ALTERATIONS IN VENTILATION

Disorder Risk Factors/ Etiology Pathophysiology Clinical Manifestation Nursing Responsibilities

Chronic Obstructive ENVIRONMENTAL ● CHRONIC BRONCHITIS (blue ● Dyspnea w/ activity Monitor respiratory system
Pulmonary Disease ● harmful irritants into lung bloaters) ● Chronic cough - productive ● Lung sounds (may need suction)
● Pulmonary disease that ● Ex. Smoking, bad air Environmental irritant → bronchial ● Smoker’s cough - in the ● Sputum production (collect Cx if ordered) @ risk for pneumonia
causes chronic obstruction pollution, occupation inflammation and damage → mucus morning ○ Usually chronic bronchitis
of airflow from the lungs (wielding) production → inability to exhale fully ● Recurrent lung infections - ● Keep O2 sat 88-93%
(inhalation ↑ volume because there is pneumonia ○ Why? Pt w/ COPD are stimulated to breathe due to LOW O2
Key Points: Happens gradually. S/S are residual air)→ hyperinflation of lungs → LEVELS rather than high carbon dioxide levels
● Limited airflow: inflamed mostly noticed at middle-aged Not enough O2 coming in and retainment “LUNG DAMAGE” ○ Giving too much O2 stops their breathing, causes
bronchioles - deformed and of CO2 → respiratory acidosis → cyanotic hypoventilation & CO2, will become toxic
narrow w/ excessive Complications: ↓O2 → ↑ RBC (to compensate) → ↑ Lack of energy ● Administer O2 as prescribed 1-2L/min
mucus) ● Heart disease: Heart pressure in the arteries from the shift of Unable to tolerate activity (SOB) ● Monitor effort of breathing and teach about:
● Inability to fully exhale failure blood due to ↓ O2 PULMONARY Nutrition poor (weight loss esp ○ Pursed lip breathing: used for dyspneic episodes to ↑ O2 lvl
(elasticity loss in alveoli ● Pneumothorax: HYPERTENSION → Right sided Heart emphysema) ■ Encourage to breathe out longer (bc of retained air)
sacs + air pockets develop) spontaneous from air sacs Failure → bloating of abdomen & legs ● Takes a lot of calories to ■ Like blowing out a bday candle
● Irreversible once (emphysema) (backflow of blood) breathe and do activity ○ Diaphragmatic breathing: Uses abdominal muscles rather than
developed…cases vary ● Lung infections: Gases abnormal (respiratory accessory muscles
among people from mild to Pneumonia acidosis PCO2 >45, PO2 <90) ○ Helps strengthen diaphragm, slows down breathing rate, eases
severe…managed with ● ↑ risk of lung cancer Dry or productive cough (esp breathing
lifestyle changes and ● EMPHYSEMA (pink puffers) chronic bronchitis) ○ Takes lesser energy to breathe
medications. Diagnostic Tests: Hyperventilate for compensation of ↓O2 Accessory muscle usage ● Administer breathing Tx:
● COPD is a term used as a Spirometry: Maintains “pink” normal complexion - no (emphysema) ○ Respiratory therapy nebulizers
“catch all” for diseases that ● How much volume the cyanosis, barrel chest from accessory Abnormal lung sounds: ○ Short-acting “Albuterol, Atrovent”
limit airflow and cause lungs can hold during muscle usage ● Diminished (esp in ○ Must know long vs short-acting inhalers, corticosteroids
dyspnea. inhalation lower bases)
● How much and how fast Environmental irritant → inflammation → ● Coarse crackles or EDUCATION
Types of COPD: air volume is exhaled alveoli sacs loss elasticity → air gets wheezing (chronic ● Nutrition needs: eat high calorie+protein meals small frequent +
● Chronic bronchitis “blue Measuring FVC: trapped in sacs → HYPERINFLATION bronchitis) start hydration 2-3L/day
bloaters” ● Largest amount of air (diaphragm flattens) → use of accessory Modification of skin color from ○ A full stomach can cause further DOB
○ Cyanosis due to exhaled after breathing muscles and hyperventilate → BARREL pink to cyanosis (chronic ○ Hydration thins the mucus
hypoxemia in deeply in 1 sec CHEST → anteroposterior diameter ↑ bronchitis) ● Avoid sick ppl, irritants, hot humid or extreme cold (smothering
○ Bloating:edema in ● if low reading → Anteroposterior diameter days)
belly and restrictive breathing Diaphragm does 80% of the breathing increases - barrel chest ● Stop smoking + avoid 2nd hand smoke
extremities; and (emphysema) ● Vaccinations up-to-date: annual flu shot + pneumovax q5yrs
increased lung Measures Forced Hyperventilation causing ↑ RR → less Gets in tripod position to breathe - ○ very hard for people with COPD to recover from illnesses
volume Expiratory Volume hypoxemia that chronic bronchitis, hence leaning forward while supporting
● Emphysema “pink puffers” ● How much air a pink puffer hands on knees or object MEDICATIONS: Regime
person can exhale Extreme dyspnea “Chronic Pulmonary Medications Save Lungs”
w/in 1 sec
● Low reading shows CORTICOSTEROIDS
severity ↓ inflammation ↓mucous production in airway
Route: oral, IV, inhaled
● used in combination with bronchodilator like:
● Symbicort: combination of steroid and long acting
bronchodilator
● Other corticosteroids: Prednisone, Solu-medrol, Pulmicort
● Side effects: easy bruising, hyperglycemia, risk of infection
(immunosuppressive), bone problems (long term use -
osteoporosis)
Patient education:
● rinse mouth after using inhaled corticosteroids (can develop
thrush)
● use corticosteroid inhaler AFTER using bronchodilator
inhaler

PHOSPHODIESTERASE-4 INHIBITORS
● Roflumilast
● Used for people with chronic bronchitis & helps ↓ COPD
exacerbation (not bronchodilater)
● Side effects: cause suicide ideation & weight loss
● “last” - could be their last day hence assess thoughts of suicide
and report to physician

METHYLXANTHINES
● Theophylline (Given orally many times)
● Type of bronchodilator, used long-term in pts w/ severe COPD
○ Narrow therapeutic range: 10-20mgc/mL

● ↑ Digoxin therapy & ↓ effects of lithium & dilantin

SHORT-ACTING BRONCHODILATORS
● Relaxes smooth muscle of bronchial tubes
● Emergency situation & quick relief
○ Beta2 agonist: Albuterol
○ Anticholinergic: Atrovent

LONG-ACTING BRONCHODILATOR
● Same action as short but effects last longer
● Used over period of time
● Scheduled: OD/BID
○ Beta2 agonist: Salmeterol
○ Anticholinergic: Spiriva
● Use before inhaled corticosteroid
○ Beta2 agonist: ↑ HR, urinary retention
○ Anticholinergic: Dry mouth, blurred vision

Patient education: let them know which drug is short and long-acting,
how to use inhaler and to use bronchodilator inhaler BEFORE steroid
inhaler (wait 5 minutes in between)
WHY? TO OPEN UP THE AIRWAYS SO THE STEROID CAN
GET IN THERE AND DO ITS JOB

Pulmonary Embolism ● Trauma Clot begins as a thrombus (usually DVT) Dyspnea Medical management:
obstruction of the pulmonary ● surgery (orthopedic, → clot grows faster than fibrinolytic Substernal chest pain - may EMERGENCY MANAGEMENT:
artery or one of its branches major abdominal, pelvic, activities can break it down → fragments mimic angina pectoris/ ● Nasal O2
by a thrombus that originates gynecologic) break off (embolize) → travel to the heart myocardial infarction ● KVO
somewhere in the venous ● Pregnancy → lodges in the pulmonary artery or Tachypnea ● Dobutamine/dopamine – for hypotension
system or ● heart failure smaller blood vessels Rapid and weak pulse, Shock, ● ECG
in the right side of the heart. ● age older than 50 years Syncope, and ● Digitalis glycosides, IV diuretics, antiarrhythmics
● hypercoagulable states Can sudden death. ● If abnormal ABGs persist → intubation + mech vent
● prolonged immobility
Anticoagulation Therapy
● continue 3-6 mos. after embolic event
● Heparin therapeutic range: 2.0-2.5

Thrombolytic Therapy
● urokinase, streptokinase, tissue plasminogen activator

Surgery: Transvenous catheter embolectomy

Nursing Management:
● Early ambulation, active & passive ROM
● DO NOT: sit/lie for too long, cross legs, wear constrictive
clothing, dangle feet, prolong IV catheters
● Sequential compression devices
● Deep breathing, incentive spirometry, nebulizer, percussion &
postural drainage

Acute Respiratory Distress Cause: MAJOR SYSTEMIC “ARDS” Early signs: subtle Medical Management: Respiratory assistance w/ PEEP to open up the
Syndrome INFLAMMATION Atelectasis (alveolar sac fill with fluid and ● Normal lung sounds or alveoli sacs
Milder form: acute lung Indirect Causes: collapse, pulmonary edema) random crackle (fluid still in
injury ● Sources is outside the | interstitium not in sac) Nursing Interventions:
lungs Refractory Hypoxemia ● Difficulty breathing “air- Maintain airway/function
Type of respiratory failure ● SEPSIS (poor prognosis | hunger” ● Mechanical ventilation w/ PEEP (high 10-20cm H2O)
that occurs when the gram-negative) Decrease in lung compliance (lung aren’t ● ↑ RR - low O2, respiratory ○ Why does it have to be high?
capillary membrane around ● Burns as elastic or stretchable + hyaline alkalosis ■ ↓lung compliance
the alveoli sac start to leak ● Blood transfusion membrane develops) | ■ Edema in sacs
fluid (multiple) | ● Full respiratory failure ■ ↓ surfactant - collapsed sac
Fluid will enter into the sac ● Pancreatitis Surfactant cell damaged (decrease in ● Refractory hypoxemia!! ■ PEEP open alveoli sacs that are collapsed, esp during
● Drug overdose surfactant production) ● Cyanosis exhalation
Gas Exchange ● Mental status changes: tired, ■ Improve gas exchange, ↑ O2, keep clear of fluid
Blood coming from Direct causes: Organs suffer fatigue, confused ○ Watch out for complications:
pulmonary artery ● Source is in the lungs ● ↑HR ■ ↑ intra-thoracic pressure
(deoxygenated) ● Pneumonia How it happens? ● Retractions ■ Compress the heart and ↓ cardiac output (watch out for
O2 crosses capillary ● Aspiration (food or ● Exudative ● Crackles throughout lungs hypotension)
membrane into the blood gastric secretions) ○ 24 hrs after injury → damage to (pulmonary edema) ■ Hemodynamic monitoring
CO2 crosses the capillary ● Inhalation injury capillary membrane → leak Diagnostic Tests: ■ If hypotension occurs, MD can prescribe:
wall into the alveoli ● Drowning-near protein-rich fluids (enters ● Chest X-ray: White-out ➢ Colloid solutions, crystalloids, IV solutions
Blood goes back to heart ● embolism interstitium → sac) = pulmonary appearance, bilateral ➢ Inotropic drugs: dobutamine
(oxygenated) by pulmonary edema infiltrates ■ Hyperinflation of llungs
vein ○ Damaged surfactant cells: ↓surface ➢ Risk for pneumothorax
tension: collapse exhalation ➢ Subcutaneous emphysema
Quick Facts: ○ ↓ surfactant = unstable sac ● PaO2 >60mmHg and O2 sat >90%
● Fast onset COLLAPSE
● Usually already ○ ATELECTASIS → hypoxemia Prone positioning
hospitalized with ○ Hyaline membrane (dead cells & ● ↑ O2 without ↑ O2 concentration
another condition protein): lung less elastic, ↓ ● Improve V/Q, airflow (heart no longer compresses the posterior
○ Burns compliance, V/Q mismatch parts of the lungs)
○ Sepsis ○ Hallmark S/S: REFRACTORY ● Moves secretions to other area
● Develop due to HYPOXEMIA = O2 ↓ even ● Improves atelectasis
systemic though receiving high amounts of
inflammation O2
○ Pt w/ severe ○ Early stage: PULMONARY ARTERY WEDGE PRESSURE
burns is at risk ■ ↑RR to blow off CO2 ● Measures left arterial pressure
for ARDS due ■ O2 ↓ CO2 ● Pulmonary catheter with balloon “wedged” in pulmonary
to the systemic ■ pH ↑ arterial branch
inflammation ■ RESPIRATORY ● < 18 mmHg → ARDS
present in the ALKALOSIS ● > 18mmHg → cardiac issue: heart failure
body. ■ Hyaline membrane formation ● Assessing other systems of the body to make sure they are
○ Increased prevents CO2 to pass through getting enough oxygen: mental status, urine output, heart
inflammatory = respiratory acidosis (blood pressure and cardiac output with PEEP)
cells circulate ● Preventing complications: pressure injury, blood clots,
to lungs and ● Proliferative infection related to ventilator, nutrition (lose weight),
causes alveolar ○ ~14 days after injury pneumothorax
damage ○ Grow & reproduce cells quickly ● Administering drugs: corticosteroids (help with systemic
● High mortality rate ○ Repair structure & reabsorption inflammation), antibiotics (preventing and treating infection
fluid [sepsis]), fluids colloids or crystalloids solutions if cardiac
○ Lung tissue becomes very dense & output decreased along with drugs like that have an inotropic
fibrous effect (helps with heart muscle contraction), GI drugs for
○ ↓ lung compliance, worsen stress ulcers
hypoxemia
● Fibrotic
○ ~3 weeks after injury
○ Fibrosis of lung tissue, dead space
in the lungs
○ Major lung damage
○ Poor prognosis
○ But not all patients will enter this
(worst case scenario)

Protein regulates water, oncotic pressure

Atel

Respiratory Failure Ventilatory failure: Early signs: Medical Management:

● Impaired function of CNS Abnormality in any component of restlessness, fatigue, headache, ● Intubation and mechanical ventilation
Acute Respiratory Failure: ● Neuromuscular respiratory system (airways, alveoli), CNS, dyspnea, air
PaO2 <50mmHg dysfunction PNS, respiratory muscles, chest wall hunger, tachycardia, and Nursing Management:
(hypoxemia) ● Musculoskeletal | increased blood pressure ● assisting with intubation and maintaining mechanical
PaCO2 > 50mmHg dysfunction Ventilatory capacity < ventilatory demand ventilation
(hypercapnia) ● Pulmonary dysfunction Late signs: ● level of responsiveness, arterial blood gases, pulse oximetry,
Arterial pH <7.35 confusion, lethargy, tachycardia, and vital signs.
Oxygenation failure: tachypnea, cen
Chronic Respiratory ● Pneumonia, ARDS, tral cyanosis, diaphoresis, and
Failure: heart failure, COPD, finally respiratory arrest.
deterioration in the gas pulmonary embolism,
exchange function of the restrictive lung diseases Physical findings:
lung that has developed Use of accessory muscles,
insidiously or has persisted Postoperative period: decreased breath sounds
for a long period after an ● Anesthetic, analgesic,
episode of acute respiratory sedative that can
failure enhance opioids
(hypoventilation)
Pneumonia Risk Factors: Pathogen → attacks alveoli → alveolar “PNEUMONIA” Nursing Interventions:
● a lower respiratory ● Prior infection: flu or cold inflammation, full of fluid, WBCs, RBCs ● Productive cough, Pleuritic Monitor respiratory system:
tract infection that ● Weak immune system: stuck & bacteria → ↓ ability to pain (chest pain that is ● Lung sound: improving?
causes inflammation of Elderly, infants, HIV, inflate/deflate → hypoxemia (O2 cant caused by coughing, ● Vital signs esp RR & O2sat
the alveoli sacs autoimmune medications transfer across capillary wall, CO2 retains) breathing etc.) ● Color of skin: cyanotic? Lips!
● Immobile: strokes or any → Respiratory acidosis ● Neuro changes (especially ● Monitor ABG results
Key Players: other condition that ELDERLY patient - may ● Collect sputum Cx (if ordered)
Germs: Bacteria, Virus, causes decrease mental Respiratory Acidosis: keep CO2 & can’t not even have a fever but ● Suction as needed
Fungi awareness or restrict get O2 fatigue and increased ● Breathing Tx: respiratory therapists, bronchodilators, chest
Lung Parenchyma: Alveoli, ability to move ABGs: respiratory rate) percussion (scheduled or prn)
Alveolar Ducts, and ● Lung problems: COPD, ● PO2 <90mmHg ● Elevated labs: PCO2 >45
Bronchioles (the trio in gas asthma, smokers ● pH: <7.35mmHg (retaining carbon dioxide Education:
exchange) ● Post-opt patient: not ● PCO2: >45mmHg because it can’t pass ● Incentive spirometer usage 10x q1-2hr while awake
coughing deep breathing To compensate: the Kidneys start to capillary of alveoli sac), ○ To properly exhale and inflate alveoli
Normal gas exchange: conserve bicarbonate (HCO3) to hopefully increased WBC (represents ● Stay hydrated 2-3L/day
● O2 → Upper respiratory Route of transmission: ↑ the blood’s pH back to normal, so HCO3 infection…body is trying to ○ To keep secretions thin
system: trachea → left & inhalation, aspiration, from becomes >26 mEq/L fight infection off) ○ Fever → dehydration
right primary bronchi → blood and attack the alveoli ● Unusual breath sounds: ○ Respirations cause 300-400mL water loss per day
splits at the carina → sacs coarse crackles, rhonchi, or ○ Contraindicated: Heart failure, renal failure
enters lungs at hilum → bronchial in the peripheral ○ Immobile pts: keep HOB > 30deg & turn
secondary (lobar) & Causes: lung fields frequently
tertiary (segmental) BACTERIA: ● Mild to high Fever (bacteria ■ Prevent aspiration esp while eating and
bronchi → bronchioles most common esp. In cause produces highest after meals
→ alveolar ducts → community-acquired fever….. greater than 104’F ○ Up-to-date vaccines:
alveolar sacs → pneumonia is [40C]) ■ Annual flu shots
In the alveoli capillary wall: “Streptococcus ● Oxygen saturation ■ Pneumovax q5yrs for pt 65+y/o and 19-
transfer of oxygen from pneumoniae” decreased (want >90%) will 64y/o with risk factors
inhalation into the need supplemental oxygen ○ Stop smoking, avoid sick ppl, crowds during peak
bloodstream and ATYPICAL BACTERIA: ● Nausea and vomiting (won’t flu season, hand washing
| Mycoplasma pneumoniae feel like eating) Administering medication per MD order:
transfer of carbon dioxide that causes “walking ● Increase heart rate and ● Antipyretics, fluids, antibiotics (if bacterial), anti-virals (if
out of the blood through the pneumonia” which is a milder respirations viral, e.g. Tamiflu)
lungs which is exhaled form of pneumonia (no need ● Aching all over with joint
| complete rest hence pain Antibiotics Groups for Bacterial Pneumonia
the fresh oxygenated blood is “walking”) Activity intolerance with “Various Medications Frequently Treat Pneumonia Cases”
taken back to the heart shortness of breath
through the pulmonary vein VIRUS: influenza, RSV Antibiotics used depend on the bacteria type that is causing the
and is pumped through the (pedia) infection, the patient’s ability to tolerate etc.
heart to the body.
FUNGI: least common → Vancomycin: treat severe cases and is one of the few that can treat
● Normally respiratory mostly affects bacteria that may be resistant to other antibiotics
system “fights off” germs immunosuppressed pts (found ● watch for HEARING LOSS “ototoxicity”
by filtering air taken from plants & animals)
through the nose but Pneumocystis jirovecii Macrolides: “Zithromax (Z-Pak)”
certain conditions ● used in patients with Penicillin allergy narrow-spectrum
decrease the body’s targets mainly gram positive bacteria
ability Diagnostic Tests:
● Notice: abnormal lungs Tetracyclines: “Doxycycline”
Types: sound when auscultating ● broad-spectrum that targets gram positive and negative
● Community-acquired with a stethoscope may bacteria.
Pneumonia (most hear coarse crackles, ● Side effects: not for pregnant women or 8 years or younger
occurring): patient rhonchi (type of due to growth retardation and teeth discoloration,
obtains the germs that wheezing) or bronchial photosensitivity of the skin and decreases effectiveness of
causes the pneumonia breath sounds which birth control, no antacids or milk product while taking this
OUTSIDE of the should be noted only in medication because it affects absorption.
healthcare system hence the tracheal area and this
in the community. represents lung Fluoroquinolones: “Levaquin”
● Hospital-acquired consolidation. ● broad-spectrum (targets gram-negative and positive)
Pneumonia: patients ● Chest x-ray, sputum ● treatment for severe infections that are found in the hospital
who are on mechanical culture that are resistant
ventilation at major ● Side effects: clos. diff infection → diarrhea (disrupts normal
risk…it is hard to treat flora of GI), tendon rupture, cardiac arrhythmias such as QT
because the bacteria tend interval prolonged
to be resistant to
antibiotics and more Cephalosporins: “Keflex, Rocephin”
likely a bacteria cause. ● watch with patients who are allergic to penicillin (can also be
Criteria: patient must allergic to cephalosporin)
have developed 48-72 ● great for community acquired pneumonia
hours after admission ● (3rd and 4th generations of cephalosporins broad-spectrum)

Penicillin: “Penicillin G”
● Narrow-spectrum (target gram positive bacteria)
● monitor if patient is allergic to cephalosporins
● decreases effectiveness of birth control

Education about antibiotics:

Take medications as prescribed and don’t stop in the middle of
treatment, even if feeling better which helps decrease resistance

Viral Cases: May be prescribed an antiviral of the virus that is causing

the pneumonia ex: Tamiflu

Pulmonary Hypertension ● Collagen vascular diseases Pulmonary Vascular bed injury ● Dyspnea at first with exertion Medical Management:
• Congenital systemic-to- | and eventually with rest ● Anticoagulation – in pt with indwelling catheter
● the mean pulmonary pulmonary shunts endothelial and vascular smooth muscle ● Supplemental oxygenation with exercise
artery pressure exceeds • Portal hypertension dysfunction ● Substernal chest pain ● Diuretics
25 mm Hg with a • Altered immune | ● Oxygen therapy reverses vasoconstriction
pulmonary capillary mechanisms (HIV infection) thickening of the wall ● weakness, fatigue, syncope, ● Calcium channel blockers
wedge pressure of less • Diseases associated with | occasional hemoptysis ● Phosphodiesterase-5 inhibitors: Sildenafil
than 15 mm Hg significant venous or advance vascular lesions formation ● Endothelin antagonists: Bosentan (BID)
● measured through a capillary involvement | ● signs of right-sided heart ○ monitor liver function!!
right-sided heart • Chronic thrombotic or ↑Pulmonary arterial pressure. failure (peripheral edema,
catheterization embolic disease | ascites, ● Prostanoids: epoprostenol, Treprostinil, iloprost
● clinical recognition in • Pulmonary venous ↑ Pulmonary vascular resistance ● distended neck veins, liver
late progression hypertension | engorgement, crackles, Surgery: Lung transplantation, atrial septostomy
• Pulmonary vasoconstriction right ventricular hypertrophy ● heart murmur)
TYPES: due to hypoxemia Nursing Management:
Idiopathic (Primary) PAH: • Chronic obstructive ● anorexia & abdominal pain ● Identify pt high risk: COPD, pulmonary emboli, congenital heart
women 20 to pulmonary disease (COPD), URQ dse, mitral valve dse
40 years of age, either interstitial ● Alert for s/s, administer O2 therapy
sporadically or in patients lung disease, sleep-disordered ● Epoprostenol – via CVA
with a family History breathing ● Treprostinil – via subq infusion
• Miscellaneous causes:
Pulmonary Arterial sarcoidosis, histiocytosis,
Hypertension scondary to compression of pulmonary
caerdiac/pulmonary dse vessels
e.g: pulmonary artery
constriction due to
hypoxemia from COPD

Pneumothorax Causes include but not Visceral pleura -attaches to the lungs “COLLAPSED” ● NCLEX TIP: Pt comes into ED with an open chest wound.
the collapsing of a lung due limited to: Parietal pleura - attaches to the chest wall ○ Nursing intervention: Place sterile occlusive dressing & tape
to air accumulating in the ● spontaneous (without Intrapleural space- between visceral and Chest pain (sharp and sudden and on 3 sides, leaving 4th side untapped
pleural space (the space warning) parietal pleura worst on inspiration), Cyanosis ■ To allow the exhaled air to leave the opening but seal over
between the visceral and ● trauma to the chest (blunt opening when inhaling
parietal pleura which is also or penetrating) The lungs LOVE NEGATIVE Overt tachycardia and tachypnea ■ Preventing tension pneumothorax
called the intrapleural space). ○ Gunshot wound, PRESSURE.
CPR, car accident Low blood pressure Tension Pneumothorax
Key Points: ● lung disease, Intrapleural space: contain small amount of ● Watch for pt on mechanical ventilation w/ PEEP
● It can be a partial or total ● medical procedures serous fluid which allows lungs to glide → Low SpO2 ● Risk for tension pneumothorax due to barotrauma
collapse of the lung ○ central line placement creates negative pressure which acts like ● Cause build-up of air in intrapleural space from rupture of
(mainly affects one ○ mechanical suction to keep lungs inflated Absent lung sounds on affected visceral pleura
lung). ventilation: PEEP → Air enters into space: object piercing chest side ● Tx: needle decompression (insert needle to aspirate air)
barotrauma wall, lung layer ruptures → barotrauma - Compare both sides Nursing Interventions:
Medical Management: Air builds in space: ↓ lungs ability to recoil ● Monitor breath sounds (equal sounds on both sides),
● A small pneumothorax Diagnostic Tests: & pushes lung away from chest leading to Pushing of trachea to unaffected ● Assess rise and fall of the chest, vital signs (HR, blood pressure,
usually resolves on its ● Chest x-ray collapse (need neg. Pressure to recoil) side (tension pneumo.) oxygen saturation), and patient effort of breathing, subq
own. ● Ultrasound emphysema (can be found on the face, abdomen, armpits, neck
● A large pneumothorax ● CT scan Types of Pneumothorax: Subcutaneous emphysema (affects breathing),
usually requires CLOSED PNEUMOTHORAX (escaping carbon dioxide ● Administering oxygen as ordered
treatment like a chest Closed Pneumothorax ● when air leaks into the intrapleural collecting in the skin…crunchy ● Maintain chest tube drainage system if placed by physician:
tube to remove air from Causes: space without any outside wound bulges on the skin), Sucking ○ Assessing for air leaks in the system, keep it secure
intrapleural space or ● Rib fracture: where the ● hence the chest wall and pleural stay sound with open pneumothorax ○ Troubleshooting if drain comes out or system breaks
needle aspiration (as sharp, bony part of the intact ○ Water seal chamber: may have intermittent bubbling as air
with a tension bone punctures the lung Expansion of chest rise and fall is drained from the pleural space. The water seal chamber
pneumothorax). causing air to be released OPEN PNEUMOTHORAX unequal fluctuates as the patient breathes in and out. If it stops
into the intrapleural space ● Opening in the chest wall & pleura that fluctuating there may be a kink somewhere or the lung has
● SPONTANEOUS causes a passage between outside air & Dyspnea re-expanded.
PNEUMOTHORAX: intrapleural space ○ NOT normal to have excessive bubbling in the water seal
defect in the alveolar wall ● Allows air to pass back & forth w/ chamber (air leak somewhere).
& visceral pleura → inspiration & expiration
causes air to form a sac- ● “Sucking chest wound” ● Keep HOB of the bed elevated → Fowler’s position
like blister “pulmonary ● Body is shunting air through chest wall
bleb” that ruptures & opening instead of trachea and will
releases air into the create “sucking sound”
pleural space ● Intrapleural pressure will become = to
○ Blebs can develop atmospheric pressure → lung collapse
over time (can have
multiple, may not TENSION PNEUMOTHORAX
rupture immediately ● Complication of pneumothorax
→ changes in air ● Can happen w/ open/closed pneumo
pressure, taking ● Medical emergency! Happens when
sudden, deep breath an opening to the intrapleural space
or smoking) creates a one-way valve: air collects
but can't escape
● Leads to ↑ intrathoracic pressure
Primary Secondary ● Compression on lungs and heart
spontaneous spontaneous ● Mediastinum shift [heart, trachea,
pneumothor pneumothor esophagus, vessels] shift to unaffected
ax ax side
● Major compression on other lung &
occurs in pt Occurs in pt venous vessels → ↓ venous return
w/o lung w/ lung dse: ● Pt tries to compensate ↑RR (tachypnea)
dse COPD,asth to maintain O2
ma ● Compression of vena cava ( theatdrain
blood to heart)
young <30 ● Heart has nothing to pump
years of age ● ↑ HR (tachycardia & reduced cardiac
and tall and output) → hypotension
thin.
“Tachycardia, Tachypnea, hypotension,
hypoxia, jugular vein distention, “shock”
LATE SIGN: tracheal deviation