Chapter 68: Respiratory Failure and ARDS

Question 1

Not a disease but a sx or an underlying pathology (bacterial, toxins..). Occurs when O2 and/or CO2 cannot be exchanged adequately. Hypoxemia- low O2 in blood. Decreased PaO2 (want 80-100), SaO2 (Hgb saturation).
Hypercapnea- increase PaCO2.
Very important to assess clinical findings int he context of the pt’s baseline.

Answer 1

Acute Respiratory Failure

Question 2

Oxygenation failure b/c of inadequate oxygen transfer between the alveoli and the pulmonary capillary bed; defined by PaO2

Answer 2

Hypoxemia respiratory failure

Question 3

Ventilatory failure b/c the primary problem is inadequate removal of CO2; defined by PaCO2 >45 and pH

Answer 3

Hypercapnic respiratory failure.

Question 4

______ ____ only tells us about oxygenation and not about ventilation- this means you need an ABG

Answer 4

Pulse oximetry

Question 5

_____ worse because no bicarb to kick in to counterbalance acidic factor of CO2

Answer 5

Acute

Question 6

PaO2

Answer 6

Hypoexmic (Oxygenation) Failure

Question 7

Causes of Hypoxemic (oxygenation failure)

Answer 7

Ventilation perfusion mismatch (V/Q mismatch): occurs when the volume of blood perfusing the lungs is not the same as the amount of gas in the alveoli or vice versa. Increased secretions, atelectasis, PE. Tx: oxygen, treat the cause
Shunt: Blood exits the heart without having gas exchange (extreme VQ mismatch). 2 types- blood bypasses the lungs or when blood passes through the pulmonary capillaries without having gas exchange (i.e. Alveoli filled with fluid, ARDS, pneumonia, pulmonary edema). Tx: oxygen won’t fix, usually need mechanical ventilation with high FiO2.
Diffusion limitation: gas exchange is compromised b/c alveolar/capillary membrane is thickened, damaged, or destroyed; severe emphysema, recurrent PE, CF, interstitial lung disease, ARDS; causes hypoxemia during exercise and not usually at rest; can also happen with high CO causing blood to flow through the pulm capillary bed so quickly that there is not time for gas exchange.

Question 8

Hypercapnic (ventilatory) failure

Answer 8

Imbalance between ventilatory supply (gas flow in/out without getting resp muscle fatigue) and demand (amount of ventilation needed to keep PaCO2 w/in normals). Normally we have far more ventilatory support than we have demand allowing us to strenuously exercise (able to compensate without seeing a net increase in PaCO2). Perfusion is normal, but ventilation is inadequate (blood flow, just issue with lungs going up and down to breathe off CO2). Thoracic pressure does not allow for enough air movement in/out of the lungs. CO2>45 in otherwise healthy lungs.

Question 9

Causes of hypercapnia (ventilatory) failure

Answer 9

Airway and alveoli: asthma, COPD; CF; causes airflow obstruction and air trapping leading to resp muscle fatigue.
CNS: opioid overdose, CVA, severe head injury. Medulla doesn’t alter the resp rate in response to the change in PaCO2 (H+ changes).
Chest wall: flail chest, kyphoscoliosis, morbid obesity; limits lung expansion or diaphragmatic movement
Neuromuscular conditions: Guillain-Barre syndrome, muscular dystrophy, myasthenia gravis, MS; causes resp muscle weakness or paralysis
Resp failure can occur despite healthy, normal lungs- pt can not inspire with enough tidal volume

Question 10

S/S of inadequate oxygenation

Answer 10

1st indicator: change in mental status. Occur before ABG changes b/c the brain is so sensitive to changes in oxygenation; restlessness, confusion, agitation, combativeness
Other early signs: Increased HR, increase RR, mild HTN d/t catecholamine release from stress
Severe morning headache: hypercapnia occurring during the night from vasodilation. Everything slows down at night. If you have an issue with oxygenation and everything is slowed, including RR, everything builds up. CO2 causes vasodilation, including in cerebral arteries.
Late sign: cyanosis. doesn’t occur until PaO2

Question 11

Tells us how much O2 is available in the alveoli to dissolve in the blood. O2 dissolved in plasma, NOT total O2. 60 is considered adequate. From 60-100 the O2 sat only increases from 90% to 98%. If it drops from 60 to 20 the oxygen sats would from from 90% to 33%.

Answer 11

PaO2

WANT 80-100 IN A NORMAL PERSON

Question 12

Oxygen’s affinity for Hgb changes based on ___ and ____ which is why we have the O2-Hgb dissociation curve. This curve shows a non-linear tendency for O2 to bind to Hgb. Blow SaO2 90% small difference in Hgb saturation reflect large changes in PaO2 (a small drop in SaO2 is a large drop in PaO2).

Answer 12

pH; temperature

Question 13

Higher sat for give PaO2 (how much O2 available in alveoli to dissolve in the blood). (i.e. cold, rest, alkalosis, CO poisoning) Hgb holds onto O2, can lead to tissue hypoxia even with sufficient O2 in the blood

Answer 13

Left shift. Alkalotic conditions.

Question 14

Lower sat for given PaO2 (i.e. heat, exercise, acidosis. O2 is released more readily- less affinity for Hgb, more O2 will be released to cells but less O2 will be carried from lungs).

Answer 14

Right shift. Acidotic conditions. Hgb looses affinity for oxygen b/c it knows you are in a hyper metabolic state for some reason or another and gives O2 to the tissues.

Question 15

S/S:

Answer 15

Rapid or slow resp rate (both cause poor CO2 removal, increased work of breathing leading to resp muscle fatigue [usu a change from rapid to slow is NOT a good sign]).
Position- lying (mild distress), sitting(moderate), sitting upright (severe), tripod
Orthopnea
Pursed-lip breathing: allows more time for expiration, prevents small bronchioles from collapsing
I:E ratio increasing- usu 1:2; increasing suggest airflow obstruction requiring more time to empty the lungs
Auscultation: crackles (pulm edema), rhonchi (COPD), wheezes (obstruction, narrowing), absent/diminished (atelectasis, pleural effusion), pleural friction rub (pneumonia)

Question 16

Oxygen therapy

Answer 16

O2 at 1-3 L/min by NC or 24-32% by simple face mask or Venturi mask.
Make sure that the pt can tolerate the oxygen delivery device.

Question 17

Mobilization of secretions

Answer 17

Effective coughing
Positioning: upright at least 45 degrees, good lung down if one lung involved
Hydration/humidification: 2-3 L/day, humidification
CPT: postural draining, percussion, vibration
Suctioning

Question 18

Positive pressure ventilation

Answer 18

Helps decrease WOB. Try BiPAP or CPAP. May need mechanical ventilation

Question 19

Relief of bronchospasm

Answer 19

Short-acting bronchodilators (i.e. Albuterol, Alupent) given with oxygen q15-30 minutes

Question 20

Reduction of airway inflammation

Answer 20

IV corticosteroids (ie methylprednisolone): immediate action. Inhaled take 4-5 days to work

Question 21

Reduction of pulmonary congestion

Answer 21

IV diuretics (ie Lasix), Tridil for HF

Question 22

Tx of pulmonary infection

Answer 22

IV antibiotics (ie vancomycin, Rocephin)

Question 23

Reduction of anxiety, pain, agitation

Answer 23

Propofol, Ativan, Versed, fetanyl, morphine, vecuronium.

Give “sedation vacation”

Question 24

Sudden, progressive form of acute respiratory failure. Alveoli fill with fluid causing severe dyspnea, refractory hypoxemia, reduced lung compliance, and pulmonary infiltrates. Mortality rate is high (50-60%). Most common cause is sepsis (not necessarily lung issue, can be anywhere in body b/c the infection in the blood eventually travels to the lungs and can stay here).
Massive inflammation. Alveoli become very permeable=edema (fluid into alveoli)=thickening of membrane=decreased VQ.

Answer 24

Acute Respiratory Distress Syndrome (ARDS)

Question 25

Injury at the alveolar-capillary membrane causes lung fluids to increase and surfactant to be decreased or diluted. Alveoli fill with fluid and can’t have gas exchange. As fluid continues to leak more blockages occur and blood cannot be oxygenated.

Answer 25

SIRS

Question 26

Hypoxia even with 100% O2

Answer 26

Refractory hypoxemia

Question 27

causes of ARDS

Answer 27

Massive SNS stimulation (i.e. trauma or hypoxia) causing constriction and large volumes of blood in the lungs circulation increasing pressure and causing injury. Also can occur from direct lung injury (i.e. aspiration, radiation, near drowning, sepsis).
NOT from chronic respiratory diseases.
Usually occurs in a healthy pt after trauma, NOT as common in pts with chronic respiratory disease.

Question 28

P/F ratio: PaO2/FiO2 (in decimal form).
Should be above 400.
In acute lung injury, PF ratio is ___-___
In ARDS, PF ratio is

Answer 28

200-300

200

Question 29

Occurs 1-7 days after the initial problem (24-48). Interstitial edema, alveolar edema, and atelectasis = VQ mismatch. Engorgement of the peribronchial/perivascular space produces interstitial edema. Interstitial edema occurs and fluid fills the alveoli. Intrapulmonary shunt develops because the fluid filled alveoli no longer allows through the thin membrane the ability for O2/CO2 exchange. Surfactant no longer works causing atelectasis. Necrotic cells, protein, and fibrin membranes line the alveoli. Hypoventilation, decreased CO , hypoxemia. Severe V/Q mismatch, shunting, less compliant lungs-decreased surfactant production, pulm edema, atelectasis. Decreased lung compliance results in increased pt WOB. Vent settings may require high inspiratory and plateau pressures. Hypoxemia, and stimulation of the juxtacapillary receptors in the stiff lungs may cause and increased RR and decrease tidal volume.
RESPIRATORY ALKALOSIS.

Answer 29

Injury (exudative phase)

Question 30

Occurs 1-2 weeks after the initial problem. Influx of monocytes, neutrophils, lymphocytes, and fibroblast proliferation. Inflammatory process causes dense, fibrous tissue. Pulmonary HTN, worsening hypoxemia

Answer 30

Reparative (proliferative) phase of ARDS

Question 31

Occurs 2-3 weeks after initial problem. Diffuse scarring, fibrosis, continue hypoxemia. The lung is completely remolded by collongous/fibrous tissues. Surface area for gas exchange is significantly reduces because the interstitial is fibrotic.
PULMONARY HTN results from pulm vascular destruction and fibrosis

Answer 31

Fibrotic (chronic or late)

Lung completely remodeled.

Question 32

S/S:

Answer 32

Hypoxemia despite increased FiO2 is hallmark sx. Initial presentation is subtle (i.e. mild or no resp dx, fine/scattered crackles, mild resp alkalosis, normal CXR). Mental status change- early sign of hypoxia. Tachypnea, retractions, tachycardia, diaphoresis, change in LOC, diffuse crackles. PAWP will NOT increase(tells us indirectly what the LV is doing but this isn’t the issue so it won’t be changed). As it progresses, the pt will have profound resp distress requiring intubation or PPV(Positive pressure ventilation) CXR with whiteout. Lung consolidation and infiltrates spread though out the lungs leaving few recognizable air spaces.
Severe hypoxemia, hypercapnea, metabolic acidosis, and manifestation of target organ dysfunction will rapidly occur.
HALLMARK SX IS REFRACTORY HYPOXIA.
Whiteout suggests fluid, consolidation in the lungs.

Question 33

Care

Answer 33

Lowest O2 concentration that results in a PaO2 of >60 to prevent O2 toxicity.