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					Heart Failure
Overview

   Heart failure is a complex progressive
    disorder in which the heart is unable to
    pump sufficient blood to meet the needs of
    the body
   1) Due to an impaired ability of the heart to
    adequately fill with blood
                    and/or
   2) An impaired ability of the heart to eject
    blood
Overview

   Heart failure is often accompanied by
    abnormal increases in blood volume
    that leads to edema
       Results in pulmonary congestion (lungs)
       Results in peripheral edema
   Often called congestive heart
    failure (CHF)
       Due to accumulation of fluid
Symptoms of Heart Failure

   Dyspnea from pulmonary congestion
       Dyspnea: difficulty breathing
   Peripheral edema or pitting edema
       Fluid retention, swelling, pitting with applied
        pressure
   Fatigue
Underlying Causes
   Arteriosclerotic cardiovascular disease (ASCVD)
       Also known as Coronary Artery Disease (CAD)
       *main thing that causes heart failure
   Myocardial Infarction (heart attack)
       Heart attack  part of the heart dies, if severe enough 
        you get inability of heart to function normally
   Less likely:
       Severe hypertension
       Disease of the valves of the heart
       Dilated cardiomyopathy
       Congenital heart disease
Underlying Causes

   Left ventricular failure secondary to
    coronary artery disease is most
    common cause of heart failure
   70% of all cases of heart failure are
    caused by CAD
Compensatory Changes
Compensatory Changes
   Failing heart activates 3 major compensatory
    changes
       Increased sympathetic activity w/hope of raising BP
           (1st thing that happens w/heart failure  BP goes down)
       Activation of renin-angiotensin-aldosterone system
           Retention of sodium and water to increase fluid
           If sxs of heart failure is fluid retention, THIS WILL MAKE IT
            WORSE
       Myocardial hypertrophy
           Cardiac pneumonally

   Initially beneficial, these alternations ultimately
    cause deterioration of cardiac function
Increased Sympathetic Activity
   Decrease in BP causes activation of sympathetic
    nervous system
   Results in increased HR, force of contraction,
    vasoconstriction, and increased in preload and
    afterload
       Afterload
       Preload:return of blood back to heart (superior vena cava)
           When you get return to heart, heart stretches, L ventricular
            diastolic pressure goes up
           But if heart isn’t pumping efficiently, can’t get extra blood out
           If heart isn’t pumping efficiently, can’t get extra blood out,
            blood has hard time pumping against pressure of vena cava
             everything backs up…into lungs, periphery
   Compensatory changes increase work of the heart
    and eventually make HF worse
Activation of RAA System
   Increased afterload
   Fall in CO decreases blood flow to kidney
   RAA system is activated
       Results in increased peripheral resistance and retention of
        sodium and water
   Blood volume increases and more blood is returned
    to heart(more preload)
       If heart is unable to pump extra volume, edema results
   Compensatory changes increase work of heart and
    eventually make HF worse
Myocardial Hypertrophy
   Heart increases in size stretching the heart
    muscle and leading to stronger contraction
   Eventually causes elongation of heart fibers
    resulting in weaker contraction
       Force of contraction goes down
       Results in inability of heart to pump blood
        eventually making heart failure worse
   Hypertrophic changes can become
    permanent
       Called cardiac remodeling
Compensated Heart Failure
   If compensatory changes restore cardiac
    function(GOOD), HF is said to be
    compensated
       if the compensatory mechs end up helping
        patient
       This isn’t normal, doesn’t occur much, if it does
        occur it doesn’t last long
   If compensatory changes fail to restore
    cardiac function, HF is said to be
    decompensate
       Patient is worse
Goals of Therapy

   Alleviate symptoms
   Slow progression of disease
   Improve patient survival
Drugs Used To Treat Heart
         Failure
Effects of Drug Therapy

   Reduce load on the heart
   Decreased extracellular fluid volume
       Ex: w/diuretics
   Improved cardiac contractility
       By decreasing afterload and preload
   Slow rate of cardiac remodeling
       BB and digoxin do this the most
ACE Inhibitors
ARBs

   Similar effect as ACE inhibitors but are
    not therapeutically identical
   Used as substitute for ACE inhibitors
    in patients who have developed
    angioedema or in patients who have
    developed severe cough
-Blockers

   Seems counterintuitive to administer a drug
    whose major therapeutic effect is to lower
    cardiac output to a patient with heart failure
   Block chronic activation of sympathetic
    nervous system
       Decreases sympathetic tone, decreased
        comepnsatory mechs
       Improved left ventricular functioning
   Reverses cardiac remodeling
Consultation (β-blockers)

   Consultation for β-blocking drugs used
    to treat patients with CHF should
    include warnings about increasing
    symptoms of heart failure early in the
    course of treatment
   Pt: can get mild worsening initially,
    BUT if it stays for a long time 
    contact PCP
Approved -Blockers for HF

   Carvedilol       Coreg
       Non-selective -blocker that also blocks -
        receptors
   Metoprolol       Toprol
       Selective 1-blocker
   Recommended for nearly all patients with
    mild to moderate HF in combination with
    diuretics, ACE inhibitors, and digoxin
Vasodilators (nitrates)
   Direct vasodilator, works directly on smooth
    muscle of the vasculature
   Causes dilation of venous blood vessels
   Causes some pooling of blood in periphery
   Leads to a decrease in cardiac preload
       Less venous return to heart
       Less LVEDP
   Reduction in symptoms of congestion
   Heart pumps more efficiently
Direct Vasodilators

   Isosorbide dinitrate   Isordil
    Thiazide Diuretics
   Promote sodium and water elimination, reduce plasma
    volume
   Relieve pulmonary and peripheral congestion
   Relieve symptoms of nocturnal dyspnea and
    orthopnea
       orthopnea: Sxs of pulmonary congestion when u lie flat
           In order to breathe, have to prop up w/a few pillows
           Diagnostic feature of heart failure (ex: pt has “2-pillow orthopnea”)

   Decrease plasma volume and decrease preload
    (reduced amt of return to heart, reduces pulmonary
    congestion)
       Decrease cardiac work and myocardial oxygen demand
Diuretics

   Hydrochlorothiazide
   Furosemide       Lasix
Potassium Sparing Diuretics

   Patient with advanced heart disease have
    elevated levels of aldosterone
   Aldosterone causes sodium and fluid
    retention
   Spironolactone is direct antagonist of
    aldosterone and prevents salt and water
    retention
   Reserved for most advanced cases of heart
    failure
Inotropic Agents

   Inamrinone
   Milrinone      Primacore
   Dobutamine     Dobutrex
   Digoxin    Lanoxin, Digitek
Digoxin

   Alkaloid from foxglove
   Has a positive inotropic effect by
    increasing contraction of atrial and
    ventricular myocardium
   Problem: Show small differences
    between therapeutic and toxic or even
    fatal levels
Therapeutic Digoxin Levels

   0.8-2.0ng/ml
   30% of patients develop signs of
    toxicity below a blood level of 2.0ng/ml
       Drug MUST be monitored closely
Clinical Effects

   Increases contractility of the heart and
    increases cardiac output
   Decreases LVEDP thus increasing
    efficiency of heart
   Improved circulation reduces sympathetic
    tone and peripheral resistance.
   Reduces heart rate by slowing conduction
    through the AV node
   Reduction in myocardial oxygen demand
         Consultation for Digoxin
   Take this medicine by mouth with a glass of water.
   it is best to take this medicine on an empty stomach.
   ***Visit your doctor or health care professional for regular checks on your progress.
   ***Do not stop taking this medicine without the advice of your doctor or health care
    professional
   Do not change the brand you are taking, other brands may affect you differently.
   Check your heart rate and blood pressure regularly while you are taking this medicine.
   Less digoxin may be absorbed if you consume a diet high in bran fiber
   Do not treat yourself for coughs, colds or allergies without asking your doctor or health care
    professional for advice
          Cold meds or antihistamines, ESP NO PSEUDOEPHEDRINE (increases heart rate, BP)
          Antihistamines: those w/significant anticholinergic proerpties- -> block vagus nerve,
           increase heart rate , and dries you out, stops secretions  SHOULD RECOMMEND 2ND
           GENERATION (loratidine, fexofenadine)
Side Effects

   Blood levels must be kept in a very
    narrow range
       0.8—2.0 ng/ml
   Side effects are associated with higher
    blood levels
Cardiac Arrhythmias

   Bradycardia
   Premature atrial contraction
   Premature ventricular contractions
   Atrial tachycardia
   Atrial tachycardia with block
   Atrial fibrillation
   Ventricular tachycardia
Normal ECG
Bradycardia
Premature Ventricular Contractions
Multifocal PVC’s
PAT With Block
Angina Pectoris
Overview
   Sudden severe pressing chest pain radiating to
    neck back jaw and arms
   Maybe associated with nausea shortness of breath,
    sweating, light-headedness, or weakness.
   Caused by imbalance between myocardial oxygen
    demand and myocardial oxygen supply
   Episodes 15-30 seconds
   Episodes do not cause myocardial cellular damage
Types of Angina
   Stable
   Unstable
   Printzmetal
       Stable Angina
   Most common form
   Symptoms occur whenever there is increased
    oxygen demand
   Usually induced by exercise, large meals, cold etc.
       Cold? Hands/feet get vasocontriction to preserve warmth heart
        increases afterload (increase vasocontriction in periphery)
   Promptly relieved by nitroglycerin
Unstable Angina

   Progressive with increasing frequency
   Takes less and less to precipitate
    episode
   May occur at rest
   May not be relieved by nitroglycerin
       A bad sign
Printzmetal’s Angina

   Rare type of angina cause by coronary
    vasospasm
   Usually occurs during periods of rest
   Episodes appear in clusters.
   In men prinzmetal's angina is often
    associated CAD, in women it is not
Drug Therapy

   Three classes of drug are useful
       Nitrates
       -blockers
       Calcium channel blockers
   All work by lowering myocardial
    oxygen demand
   In printzmetal’s angina CCB help to
    prevent coronary vasospasm
Nitroglycerin

   Nitroglycerin works by decreasing
    myocardial oxygen demand by dilating veins
   *Reduces venous return to the heart
    (preload) which lowers myocardial work and
    thus decreases oxygen demand
   Some evidence that nitroglycerin dilates
    coronary arteries thus increasing myocardial
    oxygen supply
Dose of Nitroglycerin Tablets
   Take one NTG tablet dissolved under the tongue
    immediately when symptoms of angina occur.
   During drug administration, the patient should rest,
    preferably in the sitting position.
   Symptoms typically improve within 5 minutes.
   If needed, SL NTG may be repeated every 5
    minutes as needed, up to 3 doses
   If not response after 15 minutes and 3 doses of
    NTG, call for help
Revised Recommendations
   Recommendations changed in 2004 for patients with
    STEMI
   Recommend instructing
    a patient to call for help if chest pain is persistent or
    worsened 5 minutes after ONE dose of nitroglycerin
   Self-treatment with nitrates has been identified as a
    factor resulting in delaying access to emergency care for
    patients with STEMI, including those with a history of MI
    or angina
   New guidelines stressed the importance of preventing
    delays in emergency evaluation due to self-medication.
STEMI
Adverse Effects

   All side effects are associated with
    vasodilatation
Also Flushing
Dosage Forms of NTG

   SL Tablets          Nitrostat
   Spray               Nitrolingual
   Sustained Release   Nitrobid Caps
   Topical Ointment    Nitrobid Oint
   Transdermal Patch   Nitrodur
Other Organic Nitrates

   Isosorbide Dinitrate    Isordil
   Isosorbide mononitate   Imdur
Nitrate Tolerance

   Tolerance rapidly develops
   Tolerance can be minimized by
    permitting a 10-12 hour nitrate-free
    interval each day
   Angina during nitrate free interval can
    be controlled with β-blockers and
    calcium channel blockers
Asymmetric Dosing for Imdur

   20mg po bid
   Give two doses/day 7 hours apart
   This allows 10 hour nitrate-free interval
-Blockers

   Decrease oxygen demand
       Decrease heart rate
       Decrease force of contraction
Calcium Channel Blockers

   Cause coronary vasodilatation?
   Cause peripheral vasodilatation and
    lower preload and afterload
   Good for angina caused by coronary
    vasospasm

				
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posted:8/10/2011
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