Ventilatory Mechanics
Montana Oxford
6/14/2018
RES 242
Debi J. Atchley
Ventilatory Mechanics
For this assignment, you will provide detailed responses to the following question and provide detailed responses to the case study.
1. A patient with fibrotic lung disease is on a volume control ventilator at a CMV rate of 8 breaths/min. The respiratory care practitioner notices it is taking more and more pressure to ventilate the patient. What would you recommend? Why?
I feel like this patient might benefit more from pressure control and needs to be switched from CMV to Pressure control. Patients with fibrotic lung disease have what we call “stiff lung” so they require more pressure than the typical patient that has healthy lungs. Also,
…show more content…
Over several hours the RCP notices that Cstat and Cdyn are decreasing. What is the most likely nature of the problem (Restrictive or Obstructive)? Explain your answer.
I feel like the nature of this problem would be obstructive and that this patient would greatly benefit from a DuoNeb treatment. “Due to the damage that has been done to the lungs from the fibrotic lung disease is causing narrowing of the patient’s airways which is causing the exhaled air to come out more slowly than it normally would in a patient with healthy lungs” (Mayo Clinic Staff, 2018).
3. Review the data below regarding your patient and interpret the data. Hint: Is the airway resistance and/or compliance increasing or decreasing? Why? or why not? (Support your position with formulas, calculations, and units of measure.) 0800 hrs. 1200
…show more content…
This is because the patient cannot fully exhale so some of the CO2 is remaining in the lungs when the patient is done exhaling. Plateau pressure is when there is no air in the circuit, this presser is found from the lung compliance. When lung compliance isn’t right the patients plateau pressure will go up. I feel like before we go changing a bunch of settings we need to make sure something else isn’t going on such as:
●Bronchospasm
●Retained secretions
●Mucous plug
●ET tube tip occlusion
These four things can also cause a high peak pressure.
When concerning the patients high plateau pressure. We need to look into conditions such as:
●Pneumothorax
●Pulmonary edema
●ARDS
●Pneumonia
These four conditions can cause the patients plateau pressure to be high.
After checking for bronchospasm, retained secretions, Mucous plug, and a ET tube tip occlusion if nothing was found at This point I would call x ray to get a chest x ray to check for these four conditions. After getting the x rays back we would talk to the doctor and come up with a new plan for this specific patient according to our newest findings. However, in the mean time I think that the patient would benefit from a decrease in their tidal volume and their respiratory
According to the provider, the claimant's cough has been improved. His review of systems was positive for fatigue, malaise, sleep difficulty, shortness of breath, wheezes, and a cough. His blood pressure was 115/71 mmHg and his BMI was 30.35 kg/m2. The physical examination revealed wheezes. Clonazepam was prescribed for agitation. Atorvastatin, Nystatin, Citalopram, and a probiotic were prescribed. Continued use of Aspirin and a regular inhaler were suggested. Further, a follow-up visit with Endocrinology, Cardiology, and Pulmonology. As it relates to a spot in his lung, a repeat CT scan was recommended. The bronchial washes were negative for
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.
Ms. Manock has had by and large very stable symptoms, since her last visit in February. She has had no exacerbations of her COPD. She should continue use of her Symbicort as well as her Xopenex HFA on a p.r.n. basis. She should also continue use of her supplemental oxygen with exertion and with sleep. Given the severity of her COPD, I have suggested reengagement with outpatient pulmonary rehabilitation and Fit For Life, which she is willing to do at this time. I have also encouraged self-directed exercise at home. She has also mentioned some increasing postnasal drip and I have suggested continue use of her Zyrtec as well as over the counter Nasonex to help mitigate her
Another follow up ABG at 0100 shows a small improvement on the Ph to 7.18, the Pco2 became more acidotic moved to 53, the Po2 improved to 77 which shows he is oxygenating better but still hypoxic, his Hco3 acidosis is improving at a change to 19.8, and sating 91% now. The Pt is now breathing at a rate has come down to 10 BPM on his own above and beyond the vent. After consulting with the physician we changed the Vt to 600 and the pressure support to 20 and Cpap to 15. The Pt continued on these settings till 0415. The physician then made the change to Bi-level with the settings of a rate of 14 pressure support of 25, and an H/L pressure of 35/15. The Pt at this time is pulling a Vt of 745 and a spontaneous rate of 17 and still at 100% Fio2 and sating 92%. This is the point when the Pt makes the turn. The Bi-level or APRV was the proper setting for this Pt. He continued to improve over the next several days with his peek pressure climbing to 40. The Pt continues these settings and slowly improves and eventually weaned from the ventilator till the Pt no longer needs support.
Lung function tests have revealed normal spirometry, gas transfer and static lung volumes. There appears to be a fall in pre-bronchodilator FEV1, but not so FVC and TLCO comparing back to 2007??. Maximal respiratory pressures are reduced indicative of respiratory muscle/diaphragm weakness. This is consistent with what has previously been observed and the previous diagnosis of mild left hemidiaphragm weakness. I note from Tony Dortimer’s most recent letter that the coronary angiogram
Airway pressure release ventilation (APRV) is a fairly new mode of ventilation, just becoming available in the U.S. in the mid-1990’s. APRV is “inverse ratio, pressure controlled, intermittent mandatory ventilation with unrestricted spontaneous breathing and it is based on the principle of open lung approach”. (Daoud, Farag, & Chatburn, 2012) The open lung approach is “concept of maximizing and maintaining alveolar recruitment throughout the ventilatory cycle by potentially ventilating the lung on the steep portion of the pressure-volume curve, thus avoiding over-distention on inspiration and alveolar collapse on exhalation”. (2012) APRV “was first used and described in 1987 as CPAP with an intermittent pressure release phase. Continuous airway pressure is applied to maintain adequate lung volume and improve alveolar recruitment. It is a pressure-limited, time-cycled, volume-variable mode of ventilation.” (2012)
Lungs: Mild end-expiratory wheezing. Pursed-lip breathing noted and has a prolonged expiratory phase. Chest x-ray shows pulmonary hyperinflation, flattening of the diaphragm; Pulmonary function test (after bronchodilation with 2 puffs albuterol—FEV1/FVC ratio 0.60 FEV1 60% of predicted value)
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,
Hooke’s law is directly related to the use of mechanical ventilation. If when a patient is placed on a mechanical ventilation, you can exceed the limitations cause by the lower elastance of the lung. A severe type of pneumothorax can occur in people who need mechanical assistance to breathe. The action of the
2. A 65-year-old patient is admitted to the hospital with acute shortness of breath. The patient has a respiratory rate of 28, is sitting forward to breathe, and appears anxious. According to the patient’s family, the shortness of breath has been increasing over the past
This paper will discuss the weaning of patients off of a mechanical ventilator. It will look at the problems associated with prolonged intubation vs. premature extubation, and what healthcare professionals can do to assess a patients readiness to begin the weaning process. A patient care scenario will be given and an explanation of how nursing practice can evolve with the knowledge from this study will be shown. The accountability of the nursing professional in regards to mechanical ventilation will be visited as well.
Another important intervention was to maintain the head of the bed at 30-45 degrees and position L.M.’s left lung into a dependent position to improve ventilation and perfusion. L.M.’s O2 was decreased to 63 and her CO2 was increased to 50. According to the IHI, it is recommended to elevate the bed to 30- 45 degrees to improve ventilation. Patients that lay in the supine position have lower spontaneous tidal volumes on pressure support ventilation compared to those laying at more of an angle (Institute for Healthcare Improvement, 2012). In regards to positioning, when the least damaged portion of the lung is placed in a dependent position it receives preferential blood flow. This redistribution of blood flow helps match ventilation and perfusion, therefore, improving gas exchange (Lough, Stacy & Urden, 2010). Implementing these interventions combined with respiratory therapy, significantly improved the blood gas values for oxygen and carbon dioxide levels.
Ineffective breathing pattern related to decreased oxygen saturation, poor tissue perfusion, obesity, decreased air entry to bases of both lungs, gout and arthritic pain, decreased cardiac output, disease process of COPD, and stress as evidenced by shortness of breath, BMI > 30 abnormal breathing patterns (rapid, shallow breathing), abnormal skin colour (slightly purplish), excessive diaphoresis, nasal flaring and use of accessory muscles, statement of joint pain, oxygen saturations of 85-95% 2L NP, immobility 95% of the day, and adventitious sounds throughout lungs (crackles) secondary to CHF, hypertension, pain caused by gout and arthritis, and obesity
This also affects the pressure gradient from the lungs to
High Frequency Ventilation, HFV, with its small tidal volumes appears to be ideal for ventilation within the safety zone. Dr, Alison Froese, pulmonologist, assumes that there is a window in the Pressure-Volume relation, the area between a lower zone of atelectasis and an upper zone of overdistention. If possible, ideally, Tidal Volume should fit within this area. We can achieve that by setting PEEP level above the lower inflection point and reducing Plateau Pressure to avoid over inflation. In diseased lung, the safe window may be too small to harbor conventional tidal volume. When the patient is attached to HFOV, some aspects should be mentioned. Through careful observation we can detect early evidence of changing disease or adverse effects. Auscultation during HFOV may be difficult, but very useful. For instance, reduced breath sounds can indicate pneumothorax or endotracheal tube displacement when the tube is too low. Humidification and warming of inspiratory gases are necessary to prevent necrotizing tracheobronchitis. In the article “High frequency oscillatory ventilation in children: an overview”, the authors use data gained through systematic professional literature review and current studies to provide the information about different modes of HFV, and to summarize the current knowledge about advantages of HFV. It