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
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 => Everything can cause this. 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
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.
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 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. Anything that thickens or disrupts the alveolar-capillary barrier
List the causes of type 1 and type 2 ARF
Common: COPD and ARDS (more likely type 2)
Type 1: Asthma, Pulmonary fibrosis, pneumothorax, pulmonary embolism!!, CHD (shunt), Bronchiectasis, !pneumonia, Acute asthma
Type 2: Severe asthma, pulmonary oedema, opioid/benzo/alcohol overdose, muscle disorders (myasthenia gravis), 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? What is it composed of?
Volume of air breathed out after deepest inhalation
Either Inspiratory capacity + Expiratory reserve volume
or inspiratory reserve + tidal + expiratory reserve
How is residual volume calculated?
Total lung capacity - vital capacity
What are your initial investigations to conduct for any patient with ARF?
What are some considerations for later?
Initial: (all)
1) Bedside: ECG + PEFR (peak expiratory flow rate)
2) Lab: ABG + U&E + LFTs {+Troponin if suspected ACS, +BNP if suspected HF/ARDS, + D-Dimer if suspected PE/DVT}
3) Radiological: CXR, US
4) Micro: Swab (flu and COVID - causes of ARDS), Septic screen (Blood culture, urine culture - most common cause of ARDS)
Later (3): CT thorax if findings on radiograph
Urine/serum toxicology if suspected toxic/drug as cause
CT angio if D-dimer +ve
PFT (not in acute)
Urinary antigens (legionella and S. pneumo)
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 have identified that a patient is undergoing ARF, state your initial management?
ABCDE approach
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
Briefly state how you will manage a patient with acute exacerbation of pneumonia as the cause of ARF?
How about COPD?
Pneumonia: ABCDE + antibiotics
COPD: ABCDE + bronchodilators + steroids
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
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 relative and absolute contraindications for non-invasive ventilation (NIV)
Relative (all): Serum pH <7.15 or <7.25 with GCS<8 or evidence of cognitive impairment
Absolute (4): Urgent need for intubation (cardiac/pulmonary arrest, organ failure), altered conciousness, Pneumothorax, fixed upper airway obstruction, facial burns, severe facial deformity
BiPAP is a great machine used to deliver oxygen which allowing removal of CO2. How would you set up the machine?
When is this indicated
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
What are the indications and risks of IMV (invasive mechanical ventilation)?
Indications:
ARF with failure of other therapies (O2 and NIV)
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
IMV (invasive mechanical ventilation) may cause lung injury leading to pneumothorax or sometime atelectasis. What are the two types of lung injury from IMV?
Volutrauma = distention via excessive tidal volume
Barotrauma = Alveolar distension due to high flow pressure
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?
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 = 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 were 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 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
What are the 4 different types of hypoxia (brief description of each)
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
FEV1<33% baseline –> ACHEST
Altered GCS
Cyanosis
Hypotension
Exhaustion (low or normal CO2)
Silent chest
Tachycardia
An asthmatic patient is having acute exacerbation and has an FEV1 of 60% baseline. You commence ABCDE. What severity would you classify this?
Run me through what drugs you will administer from first-line to last
Moderate exacerbation
1) Oxygen therapy to achieve 93% SpO2
2) Salbutamol 5mg every 15 minutes via nebulizer for 3 doses and then 4-6 hourly
Ipratropium bromide 0.5mg 4-6 hourly
3) PO prednisolone 40mg QDS (if can take orally)
If not then give IV hydrocortisone 200mg STAT then QDS
4) If all fails => IV magnesium 2g over 20 mins and ICU referral
An asthmatic patient is having acute exacerbation and has an FEV1 of 35% baseline. You commence ABCDE. What severity would you classify this?
Run me through what drugs you will administer from first-line to last
Severe exacerbation. Borderline of life threatening => look for ACHEST
1) Oxygen therapy to achieve 93% SpO2
2) Salbutamol 5mg + Ipratropium bromide 0.5mg back to back x3 before going 4-6 hourly
3) Assuming its too severe for PO 40 mg prednisoloine, IV hydrocortisone 200mg STAT then QDS
4) If all fails => IV magnesium 2g over 20 mins and ICU referral
You are asked to see a child with ARF. You notice there is an audible stridor. What additional precaution would you take during ABCDE assessment of this child
Do not put anything in their mouth and avoid invasive procedures unless necessary as it can cause complete airway obstruction
During B in ABCDE, CO2 retention is evident as PaCO2 is 8.5 despite oxygenation. They have a history of obesity hypoventilation syndrome but is stable now. How would you manage this hypercapnia?
BiPAP (!target 88-92% sat!)
What is the difference between intrinsic and extrinsic PEEP?
What are the most common causes (2) of intrinsic PEEP?
Explain the pathophysiology of intrinsic PEEP
Explain how intrinsic PEEP is obtained
How is this issue rectified?
Extrinsic PEEP = Pressure given by ventilator at the end of expiration
Intrinsic PEEP = Pressure left in the alveoli (without the ventilator) due to incomplete exhalation
Most common causes: Obstructive lung diseases => COPD and Asthma Why?
Bronchoconstriction leaves air in the lungs every time as there is not enough time to exhale it all out before needing another breath. => air is built up with every breath causing DYNAMIC HYPERINFLATION.
Intrinsic PEEP is calculated via the EXPIRATORY HOLD MANEUVRE. This measures the end-expiratory pressure after triggering by the machine is disabled for a while allowing for the pressure to settle at a non-zero amount.
The patient needs a longer amount of time to compensate for the intrinsic peep and hyperinflation. This is done by increasing the I:E ratio to 1:3 instead of 1:2
Explain Plateau Pressure
How is it obtained?
It is the static pressure in the alveoli and small airways at the end of inspiration. This is calculated via the INSPIRATORY HOLD MANEUVRE which measures the end-inspiratory pressure. This is done by asking the patient to take a deep breath and then stopping flow while holding their breath. The air pressure of the ventilator after this will be the plateau
