Respiratory Failure Flashcards
How does acute respiratory failure present and what diseases is part of it?
- Heterogenous disease presentation (presents differently between patients)
Can present as:
-CF
-pulmonary hypertension
-pneumonia
-COPD exacerbation
What name do we group all diseases that cause acute respiratory failure?
Acute Respiratory Distress Syndrome (ARDS)
What do we use to classify ARDS?
The Berlin definition
How can we classify respiratory failure? (3)
-Acute
-Chronic
-Acute on chronic
What do we see in type 1/ hypoxemic resp failure?
- Failure of oxygen exchange
- PaO2 <60 at sea level
-Increased shunt fraction (QS/QT)
-Hypothermia refractory to supplemental oxygen
What does an increased shunt fraction mean?
More blood transported through lungs without taking part in gas exchange
What are some causes of type 1/ hypoxemic resp failure? (6)
- Collapse of lobe
- Aspiration (inhaling foreign material)
- Fibrosis
- Pulmonary oedema
- Pulmonary embolism
- Pulmonary hypertension
What is type 2/ hypercapnic resp failure, some characteristics.
- Failure to exchange or remove CO2
- Decreased alveolar minute ventilation
- Dead space ventilation
What causes of type 2 resp failure are there? (5)
- Nervous system issues
- Neuromuscular issues
- Muscle failure- muscles too tired to maintain tidal volume
- Airway obstruction
- Chest wall deformity
Why shouldn’t patients with chronic hypercapnic resp failure be given liberal O2?
It can exacerbate resp failure,
the O2 doesn’t maintain hypoxic drive to breath.
This means O2 sats in these patients is and should be 88-92%
What is atelectasis?
collapse of entire lung or lobe
What is hypoxemia?
Hypoxemia is a medical condition in which there is an abnormally low level of oxygen in the blood.
What is hypercapnia?
Hypercapnia is a medical condition in which there is an abnormally high level of carbon dioxide (CO2) in the blood.
What is functional residual capacity?
Functional residual capacity (FRC) refers to the volume of air left in the lungs after a normal, passive exhalation
When does type 4, respiratory failure aka shock happen?
- This happens in intubated and ventilated patients during shock (septic/cardiogenic/neurologic)
- Poor perfusion of the lung so gas can’t come into blood
What does it mean when a patient becomes vasoplegic
Low systemic vascular resistance → low bp despite normal/raised cardiac output.
What happens to a vasoplegic patient. In terms of blood flow
Blood pools in the peripheral, not much return of blood to pulmonary vasculature.
Leads to significant drop in pulmonary perfusion.
What are the effects of the ventilator on the left ventricle and right ventricle?
- Good for LV because it reduces afterload on heart so stress on heart muscle wall is reduced because the pressure in the chest being raised means heart muscle does less work as the pressure gradient between LV and thorax is lower
- Bad for RV because it increases preload- as you increase pressure in thorax its harder for RV to fill with blood and its contractility is also affected
What is the overal mechanism of acute lung injury?
-Alveolar macrophages get activated by inflammation/infection, release further cytokines → IL-6 and 8, TNF alpha.
-This leads to alveolar protein rich oedema building up.
-Neutrophils migrate into the interstitium and cause some damage
-More oedema builds up increasing the distance between capillary and alveoli
-Increases the distance for gas exchange
What makes the alevoli less efficient in expanding in acute lung injury?
Activation of surfactant
What in vivo evidence do we have for acute lung injury? (5)
- TNF signalling implicated- reduced injury of alveolar lung injury by blocking TNFR-1 signalling pathway with Ab or using TNFR-1 knockouts
- Macrophage activation occurs in alveolar space and neutrophil lung migration also occurs
- DAMP release (commonest for lung are HMGB-1 and RAGE)
- Cytokines are released e.g. IL-6, 8, IL-1B, IFN-gamma (this is important for viral response and T cell differentiation)
- Cell death- there is necrosis in lung biopsies, and also apoptotic mediators e.g. FAS, FAS-I and BCl-2
What can we split therapeutic intervention for ARDS into?
-Treating the underlying disease
-Respiratory support
-Multiple organ support
What is the main ARDS specific intervention?
Positive pressure ventilation
What two things can we control in positive pressure ventilation?
-Volume
-Pressure
What 2 pressures do we have in this ventilation and why?
- Peak pressure: drives air into lung
- Underlying base pressure: keeps airway open
How does the pressure-volume loop change for ARDS from normal?
- ARDS lung is much stiffer so volume is reduced and more pressure is used at the top to get very little gain in volume increase
- Lung can drop below lower inflection point leading to lung collapse
What is the reason for high thoracic volume in COPD and asthma patients?
COPD and asthma patients have high thoracic volume because they don’t completely exhale on the ventilator.
What is breath stacking?
Breath stacking is the trapping of air in the lung, which leads to increased pressure in the lung, making it difficult to efficiently ventilate the patient.
Why does breath stacking make the control of CO2 harder?
Breath stacking makes the control of CO2 harder because minute ventilation is difficult to get right.
What do we have to set to prevent breath stacking?
We have to set a TIME for exhalation to be long enough for enough gas to leave the lung.
NOT TOO MUCH PRESSURE to drive air into the lung.
What is PEEP?
Positive end expiratory pressure,
Why do COPD and asthma patients have an intrinsic level of PEEP?
COPD and asthma patients have an intrinsic level of PEEP because their chests are always open due to their lung disease.
What happens when we use a lower pressure for COPD and asthma patients?
If we use a lower pressure, COPD and asthma patients have to work much harder, which can tire out the patient’s muscles.
What imaging is used for ARDS patients? (2)
-Lung recruitment CT
-Lung ultrasound
What system do we use for escalation of ARDS therapy?
Murray score
