BASIC Flashcards
Define respiratory failure
The inability for the respiratory system to meet the metabolic demands of the body by supplying oxygen and removing carbon dioxide
Type 1 - hypoxic - PaO2 <60
Type 2 - hypercapnic - PaCO2 >50
What are the 4 major pathophysiological mechanisms of respiratory failure?
- Low inspired partial pressure of oxygen
- Hypoventilation
- V/Q mismatch
- Diffusion abnormality
What is the Aa gradient, what is it used for?
The gradient between the partial pressure of O2 in the alveolus (PAO2) vs the arterial blood (PaO2)
Used to determine whether a shunt or diffusion abnormality is present
should be<20mmHg - affected by age and FiO2
normal implies hypoxameia is caused by hypercapnea
How is pAO2 calculated?
Alveolar gas equation:
pAO2 = FiO2 (PB-SVPH2O) - PaCO2/R+F
PB= barometric pressure 760mmHg at sea level SVPH2O= saturated vapour pressure of water 47mmHg at 37 degrees R= resp quotient carbon dioxide made from O2 consumed (usually 0.8) F= correction factor (minor and ignored)
pAO2 = (FiO2 x 713) - (PaCO2 x 1.25)
What are the causes of hypoventilation?
Resp Centre: head injury, encephalopathy, anaesthesia/drugs
Nerves: cord injury, GBS, MND
NMJ: MG, neuromuscular blockade
Muscles: myopathy, muscular dystrophy, malnutrition
Wall: kyphoscoliosis, ank spond, pleural fibrosis
lungs: APO, pneumonia, haemorrhage, ARDS
What are the causes of VQ mismatch?
V Pneumonia APO Atelectasis Haemorrhage
P
PE
Low cardiac output (and all associated causes eg Hypovolaemia)
high intrathoracic pressures
Anatomical shunting - Eisenmenger, TOF
What is the oxygen delivery equation?
O2 delivery = CO x Oxygen content
DO2 = CO x Hb x SaO2 x 1.34 + free O2 (PaO2x0.003)
What should be available for emergency airway equipment?
- O2
- Mask
- Airways - OPA/NPA/LMA
- Laryngoscopes
- ETTs
- Monitors (ECG/SaO2/ETCO2)
- Emerg drugs
- Suction
- self inflating bag mask
What size LMA would you use for a female? large male?
3 for female, 5 for large male
Sizes of Macintosh blades?
2,3,4
Sizes of ETT for male/female? normal depth?
8-9 for male, 7-8 for female
22-23cm depth
complications of ETT placement?
Meds
- hypotension
- anaphylaxis
- arrhythmias
Placement
- trauma (dental/soft tissue)
- incorrect placement (endobronchial > PTx)
- HTN/Tachycardia
- raised ICP
- hypoxaemia
- aspiration/laryngospasm
longterm
- laryngeal/tracheal stenosis
How is airway pressure calculated? Alveolar pressure?
Airway Pressure = Flow x Resistance + (volume/complicance) + PEEP
Alveolar pressure = (volume/complicance) + PEEP
Flow = Volume/time
How can shunting be reduced by mechanical ventilation?
reopening alveoli, keeping them open with PEEP, prolonging inspiration (more even distribution of ventilation)
How is alveolar ventilation calculated?
Alv Vent = RR x (Tidal Volume - Dead Space Volume)
How can O2 be improved using mechanical ventilation? CO2?
O2 improved by:
- increasing FiO2, PEEP, insp time
CO2 removal improved by:
- Increasing TV, RR (MV)
- Decreasing deadspace
What is gas trapping? what value increases with gas trapping?
- occurs with insufficient time for alveoli to empty before next breath (worse with airway obstruction Asthma/COPD). Causes progressive hyperinflation and rise in intrinsic PEEP
- can result in barotrauma and cardiovascular compromise from high ITP
What is set in Volume preset assist control?
TV + RR
same breath delivered whether pt or vent triggers
pt can breath above the prescribed rate
uncomfortable, needs sedation
risk of barotrauma with fall in compliance
difficult to set flow trigger correctlty
What is set in Pressure preset assist control?
Insp P + RR
because flow falls to zero if the breath is long enough and stays there as long as you apply pressure an insp hold is built in to each breath and improves oxygenation
pt can breath above the prescribed rate
uncomfortable, needs sedation
risk of changes in tidal volume with change in compliance
What is set in Pressure support?
insp pressure
only delivered when pt triggers a breath
(on newer vents will switch to backup if no triggers)
swaps to exp when the insp flow falls to a preset level
need some support to overcome added work of breathing through ETT and demand valve of ventilator
What is set in Synchronized intermittent mandatory ventilation (SIMV) ?
RR and either insp P or V (more common)
usually combined with pressure support
set number of mandatory breaths and pt can take additional PS breaths between
if pt breaths in SIMV period will deliver a mandatory breath
if pt breaths in spont period will PS
these periods are determined by the set RR
What are reasonable starting settings for FiO2, RR, TV, insp P, I:E, PEEP, triggering?
FiO2 - 100 then adjust to PaO2 or SaO2
RR- 12 (higher if high metabolic rate)
TV- 6-8mL/kg PREDICTED BW
Insp P - set to acheive a good TV, sum of PEEP and insp P should not be >30cmH2O
I:E - 1:2 is normal, higher (1:1) is better for oxygenation but worse for gas trapping
PEEP - 5cmH2O (unless asthma or COPD and not spont breathing then 0)
Triggering - flow or pressure. flow leads to more synchrony but is more sensitive. usually start with pressure -2cmH2O or mod sensitive flow
Describe the how the respiratory cycle time, and inspiratory time are calculated
Respiratory cycle time = 60/RR
Resp cycle time = insp time + exp time
exp time is not set
insp time = insp flow time + insp pause time
therefore you can only set 2 of insp time, insp flow time and insp pause time
remember flow = volume / time
Which lab value should be used to titrate minute ventilation?
In general pH should be used to titrate MV and not CO2 as the pathophysiological consequences of raised CO2 are mediated by acidosis.
Note raised ICP is an exception to this
What are causes of high airway pressure in volume preset modes or low TV in pressure preset modes?
Ventilator: inapp setting, malfunction
Circuit: kinking, pooling of water, wet filter
ETT: kinked, obstructed with sputum/blood, endobronchial
Pt: bronchospasm, decreased lung compliance (APO, consolidation, atelectasis), decreased pleural compliance PTx, decreased wall compliance (abdominal distension), dysynchrony (cough/hiccup)
What is the easiest way to determine if there is a problem with the vent/circuit/ETT/pt causing alarms on the vent?
Disconnect and manually ventilate
How can the ventilator be used to estimate alveolar pressure?
Insp pause pressure
Airway pressure = flow*resistence + Alveolar pressure
so if flow = 0 , Airway P = Alv P
Which pressure (airway or alveolar) is important for lung injury? haemodynamic effects?
Alveolar is what is important for both
How is Total PEEP calculated? how is it estimated using the ventilator?
PEEP Total = Intrinsic PEEP + Extrinsic PEEP
Extrinsic PEEP = PEEP applied (set on vent)
intrinsic PEEP = result of gas trapping
Estimate PEEP total with exp pause
Differentials and management for hypotension post-initiation of IPPV
DDx
- hypovolaemia (decreased vasc return due to increased ITP)
- Anaesthetic drugs
- Gas trapping from over-enthusiastic ventilating
- Tension PTx
First two are most common - give fluids, if this doesnt work disconnect from vent - this will resolve gas trapping, if that fails consider PTx
Describe the optimal ventilation strategy for ARDS with rationale
- High PEEP, low tidal volumes (6-8ml/hg predicted), plateau P <30cmH2O
- as PEEP increase so should FiO2
In ARDS there are dependent areas of lung with low compliance and relatively normal areas of lung with normal compliance. Ventilating this normally with cause barotrauma to the normal areas and cause rapid opening/closing of the alveoli in the dependent areas increasing shear injury. using high PEEP stents open alveoli and low tidal volumes prevents recurrent shear injury.
Describe the general ventilation strategy for unilateral lung disease
- low TV, low pressure as with ARDS
- increasing insp time increases gas distribution across lung
- Ventilating in lateral position with unaffected lung dependent (down) increases perfusion to normal lung and decreases its compliance (making it more similar to the bad lung) and makes it easier to ventilate
Describe the general ventilation strategy for Asthma
- Airway resistance and therefore pressure will be high but alveolar pressure will stay normal
- Volume control as Pressure control will deliver low TV as pressure is high
- maximize exp time to minimize gas trapping (this will shorten insp time and therefore increase insp flow time and airway pressure but alveolar pressure will be unaffected). Lowest RR you can to maximize exp time
- monitor plateau pressure and PEEP total (aim <10cmH2O)
How to decide if a patient should have NIV?
- Is resp failure severe enough to warrant it (pH<7.32, PaCO2 >60 or PaO2 <60 despite high FiO2)
- is resp failure so severe they should have IPPV
- are there contraindications to NIV
- what is the underlying disease and will they benefit from NIV? Benefit with COPD, APO (CPAP), Pneumonia, CF, Chest Trauma, neuromuscular disease, Caution in asthma, potentially failed extubation
Contraindications to NIV
- severe acidosis pH <7.1
- inability to protect airway
- haemodynamically unstable
- agitation
- excessive secretions/vomiting
- PTx
- Orofacial abnormalities or recent surgery to face/ airway/upper GI
Complications of NIV
- Pressure injury
- Gastric distension
- aspiration
- dryness of airway, rhinorrhea, epistaxis
What are good initial NIV settings
Insp P 8-10cmH2O
Exp P 4-6cmH2O
Back up RR 12
FiO2 100
How should NIV be adjusted if high CO2? low O2?
High CO2 - check its fit/rebreathing/synchronizing thyen increase insp P in 2cmH2O increments
Low PaO2 increase FiO2 or Exp P (PEEP) to max of 8-10cmH2O
What is a normal urine output?
Normal: 0.5-1mL/kg/hr
Oliguria: <0.3mL/kg/hr
how does blood pressure relate to blood flow
under normal circumstances blood flow to organs is autoregulated so that flow is constant despite changes in pressure - however, at extremes of pressure this is lost and autoregulation is also usually impaired in critically ill patients
How to size a NIBP cuff
width of the cuff should be 40% the circumference of the limb
the length should be twice the circumference
how does the position of the arterial line transducer change its values
- over reads BP if too low
- under reads if too high
Describe how damping effects the arterial line value and how to test for true systolic BP
- under damping overestimates systolic and underestimates diastolic BP
- over damping underestimates systolic and overestimates diastolic BP
- test true systolic BP by placing a manual manometer on the limb with an Aline and inflate the cuff until the trace is gone. When releasing pressure, when the Aline trace can just be detected the value on the manometer will be accurate
Describe how CVP can be used to gain information about fluid responsiveness
- CVP approximates RAP and therefore EDP
- preload is what we are interested in for fluid responsiveness (EDV)
- EDP and EDV are related by the ventricular compliance curve
- by knowing the CVP, then giving a fluid bolus, and reassessing in 5min you can gain an idea about where on this curve the pt is
- a change of 0-3mmHg indicates underfilled, 3-5mmHg is adequately filled, >5 overfilled
Describe how to calculate pulse pressure variation, its preconditions and what it is useful for
PP variation= (PPmax-PPmin)/((PPmax+PPmin)/2) * 100
PPmax usually during insp
PPmin usually during exp
Preconditions:
- controlled vent with no spont breaths
- TV >10mL/kg PBW unless PPV already >10% at lower tidal volumes
likely fluid responsive if PPV >10-15%
How can a passive leg raise indicate fluid responsiveness?
- reversible fluid challenge with approximately 500mL of blood
- a rise in PP by 10% suggests hypovolaemia
What are supportive therapy options for cardiogenic shock? (Non PCI/CABG)
- aimed at increasing diastolic BP to increase coronary perfusion pressure and flow
- if hypotensive NA as it will increase dBP and not have much chronotropic effect
- IABP: increases dBP, decreases afterload, inceases CO, no increase in O2 demand
- can consider judicious fluids, dobutamine
Causes of cardiogenic shock
- IHD- MI, acute MR, acute VSD, Vental wall rupture, LV aneurysm
- end-stage Cardiomyopathy
- LVOT obstruction- HOCM/AS
- LV inflow tract obstruction- MS, LA myxoma
- Trauma (myocardial contusion)
Causes of hypovolaemic shock?
- blood loss
- third spacing - pancreatitis, ascites, BO, peritonitis
- GI loss
- renal loss (DKA/DI)
- skin loss (burns, fever, dermatitis)
Causes of distributive shock
- sepsis
- anaphylaxis
- neurogenic
- acute adrenal insufficiency
Causes of obstructive shock
Tamponade
tension PTx
Massive PE
definition and causes of pulsus paradoxus
Pulsus paradoxus is defined as an inspiratory drop in blood pressure of 10mmHg or more during normal breathing.
insp hold blood in lungs (less to LV) and returns blood to RH which normally transmits pressure to RV wall, with tamponade cant put pressure to RV so goes to IVS and further reduces LV compliance and preload (therefore BP)
Causes pericardial tamponade acute asthma massive pulmonary embolism constrictive pericarditis hypovolaemia (especially during positive pressure ventilation)
Define AKI
Can use RIFLE or AKIN
RIFLE
Risk = Cr 1.5x baseline or UO <0.5mL/kg/hr for 6h
Injury = Cr 2x or UO <0.5mL/kg/hr for 12h
Failure = Cr 3x or >4mg/dL or rise of >0.5mg/dL or UO <0.3mL/kg/h for 12h or anuria for 12h
Loss = failure for >4 weeks
ESRD = end stage on dialysis
risk factors for AKI
- preexisting kidney impairment
- HTN
- DM
- Vascular disease
- nephrotoxins
Causes of AKI
Pre-renal
- volume responsive AKI -> monitor haemodynamics and challenge with volume
- sepsis-induced AKI
- hypotension – manage aggressively
- renovascular disorders (RAS, Thrombosis, Vasculitis, dissection)
Renal nephrotoxins — allopurinol, aminoglycosides, amphotericin, frusemide, NSAIDS, ACE-I, organic solvents, contrast, sulfondamides, thiazides, herbal medicines, heavy metals, pentamidine, paraquat glomerular disease (SLE, postinfectious GN, goodpastures (anti GBM), granulomatosis with polyangitis HUS crystal nephropathy tubulointerstitial disease rhabdomyolysis TTP Scleroderma
Post-renal
obstruction at any post-renal site (e.g. tumour, clot, papillary necrosis, foreign body, post-surgical, blocked IDC)
abdominal compartment syndrome
What percentage of body weight is fluid? how much of body fluid is intra vs extracellular? what amount of ECF is plasma vs interstitial fluid?
~60% of body weight is fluid (less in females and less as you age)
2/3 ICF with principle cation being K (3500mmol)
1/3 ICF with principle cation being Na (4200mmol). of ICF 1/4 is plasma and 3/4 is interstitial
what is the daily water, sodium and potassium requirements?
water 30mL/kg/day
Na 2mmol/kg/day
K 1mmol/kg/day
what is the breakdown of usual insensible losses per day?
Faeces 100mL/day
Lungs 400mL/day
Skin 600mL/day
Define sepsis and septic shock
Sepsis is life-threatening organ dysfunction due to a dysregulated host response to infection
Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
Septic shock clinical criteria: Sepsis and (despite adequate volume resuscitation) both of:
Persistent hypotension requiring vasopressors to maintain MAP greater than or equal to 65 mm Hg, and
Lactate greater than or equal to 2 mmol/L
With these criteria, hospital mortality is in excess of 40%
How is cerebral perfusion pressure calculated?
CPP=MAP-ICP
What ICP should prompt treatment?
20-25mmHg
What are some treatment options for lowering ICP?
- Osmotherapy with mannitol or 3% NS (better for hypovolaemic pts)
- hyperventilation to a pCO2 of 30-35 (reduces CBF though)
- sedation/analgesia
- nurse 30 degrees head-up neutral neck to improve venous outflow
- insert drain
Definition of generalized convulsive status epilepticus
- ≥5 minutes of continuous seizures, or
- ≥2 discrete seizures between which there is incomplete recovery of consciousness
Treatment of status epilepticus
Treat hypoglycaemia, take blood, position in left lateral and give O2. if aborts look for cause and start anticonvulsant
if does not abort give Lorazepam IV 0.1mg/kg at 2mg/min or clonazepam 1mg IV. if no IV Midazolam 10mg IM. can give repeated doses of loraz.
if not aborted give Levetiracetam 60mg/kg (max 4500) over 15min
if still not aborted treat as refractory status:
(intubate and infusion of thiopentone/propofol/midazolam)
What is Winters formula?
to calculate expected compensatory changes for metabolic acidosis
PaCO2 = (1.5*HCO3)+8 +/-2
Expected change in PaCO2 in metabolic acidosis? alkalosis?
acid CO2 down by 1.25 for each mmol decrease in HCO3
alk CO2 increase by 0.75 for each HCO3
changes to HCO3 for acute and chronic respiratory acidosis
acute HCO3 up by 1 for each 10mmHg rise in CO2 up to 30
chronic HCO3 up by 4 for each 10mmHg in CO2 up to 36
changes to HCO3 for acute and chronic respiratory alkalosis
acute HCO3 down by 2 for each fall of 10mmHg CO2 down to 18
chronic HCO3 down by 4 for each fall of 10mmHg CO@ down to 18
Types and causes of lactic acidosis
Type A (due to tissue hypoxia)
- Shock
- severe hypoxaemia
- Anaemia
- post convulsion
- severe exercise
Type B
- also shock
- Drugs (metformin, salicylates, ethanol, methanol…)
- Other disease states (DKA, renal failure, liver disease, pancreatitis, thiamine deficiency, G6PD…)
causes of metabolic alkalosis and how to differentiate them
Volume (chloride) depletion - normally bicarb excretion at high levels is very rapid, bicarb retention is normally sustained - to maintain an alkalosis volume depletion is needed as the kidneys conserve sodium requiring the reabsorption of bicarb as well to pair it. (vomiting, gastric drainage, diuretics)
hyperadrenocorticoidism - cushings, conns, steroids
severe potassium depletion
can differentiate with urine chloride levels (low <10 with volume depletion, higher >20 with hyperadrenocorticoidism
Describe the richmond agitation sedation score
+4 - combative (immediate danger to staff)
+3 - very agitated (pulling on tubes, aggressive)
+2 - agitated (frequent non-purposeful movement)
+1 - restless (anxious, not vigorous movements)
0 - alert and calm
-1 - drowsy (sustained awakenings >10s to voice)
-2 - light sed (brief <10s awakening to voice)
-3 - mod sed (moves to voice, no eye contact)
-4 - deep (no response to voice, moves to physical stim)
-5 - unrousable (no response to voice or physical stim)
compare Midazolam, Propofol, clonidine/dexmed in terms of tolerance, withdrawal, accumulation in renal failure and haemodynamic stability
- Tolerance with midaz, not prop or clon/dexmed
- withdrawal with midaz, limited with clon/dex, not with prop
- midaz accum in renal failure, not prop/clon
- midaz is haem stable, prop is not, clon/dexmed cause initial HTN, then hypo with bradycardia
dose of propofol, suxamethonium and rocuronium
prop 1-1.5mg/kg
sux 1mg/kg
roc (elective 0.6mg/kg, emerg 0.9mg/kg)
side effects of suxamethonium
- bradycardia
- hyperkalaemia
- MH
- anaphylaxis
reversal of rocuronium?
- sugammadex 16mg/kg
how is basal energy expenditure calculated?
BEE (kcal/day) = 25 x ideal BW
with fever or stress needs adjustment
fever 1.1 BEE
mod to severe stress 1.4BEE
Risks/consequences of poor nutrition in ICU?
- hypoglycaemia
- Ketosis
- muscle breakdown
- difficulty weaning
- sepsis from (gut translocation secondary to atrophy)
describe how to initiate enteral feeds
commercial feed = 1kcal/mL
- 2-1.8mL/kg/hr = 1800-2400kcal/day
- set aim based on BEE
- start at 20-30mL/hour and asp 4hourly. - stop feeds if 200-400mL asp otherwise return
- aim to reach full rate by 48hr
How to correct sodium for hyperglycaemia?
Na corrected = Na measured + 2.4( (glucose -5.5)/5.5)
Treatment for severe hyponatraemia with seizures
2mL/kg 3% Nsaline over 20min then bloods and another 2mL/kg while awaiting result
repeat until symptoms resolve or increase of 5mmol/l. limit rise to 6-8 in 24hours
Causes of SIADH
- Pulmonary (Pneumonia, TB, asthma, mech vent)
- Neuro ( CNS infection, trauma, SAH, stroke, hydrocephalus)
- Drugs (antideps, anticonvuls, antipsych, thiazides, amiodarone, NSAIDs, opiates, PPI, vasopressin, desmopressin, terlipressin, oxytocin)
- malignancy
- other (GA, nausea, pain, stress)
how to differentiate cerebral salt wasting and SIADH/adrenal insuff
- cerebral salt wasting has UO+++ and urine sodium»_space;30mmol/l
Causes of hypernatraemia
- excess sodium
- water depletion/loss
- DI
- diarrhoea/vomiting
- burns
