Discuss about the Study Of COPD associated with Coughing.
Mr.X is a 69-year-old male patient, admitted to the hospital with a history mild COPD associated with coughing which had lasted for five days. The cough is characterized with yellow-green sputum. Mr.X presented with complaints of pyrexia, poor appetite, rigors, increasing breathing difficulties and mild chest pain secondary to sepsis. As per the patient, the cough and fatigue started 5 days ago.
Shortly, the cough became productive with a yellow/green sputum and thereafter he developed mild fever. Today, fever measurement was 1100F. He walked around his home compound, he developed significant shortness of breath associated with minor exertion. Mr. X recalls the development of cold-like symptoms a week before developing the cough and fatigue. The productivity of Smith’s cough has increased progressively in the past two days. The shortness of breath is aggravated by exertion and relieved by resting. Smith has been on albuterol inhaler 2-3 times a day but he reports that it has minimally helped him.
Mr.X has a positive history of COPD which he seems it to be mild and believed it is treated with albuterol inhaler 2-3 times a week. He reports that he has had a treatment for pneumonia and bronchitis with antibiotics almost every year. Mr.X has never been admitted for pneumonia. He denies recent known sick contacts. He denies any swelling, weigh changes and lower extremity pain. Additionally, Mr.X denies chest pain but admits chest tightness, shortness of breath and increased heart rate when coughing.
Neurological observations revealed that Mr.X had an altered neurological status, was confused and agitated with a Glasgow Comma Scale of 11/15. Cardiovascular observations showed that he had hypotension with a blood pressure of 92/46mmHg, sinus tachycardia and a heart rate of 136beats/minute. Respiratory observations indicated tachypnea with a respiration rate of 34breaths per minute and reduced saturation while getting 6Litres of oxygen via Hudson Mask. Metabolic observations showed that the patient was febrile with a temperature of 39.2 centigrade. Renal assessment revealed oliguria with a urine output of 20mls per hour and indwelling catheter that had been inserted (Angus and Van der Poll, 2013).
Blood works for Mr.X revealed that he was suffering from hyperglycemia, hyperkalemia, hypernatremia, poor creatinine, elevated levels of urea, low count of platelets and in increased white blood cells. Arterial Blood Gas analysis was done and it revealed that Mr.X was having both metabolic and respiratory acidosis. Finally, Mr.X was diagnosed with sepsis with a complication of right middle lobe streptococcus pneumonia. Based on this, Mr.X needed to be intubated and put on invasive ventilation support.
Sepsis refers to a dysregulated inflammatory response which is associated with severe infection. The interchangeable definition of sepsis is Systemic Inflammatory Response syndrome (SIRS) which results from a confirmed or suspected source of infections. The SIRS concept was initially introduced by the American College of Chest Physicians (ACCP) and Society of Critical Care Medicine (SCCM) in the year 1992. SIRS is characterized some of the following symptoms (Angus and Van der Poll, 2013).
These symptoms include: fever characterized by a temperature of more than 38 degrees, hypothermia, tachypnea, tachycardia and partial pressure of arterial carbon dioxide (PaCO2) below 32 mmHg. Additionally, there is a deranged count of white blood cells of more than 12,000/µL or below 4,000/µL. Associated with Smith’s manifestations, it is clearly evident that he was experiencing sepsis. This is because Smith was febrile up to 39.2 degrees, had an elevated respiratory rate of 34 breaths/minute, tachycardia with heart rate of 136 beats/minutes and elevated level of leucocytes count of 14,000uL (Angus and Van der Poll, 2013).
These clinical manifestations are associated with the inflammation process in the body which is often activated by the immune system of the body. Because of severe infection, many proinflammatory mediators are in turn released in Extensive Tissue Damage and Serial Inflammatory Reactions. Based on various reports, SIRS is associated with increased rate of morbidity and mortality due to high occurrence of SIRS-induced Multiple Organ Dysfunction Syndrome (MODS) (Angus and Van der Poll, 2013).
Pathophysiology of sepsis is complex and few important elements need to be addressed and more emphasis put on them. These elements include inflammatory process, acute stress response and cytokine storm. To begin with, Stress Response is considered as the acute phrase reaction when the immune system of the body is making efforts to fight against pathogens or threatening triggers. In other words, the triggers are described as “stresses”. Stress results from events of daily life, physical illness and environmental factors. In Smith’s case, the stress response is said to be triggered by infection (Angus and Van der Poll, 2013).
Under stress influence, the steady state of the body is always disrupted. In order to regain and maintain an homeostatic body state, the stress response is often activated to in order to reverse the balance of the body and facilitate redistribution of energy and oxygen maintain the normal functioning of important body organs. Hypothalamus organ plays an important role in processing the signals of distress. Once the hypothalamus senses the stress, it initiates activation of Sympathetic Nervous System. The Sympathetic Nervous System in turn stimulates the adrenal gland which produces epinephrine hormone. Epinephrine is called adrenaline. The adrenaline hormones is associated with increased myocardial contractility and heart rate, pupil dilatation and bronchi dilatation and peripheral vasoconstriction. Adrenaline is also associated with accelerated rate of respiration, increased glucose production from the liver and decreased activity of the gastrointestinal system (Angus and Van der Poll, 2013).
Additionally, stress can activate an alternative pathway of Stress Response. This path is the Hypothalamic-pituitary-Adrenal (HPA) axis. This means that stress initiates the production of corticotrophin-releasing factor (CRF) from the anterior aspect of the hypothalamus. The CRF in turn promotes production of adrenocorticoid trophic hormone (ACTH) by the pituitary gland. The ACTH functions by stimulating the adrenal cortex to produce aldosterone and cortisol (Angus and Van der Poll, 2013).
Those corticosteroids result to increased rate of metabolism, water and sodium retention. Therefore, it is very obvious that Mr. was under stress influence. He was tachypnoeic, tachycardic, and hyperglycemic because of the impact of the sympathetic nervous system response. He was also oliguric due to Acute Kidney Injury secondary to the vasoconstriction. His status of hypernatremia can be associated with the effects of aldosterone. Mr. had poor oral intake which could be associated with suppressed functioning of the gastrointestinal system.
The second element of the pathophysiology of sepsis is the, the inflammatory cascade which plays a crucial role in the pathophysiology of Systemic Inflammatory Response Syndrome. The mediators of inflammation process are related to the mechanisms involved in Systemic Inflammatory Response. Excessive production of pro-inflammatory mediators lead to inflammation and inhibit the functioning of the Compensatory anti-Inflammatory Response. Pro-inflammatory mediators eventually compromise the body’s immune system.
Cytokines are one of the vital elements of the immune system. Local cytokines are immediately activated following an insult to repair the wounds and stimulate the innate immune system. Following release of local cytokines, some of the cytokines get into circulation system. Presence of cytokines in the circulation promotes release of growth factors and adhesion of platelets and macrophages which help in local damage recovery. However, severe infection and homeostasis that cannot be restored lead to occurrence of cytokine storm (Angus and Van der Poll, 2013).
Cytokine storm specifically results from complex progression. Cytokines are always made by monocytes, macrophages, platelets, mast cells and endothelial cells which make up the components of the initial immune defensive system. The multitude of cytokines induces Interleukin-1 (IL-1) and cytokine Tissue Necrosis Factor-alpha (TNF-a) and interleukin-1 (IL-1). These elements lead to removal of the Nuclear Factor-KB (NF-KB) Inhibitor which consequently prompts the release of more proinflammatory mediators like interferon gamma, Interleukin-8 (IL-8) and interleukin-6 (IL-6). Generally, cytokines do initiate the production of immune cells, which then induce more cytokines in the circulation system (Angus and Van der Poll, 2013).
The cytokines greatly impact the body. This includes indirect and direct contribution of morbidity and mortality in SIRS. TNFa is associated with fever clotting problems, abnormal hemodynamic values, low count of white blood cells and elevated level of liver enzymes. IL-1 is connected to loss of appetite, fever, haemodynamic abnormalities, general body weakness, neutrophilia and headache. IL-6 has strong relationship with impaired functioning of the lungs and fever. It also acts as a severity determinant of mortality rate associated with SIRS (Angus and Van der Poll, 2013).
The massive cytokine accumulation can lead to wide spreading vasodilatory impacts. This is because they stimulate the release of some vasodilators like nitric oxide. To add on this, cytokines are known for promoting adhesion of the endothelial cells and immune cells which lead to leaky endothelium and fluid loss from intercellular space to the extracellular space. The cytokines cascade can lead to disorders of clotting due to the high fibrinogen concentration involved in the process of inflammation. The fibrinogen produced is always converted from thrombin, generated by tissue factor. Tissue factor refers to the substance expressed by the surface of white blood cells. The tissue factor can also be induced by endotoxin and TNFa from the infection. The fibrinogen can be converted into fibrin forming clots. Therefore, excessive amount of fibrin during inflammation process leads to extensive clotting disorders (Angus and Van der Poll, 2013).
Based on all these mechanisms, it can be concluded that Mr.X’s fever is highly likely related to the production of Interleukin-1, TNFa and interleukin-6. Interleukin-1 could be the likely contributor of his reduced appetite and elevated count of white blood cells. Interleukin-6 could lead to worsening of Mr.X’s already affected lung functioning. Mr.X had increased count of white blood cells which could have been contributed by the interleukin-1 and immune response.
The hypotension (92/46mmHg) could be associated with the effects of vasodilation due to the effect of the Sympathetic nervous system. Hypotension led to reduced kidney perfusion hence causing acute kidney failure and reduced urinary output (20mls/hour). The acute kidney injury may consequently affect the patterns of potassium elimination so that Mr.X was discovered having high levels of potassium. The low count of platelets could be associated with to the massive cytokine production and endothelium damage.
Upon assessment, Mr.X was agitated, confused with a GCS of 12/15. He was febrile with a temperature of 39.1 centigrade secondary to the inflammation process and cytokine production involved in sepsis. He had poor urine output with 20mls/hour following hypotension which led to reduced kidney perfusion hence low urinary output. Mr.X had an increased heart rate (134 beats/minute) and respiration rate (34 breaths/minute) following stimulation of the sympathetic nervous system and metabolic and respiratory acidosis. Production of cytokines could also ahve led to compromised lung functioning hence leading to dyspnea. Additionally, dyspnea was also related to right lobe streptococcus pneumonia which led to compromised functioning of the lung leading to shortness of breath and coughing.
The main problems for Mr.X were hyperthermia, hypoxia, impaired gas exchange/dyspnea and risk of fluid volume deficit. The Based on assessment, the goal of nursing of nursing care was to ensure that the patient displays respiratory rate and Arterial Blood Gas Analysis (ABGs) within their normal ranges, with clear breath sounds and he experiences no dyspnea. The patient will also experience no complications associated with hyperthermia and demonstrate a temperature within the normal range of values. The problems that were addressed were impaired gas exchange and hyperthermia.
Mechanical Ventilation Management of Mr.X involved use of Synchronized Intermittent Mandatory Ventilation Volume Control. SIMV is used very commonly in Intensive Care Units (ICU). Using the volume control mode, Mr.X was given ventilation support using a set of tidal volume in mandatory breaths. For an effective ventilation support, I had to set up some specific values for the SIMV volume-controlled mode. The values were respiratory and tidal volume. Tidal volume is an amount of oxygen given by the machine or that amount in the lungs when a patient breathes without support. The respiratory rate has to be set for mandatory breaths. In the SIMV volume controlled mode, the ventilator or patient triggered ventilation.
The SIMV mode helped Mr.X reduce the energy required in breathing especially in his high energy-consuming status of sepsis. The model also allowed him get an extra breath in order to expel the accumulative level of carbon dioxide which led to respiratory acidosis hence improving the acidosis. Additionally, due to pneumonia and thee accumulative inflammatory response syndrome, the lungs could be fragile and stiff secondary to mass accumulation of cytokines and the inflammation process. Therefore, the volume controlled ventilator acted as protective strategy to prevent complications related to ventilators such as volutrauma. The tidal volume was set at 9ml/kg to avoid ventilator-related complications.
Profoundly, ventilation can compromise cardiovascular functioning via conflicting, complex, and opposite processes. The processes give a reflection of the interaction between ventricular pump function, myocardial reserve, blood flow distribution, circulating blood volume, autonomic tone, lung volume, endocrinologic responses, intrathoracic pressure (ITP), and the surrounding pressures for the remaining part of circulation.
Mechanical ventilation generates an increased airway pressure hence increased in intrathoracic pressure. This may consequently may decrease intra-abdominal organ and systemic perfusion, which may significantly affect the homeostasis an organ functioning. Therefore, critically ill patients can develop a Systemic Inflammatory Response hence culminating to multiple-organ dysfunction syndrome and mortality. Therefore, I closely monitored the patient while on mechanical ventilation.
Since Mr.X was on intubation and mechanical ventilation, I had to implement some interventions to prevent aerodigetive tract colonization which result severe complications associate with ventilation. These interventions included avoidance of unprescrtibed antibiotics, chlorhexidine mouth rinsing, stress ulcer prophylaxis, selective digestive decontamination and short-course parenteral prophylactic antibiotics in high-risk patients. I also avoided use of weaning protocols, semi-recumbent positioning, and sub-glottic suctioning.
Obviously, a very a key element is the haemodynamic monitoring, which has been very vital in the assessment of the patient. According to literature, dynamic and ongoing haemodynamic monitoring is vital in judging the response to the treatment modalities and fluid challenge. Mechanical ventilation induces cyclic variations in blood flow in the vena cava, pulmonary artery and aorta. At the bedside, changes in respiration in aortic blood flow are indicated by “swings” in blood pressure whose magnitude is dependent on volume status (Green, 2015).
From the assessment the patient had a temperature of 39.20C which hyperthermic. The aim of nursing care was to ensure that patient demonstrates a normal temperature and prevent any complications associated with hyperthermia. To achieve this, the following interventions were implemented; Monitoring his temperature–degree and pattern. A temperature of 38.90C to 41.20C it’s a suggestion of acute infection process. Consistent fever lasting for more than 24 ours is an indication of pneumococcal pneumonia. Administering antipyretics like acetaminophen. Antipyretics are useful in reducing fever due to its central action on the hypothalamus (Green, 2015).
Regarding impaired gashouse exchange, the goal of nursing care was to ensure that the patient displays respiratory rate and Arterial Blood Gas Analysis (ABGs) within normal range, with clear breath sounds. The patient should demonstrate reduced dyspnea. To achieve this goal, I monitored rate and depth of respirations noting use of accessory muscles when breathing. Rapid and shallow respirations often occur due to stress, hypoxemia and circulating endotoxins. Dyspnea and hypoventilation indicate ineffective compensatory mechanisms hence indicating the need for ventilator support. I auscultated the patient for breath sounds noting stridor, crackles, wheezes and areas of absent or decreased ventilation. Presence of respiratory distress and adventitious sounds indicate lung atelectasis, pulmonary congestion and interstitial edema. I assessed Mr.X for sensorium changes. Cerebral functioning is sensitive to decreased oxygenation such as reduced perfusion or hypoxemia (Green, 2015).
I maintained the airway of the patient by positioning him comfortably with head elevated at 30degrees. Head elevation promotes lung expansion hence reducing respiratory effort. I noted coughing and production of purulent sputum. Pneumonia is one of the commonest hospital-acquired infection that occurs via aspiration of oropharyngeal microorganisms. I frequently re-positioned Mr.X and encouraged him to cough and do breathing exercises. I also suctioned him as per the indications. Good pulmonary toilet is vital in reducing perfusion/ventilation imbalance. This also facilitated removal of secretions from the airway to ensure maximum gas exchange (Green, 2015).
I also monitored pulse oximetry and ABGs for Mr.X. Hypoxemia is associated with decreased rate of ventilation and changes in the pulmonary system such as interstitial edema, atelectasis or pulmonary shunting. Hypoxemia is also associated with increased demand for oxygen which is caused by infection or fever. Respiratory acidosis characterized by a pH of below 7.35 and PaCO2 more than 40 mm Hg, happens because of ventilation-perfusion imbalance and hypoventilation. As septic condition deteriorates, metabolic acidosis characterized by a pH of below 7.35 and HCO3 below 22-24 mEq/L, develops due to accumulation of lactic acid from anaerobic metabolism (Green, 2015).
Regarding medical treatment, Mr.X had been prescribed intravenous antibiotics by the physician such as vancomycin to treat pneumonia and infections of the skin and soft tissue. These antibiotics were administered following the nursing protocol of drug administration. The patient was also on vasopressin which was meant to constrict hence helping in increasing blood pressure to increased tissue-perfusion. Management of Mr.X was multidisciplinary whereby the nurse, doctor, nutritionist and counsellor were involved to give holistic care to the patient (Green, 2015.
After the 12 hour nursing care, Mr.X showed great improvement whereby the temperature dropped to 37.00C with a respiration rate of 26 breaths per minute. His pulse rate was 110beats per minute. The patient displays reduced use of accessory muscles when breathing and from auscultation, he has clear breath sounds. There are no major complications associated with dyspnea and hyperthermia.
Conclusion
It was a good experience providing holistic care to a patient with sepsis which is a multi-system organ dysfunction. Sepsis involves inflammation process, cytokine storm and immune system response. These key elements lead to the clinical manifestations seen in a patient with sepsis. Management of sepsis requires one to be more knowledgeable and involve the multidisciplinary team to good prognosis of patient condition. I personally played the role of a nurse in mechanical ventilation of the patient with the SIMV mode since patient was dyspneic and tachypnea. I managed the hyperthermic state of Mr.X and my interventions really worked for him since an improvement was reported based on the vitals taken in comparison to how he came to the Intensive Care Unit.
References
Angus, D.C. and Van der Poll, T., 2013. Severe sepsis and septic shock. New England Journal of Medicine, 369(9), pp.840-851.
Green, J.M., 2015. Essentials of sepsis management. Surgical Clinics, 95(2), pp.355-365.
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