ARF and ARDS Flashcards
What is Acute Respiratory Failure (ARF)?
- State of disturbed gas exchange resulting in abnormal ABG
- Condition that develops rapidly with little time for physiologic compensation
PaCO2 is the most important criteria in labelling RF
- PaCO2 < 60 mmHg
~ Hypoxemia
- PaCO2 > 50 mmHg
~ Hypercapnia
- pH <7.35 when px is on room air
What are the types of ARF?
Type I (Failure of oxygenation/perfusion)
- PaO2 < 60 mmHg but PaCO2 is normal/low
~ Hypoxemia w/o hypercapnia
Type II (Failure of ventilation)
- PaO2 < 60 mmHg + PaCO2 > 50 mmHg
~ Hypoxemia w hypercapnia
Type III (due to lung atelectasis)
- Common perioperatively
~ After GA, dec in functional capacity can lead to collapse of lung units
Type IV (due to hypoperfusion of resp. muscles in shock)
- Px in shock often experience resp. distress due to pulmonary edema, lactic acidosis and anemia
What is the pathophysiology of hypoxemia?
1) Diffusion limitation
- O2 con. is alveoli is unchanged/unaffected, but gas transfer ability is impaired
2) Alveolar hypoventilation
- Lungs do not adequately exchange gases due to insufficient ventilation of the alveoli
3) Low inspired oxygen
- eg in commercial flights
4) V/Q mismatch
- a) Impaired ventilation, preserved perfusion
~ Area of the lung can receive little ventilation in comparison to the amount that can be perfused
- b) Impaired perfusion, preserved ventilation
~ PE
What is the pathophysiology of hypercapnia?
- Due to alveolar hypoventilation
- If the capacity of muscle pump is slightly > load, uncomfortable compensation occurs
~ Dyspnoea - If capacity of pump < load, body is unable to compensate
~ Respiratory failure
What are the common causes of Type I ARF?
- V/Q mismatch
~ Imbalance between ventilation (V)—the air reaching the alveoli—and perfusion (Q)—the blood flow reaching the alveoli for gas exchange in the lungs
~ Eg PE - Alveolar hypoventilation
- Diffusion problem
- Shunt
- Bronchial asthma
- Emphysema
- Bronchitis
- Pneumonia
- PE
- HF
- ARDS Type I/II
What are the common causes of Type II ARF?
- ^ airway resistance
~ eg COPD - Reduced WOB
- Dec in area of lung for gas exchange
~ eg bronchitis - Neuromuscular problems
~ Myasthenia gravis
~ GBS
~ Spinal cord trauma - CNS depression
~ Head injuries
~ Drug overdoes
What are the early clinical signs of ARF in general?
- Restlessness, fatigue
- Headache
- Dyspnea, use of accessory muscles, paradoxical breathing
- Tachypnea
- ^ BP
What are the late clinical signs of ARF in general?
- Confusion
- Central cyanosis
- Diaphoresis
- Tachycardia
- Tachypnea, respiratory arrest
What are the complications of respiratory failure?
- Chronic RF -> Pulmonary vasoconstriction -> Pulmonary arterial hypertension -> Right ventricular function impaired -> Right heart failure
What investigations are done for respiratory failure?
- ABG
- FBC
- U/E/Cr
- CXR
- Lung CT
- Sputum, blood, urine c/s
What are the treatment goals for RF?
1) Maintain adequate air patency
- Chest PT, brochodilators, NIV, intubation
2) Correct underlying cause
3) Optimizing oxygen delivery
- Supplemental O2, positioning, blood transfusion to ensure sufficient Hb
4) Minimizing oxygen demand
- Timing of ADLs, bed rest, addressing sepsis, restlessness & px-ventilator desynchrony
5) Preventing complications
What is the treatment for hypoxemic RF?
- Long-term O2 therapy >15 hrs/day
~ If PaO2 is <7.3 kPa
What is the treatment for hypercapnic RF?
- Domiciliary (home) non-invasive ventilation
What is the treatment for Type III RF?
- Frequent changes in position, chest PT and control of pain
- NIV to reduce regional atelectasis
What is the treatment for Type IV RF?
- Intubation
- MV to redistribute CO away from respiratory muscles and back to vital organs while the shock is being treated
What is acute respiratory distress syndrome (ARDS)?
Clinical syndrome of
- severe dyspnea of rapid onset
- hypoxemia
- diffuse pulmonary infiltrates
Subset of acute lung injury (ALI)
- Condition characterized by widespread inflammation and increased permeability of the alveolar-capillary barrier, leading to pulmonary edema, hypoxemia, and reduced lung compliance
What are the 3 criteria to diagnose ARDS from ALI?
PaO2/FiO2 ratio:
- <200 (ARDS)
- <300 (ALI)
Bilateral infiltrates
- Present in ARDS
Pulmonary artery occlusion pressure (PAOP)
- <18 mmHg or no clinical evidence of left atrial hypertension in ARDS
What are the causes of ARDS?
- Bacteremia, sepsis
- Trauma, fractures, burns
- Massive transfusion
- Pneumonia
- Aspiration
- Drug overdose
- Pancreatitis
- Fat embolism
What is the pathophysiology of ARDS?
1) Injury to alveolar-capillary membrane
- Releases inflammatory mediators
~ Bronchoconstriction, vascular narrowing and obstruction, and pulmonary edema cause impairment in gas exchange
- Damages type II alveolar cell
~ Dec surfactant production causes atelectasis which dec lung compliance and impairs gas exchange
What are the complications of ARDS?
- Impaired gas exchange
~ V/Q mismatching - Dec lung compliance due to lung stiffness
- Pulmonary HTN
What are the stages of ARDS?
Stage 1 (Injury)
- Within 24 hours
- ^ dyspnoea and RR
- Coarse bilateral crackles
- Patchy infiltrates on CXR
Stage 2 (Exudative)
- 1-7 days
- Mediator induced interstitial and alveolar edema
- Damage to hyaline membrane formatio
- Increased permeability to proteins
- Hypoxia is resistant to supplemental O2
~ Requires MV
Stage 3 (Proliferative)
- 1-2 weeks after injury
- Hemodynamic instability
- Evidence of systemic inflammatory response syndrome (SIRS)
~ < 36 or >38 deg C
~ HR > 90
~ RR > 20/min
~ WBC <4000 cells/mm^3 or >12000 cells/mm^3
- Generalised edema, with denser and more fibrous lungs
- Thickened alveolar membrane
Stage 4 (Fibrotic)
- 2-3 weeks after injury
- Lung is remodelled by collagenous and fibrous tissues
- Increased dead space -> poor ventilation -> increased alveolar pressure
How to diagnose ARDS?
- During the first few days, ARDS will resemble acute cardiogenic PE
- Dx made on onset + additional tests
~ BNP (hormone released by heart failure or during ARDS)
~ Echo (can detect L ventricular dysfunction and valve abnormalities)
~ Pulmonary artery catheterisation (PAC) (only if there is pulmonary artery HTN)
What is the treatment for ARDS?
- Mainly supportive while waiting for lungs to heal
- Constant monitoring
- Treatment of underlying causes of ARDS
Ventilation vs oxygenation vs perfusion
Ventilation:
- Physiology of breathing
- Intact brain, nerves, respiratory muscles, non-collapsed alveoli
- No inflammation, bronchospasm
Oxygenation:
- O2 goes into pulmonary vessels
- Simple diffusion process at pulmonary-capillary bed
- Intact, non-thickened alveolar walls, basement membrane, no edema in interstitial space and intact capillary walls
Perfusion:
- Volume of blood to carry the oxygen
- Adequate blood volume, hemoglobin, non-occluded pulmonary capillaries and functioning heart
What is low and very low V/Q ratio?
eg in bronchospasm, bronchitis
- Impaired ventilation -> Alveoli does not get enough oxygen -> Alveoli loses its ability to exchange gases
- Perfusion is intact
- Still responsive to oxygen therapy
- Very low ratio when there are many alveoli affected (>80%)
~ Aka shunting - Not responsive to oxygen therapy as alveoli have collapsed and oxygen cannot enter
What is high V/Q ratio?
eg pulmonary embolism (?)
- Ventilation normal
- Perfusion compromised
