Chapter 39 Respiratory Failure Keypoints Respiratory failure is not a disease but a consequence of severe respiratory dysfunction Its defined

Its defined by ABG values: (these values generally indicate respiratory failure) Arterial O2 Level (PaO2) < 50 60 mmHg Arterial Carbon Dioxide level (PaCO2) > 50 mmHg

Clients w/ COPD would be alert and functional w/ above values oppose to an otherwise healthy adult. COPD clients resp. failure is indicated by an acute drop in blood O2 levels along w/ increased PaCO2 Resp failure results from Impaired gas exchange Inadequate alveolar ventilation (hypoventilation), Significant ventilation-perfusion mismatch

Cause of resp. failure: COPD, lung diseases, injury, neuromuscular disorders, inhalation trauma

Pathophysiology of Respiratory Failure Primary hypoxemia or combination of hypoxemia and hypercapnia In hypoxemic resp. failure, PaO2 is significantly reduced, PaCO2 is normal or low due to stimulation of respiratory center or tachypnea cause a drop in arterial oxygen levels (PaO2), rising more rapidly than CO2 Metabolic acidosis results from hypoxia

Impaired diffusion across the alveolar-capillary membrane and a ventilation-perfusion mismatch can

Increased breathing leads to respiratory muscle fatigue and hypoventilation (less air) Hypoventilation causes carbon dioxide retention CO2 increase in the blood leads to respiratory acidosis Hypoxemia w/o a corresponding rise in CO2 levels indicates oxygenation failure Hypoxemia w/ hypercapnia leads to lung hypoventilation

Manifestations Caused by hypoxemia and hypercapnia Hypoxemia causes dypsnea and neuro symptoms: restlessness, impaired judgement and motor function Tachycardia and hypertension develops as cardiac output increases to perfuse tissues Cyanosis is present Dysrhythmias, hypotension & decreased cardiac output may developed as hypoxemia progresses Hypercapnia depresses CNS function and cause vasodilation Dypsnea and headaches are early sign decreased LOC. Periperheral and conjuntival vasodilation, papilledema (optic disk swelling), neuromuscular irritability, Respiratory center depression, slowing respirations and Dyspnea

Administering O2 w/o ventilation support may reduce drive to breathe causing respiratory arrest

Types of Dysfunction Impaired ventilation Airway Obstruction Respiratory Disease Neuro causes Chest Wall Injury Impaired Diffusion Alveolar Disorders Pulmonary Edema Ventilation-Perfusion Mismatch

Examples Laryngospasms, foreign body aspiration, airway edema Asthma, COPD Spinal cord injury, polio, Guillaine-Barre, drug overdose, stroke Flail chest, pneumonthorax

Pnuemonia, pneumonitis, COPD Heart Failure, ARDS, near drowning Pulmonary embolism

Ventilation-Perfusion Mismatch Impaired Gas Diffusion Hypoventilation Hypoxemia Respiratory Failure Manifestations: Dyspnea, tachypnea Cyanosis Restlessness, apprehension Manifestations: Interdisciplinary Care Diagnosis

Hypoventilation Hypercapnia

Dyspnea leads to respiratory depression Headache Papilledema

Confusion, impaired judgement Tachycardia, dysrhythmias Hypertension Metabolic acidosis

Tachycardia, hypertension Drowsiness, coma Heart failure Systemic vasodilatation Respiratory acidosis

Exhaled carbon dioxide and ABGs used to diagnose and monitor respiratory failure ETco2 evaluates alveolar ventilation, Normal value is 35 to 45 mmHg, Elevated when ventilation is adequate Decreased when pulmonary perfusion is impaired

ABGs used to evaluate alveolar ventilation and gas exchange

Hypoxemic respiratory PaCo2 maybe normal (38- 42 mmHg) or low due to Tachypnea Respiratory failure rt hypoventilation PaCo2 is elevated > 50 mmHg

Medications Beta-adrenergic (sympathomimetic) or anticholinergic medications Methylxanthine bronchodilators given via intravenously Corticosteroids

Sedation and analgesia via benzodiazepines, midolozams (Versed) Intravenous morphines or fentanyl Neuro blocking agent to induce paralysis and suppress the ability to breathe

Oxygen Therapy Goal is to achieve O2 saturation > 90% PaO2 > 60 mmHg 1 to 3 Liter of O2 per nasal cannula

28% O2 via Venturi mask in advanced COPD

O2 concentration 40 60% when diffusion impairment (pneumonia, ARDS) for short periods High O2 concentration leads to toxicity: impairs surfactant production, reduce lung inflation, ARDS, atelectasis Resp. failure caused by hypoventilation need a CPAP

CPAP increases lung volume, improved ventilation, ventilation-perfusion relationships

Airway Management Obstruction of upper airway or positive-pressure mechanical is necessary an endotracheal tube is inserted To maintain positive-pressure ventilation the tube is cuffed w/ an air filled or foam sac above end of tube When cuff is inflated , it obstructs airway preventing air from escaping into nose or mouth Excess pressure of the cuff can cause tissue ischemia and necrosis of trachea Low pressure tubes can be left in place 3 4 weeks Gag, cough and swallow reflexes must be intact When client is able to maintain effective respirations the endotracheal tube is removed (extubation) Humidified O2 is provided immediately following removal

Inspiratory stridor within the first 24 hours indicate edema and necessitate reintubation

Mechanical Ventilation Indications Apnea or acute ventilator failure Hypoxemia unresponsive to O2 therapy Respiratory muscle fatigue or its potential pneumonia , ARDS

Drug overdose, neural disorders, chest wall injury, severe asthma, COPD, pulmonary contusion,

Types of Ventilators Negative Pressure ventilators create negative (sub-atmospheric) pressure drawing chest outward and air into lungs which mimics spontaneous breathing Eg are: iron lung, cuirass and pulmo wrap Positive Pressure ventilators (used more than negative pressure) Positive pressures push air into lungs rather than draw air into lungs. Invasive ventilation with a trach tube or non-invasive (tight fitting mask) may be used failure Used for clients w/ neuro muscular disorders and sleep apnea

Its primary use is for clients with obstructive sleep apnea, neuro-muscular disease, and impending resp. NIV is more successful in clients w/o significant lung disease A trigger is used to prompt ventilator to deliver a breath Clients inspiratory effort triggers ventilator assisted breaths

Modes of Ventilation Mode determines whether a breath is initiated by the client or the ventilator and the pattern of airway support Continuous Positive Airway Pressure (CPAP) Applies positive pressure to airway of a spontaneously breathing client Can be used with a trach or tight fitting face mask All breathing is spontaneous, maintains airway opening and alveoli

Bilevel Ventilator (BiPap) Provide inspiratory positive airway pressure Used w/ tight fitting mask at night spontaneous breathing fails Assisted Control Mode Ventilation (ACMV or AC) Used to initiate mechanical ventilation when client at risk for respiratory arrest Assisted breaths are triggered by inspiratory efforts, If respiratory falls below a preset number ventilator controlled breaths are delivered Synchronized intermittent Mandatory Ventilation (SIMV) Client breaths spontaneously w/o ventilator assistance between ventilator breaths Ventilator (mandatory) breaths are delivered at a preset number Used to exercise respiratory muscles Three modes can be used: Spontaneous, timed delivered at determined rates, spontaneous/times in case

Positive End Expiratory Pressure

Requires intubation can be applied to other ventilator modes Positive pressure is maintained in airways during exhalation and between breaths Lower percentages of O2 is can be used w/ PEEP Useful for treating ARDS Improves ventilator-perfusion relationship and diffusion across capillary/aveoli membrane

Pressure Support Ventilation (PSV) Ventilator assisted breaths are delivered when client initiates inspiratory Flow cycle limited Inspiration is terminated when inspiratory airflow falls below a determined rate Decreases work of breathing Can be combined w/ SIMV when respiratory drive depressed Ventilator support can be withdrawn during weaning

Pressure Control Ventilation (PCV) Control pressure within airway to reduce airway trauma Pressure is preset Ventilation timed is triggered and time cycled, pressure is limited Requires heavy sedation

Ventilator Settings Typically set between 12 15 breaths per minute ACMV or SIMV respiratory rate is higher than ventilator setting due to spontaneous breathing Exhaled CO2 (ETco2) or PaCo2 may be used to determine rate PaCo2 < 38 mmHg indicates respiratory acidosis/hyperventilation so set rate is reduced

PaCo2 > 42mmHg or an ETco2 > 45mmHg indicates hypoventilation requiring an increase in rate

Tidal volume Controls the amount of gas delivered with each ventilator breath Normal adult tidal volume = 7 mL/kg of body weight or 400 550 mL tubing dead space Complications Improper tube placement Advancement of tube into mainstream bronchus causing ventilation of one lung Noninvasive ventilation

Tidal volume is delivered by mechanical ventilation is slightly higher (500-700mL) to compensate for High tidal volumes can cause lung tissue damage

Inflated lung becomes over extended and traumatized under inflated lungs develops atelectsasis

Gastric dilation Aspiration Facial skin necrosis Stress

Drying of the eyes and mucous membrane Claustrophobia

Nonsocomial Pnuemonia Normal upper resp. tract defense mechanism are bypassed due to loss of air humidfication and trapping pathogens Oral secretions and gastric content can enter respiratory tree through epiglottis Cough reflex is inhibited or impaired Secretions become thick and tenacious increase atelectasis risks

Barotrauma (volutrauma) Lung injury due to alveolar overdistention Caused by volume and pressure of delivered gas pleural space and other tissues

Overdistened aveoli ruptures and allows air to escape in pulmonary interstitial space and mediastinum, Subcutaneous emphysema (air in subcutaneous tissue), pnuemothorax, and pneumomeditstatum can result Tissue swelling of chest, neck and face Crackling or air-bubble popping sensation is felt when palpated percussion tone

Pneumothorax identified by unequal chest expansion, significant breath decrease, hypersonant Pneunomedastitum presence of air in mediastum space between lungs, heart, trachea and great vessels Can lead to pneumopericardium (air in pericardial sac) diagnosed thru CXR

Cardiovascular effects PPV increase intrthoracic pressure which impedes venous return and ventricle filling Cardiac output falls, which can affect liver and kidney function

Gastrointestinal Effects Stress ulcers (erosive gastritis) leading to gastrointestingal hemorrhage Histamine or sucrafate used to prevent ulcers Air leaks around tracheal tube can cause gastric distention Constipation from sedation and analgesic medications

Weaning Begins only after underlying cause of respiratory failure has been corrected or stabilized T-piece or CPAP may be used for weaning Ventilator is removed for brief periods while O2 is delivered using T-piece Duration of time off of ventilator is increased gradually ETo2 and PaO2 rates closely monitored CPAP weaning is same as above Client is placed back on mechanical ventilation if respiratory distress occurs SIMV and PSV used when ventilation has been longer and reconditioning of respiratory muscles is required When client can tolerate SIMV at 4 breaths per minute without rest, they are weaned to CPAP or T-piece prior to extubation Terminal Weaning The weaning of mechanical ventilation when client is not expected to recover Decisions can be made with client prior to ventilator support Analgesics and sedation are given for comfort

Nutrition and Fluids Ventilation promotes water and sodium retention due to effects on cardiac output Renal perfusion is decreased, which stimulates rennin-angiotensin system to retain NA and H2O Swan Ganz catheter is used to monitor pulmonary artery pressures and cardiac output Arterial line monitors blood gas Electrolytes are monitored

Intake and output and daily weight monitored

Enteral or parental nutrition provided because trach prohibits eating Nasogastric, gastrotomy or jejunostotomy feeding tube is used. Jejunostomy used to reduce risk of regurgitation and aspiration

Nursing Diagnosis

Impaired Spontaneous Ventilation Assess vitals every 15 30 minutes Report immediately signs of respiratory distress Administer O2 as ordered

Report worsening ABG report and O2 saturation

Place in fowlers/high fowlers Minimize activities Prepare for trach tube placement or mechanical ventilation

Ineffective Airway Clearance Suction as needed keeping suction unit between 80 120mmhg Obtain sputum culture if it appears purulent or ordorous Perform percussion, vibration and postural drainage as ordered Evaluate trach tube pressure by measurement (no more than 20-25 pressure) Auscultate suprasternal notch for hissing sound at end of inspiration Firmly secure endotracheal tube or trach tube Assess fluid balance and maintain hydration

Risk for Injury LOC is affected by hypoxemia and hypercapnia Assess frequently: LOC, Neuromusclar blockade impairs clients breaths, communication and movement

Condition of mucosa of mouth and nose Vital signs, skin color, cap refill, pulse Bowel sounds

Respiratory lung sounds, chest excusion and ventilator pressures

Test gastric secretions and feces for blood Urine output, daily weight Turn and reposition often Passive range-of-motion Report air leaks and decrease breath sounds Keep skin and linens clean Rail side up and soft restraints Histamine and sucralfate

Anxiety Monitor anxiety level Remain with client Explain all procedures

Communicate via simple meanspicture board, slate Encourage family friends to visity Distract w/ television and radio

Promptly attend to physical needs Reassure ventilation is temporary