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PULMONARY ALTERATIONS
pulm assessment + labs -always auscultate -> you hear things before you
see it
LABS
-pH: 7.35-7.45
-PaCO2: 35-45
-HCO3: 22-26
-PaO2: 80-100
-SaO2: 95-100%
-hg transports O2 = SaO2 shows oxyhemoglobin lvl
mixed venous oxygen saturation -evaluate o2 supply and demand = % of oxygen that
(SVO2) is actually transported from hg to tissues to
utilize/offload
-measured by PA cath: distal
,Acute Respiratory Failure (ARF) Patho: inadequate gas exchange (impaired diffusion)
(aka Acute Lung Failure ALF) - not enough O2 in blood = hypoxemia
- not enough CO2 removal from blood =
hypercapnia
Causes
-VQ mismatch: when part of lung receives O2 w/o
perfusion or perfusion without enough O2
-Intrapulm shunting: extreme form of VQ mismatch -
-> blood passed pulm and arterial WITHOUT gas
exchange due to undervent of alveoli = perfusing
deoxy blood
ARF Classifications Type 1: hypoxemic normocapnic resp failure
-oxygenation failure = low O2, normal CO2
-caused: alterations in respiration/breathing
Type 2: hypoxemic hypercapnic resp failure
-ventilatory failure = low O2, high CO2
-caused: hypoventilation of alveoli
S/S of ARF hallmark sign: hypoxemia
-early: tachycardia, tachypnea, mild HTN, mental
status changes (confused)
-late: cyanosis
,ARF treatment -give O2 + intubate
-give meds:
+ bronchodilators: albuterol
+ steroids
+ sedatives: to calm pt down and normalize
breathing
+ analgesics: morphine
+ NMB
-raise HOB 30-45 + suctioning to remove secretion
-correct acidosis: give bicard
-DVT prophylaxis: SCDs compression stocks,
enoxaparin
-stress ulcer prophylaxis: PPI and H2RA
Acute Respiratory Distress Syndrome Patho: injury --> inflammation --> SIRS response
(ARDS) (increased capillary permeable + swelling) --> cause
pulm edema --> alveoli collapse --> hypoxemia
Causes
-Indirect (extrapulmonary): sepsis, CT bypass,
embolism, DIC, pancreatitis
-Direct pulmonary: aspiration, near drowning,
pneumonia, toxic inhalation, oxygen toxicity
hallmark features of ARDS 1) acute onset severe dyspnea + hypoxemia
2)bilateral patchy infiltrates on CXR --> lots white on
XR
3) pulm edema + no s/s HF
4) no improvement in O2 despite increasing O2
delivery
5) lung compliance reduced, stiff -> need higher
pressure to vent
, s/s of ARDS EARLY
-dyspnea, tachypnea, accessory muscle use,
increased WOB, restless and agitated
-chest auscultation might normal or fine, scattered
crackles/dimished breath sounds
-mild hopoxemia + respiratory alkalosis bc
hypervent initially
-CXR may be normal or scattered interstitial
infiltrates
LATE: s/s worsens as fluid builds + decreased lung
compliance
-skin from pink -> dusky -> pale -> cyanotic +
change in temp and cap refill
-diffuse crackles and rhonchi --> -infiltrates on CXR
worsens
-increased agitation: bc unable to breathe
-tachypnea changes to bradypnea
-low O2 + high CO2 = lactic acidosis
-tachycardia, low BP, high PAP
treatment + nursing intv for ARDS -need vent or positive pressure (PEEP keeps alveoli
open)
+ low Tidal Vol to avoid pneumthorax bc too much
pressure and alveoli exploded
-avoid immediately giving 100% O2 bc oxygen
toxicity and prevent reabsorption atelectasis
-permissive hypercapnia: and wait for it to normalize
-bronchodilators, sedatives, analgesics, NMB
-Prone position: help secretions fall off posterior
side of lung to better suction + reverse atelectasis
Pneumonia Patho: acute inflammation of lungs bc of an infection
-community acquired, hospital/ventilator associated