Heart Failure Flashcards
a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction
Ejection Fraction
50-70% is pumped out during each contraction (comfortable during activity)
NORMAL Ejection Fraction
41-49% is pumped out during each contraction (sx may be noticeable during activity)
BORDERLINE Ejection Fraction
<_ 40% is pumped out during each contraction (sx ate noticeable even during rest)
REDUCED Ejection Fraction
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
•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
S/Sx: of Heart Failure
DetPePue TaShoCa
• Decreased exercise tolerance
• Peripheral edema
• Pulmonary edema
• Tachycardia
• Shortness of breath
• Cardiomegaly
Neurohumoral Compensatory Mechanism
(RaSyEnNat)
• Renin-angiotensin-aldosterone system (Angiotensin II)
• Sympathetic stimulation (NE, Epi)
• Endothelin release
• Natriuretic peptides (Brain Natriuretic Peptide)
Neurohumoral Compensatory Mechanism
a.va=
b.pro=
a. vasoconstriction=↑afterload
b. Prolongedβ-activation=caspases = apoptosis
Enlargement of myocardial cells due to chronic and increased stress on the heart (release of caspases)
Myocardial Hypertrophy
• thickening of heart walls/muscle
• can lead to ischemic changes, impairment of diastolic filling, and alterations in ventricular geometry
Myocardial Hypertrophy
• dilation (other than that due to passive stretch) and other slow structural changes that occur in the stressed myocardium
Remodeling
Pathophysiology of Cardiac Performance
(PACH)
a. Preload
b. Afterload
c. Contractility
d. Heart rate
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
Patho
• Reduced by diuretics and venodilators
Preload
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
Reduced by drugs that reduces arteriolar tone
Afterload
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
Inotropic drugs increase contractility
Contractility
• 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
drugs may benefit patients with high heart rates
Bradycardic drugs
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
Classification
Symptoms:
•pulmonary symptoms (dyspnea, orthopnea, tachypnea, paroxysmal nocturnal dyspnea, Cheyne-stokes respiration),
•S3 gallop or third heart sound
•cardiomegaly
SYSTOLIC HF
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
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
