Cardiac Medications Review 2011
Upcoming SlideShare
Loading in...5
×
 

Cardiac Medications Review 2011

on

  • 3,829 views

 

Statistics

Views

Total Views
3,829
Views on SlideShare
3,829
Embed Views
0

Actions

Likes
1
Downloads
127
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Cardiac Medications Review 2011 Cardiac Medications Review 2011 Presentation Transcript

  • Cardiac Medications: What’s With the Mixing & Matching? Michele B. Collins MSN RN CCRN September 2009
  •  
  • Sodium-Potassium Pump
            • Sodium OUTSIDE cell &
            • Potassium INSIDE cell before depolarization
            • Cell has NEGATIVE charge & must CONTRACT to become POSITIVE
            • SA node has less negativity so it serves as pacemaker
    • With cell stimulation, cell permeability allows sodium INTO cell & potassium OUT of cell
    • With sodium, can only have STAT (“fast channel”) contraction
    • Calcium (“fast channel”) also enters cell,
    • leading to total controlled contraction
  • Cardiac Repolarization
    • Na+ - K+ pump uses energy (ATP) so SODIUM LEAVES cell and POTASSIUM RETURNS to cell
    • Calcium also leaves cell at this time
  • Cardiac Repolarization
    • If the S-A node does not generate an impulse, another cardiac site WILL (“reentry phenomenon”)
    • Statistically, if you take six different drugs, you have an 80% percent chance of at least one drug-drug interaction.
    Wayne K. Anderson, Dean, State University of New York School of Pharmacy
  • Medications Discussed
    • Antiarrhythmics
    • Beta Blockers Ace Inhibitors
    • Calcium Channel Blockers
    • ACE Inhibitors
    • Angiotensin II Receptor Blockers (ARB)
    • Diuretics
    • Digitalis
    • Nitrates
    • Amiodarone
  • Why so Many?
    • In atrial fibrillation, used to suppress arrhythmias
    • Often done to relieve the symptoms associated with loss of the atrial component to ventricular filling ( atrial kick ) due to atrial fibrillation or flutter .
    • In individuals with ventricular arrhythmias, used to suppress arrhythmias. Antiarrhythmic agents may be considered the first-line therapy in the prevention of sudden death in certain forms of structural heart disease
  •  
  • Automaticity
    • Refers to a cardiac muscle cell firing off an impulse on its own
    • All cardiac cells can initiate an action potential , however, only some of these cells are designed to routinely trigger heart beats
    • Found in the 'conduction system' of the heart and include the SA node, AV node, Bundle of HIS and Purkinje fibers
    • S inoatrial node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually responsible for setting the heart rate, and initiating each heart beat.
  • Re-entry
    • Occurs when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping
    • If conduction is abnormally slow in some areas, part of the impulse will arrive late and potentially be treated as a new impulse
    • Can produce a sustained abnormal circuit rhythm. Re-entry circuits are responsible for atrial flutter , most paroxysmal supraventricular tachycardia , and dangerous ventricular tachycardia .
    • Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia
    • Resulting heart rhythm depends on where the first signal begins
      • if in sinoatrial node, the rhythm remains normal but rapid
      • if an ectopic focus, many types of dysrhythmia may ensue.
  • Positive Inotropes
    • THE EFFECTS OF STIMULATING ADRENERGIC RECEPTORS
    • RECEPTOR SITE ACTION
    • alpha peripheral blood vessels vasoconstriction of peripheral arterioles
    • beta 1 myocardium increased heart rate (chronotropic)
    • increased contraction force (inotropic) inc. conduction
    • (dromotropic)
    • beta 2 peripheral blood vessels vasodilation of peripheral arterioles & veins
    • bronchioles bronchodilation
  •  
  • ANTIARRHYTMICS (Vaughan Williams classification)
    • Class I – Membrane-stabilizing agents
    • Class II – Beta-blocking agents
    • Class III – Increase time for cell to repolarize
    • Class IV – Calcium Channel blockers
    • Class I agents interfere with the sodium (Na+) channel.
    • Class II agents are anti- sympathetic nervous system agents. Most agents in this class are beta blockers .
    • Class III agents affect potassium (K+) efflux.
    • Class IV agents affect calcium channels and the AV node .
    • Class V agents work by other or unknown mechanisms.
  • Class I Antidysrhythmics:
    • slow rate of spontaneous depolarization of cardiac cells, thus decreasing automaticity, increasing refractory period, & decreasing susceptibility to escape beats
    • Prolong QT interval.
    • Widen QRS interval : decreased Na+ influx into the cell decreases conduction velocity and lengthens the QRS interval)
    • CLASS I-A (quinidine, procainamide,
    • disopyramide)
    • Not often used today
  • Class 1c
    • Increases blockage of sodium channel
    • Encainide, Tombocor, Rythmol
    • severe ventricular dysrhythmias
  • Class I: Sodium channel blockers
    • Disopyramide (Norpace) Flecainide Procainamide Propafenone (Rythmol) Quinidine Tocainide
  • Beta blockers
    • Decrease mortality in patients with myocardial infarction
      • Decrease infarct size
      • Decrease ventricular dysrhytmias
    • Slow progression of heart failure (HF) and prolong lifespan in patients with HF
    • Used in treatment of coronary artery disease, heart failure (HF), & dysrhythmia
  • Class II Agents: Beta Blockers
    • Blockage of beta-1 receptors causes
      • Decreased force of contraction (- inotrope)
      • Decreased heart rate (-chronotrope)
      • Slowed conduction (-dromotrope)
    • These 3 mechanisms of action combine to decrease myocardial oxygen demand
    • decrease cardiac workload & myocardial oxygen needs
    • Tr eatment of supraventricular tachycardias . They decrease conduction through the AV node .
  • Side Effects
    • Angina
    • Fatigue, nightmares, & slow HR
    • Males may experience impotence
    • Patients with asthma or emphysema
    • may not be able to tolerate beta
    • blockers because of an increase in symptoms of shortness of breath and wheezing
    • Depression
    • Weight gain
    • Assess for cough, fatigue, edema, and other symptoms of HF
    • may mask hypoglycemia in diabetics; check blood glucose frequently
    • Removed from blood during hemodialysis; hold dose until treatment finished
  • Cardioselectivity
    • Acebutolol Sectrol
    • Atenolol Tenormin
    • Esmolol Brevibloc
    • Metoprolol Lopressor
  • Non Cardioselectivity
    • Propranolol Inderal
    • Labetalol normodyne, Trandate (alpha properties as well)
    • Carteolol Cartrol
    • Nadolol Corgard
    • Pindolol Visken
    • Timolol Blocadren
  • Beta Blockers
    • Atenolol
    • Metoprolol
    • Propranolol
    • Sotalol
    • Bisoprolol
    • Nadolol
    Carvedilol Timolol Nadolol Betaxolol Pindolol Labetolol
  • Calcium Channel Blockers
    • Block movement of calcium into smooth muscle cells in vessel walls
      • Calcium required for muscle contraction; calcium channel blockers cause relaxation and dilatation of arteries
      • By this mechanism, lower BP
      • Dilate the coronary arteries so also used in treatment of
      • angina
    • R educe cardiac contractility, PVR, & myocardial O2 needs. Effective on reentrant dysrhythmias that require AV nodal conduction for their continuation
    • In contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.
    • Some have a slowing effect on the heart rate and are used in the treatment of arrhythmia
    • Used in treatment of hypertension, arrhythmia, and angina
  • Uses
    • Paroxysmal SVT, rate control for a-fib and flutter
    • Dilate coronary arteries/decreases BP
    • Potentiates effects of digoxin
    • Change position slowly.
  • Side Effects
    • Usually go away within a few hours to a day or so and are not said to be permanent once the medication has "washed out" of the system
    • Common side effects of these drugs include constipation, dizziness, and weakness
    • Swelling of the feet and ankles
    • Excessive lowering of the blood pressure
      • Most common with first dose
      • Change position slowly
    • Rarely an excessively slow heart beat
    • Worsening of HF
    • Many calcium channel blockers come in an extended release or sustained release preparation ( XL, SR) that is convenient for once a day dosing. These tablets should not be cut in half or crushed, as this would affect the rate of drug release into the bloodstream.
  • Diltiazem (Cardizem)
    • Less negative inotropic activity than verapamil
    • D ilates the coronary arteries
    • Treatment of supraventricular arrhythmias
    • Oral diltiazem is effective in treatment of reentry tachycardia
    • A dverse Effects : fewest adverse effects of this category of drugs
    • Hypotension
    • - AV Block if patient is on Beta Blocker therapy
    • Verapamil (Calan, Isoptin): severe hypotension & bradycardia
  • Calcium Channel Blockers
    • Drugs in this class include:
    • Nifedipine
    • Diltiazem
    • Verapamil
    • Amlodipine
    Felodipine Isradapine Nicardipene Nimodipine Bepridil
  • ACE Inhibitors (“pril”)
    • Used to treat both hypertension and Acute Coronary Syndrome
    • Inhibit conversion of angiotension I to angiotension II >>> block release of aldosterone >>> reducing sodium & water retention
  • ACE Inhibitors
    • Act to lower the blood pressure
      • Dilate blood vessels
      • Help with cardiac emptying in HF
    • Good for patients with heart failure by lowering the net resistance in the vascular bed, thereby facilitating the heart’s task of pumping blood.
  •  
  •  
  • Indications
    • Mild to severe hypertension
    • Treatment of heart failure
    • Given within 48 hours of MI to prevent ventricular remodeling & development of HF
    • Increase survival rate after MI
  •  
  • Side Effects
    • Hypotension
      • have person lie down for 3 hrs after first dose
      • temporarily D/C diuretics when starting therapya
      • avoid potassium supplements/salt substitutes, diuretics (may cause severe hypotension)
    • Hyperkalemia, renal tubular damage
    • Cough
    • Angioedema
    • Give one hour before meals
    • Hold enalapril or lisinopril until after hemodialysis (both are removed by dialysis)
  • Ace Inhibitors
    • Enalapril Vasotec
    • Lisinopril Zestril
    • Captopril Capoten
    • Quinapril Accupril
    • Benazopril
    • Fosinopril
  • ARBs
    • Related to ACE inhibitors
    • Used to treat hypertension
    • Block the action of angiotensin II to constrict blood vessels
      • lower blood pressure
      • function in a similar way as the ACE inhibitors, but do not cause the dry, hacking cough that is sometimes associated with ACE inhibitor use.
  •  
  • Angiotensin II Receptor Blockers (ARBs)
    • Losartan
    • Valsartan
    • Candesartan
    • Irbesartan
  •     Digitalis
    • First medication useful in treating disorders of the heartbeat (1800s)
    • Digitalis leaf from the foxglove plant
    • Used to treat atrial fibrillation and heart failure
  • Actions
    • Direct: increases myocardial contractility and CO
      • Vagal effect on SA & AV nodes so decreases heart rate
      • Slows conduction through AV node (positive inotrope, negative chronotrope and negative dromotrope)
    • Indirect
      • decreases diastolic cardiac size
      • reduces cardiac wall tension
      • increases renal Na+ & H2O excretion
      • decreases peripheral vasoconstriction
    • Slows HR so used in treatment of atrial fibrillation and atrial flutter
      • does not suppress or prevent arrhythmias but only works to slow them down and relieve symptoms
      • of palpitations
    • Frequently used in heart failure (HF)
      • Reduces frequency of HF exacerbations
      • Does not reduce mortality from HF
  • Digitalis Toxicity
      • anorexia, n & v, visual disturbances
      • lethargy, bradycardia, heart block, tachydysrhythmias
      • Take apical heart rate for one full minute before administering
      • Monitor digoxin levels: narrow therapeutic window: 0.8-2.0 ng/ml
      • Monitor potassium levels: hypokalemia more likely to become digtoxic
  • Drug Interactions
    • Decreased digoxin absorption with antacids & laxatives
    • Decreased digoxin effect: metoclopramide, aminoglycosides, thyroid supplements
    • Increased digoxin effect Amphotericin B, corticosteroids, non-potassium-sparing diuretics, amiodarone
  • Digoxin Fab (Digibind)
    • Used for life-threatening digoxin toxicity
    • Mechanism: antibody complex formation to digoxin
    • Adverse Events
      • exacerbation of heart failure or a-fib due to withdrawal of digoxin
      • potential for complex dissociation with repeat toxicity in end-stage renal disease
      • digoxin levels meaningless for 7 days post Digibind use.
  • Nitrates
    • Vasodilator: increases coronary blood flow by dilating coronary arteries and improving blood flow to ischemic regions of the heart
      • Decreases preload by dilating peripheral veins
      • Decreases afterload
      • Decreases myocardial oxygen demand to decrease angina
  •  
    • Used for angina, hypertension, MI
    • Used in heart failure to diminish symptoms of shortness of breath
    • Do not reduce mortality in coronary artery disease or heart failure. Their use is principally for symptom relief.
  • Short-acting: Nitroglycerin
    • For acute anginal attacks. SL dosage (0.4mg): · Instruct patient to lie down · Repeat at 5 minute intervals; if pain not
    • relieved, up to 3 tablets · If anginal pain persists after 3 doses, go to ED · Stay with patient and monitor VS (esp. BP) · Headache & hypotension are major side effects
  • Long-acting Nitrates: Isordil, nitroglycerin ointment, nitroglycerin transdermal patch
    • Ointment: use appropriate application paper; don’t “rub in”
    • Rotate sites (remove old patch, ointments)
    • Avoid contact with skin
    Nitrate-free periods (6 – 10 hrs/ 24 hr period) to prevent tolerance Remove patch before defibrillating as patch may explode
  • Side Effects
    • Hypotension, diaphoresis, nausea
    • Tachy- and bradydysrhythmias
    • Headache; reflex tachycardia
  • Drug Interactions
    • Sympathomimetics, thyroid hormones, nicotine
    • All increase cardiac workload so counteract NTG effects
  • Nitrates
    • Drugs in this class include:
    • Isosorbide Dinitrate
    • Isosorbide Mononitrate
  • Amiodarone
    • Principal effect on cardiac tissue to
    • increase time for cell to repolarize
    • Mainly block potassium channels , thereby prolonging repolarization.
    • Do not affect the sodium channel so conduction velocity is not decreased
    • Used to treat atrial arrhythmias (atrial fibrillation and atrial flutter) as well as ventricular arrhythmias (ventricular fibrillation
    • Prevent re-entrant arrhythmias
    • results in "chemical antifibrillatory" action
  • Side Effects
    • Pulmonary fibrosis
    • Abnormal thyroid function
    • Photophobia,
    • Nausea, vomiting
    • Blue-gray skin color
    • Seeing halos around objects
    • May take over 3 weeks to work; half-life about 50 days
    • Monitor with patients in HF and elderly for decreased BP and pulse
    • Assess for fluid retention
    • Have patient swallow whole
    • Do not stop abruptly
    • Take one hour before meals or 2 hours after meals
    • High fat meals elevate levels
    • Use sunscreens and sunglasses when outside
  • Drug Interactions
    • Anticoagulants increase anticoagulation
    • Increased digoxin effects
    • Avoid grapefruit juice as it will increase serum levels causing hypotension
  • Class III — Potassium Channel Blockers
    • Amiodarone (Cordarone)
    • Dofetilide (Tikosyn)
    • Ibutilide (Corvert)
  • So How Does This Relate to My Patients? HTN
    • Goal
      • Two primary regulatory factors
        • Blood flow (volume)
        • Peripheral Vascular Resistance (PVR)
      • Primary groups of drugs are used:
        • Diuretics
        • Adrenergic inhibitors (Beta-blockers)
        • Vasodilators
        • ACE inhibitors
        • Calcium antagonists
  • Pharmacologic Treatment
    • For patients with systolic dysfunction (ejection fraction <40%)
      • Angiotensin-converting enzyme (ACE) inhibitors for all patients
      • Beta blockers for all patients except
        • Hemodynamic instability or
        • Dyspnea at rest with signs of
        • congestion
      • Aldosterone antagonist (ACE inhibitor or ARB) for those with
        • dyspnea at rest or
        • symptomatic patients who have suffered a recent myocardial infarction
        • ARB as a substitute for patients intolerant of ACE inhibitors
    • Digoxin only for patients who remain symptomatic despite treatment with
      • Diuretics, ACE inhibitors, and beta blockers
      • or for those in atrial fibrillation
      • Diuretics for symptomatic patients to maintain appropriate fluid balance .
    • HF patients on multiple medications are at a risk of potential drug interactions and side effects
      • risk of hyperkalemia is increased with renal insufficiency treated with an aldosterone antagonist and an ACE inhibitor.
  • Goals for Mgt of Heart Disease
    • Maximize blood flow to heart muscle
    • Maximize preload & minimize afterload
    • Maximize cardiac contractility (inotropic effect)
    • Reduce chances of clot formation
    • Reduce overall blood volume if overload
    • Maintain heart rate between 60-80 beats/min to maximize cardiac output and filling pressures
  • What Drugs Help to Meet these Goals?
      • Maximize preload I.V. fluids, volume expanders
      • Minimize afterload ACE inhibitors
      • Maximize cardiac
      • contractility Digoxin, Dopamine
      • Decrease preload,
      • inc coronary circulation
      • & reduce pulmonary
      • congestion Nitrates
  • What Drugs Help to Meet these Goals (cont’d)?
      • Reduce chances of ASA or other anti-platelet
      • clot formation agents
      • Reduce fluid
      • volume overload Diuretics
      • Keep heart rate btw Beta blockers &
      • 60-80/min Calcium-channel blockers
      • Dysrhythmias Antidysrhytmics
  • Treatment Goals for HF
      • Relieve symptoms & improve quality of life
      • Prevent readmission to hospital, and/or recurrent ischemic events
      • Reduce mortality
      • Medications used:
        • ACE Inhibitors
        • Beta Blockers
        • Diuretics
        • Vasodilators
        • Digitalis
  • ACE Inhibitors
    • Increase lifespan of patients with heart failure
    • Effects on blood vessels that seem to counteract the process of atherosclerosis and have been shown to reduce heart attack, stroke, and mortality in CAD
  • Beta-Blockers
    • Lower blood pressure & slow heart rate (including protection against arrhythmias)
    • Helps lower risk of stroke and heart attacks
  • Nitrates
    • Used to treat angina
    • Vasodilates and
    • stops chest pain by increasing myocardial oxygen supply & decreasing demand
  • Antidysrhythmic Drugs
    • Used to bring under control abnormal rhythms of the heart (including atrial fibrillation), so the heart can pump more effectively
  • Antihypertensives
    • Used to control BP & risk of stroke & MI
    • Categories
      • ACE Inhibitors
      • Beta-Blockers
      • Calcium-Channel Blockers
  • Managing the Cost
    • Patients may be taking two to four drugs to
    • manage cardiac condition
      • in addition to meds for other health issues such
      • as diabetes
      • Med treatment for a chronic condition becomes expensive with each drug added  
    • Even with worsening condition some people try to limit costs
      • May or may not ask which can be decreased or stopped
    • Best if medication regimen is kept simple so patients without insurance can purchase generic versions without rationing their doses.
  • Refill Red Tape
    • Patients and HCPs often face red tape when it comes to refills and preapproved status.
    • If desired med is not on insurance company's preferred list
      • Must complete preauthorization form
      • Also must talk with insurance company about why that particular medication is needed
    • Patients receiving non-formulary drugs often pay more
      • May only be able to get partially filled prescriptions
      • Providers should seek generic or less expensive alternatives whenever possible
  •  
  • Simple Steps: Lifestyle Changes
    • Decrease sodium intake
    • Exercise & weight loss
  • Preload or Afterload?
    • Arterial vasoconstriction
    • BP 190/124
    • Administration of hydralazine or nitroprusside
    • Administration of Nitroglycerin
    • Diuretic therapy
    • Arterial vasodilation
    • List some positive and negative aspects to the administration of beta blockers
    • The desired effect from the use of diuretics in the patient with acute left ventricular failure is to …
    • List some medications that decrease myocardial contractility
    • What are some of the signs & symptoms of left sided heart failure?
    • Your patient on digoxin has a morning heart rate of 56 BPM and is supposed to be discharged today. Your first priority is to…
    • What are some positive and negative aspects related to Nitroglycerin administration?
    • A patient with a dysrhythmia is placed on digoxin and metoprolol (Lopressor). Because of the combined effects of these drugs, what area(s) need to be the most closely monitored?