NU 454 Acute Respiratory
What are the steps in the gas exchange process?
Ventilation – breathing in O2
Diffusion – O2/Co2 exchange
Transfer of gases in the circulation
Diffusion between systemic capillary bed and body tissue cells
What are the normal values of ABG labs?
pH = 7.35-7.45
PaO2 = 80-100
PaCO2 = 35-45
HCO3 = 22-26
SaO2 = 95-100% (don’t get confused with PaO2)
Our physiological goal in life is to maintain a normal pH. Cells don’t work as well when pH is out of whack. The two organs that control and maintain our pH are the lungs and the kidneys.
The most important blood gas to look at first is paO2.
What are the four steps in evaluating ABGs?
1. Evaluate each number. Does it indicate acidity or alkalinity?
2. Check the pH to determinie the cause of the imbalance. If it’s above 7.45 the cause is alkalosis; below 7.35, it’s acidosis. If the pH is normal but the PaCO2 or HCO3 indicate an imbalance, use 7.40 as your cutoff point.
3. Find the value that matches the acid-base status of the pH. If the PaCO2 matches, the problem is respiratory; if the HCO3 matches, it’s metabolic.
4. Determine the value the extent of compensation as follows:
Absent – the value that doesn’t match the acid-base status of the pH is normal.
Partial – both the value that doesn’t match the acid-base status of the pH and the Ph itself are above or below normal.
Complete – the value that doesn’t match the acid-base status of the pH is above or below normal, but the pH is normal.
What are the basic principles of treatment for acidosis and alkalosis?
Respiratory acidosis: Most common cause would be that the pt isn’t breathing fast enough. Need to increase rate of respirations. Could ventilate them or just get them to breath more. Typically, the best way to treat a respiratory problem is through the respiratory system.
Respiratory alkalosis: Typically, breathing too fast. Blowing CO2 off to fast. Must slow the rate down. Maybe give anti-anxiety drugs if that’s the problem.
Metabolic acidosis: Give them sodium bicarb. It’s the choice for metabolic acidosis.
Metabolic alkalosis: treated by giving fluids. Going to take a while. Typically, renal pts have this problem.
What are the characteristics of artificial airways?
◦Advantages – use for semi-coma pts, opens airway, gives guide for suction
◦Disadvantages – must be right size, can get lodged in airway
◦Advantages – can suction w/o heavy trauma
◦Used if patient requires ETT for long period of time
◦More comfy than ETT
◦Also bypass dead space from mouth to trach.
What is the nurse's role in endotracheal intubation?
Administer meds – usually anti-anxiety
Ensure adequate oxygenation
Document: Measure and chart where it is @ lip line.
What management principles should a nurse implement when caring for a patient who is intubated?
Maintain correct tube placement
- ◦Monitor exit mark
- ◦Be sure tape is secure
- ◦Emergency intervention if comes out. Have ambu bag and mask in the room just in case.
Maintain proper cuff inflation
- ◦Keep cuff pressure below 20-25 mm Hg
- ◦Measure and record every 8 hours
- ◦Too much causes necrosis; too little allows air to escape.
Maintain and monitor ventilator and oxygenation
- ◦Pulse oximeter
- ◦Clinical assessment: Nurse the pt, not the vent
Maintain tube patency by suctioning
- ◦Performed as needed
- No longer than 10 seconds
- Ambu with 100% FIO2 prior too and after
- ◦Attempt to get patient to cough first
- ◦Assess lungs before and after suctioning
- Mucosal damage- more so w/ nasal and oral suction
- Change in BP
- Raises ICP
- Don’t use saline
Mouth care and tube repositioning
- ◦Oral ETT change every shift (minimum every 24 hrs)
- ◦Mouth care every 4 hours
- ◦Oral suctioning frequently
- ◦Nasal – should not extend out of nose by more than 1 ½ to 2 inches
What are some complications of endotracheal intubation?
Injury to pharynx, larynx, and trachea
Nasal or oral pressure sores
Accidental extubation: Use soft restraints, anti-anxiety/pain meds, other comfort measures.
What are the two types of mechnical ventilation available? What ventilator modes do we use for different patients?
Negative Pressure – device surrounds the body allowing a negative pressure to be created which causes the lungs to expand for inspiration. Expiration is passive.
Positive Pressure - Pushes air into the lungs allowing for passive exhalation. These are the type we see in most health-care settings.
Controlled Mechanical Ventilation (CMV) – a set number of breaths is delivered at regular intervals regardless of patients effort. Every breath is controlled by vent, same TV.
Assist-Control Mechanical Ventilation (AC) – same as CMV, but if patient attempts to breath, it will ventilate him at that time also. Patient's own breaths are used, but also ventilated with same TV.
Synchronized Intermittent Mandatory Ventilation (SIMV) – delivers preset rate and depth, but patient can breath on their own in between vent breaths w/o assistance. Patient's own breaths are not ventilated, have different TV than vent.
Positive-End Expiratory Pressure (PEEP) – positive pressure is applied at end expiration. PEEP helps keep the alveoli open; therefore, helps oxygen diffusion into the blood. Can help raise paO2. Also helps prevent the airway from collapsing and atelectasis. Complications of PEEP is bursting of the alveoli, decreases venous return which affects BP and CO. May make a patient hemodynamically unstable. Want to check BP when the doc orders PEEP on a pt.
Pressure Support – positive pressure is applied during inhalation
Continuous Positive Airway Pressure (CPAP) – the use of PEEP in a spontaneously breathing patient. If placed on CPAP, monitor closely for respiratory rate and effort
What should a nurse document about a ventilator?
What are some complications of mechanical ventilation?
Cardiovascular – increase pressure in the thoracic cavity resulting in decreased preload, CO, and BP
Sodium and Water Balance – fluid retention occurs within about 48-72 hours after ventilation due to drop in CO and less insensible loss (humidified air)
Nutrition – feed the gut
High Pressure Vents – assess for SQ emphysema
- ◦Barotauma – due to volume and Peep
- ◦Aveolar hypoventilation usually due to inadequate settings or pulmonary plugs
- ◦Aveolar hyperventilation usually due to inadequate setting or patient is on SIMV
- ◦Ventilator associated
- Keep HOB elevate
- Oral Care a minimum of every 4 hours
- Oral suctioning frequently
- No use of saline to liquefy secretions
What would cause the ventilator alarms to sound?
Increased inspiratory pressure/increased pressure limit (sudden increase vs. gradual increase)
Low exhaled volume
What are some factors that maintain breathing regularity?
Coordination and Maturity of CNS
Stability of chest wall
What are the characteristics of transpulmonary pressure?
Is defined as the difference between alveolar and pleura pressure.
TP is at it’s minimum during end expiration (greatest risk for lung to collapse)
What are the characteristics of acute respiratory failure?
Results from inadequate gas exchange
Insufficient O2 transferred to the blood - Hypoxemia
Inadequate CO2 removal - Hypercapnia
Not a disease but a condition
Result of one or more diseases involving the lungs or other body systems
- Hypoxemic respiratory failure (oxygenation failure): PaO2 less than or equal to 60 mm Hg on 60% O2
- Hypercapnic respiratory failure (ventilatory failure): PaCO2 greater than 45 mm Hg and pH less than 7.35
Range of V/Q relationships:
1) Absolute shunt - A substance (for example, secretions) block all oxygen supply from reaching the alveoli and diffusing into the bloodstream
2) V/Q mismatch, airway - secretions or a mucus plug in the airway limits oxygenation into the alveoli. Not all, but some.
3) Normal unit has no blockage from respiratory or circulatory end. Diffusion of gases occurs without hindrance.
4) V/Q mismatch, circulation - And emboli or clot has blocked some of the blood supply from reaching the alveoli in order to receive oxygen from the lungs.
5) Dead space, no perfusion - For some reason (emboli, clot, HF, MI, etc.) blood circulation is completely halted/cut off from alveoli.
Major threat is the inability of the lungs to meet the oxygen demands of the tissues
What are some causes of a hypoxemic respiratory failure?
- Pulmonary embolus
- Severe emphysema
- Pulmonary fibrosis
- Hypoxemia present during exercise
- Restrictive lung disease
- CNS disease
- Chest wall dysfunction
- Neuromuscular disease
What causes hypercapnic respiratory failure?
Imbalance between ventilatory supply (max ventilation that the patient can sustain without developing respiratory muscle fatigue) and demand (amount of ventilation needed to keep the PaCO2 w/i normal limits).
Airways and alveoli
- Chronic bronchitis
- Cystic fibrosis
Central nervous system
- Drug overdose
- Brainstem infarction
- Spinal cord injuries
- Flail chest
- Mechanical restriction
- Muscle spasm
- Muscular dystrophy
- Multiple sclerosis
What are the clinical manifestations of respiratory failure?
Sudden or gradual onset
A sudden decrease in PaO2 or rapid increase in PaCO2 indicates a serious condition
When compensatory mechanisms fail, respiratory failure occurs
Signs may be specific or nonspecific
Rapid, shallow breathing pattern
Severe morning headache
Change in I:E ratio
Cyanosis - Late sign
Tachycardia and mild hypertension - Early signs
Consequences of hypoxemia and hypoxia
- Metabolic acidosis and cell death
- Decreased cardiac output
- Impaired renal function
What are some diagnostic studies we can perform when suspecting respiratory failure?
History and physical assessment
CBC, sputum/blood cultures, electrolytes
V/Q lung scan
Pulmonary artery catheter (severe cases)
What are some overall goals for a client in acute respiratory failure?
ABG values within patient’s baseline
Breath sounds within patient’s baseline
No dyspnea or breathing patterns within patient’s baseline
Effective cough and ability to clear secretions
How should a nurse aim to prevent respiratory failure?
Thorough history and physical assessment to identify at-risk patients
Early recognition of respiratory distress
What are some guidelines for respiratory therapy of a client in acute respiratory failure?
Oxygen therapy: Delivery system should
- Be tolerated by the patient
- Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible
Mobilization of secretions
- Hydration and humidification
- Chest physical therapy
- Airway suctioning
- Effective coughing and positioning
Positive pressure ventilation (PPV)
- BiPAP-delivers a high pressure during inhalation and a low pressure during exhalation
- CPAP-continuous pressure
What drug therapy should be considered for specific symptoms of acute respiratory failure?
Bronchodilators - Relief of bronchospasm
Corticosteroids - Reduction of airway inflammation
Diuretics, nitrates if heart failure present - Reduction of pulmonary congestion
Pulmonary infections - IV antibiotics
Reduction of severe anxiety, pain, and agitation - benzodiazepines and narcotics
Why is nutritional therapy considered for a client in acute respiratory failure?
Maintain protein and energy stores
Enteral or parenteral nutrition
What are the overall goals when treating acute respiratory failure?
Treat the underlying cause
Maintain adequate cardiac output and hemoglobin concentration
What are some gerontologic considerations in regards to acute respiratory failure?
Physiologic aging results in
- ↓ Ventilatory capacity
- Alveolar dilation
- Larger air spaces
- Loss of surface area
- Diminished elastic recoil
- Decreased respiratory muscle strength
- ↓ Chest wall compliance
Poor nutritional status
Less available physiologic reserve
- Autonomic nervous system
What are the characteristics of acute respiratory distress syndrome (ARDS)?
Sudden progressive form of acute respiratory failure
Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid
Alveoli fill with fluid
- Severe dyspnea
- Decreased lung compliance
- Diffuse pulmonary infiltrates
- 150,000 cases annually
- 50% mortality rate
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 and immune systems
Neutrophils are attracted and release mediators producing changes in lungs
- ↑ Pulmonary capillary membrane permeability
- Destruction of elastin and collagen
- Formation of pulmonary microemboli
- Pulmonary artery vasoconstriction
How does the injury/exudative phase of ARDS progress?
Injury or exudative phase:
1 to 7 days after direct lung injury or host insult
Neutrophils adhere to pulmonary microcirculation
Damage to vascular endothelium
↑ Capillary permeability
Engorgement of peribronchial and perivascular interstitial space
Fluid crosses into alveolar space
Intrapulmonary shunt develops as alveoli fill with fluid and blood passing through cannot be oxygenated
Alveolar cells type 1 and 2 are damaged
Surfactant dysfunction → atelectasis
Hyaline membranes line alveoli
Contribute to atelectasis and fibrosis
Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia
Unresponsive to increasing O2 concentrations
Lungs become less compliant
Increased airway pressures must be generated
↑ Work on Breathing
↓ Tidal volume
Produces respiratory alkalosis from increase in CO2 removal
Interstitial and alveolar edema (noncardiogenic pulmonary edema)
Atelectasis resulting in V/Q mismatch
Shunting of pulmonary capillary blood
Hypoxemia unresponsive to increasing concentrations of O2 (refractory hypoxemia)
How does the reparative or proliferative phase of ARDS progress?
Reparative or proliferative phase
1 to 2 weeks after initial lung injury
Influx or neutrophils, monocytes, and lymphocytes
Lung becomes dense and fibrous
Lung compliance continues to ↓
Thickened alveolar membrane
Diffusion limitation and shunting
If reparative phase persists, widespread fibrosis results
If phase is arrested, lesions resolve
How does the fibrotic or chronic phase of ARDS progress? What is the prognosis of ARDS?
2 to 3 weeks after initial lung injury
Lung is completely remodeled by sparsely collagenous and fibrous tissues
↓ Lung compliance
↓ Area for gas exchange
Results from pulmonary vascular destruction and fibrosis
Some persons survive acute phase of lung injury:
Pulmonary edema resolves
Survival chances are poor for those who enter the fibrotic phase. These clients require long-term mechanical ventilation.
What are the clinical manifestations of ARDS?
Dyspnea, tachypnea, cough, restlessness
Chest auscultation may be normal or reveal fine, scattered crackles
ABGs - Mild hypoxemia and respiratory alkalosis caused by hyperventilation
Chest x-ray may be normal or show minimal scattered interstitial infiltrates. Edema may not show until 30% increase in lung fluid content
Symptoms worsen with progression of fluid accumulation and decreased lung compliance
Pulmonary function tests reveal decreased compliance and lung volume
Evident discomfort and increased work of breathing (WOB)
Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor
Hypoxemia and a low PaO2 despite increased FIO2
As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation
Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs
If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue
What should a nurse look for in a thorough assessment of an ARDS patient?
History of lung disease
Exposures to lung toxins
Spinal cord trauma
Use of O2, inhalers, nebulizers, immunosuppressant therapy
Recent major surgeries
Dyspnea, wheezing, cough, sputum, palpitations, swollen feet
Changes in sleep pattern
Pale, cool, clammy or warm, flushed skin
Use of accessory muscles
Shallow breathing with increased respiratory rate
Tachycardia progressing to bradycardia
Extra heart sounds
Abnormal breath sounds
Hypertension progressing to hypotension
Abdominal distention, ascites
Somnolence, confusion, delirium
Changes in pH, PaCO2, PaO2, SaO2
Decreased tidal volume, FVC
May have a normal pulmonary artery wedge pressure (noncardiogenic pulmonary edema)
What respiratory therapy should be implemented with an ARDS patient?
- High flow systems used to maximize O2 delivery
- SaO2 continuously monitored
- Give lowest concentration that
results in PaO2 60 mm Hg or greater
- Risk for O2 tox increases when FiO2 exceeds 60% for more than 48 hrs.
- Will commonly need intubation because the PaO2 cannot be maintained at acceptable levels.
- PEEP at 5 cm H2O, opens collapsed alveoli
- Higher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater
- High levels of PEEP can compromise venous return, decrease preload, CO, and BP
- Alternative modes of mechanical ventilation if hypoxemia persists. e.g. pressure support ventilation
- Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone. Predisposes to atelectasis
- Turn from supine to prone position. May be sufficient to reduce inspired O2 or PEEP
- Fluid pools in dependent regions of lung
- Continuous lateral rotation therapy
- Proning typically reserved for refractory hypoxemia not responding to other therapies. Plan for immediate repositioning for cardiopulmonary resuscitation
What are some complications of ARDS treatment?
Hospital-acquired pneumonia: Strategies for prevention include strict infection control measures and elevation of HOB 45 degrees or more to prevent aspiration.
Barotrauma: rupture of over-distended alveoli during mechanical ventilation. Avoid by ventilating with smaller tidal volumes.
Volu-pressure trauma: Occurs when large tidal volumes are used to ventilate non-compliant lungs. Causes alveolar fractures and movement of fluids and proteins into alveolar spaces. Avoid by using smaller tidal volumes or pressure ventilation.
High risk for stress ulcers: Bleeding from stress ulcers occurs in 30% of pts with ARDS on mechanical ventilation. Manage by correction of predisposing conditions, prophylactic antiulcer agents, and early initiation of enteral nutrition.
Renal failure: occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia. May also be caused by nephrotoxic drugs used for infection associated with ARDS.
What are the principles of medical supportive therapy for ARDS patients?
Maintenance of cardiac output and tissue perfusion
- Continuous hemodynamic monitoring
- Continuous BP measurement via arterial catheter
Pulmonary artery catheter to monitor pulmonary artery pressure, pulmonary artery wedge pressures, and CO
- Administration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls
Use of inotropic drugs may be necessary (Dobutrex)
Hemoglobin usually kept at levels
greater than 9 or 10 with
Maintenance of fluid balance
May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEP
Monitor PAWP, daily weights, and I&Os to assess fluid status
What are some overall goals for an ARDS patient?
PaO2 within normal limits or at baseline
SaO2 > 90%
Clear lungs or auscultation
No abnormal breath sounds
Effective cough and expectoration
Normal respiratory rate, rhythm, and depth
Synchronous thoracoabdominal movement
Appropriate use of accessory muscles
Decreased or absent peripheral edema
Normal pulmonary artery or pulmonary artery wedge pressures
Verbalization of positive attitude toward outcome
PaO2 and PaCO2 within normal ranges or at baseline
Maintenance of weight or weight gain
Serum albumin and protein within normal ranges
What are the characteristics of severe ARDS?
Acute respiratory infection caused by coronavirus (CoV)
Spreads by close contact
Maybe spread via air
- Sore throat
- Antiviral medications
- Antibiotics (some also have bacterial infections)
Start to recover after 6-7 days of treatment
10-20% will develop respiratory failure
What are the characteristics of Middle East Respiratory Syndrome (MERS)?
Originated in Saudi Arabia
Over 600 cases worldwide
Healthcare workers vulnerable
Flulike symptoms: pneumonia, breathing problems and in sever cases, kidney failure and death
Not sure how transmitted: cough droplets, airborne, or surfaces