ACUTE RESPIRATORY 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
- Known Hypertensive for 28 years and is maintained on Metoprolol 50mg. - In 2004, patient has been hospitalized due to PTB.  2 weeks PTA:  mild episodes of dizziness  BP was elevated to 150/100

 2 days PTA:
 Productive cough with whitish sputum  Carbocisteine provided minimal relief  Weakness after walking 2 blocks

 Few hours PTA: Symptoms persisted  Upon Admission: conscious, coherent but in respiratory distress.

Physical Assessment:
 (+) subcostal retractions, (+) crackles at both lung fields  VS: BP – 140/80 mmHg, HR – 140 bpm, RR: 42, Temp: 36.6 °C

Hooked to mechanical ventilator, cardiac monitor and pulse oximeter. CXR showed confluence of densities, R lower and upper lung fields, L middle and upper lungs Furosemide drip Metabolic Acidosis NaHCO3

Tachycardia at 150s – 160s – Digoxin 0.5mg/IV Runs of Afib Hooked to Amiodarone drip ABG revealed hypoxemia Hypotensive episodes 70/40, Urine output – inadequate  Dopamine and dobutamine drip started

 A clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.  Acute Respiratory Distress Syndrome (ARDS) is also known as shock lung, wet lung, post perfusion lung and a variety of other names related to specific causes.  According to the American Lung Association, the incidence of ARDS ranges from 2 to 71 per 100,000 persons in the United States.

Clinical Disorders Commonly Associated with ARDS according to HARRISON Direct Lung Injury Indirect Lung Injury Pneumonia Sepsis Aspiration of gastric Severe trauma contents Pulmonary contusion  Multiple bone fractures Near-drowning  Flail chest Toxic inhalation injury  Head trauma    Burns   Multiple transfusions   Drug overdose   Pancreatitis   Post-cardiopulmonary bypass

• Type II pneumocyte
– proliferate – differentiate into Type I cells – reline alveolar walls

• Characterized by:
– local fibrosis – resolution

ANATOMY and PHYSIOLOGY

The Alveoli

bronchiole

alveoli

Found at the end of the terminal bronchioles, the smallest subdivisions of the bronchial tree, these are clusters of tiny air sacs in which most gas exchange takes place. The wall of each alveolus is made of a singlecell layer of squamous (flat) epithelium. This thin wall provides easy passage for the gases entering and leaving the blood as the blood circulates through the millions of tiny capillaries covering the alveoli.

The Alveolar Epithelium
Type I alveolar cells (pneumocytes) extremely thin squamous cells that line about 95% of the alveolar surface area. responsible for the gas (oxygen and carbon dioxide) exchange that takes place in the alveoli. It is a very large thin cell stretched over a very large area

Type II alveolar cells (pneumocytes) or septal cells - cuboidal cells cover about
5% of the alveolar air surface -responsible for the production and secretion of surfactant -can replicate in the alveoli and will replicate to replace damaged type 1 pneumocytes.

Surfactant -Produced by Alveolar Type II cells 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)
Thin squamous epithelial layer lining alveolar walls Pulmonary capillaries cover external surfaces of alveoli

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
Increasing the thickness of the respiratory membrane decreases the rate of diffusion. In healthy lungs, the respiratory membrane (alveolar membrane + endothelial membrane + fused basement membranes) is 0.5-1.0um thick, but the thickness can be increased by respiratory diseases.

Surface Area
The total surface area of the respiratory membrane is approximately 70 m2 (approximately the area of one half of a tennis court) in the normal adult. When the total surface area of the respiratory membrane is decreased to one third or one fourth of normal, the exchange of gases is significantly restricted even under resting conditions.

Partial Pressure Difference
 difference between the partial pressure of the gas in the alveoli and the partial pressure of the gas in the blood of the alveolar capillaries.  When the partial pressure of a gas is greater on one side of the respiratory membrane than on the other side, net diffusion occurs from the higher to the lower pressure.  Normally the partial pressure of oxygen (P02) is greater in the alveoli than in the blood of the alveolar capillaries, and the partial pres-sure of carbon dioxide (Pco2) is greater in the blood than in the alveolar air.

Partial Pressure Difference
The partial pressure difference for oxygen and carbon
dioxide can be increased by increasing the alveolar ventilation rate. The greater volume of atmospheric air exchanged with the residual volume raises alveolar Po2, lowers alveolar Pco2, and thus promotes gas exchange.  Conversely, inadequate ven-tilation causes a lower-thannormal partial pressure difference for oxygen and carbon dioxide, resulting in inadequate gas exchange.

Events of Respiration
Pulmonary ventilation – moving air in and out of the lungs External respiration – gas exchange between pulmonary blood and alveoli

Events of Respiration
Respiratory gas transport – transport of oxygen and carbon dioxide via the bloodstream Internal respiration – gas exchange between blood and tissue cells in systemic capillaries

Mechanics of Breathing (Pulmonary Ventilation)
Completely mechanical process Depends on volume changes in the thoracic cavity Volume changes lead to pressure changes, which lead to the flow of gases to equalize pressure

Inspiration

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

Alveolus (air sac)

O2 Concentration high Alveolus Alveolar Wall Capillary Wall Capillary

capillaries A Capillary bed in tissue

CO2 Concentration high Erythrocyte Capillary O2 Concentration high

Capillary Wall Interstitial Fluid B cells Body Cells CO2 Concentration high

O2

CO2

Diffusion across ALVEOLOCAPILLARY MEMBRANE
Diffusion occurs: • Large surface area and very thin membrane • partial pressure of O2 is greater in alveolar gas than in capillary blood ↑P area → ↓ P area

Determinants of arterial oxygenation
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
 Ventilation of the lungs  Diffusion of O2 from the alveoli into the capillary blood  Perfusion of systemic capillaries into the cells  Diffusion of CO2 form the cells into systemic capillaries

Transport of carbon dioxide
3 forms of transport: 3.Dissolves in plasma 4.Bicarbonate 5.Carbamino compound

CO2 + H2O
(Hgb)

carbonic anhydrase

carbonic acid

H+

(RBC)

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
1. Diffusion of carbon dioxide from the cells into the systemic capillaries 2. Perfusion of the pulmonary capillary bed by venous blood 3. Diffusion of carbon dioxide into alveoli 4. Removal of carbon dioxide from lung by ventilation

LABORATORY AND DIAGNOSTIC EXAMS
BY: FANER, NED DENEBE V. RN

Complete Blood Count
Hgb Hct Rbc Platelet Wbc Segmenters Lymph 11/ 14/ 08 143 0.43 ↓ 6.12 298 35.20 ↑ 0.83 6.09 11/ 16/ 08 119 ↓ 0.36 ↓ 5.20 282 20.40 ↑ 0.93 0.07 11/ 19/ 08 107 ↓ 0.32 ↓ 4.65 244 24.00 ↑ 0.93 0.04

 ↓ Hct level and Hgb - ↓O2 in blood  ↑RBC – compensate ↓O2 in blood  ↑ WBC – cause by infection , inflammatory response

Chest X-ray

Normal Chest X-ray

Patchy Patient with ARDS infiltrates

Chest X-ray
11/ 14/ 08 Haziness on both lung fields, confluence of densities mostly on right lower and upper lung fields, left middle and part of upper lung fields 11/ 14/ 08 Confluent densities appreaciated on both perihilar and basal regions. Heart is enlarged. Cvp line is in place. 11/ 16/ 08 Clearing of previously noted bilateral densities. Heart remains enlarged. Aorta is atheromatous. 11/ 19/ 08 There is progression of alveolar infiltrates. Cardiomegaly is present.

Arterial Blood Gases
11/14 pH 11/15 11/15 11/16 11/17 7.373 11/18 7.421 39.6 261.0 25.3
99.6% 22.9

11/19 7.390 44.5 116.9 26.3
98.2% 51

11/20 7.420

11/21 7.51

7.16 ↓ 7.145 ↓ 7.27 ↓ 7.358 39 38.4↓ 13.2↓
61.5%↓ 186.82

pCO2 38.1 pO2
HCO3 O2 sat dFiO2

36.7

26.4 ↓ 35.7 108.0 20.4↓
97.9% 73.7

48.6 ↑ 42.5 192.4 31.1↑
99.3% 29.69

74.0↓ 13.7↓
90.8% 104.8

56.8↓ 152.7 16.5↓ 14.5↓
85.8%↓ 98.9%

123.5 33.8↑
98.8% 41.19

146

51

Arterial Blood Gas
11/14 11/15 11/15 11/16 11/17 11/18 11/19 11/20 11/21 Uncompensated Metabolic Acidosis Uncompensated Metabolic Acidosis Uncompensated Metabolic Acidosis Compensated Respiratory Alkalosis Compensated Metabolic Acidosis Compensated Metabolic Acidosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Alkalosis

METABOLIC ACIDOSIS

RESPIRATORY ALKALOSIS

 SIGNS AND SYMPTOMS  Headache  Lethargy  Coma  Kussmaul’s breathing  Nausea and vomiting  Diarrhea  Abdominal discomfort

SIGN AND SYMPTOMS Dizziness Confusion Tingling sensation Convulsions

Oxygen toxicity
Pure oxygen is being breathe in and no nitrogen gas is present – maintainance of alveolar expansion is loss leading to alveolar collapse. Oxygen has toxic effects on Type II pneumocytes cells that produce surfactant. Inadequate production of surfactant leads to alveolar collapse and further fluid shifts from capillaries to alveolar sacs, aggravating the patient condition.

Arterial Blood Gas
↓O2 → hyperventilation → ↓CO2 = RESPIRATORY ALKALOSIS ↓BP and ↓O2 → lactic acid production → bicarbonate binds to acids → ↑ loss of bicarbonate = METABOLIC ACIDOSIS

ACUTE RESPIRATORY DISTRESS SYNDROME

Clinical lung injury

antibiotics

Sepsis

Endothelial damage Alveolar damage

Platelet aggregation Attract / activate neutrophils Release of mediators

Damage to type II pneumocytes ↓ surfactant production atelectasi s Impaired lung compliance

Digoxin, amiodarone
Inc vascular permeability Compensator y mechanisms Tachycardia AF

Regeneration of the alveolar membrane with thick epithelial cells

Diffuse alveolar infiltrates, crackles, cough

Tachypne a DOB retractio ns

Inc alveolar permeability

Inc permeability

Fluid and protein move into the alveoli Pulmonary edema

↓ SVR

diuretics

↓ blood volume

Eventual scarring and loss of functional lung tissue

Severe dyspnea, Hypoxemia unresponsive to O2

↓ BP
V/Q mismatch R-L shunting

↓ venous return ↓ CO

Unmet myocardial demands

pressor s
Cellular hypoxia

↓ tissue perfusion ischemia Severe organ dysfunction

MV w/ PEEP ACUTE RESPIRATORY FAILURE

Metabolic acidosis

↓ renal perfusion

Myocardial depression

↓ cerebral tissue perfusion

death

↓ UO Inc creatinine

↓ LOC

Nursing Problems
A. Ineffective Breathing Pattern 1. Dyspnea 2. Crackles 3. Cough

Nursing Problems
B. Impaired Gas Exchange 1. Hypoxemia 2. Dizziness

Nursing Problems
c. Decreased Tissue Perfusion
1. Decreased urinary output 2. Hypotension

Roger G. Spragg, M.D., James F. Lewis, M.D., Hans-Dieter Walmrath, M.D., Jay Johannigman, M.D., Geoff Bellingan, M.D., Pierre-Francois Laterre, M.D., Michael C. Witte, M.D., Guy A. Richards, M.D., Gerd Rippin, Ph.D., Frank Rathgeb, M.D., Dietrich Häfner, M.D., Friedemann J.H. Taut, M.D., and Werner Seeger, M.D.

N Engl J Med 2004;351:884-92. Copyright © 2004 Massachusetts Medical Society.

Optimal Ventilator Settings in Acute Lung Injury and Acute Respiratory Distress Syndrome
M. Yilmaz, O. Gajic Mayo Clinic College of Medicine, Division of Pulmonary and Critical Care Medicine, Rochester MN, USA Akdeniz University, Medical Faculty, Development of Anesthesiology and Intensive Care, Antalya, Turkey November 16, 2007

Overdistention injury induced by High Vt ventilation has been identified as the single most important determinant of VILI Ventilation at low lung volumes in the absence of PEEP may lead to lung injury caused by repetitive collapse and reopening of the alveolar units Better understanding of the pathophysiology of ALI/ARDS and the role of VILI prompted the use of smaller Vt with lower inspiratory pressures and a moderate amount of PEEP to prevent respiratory

Strategy: Low Vt mechanical ventilation in patients with ARDS
1990 RTC: Conventional vs Lung protective approach Villar, et al Result: The incidece of barotrauma, mortality has decreased significantly in the lung protective group The threshold of Vt of <7.7 ml Kg PBW and Ppl < 30 mmHg to be associated with improved outocmes.

USE OF PEEP
help achieve adequate oxygenation and decrease requirement for high fractions of inspired oxygen. the

Three mechanisms have been proposed to explain the improvement in gas exchange with PEEP: (1) Alveolar recruitment with increased functional residual capacity (2) Redistribution of extravascular lung water (3) Improved ventilation-perfusion matching. Computed tomography studies demonstrated PEEP induced recruitment of previously collapsed alveoli and that lung regions recruited with PEEP may not completely collapse at end-expiration . This in turn leads to more even distribution of airway pressures within the lung parenchyma.

USE OF PEEP
In conclusion, in patients with ALI/ARDS lung protective ventilation strategies yield better clinical outcomes compared to traditional approaches in which more generous tidal volumes are used. Limiting Vt to ^6-8 mLkg ' PBW, with further reductions of Vt if the Ppl is high (>30cmH2O) has been shown to improve outcomes and should be considered as a standard of care for the majority of patients with ALI/ ARDS.

Recent Developments in the Management of Acute Respiratory Distress Syndrome in Adults
Heather R. Bream-Rouwenhorst, Elizabeth A. Beltz, Mary B. Ross, and Kevin G. Moores

Corticosteroids
*ameliorate

the cytokine- and toxic-mediator release associated with ARDS *benefit would be greatest in the initial exudative phase of ARDS when neutrophils begin to invade the pulmonary epithelium * have not demonstrated clear benefit in patients with ARDS. Some trials have found increased complications and mortality related to corticosteroid use

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. Result: at day 10, 7 patients receiving methylprednisolone were extubated,compared with 0 patients in the placebo group. Inhospital mortalityrates were 12% in patients treated with methylprednisolone and 62% in those receiving

te administration of corticosteroids.
*mortality rates were higher with methylprednisolone at day 60 (35% versus 8%, p =0.02) and at day 180 (44% versus 12%, p = 0.01) *Mortality was not significantly higher in the group receiving methylprednisolone whose ARDS was present for 7–13 days at the time of study enrollment. *Hence, initiating corticosteroids more than two weeks after the onset of ARDS may actually increase mortality *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
Raksha Jain, MD and Anthony DalNogare, MD Mayo Clinic Proc February 2006

Vasodilators 2.Inhaled Nitric Oxide relaxes pulmonary vascular smooth muscle and thus has important regulatory effects on regional lung ventilation and perfusion ratios Although endogenous nitric oxide, produced from nitric oxide synthase, impairs gas exchange during ARDS, exogenous inhaled nitric oxide relaxes vascular smooth muscle that supplies ventilated alveoli and thus may improve ventilation-to-perfusion relationships. In 1993, Rossaint et al: inhaled nitric oxide reduced pulmonary artery pressures and increased arterial oxygenation without producing systemic vasodilation. Other studies showed: adverse effects of methohemoglobinemia, production of toxic compounds such as nitrogen dioxide and peroxynitrate ion, increased pulmonary edema, and rebound pulmonary hypertension. Other studies showed increased mortality with infants treated with NO. Other studies showed no oerall survival benefit

Fig. 1. A. Schematic of vasoconstriction of pulmonary bed with normal and atelectatic alveoli. B. Nitroprusside (NTP) causes non-selective vasodilation of all pulmonary arteries, which may worsen ventilation-perfusion (V/Q) matching. C. Inhaled nitric oxide (NO) dilates only ventilated alveoli, an outcome that improves V/Q matching. (From Lunn R: Subspecialty clinics: Anesthesiology; Inhaled nitric oxide therapy. (Mayo Clin Proc 1995; 70:247-255; with permission.)

Decreased Alveolar Surface Tension 2.Surfactant
Lowers surface tension and prevents alveolar collase 1 study showed: a decrease in Fio2 requirement RTC on 448 adult ARDS patients who received recombinant protein Cbased surfactant showed improved gas exchange and oxygenation, but no difference occurred in the number of ventilator-free days or 28-day mortality

References: Books •McCance. Pathohysiology: The Biologic Basis for Disease in Adults & Children, 5th ed., 2006. Mosby •Fauci et. Al.. Harrison’s Principles of Internal Medicine, 17th ed., 2008. McGraw Hill. •Bullock. Pathophysiology: Adaptations & Alterations in Function, 4th ed., 1996. Lippincott. •Apostalakos & Papadalos. The Intensive Care Manual, 2001. McGraw Hill •Rumrakhd & Moore. Oxford Handbook of Acute Medicine, 2nd ed. 2004. Oxford University Press. 6. Murray & Nadel's Textbook of Respiratory Medicine, 4th ed., 2005 Saunders, An Imprint of Elsevier 7. Mayo Clinic Internal Medicine: Concise Textbook, edited by Thomas M. Habermann, Amit K. Ghosh., 2008©

For Bibliography: 1. “Recent developments in the management of acute respiratory distress syndrome in adults”, by Heather R. Bream-Rouwenhorst et. al, American Journal of Health System Pharmacy Vol. 65 Jan 1, 2008 2. “Optimal ventilator setting in acute lung injury and acute respiratory distress syndrome”, by M. Ylmaz and O. Gajic, European Journal of Anesthesiology 2008: 25: 89-96, 2007 © 3. “Prone position in Acute Respiratory Distress Syndrome”, P. Pelosi, L. Brazzi and L. Gattinoni, European Respiratory Journal, 2002: 20: 1017 – 1028, 2002 © 4. “Effect of Recombinant surfactant protein c-Based Surfactant on the Acute Respiratory Distress Syndrome”, Roger G. Spragg et. al The New England Journal of Medicine, 2004: 351:884- 92, 2004 © 5. “Surfactant alteration and replacement in acute respiratory distress syndrome”, Andreas Gunther et. al., Respiratory Research Vol.2 No.6, Oct 2001

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