Acute Respiratory Failure + ARDS Flashcards
what is PaO2 and what is considered hypoxia?
Partial pressure of oxygen in the arteries. Hypoxia is when PaO2 <8 kPa
What is considered hypercapnia?
PaCO2 >6.7 kPa
What is the normal pH range?
7.35-7.45
Is hypoxaemia the same as saying reduced tissue perfusion?
No, shock, hypotension, and VTE also all lead to reduced tissue perfusion whereas hypoxaemia just means low O2 in blood (reduced PaO2)
What are the classifications of Acute Resp Failure (3) with the definition (cutoffs) of each
Acute Type 1: Hypoxia without hypercapnia (PaO2 <8, normal/low CO2 (hyperventilation), pH normal)
Acute type 2: Hypoxia with hypercapnia (PaO2 <8, PaCO2 >6.7, pH <7.35)
Chronic Type 2: Hypoxia with hypercapnia (PaO2 <8, PaCO2 >6.7, Ph normal)
Why is the pH normal in chronic type 2 ARF
Renal compensation with bicarbonate and elimination of H+ but this takes days to weeks compared to the acute version which is hours
What is the difference between hypoxia and hypoxemia?
Hypoxia is the reduced O2 in tissues (hypoperfusion) whereas hypoxemia is reduced PaO2 (in the arteries)
Hypoxemia occurs due to failure of gas exchange as a result of 5 mechanisms. List each of these mechanisms and their effect on PaO2 and PaCO2.
Shunt V=0 (fluid or exudate clogging alveoli) => mostly reduced PaO2
V/Q mismatch => Regional deadspace ventilation and/or intrapulmonary shunting. It reduces PaO2 while increasing PaCO2
Hypoventilation: by definition reduced ventilation leading to reduction PaO2 while increasing retention of PaCO2
Diffusion limitation: reduced PaO2
Reduced inspired O2 tension: Reduced PaO2 (high altitude)
What is normal V/Q?
There are physiological differences within the lung based on different zones which are more evident when diseased causing V/Q mismatch. Explain this
What are the 2 most common causes of this acutely?
Normal V/Q = 1
The apices of the lung receive the most ventilation but least perfusion whereas the lower regions of the lung are better perfused but more ventilated. => V/Q is highest at the apices and lowest at the bases.
Acute causes: PE, Pneumonia
Oxygen dissociation curve: Explain the curve and the factors affecting it (causing a shift)
The curve represents Hb’s affinity to oxygen at different pressures of oxygen. As PaO2 increases it is more likely to be picked up by Hb. An Hb molecule can hold up to 4 molecules of oxygen with each subsequent one being more difficult to bind to. This is affected by several factors.
Left shift: Better for picking up oxygen in an oxygenated part of the system. Better during exercise. Low acidity (high pH), CO2, Temp, and DPG will shift the curve left
Right shift: Better for tissue perfusion. High acidity (low pH), CO2, Temp, and DPG will shift the curve right. This means that oxygen will be more likely to dissociate from Hb and diffuse across the membrane in areas with low perfusion (high CO2)
What mechanisms may lead to hypercapnia (2) and their effect on PaO2 and PaCO2
Hypoventilation: reduction PaO2 while increasing retention of PaCO2
Dead space areas where Q=0. No diffusion. increases PaCO2
What does the A-a gradient stand for
Alveolar to arterial oxygen gradient
Indicate the effect of each of the following mechanisms of hypoxaemia on the A-a gradient:
Reduced inspired O2 (PiO2/FiO2):
Hypoventilation:
Diffusion limitation:
V/Q mismatch:
Reduced inspired O2 (PiO2/FiO2): Normal
Hypoventilation: Normal
Diffusion limitation: Increased
V/Q mismatch: Increased
Indicate the effect of each of the following mechanisms of hypoxaemia on the A-a gradient:
Pulmonary Embolism:
Pneumonia:
High altitude:
CNS depression:
Morbid obesity:
Emphysema:
ILD:
Pulmonary Embolism: Increased
Pneumonia: Increased
High altitude: Normal
CNS depression: Normal
Morbid obesity: Normal
Emphysema: Increased
ILD: Increased
What is the most common RF for increased physiological dead space?
COPD
What are the 2 different types of deadspace
Anatomical deadspace: Normal, space between upper airway and bronchioles where no gas exchange happens
Physiological/alveolar deadspace: pathological, dead space in alveoli where gas change should be occurring
What diseases may cause diffusion limitation?
Interstitial lung disease, fibrosis, and emphysema. Anything that thickens or disrupts the alveolar-capillary barrier
List the causes of type 1 and type 2 ARF (5 each)
Common: Acute COPD and ARDS (more likely type 2)
Type 1: Acute Asthma, Pulmonary fibrosis, ILD, pneumothorax, pulmonary embolism!!, CHD (shunt), Bronchiectasis, !pneumonia,
Type 2: Severe asthma, pulmonary oedema, opioid/benzo/alcohol overdose, Neuromuscle disorders (myasthenia gravis), CNS depression, Chest wall deformities, polyneuropathy, cervical cord injury, !obestiy hypoventilation syndrome!
Quick History questions in ARF
Dyspnea
Recent illness/Sick contacts
Cough
Wheeze
Fever
Constipation
Smoking
Head injury
Swallowing difficulties
Past med for COPD, asthma, CHD, muscular disorders
What is the tidal volume?
This is the volume of air moving in and out during normal respiration
What is the inspiratory capacity? How is it calculated?
active volume of air inhaled during maximum inhalation
Tidal volume + inspiratory reserve volume
how is inspiratory reserve volume calculated?
Inspiratory capacity - tidal volume
What is vital capacity?
Volume of air breathed out after deepest inhalation
What is PEFR?
What is the normal PEFR?
PEFR is closely related to another measure which is used to assess severity of ARF. What is that measure and how is it used to identify severity?
Peak expiratory flow rate where normal is 20-30L/min
Closely related to FEV1 which is forced expiratory volume in 1 second
FEV1 <75% of baseline is considered moderate
<50 is considered severe
<33 is considered life threatening
You begin ABCDE approach on a patient with ARF and notice their SPO2 is quite low at 85%. You decide to apply a non-rebreather mask when a colleague stops you to say theyre hypercapnic. What will you do? be very specific
Why do you think the colleague brought up that point?
Apply non-rebreather mask at 15L/min at 100% FiO2. Why?
Even if the patient is hypercapnic, hypoxemia will kill first. In this case we will use the ABG to then titrate accordingly later when the patient is stable.
The colleague brought up the point because giving oxygen to a patient who is hypercapnic (e.g. COPD) will increase the V/Q mismatch leading to CO2 being released into the blood from the RBC (called the Haldane effect) => the body has no effective way of clearing it => worsening hypercapnia. Buffering system needs to compensate
How would you manage a patient presenting with type 1 ARF. Give plan with escalation plans
aim = achieve sats of >93%
2 parameters to adjust that which are FiO2 and flow rate
start with low flow systems e.g. low flow nasal cannula, simple face mask, and venturi
before escalating to high flow systems (non-rebreather and HFNC)
CPAP only for ARF due to cardiogenic pulmonary oedema (e.g. HF)
If none of these work => intubation and ventilation
How would you manage a patient presenting with type 2 ARF. Give plan with escalation plans
Aim = controlled oxygenation to achieve sats between 88 and 92, avoid worsening hypercapnia and iatrogenic harm
Step 1: controlled oxygenation => same as type 1 in terms of starting with low flow before high flow to achieve target saturations. MUST HAVE: we must ensure that we then wean off oxygen with close monitoring of ABG
Step 2: Non-invasive ventilation
BiPAP (IPAP at 15cm H2O, EPAP at 3cm H2O and target 88-92% sat)specifically indicated for COPD with hypercapnia >6.7 and pH <7.35, neuromuscular disease, obesity hypoventilation syndrome, and ARDS (so go with this)
If this does not work escalate to Invasive mechanical ventilation
What are the contraindications for non-invasive ventilation (NIV)?
Urgent need for intubation (cardiac/pulmonary arrest, organ failure),
altered conciousness GCS <8
Pneumothorax,
Fixed upper airway obstruction,
Severe facial deformity or facial burns
Active vomiting
BiPAP is a great machine used to deliver oxygen while allowing removal of CO2. What is the target?
When is this indicated?
BiPAP (target 88-92% sat)
specifically indicated for T2RF (with hypercapnia >6.7 and pH <7.35)e.g. for COPD, neuromuscular disease, obesity hypoventilation syndrome, and ARDS
What are the indications and risks of IMV (invasive mechanical ventilation)?
Indications:
ARF with failure of other therapies (O2 and NIV)
GCS 8 or under (<9)
Work of breathing too great for patient to maintain
Respiratory arrest/ severe resp depression
Risks:
Lung injury (volutrauma and barotrauma)
VAP (ventilator associated pneumonia)
myopathy
What are the two types of lung injury from IMV?
What can they lead to?
Volutrauma = distention via excessive tidal volume
Barotrauma = Alveolar distension due to high flow pressure
these can lead to Pneumothorax, pleural effusion, atelectasis.
During respiratory acidosis, the kidneys perform 2 functions to try and compensate. What are they?
Increase production of bicarbonate
increase elimination of H+
What is used to determine the severity of ARDS? How is it calculated? What are the values for normal, mild, moderate, and severe?
P/F ratio is used to determine the severity of ARDS by comparing the inspired oxygen (FiO2) to arterial oxygen levels (PaO2)
The formula is PaO2/FiO2. PaO2 is obtained from the ABG
FiO2 = 0.21 (FiO2 without O2 therapy) + (0.03xO2 flow rate in L/min)
Measurements are taken when the patient is on CPAP/PEEP of 5cmH2O
Normal >500 mmHg
Mild <300 Moderate <200 Severe <100 mmHg
What is the A-a gradient? What is it used for?
What is the normal A-a gradient?
In a patient with respiratory distress,
What would a normal A-a gradient indicate?
What would a raised A-a gradient indicate?
The A (alveolar)-a (arterial) gradient (PAO2 - PaO2): measures the difference in pressure of oxygen within the alveoli and the arterial system.
Measures integrity of alveolar-capillary interface
Normal gradient is 10-15 mmHg
Normal gradient = Hypoventilation or reduced inspired O2 tension (FiO2)
Raised gradient = Diffusion abnormality or V/Q mismatch (shunt, deadspace)
Helps narrow ddx
You are asked to see a patient with ARF. In terms of vitals, what do you expect to see?
On inspection of the patient what do you expect to see?
What other emergency should you be aware about as it presents very similarly?
Similar to sepsis (emergency we’re worried about)
Vitals: Increased RR and HR. Reduced BP, SpO2, and GCS
Inspection: Tripod positioning, altered mental status, Signs of increased work of breathing (accessory muscles, recession, nasal flaring)
What is the target SpO2 in COPD? Hypercapnia? Type 1 RF
COPD and Hypercapnia = 88-92
Type 1 RF = <92 (93 or more)
How do you medically reverse:
Alcohol OD
Opioid
Benzo
Alcohol: Naltrexone
Opioid: Naloxone IV 400mg -> 800mg ->2g 1minute apart
Benzo: Flumazenil IV 200mg (may precipitate seizures)
What is atelectasis?
Partial or full lung collapse
For each of the following types of Hypoxia, briefly state what it means.
Hypoxic Hypoxia: Everything were studying
Anemic hypoxia:
Ischemic hypoxia:
Histotoxic Hypoxia
Hypoxic hypoxia: Everything were studying
Anemic Hypoxia: CO poisoning
Ischemic Hypoxia: Low cardiac output (cardiogenic)
Histotoxic Hypoxia: Cyanide toxicity affecting electron transport chain in mitochondria
What are the signs of a life-threatening ARF
Same as Asthma
FEV1<33% baseline –> ACHEST
Altered GCS
Cyanosis
Hypotension
Exhaustion (low or normal CO2)
Silent chest
Tachycardia