1. Tall 'tented' T waves
In the presence of hyperkalemia, the T wave on the ECG/EKG rises in amplitude (A, below). In text books, we are told that in a given lead, the T wave should be no more than half the amplitude of the preceding R wave. In reality, ‘tall’ T waves are quite common on the ECG of normal individuals, particularly young men ('normal variant' in B and see our videos on avoiding error in ECG interpretation on acadoodle.com) . However, you can see that they differ markedly in morphology (below). If we use the computer to superimpose the 'normal variant' tall T wave (red T wave, (C)) on those associated with hyperkalemia you can appreciate the difference. In the case of hyperkalemia, the tall T wave has a narrow base (C, black line) and rises rapidly to a point (C, red arrow). These features are said to result in a 'tented' appearance. The male variant T wave is broad based (D, black line) and does not rise to a point but rather to a curve at its apex (blue curve). When we superimpose these two T waves (C) you can see why people say that the hyperkalemic T wave appears to be pinched (black arrows) in the middle compared to the normal variant.
2. P wave changes
Worsening hyperkalemia is associated with progressive flattening of P waves, prolongation of the PR interval (PR interval > 200 ms) and eventually disappearance of P waves. Bradycardia is common and AV block may complicate hyperkalemia.
3. Broad QRS complexes
As serum K+ levels rise the qrs complex becomes wider eventually passing the upper limit of normal. At least think of hyperkalemia if you see this combination of wide qrs complexes and tall T waves.
4. Development of a sine wave pattern
As K+ levels rise further, the situation is becoming critical. The combination of broadening QRS complexes and tall T waves produces a sine wave pattern on the ECG readout. Cardiovascular collapse and death are imminent.
5. Endgame. Ventricular fibrillation
The end game for untreated hyperkalemia is chaotic depolarisation of ventricular myocardium: ventricular fibrillation. No cardiac output is present. This situation is not compatible with life.
As a general rule if an ECG looks utterly bizarre think of hyperkalemia.
Blockage of a coronary artery results in ischemia of the myocardium supplied by that vessel. In practice, this usually arises due to thrombosis of an atheromatous plaque in a coronary artery (yellow above). The clot formed in the lumen of the artery deprives the area of myocardium it supplies of oxygenated (arterial) blood. Ischemia of the affected region of myocardium progresses to necrosis over a period of hours. In theory, therefore, myocardial infarction (MI) is a histological diagnosis requiring the demonstration of necrotic myocardium under the microscope. In reality, we have no way of obtaining a sample of myocardium to establish the presence of myocardial necrosis. In clinical practice we, therefore, rely on a combination of imprecise indicators of the presence of myocardial necrosis to diagnose MI.
In 2012, a new universal diagnosis of MI was accepted by the European and North American cardiology societies. The 'third universal definition of myocardial infarction':
A myocardial infarction is assumed to have taken place or to be taking place if there is evidence of A) myocardial necrosis in a clinical setting consistent with B) acute myocardial ischemia.
Evidence of A) (myocardial necrosis) is a rise to (or fall from) a cTn (cardiac troponin) level above the 99th centile. (ie a dynamic change in troponin levels with at least one 'high' value)
Evidence of B) acute ischemia is at least one of the following
So, in clinical practice, MI is defined as A) plus one or more of B)
Note that there may be a retrospective element to this diagnosis. It may take time for the serum troponin level to rise. We may need to act before this and, therefore, should be able to recognise the possibility of evolving MI based purely on B) 1, 2 and 3. Proceeding to B) 5 with re-establishment of vessel patency may then be indicated and life-saving.
Disclaimer: This is a ‘pop’ article. It contains the personal views of the author and is designed to generate discussion only. It is not endorsed by any clinical body and should not guide clinical practice.
There is currently interest in the application of ECG screening to young sports people. Getting an ECG is easy, reading them in the young is challenging. Consider the ECG shown below. It is taken from a schoolboy aged 16 years. He plays multiple contact sports and trains regularly. His mother is concerned about a lack of energy obvious in several recent matches. He has no complaints. There is no significant family history. On examination, he is 6′ tall and weighs 145 pounds. Cardiovascular examination is completely normal.
As indicated by the reviewing doctor below, his ECG is strikingly different from those we are used to looking at in clinical practice but is it any cause for concern? Will he be able to play next Saturday?
The answers to these questions are no and yes (if selected). When analyzing the ECG of young men, particularly those who are physically trained we must keep 5 (maybe 6) things in mind
In general terms, the height of the R waves in the left lateral chest leads and the depth of the S waves in the right sided chest leads correlate with the muscle mass of the left ventricle. The criteria (Sokolow-Lyon criterion) for pathological ventricular hypertrophy were established in post-mortem comparisons of heart size to ante-mortem ECGs. The criteria are reasonably specific and have been validated in the old and middle aged subjects in recent years using cardiac MRI. There is some doubt, however, as to whether these criteria are in any way applicable to the young.
The young mans ECG easily satisfies the published criteria for left ventricular hypertrophy (see below). He probably does have a degree of left ventricular hypertrophy but this is expected as a normal consequence of regular training. When considered in clinical context, the R waves and S waves on his ECG are normal.
The perceived risk here is that we could miss a case of hypertrophic obstructive cardiomyopathy (HOCM), a condition associated with left ventricular hypertrophy and sudden death. However, the great majority of HOCM cases will demonstrate ST changes and/or pathological deviation of the cardiac axis in association with the R and S wave changes of hypertrophy. ECG (A) below does not cause great concern in a young sportsman. In contrast, the same findings associated with widespread repolarization abnormalities (T wave inversion) in ECG (B) would be a cause for concern and would merit further investigation.
Tall R and deep S waves in isolation, are not an indication for further investigation in a young person.
On the ECG under consideration, there is a marked sinus arrhythmia. The arrhythmias present in very fit young people may be even more dramatic but equally benign. Benign conduction abnormalities, such as the Wenkebach phenomenon or first degree AV block, are common perhaps reflecting increased vagal tone in this group, carry no risk and may disappear during exercise.
The ECG under consideration demonstrates an incomplete right bundle branch block (RBBB) that is an rSr ‘pattern’ in lead V1 with a normal qrs duration (less than 0.12s, less than 3 small squares). This is a common normal variant on the resting ECG of young people, Also, in the young, T waves are normally inverted in V1 and V2 (the ‘juvenile T wave pattern’).
Complete RBBB (qrs duration > 0.12s) is also common in the young in the absence of heart disease. The evidence suggests that this has no clinical implications. The fear amongst most doctors here is that we might miss a case of the Brugada syndrome, a cause of sudden death in the young. However, the three subtypes of Brugada syndrome are associated with upright T waves and/or ST elevation in V1/V2.
Incomplete right bundle branch block is of no concern. In the absence of ST segment elevation in V1 and V2 and provided the T waves in these leads are negative, this is probably also true of complete RBBB. However,many experts would disagree with the latter statement advocating further investigation for any case associated with a prolonged qrs duration. It’s up to you.
U waves, bifid P waves, q waves and T wave inversion (TWI), are features of many a normal ECG. These features are present on our subjects ECG.
A. U waves (blue outline) are often seen on the normal ECG. They are probably produced by the normal process of Purkinje fibre repolarization. They may become exaggerated in the presence of hypokalemia but if you look, they are present on most ECGs even in the absence of metabolic derangement.
B. Physiological q waves (blue circle) are common on the ECG in the absence of heart disease. Pathological Q waves are a recognised feature of HOCM. The criteria for distinguishing physiological q waves from pathological Q waves associated with HOCM differs from the criteria used to analyse these waves in cases of ischemic heart disease. It has been suggested that the presence of q waves greater than 3 mm in depth or greater than 40 ms in duration should raise concerns in the young. The deepest q waves on our young mans ECG are 3 mm in depth.
C. Bifid p waves are frequently seen on normal ECGs. They represent a physiological separation of right and left atrial depolarisation and are of no significance. ‘P Mitrale’ is said to exist when the separation of the right atrial and left atrial peaks is 1mm or more (> 1 small square). P mitrale, if present, is said to be highly specific for left atrial abnormality. On this ECG the separation is less than 1 mm. This is not P mitrale.
D. T wave invesrion (TWI, circled in blue) is frequently seen in lead III in normal subjects. In this context, it is of no significance. T waves are expected to be inverted in aVR and in the young they are normally inverted in leads V1 and V2.
In recent years, it has been realised that ST elevation is present on the ECG of the majority of normal young men. This ‘male pattern ST elevation’ is usually observed in the right sided chest leads and is no cause for concern. The ECG under consideration is a nice example. The ST elevation (white arrow) is about 1 to 2 mm above the TP segment (blue line) and has a characteristic morphology (‘concave upwards’ shape). ST elevation in this scenario follows a deep S wave and in turn is followed by tall upright T waves. Inverted T waves in this situation might be a cause for concern but it is worth remembering that ST elevation in the chest leads in conjunction with T wave inversion may be a normal variant in young men of sub-Saharan African origin.
We said ‘5 tips’ but we should probably factor in one more
Our profession is ruled by risk aversion. As the tyranny of preventative medicine creeps into sport, a few words of wisdom seem appropriate. Some years ago my wife and I were house-hunting in the area around Perpignan. Our driver was an elderly french gentleman, small in stature but memorably charismatic. A former paratrooper in the Free French Forces, he had fought behind German lines during the battle to liberate occupied France and had the serenity and charm of a man who had ‘seen it all’. Sitting beside a swimming pool in the small village of Fitou, at a moment of doubt, he turned to us and said, ‘don’t let fear stop you from doing anything in life, a life worth living always carries risks’. Sound advice.
Figure 1. The bicarbonate buffering system in the ECF
1. CO2 is an acid. As shown in the figure above, CO2 when dissolved in water generates carbonic acid and will, therefore, acidify any solution.
2. CO2 is a gas. Its level in the body is controlled by excretion in exhaled air. It is, therefore, referred to as 'respiratory acid'. Disturbances in extracellular fluid (ECF) pH secondary to diseases which alter the level of CO2 in the ECF are referred to as primary respiratory pH disturbances.
3. Bicarbonate is a base. Bicarbonate is a metabolite produced in several metabolic processes. The level of bicarbonate in the ECF is controlled by a balance between its rate of production in the body and its rate of excretion in the kidney. It is referred to as 'metabolic base'. Disturbances in ECF pH secondary to diseases which alter bicarbonate levels are referred to as primary metabolic pH disturbances.
4. Think of acid-base homeostasis as a balance between a respiratory acid (CO2) and an opposing metabolic base (HCO3-).
5. A disease process which elevates respiratory acid (CO2) levels in ECF results in a primary respiratory acidosis. A disease process which lowers respiratory acid (CO2) levels in the ECF results in a primary respiratory alkalosis.
6. A disease process which lowers metabolic base (HCO3-) levels in the ECF results in a primary metabolic acidosis. A disease process which elevates metabolic base (HCO3-) levels in the ECF results in a primary metabolic alkalosis.
7. The body can compensate for the change in ECF pH by adjusting the component of the bicarbonate buffering system it still controls. These secondary changes in the bicarbonate buffering system are termed compensation. How does this work?
8. In the presence of a primary metabolic pH disturbance, predictable compensatory changes occur in CO2 levels which oppose the disease-induced change in pH. This is termed respiratory compensation. In the presence of a metabolic acidosis the body will try and get rid of respiratory acid (CO2) in an attempt to bring the pH back towards normal. While in the presence of a metabolic alkalosis the body will try and retain respiratory acid (CO2).
9. In contrast in a patient with a primary respiratory pH disturbance, predictable compensatory changes occur in HCO3- levels opposing the disease-induced change in pH. As this change in bicarbonate levels is mediated by the kidney, this is termed renal compensation. So, in the presence of a respiratory acidosis the body will raise the concentration of metabolic base (HCO3-) in an attempt to bring the pH back towards normal. While in the presence of a respiratory alkalosis the body will decrease the level of metabolic base (HCO3-).
10. In most pH disturbances, compensatory mechanisms move the pH towards the normal range but usually do not succeed in returning it to the normal range. Compensation in these scenarios is said to be partial. This actually helps us to interpret blood gas abnormalities.
Considering the 10 points above, we can easily predict the four patterns of pH disturbance on the ABG
Arterial blood gas analysers are designed to measure multiple components in the arterial blood. The readout from the machine quotes normal values based on the assumption that the sample analysed is arterial (an ABG). There is currently a plague of ‘venous’ blood gases (VBG) in clinical practice. A VBG is obtained by placing a venous sample in the arterial blood gas analyser. VBGs are popular as it is far less painful for the patient to obtain a venous sample compared to an arterial sample. In addition, obtaining ABGs carries well known risks. VBGs are useful if you know how to interpret them and have a knowledge of their limitations.
An ABG has a number of uses, the VBG can be substituted for some of these uses but not for others.
The pO2 on a VBG bears no relationship to the paO2. The VBG is of no value in assessing oxygenation status.
In patients with COPD we need to detect the presence of CO2 retention. This has an important impact on treatment.
If the pCO2 on the VBG is above the normal arterial range (ie >45 mmHg, >6 kPa) the patient has CO2 retention. (100% sensitivity reported, so, at least in studies, it does not appear to miss any cases)
However, the absolute value of pCO2 on the VBG above this range correlates poorly with the paCO2 and cannot be used to monitor the response to treatment in a CO2 retainer.
This is probably where the VBG is of most use but there are still limitations.
The venous pH correlates well with the arterial pH. The venous pH tends to be more acidic than the arterial pH. Add 0.035 to the venous pH to estimate the arterial pH. In conditions such as DKA, it is probably reasonable to follow the pH response to treatment with VBGs. In addition, if there is no concern over a patient’s oxygenation status, it is reasonable to screen for pH disturbances with a VBG. Sometimes this can be very helpful. For example, in an elderly person with abdominal pain, identification of an unsuspected acidosis could drastically alter the differential.
The venous bicarbonate correlates reasonably well with the arterial bicarbonate. However, there are outliers. If in doubt do an ABG.
There are limitations to the VBG in assessment of pH status.
All correlations break down in the presence of shock. The VBG has no role in the assessment of critically ill patients.
The ‘bedside rules’ (see our video tutorial) have not been validated for VBGs, therefore, at the present time, VBGs have no role in the assessment of mixed acid-base disturbances.
Elevated venous lactate levels show no relationship with the arterial lactate. A venous lactate level elevated above the normal arterial range quoted on the arterial blood gas analyser has no meaning clinically.
The arterial blood gas analyser will measure electrolyte levels in the plasma. People often use a VBG to obtain a rapid assessment of electrolyte levels in a patient, as we can analyse the sample in the Emergency Department avoiding the time needed to send the sample to the lab. Be careful! Remember the concentration of key electrolytes is influenced by the presence of hemolysis. The most important example is K+. In vitro hemolysis of red cells in a blood sample will give rise to release of K+ from red cells and may produce an artefactual hyperkalemia on the readout. Venous samples sent to the laboratory are screened for hemolysis, VBG samples analysed in the Department are not. Be cautious when analysing K+ levels on a VBG or indeed on an ABG for that matter.
There is an excellent correlation between the levels of carboxyhemoglobin and methemoglobin on a VBG and an ABG.
Some people say that the VBG will replace the ABG in clinical practice. This is a little premature and may reflect the fact that many of us don’t know how to read an ABG properly to maximise the information available (see our detailed video tutorials).
Has this helped you? Have you any comments/suggestions? Please comment below: