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Background: Mechanical ventilation is an important tool in the management of respiratory failure in the critically ill patient. In patients with type 2 diabetes, progressive beta cell failure leads to near universal need for insulin replacement therapy. When compared specifically to basal-bolus insulin, the combination of basal insulin and GLP-1 agonists led to a greater reduction in A1c, although the proportion of patients achieving A1c goals was similar. Twice-daily analog premixed insulin (biphasic insulin aspart 30) was shown superior to once-daily basal insulin (glargine) in the INITIATE Trial. Most patients with type 2 diabetes evenutally require insulin to manage hyperglycemia and insulin intensification is the norm as beta cell function continues to decline. Edentulous patients are generally easier to intubate as there is more room within the mouth for the laryngoscope and manoeuvring the endotracheal tube. Cardiac DrugsAtorvastatin: an HMG-CoA Reductase inhibitor ("Statin") prescribed to lower cholesterol and other lipids. Urological DrugsDoxazocin: An alpha 1a selective alpha blocker used to treat hypertension as well as urinary retention secondary to benign prostatic hyperplasia. Although mechanical ventilation can be a life-saving intervention, it is also known to carry several side-effects and risks.
Joseph's Regional Medical Center, 703 Main Street, Paterson, New Jersey USASource of Support: Pulmonary division fund, St. Mechanical ventilation is required for the management of respiratory failure resulting from various clinical conditions including acute respiratory distress syndrome (ARDS), pneumonia, sepsis, chronic obstructive pulmonary disease (COPD), and asthma. Albumin administration improves organ function in critically ill hypoalbuminemic patients: A prospective, randomized, controlled, pilot study. Flexible fiberoptic bronchoscopy in the critically ill patient: Methodology and indications. Assessment of routine chest roentgenograms and the physical examination to confirm endotracheal tube position.
Relationship between ventilatory settings and barotrauma in the acute respiratory distress syndrome. Continuous aspiration of subglottic secretions in preventing ventilator-associated pneumonia. Relationship of microbiologic diagnostic criteria to morbidity and mortality in patients with ventilator-associated pneumonia. Efficacy of an expanded ventilator bundle for the reduction of ventilator-associated pneumonia in the medical intensive care unit. Prevalence of acute pulmonary embolism among patients in a general hospital and at autopsy. Pulmonary embolism in intensive care unit: Predictive factors, clinical manifestations and outcome. Oral antidiabetic agents may stall insulin initiation, but the signs that a patient is ready are clear. Atrial fibrillation is a prothrombotic condition as the atria are not contracting properly. Although mechanical ventilation can be a lifesaving intervention, it is also known to carry several side-effects and risks. Airway pressures and early barotrauma in patients with acute lung injury and acute respiratory distress syndrome.
Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. Its mode of action is incompletely understood but it decreases conduction of electrical impulses through the AV node and increases vagal activity via its central action on the central nervous system.
However, while on mechanical ventilation, patients frequently experience hypoxic events resulting from various causes, which need to be properly evaluated and treated.
Various complications of mechanical ventilation include hypotension, respiratory distress ("fighting the ventilator"), with consequent increase in airway pressure, ARDS, ventilator-associated pneumonia (VAP), and complications related to endotracheal tubes. Materials and Methods: Data were obtained by prospectively reviewing all intensive care admissions during the period from March 2009 to March 2010 at a 651-bed urban medical center. Results: During the study period, 955 patients required mechanical ventilation from which 79 developed acute hypoxia. The causes of acute hypoxia in decreasing order of occurrences were pulmonary edema, atelectasis, pneumothorax, pneumonia, ARDS, endotracheal tube malfunction, airway bleeding, and pulmonary embolism.


This study examines the causes and frequency of various hypoxic events while on mechanical ventilation. Evaluation of the endotracheal tube can immediately reveal dislodgement, bleeding, and secretions. In this study, all patients admitted to the medical intensive care unit and mechanically ventilated for any cause of respiratory failure were considered for inclusion. Patients who could not be stabilized with adequate oxygenation regardless of the mode of ventilation and inspired fraction of oxygen delivered by the ventilator were not considered for inclusion in this study.
Only stable patients on mechanical ventilation that developed acute hypoxia, not as a result of the underlying cause of respiratory failure, were further studied and included.
If on evaluation of the patient the cause of the hypoxia was considered to be secondary to the underlying cause of respiratory failure than the patient would be excluded.The three most common causes of respiratory failure among the patients developing acute hypoxic events were septic shock (22%), cardiopulmonary arrest (18%), and pneumonia (13%). The remaining causes included COPD exacerbation (8%), postoperative respiratory failure (6%), stroke (5%), myocardial infarction (5%), status epilepticus (4%), drug overdose (4%), ARDS (4%), congestive heart failure exacerbation (3%), gastrointestinal bleeding (3%), pulmonary edema (3%), aspiration pneumonia (1%), ischemic bowel (1%), pulmonary embolism (PE) (1%), and trauma (1%) in decreasing order of occurrence [Table 1].
Patients presenting with signs of systemic inflammatory response syndrome, high suspicion or evidence of infection, end organ dysfunction, and refractory hypotension were considered to have septic shock. Prior to the occurrence of each hypoxic event, all the patients had been stable with adequate oxygenation. The patients developing hypoxic events were clinically evaluated and a chest X-ray and other relevant clinical test were conducted to determine the cause of hypoxic event while on mechanical ventilation. There was a total of 79 patients (8%) who developed acute hypoxia while on mechanical ventilation. Common causes of atelectasis among the study patients were mucous plugging (20%), poor suctioning (6%), and right main-stem intubation (2%) leading to right upper lobe collapse or left lung collapse. In the pneumothorax group, five patients (6%) had COPD, three (5%) had ARDS, and two (3%) had bronchial asthma.The remaining causes of acute hypoxia included pneumonia (10%), ARDS (9%), endotracheal tube malfunction (6%), airway bleeding (3%), and PE (3%) in decreasing order of occurrence [Table 2].
While a patient is mechanically ventilated, the cause of a hypoxic event can be due to the ventilator and equipment problems, progression of the pre-existing disease that resulted in respiratory failure, and development of a new disease process or a side-effect from an intervention.
We will explore in detail the most common causes of acute hypoxia in patients on mechanical ventilation.Pulmonary edemaPulmonary edema was the leading cause of acute hypoxic events in our patients. The average ejection fraction of the patients developing pulmonary edema in our patients was 37% (ranging between 20% and 55%).
Pulmonary edema is a common complication of excessive fluid resuscitation in mechanically ventilated patients leading to an increase in intravascular volume and increased left ventricular end-diastolic pressure. Pulmonary edema develops as a result of excess fluid filtration through the capillaries into the lungs. The accumulation of this fluid is dependent on various factors including vascular permeability, hydrostatic, and oncotic pressures. Most of the study patients had multiple comorbidities including advanced age, poor nutritional status resulting in hypoalbuminemia, and a history of structural and functional heart disease. Typically, these cases of pulmonary edema responded to fluid restriction and forced diuresis with loop diuretics. In hypoalbuminemic patients, the use of intravenous albumin aids in preventing third spacing of fluids. Immobility in critically ill patient along with impaired mucociliary clearance, ineffective cough leading to mucous accumulation are risk factors for atelectasis. Atelectasis is a common cause of hypoxic events and can further lead to complications including pneumonia. Also commonly observed is left lower lobe collapse or entire left lung collapse with right main-stem intubations.Five patients (6%) developed atelectasis from poor suctioning. In addition, four patients were found to have left lower lobe atelectasis that was likely the result of poor suctioning of the left main stem bronchus due to its natural angulation.
Proper suctioning technique requires a catheter that is half the diameter of the endotracheal tube inserted at the level of the carina with minimal pressure suctioning started only after retraction 1-2 cm away from the carina for a maximum duration of 10 s. Pneumothorax results from pulmonary barotrauma leading to alveolar rupture and subsequent air leak into the pleural space due to positive pressure ventilation. In this study, nearly half of the patients who developed pneumothorax had underlying lung disease including COPD and asthma.
Average peak pressures in patients with underlying lung disease were between 30 and 35 cm H 2 O and in patients with ARDS were 40 cm H 2 O. As mentioned, controlling PIP is one of the most important steps in preventing iatrogenic barotrauma.


There are two varieties of VAP based on the time of onset: early onset and late onset with the former diagnosed during the first 3-4 days of intubation and the latter occurring after 4 days of intubation. Late onset pneumonia results from gram negative bacteria including Pseudomonas aeruginosa and Acinetobacter.
Repetitive suctioning of the airway to remove secretions leads to inflammation and eventually vascular erosion and bleeding.
Stress-induced ultrastructural changes that disrupt the capillary-alveolar endothelium can also result in pulmonary edema and alveolar hemorrhage.
Bronchoscopic examination is crucial in the workup of patients with endobronchial bleeding.Endotracheal tube malfunctionFive patients (6%) in our study developed hypoxemia due to endotracheal tube malfunction.
Cough reflex of these patients in respiratory distress led to the displacement of the endotracheal tube which led to hypoxemia requiring re-intubation. Several methods of stabilizing the endotracheal tube exist which include commercial tube holders, adhesive tape, cotton, and twill. Patients who experience sudden hypoxemia with the presence of tachycardia or hypotension may have undetected PE.
All of our patients had normal cardiac ejection fraction and central venous pressures ≤ 12. Various causes of acute hypoxic events included pulmonary edema (29%), atelectasis (28%), pneumothorax (13%), pneumonia (10%), ARDS (9%), endotracheal tube malfunction (6%), PE (3%), and bleeding (3%) in decreasing order of frequency.Pulmonary edema is the most common cause of hypoxia as a result of fluid overload either due to over-hydration, renal disease, or low ejection fraction. Physical examination findings, chest radiographs, and echocardiograms are useful in confirming the diagnosis.
Treatment with diuretics or hemodialysis, if needed, can reverse hypoxia.Atelectasis commonly results from mucous plugging as a result of poor suctioning or right main-stem intubation. A prompt chest radiograph can confirm right main-stem intubation requiring tube readjustment to reverse atelectasis.
Proper suctioning of the mucous plugs causing atelectasis can similarly relieve the endobronchial obstruction and relieve hypoxia.
Proper suctioning technique with removal of secretions can prevent eventual plugging and atelectasis. Bronchoscopy plays a significant role in the removal of retained secretions to alleviate hypoxia due to atelectasis.Pneumothorax causing hypoxia may occur in patients with COPD, asthma, ARDS, and high PEEP and after certain invasive pulmonary procedures or placement of a central line.
Early recognition of a pneumothorax, typically on a chest radiograph, can help avoid tension pneumothorax and eventual cardiopulmonary arrest.Ventilator-associated pneumonias both either early or late onset can lead to hypoxia.
Prevention of VAP may be successfully achieved with the use of strategic ventilator bundles which include various infection control techniques.Worsening hypoxia may result from the development or progression to ARDS.
In our study, most cases of ARDS resulted from pneumonia.Endotracheal tube malfunction commonly occurs as a result of tube displacement due to uncontrolled cough or struggle by the patients under inadequate sedation. The use of proper tube stabilizers and anchoring techniques along with adequate sedation can help minimize tube dislodgements.
Ruptured cuff or over-distended cuff with tracheal ballooning due to tracheomalacia requires replacement of the tube.PE is an infrequent cause of a hypoxic event in our study.
The use of thromboembolism prophylaxis in our patients may explain the low occurrence of PE and supports its use in all ventilated patients.
Lack of predictive models in the ICU can cause many cases to go undiagnosed with serious consequences. Clinical suspicion for PE must be considered in patients who suddenly develop hypoxia with otherwise unexplained tachycardia or hypotension.Bleeding in the airway, although an alarming sign, is usually the result of suction trauma.
A systematic approach to identify the cause of bleeding is essential.Appropriate evaluation of all hypoxic events must begin at the bedside. A step-by-step approach must include a thorough physical examination, in general, and chest examination, in particular, with special attention to auscultatory findings.
When presented with a hypoxic event, the physician must consider all the above outlined causes. Instead of simply increasing the fraction of oxygen in the inspired air to overcome hypoxia, a concerted effort in appropriate problem solving can reduce the likelihood of an incorrect diagnosis and inappropriate management response.



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