Refers to abnormally of muscle cells resulting in large ventricles or atria resulting in reduced functions, creating potential arrythmias, caused by:
- Dilation by volume (diastolic) overload: Increased pressure within the chamber causing dilation; this is due to the regurgitation of blood due to impaired valves or inability to pump blood forward due to afterload (hypertension)
- Hypertrophy by pressure (systolic) overload: Enlargement of muscle cells due to increased demand or pressure which requires more muscle bulk & cell expansion (usually in athletes). Other reasons include increase resistance in the aortic valve making it difficult to pump blood towards. Other causes can include pulmonary disorders where pressure can backlog the heart.
- Increased QRS amplitudes: As muscle mass increase, so does electrical potentials therefore producing a stronger impulse, furthermore, larger chamber may be near the electrodes producing higher amplitude. Exception is late dilation where ventricular function is poor = lower QRS amplitude
- Prolongation of QRS duration: Slight change due to longer depolarisation time for larger mass – Should not exceed 0.12 seconds (unless due to intraventricular conduction defects).
- Axis changes: Can shift to right (RVH) or left (LVH)
- ST-T segment changes: Secondary ST-T changes such as ST elevation & depression can occur with presence of being discordant to the QRS complex in significant hypertrophy.
Can lead to having atrial fibrillation or flutter (AF) - Usually P-wave is impacted & examined in V1 + Lead II.
Usually from mitral valve impairment causing resistance to flow, hence enlarging the left atrium – A second hump in P-wave is seen showing right atrium contraction before the left.
ECG Findings
- Biphasic p-wave in V1 with wide, deep (> 1mm) terminal component
- Left atrial hyper-terminal component is larger than .04 sec
Pressure in the pulmonary system or resistance in valve can cause right atrium hypertrophy in order to pump blood to the ventricles. This generates a stronger impulse (hence higher P-wave amplitude) where the wave can be seen as a sharp peak – P-wave amplitude is > 2.5mm
ECG Findings
- Rarely isolated finding (usually RVH/RAD also)
- P amplitude >2.5mm in II
- Large biphasic p wave in V1 (> 1.5 mm in V1 and V2)
- Right atrial hyper.-initial component is larger in V1 than V6
- p-mitrale-m notched p wave in leads 1 and 2. Greater than .12 seconds.
Implies enlargement in both left & right atrium (seen as large P-wave in Lead II, and large biphasic P-wave in V1).
Also known as left/right ventricular hypertrophy (LVH/RVH), can lead to having ventricular tachycardia (VT) – Usually QRS is impacted (often tall QRS complex due to increased muscle mass).
Usually V1-V2, & V5-V6 are impacted – Generally by aortic stenosis, insufficiency or hypertension, overloading causes broader QRS where longer depolarisation occurs in the left ventricles.
- R-Wave: V5-V6, Lead I, & aVL show larger R-waves – Usually > 30mm in V5
- S-Wave: Deeper S-waves shown in V1-V2 due to amplified vector of left ventricles
- QRS Complex: Can be notched and prolonged in duration
- V5-V6 Secondary ST-T: ST downslope & T-wave inversion can occur
- V5-V6 Secondary ST-T: ST elevation can occur, ST segment is concaved
- P-mitral may be present (as it affects hemodynamic of left atrium
- Left axis deviation may be present
- Longer QTc interval
Usually, left ventricle’s vector is larger than the right, therefore QRS is dominated by left ventricle. However, right ventricle can be seen in QES due to hypertrophy – This can be by lung or heart disease, and valve impairment.
- R-Wave: V1 & V2 show larger R-waves, wave progression is smaller from V1 to V6
- S-Wave: Small S-wave observed in V1
- QRS Complex: Prolonged slightly (< 120ms) where R-wave is 35-55ms in V1-V2
- V1-V3 Secondary ST-T: ST-T is discordant to QRS complex
- rSR’ pattern can be seen in V1 & V2, can resemble RBBB, but is not
- P-pulmonale can be present
- Electrical axis almost resembles RAD
- V5-V6, Lead I, & aVL display smaller R-waves; due to opposite R-wave progression from V1 to V6
Detection is low to detect biventricular hypertrophy due to both vectors cancelling each other out when both vectors are hypertrophied.
When LVH is shown, an examination should occur to see if RVH is present - shown by:
- Right axis deviation – This never occurs in LVH
- Deep S-wave (> 6mm) in V5 or V6
- Large RS-complex in multiple leads
- P-pulmonale present
References
College of Pre-Hospital Care. (2015). 12-Lead ECG Analysis: Self-Directed Learning Package. Version 3. St John Ambulance Ltd.
Curtis, K., & Ramsden, C. (2016). Emergency and trauma care for Nurses and Paramedics (2nd ed.). Elsevier Australia.
DeLaune, S. C., Ladner, P. K., McTier, L., Tollefson, J., & Lawrence, J. (2016). Australian and New Zealand fundamentals of nursing (1st ed.). Cengage Learning Australia Pty Limited.
ECG & ECHO Learning. (2020). Clinical ECG Interpretation. https://ecgwaves.com/topic/ecg-normal-p-wave-qrs-complex-st-segment-t-wave-j-point/
Life in the Fast Lane. (2020). ECG Library. https://litfl.com/ecg-library/
St John WA Ltd. (2017). Electrocardiography (ECG). Clinical Resources. https://clinical.stjohnwa.com.au/clinical-skills/assessment/vital-signs/electrocardiography-(ecg)
WikiEM. 2020. The Global Emergency Medicine Wiki. https://www.wikem.org
Page contributors:
 | Thanh Bui, AP60825 Event Medic, Emergency Medical Technician & Volunteer Development Officer
|
 | Andrew Moffat, AP16790 |
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