shock and awe…

the case.

Previously well 64 year male presents to ED with 90 minutes of retrosternal chest pain after riding his bike.

This is his ECG….

 

[DDET Describe & interpret his ECG.]

• Rate:
  • Atrial ~ 60/min.
  • Ventricular ~ 36/min
• Rhythm – regular. No P-QRS relationship therefore complete heart block
• Axis ~ +60* (Normal)
• Intervals;
  • PR – n/a
  • QRS ~ 90 msec
  • QTc ~ 380 msec
    
• Segments;
  • STE (II, III & aVF) [III > II]
  • STD (V2-5, I & aVL)
  • V1 isoelectric ST.
• Other;
  • Q-wave in lead III

Interpretation.

Inferior STEMI with right ventricular extension (STE III>II, isoelectric ST V1, STD V2) and complete heart block.

[/DDET]

His BP drops to 60…
What do you do now ?!?!?

[DDET You grab the ultrasound…]

Here is our patient’s ECHO…

httpv://www.youtube.com/watch?v=1IOCNWTR63I

Definite RV hypokinesis. No pericardial effusion/tamponade.

[/DDET]

[DDET He’s still hypotensive ! Now what ??]

Right Ventricular Infarction & Shock

• Right ventricular infarction rarely occurs in isolation.
  • Complicates ~ 1/3 – 1/2 of all inferior AMIs.
• RV infarction is a common cause of shock.
  • Inferior AMI, clear lung fields & hypotension…
  • ~20% of shocked patients in GUSTO-I.
  • Carries a similar in-hospital mortality rate to that of LV-infarction & shock !!
• Often complicated by bradydysrhythmias.

Simply put, the infarcting RV fails to offer a sufficient preload to the LV. Consequently reducing cardiac output & resulting in systemic hypoperfusion.

• Volume-sensitive state (in contradistinction from the pressure-sensitive state of LV-infarction).
  • Patients are dependent upon preload.
• Classically, high right atrial pressures but low systolic pulmonary artery pressures.
  • A disproportionate elevation of RV-filling due to excessive volume loading can result in marked RV dilatation, paradoxically causing high pulmonary-wedge pressures secondary to a left-ward shift of the intraventricular septum.
  • This is the physiologic concept of Biventricular Interdependence. – see image below.
• Shock can be compounded by factors that impair RV-filling such as;
  • Intravascular volume depletion
  • Concomitant atrial infarction
  • Loss of AV-synchrony

Treatment.

• Avoid nitrates
• Preload maintenance / Volume replacement
  • IV fluid boluses
  • Caution: excessive amounts may further compromise RV function.
  • Some advocate for placement of pulmonary-artery catheter.
    • Suggested target – RAP 10-14mmHg [>14mmHg associated with reduced RV function]
• Oxygen (w/ impaired gas-exchange & respiratory failure)
• Antiplatelet therapy + anticoagulation.
  • Aspirin loading
  • Clopidogrel / Ticagrelor etc.
  • Heparin / Bivalirudin etc.
• Revascularisation.
  • Early !!
  • Thrombolysis
    • ?TPA & other newer agents prevent shock better than streptokinase.
    • Thrombolytics become much less effective once shock is established (streptokinase maybe better than TPA in this instance)
  • PCI.
    • Improved survival (amongst shocked STEMI patients) over those who receive thrombolysis.
    • Typically results in successful reperfusion (1-2 vessels involved on average).
    • Early revascularisation can result in near immediate recovery of RV function.
• Intra-aortic Balloon Counterpulsation.
  • Many text-book references suggest this as a stabilisation manoeuvre for those with shock awaiting PCI.
  • Recent data (particular IABP-SHOCK II) suggest that the use of IABP heralds no significant reduction in 30-day mortality nor reduction in 12-month all-cause mortality.
• Inotropes.
  • Dobutamine, noradrenaline, milrinone, levosimendan etc.
• Electrical stabilisation.
  • Maintenance of atrioventricular synchrony.
  • Transcutaneous or transvenous pacing may be required.

[/DDET]

[DDET The conclusion]

• With the diagnosis made, our Cardiac Cath team was notified & mobilised to the hospital
  • IV fluid bolused with temporary improvement in SBP to ~ 90mmHg.
  • Atropine trialled without benefit.
• At angiography.
  • Heavy thrombosed proximal RCA lesion identified & successfully reperfused.
• Shock persisted despite reperfusion & insertion of temporary pacing wire.
• IABP placed & patient transferred to ICU on inotropes.
• DC to ward on Day 4 of admission.
• DC home well on Day 8 post-infarct.

[/DDET]

[DDET References]

1. Hasdai D et al. Cardiogenic shock complicating acute coronary syndromes. Lancet. 2000 Aug 26;356(9231):749-56.
2. Jacobs AK et al. Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry. J Am Coll Cardiol. 2003 Apr 16;41(8):1273-9.
3. Inohara T et al. The challenges in the management of right ventricular infarction. Eur Heart J Acute Cardiovasc Care. 2013 Sep;2(3):226-34.
4. Right Ventricular Myocardial Infarction – UpToDate.com
5. Thiele H et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012 Oct 4;367(14):1287-96.
6. Thiele H et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet. 2013 Sep 2. pii: S0140-6736(13)61783-3

[/DDET]