NS4P1 Exam 1: Acute Respiratory Disororder

ARDS is a syndrome, it occurs from something else.  Aka shock lung. Often fatal.

We want to avoid it.

• 50% mortality
• 70-90%  mortality if due to  septic shock

Onset is usually 24-48 hours after injury. Occurs quickly.

Alveoli-Capillary Lung Changes: due to anything. Any lung or vascular conditons. Even Overoxygenations

• Neutrophils start to flood pulmonary interstitium
• Due to aspiration. Embooli of any sort.

• Alveolar-capillary membrane changes.
• Exact cause unknown.

May be due to stimulation of the inflammatory and immune systems causing neutrophils to flood the pulmonary interstituim

Direct (primary): Aspiration, diffuse pneumonia, fat embolism (emboli of any sort), near drowning, prolonged ventilation, O2 toxicity, burns, chest trauma, radiation therapy, toxic inhalation of any type of substance whether primary or secondary inhaltion

Indirect (secondary): Gram negative sepsis, Post Op CABG, anaphylaxis, DIC, drug overdose, eclampsia, fractures, multiple blood transfusions, pancreatitis, multisystem trauma, hypotension, severe head injury, shock states.

Lung Injury

-Increased Pulonary Vascular Resistance -> Poor Perfusion of ventilated alveoli -> V/Q mismatch (poor perfusion, the alveoli doesn’t get ventilation and poor oxygenation)

-Increased Capillary permeability -> Extravasation of protein rich fluid (fluid seeping out) -> Diffusion Impairment -Loss of Surfactant -> Alveolar collapse -> Increased Shunting of the blood away from the plulmonary system

Pulmonary Vein brings in Oxygenated blood to heart

-Pulm Artery brings bad blood to lungs

Insidious onset.  S&S develop 1-2 days after initial injury (primary or secondary potential causes)

Dyspnea

Hyperventilation to be able to get more air (Alkalosis-Resp. CO2 down and pH goes up)

 Then hypoventilation (so oppositie occursAt first the lungs are Clear ,  Then crackles & rhonchi

Cough

Accessory muscles to start to breath: diaphragmatic muscles, neck, shoulders

Restlessness from Hypoxemia

• HALLMARK FEATURES:
• Bilateral infiltrates on chest x-ray
• No signs or symptoms of heart failure
• No improvement in PaO2 despite ­ O2

So we’re putting them in non-breather, intubate them with 50% oxygenation level, but ABG’s are still dropping. Put on 100% just to maintain PaO2 60-80 but this won’t last very long.

• ABG analysis
• initially decrease  PaO2, decrease PaCO2 & ­  increased pH, due to hyperventilation

later decrease PaO2, ­ INCREASE PaCO2 & DECREASED pH, due to decreased lung compliance (Resp Acidosis)

CxR : Initially normal, Progress quickly from bottom up, Basilar infiltrates : ground glass appearance (on cxr ” broken up glass inside lungs” , white patches becomes white-out

• PA catheterization: To identify pulmonary edema, PCWP < 18 mmHg (wedge pressures)
• -Pulm artery Cath: R atrium to R ventricle into Pulm artery à Wedge itself to determine pressure in the lungs. 

• Other tests (Rule out causes: infection?)
• Sputum & blood cultures
• Toxicology
• Screen
• Serum amylase to r/o pancreatitis

1.Impaired Gas Exchange RT alveolar-capillary membrane changes & alveolar collapse 2° to ARDS AEB: abgs, oxygenation, poor saturation, High level of oxygen

2.Ineffective Airway Clearance RT altered anatomic structure 2° presence of ET tube AEB: intubated unable to spectorate secretions w/o asiistance

3.Decreased CO RT impeded venAous return by PVP (pulmonary venous pressure) AEB: pulmonary pressures

4.Risk for Infection RT loss of normal protective barrier & immobility

5.Altered Nutrition, Less than Body Requirements RT inadequate oral nourishment and ­ caloric demands 2° NPO status, and effects of ARDS AEB:

6.Impaired Mobility RT restricted movement, 2° bedbound status, effects of ARDS AEB:

7.Severe Anxiety RT clinical condition, pain, fear of death, suffocation, and ICU environment AEB:8.-Most often, ARDS are paralyzed b/c we want lungs to rest.  A/C and SIMV has work load od breathing. This can increase based on if they’re going against/fighting the vent. We want to avoid this during ARDS bc you’ll damage the lungs even more.

1.Improve oxygenation (PaO2 > 60 mmHg, PaCO2 < 45 mmHg, pH 7.35-7.45 at the lowest FiO2

• SvO2 60%-80% (more sensitive indicator of oxygen availability for tissue oxygenation)
• Obtained from the PA catheter
• SvO2 < 50% impaired
• PaO2 on RA within normal limits for age or baseline values

SaO2 > 90% And return WOB to a desirable level where they can breath on their own,  with clear breath sounds

Chest xray is clearing

No s/s pulm edema

No s/s of going into HF. Controlled BP Giving antibiotics to make sure infection process is being managed

Adequate nutrition and watching their albumin

Maintain their strength, ROM, no footdrop, Family is aware. Cooperative with plan of care. Minmizing anxiety.

• 3.B/P will be maintained at >110/60 without vasopressers
• oPulses 2+ BL and BUE
• oNo edema
• oUO >30mL/hour

• 4.WBC will be WNL.
• oNo TemperatureoLung sounds clear
• oPulmonary secretions will be clear

• 5.Albumin levels will be
• oNo further weight loss
• oH/H WNL
• oConsuming >70 percent of daily nutritional offerings

6.Pt will demonstrate strength 4-5/5, and ambulate safely with minimal assistance, tolerating with minimal physical and respiratory fatigue

7.Pt./family will report anxiety to minimal level, actively participate in POC, and identify 2-3 ways to reduce/eliminate anxiety

• Mechanical Ventilation
• FiO2 < 50%, up to 100% may  be necessary.  Monitor for toxicity
• VT  4-8 ml/kg

PCV (CMV) with IP (pressure support) 10-40 cm H2O, RR 12-40,  I/E ratio 1:2 or 1:1.5

or PCV with IRV (inverse ratio ventilation) - same settings, except I/E 1:1, 2:1, 3:1, 4:1

PEEP 5-20 cm H2O

• Mech Vent: giving least amount of oxygen to minimizing overoxygenating or toxicitiy of the pt
• Maxmizing our tidal volume

Sometimes we may have to change IE ratio for inverse.

Monitor Pressure support. PEEP to keep alveoli open at the end.

• Extracorporeal Membrane Oxygenation (ECMO)
• Partially relieves lungs of the work of gas exchange
• Allows lungs to rest and heal

Current survival rates improved to 50-60%

• Selection criteria
• Neurologically intact
• Mechanical ventilation < 10 days
• No terminal illness
• No major immunosuppression
• No contraindication to systemic anticoagulation

If all else fail, they might have to go on ECHMO.

High risk factors so putting on ECMO may not have a positive outcome.

Look at criteria before. We want to allow the lungs to heal.

Fluid Therapy - goal is to maintain a minimal PAWP to provide adequate CO

Keep slightly volume depleted - mild fluid restriction

Infuse crystalloid or colloid fluids (for patients with hypoalbuminemia)

Administer dobutamine or dopamine if CO decreases.

Administer diuretics PRN

Monitor PAWP, daily weights, I&O

Be conscientious of fluids you’re giving: you don’t want to flood their system.

Keep ARDS pt on the dryer side, you don’t want to overhydrate them

Cryastaloid or colloid foluids for low albumin levels

Vasopressors for low output

• Nutritional Support - increased caloric need due to increased WOB
• Ideally enteral feeding
• NGT
• OGT
• PEG
• TPN

• Corticosteriod Therapy
• Use of steroids is controversial
• Short-term use of steroids may stabilize the alveolar-capillary membrane

Steroid therapy is controversial due to the fact that they can cause more damage to the lungs.-Try to do it right in the beginning and keep it short term if possible. Long term is bad for the lungs. 

• Positioning
• at least Q 2 hrs
• Lateral rotation therapy bed - continuous
• Redistribution of interstitial edema which may improve oxygenation

• Prone positioning - Vollman prone positioner
• Perfusion may be better matched to ventilation, less V/Q mismatch 

• Anxiety Reduction
• Anxiolytics: lorazepam (Ativan), midolazam (Versed)

Sedative: propofol (Diprivan)

Neuromuscular blocking agent:  vecuronium bromide (Norcuron)

Analgesics: Morphine, Dilaudid

When they’re in ARDs, we don’t want to give them a sedation vacation b/lc if we take them off, they’ll fight and it’s bad for their lungs -so we aren’t giving a sedation vacation until some improvement in their oxygenation and ABGs and titrate off their vent settings based on their ABGs

-Neuromusc drug is continuously running

-Paralyzed: still feel and still hear. Opioids to minimize pain

• Description
• 1. A form of acute respiratory failure that occurs as a complication of some other condition; it is caused by a diffuse lung injury and leads to extravascular lung fluid.

2. The major site of injury is the alveolar capillary membrane.

3. The interstitial edema causes compression and obliteration of the terminal airways and leads to reduced lung volume and compliance.

4. The ABG levels identify respiratory acidosis and hypoxemia that do not respond to an increased percentage of oxygen.

5. The chest x-ray shows bilateral interstitial and alveolar infiltrates; interstitial edema may not be noted until there is a 30%increase in fluid content.  


Causes include sepsis, fluid overload, shock,trauma, neurological injuries, burns, disseminated intravascular coagulation, drug ingestion, aspiration,and inhalation of toxic substances.

Assessment

• 1. Tachypnea
• 2. Dyspnea
• 3. Decreased breath sounds
• 4. Deteriorating ABG levels
• 5. Hypoxemia despite high concentrations of delivered oxygen
• 6. Decreased pulmonary compliance
• 7. Pulmonary infiltrates

• Interventions
• 1. Identify and treat the cause of the acute respiratorydistress syndrome.
• 2. Administer oxygen as prescribed.
• 3. Place the client in a Fowler’s position.
• 4. Restrict fluid intake as prescribed.
• 5. Provide respiratory treatments as prescribed.
• 6. Administer diuretics, anticoagulants, or corticosteroids as prescribed.
• 7. Prepare the client for intubation and mechanicalventilation using PEEP.

• Description
• 1. Occurs when insufficient oxygen is transported to the blood or inadequate carbon dioxide is removed from the lungs and the client’s compensatory mechanisms fail

2. Causes include a mechanical abnormality of the lungs or chest wall, a defect in the respiratory control center in the brain, or an impairment in the function of the respiratory muscles.

3. In oxygenation failure, or hypoxemic respiratory failure, oxygen may reach the alveoli but cannot be absorbed or used properly, resulting in a PaO2 lower than 60 mm Hg, arterial oxygen saturation(SaO2) lower than 90%, or partial pressure of arterial carbon dioxide (PaCO2) greater than 50 mm Hg occurring with acidemia.

4. Many clients experience both hypoxemic and hypercapnic respiratory failure and retained carbon dioxide in the alveoli displaces oxygen, contributing to the hypoxemia.

5. Manifestations of respiratory failure are related tothe extent and rapidity of change in PaO2 and PaCO2.

• Assessment
• 1. Dyspnea
• 2. Headache
• 3. Restlessness
• 4. Confusion
• 5. Tachycardia
• 6. Hypertension
• 7. Dysrhythmias
• 8. Decreased level of consciousness
• 9. Alterations in respirations and breath sounds

• Interventions
• 1. Identify and treat the cause of the respiratory failure
• 2. Administer oxygen to maintain the PaO2 level higher than 60 to 70 mm Hg.
• 3. Place the client in a Fowler’s position.
• 4. Encourage deep breathing.
• 5. Administer bronchodilators as prescribed.
• 6. Prepare the client for mechanical ventilation if supplemental oxygen cannot maintain acceptable PaO2 and PaCO2 levels.