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
Depolarizing vs. nondepolarizing NMB
Which is which?
Depolarizing = succinylcholine
-depolarize then block ACh receptors on muscle membrane
depolarization => potassium efflux from muscle => potential hyperkalemia
Nondepolarizing = rocuronium
Pts in which to avoid succinylcholine for paralysis and why
Avoid depolarizing (causes K+ efflux from muscle) NMB (succ) in patients at high risk for hyperkalemia such as- burns covering significant body surface area, existing hyperkalemia, renal failure, spinal cord injury, chronic limb paralysis, prolonged bed rest, and rhabdo
Adverse effects of induction with etomidate vs. ketamine
No mortality difference`
Etomidate- carries risk of relative adrenal insufficiency
Ketamine- risk of laryngospasm, increase BP/HR => increased myocardial O2 demand
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
Cutoff for definition of hypothermia
Hypothermia: technically under 35C, 92F
Mild 32-35 (90-95)
Moderate 28-32 (82-90)
Severe under 28C (82F)
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
Typical temperature cutoff for active rewarming
Typically actively rewarm until 32C (90F)
Typical meds causing
(a) Malignant hyperthermia
(b) Neuroleptic malignant syndrome
Medications causing
(a) Malignant hyperthermia = genetic abnormality in intracellular calcium channels, triggered typically by inhaled halogenated anesthestics
(b) NMS = anti-dopaminergic agents such as antipsychotics
Differentiate use of dantrolene for malignant hyperthermia and neuroleptic malignant syndrome
Dantrolene = inhibits intracellular calcium release => inhibiting muscle contraction
(a) First line for malignant hyperthermia from anesthetic agents
(b) First line for NMS but use in addition to replacing CNS dopamine stores with dopaminergic agent such as bromocriptine, amantadone, L/carbidopa
Where on the ECMO circuit is the heater/cooler to regulate temperature?
Regulate the temperature of air that goes into the oxygenator
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
Describe configuration of V-AV ECMO and why you’d use
To reduce North-south/harlequin syndrome- externally oxygenate (VV) and externally pump (VA) for when cardiac function is improving but lung function still stinks so LV is pumping out deoxygenated blood against VA ECMO circuit
Tx of methemoglobinemia in patient with G6PD deficiency
Vitamin C
-methylene blue make it worse
Outcome of NICE-SUGAR NEJM 2009
Higher mortality in tight glycemic control (FS 80-110) than conventional (140-180) likely due to higher hypoglycemic events
What group of patients may benefit from tighter glucose control
Target 110-140 for surgical ICU patients
vs. 140-180 for medical ICU
Differentiating euglycemic DKA from regular DKA
(a) Treatment difference
Euglycemic DKA when FS < 250, everything else the same (acidosis, +ketones)
(a) Same tx but start glucose replacement sooner
Fluid choice for volume replacement in DKA
Some data for LR over NS- faster time to DKA resolution
Initial empiric insulin bolus/gtt dosing in DKA
Insulin dosing- typically start with 0.1 U/kg bolus followed by 0.1 U/kg/hr infusion with q1h finger sticks
ex: 70kg patient- 7U bolus followed by 7 U/kg/hr infusion
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
Classic drugs that cause thyroid issues
Amio, PTU, lithium, sulfonamides, iodine therapy or contrast agents
Utility of reverse T3 lab value
Reverse T3 is a marker of thyroid function- positive in euthyroid sick thyroid syndrome (nonthyroidal illness) where thyroid function is otherwise normal but T3/4 is low
Clinical features of thyrotoxicosis
Thyroxtoxicosis- excess thyroid hormone activity on tissues
CNS- tremors, hyperpyrexia
CV- tachycardia, AFib, HTN with wide pulse pressure, can cause high-output failure
Differentiate changes in reflexes expected in
(a) Serotonin syndrome
(b) Malignant hyperthermia
(c) Neuroleptic malignant syndrome
(a) Hyperreflexia and clonus due to increase serotonergic activity
(b) Hyporeflexia b/c no intracellular calcium => can’t reflex/react and rigid
(b) Bradyreflexia b/c relative lack of dopamine, ‘lead’ pipe rigidity
Indication for cyproheptadine
(a) Mechanism of action
Cyproheptadine = antihistamine and serotonin antagonist with anticholinergic effect used in the tx of serotonin syndrome (hyperreflexia, tachycardia, clonus, agitation, diaphoresis, fever)
Explain how water deprivation test differentiates/diagnoses central vs. nephrogenic DI
Central DI- not making ADH, nephrogenic DI- don’t respond (concentrate urine) in response to ADH
Step 1: 8 hrs of water deprivation, expect reduced UOP and concentrates urine (if don’t concentrate then ADH not working and diagnosis made)
Step 2: Administer desmopressin (ADH analogue) and measure urine osmolality response. Central DI will have rapid rise in urine osm, while nephrogenic DI will not
Buzzword: masseter muscle contraction
Masseter muscle contraction- malignant hyperthermia from calcium dysregulation
When to consider osmolar gap positive?
Not just when the serum osms are high, have to calculate expected then subtract measured
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
Meaning of ESBL
(a) typical bugs
ESBL = entended-spectrum beta-lactamase producing bactereia = enzymes that hydrolyze extended-spectrum cephalosporins => resistant to CTX, cefepime
(a) gram negatives (typically E. coli, klebsiella, pseudomonas)
- first line tx = carbapenems
ESBL
(a) Typical bugs
(b) Sensitivity pattern to look for
(c) First-line agent
ESBL = entended-spectrum beta-lactamase producing bactereia = enzymes that hydrolyze extended-spectrum cephalosporins => resistant to CTX, cefepime
(a) gram negatives (typically E. coli, klebsiella, pseudomonas)
(b) ESBL not routinely tested for so nonsusceptibility to CTX (MIC > 2) is often used as a proxy for ESBL production
(c) First line tx for ESBL-producing organisms = carbapenems- ertapenem if klebs or E. coli, meropenem if pseudomonas or acinetobacter
Differentiate ESBL from CRE
For resistant gram negative bugs (klebs, E. coli, pseudomonas mainly)
-ESBL = extended-spectrum beta-lactamase producing bacteria that confers resistant to 3rd/4th gen cephalosporins (CTX, cefepime) so first line treatment is carbapenems (mero)
-taking it a step further CREs are carbapenamase-producing bugs (typically pseudomonas, steno, klebs) resistant to mero/carbapenems => need to use something with even more extended capabilities
ex: meropenem-vaborbactam, colistin
Lactose vs. non-lactose fermenting GNRs
Non-lactose fermenting = pseudomonas
Lactose-fermenting = E. coli and klebs
2 indications for early (within 48 hrs) valve replacement for native-valve L-sided endocarditis
Early valve replacement based on characteristics of the valvular vegetation
- Size over 10mm diameter
- location- particularly anterior leaflet of mitral valve given association with embolic phenomenon
-importantly: not persistent bacterermia over 72 hrs, as 72 hrs if within natural history of S. aureus bacteremia and bacteremia considered persistent only after 5-7 days
How long is consider persistent bacteremia for infective endocarditis?
-considered persistent bacteremia once blood cultrues + for 5-7 days. Within natural history of S. aureus bacteremia for blood cultures to remain positive for >72 hrs
Infection Prevention required for the following
(a) Tb
(b) SARS, Covid
(c) Varicella
(d) RSV
(e) Ebola
(f) Meningococcus
(g) C. Diff
(a) Tb = airborne only (no contact)
(b) SARS, COVID = airborne and contact
(c) Disseminated varicella = airborne and contact
(d) RSV = droplet and contact
(e) Ebola (viral hemorrhagic infections) = airborne and contact
(f) Meningococcus = droplet and contact
(g, h): C. diff and MRSA/VRE = contact
Droplet (regular surgical mask) vs. Airborne (negative pressure and n95)B
Buzzword for unusually “stick” gram negative rod
GNR- so thinking E. coli, pseudomonas, klebs
Hypervirulent klebsiella pneumoniae is specifically hypermucoviscous (ew)- often metastasizes to other organs (eyes, brain, lungs, skin, liver)
Differentiate clinical utility of DSA vs. CT perfusion of the brain
DSA- often used to look for vasculitis or mycotic aneurysms (infected aneurysms) that would infer higher risk of ICH
ex: pt with infective endocarditis and septic emboli needs AC for a PE- risk of bleed helped determine by DSA
Newest guidelines for treatment duration of GNR bacteremia
Certain gram negative bacteremias- noninferior to treat for 7 instead of 14 days
Gram negative bacteremia afebrile and HD stable after 48 hours with adequate source control- noninferior to treat for 7 days
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
Estimated loss in cardiac output in AFib
Expect drop in cardiac output 10-15% due to loss of atrial kick
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
First line treatment for thyroid storm in pregnancy
Thionamides (PTU) preferred, methimazole contraindicated due to teratogenic effects
Formal recs for prophylactic fluids to reduce risk of contrast-induced nephropathy
Nope not indicated, RCT with 660 pts, half to periprocedural fluids- no difference in AKI
First line mgmt for life-threatening ANCA vasculitis
Induction with steroids + cyclophosphamide or rituxan
(not PLEX- PLEX first line for myasthenia crisis or anti-GBM, but use is controversial in ANCA)
Differentiate lactate:pyruvate ratio in type A vs. type B lactic acidosis
(a) Ex: lactate:pyruvate seen in status asthmaticus on continuous nebs
Type A due to hypoperfusion where pyruvate metabolism is shifted to produce lactate = increased lactate:pyruvate ratio
While type B (few reasons but one being beta-adrengeric tone increase produciton of both lactate and pyruvate) => lactate/pyruvate ratio is normal
(a) Normal lactate:pyruvate ratio
Acid/base disorder caused by excessive normal saline
Hyperchloremic metabolic acidosis
-hyperchloremic b/c 154 mEq/L of Cl
-met acidosis b/c Cl- encourages renal bicarb excretion
3 cutoffs for definition of AKI
- Rise in serum Cr by 0.3 over 48 hrs
- Cr increases by 1.5x baseline
- UOP below 0.5 cc/kg/hr x6 hrs
Differentiate approach for treatment of thyroid storm with AFib with RVR
Esmolol + PTU
vs.
Amio + methimazole
Avoid amio in thyroid storm b/c metabolism releases iodine which can be used to increase thyroid hormone production!
=> beta blockade and PTU
Then yes PTU or methimazole to block production, use PTU in pregnancy (avoid methimazole in pregnancy)
First line tx for suspected ADAMS-TS 13
Both PLEX and steroids (not just PLEX)
Parts of the PLASMIC score
Pre-test probability for TTP while ADAMTS-13 activity is pending
What’s more highly associated with failure to extubate
Ultrasound evidence of diaphragm dysfunction or peripheral muscle strength as a marker of diaphragmatic muscle stregnth
Diaphragmatic thickening fraction or diaphragmatic excursion highly correlated with failure to wean from mechanical ventilation
while peripheral muscle weakness does not mirror diaphragmatic weakness
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
8 hrs after last known well CTA shows middle cerebral artery occlusion- next step IR for catheter directed intervention vs. CT perfusion scan of brain vs. IV tenecteplase
Large vessel occlusions out of window for tPA (4.5 hrs after symptom onset or from last known well) benefit from CT perfusion to risk stratify penumbra and decide who should undergo IR intervention
Current guidelines don’t recommend bypassing imaging to go straight for intervention
Pt in status epilepticus unresponsive to ativan- next best agent?
No clear answer- keppra, fosphenytoin, and valproate all shown to have equivalent efficacy for seizure control
Time window for IV tPA in ischemic stroke
4.5 hr from last known well or 3 hrs in patients over the age of 80W
Explain candidacy for interventional thrombectomy
Large vessel occlusion on CT artiography and perfusion/injury mismatch on CT perfusion within 24 hours of symptoms
=> even if pt is out of window for tPA, if has acute neurologic symptoms with normal NCHCT get CT angiography and perfusion scanning
What drug is most successful at stopping convulsions and prevent recurrence of status epilepticus?
0.1 mg/kg Lorazepam
First line tx for status- IV ativan, NOT diazepam injection with phenytoin infusion which take longer to infuse and therefore took longer to stop seizures
Second line tx for status epilepticus if 0.1 mg/kg IV lorazepam doesn’t stop seizures
ESETT trial- RCT of pts who failed 0.1 mg/kg ativan assigned to keprra, fosphenytoin, or valproate- all equivalent
So wrong answer is phenobarb or another dose of ativan
Mechanism for hyperventilation to reduce ICP
(a) Lower limit pCO2
Alkalosis => vasoconstriction via alkalization of the CSF causing vasoconstriction. However this vasoconstriction is not paired with decreased metabolism so if pCO2 below 20mmHg can lead cause ischemia
(a) pCO2 < 20 start to see ischemia from too much intracranial vasoconstriction
(guidelines say pCO2 keep > 30)
Three key components of death by neurologic criteria
- Cause
- Exam
- Apnea test
- Mechanism that explains coma- 2 mechanisms for cessation of blood flow to the brain: (a) ICP > MAP or (b) loss of metabolic demand due to cessation of brain at cellular level
- No brain activity- ex: no cranial nerve reflexes and negative cold calorics
- can maintain spinal reflexes ex: babinski - No breath triggered by CO2 (apnea test)
What to do if pt becomes hypoxic or hypotensive during apnea test for evaluation of brain death
Apnea test is to see if pt will attempt to initiate a breath with increased pCO2 (cannot let them die first of hypoxia or hypotension)- so need to treat those (preoxygenate and ensure euvolemia) or stop test if they occur. If you stop the test doesn’t mean they’re not brain dead, just test does not contribute to diagnosis
How to interpret DF and Lille Score
For EtOH hepatitis:
DF > 32- steroids (pred 40) x28 days, unless stop at 1 week if Lille > 0.45 due to infectino risk (and score showing inadequate response)
Explain use of benzos and pralidoxime in sarin gas poisoning
Sarin gas or organophosphate => cholinergic toxicity
-benzos for seizure prevention and b/c nicotinic overactivation can cause aggressive tachycardia
-prolidoxime (AChE reactivator)
Mnemonic for drugs with zero order kinetics
PEAS
Phenytoin
Ethanol
Acetaminophen
Salicylates
(while all others have stable half life = first order kinetics)
Chlorine vs. phosgene
Chlorine- more water soluble compound => upper airway, eye irritation, more immediate respiratory distress
Phosgene- noncardiogenic pulmonary edema, freshly mowed hay or green corn
Why propranolol in thyroid storm preferred beta-blocker
B/c also inhibits T4 to T3
Preferred fluid to resuscitate DKA and why
LR > NS b/c LR gives some bicarbonate to bind some ketone excretion in urine and doesn’t contribute as much to the hyperchloremic metabolic acidosis
Pts resuscitated with LR had DKA resolve 4 hrs faster than NS
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)
Main CMP abnormality to suspect
(a) During cooling
(b) During rewarming
During cooling everything shifted into cells => (a) Monitor for hypokalemia. Also metabolism slowed down so look out for (a) Hyperglycemia
During rewarming everything shifted back out of cells and glucose used up again => (b) Hyperkalemia and hypoglycemia
Utility of factor VIII in coagulopathy
Factor VIII- only clotting factor not made in the liver (made in the endothelium) => if factor VIII activity is low can be used to differentiate DIC vs. coagulopathy from liver dysfunction (normal factor VIII level)
