Discuss About The Alterations Of Cardiovascular In Children.
According 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 between 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) further adds 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 tendinae thick and shortened (Sika-Paotonu et al., 2017).
Additionally, Bernstein (2016) ascertains that an acute rheumatic fever accompanied with serious 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 function (Pike & Peterson, 2018). The increased left ventricular end-diastolic pressure leads to an increased filtration of the protein-poor fluid into the interstitium and alveoli. This increased filtration further leads to an increase in the hydrostatic pressure of the pulmonary capillary. It is further necessary to note that the left atrium enlarges due to increase in the volume load when blood regurgitates due to the insufficiency of the mitral valve that further creates soft heart sounds and a gallop rhythm (Pike & Peterson, 2018). According to Sampson (2016), we can observe an enlargement of the left atrial from the ECG diagram evidenced by bifid and widened P-waves.
Interstitial edema reduces the compliance of the lung which may lead to an increase in the work of breathing which is characterized by intermittent grunting and soft tissue retraction which is further characterized by tracheal tugging during inspiration. As ascertained by Sika-Paotonu et al. (2017), a failure of the left ventricular, an enlargement of the left atrial, and the regurgitation of the mitral valve are some of the significant contributors of pulmonary edema. This condition is responsible for the bilateral apical wheezes as a result of fluid accumulation in the peribronchial-vascular or alveoli spaces leading to the narrowing of the small airways which consequently hampers gaseous exchange (Pike & Petersin, 2018). Pulmonary edema also causes the patient to be a cough, experience shortness of breath, and become increasingly exercise intolerant. Alveolar edema, on the other hand, leads to an intrapulmonary shunting that causes peripheral cyanosis and hypoxemia. The body of the patient, therefore, responds to these conditions by increasing the rate of respiration which is characterized by tachypnea (Frey & Arain, 2017). It additionally leads to orthopnea which is a characteristic of difficulty in breathing when supine is manifested by the inability to lie flat (Pike & Peterson, 2018).
An enlargement of the patient’s left ventricle leads to a decrease in the cardiac output and the stroke volume that leads to hypotension that can be witnessed by a blood pressure of 80/50 mmHg. There are also diminished radial pulses with a cool skin having a capillary refill time that is more than 3 seconds which is an indication of poor perfusion and a heart failure characterized by a low output (Pike & Peterson, 2018). The low blood pressure causes the activation of the sympathetic nervous system and the renin-aldosterone-angiotensin system. This causes the vasoconstriction of the arteries and veins, the retention of sodium and fluid as a mechanism of compensation, and tachycardia (Pike & Peterson, 2016). Water retention leads to an increase in the systemic venous pressure.
According to Bernstein (2016), elevation of the pressure of the pulmonary artery leads to an enlargement of the right atrium and ventricle which then leads to right-sided heart failure. From the ECG diagram provided, we can note that there are dominant R waves in V1, V2, and V3. Also, there are deep S waves in V4-V6 in addition to ST depressions and inversion of the T wave in lead V1-V3. Furthermore, there is an ST elevation in V5-V6 accompanied by a deviation in the right axis which is a characteristic of right ventricular hypertrophy (Sampson, 2016). The right-sided heart failure causes hepatomegaly which is characterized by an increase in the size of the liver that leads to systemic venous congestion. We are additionally informed that the patient complains about pain in the right upper abdomen accompanied by intermittent nausea and vomiting. Furthermore, during an examination of the abdomen, there is an observation of soft liver edges which is an indication of hepatomegaly as result of an increased venous congestion and pressure from the right side of the heart into the hepatic vein via the inferior vena cava. This causes the engorgement of the liver (Pike and Peterson, 2018).
It is an antibody that targets the production of streptolysin-O that is produced by group A streptococcus (Chernecky & Berjer, 2012). They start rising after approximately seven days of infection and reach peak levels after 21-35 days before gradually returning to the baseline after 6-12 months. Since the Antistreptolysin O titers remain high in patients that have post-streptococcal infections, Chernecky & Berjer (2012), argue that the test can be used to determine whether an acute rheumatic fever is as a result of a post-streptococcal disease. As confirmed by Hanson-Manful et al. (2017), the disease specificity of Antistreptolysin O response tends to occur due to a throat infection mostly. Antistreptolysin O has a specificity of 57.6% and a sensitivity of 75% (Hanson-Manful et al., 2017). This biomarker is significant in the determination of group A streptococcus bacteria which could precipitate acute rheumatic fever (Chernecky & Berjer, 2012).
Cardiac muscles produce this biomarker due to an increase in the end-diastolic volume and pressure. It can also be produced as a result of cardiac strain (Januzzi et al., 2018). Its sensitivity is 81% while its specificity is 76%during the diagnosis of acute heart failure in pediatric patients. According to Chernecky & Berjer (2012), an NT-proBNP level that is less than 30pg/mL is an indication of unlikely heart failure. According to several pieces of evidence by Januzzi et al. (2018), the levels of NT-proBNP correlates with prognosis, clinical status, and diagnosis of patients who have congestive heart failure. NT-proBNP is normally elevated among pediatric patients with different heart failure causes and it is thus recommended as an adjunctive biomarker during a heart failure diagnosis.
According to Chernecky & Berjer (2012), the liver produces this protein during acute inflammation. It is easy to detect during the first 6-10 hours of the inflammatory response of the body which is stimulated and may even rise to as high as 4000 times during the peak of the acute phase inflammatory response. The level of C-reactive protein tends to rise as a result of various stimuli that include trauma, infection, ischemic tissue injury, and inflammation (Ansar & Ghosh, 2013). According to Paradhan et al. (2016), the sensitivity of C-reactive protein is 84.3% while its specificity is 46.15%.
This biomarker is ultrasensitive and cardiac specific. Chernecky & Berjer (2012) argue that it is detectable an hour after a myocardial injury. The specificity of this biomarker is 80% while its sensitivity is 95% (Brush, Kaul, & Krumholz, 2016). According to several pieces of evidence, Troponin I, in most cases is elevated in the blood within 3-8 hours of myocardial injury and peaks after 8-24 hours. As confirmed by Fox & Diercks (2016), Troponin I may remain elevated in the bloodstream for approximately 1-2 weeks. The elevation is significant in cases of cardiac injuries.
According to Mebazza et al. (2015), the patient needs to be closely monitored by a highly knowledgeable practitioner with the necessary expertise to respond to deteriorations. The first step towards the determination of the severity of the instability of hemodynamic is founded on the mental status, heart rhythm, hemodynamic status, and dyspnea levels. Due to the patient’s high risk of clinical deterioration, he requires a one on one nursing management in the emergency department. The continuous patient monitoring including the signs and symptoms as a result of the hemodynamic status and treatment requires close observation of the hemodynamic parameters that include assessing the vital signs of the patient after every five minutes until he is stable. This implies that the blood pressure, heart rate, heart rhythm, saturation of oxygen, respiratory rate, the temperature of the body, and pain should be stabilized (Mebazza et al., 2015). It is additionally important to observe the mental status of the patient and his level of consciousness after every five minutes thus promptly identifying the changes in the patient’s clinical status. It is important to assess the patient’s orthopnea, the rate of respiration, the degree of hypoxia, and work of breathing (Mebazza et al., 2015). Additionally, the practitioner needs to determine the signs and symptoms of hypo-perfusion inclusive of mental status, cool extremities, and narrow pulse pressure. It is also necessary to closely analyze the findings from the laboratory tests including the electrolytes that are in some instances affected by diuretic therapy. It is also significant to check the blood glucose level.
The recommended mode of delivering oxygen for hypoxic patients that have heart failure but do not require any intubation is a non-invasive positive pressure ventilation therapy. This therapy may consist of Bi-level positive airway pressure and continuous positive airway pressure (Kato, Suda, & Kasai, 2014). The non-invasive positive pressure ventilation therapy on the collapsed alveoli is helpful in sustaining the alveolar pressure thus preventing the collapse of the alveoli and at the same time improving gaseous exchange. Kato et al. (2014) further confirm that the non-invasive positive pressure ventilation induces a shift of fluids from the interstitial space and the alveoli back into the circulation of the pulmonary. This is done through the counterbalancing of the capillary or interstitial hydrostatic pressure. The shift leads to a decrease in the amount of intrapulmonary shunting and consequently improves gaseous exchange. Purvey & Allen (2014) confirm that non-invasive positive pressure ventilation should be commenced at 100% oxygen concentration and titrated until an oxygen saturation ranging between 92%-96% is achieved. It reduces the muscle load on the respiratory system thus improving the function of the lung and work of breathing. This is done through lung inflation and maintaining the functional residual capacity. Non-invasive positive pressure ventilation is fundamental in improving the cardiac output. This is done by improving the intrathoracic pressure. Kato et al. (2014) further ascertain that the increased intrathoracic pressure helps in decreasing the systemic venous return and the preload in the right ventricular thus leading to an increased cardiac output. The decrease in the preload could result in low blood pressure or hypotension, and it is therefore important to closely monitor the blood pressure (Purvey & Allen, 2014).
The primary goal of this management optimizes the delivery of oxygen by raising the cardiac input while at the same time reducing the metabolic demand. The recommended medication in during this management includes epinephrine, milrinone, and dobutamine specifically in refractory hypotension. The mode of action of milrinone is by increasing the contractility of the heart thus decreasing the resistance of the pulmonary ventricular. Additionally, this drug leads to the vasodilation thus helping in reducing afterloads and improving contraction. It is imperative to note that diuretics are used to reduce preloads but caution must be exercised during its administration so as not to worsen hypotension.
The patient’s management of pain is divided into two classes that include pharmacological and non-pharmacological. According to Newcombe & Brady (2017), pharmacological management is made up of oral pain medications that include ibuprofen and paracetamol. According to Kasowsky (2013), fentanyl exhibit minimal hemodynamic effects in getting rid of the pain. KAsowsky (2013) further adds that the administration of opioids for example morphine should be carefully done because it has the capability of causing hypotension. Nitroglycerin is believed to cause vasodilation thus reducing preload and decrease the heart’s demand for oxygen. This drug can, therefore, be administered for chest pains that result from ischemic changes. Non-pharmacological, on the other hand, constitutes pacing of activities, techniques of distraction, guided imagery, the involvement of parents or primary care, and comforting touch.
Management plans include the alleviation of the anxiety of the patient by maintaining a free and open communication between a patient and their family during patient care. It is also important to strictly adhere to the hand hygiene protocol which helps in controlling infection and managing infection prevention.
References
Ansar, W., & Ghosh, S. (2013). C-reactive protein and the biology of disease. Immunologic research, 56(1), 131-142.
Bernstein, D. (2016). Rheumatic heart disease. In R. M. Kliegman, B. F. Stanton, J. W. St Geme, & N. F. Schor (Eds.), Nelson Textbook of Paediatrics (20th ed.). (pp. 2269-2271). Philadelphia, USA: Elsevier, Inc.
Brush, J. E., Kaul, S., & Krumholz, H. M. (2016). Troponin testing for clinicians. Journal of the American College of Cardiology, 68(21), 2365-2375.
Chernecky, C. C., & Berger, B. J. (2012). Laboratory test and diagnostic procedures, Saunders. Philadelphia, 19932, 401.
Fox, W. R., & Diercks, D. B. (2016). Troponin assay use in the emergency department for management of patients with potential acute coronary syndrome: current use and future directions. Clinical and experimental emergency medicine, 3(1), 1.
Frey, T., & Arain, N. (2018). Pediatric Viral Myocarditis–A Review. South Dakota Medicine, 71(1).
Hanson-Manful, P., Whitcombe, A. L., Young, P. G., Carr, P. E. A., Bell, A., Didsbury, A., … & Moreland, N. J. (2017). The novel Group A Streptococcus antigen SpnA combined with bead-based immunoassay technology improves streptococcal serology for the diagnosis of acute rheumatic fever. Journal of Infection.
Januzzi, J. L., Chen-Tournoux, A. A., Christenson, R. H., Doros, G., Hollander, J. E., Levy, P. D., … & Peacock, W. F. (2018). N-Terminal Pro–B-Type Natriuretic Peptide in the Emergency Department: The ICON-RELOADED Study. Journal of the American College of Cardiology, 71(11), 1191-1200.
Kasowsky, J. (2013). Congestive Heart Failure. In J. G. Admas (Ed.), Emergency Medicine Clinical Essentials (2nd ed.). (pp. 476-486). Philadelphia, USA: Saunders
Kato, T., Suda, S., & Kasai, T. (2014). Positive airway pressure therapy for heart failure. World journal of cardiology, 6(11), 1175.
Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., … & McDonagh, T. (2015). Recommendations on pre?hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. European journal of heart failure, 17(6), 544-558.
Newcombe, J., & Brady, M. 2017. Paediatric pain management. In C. Burns, A Dunn, M. Brady, N. Starr, C. Blosser, & D. Garson (Eds.), Pediatric Primary Care (6th ed.). (pp. 459-473). Missouri, USA: Elsevier, Inc.
Nulu, S., Bukhman, G., & Kwan, G. F. (2017). Rheumatic heart disease: the unfinished global agenda. Cardiology clinics, 35(1), 165-180.
Pellekaan, S., & Best, O. (2015). Indigenous health issues health in Australia. In J. A. Craft (Ed), Understanding Pathophysiology – ANZ Adaptation (2nd ed.). (pp. 1156-1178). NSW, Australia: Elsevier, Inc.
Pike, N., & Peterson, J. K. (2018). Alterations of cardiovascular function in children. In K. L. McCance, & S. E. Huether (Eds.), Pathophysiology: The Biological Basis for Disease in Adults and Children (8th ed.). (pp. 1115-1142). Missouri, USA: Elsevier, Inc.
Pradhan, S., Ghimire, A., Bhattarai, B., Khanal, B., Pokharel, K., Lamsal, M., & Koirala, S. (2016). The role of C-reactive protein as a diagnostic predictor of sepsis in a multidisciplinary Intensive Care Unit of a tertiary care center in Nepal. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine, 20(7), 417.
Purvey, M., & Allen, G. (2017). Managing acute pulmonary oedema. Australian prescriber, 40(2), 59.
Sampson, M. (2016). Understanding the ECG. Part 7: Chamber enlargement. British Journal of Cardiac Nursing, 11(5), 230-238.
Sika-Paotonu, D., Beaton, A., Raghu, A., Steer, A., & Carapetis, J. (2017). Acute rheumatic fever and rheumatic heart disease.
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