ARDS & Respiratory Failure

acute RR failure (type 1) is

PaO2

can’t get enough O2

what pts or disease process do you see with type 1 RR failure

PNA

acute RR failure type 2 is

PaCO2

can’t get enough of CO2

60-70

what pts or disease process do you see with type 2 RR failure

COPD pts

altered gas exchange on ABG

pH <7.30 (severely acidotic)

paO2 <60 (severely hypoxic)

paCO2 >50 (acidotic)

failure of oxygenation

• hypoventilation

• intrapulmonary shunting ( perfusion, NO VENTILATION) blood is flowing but no air not reaching alveoli (PNA, ARDS, pulmonary edema)

• diffusion defects

• decreased barometric pressure

• LOW CO (non pulmonary hypoxemia)

• LOW Hgb (non pulmonary hypoxemia)

failure of oxygenation

• hypercapnia (increased CO2)

  • r/t —> alveolar hypoventilation, decrease in ventilation and hypoxemia

  • V/Q mismatch

buildup of CO2 since the lungs aren’t moving air in and out effectively or pt is hypoventilation (breathing too slow)

earliest sign of RR failure

neuro changes !!!!

• change in LOC

interventions for acute RR failure

• maintain patent airway (always thinks ABC’s)

• optimize O2 delivery

• minimize O2 demand (keep pt sedated enough, paralytics, keep afebrile and cool)

• identify and tx cause

• prevent further complications

acute RR failure nursing care

• Maintain patent airway

• monitor respiratory status hourly and prn

• Mechanical ventilation/ VAP prevention

• Suction as needed, monitor lung sounds

• Monitor for pneumothorax (a high PEEP may cause the lungs to collapse)

• Obtain ABGs as prescribed and following each vent change

• Continuous ECG monitoring for changes that may indicate increased hypoxemia

• Vitals hourly (BP, MAP, HR, RR, SPO2, pain)

• Manage nutritional needs

• Provide emotional support to the client and family

what is ARDS

acute respiratory distress syndrome

• fluid rushes into the lungs (NO BACTERIA)

• which can be r/t SIRS (overwhelming response to trauma, pregnancy, pancreatitis)

ARDS meaning continued

• NON CARDIOGENIC PULMONARY EDEMA (fluid is in the lungs from increased pulmonary capillary permeability !!!! usually not from L sided HF

ARDS diagnostic criteria

• PaO2/FiO2 ratio is LESS THAN 200

• BILATERAL INFILTRATES ( white out on both lungs or ground glass appearance)

ARDS pathophysiology

fluid destroys surfactant in alveoli —> no gas exchange

• ARDS kills macrophages !!! often leads to a secondary bacterial infection

• insult —> SIRS

• release of inflammatory mediators

• damage to alveolar capillary membrane

• increased capillary permeability

• non cardiogenic pulmonary edema

ARDS patho continued

• microatelactasis ( no surfactant —> closed alveoli)

• decreased compliance (stiff lungs, fill up with fluid)

• impaired gas exchange

• V/Q mismatch

what type of vent setting will a pt with ARDS need to be on

AC/PC

PRESSURE control

other pressure control settings are

• SIMV-P

• pressure support

what percentage of O2 can usually cause O2 toxicity

60% in about 48 hrs

causes fibrosis of the lungs and scarring

direct risk factors for ARDS

• * gastric aspiration

• * diffuse pneumonia

• * multi system trauma

• fat embolism

• near drowning

• O2 toxicity

• pulmonary contusion

• inhalation of toxic gases

INdirect risk factors for ARDS (big insult to the body not r/t bacteria)

• *Septicemia

• *Nonthoracic Trauma

• CABG

• DIC

• Drug overdose

• Eclampsia

• Multiple transfusions

• Pancreatitis

• Leukemia

Berlin Criteria is

mild: paO2/FiO2 ratio is 201-300 with PEEP >5

moderate: paO2/FiO2 ratio is 101-200, PEEP >5

severe: <100 paO2/FiO2 ratio, PEEP >5

need to be able to find the PaO2 /FiO2 ratio in order to classify

example” paO2 is 60 and FiO2 is 60 —> make into a decimal

so 60/.60=100 that is SEVERE ARDS

stages of ARDS

• insult

• acute exudative- SIRS, permeability, leakage, infection

• fibroproliferative begins > 24 to 48 hours, fibrosis at 7 days

• recovery

early s/s of ARDS

• ALTERED LOC

• restlessness

• refractory hypoxemia (doesn’t get better with supplemental O2)

• increased HR and Temp

• grunting

• normal lung sounds

• RR alkolosis from increased WOB

late s/s of ARDS

Severe dyspnea

• increased WOB

• Intercostal retractions

• Accessory muscles

• Pink frothy sputum

• Cough

• Cyanosis

• Increased PIP

• Severe hypoxemia

how will the CXR look with ARDS

Interstitial/alveolar infiltrations

• Diffuse, bilateral, symmetrical

• “Ground Glass” or “White-out”

labs for ARDS

• CBC with differential

• Electrolytes

• Sputum culture (r/o)

• Blood culture (r/o)

• Albumin

• Pre-albumin

CXR is best

dont tx with ABX unless secondary infection

ARDS treatment

• Treat the cause

• Oxygenation and ventilation

• Positive end-expiratory pressure (PEEP) (high PEEP can cause Barotrauma and decrease BP)

• Possible nontraditional modes of ventilation: high-frequency, pressure-control, and inverse-ratio

*PRONING helps move fluid around to not obstruct alveoli

treatment goals

• Resolution of hypoxemia

• Normal breathing pattern

• “Normal” ABG’s

• Minimal or no dyspnea

• No complications secondary to treatment therapies evident (can get a pneumo will need chest tube)

oxygenation for ARDS

• Oxygen!!!

• High Flow NC, NIPPV, BiPap, CPAP

• Ventilator

• PEEP

• Low Vt

• Permissive hypercapnia

• Non-traditional modes

• High frequency

• Pressure control

• Inverse I:E ratio

prone position benefits

Alveolar recruitment

• ↑ oxygenation

• Facilitates drainage of secretions

prone position risks

• Loss of airway

• Aspiration

• Corneal injury

• Facial edema

• Impaired skin integrity

pharmacological tx

Diuretics

• Corticosteroids

• Bronchodilators

• Statins

• Antibiotics

• Stress ulcer prophylaxis

• DVT prophylaxis