Nursing Case Study: Acute Respiratory Distress Syndrome and Severe Sepsis
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This nursing case study discusses the pathophysiology of Acute Respiratory Distress Syndrome and severe sepsis, including the interpretation of arterial blood gas and determinants of cardiac output. It also outlines proposed ventilation parameters and critically analyzes the use of low tidal volume ventilation.
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Case study: Billy, a 32-year-old male, was admitted to the Intensive Care Unit (ICU) with a suspected overdose of tricyclic antidepressants. He is obese (weight 160kg, height 172cm) and has a history of depression and chronic back pain for which he takes oxycodone. On admission to the emergency department, paramedics were maintaining Billy’s airways with a combination of jaw thrust, head tilt and guedel airway. Billy was obtunded with evidence of vomitus on his clothing. There was an attempted intubation enroute which was unsuccessful. Billy’s initial observations were: Temperature 35.5 degrees Celsius Heart rate 140bpm Blood pressure 100/50mmHg Respiratory Rate 22 beats/ min, shallow and laboured Oxygen saturation 92% breathing spontaneously via a bag valve mask with oxygen at 15L/min Auscultation of lung sounds revealed decreased air entry bilaterally and expiratory wheezes Arterial blood gas: pH 7.21, PaCO2 68mmHg, PaO2 90mmHg, HCO3 26mEq/L, SaO2 94% GCS 8 (E1, V3, M4) Question One PART A) DescribethepathophysiologyofAcuteRespiratoryDistressSyndrome,includinga systematic interpretation of the arterial blood gas (Consider PaO2/ FiO2 – P/F ratio, assume PEEP is 5cmH2O). Interpret the ABG, including determining the PaO2/FiO2 ratio. What do these results indicate for Billy? Pathophysiology of Acute Respiratory Distress Syndrome:An Acute Respiratory Distress Syndrome is generally a multifaceted syndrome of acute lung damage specifically foremosttoanon-cardiogenicpulmonaryoedemafromvariousreasonswhichis heterogeneous within its medical demonstration and are also linked with the 40% death rate. An Acute Respiratory Distress Syndrome is significantly marked by an inflammation- medicated disruption within the alveolar-capillary permeability, edema formation, decreased alveolarclearanceaswellascollapse/derecruitment,decreasedobedience,enhanced pulmonary vascular resistance as well as a resulting interchange of gases. Within this, an understandingofARDSphysiology,thatcanincludeakeycharacteristicsconsisting exchange of gas abnormalities can frequently need ventilator encouragement as well as reduced compliance with the specific regional heterogeneity, generally has inferences for the ventilator encouragement strategies(Ali and Lamont, 2019). A positive pressure ventilation consisting with the positive as well as an expiratory pressure generally decreases the breathing work as well as can prevent atelectasis of a nearly collapsed lung units in order to enhance the interchange of gases. In this, a positive pressure of the airways generally helps to decrease further ongoing edema synthesis within various oedematous states, consisting the
enhanced alveolar penetrability of the Acute Respiratory Distress Syndrome. Within acute respiratory distress syndrome, the damaged lung is generally believed to go via the specific three phases such as exudative, fibrotic and a proliferative, but the course of every part as well as entire illness development is quite variable. While talking about exudative phase, injury towards the alveolar epithelium as well as vascular endothelium creates leakage of water, inflammatory, protein as well as the red blood cells within the interstitium and an alveolar lumen. In addition, these such alterations are effectively induced by a complex interplay of a pro-inflammatory as well as an anti-inflammatory mediator. The specific type 1 alveolar cells are generally irreversibly injured as well as the denuded space is replaced by the protein deposition, cellular debris, fibrin and can produce a hyaline membrane, while damage to the type 2 cells produced by surfactant mainly contributes towards an alveolar collapse. In context with the proliferative phase, type 2 cells generally proliferate with regeneration of some of the epithelial cells, remodelling and a fibroblastic reaction as well. Among some of the patients, such things can advance towards a permanent fibrotic phase consisting the deposition of collagen within alveolar, interstitial beds and vascular with the advancement of microcyst. ABG is generally an Arterial Blood Gas that can include various steps. Within this, the initial step in an interpretation of ABG is to visualise the pH. The standard range of blood pH is 7.4, minus or plus 0.05, mainly developing the range of 7.35 to 7.45. If the pH falls from the normal range such as below 7.35 then it can be considered as acidic. Whereas, if the blood pH increased above 7.45, then it can be considered as alkalotic(Byrne, 2021). The pH range of Billy’s is about 7.21 is normal but slightly acidic. In addition to this, the another step is to determine the pCO2 level. A standard pCO2 levels are about 35 to 45 mmHg. An underneath from the normal range such as >35 is alkalotic and <45 is quite acidic. In context with provided case scenario, the pCO2 level is 68 mmHg that is quite acidic. The third step within the interpretation of Arterial Blood Gas is to aspect at the HCO3 level. In this, a standard range of HCO3 is about 22 to 26 mEq/L. And, if the HCO3 is above the level of 26, the patient is alkalotic and below of 22 then the patient is acidotic in nature. Within the provided case scenario, a HCO3 level is given about 26 mEq/L which is normal. Next will match either the HCO3 or the pCO2 with the pH in order to measure the acid-base disorders. Such that, if the pH is acidotic, and the CO2 is acidotic, then the acid-base disturbance is generally being caused by the respiratory system. Therefore, if the pH is alkalotic and the HCO3 is alkalotic, then the acid-base disturbance is being caused by the metabolic or the renal system. However, it will be a metabolic alkalosis. In the case of Jelly, while comparing the normal range of pCO2 or HCO3 with the pH, in his case pH is slightly acidotic and the CO2 is also acidotic, then the acid-base disturbance that is being caused by the respiratory system (6 Easy Steps to ABG Interpretation, 2019). The partial arterial pressure of O2 and the fraction of an inspired oxygen ratio such as PaO2/FiO2 is broadly used within the Intensive Care Units as an indicator of the oxygenation status. A PaO2/FiO2 ratio is mainly subdivided using the threshold of about 100-200-300 as per the Berlin criteria of Acute Respiratory Distress Syndrome. PaO2< 60 and>100 mmHg versus PaO2 60-100. A partial pressure level of oxygen in Jelly’s case is 90 mmHg. PART B) In view of Billy’s current clinical condition, outline the proposed ventilation parameters you would suggest including rationales.
An acute respiratory distress syndrome is mainly categorized by the fatal damage of the pulmonary gas interchange, generally outcomes in hypoxemia, respiratory acidosis, hypercapnia as well as needing an acute rescue dealing. The distribution of the oxygen towards tissues are generally essential for all the aerobic life and the tissue hypoxia will outcomes in several toxic impacts consisting a transformed vascular reactivity, cell apoptosis, infection as well as organ failure(Haeberle and et. al., 2020). A tissue hypoxia is generally an outcome of hypoxemia that is a significance of having an inadequate encouragement of the respiratorysystemandtheoxygentransportsystem.Inordertoprovidemechanical ventilation for Jelly’s condition, the specific settings are suggested such as constraint of tidal volume (6 ml/kg anticipated the body weight), having adequate high PEEP (>12 cm H2O), a balanced respiratory rate about 20 to 30 beats per minute and a manoeuvre within the special condition. The use of invasive aeration for the patients with consisting Acute Respiratory Disorder syndrome, specifically those with a severe or moderate level ARDS<= 200 mmHg on both the positive end-expiratory pressure. A patient with ARDS such as Jelly’s case will need an intubation as well as a mechanical ventilation. While having the peri-intubation period, about 95 to 100 percent of the oxygen must be provided to effectively safeguard a suitable amount of oxygen saturation. It is because an uptake of oxygen can exceed a replenishment within the region of consisting a low V/Q ratio. Once it is established, an absorptive atelectasis is not speedily reversed by the decrease of FiO2 towards a keep levels, more stressing over the desirability of limiting prolonged periods of elevated FiO2 during and following the intubation period(Haren, Byrne and Litton, 2019). PART C) Usingcurrentevidencefromtheliterature,criticallyanalyseoneofthemechanical ventilation strategies/ parameters that you have chosen. From various chosen articles or websites, it has been determined that the one of the mechanical ventilation parameter or strategies that is being chosen is Low Tidal Volume Ventilation. For the patient with involving Acute Respiratory Disorder Syndrome, a Low Tidal Volume Ventilation is being recommended and is also called as lung protective aeration having 4 to 8 mL/Kg anticipated body weight. As per the LTVV, a predicted body weight of Jelly is about 172 cm/ 68.4 Kg and the tidal volume from 4 to 8 mL/Kg should be about 274,342, 410, 479 and 547 ml/Kg. As his body weight is of 160 Kg which fall under obese category. The LTVV approach is being used and is based on various meta-analysis as well as a randomized trail which can report a mortality advantages from the LTVV approach among the patient with ARDS. It is being thought that a LTV generally mitigate an alveolar over enlargement mainly encouraged by a mechanical ventilation, that can cause a supplementary lung damage as well as death within the patients with ARDS. A PEEP is being used among patients with ARDS. The main goal to apply PEEP among patients with ARDS is generally to enhance as well as maintain an alveolar recruitment, thereby enhancing an oxygenation as well as limiting oxygen toxicity (Ventilator management strategies for adults with acute respiratory distress syndrome, 2022). Question Two Twenty-four hours after admission to the ICU, Billy’s condition deteriorates. His current observations are:
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Temperature 39 degrees Celsius Sinus Tachycardia with a heart rate 130 beats/min Arterial Blood pressure 85/55 mmHg Pulse pressure variation or systolic volume variation (PPV or SVV) 15% Central venous pressure 5mmHg Bounding peripheral pulses Urine output 20mls for the last hour and 80ml total for last 4 hours PART D) Discuss Billy’sassessment data, incorporating the determinantsof cardiacoutput and pathophysiology of severe sepsis. A severe sepsis is generally well-defined as a dysfunction of one of the main organ system or an inexplicable metabolic acidosis. In this, the inflammatory reactions are generally facilitatedbythedischargeofcytokines,consistingthetumornecrosisfactor-alpha, prostaglandins and interleukins from the macrophages and neutrophils. It includes role of cytokines, a multifaceted array of interconnecting the ways within the pathophysiology of the sepsis has been illustrated(Haukoos, Douglas and Sasson, 2021). A vascular endothelial harm,coagulationactivation,inflammationaswellassuppressionofthefibrinolysis generally appears towards contribution of the organ dysfunction advancement and consisting the risk of death as well (Pathophysiology of Sepsis, 2019).
The sepsis progression is generally from the initial insult as well as the local inflammatory and an anti-inflammatory response via a systemic spill over of the mediators. Within this, the systemic reactions might consist the characteristics of additional of either an anti-inflammatory or the inflammatory intermediaries or consisting a mixed pattern as well. In addition, the medical sequelae of the sepsis generally vary contingent on the balance of mediators. An excessive inflammatory response (SIRS) might create a shock as well as the dysfunctioning of organ. CARS specifically inhibits the immune system. Within this, a composed response of the inflammatory mediators significantly creates homeostasis. Some of its patients might die with having a reduced inflammation as an outcome of apoptosis (Kharrat and Jain, 2022). Role of coagulation: In this, an inflammation process as well as coagulation generally appears to be a closely associated with the components of SIRS and sepsis. Medically, the patients often demonstrate the low platelets counts, enhance D-dimer concentrations as well as fibrinogen degradation products as well as other features of the low- grade disseminated intravascular coagulation or the microvascular coagulopathy (Acute Respiratory Distress Syndrome, 2022). As per the Billy’s assessment, his body temperature is quite increased from the normal temperature like it should be about 37 degrees and is observed at 39 degrees Celsius. He is also noted with Sinus tachycardia with consisting heart rate about 130 beat per minute which should be about 60 to 100 beats per minute. His central venous pressure is normal including range of 5 mmHg. In addition to this, He has critical issue with the urine output of about 20 mL for the last one hour and about 80 mL in total for last 4 hours which should be about 0.5 to 1.5 mL per hour. He also has low blood pressure such as having 85/55 mmHg Arterial blood pressure. Patients having ARDS is usually characterised by the diffusion of alveolar impairment as well as is often complicated by the pulmonary hypotension. There are generally the various elements which can contribute towards the development of pulmonary hypotension among patients. In addition to this, he is anabusivepersonasheissuspectedwithoverdosageoftricyclicantidepressants (Pulmonary vascular dysfunction in ARDS, 2014). Due to which he has experienced serotonin syndrome. It is generally a critical negative drug reaction which can occurs when enough serotonin arises within the body. The syndrome can cause nausea too among people. PART E) Using current evidence critically analyse the best practice therapy in relation to fluid resuscitation and vasopressor management. A septic shock is generally a consequence of the systemic contamination which is being featured by the hypotension unresponsive to the fluid resuscitation. It is specifically a critical well-being care issue which afflicts a numerous of the people annually across the nation (Acute respiratory distress syndrome: Supportive care and oxygenation in adults, 2022). An initial management of the patients with consisting a septic shock is generally to uphold the mean arterial pressure as well as a cardiac outcome while highlighting the contamination with an antimicrobial therapy and a source control. The patients who generally fails to retort towards an aggressive fluid resuscitation are generally the participants for the vasopressor or an inotropic therapy to uphold the hemodynamic parameters. PracticetherapyinrelationtoFluidresuscitation:Inthis,anoptimumfluid management strategy for the acute respiratory distress syndrome is not known. In context with European Society of Intensive Care Medicine/American Thoracic Society, medical care
practice guidelines generally make no significant suggestions for the management of fluid among the ARDS patients (Fluid management in Acute Respiratory Distress Syndrome: A narrative review, 2019). While talking about the liberal fluid management, historically the conventionaltraining,donotlimittheadministrationofthefluidwhilehavingthe resuscitation phase or effectively seeking to remove the fluid during the deresuscitative phase. Within this, the theoretic argument for a liberal management of the fluid strategy is that it can enhance the stroke volume and thereby can enhance end organ perfusion along with oxygen delivery(Kornas and et. al., 2021). As compared with the liberal management of fluid strategy, a conservative strategy can limit the administration of fluid during the resuscitation phase as well as employs the care treatment to lower the entire body fluid balance during the deresuscitative phase. Such effective strategy can seek to decrease the pulmonary perfusion or ventilation mismatch by restricting the pulmonary edema but might risk as well as end-organ malfunction from reduced cardiac perfusion (Fluid Therapy and Acute Respiratory Distress Syndrome, 2021). Furthermore, a fluid limitation can decrease the cardiac output as well as a perfusion of tissue, that can cause or deteriorates the non- pulmonary dysfunctioning of organs. Among various patients with acute liver injury or ARDS, the dysfunctioning of the various organs along with systems can happen from a systemic inflammatory response (Fluid management in ARDS: an evaluation of current practice and the association between early diuretic use and hospital mortality, 2020). Practice therapy in relation to vasopressor management:The vasopressor is generally needed to encourage the systemic Blood pressure or to enhance the cardiac output among patientswiththeshock.In additiontothis,thereisgenerallynoclearreferenceor information that any of the vasopressor or grouping of these vasopressor is higher. Within this, the prudent methods within ARDS patients is generally to re-establish the intravascular volume towards the euvolemic levels and then to use a vasopressor like the dopamine to effectively attain a mean arterial pressure of about 55 to 65 mmHg. Therefore, both the vasopressor and fluid therapy would be effectively directed by the medical indexes of the organ perfusion. In addition, an output of urine, blood pH as well as a base discrepancy are effectively supportive to measure the competence of perfusion of organs. Among some of the patients, a pulmonary arterial catheter can give a beneficial supplementary information, more specifically when there is a left ventricular dysfunctioning or the pulmonary hypertension that is quite communal among the patients with ARDS. Furthermore, there is a new information on the problem of management of fluid as well as the value consisting a central venous Vs a pulmonary arterial catheter will be approaching from a wide perspective ARDS network trails which is recently under pathway. While talking about vasodilators, many of the patients with ARDS have a mild to moderate level of pulmonary arterial hypertension. Within this, an advanced growth within the pulmonary vascular resistance generally has been visualised by the patients who specifically die from acute lung injury. Within this, the main cause of the pulmonary arterial hypertension is generally multifacetedas well as can consist a hypoxic vasoconstriction, destruction as well as barrier of the pulmonary vascular bed and an advanced level of PEEP (Vasopressor therapy in critically ill patients with shock, 2019).
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