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
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!)
During ABCDE in a patient with decompensated congestive cardiac failure, how would you manage their circulation to address their fluid overload
Decompensated => cardiogenic cause as heart cannot pump properly => diuresis (furosemide) -> Ultrafiltration via haemodialysis
During ABCDE in adults, what are the steps in Disability step?
GCS/AVPU
Temperature
Pupils (PEARL)
Neck stiffness
Blood glucose
When inspecting the pupils during the ABCDE approach, there is no PEARL. You note constricted pupils. What is this called?
What is this a sign of?
How would you treat?
Miosis
Opioid toxicity
Naloxone IV 400mg -> 800mg ->2g 1minute apart
During ABCDE, what is done during the exposure step?
Abdomen inspection, palpation, and auscultation
Inspect for skin changes
Urinary output
Why is it crucial to examine the abdomen during the ABCDE approach?
Bowel obstruction shown via reduced bowel sounds/tinkling may cause:
1) Mass effect => Basal atelectasis
2) Precipitating vomit -> may lead to aspiration event => ARDS maybe?
What inflammatory cytokines are typically recruited when there is injury?
What causes the increased permeability?
TNF-alpha, IL1 and IL6.
These recruit neutrophils which release toxic mediators (oxygen reactive species and proteases) which increase permeability
Define ARDS. What is it? Explain via pathophysiology
Acute respiratory distress syndrome is the acute, diffuse form of lung injury causing increased alveolar-capillary permeability leading to respiratory failure and eventually non-cardiogenic pulmonary oedema
The injury causes inflammatory cytokines (TNF, IL1 and IL6) to respond to damage at the endothelium. These recruit neutrophils which release toxic mediators (oxygen reactive species and proteases) which increase permeability further.
Some will return to normal after this but many will progress to a fibroproliferative phase where the lung develops fibrous tissue and collagen deposition (barrier to diffusion) as with pulmonary fibrosis/restrictive lung disease
What are the causes/RFs to ARDS. What is the most common cause?
Sepsis is the most common cause
Viral pneumonia (COVID, Flu)
Aspiration event (from bowel obstruction?)
Inhalational injury (smoke, toxic fumes)
Burns
Pancreatitis
Fat embolism
What Criteria is used to diagnose ARDS?
Berlin Criteria
The Berlin criteria is used to diagnose ARDS. State what is included
Berlin criteria
1) acute onset within 1 week of insult
2) CXR - Bilateral diffuse opacities not explained by effusions, collapse, or nodules
3) ECG - Resp failure not fully explained by heart failure/fluid overload. !ECG (objective measure) needed to rule out hydrostatic oedema!
4) ABG - P/F ratio <300 (w/CPAP/PEEP of 5cm H2O)
What is BNP. What is it used for? What is it’s significance in ARDS?
B-type Natriuretic Peptide is released when the heart is attempting to compensate => released due to strain/stretching of the heart (increased resistance) => indicates degree of pulmonary oedema indirectly.
Typically used to diagnose HF. Used in ARDS to differentiate it from HF due to the similar sx. If <100 nanograms => ARDS as LHF unlikely. if >500 then HF
What investigations would you carry out along with expected findings in ARDS.
CXR - Bilateral diffuse opacities not explained by effusions, collapse, or nodules
ABG - P/F ratio <300 (w/CPAP/PEEP of 5cm H2O)
BNP - <100 nanograms
Septic workup: Blood/urine/sputum culture as sepsis is the most common cause
At what BNP level is it likely to be LHF instead of ARDS?
> 500 nanograms
When would you recommend a patient with ARDS to be prone? For how long?
What is the benefit of placing them in the prone position anyways?
prone position for 12hrs/day only if severe
In supine position, the majority of the lung sits beneath the weight and pressure of the heart and mediastinum => more pressure on lungs
=> in prone position, V/Q is more closely matched, there is an increased end-expiratory volume and also a reduced risk of ventilator-associated injury
When lying a patient prone for 12hrs/day. What part of the lung is most relieved with this maneuver (or most affected when in supine)?
Dorso-Caudal proportion of the lung
If all else fails, what are the rescue measure is used in ARDS?
Muscle relaxants. Why? less energy demand of muscles => less cellular resp
Vasodilators have a role but only in refractory cases as there is no evidence of it improving mortality
What is the normal FEV1 that we breathe in?
What is the normal PEFR?
FEV1 of 21% or 0.21 (which is why in the formula we assume 0.21)
normal PEFR is 20-30L, much closer to 20
What is the Haldane effect? (in the context of COPD)
How does the body compensate for it?
1) In COPD, the respiratory drive is often more dependent on hypoxemia than hypercapnia. Supplemental oxygen can blunt this drive leading to hypoventilation
2) When giving a COPD patient supplemental oxygen, Hb becomes more oxygenated => reduced affinity to CO2 (as per the oxygen dissociation curve). => Hb will dissociate from CO2 and release it into the blood stream. The body is much less efficient in removing CO2 from the blood => hypercapnia, confusion, and lethargy. Buffering systems is the way to clear the CO2 in the blood by binding with H2O to form H2CO3
What are the 3 ways that the body regulates pH
1) Buffering systems CO2 + H2O -> H2CO3 -> H+ + HCO3
2) Lungs PaCO2
3) Kidneys HCO3 and H+ elimination
What is the most common site for ABG? What are some others?
Radial is used the most often due to patient comfort and ease of access
Others: femoral, brachial, axillary
When is ABG indicated over VBG?
when accurate measurements of PaO2 and PaCO2 are needed. So basically whenever there is respiratory compromise
What is the normal range for HCO3? what is the baseline used in calculations
22-28 mmol/L
Calculations = 24mmol/L/ Used when estimating compensation
What is the normal range for PaO2 and at what point is it considered ARF?
Normal PaO2 is 11-13.5 kPa. Resp failure is <8
What is the stepwise approach to interpreting an ABG?
1) Assess oxygenation and Aa gradient
2) Check pH for acid-base disturbance
3) Is there a resp or metabolic component to it. Are they consistent with pH?
4) Is there compensation? Is it as expected?
5) Is there an anion gap? (for metabolic acidosis)
Can asthma cause respiratory alkalosis or acidosis?
Both
Give 6 causes for respiratory acidosis and 4 causes for respiratory alkalosis
Respiratory acidosis: (Think type 2 resp failure)
Restrictive: ARDS, Pulmonary fibrosis, bronchiectasis
Obstructive: Asthma, COPD
Others: Neuromuscular, polyneuropathy, chest wall deformities
Respiratory alkalosis: (Think of hyperventilation)
Pulmonary: Pulmonary embolism (PE), pneumonia, asthma, pulmonary oedema
Pregnancy
CNS: Head-injury, stroke, anxiety
Salicylates (Aspirin)
In terms of respiratory and metabolic acidosis and alkalosis. What can salicylates cause? Give an example of a salicylate.
Aspirin
Respiratory alkalosis
Metabolic acidosis (High anion gap)
Give 5 causes of metabolic acidosis with and without anion gap
No anion gap: USED CAR
Ureteral diversion
Saline infusion
Exogenous acid
Diarrhoea
Carbonic anhydrase inhibitors
Adrenal insufficiency/Addison’s disease
Renal Tubular acidosis
Anion Gap: MUDPILES
Methanol and ethanol
Uremia - Renal failure
DKA (ketones)
Propylene glycol
Isoniazid or Iron excess
Lactic acid -> dehydration
Ethylene glycol
Salicylates - Aspirin
Primary hyperaldosteronism is most likely to cause what acid-base status?
What do we expect to see in terms of serum electrolytes of K+ and Na+?
Metabolic alkalosis (H+ wasting)
K+ is also wasted => Hypokalaemia
Na+ is retained at the DCT => Hypernatraemia
Aldosterone saves sodium and water and Kicks out K+ and H+
Give 4 causes of metabolic alkalosis
H+ loss: Severe vomiting, loop and thiazide diuretics, excess mineralocorticoid (primary hyperaldosteronism)
HCO3- adminstration: Post-correction of metabolic acidosis for DKA/lactic acidosis
What is Base excess? Where is it seen?
ABG
Base excess is the amount of acid required to restore a litre of blood to a normal pH at a PaCO2 of 40mmHg
Base excess follows the direction of HCO3 as that is the base that is in excess
What is the inspired oxygen fraction in normal room air?
What is this measurement called?
21% or 0.21. Referring to FiO2
A patient is put on a non-rebreather mask at 10L/min 100%FiO2. His normal peak inspiratory flow is 30 L/min while on this. How much FiO2 is the patient receiving in total.
10L/min x 1 + 20L/min x 0.21 = 14.2L/min
There is a multitude of O2 delivery devices. They can be classified as low and high flow as well as fixed and variable. What is the difference between fixed and variable?
Fixed and variable refer to the FiO2. If it is variable that means the FiO2 can be modified.
There is a multitude of O2 delivery devices. They can be classified as low and high flow as well as fixed and variable.
1) List the variable devices (Honours + - with their FiO2 and Flow ranges) as well as whether they are low flow and high flow.
2) Only state the names of the Fixed devices and whether they are high or low flow
Variable:
Nasal Cannula (low flow) 24-40% FiO2 with flow 1-5L/min
Simple/Hudson face mask (low flow) 30-50% FiO2 with flow 5-10L/min
100% Non-rebreather mask (high flow) 60-95% FiO2 with flow 15L/min
Fixed:
Venturi mask (low)
HFNC (High flow nasal cannula)
What are the FiO2 ranges of the Venturi mask?
Although it is a fixed device, the amount of FiO2 can be modified via color coded parts which constrict the flow to a certain degree (venturi principle) but not as the patient is utilizing it
Range = 24-60% FiO2
What is the maximum flow available on HFNC?
60L/min
What are the benefits of using HFNC over the other methods of oxygen delivery (Honours +) Can put 5/5 if close to exam and useless at this point
1) Patient comfort via heat and humidification + avoids epithelial injury
2) Secretion clearance
3) Has PEEP due to high flow => reduced WOB and improved breathing pattern
Main Indications for HFNC (as part of the pathway of treating resp failure)
1) Type 1 failure as an alternative to NIV (thats why we skip NIV in the management of type 1 RF and go directly to mechanical ventilation after HFNC)
2) Post-extubation support (step down from IMV) in non-high risk groups (give BiPAP for that)
Contraindications for HFNC
Like any other device: burns, facial/nose/airway abnormality
What are some examples of NIV?
What are the different methods of administration?
CPAP and BiPAP
Can be delivered through nose plugs, nasal mask, face, mask, or helmet
What are the advantages of NIV over IMV?
Reduced lung injury (baro,volu)
Reduced risk of VAP
Reduced need for sedation
Can be managed outside ICU
When would you use CPAP instead of BiPAP?
Only for cardiogenic pulmonary oedema (Aka HF) as
Type 1 and asthmatics will go for HFNC instead
Type 2 with hypercapnia and CPAP gives no ventilation => BiPAP used instead
What are the main indications for BiPAP? (as part of the pathway of treating resp failure)
Type 2 RF after oxygenation
Post-extubation from IMV in high risk patients
When should ABG measurements be taken when commencing O2 therapy?
Before and after commencing oxygen therapy. Should be taken regularly throughout administration based on severity of the case to track improvement (and also write on the report if the patient was on room air or receiving therapy)
What are the complications of NIV
Discomfort ->Nasal bridge ulceration
Pneumonia
Barotrauma (still there although less than IMV by a lot)
Air leaks (pneumothorax)
Desynchrony
What is meant by compliance? Whats the formula?
Compliance is how elastic the lung is. If the lung is less compliant, then it wont expand much on inspiration (increased pressure) => inversely proportional to pressure and proportional to volume => compliance = Volume/pressure
What is meant by “trigger” when discussing modes of invasive ventilation
Trigger is what is used by the machine in IMV to detect when a patient is taking a breath in or out.
What are the benefits of PEEP?
PEEP provides expiratory pressure allowing for more recruitment of alveoli that are hypo ventilated => increasing compliance and preventing alveolar collapse
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
The I:E ratio or inspiratory:Expiratory ratio is an important parameter in IMV. How is it normally set? How is it normally set for patient with obstructive lung disease? Why?
In this example: I:E 1:3 and RR 10. Find the breath cycle duration and the duration in inspiration and expiration
Normally: 1:2 (1 second in inspiration followed by 2 seconds in expiration)
COPD and Asthma: 1:3 to prevent dynamic hyperinflation and intrinsic peep due to them needed more time to exhale
60s/10RR = 6s/breath cycle. Broken up into 1+3 parts => 6/4 = 1.5. => 1.5 spent in inspiration followed by 3x1.5s =4.5s in expiration
A 68yo female presents with worsening productive cough over the last 5 days. She is short of breath and unable to complete sentences PMHx: COPD, CKD Stage 3
Vitals: HR 115, BP 135/85, RR 30, SpO2 80% on RA, Temp 37.2.
On your review, she is noted to have diffuse bilateral wheeze + marked increased work of breathing. She was prescribed nebulised bronchodilators and PO prednisolone therapy in ED.
What would your immediate course of action with this patient be?
A - Apply Nasal cannula @ 4L O2 therapy
B - Apply Venturi Mask to provide 28% FiO2 therapy
C - Apply Non-rebreather 15L to provide 100% FiO2
D - Commence BiPAP at settings of IPAP 15 + EPAP 3
E - Urgent ABG to assess accurate O2 and CO2 level
15L Non Re-breather. Learning point = Hypoxia kills patients faster than hypercarbia and must be treated urgently in the acute setting.
A 77-year-old man with infective exacerbation of COPD is admitted to hospital. He is tachypnoeic, but haemodynamically stable. Results of an arterial blood gas (ABG) taken on 35% oxygen via facemask are:
pH 7.41, PO2 6.2 kPa, PCO2 5.0kPa, Bicarbonate 32mmol/L.
What does this blood gas demonstrate?
A - Metabolic acidosis with respiratory compensation
B - Respiratory acidosis with metabolic compensation
C - Type 1 hypoxaemic respiratory failure
D - Type 2 hypercapnoeic respiratory failure
E - I have no idea
The patient has COPD and the measurements of the ABG were taken as the patient was on 35% oxygen facemask
Given the patient’s arterial blood gas results:
pH is within normal range (7.35-7.45)
PO2 is low (indicating hypoxemia)
PCO2 is elevated (indicating respiratory acidosis)
Bicarbonate is within normal range
This blood gas pattern demonstrates Type 2 hypercapnic respiratory failure, which is characterized by hypoxemia and hypercapnia due to inadequate ventilation, commonly seen in patients with COPD exacerbation. Therefore, the correct answer is:
D - Type 2 hypercapnoeic respiratory failure
You are called urgently to the ward to review a 72-year-old woman who is admitted for investigation of abdominal pain. The nurses have called you as the patient is unresponsive and saturations are low.
The nurses inform you that the patient was recently given a large dose of IV sedation by one of the interns to facilitate an CT scan (as the patient has severe claustrophobia).
On review: Vitals: HR 88, BP 110/60, RR 2, SpO2 78% on RA, Temp 37.0
Which of the following is most appropriate Immediate action?
A - Apply Venturi Mask to provide 28% FiO2 therapy
B - Call for help and apply Non-rebreather to provide 100% FiO2
C - Call for help and begin bag mask ventilation
D - Commence CPAP
E - I have no idea
RR = 2 => he needs respiratory support via bag mask
A 70-year-old patient is on the respiratory ward where they are being treated with IV antibiotics + O2 therapy for a CAP on a background of COPD. On review late in the evening the patient appears tired, with increased work of breathing.
You perform an ABG (on Fi02 04) :
pH 7.28, PaO2 7.8Kpa, PaCO2 7.4Kpa, HCO3-:26 mEq/L
Vitals: HR 90, BP 120/80, RR 22, SpO2 88%, Temp 37.6.
On review she is tired but alert and orientated.
Which of the following is most appropriate in this case?
A - Apply Nasal cannula @ 4L O2 therapy
B - Apply Venturi Mask to provide 60% FiO2 therapy
C - Apply Non-rebreather to provide 100% FiO2
D - Commence BiPAP
E - Commence CPAP
D - BiPAP as she needs to ventilate the CO2 out
A 70-year-old patient is on the respiratory ward where they are being treated with IV antibiotics + O2 therapy for a CAP on a background of COPD. On review late in the evening the patient appears tired, with increased work of breathing. On review she is tired but alert and orientated.
You perform an ABG (on Fi02 04) :
pH 7.28, PaO2 7.8Kpa, PaCO2 7.4Kpa, HCO3-:26 mEq/L
Vitals: HR 90, BP 120/80, RR 22, SpO2 88%, Temp 37.6.
She has been on BiPAP for two hoursYou repeat an ABG and set of vitals to assess her progress.
pH 7.15 PaO2: 6.9 Kpa PaCO2: 11.9Kpa HCO3-30
Vitals: HR 93, BP 105/70, RR 20, SpO2 87%, Temp 37.6
She is now flexing to pain, but will not open her eyes + is only making incomprehensible sounds.
Which of the following is most appropriate in this case?
A - Apply Non-rebreather to provide 100% FiO2
B - Continue BiPAP with increased IPAP & EPAP & repeat ABG 1 hour
C - Commence CPAP
D - Urgent ICU referral for Intubation & Ventilation
Correct answer will be for ICU referral for intubation and mechanical ventilation. Learning point re: contraindications of BiPaP and when it is failing.
+
GCS is 5 => 8 or less => cannot reliably maintain airway => Intubate
