Professional Documents
Culture Documents
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)
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
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)
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
ASA make metabolic acidosis , BUT ASA overdose make respiratory alkalosis
respiratory alkalosis
primary respiratory alkalosis(ph>7,45 and pco2 less 35)
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
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
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
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
*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
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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 )
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
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
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
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
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
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
The APACHE II Scoring System is designed to measure the severity of disease in patients admitted to
the intensive care unit
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%
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
rbonate concentration >18 meq/L
=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.
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
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
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)
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.
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
or
Phenobarbitone bolus of 15-20 mg/kg
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)
in case of hypoalbuminemia
fosphenytoin vs phenytoin
fosphenytoin phenytoin
150mg/min Iv,oral
prodrug
Iv,im
Less cardiotoxic
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
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
** 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)
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);