Cardiac Medications Flashcards

(72 cards)

1
Q

Adenocard

(mechanism of action)

A

♦ 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.

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2
Q

Adenocard

(onset-duration)

A

Onset: Immediate

Half Life: < 10 sec

Duration: 1-2 min

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3
Q

Adenocard

(side effects)

A

Because adenosine decreases conduction through the AV node,

First-, Second-, or Third-degree heart blocks are possible effects

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4
Q

Adenocard

(indications)

A

♦ PSVT

♦ SVT

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5
Q

Adenocard

(contraindications)

A

♦Do not administer for wide QRS tachycardia

♦Caution in patients with WPW syndrome who present with A-fib w/ RVR

Contraindicatedsick 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.

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6
Q

Adenocard (adult dose)

A

SVT6 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-Tach12 mg rapid IO/IV bolus for stable monomorphic, regular wide complex tachycardia that may be SVT with aberrancy

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7
Q

Adenocard

(pediatric dose)

A

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

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8
Q

Adenocard

(pregnancy safe)

A

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.

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9
Q

Amiodarone

(mechanism of action)

A

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.

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10
Q

Amiodarone

(side effects)

A

Hypotension,

bradycardia,

AV block,

asystole,

PEA,

hepatoxicity

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11
Q

Amiodarone

(indications)

A

♦ Shock resistant V-Fib

♦ Pulseless V-Tach

♦ Ventricular Tachycardia

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12
Q

Amiodarone

(contraindications)

A

♦ 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

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13
Q

Amiodarone

(adult dose)

A

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.

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14
Q

Amiodarone

(pediatric dose)

A

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.

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15
Q

Amiodarone

(pregnancy safe)

A

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.)

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16
Q

Atropine

(mechanism of action)

A

♦ 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.

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17
Q

Atropine

(side effects)

A

Tachycardia,

Dry mouth, thirst,

Flushing of skin,

Blurred vision,

Headache,

Pupillary dilation,

Urinary retention

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18
Q

Atropine

(indications)

A

♦ Anticholinergic drug used in bradycardias

♦ Organophosphate poisoning (to block the parasympathetic response)

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19
Q

Atropine

(contraindications)

A

♦ Tachycardia,

♦ Glaucoma,

♦ A-Fib/Flutter w/RVR

Atropine-induced tachycardia may cause ischemia, extend or initiate myocardial infarcts, and stimulate ventricular ectopy and fibrillation.

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20
Q

Atropine

(adult dose)

A

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

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21
Q

Atropine

(pediatric dose for bradycardia)

A

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

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22
Q

Atropine

(pediatric dose for organophosphate poisoning)

A

Organophosphate Poisoning
0.02mg/kg IO/IV
(min 0.1mg / max 1mg)

♦ Repeat every as needed to
max total dose of 6 mg

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23
Q

Atropine

(pediatric dose for RSI)

A

Rapid Sequence Intubation
0.02 mg/kg IO/IV

  • *Minimum** dose of 0.1 mg
  • *Maximum** dose of 1 mg
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24
Q

Atropine

(pregnancy safe)

A

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.)

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25
**Cardizem (Diltiazem)** **(mechanism of action)**
**Class IV Antiarrthmic/Calcium Channel Blocker** ## Footnote ***_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.**_
26
**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
27
**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_**
28
**Cardizem (Diltiazem)** **(indications)**
♦ Rate control in refractory atrial fibrillation ♦ SVT
29
**Cardizem (Diltiazem)** **(contraindications)**
♦ Diltiazem ***can precipitate or exacerbate heart failure*** **or** cause **excessive bradycardia** **or cardiac conduction abnormalities** 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***. ***_should not be used_*** in patients with ***SBP _\<_*** ***_90_*** mmHg Due to its inhibitory effects on AV node conduction, diltiazem is contraindicated in patients with ***_preexisting second- or third-degree AV block or previous conduction abnormalities_***. ♦ Use of diltiazem for treatment of atrial fibrillation or flutter ***may precipitate severe ventricular arrhythmias*** and is **_contraindicated_** in patients with **_Wolff-Parkinson-White syndrome or Lown-Ganong-Levine syndrome._**
30
**Cardizem (Diltiazem)** **(adult dose)**
♦ **0.25 mg/kg** *up to _20 mg_* IO/IV **over 2 minutes** if **systolic BP \> 90** ♦ If uncontrolled after 15 minutes → **0.35 mg/kg** IV/IO **over 2 minutes**
31
**Cardizem (Diltiazem)** **(pediatric dose)**
**_Not indicated in current protocols_**
32
**Cardizem (Diltiazem)** **(pregnancy safe)**
Pregnancy **Class C** ## Footnote There are no well-controlled studies of diltiazem in pregnancy. _Administer diltiazem to pregnant women **only if the potential benefit justifies the potential risk to the fetus.**_
33
**Furosemide** **(mechanism of action)**
Furosemide is a **loop diuretic** that **inhibits** the **reabsorption** of **sodium**, **calcium**, **magnesium**, **chloride**, **water** and some **potassium**. _Increases urinary excretion of sodium_, chloride, **potassium**, and hydrogen ions. The diuresis caused by furosemide can lead to increased aldosterone production, resulting in increased sodium resorption, and **increased** _**potassium** and hydrogen excretion_. _**Excessive loss** of these electrolytes **can lead to metabolic alkalosis.**_ *Renal vasodilation occurs following administration of furosemide; renal vascular resistance decreases, and renal blood flow is enhanced.* Reduced peripheral vascular resistance and increased peripheral venous capacitance also occur, and the **subsequent decrease in left ventricular filling pressure may contribute to the drug's beneficial effect in patients with congestive heart failure.**
34
**Furosemide** **(onset and duration)**
Onset: **10 - 30 min** Half Life: 30 - 60 min Duration: **2 hrs**
35
**Furosemide** **(side effects)**
♦ Hypovolemia, hypotension, hyponatremia, hypokalemia. ## Footnote ♦ Loop diuretics **may induce metabolic alkalosis** associated with **hypokalemia** and **hypochloremia**
36
**Furosemide** **(indications)**
Acute Pulmonary Edema such as CHF
37
**Furosemide** **(contraindications)**
**♦ Absolute - Hypersensitivity** **♦ Relative** - _Excessive diuresis with furosemide_ _should be avoided in patients with acute myocardial infarction due to the **risk of precipitating shock**_. Furosemide is contraindicated in patients with anuria. It should be ***used cautiously*** in any patient ***with renal disease*** such as severe renal impairment or renal failure.
38
**Furosemide** **(adult dose)**
## Footnote **40-80 mg IV**
39
**Furosemide** **(pediatric dose)**
**OLMD Required**
40
**Furosemide** **(pregnancy safe)**
Pregnancy **Class C** ## Footnote **_Do not use_** **furosemide** during pregnancy **unless** the potential **benefit justifies the potential risk to the fetus.** Use caution when administering furosemide to a breast-feeding mother. **Furosemide is excreted in human breast milk.**
41
**Heparin** **(mechanism of action)**
♦ Heparin **exerts its anticoagulant action** by **accelerating the activity of antithrombin III** (ATIII) to **inactivate thrombin**; however, heparin does not lyse existing clots. **_♦ High doses of heparin also interfere with platelet aggregation_**, which, in turn, prolongs the bleeding time, although commonly used therapeutic doses heparin do not affect bleeding time.
42
**Heparin** **(onset and duration)**
After intravenous administration, response is almost **immediate**. The anticoagulation half-life of heparin is 1, 2.5, and 5 hours when heparin 100, 400, or 800 units/kg, respectively, is given intravenously.
43
**Heparin** **(side effects)**
No immediate side effects. Late side effects include hemorrhages.
44
**Heparin** **(indications)**
Anticoagulant therapy
45
**Heparin** **(contraindications)**
♦ Severe thrombocytopenia, ♦ Uncontrolled active bleeding
46
**Heparin** **(adult dose)**
♦ **5,000 units** IO/IV ## Footnote ♦ *Consider continuous infusion for extended transports: 12 units/kg/hr,* ***not to exceed 1,000 units/hr***
47
**Heparin** **(pediatric dose)**
Not indicated in current protocols
48
**Heparin** **(pregnancy safe)**
Pregnancy **Class C** ## Footnote In published reports, heparin exposure during pregnancy did not result in increased risk of adverse maternal or fetal outcomes in humans. Heparin _does not_ _cross_ the placental barrier.
55
**Magnesium Sulfate** **(mechanism of action)**
Effects the myocardium, bronchial tree, skeletal and smooth muscle by **reducing the release of acetylcholine at the neuromuscular junction reducing muscle contractions and promoting relaxation**.
56
**Magnesium Sulfate** **(onset and duration)**
**Onset**: Immediate **Duration**: 30 min
57
**Magnesium Sulfate** **(side effects)**
Bradycardia, Hypotension, Hyporeflexia, Diaphoresis and Drowsiness, Decreased Respiratory Rate, Flaccid Paralysis
58
**Magnesium Sulfate** **(indications)**
♦ Torsades de Pointe ♦ Digitalis induced ventricular arrhythmias ♦ Anticonvulsant in eclampsia ♦ Suspected hypomagnesium
59
**Magnesium Sulfate** **(contraindications)**
Hypermagnesium Hypocalcemia Anuria Heart block Active labor
60
**Magnesium Sulfate** **(adult dose)**
**⇒ Eclampsia / Pre-Eclampsia** ♦ ***4 grams IO/IV over 20 minutes*** **⇒ Pulseless V-Tach / V-Fib** ♦ refractory V-Tach unresponsive to Amiodarone or in Torsades de Pointes, administer ***2 grams _slow_ IO/IV push over 20 minutes***. **⇒ Reactive Airway Disease** ♦ **2 grams IO/IV over 10 minutes**. ♦ transferrs with Mag Sulfate infusing, continue at current rate. **If rate is \> 4 grams/hr, contact receiving MD**.
61
**Magnesium Sulfate** **(pediatric dose)**
⇒ **Pulseless V-Tach / V-Fib** refractory V-Tach unresponsive to Amiodarone or in Torsades de Pointes, administer **♦ 50 mg/kg slow IO/IV over 20 minutes** ♦ **Maximum 2 grams**
62
**Lidocaine** (Xylocaine) ## Footnote **(mechanism of action)**
♦ **Lidocaine's antiarrhythmic effects** result from its ability to ***inhibit the influx of sodium through the "fast" channels of the myocardial cell membrane***, ***increasing the recovery period*** after repolarization ♦ Lidocaine ***suppresses automaticity*** and ***decreases*** the effective ***refractory period*** and the ***action potential duration** **in the His-Purkinje system*** at concentrations that do not suppress automaticity at the SA node.
63
**Lidocaine** (Xylocaine) ## Footnote **(onset and duration)**
**Onset**: Immediate **Duration**: 10 to 20 minutes
64
**Lidocaine** (Xylocaine) ## Footnote **(side effects)**
Hypotension, Decreased LOC, Irritability, Muscle Twitching, Eventually Seizures
65
**Lidocaine** (Xylocaine) ## Footnote **(indications)**
Pain Management for IO insertion Cardiac Arrest
66
**Lidocaine** (Xylocaine) ## Footnote **(contraindications)**
Known sensitivity
67
**Lidocaine** (Xylocaine) ## Footnote **(adult dose)**
_**40 mg 2% for** **IO insertion**_ ⇒ **_Cardiac Arrest_** ♦ **1.5mg/kg** IV/IO ***followed*** by **0.75 mg/kg** up to **max dose of 3mg/kg** **Followed** by a _maintenance infusion of 2-4 mg/min_
68
**Lidocaine** (Xylocaine) ## Footnote **(pediatric dose)**
**0.5mg/kg** (**max dose 40 mg**) for ***_IO insertion_*** **♦ Not indicated for pediatric arrest.**
69
**Lidocaine** (Xylocaine) ## Footnote **(pregnancy safe)**
Pregnancy **Calss B** Local anesthetics are **known to cross the placenta rapidly** and, when administered for epidural, paracervical, pudendal, or caudal block anesthesia, and to cause fetal toxicity. There are, however, _no adequate and well-controlled studies in pregnant women_.
70
**Magnesium Sulfate** **(pregnancy safe)**
Pregnancy **Class D** **Positive evidence of human fetal risk** based on adverse reaction data Potential benifits may warrant use of the drug in pregnant women despite potential risks. (don't ask me, I have no idea why it is ok to give a pregnant eclamtic patient after reading this)
71
**Lidocaine (Xylocaine)** **I/O Infusion Dose** **(*adult* and pediatric dose**)
♦ 40 mg of 2% over 120 seconds prior to NS flush (***adults***) → may repeat at 20 mg ♦ 0.5 mg/kg 2% max initial dose 40 mg over 120 seconds → may repeat at half the initial dose → flush with NS 10 mL (adult) 5 mL for pediatric
72
**Nitroglycerin** **(mechanism of action)**
♦ Converts into nitric oxide in the body which in turn ***causes vasodilation*** by relaxing smooth muscle which ***decreases myocardial workload and oxygen demand*** ► Works more on veins than arteries ► Can also improve coronary collateral circulation
73
**Nitroglycerin** **(onset and duration)**
## Footnote **1 - 4 minute duration**
74
**Nitroglycerin** **(side effects)**
**Headache** **Dizziness** **Hypotension**
75
**Nitroglycerin** **(indications)**
## Footnote **Chest Pain / ACS** **CHF / Pulmonary Edema**
76
77
**Nitroglycerin** **(contraindications)**
**Increased ICP** **Hypotension/Shock** **Glaucoma** **Use of Viagra/Levitra (24 hrs)** **Cialis (36hrs)**
78
**Nitroglycerin** **(adult dose)**
Sublingual ***0.4 mg q 5 min*** **_IV Infusion_** ***5 mcg/min*** → ***increasing*** by ***5-20 mcg/min*** up to a ***max of 200 mcg/min*** ***(infusion recommended for long transports)***