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
Q

Osmotic Diuretic examples

A

Mannitol (Osmitrol)

26
Q

Mannitol (Osmitrol)

A

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
Q

Mannitol (Osmitrol) is used to prevent

A

renal failure, lowers intracranial pressure/cerebral edema in brain trauma patients (swelling on the brain/fluid on the brain)

28
Q

with Mannitol (Osmitrol) watch for onset

A

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
Q

left ventricle is important in heart failure bc

A

it pumps blood to the rest of the body

30
Q

Renin Angiotension Cycle **

A

kidney secrets renin and causes conversion of A1 - A2, makes blood vessels constrict, makes more blood flow to heart and vasoconstriction

31
Q

aldoesterone

A

hormone excreted by adrenal cortex, causes NA and H2O retention in effort to increase volume but now heart has more tp pump

32
Q

ACE inhibitors important with **

A

heart failure, block renin and vasodilation, bp drops, block na and water retention

33
Q

Digoxin (Lanoxin) used to be the

A

1 drug but not its not the 1st choice

34
Q

what does Digoxin (Lanoxin) do?

A

it slows the heart and makes it contract more efficiently (slows it down and makes it do a good job)

35
Q

Digoxin (Lanoxin) has what kind of actions

A

positive inotropic actions - make left ventricle pump more efficiently but decreases the rate, doesn’t treat what is contributing to heart failure

36
Q

what is better than Digoxin (Lanoxin)

A

ACE inhibitor

37
Q

increasing myocardial contractile force and cardiac output (Digoxin)

A

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
Q

second line agents -

A

use with caution in women - may shorten life, not drug of choice for women with heart failure (Digoxin)

39
Q

a lot of heart meds cause**

A

a lot of heart problems so have to be careful with heart meds

40
Q

adverse effects of Digoxin

A

dysrhythmias, has narrow therapeutic index

41
Q

dysrhythmias

A

alters electrical properties of the heart; the higher the does the greater the problem

42
Q

before administering Digoxin must always check

A

heart rate and rhythm; pulse should be 60 or higher; bc it slows it down

43
Q

Digoxin has a narrow **

A

therapeutic index; so risk of Digoxin toxicity is high and more likely if potassium levels are low

44
Q

monitor Digoxin levels

A

optimal range 0.5-0.8 ng/ml in order to reduce risk of dysrhythmias

45
Q

signs of Digoxin toxicity

A

loss of appetite, n/v, anorexia, diarrhea, fatigue, visual disturbances (blurred vision/ yellow/green / halos at night)

46
Q

interactions

A

diuretics, ACE inhibitors and Angiotension Receptor Blockers, sympathomimetics, quidine and verapamil

47
Q

diuretics and Digoxin

A

lead to hypokalemia

48
Q

Angiotension Receptor Blockers with Digoxin

A

can increase potassium levels, and thereby decrease response to Digoxin

49
Q

sympathomimetics and Digoxin

A

will intensify inotropic action of Digoxin and increase risk of dysrhythmias

50
Q

quinidine and verapamil will cause

A

Digoxin levels to rise

51
Q

with Digoxin monitor

A

HR, if less than 60 hold! do not double up on doses in attempt to compensate for missed dose

52
Q

with Digoxin if irregular rhythm or slowing or speeding of HR

53
Q

Digoxin teach pt

A

s/s of hypokalemia and Digoxin toxicity; bc pt now at risk for them

54
Q

with Digoxin teach pts to limit

A

salt intake to 2 gm/day and to avoid excessive fluid - weight daily

55
Q

with Digoxin avoid

A

alcohol, limit to no more than 1 drink per day

56
Q

before 1990s beta blockers were

A

contraindicated in heart failure bc they do reduce contractility

57
Q

today beta blockers with control of dosage

A

(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
Q

carvedilol (coreg), metoprolol (troprol XL), bisoprolol (Zebeta) are used

A

to improve cardiac output, increase exercise tolerance