Journal of Emergency Nursing
Added on 2021-05-31
14 Pages3967 Words46 Views
Running head: EMERGENCY NURSING1Emergency NursingNameInstitution
EMERGENCY NURSING2Emergency NursingOption 1: Pediatric CaseQuestion 1: 12 Lead ECG InterpretationsAdditional information: Calibration: 20mm/mv. Speed: 25mm/s. Negative AVR. Mild chest discomfort. Rhythm strip- V1Rate Atrial -160The p-wave is small, upright, and precedes every QRS The P-R interval is 0.08 seconds implying that it is normal. Ventricular-160The QRS interval is 0.04 seconds which is narrowRhythm Regular AtrialST depression is 2mmThe T-wave is invertedRegular ventricularThe QT interval is 0.32 seconds QTc= 0.32/√0.40=0.506secondsThe above time is an indication of a prolonged QTc12 leadAVR is a negative p wave with a positive QRS and a 1mm ST depression in addition to a negative T-waveV1- biphasic T waves, tall R waves, 2.5 mm ST depression, narrow RS, andsmall positive P waves. The bundle branch is absent.The AVL is a positive flattened p-Wave with a narrow QRS and a t-wave that is flattened uprightV2- biphasic T wave, 2.5 mm ST depression, narrows RS, and small positive P waves.Heart block is absent. AVF is a small positive p-wave an elevated ST with 1mm and a narrow V3- V2- biphasic T wave, 2.0 mm ST depression, narrows RS, and small positive P waves.
EMERGENCY NURSING3QRSI is a flattened positive p-wave, a narrow QRS, a biphasic T wave, 1mm ST elevation, and a deep Q-wave.V4- an inverted T wave, a narrow RS,and small positive P waves. II is a narrow QRS, positive p-wave, an upright T-wave and a 1mm ST elevation.V5- a narrow QRS, a 2.5mm ST elevation, and a flattened positive p waves.III is made up of small positive p-waves, flattened T-waves, and an ST elevation at 0.5mm. V6- a narrow QRS, a 2.5mm ST elevation, and a flattened positive p waves.The 12-lead ECG can be interpreted as a sinus tachycardia with a lateral (inferior) ST elevation. Additional there is an anterior (septal) ST depression with a prolonged QT.Question 2: Abnormal Findings from the CaseAccording to Bernstein (2016), a rheumatic heart disease (RHD) is a consequence of an acute rheumatic fever due to an infection by a group A streptococcus that further leads to the damage of the heart valves. Sika-Paotonu, Beaton, Raghu, Steer, & Carapetis (2016) ascertain that the rheumatic heart disease is a condition that results from single or multiple recurrent episodes of acute rheumatic fever. The acute rheumatic fever is common among children aged
EMERGENCY NURSING4between 5 years to 14 years (Sika-Paotonu et al., 2017). It is, however, important to note that there has been a dramatic reduction in the cases of the acute rheumatic fever recorded since penicillin was introduced. According to Pellekaan & Best (2015), this complication is still widely common among the Aboriginal and Torres Strait Islander communities that are found in Australia. Cross-reactivity between group A streptococcus and antigens of the cardiac is referred to as molecular mimicry. This reactivity is responsible for the immunologic activation and consequently the destruction of the heart tissues (Nulu, Bukhman, & Kwan, 2017). According to Bernstein (2016), endothelial damage mediated by antibodies results in the activation of the T-cells in addition to the infiltration and scarring of the valves of the heart. Bernstein (2016) furtheradds that the scarring witnessed in the mitral valve usually begins as a small lesion made up of blood cells and fibrin. A severe and repeated attack by an acute rheumatic fever leads to the involvement of the chordae tendinae and the endocardium walls (Bernstein, 2016). The insufficiency of the mitral is as a result of the changes in the valve structure which are mostly accompanied by the loss of the properties of the valves which further makes the chordae tendinaethick and shortened (Sika-Paotonu et al., 2017). Additionally, Bernstein (2016) ascertains that an acute rheumatic fever accompanied withserious cardiac impairments may lead to a heart failure which is caused by a dysfunction of the mitral valve in combination with an inflammation of the pericardium, endocardium, and myocardium. Hypertrophy of the left ventricular will develop due to an increase in the volume load (Bernstein, 2016). From the patient’s chest radiograph, we can observe the inflammatory process that shows an extremely dilated left ventricle. An increase in the left ventricular end-diastolic pressure and a reduced stroke volume is due to the impairment of the left ventricular
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