Acute Respiratory Failure Flashcards
If pulse ox is 89 on pneumonia with antibiotis what do you do first
Assess probe site to ensure accurate reading, apply oxygen after then tell Dr bc change condition
purpose of pursed lip breathing with COPD
reduce the overal work of breathing
ARF vs ALI
ALI is milder from of ARDSand can lead to sudden deterioration in pulmonary gas exchange resulting in CO2 retention & inadequate oxygenation
Ventilation issues
Oxygenation (gas exchange) issues
-ARF- from infection, decreased perfusion to lungs hypoxia, increased rr, doesnt have to be lung injury
ARF, ALI, ARDS
can lead to resp arrest
type 1 or hypoxemic respiratory failure PaO2<60(norm 75-100)
Failure of oxygen exchange
Abnormal O2 transport with resultant inadequate oxygenation
Hypoxemia refractory to supplemental oxygen
-COPD and CHF pt
-could have normal SAO2
Type II or Hypercapnic (PaCO2 >45) resp failure
Failure to exchange or remove carbon dioxide
Decreased alveolar minute ventilation (hypoventilation of alveoli)
-drug overdose, alcohol, chronic COPD requiring O2, emphysema, HR
Type 3 Mixed Hypoxemic-Hypercapnic
SAO2 low, CO2 high
Inadequate alveolar ventilation and abnormal O2 transport
-harder to manage
-treat with bipap- positive pressure in to control rr to blow off CO2
type 4 resp failure: SHOCK
patients who are intubated and ventilated in the process of resuscitation for shock
Goal of ventilation is to stabilize gas exchange and to unload the respiratory muscles, lowering their oxygen consumption
-almost always sedated or paralyxed to not consume extra oxygen
Goals ARF
correct cause, alleviate hypoxemia and hypercapnia
-SAO2 is low so put back in bed to decrease amt oxygen demand
cause of ARF- infection, airway obstruction(mucus plugging,anaphylaxis, pills), cardiac function
how to figure hypoxemic or hypercapnic
cant get O2 up, pt gets restless, look tired , tachypnic
Infection
If the lung injury pattern is accompanied by a significant increase in neutrophils, areas of necrosis, viral cytopathic effect, and/or granulomas, infection should lead the differential diagnosis.
-pneumonia- can lead to resp prob because wait too long
-
Resp distress problems
Asthma- bronchospasms
COPD- mucus plugging alveoli, bronchoconstriction, two classic signs - chronic bronchitis and ed stage emphysems
chronic bronhcitis- SOB, cough, steroidt reatment from chroninc inflam response causing bronchoconstriction
emphysems- alveoli dont work and lung capacity is limited so always SOB
lung cancer- tumor decreased blood and O2
-cystic fibrosis- excessive mucus plugging lead to scarring and not reversible
-pneumonia- aspiration can put int resp distrss
pleural effusion-fluid decreases lung capacity
Covid 19- into resp failure bc high oxygen demand and consumption bc large amt mucus, alveolar damage cant perfuse through them and walls collapse and dont allow blood and oxygen to get through, both sides of lungs
ARDS patho(high mortality rate)- nebulizer treatments every four hours, cant move far, alwasy sob
lung injury
Decreased blood flow to lungs
Alveolar membrane damage
Increased membrane permeability
Interstitial & intra-alveolar edema
Further impaired oxygenation
“Leaky” membranes cause osmotic pressure changes
Pulmonary edema
Inflammatory changes can lead to fibrosis
Stage 1 ARDS (first 12 hr)
increased SOB, RR, few CXR changes
Stage 2 ARDs (exudative) 24 hr
hypoxemia is resistant to supplemental oxygen (mechanical ventilation required)
Stage 3 ARDS (proliferative) day 2-10
hemodynamically unstable, evidence of SIRS(systemic inflammatory response- increased temp, HR, leUKOCYTOSIS ELEVATED WBC NOT JUST INFECTION-INFLAMMATOIN, Decreased BP bc cant diffuse and no oxygen recovery)
Satge 4 ARDS (fibrotic) over10 days
lung fibrosis issues; ventilator management issues
Symptoms ARDS
develop quickly after lung insult
Covid- headache, sore throat, muscle aches, cough, SOB
hypoxic, cough, poor oxygen exhange, TACHYPNEA, HYPOTENSION, CONFUSION, LETHARGY, SOMNOLENT
Diagnostic ARDS
PaO2 : FiO2 ratio < 200 (greater 300 optimal)
B/L infiltrates on CXR “white out”
Elevated serum lactate levels
No cardiac etiology for pulmonary edema(LINKED TO HF)
*Deterioration of ABG’s despite intervention
End of ARDS support
-Proned so lungs can expand more in lungs on belly, bad thing about proned-all drips, tube, 8 ppl to flip body sedated,
pharm-SUPPORTIVEE
Antibiotics – if known microorganisms
Bronchodilators
Corticosteroids
Diuretics-intervascular system cant support this
Neuromuscular blocking agents-paralytic to DECREASE O2 DEMAND (NIMBEX)
Mechanical ventilation
increase F1O2(at 100% baseline 40%)(fraction of inspired O2)(norm 21%) and peep(positive end expiratory pressure) to correct hypoxemia
pressure support(keep alveoli open to crrect hypoxi)- amount tidal needed inhalation
norm tidal fem400ml 500m
increase rr, tidal volume to enhance ventilation
decrease preload, afterload, metabolic demans to optimize cardiac function.
hyperventilation may be used as a short term adgustment to treat elevate ICP
-first thing to do to give body a break so it doesnt lead to resp failure
-airway protection and optimal control of organs
assistance for neural or muscle dysfunction
Correct respiratory acidosis, providing goals of lung protective ventilation are met
Match metabolic demand
Rest respiratory muscles
intubate if cant clear secretions,trauma
Guillan- barrea
autominne secondary to infection or immunization and body function shuts down
paralyzes
goes on vent
starts at bottum and goes up
Indication for intubation
Altered mental status or coma-high CO2(35-40norm) levels, drug use, do wear O2
Severe respiratory distress/arrest
Extremely low or agonal(mistaken as true breathing, looks painful deep breath in and moans, inconsisten breathing pattern) respiratory rate
Shock-cardiogenic, hypovolemic
Peripheral cyanosis-decreased perfusion to body
Acute respiratory acidosis
Inability to clear secretions with impaired gas exchange or excessive resp work
Obvious respiratory muscle fatigue-tripod,look tired
Newly diagnosed neuromuscular disease(MS,parkinsons,ALS) with vital capacity <10-15mLair /kg weight- the bigger the person, more tidal volume needd
Impending cardiopulmonary arrest-Bp low,PVCs,pulm edema-crackles, pink frothy sputum
-drug overdose reversed with narcan bt if it cant- coma
Priorities vent
- Monitor & evaluate
patient response (touch them, decrease HR, inc BP, sedate(large doe can cause neuro defiicitand stroke) may decrease bp and then do vasopressors - Manage ventilator system- nasal canula, bipap
- Prevent complications-vent pneumonia, tissue breakdown, third space fluid cap leak, foley
elevate hob, vital signs SAO2, notify provider if requiring oxygen,medication prn
-stay with pt get RN to help for orders
volume cycled
pushes air in until preset volume delivered. alveoli collapse mucuc limited o2.
ensure with every breath rihgt am according to weight is given
