Ok, so we understand the basics of our Cardiopulmonary System for the most part, at least most of us reading this.
But, if you donâ€™t, DONâ€™T WORRY, we can break it down in a few simple steps, soâ€¦
Here ya 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 â€œdeoxygenated bloodâ€. 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 asÂ 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:Â 15-25 mmHg
Diastolic:Â 8-15 mmHg
During rest (Diastole), Right Ventricular pressures are very low, close to 0, betweenÂ 1-6 mmHg, known asÂ End Diastolic Right Ventricular Pressure (EDRVP). While End Systolic Pressures range betweenÂ 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:Â â€œPulmonary Arteries carry deoxygenated bloodâ€Â is not totally true?
This is becuase, under normal circumstances, the body utilizes approximatelyÂ 25%Â of O2 delivered (DO), while 60-75%Â of this O2 in our blood goes unused, still available in venous blood. This is know asÂ Mixed Venous Blood Saturation (SvO2).Â
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.
PULMONARY ARTERY HYPERTENSION
During Pulmonary Artery Hypertension (PAH), pressures in the Pulmonary Artery increase. We wonâ€™t get into specific details right now, just understand that this changes can affect the heart. These include:
- Asthma exacerbation
- Narrowing of arteries
- Vessel disease
- Idiopathic cause
- Pulmonary Embolism
- LV failure
Pulmonary Hypertension is defined as Pulmonary Artery pressuresÂ >25 mmHgÂ during rest orÂ >30 mmHgÂ during exertion. This increased pressures increases the workload of the RV.
ECG CHANGES CONSISTENT WITHÂ PULMONARY HYPERTENSION
The combination of any of the follow ECG changes suggests increased pulmonary and RV pressures, knonw as
PULMONARY DISEASE PATTERN
- Right Ventricular Hypertrophy (RVH)
I. An R wave >7 mm in V1 or V2
II. Â A deep S wave in V6 >7 mm
Strain PatternÂ = This is an abnormal ventricular Â 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
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 asÂ P Pulmonale
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 â€œRight Atrial Abnormalityâ€ (RAA) is gaining favor over â€œEnlargmentâ€
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.Â Atrial Ectopic Rhythm:Â Identified as a Supraventricular rhythm (originating above the ventricles) with 2 different P waves.
II.Â Wwadsfandering Atrial Pacemaker (WAP):Â Identified as 3 different P waves and irregularly irregular rhythm
III.Â Multifocal Atrial Tachycardia (MAT):Â Same principal as WAP, at least 3 different P waves with irregularÂ tachycardia
What do we see?
– Irregularly irregular rhythm
– At leastÂ 3 different P waves
– Incomplete Right Bundle Branch (IRBBB) pattern
What do we see?
IV.Â Atrial Fibrillation (AF):Â 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 RBBBÂ or >.10s for incomplete RBBB (IRBBB)
III. Terminal monophasic R wave in V1. A second R wave may be present due known asÂ Râ€™ (R prime)Â being taller tha the first R wave,Â also known asÂ â€œBunny or Rabbit Earsâ€
IV. Wide and slurred lateral S waves in Leads I, aVL, V5-6 indicating delayed RV depolarization
– 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,Â 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.
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.Â This means, S1Q3T3 is not a specific sign or proved without a doubt that PE is present.
What do we see?
– Inverted T wave in V1
– Rightward frontal axis
– Low QRS voltage
This ECG above is from a 36 yom with syncopal episode while standing in line for an Halloween attraction. This patient advised he recently landed from an 18 hour flight.
Past Medical history:Â DVT and PE
He advised while standing in line, he experienced sudden shortness of breath, became sweaty and passed out.
Vital signs: HR 108-115 bmp, normotensive, SpO2 in the low 90s and tachypneic.
He was transported emergency to the closed receiving ED and CT confirmed the presence of multiple small clots. I did lost track of him after returning to service.
This ECG is from a previous case of a 56 yof with confirmed PE.
(click on the ECG to view case)
- LOW QRS VOLTAGE
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.Â 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.