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Introduction to CV Pharmacology

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

CV Pharmacology

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 CHECK YOURSELF POP QUIZ............................................................................................................................33 CHECK YOURSELF POP QUIZ -ANSWERS .................................................................................................................34 VASOPRESSOR THERAPY ...................................................................................................................................35 DOPAMINE ...............................................................................................................................................................35  2010 Orlando Health, Education & Development

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CV Pharmacology 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 CHECK YOURSELF POP QUIZ............................................................................................................................42 CHECK YOURSELF POP QUIZ -ANSWERS .................................................................................................................43 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 CHECK YOURSELF POP QUIZ............................................................................................................................50 CHECK YOURSELF POP QUIZ -ANSWERS .................................................................................................................51 DIURETIC AGENTS................................................................................................................................................53 LOOP DIURETICS .....................................................................................................................................................53 THIAZIDE DIURETICS ...............................................................................................................................................54 POTASSIUM-SPARING DIURETICS ............................................................................................................................54 ALDOSTERONE ANTAGONISTS.........................................................................................................................55 CHECK YOURSELF POP QUIZ............................................................................................................................56 CHECK YOURSELF POP QUIZ -ANSWERS .................................................................................................................57 SUMMARY................................................................................................................................................................58 CARDIOVASCULAR PHARMACOLOGY POST TEST....................................................................................59 REFERENCES ..........................................................................................................................................................66 DRUG INFORMATION RESOURCES ............................................................................................................................66

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CV Pharmacology 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. Select “SLP” under type of test. Describe the normal physiological actions of the cardiovascular system. 3.0 contact hours. and you will be asked to retake the posttest. and to provide basic guidelines for safe administration by licensed healthcare providers. This Introduction to CV Pharmacology SLP is not designed to be an all-inclusive reference or to © 2010 Orlando Health. FL 32806 For Orlando Health Team Members: Please complete testing via Online Testing Center. 7. 4. contraindications. the participant should be able to: 1. You will be notified if you do not pass. or special considerations of each drug class. Describe side effects and appropriate precautions. Use your Orlando Health Network Login and password. 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. Return to: Orlando Health. List the clinical indications for using cardiovascular pharmaceutical agents. MP14. 1414 Kuhl Ave. State the appropriate patient teaching information. Orlando. 5. broken down by classification. Be sure to complete all the information at the top of the answer sheet. Instructions In order to receive 4. Explain how cardiovascular drugs influence the cardiovascular system. Identify the mechanisms of action for each drug or class of drug. 2. Describe the role oxygen has in the cardiovascular patient. It is important to understand that although these drugs affect the cardiovascular system their use is not exclusive to cardiac departments. choose correct SLP Title. Education & Development. Introduction This self-learning packet (SLP) is designed to introduce basic information regarding some of the most commonly administered cardiovascular drugs. Objectives Upon completion of this self-learning packet. Education & Development 3 . 6. Payroll authorization is required to download test. Log on to: SWIFT Departments E-Learning Testing Center.

meaning they are used interchangeably to indicate rhythms other than normal sinus rhythms. and the PDR. © 2010 Orlando Health. Please refer to current ACLS references for these guidelines. Education & Development 4 .CV Pharmacology replace current drug references. actions and interactions. A Note about ACLS This SLP is not designed to include current ACLS algorithms. This SLP does not indorse any specific product. Go to SWIFT for links to LexiComp and Micromedex. the web based links and reference materials listed may be very helpful to you. it is vital that the healthcare provider understand the indications. In order to achieve the best patient outcomes. Please note that in current practice the terms arrhythmia and dysrhythmia are synonymous. proper administration. 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. Please refer to current comprehensive reference materials readily available for all healthcare providers such as LexiComp. and potential adverse effects of these pharmacologic agents. however. Micromedex. The vast majority of patients who receive care for cardiovascular disorders require the administration of multiple drugs during their hospital stay.

a slowing of electrical conduction through the AV node. The conduction can be altered by factors such as sympathetic or parasympathetic stimulation. Conductivity is the ability of the cardiac cell to receive an electrical stimulus and conduct the impulse to another cardiac cell. Sympathetic stimulation (the “fight or flight” response) results in peripheral vasoconstriction. Some drugs are known as sympathomimetics because they mime or mimic the actions of the sympathetic nervous system. These fibers are known as cholinergic fibers in reference to their relationship to acetylcholine. such as from a chemical. Education & Development 5 . The fibers of the sympathetic nervous system affect the organs and tissues in which they are located in by releasing norepinephrine (noradrenalin). they have a pronounced effect on the atria. including the cardiovascular system. or electrical source. The SNS and the PNS normally work together to help maintain homeostasis in the body. an increase in heart rate. While fibers of the parasympathetic nervous system do exist in both the atria and the ventricles. The autonomic nervous system is composed of two branches. The fibers of the parasympathetic nervous system affect the organs and tissues that they innervate by releasing acetylcholine. and an increase in the strength with which the heart pumps blood (contractility). Contractility is the ability of the cardiac cell to contract in response to an electrical stimulus. electrolyte imbalances and medications. These fibers are known as adrenergic fibers in reference to their relationship to norepinephrine.CV Pharmacology Autonomic Cardiovascular Innervation In order to have a better understanding of how cardiovascular drugs work. 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.  2010 Orlando Health. These drugs may also be known as adrenergic agents because they have the effects that stimulate the adrenergic fibers. a brief review of how the heart and circulation are regulated by the autonomic nervous system is needed. the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). The sympathetic nervous system innervates all chambers of the heart. while causing a minimal effect on the ventricles. faster speed of electrical impulses conducted through the heart (conductivity). Excitability is the ability of the cardiac cells to respond to an external stimulus. and a mild decrease in the pumping action of the ventricles. Parasympathetic stimulation results in a decrease in heart rate. cardiac muscle damage. mechanical.

CV Pharmacology

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 αreceptors 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 (β1) and non-cardiac (β2) receptors. The β1 receptors are located within the heart. Stimulation of the β1 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 β2 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.

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CV Pharmacology

Check Yourself Pop Quiz
Match the definitions at the bottom with the terms at the top.

1. 3. 5. 7. 9.

Conductivity Contractility Norepinephrine alpha agonist 1 stimulant effects

2. 4. 6. 8. 10.

afterload alpha effect parasympathetic stimulation alpha antagonist 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.

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CV Pharmacology

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.

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In addition. They supply a more accurate concentration (%) of oxygen. and supplies oxygen at a rate of 24-40%. it is the most important drug contained in the ACLS protocols. This concentration is used even in patients with chronic lung disease (such as COPD) until the resuscitation is over. The best CPR you can provide only yields about 25-30% of the normal cardiac output.CV Pharmacology Oxygen Oxygen is present in the air all around us at a concentration of approximately 21%. Therefore the patient must be able to inhale a sufficient amount of room air along with the oxygen provided. It is also used for patients with either demonstrated or suspected hypoxemia. and partial rebreathing masks. oxygen is delivered at a concentration of approximately 100% utilizing a bagvalve-mask (BVM) device.  2010 Orlando Health. Additionally. the oxygen concentration provided to the patient may need to be reassessed and appropriately modified. but it is considered a drug. 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. While partial rebreathing masks provide an oxygen concentration of 24-60%. All tissues within the body require oxygen and will begin to suffer damage if deprived for more than several minutes. The venturi mask is the most common high flow system. since this may lead to metabolic acidosis. nonrebreathing masks. nonrebreathing masks can provide an oxygen concentration between 55-95%. Low Flow Low flow oxygen systems include nasal cannulas. Since blood flow is diminished. 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. In fact. simple face masks. other efforts will be wasted. The practice of cardiovascular medicine revolves around assuring the proper balance between oxygen supply and demand throughout the body. if efforts fail to assure an adequate oxygen supply. as the patient’s breathing pattern changes. Education & Development 9 . oxygen is used in all cases where CPR must be implemented. Regardless of any other actions taken during cardiovascular emergencies. low flow systems do NOT supply sufficient gas volume to meet the patient’s needs. Indications Supplemental oxygen is indicated for patients who are experiencing acute chest pain regardless of the cardiac cause. one way to prevent tissue damage is to increase the oxygenation of the blood flow that you are providing. Use of the Bag-Valve-Mask Devices In a cardiac arrest. Regardless of the concentration (%).

Action Potential Q MV 0 1 2 R T S ECG 0 Inside Cell 3 Cell Membrane 4 100 ↓K ↑ Na ↑ Ca 4 ↓K & ↓ Na Outside Cell  2010 Orlando Health Education & Development 10 . and the resting period is the repolarization cycle (diastole). 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. It is identified on the AP curve as phases 0. These electrical charges are a result of specific ions (sodium. 1. To understand how antidysrhythmic drugs affect the heart. one must be familiar with the action potential curve and its reflection of the cardiac cycle. The following chart briefly explains the different phases of the action potential. and is identified on the AP as the last half of phase 3 and phase 4. Relative Refractory Period – This is the vulnerable period in which a strong stimulus may produce ectopic depolarization. and calcium) that shift between the myocardial cell and the extracellular fluid via the sodium-potassium pump mechanism. In the heart.CV Pharmacology Review of Antidysrhythmics Antidysrhythmic drugs work by affecting the action potential (AP) of the myocardial cells. potassium. regardless of strength. the working period is the depolarization cycle (systole). 2. and the first half of phase 3.During this period the cells cannot respond to any stimulus. Absolute Refractory Period . This period corresponds with the onset of the QRS complex to the peak of the T-wave. The term “Refractory” is used to describe the extent to which a cell is able to respond to a stimulus. This period corresponds with the last half of the T-wave. This activity can be compared to ourselves as we work and rest. An action potential curve refers to the electrical changes in the myocardial cell during the depolarization and the repolarization cycle.

 Class I .. Potassium begins to move back into the cell. Absolute Refractory Period Relative Refractory Period Last half of T wave as it returns to isoelectric line Phase 4 Resting Phase The cell is now ready for another depolarization stimulus.Block sodium ion channel o o o Class Ia Class Ib Class Ic    Class II (beta-blockers) . Currently there are four main classes of antidysrhythmics. not the actual contraction of the heart. This peak reflects the brief period that sodium channels close. ECG Waveform QRS Absolute Refractory Period QRS Absolute Refractory Period QRS Absolute Refractory Period Phase 3 Beginning Repolarization Phase QRS and first half of T wave Absolute refractory period until midpoint of T wave. sotalol).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. antidysrhythmics are classified based on their mechanisms of action and effects on the action potential. Relative Refractory Period Keep in mind the ECG only represents electrical heart activity.Block beta receptors Class III . Calcium plays a key role in myocardial contraction. Based on these previously mentioned principles. Calcium channels open for a slow influx of calcium ions to prolong depolarization. (Example: amiodarone. antidysrhythmic drugs are designed to modify the movement of ions in the various AP phases by altering the electrophysiology of the cardiac cell.Block potassium ion channels Class IV (calcium channel blockers) . The classification system (VaughanWilliams) can assist you in recalling the actions and adverse effects. This rapid downswing marks the closure of sodium and calcium channels to prevent any further entry of sodium or calcium into the cell. then becomes relative refractory period. Based on this principle. Potassium begins exiting cells.CV Pharmacology AP Phase Phase 0 Rapid Depolarization Phase 1 Peak Phase Phase 2 Plateau Phase Response The initial upswing indicates rapid depolarization by the influx of sodium into the myocardial cell. It is also important to note that all antidysrhythmics have the potential (some worse than others) to  2010 Orlando Health Education & Development 11 . the last half of T-wave.

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. Second. Far from perfect. or the QRS interval can be subtracted from the QTI. Note: It is essential to identify drugs that prolong the QTI. it is not clear precisely how the measurement can be used to predict and prevent sudden cardiac death. polymorphic ventricular tachycardia (torsades de pointes). Some institutions do not measure the QTI unless physician ordered. as it requires a very large population with high quality ECG data. The QTI includes the “relative refractory period. Data collection for the purpose of investigating different formulas is difficult. The QT interval. (QTI) represents depolarization and repolarization of the ventricles. and yet a standard for evaluation has not been agreed upon. Education & Development 12 .” or use a current drug reference. 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.org ECG Measurement: The QTI and QTc Introduction The interpretation of changes in the QT interval is an important aspect in the evaluation of an ECG tracing. The use of the QT interval in clinical practice is not without controversy. Data collection and interpretation: First. yet deemed important. QTI variation though 24 hours: Another problem is that the QTI changes depending on wake and sleep states. and sudden cardiac death. 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.” during which the heart is vulnerable to any ectopic foci that can initiate a stimulus. Lack of standardization: An identified problem is lack of a uniform approach to measurement.long-qt-syndrome. Underlying problems such as a bundle branch block will affect the rate. QTI and a wide QRS: A widened QRS due to a ventricular conduction block causes the QT interval to be longer without prolonged depolarization. read below for “ECG Measurement: The QTI and QTc. it is critical to closely monitor patients during initiation and usage of antidysrhythmics. and internet resources such as: http://www. This means they can either worsen the dysrhythmia or trigger new ones. Antidysrhythmics can also prolong the QT interval (QTI) resulting in lethal dysrhythmias. specific values of parameters vary depending on the population and circumstances. © 2010 Orlando Health. 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. heart rate. sympathetic and parasympathetic tone.qtdrugs. Consequently. while others measure only the QTI and not the QTC. For further information. as a prolonged QTI has been linked to monomorphic ventricular tachycardia. This includes closely monitoring the ECG measurement of the QTI or QT interval corrected (QTc).CV Pharmacology produce proarrhythmic effects on the patient.html http://www. lead selection. Accurate measurement is significant.com/ekg_readout.

The QTI may be short. it is often difficult clinically to distinguish between a normal or short QTI. 1998). normal. 1998) Q T I e n d s h e re w h e re th e T -w a v e r e t u r n s to b a s e lin e . The recommended lead for measurement is lead II. Although a short QTI may suggest hypercalcemia. Example of evaluating R-R interval. The possible problem of distinguishing the T wave from a U wave can be minimized by measuring the QTI in lead II.CV Pharmacology 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. or prolonged (>. The literature suggests that healthcare providers should not be as concerned with QT shortening as with prolongation.44). Education & Development 13 . 1998) © 2010 Orlando Health. The QTI is probably prolonged if it exceeds more than half of the R-R interval. (Grauer. Example of QTI measurement (with permission Grauer. Another method to determine if a QTI is prolonged in sinus rhythms (< 100 beats per minute) is to observe the R-R interval. it is not to be included in the measurement. Note: If a U wave is present. (with permission Grauer.

20-0.5 1.  Record the QTI and the QTC as part of the routine documentation on patients in critical care and telemetry monitoring areas.  Documentation.35-0.41-0.44 is considered prolonged Normal QT Intervals Corrected for given Heart Rate = (QTc) Heart Rate/minute 40 50 60 70 80 90 100 120 150 180 200 R-R Interval/sec 1. Example.30 QTC 0.a QTI/QTC on a patient receiving procainamide should be measured q 4 hours and prn.34 0.75 0.86 0.2 1. charge nurse) if changes are observed.46 0.23-0.67 0.  Notify the appropriate person immediately (i.  Identify conditions and drugs associated with a prolonged QT interval.38-0.0 0.41 0.39 0. nurse.43 0.60 0.32-0.28 0.33-0.40 0.CV Pharmacology 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. and report to next shift. this rule applies to a regular HR in the normal range of 60-100)  A QTc > 0.32 0.33 0. and increase frequency in documenting the QTI/QTC.50 0. continued assessment.25 0.51 0.30-0. physician.26-0.28-0.24 Recommended Actions:  Remember to treat the patient not the monitor. Evaluate all the assessment data.36 0. This strip documentation is to include the drug that patient is receiving.21-0.e.  2010 Orlando Health Education & Development 14 .

Calculate the square root of the R-R interval as shown in the diagram and the example below.The R-R interval is 24 boxes.Divide the numerator by the denominator. Step 1.Square root of the R-R is 0.96 sec. when the heart rate increases the QTI shortens. Step 4.04.98 (denominator) = QTc of 0.44 seconds (450 ms) is considered prolonged. Step 3.96 = 0.Obtain the QTI in seconds.49 seconds = prolonged © 2010 Orlando Health.) Step 3. This number is the QTc EXAMPLE: Step 1. Step 2.QTI is 0. The formula used to calculate a QTC is called Bazett’s Formula after the founding physician.48 seconds. Education & Development 15 . a QTc greater than 0. Sequential Steps to Obtain a QTc Measurement All diagrams used with permission from Long-QT-Syndrome. This square root number becomes the denominator.0.com.98.98) (Denominator) Step 4. For example. (0. This number becomes the numerator. then multiply by 0. (Numerator) Step 2.48 (numerator) divided by 0. The QTc is determined by dividing the QT interval by the square root of the R-R interval.Obtain the R-R interval by counting the number of small boxes between two R waves. This “corrected” measurement adjusts for heart rate and rhythm variability since it is known that autonomic tone influences heart rate. (24 X . Generally. and when the heart rate decreases the QTI lengthens.04 = 0.CV Pharmacology How to Obtain a QTc Measurement The QT interval (QTc) measurement is a more accurate measurement of the QT interval (QTI).

Examples of Drugs: disopyramide (Norpace) procainamide (Pronestyl) quinidine Precautions    Procainamide serum levels should be monitored in patients with renal failure or receiving constant infusion. This risk is increased in patients with hypokalemia or hypomagnesemia. Ib and Ic. it must be given no faster than 30mg/minute. and ventricular tachycardia. which may lead to profound hypotension. Class I drugs also depress automaticity by slowing the rate of spontaneous depolarization of pacemaker cells. Procainamide ( Pronestyl) is available in both oral and intravenous forms. premature ventricular complexes. 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 class of antidysrhythmics is further broken down into subclasses Ia. These drugs alter the absolute refractory period to decrease the risk of premature impulses from ectopic foci. depending on specific actions. Consequently. When used as an intravenous bolus in the ACLS algorithm. which indicates slowing of electrical conduction within the heart. Indications These antidysrhythmics are used to treat atrial dysrhythmias. These drugs are potent sodium channel blockers (prolong QRS interval).CV Pharmacology Class I Antidysrhythmics This class decreases the influx of sodium during phase 0 of depolarization. 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%. All class I drugs depress myocardial contractility resulting in a lower cardiac output. it is important to monitor the patient and the QTI or QTc intervals. Class Ia Blocks sodium to depress conductivity and prolong the refractory period of the heart.  2010 Orlando Health Education & Development 16 . and may prolong repolarization (prolong QT interval) through blockade of potassium channels.

Toxicity of lidocaine is most commonly apparent in the central nervous system resulting in drowsiness. Each of these drugs is associated with an increased overall mortality. and paresthesias. Education & Development 17 . 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". Lidocaine Since they shorten refractoriness. 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. they are used to decrease myocardial irritability and make it more difficult for ectopy or fibrillation to occur. Examples of Drugs: Propafenone (Rhythmol) Flecainide (Tambocor) © 2010 Orlando Health. so they are usually used in dysrhythmias that are resistant to other agents. therapeutic Levels of 1. Additionally.5-5mcg/ml are considered   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. confusion/disorientation. but have little effect on repolarization (no effect on QT interval). they do NOT prolong the QTI/QTc.CV Pharmacology Antidysrhythmics: Subclass Ib In comparison to other class I drugs. Lidocaine serum levels can be measured. Antidysrhyhmics: Subclass Ic Subclass Ic drugs are the most potent sodium channel blocking agents (prolong QRS interval). 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. because these drugs target irritable tissue.

prolong the PR interval. contractility. stroke volume.CV Pharmacology Antidysrhythmics: Class II Class II antidysrhythmics are beta-blockers. and reinfarction. Beta-blockers compete for receptor sites with one’s naturally occurring catecholamines such as epinephrine and norepinephrine. conductivity. with no effect on QRS or QT intervals). SVT. The early use of beta-blockers in Acute Myocardial Infraction (AMI) patients reduces the likelihood of ventricular arrhythmias. Indications Beta-blockers are used for rate control of sinus tachycardia. atrial tachycardia. carefully monitor BP. and atrial fibrillation. bradycardia. Although their actions depend propanolol (Inderal) on which catecholamine receptor (β1 versus β2) they block. heart rate. Precautions    Beta-blockers may precipitate hypotension. They act indirectly on electrophysiological parameters by blocking beta-adrenergic receptors (slow sinus rate.  2010 Orlando Health Education & Development 18 . 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 β2 receptors in the bronchial system. and heart failure. thereby decreasing mortality. During IV administration. as well as mask signs of hyperthyroidism and hypoglycemia. and ECG due to their mechanism of action. recurrent ischemia. these drugs will have effects that are directly opposite to catecholamines by decreasing automaticity. Examples of Drugs: 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. cardiac output and blood pressure and myocardial workload. heart rate.

Betapace AF®) Sotalol is used for the treatment of documented ventricular arrhythmias (i. Strict monitoring of the QTI/ QTc is essential for drugs within this class. For example. it exhibits electrophysiological characteristics of each of the other classes of antidysrhythmics. After a minimum three-day hospital stay with dose adjustment. sotalol (Betapace and Betapace AF) 19 . although amiodarone is generally prescribed because of its class III properties. Whereas sotalol combines the class III property of prolonging the refractory period with the beneficial beta-blocking effects of class II drugs. and control of hemodynamically stable VT. Contact the cardiologist immediately if adverse signs occur. Dofetilide (Tikosyn®) Dofetilide (Tikosyn) is indicated for the conversion of atrial fibrillation or atrial flutter to sinus rhythm. with specific manufacturer instructions that states  2010 Orlando Health Education & Development Examples of Drugs: Pure class III: ibutilide (Corvert).magnesium. Class III drugs are further known as either mixed or pure class III. hospital pharmacists and nurses must have received education prior to dispensing and administering this drug .50) in patients with ventricular conduction abnormalities. and for maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation or atrial flutter. Only prescribers (physicians.50) necessitates either a dosage reduction or discontinuation of dofetilide. Sotalol (Betapace®. It is also used to maintain sinus rhythm in patients with atrial fibrillation or atrial flutter. Additionally. dofetilide (Tikosyn) Mixed class III: amiodarone (Cordarone). Likewise. and renal function must be done for patients receiving dofetilide. after defibrillation and epinephrine in cardiac arrest with persistent ventricular tachycardia (VT) or ventricular fibrillation (VF). It is recommended that nursing collaborate with the hospital pharmacy for discharge planning. or wide-complex tachycardia of uncertain origin. Betapace AF® is a modified version of Betapace.CV Pharmacology Antidysrhythmics: Class III Class III drugs prolong repolarization (phase 3) by preventing any further entry of sodium or calcium into the cell. Therapy must be initiated in a hospital setting so the patient can be monitored for dysrhythmias. Potassium begins to move back into the cell.44) or greater than 500 msec (>0. the patient can be discharged home with a 7-day supply of medication. nurse practitioners. Careful monitoring of serum potassium. ECG monitoring is continuous during the initial dosing period with strict measurement and documentation of the QTc and patient tolerance. Amiodarone (Cordarone) Amiodarone is an ACLS drug used for control of rapid ventricular rate due to an accessory pathway conduction in pre-excited atrial arrhythmias. sustained ventricular tachycardia) that in the judgment of the physician are life-threatening. a baseline QTC interval must be measured and dofetilide is not be administered if the baseline QTc is greater than 440 msec (>0. An increase in the QTc measurement of greater than 15% over baseline or greater than 500 msec (0. physician assistants) who have received specialized training can prescribe dofetilide. polymorphic VT.e.

and others. and has the potential to result in lethal ventricular dysrhythmias. nurse practitioners. antifungals. Sotalol doses are further adjusted for renal dysfunction. A positive dromotropic effect would increase conductivity. 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. Dofetilide is available in a limited number of retail pharmacies. these labs should be monitored closely and replaced if necessary. Ibutilide is available in IV form only. while a negative effect would decrease conductivity. Education & Development 20 . physician assistants) who have received specialized training can prescribe dofetilide.CV Pharmacology substitutions are not to be made for Betapace AF® since it is distributed with a patient package insert specific for atrial fibrillation/flutter. while a negative inotropic effect will decrease contractility. antipsychotics. Precautions  All class III drugs prolong the QT interval to varying degrees which may result in lifethreatening ventricular dysrhythmias. The effectiveness of ibutilide has not been determined in patients with arrhythmias >90 days in duration. The risk of dysrhythmias with class III drugs increases with hypokalemia and hypomagnesemia. Ibutilide (Corvert®) Ibutilide is indicated for the acute termination of atrial fibrillation or flutter of recent onset. Hypokalemia and hypomagnesemia are contraindications for ibutilide due to the increased risk of lethal ventricular dysrhythmias. A positive inotropic effect would increase contractility. © 2010 Orlando Health. Retail pharmacies can call 1-877-TIKOSYN for further information. Chronotropic effect refers to an increase in heart rate. Likewise. and for at least 4 hours following the infusion of ibutilide. The QT interval must be closely monitored initially. The QTI and QTc must be carefully monitored and documented. a negative chronotropic is decrease in heart rate. It is important to also note that an array of drug categories other than cardiac can cause a prolonged QTI such as certain antibiotics. Dromotropic effect refers to the influence the cardiac nerves have on the conductivity of impulses across the muscle.   Important Definitions: Inotropic effect is a change in myocardial contractility. Only prescribers (physicians. A unique adverse effect profile and drug interactions with dofetilide require additional guidelines for patient selection and administration. It is vital that sotalol be avoided with other beta-blockers since it also has class II effects that can result in profound hypotension. hospital pharmacists and nurses must have received education prior to dispensing and administering the drug.

decrease heart rate. nicardipine (Cardene). and/or death. Tiazac) verapamil (Calan. and nisoldipine (Sular) The following page has a summary chart on the actions and indications for calcium channel blockers. thereby increasing the supply of oxygenated blood to the myocardium and reducing myocardial workload to reduce myocardial oxygen demand. isradipine (DynaCirc). Calcium channel blocker categories Two types of calcium channel blockers exist because they exert different effects. angina. These actions result in prolonging both the absolute and relative refractory periods. Adalat®) are not recommended for acute blood pressure reduction nor for chronic hypertension management due to risk of profound hypotension. They are utilized to treat atrial dysrhythmias. 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. cerebral ischemia or stroke. Adalat). They are utilized to manage hypertension and will be discussed later in this SLP. and decrease conduction through the SA and AV nodes.  Nifedipine should NEVER be administered sublingually or as a “bite and swallow” order. Verelan PM) Calcuim channel blockers known as (dihydropyridines): dilate peripheral blood vessels without affecting heart rate or contractility. Precautions  Short acting nifedipine capsules (Procardia®. Drugs in this class also produce vasodilation of the peripheral and coronary arteries.CV Pharmacology Antidysrhythmics: Class IV Calcium is critical to heart function due to its effect on cardiac output by increasing contractility and conductivity. Dilacor XR. Diltiazem (Cardizem. amlodipine (Norvasc). Nifedipine (Procardia. felodipine (Plendil). and hypertension. Isoptin. Calcuim channel blockers known as (nondihydropyridines): cause coronary artery vasodilation.  2010 Orlando Health Education & Development 21 .

Negative dromotropic effect. This effect is used to depress the frequency of hyperactive tissue causing arrhythmias. This effect increases coronary blood flow. This effect is due to slowing of the SA node and results in reduced myocardial oxygen consumption.CV Pharmacology Summary chart of calcium channel blocker actions and indications Calcium Channel Blockers Actions Potent vasodilator of coronary vessels. Indications Angina Hypertension Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina  2010 Orlando Health Education & Development 22 . Negative chronotropic effect. Nondihydropyridine agents cause a modest decrease in contractility and reduction of myocardial oxygen consumption. there is no significant effect on venous beds. Negative inotropic effect. This results in reduced myocardial oxygen consumption. and reduces coronary vasospasm. Dihydropyridine agents reduce peripheral resistance and afterload. Vasodilation occurs predominantly in arterioles. nondihydropyridine agents increase the time needed for each beat. Vasodilator of peripheral vessels. By slowing conduction through the AV node. Nondihydropyridine agents cause a modest lowering of heart rate.

Patients with a magnesium deficiency commonly have a high incidence of cardiac dysrhythmias. 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. including torsades de pointes (TdP) and sudden cardiac death. resulting in a brief asystolic period that allows the heart's electrical activity to "reset" and return to sinus rhythm. resulting in a prolonged relative refractory period and QT interval.CV Pharmacology 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. of 6-10 seconds. Precautions IV administration can cause hypotension and circulatory collapse if given too fast. A rapid IV push bolus of adenosine causes complete depolarization of the myocardium. Magnesium Magnesium is essential for the functioning of the sodium-potassium pump to drive myocardial electrical activity.  2010 Orlando Health Education & Development 23 . It is vital to have emergency resuscitation equipment readily available. Precautions Adenosine can induce a brief period of asystole. Because of this action. A low serum magnesium level slows the return of potassium into the cell during phase 4 of the action potential.

may also be used for PVC’s. f) A class III drug used to convert recent onset atrial fibrillation to sinus rhythm. ________ Dofetilide 9. Corresponds with the last half of the T-wave. conductivity. j) Strict monitoring of the QTI/QTc is essential for drugs within this class. ________ Class IV 6. e) A mixed class III drug that is to be avoided with beta-blocker drugs. ________ Amiodarone 4. contractility. ________ Proarrythmic 5. i) A strong stimulus may produce ectopic depolarization in the cardiac cells. d) Treatment of choice for the dysrhythmia torsades de pointes. c) Time frame when cardiac cells cannot respond to any stimulus from ectopic sources. ________ Relative Refractory Period a) A drug class known to decrease the heart rate. ________ Class II 7.CV Pharmacology Check Yourself Pop Quiz Match the definitions at the bottom with the terms at the top. ________ Sotalol 8. Healthcare providers must be inserviced prior to providing this agent.  2010 Orlando Health Education & Development 24 . corresponds with the QRS and first half of the T wave. ________ Class III 3. h) Describes a drug that may induce additional dysrhythmias. ________ Magnesium 2. 1. ________ Absolute Refractory Period 10. g) Indicated in emergency therapy for ventricular tachycardia or ventricular fibrillation. b) A drug class which decreases contractility and slows conduction though the SA and AV nodes.

6. 8.CV Pharmacology Check Yourself Pop Quiz -Answers 1. 4. 9. 3. 7.  2010 Orlando Health Education & Development 25 . i Refer to previous section as a review for any incorrect answers. 2. Reviewing your incorrect answers will benefit your learning as you proceed in this packet. d j g h b a e f c 10. 5.

Instead. and intravascular volume. Atacand® (candesartan). Renin is formed in the renal juxtaglomerular cells in response to certain types of stimuli. they bind to receptor sites to prevent the effects of angiotensin-II. angiotensin-I reaches the lungs. and stimulates aldosterone Zestril® (lisinopril). Accupril® (quinapril). These stimuli include salt depletion. It is important to understand that a number of patients who take ACE inhibitor drugs develop a persistent nonproductive cough.CV Pharmacology Antihypertensives Angiotensin Converting Enzyme (ACE) Inhibitors Before discussing the ACE inhibitors. release of norepinephrine. Unlike the ACE inhibitor drugs. they do not prevent the formation of angiotensin-II. ACE inhibitor therapy may compromise renal function and result in transient increases in BUN and creatinine. Monopril® (fosinopril). 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. arterial blood pressure. Angiotensin-II causes vasoconstriction. Mavik® angiotensin converting enzyme into angiotensin-II. aldosterone production is no longer stimulated by Angiotensin II. it is converted by the Lotensin® (benazepril). production resulting in sodium and water retention. renin mediates Capoten® (captopril). Furthermore. prevention of systemic vasoconstriction and decreased blood pressure. β2 stimulation. let us take a moment to review the renin-angiotensin system. which results in decreased intravascular volume. Vasotec® the formation of angiotensin-I in the liver. and a decrease in renal perfusion that might be found Examples of Drugs: in hypotension or hypovolemia. Altace® (ramipril). Patients are to be cautioned about these effects prior to initiating ACE inhibitor therapy. ACE inhibitors may cause hypotension or symptoms related to hypotension. Univasc® (moexipril) Additional effects of angiotensin-II include increased systemic vascular resistance. promotes the Aceon® (perindopril). Micardis® (telmisartan). Avapro® (irbesartan). This results in a decrease in norepinephrine levels.  Angiotensin II Receptor Blockers (ARBs) Angiotensin receptor blockade is a newer method of renin-angiotensin blockade. Benicar® (olmesartan). ACE inhibitor drugs work by blocking the angiotensin converting enzyme in the lungs so angiotensin-I is prevented from being converted to angiotensin-II. Teveten® (eprosartan) 26 . Diovan® (valsartan). When (enalapril). Next. such as dizziness and syncope. The outcome is a decrease in norepinephrine levels. (trandolapril). Prinivil®. Precautions   Due to their mechanism of action. prevention of  2010 Orlando Health Education & Development Examples of Drugs: Cozaar® (losartan).

Used in patients with heart failure because they block the vasoconstrictive effects of angiotension-II and the release of aldosterone.CV Pharmacology systemic vasoconstriction and a decreased blood pressure. the use of ARB therapy may result in transient increases in BUN and creatinine. Education & Development 27 . In some patients. Precautions   Angiotensin receptor antagonists may cause hypotension or symptoms related to hypotension. Indications ARBs are indicated for the treatment and management of mild to severe hypertension. © 2010 Orlando Health.

Precautions     Beta-blockers may precipitate hypotension and bradycardia. 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. and improved renal blood flow. esmolol). Coreg (carvedilol). Concurrent use of beta-blockers. ® and Tenormin (atenolol). dysrhythmias and rate control. Precautions   Due to its potent and rapid acting hypotensive properties. Oral beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD). Please review your institution’s policy regarding patient placement in an appropriate telemetry unit. sodium excretion. and/or ischemia. hypertension. Some betaExamples of Drugs: blockers are specific for beta-1 receptors (atenolol. Brevibloc® (esmolol). Toprol-XL® ® beta-1 selectivity is dose-dependent and is not seen (metoprolol). cautious use is indicated in diabetics because they can mask prominent hypoglycemic symptoms. but gradually tapered to avoid acute tachycardia. betaxolol. Trandate® (labetalol). Indications Used for hypertension. MI’s. Lopressor®. Zebeta® with high doses of beta-1 selective drugs. Likewise.CV Pharmacology 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. metoprolol. bisoprolol. It is used as an antihypertensive with the added bonus effects of natriuresis. frequent blood pressure monitoring is necessary. Indications Used for short-term management of severe or malignant hypertension when rapid reduction of blood pressure is needed. (bisoprolol). angina.Inderal ® (propranolol). or the calcium channel blockers verapamil and diltiazem because bradycardia or heart block can occur. Corgard® (nadolol)  Fenoldopam (Corlopam) Fenoldopam is a rapid acting vasodilator because of its dopamine agonist properties.  2010 Orlando Health Education & Development 28 . However. and heart failure.

are at risk for cyanide and/or thiocyanate toxicity. myocardial infarction. Sodium nitroprusside has the potential to cause severe hypotension that can lead to myocardial ischemia. Patients receiving high doses and/or prolonged infusions of nitroprusside. and decreasing preload by increasing venous capacitance and reducing blood return to the heart. Precautions  Sodium nitroprusside has a rapid onset and short duration of action making it very easy to titrate. blurred vision. tinnitus. discontinuing the drug and elevating the patient’s legs should be sufficient to return arterial blood pressure to prior levels within several minutes. or stroke.CV Pharmacology Sodium Nitroprusside (Nipride. dissecting aortic aneurysm. fast acting drug producing vasodilation of both the arteries and the veins. The preload and afterload reduction results in both decreased myocardial workload and myocardial oxygen demand. coronary bypass surgery. Nitropress) Sodium nitroprusside (Nipride) is a potent. This action results in decreasing afterload by reducing systemic vascular resistance and arterial blood pressure. twitching. which include metabolic acidosis (may be the earliest sign of toxicity). and seizures  2010 Orlando Health Education & Development 29 . changes in mental status. The effects of this drug are observed almost immediately and disappear within a few minutes after it is discontinued.   Clinical note: The patient is to be observed continuously for signs of cyanide toxicity. hyperreflexia. Cyanide is produced which is converted to thiocyanate in the liver and thiocyanate is eliminated mainly in the urine. nausea. Due to its short duration. Patients must be monitored closely during initiation and titration. Nipride is used to managed hypertensive crises and control blood pressure in patients after vascular surgeries.

Hydralazine. In some cases. They are used for angina and for heart failure in combination with hydralazine (BiDil®). interactions. Levitra®. Monoket®. so patients need to be instructed that this is an expected side effect. it should be initiated cautiously and the patient closely monitored during titration. myocardial oxygen demand. Nitrostat. Ismo®) are available orally. Isosorbide dinitrate. isosorbide mononitrate. and prinzmetal. and adverse effects. and sublingually. Cialis®).CV Pharmacology 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. unstable. As a result. stable. Headaches are common with all forms of nitroglycerin. This is important to remember since these drugs may be administered concomitantly to patients diagnosed with an acute myocardial infarction or acute coronary syndrome. Nitroglycerin decreases systemic arterial resistance and arterial blood pressure. Intermittent doses of nitrates by use of a nitrate-free interval of 10-12 hours may minimize or prevent the development of tolerance.  2010 Orlando Health Education & Development 30 . Their mechanism of action is similar to nitroglycerin so they share the same precautions. increases venous capacitance and reduces preload. an intravenous nitroglycerin preparation may antagonize an IV infusion of heparin and therefore close monitoring of its effects is required. Nitroglycerin is the drug of choice for the relief of all types of angina. and nitroglycerin are collectively known as nitrates. Precautions  Because nitroglycerin is a powerful vasodilator. The combination can worsen the hypotensive effects of nitrates. isosorbide dinitrate (Isordil®). (Imdur®. Nitrate tolerance – Tolerance to the vascular and antianginal effects of individual nitrates and cross-tolerance among the drugs may occur with repeated prolonged use. Patients receiving nitrate therapy should not take selective phosphodiesterase inhibitors used for erectile dysfunction (Viagra®. Nesiritide (Natrecor)    Isosorbide Compared to nitroglycerin. helping to relieve myocardial ischemia. isosorbide dinitrate (Isordil®) is a less potent vasodilator. Examples of Drugs: nitroglycerin decreases myocardial workload and Tridil(IV). As a result. Ismo®). it may result in profound hypotension. possibly resulting in potentially life-threatening hypotensive/hemodynamic compromise. Isosorbide dinitrate and one of its metabolites-isosorbide mononitrate (Imdur®. Monoket®. Nitro-Bid. Nitroglycerin also relieves vasospasm and dilates coronary arteries to increase blood flow to the myocardium. isosorbide mononitrate.

© 2010 Orlando Health. nitroprusside) are recommended for hypertensive crises in non-pregnant patients. Review your institution’s policy regarding placement of the patient in an appropriate telemetry unit. it is important to institute frequent blood pressure monitoring. the lab results will be altered after this drug is administered. Due to its potent hypotensive properties. Hydralazine has been used in combination with isosorbide dinitrate as a second-line treatment of heart failure. It is currently indicated for the patient in acutely decompensated heart failure who is symptomatic with either minimal activity or dyspnea at rest. which is responsible for vasodilation of veins and arteries. Nesiritide (Natrecor) Nesiritide is a synthetic human B-type natriuretic peptide (BNP) with potent vasodilator properties.. hydralazine is administered as intermittent doses. When used parenterally. Nesiritide binds to the receptor sites of vascular smooth muscle resulting in an increase in cGMP. However.CV Pharmacology Hydralazine Hydralazine has direct vasodilatory effects on the vascular smooth muscle resulting in blood pressure lowering. It promotes diuresis and natruresis. the blood must be obtained prior to the administration of nesiritide (Natrecor).e. It is one of the parenteral drugs of choice for management of pregnancyassociated hypertensive emergencies. Education & Development 31 . Since nesiritide (Natrecor) is a synthetic BNP. Precautions When B-type natriuretic peptide (BNP) lab values are ordered. other parenteral therapies (i.

 Atropine Atropine has numerous clinical applications so we will limit our discussion to those that involve the cardiovascular system. atropine affects atrial activity. Calcium replacement should be guided by ionized calcium levels to avoid hypercalcemia. and increases electrical conduction through the atria and the AV node. Calcium is available in oral and parenteral forms for a wide variety of indications. Atropine is known as a vagolytic or parasympatholytic because it counteracts the effects of the parasympathetic nervous system. © 2010 Orlando Health. Calcium Salts Calcium is an essential electrolyte for normal cardiac and vascular function. thus hypotension may occur. The effects of morphine can be reversed with naloxone (Narcan) 0. Education & Development 32 . This leaves the actions of the sympathetic nervous system unopposed so patients who have received atropine will display signs of increased sympathetic activity. Rapid administration of morphine may result in respiratory arrest. The blood pressure must be closely monitored in patients receiving morphine. Morphine is also useful in the management of cardiogenic pulmonary edema by increasing venous capacitance (capacity). to a maximum of 10mg. It is used in sinus bradycardia to increase heart rate. Calcium Chloride must be given carefully because rapid administration can result in cardiac arrest.2mg – 2. By reducing preload and afterload.CV Pharmacology Morphine Sulfate Morphine sulfate is a powerful narcotic analgesic used to relieve severe acute or chronic pain and to relieve anxiety. Careful monitoring of the respiratory rate and depth is necessary during administration of morphine. Atropine is indicated for symptomatic bradydysrhythmias. Calcium salts will not be discussed further in this packet. Morphine causes venous and arterial vasodilation. It primarily stimulates venous vasodilation and a reduction in preload (the volume of blood in the ventricles at the end of diastole). resulting in a decrease in afterload (the force the ventricles must push against to pump blood into the aorta and pulmonary vasculature). 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. Calcium Chloride is usually reserved for emergent situations requiring calcium replacement. morphine diminishes myocardial workload and oxygen demand. Precautions  The most serious adverse effect of morphine is depression of the respiratory system. An additional property is arterial vasodilation. Because parasympathetic innervation of the heart is primarily in the atria. thus decreasing the return of blood to the right side of the heart and to the lungs. Calcium Gluconate is used more frequently because it is associated with fewer side effects than Calcium Chloride. It enhances automaticity of the sinus node.0mg at 2-3 minute intervals.

Which class of drugs is used as a vasodilator and also blocks the conversion of Angiotensin I to Angiotensin II? ______________________________________________________________ 3. State the vasodilator agent that is used as a potent antihypertensive and rapid acting. Name 3 effects of Angiotensin II? ______________________________ ______________________________ ______________________________ 4. Education & Development 33 . What are the effects of this class of drugs on the heart? _________________________________________________________________ _________________________________________________________________ 2. but also has the effects of natriuresis? _________________________________________________________________  2010 Orlando Health. 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 answer) Will this have more effect on ventricular preload or afterload? (Circle correct Afterload Preload 5. Define parasympatholytic.CV Pharmacology Check Yourself Pop Quiz 1. 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.

Sodium nitroprusside is a potent. 4. The ARB therapy blocks the effects of angiotensin II after this conversion occurs. but it increases venous capacitance and reduces preload to a greater extent. 2. and stimulates aldosterone production resulting in sodium and water retention. NTG relaxes vascular smooth muscle of arteries and veins. Additional effects of angiotensin-II include increased systemic vascular resistance. Angiotensin-II causes vasoconstriction. This class of drug will enhance automaticity of the sinus node. Fenoldopam (Corlopam).CV Pharmacology Check Yourself Pop Quiz -Answers 1. fast acting drug which causes vasodilation of both arteries and veins. (Increases sinus and ventricular heart rate). This preload and afterload reduction results in decreased myocardial workload and myocardial oxygen demand.  2010 Orlando Health. it decreases afterload by reducing systemic vascular resistance and arterial blood pressure. promotes the release of norepinephrine. ACE inhibitor therapy blocks the conversion of angiotensin I to II. increase electrical conduction through the atria and the AV node and will enhance conductivity. which occurs primarily in the lungs. 3. 5. and decreases preload by increasing venous capacitance and reducing blood return to the heart. Nitroglycerin will decrease systemic arterial resistance and arterial blood pressure. arterial blood pressure. Because of this action. Education & Development 34 . Parasympatholytic is defined as counteracting the effects of the parasympathetic nervous system. and intravascular volume. but has a more pronounced effect on the venous system. 6.

Refer to your hospital’s policy regarding the use of phentolamine for intravenous extravasation of these drugs. cardiac output. renal. and dopaminergic receptors. and pulmonary edema. At low doses (1 – 4 mcg/kg/minute). dopamine may also be considered in hemodynamically significant bradycardia. and also stimulates the release of norepinephrine Indications Dopamine is used primarily for symptomatic hypotension and to increase organ perfusion. phentolamine (Regitine) may be used to help minimize tissue damage. and arterial blood pressure. β1. dopamine may be used in conjunction with positive inotropic agents and vasodilators. and myocardial workload. Dopamine stimulates alpha. At higher doses (10 – 20 mcg/kg/minute). dopamine stimulates the dopaminergic receptors to produce cerebral. The administration of vasopressors to hypovolemic patients does not increase blood pressure. This results in an increase in preload. At moderate doses (5 -10 mcg/kg/minute). This permits the beneficial β1 effects to predominate and counteracts the increases in preload and afterload caused by alpha stimulation. Should extravasation of this or any other alpha agonist occur. This increases contractility. following the use of transcutaneous pacing and/or atropine.  2010 Orlando Health. with the dose beginning at 5 mcg/kg/minute. left ventricular failure. NOTE: Many clinicians currently suggest that low dose dopamine therapy does NOT prevent or ameliorate acute renal failure in patients. then other interventions should be considered. According to the ACLS bradycardia algorithm. Dopamine Dopamine (Intropin) is a chemical precursor of norepinephrine. This dose is commonly thought to increase blood flow to the kidneys and may sometimes be referred to as the renal dose dopamine.CV Pharmacology Vasopressor Therapy Clinical Application Vasopressor drugs must not be used until the patient’s volume status has been addressed. afterload. dopamine stimulates the β1 receptors in the myocardium. In patients with cardiogenic shock. It also significantly increases myocardial oxygen demand and negates the positive β1 and dopaminergic effects. the alpha agonist properties of dopamine are much more pronounced. resulting in significant increases in peripheral and venous vasoconstriction. At doses of 20 mcg/kg/minute or more. and mesenteric vasodilation. If hypotension continues. Education & Development 35 . depending on the administered dose. significant arterial vasoconstriction results. The efficacy of dopamine for this indication is not supported in the literature. instead it can result in profound tachydysrhythmias and ventricular tachycardia or ventricular fibrillation.

Failure to do so may result in tachydysrhythmias. 1:10. and ventricular fibrillation. and may actually result in a slight decrease in blood pressure. and blocks the release of histamine (histamine is the chemical mediator that leads to the vascular changes in anaphylaxis thus leading to shock). Indications Epinephrine’s adrenergic agonist properties make it useful in any pulseless rhythm such as asystole.V.Epinephrine’s alpha agonist activity results in peripheral vasoconstriction. Epinephrine 1:1000 = 1 mg/mL and is most commonly used Sub Q for hypersensitivity reactions or as a bronchodilator. MAO inhibitors strongly potentiate dopamine so the dosage should be only 10% of the recommended dose. which increases systemic vascular resistance as well as systolic and diastolic blood pressure. ventricular tachycardia.000). It also facilitates these ventricular rhythms to be more responsive to defibrillation. Precautions and Interactions Note: Medication errors have occurred due to confusion with epinephrine products expressed as ratio strengths (i. as part of the ACLS protocol.1 mg/mL and is used I. Epinephrine is also used in the management of anaphylactic shock. causes bronchodilation. and pulseless ventricular tachycardia. the patient’s volume status should be addressed before the administration of dopamine. The arrhythmogenic potential of dopamine increases as the dose increases.CV Pharmacology Precautions and Interactions As with any of the vasopressors. Its beta-2 agonist properties result in bronchodilation. Clinical Application It is recommended that all dopamine doses be administered through a central venous catheter since extravasation of dopamine causes tissue necrosis. Epinephrine also inhibits the release of histamine. Epinephrine 1:10. is a naturally occurring catecholamine which stimulates both alpha and beta receptors. It relieves bronchospasm. Epinephrine’s beta-1 agonist activity increases automaticity and myocardial electrical activity. which is responsible for the cardiovascular collapse that occurs in severe allergic reactions and anaphylaxis. as does the increase in myocardial workload and myocardial oxygen demand. This results in increased coronary and cerebral perfusion blood flow.e. pulseless electrical activity. It is further recommended that epinephrine be administered through a central venous catheter since extravasation of epinephrine causes tissue necrosis. it tends to shunt blood to the kidneys and intestines.000 = 0. Additionally. 1:1000 vs. Since low dose dopamine causes vasodilation of the mesenteric and renal vessels. when used as a diluted continuous intravenous infusion. Epinephrine Epinephrine. epinephrine is useful for profound symptomatic bradycardia that has not responded to a pacemaker or atropine. Education & Development 36 . © 2010 Orlando Health. myocardial contractility and cardiac output. also known as Adrenalin. ventricular fibrillation.

or other conditions that result in vasodilation (decreased systemic vascular resistance). This increased stress on the heart may exacerbate myocardial ischemia and extend a myocardial infarction. © 2010 Orlando Health. the resulting increased afterload limits the beneficial inotropic effects and increases myocardial oxygen demands. and ventricular fibrillation. myocardial contractility. Failure to do so may result in tachydysrhythmias.CV Pharmacology It is important to remember that by enhancing preload. As with any of the vasopressors. Norepinephrine Norepinephrine (Levophed) is a naturally occurring catecholamine that is structurally similar to epinephrine. The beta-1 agonist effects are comparable to epinephrine with additional effects such as increasing automaticity. Additionally. It is especially beneficial in patients with septic and neurogenic shock. Norepinephrine has very little effect on beta-2 receptors so it does not produce bronchodilation. and cardiac output. afterload. epinephrine increases the myocardial oxygen demand resulting in an increased myocardial irritability that can induce ventricular ectopy. Indications Norepinephrine is indicated for hemodynamically significant hypotension (<70mmHg SBP) and is particularly helpful in the presence of decreased systemic vascular resistance. in shock states. myocardial electrical activity. However. ventricular tachycardia. the use of norepinephrine at low doses is common. norepinephrine’s alpha agonist effects result in a more pronounced peripheral vasoconstriction. Precautions and Interactions Norepinephrine increases myocardial workload and myocardial oxygen demand so it may precipitate myocardial ischemia or infarction. As the dose of norepinephrine increases. It also increases myocardial irritability and can result in ventricular dysrhythmias. the patient’s volume status should be addressed before the administration of norepinephrine. Education & Development 37 . and myocardial workload.

Dosing for Cardiac Arrest is 40 Units IV push x 1.. vasopressin cannot be administered through the endotracheal tube. Indications According to ACLS Guidelines. Education & Development 38 . Precautions The half-life of vasopressin is 10–20 minutes. after 10 minutes a decision needs to be made to give epinephrine because vasopressin can only be given once.  2010 Orlando Health. As a pharmacologic agent. septic shock). phenylephrine increases preload and afterload and resulting in increased myocardial oxygen demand. phenylephrine is used in patients with hypotension and shock. IV is the only route recommended currently by AHA guidelines. Clinical Application It is recommended that phenylephrine be administered through a central venous catheter since extravasation of phenylephrine causes tissue necrosis. it causes vasoconstriction to increase systemic vascular resistance and arterial blood pressure. In usual therapeutic doses. 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.CV Pharmacology Phenylephrine Phenylephrine (Neo-Synephrine) is a sympathomimetic agent used primarily as an alpha agonist. As a result. vasopressin has several clinical applications. Precautions and Interactions In usual therapeutic doses. or as a continuous infusion. Phenylephrine may cause a slowing of the heart rate (reflex bradycardia) and is potentiated by tricyclic antidepressants and monoamine oxidase (MAO) inhibitors. so our discussion is limited to the application of vasopressin within the ACLS guidelines as a vasopressor. At this time. Vasopressin may be useful for hemodynamic support in vasodilatory shock (e. Vasopressin Vasopressin (Pitressin) is a naturally occurring antidiuretic hormone found in the posterior pituitary. Indications From a cardiovascular perspective.g.

At doses of 2–20 mcg/kg/min. Digitek®) which is the most commonly prescribed form of digitalis. hyperkalemia. By increasing the cardiac output in the presence of mild vasodilation. Indications Digoxin is used as maintenance therapy for symptom control in patients with heart failure to increase myocardial contractility. diarrhea. it has only a minimal effect on the heart rate. It also is used to control the ventricular rate with atrial fibrillation or atrial flutter by slowing AV nodal conduction. visual disturbances. Note: For initial ventricular rate control in atrial fibrillation. Symptoms of digoxin toxicity include nausea. and changes in mental status and level of consciousness. resulting in a mild vasodilation effect. Dobutamine Dobutamine (Dobutrex) is a synthetic catecholamine. This vasodilation will decrease preload and afterload with a beneficial effect on myocardial oxygen supply and demand. including heart blocks. junctional rhythms. Clinical Application 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. renal and mesenteric perfusion. Education & Development 39 . Toxicity is precipitated by hypokalemia. It is also a mild alpha agonist. Overdose of digoxin can be treated by the drug Digibind®. and hypomagnesemia. Many patients taking digoxin for heart failure also take diuretics that can deplete potassium and lead to toxicity. the alpha effects are counteracted by the more potent β2 properties. it will increase coronary. calcium channel blockers. vomiting. Digoxin is a positive inotropic agent as it increases the strength of myocardial contraction. and ventricular dysrhythmias. Digoxin also decreases automaticity and prolongs electrical conduction through the AV node.  2010 Orlando Health. stroke volume. however. and cardiac output. In patients taking these drugs. and quinidine. Be sure to provide patient education concerning the need to take any prescribed potassium supplements if the patient is on diuretic therapy. Toxicity also causes a wide variety of dysrhythmias. It is a potent β1 agonist to increase myocardial contractility and cardiac output.CV Pharmacology Positive Inotropic Therapy Digoxin Our discussion of digitalis preparations will be limited to digoxin (Lanoxin. 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. Precautions and Interactions Digoxin has a very narrow therapeutic range and toxicity can develop rapidly. Digoxin is potentiated in such drugs as amiodarone. digoxin should be used with caution and the dose might be reduced by 50%.

tremors. the PDE inhibitors reduce preload and afterload and milrinone (Primacor) thus decrease myocardial oxygen demand. Milrinone may cause a mild thrombocytopenia. Remember that hypokalemia may increase ventricular irritability and precipitate digoxin toxicity. By increasing cardiac output. Phosphodiesterase (PDE) Inhibitors PDE’s inhibit the breakdown of cyclic AMP (cAMP) in cardiac and peripheral vascular smooth muscle. Although. The net effect is similar to dobutamine. Indications PDE inhibitors are used for patients with heart failure or systolic dysfunction cardiomyopathy. so patients receiving dobutamine should be monitored for hypokalemia. and hypokalemia. dobutamine may result in an increase in arterial blood pressure. it does so to a much lower extent than other catecholamines. resulting in potent inotropic effects while dilating both arteries and veins. Inamrinone is seldom used due its significant problems with thrombocytopenia. It is commonly used with moderate dose dopamine (510 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. hypotension can occur. Precautions and Interactions Dobutamine may cause headache. the incidence is far lower than with inamrinone. nausea. Education & Development 40 . inamrinone (Inocor) amrinone © 2010 Orlando Health. These agents are more effective in heart failure and cardiomyopathy than they are in the presence of ischemic heart disease. While dobutamine may induce tachydysrhythmias and myocardial ischemia. It is used concomitantly with volume loading in the presence of right ventricular myocardial infarction. Note: Since is rarely used. Milrinone may also cause mild to moderate headaches.CV Pharmacology Indications Dobutamine is used to increase myocardial contractility and cardiac output in patients with left ventricular systolic dysfunction. an increase in myocardial irritability may occur inducing both supraventricular and ventricular dysrhythmias. Precautions and Interactions Due to the potent vasodilation properties. our discussion will focus on milrinone. Likewise. By increasing contractility and causing Examples of Drugs: vasodilation.

computed tomography (CT). and dysrhythmias. the administration of sodium bicarbonate during a cardiac arrest situation is associated with poor resuscitation outcomes. Because it is used so rarely. it forms carbonic acid. resulting in massive diuresis and cellular dehydration. Isopreterenol produces large increases in myocardial contractility. However. It is given to patients with a preexisting metabolic acidosis such as patients in renal failure or diabetic ketoacidosis. Education & Development 41 . It can also be given to patients with hyperkalemia or those who have overdosed on tricyclic antidepressants or phenobarbital. Because of its severe side effect profile Isopreterenol is now used only for very specific indications. Isopreterenol (Isuprel) is a potent beta-adrenergic agonist with essentially no alpha adrenergic activity. which usually dissociates to water and carbon dioxide. diagnostic or therapeutic arteriography. 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. or transjugular intrahepatic portal systemic shunt (TIPS) placement. For further information please refer to Lexicomp and Micromedex. myocardial infarction. In general.CV Pharmacology Isoproterenol Sometimes called the “cardiac whip”. For this reason. Precautions and Interactions Sodium bicarbonate can lead to metabolic alkalosis if too much is administered. Isopreterenol will not be discussed further in this packet. most commonly in cardiac transplantation. 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. When bicarbonate combines with an acid. sodium bicarbonate is no longer routinely given as part of resuscitation efforts. Sodium Bicarbonate Sodium bicarbonate is used as a buffering agent in patients with a preexisting metabolic acidosis. which can lead to an intracellular acidosis and result in a decrease in myocardial contractility. Instead. it remains carbonic acid. These actions profoundly increase myocardial oxygen demand and increase the risk of myocardial ischemia. it may cause hypernatremia and increase serum osmolality. Because of the high sodium content. it is not given to patients in respiratory acidosis. Indications Sodium bicarbonate is indicated for several specific causes of pulseless electrical activity or asystole within ACLS protocols.  2010 Orlando Health. automaticity and conductivity.

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. vomiting.CV Pharmacology Check Yourself Pop Quiz 1) Choose the signs and symptoms of digoxin toxicity? a) Nausea. diarrhea b) Heart blocks. Education & Development 42 . ___________________________________  2010 Orlando Health. _______________________ 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. junctional rhythms. 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.

3.CV Pharmacology Check Yourself Pop Quiz -Answers 1. Education & Development 43 . 7. Reviewing your incorrect answers will benefit your learning as you proceed in this packet. 2. d b c Dobutamine / 5mcg/kg/min b C Phenylephrine (Neo-Synephrine) Refer to previous section as a review for any incorrect answers. 5 6. 4.  2010 Orlando Health.

It is given as a single IV push bolus over 5 seconds. The most commonly used plasminogen activator (tPa. and areas of injury. alteplase). and there is no continuous intravenous infusion to be monitored. resulting in less degradation of circulating clotting factors in comparison to other agents. They also may result in intracranial hemorrhage leading to death.50 mg/kg over the next 60 minutes not to exceed 35 mg. is a fibrinolytic enzyme that fibrinolytics include tissue Examples of Drugs: tPA. surgical sites. They also should be prepared gently to avoid foaming and should be gently swirled. then 50 mg infused over 30 minutes. Retavase (reteplase. and Retavase (reteplase r-PA) and TNKase (tenecteplase). Alteplase) the dosage is based on weight with a total maximum dose of 100mg. The risk of bleeding remains for several hours to several days following administration. All three agents have shown similar efficacy.CV Pharmacology Fibrinolytic Agents Fibrinolytic agents activate plasminogen to form plasmin.75 mg/kg infused over the next 30 minutes not to exceed 50 mg. Precautions and Interactions All fibrinolytic agents may cause bleeding from puncture sites. In all cases they are to be mixed in normal saline or D5W. activase. tPA (Activase. Tenecteplase has an enhanced specificity for fibrin and is highly clot selective. followed by 0. with the dose based on the patient’s weight. Fibrinolytics may also be used in the emergency management of acute pulmonary embolism. Alteplase (tPA) and reteplase (r-PA) are fibrin-selective agents. a 15 mg intravenous bolus is given. TNKase (tenecteplase) is provided in a kit containing a vial with 50 mg TNKase and sterile water with a needleless injection system. is not weight based. For patient’s >67 kg an intravenous bolus dose of 15 mg is given over 1-2 minutes. alteplase.  2010 Orlando Health. Education & Development 44 . Plasmin digests or dissolves fibrin clots. with an additional 10 units as an intravenous bolus given 30 minutes following the initial bolus. The total dose should not exceed 50 mg. meaning that they act primarily on plasminogen that is bound in blood clots. Indications All of the fibrinolytic agents are indicated in the management of acute myocardial infarction. Reteplase (r-PA) has the advantage of reducing the nursing time involved in administration since it requires no mixing or preparation. Activase. r-PA) TNKase (tenecteplase). They must not be mixed in bacteriostatic preparations. For patient’s < 67 kg. not shaken. When used for acute myocardial infarction. Administration Dosage and administration of fibrinolytics vary depending on the indication for which they are being used and institutional protocols. followed by 35 mg over the remaining hour. and then 0. tPA is also approved for use in the management of acute stroke and in the management of acute peripheral vascular thrombosis. Reteplase (r-PA) is generally administered as an initial 10 unit intravenous bolus over two minutes.

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.. 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. 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. the higher the INR. symptoms are to be managed with morphine and antidysrhythmics. including changes in neurological status. When used in the management of acute myocardial infarction. dementia. or hypotension. It is vital not to stop the administration of the fibrinolytic agent due to reperfusion symptoms. Education & Development 45 . 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. 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.CV Pharmacology 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.  2010 Orlando Health. NOTE: See package insert or institutional guidelines for more information. 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). These are viewed as advisory for clinical decision making and may not be all-inclusive. If needed. abdominal pain or rigidity.g.

does not work through the ADP pathway. and bivalirudin (Angiomax). Aspirin. Platelet Aggregation Inhibitors These drugs. Administration of these agents can result in reducing refractory myocardial ischemia. another antiplatelet agent. thrombocytopenia. and as an adjunct to percutaneous coronary interventions (PCI). Patients are to be monitored closely for signs of bleeding. and Integrilin are indicated in the treatment of refractory unstable angina. In addition. its use is generally reserved for patients  2010 Orlando Health. and aplastic anemia. Indications Reopro. Precautions and Interactions Also refer to fibrinolytics for the contraindications of GP IIb/IIIa inhibitors.CV Pharmacology Platelet Inhibitors IIb/IIIa GP Platelet Inhibitors Platelet inhibitors bind to the platelet receptor site named the glycoprotein IIb/IIIa site. Administration Please consult Lexi-Comp. clopidogrel (Plavix). Consequently. Please contact a pharmacist at your facility for further information. Micromedex. unfractionated heparin and enoxaparin (Lovenox). Aspirin irreversibly inactivates the COX-1 enzyme in platelets preventing the formation of thromboxane A2 (a platelet aggregating substance). such as angioplasty an planned within 24 hours. abdominal pain or rigidity. to block the ADP pathway to prevent platelet aggregation and prolong bleeding time. The effect of all of these agents is irreversible for the life of the platelets modified. These agents should not be used together and need to be used cautiously with other drugs that effect clotting. Aggrastat. Reopro is a monoclonal antibody derivative. Because ticlopidine can cause life-threatening hematological reactions including neutropenia. Drugs in this class include Reopro (abciximab). Education & Development 46 . myocardial infarction. and Integrilin (eptifibatide). include Plavix (clopidrogrel) and Ticlid (ticlopidine). work by modifying the platelet membrane. platelet function and bleeding time may take up to 2 weeks following discontinuation of the drug to return to normal. A platelet assay count should be monitored daily during therapy. 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. Aggrastat (tirofiban). and hypotension. meaning it has the potential to cause allergic and anaphylactic reactions if the patient has had this drug in the past. and mortality. Consequently. and PDR for dosage administration and usage. These receptor sites function at the end of final common pathway to block the binding of fibrinogen and other components in the clotting cascade. this action inhibits platelet aggregation and blood clotting. It is important to note that all of these agents have been administered in clinical trials with aspirin. thrombotic thrombocytopenic purpura (TTP). One must obtain a platelet count within 4 hours of the bolus therapy. agranulocytosis. changes in neurological status.

Furthermore. 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. warfarin. or for those in whom other agents have been ineffective.000 of those taking clopidrogrel.CV Pharmacology who are unable to take clopidrogrel or aspirin. heparin. nausea. Precautions and Interactions Platelet aggregation inhibitors should not be used in any patients with active pathological bleeding such as peptic ulcer or intracranial hemorrhage. Blood dyscrasias as previously listed. ticlopidine is rarely used & is usually given to patients unable to take other agents or in those for whom other agents are ineffective. are administered with extreme caution to patients taking ticlopidine or clopidrogrel. stable and unstable angina. along with heparin or enoxaparin (Lovenox). In addition to the bleeding precautions for aspirin. These reactions have resulted in discontinuing the drug in approximately 3% of patients taking clopidrogrel and 21% of patients taking ticlopidine. © 2010 Orlando Health. numerous studies have proven the efficacy with acute onset MI. In such cases an enteric coated aspirin preparation may be suitable. Because of its increased risk for adverse reactions. there may also be some notable GI distress or bleeding. The clinical indications for aspirin and clopidogrel continue to expand because platelets play such an important role in all types of vascular disease. aspirin and/or clopidogrel become part of the standard adjunct therapy. and abdominal pain. the incidence is approximately 1 out of every 2000-4000 patients taking ticlopidine and approximately 1 out of every 250. trauma or surgery. vomiting. and non-hemorrhagic strokes. may occur with either of these agents. They are also used with patients with acute coronary syndromes who are undergoing PCI. constipation. cath lab procedures. diarrhea. For example. They are to be used with caution in patients who are at risk of increased bleeding due to impaired liver function. They should also be discontinued 7-14 days prior to elective surgery. Adverse reactions include rash. When a GPIIb/IIIa inhibitor is used. and NSAIDs that may interfere with hemostasis. Education & Development 47 . drugs such as aspirin.

headache. Other adverse events that may occur include the rare but serious effects of anaphylaxis and respiratory effects (bronchospasm. and bleeding or oozing from venous access sites. stridor. retroperitoneal bleeding. Lepirudin is a derivative of hirudin (the first direct thrombin inhibitor) and is a very potent and Examples of Drugs: specific inhibitor of thrombin. including intracranial bleeding. Angiomax® (bivalirudin) Indications Bivalirudin is indicated for patients with unstable angina undergoing percutaneous transluminal coronary angioplasty. Lepirudin slowly forms a reversible Angiomax (bivalirudin) complex with two sites on the thrombin molecule. Thrombin also activates platelets. dyspnea. pain. nausea. and hypotension. and bleeding or oozing from venous access sites. bivalirudin. including oozing or bleeding from venous access sites or the presence of blood in urine or stool. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications. Patients should be monitored closely for any signs of bleeding. which is a synthetic compound. Argatroban Argatroban binds reversibly to thrombin. including intracranial bleeding. and cough). retroperitoneal bleeding.  2010 Orlando Health. binds at two sites on the Refludan (lepirudin) thrombin molecule but only acts transiently at one site.CV Pharmacology Direct Thrombin Inhibitors These drugs specifically target and bind to sites on thrombin. Education & Development 48 . Patients receiving therapy with bivalirudin need their renal function evaluated prior to administration of and upon discontinuation of the infusion. Whereas. 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. Angiomax is also recommended to be used in patients with a history of heparin induced thrombocytopenia. effectively inhibiting the conversion of fibrinogen to fibrin and interrupting the formation of the hemostatic plug. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications. Other adverse events that may occur include back pain.

The degree of anticoagulation is monitored by measuring the aPTT. the INR is to be determined during warfarin monotherapy 4-6 hours after the discontinuation of argatroban infusion. Because of a drug-laboratory interaction. Education & Development 49 . Administration 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. warfarin (Coumadin) is to be discontinued when the INR on combined therapy exceeds 4. An aPTT 1. Doses are reduced for patients with moderate to severe hepatic impairment (0. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications.5-3 times the normal value is considered therapeutic. Next. If the INR is below the desired range. argatroban can falsely elevate the INR. For an argatroban infusion rate of 2 mcg/kg/min.CV Pharmacology 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. © 2010 Orlando Health.5 mcg/kg/min). the physician should be contacted and argatroban resumed.

are indicated as an adjunct to __________________ within _____ hours. ________________. Education & Development 50 . 7. patients require close monitoring of: a) _____________________________________________________________ b) _____________________________________________________________ c) _____________________________________________________________ 3. ________________________________________________ agents block the final common pathway for platelet aggregation. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors. ____________________________________________________________________ 8. Platelet function may take up to _____________ weeks to return to normal following the discontinuation of clopidrogel or ticlopidine. and ___________________. Platelet Aggregations inhibitors are used for the following. ______________________ ______________________ 2.CV Pharmacology Check Yourself Pop Quiz 1. State 2 absolute contraindications of fibrinolytic therapy. An acute MI patient receiving fibrinolytics may experience ______________________ or __________________________ as the supply of oxygenated blood is restored. (Please state your answer below). 4. The GP IIb/IIIa platelet inhibitors named _________________. Which of the following drug category bind to sites on thrombin to inhibit the conversion of fibrinogen to fibrin. 6. a) Fibrinolytics b) Platelet Inhibitors c) Direct Thrombin Inhibitor d) Direct Fibrin Inhibitor  2010 Orlando Health. You are screening your new admission for possible fibrinolytic therapy. 5.

______________. and ______________. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors. 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. patients require close monitoring of: bleeding. An acute MI patient receiving fibrinolytics may experience ______________________ or __________________________ as the supply of oxygenated blood is restored. Aggrastat..CV Pharmacology Check Yourself Pop Quiz -Answers 1. two weeks 6. ________________________________________________ inhibitors block the final common pathway for platelet aggregation. 24 hours  2010 Orlando Health. PCI. Reopro. are indicated as an adjunct to _______________ within _____ hours. Integrilin. changes hypotension in neurological status. 3. chest pain 4. dysrhythmias. abdominal pain/rigidity.g. The GP IIb/IIIa platelet inhibitors named ______________. 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. GPIIb/IIIa platelet 5. Platelet function may take up to _____________ weeks to return to normal following the discontinuation of clopidrogel or ticlopidine. Education & Development 51 .

C.CV Pharmacology 7. 8. PVD. They are also used with patient with ACS who undergo PCI. Education & Development 52 . Which of the following drug category bind to sites on thrombin to inhibit the conversion of fibrinogen to fibrin. Direct Thrombin Inhibitor © 2010 Orlando Health. Platelet Aggregation Inhibitors are used for the following: Reduce risk of thrombotic events such as MI and stroke.

myocardial irritability. patients with sulfa allergies may demonstrate a cross-sensitivity. and ethacrynic Acid (Edecrin). For example. HCTZ and spironolactone (Aldactazide) HCTZ and amiloride (Moduretic) 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. and because these agents are ototoxic. one class acts on the loop of Henle and another on the distal nephron. loop diuretics inhibit this transport system to increase the elimination of sodium and water in the urine.  2010 Orlando Health. Edecrin® is rarely used so it may be difficult to obtain. Diuril (chlorothiazide) Zaroxolyn (metolazone) Potassium sparing: triamterene (Dyrenium) amiloride spironolactone (Aldactone ) eplerenone (Inspra) Combination: HCTZ and triamterene (Maxzide). or vasodilator therapy. This is achieved using the sodium/potassium/chloride transport system. Education & Development 53 . calcium. bumetanide (Bumex). corticosteroids. torsemide (Demadex) ethacrynic Acid (Edecrin) Thiazide: hydrochlorothiazide Lozol (indapamide). Loop diuretics may elevate the blood sugar in diabetics. Patient teaching must include education on a potassium rich diet. estrogen. The loop diuretics are named: furosemide (Lasix). there is an increased risk of tinnitus and deafness when administered too rapidly or in doses exceeding the recommended daily maximum. potassium. potassium replacement therapy may be necessary. Examples of Drugs: the degree of potency varies with the classes. and reduction of acites due to cirrhosis. or magnesium may lead to metabolic alkalosis. Consequently. Demadex. Indications for all classes The main indications for diuretics are hypertension.CV Pharmacology Diuretic Agents Diuretics are defined as any drug that increases urine flow by altering the physiologic renal mechanisms that form urine to promote diuresis. torsemide (Demadex). bumetanide (Bumex). Diuretics are divided into classes based on how they effect each of the different sections of the nephron. some are more potent than others resulting Loop: in a greater excretion of electrolytes and water. relief of heart failure symptoms. Also. for example. reduction of edema due to renal dysfunction. Specifically. Loop diuretics increase serum uric acid levels and may precipitate gout in susceptible patients. management of heart failure. Moreover. and Bumex are sulfonamide derivatives. and ventricular dysrhythmias. It is also important to note that since Lasix. the depletion of sodium. furosemide (Lasix) while others cause potassium to be retained. as well as their potency in the presence of normal or abnormal renal function. Edecrin is the most ototoxic of the loop diuretics. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. They are known for their rapid onset of action and venodilator effects.

The depletion of potassium may lead to metabolic alkalosis. there are two groups of potassium-sparing diuretics that act at the distal portion of the nephron. The advantage is that sodium loss is achieved without a major loss of potassium or magnesium. either alone or in combination with other antihypertensives. Lozol (indapamide). and ventricular dysrhythmias. © 2010 Orlando Health. Thiazide Diuretics Thiazide diuretics main actions are to inhibit the transportation of sodium and chloride in the distal nephron. myocardial irritability.CV Pharmacology It is recommended that before administering to a patient with sulfa allergies. Diuril (chlorothiazide). 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. Potassium-Sparing Diuretics Currently. which inhibit the effects of aldosterone. Commonly. Thiazide diuretics are chosen in the treatment of diabetes insipidus. Indications Thiazide diuretics are indicated for the treatment and management of hypertension. Likewise. potassium diuretics are given in combination with hydrochlorothiazide. The first group. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. and Zaroxolyn (metolazone). Education & Development 54 . or for fluid retention from premenstrual syndrome. HCTZ and spironolactone (Aldactazide). and water in the urine. These agents will be discussed separately. 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. since thiazide diuretics tend to retain calcium. and HCTZ and amiloride (Moduretic). Products include: HCTZ and triamterene (Maxzide). The other group consists of spironolactone (Aldactone) and eplerenone (Inspra). block the sodium channels to interfere with sodium reabsorption in the distal and collecting tubules of the nephron. Thiazide diuretics may increase total blood cholesterol and like loop diuretics may elevate blood sugar in diabetics. estrogen. This action results in an increased loss of sodium. chloride. triamterene (Dyrenium) and amiloride. the nurse needs to check with the pharmacy or the prescriber. Thiazide diuretics are also used when a longer (versus shorter acting loop diuretic) duration of action is needed. there is an increased risk of tinnitus and deafness when administered too rapidly or in doses exceeding the recommended daily maximum. there is a mild risk of hypercalcemia. Because all diuretic agents can be ototoxic. or corticosteroid therapy. The most commonly used thiazide agents are hydrochlorothiazide. They can also decrease excretion of uric acid resulting in an increasing risk for gout attacks in patients with this disease.

Hyperkalemia can occur with both agents and the incidence is increased in patients on potassium supplements. Concurrent use with ACEinhibitors and non-steroidal anti-inflammatory agents may cause hyperkalemia. this category of diuretics eliminates the need for gastric-irritating potassium supplementation since they do not cause potassium excretion. and ventricular dysrhythmias.e. Precautions and Interactions Because spironolactone is similar to steroids. ARBs. to be increased. Indications Both of these agents are indicated for the management of hypertension either as monotherapy or in combination with other antihypertensives. while excreting potassium in the urine. These drugs are also important heart failure therapies. These effects are seen less often with eplerenone. eplerenone was shown to improve survival in hemodynamically stable patients with left ventricular dysfunction who demonstrated clinical evidence of heart failure following AMI. The most common is GI distress. Administration Both spironolactone and eplerenone are administered orally once daily. it is considered a selective aldosterone receptor antagonist. Spironolactone is frequently used to counter the effects of elevated aldosterone in conditions such as heart failure. Aldosterone is an endogenous steroid that acts on the kidney to retain sodium and water. In men. NSAIDS).CV Pharmacology Indications For patients intolerant of oral potassium supplements. © 2010 Orlando Health. cirrhosis. In other studies. It may also counteract the rise of angiotension II and aldosterone. Spironolactone binds to the aldosterone receptor to prevent the retention of sodium and water and the excretion of potassium. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. ACE-inhibitors. Education & Development 55 .. and nephrotic syndrome. myocardial irritability. whereas spironolactone is non-selective. Patient teaching includes information about avoiding potassium rich foods or vitamin supplements containing potassium. Eplerenone shares the same pharmacologic properties as spironolactone. it has the potential to produce some of the same adverse effects. loop diuretics) reduced hospital admissions and mortality. there also may be an increased risk of gynecomastia. Aldosterone Antagonists Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. and drugs that cause potassium retention (i. digoxin. Studies of patients with severe heart failure demonstrate that spironolactone added to conventional therapy (ACE-inhibitors. The depletion of sodium or an excess retention of potassium may lead to metabolic alkalosis. Potassium sparing diuretics may cause the levels of some drugs such as digoxin. however.

__________ Drugs such as NSAIDS may be co-administered with “potassiumsparing” diuretics without the risk of adverse consequences. loop diuretics do not require potassium supplementation. 9. eplerenone. 5. __________ Thiazide diuretics may increase total serum cholesterol. 8. __________ Thiazide diuretics have a much shorter duration of action than the other diuretic classes.CV Pharmacology Check Yourself Pop Quiz Insert either TRUE or FALSE for each statement 1. 2. __________ Aldosterone acts on the kidney to retain sodium and water and excrete potassium in the urine. 6. __________ Loop diuretics are the only class of diuretics that may cause ototoxicity. __________ It is important to emphasize to the patient receiving spironolactone to eat potassium rich foods daily. 7. thiazide diuretics are the most likely to cause hyperkalemia and hypercalcemia.  2010 Orlando Health. __________ Diuretics can be divided into three major classes. __________ Some examples of drugs known as “potassium-sparing” diuretics are triamterene. 10. __________ Patients with a documented adverse reaction to sulfa drugs may not be able to safely receive loop diuretics. 4. Due to the inherent properties of this class. __________ When comparing all the classifications of diuretics. 3. Education & Development 56 . and spironolactone.

Education & Development 57 . F 10. T 3. F 8.CV Pharmacology Check Yourself Pop Quiz -Answers 1. T 6. T 7. F 4. F 5. F 2. F 9. T  2010 Orlando Health.

If a nurse receives the order “administer per protocol. contraindications. Upon successful completion of this packet.” the nurse needs to confirm the drug and dose. Education & Development 58 . Some physicians may have preferences that are not covered in this packet. It is not to be mistaken as a complete drug/nursing reference source. Many drugs may also require a dedicated IV infusion line for continuous or IV push administration. or special considerations of each drug class State patient teaching information As previously stated. as well as the physician’s orders and institutional or unit preferences. A number of the IV infusions may be concentrated if the patient receiving them is on a fluid restriction. be mindful of the dosing guidelines that have been presented. One must look up the drugs for complete information and nursing considerations. Remember that when mentioned. this packet is designed to introduce vital information regarding some of the most commonly administered cardiovascular drugs. For that reason. the mixing and administering of these drugs are general guidelines.  2010 Orlando Health. Certain units or institutions may have specific protocols they follow.CV Pharmacology Summary This completes the content of the Introduction to CV Pharmacology self-learning 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.

You have administered a dose of 17 mg/kg D. Lidocaine. You are caring for a patient in recurrent pulseless ventricular tachycardia who is receiving the initial bolus of Procainamide. Mexitil B. Which of the following is NOT a reason to stop the initial bolus dose of this drug? A. Metropolol. The dysrhythmia is terminated C. The QRS widens by 50% B. Your patient has been diagnosed with HIT (Heparin induced thrombocytopenia) Identify the drug that is the best choice to prevent further thromboembolic complications. Blocking the beta-2 receptors C. You are caring for a 40-year old male following an acute anterior myocardial infarction. The QT interval is 0. A. Sotalol C. Increasing myocardial oxygen demand B. Education & Development 59 . Decreasing myocardial work load D. Select the desired effect of giving this patient a Class II antidysrhythmic drug. A. Plavix 4. Which of the following antiarrhythmics agents is known to prolong the QTI. Retavase C.36 3. Blocking the conversion of angiotensin I to angiotensin II  2010 Orlando Health. Breviblock 2.CV Pharmacology Cardiovascular Pharmacology Post Test Instructions: Use the answer sheet provided on the previous page. Diltiazam. Reopro D. Refluden B. Calan D. thus requiring careful monitoring of both the QTI and the QTc? A. 1. Dofetilide.

bronchoconstriction 6. Suppression of ventricular ectopy 8. Bronchodilation D. Brief period of asystole C. Peripheral vasoconstriction C. You have just administered adenosine to a patient in SVT with a heart rate of 200. Partial rebreathing mask  2010 Orlando Health. brief rapid increase of the ventricular response B. Peripheral vasodilation B. The monitor alarm alerts you that the patient's rhythm has changed to polymorphic ventricular tachycardia (Torsades de pointes). Which of the following effects may occur after administration of beta blockade therapy? A. Amiodarone C. Bronchodilation. Adenosine B. Which of the following if observed is an expected response? A. You are caring for a 52-year old male following an anterior myocardial infarction. Magnesium sulfate D.CV Pharmacology 5. Increase in heart rate. Nonrebreathing mask: 100% D. alert. anxious. Education & Development 60 . Procainamide (pronestyl) 7. hypotension C. Hypertension. HR 130. Brief period of ventricular standstill D. Venturi mask: 40-50% C. decrease in heart rate B. Which of the following is an example of a high flow oxygen delivery system? A. BP 100/60. Nasal cannula B. Which of the following pharmacologic interventions should receive your highest priority? A. Hypotension. increase in respiratory rate D. Bronchoconstriction 9. Transient. The patient is awake. Stimulation of the alpha adrenergic receptors will cause what response? A.

Diuretics 12.CV Pharmacology 10. Procainamide  2010 Orlando Health. Direct thrombin inhibitors C. but extreme cautions needs to be given to which patient population when the drug is used. Non-hemorrhagic stroke 2 years ago D. Atenolol B. Intracranial bleeding 12 months ago B. Diltiazem D. To manage severe cardiomyopathy that has not responded to dobutamine B. To treat life-threatening atrial and ventricular tachyarrhythmias C. Heart failure patients D. Which of the following is a Class III antidysrhythmic that is used for the conversion of recent onset atrial fibrillation to sinus rhythm? A. To treat severe heart failure that has not responded to negative inotropics and diuretics D. Dofetilide C. Beta-blockers should be administered to patients with Acute Coronary Syndrome. Angiotensin II receptor blockers (ARBs) B. Post MI patients C. Surgery 10 weeks ago C. Which of the following drug category may increase total blood cholersterol? A. Select the statement that best reflects the current indications for Amiodarone. A. Your patient is ordered to be placed on a IIb/IIIa GP Platelet inhibitor in preparation for a percutaneous coronary intervention. The asthma and COPD patient population B. A. Education & Development 61 . Post bypass surgery patient population 11. Platelet inhibitors D. To treat junctional dysrhythmias that have not responded to atropine 13. Which of the following is a contraindication to the use of IIb/IIIa inhibitors? A. Admission 3 weeks ago for an acute peptic ulcer bleed 14.

Adenosine 18. Vasopressor therapy for severe hypotension C. ACE inhibitors D. Peripheral vasoconstriction C. Class III drugs  2010 Orlando Health. Epinephrine D. Bronchodilation D. Vasodilator therapy for acutely decompensated heart failure 19. Coronary artery vasodilation B. Stimulation of β2 adrenergic receptors will cause which of the following response? A. Adenosine 16. Norepinephrine B. Select the indication for the use of Nesiritide (Natrecor). Antidysrhythmic therapy for ventricular dysrhythmias D. Atropine B. Bronchoconstriction 17. Positive inotropic therapy for heart failure B. 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. Education & Development 62 .CV Pharmacology 15. Digoxin C. Atropine C. A. and increase electrical conduction through the AV node? A. 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. Diltiazem D. Beta blockers C. Calcium channel blockers B. Choose the drug whose action is to inhibit the parasympathetic nervous system to enhance automaticity of the sinus node. A.

Nausea.5 mg IV push C. Select the primary indications for ACE inhibitor and/or ARB therapy drugs? A. In the event of extravasation of a sympathomimetic agent. Hypokalemia.CV Pharmacology 20. Second degree heart block 24. A. Thaizde diuretic. A. Hypertension and bradycardia B. A dopamine IV infusion at (5 mcg/kg/minute) 23. vomiting. The primary physician orders a Nitroglycerin drip to be added to the patient regimen. Hypomagnesemia B. Which of the following interventions is contraindicated in a patient in sinus bradycardia (heart rate of 40) who is also hypotensive. A. Thaizde diuretic 22. Severe hypotension C. Ventricular myocardial irritability B. Digoxin toxicity is precipitated by which of the following factors. Atropine 0. Hypocalcemia. Beta Blockers. Hypermagnesemia. Heart failure and bradycardia  2010 Orlando Health. Loop diurectic C. and a headache D. Phentolamine (Regitine) C. Hypertension and heart failure C. Education & Development 63 . Phenylephrine (Neosynephrine) B. Hyperkalemia. Calcium Channel Blocker D. Epinephrine 21. Tachycardia and hypotension D. Lidocaine D. Select the possible drug to drug interaction that could occur. A. select the drug used to aid in minimizing tissue damage. A normal saline bolus of 250 ml B. Your patient is on Primacor drip for cardiomyopathy. Epinephrine 1mg IV push D.

3 weeks  2010 Orlando Health. Phenylephrine IV push followed with boluses D. Triamterene 28. Vasopressin 40 units IV push x one dose B. Select the appropriate dosage of Vasopressin for the treatment of pulseless VT or VF? A. Select the drug of choice for this problem? A. Dopamine IV infusion @ 3 mcg/kg/min B.0 units IV push x one dose C. Vasopressin 40 units IV push q3-5 minutes D. Your new orientee asks you how long the patient will need to observe bleeding precautions due to altered platelet functioning. 2 weeks D. Spironolactone B. Eplerenone C. Epinephrine 1 mg IV push C. Vasopressin 40 units IV push q10 minutes 27.CV Pharmacology 25. the systolic BP continues to remain less than 70. After addressing the patient’s volume status. A. Choose the diuretic that depletes potassium thus requiring patient education on the importance of consuming potassium rich foods. Vasopressin 4. Education & Development 64 . 6 weeks B. Furosemide D. Norepinephrine IV infusion 26. You received an order to discontinue clopidrogel on your post cath patient. 4 weeks C. Your best response would be: A.

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. Reteplase  2010 Orlando Health. Heparin B. Lepirudin C. The patient has recently been diagnoses with HIT (Heparin induced thrombocytopenia) from a prior treatment for a DVT.CV Pharmacology 29. A. Clopidrogrel D. Education & Development 65 . A cancer patient is admitted to the ED with a diagnosis of an acute inferior wall myocardial infarction.

2005 from http://www. ET AL. “Keeping Pace with Long QT”. BETHESDA MARYLAND. (2004-2005). 588-636. DALLAS : AMERICAN HEART ASSOCIATION. ANTMAN. 110. (2004). DRUGS FOR THE HEART (6TH ED. (2005). Colorado 80111-4740 Fax: 303-486-6464 American Society of Health-Systems Pharmacists AHFS DI® EssentialsTM Customer Service Department 7272 Wisconsin Avenue Bethesda. MD 20814 Toll-free: 866-279-0681 © 2010 Orlando Health. ST..com/ekg_readout. HANDBOOK OF EMERGENCY CARDIOVASCULAR CARE. SYDNEY C. AHFS DRUG INFORMATION ESSENTIALS. BERNARD J. AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. ACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION— EXECUTIVE SUMMARY. Hudson. Suite 300 Toll-free: 800-525-9083 Fax: (330) 656-4307 Greenwood Village.). 2008 FROM HTTP://CIRC.CV Pharmacology References AEHLERT. LIONEL H. BETHESDA MARYLAND.long-qtsyndrome. (2008).. PHILADELPHIA: ELSEVIER. CIRCULATION.).SAUNDERS _______________________________________ Drug Information Resources Lexi-Comp TM 1100 Terex Rd. Education & Development 66 .. DAVID (EDS. FIELD.). AHFS DRUG INFORMATION. SMITH. RETRIEVED JULY 2. BARBARA (2005). ELLIOT M.ORG/CGI/CONTENT/FULL/110/5/588 HAZINSKI. & GILMORE.html OPIE. ECGS MADE EASY (3RD ED. LOUIS : MOSBY AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. OH 44236 (877) 837-5394 Thomson Micromedex 6200 South Syracuse Way. & GERSH. MARY F. JOHN M.AHAJOURNALS. Retrieved February 2. (2004).