Management of Clients with Ventilation Problems

INTRAPULMONARY PLEURAL RESTRICTIVE DISORDER

Pleural effusion
• Pleural effusion: collection fluid in pleural space usually secondary to another
disease process
• Large effusions impair lung expansion, cause dyspnea

Pathophysiology
• Increased systemic hydrostatic pressure
• Reduced capillary oncotic pressure
• Increased capillary permeability
• Impaired lymphatic formation
• Effusion may be
o Hemorrhagic or bloody
o Chylous or thick and white
o Rich in cholesterol

A clear fluid may be a transudate or an exudates.

Causes
• Transudate pleural effusion
o Heart failure
o Hepatic disease
o Hyperalbuminemia
o Renal disease
• Exudate pleural effusion
o Fungal or bacterial pneumonitis or emphysema
o Chest trauma
o Malignancy
o Subphrenic abscess, pancreatitis
o TB
o Carcinoma, lung abscess
o Idiopathic infection

Clinical Manifestations
• Usually caused by underlying disease.
o If the effusion is small or moderate pleural effusion causes minimal or no dyspnea
o With larger effusion
• lung expansion may be restricted, dyspnea
• Difficulty lying flat
• Non productive cough
• Tactile fremitus
Assessment and Diagnostic findings
• Pleural reveals
• Effusion
• Decreased or absent breath sounds
• Decreased fremitus
• Dull, flat sound on percussion
• In extremely large pleural effusion, the assessment reveals a patient in acute
respiratory distress
• Tracheal deviation
• CXR
• Chest CT
• Thoracentesis
• Culture
• Gram stain
• AFB
• CBC
• Blood chemistries
• Cytologic exam
• Pleural biopsy

Medical Management
The objective of the treatment
are to discover the underlying
cause of pleural effusion; to
prevent reaccumulation of fluid;
and to relieve discomfort,
dyspnea and respiratory
compromise.

• Specific treatment is
directed to underlying
cause
• Thoracentesis
• CTD
• Pleurodesis
• Pleurectomy
• Pleuroperitoneal shunt

Nursing Management
Preparation and support the patient for thoracentesis.

• Proper Recording and sending of fluids for appropriate laboratory testing.

• Chest tube care and monitoring
• Pain management
• Patient teaching
 Chest Trauma
• Chest trauma is frequently life threatening.

Pathophysiology
• Penetrating injury – open wound
• Non-penetrating blunt trauma – blow injury
• Initial assessment is directed toward identifying and treating immediate life
threatening conditions.
• Any client with chest injury should be considered to have a serious injury until proven
otherwise.
• ABC’s is the primary concern.
▪ Blunt trauma
o Sternal, rib fractures
o Flail chest
o Pulmonary contusion
▪ Penetrating trauma
▪ Pneumothorax
o Spontaneous or simple
o Traumatic
o Tension pneumothorax

Blunt Trauma
• More common than penetrating trauma
• Difficult to identify extent of damage because the symptoms may be generalized
and vague.
• Patient may not seek immediate attention

Most common causes

• Motor vehicle crashes
• Falls
• Bicycle crashes
• Mechanism of blunt trauma
• Acceleration
• Decelerration
• Shearing
• Compression

Chest injuries may result to

• Hypoxemia
• Hypovolemia
• Cardiac failure
 • Time is critical in treating chest trauma, assess pt immediately to determine the
following
• Time elapsed
• Mechanism of injury
• Level of responsiveness
• Specific injuries
• Estimated blood loss
• Recent drug or alcohol use
• Prehospital treatment

Initial assessment includes assessment for

• Airway obstruction
• Tension pneumothorax
• Open pneumothorax
• Flail chest
• Cardiac tamponade

Secondary assessment
• Simple pneumothorax
• Hemothorax
• Pulmonary contusion
• Traumatic aortic rupture
• Tracheobronchial disruption
• Esophageal perforation
• Traumatuc diaphragmatic injury

Physical exam
• Inspection of the airway, thorax, neck veins and breathing difficulty
• Rate and depth of breathing for anormalities
• Chest symmetry
• Breath sounds
• Open chest wounds, entrance or exit wounds
• Tracheal shift
• Distended neck veins
• Subcutaneous emphysema (crispy sound when palpating the chest)
• Paradoxical chest wall motion
• Assess for bruishing, petechiae, lacerations and burns
• VS and skin color
• Palpated for tenderness and crepitus and position of traschea

Diagnostic work-up
• CXR, CT
• CBC, clotting studies, type and cross-matching, electrolytes, 02 saturation, ABG
analysis
 • ECG

Medical management
• Goal of treatment are to evaluate the pt’s condition and to initiate aggressive
resuscitation
• O2 therapy, intubation and ventilatory effect
• Reestablish fluid volume and negative intrapleural fluid and blood

Sternal and rib fractures

• Most common in motor vehicle crashes with a direct blow to the sternum via the
steering wheel.
• Ribs 4-9 are commonly fractured because they are less protected
• Occurs in more than 60% of patient with blunt trauma
• Manifestations: anterior chest pain, tenderness, ecchymosis, crepitus, swelling, chest
wall deformity.
• Assessment and Diagnostic findings: crackling, grating sound
• On auscultation, CXR, rib films for specific area, ECG, pulse oximetry, ABG analysis.
• Medical management: relieve pain, avoiding excessive activity,
• Treating associated injuries. Surgical fixation is rarely necessary. Sedation, intercostal
nerve block, ice pack, chest binder, epidural anesthesia, PCA, non-opoid analgesia
• Pains abates in 5 to 7 days
• Rib fractures heals in 3 to 6 weeks

Flail chest
• Occurs because of several rib fracture resulting instability of the affected chest wall.
Chest wall is no longer able to provide bony structure.
• Manifestation: Atelectasis, hypoxemia, respiratory acidosis, hypotension,
inadequate tissue perfusion
• Treatment: supportive, provides ventilatory support, clearing secretions from the
lungs, controlling pain.
• Small segment clear airway through positioning, coughing, deep breathing and
suctioning, relieve pain
• Mild to moderate monitor fluid intake & appropriate replacement, pulmonary
physiotherapy
• Severe – ET intubation, mechanical ventilator
• Surgery – rare

Acute Respiratory Distress Syndrome

• A severe form of acute lung injury
• Also referred to as shock lung and white lung.
• A syndrome characterized by sudden and progressive pulmonary edema,
increasing bilateral lung infiltrates on CXR, refractory hypoxemia, and decreased
lung compliance.
 • A form of pulmonary insufficiency more commonly encountered in adults with no
previous lung disorders than in those with existing lung disease.
• There is cell damage, a decrease in lung surfactant production, and Atelectasis.
• Patient with ARDS usually requires mechanical ventilator.
• Major cause of death in ARDS is non pulmonary multi-system organ failure, often
with sepsis.

Risk factor (Direct pulmonary trauma)

• Pneumonia
• Lung contusion
• Fat or air embolism
• Aspiration
• Massive smoke inhalation
• Inhaled toxins
• Prolonged exposure to high concentration of oxygen

Risk factor
• Systemic Sepsis
• Shock
• Multisystem trauma
• DIC
• Pancreatitis
• Uremia
• Drug overdose
• Anaphylaxis
• Idiopathic
• Prolonged heart bypass
surgery
• Massive blood
transfusion
• PIH
• Increased ICP
• Radiation therapy

The hallmark of ARDS is a massive inflammatory response by the lungs that increases
permeability of the alveolar membrane, with resultant fluid movement into the interstitial
and alveolar spaces resulting to pulmonary edema which decreases lung compliance (stiff
lungs) and impairs oxygen transport.

Surfactants: gives surface stability and alveoli becomes collapse.

Refractory: not responsive to supplemental oxygen/ treatment.

Three phases of ARDS

1. Phase 1 (exudate) - 24 hours after the initial insult.

• Injury reduces normal blood flow to the lungs.

 • Platelets aggregates and release histamine, serotonin and bradykinin.
• The released substances inflame and damage the alveolar capillary membrane,
increasing capillary permeability. Fluids the shift to the interstitial space.

2. Phase 2 (proliferative) - begins about 7-10 days later.

• Capillary permeability increased and proteins and fluids leak out, Increasing
osmotic pressure and causing pulmonary edema.
• Decreased blood flow and fluids in the alveoli damage surfactant and impairs the
cell ability to produce more.
• The alveoli then collapse, impairing gas exchange resulting in severe refractory
hypoxemia.

3. Phase 3 (fibrotic) - occurs about 2-3 weeks.

• Pulmonary edema worsens and inflammation leads to fibrosis.

• Gas exchange is further impeded

Clinical manifestations
• Increased respiratory rate, dry non productive cough and Rapid onset of severe
dyspnea -12-48 hrs after initiating event – early sign
• Cyanosis,
• Hypocapnia (decreased retention of CO2)
• Hypoxemia that does not respond to supplemental oxygen – characteristic sign of
ARDS
• Restlessness, apprehension, mental sluggishness and motor dysfunction
• Kussmaul’s breathing
• Intercostal and suprastemal retractions
• Crackles
• Tachycardia

Complications
• Decreased urine output
• Hypotension
• Metabolic acidosis
• Multisystem organ dysfunction syndrome

Diagnostics
• CXR – diffuse alveolar infiltration bilaterally (white out)
• ABGs-decrease in PaO2 with increased levels of fraction of inspired 02.
• Initially respiratory alkalosis
• ARDS worsens – respiratory acidosis
• Metabolic acidosis
• Ventilation-perfusion imbalance – indicating a shunt.
• Pulmonary function test – decrease lung compliance, lung capacity
• Pulmonary artery catheterization – is the definitive method to distinguish between HF
and permeability pulmonary edema (ARDS)
 • Plasma brain natriuretic peptide (BNP) levels – helpful in distinguishing ARDS fro
hemodynamic pulmonary edema (HF).
• Transthoracic echocardiography – may be if the BNP is not conclusive
• Blood cultures
• Sputum analysis
• Toxicology

Medical management goals

• Respiratory support
• Maintenance of hemodynamic stability
• Treatment of the underlying cause
• Prevention of complications

Medical Management
• Support respiration and ventilation
• Mechanical ventilation
• Endotracheal intubation
• Maintain hemodynamic stability
• Monitor fluids and degree of pulmonary edema
• Treat underlying condition
• Antibiotics
• Monitor for complications
• Lung fibrosis, dysrhythmias, oxygen toxicity, renal failure, sepsis, disseminated
intravascular coagulation (DIC), GI bleeding
• Intubation and mechanical ventilation with PEEP (positive end-expiratory pressure)
to treat progressive hypoxemia
• Positioning: frequent position
changes
• Supportive medications
o Prophylactic antibiotics
o Diuretics
o Sedatives
o Bronchodilators
• Neuromuscular blocking
agents
o steroids
• Nutritional support
• General supportive care

Nursing intervention
• Promote optimal Ventillatory
status
• Perform ongoing assessment of the lungs with auscultation q 1-2 hours
• Elevate head and chest
 • Administer and monitor mechanical ventilation with PEEP
o Assist with chest physical therapy as ordered
• Encourage coughing and deep breathing every hour.
o Monitor ABGS, 02 saturation and report significant changes
• Promote rest
o Spacing of activities and treatments
o Maintain fluid and electrolyte balance
• Treat the cause
• Provide client and family education concerning plan of care.

Pulmonary Edema
• Is the abnormal accumulation of the fluid in the lung tissue, the alveolar sac or both.
This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe.
• Life threatening condition.
• In most cases, heart problems cause pulmonary edema.
• Pulmonary edema that develops suddenly (acute) is a medical emergency
requiring immediate care. Although pulmonary edema can sometimes prove fatal,
the outlook may be good when you receive prompt treatment for pulmonary
edema along with treatment for the underlying problem

Pathophysiology
• Pulmonary edema occurs when the alveoli fill up with excess fluid seeped out of the
blood vessels in the lung instead of air. This can cause problems with the exchange
of gas (oxygen and carbon dioxide), resulting in breathing difficulty and poor
oxygenation of blood. Sometimes, this can be referred to as “water in the lungs”
when describing the condition to patients.

Etiology
• Pulmonary edema can be caused by many different factors.
• It can be related to heart failure, called cardiogenic pulmonary edema, or related
to other causes, referred to as non-cardiogenic pulmonary edema.

Cardiogenic causes of pulmonary edema

• Cardiogenic causes of pulmonary edema results from high pressure in the blood
vessels of the lung due to poor heart function.
• Congestive heart failure due to poor heart pumping function (arising from various
causes such as arrhythmias and diseases or weakness of the heart muscle)
• Heart attacks or abnormal heart valves can lead to accumulation of more than the
usual amount of blood in the blood vessels of the lungs. This can, in turn, cause the
fluid from the blood vessels to be pushed out to the alveoli as the pressure builds up.
Non-cardiogenic pulmonary edema can be commonly caused by the following:
• Acute respiratory distress syndrome (ARDS), a potentially serious condition caused
by severe infections, trauma, lung injury, inhalation of toxins, lung infections, cocaine
smoking, or radiation to the lungs. In ARDS, the integrity of the alveoli become
compromised as a result of underlying inflammatory response, and this leads to
leaky alveoli that can fill up with fluid from the blood vessels.
• Kidney failure and inability to excrete fluid from the body can cause fluid build-up in
the blood vessels, resulting in pulmonary edema. In people with advanced kidney
disease, dialysis may be necessary to remove the excess body fluid.
• High altitude pulmonary edema, which can happen due to rapid ascent to high
altitudes of more than 10,000 feet.
• A rapidly expanding lung can sometimes cause re-expansion pulmonary edema.
This may happen in cases when the lung collapses (pneumothorax) or a large
amount of fluid around the lung (pleural effusion) is removed, resulting in rapid
expansion of the lung. This can result in pulmonary edema on the affected side only
(unilateral pulmonary edema).
• Rarely, an overdose on heroin or methadone can lead to pulmonary edema.
• Aspirin overdose or chronic high dose use of aspirin can lead to aspirin intoxication,
especially in the elderly, which may cause pulmonary edema.
• Other more rare causes of non-cardiogenic pulmonary edema may include
pulmonary embolism (blood clot which has traveled to the lungs), transfusion-
related acute lung injury (TRALI), some viral infections, or eclampsia in pregnant
women.

Clinical Manifestations
Signs and symptoms that come on suddenly may include:

• Extreme shortness of breath or difficulty breathing

o A feeling of suffocating or drowning
o Wheezing or gasping for breath

• Anxiety, restlessness or a sense of apprehension

o A cough that produces frothy sputum that may be tinged with blood
• Excessive sweating
• Pale skin
• Chest pain, if pulmonary edema is caused by heart disease
• A rapid, irregular heartbeat (palpitations)

Signs and symptoms that develop more gradually, often due to heart failure, include:

• Having more shortness of breath than normal when you’re physically active.
• Difficulty breathing with exertion, often when you’re lying flat as opposed to sitting
up.
• Awakening at night with a breathless feeling that may be relieved by sitting up.
• Rapid weight gain when pulmonary edema develops as a result of congestive heart
failure, a condition in which your heart pumps too little blood to meet your body’s
 needs. The weight gain is from accumulation of fluid in your body, especially in your
legs.
• Loss of appetite.
• Fatigue.

Signs and symptoms of pulmonary edema caused by high-altitude generally include:

• Headache
• Insomnia
• Fluid retention
• Cough
• Shortness of breath

Pulmonary edema that comes on suddenly (acute) is life- threatening. Get emergency
assistance if you have any of the following acute signs and symptoms:

• Trouble breathing or a feeling of suffocating (dyspnea)

• A bubbly, wheezing or gasping sound when you breathe
o Pink, frothy sputum when you cough
o Breathing difficulty along with profuse sweating
o A blue or gray tone to your skin
o A severe drop in blood pressure
o A sudden worsening of any of the symptoms associated with chronic pulmonary
edema or high-altitude pulmonary edema

Assessment And Diagnostic Findings

• Auscultation reveal crackles
• CXR reveals increased interstitial markings
• Tachycardia
• Pulse oximetry reveals decrease values worsening hypoxemia
• Hypocapnia

Complications
• Leg swelling (edema)
• Abdominal swelling (ascites)
• Buildup of fluid in the membranes that surround your lungs (pleural effusion)
• Congestion and swelling of the liver

Medical management
• Correct hypoxemia
• Reduce preload and afterload
• Support perfusion

Management of Pulmonary Edema

• Prevent
 • Early recognition: monitor lung sounds and for signs of decreased activity tolerance
and increased fluid retention
• Place patient upright and dangle legs
• Minimize exertion and stress
• Oxygen
• Medications
o Morphine
o Diuretic: furosemide
o Intubation and mechanical ventilation

Diagnosis, Outcomes, Interventions

Nursing diagnosis: Impaired Gas Exchange related to capillary membrane obstruction from
fluid

Outcomes: Demonstrate improved gas exchange

Interventions

• Assess vital signs and administer oxygen

• Position with legs dependent
• Medicate with morphine and nitroglycerin

Nursing diagnosis

• Excess Fluid Volume related to excess preload

Outcomes

• Evidence of fluid balance

Interventions

• Medicate with diuretic

• Monitor urine output, weight, vital signs