A 37-year-old male has presented to the Emergency Department with a 12-hour history of central crushing chest pain. He was taken to Catheter Lab by the cardiologists who have referred him to ICU 12 hours later due to hypotension, and confusion. His ECG (ECG 23.1) is shown on page 9, and laboratory results are presented below.   

Parameter

Patient Value

Adult Normal Range

FiO2

6L Hudson Mask

pH

7.36

7.35 – 7.45

pO2 

162 mmHg (21.6 kPa)

pCO2

36.7 mmHg (4.89 kPa)

35.0 – 45.0 (4.60 – 6.00)

SpO2

99%

Bicarbonate 

20.1 mmol/L*

22.0 – 26.0 

Base Excess 

-4.4 mmol/L*

-2.0 – +2.0 

Lactate 

5.1 mmol/L*

0.5 – 1.6

Sodium 

148 mmol/L*

135 – 145 

Potassium 

4.8 mmol/L

3.5 – 5.0

Chloride 

115 mmol/L*

95 – 105

Glucose 

28.0 mmol/L*

3.5 – 6.0

Aspartate aminotransferase (AST)

3252 U/L*

< 35

Alanine aminotransferase (ALT)

6378 U/L*

< 35

Alkaline phosphatase (ALP)

58 U/L

30 – 110

-Glutamyl transferase (GGT)

32 U/L

< 40

Prothrombin time (PT)

29.8 seconds*

12.0 – 15.0

International normalized ratio (INR)

2.9*

0.8 – 1.1

Activated Partial Thromboplastin Time (APTT)

> 170.0 seconds*

25.0 – 37.0

Creatinine 

140 U/L*

45 – 90

(actual ECG image removed by examiners)

Dr Smith's ECG Blog

  1. Describe the ECG (ECG 23.1 on page 9) changes.                                     (20% marks) 
  1. Give a rationale for the biochemical abnormalities.                                     (20% marks)
  1. What is the most likely diagnosis?                                                             (10% mark)

[Click here to toggle visibility of the answers]

College answer

a) Describe the ECG changes Bradycardia 
ST elevation in Leads II, III and aVF (inferior MI acute) also in lateral leads. ST elevation also in anterior leads, I aVL (Lateral) have ST depression. 
Compete Heart Block 
 
b) Give a rationale for the biochemical abnormalities 
Metabolic acidosis with elevated Lactate, either cardiogenic shock or related to bradycardia. Lactate is relatively high considering normal pH and only minor reduction in bicarb – potentially catecholamine infusion or hepatic injury 
Elevated liver enzymes AST and ALT probably associated with hepatic congestion Elevated INR and APTT associated with hepatic congestion, or therapeutic interventions

Corrected Na is elevated, hyperglycaemia may be underlying diabetes or stress response.

Mildly elevated Creatinine 140 secondary to hypotension, and/or contrast post angiography.

May also be pre-existing. 
 
c) What is the most likely diagnosis? 
Cardiogenic shock due to Acute right ventricular Infarction with hepatic congestion, or shock related to bradycardia 
 

Discussion

Though the ECG image was removed by the examiners, and souvenir exam papers becoming forbidden to trainees (as of this paper), it is impossible to determine which Google search the examiners used to get their images. Fortunately, within fifteen seconds one is able to conjure an ECG with the described abnormalities, from Dr Smith's ECG blog. Stephen W. Smith describes it thus:

"Rhythm: There is a regular, narrow complex bradycardia, with ventricular rate of ~43 bpm. There appear to be P-waves at irregular intervals, but without relationship to the QRS.  Thus, there is third degree (complete) AV block.  The escape is narrow, thus junctional or from the bundle of HIS.  

QRST: The QRS is narrow, so any ST-T abnormalities are primary: there is significant ST elevation in leads II, III, and AVF, with reciprocal ST depression in leads I and AVL, all suggestive of an inferior STEMI. Note that the ST elevation in lead III is greater than that in lead II, but that this is not specific for culprit artery (RCA vs. Left Circumflex).  However, there is ST elevation in lead V1, the furthest right pre-cordial lead, which lies directly over the RV free wall and highly suggests a Right Ventricular MI"

This context serves to demystify the rest of the interpretation. Rationale for the rest of the abnormalities is as follows:

  • There is virtually no A-a gradient, probably because this sort of MI does not tend to produce florid pulmonary oedema (A-a = (0.30 × 713)-(36.7 / 0.8) - 162 = 6 mmHg).
  • There is no acidaemia or alkalaemia
  • There is a metabolic acidosis, which is mild (SBE -4.4)
  • The respiratory compensation is appropriate (expected CO2 is 36.3 mmHg if you use the Copenhagen method, or (1.5 × 20.1)+8 = 38.1 mmHg by Winter's formula).
  • The anion gap is raised if you calculate it with potassium (17.7) or normal without it (12.9). The delta ratio is therefore either 0.23 or 1.46 (because the bicarbonate change was so small). Because lactate is raised (5.1), one would be probably more inclined to trust the potassium-inclusive result, as it fits better into the "liver, lactate, HAGMA" narrative. 
  • Speaking of the LFTs, they are profoundly deranged, with a predominantly hepatotoxic patter, colloquially referred to as a "transaminitis". The large AST elevation can be in part attributed to the myocardial myocyte death.
  • Synthetic liver function is deranged, with elevated PT/INR and APTT.
  • The creatinine is raised (140) which the college have attributed to contrast post angiography ("He was taken to Catheter Lab").
  • There is otherwise unexplained hyperglycaemia, which given the state of cardiogenic shock could be due to anything, including the stress response and catecholamine release.

In summary, the most likely explanation which covers the ECG and biochemistry is cardiogenic shock due to right ventricular infarction, with hepatic congestion. 

References