Pathological causes of LVH

My last article looked at the assessment of Left Ventricular Hypertrophy; its contextual clinical significance and subsequent electrocardiographic findings, and concluded with possible pathological reasons for the development of LVH of which I wanted to discuss in my next article.

Sadly, due to an onslaught of assignments more intimidating than Xerxes Persian army in the film 300, I haven’t had the time to write any subsequent material.

However, now the assignments are over I have the time to explore these pathological causes of LVH.

Just as a recap, LVH is an increase in the size and proportion of the left ventricular myocardium. Just like any muscle, the more it is permitted to carry out work (contract) the greater it will increase in size (hypertrophy).

This increase in muscular size results from increased recruitment of sarcomeres (basic subunit of muscle cells) as well as extra cellular matrix remodeling (the scaffolding material of tissue). As a result of these anatomical adaptations the ventricle changes in size and proportion. Its normal conoid shape may be altered.

Concentric/Eccentric Hypertrophy

This remodeling will present as either Concentric or Eccentric hypertrophy depending on the underlying cause.

Concentric hypertrophy results from chronic pressure overload commonly associated with chronic hypertension and aortic stenosis. New sarcomeres are added in parallel to existing sarcomeres. Wall thickness greatly increases and persistence over time will significantly reduce chamber radius. The remodeled ventricle has reduced contractility  and compliance leading to diastolic and eventually systolic dysfunction (impaired filling/ejection).

Eccentric hypertrophy often occurs with volume and pressure overload; pathological associations include heart failure; aortic/mitral regurgitation (volume overload) and chronic hypertension (pressure overload). Ventricular remodeling results in increased chamber radius and moderate increases in wall thickness. Chamber dilation occurs as new sarcomeres are added in series to existing sarcomeres.



Physiological consequences of LVH

LVH usually develops as a compensatory response to the underlying pathologies mentioned above. Increased arterial pressure (afterload) as a result of chronic hypertension and/or aortic stenosis increases the pressure required of the LV to eject this blood.  Increased LV wall tension compensates via concentric hypertrophy.

Volume overload within the heart (heart failure) is often a resultant of valvular regurgitation and/or systolic dysfunction. Aortic/mitral regurgitation will increase the volume of blood left in the ventricle after systole (End Systolic Volume). During the next systolic cycle the LV has to contract with greater force to eject this increased volume of blood (End Diastolic Volume). Frank Starlings law of the heart states that increased stretch on the myocardial wall (Preload) increases strength of contraction. This pressure/volume overload induces chamber dilation and eccentric hypertrophy.

The hypertrophied LV becomes less compliant reducing its filling and contractile capacities. This culminates in systolic dysfunction. Systolic dysfunction is a significant reduction in cardiac output and will present with symptoms of dizziness, fatigue and shortness of breath. Systolic dysfunction of the LV will also lead to pulmonary congestion due to the back up of pressure generated by increased atrial and pulmonary venous pressures resulting from the increased EDV.

LVH is one of the strongest predictors of cardiac morbidity in hypertensive patients. The degree of hypertrophy correlates with the development of congestive heart failure, angina, arrhythmia, myocardial infarction and cardiac death (Lilly).

Another pathological subcategory I have not eluded to that is also a major contributor to LVH is cardiomyopathies. This is something I will look at in detail in my next article. Thanks for reading 🙂



I’d just like to take the opportunity to thank my good friend and partner in crime Christopher Wild for firstly creating this fantastic physiology based resource and secondly giving me the opportunity to participate in its progression.

3 months since creation and the TSP has already received nearly 1500 hits, recognition and support from numerous universities and academics across the country as well as our professional governing body.

My buddy deserves massive acclamation for this achievement and I know there is much more to come!

Whilst writing this article it has again reminded me how interconnected many pathologies, symptoms and clinical findings can be. About half way through writing I felt as though I’d opened a big can of worms as there are so many different tangents on which you could proceed to discuss. Added to this is the limited knowledge I have as I’m only a second year student! Therefore please don’t take this information as cardiology gospel! I have and always will, use reliable sources of information, but this is my interpretation of such material and I can’t guarantee inclusion of every detail.  Nevertheless, I have personally found writing such articles to be of great benefit; and thus if there are any other physiology students out there that may be interested in writing for TSP we would greatly welcome your support.

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Lilly, L. S. (ed.) (2010) Pathophysiology of heart disease: A collaborative project of medical students and faculty. Editor, Leonard S. Lilly. 5th edn. Philadelphia, PA: Lippincott Williams and Wilkins.
(Lilly, 2010, pp. 315 – 315)

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I Have LVH, Should I Be Worried? Normal Variants Of An ECG

As part of our course we often perform ECG’s on one another to enhance and refine our practical ECG skills. During a practical recently I volunteered to be the patient so that my fellow students could practice their electrode placement skills; whilst being filmed and critiqued by others. The group universally agreed in the value of this experience, despite the fact it felt strange performing an ECG to an audience of your friends whilst being filmed in an artificial clinical environment. After everyone had practiced we printed of a recording of my ECG. Our lecturer, whom is a senior physiologist, explained that we would as a class analyse the ECG in our following lecture.

Upon the analysis of my ECG, my lecturer broke the news to me that I had left ventricular hypertrophy (LVH) with sinus bradycardia. Considering the previous lectures we’d had on LVH and its clinical significance I was pretty scared few a seconds or so. He then thankfully reassured me that in my case this was completely normal. My lecturer emphasised the importance of always combining your ECG analysis and findings within the context of your patient.

My ECG LVH sinus brady

He explained my athletic physique (his words) and my age were enough to convince him that my development of LVH was not due to pathological reasons but that of heart remodeling as a result of prolonged physical conditioning. If presented with a 30 stone, 60 year old male, with LVH, or a 70 year old sinus bradycardic female ticking a long at 50 bpm and suffers occasional syncope; this would not fit as a normal finding in the context of these patients.

This practical highlighted the importance of always putting your ECG findings in the context of your patient and the normal ECG variants that may be encountered. The patients we see will be varied. They will be of different genders, ethnicities, ages, physical condition, possibly even pregnant. All these groups will produce significant normal variants in their ECG’s. These factors must always be taken into consideration when assessing the significance of your findings. Is your patient bradycardic and symptomatic suffering frequent dizzy spells or are they a young physically conditioned adult. We will be posting articles shortly on the normal variants expected in some of these patient demographics.

What is LVH

LVH is an increase in size and proportion of ventricular myocardium (in this case specifically the left ventricular myocardium). This can occur in any chamber of the heart but is most commonly found in the LV.

How is LVH diagnosed on an ECG

Most trained operators will spot signs of LVH relatively quickly on a ECG recording as it will be common that precordial ventricular tracings will overlap one another requiring a reduction in gain settings.

However, the Sokolow Lyon criteria is correct method of choice. This involves measuring the amplitude of the S wave in V1 and adding it to the R wave amplitude in V5 OR 6 (whichever bigger). If the sum amplitude is greater than 3.5mV LVH is suspected.

To calculate right ventricular hypertrophy (RVH): Amplitude of R wave in V1 + S wave V5 or 6. If the sum amplitude is greater than or equal to 1.1mV RVH is suspected.

However, an ECG alone cannot determine the extent of hypertrophy and its clinical consequence. An echo-cardiogram would be required to ascertain this.

Causes of LVH

LVH is a result of increased demand put on the LV to increase cardiac output. Over prolonged periods of time this increases cardiomyocyte size. As discussed earlier, this increased CO demand could be the result of exercise, and therefore sustained activity levels could lead to LVH. The upshot of this is that for every heart contraction the ventricles can force out a greater volume of blood for every beat (stroke vol) reducing the demand on the heart to supply cardiac output at rest. For this reason athletes with LVH will have a lower resting HR (sinus bradycardia).

However, there are also many pathological reasons for developing LVH, all of which result in pressure overload in the LV increasing its resting workload.

Some of the most common pathologies associated with LVH are as follows:

• Hypertension (most common cause)

• Aortic stenosis

• Aortic regurgitation

• Mitral regurgitation

• Coarctation of the aorta

• Hypertrophic cardiomyopathy

As LV hypertrophy develops, the myocardium can become so thickened that it begins to inhibit the filling of the LV reducing cardiac output leading to increased risk of mortality.

In my next article I will be looking further into some of the pathological causes of LVH and their clinical significance.


How Is Your ECG Electrode Placement?

As a student cardiac physiologist it has been drilled into our heads from an early stage the importance of correct anatomical electrode placement in obtaining an accurate ECG recording. An ECG measures the electrical activity of a patient’s heart from many different angles, and is achieved by placing 10 sticky electrodes on the patient; four on the limbs and six on the chest. For correct electrode placement we follow the clinical body guidelines set out by the our governing body, the SCST. As specialists within the field, we have a duty to perform these tests in a standardised, methodical manner to produce reliable and accurate diagnostic information, as the ECG is the first port of call when assessing heart abnormality.

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Unfortunately, from my experience, and from that of my colleagues, the misplacement of these electrodes has become somewhat commonplace. To the unassuming operator this may seem superficial but incorrect placement of electrodes can alter the ECG patterns displayed simulating or concealing abnormalities, such as myocardial ischemia/infarction.

There is evidence that many health professionals who record ECG’s have not been suitably trained or assessed in the technique: A study by Kings College London into electrode misplacement highlighted that only 50% of nurses and less than 20% of cardiologists correctly place leads V1 and V2 during a standard 12-lead ECG. These numbers are quite shocking and highlight the widespread misunderstanding of this key diagnostic tool.

An example of how NOT to perform an ECG. V1 and 2 are incorrectly placed, as are 3 and 5.

I personally witnessed an example of this whilst on my first week of placement. I was performing an ECG on a patient within the cardiac ward under the supervision of an assistant technical officer who regularly performs ECGs. I correctly located the anatomical landmarks on the patient’s chest and applied the electrodes, as per the official guidelines. At this point, the ATO interrupted me and challenged the placement of my V1+V2 electrodes, stating they were too low. She then took over control of the procedure and removed the electrodes. She began to count the intercostal spaces, beginning from the clavicle. The guidelines state the operator should identify the manubriosternal joint, or angle of Louis, on the patient to locate the second intercostal space as their first anatomical landmark. This subsequently meant her V1 and V2 electrodes were placed too high and  my original placement was in fact correct. After the procedure I challenged my colleague about this explaining we were taught to follow the SCST guidelines in our electrode placement. The ATO responded by saying that this was “how they had always done it.” I discussed this with my clinical educator and the issue was later addressed with my colleague.

The consequence of incorrect ECG recording can lead to potentially incorrect diagnoses and inappropriate treatment leading to wasteful use of healthcare resources and even cause harm to patients. Evidence suggests that adequate training of operators reduces ECG recording errors. However as the SCST highlights in their guidelines, the indications there is little awareness in many practitioners of the need for training.

Clearly, the solution to this issue is to increase awareness in health professionals exposed to ECG practice about the importance of correct electrode placement.  This could be achieved by increased collaboration between cardiac physiologists and other healthcare professionals. As specialists within the field we have duty to share our expertise and knowledge to ensure our patients receive the best standard of care. As a profession we should be much more active in teaching and increasing awareness of what we do and why it is so important. Relevant staff should be confident in performing ECGs not because of experience, but due to high quality training and continual auditing.

To achieve this I feel our profession needs to embrace this responsibility and be far more active in the support and training of other health professionals.

Khunti, K. (2013) Accurate interpretation of the 12-lead ECG electrode placement: A systematic review. Health education journal . 73 (5) pp. 610-623.

Harrigan, H., Chan, TC., Brady, JW. (2012) Electrocardiographic Electrode Misplacement, Misconnection, and Artifact. The Journal of Emergency Medicine [online]. 43 (6), pp. 1038–1044.

Baxter, S, Blackman, S, Breen, C, Brown, C, Campbell, B, Cox, C, Eldridge, J, Hutchinso, J, Rees, E, Richley, D, Ross, C. Society for Cardiological Science and Technology (2014) Recording a standard 12-lead electrocardiogram. Available from:

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