Teaching clinic: Acute respiratory failure Flashcards
What is type 1 RF?
T1RF: Hypoxemic (decreased sO2 –> increased tissue hypoxia –> serum lactate)
T2RF: Hypercapnic
covid 19 patient who needs 6LPM of O2 via nasal cannulas to keep his SpO2 at 88%?
Requires ABG to diagnose respiratory failure: likely T1RF.
Tissue hypoxia causing increased lactate (hypoxemic but tissue can be well perfused)
mechanisms of oxygenation failure (type 1 RF)
- Hypoxia
- Alveolar hypoventilation
- Alveol-arterial block
- Ventilation perfusion mismatch (most common in clinical practise)
- Shunting
type 2 RF mechanism
PaCO2 inversely related to Minute Alveolar Ventilation
– increases alveolar dead space: e.g. COPD
Drugs: sedatives, neuromuscular blockers
Muscle weakness: myasthenia gravis
Central apnoea: idiopathic, COPD
Restrictive Lung Diseases: Kyphoscoliosis
Diaphragm fatigue: during weaning from ventilators
VQ mismatch mechanism
- areas with high ventilation and low perfuson: alveolar dead space
Areas with low ventilation and high perfusion
* Blood not oxygenated
* Venous blood return to arteries = shunt
* Results in hypoxemia
What is the VQ mismatch in APO?
What is Mx?
O2 therapy doesnt help: cant reach blood vessel
Mx: CPAP
What is expected changes in ABG of patient after R upper lobectomy, if the rest of his lungs are normal?
What about lung function parameters?
- Test for this patient upon recovery from surgery: should be no changes
- TLC will decrease, FEV1/FVC ratio same, FVC decrease, DLCO will decrease (difusing area less), transfer factor (same as it measures the capacity to transfer gas from alveolar spaces into the alveolar capillary blood)
Patient with pneumonia, what would you expect of the blood gases of this patient
pO2 low (marker of severe pneumonia: degree of shunting)
pcO2 normal
VQ shunting (through area of consolidation the blood doesnn’t pick up O2)
L lung collapse due to L main bronchus obstruction by a tumor
What would you expect of the ABG?
pO2 low (massive shunting T1RF)
pCO2 normal (there is no dead space, hypoventilation) even if 1 lung
One breath of 600ml vs 2 breaths of 300ml which is better if want to exhale CO2
One breath of 600ml is better than 2 breaths of 300ml (wasting 150ml with dead space)
Physiological dead space:150 ml (upper airway to respiratory bronchial –> anatomical deadspace)
If 2 breaths of 300ml –> more prone to T2RF
- A normal young male patient sustained multiple ribs fractures in a blunt contusion to the R chest in a traffic accident.
- Will he have Respiratory Failure if 4 ribs were broken?
- Depends on if its complicated rib fracture
- Tension pneumothorax (air goes in, can’t come out): will likely cause lung collapse (increased intrapleural pressure) –> resulting in T1RF
- Flail chest: 2 consecutive ribs broken at the same site. There will be collateral ventilation (some fresh air and dead air from the flail lung side) and shallow breathing (wasted lots of ventilation) –> T2RF. Likely to go into respiratory arrest. Give CPAP (no more cross ventilation)
does moderately sized primary spontaneous pneumothorax typically have respiratory failure?
What is the ABG?
pO2 normal
if other lung is normal pCO2 will be normal
Uncomplicated pleural effusion and pneumothorax will not affect gaseous exchange
If pO2 low think about another underlying disease: can be secondary pneumothorax, COPD, underlying shunt (collapsed lung)
ABG of severe acute asthma
low pO2 (more alveolar shut so more VQ shunting): degree of shunting reflects degree of bronchospasm
high pCO2: hypoventilation
ARDS definition
Berlin definition 2012
if on CPAP and pulmonary edema –> decreases shunting as expands the alveoli –> should improve
ARDS pharmacological treatment
- So far, no drugs proven to improve prognosis in ARDS
– Standard of Care now involves proper care of Ventilation and Care for Respiratory Failure - Drugs that have been shown NOT useful
– Nitric oxide (NO)
– Surfactant
– Systemic Steroids
Can Patients Have Type I Respiratory Failure with Normal/Near Normal Looking Lungs on CXR?
- Asthma
- COPD (can have normal CXR but abnormal physiology)
- Early stage ILD (dx by HRCT and lung function test)
- Pulmonary embolism (T1RF due to pulmonary-systemic shunting): post op patients
- R to L shunt (intracardiac): eisenmenger syndrome, TOF (VSD, pulmonary stenosis, overriding aorta, RVH)
- Primary pulmonary hypertension (30-60 yo female): normal lungs but PAH causing right heart failure
- Intrapulmonary shunting: AV malformations –> Hereditary hemorrhagic telangiecasia (osler weber randu syndrome). Fatal intracerebral bleed (cerebral AVM), haemostasis, haemoptysis. Inheritance: autosomal dominant. Can do prophylactic embolization.
COPD: dx by spirometry (show obstructive pattern that is not fully reversible). Does not require CXR to diagnose.
Forms of non invasive positive pressure ventilation
More pressure cycled ventilators for NIPPV now are semi closed circuits
Approach for type 1 respiratory failure?
Algorithm for acute cardiogenic pulmonary edema
Algorithm for mx of acute exacerbation of COPD
Algorithm for severe acute asthma
What is the oxygen cascade?
When doing ABG it is to detect the issue above the tissues.
There is massive reserve in tissues before becoming hypoxic tissue
