23 Restrictive Pulmonary Disorders Flashcards
obstructive vs restrictive pulmonary disorders
obstructive have problems w emptying their lungs
restrictive have problem opening/expanding their lungs
Restrictive Pulmonary Disorders
- results fr DECREASED LUNG EXPANSION
- alterations in lung parenchyma, pleura, chest wall, or neuromuscular function
- –represent acute or chronic patterns of lung dysfunctions (not a single disease)
Restrictive Pulmonary Disorders
classifications
Pulmonary
Extrapulmonary
Restrictive Pulmonary Disorders
ABG
DECR PaO2
normal/DECR PaCO2
INCR pH (alkalosis)
Restrictive Pulmonary Disorders
PFT
DECR: VC, TLC, FRC, RV
FEV1/FVC: slight decrease in each but ratio is about normal
Atelectasis
complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid
Acute (Adult) Respiratory Distress Syndrome
[ARDS]
- type of atelectatic disorder
- damage to alveolar-capillary membrane
- –causes widespread protein-rich alveolar infiltrates
- occurs in assoc w other pathophysiologic processes
3 most important effects of AARDS
1 lung is filled w water + protein
2 decr in surfactant > collapse
3 fibrosis of lung > cannot expand
4 fibrosis of common membrane > cannot diffuse O2/CO2 thru blood vessels > low O2, high CO2
ARDS
etiology
- mortality rt 30-63%
- more than 150,000 cases/yr in US
- assoc w decline in PaO2 that is REFRACTORY to supplemental O2 therapy
refractory
- resistant to stimulus
- does not respond
ARDS
causes
1 sepsis (>40%) 2 severe trauma 3 aspiration of gastric acid (>30%) 4 fat emboli syndrome 5 shock
ARDS
inflamation + fibrosis
- increased permeability of the pulmonary vasculature
- flooding of alveoli w proteinaceous fluid/protein-rich pulmonary edema
- triggers the immune system to activate the complement system + initiate neutrophil sequestration in the lung
flooding of alveoli w proteinaceous fluid/protein-rich pulmonary edema
(hyaline membrane i.e. fibrosis)
- diffuse, fluffy alveolar infiltrates
- disruptions in O2 transport + utilization
- —severe hypoxemia
lack of surfactant in ARDS
causes atelectasis + decrease in lung compliance
ARDS
clinical manifestation
-Hx of a precipitating event that has led to a low blood volume state [SHOCK state] + low BP 1-2 days prior to the onset of respiratory failure
ARDS
EARLY clinical manifestation
- sudden marked respiratory distress (high vent rt)
- slight increase in pulse rate
- dyspnea
- low PaO2
- shallow, rapid breathing
ARDS
LATE clinical manifestation
- FROTHY SECRETION (too much mucus + fluid)
- CRACKLES, RHONCHI ON AUSCULTATION
- tachycardia
- tachypnea
- hypotension
- marked restlessness
- use of accessory muscles: intercoastal + sternal retraction
- cyanosis (severe)
ARDS
diagnosis
1 Hypoxemia Refractory 2 ABG 3 Chest X-Ray 4 PFT 5 Open-lung biopsy shows
ARDS
Hypoxemia Refractory
hallmark diagnosis for ARDS
-hypoxemia refractory to increased levels of supplemental O2
ARDS
ABG
- hypoxia
- acidosis (bc retaining CO2)
- hypercapnia
ARDS
chest x-ray
normal progression to DIFFUSE “WHITEOUT”
whiteout=filled w water
ARDS
PFT
DECR: FVC, lung vol, lung compliance
VA/Q mismatch w large right-to-left shunt
ARDS
open-lung biopsy
- ateclasis
- hyaline membranes
- cellular debris
- interstitial + alveolar edema
ARDS
treatment
1 Inhaled Nitric Oxide
2 Supplemental O2
3 ID + treat underlying cause
4 maintain fluid + electrolyte balance
most supportive treatments for ARDS
inhaled nitric oxide + supplemental O2
supplemental O2 ARDS
- high-frequency jet ventilation [HFJV]
- inverse ratio ventilation [IRV]
- vol ventilator using pressure support
- mechanical ventilation w positive end-expiratory pressure [PEEP]
- –increases FRV and prevents alveolar collapse at end-expiration
- –forces edema out of alveoli