Cardiac Medications

Margaret Glembocki RN, MSN, ACNP-CSC

Acute Care Nurse Practitioner

Objectives

To define drug classes specific to cardiovascular system

To be able to verbalize safe administration of cardiac medications.

To be able to verbalize safe titration of cardiac medications

To identify potential outcomes and side effects of cardiac medication

It is our duty and responsibility as nursing professionals to ensure health care quality and patient safety. According to The Institute of Medicine, “Medical errors cause as many as 98,000 deaths at costs up to $29 billion a year in hospitals alone.” Alarming isn’t it?

5 Rights of Medication Administration

Right Patient Right Route Right Dose Right Time Right Medication

How do Inotropic Drugs work??

Alters the force or strength of the heart’s muscular contractions.

2 types: Negative and PositiveNegative Inotropic drugs make the heart beat

less stronglyPositive Inotropic drugs make the heart beat

more strongly

Calcium Channel Blockers (-)

Decrease the force of contraction of the myocardium.

Slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart.

This results in a negative chronotropic effect resulting in a lowering of the heart rate and the potential for heart block.

Thinkers…..

It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with __________________.

The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with _____________________ in whom control of the heart rate is an issue.

Beta receptors…..

Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart & increases cardiac conduction velocity and automaticity.

Stimulation of β1 receptors on the kidney causes renin release.

Stimulation of β2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle.

Stimulation of β3 receptors induces lipolysis.

What Beta-blockers do…

Beta blockers inhibit these normal epinephrine-mediated sympathetic actions. Reduce the effect of excitement/physical exertion on

heart rate & force of contraction Dilation of blood vessels Opening of bronchi Reduce tremor Reduce breakdown of glycogen

Renin-Angiotensin-Aldosterone System (RAAS) This system is activated in response to hypotension,

decreased sodium concentration in the distal tubule, decreased blood volume and renal sympathetic nerve stimulation.

In such a situation, the kidneys release renin which cleaves the liver-derived angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II via the ACE in the pulmonary circulation as well as in the endothelium of blood vessels in many parts of the body.

The system in general aims to increase blood pressure

Angiotensin-Converting Enzyme Inhibitors(ACE inhibitors)

Lower arteriolar resistance and increase venous capacity; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis (excretion of sodium in the urine).

Indications for ACE inhibitors include: CHF, HTN, LV dysfunction, prevention of nephropathy in DM

Captopril, Norvasc, Lotensin

Case Study

52 y/o female with history of HTN, EF= 50% and diet controlled DM presented to the ED with fatigue. Admitted for observation and stress test the following day. Home meds: Lisinopril and MVI.

Now c/o nausea and diaphoretic. 12- lead EKG ST inversion in Lateral leads…Call the doctor & get ready for________.

What should we prepare for?

Cath lab bound….. Blood work pending Consent Oxygen Morphine Anti-Platelets: Aspirin (COX inhibitor) and

Plavix (ADP)

Heparin

Anticoagulation action by accelerating the activity of antithrombin III to inactive thrombin. Does NOT lyse existing clots.

Measures: aPTT goal 1.5-2 times control (50-70)

25,000 units in 250mL of D5W. Concentration: 100units/mL. Dosing: units/hour

Integrilin (Eptifibatide)

Inhibits platelet aggregation, with specificity for the platelet receptor GP IIb-IIIa. Initial onset of inhibition of platelet aggregation was observed within 15 minutes after the IV bolus.

Reversible: platelet function was restored toward baseline (<50% inhibition) within 4 hours of discontinuation of infusion. Primarily renally excreted

Indications: MI, PCI, USA Dose:

180mcg/kg bolus (max 22.6mg) 2mcg/kg/min

CrCL <50: reduce maintenance to 1mcg/kg/min

Intergrelin Adverse Reactions

Anaphylactic shock Bleeding GI bleed Hematuria Hypotension IC bleed

Platelet dysfunction Stroke Thrombocytopenia

Nitroglycerin

Correct myocardial oxygen imbalances by reducing systemic & pulmonary artery pressure (afterload) and decreasing CO secondary to peripheral dilation rather than coronary artery dilatation

Decreased venous return, which decreases preload

Dose: 50mg in 250mL D5W (glass bottle) Infusion rate 5-200 mcg/mim

Nitroglycerin Adverse Reactions

Diaphoresis Flushing Headache Hypotension Nausea/Vomiting Orthostatic

hypotension

Palpitations Rash Sinus Tachycardia Syncope Tolerance Weakness

Metoprolol (Lopressor)

Beta 1-receptor: decrease in heart rate, decrease in both systolic and diastolic blood pressure (chron). Decreased CO (-)

Indications: MI, angina, atrial fibrillation and flutter, HF, HTN

Dose: 25-100mg po twice daily2.5-5mg IV

Metoprolol Adverse Reactions

AV block Blurred vision Bradycardia Constipation Hypotension Impotence Insomnia

Jaundice Peripheral edema Jaundice Depression Dyspnea Headache

Dopamine

Mechanism of Action: Stimulates both adrenergic & dopaminergic receptors. Lower doses: mainly dopaminergic stimulating && produce renal and

mesenteric vasodilation. Higher doses: both dopaminergic and beta1-adrenergic stimulating and

produce cardiac stimulation and renal vasodilation. Large doses: stimulate alpha-adrenergic receptors

Indications: Bradycardia, Cardiac arrest, Cardiogenic shock, CPR, HF, HypoTN, Septic shock

400mg in 250mL D5W Dose: 1-50mcg/kg/min

0.5-2mcg/kg/min: Vasodilatation 2-10mcg/kg/min: Increased HR, CO, BP >10mcg/kg/min: PVR, renal vasoconstriction

Dopamine – Hemodynamic effects

Low-dose: 1-3 mcg/kg/minute, increased renal blood flow and urine output

Intermediate-dose: 3-10 mcg/kg/minute, increased renal blood flow, heart rate, cardiac contractility, and cardiac output

High-dose: >10 mcg/kg/minute, alpha-adrenergic effects begin to predominate, vasoconstriction, increased blood pressure

Dopamine Adverse Reactions

Angina Anxiety Arrhythmia Bradycardia Dyspnea Hypertension Hypotension

Palpitations Nausea/Vomiting Sinus Tachycardia V- tach V-fib

Dobutamine

Stimulates beta1-adrenergic receptors, causing increased contractility and heart rate, with little effect on beta2- or alpha-receptors

Indications: Cardiac surgery, Cardiogenic shock, HF

Dose: 250mg in 250mL D5W (1:1)0.5-40mcg/kg/min

Dobutamine Adverse Reactions

Angina Arrhythmia Fatigue Headache HTN Hypokalemia Nausea/vomiting

Palpitations Phlebitis Skin necrosis Sinus tachycardia Ventricular

tachycardia

Primacor (Milrinone)

Bipyride inotropic/vasodilator agent. (+) Increases Myocardial contractibility, decreases preload and afterload by direct dilating effect on vascular smooth muscles (smooth muscle relax).

Indications: Heart Failure Dose: 20mg in 100mL D5W (0.2mg/ml)

Loading: 50mcg/kg over 10 mins Maintenance: 0.2-0.75mcg/kg/min

Primacor Adverse Reactions

Angina Atrial fibrillation/flutter Atrial tachycardia Headache Hypotension Palpitations

PVCs Syncope Thrombocytopenia

Amiodarone

Antiarrhythmic with predominant class III effects of lengthening cardiac action potential and blocking myocardial potassium channels leading to slowed conduction and prolonged refractoriness.”

Slows SR, increases PR & QT intervals, decreases PVR. Peripheral line ok to use.

Indications: A-fib/flutter, V-tach/fib, Cardiac arrest, PSVT, WPW

Dose: 450mg in 250 D5W Load: 150mg IVBP over 10 mins Maintenance: 1mg/min x 6 hrs, then 0.5mg/min x 18hrs

Amiodarone Adverse Reaction

Bradycardia Heartblock Hypotension Tremors Headaches Abnormal LFTs

Visual disturbances Optic neuritis Neuropathy Blue discoloration of

the skin Pulmonary fibrosis

Diltiazem Calcium channel blocker that blocks calcium ion

influx during depolarization of cardiac and vascular smooth muscle.

Decreases PVR and causes relaxation of the vascular smooth muscle resulting in a decrease of both systolic and diastolic blood pressure

Indications: A-fib, HTN, angina, Dose: 125mg in 125 D5W (1:1)

Load: 0.25mg/kg over 2mins repeat: 0.35mg/kg

Maintenance: 5-15mg/hr

Diltiazem Adverse Reaction

Hypotension Flushing Peripheral edema Heart failure Bradycardia

May see pronounced bradycardia if given concurrently with digoxin or beta-blockers.

Digoxin

Inhibits Na-K ATPase membrane pump. Indications: Atrial fibrillation/flutter, HF,

PSVT Dose: 10-15mcg/kg IV or PO in 3 divided

doses q6-8 hrs with first dose = ½, then po q6 x2 (ie: 500mcg x1, then 250mcg q6 x2. Then 125-350mcg per day

Digoxin Adverse Reaction

Hypokalemia Nausea/vomiting SJS PVCs Syncope Psychosis Bradycardia

AV block Fatigue Depression Headache Sinus tachycardia Weakness