ECG 1 Analysis, Interpretation and Management
| 1.Other | Initial impression | The above ECG is a 12-lead since the information is recorded from 12 different views of that heat that provides the entire picture of electrical activity. The 12 views are generated by placing the electrode on limbs and chest of the patient. It contains 6 precordial leads that are V1, V2, V3, V4, V5, and V6 that provide the horizontal information of the heart. The resent precordial leads are unipolar such that they only require a single electrode. |
| 2. Rate | Heart rate | The heart rate is 68; the atrial kick contributes 30% of the output in the cardiac. |
| 3.Rhythm | Regular/Irregular | The rhythm is regular |
| 4.P Waves | Wave presence | The P wave is present, and it precedes the QRS with an amplitude of between 2 and 3 mm and period of between 0.06 and 0.12 seconds. It also has a rounded and upright configuration. |
| 5. QRS | Is QRS Present? | The ECG has a QRS complex that accompanies P wave with an interval of 0.03 – 0.09 seconds. It has an amplitude of 5 to 30 mm and follows the PR interval, taking the duration from the start of Q wave up to the terminal of the S wave. The Q wave signifies a negative reflection of P wave, while R wave resembles a positive reflection of either P or Q waves. |
| 6. T wave | Are T waves present? | T waves are present and elevate in the anterior leads. The T waves are inverted with the first half moving slowly that the other half. It is upright in V3 to V6 and leads I and II. |
| 6. Interpretation and Management The ECG shows regular rhythms. The intervals are consistently similar. The hate rate was calculated using rapid estimation approach also known as countdown method (Corrado et al., 2009). The measure was estimated using the more extensive box between R wave and P wave. The ECG indicates the presence of sinus arrest whereby SA node is the pacemaker. The rhythm is regular with heart rates that are within the normal, but vary according to the pauses and the activity of the patient. P. waves, in this case, are normal and constant, while QRS complex is standard if presence, but absent during the pause (Uberoi et al., 2015). Similarly, T wave is standard if present and missing during the pause. The rhythm may nonetheless give the impression of a third degree AV block due to the lack of the QRS complex at some interval. However there is relation between the P and the QRS implying that the atria and the ventricles are still connected with each other. Additionally, third degree sinoatrial block cannot be diagnosed using a surface ECG as highlighted by Romanò (2015), this is because the electrical potentials generated by the sinoatrial node are much too small to be detected o the ECG surface. It is also worth that the QRS complex and the P waves in sinus arrest are usually absent during pause. Patient with sinus arrest is at risk of developing syncope. Therefore, it is essential to inquire from the patient whether he or she has ever passed out or had a feeling of passing out. The patient requires immediate treatment (Drezner et al., 2013). The procedure may involve the use of temporary pacemaker as well as the administration of atropine or epinephrine. However, a permanent pacemaker may be used for long-term management. The primary goal of treatment is to ensure the patient has adequate cardiac output and perfusion. This is accompanied by recording the frequency and duration of pauses to determine whether the pause results in SA block. It is also advisable to check with the individual who witnessed the episode to identify what happens and the duration of the unconsciousness (Baquero et al., 2015). The information is crucial in determining whether that patient experienced a vagal mechanism. The presence of sinus pauses on ECG indicates that there is a need for extensive electrophysiologic assessment. |
ECG 2: Analysis, Interpretation, and Management
| 1.Other | Initial impression | The above image shows the results of a 12-lead ECG that was produced through physical examination of the heart. However, when analyzing ECG, it is essential to follow the sequence of steps to avoid missing the abnormality being traced, which have clinical significance. The frontal QRS axis is used to indicate the average direction of ventricular activation situated in the frontal plane. The normal range is presented by 30 to 90 degree. From the above diagram, the QRS axis is positioned perpendicularly to the lead’s orientation. |
| 2. Rate | Heart rate | The heart rate is 50 beats/minute. The rate is below the normal 65 to 70 beats/minute. |
| 3.Rhythm | Regular/Irregular | The rhythm is regular |
| 4. P Waves | Wave presence | The P wave is present and normal. |
| 5. QRS | Is QRS Present? | The QRS complex of 0.08 is present. The ECG does not show any isoelectric lead; it presents two leads that are 30 degrees apart. The QRS axis within 30 degrees is used to find the perpendiculars for each lead. |
| 6. T wave | Are T waves present? | The T wave is present and Normal |
| Interpretation and Management The ECG waves indicate the presence of Sinus bradycardia. This is because the heart rate is at 50 beats/minutes which is below 60 beats/minute with a regular rhythm. The conditions mostly happen during sleep or when a person has a well-conditioned hear such as an athlete. In this case, the heart can maintain normal stroke volume with less effort. Sinus bradycardia may also occur during sleep as a result of reduced metabolic demands. The condition is a normal response to the decreased demand for the flow of blood (Mattu and Brady, 2011). However, there is an increase in vagal stimulation, while the sympathetic stimulation reduces. There is also the presence of peaked the T waves. This may indicate a sign of hyperkalemia Alboni, Stucci and Parisi (2017) highlights that the condition is not critical unless the QRS complex shows some widening. One important thing to note however is that peaking T waves also occur in other conditions other than in hyperkalemia for instance early repolarization hence comparison with previous ECG should be done. The clinical significance of sinus bradycardia is based on how low the rate is as well as the symptomatic condition of the patient. Most adult patients may be tolerant to the heartbeat between 45 and 59 beats/minute. However, it is rare for a patient to be tolerant to the pulse less than 45beats/minute (Brosnan et al., 2015). Sinus bradycardia may be caused by noncardiac conditions such as hyperkalemia, high intracranial pressure, sleep, hypothyroidism, glaucoma, and hypothermia. It may also result from excess vagal stimulation or inadequate sympathetic stimulation as a result of sleep, Valsalva maneuver or vomiting. The patients who cannot tolerate symptomatic bradycardia may develop symptoms such as hypotension, dizziness, blurred vision, chest pain, clammy skin, syncope and mental complications. The management of bradycardia focuses on identifying and correcting the underlying cause. The first step is to ensure that the heart rate is maintained within the transcutaneous pacing of between 65 and 70 beats/minute. The observation involves assessing the P wave preceding each QRS complex as well as the normal PR interval, T wave, QRS complex and QT interval. The correction is achieved through the use of drugs such as epinephrine, dopamine or atropine as the patients wait for the pacemaker (Houghton and Gray, 2014) The recommended dose include 0.5 mg dose administered through rapid injection, which may be given in every 3 to 5 minutes to attain a maximum of 3 mg. Epinephrine is administered if atropine proves ineffective at a rate of 2 to 10 mcg/minute (Brosnan et al., 2015). The symptomatic sinus bradycardia is treated through the insertion of a permanent pacemaker. |
References
Baquero, G.A., Banchs, J.E., Ahmed, S., Naccarelli, G.V. and Luck, J.C., 2015. Surface 12 lead electrocardiogram recordings using smart phone technology. Journal of electrocardiology, 48(1), pp.1-7.
Brosnan, M., La Gerche, A., Kumar, S., Lo, W., Kalman, J. and Prior, D., 2015. Modest agreement in ECG interpretation limits the application of ECG screening in young athletes. Heart Rhythm, 12(1), pp.130-136.
Corrado, D., Pelliccia, A., Heidbuchel, H., Sharma, S., Link, M., Basso, C., Biffi, A., Buja, G., Delise, P., Gussac, I. and Anastasakis, A., 2009. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. European heart journal, 31(2), pp.243-259.
Drezner, J.A., Ackerman, M.J., Anderson, J., Ashley, E., Asplund, C.A., Baggish, A.L., Börjesson, M., Cannon, B.C., Corrado, D., DiFiori, J.P. and Fischbach, P., 2013. Electrocardiographic interpretation in athletes: the ‘Seattle criteria’. Br J Sports Med, 47(3), pp.122-124.
Houghton, A. and Gray, D., 2014. Making sense of the ECG: a hands-on guide. CRC Press. Hill, A.C., Miyake, C.Y., Grady, S. and Dubin, A.M., 2011. Accuracy of interpretation of preparticipation screening electrocardiograms. The Journal of pediatrics, 159(5), pp.783-788.
Mattu, A. and Brady, W.J., 2011. ECGs for the emergency physician 2. John Wiley & Sons.
Uberoi, A., Stein, R., Perez, M.V., Freeman, J., Wheeler, M., Dewey, F., Peidro, R., Hadley, D., Drezner, J., Sharma, S. and Pelliccia, A., 2011. Interpretation of the electrocardiogram of young athletes. Circulation, 124(6), pp.746-757.
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