week 2 Flashcards
cardiac arrest
unable to geenrate adequate CO to support o2 demands of tissue
four rhythms:
v fib
pulseless ventriculat rachycardia
pulseless electrical activity (PEA)
asystole
survivial depends on acs or bcls
only proven benefit of cardiac arrest
quality chest compressions
cardiac arrest treatments
1, start CPR
- determine rhythm
shockable: VF and pVT
non shockable: asystole, PEA
VF or VT arrest
- provide shock
work on establishing iv access,
if still in shockable environent, give another shock….
then can give epinephrine…
if pt is still in shockable rhythm.. can give another shock, then give antiaryhmics like amiodarone or lidocaine
pea/asystole
non shockable
if asytole or pea admin epinehrine asap and perform cpr for 2 min
if pt still in nonshockable rhhtm, continue cpr
*note: EPNIPHERINE ONLY. vasopressin no longer epinephrine
cardiac arrest med admin routes
iv
io (intraosseous)
endotracheal (et)
NAVEL
naloxone
atropine
vasopressin
epinephrine
lidocaine
vasoactive agents
enhance organ profusion by increasing arterial and aortic diastolic pressures resulting in increases incoronary and cerebral perfusion pressures
ex: epineohrine
epinephrine
indications:
vf and pulseless vt
pea and asystole
dose: 1mg iv/ io q3-5 min
admin as soon as possible in pea/asystole
antiarrhythmics
no high quality evidence to suggest that any antiarryhtmics routinely during crdiac arrest increases survival
amiodarone
lidocaine
amiodarone
indications
dose
considerations
indications: vf and pulseless vt
dose: 300 mg iv bolus. may repeat 150mg iv bolus
considerations: caution in bradycardia and hypotension, possible qt prolongation
lidocaine
indications
dose
considerations
indications: vf an dpulseless vt
dose: 1.1.5 mg/kg IV/IO
considerations:
consider if amiodarone unavailable, risk/ hx of qt prolongation. study not suggests beenfit of lidocaine
magnesium
indications
dose
considerations
indications: vf, pvt associated with torsades des pointes. NOT TO BE USED IN VF,PVT W. NORMAL QT INTERVAL
dose: 2g iv bolus
considerations
reversible causes of arrest Hs
H
hypovolemia- give fluids
hypoxia-give 100% o2 by mask
hydrogen ions(acidosis)-bicarb not recomomended during o2 arrest
hyperkalemia:suspect in dialysis pts, renal insufficicnecy, drug induced (trt w. calcium chloride or gluconate
temporary measures: (bicarb, insulin and dextrose)
long term: diuresis, kayexalate
hypothermia
reversible causes of cardiac arrest
Toxins (opioids, TCA, etc.)
*give naloxone if suspected I
cardiac Tamponade:
Tenstion pneomothorax
thrombosis(PE and MI)
ischemic stroke SS
sudden onset of focal neurological defecit
dysphasia/dysarthria
hemianopia
weakness
ataxia
sensory
neglect
symptoms are unilateral
NIHSS stroke severity
0: no strok esymptons
1-4: minor stroke
5-15: moderate stroke
16-20: mod-sveere stroke
21-42 seevre stroke
treatment options for ischemic stroke
within 4.5 hr of symptom onset
*fibrinolysis +/- thrombectomy
iv fibronylitics
contraindications
iv fibrinolytics ci
<18
ischemic throjke w.i 3 months
intrcranial surgery w.in 3 months
gi malignancy or hib within 21 days
lmwh within 24hrs
unclear onset time >4.5
intracranial hemmorhage
iv fibrinolytics
alteplase,
tenacteplase
moa: tpa activator, dissolves fibrin
dose:
alteplase: 0.9mg/kg
short acting. can give bolus
tenacteplase: 0.25mg/kg
can give iv push, longer t/2
iv fibrinolytics blood pressure control
goal for bolus: <185/110
goal for infusion <180/105
if pt meets exclusion criteria and alteplase not given, permissive htn is allowed
bp not treated unless >220/110 in effort to perfuse brain
ischemic stroke htn treatment
1st line: labetalol
nicardipine
fibrinolytic complications
systomatic ICH:
d/c alteplas einfusion
treat w. cryocepitate 10u
angioedema
-miantaine airway, hold acei-
post fibrinolytic care
neuro and bp monitoing for 24 hrs
dysphagia and aspiration risk
high dose statin all apts
anti platelets
dvt prophylaxis >24hr post alteplase
anticoags if cardioembolic stroke or hx of a fib
secondary strok erevention
lifestyle and nutrition
smoking cessation
limit alcohol consumption
ocunsel on substance abuse
risk factor for breakthorugh seizures
provoked:
intoxication
withdrawal, etoh, benzos
trauma
meningitis
psychiatric
metabolic derangements
unprovoked
*difficultto determine
1st line agents to stop seizures
benzos (lorazepan, diazepam, midazolam)
antiepileptics for seizures
not first lines
do not stop seizures
prevent more seizures from occuring
treatment of seizures
stage 1(0-10 min): lorazepam or midazolam
stage2: 10-30 min
phenytoin, foshenytoin
stage 3: 30-90 min
midazolam or propofol
stage 4 (90 min-many hours to days): pentobarbitokl
benzos for seizures
1st line: lorazepam 4mg
second line: diazepam 5-20 mg
moa: bind to gaba receptor
ae: impaired conciousness
hypotension
resp depression
antiepileptics for seizures
second seizure indicates epileptic
if on epileptic, can give small dose of at home antiepileptic
phenytoin
fosphenytoin
pneumonic for phenytoin adr
PHENYTOIN
p-450 reactin
hirsutism
enalarged gums
nystahmus
yellow borwning of skin hepaptiis
teratogenecity
osteomalaciaa
inteferance w. metabolsm
neuropathies
cardio: hypotension, bradycardia, qt prolongation
saturable pk
monitinrg: goal 10-20. if seizing, goal 15-25
must correct for low for albumin
levetiracetam
dose: 60mg/kg for status epilepticus
levels do not correlate w. efficacy
AE: agitation, drowsiness
valproic acid
LD: 50 mg/kg
goal levels 50-100
AE: hyperamonemia
thrombocytopenia
DDI: phenytoin and valproic acid both strongly protein bound
lacosamide
dose: 100-200 mg
adr: dizziness, abnormal vision
refractory status epilepticus
no response to inticial anticonvulsants
seizure lasting>2 hrs OR occuring at 2 more incidences per hour
high dose benzos: ex.midazolam2mg iv bolus
propofol infusion
phenobabrb and pentobarb coma (only use dif intubated because causes severe respiratory supression
post intubation treatment
paralytic used during intubation
goal of status epilepticus
to attai n burst supression
super refactory status epilepticus
treatment: ketamine infusion.
how to wean off antiepileptics for seizures
wean off meds tht have high risk AE
status epilepticus outcomes
repeat full neuro examinations
shock
sbp<90 mmhg
decrease by 40 mmhg from baseline
end organ dysfunctions in shock
cns
cardiac
pulmonary (acute resp failure)
renal(AKI, ATN
GI(erosive gastritis)
hepatic
hematologic
metabolic
immune system
hemodynamic parametes
BP=COxSVR(systemic vascular resistance)
CO: HR x SV
stroke volume: preload, instrinsic contractility, afterload
mean arterial pressure(MAP)
calculation= 1//3SBP+2/3DBP
mean arterial pressure calculation
1/3 SBP+2/3 DBP
goals for shochk mgt
determien etiology (hypovolemic, cardiogenic, distributive, obstructive
maintian adequate perfusion (assess preload, restore mean artieral pressure (GOALMAP
normalize lactate: goal<2
devices used in recognizing and magaing shock states
central venous catheyer
*measures central venous o2 sat
admin of fluids
pulmonary artery catheters
*measures pulmonary pressure, CO, mixed venous sat
not commonly used due to severe complications
Shocks
hypovolemic
what is it
cause
treatment
Shocks
what is it: low and sudden loss of iv volume
cause: hemorrhage, gi loss, severe dehydration, burns
#1 cause of death<45y.o
preload:decrease
CO: decrease
SVR increase
o2 sat decreases
treatment
REPLACE blood loss(PRBCS)
aniticoag reversal etc.
Shocks
CARDIOGENIC SHOCK
what is it
cause
treatment
Shocks
what is it: failure of left ventricle
cause: ACUTE MI
arrythimas, etc.
treatment.
preload increase
CO: decreaseSVR: increase
treatment: treat underlying cause (mi:recatheterization)
Shocks
disitributive shock
what is it
cause
treatment
Shocks
what is it: septic shock classic. pronounced vasodilation
cause: septic shock most common cause
preload: low
aterload: decrease
decreased or increased CO
decreased or increased tissue perfusion
treatment
Shocks
obstructive
what is it
cause
treatment
Shocks
what is itdecrease din lv stroke volume
cause
PE
pulmonary hypertension
tension pneumothorax
treatment
preload: high
CO:decrease
svr: increase
tissue perfusion: decreased
shock therapy
fluid challenge(generlly w. sepsis): crystalloid 30ml/kg over 25 min-30 min
pharm theraoy of shock
initiation of vasoactive agents when map remains <65 despite fluid admin
vasopressors: norepinehpine
epinehorine
dopamine
phenylephrine
vasopressin
NE for shock theraopy
alpha adrenergic agonist: causes peripheral vasoconstriction
epinephrine
b2 agonists
may increase aerobic lactate production
also useful in anaphylactic shock
dopamine in use for shock
dose dependent pharm
most effective in hypotensive ots w. depressed function
phenylephrine
reflex bradycardia
CO is hih and bp is low
dobutamine:
inotrope
vasopressin
goal: reduce concurrent vasopressor doses
o.3-0.4 u/min
septic shock mgt
correction of underliying cause (abx, source control)
abx timing: sepsis is deifnite: admin abx immediately
sepsis is possible: if present, give abx w.in an hour, if not present, reassess, admin abx w.in 3 hrs if ocncern of infeciton persisst
fluid resucitation: crystalloid 30ml/kg bolus (fluid of choice for initial recussiatiairon
1L of crystallid gives ~250ml o fintravascular volume
vasopressors
inotropes
corticosteroids
what is sepsis
lifethreartening organ dysfunction caused by a dysregulated host response to infection
SIRS criteria for spetic shock
atleast 2 of following
1. temp >38 C or < 36 C
hr: > 90 bpm
Rr: >20
wbc>12 or <4
pharm of septic shock
initiate when map <65 despite fluid amdin
1dt line: norepinehprine
vasopressin: an be added if pt has inadequate map while on norepinephrine
glucocorticoids( hydrocortisone)
improves ohysiologic response to sepsis, regulation of proinflammatory state
improve time to shock resolution
added when pt is still hypotensice despite increasing norepinephrine and assing
