44: AGENTS FOR TREATING HEART FAILURE Flashcards
resistance/pressure against which the heart has to push
afterload
volume of blood being pumped by the heart; cardiac output = heart rate x stroke volume
cardiac output
enlargement of the heart, commonly seen with chronic hypertension, valvular disease, and heart failure
cardiomegaly
disease of the heart muscle that leads to a weakened heart and can eventually lead to complete heart muscle failure and death
cardiomyopathy
discomfort with respirations, often with a feeling of anxiety and inability to breathe; seen often with left- sided heart failure
dyspnea
condition in which the heart muscle has less ability to adequately pump blood around the cardiovascular system, leading to a backup or congestion of blood in the system
heart failure (HF)
blood-tinged sputum seen in left-sided heart failure when blood backs up into the lungs and fluid leaks out into the lung tissue (coughing up of blood)
hemoptysis
getting up to void at night, reflecting increased renal perfusion with fluid shifts in the supine position when a person has gravity-dependent edema related to heart failure or other medical conditions, including urinary tract infection, increasing the need to get up and void
nocturia
difficulty breathing when lying down, oftenreferred to by the number of pillows required to allow a person to breathe comfortably
orthopnea
describes an agent that causes an increased force of muscle contraction
positive inotropic
amount of blood that is brought back to the heart to be pumped throughout the body; this blood exerts pressure on the heart ventricles
preload
increased fluid in the lung tissue that can be due to left-sided heart failure
pulmonary edema
rapid and shallow respirations that can be seen with left-sided heart failure
tachypnea
are often used to decrease the workload and oxygen consumption of the heart
antianginal medications
are drugs used to increase the contractility of the heart muscle for patients experiencing heart failure
cardiotonic agents
These are the medications that are used if the patient is not able to tolerate medications that lower heart rate and blood pressure due to weakening of the heart muscle
cardiotonic agents and hyperpolarization-activated cyclic nucleotide-gated channel blockers (HCN blockers)
at high risk for HF but without structural heart disease or symptoms of HF
Stage A
Structural heart disease but without signs or symptoms of HF
Stage B
Structural heart disease with prior or current symptoms of HF
Stage C
Refractory HF requiring specialized interventions
Stage D
No limitation on physical activity. ordinary physical activity does not cause symptoms of HF
Class I
Slight limitation of physical activity. comfortable at rest, but ordinary physical activity results in symptoms of HF
Class II
Marked limitations of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF
Class III
Unable to perform any physical activity without symptoms of HF, or there are symptoms of HF at rest
Class IV
Normal ejection fraction of the left ventricle is about?
55% - 70%
what are the two contractile proteins of sarcomere?
Actin and Myosin
Actin and myosin are highly reactive with each other but at rest are kept apart by this chemical
Troponin
it enters the cell and inactivates the troponin when a cardiac muscle is stimulated, allowing the actin and myosin to form actomyosin bridges
Calcium
The formation of these bridges allows the muscle fibers to slide together or contract
actomyosin bridges
is one of the leading causes of heart failure
coronary artery disease
results in an insufficient supply of blood to meet the oxygen demands of the myocardium
coronary artery disease
there is enlarged liver (hepatomegaly),
enlarged spleen (splenomegaly), decreased blood flow to the gastrointestinal
(GI) tract causing feelings of nausea and abdominal pain, swollen legs and
feet, and dependent edema in the coccyx or other dependent areas with
decreased peripheral pulses and hypoxia of those tissues.
right side heart failure
RIGHT SIDE HEART FAILURE
1. elevated jugular venous presssure
2. splenomegaly
3. hepatomegaly
4. decreased renal perfusion when upright
5. increase renal perfusion when supine = nocturia
6. pitting edema
7. weakness/fatigue
LEFT SIDE HF
1. anxiety
2. tachypnea, dyspnea, orthopnea, hemoptysis, rales
3. cardiomegaly
4. increased heart rate
5. GI upset, nausea, abdominal pain
6. decreased peripheral pulses
7. hypoxia
usually occurs as a result of chronic obstructive pulmonary
disease or other lung diseases that elevate the pulmonary pressure.
right side heart failure
affect the intracellular calcium levels in the
heart muscle, leading to increased contractility to improve the heart’s ability to pump blood effectively.
cardiotonic agents or drugs
increased contraction > increased cardiac output (amount of blood pump to the heart) > increased renal blood flow and urine production > decrease renin release > increase urine output > decreased blood volume
increases intracellular calcium and allows more calcium to enter
myocardial cells during depolarization
digoxin
Increases intracellular calcium and allows more calcium to
enter the myocardial cell during depolarization; this causes a positive
inotropic effect (increased force of contraction), increased renal
perfusion with a diuretic effect and decrease in renin release, a negative
chronotropic effect (slower heart rate), and slowed conduction through
the AV node.
digoxin
belong to a second class of
drugs that act as cardiotonic (inotropic) agents.
phosphodiesterase inhibitors
the only phosphodiesterase inhibitors drugs that is currently available
milrinone
block the enzyme phosphodiesterase and this blocking effect leads to an increase in myocardial cell cyclic adenosine
monophosphate (cAMP), which increases calcium levels in the cell
phosphodiesterase inhibitors
Short-term treatment of HF in patients who have not
responded to digitalis, diuretics, or vasodilators
milrinone
Blocks the enzyme phosphodiesterase, which leads to an
increase in myocardial cell cAMP, which increases calcium levels in the
cell, causing a stronger contraction and prolonged response to
sympathetic stimulation; directly relaxes vascular smooth muscle.
milrinone
does not
affect muscle contraction but does affect the pacemaker (slows down) of the heart to reduce
heart rate.
hyperpolarization activated nucleotide gated channel blockers
Slowing the heart rate allows more time for ventricular filling and
improves cardiac output
Treatment of chronic heart failure in stable patients at
maximum beta-blocker doses, to prevent rehospitalizations.
ivabradine
increases the movement of calcium into
the heart muscle. This results in increased force of contraction, which
increases blood flow to the kidneys (causing a diuretic effect), slows
the heart rate, and slows conduction through the AV node. All of these
effects decrease the heart’s workload
cardiac glycoside (digoxin)
block the breakdown of cAMP in the
cardiac muscle. This allows more calcium to enter the cell (leading to
more intense contraction) and increases the effects of sympathetic
stimulation (which can lead to vasodilation but also can increase pulse,
blood pressure, and workload on the heart)
phosphodiesterase inhibitors
the only phosphodiesterase inhibitor available, is associated
with severe effects. It is reserved for use in extreme situations. It is
only available for IV use.
milrinone
is the first HCN blocker, which is used with stable, chronic
HF to slow the pacemaker of the heart, reducing heart rate without the
systemic effects that occur with beta-blockers. Slowing the heart rate
allows more time for ventricular filling and improves cardiac output
without the systemic effects seen with beta-blockers
ivabradine
is the functioning unit of the heart
sarcomere
