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Pharmacology > Cardiac pt 3 > Flashcards

Cardiac pt 3 Flashcards

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1
Q

why are nitrates used to treat chronic HF

A

to reduce preload

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2
Q

how does the diuretic effect with SGLT-2 inhibitors occur

A

through inc loss of Na and glucose -> osmosis leading to dec circulating volume + reduced preload

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3
Q

why are beta blockers used to treat chronic HF

A

to protect heart from effects of sympathetic overstimulation

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4
Q

for acute HF, what will the drugs used usually seek to do

A

increase force of contraction

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5
Q

what are the two aims of chronic HF treatment

A

reduce symptoms
reduce workload on heart

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6
Q

what do BNP peptides do

A

reduce volume overload by inc urinary excretion of sodium and water

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7
Q

why are angiotensin receptor neprilysis inhibitors (ARNI) used to treat chronic HF

A

to reduce peripheral resistance and venous return (pre and afterload)

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8
Q

what is HF

A

heart unable to pump sufficiently to maintain blood flow to supply body’s O2 requirement

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9
Q

whats the electrical effect of cardiac glycosides

A

dec HR
dec AV conduction

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10
Q

why are sodium-glucose transport inhibitor diuretics used to treat chronic HF

A

to reduce blood volume (preload)

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11
Q

in vascular SM, inc of cAMP or cGMP causes what

A

relaxation of BVs

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12
Q

why would you used ivabradine for HF symptoms

A

if your pt has a HR over than 77bpm

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13
Q

what are two symptoms of excessive congestion

A

oedema
dyspnea

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14
Q

how does digoxin cause inc Ca
intracellular levels

A

The poisoning of Na-K-ATPase pump by digoxin leads to increased intracellular sodium levels and this decreases the activity of the Na-Ca exchanger – ultimately leading to increased intracellular calcium levels

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15
Q

what are 3 drug classes used for HF

A

cardiac glycosides (chronic HF)
phosphodiesterase inhibitors (acute HF)
adrenergic agonists (acute HF)

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16
Q

how do you treat an overdose of cardiac glycosides

A

administration of neutralizing anti-digoxin antibody fragments (Digibind)

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17
Q

why would you used hydralazine and nitrates for HF symptoms

A

if ARNI, ACEi, ARBs
not tolerated

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18
Q

why is there limited use of Beta agonists

A

due to adverse effects and short half life

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19
Q

why are loop diuretics used to treat chronic HF

A

to reduce pulmonary or peripheral oedema

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20
Q

dapagliflozin
empaglifozin
canaglifozin are examples of what kind of drug

A

SGLT-2 inhibitors

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21
Q

what are the initial therapies to treat patients with HF symptoms and a reduced EF

A

ARNI, ACEi, ARBs
Beta blockers
MRAs
SGLTi

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22
Q

what are the two mechanisms of action for cardiac glycosides

A

blocks Na/K ATPase
results in inc intracellular Ca levels

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23
Q

why are neprilysin inhibitors used with an AngII receptor blockers?

A

to prevent unwanted increases in AngII

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24
Q
A
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25
why are mineralocorticoid receptor antagonists used to treat chronic HF
to reduce blood volume (preload)
26
in the heart, inc of cAMP causes what
inc force of contraction
27
name 3 additional interventions for pts with HF symptoms and reduced EF
ivabradine hydralazine/nitrate digoxin
28
what does an intermediate dose of dopamine do
it has a positive inotropic effect
29
name 2 drugs that cause early afterdepolarization
class 3 antiarrhytmic drugs -> sotalol amiodarone
30
why is ivabradine used to treat chronic HF
for control of inc HR
31
why is hydralazine used to treat chronic HF
to reduce afterload
32
what are some adverse effects of SGLT-2 inhibitors
fungal infections polyuria hypotension euglyemic diabetic ketoacidosis
33
inhibition of neprilysin results n an acculmulation of what
AngII
34
name 3 drugs used to treat acute HF that inc contracility and BP
dobutamine dopamine milrinone
35
what is phosphodiesterase
the enzyme responsible for the degredation of cAMP and cGMP
36
what inhibits neprilysin
sacubitril
37
what type of drugs cause delayed afterdepolarizations
mostly inotropic drugs that inc intracellular Ca levels
38
how does ivabradine slow accelerated cardiac rythym
it blocks an ion channel that is responsible for generating the SA node pacemaker current
39
what are afterdepolarizations
unwated depolarizations that occur after the AP
40
whats the mechanical effect of cardiac glycosides
inc force of contraction (ie positive inotropic effect)
41
name 4 signs of HF
dec force of contraction dec tissue perfusion oedema diaphoresis
42
what do SGLT-2 inhibitors do
inhibit Na/glucose reabsorption in proximal tubule of the kidney
43
what are the 3 areas of focus for treatment of acute HF
inc O2 sat reduce volume overload inc contractility and BP
44
what do low doses of dopamine do
dilates BV in kidneys for better filtration
45
what are two phosphodiesterase inhibitors
milrinone inamrinone
46
what is the mechanism of action for beta agonists
inc force of contraction and HR dobutamine stimulates B1 receptors
47
name some causes of HF
cardiomyopathies MI HTN valvular disease
48
what does a high dose of dopamine do
peripheral vasoconstriction
49
name 2 adverse effects of cardiac glycosides
nausea/vomiting arrhythmias (late afterdepolarizations)
50
why are cardiac glycosides dangerous if patients are hypokalemic
it has a narrow therapeutic index and low extracellular K increases effect of cardiac glycosides
51
name 3 SGLT-2 inhibitors
dapagliflozin empaglifozin canaglifozin
52
name 2 beta agonists
dopamine dobutamine
53
why would you used digoxin for HF symptoms
if suboptimal control of afib
54
when are BNP natriuretic peptides released
when our effective circulating volume is too high (like during HF)
55
what is neprilysin responsibe for
degradation of BNP natriuretic peptides and vasodilatory peptides degradation of circulating AngII
56
why are cardiac glycosides used to treat chronic HF
they're helpful against HF with afib (idk why tho)
57
what does sacubitril do
inhibits neprilysin
58
what are two symptoms of inadequate CO
fatigue poor perfusion
59
what is the danger of Beta agonists
can result in arrhythmias
60
why are ACEi or ARBs used to treat chronic HF
to reduce peripheral resistance and venous return (pre and afterload)
61
what are the 4 methods of compensation for reduced CO
dilation of the heart activation of SNS to inc contractility, HR and BP activation of RAA system water retention
62
when the body compensates for HF, what 3 things inc
HR venous return (preload) peripheral resistance (afterload)
63
name an example of a cardiac glycoside
digoxin
64
what is the mechanism of action of cardiac glycosides
they block Na-K ATPase
65
what does the mechanism of action for cardiac glycosides result in
increased intracellular Ca levels
66
what is the mechanical effect of cardiac glycosides
inc force of contraction
67
what are the electrical effects of cardiac glycosides
dec HR dec AV conduction
68
what is phosphodiesterase
the enzyme responsible for cAMP and cGMP degredationi
69
higher levels of cAMP does what
inc the force of contraction of the heart and inc relaxation of vascular SMH
70
name 2 phosphodiesterase inhibitors
milrinone inamirone
71
milrinone and inamirone are examples of what
phosphodiesterase inhibitors

Pharmacology (22 decks)

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