Acute Pulmonary failure

Gastrointestinal surgical department

of affiliated hospital of jining medical college
 Basic Concepts
 Respiration: Exchange of gases
 Tidal Volume: Volume of gas
inspired & expired in one normal breath
 Ventilation: Movement of air
 Perfusion: Circulation of blood
through the lungs with normal
Hemoglobin level
 Compliance: Ability of the lungs to
“stretch”
 Basic Concepts
 Va/Q Ratio: The relationship between
alveolar ventilation & perfusion. The
normal is 0.8 & alterations lead to
hypoxemia
 Shunting: When a portion of the
cardiac output is shunted through the
pulmonary capillary bed without
becoming oxygenated. Therefore,
nonoxygenated blood is deposited in the
 Acute Pulmonary failure
 Acute Respiratory Distress syndrome(ARDS)
 Mechanical failure
 Atelectasis
 Aspiration
 Pulmonary contusion
 Pulmonary embolism
 Pneumonia
 Cardiogenic pulmonary edema
 Neurogenic pulmonary edema
 Acute Respiratory Distress syndrome
 Acute hypoxia respiratory failure in one or both gas
exchange functions: oxygenation and carbon dioxide
elimination
 Noncardiogenic pulmonary edema
 Decreased lung compliance
 Ventilation-perfusion abnormalities
 Decreased functional residual capacity
 Progressive dyspnea
 Refractory hypoxemia
 Diffuse Infiltrates on chest
Acute Respiratory Distress syndrome
 Hypoxia
 • Decreased concentration of O2 in
inspired air
 Hypoxemia
 • Decreased arterial 02 tension (Pa02)
 • Decreased arterial 02 saturation
(Sa02)
 Hypercapnia
 Diagnostic Criteria
 Acute onset(usually development
approximately 24h after resuscitation
from shock)
 PaO2/FiO2≤200mmHg
 Bilateral lung diffuse infiltrating change
on X-ray
 Pulmonary capillary wedge
pressure(PCWP) ≤18mmHg,or No
cardiac factors
` Diagnostic Criteria

 _ Hypoxemia - Pa02 60mm Hg or less

when receiving 02 in concentration
60% or greater
 _ Hypercapnia – PaC02 greater than
46mm Hg in combination with arterial
ph less than 7.35
Acute Respiratory Distress syndrome
 Severe trauma
 Sepsis
 Aspiration
 Lung contusion
 Acute pancreatitis
 Multiple transfusions
 Ventilator induced lung injury
 Ventilation & Perfusion
Balance
 Normal ventilation & perfusion:
 The normal function of the lungs to move
oxygen from the air to the blood & CO2 from
the blood to the air.
 Even in normal lungs, there are regional
differences in ventilation, perfusion & gas
exchange. These difference are due to
gravity,to variations in pleural pressures &
complexity of normal anatomy
 Ventilation & Perfusion
Balance
 In the normal lung, both ventilation
&perfusion are greatest at the base of the
lung & decrease toward the apices
 However, the gradient for perfusion from
the bottom to the top of the lung is greater
than the gradient for ventilation.
 End result: In an normal, upright
patient:Upper segments are relatively
hypoperfused;(V/Q is high)
 Ventilation & Perfusion
Balance
 Lower segments are relatively hypo-
ventilated
(V/Q is low)
 Thus, V/Q values show marked
variations in different lung units, even
though V/Q may be normal for the
overall lung !
 Ventilation & Perfusion
Balance

 Four Common Causes of Hypoxemia:

 Hypoventilation, V/Q Mismatch,
Diffusion Abnormalities & Shunt
Acute Respiratory Distress syndrome
Exchange of gas
 Hypoxemia due to
Hypoventilation
 Pathophysiology: Hypoxemia always
accompanied by
 hypercarbia
 Etiology: damage to brain’s respirotary-center
 (trauma, strokes, CNS depressant drugs) & Neuro-
muscular
 defects (myasthenia gravis or Guillian-Barre
Syndrome) In
 abnormal lungs; bronchitis & emphysema
 Diagnosis: Hypoxemia with a increased PCO2
 Therapy: Improve oxygenation by increasing
alveolar

 Hypoxemia due to Diffusion
Abnormalities
 Pathophysiology:
 1.Increased diffusion pathway (prevents
equilibrium between alveolar oxygen &
pulmonary capillary
 2.Decreased diffusion area(destruction of
membrane surface available for diffusion ,
loss of pulmonary capillary bed
 Etiology: Pneumonia,ARDS, interstitial lung
)
 Diagnosis: H&P, Lab findings ,X-Ray
 Treatment: Oxygen administration
Hypoxemia due to V/Q Mismathching
 Pathophysiology: HighV/Q , units perfusion in
 excess of ventilation,Gases traversing these units is
not fully exchanged or Low V/Q
 units may result from partial obstruction of airways
 (secretions, edema, foreign object, etc.)
 Etiology: Obstructive airway (chronic bronchitis,
 emphysema, asthma); pulmonary vascular embolism
 Diagnosis: H& P, ABG’s (widened DaO), CXR,
 PFT’s, V/Q Scan
 Treatment: Oxygen administration, identify cause
 Hypoxemia due to Shunting (R to L)
 Pathophysiology: Venous admixture occurs when
 deoxygenated, mixed venous bypasses functional
alveolarcapillary
 units & mixes with normally oxygenated blood in
 circulation; shunts may be anatomic or physiologic
 Etiology: Anatomic shunts: normal shunts
(bronchial, pleural
 or thebesian veins), intrapulmonary shunts
(pulmonary A-V
 fistula), intracardiac shunts (Tetrology of Fallot,
 Eisenmenger’s syndrome) or other shunts assoc.
with
 Neoplasms or Physiologic shunts: Alveolar collapse
 (atelectasis, pneumonia, pleural effusion), alveoli
 Hypoxemia due to Shunting

 Diagnosis: Hypoxemia with a normal

or
 decreased PaCo2,
 Treatment: Oxygen administration
has little
 effect; proper therapy depends on
specific
 etiology
Acute Respiratory Distress syndrome
 _ Alveolar capillary membrane becomes
damaged and more permeable to
intravascular fluid.
 _ Results in Severe dyspnea
 -Hypoxia that is not altered by
supplemental 02 Reduced lung
compliance
 -Diffuse pulmonary infiltrates
Acute Respiratory Distress syndrome
 _ 1. Injury or exudates
 • Within 24 - 48 hours
 • Interstitial and alveolar edema
 • Atelectasis
 • Severe ventilation perfusion ratio
(V/Q)
 mismatch
 • Shunting of pulmonary capillary blood
Acute Respiratory Distress syndrome
 _ 2. Reparative or Proliferative phase
 • Within 1 - 2 weeks after initial injury
 • Diseased lung characterized by dense
fibrous tissue
 • pulmonary vascular resistance
 • Pulmonary hypertension
 • Decreased lung compliance
 • Hypoxemia worsens
Acute Respiratory Distress syndrome
 _ 3. Fibrotic phase
 • 2 to 3 weeks after initial injury
 • Lung remodeled by collangenous fibrous
tissue
 • Diffuse scaring and fibrosis
 • Decreased lung compliance
 • Surface area for gas exchange significantly
reduced
 • Pulmonary hypertension
Acute Respiratory Distress syndrome
 Initial signs
 • Restlessness
 • Change in personality
 • Disorientation
 • Change in LOC
 • X-ray normal or minimal scattered
infiltrates
Acute Respiratory Distress syndrome
 Worsening signs
 • Tachypnea
 • Intercostals and suprasternal retractions
 • Decreased compliance (“stretchiness”)
 • Decreased lung volumes
 • Decreased Functional Residual Capacity
(FRC)
 • Diaphoresis
 • Diffuse crackles and rhonchi
Acute Respiratory Distress syndrome
 Decreased mentation
 • X-ray = diffuse and extensive
bilateral
 interstitial and alveolar infiltrates
 • Hypoxia despite increase in oxygen
 • Hypercapnia
 • Pleural effusion
 • White lung
Acute Respiratory Distress Syndrome

 Severe ALI
 B/L radiographic
infiltrates
 PaO2/FiO2 <200mmHg
(ALI 201-300mmHg)
 No e/o ↑L Atrial P;
PCWP<18
Acute Respiratory Distress Syndrome

 Develops ~4-48h
 Persists days-wks
 Diagnosis:
 Distinguish from
cardiogenic edema
 History and risk
factors
 Acute Respiratory Distress Syndrome

Exudative phase Proliferative phase Fibrotic phase

Diffuse alveolar damage
Acute Respiratory Distress syndrome
 Indications for Endotracheal
Intubation
 Cardiopulmonary Resuscitation
 Airway Protection
 Need for mechanical ventilation
 Control of copious secretions
 Sever upper airway obstruction
Acute Respiratory Distress syndrome
 _ Patient at-risk
 • Teach respiratory interventions
 • Coughing
 • Deep breathing
 • Incentive spirometer
 • ambulation
 • Hydration and nutrition
 O2 Delivery Systems

 Nasal cannula: Low concentrations

of O2 (up to 50% , 6-8L/min). In a low
flow system,the larger the tidal volume,
the lower the FiO2;or the smaller the
tidal volume the larger the FIO2. More
than 6L/min does little to inc O2
concentration,because the anatomic
reservoir is filled. This device beneficial
in correction mild hypoxemia, ACS,
COPD
 O2 Delivery Systems

 Simple Face Mask: Should not run less

than
 5L/min…otherwise exhaled gas will
accumulate in
 the mask reservoir, might be rebreathed.
Flow rates
 above 8L/min result in little inc inspired O2
 concentration because the reservoir is filled.
Useful
 with correction with moderate hypoxemia.
Acute Respiratory Distress syndrome
 Supplemental 02
 _ Positive Pressure Ventilation
 _ Huff cough
 _ Staged cough
 _ Chest physical therapy
ventilator
Acute Respiratory Distress syndrome
 _ Bronchodilators – Ventolin, Alupent
 _ Corticosteroids – methylprednisolone
 (solu medrol)
 _ Diuretics
 _ Antibiotics
 _ Anxiety, pain, agitation rx. – Ativan,
 Versed, Morphine
 Summary
 ARDS is the end result of multiple
types of
 lung injury
 Severe trauma,Aspiration, sepsis
(Gram negative) likely causes
 Attention to patient support in the ICU
appears to improve mortality
 Mechanical ventilation to limit
barotrauma