critical care pulmonary lecture

lateral visualizaton of lungs

atelactasis

collapse of alveoli leading to reduced gas exchange

types of atelactasis

• obstructive: mucus plug (COPD, PF), forgien body, tumor

• non obstructive:

  • most commonly caused by anesthesia

  • compressive - pneumothorax, hernia

  • contraction - scar tissue

  • adhesice - surfactacnt deficiency

• CM:

  • dyspnea

  • hypoxia (O2sat 90%)

  • reduced breath sounds

  • crackles over area

diagnosing atelectasis

• chest Xray: colume loss, shift of fissuresm elebated hemidiaphram

• ct when unclear: consider risk factors

nurisng interventions for ateleactasis

•Prevention

–Frequent turning

–Early mobilization

–Strategies to expand lungs and manage secretions

–Incentive spirometer

–Voluntary deep breathing

–Secretion management

–Pressurized metered-dose inhaler

-oral care

•Treatment: bronchial hygiene, bronchoscopy for mucus plugging, address underlying cause.

• complications and pearls: can predipose to PNA and hypoxemia

acute tracheobronchitis

infammation of the mucus membranes of the trachea usually after a viral infection

patho of tracheobronchitis

• Viral: “PAIR”

  • parainfluenza, advenovirus, influenza, rhinovirus

• Bacterial

  • strep, pneumonea, haemophilus influenza (more likely COPD and smokers

• SM

  • initially dry cough with mucoid sputum

  • as progresses, dyspnea, stridor, wheezes, purulent sputum

pneumonia

• = inflammation of the lung parenchyma

  • exudate accumulates in teh alveoli

classifications of pneumonia

• bacterial

• viral

• atypical

typical bacterial PNA

• bacteria that normally resides in the nasopharynx of healthy people and do not cause a problem

• through coughing and sneezing bacteria can travel to lungs causing infection

• ss: fever, chills, productive cough, chest pain, dyspnea, shortness of breath.

• need chest XR

• streptococcal is what causes most of PNA*

viral PNA

• determined by genetic material they carry

• influenza, covid - the virus that causes covid 19, RSV

atypical PNA

• mycoplasma or legionella or chlamydial

• ss: beyond lungs

  • HA, fever, pharyngitis, rash joint pain, stomach ss NVD

physcial exam for PNA / ss

• assessment: orthopnea (SOB when laying), crackles, increased tactile fremitus (palpable vibration in chest wall), purulent sputum

• symptoms: Cough, fever, chills, HA, malaise, fatigue, leuritic chest pain, dyspnea

• signs: tachycardia, tachypnea, use of accessory muscles, sputum, abnormal breath sounds

community aquired PNA

• Community setting or within first 48 hours post hospitalization

• Older more at risk

• S. Pneumoniae is the most common cause among adults

• Viral cause in infants and children

health care associated PNA

• Occurs in long term care facilities

• Often caused by multidrug‐resistant organisms

• Early diagnosis and treatment are critical

hospital aquired PNA

• Develops 48 hours or more after hospitalization

• Subtype of health care–associated pneumonia

• Potential for infection from many sources

• High mortality rate

• Colonization by multiple organisms due to overuse of antimicrobial agents

• Pleural effusion, high fever, and tachycardia

• Common with debilitated, dehydrated patients with minimal sputum production

ventilator associated PNA

• Develops 48 hours or more after hospitalization

• Subtype of health care–associated pneumonia

• Potential for infection from many sources

• High mortality rate

• Colonization by multiple organisms due to overuse of antimicrobial agents

• Pleural effusion, high fever, and tachycardia

• Common with debilitated, dehydrated patients with minimal sputum production

Pneumonia in the immunocompromised host

•Common agents include pneumocystis, fungi, and tuberculosis

•Receiving immunosuppressive agents, history of immunosuppressive condition

•Subtle onset with progressive dyspnea, fever, and nonproductive cough

risk factors for PNA

– Heart failure, diabetes, alcoholism, COPD, and AIDS

– Influenza

– Smokers

– Depressed cough reflex: age, anesthesia, sedation, medications, head injury, abnormal; swallow, Intubation

– ABX treatment… secondary infection in oropharynx

– Prolonged immobility

– Supine position ( Pt unable to protect airway)

– ETOH intoxication

– Cystic fibrosis

diagnosing PNA

• hostory and hyscial exam

• imaging

• sputum examination

• blood work

treatment for PNA

• depending on what type: pharm” ABX or antiviral

• oxygen

• fluids

• bed rest until clinically stable

• nursing interventions: small frequent feedings, cough suppressants, antipyretics, bronchodolator’s, montir vs, rest/activity balance, hydration

nursing assessment and complicaions with bacterial Pneumonia

• assessment:

  • •Vital signs

    •Secretions: amount, odor, color

    •Cough: frequency and severity

    •Tachypnea, shortness of breath

    •Inspect and auscultate chest

    •Changes in mental status, fatigue, edema, dehydration, concomitant heart failure, especially in older adult patients

• complications:

  • Continuing symptoms after initiation of therapy

    •Sepsis and septic shock

    •Respiratory failure

    •Atelectasis

    •Pleural effusion

    •Delirium

planning and goals for pt with bacterial PNA

• improved airway patency

• increased activity

• maintenance of proper fluid volume

• maintenance of adequate nutrition

• absense of complications

• based on patient outcomes plan for home, community, and transitional care

nursing interventions for patient with bacterial PNA *

• oxygen with humidification to loosen secretions

  • face mask or nasal cannula

• coughing techniques

• chest physiotherapy *

• position changes

• incentice spirometry

• nutrition

• hydration * (infection takes up fluid)

• rest

• activity as tolerated

• pt education

• self care

expected outcomes for patient with bacterial PNA

•Demonstrates improved airway patency

•Rests and conserves energy and then slowly increases activities

•Maintains adequate hydration; adequate dietary intake

•Verbalizes increased knowledge about management strategies

•Complies with management strategies

•Exhibits no complications

aspiration PNA

occurs when inhaled food, drink, vomit or saliva into the lungs. more likely if something disturbs your normal gag reflex, such as a brain injury or swallowing problem, or excessive use of alcholhol or drugs

risk factors for aspiration PNA and ss

• age >65

• chronic disease: CAD, COPD

• smoking

• weakened 0r suppression of immune system

• ss:

  • coughing episodes with eating

  • increased fatigue

  • low grade fever

  • change in MS

  • imaging: CXR: infiltrate usually lower lobes RLL>LLL (can see as soon as 2 hours after aspiration

prevention of aspiration PNA

• thickened liquids

  • making sure they go down esophagus

• sit upright when eating

• good oral hygiene

aspiration management

• supportive care, airway protection, consider early antibiotics if bacterial infection suspected

• bronchoscopy for large particulate aspiration

  • standard for removing forgien objects other blockages

aspiration prevention

• HOB elevated between 30-45 degrees

• limit sedation

• avoid stimulation of gag reflex

• swallow eval

• soft diet, small bites, no straws

critical care clinical practice to prevent tube feeding aspiration

•Before initiating tube feeding, confirm tip location.

•Tube feed patients: residuals Q4h, <150mL before next feeding.

•Avoid bolus Tube feeding

•Draw back 1-2 cc of fluid from tube and check ph.

•Ph of 5.5 =likely in the stomach (where it is more acidic)

•Ph of 6= likely respiratory tract or intestines and repeat x-ray.

pt education/PNA healing timeline

• 1 week - fever shhould begin to resolve

• 4 wekks - chest pain and sputum should decrease

• 6 weeks - cough and SOB decrease, if persists, concider further w/u and alternate diagnosis

• 3 mo - all ss should be resolved, may still have soem fatigue

• 6 months - back to normal

what is a lung abcess

• pocket of pus in the lung surrounded by inflamed tissue

• most are complication of bacterial pna

• ss: vary from a mild productive cough to acute illness with foul sputum, leukocytosis, pleurisy, dyspnea, weakness, anorexia, and weight loss,

lung abcess assessment/physical exam

• pleural friction rub/ crackles

• test: chest XR, sputum culture, bronchoscopy, ct of chest

pleurisy

= inflammatiom of both layers of pleurae

• lungs have two layers

  • visceral pleura – inner

  • parietal pleura – outer

• key characteristic: pleuritic pain and its realtion to resp movement

  • friction rub can be heard with stethoscope

• test: chest XR, sputum, thoracentesis

empyema

•: infected pleural fluid—pus, positive gram stain/culture, low pH, low glucose.

Tuberculosis

• caused by a bacterium called Mycobacterium tuberculosis transmitted through aerosolized droplets.

• 20-40% wold population is effected

• higher risk in disadvantages communities

• primarily attacks lungs but may effect otehr areas (ei; kidney, spine, brain)

TB disease/active TB

• with infection and symptoms

• may occur 2-3 months or years after exposure

• changes from latent to active due to immune compromise of chronic illness

• infectios ss:

  • cough over 3 weeks

  • hemoptysis (coughing up blood )

  • wt loss

  • night sweats

  • weakness

  • fever

Latent TB

• person expose to bacteria but immune system keeps under control

  • bacteria are encapsulated

• NOT infetious

• 10-15% will develop active without treatment

length of treatment for TB

once a week treatment for 12 weeks

pleural effusion

fluid build up in the lungs

assessment of pleural effusion

• inspection: anxious, in distress, trachea may deviate tawards inaffected side

• palpation: decreased tactile fremitis and decreased expansion of effected side

• percussion: dullness

• auscultation: decreased/absent breath sounds or possible rub on affected side

diagnostic studies of pleural effusion

Chest CT gold standard

CXR

U/S

Diagnostic thoracentesis

Pleural biopsy

Bronchoscopy

Malignancy workup

treat: fluid must be tapped

management of empyema

•: antibiotics and surgical drainage (small-bore chest tube +/- fibrinolytics; VATS if loculated)

acute respiratory failure

• type 1: hypoxemic —> oxygenation failure

• type 2: hypercapnia —> ventilatory failure

type 1 of acute respiratory failure

• oxyegenation failure —> impaired oxygen diffusion at the alveolar capilary membrane

  • breathing air with reduced oxygen content

  • abnormal hemoglobin

  • thickening or desteiction of alveolar capilar membrane

  • PNA, ARDS, HF, Pulmonary embolism

type 2 of acute respiratory failure

• ventilatory failure —> inability to blow off CO2

  • increases resistance to breathing (asthma)

  • reduced breathing effort due to resp muscle weakness

  • increased area of the lung that is not available for gas exchange (COPD, obesity hypoventilation syndrome)

clinical manifestions of acute respiratory failure

• rapid deterioration to hypoxemia, hypercapnia, and resp acidosis

• impaired ventilation of perfused mechanisms

• CM: use of accessory muscles and decreased breath sounds

• dyspnea is the hallmark of acute respiratory failure

early signs of oxygen failure in acute respiratory failure ***

• dyspnea/tachycpnea - use of accessory muscles

• restlessness

• tachycardia/HTN/diaphoresis

• changes LOC/mentation restlessness/agitation

• HA and fatigue

late signs of oxygen failure in acute resp failure ***

• confusion, lethergy

• tachypnea - resp arrest

• tachycardia - dysrhythmias- bradycardia

• central cyanosis (bodies core turns blue ie lips, tongue, mucous membrane)

• cool, clammy skin

nursing management of acute resp failure

• identify and treat underlying cause

• intonation, mechanical vent

• nutrition- enteral feedings preffered

• reduce anxiety

• provide pt a form of communication

• prevent complications (turning, ROM, mouth care, skin care)

• do imaging and labs - see what electrolytes are

• when to intubate:

  • worsening hypoxemia despite O2

  • resp fatigue

  • hypercapnia with acidosis *

  • altered mental status

  • prepare for rapid sequence intubation and post intunation strategy

what is ARDS

• = a severe form of Acute Resp Failure

• Alveolar capillary injury (not caused by cardiac issue)

• Damage to the endothelial lining of the alveolar capillary membrane, which increases its permeability

  • Plasma and proteins leak from capillaries into the interstitial spaces and alveoli

  • Diffuse alveolar damage

  • Reduces lung compliance, volume, and normal gas exchange

• Rapidly progressive hypoxemia

• Noncardiogenic pulmonary edema

  • (fluid accumulates in the lungs but not caused by a problem with the heart)

significance of ARDS

• mortality rate 27-50% unless accurately diagnosed it can prove fatal in the first 48 hours

(covid resemebles )

• causes: COPD, PNA, neuromusclar failure, drug OD

etiolofy of ARDS

• common causes* =

• Aspiration of Gastric Contents*

• Pneumonia (COVID) (Bacterial/Viral)*

• Inhalation Injury

• Oxygen Toxicity

• Pulmonary Contusion

• Chest Trauma

• Fat Emboli

• Near Drowning

• Shock of Any Etiology *

• Sepsis *

• Massive Trauma

• Disseminated Intravascular Coagulation

• Massive Transfusion

• Drug Overdose

• Acute Hemorrhagic Pancreatitis

• Burns

• Anaphylaxis

CM/physical assessmemt of ARDS

• Hypoxia that doesnt improve with O2!!**

• tachypnea

• increasing dyspnea.. hyperventilation.. resp distress

• initially no adventotious breath sounds

• tachycardia

• hypertension

• restlessness, anxiety

• chest XR

• chest x-ray appears to resemble pulmonary edema

• BNP to distinguish pulmonar edema from ARDS cersis from heart failure

  • BNP higher in pulmonary edema due to HF

• visible bilateral infilrates that quickly worsen

BNP

= brain natiritic peptide

• hormone released from the heart when under stress in respinse to increased venticlar pressue and volume

• high BNP = heart failure with pulomary edema (but NOT with ARDS)

medical management of ARDS

• Intubation, mechanical ventilation with Positive End Expiratory Pressure (PEEP) to keep alveoli open (normally alveoli deflate with breathing out, this keeps them open during expiration to increase gas exchange ie: o2 in and Co2 out)

• Treat hypovolemia to keep hemodynamically stable

• Turn patient to Prone position

  • is best for oxygenation,

  • the weight of the heart, abdominal organs, and diaphragm is shifted away from the lungs,

  • allowing for better ventilation of the dorsal (back) lung regions that have collapsed d/t atelectasis.

  • Also Increases end-expiratory lung volume

  • Improves bronchial draining

  • Improves functional residual capacity

  • Improves gas exchange

  • Opens collapsed alveoli

• frequent repositioning to safeguard integumentary system. Improves oxygenation 

  • Nutritional support, enteral feedings preferred

  • Reduce anxiety, sedation, paralysis

  • Supportive care

halmark sign of ARDS

hypoxia that doesnt improve with O2

non-invasive positive pressure ventilation

• ventilatory support without intubation

• positive pressure keeps airways & alvioli

• CPAP: pushes O2 in using single continuous pressure

  • improves oxygenation (does not remove co2)

  • used for sleeo apnea

• BIPAP: helps move air in and out

  • high pressure on inhalation, lower pressure on exhaltion

  • helps remove CO2

  • used for COPD

critical lab values for mechanical ventilation

• PaO2 <55 mm HG   (norm values 80-100 mmHg)

• PaCO2 >50 MM HG  (norm values 35-45 mmHg)

• Vital capacity <10ml/kg  (norm 50 ml/kg)   

  • (reduced vital capacity= weakness of respiratory and diaphragm muscles to have enough force to draw air in and out of lungs)

• Negative inspiratory force (NIF) < - 25 cm H2O (norm NIF is - 60 to  -100 cm H20)

  • The NIF= measures the strength of respiratory muscles and diaphragm, by quantifying the maximum negative pressure generated during inhalation effort

  • FEV <10ml/KG ( Forced Expiratory Volume)

ss that indicate a need for mechanical ventilation

•Typically…Dyspnea(SOB),Tachypnea, LOC changes

•Apnea or bradypnea

•Respiratory Failure /Compromised airway

•Emergency

•Respiratory distress with confusion

•Increased work of breathing when other interventions have failed.

•Confusion with the need to protect the airway.

•Shock

•Control patient’s respirations during Surgery or Procedures

medications for patients of mechanical ventilation

• Narcotics/ Opioids

  • Pain Management

• Benzos

  • Sedation, amnesia, muscle relaxants

• Paralytics

  • Paralytics/Versed paralyze respiratory muscles, Patient MUST HAVE a Sedative 

• Corticosteroids

  • Reduce inflammation, suppress immune system, studies are +/– for use of steroids

• Inotropes

  • Balance carefully: Nitrates/ Pulmonary HTN, and Dopamine will maintain BP

• Bronchodilators

  • Albuterol, DuoNeb treatments allow smooth airways to relax.

• Diuretics

  • Help to increase renal excretion, decrease pulmonary edema & reduce preload.

• Dobutamine/Dopamine

  • for Hypotension

• Nitroglycerine / Nitroprusside

  • For Pulmonary Hypertension

potential complications/things to look for when monitoring ventilator

• vent problems:

  • volume/rate depending of pt condition/ARDS

  • oxygen is priority!

• alteractions in cardiac finction

  • decrease in venous return

  • VS and fluid volume assessment

• barotrauma/Pneumothorax

  • high airway pressure may cause alveoli to rupture

• pulmonary infection

weaning from ventilator

• process is dependant on spontaneous breathing

• vent rate is gradually decreased until pt breathes on own without use of vent

• pressure support is maintained during weaning

nursing management of ventilation patients

• improving O2 and ventilation

• positioning

  • least affected area of lung is most dependent position

  • semi recombent/elevate HOB

  • reposition every 2 hours

• prevent desaturation

  • hyper oxygenate before suctioning

  • minimize acticity

• secretion clearence

  • hydrate, humidifym neb treatment, mucolytics, chest PT, suction

• prevent complications

  • hospital and ventilator aquired PNA

    • oral care: 12% chlorohexidine swabs and brush teeth

endotracheal intubation

•Passing an endotracheal tube through the nose or mouth into the trachea

•Protects airway, provides patent airway, access for mechanical ventilation

•Facilitates removal of secretions,

•Maintain cuff pressure between 20- and 25-mm Hg

•Intubation for no longer than 14 to 21 days (after will require a tracheostomy)

• short term

tracheotomy

• long term breathing support

• surgical procedure where an opening is make into the tracheo

• allow removal of secretions

• reasons for it:

  • long term mechanical ventilation for weeks or longer

  • severe COPD, ICU stay, neuro disease

  • may have upper resp obstriction

• benifits

  • more comfortable long term

  • decrease risk of vocal injury

  • easier suctining and airway care

• high risk for aspiration - keep HOB elevated at >30%-45%

suctioning w/ trache

• patient should NOT be routinely suctioned

  • invasive procedure: can cause infection (PNA), atelectasis, airway injury, hypoxia, dry membraines

• pt are suctioned ONLY AS NEEDED basis if:

  • visable secretion in andotracheal tube

  • onset of resp distress

  • suspected aspiration of secretions

  • increase in airway pressure

  • adventitious vreath sounds

  • increase in resp rate/sustained coughing (normal RR = 12-22)

  • sudden decrease in O2 levels

responding to alarms/patient saftey

• if cause of an alarm cannot be determoned, ventilate the pt manually until problem is corrected (with ambu bag)

• oxygen is priority

• check the pt 1st!!

potential complications for mechanical ventilation

• shock:

• resp failure

• pleurisy: inflamation of the pleura (membrane around lungs)

• pleural effusion: accumulation of excess fluid

• empyema: accumulation of puss in pleural space

Pneumothorax

• air in the pleural space

• inspection: trachea is deciated towards unaffected side, anxious, holding chest

• palpiation decrease in tactile fremitis and decrease in thoracic expansion of affected side

• percussion: hyper resonance over chest wall (loud percussion)

• auscultation: decreased or absent breath sounds of affected side

• need chest XR and CT scan

• treat: chest tube, O2

pulmonary embolism

Occurs when a blood clot gets wedged into an artery in the lungs. Most caused by blood clots from the deep veins in the legs causes a Deep Vein Thrombosis (DVT) that gets released and travels to lungs. Multiple clots may be involved.

SS of puomonary embolism

•  tachycardia, S3 or S4 gallop

•   dyspnea

•   rales

•   pleuritic chest pain

•   cough

•   hemoptysis

•   diaphoresis 

•   leg pain

•   cyanosis 

•   fever

•   anxiety/fear

•    syncope

• asymmetric pitting lower extremity edema

• prominent superficial collateral vessels

• tenderness to palpation along the deep venous system

• + Homans’ sign

  • (calf pain with dorsiflexion of foot with knee straight)

  • (poor predictive value; reliability only 50%)

diagnostic testing for PE

• D-dimer

  • indicated in there is a clot

  • fibrin * from clot shows up

• ECG

• CXR

• ABG

• spiral ct

• pulmonary arteriogram

risk factors for PE

• venous stasis

• sedentary lifestyle

• prolonged immobilization

• periods of sitting/traveking

• vericose veins

• hypercoagubility

• injury

• tumor

• increased platelet count

• venous enothelial disease

• thrombophlebitis

• vascular disease

• forgien bodies

• HF

• Postoperative/postpartum

prevention and treatment of PE

• in hospital

  • active leg expercises

  • mobility with PT

  • early ambulation

  • anticoagulant therapy

  • compression devices

• treatment

  • measures to improve resp and vascular stasus

    • provide O2

    • ECG monitoring

    • IV access

  • anticoagulation therapy

    • heparin/warfarin

  • thrombilytic therapy

    • streptokinase alteplase

  • sugical

    • embolectomy

nursing managemnt for PE

• encourage ambulation

• passive leg exercise

• moniter thrombolytic therapy

  • VS q2 hours

  • PTT q 4 hours (make sure we are not thinning blood too much)

• O2 therapy

  • cough and deep breathing

  • IS

  • pulse ox

sarcoidosis - pleural involvement

• Sarcoidosis is an immune disorder meaning the immune system is dysfunctional and forms granulomas.

• What is a granuloma?

  • A granuloma is a small clump of immune cells that forms when the body tries to wall off something it sees as foreign but can’t get rid of.  Granulomas are made up of macrophages and other immune cells.

  • Think of it as the body building a fence around a problem

• Sarcoidosis is an interstitial lung disease that is inflammatory multisystem, granulomatous

why are granulomas a problem?

take up space in the lungs, make lung tissue stiff, restricting lung expansion and impair gas exchange

• cause: unknown

• occurs between ages of 20-40

treatment of granulomas

• no ss= no treatment

• moderate to severe ss = corticosteroids

  • supress immune system

pulmonary arterial hypertension

= progressive disease characterized by high blood pressure in the pulmonary arteries, leading to symptoms like shortness of breath, fatigue, and chest pain.

• pulmonary artery mean pressure > 25 mmHg

  • normal = 8-20

• idopathic or secondary to existing cardiac or pulmonary conditions like COPD

CM and diagnostic testing of Pulmonary Arterial HTN

CM:

• dyspnea

• substernal chest pain

• weakness, fatigue, syncope, and signs of right heart failure

Diagnostic tests

• chest XR

• pulmonary function test

• ECG and echocardiogram

• cardiac catheterization with measurement of right heart pressure

management of pulmonary HTN

• supplemental O2 with activity

• central venous access for prostanoids: active lipid mediators that regulate inflammatory respinse

• meds:

  • calcium channel blockers

  • Phosphodiesterase inhibitors: medications that cause blood vessels to relax and widen, improving circulation and lowering blood pressure.

  • Prostanoids ( prostaglandins mediate inflammation).

Cor Pulmonale

• restriction of pulmonary arteries leading to pulmoary HTN —> inceased resistance to right ventricle

• = enlargement of right ventricle leads to increased resistance and right sided HF

  • does not eject as much blood bc the muscle is larger and not enough blood can get in

types of thoracic surgery

• pneumonactomy

• lobectomy

• segmental resection

• wedge resection

• lung colume reduction - end stage emphysema

post op nursing care following thoracic surgery

• positioning

  • elecate HOB 30-45 desgrees

  • change position from back to side frequently

• self care

  • arm and shoulder exercises

  • pain relief pedalities

  • acticity - rest balce

  • avoid bronchial irritats

  • follow up care

  • smoke cessation

nursing care wth chest tube

•Pain Control**

•Narcotics/ Local for tube placement 

•NSAIDS for tube duration

•Anxiety treatments prn

•Nurses are responsible for keeping tubing connections patent and ensuring they are not compressed or kinked - position your patient well

•Ensure the drainage system is always below the level of the client’s chest to use gravity to drain air and fluid from the pleural space.

•Monitor the levels of fluid in water seal and suction control chambers – sterile water may need to be added prn

•Vital signs, pulmonary assessment, insertion site evaluation

•Daily x-rays

•Q Shift (or sooner) measurements of drainage

•Document the quality of drainage – sanguineous, serosanguinous, yellow, clear or opaque

• encourage IS and ROM with arms

chest tube complications

• bubbling in water seal chamber of chest tube system —> indicates air leak

• subQ emphysema or crepitis —> leakage of air into the sub Q tissue

chest tube emergency care

• if drainage system spills over —> encoruage p to take a few deep breaths with forceful exhalations and coughs

• sett up a new system and change pt over

• should the drainage system break, submerg the distal end of tubing into a bottle of sterile water (kept at bedside)

complications of chest tubes

infection at insertion site

PNA from poor pulmonary toilet

frozen shoulder

systemic hypotesion with rapid high volume drainage

chest tube removal

• Suction usually discontinued, patient on water seal for 6-24 hours prior to removal

• Chest x-ray prior

• Lungs re-expanded; pleural drainage ceased

• Pre-medicate*

• Pre-educate about upcoming events

• Sutures holding tube in place are cut, as patient exhales a deep breath the tube is   removed.

• Occlusive dressing placed over the wound

• Pleura self-seals usually – wound heals in several days – offer NSAIDS prn

blunt chest trauma

•involves forceful impact from dull objects (like car crashes, falls) causing compression/shearing, leading to bruises, fractures, internal damage without skin break

penetrating chest trauma

pierces the skin with sharp objects (knives, bullets) creating open wounds, causing direct tissue damage, infection risk, and potential organ perforation, with mechanisms differing in energy transfer and injury pattern.

pulmonary contusion and rib fractires

•Contusion causes alveolar hemorrhage/edema; rib fractures cause pain and hypoventilation leading to atelectasis.

•Manage with pain control, pulmonary hygiene, and respiratory support as needed.

Flail Chest

• multiple contiguous rib fractures causeing paradoxical chest wall motion - creating a loose, disconnected piece of bone that moves opposite way you breathe

• ribs are floating

  • paradoxical movement - making it hard to breathe

  • inhale = chest moves out

  • exhale = chest moves in

• high risk for resp failure

open pneumothorax

penetrating thoracic injury that causes air to enter from the outside in

closed pneumothorax

air enters the pleura space without an outside wound

causes:

• traumatic impact (MVA) or

• spontaneous rupture of lung tissue

  • primary spontaneous: without history of lung diease

  • secondary: with history of lung disease

tension pneumothorax

complication of open and closed

• worsening pneumothorax where air connot escape

• increaing intrathoracic pressure

• pressure starts to displace heart, good lung, and trachea

  • —> tracheal deviation*

• emergceny situation

diagnosis & CXR findings

• absent lung parkings, visceral pleural line of CXR, ultrasounds shows “lung point” (location of chest wall)

• ct more sensitive for small pneumothorax

• ABG

  • decrease in PaO2

  • increase in PaCO2

hemothorax

blood in pleural space collapsing ling - trauma or post op