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1) Increased work of breathing with gas exchange function near normal 2) Inability to maintain normal ABGs with development of hypoxemia & acidosis as a result of CO2 retention

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What 2 things cause respiratory insufficiency?

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Apnea Respiratory Failure Respiratory Arrest

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Terminology

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Difficulty breathing, also causes psychological issues with inability to breathe

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What is respiratory distress?

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Temporary cessation of breathing, especially during sleep

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Apnea is?

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The end result from inadequate gas exchange by the respiratory system (arterial O2, CO2, or both O2 & CO2 can't be kept at normal levels) (*results in hypoxemia & hypercapnia*)

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Respiratory failure is?

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Normally increase in number from 20-70 million at birth to as many as 300-400 million at 2-8 yo

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Alveoli

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Type I alveolar cells Type II alveolar cells Type III alveolar cell macrophages

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Types of Alveolar Cells

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-Is made up of Lipoproteins -Provides alveolar stability -Adequate levels lead to better lung compliance & decrease work of breathing

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Surfactant

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Coat inner surfaces of alveoli

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What do lipoproteins do?

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-When ventilation & perfusion are matched, un-oxygenated blood from the venous system returns to the RT Ventricle through the Pulmonary Artery to the Lungs. -Carrying CO2.

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V/Q Ratio (*Normal Ventilation & Perfusion*)

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In the alveolar capillaries

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Where does gas exchange occur?

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-Pulmonary circulation is adequate but not enough oxygen is available to the alveoli for normal diffusion -A portion of the blood flowing through the pulmonary vessels does not become oxygenated

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Low V/Q Ratio

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Inadequate ventilation/shunt

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What is Low V/Q ratio called?

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(*Any obstruction of distal airways*) -PNA, Atelectasis, Tumor, & Mucus plug

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Disorders Resulting in Low V/Q Ratios?

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-Ventilation is normal, but alveolar perfusion is reduced or absent. -Capillaries narrow, indicating poor perfusion

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High V/Q Ratio

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(*A perfusion defect*) -Pulmonary embolism -Pulmonary infarction or any d/o that decreases CO

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What causes capillaries to narrow from high V/Q ratio?

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Inadequate perfusion/dead-space ventilation

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What is High V/Q ratio called?

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-Pulmonary emboli -Pulmonary infarct

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Disorders Resulting in High V/Q Ratios

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-Absence of ventilation & perfusion to the lung area -May help compensate for a V/Q imbalance by delivering blood flow to better ventilated lung areas.

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Silent Unit is?

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Inadequate ventilation & perfusion

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What is a Silent Unit referred to as?

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-Pneumothorax -Severe acute respiratory distress syndrome (ARDS)

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Disorders Resulting in Silent Unit

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-Lung volume & capacity -Compliance -Resistance to air flow -Diffusion & perfusion -Responsiveness of respiratory center in brain

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Effective gas exchange is dependent on?

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Chemoreceptors & integrity of respiratory centers in brain

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What does the responsiveness of the respiratory center in the brain consist of?

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-History (any co-morbidities: asthma, trauma, cardiac issues, meds) -Onset (sudden or gradual) -Duration -Precipitating factors -Aggravating factors -Alleviating factors -Risk factors -Signs & symptoms

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Patient assessment for respiratory failure/distress

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-Behavior changes -Fatigue/Weakness -Dyspnea -Tachypnea -Orthopnea -Pain -Cough -Sputum production -Edema of lower extremities -Lung sounds -Asymmetrical chest movement -Use of accessory muscles -Skin

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As a nurse, what would you assess in a patient with respiratory failure/distress?

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You're looking to see if the patient is cyanotic, looking for skin color changes.

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When assessing the patient for respiratory insufficiency, what are you looking for in the skin?

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-Retractions -Flaring of nares -Grunting

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Use of accessory muscles in pedi patients with respiratory distress/failure consists of?

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A drop in the oxygen that's carried in the blood (*oxygenation failure*)

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What is Hypoxemia?

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-A rise in arterial carbon dioxide levels (*Failure of ventilation causes inadequate CO2 removal from the lungs/Ventilatory Failure*)

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What is Hypercapnia?

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-Mood change (subtle mental status changes) -Headache -Respiratory depth & pattern change -Hypertension -Exertional dyspnea (DOE) -Anorexia

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What are the *early s/s* of Hypoxia?

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Hypoxia, & they are the cardinal s/s of hypoxia (restlessness, tachypnea, tachycardia, diaphoresis)

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RTTD are signs of what condition, & what are they?

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-Restlessness -Tachypnea -Tachycardia -Diaphoresis

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what are the *cardinal s/s* of Hypoxia?

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-HTN changing to hypotension -Vision changes -Change in LOC -Dyspnea -Bradypnea -Bradycardia -Cyanosis that's peripheral &/or central

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Signs of More Severe Hypoxia

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Respiratory failure

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Decompensation/changes of initial s/s of Hypoxia indicate what?

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Decrease dyspnea & promote gas exchange

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What is the goal for managing Hypoxia?

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-Oxygen therapy -Positioning -Pharmacologic therapy (give meds as ordered) -Energy conservation (frequent rest periods, pursed lip breathing?) -Nutritional therapy

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What interventions do you perform when trying to decrease dyspnea & promote gas exchange with Hypoxia?

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-Elevate HOB (*1st thing to do is this!*) -Administer O2 (*2nd thing to do is this!*) -Check VS & SpO2 (at least q ~15 min & prn) -Lung sounds -Do head to toe assessment -Notify MD & family of change in patient status -Obtain IV access

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What are the *immediate* nursing interventions for Hypoxia?

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-Constant reassessment (looking for trends of VS, alert MD if changes) -Monitor: VS, I&O, Fluid status, Nutritional status, labs, & responsiveness to treatment & care

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What are the *ongoing* nursing interventions for Hypoxia?

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Notify MD!

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With regards to ongoing nursing interventions with Hypoxia, what do you do if there's a change in the patient's status?

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-Pulse oximetry -ABGs -Chest X-ray -CBC with differential -Electrolytes -Bronchoscopy -Sputum studies -PFTs -V/Q scan -CT -CTA

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Diagnostic testing for respiratory distress/failure?

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-When oxygenation &/or ventilation is inadequate to meet the body's needs. -Not a disease but a condition resulting from other disease processes

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Acute Respiratory Failure is?

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Assess clinical assessment findings as well as the patient's baseline

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What's an important thing to consider with Acute Respiratory Failure?

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Inadequate gas exchange via: -Hypoxemia -Hypercapnia

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What does Acute Respiratory Failure result from?

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-PaO2 60%

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What is the PaO2 range in Hypoxemia?

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Increase in PaCO2 above normal (>45 mm Hg)

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What is the PaCO2 range in Hypercapnia?

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Causes: -Ventilation-perfusion (V/Q) mismatch -Diffusion limitation -Alveolar hypoventilation

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Hypoxemic Respiratory Failure (Etiology & Pathophysiology)

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COPD, Pneumonia, Asthma, Atelectasis, Pulmonary embolus

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V/Q Mismatch (hypoxemic respiratory failure) happens from?

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-Severe emphysema -Pulmonary fibrosis

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Diffusion Limitation (hypoxemic respiratory failure) happens from?

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-Restrictive lung disease -CNS disease -Chest wall dysfunction -Neuromuscular disease

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Alveolar Hypoventilation (hypoxemic respiratory failure) happens from?

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-Airways & alveoli -CNS -Neuromuscular conditions -Chest wall

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Hypercapnic Respiratory Failure (Etiology & Pathophysiology ) is caused from?

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Asthma, Emphysema, Chronic Bronchitis, Cystic Fibrosis

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What are the *airway & alveoli* causes for Hypercapnic?

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Drug overdose, Brainstem infarction, Spinal Cord injuries

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CNS causes for Hypercapnic Respiratory Failure?

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Muscular dystrophy, Multiple sclerosis

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Neuromuscular conditions that cause Hypercapnic Respiratory Failure?

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Fractures, Mechanical restriction, trauma

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Chest wall causes for Hypercapnic Respiratory Failure?

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The inability of the lungs to meet the oxygen demands of the tissues

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What is the major threat with Acute Respiratory Failure?

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-Metabolic acidosis & cell death -Decreased cardiac output -Impaired renal function -GI tissue ischemia

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Consequences of Hypoxemia & Hypoxia

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A build up of lactic acid

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Metabolic Acidosis & cell death cause what to happen?

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Shock results from cells shifting from aerobic to anaerobic metabolism

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A build up of lactic acid causes what to happen & how?

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-Has a sudden or gradual onset (can be from mins, to hours, to days) -Signs may be specific or nonspecific (low O2, slight mental status changes)

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Acute Respiratory Failure (*Clinical Manifestations*)

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Respiratory Failure

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When compensatory mechanisms fail, what results?

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The patient's VS (trends) & behavior

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What is extremely important to monitor in Acute Respiratory Failure?

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-Mental status changes -Restlessness, fatigue, HA -Tachycardia, tachypnea, & mild HTN -Dyspnea

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Early signs of respiratory failure

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-Cyanosis, diaphoresis, confusion, lethargy -Worsening tachycardia &/or tachypnea -Use of accessory muscles -Decreased breath sounds -*Finally respiratory arrest*

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Late signs of respiratory failure

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Respiratory Arrest

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Respiratory Failure results in?

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-History & physical assessment (any hx that could trigger ARF) -Diagnostic Studies (is specific to what's going on) +ABG analysis +Chest x-ray +CBC, sputum/blood cultures, electrolytes +ECG +V/Q lung scan +Pulmonary artery catheter

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Diagnostic Testing for Acute Respiratory Failure

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Severe cases of Acute Respiratory Failure

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A pulmonary artery catheter is used as a diagnostic tool in?

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-Treat the underlying cause -Restore adequate gas exchange -Oxygen therapy -Mobilization of secretions -Positive pressure ventilation (PPV)

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Acute Respiratory Failure *Treatment*

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Intubation & mechanical ventilation

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In Acute Respiratory Failure, what is used to help restore adequate gas exchange while the cause of failure is being corrected?

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*Restore adequate gas exchange*

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What is the main objective with treating Acute Respiratory Failure?

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-Delivery system needs to be tolerated by the patient -Maintain PaO2 at 55-60 mmHg or more & SaO2 at 90% or more at the lowest O2 concentration possible

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Acute Respiratory Failure: Oxygen Therapy

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-PaO2: greater than or equal to 55-60mmHg -SaO2: greater than or equal to 90% at the lowest O2 concentration possible

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What should the PaO2 & SaO2 be maintained at when treating Acute Respiratory Failure?

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-Hydration & humidification (*IV fluids!*) -Chest PT -Airway suctioning -Encourage effective coughing & positioning

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Acute Respiratory Failure: Mobilization of Secretions

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BIPAP & CPAP (*allows you to give respiratory support without invasive intubation*)

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Acute Respiratory Failure: Positive Pressure Ventilation (PPV)

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-Bronchodilators (albuterol) -Corticosteroids (solumedrol) -Diuretics -IV antibiotics -BZD/Narcotics (relax the pt & decrease anxiety & pain)

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Acute Respiratory Failure: Pharmacologic Therapy

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-Maintain protein & energy stores -Enteral or parenteral nutrition -Nutritional supplements

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Acute Respiratory Failure: Nutritional Therapy

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-Assist with intubation & maintaining mechanical ventilation -Assess respiratory status -Monitor: +Level of response +ABGs +Pulse oximetry (SpO2) (document if O2 goes up or stays down) +Vital signs +Assess respiratory system -Implement strategies to prevent complications -Assess patient's understanding of management strategies -Initiate some form of communication to enable patient to express needs to team -Address problems that led to respiratory failure -As improves, assess knowledge of underlying disorder -Provide teaching as appropriate -Continuous reassessment -Notify physician if unable to maintain adequate oxygenation -Position for comfort -Encourage relaxation, guided imagery, & diversion -Administer medications as ordered to promote gas exchange & maximize oxygenation -Address nutritional needs

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Acute Respiratory Failure: Nursing Management

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-Level of response -ABGs -Pulse oximetry (SpO2) (document if O2 goes up or stays down) -Vital signs -Assess respiratory system (lung sounds, symmetrical breathing, accessory use, pain?)

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What do you need to monitor with Acute Respiratory Failure?

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-Thorough H&P to ID at-risk patients -Early recognition of respiratory distress -*The biggest thing to do, *prevention**

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Prevention of Acute Respiratory Failure consists of?

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AMS, tachycardia, tachypnea, HTN

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What s/s would a nurse ID as early Acute Respiratory Failure?

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-Sudden, progressive form of acute respiratory failure -Alveolar capillary membrane becomes damaged & more permeable to intravascular fluid -Alveoli fill with fluid -150,000 causes annually -50% mortality rate

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Acute Respiratory Distress Syndrome (ARDS) is?

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Adult Respiratory Distress Syndrome, Noncardiogenic Pulmonary Edema & Shock Lung

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ARDS is formerly called what?

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-Severe dyspnea -Hypoxia -Decreased lung compliance -Diffuse pulmonary infiltrates -Pulmonary artery vasoconstriction

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With ARDS, alveoli no longer function resulting in?

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-Develops from a variety of direct or indirect lung injuries -*Most common cause is sepsis* -Exact cause for damage to alveolar-capillary membrane not known -Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory & immune systems -Inflammatory trigger initiates release of cellular & chemical mediators -Neutrophils are attracted & release mediators producing changes in lungs -↑ Pulmonary capillary membrane permeability -Destruction of elastin & collagen -Formation of pulmonary microemboli (*Results in Pulmonary artery vasoconstriction*)

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ARDS Pathophysiology & Etiology

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Pulmonary Disease & Sepsis (*sepsis is the most common cause*)

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What are examples of direct lung injuries resulting in ARDS?

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-Injury or exudative phase -Reparative or proliferative phase -Fibrotic phase

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ARDS has 3 phases

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-Occurs 1-7 days after direct lung injury or host insult -Neutrophils adhere to pulmonary microcirculation -Damage to vascular endothelium -↑ Capillary permeability -Fluid crosses into alveolar space -Intrapulmonary shunt develops as alveoli fill with fluid -Blood passing through cannot be oxygenated -Alveolar cells type 1 & 2 are damaged -Severe V/Q mismatch & shunting of pulmonary capillary blood result in hypoxemia -Lungs become less compliant (↑ Work of breathing, ↑ RR)

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ARDS (*Injury or Exudative Phase*)

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Unresponsive to increasing O2 concentration interventions because lungs are less compliant further increasing work of breathing & RRs.

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Severe V/Q Mismatch & shunting of pulmonary capillary blood resulting in *Hypoxemia* is what?

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Type I & II, causing surfactant dysfunction, leading to atelectasis

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What alveolar cell types are damaged in the Injury/Exudative Phase of ARDS?

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-Occurs 1-2 weeks after initial lung injury -Influx of neutrophils, monocytes, & lymphocytes -Lung becomes dense & fibrous -Lung compliance continues to ↓ -Hypoxemia worsens

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ARDS (*Reparative or Proliferative Phase (scar tissue forms) *)

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Scar tissue/widespread fibrosis forms if the phase continues, if phase is stopped, lesions/scarring resolves

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The Reparative/Proliferative Phase of ARDS causes what to develop in the lungs?

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-Occurs 2-3 weeks after initial lung injury -Lung is completely remodeled by sparsely collagenous & fibrous tissues -Decrease in lung compliance & area for gas exchange -Pulmonary HTN

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ARDS (*Fibrotic or Chronic/Late Phase*)

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Pulmonary vascular destruction & fibrosis (survival chances are poor for patients in this phase_

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The Fibrotic/Chronic-Late Phase of ARDS results from?

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-Dyspnea, tachypnea, cough, restlessness (*early general respiratory failure signs*) -Lung sounds: initially may be normal or fine, scattered crackles (as alveoli fill with fluid) -ABGs -Mild hypoxemia & respiratory alkalosis caused by hyperventilation (*increased RR*) -Chest x-ray needed (may be normal or show minimal scattered interstitial infiltrates) (*there's no specific test to dx respiratory hypoxemia/failure*)

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ARDS Early S/S

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-Symptoms worsen with progression of fluid accumulation & decreased lung compliance -Increased work of breathing -Hypoxemia -ARDS continues to progress -Chest x-ray shows whiteout or white lung because of consolidation & widespread infiltrates throughout lungs

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ARDS Late S/S

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Severe Respiratory Distress requiring ET intubation & PPV to maintain PaO2 at an acceptable level (>60mmHg)

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As ARDS progresses, what develops & what's needed?

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-Supplemental O2 (O2 sats will not improve the way they normally would in a person without ARDS) -Intubation & mechanical ventilation -Circulatory support -Adequate fluid volume -Nutritional support

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ARDS Treatment (*Supportive Therapy*)

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To identify ARDS & treat underlying condition & to support respiratory function

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What is the goal for ARDS treatment?

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-Correct hypoxemia -Initially, use NC or face mask with high-flow systems used to maximize O2 delivery -SpO2 is continuously monitored -Give lowest concentration that results in PaO2 >60mmHg -As ARDS progresses, intubation with mechanical ventilation to maintain the PaO2 at acceptable levels will be required

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ARDS Collaborative Treatment (Oxygenation)

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To correct hypoxemia, by giving the lowest concentration of O2 that results in PaO2 >60mmHg

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What is the primary goal with ARDS Oxygenation treatment?

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Give lowest concentration that results in PaO2 > 60 mmHg

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What should you set the oxygen concentration at with ARDS?

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Admin Positive End-Expiratory Pressure (PEEP)

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ARDS Collaborative Treatment (*Mechanical Ventilation*)

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Improves oxygenation & keeps alveoli open minimizing collapse, improving gas exchange, & reducing V/Q imbalance

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What does treatment of ARDS using PEEP do?

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PaO2 >60 mm Hg or SaO2 >90% at lowest possible FiO2

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What is the goal for mechanical ventilation with ARDS?

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This position shifts fluid from dorsal part of lungs & allows undamaged alveoli to be ventilated, thus improving oxygenation

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ARDS Collaborative Treatment (*Prone Position*)

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-Maintains perfusion/no decrease in blood flow to aerated areas -Improves V/Q match & decreases shunting, resulting in better oxygenation

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What does the prone position maintain & improve?

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The dorsal aspects of the lung regardless of position

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Where is perfusion greater in the lungs, with a patient that has ARDS?

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The dorsal areas

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Where is lung damage & edema greatest in patients with ARDS?

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Refractory hypoxemia that's not responding to other therapies

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What is the prone position reserved for in patients that have ARDS?

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-Hemodynamic monitoring -Treatment of systemic hypotension, hypovolemia via PEEP ventilation -Inotropic or vasopressor agents used to increase BP

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ARDS Collaborative Treatment (*Maintenance of cardiac output & tissue perfusion*)

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Fluid status

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What do you monitor with admin of inotropic & vasopressor agents?

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Central Venous or Pulmonary Artery Catheter used to monitor CO, BP, & sample blood for ABG tests

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Hemodynamic monitoring is done via what devices & are they used for?

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-Enteral or parenteral feedings are started (*early enteral feedings if tolerated*) -Monitor daily weight, I&O

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ARDS Collaborative Treatment (*Maintenance of nutrition/fluid balance*)

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1) Hospital-acquired pneumonia 2) Barotrauma 3) Volu-pressure trauma 4) Stress ulcers 5) Renal failure

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ARDS Treatment Complications

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Decreased renal tissue oxygenation

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Renal Failure with ARDS occurs from?

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Support kidney function, monitor trends, short term dialysis

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What nursing interventions are done with renal failure resulting from ARDS?

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-Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation

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Stress Ulcers with ARDS are caused from?

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-Correction of predisposing conditions -Prophylactic anti-ulcer agents (*PPIs, H2 blockers for pts who can't tolerate PPIs*) -Early initiation of enteral nutrition (*to increase GI motility to prevent ulcer formation*)

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What nursing interventions do you perform with GI stress ulcers resulting from mechanical ventilation?

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Rupture of over distended alveoli during mechanical ventilation (*monitor ventilator to prevent this from happening*)

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What is barotrauma?

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-Occurs when large tidal volumes are used to ventilate noncompliant lungs. -Alveoli fractures & allows movement of fluids & proteins into alveolar spaces

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What is Volu-pressure trauma?

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Fluid that sits in lungs

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What is Hospital-Acquired PNA?

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Strict aseptic techniques used at all times

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What strategies are used to prevent Ventilator-Associated PNA?

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-Patient centered care -Continuous monitoring -Respiratory therapy -Implementing medical plan of care -Positioning (turn q2h) -Explain procedures & plan of care (include teaching this to families) -Encourage rest -Bronchodilators, corticosteroids, BBs, antibiotics (as stated in earlier slide)

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ARDS Overall Nursing Management

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-Used for patients with difficulty breathing or that need assistance maintaining their airway or that may require mechanical ventilation 1) Endotracheal (ET) intubation (via mouth or nose past larynx) 2) Tracheostomy (via stoma in neck) 3) Tracheotomy (surgical incision in neck)?

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What are artificial airways used for & what types are there?

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When there's a placement of a tube into the trachea to bypass the upper airway & laryngeal structures (*maintain patent airway at all times!)

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What is considered an artificial airway?

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-Upper airway obstruction (tumor/cancer dx) -Apnea -Inability to protect airway (drug overdose) -Ineffective clearance of secretions (PNA & non-productive cough) -Respiratory distress

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Indications for artificial airways

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(*Procedure of choice/best procedure*) -Airway can be secured rapidly -Larger diameter tube can be used -Decreases work of breathing (WOB) -Easier to remove secretions & perform bronchoscopy -Explain associated risks

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Oral ET Intubation

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Cervical spine injury, dislodging of teeth, risk of infection

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What are the associated risks with oral ET intubation?

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-ET tube placed blindly -Used when oral intubation is not possible

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Nasal ET intubation

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-Requires informed consent/pt teaching -*elective intubation: for COPD* -*non-elective: respiratory distress/failure* -Equipment: +Self-inflating bag-valve-mask (BVM) attached to oxygen (AMBU bag needed to give breaths to patient) +Suctioning equipment available +IV access (especially if sedation is needed prior to intubation)

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ET Intubation Procedure

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-*Pre-oxygenate using BVM with 100% O2 for 3-5 minutes* -Limit each intubation attempt to <30 seconds -Ventilate patient between successive attempts using BVM with 100% O2 -(*Priority: maintaining airway over IV access!*)

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ET Intubation Procedure (*before procedure*)

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-Rapid, concurrent admin of a paralytic agent & sedative agent during emergency airway management -Has increased risks of aspiration, combativeness, & injury to patient

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Rapid sequence intubation (RSI) in a pt whose awake (*ET Intubation*)

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Comatose or cardiac arrest patients

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RSI is contraindicated in which type of patients?

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-Inflate cuff & confirm placement of ET tube while manually ventilating patient with 100% O2 -End-tidal CO2 detector measures amount of exhaled CO2 from lungs +Place it between BVM & ET tube +Observe for a color change or a number indicating CO2 +If no CO2 is detected, ET tube is in esophagus & needs to be re-positioned -Record & document position of tube at the lip of the pt in cm to observe for migration of tube -Auscultate lung for bilateral breath sounds -Observe chest for symmetric chest wall movement -Obtain portable chest x-ray to confirm tube location -Connect ET tube to either humidified air, O2, or mechanical ventilator -Obtain ABGs within 25 minutes after intubation to determine oxygenation & ventilation status -Continuously monitor pulse oximetry as estimate of arterial oxygenation

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Following ET intubation

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Record & document position of tube at the lip of the patient in *cm* to observe for migration of the tube

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What is very important to do with ET intubation placement?

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CO2

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End-tidal CO2 detector shows color change or number indicating what?

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Pulse oximetry

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With ET intubation, what do you continuously monitor as an estimate of arterial oxygenation?

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Within 25 minutes *after* intubation to determine oxygenation & ventilation status

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When do you obtain ABGs with ET intubation?

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Obtain a portable chest x-ray

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How do you confirm proper ET tube placement?

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No CO2 is detected, meaning the ET tube is in the esophagus & will need to be repositioned

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If the End-Tidal CO2 detector doesn't show color or number change, what does this indicate?

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-Monitor ET tube every 2-4 hours -Confirm exit mark on ET tube remains constant -Observe for symmetric chest wall movement -Auscultate to confirm bilateral breath sounds

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Maintaining correct tube placement

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-Stay with patient & maintain airway -Support ventilation -Secure help immediately -If necessary, ventilate with BVM & 100% O2/Incorrect ET tube placement is an emergency!

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What do you do if the ET tube is placed incorrectly?

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-Cuff is an inflatable, pliable sleeve encircling outer wall of ET tube -Stabilizes & seals ET tube within trachea -Prevents escape of ventilating gases -Cuff can cause tracheal damage

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Maintaining proper ET cuff inflation

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-Cuff pressure is measured & recorded after intubation & on a routine basis (often q8H usually by respiratory therapy) -Normal arterial tracheal perfusion is estimated at 30 mm Hg -Cuff pressure should be maintained at 20-25 mm Hg

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Measures to avoid tracheal damage with ET intubation

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30mmHg

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What is the normal arterial tracheal perfusion rate with ET intubation?

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20-25mmHg

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What is the normal cuff pressure maintained at with ET intubation?

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-Assessment -ABGs -SpO2 -Clinical signs of hypoxemia -Clinical signs of respiratory distress -*Remember to monitor trends*

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Monitoring oxygenation & ventilation with ET intubation

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Assess patient routinely to determine need for suctioning, but do not suction routinely

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Maintaining tube patency in an artificial airway

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-Visible secretions in ET tube -Sudden onset of respiratory distress -Increased RR, adventitious lung sounds, decreased SaO2, accessory muscle use etc.. -Suspected aspiration of secretions

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What are indications for suctioning the artificial airway?

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*Used for mechanically ventilated patients* -Enclosed in a plastic sleeve connected directly to patient-ventilator circuit (Less risk of infection) -CST maintains oxygenation & ventilation & decreases exposure to secretions

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Closed-suction technique (CST) for artificial airway

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-Hypoxemia -Bronchospasm -Increased intracranial pressure -Dysrhythmias (especially if hypoxemia during suction) -HTN/hypotension -Mucosal damage, bleeding -Infection (highest risk)

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What are potential complications associated with suctioning with artificial airways?

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Infection

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What is the highest complication associated with suctioning an airway?

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-Assess patient before, during, & after suctioning -If patient does not tolerate suctioning: +Stop procedure & manually hyperventilate with 100% oxygen +If performing CST, hyper oxygenate (ventilator setting...maintains closed system between ET tube & ventilator, decreased risk of infection)

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How do you *prevent* suctioning complications with artificial airways?

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-Hyper oxygenate before & after each suctioning pass -Limit each suctioning pass to ≤10 seconds -Assess trends in SpO2 throughout suctioning -Limit suction pressures to <120 mm Hg -Avoid overly vigorous catheter insertion

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How do you *limit* suctioning complications with artificial airways?

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-Provide adequate hydration & supplemental humidification -No installation of NS into ET tube -Treatment of infections with antibiotics -Provide postural drainage, percussion, & turn patient q2h

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How do you manage thick secretions with artificial airways?

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-Mouth care -Suction oral/pharyngeal cavity every 2-4 hours & PRN

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Providing oral care & maintaining skin integrity with artificial airways

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-*Anxiety d/t inability to communicate requires emotional support (letter boards, paper/pencil, electronic methods of communication)* -Physical discomfort associated with ET intubation & mechanical ventilation necessitates sedation & analgesia -Consider alternative therapies to complement drug therapy (*relaxation & pain control*)

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Providing comfort & communication with artificial airways

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-Ensure adequate securement of ET tube -Support ET tube during repositioning & procedures -Use soft wrist restraints -Provide sedation & analgesia as ordered

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Preventing unplanned extubation with artificial airways

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-Stay with patient -Call for help -Manually ventilate patient with 100% O2 (ambu bag) -Provide psychologic support

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What do you do if an unexpected extubation occurs?

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-Improper cuff inflation -Patient positioning

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What are the risk factors for aspiration with artificial airways?

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-Proper patient positioning -Proper cuff inflation -Suction oral cavity frequently -Keep HOB elevated 30-45 degrees

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How do you prevent aspiration with artificial airways?

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Surgical incision into the trachea to establish an airway

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What is a Tracheotomy?

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Stoma that results from tracheotomy

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What is a tracheostomy?

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-Bypass upper airway obstruction -Facilitate removal of secretions -Long-term mechanical ventilation -Permit oral intake & speech in patients who require long-term mechanical ventilation

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Tracheostomy Indications

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-Less risk of long-term damage to airway -Increased comfort -Patient can eat. -Increased mobility because tube is more secure

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Tracheostomy Advantages

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-Suctioning the airway to remove secretions -Cleaning around stoma (*monitor skin integrity around the stoma*) -Changing ties (*have someone else helping secure teach while you're cleaning & changing it*) -Providing inner cannula care -Tube with inflated cuff is used for risk of aspiration or in mechanical ventilation. -Inflate cuff with minimum volume required to create an airway seal. -When patent, can protect against aspiration & does not require mechanical ventilation, a cuff less tube is used.

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Tracheostomy care involves?

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-Tube of equal or smaller size kept at bedside for emergency reinsertion (*have emergency trach tray at bedside at all times even if they already have a trach inserted*) -Tapes not changed for at least 24 hours after insertion

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What are the precautions for tracheostomy tube placement?

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Process by which fraction inspired oxygen (FIO2) at ≥21% (room air) is moved in & out of lungs by a mechanical ventilator

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What is mechanical ventilation?

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-Apnea or impending inability to breathe -Acute respiratory failure -Severe hypoxia -Respiratory muscle fatigue

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What are indications for mechanical ventilation?

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-Regulate rate, depth, & other characteristics of ventilation -Are based on patient's status (ABGs, body weight, LOC, muscle strength) -Ventilator is tuned to match patient's ventilatory pattern/status

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Settings of mechanical ventilators

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Negative Pressure (NPV) & Positive Pressure Ventilation (PPV)

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What are the different types of mechanical ventilators?

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-Uses chambers that encase chest or body & surround it with intermittent negative pressure -It's a noninvasive ventilation that does not require an artificial airway (like an iron lung?)

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Negative Pressure Ventilation (NPV)

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Acutely ill patients

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NVP isn't used extensively for what type of patients?

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-Pushes air into lungs under positive pressure during inspiration -Expiration occurs passively -PPV has many different settings (which can cause complications?)

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Positive pressure ventilation (PPV)

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Acutely ill patients

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What is PPV used primarily for what type of patients?

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*PPV affects circulation due increased intra-thoracic pressure causing:* -↑ Intrathoracic pressure compresses thoracic vessels -↓ Venous return to heart, ↓ left ventricular end- diastolic volume (preload), ↓ cardiac output -Hypotension because of lack of blood flow return

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What are complications of PPV (*cardiovascular effects)?

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1) Barotrauma 2) Pneumo-mediastinum 3) Volu-trauma 4) Ventilator-associated pneumonia

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What are complications of PPV (*pulmonary effects*)

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-Is when air can escape into pleural space from alveoli & become trapped causing pneumothorax -Chest tubes may be placed prophylactically for barotrauma

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What is Baro-trauma?

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-Begins with rupture of alveoli into lung interstitium -Progressive air movement into mediastinum & subcutaneous neck tissue & is commonly followed by pneumothorax

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What is Pneuma-Mediastinum?

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fever &/or elevated WBCs, crackles or rhonchi on auscultation, & pulmonary infiltrates on chest x-ray

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What are the clinical s/s of VAP?

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-Pneumonia that occurs 48 hours or more after ET intubation -Clinical evidence s/s: fever &/or elevated WBCs, crackles or rhonchi on auscultation, & pulmonary infiltrates on chest x-ray

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What is Ventilator-Associated PNA (VAP)?

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(*lung fracture*) -Lung injury that occurs when large tidal volumes are used to ventilate noncompliant lungs -Results in alveolar fractures & movement of fluids & proteins into alveolar spaces

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What is Volu-trauma?

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-Hypoventilation -Hyperventilation

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Overall complications of PPV

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ABGs

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What is the best diagnostic test to diagnose respiratory failure?

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-HOB elevation at least 30-45 degrees unless medically contraindicated -No routine changes of ventilator circuit tubing -Drain condensation that collects in ventilator tubing

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What are the guidelines to prevent VAP?

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-Risk for stress ulcers & GI bleeding -↑ Risk of translocation of GI bacteria -Gastric & bowel dilation as a result of gas accumulation & constipation

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Complications of PPV (*GI effects*)

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*Via peptic ulcer prophylaxis* Histamine (H2)-receptor blockers, proton pump inhibitors, tube feedings, & NG tube for decompression

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How do you treat stress ulcers & GI bleeding from PPV?

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(*Early tube feeding is important*) -If patient is likely to be without food for 3-5 days, a nutritional program should be initiated -*Enteral feeding via a small-bore feeding tube is the preferred method to meet caloric needs of ventilated patients*

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Nutritional therapy for mechanical ventilation

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-Delay weaning -Decrease resistance to infection -Decrease speed of recovery

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What can inadequate nutrition do to someone who is on mechanical ventilation?

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(*Maintain muscle strength & prevent problems associated with immobility*) -Perform passive & active exercises -Prevention of contractures, pressure ulcers, & foot drop

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Complications of PPV (*Musculoskeletal effects*)

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PPV

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Contractures, pressure ulcers, & foot drop are musculoskeletal complications of what?

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-Physical & emotional stress due to inability to speak, eat, move, or breathe normally -Pain, fear, & anxiety related to tubes/machines -*Ordinary ADLs are complicated or impossible* -Involve patients in decision making -Encourage hope & build trusting relationships with patient & family -Provide sedation &/or analgesia to facilitate optimal ventilation -If necessary, provide paralysis to achieve more effective synchrony with ventilator & increase oxygenation -Paralyzed patient can hear, see, think, feel

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Mechanical Ventilation (*Psychological Needs*)

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-Pause alarms during suctioning/removal from ventilator -Reactivate alarms before leaving -If machine malfunctions: +Disconnect patient from ventilator +Manually ventilate with 100% O2

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Machine disconnection or malfunction interventions

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Between the tracheal tube & adapter

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What is the most common site for disconnection of machine disconnection/malfunction?

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-Process differs for short-term vs long-term ventilated patients -Requires a team approach -Occurs in 3 phases: +Pre-weaning phase +Weaning process +Outcome phase

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Mechanical Ventilation: Weaning & Extubation

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The process of decreasing ventilator support & resuming spontaneous breathing

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What is weaning & extubation?

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1) *Determine the patient's ability to breathe spontaneously via*: -Assess muscle strength & endurance -Auscultate lungs -Assess chest x-ray 2) *Assess non-respiratory factors preventing weaning/extubation* -Assessment of neurologic status, hemodynamics, fluid & electrolytes/acid-base balance, nutrition, & hemoglobin

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Pre-weaning/Assessment Phase of weaning/extubation

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(*Awakening/Breathing Coordination, Delirium Monitoring/Management, & Early Mobility bundle*) -*SBT* (spontaneous breathing trial) should be at least 30 minutes but not >120 minutes -*SAT* (spontaneous awakening trial) done by stopping all sedatives -Use of weaning protocol decreases ventilator days -Important to rest between weaning trials -Provide explanations regarding weaning & ongoing psychologic support -Comfortable position (sitting or semi-recumbent) -Obtain baseline assessment +Vital signs +Respiratory assessment -Monitor for signs & symptoms +Tachypnea, dyspnea, tachycardia, dysrhythmias +Sustained desaturation [SpO2 <90%] +HTN or hypotension, diaphoresis +Agitation, anxiety or changes in mentation

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Weaning Process Phase of weaning/extubation

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-Weaning stops & patient is extubated --OR-- -Weaning is stopped because no further progress is made

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Weaning Outcome Phase of weaning/extubation

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-Hyper-oxygenate & suction -Loosen ET tapes or holder -Deflate cuff & remove tube at peak of deep inspiration -Encourage patient to deep breath & cough -Supplemental O2 -*Careful monitoring after extubation*

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How to extubate with mechanical ventilation

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