Chronic Respiratory Failure Lab Report

Both rapid, shallow breathing patterns and hypoventilation effect gas exchange. Arterial blood gases will be monitored and changes discussed with provider. Alteration in PaCO2 and PaO2 levels are signs of respiratory failure. Patient’s body position will be properly aligned for optimum respiratory excursion, this promotes lung expansion and improved air exchange. Patient will be suctioned as needed to clear secretions and maintain patent airways. The expected outcome is that the patient’s airway and gas exchange will be maintained as evidence by normal arterial blood gases (Herdman,

History of Present Illness: Mr. Olson is a very pleasant 57-year-old gentleman with multiple medical problems to include severe COPD, who is here today for an initial consultation for his shortness of breath. He is followed by a pulmonologist Dr. William Goodman, at the Veteran Affairs Administration. His last evaluation there was in February 2015. Mr. Olson states he has had ongoing dyspnea on exertion over the last two years. He complains of minimal cough. He does note some sinus problems for which he is on Flovent. In the past, he has had pulmonary function testing that did demonstrate reversible airflow obstruction, therefore he likely has some component of asthma overlay. He states that occasionally has chest tightness and chest heaviness. He has gained about 25 pounds over the last year. He is currently using Spiriva, albuterol as needed as well as Symbicort. He is also using supplemental oxygen at 2.5L per minute at night as well as on an as needed basis during the day. Mr. Olson admits to continued tobacco use with about a half pack to a pack a day. He states that when he is feeling depressed, he will smoke more.

Jane’s asthma was acute severe. Initially to alleviate some of Jane’s breathlessness she was sat up right in the bed and supported with pillows to improve air entry. Due to her low oxygen saturations she was placed on 40% oxygen via Hudson mask (BTS 2006), as Jane was mouth breathing the mask was the appropriate device to use to ensure adequate oxygenation (Walsh 2002). According to Inwald et al (2001) hypoxemia is frequently a primary cause in numerous asthma related deaths. By administering oxygen promptly, for acute severe asthma, serious hypoxemia

Patient is a high school counselor. He participates in physical activities by running 2 to 3 times a week, playing golf, and volunteering at a nursing home. The patient is married with one daughter and one son. He does not use tobacco and periodically drinks at

Data: Pulmonary function testing dated 2010 showed moderately severe obstruction with positive bronchodilators response. Normal lung volumes. Evidence of air trapping. Severely reduced diffusing capacity for carbon monoxide.

My patient is 79-year old, male that was brought the University of Kentucky medical center emergency department via ambulance on January 14, 2017. The patient was smoking while using home oxygen, when he fell asleep. The EMS responded to a home fire.

On the early morning of August 17, 2002, James C., a patient in one of the wards under the supervision of Ellen Hughes Finnerty, RN, went into respiratory depression. Between 3:00 and 4:00 a.m., Ann Mugi, the patient’s primary nurse, sought the assistance of a respiratory therapist, Hiran Obeyesekere, to help her care for the patient. As Obeyesekere suctioned the patient airway, Mugi called the service of the patient’s primary care physician, Dr. Jackson, to report the changes in the patient’s respiratory status, e.g., respiratory rate of 40 breaths per minute and low urine output.

HISTORY OF PRESENT ILLNESS: David Lockman is here for followup for his traumatic saw injury to his right knee. He is about two and half weeks out now. He was seen, I believe a week or so ago or two weeks ago perhaps, by one of my partners. He was sent for therapy, although he has had some delay in therapy. He just started therapy. He did get a blood clot, I believe recently, and is now on Xarelto for that. He states that the swelling in his leg is much better, at this point. He does continue to smoke, however. I believe he is a half a pack or one pack per day smoker. Again, I went over smoking cessation with him, as well as the risks of uncontrolled bleeding with the Xarelto that he currently on. He understands this, so he should

The incident happened on Nov 21st, 2017. The patient has sleep apnea and a health history of chronic bronchitis (no episode in recent 2 years). Her respiration rate was 16 and all lung fields were clear upon auscultation. After I took the patient’s vital signs, I noticed that her oxygen saturation was low (83%). Then, I notified the nurse and asked the patient to do take some deep breath. After that, we put her on 2L of oxygen and her oxygen saturation went up to above 90s. However, the patient had a bladder control problem (was incontinent), so I took the oxygen off because she went to the toilet for around 4-5 times in an hour. However, I forgot to monitor her O2 saturation right away. Instead, I checked her oxygen saturation after she finished her dinner, and it dropped to 86%. The instructor showed me how deep breathing exercise can help the patient increase her oxygen level quickly. I notified the nurse and we put the patient on 2L of oxygen, but again I forgot to check her oxygen saturation right away. Instead, I checked her oxygen around 7pm later.

To ensure that adequate oxygen is available to the tissues, supplemental oxygen may be needed. Pulmonary injuries fall into several categories: upper airway injury; inhalation injury below the glottis, including carbon monoxide poisoning; and restrictive defects. Upper airway injury results from direct heat or edema. It is manifested by mechanical obstruction of the upper airway, including the pharynx and larynx. Because of the cooling effect of rapid vaporization in the pulmonary tract, direct heat injury does not normally occur below the level of the bronchus. Upper airway injury is treated by early intubation. Inhalation injury below the glottis results from inhaling the products of incomplete combustion or noxious gases. These products include carbon monoxide, sulfur oxides, nitrogen oxides, aldehydes, cyanide, ammonia, chlorine, phosgene, benzene, and halogens. The injury results directly from chemical irritation of the pulmonary tissues at the alveolar level. Inhalation injuries below the glottis cause loss of ciliary action, hypersecretion, severe mucosal edema, and possibly bronchospasm. The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli). Expectoration of carbon particles in the sputum is the cardinal sign of this injury. Carbon monoxide is probably the most common cause of inhalation injury because it is a

➢ The patient may have no respiratory problems, but may still have inhaled carbon monoxide.

Introduction: Late onset obese asthmatics are associated with reduced L-arginine and greater levels of asymmetric di-methyl arginine (ADMA). This imbalance increases nitric oxide synthase (NOS) uncoupling leading to reduced nitric oxide (NO) and increased oxidative and nitrosative stress. However, the role of the human bronchial epithelial cells (HBECs) in regulating this process in asthma is unknown.

I have to consider that he has COPD, and low levels of oxygen therapy are essential, because high levels of oxygen may suppress breathing stimulus, cause hypoventilation and CO2 retention, and can lead to respiratory arrest due to CO2 narcosis. He had (ABG) arterial blood gases analysis drawn earlier in the E.R. Evidence-Based Practice of pulse oximetry measures the arterial saturation of available hemoglobin. The anemic client may have a normal Sp02 and not have adequate tissue oxygenation because available hemoglobin is maximally saturated with oxygen. His pulse oximetry reading is 90-92% on oxygen at 2 liters/minute. Using pulse oximetry technology allows for more cost and time efficient PRN or continuous monitoring of arterial oxygen saturation( Sa02). I place a Nicotine patch to his upper right arm, as prescribed. The client and I discuss the use for the Nicotine patch as well as smoking cessation. I give him written information and explain alternative choices that he may want to try. He voices,” Look lady, no one will ever get me to quit smoking, so, stop trying!” I inform him that he can not smoke in the hospital and that concentrated oxygen is highly flammable when it interacts with smoke/fire. He voiced that he does not have any cigarettes or matches. I check his lab work (Quantitative D-dimer, C-reactive protein,

BCD Biology the variety of life: Layout of report Title: Background information: Research question: Hypothesis: Variables: Method: Data collection: Data processing: Conclusion: Evaluation: Research Question: Does height affect lung capacity in humans? Aim: To Establish a statistical relationship between two characteristics of individuals from a population.

In the experiment you must ask a question that can be tested. Does the mount of physical exertion that a sport demands affect the players lung capacity? Based on previous knowledge of the pulmonary system and the physical demands of sports, a hypothesis was produced. If the physical demand of the sport increases, then the lung capacity of the athlete will increase when lung capacity is a function of physical demand. To test this prediction, an experiment must be conducted. The independent variable in this experiment is playing a sport; since there are not units of this variable, it will be rated on a scale. The test subjects will be asked to rate the physical demand of their sport on a scale of one to five: one being the lowest physical demand a sport requires and five being the greatest. The sports that will be tested are football, basketball, and soccer. An experimental control is needed to compare results; therefore, we will include non-athletic subjects as well. The dependent variable of the experiment is lung capacity, which will be measured using a Spirometer in FVE1; FVE1 is the force of air one can blow out in one second.