What is an Electrocardiogram?
Question:
Discuss about the Electrode placement and Cardiac monitoring.
Hannibal, G (2009); Moses, et al., (2008) defines electrocardiogram as the graphical representation of the electrical conduction of the heart muscles. This is achieved by attaching electrodes to the body surface. It is a tool for diagnosis and management of any cardiac rhythms that are abnormal. It can also be used in the diagnosis of the causes of chest pain. Thrombosis management of myocardial infarction depends on it. It can also be used in identifying the causes of breathlessness in a patient (Hampton, J 2013).
An electrocardiogram for easy interpretation can be grouped into segments, waves, and intervals. P, Q, R, S, T, U waves. The QRS complex segment, PR segment, and ST segment. RR interval, QRS complex interval, PR interval, QT interval and ST interval. A deviation on any of the above is indicative of a problem in cardiac muscles electric conduction (Davidson, 2014).
In electrocardiogram interpretation the following factors are analyzed; rhythm, conduction interval, cardiac axis, description of ST segment, QRS complexes and the T waves (Hampton, J 2013).
- There is a normal sinus rhythm with a heart rate of 50beats/minute because;
Every cycle starts with a P wave, a QRS complex follows the P waves. The PR intervals remain the same. This shows that the electrical conduction starts at the Sinoatrial node. The heart rate is regular and bradycardic.
- There is a normal cardiac axis.
The ventricular depolarization that is seen on the front is called cardiac axis. It is deduced from the interpretation of the QRS complexes on lead I, II, III. A normal cardiac axis looks like a clock moving from 1100hrs to 0500hrs. The deflections on these leads are usually upright. For a normal cardiac axis, the lead II is more positive than the rest (Currey et al., (2005). All of them shows a positive deflection and the lead II deflection is most positive.
- Prolonged PR interval 240ms.
PR interval is measured from the start atrial depolarization that is the P wave to the start of ventricular depolarization that is QRS complex. The normal ranges are 120ms-200ms.
- The QRS segment is normal.
A representation of ventricular depolarization. Has the Q, R, S waves. In V1, V2, V3, and V4 the S waves are deeper than the R waves which is normal. V5, V6 the R waves are longer than S waves which are normal.
- QRS interval is normal, 120ms.
This represents the ventricular contraction, both the left and the right ventricles. It should not 120 milliseconds.
- ST segment is normal.
It is isoelectric that is, it lies on the same level as the sections between the T waves and that of the subsequent P wave. It is an indication of sufficient cardiac muscle perfusion.
This is indicative of first-degree heart block. This is because each depolarization wave originates from the Sino-atrial node, P wave. The P waves atrial depolarization) is followed by a ventricular depolarization QRS complex wave. This is conduction in the ventricles.
Although the above is normal. There is a delay in conduction. The PR interval is prolonged. The start of P wave (atrial depolarization) and the start of ventricular depolarization is prolonged. It is 240milliseconds. The normal range is 120ms to 200ms.
- There is a sinus rhythm with a heart rate of 45beats per minute which is regular.
Interpreting an Electrocardiogram
The depolarization cycle starts with the atrial depolarization that is P wave, at the Sino-atrial node which is conducted to the ventricles which is, ventricular depolarization, the QRS complex wave.
The heartbeat is bradycardic. It is below the normal range of 60-100 beats per minute.
- A normal cardiac axis.
The ventricular depolarization that is seen on the front is called cardiac axis. It is deduced from the interpretation of the QRS complexes on lead I, II, III. A normal cardiac axis looks like a clock moving from 1100hrs to 0500hrs. The deflections on these leads are usually upright. For a normal cardiac axis, the lead II is more positive than the rest (Currey et al., (2005). This is the case on ECG strip two.
- Normal PR interval, 200ms
As mentioned earlier PR interval represents the start of the P wave that is atrial depolarization and the electrical impulse conduction in the ventricles. It is measured from start of P wave and the Q wave. The normal range is 120ms to 200ms. The PR interval on the ECG strip is 200ms which is within the normal range. This shows that the firing of the Sino-atrial node and the electrical conduction is normal.
- The QRS complex segment is normal.
As mentioned early the QRS complex segment is a representation of ventricular depolarization. It is a combination of the Q wave, R wave, and the S wave. On the ECG strip, they are all present although the R waves are longer than 25mm on electrodes V5 and V6.
- QRS interval is normal, 120ms
This represents the time the ventricles take to repolarize. It should not exceed 120milliseconds. In our case, it is normal as repolarization takes 120milliseconds.
- ST segment is normal.
ST segment is measured from the end of ventricular depolarization and the start of ventricular depolarization. On the ECG strip, it is normal as it is isoelectric with the T wave and the P wave. In other words, it is on the same level as the waves mentioned above.
From the electrocardiogram, R waves are longer than 25mm on electrodes V5 and V6. The summation of the V1 and V5 is more than 35mm, it is 53mm. On the 12 lead ECG, V5 is located between the V4 and the V6 on the left 5th intercostal space and V6 is usually on the mid-axillary line on the left intercostal space. They are located in the left ventricle. Their readings show the depolarization of the ventricles (Brunner and Suddath, 2013).
All the above indicates that the patient from which the electrocardiogram was done on has left ventricular hypertrophy.
MacFanane et al., (2010) atria-ventricular block that is first degree just implies that there is a delay in electrical impulse conduction. Despite this, all the impulses are conducted to the ventricles. In most cases it is asymptomatic.
First-degree block is more of a sign than a diagnosis. It can be as a result of coronary artery disease, digoxin toxicity, acute rheumatic carditis, and electrolyte imbalance. Therefore, management of first heart block entails identifying the underlying causes and treating it. For a diagnosis, an echocardiogram is done, cardiac catheterization, blood analysis (in case of toxicity), electrolytes analysis.
Analysis of Electrocardiogram Factors
For example, in cases of electrolyte imbalances, in most cases, it is usually hyperkalemia or hypokalemia. The deficiency should be dealt with appropriately. In hyperkalemia, it is reversed by giving the patient 10Iu soluble insulin intravenously, 10ml calcium gluconate and 50ml 50% dextrose. The patient is advised not to take foods rich in potassium (Brunner and Suddath, 2013)
Example, 2. In case of coronary artery diseases (ischemic heart diseases) which results from atherosclerosis. This causes angina, myocardial infarction, and cardiac arrest. The root of all these problems is atherosclerosis, the formation of cholesterol plaques in the coronary arteries. Treatment involves a change in lifestyle, reduce cholesterol intake, avoid smoking, exercise regularly. Cholesterol-modifying drugs, aspirin, Beta- blockers can also be used in its management. in severe conditions, angioplasty or stents placement is done. The defective coronary arteries are repaired in theatre (Ferri, 2016).
Ventricular hypertrophy eventually translates to congestive cardiac failure which leads to heart failure. Heart failure is the inability is the hearts’ inability to pump sufficient blood so as to meet the tissues need. The oxygen and the nutrients requirement by tissues (Brunner and Suddath, 2013). The management of heart failure targets at reducing the workload of the heart by reducing the preload and afterload. Secondly, it aims at reducing or eliminating the causal factors. Further diagnosis is done through an echocardiogram, cardiac scans, chest X rays, and the management modalities follow the findings (Larvie, 2014).
The management involves modification in the lifestyle; have regular exercises, low-fat diets, low sodium diets and stop smoking. These modifications help in reducing heart pressures. With reduced heart pressure the heart’s workload is reduced (Kaplan, 2015).
The medical management includes Angiotensin-converting enzyme inhibitors. These drugs cause vasodilation, which causes an improvement in blood flow and reduces the workload of the heart. Angiotensin II receptor blockers have similar effects as the drug above. Calcium channel blockers. These drugs are used to prevent calcium influx into the cardiac cells. This reduces blood pressure. Diuretics help in reducing the congestion. They also help in reducing the blood pressure hence reduced workload and better perfusion of the tissues. In the case that aortic stenosis is the case, the aortic valve replacement or repair is done in theatre (Douglas, 2015; Kaplan, 2015).
References
Brunner and Suddath (2013). Cardiovascular system. Medical-surgical nursing. Pg. 600-900, ed 23.
Coronary heart disease (2014). Retrieved from: https://www.nhlbi.nih.gov/health/health-topics/topics/cad. Accessed 12th March 2018.
Currey, A., Leanne M., (2005). Cardiovascular assessment. Nurses guide. Collegian, 12, 1, 34-40
Hannibal, B., (2014). Electrode placement and Cardiac monitoring. Advanced critical care AACN, 25, 2, 188-192
Moser, D., Riegel, B., (2007). Cardiac nursing. Braunwald’s heart disease companion guide.
Davidsons, J., (2014). Cardiovascular system. Principles and practices of medicine. Pg. 67-98, 22nd edition.
Douglas, P., et al. (2015). Pathogenesis of ventricular hypertrophy. Retrieved from https://www.uptodate.com/home accessed on 12th March 2018.
Ferri FF (2015). Coronary artery disease CAD. Clinical Advisor. Retrieved from: https://www.clinicalkey.com. Accessed on 12th March 2018.
Goldberger, L., (2013). Left ventricular hypertrophy diagnosis by electrocardiogram. https://www.uptodate.com/home. Accessed on 12th March 2018.
Kaplan NM (2015). Clinical implications and treatment of left ventricular hypertrophy in hypertension. https://www.uptodate.com/home accessed on 12th March 2018.
Larvie, J., et al (2014). Impact of echocardiographic left ventricular geometry on clinical prognosis. Progress in Cardiovascular Diseases. Pg.57:3.
Maron, M., et al (2012). Clinical manifestations, diagnosis, and evaluation of hypertrophic cardiomyopathy. https://www.uptodate.com/home. Accessed March 12, 2018.
Podrid, P., (2015). Left ventricular arrhythmia and hypertrophy. https://www.uptodate.com/home accessed on 12th Match 2018.
MacFariane et al., (2010). Comprehensive electrocardiology. Springer.
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