Critical Care Flashcards
Differentiate accessory muscles used for inhalation and exhalation
Inhalation- intercostals, scalene, sternocleinomastoid, parasternals
(become even more important when diaphragm is flattened as in COPD/hyperinflation)
vs.
Exhalation- typically passive due to recoil, then if exaggerated can use obliques and abdominal muscles
Differentiate mechanism toxin-induced paralysis:
tetanus vs. botulism
Tetanus- blocks inhibitory neurotransmitters => get spastic paralysis (can’t relax)
Botulism- binds to ACh-R at neuromuscular junction => descending flaccid paralysis
Infections aside from C. jejuni associated with Guillain-Barre
Guillain-Barre also has association with viruses: EBV, HIV, Zika, CMV
Differentiate pattern of paralysis of guillain-barre vs. botulism
Guillain-Barre (progressive demyelinating neuropathy) typically starts with lower extremity symmetric weakness then ascends
While botulism typically starts up top (ocular, facial, bulbar weakness) then descends
Complete injury above what spinal level will definitely result in respiratory failure?
Above C3 => guaranteed respiratory failure because C3-5 innervate the diaphragm (C3-4-and 5 keep the diaphragm alive)
Describe how injury to cranial nerve may cause breathing accessory muscle weakness
CN XI innervates trapezius and SCM- sternocleinomastoid used as an accessory muscle during inspiration
Describe type of abnormal breathing seen in stroke (classically lesions of pons or lower medulla)
Cluster breathing or Biot respirations where there are irregular clusters of breaths and apneas (not the predictable crescendo-descrendo of cheyne stokes)
Location of central respiratory center
Medulla
What does acute hypercapnia do to the Hb-dissociation curve
Shift to the R- increases O2 offloading onto tissues
As make more CO2, tissues need more oxygen
What does acute hypercapnia do to cerebral blood flow
Acute hypercapnia causes cerebral vasodilation- increases cerebral blood flow => increases ICP
Change in bicarb expected for acute vs. chronic respiratory acidosis
Changes in bicarb (kidney compensation for respiratory acidosis)
For every 10 increase in pCO2:
acutely: 1 increase in bicarb
chronically: 3-4 increase in bicarb
ex: chronic hypercapnic can live in pCO2 of 70 with CO2 of 33-35ish
When expect to see CO2 narcosis in someone with a normal baseline bicarb
pCO2 above 60-70 if baseline is normal, of course much higher if baseline is higher (chronic compensation)
Answer = D
Trick with C- MG responds to CHOLINERGIC (not anticholinergic) agent such as pyridostigmine
Answer = D
- cranial nerves generally spared in critical illness
- Not C b/c typically recovers within weeks to months => is reversible
- most notable symptoms are limb and diaphragmaic weakness, decreased DTRs
Describe concept of stress index during mechanical ventilation
Stress index- changes in the pressure slope throughout inspiration which signify increasing, constant, or decreasing chest compliance
Way of telling you if too much PEEP (overdistended at Pplat) or driving pressure
-requires square waveflow pattern on volume control
-seeing if airway pressure increases disproportionately at end of the breath
Trial that showed proning improved mortality had what criteria
(a) P:F ratio
(b) Duration of proning
NEJM 2013 (PROSEVA)
(a) P:F under 150
(b) Prone for at least 16 hrs a day
Why doesnt inhaled NO typically cause systemic hypotension?
Such a potent vasodilator- but inhaled gets rapidly inactivated => not systemically absorbed => no systemic hypotension and just the pulmonary vasodilation
6 cc/kg or whhhhat kind of body weight?
6 cc/kg of predicted body weight (not ideal or actual)
-ARDSnet used predicted rather than actual b/c lung size has shown to depend most strongly on height and sex
pH of 7.4 correlates to what concentration of hydrogen ions?
(a) How does [H+] change with change in pH?
pH of 7.4 = 40 nmol/L of [H+]
(a) Then every 0.01 drop in pH increases [H+] by 1 nml/oL
so pH of 7.30 = 50 nmol/L of [H+]
Explain delta-delta gap
Comparing the change in the anion gap to the change in bicarb
Tells you in a AGMA if the anion gap accounts for all of the acidosis, if not then there is an additional disorder
-if change in anion gap more than change in bicarb (gap over 2) then concomitant metabolic alkalosis
-change in bicarb more than change in AG (ratio under 1) then additional NAGMA
How to calculate serum osmolarity
(a) Normal/expected osmolar gap
Serum osms = 2Na + glucose/18 + BUN/2.8
(a) Expect osmolar gap under 10
-if elevated think toxic alcohols
Causes of elevated osmolar gap
Toxic alcohols: methylene glycol, propylene glycol
Also drugs that have propylene glycol in their diluent including etomidate, diazepam, lorazepam, phenobarb, bactrim
Etiologies of non-anion gap metabolic acidosis (NAGMA)
NAGMA- lose bicarb with chloride
- Addition of HCl with normal saline
- Loss of bicarbonate
-Renal bicarb loss = RTAs
-GI bicarb loss = diarrhea
Etiologies of metabolic alkalosis
Metabolic alkalosis-
- GI loses of acid- vomiting
- Renal loss of acid- mineralocorticoid excess, licorice ingestion, Liddle syndrome, loop or thiazide diuretics, milk alkali, contraction alkalosis
Use for Winter’s formula
(a) Write it out
Winter’s formula to determine if change in pCO2 is appropriate for the change in pH in a metabolic acidosis
(if respiratory compensation is adequate to compensate for the entirety of metabolic acidosis)
-if pCO2 change in enough to explain the entire change in pH
(a) change in pH = 0.08 in opposite direction for every 10mmHg change in pCO2 from 40
ex] metabolic acidosis with pH of 7.24, would expect pCO2 of 20 for appropriate compensation.
If pCO2 over 20, not fully compensated so look for another disorder
If kidneys work differentiate change in HCO3 for compensation of acute vs. chronic respiratory acidosis
Compensation for respiratory acidosis by kidneys holding onto bicarb
For every 10mmHg increase in pCO2
-acutely: bicarb increases by 1
-chronically: bicarb increases by 4
If kidneys work differentiate change in HCO3 for compensation of acute vs. chronic respiratory alkalosis
Compensation for respiratory alkalosis by kidneys getting rid of bicarb
For every 10mmHg drop in pCO2
-acutely: bicarb drops by 2
-chronically: bicarb drops by 5
Expected change in pCO2 to compensate for metabolic acidosis
Winter’s formula to see if pCO2 change compensates for entirety of metabolic acidosis
Expected pCO2 = 1.5 (HCO3) + 8 +/- 2
Or change in pCO2 = 1.2 (change in bicarb)
4 systematic steps to detect triple acid-base disorders
- Determine primary disorder (acidemic or alkalemic)
- Primarily respiratory or metabolic
- Appropriate compensated?
- If initial compensation does not acocunt for entire change in pH, is another disorder present (delta-delta- is change in anion gap = change in bicarb)
In PSAX which walls correlate with which ischemic cardiac vessel?
Anterior- LAD
Inferior/septal- RCA
Inferolateral- LAD or LCx
EKG changes of what leads correlate with which ischemic vessel?
Anterior (V1-V2) = LAD classically
Lateral (V5-V6, I, aVL) = LCx
Inferior (I, III, aVF) = RCA
Explain requirements for ICU patient to use pulse pressure variation of volume responsiveness
(a) Cutoff
Look at change in pulse pressure (SBP - DAP) from max just before a breath to minimum several beats after breath
-Need pt to be passive on vent
-Need pt in sinus rhythm
-Need large TVs (like 700-800cc, none of that LPV stuff)
(a) 13% change between min and max predicts increase in cardiac output to fluid challenge
Cutoff for change in pulse pressure considered fluid responsive during passive leg raise
Change in pulse pressure by more than 9% (8-14% depending on study) considered an indication of fluid responsiveness
When to use fidaxomicin over PO vanc in C. Diff
Fidaxomicin preferred for patients with nonfulminant disease (no shock, ileus, or megacolon) given lower rates of recurrence and increased sustained response after therapy
For fulminant disease (shock, ileus, or megacolon)- PO vanc preferred
Serotonin syndrome vs. NMS vs. malignant hyperthermia
(a) Timeline from exposure
(b) Pupils
(c) Compare reflexes
Serotonin syndrome
(a) Rapid onset within 12 hrs
(b) Mydriasis (dilated pupils)
(c) Hyperreflexic, clonus
NMS (from dopamine antagonists like antipsychotics)
(a) Slower/insidious onset, 24-73 hrs
(b) Normal pupils
(c) Bradyreflexic
Malignant hyperthermia from inhaled anesthetics
(a) 1-24 hrs
(b) Normal pupils
(c) Hyporeflexia
-All rigid
Compare the common triggers of Serotonin syndrome vs. NMS vs. malignant hyperthermia
Common triggers for hyperthermic disorders
Serotonin syndrome- multiple serotoninergic agents
NMS- dopamine antagonists (ex: haldol, other antipsychotics, withdrawal of dopamine agonists)
Malignant hyperthermia- inhaled anesthetics
Benefits of APRV
APRV often does improve oxygenation, also less sedation/paralysis used
But in RCTs that didn’t correlate to shorter duration of mechanical ventilation or improved mortality
Pitfalls of APRV
Despite improved oxygenation and less sedation not shown to have improvement in outcomes (same duration of mechanical ventilation, same survival)
Beware of
-autoPEEP/gas trapping b/c very little time spent exhaling- so beware of flow not returning to 0
-lung overinflation and volume swings
The concept of stress index would suggest that which PEEP is ideal for this patient?
PEEP 15 = appropriate
Stress index- slope of airway pressure in a volume controlled breath, mostly at the end of the breath (see if pressure has to go up a lot to get that last bit of volume in)
(A) tracing at PEEP of 5- airway pressure slope decreases showing more recruitment could be done
(B) linear- compliance constant during the breath = appropriate PEEP
(C) airway pressure slope upward = overdistention
Differentiate flumazenil and fomepizole
Both antidotes
Fomepizole = for methanol and ethylene glycol toxicity by inhibiting EtOH dehydrogenase
Flumazenil = for benzo overdose, benzo receptor antagonist
Tracing that could reflect pulmonary edema for patient on pressure control
B- reduced volume delivered (so not C)
(not A) b/c much longer expiratory time indicative of obstruction, while would expect stiffer lung with more rapid expiratory flow (thick arrow)
What could vent tracing C indicate?
Same inspiratory pressure and flow delivered but less expiratory volume delivered = circuit leak
Differentiate mechanism/use of andexanet alpha and idarucizumab
Andexanet alpha = structurally similar to Xa to acte as decoy (bind) to Xa-inhibitors
-reverse severe bleeds due to apixaban and rivaroxaban
Idarucizumab = mAb that binds and inactivates dabigatran (direct thrombin inhibitor so not affected by Xa decoy)
One benefit of vaso over levo
Potentially less need for dialysis (renal replacement) when vaso used early vs. levo
But no change in mortality, digital ulceration, MI
Describe McKonnel’s sign
Pattern of regional RV dysfunction-
akinesia of the RV free wall but normal movement of the RV apex (b/c apex also tethered to the LV)
What does McKonnel’s sign indicate?
RV free wall akinesis with RV apex normal movement (b/c LV also tethers/moves the apex) indicative of RV strain seen in PE or RV infarct
Pt not on high PEEP- estimate RA pressure based off this subcostal view of the IVC
IVC diameter over 2.5cm (using M-mode) with less than 50% collapsibility on inspiration: RA pressure estimated 16-20 cm
IVC diameter and collapsibility for estimated RA pressure of 0-5cm
IVC diameter less than 1.5cm diameter and greater than 50% collapsibility with inspiration
(inspiration = increased intrathoracic pressure = lower R heart venous return = IVC collapses)
Differentiate IVC appearance on subcostal view for estimated RA pressure of 5-10cm vs. 11-15cm
IVC diameter 1.5-2.5cm estimated RA pressure at 5-15
(IVC diameter under 1.5 with collapsibility suggests RA pressure under 5, IVC diameter over 2.5 w/o collapsibility suggests RA pressure over 16)
Then collapsibility
1.5-2.5cm with greater than 50% collapsibility on inspiration estimates RAP at 5-10cm
1.5-2.5cm with less than 50% collapsibility on inspiration estimates RAP at 11-15cm
Big caveat for when you can’t use IVC diameter and collapsibility to estimate RA pressure
Large swings in intrathoracic pressure (high pressure control settings) or pt on ventilator with high PEEP (won’t expect as much IVC collapsibility with inspiration)
Histology buzzword for amiodarone-induced lung toxicity
Lipid-laiden foamy macrophages in the alveolar space
Sensitive but NOT specific- if they’re absent it makes amio-toxicity unlikely, but presence doesn’t mean amio AND doesn’t mean toxicity (can be present in pt taking amio w/o toxicity)
Effect of A-line transducer above vs. below level of the heart
A-line reading underestimated if transducer is above the level of the heart (b/c have to pump all that extra way up)
Hydrostatic pressure difference easily calculated as 10cm water height = 7.4 mmHg
-so transducer 10cm above level of the heart means A-line will underestimate MAP by 7.5mmHg
Describe a normally dampened A-line tracing during flushing maneuver
Pressure shoots up briefly when exposed to pressure straight from counter bag (typically inflated at 300mmHg), then transducer should oscillate no more than 2-3 times before returning to natural frequency with clear dicrotic notch
Describe what a fast-flush test will show for an underdamped A-line vs. overdamped A-line
After a square wave of high amplitude (exposed to counter bag), underdamped will show more than 2 oscillations before returning to baseline
While overdamped will have 0-1 oscillations
Describe effect on SBP, DBP, and MAP for under and overdamped A-lines
Underdamped- more than 2 oscillations after fast-flush. Will overestimate SBP and underestimate DBP (so falsely widened pulse pressure), MAP remains accurate
Overdamped- 0-1 oscillations after fast flush. Will falsely narrow pulse pressure underestimating SBP and overestimating SBP but MAP remains accurate
Pt on pressure control with acute tachypnea and this vent tracing- likely cause?
Circuit leak from a few things: circuit disconnect, rupture of ETT cuff, large bronchopleural fistula
Delivered inspired volume RTS but then exhaled volume considerably less (end of expiration when volume tracing resets to 0)
What percent change in VTI is considered volume responsive after passive leg raise?
10% or greater increase in VTI is considered volume responsive after passive leg raise
What way would you expect EtCO2 to change if patient who is volume responsive undergoes passive leg raise?
Passive leg raise in volume-responsive person will transiently increase cardiac output => transient increase in EtCO2
What ultrasound measurements are needed to calculate stroke volume?
- LVOT VTI (ideally in apical 5 chamber view)
- LVOT diameter
SV = VTI x LVOT area
Get LVOT area by pie x r^2
ex attached] SV = VTI x LVOT area = 6.5 x 3 = ~20
Pt on volume control has sudden desat with vent circuit intact and normal EtCO2 tracing- what’s wrong?
Mucus plug, PTX, or ET tube cuff rupture?
ET tube cuff rupture => reintubate w/ a new tube
Inhaled volume remains stable but exhaled volume is way lower so some air is getting exhaled not through the ventilator flow sensor => leak in the circuit, ET cuff leak, or large BPF
Mucus plug and PTX would expect increase in pressure for same given volume
Placement of pulse wave doppler box with respect to the aortic valve
(A) Which will underestimate VTI
(b) Which will overestimate VTI
(a) Underestimate VTI if pulse wave box is too far into the LV cavity
(b) Overestimate VTI if pulse wave box is too far into the aortic valve
What’s wrong with the tracing in figure 2 for LVOT VTI?
Pulse wave doppler too close to the aortic valve- in the flow acceleration zone and DOppler tracing displays messy profile with spectral broadening => overestimates VTI
What’s wrong with the tracing in figure 3 for LVOT VTI?
Pulse wave doppler too far into the LV cavity => doppler tracing displays flat profile with no closing click => VTI underestimated
Are A-lines or B-lines expected in pneumothorax?
B-lines rules out PTX even if lung sliding not seen
-PTX will always give an A-line pattern (just reverberation of pleura)
Mechanism for TXA use in nonmassive hemoptysis
TXA = antifibrinolytic
Displaces plasminogen from fibrin to inhibit fibrinolysis (breakdown of fibrin)
also inhibits protelytic activity of plasmin
So basically stops clot breakdown
Differentiate lactose vs. non-lactose fermenting GNRs
Lactose fermenters = E. coli, Klebs
NLFs = pseudomonas, proteus
Differentiate decelerating ramp vs. square wave flow during mechanical ventilation
On volume control (AC-VC) you set the volume then the max flow, then can set the shape at which the flow is delivered
-decelerating ramp typically more comfortable
-square wave can help reduce i-time but at risk of higher airway pressure
How can SIMV tell you what settings the patient is most comfortable with?
SIMV = combined assisted and supported breaths
Can look at the supported breaths (pt triggers spontaenous, gets a little bit of pressure support) compared to assisted breath (equal to the controlled breath with set pressure or volume) to see what flow pattern pt prefers to improve vent synchrony
What is this vent tracing trying to show?
Too long an i-time
(aka delayed termination)
Patient trying to exhale (see outward flow below x-axis) while vent is still delivering breath => little pop up in pressure
Formula for oxygen delivery to tissues
DO2 = CO x CaO2 (arterial oxygen content)
CO = HR x SV
CaO2 = (1.39 x Hb x SpO2) + (0.003 x PaO2)
Will the following over or under dampen an A-line tracing
(a) Bubbles in tubing
(b) Kinked catheter
(c) Longer/excess tubing
(a, b) Bubbles in tubing and kinked catheter = overdampen
(c) Excess tubing underdampens S
Regardless MAP should be ok but pulse pressure will vary
Differentiate a, c, v waves of a CVP tracing
A wave = R atrial contraction (right after P-wave)
C = tricuspid valve closure (right after QRS/systole begins)
-‘cusps’ of tricupid valve bulging into the RA (closing)
V wave = atrial filling against closed tricuspid valve in beginning of diastole
Differentiate x and y-descent on CVP tracing
x-descent = RA relaxation during systole
y-descent = ventricular filling in diastole
Describe change in CVP tracing in response to 3rd degree heart block
Cannon a-waves: atrial contraction against closed tricuspid valve
Describe change in CVP tracing in response to Afib or Aflutter
Loss of a-wave b/c not synchronized atrial contraction
Describe change in CVP tracing in response to tamponade
Tall a-wave (RA contracting against stiff RV) and tall v-wave (rapid RA filling b/c of RV backpressure)
Tamponade- ventricular filling impaired => minimized y-descent
Describe change in CVP tracing in response to constrictive pericarditis
Accentuated x-descent (RA relaxation) in constrictive pericarditis
Things that increase CVP’s a-wave
A-wave = RA contraction, increased whenever there is increased resistance to RV filling
-tricuspid stenosis
-R heart failure
-pulmonary stenosis
-pulmonary HTN
Ways to differentiate RV pressure and PA pressure tracings
- diastolic pressure higher on PA tracing
- diastolic pressure upsloping in the RV (b/c ventricle filling during diastole), PAP tracing downsloping during diastole (pulmonary artery draining blood during diastole)
- PA (arterial now) has very distinct dicrotic notch, while RV does not have a dicrotic notch (= closure of pulmonic valve)
Upon advancing PA catheter where do you start to see a dicrotic notch?
Once enter the PA
Dicrotic notch = separates systole and diastole, so starts once get into the arterial system (not present in the RV!)
Dicrotic notch = closure of pulmonic valve when in the PA
-on an A-line, dicrotnic notch = closure of aortic valve
Differentiate the three west zones of the lung
Comparing arteriole (a), alveolar (A), and venuole (v) pressure
Zone 1 = Palveolar exceeds both arteriole and venule (ex: positive pressure ventilation) so not much gas exchange occuring here, debatable if all dead space
Zone 2 = majority of lung, Part > Palv > Pven so during systole the alveoli are perfused
Zone 3 = basilar predominant, most blood flow
Majority of the lung is which west zone? (What this means for Palv, Part, and Pvenous
Majority of lung in zone 2: where Part > Palv > Pven so blood flow is dependent on the gradient between arteriole and alveolar pressure, most of the flow through pulmonary capillaries occurs during systole
Effect on PA pressure if PA catheter is in zone west 1 of the lung
Can falsely elevate PA pressure and wedge b/c alveoli compressing arteriole
Describe the concept of stressed vs. unstressed body volume
Unstressed volume = blood volume where blood vessels are not at all stretched
Once blood volume is enough to put pressure on blood vessel walls = stressed volume
-important b/c this is the pressure that works against CVP to fill the R heart
Describe the mean systemic filling pressure and how that works against CVP to fill the heart
Pmsf = pressure (mean systemic filling)
-unstressed volume = volume to fill vascular bed without distending vessels
-once that’s met extra volume becomes stressed volume = volume that exerts pressure on the vessel walls which drives venous return
Pmsf works against CVP to fill the R heart
Cutoff considered fluid responsive for pulse pressure variation
12-15% change in pulse pressure from minimum (exhalation) to maximum (inspiration) correlates with fluid responsive (increase in cardiac output to increase in intravascular volume )
Formula for SVR
V = IR, so dP = (CO)(SVR), SVR = dP / CO
Change in pressure for systemic vasculature is MAP - CVP
so SVR = (MAP - CVP) / CO x 80
(x 80 for conversion from Woods to metric)
What lung volume should PAWP be measured at?
FRC, aka end exhalation
2 modifiable risk factors for west zone 1 (similar to dead space, aka not perfused) lung physiology
Zone 1 = Palv > Parteriole > Pvenuole, so basically alveolar pressure exceeds the pressure in the arterioles => reducing blood flow
Modifiable risk factors
1. High positive pressure ventilation
2. Volume depletion
