Mechanical ventilation in Infective airway diseases
Introduction
Nearly 50% of patients with infective airway diseases are at an increased risk of developing Acute Lung Injury or Acute Respiratory Distress Syndrome (ALI/ARDS). Endotracheal intubation may be lifesaving in these situations, as they allow provision of adequate tissue oxygenation, reduce the respiratory muscle effort and avert hemodynamic embarrassment. Over the last 20 years, many clinical evidences have highlighted the harmful consequences of invasive mechanical ventilation such as Ventilator associated pneumonia (VAP) and excessive mechanical stress leading to perpetuation of lung injury.
Unavailability of robust clinical data fails to provide enough evidence-based data on
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Common indications for institution of mechanical ventilation may include profound tachypnea (respiratory rate > 40), failure of respiratory muscles (use of accessory muscles), refractory hypoxemia on high levels of inspired FIO2, compromised cardiac performance, life-threatening metabolic acidosis, and altered mental status.
4. Is normalization of 1) pH or 2) PCO2 necessary in sepsis induced ALI/ARDS, and 3) should permissive hypercapnia be used in patients with sepsis induced ALI/ARDS?
Recommendation:
Hypercapnia (allowing PaCO2 to increase above normal, so-called permissive hypercapnia) can be tolerated in patients with sepsis induced ALI/ARDS if required to minimize plateau pressures and tidal volumes.
5. Does the use of 1) small tidal volume ventilation or 2) pressure-limited ventilation strategies affect outcome in ALI related to infective airway diseases?
Recommendation:
High tidal volumes that are coupled with high plateau pressures should be avoided in ALI/ARDS. Clinicians should use as a starting point a reduction in tidal volumes over 1 to 2 hrs to a “low” tidal volume (6 mL/kg•lean body weight) as a goal in conjunction with the goal of maintaining end-inspiratory plateau pressures of < 30 cm
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Does prone positioning affect 1) gas exchange or 2) outcome in sepsis related ALI, and 3) should prone positioning be used for patients with ARDS requiring potentially injurious levels of FIO2 or plateau pressure?
Recommendation:
In facilities with adequate experience, prone positioning should be considered in patients requiring potentially injurious levels of FIO2 or plateau pressure who are not at high risk for adverse positional changes.
6. Is there a defined fluid management strategy in sepsis-related ALI/ ARDS?
Recommendation:
Avoid administration of fluids in excess of those amounts needed to maintain appropriate vital organ perfusion. Consider use of colloids in hypoproteinemic patients with ALI/ ARDS.
7. Are corticosteroids indicated in the 1) prevention, 2) early treatment (exudative phase), or 3) late treatment (fibroproliferative phase) of sepsis induced
It has been repeatedly stated that oral care is important in the prevention of ventilator-associated pneumonia (VAP). Endotracheal intubation predisposes patients to developing VAP. The tube acts as a conduit from the mouth to the lungs – a perfect track for bacteria to descend upon. Khezeri, et al. (2014) suggest that “the presence of an endotracheal tube (ETT) inhibits normal coughing, normal swallowing, and the protection of the trachea contact by epiglottis closure.” In addition, an endotracheal tube keeps the patients mouth open – leading to dryness. Bacteria are not washed away by saliva. Also, Landgraf, et al. (2017) mention that the presence of an endotracheal tube in the mouth causes “changes in the oral epithelium” which “might indicate risk for infection in intensive care patients
The early intravenous fluid administration for resuscitation of the critically ill hypovolemic patient is the corner stone of shock therapy (Kruemer & Ensor 2012). The Surviving Sepsis recommends early optimization in the first six hours, followed with fluid challenges in the case of persistent hypo
ICU patients suffer from a broad range of pathologies, requiring MV, sedation and use of multiples devices, which do not allow patients to protect their airway (Augustyn. 2007; Kollef. 2004).
The nurse found Mrs Smith to be tachypnoeic, her respirations were recorded as 24 breaths per minute it was observed as being fast and it appeared that her accessory muscles were being used. Mrs Smith’s pallor also appeared flushed and her saturations were documented as 93%. The nurse used the stethoscope to check for wheeze the patient’s lungs were clear and chest rise was symmetrical. Mrs Smith was commenced on 100% oxygen through a non-rebreathe mask, oxygen as an intervention is necessary as Creed & Spiers (2010) highlight ‘metabolic demand for oxygen throughout the body is hugely increased by sepsis and is essential to ensure the supply of oxygen is maximized’ .The nurse monitored the patient closely because in her confused state the patient may try to remove the oxygen mask.
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,
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.
From investigation in health practices, ventilator associated pneumonia caught my attention. “Ventilator Associated Pneumonia (VAP) is a leading cause of morbidity and mortality in intensive care units. Most episodes of VAP are thought to develop from the aspiration of oropharyngeal secretions containing potentially pathogenic organisms. Aspiration of gastric secretions may also contribute, though likely a lesser degree. Tracheal intubation interrupts the body’s anatomic and physiologic defenses against aspiration, making mechanical ventilation a major risk for Ventilator Associated Pneumonia. Semi-recumbent positioning of mechanically ventilated patients may help reduce the incidence of gastroesophageal reflux and lead to a decreased incidence of VAP. The one randomized trial to date of semi- recumbent positioning shows it to be an effective method of reducing VAP. Immobility in critically ill patients leads to atelectasis and decreased clearance of bronchopulmonary secretions. The accumulation of contaminated oropharyngeal secretions above the endotracheal tube cuff may contribute to the risk of aspiration. Removing these
Home mechanical ventilation (HMV) has been used as long-term ventilation for over 70 years to manage chronic ventilatory failure. In the United States, the first introduce of mechanical ventilation was by the use of the iron lung which used with polio victims (Tobin, 2006). Iron lung was the only way available that time to ventilate Poliomyelitis patients and injured army soldiers (Goldberg, 2002).In 1950s, the use of intermittent positive-pressure ventilation with mouth piece have began ,and in 1952, the use of intermittent positive-pressure ventilation (SIMV) via tracheostomy was introduced (Tobin, 2006). In France, professor Rideau had tried applying another method of mechanical ventilation for some of his patients who were suffering
Effect of a Protective-Ventilation Strategy on Mortality in the Acute Respiratory Distress Syndrome (Amato et al.,). The topic of the article is the use of protective lung strategies and the effects they have on mortality rates for patients with Acute
Effect of a Protective-Ventilation Strategy on Mortality in the Acute Respiratory Distress Syndrome (Amato et al.,). The topic of the article is the use of protective lung strategies and the effects they have on mortality rate for patients with Acute Respiratory Distress Syndrome (ARDS). The problem the authors, and practitioners around the world, face is that traditional methods for mechanical ventilation damage already diseased lungs which increases the mortality rate of patients with ARDS. The purpose of this study is to define what lung protective strategies are comprised of and to determine if using these strategies will reduce pulmonary complications which will ultimately decrease mortality rates. The questions the authors focused on were:
The European Society of Intensive Care Medicine (ESICM) and its American counterpart (SCCM) recently unveiled an updated definition of sepsis syndrome in adults (Sepsis-3) [1]. Previous diagnostic criteria have been revalued and retrospectively validated in several large patient databases. The consensus document, published in the journal JAMA, have been produced by a working group of 19 experts in critical care, infectious diseases, surgery and respiratory medicine.
The indication of tracheostomy includes (1) needed or long-term ventilator dependent due to acute respiratory failure (2) traumatic injury or neuromuscular disease requiring airway, or mechanical ventilator support or both(Cheung & Napolitano, 2014). However, we should also consider the patient's physiological needs, the patient's expectations, the characteristics of the disease, and the side effects and surgical risk posed by intubation vs. tracheostomy.
Sepsis is a clinical syndrome defined as a potentially fatal systemic response to an infection. It can affect patients across their life span. And it is usually caused by both gram positive and gram negative bacterial infections. Sepsis can develop from a systemic inflammatory response syndrome (SIRS) which is used to describe the early response to injury, which might be infective or non-infective, to a severe sepsis and septic shock if it was not recognized early and promptly, and effectively managed (2). Abnormalities in the inflammation, immune, coagulation, oxygen delivery, and utilization pathways play a role in organ dysfunction and death. Sepsis is a cause of considerable mortality, morbidity, health care utilizations and cost
Understanding vasopressor therapy in sepsis for being able to understand the lactate measurements the provider attains throughout the course of disease. In addition to a lactic acidosis, early sepsis is characterised by other aspects of poor perfusion such as cold acral parts, altered mental status, oliguria. Initial treatment as described by the Surviving Sepsis Campaign is early and empirical antibiotics along with a fluid challenge of 30ml/kg . We do this is order to maintain the MAP of 65mmHg. If this fails, then this is the standard time to add on a vasopressor. Levy et al in 2010 looked at the performance of sepsis therapy and found that as providers began to adopt the guidelines, that the plurality of patients responded to fluids and
Ninety-four NIRS VOT measurements were undertaken in 35 children accounting for 94 recordings. Eighty-two percent (29/35) of the children survived to intensive care unit discharge. Just over half the children recruited were admitted with sepsis (51.4\%). The PELOD2 score ranged from 7-16 (Figure 6.1). Demographics and clinical information are presented in table 6.2.\\