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


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


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

[DDET You grab the ultrasound…]

Here is our patient’s ECHO…


Definite RV hypokinesis. No pericardial effusion/tamponade.


[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

RV infarct septal mment


  • 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 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 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


Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.