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Ch. 37: Disorders of Ventilation and Gas Exchange

Terms in this set (79)

Pleurisy
an inflammation of the pleura
causes pleuritic chest pain.
Pleural effusion
• Abnormal collection of fluid in the pleural cavity as a result of a disease process.

• Types:
- Transudates (renal failure, etc)
- Exudates (protein enriched)
- Empyema (local infection)
- Blood (hemothorax)
- Chyle (chylothorax) (from lymph system)

fluid will settle to bottom of pleural space; fluid cannot be controlled with diuretics; has to be controlled by manually pulling out with a needle

exudate: seen with malignant types of pleural space

hemothorax: common in trauma (rapid deceleration/exceleration injury); or after surgery

pleural space: around lungs
pleural effusion: something in there that doesn't belong
pleuritic chest pain
pain from pleurisy/ pleural friction rub:
severe stabbing pain
pointed pain
relieved by leaning forward
gets worse with deep breaths
Pleural Effusion: Pathophysiology
• Increased capillary pressure
• Increased capillary permeability
• Decreased colloid osmotic pressure
• Increased negative intrapleural pressure
• Impaired lymphatic drainage
Pleural Effusion: Diagnosis
Clinical Manifestations:
• Dullness to percussion
• Absence of breath sounds over affected area
• Dyspnea
• Pleuritic pain
• Hypoxemia

Diagnostic Studies:
• CXR, CT, ultrasound
• Thoracentesis
• Analysis of pleural fluid
Pleural Effusion: Treatment
• Treat the cause
• Thoracentesis
• Chest Tube (to drain when it is bad; might have to leave chest tube in)
Pneumothorax
air in the chest

• Accumulation of air in the pleural cavity
• Partial or complete collapse of lung
• Classifications:
- Spontaneous
-Traumatic
-Tension
Pneumothorax: Pathophysiology
• Normal pressure in the pleural space is negative (subatmospheric)
• Negative pressure is required to keep the lungs inflated.
• Breach in the lung or pleura, allows air to enter the pleural space and the lung or a portion of the lung collapses

stab wound, GSW, intentional trauma from surgery
Spontaneous Pneumothorax
can happen all by itself; for some reason, alveoli pop and leak into pleural space

common in COPD patients bc of inflated chest

more common in tall/thin ppl; lungs hang more freely/maybe have more pressure
Pneumothorax: Diagnosis
Clinical Manifestations:
• Tachycardia
• Decreased or absent breath sounds
• Dyspnea
• Tachypnea
• Chest asymmetry (**** classic sign: chest won't rise when there is no air in there)
• Hypoxemia

Diagnostic Tests:
• CXR
• CT scan (can confirm diagnosis)
• ABG (not specific, but can confirm diagnosis)

if small (not whole lung, ~ 20%), it may resolve on itself
Pneumothorax: Treatment
• Supplemental 02
• Evacuation of the air from the pleural space
• Chest tube insertion - 2nd intercostal space, mid-clavicular line
• Placed to chest drainage system that provides water-seal and suction (Pleuravac)
Tension Pneumothorax: Diagnosis
Clinical Manifestations:
• Tachycardia
• Hypotension
• Distended neck veins
• Tracheal shift
- Mediastinal shift/Trachea not midline

Treatment:
• Immediate decompression of lung by insertion of chest tube

IE: stab wound, GSW

all air accumulating rapidly in pleural space, ticking time bomb, needs immediate decompression

chest tube reestablishes pressure

"Tension pneumothorax is the progressive build-up of air within the pleural space, usually due to a lung laceration which allows air to escape into the pleural space but not to return. Positive pressure ventilation may exacerbate this 'one-way-valve' effect.

Progressive build-up of pressure in the pleural space pushes the mediastinum to the opposite hemithorax, and obstructs venous return to the heart. This leads to circulatory instability and may result in traumatic arrest. The classic signs of a tension pneumothorax are deviation of the trachea away from the side with the tension, a hyper-expanded chest, an increased percussion note and a hyper-expanded chest that moves little with respiration. The central venous pressure is usually raised, but will be normal or low in hypovolaemic states.

However these classic signs are usually absent and more commonly the patient is tachycardic and tachypnoeic, and may be hypoxic. These signs are followed by circulatory collapse with hypotension and subsequent traumatic arrest with pulseless electrical activity (PEA). Breath sounds and percussion note may be very difficult to appreciate and misleading in the trauma room." (trauma.org)
Hemothorax
blood collection in pleural space
after accident, blunt force trauma, surgery, etc.
chest tube drains the blood

"Most small-moderate haemothoraces are not detectable by physical examination and will be identified only on Chest X-ray, FAST or CT scan. However, larger and more clinically significant haemothoraces may be identified clinically. If a large haemothorax is detected clinically it should be treated promptly...
The classic signs of a haemothorax are decreased chest expansion, dullness to percussion and reduced breath sounds in the affected hemithorax. There is no mediastinal or tracheal deviation unless there is a massive haemothorax. All these clinical signs may be subtle or absent in the supine trauma patient in the emergency department, and most haemothoraces will only be diagnosed after imaging studies." (trauma.org)
Atelectasis: Pathophysiology
Incomplete lung expansion
Inadequate surfactant

2 types:
1. *Obstructive atelectasis* (blocked airway by foreign body, tumor, mucus plug,etc.)
Obstructive atelectasis can be *absorptive atelectasis* because the obstruction "creates a pocket of trapped gas in the distal lung unit. The pressure in the pocket initially is close to atmospheric pressure. Mixed venous blood continues to perfuse the pocket, and since the sum of the gas partial pressures in the mixed venous blood is subatmospheric, gas uptake from the pocket by the blood continues and the pocket collapses." (British Journal of Anesthesia)

2. Non-obstructive atelectasis (Injury, Pleural Effusion, Pneumonia, Pneumothorax, Scarring of lung tissue, tumor on outside, surfactant deficiency)
Non-obstructive atelectasis includes: *Compression* (tumor puts pressure on lung)

• Cause - inadequate ventilation, mucus plug, external compression by fluid, mass, exudate

• Patho: decreased ciliary function → secretion retention → airway obstruction → impaired cough reflex → hypoventilated alveoli → hypoxemia → acute respiratory failure

gas exchange cannot take place bc alveoli are collapsed and not touching capillaries

at risk: obese patient, pregnant patient, patient not taking normal breaths, post-op
(ie. in pain after surgery, not breathing normally bc it hurts too much)

usually occurs regionally and can be treated

tumor can cause compression--causes alveoli to collapse
Which type of commonly-encountered patient would be at risk for atelectasis?
surgical patients!! atelectasis can lead to pneumonia--not deep breathing bc of pain
ANY post-op patient (when under anesthesia, no periodic deep breaths to vent alveoli AND pain from breathing after surgery--no deep breaths)
early signs: cough, sputum production, tachycardia, low grade fever
LATE sign: cyanosis
give pain medication to ease breathing, but too much pain meds can cause atelectasis bc they don't breathe deeply and lay around
Post-Op Atelectasis: Diagnosis
Clinical Manifestations:
• Cough
• Sputum production
• Low-grade fever
• Dyspnea, tachypnea
• Tachycardia
• Anxiety
• Cyanosis
• Decreased breath sounds/crackles

Diagnosis:
• Based on sx/sx
• CXR
Post-Op Atelectasis: Treatment
Treatment:
• Prevention!!!!!
- pre-op education
- turn, cough, deep breathe
- early ambulation
- incentive spirometry

• Improve ventilation and remove secretions

• Nebulizer treatment/dilators

• Bronchoscopy (in very bad cases)
Chronic Obstructive Airway Disease (3)
Caused by disorders that increase the resistance to airflow:
• Bronchial Asthma
• Bronchitis
• Emphysema
Bronchial Asthma
• Chronic inflammatory airway disease
• Recurrent episodes of airway obstruction and bronchial hyperresponsiveness, usually reversible
• May be triggered by extrinsic causes (atopic), intrinsic causes (nonatopic) or exercise
(allergic responses--usually reversible)
• Cartilaginous layers of upper airway are gradually replaced by smooth muscle
(want to minimize change in cells between cartilaginous layers and smooth muscle)
• Better disease management has decreased mortality and hospitalizations
Asthma: Pathophysiology
everything leads to bronchospasms--patients presents with WHEEZING

Early phases:
Allergen --> Mast Cells released --> bronchospasm

Mast cells --> inflammatory cells --> airway inflammation

Late phase:
airway inflammation --> more inflammatory cells

airway inflammation --> Edema, Epithelial injury, impaired mucociliary function (secretions retained, not expectorated)

airway inflammation --> airflow limitation, increased airway responsiveness --> more BRONCHOSPASMS
In bronchial asthma, which WBC would be elevated on the CBC?
Eosinophils--more specific for allergic responses

(IgE is increased in asthma)
Asthma: airways
asthma: assymetric shape
Asthma: Diagnosis
Clinical Manifestations *
• Cough
• Wheezing
• Chest tightness
• Prolonged expiration
• Tachycardia
• Tachypnea
• Dyspnea

Diagnostic Test:
• ABG
• Pulmonary Function Test (not done in acute setting)
• Determination of allergens → skin testing
• CBC (presence of eosinophils)
Asthma: Management
• Four classifications of chronic asthma:
- Mild intermittent
- Mild persistent
- Moderate persistent
- Severe persistent

• Stepwise approach:
- Prevent symptoms, reduce triggers
- Daily meds for long-term control
- "Rescue" medications for quick relief
Chronic Obstructive Pulmonary Disease (COPD)
also known as Chronic Recurrent Airway Obstruction

• Caused mainly by smoking
• Progressive, debilitating, irreversible
• Affects 11 million Americans
• 4th leading cause of death in US
• Males more than females
• Occupational exposure
• Familial tendency
COPD: Chronic Bronchitis
Blue Bloater

• Obstruction of airways caused by chronic inflammation and fibrosis of bronchial wall

• Hypertrophy of submucosal glands with hypersecretion of mucus with excessive bronchial secretions

disease of bronchi: too much mucus
COPD: Emphysema
Pink Puffer

• Enlargement of air spaces caused by destruction of alveolar walls and capillary beds

• Loss of alveolar tissue → decreased surface area for gas exchange

• Loss of elastic lung fibers → airway collapse, air-trapping

• Retained CO2

disease of air space
COPD: Chronic Bronchitis: Pathophysiology
• Chronic productive cough for 3 months in 2 consecutive years
• Hypersecretion of mucus in large airways
• Hypertrophy of submucousal glands in trachea and bronchi
• Increase in goblet cells and excess mucus production in small airways
COPD: Chronic Bronchitis: Clinical Manifestations
blue bloater

Clinical Manifestations:
-excess body fluids
-chronic cough
-shortness of breath on exertion
-increased sputum
-cyanosis (late sign)

chronic hypoxemia
In Chronic Bronchitis, why would the RBC count be elevated?
polycythemia: the bone marrow makes stem cells of RBC, differentiated in bone marrow based on what body needs,
chronically low O2= chronic prompting for stem cells to turn into RBC, to carry more O2
COPD: Chronic Bronchitis: Diagnostic Testing
Pulmonary Function Testing:
increased residual volume
decreased vital capacity
(may have decreased inspiratory and expiratory flow rates)

**Arterial Blood Gases (ABGs):**
mild to severe hypoxemia
mild to severe hypercapnea
compensated respiratory acidosis

Complete Blood Count:
Polycythemia
COPD: Emphysema: Pathophysiology
Pink Puffers

caused by smoking and genetics
alpha 1- antitrypsin is very important in this disease process;

smoking attracts inflammatory cells that release elastase, smoking causes a decrease in alpha 1- antitrypsin (the inhibitor responsible for counteracting elastase)

elastase, partially uninhibited by decreased alpha 1-antitrypsin, causes destruction of elastic fibers in the lung which causes emphysema

the alpha 1- antitrypsin deficiency can also be genetically inherited and not caused by smoking
COPD: Emphysema: Alveolar Changes
Emphysema: weakened and collapsed alveoli with excess mucus; air sacs grow together and form blebs

decreased area for gas exchange

problems:
1) a lot less surface area - hypoxemia
2) over distended with retained CO2 - air trapping --- they can rupture and cause pneumothorax

Destruction of alveolar septa → elimination of portions of the capillary bed → loss of elastic tissue → air trapping→ enlarged air sacs → hyperinflated lungs

elastic tissue lost-- hyperexpanded: wasted air not participating in gas exchange
hyperinflated lungs stretch out rib cage
COPD: Emphysema: Barrel Chest
• Loss of lung tissue elasticity results in
hyperinflation of lungs with increased chest diameter

barrel chest develops when lungs become more and more inflated

AP diameter to transverse 1:2 ratio;
in emphysema becomes 1:1
COPD: Emphysema: Clinical Manifestations
Pink Puffers

- use of accessory muscles to breathe
- pursed-lip breathing
- minimal or absent cough
- leaning forward to breathe
- Dyspnea on exertion (late sign)

metabolic rate in patients is very rapid--uses a lot of energy to breathe

PROBLEM: air trapping; can't get it out--"pursed lip breathing" to get more air out of the lungs
COPD: Obstructive Disorders: Diagnosis and Treatment
treatment is supportive, not curative

Diagnosis:
• H&P
• Pulmonary function
• CXR, shows dark air
• Labs

Treatment:
• Smoking cessation
• Bronchodilators, anticholinergics, expectorants
• Steroids (acute)
• O2 - low dose, SaO2>90%
• Nutrition
• Immunizations
COPD: Diagnosing with spirometry
• Spirometry to measure:
- Forced Vital Capacity (FVC)
- Forced Expiratory Volume in one second (FEV1)

take in a deep breath and they can't blow out in one long puff

Typical findings include:
- Decreased FEV1
- Reduced FEV1/FVC ratio (< 70%)*
- Increased residual volume
- Increased total lung capacity
Cystic Fibrosis
a hereditary disorder characterized by lung congestion and infection and malabsorption of nutrients by the pancreas
Cystic Fibrosis: Symptoms
• Causes thick mucus with impaired clearance in bronchi and frequent lung infections
• Clubbing may be present (painless bulbous enlargement of the end of the digit (finger or toe)
• Due to chronic hypoxemia
Cystic Fibrosis: Treatment
supportive treatment, not curative

antibiotics, postural drainage, and percussion
Which chronic pulmonary diseases are considered obstructive in nature?
asthma, emphysema, and bronchitis
Which chronic pulmonary disease is due to a hypersensitivity reaction causing bronchospasm?
asthma
Which two chronic pulmonary diseases are classified as "COPD"?
emphysema and chronic bronchitis
Out of two COPD diseases, which one causes increased mucus production?
chronic bronchitis
Out of two COPD diseases, which one causes retention of CO2, air trapping and destruction of alveolar walls?
emphysema
How does pursed lip breathing help the dyspnea associated with COPD?
it helps control emptying of alveoli through prolonged expiration
A nonsmoker who develops emphysema needs to be evaluated for a decreased level of which enzyme?
alpha 1 antitripsin
Pulmonary Emboli
Undissolved, detached material that occludes blood vessels of the pulmonary vasculature

What can be an emboli?
* Thrombus
* Fat globules
* Air
* Amniotic fluid
* Foreign material
Pulmonary Emboli: Virchow's Triad
Venous Stasis: ie. bedridden patient

Hypercoagulability: sluggish blood: dehydration, primary clotting disorders, post op

Vascular wall damage: injury, surgery
Pulmonary Emboli: Risk Factors
• Immobility
• Previous DVT
• Recent surgery
• Previous CVA, SCI
• Malignancy
• Smoking
• Obesity
Pulmonary Emboli: Pathophysiology
• Emboli released from DVT
• Travel toward the heart and lungs
• Lodge in the pulmonary vasculature
• Vasoconstriction → increased pulmonary artery pressures
• Increase workload for right ventricle → right sided heart failure
• Hypotension from decreased CO
• Shock

small: sometimes no problem
large: can obstruct and cause pulmonary infarct
Pulmonary Emboli: Diagnosis
Signs & Symptoms:
• Restlessness, anxiety
• Tachycardia, tachypnea
• Sudden dyspnea
• Chest pain
• Hemoptysis
• Heart failure, shock, respiratory arrest

*don't always know that symptoms are of PE, so we should always be highly suspicious
in post op: sudden onset, fine before

Diagnostic Tests:
• V/Q scan
• ABG's
• Pulmonary arteriography** (best test)
• Spiral CT
Pulmonary Emboli: Treatment
Goals:
• Prevention - primary treatment - HOW?? (compression hoses, prophylactic treatment, ambulation after surgery)
• When occurs → stabilize patient condition
• Dissolve existing emboli and prevent new ones from forming (location that matters; don't cause problems until they are caught in the lung)

• Measures to improve respiratory and vascular
status:
- Oxygen
- Bedrest
- Ventilator support

• Pharmacologic Treatment:
- Anticoagulants - Heparin, Coumadin (warfarin)
- Thrombolytic therapy

• Surgical Intervention:
- Embolectomy
- IVC (inferior vena cava) filter (catches clot on way to lungs; dissolve in cage)
A blood clot that becomes a pulmonary embolus → is it a V or Q problem?
bc its a blood clot, it deals with Q (perfusion)
Pulmonary Hypertension
• Normal pulmonary circulation - high flow, low pressure system
• Pulmonary hypertension = mean PAP > 25 mm Hg
• Increases workload of right heart
• May be primary or secondary (chronic hypoxemia)

"Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of your heart.

Pulmonary hypertension begins when tiny arteries in your lungs, called pulmonary arteries, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through your lungs, and raises pressure within your lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and eventually fail." (mayoclinic)

(can be caused by: pulmonary embolism, COPD, lupus, sleep apnea, heart abnormalities, sickle cell anemia, AIDS, cocaine, etc.)
Name a cause of chronic hypoxemia.
1. Sleep apnea; stop breathing during the night & overtime and will cause pulmonary hypertension -- get bigger & tighter & increase in workload of right ventricle
Pulmonary Hypertension: Pathophysiology
• Chronic exposure to increased pressures
• Changes in the small vessels lumen → local tissue hypoxia, acidosis
• Small vessel walls thicken → increase in muscle
• Pulmonary artery wall fibrosis
***• Ability to handle increased RV flow is impeded (vessel constriction)
***• Right ventricular demands exceed capacity
***• RV enlarges → hypertrophy → failure
Pulmonary Hypertension: Diagnosis
Signs/Symptoms:
• Dyspnea
• Exercise intolerance
• Chest pain on exertion
• Fatigue
• Hemoptysis
• Pulmonary edema
• Right sided heart failure (cor pulmonale)

Diagnostic Tests
• Right heart cath **** (standard)
• CXR
• EKG
• Echocardiogram
• ABG
• VQ scan

*usually a secondary diagnosis; don't even know they have it; right heart cath has to be done to really know whats going on
Pulmonary Hypertension: Treatment
not curable

• Early identification and control of underlying cause (ie. CPAP for sleep apnea)
• Oxygen
• Vasodilators → calcium channel blockers, prostacyclin
• Diuretics
• Lung transplants
Pulmonary Hypertension: Cor Pulmonale
right sided heart failure
an enlargement of the right ventricle due to the high blood pressure in the lungs, usually caused by chronic lung disease

Pure right sided heart failure caused by chronic lung disease = so pulmonary hypertension can lead to cor pulmonale

not caused by left-sided heart failure
Acute Respiratory Failure
• Rapidly occurring inability of the lungs to maintain adequate oxygenation of blood and/or impairment of CO2 elimination

• Inadequate gas exchange ***
- PaO2 < 60 mm Hg (oxygenation)
- Pa CO2 > 45 (ventilation)
- pH < 7.35 (resp. acidosis)

• Not a disease state but a blood gas diagnosis

• Need to look deeper - for CAUSE

Lungs fail to adequately oxygenate the blood and/or prevent carbon dioxide removal.

"Respiratory failure is a condition in which not enough oxygen passes from your lungs into your blood. Your body's organs, such as your heart and brain, need oxygen-rich blood to work well.

Respiratory failure also can occur if your lungs can't properly remove carbon dioxide (a waste gas) from your blood. Too much carbon dioxide in your blood can harm your body's organs.

Both of these problems—a low oxygen level and a high carbon dioxide level in the blood—can occur at the same time." (NIH)
Acute Respiratory Failure: Hypoxemia
• Oxygenation parameters are the paO2 and O2 saturation
• Remember the oxygen hemoglobin dissociation curve
• Normal paO2 is 80-100
• Normal saO2 is 95 - 100%
• Absolute minimal acceptable level for paO2 is 60
• Absolute minimal acceptable level for saO2 is 90

Anything less than 80 is really hypoxemia but don't actually say that unless its less than 60 (so basically 60-80 with a patient who has COPD)
Acute Respiratory Failure: Oxygen Hemoglobin Dissociation Curve
shift to right = most often seen in increased oxygen demand situations

right: increased PCO2, decreased pH
left: decreased PCO2, increased pH
Acute Respiratory Failure: Causes
Ventilatory (Acute Hypoventilation):
* Atelectasis
* Oversedation
* Respiratory muscle fatigue
* Neuromuscular disorders
* COPD

Oxygenation Failure (Diffusion):
• Atelectasis
• Pneumonia
• Pulmonary edema
• ARDS
• COPD
• Pneumothorax


PaCO2 > 45 = hypercapnea
paO2 < 60 mm Hg hypoxemia

Hypoventilation is the ONLY cause of hypercapnea
prolonged=acute respiratory failure
Eupnea
normal tidal volume in and out
Dyspnea
labored breathing
Orthopnea
can't breathe laying flat
Kussmaul Respiration pattern
hypercapnea
getting rid of CO2, think about breathing
Cheynes-Stokes pattern
clustered breathing; periods of apnea; not the worst breathing pattern possible; ventilator
Ventilation-Perfusion Relationships
Pulmonary Embolus (V>Q) mismatch: Ventilation without Perfusion

Atelectasis (Q>V):
Perfusion without Ventilation
"dead space"; shunt
Acute Respiratory Failure: Oxygenation Failure: Transport
perfusion problem

- Decreased cardiac output
• HR, SV, BP, PEEP, drugs

- Decreased hemoglobin
• Bleeding, anemia

- Decreased ability to bind
• Carbon monoxide

- Pulmonary embolus
• `VQ mismatch ( also a diffusion problem)--->can lead to a diffusion problem, due to wasted ventilation
Acute Respiratory Failure: Hypoxemia: Clinical Findings
• Earliest signs: restlessness, agitation, apprehension , confusion***
• Increased work of breathing (tachypnea, tachycardia, ↑BP, use of accessory muscles) **
• Decrease in spO2; delayed capillary refill
• Cyanosis is a LATE SIGN!
Acute Respiratory Failure: Treatment
• Hypercapnea:
Ventilate

• Hypoxemia:
Oxygen - BIPAP
Mechanical ventilation
PEEP

*TREAT THE CAUSE!*
You are caring for a post-op patient who
has developed pneumonia. The spO2 is
88% on 40% FIO2 and the health care
provider orders an ABG and a
nonrebreather mask. The PaO2 comes
back as 50 mm Hg and the O2 sat as 88%
despite supplemental oxygen therapy with
a nonrebreather mask. What is this
condition called? What action would you
expect to be taken?
refractory hypoxemia (give 100% O2 and they don't get better=shunting=alveoli collapsed, etc)

they need a ventilator or BiPap
Adult Respiratory Distress Syndrome
a complication, not a disease

• Acute lung injury causes inflammatory response &
increased capillary permeability
• Fluid leaks into ICS and alveoli
• Surfactant is decreased - alveoli collapse
• Causes "refractory hypoxemia"

capillaries become leaky; cells and water squeezes and you have pulmonary edema; surfactant decreases; alveoli collapse

"Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. More fluid in your lungs means less oxygen can reach your bloodstream. This deprives your organs of the oxygen they need to function.

ARDS typically occurs in people who are already critically ill or who have significant injuries. Severe shortness of breath — the main symptom of ARDS — usually develops within a few hours to a few days after the original disease or trauma." (mayoclinic)
Adult Respiratory Distress Syndrome: Stages of Edema formation and Symptoms
A. Latent stage - slight changes in alveolar-capillary membrane - no symptoms

B. Interstitial edema occurs with increased flow of fluid into the interstitial space - only symptom = SOB, anxiety

C. Alveolar edema occurs when the fluid crosses the blood-gas barrier - classic signs of respiratory distress

---occurs all over the lungs (unlike pneumonia); need to be ICU and put on ventilator
Adult Respiratory Distress Syndrome: Risk Factors and Causes
Direct Causes:
• Aspiration
• Pneumonia **
• Pulmonary contusions
• Airway burns
• Chemical inhalation

Indirect Causes:
• Sepsis/ SIRS
• Pancreatitis
• Blood transfusion-PRBC
• Fat emboli
• Burns > 30% BSA
• Drug overdose

*anybody that has had injury need to suspect them of ARDS; and any suspection you would start to asses the oxygen sat.
Adult Respiratory Distress Syndrome: Treatment
symptoms: (mayoclinic)
Severe shortness of breath
Labored and unusually rapid breathing
Low blood pressure
Confusion and extreme tiredness

• Similar to ARF
• Oxygen high flow
• Mechanical Ventilation with PEEP (positive end expiratory pressure)
• Positioning (head of the bed is up)
• Treatment of pulmonary edema (diuretics)
What is an early sign of hypoxemia?
A. Cyanosis
B. Bradycardia
C. Restlessness
D. Palpitations
C. Restlessness
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