Aortic Stenosis

Clinical examination

  • Ejection systolic murmur
  • Carotid radiation
  • Louder on expiration (positive intrapleural pressure helps push blood out)
  • Softer with isometric handgrips (increased afterload)
  • Softer with Valsalva (decreased preload so less blood flow)
  • Louder with leg raise (increased preload from autoinfusion so more blood flow)



  • Valve area
    • Severe <1cm2
    • Critical <0.8cm2
    • Consider indexing to BSA
  • Mean pressure gradient
    • Severe disease unlikely if gradient <40mmHg and CO is normal
    • When small valve area and gradient <40mmHg, low dose dobutamine echo may be an option
      • Small valve area may be an artefact of valves not opening fully
      • True severe AS shows an increase <0.2cm2  with dobutamine, the total remaining <1.0cm2
  • TOE generally not helpful except to quantify associated mitral disease
  • Stress echo contraindicated in symptomatic AS
  • CT and cardiac MRI useful adjuncts


Natural history

  • Chronic, progressive disease
  • In asymptomatic severe AS patients, event-free rate is 20-50% at2 years
  • As soon as symptoms begin, survival is between 15-50% at 5 years



  1. Aortic valve replacement surgery
    1. Intervention of choice
    2. Indications for intervention
      1. Symptomatic
      2. Caveat: careful consideration for low flow, low gradient AS
      3. Asymptomatic patients with severe AS and LVEF<50% not due to another cause
      4. When heart surgery for other indications is being performed anyway
    3. Types of valves
      1. Metallic
        1. INR – depending on risk factors, from 2-3 to 3.5 to 4.5
      2. Bioprosthetic
        1. Low dose aspirin
        2. If high risk, aim for INR 2-3
  2. Transcatheter aortic valve implantation
    1. Indicated in symptomatic severe AS patients considered not fit for surgery
  3. Medical management
    1. None show benefit compared to natural history

Atrial Fibrillation

Mechanism and causes

  • Focal activation – increased automaticity or micro-re-entry commonly located in the pulmonary veins
  • Multiple wavelet – dilated atrium -> multiple wavelets -> re-entrant circuits
  • Causes
    • V – IHD, HTN, valvular HD, cardiomyopathy, PE
    • I – acute infections
    • T – direct trauma
    • A – pericarditis
    • M – hypokalemia, hypomagnesaemia, alcohol
    • I – sympathomimetics
    • N – phaeochromocytoma


  • You should know the basics by now
  • Coarse fibrillation waves in V1 often mimic flutter
  • Ashman’s phenomenon – aberrantly conducted beats with RBBB morphology in a long refractory period


  • EHRA class roughly parallels NYHA (convenient for regurgitation in exams)
    • I – asymptomatic
    • II – mild
    • III – daily activities affected
    • IV – symptoms at rest


  1. No difference between rate and rhythm control – AFFIRM, RACE
  2. Strict rate control no better than lenient control (<110 bpm) RACE II

Rhythm control

  1. Electrical cardioversion – requires sedation
    1. AF <48 hours -go ahead and zap if <48 hours and then you’re done
    2. AF>48 hours
      1. Perform a TOE – if LAA absent, cardiovert under heparin, if LAA present, OAC for 3/52 then review, if still present, long term OAC, if resolved, proceed to cardioversion
      2. If TOE not performed, OAC for 3/52 then cardiovert
      3. Cover for 4/52 of OAC after cardioversion
  2. Chemical cardioversion
    1. Two main agents used in Australia
      1. Amiodarone  – takes a while, avoid in thyroid disease
      2. Flecainide – requires structurally normal heart
    2. Same need for TOE/OAC strategy as cardioversion
    3. Facilitates patient-initiated pill in the pocket therapy

Rate control

  1. Determine need for anithrombotic therapy with CHADSVASC score
    1. CHADSVASC is annoying to calculate. Pretty much everyone scores over2 though, which is nice
    2. 0 – no antithrombotics
    3. 1 – apixaban or warfarin or nothing (traditionally aspirin) AVERROES, JAST
    4. 2 up – warfarin BAFTA, WASPO
  2. Asses bleeding risk with the HASBLED score (use a calculator)
    1. Hypertension, abnormal liver function, renal impairment, stroke, bleeding, labile INR, age>65, drugs, alcohol
  3. Choose a rate control agent
    1. BB
    2. Non-dihydropyridine CCB (verapamil, diltiazem)
    3. Digoxin (useful at rest but not in exercise)

Operative intervention

  1. AVN ablation – palliative
  2. Left atrial catheter ablation
    1. Better quality of life and AF-free time at 2 years but no difference in total AF burden MANTRA-PF, RAAFT II
    2. Reasonable first line option in patients with low risk for peri-procedural complications preferring interventional management
    3. OAC for minimum of 3 months after procedure, then continue OAC in keeping with CHADSVASC score
    4. Other indication is failed trial of antiarrhythmic medication
  3. Surgical ablation only if concomitant heart surgery

Hypertension management

Treatment targets

  • >80 yrs old SBP 140-150 mmHg
  • <80 yrs old SBP<140 mmHg
  • Diastolic <90mmHg always recommended
  • T2DM BP <130/85 mmHg
  • Nephropathy SBP<130  mmHg

Treatment approach

  1. Exclude endocrine causes
  2. Lifestyle modification
    1. Salt restriction 5g a day
    2. <30g of EtOH a day
    3. SNAP
  3. Diuretics, BB, CCB, ACE-I and ARB are ALL suitable as initial monotherapy
  4. Choose initial agent based on SE profile and other effects
  5. Special cases
    1. Elderly with isolated systolic hypertension – CCB/diuretics
    2. Pregnancy – methyldopa, labetalol, nifeipine
    3. Nephropathy – ACE-I
    4. Angina pectoris – BB and CCB
    5. LVH – ACE-I, CCB
  6. Resistant hypertension
    1. Mineralocorticoid receptor antagonist
    2. Amiloride
    3. Doxazocin


  • 4 weekly after initiation of drug therapy
  • 3 monthly after taget BP reached
  • Asses risk factors and asymptomatic organ damage every 2 years

Treatment of associated risk factors

  • Low dose aspirin in patients with previous CVD
  • Aspirin only for primary prevention in high risk patients
  • GP to review for hypertensive nephropathy and retinopathy

Infective Endocarditis


  • Fairly nonspecific
  • New murmurs and classic peripheral stigmata are uncommon signs

Duke Criteria

  • 2 major OR 1 major + 3 minor OR 5 minor
  • Major criteria
    • Culture evidence of IE organisms
      • 2X blood cultures positive for typical organisms
      • Cultures persistently positive 12 hours apart
      • Cultures should be drawn 1 hour apart and at least 3 should be peformed
    • Echocardiographic evidence
      • Intracardiac mass
      • Myocardial abscess
      • Partial dehiscence of prosthetic valve
      • New-onset valvular regurgitation
  • Minor criteria
    • Predisposing heart condition or drug use
    • Fever >38C
    • Vascular phenomenon (septic embolic, mycotic aneurysm, Janeway lesions)
    • Immunological phenomenon (GN, Osler nodes, Roth spots, RF positive)
    • Blood cultures consistent for dx but not meeting major criteria requirements
    • Echo results consistent for dx but not meeting major criteria requirements


  • Standard empirical regimen
    • Benzylpenicillin 1.8g IV q4hours
    • Flucloxacillin 2g IV q4hours
    • Gentamicin 6mg/kg IV for 1 dose, then either 1 or 2 further doses based on renal function
  • Subsititute vancomycin 1.5g IV bd for benzylpenicillin and flucloxacillin if
    • Cardiac device in situ (prosthetic valve, ICD etc.)
    • Hospital-acquired
    • Clinical suspicion of MRSA
  • Cease gentamicin once susceptibilities known; howeevr,  mantain low dose for streptococcal or enterococaal endocarditis
  • Uncomplicated viridans streptococci, treat for 2 weeks
    • Benzypenicillin 1.8g IV q4hours
    • Gentamicin 1mg/kg IV q8hours

Social issues

  • Requires PICC line; not ideal for a druggie with a craving for a hit of his favourite stuff


A bit disorganised; reflects how I think about these drugs. Basically, it boils down to amiodarone is safe-ish and requires less clever thinking then other options. I’d talk more about the other options in the guidelines but no-one in Australia seems to use anything other than amiodraone, beta blockade, lignocaine and occasionally CCBs and dig.

 Class I – Sodium channel blockade

  • Class Ia affects the QRS – not avilable in Australia (I think); Class Ib and Ic don’t affect the QRS
  • Class Ib
    • Fast association/disassociation
    • Lignocaine 1mg/kg for VT
  • Class Ic
    • Slow association/disassociation
    • Flecainide
      • Not great acutely: oral form + need to confirm structurally normal heart
      • PSVT / PAFib 50mg PO bd
      • VT 100mg bd

Class III – K+ efflux

  • Amiodarone
    • AF: 300mg in 100ml bag of D5W over 30 minutes + 900mg over remaining 24 hours
    • VT: 300mg in 10ml D5W over 3 minutes

Class IV – Calcium channel blockade

  • Verapamil – personally not first line due to lack of experience
    • PSVT / PAFib / PAFlutter – 5mg IV over 2 minutes



Pulmonary Arterial Hypertension


  • Pulmonary hypertension is present when mean pulmonary artery pressure exceeds 25 mm Hg at rest or 30 mm Hg with exercise
  • Primary PAH is rare, usually secondary to cardiac or respiratory causes
  • Don’t miss when planning an operation


  • Hypoxic or mediator-induced vasoconstriction
    • OSA
    • Chronic lung disease
    • Sepsis
    • Cardiac surgery
  • LV-mediated volume or pressure overload
    • Effectively, any cause of HF
    • VSD
  • Vessel obstruction
    • Embolus, luminal narrowing processes or mass effect compression


  • History
    • Progressive SOB
    • Angina-like chest pain
    • Syncope
    • Elicit history of likely aetiologies
  • Exam
    • Palpable P2
    • Signs of right-sided HF
    • Hypoxaemia


  • ECG – RVH, RAD, RV strain pattern, P-pulmonale
  • Echo – RVH, allows PAP estimation
  • Low DLCO
  • Catheterisation of right side
  • iNO provocation test directs treatment with calcium channel blockade
  • LFTs – hepatic congestion
  • Hunt for the aetiology


  • Reduce PAP
    • Phosphodiesterase inhibitors
    • Endothelin receptor antagonists (bosentan)
    • Prostanoids
    • Oxygen
    • Calcium channel blockade is selected patients
  • Optimise preload
    • Diuresis
  • Manage exacerbations and complications
    • Warfarinise
    • Vaccination against influenza
    • Avoid hypercarbia, acidosis, hypothermia


Cardiac Arrest


  • Run through basic DRS ABCDE first, then do the extended version to cover the Hs and Ts
  • A: BVM, early use of LMA. Consider hooking up BVM to a CPAP machine and using both hands to mask to get better ventilation (two hands thumbs down > one hand C-grip). Look for tracheal deviation (pneumothorax)
  • B: Auscultate both lungs for airways entry (pneumothorax). Percuss if unsure. Get a sats probe on.
  • C: Fingers on femorals. Feel peripheries (hypovolemia), skin turgor and capillary refill. Early use of adrenaline (1mg IV) or atropine (0.6mg IV for bradycardia)
  • D: Defibrillator pads on. Get a 12 lead where you can. Eyes out for low voltage, electrical alterans (tamponade) or infarct. Auscultate briefly for muffled heart sounds (tamponade)
  • E: Electrolytes – VBG as soon as possible (toxins indirectly through the AG, severe acidosis, K and glucose)
  • F: Four chamber view + pneumothroax scan
  • G: Glucose. Please don’t forget.


Some Hs and Ts specifics

  • Hypokalemia
    • 10mmol of K by IV over 5 minutes; consider early CVL
  • Hyperkalemia
    • 10mL of 10% calcium (chloride > gluconate, risks for extravasation injury present but good large bore peripheral IV should be OK temporarily)
    • 0.5mg IV salbutamol
    • Adrenaline (1mg IV resus dosing) helps
    • Bicarb if in acidosis
    • 10U actrapid, 50mL of 50% glucose once ROSC
    • Intra-CPR CVVHD well-documented
  • Tension pneumothorax
    • Finger or needle  thoracostomy
  • Tamponade
    • Pericardiocentesis +/- US guidance
  • Thrombosis
    • Thrombolyse: rTPA 1.5mg/kg is maximum dose