Question 18

College Answer

a)

Probably multifactorial but potential causes:

• Distributive shock
  • Septic shock
• Cardiogenic shock/cardiac depression from sepsis/drugs
• Obstructive shock- 
  • pneumothorax
  • High PEEP 
  • Dynamic hyperinflation
  • Tamponade less likely
  • PE unlikely
• Hypovolaemic shock less likely but patient may be fluid responsive
• Drug delivery failure – misplaced CVC / kinked or leaking line
• Administration of drugs causing hypotension e.g. propofol, IV paracetamol

b)

Clinical exam (ABCs) to assess for cause and resuscitate simultaneously

• Rapid check to verify BP – non-invasive, check transducer position, check arterial pressure trace not damped
• Recent CXR / lung U/S for pneumothorax
• Associated oxygen requirements
• CVP – baseline and change with fluid responsiveness
• Evidence of end organ perfusion: lactate, urine output, LFTs
• Response to dynamic manoeuvres (e.g. straight leg raise)

Management options:

• Assess for and treat reversible causes: 
• If possible minimise PEEP and sedation o Check ventilator settings
• Judicious fluid filling but conflicting goals given oxygenation difficulties
• Urgent echocardiogram to exclude cardiac cause and assess fluid responsiveness +/- cardiac output monitor (PAC/PiCCO/Vigileo)
  • If hyperdynamic consider addition of steroid therapy and vasopressin
  • If low cardiac output state consider addition of adrenaline +/- other inotrope e.g. milrinone/dobutamine
  • If hypovolaemic appropriate fluid resus
• Maintain adequate oxygenation, ventilation
• Review micro and check sensitivities
• Broad spectrum antibiotics
• Consider fresh bag of noradrenaline

Discussion

a)

Broadly, differential diagnosis for shock would have to include the following categories:

• Neurogenic: another form of “distributive” shock
• Anaphylactic: also “distributive” shock
• Cardiogenic: pump failure. No pumping = no blood flow
• Hypovolemic: loss of blood or water
• Obstructive: eg. tension pneumothorax or cardiac tamponade
• Septic: “distributive” shock; stagnation of blood flow owing to vasodilation

In the context of the history we are offered, one may need to reframe the answer and order it in reference to the likelihood of each cause. The college love it when you prioritise your answer. Thus:

• Septic shock  is the most likely answer, as the patient already has a diagnosed
• Cardiogenic shock is the next most likely, as the patient is in the right age group for coronary artery disease, is at risk of MI, and may have a degree of septic cardiomyopathy
• Hypovolemic shock is the next most likely, and may represent a sudden GI bleed ( as patients with high PEEP are at greater risk of gastric ulceration) or another
• Obstructive shock is possible, given that the PEEP is very high
• Artifactual shock: the blood pressure is being measured incorrectly, or the noradrenaline line has become accidentally disconnected

b)

This approach assumes that the patient does not have any fancy PiCCO or PA catheter in situ.

• Rule out artifactual and spurious causes
  • Re-zero/recalibrate arteral line
  • Ensure vasopressor infusion line is connected
  • Exclude drug error ("is that really noradrenaline?")
  • Ensure sedation infusion rate is not accidentally excessive
• Assess the airway
  • Rule out airway obstruction
  • Examination of the patient'sface to rule out angioedema and anaphylaxis can take place at this stage, as it would be important to exclude these early.
• Assess the respiratory system
  • Examine chest expansion
  • Auscultate the chest
    • Rule out tension pneumothorax
    • Rule out dynamic hyperinflation
  • End-tidal CO2:
    • Rule out hypercapneic vasodiation
    • Consider massive PE if EtCO₂ is suddenly lower than the last PaCO₂
  • Drop PEEP to 8-10, to exclude the contribution of high PEEP
• Assess the circulation in detail, focusing on the following
  • Capillary refill
  • Tachycardia or bradycardia (i.e. is the rate responsible for the hypotension)
  • Arrhythmia (i.e. AF with loss of atrial kick)
  • Heart sounds and murmurs (new murmur? Did the mitral valve just die on me? Are the heart sounds muffled, suggestive of a pericardial effusion?)
  • CVP and its trend: did the CVP just suddenly drop, or rise?
  • Urine output in the last hour
  • Aspirate the NG tube, to look for blood or coffee grounds
• Assess dynamic predictors of fluid responsiveness
  • Pulse pressure variation, arterial line"swing"
  • Passive leg raise test
• At this stage, one should decide whether one wants to give a fluid bolus of 10ml/kg
• Perform a rapid bedside TTE, looking for:
  • LV contractility (grossly: "good, bad, not too bad")
  • RV dilatation (grossly: is it bigger than the LV on a 4-chamber view?)
  • Pericardial effusion and tamponade
  • IVC diameter (although this resembles black magic, because nobody knows what the normal appearance should be. A dry collapsed IVC is more informative than a vaguely mid-sized one).
• At this stage, one should decide whether one wants to add an inotrope, eg. milrinone or dobutamine
• At this stage one should also have come to the conclusion as to what short of shock state this is.
  • If the shock is of a distributive sort, one should consider adding vasopressin to noradrenaline, and giving the patient a "stress dose" of corticosteroids.
• Investigations:
  • Perform a CXR to ensure the CVC tip is in an appropriate position and that no new pathology has emerged beyond the pneumonia
  • Perform an ECG, looking for new change suspicious of MI
  • Perform an ABG and a set of bloods to look for lactic acidosis and to establish any organ system failures
  • Perform a septic screen, including blood cultures and inflammatory markers
• If the cause of haemodynamic instability is still not apparent form these manoeuvres, or a TTE is not available, one may need to resort to advanced haemodynamic monitoring techniques:
  • PA catherisation
  • PiCCO monitoring
  • ScvO₂ sampling