Lower Respiratory Infections [ Atelectasis , Pneumonia, T.B., Respiratory Failure etc.

1. LOWER RESPIRATORY
DISORDER
Dr. PALLAVI PATHANIA

2. LOWER RESPIRATORY DISORDER
• ATELECTASIS 519
• RESPIRATORY INFECTIONS 521
• Acute Tracheobronchitis 521
• Pneumonia 522
• Nursing Process: The Patient With Pneumonia 531
• Pulmonary Tuberculosis 534
• Nursing Process: The Patient With Tuberculosis 538
• Lung Abscess 540
• PLEURAL CONDITIONS 542
• Pleurisy 542
• Pleural Effusion 542
• Empyema 543
• PULMONARY EDEMA 544
• ACUTE RESPIRATORY FAILURE 545
• ACUTE RESPIRATORY DISTRESS SYNDROME 546
• PULMONARY HYPERTENSION 548
• PULMONARY HEART DISEASE (COR PULMONALE) 549
• PULMONARY EMBOLISM 550
• SARCOIDOSIS 554
• OCCUPATIONAL LUNG DISEASES: PNEUMOCONIOSES 554
• Silicosis 555
• Asbestosis 555
• Coal Workers’ Pneumoconiosis 555
• CHEST TUMORS 556
• Lung Cancer (Bronchogenic Carcinoma) 556
• Tumors of the Mediastinum 559
• CHEST TRAUMA 559
• Blunt Trauma 560
• Penetrating Trauma: Gunshot and Stab Wounds 562
• Pneumothorax 563
• Cardiac Tamponade 564
• Subcutaneous Emphysem

3. ATELECTASIS

4. • Atelectasis is defined as the
collapse or closure of the lung
resulting in reduced or absent
gas exchange. It may affect part
or all of one lung.
• It is the collapse or incomplete
expansion of lung or parts of
lung.
• Atelectasis is caused by
blockage of the air passages or
absent of gas exchange.

5. Causes
• Inhalation of irritants
• Chest wall disorders
• Atelectasis is caused by a blockage of the air passages (bronchus or
bronchioles) or by pressure on the outside of the lung.
• Another type of collapsed lung is called pneumothorax. It occurs
when air escapes from the lung. The air then fills the space outside
of the lung, between the lung and chest wall.
• Atelectasis is common after surgery or in patients who were in the
hospital.

6. Risk factors for developing atelectasis include:
• Anesthesia
• Foreign object in the airway (most common in children)
• Lung diseases
• Mucus that plugs the airway
• Pressure on the lung caused by a buildup of fluid
between the ribs and the lungs (called apleural effusion)
• Prolonged bed rest with few changes in position
• Shallow breathing (may be caused by painful breathing)
• Tumors that block an airway

8. Signs and symptoms
• cough, but not prominent;
• chest pain (not common);
• breathing difficulty (fast and shallow);
• low oxygen saturation;
• pleural effusion (transudate type);
• cyanosis (late sign);
• increased heart rate.
• increased temperature.

9. Exams and Tests
• To confirm if you have atelectasis, the following
tests will likely be done:
• Bronchoscopy
• Chest CT scan
• Chest x-ray
•

10. Treatment
• The goal of treatment is to re-expand the collapsed lung tissue. If fluid is putting pressure on the
lung, removing the fluid may allow the lung to expand.
• Oxygen therapy
• Clap (percussion) on the chest to loosen mucus plugs in the airway
• Chest physiotherpy
• Perform deep breathing exercises (with the help of incentive spirometry devices)
• Remove or relieve any blockage in the airways by bronchoscopy.
• Tilt the person so the head is lower than the chest (called postural drainage). This allows mucus to
drain more easily.
• Treat a tumor or other condition, if there is one
• Turn the person to lie on the healthy side, allowing the collapsed area of lung to re-expand
• Use aerosolized respiratory treatments (inhaled medications) to open the airway
• Use other devices that help increase positive pressure in the airways and clear fluids (positive
expiratory pressure [PEP] devices)

11. PNEUMONIA

12. INTRODUCTION
• Pneumonia is an inflammation and infection of the lungs.
• Inflammation is the immune system normal response to
injury or contaminants.
• Germs, bacteria and viruses are contaminants and can cause
inflammation.
• There are more than 50 kinds of pneumonia.
• Pneumonia can affect one or both lungs. when it affects both
lungs ,it sometimes called double pneumonia.

13. PNEUMONIA
• Pneumonia is an inflammation of the lung
parenchyma that is caused by a microbial agent.
• Pneumonia is an inflammatory process, involving
the terminal airways and alveoli of the lung, caused
by infectious agents. It is classified according to its
causative agent

14. CAUSES
• Bacteria
• Viruses
• Fungal infections
• Aspiration of food, fluids or vomitus
• Inhalation of toxins { chemicals, smoke, dust, gases}

15. RISK FACTORS
• Advanced age
• A history of smoking
• Upper respiratory infections
• Tracheal intubation
• Malnutrition
• Chronic lung diseases
• Renal diseases

16. CLASSIFICATION
• SITE OF INFECTION
– Lober Pneumonia { lobes one or more entire lobe may affected}
– Broncho Pneumonia
• ORIGION OF INFECTION
– Community acquired pneumonia
– Nosocomial pneumonia
– Aspiration pneumonia
– Immunocompromised pneumonia
• BASED ON ETIOLOGY
– Bacterial, viral, fungal, atypical

17. TYPES OF PNEUMONIA

18. Community acquired pneumonia refers to pneumonia you
get, or acquire from your community such as school ,
work.
Hospital acquired pneumonia or nosocomial pneumonia is
a serious pneumonia acquired at a hospital or a health
care facility it usually effects patients who are
• Mechanical ventilators.
• I cu unit.
• Or having weak immune system.

19. Bacterial Pneumonia: occurs when pneumonia-
causing bacteria masses and multiplies in the lungs.
The alveoli become inflamed and pus is produced,
which spreads around the lungs. The bacteria that
caused Bacterial Pneumonia are:
• streptococcus pneumonia,
• hemophilus influenza,
• and staphylococcus aureus.

20. Viral Pneumonia:
Viral Pneumonia is believed to be the cause of half
of all pneumonias. The viruses invade the lungs and
then multiply- causing inflammation
Aspiration pneumonia happens when any thing other
than air gets in to the lungs.

21. PATHOPHYSIOLOGY

22. • Due to causing factor{ when foreign matter such as viruses, bacteria, parasites, or
fungus enters the lungs and causes inflammation}
• Decrease resistance
• Decreases immune system
• Inflammation
• Decrease cell permiability
• Impaired cilliary function
• Increase mucus production
• Collection of fluid
• Bacterial growth
• Pneumonia

23. SIGN AND SYMPTOMS
• Fever
• Chills, sweating
• Cough, sputum production,
• Haemoptysis, Pleuritic chest pain,
• Wheezing, difficulty in breathing
• Nausea , vomiting
• Tactile fermitus increased

24. DIAGNOSIS
• Clinical history and Physical exam
• Blood & Urine Culture
• Chest x ray
• Sputum Analysis
• Bronchoscopy

25. MEDICAL MANAGEMENT
• CAP
– IV-beta lactum antibiotic plus
• NOSOCOMIAL PNEUMONIA
– Cephalosporin 2nd generation
• ASPIRATION PNEUMONIA
– Cephalosporin 2nd generation + metronidazole
• ANTIBIOTIC THERAPY
• OXYGEN THERAPY
• BRONCHODILATORS {SALBUTAMOL}
• SUCTIONING
• CHEST PHYSIOTHERAPY

26. VACCINES
•
Vaccines help prevent pneumococcal pneumonia but
cannot prevent all cases of infection. The following
vaccines are recommended to help protect you
against pneumonia.
• Haemophilus influenzae type b (Hib)
• Influenza vaccine -
• Pneumococcal pneumonia vaccine -.

27. PATIENT COUNSELLING
• LIFE STYLE MODIFICATIONS:
• Eat healthy.
• Sleep well.
• Avoid smoking.
• Exercise.
• Reduce stress.
• Avoid drinking alcohol excessively

29. PULMONARY TUBERCULOSIS

30. • TB is an infectious disease caused by bacteria
(Mycobacterium tuberculosis) that are usually spread
from person to person through the air. It usually
infects the lung but can occur at virtually any site in
the body. HIV-infected patients are especially at risk.
Drug-resistant TB is of particular concern in certain
parts of the United States

33. CAUSES
• MYCOBACTERIUM TUBERCULOSIS
• Mycobacterium bovis
• Mycobacterium africanum
• Mycobacterium conctti
• Mycobacterium microti

38. PATHOPHYSIOLOGY
• Due to etiological factor
• Decrease immune response
• Decrease resistance
• Inflammatory reactions occur
• Impaired cillary function
• Collection of fluid
• Macrophages
• Phagocytosis
• Necrosis
• Cavity formation
• Cheesy material
• WBC’s mycobacterum tuberculii
• Symptoms of Primary T.B.
• Many infection tuberculi
• Hypersensitivity
• Reactivation of T.B.
• Coughed out with foul smelling
• Weak immunity
• Secondary T.B.

46. PPD: PURIFIED PROTIEN DERIVATIVE

60. LUNG ABSCESS

61. • Lung abscess is a type of liquefactive necrosis of the lung tissue
and formation of cavities (more than 2 cm) containing necrotic
debris or fluid caused by microbial infection.
• This pus-filled cavity is often caused by aspiration, which may
occur during altered consciousness. Alcoholism is the most
common condition predisposing to lung abscesses.
• A lung abscess is a localized, pus-containing, necrotic lesion in the
lung characterized by cavity formation.
• Lung abscess is defined as necrosis of the pulmonary tissue and
formation of cavities containing necrotic debris or fluid caused by
microbial infection.

62. Causes
– Aspiration of foreign body into lung.
– Pulmonary embolus.
– Trauma.
– TB, necrotizing pneumonia.
– Bronchial obstruction (usually a tumor) causes obstruction to
bronchus, leading to infection distal to the growth.
– Necrotizing pneumonia
– Necrotizing tumors
– Anaerobic bacteria: Actinomyces, Bacteroides,
– Aerobicbacteria: Staphylococcus, Klebsiella, , Pseudomonas, Strepto
coccus, Mycobacteria
– Fungi: Candida,
– Septic emboli

63. Signs and symptoms
• Cough, fever, and malaise
• Headache, anaemia, weight loss, Dyspnea,
weakness.
• Pleuritic chest pain
• Production of mucopurulent sputum, usually foul-
smelling.
• Chest may be dull to percussion, decreased or
absent breath sounds, intermittent pleural friction
rub.

64. Diagnosis
• Chest X-ray and other imaging studies
• Laboratory studies
• bronchoscopy aspirates can also be cultured.

65. Management
• Administration of appropriate antimicrobial agent, usually by
I.V. route, until clinical condition improves; then oral
administration.
• Chest postural drainage to drain cavity.
• Bronchoscopy to drain abscess is controversial.
• Nutritional management is usually a high-calorie, high-
protein diet.
• Pulmonary physiotherapy
• postural drainage .
• Surgical procedures are required in selective patients for
drainage or pulmonary resection.

66. Nursing Diagnoses
• Ineffective Breathing Pattern related to presence of
suppurative lung disease
• Acute or Chronic Pain related to infection
• Imbalanced Nutrition: Less Than Body
Requirements related to catabolic state from
chronic infection

67. CANCER OF THE LUNG
(BRONCHOGENIC CANCER)

68. • Bronchogenic cancer refers to a malignant tumor of the lung
arising within the wall or epithelial lining of the bronchus.
• The lung is also a common site of metastasis by way of
venous circulation or lymphatic spread.
• Bronchogenic cancer is classified according to cell type:
– Epidermoid (squamous cell) most common
– Adenocarcinoma
– Small cell (oat cell) carcinoma
– Large cell (undifferentiated) carcinoma

69. Predisposing Factors
– Cigarette smoking amount, frequency, and duration of smoking have
positive relationship to cancer of the lung.
– Occupational exposure to arsenic, chromium, nickel, iron,
radioactive substances, isopropyl oil, coal tar products, petroleum oil
mists alone or in combination with tobacco smoke.
– Age younger than 50 years
– Radiation exposure

70. Warning signals of lung cancer
– Any change in respiratory pattern
– Persistent cough
– Sputum streaked with blood
– Hemoptysis
– Rust color or purulent sputum
– Fatigue
– Chest, shoulder, back or arm pain
– Recurring episodes of pleural effusion, pneumonia or
bronchitis.
– Unexplained dyspnea

71. Staging
– Refers to anatomic extent of tumor, lymph node involvement, and
metastatic spread.
– Staging done by:
• Tissue diagnosis
• Lymph node biopsy
• Mediastinoscopy

72. Clinical Manifestations
• Usually occur late and are related to size and location of tumor, extent of spread,
and involvement of other structures
– Cough, especially a new type or changing cough, results from bronchial
irritation.
– Dyspnea, wheezing (suggests partial bronchial obstruction).
– Chest pain (poorly localized and aching)
– Excessive sputum production, repeated upper respiratory infections
– Haemoptysis
– Malaise, fever, weight loss, fatigue, anorexia
– Paraneoplastic syndrome metabolic or neurologic disturbances related to the
secretion of substances by the neoplasm
– Symptoms of metastasis bone pain; abdominal discomfort, nausea and
vomiting from liver involvement; pancytopenia from bone marrow
involvement; headache from CNS metastasis
– Usual sites of metastasis ”lymph nodes, bones, liver

73. Diagnostic Evaluation
– Computed tomography (CT) scan and positron-emission tomography
(PET) scan are indicated because lung cancers may be partly or
completely hidden by other structures on chest X-ray.
– Cytologic examination of sputum/chest fluids for malignant cells.
– Fiber-optic bronchoscopy for observation of location and extent of
tumor; for biopsy.
– PET scan—sensitive in detecting small nodules and metastatic
lesions.
– Lymph node biopsy; mediastinoscopy to establish lymphatic spread;
to plan treatment.
– Pulmonary function tests (PFTs) combined with split-function
perfusion scan to determine if patient will have adequate pulmonary
reserve to withstand surgical procedure.

74. Management
• The treatment depends on the cell type, stage of disease, and the
physiologic status of the patient. It includes a multidisciplinary approach
that may be used separately or in combination, including:
– Surgical resection.
• Lobectomy
• pneumonectomy
– Radiation therapy.
– Chemotherapy.
– Immunotherapy.

75. Nursing Diagnoses
– Ineffective Breathing Pattern related to obstructive and restrictive
respiratory processes associated with lung cancer
– Imbalanced Nutrition: Less Than Body Requirements related to hyper
metabolic state, taste aversion, anorexia secondary to
radiotherapy/chemotherapy
– Acute or Chronic Pain related to tumor effects, invasion of adjacent
structures, toxicities associated with radiotherapy/chemotherapy
– Anxiety related to uncertain outcome and fear of recurrence

76. PULMONARY
EMBOLISM

77. • Pulmonary embolism (PE) is a blockage of
the lung's main artery or one of its branches by a
substance that has traveled from elsewhere in the
body through the bloodstream (embolism).
• PE results from deep vein thrombosis (commonly a
blood clot in a leg) that breaks off and migrates to
the lung, a process termed venous thrombo
embolism (VTE).

79. • Pulmonary embolism refers to the obstruction of one
or more pulmonary arteries by a thrombus (or
thrombi) originating usually in the deep veins of the
legs, the right side of the heart or, rarely, an upper
extremity, which becomes dislodged and is carried to
the pulmonary vasculature.
• Pulmonary infarction refers to necrosis of lung tissue
that can result from interference with blood supply.

80. Causes
• Predisposing factors include:
– Stasis, prolonged immobilization.
– Concurrent phlebitis.
– Previous heart (heart failure, myocardial infarction
[MI]) or lung disease.
– Injury to vessel wall.
– Coagulation disorders.
– Metabolic, endocrine, vascular, or collagen disorders.
– Malignancy.
– Advancing age, estrogen therapy.

81. Pathophysiology
– Obstruction, either partial or full, of pulmonary
arteries,
– which causes decrease or absent blood flow;
– there is ventilation but no perfusion
– Increased pulmonary vascular resistance
– Increased pulmonary artery pressure (PAP)
– Increased right ventricular workload to maintain
pulmonary blood flow
– Decreased cardiac output
– Decreased blood pressure
– Shock

82. Clinical Manifestations
• Dyspnea, Pleuritic pain, tachypnea,
• Chest pain
• Cyanosis, tachyarrhythmia's, syncope, circulatory collapse
• Pleural friction rub
• cough and hemoptysis (coughing up blood).
• More severe cases can include signs such as cyanosis (blue
discoloration, usually of the lips and fingers),
• collapse, and circulatory instability because of decreased
blood flow through the lungs and into the left side of the
heart.

83. Diagnostic Evaluation
• ABG levels : decreased Pao2 is usually found, due to
perfusion abnormality of the lung.
• Chest X-ray
• Pulmonary angiogram

84. Management
• Oxygen is administered to relieve hypoxemia, respiratory distress, and cyanosis.
• An infusion is started to open an I.V. route for drugs and fluids.
• Vasopressors, inotropic agents such as dopamine (Intropin), and antidysrhythmic
agents may be indicated to support circulation if the patient is unstable.
• ECG is monitored continuously for right-sided heart failure, which may have a
rapid onset.
• Small doses of I.V. morphine are given to relieve anxiety, alleviate chest
discomfort (which improves ventilation), and ease adaptation to mechanical
ventilator, if this is necessary.
• Pulmonary angiography, hemodynamic measurements, ABG analysis, and other
studies are carried out.

85. • Oral anticoagulation with warfarin (Coumadin) is
usually used for follow-up anticoagulant therapy
after heparin therapy has been established
• Thrombolytic agents, such as streptokinase
(Streptase), may be used in patients with massive
pulmonary embolism.

86. Surgery
• Used inferior vena cava filter.
• If anticoagulant therapy is contraindicated (e.g.
shortly after a major operation), an inferior vena
cava filter may be implanted to prevent new emboli
from entering the pulmonary artery and combining
with an existing blockage. It should be removed as
soon as it becomes safe to start using
anticoagulation.
• (pulmonary thrombectomy).

87. Nursing Diagnoses
• Ineffective Breathing Pattern related to acute increase in
alveolar dead airspace and possible changes in lung
mechanics from embolism
• Ineffective Tissue Perfusion (Pulmonary) related to
decreased blood circulation
• Acute Pain (pleuritic) related to congestion, possible pleural
effusion, possible lung infarction
• Anxiety related to dyspnea, pain, and seriousness of
condition
• Risk for Injury related to altered hemodynamic factors and
anticoagulant therapy

88. RESPIRATORY
FAILURE

89. Respiratory failure
• It is inadequate gas exchange
by respiratory system.
• It is a broad, non-specific
clinical diagnosis indicating
that the respiratory system is
unable to supply the oxygen
necessary to metabolism or
can not eliminate sufficient
carbon dioxide.

90. Classification
Acute respiratory failure
• It is defined as a partial pressure of arterial oxygen {PaO2} of
55 mmHg or less on room air or PaCo2 of 55 mmHg or more.
• It may be classified as :
– Hypoxemic respiratory failure
– Ventilatory failure

91. • Hypoxemic respiratory failure / low blood oxygen level :
• It may be caused by diffuse problem such as pulmonary edema,
ARDS, or localized problem such as pneumonia, bleeding from chest,
or lung tumor.
• Ventilatory or hypercapnic respiratory failure :
• When the client is unable to support adequate gas exchange that can
result from CNS depression, inadequate neuromuscular ability to
sustain breathing or respiratory system overload.

92. • HYPOXEMIC RESPIRATORY FAILURE
–Pulmonary edema

93. PULMONARY
EDEMA

95. Pulmonary Edema
• Pulmonary edema is an abnormal buildup of fluid in the
lungs. This buildup of fluid leads to shortness of breath.
Pulmonary edema or oedema is fluid accumulation in
the air spaces and parenchyma of the lungs. It leads to
impaired gas exchange and may cause respiratory
failure.
• Pulmonary edema is defined as abnormal
accumulation of fluid in the lung tissue and/or alveolar
space. It is a severe, life threatening condition

96. Causes
• Bacterial infections
• Hypervolemia Or A Sudden Increase In The Intravascular
Pressure In The Lung.
• Pneumothorax
• Pleural Effusion
• Inhalation of hot or toxic gases
• Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)
• Aspiration, e.g., gastric fluid
• thoracocentesis,
• removal of endobronchial obstruction
• Reperfusion injury, or lung transplantation
• Multiple blood transfusions
• Pulmonary Hypertension
• Other respiratory disease condition

97. • Pathophysiology
– Due to etiological factor
– Result Of Increased Microvascular Pressure From Abnormal
Cardiac Function.
– The Backup Of Blood Into The Pulmonary Vasculature Resulting
From Inadequate Left Ventricular Function
– An Increased Microvascular Pressure,
– Fluid Begins To Leak Into The Interstitial Space And The Alveoli.
– Impaired gas exchange
– Decrease PaO2 & increased Paco2
– Ischemic lung injury
– Reduce air flow
– Brain stem infarction
– Neuro musculer diseases
– Muscle weaknes
– Decreased Co2 excretion
– Increased PaCo2

98. Clinical Manifestations
Symptoms of pulmonary edema may include:
• Dyspnea
• Coughing up blood or bloody froth
• Chest pain
• Excessive sweating
• Anxiety
• Pale skin
• Pink frothy sputum (which may be coughed up)
• Anxiety or restlessness
• Decrease in level of alertness (consciousness)
• Leg or abdominal swelling

99. Diagnostic investigation
– History collection
– Physical examination
– Blood chemistries
– Blood oxygen levels(oximetry or arterial blood gases)
– Chest x-ray
– Complete blood count (CBC)
– Echocardiogram (ultrasound of the heart) to see if
there are problems with the heart muscle
– Electrocardiogram (ECG) to look for signs of a heart
attack or problems with the heart rhythm

100. Treatment
• Pulmonary edema is almost always treated in the emergency room or hospital. You may need to
be in an intensive care unit (ICU).
• Oxygen is given through a face mask or tiny plastic tubes are placed in the nose.
• A breathing tube may be placed into the windpipe (trachea) so you can be connected to a
breathing machine (ventilator) if you cannot breathe well on your own.
• The cause of edema should be identified and treated quickly. For example, if a heart attack has
caused the condition, it must be treated right away.
• IABP intra aortic balloon pump
• Diuretics that remove excess fluid from the body
• Medicines that strengthen the heart muscle, control the heartbeat, or relieve pressure on the
heart

101. ACUTE VENTILATORY FAILURE

102. • Ventilatory failure is rise in PaCo2 [hypercapnia]that occurs when
the respiratory load can no longer be supported by the strength or
activity of the system.
Causes
– Drug overdose
– Stroke
– Tumors
– Tetanus
– Pneumothorax
– Pneumonia
– Chronic obstructive pulmonary disease (COPD) (chronic
bronchitis, emphysema).
– Severe asthma.
– Cystic fibrosis.

103. Clinical Manifestations
• Hypoxemia restlessness, agitation, dyspnea,
disorientation, confusion, delirium, loss of
consciousness.
• Hypercapnia headache, dizziness, confusion.
• Tachypnea initially; then when no longer able to
compensate, bradypnea
• Accessory muscle use
• Pulsus paradoxus

104. Diagnostic Evaluation
– ABG analysis show changes in Pao2, Paco2, and pH
from patient's normal; or Pao2 less than 50 mm Hg,
Paco2 greater than 50 mm Hg, pH less than 7.35.
– Pulse oxymetery decreasing Sao2.
– End tidal CO2 monitoring elevated.
– Complete blood count, serum electrolytes, chest X-
ray, urinalysis, electrocardiogram (ECG), blood and
sputum cultures to determine underlying cause and
patient's condition

105. Management
– Oxygen therapy to correct the hypoxemia.
– Chest physical therapy and hydration to mobilize secretions.
– Bronchodilators and possibly corticosteroids to reduce bronchospasm and
inflammation.
– Diuretics for pulmonary congestion.
– Mechanical ventilation as indicated. Non-invasive positive-pressure
ventilation using a face mask may be a successful option for short-term
support of ventilation.
– Provide E.T.
• Oral- short term
• Nasal- long term

106. ACUTE
RESPIRATORY
DISTRESS
SYNDROME

107. Previously known as RDS
• RESPIRATORY DISTRESS SYNDROME OR SHOCK LUNG
• It is a sudden progressive form of respiratory failure,
characterized by severe Dyspnea, hypoxia & diffuse
bilateral infiltration.
• ARDS is a disease of lung parenchyma that leads to
impaired gas exchange.

108. Causes
• Direct pulmonary trauma
– Viral infection
– Bacterial infection
– Fungal infection
– Pneumonia
– Fat emboli
– Inhaled toxins
• Direct pulmonary trauma
– Sepsis shock
– Drugs over dose
– Radiation therapy

109. Phases
• Phase -1 exudative
– It is approximately 24 hours after the initial insult &
consist of damage to the capillary endothelium & leakage
of fluid into pulmonary interstistium which increases
pulmonary artery pressure.
– Exudates move or pass slowly as it through a small
opening or passages.
– Inflammatory responses of parenchyma damage

110. • Phase -2 proliferative
– It begins about 7-10 days. In this phase growing and
increasing in number rapidly.
– Alveolar cell r ultimately damaged.
– Hypoxemia is present & decreased surfactant production
which leads to V/Q mismatch.

111. • Phase -3 fibrotic
– It occurs in about 2-3 weeks. There is deposition of fibrin
into the lungs than cause lung compliance & worsening
hypoxemia, V/Q mismatch.

112. Pathophysiology
– Lung injury
– Release of vasoactive substance
– Increased permeability of alveolar membrane
– Fluid and proteins move into the alveoli
– Altered V/Q
– Damage alveolar epithelium
– Decrease surfactant production
– Atelectasis
– Regeneration of alveolar membrane with thick epithelial cell
– Scarring & loss of lungs function

113. Clinical manifestation
• Hypoxemia
• Dyspnea
• Thick frothy sputum
• Atelectasis
• Tachypnea
• Cough
• Crackle sound hear
on auscultation

114. Diagnostic investigations
– The hallmark sign for ARDS is a shunt; hypoxemia remains
despite increasing oxygen therapy.
– Decreased lung compliance; increasing pressure required
to ventilate patient on mechanical ventilation.
– Chest X-ray exhibits bilateral infiltrates.
– Pulmonary artery catheter readings: pulmonary artery
wedge pressure >18 mm Hg

115. Management
– The underlying cause for ARDS must be determined so appropriate treatment
can be initiated.
– Ventilator support with PEEP will be instituted. PEEP keeps the alveoli open,
thereby improving gas exchange.
– Fluid management must be maintained
– Pulmonary artery catheter monitoring and inotropic medication can be
helpful.
– Medications are aimed at treating the underlying cause. Corticosteroids are
used infrequently due to the controversy regarding benefits of usage.
–
Adequate nutrition should be initiated early and maintained.

116. – Provide nitric oxide to dilate the capillary bed of lungs & help in
vasodilatation.
– Oxygen therapy
– Antibiotic therapy
– Steroids

117. CHEST
TRAUMA

118. • IT is injury of the thoracic cage & can restrict the
heart ability to pump blood or the lungs ability to
exchange air & oxygenated blood.
• Major danger associated with chest injuries r:
– Interstitial bleeding
– Punctured organs

119. CHEST INJURIES
BLUNT INJURIES PENETRATING INJURIES

120. • BLUNT INJURIES: r most commonly deceleration injuries
associated with motor vehicle, crashes. It may result from falls or
blows of the chest.
• PENETRATING INJURIES: it is an open chest wound
permitting atmospheric air into the pleural space & disrupting the
normal vacuum ventilation mechanism.

121. BLUNT
• RIB FRACTURE
• FRACTURED STERNUM
• FLAIL CHEST
PENETRATING
• PNEUMOTHORAX
• TRAUMATIC
PNEUMOTHORAX
• TENSION PNEUMPTHORAX
• HEMOTHORAX

122. Rib Fracture
– Most common chest injury.
– May interfere with ventilation and may lacerate
underlying lung.
– Causes pain at fracture site; painful, shallow respirations;
localized tenderness and crepitus (crackling) over fracture
site

123. • Fracture in ribs associated with any kind of blunt injury. The 5 -9th r
most commonly affected.
• It is associated with blunt injury such as a fall, etc.
S/S
– Localized pain & tenderness over the fracture area on
inspiration & expiration.
– Dislocation, protruding bone
– Shallow respiration
– Click sound sensation on inspiration
– Ineffective cough
– Dyspnea
– Weak lungs
– Abnormal V/Q
– Infection

124. Management
• Rapid mobilization to hospital.
• Pain control
• Give analgesics (usually nonopioid) to assist in effective coughing and deep breathing.
• Encourage deep breathing with strong inspiration; give local support to injured area by splinting
with hands.
• Assist with intercostal nerve block to relieve pain so coughing and deep breathing may be
accomplished. An intercostal nerve block is the injection of a local anesthetic into the area around
the intercostal nerves to relieve pain temporarily after rib fractures, chest wall injury, or
thoracotomy.
• For multiple rib fractures, epidural anesthesia may be used.
• Pulmonary physiotherapy

125. FRACTURED STERNUM
• IT Is usually result from blunt deceleration injuries such
as impact from a steering wheel.
C/M:
-- sharp, stabbing pain, swelling & discoloration over
the fractured site & creptius
Management
-Analgesics
-Intercostals nerve blocks
-Surgical fixation

127. Flail Chest{ portion of the rib cage is seprated from the rest of chest}
– Loss of stability of chest wall as a result of multiple rib fractures, or
combined rib and sternum fractures.
– When this occurs, one portion of the chest has lost its bony connection to
the rest of the rib cage.
– During respiration, the detached part of the chest will be pulled in on
inspiration and blown out on expiration (paradoxical movement)
– Normal mechanics of breathing are impaired to a degree that seriously
jeopardizes ventilation, causing Dyspnea and cyanosis,creptius, hypoxia,
– Hypercapnia, abnormalV/Q.
– Generally associated with other serious chest injuries; lung contusion, lung
laceration, diffuse alveolar damage

129. Management
– Stabilize the flail portion of the chest with hands; apply a pressure
dressing and turn the patient on injured side, or place 10-lb sandbag at
site of flail.
– Thoracic epidural analgesia may be used for some patients to relieve
pain and improve ventilation.
– If respiratory failure is present, prepare for immediate ET intubation and
mechanical ventilation—treats underlying pulmonary contusion and
serves to stabilize the thoracic cage for healing of fractures, improves
alveolar ventilation, and restores thoracic cage stability and intrathoracic
volume by decreasing work of breathing.
– Prepare for operative stabilization of chest wall in select patients.

130. PNEUMOTHORAX

131. • It is the presence of air in the pleural space
that prohibits complete lung expansion.
• It is an abnormal collection of air or gas in the
pleural space that separate the lung from the
chest wall.
• It is often called collapsed
lung.

132. PNEUMOTHORAX CLASSIFICATION
• A SPONTANEOUS PNEUMOTHORAX: it may be idiopathic. A spontaneous
Pneumothorax onset of air in the pleural space with deflation of the
affected lung in the absence of trauma.
• OPEN PNEUMOTHORAX: (sucking wound of chest) implies an opening in
the chest wall large enough to allow air to pass freely in and out of
thoracic cavity with each attempted respiration.
• TRAUMATIC PNEUMOTHORAX : is a collapse lung resulting from either
blunt force trauma to the chest wall or the creation of an open sucking
chest wound caused by motor-vehicle accidents etc.
• TENSION PNEUMOTHORAX: build up of air under pressure in the pleural
space resulting in interference with filling of both the heart and lungs

133. CAUSES
Spontaneous Pneumothorax
• Bleb or bulla
• Emphysema
• AIDs
• T.B.
• Cocaine use
Traumatic Pneumothorax
• Chest surgery
• Thoracentsis
• Gun shot wound
• Knife wound
• Motor vehicle accidents
• Fractured Rib

134. Clinical manifestation
– Hyper resonance; diminished breath sounds.
– Reduced mobility of affected half of thorax.
– Tracheal deviation away from affected side in tension Pneumothorax
– Clinical picture of open or tension Pneumothorax is one of air hunger,
agitation, hypotension, and cyanosis
– Mild to moderate Dyspnea and chest discomfort may be present with
spontaneous Pneumothorax
– Decreased tactile fermitus

135. Diagnostic Evaluation
• Chest X-ray confirms presence of air in pleural
space.

136. Management
Spontaneous Pneumothorax
• Treatment is generally non operative if Pneumothorax is not too
extensive.
– Observe and allow for spontaneous resolution for less than 50%
Pneumothorax in otherwise healthy person.
– Needle aspiration or chest tube drainage may be necessary to
achieve re expansion of collapsed lung if greater than 50%
Pneumothorax.
• Surgical intervention by pleurodesis or thoracotomy with resection
of apical blebs is advised for patients with recurrent spontaneous
Pneumothorax.

139. Tension Pneumothorax
– Immediate decompression to prevent cardiovascular collapse by
Thoracentsis or chest tube insertion to let air escape.
– Chest tube drainage with underwater-seal suction to allow for full
lung expansion and healing

141. Open Pneumothorax
– Close the chest wound immediately to restore
adequate ventilation and respiration.
• Patient is instructed to inhale and exhale gently against a
closed glottis (Valsalva maneuver) as a pressure dressing
(petroleum gauze secured with elastic adhesive) is applied.
This maneuver helps to expand collapsed lung.
– Chest tube is inserted and water-seal drainage set up
to permit evacuation of fluid/air and produce
reexpansion of the lung.
– Surgical intervention may be necessary to repair
trauma.

142. Hemothorax
– Blood in pleural space as a result of penetrating or blunt chest trauma.
– Accompanies a high percentage of chest injuries.
– Can result in hidden blood loss
– Patient may be asymptomatic, dyspneic, apprehensive, or in shock

143. HEMOTHORAX
• It may be present in client with chest injuries.
• A small amount of blood more than 300 ml in the pleural
space may cause no clinical manifestation and may require
no intervention with the blood being reabsorbed
spontaneously.
• Severe Hemothorax {1400-2500ml} may be life threatening
becoz of resultant hypovolemia & tension.

144. Clinical manifestation
– Respiratory distress
– Shock
– Dullness upon percussion of the affected side.

145. Management
– Assist with Thoracentsis to aspirate blood from pleural space, if
being done before a chest tube insertion.( 7th & 8th intercostal
space)
– Assist with chest tube insertion and set up drainage system for
complete and continuous removal of blood and air.
• Auscultate lungs and monitor for relief of dyspnea.
• Monitor amount of blood loss in drainage.
– Replace volume
with I.V. fluids or blood products.

148. PULMONARY HEART DISEASE
/COR PULMONALE

149. COR PULMONALE
• Pulmonary heart disease (cor
pulmonale) is an alteration in
the structure or function of
the right ventricle resulting
from disease of lung
structure or function or its
vasculature (except when this
alteration results from
disease of the left side of the
heart or from congenital
heart disease). It is heart
disease caused by lung
disease.

150. Pathophysiology and Etiology
– Condition that deprives lungs of oxygen: hypoxemia,
hypercapnia, acidosis, circulatory complications,
pulmonary hypertension, right heart enlargement, right-
sided heart failure.
– Etiology includes:
• Pulmonary vascular disease.
• Pulmonary embolism.
• COPD.

151. Clinical Manifestations
– Increasing dyspnea and fatigue; progressive dyspnea
(orthopnoea, paroxysmal nocturnal dyspnea), chronic cough.
– Distended jugular veins, peripheral edema, hepatomegaly.
– Bibasilar crackles and split second heart sound on
(auscultation of chest , lung sound on the base of right and left
lung)
– Manifestations of CO2 narcosis headache, confusion,
somnolence{ strong desire for sleep bcoz of drowsiness), coma

152. Diagnostic Evaluation
– ABG levels decreased Pao2 and pH, increased
Paco2.
– PFTs may show airway obstruction.
– ECG changes are consistent with right ventricular
hypertrophy.
– Chest X-ray shows right heart enlargement.
– Echocardiogram shows right heart enlargement.

153. ABG Analysis

154. Management
• Goal: treatment of underlying lung disease and management of heart
disease.
– Long-term, low-flow oxygen to improve oxygen delivery to
peripheral tissues, thus decreasing cardiac work and lessening
sympathetic vasoconstriction. Liter flow individualized during
activities, rest, and sleep.
– Diuretics to lower PAP by reducing total blood volume and excess
fluid in lungs.
– Pulmonary vasodilators such as nitroprusside (Nitropress);
hydralazine (Apresoline); calcium channel blockers to dilate
pulmonary vascular bed and reduce pulmonary vascular resistance;
use is controversial.
– Bronchodilators to improve lung function.
– Mechanical ventilation, if patient in respiratory failure.
– Sodium restriction to reduce edema.