NURSING 2571 /CARDIAC ANSWERS | DETAILED SOLUTION | Rasmussen College

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Initial Evaluation Go to: Initial evaluation to elucidate the source of dyspnea was performed and included CBC to establish if an infectious or anemic source was present, CMP to review electrolyte ba... lance and review renal function, and arterial blood gas to determine the PO2 for hypoxia and any major acid- base derangement, creatinine kinase and troponin I to evaluate presence of myocardial infarct or rhabdomyolysis, brain natriuretic peptide, ECG, and chest x-ray. Considering that it is winter and influenza is endemic in the community, a rapid influenza assay was obtained as well. CBC Largely unremarkable and non-contributory to establish a diagnosis. CMP Showed creatinine elevation above baseline from 1.08 base to 1.81 indicating possible acute injury. EGFR at 28 is consistent with the chronic renal disease. Calcium was elevated to 10.2. However, when corrected for albumin this corrected to 9.8 mg/dL. Mild transaminitis present as seen in Alkaline Phosphatase, AST, and ALT measurements which could be due to liver congestion from volume overload. Initial arterial blood gas with pH 7.491, PCO2 27.6, PO2 53.6, HCO3 20.6, and oxygen saturation 90% on room air indicating respiratory alkalosis with hypoxic respiratory features. Creatinine kinase was elevated along with serial elevated troponin I studies. In the setting of her known chronic renal failure, and in the setting of acute injury indicated by the above creatinine value, a differential of rhabdomyolysis is set. Influenza A and B: Negative ECG Normal sinus rhythm with non-specific ST changes in inferior leads. Decreased voltage in leads I, III, aVR, aVL, aVF. Chest X-ray Findings: Bibasilar airspace disease that may represent alveolar edema. Cardiomegaly noted. Prominent interstitial markings noted. Small bilateral pleural effusions Radiologist Impression: Radiographic changes of congestive failure with bilateral pleural effusions greater on the left compared to the right See reviews... See all... Recent Activity Turn Off Clear Case Study: 60-Year-Old Female Presenting With Shortness of Breath - StatPearls Dietary Recommendations - Improving America's Diet and Health Practical approach to the management of catheter- related bloodstream infection Clinical impact of delayed catheter removal for patients NSTEMI - NSTEMI stands for Non-ST-elevation myocardial infarction. used to evaluate for left ventricular ejection fraction, right ventricular function, pulmonary artery pressure, valvular function, pericardial effusion and any hypokinetic area. TSH: 112.717 (H) Free T4: 0.56 (L) TSH and Free T4 values indicate severe primary hypothyroidism. BNP: 187 BNP can be falsely low in obese patients due to the increased surface area. Additionally, adipose tissue has BNP receptors which augment the true BNP value. Also, African American patients more excretion may have falsely low values secondary to greater excretion of BNP. This test is not that helpful in renal failure due to the chronic nature of fluid overload. This allows for desensitization of the cardiac tissues with a subsequent decrease in BNP release. Repeat arterial blood gas on BiPAP ventilation shows pH 7.397, PCO2 35.3, PO2 72.4, HCO3 21.2, and oxygen saturation 90% on 2 L supplemental oxygen. CT chest without contrast was mainly obtained to evaluate left hemithorax especially retrocardiac area. Radiologist Impression: Tiny bilateral pleural effusions. Pericardial effusion. Coronary artery calcification. Some left lung base atelectasis with minimal airspace disease. Echocardiogram The left ventricular systolic function is normal. The left ventricular cavity is borderline dilated. The pericardial fluid is collected primarily posteriorly, laterally but not apically. There appeared to be a subtle, early hemodynamic effect of the pericardial fluid on the right-sided chambers by way of an early diastolic collapse of the RA/RV and delayed RV expansion until late diastole. Dedicated tamponade study was not performed. Estimated ejection fraction appears to be in the range of 66% to 70%. The left ventricular cavity is borderline dilated. The aortic valve is abnormal in structure and exhibits sclerosis. The mitral valve is abnormal in structure. Mild mitral annular calcification is present. There is bilateral thickening present. Trace mitral valve regurgitation is present. Diagnosis 1. Myxedema coma or severe hypothyroidism 2. Pericardial effusion secondary to myxedema coma 3. COPD exacerbation 4. Acute on chronic hypoxic respiratory failure 5. Acute respiratory alkalosis 6. Bilateral community-acquired pneumonia 7. Small bilateral pleural effusions 8. Acute mild rhabdomyolysis 9. Acute chronic, stage IV, renal failure 10. Elevated troponin I levels, likely secondary to Renal failure 11. Diabetes mellitus type 2, non-insulin dependent 12. Extreme obesity 13. Hepatic dysfunction Management Go to: Go to: The patient was extremely ill and rapidly decompensating with multisystem organ failure including respiratory failure, altered mental status, acute on chronic renal failure, and cardiac dysfunction. The primary concerns for the stability of the patient revolved around the respiratory failure coupled with altered mental status. In the intensive care unit (ICU), she rapidly began to fail BiPAP therapy. Subsequently, the patient was emergently intubated in the ICU. A systemic review of therapies and hospital course is as follows: Endocrine Considering the primary diagnosis of myxedema coma, early supplementation with thyroid hormone is essential. Healthcare providers followed the American Thyroid Association recommendations which recommend giving combined T3 and T4 supplementation; however, T4 alone may also be used. T3 therapy is given as a bolus of 5 to 20 micrograms intravenously and continued at 2.5 to 10 micrograms every 8 hours. An intravenous loading dose of 300 to 600 micrograms of T4 is followed by a daily intravenous dose of 50 to 100 micrograms. Repeated monitoring of TSH and T4 should be performed every 1 to 2 days to evaluate the effect and to titrate the dose of medication. The goal is to improve mental function. Until coexistent adrenal insufficiency is ruled out using a random serum cortisol measurement, 50 to 100 mg every 8 hours of hydrocortisone should be administered. In this case, clinicians used hydrocortisone 100 mg IV every 8 hours. Dexamethasone 2 to 4 mg every 12 hours is an alternative therapy. Neurologic The patient’s mental status rapidly worsened despite therapy. In the setting of her hypothyroidism history, this may be myxedema coma or due to the involvement of another organ system. The thyroid supplementation medications and hydrocortisone were continued. A CT head without contrast was normal. Respiratory For worsening metabolic acidosis and airway protection, the patient was emergently intubated. Her airway was deemed high risk due to having a large tongue, short neck, and extreme obesity. As the patient’s heart was preload dependent secondary to pericardial effusion, a 1- liter normal saline bolus was started. Norepinephrine was started at a low dose for vasopressor support and ketamine with low dose Propofol was used for sedation. Ketamine is a sympathomimetic medication and usually does not cause hypotension as all other sedatives do. The patient was ventilated with AC mode of ventilation, tidal volume of 6 ml/kg ideal body weight, flow 70, initial fio2 100 %, rate 26 per minute (to compensate for metabolic acidosis), PEEP of 8. Cardiovascular She was determined to be hemodynamically stable with a pericardial effusion. This patient’s cardiac dysfunction was diastolic in nature as suggested by an ejection fraction of 66% to 70%. The finding of posterior pericardial effusion further supported this conclusion. The posterior nature of this effusion was not amenable to pericardiocentesis. As such, this patient was preload dependent and showed signs of hypotension. The need for crystalloid fluid resuscitation was balanced against the impact increased intravascular volume would have on congestive heart failure and fluid overload status. Thyroid hormone replacement as above should improve hypotension. However, vasopressor agents may be used to maintain vital organ perfusion targeting a mean arterial pressure of greater than 65 mm Hg as needed. BP improved after fluid bolus and eventually the norepinephrine was stopped. Serial echocardiograms were obtained to ensure that the patient did not develop tamponade physiology. Total CK was elevated which was likely due to Hypothyroidism compounded with the chronic renal disease. Infectious Disease Blood cultures, urine analysis, and sputum cultures were obtained. The patient's white blood cell count was normal. This is likely secondary to her being immunocompromised due to hypothyroidism and diabetes. In part, the pulmonary findings of diffuse edema and bilateral pleural effusions can be explained by the cardiac dysfunction. Thoracentesis of pleural fluid was attempted and the fluid analyzed for cytology and gram staining to rule out infectious or malignant causes as both a therapeutic and diagnostic measure. Until these results return, broad- spectrum antibiotics are indicated and may be discontinued once the infection is ruled out completely. Gastrointestinal Nasogastric tube feedings were started on the patient after intubation. She tolerated feedings well. AST and ALT were mildly elevated which was thought to be due to hypothyroidism and as the TSH and free T4 improved her AST and ALT improved. Eventually, these values became normal once her TSH level was close to 50. Renal Her baseline creatinine was found to be close to 1.08 in prior medical records. She presented with a creatinine of 1.8 in the emergency department. As hypothyroidism causes fluid retention in part due to the fact that thyroid hormone encourages excretion of free water and partly due to decreased lymphatic function in returning fluid to vascular circulation. Aggressive diuresis was attempted. As a result, her creatinine increased initially but improved on repeated evaluation and patient had a new baseline creatinine of 1.6. Overall she had a net change in the fluid status of 10 liters negative by her ten days of admission in the ICU. Hematology Mildly anemic otherwise WBC and platelet counts were normal. Electrolyte balance should be monitored closely paying attention to sodium, potassium, chloride, and calcium specifically as these are worsened in both renal failure and myxedema. Daily sedation vacations were done, patients mental status improved and was much better when TSH was around 20. The bilateral pleural effusions improved with aggressive diuresis. Breathing trials were initiated when the patient's fio2 requirements decreased to 60% and a PEEP of 8. She was eventually extubated on to BiPAP and then high flow nasal cannula while off of BiPAP. Pericardial fluid remained stable, and no cardiac tamponade pathology developed. As a result, it was determined that a pericardial window was unnecessary. Furthermore, she was not a candidate for pericardiocentesis as the pericardial effusion was located posterior to the heart. Her renal failure improved with improved cardiac function, diuretics, and thyroid hormone replacement. After extubation patient had speech and swallow evaluations and was able to resume an oral diet. The patient was eventually transferred out of the ICU to the general medical floor and then eventually to a rehabilitation unit. Discussion Go to: Despite the name myxedema coma, most patients will not present in a coma status. This illness is at its core a severe hypothyroidism crisis that leads to systemic multiorgan failure. Thyroid hormones T3, and to a lesser extent, T4 act directly on a cellular level to upregulate all metabolic processes in the body. Therefore, deficiency of this hormone is characterized by systemic decreased metabolism and decreased glucose utilization along with increased production and storage of osmotically active mucopolysaccharide protein complexes into peripheral tissues resulting in diffuse edema and swelling of tissue. [1] Myxedema coma is an illness that occurs primarily in females at a rate of 4:1 compared to men. It typically impacts the elderly at the age of greater than 60 years old and approximately 90% of cases occur during winter months. Myxedema coma is the product of longstanding unidentified or undertreated hypothyroidism of any etiology. Thyroid hormone is necessary throughout the body and acts as a regulatory hormone, that affects many organ systems.[2]In cardiac tissues, myxedema coma manifests as decreased contractility with subsequent reduction in stroke volume and overall cardiac output. Bradycardia and hypotension are typically present also. Pericardial effusions occur due to the accumulation of mucopolysaccharides in the pericardial sac which leads to worsened cardiac function and congestive heart failure from diastolic dysfunction. Capillary permeability is also increased throughout the body leading to worsened edema. Electrocardiogram findings may include bradycardia and low-voltage, non-specific ST waveform changes with possible inverted T waves. Neurologic tissues are impacted in myxedema coma leading to the pathognomonic altered mental status as a result of hypoxia and decreased cerebral blood flow secondary to cardiac dysfunction as above. Additionally, hypothyroidism leads to decreased glucose uptake and utilization in neurological tissue thus worsening the cognitive function. The pulmonary system typically manifests this disease process through hypoventilation secondary to central nervous system (CNS) depression of the respiratory drive with blunting of the response to hypoxia and hypercapnia. Additionally; metabolic dysfunction in the muscles of respiration leads to respiratory fatigue and failure, macroglossia from mucopolysaccharide driven edema of the tongue leads to mechanical obstruction of the airway, and obesity hypoventilation syndrome with the decreased respiratory drive as most hypothyroid patients suffer from obesity. Renal manifestations include decreased glomerular filtration rate from the reduced cardiac output and increased systemic vascular resistance coupled with acute rhabdomyolysis lead to acute kidney injury. In the case of our patient above who has a pre-existing renal disease status post-nephrectomy, this is further worsened. The net effect is worsened fluid overload status compounding the cardiac dysfunction and edema. [3] The gastrointestinal tract is marked by mucopolysaccharide driven edema as well leading to malabsorption of nutrients, gastric ileus, and decreased peristalsis. Ascites are a common occurrence because of increased capillary permeability in the intestines coupled with coexistent congestive heart failure and congestive hepatic failure. Coagulopathies are common to occur as a result of this hepatic dysfunction. Evaluation: The diagnosis of myxedema coma, as with all other diseases, is heavily reliant on the history and physical exam. A past medical history including hypothyroidism is highly significant whenever decreased mental status or coma is identified. In the absence of identified hypothyroidism myxedema coma is a diagnosis of exclusion when all other sources of coma have been ruled out. If myxedema coma is suspected, evaluation of thyroid stimulating hormone (TSH), free thyroxine (T4), and serum cortisol is warranted. T4 will be extremely low. TSH is variable depending on the etiology of hypothyroidism with a high TSH indicating primary hypothyroidism and a low or normal TSH indicating secondary etiologies. Cortisol may be low indicating adrenal insufficiency because of the hypothyroidism. [4] Prognosis: Myxedema coma is a medical emergency. With proper and rapid diagnosis and initiation of therapy the mortality rate is still as high as 25% to 50%. The most common cause of death is due to respiratory failure. The factors which suggest a poorer prognosis include increased age, persistent hypothermia, bradycardia, low score Glasgow Coma Scale, or multi-organ impairment indicated by high APACHE (Acute Physiology and Chronic Health Evaluation) II score. For these reasons, placement in an intensive care unit with a low threshold for intubation and mechanical ventilation can improve mortality outcomes.[3][5] Pearls of Wisdom Go to: Not every case of shortness of breath is COPD or congestive heart failure (CHF). While less likely, a history of hypothyroidism should raise suspicion of myxedema coma in a patient with any cognitive changes. Myxedema is the great imitator illness that impacts all organ system. It can easily be mistaken for congestive heart failure, COPD exacerbation, pneumonia, renal injury or failure, or neurological insult. Initial steps in therapy include aggressive airway management, thyroid hormone replacement, glucocorticoid therapy, and supportive measures. These patients should be monitored in an intensive care environment with continuous telemetry.[6] [Show More]

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