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 isnt 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 hearts
muscular contractions.
2 types: Negative and Positive

Negative

Inotropic drugs make the heart beat

less strongly
Positive 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 1 receptors by epinephrine induces a

positive chronotropic and inotropic effect on the heart &
increases cardiac conduction velocity and automaticity.
Stimulation of 1 receptors on the kidney causes renin
release.
Stimulation of 2 receptors induces smooth muscle
relaxation, induces tremor in skeletal muscle, and
increases glycogenolysis in the liver and skeletal muscle.
Stimulation of 3 receptors induces lipolysis.

What Beta-blockers do

Beta blockers inhibit these normal epinephrinemediated 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 leadsCall
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 daily
2.5-5mg 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, alphaadrenergic 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 alphareceptors
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 betablockers.

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 = , 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