NCM 118 Altered Ventilatory Function

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Benedicite Nomini Eius

HOLY NAME
UNIVERSITY
NCM 118
NURSING CARE OF
CLIENTS WITH
ALTERED
VENTILATORY
FUNCTION
Prepared by:
Prof. Judith L. Godinez, RN, MAN
“The task ahead of us is not greater than the power and love of God that is behind us”.

HOLY NAME
UNIVERSITY
NCM 118
CLIENTS WITH ALTERED VENTILATORY
FUNCTION
Acute and Chronic Obstructive Pulmonary Disease
Pulmonary Embolism
Acute Respiratory Syndrome/Acute Lung Injury
Respiratory Failure
Pneumonia (Community or Ventilator Acquired)
Respiratory Pandemics
Pulmonary Hypertension
Pneumothorax

HOLY NAME
UNIVERSITY
NCM 118
Acute and C O P D
● COPD – chronic obstructive lung dse. and chronic airflow
limitation.
● Mortality/Morbidity – 4th leading cause of death in the US,
and the 6th worldwide.
- More in men than women
- Predominantly in individuals more than 40 years old.

HOLY NAME
UNIVERSITY
NCM 118
ASTHMA
● Chronic inflammatory airway disorders that cause
episodic air obstruction and hyperresponsiveness of the
airway to multiple stimuli.

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UNIVERSITY
NCM 118
Causes/Pathophysio/S&S
Allergy(extrinsic)inflammation(intrinsic)
histamine,bradykinin,prostaglandin,serotonin, leukotrienes
bronchospasm,bronchoconstriction
Edema of the mucous membrane
hypersecretion of mucus

HOLY NAME
UNIVERSITY
NCM 118
narrowing of airways
orthopnea, restlessness, tachypnea, dyspnea, nasal flaring, tachycardia,

diaphoresis, cold clammy skin, wheezing, retractions, pallor, cyanosis
Air trapping
RESPIRATORY ACIDOSIS, HYPOXIA

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UNIVERSITY
NCM 118
Management
- Epinephrine
- Steroids
- Bronchodilators

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UNIVERSITY
NCM 118
CHRONIC BRONCHITIS
- productive cough present for a period of three months
in each of two consecutive years in the absence of
another identifiable cause of excessive sputum
production.

HOLY NAME
UNIVERSITY
NCM 118
Cigarettes smoking, RT infection, pollutants
histamine,bradykinin,prostaglandin
inflammation
Increased capillary permeability

HOLY NAME
UNIVERSITY
NCM 118
Fluid/Cellular Exudation
Edema of the mucous membrane
Hypersecretion of mucus
Persistent cough

HOLY NAME
UNIVERSITY
NCM 118
In addition, S&Sx
- Fatigue
- Sore throat
- Muscle aches
- Nasal congestion
- Headaches
- Severe coughing may cause chest pain
- cyanosis

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UNIVERSITY
NCM 118
Management
- Antibiotics
- Steroids
- Inhaled meds

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UNIVERSITY
NCM 118
EMPHYSEMA
Abnormal, permanent enlargement of acini
accompanied by destruction of alveolar walls, occurs
when alveolar gas is trapped and gas exchange is
compromised.

HOLY NAME
UNIVERSITY
NCM 118
Release of proteolytic enzyme from the lung cells causes
breakdown of lung tissues
inflammation
Enlargement of airspaces distal to terminal

bronchioles(acini)

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UNIVERSITY
NCM 118
Destroys the alveolar wall, breakdown/loss of elasticity
Making the lung less compliant
Hypoxia, Respiratory Acidosis(increased CO2

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UNIVERSITY
NCM 118
ASSESSMENT IN COPD, S&Sx
- Cough
- Dyspnea
- Sputum production
- Adventitious breath sounds
- Pursed-lip breathing
- Orthopnea
- Altered LOC

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UNIVERSITY
NCM 118
ASSESSMENT IN COPD, S&Sx
- Pallor to cyanosis
- Cold clammy skin
- Barrel chest
- Clubbing of fingers
- Polycythemia
- Decreased metabolism due to decreased O2
weakness fatigue, anorexia, weight loss

HOLY NAME
UNIVERSITY
NCM 118

HOLY NAME
UNIVERSITY
NCM 118
MEDICAL MANAGEMENTS
- Expectorants (guaiafenesin)
- Mucolytic(mucomyst/mucosolvan)
- Antitussives
Examples:
: Dextromethorphan
: Codeine

HOLY NAME
UNIVERSITY
NCM 118
MEDICAL MANAGEMENTS
- Bronchodilators
:Aminophylline (Theophyline)
:Ventolin (Salbutamol)
:Bricanyl (Terbutaline)
:Alupent (metaprotelenol)
- Antihistamines
- Steroids
- Antimicrobials

HOLY NAME
UNIVERSITY
NCM 118
NURSING MANAGEMENTS
- Rest
- Increased fluid intake
- Good oral hygiene
- Diet – hi caloric, hi CHON, low CHO
- O2 Therapy – 1 to 3L/min.
- Avoid cigarette smoking, alcohol and environmental pollutants
- CPT
- Bronchial hygiene

HOLY NAME
UNIVERSITY
NCM 118
NURSING MANAGEMENTS
- Rest
- Increased fluid intake
- Good oral hygiene
- Diet – hi caloric, hi CHON, low CHO
- O2 Therapy – 1 to 3L/min.
- Avoid cigarette smoking, alcohol and environmental pollutants
- CPT
- Bronchial hygiene

HOLY NAME
UNIVERSITY
NCM 118
CPT
- Assess the area of accumulation of mucus secretions
- Position to allow expectoration of mucus secretions by gravity
- Place the client in each position for 10 to 15 mins
- Percussion and vibration done to loosen secretions
- Change position gradually to prevent postural hypotension
- Done 60 to 90 min AC or in am upon awakening and at
bedtime.

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UNIVERSITY
NCM 118
CPT
https://www.youtube.com/watch?v=LJU_zVMnF3o

HOLY NAME
UNIVERSITY
NCM 118
Pulmonary Embolism

HOLY NAME
UNIVERSITY
NCM 118
Pulmonary Embolism
– an obstruction of one or more pulmonary arteries by

a thrombus or thrombi, originating somewhere in the
venous system or on the right side of the heart.

HOLY NAME
UNIVERSITY
NCM 118
Causes/Pathophysiology
Virchow’s triad of factors for venous thrombosis:

1. Venous stasis
2. Injury to the intima
3. hypercoagulability

HOLY NAME
UNIVERSITY
NCM 118
Thrombosis usually originates as a platelet nidus in the region of
venous valves located in the veins of the lower extremities. Further
growth occurs by accretion of platelets and fibrin and progression
to red fibrin thrombus w/c may either break off and embolize or
result in total occlusion of the vein. The endogenous thrombolytic
system leads to partial dissolution; then thrombus becomes
organized and is incorporated into the venous wall.

HOLY NAME
UNIVERSITY
NCM 118
P.E. usually arises from the thrombi originating from the deep venous
system of the lower extremities; however, rarely they may originate in the
pelvic, renal, or upper extremity veins and the right heart chambers. After
traveling to the lung, large thrombi lodge at the bifurcation of the main
pulmonary artery or the lobar branches and cause hemodynamic
compromise. Smaller thrombi continue travelling distally occluding a
smaller vessel in the lung periphery. These are more likely to produce
pleuritic chest pain by initiating an inflammatory response adjacent to
the parietal pleura. Most pulmonary emboli are multiple, and the lower
lobes are involved more commonly than the upper lobes.

HOLY NAME
UNIVERSITY
NCM 118
Acute respiratory consequences of P.E. include increased alveolar dead
space, pneumoconstriction, hypoxemia, and hyperventilation. Later, 2
additional consequences may occur: regional loss of surfactant and
pulmonary infarction. Arterial hypoxemia is a frequent but not universal
finding in patients with acute embolism. The mechanisms of hypoxemia
include ventilation–perfusion mismatch, intrapulmonary shunts, reduced
cardiac output, and intracardiac shunt via patent foramen ovale.
Pulmonary infarction is an uncommon consequence because of the
bronchial arterial collateral circulation.

HOLY NAME
UNIVERSITY
NCM 118
S & Sx
The presentation of P.E. may vary from a sudden onset of catastrophic
hemodynamic collapse to gradually progressive dyspnea. The dx of P.E.
should be sought actively in patients with respiratory symptoms
unexplained by alternate dx. The symptoms of P.E. Are nonspecific,
therefore, a high index of suspicion is required, particularly when a
patient has risk factors, which include recent surgery, immobility, or
hypercoagulable state.

HOLY NAME
UNIVERSITY
NCM 118
S & Sx
The second subset has no previously documented pulmonary emboli but
has a widespread obstruction of the pulmonary circulation with a clot.
They present with gradually progressive dyspnea, intermittent exertional
chest pain, and eventually, features of pulmonary hypertension and cor
pulmonale.

HOLY NAME
UNIVERSITY
NCM 118
S & Sx
Patients with P.E. may present with atypical symptoms, where strong
suspicion in a high risk patient often leads to consideration of P.E. In the
differential dx. These symptoms include the following.
- Seizures - Wheezing
- Syncope - Decreasing LOC
- Abdominal pain - New onset of AF
- Fever - Pleuritic chest pain w/o
- Productive cough symptoms of risk factors may
be a presentation of P.E.

HOLY NAME
UNIVERSITY
NCM 118
Surgical Mgt.
Inferior vena cava (IVC) interruption - (Greenfield filter)
Indications:
- Patients with acute venous thromboembolism who have an absolute
contraindication to anticoagulant therapy, e.g. recent surgery,
hemorrhagic stroke, or significant active or recent bleeding
- Patients who have objectively documented recurrent venous
thromboembolism, adequate anticuagulant therapy notwithstanding.

HOLY NAME
UNIVERSITY
NCM 118
Surgical Mgt.

HOLY NAME
UNIVERSITY
NCM 118
Medical Mgt.
- Thrombolytic therapy
Goals of anticoagulation therapy:
N - 30 to 50 seconds
PT – 10 to 14 sec / 11-14
PTT – 32 to 45 sec 25-35 most commonly used test to monitor heparin therapy
BT – 3-7 mins/ 2-7
CT – 5 – 15 mins/ 8-15
INR – 0.8 – 1.2
aPTT: More than 70 seconds (signifies spontaneous bleeding)
PTT: More than 100 seconds (signifies spontaneous bleeding)

HOLY NAME
UNIVERSITY
NCM 118
Medical Mgt.
Heparin therapy generally is overlapped with warfarin for a minimum of 4 – 5 days.
Duration of anticoagulation
A patient with a first thromboembolic event occurring in the setting of reversible risk
factors such as immobilization, surgery or trauma should receive warfarin therapy for 3-6
months. In the absence of an identifiable risk factor, the first ideopathic
thromboembolic event should be treated for a minimum of 6 months and 3 months of
anticuagulation is insufficient in this setting.
Warfarin tx for longer than 6 months is indicated in patients with recurrent venous
thromboembolism or in those in whom a continuing risk factor for venous
thromboembolism exists including malignancy, immobilization or morbid obesity.

HOLY NAME
UNIVERSITY
NCM 118
ACUTE RESPIRATORY DISTRESS SYNDROME

HOLY NAME
UNIVERSITY
NCM 118
ACUTE RESPIRATORY DISTRESS SYNDROME
Characterized by a severe inflammatory process, alveolar & capillary
membrane damage, resulting to:
A - atelectasis (fluid accumulation in the alveoli & dec. surfactants)
- absence of elevated left atrial pressure (LAP) – PCWP
R - reduce lung compliance (hyaline membrane)
- refractory hypoxemia ( hallmark sign of ARDS), low O2 in blood circ. to organ
D - developing bilateral infiltrates in the CXR
- decreased gas exchange
S - sudden & progressive pulmonary edema

HOLY NAME
UNIVERSITY
NCM 118
ARDS
Alveolar & capillary

damage, leakage of
fluids

HOLY NAME
UNIVERSITY
NCM 118
ARDS: Pathophysiology
Causes: (leads to systemic inflammation)
Injuries excluding lungs:
Indirect Injury:
Sepsis
Burns
Multiple blood transfusions
Pancreatitis

HOLY NAME
UNIVERSITY
NCM 118
Causes: (leads to systemic inflammation)
Lung related injuries:
Direct Injury: COVID 19
Pneumonia
Inhalation injury (smoke/chemical)
Near drowning
Aspiration
Triggers the immune 🡪 Releasing cellular &
Causes: (direct/indirect) 🡪 system to stimulate chemical mediators
inflammatory responses
🡪
Recruit/invite
more/other
immune cells
🡪
Injury to the tissues Through the • Inc. capillary
🡪 Injury to the blood to the permeability
🡪 🡪
alveolar-capillary affected area • Inc. blood flow
membrane
LUNGS: V/Q mismatch
Alveolar collapse (atelectasis)
Due to: Non functional
🡪
• inflammatory infiltrates alveoli 🡪 alveoli
• Blood/fluid accumulation dead space Shunting of blood
• Surfactant cell damage (the flow of blood to
unventilated alveoli)
🡪
Goes back to the
HYPOXEMIA heart and system
🡪 🡪
HYPOXIA
less/without O2.
Phases:
Exudative 🡪 24 hrs / <72hrs (1-7 days) 🡪 damage to membrane
🡪 leakage of fluid (protein-rich) to the
interstitium and alveolar sac
🡪 Pulmonary edema (ARDS/CHF)
🡪 damaged type 1 & 2 epithelial cells
🡪 damage surfactant cells 🡪 atelectasis
🡪 O2 falls – hypoxemia
🡪 hyaline membrane formation
🡪 dec. lung compliance (V/Q mismatch)
Manifestations 🡪 • refractory hypoxemia

(characteristic/hallmark sign)
• Dyspnea (SOB)
• Inc. RR 🡪 low O2; low CO2 🡪
Respiratory Alkalosis
• CXR: bilateral infiltrates
Phases:
Proliferative 🡪 14 days / 2weeks 🡪 repair structures (reproduction of cells)
🡪 tissue dense & fibrous (scarring)
🡪 dec. lung compliance & hypoxemia worsens
Fibrotic 🡪 3 wks 🡪 fibrotic lung tissue

🡪 inc. alveolar dead space
🡪 dec. lung compliance – “stiff lung”
🡪 poor prognosis
Manifestations 🡪 • Central cyanosis

• Altered mental status
• Inc. HR
• Intercostal retractions
• crackles
ARDS: Assessment & Diagnostic Findings
• Physical Examination
• Diagnostic Tests 🡪 BNP Levels – distinguish ARDS
from cardiogenic pulmonary edema
🡪 Echocardiography
🡪 Pulmonary Artery
Catheterization
● Right pulmonary systolic and diastolic
pressures (PAP),
● Pulmonary Artery Wedge Pressure (PAWP),
● Cardiac Index (CI),
● Systemic and Pulmonary Vascular
Resistance (SVR & PVR),
● Core body temperature
● Mixed venous oxygen saturation.
ARDS: Medical Management
GOALS:
● Treatment of the underlying condition
● Gas exchange function
Supportive care/therapy:
1. Respiratory assistance/support
● O2 supplementation – High Flow (High concentration)
● Endotracheal Intubation
● Mechanical ventilation
Note: monitor respiratory status 🡪 ABG, pulse oximeter, V/S

monitoring
MV with PEEP (Positive End-Expiratory Pressure) – 10-20mm H2O

🡪 reverse alveolar collapse during expiratory
🡪 get rid of fluid accumulation 🡪 improves gas exchange
Complications: High level PEEP depresses cardiac output

🡪 systemic hypotension
Nursing consideration:
● Monitor BP
● Administer inotropes/vasopressors
MV with PEEP (Positive End-Expiratory Pressure)
Complications: high-level PEEP hyperinflation of

lungs
🡪 pneumothorax, subcutaneous emphysema
Nursing consideration:
• Assess for respiratory problems
Nursing consideration MV with PEEP:
• Relieve pt anxiety
• Check for tube blockage – kinking or retained
secretions
• Assess for respiratory problems & complications
• Assess for a decreased O2 level
• Assess for level of dyspnea
• Assess for ventilatory malfunction
Pharmacologic Interventions
🡪 No specific medication/tx for ARDS except supportive
care.
ex.: GI drugs, corticosteroids, sedatives, neuromuscular
blocking agents, analgesics
Nutrition Therapy
🡪 DAT
🡪 If on MV 🡪 Enteral feeding
🡪 Parenteral feeding
ARDS: Nursing Management
1. Closely monitor the patient – ICU.
2. Administer respiratory assistance/support.
🡪 O2 supplementation
🡪 nebulization
🡪 chest physiotherapy
🡪 ET intubation/tracheostomy
🡪 Mech Vent
🡪 Suctioning
3. Frequent ax of pt’s status 🡪 evaluate the effectiveness of tx
4. Positioning
🡪 HBR
🡪 side-lying position
4. Positioning
🡪 PRONE POSITION
🡪 oxygenation improves (V/Q ratio)
🡪 improve airflow (heart position)
🡪 move secretions
🡪 improve atelectasis
🡪 turning to sides (proper ventilation and enhanced secretion
drainage)
NOTE: Deterioration in O2 level due to changing the position
5. Reduce the anxiety level of pt.
6. Keep the patient well rested.
7. Mouth care, and hygiene.

8. Assess skin integrity 🡪 ROM exercises.

HOLY NAME
UNIVERSITY
NCM 118
Acute Respiratory Failure
ACUTE RESPIRATORY
FAILURE
• Sudden and life-threatening deterioration
of the gas exchange function of the lungs
• Indicates failure of the lungs to provide

adequate OXYGENATION and
VENTILATION for the blood
HYPOXEMIC RESPIRATORY
FAILURE
HYPERCAPNEIC
• Inadequate oxygenation
• Defined through the
RESPIRATORY FAILURE
measurement of the • Ventilatory failure
partial arterial pressure of • Defined through the
oxygen (PaO2) measurement of the partial
• < 50 / <60 mm Hg arterial pressure of carbon
dioxide (PaCO2)
• PaCO2 : > 50 / > 45 mmm Hg
• pH : > 7.35
HYPOXEMIC HYPERCAPNIC
RESPIRATORY FAILURE RESPIRATORY FAILURE
• CAUSES
• Respiratory • Respiratory
• ARDS
• Asthma
• Pneumonia
• COPD
• Smoke inhalation
• Cystic Fibrosis
• Pulmonary Embolism
• CNS
• Pulmonary hemorrhage
• Decreased respiratory drive
• Cardiac
• Chest Wall Dysfunction
• Heart failure (cardiogenic
• Neuromuscular disorders
pulmonary edema) • Obesity
• Trauma
RESPIRATORY FAILURE
Clinical Manifestations
Early signs are those associated with
impaired oxygenation:
1. Restlessness
2. Fatigue
3. headache
4. dyspnea (air hunger)
5. tachycardia
6. increased blood pressure

RESPIRATORY FAILURE
As the hypoxemia progresses, more obvious signs
may be present:
1. Confusion
2. lethargy
3. Tachycardia
4. Tachypnea
5. central cyanosis
6. Diaphoresis
7. respiratory arrest
RESPIRATORY FAILURE
1. Physical findings are those of acute
respiratory distress, including:

2. use of accessory muscles
3. Decreased breath sounds if the patient
cannot adequately ventilate
4. other findings related specifically to the
underlying disease process and cause
of ARF.
RESPIRATORY FAILURE
Medical Management
The objectives of treatment:
❑ to correct the underlying cause
❑ to restore adequate gas exchange in
the lung
⮚ Intubation
⮚ Mechanical ventilation
RESPIRATORY FAILURE
Nursing Management
1. Assisting with intubation
2. Maintaining mechanical ventilation
3. Assessing the patient’s respiratory status
RESPIRATORY FAILURE
STRATEGIES IMPLEMENTED BY THE NURSE TO

PREVENT COMPLICATIONS:
1. turning schedule
2. mouth care
3. skin care
4. range of motion of extremities

HOLY NAME
UNIVERSITY
NCM 118
Pneumonia (Community or Ventilator

Acquired)

HOLY NAME
UNIVERSITY
NCM 118
Pneumonia (Community or Ventilator
Acquired)
An infection of the pulmonary tissue, including the
interstitial spaces, the alveoli, and the bronchioles.
An edema associated with the inflammation, stiffens the
lungs, decreasing lung compliance and vital capacity
and causing hypoxemia.
Can be CAP or HAP

HOLY NAME
UNIVERSITY
NCM 118
Classification
CAP
HAP
Aspiration pneumonia
Pneumonia caused by opportunistic organisms
Other pathogens – H5N1 influenza, SARS, AH1N1,
tularemia, anthrax, plague

HOLY NAME
UNIVERSITY
NCM 118
Inflammation of the pleura
- chest pain
- pleural effusion
- dullness
- decreased breath sounds
- decreased vocal fremitus

HOLY NAME
UNIVERSITY
NCM 118
Hypoventilation
- decreased chest expansion
- respiratory acidosis
Protective mechanism
- increased WBC
- increased RR
- fever

HOLY NAME
UNIVERSITY
NCM 118
Pathophysio/ S & S
Hypertrophy of mucous membrane
- increased sputum
- wheezing
- dyspnea
- cough
- rales
- rhonchi

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UNIVERSITY
NCM 118
Med’l Mgts.
- Antibiotics
- Antipyretics
- Bronchodilators

HOLY NAME
UNIVERSITY
NCM 118
Nsg. Mgts.
- Rest
- Fluids
- Incentive spirometry
- O2 therapy
- Semi Fowler’s
- Bronchial hygiene

HOLY NAME
UNIVERSITY
NCM 118
Nsg. Mgts.
- Oral hygiene
- Humidifier
- Splint chest when coughing
- CXR
- Monitor V/S

HOLY NAME
UNIVERSITY
NCM 118
Respiratory Pandemics
COVID -19:
CORONAVIRUS
DISEASE
1.
DEFINITION
INFECTIOUS DISEASE CAUSED
BY THE EXPOSURE TO
CORONAVIRUS CALLED
SARS-COV-2.
2.
RISK FACTORS
▪ Most people – MILD TO MODERATE
respiratory illness (asymptomatic and does
not require hospital care).
▪ Serious cases – evident S/Sx
▪ older people
▪ with comorbidities – cardiovascular
diseases, diabetes, cancer, chronic
respiratory dx
▪ Immunocompromised
▪ UNVACCINATED
3.
MODE OF TRANSMISSION
▪ Droplets or aerosols
▪ Direct contact with
infected people
4.
SIGNS & SYMPTOMS
COMMON
▪ Fever
▪ Cough
▪ Tiredness
▪ Loss of taste/smell
4.
SIGNS & SYMPTOMS
LESS COMMON
▪ Sore throat
▪ Headache
▪ Aches & pains
▪ Diarrhea
▪ Rashes on skin
4.
SIGNS & SYMPTOMS
SERIOUS
▪ Difficulty breathing /
SOB
▪ Loss of speech/mobility
▪ Confusion
COVID-19: SEVERELY ILL
▪ Admitted to a COVID facility for an

intensive care.
▪ ER – cohorting of patients
▪ Zone 1
▪ Zone 2
▪ Zone 3
85
5.
DIAGNOSTIC EXAMS
CRP Level
Ferritin test
▪ Inflammatory biomarkers
LDH
▪ Severity of tissue damage
5.
DIAGNOSTIC EXAMS
Procalcitonin
▪ Serious bacterial infection
D-dimer test
▪ Risk for clot formation
PCR test
▪ Positive of COVID-19
ABG
6.
MEDICAL MANAGEMENT
Pharmacology interventions
▪ Tocilizumab
▪ Remdesivir
▪ Favipiravir
▪ Melatonin
6.
MEDICAL MANAGEMENT
Pharmacology interventions
▪ Dexamethasone
▪ Anti-biotics
▪ Bronchodilators
▪ Antihistamines
▪ Vitamins
7.
NURSING MANAGEMENT
▪ Position: HBR & Prone position
(16-20hrs)
▪ Coughing technique (every
movement)
▪ Assist with ROM’s & ADL’s
▪ CBR w/o TP
▪ Monitor Intake and Output
▪ Personal hygiene & care
8.
NURSING MANAGEMENT
PREVENTIVE MEASURES
C – lean your hands properly.
O – bserve 1 meter distance; open,
well-ventilated spaces
V – accine & vitamins for immunity
I – n coughing & sneezing, always
cover your nose and mouth
D – on a well fitted mask.

HOLY NAME
UNIVERSITY
NCM 118
Pulmonary Hypertension

HOLY NAME
UNIVERSITY
NCM 118
Pneumothorax

HOLY NAME
UNIVERSITY
NCM 118
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Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

orthopnea, restlessness, tachypnea, dyspnea, nasal flaring, tachycardia,

RESPIRATORY ACIDOSIS, HYPOXIA

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Benedicite Nomini Eius

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Increased capillary permeability

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Edema of the mucous membrane

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Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Enlargement of airspaces distal to terminal

Benedicite Nomini Eius

Destroys the alveolar wall, breakdown/loss of elasticity

Making the lung less compliant

Hypoxia, Respiratory Acidosis(increased CO2

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

– an obstruction of one or more pulmonary arteries by

Benedicite Nomini Eius

Virchow’s triad of factors for venous thrombosis:

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

Benedicite Nomini Eius

ACUTE RESPIRATORY DISTRESS SYNDROME

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Alveolar & capillary

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Manifestations 🡪 • refractory hypoxemia

Fibrotic 🡪 3 wks 🡪 fibrotic lung tissue

Manifestations 🡪 • Central cyanosis

Note: monitor respiratory status 🡪 ABG, pulse oximeter, V/S

MV with PEEP (Positive End-Expiratory Pressure) – 10-20mm H2O