Pulmonary Edema - Coursework Example

Critical Thinking Questions: Part I Name Institution 1. Explain three possible causes of pulmonary oedema. Include a brief pathophysiological overview of the condition, exacerbating factors, significant contributing co-morbidities and a full pre-hospital management plan (including recommended medications). Introduction Pulmonary oedema occurs when the extravascular water content in the lungs dramatically increases. This increase in water content level affects lymphatic drainage because the fluid filtration rate is higher than the lymphatic removal rate (Murray, 2011). Pulmonary oedema may be cardiogenic or noncardiogenic. Cardiogenic pulmonary oedema results from an increase in pressure in the pulmonary capillary due to heart failure. Noncardiogenic pulmonary oedema is characterized by elevated permeability resulting from injury to epithelial barriers or endothelial barriers (Murray, 2011). Discussion Three types of pulmonary oedema are high-altitude pulmonary oedema, neurogenic pulmonary oedema and cardiac pulmonary oedema. High-altitude pulmonary oedema (HAPE) is a non-cardiogenic pulmonary oedema that causes pressure increase in the normal left atrial and pulmonary artery. HAPE is caused by capillary pressure brought about by rapid change in altitude above 2,500 (Maggiorini et al., 2001). This condition occurs between two and five days of arriving at a high altitude. These pressure changes affect pulmonary capillaries because they lead to overperfusion and hypoxic vasoconstriction. Early symptoms include dyspnoea, non-productive cough and reduced ability to exercise. As the condition progresses, symptoms include worsened cough, orthopnea, pink sputum and gurgling. Clinical features of HAPE are tachycardia, tachypnoea, increased body temperature and cyanosis (Paralikar, 2012). The pathophysiology of HAPE is the constriction of pulmonary blood vessels. The constriction is non-homogenous because it affects the smooth muscle arterial walls. The smooth muscle cells inhibit potassium channels that are dependent on voltage, entry of calcium through L-type channels and membrane depolarization. Elevated hypoxic pulmonary vasoconstriction (HPV) is caused by high endotheline-1 levels and susceptibility of pulmonary vasculature-to-sympathetic activity. The elevated hypoxic pulmonary vasoconstriction leads to overdistension of vessel walls that open cellular junctions and lead to stress failure of alveolo-capillary membrane. (Paralikar, 2012). Neurogenic pulmonary oedema (NPE) is a non-cardiogenic type of pulmonary oedema that occurs from a rapid increase in catecholamines that leads to cardiopulmonary dysfunction (Davison, Terek & Chawla, 2012). Neurogenic pulmonary oedema (NPE) is characterised by acute pulmonary oedema that occurs from a significant insult of the central nervous system such as a spinal cord injury, intracranial haemorrhage, meningitis or traumatic brain injury. The origin of NPE is believed to be trigger zones such as the medulla and the hypothalamus (Davison, Terek & Chawla, 2012). For instance, an injury to medulla area A1 has been shown to cause pulmonary oedema. The pathophysiology of NPE is that a neurologic condition produces rapid and excessive increase in intracranial pressure (ICP). This increase in intracranial pressure is correlated with NPE and an increase in extravascular lung water level. Furthermore, elevated ICP causes ischemia or neuronal compression results in discharge of catecholamines and activation of sympathetic nervous system (Davison, Terek & Chawla, 2012). Cardiogenic pulmonary oedema (CPO) is caused by pump failure or stiff left ventricle (Henson, 2011). CPO has two main clinical causes. The first cause is pump failure characterized by systolic dysfunction and lower ejection fraction. The second cause is diastolic dysfunction characterized by preserved ejection fraction. This diastolic dysfunction occurs in individuals with stiff left ventricles or are hypertensive (Henson, 2011). Symptoms of CPO are cough with pink sputum, palpitations, sweating and acuity. The pathophysiology of CPO is based on changes within the host’s circulatory system where one problem causes another problem, which spirals into an increase in the accumulation of fluid in the lungs (Henson, 2011). This fluid accumulation restricts gas exchange resulting in hypoxia or respiratory failure. When the left ventricle fails to empty blood from the lungs, it increases end diastolic pressure and volume. This change increases the pulmonary vasculature that then increases hydrostatic pressure above the oncotic pressure. These pressure changes cause fluid to accumulate in the interstitium and alveoli. The lymphatic system’s failure to re-absorb this fluid affects gaseous exchange and causes hypoxia and breathing difficulties. Hypoxia induces a release of catecholamine that leads to vasoconstriction and systemic vascular resistance. The result is difficulty in ventricular emptying and relaxation. The activation of renin, aldosterone and angiotensin causes water and salt retention, increases sympathetic tone and results in a rise in preload and the afterload. These changes increase oxygen consumption and demand, leading to further respiratory load that cannot be met by the failing lungs. Tissue hypoxia then occurs (Henson, 2011). Treatment Plan This treatment plan provides individual treatment options for HAPE, NPE and CPO. Early treatment can reverse HAPE. Treatment for HAPE includes rapid descent from the high altitude or supplemental oxygen. If no medical care is available, rapid descent is proposed. Where medical care is available, 20mg nifedine should be administered every six hours to relieve symptoms and improve gas exchange (Paralikar, 2012). Supplemental oxygen should be provided for up to 48 hours and bed rest recommended for a few days within the same altitude. Treatment for NPE includes reducing intracranial pressure through decompression, tumour resection, anti-epileptics steroids and osmotic diuretics to improve oxygenation. Pharmacological treatment for NPE is anti-α-adrenergic agent that interrupts hemodynamic instability and the cycle of respiratory failure. Alternatively, an α-blocking agent such as chlorpromazine is recommended because it rapidly improves oxygenation (Davison, Terek & Chawla, 2012). Treatments for CPO include oxygen supplementation, morphine, airway positioning, nitrates and furosemide (Henson, 2011). Symptoms of CPO can be improved by positioning the patient for better breathing or non-invasive ventilation where pulmonary oedema fluid is exuded from lungs. Supplemental oxygen at a rate of 15L/minute is recommended when saturation is less than 95%, the patient has shortness of breath or has hypoxia. To improve circulation in patients with fluid overload, loop diuretics such as 40mg of furosemide are proposed. Vasodilators such as nitrates and nitroprusside reduce afterload and/or preload but should not be used on patients whose systolic blood pressure is lower than 90mmHG. At least 10mcg/min of nitrates is administered every 5 minutes as needed. Alternatively, an infusion of 0.3mcg/Kg/min of nitroprusside could reduce afterload and preload in CPO patients in hypertensive emergency. In case the patient is agitated or has chest pain, opiates such as morphine are recommended. Small doses of 2.5mg to 5mg have a vasodilatory effect and reduce preload (Henson, 2011). Conclusion Pulmonary oedema is a critical condition that needs immediate treatment. This conduction occurs when fluid moves from the pulmonary capillaries to interstitital space then the accumulates in the alveoli. Pulmonary oedema may be cardiogenic or noncardiogenic. All three types of pulmonary oedema require oxygen supplementation, mechanical ventilation in some cases and pharmacological interventions (such as opiates for CPO). Treatment should be administered to prevent patient mortality. 2) Investigate the progression of infection, through various stages, to septic shock. Include a discussion of the ‘Four Stages of Shock’, major causative factors, effects on perfusion and microcirculation and the involvement of major organs. Introduction Sepsis affects 750,000 people in the United States (US) and causes more than 215,000 deaths every year. Mortality from sepsis accounts for 9.3 percent of all deaths in the country (Sharma & Kumar, 2003). This mortality rate exceeds deaths related to breast cancer or AutoImmune Deficiency Syndrome (AIDS). Sepsis refers to a clinical syndrome that arises from systemic inflammatory response syndrome (SIRS). Discussion The three stages of shock are compensated shock, decompensated chock and irreversible shock. Compensated shock, also called non-progressive shock, occurs when there is low blood flow or perfusion. When perfusion occurs, the body activates different systems to restore its status. The diameter of the blood vessels reduces, the heart rate increases and fluid retention is increased by the kidneys. The purpose of this change is to improve blood flow to body organs and systems. At this phase, the patient does not exhibit many symptoms. Treatment at this phase can prevent further progression of shock. The second stage of shock, also referred to as progressive shock, occurs when treatment is not provided in the first stage. This process is characterised by failed compensation. The body has problems improving perfusion leading to severe symptoms in the patient such as disorientation or chest pain. Inability to improve perfusion deprives the brain of oxygen, which causes disorientation and confusion in the patient. The patient experiences chest pain when the heart is deprived of oxygen. Symptoms include clammy skin, elevated shock index where the systolic blood pressure is above 0.9 and mottling. This progresses to cardiovascular dysfunction and results in hypotension and shock. At this phase, quick treatment is very important. Early treatment can reverse this phase of shock. The third phase is the irreversible stage of shock. This phase occurs when poor perfusion has occurred for a long period, which may have a permanent effect on body organs. At this stage, the heart function continues to decline while the kidneys completely shut down. Tissues and organ cells become injured and begin dying. The end result is death. Multiple organ dysfunction is the final phase of septic shock. Septic shock reduces the peripheral arterial vascular tone, which results in vasodilatation. This arterial vasodilatation causes hypotension which may lead to an increase in cardiac output if the condition is not compensated (Thooft et al., 2011). In the early phases of septic shock, hypovolemia and a preload decrease limits an increase in cardiac output. The hyperdynamic phase occurs from the augmentation of the intravascular volume that causes an increase in cardiac output. This change in cardiac output depresses the performance of the patient’s heart. Other factors that may lead to myocardial depression are abnormalities in coronary blood flow, nitric oxide, pulmonary hypertension and myocardial depressants (Wenzel & Edmond, 2012). The pathogenesis of the condition involves interactions of inflammatory mediators, suppressed endogenous fibrinolysis, the release of counter-inflammatory mediators and the trigger of coagulant response by tissue factors (Sharma & Kumar, 2003). Bacteria, fungus, virus parasite or endtoxins invade the host cell. The host cell produces tissue factors and releases cytokine, which leads to coagulopathy. Cytokine release causes an inflammatory response such anorexia and fever. These responses trigger thrombotic and fibrinolytic response. Fibrin produced from these responses causes microvascular thrombosis and fibrin clot. The bacterial/fungal/virus or parasitic infection also triggers the production of elastase and inhibition of thrombomedulin. These processes suppress fibrinolysis which leads to microvascular thrombosis or fibrin clot (Sharma & Kumar, 2003). Sepsis causes significant microcirculatory alternations. While normal conditions have perfused network capillaries, sepsis has a lower capillary density and higher heterogeneity of perfusion. These changes are caused by the presence of not-perfused capillaries that are close to the well-perfused capillaries (Backer, Cortes, Donadello & Vincent, 2014). The dynamic alterations occur after live bacteria or endotoxin have been administered. Reduced capillary density in sepsis causes an increase in the oxygen diffusion distance. This increase in oxygen diffusion distance reduces oxygen saturation in capillaries to indicate tissues use delivered oxygen. This change affects oxygenation and oxygen extraction capabilities. As hypoperfusion occurs, heterogeneity of microvascular perfusion continues to increase in sepsis rather than reduces as in a normal condition. These alterations cause cellular injury and contribute to organ dysfunction (Backer, Cortes, Donadello & Vincent, 2014). Septic shock is depicted by hemodynamic alterations (such as myocardial depression, reduced vascular tone and hypovolemia) from organ dysfunction (Thooft et al., 2011). The hemodynamic alterations are associated with arterial hypotension, or a systolic arterial pressure that is lower than 90mm Hg. This low arterial pressure induces alterations in the autoregulation of organ flow, which implies that tissue perfusion depends on arterial pressure level. Fluid resuscitation at this stage does not help in restoring hemodynamic stability. Vasopressor therapy is more effective in restoring organ perfusion. However, this intervention may not be effective in changing urinary output, gastric intramucosal partial pressure of carbon dioxide (PCO2) or blood lactate levels. This is because previous studies have shown that increasing mean arterial pressure from 65mm HG to 85 mm HG in patients experiencing septic shock does not affect blood lactate level or urinary output. However, an increase in mean arterial pressure using neropinephrine leads to a positive change in cardiac output, improved microcirculatory function and reduced blood lactate level (Thooft et al., 2011). This is because neropinephrine is a vasopressor agent for patients with septic shock. It contains alpha-adrenergic properties that make it viable vasopressor agent. Alterations to the microcirculatory system lead to endothelial cellular dysfunction for a number of reasons. According to Backer, Cortes, Donadello and Vincent (2014), the alternations are characterised by co-localization of low PO2 and hypoxia-inducible factor production. Low oxygen saturation in well-perfused capillaries confirms that tissues use existing oxygen. In addition, tissue to the arterial PCO2 gradient has a higher PCO2 gap in sepsis. This increase in the PCO2 gap is inverse to the sublingual microvascular perfusion. Furthermore, the abnormalities in microvascular perfusion influence changes in organ function (Backer, Cortes, Donadello & Vincent, 2014). Conclusion Sepsis remains the leading cause of mortality. Microcirculatory alterations such as changes in inter-cell communication, deformed red blood cells and endothelial dysfunction occur in sepsis. Early administration of treatment is required to reverse or prevent further complications from sepsis and septic shock such as end-organ failure. Intravenous administration of antibiotics such as neropinephrine can address the effects of septic shock. References Backer, D., Cortes, D., Donadello, K., & Vincent, J. (2014). Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock. Virulence, 5(1), 73-79. Davidson, D., Terek, M., & Chawla, L. (2012). Neurogenic pulmonary oedema. Critical Care, 16, 212-218. Henson, V. L. (2011). Cardiogenic pulmonary oedema. Retrieved from http://www.rcemlearning.co.uk Maggiorini, M., Melot, C., Pierre, S., Pfeiffer, F., Greve, I., Sartori, C., Lepori, M., Hauser, M., Scherrer, U., & Naeije, R. (2001). High-altitude pulmonary oedema is initially caused by an increase in capillary increase. Circulation, 103, 2078-2083. Murray, J. (2011). Pulmonary oedema: Pathophysiology and diagnosis. The International Journal of Tuberculosis and Lung Disease, 15(2), 155-160. Paralikar, S.J. (2012). High altitude pulmonary oedema-clinical features, pathophysiology, prevention and treatment. Indian Journal of Occupational and Environmental Medicine, 16(2), 59-62. Sharma, S., & Kumar, A. (2003). Septic shock, multiple organ failure, and acute respiratory distress syndrome. Current Opinion in Pulmonary Medicine, 9, 199-209. Thooft, A., Favory, R., Salgado, D., Taccone, F., Donadello, K., Backer, D., Creteur, J., & Vincent, J. (2011). Effects of changes in arterial pressure on organ perfusion during septic shock. Critical Care, 15, R222-R230. Wenzel, R. P., & Edmond, M. (2012). Septic shock – Evaluating another failed treatment. The New England Journal of Medicine, 1-3. Read More