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DISTRESS SYNDROME
FANER, Ned Denebe
LACANILAO, Sunshine
PAGADUAN, Maribec
PUA, Monalisa
NUCUM, Billie Kim
B.V., 63 Years old
Chief Complaint: Difficulty of breathing
Diagnosis: ARDS 2° to Pneumonia, Septic
Shock
History
Alveoli alveoli
Functions
5.Lowers surface tension & provide
alveolar stability
6.Prevents alveolar flooding
7.Maintains patency & stabilization of
small airways
8.Plays an important role in host defense
Critical components :
2.Dipalmitoylphosphatidylcholine
3.Surfactant Proteins
a. SP-A
b. SP-B
c. SP-C
d. SP-D
Metabolic trafficking of surfactant
phospholipids
Surfactant
secreting
cell
Respiratory Membrane (Air-Blood Barrier)
Figure 13.6
4 layers:
a layer of type 1 and
2 alveolr cells and
associated alveolar
macrophage=
alveolar wall
Epithelial basement
membrane
underlying the
alveolar wall
Capillary basement
membrane
Endothelial cells of
the capillary
Respiratory membrane thickness
Figure 13.7a
Expiration
Figure 13.7b
Pressure Differences in the Thoracic
Cavity
Normal pressure within the pleural space
is always negative (intrapleural pressure)
Differences in lung and pleural space
pressures keep lungs from collapsing
Boyle’s Law
Pressure Changes in Pulmonary Ventilation
Other Factors affecting Pulmonary
Ventilation:
Surface tension of alveolar fluid
Compliance of lungs
Airway resistance
Transport of Oxygen
2 FORMS of TRANSPORT
3.Small amount dissolves in plasma
4.Binds to hemoglobin
O2 Concentration high
Alveolus (air sac)
Alveolus
Alveolar
Wall
Capillary
Wall
capillaries
Capillary
A CO2 Concentration high
Erythrocyte
Capillary bed
in tissue O2 Concentration high
Capillary
Capillary
Wall
Interstitial
O2 CO2 Fluid
Partial Pressure of O2
- pressure exerts by O2 dissolved in
plasma
- as PaO2 increases oxygen moves
from plasma to bind with hemoglobin
- continues to bind until hemoglobin
binding sites are saturated
Oxygen saturation
- percentage of available hemoglobin that
is bound to oxygen
Hemoglobin concentration
- amount of hemoglobin available for
binding
- as amount of hemoglobin decreases, O2
content also decreases
Oxyhemoglobin association and
dissociation
hemoglobin binds with O2 (lungs) –
OXYHEMOGLOBIN
hemoglobin released O2 (tissues) –
HEMOGLOBIN DESATURATION
BOHR Effect – shift in the oxyhemoglobin
dissociation curve caused by changes in
CO2 and H ion concentrations in the blood.
↑CO2 → ↓O2 affinity
↓CO2→ ↑O2 affinity
4 steps transport of oxygen
3 forms of transport:
3.Dissolves in plasma
4.Bicarbonate
5.Carbamino compound
carbonic
anhydrase
CO2 + H2O carbonic acid H+
(RBC)
(Hgb)
HCO3
(plasma)
↓ O2 in hgb = ↑ CO2 binds in hgb
↑O2 in hgb = ↓ CO2 binds in hgb
HALDANE EFFECTS
4 steps in transport of carbon dioxide
Patchy
Normal Chest X-ray Patient with ARDS infiltrates
Chest X-ray
11/ 14/ 08 11/ 14/ 08 11/ 16/ 08 11/ 19/ 08
Haziness on Confluent Clearing of There is
both lung densities previously progression
fields, appreaciated noted of alveolar
confluence of on both bilateral infiltrates.
densities perihilar and densities. Cardiomegaly
mostly on basal regions. Heart remains is present.
right lower Heart is enlarged.
and upper enlarged. Aorta is
lung fields, Cvp line is in atheromatous.
left middle place.
and part of
upper lung
fields
Arterial Blood Gases
11/14 11/15 11/15 11/16 11/17 11/18 11/19 11/20 11/21
pO2 74.0↓ 38.4↓ 56.8↓ 152.7 108.0 261.0 116.9 192.4 123.5
HCO3 13.7↓ 13.2↓ 16.5↓ 14.5↓ 20.4↓ 25.3 26.3 31.1↑ 33.8↑
O2 sat 90.8% 61.5%↓ 85.8%↓ 98.9% 97.9% 99.6% 98.2% 99.3% 98.8%
Endothelial damage
Alveolar damage
Platelet
aggregation
Damage to type Attract / activate
II pneumocytes neutrophils
Release of
↓ surfactant
mediators Digoxin,
production
amiodarone
atelectasi Tachypne Inc Inc vascular
s Inc alveolar permeability
a permeability
DOB permeability
Impaired lung
compliance
retractio Compensator
ns y
Diffuse Fluid and protein ↓ SVR mechanisms
alveolar move into the Tachycardia
Regeneration of the infiltrates, alveoli diuretics AF
alveolar membrane with crackles, cough ↓ blood volume
thick epithelial cells Pulmonary edema
↓ BP ↓ venous Unmet
Severe
return myocardial
dyspnea,
Eventual scarring and Hypoxemia V/Q mismatch demands
loss of functional lung R-L shunting ↓ CO
tissue
unresponsive pressor
to O2
s
↓ tissue perfusion
Cellular ischemia
hypoxia
↓ UO
death Inc
creatinine
↓
LOC
Nursing Problems
Villar, et al
High-dosage, short-course
regimens.
*Two meta-analyses (1990s)=no benefit with high-dosage, short-course
administration of corticosteroids in patients who had various stages of
ARDS
*Therefore, the current standard of practice is to avoid these regimens.
oderate-dosage, tapering regimens.
Research: Methylprednisolone versus placebo at
day 7 of ARDS
*Intravenous methylprednisolone was dosed as 2
mg/kg once, 2 mg/kg/day on days1–14, 1
mg/kg/day on days 15–21, 0.5 mg/kg/day on days
22–28, 0.25 mg/kg/day on days 29 and 30, and
0.125 mg/kg/day on days 31 and 32.
*Patients who survived 14 days of ARDS may have had less active
fibroproliferation and hence a lesser response to corticosteroids.
SUMMARY
Corticosteroids should be started early in the course of ARDS (before
day14), at moderate dosages (i.v. methylprednisolone <2 mg/kg/day), and
tapered over three to four weeks. Initiation of corticosteroid therapy on day
14 or later in patients with ARDS should be discouraged due to the
increased mortality rates found
Pharmacological Therapy
for Acute Respiratory
Distress Syndrome
In 1993, Rossaint et al: inhaled nitric oxide reduced pulmonary artery pressures
and increased arterial oxygenation without producing systemic vasodilation.