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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
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, broken down by classification, and to provide basic guidelines for safe administration by licensed healthcare providers.
Objectives
Upon completion of this self-learning packet, the participant should be able to: 1. Describe the normal physiological actions of the cardiovascular system. 2. Explain how cardiovascular drugs influence the cardiovascular system. 3. Describe the role oxygen has in the cardiovascular patient. 4. List the clinical indications for using cardiovascular pharmaceutical agents. 5. Identify the mechanisms of action for each drug or class of drug. 6. Describe side effects and appropriate precautions, contraindications, or special considerations of each drug class. 7. State the appropriate patient teaching information.
Instructions
In order to receive 4.0 contact hours, you must: complete the posttest at the end of this packet achieve an 84% on the posttest
For Non-Orlando Health employees: Complete the test using the bubble sheet provided. Be sure to complete all the information at the top of the answer sheet. You will be notified if you do not pass, and you will be asked to retake the posttest. Return to: Orlando Health, Education & Development, MP14, 1414 Kuhl Ave, Orlando, FL 32806 For Orlando Health Team Members: Please complete testing via Online Testing Center. Log on to: SWIFT Departments E-Learning Testing Center. Use your Orlando Health Network Login and password. Select SLP under type of test; choose correct SLP Title. Payroll authorization is required to download test.
Introduction
This self-learning packet (SLP) is designed to introduce basic information regarding some of the most commonly administered cardiovascular drugs. It is important to understand that although these drugs affect the cardiovascular system their use is not exclusive to cardiac departments. This Introduction to CV Pharmacology SLP is not designed to be an all-inclusive reference or to
CV Pharmacology
replace current drug references. Please refer to current comprehensive reference materials readily available for all healthcare providers such as LexiComp, Micromedex, and the PDR. This SLP does not indorse any specific product, however, the web based links and reference materials listed may be very helpful to you. Go to SWIFT for links to LexiComp and Micromedex, and check in your work area or the medical library regarding availability of the other information sources found in the References section of this SLP. The vast majority of patients who receive care for cardiovascular disorders require the administration of multiple drugs during their hospital stay. In order to achieve the best patient outcomes, it is vital that the healthcare provider understand the indications, actions and interactions, proper administration, and potential adverse effects of these pharmacologic agents. Please note that in current practice the terms arrhythmia and dysrhythmia are synonymous, meaning they are used interchangeably to indicate rhythms other than normal sinus rhythms.
A Note about ACLS

This SLP is not designed to include current ACLS algorithms. Please refer to current ACLS references for these guidelines.
CV Pharmacology
Autonomic Cardiovascular Innervation

In order to have a better understanding of how cardiovascular drugs work, a brief review of how the heart and circulation are regulated by the autonomic nervous system is needed. The autonomic nervous system is composed of two branches; the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). The SNS and the PNS normally work together to help maintain homeostasis in the body, including the cardiovascular system. The fibers of the sympathetic nervous system affect the organs and tissues in which they are located in by releasing norepinephrine (noradrenalin). These fibers are known as adrenergic fibers in reference to their relationship to norepinephrine. Some drugs are known as sympathomimetics because they mime or mimic the actions of the sympathetic nervous system. These drugs may also be known as adrenergic agents because they have the effects that stimulate the adrenergic fibers. The sympathetic nervous system innervates all chambers of the heart. Sympathetic stimulation (the fight or flight response) results in peripheral vasoconstriction, an increase in heart rate, faster speed of electrical impulses conducted through the heart (conductivity), and an increase in the strength with which the heart pumps blood (contractility). While fibers of the parasympathetic nervous system do exist in both the atria and the ventricles, they have a pronounced effect on the atria, while causing a minimal effect on the ventricles. The fibers of the parasympathetic nervous system affect the organs and tissues that they innervate by releasing acetylcholine. These fibers are known as cholinergic fibers in reference to their relationship to acetylcholine. Parasympathetic stimulation results in a decrease in heart rate, a slowing of electrical conduction through the AV node, and a mild decrease in the pumping action of the ventricles.
Properties of Cardiac Cells

Automaticity is the ability of the cardiac pacemaker cells to spontaneously initiate an electrical impulse without being stimulated from another source such as a nerve. Excitability is the ability of the cardiac cells to respond to an external stimulus, such as from a chemical, mechanical, or electrical source. Conductivity is the ability of the cardiac cell to receive an electrical stimulus and conduct the impulse to another cardiac cell. The conduction can be altered by factors such as sympathetic or parasympathetic stimulation, cardiac muscle damage, electrolyte imbalances and medications. Contractility is the ability of the cardiac cell to contract in response to an electrical stimulus.
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 () Alpha () receptors are most abundant in the peripheral arteries and veins, although some receptors are located in the coronary arteries. Stimulation of -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 () Beta () receptors are divided into cardiac (1) and non-cardiac (2) receptors. The 1 receptors are located within the heart. Stimulation of the 1 receptors are responsible for the cardiac effects caused by the sympathetic nervous system, such as increased heart rate, increased conductivity, and increased strength of myocardial contraction. Stimulation of the 2 receptors results in dilation of the peripheral arteries and dilation of the bronchial system in the lungs. Dopaminergic Dopaminergic receptors are located within the blood vessels of the kidneys, intestines, heart, and brain. Stimulation of the dopaminergic receptors has a vasodilatory effect in these blood vessels, increasing blood flow to those organs.
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.
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.
CV Pharmacology
Oxygen
Oxygen is present in the air all around us at a concentration of approximately 21%, but it is considered a drug. In fact, it is the most important drug contained in the ACLS protocols. All tissues within the body require oxygen and will begin to suffer damage if deprived for more than several minutes. The practice of cardiovascular medicine revolves around assuring the proper balance between oxygen supply and demand throughout the body. Regardless of any other actions taken during cardiovascular emergencies, if efforts fail to assure an adequate oxygen supply, other efforts will be wasted. Indications Supplemental oxygen is indicated for patients who are experiencing acute chest pain regardless of the cardiac cause. It is also used for patients with either demonstrated or suspected hypoxemia, since this may lead to metabolic acidosis. In addition, oxygen is used in all cases where CPR must be implemented. The best CPR you can provide only yields about 25-30% of the normal cardiac output. Since blood flow is diminished, one way to prevent tissue damage is to increase the oxygenation of the blood flow that you are providing. Administration Supplemental oxygen is given in a wide variety of doses and delivered in a number of ways depending on the patients particular need. Low Flow Low flow oxygen systems include nasal cannulas, simple face masks, nonrebreathing masks, and partial rebreathing masks. While partial rebreathing masks provide an oxygen concentration of 24-60%, nonrebreathing masks can provide an oxygen concentration between 55-95%. Regardless of the concentration (%), low flow systems do NOT supply sufficient gas volume to meet the patients needs. Therefore the patient must be able to inhale a sufficient amount of room air along with the oxygen provided. Additionally, as the patients breathing pattern changes, the oxygen concentration provided to the patient may need to be reassessed and appropriately modified. High Flow High flow oxygen systems provide a high volume of gas that is sufficient to meet the patients inspiratory need without inhaling additional room air. They supply a more accurate concentration (%) of oxygen. The venturi mask is the most common high flow system, and supplies oxygen at a rate of 24-40%. Use of the Bag-Valve-Mask Devices In a cardiac arrest, oxygen is delivered at a concentration of approximately 100% utilizing a bagvalve-mask (BVM) device. This concentration is used even in patients with chronic lung disease (such as COPD) until the resuscitation is over.
CV Pharmacology
Review of Antidysrhythmics
Antidysrhythmic drugs work by affecting the action potential (AP) of the myocardial cells. To understand how antidysrhythmic drugs affect the heart, one must be familiar with the action potential curve and its reflection of the cardiac cycle. An action potential curve refers to the electrical changes in the myocardial cell during the depolarization and the repolarization cycle. This activity can be compared to ourselves as we work and rest. In the heart, the working period is the depolarization cycle (systole), and the resting period is the repolarization cycle (diastole). These electrical charges are a result of specific ions (sodium, potassium, and calcium) that shift between the myocardial cell and the extracellular fluid via the sodium-potassium pump mechanism. The end result is the myocardial electrical activity known as the cardiac cycle (depolarization-repolarization phases) observable on the cardiac monitor or 12-lead EKG. The term Refractory is used to describe the extent to which a cell is able to respond to a stimulus. Absolute Refractory Period - During this period the cells cannot respond to any stimulus, regardless of strength. This period corresponds with the onset of the QRS complex to the peak of the T-wave. It is identified on the AP curve as phases 0, 1, 2, and the first half of phase 3. Relative Refractory Period This is the vulnerable period in which a strong stimulus may produce ectopic depolarization. This period corresponds with the last half of the T-wave, and is identified on the AP as the last half of phase 3 and phase 4. The following chart briefly explains the different phases of the action potential.
Action Potential Q MV 0 1 2 R T S ECG
Inside Cell 3 Cell Membrane
4 100 K Na Ca
4 K & Na Outside Cell
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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. Potassium begins exiting cells. This peak reflects the brief period that sodium channels close. Calcium channels open for a slow influx of calcium ions to prolong depolarization. Calcium plays a key role in myocardial contraction. This rapid downswing marks the closure of sodium and calcium channels to prevent any further entry of sodium or calcium into the cell. Potassium begins to move back into the cell.
ECG Waveform
QRS
Absolute Refractory Period
QRS

QRS
Phase 3 Beginning Repolarization Phase
QRS and first half of T wave Absolute refractory period until midpoint of T wave, then becomes relative refractory period, the last half of T-wave.
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.
Relative Refractory Period
Keep in mind the ECG only represents electrical heart activity, not the actual contraction of the heart. Based on these previously mentioned principles, antidysrhythmic drugs are designed to modify the movement of ions in the various AP phases by altering the electrophysiology of the cardiac cell. Based on this principle, antidysrhythmics are classified based on their mechanisms of action and effects on the action potential. Currently there are four main classes of antidysrhythmics. The classification system (VaughanWilliams) can assist you in recalling the actions and adverse effects.
Class I - - Block sodium ion channel

o o o
Class Ia Class Ib Class Ic
Class II (beta-blockers) - Block beta receptors Class III - Block potassium ion channels Class IV (calcium channel blockers) - Block calcium ion channels
In general, drugs within the same class are similar in action and adverse effects and some drugs may have properties of more than one class category. (Example: amiodarone, sotalol). It is also important to note that all antidysrhythmics have the potential (some worse than others) to
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produce proarrhythmic effects on the patient. This means they can either worsen the dysrhythmia or trigger new ones. Antidysrhythmics can also prolong the QT interval (QTI) resulting in lethal dysrhythmias. Consequently, it is critical to closely monitor patients during initiation and usage of antidysrhythmics. This includes closely monitoring the ECG measurement of the QTI or QT interval corrected (QTc). Note: It is essential to identify drugs that prolong the QTI. For further information, read below for ECG Measurement: The QTI and QTc, or use a current drug reference, and internet resources such as: http://www.long-qt-syndrome.com/ekg_readout.html http://www.qtdrugs.org
ECG Measurement: The QTI and QTc

Introduction The interpretation of changes in the QT interval is an important aspect in the evaluation of an ECG tracing. The QT interval, (QTI) represents depolarization and repolarization of the ventricles. The QTI includes the relative refractory period, during which the heart is vulnerable to any ectopic foci that can initiate a stimulus. Accurate measurement is significant, as a prolonged QTI has been linked to monomorphic ventricular tachycardia, polymorphic ventricular tachycardia (torsades de pointes), and sudden cardiac death. The use of the QT interval in clinical practice is not without controversy. The literature clearly indicates that prolongation of the QTI in certain situations is associated with dysrhythmias or sudden cardiac death within 6-48 hours of lengthening. Far from perfect, yet deemed important, evaluation of the QTI/QTc remains a hot topic as researchers strive to discover methods that will provide better sensitivity and specificity for detecting the electrophysiologic changes that increase the risk of arrhythmias and sudden death. Lack of standardization: An identified problem is lack of a uniform approach to measurement. Some institutions do not measure the QTI unless physician ordered, while others measure only the QTI and not the QTC. Underlying problems such as a bundle branch block will affect the rate, and yet a standard for evaluation has not been agreed upon. Data collection and interpretation: First, it is not clear precisely how the measurement can be used to predict and prevent sudden cardiac death. Second, specific values of parameters vary depending on the population and circumstances. Data collection for the purpose of investigating different formulas is difficult, as it requires a very large population with high quality ECG data. QTI variation though 24 hours: Another problem is that the QTI changes depending on wake and sleep states, lead selection, heart rate, sympathetic and parasympathetic tone. QTI and a wide QRS: A widened QRS due to a ventricular conduction block causes the QT interval to be longer without prolonged depolarization. Two methods are available for measuring the QTI in the presence of a wide QRS due to a conduction block: it can be measured from the end of the QRS (at the J point) to the end of the T wave, or the QRS interval can be subtracted from the QTI. It is important to note that many different pharmaceutical agents other than CV agents have the potential to prolong the QTI. Please refer to current drug references and the links listed below.
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Measurement of the QTI in stable sinus rhythm The QTI is measured from the beginning of depolarization of the QRS complex to the end of the T wave representing repolarization. The QTI may be short, normal, or prolonged (>.44). Although a short QTI may suggest hypercalcemia, it is often difficult clinically to distinguish between a normal or short QTI. The literature suggests that healthcare providers should not be as concerned with QT shortening as with prolongation. (Grauer, 1998). The recommended lead for measurement is lead II. Note: If a U wave is present, it is not to be included in the measurement. The possible problem of distinguishing the T wave from a U wave can be minimized by measuring the QTI in lead II. Example of QTI measurement (with permission Grauer, 1998)
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 .
Another method to determine if a QTI is prolonged in sinus rhythms (< 100 beats per minute) is to observe the R-R interval. The QTI is probably prolonged if it exceeds more than half of the R-R interval.
Example of evaluating R-R interval. (with permission Grauer, 1998)
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General Rules The QTI is normal if it is less than half of the R-R interval The QTI is prolonged if it is more than half of the R-R interval The QTI is borderline if it is approximately half of the R-R interval (Remember, this rule applies to a regular HR in the normal range of 60-100) A QTc > 0.44 is considered prolonged
Normal QT Intervals Corrected for given Heart Rate = (QTc) Heart Rate/minute
40 50 60 70 80 90 100 120 150 180 200
R-R Interval/sec
1.5 1.2 1.0 0.86 0.75 0.67 0.60 0.50 0.40 0.33 0.30
QTC
0.41-0.51 0.38-0.46 0.35-0.43 0.33-0.41 0.32-0.39 0.30-0.36 0.28-0.34 0.26-0.32 0.23-0.28 0.21-0.25 0.20-0.24
Recommended Actions: Remember to treat the patient not the monitor. Evaluate all the assessment data. Record the QTI and the QTC as part of the routine documentation on patients in critical care and telemetry monitoring areas. Identify conditions and drugs associated with a prolonged QT interval, and increase frequency in documenting the QTI/QTC. Example- a QTI/QTC on a patient receiving procainamide should be measured q 4 hours and prn. This strip documentation is to include the drug that patient is receiving. Notify the appropriate person immediately (i.e. physician, nurse, charge nurse) if changes are observed. Documentation, continued assessment, and report to next shift.
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How to Obtain a QTc Measurement The QT interval (QTc) measurement is a more accurate measurement of the QT interval (QTI). This corrected measurement adjusts for heart rate and rhythm variability since it is known that autonomic tone influences heart rate. For example, when the heart rate increases the QTI shortens, and when the heart rate decreases the QTI lengthens. The QTc is determined by dividing the QT interval by the square root of the R-R interval. Generally, a QTc greater than 0.44 seconds (450 ms) is considered prolonged. The formula used to calculate a QTC is called Bazetts Formula after the founding physician. Sequential Steps to Obtain a QTc Measurement
All diagrams used with permission from Long-QT-Syndrome.com.
Step 1- Obtain the QTI in seconds. This number becomes the numerator. Step 2- Obtain the R-R interval by counting the number of small boxes between two R waves, then multiply by 0.04. Step 3- Calculate the square root of the R-R interval as shown in the diagram and the example below. This square root number becomes the denominator. Step 4- Divide the numerator by the denominator. This number is the QTc
EXAMPLE: Step 1- QTI is 0.48 seconds. (Numerator) Step 2- The R-R interval is 24 boxes. (24 X .04 = 0.96 sec.) Step 3- Square root of the R-R is 0.98. (0.96 = 0.98) (Denominator) Step 4- 0.48 (numerator) divided by 0.98 (denominator) = QTc of 0.49 seconds = prolonged
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CV Pharmacology
Class I Antidysrhythmics
This class decreases the influx of sodium during phase 0 of depolarization. These drugs alter the absolute refractory period to decrease the risk of premature impulses from ectopic foci. Class I drugs also depress automaticity by slowing the rate of spontaneous depolarization of pacemaker cells. This class of antidysrhythmics is further broken down into subclasses Ia, Ib and Ic, depending on specific actions.
Class Ia
Blocks sodium to depress conductivity and prolong the refractory period of the heart. These drugs are potent sodium channel blockers (prolong QRS interval), and may prolong repolarization (prolong QT interval) through blockade of potassium channels. Indications These antidysrhythmics are used to treat atrial dysrhythmias, premature ventricular complexes, and ventricular tachycardia. Procainamide ( Pronestyl) is available in both oral and intravenous forms. When used as an intravenous bolus in the ACLS algorithm, it must be given no faster than 30mg/minute. Indications that procainamide must be stopped: Termination of the dysrhythmia Hypotension Reaching a total dose of 17 mg/kg Widening of the QRS complex by 50%, which indicates slowing of electrical conduction within the heart.
Examples of Drugs: disopyramide (Norpace) procainamide (Pronestyl) quinidine
Precautions Procainamide serum levels should be monitored in patients with renal failure or receiving constant infusion. All class I drugs depress myocardial contractility resulting in a lower cardiac output, which may lead to profound hypotension. Class Ia agents can prolong the QRS and QT intervals putting the patient at risk for ventricular dysrhythmias such as ventricular tachycardia or torsades de pointes. This risk is increased in patients with hypokalemia or hypomagnesemia. Consequently, it is important to monitor the patient and the QTI or QTc intervals.
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Antidysrhythmics: Subclass Ib
In comparison to other class I drugs, as sodium channel Example of Drug: blockers subclass Ib have the lowest potency because they produce little or no change in the action potential duration. Lidocaine Since they shorten refractoriness, they do NOT prolong the QTI/QTc. Additionally, because these drugs target irritable tissue, they are used to decrease myocardial irritability and make it more difficult for ectopy or fibrillation to occur. Indications Subclass Ib drugs are used to treat ventricular dysrhythmias Precautions Lidocaine should not be given to anyone allergic to local anesthetic agents such as "Novocaine". Toxicity of lidocaine is most commonly apparent in the central nervous system resulting in drowsiness, confusion/disorientation, and paresthesias. Lidocaine serum levels can be measured. therapeutic Levels of 1.5-5mcg/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.
Antidysrhyhmics: Subclass Ic
Subclass Ic drugs are the most potent sodium channel blocking agents (prolong QRS interval), but have little effect on repolarization (no effect on QT interval). Each of these drugs is associated with an increased overall mortality, so they are usually used in dysrhythmias that are resistant to other agents. 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.
Examples of Drugs: Propafenone (Rhythmol) Flecainide (Tambocor)
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Antidysrhythmics: Class II
Class II antidysrhythmics are beta-blockers. They act indirectly on electrophysiological parameters by blocking beta-adrenergic receptors (slow sinus rate, prolong the PR interval, with no effect on QRS or QT intervals). Beta-blockers compete for receptor sites with ones naturally occurring catecholamines such as epinephrine and norepinephrine.
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. Although their actions depend propanolol (Inderal) on which catecholamine receptor (1 versus 2) they block, these drugs will have effects that are directly opposite to catecholamines by decreasing automaticity, heart rate, conductivity, contractility, stroke volume, cardiac output and blood pressure and myocardial workload. Indications Beta-blockers are used for rate control of sinus tachycardia, SVT, atrial tachycardia, and atrial fibrillation. The early use of beta-blockers in Acute Myocardial Infraction (AMI) patients reduces the likelihood of ventricular arrhythmias, recurrent ischemia, and reinfarction, thereby decreasing mortality. Precautions Beta-blockers may precipitate hypotension, bradycardia, and heart failure, as well as mask signs of hyperthyroidism and hypoglycemia. During IV administration, carefully monitor BP, heart rate, and ECG due to their mechanism of action. Beta-blockers are used with extreme caution in patients with asthma and COPD because they may lead to bronchospasms when non-selective beta-blockers interfere with the stimulation of 2 receptors in the bronchial system.
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Antidysrhythmics: Class III

Class III drugs prolong repolarization (phase 3) by preventing any further entry of sodium or calcium into the cell. Potassium begins to move back into the cell. Class III drugs are further known as either mixed or pure class III. For example, although amiodarone is generally prescribed because of its class III properties, it exhibits electrophysiological characteristics of each of the other classes of antidysrhythmics. Whereas sotalol combines the class III property of prolonging the refractory period with the beneficial beta-blocking effects of class II drugs. Strict monitoring of the QTI/ QTc is essential for drugs within this class. Amiodarone (Cordarone) Amiodarone is an ACLS drug used for control of rapid ventricular rate due to an accessory pathway conduction in pre-excited atrial arrhythmias; after defibrillation and epinephrine in cardiac arrest with persistent ventricular tachycardia (VT) or ventricular fibrillation (VF); and control of hemodynamically stable VT, polymorphic VT, or wide-complex tachycardia of uncertain origin. Dofetilide (Tikosyn) Dofetilide (Tikosyn) is indicated for the conversion of atrial fibrillation or atrial flutter to sinus rhythm. It is also used to maintain sinus rhythm in patients with atrial fibrillation or atrial flutter. Only prescribers (physicians, nurse practitioners, physician assistants) who have received specialized training can prescribe dofetilide. Likewise, hospital pharmacists and nurses must have received education prior to dispensing and administering this drug . Therapy must be initiated in a hospital setting so the patient can be monitored for dysrhythmias. Careful monitoring of serum potassium,magnesium, and renal function must be done for patients receiving dofetilide. Additionally, a baseline QTC interval must be measured and dofetilide is not be administered if the baseline QTc is greater than 440 msec (>0.44) or greater than 500 msec (>0.50) in patients with ventricular conduction abnormalities. An increase in the QTc measurement of greater than 15% over baseline or greater than 500 msec (0.50) necessitates either a dosage reduction or discontinuation of dofetilide. Contact the cardiologist immediately if adverse signs occur. ECG monitoring is continuous during the initial dosing period with strict measurement and documentation of the QTc and patient tolerance. After a minimum three-day hospital stay with dose adjustment, the patient can be discharged home with a 7-day supply of medication. It is recommended that nursing collaborate with the hospital pharmacy for discharge planning. Sotalol (Betapace, Betapace AF) Sotalol is used for the treatment of documented ventricular arrhythmias (i.e. sustained ventricular tachycardia) that in the judgment of the physician are life-threatening, and for maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation or atrial flutter. Betapace AF is a modified version of Betapace, with specific manufacturer instructions that states
Examples of Drugs: Pure class III: ibutilide (Corvert), dofetilide (Tikosyn) Mixed class III: amiodarone (Cordarone), sotalol (Betapace and Betapace AF)
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substitutions are not to be made for Betapace AF since it is distributed with a patient package insert specific for atrial fibrillation/flutter. It is vital that sotalol be avoided with other beta-blockers since it also has class II effects that can result in profound hypotension. Sotalol doses are further adjusted for renal dysfunction. Ibutilide (Corvert) Ibutilide is indicated for the acute termination of atrial fibrillation or flutter of recent onset. The effectiveness of ibutilide has not been determined in patients with arrhythmias >90 days in duration. Ibutilide is available in IV form only, and has the potential to result in lethal ventricular dysrhythmias. Hypokalemia and hypomagnesemia are contraindications for ibutilide due to the increased risk of lethal ventricular dysrhythmias. The QT interval must be closely monitored initially, and for at least 4 hours following the infusion of ibutilide. Precautions All class III drugs prolong the QT interval to varying degrees which may result in lifethreatening ventricular dysrhythmias. The QTI and QTc must be carefully monitored and documented. It is important to also note that an array of drug categories other than cardiac can cause a prolonged QTI such as certain antibiotics, antifungals, antipsychotics, and others. The risk of dysrhythmias with class III drugs increases with hypokalemia and hypomagnesemia; these labs should be monitored closely and replaced if necessary. A unique adverse effect profile and drug interactions with dofetilide require additional guidelines for patient selection and administration. Only prescribers (physicians, nurse practitioners, physician assistants) who have received specialized training can prescribe dofetilide. Likewise, hospital pharmacists and nurses must have received education prior to dispensing and administering the drug. Dofetilide is available in a limited number of retail pharmacies. Patients need to contact their local pharmacy prior to discharge to see if the pharmacy is enrolled in the TIPS (Tikosyn in Pharmacy System) program. Retail pharmacies can call 1-877-TIKOSYN for further information.
Important Definitions: Inotropic effect is a change in myocardial contractility. A positive inotropic effect would increase contractility, while a negative inotropic effect will decrease contractility. Chronotropic effect refers to an increase in heart rate; a negative chronotropic is decrease in heart rate. Dromotropic effect refers to the influence the cardiac nerves have on the conductivity of impulses across the muscle. A positive dromotropic effect would increase conductivity, while a negative effect would decrease conductivity.
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Antidysrhythmics: Class IV
Calcium is critical to heart function due to its effect on cardiac output by increasing contractility and conductivity. Calcium channel blockers decrease contractility of the myocardium and slow conduction through the SA and AV nodes by inhibiting the influx of calcium and sodium during phase 2 of the action potential. These actions result in prolonging both the absolute and relative refractory periods. Drugs in this class also produce vasodilation of the peripheral and coronary arteries, thereby increasing the supply of oxygenated blood to the myocardium and reducing myocardial workload to reduce myocardial oxygen demand. Calcium channel blocker categories Two types of calcium channel blockers exist because they exert different effects.
Calcuim channel blockers known as (nondihydropyridines): cause coronary artery vasodilation, decrease heart rate, and decrease conduction through the SA and AV nodes. They are utilized to treat atrial dysrhythmias, angina, and hypertension. Diltiazem (Cardizem, Dilacor XR, Tiazac) verapamil (Calan, Isoptin, Verelan PM) Calcuim channel blockers known as (dihydropyridines): dilate peripheral blood vessels without affecting heart rate or contractility. They are utilized to manage hypertension and will be discussed later in this SLP. Nifedipine (Procardia, Adalat), amlodipine (Norvasc), felodipine (Plendil), isradipine (DynaCirc), nicardipine (Cardene), and nisoldipine (Sular)
The following page has a summary chart on the actions and indications for calcium channel blockers. Precautions Short acting nifedipine capsules (Procardia, Adalat) are not recommended for acute blood pressure reduction nor for chronic hypertension management due to risk of profound hypotension, cerebral ischemia or stroke, and/or death. Nifedipine should NEVER be administered sublingually or as a bite and swallow order.
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Summary chart of calcium channel blocker actions and indications

Calcium Channel Blockers Actions Potent vasodilator of coronary vessels. This effect increases coronary blood flow, and reduces coronary vasospasm. Vasodilator of peripheral vessels. Vasodilation occurs predominantly in arterioles; there is no significant effect on venous beds. Dihydropyridine agents reduce peripheral resistance and afterload. Negative inotropic effect. Nondihydropyridine agents cause a modest decrease in contractility and reduction of myocardial oxygen consumption. This effect is used to depress the frequency of hyperactive tissue causing arrhythmias. Negative chronotropic effect. Nondihydropyridine agents cause a modest lowering of heart rate. This effect is due to slowing of the SA node and results in reduced myocardial oxygen consumption. Negative dromotropic effect. By slowing conduction through the AV node, nondihydropyridine agents increase the time needed for each beat. This results in reduced myocardial oxygen consumption. Indications Angina
Hypertension
Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina
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Miscellaneous Antidysrhythmics Adenosine (Adenocard)

Adenosine interrupts electrical conduction in the AV nodal reentry pathways making it effective against supraventricular tachyarrhythmias and narrow complex tachyarrhythmias of unknown origin. A rapid IV push bolus of adenosine causes complete depolarization of the myocardium, resulting in a brief asystolic period that allows the heart's electrical activity to "reset" and return to sinus rhythm. Because of this action, administration of adenosine is often referred to as a "chemical cardioversion. Indications Generally slow the rhythm down sufficiently to allow for correct interpretation of atrial fibrillation or atrial flutter so that appropriate intervention may be made. Precautions Adenosine can induce a brief period of asystole, of 6-10 seconds. It is vital to have emergency resuscitation equipment readily available.
Magnesium
Magnesium is essential for the functioning of the sodium-potassium pump to drive myocardial electrical activity. A low serum magnesium level slows the return of potassium into the cell during phase 4 of the action potential, resulting in a prolonged relative refractory period and QT interval. Patients with a magnesium deficiency commonly have a high incidence of cardiac dysrhythmias, including torsades de pointes (TdP) and sudden cardiac death. Precautions IV administration can cause hypotension and circulatory collapse if given too fast.
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Match the definitions at the bottom with the terms at the top.
1. ________ Magnesium 2. ________ Class III 3. ________ Amiodarone 4. ________ Proarrythmic 5. ________ Class IV 6. ________ Class II 7. ________ Sotalol 8. ________ Dofetilide 9. ________ Absolute Refractory Period 10. ________ Relative Refractory Period
a) A drug class known to decrease the heart rate, conductivity, contractility. b) A drug class which decreases contractility and slows conduction though the SA and AV nodes. c) Time frame when cardiac cells cannot respond to any stimulus from ectopic sources, corresponds with the QRS and first half of the T wave. d) Treatment of choice for the dysrhythmia torsades de pointes. e) A mixed class III drug that is to be avoided with beta-blocker drugs. f) A class III drug used to convert recent onset atrial fibrillation to sinus rhythm. Healthcare providers must be inserviced prior to providing this agent. g) Indicated in emergency therapy for ventricular tachycardia or ventricular fibrillation. may also be used for PVCs. h) Describes a drug that may induce additional dysrhythmias. i) A strong stimulus may produce ectopic depolarization in the cardiac cells. Corresponds with the last half of the T-wave. j) Strict monitoring of the QTI/QTc is essential for drugs within this class.
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Check Yourself Pop Quiz -Answers

1. 2. 3. 4. 5. 6. 7. 8. 9. d j g h b a e f c
10. i
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Antihypertensives Angiotensin Converting Enzyme (ACE) Inhibitors

Before discussing the ACE inhibitors, let us take a moment to review the renin-angiotensin system. Renin is formed in the renal juxtaglomerular cells in response to certain types of stimuli. These stimuli include salt depletion, 2 stimulation, and a decrease in renal perfusion that might be found Examples of Drugs: in hypotension or hypovolemia. Next, renin mediates Capoten (captopril), Vasotec the formation of angiotensin-I in the liver. When (enalapril), Monopril (fosinopril), angiotensin-I reaches the lungs, it is converted by the Lotensin (benazepril), Mavik angiotensin converting enzyme into angiotensin-II. (trandolapril), Accupril (quinapril), Angiotensin-II causes vasoconstriction, promotes the Aceon (perindopril), Prinivil, release of norepinephrine, and stimulates aldosterone Zestril (lisinopril), Altace (ramipril), production resulting in sodium and water retention. Univasc (moexipril) Additional effects of angiotensin-II include increased systemic vascular resistance, arterial blood pressure, and intravascular volume. ACE inhibitor drugs work by blocking the angiotensin converting enzyme in the lungs so angiotensin-I is prevented from being converted to angiotensin-II. The outcome is a decrease in norepinephrine levels, prevention of systemic vasoconstriction and decreased blood pressure. Furthermore, aldosterone production is no longer stimulated by Angiotensin II, which results in decreased intravascular volume. Indications ACE inhibitors are used in the management of hypertension either alone or in combination with other anti-hypertensive classes and also for patients with type 1 diabetes mellitus to slow the progression of diabetic nephropathy. Precautions Due to their mechanism of action, ACE inhibitors may cause hypotension or symptoms related to hypotension, such as dizziness and syncope. It is important to understand that a number of patients who take ACE inhibitor drugs develop a persistent nonproductive cough. Patients are to be cautioned about these effects prior to initiating ACE inhibitor therapy. ACE inhibitor therapy may compromise renal function and result in transient increases in BUN and creatinine.
Angiotensin II Receptor Blockers (ARBs)

Angiotensin receptor blockade is a newer method of renin-angiotensin blockade. Unlike the ACE inhibitor drugs, they do not prevent the formation of angiotensin-II. Instead, they bind to receptor sites to prevent the effects of angiotensin-II. This results in a decrease in norepinephrine levels, prevention of
Examples of Drugs: Cozaar (losartan), Diovan (valsartan), Atacand (candesartan), Benicar (olmesartan), Avapro (irbesartan), Micardis (telmisartan), Teveten (eprosartan)
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systemic vasoconstriction and a decreased blood pressure. Indications ARBs are indicated for the treatment and management of mild to severe hypertension. Used in patients with heart failure because they block the vasoconstrictive effects of angiotension-II and the release of aldosterone. Precautions Angiotensin receptor antagonists may cause hypotension or symptoms related to hypotension. In some patients, the use of ARB therapy may result in transient increases in BUN and creatinine.
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Beta-Adrenergic Blockers
Beta-blockers inhibit the response to adrenergic stimuli by competitively blocking beta-1 adrenergic receptors within the myocardium and by blocking beta-2 adrenergic receptors within the bronchial and vascular smooth muscle. Some betaExamples of Drugs: blockers are specific for beta-1 receptors (atenolol, metoprolol, betaxolol, bisoprolol, esmolol). However, Lopressor, Toprol-XL beta-1 selectivity is dose-dependent and is not seen (metoprolol), Coreg (carvedilol), and Tenormin (atenolol). Zebeta with high doses of beta-1 selective drugs. Indications Used for hypertension, angina, MIs, and heart failure, dysrhythmias and rate control. Precautions Beta-blockers may precipitate hypotension and bradycardia. Oral beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. Concurrent use of beta-blockers, or the calcium channel blockers verapamil and diltiazem because bradycardia or heart block can occur. Beta-blockers should be avoided in patients with asthma and COPD because they may lead to bronchospasm when non-selective beta-blockers interfere with the stimulation of beta-2 receptors in the bronchial system. Likewise, cautious use is indicated in diabetics because they can mask prominent hypoglycemic symptoms.
(bisoprolol),Inderal (propranolol), Brevibloc (esmolol), Trandate (labetalol), Corgard (nadolol)
Fenoldopam (Corlopam)
Fenoldopam is a rapid acting vasodilator because of its dopamine agonist properties. It is used as an antihypertensive with the added bonus effects of natriuresis, sodium excretion, and improved renal blood flow. Indications Used for short-term management of severe or malignant hypertension when rapid reduction of blood pressure is needed. Precautions Due to its potent and rapid acting hypotensive properties, frequent blood pressure monitoring is necessary. Please review your institutions policy regarding patient placement in an appropriate telemetry unit.
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Sodium Nitroprusside (Nipride, Nitropress)

Sodium nitroprusside (Nipride) is a potent, fast acting drug producing vasodilation of both the arteries and the veins. This action results in decreasing afterload by reducing systemic vascular resistance and arterial blood pressure, and decreasing preload by increasing venous capacitance and reducing blood return to the heart. The preload and afterload reduction results in both decreased myocardial workload and myocardial oxygen demand. Nipride is used to managed hypertensive crises and control blood pressure in patients after vascular surgeries, coronary bypass surgery, dissecting aortic aneurysm. Precautions Sodium nitroprusside has a rapid onset and short duration of action making it very easy to titrate. The effects of this drug are observed almost immediately and disappear within a few minutes after it is discontinued. Sodium nitroprusside has the potential to cause severe hypotension that can lead to myocardial ischemia, myocardial infarction, or stroke. Patients must be monitored closely during initiation and titration. Due to its short duration, discontinuing the drug and elevating the patients legs should be sufficient to return arterial blood pressure to prior levels within several minutes. Cyanide is produced which is converted to thiocyanate in the liver and thiocyanate is eliminated mainly in the urine. Patients receiving high doses and/or prolonged infusions of nitroprusside, are at risk for cyanide and/or thiocyanate toxicity.
Clinical note: The patient is to be observed continuously for signs of cyanide toxicity, which include metabolic acidosis (may be the earliest sign of toxicity), nausea, tinnitus, blurred vision, changes in mental status, hyperreflexia, twitching, and seizures
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Vasodilators Nitroglycerin
Nitroglycerin is a potent vasodilator relaxing both the vascular smooth muscle of the arteries and veins and has a more pronounced effect on the venous system. Nitroglycerin decreases systemic arterial resistance and arterial blood pressure, increases venous capacitance and reduces preload. As a result, Examples of Drugs: nitroglycerin decreases myocardial workload and Tridil(IV), Nitro-Bid, Nitrostat, myocardial oxygen demand. isosorbide dinitrate (Isordil), Nitroglycerin also relieves vasospasm and dilates coronary arteries to increase blood flow to the myocardium, helping to relieve myocardial ischemia. Nitroglycerin is the drug of choice for the relief of all types of angina, stable, unstable, and prinzmetal. Precautions Because nitroglycerin is a powerful vasodilator, it may result in profound hypotension. As a result, it should be initiated cautiously and the patient closely monitored during titration. Headaches are common with all forms of nitroglycerin, so patients need to be instructed that this is an expected side effect. Patients receiving nitrate therapy should not take selective phosphodiesterase inhibitors used for erectile dysfunction (Viagra, Levitra, Cialis). The combination can worsen the hypotensive effects of nitrates, possibly resulting in potentially life-threatening hypotensive/hemodynamic compromise. In some cases, an intravenous nitroglycerin preparation may antagonize an IV infusion of heparin and therefore close monitoring of its effects is required. This is important to remember since these drugs may be administered concomitantly to patients diagnosed with an acute myocardial infarction or acute coronary syndrome.
isosorbide mononitrate, (Imdur, Monoket, Ismo), Hydralazine, Nesiritide (Natrecor)
Isosorbide
Compared to nitroglycerin, isosorbide dinitrate (Isordil) is a less potent vasodilator. Isosorbide dinitrate, isosorbide mononitrate, and nitroglycerin are collectively known as nitrates. Isosorbide dinitrate and one of its metabolites-isosorbide mononitrate (Imdur, Monoket, Ismo) are available orally, and sublingually. They are used for angina and for heart failure in combination with hydralazine (BiDil). Their mechanism of action is similar to nitroglycerin so they share the same precautions, interactions, and adverse effects. Nitrate tolerance Tolerance to the vascular and antianginal effects of individual nitrates and cross-tolerance among the drugs may occur with repeated prolonged use. Intermittent doses of nitrates by use of a nitrate-free interval of 10-12 hours may minimize or prevent the development of tolerance.
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Hydralazine
Hydralazine has direct vasodilatory effects on the vascular smooth muscle resulting in blood pressure lowering. It is one of the parenteral drugs of choice for management of pregnancyassociated hypertensive emergencies. However, other parenteral therapies (i.e., nitroprusside) are recommended for hypertensive crises in non-pregnant patients. When used parenterally, hydralazine is administered as intermittent doses. Hydralazine has been used in combination with isosorbide dinitrate as a second-line treatment of heart failure.
Nesiritide (Natrecor)
Nesiritide is a synthetic human B-type natriuretic peptide (BNP) with potent vasodilator properties. Nesiritide binds to the receptor sites of vascular smooth muscle resulting in an increase in cGMP, which is responsible for vasodilation of veins and arteries. It promotes diuresis and natruresis. It is currently indicated for the patient in acutely decompensated heart failure who is symptomatic with either minimal activity or dyspnea at rest. Precautions When B-type natriuretic peptide (BNP) lab values are ordered, the blood must be obtained prior to the administration of nesiritide (Natrecor). Since nesiritide (Natrecor) is a synthetic BNP, the lab results will be altered after this drug is administered. Due to its potent hypotensive properties, it is important to institute frequent blood pressure monitoring. Review your institutions policy regarding placement of the patient in an appropriate telemetry unit.
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Morphine Sulfate
Morphine sulfate is a powerful narcotic analgesic used to relieve severe acute or chronic pain and to relieve anxiety. It primarily stimulates venous vasodilation and a reduction in preload (the volume of blood in the ventricles at the end of diastole). An additional property is arterial vasodilation, resulting in a decrease in afterload (the force the ventricles must push against to pump blood into the aorta and pulmonary vasculature). By reducing preload and afterload, morphine diminishes myocardial workload and oxygen demand. Morphine is the drug of choice to relieve the pain and anxiety associated with ischemic chest discomfort and myocardial infarction because it decreases the myocardial oxygen. Morphine is also useful in the management of cardiogenic pulmonary edema by increasing venous capacitance (capacity), thus decreasing the return of blood to the right side of the heart and to the lungs. Precautions The most serious adverse effect of morphine is depression of the respiratory system. Careful monitoring of the respiratory rate and depth is necessary during administration of morphine. Rapid administration of morphine may result in respiratory arrest. Morphine causes venous and arterial vasodilation, thus hypotension may occur. The blood pressure must be closely monitored in patients receiving morphine. The effects of morphine can be reversed with naloxone (Narcan) 0.2mg 2.0mg at 2-3 minute intervals, to a maximum of 10mg.
Atropine
Atropine has numerous clinical applications so we will limit our discussion to those that involve the cardiovascular system. Atropine is known as a vagolytic or parasympatholytic because it counteracts the effects of the parasympathetic nervous system. This leaves the actions of the sympathetic nervous system unopposed so patients who have received atropine will display signs of increased sympathetic activity. Because parasympathetic innervation of the heart is primarily in the atria, atropine affects atrial activity. Atropine is indicated for symptomatic bradydysrhythmias. It enhances automaticity of the sinus node, and increases electrical conduction through the atria and the AV node. It is used in sinus bradycardia to increase heart rate.
Calcium Salts
Calcium is an essential electrolyte for normal cardiac and vascular function. Calcium is available in oral and parenteral forms for a wide variety of indications. Calcium Chloride is usually reserved for emergent situations requiring calcium replacement. Calcium Chloride must be given carefully because rapid administration can result in cardiac arrest. Calcium Gluconate is used more frequently because it is associated with fewer side effects than Calcium Chloride. Calcium replacement should be guided by ionized calcium levels to avoid hypercalcemia. Calcium salts will not be discussed further in this packet.
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1. Define parasympatholytic. What are the effects of this class of drugs on the heart? _________________________________________________________________ _________________________________________________________________ 2. Which class of drugs is used as a vasodilator and also blocks the conversion of Angiotensin I to Angiotensin II? ______________________________________________________________ 3. Name 3 effects of Angiotensin II? ______________________________ ______________________________ ______________________________ 4. Does Nitroglycerin have more effect on the venous or arterial system or equally on both? (Circle correct answer) Arterial system Venous system Equally on both system
answer)
Will this have more effect on ventricular preload or afterload? (Circle correct Afterload
Preload
5.
Select which system Nitroprusside has more effect on: (Circle correct answer) Venous system Arterial system Equally on both systems
List the effects Nitroprusside has on ventricular preload and afterload? _________________________________________________________________ _________________________________________________________________ 6. State the vasodilator agent that is used as a potent antihypertensive and rapid acting, but also has the effects of natriuresis? _________________________________________________________________
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1. Parasympatholytic is defined as counteracting the effects of the parasympathetic nervous system. This class of drug will enhance automaticity of the sinus node, increase electrical conduction through the atria and the AV node and will enhance conductivity. (Increases sinus and ventricular heart rate). 2. ACE inhibitor therapy blocks the conversion of angiotensin I to II, which occurs primarily in the lungs. The ARB therapy blocks the effects of angiotensin II after this conversion occurs. 3. Angiotensin-II causes vasoconstriction, promotes the release of norepinephrine, and stimulates aldosterone production resulting in sodium and water retention. Additional effects of angiotensin-II include increased systemic vascular resistance, arterial blood pressure, and intravascular volume. 4. NTG relaxes vascular smooth muscle of arteries and veins, but has a more pronounced effect on the venous system. Nitroglycerin will decrease systemic arterial resistance and arterial blood pressure, but it increases venous capacitance and reduces preload to a greater extent. 5. Sodium nitroprusside is a potent, fast acting drug which causes vasodilation of both arteries and veins. Because of this action, it decreases afterload by reducing systemic vascular resistance and arterial blood pressure, and decreases preload by increasing venous capacitance and reducing blood return to the heart. This preload and afterload reduction results in decreased myocardial workload and myocardial oxygen demand. 6. Fenoldopam (Corlopam).
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Vasopressor Therapy Clinical Application

Vasopressor drugs must not be used until the patients volume status has been addressed. The administration of vasopressors to hypovolemic patients does not increase blood pressure; instead it can result in profound tachydysrhythmias and ventricular tachycardia or ventricular fibrillation.
Should extravasation of this or any other alpha agonist occur, phentolamine (Regitine) may be used to help minimize tissue damage. Refer to your hospitals policy regarding the use of phentolamine for intravenous extravasation of these drugs.
Dopamine
Dopamine (Intropin) is a chemical precursor of norepinephrine. Dopamine stimulates alpha, 1, and dopaminergic receptors, depending on the administered dose, and also stimulates the release of norepinephrine Indications Dopamine is used primarily for symptomatic hypotension and to increase organ perfusion. According to the ACLS bradycardia algorithm, dopamine may also be considered in hemodynamically significant bradycardia, with the dose beginning at 5 mcg/kg/minute, following the use of transcutaneous pacing and/or atropine. In patients with cardiogenic shock, left ventricular failure, and pulmonary edema, dopamine may be used in conjunction with positive inotropic agents and vasodilators. This permits the beneficial 1 effects to predominate and counteracts the increases in preload and afterload caused by alpha stimulation. At low doses (1 4 mcg/kg/minute), dopamine stimulates the dopaminergic receptors to produce cerebral, renal, and mesenteric vasodilation. This dose is commonly thought to increase blood flow to the kidneys and may sometimes be referred to as the renal dose dopamine. The efficacy of dopamine for this indication is not supported in the literature. NOTE: Many clinicians currently suggest that low dose dopamine therapy does NOT prevent or ameliorate acute renal failure in patients. At moderate doses (5 -10 mcg/kg/minute), dopamine stimulates the 1 receptors in the myocardium. This increases contractility, cardiac output, and arterial blood pressure. At higher doses (10 20 mcg/kg/minute), the alpha agonist properties of dopamine are much more pronounced, resulting in significant increases in peripheral and venous vasoconstriction. This results in an increase in preload, afterload, and myocardial workload. It also significantly increases myocardial oxygen demand and negates the positive 1 and dopaminergic effects. At doses of 20 mcg/kg/minute or more, significant arterial vasoconstriction results. If hypotension continues, then other interventions should be considered.
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Precautions and Interactions As with any of the vasopressors, the patients volume status should be addressed before the administration of dopamine. Failure to do so may result in tachydysrhythmias, ventricular tachycardia, and ventricular fibrillation. MAO inhibitors strongly potentiate dopamine so the dosage should be only 10% of the recommended dose. The arrhythmogenic potential of dopamine increases as the dose increases, as does the increase in myocardial workload and myocardial oxygen demand. Since low dose dopamine causes vasodilation of the mesenteric and renal vessels, it tends to shunt blood to the kidneys and intestines, and may actually result in a slight decrease in blood pressure.
Clinical Application
It is recommended that all dopamine doses be administered through a central venous catheter since extravasation of dopamine causes tissue necrosis.
Epinephrine
Epinephrine, also known as Adrenalin, is a naturally occurring catecholamine which stimulates both alpha and beta receptors.Epinephrines alpha agonist activity results in peripheral vasoconstriction, which increases systemic vascular resistance as well as systolic and diastolic blood pressure. This results in increased coronary and cerebral perfusion blood flow. Epinephrines beta-1 agonist activity increases automaticity and myocardial electrical activity, myocardial contractility and cardiac output. Its beta-2 agonist properties result in bronchodilation. Epinephrine also inhibits the release of histamine, which is responsible for the cardiovascular collapse that occurs in severe allergic reactions and anaphylaxis. Indications Epinephrines adrenergic agonist properties make it useful in any pulseless rhythm such as asystole, pulseless electrical activity, ventricular fibrillation, and pulseless ventricular tachycardia. It also facilitates these ventricular rhythms to be more responsive to defibrillation. Additionally, when used as a diluted continuous intravenous infusion, epinephrine is useful for profound symptomatic bradycardia that has not responded to a pacemaker or atropine. Epinephrine is also used in the management of anaphylactic shock. It relieves bronchospasm, causes bronchodilation, and blocks the release of histamine (histamine is the chemical mediator that leads to the vascular changes in anaphylaxis thus leading to shock). It is further recommended that epinephrine be administered through a central venous catheter since extravasation of epinephrine causes tissue necrosis. Precautions and Interactions Note: Medication errors have occurred due to confusion with epinephrine products expressed as ratio strengths (i.e. 1:1000 vs. 1:10,000). Epinephrine 1:1000 = 1 mg/mL and is most commonly used Sub Q for hypersensitivity reactions or as a bronchodilator. Epinephrine 1:10,000 = 0.1 mg/mL and is used I.V. as part of the ACLS protocol.
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It is important to remember that by enhancing preload, afterload, and myocardial workload, epinephrine increases the myocardial oxygen demand resulting in an increased myocardial irritability that can induce ventricular ectopy.
Norepinephrine
Norepinephrine (Levophed) is a naturally occurring catecholamine that is structurally similar to epinephrine. Norepinephrine has very little effect on beta-2 receptors so it does not produce bronchodilation. The beta-1 agonist effects are comparable to epinephrine with additional effects such as increasing automaticity, myocardial electrical activity, myocardial contractility, and cardiac output. Additionally, norepinephrines alpha agonist effects result in a more pronounced peripheral vasoconstriction. As the dose of norepinephrine increases, the resulting increased afterload limits the beneficial inotropic effects and increases myocardial oxygen demands. This increased stress on the heart may exacerbate myocardial ischemia and extend a myocardial infarction. However, in shock states, the use of norepinephrine at low doses is common. It is especially beneficial in patients with septic and neurogenic shock, or other conditions that result in vasodilation (decreased systemic vascular resistance). Indications Norepinephrine is indicated for hemodynamically significant hypotension (<70mmHg SBP) and is particularly helpful in the presence of decreased systemic vascular resistance. As with any of the vasopressors, the patients volume status should be addressed before the administration of norepinephrine. Failure to do so may result in tachydysrhythmias, ventricular tachycardia, and ventricular fibrillation. Precautions and Interactions Norepinephrine increases myocardial workload and myocardial oxygen demand so it may precipitate myocardial ischemia or infarction. It also increases myocardial irritability and can result in ventricular dysrhythmias.
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Phenylephrine
Phenylephrine (Neo-Synephrine) is a sympathomimetic agent used primarily as an alpha agonist. In usual therapeutic doses, it causes vasoconstriction to increase systemic vascular resistance and arterial blood pressure. Indications From a cardiovascular perspective, phenylephrine is used in patients with hypotension and shock.
It is recommended that phenylephrine be administered through a central venous catheter since extravasation of phenylephrine causes tissue necrosis.
Precautions and Interactions In usual therapeutic doses, phenylephrine increases preload and afterload and resulting in increased myocardial oxygen demand. Phenylephrine may cause a slowing of the heart rate (reflex bradycardia) and is potentiated by tricyclic antidepressants and monoamine oxidase (MAO) inhibitors.
Vasopressin
Vasopressin (Pitressin) is a naturally occurring antidiuretic hormone found in the posterior pituitary. As a pharmacologic agent, vasopressin has several clinical applications, so our discussion is limited to the application of vasopressin within the ACLS guidelines as a vasopressor. Indications According to ACLS Guidelines, vasopressin is an effective vasopressor and can be used as an alternative for the first or second dose of epinephrine in the pulseless arrest algorithm. Dosing for Cardiac Arrest is 40 Units IV push x 1. IV is the only route recommended currently by AHA guidelines. Vasopressin may be useful for hemodynamic support in vasodilatory shock (e.g., septic shock). Precautions The half-life of vasopressin is 1020 minutes. As a result, after 10 minutes a decision needs to be made to give epinephrine because vasopressin can only be given once. At this time, vasopressin cannot be administered through the endotracheal tube, or as a continuous infusion.
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CV Pharmacology
Positive Inotropic Therapy Digoxin

Our discussion of digitalis preparations will be limited to digoxin (Lanoxin, Digitek) which is the most commonly prescribed form of digitalis. Digoxin is a positive inotropic agent as it increases the strength of myocardial contraction. Digoxin also decreases automaticity and prolongs electrical conduction through the AV node. Indications Digoxin is used as maintenance therapy for symptom control in patients with heart failure to increase myocardial contractility, stroke volume, and cardiac output. It also is used to control the ventricular rate with atrial fibrillation or atrial flutter by slowing AV nodal conduction. Note: For initial ventricular rate control in atrial fibrillation, IV calcium channel blockers and beta-blockers are used before digoxin due to the length of time digoxin takes to produce a slowing of the ventricular rate. Precautions and Interactions Digoxin has a very narrow therapeutic range and toxicity can develop rapidly. Symptoms of digoxin toxicity include nausea, vomiting, diarrhea, visual disturbances, and changes in mental status and level of consciousness. Toxicity also causes a wide variety of dysrhythmias, including heart blocks, junctional rhythms, and ventricular dysrhythmias. Toxicity is precipitated by hypokalemia, hyperkalemia, and hypomagnesemia. Many patients taking digoxin for heart failure also take diuretics that can deplete potassium and lead to toxicity. Be sure to provide patient education concerning the need to take any prescribed potassium supplements if the patient is on diuretic therapy. Digoxin is potentiated in such drugs as amiodarone, calcium channel blockers, and quinidine. In patients taking these drugs, digoxin should be used with caution and the dose might be reduced by 50%. Overdose of digoxin can be treated by the drug Digibind.
Digoxin should be avoided with those patients with sick sinus syndrome or significant atrioventricular nodal heart blocks such as complete heart block and second degree AV block.
Dobutamine
Dobutamine (Dobutrex) is a synthetic catecholamine. It is a potent 1 agonist to increase myocardial contractility and cardiac output. It is also a mild alpha agonist; however, the alpha effects are counteracted by the more potent 2 properties, resulting in a mild vasodilation effect. This vasodilation will decrease preload and afterload with a beneficial effect on myocardial oxygen supply and demand. At doses of 220 mcg/kg/min, it has only a minimal effect on the heart rate. By increasing the cardiac output in the presence of mild vasodilation, it will increase coronary, renal and mesenteric perfusion.
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CV Pharmacology
Indications Dobutamine is used to increase myocardial contractility and cardiac output in patients with left ventricular systolic dysfunction. By increasing cardiac output, dobutamine may result in an increase in arterial blood pressure. It is used concomitantly with volume loading in the presence of right ventricular myocardial infarction. It is commonly used with moderate dose dopamine (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. Precautions and Interactions Dobutamine may cause headache, nausea, tremors, and hypokalemia. Remember that hypokalemia may increase ventricular irritability and precipitate digoxin toxicity, so patients receiving dobutamine should be monitored for hypokalemia. While dobutamine may induce tachydysrhythmias and myocardial ischemia, it does so to a much lower extent than other catecholamines.
Phosphodiesterase (PDE) Inhibitors

PDEs inhibit the breakdown of cyclic AMP (cAMP) in cardiac and peripheral vascular smooth muscle, resulting in potent inotropic effects while dilating both arteries and veins. The net effect is similar to dobutamine. By increasing contractility and causing Examples of Drugs: vasodilation, the PDE inhibitors reduce preload and afterload and milrinone (Primacor) thus decrease myocardial oxygen demand. Note: Since is rarely used, our discussion will focus on milrinone. Inamrinone is seldom used due its significant problems with thrombocytopenia. Indications PDE inhibitors are used for patients with heart failure or systolic dysfunction cardiomyopathy. These agents are more effective in heart failure and cardiomyopathy than they are in the presence of ischemic heart disease. Precautions and Interactions Due to the potent vasodilation properties, hypotension can occur. Likewise, an increase in myocardial irritability may occur inducing both supraventricular and ventricular dysrhythmias. Although, Milrinone may cause a mild thrombocytopenia, the incidence is far lower than with inamrinone. Milrinone may also cause mild to moderate headaches.
inamrinone (Inocor) amrinone
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CV Pharmacology
Isoproterenol
Sometimes called the cardiac whip, Isopreterenol (Isuprel) is a potent beta-adrenergic agonist with essentially no alpha adrenergic activity. Isopreterenol produces large increases in myocardial contractility, automaticity and conductivity. These actions profoundly increase myocardial oxygen demand and increase the risk of myocardial ischemia, myocardial infarction, and dysrhythmias. Because of its severe side effect profile Isopreterenol is now used only for very specific indications, most commonly in cardiac transplantation. Because it is used so rarely, Isopreterenol will not be discussed further in this packet. For further information please refer to Lexicomp and Micromedex.
Sodium Bicarbonate
Sodium bicarbonate is used as a buffering agent in patients with a preexisting metabolic acidosis. When bicarbonate combines with an acid, it forms carbonic acid, which usually dissociates to water and carbon dioxide. In the presence of inadequate respiratory function (when carbon dioxide is not rapidly cleared from the system) carbonic acid does not dissociate to carbon dioxide and water. Instead, it remains carbonic acid, which can lead to an intracellular acidosis and result in a decrease in myocardial contractility. In general, the administration of sodium bicarbonate during a cardiac arrest situation is associated with poor resuscitation outcomes. For this reason, sodium bicarbonate is no longer routinely given as part of resuscitation efforts. Indications Sodium bicarbonate is indicated for several specific causes of pulseless electrical activity or asystole within ACLS protocols. It is given to patients with a preexisting metabolic acidosis such as patients in renal failure or diabetic ketoacidosis. However, it is not given to patients in respiratory acidosis. It can also be given to patients with hyperkalemia or those who have overdosed on tricyclic antidepressants or phenobarbital. A continuous infusion of sodium bicarbonate given immediately prior to and post procedure has been shown to reduce the incidence of contrast-induced nephropathy for patients undergoing cardiac catheterization, computed tomography (CT), diagnostic or therapeutic arteriography, or transjugular intrahepatic portal systemic shunt (TIPS) placement. Precautions and Interactions Sodium bicarbonate can lead to metabolic alkalosis if too much is administered. Because of the high sodium content, it may cause hypernatremia and increase serum osmolality, resulting in massive diuresis and cellular dehydration.
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CV Pharmacology

1) Choose the signs and symptoms of digoxin toxicity? a) Nausea, vomiting, diarrhea b) Heart blocks, junctional rhythms, ventricular dysrhythmias c) Visual disturbances and changes in mental status d) All of the above 2) Which of the following is an indication for the administration of sodium bicarbonate? a) Hypokalemia b) Tricyclic antidepressant overdose c) Respiratory acidosis d) Asystole 3) You are caring for a 71-year old male patient in heart failure. Which class of drugs is used to increase contractility? a) Beta blockade b) Calcium channel blocker c) Positive inotrope d) Negative inotrope 4) Name a drug that has potent 1 agonist properties and is indicated for treatment of left ventricular systolic dysfuntion. _______________________ What is the usual starting dose? _____________ 5) Stimulation of the dopaminergic receptors will cause which effect? a) Peripheral vasoconstriction b) Renal and mesenteric vasodilation c) Bronchodilation d) Bronchoconstriction 6) Choose the answer that best states the current ACLS Vasopressin dosage: a) 80 units b) 65 units c) 40 units d) 20 units 7) Identify a sympathomimetic drug that is used primarily as an alpha agonist. ___________________________________
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CV Pharmacology

1. 2. 3. 4. 5 6. 7. d b c Dobutamine / 5mcg/kg/min b C Phenylephrine (Neo-Synephrine)
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CV Pharmacology
Fibrinolytic Agents
Fibrinolytic agents activate plasminogen to form plasmin. Plasmin digests or dissolves fibrin clots. The most commonly used plasminogen activator (tPa, activase, alteplase, and Retavase (reteplase r-PA) and TNKase (tenecteplase). Alteplase (tPA) and reteplase (r-PA) are fibrin-selective agents, meaning that they act primarily on plasminogen that is bound in blood clots. Tenecteplase has an enhanced specificity for fibrin and is highly clot selective, resulting in less degradation of circulating clotting factors in comparison to other agents. All three agents have shown similar efficacy. Indications All of the fibrinolytic agents are indicated in the management of acute myocardial infarction. tPA is also approved for use in the management of acute stroke and in the management of acute peripheral vascular thrombosis. Fibrinolytics may also be used in the emergency management of acute pulmonary embolism. Administration Dosage and administration of fibrinolytics vary depending on the indication for which they are being used and institutional protocols. In all cases they are to be mixed in normal saline or D5W. They must not be mixed in bacteriostatic preparations. They also should be prepared gently to avoid foaming and should be gently swirled, not shaken. When used for acute myocardial infarction, tPA (Activase, Alteplase) the dosage is based on weight with a total maximum dose of 100mg. For patients >67 kg an intravenous bolus dose of 15 mg is given over 1-2 minutes, then 50 mg infused over 30 minutes, followed by 35 mg over the remaining hour. For patients < 67 kg, a 15 mg intravenous bolus is given, followed by 0.75 mg/kg infused over the next 30 minutes not to exceed 50 mg, and then 0.50 mg/kg over the next 60 minutes not to exceed 35 mg. Reteplase (r-PA) is generally administered as an initial 10 unit intravenous bolus over two minutes, with an additional 10 units as an intravenous bolus given 30 minutes following the initial bolus. Reteplase (r-PA) has the advantage of reducing the nursing time involved in administration since it requires no mixing or preparation, is not weight based, and there is no continuous intravenous infusion to be monitored. TNKase (tenecteplase) is provided in a kit containing a vial with 50 mg TNKase and sterile water with a needleless injection system. It is given as a single IV push bolus over 5 seconds, with the dose based on the patients weight. The total dose should not exceed 50 mg. Precautions and Interactions All fibrinolytic agents may cause bleeding from puncture sites, surgical sites, and areas of injury. They also may result in intracranial hemorrhage leading to death. The risk of bleeding remains for several hours to several days following administration. is a fibrinolytic enzyme that fibrinolytics include tissue
Examples of Drugs: tPA, Activase, alteplase), Retavase (reteplase, r-PA) TNKase (tenecteplase).
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The American College of Cardiology/American Heart Association Guidelines for the Management of Patients with ST-Elevation MI guidelines list the absolute and relative contraindications of fibrinolytic therapy. These are viewed as advisory for clinical decision making and may not be all-inclusive. NOTE: See package insert or institutional guidelines for more information, as well as the ACC/AHA Guidelines for the Management of Patients with ST Elevation Myocardial Infarction (updated 7/1/04) via the ACC website as listed in the References section of this SLP.
Absolute contraindications to the use of fibrinolytics include:

ANY HISTORY OF INTRACRANIAL HEMORRHAGE
Known malignant intracranial neoplasm (primary or metastatic) Known structural cerebral vascular lesion (e.g., AVM) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Active internal bleeding or bleeding diathesis (excluding menses) Suspected aortic dissection Acute pericarditis Significant closed head or facial trauma within 3 months
Relative contraindications must be weighed against potential benefits and include:

Severe uncontrolled hypertension (>180/110) or history of chronic severe hypertension History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications Pregnancy Active peptic ulcer or recent internal bleeding within the previous 2-4 weeks Non-compressible vascular punctures Current use of anticoagulants, the higher the INR, the higher the risk of bleeding Traumatic or prolonged (greater than 10 minutes) CPR or major surgery with the previous 3 weeks For streptokinase/anistreplase: Prior exposure ( more than 5 days) or prior allergic reaction to these agents
All patients are to be monitored closely for signs of bleeding, including changes in neurological status, abdominal pain or rigidity, or hypotension. When used in the management of acute myocardial infarction, the patient may experience chest pain or dysrhythmias when the coronary artery opens and the supply of oxygenated blood to the myocardium is restored (reperfusion). It is vital not to stop the administration of the fibrinolytic agent due to reperfusion symptoms. If needed, symptoms are to be managed with morphine and antidysrhythmics.
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Platelet Inhibitors IIb/IIIa GP Platelet Inhibitors

Platelet inhibitors bind to the platelet receptor site named the glycoprotein IIb/IIIa site. These receptor sites function at the end of final common pathway to block the binding of fibrinogen and other components in the clotting cascade. Consequently, this action inhibits platelet aggregation and blood clotting. Drugs in this class include Reopro (abciximab), Aggrastat (tirofiban), and Integrilin (eptifibatide). Administration of these agents can result in reducing refractory myocardial ischemia, myocardial infarction, and mortality. Recent research indicates a significant decrease in complications and mortality from ischemic stroke, even when administered up to 24 hours following the onset of symptoms. Indications Reopro, Aggrastat, and Integrilin are indicated in the treatment of refractory unstable angina, and as an adjunct to percutaneous coronary interventions (PCI), such as angioplasty an planned within 24 hours. These agents should not be used together and need to be used cautiously with other drugs that effect clotting. It is important to note that all of these agents have been administered in clinical trials with aspirin, clopidogrel (Plavix), unfractionated heparin and enoxaparin (Lovenox), and bivalirudin (Angiomax). Administration Please consult Lexi-Comp, Micromedex, and PDR for dosage administration and usage. Please contact a pharmacist at your facility for further information. Precautions and Interactions Also refer to fibrinolytics for the contraindications of GP IIb/IIIa inhibitors. Patients are to be monitored closely for signs of bleeding, changes in neurological status, abdominal pain or rigidity, and hypotension. A platelet assay count should be monitored daily during therapy. One must obtain a platelet count within 4 hours of the bolus therapy. In addition, Reopro is a monoclonal antibody derivative, meaning it has the potential to cause allergic and anaphylactic reactions if the patient has had this drug in the past.
Platelet Aggregation Inhibitors

These drugs, include Plavix (clopidrogrel) and Ticlid (ticlopidine), work by modifying the platelet membrane, to block the ADP pathway to prevent platelet aggregation and prolong bleeding time. Aspirin, another antiplatelet agent, does not work through the ADP pathway. Aspirin irreversibly inactivates the COX-1 enzyme in platelets preventing the formation of thromboxane A2 (a platelet aggregating substance). The effect of all of these agents is irreversible for the life of the platelets modified. Consequently, platelet function and bleeding time may take up to 2 weeks following discontinuation of the drug to return to normal. Because ticlopidine can cause life-threatening hematological reactions including neutropenia, thrombocytopenia, thrombotic thrombocytopenic purpura (TTP), agranulocytosis, and aplastic anemia, its use is generally reserved for patients
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who are unable to take clopidrogrel or aspirin, or for those in whom other agents have been ineffective. Indications Platelet aggregation inhibitors are used to reduce the risk of thrombotic events such as myocardial infarction and stroke in patients with previously diagnosed atherosclerotic vascular disease. They are also used with patients with acute coronary syndromes who are undergoing PCI. When a GPIIb/IIIa inhibitor is used, aspirin and/or clopidogrel become part of the standard adjunct therapy, along with heparin or enoxaparin (Lovenox). The clinical indications for aspirin and clopidogrel continue to expand because platelets play such an important role in all types of vascular disease. For example, numerous studies have proven the efficacy with acute onset MI, stable and unstable angina, cath lab procedures, and non-hemorrhagic strokes. Precautions and Interactions Platelet aggregation inhibitors should not be used in any patients with active pathological bleeding such as peptic ulcer or intracranial hemorrhage. They are to be used with caution in patients who are at risk of increased bleeding due to impaired liver function, trauma or surgery. They should also be discontinued 7-14 days prior to elective surgery. Furthermore, drugs such as aspirin, heparin, warfarin, and NSAIDs that may interfere with hemostasis, are administered with extreme caution to patients taking ticlopidine or clopidrogrel. Adverse reactions include rash, nausea, vomiting, diarrhea, constipation, and abdominal pain. These reactions have resulted in discontinuing the drug in approximately 3% of patients taking clopidrogrel and 21% of patients taking ticlopidine. Blood dyscrasias as previously listed, may occur with either of these agents; the incidence is approximately 1 out of every 2000-4000 patients taking ticlopidine and approximately 1 out of every 250,000 of those taking clopidrogrel. Because of its increased risk for adverse reactions, ticlopidine is rarely used & is usually given to patients unable to take other agents or in those for whom other agents are ineffective. In addition to the bleeding precautions for aspirin, there may also be some notable GI distress or bleeding. In such cases an enteric coated aspirin preparation may be suitable.
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Direct Thrombin Inhibitors

These drugs specifically target and bind to sites on thrombin, effectively inhibiting the conversion of fibrinogen to fibrin and interrupting the formation of the hemostatic plug. Thrombin also activates platelets. Lepirudin is a derivative of hirudin (the first direct thrombin inhibitor) and is a very potent and Examples of Drugs: specific inhibitor of thrombin. Lepirudin slowly forms a reversible Angiomax (bivalirudin) complex with two sites on the thrombin molecule. Whereas, bivalirudin, which is a synthetic compound, binds at two sites on the Refludan (lepirudin) thrombin molecule but only acts transiently at one site. Argatroban Argatroban binds reversibly to thrombin.
Angiomax (bivalirudin)
Indications Bivalirudin is indicated for patients with unstable angina undergoing percutaneous transluminal coronary angioplasty. Angiomax is also recommended to be used in patients with a history of heparin induced thrombocytopenia. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications, including intracranial bleeding, retroperitoneal bleeding, and bleeding or oozing from venous access sites. Other adverse events that may occur include back pain, pain, nausea, headache, and hypotension. Patients receiving therapy with bivalirudin need their renal function evaluated prior to administration of and upon discontinuation of the infusion. Patients should be monitored closely for any signs of bleeding, including oozing or bleeding from venous access sites or the presence of blood in urine or stool.
Refludan (lepirudin)
Indications It is indicated for anticoagulation in patients with heparin-induced thrombocytopenia (HIT) and associated thromboembolic disease in order to prevent further thromboembolic complications. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications, including intracranial bleeding, retroperitoneal bleeding, and bleeding or oozing from venous access sites. Other adverse events that may occur include the rare but serious effects of anaphylaxis and respiratory effects (bronchospasm, stridor, dyspnea, and cough).
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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. 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. Doses are reduced for patients with moderate to severe hepatic impairment (0.5 mcg/kg/min). The degree of anticoagulation is monitored by measuring the aPTT. An aPTT 1.5-3 times the normal value is considered therapeutic. Precautions and Interactions The major adverse effects associated with this drug are bleeding and bleeding-related complications. Because of a drug-laboratory interaction, argatroban can falsely elevate the INR. For an argatroban infusion rate of 2 mcg/kg/min, warfarin (Coumadin) is to be discontinued when the INR on combined therapy exceeds 4. Next, the INR is to be determined during warfarin monotherapy 4-6 hours after the discontinuation of argatroban infusion. If the INR is below the desired range, the physician should be contacted and argatroban resumed.
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1. You are screening your new admission for possible fibrinolytic therapy. State 2
absolute contraindications of fibrinolytic therapy. ______________________ ______________________
2. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors, patients require
close monitoring of: a) _____________________________________________________________ b) _____________________________________________________________ c) _____________________________________________________________

3. An acute MI patient receiving fibrinolytics may experience
______________________ or __________________________ as the supply of oxygenated blood is restored.

4. ________________________________________________ agents block the final
common pathway for platelet aggregation.

5. Platelet function may take up to _____________ weeks to return to normal
following the discontinuation of clopidrogel or ticlopidine.
6. The GP IIb/IIIa platelet inhibitors named _________________, ________________,
and ___________________, are indicated as an adjunct to __________________ within _____ hours.
7. Platelet Aggregations inhibitors are used for the following. (Please state your answer
below).
____________________________________________________________________
8. Which of the following drug category bind to sites on thrombin to inhibit the
conversion of fibrinogen to fibrin. a) Fibrinolytics b) Platelet Inhibitors c) Direct Thrombin Inhibitor d) Direct Fibrin Inhibitor
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1. Name two absolute contraindications of fibrinolytics:
Absolute contraindications to the use of fibrinolytics include:

ANY HISTORY OF INTRACRANIAL HEMORRHAGE
Known malignant intracranial neoplasm (primary or metastatic) Known structural cerebral vascular lesion (e.g., AVM) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Active internal bleeding or bleeding diathesis (excluding menses) Suspected aortic dissection Acute pericarditis Significant closed head or facial trauma within 3 months
2. Upon administration of fibrinolytics or GPIIb/IIIa platelet inhibitors, patients require
close monitoring of:
bleeding, changes hypotension
in
neurological
status,
abdominal
pain/rigidity,
3. An acute MI patient receiving fibrinolytics may experience
______________________ or __________________________ as the supply of oxygenated blood is restored. dysrhythmias, chest pain
4. ________________________________________________ inhibitors block the final
common pathway for platelet aggregation. GPIIb/IIIa platelet
5. Platelet function may take up to _____________ weeks to return to normal
following the discontinuation of clopidrogel or ticlopidine. two weeks
6. The GP IIb/IIIa platelet inhibitors named ______________, ______________, and ______________, are indicated as an adjunct to _______________ within _____ hours. Reopro, Integrilin, Aggrastat, PCI, 24 hours
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7. Platelet Aggregation Inhibitors are used for the following: Reduce risk of thrombotic events such as MI and stroke, PVD. They are also used with patient with ACS who undergo PCI. 8. Which of the following drug category bind to sites on thrombin to inhibit the conversion of fibrinogen to fibrin. C. Direct Thrombin Inhibitor
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Diuretic Agents
Diuretics are defined as any drug that increases urine flow by altering the physiologic renal mechanisms that form urine to promote diuresis. Diuretics are divided into classes based on how they effect each of the different sections of the nephron. For example, one class acts on the loop of Henle and another on the distal nephron. Also, Examples of Drugs: the degree of potency varies with the classes; for example, some are more potent than others resulting Loop: in a greater excretion of electrolytes and water, furosemide (Lasix) while others cause potassium to be retained. bumetanide (Bumex), Indications for all classes The main indications for diuretics are hypertension, management of heart failure, relief of heart failure symptoms, reduction of edema due to renal dysfunction, corticosteroids, estrogen, or vasodilator therapy, and reduction of acites due to cirrhosis.
torsemide (Demadex) ethacrynic Acid (Edecrin) Thiazide: hydrochlorothiazide Lozol (indapamide), Diuril (chlorothiazide) Zaroxolyn (metolazone) Potassium sparing: triamterene (Dyrenium) amiloride spironolactone (Aldactone ) eplerenone (Inspra) Combination: HCTZ and triamterene (Maxzide), HCTZ and spironolactone (Aldactazide) HCTZ and amiloride (Moduretic)
Loop Diuretics
The loop of Henle is a portion of the nephron responsible for the concentration or dilution of urine by means of the tubular reabsorption process. This is achieved using the sodium/potassium/chloride transport system. Consequently, loop diuretics inhibit this transport system to increase the elimination of sodium and water in the urine.
The loop diuretics are named: furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), and ethacrynic Acid (Edecrin). They are known for their rapid onset of action and venodilator effects, as well as their potency in the presence of normal or abnormal renal function. Edecrin is rarely used so it may be difficult to obtain. Edecrin is the most ototoxic of the loop diuretics. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. Moreover, the depletion of sodium, potassium, calcium, or magnesium may lead to metabolic alkalosis, myocardial irritability, and ventricular dysrhythmias. Specifically, potassium replacement therapy may be necessary. Patient teaching must include education on a potassium rich diet. Loop diuretics may elevate the blood sugar in diabetics, and because these agents are ototoxic, there is an increased risk of tinnitus and deafness when administered too rapidly or in doses exceeding the recommended daily maximum. Loop diuretics increase serum uric acid levels and may precipitate gout in susceptible patients. It is also important to note that since Lasix, Demadex, and Bumex are sulfonamide derivatives, patients with sulfa allergies may demonstrate a cross-sensitivity.
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It is recommended that before administering to a patient with sulfa allergies, the nurse needs to check with the pharmacy or the prescriber.
Thiazide Diuretics
Thiazide diuretics main actions are to inhibit the transportation of sodium and chloride in the distal nephron. This action results in an increased loss of sodium, chloride, and water in the urine. The most commonly used thiazide agents are hydrochlorothiazide, Lozol (indapamide), Diuril (chlorothiazide), and Zaroxolyn (metolazone). Indications Thiazide diuretics are indicated for the treatment and management of hypertension. The most recent national guidelines for hypertension management (JNC 7) recommends that thiazide diuretics be used as initial monotherapy for the treatment of uncomplicated hypertension in most patients, either alone or in combination with other antihypertensives. They can be used alone to manage mild edema in patients with heart failure or in combination with loop diuretics to manage more severe edema. Thiazide diuretics are also used when a longer (versus shorter acting loop diuretic) duration of action is needed, or for fluid retention from premenstrual syndrome, estrogen, or corticosteroid therapy. Thiazide diuretics are chosen in the treatment of diabetes insipidus. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. The depletion of potassium may lead to metabolic alkalosis, myocardial irritability, and ventricular dysrhythmias. Likewise, since thiazide diuretics tend to retain calcium, there is a mild risk of hypercalcemia. Thiazide diuretics may increase total blood cholesterol and like loop diuretics may elevate blood sugar in diabetics. They can also decrease excretion of uric acid resulting in an increasing risk for gout attacks in patients with this disease. Because all diuretic agents can be ototoxic, there is an increased risk of tinnitus and deafness when administered too rapidly or in doses exceeding the recommended daily maximum.
Potassium-Sparing Diuretics
Currently, there are two groups of potassium-sparing diuretics that act at the distal portion of the nephron. The first group, triamterene (Dyrenium) and amiloride, block the sodium channels to interfere with sodium reabsorption in the distal and collecting tubules of the nephron. The advantage is that sodium loss is achieved without a major loss of potassium or magnesium. The other group consists of spironolactone (Aldactone) and eplerenone (Inspra), which inhibit the effects of aldosterone. These agents will be discussed separately. Commonly, potassium diuretics are given in combination with hydrochlorothiazide. Products include: HCTZ and triamterene (Maxzide), HCTZ and spironolactone (Aldactazide), and HCTZ and amiloride (Moduretic).
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Indications For patients intolerant of oral potassium supplements, this category of diuretics eliminates the need for gastric-irritating potassium supplementation since they do not cause potassium excretion. Precautions and Interactions It is important to remember that large amounts of excreted urine may lead to hypotension and hypovolemia. The depletion of sodium or an excess retention of potassium may lead to metabolic alkalosis, myocardial irritability, and ventricular dysrhythmias. Potassium sparing diuretics may cause the levels of some drugs such as digoxin, to be increased. Concurrent use with ACEinhibitors and non-steroidal anti-inflammatory agents may cause hyperkalemia. Patient teaching includes information about avoiding potassium rich foods or vitamin supplements containing potassium.
Aldosterone Antagonists
Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. Aldosterone is an endogenous steroid that acts on the kidney to retain sodium and water, while excreting potassium in the urine. Spironolactone binds to the aldosterone receptor to prevent the retention of sodium and water and the excretion of potassium. Eplerenone shares the same pharmacologic properties as spironolactone; however, it is considered a selective aldosterone receptor antagonist, whereas spironolactone is non-selective. Indications Both of these agents are indicated for the management of hypertension either as monotherapy or in combination with other antihypertensives. These drugs are also important heart failure therapies. Studies of patients with severe heart failure demonstrate that spironolactone added to conventional therapy (ACE-inhibitors, digoxin, loop diuretics) reduced hospital admissions and mortality. In other studies, eplerenone was shown to improve survival in hemodynamically stable patients with left ventricular dysfunction who demonstrated clinical evidence of heart failure following AMI. Spironolactone is frequently used to counter the effects of elevated aldosterone in conditions such as heart failure, cirrhosis, and nephrotic syndrome. It may also counteract the rise of angiotension II and aldosterone. Administration Both spironolactone and eplerenone are administered orally once daily. Precautions and Interactions Because spironolactone is similar to steroids, it has the potential to produce some of the same adverse effects. The most common is GI distress. In men, there also may be an increased risk of gynecomastia. These effects are seen less often with eplerenone. Hyperkalemia can occur with both agents and the incidence is increased in patients on potassium supplements, and drugs that cause potassium retention (i.e., ACE-inhibitors, ARBs, NSAIDS).
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Insert either TRUE or FALSE for each statement
1. __________ Diuretics can be divided into three major classes. Due to the inherent properties of this class, loop diuretics do not require potassium supplementation. 2. __________ Some examples of drugs known as potassium-sparing diuretics are triamterene, eplerenone, and spironolactone. 3. __________ When comparing all the classifications of diuretics, thiazide diuretics are the most likely to cause hyperkalemia and hypercalcemia. 4. __________ Drugs such as NSAIDS may be co-administered with potassiumsparing diuretics without the risk of adverse consequences. 5. __________ Patients with a documented adverse reaction to sulfa drugs may not be able to safely receive loop diuretics. 6. __________ Aldosterone acts on the kidney to retain sodium and water and excrete potassium in the urine. 7. __________ Thiazide diuretics have a much shorter duration of action than the other diuretic classes. 8. __________ Loop diuretics are the only class of diuretics that may cause ototoxicity. 9. __________ It is important to emphasize to the patient receiving spironolactone to eat potassium rich foods daily. 10. __________ Thiazide diuretics may increase total serum cholesterol.
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1. F 2. T 3. F 4. F 5. T 6. T 7. F 8. F 9. F 10. T
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Summary
This completes the content of the Introduction to CV Pharmacology self-learning packet. Upon successful completion of this packet, the participant should now be familiar enough with the content presented to do the following: Explain how cardiovascular drugs influence the cardiovascular system Describe the role oxygen has in the cardiovascular patient List clinical indications for using cardiovascular pharmaceutical agents Identify the mechanisms of action for each drug or class of drug Describe side effects and appropriate precautions, contraindications, or special considerations of each drug class State patient teaching information As previously stated, this packet is designed to introduce vital information regarding some of the most commonly administered cardiovascular drugs. It is not to be mistaken as a complete drug/nursing reference source. One must look up the drugs for complete information and nursing considerations. Remember that when mentioned, the mixing and administering of these drugs are general guidelines. Certain units or institutions may have specific protocols they follow. If a nurse receives the order administer per protocol, the nurse needs to confirm the drug and dose. A number of the IV infusions may be concentrated if the patient receiving them is on a fluid restriction. Many drugs may also require a dedicated IV infusion line for continuous or IV push administration. Some physicians may have preferences that are not covered in this packet. For that reason, be mindful of the dosing guidelines that have been presented, as well as the physicians orders and institutional or unit preferences.
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CV Pharmacology
Cardiovascular Pharmacology Post Test

Instructions: Use the answer sheet provided on the previous page. 1. Which of the following antiarrhythmics agents is known to prolong the QTI, thus requiring careful monitoring of both the QTI and the QTc? A. Lidocaine, Mexitil B. Dofetilide, Sotalol C. Diltiazam, Calan D. Metropolol, Breviblock 2. You are caring for a patient in recurrent pulseless ventricular tachycardia who is receiving the initial bolus of Procainamide. Which of the following is NOT a reason to stop the initial bolus dose of this drug? A. The QRS widens by 50% B. The dysrhythmia is terminated C. You have administered a dose of 17 mg/kg D. The QT interval is 0.36 3. Your patient has been diagnosed with HIT (Heparin induced thrombocytopenia) Identify the drug that is the best choice to prevent further thromboembolic complications. A. Refluden B. Retavase C. Reopro D. Plavix 4. You are caring for a 40-year old male following an acute anterior myocardial infarction. Select the desired effect of giving this patient a Class II antidysrhythmic drug. A. Increasing myocardial oxygen demand B. Blocking the beta-2 receptors C. Decreasing myocardial work load D. Blocking the conversion of angiotensin I to angiotensin II
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CV Pharmacology
5. Which of the following effects may occur after administration of beta blockade therapy? A. Hypertension, decrease in heart rate B. Increase in heart rate, hypotension C. Bronchodilation, increase in respiratory rate D. Hypotension, bronchoconstriction 6. You are caring for a 52-year old male following an anterior myocardial infarction. The monitor alarm alerts you that the patient's rhythm has changed to polymorphic ventricular tachycardia (Torsades de pointes). The patient is awake, alert, anxious, BP 100/60, HR 130. Which of the following pharmacologic interventions should receive your highest priority? A. Adenosine B. Amiodarone C. Magnesium sulfate D. Procainamide (pronestyl) 7. You have just administered adenosine to a patient in SVT with a heart rate of 200. Which of the following if observed is an expected response? A. Transient, brief rapid increase of the ventricular response B. Brief period of asystole C. Brief period of ventricular standstill D. Suppression of ventricular ectopy 8. Stimulation of the alpha adrenergic receptors will cause what response? A. Peripheral vasodilation B. Peripheral vasoconstriction C. Bronchodilation D. Bronchoconstriction 9. Which of the following is an example of a high flow oxygen delivery system? A. Nasal cannula B. Venturi mask: 40-50% C. Nonrebreathing mask: 100% D. Partial rebreathing mask
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10. Beta-blockers should be administered to patients with Acute Coronary Syndrome, but extreme cautions needs to be given to which patient population when the drug is used. A. The asthma and COPD patient population B. Post MI patients C. Heart failure patients D. Post bypass surgery patient population 11. Which of the following drug category may increase total blood cholersterol? A. Angiotensin II receptor blockers (ARBs) B. Direct thrombin inhibitors C. Platelet inhibitors D. Diuretics 12. Select the statement that best reflects the current indications for Amiodarone. A. To manage severe cardiomyopathy that has not responded to dobutamine B. To treat life-threatening atrial and ventricular tachyarrhythmias C. To treat severe heart failure that has not responded to negative inotropics and diuretics D. To treat junctional dysrhythmias that have not responded to atropine 13. Your patient is ordered to be placed on a IIb/IIIa GP Platelet inhibitor in preparation for a percutaneous coronary intervention. Which of the following is a contraindication to the use of IIb/IIIa inhibitors? A. Intracranial bleeding 12 months ago B. Surgery 10 weeks ago C. Non-hemorrhagic stroke 2 years ago D. Admission 3 weeks ago for an acute peptic ulcer bleed 14. Which of the following is a Class III antidysrhythmic that is used for the conversion of recent onset atrial fibrillation to sinus rhythm? A. Atenolol B. Dofetilide C. Diltiazem D. Procainamide
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15. Which of the following is the initial antidysrhythmic drug of choice for narrow-complex tachycardias when it is known that the origin is supraventricular? A. Atropine B. Digoxin C. Diltiazem D. Adenosine 16. Stimulation of 2 adrenergic receptors will cause which of the following response? A. Coronary artery vasodilation B. Peripheral vasoconstriction C. Bronchodilation D. Bronchoconstriction 17. Choose the drug whose action is to inhibit the parasympathetic nervous system to enhance automaticity of the sinus node, and increase electrical conduction through the AV node? A. Norepinephrine B. Atropine C. Epinephrine D. Adenosine 18. Select the indication for the use of Nesiritide (Natrecor). A. Positive inotropic therapy for heart failure B. Vasopressor therapy for severe hypotension C. Antidysrhythmic therapy for ventricular dysrhythmias D. Vasodilator therapy for acutely decompensated heart failure 19. Select the pharmacologic agent that may be used as adjunct therapy in the presence of heart failure due to its preload and afterload reducing effects. A. Calcium channel blockers B. Beta blockers C. ACE inhibitors D. Class III drugs
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20. In the event of extravasation of a sympathomimetic agent, select the drug used to aid in minimizing tissue damage. A. Phenylephrine (Neosynephrine) B. Phentolamine (Regitine) C. Lidocaine D. Epinephrine 21. Digoxin toxicity is precipitated by which of the following factors. A. Hypokalemia, Hyperkalemia, Hypomagnesemia B. Hypermagnesemia, Hypocalcemia, Loop diurectic C. Thaizde diuretic, Calcium Channel Blocker D. Beta Blockers, Thaizde diuretic 22. Which of the following interventions is contraindicated in a patient in sinus bradycardia (heart rate of 40) who is also hypotensive. A. A normal saline bolus of 250 ml B. Atropine 0.5 mg IV push C. Epinephrine 1mg IV push D. A dopamine IV infusion at (5 mcg/kg/minute) 23. Your patient is on Primacor drip for cardiomyopathy. The primary physician orders a Nitroglycerin drip to be added to the patient regimen. Select the possible drug to drug interaction that could occur. A. Ventricular myocardial irritability B. Severe hypotension C. Nausea, vomiting, and a headache D. Second degree heart block 24. Select the primary indications for ACE inhibitor and/or ARB therapy drugs? A. Hypertension and bradycardia B. Hypertension and heart failure C. Tachycardia and hypotension D. Heart failure and bradycardia
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25. After addressing the patients volume status, the systolic BP continues to remain less than 70. Select the drug of choice for this problem? A. Dopamine IV infusion @ 3 mcg/kg/min B. Epinephrine 1 mg IV push C. Phenylephrine IV push followed with boluses D. Norepinephrine IV infusion 26. Select the appropriate dosage of Vasopressin for the treatment of pulseless VT or VF? A. Vasopressin 40 units IV push x one dose B. Vasopressin 4.0 units IV push x one dose C. Vasopressin 40 units IV push q3-5 minutes D. Vasopressin 40 units IV push q10 minutes 27. Choose the diuretic that depletes potassium thus requiring patient education on the importance of consuming potassium rich foods. A. Spironolactone B. Eplerenone C. Furosemide D. Triamterene 28. You received an order to discontinue clopidrogel on your post cath patient. Your new orientee asks you how long the patient will need to observe bleeding precautions due to altered platelet functioning. Your best response would be: A. 6 weeks B. 4 weeks C. 2 weeks D. 3 weeks
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29. A cancer patient is admitted to the ED with a diagnosis of an acute inferior wall myocardial infarction. The patient has recently been diagnoses with HIT (Heparin induced thrombocytopenia) from a prior treatment for a DVT. What specific drug will target and bind to sites on thrombin effectively inhibiting the conversion of fibrinogen to fibrin interrupting the formation of a clot. A. Heparin B. Lepirudin C. Clopidrogrel D. Reteplase
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References
AEHLERT, BARBARA (2005). ECGS MADE EASY (3RD ED.). ST. LOUIS : MOSBY AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. (2004). AHFS DRUG INFORMATION. BETHESDA MARYLAND. AMERICAN SOCIETY OF HEALTH-SYSTEM PHARMACISTS. (2004-2005). AHFS DRUG INFORMATION ESSENTIALS. BETHESDA MARYLAND. ANTMAN, ELLIOT M., SMITH, SYDNEY C., ET AL. (2004). ACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION EXECUTIVE SUMMARY. CIRCULATION. 110, 588-636. RETRIEVED JULY 2, 2008 FROM HTTP://CIRC.AHAJOURNALS.ORG/CGI/CONTENT/FULL/110/5/588 HAZINSKI, MARY F., FIELD, JOHN M. & GILMORE, DAVID (EDS.). (2008). HANDBOOK OF EMERGENCY CARDIOVASCULAR CARE. DALLAS : AMERICAN HEART ASSOCIATION.
Keeping Pace with Long QT. Retrieved February 2, 2005 from http://www.long-qtsyndrome.com/ekg_readout.html
OPIE, LIONEL H. & GERSH, BERNARD J. (2005). DRUGS FOR THE HEART (6TH ED.). PHILADELPHIA: ELSEVIER- SAUNDERS
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Drug Information Resources
Lexi-Comp TM 1100 Terex Rd. Hudson, OH 44236 (877) 837-5394 Thomson Micromedex 6200 South Syracuse Way, Suite 300 Toll-free: 800-525-9083 Fax: (330) 656-4307 Greenwood Village, 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
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Introduction to CV Pharmacology

2010 Orlando Health, Education & Development

A Note about ACLS

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Autonomic Cardiovascular Innervation

Properties of Cardiac Cells

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The Adrenergic Receptor System

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Check Yourself Pop Quiz

Conductivity Contractility Norepinephrine alpha agonist 1 stimulant effects

afterload alpha effect parasympathetic stimulation alpha antagonist 2 stimulant effects

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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

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Inside Cell 3 Cell Membrane

4 K & Na Outside Cell

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Absolute Refractory Period

Absolute Refractory Period

Absolute Refractory Period

Phase 3 Beginning Repolarization Phase

Absolute Refractory Period Relative Refractory Period

Phase 4 Resting Phase

The cell is now ready for another depolarization stimulus.

Relative Refractory Period

Class I - - Block sodium ion channel

Class Ia Class Ib Class Ic

ECG Measurement: The QTI and QTc

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

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Antidysrhythmics: Class III

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Summary chart of calcium channel blocker actions and indications

Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina Supraventricular Dysrhythmias Angina

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Miscellaneous Antidysrhythmics Adenosine (Adenocard)

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Check Yourself Pop Quiz

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Check Yourself Pop Quiz -Answers

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Antihypertensives Angiotensin Converting Enzyme (ACE) Inhibitors

Angiotensin II Receptor Blockers (ARBs)

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Sodium Nitroprusside (Nipride, Nitropress)

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Check Yourself Pop Quiz

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Check Yourself Pop Quiz -Answers

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Vasopressor Therapy Clinical Application

absolute contraindications of fibrinolytic therapy.

close monitoring of: a) _______________________________ b) _ c) _______________________________

or ____ as the supply of oxygenated blood is restored.

6. The GP IIb/IIIa platelet inhibitors named _, ,

and _____, are indicated as an adjunct to within _ hours.