Week 6; Acute Care Respiratory Flashcards
ARDS
Characterized by rapid onset of noncardiac pulmonary edema, progressive refractory hypoxemia, extensive lung tissue inflammation, small blood vessel injury, multisystem organ malfunction, and varied initial admitting diagnoses.
ARDS is caused by
acute lung injury from unregulated systemic inflammatory response to acute injury or inflammation
ARDS patho after acute lung injury
Damaged capillary membranes → plasma, blood cells leak into interstitial space
Damage to alveolar membrane → fluid enters alveoli
Dilutes, inactivates surfactant → damage to surfactant-producing cells
Deficit of surfactant, increased alveolar surface tension, alveolar collapse with atelectasis
Lungs become less compliant, gas exchange impaired
Hyaline membranes form → further reduced gas exchange, compliance
Fibrotic changes in lungs → less surface area for gas exchange
Hypoxemia becomes resistant to improvement with supplemental O2
PaCO2 rises as diffusion further impaired
ARDS causes
Hypoxemia, metabolic acidosis, sepsis, multiple organ system dysfunction
ARDS risk factors
Greater for men than women
Greater for African Americans
Patients who develop ARDS from sepsis have poorer outcomes than those who develop ARDS from pulmonary infections or trauma
Direct insults that can cause ARDS
Pulmonary infections
Aspiration of gastric contents
Inhalation injuries
Smoke inhalation
Saltwater inhalation
Indirect insults that can cause ARDS
Overall body sepsis
Trauma
Gastrointestinal (GI) infections
Drug overdose
Multiple blood transfusions
ARDS s/s
Dyspnea and tachypnea are early signs
Chest x-ray, arterial blood gases (ABGs) often normal
Respiratory rate, intercostal retractions, use of accessory muscles of respiration increase
Tachypnea
Rales, rhonchi develop
Chest x-ray shows interstitial changes, patchy infiltrates
Pulse oximetry, ABG levels show refractory hypoxemia
Agitation, confusion, and lethargy
Nurse’s focus for the pt with ARDS
Constantly monitor patient’s condition, respond to subtle cues indicating changes, and intervene appropriately
ARDS dx tests
ABG analysis to determine O2 levels in blood, chest x-ray or chest CT to determine fluid in lungs, CBC, blood chemistry, blood cultures to help find cause of ARDS, and sputum culture to determine cause of infection
Pharmacologic therapy for ARDS
No definitive drug therapy for ARDS
Nitric oxide reduces intrapulmonary shunting and improves oxygenation
Surfactant therapy
Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are being studied
Corticosteroids may be used late in disease course when fibrotic changes occur to improve oxygenation, lung mechanics
Mainstay of ARDS management
Endotracheal intubation, rarely possible to maintain adequate oxygenation with O2 therapy alone. Mechanical ventilation does not cure ARDS
Supports respiratory function while underlying problem is found, treated
Vent support complications
Ventilator-associated pneumonia (VAP), barotrauma, pneumothorax, cardiovascular effects, GI effects
Negative pressure ventilators
Create negative pressure externally to draw chest outward and air into lungs
Positive pressure ventilators
Push air into lungs, used more often than negative pressure ventilators
Noninvasive positive pressure ventilation (NIPPV)
Tight-fitting face mask, nasal mask, nasal shield, or nasal pillows, may prevent need for tracheal intubation. Ventilatory support for patients with sleep apnea, neuromuscular disease, or impending respiratory failure.
Weaning from ventilator support
When underlying process causing respiratory failure is corrected or stabilized. Process and time required depend on several factors:
Preexisting lung condition
Duration of mechanical ventilation
Patient’s general physical and psychologic condition
Vital signs, respiratory rate, extent of dyspnea, blood gases, clinical status used to evaluate weaning and its progress
T-piece, CPAP may be used for weaning
SIMV, PSV
When duration of ventilation long enough that respiratory muscles need to be reconditioned
Weaning is a primary use for PSV
Terminal weaning:
when survival without assisted ventilation is not expected
Artificial airways
Inserted to maintain patent air passage
Oropharyngeal airways
Stimulate gag reflex, used only for semiconscious, unconscious patients
Nasopharyngeal airways
Usually well tolerated by alert patients, frequent oral and nares care needed
Endotracheal tubes
In patients under general anesthesia or in emergency situations. Insertion requires specialized education, patient unable to speak while tube in place
Tracheostomies
For long-term airway support, opening into trachea through neck
Open surgical method: done in operating room
Percutaneous method: can be done at bedside in critical care unit
Nursing care: maintain airway patency and precautions to provide humidity
Swan-Ganz catheter
Monitor pulmonary artery pressures and cardiac output
Arterial line
Repeated blood gas analysis and continuous arterial pressure monitoring
Nutrition and fluids for pt with ARDS
Serum electrolytes drawn frequently, monitor intake and output (I&O), daily weight, fluid and electrolyte status, enteral or parenteral nutrition during mechanical ventilation, jejunostomy tube may be used to reduce risk of regurgitation, aspiration
ARDS nursing cares
Prone positioning in conjunction with mechanical ventilation, treatment of any infection with IV antibiotic therapy, correction of underlying condition, careful fluid replacement, low-molecular-weight heparin to prevent thrombophlebitis, pulmonary embolus and DIC
Possible ARDS complications
Thrombophlebitis, pulmonary embolus, DIC
Children and ARDS
Low incidence, may be underdiagnosed. Immunocompromised children at increased risk
Clinical guidelines reflect differences between adult, pediatric patients: more compliant chest walls in children, higher sedation requirements, baseline airway resistance
Lower hematocrit, functional residual capacity
Lungs not yet fully developed
Advise against routine use of inhaled nitric oxide (NO), exogenous surfactant, corticosteroids, prone positioning. Intubation to be used only in patients who do not respond to other measures or have worsening signs, symptoms
Pregnant women and ARDS
Low incidence rates but devastating results; maternal mortality rate as high as 44%
Common obstetric causes: preeclampsia, amniotic fluid embolism, obstetric hemorrhage, sepsis from infection of uterus, fetal membranes, kidneys, influenza during pregnancy.
Goals: adequate ventilation, nutritional support
Prone positioning but with caution during third trimester, close fetal monitoring
Older adults and ARDS
Greater risk than rest of adult population, especially over age 40
Due partly to age-related changes in respiratory physiology, higher mortality rate. Less likely to receive same intensity of care as other ARDS patients. Significantly more likely to die from multiple organ failure, other complications. Treatments aimed at prevention of nonpulmonary organ complications help improve overall outcomes. Adequate nutrition contributes to improved O2 levels, lung function, diet high in omega-3 and -6 fatty acids
Nursing process with ARDS
Careful, continuous monitoring of airway, breathing, circulation, monitor for changes in level of consciousness (LOC), oxygenation, perfusion require rapid intervention.
Assessment of the patient with ARDS
Respiratory rate, rhythm, auscultation of lungs, LOC, including orientation, baseline vital signs, peripheral perfusion
In the pt with ARDS, monitor
Vital signs hourly, oxygenation status with ABG, pulse oximetry, neurologic status, including orientation and LOC, lung and heart sounds
Interventions for the pt with ARDS
Analgesia, anxiolytics, sedation, provide beta-agonist to maintain patent airways, maintain head of bed at 30 degrees or higher, prone position as tolerated 3–4x/day, suction airways as needed, monitor hemodynamic status with central venous catheters or pulmonary artery catheter as ordered, monitor renal function by I&O, blood urea nitrogen (BUN) and creatinine levels, foley, IV fluids as needed but avoid fluid overload, monitor glucose levels, maintain within normal limits
Maintaining a patent airway in the pt with ARDS
Perform postural drainage (PVD) as ordered, assess fluid balance, maintain adequate hydration, suction as needed, obtain sputum for culture if sputum appears purulent or is odorous, secure endotracheal or tracheostomy tube with adequate slack on tubing, restrain patient’s hands if necessary
Promote spontaneous ventilation in the pt with ARDS
Place patient in Fowler or high-Fowler position, minimize activities, energy expenditures, assist with activities of daily living (ADLs), space procedures, activities, allow uninterrupted periods of rest, assess, document respiratory rate, VS, O2 saturation every 15–30 minutes, promptly report worsening data, administer O2 as ordered, monitor response
Enhance cardiac output in the pt with ARDS
Assess LOC at least every 4 hours, monitor pulmonary artery pressure, central venous pressure, cardiac output every 1–4 hours, assess heart and lung sounds frequently, weigh daily at same time, provide frequent skin care, maintain IV fluids as ordered, administer analgesics, sedatives, neuromuscular blockers as ordered
Interventions for dysfunctional ventilatory weaning response
Assess vital signs every 15–30 minutes
Place in Fowler or high-Fowler position
Explain weaning procedures, expected changes in breathing
Remain with patient during initial periods following changes of setting
Limit procedures, activities during weaning periods
Provide diversion
Begin weaning in morning
May discontinue overnight to provide rest
When SIMV used for weaning, decrease rate by increments of 2 breaths/min
Avoid drugs that may depress respiratory
Keep oxygen at bedside
Provide pulmonary hygiene
ARDS teaching
Need to tailor activities until maximal respiratory function returns, avoid smoking, exposure to smoke and other pollutants, immunizations for pneumonia, influenza
Cystic fibrosis:
Inherited disorder that affects secretory glands, particularly glands responsible for secreting mucus, digestive enzymes, sweat (exocrine glands). In turn, affects lungs, sinuses, digestive organs, reproductive organs.
CF patho
CF stems from mutation of CFTR gene. This protein is central to movement of chloride into, out of body cells. Mutation affects movement of salt and water into, out of cells. Entry of too much salt, not enough water causes production of thick, sticky mucus that obstructs ducts and passageway, including airways, pancreatic duct. Causes airway occlusion and creates environment that supports bacterial growth. Immune response causes WBCs to release sticky chemical substances into mucus. This worsens obstruction and exacerbates inflammation, infection. Often diagnosed before 2 years of age, but manifestations vary, may occur later
CF prevention
Genetic testing
CF clinical manifestations: hallmark and respiratory
Increased level of chloride in sweat: hallmark manifestation
Respiratory manifestations include chronic cough, chronic sinusitis, recurrent infection, including bronchiectasis, pneumonia
Recurrent respiratory infections → scar tissue, cysts in lungs
Pneumothorax in later stages of disease
Pulmonary damage may lead to respiratory failure and death
Other s/s of CF
Chronic diarrhea, nutritional deficiencies, obstruction of pancreatic ducts, impaired production of enzymes needed for food digestion, malnutrition, delays in growth and development, impaired insulin production, impaired blood glucose control, blockage and inflammation of bile duct, hepatic dysfunction, gallstones, Men with CF absence of vas deferens, obstruction and impaired development of vas deferens, fertility treatment or surgical procedures may be needed, women with CF have decreased fertility, changes of pregnancy may exacerbate effects of CF
CF dx tests
Prenatal screening: if mother has abnormal CFTR gene, father is tested, if both parents are carriers, fetus may be tested
Amniocentesis: chorionic villus sampling, newborns screened at birth in United States
Sweat test: older children or adults may be tested if they show warning signs, such as:
Bronchiectasis
Chronic lung or sinus infections
Nasal polyps
Pancreatitis
Male infertility
Surgery for CF
Removal of nasal polyps to improve breathing, removal of mucus via endoscopic lavage to improve breathing, oxygen therapy for advanced lung disease, feeding tube insertion to administer additional nutrients, bowel surgery in case of bowel blockage or intussusception
Pharmacologic therapy for CF
Bronchodilators for patients with mild disease for specific purposes
Mucolytics, antibiotics, CFTR modulators, vaccination, anti-inflammatory drugs, digestive drugs, including vitamin and mineral supplements
CFTR modulators
Revolutionary treatment targeting cause of problem, patients age ≥12 with two copies of most common mutation. Relatively new, may be prohibitively expensive
Nonpharmacologic therapy for CF
Airway clearance techniques such as coughing, huffing, chest physical therapy, percussion, vibration, deep breathing, pulmonary rehabilitation, lifestyle interventions, healthy, well-balanced diet, high fluid intake, regular exercise, fitness training, refraining from smoking, avoiding secondhand smoke, good hygiene, coughing into tissue, disposing immediately, cleaning hands afterward
Children and infants CF considerations
Prenatal indicators of CF: prenatal testing, hyperechoic or echogenic bowel on ultrasound
Neonates: meconium ileus
Children: intussusception, poor weight gain, delayed growth and development, failure to thrive, respiratory difficulties
Vigilant assessment, monitoring of airway patency, respiratory status required to protect safety of neonatal, pediatric patients
Staying up to date on immunizations is critical
Children and infants CF considerations
Prenatal indicators of CF: prenatal testing, hyperechoic or echogenic bowel on ultrasound
Neonates: meconium ileus
Children: intussusception, poor weight gain, delayed growth and development, failure to thrive, respiratory difficulties
Vigilant assessment, monitoring of airway patency, respiratory status required to protect safety of neonatal, pediatric patients
Staying up to date on immunizations is critical
CF in adolescence
Continue to require CPT, enzymes, vaccines, other medications
Nutritional supplementation: extra calcium, vitamin D
Puberty may be delayed, teens can live normally as long as they engage in appropriate self-care, adequate nutrition and sleep, scheduling provider appointments, managing medication regimens, healthcare decisions, parents should encourage autonomy while providing emotional, social support. Adolescents should be encouraged to think about future education, career plans
CF in adults
Long-term damage to lungs, pancreas, liver → organ transplantation may be needed
Surgery may be needed to promote normal bowel function, proper sinus drainage
Kegel exercises to strengthen pelvic floor muscles
Women: normal fertility rates if get adequate nutrition, have good lung function
Men: only 2–3% are fertile
Intracytoplasmic sperm injection to help partner conceive. Sperm extracted, used for in vitro fertilization
CF in pregnant women
Outcome of pregnancy for woman with CF depends heavily on respiratory health
Good lung function = less likely to experience preterm delivery
Lower than average weight gain during pregnancy
Nutritional supplementation often necessary
Higher risk of gestational diabetes
Therapeutic regimen might need to be changed
Some drugs may need to be discontinued until postpartum period
Promote effective breathing for the pt with CF
Teach patient to call primary care provider if pulmonary exacerbation occurs
Administer bronchodilators before beginning airway clearance techniques or administering inhaled mucolytics
Teach patient to use incentive spirometer
Administer pure O2 as prescribed
Promote effective breathing for the pt with CF
Teach patient to call primary care provider if pulmonary exacerbation occurs
Administer bronchodilators before beginning airway clearance techniques or administering inhaled mucolytics
Teach patient to use incentive spirometer
Administer pure O2 as prescribed
