The role of 12 lead ECG in Pediatric Pulmonary Hypertension

An 11  year old male presents with complaint of substernal chest pain, 6/10, unable to describe the sensation but non-radiating, which  started while running.

Primary assessment:

  • Patent airway
  • Adequate respiratory effort with no signs of distress
  • skin is pink, warm and dry, with no signs of hypoperfusion

Pertinent medical Hx:

  • Chronic Interstitial Lung Disease
  • Secondary  Pulmonary Hypertension

No allergies reported

Medications:

  • Acetaminophen PRN
  • Furosemide  20mg
  • Flovent

Baseline vital signs:

  • Heart rate: 112 beats/min
  • Respiratory rate: 24 breaths/min
  • SpO2: 97% on 2 lpm O2
  • Capillary refill: < 2 seconds

The patient is evaluated in the ED and admitted or further evaluation. The following 12 lead ECG is obtained:

 

ECG1

  • Sinus rhythm
  • Biatrial Enlargement or Abnormality
  • Right Ventricular Hypertrophy (R > 7mm in V1-2)
  • Rightward Frontal Axis (QRS axis approximately 121 degrees)
  • Right Precordial ST segment depression

As many prehospital and in-hospital providers are initially taught, ST segment depression and T wave inversion indicates myocardial ischemia. However, there are other conditions which can present with ST segment depression  and T wave inversion,  and not be ischemia related. These are  commonly due to ventricular repolarization abnormalities, electrolyte imbalances such as Hypokalemia (low serum Potassium) and Hypomagnesemia (low serum Magnesium) and in the pediatric setting, Juvenile T waves or Juvenile T wave Inversion.

Reponarization abnormalities, such as the ones seen in ventricular hypertrophy, ventricular beats, Bundle Branch Blocks or ventricular paced rhythms, are knows as Secondary ST-T changes, which again, are not due to ischemia but the altered repolarization conduction. At times, it might be hard to differentiate between the two, however, in this case,  the patient is admitted and diagnosed with Cor Pulmonale, treated for Pulmonary HTN and mild Hypokalemia of 3.0 mEq/L following blood work. Cath performed show no structural coronary artery deffects or occlusion.

28 days later, the same patient presents to the Emergency Department complaining of chest pressure and is again admitted. The following 12 lead ECG is obtained:

first

  • Sinus rhythm
  • Biatrial enlargement or abnormality
  • Rightward Frontal Axis at 112 degrees
  • Biventricular Hypertrophy voltage criteria
  • Secondary ST-T changes

  An Echocardiogram study is performed which showed mild dilated Right Atrium (RA) and dilated Right Ventricle (RV) with decreased RV systolic function and tricuspid valve regurgitation. Normal Left Ventricular function and size noted.

  The patient is admitted and treatment remained with Viagra (sildenafil) 20mg, Ambrisentan 10mg, Lasix 20mg and shceduled Bipap. Hemodynamic monitoring was established with Central Venous Pressures (CVP) and Pulmonary Artery Pressures (PAP) assessed and controlled.

16 days later, the following 12 lead ECG is obtained, with no complaint or symptoms:

Untitled

  •  Sinus rhythm
  • Biventricular Hypertrophy voltage criteria
  • Rightward Frontal Axis at 98 degrees
  • Secondary ST-T changes

This time, Echo showed thickened RV free wall with improved systolic function and tricuspid valve insufficiency.  There is a  dilated  main pulmonary artery with normal branches.  The LV remained within normal limits.

 

Take home value:

In the emergency medicine setting,  a large portion of pediatric population will present  with pulmonary  and   cardiac related complications, which mostly arise from congenital etiology. The pulmonary and cardiac systems (Cardiopulmonary) are unavoidably  related for normal physiologic function. Although RV forces are typically predominant in the early stages of life and often normalizes as the LV increases in workload and size, pathologic RV  changes  are one of the most common abnormal findings  during pediatric ECG evaluation, which often, not only reflect cardiac abnormalities, but pulmonary system deffects.

For further, click on the link below:

Pulmonary artery pressures and ECG patterns

4 Comments

  • Tyler says:

    Can you explain how these ST segment and T wave changes can be differentiated from right strain pattern?

    • Ivan Rios says:

      Thanks for writing Tyler. They are the same thing. Strain pattern is just the result of increased pressures against the ventricles which alters the way repolarization occurs from epicardium to endocardium. Similar to stepping on a puddle of water. Your show spreads the water away from the area of pressure. The ST segment is slightly depressed, sometime more prominent depending on how high the voltage is (the taller the R wave, the deeper the ST segment), and the T wave is inverted but remains asymmetric (slow downstroke and fast upstroke), like an normal upright T wave would be. I just happened to not use the term “strain pattern” here. I hope it helps!

  • Shaheedul Islam says:

    Precision of discussion is noteworthy. It helped a lot to understand PAH in an ECG. Thanx much Ivan Rios.

  • NICE case and discussion by Ivan Rios! I’ll just add a few points.

    #1) It is of interest how dynamic QRST changes are for this series of tracing in this pediatric patient with RVH and pulmonary hypertension. I “take home” several pearls from awareness of how much these serial ECGs change including the point that effective treatment may greatly alter the ECG picture, especially in these younger patients with congenital heart disease – AND – that some of the changes probably reflect not only alteration in the extent of “hypertrophy” of heart chambers – but rather volume and pressure changes that occurred during the course of treatment. This IS clinically helpful – because in THIS particular patient, should he present again – all it would take is a quick glance at his ECG to get an excellent idea of his cardiopulmonary status (since we’ve seen the extremes of ECG manifestations during our previous treatment).

    #2) The diagnosis of RVH is MUCH easier in children than in adults. This is because the pediatric right ventricle is relatively larger compared to the left ventricle than it is in adults. Therefore – increases in RV dimensions are much easier to see – whereas in adults, even when the RV dramatically increases in size, it is still usually no where near the amount of LV mass. By the time you see a tall R wave in V1 and RV “strain” in an adult – it is almost always near end-stage disease.

    #3) One needs to refer to Tables in assessing Pediatric Voltage limits. For example – the initial R wave in V1 of ~ 9mm is barely above the mean for a 12-year old boy – and no where near the 98% percentile for voltage in this lead for this age group (GO TO – http://tinyurl.com/ECG-Peds-R-Wave). So while slightly-taller-than-expected – I would make the diagnosis of RVH on the TOP ECG NOT because of QRS amplitude in lead V1 – but rather because of associated marked right axis -RAA (Right Atrial Abnormality – persistent precordial S waves in V5,V6 – and ST-T wave changes consistent with RV “strain”.

    #4) For free On-Line access to Upper Normal Limits for ALL Age Groups – GO TO – http://www.normalecg.org

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