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0
Q

Digoxin

A
  1. Cardiac glycoside, that increases the influx of calcium from extracellular to intracellular
  2. Therapeutic effect: .
  • increase force of myocardial contraction (positive ionotropy) by increasing intracellular calcium ,results in greater activation of contractile proteins .
  • Slows heart rate by decreasing conduction from SA node to AV node, lengthening the refractory period of AV node by increasing phase 4 depolarization and shortening of action potential
  1. onset: 5-30 min/ peak:2-4 hours/ Duration: 3-4 days
    note: digoxin has low theraputic/ toxic ratio especially in presence of hypokalemia .. high serum levels can cause dysrhythmias ..

diseases that contribute to toxicity: hypothyroidism, hypokalemia, renal dysfunction .. digoxin sensitive antibody is available for tx o toxicity

  1. Metabolized partially in liver
  2. excreted in urine
  3. Indication: Management and treatment of CHF control ventricular rate in patients with A-fib note: dose not convert A-fib to sinus rhythm control of recurrent paroxysmal atrial tachycardia
  4. Dosing: . CHF, Atrail fibrilation: 2.4-3.6 mcg/kg IV qid
  5. Vial: 500 mcg/2ml (so for 100 kg person, you use 1 cc)
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1
Q
  1. Ephedrine
A
  1. non- catacholamine sympathomimetic
  2. effects similar to that of epinephrine
  3. increases arterial Bp and it is a positive ionotrop (increases contaction), chronotropand thus increase cardiac output. Also a Bronchodilator.

** a. Due to B1 adrenergic stimulation, helpful in treating moderate hypotension,**

** especially when accopmanied by bradycardia**

  1. Difference between ephedrine and epinephrine:
    a. Ephedrine has longer duration of action
    b. Less potant
    c. Has both direct and indirect actions
    i. Indirect effects could be either by a. peripheral postsynaptis release of norepi
    b. inhibition of norepi reuptake
    d. Stimulate central nervous system ( raises minimum alveolar concentration)
  2. Ephedrine has also been reported for antiemetic properties particulrly is associationwith hypotension following spinal anesthesia
  3. Clonidine premed augments the effect of ephedrine
  4. Used as pressor in hypotensive pregnenat women as it does not effect uterine bloodflow ( however phenilephrine is now prephered due to decreased risk of fetalacidosis

Recommended dose:

  1. Vial is 50 mg/ ml u dispute 1 ml with 4 ml saline then u would have 10 mg/ cc
  2. Adults: bolus of 2.5-10 mg
  3. Children: 0.1 mg/kg
  4. Metabolized in liver and excreted in urine
  5. Half life 3-6 hours
  6. Context sensitive half life 20 min
  7. Onset of bronchodilation: 15 - 1 hour
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2
Q

Cyklokapron (tranexamic acid)

A

Tranexamic acid (\ˌtran-eks-ˌam-ik-)

  1. synthetic analog of the amino acid lysine.
  2. It is used to treat or prevent excessive blood loss during surgery and in various medical conditions or disorders (helping hemostasis).
  3. It is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin, by binding to specific sites of both plasminogen and plasmin, a molecule responsible for the degradation of fibrin, a protein that forms the framework of blood clots.
  4. Tranexamic acid has roughly eight times the antifibrinolytic activity of an older analogue, ε-aminocaproic acid.
  5. Tranexamic acid is frequently used in surgeries with high risk of blood loss such as cardiac, liver, vascular and large orthopedic procedures. Its oral form is now being evaluated for use in outpatient conditions involving heavy bleeding.
  6. Tranexamic acid is used in dentistry in the form of a 5% mouth rinse after extractions or surgery in patients with prolonged bleeding time, e.g. from acquired or inherited disorders.
  7. Rare in general, including gastrointestinal effects, dizziness, fatigue, headache, and hypersensitivity reactions. Use of tranexamic acid has a potential risk of thrombosis.[4]
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3
Q

Isoproternol (Isuprel)

A
  1. potent bronchodilator and sympathomimetic
  2. structurally similar to epinephrine
  3. Potant B1 and B2 agonist, lacks a adrenergic properties. More B1 activity than B2
  4. positive ionotrop and chronotrop (increase heart rate and contraction)
  5. Action is mediated intracellularly by cAMP
  6. Administration caused increase in systolic BP and decrease in Diastolic BP

. This is attributed to drug induced peripheral vasodilation

. This effect increaes myocardial blood flow, however increase in heart rate and

increase in O2 demand of heart overweighs the benefit of any increase in

myocardial blood flow

  1. increases myocardial excitability and automaticity, which favors dysrhythmias. Popularity has declined bc of adverse effects such as tachycardia and arrhythmias
  2. Second line of treatment for symptomatic bradycardia that does not respond to

Atropine

. Dosage: 2-10 mcg/ min infusion titrated to heart rate effect

  1. B/c of its direct effect on B receptors (mainly chronotropic effect), it is useful in treatment of symptomatic bradycardia in heart transplant recipients (Main use now)

. Dosage : 1 mcg/min is titrated upward until desired effect is achieved

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4
Q

Dobutamine

A
  1. Synthetic analogue of Dopamine
  2. Mostly B1 adrenergic effect
  3. Compared to isoproternol Ionotropy is more effected than chronotropy
  4. Less of B2 than Iso and less of a1 than norepi
  5. Theraputic use:
  • CHF
  • MI
  • Both complicated with low cardiac output
  1. Dobutamine directly effects B1 receptors and does not rely on endogenus

catacolamines

  • May be useful in catacolamine depeleted states such as chronic CHF
    7. Prolonged treatmet produces tolerance to hemodynamic effects of dobutamine
  • bc of down regulation of B-receptors
  • mostly after 3 days
  • hence intermittent infusaion of dobutamine have been used in treatment of CHF
  • Treatment improved excecise tolerance but not survival rate

8.Dose:

  • Doses smaller than 20 mcg/kg/min do not produce tachycardia
  • Adult and pediatric: 2-20 mcg/kg/min
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5
Q

Adenosine

A
  1. cardiac agent:
  • slows impulse formation in SA node
  • slows conduction time through AV node
  1. Effect: depresses left ventricular function and restore normal sinus rhythm
  2. Half life: 10 seconds
  • Rapidly cleared from blood after iv administration
  • metabolized by red blood cells and vascular enothelial cells
  1. Indication:
  • Paroxysmal supraventicular tachycardia
  • Dose: 6 mg ivx1 then 12 mg iv q1-2 minx 1-2 doses
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6
Q

Etomidate

A
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