Heart Failure[1][2]

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  • Heart failure is the heart’s inability to pump enough blood to meet the body’s metabolic demands which may be caused by any structural or functional abnormality. The body undergoes a variety of compensatory mechanisms including the RAAS and SNS to maintain homeostasis which leads to a perpetual cycle of cardiac deterioration. There are many different forms of heart failure because it is a common end-point for many cardiovascular disorders. The most common forms we may see in an acute care hospital are chronic, acute, systolic and not so commonly diastolic.
  • Approximately 5 million Americans have HF and almost ½ million cases are diagnosed each year. Is affects men more than women until the age of 65 when there is no gender difference. Almost 10% of the population over 75 have heart failure and this number is expected to increase as the population ages. And it is the #1 cause of hospitalization among Medicare patients.
  • We classify heart failure by stage and class. The ACC/AHA staging system stratifies patients based on the progression of the disease. Patients in stage A do not have heart failure but are at risk of developing the disease because they have conditions that affect the cardiovascular system such as CAD, HTN, and DM. Stage B patients have structural heart disease such as LV hypertrophy or cardiomyopathies but do not have symptoms of heart failure like patients in stage C. Stage D patients have heart failure that is refractory to treatment. The functional class describes the severity of patient’s symptoms. In Class I, there are no limitations on physical activity. In Class II, ordinary physical activity like climbing stairs causes symptoms. In Class III, less than ordinary activity such as taking a few steps causes symptoms. In Class IV, symptoms are present even at rest. It is important to note that patients may be downgraded in class, but never in stage. So, the patient may never be a stage C one day and after treatment be downgraded to stage B, although they may move from Class III to Class II.
  • Chronic heart failure patients are in a state of constant compensation and adaptive changes that allows them to live with the disease. These adaptive changes may include enlargement of the LV, ventricle wall thickening, and dilation of the ventricle. This process occurs over months to years in contrast to acute HF which occurs over hours days and is a medical emergency. In acute HF, a precipitating event causes rapid fluid overload or vasoconstriction in such a short amount of time that the body does not have enough time to mount an adequate compensatory response.
  • systolic dysfunction is the most common and most studied form of HF. Systolic dysfunction occurs when the ventricle does not contract normally which decreases the amount of blood expelled from the ventricle with each contraction (EF). This leads to an increased afterload and preload and decreased cardiac output. 2/3 of cases are due to CAD, 1/3 are due to HTN, hyperthyroidism, cardiotoxins such chemotherapeutic agents or poisions, or it may be idiopathic.
  • Diastolic dysfunction is less common, representing about 30% of cases. Diastolic dysfunction is impairment of ventricular relaxation which increases preload and decreases cardiac output. It may be caused by HTN, cardiomyopathies, and loss of the heart’s instrinsic elastic recoil due to aging.
  • An index event either damages the heart muscle or disrupts the ability of the heart muscle to generate enough force for contraction. This event may be abrupt or gradual. When the heart does not supply the rest of the body with an adequate blood supply, the body will compensate by activating the RAAS and SNS in an effort to increase cardiac output. In the short-term, this is ok because these systems are able to restore cardiac function, however over time, the sustained activation causes persistent tachycardia, fluid retention, myocardial cell death, and ventricular remodeling which will also potentiate a decrease in cardiac output due to increased preload (pressure at end of diastole) and afterload (pressure the heart must pump against). In addition to causing hemodynamic stress, the neurohormones (NE, angiotensin II, aldosterone, vasopressin, endothelin-1, and cytokines) may have direct toxic effects on the heart tissue such as promoting myocardial fibrosis. The natriuretic peptides, NO, and bradykinin are released to cause increased sodium and water excretion and vasodilation which would counter the effects of the RAAS and SNS, however in HF these systems become overwhelmed.
  • Patients with HF may present w/dyspnea that is brought about by exertion or, in more severe cases, patients may have dyspnea by just getting getting out of bed or taking a few steps. Edema of the lower extremities is also a hallmark of HF as is exertional fatigue.
  • The goals of therapy for chronic HF is to block the activity of neurohoromes that cause vasoconstriction and fluid retention. We also want to minimize fluid retention. The treatment approach is based on the patient’s stage. Stage A patients should be on an ACEI or ARB unless they have a contraindication to them or cannot tolerate them. Stage B patients should also be on ACEIs or ARBs in addition to beta-blockers. Stage C patients should be on the same medications as patients in stage B, although they may also benefit from diuretics, digoxin, and aldosterone antagonists. Stage D represents the end-stage of the disease so all medications known to be beneficial should be given in addition to positive inotropes.
  • ACEIs, ARBs, beta-blockers, hydralazine+isosorbide dinitrate, and aldosterone antagonists have been shown to decrease mortality in patients with HF. ACEIs or ARBs can also reduce the risk of developing HF. Beta blockers are also beneficial because they have been shown to slow disease progression. Diuretics are the most effective at improving systems related to fluid overload. Digoxin may also be used to control symptoms but it is not as effective as diuretics although it has been shown to decrease hospitalizations due to exacerbations of HF.
  • Infections, arrhythmias, an acute MI or medication noncompliance can lead to exacerbations of HF because these events increase stress on the heart and further decrease cardiac function.
  • When the heart fails acutely, two things can happen. #1 is pulmonary congestion caused by increased fluids in the lungs, which we call “wet”. #2 is hypoperfusion because of increased vasoconstriction or the heart’s inability to pump effectively, which we call “cold”. Most patients will present with pulmonary congestion only (warm & wet). Less commonly we may see hypoperfusion by itself (cold & dry) and even less commonly and more severe, we can see pulmonary congestion along with hypoperfusion (cold & wet).
  • When patients are cold, we need to increase perfusion with inotropes and vasodilators. When patients are wet, we need to get rid of the excess fluid with diuretics.
  • The diuretic of choice is furosemide because it is the most effective diuretic and may be used even when the patient has poor renal function. If bolus doses of furosemide are not effective, we can consider restricting fluids and giving an IV drip. If stil not effective, we can add another diuretic or a vasodilator.
  • If the patient is not hypotensive, we can give them vasodilators to increase perfusion. The vasodilator of choice is nesiritide which is recombinant BNP which will promote sodium and water loss in addition to its vasodilating properties. The dosing is… One of the advantages of nesiritide over other vasodilators is that is not eliminated by the kidneys or the liver, it is metabolized intracellularly. Sodium nitroprusside is another option, but it may cause cyanide toxicity. IV NTG may also be used however, it may cause tachyphylaxis.
  • If fluid overload does not respond to other treatments, we can use inotropes to increase cardiac output. Dobutamine is a β agonist that can increase the force of contraction and increase heart rate. Milrinone is a cardioselective PDE inhibitor that increases the force of contraction. These medications should be used with caution because they have been associated with causing arrhythmias.
  • Patients with HF have a poor prognosis overall. 50% of patients will die 5 years post-diagnosis and 75% will die 10 years post-diagnosis.
  • Heart Failure[1][2]

    1. 1. Heart Failure Trennette R. Gilbert University of Southern Nevada College of Pharmacy
    2. 2. Definition <ul><li>Inability of the heart to circulate blood effectively enough to meet the body’s needs </li></ul><ul><ul><li>May result from any abnormality of cardiac structure or function </li></ul></ul><ul><li>A state of increased SNS (sympathetic nervous system) and RAAS (renin-angiotensin-aldosterone system) activation that promotes further cardiac deterioration </li></ul><ul><li>Forms of heart failure (HF) </li></ul><ul><ul><li>Chronic vs. acute </li></ul></ul><ul><ul><li>Diastolic vs. systolic </li></ul></ul>
    3. 3. Epidemiology <ul><li>Approximately 5 million Americans have HF </li></ul><ul><ul><li>Approximately 500,000 newly diagnosed each year </li></ul></ul><ul><li>Men > women (until age 65) </li></ul><ul><ul><li>Affects nearly 10% of individuals ≥ 75 years old </li></ul></ul><ul><li>#1 cause of hospitalization among Medicare patients </li></ul>
    4. 4. Classification of HF <ul><li>ACC/AHA Staging </li></ul><ul><li>Stage A </li></ul><ul><ul><li>At high risk of developing HF </li></ul></ul><ul><li>Stage B </li></ul><ul><ul><li>Structural heart disease - symptoms </li></ul></ul><ul><li>Stage C </li></ul><ul><ul><li>Structural heart disease + symptoms </li></ul></ul><ul><li>Stage D </li></ul><ul><ul><li>Refractory HF </li></ul></ul><ul><li>NYHA Functional Class </li></ul><ul><li>Class I </li></ul><ul><ul><li>No limitations on ordinary physical activity </li></ul></ul><ul><li>Class II </li></ul><ul><ul><li>Ordinary physical activity causes fatigue, dyspnea, palpitation </li></ul></ul><ul><li>Class III </li></ul><ul><ul><li>Less-than ordinary activity leads to symptoms </li></ul></ul><ul><li>Class IV </li></ul><ul><ul><li>Symptoms are present at rest </li></ul></ul>
    5. 5. Chronic vs. Acute <ul><li>Chronic HF (months – years) </li></ul><ul><ul><li>An index event causes the heart to undergo adaptive changes over a long period of time </li></ul></ul><ul><li>Acute HF (hours – days) </li></ul><ul><ul><li>Rapid failure due to a precipitating event </li></ul></ul><ul><ul><li>Heart does not have time to undergo compensatory adaptations </li></ul></ul>
    6. 6. Systolic vs. Diastolic <ul><li>Systolic dysfunction </li></ul><ul><ul><li>Ejection fraction (EF) < 40% </li></ul></ul><ul><ul><li>Ventricular contraction impaired </li></ul></ul><ul><li>Etiology </li></ul><ul><ul><li>2/3 of cases due to CAD </li></ul></ul><ul><ul><li>1/3 due to HTN, hyperthyroidism, cardiotoxins, idiopathic </li></ul></ul><ul><li>Prevalence </li></ul><ul><ul><li>Most common form </li></ul></ul>
    7. 7. Systolic vs. Diastolic cont… <ul><li>Diastolic </li></ul><ul><ul><li>EF normal </li></ul></ul><ul><ul><li>Ventricular relaxation/filling impaired </li></ul></ul><ul><li>Etiology </li></ul><ul><ul><li>HTN, age-related decreases in elasticity, cardiomyopathies </li></ul></ul><ul><li>Prevalence </li></ul><ul><ul><li>Approximately 30% of cases </li></ul></ul>
    8. 8. Pathophysiology of HF <ul><li>An index event causes LV dysfunction </li></ul><ul><ul><li>LV unable to fill with blood or generate enough force to expel blood forward -> ↓ cardiac output </li></ul></ul><ul><li>Body compensates by activating RAAS and SNS </li></ul><ul><ul><li>Results in tachycardia and fluid retention </li></ul></ul><ul><ul><li>Neurohormones also have direct toxic effects </li></ul></ul><ul><ul><li>Naturietic peptides (ANP, BNP), nitric oxide, and bradykinin counter effects of RAAS and SNS </li></ul></ul><ul><ul><ul><li>In HF, these mechanisms become overwhelmed </li></ul></ul></ul>
    9. 9. Presentation of Chronic HF <ul><li>Dyspnea </li></ul><ul><li>Fatigue </li></ul><ul><li>Edema </li></ul><ul><li>Exercise intolerance </li></ul>
    10. 10. Drug Therapy for Chronic HF <ul><li>Goals of therapy </li></ul><ul><ul><li>Neurohormonal blockade </li></ul></ul><ul><ul><li>Prevent/minimize fluid retention </li></ul></ul><ul><ul><li>Manage symptoms </li></ul></ul><ul><ul><li>Slow progression </li></ul></ul><ul><ul><li>Decrease mortality </li></ul></ul>Stage Medications A ACEIs or ARBs in some patients B ACEIs or ARBs in all patients + β -blocker in some patients C ACEIs or ARBs + β -blocker in all patients +diuretics, digoxin, or aldosterone antagonists in some patients D Same as C + chronic inotropes, end-of-life care
    11. 11. Rationale for Medications Used in HF Medication Benefits ACEIs ↓ morbidity & mortality ↓ risk of developing HF Prevents post-MI remodeling ARBs As or slightly less effective than ACEIs β -blockers ↓ morbidity & mortality (nebivolol for elderly patients) Slow disease progression ↑ ejection fraction Digoxin ↓ hospitalizations Diuretics Most effective at improving symptoms Hydralazine/nitrates Alternative to ACEI or ARB ↓ morbidity & mortality Aldosterone antagonists ↓ morbidity & mortality in moderate – severe HF
    12. 12. Etiology of Acute HF <ul><li>Acute exacerbation of chronic HF </li></ul><ul><ul><li>Infection </li></ul></ul><ul><ul><li>Acute MI </li></ul></ul><ul><ul><li>Severe arrhythmia </li></ul></ul><ul><ul><li>Noncompliance with medications </li></ul></ul>
    13. 13. Presentation of Acute HF <ul><li>PCWP (mm Hg) </li></ul>Warm & dry Cold & dry Warm & wet Cold & wet
    14. 14. Drug Therapy for Acute HF <ul><li>Cold & dry </li></ul><ul><ul><li>Inotropes, vasodilators </li></ul></ul><ul><li>Cold & wet </li></ul><ul><ul><li>Diuretics, inotropes, vasodilators </li></ul></ul><ul><li>Warm & wet </li></ul><ul><ul><li>Diuretics, vasodilators </li></ul></ul>
    15. 15. Diuretics <ul><li>IV loop diuretics (furosemide) recommended </li></ul><ul><ul><li>Most effective, even at low Crcl </li></ul></ul><ul><li>Minimal response, consider: </li></ul><ul><ul><li>Fluid and sodium restriction </li></ul></ul><ul><ul><li>Increase dose of loop diuretic or IV drip </li></ul></ul><ul><ul><ul><li>Furosemide ceiling effect at 160 – 200 mg </li></ul></ul></ul><ul><ul><ul><li>Continuous infusion 0.1 mg/kg/hr, double q 4-8h [maximum: 0.4 mg/kg/hr] </li></ul></ul></ul><ul><ul><li>Add a thiazide </li></ul></ul>
    16. 16. Vasodilators <ul><li>Consider in addition to diuretics if persistent fluid overload w/o symptomatic hypotension </li></ul><ul><li>Nesiritide </li></ul><ul><ul><li>Recombinant BNP </li></ul></ul><ul><ul><li>Has natriuretic effects and balances RAAS, SNS </li></ul></ul><ul><ul><ul><li>Use in cold & wet or warm & wet patients </li></ul></ul></ul><ul><ul><li>Dosing: 2 mcg/kg bolus, 0.01 mcg/kg/min </li></ul></ul><ul><ul><li>Requires no renal or hepatic elimination </li></ul></ul>
    17. 17. Inotropes <ul><li>Consider if hypoperfusion,end-organ damage, or fluid overload refractory to diuretics and vasodilators </li></ul><ul><ul><li>Increase cardiac output </li></ul></ul><ul><li>Dobutamine </li></ul><ul><ul><li>Positive inotropic, chronotropic effects </li></ul></ul><ul><ul><li>Dosing: 2.5-5 μ g/kg/min, titrate to max 20 μ g/kg/min </li></ul></ul><ul><li>Milrinone </li></ul><ul><ul><li>Positive inotropic effects </li></ul></ul><ul><ul><li>Dosing: 50 μ g/kg, then 0.375 μ g/kg/min titrate to max 0.75 μ g/kg/min </li></ul></ul>
    18. 18. Inotropes cont… <ul><li>Levosimendan </li></ul><ul><ul><li>An investigational inotrope </li></ul></ul><ul><ul><li>Increases contractility by increasing the sensitivity of contractile proteins to intracellular calcium </li></ul></ul><ul><ul><li>Also stimulates peripheral vasodilation </li></ul></ul><ul><ul><li>Does not predispose to arrhythmias </li></ul></ul><ul><ul><li>Not currently available in the US </li></ul></ul>
    19. 19. Prognosis of HF <ul><li>At 5 years post-diagnosis: </li></ul><ul><ul><li>Less than 50% of patients will be alive </li></ul></ul><ul><li>At 10 years post-diagnosis: </li></ul><ul><ul><li>Less than 25% will be alive </li></ul></ul>
    20. 20. Drugs to Avoid in HF <ul><li>NSAIDs </li></ul><ul><ul><li>Associated with increased risk of exacerbations </li></ul></ul><ul><li>Thiazolidinediones </li></ul><ul><ul><li>Cause fluid retention </li></ul></ul><ul><li>Metformin </li></ul><ul><ul><li>Increased risk of lactic acidosis </li></ul></ul><ul><li>Antiarrhythmics </li></ul><ul><ul><li>Ibutalide, sotalol have – inotropic effects </li></ul></ul><ul><li>Chemotherapeutic agents </li></ul><ul><ul><li>Doxorubicin, trastuzumab, bevacizumab are toxic to heart </li></ul></ul>
    21. 21. Role of Pharmacists <ul><li>Ensure heart failure patients are on appropriate medications </li></ul><ul><ul><li>Most should be on ACEI or ARB </li></ul></ul><ul><ul><li>Know which medications should be avoided </li></ul></ul><ul><li>Stress medication compliance </li></ul><ul><ul><li>Lack of compliance can lead to acute HF, hospitalization and ↑ costs </li></ul></ul>
    22. 22. References <ul><li>Kusumoto Fred M, &quot;Chapter 10. Cardiovascular Disorders: Heart Disease&quot; (Chapter). McPhee, SJ, Hammer, GD: Pathophysiology of Disease: An Introduction to Clinical Medicine, 6e: http://nv-ezproxy.usn.edu:2062/content.aspx?aID=5367630. </li></ul><ul><li>Parker Robert B, Rodgers Jo E, Cavallari Larisa H, &quot;Chapter 16. Heart Failure&quot; (Chapter). Joseph T. DiPiro, Robert L. Talbert, Gary C. Yee, Gary R. Matzke, Barbara G. Wells, L. Michael Posey: Pharmacotherapy: A Pathophysiologic Approach, 7e: http://nv-ezproxy.usn.edu:2062/content.aspx?aID=3189842. </li></ul><ul><li>Mann Douglas L, &quot;Chapter 227. Heart Failure and Cor Pulmonale&quot; (Chapter). Dennis L. Kasper, Eugene Braunwald, Anthony S. Fauci, Stephen L. Hauser, Dan L. Longo, J. Larry Jameson, Kurt J. Isselbacher: Harrison's Principles of Internal Medicine, 17e: http://nv-ezproxy.usn.edu:2062/content.aspx?aID=2902061. </li></ul><ul><li>Colucci, WS, Gottlied, SS, Yeon, SB. Evaluation and management of asymptomatic left ventricular systolic dysfunction. Up to date online. Feb 2009. </li></ul><ul><li>MS Nieminen. Pharmacological options for acute heart failure syndromes: current treatments and unmet needs. Eur Soc Cardiology. Vol 7, Suppl B. pp. B20-B24. 2005. </li></ul>

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