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supply & demand…

Case:

74 year old female is placed in the acute-area of our ED with a complaint of retrosternal chest tightness at approximately 9am. Her symptoms sound very typical for ACS. She looks clammy and pale.

My colleague has placed her on telemetry, high flow oxygen and has prescribed 300mg aspirin &  600mcg sublingual anginine.

I am handed her ECG, which shows a sinus tachycardia and evidence of left ventricular hypertrophy with a repolarisation pattern. Of concern is the associated anterior ST depression, so I make my way to the bedside….

…as I approach her bed I witness her telemetry deteriorate from a sinus tachycardia to ventricular fibrillation !!

There is a defibrillator 15 metres away, across the department. The following takes place…

    • Precordial thump (by me. did nothing except hurt my hand).
    • Immediate CPR until defib pads placed.
    • 200J shock
    • 2 further minutes of CPR with 1mg IV adrenaline.
    • 3 minutes post arrest she has return of spontaneous circulation.

Cardiology are notified of this and want her in their Cath-lab immediately….

…I receive a call from the Cardiology Reg an hour later with the angio results !

    • Normal coronary arteries.
    • Critical aortic stenosis with valve area of 0.5cm2.
    • Seen by Cardiothoracic surgeons already
    • Going for aortic valve replacement this afternoon.

Discussion: CRITICAL AORTIC STENOSIS.

Causes:

    • Calcific degeneration (most common)
    • Bicuspid aortic valves
    • Rheumatic heart disease
    • Congenital heart disease

Natural history / Pathophysiology:

    • Long latent period with decades of slowly progressive obstruction.
        • Normal valve area = 3cm2
        • Critical aortic stenosis = < 0.8cm2
          or pressure gradient > 50mmHg.
    • Left ventricle hypertrophies to preserve ejection fraction.
    • Further progression = LV dysfunction, LA enlargement & atrial fibrillation.
    • These patients are preload dependent & have little cardiovascular reserve.
        • Delicate balance between myocardial oxygen supply & demand !
        • Precipitous decompensation w/ ischaemia, rapid AF, volume depletion or anaemia.
    • With symptom onset, average survival is 2-3 years.
        • High risk of sudden death.

Clinical Features:

Classically:

    • Angina (demand ischaemia)
        • decreased supply (reduced perfusion pressure)
        • increased demand (high wall stress)
    • Exertional syncope
        • Fixed cardiac output & vasodepressor response.
    • CCF / dyspnoea
        • Diastolic & systolic dysfunction.

The Murmur: crescendo-decrescendo systolic murmur, radiates to carotids.

      • Loudest at right 2nd intercostal space.
      • Associated S4 gallop & soft S2.
      • As disease severity increases; the murmur peaks later & is less apparent.

The ECG.

The ECHO – required to assess for severity

  

Treatment.

Essentially medical therapy is ineffective & valve replacement should be performed as soon as the patient is symptomatic. Negative inotropic agent, beta-blockers, vasodilators and nitrates should be used with caution due to reduction in preload or afterload causing significant hypotension.

The decompensated patient with critical aortic stenosis in the acute setting requires;

  • Judicious fluid resuscitation
  • Blood transfusion
  • Restoration of sinus rhythm
  • Refractory cases may require intra-aortic balloon pump as a bridge to surgery.

I hope you find this helpful,

Chris.

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