This 79 year old lady presented to emergency with abdominal pain, nausea and vomiting. On examination, she appeared shocked, with cool mottled extremities and a weak thready pulse. The heart rate was 150 (in AF, but apparently that is long-standing) and the non-invasive blood pressure cuff generated improbable numbers (Pfft, 52/35mmHg? Really?).
A CT of the abdomen was ordered, which revealed the following findings:
Shortly after returning from CT, the surgical team were disappointed to find her breathless and semicomatose. A rapid sequence induction and intubation were carried out, and a post-intubation blood gas was collected.
Though this patient has a reasonable oxygen saturation, one cannot help but notice that in spite of receiving 100% FiO2, their PaO2 is only 144. From the a/A ratio it would appear that only 22% of alveolar oxygen is appearing in the arterial circulation. On the basis of these findings, one might conclude that this patient has some sort of severe respiratory pathology.
There is a severe acidaemia; the pH is 7.069.
The PaCO2 is on the high end of normal. Given that the patient is acidotic, this is inappropriate.
More than likely, the ventilator settings have been left at their default (VT 500ml, rate 12) abolishing any attempts at respiratory compensation.
The Actual Base Excess is strongly negative, suggesting a severe metabolic acidosis.
Copenhagen interpretation of acid-base compensation:
With this massively negative actual base deficit, one predicts that the PaCO2 should be around 22.3mmHg. Since the measured PaCO2 is higher than this, there must also be a respiratory acidosis.
Boston interpretation of acid-base compensation:
Note that this ABG machine reports the actual bicarbonate rather than the standard bicarbonate, which saves the Boston supporter from having to calculate the actual bicarbonate themselves. The actual bicarbonate for this scenario is 12.2mmol/L.
Using the "1.5 plus8 " rule, the expected PaCO2 for this scenario is 26.3 mmHg, much lower than the measured value. Therefore there is a coexisting respiratory acidosis, due to a failure of respiratory compensation (we can blame the anaesthetist).
The anion gap is 27.3
The albumin was 20. With this value, the "normal" anion gap should be 7
The delta ratio is therefore 1.71
This suggests that the metabolic acidosis is a pure high anion gap metabolic acidosis. The lactate is 14.4, which is close enough to the base excess - suggesting that the lactate is almost wholely responsible for the titratable acidity.
There is a massively raised p50. At 47.95, it represents a significant right shift, which can be explained by the severe acidosis. The implications of this change in oxygen-haemoglobin dissociation mechanics for tissue oxygen delivery is profound; the haemoglobin will only reluctantly bind oxygen, and in a sluggish septic circulation there will be little oxygen transport to the capillaries.
This hypoxic patient has a severe high anion gap metabolic acidosis, largely due to lactate generated in her ischaemic bowel. Laparotomy findings suggested an embolic cause, and sure enough there was a thrombus in the left atrium, which can be traced to poor compliance with warfarin.
But why was she so hypoxic? The CT findings of atelectatic bases were not in proportion to the severity of this hypoxia. Another explanation is required. Most likely, in this state of severe sepsis, the reversal of hypoxic pulmonary vasoconstriction by increased nitric oxide synthase activity had resulted in a shunt of blood though the collapsed bases.
Siegel, John H., Ivo Giovannini, and Bill Coleman. "Ventilation: perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis." Journal of Trauma-Injury, Infection, and Critical Care 19.6 (1979): 432-460.
Fischer, Stefanie R., et al. "Nitric oxide synthase inhibition restores hypoxic pulmonary vasoconstriction in sepsis." American journal of respiratory and critical care medicine 156.3 (1997): 833-839.