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110 Cards in this Set

  • Front
  • Back
What is the definition of Chronic Heart Failure?
Heart is unable to pump blood at a rate sufficient to meet requirements of metabolizing tissues
What is the primary cause of Chronic Heart Failure?
Impairment of heart's ability to empty (systolic dysfunction) and/or fill properly (diastolic dysfunction)
What is Chronic Heart Failure the end-product of?
- Coronary Artery Disease
- Hypertension
- Valvular Diseases
- Idiopathic / Familial Cardiomyopathies
- Infection
- Toxicity
What is the 5-year survival rate of Chronic Heart Failure?
50%
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)
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)
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)
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)
If a patient can't walk to mailbox without causing fatigue and breathlessness, what stage of heart failure are they in?
Class III (Moderate Heart Failure)
What is the name for heart failure due to systolic dysfunction? How is the ejection fraction affected?
- Heart Failure w/ Reduced Ejection Fraction (HFrEF)
- EF < 40-50% → ↓CO
What typically causes Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Injury to myocardium causing systolic dysfunction
What are the characteristics of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
- Progressive ventricular dilation
- Wall thinning
= Eccentric hypertrophy / remodeling
(Systolic Dysfunction)
What is the name for heart failure due to diastolic dysfunction? How is the ejection fraction affected?
- Heart Failure w/ Preserved Ejection Fraction (HFpEF)
- Normal or near normal EF (>50%)
What are the characteristics of Heart Failure w/ Preserved Ejection Fraction (HFpEF)?
- Impaired relaxation of ventricle
- Ventricular hypertrophy / remodeling
= Concentric Hypertrophy
(Diastolic Dysfunction)
What are some compensatory mechanisms for Heart Failure w/ Reduced Ejection Fraction (HFrEF) = systolic dysfunction?
- Neurohumoral activation (SNS, Renin-Ang-Aldosterone Axis, Vasopressin, Endothelin)
- Ventricular remodeling (hypertrophy and dilation)
How does the neurohumoral system compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)? Outcomes?
- Activates SNS
- Activates Renin-Angiotensin-Aldosterone Axis
- Releases Vasopressin and Endothelin

- ↑Contractility, ↑Rate, ↑Preload, ↑Afterload, Remodeling
- ↑CO via compensation
How does the ventricle remodel to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)? Outcomes?
- Hypertrophy
- Dilation
What are the effects of the activated SNS for compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
↑Contractility, ↑Rate, ↑Preload, ↑Afterload
What are the effects of the activated Angiotensin II for compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
↑Preload, ↑Afterload, Remodeling
Acutely, what are the functions of the neurohumoral activation and ventricular remodeling in Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Help to maintain perfusion of vital organs by ↑preload, stimulating contractility, ↑arterial tone, ↑stroke volume
Chronically, what are the effects of the neurohumoral activation and ventricular remodeling in Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Contribute to disease progression
- Volume expansion (dilation)
- Abnormal Ca2+ homeostasis
- β-Receptor expression changes
- Hypertrophy
- Adverse remodeling
What are the long-term effects of ventricular dilation to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Volume expansion →
↑Diastolic and Systolic Wall Stress →
Disrupts myocardial energetics (↑O2 demand)
What are the long-term effects of altered calcium homeostasis in the compensation of Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Leads to alterations in contractile activity and arrhythmias (sudden death)
What are the long-term effects of ventricular hypertrophy to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
Initially maintains performance, but leads to ischemic changes
What are the long-term effects of remodeling to compensate for Heart Failure w/ Reduced Ejection Fraction (HFrEF)?
- Excessive dilation and altered ventricular geometry
- Fibrosis
- Myocyte apoptosis
- Fetal gene expression
What increases preload?
- ↑ Blood Volume
- ↑ Venous Tone
How can you decrease a high filling pressure (↓ preload)?
- Salt restricted diet (↓ blood volume)
- Diuretic therapy (↓ blood volume)
- Venodilators / nitrates (↓ venous tone)
What is the effect of an inotrope on a stroke volume vs ventricular filling pressure (preload) graph?
- Increases stroke volume
- No change in ventricular filling pressure

(same as an arterial dilator)
What is the effect of a venous dilator on a stroke volume vs ventricular filling pressure (preload) graph?
- Decreases ventricular filling pressure
- No change on stroke volume

(same as a diuretic)
What is the effect of a mixed vasodilator on a stroke volume vs ventricular filling pressure (preload) graph?
- Decreases ventricular filling pressure
- Increases stroke volume
What is the effect of a diuretic on a stroke volume vs ventricular filling pressure (preload) graph?
- Decreases ventricular filling pressure
- No change on stroke volume

(same as a venous dilator)
What is the effect of an arterial dilator on a stroke volume vs ventricular filling pressure (preload) graph?
- Increases stroke volume
- No change in ventricular filling pressure

(same as an inotrope)
How does afterload affect a failing heart?
A failing heart is very sensitive to changes in afterload because of poor contractile function
How can you decrease afterload?
- Arterial vasodilators (hydralazine)
- ACE Inhibitors
- ARBs
What factor influences the contractility of the heart?
Availability of intracellular Ca2+
What drugs influence the contractility of the heart? How?
Positive inotropic drugs:
- Digoxin
- β-adrenergic AGONISTS

Act by increasing intracellular Ca2+ (↑contractility)
What is the major determinant of cardiac output?
HR
What is the determinant of myocardial perfusion during diastolic interval?
HR
How can you increase / decrease HR?
Increase: SNS stimulation

Decrease:
- β-blockers directly
- Indirectly by ACE-I, ARBs, Digoxin
What drugs are used for treatment of systolic heart failure?
- Diuretics
- Inhibitors of Renin-Ang-Aldosterone System
- β-blockers
- Vasodilators
- Positive Inotropic Agents (Digoxin)
What are the goals of therapy for systolic heart failure?
- Clinical improvement and stabilization
- Improve quality of life (↓morbidity)
- Increase length of life (↓mortality)
What cardiac glycoside is available in the US?
Digoxin / Digitalis
What are the direct effects of Digoxin?
- Positive inotropic effect (direct effect on contractile state of myocardium; ↑SV)
- Increases vagal tone (↓HR)
What are the indirect effects of Digoxin?
- ↓HR (via increased vagal tone)
- Arterial and venous dilation
- ↓Venous pressure
- Normalized arterial baroreceptors
What is the mechanism of Digoxin?
- Inhibits Na+/K+ ATPase
- ↑ intracellular [Na+]
- ↓ driving force for Ca2+ extrusion by Na+/Ca2+ exchanger
- Indirectly results in ↑ intracellular [Ca2+]
How do K+ levels affect Digoxin mechanism / effect?
- K+ competes for binding of Digoxin to Na+/K+ ATPase (main site of action)
- If there is hypkalemia, can have Digoxin toxicity
What are the effects of increased vagal tone d/t Digoxin?
- Reduced firing rate of SA node → ↓HR
- ↓ Conduction velocity in AV node
- Heart block can develop
What happens to the EKG while taking Digoxin? Why?
↑PR interval (d/t ↓conduction velocity in AV node - can lead to heart block)
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
What are the adverse effects of Digoxin?
- 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
What are the clinical uses of Digoxin?
- 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
What dosing should be used for Digoxin?
Low doses (for neurohormonal benefits); will be too low to get max ↑ contractility but want to avoid severe side effects (low therapeutic index)
What is the action of diuretics in systolic heart failure?
- ↓ fluid volume and preload
- ↓ heart size, improves efficiency and reduces wall stress
- ↓ edema (and sx)
* ↓ ventricular filling pressure without change in stroke volume
What are some diuretics / types?
- Loop: Furosemide
- Thiazide: HCTZ
- K+ Sparing: Amiloride, Triamterene
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)
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)
What are the characteristics of Amiloride and Triamterene?
- Type?
- Use?
- Benefits?
- K+ Sparing diuretics
- Weak diuretic activity
- Limited K+ wasting
What are the actions of Angiotensin II?
- Potent arterial constrictor (↑afterload)
- Na+ / H2O retention (via glomerular filtration and aldosterone secretion)
- ↑SNS activity by ↑catecholamine release
- Arrhythmogenic
- Promotes myocardial hypertrophy and apoptosis
What are the actions of Aldosterone?
- Na+ / H2O retention, K+ secretion
- Stimulates fibrosis in heart and vasculature
- Cardiac hypertrophy
What are the actions of ACE Inhibitors in heart failure?
- ↓ Systemic vascular resistance (↓afterload)
- ↓ LV filling pressure (↓preload)
- ↓ Na+ retention
- ↓ Cardiac fibrosis and hypertrophy
What are the benefits / side effects of ACE inhibitors in heart failure?
- Increases survival
- Can decrease renal function, cough, angioedema, hypoTN, hyperkalemia
How do ARBs compare to ACE-Inhibitors?
- Similar action to ACE-inhibitors
- Beneficial effect on survival
- Alternative for patients that can't tolerate ACE-Inhibitors
Why might ARBs be better than ACE-Inhibitors?
- 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
What are the effects of Ang-II binding the AT1 receptor?
- Vasoconstriction
- Vascular proliferation
- Aldosterone secretion
- Cardiac myocyte proliferation
- Increased sympathetic tone
What are the effects of Ang-II binding the AT2 receptor?
- Vasodilation
- Anti-proliferation
- Apoptosis
What are the Aldosterone Antagonists?
- Spironolactone
- Eplerenone
What are the actions of Aldosterone Antagonists in heart failure?
- ↓ Edema
- ↓ Fibrosis in myocardium and vessels (counteracts some aspects of adverse remodeling)
What are the benefits / side effects of Aldosterone Antagonists in heart failure?
- Improves mortality rate and reduces symptoms (even in presence of ACE-inhibitors)
- Hyperkalemia (need to monitor K+ levels)
When should Aldosterone Antagonists be used?
Moderate to severe symptoms of heart failure (Class III and IV)
What are the actions of β-blockers in heart failure?
- ↓ Arrhythmias
- ↓ O2 demand
- ↓ BP
- Prevents disease progression (remodeling)
- Inhibits cardiotoxic actions of catecholamines
- Reduces β1 receptor down-regulation
What are the benefits / side effects of β-blockers in heart failure?
- Initially worsens cardiac function (d/t initial cardiac depression)
- Must start at low dose and gradually increase to max tolerated dose
Which β-blockers have shown benefit for heart failure?
- Metoprolol Succinate (extended release form)
- Carvedilol
- Bisoprolol
What are the actions of vasodilators in heart failure?
- ↓ Preload and ↓ Afterload
- ↑ CO
What are the benefits / side effects of vasodilators (isosorbide dinitrate and hydralazine) in heart failure?
- Improve survival rate
- Use when ACE-I and ARBs are not tolerated
- Particularly useful for African Americans
- Less drug tolerance w/ combination
- Headache
How do Prazosin (α antagonist) and dihydropyridine CCBs affect heart failure?
Do not provide benefit, but do not worsen disease (can be used if for other indications)
What are some non-drug therapies for systolic heart failure?
- Salt restriction
- Bi-ventricular pacing
- Implantable Cardiodefibrillator Devices (ICD)
- Heart transplant
- LVAD (left ventricular assist device)
- Stem cell therapy?
What happens in bi-ventricular pacing? Use?
- Synchronizes the contraction of RV and LV
- Increases efficiency of heart
- Used in systolic heart failure
What happens with an LVAD? Use?
- Left Ventricular Assist Device
- Blood from LV enters LVAD
- LVAD pumps blood into aorta (to body)
- Used in systolic heart failure
What are patients with Heart Failure with Preserved Ejection Fraction (HFpEF) vulnerable to?
Certain types of hemodynamic stress
- Eg, A. Fib., tachycardia, abrupt changes in systemic blood pressure, ischemia
How should Heart Failure with Preserved Ejection Fraction (HFpEF) be treated?
- 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
How can you categorize the symptoms of Heart Failure?
- Forward failure
- Backward failure
What are the heart failure symptoms categorized as forward failure?
↓ CO, which leads to:
- Fatigue
- ↓ Exercise tolerance
- Lightheadedness
What are the heart failure symptoms categorized as backward failure?
↑ VR and Congestion, which leads to:
- Lower extremity edema
- Shortness of breath w/ exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Cough
How can you categorize the types of Heart Failure?
- Systolic Dysfunction
- Diastolic Dysfunction
What can cause systolic dysfunction heart failure?
Dilated CM (ischemic, idiopathic, alcoholic, viral, etc)
What can cause diastolic dysfunction heart failure?
- Hypertrophic CM
- Restrictive CM (infiltrative like amyloid or hemochromatosis)
- Constrictive pericarditis
- HFpEF (preserved EF)
What drugs can / should be used for Stage 1 (asymptomatic) Systolic Heart Failure?
- β-blockers
- ACE-I
What drugs can be used for Stage 2 (Mild) Systolic Heart Failure?
- β-blockers
- ACE-I
- Possibly diuretics
What drugs can be used for Stage 3 (Moderate) Systolic Heart Failure?
- β-blockers
- ACE-I
- Diuretics
- Aldosterone Antagonists (Spironolocatone)
- Vasodilators: hydralazine, nitrates
What drugs can be used for Stage 4 (Severe) Systolic Heart Failure?
- β-blockers (not at very severe end)
- ACE-I
- Diuretics (combinations)
- Aldosterone Antagonists (Spironolocatone)
- Vasodilators: hydralazine, nitrates
- Inotropes
When should transplantation and LVAD be considered in heart failure?
- Transplant: Stage IV systolic heart failure
- LVAD: Late Stage IV systolic heart failure
How should you treat a patient that comes in with signs of an acute STEMI (on EKG)?
- Give aspirin
- Take immediately for emergency catheterization
How should you treat a patient that has coronary artery disease (hx of STEMI) and heart failure w/ low ejection fraction (30%)?
- Diuretics
- Digitalis (inotropic effect - use acutely)
What does a U wave indicate? What should you do?
Hypokalemia (check if they are on diuretics)
What might be the danger of having a patient on a diuretic and Digoxin?
Diuretic may cause hypokalemia which can increase Digoxin Toxicity
If a patient on Digoxin presents w/ hypokalemia, what should you do?
- 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)
What are the hemodynamic effects of Digoxin?
- ↑CO
- ↓LV EF
- ↓LV EDP
- ↑Exercise Tolerance
- ↑Natriuresis
- ↓Neurohormonal activation
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
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
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)
What combination of drugs works well to decrease mortality of systolic heart failure?
- β-blcokers
- ACE-I
What are the side effects of Aldosterone Antagonists? Why?
- Edema: d/t retention of Na+ and H2O
- Arrhythmias: d/t excretion of K+ and Mg2+
- Fibrosis: d/t collagen deposition
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
What can predict the hyperkalemia effect of Aldosterone Antagonists (eg, Spironolactone)?
- Dose of spironolactone
- Use of ACE-I
- Baseline serum creatinine and K+
- Concomitant use of ACE-I, β-blocker, NSAID, or K+ supplement
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
Which drugs / combos can be used to improve mortality rates of systemic heart failure?
- β-blockers
- ACE-I
- Angiotensin Receptor Blocker
- Aldosterone Antagonists
- Hydralazine + Isordil
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
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
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
What is the summary of treatments for CHF?
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