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ARDS
Statistics
Approximately 190,000 Americans are affected by ARDS annually.
Up to 30% of ARDS cases can be fatal
◦ improvement from the 50%-70% death rate just 20 years ago.
Patients who develop ARDS due to trauma or a lung infection usually do better than those who
develop the condition due to sepsis (infection of the blood).
Ranges from1.5 to 75 cases per 100,000 persons
What is ARDS?
Occurs when fluid builds up in the alveoli of the lungs.
With increased fluid, less oxygen can reach the bloodstream.
Organs become oxygen deprived.
ARDS usually follows a major illness or injury
◦ Most patients are already hospitalized.
Symptoms
Severe shortness of breath.
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Usually develops within a few hours to a few days after the original disease or trauma.
Risk of death increases with age and severity of illness.
Survivors may recover completely
◦ Lasting lung damage can occur.
Symptoms Continued
Labored and unusually rapid breathing
Low blood pressure
Confusion and extreme tiredness
Causes
Bacteremia
Sepsis
Trauma, with or without pulmonary contusion
Fractures, especially multiple fractures and long bone fractures
Burns
Massive transfusion
Pneumonia
Causes Continued
Inhalation of harmful substances
Head, chest or other major injury
Aspiration
Drug overdose
Near drowning
Post perfusion injury after cardiopulmonary bypass
Pancreatitis
Fat embolism
Risks
People with history of chronic alcoholism are at higher risk of developing ARDS
◦ They are also more likely to die from ARDS
MODS
ARDS is a prominent manifestation of Multiple Organ Dysfunction Syndrome (MODS)
MODS occurs when the organ systems fail
Acute respiratory distress syndrome (ARDS) is a rapidly progressive disorder that initially
manifests as dyspnea, tachypnea, and hypoxemia, then quickly evolves into respiratory failure.
Because the presenting symptoms of ARDS are nonspecific, physicians must consider other
respiratory, cardiac, infectious, and toxic etiologies
Patient history (i.e. comorbidities, exposures, medication) in conjunction with a physical
examination focusing on the respiratory and cardiovascular systems can help narrow the
differential diagnosis and determine the optimal course of treatment.
Difference in diagnosing CHF and ARDS
Congestive heart failure is characterized by fluid overload
Patients diagnosed with ARDS, by definition, do not show signs of left atrial hypertension or
overt volume overload.
Patients with congestive heart failure may have edema, jugular venous distension, third heart
sound, an elevated brain natriuretic peptide level, and a salutary response to diuretics.
Jugular Venous Distention – this occurs in HF, not ARDS
Distinguishing between Pneumonia and
ARDS
Patients with uncomplicated pneumonia may have signs of systemic and pulmonary
inflammation (i.e., fever, chills, fatigue, sputum production, pleuritic chest pain, and localized or
multifocal infiltrates);
◦ If hypoxia is present, the patient should be given oxygen.
If oxygen administration does not correct the hypoxia, ARDS should be suspected and confirmed
based on AECC diagnostic criteria.
Patients with combined pneumonia and ARDS should receive treatment with antibiotics and
ventilator management.
Physical
ARDS may cause abnormal breathing sounds, such as crackling.
signs of extra fluid in other parts of your body. Extra fluid may mean there are heart or kidney
problems.
Cyanosis - bluish color on skin and lips
Initial Tests
An arterial blood gas test. This blood test measures the oxygen level in your blood using a
sample of blood taken from an artery. A low blood oxygen level might be a sign of ARDS.
Chest X-ray
Blood Tests
Other Tests
Chest Computed Tomography
Heart tests that look for signs of heart failure.
Pathophysiology
ARDs is characterized a sudden respiratory failure.
Clinical signs of ARDS can be seen within the first few hours:
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dyspnea,
tachypnea,
pallor,
diaphoresis.
an increase in the use of the accessory muscles, including the internal intercostal muscles, pectoralis
major, scalene, trapezius and the sternocleidomastoid muscles.
Pathophysiology
Injury to the vascular system of the lungs is typically the most significant cause of ARDs
Neutrophils are then seen to accumulate in the area of injury. There they release toxic
mediators such as pro inflammatory cytokines, reactive oxygen species, proteases, and
procoagulant molecules.
Essentially, it is a large inflammatory response.
Pathophysiology
While injury to the epithelium of the lung causes damage, it is the harm done to the alveoli that
causes the biggest problem
Neutrophils migrate from their residence in the lung epithelium and move into the air spaces.
From there they continue their course into the epithelium of the alveoli.
The Exudative Phase
In this phase, one experiences hypoxemia due to the pulmonary edema in the alveoli.
The large number of neutrophils release toxic molecules that can destroy the tight junctions
and induce apoptosis of the type I and type II alveolar cells
◦ As the Type II cells are destroyed, surfactant production in decreased which leads to the collapse of the
alveoli.
This is the point at which mechanical ventilation (which will be discussed later) would be used.
Increasing complications in this phase
The increase in pulmonary resistance leads to hypertension which can lead to right ventricular
failure
The next phase….
If ARDS is not resolved in the first week, a patient can enter the fibroproliferation phase.
During this period, the patient can develop fibrosing alveolitis, or inflammation between the
fibrous tissue between the alveoli and the lung that causes fibrogenesis.
◦ This creates a closely woven tissue that isn’t as elastic. That poses a problem when trying to breathe,
doesn’t it.
The resolution phase
The next phase is the resolution phase. At this time, the lungs are returning to their normal
histology. While much of this stage remains unclear, researchers have seen the epithelium
become repaired and the neutrophils undergo apoptosis.
The edema is the lungs is transferred from the alveoli into the lung interstitium and the protein
is removed. The fibrotic changes that occur also require remodeling but little is known about
this process.
There is still so much that we don’t
know…
Acid Base Disorder
Often present in patients
Acid-base homeostasis involves the lungs, the kidneys and endogenous buffers.
Normal Body pH is 7.4
Buffers
Buffering is the “…ability of a weak acid and its corresponding base to resist change in the pH
upon the addition of a strong acid or base”
Principle buffer in the body is the carbonic acid/bicarbonate base.
◦ Almost all of the carbonic acid in the body exists as carbon dioxide.
However, the concentration of acid or base in your blood can reach levels which exceeds
buffering capacity.
The Role of the Kidneys
This is considered the metabolic parameter.
The primary role of the kidneys in this system is to regulate the concentration of bicarbonate,
which is a base.
◦ HCO3 binds with the free H+ to reduce its concentration
Bicarbonate is reabsorbed in the proximal tubule
Metabolic Acidosis
Metabolic acidosis is considered a blood pH of <7.35 and/or a low serum bicarbonate
concentration.
If we don’t have enough HCO3 in our blood we will have more H+ floating around which will
make it acidic.
Compensation for Metabolic Acidosis
When the body is in metabolic acidosis the lungs will often compensate by causing
hyperventilation. This hyperventilation causes the release of more CO2.
The release of this CO2 is the lungs effort in decreasing the acidity of the blood.
Metabolic Alkalosis
Marked by an elevated pH and an increase in serum bicarbonate levels.
The bicarbonate is binding to all the free H+ and therefore making the blood more alkaline
Causes include:
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Loss of gastric acid secondary to vomiting
Nasogastric suctioning
Diuretic use
Parenteral nutrition has excessive acetate and chloride.
Compensation for Metabolic Alkalosis
Respiratory compensation is relatively minor
The role of the lungs
This is the respiratory parameter.
CO2 will combine with water to make carbonic acid, so CO2 itself is considered an acid.
The lungs play a role in regulating how much CO2 is in the body.
Respiratory Acidosis
Can be due to hypoventilation
Other causes include
◦ Central nervous system depression
◦ Chronic pulmonary diseases
Side effects include altered mental status, motor disturbances and dyspnea
Respiratory Acidosis
Patients who have a severe problem with excreting CO2 or have hypoxemia will need to be
provided with adequate oxygen.
This often requires mechanical ventilation.
◦ In an extremely severe case, sodium bicarbonate may be administered. However, many complications
can arise so it should be used with caution.
Compensation for Respiratory Acidosis
The proximal tubule of the kidney will begin to reabsorb more bicarbonate.
Respiratory Alkalosis
Occurs because of a decrease in CO2 and an increase in pH due to hyperventilation
Causes:
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Hypoxemia
Stimulation of respiration
Pneumonia
Interstitial lung disease
Pulmonary emboli
Compensation for Respiratory Alkalosis
Chemoreceptor in the brain stem, carotid arteries and aortic bodies sense the change in the pH .
The kidneys will then try to compensate by excreting more bicarbonate rather than reabsorbing
it.
With these imbalances and compensations
how are we able to diagnose the actual
problem?
This can be easily done by asking three questions
◦ Does the pH indicate acidosis or alkalosis?
◦ Is the cause of pH imbalance respiratory or metabolic?
◦ Is there compensation for the imbalance?
Acid
Normal
Alkaline
pH
<7.35
7.35-7.45
>7.45
PaCO2
>45
35-45
<35
HCO3
<22
22-26
>26
In order to answer those questions we can
use a tic-tac-toe chart organize what we
know…
Acid
Normal
Alkaline
We fill out this chart using the our patient’s Arterial Blood Gas (ABG) results, which include the pH, PaCO2,
and HCO3 like we saw on the last chart.
Patient: RM
◦ pH: 7.26
◦ PaCO2: 33
◦ HCO3: 17
Acid
pH
Acid
Normal
Alkaline
pH
<7.35
7.35-7.45
>7.45
PaCO2
>45
35-45
<35
HCO3
<22
22-26
>26
Normal
Alkaline
PaCO2
HCO3
So, this means that he is in a state of acidosis because of a decreased level of bicarbonate. We see that his PaCO2 is
more alkaline than what is normal. What does this mean?
Now for one on your own…
Patient: LR
Acid
Normal
Alkaline
pH: 7.48
pH
<7.35
7.35-7.45
>7.45
PaCO2: 31
PaCO2
>45
35-45
<35
HCO3: 21
HCO3
<22
22-26
>26
Acid
Normal
Alkaline
Interventions
Medicine to prevent and treat infections and to relieve pain
Oxygen Therapy & Support
Ventilation
Tracheostomies ( incision in the windpipe)
MNT
Treatment of underlying disease or trauma
Medications
Corticoid steroids to decrease inflammation and immune response and WBC movement into alveoli
◦ Prednisone
Antibiotics
◦ Prevent Sepsis  MODS
Diuretics
◦ Control fluid levels
Immunosuppressant
◦ To decreases inflammation
Blood pressure supporting medications
◦ Dopamine – increases blood pressure
◦ Neosynephrine – increases blood pressure
sedative and paralytic medications are used to decrease metabolism
Medications & Things to Avoid
Too much CHO
◦ Stress on lungs due to increase O2 needs
Too much fluid
Blood thinners
◦ Decreases blood pressure
Oxygen Therapy & Support
Nasal cannula: Oxygen through tubes in your nose or through a mask
◦ Supplemental oxygen
Non-invasive
Machine Ventilation
When?
◦ When lungs are no longer able to work on their own
◦ Why not immediately?
◦ Ventilation causes atrophy of the lung muscles and other complications
Goal?
◦ support the patient’s breathing during the time needed for the lungs to recover
◦ Get carbon dioxide out of the body
What is it?
Mechanical ventilator: Oxygen through a breathing tube. The tube is flexible and goes through
your mouth or nose into your windpipe. The tube is connected to a ventilator
◦ The ventilator does the actual breathing for you or assists you in breathing
Mechanical Ventilator
How Does It work?
The patient is connected to the ventilator by a tube, which goes through their mouth or nose to
the trachea. This tube (referred to as an endotracheal tube) passes through the vocal cords
https://www.youtube.com/watch?v=V8VIw0fk4X0
Problems with Ventilation
Respiratory muscle weakness
Retention of CO2
Patient is unable to speak due to tube blocking vocal chords
Pt put on sedatives and pain medication
◦ Ativan or Versed
Risk of infection
◦ Ventilation associated Pneumonia (VAP)
Coughing risk to irritate lungs
Other Risks of Ventilators
Pneumothorax
◦ What is it?
◦ Air leaks out of the lungs into the space between the lungs and the chest wall
◦ Problems?
◦ Pain, shortness of breath, and lungs can collapse
◦ Cause?
◦ Forced airflow
Increase Risk Fatcors
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Cystic Fibrosis
Emphysema
Medically compromised
Malnourished
Older
Feeding on Ventilation
Enteral Feeding
◦ Until the patient can eat again by mouth, food is given into the stomach or intestine
through a feeding tube by enteral nutrition.
◦ If liquid feeding is required for longer than one or two weeks, a surgical procedure
may be performed to place a tube through the abdominal wall directly into the
stomach or intestine (“G-tube”, “J-tube”, or “PEG”).
Parenteral Feeding
◦ Given if the esophagus is obstructed and feeding cannot be done enterally
How feeding works
Pulmonary Enteral Formulas
Pulmonary
Kcal/ml
Protein (g/L) CHO (g/L)
Fat (g/L)
mOsm
Free H2O
(mL/L)
1.5
63-68
93-95
3300-785
535-785
100-106
PEPTAMEN AF®
◦ Helps with inflammatory response and GI absorption/ high protein/ antioxidants
Oxepa®
◦ Calorically dense/ helps inflammatory response
Energy Requirements on Ventilation
1.
PSU (HBE) = HBE(.85) + Tmax(175) + Ve(33) – 6344 (mechanically ventilated, non-obese,
critically ill patients)
2.
PSU (HBEa) = HBEa(1.1) + Tmax(140) + Ve(32) – 5340 (mechanically ventilated, obese,
critically ill patients)
3.
PSU (m) = Mifflin(0.96) + Tmax(167) + Ve(31) – 6212 (most precise expect for obese elderly)
Tmax = maximum body temp in 24 hours
Ve = expired minute ventilation
Tracheostomies
Tracheostomies
What is it?
◦ A breathing tube, also called a trach tube, is put through the tracheostomy and directly into the
windpipe to give more oxygen from the ventilator
When?
◦ Usually done 14 days after ventilation and if patient will be on ventilation for a couple of weeks
How long?
◦ Usually temporary until off the ventilator but can be permanent
Tracheostomies
Why?
◦ Patient is unable to do the nasal or oral route for mechanical ventilation
◦ Patient is sensitive to coughing
◦ Patients with swallowing problems
Risks
◦ Infection
Feeding
◦ Enteral
Extracorporeal Membrane Oxygenation
(ECMO)
ECMO
Why?
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Individuals with gas-exchange abnormalities
Individuals with cardiac dysfunction
Lung dysfunctions
Septic shock
What?
◦ Blood is taken from the veins through a cannula and put into an oxygenator that puts O2 in the blood
and takes out Co2
◦ Another cannula brings the blood into the superior vena cava
Complications
◦ Hemorrhage
◦ Infection
MNT
Factors
◦ Underlying disease, age, and prior nutrition status
Increase caloric needs
◦ Due to hypercatabolism or hypermetabolism
Cautions
◦ Malnourishment and underweight
Feeding Methods
Small portions of favorite foods
◦ If not ventilated or has tracheostomy
Intubated
◦ Enteral feeding or parenteral
STUDY
-bolus administration may not be as efficient as continuous administration.
Nutritional Assessment
Indirect calorimetry measurements
Anthropometric measurements
Labs can be thrown off
◦ Fluid imbalances, mediations, and ventilator support
Immunocommpetence
Chronic mouth breathing
Aerophagia
◦ Swallowing too much air
Dyspnea
◦ Difficulty or labored breathing
Depression
Exercise tolerance
Goals
Meet basic nutritional requirements
Preserve LBM
Restore respiratory muscle mass and strength
Maintain fluid balance
Improve resistance to infection
Facilitate weaning form oxygen support and ventilation
Energy Requirements
Energy needs are elevated
◦ Hypercatabolism and hypermetabolism from immune system
◦ Inflammation and cytokines can lead to increased daily energy expenditure by up to 20%
DAILY MONITORING IS CRUCIAL
Requirements best determined by continuous assessment due to fluctuation
Determining Energy Requirements
Indirect calorimetry (IC) is the “gold standard”
◦ O2 and Co2 are measured by breathing into a mouthpiece, mask or canopy
Contraindications for using IC on ventilated patients
◦ Bias flow
◦ Air leaks in tubing or ventilator
Determining Energy Requirements
The Weir
◦ [3.94(VO2) + 1.11(VCO2)] 1.44 = 24 hr KCAL
◦ equation respiratory quotient value 0.85 constant is used
◦ [[( 3.94 (VCO2/0.85)) + (1.106 VCO2)]]X 1.44–2.17 UN
PENN Equations
◦ Most reliable next to indirect calorimetry
Harris–Benedict equation multiplied by stress factor (least reliable)
CHO Requirements
Influenced by
◦ Organ system decompensation – inability to compensate the load created by the disease
◦ Respiratory status
◦ Ventilation methods
Fat Requirements
Determined by calories left over after protein requirements are met
Often split evenly with CHO
immunomodulatory properties of lipid emulsions, as shown by their ability to alter cytokine
release, to modify leukocyte function, and to influence the generation of lipid mediators that
display both pro- and anti-inflammatory properties
Protein Requirements
Increase protein needs due to negative nitrogen balance
◦ WHY? Not using their muscles = LBM breakdown and trauma/sepsis/inflammation/underlying disease
Calculated
◦ 1.5 to 2 g/kg body weight
Overfeeding
Complications
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Increased oxygen demand causes unneeded stress on respiratory system
Hypercapnea: increase CO2 in the body that the body cannot get out
lipogenesis
increased glucose levels
◦ Inflammation increased oxygen demand
◦ inability to wean from the ventilator
MNT: Overfeeding
Decrease CHO intake and lipid intake
Increase protein intake
Monitor and access energy needs daily
◦ STUDY: Total calories is more important than percent calories from CHO
MNT: Restore Respiratory Muscle Mass &
Strength
Respiratory muscle strength begins to decline after only a few days of suboptimal nutrition
Use a high protein enteral formula to preserve LBM
Lower CHO formula
◦ Decreases strain to metabolize CHO
Monitor caloric needs daily
MNT: Preserving LBM
The body is in a pro-inflammatory catabolic state
Increase protein intake
◦ Enteral formulas with higher protein content
Increase ω-3 FAs (EPA/DHA) through supplements or fish oil
◦ Decreases stress response through changes in cell membrane phospholipids
Use PN if nutritional requirements cannot be met
Vitamin & Mineral Requirements
Exact requirements are unknown
Supply to DRI plus repletion
Those with antioxidant, healing, immunity and anabolism functions may be increased
◦ Vitamin E & C, Selenium
MNT: Improve Resistance to Infection
Omega-3 fatty acid in fish oils
◦ eicosapentaenoic acid (EPA)
◦ docosahexaenoic acid (DHA)
γ-linolenic acid
Antioxidant enriched diets
◦ Vitamin C & E added to diet
Fluids Requirements
Too much fluid will fill the lungs
Not enough fluids will limit blood flow to organs = decrease in oxygen to organs
Usually given intravenously
Carefully monitored
MNT: Fluid Balance
Diuretics are used to maintain fluid balance
Electrolytes are monitored closely
◦ Fluid imbalances
◦ Respiratory acidosis or alkalosis
K+, Ca, Mg loss in urine due to medications
◦ Monitor closely and replace losses through supplements supplements
Feeding Complications From Low Oxygen
Anorexia
Early satiety
Malaise (discomfort or illness)
Bloating
Constipation
diarrhea
MNT: Low Oxygen
Do not overfeed
◦ Decrease the oxygen load needed to metabolize food
Continuous enteral feeding is better than bolus
If oral feeding give them appealing foods in small portions
Fiber for the constipation
Medicine for the bloating
Supportive & Alternative Therapy
Supportive breathing technique called positive end expiratory pressure (PEEP)
Supportive: Noninvasive positive pressure ventilation (NPPV)
◦ Wear a mask connected to a device that uses mild air pressure to keep your airways open while you
sleep
Supportive: Rocking bed
◦ A mattress on a motorized platform rocks back and form as you sleep
Alternative
◦ ECMO
Case Study
Case Study: Anthropometrics
Ht: 5’ 4”
Wt: 122 lbs
◦ UBW: 135 lb
◦ 10% recent wt. loss
BMI: 21.1
Age: 65 years
Case Study: Biochemical
pH: 7.2
◦ Acidic
Co2: 65
◦ Acidic
O2: 56
◦ Low
HCO3: 38
◦ Basic
Case Study: Clinical
Cyanosis
Pitting edema
Distended jugular veins
Hyper resonate breath sounds
Trachea shifted to the right
Using his accessory muscles
Pulse on right side of body is absent
Case Study: Dietary
Retaining fluids
◦ Input: 650 mL/kg
◦ Outputting 525 mL
◦ Net gain of 125 mL per day
Poor appetite
Insufficient calorie intake
Case Study: PES
Problem:
◦ Insufficient caloric intake related to respiratory complications from COPD leading to ARDS as evidenced
by his 24 recall and 13# wt. loss.
Case Study: Nutrition Support
Harris Benedict Equation with stress factor
◦ 66+(6.23*122)+(12.7*64)-(6.8*65)=1,196.86
◦ Multiple by 1.3 stress factor = 1,556
Enteral feeding with PEPTAMEN AF®
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1556kcal/1.2kcal/mL= 1,297mL=54mL/hr
Continuous drip
1297mL/250mL =5.1 bottles*19g of protein=98.5 grams of protein/day
5.1 bottles*26.7 grams CHO=136.1grams/day
5.1 bottles*13.7grams of fat=70 g fat /day
Formula includes omega-3 fatty acids and antioxidants (vitamins C & E and
selenium)
Case Study: Evaluation and Monitoring
Check wt. daily to assess wt. increase or loss
◦ Change caloric intake accordingly
Monitor fluids to determine if he needs a more calorie dense formula or diuretics
Monitor K, Mg, Na due to diuretics
Goal is to preserve LBM through adequate caloric intake