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Applied Physiology ECG Report
An electrocardiogram (ECG) records the electrical activity of the heart. Electrodes are placed on the surface of the body and the net spread of electrical signals are detected from an area of depolarised myocytes. The shape of a wave can vary depending on the orientation of the wave-front. The duration of myocyte depolarisation and repolarisation is shown on the ECG, the amplitude shows the amount of depolarisation and repolarisation.
There are twelve leads that are seen on the ECG, from the placement of ten electrodes. There are four limb leads which are placed the right arm (RA), left arm (LA), right leg (RL) and left leg(LL) and there are also the six precordial leads which are placed on the chest.
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In the main limb leads the RA, LA, and LL electrodes are used. The RL electrode is used as a neutral lead. It is used to complete the circuit and as a reference for the other leads. Lead I, II and III are formed from the three electrodes used on the arms and left leg. Lead I is formed from the RA and LA electrodes. Any angles are measured clockwise from lead I, as this lead is taken as 0°. Lead II is formed from the RA and LL, giving an axis of 60° to lead I. Lead III is formed from LA and LL, giving an axis of 120° to lead I. These leads are describes as being bipolar (Khunti, 2013).
Figure 1: https://www.cablesandsensors.eu/pages/12-lead-ecg-placement-guide-with-illustrations
The augmented limb leads are produced by combining pairs of electrodes to produce ‘virtual’ electrodes. These leads are describes as being unipolar (Khunti, 2013). Limb leads provide information about the depolarisation wave-front in the coronal plane. aVR moves toward the right arm, aVL moves towards the left arm, and aVF moves towards the left leg.
Figure 2: https://www.cablesandsensors.eu/pages/12-lead-ecg-placement-guide-with-illustrations
The precordial/chest leads are placed on the chest provide information about the depolarisation wavefront in the transverse plane. The precordial electrodes record the movement of depolarisation wavefront from the virtual electrode, towards the outward direction of the chest.
There are pairs of main and augmented leads which lay at right angles to each other, called orthogonal components, these are: lead I and aVF, lead II and aVL and lead III and aVR. Einthoven’s formula is lead I + lead III = lead II. The axis of Einthoven’s triangle can be estimated by looking at orthogonal axes, the easiest to look at are lead I and aVF.
The patient is in sinus rhythm and has a normal heart rate of 78 bpm. The P wave is seen to be longer than 120 ms with notches. The PR interval is prolonged, there is an absence of Q waves in V5-V6 and there is ST elevation in V2-V4.
A standard ECG has a paper speed of 25 m/s, each small 1 mm square is 0.04s (40 ms) and each large box is 0.2s (200 ms). By counting the number of R waves in the 10 second rhythm strip (lead II), the heart rate can be calculated. This shows if the SA (sinoatrial) node is depolarising at an appropriate time. The SA node is known as the “natural pacemaker” (Guyton and Hall, 2006) due to it being the first group of cells creating rhythmic impulses and sending them throughout the heart, to other cardiomyocytes. The SA node controls the depolarisation of other nodes, directly controlling the heart rate. There are 13 R waves on the rhythm strip, there is a heart rate of 78 bpm (beats per minute). This heart rate is within the normal range for an adult, as it is between 60-100 bpm.
The rhythm of the heart can be seen in the rhythm strip (lead II). There should be a P wave seen before every QRS, the QRS complex should not be too wide or narrow (between 70-100ms), and there should be a T wave after every QRS complex. The morphology of the P wave, QRS complex and T wave should be smooth. The rhythm is regularly regular in lead II, with a P wave before every QRS complex, the QRS is not too wide or narrow, and the T wave is seen after every QRS complex. The rhythm was measured by calculating the time between each R wave.
There are four different axis; the normal axis deviation is between -30° and +90°, left axis deviation (LAD) which is less than -30°, right axis deviation (RAD) which is greater than +90° and extreme axis deviation between -90° and 180°. There are three main ways to determine the axis of the heart; the quadrant method, the three-lead analysis, or the isoelectric lead analysis.
From the quadrant method, lead I and aVF are examined. Lead I is positive and aVF is negative. There is a left axis deviation in the ECG.
In the three-lead analysis, lead I, lead II and aVF. Lead I is positive, aVF is negative and lead II is isoelectric. This means that the left axis deviation is physiological rather than pathological, between 0° and -30°. The axis would have been pathological if lead II was also negative.
Figure 5 & 6: https://litfl.com/ecg-axis-interpretation/
The PR interval is usually between 120-200 ms, which is 3-5 small boxes on the ECG graph. The ECG shows the PR interval to be between 5-6 small boxes, or 200 – 240 ms which is not within normal range, there is First-Degree Heart Block.
There is slight PR depression of the PR segment in lead II, but no PR elevation in aVR and V1 which would be signs of pericarditis. There is widespread ST elevation which looks “saddle-shaped” in V2-V4. Pericarditis is a differential diagnosis in this case. Only a few points for the criteria of diagnosing atrial ischemia or infarction have been met. These are that there is PR depression in lead II and that there is abnormal P wave morphology due to notches being present. This may be a differential diagnosis.
The QTc (corrected QT Interval) is 433 which is within normal range, using the Bazett formula (QTc = QT / √ RR). The QTc is used to compare the QT interval over time and to identify any arrhythmia. This is obtained from an average QT interval of 380 ms (9.5 small squares) and a heart rate of 78 bpm. If the patient is a female this would be a normal QTc. The QTc is prolonged if it is larger than 440 ms in men, larger than 460 ms in women, or shorter than 350 ms.
QT = 9.5 x 40
QT = 380
RR = √60/78
RR = 0.8770580193
QTc = 380/0.877
QTc = 433
There is ST segment elevation in the precordial leads, most notably in V2-V4. The ST elevation is also paired with deep S waves. This is linked to LBBB and LVH. LVH would not be present due to there being ST depression or inverted T waves in leads with tall R waves (lead I, aVL, V5 and V6). The ST elevation in V2 is linked to a septal STEMI and an anterior STEMI in V3 and V4. Therefore, an anteroseptal STEMI is present. There ST segment is not elevated in lead I, aVR, V5 and V6. There are no J point abnormalities seen.
Problems within the P wave can be found in the inferior leads II, III, aVF and V1, since the P waves are the most prominent here. The P wave is upright and monophasic in lead II and biphasic in V1. There are a few notches seen on the left side of the P wave, with a steeper side on the right. The average length of a P wave is normally less than 120 ms, however, on lead II it it is around 120-160 ms. The duration lasts longer than usually seen, but the amplitude remains unchanged. The amplitude of the P wave is typically less than 2.5 mm in the limb leads and less than 1.5 mm in the precordial leads, which is seen. The notches, long duration and unchanged amplitude support the diagnosis of left atrial enlargement (LAE). However, negative deepening in V1 is less than 1 mm which is normal.
Q waves are normally seen on leads I, aVL, V5 or V6. The absence of Q waves in V5 and V6 is abnormal and is commonly due to Left Bundle Branch Block (LBBB).
Generally, when looking at the QRS complex, V1 and V2 are negative, V3 and V4 are equiphasic and V5 and V6 are positive. The QRS complex has a normal duration of 70-100 ms or 3.5-5 small boxes. A normal amplitude which is bigger than 5mm in limb leads, bigger than 10 mm in precordial leads, or smaller than 35mm precordial leads is normal. There are Delta waves, upstrokes in the QRS complex, seen in V1 and V2 which are associated which Wolff-Parkinson-White Syndrome (WPW).
The R waves show the early repolarisation of the ventricles, abnormalities can be seen in aVR and V1. Poor R wave progression can be seen in leads I, aVR, and V1-V4. On the ECG it can be seen clearly in V2 and V3.
T Waves and U Waves
There are no T wave abnormalities and the U waves cannot be seen.
The ECG shows LAE from the prolonged P wave and the notches seen on the right-hand side of the wave. LAE is related to stroke and cardiovascular disease (Ou, Chen, Yu, Guo, Zhao, and Sun, 2016).
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The ECG shows First-Degree Heart Block from the prolonged PR interval. First-Degree Heart Block can be congenital, but in most cases, it develops in later life. The electrical signal travelling from the SA node, located at the top of the right atrium, to the AV node, located in the lower back section of the interatrial septum.
The ECG shows LBBB from the absence of Q waves, that means that the depolarisation of the septum would not be in the normal direction, left to right, but in this case from right to left. LBBB can also be diagnosed from elevated ST segments. LBBB is a common abnormality in which the electrical impulse does not travel on the left fascicles of the His and Purkinje fibres. LBBB is often the result of myocardial injury, strain or hypertrophy (Scherbak and Hicks, 2018).
Poor R wave progression shows early ventricular depolarisation, it is linked to prior anteroseptal (myocardial infarction) MI and ST elevation shows the presence of an anteroseptal STEMI. The pattern of the ST segment indicates prior infarction of the anteroseptal and lateral walls.
Delta waves are upstrokes in the QRS complex, seen in V1 and V2 which are associated which WPW syndrome.Wolff-Parkinson-White Syndrome occurs from extra electrical impulses bypassing the usual route, travelling through a shorter route (NHS). The patient may not have WPW due to having a normal heart rate and long PR intervals, but this could develop.
The ST elevation shows signs of pericarditis, however, not all the criteria were met for this to be diagnosed. There should also be reciprocal ST depression and PR elevation in leads aVR for pericarditis to be present.
LBBB has no specific treatment due to it being caused by underlying disorders (Scherbak and Hicks, 2018). A pacemaker can be placed to return the heart back to normal sinus rhythm.
A STEMI occurs when there is a blood clot (thrombus) in the coronary artery. There is then no blood supply to myocardial cells, leading to myocardial heart muscle loss. No oxygen can reach the myocardial cells, causing cell death. Infarcted muscle is gradually replaced with replaced with scar tissue, called fibrosis. “The extent of damage will determine the overall pumping ability of the heart, and is a determinant of ‘heart failure’” (Acute Management of Myocardial Infarction with ST-Segment Elevation, 2013). A STEMI can be diagnosed with a blood test (NHS). The blood test will measure cardiac biomarkers. One example would be cardiac troponin enzymes, that enter the blood from damage to the heart. In less serious cases of a STEMI, blood anti-clotting medication is usually prescribed such as: aspirin, heparin, clopidogrel, prasugrel, ticagrelor, and bivalirudin. If the STEMI becomes serious, the patient can undergo primary percutaneous coronary intervention (PCI). This surgery widens the coronary artery (coronary angioplasty), allowing there to be a better blood supply to the heart muscles. If left untreated a STEMI can worsen and lead to heart damage.
Abnormal heart activity of a heart with Wolff-Parkinson-White Syndrome is harmless and it is said to settle down without treatment (NHS).
The patient has left axis deviation, left atrial enlargement, left bundle branch block, a first-degree heart block, and anteroseptal MI.
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