergy to contrast or renal impairment (eGFR<30) or pregnant or woman <40

o If negative D-dimer or positive D-dimer and negative CTPA, then excluded

148
Q

What other tests are performed upon initial assessment of someone suspected of PE?

A

 Bloods
• FBC, U&Es, baseline clotting, D-Dimer (if Wells of <4 to exclude PE)

 ABG (if hypoxic, SOB)
• Low PaO2, Low PaCO2, pH often raised

 ECG (if tachycardic or chest pain)
• Commonly normal – can have sinus tachycardia, RBBB, RV strain pattern (S1Q3T3), RAD, AF
• S1Q3T3 – in up to 50% (sign of Cor Pumonale)

149
Q

when to perform diagnostic imaging in PE?

A

CTPA
 First-line
 When Wells >4 or, elevated D-Dimer

V/Q Scanning
 Used in pregnancy or young people (women<40)
 Usually need CTPA afterwards to confirm

150
Q

Management of PE - initial management?

A

o If hypoxic – 15L/min Oxygen
o Analgesia (Morphine) + Antiemetic – if in pain or very distressed
o If massive PE/haemodynamically unstable (BP <90mmHg, hypoxic, tachycardia, tachypnoea):
 Urgent ICU help
 Rapid colloid infusion
 If BP still <90mmHg – consider dobutamine then IV noradrenaline infusion
 Alteplase 100mg over 2 hour or 0.6mg/kg over 15 mins

151
Q

Management of PE - pharmacological interventions?

A

 LMWH (175U/kg Tinzaparin SC/24h) as soon as possible for at least 5 days or until INR >2 for at least 24 hours, whichever is longer
• For severe renal impairment (eGFR <30) – Unfractionated heparin (UFH)
• If PE and haemodynamically unstable – offer UFH and thrombolytic therapy

 Warfarin offered within 24 hours of diagnosis and continue for 3 months with unprovoked PE
• Alternatives: NOACs (Apixaban, dabigatran, rivaroxaban)

 If cannot have anticoagulation therapy:
• Temporary inferior vena cava filter

 If recurrent DVT:
• Inferior vena cava filter after alternatives (raise INR 3-4, switching to LMWH)

152
Q

Follow up advice for diagnosed PE?

A

 Follow-up appointment to anticoagulation services and medical outpatient
 Advise to return immediately if become breathless or chest pain

153
Q

Management of PE - thrombolytic therapy?

A
  • Consider systemic thrombolytic therapy for patient with haemodynamic instability
  • Alteplase 100mg over 2 hour or 0.6mg/kg over 15 mins
154
Q

Investigations to perform following management of patient with PE? When to perform thrombophilia testing?

A

 Cancer investigations for unprovoked DVT:
• Examination
• CXR
• Bloods (FBC, serum Ca, LFTs)
• Urinalysis
• Consider abdomino-pelvic CT scan if >40 with 1st unprovoked DVT

 Thrombophilia testing
• Antiphospholipid antibodies in patients with unprovoked DVT if it is planned to stop anticoagulation therapy
• Hereditary thrombophilia testing – unprovoked DVT with 1st degree relative with DVT/PE if planned to stop anticoagulation

155
Q

Definition of varicose veins?

A
  • Dilated, tortuous, superficial veins

- Most commonly found in legs, visible and palpable

156
Q

Causes of varicose veins?

A

o Indication of superficial lower extremity venous insufficiency
 Incompetent valves in vein lead to reflux of blood and increased pressure in vein distally
 Weakness or degeneration of vein wall may contribute
o Unknown, congenital

157
Q

Risk factors of varicose veins?

A 
o	Increasing age
o	FHx of varicose veins
o	Females
o	Pregnancy
o	Obesity
o	Prolonged standing/sitting
o	Hx of DVT
158
Q

Symptoms of varicose veins?

A

o Dilated veins on leg
o Pain, itching, swelling
 Especially after prolonged standing
o Restless legs and leg cramps

159
Q

Signs of varicose veins?

A

o Irregular bulges consistent with varicose veins
o Telangiectasias
o Skin changes – hyperpigmented, venous eczema, lipodermatosclerosis
o Ulcers or thrombophlebitis

160
Q

Examination of varicose veins?

A

o Inspect patient standing
o Feel for cough impulse at saphenofemoral junction
o Trendelenberg test – assess SFJ incompetence – patient lying down, elevate leg and empty vein by massaging distal to proximal – occlude superficial veins using tourniquet – patient stands
 If veins do not re-fill – incompetent valve above this level
 If veins re-fill – incompetent valve lower down
 Test then above knee, below knee

161
Q

Management of varicose veins - bleeding varicose veins?

A

o First aid and admit to vascular service

162
Q

Management of varicose veins - non-bleeding varicose veins - general advice?

A 
	Reassure complications uncommon
	Lose weight
	Light-to-moderate physical activity
	Avoid standing for too long
	Elevate legs where possible
163
Q

Management of varicose veins - non-bleeding varicose veins - when to refer to vascular surgeons?

A

 Symptomatic varicose veins
 Skin changes (pigmentation or eczema)
 Superficial vein thrombosis (hard painful veins)
 Leg ulcer – active or healed

164
Q

Management of varicose veins - non-bleeding varicose veins - secondary care investigations?

A

• Duplex US

165
Q

Management of varicose veins - non-bleeding varicose veins - secondary care treatment?

A
  • Endothermal ablation – seal affected veins
  • US-guided Foam Sclerotherapy – injection of irritant foam, inflammation closes vein
  • Surgery – Ligation and stripping of affected vein
166
Q

Management of varicose veins - non-bleeding varicose veins - primary care treatment?

A

 Compression stockings following Doppler
• If compression stockings considered:
o Doppler to assess ABPI to exclude arterial insufficiency
 <0.5 – severe PAD and stocking contraindicated
 0.8-0.5 – avoid stockings – refer
 0.8-1.3 – safe to wear
 >1.3 – refer as incompressible arteries

167
Q

Management of varicose veins - non-bleeding varicose veins - safety net?

A

 Seek medical advice if hard and painful, skin changes, venous ulcer, bleeding

168
Q

Complications of varicose veins?

A 
o	Bleeding (after trauma)
o	Thrombophlebitis (hard, painful veins)
o	DVT
o	Skin changes (pigmentation caused by hemosiderin, venous eczema, lipodermatosclerosis)
o	Skin Ulceration
o	Decreased QoL
169
Q

Definition of peripheral artery disease?

A
  • Peripheral artery disease describes narrowing or occlusion of peripheral arteries, affecting blood supply to lower limbs
  • Chronic limb ischaemia can present as:
    o Intermittent claudication (most common)
    o Critical limb ischaemia/Rest Pain
170
Q

Causes of peripheral artery disease?

A

o Atherosclerosis
o Vasculitis
o Embolism
o Buerger’s disease

171
Q

Risk factors of peripheral artery disease?

A 
o	Smoking
o	DM
o	Age
o	Hypertension
o	Hypercholesterolaemia
o	Atherosclerosis elsewhere (coronary, carotid)
172
Q

When to suspect peripheral artery disease?

A

o Progressive cramping pain in calf, thigh or buttock on walking which is relieved by rest
o Non-healing wounds

173
Q

What is the Fontaine Classification of peripheral artery disease?

A

o Asymptomatic
 ABPI <0.9

o	Intermittent Claudication
	Felt in calfs, thighs, buttocks
	Tightness/cramping pain developing after certain distance
	Worse on uphill
	Pain disappears when resting
o	Ischaemic Rest Pain
	Woken up by pain
	Occurs due to gravitational effect lost when lying flat
	Relief by swinging legs over bed
	Dependent oedema

o Ulceration/Gangrene

174
Q

Signs of peripheral artery disease?

A 
o	Absent pulses
o	Cold, hairless, dry, white legs
o	Atrophic skin
o	Punched out ulcers (painful)
o	CRT prolonged
o	Buerger’s angle <20o
175
Q

Assessment of peripheral artery disease?

A

o Examine ulcers, temperatures, skin changes, pulses, CRT
o ABPI
 <0.9 means peripheral artery disease
 <0.5 critical limb ischaemia
 >1.2 means vessels not compressible – calcifications - DM likely

176
Q

Management of intermittent claudication - primary care?

A

 Smoking cessation
 Diet and weight modification
 Clopidogrel 75mg OD (aspirin 75mg OD if clopidogrel CI or not tolerated)
 Supervised exercise programme – 3 months twice a week
 Refer for vascular surgery
 If not for surgery – Praxaline (naftidrofuryl oxalate)

177
Q

Management of intermittent claudication - secondary care?

A

 Supervised exercise programme – 3 months, 2hours, twice a week
 Duplex US if revascularisation considered
• +/- contrast-enhanced MR angiography
 Angioplasty and stenting
 Bypass Surgery and grafts

178
Q

Management of critical limb ischaemia - primary care?

A

 Refer to vascular MDT
 PRN paracetamol + weak/strong opioids (+/- antiemetic)
• Refer to pain management services if pain not controlled and revascularisation inappropriate
 Manage cardiovascular risk
• Smoking cessation
• Diet and weight modification
• Clopidogrel 75mg OD (aspirin 75mg OD if clopidogrel CI or not tolerated)

179
Q

Management of critical limb ischaemia - secondary care?

A

 Duplex US if revascularisation considered
• +/- contrast-enhanced MR angiography (CT if CI)
 Angioplasty and stenting
 Bypass Surgery and grafts
 Amputation if ALL options have been considered by MDT

180
Q

Prognosis of peripheral artery disease?

A

o Amputation required in 1-2% of intermittent claudication patients
o Critical limb ischaemia risk of amputation and premature death
o 3x more likely to die from CVD

181
Q

Complications of peripheral artery disease?

A

o Impaired QoL
o Ulceration and gangrene
o Amputation
o CVD, CVA

182
Q

Definition of AAA?

A
  • Artery with dilatation >50% of its original diameter
    o True aneurysms – abnormal dilatations that involve all layers of arterial walls
    o False aneurysm – Collection of blood in outer layer only (adventitia)
  • May be fusiform (most AAA) or sac-like (Berry aneurysms)
183
Q

Definition of unruptured AAA?

A
  • Unruptured AAA definition >3cm
    o 3% of those >50 years
    o Males 3:1 Females
    o Majority infrarenal
184
Q

Definition of ruptured AAA?

A

o Majority found infrarenal and haemorrhage into retroperitoneum
o Mortality 41% and untreated 100%

185
Q

Risk factors of AAA?

A 
o	Hypertension
o	Smoker
o	Male
o	Increasing age
o	COPD 
o	Hyperlipidaemia
o	Family history
186
Q

Causes of AAA?

A

o Degeneration of elastic lamellae and smooth muscle loss

187
Q

Symptoms and signs of unruptured AAA?

A
  • Unruptured often have no symptoms – incidental finding
    o Pulsatile mass in abdomen
    o May have pain in back, abdomen or groin
  • Unruptured Signs
    o Expansile abdominal mass
    o Abdominal bruit
188
Q

Symptoms and signs of ruptured AAA?

A 
-	Ruptured Symptoms
o	Classical central abdominal and lower back pain in patient with known aneurysm
o	Sudden onset and severe pain
o	PEA cardiac arrest
o	Sudden painless collapse
-	Ruptured Signs
o	Pale, sweating, tachycardia, hypotensive
o	Mottled skin of lower body
o	Tender pulsatile abdominal mass
o	Pulses in femoral region may be absent
189
Q

Investigations in AAA?

A
  • Low clinical suspicion
  • USS
  • CT Scan
    o Used if evaluated for surgery
190
Q

Screening in AAA?

A

o All men aged 65 years screened USS of abdomen

191
Q

When to refer unruptured AAA to vascular surgeons?

A

 AAA 5.5cm or larger to vascular surgeon within 2 weeks

 AAA 3-5.4cm to vascular surgeon within 12 weeks

192
Q

General management of unruptured AAA?

A

 Stop smoking service

 Treat hypertension

193
Q

Surveillance of unruptured AAA?

A

 Asymptomatic AAA
• Every 3 months if AAA 4.5-5.4cm
• Every 2 years if AAA 3.0-4.4cm

194
Q

Surgical management of unruptured AAA - when and what?

A

 When?
• Aneurysms >5.5cm, larger than 4cm and expanding at >1cm/year or symptomatic

 What?
• Open Repair
• Stenting (EVAR)

195
Q

Management of ruptured AAA?

A

o Get vascular surgeon and anaesthetist, warn theatre
o High flow Oxygen
o 2 large bore cannulas, Bloods (FBC, LFTs, U&Es, amylase, glucose, coagulation screen, Crossmatching (Emergency – 10U Red cells, 8U platelets, 8U FFP)
o IV morphine & 50mg Cyclizine
o IV Fluids (aim BP >90mmHg but <100mmHg due to risk of rupture)
o Portable USS, CXR, Urinary catheter and radial artery line, ECG
o Prophylactic Abx – Cefuroxime + Metronidazole IV
o Vascular surgeon - Aortic cross clamping
 Endovascular repair or open surgery

196
Q

Prognosis of AAA?

A
  • No more than 1 in 3 patients with ruptured AAA will reach hospital alive and 20% of those who do, fail to reach theatre

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