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AE1 > PHARM WEEK 4 CARDIO AGENTS II > Flashcards

PHARM WEEK 4 CARDIO AGENTS II Flashcards

1
Q

The CNS which consists of the __ and __ __ are protected by the __, __, and __

A

brain & spinal cord

skull, spine, meninges

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2
Q

The Peripheral Nervous System (connects CNS to __ and __) are comprised of the __ __ system and __ __ system

A

Limbs and organs

Autonomic Nervous system

Somatic Nervous system

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3
Q

The Autonomic Nervous System is composed of:
1.
2.

A
  1. sympathetic nervous system (fight/flight)

2. parasympathetic nervous system (rest/digest)

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4
Q

the autonomic nervous system is also called the

A

visceral nervous system

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5
Q

Somatic nervous system =

A

voluntary control of body movements via skeletal musculature and with sensory reception of external stimuli, cranial, and spinal nerves

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6
Q

Sympathetic Nervous System (Adrenergic system) - prepares the body to cope with __ __

A

stress situations

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7
Q

SNS secretes :

A

epinephrine and norepinephrine

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8
Q

Epinephrine/Norepinephrine in the SNS has these effects on the body : (8)

A
  1. Increases HR
  2. Dilates the bronchioles
  3. Dilates the pupils
  4. Vasoconstricts blood vessels
  5. Vasodilates the skeletal muscles
  6. Slows peristalsis
  7. Relaxes uterus and bladder
  8. Converts glycogen to glucose by the liver
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9
Q

The parasympathetic nervous system secretes

A

acetylcholine

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10
Q

Acetylcholine from the PNS has these effects on the body: (7)

A
  1. Constricts pupils
  2. Contracts smooth muscle of the GI tract
  3. Constricts bronchioles
  4. Slows the heart rate
  5. Increases secretions/motility of the digestive tract
  6. contractions of bladder
  7. glycogen synthesis
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11
Q

What are the three types of angina pectoris?

A
  1. classic (or stable)
  2. unstable (pre-infarction)
  3. variant (Prinzmetal, vasospastic)
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12
Q

Classic (or stable) angina pectoris

A

reproducible symptom pattern; no change in pattern for 2 months or more

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13
Q

Unstable (pre-infarction) angina pectoris

A

occurs frequently over course of a day with increased severity due to coronary artery narrowing or partial occlusion

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14
Q

Variant angina pectoris

A
  • occurs with rest, caused by vasospasm, rare

- some medications can stimulate vasospasms

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15
Q

What are the three types of antianginal drugs?

A
  1. nitrates
  2. beta-blockers
  3. calcium channel blockers
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16
Q

these antianginal drugs increase myocardial blood flow by: (2)

A
  1. increasing O2 supply (increasing oxygenated blood to the heart) OR
  2. decreasing O2 demand (decreasing workload)
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17
Q

Nitrates (6)

A
  1. Dilate peripheral blood vessels
  2. Decrease systemic vascular resistance (after load)
  3. decrease venous return to heart
  4. cause coronary artery dilation -> increase oxygen supply to the heart
  5. decrease left ventricular end diastolic pressure (pre-load)
  6. decreases preload -> decreases workload of heart and demand of oxygen from the heart
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18
Q

Beta-blockers: blockade of beta adrenergic receptors which leads to

A
  1. decrease in HR
  2. decrease in rhythm disturbance
  3. decreased incidence of angina
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19
Q

Beta-blockers can increase __ __, __ __ - this can be problematic for the asthma patient

A

airway resistance

bronchial constriction

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20
Q

Most common beta-blockers are:

A

metoprolol, atenolol

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21
Q

Blocking beta 1 receptors does what things?

A
  1. decreases HR

2. rhythm disturbances (prolongs action potential)

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22
Q

Selective beta blockers block with receptors?

A

beta 1 adrenergic receptors

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23
Q

Beta 1 =

A

heart

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24
Q

Beta 2 =

A

lungs (bronchial receptors)

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25
Q

Calcium activates __ __, increases the __ of the heart, and increases __ __

A

myocardial contraction
workload
oxygen demand

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26
Q

Calcium channel blockers inhibits __ from moving __ the heart and vessels. The smooth muscle contraction is reduced which causes__ __ which __ venous return to the heart (preload) and __ oxygen demand

A

Ca+

into

peripheral vasodilation
decreases
decreases

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27
Q

Calcium channel blockers decrease __ __ __

A

coronary artery spasm

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28
Q

Calcium channel blockers relax __ __ decreasing cardiac oxygen demand

A

peripheral arterioles

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29
Q

Common calcium channel blocker:

A

Amlodipine (Norvasc)

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30
Q

What are the 8 types of antihypertensive meds?

A
  1. Diuretics
  2. Beta (adrenergic) blockers
  3. centrally acting Alpha 2 Agonists
  4. Alpha (adrenergic) blockers
  5. Calcium channel blockers
  6. Angiotensin Converting Enzyme (ACE) inhibitors
  7. Angiotensin II Receptor Blockers (ARBs)
  8. Direct Renin Inhibitor
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31
Q

Diuretics promote __ and __ depletion which decreases __ __ __

A

Na+ ; water ;

extracellular fluid volume

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32
Q

Diuretics are effective as the __ __ __ for __ HTN

A

1st line treatment

mild

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33
Q

Loop Diuretics: give an example

A

Furosemide

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34
Q

Loop Diuretics: works __ and __

A

fast; effective

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35
Q

Loop Diuretic side effects:

A
  1. nausea
  2. diarrhea
  3. electrolyte imbalances (hypokalemia)
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36
Q

Loop diuretics are used in emergencies for __ and __ __

A

CHF, pulmonary edema

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37
Q

Thiazides: give an example

A

Hydrochlorothiazide (HCTZ)

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38
Q

Thiazides are associated with __ __

A

electrolyte imbalances

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39
Q

Thiazides compared to loop diuretics: (3)

A
  1. not as effective
  2. do not work as fast
  3. does not promote as much Na+ and water depletion
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40
Q

Thiazides inhibit active exchange of ___ in the cortical diluting segment of the __ __ __ __

A

Cl-Na

ascending loop of Henle

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41
Q

When thinking about Thiazides, only __ Na is going in urine b/c __ of Na has already been __ prior to the cortical diluting segment of the ascending loop of Henle

A

10%

90%
reabsorbed

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42
Q

K-sparing diuretics inhibit the reabsorption of __ in the __ __ and __ __

A

Na+

distal convoluted; collecting tubule

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43
Q

Loop diuretics inhibit exchange of _____ in the __ __ of the __ __ __ __

A

Cl-Na-K

thick segment
ascending loop of Henle

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44
Q

The category “Diuretics” does not include __ __

A

“secondary” diuretics - any drug whose primary target is not to diurese

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45
Q

The diuretics are the primary line of therapy for the majority of patients with __ __ and __ __. They decrease __ and __ which result from fluid retention

A

heart failure

pulmonary congestion

dyspnea, edema

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46
Q

Diuretic drugs are divided into what 3 categories?

A
  1. Thiazides
  2. Loop Diuretics
  3. Potassium-sparing
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47
Q

Where are aldosterone receptors found? (3)

A
  1. myocardium
  2. arterial walls
  3. kidneys
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48
Q

Aldosterone is a hormone that

A

promotes sodium/water retention and potassium/magnesium excretion

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49
Q

Aldosterone receptor antagonists block the action of aldosterone and inhibit the __-__ __ . Here, __ is retained and __ is excreted.

A

sodium-potassium pump

potassium ; sodium

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50
Q

Give an example of an aldosterone receptor antagonist:

A

spironolactone

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51
Q

Aldosterone increases the elimination of potassium and magnesium, creating an __ __ which may be responsible in part for __ __.

A

electrolyte imbalance

cardiac arrhythmias

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52
Q

At the tissue level, aldosterone stimulates the production of __, therefore being responsible for the __ that is found in hypertrophied myocardium and in the arterial walls of patients with heart failure

A

collagen

fibrosis

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53
Q

What three types of effects do aldosterone inhibitors exert?

A
  1. diuretic effect
  2. anti arrhythmic effect - mediated by the correction of hypokalemia and hypomagnesemia
  3. antifibrotic effect - can contribute to a decrease in the progression of structural changes in patients with HF
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54
Q

Beta- Adrenergic Blockers are also called what things?

A
  1. Sympatholytics
  2. Sympathetic depressants
  3. Beta (1,2) blockers
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55
Q

What do selective Beta1 blockers do? (4)

A
  1. decreases cardiac output
  2. decreases systemic vascular resistance
  3. lowers BP
  4. decreases HR, contractility and renin release
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56
Q

What is the prototype drug for beta blockers?

A

metoprolol (Lopressor)

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57
Q

What are adverse effects of beta blockers? (6)

A
  1. Hypotension
  2. Fluid retention - can worsen heart failure
  3. Fatigue
  4. Bradycardia - to the point of heart block
  5. In asthmatics (can worsen asthma)
  6. In Diabetics (masks hypoglycemic effects) - increased HR, beta blockers, decrease HR
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58
Q

Centrally acting alpha2 agonists: (4)

A
  1. These agonists ↓ sympathetic activity – causes a decrease in heart rate and blood pressure
  2. ↓ CO, serum epinephrine, norepinephrine, & renin release (causes vasodilation and decreased vascular resistance)
  3. Reduces peripheral vascular resistance and increases vasodilation
  4. Are never given with Beta Blockers because both could cause accentuation of bradycardia
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59
Q

Side effects/ Adverse reactions for Centrally Acting Alpha2 Agonists:

A
  1. drowsiness
  2. dry mouth
  3. dizziness
  4. bradycardia
  5. rebound hypertensive crisis if D/C abruptly
    (if need to stop immediately, prescribe another antihypertensive)
  6. Peripheral edema d/t Na+ and H2O retention
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60
Q

Give two examples of centrally acting alpha2 agonists:

A
  1. aldomet (older drug, given IV)

2. clonidine (PO and via patch, more common)

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61
Q

Alpha-adrenergic blockers causes

A

vasodilation and decreases BP

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62
Q

Alpha-adrenergic blockers do NOT affect __ __ or __ __

A

glucose metabolism or

respiratory function

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63
Q

Selective alpha1 adrenergic blockers are used to __ __ (and in BPH to relax the __ __ )

A

decrease BP

urethral constriction

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64
Q

Name the alpha-adrenergic blocker prototype:

A

Prazosin HCl (Minipress)

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65
Q

Alpha-adrenergic blockers: side effects/adverse reactions

A
  1. orthostatic hypotension
  2. nausea
  3. drowsiness
  4. edema
  5. weight gain
  6. impotence
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66
Q

What drug interaction occurs between alpha-adrenergic blockers and nitrates:

A

decreases BP

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67
Q

Alpha-adrenergic blockers are often given at __ to pas s the initial orthostatic hypotension

A

night

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68
Q

Angiotensin-converting enzymes (ACE) inhibitors inhibit the formation of __ __ which is a __ __

A

angiotensin II ; potent vasoconstrictor

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69
Q

ACE inhibitors block the release of __, which then causes __ excretion and __ retention

A

aldosterone

Na+
K+

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70
Q

ACE inhibitors cause (a major change/little change) in CO. Which one?

A

little change

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71
Q

ACE inhibitors lower the __ __ __

A

peripheral vascular resistance

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72
Q

What 3 other enzymes can be used to convert angiotensin I to angiotensin II BESIDES angiotensin-converting enzyme (ACE)?

A
  1. chymostatin-sensitive angiotensin-generating enzyme (CAGE)
  2. cathepsin G
  3. chymase
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73
Q

Is this true or false? Several nonrenin enzymes have been found that directly cleave angiotensin II from angiotensinogen without forming angiotensin I.

A

TRUE

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74
Q

The effects of angiotensin II are mediated through the __ __ divided into the __ and __ subclasses. The majority of deleterious effects of angiotensin II are provoked through the __ receptors. Angiotensin receptor blockers exert their effects through specific blockade of the __ receptors.

A

AT receptors

AT1 and AT2

AT1

AT1

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75
Q

What else do agents that block the RAAS accomplish besides lowering bp? (2)

A
  1. they slow the progression of renal disease in patients with DM
  2. beneficial in hypertensive patients with heart failure, recent myocardial infarction, and chronic kidney disease
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76
Q

common side effect of ACE inhibitors:

A
  1. nagging cough - angiotensin converting enzyme blocks bradykinin (more active bradykinin leads to nagging cough)
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77
Q

__ don’t have the nagging cough, but the effects of anti-hypetensive aren’t as effective as ACE inhibitors

A

ARBs

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78
Q

Do african-americans respond well to ACE inhibitors alone?

A

NO

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79
Q

Do elderly respond well to ACE inhibitors alone?

A

NO

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80
Q

ACE inhibitors are primarily used to treat

A

HTN

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81
Q

Some ACE inhibitors also treat

A

heart failure

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82
Q

ACE inhibitors should not be used in __

A

pregnancy

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83
Q

Can ACE inhibitors be taken with food?

A

yes, most can

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84
Q

what is the prototype drug for ACE inhibitors?

A

Captopril (Capoten)

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85
Q

__ is the most abundant intracellular cation

Under normal conditions, __ can adjust __ excretion

A

Potassium

kidneys; potassium

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86
Q

Hypokalemia - etiology (3)

A
  1. renal or nonrenal wasting
  2. decreased intake
  3. redistribution (e.g. insulin)
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87
Q

Hypokalemia increases the risk for

A

cardiac arrhythmias

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88
Q

Hypokalemia treatment

A

replacement either oral or IV (many instances given IV - however can be irritating, causing IV site to extravasate)

telemetry during severe hypokalemia

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89
Q

Hyperkalemia =

A

K+ > 5.0 mmol/ L

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90
Q

Hyperkalemia etiology (3)

A
  1. redistribution
  2. reduced K+ excretion
  3. Increased K+ intake
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91
Q

Pseudohyperkalemia

A

occurs with RBC hemolysis, leukocytosis (>70,000/mm^3) or thrombocytosis (>500,000mm^3)

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92
Q

Hyperkalemia Emergency

A

renal failure in setting of tumor lysis syndrome, rhabdomyolysis, tissue necrosis, large hematomas

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93
Q

What would you do if someone was in pseudohyperkalemia?

A 
You would assume it was an emergency. 
You would get: 
1. an EKG 
2. look for peak T waves 
If those are there, you will treat assuming patient has hyperkalemia and redraw lab specimen
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94
Q

Hyperkalemia signs and symptoms (2)

A
  1. cardiac arrhythmias

2. lower extremity weakness

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95
Q

Hyperkalemia treatment

A
  1. Kayexalate - slow way to treat; drink, or thru enema
  2. Insulin - drives the K+ into the cells so we lower serum K+
  3. Calcium - stabilize heart to prevent heart dysrhythmias
  4. Renal dialysis
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96
Q

What is the 2nd most prevalent intracellular cation?

A

magnesium

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97
Q

Magnesium acts as a __ __ __

A

calcium channel antagonist

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98
Q

What are magnesium’s key roles? (2)

A
  1. muscle contraction

2. insulin release

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99
Q

What organ maintains magnesium balance?

A

kidneys

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100
Q

hypomagnesemia is present in __-_% of ICU patients

A

11-65%

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101
Q

Hypomagnesemia is due to __ or __ __

A

renal (increased tubular flow) or GI (diarrhea) losses

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102
Q

Hypomagnesemia can produce __ ___ –> __ __ __

A

cardiac arrhythmias

Torsade de Pointes

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103
Q

__ __ can occur when magnesium level

A

Neuromuscular irritability

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104
Q

_____ occurs in ~ __% of those with hypomagnesemia

A

hypokalemia; 40%

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105
Q

Treatment for hypomagnesemia (2)

A
  1. IV Magnesium Sulfate
    - caution in patients with renal insufficiency (decreased doses)
  2. Oral supplementation for long term replacement
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106
Q

Hypermagnesemia is __ and is usually due to __ __

A

rare

renal insufficiency

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107
Q

Typical setting of hypermagnesemia is treatment of __-__ __ or ____/____

A

pre-term labor

pre-eclampsia/eclampsia

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108
Q

What are symptoms of hypermagnesemia (5)

A
  1. loss of deep tendon reflex
  2. flaccid paralysis
  3. apnea
  4. bradycardia
  5. hypotension
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109
Q

Hypermagnesemia

treatment

A
  1. prevention
    -do not give magnesium-containing antacids or cathartics
    - stop infusion or
    administering oral medications
  2. Dialysis
    - peritoneal or
    hemodialysis
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110
Q

What are the two types of cardiovascular agents?

A
  1. Antidysrhythmics

2. Drugs for circulatory disorders

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111
Q

Cardiac action potential has __ phases

A

5

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112
Q

Cardiac Action Potential:

The movement of __ across the membrane allows for muscles to contract and relax

A

electrolytes

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113
Q

Phase 0 of Cardiac Action Potential:

A

Na enters cell -> this causes rapid depolarization -> sub sequential contraction

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114
Q

Phase 1 of Cardiac Action Potential:

A

Initial repolarization; Na stops entering the cell

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115
Q

Phase 2 of Cardiac Action Potential :

A

Plateaus, evens out
Ca++ enters, makes the contraction a little bit longer (calcium channel blockers block calcium making contraction shorter)

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116
Q

Phase 3 of Cardiac Action Potential:

A

Rapid repolarization, beginning of relaxation -> K+ exits the cell into the extracellular

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117
Q

Phase 4 of Cardiac Action Potential:

A

Resting membrane potential between heartbeats

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118
Q

what are the two types of dysrhythmia?

A
  1. atrial dysrhythmia

2. ventricular dysrhythmia

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119
Q

Atrial dysrhythmia:

A
  • prevents proper filling of ventricles
  • decrease CO by 1/3
  • quivering of the atria doesn’t allow the heart to fully contract
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120
Q

Ventricular dysrhythmia:

A
  • life threatening
  • ineffective ventricular filling results in decreased or absent CO
  • entire heart is quivering!
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121
Q

Examples of ventricular dysrhythmias:

A
  1. Premature Ventricular Complexes (PVC)
  2. Ventricular tachycardia
  3. Ventricular Fibrillation
    • follow BCLS and ACLS
      algorithm
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122
Q

Dysrhythmias are also called

A

arrhythmias

123
Q

Must give __ __ prior to and after surgery even if the patient is NPO (give with a sip of water)

__ causes side effects postoperatively

A

beta blockers

tachycardia

124
Q

Causes of Dysrhythmia:

A 
REMEMBER "TECH" 
T- 
Tension PTX 
Tamponade (cardiac) 
Toxins
Thrombosis (pulmonary or coronary) 
Thyroid disease

E -
Excess catecholamines
Electrolyte imbalances

C-
Coronary artery disease
Cardiac Surgery

H- 
Heart attack 
Hypoxia 
Hypercapnia
Hypovolemia 
Hydrogen ions (acidosis) 
Hypo-Hyperkalemia 
Hypothermia
125
Q

Dysrhythmias are due to an influx of electrolytes affecting __ __

A

action potentials

126
Q

Antidysrhythmics: Pharmacodynamics

A
  1. Block adrenergic stimulation of heart
  2. Depress myocardial excitability & contractility
  3. Decrease conduction velocity in cardiac tissue
  4. Increase myocardial recovery time (repolarization)
  5. Suppress automaticity (spontaneous depolarization to initiate beats)

Note: Most Antidysrhythmics are also proarrhytmic

127
Q

antidysrhythmics prolong the __ __

A

refractory period

128
Q

Antidysrhythmics: Class I

A

Fast (Sodium) Channel Blockers

  • IA: procainamide (Pronestyl, Procan SR)
  • IB: lidocaine (Xylocaine)
  • IC: Propafenone (Rythmol), Flecainide (Tambocor)
129
Q

Antidysrhythmics: Class II

A

Beta-Blockers:
Acebutolol (Sectral)
Esmolol (Brevibloc)
Sotalol (Betapace)

130
Q

Antidysrhythmics: Class III

A

Drugs that Prolong Repolarization:

-Amiodarone (Cordarone)

131
Q

Antidysrhythmics: Class IV

A

Slow (Calcium) Channel Blockers -

Verapamil (Calan, Isoptin) and Diltiazem (Cardizem)

132
Q

Class 1A antidysrhythmic mechanism of action :

A

depress the phase 0 of the action potential leading to slow conduction, prolonged repolarization. Decreases automaticity and likelihood of ectopic foci, ↓ conduction velocity in cardiac tissues and increases refractory period. Slow conduction and prolonged repolarization

133
Q

Class 1A uses:

A

Wide variety of ventricular & atrial dysrhythmias

Paroxysmal atrial tachycardia, supraventricular dysrhythmia

134
Q

Examples of Class IA antidysrhythmics:

A
  1. Procainamide (Pronestyl)
  2. quinidine (Quinoglute)
  3. disopyramide (Norpace)
    (these are drugs given for rapid heart rates)
135
Q

Class 1A Procainamide absorption:

A
  • oral extended release - 90 to 120 minutes

- IM - 15-60 minutes

136
Q

Class 1A Procainamide metabolism and excretion:

A
  • converted by liver to N-acetylprocainamide (NAPA), an active anti arrhythmic compound
    • may vary among population
  • 30-60% excreted unchanged by kidney
137
Q

Class 1A Procainamide: Half life

A

Half-life - 2.5 to 4.7 hours (NAPA - 6 to 8 hours)

*prolonged in renal impairment

138
Q

Procainamide: side effects

A
  1. Dose-related nausea
  2. anorexia
  3. vomiting
  4. dizziness
  5. drowsiness
  6. heart blocks
  7. hypotension
  8. CHF
    Note: avoid citrus juices and fruits when taking quinidine
139
Q

Procainamide: Side Effects during long-term therapy

A
  1. Lupus-like syndrome with rash and small joint pain
  2. Pericarditis with tamponade
  3. Notify prescribing provider immediately as may need to discontinue
140
Q

Procainamide: Adverse Reactions

A
  1. Life threatening: caused by high concentrations (>19 micrograms/ml)
  2. hypotension
  3. marked slowing of conduction
  4. Torsade de pointes
141
Q

What is Torsade de points?

A

Uncommon form of ventricular tachycardia (VT) characterized by changes in QRS complexes

It is associated with a prolonged QT interval. May evolve into V fib (cardiac arrest)

142
Q

What else can procainamide be used for?

A

It can act as an anti-hypertensive.

It vasodilates the blood vessels (blocks phase 0)

143
Q

PR interval

A

0.12-0.20 sec

144
Q

QRS duration

A

0.08-0.10 sec

145
Q

QT interval

A

0.4-0.43 sec

146
Q

QT interval greater than __ seconds leads to higher risk of v-tach and v-fib

A

0.43

147
Q

Drugs that can prolong QT interval (18)

A
  1. Amiodarone
  2. Erythromycin
  3. Ciprofloxacin
  4. Clarithromycin
  5. Cisapride
  6. Droperidol
  7. Famotidine (Pepcid)
  8. Fluconazole
  9. Haloperidol
  10. Lithium
  11. Methadone
  12. Octreotide
  13. Pentamidine
  14. Sotalol
  15. Tacrolimus
  16. Thioridazine
  17. Zofran (for vomiting)
  18. Fluoxetine (Prozac)
148
Q

Procainamide: toxicity
What do you monitor?
What is the therapeutic level of procainamide & napa levels?

A
  1. Monitor serum procainamide & NAPA levels
  2. Therapeutic level:
    Procainamide: 4-10 mcg/mL

NAPA: 15-25 mcg/mL

Combined levels: 10 – 30 mcg/mL

Toxicity may occur at procainamide
levels > 10 mcg/ml

149
Q

which three signs signify a wide QRS and requires procainamide or amiodarone?

A

Vtach
Vfib
Torsade de pointes

150
Q

Class II Antiarrhythmics prolongs which phase of the cardiac action potential?

A

Prolongs phase 4

151
Q

Class II Antiarrhythmics mechanism of action:

A

blocks beta-adrenergic receptors, causing depression of phase 4 of the action potential. Slows the recovery of the cells, leading to slowing of conduction and automaticity. Can also reduce renin release (↓ BP)

152
Q

Class II Antiarrhythmic uses

A

wide variety of ventricular and atrial dysrhythmias

- paroxysmal supraventricular tachycardia ( PSVT) and PVCs

153
Q

Class II Antiarrhythmic examples

A
  1. Acetabutol (Sectral)
  2. emolol (Brevibloc)

see used in critical care

154
Q

Class II Antidysrhythmics side effects, adverse reactions, and drug-drug interactions

A

1.Same as those of Class I and
III
2.Watch for bronchospasm and dyspnea

155
Q

Class III Antidysrhythmics mechanism of action

A

Unclear mechanism. Blocks potassium and slows the upward movement of potassium during phase 3 of the action potential; prolongs the repolarization and slows the rate and conduction of the heart. Structurally similar to thyroid hormone.

156
Q

Class III Antidysrhythmics uses

A

Ventricular tachycardia/fibrillation, atrial flutter/fibrillation. For treatment and maintenance.

157
Q

Examples of Class III Antidysrhythmics

A
  1. Amiodarone (Cordarone)
  2. Brytelium
  3. Ibutiliade (Corvert)
  4. dofetilide (Tikosyn)
  5. satolol (Betapace)
158
Q

Amiodarone side effects

A
  1. Related to size of dose and cumulative dose
  2. N/V GI distress, dizziness, hypotension, arrhythmia
  3. ↓ HR can proceed to 2nd or 3rd degree heart block (increases PR interval, QRS duration, and QT intervals
159
Q

Amiodarone adverse reactions

A
  1. Hypothyroidism or hyperthyroidism
  2. Corneal microdeposits
  3. Hepatic dysfunction
  4. Pulmonary fibrosis (Destroys the capillaries in your lungs )
    - Rarely seen with low dose 200mg/day
  5. Peripheral neuropathy
  6. Proximal muscle weakness
160
Q

Part of Amiodarone gets deposited in the __ after long term use (after __ year/s)

A

cornea

1

161
Q

What is a rare adverse reaction of Amiodarone?

A

Blue-Gray Hyperpigmentation

they look cyanotic; for darker skinned people, the skin will become darker

162
Q

amiodarone drug interactions

A
  1. Long half-life (weeks to months)
  2. Interacts with multiple drugs such as quinidine or digoxin
    • Increased risk of QT prolongation with fluoroquinolones, macrolides, and azole antifungals
      - Increases blood levels of Class I Antidysrhythmics including procainamide
      - Increases blood level warfarin (Coumadin)

Note: Grapefruit juice inhibits enzymes in GI tract that metabolize amiodarone. Avoid concurrent use ↑ levels & risk of toxicity

163
Q

Nursing considerations/patient education for Amiodarone

A
  1. For IV amiodarone – monitor IV site frequently
  2. Teach patient how to take pulse, monitor vitals
  3. Assess for neurotoxicity, monitor thyroid function, eye exams
  4. Note timing of meds – with or without food
  5. Monitor ECG during IV therapy or initiation of PO therapy
    Heart rate & rhythm, prolonged PR & QT intervals, QRS widening
  6. Assess for signs of pulmonary toxicity (shortness of breath)
    Monitor Chest X-Ray & Pulmonary Function Tests
164
Q

Amiodarone has a risk for causing ___ because it is very acidic

A

infiltration

165
Q

Class IV Antidysrhythmics mechanism of action

A

blocks calcium channel in the heart muscle cells, leading to depression of depolarization and prolongation of phases 1 and 2 of repolarization, slowing conduction through the AV node. Think Ca channel blockers

166
Q

Class IV Antidysrhythmic Uses

A

Ventricular tachycardia/fibrillation, atrial flutter/fibrillation and PSVT. Treatment and maintenance

167
Q

Class IV Antidysrhythmic examples

A
  1. diltiazem (Cardizem)

2. verapamil (Calan) – given P.O. or IV

168
Q

Class IV Antidysrhythmics prolongs __ __ and __. Slows down ___. Relaxes the __ __

A

phase 1 and 2
HR
blood vessels

169
Q

Verapamil causes __ __. If you lower the bp too low, the HR will go up

A

rebound tachycardia

170
Q

Antidysrhythmics: nursing interventions

A
  1. Give medications as scheduled
  2. Monitor vital signs
  3. Monitor ECG, liver & renal function
  4. Monitor drug levels of Procainamide and NAPA (metabolite)
  5. Check signs & symptoms of toxicity
171
Q 
Amiodarone is a Class III Antidysrhythmic because it has one of the following actions: 
A. Prolonged action potential duration
B. Decreased action potential duration
C. Prolonged NAPA excretion
C. Decreased NAPA excretion
A

A. Prolonged action potential duration

172
Q 
A life threatening adverse reaction of the medication  procainamide (Pronestyl, Procan SR) is:
A. Nausea
B. Anorexia
C. Torsades de Pointes
D. Vomiting
A

C. Torsades de Pointes

173
Q

Anticoagulants: (3)

A
  1. antiplatelets
  2. antithrombin
  3. low-molecular weight heparin(LMWH) (Lovenox)
174
Q

Thrombolytics examples

A
  1. r-tPA

2. streptokinase

175
Q

Antihemophilic Agents example

A

coagulation factor VIIa

176
Q

Systemic Hemostatic Agents

A

Aminocaproic acid

177
Q

Topical Hemostatic Agents

A

Absorbable gelatin

178
Q

What can you use to stop nosebleeds?

A

Aminocaproic acid

179
Q

Thrombus Formation

How does a clot form in an artery or vein?

A

Caused by decreased circulation, platelet aggregation on vessel wall, blood coagulation

180
Q

Arterial clot formation

A
  1. platelets initiate process
  2. fibrin formation occurs
  3. RBCs are trapped in fibrin mesh
181
Q

Venous clot formation

A

platelet aggregation with fibrin that attaches to RBCs

venous clots are caused by RBCs by sluggish flow and they eventually become stuck together

182
Q

If you have an MI, what do you give?

A

an ANTIPLATELET like aspirin

183
Q

If you have a DVT, what can you give?

A

Plavix, heparin, compression socks

184
Q

Clotting Cascade: Extrinsic Pathway

A

activated by external trauma that causes blood to escape from vascular system (bleeding)
Quicker than intrinsic pathway

185
Q

Clotting Cascade: Intrinsic Pathway

A

activated by trauma inside vascular system. Activated by platelets, exposed endothelium, chemicals. Slower than extrinsic pathway

186
Q

Clotting Cascade: Common pathway

A

completes clot production

187
Q

Any form of blood escaping vessel activates the extrinsic pathway which will stimulate __ __. __ __ will be activated to __. __ will stimulate tissue factor and will be converted to factor __ (look at slide 63)

A 
factor 7 
factor 7 
7A 
7A 
10A
188
Q

When you are septic, you clot due to the __ __

A

intrinsic pathway

189
Q

Composed of platelets and fibrin. Forms in vessels with high blood flow or in areas with atherosclerosis or plaque rapture. Activates the clotting cascade and platelet aggregation.

What kind of clot is this?

A

arterial thrombi

190
Q

Composed of coagulated RBC and fibrin, few platelets and more fibrin. Forms in areas of low blood flow or stasis like the legs. Often associated with inflammation.

What kind of clot is this?

A

venous thrombi

191
Q

The Joint Commission says:

A
  1. Take extra care with patients who take medicines to thin their blood.
  2. “High Alert” warning for blood thinners
    3.Reported Sentinel Events Related to Anticoagulants (1997-2007)
    Drugs Involved: Heparin 21, Warfarin 6, Enoxaparin 3, Unknown 2
    Outcome: 34 Deaths= 28,lLoss of function= 6
    Cause of Event: Wrong drug, wrong dose, improper monitoring, pump malfunction, given without order and meds not reordered
192
Q

Anticoagulants do not

A

dissolve clots already formed

193
Q

Anticoagulants prevent __ __ from __

A

new clots

forming

194
Q

What activates platelet aggregation in the first place?

A

a ruptured plaque (atherosclerosis)

195
Q

Heparin (unfractionated)

mechanism of action

A

Natural substance in liver & prevents clot formation; Inhibits thrombin (see next slide). Prevents conversion of fibrinogen to fibrin. Variable effect

196
Q

Heparin (unfractionated) uses

A

for rapid anticoagulant effect in:

  1. DVT, Pulmonary Embolus (PE), or evolving stroke, DIC, atrial fib/flutter, MI, valve replacement and other thromboembolic states
  2. SQ prophylaxis - 5000 to 7500 units every 8 -12 hours (weight-based)
  3. IV therapy - acute thrombosis (MI/PE). Initial bolus of 80 units per kg, then 18 units per kg per hour by infusion based on aPTT. An aPTT of 1.5 to 2.0 times the control is desirable (60-80 seconds).
197
Q

How does Heparin work?

A
  1. Heparin binds with Antithrombin III
  2. Antithrombin III inactivates thrombin
  3. Thrombin inhibits the conversion of fibrinogen to decrease fibrin
  4. clot prevented
198
Q

Heparin (unfractionated) side effects

A

Itching, burning, and ecchymosis on the injection site

199
Q

Heparin (unfractionated) adverse effects

A

Heparin -Induced Thrombocytopenia (HIT), bleeding. Highest in patients with any of the following: age >65, recent surgery, or conditions such as peptic ulcer disease, liver disease, neoplasia, and bleeding diathesis

200
Q

Heparin (unfractionated) Interactions

A

Increased effect with aspirin, NSAIDs, thrombolytics, and probenecid

201
Q

Heparin (unfractionated) Antidote:

A

Protamine Sulfate. 1-1.5 mg per 100 USP units of heparin; not to exceed 50 mg. Monitor aPTT 5-15 min after dose then in 2-8 hours.

202
Q

How does a heparin injection produce a bruise?

A

Portion of the drug goes back up into the injection puncture site into the epidermis which causes a bruise

To prevent this, count to 5 before removing the plunger. Inject heparin where there is fat

203
Q

If you give subQ heparin do you need to monitor PTT and aPTT?

A

No, because the heparin half life is only 30 minutes to 1 hours

204
Q

We only monitor aPTT if we give __ __ . The goal is to make the aPTT __-__ seconds. You will do a blood draw every __-__ hours.

A

IV Heparin

60-80 seconds

4-6 hours

205
Q

What is normal platelet levels

A

140,000 to 400,000

206
Q

Heparin-induced Thrombocytopenia (HIT)

A
  1. It is a thrombotic disorder in 5-25% of patients on Heparin. An Allergic reaction
  2. Venous thrombosis is the main feature
  3. Immune-mediated response to Heparin
  4. Platelet factor 4 binds to Heparin, combined with IgG and creates an immune complex.
  5. This immune complex binds to circulating platelets (reducing the level and causing thrombosis).
207
Q

For a patient with HIT, what can you give them ?

A

give them antithrombins

208
Q

Why don’t use normally give blood thinners like heparin to patients who have liver failure?

A

b/c there is less production of certain clotting factors

209
Q

Do not give heparin if the platelet is _____

A
210
Q

For Heparin IV drip, ensure that a __ IV line and an __ __ is used.
Avoid ___ __ __ __

A

dedicated
infusion pump
interruption of the infusion

211
Q

For Heparin IV drip, don’t __ anything with heparin

A

piggyback

212
Q

HIT

Results in activation of more platelets and PF4 release =

A

thrombin forms

213
Q

How can you rule out HIT?

A

if the level of platelets is less than 100,000 within 5-14 days of heparin tx

214
Q

what is contraindicated in a person with HIT?

A

platelet transfusion

215
Q

HIT can re-occur each time a patient receives heparin. This should be listed as a/an ___

A

allergy

216
Q

What is the treatment for HIT?

A

Lepirudin inhibits thrombin and it’s thromboembolic effects. Given IV.

217
Q

Low molecular weight heparin is __ which means :

A

fractionated

made of fragments/derivatives of unfractionated heparin

218
Q

Mechanism of action for LMWH

A

Binds with antithrombin and accelerates the rate at which antithrombin inhibits Factor Xa and thrombin

219
Q

LMWH uses

A

similar to heparin

220
Q

example of a LMWH

A

Enoxaparin (Lovenox)

221
Q

antidote for LMWH

A

Protamine Sulfate

222
Q

compared to unfractionated heparin, LMWH: (4)

A
  1. less risk for bleeding
  2. more stable response
  3. does not require frequent aPTT monitoring
  4. 1/2 life 2-4X heparin
  5. thrombocytopenia less likely
223
Q

Indications for LMWH

A

DVT prophylaxis

224
Q

When you are stressed out, you are activating __ __ like __ and __. This makes you’re blood ___.

A

inflammatory mediators
cytokines, interleukins
hypercoagualable

225
Q

Mechanism of action for Warfarin (Coumadin)

A

Inhibits the hepatic synthesis of coagulation factors dependent on Vitamin K: Factors II, VII, IX and X

226
Q

Warfarin (Coumadin) 1/2 life

A

long 1/2 life and very long duration - (2-3 days?)

227
Q

Warfarin (Coumadin) uses

A

mainly to prevent thromboembolic conditions such as embolism caused by atrial fibrillation, which can lead to a stroke (CVA), DVT, PE

228
Q

Which clotting factors need vitamin K?

A

II
VII
IX
X

229
Q

__ synthesizes and manufactures vitamin K

A

Liver

230
Q

Coumadin aka Warfarin stems from the acronym WARF which stands for:

A

Wisconsin Alumni Research Foundation

231
Q

Normal PT is

A

10-12 secodns

232
Q

Normal INR (international Normalized ratio) -

A

0.7-1.7

233
Q

Goals of Coumadin therapy:

A
  1. Atrial fibrillation - (2-3)
  2. Artificial valves - (2.5-3.5)
  3. DVT and PE - (2-3)
234
Q

Goals of Coumadin therapy: start treatment at __ mg per day and titrate the dosage every __ to __ days to achieve goal

A

5 mg

3-7 days

235
Q

Side effects of Coumadin

A

Anorexia, nausea, vomiting, diarrhea, abdominal cramps, rash, and fever

236
Q

Adverse Effects of Coumadin

A

May increase AST (aspartate aminotransferase), ALT (alanine aminotransferase), and bleeding

237
Q

Coumadin Antidote

A

Antidote: Vitamin K (2.5 to 10 mg IM or SQ). Fresh frozen plasma (FFP) is indicated for acute bleeding

238
Q

What drugs if used with Coumadin would increase bleeding?

A 
ASA
H2 Blockers
Erythromycin
Cefoxitin
Disulfiram
Amiodarone
Thyroid drugs
Cotrimoxazole (Bactrim)
239
Q

What drugs if used with Coumadin would decrease anticoagulation?

A 
Vitamin K and E
Rifampin
Phynetoin
Barbiturates
Cholestyramine
240
Q

Antiplatelet: Aspirin was discovered in the ___. Anti platelet properties was known in __.

A

1800s

1960s

241
Q

Aspirin mechanism of action:

A

Inhibits platelet aggregation by interfering with thromboxane A2

242
Q

Aspirin uses:

A

MI (bite and chew), CVA (tx or prophylaxis), CAD prophylaxis. Maybe used within 48 hours of stroke, recommended before and after endarterectomy

243
Q

Aspirin side effects

A

tinnitus, bleeding

244
Q

Aspirin adverse effects

A

nausea, dyspepsia, heartburn, GI bleed, tinnitus, toxicity, headache, anaphylactoid reaction.

245
Q

Aspirin antidote

A

No Antidote. Discontinue 1wk before surgery

246
Q

Aspirin is rapidly absorbed in the GI tract

onset: __-__minutes

A

5-30 minutes

247
Q

Aspirin inhibits platelets within __ minutes (Peak: __ min to __ hours)

A

60 minutes

25 minutes - 2 hours

248
Q

Duration of Aspirin

A

3-6 hours

249
Q

Plavix is a __ which is an _____ drug

A

thienophyridine

anti platelet drug

250
Q

Plavix mechanism of action

A

Prevents platelet aggregation by blocking Adenosine Diphosphate from binding to platelet receptor

251
Q

Examples of Thienophyridines

A
  1. dipyridamole (Persantine)
  2. ticlopidine (Ticlid)
  3. clopidogrel (Plavix)
252
Q

Plavix has similar side effects and adverse reactions with __

A

Aspirin

253
Q

Onset of action for Plavis is __ __ and drug effects last for __ __

A

several days

7 days

254
Q

Patients allergic to Aspirin can take __

A

Plavix

255
Q

__ also allows for platelets to stick together

A

ADP

256
Q

Direct acting thrombin inhibitors are ___ (_) __

A

Parenteral (IV) Anticoagulants

257
Q

Direct Acting Thrombin Inhibitors mechanism of action

A

directly inhibit thrombin from converting fibrinogen to fibrin

258
Q

Direct Acting Thrombin Inhibitors Uses

A

Heparin-induced thrombocytopenia, unstable angina, angioplasty

259
Q

Direct Acting Thrombin Inhibitors examples

A
  1. Argatroban (Acova)
  2. bivalirudin (Angiomax)
  3. lepirudin (Refludan).

SQ: Desirudin (Iprivask).

PO: Pradaxa

260
Q

__ __ is a contraindication for lepirudin

A

Liver failure

261
Q

Dabigatran Etexilate (Pradaxa) category

A

direct thrombin inhibitor

262
Q

Dabigatran Etexilate (Pradaxa) uses

A

non-valvular atrial fibrillation and stroke treatment and prophylaxis, HIT, DVT, and PE

263
Q

Dabigatran Etexilate (Pradaxa) is metabolized in the

A

liver

264
Q

Dabigatran Etexilate (Pradaxa) 1/2 life

A

12 – 17 hours (longer in the elderly) and renal impairment

265
Q

Dabigatran Etexilate (Pradaxa) excreted in the urine. Severe Renal failure =

A

risk for bleeding

266
Q

Dabigatran Etexilate (Pradaxa) dosage

A

150 mg twice daily P.O.

267
Q

Factor XA Inhibitor Oral Anticoagulants examples

A

Rivaroxaban (Xarelto) and Apixaban (Eliquis

268
Q

Factor XA Inhibitor Oral Anticoagulant uses

A

DVT and PE prophylaxis in patients

going for hip/knee surgery, stroke, atrial fibrillation, and non-valvular fibrillation

269
Q

Does Factor XA Inhibitor Oral Anticoagulant require routine coagulation monitoring?

A

no

270
Q

Factor XA Inhibitor Oral Anticoagulant is administered:

A

once daily or twice a day P.O. (10-20 mg depending on indication)

271
Q

General contraindications for anticoagulants:

A
  1. Bleeding disorders
  2. Peptic ulcer
  3. Severe hepatic or renal disease
  4. Hemophilia
  5. CVA
  6. Eye, brain, or spinal surgery
  7. Risk for injury from fall
272
Q

Nursing assessment for Anticoagulants

A

Hx clotting or bleeding
Drug & herb use
Baseline labs: CBC, Coags, LFTs, renal labs
Heparin:
Activated partial thromboplastin time (aPTT)
Warfarin: PT or INR

273
Q

Nursing Diagnoses for Anticoagulants

A

Risk for injury (bleeding)
Knowledge deficit
Evaluation
aPTT, PT/INR are within therapeutic range

274
Q

Nursing Care (8)

A
  1. Use soft toothbrush, electric razor, ID bracelet
  2. Observe the Five “Rs” and Right “REASON”
  3. Assess for allergies and history of Heparin induced thrombocytopenia (HIT)
  4. Assess fro S/S of bleeding, thrombosis and embolism (Pulmonary)
  5. Current medication regimen including OTC (Ginko, Garlic, Ginseng= increase bleeding with Coumadin)
  6. Increase effect=NSAIDS, Tylenol, PCN, Prilosec
  7. Check for baseline INR,PT, aPTT, CBC and Platelet count
  8. Do not give IM injections of any drugs?
275
Q

Thrombolytics mechanism of action

A

Promote fibrinolytic mechanism. Convert plasminogen to plasmin to dissolve clot

276
Q

Thrombolytics uses:

A

A. Myocardial infarction (best within 1 hour)
B. thromboembolic stroke (best within 3 hours)
C. pulmonary embolism
D. DVT
E. non-coronary arterial occlusion from an acute thromboembolism
F. restore patency of central lines

277
Q

Examples of Thrombolytics

A
  1. Streptokinase (Streptase)
  2. Alteplase tPA (Activase)
  3. Reteplase rPA (Retavase)
278
Q

Indications for tPA

A

heart attack

strokes

279
Q

You don’t want to give thrombolytics platelets is >

A

1.7

280
Q

Thrombolytics prototype:

A

Alteplase

281
Q

Thrombolytics short 1/2 life

A

30-45 minutes

282
Q

Excretion of Thrombolytics

A

urine

283
Q

Thrombolytics side effects

A

bleeding

284
Q

thrombolytics adverse reactions

A
  1. intracerebral hemorrhage
  2. stroke
  3. dysrhythmia
285
Q

Thrombolytics assessment

A

Baseline vital signs, CBC, PT, INR, PTT, obtain medical and drug history

286
Q

Thrombolytics Nursing diagnoses

A

Patient hemodynamically unstable due to clot

287
Q

Thrombolytics Interventions

A

Administer drug, monitor for bleeding, neuro status, labs

288
Q

Thrombolytics

What do you evaluate for?

A

Vital signs remain stable, labs within acceptable range

289
Q

The nurse is preparing to administer heparin sodium to a client diagnosed with a deep vein thrombosis. The nurse should ensure that which of the following is available if the client develops a significant bleeding problem?

A. Phytonadione (vitamin K)
B. Fresh frozen plasma (FFP)
C. Protamine sulfate
D. Reteplase (Retavase)

A

C. Protamine sulfate

290
Q 
The nurse will expect to draw the following laboratory value 6 hours after starting the heparin drip?
 A. PT/INR
 B. aPTT
 C. Serum potassium
 D. Serum sodium
A

B. aPTT

291
Q 
The patient is now taking Coumadin in preparation for discharge. The nurse knows that which of the following nursing diagnoses takes priority?
A. Risk for imbalanced fluid volume
B. Risk for injury
C.Constipation
D. Risk for unstable blood glucose
A

B. risk for injury

(MY GUESS) answer was not provided

292
Q

The nurse is preparing to discharge the client to home on warfarin (Coumadin) therapy. The nurse’s discharge teaching should include which of the following instructions?
A. The intake of foods containing vitamin K should not be altered from baseline
B. Herbal medications may interfere with the effectiveness of Coumadin
C. Alcohol can increase the anticoagulant effect of Coumadin and should be avoided
D. Coumadin can be taken without regard to food intake, although gastrointestinal upset may be diminished if taken with food

A

B. Herbal medications may interfere with effectiveness of Coumadin

(MY GUESS) answer was not provided

293
Q

Clotting Factor I

A

Fibrinogen

294
Q

Clotting Factor II

A

Prothrombin

295
Q

Clotting Factor III

A

Tissue Thromboplastin

296
Q

Clotting Factor IV

A

Calcium Ions

297
Q

Clotting Factor V

A

Labile Factor

298
Q

Clotting Factor VII

A

Stable Factor

299
Q

Clotting Factor VIII

A

Antihemophilic Factor

300
Q

Clotting Factor IX

A

Christmas Facor of Plasma Thromboplastin Component (PTC)

301
Q

Clotting Factor X

A

Stuart-Prower Factor

302
Q

Clotting Factor XI

A

Plasma Thromboplastin Antecedent (PTA)

303
Q

Clotting Factor XII

A

Hageman Factor

304
Q

Clotting Factor XIII

A

Fibrin Stabilizing Factor

AE1 (12 decks)

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