Вы находитесь на странице: 1из 11

Gas Exchange

Book Notes

A. Normal ABGs

a. pH 7.35-7.45
PaCO2 35-45
>95% Base exc. +- 2.0

Bicarb 22-26

PaO2 80-100 SaO2

B. Critical Care and Ventilated/ Intubated patients

a. Endotracheal (ET) intubation

i. Tube is placed into the trachea via the mouth or nose past the
larynx with the help of a laryngoscope or bronchoscope. Placed
in at bedside
ii. A nasal ET intubation is placed in blindly through nose,
nasopharynx, and vocal cords. This is rarely done but needed if
neck and head movement is risky
1. Contraindication in pts. w/ facial fractures or suspected
fracture of skull. WOB is greater, suction and secretion
removal are difficult, and linked to increase of infection
and ventilator-associated pneumonia
iii. Indications:
1. Upper airway obstruction, apnea, high risk of aspiration,
ineffective clearance of secretions, respiratory distress
iv. Risks:
1. If head and neck mobility is limited, teeth chipped or
accidently removed, swallowing is difficult, increased
2. Mouth care may be a challenge due to the tube
a. Use a smaller or pediatric-sized oral products for
suctioning, brushing, cleaning
3. Can become obstruct from pt. biting on tube
a. sedation and bit block is used to prevent this
v. the procedure
1. will need consent before performing, unless emergency
2. inform them how it will happen and that they wont be
able to speak
3. keep ambu bag available, suction, and IV access
4. premedicate the pt. for pain and anxiety
a. Rapid-sequence intubation (RSI)is administration of
both a sedative and paralytic agent for
1. A sedative-hypnotic-amnesic
(Midazolam[Versed}, etomidate
[Amidate]) is used for unconsciousness,
along w/ an opioid (fentanyl) for pain.
Paralytic (succinylcholine [Anectine]) for
muscle relaxer
5. Monitor the pts O2 during procedure and place the pt. in
supine w/ head extended and neck flexed (sniffing

a. For nasal intubation, nasal passage way may be

sprayed w/ (lidocaine[Xylocaine] w/
epinephrine) to reduce trauma and bleeding
6. Preoxygenate the pt. with the BVM for 3-5 mins before.
Each intubation attempt is 30 sec. so ventilate between
each attempt.
7. After attempt, inflate the cuff and confirm placement
while pt. is manual ventilated using the BVM
a. Use CO2 detector to confirm proper placement by
noting the presence of exhaled CO2 from lungs.
Place between BVM and ET tube and observe for
color change or a number. If nothing occurs, may
be in esophagus so attempt to reinsert
8. Auscultate lungs for bilateral breath sounds and
epigastrium for the absence of air sounds. Observe chest
for symmetric chest wall movement and SpO2 should be
9. Once supported place tube on O2 source, suction ET tube
and insert a bite block as needed. Obtain chest x-ray
immediately to confirm tube location.
10.Once confirmed, record and mark the position of the tube
at the lip or teeth and cut excess tubing to reduce dead
air space.
11.Tube is either connected to O2, humidified air, or
mechanical ventilator. Obtain ABGs immediately and
determine baseline oxygen and ventilator status
vi. Nursing care
1. Maintain correct tube placement: If chest tube has moved
it is an emergency. Stay w/ pt., maintain airway, support
ventilation, and call for help to reposition the tube.
2. Maintain proper cuff inflation
3. Monitor oxygenation and ventilation:
a. Assess for hypoxemia: confusion, anxiety, dusky
skin, and dysrhythmia.
b. Hypoventilation: breathing shallow and slowly, may
appear dusk
c. Hyperventilation: breath rapid and deep, may have
numbness and tingling in peripherals. PaCO2 is best
indicator for this.
4. Maintain tube patency: do not routinely suction pt.
a. Indication for suction: visible secretion, sudden
respiratory distress, suspect aspiration, increase
peak airway pressure, auscultation of adventitious
breath sounds, increase respiratory rate/ coughing,
sudden decrease in PaO2 or SpO2
b. Two types of suction: CST (closed suction
technique) or OST (open suction technique) pg.
1616 shows technique
5. Assess for complication

a. Unplanned Extubation: pt. talking, activation of lowpressure ventilator alarm, diminished or absent
breath sounds, resp. distress, gastric distention
1. soft mittens or restraints may be necessary
or sedation
b. Aspiration: prevent vomiting, NG tube on suction,
enteral feeding and keep HOB elevated at mi of 3045o
6. Provide oral care and skin integrity pg. 1617 table 66-9
7. Foster comfort and communication
a. Morphine, lorazepam, proprofol, or other sedatives
to help w/ anxiety
8. Drug therapy
a. Opioid Narcotics
1. Morphine or Fentanyl:
1. Monitor for resp. depression, ortho
hypotension, sedation ,constipation,
urinary retention, N/V
2. Toxicity can be reversed w/ Narcan
b. Muscle relaxants:
1. Succinylcholine [Anectine] is drug of
1. AE: prolonged apnea due to toxicity,
malignant hyperthermia, hyperkalemia
b. Tacheostomy
i. Tube is placed into the trachea via stoma in the neck. Surgical
procedure that is performed when the need for an artificial
airway is expected to be long term
ii. Early tracheostomy (2-10 days) may have advantages over
delayed, especially when ventilation may be needed for longer
than 10-14 days.
c. Mechanical ventilation
i. Process by which FIO2 (21% room air) is moved in and out of the
lungs by a mechanical ventilator
1. It is not curative and it just a means of supporting pt until
ii. Indications: apnea, inability to breathe, acute respiratory failure,
severe hypoxia, respiratory muscle fatigue
iii. Types:
1. Negative pressure vent:
a. Involves the use of chambers that encase the chest
or body and surround it w/ intermittent
subatmospheric pressure. Expiration is passive and
is a noninvasive ventilation (does not require
artificial airway)
2. Positive pressure vent:
a. During inspiration, vent pushes air into the lungs
and expiration is passive.
b. Two different modes:

1. Volume ventilation: predetermined tidal

volume (VT) is delivered w/ each inspiration
2. Pressure ventilation: the peak inspiratory
pressure is predetermined, and the tidal
volume delivered to pt. varies based on the
selected pressure and compliance
iv. Modes of mechanical Ventilation: Table 66-12 pg. 1620
1. Volume modes
a. Intermittent mandatory vent (IMV) and
synchronized intermittent mandatory vent (SIMV)
1. Requires rate, VT, inspiratory, sensitivity, and
PEEP are set
2. In between mandatory breaths pt
spontaneously breathe at their own rate.
3. W/ SIMV, the vent synchronizes the
mandatory breathe w/ pts inspiration
b. Assist-control (AC) or assisted mandatory
ventilation (AMV)
1. Require rate, VT, inspiratory time, PEEP be
2. When pt. initiates a breathe, a full-volume
breath is given
2. Pressure modes
a. Airway pressure release vent (APRV)
1. Provides two levels of continuous positive
airway pressure w/ time release, and permits
spontaneous breathing
b. Pressure- controlled inverse ration ventilation (PCIRV)
1. Combines pressure-limited vent w/ inverse
ration of inspiration to expiration
c. Pressure support ventilation (PSV)
1. Provides augmented inspiration and to a
spontaneous breathing pt.
2. Clinician selects an inspiratory pressure,
PEEP, and sensitivity
3. When pt. breathe, a high flow of gas is given
3. Positive end-expiratory pressure and continuous positive
airway pressure
a. PEEP- creates psotive pressure at end exhalation
and restore function residual capacity
b. CPAP- similar to PEEP, CPAP restores FRC
v. Settings of vent
vi. Nursing care:


1. Pt. w/ chronic pulmonary disease and their caregivers

should be given the opportunity to discuss mechanical
vent and withholding ventilation and place in advanced

C. Chest Tubes
a. Chest tube may be put in place if caused by pneumothorax or collapse
of lungs occur
i. Insertion & removal
a. Insertion: Can be put in place in ED, at pt.s bedside, or in
operating room. Pt. is positioned with arm raised on
affected side and HOB at 30-60 degrees. Chest x-ray is to
confirm placement. Occlusive dressing is used to cover
but some physician prefer petroleum gauze
2. Removal: suction is discontinued and chest drain is on
gravity draining for 24hrs before removal. Give pain meds
before removal. Tube removed by physician. Pt will hold
breath, then tube is removed. Site is immediately coved
w/ sterile dressing. Chest x-ray is performed to evaluate
ii. Whenever fluid or air accumulates in the pleural space, the
pressure becomes positive instead of negative causing the lung
to collapse. Chest tubes are put in place to relieve pressure.
a. Large are used to drain blood, Med to drain fluid, small to
drain air
b. Chest tubes are painful so monitor comfort measures
c. Flutter or Heimlick Valve is used to evacuate air from the
pleural space. The device consist of a one-way rubber
valve w/I a rigid plastic tube. It is very small and portable.
Patient is able to move w/ this device
iii. Drainage may also be put in pleural space to reestablish
negative pressure

a. Collection chamber receives

fluid and air from pleural or
mediastinal space
b. Water-seal chamber contains
water. The incoming air enters
from the collection chamber
and bubbles up through the
water also known as tidaling. If
any sudden cessation of
tidaling has occurred,
investigate in what is causing
this. As lung reexpand gradual
reduction and eventual
cessation will occur.
c. Control chamber applies suction to the chest drainage
system. Can either be water (20cm) or dry.
iv. Nursing care:
1. clamp chest tube during transport.
2. If chest tube becomes disconnected, immediately
reestablish the water-seal system and attach anew
drainage system as soon as possible.
3. If 1-1.5L of pleural fluid has been removed rapidly
pulmonary edema, hypotension or vasovagal response can

D. Acute Respiratory distress Syndrome

a. Definition
i. Sudden and progressive respiratory failure in which alveolarcapillary interface becomes damaged and more per-meable to
intravascular fluid.
1. Characterized by refractory hypoxemia and have noncardiac pulmonary edema.
b. Causes:
i. Aspiration of gastric content, viral/bacterial pneumonia, sepsis,
severe head trauma, chest trauma (Blunt struck by an
object or penetrating- foreign object impales or passes
through body tissue), SIRS/ MODS, anaphylaxis, DIC, opioid
overdose, severe head injury, pancreatitis, embolism, neardrowning, oxygen toxicity
c. Three phases of ARDS
i. Injury/exudative phase
1. Typically 1-7 days after initial direct lung injury. Produces
interstitial edema and then fluid from interstitial space
crosses the alveolar membranes.
ii. Reparative/proliferative phase
1. Begins 1-2 wks after lung injury. In this phase there is an
influx of neutrophils, monocytes, lymphocytes, and
fibroblast proliferation due to inflammatory response.
1. Hypoxemia worsens due to thickened alveolar
iii. Fibrotic phase-





1. Begins 2-3 wks after lung injury. Also known as chronic or

late phase of ARDS. The lung is completely remodeled by
collagenous and fibrous tissues. Hypoxemia and
pulmonary hypertension occurs.
i. Ventilator-associated pneumonia, barotauma, volutrauma, stress
ulcers, renal failure,
i. 1-2 days after: dyspnea, tachypnea, cough, and restlessness.
May have normal or fine/ scattered crackles. Mild hypoxemia in
ABGs. chest x-ray may be normal, reveal minimal scattered
interstitial infiltration, or edema may not show until 30%
increase in fluid content in lungs .
ii. As it progresses: tachypnea/dyspnea, tachycardia, diaphoresis,
change in mental status, cyanosis/pallor, intercostal retractions
and use of accessory muscles. Rhonchi and crackles in chest
auscultation. Hypoxemia despite increased FIO2 by mask,
cannula, or endotracheal tube is hallmark sign. Chest xray indicated whiteout or white lung because consolidation and
infiltrates are widespread through the lungs, leaving few
recognizable air spaces.
i. One way to assess the degree of impaired gas exchange is
measurement of PaO2/FIO2 (P/F) ratio.
1. PaO2 should be 85-100
FIO2= 0.21
2. If less than 200 then it is determined as ARDS
ii. ABGs= decreased PO2, respiratory alkalosis initially.
iii. Chest x-ray may reveal whiteout or white lung
i. Correct underlying disorder.
ii. Will be on ventilator and PEEP w. lowest setting oxygen
1. Decreases cardiac output by decreasing venous return.
iii. Medications are usually not helpful
1. May be on low dose steroids and anti-inflammatory
i. Oxygen therapy
ii. Endotracheal intubation and PPV provide additional respiratory
iii. Changing positions from supine to prone may help.
Continuous lateral rotation therapy and kinetic therapy may also
iv. Monitor daily weights and lung sounds
v. Maintaining nutrition and fluid balance
1. Enteral or parenteral feedings are started to meet high
energy requirements
2. Drug therapy
a. Diuretics may be administered to reduce pulmonary
b. Vasodilators to decrease pulmonary vascular

vi. Once in a better state, will begin weaning from ventilator

1. Monitor for dyspnea, anxiety, decreased O2 sats,
cyanosis/pallor, diaphoresis, increased BP/HR/RR,
accessory muscle use, decreased LOC, bad ABGs,
shallow/grasping breaths.
2. Keep pt. in high fowlers position, limit procedures, dont
wean at night, explain procedures to help with anxiety,
3. decrease breaths by 2/minute to help with reconditioning,
4. Avoid respiratory depressants except at night w/ rest.
vii. Extubation is ultimate goal
1. Keep intubation kit handy, provide supplemental oxygen,
and perform pulmonary hygiene before extubating.

E. Cystic Fibrosis
a. Definition
i. Autosomal recessive, multisystem disease in which sodium and
chloride ions are not properly being transported in and out of
epithelial cells.
1. Primarily affects the lungs, GI(pancreas and biliary tract),
and reproductive tract.
b. Patho
i. Is autosomal recessive and located on chromosome 7 as cystic
fibrosis treansmembrane regulator (CFTR) being the protein .
ii. Sodium chloride content line the passageways making mucus
abnormally thick and sticky. This can lead to plugging of glands
and eventual organ failure
iii. Progresses from being a disease of the small airway, to
involvement of the larger airways. Characterized by chronic
airways infection: bronchiolitis, bronchitis, bronchiectasis, blebs,
large cyst, hemoptysis
iv. Secrete normal volumes of seat, but unable to absorb sodium
chloride from seat as it moves through sweat ducts, so they
excrete four times the normal amount of sodium an d chloride in
their sweat.
v. Pancreatic insufficiency occurs due to mucus plugging the
pancreatic duct
1. CFRD occurs because fibrotic scarring of pancreas
c. Complication
i. CFRD(cystic fibrosis related diabetes), bone disease, sinus
disease, liver disease, pneumothorax, hemoptysis, digital
clubbing, cor pulmonale, respiratory failure
d. S&S
i. Wheezing, frequent coughing, failure to thrive, malnutrition,
steatorrhea. Productive cough with purulent or yellow/green
sputum, Delayed puberty, frequent lung infections, failure to
ii. Skin will taste salty when kissing child, mouth will also be dry
iii. Abnormally thick secretions and mucus. Decreased cilia motility,
hyperinflation of lungs, organ failure, bronchitis or bronchiolitis
are typical occurrences found
iv. Upper respiratory: chronic sinusitis and nasal polyposis

v. If development of DIOS (distal intestinal obstruction syndrome)

occurs- Right lower quadrant pain, loss of appetite, nausea,
emesis, and palpable mass may occur
vi. Staph aureus (in the young), haemophilus influenza, and
pseudomonas aeruginosa (in the elderly) are common organisms
vii. Malabsorption of fat, protein, and fat-soluble vitamins (A,D,E,K)
viii. CF-related diabetes mellitus may occur.
ix. Males and females have delayed puberty
x. In newborns: it is characterized by meconium ileus: small
intestine is blocked w/ thick, puttylike, tenacious, mucilaginous
e. Diagnosis:
i. Typically discovered through testing of sweat gland. They will
have four times the normal amount of sodium and chloride
excreted in sweat.
ii. Fecal fat test can also be done
iii. Genetic testing, family history, clinical presentation are also
iv. Pancreatic enzymes will be decreased
f. Treatment
i. Draining of thick bronchial mucus by aerosol and nebulization
treatment. Inhaled hypertonic saline also help with clearing
ii. Antibiotic use to prevent infections.
g. Interventions
i. Medications
1. Mycolytics
2. CFTR agents (ivacaftor(Kalydeco))
3. Bronchodilators
a. (Salmeterol or Albuterol)- monitor for
hyperglycemia and tachycardia
4. Anti-inflammatory
a. High dose ibuprofen can slow progression of
pulmonary damage
5. Inhaled dornase alfa
a. Dornase alfa (Pulmonzyme), is a purified
preparation of recombinant human DNA- it
decreases viscosity of sputum
b. It is inhaled w/ nebulizer and given daily
6. Pancreatic enzymes (pancrelipase(Creon)) and fatsoluble vitamins (A,D,E,K)
a. Give pancreatic enzymes before each meal and
b. Main concern in fibrosing colopathy
7. INHALED Antibiotics
a. Is typically long-term to suppress chronic infection
w/ P. aeruginosa.



b. Inhalation is preferred because provided high

concentratin in airway while minimizing the risk of
systemic toxicity. Resistance is still a concern
c. If pt. has pseudomonas- aerosolized tobramycin
or aztreonam is typically used
8. IV antibiotics for acute therapy
a. Ciprofloxacin, tobramycin, gentamicin
Provide oxygen therapy 1-2 times a day before meals
Good nutrition: encourage good intake of fat, calories, protein,
and vitamins (A,D,E,K)
1. Add salt into diet if sweating is excessive (such as in hot
weather, fever, or intense physical activity)
Teach avoidance of infections
Educated about sexuality issues and self confidence
Encourage aerobic exercise to clear airways
1. Drink large amounts of water and replace salt loss,
observe for dehydration, and make sure they are meeting
increased nutrition demands for exercise

F. Pulmonary Emboli
1. Definition:
i. Blockage of pulmonary arteries by a thrombus, fat or air embolus,
or tumor tissue
b. Etiology:
i. 10% of pt. die w/I the first hour and 30% die from recurrent
i. 90% of PE arise from DVT in legs. May also be from Right heart (A
fib), upper extremities, and pelvic veins (surgery and childbirth)
c. Risks factors
i. DVTS, Immobilization, surgery, stroke, malignancy, cigarette
smoking, hypertension, oral contraceptives, heart failure,
pregnancy, clotting disorders
d. Complications
i. Pulmonary infarction (Death of lung tissue) which eventually
becomes infected, and an abscess may develop.
1. Occurs when occlusion of large/medium pulmonary vessel
2. Insufficient collateral blood flow
3. Preexisting lung disease
ii. Pulmonary hypertension does not occur unless massive PE.
Recurrent emboli may cause chronic pulmonary hypertension
e. S&S
i. Symptoms may begin slowly or suddenly
i. Dyspnea is most common symptom. Mild to moderate
hypoxemia w/ low PaCO2 is common
ii. Tachypnea, cough, chest pain, hemoptysis, crackles, wheezing,
fever, accentuation of pulmonic heart sound, tachycardia,
sudden change in mental status, petechial rash
iii. Massive emboli= low BP & shock.
Small emboli= undetected
& vague symp
f. Diagnostic studies
i. Spiral/ Helical CT scan is the most frequently used to test for PE

1. If pt. is allergic to contrast they can have a ventilationperfusion (V/Q) scan. Most accurate when these are
a. Perfusion scanning: IV injection radioisotope
b. Ventilation scanning: radioactive gas is inhaled
ii. Pulmonary angiography is most sensitive and specific test but it
is expensive and invasive.
1. Insertion of catheter into artery and contrast in injected
iii. D-dimer measure the amount of cross-linked fibrin fragment but
it is neither specific nor sensitive.
1. Abnormal: greater than 250 mcg/L
iv. Troponin: identifies right heart overload.
v. ABG analysis is important but it is not diagnostic
1. PaO2 is low, pH remains normal unless respiratory
alkalosis occurs
f. Treatment
i. Infertio vena cava filter is treatment of choice in pt. who remain
at high risk and antigcoagulation is contraindication.
1. Device is percutaneously placed at level of diaphragm and
prevent migration of large clots.
ii. Prevention with anticoagulants
ii. Pulmonary embolectomy:
1. used for pts. That are hemodynamically unstable and
contraindication for fibrinolytic therapy. Typically has high
mortality rate so last case scenario
g. Interventions
i. Key is prevention of DVT by applying sequential compression
devices, early ambulation, and anticoagulants
1. (Lovenox) is drug of choice over heparin
2. Warfarin(Coumadin) should be initiated w/I first 3 days
after heparin use and continue taking for 3-6 mo
ii. Monitor INR levels (warfarin) and aPTT(heparin)
1. Monitor green leafy vegetable intake due to vitamin K can
affect warfarin intake
iii. Objective is to prevent further growth or multiplication of thrombi
in lower extremities, prevent embolization form upper or lower
extremities, provide cardiopulmonary support if indicated
iv. Once pt. has developed a PE keep them on bed rest and in semiFowlers
v. Oxygen provided via mask or cannula
vi. Encourage turning, coughing, deep breathing, and using
incentive spirometer
vii. Diuretics may be prescribed if heart failure occurs
viii. IV fluids are admitted if manifestations of shock begins followed
by vasopressor agents