Essential Pharmacology For Inpatient Care

adherence.

CARDIAC INTENSIVE CARE

Matthew C. Konerman, Sarah Hanigan, Kristen Pogue, Hitinder S. Gurm,

ANTI-PLATELET AGENTS OVERVIEW

Aspirin

Clopidogrel

Prasugrel

Ticagrelor

GP IIb/IIIa Inhibitors

INOTROPES & VASOPRESSORS OVERVIEW

Dobutamine

Milrinone

Norepinephrine

Dopamine

Phenylephrine

Vasopressin

Epinephrine

ARRHYTHMIA MANAGEMENT

Isoproterenol

Atropine

Adenosine

Esmolol

Diltiazem

Amiodarone

Lidocaine

PULMONARY HYPERTENSION MANAGEMENT OVERVIEW (FIGURE)

Endothelin Receptor Antagonists

Prostanoids

Phosphodiesterase-5 Inhibitors

Riociguat

HYPERTENSIVE EMERGENCY & VASODILATORS OVERVIEW

Nitroprusside

Nicardipine

Clevidipine

Fenoldopam

Nitroglycerin

Nesiritide

SEDATION IN THE CICU

Midazolam

Fentanyl

Propofol

GENERAL CONCEPTS

Extensive evidence, beyond the scope of this text, supports the use of Aspirin in ACS. It should be given ASAP in possible ACS.

AHA/ACC Guidelines do not favor any one P2Y12 inhibitor over another. They are all class I recommendations. Consider patient-specific factors and adverse effects in selection of agent.

12 months of dual-antiplatelet therapy (DAPT) is recommended even for conservatively managed (no PCI) ACS patients.

In patients receiving fibrinolytics, choose Clopidogrel for DAPT.

The data supporting the use of GP IIb/IIIa inhibitors in ACS was gathered prior to routine use of DAPT in ACS. Routine upstream use of GP IIb/IIIa agents pre-PCI is no longer recommended.

Aspirin (Acetylsalicylic Acid, ASA)

By irreversibly inhibiting COX-1 within platelets, Aspirin prevents the formation of thromboxane A2 which leads to diminished platelet aggregation.

Indications/Dosing: Give to all STEMI and UA/NSTEMI patients (Class I). Recommended treatment for pericarditis following STEMI (Class I). Used for CVA prophylaxis in low-risk patients with atrial fibrillation (CHADS2 ≤ 1).

Load with 162-325 mg on presentation and prior to PCI (Class I)

Continue indefinitely at a dose of 81-325 mg daily (Class I)

Preferred maintenance dose is 81 mg daily (Class IIa, see below)

Use non-enteric-coated formulations for more rapid absorption

Load and continue P2Y12 inhibitor if patient cannot tolerate Aspirin (Class I).

Kinetics

Peak concentration: 1-2 hours

*If chewed and swallowed, 1-10 minutes*

Lasts duration of platelet life (∼5 days)

Give loading dose to all suspected ACS pts

Documented mortality benefit in CAD

Maintenance dose of 81 mg is reasonable

Continue in the pre-CABG period

Adverse Effects

Bleeding

PUD/gastritis

Angioedema

Reye’s syndrome

Tinnitus

Precautions: GI symptoms, PUD, severe hepatic disease, bleeding disorders. Avoid use of other NSAIDs as may impair Aspirin effect and/or increase GI side effects

CURRENT-OASIS 7: Evaluation of Clopidogrel and ASA dosing in ACS

All patients received an ASA load followed by 75-100 mg vs. 300-325 mg daily

No difference in CV death, MI, and CVA or major bleeding at 30 days.

ISIS-2: Comparison of ASA vs. placebo in 17,187 patients with acute MI

Significant reduction in vascular death at 35 days (11.8 to 9.4%).

Clopidogrel (Plavix)

A thienopyridine that irreversibly inhibits the platelet P2Y12 ADP receptor. Clopidogrel inhibits platelet activation and aggregation both of which play a role in the pathophysiology of ACS and stent thrombosis.

Indication/Dosing: Class I indication in STEMI and UA/NSTEMI

Indicated in both invasive and conservatively managed patients

Only P2Y12 inhibitor recommended for use with fibrinolytics (Class I)

Class I: Loading dose of 600 mg PO in patients undergoing PCI

Conservatively managed patients should receive at least a 300 mg load

Class I: Maintenance dose of 75 mg PO daily

Kinetics: Requires conversion from prodrug to active metabolite via liver CYP2C19 isoenzyme. Loss of function polymorphisms associated with increased risk of adverse cardiovascular events.

Tmax = 60 minutes; t1/2 = 6 hours. Lasts duration of platelet life (∼5 days).

Avoid use with strong inhibitors of CYP2C19

Monitoring: P2Y12 assay No trial supports altering therapy based on assay. (Class IIb recommendation)

Adverse Effects

Bleeding

Stevens-Johnson’s

TTP

DAPT is essential after coronary stenting

Conservative Treatment: Up to 12 mo. DAPT

Hold for 5 days prior to elective surgery

Benefit of P2Y12 assay unclear

Interaction: Retrospective data suggests Clopidogrel is less effective in setting of PPI use though this has not been confirmed with randomized data. Omeprazole and Lansoprazole inhibit CYP2C19 decreasing response to drug.

COGENT: RCT of 3761 patients on Clopidogrel randomized to Omeprazole vs. Placebo.

Omeprazole use associated with reduced rate of upper gastrointestinal bleeding.

Omeprazole use associated with no difference in composite endpoint of CV death, nonfatal MI, CVA, and revascularization.

CURE: RCT of 12,562 patients with UA/NSTEMI

Reduction in CV death, MI, and CVA when Clopidogrel added to Aspirin.

Increased major/minor but not life-threatening bleeding with Clopidogrel

Prasugrel (Effient)

A thienopyridine that irreversibly inhibits the platelet P2Y12 ADP receptor. Prasugrel inhibits platelet activation and aggregation both of which play a role in the pathophysiology of ACS and stent thrombosis.

Indications: Class I in STEMI patients undergoing PCI. Class I in UA/NSTEMI patients undergoing PCI once coronary anatomy known.

Can give prior to angiography in patients with STEMI

Use discouraged in UA/NSTEMI patients prior to angiography

No evidence for use in medically managed UA/NSTEMI

Dosing: Loading dose of 60 mg PO once (Class I)

Maintenance dose of 10 mg PO daily (Class I)

Consider alternative drug or maintenance dose of 5 mg daily if <60 kg, age >75, or high bleeding risk

Kinetics: Prodrug that requires activation via CYP enzyme system.

Unlike Clopidogrel, genetic polymorphisms do not impact efficacy.

Tmax = 30 minutes

t1/2 = 7-8 hours

Effect lasts duration of platelet life

Monitoring: No role for platelet function testing.

No evidence of benefit without PCI.

Do not use if prior TIA/CVA, CNS bleed

No benefit if age > 75 or weight < 60 kg

Hold for 7 days prior to elective surgery

Adverse Effects: Increased bleeding vs. Clopidogrel

Contraindications

Evidence of harm if prior CVA/TIA, prior CNS bleed, or current bleeding

No evidence of benefit in patients over age 75

No evidence of benefit in patients < 60 kg

TRITON-TIMI 38: Prasugrel vs. Clopidogrel in high-risk ACS treated with PCI

Prasugrel (60 mg → 10 mg daily) vs. Clopidogrel (300 mg → 75 mg daily)

Lower rates of CV death, nonfatal MI/CVA, stent thrombosis with Prasugrel

Increased rates of major bleeding with Prasugrel compared to Clopidogrel

Net clinical benefit with Prasugrel in patients without above risk factors

TRILOGY ACS: Prasugrel vs. Clopidogrel for ACS without revascularization

No benefit of Prasugrel over Clopidogrel with similar risks of bleeding

Ticagrelor (Brilinta)

Ticagrelor is a potent, reversible antagonist of the P2Y12 ADP receptor. Ticagrelor inhibits platelet activation and aggregation both of which play a role in the pathophysiology of ACS and stent thrombosis.

Indications: Class I recommendation for use in STEMI and UA/NSTEMI

Acceptable for use if initial conservative strategy selected

Recommended maintenance Aspirin dose is 81 mg daily

Dosing

Loading dose of 180 mg PO once (Class I)

Maintenance dose of 90 mg PO twice daily (Class I)

Kinetics: Does not require activation via CYP enzyme system.

Tmax = 1.5-2 hours

t1/2 = 7 hours

Monitoring: No role for platelet function testing.

Consider patient compliance (BID dosing!)

Maintenance Aspirin dose of 81 mg daily

Hold for 5 days prior to elective surgery

Associated with all-cause mortality benefit

Adverse Effects

Bleeding

Ventricular pauses

Dyspnea

Elevated uric acid

Contraindications

FDA cautions against use in patients with active bleeding

FDA cautions against use if history of intracranial bleeding

Avoid use with concomitant use of strong CYP3A inducers/inhibitors.

Avoid doses of greater than 40 mg of Simvastatin or Lovastatin.

PLATO: Ticagrelor vs. Clopidogrel in patient with STEMI and UA/NSTEMI

Over 60% of patients underwent PCI. Followup of 12 months.

Reduction in vascular death, MI, CVA, stent thrombosis with Ticagrelor

Benefit in both invasive and medically-managed patients

No benefit observed in North America (attributed to high Aspirin dosing)

Reduction in death from any cause observed with Ticagrelor.

No difference in rate of major, fatal, or life-threatening bleeding

Increased non-CABG and fatal intracranial bleeding with Ticagrelor

GP IIb/IIIa Inhibitors

These agents bind to GP IIb/IIIa receptors, preventing binding of fibrinogen, vWF, and other adhesion molecules. Inhibition of platelet aggregation results.

Abciximab: Chimeric human-murine monoclonal antibody Fab

Noncompetitive, irreversible inhibitor of GP IIb/IIIa receptors

Eptifibatide/Tirofiban: Low molecular weight competitive, reversible antagonists.

Indications: ACS (most benefit in high-risk patients with positive biomarkers)

To support PCI in patients not receiving P2Y12 inhibition (Class I)

Chest pain refractory to therapy with ASA, P2Y12 inhibitor, UFH (Class IIa)

Eptifibatide and Tirofiban preferred in this setting

Limited role for upstream use in patients chest pain free with low bleeding risk (Class IIb)

Abciximab should not be used if PCI is not planned (Class III)

Dosing/Kinetics: Should be given with UFH. Infusion duration 12-18 hours.

Eptifibatide (Integrilin): 180 mcg/kg IV bolus, then 2 mcg/kg/min, then a second 180 mcg/kg bolus is given 10 minutes after the first bolus. Half-life = 2.5 hours.

Renal clearance. ↓ infusion by 50% if CrCl < 50 mL/min. Avoid in dialysis pts.

Reversal: Discontinuing drug leads to marked diminution of effect in 2-4 hours.

Tirofiban (Aggrastat): 25 mcg/kg IV bolus then 0.15 mcg/kg/min

Renal Clearance (half-life 2 hrs.). ↓ infusion by 50% if CrCl < 30 mL/min

Reversal: Discontinuing drug leads to marked diminution of effect in 2-4 hours.

Abciximab (ReoPro): 0.25 mg/kg IV then 0125 mcg/kg/min (max 10 mcg/min)

>80% of platelets at two hours. Long infusion half-life of approximately 12 hours.

Reversal: Platelet transfusions

Adverse Effects

Bleeding, intracranial hemorrhage. Alveolar hemorrhage is a rare complication of Abciximab.

Thrombocytopenia (esp. Abciximab). Can occur within hours of starting therapy.

Hypotension

Contraindications

Increased bleeding risk

Recent CVA, prior hemorrhagic CVA

Intracranial malformation/aneurysm

Severe hypertension

Dialysis (Abciximab can be used)

Recent surgery

Thrombocytopenia

Benefit in PCI patients yet to receive P2Y12 inhibition

Limited role for upstream use in ACS

Dose adjustment required in renal disease

EARLY ACS: Compared early vs. delayed (at PCI) Eptifibatide in UA/NSTEMI

Early Eptifibatide did not improve rates of death, MI, recurrent ischemia

No benefit even in absence of Clopidogrel (25% of study population)

Higher rates of non-life-threatening bleeding and transfusion with early use.

INOTROPES AND VASOPRESSORS

α1: vascular smooth muscle contraction → vasoconstriction

β1: inotropy, chronotropy → increased contractility and heart rate

β2: vascular smooth muscle relaxation → vasodilatation

DA: vasodilatation of the renal, splanchnic, and coronary vasculature

GENERAL CONCEPTS

Through their effects on inotropy, afterload, and chronotropy, inotropes and vasopressors increase cardiac demand, potentiate ischemia, and may even have direct toxic effects on myocytes. Therefore, use the lowest necessary dose of these agents!

These agents commonly trigger arrhythmias. Monitor closely.

Randomized data supporting the use of one inotrope or vasopressor over another is lacking. Agents are typically selected based on the patient’s hemodynamic profile, underlying comorbidities, and potential for adverse effects with particular agents.

Recent data support use of nor-epinephrine over Dopamine as the first line agent for shock.

Dobutamine (Dobutrex)

Dobutamine is a synthetic catecholamine that activates beta receptors.

β1 Stimulation: Potent ↑ inotropy with weaker ↑ chronotropy.

β2 Stimulation: Mild systemic vasodilatation (↓ SVR) at lower doses

Increased vasoconstriction (↑ SVR) at higher infusion rates (α1 matches β2 stimulation).

Indications: Decompensated HF, Cardiogenic Shock, Symptomatic Bradycardia

ACC/AHA 2004 Guidelines: First-line if low output, no shock, SBP 70-100

Preferred inotrope in setting of hypotension (less ↓ in SVR vs. Milrinone)

Preferred inotrope in the setting of renal insufficiency

Preferred agent in the setting of acute RV infarction

Dosing: 2.5 – 20 mcg/kg/min. Can titrate every 5 minutes by 2.5 mcg/kg/min

Half-Life: 2 minutes

Adverse Effects

Tachycardia

Ventricular arrhythmia

Cardiac ischemia

Tachyphylaxis

Nausea, vomiting

Headache

First-line agent for RV infarction

Monitor for arrhythmias!

Agent utilized in stress-testing.

Option for palliation in end-stage HF

Randomized data associate inotropic agent use with ↑ mortality.

PROMISE: Increased mortality with oral Milrinone

FIRST: Increased mortality with Dobutamine

These findings have been corroborated in registry studies where use of inotropes has been associated with increased mortality.

Milrinone (Primacor)

Milrinone exerts its effect via inhibition of phosphodiesterase III within cardiac myocytes. Increased levels of cAMP result leading to increased cardiac contractility. In addition to potent inotropy, this agent decreases afterload via systemic vasodilatation. It also decreases preload via improved lusitropy.

The net effect is increased contractility, decreased afterload, and preload. Milrinone also has a vasodilatory effect on the pulmonary vasculature.

Indications: Decompensated Heart Failure

Beneficial in end-stage HF as β-adrenergic receptor response is often blunted

More potent ↓SVR compared to Dobutamine (use caution if borderline BP)

Greater effect on lowering filling pressures than Dobutamine

Provides RV afterload reduction → consider in RV failure

Dosing: 0.125 – 0.50 mcg/kg/min (dose-adjust for renal impairment!). Maximum dose 0.75 mcg/kg/min

Loading dose of 50 mcg/kg can be given if immediate inotropy needed

Maintains effect despite concurrent beta-blockade

Kinetics

Renal clearance

t1/2 = 3 hours

Dose carefully in renal insufficiency

Monitor BP closely (↓↓ SVR)

Option for palliation in end-stage HF

Provides RV and LV afterload reduction

Adverse Effects

Ventricular arrhythmia

Cardiac ischemia

Hypotension

PROMISE: Milrinone PO in 1,088 HF with reduced EF patients (NYHA III/IV)

Increased all-cause (28%), CV (34%) mortality with Milrinone (6 mo. FU)

Milrinone associated with ↑ hospitalizations, hypotension, syncope

OPTIME-CHF: No role in ADHF with preserved end-organ perfusion

Randomized to 48-hr Milrinone vs. Placebo. Followup of 60 days.

No difference in length of hospitalization or mortality with Milrinone.

Increased rates of atrial arrhythmias and hypotension with Milrinone

Norepinephrine (Levophed)

Norepinephrine is an endogenous neurotransmitter with potent α1-adrenergic activity along with moderate β-receptor activity.

Results in ↑ SBP/DBP/PP with less net impact on CO and HR.

Indications: Vasodilatory Shock, Cardiogenic Shock

ACC/AHA 2004 Guidelines: First-line for cardiogenic shock if SBP < 70

Dosing: Start at 0.1 mcg/kg/min. Titrate by 0.01 - 0.05 mcg/kg/min every 5 minutes.

Maximum dose 1 mcg/kg/minute

Kinetics

Onset: 1-2 minutes

t1/2 = 2 minutes

First-line agent for cardiogenic shock if SBP < 70

First-line agent for septic shock

Delivery via central access preferred

May be less arrhythmogenic than Dopamine

Monitoring: Consider arterial line for BP monitoring

Adverse Effects

Arrhythmias

Tissue necrosis (limit with central line delivery)

Increased doses cause more α1 stimulation and may decrease renal perfusion.

Precautions: Concomitant use with TCA, SSRI, and MAO inhibitors may increase the alpha-adrenergic effects of the drug.

De Backer NEJM Norepinephrine vs. Dopamine in shock

RCT including 1679 patients requiring initiation of vasopressor for shock

No difference in primary outcome of death at 28 days

Significant increase in rates of arrhythmia with Dopamine

Cardiogenic shock subgroup → increased mortality with Dopamine

Dopamine (Intropin)

Dopamine, the precursor to norepinephrine in catecholamine synthesis, exerts dose-dependent effects on both dopaminergic and adrenergic receptors. It also causes release of norepinephrine at nerve terminals.

Indications: Cardiogenic/Septic Shock, Symptomatic Bradycardia, Diuresis

ACC/AHA 2004 Guidelines: First-line for cardiogenic shock if SBP 70-100

ACC/AHA 2013 HF Guidelines: Class IIb to facilitate diuresis.

Dosing: Start at 2 – 5 mcg/kg/min. Titrate by 1 – 5 mcg/kg/min every 5 min. Maximum 20 mcg/kg/min.

Half-Life: 2 minutes

Monitoring: Consider arterial line for BP monitoring

Adverse Effects

Tachycardia

Ventricular arrhythmia

Tissue necrosis

Cardiac ischemia

Nausea, vomiting

Recognize dose-dependent effects

Temporizing measure for bradycardia

Monitor for arrhythmias!

Low-dose may facilitate diuresis in HF

Havel Cochrane Review (2011): Vasopressors for hypotensive shock

Review of 23 RCTs evaluating vasopressors in shock

No evidence to prove one vasopressor is superior in regards to mortality.

Dopamine appears to increase the risk of arrhythmia

Phenylephrine (Neo-Synephrine)

Phenylephrine is a synthetic agent that activates α1-receptors without any stimulation of beta receptors.

Indications: Hypotension (medication-induced, vagally-mediated), shock

Consider for treatment of hypotension with concomitant severe AS

Consider for pressor support in setting of tachyarrhythmias.

Theoretical benefit in pulmonary hypertension – increased afterload can facilitate LV filling against high RV pressures.

Reduces LVOT gradient in obstructive hypertrophic cardiomyopathy

Dosing

Bolus: 50 – 200 mcg bolus

Infusion: 50 – 300 mcg/min

Titration: 20 mcg/min every 5 min.

Use as bolus for rapid BP improvement

Consider in pulmonary hypertension, AS

Monitor for peripheral ischemia!

Provides ↑ afterload without ↑ inotropy

Reflex bradycardia can lower CO

Half-Life: 2-3 hours

Duration of Action: 15-20 min.

Monitoring: Consider arterial line for BP monitoring

Adverse Effects: Phenylephrine may cause reflex bradycardia which may decrease cardiac output as it has no inotropic effect. Phenylephrine also may cause narrowing of the pulse pressure. It is also associated with tissue necrosis.

Vasopressin (Pitressin)

Vasopressin is an endogenous hormone stored primarily in the posterior pituitary gland. At greater than physiologic doses, it exerts circulatory effects.

V1A Stimulation: Constriction of vascular smooth muscle (↑ SVR)

V2 Stimulation: Increases water reabsorption at renal collecting ducts.

Indications: Shock, Cardiac Arrest

Increases vascular sensitivity to Norepinephrine (enhances pressor effect)

ACLS: Can replace first or second dose of Epinephrine (give IV/IO).

Dosing

Bolus: 40 units IV

Infusion: Fixed at 0.04 units/min

Can be given via endotracheal tube

ACLS agent for cardiac arrest

Do NOT titrate this vasopressor infusion

Potentiates the effect of Norepinephrine

Remains effective in acidosis and hypoxia

Catecholamine-sparing pressor support

Half-Life: 10-20 minutes

Adverse Effects:

Arrhythmias

Cardiac/peripheral ischemia

Tissue necrosis.

Jolly Am J Cardiology (2005): Vasopressin in cardiogenic shock

Retrospective study of 36 patients with cardiogenic shock post-MI

Vasopressin ↑ MAP without affecting PCWP, CI, UOP, or inotrope needs

VASST: Vasopressin vs. Norepinephrine in Septic Shock

Included 778 pts with septic shock. Primary endpoint 28-day mortality.

Vasopressin (max 0.03 U/min) vs. Norepinephrine (max 15 μg/min)

Patients received other open-label vasopressors to maintain goal MAP.

No significant difference in mortality rate between the two groups.

Epinephrine

Epinephrine is an endogenous neurotransmitter with activity at β1, β2, and α1-receptors. At lower doses, beta receptors are mostly affected; as dose increases, activity at the α1 receptor dominates leading to peripheral vasoconstriction. B2 activity relaxes smooth muscle of the bronchi.

Indications:

Utilized in ACLS protocols for cardiac arrest

Can administer for hypotension and shock

Bradycardia unresponsive to atropine

Anaphylactic reactions and severe bronchospasm

Dosing

Bolus (ACLS): 1 mg IV or intraosseously every 3-5 minutes

IM Injection (Anaphylaxis): 0.1 – 0.5 mg (max 1 mg)

Infusion (Shock): Start at 0.1 mcg/kg/min. Titrate by 0.01 - 0.05 mcg/kg/min every 5 minutes.

Maximum dose 1 mcg/kg/minute

May be administered via an endotracheal tube (2 – 2.5 mg).

Half-Life: 2 minutes Monitoring: Arterial Line.

Adverse Effects

Arrhythmias

Cardiac ischemia

Splanchnic vasoconstriction

Tissue necrosis

ACLS agent for cardiac arrest, bradycardia

Most potent alpha-receptor activator

Preferred agent in Anaphylaxis

Precautions: Concomitant use with TCA, SSRI, and MAO inhibitors may increase the alpha-adrenergic effects of the drug.

Lin Circulation (1995): Effect of Epinephrine on coronary thrombosis

In canine models, epinephrine use associated with increased coronary thrombosis; norepinephrine inhibited coronary thrombosis.

Isoproterenol (Isuprel)

Isoproterenol is a synthetic, potent agonist of β1 and β2 receptors. This agent has significant chronotropic and inotropic activity. β2 stimulation results in systemic and pulmonary vasodilatation that can lead to hypotension. It can increase pulse pressure due to reductions in diastolic blood pressure.

Indications: Bradyarrhythmias, AV Block, refractory torsades de pointes

Temporizing agent while awaiting pacing for bradyarrhythmias, heart block

Class IIa: Temporary treatment in patients with recurrent pause-depended torsades de pointes who do not have congenital Long QT syndrome.

Class IIa: Treatment of torsades de pointes due to QT prolonging agents

Class IIa: Treatment of VT storm in the Brugada syndrome

Dosing: 0.5 – 10 mcg/min

Kinetics

Onset: Immediate.

t1/2 = 2.5 – 5 min.

Temporizing measure for bradycardia

Consider in recurrent torsades de pointes

Hypotension is a potential adverse effect

Adverse Effects

Arrhythmias

Palpitations

Cardiac ischemia

Hypotension.

Atropine

Atropine is a competitive antagonist of acetylcholine at muscarinic receptors. Acetylcholine is the main neurotransmitter of the parasympathetic nervous system. Atropine blocks vagal stimulation of the heart; this results in increased firing of the SA and increased AV node conduction (increased HR).

Indications

Class IIa: Acute, symptomatic bradycardia including symptomatic sinus bradycardia, conduction block at the AV node, and sinus arrest.

Less effective if location of heart block is below the AV node (Mobitz II second-degree block, third-degree AV block, wide QRS).

Serves as a temporizing measure while preparing for pacing

Dosing: Give 0.5 mg IV every 3-5 minutes (maximum dose 3 mg)

Can be administered via endotracheal tube.

Kinetics

Onset: Rapid.

t1/2 = 2-3 hours

Adverse Effects

Dysrhythmia

Tachyarrhythmia

Constipation

Dry mouth

Flushing

Blurred vision (dilated pupils)

Disorientation

*Antidote: Physostigmine*

ACLS agent for bradycardia with a pulse

No longer in PEA/Asystole ACLS algorithm

Less effective if block below AV node

Precautions

Atropine can exacerbate cardiac ischemia in ACS