Drugs HF and H 3 Flashcards

1
Q

arthomia

A

have to sit up to breath

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2
Q

paroxymal nocturnal dyspnea

A

wake up in the middle of the night gasping for breath, sign of retaining fluid

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3
Q

for fluid overload check

A

the RIGHT jugular vein distension in the older patient

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4
Q

why check the RIGHT jugular vein distension in the older patient

A

The left inominate vein dumps into the left jugular; this vein may be compressed between an elongated and unfolded aortic arch and the back of the sternum; increased mechanical pressure of the inominate vein may lead to increased left jugular vein distention continuously.

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5
Q

if S3

A

Indicates an elevated left ventricular diastolic pressure- blood on top of blood that didn’t get emptied the last time; lower sodium and water retention so that s3 goes away

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6
Q

if pt seems very anxious

A

give pt touch of morphone bc it vasodilates, so it will chill out pt and well make them relax and breath better; so morphine, lasix and ACE inhibitor

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7
Q

FVE (fluid volume excess)

A

edema, increase bp, sob, decrease u/o, rales, crackles, infiltrates/pleural infusion

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8
Q

the weakling of diuretics

A

potassium sparing diuretics

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9
Q

Spironolactone inhibits the action of

A

aldosterone. Blocks sodium and water retention; conserves potassium; (also used for hirsutism in women);

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10
Q

potassium sparing diuretics examples

A

This group consists of spironolactone (Aldactone), eprelrenone (Inspra), amiloride, and triamterene.

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11
Q

side effects of potassium sparing diuretics

A

gynecomastia (increase in breast tissue) in men, hyperkalemia

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12
Q

hyperkalemia

A

when levels are higher than 3.5 - 5.0 mEq/L; • Ventricular dysrhythmias, peaked T waves (tall tented T waves), prolonged PR interval on EKG)

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13
Q

Disruption of electrical activity of heart:

A

asystole (occurs when levels reach 8-9 mEq/L)

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14
Q

S/S of hyperkalemia

A

• Confusion, anxiety, dyspnea, weaknes or heaviness of legs, numbness/tingling of hands, feet, lips, bradycardia, changes in bp

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15
Q

Treatment of Hyperkalemia ***

A
  1. Withold foods containing potassium and medications that promote potassium accumulation 2. Calcium gluconate IV to promote cardiac contraction 3. Infusion of glucose and insulin 4. Sodium bicarbonate 5. Sodium polystyrene sulfonate 6. Dialysis
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16
Q

Calcium gluconate IV to promote cardiac contraction

A

won’t decrease potassium but will protect heart and makes it contract

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17
Q

Infusion of glucose and insulin:

A

As insulin carries glucose into the cells, it also carries K+ from the serum into the cell

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18
Q

Sodium bicarbonate:

A

By making the blood more alkalotic (raising the pH), the cells take up more K+ from the blood

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19
Q

Sodium polystyrene sulfonate

A

Kayexalate: an exchange resin (exchanges Na for K, works in GT tract so then increase in stool) that exchanges sodium for potassium in the GI tract, causing K+ to be eliminated in the stool

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20
Q

dialysis

A

will give amp of dextrose 50% then administer IV insulin

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21
Q

so if bump up glucose then**

A

will pull glucose in cell and K

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22
Q

in and outside cell elements

A

outside cell more Na inside more K, Hydrogen in cell and when K leaves starts moving in Hydrogen moves out

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23
Q

when at risk for hyperkalemia then at risk

A

for metabolic acidases; ph goes down but hydrogen ion concentration will be high

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24
Q

so to correct acidassis

A

give sodium bicarbonate

25
Osmotic Diuretic examples
Mannitol (Osmitrol)
26
Mannitol (Osmitrol)
Most of this drug remains within the nephron creating an osmotic force keeping water in the nephron tubules until they “dump” fluid out through the collecting duct into the urine
27
Mannitol (Osmitrol) is used to prevent
renal failure, lowers intracranial pressure/cerebral edema in brain trauma patients (swelling on the brain/fluid on the brain)
28
with Mannitol (Osmitrol) watch for onset
of congestive heart failure. Mannitol can exit capillaries and move into tissues drawing water with it. Fluid builds in heart and lung tissue. (can have fluid shifts and put pt on heart failure)
29
left ventricle is important in heart failure bc
it pumps blood to the rest of the body
30
Renin Angiotension Cycle **
kidney secrets renin and causes conversion of A1 - A2, makes blood vessels constrict, makes more blood flow to heart and vasoconstriction
31
aldoesterone
hormone excreted by adrenal cortex, causes NA and H2O retention in effort to increase volume but now heart has more tp pump
32
ACE inhibitors important with **
heart failure, block renin and vasodilation, bp drops, block na and water retention
33
Digoxin (Lanoxin) used to be the
#1 drug but not its not the 1st choice
34
what does Digoxin (Lanoxin) do?
it slows the heart and makes it contract more efficiently (slows it down and makes it do a good job)
35
Digoxin (Lanoxin) has what kind of actions
positive inotropic actions - make left ventricle pump more efficiently but decreases the rate, doesn't treat what is contributing to heart failure
36
what is better than Digoxin (Lanoxin)
ACE inhibitor
37
increasing myocardial contractile force and cardiac output (Digoxin)
alters electrical activity of the heart - increases the firing rate of vagal fibers (parasympathetic system); increases the repsonsiveness of the SA node to ACH (neurotransmitter of para symp), lowers hr; favorably affects neurohormonal systems - suppresses renin release (not as well as ACE inhibitor), decreases SNS flow
38
second line agents -
use with caution in women - may shorten life, not drug of choice for women with heart failure (Digoxin)
39
a lot of heart meds cause**
a lot of heart problems so have to be careful with heart meds
40
adverse effects of Digoxin
dysrhythmias, has narrow therapeutic index
41
dysrhythmias
alters electrical properties of the heart; the higher the does the greater the problem
42
before administering Digoxin must always check
heart rate and rhythm; pulse should be 60 or higher; bc it slows it down
43
Digoxin has a narrow **
therapeutic index; so risk of Digoxin toxicity is high and more likely if potassium levels are low
44
monitor Digoxin levels
optimal range 0.5-0.8 ng/ml in order to reduce risk of dysrhythmias
45
signs of Digoxin toxicity
loss of appetite, n/v, anorexia, diarrhea, fatigue, visual disturbances (blurred vision/ yellow/green / halos at night)
46
interactions
diuretics, ACE inhibitors and Angiotension Receptor Blockers, sympathomimetics, quidine and verapamil
47
diuretics and Digoxin
lead to hypokalemia
48
Angiotension Receptor Blockers with Digoxin
can increase potassium levels, and thereby decrease response to Digoxin
49
sympathomimetics and Digoxin
will intensify inotropic action of Digoxin and increase risk of dysrhythmias
50
quinidine and verapamil will cause
Digoxin levels to rise
51
with Digoxin monitor
HR, if less than 60 hold! do not double up on doses in attempt to compensate for missed dose
52
with Digoxin if irregular rhythm or slowing or speeding of HR
notify MD
53
Digoxin teach pt
s/s of hypokalemia and Digoxin toxicity; bc pt now at risk for them
54
with Digoxin teach pts to limit
salt intake to 2 gm/day and to avoid excessive fluid - weight daily
55
with Digoxin avoid
alcohol, limit to no more than 1 drink per day
56
before 1990s beta blockers were
contraindicated in heart failure bc they do reduce contractility
57
today beta blockers with control of dosage
(start low and gradual increase) they improve long term outcome of heart failure pt, slowing progression of heart failure, protecting heart from s/s of stimulation and dysrhythmias
58
carvedilol (coreg), metoprolol (troprol XL), bisoprolol (Zebeta) are used
to improve cardiac output, increase exercise tolerance