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introduction

we dont use antacid like calcium carbonate in icu pt cuz it oral agent and pt cant take it and cuz
its continue minerals and most pt in icu have renal abnormality ,and cuz not effective as ppi and h2
hold enoxaparin when platelet less than 100,000 dose adj crcl les than 30
electrolyte disturbances , sodium and potasum
hypo ,hyper natremia kalemia underlying cause
Disseminated intravascular coagulation (DIC) criteria

evaluation number 1
how to do case presentation :
*B3d history of present illness > Wight and height an crcl >medication (for dm for htn at home )
*start medication presentation with acute problem medication and for what indication and if u
agree or not wbhmni a3ref etha el drug dafo jded wla mashi 3aleh mn el home ex gemfibrozil <TG
then we statrt interpret lab test

* any pt with GI pleading always mast be in IV PPI in treatment dose (not on h2 blocker )
omeprazole for stress ulcer prophylaxis 40mg once daily >
in GI bleeding treatment dose 40mg IV twice

H2 VS PPI on active gi pleading (ppi can make healing ,h2 not ) cuz : platelet aggregation need ph 6
and this achieved by PPI
another different ppi given once daily , h2 tolerance after 30 day , s/e h2 thrombocytopenia (so
always should monitor platelet when pt on ranitidine ) , h2 need renal dose adj but ppi need hepatic
adj especially omeprazole .lanzoprazol bt9eer max 30 mg which is bel a2sas given 30 mg once
another different h2 can make headache and diarrhea ,and increase risk of aspiration pneumonia
(both h2 and ppi) ppi on long term can cause osteoporosis cuz decrease vit d absorption
you should know when to use ppi or h2 blocker for stress ulcer prophylaxis

main use for metoprolol for HR and migraines prophylaxis (not common for htn)
the main complication for gi bleeding is hypotension so for any pt have active gi bleeding always
check BP anf u mast give fluid
any pt on icu should not receive any po medication
RBG in icu should be less than 180
on care plan u should right : pt have blood glucose higher than goal which is <180 so start sliding
scale with coverage
any oral hyperglycemia agent should be avoided in icu why ? to avoid glucose level fluctuation
to achieve beter blood glucose level , oral agent need dose adj in renal impaired
Glasgow Coma Scale (GCS) to detriment level of conscious or conscious state
1Eye response(E)2 Verbal response (V) 3 Motor response (M ) EVM
gemfibrozil and statin Category x > rhabdomyopathy >aki

basic steppes in management upper gi bleeding : 1-ppi treatment dose 2- any patient have
active bleeding regardless HGB should take packed rbc
indication for packed rbc: active bleeding regardless HGB 2-hgb less than 7 3- hgb less than 10
with pt have solid tumor (cancer)
packed rbc complication : fluid overload 2-viral infection(hiptits) 3. anaphylaxis 4- iron overload
insensible loss ; water loss from skin and lungs in healthy adults ( evaporation) and it calculate by
adding 10ml/kg on output
balance should be zero but we accept +- 1000
gi bleeding underlying cause:cancer , Esophageal varices, ulcer
leukocytes increase in infection ,stressful condition ,corticosteroid
Corrected calcium = serum calcium + 0.2 * (40 - serum albumin) if mg/dl 0,8 =4

Decompensated Heart Failure : we should not be uprtly d/c BB blocker cuz its may case Broncho
spasm and exacerbation edema
maximum dose of lactulose 60 ml more dose in liver cirrhosis (encephalopathy) becose it not
absorbed and it useful in decrease ammonia
to say the diuretic is effective : fluid balance with insensible loss mast be negative (-500 ml)

tolerance for furosemide how to solve it?


first thing in workup anemia is reticulocyte : precursor rbc
LDL,HDL,TC *38.6
-TGC *88.5
-GLS *18
UREA /59.5
Left Bundle Branch Block (LBBB)
need to mummeries cocroft and gault equation
in dka (icu ) type of insulin givin is regular >nph not given why ?
enoxaparin treatment dose 1/kg twice or once if crcl less than 30 ,prophylaxis dose 40 mg once
daily
enoxaparin maximum dose 225
empirical and hospital acquired need duple coverage with different mechanism
tecoplanin indication : mrsa > catheter>gram positive
manistifation of mrsa is hypotension so if pt On antibiotic and still hypotensive so we
empirically add tecoplanin
Tamiflu> Oseltamivir :75 mg twice daily , prophylaxis dose once daily when h1n1 negative d/c
KCL given peripheral and central line but it prefer to give peripheral
kcl deferent in maximum infusion rate and maximum concentration in peripheral and central line
peripheral line maximum concentration for peripheral infusion is 10 mEq/100 mL and maximum rate
of administration is 10 mEq/hour
*central line Concentrations of 20 to 40 mEq/100 mL at a maximum rate of 40 mEq/hour via central
line have been safely administered

w e dont give KCL as polus cuz it cause Extravasation(irritant) and cause tachycardia arrhythmia
piperacillin/tazopcatm :s/e hypokalemia and hypernatremia ,thrombocytopenia , seizure so give
lower dose
we should know if antibiotic bacteriostatic and bactericidal
final Q Acinetobacter and choice between tigecycline , colistin : cuz its bactericidal or we use
combination
main s/e for fluoroquinolones is hallucination ,nephrotoxic ,qt prolongation
*acid base disturbances
first thing we should know the normal range of ABG
PH :7,35-7,45
HCO3:22-26
PCO2: 35-45
ABG sample O2% should be more than 90 to say the result of ABG reliable
primary acid base disturbances include primary acidosis(ph <7.35) and primary alkalosis (ph>7.45)
metabolic acidosis or alkalosis related to hco3
primary metabolic acidosis(hco3 less 22), respiratory acidosis( pco2 more 45)
primary metabolic alkalosis(hco3 more 26) , respiratory alkalosis(pco2 less 35)

metabolic acidosis: two type ionic gap metabolic acidosis and NON-Anion Gap Metabolic Acidosis
ionic gap normal range 8-16 : if more 16 ionic gap metabolic acidosis
some pt have both ionic gap plus NON-Anion gap : like dka pt and have vomiting
we have 3 method to r/o ionic gap plus NON-Anion gap
method #1
ionic gap = Na - (Cl + HCO3)
ionic gap = pt ionic gap -12
ionic gap+ HCO3
if the result less 22 : have both ionic gap plus NON-Anion gap
if between 22-30 : ionic gap metabolic acidosis
if more 30 : ionic gap metabolic acidosis plus metabolic alkalosis

method #2
comparison between ionic gap and HCO3
HCO3=24 - pt HCO3
if the HCO3 less ionic gap: have both ionic gap plus anionic gap
if = : ionic gap metabolic acidosis
if more ionic gap: ionic gap metabolic acidosis plus metabolic alkalosis

method #3
ionic gap - HCO3
if the result less -6 : have both ionic gap plus anionic gap
if between -6-6: ionic gap metabolic acidosis
if more 6 : ionic gap metabolic acidosis plus metabolic alkalosis
compensation for metabolic acidosis
after we check acid base disturbances we should check Compensatory Responses
The body responds to metabolic acidosis by trying to restore the PCO2 / [HCO3-] ratio. This is
done by reducing the PCO2. by hyperventilation
example if pt have metabolic acidosis ,he will develop respiratory alkalosis by hyperventilation
if PCO2 in normal range : 35-45 we can say non compensation
Compensatory Responses type: well compensation, under compensation ,over compensation
we can determine Compensatory Responses by calculate expected pco2
expected pco2= 35 - (1.2xHCO3)
HCO3=24 - pt HCO3
make expected plus mines 2
if pt pco2 less than 35 but still above the expected range we say under Compensatory
if within the range we say well Compensatory
if less the range over Compensatory

underlying cause of anionic gap metabolic acidosis( acat mudpiles) back to handbook page 773
A:analgesia C:carbon monoxide T:toluene m:metformin u: uremia D:dkaP: paraldehyde I: iron lactic

underlying cause of non-anionic gap metabolic acidosis:1-loss of hco3 like renal impairment ,
acetazolamide, diuretic,2- gaining of acid like hcl and nh4cl 3- any thing can cause hypokalemia like
Adison diseases 4- any thing can cause hyperkalemia
management of metabolic acidosis :treating underlying case

criteria to give sodium bicarbonate:


in non-dka case : ph less 7,2 or phco3 less 8
in case of DKA ph less( 7 or 6,9) or phco3 less 8

how to give sodium bicarbonate in non-DKA cases (nahco3) :


Nahco3 dose = wt x0.5 x(24-hco3)
half the dose over 30-60 min and the other half over 12-24 h

in case of DKA the dose of Nahco3 depend on ph value


if PH <6.9 100meq in 400cc N.S over 2 hours
if PH 6.9-7 50meq in 200cc N.S over 2 houre

final q :pt(weight not known) with non ionic gap metabolic acidosis secondary to hyperkalemia and
criteria to give sodium bicarbonate not applicable fkan el jawab bs treatment hyperkalemia

metabolic alkalosis ph more 7.45 hco3 more 26


underlying cause of metabolic alkalosis
1hypokalima a-insulin b-albetarol c- diuretic d- Cushing syndrome-e vomting
2- nasogastric tube suctioning

compensation metabolic alkalosis

The body responds metabolic alkalosis by trying to restore the PCO2 / [HCO3-] ratio. This is done
by increase the PCO2. by hypoventilation (respiratory acidosis)

management for metabolic alkalosis (handbook algortham)


we determine if Sodium chloride responsive or not by calculate chloride in urine

treatment of choice for metabolic alkalosis is normal saline but if pt contraindication to normal
saline like pt have hyponatremia ,fluid overload we give Acetazolamide PO 250375 mg QD or BID
plus potassium if K <3.5 mEq/
if pt have sever metabolic alkalosis ph >7.6 we give hcl or nh4cl( Ammonium chloride)
hcl complication :1 irritant and cause hemolysis <> nh4cl cause encephalopathy

if pt Sodium chloride resistant type: the best management is treat underlying cause las choice is
amiloride

we can determine Compensatory Responses to for metabolic alkalosis by calculate expected


pco2

expected pco2= 45 + (1.6xHCO3)


if pt pco2 less than more 45 but still less the expected range we say under Compensatory
if within the range we say well Compensatory
if more the range: over Compensatory

primary respiratory acidosis(ph <7.35 and pco2 more 45)


* compensation for primary respiratory acidosis done by metabolic alkalosis
if hco3 within the normal range(:22-26) no compensatory response

in acute: each 10 in pco2 (above 45)--------- 1 hco3

in chronic : each 10 in pco2 (above 45)--------- 4 hco3(


example if pt have pco2 75 so we expect that hco3 in acute will be 29(26+3)
and in chronic 38 (26+12)

Causes of respiratory acidosis : opioid ,BDZ ,COPD(ASTHMA cause of respiratory alkalosis )

ASA make metabolic acidosis , BUT ASA overdose make respiratory alkalosis

management :treat underlying cause

we should know when to start O2 thereby : Po2 less 55 (hypoxia)

respiratory alkalosis
primary respiratory alkalosis(ph>7,45 and pco2 less 35)

compensation for primary respiratory alkalosis done by metabolic acidosis


if hco3 within the normal range(:22-26) no compensatory response

in acute: each v 10 in pco2 (uder 35) 2 v hco3(3n the upper limit 35)

in chronic : each 10 v in pco2 (above 35)--------- v 5 hco3(3n the upper limit 35)
example pco2 15 >>>>22-4=18
more than 18 over compamsatory
if less undr

hypokalemia(k <3,5)
mild hypokalemia 3__3,5
moderate hypokalemia 2,5__3
severe hypokalemia less 2,5

k daily need 1- meq/kg


potassium deficit = wt x 0.4(4-k level for the pt )
total= deficit +daily
peripheral line maximum concentration for peripheral infusion is 10 mEq/100 mL and maximum rate
of administration is 10 mEq/hour
*we can give maximam 200 meq over 24 h
*central line Concentrations of 20- 40 mEq/100 mL at a maximum rate of 40 mEq/hour via central
line have been safely administered
we can give maximam 400 meq over 24h

w e give KCL as continues infusion cuz it cause Extravasation(irritant) and cause tachycardia
arrhythmia and cerebral edema
Evaluation
criteria for machine ventilator : O2,ABG

Gestational diabetes develops during pregnancy (gestation) between the 24th and 28th weeks of
pregnancy and we should test HBA1C After 6 month of delivery to rollout dm2 secondary to
gestational dm
criteria for increase risk of dvt ?
Tamiflu (oseltamivir):prodrug when active is a neuraminidase inhibitor treatment dose( when
h1n1 positive not flu a) 75 bid for 10 days prophylaxis dose :75 mg once for 5 day
we should know equivalent between cortisone since hydrocortisone 250mg minor criteria for
stress ulcer prophylaxis
the main reason for stress ulcer prophylaxis in ICU ,that pt on NPO and this lead to increase acid
excretion without food in stomach and this increase risk for stress ulcer

nifedipine formulation available at icu ??>extended release 20 mg >> what max dose?? 90-120mg
max dose of atenolol 25-50 mg but they find 50mg of atenolol in icu pt not increase risk of S/E s
hydralazine must be given continues infusion in HTN crises
all vasodilator including hydralazine not used in strok cuz its increase intrarenal pressure
so labetalol iv is DOC in case of strok but Unfortunately its not available in KAUH so we use
hydralazine
maximum infusion rate of hydralazine is 10 mg/h
the major s/e of hydralazine lupus like syndrome(type of allergy)
if pt Afebrile and blood culture show gram positive cocci we dont start vanco or tecoplanin
immediately cuz the blood sample contaminated blood sample is common ,since gram postive cocci
in skin so we need clinical sign of infection

Tecoplanin need dose adjustment in loading dose (not in maintenance dose ) if crcl less 20
one complication of intracranial hemorrhage is seizure so we should give phenytoin as
prophylaxis's
Nimodipine is a dihydropyridine calcium channel blocker originally developed for the treatment
of high blood pressure. It is not frequently used for this indication, but has shown good results in
preventing a major complication of subarachnoid hemorrhage ,termed vasospasm; this is now the
main use of nimodipine.
= one complication of subarachnoid hemorrhage rebleeding
Pneumatic compression devices (PCD) for dvt prophylaxis in stork pt

how to write formal case


write problem by problem (daily not within the problem) 30:30 icu 3

phenytoin s/e : hypotension ,gingival hyperplasia hepatotoxicity. Arrhythmia, qt prolongation


all anti epileptically agent can effect vitmin d and calcium
amlodipine and nifedipine also cause gingival hyperplasia
metoprolol not need dose adj in renal impairment >>which one of bb need dose adj ?
colistin moa? interact with the bacterial outer membrane>> a detergent
what is the underlying cause of dvt and type of dvt
when to give antibiotic in COPD pt ? 1-incrasing volume of sputum 2- color and dyspnea 3
fever
morphen never used as analgesic in intubation pt cuz s/e : respiratory distress, dependence ,
increase histamine release so cause hypotension ,increase intrcranial pressure

fentanyl not require renal or hepatic dos adj


spironolactone moa and side effect
theophylline s/e seizure and arrhythmia level 5-20 not exeed 15
side effect of opioid
valporic acid moa ? sodium channel booker % gaba inhancer
ticagrelor vs clopidogrel
hyponatremia and evaluation
#Fluid calculation
balance in fluid =input-output
input example :iv fluid ,oral or nasogastric intake ,iv medication
*don't forget to consider amount of fluid used to reconstitute medication in calc balance
*output example : urine , sweeting ,berthing , lachrymation
normal balance should be zero but we accept 1000cc
example of positive and negative balance
how to calculate maintenance fluid(total daily requirement over 24h) ?
method #1 :
maintenance fluid=35cc/KG/Day (over 24h)
method #2 :
we can use it in adult and pediatric
the first 20 kg give 1500 cc then any KG multiple it by 20cc

type of fluid :
1-crystalloid fluid like normal saline , Lactated Ringer's ,dextrose
* ( Lactated Ringers, dextrose):source of enrage ,contain minerals like ca
normal saline : zero enrage
type of normal saline(different osmolarity) : 1- hypotonic 0.45% nacl 2- isotonic 0.9% nacl 3-
hypertonic saline 3%
* glucose : glucose 5% , glucose 4.3

2-calloid : albumin , Hetastarch ,dextran , gelatin

crystalloid :cheaper ,more easier to administration ,more Compatible with medication ,lower s/e
like allergic reaction(serum sickens) ,bleeding ,infection ,kidney injury
disadvantage: increase risk to developed Hyperchloremic acidosis(non anion gap metabolic acidosis)
when we give more than 3L of crystalloid

colloid:more viscous so we need less volume,, so its favorite for HF pt .(have higher retention site

normal osmolarity in blood : range of 285 to 310 mosmoles/liter


always we should calc osmolarity in blood in pt have DKA (hyperglycemia increase osmolarty ) ,pt
with change in sodium ,pt with change blood urea nitrogen
osmolarity in blood= 2 X Na + Glucose + Urea ( all in mmol/L)
OR= 2* Na + [Glucose]/18 + [ BUN ]/2.4 where [Glucose] and [BUN] are measured in mg/dl

fluid osmolarty = % X 106 X (equivalent /M.W)


example :normal sline 0.45%
(0.45/100)x106x(2/58.44)=154 mosmoles/liter (hypo)

*if pt osmolarity in blood hypo give hypo fluid if hyper give hyper if normal range give iso fluid
example #2 :glucose saline 0.18 (in this case we calc osmolarity for glu and saline separately b3den
mnjm3ahom lab3d)

hypernatremia hyponatremia calculator

Na normal level is 135-145 so hyponatremia less than 135


*we should know the type of hyponatremia:
1-hypotonic hyponatremia:
a- euvolemic : (SIADH) syndrome of inappropriate secretion of antidiuretic hormone
b- hypovolemic :diuretic use
c- hypervolemia (dilutional hyponatremia): volume over load like HF, nephrotic syndrome liver crosi
2- isotonic hyponatremia : hyperlipidemia or hyperproteinemia> increase extracellular volume
3- hypertonic hyponatremia: like in case elevated glucose: glucose increase osmalirty and work as
osmotic diuretic

management of hyponatremia
in general we give normal saline
sodium daily 1-2meq /kg (1)
sodum deficit =total body water(TBW) x (sodium Desired-serium sodium=12)
total body water(TBW)= pt Weight x 0,6 for male and 0,5 for female

in acute sodium deficit the correction should not be exceed 8-12meq daily (increase or decrase) cuz
risk of Osmotic demyelination syndrome

total Na requirement = sodium daily(1/kg) + sodum deficit(TBWx12meq)


we give it as 0,45 nacl in dka pt cuz they are dehydration > 0.9nacl or 3% in case HF and.
each letter of 0,45% contain 77na
each letter of 0,9% contain 154na
each letter of 3% contain 513na

24
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hypernatremia and evaluation
Hypernatremia Na >145 mmol/l
most common cusses for Hypernatremia : water deficiency(fluid loss),diuretic (can cause both
hypo and Hypernatremia bt3tmed sho 6ala3 akther water wla na )

for Hypernatremia pt we calculate water deficit:

0.6 x for male


0,5x for female

Na desired =na measured -12


Water deficit(L) x1000 given q8h or q6h or q4h example 2L x1000=2000cc so give 500cc every 4h
***keep in mind the volume of fluid of other type that used for medication administration
example : if we use 500ml of .9% to reconstructed levofloxacin so should be 2000cc-500cc

Type of fluid that given in Hypernatremia : tap water ,dextrose(if pt have hypoglycemia)
if the pt was on 0,9% normal saline and developed Hypernatremia so we convert him to 0.45%
or ,dextrose(if pt have hypoglycemia)

evaluation :

octreotide : somatostatin analog used in GI bleeding: octreotide inhibit secretion gastrin so this
reduce aced secretion also can be used as antidiarrheal
given as iv bolus 50-100mic then 25-50mic per hour as continues infusion for 5 day

if pt have history of ESBL so impirc thereby should be carpanem


critiria for dka diagnosis
dka fluid bnefti to wash keton and uti
dka fluid 500-1000 n.s 0.9% over 30 min bolus then maintenance 150-250 ml per h
or 4-14ml/kg/h
type of fluid detetermination affected by two fctor glucose level ,and corrected Na

dopamine :
low dose (renal dose) :work on dopamine receptor and increase kidney perfusion (5mic/kg/min)
we dont exceed 20 mic cause increase risk of arrthimia without addition advantage
Dose dependent effect
Low doses( 0.5- 3 microgram/kg/min)
Intermediate doses (3-10 mcg/kg/min)
Higher doses (10-20 mcg/kg/min)

dopamine calculation
convert ml/h to mic/kg/min
rate(ml/h)= dose(mic/min) xwt
1ampule of dopamine contain 250mg reconstituted by 500ml

the most common is the adpdominal pain


Metoclopramide bind to dopamine D2 receptors Antagonist
S/E of antagonist dopamine : extrapyramidal effects , restlessness (akathisia), and focal
dystonia
antidote: anticholinergic :benztropine

when we give potassium we should monitor urine output befor start and ECG Whin we givet
k is contraindication in anuria

final q :potassium is low so first correct k by giving 40 meq in 400ml n,s over 4h befor start
insulin then after cortication start insulin
we reduice level of gls by 60-70 /h to avoid cerebral edema

complication of sodium bicarbonate :hypernatremia 2-fluid overload 3-metabolic alkalosis 5-


inercullr acidosis 6-hypocalcemia 7- hypoxia

calcium gluconate in hyperkalemia as cardiac muscle stabilization just! Zero effect on k level
also we give insulin and albuterol
in chronic hyperkaliemia we use sodium resonium and calcium resonium

why we choose levofloxacin in rs infection cuz its cover pseudomonas and atypical
in case of AKI we wait 48 h before we make dose adj
digoxin reduce HR and not effect BP
Evaluation and quiz topics number 1:
Warfarin acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include
Factors II, VII, IX, and X, and the anticoagulant proteins C and S 1972
.the longest half life for this factor 7 day ,, so this way we see the effect of warfarin after 7 d
when we use enoxaparin as bridge therapy with warfarin we can stop it two constitutive INR
within the goal
levofloxacin it functions by inhibiting DNA gyrase and topoisomerase IV
levofloxacin s/e : hallucination , photosensitivity, nephrotoxicity, QT prolongation
glargine insulin :given on fixed time , peakless,
psychiatric pt with obstructive sleep apnea ,oxygen thereby due to sever obesity ,infection , DIC
d/5 wter and have metabolic acidosis >give normak sline, positive budding yeast in urine, acino
bacter >colstin dose actul wt

Criteria for brain death: fixed pupil , irreversible loss of brain function (functional brain death ) loss
of the brain nerve reflexes including the light reflex

Tamiflu (oseltamivir):prodrug when active is a neuraminidase inhibitor


treatment dose( when h1n1 positive not flu a) 75 bid for 10 days
prophylaxis dose :75 mg once for 5 days

ticoplanin Glycopeptide antibiotics: inhibits peptidoglycan synthesis


Initial: IV: 400-800 mg every 12 hours for 3-5 doses maintenenance 6-12 mg/kg once daily
Tecoplanin need dose adjustment in loading dose (not in maintenance dose ) if crcl less 20
adj CrCl 30-80 mL/minute: maintenance dose once every 48 hours, or administer one-half of previous
maintenance dose once daily
CrCl <30 mL/minute (including hemodialysis patients): Administer previous maintenance dose once
every 72 hours, or administer one-third of previous maintenance dose once daily
tecoplanin indication : mrsa > catheter>gram positive

not all pt have fever with budding yeast positive in urine should start fluconazole
we should r/o bacterial infection first by covers all thing then if still febrile and hymodynmic unstable
we can start
fluconazole 200mg iv once daily require dis adj renal 50% dose
fluconazole maxim dose 800

normally we can find pt with sepsis with normal wbc since the criteria for sepsis is wbc>12 or less
4

nifedipine>CCB> dihydropyridine>S/E >edema ,constipation when given with vepramil diltiazem


reflex tachycardia , in long term gingival hyperplasia
moxonidine> antihypertensive> selective agonist at the imidazoline receptor subtype 1
intial dose 0,2 maximum daily dose of 0.6 mg>>GFR 30-60 mL/minute: Maximum single dose: 0.2
Maximum daily dose: 0.4 mg ; GFR <30 mL/minute: Use is contraindicated

Haloperidol> typical antipsychotic medication> prn >


s/e wt gain , Extrapyramidal s/e including: Distonia ,Muscle rigidity Akathisia, Parkinsonism
Extrapyramidal antidote> diphenhydramine>BZD>BB>cholinergic
final Q : Haloperidol s/e Neuroleptic malignant syndrome (NMS)( consists of muscle rigidity,
fever, autonomic instability) what is the antidote ? . Dantrolene

the major s/e of hydralazine lupus like syndrome(type of allergy)


allopurinol > allopurinol for tumor lysis syndrome (TLS) prophylaxis
TLS >increase uric aced ,phosphors ,ca
allopurinol is a purine analog; of the enzyme xanthine oxidase inhibitor
daily dose 300-600 mg in divided dose the maximum daily dose 800mg/daily
CrCl 10 to 20 mL/minute: 200 mg/day
CrCl 3 to 10 mL/minute: Do not exceed 100 mg/day.
CrCl <3 mL/minute: The dosing interval may need to be extended; do not exceed 100 mg/day
major s/e allopurinol skin allergy ,kft monitoring

digoxin :nhibition of the sodium/potassium ATPase pump, Direct suppression of the AV node
digoxin toxicity sign :gi s/e ,cardiovascular>brady or tache arthmia ,vf ,cnc s/e ,,ophthalmic s/e>green
yellow spoting ,
antidote :fab antibodi

dexamethasone
Extubation or airway edema: Oral, IM, IV: 0.5 to 2 mg/kg/day in divided doses every 6 hours
beginning 24 hours prior to extubation and continuing for 4 to 6 doses afterwards
Cerebral edema: IV: 10 mg stat, 4 mg IM/IV (should be given as sodium phosphate) every 6 hours
until response is maximized, then switch to oral regimen, then taper off if appropriate; dosage may
be reduced after 2 to 4 days and gradually discontinued over 5 to 7 days

enxoparin max dose 225


hydrocortisone:14 days then oral
hydrocortisone tapering : every 3days decrease the dose 2.5-5 mg until to reach the lowest dose
which is 5mg then u d/c it
dic management
in dic fibrinogen level is low and high FDB (degradation product of fibrinogen)
but in some condition like sepsis fibrinogen level will be normal or high
DIC is suspected, platelet count, PT, PTT, plasma fibrinogen level, and plasma d-dimer level
rbc indication
fresh frozen plasma contain clotting factor so given in case bleeding
indication for fresh frozen plasma (FFP):1-elevation in INR(1,5) 2- PT(apove 45) 3-active bleed all3
in case we give FFP and the patient still bleeding and the fibrinogen less than 1 ,so we give
cryoprecipitated (antihaemophilic factor(factor a))
indication for platelet ? 1- platelet cunt less 10.000 regardless if there is bleeding or no
2- platelet cunt less 30,000 and their is risk of bleeding 3-pletelet less 50.000 and have active
bleeding
condition cause of dic :sepsis ,cancer ,hepatitis, snake bite

Topic in quiz : 1-shock and sepsis and septic shock


DVT and stress ulcer prophylaxis
DVT :contraindication for enoxaparin 2-dose enoxaparin in DVT treatment and prophylaxis dose adj
unfractionated heparin prophylaxis dose
stress ulcer : major/minor criteria (one major or two minor)5726

topic 2
head trauma and sub-arachnoid hemorrhage
(head trauma >falling down or rod traffic accident(rta) and this may led to fracture)
we have types of fracture:1- simple skull fracture 2- depressed skull fracture 3-compound depressed
skull fracture 4- Basal fracture (the most dangerous one cuz of risk of leakage of CF fluid and risk of
meningitis
Basal fracture have two sign : Raccoon eyes(ecchymosis around eyes) and battle sign(ecchymosis
temporal eria)
management :
mainly we do management for complication
1-sizure : we give seizure prophylaxis
phenytoin : for 7 days >>>>if he developed seizure 6-12month
note :if pt exceed 7 days and still on phenytoin but he on Mechanical ventilation and not stable so
we keep him on phenytoin
* we should know phenytoin vs levetiracetam dose and every thing

2-elevation intracranial pressure So we expected ischemic or hemorrhage


cerebral perfusion pressure = MAP - ICP
if ICP >MAP so cerebral perfusion well decrease and we expected ischemic
*how we decrease intracranial pressure ?
non pharma :surgery+ cefazolin surgery prophylaxis
pharmalogical :
first line :hypertonic saline 3%
second line :mannitol (dose, contraindications, duration of treatment not exeed 3 day why ?)
in mannitol we should calc serum osmalirety if the result more 325: mannitol contraindication

some study recommend to give combination mannitol and furosemide low dose 10-20mg since its
give synergistic diuretic effect to decreases cerebral edema

3- meningitis: we should know when to start meningitis prophylaxis and what ?


we usually give ceftriaxone and vancomycin but if frontal area involve we add metronidazole to
cover anaerobic

*criteria for meningitis prophylaxis


4- sub-arachnoid hemorrhage: the main complication vasospasm so we give nimodipine (dose: 60mg
po q ? duration 21 days) after the pt be com stable
other complication include :1-rebleeding2-sizure 3- hemorrhage 4-( hyponatremia ??)

Two mechanisms have been proposed as causes: syndrome of inappropriate anti -diuretic hormone
and cerebral salt wasting

topic 3
glycemic control
we give regular insulin as continues infusion cuz mixterid contain NPH ,and particles occlusion iv line

topic 4
acid-and base disturbances and electrolyte disturbances
antibiotic case

sepsis:
we treat :hypotension ,infection and supportive (stress ulcer and DVT prophylaxis)
hypotension: 500-1000 bolus normal saline then maintenance *
if pt still hypotension despite adequate fluid resuscitation so we give vasopressors:
norepinephrine first line why ? cuz it work both in alpha and beta resptor but more in alpha so less risk of
tachycardia and more vasoconstriction
epinephrine a=b
dopamine=low dose dopamine receptor mod dose :b high :alpha
the most risk for elevate hr with dopamine so not use in arrhythmia

bp=co x pvr
to give dobutamine 1-SBP>90 2-hct>30%(cuz its increase risk of hypoxia) 3-cardic index low(EF Less 45)

dose and when to use each one


norepinephrine maximum dose In septic shock 3mic/kg/min
other type of shock :30mic/min
dose range
dopamine :max dose practically 20mic/kg/min theoretically 50
dobutamine : max dose practically 20mic/kg/min theoretically40

==.S/E of dopamine and norepinephrine is renal failure and skin necrosis so we make irrigation and give (
antidote nitroglycerine topical or phentolamine topical ) alpha antagonist

last option is hydrocortisone 100mg q8h max 300 for 7days

infection
FINAL Q :culture with Pseudomonas and positive cocci's :to antibiotic should be given
homework four indication for double coverage for pseudomonas?
supportive

what is complications for sepsis? End organ damage ,dic Acute Respiratory Distress

The APACHE II Scoring System is designed to measure the severity of disease in patients admitted to
the intensive care unit

type of shock cardiogenic shock ,


DKA

aki diagnosis criteria: Increase in serum creatinine to 1.5 times baseline or Increase in
serum creatinine by 0.3mg/dL or more within 48 h
criteria for dka :1- Hyperglycemia: >250 mg/dL 2- Metabolic acidosis: pH < 7.3
3- serum bicarbonate < 18 mmol/l 4- positive Urine or serum ketones
non-dka ketones in urine : pregnancy , infection ,dehydration ,stress
the major source of energy for the body is glucose , insulin is required for glucose uptake
in tissue ,anyway as consequence of absolute or relative insulin deficiency body
accompanied that by an increase lipolysis result in increases serum ketones
symptoms of dka Abdominal pain and vomiting
Ketone bodies have generally included acetone, beta-hydroxybutyrate, and acetoacetate
acetoacetate is the predominant ketone bodies
nitroprusside is used as reagent for the detection of beta-hydroxybutyrate (not the
predominant ketone acetoacetate) so same patent have DKA but negative ketone because
theres no adequate amount of beta-hydroxybutyrate
dka causes : infection, hyperthyroidism ,stressful condition medication (isotretinoin,
corticosteroids, beta blocker ,oral contraceptive , antimalarial) hyperthyroidism
beta blockers can cause hypoglycemia or hyperglycemia depend on beta blocker receptor
selectivity (beta 1, beta 2, beta 3 )
hyperglycemia in dka can cause pseudohyponatremia so we should calculate corrected
sodium .Na = Measured Sodium + 0.016 * (Glucose - 100)

the first step in management in dka is rehydration : 500-1000cc normal saline iv bolus
over 30 min regardless sodium level
then we give maintenance(125-250cc /hour) (N.S or N.S) with or without D5% depend on
corrected sodium and glucose level (if corrected sodium normal or hypernatremia give N.S
,IF hyponatremia give N.S) and if glucose level less than 250 add D5% if glucose less 150
hold insulin and give D5%

the second step check potassium level


if potassium level is normal we can immediately start insulin and we give 20-30 meq
potassium
if the patient have hypokalemia so we should first correct potassium level before start
insulin
if K level 3.3 -5.5 give 20-30 meq for each liter of maintenance fluid
if K level 3.3 to 3.5 give 30 meq KCL as bolus +insuln
if K level less than 3.3 give 40 meq as bolus , after k level correction add insulin
if K level more 5.5 dont give kcl and start insulin
type of insulin is regular dose: 1-10 unit/kg/h as continues infusion
glucose level is measured every hour
electrolyte is measured Q 2h if abnormal and Q 4h if normal

criteria to give sodium bicarbonate:


in non-dka case : ph less 7,2 or phco3 less 8
in case of DKA ph less( 7 or 6,9) or phco3 less 8

how to give sodium bicarbonate in non-DKA cases (nahco3) :


Nahco3 dose = wt x0.5 x(24-hco3)
half the dose over 30-60 min and the other half over 12-24 h

in case of DKA the dose of Nahco3 depend on ph value


if PH <6.9 100meq in 400cc N.S over 2 hours
if PH 6.9-7 50meq in 200cc N.S over 2 houre

S/E OF sodium bicarbonate : metabolic alkalosis ,cerebral edema , hypernatremia ,hypoxia


,intracellular acidosis ,fluid over load ,hypocalcemia

hypokalemia(k <3,5)
mild hypokalemia 3__3,5
moderate hypokalemia 2,5__3
severe hypokalemia less 2,5

k daily need 1- meq/kg


potassium deficit = wt x 0.4(4-k for the pt )
total= deficit +daily
peripheral line maximum concentration for peripheral infusion is 10 mEq/100 mL and maximum rate
of administration is 10 mEq/hour
*we can give maximam 200 meq over 24 h
*central line Concentrations of 20- 40 mEq/100 mL at a maximum rate of 40 mEq/hour via central
line have been safely administered
we can give maximam 400 meq over 24h

w e give KCL as continues infusion cuz it cause Extravasation(irritant) and cause tachycardia
arrhythmia and cerebral edema

DKA means diabetic ketoacidosis and HHS means Hyperosmolar Hyperglycemic Syndrome.
what the different between DKA and HHS?
ceftriaxone: biliary excretion
Resolution of DKA:
clinical symptom improvement with Plasma glucose <200 mg/dl
rbonate concentration >18 meq/L

=12 2

--------------------------------------------------------------------------------------------------------------------------------------
SEPSIS AND VAP
Old definition

infection>SIRS>Sepsis>Severe Sepsis>Septic Shock

SIRS (Systemic inflammatory response syndrome) criteria


two or more of the following conditions :

temperature >38C or < 36C;


HR > 90 beats/min;
RR >20 breaths/min
PaCO2 <32 torr; WBC >12,000 cells/mm3,<4,000cells/mm3

New definitions
Sepsis: A life-threatening organ dysfunction caused by a dysregulated host response to infection.

Septic shock: Sepsis in which underlying circulatory and cellular/metabolic abnormalities are
profound enough to substantially increase mortality.

Terms like severe sepsis/ septicemia removed


Criteria for new definitions SOFA score 2 points consequent to the infection

norepinephrine ampule available at icu 4mg/4ml so the total dose in 1 ampule is 16 mg

management of sepsis :
first step : Fluid therapy
septic patients who initially present with hypotension, fluids alone will reverse hypotension and
restore hemodynamic stability
Resuscitation with IV bolus normal saline 500-1000 mL over 15-30 min then start maintenance
fluid
challenge test :maintenance fluid + IV boluses normal saline 500 mL every 15 minutes until the
target central venous pressure (CVP)is reached.

if challenge test started and 3 boluses was given and patient still hypotension or patent become
edematous so in these case we keep patient on maintenance fluid and Vasopressor should be
started

type of fluid depend on glucose and Na level

norepinephrine maximum dose In septic shock 3mic/kg/min


other type of shock :30mic/min
dose range
dopamine :max dose practically 20mic/kg/min theoretically 50
dobutamine : max dose practically 20mic/kg/min theoretically40
we treat :hypotension ,infection and supportive (stress ulcer and DVT prophylaxis)
hypotension: 500-1000 bolus normal saline then maintenance *
if pt still hypotension despite adequate fluid resuscitation so we give vasopressors:
norepinephrine first line why ? cuz it work both in alpha and beta receptor but more in alpha so less risk of
tachycardia and more vasoconstriction
epinephrine a=b
dopamine=low dose work on dopamine receptor ,,,mod dose :work on B>>> high dose :alpha
the most risk for elevate hr with dopamine so not use in arrhythmia

in case AF the first choice is phenylephrine cuz its have zero effect on BETA receptor so no risk of increase
HR
BP=CO x PVR
to give dobutamine 1-SBP>90 2-hct>30%(cuz its increase risk of hypoxia) 3-cardic index low(EF Less 45)

dose and when to use each one


norepinephrine maximum dose In septic shock 3mic/kg/min
other type of shock :30mic/min

dopamine :max dose practically 20mic/kg/min theoretically 50


dobutamine : max dose practically 20mic/kg/min theoretically40

S/E of dopamine and norepinephrine is renal failure and skin necrosis so we make irrigation and give (
antidote nitroglycerine topical or phentolamine topical ) alpha antagonist

last option is hydrocortisone 100mg q8h max 300 for 7days


Ventilator-associated pneumonia (VAP) is pneumonia that develops 48 hours or longer after
mechanical ventilation
to determine empiric thereby we should know if patient have risk factor for MDR or not
Initiate empiric antibiotic within firs hour in sepsis

Risk Factors for MDR Pathogens:


recent or Current hospitalization of 5 days
2 immunocompromised patients : Immunosuppressive disease or therapy
3- High Institution antibiotic resistance rate
4 Antimicrobial therapy in preceding 90 days

if the patient have Risk Factors for MDR so double anti-pseudomonal coverage and if the pt have
risk for MRSA so we add vancomycin (2 anti-pseudomonal +vanco or tecoplanin)
if nor risk factor for MDR :empiric >ceftriaxone or one anti-pseudomonal
if source of infection is skin: add vanco as empiric
if source of infection is skin with Abscess and foul smelling : carbapenem to cover anaerobic

Risk Factors for VAP :


1-Age
2- immunocompromised patients
3- respiratory disease
4- nasogastric tube suctioning
5- prolonged m.ventilation

how to decrease Risk Factors for VAP


1- decrease duration m.ventilation > tracheostomy if needed
2- hygiene and good Aseptic technique
3- semi sitting position

if source of infection is skin add vanco as empiric

The goals during the first 6 hours


1)CVP of 8 to 12 mm Hg.
2) MAP 65 mm Hg.
3) urine output 0.5 mL/kg/h.
4) central venous or mixed venous oxygen saturation 70%.
5) lactate less than 4 mmol/L

Early Sepsis (at the first 6 hours) vs Late Sepsis

Early Sepsis: Hyperglycemia, Tachycardia Tachypnea, Hyperbilirubinemia, Fever or hypothermia

Late Sepsis: Hypoglycemia, Hypotension, Leukopenia, Pulmonary edema, Oliguria,DIC, Lactic acidosis
Sepsis caused by Candida albicans DOC is Fluconazole
Sepsis caused by Candida non-albicans(C. glabrata, C. krusei, and Candida lusitaniae) DOC is
Caspofungin (Echinocandin)

sulfamethoxazole/trimethoprim : Pneumocystis jirovecii (previously Pneumocystis carinii)


Voriconazole : Aspergillus species

risk factor for fungal infection :


1)Those receiving total parenteral nutrition. 2) With bowel perforation. 3)With persistent or new
signs and symptoms of infections despite receiving broad-spectrum antibacterial therapy 4-
immunocompromised patients
Status epileptic

** underlying causes for seizures : electrolyte disturbances, hypo or hyperglycemia , Intracranial


hemorrhage , Brain tumor , Maternal drug use, Fever (febrile seizures) ,infection

old definition : seizure needed to last longer than 30 minutes to be considered status
epilepticus, it is now defined as any seizure greater than 5 minutes.

Pathophysiology : increasing in Glutamate ( the most common excitatory) or redaction


in (GABA) is the most common inhibitory neurotransmitter thought to be the major mechanism
leading to status epilepticus

management at home should assess the patient's airway ( maintenance Airway, Breathing, and
Circulation) And make sure the airway is clear
at home : rectal diazepam or im midazolam if the patient still seizing prompt emergency
treatment is necessary

emergency work-up:Complete blood count (CBC).,,Serum chemistry profile (e.g., electrolytes,


calcium, magnesium, glucose, serum creatinine, ALT, AST.
-Urine drug/alcohol screen : help eliminate illicit drug use or drug overdose.
-Blood cultures : e.g albumin , that affect anticonvulsant dosing.
-Arterial blood gas to assess for metabolic and respiratory acidosis, oxygenation.
-Serum drug concentration if previous anticonvulsant suspected or known : low concentrations can
reflect partial adherence or rapid drug withdrawal

Flumazenil (Romazicon) is a specific antidote for BZDs


naloxone >opioids

oxygen saturation in status epilepticus sold be 100%

three stages of status epilepticus :


the early status epilepticus stage from 030 minutes, the stage of established status epilepticus from
3060/90 minutes and then the refractory (late) stage during which substantial neuronal damage
can occur.
emergency antiepileptic drug regimen for status in newly presenting adult patients.

prehospital rectal diazepam A dose of 0.51 mg/kg or im


midazolam 200mcg/kg rat 0.5-1mg/min
if the patient still seizing prompt emergency
treatment is necessary
Early status(0-30 min) 0-10 min Lorazepam (i.v.) 0.1 mg/kg (usually
a 4 mg bolus, repeated once after 5 minutes;
rate 4mg/2min) If seizures continue 10 minutes
after first injection, treat as below

10-30 min Phenytoin or fosphenytoin at a


dose of 15-20 mg/kg at a rate of 50 mg/minute

Established staus(30-60min) Phenytoin at a dose of 5-10 mg/kg at a rate of


50 mg/minute

or
Phenobarbitone bolus of 15-20 mg/kg

in case of allergic to phenytoin :Valproate at a


dose of 2040 mg/kg at rate 3-6mg/kg/min
Refractory status( after 60 min) Try other Phenobarbitone bolus of 15-20 mg/kg
or
Induce coma :
Phenobarbitone or General anaesthesia, with
either propofol, midazolam or thiopentone.
Anaesthetic continued for 1224 hours after
the last clinical or electrographic seizure, then
dose tapered

dextrose solution if hypoglycemic (< 60 mg/dL).

in case of alcohol patient :chronic alcoholics can develop encephalopathy (due to thiamine
deficiency), so should receive IV thiamine (100 mg) prior to glucose(kreb cycle to produce energy)

benzodiazepines advantage and disadvantage


advantage BDZ :rapid onset
anxiolytic and calming effect
retrograde amnesia

disadvantage: no analgesia 2- tolerance 3- respiratory suppression, hypotension, sedation, and


local tissue irritation , The vehicle (propylene glycol) can cause administration-related hypotension
and cardiac arrhythmias.

why lorazepam is the first choice among All benzodiazepines ?


no renal or hepatic adjustment 2-rapid onset,and long duration ,,,, disadvantage> propylene glycol

propylene glycol toxicity > lorazepam , Phenytoin , midazolam

corrected phenytoin in to case : crcl <10 and hypoalbuminemia

in case crcl <10:

in case of hypoalbuminemia

Phenytoin reference level in blood 10-20


adj dose by 25%-50% increase or decrease

valproic acid mechanism of action :GABA analog , sodium channels inhibitor


Valproate at a dose of 2040 mg/kg at rate 3-6mg/kg/min

fosphenytoin vs phenytoin

fosphenytoin phenytoin
150mg/min Iv,oral
prodrug
Iv,im
Less cardiotoxic

memorize all levecetam Characteristics


Hypertensine crisis

SBP>180 , DBP>120
emergency :end organ damge (MI,strok,AKI, encephalopathy, pulmonary edema,
pheochromocytoma)
*IV meds
* goal of BP redaction:
reduce BP 25% of the MAP (1/3 SBP + 2/3 DBP) within the first our
then reduce BP not less than 160/100-110 within the next 2-6 hour
then reduce BP to goal within 24-48 h
abrupt reduction of blood pressure lead to ischemia so in case of stroke we need slower
reduction anyway in case aortic dissection we need more rapid and aggressive reduction so in this
case we give nitroprusside+BETA BLOCKER >>justification:BB to prevent reflex tachycardia

blood pressure goal in acute subarachnoid hemorrhage :140-160/90

what characteristics are most important in medication used in HTN emergency


1-rapid onset/offset 2- given as continuous infusion by bump

medication in emergency :
**nitroglycerin
-first line in MI and PE
-vasodilator
-dose : 5-300 mcg/min theoretically :max 400mcg/min
s/e :headache ,vomiting , methemoglobinemia
Methylene blue is the antidote for methemoglobinemia as well as for disulfiram like reaction

- in case of PE : (nitroglycerin + furosemide) and we need avoid beta blocker cuz its increase SOB
- in case of encephalopathy :we can use nitroglycerin or nitroprusside but is preferred to use
hydralazine
- in case of renal impairment :fenoldopam (dopamine analog )
- in case of pheochromocytoma : phentolamine
in case of pregnancy : hydralazine or labetalol and we add magnesium sulfate to prevent eclampsia

nitroglycerin disadvantage :tolerance , disulfiram like reaction


to solve tolerance problem :12 h free interval
**labetalol
-first line in stroke
-dose :20-80 mg iv bolus every 5-10 min(2 bolus dose) then maintenance :0.5-2mg /min as iv
infusion

** nitroprusside

thiocyanate toxicity : hig dose more 3g , using as contains infusion more 72hr , renal impairment
- D/C if more 12mg/dl in blood
- thiocyanate antidote :sodium thiosulphate
-CI in ckd
urgency : no organ damage
*po meds
* goal of BP redaction: reduce BP toward goal within (3-7 days ) preferred 3 days
-management :1-maximized or optimized antihypertensive medication
2- add short acting antihypertensive :captopril 25 mg, may repeat as needed; ,labetalol
clonidine : we use it only in case that the patient already on clonidine and he abruptly D/C it

Isolated systolic hypertension can be caused by underlying conditions such as HF, artery
stiffness, heart valve problems or an overactive thyroid (hyperthyroidism)

**** check and memorize all doses


ng:
Manufacturer's labeling: 5 mcg/minute, increase by 5 mcg/minute every 3 to 5 minutes to 20
mcg/minute. If no response at 20 mcg/minute, may increase by 10 to 20 mcg/minute every 3 to 5
minutes (generally accepted maximum dose: 400 mcg/minute)

furosemide
IV: 40 mg over 1 to 2 minutes. If response not adequate within 1 hour, may increase dose to 80
mg. Note: Minimal additional response is gained by single doses over 160 to 200 mg; maximum
dose: 200 mg

hydralazine
IM, IV: 10 to 20 mg every 4 to 6 hours as needed (Rhoney, 2009)

fenoldopam
IV: Initial: 0.01 to 0.3 mcg/kg/minute; may increase in increments of 0.05 to 0.1 mcg/kg/minute every
15 minutes until target blood pressure is reached; the maximum infusion rate reported in clinical
studies was 1.6 mcg/kg/minute; limit for short-term use (up to 48 hours)

nitroprusside
Acute hypertension: Initial: 0.3-0.5 mcg/kg/minute; may be titrated by 0.5 mcg/kg/minute every few
minutes to achieve desired hemodynamic effect (Rhoney, 2009); maximum dose: 10 mcg/kg/minute.
To avoid toxicity, some recommend a maximum dose of 2 mcg/kg/minute (Marik, 2007).

labetalol
IV bolus: Per the manufacturer: Initial: 20 mg IV push over 2 minutes; may administer additional
injection of 40 or 80 mg at 10-minute intervals, up to 300 mg total cumulative dose;

or
2 mg/minute; titrate to response up to 300 mg total cumulative dose (eg, discontinue after 2.5 hours of
2 mg/minute);