Symptoms And Treatment Of Respiratory Distress

Her drug screen showed positive benzodiazepines and blood alcohol was negative. Troponins were negative. Also, her initial work up showed acute kidney injury with a creatinine of 1.84, and potassium of 5.8. Her chest x-ray showed small amount of infiltrate in the right lower lobe. The CT scan of the head did not show any acute changes. The abdominal CT scan showed constipation and 6 mm opacity in her bladder. She had an electroencephalogram (EEG) which revealed diffuse generalized nonspecific encephalopathy. In addition, there was slowing of the left hemisphere consistent with left intracerebral lesion. The assessment diagnoses were acute respiratory failure (ABG of 87.287, pCO2 of 45.2, pO2 of 380 and biacarbonate of 20 on vent settings), altered mental status, attempted suicide, infectious process, medication use, hyperglycemic nonketotic, and less likely cerebrovascular accident given that her CT scan of the head was normal. She was admitted to the Intensive Care Unit under the care of Dr. Modupe Kehinde. She was intubated for airway protection and remained intubated until 5/23/2016 (7 days). She was on ventilator and was given nutritional support

Throughout my clinical rotation, the only concern for this patient was pain management and discomfort from the chest tube site. The patient was given Ketorolac for a pain of 4/10 using the numeric pain sale. The patient was also at risk for pneumonia and pressure ulcers from immobility and not coughing/deep breathing. Nursing interventions were getting the patient up to the chair and using the incentive spirometer ten-times per hour. Another concern was SOB and fatigue with activities.

Patient 1: monitor B/P, pulse, respirations, skin appearance and touch, notable changes in neurologic function, ECG, lab

The patient is an 85-year-old female who is brought to the ED by her family because of increasing confusion and supposedly she had a degree of altered mental status of two hours previous to presentation. In the ED she is completely worked up. CT shows advanced atrophy with microvascular changes and several lacunar infarcts nothing acute. Specific gravity in the urine reveals her to be markedly dehydrated. She culture completely, started on IV antibiotics, IV fluids and B12. On the day after admission she still presents as persistently confused. She is evaluated by PT. The patient who was formerly ambulating with a walker and allegedly driving a car is unable to be ambulated. Before the history indicates that she has a slow downward

The patient is alert and oriented to person, place, and time. Upon initial interaction, the patient is easy to communicate with and states she is doing well. Facial features are uneven and asymmetrical, as she has a slight left facial droop due to her stroke, which she states happened a couple of years ago. DG expresses multiple times that she has a hard time seeing and she wears prescription eyeglasses. PERRLA. Skin is pink, warm, dry; temperature is 97.5 and turgor is brisk. There is a 20 gauge IV in the right hand infusing Lactated Ringers at 20ml/hour per pump, no redness or edema noted at the insertion site. Respirations are even and non-labored at 22 breaths per minute. Lung sounds are bilaterally clear. The client has a nasal cannula infusing 2 liters of oxygen with an oxygen saturation of 96%. DG tells me she is a current smoker and she smokes

The patient reports being sick with the flu for the past 8 days. She has been vomiting several times a day and has been using more than the recommended dose of antacids in an attempt to calm the nausea. She has become severely dehydrated. After fainting at home she was taken to the hospital. An arterial blood gas sample was drawn and then an IV was placed to help rehydrate her.

The primary nursing diagnosis for this patient is impaired gas exchange, related to abnormal ventilation and perfusion ratio, as evidenced by restlessness, irritability, anxiety, decreased level of consciousness, abnormal arterial blood gases, and abnormal skin color (Gulanick & Myers, 2014, p. 82). A.C. has an endotracheal tube (ETT), and there is a note for the next day to have surgery to put in a tracheostomy. She is currently a smoker, her C02 is 74.6mEq/L which is high, her pH is low at 7.19, and the bicarbonate is 28.6mEq/L which is high. Her oxygen saturation is maintaining at 90%. Her PA02 is 56mm Hg and FI02 is 0.60. The patient is very anxious and restless in the bed, despite sedation and pain medication, and her skin is pale in color and she is diaphoretic.

Prior to my entrance into the patients’ room, I had to look up the patients chart to see what her current status and past Hx was. As I as reviewed my patients chart, I saw that she is a paraplegic who is paralyzed from the waste down with no smoking History or pulmonary dysfunction. My patient had been on SVN Pulmicort treatment

Mrs. Weeks is a 44-year-old female here today to discuss a recent hospitalization with chest discomfort.

Medication that were given to this patient were continual sulbutamol nebulizer and as well as an infusion, hydrocortisone (steroid) adrenalin infusion, potassium intravenously as life in the fast lane (2016) states that “hypokalaemia will occur with continuous beta-agonist use” and magnesium this “Involve a combination of smooth muscle relaxation,” life in the fast lane (2016). I cannot tell you in what order these medications were given as it was a very intense and stressful resus but well run and great outcome in the end.

In the article, Acute lung injury and acute respiratory distress syndrome: Two challenging respiratory disorders, I learned about how difficult it is to diagnose a deadly respiratory disorder. Acute lung injury and acute respiratory distress (ARDS) is a secondary illness resulting from a primary disease that has been largely ignored by the veterinary community, but initial early recognition of the disease is paramount to providing a full recovery. This compounding disorder primarily affects the lungs and its associated passages and membranes in the respiratory system which becomes deadlier as it progresses. The three phases of this disease are the exudative phase, the proliferative phase, and the fibrotic phase. In order to suspect this

Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the bloodstream. According to Kacmarek, Stoller and Heuer, “ it has been proposed that ARDS can develop via different mechanisms and the risk factors for ARDS should be categorized either by direct injury to the alveolar space or indirect injury initiated by systemic disease (2014, p. 601)”. Common direct injuries to the lungs can include pneumonia, lung transplant, trauma, septic shock and aspiration among others. Without enough oxygen, an individual’s brain and other organs can be severely damaged. The brain is what controls the rate and depth of respiration. ARDS can lead to a buildup of fluid

Respiratory distress syndrome (RDS) is an important disease due to a paucity of surfactant and structural immaturity of the lungs in premature neonates. Because the lower gestational age increases the risk of RDS, it is generally seen in the preterm infants. RDS in neonates is managed with the intention to supply interventions that enhance survival as well as lessen potential complications, such as the risk of bronco- pulmonary dysplasia (BPD)

Respiratory distress syndrome (RDS), “is a developmental deficiency in surfactant synthesis accompanied by lung immaturity and hypoperfusion” (Blackburn, 2013, p. 342). Based on the above scenario, there are so many factors that could lead to surfactant deficiency and I would like to discuss on three factors like preterm birth, poorly controlled diabetes, and cesarean section as the reasons for RDS.

Respiratory distress syndrome (RDS) is a common lung disorder that mostly affects preterm infants. RDS is caused by insufficient surfactant production and structural immaturity of the lungs leading to alveolar collapse. Clinically, RDS presents soon after birth with tachypnea, nasal flaring, grunting, retractions, hypercapnia, and/or an oxygen need. The usual course is clinical worsening followed by recovery in 3 to 5 days as adequate surfactant production occurs. Research in the prevention and treatment of this disease has led to major improvements in the care of preterm infants with RDS and increased survival. However, RDS remains an important cause of morbidity and mortality especially in the most preterm infants. This chapter reviews the most current evidence-based management of RDS, including prevention, delivery room stabilization, respiratory management, and supportive care.