RESPIRATORY SYSTEM

ANATO
MY
AND
PHYSIO
LOGY
 UPPER RESPIRATORY
Nose

Paranasal Sinuses

Pharynx

Larynx
 LOWER RESPIRATORY

LUNGS

PLEURA

MEDIASTINUM
Function of Respiratory
System
LUNG VOLUME AND
CAPACITIES
 LUNG VOLUME NORMAL VALUE SIGNIFICANCE

Tidal Volume The tidal volume may

(TV or VT) 500ml or 5-10ml/kg not vary, even with
severe disease.
Inspiratory Reserve
volume(IRV) 3000ml
Expiratory reserve Decreased with
volume(ERV) 1100ml restrictive condition
such as obesity
,ascites, and preg.
Residual 1200ml It may increased with
obstructive disease.
Volume(RV)
 Lung Capacity Normal Value Significance

Vital Capacity 4600 ml if ↓ may be found

neuromuscular dse.
Generalized fatigue,
atelectasis,pulmonary
edema , COPD, obesity.
Inspiratory Capacity 3500 ml If ↓ may indicate restrictive
dse and also may ↓ in
obesity

Functional residual 2300 ml It may ↑ COPD and ↓

Capacity ARDS and obesity.

Total Lung Capacity 5800 ml If ↓ with restrictive

( atelectasis, pneumonia,
and ↑ in COPD)
GAS
EXCHANGE
PULMONARY DIFFUSION
 P Pressure
PO
PARTIAL PRESSURE ABBREVIATIONS
Partial pressure of oxygen
2

PCO2 Partial pressure of carbon dioxide

PAO2 Partial pressure alveolar Oxygen
PACO2 Partial pressure of carbon dioxide
PaO2 Partial pressure of the arterial oxygen
PaCO2 Partial pressure of the arterial carbon dioxide
PvO2 Partial pressure of venous Oxygen
PvCO2 Partial pressure of venous Carbon dioxide

P50 Partial pressure of oxygen when the hemoglobin is 50 %

saturated.
DISTURBANCES
IN
OXYGENATION
PUL
MO
NAR
Y
EDE
MA
PUL
MON
Cause:
ARY
EDE 1. abnormal cardiac function
MA
2. hypervolemia
a. Post-pneumonectomy
b. Re-expansion
pulmonary edema
PATHOPHYSIOLOGY
Inadequate Backup of ↑ microvascular
left blood into pressure from
ventricular pulmonary abnormal cardiac
function vasculature function

PULMONAR Fluid leaks into the

intertitial space and
Y EDEMA alveoli
MANIFESTATIO
N
Dyspnea Anxiety/agitated

Air hunger Foamy, frothy,

blood-tinged
Central cyanosis secretion/sputum

Tachycardia.
ASSESSMENT AND
DIAGNOSTIC FINDINGS
(+) crackles in the lung bases.

CXR: Increase in interstitial

makings.

ABG: Increasing Hypoxemia

MEDICAL
MANAGEMENT
Cardiac origin-vasodilators inotropic

Fluid overload-diuretics fluid restrictions

O2 inhalation

Morphine- reduces anxiety and controls pain.

NURSING INTERVENTIONS
Assist O2 administration/intubation
and mechanical
ventilation if respiratory failure occurs.
Administer meds. as order(morphine,
vasodilators, inotropics)
PUL
MON
ARY
EDE
MA
COPD
CHRONIC
OBSTRUC
TIVE
PULMONA
RY
DISEASE
PATHOPHYSIOLOGY
↑numbers of the
goblet cells and
enlarged PROXIMAL Trigger the
submucosal compensatory
PERIPHERAL mechanism of the body
glands AIRWAYS

INFLAMMATORY LUNG
RESPONSE OF PARENCHYMA Narrowing the
THE LUNGS
airways
PULMONARY
VASCULATURE
Loss of alveolar
attachments
Thickening of the ↓in elastic recoil
PULMONARY lining of the vessel
HYPERTENSION Hypertrophy of
smooth muscle
 a lung disease characterized by
chronic obstruction of lung
airflow that interferes with
CHRONI normal breathing and is not
C fully reversible
OBSTRU
CTIVE
PULMON
ARY
DISEASE
 Bronchial asthma

Chronic Bronchitis
CHRONI
C
OBSTRU
Bronchoectasis
CTIVE
PULMON
ARY Pulmonary emphysema
DISEASE
BRO
NCHI
AL A reversible inflammatory
AST
HMA disorder of lung tissue due to
hypersensitivity to allergens
narrowing smaller airways.
ONCHIALPREDISPOSING FACTORS
THMA
Extrinsic (atopic/allergic)
Pollen, dust ,furs, fumes, gases,
smoke, dander ,lint.
Intrinsic(non atopic/ nonallergic)
Hereditary
Drugs(ASA, Pen, PhenylButazone,
Beta blockers)
BRONC Foods: seafoods, eggs, chicken,
HIAL
chocolate,milks and its products.
ASTHM
A Food additives- nitrates(cause CA.)
Sudden change in T, air pressure
and Humidity
Extreme emotion
Physical stress
CLINICAL
MANIFESTATION
Non-productive cough
Dyspnea
Wheezing on expiration
Slight cyanosis
Mild restlessness and
apprehension
Tachycardia and palpitation
Diaphoresis
ASSESSMENT AND
DIAGNOSTIC FINDINGS
In ASSESSMENT:
(+) Episodic symptoms of airflow
obstruction
(+) Family history and environmental factors
Variety of occupation related chemicals and
compounds
Comorbid conditions like GERD,drug-
induced asthma etc.
ASSESSMENT AND
DIAGNOSTIC FINDINGS
In DIAGNOSTIC:
ABG-↓Po2
PFT-↓ Vital lung capacity (Maximum volume
of air that can be exhale with the deepest
breath possible
Pulse oximetry
Blood test
Sputum test
NURSING MANAGEMENT
Calm approach to the family
Assess the patient’s respiratory status
Monitor VS
Administer medication as ordered:
- Bronchodilators
- Anti-histamine
- Mucolytics/expectorant
Administer O2 as ordered
BRONCHOECTASIS

chronic, irreversible dilation of

the bronchi and bronchioles.

It is considered a disease
process separate from COPD
PREDISPOSING FACTORS

Recurrent URTI and LRTI

Congenital anomalies(LTB)

Lung Tumors
CLINICAL
MANIFESTATION
Chronic cough
Production of purulent sputum
Dyspnea

Clubbing of the finger

Hemoptysis
ASSESSMENT AND DIAGNOSTIC
FINDINGS
In ASSESSMENT:
-determine the prolonged history of
productive cough
In DIAGNOSTIC:
ABG-↓Po2
CT scan – reveals bronchial dilation
Bronchoscopy
NURSING MANAGEMENT
Helping patients clear pulmonary
secretions

Educate the patient and the family to

perform drainage

Inform the pt and the family to avoid

exposure to people with URTI
NURSING MANAGEMENT

Pre-operative:
-Maintain on NPO
-Informed consent
-Monitor VS
NURSING MANAGEMENT
Post-operative
- Feed when gag reflex return
- Avoid talking, coughing, smoking
- Monitor for S/ of gross/frank
bleeding
- Edema & WOF laryngospasm
 Inflammation of the bronchi

The presence of cough and

sputum production for
CHR
ONI atleast 3 months in each of 2
C consecutive years.
BRO
NCH
ITIS
PATHOPHYSIOLOGY
hyperplasia of
Inflammation of goblet mucus- ↑mucus
Bronchi producing production
cells

CHRONIC
BRONCHITIS

More susceptible to Altered function of the Narrowing of

respiratory infection alveolar macrophages smaller airways
PREDISPOSING
FACTORS

Excessive,chronic
smoking

Air pollution.
CLINICAL
MANIFESTATION
Productive cough
Dyspnea at exertion
Prolonged expiratory grunt
Scattered rales,rhonchi
Anorexia & general body malaise.
CLINICAL MANIFESTATION
Cyanosis-blue Bloaters
Feeling of breathlessness
Pulmonary HTN leading to
peripheral adema and Cor
pulmonate(most feared
complication.)
 A pathologic term that describes
an abnormal distention of the
airspaces beyond the terminal
PUL bronchioles and destruction of
MO the walls of the alveoli
NAR
Y
EMP
HYS
EMA
PREDISPOSING FACTORS

Excessive,chronic smoking
Allergy
Air pollution
Hereditary-Deficiency of Alpha-1
antitrypsin→elastase/elastin→
alveolar recoil.
Elderly- high risk group.
PATHOPHYSIOLOGY

Inelasticity of Air
alveolar wall Maldistribution
trapping of gases

PULMONARY
EMPHYSEMA
↑A:P diameter over distension of
(barrel-chest) thoracic cavity
 TYPES OF
EMPHYSEMA
Centrilobular/Panlobular
• Blue bloaters
• PCO2↑,PO2↓, respiratory
alkalosis with hypoxemia
TYPES OF EMPHYSEMA

Centriacinar/Panacinar
• Pink puffers
• PCO2↓, PO2↑,
respiratory alkalosis
with hypoxemia.
CLINICAL MANIFESTATION
Productive cough

Dyspnea at rest

Anorexia

On lung percussion-resinance to
hyperresonance.
CLINICAL MANIFESTATION
(+) alar flaring
Rales,rhonchi
↓Breath sounds
Barrel chest-Pathognomonic
Sign.
(+)Pursed-lip dreathing.
NURSING
MANAGEMENT
• CBR
• Administration of medication as
ordered:
-Bronchodilator
-Corticosteriod
- Antibiotic
- Mucolitics/expectorants.
NURSING MANAGEMENT
• Low flow: fixed concentration of O2
inhalation as ordered not to remove the
hypoxic Drive.
• Nebulize and suction secretions prn.
• Discharge health teaching:
-Stop smoking
-Regular adherence to the meds.
Restrictive
Lung
Disorder
 category of extrapulmonary, pleural,
or parenchymal respiratory disease
that restrict lung expansion,
resulting in a decreased lung
volume, an increased work of
breathing, and inadequate
ventilation and/or oxygenation
Restrictiv
e Lung
Disorder
Restrictiv
e
Lung Pneumonia
Disorder

Pleural effusion

Tubercolosis
P • An Inflammation of the lung
N Parenchyma caused by various
E microorganism.
U
M • PNEUMONITIS is more general term
O
that describes an inflammatory process
N
in the lung tissue
I
A
 PNEUMONIA

COMMUNITY NOSOCOMIA IMMUNOCOMPROMISE ASPIRATIO

ACQUIRED L D HOST N
PNEUMONIA PNEUMONI
PNEUMONIA A
• Enterobacter • Pneumocysti Anaerobic
• S.Pneumonia species
s pneumonia bacteria(S.Pn
• E.Coli
e • H.Influenzae • Fungal eumonia,
• H.Influenzae • Klebsiella species pneumonias H.Influenzae,
• Legionella • Proteus • Mycobacteri
• Serratia marcescens S. Aureus.
• Pseudomonas um
• P.aeruginosa
tuberculli
Aeruginosa • MRSA
SEVE
RE
PNE
UMO
NIA
PATHOPHYSIOLOGY
Will cause
acute and
Altered normal
flora /aspiration
chronic
of flora in the diseases
oropharynx

PNEUMONI
Impair host
A defenses
 PREDISPOSING FACTORS
Travel or exposure to certain
environment.
Air pollution
Excessive smoking
Residence in a long term care
facility.
Immunocompromised state
CLINICAL
MANIFESTATION
Sudden onset of chills,fever
Productive cough
Rapidly rising fever
Anorexia
Cyanosis
Pleuritic chest pain
Abdominal distention
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Physical Examination
Chest X-ray
Blood Culture
Sputum examination
CBC
ABG analysis
NURSING MANAGEMENT
CBR
Administer medicines
as ordered
Educate the patient on
healthy lifestyle
 A collection of fluid in the pleural
space
PLE It usually secondary to other
URA diseases
L The most common malignancy
EFF associated with Pleural Effusion is
USIO BRONCHOGENIC
N CARCINOMA.
PATHOPHYSIOLOGY
ACCUMULATI
ALTERED
ON OFF FLUID
PLEURAL FLUID
IN THE
REABSORPTION
PLEURAL
SPACE

a
PLEURAL
EFFUSION
MANIFESTATION
It is caused by the underlying disease like
Pneumonia it causes:
• Fever
• Chills
• Pleuritic pain
If malignant effusion, it may result to:
• dyspnea
• difficulty lying flat
• coughing.
ASSESSMENT AND
DIAGNOSTIC FINDINGS
In ASSESSMENT:
↓ fremitus
decreased or absent
of breath sounds
a dull and flat sound
on percussion
In DIAGNOSTIC:
Physical Examination
Chest X – ray
Chest CT
Thoracentesis
MEDICAL MANAGEMENT

THORACOCENTESIS
is performed to remove
fluid and to relieve dyspnea
& respiratory compromise
NURSING MANAGEMENT
Implementing the medial regimen
Prepare and positions the patient for
thoracentesis
Offers support throughout the procedure
Responsible for making sure the
thoracentesis fluid amount is recorded and
sent for appropriate laboratory testing.
NURSING MANAGEMENT
Assumes least painful position after
procedure
Evaluate the patient’s pain level and
administer analgesic agents as prescribed
and as needed.
Educate the patient and the family about
the management and care of the catheter
and drainage before discharge.
 An infectious disease the
primarily affect the lung
parenchyma
It also may be transmitted to
other parts of the body
PUL
MON
Causative agent:
ARY Mycobacterium tuberculosis
TUB
ERC
ULO
MYCOBACTERIUM
TUBERCULOSIS
FACTORS
Close contact
Immunocompromised status
Substance abuse ( IV/injection drug
users and alcoholics)
Preexisting medical conditions or
special treatment
Living in crowded, substandard
housing
PATHOPHYSIOLOGY KIDNEY
TRANSMITTE INHALATION OF
D MYCOBACTERIU BONE
THROUGHOU M
CEREBRAL
T THE TUBERCULOSIS
CORTEX
ALVEOLI LUNGS
UPPER
DESTROY TISSUE OF LOBES
IMMUNE SYSTEM
CAUSING NON TUBERCLE
BRONCHOPNEUMONIA PRODUCE

INFECTED LUNG
TUBERCULOSIS BECOME MORE
INFLAMED
CLASSFICATION INTERPRETATION
CLASS 0 No exposure; no infection
CLASS 1 Exposure; no evidence of infection

CLASS 2 Latent infection; no disease ( eg, + PPD

reaction but – clinical evidence of TB)

CLASS 3 Disease; clinically active

CLASS 4 Disease; not clinically active

CLASS 5 Suspected disease; diagnosis pending

CLINICAL MANIFESTATION
Low grade fever
Cough
Night sweats
Fatigue
Weight loss
Hemoptysis
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Complete history
Physical examination
Tuberculin skin test
Chest X-ray
Acid-fast bacillus smear
Sputum culture
MANAGEMENT
Promoting airway clearance
Advocating treatment regimen
Promoting activity and
nutrition
Preventing transmission
MANAGEMENT

Treated primarily with

anitituberculosis agents
for 6 to 12 months
FIRST LINE ANTITUBERCULOSIS
AGENTS
DRUGS ADULT DOSAGE
Isoniazid (INH) 5mg/kg ( 300 mg maximum daily)

Rifampicin 10 mg/kg (600 mg maximum daily)

( Rifadin)
Pyrazinamide 15-30mg/kg ( 2.0 maximum daily)
(PZA)
Ethambutol 15-25 mg/kg ( no maximum daily dose
but base on lean body weight)
CHEST TRAUMA
 CHEST TRAUMA

BLUNT PENETRATIN
CHEST TRAUMA
TRAUMA G TRAUMA

Strenal and Gunshot and

RibFracture Stab wounds
Flial Chest Pneumothorax
 More common than penetrating
trauma
It is often difficult to identify the
extent of the damage because the
BLU symptoms may be generalized and
NT vague
TRA Patients may not seek immediate
UMA medical attention which may
complicate the problem
 ACCELERATIO
PATHOPHYSIOLOGY
MECHANISM
N
DECELERATIO
OF BLUNT
N
ACCIDENTS CHEST
TRAUMA SHEARING
COMPRESSIO
N
ARF, HYPOVOLEMIC
SHOCK AND worst INJURIES TO
DEATH THE CHEST

WILL RESULT IN
IMPAIRED HYPOXEMIA OR
VENTILATION HYPOVOLEMIA
AND AND CARDIAC
PERFUSION FAILURE
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Initial Assessment:
Airway Massive
obstruction hemothorax

Tension Flail chest

pneumothorax
Cardiac
Open tamponade
pneumothorax
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Secondary Assessment:
Pulmonary contusion
Traumatic aortic rupture
Tracheobronchial disruption
Esophageal perforation
Traumatic diaphragmatic injury
Penetrating wounds to the
mediastinum
ASSESSMENT AND
DIAGNOSTIC FINDINGS
In Diagnostic: Electrolytes
Physical
Examination O2 saturation
Chest X-ray
CT Scan ABG analysis
CBC ECG
Clotting
studies,type and
cross- match
MEDICAL
MANAGEMENT
O2 support
Reestablishing fluid volume
and negative intrapleural
pressure
Draining intrapleural fluid and
blood
 STERNAL and RIB
FRACTURE
STERNAL FRACTURE most common in
motor vehicle crashes
RIB FRACTURE most common type of
chest trauma
Most common fracture of the ribs are FIFTH
through NINTH
Fracture of the lower ribs are associated with
injury in liver and spleen
CLINICAL MANIFESTATION
In STERNAL FRACTURE:
Swelling
Crepitus
Anterior chest pain
Possible chest wall deformity
Ecchymosis
O!!verlying tenderness
CLINICAL MANIFESTATION

In RIB FRACTURE:
Point tenderness
Muscle spasm
Severe pain
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Physical Examination
Chest X-ray
Rib films of a specific area
ECG
Continuous pulse oximetry
ABG analysis
MEDICAL
MANAGEMENT
Surgical fixation
Chest binder
Sedation – for
relieving pain
 A frequently complication of
blunt chest trauma
FLA
IL It occurs when 3 or more
CHE adjacent ribs are fractured
ST It may also result as a
combination fracture of ribs
and costal cartilages or
sternum
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Chest X-ray
Physical Examination
ABG analysis
Bedside pulmonary function
monitoring
Pulse oximetry
MEDICAL MANAGEMENT
For mild to moderate flail chest
Monitoring fluid intake
Appropriate fluid replacement
Relieving chest pain
Pulmonary physiotherapy
Secretion management technique
 MEDICAL MANAGEMENT
For severe flail chest injuries
-endotracheal intubation
-mechanical ventilation
Administration of Patient-controlled
analgesia
Intercostal nerve block
Epidural analgesia and intrapleural
Opiods ( for relieving pain)
 Occurs when the parietal
or visceral pleura is
PN breached.
EU Pleural space is exposed to
M
O
(+) atmospheric pressure
TH
OR
AX
 HEMOTHORAX

HYDRO
THORAX
 TYPES of PNEUMOTHORAX
Simple pneumothorax- occurs when air
enters pleural space through breach of
either parietal or visceral pleura
Traumatic pneumothorax -occurs when air
escapes from a laceration in the lung itself
Tension pneumothorax - occurs when air is
drawn into the pleural space from a
lacerated lung
CLINICAL MANIFESTATION

Sudden pain
Respiratory distress
Chest discomfort
Tachypnea
Hypoxemia
MUSCULAR
WEAKNESSES
 MYASTRENIA
GRAVIS
GUILLAIN – BARRE
MUS SYNDROME
CULA
R AMYOTROPHIC
WEA LATERAL
KNES
SES
SCLEROSIS
 • an autoimmune disorder
affecting the myoneural
junction.
• characterized by varying
MYAS degrees of weakness of the
TRENI voluntary muscle
AGRA
VIS
CLINICAL MANIFESTATION
• Diplopia ( double vision)
• Ptosis (drooping of the eyelids
• Muscle weakness
• Dysphonia(voice impairment)
• Aspiration and choking
 • An autoimmune attack on the
peripheral nerve myelin
• Causative agents:
- Campylobacter jejuni
GUILLAIN
BARRE - H.influenzae
YNDROM - Mycoplasma pneumoniae
E - HIV
CLINICAL
MANIFESTATION
• Muscle weakness
• Hyporeflexia + weakness
TETRAPLEGIA
• Paresthesia of the hand and feet
• Pain –related to demyelination of
sensory fibers
MY
OT
RO
• is a form of motor neuron
PHI disease.
C
LA • a progressive, fatal,
TE
RA neurodegenerative disease
L caused by the degeneration
SC
LE of motor neurons.
RO
SIS
CLINICAL MANIFESTATION
• Muscle atrophy
• Twitching, cramping, or
stiffness of affected muscles
• Muscle weakness
• Slurred and nasal speech
CLINICAL MANIFESTATION
• Pulmonary edema
• Increasing bilateral
infiltrates on chest X-ray
• Arterial hypoxemia
• Absence of elevated left
atrial pressure
ASSESSMENT AND
DIAGNOSTIC FINDINGS
Physical Examination – check for
intercostal retractions and crackles
Plasma brain natriuretic peptide (BNP)
level
Echocardiography
Pulmonary artery catheterization
MEDICAL MANAGEMENT
Supportive therapy (intubation
and mechanical ventilaton)

Identification and treatment of

the underlying condition

Supplemental O2
MANAGEMENT
• Frequent assessment of
patient’s status
• Consider other needs of the
patient
• Positioning of the patient
ACUTE RESPIRATORY
DISTRESS SYNDROME
 • Severe form of acute
lung injury
• Nonpulmonary
multiple-system organ
ACUTE
RESPIRAT failure – major cause
ORYDISTR of death
ESS
SYNDROM
PATHOPHYSIOLOGY
Release of mediators

Initiation of ↓In airway diameter

Acute inflammatory –
lung immune ↑Airway resistance
injury response ↓Lung compliance

↑ Work of breathing

Alveolar hypoventilation
HYPOXEMIA Intrapulmonary shunting
 • PULMONARY
EMBOLISM
• LUNG RESECTION
ACUTE
RESPIRATO
RY
DISTRESS
 • Obstruction of the pulmonary artery
or one of its branches by a thrombus
• Deep Vein Thrombus (DVT) refers to
a thrombus formation in the deep vein
PUL • Venous thromboembolism (VTE)
MON term that includes both PE and DVT
ARY
EMB
OLIS
M
PATHOPHYSIOLOGY
Thrombus ↑ Alveolar
obstruction space

Contricted
↓/no blood flow blood vessels and
bronchioles

IMPAIRED GAS
EXCHANGE
CLINICAL
MANIFESTATION
• Dyspnea • Cough
• Chest pain • Diaporesis
• Anxiety • Hemoptysis
• Fever • Syncope
• Tachycardia • Tachypnea
• Apprehension
ASSESSMENT AND
DIAGNOSTIC FINDINGS
• Chest X-ray
• ECG
• ABG analysis
• Ventilation-perfusion (V/Q) scan
• Pulmonary angiography- best
method to diagnose PE
NURSING MANAGEMENT
• Minimizing the risk of pulmonary embolism
• Preventing thrombus formation
• Assessing potential for PE
• Managing pain
• Managing O2 therapy
• Monitoring for complications
• Relieving anxiety
• Providing post-op nursing care
• Promoting home and community-based care
LUNG RESECTION
 TYPES OF LUNG RESECTION
• LOBECTOMY
SINGLE lobe of the lung is removed
• BILOBECTOMY
TWO lobes of the lung are removed
LUN
• SEGMENTECTOMY
G
RES A SEGMENT OF THE LUNG is
ECT removed
ION
NG TYPES OF LUNG RESECTION
SECTION
• SLEEVE RESECTION
CANCEROUS LOBES are
removed and segment of the main
broncus is resected
• PNEUMONECTOMY - removal
of the ENTIRE LUNG
LUN TYPES OF LUNG RESECTION
G • WEDGE RESECTION
RESE
CTIO REMOVAL OF A SMALL, PIE-
N SHAPED AREA OF THE SEGMENT
• CHEST WALL RESECTION
REMOVAL OF CANCEROUS LUNG
TISSUE;FOR CANCER THAT HAVE
INVADED THE CHEST WALL