Nursing 220: Pharmacology Module II Part B: Cardiovascular Drugs

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Nursing 220 PharmacologyModule II Part B
Cardiovascular Drugs

• Presented by
• Ronda M. Overdiek, MSN, CCRN, RNC

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Overview

• Anti-Hypertension Drugs
• Vasodilators
• Cardiac Glycosides
• Antidysrhythmic Medications

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Anti-Hypertensive Drugs

• Diuretics
• ACE Inhibitors
• Calcium Channel Blockers
• Sympatholytics (Adrenergic Antagonists)
• Beta-Adrenergic Blockers
• Alpha1 Blockers
• Alpha/Beta Blockers
• Centrally Acting Alpha2 Agonists
• Adrenergic Neuron Blockers

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Calcium Channel Blockers

• Drugs the prevent calcium ions from entering
  cells
• Vascular Smooth Muscle
• Calcium channels regulate contraction
• If channels are blocked, contraction will be
  prevented and vasodilation will result
• Act selectively on peripheral arterioles and
  arteries and arterioles of the heart (no effect
  on veins)

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Calcium Channel Blockers

• Heart
• Regulate function of myocardium, SA AV nodes.
• Myocardium
• Positive inotropic effect (increases force of
  contraction)
• Calcium is blocked, contractile force will
  diminish
• SA Node
• Pacemaker activity regulated by calcium influx
• Calcium is blocked, heart rate is reduced
• AV Node
• Excitability of AV nodal cells is regulated by
  calcium entry
• Calcium is blocked, discharge of Av nodal cells
  is suppressed (decreases the velocity of
  conduction through the AV node).

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Calcium Channel Blockers

• Three chemical families in CCBs (Prototypes)
• Verapamil
• Blocks calcium channels in blood vessels and in
  the heart
• Peripheral arteriole dilation, reducing arterial
  pressure
• Arteries/arterioles of heart dilation, increasing
  coronary perfusion
• Blocks SA node, reducing heart rate
• Blocks AV node, decreases AV nodal conduction
• Blockade in the myocardium decreases force of
  contraction
• Used for
• Angina Pectoris (vasodilation)
• Hypertension
• Cardiac dysrhythmias
• Careful administration/contraindications
• Cardiac failure, AV block, sick sinus syndrome
• Diltiazem similar to Verapamil (page 437)

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Utilizing the Nursing Process

• Assessment
• Why is my patient getting this drug?
• Assess other drugs patient is getting
• Baseline data
• Blood pressure, pulse rate, laboratory values for
  liver/kidney function
• Identify high risk patients
• Contraindicated patients hypotension, sick sinus
  syndrome, AV block

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Utilizing the Nursing Process

• Nursing Diagnosis
• Knowledge Deficit
• Altered Nutrition, more than body requirements
• Impaired adjustment
• Decreased cardiac output
• Noncompliance
• Planning
• Patient education, blood pressure control,
  lifestyle changes (dietary/weight
  management/exercise)

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Utilizing the Nursing Process

• Implementation
• Administration ( 7 rights)
• Know bp range for the patient
• Evaluation
• Evaluate effectiveness of medication (drop bp,
  less chest pain)
• Teach pt to monitor bp
• Minimize Adverse Effects
• Bradycardia, AV block, heart failure, peripheral
  edema, constipation
• Minimize Adverse Interactions
• Digoxin, beta blockers

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Calcium Channel Blockers

• Nifedipine
• Produces significant blockade of calcium channels
  in blood vessels and minimal blockade of calcium
  channels in the heart.
• Promotes vasodilation
• Cannot be used to treat dysrhythmias, does not
  cause adverse cardiac suppression.
• Reflex effect lowers bp, activates the
  baroreceptor reflex causing sympathetic
  stimulation of the heart
• Effect
• Lowers blood pressure
• Increases heart rate
• Increases contractile force
• Uses
• Hypertension

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Utilizing the Nursing Process

• Assessment, Diagnosis, Planning, Implementation
• Same as for Verapamil/Diltiazem
• Evaluation
• Minimize Adverse Effects
• Reflex tachycardia (beta blocker)
• Peripheral Edema

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Sympatholytics (Adrenergic Antagonists)

• Suppress the influence of the sympathetic nervous
  system on the heart, blood vessels, and other
  structures
• Five Subcategories
• Beta blockers
• Alpha1 blockers
• Alpha/beta blockers
• Centrally acting alpha2 agonists
• Adrenergic neuron blockers

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Beta-Adrenergic Blockers

• Most widely used antihypertensive drugs
• Four useful actions in hypertension
• Blockade of cardiac beta1 receptors
• Decreases heart rate and contractility (decreases
  cardiac output)
• Suppress reflex tachycardia caused by
  vasodilators in the regimen
• Blockade of beta1 receptors on juxtaglomerular
  cells of kidney reduce release of renin
• Reduces Angiotensin II vasoconstriction,
  aldosterone mediated volume expansion
• Long term use reduces peripheral vascular
  resistance
• Adverse effects
• Bradycardia, decreased AV conduction, reduced
  contractility
• Contraindicated
• Sick sinus syndrome/ AV blocks/ asthma
  (bronchoconstrictive effects)

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Beta-Adrenergic Blockers

• Two subgroups
• Nonselective Beta Blockers (Propanolol Beta1
  Beta2)
• Reduce heart rate, decrease force of ventricular
  contraction, suppress impulse conduction through
  the AV node, suppress secretion of renin,
  bronchoconstriction, inhibition of
  glycogenolysis.
• Cardioselective Agents (Metoprolol-Beta1 only)
• Same as nonselective except it does not block
  bronchial beta2 receptors so does not increase
  airway resistance.

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Alpha1 Blockers

• Prevent stimulation of alpha1 receptors on
  arterioles and veins, thereby preventing
  sympathetically mediated vasoconstriction.
• Resultant vasodilation results in lowered bp
• Blockade of Alpha1 receptors can cause
  orthostatic hypotension, reflex tachycardia.
• 1 of patients lose consciousness 30-60 minutes
  after receiving their first dose
• The American College of Cardiology recommends
  that alpha blockers NOT be used as first line
  therapy for hypertension. (ALLHAT studydiuretics
  more effective, less side effects)

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Alpha/Beta Blockers

• Block Alpha1 and Beta receptors
• Prototypes Carvedilol, Labetalol
• Blood pressure drops
• Alpha1 blockade promotes dilation of
  arterioles/veins
• Blockade of cardiac beta1 receptors reduced heart
  rate and contractility
• Blockage of beta1 receptors on juxtaglomerular
  cells suppresses release of renin
• Reduce peripheral vascular resistance
• Watch for
• Bradycardia, AV heart block, asthma, postural
  hypotension

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Adrenergic Neuron Blockers

• Decrease blood pressure through actions in the
  terminals of the postganglionic sympathetic
  neurons.
• Inhibit/deplete norepinephrine release
• Resulting in decreased sympathetic stimulation of
  the heart and blood vessels
• Watch for
• Severe orthostatic hypotension

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Utilizing the Nursing ProcessAntihypertensive
Therapy

• Assessment
• Why is the patient taking this drug?
• Assess medication history of drugs currently
  taken, including nonprescriptive drugs
• Baseline Data
• Blood pressure, electrocardiogram, complete
  urinalysis, hemoglobin/hematocrit, blood levels
  of sodium, potassium, calcium, creatinine,
  glucose, uric acid, triglycerides, cholesterol.
• History AV block, gout, diabetes, etc.

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Utilizing the Nursing ProcessAntihypertensive
Therapy

• Nursing Diagnosis
• Planning
• Determine nursing goals derived from nursing
  diagnosis
• Plan of care is individualized to patient
• Implementation
• Administration (7 rights)
• Teachinglifestyle modifications compliance

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Utilizing the Nursing ProcessAntihypertensive
Therapy

• Evaluation
• Monitor blood pressure! Check LOC!
• Minimize Adverse interactions
• Be careful when two or more regimes are employed
  at one time
• If the evaluation does not prove to be what the
  expected outcome in the plan of care was, start
  the nursing process over again!

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Question 1

• Mr. Smith is a 59-year-old who is diagnosed with
  hypertension. The physician orders an alpha1
  blocker, Minipress 1 mg po daily. One of the most
  important things you can do for Mr. Smith is
• Teach Mr. Smith to take his medication with meals
• Advise Mr. Smith to call for help if he needs to
  get up to go to the bathroom
• Check for increasing heart rate
• Tell Mr. Smiths wife that he needs his rest and
  to leave the room to allow him to sleep

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Question 2

• Mrs. Jones is a 75 year old female diagnosed in
  your clinic today with hypertension. She has a
  history of asthma and AV block. The physician
  orders a beta blocker to help with her blood
  pressure. You should
• Give the dose as ordered
• Check her blood pressure after the dose has been
  given
• Remind the physician of the patients history
• Tell Mrs. Jones to use her inhaler when she takes
  her newly prescribed medication

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Vasodilators

• Hydralazine
• Sodium Nitroprusside
• ACE Inhibitors
• Calcium Channel Blockers
• Sympatholytics
• Nitroglycerin

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Vasodilators

• Vasodilators differ in respect to the types of
  blood vessels they affect.
• Dilation of arterioles cause decrease in
  afterload
• Dilation of veins causes decrease in preload,
  in turn decreases ventricular contraction
• Uses
• Hypertension, Angina, heart failure, myocardial
  infarction.
• Adverse Effects
• Orthostatic hypotension caused by relaxation of
  smooth muscle in veins. (Teach pts symptoms
  dizziness, lightheadedness)
• Reflex tachycardia (page 444) places unacceptable
  burden on heart, tachycardia rises blood pressure
• Expansion of blood volume-secretion of
  aldosterone(diuretic may need to be added)

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Vasodilators

• Hydralazine
• Causes selective dilation of arterioles, has
  little or not effect on veins
• Peripheral resistance and arterial blood pressure
  fall
• Heart rate and myocardial contractility increase
• Uses
• Hypertension, heart failure (reduce afterload)
• Adverse Effects
• Reflex tachycardia, increased blood volume
  (sodium/water retention), Systemic Lupus
  Erythematosus-like syndrome (muscle pain, joint
  pain, fever, nephritis, pericarditis).
• Note Inactivated by process called acetylation,
  which is genetically determined.

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Vasodilators

• Sodium Nitroprusside
• Potent and efficacious vasodilator
• Fastest acting antihypertensive agent available
• Causes venous and arteriolar dilation
• IV infusion, onset is immediate
• Uses
• Hypertensive emergencies
• Adverse Effects
• Excessive hypotension
• Thiocyanate Toxicity (patients on med gt 3 days)
• Administration
• Degraded by light--cover

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Vasodilators

• Nitroglycerin
• Acts directly on vascular smooth muscle (VSM) to
  promote vasodilation
• Acts primarily on veins (nitric oxide), dilation
  of arterioles is only modest
• Use
• Angina decreases cardiac oxygen demand by
  dilating veins, decreasing venous return to the
  heart, decreasing ventricular filling, decreasing
  wall tension (preload) which decreases oxygen
  demand.
• Pharmacokinetics
• High lipid soluble some routes are
  uncommonsublingual, buccal, transdermal, oral or
  IV
• Metabolism rapid inactivation by liverhalf life
  of only 5-7 minutes

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Vasodilators

• Nitroglycerin
• Adverse Effects
• Orthostatic hypotension
• Headache
• Reflex tachycardia (treat w/beta blocker or
  calcium channel blocker)
• Sildenafil (Viagra) greatly intensity
  nitroglycerin-induced hypotension causing life
  threatening hypotension
• Nurse administration be careful when giving
  transdermal administration!

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Question 1

• Mr. Armstrong is a 74-year-old admitted to the
  CCU with a diagnosis of unstable angina. He has
  a history of mild hypertension and is currently
  taking propranolol (non-selective beta
  adrenergic). When monitoring Mr. Armstrongs
  ECG, the following effect may be observed related
  to nitroglycerin therapy
• Rebound bradycardia
• Widened Q-T interval
• Shortened P-R interval
• Reflex tachycardia

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Question 2

• Mr. Armstrong tells the nurse that he has a
  sudden pounding headache. The nurse is aware
  that this represents
• An allergic reaction
• An adverse effect
• A toxic effect
• An impending seizure

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Cardiac Glycosides

• Cardiac Glycosides
• Profound effects on the mechanical/electrical
  properties of the heart
• Most widely used prescription drugs, they are the
  most dangerous (toxicdysrhythmias)
• Prototype (Digoxinonly cardiac glycoside
  available in the United States)
• Uses
• Heart failure, dysrhythmias

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Cardiac Glycoside Digoxin

• Digoxin
• Exerts a positive inotropic action on the heart
  (increases the force of ventricular contraction,
  enhancing cardiac output)
• Inhibits enzyme sodium/potassium ATPase which
  promotes calcium accumulation inside myocytes
• Calcium augments contractile force by
  facilitating interaction between myosin and actin
• Potassium ions compete with digoxin for binding
  to sodium/potassium ATPase
• When potassium levels are low binding of digoxin
  increases resulting in toxicity
• When potassium levels are high, binding of
  digoxin decreases, resulting in reduction of
  therapeutic response

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Digoxin

• Digoxin Uses
• Heart failure
• Increased cardiac output by increasing myocardial
  contractility
• Sympathetic tone declines
• Because Digoxin increases arterial pressure.
• Heart rate is reduced, allowing more complete
  ventricular filling
• Afterload is decreased, allowing more complete
  ventricular emptying
• Venous pressure is reduced, reducing cardiac
  distention, pulmonary congestion, and peripheral
  edema
• Increased urine production
• Increased cardiac output increases renal blood
  flow
• Loss of water (urine) decreases blood volume
  which reduces cardiac distension, pulmonary
  congestion, and peripheral edema.
• Decreased Renin Release
• In response to increased arterial pressure,
  decrease in Angiotensin II-less
  vasoconstriction-reducing afterload and venous
  pressure. Decreased aldosterone decreases
  retention of sodium/water, reducing blood volume,
  further reducing venous pressure.

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Digoxin

• Digoxin overall effects on CHF
• Cardiac output improves, heart rate decreases,
  heart size declines, constriction of arterioles
  and veins decrease, water retention reverses,
  blood volume declines, peripheral and pulmonary
  edema decrease, weight is lost, exercise
  tolerance improves, fatigue is reduced.

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Digoxin

• Digoxin treats dysrhythmias
• Through a combination of actions, digoxin can
  alter the electrical activity in noncontractile
  tissue (SA AV nodes, Purkinje fibers), as well
  as the ventricular muscle.
• Alters automaticity, refractoriness, and impulse
  conduction
• Therapeutic/Toxic
• SA node decreases automaticity
• AV node decreases conduction velocity and
  prolongs the effective refractory period
• Purkinje fibers increases automaticity
• Ventricular myocardium shorten the effective
  refractory period and increase automaticity

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Digoxin

• Toxicity
• Dysrhythmias AV block, ventricular flutter,
  ventricular fibrillation
• Predisposing factors
• Hypokalemia (usually secondary to the use of
  diuretics)
• Elevated digoxin levels
• Narrow therapeutic range
• Heart disease
• Side Effects anorexia, nausea, vomiting,
  fatigue, visual disturbances
• Administration Count heart rateless than 60 or
  change in rhythm detected HOLD THE DOSE AND CALL
  THE PHYSICIAN!
• Digoxin orders should be signed by two licensed
  prescribing health care providers.
• Loading dose is given to achieve high plasma
  levels (otherwise it takes 6 days to get a
  therapeutic level)

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Question 1

• Juliana Fortham, a 66-year-old is admitted to the
  CCU with symptoms of nausea, vomiting, and a
  heart rate of 43 beats per minute. Medications
  that Mr. Fortham currently takes include digoxin,
  furosemide (Lasix) and a potassium supplement. A
  diagnosis of digoxin toxicity is made according
  to serum digoxin concentrations. The nurse is
  aware of the following
• Digoxin will be decreased slowly to prevent
  rebound arrhythmias
• Electrolyte values should be checked
• High doses of potassium will be necessary to
  restore automaticity
• Cardioversion is the treatment of choice for Mrs.
  Fortham

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Question 2

• The nurse would check Ms. Forthams laboratory
  results for which of the following conditions
  that would potentiate digoxin toxicity
• Hyperthyroidism
• Hypocalcemia
• Hypokalemia
• Hyperkalemia

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Question 3

• After several days, Ms. Forthams serum digoxin
  level reflects a therapeutic level, and she is to
  be discharged on 0.125 mg po daily dosage. Which
  of the following would be included in patient
  teaching?
• Taking the medication in the morning before
  rising
• Monitoring pulse rate daily
• Discontinuing the medication if the pulse rate is
  stable
• Eating a diet that is high in bran fiber

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Antidysrhythmics

• Dysrhythmia (Arrhythmia)
• Defined as abnormality in the rhythm of the
  heartbeat.
• Associated with high degree of morbidity/mortality
  
• Types
• Tachydysrhythmias
• Largest group/responds best to drugs
• Bradydysrhythmias
• Atropine/Isoproterenol/ pacing
• Arise from
• Disturbances of automaticity (impulse formation)
• Disturbances of impulse conduction

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Antidysrhythmics

• Vaughan Williams Classification
• Class I Sodium Channel Blockers
• Class II Beta Blockers
• Class III Potassium Channel Blockers
• Class IV Calcium Channel Blockers
• Class V Other Antidysrhythmic Drugs

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Class I Sodium Channel Blockers

• Sodium Channel Blockers
• Block cardiac sodium channels
• Decrease conduction velocity in the atria,
  ventricles, and Purkinje system
• Class IA agents delay repolarization (Quinidine)
• Class IB agents accelerate repolarization
  (Lidocaine)
• Class IC agents have pronounced prodysrhythmic
  actions

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Class III Potassium Channel Blockers

• Potassium Channel Blockers
• Delay repolarization of fast potentials
• Bretylium
• Short term therapy of ventricular dysrhythmias,
  s/e is profound hypotension
• Amiodarone
• Effective against both atrial and ventricular
  dysrhythmias (only for life-threatening because
  of toxicitylung damage/visual impairment)

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Other Antidysrhythmic Drugs

• Adenosine
• Decreases automaticity in the SA node and greatly
  slows conduction through the AV node
• Treats SVT
• Short plasma half life (less than 10 seconds)
• Given IVPclosest IV site to the heart, followed
  by push of saline
• Digoxin

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Principles of Antidysrhythmic Drugs

• Treat only if there is a clear benefit and then
  only if the benefit outweighs the risks
• Treatment reduces
• Symptoms (palpitations, angina, dyspnea, and
  faintness)
• Mortality (may increase mortality due to
  prodysrhythmic properties)

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Antidysrhythmics Bradydysrhythmias

• Atropine
• Muscarinic Antagonist
• Competitively block the actions of acetylcholine
• Stimulation of muscarinic receptors decreases
  heart rate
• Blocking these receptors will INCREASE heart rate
• Isoproterenol
• Acts on Beta-adrenergic receptors
• Activates Beta1 receptors on the heart-overcomes
  AV block, restarts the heart following cardiac
  arrest, increases cardiac output during shock