College Answer

Consider mixed aetiology for shock
•    Cardiogenic (cardiac history, severe sepsis, rhythm)
•    Distributive shock (sepsis)
•    Obstructive  shock (PE, tamponade)  – less likely but will probably  get mentioned.
Maybe give less marks for this than the other causes

Establishing relative contribution of each to the hypotension
•    Clinical Signs
•    Distributive;  warm  and  dilated  (if  adequate  filling),  temperature,  potential  source sepsis

•     Cardiogenic
•    LVF; tachycardia, bibasal crepitations, gallop
•    RVF; JVP, hepatomegaly, oedema
•    Escalating monitoring
•    Minimal: ECG, NIBP, SpO2
•    ABP, CVP progressing to Central Venous O2 Sat / TTE / PICCO / PAC as indicated

•    Laboratory Investigations directed at cause
•    Lactate, Troponin, ECG, CXR, Sepsis screen, UA
•    Collateral history

Interventions
•    Optimise preload
•     Cardiogenic
•    Optimize preload (low from redistribution
•    Optimize contractility
•    Rhythm; rate control / normalization (cardioversion?)
•    Inotropic support
•    Dobutamine / Milrone / Levosimenden / Adrenaline / Nor Ad (increases coronary art perfusion pressure) Caution with inodilators while still hypotensive

•     IABP
•    CPAP
•    Reversible / Specific factors

•    Exclude / treat ischaemia (heparin / angio , revascularisation etc.)
•     Distributive
•    Optimize preload
•    Vasopressor support
•     Noradrenaline
•    Adjuncts: Vasopressin / Steroid (infusion or bolus)
•    Mixed pathology issues
•    Risk of Noradrenaline  alone is an increased  afterload  with worsening  cardiogenic shock / peripheral perfusion

•    Start with inotrope and then add vasopressor; dobutamine / norad combination

•    Adrenaline may a safer choice (inotrope + vasoconstriction)

Discussion

This is a question about undifferentiated shock. The question really should read "how do you assess a patient in a non-specific shock state, and maintain their organ perfusion while looking for a cause?" It would probably be useful to mention a rapid focused bedside echo. Obvious hints in terms of fever and a history of crusty coronaries have been given. The examiners would mainly be looking for a systematic approach to diagnosis and treatment, without overcommitment to any specific diagnosis.

The following is really just a rearrangement of the college answer. A standard template of shock assessment should exist; it can be applied here with minimal variation.

Immediate management:

• Attention to airway and breathing
• Establish secure venous access
• Introduce invasive monitoring tools - arterial/central line

Rapid assessment:

• Focused history to differentiate a source of sepsis, and to assess the contribution of cardiac ischaemia
• Physical examination to assess adequacy of peripheral perfusion
• ABG, ECG, CXR, cardiac enzymes, blood and urine cultures
• Rapid bedside TTE to rule out cardiac tamponade and to assess contractility
• Fluid challenge 20-40ml/kg of crystalloid, to assess fluid responsiveness - plus/minus dynamic bedside manoeuvres
• Consider advanced hemodynamic monitoring, eg. SvO2 PAC or PiCCO

Decisive management for this mixed shock state:

• Control sepsis
  • Broad spectrum antibiotics, given early
  • Consider "stress dose" steroids
• Optimise preload
  • Fluid boluses to continue, as permitted by measures of fluid responsiveness
• Optimise afterload
  • Maintain organ perfusion and coronary filling by maintaining a MAP > 65 and a reasonable diastolic pressure, using vasopressors such as noradrenaline and vasopressin
• Optimise rhythm
  • Consider early DC cardioversion if the rhythm is atrial fibrillation, to recover the "atrial kick"
• Optimise contractility
  • If there is concern regarding contractility, consider inotropes eg. dobutamine milrinone or levosimendan
• Use adjuncts to resuscitation
  • Consider IV thiamine, perticularly if there is lactic acidosis
• Reverse any reversible factors
  • Early angiography or thrombolysis
  • Surgical source control for septic foci