Question 15

College Answer

This man is profoundly hypoxic with a PaO2 of only 50 mmHg on 100% oxygen (AaDO2=596 mmHg; PaO2/FiO2 ratio 50).

He is alkalemic, with an elevated bicarbonate (metabolic alkalosis) and an elevated PaCO2 (higher than predicted = respiratory acidosis)

Electrocardiographic features of 1st degree heart block and RVH: Right axis, R wave in V1>5mm, R/S in V1>1 and R/S in V6 >2.5.

Further information that may help clarify the cardiac status include:

Clinical examination (RV heave, loud P2, raised JVP, giant v waves, pulsatile liver, ascites, peripheral oedema).

CXR may show lung disease, and show evidence of pulmonary arterial hypertension (prominent pulmonary arteries with peripheral pruning).

Echocardiogram (TTE vs TOE)- will show RV hypertrophy, may reveal PA pressures if there is some TR (which is usual in pulmonary hypertension). Exclude Ostium primum ASD, Eisenmengers complex.

Pulmonary artery catheter will reveal PA pressures and cardiac output. V/Q is a poor test to investigate chronic RV hypertrophy.

Discussion

The ECG features of RVH are explored in this excellent article from LITFL. Thank you, Ed Burns!

In summary, the changes are as follows:

• Right axis deviation
• Dominant R wave in V1
• Dominant S wave in V5-V6
• Normal QRS duration (i.e. not a right bundle branch block)

Right ventricular strain patterns is also well covered there:

• ST depression / T wave inversion in the anterior leads, V1 - V2
• ST depression / T wave inversion in the inferior and right-facing limb leads ( II, III and aVF)

Now, as to what the college means by "clarify the cardiac status" - this is uncertain.

I guess that must mean "investigate the cardiac causes of these ECG changes and blood gas abnormalities".

That would have been a better way to word this question.

Thus, we have RVH on the ECG and a metabolic alkalosis, respiratory acidosis and profound hypoxia on the ABG.

One immediately begins thinking about some sort of pulmonary arterial hypertension, pulmonic valve stenosis, massive PE, or a cyanotic heart defect with a right-to-left shunt.

How would one discriminate among these differentials?

By taking a thorough history, performing a complete examination, and requesting appropriate investigations.

• History:
  • Features of pulmonary hypertension, incl. SOB, cyanosis, exercise in tolerance
  • History of foetal alcohol exposure or a family history of congenital heart defects
  • History of exposure to volatile toxins, disease-causing dust (eg. asbestos) or heavy smoking
  • History of thromboembolic disease, prothrombotic diathesis
• Examination:
  • Features of pulmonary hypertension: split P2, opening snap of pulmonic valve, flow murmur though pulmonic valve, prominent a waves
  • Features of RVH: right parasternal heave, prominent a waves, tricuspid regurgitation murmur, cannon v waves
  • Features of RV failure: pulsatile liver, engorged pulsatile veins
  • Congential syndromic features which might lead one to investigate for congenital heart disease
• Investigations
  • CXR to interrogate the mediastinal contour and to look for features of poulmonary hypertension
  • TTE to observe the characteristic echocardiographc features of the above
  • CTPA and bilateral lower limb dopplers to exclude thromboemolic cause for hypertension
  • Right heart study to measure the oxygen saturation in each chamber, looking for a ventricular septal defect - as well as measuring the pressures.

Myers, Gordon B., Howard A. Klein, and Bert E. Stofer. "The electrocardiographic diagnosis of right ventricular hypertrophy." American heart journal 35.1 (1948): 1-40. - this goes back to well before the lazyness of transthoracic echo.

CHEST has an old 1993 article about pulmonary hypertension, which has some relevance to this very day;
Rubin, L. J. "Primary pulmonary hypertension." CHEST Journal 104.1 (1993): 236-250.

If one wishes to avoid the right heart study, one may wish to examine these European guidelines:
Grünig, Ekkehard, et al. "Non-invasive diagnosis of pulmonary hypertension: ESC/ERS Guidelines with Updated Commentary of the Cologne Consensus Conference 2011." International journal of cardiology 154 (2011): S3-S12.