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Y5 Cardiovascular System > List I - Core Conditions > Flashcards

List I - Core Conditions Flashcards

1
Q

What is atrial fibrillation?

A
  • Cardiac arrhythmia with:
  • Absolutely irregular RR intervals
  • No distinct P waves on the surface ECG
  • Rapid and chaotic atrial activity
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2
Q

What is the prevalence of atrial fibrillation?

A
  • AF is the most common sustained arrhythmia
  • Occurs in 1-2% of the population
  • > 6 million europeans affected
  • <0.5% prevalence 40-50 years
  • 5-15% prevalence at 80 years
  • Males to females 1.5:1
  • Lifetime risk of ~25% at age 40 years
  • Prevalence is set to double in the next 50 years
  • Present in 3-6% of acute medical admissions
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3
Q

What are the classifications of atrial fibrillation?

A
  • Initial episode - AF > 30s diagnosed by ECG
  • Paroxysmal - recurrent >2 episodes that terminate within 7 days (<48h terminated with CV)
  • Persistent - continuous >7 days or AF >48h in which decision made to perform CV
  • Long standing persistent - continuous AF of >12 months duration
  • Permanent - joint decision by patient and clinician to cease further attempts to restore or maintain SR
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4
Q

What are the related symptoms as a result of AF?

A
  • Palpitations
  • Shortness of breath (loss of atrial contraction)
  • Fatigue
  • Dizziness
  • Syncope
  • (None)
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5
Q

Which other conditions are associated with AF (can increase chance)?

A
  • Hypertension
  • Heart failure
  • Diabetes
  • Obesity
  • Sleep apnoea/ chronic lung disease
  • Valvular heart disease (MV disease)
  • Congenital heart disease
  • Coronary artery disease
  • Thyroid disease
  • Chronic kidney disease
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6
Q

What are the objectives of AF management?

A
  • Stroke prevention
  • Symptom relief
  • Ventricular rate control
  • Correction of rhythm disturbance in some
  • Optimal management of concomitant cardiovascular disease
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7
Q

What are the associations between AF and stroke?

A
  • Increases stroke risk by 5%
  • Present in 15-20% of acute strokes
  • Strongest risk factor for stroke in 80-89 yo’s (accounts for 24% of strokes)
  • Associated with larger size infarcts, increased disability, death, long term care and recurrence
  • Associated with impaired cognitive function and dementia
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8
Q

What is used for assessing stroke risk in AF?

A
  • CHA2DS2-VASc Score
  • 2 or more in females give or offer anti-coagulation
  • 1 or more in males give or offer anti-coagulation
  • Don’t give aspirin
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9
Q

What is used to assess bleeding risk in AF?

A
  • HASBLED

* Modify risk factors where possible

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10
Q

What is the purpose of the HASBLED score?

A
  • To identify modifiable risk factors to improve safety of anticoagulation
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11
Q

How is HASBLED scored?

A
  • Hypertension = uncontrolled
  • Renal disease = dialysis/transplant/creatinine >200
  • Liver disease = cirrhosis/bilirubin > x2, AST/ALT > 3x normal
  • Stroke history
  • Bleeding = previous major bleed or predisposition to bleeding
  • INR’s = unstable /high/TTR< 60%
  • Drugs = antiplatelets/NSAID’s
  • Alcohol = >8 drinks/week
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12
Q

How should anticoagulation be managed in AF?

A
  • CHA2DS2Vasc >2 offer oral anticoagulation
  • Vitamin K antagonist (warfarin)
  • Novel anticoagulants (dabigatran, rivaroxaban, apixaban)
  • CHA2DS2Vasc >1 Consider oral anticoagulation
  • CHA2DS2Vasc 0 Do not offer anticoagulation
  • Do not use aspirin as an anti-coagulant
  • Stroke risk needs to be reviewed regularly
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13
Q

When is rate and rhythm control indicated in AF?

A
  • Should be offered as a first line strategy except in people:
  • Whose AF has a reversible cause
  • Who have heart failure thought to be primarily due to AF
  • Who have new onset AF
  • For whom a rhythm control strategy is more suitable based on clinical judgement
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14
Q

How should rate be controlled in AF?

A
  • Standard beta-blocker (other than sotalol)
  • Rate limiting calcium channel blocker (verapamil or diltiazem)
  • Digoxin only in non-paroxysmal AF for sedentary patients or if in heart failure
  • Combination therapy often required
  • Beta blocker
  • Diltiazem
  • Digoxin

NB - do not use amiodarone for long term rate control

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15
Q

How should rhythm be controlled in AF?

A
  • Antiarrhythmic drug therapy
  • Beta blockers
  • Flecainide - normal heart (not for ischaemic), propafenone
  • Sotalol, dronedarone, amiodarone
  • Cardioversion
  • Chemical
  • Electrical
  • Catheter ablation
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16
Q

What is the indication of cardioversion for AF?

A
  • DC cardioversion if AF <48 hours
  • Arbitrary cut off - could cause a clot to fire off
  • AF > 48 hours requires a period of therapeutic anticoagulation minimum 3 weeks before and 4 weeks afterwards (warfarin with INR >2 or NOAC)
  • 50% recurrence at 12 months
  • Amiodarone pre-treatment 4 weeks before can improve success rates
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17
Q

What is the method of catheter ablation for AF treatment?

A
  • Electrical isolation of the pulmonary veins
  • Prevents “triggers” and “drivers” of AF
  • Creates electrically inexcitable “scar” around the PV’s which blocks PV ectopics from entering the left atrium
  • 2-3 hour procedure under conscious sedation with opiate analgesia
  • Prior anticoagulation with warfarin (or NOAC)
  • Percutaneous access via femoral veins
  • Trans-septal puncture to access the left atrium
  • ~70% success rates with need for multiple procedures in 25%
  • 2-3% major complication (stroke, tamponade, PV stenosis)
  • Patient may require multiple procedures
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18
Q

What are the mechanisms of AF?

A
  • More commonly ectopic beats in the left (inferior) pulmonary vein
  • Pulmonary vein ablation leads to a scar around the pulmonary vein - this is done empirically to treat
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19
Q

What is a procedural option for patients who cannot have anti-coagulation?

A
  • Left atrial appendage occlusion
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20
Q

What are the long term side effects of amiodarone?

A
  • Lung fibrosis
  • Thyroid disease
  • Liver fibrosis
  • Photo-sensitivity (slate grey complexion)
  • Cataracts
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21
Q

What are the reversible causes of AF?

A
  • Hyperthyroidism
  • Infection
  • Drugs & alcohol
  • Hypertension
  • Hyperkalaemia - but more commonly leads to VF
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22
Q

What are the investigations for AF?

A
  • TFT
  • BM
  • U&E
  • Ca
  • Mg
  • CXR
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23
Q

What is the management for AF?

A
  • Anticoagulation - DOAC or warfarin
  • Rate control - beta blocker or rate limiting (CCB)
  • Aim 60-90 bpm
  • Max <120bpm
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24
Q

What is the most important feature to manage during AF?

A
  • Anticoagulation - it can improve longevity by reducing the chance of stroke
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25
Q

Where do the triggers come from in most AF?

A
  • Pulmonary veins
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26
Q

How is CHA2DS2VASC score done?

A

Used to assess a person’s stroke risk. Adding together the points allocated to each risk factor gives a total which guides the decision to offer anti-thrombotic treatment

  • CHF/LVHF with REF or people with recent HF requiring hospital = 1
  • HTN (defined as 140/90 on at least 2 occasions) or current anti-hypertension treatment = 1
  • Age > or equal to 75 years = 2
  • Diabetes mellitus (fasting glucose > 7mmol/L or more or treatment with oral hypoglycaemic drugs and/or insulin = 1
  • Stoke/TIA = 2
  • Vascular disease (prior MI, peripheral arterial disease or aortic plaque) = 1
  • Age 65-74 = 1
  • Sex (female) = 1
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27
Q

What is the reason for doing the HASBLED score?

A
  • Identifies modifiable bleeding risk factors that can help you to advise patients to manage
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28
Q

How is a HASBLED score done?

A

Identifies people at high risk of bleeding who could benefit from increased vigilance and correction of modifiable risk factors
1 point score for each of the following risk factors:
* Hypertension (uncontrolled >160 systolic)
* Abnormal liver function
* Abnormal renal function
* Stroke (previous history, particularly lacunar strokes)
* Bleeding (history or predisposition)
* Labile INR’s <60% of time in therapeutic range
* Elderly (aged over 65 years)
* Drugs (antiplatelet agents or NSAID’s)
* Harmful alcohol consumption

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29
Q

What are the rules on flying after AF diagnosis?

A
  • No flying restrictions provided AF is stable and has not recently worsened or become more symptomatic
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30
Q

What are the rule on driving after AF diagnosis?

A
  • Advise the patient it is their responsibility to inform the DVLA of any condition that may affect their ability to drive
  • Group 1 (cars and motor bikes) - driving must cease if the arrhythmia is likely to cause incapacity, driving may be permitted when the underlying cause has been identified and controlled for at least 4 weeks, DVLA need not be notified unless there are distracting or disabling symptoms
  • Group 2 ( lorries and buses) - disqualified if the arrhythmia has caused or is likely to cause incapacity, driving may be permitted when the arrhythmia is controlled for at least 3 months, LV fraction is equal to or greater than 0.4 and there is no other disqualifying condition
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31
Q

How often should a person with AF be reviewed?

A
  • At least annually
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32
Q

How should a person with AF be followed up after starting rate control treatment?

A
  • Within 1 week of starting the rate control treatment (or any dose alteration), check that the person is tolerating the drug and review the symptoms (palpitations, SOB, fatigue), heart rate and BP
  • Target resting ventricular rate at 60 to 80 BPM at rest and between 90 and 115 BPM during moderate exercise
  • Alternative rate control drug if they are not tolerating the current one
  • If HR and/or BP are not controlled consider one of the following:
  • Increase dose
  • Combination treatment (beta blocker, digoxin, diltiazem - seek specialist advice)
  • If symptoms are not controlled by combination treatment, refer promptly (within 4 weeks) to a cardiologist
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33
Q

How should a person with AF on warfarin be followed up after starting anticoagulant treatment?

A
  • For people taking warfarin - assess INR, daily or alternate days initially until within the therapeutic range (between 2 and 3) on two consecutive occasions, then monitor twice weekly for 1-2 weeks, followed by weekly measurements untilat least two INR measurements are within therapeutic range, then longer intervals e.g. 12 weeks agreed locally
  • Calculate the time in therapeutic range at each subsequent visit to ensure that the person is maintaining an INR between 2 and 3 over a longer period of time
  • Calculate the TTR over a maintenance period of at least 6 months
  • Use a validated method of measurement such as the Rosendaal method for computer based dosing or proportion of tests in range for manual dosing
  • Exclude measurements taking in the first 6 weeks of treatment
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34
Q

How is poor anticoagulation control indicated for patients on warfarin for AF?

A
  • TTR <65%
  • Two INR values of 5 or higher or one INR value higher than 8 within the past 6 months
  • Two INR values <1.5 within the past 6 months
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35
Q

For people with poor anticoagulation control on warfarin for AF, how should they be managed?

A
  • Correct the factors contributing to poor control if possible:
  • Impaired cognitive function
  • Poor adherence to prescribed treatment
  • Illness
  • Use of concurrent medications that may interact with warfarin
  • Diet and alcohol
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36
Q

If poor anticoagulation control cannot be improved for people with AF on warfarin what is the management?

A
  • Consider switching to a DOAC (apixaban, edoxaban, dabigatran or rivaroxaban)
  • Good compliance is required for DOAC due to shorter half life
  • No specific anti-dote to DOAC
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37
Q

What should be including in the annual review of a patient with AF?

A
  • Check for symptoms of AF at rest and during exercise and assess HR
  • Review the medications - symptom control, compliance and identify and manage any drug interactions
  • Increase dose/alter medication if symptom control is poor
  • Review CHA2DS2VASC stroke risk and HASBLED annually (routinely when a person is 65 + or develops DBM, HF, CVD, stroke, TIA or VTE)
  • Anticoagulate if needed
  • If already taking anticoagulant manage any modifiable bleeding risks
  • Assess and manage CVD risk - QRISK2
  • Assess and manage complications of AF
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38
Q

What is the anticoagulant of choice for AF that does not require regular monitoring?

A
  • DOAC’s

- Apixaban, Rivaoxaban, Dabigadran

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39
Q

For patients with AF post stroke or TIA, how should their anticoagulation be managed?

A
  • DOAC or warfarin

- Antiplatelets only given if needed in the management of other comorbidities

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40
Q

For acute stroke patients when should anticoagulation therapy be started (in the absence of haemorrhage)?

A
  • 2 weeks after the stroke

- If the imaging shows a very large cerebral infarct, anticoagulation may be delayed

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41
Q

Which medications are used to control rate in patients with AF?

A
  • Beta blockers
  • Calcium channel blockers
  • Digoxin (not first line but considered if the patient has coexistent heart failure)
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42
Q

Which drugs may be used in the pharmacological cardioversion of patients with paroxysmal atrial fibrillation?

A
  • Amiodarone (if structural heart disease)

* Flecanide (if no structural heart disease)

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43
Q

What can be prescribed to patients with AF who have a co-existing asthma diagnosis and require rate control?

A
  • Calcium channel blocker - diltiazem
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44
Q

If a patient with AF has a CHA2DS2-VASc score of 0, what is the treatment for anticoagulation?

A
  • No treatment required
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45
Q

Under which circumstances is rhythm control more appropriate than rate control for AF?

A
  • Coexistent heart failure
  • First onset AF
  • Obvious reversible cause
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46
Q

What are the options for rhythm control in AF?

A
  • Treat the underlying cause if there is one e.g. infection
  • DC cardioversion when there is life threatening haemodynamic instability caused by new onset AF
  • Pharmacological cardioversion
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47
Q

What is the second line medication for rate control in AF if a patient has co-existing heart failure?

A
  • Digoxin
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48
Q

What is re-entrant supra-ventricular tachycardia?

A
  • Group of paroxysmal SVT (junctional arrhythmias) with accessory pathways of specialized conducting tissue between atria and ventricles
  • Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT)
  • Atrio-ventricular re-entry tachycardia (AVRT) are extranodal
  • Wolf-Parkinson-White Syndrome (WPW) - is pre-excitation with accessory pathway (bundle of Kent) conducting atrial depolarisation directly into ventricular myocardium
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49
Q

How common is SVT?

A
  • 35/100,000/year
  • M:F = 1:2 (<65yrs)
  • M:F = 3:1 (>65yrs)
  • AVNRT:AVRT = 2:1
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50
Q

If assessed to be in narrow QRS (<0.12s) how should the patient further be assessed to decide management?

A
  • Is the rhythm regular or irregular?
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51
Q

If the SVT is regular - what is the approach to management?

A
  • Vagal manoeuvres
  • Adenosine 6 mg rapid IV bolus
  • No effect give 12mg
  • No effect give further 12mg
  • Monitor ECG continuously
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52
Q

After treatment with adenosine, how should the patient be further assessed?

A
  • Sinus rhythm achieved?
  • Yes - Probable re-entry paroxysmal SVT
  • Record 12 lead ECG in sinus rhythm
  • If SVT recurs consider anti-arrhythmic prophylaxis
  • No - Seek expert help
  • Possible atrial flutter
  • Control rate e.g. beta blocker
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53
Q

If the SVT is irregular - what is the approach to management?

A
  • Probably AF
  • Control rate with beta-blocker or diltiazem
  • If in heart failure consider digoxin or amiodarone
  • Assess thromboembolic risk and consider anticoagulation
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54
Q

What are the investigations for a patient with SVT?

A
  • ECG - regular P waves may be visible between QRS, regular narrow QRS tachycardia (c.150-200bpm), compare to previous ECG
  • Screen for WPW - short PR, delta wave (slurred upstroke of QRS due to myocyte-myocyte transmission as opposed to conduction via specialised conducting tissue
  • Electrophysiological study - induces a tachycardia to map the site of the re-entrant pathway
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55
Q

What are vagal manouvers?

A
  • Valsalva maneuver - hold nose, blow out
  • Cough
  • Gag
  • Cold water on face
  • Carotid sinus massage - one side only
  • Lateral to thyroid, massage the carotid artery - this triggers baroreceptor reflex and increases vagal tone, affecting SA and AV nodes
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56
Q

What are the risks of SVT?

A
  • Paroxysmal SVT - often self terminating narrow complex tacycardia’s
  • Recurrence - 80% with 1 month (20% 2 yrs)
  • Usually self terminating in the young and with no other structural heart disease
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57
Q

What is ventricular tachycardia?

A
  • Broad complex tachycardia (<0.12s) originating from a ventricular ectopic focus
  • Has the potential to precipitate ventricular fibrillation and hence requires urgent treatment
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58
Q

What are the two main types of ventricular tachycardia?

A
  • Monomorphic VT: Most commonly caused by myocardial infarction
  • Polymorphic VT: Subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval
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59
Q

What are the causes of a prolonged QT interval?

A
  • Congenital
  • Jervell-Lange-Nielsen syndrome (includes deafness and is due to abnormal potassium channel)
  • Romano-Ward syndrome (no deafness)
  • Drugs
  • Amiodarone, sotalol, class 1a antiarrhythmic drugs
  • TCA’s, fluoxetine
  • Chloroquine
  • Terfenadine
  • Erythromycin
  • Others
  • Hypocalcaemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Acute MI
  • Myocarditis
  • Hypothermia
  • Subarachnoid haemorrhage
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60
Q

What is the pathophysiology of ventricular tachycardia?

A
  • Monomorphic VT: Re-entrant circuits in anatomically abnormal substrate e.g. MI scar tissue
  • Polymorphic VT: Abnormal activity in ventricular myocardium, often resulting from triggers that increase the QT interval
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61
Q

What are the symptoms/signs of VT?

A

Symptoms

  • Palpitations, especially if post MI, collapse, angina (underlying IHD), SOB (underlying heart valve disease/cardiomyopathy)
  • PMH - recent MI, valvular disease
  • DH - anti-arrhythmics

Signs
* Weak pulse (or absent), RJVP (cannon waves), HS1 variable intensity, +/- hypotension

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62
Q

What are the differential diagnoses for VT?

A
  • SVT with aberrant conduction e.g. atrial fibrillation/flutter
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63
Q

What are the investigations for VT?

A
  • Bloods - U and E’s, Mg2+, cardiac markers (if chest pain)
  • Radiology - transthoracic echocardiogram if suspected HF/heart valve disease
  • St - ECG and compare with previous to determine QT baseline
  • Monomorphic VT: regular, 120-190bpm (may be independent electrical activity: dissociated P waves)
  • Polymorphic VT: less regular, more chaotic, phasic variation in QRS (torsades des pointes: twisting of the points)
  • Electrophysiological studies if recurrent, symptomatic VT
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64
Q

What is the management of VT with adverse features?

A
  • If the patient has adverse signs
  • Systolic BP <90 mmHg
  • Chest pain
  • Heart failure
  • Syncope
  • Immediate synchronised DC shock is indicated
  • Conscious patients require sedation or GA for cardioversion
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65
Q

What is the management of VT with no adverse features?

A
  • Broad QRS (>0.12s), regular
  • Amiodarone 300mg IV over 20 - 60 mins, then 900mg over 24 hrs
  • Ideally administered through a central line
  • Alternatives
  • Lidocaine: use with caution in severe LV impairment
  • Procainamide
  • If drug therapy fails
  • Electrophysiological study
  • Implantable cardioverter-defibrillator (ICD)
  • Particularly indicated in patients with significantly impaired LV function
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66
Q

What are the potential complications of VT?

A
  • Risk of syncope
  • Cardio-genic shock
  • Cardiac arrest
  • Sudden cardiac death
  • Torsades de pointes
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67
Q

What is the preventative management of VT?

A
  • Long term medication (all shown to improve LV function)
  • Beta blockers
  • Amiodarone
  • ACEi
  • Spironolactone
  • Revascularisation
  • For severe CAD (PTCA/CABG)
  • Implantable cardioverter defibrillator (ICD)
  • If had cardiac arrest
  • Spontaneous sustained VT with LV dysfunction
  • Haemodynamically significant sustained VT resistant to drug therapy
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68
Q

What is mitral regurgitation?

A
  • Compromised mitral valve competence by disease affecting any part of the mitral apparatus (annulus, leaflets, chordae, papillary muscles, LV function)
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69
Q

What is mitral stenosis?

A
  • Narrowing of mitral valve orifice (treatment required if <2.5cm : normally 4-6cm)
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70
Q

What are the causes of mitral regurgitation?

A
  • Primary
  • Myxomatous degeneration (Ehler’s Danlos/Marfan’s)
  • IHD
  • Endocarditis
  • Rheumatic fever
  • Cardiomyopathy
  • Congenital
  • Appetite suppressants: fenfluramine
  • Secondary (functional)
  • Ventricular dilation due to HF
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71
Q

What are the causes of mitral stenosis?

A
  • Rheumatic fever
  • Congenital
  • Mucopolysaccharidoses
  • Endocardial fibroelastosis
  • Malignant carcinoid
  • Prosthetic valve
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72
Q

How common is mitral stenosis?

A
  • F>M
  • More common in India due to rheumatic fever
  • Usually presents >40 yrs
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73
Q

What is the pathophysiology of mitral regurgitation?

A
  • Myxomatous degeneration
  • Fibroelastic tissue defect (mitral valve prolapse/Barlow’s syndrome)
  • Annular dilatation
  • Posterior leaflet prolapse
  • Elongated chordae
  • IHD
  • Episodic/reversible MR
  • Posterior papillary muscle ischaemia +/- papillary muscle infarct (MI)
  • Rupture
  • Acute MR
  • Acute LVF
  • Acute rheumatic fever
  • Annular dilatation
  • Leaflet thickening/calcification
  • Acute endocarditis
  • Bacterial destruction
  • Perforates leaflet
  • Chordae rupture
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74
Q

What is the pathophysiology of mitral stenosis?

A
  • Rheumatic fever
  • Rheumatic carditis
  • Leaflet thickening/commissural of chordal fusion
  • Narrowed orifice
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75
Q

How does MR affect haemodynamic status?

A
  • LV dilatation
  • Increases end diastolic volume
  • Increases stroke volume
  • Leads to irreversible LV dysfunction
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76
Q

How does MS affect haemodynamic status?

A
  • Reduced cardiac output
  • Severe left atrial enlargement
  • Pressure on organs (oesophagus, dysphagia/Ortner’s syndrome; recurrent laryngeal: hoarse voice)
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77
Q

What are the symptoms of MR and MS?

A
  • Both
  • Asymptomatic or SOB
  • Fatigue
  • Palpitations (AF)
  • CVA (thrombus)
  • Haemoptysis (pulmonary HTN)
  • MS
  • Chest pain
  • Pressure symptoms
  • Hoarseness
  • Dysphagia
  • Chest infections
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78
Q

What are the signs of MR and MS?

A
  • MR
  • Displaced thrusting apex
  • RV heave
  • Soft S1, loud S2
  • Pansystolic murmur (apex in axilla)
  • MS
  • Low volume pulse
  • Malar flush (reduced CO)
  • Undisplaced tapping apex (palpable S1)
  • Loud S1
  • Opening snap (pliable valve)
  • Mid diastolic rumbling murmur (apex in L lateral position)
  • Graham-Steell murmur (systolic murmur of PR due to pulmonary HTN in severe MS)
  • Causes
  • IHD, endocarditis
  • Complications
  • AF
  • RHF from pulmonary hypertension (RJVP, loud P2, RV heave, peripheral oedema)
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79
Q

What are the differential diagnoses for MR/MS?

A
  • Left heart murmurs

- MR, MS, AR, AS, flow murmurs (infection), valve replacements

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80
Q

What are the radiological investigations for MS/MR?

A
  • Chest x-ray (both)
  • LA enlargement (double R heart shadow)
  • Calcified mitral annulus in rheumatic heart disease
  • Features of CCF
  • MR
  • Cardiomegaly
  • MS
  • Splaying of carina
  • Tenting of L heart border
  • Transthoracic echocardiogram (TTE) / Transoesophageal echocardiogram (TOE)
  • Quantify extent of LV function (ejection fraction)
  • Measure LV dimensions (end diastolic and end diastolic diameter)
  • MR - Doppler to assess size/site of regurgitant jet
  • MS - Measure size of mitral orifice
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81
Q

What are the special tests for MR/MS?

A
  • Both
  • ECG
  • AF, P-mitrale if sinus rhythm (LA enlargement)
  • MR - Previous MI, LVH (S wave in V1 and R wave in V5/6 >35mm)
  • MS - RVH from chronic pulmonary HTN - R wave taller than S wave in V1 and RAD
  • Left heart catheterisation/LV angiography
  • Replaced by TTE (but used with coronary angiography before valve surgery in selected patients, previous valvotomy, other valve disease, angina, calcified mitral valve, pulmonary HTN
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82
Q

What is the conservative approach to the management of MS/MR?

A
  • Both
  • Antibiotic prophylaxis before dental treatment
  • MR - stable in most cases of mild MR, only selected patients require surgery
  • Surveillance - yearly clinical and TTE assessment if MR (mild/moderate without LV dysfunction/pulmonary HTN) or MS (asymptomatic mild: orifice >1.5cm without evidence of pulmonary HTN)
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83
Q

What is the medical approach to the management of MR/MS?

A
  • Warfarin - if AF (plus rate control)

* Loop diuretic - if pulmonary oedema

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84
Q

What are the surgical indications for MR/MS?

A
  • Indications
  • MR - NYHA 2-4 SOB, TTE evidence of LV dysfunction/ejection fraction <60%, LV end diastolic diameter >50mm
  • MS - Treat with moderate to severe <1.5cm or mild-moderate with increased pulmonary artery pressure >60mmHg or PCWP >25mmHg, transmitral gradient pressure >15mmHg
  • Benefits
  • Prolonged survival by improved LV function (repair/replacement), avoidance of long term warfarin in patients with sinus rhythm (repair/replacement)
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85
Q

What are the surgical treatment options for MR/MS?

A

1) Percutaneous balloon mitral commissurotomy
* Indications - MS only if favourable anatomy (pliable, non-calcified valve, minimal chordae fusion
* Procedure - Balloon tipped catheter via femoral artery into mitral valve, inflate balloon to widen orifice
* Problems - severe MR 10%, embolism, MI, mortality 2%

2) Mitral valve repair
* Indications - Procedure of choice for both MR/MS
* Procedure - Median sternotomy, cardiopulmonary bypass, heart stopped with cardioplegia solution, access via LA
- Repair - MR: resection/patch repair/chordae shortening/annuloplasty ring, MS: Commissurotomy
* Problems - 5% risk conversion to valve replacement

3) Mitral valve replacement
* Indications - If repair impossible (multiple extensive lesions, severe calcification)/failed
* Types - Mechanical (young: durable, need warfarin), tissue (old: shorter lifespan, no anticoagulation)
* Problems - Disruption by sutures (3rd degree heart block, MI, ischaemia)
* Post op - on ICU, warfarin for 6 weeks (or life if mechanical valve)

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86
Q

What are the risks of MR/MS?

A
  • Both
  • AF, emboli (CVA), pulmonary HTN
  • MS - bronchial/oesophageal obstruction, infective endocarditis
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87
Q

What is the prognosis of MR/MS?

A
  • MR - poor if pulmonary HTN, surgery (5-10 yr survival rates for repair vs replacement: 83%-68% vs 69%-52%)
  • MS - 60% 10 yr survival - reduced to 15% with functionality limiting symptoms, post surgery 5-10 yrs survival is 75%-56%
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88
Q

What preventative measures are there for patients with MR/MS?

A
  • Antibiotic prophylaxis

- Before dental treatment (and oral penicillin against recurrent rheumatic fever if that is the cause)

89
Q

What is aortic stenosis?

A
  • Narrowing of the aortic valve orifice
  • Severe <1cm
  • Moderate 1-1.5cm
  • Mild 1.5-3cm
  • Normal 3-4cm
  • Better measurement is aortic valve orifice area index
  • Orifice area/body surface area - normal 2.2, severe <0.6
90
Q

What is aortic regurgitation?

A
  • Incompetence due to any disease affecting the aortic valve or aortic root
91
Q

What are the causes of AS/AR?

A
  • AS - Calcific degeneration
  • Senile
  • Congenital - bicuspid valve leads to fibrosis/calcification, William’s syndrome
  • Rheumatic fever
  • AR
  • Aortic valve disease - calcific degeneration, infective endocarditis, rheumatic fever, congenital bicuspid valve
  • Aortic root disease - dilatation (idiopathic including age related?Marfan’s, aortic dissection, Takayasu’s arteritis
  • Rare - Trauma, RA, SLE, AS, Reiter’s syndrome, psoriatic arthropathy, IBD
92
Q

How common is AS/AR?

A
  • AS - increases with age, 3% 75-86 yrs

* AR - mild is common, M:F = 1:1.5

93
Q

What is the pathophysiology of AS?

A
  • Chronic (compensated)
  • AS progressing at 0.12cm/yr
  • LV compensates with concentric hypertrophy
  • Increased force of contraction to increase pressures
  • Reduced LV compliance
  • LV unable to relax/refill properly
  • Diastollic dysfunction
  • Eventually hypertrophy cannot match progression
  • Systolic HF
  • Angina (unable to meet O2 demand of hypertrophied muscle
  • Subaortic stenosis - Congenital membrane
  • Supra-valvular aortic stenosis
  • Williams syndrome
  • HCM (narrow LV outflow tract from gross septal hypertrophy (not true AS))
94
Q

What is the pathophysiology of AR?

A
  • Severe acute (endocarditis, ascending aortic dissection, chest trauma)
  • Limited capacity of LV to adapt to sudden volume overload
  • Pulmonary oedema
  • Chronic (compensated)
  • LV dilatation (compliance)
  • Increased SV and CO, often normal ejection fraction and LV dysfunction usually reversible in early stages
95
Q

What are the symptoms/signs of AS?

A
  • Symptoms
  • Asymptomatic or angina
  • Exertional syncope
  • SOB (also dizzy faints)
  • Signs
  • Low volume slow rising pulse
  • Narrow pulse pressure
  • Palpable thrill over A area
  • Undisplaced heaving apex (palpable S2)
  • Quiet A2 (with progression S2 may reverse)
  • Ejection systolic murmur (A area - carotids, length correlates with severity not intensity)
  • Ejection click (if pliable valve)
96
Q

What are the symptoms/signs of AR?

A
  • Symptoms
  • Asymptomatic (many years)
  • SOB on exertion
  • Orthopnoea
  • Fatigue
  • Palpitations
  • Angina
  • Syncope
  • CCF
  • Signs
  • Quincke’s sign (capillary pulsations of nail bed)
  • Large volume collapsing pulse
  • Wide pulse pressure
  • Corrigan’s/De Musset’s signs (head bobbing)
  • Displaced thrusting apex
  • Early diastolic blowing murmur at LSE with bell sitting forward (may also hear ejection systolic flow murmur at A area from increased flow)
  • Duroziez’s sign (occlude temporal artery with 2cm prox. to stethoscope gives systolic murmur/2cm distal give diastolic murmur)
  • Traube’s sign - pistol shot sound over femoral arteries
  • Austin-Flint murmur - flutter of anterior mitral valve cusp from regurgitant stream: severe AR
  • Complications
  • CCF, RJVP (later as RHF develops)
  • Causes of AR
  • Endocarditis, Marfan’s (aortic dissection/dilation, mitral valve prolapse, lens dislocation, flat cornea, increased axial length, tall stature, pectus carinatum/excavatum, arm span-height ratio >1.05, scoliosis, joint hypermobility, Steinberg’s sign, high arched palate, elongated asymmetrical face
97
Q

What are the differential diagnoses for AR/AS?

A
  • Best heard on expiration

- AS, AR, MS, MR, flow murmurs (infection), valve replacements, HCM

98
Q

What are the appropriate radiological investigations for AR/AS?

A
  • Chest x-ray (both)
  • AS - post stenotic aortic dilatation, calcified aortic arch, cardiomegaly (late)
  • AR - dilatation of ascending aorta, cardiomegaly
  • TTE - to confirm grade/severity
99
Q

What special tests can be done for AR/AS?

A
  • ECG (both)
  • LVH and LV strain (poor R wave progression from V1-V6)
    AS - P-mitrale, LAD (L anterior hemi block), LBBB, 3rd degree heart block (calcified ring)
  • Left heart catheterisation
  • Before cardiac surgery to assess coronary arteries if IHD suspected or when non-invasive assessment of AS inconclusive (can make direct measurements of aortic ventricular gradient)
100
Q

What is the conservative approach to the management of AR/AS?

A
  • Patient education
  • Both need antibiotic before dental treatment
  • AS moderate/severe should avoid competitive sports
  • Surveillance (clinical and TTE assessment)
  • AS 5 yearly (asymptomatic/mild), 2 yearly (moderate), yearly (severe)
  • AR - Yearly (asymptomatic with normal ejection fraction >50%)
101
Q

What is the medical management of AR/AS?

A
  • Severe AS - Diuretics, digoxin, cautious ACEi use (relieve pulmonary oedema)
  • Severe AR - Vasodilators to reduce SBP (nifedipine, ACEi)
102
Q

What are the surgical indications for AR/AS?

A
  • AS - severe with symptoms
  • AR - NYHA 3-4, SOB or CCS 2-4 angina, LV impairment (ejection fraction <49% or LV end diastolic diameter >55cm, or NYHA 2 SOB with progressive LV dilation/declining ejection fraction
103
Q

What are the options for surgery for AR/AS?

A
  • Percutaneous valvuloplasty
  • AS - not fit for surgery
  • Aortic valve replacement
  • Tissue valve (better for >65yrs, women of child bearing age, contact sports)
  • Mechanical valve (anticoagulation needed, lasts longer)
  • Procedure
  • Median sternotomy
  • Cardiopulmonary bypass
  • Heart stopped with cardioplegia solution
  • Native valve excised (excess Ca2+ removed)
  • New valve sutured into place
  • Problems
  • CVA
  • Permanent pacemaker required if injury to conduction system
  • Mortality 2%
104
Q

What are the risks of AS/AR?

A
  • AS - CVA (embolisation of calcific debris), sudden death (ventricular arrhythmias)
  • AR - LV dysfunction, CCF (worse outcome if CCF >12 months)
105
Q

What is the mortality of AS/AR?

A
  • AS
  • Life expectancy reduced by 5 yrs (with angina), 3 yrs (with syncope), 2 yrs (with SOB)
  • After surgery 5-10 yrs survival 78-55%
  • AR - 10% following symptom onset
106
Q

What are the preventative treatments for complications for people with AS/AR?

A
  • Antibiotic prophylaxis before dental treatment

* Avoid competitive sports if moderate to severe AS

107
Q

What is infective endocarditis?

A
  • Microbial infection of the endothelial lining of the heart (heart valve infection is most common clinical manifestation)
108
Q

What are the risk factors for developing infective endocarditis?

A
  • Strongest RF is previous episode of endocarditis
  • Following types of patients are affected:
  • Previously normal valves (50%, typically acute presentation)
  • Mitral valve is most commonly affected
  • Rheumatic valve disease (30%)
  • Prosthetic valves
  • Congenital heart defects
  • IVDU - typically causing a tricuspid lesion
  • Others - recent piercings
109
Q

What are the causes of infective endocarditis?

A
  • Staphylococcus aureus (most common in developed countries and particularly common in acute and IVDU presentations)
  • Coagulase negative staphylococci such as staphylococcus epidermis commonly colonize indwelling lines and are most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination (After 2 months the spectrum of endocarditis causing organisms returns to normal i.e. staph aureus most common
  • Streptococcus viridans (most common in developing countries) and accounts for around 20% of cases
  • Two most notable viridans streptococci are:
  • Streptococcus mitis
  • Streptococcus sanguinis
  • Both commonly found in the mouth in dental plaque so endocarditis caused by these are due to poor dental hygiene or following a dental procedure
  • Streptococcus bovis is linked to colorectal cancer
  • Subtype streptococcus gallolyticus is most linked with colorectal cancer
  • Non-infective: SLE (Libman-Sacks), malignancy: marantic endocarditis
  • Culture negative causes
  • Prior antibiotic therapy
  • Coxiella burnetii
  • Bartonella
  • Brucella
  • HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
110
Q

How common is infective endocarditis?

A
  • 4/100000/year (up to 15/100,000 >50yrs
  • M:F = 1:1
  • 50% occur on normal valves, 10% cultures are negative
111
Q

What are the presenting clinical features of infective endocarditis?

A

Symptoms

  • Non specific flu like symptoms (septic signs)
  • Fever, night sweats, rigors, malaise, weight loss, anaemia
  • Acute heart failure, embolic effects
  • Neurological deficits (CVA), abdominal pain (splenic infarcts), lung (if R sided)
  • Immune complex mediated
  • Haematuria (glomerulonephritis), arthralgia
  • Heart block (aortic root abscess)
  • Syncope, dizzy, palpitations

Signs

  • Clubbing
  • Splinter haemorrhages (>5)
  • Osler’s nodes
  • Janeway lesions
  • Skin petechiae
  • Pale conjunctivae (anaemia)
  • Roth spots (boat shaped retinal haemorrhages with pale centres)
  • New/changing murmur (AR/MR)
  • Signs of LVF (rare)
  • Abdominal distention (splenomegaly)
  • Signs of renal failure
112
Q

How is a diagnosis of infective endocarditis made?

A

Modified Dukes Criteria

  • Diagnosis of infective endocarditis can be made if:
  • Pathological criteria positive, or
  • 2 major criteria, or
  • 1 major and 3 minor criteria, or
  • 5 minor criteria
113
Q

What are the pathological Modified Dukes criteria for infective endocarditis?

A
  • Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
114
Q

What are the major Modified Dukes criteria for infective endocarditis?

A
  • Positive blood cultures
  • Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
  • Persistent bacteraemia from two blood cultures taken >12 hours apart or 3 or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
  • Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
  • Positive molecular assays for specific gene targets
  • Evidence of endocardial involvement
  • Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
  • New valvular regurgitation
115
Q

What are the minor Modified Dukes criteria for infective endocarditis?

A
  • Predisposing heart conditions or IVDU
  • Microbiological evidence does not meet major criteria
  • Fever >38c
  • Vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  • Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
116
Q

What are the blood investigations for IE?

A
  • FBC (low Hb, normal MCV, raised WCC)
  • U and E (cause or aminoglycosides use)
  • LFT
  • CRP raised/ESR
  • Mg2+
  • Blood cultures (liase with micro) x3 from different sites (6hrs apart) at peak fever (over 24h, or 12h if severely ill)
  • If severe sepsis or septic shock, take 2 sets of blood cultures at different times in the first hour before starting empirical therapy
Paired serology (if culture -ve) 
- Detect Abs - Coxiella burnetti, Chlamydia psittaci, Mycoplasma, Bartonella, Candida
117
Q

What are the urine investigations for IE?

A
  • MSU - Dipstick (haematuria, proteinuria, glomerulonephritis/renal infarct)
118
Q

What are the radiological investigations for IE?

A
  • Chest x-ray - cardiomegaly
  • TTE - oscillating masses on valve/supporting structures (if >2mm), regurgitation jets, intracardiac fistulae, abscesses (TOE better for aortic root abscess/mitral lesions), mycotic aneurysms of aortic root
  • TOE - if TTE inadequate from poor images/-ve despite strong clinical suspicion (use if suspect prosthetic valve IE)
119
Q

What further tests can be done for IE?

A
  • ECG (liase early with cardiology)

- Prolonged PR, 3rd degree AV block (aortic root abscess)

120
Q

What is the conservative approach to the management of IE?

A
  • Patient education

- Maintain good oral health, risks of invasive procedures (piercings, tattooing, IVDU)

121
Q

What is the medical approach to the management of IE?

A
  • Empirical treatment (Leeds Pathways)
  • Ideally blood cultures first
  • Native valve
  • Vancomycin IV and Ciprofloxacin IV
  • Prosthetic valve
  • Vancomycin IV, Gentamicin and Rifampicin
122
Q

What are the indications for surgery for IE?

A
  • Severe valvular incompetence
  • Aortic abscess (often indicated by a lengthening PR interval)
  • Infections resistant to antibiotics/fungal infections
  • Cardiac failure refractory to standard medical treatment
  • Recurrent emboli after antibiotic therapy
  • Haemodynamic instability (emergency: acute HF from free MR, AR)
123
Q

How common is surgery required for IE?

A
  • 1/3 patients require surgery for IE, risks of the surgery are similar to normal valve replacement but increase with severity of infection
124
Q

What are the complications of IE?

A
  • Cardiac - perforated valve leaflets, papillary muscle rupture, AR/MR (acute LVF/cardiogenic shock), fistulae (from infection extension), abscess (if involves fibrous skeleton of heart, usually aortic root - heart block may result), mycotic aortic aneurysm
  • Embolism (sterile/septic emboli from valve vegetations) - CVA, cerebral abscess, skin/mucous membranes (petechiae), eye (retinal haemorrhages), lung (septic emboli from R sided endocarditis), spleen (splenic infarcts), kidneys (renal infarcts), coronary arteries (MI: rare)
  • Immunological - Glomerulonephritis, arthralgia, arthritis, (RhF may be falsley +ve)
125
Q

What is the mortality of IE?

A
  • 5-50% overall
  • 30% staphylococci
  • 14% enterococci
  • 6% streptococci
126
Q

What is the guidance regarding prophylaxis with antibiotic for patients at risk of IE?

A
  • NICE recommend the following do not require prophylaxis:
  • Dental procedures
  • Upper and lower GI tract procedures
  • GU tract including urological, gynaecological and obstetric procedures and childbirth
  • Upper and lower respiratory tract, includes ENT and bronchoscopy procedures
  • Guidelines do however suggest:
  • Any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
  • If a person at risk of developing endocarditis is receiving antimicrobial therapy due to a procedure at a site where there is suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
127
Q

What is pulmonary embolism?

A
  • Blockage of the main lung artery or one of its branches
  • Usually embolism has travelled from elsewhere to reach the lung
  • Common source is DVT
  • 15% of DVT’s migrate to form PE’s
  • Two are often combined in the term venous thromboembolism (VTE)
  • Other causes include air, fat, talc and amniotic fluid
128
Q

What are the signs of PE?

A

Signs:

  • Tachycardia
  • Hypotension (massive PE)
  • Raised JVP
  • Pleural rub (rare)
  • May have no signs
129
Q

What are the symptoms of PE?

A
  • Classically the chest will be clear
  • SOB
  • Chest pain (usually pleuritic)
  • Cough
  • Haemoptysis (<5%)
  • Associated leg swelling
  • Collapse
130
Q

What are the risk factors for PE/DVT?

A
  • Current DVT
  • Immobility
  • Major surgery
  • Long bone fracture
  • Active malignancy
  • Oral contraceptive pill
  • Pregnancy
131
Q

What is the PESI score?

A
  • Pulmonary Embolism Severity Index

- Predicts 30-day mortality of patients with pulmonary embolism using 11 clinical criteria

132
Q

What are the key differentials for PE?

A
  • Pneumonia
  • LRTI
  • ACS
  • Pleurisy
  • MSK chest pain
  • Upper GI symptoms
133
Q

What is the gold standard for a definitive diagnosis of PE?

A

[Plain film x-ray is necessary before both]

    • CT pulmonary angiogram
  • V/Q scanning (women age 40 and younger and pregnant women)
134
Q

What can be seen on CT pulmonary angiogram and what could be the danger?

A
  • Saddle embolus seen

* Danger is a piece could break off

135
Q

What are the levels of PESI?

A

30 mortality after a PE

  • I 0-1.6%
  • II 1.7-3.5%
  • III 3.2-7.1%
  • IV 4.0-11.4%
  • V 10-25%
136
Q

What other score can be used to assess likelihood of PE?

A
  • Wells score
137
Q

How is the Wells score interpreted?

A
  • Score 4 or greater = high chance of PE diagnosis

* Score <4 = low chance of PE diagnosis

138
Q

What is the treatment for PE?

A
  • DOAC’s are first line treatment for most people with VTE e.g. Apixaban, Rivaroxaban
139
Q

Where should patients who have had a PE be managed?

A
  • NICE support the use of a validated risk stratification tool e.g. PESI score
  • Key requirements for outpatient management would clearly be haemodynamic stability, lack of comorbidities and support at home
140
Q

What is the approach to the management of a patient with a massive PE in which there is haemodynamic instability?

A
  • Thrombolysis
  • Now recommended as the first line treatment for massive PE where there is circulatory failure e.g. hypotension
  • Other invasive approaches should be considered where appropriate facilities exist
141
Q

What is the management for patients who have repeat PE’s despite adequate anti-coagulation therapy?

A
  • Consideration for an IVC filter
  • Work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries
  • IVC filter use is currently supported by NICE guidelines, other studies suggest weak evidence base
142
Q

Which features make a PE more likely?

A
  • Text book triad is pleuritic chest pain, dyspnoea and haemoptysis
  • PIOPED study 2007 looked at frequency of different symptoms and signs in patients with PE and reported the following:
  • Tachypnea (respiratory rate >20/min) - 96%
  • Crackles - 58%
  • Tachycardia (heart rate >100/min) - 44%
  • Fever (temperature >37.8c - 43%
143
Q

Which other decision tool do NICE recommend to rule out PE in low risk patients?

A
  • PERC rule
  • Low probability is defined as <15% although it is clearly difficult to quantify such judgements
  • If suspicion of PE is greater than this then patients should be assessed using the 2 step Wells score
144
Q

How can the use of D-dimer be improved?

A
  • Only use in patients with a useful result
  • Not after surgery
  • Not in pregnancy
  • Not after trauma
  • Not in sepsis
  • Use a risk score (Wells) to identify patients level of risk
145
Q

How can the improved use of D-dimer as outlined be put into practice?

A

1) PE possible
2) Stratify risk 4+high or <4 low using Wells score
3) High=CTPA, Low=D-Dimer
4) Positive D-Dimer= CTPA, Negative D-Dimer= PE excluded

146
Q

What are the ECG findings for PE?

A
  • SI, QIII, TIII

* Sinus tachycardia most common ECG finding

147
Q

What is the anatomical location of the abdominal aorta?

A
  • Enters the abdomen at T12 via the aortic hiatus, bifurcates L4 (umbilicus)
148
Q

What are the histological layers of the abdominal aorta?

A
  • Tunica intima (endothelial cells)
  • Elastin
  • Tunica media (smooth muscle)
  • Tunica adventitia (loose fibrous connective tissue)
  • Serosa (epithelial cells)
149
Q

What is an aneurysm?

A
  • Permanent localized dilatation >50% original diameter
  • True aneurysm - all 3 layers of wall involved
  • False aneurysm - only part of wall (blood collects outside vessel wall post trauma and communicates with vessel lumen)
150
Q

What are the common sites of an aneurysm?

A
  • Abdominal aorta
  • Infra-renal between renals and iliacs - most common, juxtarenal, suprarenal
  • Thoracic aorta
  • Ascending arch/descending (most common thoracic type)
  • Others
  • Iliac, femoral, popliteal

Morphology
* Fusiform, saccule e.g. Berry, expansile, dissecting

151
Q

How is an aortic dissection classified?

A
  • Stanford Classification
  • Type A - Involves ascending aorta
  • Type B - Does not involve ascending aorta
152
Q

What are the causes of aneurysms?

A
  • Atherosclerosis (abdominal, thoracic descending arch)
  • Connective tissue disorder (thoracic asccending/dissection)
  • Marfan’s, Ehler’s Danlos
  • Hypertension (thoracic ascending)
  • Infection (mycotic aneurysm)
  • Infective endocarditis
  • Tertiary syphilis
  • Brucellosis
  • Salmonellosis
  • TB
  • Others
  • Inflammatory (Behcet’s/Takayasu: smooth muslce reduced)
  • Congenital
  • Traumatic
153
Q

What are the risk factors for developing aneurysms?

A
  • IHD
  • Smoking
  • FH (12x increase)
  • HTN
  • Hyperlipidaemia
  • Male
  • Increasing age

Rupture

  • Smoking
  • Female
  • Low FEV1
154
Q

How common are aneurysms?

A
  • Abdominal (AAA)
  • Increases with age, M:F = 5:1
  • 5% male >65 yrs
  • Unruptured 3% >50 yrs
  • Sites 95% infrarenal, 5% suprarenal, 30% involve iliacs
  • Ruptured AAA - 13th commonest cause of death world wide
155
Q

What is the pathophysiology of aneurysm formation?

A
  • Artheromatous degeneration
  • Main contributor to true aneurysms (associated with periadventitial inflammation/fibrotic response)
  • Cystic medial necrosis (thoracic ascending):
  • Mucosal degeneration (from immune response, wall stress, proteolytic degradation of connective tissue
  • Increased matrix metalloprotease activity/inflammation
  • Degrades extracellular matrix protein of medial collagen/elastic tissue +/- cystic changes
  • Leads to increased lymphocyte/macrophage infiltration
156
Q

What is the pathophysiology of a dissection?

A
  • Initimal tear
  • Blood enters diseased media/cleaves it from intima
  • Dissection of variable length with true and false lumens (if no tear found, may be due to haemorrhage in media)
157
Q

What is the Law of La Place?

A
  • T = PR

* Tension in arterial wall = pressure x radius of arterial conduit

158
Q

What are the symptoms of an aneurysm?

A
  • Asymptomatic
  • 75% abdominal (expansile O/E, calcification on x-ray)
  • 40% thoracic
  • AAA
  • Expanding - epigastric/back pain, blue toes (atheroembolism)
  • Rupture - intermittent/continuous severe epigastric pain (back, iliac fossa, groins), collapse, shock, visual disturbance, embolisation (shedding of thrombus), others (pressure symptoms, fistulation)
  • Thoracic (if large) - chest pain, SVC, oesophageal pressure
  • Dissection - severe, sudden, tearing central chest pain (back/arms/neck)
159
Q

What are the signs of an aneurysm?

A
  • AAA
  • Expanding - expansile/pulsatile mass (>3cm)
  • Rupture - Tachycardia, hypotension, flank/scrotal bruising
  • Dissection (sequential branch occlusion due to unfolding) - hemiplegia (carotid artery), unequal arm pulses/BP, acute limb ischaemia, paraplegia (anterior spinal artery), anuria (renal arteries), absent peripheral pulses
160
Q

What are the differentials for AAA/other aneurysm?

A
  • MI
  • Renal colic
  • Acute abdomen
161
Q

What are the appropriate blood investigations for AAA?

A
  • CRP
  • Cardiac markers (dissection)
  • FBC (low Hb), clotting screen, cross match 10U packed red cells, 2U platelets and FFP
  • U and E’s, LFT’s, amylase
162
Q

What are the radiological investigations for AAA?

A
  • CT/USS - Size, aortic wall thickness +/- rupture
  • Thoracic - TOE accurate in diagnosis
  • Dissection - MRI gold standard
  • CT and TOE - diagnostic
  • Chest x-ray - may show widened mediastinum (rare)
  • Rupture - chest x-ray +/- abdominal x-ray
  • Calcified aneurysm
163
Q

What is the approach to the management of a ruptured AAA?

A
  • Call for vascular surgeon/anaesthetist/theatre
  • A - Maintain
  • B - (SpO2, RR) 15L NRBM
  • C - (pulse, HR, BP, JVP, ECG, UO - catheter)
  • IV access x2 bloods)
  • Treat shock with O negative blood (keep SBP <100mmHg as increased risk of leak if BP too high
  • Morphine 10mg IV and cyclizine 50mg IV
  • Straight to theatre
  • Prophylactic cefuroxime 1.5g and metronidazole 500mg IV
  • Insert arterial line
  • Open surgical repair
  • Clamp aorta above leak
  • Insert Dacron graft (tube graft if aortic/trouser graft if iliac involved, durable for 20-30 yrs)
  • Monitor on ICU
164
Q

What is the conservative approach to the management of AAA?

A
  • Examination
  • USS/CT monitoring for size
  • 3.5-4cm yearly
  • 4-5cm 6 monthly
  • > 5.5cm offer surgery
  • Lifestyle
  • Stop smoking
  • Low fat intake
  • Regular exercise
  • Cardio-pulmonary testing for suitability for surgery
  • Driving
  • Group 1 notify DVLA if >6cm (license subject to annual review)
  • Disqualified if >6.5cm
  • Can drive after successful treatment
  • Group 2 disqualified after >5.5cm
  • Can drive post successful treatment and with evidence of fitness
165
Q

What is the medical approach to the management of AAA?

A
  • Optimise risk factors
  • BP/DM
  • Statins (if >4)
  • Aspirin
  • Steroids
  • Relieve symptoms of periadventitial inflammation
166
Q

What are the indications for surgery for AAA?

A
  • Large asymptomatic
  • > 5.5cm or <5.5cm and saccular, consider fusiform
  • Rapidly expanding (>1cm/year)
  • Symptomatic
  • Ruptured/leaking
  • Active atheroembolism
  • Female <5.5cm
167
Q

What are the options for surgery for AAA?

A
  • Open surgery

* EVAR

168
Q

What does open surgery entail for AAA?

A
  • Revascularisation
  • Indications - young, fit, as long term durability required
  • Benefits
  • Gold standard (>50yr proven results)
  • Complete repair
  • <0.5% failure rate
  • 1 post operative scan then no more follow up
  • Procedure
  • Midline abdominal incision
  • Clamp aorta above leak
  • Aneurysm resected
  • Insert Dacron graft (tube graft if aortic, trouser if iliac)
  • Problems
  • During
  • GA needed
  • Aortic clamping
  • Long procedure
  • After
  • Haemorrhage
  • Infection
  • VTE
  • Distal rash
  • Ischaemia of leg/colon/mesentery/spine: paraparesis
  • False aneurysm/rupture
  • Aorto-enteric fistula
  • Anastomotic aneurysm
  • MI
  • ARF
  • Multi-organ failure
  • DIC
  • ARDS
  • Pneumonia
  • CVA
  • DVT/PE
  • Long ICU stay (10d)
  • 6wks - 4 months to recover
  • 5-8% mortality
  • 5% if elective, 10-20% severe morbidity
169
Q

Which factors can influence the outcome of open surgery for AAA?

A
  • Raised creatinine
  • Heart failure
  • ECG evidence of ischaemia
  • FEV1
  • Increasing age
  • Female gender
170
Q

What does EVAR entail for AAA?

A
  • Endovascular aneurysmal repair/stenting
  • Indications
  • Unfit for open major surgery
  • Contraindications
  • If <1.5cm below renal arteries (stent has no support)
  • Iliaces <8mm diameter (stent cannot be passed)
  • Conical aneurysmal neck
  • Benefits (vs open)
  • Less invasive/no clamping
  • Shorter stay (2 days on normal ward, 2-4 wks for full recovery)
  • Less morbidity/mortality
  • Fewer transfusions (less blood loss)
  • Can be done under LA or regional (maybe GA)
  • Takes pressure off aneurysm which can thrombose in time
171
Q

What is the procedure of EVAR for AAA?

A
  • Insert stent via femoral artery
  • Problems during
  • Distal embolism
  • After
  • Stent graft migration
  • Femoral false aneurysm
  • Endo-leak
    I at proximal or distal attachment
    II sac filling via branch vessel - most common 80%
    III from defect in graft fabric between joints in endograft
    IV generally porous graft
  • Not everyone suitable
  • Lifelong monitoring required (USS/CT contrast)
  • ARF if blocks renal arteries (and CT contrast scans needed for follow up)
  • High cost
  • May not be durable in long term (may still need open)
172
Q

What is the approach to the management of other types of aneurysms?

A
  • Thoracic
  • Open surgery if large 6-7cm
  • Smaller if Marfan’s

Dissection
- Conservative - acute type B (treat hypertension as occurs in 50%), control pain
- Surgery - acute type B
A to E management - get urgent cardiothoracic help
- Cross match 10U
- Surgery
- Take to ICU
- Antihypertensives - keep SBP 100-110 using IV labetalol or esmolol

173
Q

What are the potential complications of AAA?

A
  • Rupture
  • 1%/yr if <5.5cm vs 25%/yr if >6cm
  • Thrombosis
  • Embolism
  • Pressure on other organs/structures
  • Aortic valve incompetence
  • Inferior MI (if dissection moves proximally)
  • Fistula between SVC/bowel
174
Q

What are the potential complications of a type A dissection?

A
  • CVA (carotid artery)
  • Exanguination (rupture)
  • MI (coronary artery)
  • Tamponade (rupture into pericardium)
  • AR (stretched aortic valve)
175
Q

What are the potential complications of a type B dissection?

A
  • Renal failure (renal artery)
  • Gut ischaemia (celiac/mesenteric)
  • Lower limb ischaemia (iliac arteries)
176
Q

What is the mortality of aneurysms?

A
  • Thoracic - 5 yr survival 70-80%
  • AAA - elective surgery 5%, open surgery 5-8% (10-20% severe morbidity)
  • Ruptured AAA
  • 90-95% if untreated (only 33% reach hospital, 80% of which reach theatre, 50% of which survive) 40-50% if treated
  • Dissection
  • Emergency surgery <25%
177
Q

How is AAA prevented / reduced?

A
  • AAA screening programme
  • Consists of a single abdominal USS for males aged 65 years
  • Outcome of screening is as follows:
  • <3cm - normal, no further action
  • 3-4.4cm - small aneurysm - re-scan every 12 months
  • 4.5-5.4cm - medium aneurysm - re-scan every 3 months
  • > =5.5cm - large aneurysm - refer within 2 weeks to vascular surgery for probable intervention
  • Only found 1/1000 patients screened
178
Q

What is the management of AAA according to determined size?

A
  • Low risk rupture
  • Asymptomatic, aortic diameter <5.5cm i.e. small and medium
  • Abdominal surveillance as per indicated according to size
  • Optimise CV risk factors (e.g. stop smoking)
  • High risk rupture
  • Symptomatic, aortic diameter >=5.5cm or rapidly enlarging (>1cm/year)
  • Refer within 2 weeks to vascular surgery for probable intervention
  • Treat with EVAR or open repair
179
Q

What are the classifications of aortic dissection?

A
  • Stanford classification
  • Type A - ascending aorta, 2/3 of cases
  • Type B - descending aorta, distal to left subclavian origin, 1/3 of cases
  • DeBakey classification
  • Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
  • Type II - originates in and is confined to the ascending aorta
  • Type III - originates in descending aorta, rarely extends proximally but will extend distally
180
Q

What is the management of aortic dissection?

A
  • Type A
  • Surgical management, but BP controlled to a target systolic of 100-120mmHg whilst waiting intervention
  • Type B
  • Conservative management
  • Bed rest
  • Reduce BP IV labetalol to prevent progression
181
Q

What are the possible complications of aortic dissection?

A
  • Complications of a backward tear
  • Aortic incompetence/regurgitation
  • MI: inferior pattern often seen due to right coronary involvement
  • Complications of forward tear
  • Unequal arm pulses and BP
  • Stroke
  • Renal failure
182
Q

What are the associations/risk factors for aortic dissection?

A
  • Hypertension - most important
  • Trauma
  • Bicuspid aortic valve
  • Collagens: Marfan’s syndrome, Ehler’s-Danlos syndrome
  • Turner’s and Noonan’s syndrome
  • Pregnancy
  • Syphillis
183
Q

What are the presenting features of aortic dissection?

A
  • Chest pain: typically severe, radiates through to the back and tearing in nature
  • Aortic regurgitation
  • Hypertension
  • Other features
  • Coronary arteries - angina
  • Spinal arteries - paraplegia
  • Distal aorta - limb ischaemia
  • Majority of patients have no or non-specific ECG changes
  • Minority of patients, ST segment elevation may be seen in the inferior leads
184
Q

What are the two main veins in the lower limb?

A
  • Long saphenous vein

* Short saphenous vein

185
Q

What is the anatomy of the long saphenous vein?

A
  • Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the foot
  • Passes anterior to the medial malleolus and runs up the medial side of the leg
  • At the knee it runs over the posterior border of the medial epicondyle of the femur bone
  • Then passes laterally to lie on the anterior surface of the thigh before entering an opening in the fascia lata called the saphenous opening
  • It joins with the femoral vein in the region of the femoral triangle at the sapheno-femoral junction in the saphenous ring (SFJ)

Tributaries

  • Medial marginal
  • Superficial epigastric
  • Superficial iliac circumflex
  • Superficial external pudendal veins
186
Q

What is the anatomy of the short saphenous vein?

A
  • Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the foot which attaches to the great saphenous vein
  • Passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along the posterior aspect of the leg (with the sural nerve)
  • Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein (SPJ), approximately at or above the level of the knee joint
187
Q

What is the physiology of veins?

A
  • Venous return - calves, venomotor tone, cardiac output
  • Perforating veins - blood carried from superficial to deep veins via deep fascia
  • Valves - prevent blood going from deep to superficial
188
Q

What are varicosities?

A
  • Long saccular dilations of superficial veins (often tortuous)
  • Classifications
  • Trunk varicosities
  • Reticular varicosities
  • Telangiectasia (thread veins)
189
Q

What are the causes of varicose veins?

A
  • Primary
  • Idiopathic 95% - inherent vein wall weakness
  • Congenital valve absence (rare)
  • Secondary
  • Venous obstruction 5% - DVT, fetus, ovarian/pelvic tumour
  • Valve destruction - DVT
  • AV malformation - increased pressure
  • Constipation
  • Overactive muscle pumps
190
Q

What are the risk factors for varicose veins?

A
  • Increasing age
  • Female
  • COCP
  • Prolonged standing
  • Obesity
  • FH
  • Pregnancy
191
Q

How common are varicose veins?

A
  • F>M (31% vs 17% 35-70yrs)
  • Increase with age
  • More common in developed countries
192
Q

What is the pathophysiology of varicose veins?

A
  • Vein wall weakness
  • Dilatation
  • Separation of valve cusps
  • Incompetence
  • Increased hydrostatic pressure (gravitational) vs hydrodynamic (muscle pump) forces
  • Venous reflux
  • Venous HTN
  • Dilatation of superficial veins/venous pooling
193
Q

What are the symptoms of VV?

A
  • Aymptomatic
  • Pain
  • Cramps
  • Tingling
  • Heaviness
  • Restless legs
  • Itching especially male
    PMH
  • Previous varicose vein surgery
  • DVT
  • Thrombophlebitis
194
Q

What are the general signs of VV?

A

Inspection

  • Varicosities (distribution)
  • Oedema
  • Thin skin
  • Venous eczema (red/flakey/itchy)
  • Ulcers (gaiter’s area above medial malleolus)
  • Brown staining (haemosiderin)
  • Oedema
  • Haemorrhage
  • Phlebitis
  • Atrophie blanche (white scarring of healed ulcer)
  • Lipodermatosclerosis (purple plaques from SC fibrous caused by chronic inflammation/fat necrosis)

Palpation

  • Course of vein for tenderness (phlebitis) or hardness (thrombosis)
  • Pulses - if ulcer, exclude arterial disease

Cough impulse
* SFJ/SPJ for incompetence

Percussion
* Tap VV distally - palpate transmitted impulse at SFJ (normally interrupted by competent valves)

Auscultation
* Over VV for bruits (AV malformation)

195
Q

What is Trendelenberg’s test in relation to VV?

A

Assess for SFJ competence

  • Patient supine
  • Raise leg to empty vein
  • 2 fingers on SFJ (5cm inferior and medial to femoral pulse)
  • Stand (keep fingers in place)

If incompetent SFJ
* VV do not refill until fingers removed

If competent SFJ
* VV refill lower down before fingers removed

196
Q

How are VV classified?

A
  • CEAP classification (for treatment/progression assessment)
  • Clinical findings
  • No disease
  • Telangiectasia
  • VV
  • Oedema
  • Skin changes
  • Ulcers (active/healing)
  • Etiology
  • Congenital, 1st, 2nd
  • Anatomy
  • Superficial
  • Deep
  • Perforating
  • Pathology
  • Reflux
  • Obstruction
  • Both
197
Q

What are the differentials for VV?

A
  • Saphena varix (dilated GSV where it meets femoral vein: blue tinge)
198
Q

What are the appropriate investigations for VV?

A
  • Hand held Doppler USS (identify flow in incompetent valves)
  • Probe applied to SFJ/SPJ
  • Squeeze calf or tap VV with fingers
  • Flow >0.5-1s indicates significant reflux
  • Duplex Doppler USS
  • Assess real time blood flow
  • Measure lumen diameter, compressibility, flow direction, velocity
  • Colour Doppler USS
  • If recurs
  • Skin changes
  • History of DVT/thrombophlebitis
  • Photoplethysmography
  • If suspect deep and superficial venous reflux
  • Measures venous filling time/efficiency of calf pump
199
Q

What is the conservative approach to the management of VV?

A
  • Patient education
  • Exercise (ankle flexion)
  • Elevation (15-30 mins above level of the heart)
  • Avoid prolonged standing
  • Compression stockings (grades I-IV)
  • Lose weight
  • Regular walks (calf muscle aids venous return)
  • Referral (vascular surgeon)
  • If bleeding, pain, ulceration, superficial thrombophlebitis, severe impact on QOL
200
Q

What are the medical options for the treatment of VV?

A
  • Treat any underlying cause if known
  • Injection scleropathy
  • Indications - below knee varicosities, no gross SFJ incompetence (not for perforator sites)
  • Procedure - ethanolamine (sclerosant) injected at multiple sites (intravascular granulation tissue causes fibrosis/obliterates the lumen)
  • Vein compressed for 1-2 wks (avoids thrombosis)
  • Problems - skin staining, risk of ulcers/DVT
  • Laser coagulation therapy
  • Indications - small, isolated varicosities, venous flaring, telangiectasia
  • Contraindications - coloured skin
201
Q

What are the surgical options for VV?

A
  • Types - Depend on anatomy/surgical preference
  • High tie strip and/or avulsions
  • Ligate 5 tributaries of GSV, avulse the vein distal to proximal at various points
  • Trendelenberg procedure - saphenofemoral ligation
  • Pre-procedure - venous mapping, mark varicosities on either side with indelible ink
  • Post-procedure - bandage legs tightly, elevate for 24 hrs
  • Encourage regular walking (3 miles per day - many short walks)
202
Q

What are the complications of VV?

A
  • Bleeding, ulceration, superficial thrombophlebitis
  • Complications of high venous BP
  • Brown pigmentation (haemosiderin)
  • Lipodermatosclerosis
  • Oedema
  • Eczema

Others
- DVT if proximally spreading phlebitis of long saphenous vein

203
Q

How is VV prevented?

A
  • Lifestyle measures
  • Regular exercise
  • Elevation of legs
204
Q

What is chronic lower limb ischaemia?

A
  • Gradual onset of ischaemia in limbs > 2 weeks
  • Claudication
  • Critical chronic limb ischaemia
  • > 2 weeks recurrent rest pain needing regular analgesia
  • Non-healing ulcer/gangrene of foot with ankle SBP <50mmHg or toe SBP <30mmHg
205
Q

What are the causes of CLLI?

A
  • Atherosclerosis
  • Rare - fibromuscular dysplasia, vasculitis (thromboangitis obliterans/Beurger’s: young heavy smokers)
  • Anaemia - trigger
206
Q

How common is CLLI?

A
  • 10% >65 yrs increases with age
  • Initially M>F, but M:F = 1:1 by 80 yrs
  • 1/3 patients are DBM
207
Q

What is the pathophysiology of atherosclerosis?

A
  • Subcritical stenosis
  • Critical stenosis
  • Occlusion
  • Ischaemia
  • Necrosis
  • Ulceration
  • Gangrene (dry or wet if superadded infection)
  • Septicaemia
208
Q

What are the presenting symptoms of CLLI?

A
  • Intermittent claudication
  • Rest pain
  • Ulceration
  • Gangrene

PMH

  • DM
  • MI
  • Angina
  • CVA/TIA
  • HTN
  • High cholesterol

SH

  • Smoking
  • Alcohol
  • Diet
209
Q

What are the signs of CLLI?

A

Signs

  • Prolonged CRT
  • Calves
  • Pain
  • Pallor
  • Pulseless
  • Perishingly cold
  • Atrophic skin
  • Ulcers (pain, punched out)
  • Buerger’s test
  • Reactive hyperaemia (postural/dependent colour change
210
Q

How is chronic lower limb ishcaemia classified?

A
  • Fontaine classification
  • I asymptomatic (but ABPI <1.0)
  • IIa mild claudication (walk >200m)
  • IIb moderate-severe claudication (walk >200m)
  • III rest pain
  • IV (critical ischaemia) - ulceration/gangrene
211
Q

What are the differential diagnoses for CLLI?

A
  • Leg pain - MSK - OA/RA
  • Neurological
  • Sciatica
  • Radiculopathy
  • Neurogenic/spinal claudication
  • Cauda equina stenosis
  • Nerve entrapment
212
Q

What are the appropriate blood investigations for CLLI?

A
  • FBC (low Hb, raised WCC)
  • Clotting screen
  • Group and save if angiography planned
  • U and E’s - raised creatinine in reno-vascular disease
  • Lipids - risk factor
  • Glucose - DBM
  • ESR/CRP - arteritis
  • Syphilis serology if suspected
213
Q

What are the radiological investigations for CLLI?

A
  • Colour duplex USS
  • For localised disease to determine if the lesion is suitable for angioplasty
  • Contrast angiography (DSA, MRI/CT)
  • Pre-procedure - stop metformin on morning of procedure to avoid lactic acidosis (combined stress on kidneys of metformin and contrast)
  • Procedure - access site/extent of stenoses and quality of distal vessels
  • Post-procedure - resume metformin when renal function ok
214
Q

What are the special tests for CLLI?

A
  • ABPI
  • Claudicaton 0.6-0.9
  • Rest pain 0.5-0.6
  • Critical ischaemia <0.5
  • Impending gangrene <0.3 (if >1.0 but claudication suspected, repeat ABPI after treadmill test)
  • False -ve (calcified incompressible vessels in DM/CRF/severe atherosclerosis)
  • ECG - cardiac ischaemia (risk factor)
215
Q

What is the conservative approach to CLLI?

A
  • Patient education
  • Exercise (supervised: 1/3 improve, 1/3 stay same, 1/3 deteriorate)
  • Modify risk factors - stop smoking, treat DBM/HTN, avoid beta blockers
216
Q

What is the medical approach to the treatment of CLLI?

A
  • Statin - treat to target cholesterol <4-5, LDL <2-2.5)

* Aspirin 75mg/24 h po (clopidogrel if sensitive)

217
Q

What are the surgical options for the management of CLLI?

A
  • Percutaneous transluminal angioplasty
  • For short stenoses, big arteries e.g. iliacs
  • Balloon via femoral artery in narrow segment
  • Stent maintains patency
  • Bypass graft +/- endarterectomy
  • For extensive atheromatous disease but good run off
  • Aspirin post procedure helps maintain patency in prosthetic grafts
  • Sympathectomy
  • To relieve rest pain if revascularisation is impossible
  • Amputation
  • To relieve intractable pain, prevent death from sepsis
  • Level must be high enough to allow healing of stump
  • Above knee heals better, worse rehab
  • Below knee heals worse, better rehab
  • Gabapentin for post operative phantom limb pain - may be more effective if started before surgery
218
Q

What is the mortality of CLLI?

A
  • Worse 5 survival for above knee vs below knee amputation (22.5% vs 37.8%)
219
Q

What are the preventative measures for CLLI?

A
  • Conservative
  • Patient education - exercise and risk factor modification
  • Medical
  • Statins and aspirin

Y5 Cardiovascular System (3 decks)

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