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36 Cards in this Set

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(+) Inotrope
Increase force of contraction

How?
An increase in intracellular calcium
chronotropic effect
rate of contraction
dromotropic effect
conduction velocity
THIAZIDE
ADVERSE-REACTIONS
include:


H+
ADVERSE-REACTIONS
from ( __class__?) Rxs include:

Hypokalemia
and
Intravascular Volume Depletion with resulting:
:
Hepatic Dysfunction-emia.
Hyperglycemia
Hyperuricemia
Neutropenia
Prerenal Azotemia
Skin Rash-emia.
Thrombocytopenia
9ct
1+1(+7) = 9

H
IVVD:
:
H D
H G
H U
N
P A
S R
T-C-P
Positive Inotropic Drugs:

3ct
Positive Inotropic Drugs:

-Digitalis
-Beta-Adrenoceptor Agonist ?
-Phosphodiesterase Inhibitors ?
Beta-Adrenoceptor Agonist (Dobutamine)
Phosphodiesterase Inhibitors. (Milrinone)
Digitalis
Beta adrenoceptor Agonists (?)
Phosphodiesterase Inhibitors (?)

Positively
or
Negative
Inotropic drugs:
Positive Inotropes

Beta adrenoceptor Agonists (Name ?)
Phosphodiesterase Inhibitors. (Name ?)
Beta adrenoceptor Agonists (Dobutamine)
Phosphodiesterase Inhibitors. (Milrinone)
Digoxin
Produces Modest +/- inotrope effect
Modest + inotrope effect
(increase force of contraction)

How
caused by an increase in intracellular calcium
Digoxin
Produces a +/- chronotropic effect of contraction
Produces a (-) chronotropic effect of contraction
(decreased rate)
Digoxin
Produces a +/- dromotropic effect
Produces a (-) dromotropic effect
(a decrease in the conduction velocity).
Digoxin Toxicity S/S

6ct
-Arrhythmias: are Most-Serious-Manifestations.
-Siezures

The earliest signs are :
-Anorexia
-Nausea
-Vomiting
-Blurred vision
-Chromotropsia Yellow Green or Blue
Beta-blockers
prevent what cardiac issues from occurring?

8ct
Prevent excessive-stimulation leading to:
:
Cardiac Remodeling
Dilatation
Hypertrophy
Increases O2 demand
Increases infarct size
RAAS Activation (renin-angiotensin-aldo-system)
Tachycardia
Ventricular wall thinning/rigidity
C
D
H
I
I
R
T
V
These Rx sub catagories can cause

Reflex Tachycardia
2ct
Nitrates
or
Dihydropyridine - CCBs.

They cause what?
Reflex Tachycardia
Major contraindications for BB

3ct
-Bradyarrhythmias

-Bronchospastic Disease (Severe)

-Decompensated Heart Failure.
Digoxin Causes a decrease or increase in parasympathetic tone
Causes an Increase
Digoxin
Causes an increase or decrease in
conduction
and
AV node conduction velocity
Decreases
Digoxin Causes an increase or decrease in the
AV Node Refractory Period
Increases the AV-Node Refractory Period.
This drug is MOST HELPFUL in
Heart Failure(CHF) combined with
Atrial Fibralation.
Digoxin



This drug is MOST HELPFUL in ?
Heart Failure(CHF)
combined with
Atrial Fibralation.
the Dihydropyridine CCBs:
2ct
the Dihydropyridine CCBs:
Amlodipine
Nifedipine

the NON-Dihydropyridine
CCBs: ?
2ct
the NON-Dihydropyridine CCBs:
Diltiazem
Verapamil
Major -Contraindications for:

BB

3ct
- Bradyarrhythmias
- (severe) Bronchospastic Disease
- Decompensated Heart Failure.

Name the BB?
2ct
Carvedilol/Metoprolol XL
B-Blockers w\ Verapramil cause what?
they significantly reduce
Cardiac Output.

What 2 Rxs do this?
B-Blockers w\ Verapramil
Oraganic Nitrates\Nitrites
Release what?
&
have what effect on:
Vascular and Smooth Muscle Cells?
release Nitric Oxide
in
vascular and smooth muscle cells

Relaxation
Oraganic Nitrates\Nitrites have what effect on:

Venous Smooth Muscle?
Relax venous smooth muscle
Oraganic Nitrates\Nitrites have what effect on:

Arteriolar Smooth Muscle?
Relax Venous Smooth Muscle
but
relatively small-to-little-effect on
Arteriolar Smooth Muscle.

ref+
Brenner 113 top Right
Firstline Rx for Chronic Angina
BB

Name the two?
Carvedilol

Metoprolol XL
identify common adverse effects for
hydrochlorothiazide
AEs =
hypokalemia,
electrolyte imbalances,
pH disturbance,
increase blood glucose, hyperuricemia (causing gout).
identify common adverse effects for
furosemide
AEs =
iuresis,
dehydration,
electrolyte imbalances.
identify common adverse effects for

spironolactone
AEs =
gynecomastia
impotence;
hyperkalemia.
Describe the use of spironolactone as an aldosterone antagonist in patients with advanced HF
Competes with aldosterone at the renal tubule and other tissues (heart).

Increase sodium excretion,

decrease potassium excretion,

has a moderate diuretic effect.
Potassium-sparing diuretic.

Prevents adverse effects of excessive aldosterone levels on the heart, and having high serum potassium.

Good for mild to moderate HF. Bad for elderly due to hyperkalemia.
,
most commonly used
treatment of angina
describe
mechanism of action
Organic Nitrites & Nitrates
increase total blood flow to heart, especially subendocardial tissue,

dilate collateral vessels, which decreases intraventricular pressure and decreases the resistance to perfusion.

Reduce wall tension via their effects on ventricular volume and pressure.

Act primary on venous tissue, and predominantly affect afterload.
,
most commonly used
treatment of angina
describe
mechanism of action
Calcium Channel Blockers (CCBs):
same Nitrites/Nitrates, but act on arteriolar muscle to reduce afterload.
,
most commonly used
treatment of angina
describe
mechanism of action
reduce intraventricular pressure. decrease heart rate & contractility
(β-Blockers): are not used for
What?
&
Why?
Not effective to tx
variant angina

because they cannot counteract vasospasm and increase coronary blood flow.

May actually reduce coronary blood flow by blocking the vasodilative effect of epinephrine.
Describe why calcium channel blockers are generally avoided in patients with HF
They suppress cardiac contractility
beta-blockers ...concomitant conditions that may limit their use.
NOT used in management of
vasospastic angina
or
acute anginal attacks.
Ranolazine
Works
by
modifying myocardial metabolism

What is another mechanical benifit?
reduces angina episodes without causing significant changes in
BP
or
Heart Rate
platelet-inhibiting agents that are recommended for all patients with angina, unless contraindicated
Aspirin
Clopidogrel