Nursing 460, Management of Patients with Respiratory Failure
Nursing 460, Management of Patients with Respiratory Failure 460
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Date Created: 07/06/16
Chapter 23 -Oxyhemoglobin dissociation curve Shift to left (lower PaO2 saturations)=it is more difficult for hemoglobin to release O2 Shift to left (higher O2 saturations) = more easy for hemoglobin to release O2 Conditions for shift to left: o Increase pH o Decrease temp (hypothermia) o Decrease PaCO2 (decreased CO2) Condition for shift to right: o Decrease pH o Increase temp (hyperthermia) o Increase PaCO2 (increased CO2) Note: oxygen saturation does not change significantly above PaO2 above 60 mmHg -shunts: Most patients don’t have increased CO2 levels, b/c respiratory center is responding to hypoxemia by increasing RR Anatomic or physiological Anatomic o Blood bypasses lungs o seen through ventricular septal defect (blood passes through open chamber between right and left ventricles) or pulmonary anomaly (blood flow directly from pulmonary artery to pulmonary vein) Physiologic o Blood passes directly into vasculature o Blood does not come into contact with alveoli o seen in pulmonary edema, pneumonia, atelectasis -Acute respiratory failure (ACR) syndrome of failure of lungs to oxygenate blood and/or remove CO2 from blood, d/t failure of heart, lungs ,or both -Hypoxemic respiratory failure causes hypoventilation ventilation/perfusion mismatch (airway disease (COPD,asthma), ILD, disease of pulmonary vasculature (PE, pulmonary HTN) anatomic shunt decreased fraction of inspired air (O2) at high altitudes -Etiology of hypoxic respiratory failure: Acute lung injury, pneumothorax, atelectasis ARDS Pneumonia Pulmonary thromboembolism Cardiogenic pulmonary edema Acute collagen vascular disease (Goodpastures’s lupus) -Etiology of hypercapnic respiratory failure: Medications causing respiratory depression Pulmonary disease: COPD, asthma Neuromuscular, Guillan-Barre syndrome, Acute myasthenia gravis Sprinal cord tumors Kyphoscoliosis Obesity -Hypoventilation -decreased gas entering alveoli per unit of time; mat of gas exchanged at alveolar level *Alveolar ventilation can lead to hypercapnic respiratory failure -Clinical manifestations of ARF: SOB, tachypnea Cough, sputum, rales Decreased neurological function can lead to fatigue and respiratory arrest -Big difference in sx b/t hypoxemic and hypercapnic respiratory failure: Patient will rarely become sleepy, have decreased LOC, and difficult to arouse in hypoxemic respiratory failure Central cyanosis in hypoxemic respiratory failure Muscle twitching (caused by acidosis) in hypercapnic respiratory failure Also, tachycardia, dysrhythmias, hypertension or hypotension in hypoxemic respiratory failure -Diagnostic tests for Acute respiratory failure: ABGs o pH 7.35-7.45, PaCO2 35-45, PaO2 75-100, HCO3 24-28 o Patient hx and physical assessment o Chest radiography (to identify possibly cause of respiratory failure (eg pulmonary edeam, ARDS, pneumonia, HF, COPD/asthma, neoplasma, etc) -Acute pulmonary edema = abnormal accumulation of fluid in lungs that can lead to ARF, can accumulate from dysfunction of lungs, and/or heart Cardiogenic or noncardiogenic -Cardiogenic pulmonary edema Results from left ventricular pump failure , fluid backs up increased left ventricular pressure and pulmonary pressures From cardiac muscle (systolic or diastolic) dysfuction or valvular prob or cardiac tamponade Fluid forced into interstitial space and into alveoli when lymphatic system can’t drain excess fluid built up Can be precipitated by dysrhythmias -Noncardiogenic pulmonary edema Not caused by heart dysfunction Commonly caused by ARDS or acute lung injury (ACI) Increased capillary permeability, lymphatic insufficiency, decreased oncotic P, increased negatic interstitial P, idiopathic Fluid accumulates in interstitial space and alveoli Different forms: o Neurogenic pulmonary edema o Negative pressure pulmonary edema (attempting to breathe against airway obstruction, and intrathoracic P becomes more negative, blood return to right heart increases ) o High-altitude pulmonary edema (from hypoxia at low atmosphteric pressures and high altitude pulmonary constriction may occure) o Heroin-induced pulmonary edema: within 24 hrs, injury to pulmonary- capillary membrane o Excessive intravenous fluid administration o Transfusion-related injury – increased pulmonary pressures o Toxin and drug-related pulmonary edema (includes injuries from inhalants and toxic gases) -Common causes of acute pulmonary edema Increased pulmonary capillary pressure o Cardiogenic: left ventricular failure o Noncardiogenic: pulmonary venous fibrosis, pulmonary occlusive disease Increased negative o Upper airway obstruction (croup, epiglottis, laryngospasm) Increased pulmonary capillary permeability o Pneumonia o ARDS/ALI o Toxins o Immunologic reactions, such as transfusion reactions o Smoke inhalation o Sepsis o Immersion injury (near drowning) o Uremia -Clinical manifestations of acute pulmonary edma Initial sx include cough, dyspnea, tachypnea, fatigue When fluid invades alveoli: severe dyspnea, tachypnea, frothy sputum production Decreased saturations Crackles, wheezes, rhonchi Central cyanosis, circumoral pallor Agitation, confusion sx of hypoxemia -Different sx b/t CPE and NCPE: CPE: tachycardia w/ hypotension, cool, diaphoretic skin; jugular vein distention NCPE: tachycardia w/ HTN; bounding pulses, dry skin; warm skin (in sepsis) -Other differences b/t CPE and NCPE: History o CPE: cardiac event (eg ischemic chest pain or HTN) o NPE: preceipitating event (eg sepsis, aspiration, pneumonia, trauma, multiple transfusions) Pulmonary capillary wedge pressure (normal 6-12 mmHg): o CPE: > 18 mmHg o NCPE: < 18mmHg New S3, S4 heart sounds o CPE: associated w/ left heart failure o NCPE: not common New or changed murmur o CPE: associated w/ left heart failure o NCPE: not common Echo o CPE: weak heart muscle or valvular abnormalities that would indicate heart failure o NCPE: no cardiac muscle or valvular defects Brain natriuretic peptide (BNP) o CPE: >500 pg/mL suggests HF o NCPE: <100 pg/mL suggests unlikely cardiac cause Chest x-ray o CPE: even or central distribution of edema o NCPE: diffuse bilateral patchy infiltrate pattern -Medication management of acute pulmonary edema Supplemental O2 titrated to increase SpO2 Intubation with mechanical ventilation if necessary Blood pressure support Noninvasive positive pressure ventilation (NPPV) Airway management Diuretics but not in hypotensive patients Vasodilators (eg nitroglycerin) to decrease preload by redistributing blood peripherally or in decreasing afterload, letting heart work more efficiently Inotrope (eg dopamine and dobutamine) : decrease cardiac contractility and improve CO o Dopamine given at lower dosage, decreased vascular resistance (afterload) and increased renal perfusion Morphine: reduces pulmonary capillary pressure w/o depressing myocardial contractility Nursing interventions for acute pulmonary edema: Positioning (HOB >30) to promote lung expansion, prevent aspiration Monitor oxygen saturations > 90% Review ABGs Provide suctioning as needed to clear secretions Notify health care provider of increasing oxygen requirements Monitor patients’ energy level Diet: limit amount of high fat and salty foods, processed, canned, and fried food Watch for signs of cardiac condition deterioration: weight gain of 3 or more pounds over 1-3 days; swollen ankles, feet -Acute Respiratory Distress Syndrome (ARDS) and Acute Lung Injury (ALI) Both types of ARF ARDS is a syndrome of hypoxemic respiratory failure that leads to alveolar- capillary inflammation and damage ALI is a less severe form of ARDS, differentiated by lesser degree of abnormal oxygenation May take 6-12 months to regain normal function -Criteria that define ALI and ARDS: ALI o PaO2/FiO2<300mG (regardless of PEEP level) o Bilateral patchy infiltrates on chest x-ray o PCWP < 18 mmHg if available or no evidence of left atrial hypertension ARDS o PaO2>FiO2<200 mmHg (regardless of PEEP level) o Bilateral patchy infiltrates on chest x-ray o PCWP <18 mmHg if available or no evidence of left atrial hypertension -sx of ARDS and ALI Sx of RF (SOB, tachypnea; cough, sputum, rales) Early sx: hyperventilation w/ corresponding respiratory alkalosis Progression: o As hypoxemia increases, dyspnea, SOB, and tachypnea, with use of accessory muscles o Skin may appear cyanotic or mottle o Respirations are rapid and shallow with intercostal and suprasternal retractions on inspiration o Crackles, coarse rhonchi or wheezes o Late findings: hypotension and decreased CO -Nursing interventions for ARDS and ALI: Mechanical ventilation if severely hypoxemia: volume or pressure-targeted o Volume targeted: uses a set inspiratory volume of gas (tidal volume) moving into lungs with each breath; the stiffer the lung, the higher the pressure needed to reach the volume for that lung o Pressure-targeted: involves delivery of breath until set inspiratory pressure is reached; the stiffer the lung, the less volume will be delivered before the set pressure is reached Demonstrate use of AMBU bag and suctioning, with HOB elevated >30 degrees to prevent aspiration and HAP Cough,deep-breathing exercises Spirometry Supportive care, including feeding -Terms associated with mechanical ventilation: Tidal volume (TV) = amount of gas inspired with eac hbreath o For ventilation, ventilator delivers certain volume of breaths in volume- targeted ventilation modes; ventilator will deliver a breath until set volume is reached; should be based on ideal body weight rather than actual body weight of patient Residual volume (RV) = amount of gas remaining in lungs after maximal respiration Functional residual capacity (FRC) = total amount of gas left in lungs after normal expiration Fraction of inspired air (FiO2) = prevent of oxygen delivered to patient; prolonged > 60% can lead to lung injury Rapid shallow breathing index (RSBI) o Respiratory rate/spontaneous tidal volume o Used to determine weaning success Ventilator rate o Set rate delivered by ventilator, patients can breathe over set rate; Increasing rate on ventilator will decreased PaCO2 and raise pH; monitor for auto-PEEP and hyperventilation -Positive end-expiratory pressure (PEEP): Pressure exerted on airway throughout respiratory cycle that prevents alveolar collapse Exerts continuous pressure above atmpsphericelvesl on airways during both inspiration and expiration 5cm H2O to compensate for endotracheal tube resistance Ideal PEED prevents atelectasis Can improve oxygenation and reduce oxygen requirements (FiO2) Increases inthrothoracic pressure and can cause hypotension at high levels (b/c venous return is reduced); monitor BP Can lead to hemodynamic instability in cardiac patients -continuous positive airway pressure (CPAP) Used in spontaneous ventilatory modes to maintain a positive pressure in airway to reduce or prevent alveolar collapse Patient breathes at own rate and own tidal volume until ventilator places continuous positive pressure in airway Apnea alarms must be set Assess for hypoventilation -Endotracheal tube insertion Patient on back with blanket under shoulders to hyperextend neck and open airway Confirm equipment is working Provide 100% O2 via nonbreather mask or AMBU Document: size of tube and location in airway (by # of cm printed on tube) Cuff occlude space above tip of tube so air doesn’t escape from mouth when pt is ventilated, also prevents secretions from entering lungs o Is located below vocal cords Pilot balloon is small diameter tube that runs from cuff and leads outside mouth so that it can be inflated with syringe after tube is inserted Pressures should be set for minimal occlusion and monitored regularly *Note: Noninvasive positive pressure ventilation can be used to treat ARF (Esp in COPD) -Inspection of ET tube/ventilation Size of tube and depth of insertion Ventilator circuit should be free of fluid (or else, contamination) Amount and color of secretions in ET tube Mental status, sx of hypoxemia (eg cyanosis) Chest wall (movement, symmetry, size of chest wall) Accessory muscles used? Distended abdomen? Can prevent adequate ventilation Mottling of extremities signifies vasoconstriction Sx of infection -Palpation of ET tube/ventilation: Deviation of trachea Pleural friction fremitus (produced when swollen, inflamed pleural surfaces come in contact with each other) -Auscultation Bronchilal or bronchiovesicular lung sounds over peripheral fields can indicate pneumonia or atelectasis Check for suctioning if hear gurgles or rhonichi over large airways Diminished sounds = obesity, pleural fluid accumulation, or pneumothorax Tension pnuemo more common in patients on positive pressure ventilation Weaning from Mechanical Ventilation: Criteria: o Hemodynamically stable (low or low dose vaspopressors) on low PEEP and low FiO2 requirements o PaO2/FiO2 at least 150 or SpO2 at least 90% on FiO2 at least less than 40%and PEEP at least less than 5 cm H2O o Test for weaning by using rapid shallow breathing index; if < 105, patient will probably fail to wean o Patient must be able to initiate inspiratory effort ABGs done after app 30 min, verify ph Monitor SpO2, RR, HR, any increases in respiratory effort, breath sounds, and BP o HR and RR increased while BP and SaO2 decrease; help prevent myocardial ischemi d/t lack of O2 -Mechanical ventilation/ET tube components Inspiratory and expiratory tubing (each of own circuit) that connect to ventilator Humidifier before O2 is delivered to patients on ventilation in order to prevent drying of airways, mucous plugging o Methods by heat and moisture exchanger and heater-humidifiers FiO2 should be titrated to lowest concentration that produces PaO2 of 55-60 mmHg in patients with lung disease, in order to prevent oxygen toxicity Hypoxia may not be tolerated in patients with cardiac disease or neurological injury; patients needs PaO2 of at least 60 mmHg and saturation <90% Life-threatening hypoxia: 100% O2 should always be administered Suctioning a procedure: open and closed system suctioning o Closed system suctioning: patient doesn’t have to be disconnected from ventilator, maintains PEEP and O2 delivery and sterility of suction catheter o Open system suctioning: requires disconnection from ventilator using sterile suction catheter -Suctioning procedure Position patient and bed to comfortable working position Adjust suction to between 80 and 110 mmHg Select suction catheter that doesn’t exceed more than half the inner diameter of artificial airway Monitor patient’s pulse ox and EKG Hyperoxygenate patient with 100% oxygen for 30-60 seconds prior to suctioning by either adjusting the FiO2 on the ventilator or using temporary oxygen enrichment program.. do NOT use manual bag ventilation o If manual bad is only alternative, ensure that PEEP is maintained; use a PEEP valve attachment for PEEP-dependent in that when PEEP is removed, it can be difficult to oxygenate back to baseline Check suction power by occluding end of suction tubing prior to attaching catheter; power in adults should not occlude > 100 mmHg Use shallow, not deep suction (don’t advance until resistance is met) Withdraw catheter, applying intermittent suction, which should not exceed 15 seconds Follow-up care: o Hyperoxygenate for 1 minute o Patients should not be routinely hyperventilated o Monitor for adverse reactions (eg hypoxia, dysrhythmias, hypo- hypertension, bradycardia). -Complications of mechanical ventilation: Barotrauma = damage to lung tissue, can lead to alveolar rupture from increased pressure from high ventilation pressures Volutrauma = lung damage from increased volume that causes hyperinflation of alveoli Pneumothorax, hypoxia GI: gastric distention, abdominal distention (from swallowed air); gastric ulcer; bleeding Ventilator-associated pneumonia o (from ET tube insertion and pathogens in oropharynx, leakage of secretions, lack of oral care q2-4 hours) o Duration of ventilation -Volume-targeted modes of mechanical ventilation Continuous mandatory ventilation (CMV) o Breathes initiated, controlled, and terminated by ventilator o Patient cannot initiate any breathes spontaneously o Monitor for patient attempts to breathe beyond set ventilated breathes; consult with resp therapist if patients’ effort to breathe is causing agitation or discomfort o Sedate patient if necessary Assist-control ventilation (AC) o Both patient and ventilator can initiate breathes o Each breath, whether patient or machine triggered, receives full set tidal volume o Monitor PEEP levels to id auto-PEEP and breath stacking o Assess for patient-ventilator asynchrony could lead to hypoxea or hypercarbia o Ventilator alarms should include high-pressure limit, or else, pressure needed to deliver tidal volume could rise to dangerous levels (as lungs become less compliant) o Patient’s inspiratory pressure on ventilator may be reached, and ventilator may not deliver rest of tidal volume, patient may attempt to breathe against above set limit Synchronized intermittent mandatory ventilation o Both patient and ventilator can initiate breaths o Patient sets tidal volume (spontaneous breaths are not assisted) o Monitor for respirator effort, since patient does more of work (of breathing) than ventilator o If respiratory alkalosis, then pressure is too high o Decreasing rate may allow more opportunity for patient to take breath -Pressure-targeted ventilation = set inspiratory pressure Pressure control ventilation (PCV) o Set rate, volume o Both patient and ventilator can intiate breathes, each breathe receives full inspiratory pressure o Monitor tidal volume (with decreased lung compliance, tidal volume delivered by ventilator will decrease and may not meet respiratory demands) Pressure-support ventilation (PSV) o No set rate or volume o Each of patient’s spontaneous breathes receives support from ventilator o The higher the set pressure support, the more the ventilator is doing the work of breathing o IF patient is too sedated and does not attempt to breathe, no support is received. PAtiet must have a reliable respiratory rate. o Used for weaning o *Used for spontaneous breathing patients only o Monitor for hypoventilation o Set apnea alarm and back-up rate if available -mechanical ventilation alarms – according to nursinglabs.com Conditions that trigger high-pressure alarms: o Kinking of ventilator tubing, but not disconnected tubing o Bronchospasm or PE o Mucous plugging or water in tube o Coughing or biting on tube o Client’s being out of rhythm with ventilator Conditions that trigger low-pressure alarms: o Disconnected tubing o ET cuff leak Oxygen alarm o Changing oxygen concentration without resetting oxygen level alarm -if chest tube disconnects, according to nurselabs.com: Place tube in bottle of sterile water Placing sterile dressing over where tube was disconnected will not prevent complications System is replaced if it breaks or if collection chamber is full -fluctuations in water-seal chamber, according to nurselabs.com If lung has been removed -initial action for sucking stab wounds, according to nursinglabs.com Cover wound with dressing, to prevent air from entering space THEN draw blood, assist with chest tube, and start an IV -Complication from receiving a high O2 concentration Apnea Not respiratory alkalosis -Suctioning – see suctioning procedures as described above