هذه بعض الادوية التي تستخدم في وحدة العناية المركزة للاطفال

هذه بعض الادوية التي تستخدم في وحدة العناية المركزة للاطفال




Medication




Analgesics


Morphine sulfate (MSO4) (0.05 - 0.2 mg/kg initial dose)

Class: Opiate Analgesic
Half-life: 2-4 hours (4.5-13.3 hours in neonates)
Duration of action: 3-4 hours
Metabolism: by liver, excreted in urine and bile
Dosing Frequency: Q1-4 hours or as a continuous drip
Precautions: respiratory suppression with increasing doses, histamine release, has caused seizures in neonates
Uses: post-operative pain control, sedation, tet spells, can also increase cardiac output


Fentanyl (1-2mcg/kg per dose initially)

Class: opioid analgesic
Half-life: 2-4 hours
Duration of action: 1-2 hours
Metabolism: by liver, excreted by kidney (<10%)
Dosing Frequency: Q30min-1hour, continuous drip
Precautions: may cause chest wall rigidity in neonates at high doses.
Uses: Post-operative pain management, rapid tolerance develops, may need to increase drip rate daily to maintain equianalgesic dose.


Nalbuphine (Nubain) (0.05-0.1mg/kg initial dose)

Class: Partial opioid agonist (mixed agonist/antagonist)
Half-life: 5 hours
Duration of action: 3-6 hours
Metabolism: by liver, excreted in urine
Dosing Frequency: Q1-4 hours (as with MSO4) can be in drip
Precautions: equal respiratory depression in standard doses as MSO4, at higher doses the effect plateaus.
Uses: in post-operative pain management or to relieve itching related to narcotics. Frequently used with epidural opiods


Sedatives


Midazolam (Versed) (0.05-0.1mg/kg initial dose)

Class: benzodiazepine
Half-life: 1-4 hours
Metabolism: extensively by liver (microsomally), excreted in urine, some in feces
Dosing Frequency: Q1-2 hours, to continuous drip
Precautions: respiratory depression, when used alone in some patients can produce paradoxical effect. Cimetidine can prolong half life when used concomitantly
Uses: as anxiolytic/sedative in association with analgesic agents for patients with severe pain, or in whom sedation is desired for various reasons.


Lorazepam (Ativan) (0.03-0.09mg/kg/dose)

Class: benzodiazepine
Half-life: 10-12 hours (40 hours in neonates)
Metabolism: liver, excreted in urine
Dosing Frequency: Q4-8 hours
Precautions: as with Versed, longer acting so prolonged effect of respiratory suppression
Uses: Sedative for patients who will need prolonged sedation. Can also be used to help wean patients from Versed drips


Chloral Hydrate (25-75mg/kg max dose 2gm/day)

Class: sedative hypnotic
Half-life: around 8 hours
Metabolism: by liver to trichloroethanol (active metabolite) then excreted in urine
Dosing Frequency: Q6hours to Qday
Precautions: Trichloroethanol is carcinogenic in mice, prolonged usage may put patient at risk. Arrhythmias with high levels, withdrawal similar to EtOH withdrawal after prolonged, regular usage.
Uses: additional sedation of a different class, sedation for procedure


Propofol (Diprivan) (25-50 mcg/kg/min drip, 0.5-1mg/kg bolus)

Class: sedative hypnotic
Half-life: minutes, increases with increasing duration of therapy
Metabolism: by liver excreted in urine
Dosing Frequency: Only used as continuous drip or short acting bolus
Precautions: severe myocardial depressant proportionate to dose. No preservatives in solution so at high risk for infection unless aseptic technique is adhered to, particularly for prolonged drips.
Uses: Insoluble in water so supplied in solution of 10% Intralipid. Used for short term sedation when extra sedation is needed. Also used overnight prior to extubation on patients who have had prolonged sedation to allow decreasing other sedatives, rapid wean prior to extubation. FDA does not approve use in pediatric patients for sedation in the PICU



Paralytic Agents


Vecuronium (Norcuron) (0.1mg/kg, 0.2mg/kg for rapid sequence intubation)

Class: non-depolarizing neuromuscular blocker
Duration of action: 30-40 minutes
Metabolism: excreted primarily in bile, partially in urine
Dosing Frequency: Q1-2 hours prn to continuous drip
Precautions: must be prepared to manage airway or intubated prior to use. Do not use without adequate sedation/pain control. Prolonged administration can produce prolonged muscle weakness after stopage
Uses: as a paralytic in patients who need prolonged mechanical ventilation with significant lung disease, those with significant pulmonary hypertension,


Pancuronium (Pavulon) (0.04-0.1mg/kg initially then 0.01mg/kg per dose as needed)

Class: non-depolarizing neuromuscular blocker
Duration of action: 35-45 minutes
Metabolism: excreted mostly unchanged in urine, some metabolism by liver and elimination in bile
Dosing Frequency: Q25-60minutes
Precautions: must be prepared to manage airway or intubated prior to use. Do not use without adequate sedation/pain control.
Uses: as a paralytic in patients



Cisatracurium (Nimbex) (0.1mg/kg)

Class: non-depolarizing neuromuscular blocker
Duration of Action: 20-35 minutes, up to 45 minutes
Metabolism: rapid non-enzymatic degradation (Hofman elimination) in bloodstream
Dosing Frequency: usually a continuous drip or prn
Precautions: Cis form minimizes Histamine release caused by Atracurium
Uses: ideal as neuromuscular blocker in patient with compromised renal and/or hepatic function

Diuretics


Furosemide (Lasix) (0.5-1mg/kg, Max Dose 10mg/kg/day)

Class: loop diuretic
Half-life: 30min-2 hours, duration of action 2 hours
Metabolism: minimally by liver, 50-80% excreted in urine
Dosing Frequency: Q2 hours to Qday
Precautions: Ototoxicity, hypokalemia, hypocalcemia
Uses: diuresis, treatment of hyperkalemia



Bumetadine (Bumex) (0.02-0.1mg/kg, Max Dose 0.35mg/kg/d)

Class: loop diuretic
Half-life: 1-1.5 hours duration of effect 2-4 hours
Metabolism: by liver, excreted in urine (80%) and feces (10-20%)
Dosing Frequency: can be continuous drip to prn
Precautions: same as for Furosemide
Uses: Diuresis when not responding to Furosemide; has less ototoxicity at equi-therapeutic doses, should change usage when Furosemide dose gets high



Metolazone (Zaroxylyn) (0.2-0.4mg/kg/day)

Class: Thiazide-like diuretic
Half-life: approximately 14 hours, slowly absorbed from GI tract
Metabolism: 70-95% excreted unchanged in urine, also in bile, may undergo
enterohepatic recycling
Dosing: oral/enteral only
Precautions: dumps both Na and K, can cause bone marrow suppression
Uses: compliments activity of loop diuretics by functioning with a different mechanism. Has been shown to improve urine output even with very low GFR not found in other thiazides. Can improve urine output in patients whose renal function is not responding to high dose loop diuretics. Does not decrease GFR as other thiazides can.


Antiarrhythmic Agents

Adenosine (Adenocard) (50mcg/kg initial dose, then increase by 50 for each subsequent dose)

Class: endogenous nucleoside
Half-Life: <10 seconds
Metabolism: rapidly taken up by erythrocyes and vascular endothelial cells, becomes part of body pool of nucleosides
Dosing Frequency: repeat doses can be given as early as 2 minutes after initial dose
Administration: should be given in most central venous access site as rapidly as possible. Central venous access is preferred but not essential
Precautions: may produce a short-lasting first, second or third degree av block.
Use: Adenosine works by decreasing conduction through the av node. It is used
exclusively in supraventricular tachycardia to convert to sinus rhythm. If unsuccessful after 3 doses, or patient becomes unstable, synchronized cardioversion should be performed (This would include fresh post-op heart patients as they may not be able to withstand the significant transient decrease in BP that can occur with this agent).



Lidocaine (1mg.kg iv slowly, 20-50mcg/kg/min as a drip)

Class: a Class 1b anti-arrhythmic agent (membrane stabilizing), also an amide local anesthetic
Half-Life: Initial 7-30minutes, terminal 1.5-2 hours
Metabolism: by liver to active metabolites GX and MEGX, which are later metabolized by the liver
Dosing Frequency: bouses can be given Q3-5 minutes, otherwise can be used as a drip
Precautions: CNS depressant, may cause seizures at high doses (although does have anti-convulsant properties), can cause respiratory arrest. Also supresses cough and gag reflexes.
Uses: treatment of choice for premature ventricular contractions, used for ventricular dysrhythmias



Procainamide (15mg/kg over 15 minutes, 20-80mcg/kg/min as continuous drip)

Class: a Class 1a anti-arrhythmic agent
Half-life: 3-4 hours
Metabolism: acetylated to active form N-acetyl procainamide (NAPA), actively secreted in urine as well as filtered. All forms are excreted in urine.
Dosing Frequency: may be administered as frequently as Q5 minutes or as continuous infusion.
Precautions: contraindicated in complete heart block, Lupus, and Torsades des Pointes. Can cause transient hypotension
Uses: for lidocaine resistant ventricular tachycardia, reentrant tachycardias, atrial fibrillation and flutter associated with WPW

Amiodarone (5mg/kg IV over 30 minutes)



Antihypertensives


Nifedipine

Class: Calcium Channel blocker, ( a dihydropyridine)
Half-life: 2-5 hours
Metabolism: primarily hepatic
Dosing: must be drawn from capsule with TB syringe then dose is calculated from total extracted.
Precautions:
Uses: in patients who can take oral, or sublingual meds, can be used for acute
hypertensive episodes




Esmolol (as a drip 25-250mcg/kg/min)

Class:  blocker
Half-life:
Metabolism:
Dosing:
Precautions:
Uses: Hypertension, frequently after coarctation repair



Nitroprusside (as a drip, usual range 0.1-10 mcg/kg/min)

Class: arteriolar vasodilator, NO donor
Half-life:
Metabolism:
Dosing:
Precautions: Monitor cyanide levels, especially in the setting of renal failure
Uses: Hypertension, afterload reduction


Hydralazine

Half-life: about 4 hours, although serum levels don't correlate well with activity
Metabolism: extensively by the liver
Dosing:
Precautions: can cause a Lupus like syndrome in as many as 10-20% of patients who receive a prolonged course.
Uses: can be used for acute hypertensive episodes, but it is not the drug of choice



Cardioactive Drips

Adrenergic Receptors
Alpha - peripheral vasculature

stimulation causes vasoconstriction

Beta - (remember 1 heart, two lungs)

Receptor stimulation acts through adenylate cyclase forming cAMP

Beta 1 - cardiac receptors

stimulation increases contractile strength

and increases heart rate

Beta 2 - pulmonary receptors, and peripheral vasculature

stimulation causes smooth muscle relaxation of bronchial walls

smooth muscle relaxation in peripheral vasculature




Drugs to Improve Cardiac output
Dobutamine (3-20mcg/kg/min)

MOA: almost exclusively a Beta-1 agonist with no alpha effect, and minimal beta-2 effect
Effect: inotropic and chronotropic effects on the heart, some decrease in peripheral vascular resistance and some improvement of AV node conduction
Use: to improve cardiac output and blood pressure, can be administered peripherally
Risk: increases myocardial oxygen demand, may increase heart rate excessively


Dopamine (2-20mcg/kg/min)

MOA: precursor of norepinephrine, stimulates dopaminergic, alpha and beta adrenergic receptors (little or no beta-2 effect)
Effect: at low doses (2-5mcg/kg/min) minimal alpha effects, causes more splanchnic dilatation, improving renal blood flow (a dopaminergic response). At medium doses (5-10mcg/kg/min) beta effects start to predominate. At high doses (10-20mcg/kg/min) alpha effects more prevalent
Use: good first line to improve cardiac output when used in mid-range
Risk: high doses may cause vasoconstiction. Adverse effects on immune function.


Epinephrine (0.01 to 1 mcg/kg/min, or higher in very critical situations, usual dose range in cardiac patients is 0.03-0.3, in septic patients doses may be higher)

MOA: potent non-selective beta agonist also an alpha agonist (Beta>alpha)
Effect: increases inotropic and chronotropic cardiac activity also causes peripheral vasoconstriction, decreasing peripheral perfusion
Use: to increase cardiac output and blood pressure, at lowest doses (<0.1mcg/kg/min has primarily beta-1 effects)
Risk: can cause profound peripheral vasoconstriction, compromising tissue perfusion. Long term use downregulates catecholamine receptors, decreasing effect, also increases myocardial oxygen demand

Drugs to Improve Cardiac Output and cause Vasodilation
Milrinone (0.30-1.0mcg/kg/min)

MOA: phosphodiesterase inhibitor, prolonging the effect of cAMP, allowing increasing ionized calcium entry into cardiac cells, increasing myocardial contractility, and cAMP dependent vascular relaxation
Effect: peripheral vasodilator and positive inotropic effect on heart, improved diastolic relaxation. May cause reflex tachycardia due to vasodilation
Use: afterload reduction, additional inotropic support when catecholamines already in use.
Risk: as with other inotropes, can also potentially cause too much vasodilation leading to hypotension, use caution in severely hypovolemic patients



Drugs to cause vasodilation
Nitroprusside (Nipride) (0.5-10mcg/kg/min)

MOA: it has direct activity on vascular smooth muscle (donates an NO group to be specific)
Effect: peripheral vasodilator by relaxation of smooth muscles in vessels
Use: used as an afterload reducer, primarily an arterioloar vasodilator, can increase tissue perfusion in patients receiving vasoconstrictors, can be given peripherally.
Risk: Cyanide and Thiocyanate toxicity from prolonged usage of high doses (using Na thiosulfate decreases risk 10mg/mg nitroprusside). Risk of severe hypotension in patient who is intravascularly dry. Overcomes hypoxic vasoconstriction in the lungs, so initiation can cause increased VQ mismatch and therefore more difficulty in oxygenation.


Nitroglycerin (0.5-5mcg/kg/min)

MOA: relaxes peripheral vascular smooth muscle by donating an NO group
Effect: causes peripheral vasodilatation, decreasing pre-load and decreasing blood pressure, helps prevent vasospasm
Use: most commonly used in post-operative arterial switches to help prevent coronary vasospasm, sometime used as a preload reducer, can be given peripherally.
Risk: can cause severe hypotension in patient who is intravascularly dry, risk of methemoglobinemia, otherwise similar to nitroprusside.



Drugs to cause pulmonary vasodilation
Nitric Oxide (0-80ppm inhalation)

MOA: Activates cGMP pathway causing direct smooth muscle relaxation in local vascular bed
Effect: since given as inhalational agent, causes relaxation of pulmonary vascular bed only, with no systemic effect
Use: used to decrease pulmonary vascular resistance in patients in whom pulmonary hypertension is a problem, either from a cardiac output standpoint or from a oxygenation standpoint
Risk: can combine with Hgb to form methemoglobin, needs closed ventilatory circuit and constant monitoring. NO is now FDA approved for PPHN, but the cost is $3000/day for up to 4 days.


Drugs to increase systemic vascular resistance (increase afterload)
Norepinephrine (Levophed) (initial dose 0.05-0.1mcg/kg/min, titrate to effect)

MOA: Potent alpha adreneric agonist and beta agonist (alpha>beta)
Effect: vasoconstriction and inotropic and chronotropic effects, increasing blood pressure, both by increasing SVR and by increasing CO
Use: in patients already on vasopressors requiring more support to maintain blood pressures
Risk: decreases blood flow to all organs and tissues, can cause worsening metabolic acidosis due to ischemia


Phenylephrine (Neo-Synephrine) (0.1-0.5mcg/kg/min as drip, 5-20mcg/kg as bolus)

MOA: alpha adrenergic agonist
Effect: constricts both arterial and venous blood vessels, increasing systemic vascular resistance without changing cardiac dynamics
Use: In patients who need blood pressure support, where muscular outflow obstruction may be worsened by the use of Beta agonists, such as unrepaired TOF or hypertrophic cardiomyopathy.
Risk: decreases flow of blood to all organs, reducing oxygen supply and potentiating ischemia at very high doses can have some beta effect.


Also Epinephrine and Dopamine to some extent



Adjunct:

Steroids - can upregulate catecholamine receptors, improving function and decreasing dose

requirements of vasopressors