NURSING 265 Adv MedSurg Exam2-1 Questions with Answers
CARE OF PATIENTS WITH COMPLEX RESPIRATORY PROBLEMS
Structures of the lungs
- Trachea,
... [Show More] left/right bronchus, segmental bronchus, subsegmental bronchus, alveoli
- Visceral pleura/parietal pleura lubrication
- Right side of lung (3 lobes)
o Usually aspirate on this side r/t longer/straighter airway Gas Exchange Structures
- Bronchiole, terminal bronchiole, respiratory bronchioles, alveoli The Alveoli
- Have about 290 million
- Type 2 pneumocytes secrete surfactant (fatty protein) to keep the alveoli open and keep fluid away from alveoli
Gas Exchange
- Breath O2 in O2 goes into blood stream CO2 releases from blood stream blow CO2 out COPD: effect on lungs
- Healthy alveoli expand and contract giving adequate perfusion
- COPD alveoli have lost elasticity and rely on the impulse from the brain when the CO2 in their blood is too high causing their drive to breath to happen automatically (like kussmaul respirations)
o COPD consists of Emphysema and Chronic Bronchitis
▪ Causing bronchial spasms and dyspnea Bronchitis and Emphysema
- Chronic Bronchitis
o Caused by smoking, characterized by inflammation and structural changes
o Causes excessive secretions (mucous plug)
- Emphysema
o Elastic fibers destroyed leading to hyperinflation
Acute Respiratory Failure
- Progressive or sudden
- Deterioration of gas exchange function in the lungs
o Hypoxemia – PaO2 of less than 50 mmHg (normal 80-100)
o Hypercapnia – PaCO2 greater than 50 mmHg
▪ Decreased LOC if this happens call the Doc to get blood gas
o Acidosis – pH less than 7.35 (normal 7.35 – 7.45)
- Ventilatory failure – Can’t get O2 in
o Asthma, sleep apnea, myasthemia gravis
- Oxygen failure – O2 getting in but it isn’t getting picked up
o Pneumonia, ARDS, PE, shock
CORRECT
respiratory excursion. Clients with cervical and thoracic spinal cord injuries are at high risk for respiratory failure because spinal nerves that affect intercostal muscles are affected. Opiates, which can depress the brainstem, present risk factors for respiratory failure. All of these clients should be monitored closely for respiratory failure. Cocaine is a stimulant, which would not cause respiratory failure unless a stroke ensued.
CORRECT
• Client with acute pancreatitis
Pressure on the brainstem may depress respiratory function. Acute pancreatitis is a risk factor for acute respiratory distress syndrome; abdominal distention also ensues, which can limit respiratory excursion. Clients with cervical and thoracic spinal cord injuries are at high risk for respiratory failure because spinal nerves that affect intercostal muscles are affected. Opiates, which can depress the brainstem, present risk factors for respiratory failure. All of these clients should be monitored closely for respiratory failure. Cocaine is a stimulant, which would not cause respiratory failure unless a stroke ensued.
CORRECT
• Client with a T3 spinal cord injury
Pressure on the brainstem may depress respiratory function. Acute pancreatitis is a risk factor for acute respiratory distress syndrome; abdominal distention also ensues, which can limit respiratory excursion. Clients with cervical and thoracic spinal cord injuries are at high risk for respiratory failure because spinal nerves that affect intercostal muscles are affected. Opiates, which can depress the brainstem, present risk factors for respiratory failure. All of these clients should be monitored closely for respiratory failure. Cocaine is a stimulant, which would not cause respiratory failure unless a stroke ensued.
CORRECT
• Client using patient-controlled analgesia
Pressure on the brainstem may depress respiratory function. Acute pancreatitis is a risk factor for acute respiratory distress syndrome; abdominal distention also ensues, which can limit respiratory excursion. Clients with cervical and thoracic spinal cord injuries are at high risk for respiratory failure because spinal nerves that affect intercostal muscles are affected. Opiates, which can depress the brainstem, present risk factors for respiratory failure. All of these clients should be monitored closely for respiratory failure. Cocaine is a stimulant, which would not cause respiratory failure unless a stroke ensued.
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Blood Gas Values
- pH = 7.35 – 7.45, pCO2 = 35 – 45 (respiratory), HCO3 = 22 – 28 (metabolic)
- Increased CO2 = acid build-up, acidosis; Increased HCO3 = alkaline build-up, alkalosis
- ROME (Respiratory Opposite, Metabolic Equal) Pathophysiology of Respiration
- Occurs at the alveolar capillary units exchange of oxygen and carbon dioxide oxygen attaches to the circulating hemoglobin molecules 2 processes occur, ventilation and perfusion
- V/Q scan measures how well the alveoli are being ventilated and perfused
o Radioactive dye used to find PE
o Ventilation – perfusion mismatch = PE Causes of Acute Respiratory Failure
- Decreased respiratory drive (narcotics, COPD w/ too much O2)
- Obstruction of the airways (Bronchitis, sleep apnea, asthma)
- Trauma (Injury to the lung tissue or chest wall)
- Dysfunction of the chest wall (spinal cord injury, any condition that affects breathing)
- Disorders (sleep apnea, PE, overdose of opiods/alcohol) Clinical Manifestations of Acute Respiratory Failure
- Early: Impaired O2 (give O2), restlessness, fatigue (promote rest), headache, dyspnea, air hunger, tachycardia, increased BP
o Use interventions
- Progressive: Confusion, lethargy, tachycardia, tachypnea, central cyanosis, diaphoresis, respiratory arrest
o Call rapid response
- Intervention Rapid response ICU Medical Management
- Increased oxygenation, intubation, mechanical ventilation, ICU, bronchodilators, antibiotics, anti- inflammatories
Nursing Management
- Anticipate and assist with intubation
- Monitor (assess): LOC, RR, O2, ABGs continuous pulse oximetry
- Prevent ventilator associated pneumonia
Acute Respiratory Distress Syndrome (ARDS)
- Severe form of acute lung injury, usually results in death
- Starts with Acute Respiratory Failure sudden, progressive pulmonary edema with increasing bilateral infiltrates in lungs
- Refractory hypoxemia – giving pt 100% FiO2 but it isn’t making a difference in O2 stat
- Reduced lung compliance
Causes of Acute Respiratory Distress Syndrome (ARDS)
- Aspiration – acid destroys alveoli/surfactant leads to inflammation
- Drug ingestion and overdose
- Hematologic disorders (DIC massive transfusions)
o TRALI – Transfusion related acute lung injury
- Prolonged inhalation of smoke or corrosive substances, near drowning
- Infection (pneumonia)
- Metabolic disorders
- Shock, trauma, major surgery Clinical Manifestations
- Rapid onset of severe dyspnea
- Arterial hypoxemia
o ABG’s show respiratory acidosis
- Bilateral infiltrates in lungs white out on x-ray
- Intercostal retractions
- Persistent, severe hypoxemia
- Increased alveolar dead space Alveoli collapsed (Atelectasis)
- Hallmark sign refractory hypoxemia 100% O2 no change on ABGs
Medical Management
- Intubation ALWAYS!
o Aggressive supportive care
o If pt declines intubation give Bipap
- Mechanical ventilation
o PEEP – Positive End Expiratory Pressure
▪ Pushes air in to open up alveoli, helps push fluid out of alveoli
▪ Watch for pneumothorax (too much pressure can push air into chest wall causing air to push up against your lungs causing a collapsed lung)
o Prone position (on stomach) to improve ventilation perfusion
- Circulatory support
o Adequate fluid volume
▪ Fluid and diuretics to maintain proper fluid volume
- Nutritional support
o 35-45 kcal/kg per day
o Enteral feeding feeding through gut keeps everything working so you don’t have peristalsis
Pharmacologic Therapy
- Pulmonary specific vasodilators (Nitric Oxide)
- Corticosteroids (to decrease inflammation)
- Anti-inflammatories, Antibiotics
- Surfactant replacement (replace type 2 pneumocytes) Understanding Acute Respiratory Distress Syndrome (ARDS)
- Starts with lung injury
o Antibiotics, anti- inflammatory agents
- Release of vasoactive substances (lungs fill up with fluid)
- Increased permeability of alveoli
- Fluid and protein move into alveoli
o Crackles, dyspnea, tachypnea, hypoxemia r/t fluid build up, possible mechanical ventilation
- Altered ventilation, perfusion
o Use prone position
- Early on CO2 may be in normal range until fluid builds up, O2 goes down early
- Damage to alveolar epithelium
o Causes hemoptysis (coughing up blood)
- Decreased surfactant production
o Decreases compliance of lungs, may need to administer surfactant
- Atelectasis occurs (collapse of alveoli)
o Mechanical ventilation with PEEP (keeps alveoli open, pushes fluid out of alveoli)
- Eventually scarring occurs with loss of functional lung tissue once fibrotic highland membrane is formed, lung damage is permanent
- Interdisciplinary team for this pt consists of social work, resp therapist, pulmonologist, palliative care, dietary
Pulmonary Hypertension
- Can lead to right sided HF Cor Pulmonale
- Increased blood pressure and vasoconstriction in the pulmonary vasculature
- May be arterial, venous, hypoxic, or thromboembolic
- Causes: lung disease, obesity, sleep apnea, narcosis
- Leads to non-ischemic hypertensive cardiomyopathy and right-sided heart failure
Clinical Manifestations
- Signs of right-sided heart failure (Cor Pulmonale)
o SOB (especially with exertion), chest pain, JVD, peripheral edema
- Decreased O2 saturation
- Loud S2 heart sound
Medical Management
- Oxygen, vasodilators, diuretics for edema
- HTN control
o ACE inhibitors, Calcium Channel Blockers
- DVT prophylaxis
- Pain management
- Treat the underlying problem Nursing Management
- Monitor VS every 4 hours, and EKG
- I+O to prevent Cor Pulmonale
- Pain assessment
- Monitor electrolyte levels
- Titration of critical care infusions
- Activity, allow for rest periods, cluster care if possible
Cor Pulmonale
- Pulmonary heart disease
- Originates in the lungs and eventually damages the right side of heart from increased pressure
- Acute – rapid dilation of right ventricle; caused by too much right ventricular stretch
- Chronic – progressive; results in right ventricular hypertrophy
- Can lead to left sided heart failure and death
Causes:
- COPD – Most common
- Deformities of thoracic cage
- Injuries to chest wall; tissue damage
- Chemical agents
- Massive obesity
- PE
- Disorders in the nervous system, respiratory muscles, chest wall, and pulmonary tree Clinical Manifestations
- Peripheral edema, JVD, enlarged liver, ascites, pleural effusion (buildup of fluid between the tissues that line the lungs and the chest), cough, SOB, wheezing, crackles, heart murmurs, fatigue, headache, confusion, Ruddy (greyish/reddish, blotchy skin r/t hypoxemia)
Medical Management
- Treat underlying cause (Supplemental O2, Intubation if necessary, sodium restriction, diuretic therapy, bed rest to promote diuresis)
Pharmacologic Therapy
- Nitrates, diuretics, digitalis, bronchodilators, calcium channel blockers, anticoagulants, inotropes (dobutamine, dopamine, digitalis)
Nursing management
- Client teaching, fluid balance, daily weights, edema, nutrition, sodium restrictions, diuretics, smoking cessation
Pulmonary Embolism (PE) Respiratory Alkalosis
- Thrombus, air, fat (from breaking femur), amniotic fluid
- Clot travels into pulmonary circulation
- Complete or partial obstruction of pulmonary blood vessels
- Increased risk with:
o Prolonged bed rest, after surgery, smokers, cancer (r/t immobilization, meds), venous stasis (make sure pt wearing TED hose, possible SubQ Heparin, do ROM exercises), A fib (blood just sitting in the atrium), obesity
- Potentially lethal, depends on amount of occlusion and location
Clinical Manifestations
- Dyspnea, tachypnea, Sudden SOB, cough, (inspiratory)chest pain, anxiety, petechiae (across chest and upper body), fever, diaphoresis, syncope, hemoptysis (coughing up blood, indicates alveolar damage), crackles, tachycardia, (hypotension dizziness and fainting) low CO2
o If pt has JVD, syncope, cyanosis, and hypotension or dyspnea and chest pain call rapid responses, elevate HOB, and put on O2
o It is important to remember that many pts with PE do not have the “classic”
manifestations but instead have vague symptoms resembling the flu, such as nausea, vomiting, and general malaise.
Diagnostic Tests for PE:
- Ct scan and ABGs
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- V/Q scan (for definite diagnosis)
o Radioactive compound inhaled into airspace of lung (normal lung distributes equally)
o Radioactive compound injected into vein. Travels to lung tissues in blood vessels
▪ If there is a clot in an artery the dye will stop short of the end of the artery
o Mismatch of inhaled and injected compounds on the lung scan images = PE
- D-dimer (tells you if pt has any blood clots, but not specific to PE) Prevention is KEY! [Show Less]