Critical Care Flashcards
MAP Calculation
[SBP + 2*DBP] / 3
Normal MAP
70 - 100mmHg
MAP >65 is essential for what function?
cerebral perfusion pressure
urine output indicative of hypoxia
UR < 0.5ml/kg/hr
when does lactic acid rise?
anaerobic metabolism
hypoperfusion - as air runs out for the organs they start to use other sources
normal lactic acid level
< 1 mmol/L
hemodynamics of hypovolemic shock
low cardiac index and wedge pressure
reduced preload (lack of volume) means less to pump
SVR reflexively increases to compensate
cardiogenic shock hemodynamics
acute HF (low cardiac index)
heart is not pumping correctly so it causes congestion (increased wedge pressure)
this in turn decreases volume in circulation leading to hypoperfusion which will reflexively increase SVR which in turn hurts the pumping of blood more (increased afterload)
causes decrease in renal excretion of sodium and water
Obstructive Shock Hemodynamics
massive PE, tamponade filling pleural space, aortic stenosis, etc
puts too much pressure on the diastolic chambers so they cannot fill well to then be pumped out, same hemodynamics as cardiac
distributive shock hemodynamics
sepsis, anaphylaxis, intoxication, pancreatitis, could even be endocrine - could be all over the map here
usually have increased cardiac index with leaky capillaries to fill with fluid and decreased BP
definition of septic shock (2 requirements)
MAP < 65 requiring vasopressors
Lactic acid >2 mmol/L
when to administer IVF in sepsis and what fluid volume to give?
30ml/kg x 1 and give if hypotension or Lactate > 4mmol/L
sepsis vasopressor of choice and dose
Levophed - typical is 0.01 - 3 mcg/kg/min (ours is a flat 8mcg/min)
when to add vasopressin to levophed and what dose?
infuse at a fixed rate of 0.03units/min usually
when flow rates are around 0.25 - 0.5mcg/kg/min
when to use phenylephrine as a vasopressor
if severe tachyarrhytmias develop w/levophed and vasopressin
duration of peripheral vasopressor until you NEED a central line
> 6 hours
extravasation of vasopressor treatment
phentolamine injected around the site
may sub w/nitroglycerin paste q6h or SC terbutaline
dopamine ADRs
arrhythmias
endocrine changes (decreased prolactin, GH, and TH)
depletes endogenous levophed (precursor to levophed)
when do you use antifungals in sepsis?
recent broad spectrum antibiotics
indwelling Central line
long-term PN
recent abdominal surgery
immunocompromised
when to use hydrocortisone
varying opinions
possible add 200mg IV daily once levophed doses > 0.25mcg/kg/min for at least 4 hours
Bicarb Normal Range
22 - 26 meq/L
acidosis means more or less bicarb
acidosis means less bicarb (bicarb is basic)
respiratory acidosis means higher or lower PCO2
acidosis is increased PCO2 and alkalosis is a decrease
normal range of PCO2
35 - 45 mmHg
respiratory compensation shift
blood that is pH < 7.35 will result in an increased respiratory rate to get rid of more CO2 and raise the pH
acidosis/alkalosis and the respiratory/urinary response
immediately -respiratory compensation occurs
acidosis results in respiratory increased breathing rate to get rid of CO2 (acid)
alkalosis results in respiratory slowing to decrease loss of CO2
kidneys take longer to compensate
bicarb excretion or retention will change the pH
differentiate b/w metabolic or respiratory alkalosis/acidosis
pH <7.35:
pCO2 elevated is respiratory, bicarb is low its metabolic
pH >7.45:
pCO2 decreased is respiratory, bicarb is high its metabolic
Anion Gap Calculation
Sodium - Chloride - Bicarb
Anion Gap Normal Range
6 - 12 meq/L
what causes respiratory acidosis?
PE
pulmonary edema
over-sedation, CNS depression
stroke
PNA
bronchospasm
spinal cord injury
what causes respiratory alkalosis?
stimulants
anxiety
pain
head injury
decreased O2 carrying in blood
reduced alveolar O2 extraction
respiratory rate
extracorporeal removal
hyperventilation
metabolic acidosis with anion Gap causes
MUDPILES
methane
uremia
DKA
propylene glycol
intoxication/infection
lactic acidosis
ethanol
salicylate
metabolic acidosis without anion Gap causes
F-USED CARS
fistula (pancreatitis)
uteroenteric conduits
saline excess
endocrine (hypo-parathyroid)
diarrhea
carbonic anhydrase inhibitors
arginine, lysine, Cl
renal tubular necrosis
spironolactone
metabolic alkalosis causes
Urine Cl >25:
hyperaldosteronism
high mineralocorticoid
urine Cl <25:
vomiting
NG suction
diuretic
treatment for respiratory acidosis
ventilation
correct causet
treatment for respiratory alkalosis
slow breathing
sedation
ventilation
oxygen
treatment for metabolic acidosis
treat cause
bicarb not as effective but is used sometimes for non-AG
treatment for metabolic alkalosis
Urine Cl >25:
potassium
aldosterone antagonist
acetazolamide
Urine Cl < 25
NS
acetazolamide
HCl if severe
normal PaCO2
35 to 45 mmHg
EtCO2 level to determine if good outcomes can be hoped for after ROSC
EtCOS < 10 is a poor prognostic factor after intubation or 20 mins after ROSC
longest duration for breaks in chest compressions
10 seconds
drugs and doses that can be given endotracheal tube
NALE
naloxone
atropine
lidocaine
epinephrine
2 - 2.5x the standard dosing
targeted temperature management goal temps
32 - 36 C for at least 24 hours if still unconscious after ROSC
how to treat shivering with TTM
preceded, ketamine, opioids, anesthetics, bupsirone, paralytics (use last)
effects of TTM on drug metabolism
CYP 3A4 and 3A5 are hindered
sites of delivery are hindered (propofol for example)
use bolus dosing in this setting
reduce doses of all sedatives for tx during this time
heart effects with TTM
bradycardia
shifts in electrolytes and glucose during TTM
during cooling - hyperglycemia as insulin secretion slows, K-Phos-Mag go low as they seep into the cells
during rewarming - hyperkalemia, hypoglycemia as insulin increases
replace electrolytes slowing so not to overshoot on rewarming and monitor glucose q1h
rewarming goal rates
increase by 0.25 to 0.5 degrees/hr
causes of hypoventilation
drug overdose
neuromuscular disease
CPR
CNS injury
hypoxemia causes that can lead to respiratory failure
pulmonary injury
PNA
pulmonary edema
pulmonary embolus
ARDS
2 bets pain scales for ICU and one patient set it is bad for
bad if patients have TBI
Behavioral Pain Scale
Critical-Care Pain Observation Tool
sedation scales and goals
RASS goals 0 to -1
SAS goals 3 to 4
morphine opioid highlights
prolonged duration of action with renal failure
active metabolites
can cause bronchospasm
fentanyl highlights
no hypotension or flushing
longer you use it the longer the 1/2 life gets
continuous sedation benzos
lorazepam can cause propylene glycol toxicity
measure osmolal Gap to monitor
lorazepam preferred due to no metabolites, no effects if renal/hepatic failure or CYP enzymes
midazolam - greater lipophilicity and active metabolites but rapid onset for dressing changes, etc
diazepam - accumulates, rarely used, only used for alcohol withdrawal usually
propofol highlights
initial dose 5mcg/kg/min titrated by 5 q5 min
avoid >80mcg/kg/min - may develop propofol related infusion syndrome, no loading dose b/c of hypotension usually
no pain control
Monitor:
BP, Triglycerides if over 48 hours
propofol related infusion syndrome (PRIS)
metabolic acidosis, cardiac failure, arrhythmias, cardiac arrest, rhabdo, hyper-Kalemia, kidney failure
Preceded highlights
prolonged duration in hepatic failure
usual dose 0.2 - 0.7 mcg/kg/hr depending on intubation or light sedation
ketamine highlights
has some sedation and analgesia properties
NMDA and partial MU receptors
ADR - HTN, tachy, delirium (30% of pts) treat w/benzos
haldol for delirium
give 1 - 2.5mg IV in elderly, double dose every 20 minutes until it works
not proven to shorter delirium
antipsychotics for delirium
measure all for QT prolongation
risperidone and olanzapine have less QTc
haloperidol and risperidone - higher EPS
neuromuscular blockade use
cisatricurium 15mg x1, then 37.5mg/hr for those on analgesics and sedatives and still not recovering from intubation
can lower intracranial HTN in TBI
should use artificial tears
precedex is not deep enough sedation for nmb
who should not receive SC insulin? IV is prefered
if they have significant peripheral edema
vasopressors
rapid correction of blood sugar preferred
Behavioral Health Pain Score treat score
6 or higher means unacceptable pain
CPOT score meaning
> 3 is unacceptable pain
drugs that increase neuromuscular blockade
steroids
aminoglycosides
clinda
TCN
polymyxins
CCB
antiarrhthmics
furosemide
lithium
drugs that decrease neuromuscular blockade
aminophylline
theophylline
carbamazepine
phenytoin
electrolytes and neuromuscular blockade
low electrolytes increase block
high electrolytes block blockade
when is POC glucose testing least accurate?
hypotension
high highs or low lows
anemia
hypoperfusion
does POC glucose testing OVER estimate or UNDER estimate levels?
over estimate
any of these designate SUP by themselves
mechanical ventilation x 48 hours
platelets < 50, INR > 1.5 or aPTT x 2 ULN
GI bleed within last one year of admission
any 2 of these risk factors would designate SUP
spinal cord injury
hypoperfusion
severe burns
organ dysfunction acutely
>250mg/day of hydrocortisone
liver failure causing coagulopathy
transplant
AKI
major surgery
multiple traumas
sucralfate can cause what toxicity?
aluminum in renal failure
H2RA’s for SUP and doses
famotidine 20mg IV/PO daily or BID
Nizatidine 150mg PO q12h
cimetidine 300mg q6h PO
PPI for SUP and doses
omeprazole 20mg daily
esomeprazole 20-40mg PO/IV daily
lansoprazole 30mg PO/IV daily
pantoprazole 40mg PO/IV daily
PPI Side effects
HA
diarrhea/constipation/ab. pain/nausea
C diff / PNA risk increased
H2RA side effects
thrombocytopenia
mental status changes
renal function dose adjustments
PNA risk increased
epidural access and LMWH
can place an epidural 12 hours after last LMWH dose I for VTE
can maintain a catheter with daily dosing
if BID, cannot keep an epidural in
remove catheter at least 10-12H after LMWH dose
EN residual volume to start worrying
250 - 500 ml residuals
DOC to prevent vasospasm after intracranial hemorrhage
nimodipine PO 60mg q4h x 21 days
