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110 Cards in this Set
- Front
- Back
What is the definition of Chronic Heart Failure?
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Heart is unable to pump blood at a rate sufficient to meet requirements of metabolizing tissues
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What is the primary cause of Chronic Heart Failure?
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Impairment of heart's ability to empty (systolic dysfunction) and/or fill properly (diastolic dysfunction)
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What is Chronic Heart Failure the end-product of?
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- Coronary Artery Disease
- Hypertension - Valvular Diseases - Idiopathic / Familial Cardiomyopathies - Infection - Toxicity |
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What is the 5-year survival rate of Chronic Heart Failure?
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50%
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What class of heart failure is described as:
- Cardiac disease w/ no limitation in physical activity - Ordinary activity (walking/climbing stairs) does not cause undue breathlessness, fatigue, or palpitations |
Class I (Mild Heart Failure)
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What class of heart failure is described as:
- Slight limitation of physical activity - Comfortable at rest, but ordinary physical activity results in undue breathlessness, fatigue, or palpitations |
Class II (Mild Heart Failure)
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What class of heart failure is described as:
- Marked limitation of physical activity - Comfortable only at rest, but less than ordinary physical activity (ie, walking 20-100 m) results in undue breathlessness, fatigue, or palpitations |
Class III (Moderate Heart Failure)
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What class of heart failure is described as:
- Unable to carry on any physical activity without discomfort - Symptoms at rest can be present - If any physical activity is undertaken, discomfort is increased |
Class IV (Severe Heart Failure)
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If a patient can't walk to mailbox without causing fatigue and breathlessness, what stage of heart failure are they in?
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Class III (Moderate Heart Failure)
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What is the name for heart failure due to systolic dysfunction? How is the ejection fraction affected?
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- Heart Failure w/ Reduced Ejection Fraction (HFrEF)
- EF < 40-50% → ↓CO |
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What typically causes Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Injury to myocardium causing systolic dysfunction
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What are the characteristics of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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- Progressive ventricular dilation
- Wall thinning = Eccentric hypertrophy / remodeling (Systolic Dysfunction) |
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What is the name for heart failure due to diastolic dysfunction? How is the ejection fraction affected?
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- Heart Failure w/ Preserved Ejection Fraction (HFpEF)
- Normal or near normal EF (>50%) |
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What are the characteristics of Heart Failure w/ Preserved Ejection Fraction (HFpEF)?
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- Impaired relaxation of ventricle
- Ventricular hypertrophy / remodeling = Concentric Hypertrophy (Diastolic Dysfunction) |
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What are some compensatory mechanisms for Heart Failure w/ Reduced Ejection Fraction (HFrEF) = systolic dysfunction?
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- Neurohumoral activation (SNS, Renin-Ang-Aldosterone Axis, Vasopressin, Endothelin)
- Ventricular remodeling (hypertrophy and dilation) |
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How does the neurohumoral system compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)? Outcomes?
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- Activates SNS
- Activates Renin-Angiotensin-Aldosterone Axis - Releases Vasopressin and Endothelin - ↑Contractility, ↑Rate, ↑Preload, ↑Afterload, Remodeling - ↑CO via compensation |
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How does the ventricle remodel to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)? Outcomes?
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- Hypertrophy
- Dilation |
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What are the effects of the activated SNS for compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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↑Contractility, ↑Rate, ↑Preload, ↑Afterload
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What are the effects of the activated Angiotensin II for compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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↑Preload, ↑Afterload, Remodeling
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Acutely, what are the functions of the neurohumoral activation and ventricular remodeling in Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Help to maintain perfusion of vital organs by ↑preload, stimulating contractility, ↑arterial tone, ↑stroke volume
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Chronically, what are the effects of the neurohumoral activation and ventricular remodeling in Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Contribute to disease progression
- Volume expansion (dilation) - Abnormal Ca2+ homeostasis - β-Receptor expression changes - Hypertrophy - Adverse remodeling |
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What are the long-term effects of ventricular dilation to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Volume expansion →
↑Diastolic and Systolic Wall Stress → Disrupts myocardial energetics (↑O2 demand) |
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What are the long-term effects of altered calcium homeostasis in the compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Leads to alterations in contractile activity and arrhythmias (sudden death)
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What are the long-term effects of ventricular hypertrophy to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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Initially maintains performance, but leads to ischemic changes
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What are the long-term effects of remodeling to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
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- Excessive dilation and altered ventricular geometry
- Fibrosis - Myocyte apoptosis - Fetal gene expression |
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What increases preload?
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- ↑ Blood Volume
- ↑ Venous Tone |
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How can you decrease a high filling pressure (↓ preload)?
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- Salt restricted diet (↓ blood volume)
- Diuretic therapy (↓ blood volume) - Venodilators / nitrates (↓ venous tone) |
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What is the effect of an inotrope on a stroke volume vs ventricular filling pressure (preload) graph?
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- Increases stroke volume
- No change in ventricular filling pressure (same as an arterial dilator) |
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What is the effect of a venous dilator on a stroke volume vs ventricular filling pressure (preload) graph?
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- Decreases ventricular filling pressure
- No change on stroke volume (same as a diuretic) |
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What is the effect of a mixed vasodilator on a stroke volume vs ventricular filling pressure (preload) graph?
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- Decreases ventricular filling pressure
- Increases stroke volume |
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What is the effect of a diuretic on a stroke volume vs ventricular filling pressure (preload) graph?
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- Decreases ventricular filling pressure
- No change on stroke volume (same as a venous dilator) |
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What is the effect of an arterial dilator on a stroke volume vs ventricular filling pressure (preload) graph?
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- Increases stroke volume
- No change in ventricular filling pressure (same as an inotrope) |
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How does afterload affect a failing heart?
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A failing heart is very sensitive to changes in afterload because of poor contractile function
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How can you decrease afterload?
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- Arterial vasodilators (hydralazine)
- ACE Inhibitors - ARBs |
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What factor influences the contractility of the heart?
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Availability of intracellular Ca2+
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What drugs influence the contractility of the heart? How?
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Positive inotropic drugs:
- Digoxin - β-adrenergic AGONISTS Act by increasing intracellular Ca2+ (↑contractility) |
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What is the major determinant of cardiac output?
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HR
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What is the determinant of myocardial perfusion during diastolic interval?
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HR
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How can you increase / decrease HR?
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Increase: SNS stimulation
Decrease: - β-blockers directly - Indirectly by ACE-I, ARBs, Digoxin |
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What drugs are used for treatment of systolic heart failure?
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- Diuretics
- Inhibitors of Renin-Ang-Aldosterone System - β-blockers - Vasodilators - Positive Inotropic Agents (Digoxin) |
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What are the goals of therapy for systolic heart failure?
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- Clinical improvement and stabilization
- Improve quality of life (↓morbidity) - Increase length of life (↓mortality) |
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What cardiac glycoside is available in the US?
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Digoxin / Digitalis
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What are the direct effects of Digoxin?
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- Positive inotropic effect (direct effect on contractile state of myocardium; ↑SV)
- Increases vagal tone (↓HR) |
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What are the indirect effects of Digoxin?
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- ↓HR (via increased vagal tone)
- Arterial and venous dilation - ↓Venous pressure - Normalized arterial baroreceptors |
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What is the mechanism of Digoxin?
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- Inhibits Na+/K+ ATPase
- ↑ intracellular [Na+] - ↓ driving force for Ca2+ extrusion by Na+/Ca2+ exchanger - Indirectly results in ↑ intracellular [Ca2+] |
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How do K+ levels affect Digoxin mechanism / effect?
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- K+ competes for binding of Digoxin to Na+/K+ ATPase (main site of action)
- If there is hypkalemia, can have Digoxin toxicity |
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What are the effects of increased vagal tone d/t Digoxin?
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- Reduced firing rate of SA node → ↓HR
- ↓ Conduction velocity in AV node - Heart block can develop |
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What happens to the EKG while taking Digoxin? Why?
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↑PR interval (d/t ↓conduction velocity in AV node - can lead to heart block)
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What are the pharmacokinetic properties of Digoxin?
- t1/2 =? - Absorption? - Excretion? - Conc. effects? |
- t1/2 = 36 hours (daily dosing)
- Orally absorbed (60-75%) - Eliminated unchanged renally - Max ↑ contractility at 1.4 ng/mL - Neurohormonal benefits at lower dose |
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What are the adverse effects of Digoxin?
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- Low therapeutic index (~2)
- GI tract: anorexia, nausea, vomiting, diarrhea - Vision: blurred, photophobia, color changes - Neuro: disorientation, hallucinations - Muscular: weakness, fatigue - Cardiac: arrhythmias Toxicity enhanced w/ hypokalemia |
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What are the clinical uses of Digoxin?
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- NOT 1st line
- Heart failure patients w/ lV systolic dysfunction in A. Fib. - Or in some cases to patients in sinus rhythm who remain symptomatic despite max dosing of other therapies |
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What dosing should be used for Digoxin?
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Low doses (for neurohormonal benefits); will be too low to get max ↑ contractility but want to avoid severe side effects (low therapeutic index)
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What is the action of diuretics in systolic heart failure?
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- ↓ fluid volume and preload
- ↓ heart size, improves efficiency and reduces wall stress - ↓ edema (and sx) * ↓ ventricular filling pressure without change in stroke volume |
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What are some diuretics / types?
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- Loop: Furosemide
- Thiazide: HCTZ - K+ Sparing: Amiloride, Triamterene |
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What are the characteristics of Furosemide?
- Type? - Use? - Side Effects? |
- Loop diuretic
- Widely used, most heart failure patients require chronic therapy to maintain euvolemia (fluid balance) - Promotes K+ loss (hypokalemia) |
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What are the characteristics of Hydrochlorothiazide?
- Type? - Use? - Side Effects? |
- Thiazide diuretic
- Rarely used alone; in combination w/ loop diuretics in patients refractory to loop alone - Promotes K+ loss (hypokalemia) |
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What are the characteristics of Amiloride and Triamterene?
- Type? - Use? - Benefits? |
- K+ Sparing diuretics
- Weak diuretic activity - Limited K+ wasting |
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What are the actions of Angiotensin II?
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- Potent arterial constrictor (↑afterload)
- Na+ / H2O retention (via glomerular filtration and aldosterone secretion) - ↑SNS activity by ↑catecholamine release - Arrhythmogenic - Promotes myocardial hypertrophy and apoptosis |
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What are the actions of Aldosterone?
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- Na+ / H2O retention, K+ secretion
- Stimulates fibrosis in heart and vasculature - Cardiac hypertrophy |
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What are the actions of ACE Inhibitors in heart failure?
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- ↓ Systemic vascular resistance (↓afterload)
- ↓ LV filling pressure (↓preload) - ↓ Na+ retention - ↓ Cardiac fibrosis and hypertrophy |
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What are the benefits / side effects of ACE inhibitors in heart failure?
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- Increases survival
- Can decrease renal function, cough, angioedema, hypoTN, hyperkalemia |
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How do ARBs compare to ACE-Inhibitors?
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- Similar action to ACE-inhibitors
- Beneficial effect on survival - Alternative for patients that can't tolerate ACE-Inhibitors |
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Why might ARBs be better than ACE-Inhibitors?
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- ARB selectively blocks the negative effects of Ang-II that are mediated via AT1 receptor
- Leaves positive effects of AT2 receptor intact (vasodilation, anti-proliferation, apoptosis) - Decreases adverse effects mediated by bradykinin - Overcomes problem of angiotensin escape |
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What are the effects of Ang-II binding the AT1 receptor?
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- Vasoconstriction
- Vascular proliferation - Aldosterone secretion - Cardiac myocyte proliferation - Increased sympathetic tone |
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What are the effects of Ang-II binding the AT2 receptor?
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- Vasodilation
- Anti-proliferation - Apoptosis |
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What are the Aldosterone Antagonists?
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- Spironolactone
- Eplerenone |
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What are the actions of Aldosterone Antagonists in heart failure?
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- ↓ Edema
- ↓ Fibrosis in myocardium and vessels (counteracts some aspects of adverse remodeling) |
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What are the benefits / side effects of Aldosterone Antagonists in heart failure?
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- Improves mortality rate and reduces symptoms (even in presence of ACE-inhibitors)
- Hyperkalemia (need to monitor K+ levels) |
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When should Aldosterone Antagonists be used?
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Moderate to severe symptoms of heart failure (Class III and IV)
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What are the actions of β-blockers in heart failure?
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- ↓ Arrhythmias
- ↓ O2 demand - ↓ BP - Prevents disease progression (remodeling) - Inhibits cardiotoxic actions of catecholamines - Reduces β1 receptor down-regulation |
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What are the benefits / side effects of β-blockers in heart failure?
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- Initially worsens cardiac function (d/t initial cardiac depression)
- Must start at low dose and gradually increase to max tolerated dose |
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Which β-blockers have shown benefit for heart failure?
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- Metoprolol Succinate (extended release form)
- Carvedilol - Bisoprolol |
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What are the actions of vasodilators in heart failure?
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- ↓ Preload and ↓ Afterload
- ↑ CO |
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What are the benefits / side effects of vasodilators (isosorbide dinitrate and hydralazine) in heart failure?
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- Improve survival rate
- Use when ACE-I and ARBs are not tolerated - Particularly useful for African Americans - Less drug tolerance w/ combination - Headache |
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How do Prazosin (α antagonist) and dihydropyridine CCBs affect heart failure?
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Do not provide benefit, but do not worsen disease (can be used if for other indications)
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What are some non-drug therapies for systolic heart failure?
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- Salt restriction
- Bi-ventricular pacing - Implantable Cardiodefibrillator Devices (ICD) - Heart transplant - LVAD (left ventricular assist device) - Stem cell therapy? |
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What happens in bi-ventricular pacing? Use?
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- Synchronizes the contraction of RV and LV
- Increases efficiency of heart - Used in systolic heart failure |
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What happens with an LVAD? Use?
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- Left Ventricular Assist Device
- Blood from LV enters LVAD - LVAD pumps blood into aorta (to body) - Used in systolic heart failure |
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What are patients with Heart Failure with Preserved Ejection Fraction (HFpEF) vulnerable to?
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Certain types of hemodynamic stress
- Eg, A. Fib., tachycardia, abrupt changes in systemic blood pressure, ischemia |
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How should Heart Failure with Preserved Ejection Fraction (HFpEF) be treated?
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- Control HTN (ACE-inhibitors, ARBS, β-blockers, CCBs)
- Control ventricular rate (β-blockers, CCBs) - Control pulmonary and peripheral edema (diuretics) - No specifics as there are no clinical trials related to this form of heart failure |
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How can you categorize the symptoms of Heart Failure?
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- Forward failure
- Backward failure |
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What are the heart failure symptoms categorized as forward failure?
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↓ CO, which leads to:
- Fatigue - ↓ Exercise tolerance - Lightheadedness |
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What are the heart failure symptoms categorized as backward failure?
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↑ VR and Congestion, which leads to:
- Lower extremity edema - Shortness of breath w/ exertion - Orthopnea - Paroxysmal nocturnal dyspnea - Cough |
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How can you categorize the types of Heart Failure?
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- Systolic Dysfunction
- Diastolic Dysfunction |
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What can cause systolic dysfunction heart failure?
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Dilated CM (ischemic, idiopathic, alcoholic, viral, etc)
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What can cause diastolic dysfunction heart failure?
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- Hypertrophic CM
- Restrictive CM (infiltrative like amyloid or hemochromatosis) - Constrictive pericarditis - HFpEF (preserved EF) |
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What drugs can / should be used for Stage 1 (asymptomatic) Systolic Heart Failure?
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- β-blockers
- ACE-I |
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What drugs can be used for Stage 2 (Mild) Systolic Heart Failure?
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- β-blockers
- ACE-I - Possibly diuretics |
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What drugs can be used for Stage 3 (Moderate) Systolic Heart Failure?
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- β-blockers
- ACE-I - Diuretics - Aldosterone Antagonists (Spironolocatone) - Vasodilators: hydralazine, nitrates |
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What drugs can be used for Stage 4 (Severe) Systolic Heart Failure?
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- β-blockers (not at very severe end)
- ACE-I - Diuretics (combinations) - Aldosterone Antagonists (Spironolocatone) - Vasodilators: hydralazine, nitrates - Inotropes |
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When should transplantation and LVAD be considered in heart failure?
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- Transplant: Stage IV systolic heart failure
- LVAD: Late Stage IV systolic heart failure |
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How should you treat a patient that comes in with signs of an acute STEMI (on EKG)?
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- Give aspirin
- Take immediately for emergency catheterization |
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How should you treat a patient that has coronary artery disease (hx of STEMI) and heart failure w/ low ejection fraction (30%)?
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- Diuretics
- Digitalis (inotropic effect - use acutely) |
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What does a U wave indicate? What should you do?
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Hypokalemia (check if they are on diuretics)
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What might be the danger of having a patient on a diuretic and Digoxin?
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Diuretic may cause hypokalemia which can increase Digoxin Toxicity
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If a patient on Digoxin presents w/ hypokalemia, what should you do?
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- Admit, place on heart monitoring
- Treat w/ oral K+ (can give as much as you want) - Treat w/ IV K+ (slowly so that you don't stop heart) - Need to increase K+, because hypokalemia is associated w/ Digoxin toxicity (narrow therapeutic window) |
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What are the hemodynamic effects of Digoxin?
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- ↑CO
- ↓LV EF - ↓LV EDP - ↑Exercise Tolerance - ↑Natriuresis - ↓Neurohormonal activation |
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What did the ELITE Trial determine about:
- ACE-I (Captopril) vs ARB (Losartan) Effect on how patients w/ CHF should be treated? |
- Overall mortality in ARB group similar to ACE-I group
- ARB was better tolerated than ACE-I (cough) - ARB similarly efficacious in treating patients w/ CHF - Use ACE-I first, but try ARB if there are problems |
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What did the COPERNICUS Trial determine about:
- Carvedilol Effect on how patients w/ CHF should be treated? |
- 30% decrease in mortality rate in carvedilol group
- Effect was present in patients w/ all degrees of CHF - Carvedilol is very effective when added to existing therapeutic regimen in reducing death in patients w/ severe CHF |
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What did the COMET Trial determine about:
- Carvedilol vs Metoprolol Effect on how patients w/ CHF should be treated? |
- Mortality was 34% (carvedilol) vs 40% (metoprolol)
- In patients w/ CHF, carvedilol when added to existing tx regimen was better at improving mortality than metoprolol (Granted metoprolol dose was small and short-acting; long-acting normal dose is considered equivalent to carvedilol) |
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What combination of drugs works well to decrease mortality of systolic heart failure?
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- β-blcokers
- ACE-I |
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What are the side effects of Aldosterone Antagonists? Why?
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- Edema: d/t retention of Na+ and H2O
- Arrhythmias: d/t excretion of K+ and Mg2+ - Fibrosis: d/t collagen deposition |
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What did the RALES Trial determine about:
- Spironolactone vs Placebo Effect on how patients w/ CHF should be treated? |
- Overall mortality in spironolactone group was significantly lower than placebo group (35% vs 46%)
- Study was terminated early - Spironolactone is effective in reducing death in patients w/ moderate to severe, symptomatic CHF w/ low EF |
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What can predict the hyperkalemia effect of Aldosterone Antagonists (eg, Spironolactone)?
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- Dose of spironolactone
- Use of ACE-I - Baseline serum creatinine and K+ - Concomitant use of ACE-I, β-blocker, NSAID, or K+ supplement |
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What did the V-HeFT I and II Trials determine about:
- Vasodilators Effect on how patients w/ CHF should be treated? |
- Isosordil + Hydralazine >> superior to placebo
- Enalapril superior to Isordil + Hydralazine and to placebo - Prazosin not effective vs placebo *ACE-I is the preferred vasodilator therapy for moderate CHF but Hydralazine + Isordil is a effective substitute especailly w/ renal fxn |
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Which drugs / combos can be used to improve mortality rates of systemic heart failure?
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- β-blockers
- ACE-I - Angiotensin Receptor Blocker - Aldosterone Antagonists - Hydralazine + Isordil |
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What did the MADIT-II Trial determine about:
- Mortality Effect on how patients w/ CHF should be treated? |
- Mortality was 14% in AICD group
- Mortality as 20% in conventional group * Prophylactic implantation of AICD post-MI in patients w/ CHF (EF <30%) prolongs survival |
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What did the MIRACLE Trial determine about:
- Bi-Ventricular Pacing Effect on how patients w/ CHF should be treated? |
In select patients, biventricular pacing is effective when added to an existing therapeutic regimen, in improving exercise time and LVEF in patients w/ moderate CHF
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What did the REMATCH Trial determine about:
- LVAD Effect on how patients w/ CHF should be treated? |
- Mortality was 48% less in the LAD group
- Insertion of LVAD device in patients w/ severe CHF prolongs survival for up to 2 years |
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What is the summary of treatments for CHF?
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1. Use ACE-I if possible, or ARBs as second line choice
2. β-blocker (carvedilol = metoprolol succinate) 3. For very low EF, w/ sx, add Spironolactone 4. Consider, statins, aspirin, AICD, resynchronization therapy, - Hydralazine + Isordil if African-American or if ACE-I / ARB contraindicated |