Week 6: Toxicology Part II Flashcards
cannabinoid types
compounds that bind to and agonize the cannabinoid receptors
*phytocannabinoids
*synthetic cannabinoids
*endocannabinoids
what is the main component of marijuana that is responsible for the major psychoactive effects
THC
*mood elevation, euphoria, relaxation, creative thinking, and increased sensory awareness
cannabinoid receptors
CB1: high levels in the brain regions expected from psychoactive effects
*lack of coma and respiratory depression seen w. cannabis use
CB2: high levels expressed in periphery
*expressed on a number of immune cells
*isolated agonism of CB2 receptors has been the target for novel pharmaceutical candiates as anti-inflammatory agents
ex of medical conditions claim to be treated by marijuana
anorexia
anxiety
asthma
depression
epilepsy
glaucoma
head injury
insomnia
migraine headaches
multiple sclerosis
muscle spaciity and spasms
nausea and vomiting
neurologic disorders
pain
parkisons disase
tourette syndrome
cannabis plant parts
Hemp:
*cbd oil, hemp oil, cannabis oil (made form industrial hemp)
* contains 0.3% THC
Marijuana
*thc oil, marijuana oil, cannabis oil (made from marijuana plant)
contains 10% THC
wanted clinical effects of phytcannabinoids
mood elevation
euphoria
relxation
creative thinkning
increased sensory awareness
appetite stimuation
nausea supression
unwanted clinical effects of phytocannabinoids
short term memory difficulties
agitation
feeling tense
anxiety
dizziness
lightheadedness
confusion
loss of coodination
synthetic cannabinoids
thc is a partial agoinst at cb1 RECEPTOR
*EX: ab-chiminaca
*amb-FUBINACA
differences in cannabinoids
thc is a partial agonist at cb1
synthetic cannabinoids are full agoinsts
*higher receptor affinity
*longer half lives
desired clinical effects of synthetic cannabinoids
mood elevation
euphoria
relaxation
creative thinking
increased sensory awareness
clinical presenttion of synthetic canabinoid poisoning
SS:
Lab abnormalities
SS:
cns depression
disorientation
restlessness/agitation
hallucinations
seizures, generalized
conbativeness
anxiety
mydriasis
tachycardia
vomitingss
lab abnormalities:
*dec. K+
increased blood glucose
inc. creatinine kinase
inc. white bloos cells
inc. creatinine
management of synthetic cannabinoids
supportive, symptomatic care
*fluid electrolyte replacement
*antiemetics
*benzos
*ketamine
*intubation
Cannabinoid hyperemesis syndrome
patho
dx
patho: dysregulation of endocannabinoid system
*desensitization and downregulation of cb1 receptors that generally have antiemetic effects
*alteration in TRPV1 receptor after chronic cannabinoid use
dx:
hx of reg cannabinoid use
*cyclic N/V
*generalized diffuse abdominal pain
*compulsive hot showers w. symptom imrpovement
phases of CHS
preemetic/prodromal phase
pre metic /prodromal phase
*months-years
*diffuse abdom. disocmfort, feelings or agitation or stress, morning nausea, and fear of vomitinf
phases of CHS
hyperemetic phase
hyperemtic phase
*24-48 hrs
*cyclic episodes of N/V
*diffuse, severe abdom pain
phases of chs
recovery phase
upon total cessation of cannabis
bowel regimens, fluids , electrolyte replacement
full resolution may take ~ 1month
CHS management
clnical management;
* hot showers (activate trpv1)
*CAPSAIcin topical cream (activate trpv1
antinausea:
*haloperidol, ondansetron
*HaVOC trial found haloperidol was superior to ondansetron for improvement of N and abdom pain of 120 min
benzos:
*inhibitoy effects on medulary and vestibular nuclei associated w. n/v
supportive care:
*fluids and electrolytes
Sympathomimetic
inhibtion of norepineprine and dopamine reuptake, or increased release of neurotransmitters
“uppers”
adrenorecptor activation effects
a1:
*vasoconstriction
*inc peripheral resistance
*mydriasis
*inc closure of internal bladder sphincter
a2:
inhibitoin of norepinephrine relase
*inhibition of catecholamine release
*inhibition of insulin release
b1:
*tachycardia
*increased lipolysis
*increased myocardial contractility
*increased release of renin
b2:
*vasodilation
*decreased peripheral resistance
*bronchodilation
*increased muscle and liver glycogenolysis
*increased release of glucagon
*relaxed uterine smooth muscle
sympathomimetic toxidrome
inc vitals (bp, hr, rr, temp)
mental sttaus: agitated, hyperalert
pupil size: increases
bowel sounds: increased
diaphoresis: increased
other: tremor, seizures
general management of sympathomimetic toxirome
SUPPORTIVE CARE!
elmimination strategies (i.e activated charcoal)
benzos
anti-hypertensives
fluids
antipsychotics
electrolyte management
ice baths
sodium bicarb
substances that can cause sympathimometic toxidromes
cocaine
amphetamines
bath salts
pseudoephedrine
nootropics
buproprion
psuedoephedrine
cocaine
toxic dose: typical line=20-30 mg
*ingestion of 1 g is likely to be ftal
SS: euphoria, seizures, dysrhthmias, htn
CORNOARY ARTERY SPASM/mi
adulterants (laced w.)
*levimasole (antiparasitic agent): can cause neutropenia, vasculitis, urpura
management:
*benzos, supportive care
notes:
*be aware of body packers.
amphetamines
moa:release catecholamines
SS: adrenergic: similar to cocaine though longer lasting
*agitation, seizures, hyperhermia, htn, delerium
management: benzos,barbiturates, anti-HTN
*supportive care
Bath Salts
synthetic cathinones
ex: cathinone, methcathinone, mephedrome, methylone, MDPV
SS:
agitation, tachycardia, insomnia, paranoia, seizures, violen unpredictable behavior
Management: supportive care
buproprion and pseudoephedrien
have similar chemicalstructure to epinephrine or amphetamines, so when overdosed, can exibit sympathomimetic toxidromes
supportive care for sympathomimetic toxidrome
clinical effects: benzos
airway protection: intubation
hyperthermia: ice packs, cool fluids, antipyretics, benzos
dysrhythmias: sodium bicarb, lidocaine
rhabdomyolysis: fluids
where can salicylates be found
aspirin
methyl salicylate (oil of wintergreen)
topical salicylates
bismuth subsalicylate (peptobismol)
1ml=8.7 mg of Salicylic acid
epidemiology of salicylate exposure
ranked first amoung pharmaceuticals most frequently reported in human exposure
PK of aspirin
A: rapidly bsorped in non ionized form due to acidic ph
D: small Vd (-0.2L/kg) and highly protein bound
M: metabolized by liver. hydrolized to salicylic acid
E: excretes renally
t1/2 at low doses (antiplatelet effects)=2-3 hrs
t1/2 at high doses (anti-inflammatory)= 12 hours
toxicokinetics of aspirin
delayed absorption due to pylorospasm and bezoar formation in the stomach (immediate release stomach)
peak ocnc may not be seen until 24-36 hrs after ingestion w. enteric coated products
decreased protein binding and larger vd
*higher conc and low pH
*larger amounts of free drugs reach the tissue
prolonges t1/2 due to hepatic metabolism saturation saturation
*elmimnatino changes from irstorder kinetics tozero order kinetics
patho of SA overdose
serum ph faks and SA acid shifts to a nonioned state than can readily cross lipid bilayers and cell membranes effecting s variety of organs
krebs cycle inhibition impairs cellular respiration and uncoupling of oxidative phosphorylation leading to accumulation of pyurivc and lactic acid release of energy as heat
Acid base disturbances
*depend on time from exposure
*anion gap metabolic acidosis from presence of SA, production of lactate, ketones, and inorganic acids
neurologic; neuronal dysfunction causing cerebral edema
*discordance btw serum and cfs glucose
ototoxicity and tinnitus
hematologic
*plaelet dysfunction and hypoprothombinemia
pulmonary
*stimualte resp. driving causing hyperpnea and tachypnea
*acutre resp. distress syndrome (ARDS)
GI
*N/V
Renal
*prerenal AKi due to volume losses
8excrete large quantities of bicard, Na, and K
Acute toxicity of SA Signs and symptoms
n/v
gi irritation
tinnitus
tachypnea,hyperpnea
resp alkalosis or resp acidosiss
metabolic acidosis(anion gap or non-anion gap)
altered mental status/halucinations
coma
seizures
hyperglycemia or hypoglycemia (neuroglycopenia)
pulmonary edema
hepatic injury
HUGE CONSEQUENCES
*coagulopathy
*cerebral edema
*acure resp distress syndrome (ARDS)
*hyperthermia
acid base abnormality stages of ASA overdose
early: primary resp alkalosis, alkalemia, alkauria
intermediate: mixed resp alkalosis and anion gap metabolic acidosis, alkalemia, and aciduria
late: metabolic acidosis w. either a resp alkalosis or resp acidossi, acidemia, and aciduria
chronic toxicity of ASA
non specific and often misiagnosed
severe toxicity is associated w. serum conc.>60 mg/dl, altered mental sttaus, and acid base disturbances
cerbral edema and acutelung injury may be present
Acute vs chronic ASA toxicity
acute:
*younger
*intentional
*early dx
*suicial ideation
*severely elevated serum conc
*death is uncommen
chornic
*older
*Iatrogenic/unintentional
*underrecognized as a dx
*intermediate elevation in serum conc
*death is more common due to delayed recognition
evaluation and dx of asa testing
- serum salicylate level
*toxiicty associated w. conc >30 mg/dL
*THEREPEUTIC RANGE (INFLAMMATORY CONDITIONS(15-30g/dL)
*therepeutic range for analgesia (5-10 mg/dL)
acute toxicity
*mild symptoms seen in 150-200 mg/kg or 6.5 g of spirin
*severe symptoms>300-500 mg/kg
chronic toxicity>100 mg/kg/day for several days
- blood gas and anion gapto classify acid-base disorder
general treatment of ASA toxicity
no true antidote:
tratment based on supportive therapies
1. GI decontamination
2. IV fluids
3. glucose amdinisistration
Supportive therapies for asa toxicity
- multiple-dose activated charcoal(MDAC)
*prevents absoprtion of salicyates, can consider if pharmcobezoar or XR preparation suspected
2.hypovolemia should be corrected w. iv crystalloids
3.0.5-1g/kg of dextrose followed by additional bolus doses or continuous infusion for severe salicylate toxicity
Serum and Urine Alkalization
cornerstone of management for ASA toxicity.
shifts ASA out of brain and intro the serum to promote renal elimination
ion trapping of salicylate into serum and urine by alkalination. promotes excretion once ionized.
iv sodium bicarb is recommended for all symptomatic pts
*bolus dose: 1-2mEq/kg
continuous in fusion: 150mEq sodium biacrb in 1000mL of 5% dextrose at a rate of 1.5-2x maintenance rate
*goal urine pH 7.5-8
maintain normal K+ levels (due to shifts of K+ into intracellular space by admin of sodium bicarb)
hemodialysis in sa toxicity
can be considerd in severe toxicity and is recommended in the following ocnditions
*serum salicylate level >100 mg/dL
*serum salicylate level>90 w. impaired renal function OR failure of supportive therapies
serum salicylate level >80 w. imapired renal function AND failure of supportive therapies
supplemental o2 required due to altered mental status form hypoxemia
d/c HD when serum salicylate level is <19 mg/dL and pt is clinically improving
monitoring during treatment of SA
serum salicylate conc q2-4 hrs until pt is improving clinically
urine pH
serum pH
more frequent monitoring may be needed in critically ill patients
epedemiology of alcohol poisoning
methanol containing consumer products
*windshield wiper fuid (>60% of cases)
ethylene glycol
*engine coolant (antifreeze) in car radiators. it has sweet taste, but bittering agents have been added
isopropanol
*rubbing alcohol
*solvent used in household products, cosmetics, and topical pharmaceuticals
toxic alcohols =not intended for ingestion
primary alcohols
*methanol
*ethylene glycol
secondary alcohols
*isopropanol
toxicokinetics of toxic alcohols
A:
ingestion: rapidly absorpbed. F=92-100%
inhalation: occupational or intentional inhalation of methanol (huffing)
athylene glycol inhalation does not cause poisoning
transdermal: isopropanol and methanol penetrate skin better than EG
D: rapidly to total body water
0.5-0.77L/kg
Metab and elminiation:
(alcohol dehydrogenous and/or aledhyde dehydgrogenase (ALDH) couples to the reduction of NAD+ to NADH
*EG is eliminated via kidney unchanged
*methanol eliminated as vapor in expired air
toxic metabokites of toxic alcohols
methanol: formic acid formed by conversion by alcohol dehydrogenase and then aldehyde dehydrogenase
*formic acid causes metabolic acidosis w. minimally elevated latate
EG: metabolized by alcohol and then aldehyde dehygrognse.
toxic metab is glyoxilic acid
Isopropanol: acetone is toxic metabolite whihc is formed by alcohol dehydrogenase
clinical manifestations of toxic alcohol
cns
*iINEBRIATION is dependenton dose and mlecular-weight
*absense of inebriation doe snot include ingestion
metabolic acidosis
*toxic alcohols are metabolized to toxic organic acids [methanol->formic acid; EG->glycolic acid] which cause high anion gap metabolic acidosis
*exception: isopropanol’s metabolite acetone does not cause metabolic acidoses. it causes ketosis w.o an acidosis
methanol clinical manifestations
retinl toxicity
*blurry vision to complete blindness which can be asymptomatic
neurotixicity
*basal ganglia lesions bilaterally which can lead to parkinsonism
AKI
pancreatitis
ethylene glycol tox. clinical maninfestations
neurotoxicity
*oxalic acid+calcium=calcium oxalate monohydrate crystals which deposit renal tubules
*this precipitation can cause hypocalcemia
isopropanol clinincal mainfestations
hemorrhagic gastritis
dx testing for toxic alcohol poisonings
serum conc.
*results may not e availbale in timely manner
*prolonged time from ingestion?formate levels may be helpful
serum and urine oxalate conc are usually not clinically relevant
handle samples w. care (put in airtight container to prevent evaporation (isopropanol and ethanol)
toxic conc of methanol and eg>25 mg/dL
obtain electrolytes, Ca, BUN, Cr, UA, VBG or ABG, lactate, measured serum osmolality and serum ethanol concentration
anion gap and osmol gap and time of ingestion
! ANION GAP AND OSMOL GAP CAN BE USED TO INITIATE TREATMENT WHILE AWAITING RESULTS ON SERUM CONCENTRATION!
high anin gap metabolkic acidosis of unkown etiology
*lack of high anion gap metabolic acidosis can be seen with recent ingestion of toxic
alcohol
extrememly elevated osmal gap (>50 mOsm/L)
*normal osmol gap ranges from -14+10 mOsm/L
**a baseline osm gap is needed to compare current value as results maybe within normal range, but abnormal for the pt (i,e osmol gap=12, currentlyosmol gap=+6)
serum ethanol conc can prevent metbaolism to the organic acid and is consider protective
elevated lactate leves can be seen wih methanol and ethylene glycol poisoning
management of toxic alcohol poisoings
for antidotes
a: moa
b:dosing:
c:target conc:
d:AE:
resucitation
inhibition of ADH: cornerstone of therpy
*indicated for methanol and EG toxicity
1)IV ETOH10%continous infusion (rarely used in US)
*serum conc
*many complication s including hypotension, respiratory depression, cns depression and inebriation, flushing, hypoglycemia, hyponatreia, pancreatitis and gastrititis
2)fomepizole
*competitive inhibition of ADH
*intial boud: 15mg/kg IV piggyback over 30 in
*maintnenance dose: 10mg/kg iv piggyback q12 hours x4 doses hours then increase dose to 15mg/kg iv piggyback q 12 hours(induced its own metabolism after ~48hrs)
*continue until serum toxic alcohol conc is <20mg/dL+ asymptomatic w. normal serum pH
AE: hypotension and bradycardia
hemodyalisys preffered over renal replacement therapy
adjunctie therapy for methanol toxicities
methanol:
folic acid: enhances formate elmination
*methylprednisolone 1 g(high dose) q24 hrs for 3 days may improve the amount o vision loss experienced
*sodium bicarb continuous infusion: shifts formic acid to formate and causes ion trapping in the urine
Goal serum pH:>7.2
adjunctive therapies for ethylene glycol toxicities
thiamine: promotes coversion of EG to ketodipate
pyridoxine: promotes conversion of glycine to hippuric acid
sodium bicarb continuous infusion can be administered in pts w. ph <7.15
Examples of TCAs
imipramine (1st approved)
desipramine
amitriptalyine
nortriptyline
doxepine
trimipramine
protriptyline
epidemiology of tca overdoes
higher incidence of hospitalization and fatality in comparison to SSRI’s
pharmacoloy of TCA’s
classified at tertiary or secondary amines
inhibit reutake of NE and seretonin, incrasing amount at cns receptors
competitive antags of muscuranic ach receptots
peripheral a1 receptor antsgonists
inhibit periheral and central postsynaptic histaminr receptos
interfere w. chloride conductance
PK of tcas
A: completely and rapidly absorbed i gi tract
d: 10-40L/kg and variable
lipophillic
rapidly distribute to other organs
M:demtyhlat
E: 7-58 hrs
toxicokinetics
delayed absoprtion due to decreased gastric motility
severe overdoses leas to low blood ph increasing amount of free drug
saturable metabolisms prolong t1/2
clinicaltoxiicty is rapid and unpredictale: therepeutic dose: 2-4 mg/kg/day; conc. 50-300 ng/mL
NARROW therepeutic index
Acute ingestino causing cardiotoxicity and cns toxicity
dose: 10-20 mg/kg; conc 300-1000ng/mL
PAtho of tca toxiity
EEG findings
*prolonged qrs complex
*ight bundle branch bloc pattern
Sinus bradycardia
*antimuscarinic, vasodilatory, and sympathomimetic effects
Hypotnsino
*dirct myocardial depression from alterations in sodium channels
*alpha 1 blockade cuasing peripheral vaso dilation
binding to na channels occurs in ionized state
*tcas weak bases and become increasingly ionized in acidic environment
agitation, delerium, and depressed sensorium
seizures
*increases conc of monoamines, muscarinic antagonism, na channel alterations, and gaba inhibiton
acute clinical maniestatins of tca tox
cv
*hypotension and ventricular dysrythmias
*prolonges pr interval, qrs and qt interval
cns
*delerium, agitatoin, psychotic behaviors w. hallucinations, seizures lethargy, and ocma
other
*anticholinergic: dilated pupils minimally responseive to light, dry moutg, drug flushed skin, urinary retention and ileus
*ARDS aspiration oneumonitis, and multisympton organ fialure
chronic toxiity of tca
not life threatening
sedation and sinus tachycardia
dx testing for tca toxiicty
ECG
TCA conc : limited utility early after ingestion
electrolytes
glucose
venous or arrterial blood gas
tca overdose management
GI decom.
*actiated charcoal given to pts within 2 hrs and pt must have normal mental status and protected airway
serum alkanalization: membrane stbailization effect
*sodium stabilizing effect
control arrthmias, hypotension and seizures
IV lipid emulsion (ILE)
salavge therapy when cv therapy is refractory standard therapues
*only effective for lipophillic drugs (amitriptylie and clopiramine
8AE: ARDS and pancreatitis
membrane stabilizing effect in tca overdose treatment
in presence of tcas na channel is altered slowing the rate of rise of action potentioal
increase in sodium gradient 9by giving sodium bicarb) speeds rate of rise of action potential
drug induced effects are counteracted
increasing ph removes tcas from binding to sodium channels
serum alkalination and sodium loading
effective for wide comples dysrthrimas (qrs compex duraion>100ms) w. ocnduction delays and hypotenion
sodium bicarb preffered
*BOLUS OR RPAID INFUSION OVER SEVERAL MINUTE 1-2 MEQ/KG
*ADDITIONAL BOLUSES Q 3-5 MIN UNTIL QRS DURATION NARROWS AND HYPOTENSION IMPROVES, THEN consider initiatinf continuous infusion to maintain ph
target ph: 7.5-7.55
monitor K and ionized calcium
alternative: hypertonic saline 1-2 meq/kg bolus
only used with alkanization when sodium bicarb admin is not possible or ci
ANTIDYSRHThmic therapy for tca overdose
if pt not responsive to sodium bicarb therapy
Lidocaine:
*Class 1b
*for pts who not responsive to sodium bicarb therapy
Magnesium sulfate:
consider after alkalinzation, sodium loading and trial of lidocaine fails
CI antidysthrmics in pts w. tca overdose
class 1a: (procainamide-similar pharm action to tcas
class 1c: (flecainide-similar pharm action to tcas)
class III: amiodarone and sotalo prolongn qtc
hypotension treatment in tca overdose
*0.9% NaCl or sodium bicarab bolus doses
if hyotension continues dispite volume resucitation
*norepinephrine
vasopression
Extracorporeal membrane oxygenation
seizures
first line: benzos
second line:propofol or barbiturate
CI agents in tca overdose in pts being treated for seizures
phenytoin
*fails to temrinate seizures
*enhances cv toxicity
flumezanil
*induces seizures
physostigmine
*induces seizures
digoxin-specific antibody fragments indication
indictated when exposed to digoxin or digitoxins including cardioacive steroids
ex: lilly of the valley
epidemiology of digoxin toxiitcty
causes most cases of pharm induced cardioacctive steroid toxicity (CAS)
more ocmmonly seen in pts at extremes of age or with ckd
pk of digoxin
onset of action
*po: 1.5-6 hrs
IV: 5-30 min
max effect:
po:4-6 hrs
iv: 1.5-3 hrs
intestinal absorption : 40-90%
plasma protein binding: 25%
Vd:
*adults:5-7 days
*4-5
route of elimination :60-80% w. limited hepatic metabolism
enterohepatic circulation: 7%
toxicokinetics of digoxin tox
elevated serum conc result in greater renal cl before distribution to tissues , dec. t1/2
hypokalemia and hypomagnesemia enhances efffects on myocardim leading to toxicity at lower serum conc
tox can be seen w. changes in liver, kidney, or heart function, aong w. drgu-drug interactions including quinidine, verapamil,carvedilol, amiodarone and spirinolactone
digoxin moa of effects on heart
in presence of dgoxin, sodium-K ATP-ASE is inhibited, causing increase in intracellular sodium conc, preventing antiporter calcium and enhanced inotropy
excessive elevations in calcium inc resting potential, leading to dysrhtmias
electrophysilogical effects of cardioactive steroids on myocardium
increase excitability
increase automaticity
decrease conduction velocity
decrease refractory time
toxiciy causes increased dysryhtmias and mocardial irritability
acute ss of CAS toxiicity
asymptomatic period of min -sev hours
n/v, abdominal pain, lethargy, confusion , and weakness
chornic ss of CAS tox
difficult to dx
loss of appetite, weakness, anoriexia, n/v abdominal pain, weightloss, delerium, confusion, drowsiness, headache, visual disturbances, andrarely seizures
other ss of cas
electrolyte abnormalities (hyperkaemia)
cardiac abnormalities includuing ventricular tachy dys. or brady dys , a flutter, a fib w. av block, etc.
dx tests for cas toxiity
gi decomtam:
AC 1g/kg q2-4 hrs up to 4 doses
electrolyte therapy
(hypo/hyperkalemi)
*do not admin calcium, could exagerate cardiac effects
hypomag:
*mg sulfate 2g iv over 20 min followed by 1-2 grams/hrs if needed
dig-specific antibody fragments
CORNERSTONE
indications for dic-specific antibody fragment
lifethreatenning dysrthmias regardless of digoxin serum conc
K+ more than 5meq in setting of acute digoxin tocitiy
chornic levls of serum dig w. dysrhtmias, gi symptoms, and ams
serum digoxin conc
at anytime:>15
6hrs after injestion>10
acute ingestion of 10mg of digoxin in an adult
moa of digifab
antigen binding fragments binds to free digoxin in iv and interstitial space
*movement of free intracellular and dissociated digoxin into II or IV space due to concentration gradient which is established
immediate decl.ien in free digoxin
massive increase in serum dig conc(clinically unimportant)
increases renal cl
dec serum potassium conc
dosing of digifab
emperic
if dig serum conc unknown:
give 3-6 vials for chrnoic toxicity
give 10 vials for acute “
dig-secific fab dosing
*if serum conc known
[serum dig conc (ng/mL)x pt weight (kg)]/100=# of vials
*known amount ingested
[amount ingested mg/0.5 mg/vial]x 80% bioavailability=# of vials
ROUND U TO A WHOLE VIAL
other cardiac therpaied for digoxin tox
atropine:early bradydysryhtmias
05 mg iv push q5min
phenytoin and lidocaine:ventricular tachydysrythmias
pacemaker
cardioverison
clinical manifestatatins of bb tox
hypotension
bradyardia
dysryhtmias
hypoglycemia
seizures
resp depression and apnea
coma
ccb overdose SS
halmark SS:hypotension and bradycardia
lack of perfusion to cns can cause fatigue, dizziness, lighthededness
hyperglycemia
severe overdose can cause syncope, coma, sudden death, ARDS
dx testing for bb or ccb testing
ecg
cardiac and hemodynamic miint=oting
chest xray and o2 sat
digoxin level
thyroid function
cardiac enyzymes
lactate
mgt of ccb/bb tox
gi decom: ac!!, mdac, whole bowel irrigation
hypotensive: crystalloid fluid
bradycardia: atropine 0.5-1mg IV titrate
in severe posioning, wont respond to above therapies, need to move on to these next therapies
calcium:
calcium chloride 10% : increase extracellular calcium and leading to improvements in hypotensino and reverses impairs inotropy and conduction
glucagon
*3-5 mg iv over 1-2 min; may repeat with 4-10 mg after 1-2 minutes; may repeat with 4-10 mg after 5 min w. no improvement in hemodynamics
(glucagon has ionotrpoic and chronotropic effects bypassing adrenergic receptors)
IN CCB overdose: calcium should be given beforegglucagon
BB overdose: glucagon before calcium
REMEMBER: do not use calcium if digoxin tox is suspected or confirmed due to stone heart phenomena
IV lipid emulsion-salvage therapy. only done if above therapies failed
mgt of ccb/bb -HIGH DOSE INSULIN
trt of choice
HDI impairs sodium calcium antiporter resulting in an increase of intracellular calcium which increases calcium in sarcoplasmic reticulum increasing cardiac contractility
delayed onset of action 15-40 min
bolus:
1 u/kg iv push w. 0.5g/kg of dextrose infusion at 0.5 /kg/hr
continuous infusion
1u/kg/hr titrated to effect in combo w. dextrose infusion at 0.5g/kg/hr
monitor bg q 30 min for the first 4 hours and then every hr
monitor more frequently of bloog glucose if pt has renal failure
adverse reactions” hypoglycemia and kyopkalemia
adjunctive hemodynamic support
inotropes and vasopressors
cardiac pacing
intraaortic balloon pump
extracorpeal membrane oxygenation
