Pulmonary Pressures and ECG Patterns

Ok, so we understand the basics of our Cardiopulmonary System for the most part, at least most of us reading this.

But, if you don’t, DON’T WORRY, we can break it down in a few simple steps…

Here we  go!!!

  • The Right Ventricle (RV) pumps blood to the lungs via the Main Pulmonary Artery Trunk which divides into the left and right Pulmonary Arteries

(Remember the Pulmonary Arteries carry “deoxygenated blood”. The little parenthesis represents finger quotes because this is not totally true, but we will discuss that ahead.)

  • The Pulmonary Arteries continue into arterioles and capillaries which surround the alveoli, where Oxygen (O2) exchange occurs
  • Once this occurs, oxygenated blood moves forward via Pulmonary Veins coming from both right and left lungs, to the Left Atrium (LA) which then continues to enter the Left Ventricle (LV) and to the body

***An increase in the Pulmonary pressures will eventually affect the heart, initially and predominantly the Right Ventricle (RV). RV failure secondary to Pulmonary Hypertension is know as  Cor Pulmonale***

***Changes in Left Ventricular pressures will affect the Pulmonary system, which will eventually affect the RV***

Normal Pulmonary Artery Pressures (PAP): (may vary based on clinician)

Systolic:  15-25 mmHg

Diastolic:  8-15 mmHg

During rest (Diastole), Right Ventricular pressures are very low, close to 0, between  1-6 mmHg(value may differ among clinicians), known as  End Diastolic Right Ventricular Pressure (EDRVP). While End Systolic Pressures range between  15-25 mmHg.

This systolic RV pressure is the same as the Pulmonary Artery Pressure because when the Pulmonic Valve opens, these pressures equalize.

Now, remember how we mentioned above that the statement: Pulmonary Arteries carry deoxygenated blood is not totally true?

This is becuase, under normal circumstances, the body utilizes approximately  25%  of O2 delivered (DO), while 60-75%  of this O2 in our blood goes unused, still available in venous blood. This is know as  Mixed Venous Blood Saturation (SvO2).

Again, Right Ventricular pressures are low compared to Left Ventricular Pressures, therefore, increased PAP will increase the workload of the RV, which can alter cardiac depolarization, repolarization and conductivity, which can produce ECG changes.


During Pulmonary Artery Hypertension (PAH), pressures in the Pulmonary Artery increase. We won’t get into specific details right now, just understand that this changes can affect the heart. These include:

  • COPD
  • Asthma exacerbation
  • Narrowing of arteries
  • Vessel disease
  • Idiopathic cause
  • Pulmonary Embolism
  • LV failure

Pulmonary Hypertension is defined as Pulmonary Artery pressures  >25 mmHg  during rest or  >30 mmHg  during exertion. This increased pressures increases the workload of the RV.


The combination of any of the follow ECG changes suggests increased pulmonary and RV pressures, knonw as


  • Right Ventricular Hypertrophy (RVH)

I. An R wave >7 mm in V1 or V2


II. Deep S wave in V6 >7 mm

Strain Pattern = This is an abnormal ventricular  repolarization due to hypertrophy or dilation of the ventricle. This produces Discordant or inverted asymmetric T wave (the opposite direction of the QRS) with slight ST Segment depression in those leads reflecting hypertrophy.

In these cases, RVH occurs due to increased workload of the RV in an attempt to overcome the greater pulmonary artery pressures

axis part iv RVH wm

What do we see?

– RVH with Strain Pattern

– Right Axis Deviation

  • Right Atrial Enlargement (RAE)

I. Peaked P wave taller than 2.5 mm (>2 1/2 boxes height) in lead II


II. A P wave taller than 1.5 mm in V1. This P wave is known as  P Pulmonale

Right Atrial Abnormality Lead II

Right Atrial Abnormality V1

Keep in mind, on the surface ECG, we can not truly tell if the abnormal P wave morphology is due to enlargement or conduction deffect of the atria, therefore, the term “Right Atrial Abnormality  (RAA) is gaining favor over Enlargment

RAE or RAA, occurs when the Right Atrium (RA) has to work harder to open the Tricuspid Valve against the already increased RV pressures

  • Atrial ectopi and arrhythmias

I.  Atrial Ectopic Rhythm: Identified as a Supraventricular rhythm (originating above the ventricles) with 2 different P waves.

II.  Wandering Atrial Pacemaker (WAP):  Identified as 3 different P waves and irregularly irregular rhythm

III. Multifocal Atrial Tachycardia (MAT):  Same principal as WAP, at least 3 different P waves with irregular  tachycardia

MAT wm

What do we see?

– Irregularly irregular rhythm

– At least  3 different P waves

– Incomplete Right Bundle Branch (IRBBB) pattern

Multifocal Atrial Tachycardia

What do we see?


IV.  Atrial Fibrillation (AF):  Identified as an irregularly irregular rhythm with lack of P waves and fibrillatory isoelectric segments due to chaotic electrical activity in the atria, with variant vectors

  • Right Bundle Branch Block (RBBB)

I. Supraventricular origin

II. Wide QRS complex >.12s (>3 small boxes wide) for complete RBBB  or >.10s for incomplete RBBB (IRBBB)

III. Terminal monophasic R wave in V1. A second R wave may be present  known as  R (R prime)  being taller tha the first R wave,  also known as Bunny or Rabbit Ears

IV. Wide and slurred lateral S waves in Leads I, aVL, V5-6 indicating delayed RV depolarization

RBBB AFWhat do we see?

– Atrial Fibrillation with Rapid Ventricular Response

– Right Bundle Branch Block

  • Rightward Axis deviation (RAD)

The mean direction of impulses in the frontal plane (limb leads), moving inferiorly and rightward due to the increase muscle requiring more conduction. This gives rise to a QRS axis > 90 degrees in the right quadrant of the Hexaxial System, NOT due to a Left Posterior Fascicular Block (LPFB)

This is easily seen as negative QRS in lead I and positive in the inferior leads.

  • S1Q3T3

I. Deep S wave in lead I due to greater vectors moving towareds the RV, away from lead I

II. Q wave in lead III due to right to left depolarization

III. Inverted T wave in lead III due to alteration of ventricular repolarization vectors

This finding is known by many to be an indicator of PE, however, it is not pathognomonic of PE.  This means, S1Q3T3 is not a specific sign or proves  without a doubt that PE is present.

This ECG is from a previous case of a 56 yof with confirmed PE.

Other findings:


Low voltage is seen when there is reduced amplitude (size) of QRS complexes. Increased intra-thorasic pressures and air volume build up alter voltage reading during ECG evaluation. Think of it as dampening or the heart.

I. QRS <5mm in Limb Leads


II. QRS <10mm in Precordial Leads


Obtaining a 12 lead ECG is an important aspect of our pre-hospital and in-hospital setting evaluation of both cardiac and respiratory patients, as increased pulmonary pressure changes can dramatically alter cardiac function with or without prior cardiac history.


  • qwert says:


  • ilies2000 says:

    thank you it's very interressant ..!!!

  • Tyler says:

    How are we supposed to differentiate between right axis deviation and left posterior fascicular block?

  • Ivan Rios says:

    A few tips might help ruling in or out LPFB, such as the absence of RVH which can cause a Rightward frontal axis >90 degrees can support the presence of LPFB, pathological high lateral Q waves can cause severe rightward axis as well which suggest the axis is not due to LPFB. There is no 100% definite saying with the ECG alone, however, along with patient history and current event, your “differential diagnosis” accuracy increases.

  • tolesa says:

    Thank you.

4 Trackbacks

Leave a Reply

Your email address will not be published. Required fields are marked *