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Respiratory functions
VENTILATION:
● Breathing
● Air flow into and out of the lungs through the conducting passages
● Inspiration--involves muscle contraction increasing the size of the thoracic cavity
● Expiration--passive process involving relaxation of respiratory muscles and elastic recoil of the lungs - increase in thoracic
pressure —> lung deflation
● Compliance--measure of the force required to distend the lungs - pulmonary fxn (the ability of lungs to expand), you will lose
compliance of the lungs (the ability to expand); low compliance - difficulty for lungs to inflate, a lot of fluid buildup, conditions
that make it last elastic ex scar tissue, pneumothorax —> low compliance
● ? What are stiff lungs? ARDS What substance reduces surface tension and therefore increases compliance? -+++
surfactant+++
SPEAKER NOTES:
Listen to the lecture
Inhalation decrease in thoracic pressure —> inflation and expansion of lungs
Relaxation of chest muscles
Elastic recoil

● Diffusion - +++exchange of o2 and co2 in alv capillary mb (dx: impaired gas exchange, need to see ABG, o2 and co2 levels;
ex fluid in the way, lungs cant expand)
● Relationship between ventilation (air flow) and perfusion (blood flow) -co2 from arterial blood to environment; o2 from
environment to arterial blood; homeostasis
● Gravity affects ventilation and perfusion
○ Blood flows to the more dependent lung segments
○ Air flows to upper lung segments

Respiratory control
● Medulla oblongata = the respiratory center - control rate and depth of respirations, communicates with respiratory muscles via
sp cord and phrenic nerves
● Chemoreceptors - in medulla and carotid bodies, communicate with medulla oblongata, co2, ph, o2 and hydrogen levels are
detected
● Chemoreceptors and the medulla oblongata - ex too much co2, chemoreceptors sense —> medulla will change respirations to
blow off co2
● How happen to RR r/t resp acidosis: increases RR

Gero Changes
● Deterioration of the cilia lining - hairlike projections to expectorate (cialis fxn); supposed to expel stuff from resp tract; —> poor
removal of mucus in geros
● Diminished effectiveness of the immune system. - macrophages less effective at phagocytosis
● Loss of elasticity (elastic recoil) in respiratory tract
○ Calcification of trachea and bronchi
○ Smooth muscle fibers replaced by fibrous tissue making them less able to stretch and contract fibrous tsu prevents
good expansion
○ Alveoli lose recoil and adjacent walls deteriorate reducing surface area for diffusion of gases
● For these 3 reasons, they are more prone to resp tract infections
● May have poor tolerance to exertion as a result

Ventilation Perfusion Ratio

● Normal V/Q ratio is 1:1 - for every 1 L of air, there should be 1 L of blood flowing through as well
● V/Q mismatches
○ High V/Q ratio = normal to increased alveolar ventilation associated with decreased perfusion -ex pt with poor oxy
status; ex CHF, Pulm Embolism, pneumothorax; (theme: decreased cardiac output)
○ Low V/Q ratio = decreased alveolar ventilation associated with normal to increased perfusion - ex. pneumothorax,
COPD, hypoventilation, asthma, PNA
○ VQ scans are common, so understand it!

RESPIRATORY ASSESSMENT
● LOC - change of loc, decreased loc & lethargy, poor oxygenation (agitation, restlessness) —> indicates emergency coming!!
● Vital signs and hemodynamic values (CVP, PA pressure--systolic and diastolic, MAP, CO and PCWP) - RR, o2 sat

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● Inspection (cyanosis, use of accessory muscles) and palpation (subq emphysema) - is pt cyanotic? 1st place you see is in the
lips!! Are they using accessory muscles to breathe? Neck and shoulders pronounced when they breathe? looks like a flex;
t\orthopneic/ tripod breathing (making room so they can breathe better);; palpation - tracheal repositioning —> Pneumothorax
may move the tracheal from midline, fade to the unaffected side; palpate for bulges in the skin and see if it makes a crackling
sensation (subcutaneous emphysema; air trapped in the tissue); if air in SC tissue —> there’s a puncture or tear in the tissue
can be suspected, and doc may order radiologic test to figure out if there is
● Auscultation - listen for adventitious sounds; get baseline
● Pain - with breathing? If so, can be pulm embolism, or frx rib, or pressure on that rib
● Cough/sputum - assess and doc amt and characteristics (suction a lot in ICU); hyperoxygenate prior to suction
● Labs including ABGs, Hgb/Hct - ABGs gives info about ventilation status (o2/co2), acid base balance (acidosis probs); H/H -
hgb carries o2
SPEAKER NOTES;
Those acronyms should be explained in hemodynamics lecture
Pulm artery pressure
PCWP - pul cap w___ pressure

ACUTE RESPIRATORY FAILURE

● Defined as a life-threatening state in which the cardiopulmonary system is unable to maintain adequate gas exchange - (resp
= gas exchange, diffusion of o2/co2) -two possible probs: inadequate xfr o2 to the blood or unable to remove co2 from the
blood
● Imbalanced supply and demand either a failure of oxygenation (hypoxemia) or failure of ventilation (hypercapnia)
○ Hypoxemic respiratory failure (oxygen failure) - definition: paO2 under 60 even with admin of 60% o2
■ Happens One of 4 ways: ventilation perfusion mismatch (any inadequacy in ventilation or perfusion; 2)
shunting - blood exits the heart without doing gas exchange (alv may have too much fluid that blood passes
through but due to fluid it cant do gas exchange; 3) diffusion limitation (alv cap mb is insufficient in gas
exchange, so maybe scar tsu in excess, that alv cap mb is too damaged that it's ineffective; thickened or
damaged alveoli); 4) alveolar hypoventilation - generalized decrease in ventilation
○ Hypercapnic respiratory failure (ventilatory failure; high CO2) - def: paCO2 level greater than 45 with a pH less than
7.35
■ causes: body's inability to remove co2, so it just builds up —> ph will change
● Hypoventilation - not breathing well
● Cns depression or injury (brain, so resp status decreases, co2 builds up)
● Chest wall abnormalities (MVA, massive rib breakage, unable to breathe due to poor expansion
and severe pain)
● r/t to neuromuscular condition. Which weaken or paralyze resp muscles (GBS)

Pt with Resp Failure —>. Look for s/s —>. Look for resp and acidosis
● Clinical manifestations - sudden or gradual dep on severity (acute or chronic til failure)
● - 1st indication: Altered mental status —> tend to it and report ASAP
● Decreased LOC - used to be alert now lethargic; maybe LOC x4, now it’s just to LOCx1
● restless, agitated
● Unable to breathe —> anxiety, restless, agitated
● Dyspnea —> tachypnea (trying to compensate, increase RR up to 30/40s)
● Accessory muscle use (flexing pronounced muscles)
● Tripod breathing - room to breathe
● hear adventitious breath sounds (a lot of fluid buildup, crackles
● Poor oxygenation of blood, so may see TACHYCARDIA
● May see HTN as a result as well
● +++ Prolonged hypoxia —> anaerobic metabolism —> see increase in lactic acid —> be wary of metabolic acidosis —>
cellular dysfunction and death —> death of pt +++

Goals:
● m/t Adeq oxygenation and ventilation (good gas exchange)
● Via oxygenation therapy
● Mobilize secretion - cough and Deep breathing, hydration, CPT (there are beds that do CPT now!)
● Suction
● Positive pressure ventilation
● Force O2 to the pt (mask, endotrach tube, etc, fireman’s mask covers entire face)

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● Bronchodilators, corticosteroids (solu medrol/ methylprednisolone) for the inflammation ; diuretics to remove the xs fluids; anti
anxiety (benzodiazepine); sedation - to reduce agitation and restlessness because they increase o2 consumption (decrease
need for more o2)

ARDS - ACUTE RESP DISTRESS SYNDROME

● alveolar-capillary interface becomes damaged —> more permeable to intravascular fluids - more fluids in alv space
○ Alveoli fill with fluid also known as pulmonary edema. Xs pulm edema —>
○ +++This results in:
■ Severe dyspnea
■ Hypoxia
■ Decreased lung compliance
■ Diffuse pulmonary infiltrates
● +++don't need to know other names - Called “shock lung,” wet lung, congestive atelectasis, capillary leak syndrome and adult
hyaline membrane disease, Da Nang lung, adult respiratory distress syndrome
● Can affect children as well as adults
● 150,000 cases/year
● Mortality rate 30 to 60% with 90% of those deaths occurring within 2 weeks of disease onset
● Cause of death = MODS (multiorgan)
● Mb is permeable to fluids

CAUSE
● Syndrome develops as a result of an insult, condition or noxious event that traumatizes the lung tissue
● Direct or indirect insult (i.e., occurring in other body areas)
○ Most common cause is sepsis - sepsis checks/ scales once per shift now (sepsis is now a core measure now, but not
5 yrs ago)
● Direct pulmonary trauma
○ Viral, bacterial, or fungal infection
○ Lung contusion
○ Fat embolus
○ Aspiration (foreign body, drowning, vomitus)
○ Massive smoke inhalation
■ Inhaled toxins
Prolonged exposure to high concentrations of oxygen
SPEAKER NOTES:
High ventilation what??? Listen to recording!!

● Indirect pulmonary trauma

○ Sepsis (most common) +++
○ Shock
○ Multisystem trauma
○ DIC - disseminated intravascular coagulation
○ Pancreatitis
○ Uremia
○ Drug overdose
○ Anaphylaxis
○ Prolonged cardiac bypass surgery - CABG
○ Massive blood transfusions
○ PIH, IICP
○ Radiation tx

PATHOPHYSIOLOGY OF ARDS
3 STAGES
● 1) “Injury or exudative phase”
○ 1-7 days after insult
○ How does inflammation and immune response activity affect capillary permeability? -increase in inflammation and I/R
in lungs —> lots of neutrophils in the pulm vascular system (microcirculation) & increased capillary permeability (now
fluid shift)—> fluid shift to alveolar space —> too much fluid, no gas exchange (shunting)
■ ↑ Capillary permeability

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■ Fluids in alveolar space
● “intrapulmonary shunt” or “shunting”
○ Hypoxemia - from the pulm shunting
■ REFRACTORY HYPOXEMIA +++identifying characteristic: The pt cannot positively respond to increases in
O2 admin - once supplement with O2, the pt doesn’t respond to it d/t too much fluid, blood keeps shunting
through despite how much O2
● AKA refractory hypoxemia - If we give o2 and it doesn’t improve the condition
SPEAKER NOTES:
What refractory ______ means
refractory = certain condition that the treatment didn’t improve the problem
- refractory ascites - diuretics don't help the ascites

○Damaged alveolar cells

■ insufficient surfactant production —> increased surface tension —> collapsing alveoli
● Results in ATELECTASIS (collapsing alveoli)
○ With inadequate treatment —>. May lead to fibrosis
■ Necrotic cells, protein and hyaline ____ scar tissue —> FIBROSIS
■ Decreased compliance —> as more fibrosis occurs, more E will be needed for inhalation —> more force
needed
○ Lungs become less compliant for the above reasons
■ Symptoms
■ ↑ Work of breathing (WOB), accessory muscle use
■ ↑ Respiratory rate
■ ↓ Tidal volume - amt of air you intake or amt of air forced into pt for ventilation
● 2) The 2nd stage is the “reparative or proliferative phase”:
○ Occurs 1-2 weeks after initial lung injury
○ With continued neutrophil activity
■ Lungs become more dense and fibrous
■ Compliance decreases -stage 1 worsening
○ Hypoxemia will worsen (d/t diffusion limitation and shunting)
○ +++when surface area for active alveolar gas exchange if the amt decreases, then it’s called diffusion limitation +++
○ Understand 1st stage, and 2nd and 3rd is continuation and worsening.
● 3) The 3rd stage is the “fibrotic or late phase”
○ Occurs 2-3 weeks after initial lung injury
■ Continued damage results in collagenous and fibrous tissues
● Lung compliance worsens -extremely low
● Largely inadequate gas exchange -severely lmtd
● Pulmonary HTN - a lot of pulm vasc destruction
● Mech vent is mandatory at this point - tx was insufficient or it was caught late
EARLY S/S
● Dyspnea
● tachypnea
● cough, restlessness
● Early on: may hear normal or fine, scattered crackles
● ABGs
○ Mild hypoxemia and respiratory alkalosis caused by hyperventilation
● Chest x-ray may be normal or may show minimal scattered interstitial infiltrates
● Edema will present at 30% lung fluid content

LATE S/S
● Symptoms worsen with progression of fluid accumulation and decreased lung compliance - lots of fluid and decreased
compliance:
● Diffuse crackles and rhonchi
● Tachycardia -lungs trying to perfuse
● diaphoresis
● decreased mentation d/t decreased hypoxia
● cyanosis (lips 1st place), pallor
● Hypoxemia despite increased FIO2
● Chest x-ray termed “whiteout” - lots of fibrous tissue, more fluid, more white, more dense
DX:

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● Arterial oxygen levels do not respond to increased oxygen levels (FIO2)
● Hyperventilation in early phases result in (mild) respiratory alkalosis
● Metabolic acidosis develops from hypoxemia - buildup of lactic acid
TREATMENT
● 2 goals: PaO2 level above 60, and ph level WNL
● Will be in ICU and will need mech ventilation, will be endotrach intubation
● ETT and mechanical ventilation with PEEP to maintain adequate PaO2 levels - PEEP positive end expiratory pressure (when
you breathe out, want some end pressure still there); exhalation at 5 cm??, commonly during tx, want to see PEEP setting at 5
(this is normal) = o2 level above 60
○ Peep 5 = expansion, prevents alv collapse, and improves shunting
○ rationale: Want to give lowest o2 concentration d/t risk for o2 toxicity when FIO2 is over 60% for greater than 48
hours; so high settings for over 2 days, it increases risk of o2 tox
○ Monitor PAO2 and SaO2; be aware that vent will increase intrathoracic and intrapulmonic pressure —> may affect
venous pressure to the heart, reducing preload and CO to heart; hyperinflation of alveoli may lead to barrel trauma or
volutrauma
○ +++HOMEWORK: on barrel trauma or volutrauma, read up on this!! Take it seriously!! Read carefully
■ Barrel trauma - induce so much positive pressure that we are damaging alveoli (HCP is the cause of the
damage)
● Sedation - to control restlessness and reduce anxiety —> (decrease O2 consumption); many vent ppt are sedated and on
ETT
● Positioning--continuous lateral rotation tx or prone position tx (phase I); -prone positions increases paO2; rotation beds are
useful (2 ways: prevents pooling of fluids; romoites mobilization of fluids)
● Pharmacologic paralysis (Norcuron or Pavulon) - to manage ventilation - better control of ventilation or I:E ratio
● Abx for infection (if initial cause is sepsis (most common), so ARDS won't worsen),
● inotropes (Dopamine)- to increase CO - ensure Adeq CO
● d/t all the NP activiity, some MD use steroids as well (may or may not RX steroids)

NANDA
● Impaired gas exchange
● Ineffective airway clearance - lots of pulm edema, fluid buildup, pooling at the base
● Ineffective breathing pattern - d/t compliance is low (TV is low)
● Anxiety - SOB, increases o2 consumption
● Altered comfort: pain (trauma situations)
● Decreased CO
● Altered nutrition less than body requirements - too tired to eat

PROGNOSIS
● Mortality rates highly correlate with the severity of lung injury at 72 hours post onset
● Lung repair occurs slowly and terminates by about 6 months following onset of ARDS
○ 50% have no significant permanent lung damage
○ Many survivors have significantly reduced health-related quality of life, physical function and continued pulm prob
(fibrous tsu)
■ Pulm HTN due to thickening ?? Listen to lecture!!!
■ Ongoing cough and dyspnea
● MAIN THING: how it occurs, most common is sepsis, know pathophysiology know why they are having problems and why
they are getting tx; progression of sickness on the floor (ARDS, sepsis) 3 ways go getting ARDS (on the floor, rapid code, ICU)

OXYGEN TOXICITY
● Medically induced, potentially fatal, worsen pt original condition
○ high O2 amounts over a prolonged time period —> pulm prob, induces ventilatory failure
■ O2 levels above 50% and >24hrs are potentially toxic (baseline)
■ RISKS significantly increases when >60% for >48hrs
■ At risk are pts on steroids, bleomycin, hyperthermia, hyperthyroidism, protein deficiency (albumin levels),
vitamin E deficiency and adrenergic stimulation (stress)
■ Prolonged exposure causes pathophys changes
○ pathophysiologic changes
■ Interstitial edema, thickening of alveolar capillary membranes, damage alveoli (intra-alveolar hemorrhage),
atelectasis (collapse alveoli) —> determine presentation

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S/S OXYGEN TOXICITY

● Due to changes in the oxygen transport system
○ Mild substernal soreness - chest pain
○ Nasal congestion
○ Pain on inspiration - damaged tsu
○ Increased coughing
○ Progressive dyspnea develops -d/t damaged alv
○ consolidation and fibrosis of the lungs--decreased compliance —>. CXR

○ CXR increasing pulmonary opacification (from consolidation and edema)
○ Crackles and diminished breath sounds
○ ABGs - hypoxemia
TREATMENT
● Monitor ABGs - hypoxemia
● + Maintain FIO2 at lowest possible level
● Treat underlying disease - so we don’t need to use vent anymore, lower the use of the vent
N/I
● Emotional support - those on mech vent who are sick, be empathetic
● Monitor fluid and electrolyte status
○ Daily weights - provide the most accurate indicator for fluid volume - d/t fluid buildup for pt with ARDS who have o2
tox
● Aseptic airway care (VAP increases risks)
○ Anyone on vent, do oral care every 2 hr (in add to make sure vent rate is right, plugged in, works, etc)
● PEEP to reduce FIO2 - peep MAY reduce fiO2
● Early ambulation
● Deep breathing/coughing, IS - reduce congestion
● Position changes - to decrease intrapulmonary shunting
○ Two things we discussed earlier to reduce ARDS: review it from earlier!!!

CHEST TRAUMA
● def: Injury to thoracic cage and its contents can restrict heart’s ability to pump or lungs’ ability to oxygenate blood - (heart,
lungs, associated vasculature/ greater vessels) ; may be simple or severe (fractured rib vs ruptured organ from MVA, ripping
greater vessel)
○ Penetrating (GSW, knives, shrapnel, fell off roof and onto a pole/ fence, etc.) - open injury
■ May cause open chest wound with air entering pleural space and compressing lung -foreign obj puncture,
risking of atmospheric air entering pleural space —> lung compression (too much positive pressure,
compresses lung)
● Nonpenetrating (blunt, MVA hit sterling well) - chest struck with severe amt force but doesn’t go through, bruising; can be
internal organ injury/ damage (tear laceration contusion or organ dysfunction); rupture of heart tsu (heart is like a water
balloon/ orange, when you lean on it, it ruptures)
○ Deceleration injuries associated with motor vehicle accidents, also falls or blows to chest
SPEAKER NOTES:
● When someone has physical chest trauma, in the ER —> assess AIRWAY 1st! ABC!!! Set up room to accommodate ABC
● How well can pt oxygenate blood , pump blood throughout the body?
● stat: chest trauma is 75% of all traumatic deaths
● 2 ways to classify: penetrating vs non penetrating

COMPLICATIONS
1. Pneumothorax
2. Tension pneumothorax and mediastinal shift
3. Open pneumothorax and mediastinal flutter
4. Hemothorax or hemopneumothorax
5. Fractured ribs
6. Flail chest - a section of ribs!

PNEUMOTHORAX
● Air enters pleural space

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● Presence of air in pleural space that prohibits complete lung expansion
● Two types:
A. Open pneumothorax-open chest wall or diaphragm, atm air enters through open wound
B. Closed or spontaneous pneumothorax - internal damage (rib frx—> puncture lungs) puncture of tear in an internal
respiratory structure ; burst bleb (air pocket from emphysema)-> air escapes into pl space; or d/t fault of medical team
(increased + ventilation over long time—>barrel trauma)

S/S
● Tachypnea and tachycardia - trying to compensate for perfusion
● Dyspnea, progressive cyanosis - see in the lips
● Sudden sharp pain on affected side with chest movement, breathing or coughing - + pressure
● Asymmetric chest expansion - + pressure on one side, unaffected side normal expansion
● Diminished or absent breath sounds on the affected side
● Hyper-resonance (tympany) to percussion on affected side - will sound hollow vs dense (sounds like mini knock)
● Restlessness or anxiety - d/t diff breathing
● JVD, - pressure on great vessels
● PMI shift, - point of maximal impulse (mid clavicular b/t 5-6th intercostal); things are moving organs, and trachea to the side,
heart to the side, so PMI shifted (PMI = apex of the heart)
● subq emphysema, - in neck and shoulders (crackly), can feel it, feels like rice krispies
● tracheal deviation toward unaffected side - if rt lung affected, tracheal deviation to the left
● SPEAKER NOTES: Air in pleural space, pressure on lungs —> fast RR, fast HR

TREATMENT
● goal: optimize gas exchange
● 2 ways:
○ remove abnormal + pressure pushing against lungs
○ reestab - pressure
○ So insert chest tube! Most definitive way to release pressure
○ If pt in ER/ ICU - insert chest tube or EMT use decompression needles
● Chest tube via 3rd-4th intercostal space at mid- axillary line (for chest tube) or anterior for decompression needle
○ Attached to Closed-chest drainage system -we are removing air from pleural space and no more atmospheric air will
go into pleural space (1 way valve)
○ Thoracotomy - to explore chest and repair site of origin of air or blood leak - first hand view to see whats going on;
shows where origin of leak is coming from (ex tear? They will correct the tear); reserved for trauma pts only (super
severe, high falls, MVA, etc)
■ If less severe like long standing severe emphysema and has many burst blebs —> pneumothorax —> no
thoracotomy

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TENSION PNEUMOTHORAX AND MEDIASTINAL SHIFT - more severe with

mediastinal shift
● MEDICAL EMERGENCY!
● When Air enters pleural space with inspiration and becomes trapped (one-
way valve effect), - no route of escape! HCP can cause this by accident too
● As air increases, pressure builds in the chest -keeps adding and never
decreases whether caused naturally or from medical team —> MEDIAstinal
spinal shift
● Untreated, affected lung will collapse
● Mediastinal Shift of heart, trachea, esophagus, and great vessels toward
unaffected side--decreases CO and BP
○ Compresses “good” lung
○ Compression, traction,
torsion or kinking of great
vessels

Complications
● Risk of tearing of great vessel,
tearing of pericardium in severe
cases
● High priority - may deteriorate pt
quickly!!! ACT QUICK!!! If tear in
aorta or pericardium —> decr CO —
> immediate code!!
● Compression of the good lung
● Lung expansion decreased over all
● Poor gas exchange
● Poor oxygenation
● Compression of heart and greater
vessels
● Decreased CO , restriction of
pumping ability
● Circ flow and perfusion is decreased
● BP decreased

CAUSES:
● Causes: open chest wound
A. ex. Guy tried to jump off building and landed on fence and pierced their chest —> causing a flap, broke through the
pleural space, the lungs, so when they breathe, the flap closes, air enters but can't escape. Pleural space like a
balloon
PRESENCE OF A FLAP
B. INTERNAL LUNG TSU DAMAGE THROUGH USE OF MECH VENTILATION (+ PRESSURE TOO HIGH —>
CAUSE DAMAGE); air keeps pumping in causing tension pneumothorax
C. WE INSERTED CHEST TUBE, BUT RN MAY HAVE FORGOTTEN THE LOCK, NOW IT’S JUST BUILDING AND
BUILDING AND BUILDING —> TENSION PNEUMOTHORAX (CLAMPED OR KINKED)

SYMPTOMS - way more severe, x3 of a pneumothorax

● Marked, severe dyspnea, tachypnea - higher RR
● Crepitus of neck and upper chest
● Progressive cyanosis,
● muffled heart sounds - heart is being compressed
● Acute chest pain on affected side
● Tympany to percussion - affected side
● Asymmetric chest wall movement with absent breath sounds on affected side
● ALOC,
● JVD,
● laryngeal and tracheal shift to unaffected side,

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● shifted PMI
● C/O pressure or tightness within the chest
● Severe hypotension leading to shock - d/t increased pressure on the
heart

TREATMENT
● Release + pressure —> initially, 18 gauge decompression needle mid
clav 2nd intercostal (anterior) according to book; in hospital, usually chest
tube is inserted
● Create open pneumothorax with 18 gauge needle into pleural space at
the level of the second intercostal space, midclavicular line
● Release of trapped air allows lung to re-expand and mediastinal shift
corrects itself
● CT (chest tube) - in hospital they go straight for the test tube but go with
the textbook info (18 gauge)
 


semi-fowlers (30 degrees) and up

SPEAKER NOTES: 3 kings movie: pneumothorax with decomp needle

SUCKING CHEST WOUND

● Occurs in open chest wounds - lg enough for air to move in freely during
breathing —> creates audible sounds
● Open pneumo with traumatic opening in chest wall large enough for air to
move freely in and out of the chest cavity during ventilation
● Creates a slurping or sucking noise - see bubbling

TREATMENT
● Cover wound immediately with anything available (e.g., towel) - something sterile preferably, but if can't a shirt, your hand,
anything
● Airtight covering usually prevent tension pneumo and preserves ventilation of opposite lung--ideal dressing sterile petroleum
gauze - sterile equipment (sterile yellow petroleum gauze post exhalation before inhalation), +++secure on 3 sides only!!++,
upon inspiration, the dressing is pulled into the wound but on exhalation, it allows extra space on untaped side for air to exist
—> outcome: increase in - pressure , at high risk for tension pneumothorax (caution!)
● Instruct pt to blow against a closed glottis and place dressing before next inhalation
● Continue to check for tension pneumo/mediastinal shift
● if tracheobronchial leakage (internal) If leak within tracheobronchial tree, air can still come in and cant exit, tension pneumo
more likely—remove the dressing/ open the seal to release air; -radiology will determine if leakage in tracheobronchial tree
● CT placement is ideal - for air removal and to allow lung to re-expand

● OPEN PNEUMOTHORAX AND MEDIASTINAL FLUTTER (MISSING!!)

HEMOTHORAX OR HEMOPNEUMOTHORAX
● Less than 300 ml in pleural space may cause no symptoms therefore, no CT needed - blood filling up pleural space d/t injury
to chest wall, diaphragm, the lungs itself or the great vessels
● If less than 300 ml —> may be asymptomatic, no CT needed
● If over 300 —> CT,
● Severe hemothorax (1400 - 2500 ml) life-threatening
A. Results in hypovolemia and tension pneumo and will see tachycardia, hypotension, shock —> at risk of death
● Hemopneumothorax =

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S/S
● more blood in pleural space —>. Dyspnea
● Diminished lung sounds
● Upon percussion —>. DULLNESS d/t fluid
● Hypotensive d/t loss of fluid
● To compensate, body becomes tachycardic

● Risk for SHOCK

TREATMENT
● goal: remove blood from pleural space
○ Needle aspiration
○ CT
● Aspirate blood using large gauge needle (16+) at 5th or 6th intercostal space, midaxillary line (returns of 500 to 1000 ml not
usually a problem but 1500+ indicates need for surgery - like thoracentesis; use U/S for guidance,
○ 16 gauge, need bigger bore size
○ For air they go high, for blood they go low (d/t gravity)
● CT - will be inserted
● 200 ml or more per hour may indicate need for thoracotomy
● High alert situ may indicate severe internal injury or an active bleed
○ If initial vac is 1500 ml or greater—> may indicate severe internal injury or an active bleed
○ If initial vac and subs vac is 200 ml/ hr - its not slowing down, may indicate something active bleed —> risk for shock
—> Repair ASAP! Thoracotomy and tissue repair (d/t rupture or tear —> sew/cauterize)
○ Autotransfusion of blood loss —> reinfuse OR PRBC infusion
○ Supplement with IVF (due to low FV)
○ Frequent CXR to monitor progress
○ keep close eye on ABC

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FRX RIBS
● Usually associated with blunt injury usually breaking a point of maximal force or at costochondral joint - break in the ribs, most
common type of chest injury, assoc with blunt force trauma, occurs at costochondral Jxn
A. May damage pleura in lungs
B. May lead to pneumothorax or hemothorax
● Bone splinters may cause pneumothorax or hemothorax

S/S
● Chest pain Pain/tenderness over the fx area especially on inspiration and palpation - upon breathing and movement, self
splinting, may have shallow breathing for extended periods of time( may lead to atelectasis)
● Tendency to hold chest protectively or breathe shallowly to minimize chest movements--decreases lung compliance
● Bruising at site of injury - blunt force trauma (common)
● Protruding bone splinters
● Clicking sensation if costochondral separation or dislocation is present
● Predisposes to atelectasis and pneumonia

TREATMENT
● simple: pain control is #1
● Rest, local heat, analgesics, splinting chest when coughing and deep breathing
● Pain lasts generally 5 - 7 days with complete healing in approximately 6 weeks -pain preset for 1 wk, complete healing in 6
wks
● With severe pain and hypoventilation d/t pain and shallow breathing, local may be given at fx site or intercostal nerve block -
md will order nerve block —> will allow for better breathing, complete deep breathing and cough more effectively and I/S
● Splinting of chest during coughing and deep breathing helps pt to avoid atelectasis/pneumonia

FLAIL CHEST
● def: fractured ribs several consecutive ribs in 2 or more places (rack of ribs); segment that breaks off becomes separated from
chest wall —>. Fractured off ribs FLOATS during ventilation
● Paradoxical movement (ribs are sucked in during inspiration, on exhalation it’s pushed out) —>. EMERGENT!!!
● Disrupts normal lung expansion
● Tidal volume will be decreased, ventilation impaired, poor coughing
● Crushed chest with ribs pushed in on lung tissue
● Consists of two or more adjacent ribs on the same side and possibly the sternum with each bone fractured into two or more
segments
● Usually lateral chest wall
● Pulmonary edema, pneumonitis and atelectasis often develop rapidly as fluids tend to increase and collect at the injured site

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S/S:
● Hypoventilation
● hypoxemia
● Pulmonary contusion leading to
accumulation of fluid in affected
alveoli and causes
intrapulmonary shunting and
further hypoxia
● Mediastinal flutter--swinging
may affect circulatory dynamics
with elevated diastolic BP,
impaired filling right heart and
decreased systolic pressure -
(abnormal mvmd of organs and
vessels during inhalation and
exhalation—> pressure
abnormal )
● Anxiety,
● cyanosis,
● dyspnea,
● tachypnea (shallow),
● grunting,
● paradoxical movement of chest
wall
● Untreated, —> hypercapnia and
hypoxia
● Paradoxical chest wall movement
● Rapid shallow breathing

CAUSE:
● Cause: blunt trauma —>. Fluid in alveoli accumulates —> if signify —>. Think of pulmonary shunting —>shutning further
adds to hypoxia

TREATMENT:
● goal: airway mgmt, pain control
● Restores adequate ventilation reducing hypoxia and hypercapnia -ensure vent is maximized, supplemental o2
● Decreases paradoxical motion by using positive pressure to stabilize chest wall internally
● Relieves pain by decreasing movement of fx’d ribs
● Provides avenue for removal of secretions
● End goal: re-expansion of lungs and reoxygenation
● If pt doesn’t improve —> intubated, mech ventilator

● Muscle relaxants or musculoskeletal paralyzing agents

● ABGs, - monitor gas exchange
● postural drainage, positioning - semi fowlers
● Surgical fixation may be completed - fix the flail

THORACIC SURGERY
● Thoracotomy--pulmonary resection, wedge resection, lobectomy, pneumonectomy -for exploration or remove foreign object or
repair certain tsu, may enter medially or laterally dep on where base of problem is ; special tech is video-assisted thoracic
surgery
○ benefits: it is minimally invasive (MIS), post op discomfort is at a minimum, quicker return to baseline
○ May do pulmonary resection (remove lung section), wedge resection (remove small or localized lesion), lobectomy
(remove one lobe), pneumonectomy (remove entire lung)
○ Expect CT placement
● CT - placed for air drainage (superior, anterior), and fluid removal (inferior, posterior)
○ -post op: chest tube placement for air and blood removal

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 297 RESP
○ N/I: How is resp fxn? what is the RR? What is the effort? Lung sounds? Do complete CT asmt, if pt on ventilator
(good vent mgmt - conn, alarms, settings, see ET line, circulation under all the connections)
● Airway critical--from oxygen via cannula to ventilator, pulmonary hygiene
● Pain control -high pain scores expected d/t cutting resp muscles, those muscles always moving
○ Intercostal nerve blocks maybe
○ Opioids common
● Fluids/labs
● Positioning -frequent, keep HOB elevated, encourage ambulation TID (d/t promoting lung expansion)
● Nutrition - d/t surgery

Swan-Ganz catheterization is the passing of a thin tube (catheter) into the right side of the heart and the arteries leading to the lungs. It
is done to monitor the heart's function and blood flow and pressures in and around the heart
● Discussed in hemodynamics LECTURE
● 4-5 ports on Swan-ganz

NURSING IMPLICATIONS
● Only when obtaining further PCWP, should the balloon be inflated. If fixed-wedge waveform occurs:
○ Check to see if balloon inflated

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 297 RESP
○ Change the pt’s position
○ Instruct pt to cough
○ Perform chest percussion
○ Notify MD for catheter repositioning or follow unit protocols to pull catheter back

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