Rhythm Nation: August 2016 ANSWER

Good job, Eden Kim, for correctly Identifying pulmonary hypertension on EKG!! Let’s talk about pulmonary fibrosis and pulmonary hypertension and their prominent electrocardiographic findings.

Idiopathic Pulmonary Fibrosis

History

• usually >50 years old
• progressively worsening dyspnea and non-productive cough
• history of cigarette smoking seems to be a risk factor

Pulmonary Hypertension

• Pulmonary hypertension is present when mean pulmonary artery pressure exceeds 25 mm Hg at rest or 30 mm Hg with exercise

Severity

• Mild = 25-40mmHg
• Moderate = 41-55mmHg
• Severe = > 55mmHg

Mechanism

• Chronic hypoxemia causes reflex vasoconstriction in the pulmonary arterioles with consequent elevation of pulmonary arterial pressures.
• Destruction of lung tissue with loss of pulmonary capillaries increases the resistance of the pulmonary vascular bed by reducing its effective surface area.
• Over time, this chronic elevation of pulmonary arterial pressures results in compensatory right atrial and right ventricular hypertrophy.

This leads to:

• Chronic vasoconstriction
• Altered vascular endothelium and smooth muscle function
• Cellular remodelling
• Increased vascular contractility
• Lack of relaxation in response to various endogenous vasodilators
• Fibrosis of vascular tissue

Lets take a look at our EKG

ECG changes in Pulmonary Hypertension and Pulmonary Fibrosis

• Rightward shift of the P wave axis with prominent P waves in the inferior leads and flattened or inverted P waves in leads I and aVL

• Rightward shift of the QRS axis towards +90 degrees (vertical axis) or beyond (right axis deviation).

• Exaggerated atrial depolarization causing PR and ST segments that “sag” below the TP baseline. (STRAIN!)

• Clockwise rotation of the heart with delayed R/S transition point in the precordial leads +/- persistent S wave in V6. There may be a complete absence of R waves in leads V1-3 (the “SV1-SV2-SV3” pattern).

• Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude:
  • > 2.5 mm in the inferior leads (II, III and AVF)
  • > 1.5 mm in V1 and V2

• Right Ventricular Hypertrophy
  • Right axis deviation of +110° or more.
  • Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
  • Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
  • QRS duration < 120ms (i.e. changes not due to RBBB).

• Right bundle branch block (usually due to RVH) or incomplete RBBB
  • Broad QRS > 120 ms
  • RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
  • Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
  • Incomplete RBBB is defined as an RSR’ pattern in V1-3 with QRS duration < 120ms.

Back to our patient:

• The patient had right heart catheterization showing PA pressure of > 100mm Hg, and was started on treatment for pulmonary hypertension

References:

• Bassily-Marcus AM, Yuan C, Oropello J, Manasia A, Kohli-Seth R, Benjamin E. Pulmonary hypertension in pregnancy: critical care management. Pulmonary medicine. 2012:709407. 2012.
• Burns E. The ECG in Chronic Obstructive Pulmonary Disease. Life In The Fast Lane.  http://lifeinthefastlane.com/ecg-library/copd/
• Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
• Harrigan RA, Jones K. ABC of clinical electrocardiography. Conditions affecting the right side of the heart. BMJ. 2002 May 18;324(7347):1201-4. Review. PMID: 12016190
• Nickson C. Pulmonary Hypertension. Life In The Fast Lane. Reviewed and Revised through 12/21/15. http://lifeinthefastlane.com/ccc/pulmonary-hypertension/
• Price LC, McAuley DF, Marino PS, Finney SJ, Griffiths MJ, Wort SJ. Pathophysiology of pulmonary hypertension in acute lung injury. American journal of physiology. Lung cellular and molecular physiology. 302(9):L803-15. 2012.

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