Introduction to CV Pharmacology - Orlando Health

Introduction 

to 

CV Pharmacology 

* See SWIFT for list of qualifying boards for continuing education hours


Table of Contents 

INTRODUCTION .......................................................................................................................................................3 

A NOTE ABOUT ACLS...............................................................................................................................................4 

AUTONOMIC CARDIOVASCULAR INNERVATION.........................................................................................5 

PROPERTIES OF CARDIAC CELLS................................................................................................................................5 

THE ADRENERGIC RECEPTOR SYSTEM ......................................................................................................................6 

CHECK YOURSELF POP QUIZ..............................................................................................................................7 

CHECK YOURSELF POP QUIZ - ANSWERS ..................................................................................................................8 

OXYGEN......................................................................................................................................................................9 

REVIEW OF ANTIDYSRHYTHMICS ..................................................................................................................10 

ECG MEASUREMENT: THE QTI AND QTC..............................................................................................................12 

CLASS I ANTIDYSRHYTHMICS..........................................................................................................................16 

CLASS IA .................................................................................................................................................................16 

ANTIDYSRHYTHMICS: SUBCLASS IB........................................................................................................................17 

ANTIDYSRHYHMICS: SUBCLASS IC .........................................................................................................................17 

ANTIDYSRHYTHMICS: CLASS II......................................................................................................................18 

ANTIDYSRHYTHMICS: CLASS III ....................................................................................................................19 

ANTIDYSRHYTHMICS: CLASS IV.....................................................................................................................21 

MISCELLANEOUS ANTIDYSRHYTHMICS ......................................................................................................23 

ADENOSINE (ADENOCARD)......................................................................................................................................23 

MAGNESIUM............................................................................................................................................................23 

CHECK YOURSELF POP QUIZ............................................................................................................................24 

CHECK YOURSELF POP QUIZ -ANSWERS .................................................................................................................25 

ANTIHYPERTENSIVES..........................................................................................................................................26 

ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS .......................................................................................26 

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS)......................................................................................................26 

BETA-ADRENERGIC BLOCKERS ...............................................................................................................................28 

FENOLDOPAM (CORLOPAM) ....................................................................................................................................28 

SODIUM NITROPRUSSIDE (NIPRIDE, NITROPRESS) ...................................................................................................29 

VASODILATORS .....................................................................................................................................................30 

NITROGLYCERIN......................................................................................................................................................30 

ISOSORBIDE .............................................................................................................................................................30 

HYDRALAZINE.........................................................................................................................................................31 

NESIRITIDE (NATRECOR) .........................................................................................................................................31 

MORPHINE SULFATE ...........................................................................................................................................32 

ATROPINE................................................................................................................................................................32 

CALCIUM SALTS....................................................................................................................................................32 



VASOPRESSOR THERAPY ...................................................................................................................................35 

DOPAMINE...............................................................................................................................................................35 

2010 Orlando Health, Education & Development 1


EPINEPHRINE ...........................................................................................................................................................36 

NOREPINEPHRINE ....................................................................................................................................................37 

PHENYLEPHRINE......................................................................................................................................................38 

VASOPRESSIN ..........................................................................................................................................................38 

POSITIVE INOTROPIC THERAPY......................................................................................................................39 

DIGOXIN ..................................................................................................................................................................39 

DOBUTAMINE ..........................................................................................................................................................39 

PHOSPHODIESTERASE (PDE) INHIBITORS ................................................................................................................40 

ISOPROTERENOL ..................................................................................................................................................41 

SODIUM BICARBONATE ......................................................................................................................................41 



FIBRINOLYTIC AGENTS ......................................................................................................................................44 

PLATELET INHIBITORS.......................................................................................................................................46 

IIB/IIIA GP PLATELET INHIBITORS ..........................................................................................................................46 

PLATELET AGGREGATION INHIBITORS.....................................................................................................................46 

DIRECT THROMBIN INHIBITORS.....................................................................................................................48 

ANGIOMAX ® (BIVALIRUDIN)....................................................................................................................................48 

REFLUDAN (LEPIRUDIN)...........................................................................................................................................48 

ARGATROBAN..........................................................................................................................................................49 



DIURETIC AGENTS................................................................................................................................................53 

LOOP DIURETICS .....................................................................................................................................................53 

THIAZIDE DIURETICS...............................................................................................................................................54 

POTASSIUM-SPARING DIURETICS ............................................................................................................................54 

ALDOSTERONE ANTAGONISTS.........................................................................................................................55 



SUMMARY................................................................................................................................................................58 

CARDIOVASCULAR PHARMACOLOGY POST TEST....................................................................................59 

REFERENCES ..........................................................................................................................................................66 

DRUG INFORMATION RESOURCES............................................................................................................................66 

© 2010 Orlando Health, Education & Development 2


Purpose 

The purpose of the Introduction to Cardiovascular Pharmacology Self-Learning Packet is to 

present an overview of some of the more commonly used cardiovascular drugs, broken down by 

classification, and to provide basic guidelines for safe administration by licensed healthcare 

providers. 

Objectives 

Upon completion of this self-learning packet, the participant should be able to: 

1. Describe the normal physiological actions of the cardiovascular system. 

2. Explain how cardiovascular drugs influence the cardiovascular system. 

3. Describe the role oxygen has in the cardiovascular patient. 

4. List the clinical indications for using cardiovascular pharmaceutical agents. 

5. Identify the mechanisms of action for each drug or class of drug. 

6. Describe side effects and appropriate precautions, contraindications, or special considerations 

of each drug class. 

7. State the appropriate patient teaching information. 

Instructions 

In order to receive 4.0 contact hours, you must: 

complete the posttest at the end of this packet 

achieve an 84% on the posttest 

For Non-Orlando Health employees: Complete the test using the bubble sheet provided. Be 

sure to complete all the information at the top of the answer sheet. You will be notified if you do 

not pass, and you will be asked to retake the posttest. 

Return to: Orlando Health, Education & Development, MP14, 1414 Kuhl Ave, Orlando, FL 

32806 

For Orlando Health Team Members: Please complete testing via Online Testing Center. 

Log on to: SWIFT Departments E-Learning Testing Center. Use your Orlando Health 

Network Login and password. Select “SLP” under type of test; choose correct SLP Title. Payroll 

authorization is required to download test. 


This self-learning packet (SLP) is designed to introduce basic information regarding some of the 

most commonly administered cardiovascular drugs. It is important to understand that although 

these drugs affect the cardiovascular system their use is not exclusive to cardiac departments. 

This Introduction to CV Pharmacology SLP is not designed to be an all-inclusive reference or to 



replace current drug references. Please refer to current comprehensive reference materials readily 

available for all healthcare providers such as LexiComp, Micromedex, and the PDR. This SLP 

does not indorse any specific product, however, the web based links and reference materials 

listed may be very helpful to you. Go to SWIFT for links to LexiComp and Micromedex, and 

check in your work area or the medical library regarding availability of the other information 

sources found in the References section of this SLP. 

The vast majority of patients who receive care for cardiovascular disorders require the 

administration of multiple drugs during their hospital stay. In order to achieve the best patient 

outcomes, it is vital that the healthcare provider understand the indications, actions and 

interactions, proper administration, and potential adverse effects of these pharmacologic agents. 

Please note that in current practice the terms arrhythmia and dysrhythmia are synonymous, 

meaning they are used interchangeably to indicate rhythms other than normal sinus rhythms. 

A Note about ACLS 

This SLP is not designed to include current ACLS algorithms. Please refer to current ACLS 

references for these guidelines. 



Autonomic Cardiovascular Innervation 

In order to have a better understanding of how cardiovascular drugs work, a brief review of how 

the heart and circulation are regulated by the autonomic nervous system is needed. The 

autonomic nervous system is composed of two branches; the sympathetic nervous system (SNS) 

and the parasympathetic nervous system (PNS). The SNS and the PNS normally work together 

to help maintain homeostasis in the body, including the cardiovascular system. 

The fibers of the sympathetic nervous system affect the organs and tissues in which they are 

located in by releasing norepinephrine (noradrenalin). These fibers are known as adrenergic 

fibers in reference to their relationship to norepinephrine. 

Some drugs are known as sympathomimetics because they mime or mimic the actions of the 

sympathetic nervous system. These drugs may also be known as adrenergic agents because they 

have the effects that stimulate the adrenergic fibers. 

The sympathetic nervous system innervates all chambers of the heart. Sympathetic stimulation 

(the “fight or flight” response) results in peripheral vasoconstriction, an increase in heart rate, 

faster speed of electrical impulses conducted through the heart (conductivity), and an increase in 

the strength with which the heart pumps blood (contractility). 

While fibers of the parasympathetic nervous system do exist in both the atria and the ventricles, 

they have a pronounced effect on the atria, while causing a minimal effect on the ventricles. The 

fibers of the parasympathetic nervous system affect the organs and tissues that they innervate by 

releasing acetylcholine. These fibers are known as cholinergic fibers in reference to their 

relationship to acetylcholine. Parasympathetic stimulation results in a decrease in heart rate, a 

slowing of electrical conduction through the AV node, and a mild decrease in the pumping action 

of the ventricles. 

Properties of Cardiac Cells 

Automaticity is the ability of the cardiac pacemaker cells to spontaneously initiate an electrical 

impulse without being stimulated from another source such as a nerve. 

Excitability is the ability of the cardiac cells to respond to an external stimulus, such as from a 

chemical, mechanical, or electrical source. 

Conductivity is the ability of the cardiac cell to receive an electrical stimulus and conduct the 

impulse to another cardiac cell. The conduction can be altered by factors such as sympathetic or 

parasympathetic stimulation, cardiac muscle damage, electrolyte imbalances and medications. 

Contractility is the ability of the cardiac cell to contract in response to an electrical stimulus. 



The Adrenergic Receptor System 

Adrenergic receptors are sites located within cell membranes that are sensitive to the 

catecholamines, epinephrine and norepinephrine, as well as other sympathomimetic agents. 

When an adrenergic agent reaches the adrenergic receptor site, it selectively changes the 

permeability of the cell to various ions, thus causing the cell to react. This reaction is known as a 

sympathetic response, since it is caused by the sympathetic nervous system, or a drug that 

mimics it (sympathomimetic). 

Adrenergic receptors are known by different names depending on where they are located, what 

their primary action is, and which agents they respond to. Drugs that stimulate adrenergic 

receptors are known as adrenergic agonists, while drugs that block the effect of adrenergic 

stimulation are known as adrenergic antagonists. 

Alpha (α) 

Alpha (α) receptors are most abundant in the peripheral arteries and veins, although some α- 

receptors are located in the coronary arteries. Stimulation of α-receptors results in a 

vasoconstrictive response which increases blood pressure and afterload (the force the ventricles 

must push against to pump blood into the aorta and pulmonary vasculature). 

Beta (β) 

Beta (β) receptors are divided into cardiac (β 1 ) and non-cardiac (β 2 ) receptors. The β 1 receptors 

are located within the heart. Stimulation of the β 1 receptors are responsible for the cardiac 

effects caused by the sympathetic nervous system, such as increased heart rate, increased 

conductivity, and increased strength of myocardial contraction. Stimulation of the β 2 receptors 

results in dilation of the peripheral arteries and dilation of the bronchial system in the lungs. 

Dopaminergic 

Dopaminergic receptors are located within the blood vessels of the kidneys, intestines, heart, and 

brain. Stimulation of the dopaminergic receptors has a vasodilatory effect in these blood vessels, 

increasing blood flow to those organs. 



Check Yourself Pop Quiz 

Match the definitions at the bottom with the terms at the top. 

1. Conductivity 2. afterload 

3. Contractility 4. alpha effect 

5. Norepinephrine 6. parasympathetic stimulation 

7. alpha agonist 8. alpha antagonist 

9. 1 stimulant effects 10. 2 stimulant effects 

a) The force the ventricles must push against to pump blood into the aorta and pulmonary 

vasculature. 

b) Blocks effects of adrenergic stimulation. 

c) Dilation of peripheral arteries and the pulmonary bronchial system. 

d) Faster speed of electrical impulses through the heart. 

e) Vasoconstriction. 

f) Stimulates adrenergic receptors. 

g) Increased myocardial contraction and conductivity. 

h) Refers to the strength with which the heart pumps blood. 

i) Decreased AV node conductivity and myocardial contraction. 

j) Drug released by the sympathetic nervous system. 



Check Yourself Pop Quiz - Answers 

1. d 

2. a 

3. h 

4. e 

5. j 

6. i 

7. f 

8. b 

9. g 

10. c 

Refer to previous section as a review for any incorrect answers. Reviewing 

your incorrect answers will benefit your learning as you proceed in this 

packet. 



Oxygen 

Oxygen is present in the air all around us at a concentration of approximately 21%, but it is 

considered a drug. In fact, it is the most important drug contained in the ACLS protocols. All 

tissues within the body require oxygen and will begin to suffer damage if deprived for more than 

several minutes. The practice of cardiovascular medicine revolves around assuring the proper 

balance between oxygen supply and demand throughout the body. Regardless of any other 

actions taken during cardiovascular emergencies, if efforts fail to assure an adequate oxygen 

supply, other efforts will be wasted. 

Indications 

Supplemental oxygen is indicated for patients who are experiencing acute chest pain regardless 

of the cardiac cause. It is also used for patients with either demonstrated or suspected 

hypoxemia, since this may lead to metabolic acidosis. In addition, oxygen is used in all cases 

where CPR must be implemented. The best CPR you can provide only yields about 25-30% of 

the normal cardiac output. Since blood flow is diminished, one way to prevent tissue damage is 

to increase the oxygenation of the blood flow that you are providing. 

Administration 

Supplemental oxygen is given in a wide variety of doses and delivered in a number of ways 

depending on the patient’s particular need. 

Low Flow 

Low flow oxygen systems include nasal cannulas, simple face masks, nonrebreathing masks, and 

partial rebreathing masks. While partial rebreathing masks provide an oxygen concentration of 

24-60%, nonrebreathing masks can provide an oxygen concentration between 55-95%. 

Regardless of the concentration (%), low flow systems do NOT supply sufficient gas volume to 

meet the patient’s needs. Therefore the patient must be able to inhale a sufficient amount of 

room air along with the oxygen provided. Additionally, as the patient’s breathing pattern 

changes, the oxygen concentration provided to the patient may need to be reassessed and 

appropriately modified. 

High Flow 

High flow oxygen systems provide a high volume of gas that is sufficient to meet the patient’s 

inspiratory need without inhaling additional room air. They supply a more accurate 

concentration (%) of oxygen. The venturi mask is the most common high flow system, and 

supplies oxygen at a rate of 24-40%. 

Use of the Bag-Valve-Mask Devices 

In a cardiac arrest, oxygen is delivered at a concentration of approximately 100% utilizing a bagvalve-mask 

(BVM) device. This concentration is used even in patients with chronic lung disease 

(such as COPD) until the resuscitation is over. 



Review of Antidysrhythmics 

Antidysrhythmic drugs work by affecting the action potential (AP) of the myocardial cells. To 

understand how antidysrhythmic drugs affect the heart, one must be familiar with the action 

potential curve and its reflection of the cardiac cycle. 

An action potential curve refers to the electrical changes in the myocardial cell during the 

depolarization and the repolarization cycle. This activity can be compared to ourselves as we 

work and rest. In the heart, the working period is the depolarization cycle (systole), and the 

resting period is the repolarization cycle (diastole). These electrical charges are a result of 

specific ions (sodium, potassium, and calcium) that shift between the myocardial cell and the 

extracellular fluid via the sodium-potassium pump mechanism. The end result is the myocardial 

electrical activity known as the cardiac cycle (depolarization-repolarization phases) observable 

on the cardiac monitor or 12-lead EKG. The term “Refractory” is used to describe the extent to 

which a cell is able to respond to a stimulus. 

Absolute Refractory Period - During this period the cells cannot respond to any stimulus, 

regardless of strength. This period corresponds with the onset of the QRS complex to the peak 

of the T-wave. It is identified on the AP curve as phases 0, 1, 2, and the first half of phase 3. 

Relative Refractory Period – This is the vulnerable period in which a strong stimulus may 

produce ectopic depolarization. This period corresponds with the last half of the T-wave, and is 

identified on the AP as the last half of phase 3 and phase 4. 

The following chart briefly explains the different phases of the action potential. 

Action Potential 

Q 

R 

S 

T 

ECG 

MV 

0 

1 

2 

0 

3 

Inside Cell 

Cell Membrane 

4 

4 

100 

↓ K ↑ Na ↑ Ca 

↓K & ↓ Na 

Outside Cell 

2010 Orlando Health Education & Development 10


AP Phase Response ECG Waveform 

Phase 0 

Rapid 

Depolarization 

Phase 1 

Peak Phase 

Phase 2 

Plateau Phase 

Phase 3 

Beginning 

Repolarization 

Phase 

Phase 4 

Resting Phase 

The initial upswing indicates rapid depolarization 

by the influx of sodium into the myocardial cell. 

Potassium begins exiting cells. 

This peak reflects the brief period that sodium 

channels close. 

Calcium channels open for a slow influx of calcium 

ions to prolong depolarization. 

Calcium plays a key role in myocardial contraction. 

This rapid downswing marks the closure of sodium 

and calcium channels to prevent any further entry 

of sodium or calcium into the cell. 

Potassium begins to move back into the cell. 

The cell is now ready for another depolarization 

stimulus. 

QRS 

Absolute Refractory Period 

QRS 


QRS 


QRS and first half of T wave 

Absolute refractory period until 

midpoint of T wave, then becomes 

relative refractory period, the last 

half of T-wave. 


Relative Refractory Period 

Last half of T wave as it returns to 

isoelectric line 

Relative Refractory Period 

Keep in mind the ECG only represents electrical heart activity, not the actual contraction 

of the heart. 

Based on these previously mentioned principles, antidysrhythmic drugs are designed to modify 

the movement of ions in the various AP phases by altering the electrophysiology of the cardiac 

cell. Based on this principle, antidysrhythmics are classified based on their mechanisms of 

action and effects on the action potential. 

Currently there are four main classes of antidysrhythmics. The classification system (Vaughan- 

Williams) can assist you in recalling the actions and adverse effects. 

 

 

 

 

Class I - - Block sodium ion channel 

o 

o 

o 

Class Ia 

Class Ib 

Class Ic 

Class II (beta-blockers) - Block beta receptors 

Class III - Block potassium ion channels 

Class IV (calcium channel blockers) - Block calcium ion channels 

In general, drugs within the same class are similar in action and adverse effects and some drugs 

may have properties of more than one class category. (Example: amiodarone, sotalol). It is also 

important to note that all antidysrhythmics have the potential (some worse than others) to 



produce proarrhythmic effects on the patient. This means they can either worsen the 

dysrhythmia or trigger new ones. Antidysrhythmics can also prolong the QT interval (QTI) 

resulting in lethal dysrhythmias. Consequently, it is critical to closely monitor patients during 

initiation and usage of antidysrhythmics. This includes closely monitoring the ECG 

measurement of the QTI or QT interval corrected (QTc). 

Note: It is essential to identify drugs that prolong the QTI. For further information, read below 

for “ECG Measurement: The QTI and QTc,” or use a current drug reference, and internet 

resources such as: 

http://www.long-qt-syndrome.com/ekg_readout.html 

http://www.qtdrugs.org 

ECG Measurement: The QTI and QTc 


The interpretation of changes in the QT interval is an important aspect in the evaluation of an 

ECG tracing. The QT interval, (QTI) represents depolarization and repolarization of the 

ventricles. The QTI includes the “relative refractory period,” during which the heart is 

vulnerable to any ectopic foci that can initiate a stimulus. Accurate measurement is significant, 

as a prolonged QTI has been linked to monomorphic ventricular tachycardia, polymorphic 

ventricular tachycardia (torsades de pointes), and sudden cardiac death. 

The use of the QT interval in clinical practice is not without controversy. The literature clearly 

indicates that prolongation of the QTI in certain situations is associated with dysrhythmias or 

sudden cardiac death within 6-48 hours of lengthening. Far from perfect, yet deemed important, 

evaluation of the QTI/QTc remains a hot topic as researchers strive to discover methods that will 

provide better sensitivity and specificity for detecting the electrophysiologic changes that 

increase the risk of arrhythmias and sudden death. 

Lack of standardization: An identified problem is lack of a uniform approach to measurement. 

Some institutions do not measure the QTI unless physician ordered, while others measure only 

the QTI and not the QT C . Underlying problems such as a bundle branch block will affect the 

rate, and yet a standard for evaluation has not been agreed upon. 

Data collection and interpretation: First, it is not clear precisely how the measurement can be 

used to predict and prevent sudden cardiac death. Second, specific values of parameters vary 

depending on the population and circumstances. Data collection for the purpose of investigating 

different formulas is difficult, as it requires a very large population with high quality ECG data. 

QTI variation though 24 hours: Another problem is that the QTI changes depending on wake 

and sleep states, lead selection, heart rate, sympathetic and parasympathetic tone. 

QTI and a wide QRS: A widened QRS due to a ventricular conduction block causes the QT 

interval to be longer without prolonged depolarization. Two methods are available for 

measuring the QTI in the presence of a wide QRS due to a conduction block: it can be measured 

from the end of the QRS (at the J point) to the end of the T wave, or the QRS interval can be 

subtracted from the QTI. 

It is important to note that many different pharmaceutical agents other than CV agents have the 

potential to prolong the QTI. Please refer to current drug references and the links listed below. 



Measurement of the QTI in stable sinus rhythm 

The QTI is measured from the beginning of depolarization of the QRS complex to the end of the 

T wave representing repolarization. The QTI may be short, normal, or prolonged (>.44). 

Although a short QTI may suggest hypercalcemia, it is often difficult clinically to distinguish 

between a normal or short QTI. The literature suggests that healthcare providers should not be as 

concerned with QT shortening as with prolongation. (Grauer, 1998). The recommended lead for 

measurement is lead II. 

Note: If a U wave is present, it is not to be included in the measurement. The possible problem 

of distinguishing the T wave from a U wave can be minimized by measuring the QTI in lead II. 

Example of QTI measurement (with permission Grauer, 1998) 

QTI ends here 

where the T-wave 

returns to baseline. 

Another method to determine if a QTI is prolonged in sinus rhythms (< 100 beats 

per minute) is to observe the R-R interval. The QTI is probably prolonged if it 

exceeds more than half of the R-R interval. 

Example of evaluating R-R interval. (with permission Grauer, 1998) 



General Rules 

The QTI is normal if it is less than half of the R-R interval 

The QTI is prolonged if it is more than half of the R-R interval 

The QTI is borderline if it is approximately half of the R-R interval 

(Remember, this rule applies to a regular HR in the normal range of 60-100) 

A QTc > 0.44 is considered prolonged 

Normal QT Intervals Corrected for given Heart Rate = (QTc) 

Heart Rate/minute R-R Interval/sec QT C 

40 1.5 0.41-0.51 

50 1.2 0.38-0.46 

60 1.0 0.35-0.43 

70 0.86 0.33-0.41 

80 0.75 0.32-0.39 

90 0.67 0.30-0.36 

100 0.60 0.28-0.34 

120 0.50 0.26-0.32 

150 0.40 0.23-0.28 

180 0.33 0.21-0.25 

200 0.30 0.20-0.24 

Recommended Actions: 

Remember to treat the patient not the monitor. Evaluate all the assessment data. 

Record the QTI and the QT C as part of the routine documentation on patients in critical care 

and telemetry monitoring areas. 

Identify conditions and drugs associated with a prolonged QT interval, and increase 

frequency in documenting the QTI/QT C . Example- a QTI/QT C on a patient receiving 

procainamide should be measured q 4 hours and prn. This strip documentation is to include 

the drug that patient is receiving. 

Notify the appropriate person immediately (i.e. physician, nurse, charge nurse) if changes are 

observed. 

Documentation, continued assessment, and report to next shift. 



How to Obtain a QTc Measurement 

The QT interval (QTc) measurement is a more accurate measurement of the QT interval (QTI). 

This “corrected” measurement adjusts for heart rate and rhythm variability since it is known that 

autonomic tone influences heart rate. For example, when the heart rate increases the QTI 

shortens, and when the heart rate decreases the QTI lengthens. 

The QTc is determined by dividing the QT interval by the square root of the R-R interval. 

Generally, a QTc greater than 0.44 seconds (450 ms) is considered prolonged. The formula used 

to calculate a QT C is called Bazett’s Formula after the founding physician. 

Sequential Steps to Obtain a QTc Measurement 

Step 1- Obtain the QTI in seconds. 

This number becomes the numerator. 

All diagrams used with permission from Long-QT-Syndrome.com. 

Step 2- Obtain the R-R interval by counting the number 

of small boxes between two R waves, then multiply by 

0.04. 

Step 3- Calculate the square root of the R-R interval as 

shown in the diagram and the example below. 

This square root number becomes the denominator. 

Step 4- Divide the numerator by the denominator. 

This number is the QTc 

EXAMPLE: 

Step 1- QTI is 0.48 seconds. (Numerator) 

Step 2- The R-R interval is 24 boxes. (24 X .04 = 0.96 sec.) 

Step 3- Square root of the R-R is 0.98. (0.96 = 0.98) (Denominator) 

Step 4- 0.48 (numerator) divided by 0.98 (denominator) = QTc of 0.49 seconds = prolonged 



Class I Antidysrhythmics 

This class decreases the influx of sodium during phase 0 of depolarization. These drugs alter the 

absolute refractory period to decrease the risk of premature impulses from ectopic foci. Class I 

drugs also depress automaticity by slowing the rate of spontaneous depolarization of pacemaker 

cells. This class of antidysrhythmics is further broken down into subclasses Ia, Ib and Ic, 

depending on specific actions. 

Class Ia 

Blocks sodium to depress conductivity and prolong the refractory Examples of Drugs: 

period of the heart. These drugs are potent sodium channel 

blockers (prolong QRS interval), and may prolong repolarization disopyramide (Norpace) 

(prolong QT interval) through blockade of potassium channels. procainamide (Pronestyl) 

Indications 

quinidine 

These antidysrhythmics are used to treat atrial dysrhythmias, 

premature ventricular complexes, and ventricular tachycardia. 

Procainamide ( Pronestyl) is available in both oral and intravenous forms. When used as an 

intravenous bolus in the ACLS algorithm, it must be given no faster than 30mg/minute. 

Indications that procainamide must be stopped: 

Termination of the dysrhythmia 

Hypotension 

Reaching a total dose of 17 mg/kg 

Widening of the QRS complex by 50%, which indicates slowing of electrical 

conduction within the heart. 

Precautions 

Procainamide serum levels should be monitored in patients with renal failure or receiving 

constant infusion. 

All class I drugs depress myocardial contractility resulting in a lower cardiac output, 

which may lead to profound hypotension. 

Class Ia agents can prolong the QRS and QT intervals putting the patient at risk for 

ventricular dysrhythmias such as ventricular tachycardia or torsades de pointes. This risk 

is increased in patients with hypokalemia or hypomagnesemia. Consequently, it is 

important to monitor the patient and the QTI or QTc intervals. 



Antidysrhythmics: Subclass Ib 

In comparison to other class I drugs, as sodium channel 

Example of Drug: 

blockers subclass Ib have the lowest potency because they 

produce little or no change in the action potential duration. Lidocaine 

Since they shorten refractoriness, they do NOT prolong the 

QTI/QTc. Additionally, because these drugs target irritable tissue, they are used to decrease 

myocardial irritability and make it more difficult for ectopy or fibrillation to occur. 

Indications 

Subclass Ib drugs are used to treat ventricular dysrhythmias 

Precautions 

 

 

 

Lidocaine should not be given to anyone allergic to local anesthetic agents such as 

"Novocaine". Toxicity of lidocaine is most commonly apparent in the central nervous 

system resulting in drowsiness, confusion/disorientation, and paresthesias. 

Lidocaine serum levels can be measured. Levels of 1.5-5mcg/ml are considered 

therapeutic 

Muscle twitching in patients on lidocaine indicates advanced toxicity and warns the nurse 

of the almost certain probability of imminent focal or grand mal seizures. 

Antidysrhyhmics: Subclass Ic 

Subclass Ic drugs are the most potent sodium channel blocking 

agents (prolong QRS interval), but have little effect on 

repolarization (no effect on QT interval). Each of these drugs is 

associated with an increased overall mortality, so they are 

usually used in dysrhythmias that are resistant to other agents. 

Examples of Drugs: 

Propafenone (Rhythmol) 

Flecainide (Tambocor) 

Indications 

These drugs are used to treat supraventricular dysrhythmias and life-threatening ventricular 

dysrhythmias 

Precautions 

Class Ic are known to have proarrhythmic effects due to the prolongation of the action potential 

and QRS interval. The term proarrhythmic means that these drugs may induce or aggravated the 

dysrhythmias. 



Antidysrhythmics: Class II 

Class II antidysrhythmics are beta-blockers. They act indirectly on electrophysiological 

parameters by blocking beta-adrenergic receptors (slow sinus rate, prolong the PR interval, with 

no effect on QRS or QT intervals). 

Beta-blockers compete for receptor sites with one’s naturally 

occurring catecholamines such as epinephrine and 


norepinephrine. 

metoprolol (Lopressor) 

The beta-blockers that are chosen for antidysrhythmic therapy esmolol (Brevibloc) 

have a potent antidysrhythmic effect to inhibit dysrhythmias that 

result from the increased irritability and automaticity caused by 

atenolol (Tenormin) 

the sympathetic nervous system. Although their actions depend propanolol (Inderal) 

on which catecholamine receptor (β 1 versus β 2 ) they block, these 

drugs will have effects that are directly opposite to catecholamines by decreasing automaticity, 

heart rate, conductivity, contractility, stroke volume, cardiac output and blood pressure and 

myocardial workload. 

Indications 

Beta-blockers are used for rate control of sinus tachycardia, SVT, atrial tachycardia, and atrial 

fibrillation. The early use of beta-blockers in Acute Myocardial Infraction (AMI) patients 

reduces the likelihood of ventricular arrhythmias, recurrent ischemia, and reinfarction, thereby 

decreasing mortality. 

Precautions 

Beta-blockers may precipitate hypotension, bradycardia, and heart failure, as well as 

mask signs of hyperthyroidism and hypoglycemia. 

During IV administration, carefully monitor BP, heart rate, and ECG due to their 

mechanism of action. 

Beta-blockers are used with extreme caution in patients with asthma and COPD because 

they may lead to bronchospasms when non-selective beta-blockers interfere with the 

stimulation of β 2 receptors in the bronchial system. 



Antidysrhythmics: Class III 

Class III drugs prolong repolarization (phase 3) by preventing any further entry of sodium or 

calcium into the cell. Potassium begins to move back into the cell. 

Class III drugs are further known as either mixed or pure 

class III. For example, although amiodarone is generally 

prescribed because of its class III properties, it exhibits 

electrophysiological characteristics of each of the other 

classes of antidysrhythmics. Whereas sotalol combines the 

class III property of prolonging the refractory period with 

the beneficial beta-blocking effects of class II drugs. Strict 

monitoring of the QTI/ QTc is essential for drugs within 

this class. 

Amiodarone (Cordarone) 


Pure class III: ibutilide (Corvert), 

dofetilide (Tikosyn) 

Mixed class III: amiodarone 

(Cordarone), sotalol (Betapace 

and Betapace AF) 

Amiodarone is an ACLS drug used for control of rapid ventricular rate due to an accessory 

pathway conduction in pre-excited atrial arrhythmias; after defibrillation and epinephrine in 

cardiac arrest with persistent ventricular tachycardia (VT) or ventricular fibrillation (VF); and 

control of hemodynamically stable VT, polymorphic VT, or wide-complex tachycardia of 

uncertain origin. 

Dofetilide (Tikosyn ® ) 

Dofetilide (Tikosyn) is indicated for the conversion of atrial fibrillation or atrial flutter to sinus 

rhythm. It is also used to maintain sinus rhythm in patients with atrial fibrillation or atrial flutter. 

Only prescribers (physicians, nurse practitioners, physician assistants) who have received 

specialized training can prescribe dofetilide. Likewise, hospital pharmacists and nurses must 

have received education prior to dispensing and administering this drug . 

Therapy must be initiated in a hospital setting so the patient can be monitored for dysrhythmias. 

Careful monitoring of serum potassium,magnesium, and renal function must be done for patients 

receiving dofetilide. 

Additionally, a baseline QT C interval must be measured and dofetilide is not be administered if 

the baseline QTc is greater than 440 msec (>0.44) or greater than 500 msec (>0.50) in patients 

with ventricular conduction abnormalities. An increase in the QTc measurement of greater than 

15% over baseline or greater than 500 msec (0.50) necessitates either a dosage reduction or 

discontinuation of dofetilide. Contact the cardiologist immediately if adverse signs occur. 

ECG monitoring is continuous during the initial dosing period with strict measurement and 

documentation of the QTc and patient tolerance. After a minimum three-day hospital stay with 

dose adjustment, the patient can be discharged home with a 7-day supply of medication. It is 

recommended that nursing collaborate with the hospital pharmacy for discharge planning. 

Sotalol (Betapace ® , Betapace AF ® ) 

Sotalol is used for the treatment of documented ventricular arrhythmias (i.e. sustained ventricular 

tachycardia) that in the judgment of the physician are life-threatening, and for maintenance of 

normal sinus rhythm in patients with symptomatic atrial fibrillation or atrial flutter. Betapace 

AF ® is a modified version of Betapace, with specific manufacturer instructions that states 



substitutions are not to be made for Betapace AF ® since it is distributed with a patient package 

insert specific for atrial fibrillation/flutter. 

It is vital that sotalol be avoided with other beta-blockers since it also has class II effects that can 

result in profound hypotension. Sotalol doses are further adjusted for renal dysfunction. 

Ibutilide (Corvert ® ) 

Ibutilide is indicated for the acute termination of atrial fibrillation or flutter of recent onset. The 

effectiveness of ibutilide has not been determined in patients with arrhythmias >90 days in 

duration. Ibutilide is available in IV form only, and has the potential to result in lethal 

ventricular dysrhythmias. Hypokalemia and hypomagnesemia are contraindications for ibutilide 

due to the increased risk of lethal ventricular dysrhythmias. The QT interval must be closely 

monitored initially, and for at least 4 hours following the infusion of ibutilide. 

Precautions 

All class III drugs prolong the QT interval to varying degrees which may result in lifethreatening 

ventricular dysrhythmias. The QTI and QTc must be carefully monitored and 

documented. It is important to also note that an array of drug categories other than 

cardiac can cause a prolonged QTI such as certain antibiotics, antifungals, antipsychotics, 

and others. 

The risk of dysrhythmias with class III drugs increases with hypokalemia and 

hypomagnesemia; these labs should be monitored closely and replaced if necessary. 

A unique adverse effect profile and drug interactions with dofetilide require additional 

guidelines for patient selection and administration. Only prescribers (physicians, nurse 

practitioners, physician assistants) who have received specialized training can prescribe 

dofetilide. Likewise, hospital pharmacists and nurses must have received education prior 

to dispensing and administering the drug. Dofetilide is available in a limited number of 

retail pharmacies. Patients need to contact their local pharmacy prior to discharge to see 

if the pharmacy is enrolled in the TIPS (Tikosyn in Pharmacy System) program. Retail 

pharmacies can call 1-877-TIKOSYN for further information. 

Important Definitions: 

Inotropic effect is a change in myocardial contractility. A positive inotropic effect would 

increase contractility, while a negative inotropic effect will decrease contractility. 

Chronotropic effect refers to an increase in heart rate; a negative chronotropic is decrease in 

heart rate. 

Dromotropic effect refers to the influence the cardiac nerves have on the conductivity of 

impulses across the muscle. A positive dromotropic effect would increase conductivity, while a 

negative effect would decrease conductivity. 



Antidysrhythmics: Class IV 

Calcium is critical to heart function due to its effect on cardiac output by increasing contractility 

and conductivity. Calcium channel blockers decrease contractility of the myocardium and slow 

conduction through the SA and AV nodes by inhibiting the influx of calcium and sodium during 

phase 2 of the action potential. These actions result in prolonging both the absolute and relative 

refractory periods. Drugs in this class also produce vasodilation of the peripheral and coronary 

arteries, thereby increasing the supply of oxygenated blood to the myocardium and reducing 

myocardial workload to reduce myocardial oxygen demand. 

Calcium channel blocker categories 

Two types of calcium channel blockers exist because they exert different effects. 

Calcuim channel blockers known as (nondihydropyridines): cause coronary artery 

vasodilation, decrease heart rate, and decrease conduction through the SA and AV nodes. They 

are utilized to treat atrial dysrhythmias, angina, and hypertension. 

Diltiazem (Cardizem, Dilacor XR, Tiazac) verapamil (Calan, Isoptin, Verelan PM) 

Calcuim channel blockers known as (dihydropyridines): dilate peripheral blood vessels 

without affecting heart rate or contractility. They are utilized to manage hypertension and will 

be discussed later in this SLP. 

Nifedipine (Procardia, Adalat), amlodipine (Norvasc), felodipine (Plendil), isradipine 

(DynaCirc), nicardipine (Cardene), and nisoldipine (Sular) 

The following page has a summary chart on the actions and indications for calcium channel 

blockers. 

Precautions 

Short acting nifedipine capsules (Procardia ® , Adalat ® ) are not recommended for acute 

blood pressure reduction nor for chronic hypertension management due to risk of 

profound hypotension, cerebral ischemia or stroke, and/or death. 

Nifedipine should NEVER be administered sublingually or as a “bite and swallow” order. 



Summary chart of calcium channel blocker actions and indications 

Calcium Channel Blockers Actions 

Potent vasodilator of coronary vessels. This effect 

increases coronary blood flow, and reduces coronary 

vasospasm. 

Vasodilator of peripheral vessels. Vasodilation occurs 

predominantly in arterioles; there is no significant effect on 

venous beds. Dihydropyridine agents reduce peripheral 

resistance and afterload. 

Negative inotropic effect. Nondihydropyridine agents cause 

a modest decrease in contractility and reduction of myocardial 

oxygen consumption. This effect is used to depress the 

frequency of hyperactive tissue causing arrhythmias. 

Negative chronotropic effect. Nondihydropyridine agents 

cause a modest lowering of heart rate. This effect is due to 

slowing of the SA node and results in reduced myocardial 

oxygen consumption. 

Negative dromotropic effect. By slowing conduction through 

the AV node, nondihydropyridine agents increase the time 

needed for each beat. This results in reduced myocardial 

oxygen consumption. 

Indications 

Angina 

Hypertension 

Supraventricular 

Dysrhythmias 

Angina 


Dysrhythmias 

Angina 


Dysrhythmias 

Angina 



Miscellaneous Antidysrhythmics 

Adenosine (Adenocard) 

Adenosine interrupts electrical conduction in the AV nodal reentry pathways making it effective 

against supraventricular tachyarrhythmias and narrow complex tachyarrhythmias of unknown 

origin. A rapid IV push bolus of adenosine causes complete depolarization of the myocardium, 

resulting in a brief asystolic period that allows the heart's electrical activity to "reset" and return 

to sinus rhythm. Because of this action, administration of adenosine is often referred to as a 

"chemical cardioversion.” 

Indications 

Generally slow the rhythm down sufficiently to allow for correct interpretation of atrial 

fibrillation or atrial flutter so that appropriate intervention may be made. 

Precautions 

Adenosine can induce a brief period of asystole, of 6-10 seconds. It is vital to have emergency 

resuscitation equipment readily available. 

Magnesium 

Magnesium is essential for the functioning of the sodium-potassium pump to drive myocardial 

electrical activity. A low serum magnesium level slows the return of potassium into the cell 

during phase 4 of the action potential, resulting in a prolonged relative refractory period and QT 

interval. Patients with a magnesium deficiency commonly have a high incidence of cardiac 

dysrhythmias, including torsades de pointes (TdP) and sudden cardiac death. 

Precautions 

IV administration can cause hypotension and circulatory collapse if given too fast. 




Match the definitions at the bottom with the terms at the top. 

1. ________ Magnesium 

2. ________ Class III 

3. ________ Amiodarone 

4. ________ Proarrythmic 

5. ________ Class IV 

6. ________ Class II 

7. ________ Sotalol 

8. ________ Dofetilide 

9. ________ Absolute Refractory Period 

10. ________ Relative Refractory Period 

a) A drug class known to decrease the heart rate, conductivity, contractility. 

b) A drug class which decreases contractility and slows conduction though the SA and AV 

nodes. 

c) Time frame when cardiac cells cannot respond to any stimulus from ectopic sources, 

corresponds with the QRS and first half of the T wave. 

d) Treatment of choice for the dysrhythmia torsades de pointes. 

e) A mixed class III drug that is to be avoided with beta-blocker drugs. 

f) A class III drug used to convert recent onset atrial fibrillation to sinus rhythm. Healthcare 

providers must be inserviced prior to providing this agent. 

g) Indicated in emergency therapy for ventricular tachycardia or ventricular fibrillation. may 

also be used for PVC’s. 

h) Describes a drug that may induce additional dysrhythmias. 

i) A strong stimulus may produce ectopic depolarization in the cardiac cells. Corresponds with 

the last half of the T-wave. 

j) Strict monitoring of the QTI/QTc is essential for drugs within this class. 



Check Yourself Pop Quiz -Answers 

1. d 

2. j 

3. g 

4. h 

5. b 

6. a 

7. e 

8. f 

9. c 

10. i 



packet. 



Antihypertensives 

Angiotensin Converting Enzyme (ACE) Inhibitors 

Before discussing the ACE inhibitors, let us take a moment to review the renin-angiotensin 

system. Renin is formed in the renal juxtaglomerular cells in response to certain types of stimuli. 

These stimuli include salt depletion, β 2 stimulation, 

and a decrease in renal perfusion that might be found Examples of Drugs: 

in hypotension or hypovolemia. Next, renin mediates 

the formation of angiotensin-I in the liver. When 

angiotensin-I reaches the lungs, it is converted by the 

angiotensin converting enzyme into angiotensin-II. 

Angiotensin-II causes vasoconstriction, promotes the 

release of norepinephrine, and stimulates aldosterone 

production resulting in sodium and water retention. 

Additional effects of angiotensin-II include increased 

systemic vascular resistance, arterial blood pressure, and intravascular volume. 

Capoten ® (captopril), Vasotec ® 

(enalapril), Monopril ® (fosinopril), 

Lotensin ® (benazepril), Mavik ® 

(trandolapril), Accupril ® (quinapril), 

Aceon ® (perindopril), Prinivil ® , 

Zestril ® (lisinopril), Altace ® (ramipril), 

Univasc ® (moexipril) 

ACE inhibitor drugs work by blocking the angiotensin converting enzyme in the lungs so 

angiotensin-I is prevented from being converted to angiotensin-II. The outcome is a decrease in 

norepinephrine levels, prevention of systemic vasoconstriction and decreased blood pressure. 

Furthermore, aldosterone production is no longer stimulated by Angiotensin II, which results in 

decreased intravascular volume. 

Indications 

ACE inhibitors are used in the management of hypertension either alone or in combination with 

other anti-hypertensive classes and also for patients with type 1 diabetes mellitus to slow the 

progression of diabetic nephropathy. 

Precautions 

Due to their mechanism of action, ACE inhibitors may cause hypotension or symptoms 

related to hypotension, such as dizziness and syncope. 

It is important to understand that a number of patients who take ACE inhibitor drugs 

develop a persistent nonproductive cough. Patients are to be cautioned about these effects 

prior to initiating ACE inhibitor therapy. 

ACE inhibitor therapy may compromise renal function and result in transient increases in 

BUN and creatinine. 

Angiotensin II Receptor Blockers (ARBs) 

Angiotensin receptor blockade is a newer method of 

renin-angiotensin blockade. Unlike the ACE inhibitor 


drugs, they do not prevent the formation of Cozaar ® (losartan), Diovan ® 

angiotensin-II. Instead, they bind to receptor sites to (valsartan), Atacand ® (candesartan), 

prevent the effects of angiotensin-II. This results in a Benicar ® (olmesartan), Avapro ® 

decrease in norepinephrine levels, prevention of (irbesartan), Micardis ® (telmisartan), 

Teveten ® (eprosartan) 



systemic vasoconstriction and a decreased blood pressure. 

Indications 

ARBs are indicated for the treatment and management of mild to severe hypertension. Used in 

patients with heart failure because they block the vasoconstrictive effects of angiotension-II and 

the release of aldosterone. 

Precautions 

Angiotensin receptor antagonists may cause hypotension or symptoms related to 

hypotension. 

In some patients, the use of ARB therapy may result in transient increases in BUN and 

creatinine. 



Beta-Adrenergic Blockers 

Beta-blockers inhibit the response to adrenergic stimuli by competitively blocking beta-1 

adrenergic receptors within the myocardium and by blocking beta-2 adrenergic receptors within 

the bronchial and vascular smooth muscle. Some betablockers 

are specific for beta-1 receptors (atenolol, 

metoprolol, betaxolol, bisoprolol, esmolol). However, 

beta-1 selectivity is dose-dependent and is not seen 

with high doses of beta-1 selective drugs. 

Indications 

Used for hypertension, angina, MI’s, and heart failure, 

dysrhythmias and rate control. 

Precautions 

Beta-blockers may precipitate hypotension and bradycardia. 

Oral beta-blocker therapy should not be withdrawn abruptly (particularly in patients with 

CAD), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. 

 

 

 


Lopressor ® , Toprol-XL ® 

(metoprolol), Coreg ® (carvedilol), 

and Tenormin ® (atenolol). Zebeta ® 

(bisoprolol),Inderal ® 

(propranolol), Brevibloc ® 

(esmolol), Trandate ® (labetalol), 

Corgard ® (nadolol) 

Concurrent use of beta-blockers, or the calcium channel blockers verapamil and diltiazem 

because bradycardia or heart block can occur. 

Beta-blockers should be avoided in patients with asthma and COPD because they may 

lead to bronchospasm when non-selective beta-blockers interfere with the stimulation of 

beta-2 receptors in the bronchial system. 

Likewise, cautious use is indicated in diabetics because they can mask prominent 

hypoglycemic symptoms. 

Fenoldopam (Corlopam) 

Fenoldopam is a rapid acting vasodilator because of its dopamine agonist properties. It is used as 

an antihypertensive with the added bonus effects of natriuresis, sodium excretion, and improved 

renal blood flow. 

Indications 

Used for short-term management of severe or malignant hypertension when rapid reduction of 

blood pressure is needed. 

Precautions 

Due to its potent and rapid acting hypotensive properties, frequent blood pressure 

monitoring is necessary. 

Please review your institution’s policy regarding patient placement in an appropriate 

telemetry unit. 



Sodium Nitroprusside (Nipride, Nitropress) 

Sodium nitroprusside (Nipride) is a potent, fast acting drug producing vasodilation of both the 

arteries and the veins. This action results in decreasing afterload by reducing systemic vascular 

resistance and arterial blood pressure, and decreasing preload by increasing venous capacitance 

and reducing blood return to the heart. The preload and afterload reduction results in both 

decreased myocardial workload and myocardial oxygen demand. Nipride is used to managed 

hypertensive crises and control blood pressure in patients after vascular surgeries, 

coronary bypass surgery, dissecting aortic aneurysm. 

Precautions 

 

 

 

Sodium nitroprusside has a rapid onset and short duration of action making it very easy to 

titrate. The effects of this drug are observed almost immediately and disappear within a 

few minutes after it is discontinued. 

Sodium nitroprusside has the potential to cause severe hypotension that can lead to 

myocardial ischemia, myocardial infarction, or stroke. Patients must be monitored closely 

during initiation and titration. Due to its short duration, discontinuing the drug and 

elevating the patient’s legs should be sufficient to return arterial blood pressure to prior 

levels within several minutes. 

Cyanide is produced which is converted to thiocyanate in the liver and thiocyanate is 

eliminated mainly in the urine. Patients receiving high doses and/or prolonged infusions 

of nitroprusside, are at risk for cyanide and/or thiocyanate toxicity. 

Clinical note: The patient is to be observed continuously for signs of cyanide toxicity, 

which include metabolic acidosis (may be the earliest sign of toxicity), nausea, tinnitus, 

blurred vision, changes in mental status, hyperreflexia, twitching, and seizures 



Vasodilators 

Nitroglycerin 

Nitroglycerin is a potent vasodilator relaxing both the vascular smooth muscle of the arteries and 

veins and has a more pronounced effect on the venous system. Nitroglycerin decreases systemic 

arterial resistance and arterial blood pressure, increases 

venous capacitance and reduces preload. As a result, 

nitroglycerin decreases myocardial workload and 

myocardial oxygen demand. 

Nitroglycerin also relieves vasospasm and dilates coronary 

arteries to increase blood flow to the myocardium, helping 

to relieve myocardial ischemia. Nitroglycerin is the drug 

of choice for the relief of all types of angina, stable, 

unstable, and prinzmetal. 

Precautions 

 

 

 

 


Tridil(IV), Nitro-Bid, Nitrostat, 

isosorbide dinitrate (Isordil ® ), 

isosorbide mononitrate, 

(Imdur ® , Monoket ® , Ismo ® ), 

Hydralazine, Nesiritide 

(Natrecor) 

Because nitroglycerin is a powerful vasodilator, it may result in profound hypotension. 

As a result, it should be initiated cautiously and the patient closely monitored during 

titration. 

Headaches are common with all forms of nitroglycerin, so patients need to be instructed 

that this is an expected side effect. 

Patients receiving nitrate therapy should not take selective phosphodiesterase inhibitors 

used for erectile dysfunction (Viagra®, Levitra®, Cialis®). The combination can worsen 

the hypotensive effects of nitrates, possibly resulting in potentially life-threatening 

hypotensive/hemodynamic compromise. 

In some cases, an intravenous nitroglycerin preparation may antagonize an IV infusion of 

heparin and therefore close monitoring of its effects is required. This is important to 

remember since these drugs may be administered concomitantly to patients diagnosed 

with an acute myocardial infarction or acute coronary syndrome. 

Isosorbide 

Compared to nitroglycerin, isosorbide dinitrate (Isordil®) is a less potent vasodilator. Isosorbide 

dinitrate, isosorbide mononitrate, and nitroglycerin are collectively known as nitrates. Isosorbide 

dinitrate and one of its metabolites-isosorbide mononitrate (Imdur®, Monoket®, Ismo®) are 

available orally, and sublingually. They are used for angina and for heart failure in combination 

with hydralazine (BiDil®). Their mechanism of action is similar to nitroglycerin so they share 

the same precautions, interactions, and adverse effects. 

Nitrate tolerance – Tolerance to the vascular and antianginal effects of individual nitrates and 

cross-tolerance among the drugs may occur with repeated prolonged use. Intermittent doses of 

nitrates by use of a nitrate-free interval of 10-12 hours may minimize or prevent the development 

of tolerance. 



Hydralazine 

Hydralazine has direct vasodilatory effects on the vascular smooth muscle resulting in blood 

pressure lowering. It is one of the parenteral drugs of choice for management of pregnancyassociated 

hypertensive emergencies. However, other parenteral therapies (i.e., nitroprusside) are 

recommended for hypertensive crises in non-pregnant patients. When used parenterally, 

hydralazine is administered as intermittent doses. Hydralazine has been used in combination with 

isosorbide dinitrate as a second-line treatment of heart failure. 

Nesiritide (Natrecor) 

Nesiritide is a synthetic human B-type natriuretic peptide (BNP) with potent vasodilator 

properties. Nesiritide binds to the receptor sites of vascular smooth muscle resulting in an 

increase in cGMP, which is responsible for vasodilation of veins and arteries. It promotes 

diuresis and natruresis. It is currently indicated for the patient in acutely decompensated heart 

failure who is symptomatic with either minimal activity or dyspnea at rest. 

Precautions 

When B-type natriuretic peptide (BNP) lab values are ordered, the blood must be obtained prior 

to the administration of nesiritide (Natrecor). Since nesiritide (Natrecor) is a synthetic BNP, the 

lab results will be altered after this drug is administered. 

Due to its potent hypotensive properties, it is important to institute frequent blood pressure 

monitoring. Review your institution’s policy regarding placement of the patient in an 

appropriate telemetry unit. 



Morphine Sulfate 

Morphine sulfate is a powerful narcotic analgesic used to relieve severe acute or chronic pain 

and to relieve anxiety. It primarily stimulates venous vasodilation and a reduction in preload (the 

volume of blood in the ventricles at the end of diastole). An additional property is arterial 

vasodilation, resulting in a decrease in afterload (the force the ventricles must push against to 

pump blood into the aorta and pulmonary vasculature). By reducing preload and afterload, 

morphine diminishes myocardial workload and oxygen demand. 

Morphine is the drug of choice to relieve the pain and anxiety associated with ischemic chest 

discomfort and myocardial infarction because it decreases the myocardial oxygen. Morphine is 

also useful in the management of cardiogenic pulmonary edema by increasing venous 

capacitance (capacity), thus decreasing the return of blood to the right side of the heart and to the 

lungs. 

Precautions 

 

 

The most serious adverse effect of morphine is depression of the respiratory system. 

Careful monitoring of the respiratory rate and depth is necessary during administration of 

morphine. Rapid administration of morphine may result in respiratory arrest. 

Morphine causes venous and arterial vasodilation, thus hypotension may occur. The 

blood pressure must be closely monitored in patients receiving morphine. The effects of 

morphine can be reversed with naloxone (Narcan) 0.2mg – 2.0mg at 2-3 minute intervals, 

to a maximum of 10mg. 

Atropine 

Atropine has numerous clinical applications so we will limit our discussion to those that involve 

the cardiovascular system. 

Atropine is known as a vagolytic or parasympatholytic because it counteracts the effects of the 

parasympathetic nervous system. This leaves the actions of the sympathetic nervous system 

unopposed so patients who have received atropine will display signs of increased sympathetic 

activity. Because parasympathetic innervation of the heart is primarily in the atria, atropine 

affects atrial activity. 

Atropine is indicated for symptomatic bradydysrhythmias. It enhances automaticity of the sinus 

node, and increases electrical conduction through the atria and the AV node. It is used in sinus 

bradycardia to increase heart rate. 

Calcium Salts 

Calcium is an essential electrolyte for normal cardiac and vascular function. Calcium is available 

in oral and parenteral forms for a wide variety of indications. Calcium Chloride is usually 

reserved for emergent situations requiring calcium replacement. Calcium Chloride must be given 

carefully because rapid administration can result in cardiac arrest. Calcium Gluconate is used 

more frequently because it is associated with fewer side effects than Calcium Chloride. Calcium 

replacement should be guided by ionized calcium levels to avoid hypercalcemia. Calcium salts 

will not be discussed further in this packet. 




1. Define parasympatholytic. What are the effects of this class of drugs on the 

heart? 

_________________________________________________________________ 

_________________________________________________________________ 

2. Which class of drugs is used as a vasodilator and also blocks the conversion of 

Angiotensin I to Angiotensin II? 

______________________________________________________________ 

3. Name 3 effects of Angiotensin II? 

______________________________ ______________________________ 

______________________________ 

4. Does Nitroglycerin have more effect on the venous or arterial system or equally on 

both? (Circle correct answer) 

Arterial system Venous system Equally on both system 

Will this have more effect on ventricular preload or afterload? (Circle correct 

answer) 

Preload 

Afterload 

5. Select which system Nitroprusside has more effect on: (Circle correct answer) 

Venous system Arterial system Equally on both systems 

List the effects Nitroprusside has on ventricular preload and afterload? 

_________________________________________________________________ 

_________________________________________________________________ 

6. State the vasodilator agent that is used as a potent antihypertensive and rapid 

acting, but also has the effects of natriuresis? 

_________________________________________________________________ 




1. Parasympatholytic is defined as counteracting the effects of the parasympathetic 

nervous system. This class of drug will enhance automaticity of the sinus node, 

increase electrical conduction through the atria and the AV node and will enhance 

conductivity. (Increases sinus and ventricular heart rate). 

2. ACE inhibitor therapy blocks the conversion of angiotensin I to II, which occurs 

primarily in the lungs. The ARB therapy blocks the effects of angiotensin II after 

this conversion occurs. 

3. Angiotensin-II causes vasoconstriction, promotes the release of norepinephrine, 

and stimulates aldosterone production resulting in sodium and water retention. 

Additional effects of angiotensin-II include increased systemic vascular 

resistance, arterial blood pressure, and intravascular volume. 

4. NTG relaxes vascular smooth muscle of arteries and veins, but has a more 

pronounced effect on the venous system. Nitroglycerin will decrease systemic 

arterial resistance and arterial blood pressure, but it increases venous capacitance 

and reduces preload to a greater extent. 

5. Sodium nitroprusside is a potent, fast acting drug which causes vasodilation of both 

arteries and veins. Because of this action, it decreases afterload by reducing 

systemic vascular resistance and arterial blood pressure, and decreases preload 

by increasing venous capacitance and reducing blood return to the heart. This 

preload and afterload reduction results in decreased myocardial workload and 

myocardial oxygen demand. 

6. Fenoldopam (Corlopam). 



Vasopressor Therapy 

Clinical Application 

Vasopressor drugs must not be used until the patient’s volume status has been addressed. 

The administration of vasopressors to hypovolemic patients does not increase blood 

pressure; instead it can result in profound tachydysrhythmias and ventricular tachycardia or 

ventricular fibrillation. 

Should extravasation of this or any other alpha agonist occur, phentolamine (Regitine) may be 

used to help minimize tissue damage. Refer to your hospital’s policy regarding the use of 

phentolamine for intravenous extravasation of these drugs. 

Dopamine 

Dopamine (Intropin) is a chemical precursor of norepinephrine. Dopamine stimulates alpha, β 1 , 

and dopaminergic receptors, depending on the administered dose, and also stimulates the release 

of norepinephrine 

Indications 

Dopamine is used primarily for symptomatic hypotension and to increase organ perfusion. 

According to the ACLS bradycardia algorithm, dopamine may also be considered in 

hemodynamically significant bradycardia, with the dose beginning at 5 mcg/kg/minute, 

following the use of transcutaneous pacing and/or atropine. 

In patients with cardiogenic shock, left ventricular failure, and pulmonary edema, dopamine may 

be used in conjunction with positive inotropic agents and vasodilators. This permits the 

beneficial β 1 effects to predominate and counteracts the increases in preload and afterload caused 

by alpha stimulation. 

At low doses (1 – 4 mcg/kg/minute), dopamine stimulates the dopaminergic receptors to produce 

cerebral, renal, and mesenteric vasodilation. This dose is commonly thought to increase blood 

flow to the kidneys and may sometimes be referred to as the renal dose dopamine. The efficacy 

of dopamine for this indication is not supported in the literature. 

NOTE: Many clinicians currently suggest that low dose dopamine therapy does NOT prevent or 

ameliorate acute renal failure in patients. 

At moderate doses (5 -10 mcg/kg/minute), dopamine stimulates the β 1 receptors in the 

myocardium. This increases contractility, cardiac output, and arterial blood pressure. 

At higher doses (10 – 20 mcg/kg/minute), the alpha agonist properties of dopamine are much 

more pronounced, resulting in significant increases in peripheral and venous vasoconstriction. 

This results in an increase in preload, afterload, and myocardial workload. It also significantly 

increases myocardial oxygen demand and negates the positive β 1 and dopaminergic effects. 

At doses of 20 mcg/kg/minute or more, significant arterial vasoconstriction results. If 

hypotension continues, then other interventions should be considered. 



Precautions and Interactions 

As with any of the vasopressors, the patient’s volume status should be addressed before the 

administration of dopamine. Failure to do so may result in tachydysrhythmias, ventricular 

tachycardia, and ventricular fibrillation. MAO inhibitors strongly potentiate dopamine so the 

dosage should be only 10% of the recommended dose. 

The arrhythmogenic potential of dopamine increases as the dose increases, as does the increase 

in myocardial workload and myocardial oxygen demand. Since low dose dopamine causes 

vasodilation of the mesenteric and renal vessels, it tends to shunt blood to the kidneys and 

intestines, and may actually result in a slight decrease in blood pressure. 


It is recommended that all dopamine doses be administered through a central venous 

catheter since extravasation of dopamine causes tissue necrosis. 

Epinephrine 

Epinephrine, also known as Adrenalin, is a naturally occurring catecholamine which stimulates 

both alpha and beta receptors.Epinephrine’s alpha agonist activity results in peripheral 

vasoconstriction, which increases systemic vascular resistance as well as systolic and diastolic 

blood pressure. This results in increased coronary and cerebral perfusion blood flow. 

Epinephrine’s beta-1 agonist activity increases automaticity and myocardial electrical activity, 

myocardial contractility and cardiac output. Its beta-2 agonist properties result in 

bronchodilation. Epinephrine also inhibits the release of histamine, which is responsible for the 

cardiovascular collapse that occurs in severe allergic reactions and anaphylaxis. 

Indications 

Epinephrine’s adrenergic agonist properties make it useful in any pulseless rhythm such as 

asystole, pulseless electrical activity, ventricular fibrillation, and pulseless ventricular 

tachycardia. It also facilitates these ventricular rhythms to be more responsive to defibrillation. 

Additionally, when used as a diluted continuous intravenous infusion, epinephrine is useful for 

profound symptomatic bradycardia that has not responded to a pacemaker or atropine. 

Epinephrine is also used in the management of anaphylactic shock. It relieves bronchospasm, 

causes bronchodilation, and blocks the release of histamine (histamine is the chemical mediator 

that leads to the vascular changes in anaphylaxis thus leading to shock). 

It is further recommended that epinephrine be administered through a central venous catheter 

since extravasation of epinephrine causes tissue necrosis. 


Note: Medication errors have occurred due to confusion with epinephrine products expressed as 

ratio strengths (i.e. 1:1000 vs. 1:10,000). 

Epinephrine 1:1000 = 1 mg/mL and is most commonly used Sub Q for hypersensitivity reactions 

or as a bronchodilator. Epinephrine 1:10,000 = 0.1 mg/mL and is used I.V. as part of the ACLS 

protocol. 



It is important to remember that by enhancing preload, afterload, and myocardial workload, 

epinephrine increases the myocardial oxygen demand resulting in an increased myocardial 

irritability that can induce ventricular ectopy. 

Norepinephrine 

Norepinephrine (Levophed) is a naturally occurring catecholamine that is structurally similar to 

epinephrine. Norepinephrine has very little effect on beta-2 receptors so it does not produce 

bronchodilation. The beta-1 agonist effects are comparable to epinephrine with additional effects 

such as increasing automaticity, myocardial electrical activity, myocardial contractility, and 

cardiac output. Additionally, norepinephrine’s alpha agonist effects result in a more pronounced 

peripheral vasoconstriction. 

As the dose of norepinephrine increases, the resulting increased afterload limits the beneficial 

inotropic effects and increases myocardial oxygen demands. This increased stress on the heart 

may exacerbate myocardial ischemia and extend a myocardial infarction. However, in shock 

states, the use of norepinephrine at low doses is common. It is especially beneficial in patients 

with septic and neurogenic shock, or other conditions that result in vasodilation (decreased 

systemic vascular resistance). 

Indications 

Norepinephrine is indicated for hemodynamically significant hypotension (


Phenylephrine 

Phenylephrine (Neo-Synephrine) is a sympathomimetic agent used primarily as an alpha agonist. 

In usual therapeutic doses, it causes vasoconstriction to increase systemic vascular resistance and 

arterial blood pressure. 

Indications 

From a cardiovascular perspective, phenylephrine is used in patients with hypotension and 

shock. 


It is recommended that phenylephrine be administered through a central venous catheter 

since extravasation of phenylephrine causes tissue necrosis. 


In usual therapeutic doses, phenylephrine increases preload and afterload and resulting in 

increased myocardial oxygen demand. Phenylephrine may cause a slowing of the heart rate 

(reflex bradycardia) and is potentiated by tricyclic antidepressants and monoamine oxidase 

(MAO) inhibitors. 

Vasopressin 

Vasopressin (Pitressin) is a naturally occurring antidiuretic hormone found in the posterior 

pituitary. As a pharmacologic agent, vasopressin has several clinical applications, so our 

discussion is limited to the application of vasopressin within the ACLS guidelines as a 

vasopressor. 

Indications 

According to ACLS Guidelines, vasopressin “is an effective vasopressor and can be used as an 

alternative for the first or second dose of epinephrine in the pulseless arrest algorithm. 

Dosing for Cardiac Arrest is 40 Units IV push x 1. IV is the only route recommended 

currently by AHA guidelines. 

Vasopressin may be useful for hemodynamic support in vasodilatory shock (e.g., septic shock). 

Precautions 

The half-life of vasopressin is 10–20 minutes. As a result, after 10 minutes a decision needs to 

be made to give epinephrine because vasopressin can only be given once. At this time, 

vasopressin cannot be administered through the endotracheal tube, or as a continuous infusion. 



Positive Inotropic Therapy 

Digoxin 

Our discussion of digitalis preparations will be limited to digoxin (Lanoxin, Digitek®) which is 

the most commonly prescribed form of digitalis. Digoxin is a positive inotropic agent as it 

increases the strength of myocardial contraction. Digoxin also decreases automaticity and 

prolongs electrical conduction through the AV node. 

Indications 

Digoxin is used as maintenance therapy for symptom control in patients with heart failure to 

increase myocardial contractility, stroke volume, and cardiac output. It also is used to control the 

ventricular rate with atrial fibrillation or atrial flutter by slowing AV nodal conduction. 

Note: For initial ventricular rate control in atrial fibrillation, IV calcium channel blockers and 

beta-blockers are used before digoxin due to the length of time digoxin takes to produce a 

slowing of the ventricular rate. 


Digoxin has a very narrow therapeutic range and toxicity can develop rapidly. Symptoms of 

digoxin toxicity include nausea, vomiting, diarrhea, visual disturbances, and changes in mental 

status and level of consciousness. Toxicity also causes a wide variety of dysrhythmias, including 

heart blocks, junctional rhythms, and ventricular dysrhythmias. Toxicity is precipitated by 

hypokalemia, hyperkalemia, and hypomagnesemia. Many patients taking digoxin for heart 

failure also take diuretics that can deplete potassium and lead to toxicity. Be sure to provide 

patient education concerning the need to take any prescribed potassium supplements if the 

patient is on diuretic therapy. 

Digoxin is potentiated in such drugs as amiodarone, calcium channel blockers, and quinidine. In 

patients taking these drugs, digoxin should be used with caution and the dose might be reduced 

by 50%. Overdose of digoxin can be treated by the drug Digibind ® . 


Digoxin should be avoided with those patients with sick sinus syndrome or significant 

atrioventricular nodal heart blocks such as complete heart block and second degree AV 

block. 

Dobutamine 

Dobutamine (Dobutrex) is a synthetic catecholamine. It is a potent β 1 agonist to increase 

myocardial contractility and cardiac output. It is also a mild alpha agonist; however, the alpha 

effects are counteracted by the more potent β 2 properties, resulting in a mild vasodilation effect. 

This vasodilation will decrease preload and afterload with a beneficial effect on myocardial 

oxygen supply and demand. At doses of 2–20 mcg/kg/min, it has only a minimal effect on the 

heart rate. By increasing the cardiac output in the presence of mild vasodilation, it will increase 

coronary, renal and mesenteric perfusion. 



Indications 

Dobutamine is used to increase myocardial contractility and cardiac output in patients with left 

ventricular systolic dysfunction. By increasing cardiac output, dobutamine may result in an 

increase in arterial blood pressure. It is used concomitantly with volume loading in the presence 

of right ventricular myocardial infarction. It is commonly used with moderate dose dopamine (5- 

10 mcg/kg/minute) to increase blood pressure and enhance organ perfusion rather than using 

higher doses of dopamine and risking the adverse effects of dopamine. 


Dobutamine may cause headache, nausea, tremors, and hypokalemia. Remember that 

hypokalemia may increase ventricular irritability and precipitate digoxin toxicity, so patients 

receiving dobutamine should be monitored for hypokalemia. While dobutamine may induce 

tachydysrhythmias and myocardial ischemia, it does so to a much lower extent than other 

catecholamines. 

Phosphodiesterase (PDE) Inhibitors 

PDE’s inhibit the breakdown of cyclic AMP (cAMP) in cardiac and peripheral vascular smooth 

muscle, resulting in potent inotropic effects while dilating both arteries and veins. The net effect 

is similar to dobutamine. By increasing contractility and causing 


vasodilation, the PDE inhibitors reduce preload and afterload and 

thus decrease myocardial oxygen demand. 

milrinone (Primacor) 

Note: Since is rarely used, our discussion will focus on inamrinone (Inocor) 

milrinone. Inamrinone is seldom used due its significant problems amrinone 

with thrombocytopenia. 

Indications 

PDE inhibitors are used for patients with heart failure or systolic dysfunction cardiomyopathy. 

These agents are more effective in heart failure and cardiomyopathy than they are in the presence 

of ischemic heart disease. 


Due to the potent vasodilation properties, hypotension can occur. Likewise, an increase in 

myocardial irritability may occur inducing both supraventricular and ventricular dysrhythmias. 

Although, Milrinone may cause a mild thrombocytopenia, the incidence is far lower than with 

inamrinone. Milrinone may also cause mild to moderate headaches. 



Isoproterenol 

Sometimes called the “cardiac whip”, Isopreterenol (Isuprel) is a potent beta-adrenergic agonist 

with essentially no alpha adrenergic activity. Isopreterenol produces large increases in 

myocardial contractility, automaticity and conductivity. These actions profoundly increase 

myocardial oxygen demand and increase the risk of myocardial ischemia, myocardial infarction, 

and dysrhythmias. Because of its severe side effect profile Isopreterenol is now used only for 

very specific indications, most commonly in cardiac transplantation. Because it is used so rarely, 

Isopreterenol will not be discussed further in this packet. For further information please refer to 

Lexicomp and Micromedex. 

Sodium Bicarbonate 

Sodium bicarbonate is used as a buffering agent in patients with a preexisting metabolic acidosis. 

When bicarbonate combines with an acid, it forms carbonic acid, which usually dissociates to 

water and carbon dioxide. In the presence of inadequate respiratory function (when carbon 

dioxide is not rapidly cleared from the system) carbonic acid does not dissociate to carbon 

dioxide and water. Instead, it remains carbonic acid, which can lead to an intracellular acidosis 

and result in a decrease in myocardial contractility. 

In general, the administration of sodium bicarbonate during a cardiac arrest situation is 

associated with poor resuscitation outcomes. For this reason, sodium bicarbonate is no longer 

routinely given as part of resuscitation efforts. 

Indications 

Sodium bicarbonate is indicated for several specific causes of pulseless electrical activity or 

asystole within ACLS protocols. It is given to patients with a preexisting metabolic acidosis such 

as patients in renal failure or diabetic ketoacidosis. However, it is not given to patients in 

respiratory acidosis. It can also be given to patients with hyperkalemia or those who have 

overdosed on tricyclic antidepressants or phenobarbital. A continuous infusion of sodium 

bicarbonate given immediately prior to and post procedure has been shown to reduce the 

incidence of contrast-induced nephropathy for patients undergoing cardiac catheterization, 

computed tomography (CT), diagnostic or therapeutic arteriography, or transjugular intrahepatic 

portal systemic shunt (TIPS) placement. 


Sodium bicarbonate can lead to metabolic alkalosis if too much is administered. Because of the 

high sodium content, it may cause hypernatremia and increase serum osmolality, resulting in 

massive diuresis and cellular dehydration. 




1) Choose the signs and symptoms of digoxin toxicity? 

a) Nausea, vomiting, diarrhea 

b) Heart blocks, junctional rhythms, ventricular dysrhythmias 

c) Visual disturbances and changes in mental status 

d) All of the above 

2) Which of the following is an indication for the administration of sodium bicarbonate? 

a) Hypokalemia 

b) Tricyclic antidepressant overdose 

c) Respiratory acidosis 

d) Asystole 

3) You are caring for a 71-year old male patient in heart failure. Which class of drugs is 

used to increase contractility? 

a) Beta blockade 

b) Calcium channel blocker 

c) Positive inotrope 

d) Negative inotrope 

4) Name a drug that has potent 1 agonist properties and is indicated for treatment of 

left ventricular systolic dysfuntion. 

_______________________ What is the usual starting dose? _____________ 

5) Stimulation of the dopaminergic receptors will cause which effect? 

a) Peripheral vasoconstriction 

b) Renal and mesenteric vasodilation 

c) Bronchodilation 

d) Bronchoconstriction 

6) Choose the answer that best states the current ACLS Vasopressin dosage: 

a) 80 units 

b) 65 units 

c) 40 units 

d) 20 units 

7) Identify a sympathomimetic drug that is used primarily as an alpha agonist. 

___________________________________ 




1. d 

2. b 

3. c 

4. Dobutamine / 5mcg/kg/min 

5 b 

6. C 

7. Phenylephrine (Neo-Synephrine) 



packet. 



Fibrinolytic Agents 

Fibrinolytic agents activate plasminogen to form plasmin. Plasmin is a fibrinolytic enzyme that 

digests or dissolves fibrin clots. The most commonly used fibrinolytics include tissue 

plasminogen activator (tPa, activase, alteplase, and Retavase 

(reteplase r-PA) and TNKase (tenecteplase). Alteplase (tPA) and Examples of Drugs: 

reteplase (r-PA) are fibrin-selective agents, meaning that they act 

tPA, Activase, alteplase), 

primarily on plasminogen that is bound in blood clots. 

Tenecteplase has an enhanced specificity for fibrin and is highly Retavase (reteplase, r-PA) 

clot selective, resulting in less degradation of circulating clotting TNKase (tenecteplase). 

factors in comparison to other agents. All three agents have 

shown similar efficacy. 

Indications 

All of the fibrinolytic agents are indicated in the management of acute myocardial infarction. 

tPA is also approved for use in the management of acute stroke and in the management of acute 

peripheral vascular thrombosis. Fibrinolytics may also be used in the emergency management of 

acute pulmonary embolism. 


Dosage and administration of fibrinolytics vary depending on the indication for which they are 

being used and institutional protocols. In all cases they are to be mixed in normal saline or D 5 W. 

They must not be mixed in bacteriostatic preparations. They also should be prepared gently to 

avoid foaming and should be gently swirled, not shaken. 

When used for acute myocardial infarction, tPA (Activase, Alteplase) the dosage is based on 

weight with a total maximum dose of 100mg. For patient’s >67 kg an intravenous bolus dose of 

15 mg is given over 1-2 minutes, then 50 mg infused over 30 minutes, followed by 35 mg over 

the remaining hour. For patient’s < 67 kg, a 15 mg intravenous bolus is given, followed by 0.75 

mg/kg infused over the next 30 minutes not to exceed 50 mg, and then 0.50 mg/kg over the next 

60 minutes not to exceed 35 mg. 

Reteplase (r-PA) is generally administered as an initial 10 unit intravenous bolus over two 

minutes, with an additional 10 units as an intravenous bolus given 30 minutes following the 

initial bolus. Reteplase (r-PA) has the advantage of reducing the nursing time involved in 

administration since it requires no mixing or preparation, is not weight based, and there is no 

continuous intravenous infusion to be monitored. 

TNKase (tenecteplase) is provided in a kit containing a vial with 50 mg TNKase and sterile 

water with a needleless injection system. It is given as a single IV push bolus over 5 seconds, 

with the dose based on the patient’s weight. The total dose should not exceed 50 mg. 


All fibrinolytic agents may cause bleeding from puncture sites, surgical sites, and areas of injury. 

They also may result in intracranial hemorrhage leading to death. The risk of bleeding remains 

for several hours to several days following administration. 



The American College of Cardiology/American Heart Association Guidelines for the 

Management of Patients with ST-Elevation MI guidelines list the absolute and relative 

contraindications of fibrinolytic therapy. These are viewed as advisory for clinical decision 

making and may not be all-inclusive. 

NOTE: See package insert or institutional guidelines for more information, as well as the 

ACC/AHA Guidelines for the Management of Patients with ST Elevation Myocardial Infarction 

(updated 7/1/04) via the ACC website as listed in the References section of this SLP. 

Absolute contraindications to the use of fibrinolytics include: 

 

 

 

 

 

 

 

 

ANY HISTORY OF INTRACRANIAL HEMORRHAGE 

Known malignant intracranial neoplasm (primary or metastatic) 

Known structural cerebral vascular lesion (e.g., AVM) 

Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours 

Active internal bleeding or bleeding diathesis (excluding menses) 

Suspected aortic dissection 

Acute pericarditis 

Significant closed head or facial trauma within 3 months 

Relative contraindications must be weighed against potential benefits and include: 

Severe uncontrolled hypertension (>180/110) or history of chronic severe 

hypertension 

History of prior ischemic stroke greater than 3 months, dementia, or known 

intracranial pathology not covered in contraindications 

Pregnancy 

Active peptic ulcer or recent internal bleeding within the previous 2-4 weeks 

Non-compressible vascular punctures 

Current use of anticoagulants, the higher the INR, the higher the risk of bleeding 

Traumatic or prolonged (greater than 10 minutes) CPR or major surgery with 

the previous 3 weeks 

For streptokinase/anistreplase: Prior exposure ( more than 5 days) or prior 

allergic reaction to these agents 

All patients are to be monitored closely for signs of bleeding, including changes in neurological 

status, abdominal pain or rigidity, or hypotension. When used in the management of acute 

myocardial infarction, the patient may experience chest pain or dysrhythmias when the coronary 

artery opens and the supply of oxygenated blood to the myocardium is restored (reperfusion). It 

is vital not to stop the administration of the fibrinolytic agent due to reperfusion symptoms. If 

needed, symptoms are to be managed with morphine and antidysrhythmics. 



Platelet Inhibitors 

IIb/IIIa GP Platelet Inhibitors 

Platelet inhibitors bind to the platelet receptor site named the glycoprotein IIb/IIIa site. These 

receptor sites function at the end of final common pathway to block the binding of fibrinogen 

and other components in the clotting cascade. Consequently, this action inhibits platelet 

aggregation and blood clotting. Drugs in this class include Reopro (abciximab), Aggrastat 

(tirofiban), and Integrilin (eptifibatide). Administration of these agents can result in reducing 

refractory myocardial ischemia, myocardial infarction, and mortality. Recent research indicates a 

significant decrease in complications and mortality from ischemic stroke, even when 

administered up to 24 hours following the onset of symptoms. 

Indications 

Reopro, Aggrastat, and Integrilin are indicated in the treatment of refractory unstable angina, and 

as an adjunct to percutaneous coronary interventions (PCI), such as angioplasty an planned 

within 24 hours. These agents should not be used together and need to be used cautiously with 

other drugs that effect clotting. It is important to note that all of these agents have been 

administered in clinical trials with aspirin, clopidogrel (Plavix), unfractionated heparin and 

enoxaparin (Lovenox), and bivalirudin (Angiomax). 


Please consult Lexi-Comp, Micromedex, and PDR for dosage administration and usage. Please 

contact a pharmacist at your facility for further information. 


Also refer to fibrinolytics for the contraindications of GP IIb/IIIa inhibitors. 

Patients are to be monitored closely for signs of bleeding, changes in neurological status, 

abdominal pain or rigidity, and hypotension. A platelet assay count should be monitored daily 

during therapy. One must obtain a platelet count within 4 hours of the bolus therapy. 

In addition, Reopro is a monoclonal antibody derivative, meaning it has the potential to cause 

allergic and anaphylactic reactions if the patient has had this drug in the past. 

Platelet Aggregation Inhibitors 

These drugs, include Plavix (clopidrogrel) and Ticlid (ticlopidine), work by modifying the 

platelet membrane, to block the ADP pathway to prevent platelet aggregation and prolong 

bleeding time. 

Aspirin, another antiplatelet agent, does not work through the ADP pathway. Aspirin irreversibly 

inactivates the COX-1 enzyme in platelets preventing the formation of thromboxane A 2 (a 

platelet aggregating substance). 

The effect of all of these agents is irreversible for the life of the platelets modified. 

Consequently, platelet function and bleeding time may take up to 2 weeks following 

discontinuation of the drug to return to normal. Because ticlopidine can cause life-threatening 

hematological reactions including neutropenia, thrombocytopenia, thrombotic thrombocytopenic 

purpura (TTP), agranulocytosis, and aplastic anemia, its use is generally reserved for patients 



who are unable to take clopidrogrel or aspirin, or for those in whom other agents have been 

ineffective. 

Indications 

Platelet aggregation inhibitors are used to reduce the risk of thrombotic events such as 

myocardial infarction and stroke in patients with previously diagnosed atherosclerotic vascular 

disease. They are also used with patients with acute coronary syndromes who are undergoing 

PCI. 

When a GPIIb/IIIa inhibitor is used, aspirin and/or clopidogrel become part of the standard 

adjunct therapy, along with heparin or enoxaparin (Lovenox). The clinical indications for aspirin 

and clopidogrel continue to expand because platelets play such an important role in all types of 

vascular disease. For example, numerous studies have proven the efficacy with acute onset MI, 

stable and unstable angina, cath lab procedures, and non-hemorrhagic strokes. 


Platelet aggregation inhibitors should not be used in any patients with active pathological 

bleeding such as peptic ulcer or intracranial hemorrhage. They are to be used with caution in 

patients who are at risk of increased bleeding due to impaired liver function, trauma or surgery. 

They should also be discontinued 7-14 days prior to elective surgery. Furthermore, drugs such as 

aspirin, heparin, warfarin, and NSAIDs that may interfere with hemostasis, are administered with 

extreme caution to patients taking ticlopidine or clopidrogrel. 

Adverse reactions include rash, nausea, vomiting, diarrhea, constipation, and abdominal pain. 

These reactions have resulted in discontinuing the drug in approximately 3% of patients taking 

clopidrogrel and 21% of patients taking ticlopidine. Blood dyscrasias as previously listed, may 

occur with either of these agents; the incidence is approximately 1 out of every 2000-4000 

patients taking ticlopidine and approximately 1 out of every 250,000 of those taking 

clopidrogrel. Because of its increased risk for adverse reactions, ticlopidine is rarely used & is 

usually given to patients unable to take other agents or in those for whom other agents are 

ineffective. 

In addition to the bleeding precautions for aspirin, there may also be some notable GI distress or 

bleeding. In such cases an enteric coated aspirin preparation may be suitable. 



Direct Thrombin Inhibitors 

These drugs specifically target and bind to sites on thrombin, effectively inhibiting the 

conversion of fibrinogen to fibrin and interrupting the formation of the hemostatic plug. 

Thrombin also activates platelets. Lepirudin is a derivative of 

hirudin (the first direct thrombin inhibitor) and is a very potent and Examples of Drugs: 

specific inhibitor of thrombin. Lepirudin slowly forms a reversible 

Angiomax (bivalirudin) 

complex with two sites on the thrombin molecule. Whereas, 

bivalirudin, which is a synthetic compound, binds at two sites on the Refludan (lepirudin) 

thrombin molecule but only acts transiently at one site. Argatroban Argatroban 

binds reversibly to thrombin. 

Angiomax ® (bivalirudin) 

Indications 

Bivalirudin is indicated for patients with unstable angina undergoing percutaneous transluminal 

coronary angioplasty. Angiomax is also recommended to be used in patients with a history of 

heparin induced thrombocytopenia. 


The major adverse effects associated with this drug are bleeding and bleeding-related 

complications, including intracranial bleeding, retroperitoneal bleeding, and bleeding or oozing 

from venous access sites. Other adverse events that may occur include back pain, pain, nausea, 

headache, and hypotension. 

Patients receiving therapy with bivalirudin need their renal function evaluated prior to 

administration of and upon discontinuation of the infusion. Patients should be monitored closely 

for any signs of bleeding, including oozing or bleeding from venous access sites or the presence 

of blood in urine or stool. 

Refludan (lepirudin) 

Indications 

It is indicated for anticoagulation in patients with heparin-induced thrombocytopenia (HIT) and 

associated thromboembolic disease in order to prevent further thromboembolic complications. 



complications, including intracranial bleeding, retroperitoneal bleeding, and bleeding or oozing 

from venous access sites. Other adverse events that may occur include the rare but serious effects 

of anaphylaxis and respiratory effects (bronchospasm, stridor, dyspnea, and cough). 



Argatroban 

Indications 

Argatroban is indicated for prophylaxis or treatment of thrombosis in adults with heparininduced 

thrombocytopenia (HIT) and as adjunct to percutaneous coronary intervention (PCI) in 

patients who have or are at risk of thrombosis associated with HIT. 


Dosing is weight based and is administered as a continuous infusion starting at 2 mcg/kg/min. 

No loading dose is required and there are no adjustments for patients with renal impairment. 

Doses are reduced for patients with moderate to severe hepatic impairment (0.5 mcg/kg/min). 

The degree of anticoagulation is monitored by measuring the aPTT. An aPTT 1.5-3 times the 

normal value is considered therapeutic. 



complications. Because of a drug-laboratory interaction, argatroban can falsely elevate the INR. 

For an argatroban infusion rate of 2 mcg/kg/min, warfarin (Coumadin) is to be 

discontinued when the INR on combined therapy exceeds 4. 

Next, the INR is to be determined during warfarin monotherapy 4-6 hours after the 

discontinuation of argatroban infusion. If the INR is below the desired range, the physician 

should be contacted and argatroban resumed. 




1. You are screening your new admission for possible fibrinolytic therapy. State 2 

absolute contraindications of fibrinolytic therapy. 

______________________ 

______________________ 

2. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors, patients require 

close monitoring of: 

a) _____________________________________________________________ 

b) _____________________________________________________________ 

c) _____________________________________________________________ 

3. An acute MI patient receiving fibrinolytics may experience 

______________________ or __________________________ as the supply of 

oxygenated blood is restored. 

4. ________________________________________________ agents block the final 

common pathway for platelet aggregation. 

5. Platelet function may take up to _____________ weeks to return to normal 

following the discontinuation of clopidrogel or ticlopidine. 

6. The GP IIb/IIIa platelet inhibitors named _________________, ________________, 

and ___________________, are indicated as an adjunct to __________________ 

within _____ hours. 

7. Platelet Aggregations inhibitors are used for the following. (Please state your answer 

below). 

____________________________________________________________________ 

8. Which of the following drug category bind to sites on thrombin to inhibit the 

conversion of fibrinogen to fibrin. 

a) Fibrinolytics 

b) Platelet Inhibitors 

c) Direct Thrombin Inhibitor 

d) Direct Fibrin Inhibitor 




1. Name two absolute contraindications of fibrinolytics: 

Absolute contraindications to the use of fibrinolytics include: 

 

 

 

 

 

 

 

 

ANY HISTORY OF INTRACRANIAL HEMORRHAGE 

Known malignant intracranial neoplasm (primary or metastatic) 

Known structural cerebral vascular lesion (e.g., AVM) 

Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 

3 hours 

Active internal bleeding or bleeding diathesis (excluding menses) 

Suspected aortic dissection 

Acute pericarditis 

Significant closed head or facial trauma within 3 months 

2. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors, patients require 

close monitoring of: 

bleeding, changes in neurological status, abdominal pain/rigidity, 

hypotension 

3. An acute MI patient receiving fibrinolytics may experience 

______________________ or __________________________ as the supply of 

oxygenated blood is restored. 

dysrhythmias, chest pain 

4. ________________________________________________ inhibitors block the final 

common pathway for platelet aggregation. 

GPIIb/IIIa platelet 

5. Platelet function may take up to _____________ weeks to return to normal 

following the discontinuation of clopidrogel or ticlopidine. 

two weeks 

6. The GP IIb/IIIa platelet inhibitors named ______________, ______________, and 

______________, are indicated as an adjunct to _______________ within _____ hours. 

Reopro, Integrilin, Aggrastat, PCI, 24 hours 



7. Platelet Aggregation Inhibitors are used for the following: Reduce risk of 

thrombotic events such as MI and stroke, PVD. They are also used with 

patient with ACS who undergo PCI. 

8. Which of the following drug category bind to sites on thrombin to inhibit the 

conversion of fibrinogen to fibrin. 

C. Direct Thrombin Inhibitor 



Diuretic Agents 

Diuretics are defined as any drug that increases urine flow by altering the physiologic renal 

mechanisms that form urine to promote diuresis. Diuretics are divided into classes based on how 

they effect each of the different sections of the nephron. For example, one class acts on the loop 

of Henle and another on the distal nephron. Also, 

the degree of potency varies with the classes; for 

example, some are more potent than others resulting 

in a greater excretion of electrolytes and water, 

while others cause potassium to be retained. 

Indications for all classes 

The main indications for diuretics are hypertension, 

management of heart failure, relief of heart failure 

symptoms, reduction of edema due to renal 

dysfunction, corticosteroids, estrogen, or 

vasodilator therapy, and reduction of acites due to 

cirrhosis. 

Loop Diuretics 

The loop of Henle is a portion of the nephron 

responsible for the concentration or dilution of urine 

by means of the tubular reabsorption process. This 

is achieved using the sodium/potassium/chloride 

transport system. Consequently, loop diuretics 

inhibit this transport system to increase the 

elimination of sodium and water in the urine. 


Loop: 

furosemide (Lasix) 

bumetanide (Bumex), 

torsemide (Demadex) 

ethacrynic Acid (Edecrin) 

Thiazide: 

hydrochlorothiazide 

Lozol (indapamide), 

Diuril (chlorothiazide) 

Zaroxolyn (metolazone) 

Potassium sparing: 

triamterene (Dyrenium) 

amiloride spironolactone (Aldactone ) 

eplerenone (Inspra) 

Combination: 

HCTZ and triamterene (Maxzide), 

HCTZ and spironolactone (Aldactazide) 

HCTZ and amiloride (Moduretic) 

The loop diuretics are named: furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), 

and ethacrynic Acid (Edecrin). They are known for their rapid onset of action and venodilator 

effects, as well as their potency in the presence of normal or abnormal renal function. Edecrin® 

is rarely used so it may be difficult to obtain. Edecrin is the most ototoxic of the loop diuretics. 


It is important to remember that large amounts of excreted urine may lead to hypotension and 

hypovolemia. Moreover, the depletion of sodium, potassium, calcium, or magnesium may lead to 

metabolic alkalosis, myocardial irritability, and ventricular dysrhythmias. Specifically, potassium 

replacement therapy may be necessary. Patient teaching must include education on a potassium 

rich diet. 

Loop diuretics may elevate the blood sugar in diabetics, and because these agents are ototoxic, 

there is an increased risk of tinnitus and deafness when administered too rapidly or in doses 

exceeding the recommended daily maximum. Loop diuretics increase serum uric acid levels and 

may precipitate gout in susceptible patients. It is also important to note that since Lasix, 

Demadex, and Bumex are sulfonamide derivatives, patients with sulfa allergies may demonstrate 

a cross-sensitivity. 



It is recommended that before administering to a patient with sulfa allergies, the nurse needs to 

check with the pharmacy or the prescriber. 

Thiazide Diuretics 

Thiazide diuretics main actions are to inhibit the transportation of sodium and chloride in the 

distal nephron. This action results in an increased loss of sodium, chloride, and water in the 

urine. The most commonly used thiazide agents are hydrochlorothiazide, Lozol (indapamide), 

Diuril (chlorothiazide), and Zaroxolyn (metolazone). 

Indications 

Thiazide diuretics are indicated for the treatment and management of hypertension. The most 

recent national guidelines for hypertension management (JNC 7) recommends that thiazide 

diuretics be used as initial monotherapy for the treatment of uncomplicated hypertension in most 

patients, either alone or in combination with other antihypertensives. They can be used alone to 

manage mild edema in patients with heart failure or in combination with loop diuretics to 

manage more severe edema. Thiazide diuretics are also used when a longer (versus shorter acting 

loop diuretic) duration of action is needed, or for fluid retention from premenstrual syndrome, 

estrogen, or corticosteroid therapy. Thiazide diuretics are chosen in the treatment of diabetes 

insipidus. 



hypovolemia. The depletion of potassium may lead to metabolic alkalosis, myocardial 

irritability, and ventricular dysrhythmias. Likewise, since thiazide diuretics tend to retain 

calcium, there is a mild risk of hypercalcemia. 

Thiazide diuretics may increase total blood cholesterol and like loop diuretics may elevate blood 

sugar in diabetics. They can also decrease excretion of uric acid resulting in an increasing risk 

for gout attacks in patients with this disease. Because all diuretic agents can be ototoxic, there is 

an increased risk of tinnitus and deafness when administered too rapidly or in doses exceeding 

the recommended daily maximum. 

Potassium-Sparing Diuretics 

Currently, there are two groups of potassium-sparing diuretics that act at the distal portion of the 

nephron. The first group, triamterene (Dyrenium) and amiloride, block the sodium channels to 

interfere with sodium reabsorption in the distal and collecting tubules of the nephron. The 

advantage is that sodium loss is achieved without a major loss of potassium or magnesium. 

The other group consists of spironolactone (Aldactone) and eplerenone (Inspra), which inhibit 

the effects of aldosterone. These agents will be discussed separately. 

Commonly, potassium diuretics are given in combination with hydrochlorothiazide. Products 

include: HCTZ and triamterene (Maxzide), HCTZ and spironolactone (Aldactazide), and HCTZ 

and amiloride (Moduretic). 



Indications 

For patients intolerant of oral potassium supplements, this category of diuretics eliminates the 

need for gastric-irritating potassium supplementation since they do not cause potassium 

excretion. 



hypovolemia. The depletion of sodium or an excess retention of potassium may lead to metabolic 

alkalosis, myocardial irritability, and ventricular dysrhythmias. Potassium sparing diuretics may 

cause the levels of some drugs such as digoxin, to be increased. Concurrent use with ACEinhibitors 

and non-steroidal anti-inflammatory agents may cause hyperkalemia. Patient teaching 

includes information about avoiding potassium rich foods or vitamin supplements containing 

potassium. 

Aldosterone Antagonists 

Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. Aldosterone is 

an endogenous steroid that acts on the kidney to retain sodium and water, while excreting 

potassium in the urine. Spironolactone binds to the aldosterone receptor to prevent the retention 

of sodium and water and the excretion of potassium. Eplerenone shares the same pharmacologic 

properties as spironolactone; however, it is considered a selective aldosterone receptor 

antagonist, whereas spironolactone is non-selective. 

Indications 

Both of these agents are indicated for the management of hypertension either as monotherapy or 

in combination with other antihypertensives. These drugs are also important heart failure 

therapies. Studies of patients with severe heart failure demonstrate that spironolactone added to 

conventional therapy (ACE-inhibitors, digoxin, loop diuretics) reduced hospital admissions and 

mortality. In other studies, eplerenone was shown to improve survival in hemodynamically stable 

patients with left ventricular dysfunction who demonstrated clinical evidence of heart failure 

following AMI. 

Spironolactone is frequently used to counter the effects of elevated aldosterone in conditions 

such as heart failure, cirrhosis, and nephrotic syndrome. It may also counteract the rise of 

angiotension II and aldosterone. 


Both spironolactone and eplerenone are administered orally once daily. 


Because spironolactone is similar to steroids, it has the potential to produce some of the same 

adverse effects. The most common is GI distress. In men, there also may be an increased risk of 

gynecomastia. These effects are seen less often with eplerenone. Hyperkalemia can occur with 

both agents and the incidence is increased in patients on potassium supplements, and drugs that 

cause potassium retention (i.e., ACE-inhibitors, ARBs, NSAIDS). 




Insert either TRUE or FALSE for each statement 

1. __________ Diuretics can be divided into three major classes. Due to the 

inherent properties of this class, loop diuretics do not require potassium 

supplementation. 

2. __________ Some examples of drugs known as “potassium-sparing” diuretics 

are triamterene, eplerenone, and spironolactone. 

3. __________ When comparing all the classifications of diuretics, thiazide 

diuretics are the most likely to cause hyperkalemia and hypercalcemia. 

4. __________ Drugs such as NSAIDS may be co-administered with “potassiumsparing” 

diuretics without the risk of adverse consequences. 

5. __________ Patients with a documented adverse reaction to sulfa drugs 

may not be able to safely receive loop diuretics. 

6. __________ Aldosterone acts on the kidney to retain sodium and water and 

excrete potassium in the urine. 

7. __________ Thiazide diuretics have a much shorter duration of action than 

the other diuretic classes. 

8. __________ Loop diuretics are the only class of diuretics that may cause 

ototoxicity. 

9. __________ It is important to emphasize to the patient receiving 

spironolactone to eat potassium rich foods daily. 

10. __________ Thiazide diuretics may increase total serum cholesterol. 




1. F 

2. T 

3. F 

4. F 

5. T 

6. T 

7. F 

8. F 

9. F 

10. T 



Summary 

This completes the content of the Introduction to CV Pharmacology self-learning packet. Upon 

successful completion of this packet, the participant should now be familiar enough with the 

content presented to do the following: 

Explain how cardiovascular drugs influence the cardiovascular system 

Describe the role oxygen has in the cardiovascular patient 

List clinical indications for using cardiovascular pharmaceutical agents 

Identify the mechanisms of action for each drug or class of drug 

Describe side effects and appropriate precautions, contraindications, or special considerations of 

each drug class 

State patient teaching information 

As previously stated, this packet is designed to introduce vital information regarding some of the 

most commonly administered cardiovascular drugs. It is not to be mistaken as a complete 

drug/nursing reference source. One must look up the drugs for complete information and nursing 

considerations. 

Remember that when mentioned, the mixing and administering of these drugs are general 

guidelines. Certain units or institutions may have specific protocols they follow. If a nurse 

receives the order “administer per protocol,” the nurse needs to confirm the drug and dose. 

A number of the IV infusions may be concentrated if the patient receiving them is on a fluid 

restriction. Many drugs may also require a dedicated IV infusion line for continuous or IV push 

administration. 

Some physicians may have preferences that are not covered in this packet. For that reason, be 

mindful of the dosing guidelines that have been presented, as well as the physician’s orders and 

institutional or unit preferences. 



Cardiovascular Pharmacology Post Test 

Instructions: Use the answer sheet provided on the previous page. 

1. Which of the following antiarrhythmics agents is known to prolong the QTI, thus requiring 

careful monitoring of both the QTI and the QTc? 

A. Lidocaine, Mexitil 

B. Dofetilide, Sotalol 

C. Diltiazam, Calan 

D. Metropolol, Breviblock 

2. You are caring for a patient in recurrent pulseless ventricular tachycardia who is receiving the 

initial bolus of Procainamide. Which of the following is NOT a reason to stop the initial bolus 

dose of this drug? 

A. The QRS widens by 50% 

B. The dysrhythmia is terminated 

C. You have administered a dose of 17 mg/kg 

D. The QT interval is 0.36 

3. Your patient has been diagnosed with HIT (Heparin induced thrombocytopenia) Identify the 

drug that is the best choice to prevent further thromboembolic complications. 

A. Refluden 

B. Retavase 

C. Reopro 

D. Plavix 

4. You are caring for a 40-year old male following an acute anterior myocardial infarction. Select 

the desired effect of giving this patient a Class II antidysrhythmic drug. 

A. Increasing myocardial oxygen demand 

B. Blocking the beta-2 receptors 

C. Decreasing myocardial work load 

D. Blocking the conversion of angiotensin I to angiotensin II 



5. Which of the following effects may occur after administration of beta blockade therapy? 

A. Hypertension, decrease in heart rate 

B. Increase in heart rate, hypotension 

C. Bronchodilation, increase in respiratory rate 

D. Hypotension, bronchoconstriction 

6. You are caring for a 52-year old male following an anterior myocardial infarction. The monitor 

alarm alerts you that the patient's rhythm has changed to polymorphic ventricular tachycardia 

(Torsades de pointes). The patient is awake, alert, anxious, BP 100/60, HR 130. Which of the 

following pharmacologic interventions should receive your highest priority? 

A. Adenosine 

B. Amiodarone 

C. Magnesium sulfate 

D. Procainamide (pronestyl) 

7. You have just administered adenosine to a patient in SVT with a heart rate of 200. Which of the 

following if observed is an expected response? 

A. Transient, brief rapid increase of the ventricular response 

B. Brief period of asystole 

C. Brief period of ventricular standstill 

D. Suppression of ventricular ectopy 

8. Stimulation of the alpha adrenergic receptors will cause what response? 

A. Peripheral vasodilation 

B. Peripheral vasoconstriction 

C. Bronchodilation 

D. Bronchoconstriction 

9. Which of the following is an example of a high flow oxygen delivery system? 

A. Nasal cannula 

B. Venturi mask: 40-50% 

C. Nonrebreathing mask: 100% 

D. Partial rebreathing mask 



10. Beta-blockers should be administered to patients with Acute Coronary Syndrome, but extreme 

cautions needs to be given to which patient population when the drug is used. 

A. The asthma and COPD patient population 

B. Post MI patients 

C. Heart failure patients 

D. Post bypass surgery patient population 

11. Which of the following drug category may increase total blood cholersterol? 

A. Angiotensin II receptor blockers (ARBs) 

B. Direct thrombin inhibitors 

C. Platelet inhibitors 

D. Diuretics 

12. Select the statement that best reflects the current indications for Amiodarone. 

A. To manage severe cardiomyopathy that has not responded to dobutamine 

B. To treat life-threatening atrial and ventricular tachyarrhythmias 

C. To treat severe heart failure that has not responded to negative inotropics and diuretics 

D. To treat junctional dysrhythmias that have not responded to atropine 

13. Your patient is ordered to be placed on a IIb/IIIa GP Platelet inhibitor in preparation for a 

percutaneous coronary intervention. Which of the following is a contraindication to the use of 

IIb/IIIa inhibitors? 

A. Intracranial bleeding 12 months ago 

B. Surgery 10 weeks ago 

C. Non-hemorrhagic stroke 2 years ago 

D. Admission 3 weeks ago for an acute peptic ulcer bleed 

14. Which of the following is a Class III antidysrhythmic that is used for the conversion 

of recent onset atrial fibrillation to sinus rhythm? 

A. Atenolol 

B. Dofetilide 

C. Diltiazem 

D. Procainamide 


15. Which of the following is the initial antidysrhythmic drug of choice for narrow-complex 

tachycardias when it is known that the origin is supraventricular? 

A. Atropine 

B. Digoxin 

C. Diltiazem 

D. Adenosine 


16. Stimulation of β 2 adrenergic receptors will cause which of the following response? 

A. Coronary artery vasodilation 

B. Peripheral vasoconstriction 

C. Bronchodilation 

D. Bronchoconstriction 

17. Choose the drug whose action is to inhibit the parasympathetic nervous system to enhance 

automaticity of the sinus node, and increase electrical conduction through the AV node? 

A. Norepinephrine 

B. Atropine 

C. Epinephrine 

D. Adenosine 

18. Select the indication for the use of Nesiritide (Natrecor). 

A. Positive inotropic therapy for heart failure 

B. Vasopressor therapy for severe hypotension 

C. Antidysrhythmic therapy for ventricular dysrhythmias 

D. Vasodilator therapy for acutely decompensated heart failure 

19. Select the pharmacologic agent that may be used as adjunct therapy in the presence of heart 

failure due to its preload and afterload reducing effects. 

A. Calcium channel blockers 

B. Beta blockers 

C. ACE inhibitors 

D. Class III drugs 


20. In the event of extravasation of a sympathomimetic agent, select the drug used to aid in 

minimizing tissue damage. 

A. Phenylephrine (Neosynephrine) 

B. Phentolamine (Regitine) 

C. Lidocaine 

D. Epinephrine 


21. Digoxin toxicity is precipitated by which of the following factors. 

A. Hypokalemia, Hyperkalemia, Hypomagnesemia 

B. Hypermagnesemia, Hypocalcemia, Loop diurectic 

C. Thaizde diuretic, Calcium Channel Blocker 

D. Beta Blockers, Thaizde diuretic 

22. Which of the following interventions is contraindicated in a patient in sinus bradycardia (heart 

rate of 40) who is also hypotensive. 

A. A normal saline bolus of 250 ml 

B. Atropine 0.5 mg IV push 

C. Epinephrine 1mg IV push 

D. A dopamine IV infusion at (5 mcg/kg/minute) 

23. Your patient is on Primacor drip for cardiomyopathy. The primary physician orders a 

Nitroglycerin drip to be added to the patient regimen. Select the possible drug to drug 

interaction that could occur. 

A. Ventricular myocardial irritability 

B. Severe hypotension 

C. Nausea, vomiting, and a headache 

D. Second degree heart block 

24. Select the primary indications for ACE inhibitor and/or ARB therapy drugs? 

A. Hypertension and bradycardia 

B. Hypertension and heart failure 

C. Tachycardia and hypotension 

D. Heart failure and bradycardia 



25. After addressing the patient’s volume status, the systolic BP continues to remain less than 70. 

Select the drug of choice for this problem? 

A. Dopamine IV infusion @ 3 mcg/kg/min 

B. Epinephrine 1 mg IV push 

C. Phenylephrine IV push followed with boluses 

D. Norepinephrine IV infusion 

26. Select the appropriate dosage of Vasopressin for the treatment of pulseless VT or VF? 

A. Vasopressin 40 units IV push x one dose 

B. Vasopressin 4.0 units IV push x one dose 

C. Vasopressin 40 units IV push q3-5 minutes 

D. Vasopressin 40 units IV push q10 minutes 

27. Choose the diuretic that depletes potassium thus requiring patient education on the importance 

of consuming potassium rich foods. 

A. Spironolactone 

B. Eplerenone 

C. Furosemide 

D. Triamterene 

28. You received an order to discontinue clopidrogel on your post cath patient. Your new orientee 

asks you how long the patient will need to observe bleeding precautions due to altered platelet 

functioning. Your best response would be: 

A. 6 weeks 

B. 4 weeks 

C. 2 weeks 

D. 3 weeks 



29. A cancer patient is admitted to the ED with a diagnosis of an acute inferior wall myocardial 

infarction. The patient has recently been diagnoses with HIT (Heparin induced 

thrombocytopenia) from a prior treatment for a DVT. What specific drug will target and bind to 

sites on thrombin effectively inhibiting the conversion of fibrinogen to fibrin interrupting the 

formation of a clot. 

A. Heparin 

B. Lepirudin 

C. Clopidrogrel 

D. Reteplase 



References 

AEHLERT, BARBARA (2005). ECGS MADE EASY (3 RD ED.). ST. LOUIS : MOSBY 

AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. (2004). AHFS DRUG INFORMATION. 

BETHESDA MARYLAND. 

AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. (2004-2005). AHFS DRUG INFORMATION 

ESSENTIALS. BETHESDA MARYLAND. 

ANTMAN, ELLIOT M., SMITH, SYDNEY C., ET AL. (2004). ACC/AHA GUIDELINES FOR THE 

MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION— 

EXECUTIVE SUMMARY. 

CIRCULATION. 110, 588-636. RETRIEVED JULY 2, 2008 FROM 

HTTP://CIRC.AHAJOURNALS.ORG/CGI/CONTENT/FULL/110/5/588 

HAZINSKI, MARY F., FIELD, JOHN M. & GILMORE, DAVID (EDS.). (2008). HANDBOOK OF EMERGENCY 

CARDIOVASCULAR CARE. DALLAS : AMERICAN HEART ASSOCIATION. 

“Keeping Pace with Long QT”. Retrieved February 2, 2005 from http://www.long-qtsyndrome.com/ekg_readout.html 

OPIE, LIONEL H. & GERSH, BERNARD J. (2005). DRUGS FOR THE HEART (6 TH ED.). PHILADELPHIA: 

ELSEVIER- SAUNDERS 

_______________________________________ 

Drug Information Resources 

Lexi-Comp TM 

1100 Terex Rd. Hudson, OH 44236 

(877) 837-5394 Fax: (330) 656-4307 

Thomson Micromedex 

6200 South Syracuse Way, Suite 300 Greenwood Village, Colorado 80111-4740 

Toll-free: 800-525-9083 Fax: 303-486-6464 

American Society of Health-Systems Pharmacists 

AHFS DI® Essentials TM 

Customer Service Department 

7272 Wisconsin Avenue Bethesda, MD 20814 

Toll-free: 866-279-0681

Introduction to CV Pharmacology - Orlando Health

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