Heart Failure Flashcards by lourize lanuza

a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction

Ejection Fraction

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50-70% is pumped out during each contraction (comfortable during activity)

NORMAL Ejection Fraction

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41-49% is pumped out during each contraction (sx may be noticeable during activity)

BORDERLINE Ejection Fraction

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<_ 40% is pumped out during each contraction (sx ate noticeable even during rest)

REDUCED Ejection Fraction

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T/F:
it is also possible to have a diagnosis of heart failure with a seemingly normal (or preserved) ejection fraction of greater than or equal to 50%

TRUE

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•Occurs when cardiac output is inadequate to provide the oxygen needed by the body

• The heart cannot meet the metabolic requirements of the peripheral systems

• Heart’s inability to fill or empty the left ventricle properly

Heart Failure

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S/Sx: of Heart Failure
DetPePue TaShoCa

• Decreased exercise tolerance
• Peripheral edema
• Pulmonary edema
• Tachycardia
• Shortness of breath
• Cardiomegaly

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Neurohumoral Compensatory Mechanism
(RaSyEnNat)

• Renin-angiotensin-aldosterone system (Angiotensin II)
• Sympathetic stimulation (NE, Epi)
• Endothelin release
• Natriuretic peptides (Brain Natriuretic Peptide)

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Neurohumoral Compensatory Mechanism
a.va=
b.pro=

a. vasoconstriction=↑afterload
b. Prolongedβ-activation=caspases = apoptosis

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Enlargement of myocardial cells due to chronic and increased stress on the heart (release of caspases)

Myocardial Hypertrophy

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• thickening of heart walls/muscle
• can lead to ischemic changes, impairment of diastolic filling, and alterations in ventricular geometry

Myocardial Hypertrophy

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• dilation (other than that due to passive stretch) and other slow structural changes that occur in the stressed myocardium

Remodeling

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Pathophysiology of Cardiac Performance
(PACH)

a. Preload
b. Afterload
c. Contractility
d. Heart rate

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Patho

•is usually increased in heart failure because of increased blood volume and venous tone
• Increased blood volume and venous tone increases fiber length or filling pressure, and increases oxygen demand in the myocardium.

Preload

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Patho

• Reduced by diuretics and venodilators

Preload

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Decreased CO in chronic failure results to reflex increased in SVR (__) mediated by:

•increased sympathetic outflow and circulating catecholamines (baroreceptor reflex)
•activation of the renin-angiotensin system § endothelin

Afterload

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Reduced by drugs that reduces arteriolar tone

Afterload

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Chronic heart failure demonstrates a reduction in_____
• Decreased ___result in:

•decreased velocity of muscle shortening
•decreased rate of intraventricular pressure development
•reduced stroke output

Contractility

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Inotropic drugs increase contractility

Contractility

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• Major determinant of cardiac output
• First compensatory mechanism that comes into play to maintain cardiac output
• _______(2) limits diastolic filling time and coronary flow, further stressing the heart

Heart rate

Tachycardia

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drugs may benefit patients with high heart rates

Bradycardic drugs

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Classification of HF

• aka left-sided HF or left ventricular HF
• Reduced mechanical pumping action (contractility) of the heart
• reduced CO and significantly reduced EF
• Resulting from myocardial ischemia/infarction
• Responds with inotropic agents

SYSTOLIC HF

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Classification
Symptoms:
•pulmonary symptoms (dyspnea, orthopnea, tachypnea, paroxysmal nocturnal dyspnea, Cheyne-stokes respiration),
•S3 gallop or third heart sound
•cardiomegaly

SYSTOLIC HF

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Classification:
• aka right-sided HF or right ventricular HF
• Stiffening and loss of adequate ventricular relaxation to permit normal filling and cardiac output
• CO is reduced, EF may be normal
• Resulting from hypertrophy and stiffening of myocardium
• Does not respond with inotropic agents

DIASTOLIC HF

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Symptoms: •peripheral edema •neck-vein engorgement •hepatomegaly

DIASTOLIC HF

Cardiac output is below the normal range, but demand for blood flow is normal

Low output HF

• the demands of the body for blood is unusually high, that even increased CO is insufficient • result from hyperthyroidism, beriberi, anemia, and arteriovenous shunts • responds poorly to drugs, thus, management is by correcting the underlying cause

High Output HF

Causes of high output HF SaHyArfBerPa

Severe anemia Hyperthyroidism Arteriovenous fistula Beriberi Paget’s disease

Blood contains too few oxygen-carrying bv

Severe anemia

Thyroid gland produces too much thyroid hormone.

Hyperthyroidism

An abnormal connection between an artery and a vein

Arteriovenous fistula

Deficiency of thiamine (vitamin B1)

Beriberi

Abnormal breakdown and regrowth of bones, which develop an excessive amount of blood vessels

Paget’s disease

New York Heart Association Functional Classification Patients with cardiac disease but resulting in no limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea or anginal pain.

Class l

New York Heart Association Functional Classification Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain.

Class ll

New York Heart Association Functional Classification Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain.

Class lll

New York Heart Association Functional Classification Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort increases.

Class IV

American College of Cardiology/American Heart Association classification Px are high risk for HF but w/o structural hdx or sx of Hf

Stage A

American College of Cardiology/American Heart Association classification Px w/ structural hdx but w/o s/sx of hf

Stage B

American College of Cardiology/American Heart Association classification Px w/ structural hdx w/ prior or current sx of hf

Stage C

American College of Cardiology/American Heart Association classification Px w/ refractory hf requires specialized intervention

Stage D

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium reduces the actions of cardiac glycosides; increased cardiac automaticity is inhibited

Hyperkalemia

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium enhances the actions of cardiac glycosides; increases risk of digoxin toxicity

Hypokalemia

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium enhances the actions of cardiac glycosides; increases risk of digoxin toxicity

Hypokalemia

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium increases the risk of a digitalis-induced arrhythmia

Hypercalcemia

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium increases risk of digoxin toxicity

Hypomagnesemia

Management of Digoxin Toxicity Administration of antiarrhythmics for ventricular and atrial arrhythmias

Phenytoin

Management of Digoxin Toxicity Administration of antiarrhythmics for ventricular tachyarrhythmias

Lidocaine and procainamide

Management of Digoxin Toxicity Administration of antiarrhythmics for ventricular and supraventricular tachycardia but not in the presence of AV block

Propranolol

Management of Digoxin Toxicity Administration of antiarrhythmics for Sinus bradycardia and various degrees of AV block

Atropine

Management of Digoxin Toxicity Administration of Digoxin-specific antibody fragment for • Life-threatening digoxin or digitoxin overdosage • Patients exhibiting shock or cardiac arrest, ventricular arrhythmias, progressive bradyarrhythmias, or severe hyperkalemia

DigiFab & DigiBind

MOA: inhibits phosphodiesterase isozyme 3 (PDE3) leading to ↑cAMP → Protein kinase A (PKA) activation → ↑influx of Ca2+ into the cell = (+) inotropy, chronotropy and dromotropy

Bipyridines

• Increase contractility and promote vasodilation • Used only intravenously • Only for acute heart failure or severe exacerbation of chronic heart failure

Bypiridines

Adverse Effects of specific bypitiridines nausea and vomiting, arrhythmias, thrombocytopenia, hepatoxicity = already withdrawn

Inamrinone

Adverse Effects of specific bypitiridines arrhythmias; less likely to cause thrombocytopenia and hepatoxicity

Milrinone

Adverse Effects of specific bypitiridines arrhythmias; less likely to cause thrombocytopenia and hepatoxicity

Milrinone

MOA: stimulates β1-receptors = ↑cAMP → Protein kinase A (PKA) activation → ↑influx of Ca2+ into the cell = (+) inotropy, chronotropy and dromotropy

β1-receptor Agonists

B1 receptor agonist increaseinCO,decreaseinventricularfillingpressure

Dobutamine (β1-selective)

B1 receptor agonist acuteheartfailure,ifthereisaneedtoraisebloodpressure

Dopamine (non-selective)

Investigational Positive Inotropic Drugs IsLeOm

Istaroxime Levosimendan Omecamtiv mecarbil

Investigational Positive Inotropic Drugs • steroid derivative that inhibits Na+/K--ATPase • in addition, appears to facilitate sequestration of Ca2+ by the SR = less arrhythmogenic than digitalis

Istaroxime

Investigational Positive Inotropic Drugs • sensitizes the troponin system to Ca2+ and inhibits phosphodiesterase

Levosimendan

Investigational Positive Inotropic Drugs • parenteral agent that activates cardiac myosin and prolongs systole without increasing oxygen consumption of the heart

Omecamtiv mecarbil

Agents With No Positive Inotropic Effects DiAcArVBb

Diuretics Ace/Arbs Vasodilators Beta blockers

Agents With No Positive Inotropic Effects • Reduce left ventricular filling pressure and decrease left ventricular volume and myocardial wall tension (lower oxygen demand) • Reduce salt and water retention, edema, and symptoms

Diuretics

Agents With No Positive Inotropic Effects “balanced unloaders” • Arteriolar vasodilation = ↓ SVR = ↓ afterload • Venous vasodilation = ↓ venous return/ventricular filling pressure = ↓ preload • reduce salt and water retention = ↓ preload

ACE/ARBs

Specific vasodilators • Used in patients who cannot tolerate ACE inhibitors • African Americans respond better than with ACEis and ARBs • Balanced unloader if combined

Isosorbide dinitrate Hydralazine

Heart Failure Flashcards

(67 cards)