SEEK Qs Flashcards
Amount of blood in Morrison’s pouch for +FAST
500cc between liver and kidney (hepatorenal recess = Morrison’s pouch) before typically detectable on FAST
Hence why FAST highly specific but not sensitive- so if HD stable but injury suggesting abd. trauma still get CT A/P
Why difficult to assess diastolic function on ACCE in AFib
Diastolic dysfunction determination depends on synchronized atrial and ventricular contraction to give E and A waves (blood moving into LV during diastole)
Interpretation of E/a ratio
E and A waves are blood inflow during pulse wave doppler through mitral valve (apical 4 chamber view)
-reflects on diastolic function of the LV (b/c is showing blood filling the LV)
E = early LV passive filling due to LV relaxation (in normal this is where most blood comes into LV)
A = late LA active contracting pushing blood into LV (in diastolic dysfunction this is bigger than E)
Differentiate tissue doppler from pulse wave doppler
Tissue doppler is a type of pulse wave doppler optimized for much slower speed
Tissue doppler- detects slower speeds of tissue/muscle at 1-20 cm/s
While pulse wave doppler detects faster speed of blood at 30-200 cm/s
Differentiate E and e’ when assessing diastolic dysfunction of LV
Using pulse wave doppler (measures blood movement) can measure velocity of blood into LV during diastole (E and A-waves)- will be towards the probe (above the x-axis) in apical 4 chamber view
vs.
TDI (tissue doppler) measures slower movement of muscle/tissue, showing movement of LV away from the probe (below x-axis) as it allows blood to fill the LV
Differentiate the two phases of LV filling in diastole and how that is seen on TTE
- Early diastolic filling due to pull from LV relaxation = E-wave
- in healthy heart this is majority of the blood flow into LV - Late diastolic filling due to push from LA contraction = A-wave
What is a normal E/A ratio?
More blood moves into LV during passive ventricular relaxation than during active LA contraction = so E wave > A wave (so E/A > 0.8)
The larger A is than E, the more severe the diastolic dysfunction
What is a normal E/e’ ?
More movement of LV during relaxation (larger e’) is better, so E/e’ smaller (under 8-10) is more normal
E/e’ < 8 indicates normal LA pressure
while E/e’ > 14 indicates elevated LA pressure
How RAP is estimated on TTE
How RVSP is typically calculated on TTE
Modified Bernoulli’s equation (relating pressure difference to velocity across valve)
RSVP = 4 (TRV)^2 + RAP
TRV = tricuspid regurg jet velocity
-take max velocity on continuous wave doppler across tricuspid valve, flow will be below x-axis (b/c away from probe)
Key finding of tamponade on RHC
Equalization of end-diastolic pressures (b/c fixed pressure in the pericardium)
RA pressure = RVEDP = dPAP
What clinical entity is this ACCE finding suggestive of?
Pulse wave doppler through mitral valve showing mitral valve inflow (diastolic filling of the LV).
-Big drop in LV filling during inspiration = respiophasic reduction of mitral valve inflow
Finding of pericardial tamponade
Cutoff is technically >25% reduction in LV inflow during diastole is consistent with tamponade
Define pulsus paradoxus
Finding of SBP drop > 10mmHg with inspirations suggestive of impaired cardiac filling (pericardial tamponade)
Seen where intrathoracic pressure swings are exaggerated or RV is distended
What is this ACCE M-mode through PLAX showing?
M-mode through mitral valve. Mitral valve should be closed during systole, when there’s systolic opening suggestive of LVOT obstruction
Suggests LV septal hypertrophy or can be see in hypovolemia
Explain change in PA acceleration time expected in PH
(a) Formula for mPAP
PA acceleration time = pulse wave doppler across pulmonic valve. High pulmonary vascular resistance = shorter time to reach max speed = shorter PAAT
(a) mPAP = 90 - (PAAT x 0.62)
Ex: PAAT 80 m/s, mPAP = 41
Outcome of trial looking at trained communication facilitator in the ICU
- no change in mortality or patient/caregiver satisfaction/anxiety
- decrease ICU LOS for nonsurvivors
HLH
(a) Clinical features
(b) Risk factors
(c) Trigger
(d) Lab findings
HLH
(a) Macrophage activation => cytokine storm, mimics septic shock with fever and multi-organ dysfunction
(b) Lymphoma/leukemia
(c) Triggered by infections most common EBV
(d) Hyper-TG, ferritin > 500 more specific if > 3,000. Bi-cytopenia (or pan-cytopenia)
Degree (percentage and actual #) drop in platelet count most consistent with HIIT
HIIT
4 T’s score:
0 points: < 30% drop or nadir under 10
1 point: 30-50% drop or nadir 10-19
2 points: >50% drop or nadir> 20
2 features to trigger consideration of thrombotic microangiopathy
Consider TMAs (TTP or HUS) when
-thrombocytopenia
-fragmented RBCs (schistocytes) present
PLASMIC score
What is it?
PLASMIC score used in pts with thrombocytopenia and schistocytes (fragmented RBCs) to predict risk of TTP
plt < 30,000
Hemolysis (LDH, hepatoglobin, retic)
No active cancer
No recent transplant
MCV < 90
INR < 1.5
Cr < 2.0
1 point per criteria, 5-7 = intermediate/high risk of TTP- start empiric treatment with therapeutic plasma exchange, steroids, and rituximab
Mechanism of thrombocytopenia in TTP
TTP = genetic or more commonly acquired deficiency (auto-antibody in immune TTP) of vWF cleaving protein ADAMTS13 => small vessel platelet rich thrombi
thrombocytopenia (plts all used up in the clots)
hemolytic anemia (hemolysis thru clots)
end organ damage (CNS, liver, kidneys)
Clinical features of TTP
Neurologic- confusion, headache
Empiric TTP treatment
Very high mortality if left untreated so if high clinical suspicion (PLASMIC score > 5) for TTP start:
-therapeutic plasma exchange
-steroids
-rituximab
Clinical features: AMS/headache, thrombocytopenia, hemolytic anemia
Two most common causes of acquired long QTc
- electrolyte abnormalities- hypokalemia, hypomag
- meds
Categorize the following patient by Sepsis-2 vs. sepsis-3 criteria:
75F hypotension resolves with fluids but AKI, a bit altered, and hypoxic. +consolidation on CXR
Severe sepsis by Sepsis-2 b/c meets sepsis (infection + 2 SIRS criteria) and severe b/c has organ dysfunction. Not septic shock by sepsis-2 b/c not hypotension or lactate refractory to fluid resuscitation
Sepsis, NOT septic-shock by SEPSIS-3
Sepsis = infection + evidence of organ dysfunction
septic shock = need for vasopressors/hypotension unresponsive to fluids
delta P for oxygenator of ECMO circuit that should prompt oxygenator change
pressure gradient of 70mmHg should prompt oxygenator changeP
Positioning maneuver to reduce obstructive shock picture from vascular air embolism in the RV/RVOT
L lateral decubitus and trendelenerg- thought is to position the RVOT lower than the RV to encourage gas migration to the RV apex, reducing RVOT obstruction
Ways venous air can enter arterial circulation
- intracardiac shunt- PFO, ASD
- intrapulmonary shunt- AVM
- absorptive capacity of the pulmonary capillary bed is overwhelmed
Post-cardiac arrest surgery algorithm for VT/VF
For up to 10 days post-op different algorithm is in play- main thing is to open the chest quickly (even if by non-cardiac surgeon but experienced provider) b/c high c/f cardiac tamponade or intrathoracic bleeding and often relieving the pressure can prompt ROSC
VT/VF post-cardiac surgery:
shock x3
call cardiac surgery
amiodarone
Avoid crash cart epi
How does post-CT surgery algorithm for asystolic arrest differ from regular?
Avoid push dose epi- precipitate HTN and severe bleeding in pts who regain ROSC
Pace if wires available, consider external pacing, open chest ASAP to relieve most common causes (cardiac tamponade and intrathoracic bleeding)
Explain how fluids can worsen shock after RV myocardial infarction
If RV is infarcted can’t handle the volume load- worsened interventricular dependence
Characteristic EKG finding of Brugada syndrome
Na channelopathy causing coved ST segment elevations with inverted T-waves in V1-V3
First line management for SCAD
Spontaneous coronary artery dissection- first line management is conservative if pt is HD stable
- PCI can make it worse so not worth risk if HD stable
- Common in postpartum F in first month after pregnancy, first line conservative management
Use of methylpred and vaso in in-hospital cardiac arrest
RCT of adding methylpred + vaso to standard resuscitation => increased rate of ROSC with no improvement in survival to discharge or good neurologic outcome at 30 days.
Which measure of volume responsiveness requires 8 vs. 10 cc/kg passive ventilation
IVC diameter as measure of volume responsiveness performs best with passive ventilation and 8cc/kg tidal volume
(very altered by the negative pleural pressure during spontaneous breathing)
PPV requires at least 10 cc/kg tidal volume for enough intrapleural pressure swing to alter venous return
-also requires sinus rhythm
Which measure of volume responsiveness requires
(a) very passive ventilation
(b) sinus rhythm
Volume responsiveness
(a) Passive ventilation very key in using IVC diameter as negative pleural pressure during spontaneous breathing can alter diameter
(b) Sinus rhythm required in PPV
- while not as important in VTI since should be averaged over multiple
Explain components of LVAD (where blood goes in/out)
Inflow cannula removes blood from LV –> implanted pump –> outflow cannula returns blood into aorta.
continuous (not pulsatile) flow)
Sign on LVAD monitor of incipient thrombosis
Rising pump power
Pump power = wattage needed by LVAD to maintain the pump speed (which generates the flow)
What parameter is set on the LVAD
Only set the pump speed (rpm) which generates a certain flow (LPM)
- then cardiac output dependent on preload (volume status) and afterload (SVR)
Primary cause of death at 6-24 months for LVAD patients
Stroke
What is the pulse index/pulsatility on an LVAD
Dimensionless measure of magnitue
Explain how LVADs generate flow
Continuous flow (so not pulsatile)
Most common is the heartmate 3 that uses magnetically levitated centrifugal flow- contactless rotor enables higher flow rates at lower risk of hesmolysis and thrombosis
Describe difference in TEG appearance from
(a) Increased thrombolytic activity
(b) Fibrinogen deficiency
(a) Increased thrombolysis = increased amount of cot is gone at 30 minutes so higher LY-30 percentage
(b) Fibrinogen = shorert K-time and less steep alpha angle because fibrin accumulates slowly so takes a while for clot to reach fixed strength
Describe difference in TEG appearance from
(a) Inadequate platelet function
(b) Presence of anticoagulant or depletion of clotting factors
TEG
(a) Reduced platelets = clot is smaller/less strong = low MA
(b) Longer R-time because prolonged time to start forming clot
ATS guidelines for who to perform pre-exubation cuff leak on
(a) What if they fail…
ATS guidelines- perform cuff leak test in patients with high risk of post-extubation stridor = Female, intubated for over 6 days, previous unplanned extuation
(a) If fail give steroids to reduce risk of reintubation, wait at least 4 hours then still extubate (don’t need to repeat the cuff leak test)
How to extubate someone via guidelines who fails cuff leak test
Steroids, wait at least 4 hours, then prepare for high risk of reintubation
Utility of transesophageal pressure monitoring
Typically we use airway pressure (Pplat) as surrogate for transpulmonary pressure to prevent overinflation.
but TPP = Pairway - Ppleural (just typically can ignore pleural pressure b/c is so small)
however in obesity where chest wall compliance is reduced, pleural pressure can be more negative, leading to overestimation of TPP by using surrogate Pairway
Therefore use esophageal monitor to measure more accurate transpulmonary pressure and prevent under-recruitment
When is exchange transfusion indicated for acute chest syndrome?
When is hydroxyurea indicated for acute chest syndrome?
Nope not used in the acute setting, role is in the outpatient setting as prophylaxis against acute chest
Liver or kidney failure causes prolonged paralysis 2/2
(a) Nimbex
(b) Rocuronium
(a) Nimbex- Hoffman elimination, nonenzymatic breakdown independent of liver or renal function => good for our ICU patients with shock liver/kidneys etc
(b) Rocuronium- hepatically metabolized so can cause prolonged paralysis in liver failureBl
Blood test to help confirm diagnosis of anaphylaxis
Serum tryptase- tryptase released by mast cell degranulation
Peak at around 30-60 minutes and remain elevated for 5+ hours, while histamine does peak faster (and is more specific) but is transient (gone in 30-60 mins)
Effect of CPAP on
(a) LV afterload
(b) Venous return (RV/LV preload)
(c) RV afterload
Reduced LV afterload, reduces preload (torniquet effect on the great veins). Increases RV afterload
Describe the classic asynchronies in each of the three phases of ventilation
1. trigger
2. flow
3. cycle
- ineffective trigger = inspiratory effort does not trigger ventilator breath
- see negative pressure dip not followed by breath - flow hunger = inspirator flow is less than what the patient desires
- see negative pressure during effort = concave appearance to inspiratory pressure waveform - delayed cycling asynchrony when inspiratory time of mandatory breath is longer than what patient desires (patient wants to exhale sooner than allowed)
-pt begins exhaling early generating additional positive pressure = abrupt peak in pressure
What type of vent asynchrony is seen in this waveform?
delayed cycling asynchrony when inspiratory time of mandatory breath is longer than what patient desires (patient wants to exhale sooner than allowed)
-pt begins exhaling early generating additional positive pressure = abrupt peak in pressure
Differentiate double triggering from reverse triggering
Double triggering = both paired breaths are initiated by the patient
vs.
Reverse triggering = passive mandatory breath (passive thoracic insufflation) triggers reflexive patient-initiated breath
What type of vent asynchrony is seen in this waveform?
Reverse triggering = passive mandatory breath (passive thoracic insufflation) triggers reflexive patient-initiated breath
*not double triggering in which both paired breaths are initiated by the patient
What is a stress index on ventilator?
Stress index = slope of pressure/time at a constant flow (slope of the pressure curve)
Straight line = 1
Concave down (less pressure to continue providing flow) is a stress index < 1- indicating
concave up, SI > 1 indicating alveolar overdistentionH
Helpful test on ventilator to see if adding PEEP caused improved recruitment or overdistention
Stress index
Define pulsus paradoxus
Drop in SBP by > 10mmHg during inspiration- due to some abnormality in interventricular dependence
-During inspiration venous return is increased => RV fills, if there is a fixed space then this limits LV filling => limits LV stroke volume
Seen in cardiac tamponade
EKG findings seen in hypothermia
-Bradycardia (sinus or other bradyarrythmias
-Osborne or J waves = elevation at end of QRS and QT interval: typically most apparent in precordial leads
-shivering
Why measure blood preferentially from R. vs. L radial A-line in patient on VA ECMO
Are reverse perfusing the aortic arch, want to prevent north/south syndrome.
Most proximal branch of the aortic arch is the innominate artery which branches into the R radial
What is North-South syndrome?
Also called Harlequin syndrome- as native cardiac output recovers but lungs are still not working, deoxygenated blood from LV works against VA ECMO return
Labs to differentiate etiology of hypoglycemia: exogenous insulin vs. insulinoma
Exogenous insulin: elevated serum insulin level but low C-peptide (cleaved from (endogenous pro-insulin)
vs.
Insulinoma- high insulin and high C-peptide
TSH/T4/T3 in
(a) Myxedema Coma
(b) Euthyroid sick syndrome (nonthyroidal illness)
(c) Thyrotoxicosis
(a) Myxedema coma: high TSH, low T3/4
(b) Euthyroid sick syndrome: normal/low TSH, normal/low T4, low T3
(c) Tyrotoxicosis: high T3/4, low TSH
Differentiate droplet from airborne precautions
Droplet- simple surgical facemask, for things transmitted by close respiratory secretions and mucus membrane contact. influenza, RSV
vs. airborne = n95, negative pressure room for things transmitted by droplets in air over longer distance such as coronvairus and Tb
Differentiate contact from droplet precautions
Contact- gown/gloves with PPE donned on entry and removed before exit- for infection, colonization with MDRs, transmission due to excretions (C. Diff)
While droplet is a type of respiratory precaution- wear surgical mask to prevent Transmisson of disease by close respiratory secretions
Lactose vs. non-lactose fermenting GNRs
Non-lactose fermenting = pseudomonas
Lactose-fermenting = E. coli and klebs
What change in stroke volume index suggests volume responsiveness?
> 10%
ex: PLR with 7% increase in SV: start pressors not more fluids
Describe the change in JVP tracing with respiration seen in constrictive vs. restrictive cardiomyopathy
Key feature is ventricular dependence in constriction (differs from restriction). See paradoxical increase in JVP with inspiration with constriction
- negative intrathoracic pressure during inhalation not transmitted to the heart
- pulmonary veins are intrathoracic but not intracardiac => with negative intrathoracic pressure this reduces LV filling pressures, allowing RV to bow into LV (allowing RV filling at expense of the LV)
Classic disjunction of RV and LV pressure with respiration
Describe the characteristic square wave sign seen in constrictive cardiomyopathy
Rapid y (diastolic) descent of CVP (and LA filling/diastole) followed by abrupt halt in filling as stiff pericardium limits ventricular expansion
Explain echocardiographic equivalent of pulsus paradoxus with mitral/tricuspid inflow
Pulsus paradoxus = exaggerated fall in BP with inspiration due to impaired cardiac filling (Ex: pericardial effusion)
Echocardiographic equivalent = exaggeration of respiratory variation of mitral and tricuspid inflow velocities:
> 30% variation in mitral inflow and > 60% variation in tricuspid inflow (similar pattern but to less extent in constrictive cardiomyopathy)
Winter’s formula
Addition to MUDPILES as cause of high anion gap metabolic acidosis to consider inpatient taking acetaminophen
5-oxoproline = organic acid
Parts of the PLASMIC score
Pre-test probability for TTP while ADAMTS-13 activity is pending
Use of ICH score for stroke mortality prediction
ICH score- grades ICH severity and correlates to 30 day mortality
GCS
Age
ICH volume > 30ml
Extension to intraventricular hemorrhage
Infratentorial origin of hemorrhage
What is the triad of Cushing’s reflex of increased ICP
- Bradycardia
- Increased pulse pressure (increased systolic)
- Irregular breathing (slow breathing)C
A/b/c/d chart, formula for sensitivity and specificity
A/b/c/d chart, formula for NPV and PPV
A/b/c/d chart, formula for prevalence
Prevalence = positive / all, so (a + c) / (a+b+c+d)
