commit 4c7da8dc1faa827bf22d1c9546d5e8426aba211d
parent 7fd47dab53c1d71fcf6eee25b0eac283ff52bc5e
Author: Beau <cbeauhilton@gmail.com>
Date: Fri, 13 May 2022 08:33:58 -0500
lectures
Diffstat:
5 files changed, 258 insertions(+), 1 deletion(-)
diff --git a/learn/2022-04-28-anxiety-psychopharmacology.md b/learn/2022-04-28-anxiety-psychopharmacology.md
@@ -107,6 +107,35 @@ and afterward consider whether a taper of medicine is likely to allow the person
# psychopharmacology
FDA labels for drugs are general.
-50mg of IR quetiapine, 37.5mg XR venlafaxine do not map exactly onto what we usually call them.
+50mg of IR quetiapine, 37.5mg XR venlafaxine
+do not map exactly onto what we usually call them
+(second generation antipsychotic and SNRI).
+
+## second generation/atypical antipsychotics
+
+## pathways of clinical relevance
+
+- Mesolimbic - D2 (need >=60% blockage for efficacy)
+- Nigrostriatal - Parkinsonism, akathisia, tardive dyskinesia
+- Mesocortical - apathy, inattention
+- Tubuloinfundibular - galactorrhea
+
+## receptors "" ""
+
+- D2 - agonism increases nausea (carbidopa-levodopa brand name chosen as marketing tactic for having less GI adverse effects "Sinemet" == "no puke")
+- 5HT2a - antagonism: decreases EPS
+- H1 - antagonism: sedation, decrease itching, wt gain, anxiolysis, weight gain, decreases nausea
+- M1 - antagonism: confusion, sedation, dries, decreases nausea
+- alpha1 - antagonism: orthostatic hypotension, sedation
+
+Drug naming schemes reflect receptor targets.
+
+- cloza | pine
+- olanza | pine | H1, 5HT2a, M1, D2 (great for chemo-induced nausea, hits three relevant nausea receptors at low doses)
+- quetia | pine | H1, 5HT2a, M1 (less D2, not quite as good for nausea, but pretty great for agitation)
+- zipras | idone
+- risper | idone | 5HT2a, alpha1, D2 (less weight gain, not much of a nausea medicine)
+
+## depression
diff --git a/learn/2022-05-06-hemoptysis.md b/learn/2022-05-06-hemoptysis.md
@@ -0,0 +1,49 @@
+# hemoptysis
+
+Scott McCall
+
+
+## when to intubate
+
+if they've already coded, or are very close to it
+
+if a person is awake enough to cough,
+they are better at clearing the small airways than we are with suction
+
+
+## ABCs
+
+A - late intubation
+A - mainstem/positioning (intubate the clear side, put the sick side down)
+
+B -
+
+C - ~3L of blood can fit in a typical lung, may need massive transfusion protocol
+
+
+## meds
+
+TXA - if the inhaled drug can get to the problematic areas, e.g. bronchitis/bronchiectasis
+ - literature suggests TXA is helpful if the coagulation cascade is relatively normal (e.g. no mortality benefit in cirrhosis)
+
+PCC vs FFP -
+no in vivo or in vitro evidence that
+drug levels or coagulation parameters are meaningfully improved with PCC,
+Xa decoy (Andexanet Alfa) does work but is expensive and not often stocked
+
+Cryo
+
+
+## imaging
+
+CT bronchial artery protocol (CT angio w relatively early shots)
+
+GGO, can be tree-in-bud (clot)
+
+## causes
+
+- bronchitis/bronchiectasis (in bronchiectasis the vessels are closer to the surface)
+- PNA
+- PE (usu late, distal, scant, r/t necrosis)
+- malignancy - things that recruit VEG-F - thymic, thyroid (papillary), melanoma, Kaposi
+- cavitary lung lesions (TB, fungal balls, Erasmus formation)
diff --git a/learn/2022-05-09-vents.md b/learn/2022-05-09-vents.md
@@ -0,0 +1,86 @@
+# vents
+
+Alex Dragnich
+
+
+## overall
+
+Art Wheeler (paraphrased) - the best mode of ventilation is the mode you know best.
+
+
+## knobs
+
+Many!
+- FiO2
+- rate(t)
+- Pi
+- PEEP
+- I:E ratio
+- TV (Vt)
+- etc.
+
+but really:
+- FiO2
+- triggers
+- Q (flow)
+- C (cycle)
+
+and cannot perfectly control pressure and volume at the same time,
+though modes like PRVC attempt to strike an automated balance.
+
+oxygenation: FiO2 (directly) and PEEP (via mean airway pressure)
+
+ventilation: R(t), Vt, Pi
+
+
+## APRV
+
+Type of inverse ratio ventilation,
+based on time constants of collapse/expiration.
+
+e.g. expire ~75% of TV in a time constant.
+
+
+## SIMV
+
+supported intermittent mechanical ventilation.
+
+Background of VC at a certain rate,
+allowed to take supported breaths in between.
+
+~CMV w BiPAP
+
+
+## AC
+
+assist control.
+
+volume control, people are allowed to take breaths and then volume is delivered
+
+set: Vt, PEEP, R(t), FiO2
+
+measure: peak inspiratory pressures, plateau pressures, MV, driving pressure (plateau minus PEEP)
+
+triggers: P or Q (e.g. neuromuscular, may not be able to generate much flow so set pressure trigger, COPD often the opposite)
+
+cycle: time
+
+
+## PC
+
+set: P(high), P(low), Pi, R(t)
+
+measure: Vt, V
+
+triggers: P or Q
+
+cycle: time
+
+set a MV alarm (ideally, set at what has been maintaining ventilation for that pt)
+
+
+## PRVC
+
+set target volume, generates pressures, adjusts based on calculation of last three breaths
+
+is actually pressure control mode
diff --git a/learn/2022-05-10-troubleshooting-vents.md b/learn/2022-05-10-troubleshooting-vents.md
@@ -0,0 +1,34 @@
+# troubleshooting vents
+
+Scott McCall
+
+## high peak pressures
+
+Start at the machine.
+
+Make sure the system is working well -
+check tubes for kinks,
+follow it all the way from the vent to the patient,
+look for biting, etc.
+
+Within the patient,
+think about mucus plugs at the end of the ETT,
+single-lung intubation,
+mainstem intubation,
+PTX,
+hemothorax,
+ARDS.
+
+Get: CXR, plateau pressure
+
+## low minute ventilation
+
+vent problem vs patient problem
+
+vent problem (are we actually having high peak pressures?)
+
+patient problem
+- is the cuff inflated?
+- has the patient been intubated for a long time (balloon migration, tube breakdown)?
+- bronchopleural fistula
+
diff --git a/learn/2022-05-13-pressors.md b/learn/2022-05-13-pressors.md
@@ -0,0 +1,59 @@
+# pressors
+
+
+MAP = SVR * CO
+
+CO = HR * SV
+
+# receptors
+
+alpha1, beta1, beta2
+
+alpha1 = vessel walls, contracts
+
+beta1 = contractility
+
+beta2 = vasodilation, bronchodilation
+
+vasopressin/ADH = V1 (vasoconstriction in the periphery), V2 (in kidneys)
+
+AngII = inc aldosterone, peripheral vasoconstriction.
+
+# drugs
+
+epi = +++alpha1, +++beta1, ++beta2.
+Useful during codes, anaphylaxis (bronchodilation), third(ish)-line in sepsis.
+
+norepi = ++alpha1, ++beta1, no beta2.
+Go-to pressor.
+
+phenylephrine = +++alpha1, no beta1, no beta2.
+Useful pressor if tachyarrhythmia and not in cardiogenic shock.
+
+dobutamine = no alpha1, ++beta1, +beta2.
+Used in cardiogenic shock (+chronotropy, +inotropy), pHTN.
+
+dopamine = not really used any more
+
+vasopressin (ADH) = mostly looking for V1 effects
+
+AngII = Used in septic shock.
+Very pt-dependent,
+"super-responders" (~10%) can sometimes come off all other pressors,
+most folks don't respond much.
+C/i in heart failure.
+Increases clotting (cannot use if cannot use DVT ppx).
+
+also think about:
+stress-dose steroids (little downside, cortisol testing is useless in critically ill pts),
+acidosis (do they need bicarb drip/post-replacement bicarb?)
+
+
+# access
+
+Pressors via PIVs are usually fine.
+No actual dosage cutoff,
+some institutions will create cutoffs
+but there's no data for that.
+
+Extravasation rate ~3/1000 in one retrospective study of ~14,000 pts.
