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Chp 68- Respiratory failure & ARDS

Terms in this set (64)

Respiratory failure
results when one or both gas-exchanging functions are inadequate
-Insufficient O2 is transferred to the blood
OR
-Inadequate CO2 is removed from the lungs
Hypoxemia
-results from inadequate O2 transfer to the blood
-produces a decrease in arterial O2 (PaO2) and saturation (SaO2)
Hypercapnia
-results from inadequate CO2 removal from the lungs
-produces an increase in arterial CO2 (PaCO2)
Acute Respiratory Failure-Classifications
-Hypoxemic respiratory failure
-Hypercapnic Respiratory failure
Hypoxemic respiratory failure
-aka oxygenation failure
-commonly defined as a PaO2 less < 60 mmHg when the patient is receiving an inspired O2 concentration of 60% or more

*this PaO2 level indicates inadequate O2 saturation of hemoglobin
Hypercapnic Respiratory failure
-aka ventilatory failure b/c respiratory system is unable to remove sufficient CO2 to maintain a normal PaCO2

-commonly defined as PaCO2 > 45 mmHg in combo with academy (arterial pH <7.35)

*Indicates PaCo2 is higher than normal (45 mmhg) and body is unable to compensate (ph < 7.35)
Hypoxemic respiratory failure-Etiology
1. Mismatch between ventilation (V) and perfusion (Q)
2. Shunt
3. diffusion limitations
4. Alveolar hypoventilation
Mismatch between ventilation (V) and perfusion (Q)-Causes
1. Limit ventilation
-COPD
-Pneumonia
-Asthma
-Atelectasis
-Result of pain

2. Limit perfusion
-Pulmonary embolus
Shunt
occurs when blood exits the heart without having participated in gas exchange

-there are 2 types: anatomic and intrapulmonary

-these pt are oftentimes more hypoxic and require mechanical ventilation
Anatomic shunt
occurs when blood passes through an anatomic channel in the heart and bypasses the lungs
Intrapulmonary shunt
occurs when blood flows through the pulmonary capillaries without participating in gas exchange
Diffusion limitation
occurs when gas exchange across the alveolar-capillary interface is compromised by a process that thickens, damages, or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries

-classic sign: hypoxemia present during exercise
Diffusion limitation-causes
-Severe COPD
-Recurrent pulmonary emobli
-pulmonary fibrosis
-ARDS
-interstitial lung disease
Alveolar hypoventilation
is a generalized decrease in ventilation that results in an increase in the PaCO2 and a consequent decrease in PaO2
Alveolar hypoventilation-causes
-restrictive lung disease
-CNS disease
-Chest wall dysfunction
-neuromuscular disease
Hypercapnic Respiratory failure-explaination
-occurs when ventilatory demand exceeds ventilatory supply and PaCO2 cannot be sustained within normal limits

-normally, ventilatory supply outweighs ventilatory demand
Ventilatory supply
the maximum ventilation (gas flow in and out of lungs) that the patient can sustain without developing respiratory muscle fatigue
Ventilatory demand
the amount of ventilation needed to keep the PaCO2 within normal limits
Hypercapnic Respiratory failure-Etiology
1. abnormalities of the airways and alveoli
2. abnormalities of the CNS
3. abnormalities of the chest wall
4. neuromuscular conditions
Abnormalities of the airway and alveoli
Patients with asthma, COPD and cystic fibrosis are at high risk b/c these conditions result in airflow obstruction and air trapping

-leads to respiratory muscle fatigue and ventilatory failure
CNS abnormalities
can suppress the drive to breath. Brain won't respond to altered PaCO2

Problems: drug overdose, brainstem infarction, spinal cord injuries
Chest wall abnormalities
several conditions prevent normal movement of the chest wall and limit lung expansion

-flail chest
-rib fractures
-pain
-mechanical respiration
-muscle spasms
-kyphoscoliosis
-obesity
Neuromuscular conditions
-conditions may result in respiratory muscle weakness or paralysis therefore patients are unable to maintain normal PaCO2

-muscular dystrophy
-Guillain-Barré syndrome
-multiple sclerosis
-exposure to toxins
-muscle wasting
The major cause of respiratory failure..
is the lung's inability to meet the O2 needs of the tissues
What are the 2 main reasons lungs cannot meet tissue's O2 needs?
1. inadequate O2 delivery to tissues
2. tissues cannot use the O2 delivered to them (seen in septic shock)
Tissue O2 delivery is determined by...
-cardiac output
-amount of O2 carried in the hemoglobin
Respiratory failure-clinical manifestations
-can be sudden or gradual
-changes in mental status (restlessness, confusion, agitation, and combative behavior)
-rapid respiratory muscle fatigue
-acidemia
-tachycardia, tachypnea, and mild HTN (can be early signs
-severe morning headache
-cyanosis (late sign)
Consequences of hypoxemia & hypoxia
-metabolic acidosis
-cell death
-decreased cardiac output & BP
-impaired renal function
-possible permanent brain death
Respiratory failure-Specific Clinical manifestations
-rapid, shallow breathing pattern
-orthopnea
-tripod position
-dyspnea
-pursed-lip breathing
-retractions
-increase in I:E ratio (inspiratory to expiratory ratio)
Respiratory failure-diagnostic studies
-ABG analysis
-Chest xray: determines passable causes of respiratory failure
-CBC, sputum/blood cultures, electrolytes
-ECG
-Urinalysis
-V/Q lung scan
-pulmonary artery catheter
Respiratory failure-Therapeutic goals
1. normal ABG values
2. normal breath sounds (w/in baseline)
3. no dyspnea
4. independent maintenance of the airway
5. effective cough and ability to clear secretions
Respiratory failure-Components of respiratory therapy
1. Oxygen therapy
2. Mobilizations of secretions
3. Positive pressure ventilation
Oxygen therapy:
-delivery system should be tolerated by the patient
-needs to maintain PaO2 at 55-60mmHg or more and SaO2 at 90% or more at the lowest O2 concentration possible
Mobilization of secretions:
-Effective coughing and positioning
-Hydration and humidification
-Chest physiotherapy
-Airway suctioning
Effective coughing and positioning to mobilize the secretions:
-Augmented coughing
-Huff coughing
-Staged cough

-position the patient lateral or side-lying with good lung down
-upright position also effective
Hydration & humidification to mobilize the secretions:
-adequate fluid intake (2-3 L/day)
-IV hydration
-O2 via aerosol mask
Types of Positive pressure ventilation
-BiPAP
-CPAP

-most useful in managing chronic respiratory failure in patients with chest wall and neuromuscular disease
Respiratory failure-Drug therapy goals
1. relief of bronchospasm
2. reduction of airway inflammation
3. reduction of pulmonary congestion
4. drugs for infections
5. drugs to reduce severe anxiety, pain, and agitation
Drugs to relieve bronchospasm
-bronchodilators (SABAs: albuterol & metaproterenol)
Drugs to reduce airway inflammation
-corticosteroids (methylprednisolone)
Drugs to reduce pulmonary congestion
-diuretics (furosemide)
-nitrates
Drugs to treat pulmonary infections
-IV antibiotics (azithromycin or ceftriaxone)
Drugs to reduce severe anxiety, pain and agitation
-Benzodiazepines (lorazepam)
-opioids (morphine)
Medical supportive therapy goals:
maintain adequate CO and hemoglobin concentration
Respiratory Failure-Gerontologic considerations
-dec ventilatory capacity
-alveolar dilation
-larger air spaces
-loss of SA
-diminished elastic recoil
-decreased respiratory muscle strength
-dec chest wall compliance

-in older patients, the PaO2 falls further and the PaCO2 rises to a higher level before the respiratory system is stimulated to alter the rate and depth of breathing
A patient's ABG results include pH 7.31, Paco2 50 mm Hg, Pao2 51 mm Hg, and HCO3 24 mEq/L. Oxygen is administered at 2 L/min, and the patient is placed in high-Fowler's position. An hour later, the ABGs are repeated with results of pH 7.36, Paco2 40 mm Hg, Pao2 60 mm Hg, and HCO3 24 mEq/L. What is most important for the nurse to do?

a. Increase the oxygen flow rate to 4 L/min.

b. Document the findings in the patient's record.

c. Reposition the patient in a semi-Fowler's position.

d. Prepare the patient for endotracheal intubation and mechanical ventilation.
a. Increase the oxygen flow rate to 4 L/min.
A patient with severe chronic lung disease is hospitalized with respiratory distress. Which finding would suggest to the nurse that the patient has developed rapid decompensation?

a. An Spo2 of 86%

b. A blood pH of 7.33

c. Agitation or confusion

d. Paco2 increases from 48 to 55 mm Hg
c. Agitation or confusion
Which patient is at highest risk for hypoxemic respiratory failure?

a. A patient who has respiratory muscle paralysis

b. A patient who has fractured ribs and a flail chest

c. A patient who has a massive pulmonary embolism

d. A patient who has slow breathing from a drug overdose
c. A patient who has a massive pulmonary embolism
Acute Respiratory Distress Syndrome (ARDS)
-Sudden progressive form of acute respiratory failure in which the alveolar-capillary interface becomes damaged and more permeable to intravascular fluid-->alveoli fill with fluid

-diagnosed when PaO2/FiO2 (P/F) ratio is less than 200
Acute Respiratory Distress Syndrome (ARDS)-Etiology
-sepsis
-multiple organ dysfunction syndrome (MODS)

-thought to be caused by stimulation of the inflammatory and immune systems (neutrophils attracted and release mediators)
Pathophysiologic changes in ARDs is divided into 3 phases:
1. injury or exudative phase
2. reparative or proliferative phase
3. fibrotic phase
ARDS-injury or exudative phase
-occurs approximately 1-7 days after the initial direct lung injury or host insult
-primary change: interstitial and alveolar edema and atelectasis
ARDS-reparative or proliferative phase
-begins to 1-2 weeks after the initial lung injury -phase is complete when the diseased lung is dense and fibrous
-hypoxia worsens
-if proliferative phase persists, widespread fibrosis results
ARDS-fibrotic phase
-occurs 2-3 weeks after initial lung injury-->survival chances are poor at this point
-lung is completely remodeled by sparsely collagenous and fibrous tissues

-characteristics: decreased lung compliance, decreased SA, continued hypoxemia, pulmonary HTN
ARDS-early clinical manifestations
-dyspnea, tachypnea, cough, restlessness
-fine, scattered crackles
-ABGs indicates mild hypoxemia & respiratory alkalosis
-Inc WOB
-Inc Respiratory rate
-Dec Tidal Volume
ARDS-late clinical manifestations
-worsened symptoms with progression of fluid accumulation and decreased lung compliance
-diffuse crackles and rhonchi
-tachycardia, diaphoresis
-changes in mental status
-cyanosis
-pallor
-hypoxemia and a PaO2/FiO2 (P/F) ratio <200 despite increased FiO2
-chest xray (white lung or whiteout)
ARDS-complication
-Ventilator-associated pneumonia
-Barotrauma (rupture of over distended alveoli during mechanical ventilation)
-Volutrauma (alveolar fracture and movements of fluids and proteins into alveolar spaces)
-high risk for stress ulcers
-renal failure (monitor I &O)
ARDS-Therapeutic goals
-PaO2 within normal limits or at baseline
-SaO2 > 90%
-patent airway
-clear lungs on auscultation
ARDS-Components of Respiratory Therapy
-Oxygen
-Mechanical ventilation (PEEP at 5)
-Positioning strategies (prone position)
Mechanical ventilation
-higher levels of PEEP are often needed to maintain PaO2 at 60 mmhg
-high levels of PEEP can compromise venous return (causes dec preload, CO, and BP)
-high peep can result in barotrauma and volutrauma
Risk for O2 toxicity occurs:
-FIo2 exceeds 60% for > 48 hrs
When assessing a patient with sepsis, which finding would alert the nurse to the onset of acute respiratory distress syndrome (ARDS)?

a. Spo2 of 80%

b. Use of accessory muscles of respiration

c. Fine, scattered crackles on auscultation of the chest

d.ABGs of pH 7.33, Paco2 48 mm Hg, and Pao2 80 mm Hg
c. Fine, scattered crackles on auscultation of the chest
A patient with severe chronic lung disease is hospitalized with respiratory distress. Which finding would suggest to the nurse that the patient has developed rapid decompensation?

a. An Spo2 of 86%

b. A blood pH of 7.33

c. Agitation or confusion

d. Paco2 increases from 48 to 55 mm Hg
c. Agitation or confusion
Indications for mechanical respiration
-hypoxemia: paO2 ≤ 60 mmhg on fiO2 > 0.50
-hypercapnia: PCO2 ≥50 w/ pH ≤ 7.25

progression deterioration:
-increasing RR
-decreasing Vt (tidal volume)
-Increase WOB
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