Cardiac Medications Flashcards
Adenocard
(mechanism of action)
♦ Blocks the transmission of impulses through the AV node by binding to the Adenosine-1 receptor. Slows conduction time through the AV node. Finally causes arterial vasodilation by binding to vascular endothelial tissue.
♦ Hyperpolarizes atrial tissues, reducing the duration of the atrial action potential.
♦ Adenosine reduces the diastolic depolarization phase of the sinoatrial nodal pacemaker cells.
Adenocard
(onset-duration)
Onset: Immediate
Half Life: < 10 sec
Duration: 1-2 min
Adenocard
(side effects)
Because adenosine decreases conduction through the AV node,
♦ First-, Second-, or Third-degree heart blocks are possible effects
Adenocard
(indications)
♦ PSVT
♦ SVT
Adenocard
(contraindications)
♦Do not administer for wide QRS tachycardia
♦Caution in patients with WPW syndrome who present with A-fib w/ RVR
Contraindicated → sick sinus node syndrome or symptomatic bradycardia, →2nd or 3rd-degree AV block, except in patients with a functioning artificial pacemaker in place.
Avoid adenosine with S/S of unstable angina or cardiovascular instability because they may be at increased risk for cardiovascular adverse events.
Adenocard (adult dose)
♦ SVT → 6 mg rapid IO/IV bolus initial dose
If SVT rhythm has not changed after 5 minutes, repeat second dose of 12 mg rapid IO/IV bolus
♦ V-Tach → 12 mg rapid IO/IV bolus for stable monomorphic, regular wide complex tachycardia that may be SVT with aberrancy
Adenocard
(pediatric dose)
Supraventricular Tachycardia
♦ 0.1 mg/kg (over 1-2 seconds) IO/IV followed by rapid saline flush; max initial dose of 6 mg
♦ 0.2 mg/kg within 1-2 minutes of continuing SVT=given rapid IO/IV; max single dose of 12 mg
Adenocard
(pregnancy safe)
Pregnancy Class C
There are no adequate human studies of the effects of this drug on the fetus; however, adenosine is a naturally occurring material and dispersed widely in the body; fetal effects are not anticipated.
Adenosine should be used during pregnancy only if clearly needed.
Amiodarone
(mechanism of action)
Class III antiarrhythmic agent
♦ Blocks sodium, potassium and calcium channels
♦ Decreases AV conduction and sinus node function
(also depresses automaticity of both the SA and AV nodes directly (class II effect) and slows conduction in the His-Purkinje system and in the accessory pathway of patients with Wolff-Parkinson-White syndrome)
The drug relaxes both smooth and cardiac muscle, causing decreases in coronary and peripheral vascular resistance, left ventricular end-diastolic pressure and systolic blood pressure, thereby decreasing afterload.
Amiodarone
(side effects)
Hypotension,
bradycardia,
AV block,
asystole,
PEA,
hepatoxicity
Amiodarone
(indications)
♦ Shock resistant V-Fib
♦ Pulseless V-Tach
♦ Ventricular Tachycardia
Amiodarone
(contraindications)
♦ Iodine hypersensitivity
Due to the incorporation of iodine into its chemical structure, it is contraindicated in patients with iodine hypersensitivity.
♦ Cardiogenic shock - due to potential negative inotropic effects
♦ Marked Sinus Bradycardia
♦ 2nd or 3rd degree AV Block
Amiodarone
(adult dose)
Pulseless V-Tach / V-Fib
♦ Rapid 300 mg IO/IV
♦ Repeat once at 150 mg IO/IV
V-Tach with a pulse
♦ Rapid 150 mg IO/IV bolus.
May repeat once if patient remains in unstable V-Tach to a total dose of 300 mg over 20 minutes.
Amiodarone
(pediatric dose)
Pulseless V-Tach / V-Fib
♦ Rapid 5 mg/kg IO/IV bolus
Ventricular Rhythm – Post Resuscitation
♦ 5 mg/kg IO/IV over 20 minutes.
Repeat doses of 5 mg/kg IO/IV over 20 minutes; maximum 15 mg/kg.
Amiodarone
(pregnancy safe)
Pregnancy Class D
Amiodarone crosses the placenta and can cause fetal harm when administered to a pregnant woman.
Reported risks include neonatal bradycardia; QT prolongation; periodic ventricular extrasystoles; neonatal hypothyroidism
(Amiodarone and a major metabolite, desethylamiodarone (DEA), are excreted in human milk, suggesting that breast-feeding could expose the nursing infant to a significant dose of the drug.)
Atropine
(mechanism of action)
♦ Increases the firing of the SA node and AV node opposing the actions of the vagus nerve by blocking the acetylcholine receptor sites.
♦ Increases cardiac output, dries secretions. Atropine reverses the muscarinic effects of cholinergic poisoning due to agents with acetylcholinesterase inhibitor activity by acting as a competitive antagonist of acetylcholine at muscarinic receptors.
Atropine
(side effects)
Tachycardia,
Dry mouth, thirst,
Flushing of skin,
Blurred vision,
Headache,
Pupillary dilation,
Urinary retention
Atropine
(indications)
♦ Anticholinergic drug used in bradycardias
♦ Organophosphate poisoning (to block the parasympathetic response)
Atropine
(contraindications)
♦ Tachycardia,
♦ Glaucoma,
♦ A-Fib/Flutter w/RVR
Atropine-induced tachycardia may cause ischemia, extend or initiate myocardial infarcts, and stimulate ventricular ectopy and fibrillation.
Atropine
(adult dose)
Bradycardia
♦ 0.5 mg IO/IV;
♦Repeat every 3 – 5 minutes to a total of 3 mg
Organophosphate Poisoning
♦ 1–2 mg IO/IV;
♦Repeat dose every 5 minutes as needed
Max total dose of 6 mg
Atropine
(pediatric dose for bradycardia)
Bradycardia
♦ 0.02 mg/kg IO/IV
♦ Minimum dose of 0.1 mg
♦ Maximum single dose of 0.5 mg (child) and 1 mg (adolescent)
♦ May repeat once
Atropine
(pediatric dose for organophosphate poisoning)
Organophosphate Poisoning
♦ 0.02mg/kg IO/IV
(min 0.1mg / max 1mg)
♦ Repeat every as needed to
max total dose of 6 mg
Atropine
(pediatric dose for RSI)
Rapid Sequence Intubation
♦ 0.02 mg/kg IO/IV
- *Minimum** dose of 0.1 mg
- *Maximum** dose of 1 mg
Atropine
(pregnancy safe)
Pregnancy Class C
There are risks to the fetus and mother associated with untreated severe or life-threatening muscarinic effects; life-sustaining therapy for the pregnant woman should not be withheld due to potential concerns regarding the effects of atropine on the fetus.
(There are no data on atropine concentrations in human milk after intravenous or ocular administration, the effects on the breast-fed infant, or the effects on milk production.)
Cardizem (Diltiazem)
(mechanism of action)
Class IV Antiarrthmic/Calcium Channel Blocker
Decreases heart rate and B/P by inhibiting calcium ion influxes across the cell membrane during cardiac depolarization.
♦ Dilates coronary arteries, peripheral vessels; reduces myocardial oxygen consumption and slows SA/AV node conduction times through its negative inotropic, chronotropic and dromotropic effects.
In addition, total peripheral resistance, systemic blood pressure, and afterload are decreased effectively increasing coronary blood flow.
Cardizem (Diltiazem)
(onset and duration of action)
Onset: 2-5 min
time to peak effect is 15 minutes.
Half Life: 3.5 - 9 hrs
Duration: 1 - 3 hrs after IV ggt up to 10 hours
Cardizem (Diltiazem)
(side effects)
Diltiazem can precipitate or exacerbate heart failure or cause excessive bradycardia or cardiac conduction abnormalities (heart blocks) in patients with ventricular dysfunction, severe bradycardia, cardiogenic shock, or congestive heart failure and/or patients taking beta-adrenergic blocking agents.
Diltiazem decreases peripheral resistance and can worsen hypotension
Cardizem (Diltiazem)
(indications)
♦ Rate control in refractory atrial fibrillation
♦ SVT