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    5-Heart Failure

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    Jericho De Guzman
    The document discusses heart failure and its treatment. It begins by describing the physiology of cardiac contraction and relaxation. It then defines heart failure and lists its cardinal symptoms. There are two main types of heart failure - diastolic and systolic - which are distinguished by their effects on ejection fraction and heart contractility. As a compensatory mechanism, heart failure triggers the release of substances like norepinephrine that increase blood pressure but also increase the heart's workload. The goals of treatment are to decrease the heart's workload and increase its contractility. Drugs used for treatment include diuretics, ACE inhibitors, beta-blockers, digoxin, dobutamine, and bipyridines like inamrinone

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    5-Heart Failure

    Uploaded by

    Jericho De Guzman
    39 views12 pages
    The document discusses heart failure and its treatment. It begins by describing the physiology of cardiac contraction and relaxation. It then defines heart failure and lists its cardinal symptoms. There are two main types of heart failure - diastolic and systolic - which are distinguished by their effects on ejection fraction and heart contractility. As a compensatory mechanism, heart failure triggers the release of substances like norepinephrine that increase blood pressure but also increase the heart's workload. The goals of treatment are to decrease the heart's workload and increase its contractility. Drugs used for treatment include diuretics, ACE inhibitors, beta-blockers, digoxin, dobutamine, and bipyridines like inamrinone

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    Heart failure drugs

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    The document discusses heart failure and its treatment. It begins by describing the physiology of cardiac contraction and relaxation. It then defines heart failure and lists its cardinal symptoms. There are two main types of heart failure - diastolic and systolic - which are distinguished by their effects on ejection fraction and heart contractility. As a compensatory mechanism, heart failure triggers the release of substances like norepinephrine that increase blood pressure but also increase the heart's workload. The goals of treatment are to decrease the heart's workload and increase its contractility. Drugs used for treatment include diuretics, ACE inhibitors, beta-blockers, digoxin, dobutamine, and bipyridines like inamrinone

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    39 views12 pages

    5-Heart Failure

    Uploaded by

    Jericho De Guzman
    The document discusses heart failure and its treatment. It begins by describing the physiology of cardiac contraction and relaxation. It then defines heart failure and lists its cardinal symptoms. There are two main types of heart failure - diastolic and systolic - which are distinguished by their effects on ejection fraction and heart contractility. As a compensatory mechanism, heart failure triggers the release of substances like norepinephrine that increase blood pressure but also increase the heart's workload. The goals of treatment are to decrease the heart's workload and increase its contractility. Drugs used for treatment include diuretics, ACE inhibitors, beta-blockers, digoxin, dobutamine, and bipyridines like inamrinone

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    HEART FAILURE

    Physiology of Cardiac Contractility

    CONTRACTION: Action potential from the brain opens the L-type calcium
    channels in myocardium, for trigger calcium to stimulate Ryanodine receptors in
    SR. Stimulated RYR-II will induce sarcoplasmic Reticulum to release more calcium
    ions in the cytoplasm of the heart. The Calcium ions will eventually bind to
    myosin-actin filaments to contract the muscles
    RELAXATION: For the muscle to relax. The calcium ions will diffuse back into
    sarcoplasmic reticulum through Sarcoplasmic Endoplasmic reticulum ATPase
    (SERCA) and Na-K+ ATPase pump. The Na-K+ ATPase pumps 2 potassium ions
    inside the cytoplasm and 3 sodium ions outside the extracellular matrix. Once
    Sodium ions are concentrated enough in the extracellular matrix; it will go back
    again to the myocardium cells through Sodium-Calcium Exchanger (NCX)
    Ejection Fraction
    Heart Failure – is a long-term progressive effects in which the heart cannot pump out the blood in the
    ventricles properly, resulting to accumulation of blood in the heart and may cause valve regurgitation.

    CARDINAL SYMPTOMS OF HEART FAILURE

    1. Dyspnea
    a.. Dyspnea upon exertion
    b. Orthopnea – Dyspnea when lying flat
    c. Paroxysmal nocturnal – dyspnea when sleeping
    2. Edema
    A. Peripheral edema – the right side of the ventricle have difficulty in contracting due to large
    amount of fluid (blood).
    B. Pulmonary Edema – The left ventricle of the heart is affected because the lungs is
    transferring too much fluid (blood)
    3. Fatigue

    Two types of heart failure

    Diastolic heart failure Systolic Heart failure


    The heart is contracting normally except the The left ventricle does not generate enough
    ventricles are very stiff and do not relax properly contractile force thus there will be accumulation
    and there is lesser amount of cardiac preload is of residual blood in the heart and it will
    entering the heart. eventually build up over time.

    Hypertrophy of heart muscles Ejection Fraction <45%


    Stiffening of heart muscles
    Normal ejection fraction – but there is a
    significant reduce stroke volume since there is
    not enough cardiac preload

    Compensatory mechanism for Heart Failure

    Due to weak ventricular


    performance of the heart; it will
    eventually result in less cardiac
    preload and thus the brain will
    activate sympathetic activity which
    will enhance Sodium and H2O
    retention to increase the blood
    pressure, however it will also
    increase the oxygen demand of
    the heart.
    1.) Decrease in Cardiac Output will trigger the release of Norepinephrine, Angiotensin II, and
    endothelin to facilitate vasoconstriction. However, the vasoconstriction will cause the
    heart to pump even more harder because the arteries also constrict.
    2.) Due to increased pressure in artery; it will result again in decrease cardiac output and
    then the substances such as NE will be released again
    3.) This process repeats repeatedly and will eventually wear the heart muscles.

    OTHER CAUSES OF HEART FAILURE

    1. Hypertrophy – Enlargement of heart contractile heart cells due to ischemia and heart caspases
    2. Remodeling– Structural changes in the heart i.e. dilation of left ventricles

    CLASIFICATION OF HEART FAILURE IN NYHA


    CLASSIFICATIONOF HEART FAILURE IN ACC/AHA
    Pharmacologic goal of treatment in the heart failure

    1. Decrease the workload of heart due to compensatory mechanisms


    2. Increase the contractional ability of the heart so the blood will not accumulate in the ventricle

    DRUGS FOR HEART FAILURE

    POSITVE INOTROPES – Compounds that increases the contractile force of the myocardium

    Drugs with inotropic effect Drugs without inotropic effect


    Aka unloader mechanism – inhibits the
    compensatory mechanism

    (First line agent for Chronic HF)


    Cardiac glycosides – digoxin ACE and ARBS
    Beta-receptor stimulants – Dobutamine Diuretics – Thiazides
    Bipyridines Vasodilators
    - Inamrinone
    - Milrinone
    Beta-Blockers

    Miscellaneous inotropic drugs

    1. Istaroxime – Inhibits the NA+-K+ ATPase and facilitates the sequester of Calcium ions and
    calmodulin
    2. Levosimendan – Sensitize the troponin system to calcium and thus reduces PDE5
    CARDIAC GLYCOSIDES
    DIGITOXIN – Are not use anymore due to its long pharmacokinetics
    DIGOXIN MOA: Are concentrated in the heart cells and inhibits the Na-K ATPase
    to inhibit the NCX from functioning. Thus calcium ions will be retain in the
    intracellular and further stimulates actin-myosin action.

    Pharmacological effects of Digoxin

    1. Cardiac effects
    Mechanical effects – Enhance the level of calcium in the intracellular matrix of the heart thus
    increasing contraction of sarcomere. The extra calcium ions will also be stored in SERCA, as a
    reservoir. And so if trigger calcium stimulates RYR-II, SR can release calcium ions again
    2. Electrophysiological effects (DOSE DEPENDENT)
    THERAPEUTIC DOSE
    A. Stimulates Central Vagus Nerve - Increase the refraction period of Atrio-ventricular node
    thus it decrease the heart rate.
    Vagus nerve also slows SA node
    (Digoxin have positive inotropy and negative chronotropy)
    B. Also decrease the sympathetic tone by activating baroreceptor

    HIGH DOSE

    Ventricular Tachycardia

    Enhance automaticity
    PLASMA CONCENTRATION OF DIGOXIN

    3. Extra-cardial effect of Digoxin


     Most common is GIT disturbance such as N&V, Anorexia, Diarrhea
     Visual Disturbance = yellow-green visual discoloration
     Gynecomastia

    Interactions of Digoxin to Ions


    1. Potassium
    A. HYPERKALEMIA – Reduces the effect of cardiac glycosides
    B. HYPOKALEMIA – Facilitates the action of cardiac glycosides
    2. Calcium
    A. Hypercalcemia – Abnormal amount of trigger calcium and accumulation in the
    intracellular myocardia cells
    3. Magnesium
    A. Hypomagnesemia – enhances the effect of digoxin because Magnesium are
    considered as natural calcium channel blocker, and lower levels of it means more L-
    type calcium channels are open. (NATURAL CCBs)
    Drug Interactions of Digoxin
    1. Additive effect – Amiodarone, Erythromycin, Quinidine, Tetracycline, Verapamil
    2. Induces hypokalemia – Corticosteroids, Thiazide diuretics, Loop diuretics
    Digoxin Toxicity Treatment
    1. Withdraw the use of cardiac glycosides and drugs such as thiazides to prevent the
    residual concentration of digoxin for further drug interaction.
    2. Introduce KCl IV infusions or Magnesium to counter the effect of digoxin
    3. Anti-arrhythmic drug
    A. Phenytoin – Ventricular and Atrial Arrythmias
    B. Lidocaine and Procainamide – Ventricular arrythmias
    C. Propranolol – Ventricular and supraventricular arrythmias
    D. Atropine – Sinus Bradycardia and AV blocks
    4. DIGIBIND – An antibody that specifically binds and neutralize digoxin

    BETA-1 AGONIST : Dobutamine MOA

    1. Beta-Agonist stimulates Beta-1


    receptors that will activate Gs
    protein.
    2. Gs Protein will stimulate Adenyl
    cyclase from converting ATP into
    c-AMP
    3. Enhance level of c-AMP with
    stimulate PK-A (protein kinase A)
    4. PK-A facilitates the opening of L-
    type calcium channel in the heart

    Clinical Uses of Dobutamine

    - Use as treatment for acute heart failure


    - Unlike digoxin; it have a positive chronotropic and inotropic effect
    Phosphodiesterase-3 inhibitors: (Bipyridines) Inamrinone and Milrinone
    Function of PDE-5: Metabolize c-AMP
    MOA OF PDE-5 Inhibitors: Inhibits PDE-5

    Inamrinone and Milrinone


     Only used in ACUTE heart failure or severe exacerbation of chronic heart
    failure
     IV administration only

    Adverse effects of Inamrinone and Milrinone


     Arrythmias
     Hypotension
     Abdominal pain
     Fever
     Dizziness
     N&V
     Hepatotoxicity
     Thrombocytopenia
    ACTION OF DIURETICS IN CHF
     Reduce venous return and ventricular preload by decreasing blood
    volume and tone of veins
    Spironolactone
    Aldosterone antagonists
    Prevents Potassium wasting especially when patient is on digoxin
    ACTION OF ACE inhibitors in CHF
     Reduce preload
     Reduce afterload
     Reduce aldosterone secretion
     Inhibits cardiac and vascular remodeling
    ACTION OF ARBs
    These are ARBs drugs considered for HF: Losartan, Irbesartan, Candesartan
    SPECIAL BETA-BLOCKERS FOR HEART FAILURE
     Blocks the Beta-mediated RAAS pathway
    1. Bisoprolol
    2. Carvedilol
    3. Metoprolol succinate
    4. Nebivolol

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