Heart failure (exam 2) Flashcards
(104 cards)
1
Q
heart failure is a
A
cardiomyopathy
2
Q
heart failure
A
inadequate ability of the heart to pump enough blood to meet the metabolic demands of the body
3
Q
HF results from a _________________ due to a _______________
A
reduction in cardiac output
reduction in stroke volume
4
Q
common symptoms of HF
A
fatigue
tachycardia
edema
dyspnea
exercise intolerance
5
Q
Ejection fraction =
A
stroke volume/end diastolic volume
6
Q
heart failure with reduced ejection fraction (HFrEF)
A
systolic HF
dilation of ventricles (dec SV, inc EDV)
EF under 40%
7
Q
heart failure with preserved ejection fraction (HFpEF)
A
diastolic HF
stiffening of myocardium (dec SV, dec EDV)
EF over 50%
8
Q
cardiac output =
A
stoke volume x HR
9
Q
stroke volume is affected by
A
preload
afterload
contractility
10
Q
preload is dependent on
A
venous return
11
Q
venous return is dependent on
A
fluid volume and venous tone
12
Q
preload
A
the pressure within the ventricle
stretching of the myocytes at the end of diastole
13
Q
increase in fluid volume or venous vasoconstriction leads to
increase in venous return leads to
A
increase in preload
increase in preload and SV
14
Q
afterload
A
resistance to ejection of blood from the ventricle
15
Q
after load is dependent on
A
arterial tone
16
Q
arterial vasoconstriction leads to
A
increase in after load and decrease in SV
17
Q
contractility is dependent on
A
ANS and Calcium
18
Q
activation of beta1 receptors and intracellular Ca leads to
activation of M2 receptors leads to
A
increase contractility and SV
dec contractility and SV
19
Q
Frank starling law
A
volume of ejected blood by the ventricle depends on volume/pressure present in the ventricle at the end of diastole
20
Q
when the myocardial fibers are stretched more, the blood ejected from the heart
A
increases due to greater force of contraction
21
Q
is increase in preload sufficient for patients with HF to maintain SV?
A
no
22
Q
compensatory mechanisms in HF
A
increased preload
vasoconstriction
tachycardia and increased contractility
ventricular hypertrophy and remodeling
23
Q
cardiac remodeling
A
changes in size, shape and function of the heart following injury
24
Q
cardiac remodeling is associated with the development and progression of
A
ventricular dysfunction and arrhythmias
25
neurohormones that promote cardiac remodeling
angiotensin II
aldosterone
ADH
NE/E
inflammatory cytokies
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neurohormones that reduce cardiac remodeling
B-type natriuretic peptide (BNP)
27
B-type natriuretic peptide (BNP)
secreted by cardiomyocytes in response to pressure or volume overload
28
BNP causes
vasodilation, enhances renal sodium and water excretion and reduces cardiac remodeling
29
BNP is used as a
high levels of BNP correlates with
biomarker for HF
severity of HF
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chronic HF
compensated HF
symptoms not severe enough for hospitalization
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chronic HF medications focus to
decrease fluid overload and to counteract compensatory mechanisms
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exact medication regimen depends on
HF stage (A-D) and functional classification (I-IV)
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acute decompensated HF
sudden worsening of HF that requires hospitalization
34
acute decompensated HF occurs due to
excessive fluid overload and/or excessive reduction in cardiac output
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drugs used for acute decompensated HF
diuretics, possible vasodilators
positive inotropes
36
RAAS inhibitors for HF
ACEIs
ARBs
ARNI
aldosterone antagonists
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Angiotensin receptor neprilysin inhibitor (ARNI) example
sacubitril/valsartan (entresto)
38
combination vasodilator for HF
isosorbide dinitrate and hydralazine (BiDil)
39
cardiac glycoside for HF
Digoxin (Lanoxin)
40
HCN channel blocker for HF
Ivabradine (Corlanor)
41
medications used for Chronic HF
RAAS inhibitors
Beta blockers
Loop diuretics
combination vasodilator
cardiac glycoside
HCN channel blocker
SGLT2 inhibitor
soluble guanylate cyclase stimulator
42
SGLT2 inhibitor used for HF
dapagliflozin
empagliflozin
43
soluble guanylate cyclase stimulator used for HF
vericiguat
44
major affect of angiotensin I activation
vasoconstriction
increase in aldosterone
increase in ADH secretion
45
inhibiton of RAAS system reduces
morbidity and mortality in patients with HF
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for most patients with HF, an ___________________ is recommended
ACEI/ARB/ARNi and aldosterone antagonist
47
ACEIs effects in HF
dec preload (dec aldosterone, ADH)
dec afterload (dec angiotensin II)
reduces cardiac remodeling (dec aldosterone, ADH, AGII)
48
ACEIs and ARBs are contraindicated in
pregnancy
49
ARBs effects in HF
dec preload (dec aldosterone, ADH)
dec afterload (dec AT1 activation)
reduces cardiac remodeling (dec AT1 activation)
50
ACEIs and ARBs should be started at ___________________ due to lower renal perfusion in patients with HF
a lower dose and titrated up slowly
51
sacubitril is a
neprilysin inhibitor
52
inhibition of neprilysin increases ______________ and leads to __________________
concentration of natriuretic peptides like BNP
arterial vasodilation (dec afterload)
Na/water excretion (dec preload)
reduction in cardiac remodeling
53
neprolysin also breaks down ________________ which inhibiting this then can be counterproductive. ____________ is added because it blocks _______ receptors
angiotensin II
an ARB
angiotensin 1
54
sacubitril is a ____________ that is converted into ____________
ester prodrug
the active form LBQ657 by esterase enzymes
55
ADRs of entresto
from valsartan -- increased SCr, hyperkalemia
from sacubitiril -- cough, angioedema and inc BNP levels
56
when switching from an ACEI to ARNi or vice versa, have a ___________________ to reduce the risk of ____________
36 hour washout period
angioedema
57
entresto is contraindicated in
pregnancy
58
effects in HF due to aldosterone antagonism
reduction in fluid volume (dec preload)
reduction in cardiac remodeling
59
what needs to be monitored when taking an aldosterone antagonist with an ACEI/ARB?
serum K
60
ADRs of aldosterone antagonists
N/V/D
hyperkalemia
gynecomastia
ED
alterations in menstrution
61
beta blockers effects in HF
dec HR and contractility --> dec cardiac output
reduce cardiac remodeling
62
which are the current recommended beta blockers for HF?
bisoprolol
metoprolol
carvedilol
63
antagonism at beta1 receptors reduces cardiac output, but over time this has a
cardioprotective effect
64
carvedilol and metoprolol are metabolized by
bisoprolol is metabolized by
CYP2D6
CYP3A4
65
ADRs of beta blockers
dizziness
fatigue
bradycardia
only use cardioselective BB in people w asthma/COPD
66
loop diuretics effect in HF
reduce fluid overload - pulmonary and peripheral
(dec preload)
67
loop diuretics are recommended fr
symptomatic control of HF
68
what can be added to overcome loop diuretic resistance?
thiazide diuretic
69
what risk is reduced when combining hydralazine with ISDN?
peripheral edema
70
patients should be on a __________ before initiating combination vasodilator therapy which reduces risk of _______________
beta blocker
reflex tachycardia
71
combination vasodilator effects on HF
hydralazine - arterial vasodilation (dec afterload)
ISDN - reduce cardiac remodeling and venous vasodilation (dec preload)
72
cardiac glycoside (digoxin) MOA
increases intracellular Ca by inhibition of Na/K/ATPase leading to a positive inotropic effect
73
effects of digoxin in HF
inc contractility
dec HR
inc cardiac output
74
digoxin consists of
a steroid core with a lactone ring and 3 saccharides
75
antidote for digoxin therapy
digoxin immune FAB (digibind, digifab)
76
digoxin has a __________________ and recommended therapeutic plasma levels are ____________ in HF. Toxicity is around __________________ due to inhibition in various tissues
narrow therapeutic index
0.5-0.9 ng/ml
over 2 ng/ml
77
signs and symptoms of digoxin toxicity
N/V/D, abdominal pain
blurred/yellow vision
halos
dizziness
headache
confusion/delirium
arrhythmias
hyperkalemia
78
risk of toxicity of digoxin is higher when these specific electrolyte abnormalities are present
hypokalemia
hypomagnesemia
hypercalcemia
79
digoxin has a half life around
36-40 hours
80
common ADRs of digoxin
bradycardia
N/D
abdominal pain
loss of appetite
dizziness
headache
fatigue
81
rare ADRs of digoxin
gynecomastia
vision disturbance
arrhythmias
82
electrolyte abnormalities caused by _________ may increase risk of digoxin toxicity
loop diuretics
83
HCN channel blocker MOA
selectively inhibits hyper polarization cyclic nucleotide gated transmembrane channel in SA node
84
HCN channel blockers effects in HF
dec HR
dec cardiac output
84
HCN channel blockers prolong
diastole and reduce HR
85
HCN channel blockers are metabolized by
CYP3A4
86
ADRs of HCN channel blockers
bradycardia
increased risk of a fib
dizziness
fatigue
visual disturbance
87
treatment for warm and dry ADHF
nothing
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treatment for warm and wet ADHF
loop diuretics and vasodilators (to reduce PCWP)
89
treatment for cold and dry ADHF
increase cardiac index with positive inotropes and/or fluid replacement
90
treatment for cold and wet ADHF
delicate balance between diuretics, vasodilators, and inotropes
may use vasopressors
91
which is the most challenging form of ADHF to treat?
cold and wet
92
medications used in ADHF when the patient has fluid overload
loop diuretics
vasodilators
93
medications used in ADHF when the patient has hypoperfusion
positive inotropes
94
examples of positive inotropes
dobutamine (dobutrex)
dopamine (intropin)
milrinone (primacor)
95
dobutamine MOA
agonist at adrenergic receptors (beta 1>beta2>alpha1)
inc HR and contractility --> inc cardiac output
slight vasodilation
96
which drugs are less effective if the patient is on beta blocker therapy?
dobutamine
dopamine
97
dobutamine and dopamine are metabolized by _________ and go through ______________-
COMT (both)
glucuronidation (dobutamine) & MAO (dopamine)
98
what does dopamine do at low doses?
activates D1 receptors -> vasodilation
99
what does dopamine do at moderate doses?
activates B1 receptors --> inc HR and contractility (inc CO)
100
what does dopamine do at high doses?
activates alpha1 receptors --> vasoconstriction
101
moderate to high doses are used for treatment of which type of ADHF?
cold
102
Milrinone MOA
PDE3 inhibitor
inhibits breakdown of cAMP > cGMP
103
when milrinone is used, there is an increase in cAMP, which leads to
increased intracellular Ca
increased cardiac contractility
increased cardiac output
venous vasodilation
