Mod 4 Flashcards

1
Q

Inotropic

A

An agent that increase the force of muscular contracture.

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2
Q

Dromotropic

A

Affecting the conductivity of nerve or muscle fibers

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3
Q

Chronotropic

A

Influencing the rate of occurrence of an event such as the heart beat.

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4
Q

Cardiac output

A

the amount of blood pumped from the heart in 1 minute. (S/V x H/R= CO)

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5
Q

Stroke volume

A

the amount of blood ejected by the left ventricle (oxygenated blood) with each contraction.

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6
Q

Preload

A

is volume of unoxygenated blood coming into the heart (rt atrium). Increased in hypervolemia and regurgitation of valves

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7
Q

Afterload

A

is the resistance in the arterial system against which the left ventricle must contract to get oxygenated blood out the body. It is increased in hypertension and vasoconstriction.

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8
Q

BNP Lab-b-type natriuretic peptide

A

elevated BNP levels are noted in heart failure. It is used to diagnose heart failure and grade the severity of heart failure

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9
Q

Cardiac Glycosides originate for what plant?

A

foxglove plant

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10
Q

How are Cardiac Glycosides given?

A

because of their long half life it take them days to reach therapeutic blood levels. So a loading or digitalizing dose is given, followed by maintenance doses.

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11
Q

How do Cardiac Glycosides work?

A

They make increased intracellular calcium available to the myocardium, thus an enhanced force of contraction. They stimulate the parasympathetic nervous system, increasing vagal tone and slowing the heart rate

  • Positive Inotropic- increase the force of the cardiac contraction
  • Negative dromotropic- slow or delays conduction of the heart.
  • Negative chronotropic- deceleration of the rate of the heartbeat
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12
Q

If Cardiac Glycosides are re administered they are eliminated after how many half lives?

A

5 half lives

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13
Q

what are Cardiac Glycosides used to TX?

A

CHF, atrial fibrillation / flutter and paroxysmal atrial tachycardia. (PAT)

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14
Q

Digoxin ( Lanoxin, Lanoxicaps)

A
  • commonly used; PO or IV
  • not used IM - severe pain at site with increased CPK – complicating interpretation of enzyme levels. –Therapeutic serum concentration 0.5-2ng/ml.
  • half life is 1.6 days, can’t wait 8 days to reach a steady state for life threatening arrthymias
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15
Q

what is the antidote for digoxin?

A

digibind- but because of high cost it is used only in life threatening situations. Hold dig, hydrate to flush out of body.

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16
Q

Digitoxin (Crystodigin)

A

used rarely because of long half life with prolongs duration of adverse effects; PO, therapeutic range is 14-26 ng/ml

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17
Q

what are the adverse effects of Cardiac Glycosides?

A
  • they have a narrow therapeutic range and may produce digitalis toxicity.
  • These conditions may predispose a client; hypokalemia
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18
Q

what are early S/S of digitalis toxicity?

A

visual changes (blue green vision), difficulty reading, GI complaints –N/V, anorexia, diarrhea, bradycardia, headache, malaise, confusion

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19
Q

what drug has a synergistic effect with digoxin?

A

Quinidine: will cause increased glycoside serum level

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20
Q

what are Bipyridine used to TX?

A

It is used for short term management of CHF in clients who haven’t responded well to digitalis, positive inotropic effects

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21
Q

Primacor

A

IV only, pos inotropic and vasodilator, decreases preload and afterload, increases myocardial contractility, increases CO and diastolic function, short term tx for CHF, ordered mcq/kg of body wt

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22
Q

nesiritide (Natrecor)

A
  • formulation of BNP ( b-type natriuretic peptide)
  • Elevated BNP levels are noted in HF
  • Effects are to reduce preload and afterload which are beneficial in HF
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23
Q

what must the nurse do before giving a cardiac glycoside?

A

Take apical pulse before administering each cardiac glycoside dose: do not administer if pulse is less than 60.(not radial pulse).

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24
Q

when giving digoxin you will never give it how?

A

IM

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25
Q

What will the nurse need to monitor while giving a cardiac glycoside?

A
  • -monitor dig levels- draw blood at least 8 hours after last oral dose and preferably immediately before administering daily maintenance dose.
  • Monitor client’s blood urea nitrogen (BUN), potassium and creatinine.
  • Measure client’s fluid intake and output and weight.
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26
Q

what dose the nurse want to teach a patient taking cardiac glycoside?

A
  • Teach client to take pulse.
  • Ensure that client is familiar with symptoms that should be reported immediately, especially sudden weight gain, edema, shortness of breath, nausea and vomiting, and visual disturbances.
  • Advise client to prevent deterioration of inotropic agents by always storing medication in a tightly fitting, light- and moisture- resistant container.
  • Instruct client to check with physician before taking any nonprescription drug, such as an antacid.
  • Do not give Lanoxin with high fiber meals.
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27
Q

Dopamine

A
  • Part of the sympathomimetics system, is -used to: treat shock, & CHF to increase CO.
  • It is given IV.
  • When administering monitor v/s at least q 15-30 min, especially bp & pulse.
  • Systolic should be greater than 90.
  • There should be an increase in urine output (assess hourly).
  • It improves perfusion to vital organs. It is a vasodilation.
  • -Monitor for extravasation & peripheral pulses 2-4 hour.
  • Titrate off & monitor for decreased b/p.
    • Never use a gravity drip & always used a dedicated line.
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28
Q

what is Antiarrhythmic agents (Antidysrhythmics) used to TX?

A

Used to treat abnormal electrical activity in the heart by limiting cardiac electrical activity to normal conduction pathways and decreasing abnormally rapid heart rates.

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29
Q

what electrolytes play a major role in myocardial contraction or depolarization?

A

NA, CA, and K

30
Q

what does the normal conduction system of the heart consists of?

A

SA node, atrial pathways, the AV node, the bundle of His, the right and left bundle branches and the Purkinje fibers.

31
Q

what four groups are Antiarrhythmic agents divided into?

A
  • Group I - sodium channel blockers
  • Class II - beta adrenergic blockers
  • Class III - prolong cardiac repolarization
  • Class IV - Calcium channel blockers
32
Q

moricizine (Ethmozine) class I

A
  • is a class I sodium channel blocker used to manage life threatening ventricular arrhythmias, such as sustained ventricular tachycardia.
  • adverse reactions- the appearance of a proarrhythmia that occurs when another arrhythmia is present
33
Q

what do class 1A NA Channel Blockers do?

A
  • treat electrical activity abnormalities by blocking NA channels and slowing electrical conduction.
34
Q

why are class 1A NA Channel Blockers prescribed?

A

to treat various atrial and ventricular arrhythmias. The drugs ( esp quinidine) are synergistic with digoxin.

35
Q

Disopyramide ( Norpace) class 1A

A

) suppresses frequency of ectopic ventricular beats (even ventricular tachycardia); only po

36
Q

Procainamide ( Procan SR, Pronestyl) Class 1A

A

suppresses frequency and duration of atrial and ventricular tachycardia, used to convert atrial fibrillation; po, IV.

37
Q

Prototype: quinidine (Quinidex, Quinaglute) class 1A

A

after converting atrial fib to a regular rhythm, prevents recurrence, po

38
Q

what are the adverse effects of class1A NA Channel Blockers?

A

Anticholingeric effects (3 D effects) and GI changes (diarrhea, anorexia, GI distress)

39
Q

what is cinchonism?

A

quinidine overdose

40
Q

what are the S/S of cinchonism?

A
  • Tinnitus
  • headache
  • vertigo
  • fever
  • visual disturbances
  • syncope.
41
Q

what dose Class 1B lidocaine do?

A

used to treat ventricular arrhythmias, depress depolarization in myocardial cells.

42
Q

prototype: Lidocain (Xylocaine) class 1B

A

ventricular arrhythmias; usually IV only; Mg/kg. Treats premature ventricular contractions. (PVC)
( can not be given po due to first pass)

43
Q

What dose SAMS stand for?

A

Slurred speech
Altered CNS
Muscle Twitching
Seizures

Lidocaine Toxicity

44
Q

how do you correct lidocaine toxicity?

A

Lowering dose or stopping drug reverses these reactions.

45
Q

What do class 1C NA Channel Blockers do?

A

blocks sodium channels, depressing automaticity and slowing spontaneous depolarization

46
Q

Propafenone ( Rythmol)

A

ventricular tachycardia

47
Q

What are class 1C NA Channel Blockers used to TX?

A

used to treat life - threatening ventricular arrhythmias

48
Q

What are the adverse effects of class 1C NA Channel Blockers?

A

Proarrhythmias - limit their use.

49
Q

what do Class II Beta Blockers do?

A

block beta at the receptors and decrease sympathetic activity at SA and AV nodes. Negative inotropic effect decreasing myocardial 02 demand and may decrease myocardial ischemia

50
Q

acebutolol ( Sectral)

A

po

51
Q

What are the adverse effects of beta Blockers?

A
  • bradycardia, ( will block the tachycardia associated with hypoglycemia) -hypotension
  • exacerbate CHF
  • bronchoconstriction
  • bronchospasm
52
Q

what do class III potassium blockers do?

A

prolong action potential of myocardial cells (repolarization), delaying depolarization, thus decreasing ventricular ectopic beats.

53
Q

amiodarone ( Cordarone)

A

requires a loading dose; po or IV,

Used for V-FIB, will see used in CCU

54
Q

adenosine (Adenocard)

A

injectable ( IV) agent, short acting used to convert PSVT (paroxysmal supraventricular tachycardia). ( asystole will occur first then converts to NSR)
remember: to have the crash cart they will flatline

55
Q

what are the adverse affects of class III potassium blockers?

A
  • tremor
  • ataxia
  • N/V (watch for aspiration)
56
Q

what do Class IV Calcium channel blockers do?

A

decreasing force of myocardial contraction by blocking flow of calcium ions through cell membranes

57
Q

what are Class IV Calcium channel blockers used to TX?

A

tx supraventricular arrhythmias with rapid ventricular response (RVR)

58
Q

what is rapid ventricular response (RVR)?

A

it is when A-fib causes the ventricles to beat to fast to keep up with the atria

59
Q

verapamil ( Calan, Isoptin)

A

used when vagal stimulation unsuccessful in treating paroxysmal supraventricular tachycardia (PSVT); IV, po.

60
Q

what are the adverse effects of Class IV Calcium channel blockers?

A

-dizziness
-headache
-hypotension
- bradycardia
common side effecets: ankle edema, flushing, constipation

61
Q

should you administer Quinidine with food?

A

no, May affect absorption

62
Q

When adm any drug IV what should you monitor?

A

V/S closely and monitor EKG pattern for new arrhythmias. Have emergency equipment and oxygen available

63
Q

what are signs of congestive heart failure?

A
  • hypotension
  • peripheral edema
  • irregular heartbeat
  • shortness of breath
  • crackles
  • jugular vein distention
64
Q

why should you monitor electrolyte levels Esp K?

A

hypokalemia exacerbates arrhythmias

65
Q

what should you teach a patient about taking Antiarrhythmic agents?

A
  • Have clients weigh themselves daily and report a gain or loss of more than 2 – 3 lb per day or 5 lbs in one week.
  • Teach clients the signs of hypokalemia and congestive heart failure
  • Teach clients how to take a pulse, esp when taking beta blockers. HR over 50
  • Teach diabetic clients that beta blockers will block tachycardia associated with hypoglycemia.
66
Q

when does Angina occur?

A

when myocardial 02 demand exceeds 02 supply, areas become ischemic causing chest pain.

67
Q

what are S/S of Angina?

A
  • crushing sensation or feeling of pressure behind sternum

- may radiate to neck, jaw shoulders, down arms. -May confuse with indigestion, heartburn, or chest muscle strain.

68
Q

Classic angina

A

stable or effort, occurs with exercise or stress,relieved by rest

69
Q

Unstable angina

A

more severe, prior to MI – myocardial ischemia, unrelated to activity

70
Q

Variant angina

A

pain occurs while at rest and resembles unstable angina, spasms of coronary arteries, usually occurs with coronary stenosis.

71
Q

what are the classes of Antianginal agents?

A
  • Nitrates
  • Beta blockers
  • Calcium channel blockers