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
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
3
Q
The Autonomic Nervous System is composed of:
1.
2.
A
- sympathetic nervous system (fight/flight)
2. parasympathetic nervous system (rest/digest)
4
Q
the autonomic nervous system is also called the
A
visceral nervous system
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
6
Q
Sympathetic Nervous System (Adrenergic system) - prepares the body to cope with __ __
A
stress situations
7
Q
SNS secretes :
A
epinephrine and norepinephrine
8
Q
Epinephrine/Norepinephrine in the SNS has these effects on the body : (8)
A
- Increases HR
- Dilates the bronchioles
- Dilates the pupils
- Vasoconstricts blood vessels
- Vasodilates the skeletal muscles
- Slows peristalsis
- Relaxes uterus and bladder
- Converts glycogen to glucose by the liver
9
Q
The parasympathetic nervous system secretes
A
acetylcholine
10
Q
Acetylcholine from the PNS has these effects on the body: (7)
A
- Constricts pupils
- Contracts smooth muscle of the GI tract
- Constricts bronchioles
- Slows the heart rate
- Increases secretions/motility of the digestive tract
- contractions of bladder
- glycogen synthesis
11
Q
What are the three types of angina pectoris?
A
- classic (or stable)
- unstable (pre-infarction)
- variant (Prinzmetal, vasospastic)
12
Q
Classic (or stable) angina pectoris
A
reproducible symptom pattern; no change in pattern for 2 months or more
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
14
Q
Variant angina pectoris
A
- occurs with rest, caused by vasospasm, rare
- some medications can stimulate vasospasms
15
Q
What are the three types of antianginal drugs?
A
- nitrates
- beta-blockers
- calcium channel blockers
16
Q
these antianginal drugs increase myocardial blood flow by: (2)
A
- increasing O2 supply (increasing oxygenated blood to the heart) OR
- decreasing O2 demand (decreasing workload)
17
Q
Nitrates (6)
A
- Dilate peripheral blood vessels
- Decrease systemic vascular resistance (after load)
- decrease venous return to heart
- cause coronary artery dilation -> increase oxygen supply to the heart
- decrease left ventricular end diastolic pressure (pre-load)
- decreases preload -> decreases workload of heart and demand of oxygen from the heart
18
Q
Beta-blockers: blockade of beta adrenergic receptors which leads to
A
- decrease in HR
- decrease in rhythm disturbance
- decreased incidence of angina
19
Q
Beta-blockers can increase __ __, __ __ - this can be problematic for the asthma patient
A
airway resistance
bronchial constriction
20
Q
Most common beta-blockers are:
A
metoprolol, atenolol
21
Q
Blocking beta 1 receptors does what things?
A
- decreases HR
2. rhythm disturbances (prolongs action potential)
22
Q
Selective beta blockers block with receptors?
A
beta 1 adrenergic receptors
23
Q
Beta 1 =
A
heart
24
Q
Beta 2 =
A
lungs (bronchial receptors)
25
Calcium activates __ __, increases the __ of the heart, and increases __ __
myocardial contraction
workload
oxygen demand
26
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
Ca+
into
peripheral vasodilation
decreases
decreases
27
Calcium channel blockers decrease __ __ __
coronary artery spasm
28
Calcium channel blockers relax __ __ decreasing cardiac oxygen demand
peripheral arterioles
29
Common calcium channel blocker:
Amlodipine (Norvasc)
30
What are the 8 types of antihypertensive meds?
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
31
Diuretics promote __ and __ depletion which decreases __ __ __
Na+ ; water ;
| extracellular fluid volume
32
Diuretics are effective as the __ __ __ for __ HTN
1st line treatment
| mild
33
Loop Diuretics: give an example
Furosemide
34
Loop Diuretics: works __ and __
fast; effective
35
Loop Diuretic side effects:
1. nausea
2. diarrhea
3. electrolyte imbalances (hypokalemia)
36
Loop diuretics are used in emergencies for __ and __ __
CHF, pulmonary edema
37
Thiazides: give an example
Hydrochlorothiazide (HCTZ)
38
Thiazides are associated with __ __
electrolyte imbalances
39
Thiazides compared to loop diuretics: (3)
1. not as effective
2. do not work as fast
3. does not promote as much Na+ and water depletion
40
Thiazides inhibit active exchange of ___ in the cortical diluting segment of the __ __ __ __
Cl-Na
ascending loop of Henle
41
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
10%
90%
reabsorbed
42
K-sparing diuretics inhibit the reabsorption of __ in the __ __ and __ __
Na+
distal convoluted; collecting tubule
43
Loop diuretics inhibit exchange of _____ in the __ __ of the __ __ __ __
Cl-Na-K
thick segment
ascending loop of Henle
44
The category "Diuretics" does not include __ __
"secondary" diuretics - any drug whose primary target is not to diurese
45
The diuretics are the primary line of therapy for the majority of patients with __ __ and __ __. They decrease __ and __ which result from fluid retention
heart failure
pulmonary congestion
dyspnea, edema
46
Diuretic drugs are divided into what 3 categories?
1. Thiazides
2. Loop Diuretics
3. Potassium-sparing
47
Where are aldosterone receptors found? (3)
1. myocardium
2. arterial walls
3. kidneys
48
Aldosterone is a hormone that
promotes sodium/water retention and potassium/magnesium excretion
49
Aldosterone receptor antagonists block the action of aldosterone and inhibit the __-__ __ . Here, __ is retained and __ is excreted.
sodium-potassium pump
potassium ; sodium
50
Give an example of an aldosterone receptor antagonist:
spironolactone
51
Aldosterone increases the elimination of potassium and magnesium, creating an __ __ which may be responsible in part for __ __.
electrolyte imbalance
cardiac arrhythmias
52
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
collagen
fibrosis
53
What three types of effects do aldosterone inhibitors exert?
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
54
Beta- Adrenergic Blockers are also called what things?
1. Sympatholytics
2. Sympathetic depressants
3. Beta (1,2) blockers
55
What do selective Beta1 blockers do? (4)
1. decreases cardiac output
2. decreases systemic vascular resistance
3. lowers BP
4. decreases HR, contractility and renin release
56
What is the prototype drug for beta blockers?
metoprolol (Lopressor)
57
What are adverse effects of beta blockers? (6)
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
58
Centrally acting alpha2 agonists: (4)
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
59
Side effects/ Adverse reactions for Centrally Acting Alpha2 Agonists:
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
60
Give two examples of centrally acting alpha2 agonists:
1. aldomet (older drug, given IV)
| 2. clonidine (PO and via patch, more common)
61
Alpha-adrenergic blockers causes
vasodilation and decreases BP
62
Alpha-adrenergic blockers do NOT affect __ __ or __ __
glucose metabolism or
| respiratory function
63
Selective alpha1 adrenergic blockers are used to __ __ (and in BPH to relax the __ __ )
decrease BP
urethral constriction
64
Name the alpha-adrenergic blocker prototype:
Prazosin HCl (Minipress)
65
Alpha-adrenergic blockers: side effects/adverse reactions
1. orthostatic hypotension
2. nausea
3. drowsiness
4. edema
5. weight gain
6. impotence
66
What drug interaction occurs between alpha-adrenergic blockers and nitrates:
decreases BP
67
Alpha-adrenergic blockers are often given at __ to pas s the initial orthostatic hypotension
night
68
Angiotensin-converting enzymes (ACE) inhibitors inhibit the formation of __ __ which is a __ __
angiotensin II ; potent vasoconstrictor
69
ACE inhibitors block the release of __, which then causes __ excretion and __ retention
aldosterone
Na+
K+
70
ACE inhibitors cause (a major change/little change) in CO. Which one?
little change
71
ACE inhibitors lower the __ __ __
peripheral vascular resistance
72
What 3 other enzymes can be used to convert angiotensin I to angiotensin II BESIDES angiotensin-converting enzyme (ACE)?
1. chymostatin-sensitive angiotensin-generating enzyme (CAGE)
2. cathepsin G
3. chymase
73
Is this true or false? Several nonrenin enzymes have been found that directly cleave angiotensin II from angiotensinogen without forming angiotensin I.
TRUE
74
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.
AT receptors
AT1 and AT2
AT1
AT1
75
What else do agents that block the RAAS accomplish besides lowering bp? (2)
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
76
common side effect of ACE inhibitors:
1. nagging cough - angiotensin converting enzyme blocks bradykinin (more active bradykinin leads to nagging cough)
77
__ don't have the nagging cough, but the effects of anti-hypetensive aren't as effective as ACE inhibitors
ARBs
78
Do african-americans respond well to ACE inhibitors alone?
NO
79
Do elderly respond well to ACE inhibitors alone?
NO
80
ACE inhibitors are primarily used to treat
HTN
81
Some ACE inhibitors also treat
heart failure
82
ACE inhibitors should not be used in __
pregnancy
83
Can ACE inhibitors be taken with food?
yes, most can
84
what is the prototype drug for ACE inhibitors?
Captopril (Capoten)
85
__ is the most abundant intracellular cation
| Under normal conditions, __ can adjust __ excretion
Potassium
kidneys; potassium
86
Hypokalemia - etiology (3)
1. renal or nonrenal wasting
2. decreased intake
3. redistribution (e.g. insulin)
87
Hypokalemia increases the risk for
cardiac arrhythmias
88
Hypokalemia treatment
replacement either oral or IV (many instances given IV - however can be irritating, causing IV site to extravasate)
telemetry during severe hypokalemia
89
Hyperkalemia =
K+ > 5.0 mmol/ L
90
Hyperkalemia etiology (3)
1. redistribution
2. reduced K+ excretion
3. Increased K+ intake
91
Pseudohyperkalemia
occurs with RBC hemolysis, leukocytosis (>70,000/mm^3) or thrombocytosis (>500,000mm^3)
92
Hyperkalemia Emergency
renal failure in setting of tumor lysis syndrome, rhabdomyolysis, tissue necrosis, large hematomas
93
What would you do if someone was in pseudohyperkalemia?
```
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
```
94
Hyperkalemia signs and symptoms (2)
1. cardiac arrhythmias
| 2. lower extremity weakness
95
Hyperkalemia treatment
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
96
What is the 2nd most prevalent intracellular cation?
magnesium
97
Magnesium acts as a __ __ __
calcium channel antagonist
98
What are magnesium's key roles? (2)
1. muscle contraction
| 2. insulin release
99
What organ maintains magnesium balance?
kidneys
100
hypomagnesemia is present in __-_% of ICU patients
11-65%
101
Hypomagnesemia is due to __ or __ __
renal (increased tubular flow) or GI (diarrhea) losses
102
Hypomagnesemia can produce __ ___ --> __ __ __
cardiac arrhythmias
Torsade de Pointes
103
__ __ can occur when magnesium level
Neuromuscular irritability
104
_____ occurs in ~ __% of those with hypomagnesemia
hypokalemia; 40%
105
Treatment for hypomagnesemia (2)
1. IV Magnesium Sulfate
- caution in patients with renal insufficiency (decreased doses)
2. Oral supplementation for long term replacement
106
Hypermagnesemia is __ and is usually due to __ __
rare
| renal insufficiency
107
Typical setting of hypermagnesemia is treatment of __-__ __ or ____/____
pre-term labor
| pre-eclampsia/eclampsia
108
What are symptoms of hypermagnesemia (5)
1. loss of deep tendon reflex
2. flaccid paralysis
3. apnea
4. bradycardia
5. hypotension
109
Hypermagnesemia
| treatment
1. prevention
-do not give magnesium-containing antacids or cathartics
- stop infusion or
administering oral medications
2. Dialysis
- peritoneal or
hemodialysis
110
What are the two types of cardiovascular agents?
1. Antidysrhythmics
| 2. Drugs for circulatory disorders
111
Cardiac action potential has __ phases
5
112
Cardiac Action Potential:
| The movement of __ across the membrane allows for muscles to contract and relax
electrolytes
113
Phase 0 of Cardiac Action Potential:
Na enters cell -> this causes rapid depolarization -> sub sequential contraction
114
Phase 1 of Cardiac Action Potential:
Initial repolarization; Na stops entering the cell
115
Phase 2 of Cardiac Action Potential :
Plateaus, evens out
Ca++ enters, makes the contraction a little bit longer (calcium channel blockers block calcium making contraction shorter)
116
Phase 3 of Cardiac Action Potential:
Rapid repolarization, beginning of relaxation -> K+ exits the cell into the extracellular
117
Phase 4 of Cardiac Action Potential:
Resting membrane potential between heartbeats
118
what are the two types of dysrhythmia?
1. atrial dysrhythmia
| 2. ventricular dysrhythmia
119
Atrial dysrhythmia:
- prevents proper filling of ventricles
- decrease CO by 1/3
- quivering of the atria doesn't allow the heart to fully contract
120
Ventricular dysrhythmia:
- life threatening
- ineffective ventricular filling results in decreased or absent CO
- entire heart is quivering!
121
Examples of ventricular dysrhythmias:
1. Premature Ventricular Complexes (PVC)
2. Ventricular tachycardia
3. Ventricular Fibrillation
- follow BCLS and ACLS
algorithm
122
Dysrhythmias are also called
arrhythmias
123
Must give __ __ prior to and after surgery even if the patient is NPO (give with a sip of water)
__ causes side effects postoperatively
beta blockers
tachycardia
124
Causes of Dysrhythmia:
```
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
Dysrhythmias are due to an influx of electrolytes affecting __ __
action potentials
126
Antidysrhythmics: Pharmacodynamics
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
antidysrhythmics prolong the __ __
refractory period
128
Antidysrhythmics: Class I
Fast (Sodium) Channel Blockers
- IA: procainamide (Pronestyl, Procan SR)
- IB: lidocaine (Xylocaine)
- IC: Propafenone (Rythmol), Flecainide (Tambocor)
129
Antidysrhythmics: Class II
Beta-Blockers:
Acebutolol (Sectral)
Esmolol (Brevibloc)
Sotalol (Betapace)
130
Antidysrhythmics: Class III
Drugs that Prolong Repolarization:
| -Amiodarone (Cordarone)
131
Antidysrhythmics: Class IV
Slow (Calcium) Channel Blockers -
| Verapamil (Calan, Isoptin) and Diltiazem (Cardizem)
132
Class 1A antidysrhythmic mechanism of action :
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
Class 1A uses:
Wide variety of ventricular & atrial dysrhythmias
| Paroxysmal atrial tachycardia, supraventricular dysrhythmia
134
Examples of Class IA antidysrhythmics:
1. Procainamide (Pronestyl)
2. quinidine (Quinoglute)
3. disopyramide (Norpace)
(these are drugs given for rapid heart rates)
135
Class 1A Procainamide absorption:
- oral extended release - 90 to 120 minutes
| - IM - 15-60 minutes
136
Class 1A Procainamide metabolism and excretion:
- converted by liver to N-acetylprocainamide (NAPA), an active anti arrhythmic compound
- may vary among population
- 30-60% excreted unchanged by kidney
137
Class 1A Procainamide: Half life
Half-life - 2.5 to 4.7 hours (NAPA - 6 to 8 hours)
| *prolonged in renal impairment
138
Procainamide: side effects
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
Procainamide: Side Effects during long-term therapy
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
Procainamide: Adverse Reactions
1. Life threatening: caused by high concentrations (>19 micrograms/ml)
2. hypotension
3. marked slowing of conduction
4. Torsade de pointes
141
What is Torsade de points?
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
What else can procainamide be used for?
It can act as an anti-hypertensive.
| It vasodilates the blood vessels (blocks phase 0)
143
PR interval
0.12-0.20 sec
144
QRS duration
0.08-0.10 sec
145
QT interval
0.4-0.43 sec
146
QT interval greater than __ seconds leads to higher risk of v-tach and v-fib
0.43
147
Drugs that can prolong QT interval (18)
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
Procainamide: toxicity
What do you monitor?
What is the therapeutic level of procainamide & napa levels?
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
which three signs signify a wide QRS and requires procainamide or amiodarone?
Vtach
Vfib
Torsade de pointes
150
Class II Antiarrhythmics prolongs which phase of the cardiac action potential?
Prolongs phase 4
151
Class II Antiarrhythmics mechanism of action:
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
Class II Antiarrhythmic uses
wide variety of ventricular and atrial dysrhythmias
| - paroxysmal supraventricular tachycardia ( PSVT) and PVCs
153
Class II Antiarrhythmic examples
1. Acetabutol (Sectral)
2. emolol (Brevibloc)
see used in critical care
154
Class II Antidysrhythmics side effects, adverse reactions, and drug-drug interactions
1.Same as those of Class I and
III
2.Watch for bronchospasm and dyspnea
155
Class III Antidysrhythmics mechanism of action
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
Class III Antidysrhythmics uses
Ventricular tachycardia/fibrillation, atrial flutter/fibrillation. For treatment and maintenance.
157
Examples of Class III Antidysrhythmics
1. Amiodarone (Cordarone)
2. Brytelium
3. Ibutiliade (Corvert)
4. dofetilide (Tikosyn)
5. satolol (Betapace)
158
Amiodarone side effects
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
Amiodarone adverse reactions
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
Part of Amiodarone gets deposited in the __ after long term use (after __ year/s)
cornea
1
161
What is a rare adverse reaction of Amiodarone?
Blue-Gray Hyperpigmentation
| they look cyanotic; for darker skinned people, the skin will become darker
162
amiodarone drug interactions
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
Nursing considerations/patient education for Amiodarone
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
Amiodarone has a risk for causing ___ because it is very acidic
infiltration
165
Class IV Antidysrhythmics mechanism of action
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
Class IV Antidysrhythmic Uses
Ventricular tachycardia/fibrillation, atrial flutter/fibrillation and PSVT. Treatment and maintenance
167
Class IV Antidysrhythmic examples
1. diltiazem (Cardizem)
| 2. verapamil (Calan) – given P.O. or IV
168
Class IV Antidysrhythmics prolongs __ __ and __. Slows down ___. Relaxes the __ __
phase 1 and 2
HR
blood vessels
169
Verapamil causes __ __. If you lower the bp too low, the HR will go up
rebound tachycardia
170
Antidysrhythmics: nursing interventions
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
```
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. Prolonged action potential duration
172
```
A life threatening adverse reaction of the medication procainamide (Pronestyl, Procan SR) is:
A. Nausea
B. Anorexia
C. Torsades de Pointes
D. Vomiting
```
C. Torsades de Pointes
173
Anticoagulants: (3)
1. antiplatelets
2. antithrombin
3. low-molecular weight heparin(LMWH) (Lovenox)
174
Thrombolytics examples
1. r-tPA
| 2. streptokinase
175
Antihemophilic Agents example
coagulation factor VIIa
176
Systemic Hemostatic Agents
Aminocaproic acid
177
Topical Hemostatic Agents
Absorbable gelatin
178
What can you use to stop nosebleeds?
Aminocaproic acid
179
Thrombus Formation
| How does a clot form in an artery or vein?
Caused by decreased circulation, platelet aggregation on vessel wall, blood coagulation
180
Arterial clot formation
1. platelets initiate process
2. fibrin formation occurs
3. RBCs are trapped in fibrin mesh
181
Venous clot formation
platelet aggregation with fibrin that attaches to RBCs
venous clots are caused by RBCs by sluggish flow and they eventually become stuck together
182
If you have an MI, what do you give?
an ANTIPLATELET like aspirin
183
If you have a DVT, what can you give?
Plavix, heparin, compression socks
184
Clotting Cascade: Extrinsic Pathway
activated by external trauma that causes blood to escape from vascular system (bleeding)
Quicker than intrinsic pathway
185
Clotting Cascade: Intrinsic Pathway
activated by trauma inside vascular system. Activated by platelets, exposed endothelium, chemicals. Slower than extrinsic pathway
186
Clotting Cascade: Common pathway
completes clot production
187
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)
```
factor 7
factor 7
7A
7A
10A
```
188
When you are septic, you clot due to the __ __
intrinsic pathway
189
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?
arterial thrombi
190
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?
venous thrombi
191
The Joint Commission says:
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
Anticoagulants do not
dissolve clots already formed
193
Anticoagulants prevent __ __ from __
new clots
| forming
194
What activates platelet aggregation in the first place?
a ruptured plaque (atherosclerosis)
195
Heparin (unfractionated)
| mechanism of action
Natural substance in liver & prevents clot formation; Inhibits thrombin (see next slide). Prevents conversion of fibrinogen to fibrin. Variable effect
196
Heparin (unfractionated) uses
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
How does Heparin work?
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
Heparin (unfractionated) side effects
Itching, burning, and ecchymosis on the injection site
199
Heparin (unfractionated) adverse effects
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
Heparin (unfractionated) Interactions
Increased effect with aspirin, NSAIDs, thrombolytics, and probenecid
201
Heparin (unfractionated) Antidote:
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
How does a heparin injection produce a bruise?
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
If you give subQ heparin do you need to monitor PTT and aPTT?
No, because the heparin half life is only 30 minutes to 1 hours
204
We only monitor aPTT if we give __ __ . The goal is to make the aPTT __-__ seconds. You will do a blood draw every __-__ hours.
IV Heparin
60-80 seconds
4-6 hours
205
What is normal platelet levels
140,000 to 400,000
206
Heparin-induced Thrombocytopenia (HIT)
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
For a patient with HIT, what can you give them ?
give them antithrombins
208
Why don't use normally give blood thinners like heparin to patients who have liver failure?
b/c there is less production of certain clotting factors
209
Do not give heparin if the platelet is _____
210
For Heparin IV drip, ensure that a __ IV line and an __ __ is used.
Avoid ___ __ __ __
dedicated
infusion pump
interruption of the infusion
211
For Heparin IV drip, don't __ anything with heparin
piggyback
212
HIT
| Results in activation of more platelets and PF4 release =
thrombin forms
213
How can you rule out HIT?
if the level of platelets is less than 100,000 within 5-14 days of heparin tx
214
what is contraindicated in a person with HIT?
platelet transfusion
215
HIT can re-occur each time a patient receives heparin. This should be listed as a/an ___
allergy
216
What is the treatment for HIT?
Lepirudin inhibits thrombin and it’s thromboembolic effects. Given IV.
217
Low molecular weight heparin is __ which means :
fractionated
made of fragments/derivatives of unfractionated heparin
218
Mechanism of action for LMWH
Binds with antithrombin and accelerates the rate at which antithrombin inhibits Factor Xa and thrombin
219
LMWH uses
similar to heparin
220
example of a LMWH
Enoxaparin (Lovenox)
221
antidote for LMWH
Protamine Sulfate
222
compared to unfractionated heparin, LMWH: (4)
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
Indications for LMWH
DVT prophylaxis
224
When you are stressed out, you are activating __ __ like __ and __. This makes you're blood ___.
inflammatory mediators
cytokines, interleukins
hypercoagualable
225
Mechanism of action for Warfarin (Coumadin)
Inhibits the hepatic synthesis of coagulation factors dependent on Vitamin K: Factors II, VII, IX and X
226
Warfarin (Coumadin) 1/2 life
long 1/2 life and very long duration - (2-3 days?)
227
Warfarin (Coumadin) uses
mainly to prevent thromboembolic conditions such as embolism caused by atrial fibrillation, which can lead to a stroke (CVA), DVT, PE
228
Which clotting factors need vitamin K?
II
VII
IX
X
229
__ synthesizes and manufactures vitamin K
Liver
230
Coumadin aka Warfarin stems from the acronym WARF which stands for:
Wisconsin Alumni Research Foundation
231
Normal PT is
10-12 secodns
232
Normal INR (international Normalized ratio) -
0.7-1.7
233
Goals of Coumadin therapy:
1. Atrial fibrillation - (2-3)
2. Artificial valves - (2.5-3.5)
3. DVT and PE - (2-3)
234
Goals of Coumadin therapy: start treatment at __ mg per day and titrate the dosage every __ to __ days to achieve goal
5 mg
3-7 days
235
Side effects of Coumadin
Anorexia, nausea, vomiting, diarrhea, abdominal cramps, rash, and fever
236
Adverse Effects of Coumadin
May increase AST (aspartate aminotransferase), ALT (alanine aminotransferase), and bleeding
237
Coumadin Antidote
Antidote: Vitamin K (2.5 to 10 mg IM or SQ). Fresh frozen plasma (FFP) is indicated for acute bleeding
238
What drugs if used with Coumadin would increase bleeding?
```
ASA
H2 Blockers
Erythromycin
Cefoxitin
Disulfiram
Amiodarone
Thyroid drugs
Cotrimoxazole (Bactrim)
```
239
What drugs if used with Coumadin would decrease anticoagulation?
```
Vitamin K and E
Rifampin
Phynetoin
Barbiturates
Cholestyramine
```
240
Antiplatelet: Aspirin was discovered in the ___. Anti platelet properties was known in __.
1800s
| 1960s
241
Aspirin mechanism of action:
Inhibits platelet aggregation by interfering with thromboxane A2
242
Aspirin uses:
MI (bite and chew), CVA (tx or prophylaxis), CAD prophylaxis. Maybe used within 48 hours of stroke, recommended before and after endarterectomy
243
Aspirin side effects
tinnitus, bleeding
244
Aspirin adverse effects
nausea, dyspepsia, heartburn, GI bleed, tinnitus, toxicity, headache, anaphylactoid reaction.
245
Aspirin antidote
No Antidote. Discontinue 1wk before surgery
246
Aspirin is rapidly absorbed in the GI tract
| onset: __-__minutes
5-30 minutes
247
Aspirin inhibits platelets within __ minutes (Peak: __ min to __ hours)
60 minutes
25 minutes - 2 hours
248
Duration of Aspirin
3-6 hours
249
Plavix is a __ which is an _____ drug
thienophyridine
anti platelet drug
250
Plavix mechanism of action
Prevents platelet aggregation by blocking Adenosine Diphosphate from binding to platelet receptor
251
Examples of Thienophyridines
1. dipyridamole (Persantine)
2. ticlopidine (Ticlid)
3. clopidogrel (Plavix)
252
Plavix has similar side effects and adverse reactions with __
Aspirin
253
Onset of action for Plavis is __ __ and drug effects last for __ __
several days
| 7 days
254
Patients allergic to Aspirin can take __
Plavix
255
__ also allows for platelets to stick together
ADP
256
Direct acting thrombin inhibitors are ___ (_) __
Parenteral (IV) Anticoagulants
257
Direct Acting Thrombin Inhibitors mechanism of action
directly inhibit thrombin from converting fibrinogen to fibrin
258
Direct Acting Thrombin Inhibitors Uses
Heparin-induced thrombocytopenia, unstable angina, angioplasty
259
Direct Acting Thrombin Inhibitors examples
1. Argatroban (Acova)
2. bivalirudin (Angiomax)
3. lepirudin (Refludan).
SQ: Desirudin (Iprivask).
PO: Pradaxa
260
__ __ is a contraindication for lepirudin
Liver failure
261
Dabigatran Etexilate (Pradaxa) category
direct thrombin inhibitor
262
Dabigatran Etexilate (Pradaxa) uses
non-valvular atrial fibrillation and stroke treatment and prophylaxis, HIT, DVT, and PE
263
Dabigatran Etexilate (Pradaxa) is metabolized in the
liver
264
Dabigatran Etexilate (Pradaxa) 1/2 life
12 – 17 hours (longer in the elderly) and renal impairment
265
Dabigatran Etexilate (Pradaxa) excreted in the urine. Severe Renal failure =
risk for bleeding
266
Dabigatran Etexilate (Pradaxa) dosage
150 mg twice daily P.O.
267
Factor XA Inhibitor Oral Anticoagulants examples
Rivaroxaban (Xarelto) and Apixaban (Eliquis
268
Factor XA Inhibitor Oral Anticoagulant uses
DVT and PE prophylaxis in patients
| going for hip/knee surgery, stroke, atrial fibrillation, and non-valvular fibrillation
269
Does Factor XA Inhibitor Oral Anticoagulant require routine coagulation monitoring?
no
270
Factor XA Inhibitor Oral Anticoagulant is administered:
once daily or twice a day P.O. (10-20 mg depending on indication)
271
General contraindications for anticoagulants:
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
Nursing assessment for Anticoagulants
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
Nursing Diagnoses for Anticoagulants
Risk for injury (bleeding)
Knowledge deficit
Evaluation
aPTT, PT/INR are within therapeutic range
274
Nursing Care (8)
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
Thrombolytics mechanism of action
Promote fibrinolytic mechanism. Convert plasminogen to plasmin to dissolve clot
276
Thrombolytics uses:
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
Examples of Thrombolytics
1. Streptokinase (Streptase)
2. Alteplase tPA (Activase)
3. Reteplase rPA (Retavase)
278
Indications for tPA
heart attack
| strokes
279
You don't want to give thrombolytics platelets is >
1.7
280
Thrombolytics prototype:
Alteplase
281
Thrombolytics short 1/2 life
30-45 minutes
282
Excretion of Thrombolytics
urine
283
Thrombolytics side effects
bleeding
284
thrombolytics adverse reactions
1. intracerebral hemorrhage
2. stroke
3. dysrhythmia
285
Thrombolytics assessment
Baseline vital signs, CBC, PT, INR, PTT, obtain medical and drug history
286
Thrombolytics Nursing diagnoses
Patient hemodynamically unstable due to clot
287
Thrombolytics Interventions
Administer drug, monitor for bleeding, neuro status, labs
288
Thrombolytics
| What do you evaluate for?
Vital signs remain stable, labs within acceptable range
289
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)
C. Protamine sulfate
290
```
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
```
B. aPTT
291
```
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
```
B. risk for injury
(MY GUESS) answer was not provided
292
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
B. Herbal medications may interfere with effectiveness of Coumadin
(MY GUESS) answer was not provided
293
Clotting Factor I
Fibrinogen
294
Clotting Factor II
Prothrombin
295
Clotting Factor III
Tissue Thromboplastin
296
Clotting Factor IV
Calcium Ions
297
Clotting Factor V
Labile Factor
298
Clotting Factor VII
Stable Factor
299
Clotting Factor VIII
Antihemophilic Factor
300
Clotting Factor IX
Christmas Facor of Plasma Thromboplastin Component (PTC)
301
Clotting Factor X
Stuart-Prower Factor
302
Clotting Factor XI
Plasma Thromboplastin Antecedent (PTA)
303
Clotting Factor XII
Hageman Factor
304
Clotting Factor XIII
Fibrin Stabilizing Factor
