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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
PPI on active gi pleading (ppi can make healing ,h2 not ) cuz : platelet
aggregation need ph 6 H2 VS
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
Eye response(E)2 Verbal response (V) 3 Motor response (M ) EVM1
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)
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
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
The body responds metabolic alkalosis by trying to restore the PCO2 / [HCO3-]
ratio. This is done by increase the PCO2. by hypoventilation (respiratory acidosis)
ASA make metabolic acidosis , BUT ASA overdose make respiratory alkalosis
respiratory alkalosis
primary respiratory alkalosis(ph>7,45 and pco2 less 35)
:each v 10 in pco2 (uder 35) 2 v hco3(3n the upper limit 35) in acute
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
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
: type of fluid
crystalloid fluid like normal saline , Lactated Ringer's ,dextrose-1
source of enrage ,contain minerals like ca :(Lactated Ringers, dextrose ) *
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
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)
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
/ 24
: evaluation
: 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
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
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
Criteria for brain death: fixed pupil , irreversible loss of brain function (functional brain death )
loss of the brain nerve reflexes including the light reflex
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
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
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
sizure : we give seizure prophylaxis -1
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 *
some study recommend to give combination mannitol and furosemide low dose
10-20mg since its give synergistic diuretic effect to decreases cerebral edema
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)
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
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
hypokalemia(k <3,5)
mild hypokalemia 3__3,5
moderate hypokalemia 2,5__3
severe hypokalemia less 2,5
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
Serum bicarbonate concentration >18 meq/L
Venous blood PH >7.3
Anion gap =12 2
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SEPSIS AND VAP
Old definition
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
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
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)
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
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