Glossary of Pharmacology Midterm I slides

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bleeding stopped, initiated by bl. vessel injury.
2 stages of hemostasis
1. platelet plug formation
2. coagulation
platelet plug formation
platelets activated when exposed to interstitial collagen from injury. Platelets stick, form plug. NOT STRONG, NEEDS FIBRIN
reinfirocement of plug w/ fibrin. to prevent widespread coagulation - antithrombin. removal of cluts done by plasmin - activated by plasminogen
blood clot formed w/in bl. vessel
3 types of thrombosis
ARTERIAL: caused by adhesion of platelets to arterial wall. Leads to occlusion.
VENOUS: develop at sites where bl. flow is slow, or pooling of bl.
HEART: form on heart valves, chambers. Fibrilations of heart.
-Anticoagulants (heparin, low-molecular wt heparin, warfarin/coumadin)
-Antiplatelets (aspirin, adenosine diphosphate (ADP) Receptor Antagonist, glycoprotein IIB/IIIA receptor antagonist)
-Thrombolytics ( all end in -ase but focus on streptokinase)
Anticoagulants (3)
heparin, lmwh, warfarin/coumadin

rapid acting. IV or SQ in units.
MOA - Heparin
enhances activity of antithrombin, leads to inactivation of thrombin and factor Xa. Fibrin is reduced.
IND (5) - Heparin
1. PE
2. DVT
3. renal dialysis: prevent clots in machine.
4. evolving stroke: not on all strokes.
5. open heart surgery
CI - Heparin
any condition which causes bleeding. Used w/ caution with liver or kidneys b/c affects metabolism & excretion of bl.
AE (3) - Heparin
1. hemorrhage
2. hypersensitivity rxn b/c of pork or cow tissue
3. heparin-induced thrombocytopenia (HIT) low RBC count
DI - Heparin
other drugs that cause bl. inc risk of bleeding. ASPIRIN!
Antidote - Heparin
protamine sulfate. If dose is too high or need surgery. Binds w/ heparin
Nurs. considerations (2) - Heparin
1. Lab monitoring: coagulation time: activated partial thromboplastin time (aPTT) Normal is 40 sec. Want to increase by 1.5-2x or 60 to 80 sec. Measure q 4-6hrs. Adjust PRN, once therapeutic check q day.

2. Monitor signs of bleeding: check VS - dec. BP, inc HR, headache, easy bruising
LMWH - most common
similar to heparin DON"T HAVE TO MONITOR. Administer SQ. Most common one enoxaparin/Lovenox

Doesn't req. aPTT. Less side effects, bleeding. Can be taken at home.
Inactivates clotting factor Xa - fibrin reduced
Tx and prevention of DVT for p/c who are on bedrest for < 5 days, or immobile p/c, used following surgery esp. w/ hip or knee
bleeding, thrombocytopenia
PO. Delayed action, long-term prophylaxis.
MOA - Warfarin/Coumadin
inteferes w/ biosynthesis of Vit. K dependent clotting factors - acts as an antagonists to Vit. K (factors VII, IX, X, prothrombin).

Delayed onset, overlap w/ heparin.

IND - warfarin/coumadin (4)
long-term prophylaxis
1. A-Fib
2. valve replacement
3. PE
4. dec. risk of recurrent MI
AE - warfarin/coumadin(4)
CI - Warfarin/Coumadin
same as heparin
DI - Warfarin/Coumadin - meds that dec effects on coumadin:
seizure meds, oral contraceptives, foods high in Vit. K
DI - Warfarin/Coumadin - meds that inc effects of coumadin:
ASA (give tylenol), heparin, anti-fungals, some ABX (erythromyocin)
Antidote - Warfarin/Coumadin
vitamin K injection
Nursing Considerations - Warfarin/Coumadin
1. Lab monitoring: prothrombin time (PT) and international normalization ratio (INR) Normal INR is 1. Target is 2-3.5.

Check DAILY for therapeutic range.
1. aspirin
2. adenosine diphosphate (ADP) Receptor Antagonist
3. glycoprotein IIB/IIIA Receptor antagonist
MOA - Aspirin
causes inhibition of an enzyme CYCLOOXYGENASE, req for platelet activation.

Low doses: 81-325 mg.
IND - Aspirin
prevent MI and stroke. Better for MIs.

AE - Aspirin
GI upset
bleeding GI or inc risk hemorrhagic stroke
MOA - ADP Receptor Antagonist

When what can't be used??
blocks ADP receptors on platelets PREVENTING AGGREGATION - inactivates platelets.

For p/c who can't tolerate ASA or don't respond.

More effective than ASA but more expensive and PERMANENT
IND - ADP Receptor Antagonist

prevent strokes, MI

Ex: clopidogrel/Plavix (plavix better for CVAs)
AE - ADP Receptor Antagonist
similar to ASA but less bleeding
MOA - glycoprotein IIB/IIIA Receptor antagonist
cause reversible blockage of platelet receptors, inhibits final step in platelet aggregation.

not long term
IND - glycoprotein IIB/IIIA Receptor antagonist

Prevent what?
acute short term use, IV only to prevent ischemic events in p/c with acute coronary syndrome, coronary interventions.

Ex: Abciximab/ReoPro
AE - glycoprotein IIB/IIIA Receptor antagonist
Thrombolytics - def & types
break up clots , for severe thrombotic disease.

Fibrinolytics - PE

Types: END IN "-ASE"
MOA - Thrombolytics
streptokinase converts plasminogen to plasmin which digests thrombi

Given w/in 6 hours of Sx - IV to break up clot
IND (4) - Thrombolytics
acute MI
massive PE
used in clotted vascular catheters - central line
AE - Thrombolytics
intracranial hemorrhage
antibody production - allergic rxn. Foreign protein from streptococcous, form antibodies
ANEMIA - def
dec in RBC, hematocrit, hemoglobin. Caused by bl. loss, impaired production of RBC or inc destruction of RBC.

Production: regulated by cellular O2 requirements and hormone erythropoietin - kidneys.

Nutrition: Fe, Folic Acid
Fe deficiency anemia

Most common?
What's needed?
lack of Fe - needed for hemoglobin. P/o

AE - Fe deficiency anemia

GI upset
staining of teeth

Antidote DEFUROXAMINE - absorbs Fe
DI - Fe deficiency anemia
Ca, antacids
ABX - Fe affects absorption
Vitamin C - inc absorption of Fe.
Fe IV or IM

What's used since it's Fe?
Fe Dextran: painful, tissue discoloration - damage
IND - IV/IM Fe deficiency anemia

Used when what's ineffective?
used when po Fe is ineffective, or cannot absorb po
AE (4) - IV/IM Fe deficiency anemia
anaphylaxis from dextran
hypotension, cardiac arrest
Vitamin B12 deficiency anemia - pernicious anemia

Vit B12 prep drug? (Think blue)
Vitamin B12 needed for DNA synthesis leading to RBC maturation.

Most common cause - imapired absorption due to loss of intrinsic factor

Vitamin B12 preparation: cyanocobalamin. Can be po, most require monthly IM
AE - Vitamin B12 deficiency anemia

hypokalemia: due to inc RBC production
Folic acid deficiency anemia
Folic acid needed for RBC maturation

Most common cause: poor diet or malabsorption

Replacement therapy: folic acid, folate, pteroylglutamic acid
AE - folic acid deficiency anemia

Can mask what?
none, non-toxic even at high doses

DANGER! Can mask Vit B12 deficiency
Hematopoietic Growth Factors (4)
1. Hematopoiesis
2. Erythropoietic Growth Factors
3. leukopoietic growth factors
4. thrombopoietic growth factors
bl. cell production, regulated by growth factors - colony - stimulating factors. Act on bone marrow to produce bl. cells
Erythropoietic Growth Factors

Names of most common? Think of erythropoietin
stimulate production of RBC.

Most common: Epoetin Alpha/Epogen, Procrit. Given IV of SQ 3x q week
MOA - Erythropoietic Growth Factors

what does it stimulate?
stimulates bone marrow to produce RBC
IND - Erythropoietic Growth Factors
1. chronic renal failure - kidneys produce erythropoietin, need supplements
2. HIV pts who are taking antivirals that cause anemia
3. chemotherapy pts
4. surgical pts who are anemic
AE - Erythropoietic Growth Factors

What happens w/ inc RBC/bl. vol?
Nursing considerations - Erythropoietic Growth Factors

Don't do what?
1. monitor hemoglobin level
2. do not shake vial - destroys the protein
Leukopoietic Growth Factors

What common drug?
stimulate production of WBC.

Most common one: FILGRASTIM (Granulocute Colony-Stimulating Factor-G-CSF)/Neupogen. Given IV or SQ q day.
MOA - Leukopoietic Growth Factors
acts on cells in bone marrow to inc production of neutrophils. Enhances mature neutrophils more effective - cancer pts
IND - Leukopoietic Growth Factors

All pts
1. cancer pts on chemo
2. bone marrow transplant pts(BMT)
3. pts with severe chronic neutropenia
AE - Leukopoietic Growth Factors

What does it act on?
bone pain b/c acts on bones
Nursing considerations - Leukopoietic Growth Factors
1. monitor WBC count
2. do not shake vial
Thrombopoietic Growth Factors

What does thrombin do?

Drug? Christen's fav. #
stimulate platelet production

Oprelvekin/Interleukin-11. Given SQ q day.

MOA - Thrombopoietic Growth Factors

Stimulates what and what? Not w/ RBCs
stimulates production of stem cells and megakaryocytes
IND - Thrombopoietic Growth Factors

cancer pts on chemo that causes bone marrow suppression
AE - Thrombopoietic Growth Factors
1. fluid retention - edema, inc plasma vol. Pts w/ CHF used caustiously
2. cardiac dysrhythmias - inc plasma vol., inc work
Nursing considerations:
monitor platelet count - use until counts >50k but not to exceed 21 days.
Lipid-lowering agents
Dec LDLs. Prevent CAD, atheriosclerosis
component of cell membranes, req. for synthesis of hormones and bile salts.
function as carriers for transporting lipids.
Meds - cholesterol/lipoproteins (4)
1. HMG CoA Reductase Inhibitors
2. Bile-Acid Binding Resins
3. Nicotinic Acid (Niacin)
4. Fibric Acid Derivatives
HMG CoA Reductase Inhibitors
inhibits HMB CoA reductase, enzyme in cholesterol biosynthesis.

Causes inc in LDL receptors in liver so removes more LDLs from bl.

LDL dec. HDL inc.
Types - HMG CoA Reductase inhibitors
end in "statin"
AE - HMG CoA Reductase inhibitors
1. HA
2. GI disturbances
3. myopathy
4. hepatomegaly
5. muscle weaknses, aches
DI - HMG CoA Reductase inhibitors
1. meds that inhibit hepatic microsomal enzymes (systems that metabolizes drugs): raise statin levels
2. do not use during pregnancy
Bile-Acid Binding Resins
dec LDLs, alone or w/ statin if statin isn't enough
MOA - Bile-Acid Binding Resins
prevent absorption of bile acid, bind w/ bile acids in GI tract.

Dec production of LDLs, doesn't affect HDLs
Types - Bile-Acid Binding Resins
1. cholestyramine/ Questran
2. colestipol/Colestid
3. colesevelam/Welchol
AE - Bile-Acid Binding Resins

On what system?
GI: constipation, bloating
DI - Bile-Acid Binding Resins
1. can dec absorption of fat soluble vitamines b/c binds to things.

Time frame: use 1-4 hours before other drugs

2. can form complexes w/ other drugs and affect their absorption
Nicotinic Acid (Niacin)
not used frequently
MOA - Nicotinic Acid (Niacin)
dec production of VLDL which then cause dec LDL. Inc HDL
AE - Nicotinic Acid (Niacin)
1. skin
2. GI
3. hepatotoxicity
4. hyperglycemia
MOA - Fibric Acid Derivatives
dec triglyceride levels, inc HDL, no effect on LDLs

Ex. Gemifibrozil/Lopid
AE - Fibric Acid Derivatives
GI, gallstones
DI - Fibric Acid Derivatives

One Lipoprotein drug and anticoagulant
statins, warfarin
Consequenes of HTN (4)
1. heart diesease
2. stroke - at high elvels, #1 cause of stroke is HTN.
3. kidney disease
4. blindness
Non-pharmacological MGMT of HTN:
lifestyle modifications - smoking cessation, alcohol restrictions, maintenance of K & Ca
ARTERIAL BP - Regulation of BP (3)
2 main factors influence BP:

CO (HR x SV) & SVR (peripheral resistance)
1. Nervous sys - Regulation of BP
1. baroreceptors: stimulates NS also chemoreceptors for changes in O2
2. hormones - stimulate NS RAAS - renin
3. CNS - ischemia of brain
2. Renal sys - Regulation of BP
control Na excretion and ECF volume.

Renin -> angiotensinogen -> angeiotensin I -> angeiotensin II -> aldosterone.
3. Endocrine sys - Regulation of BP
ADH released, inc ECF volume -> inc BP
Anti-hypertensive sites of action (2)
1. Nervous system
2. Renal system
Nervous sys - Anti-hypertensive sites of action

Think ABCD
1. Sympatholytics: suppress sympathetic action
a. beta-adrenergic blockers
b. alpha1 - adrenergic receptor blockers
c. alpha2 - agonists
2. Ca channel blockers: affect vascular smooth muscle, heart (vasodilation)
3. Direct-acting Vasodilators: relax vasular smooth muscle
Renal sys - Anti-hypertensive sites of action

What's made in the kidneys?
a. Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors): prevent conversion of angiotensin I into angiotensin II

b. Angiotensin II Receptors (ARB): block angiotensin II receptors so prevents action of angeiotensin II.

c. Diuretics: acts on renal tubules to promote Na and water excretion
Anti-hypertensive Meds (8)
1. beta-adrenergenic blockers
2. Alpha 1 - Adrenergic Receptor Blockers
3. Alpha 2 - Agonists
4. Ca Channel Blockers (CCB)
5. Vasodilators
6. ACE Inhibitors
8. Diuretics
MOA - beta-adrenergenic blockers
block Beta1 receptors in heart, blocks/dec sympathetic effects on heart (Fight of flight). Blocks Beta1 receptors in the kidney causing dec in renin.
1. dec heart rate
2. dec force of contraction
3. red velocity of pulse conduction
IND - beta-adrenergenic blockers
end in "-pril"
AE - beta-adrenergenic blockers
reduced CO
AV heart block - slows impulse of AV node
MOA - Alpha1 - adrenergenic receptor blockers
block the effects of Alpha 1 receptors. Results:
1. dilated bl. vessels: dec BP
2. CO dec
IND - Alpha1 - adrenergenic receptor blockers


Ex. prazosin/minipress - used quite often
AE - Alpha1 - adrenergenic receptor blockers
1. orthostatic hypotension since a lot of vasodilation in periphery, dec BP in center
2. reflex tachycardia - HR inc b/c dec OC -> body tries to compensate
3. Na retention and inc bl. volume - dec CO & body needs inc bl. -> fluid from extracellular spaces -> maybe use diuretics if happens
MOA - Alpha2 - agonists
centrally acting - red firing of sympathic neurons - suppresses sympathetic outflow to heart and bl. vessels.

Results in dec vasoconstriction - dec BP

Uses: HTN, severe pain

Ex. clonidine/catapres
AE - Alpha2 - agonists
rebound HTN
xerostomia - dry mouth
blocks entry of Ca into cells - bl. vessels and heart.
Effects of CCB on bl. vessels
Ca regulates smooth muscle contraction. If blocked - smooth muscle contraction prevented -> vasodilation (acts on arterial walls)
Effects on CCB on heart
Ca regulates function of myocardium, SA node, AV node

Myocardium: Ca inc force of contraction, if blocked - dec force of contraction

SA node: Ca regulates HR, inblocked HR dec

AV node: Ca regulates excitability of AV node, if blocked dec velocity of contraction
Classifications - CCB (2)
1. dihydropyridines - ends in "dipines"

2. others nondihydropyridines
verapamil/isoptin, calan
AE - CCB - both types
peripheral edema
gingival hyperplasia

Dihydropyridines: reflex tachycardia
Others: bradycardia, AV block
DI - CCB - others
Digoxin CAN'T BE ON!!!
MOA - vasodilators (aterio-dilators & Venous-dilators)
relax smooth muscle in bl. vessels.
cause dec in peripheral vascular resistance, dec afterload -> dec work of the heart, inc CO, inc tissue perfusion.
red force with which bl. is returned to heart so dec ventricular filling, dec preload -> dec force of contraction
Net effect on vasodilators
DEC CO!!!!
IND - vasodilators
heart failure
Peripheral vascular disease
Types - vasodilators
Acts on aterioles

hydralazine/apresoline: aterio-dilator

minoxidil/loniten: arterio-dilator, more potent, more severe SE rxns.

Na Nitroprusside/Nitropress - aterio & venous. Once stopped, BP can return.
AE - vasodilators
postural hypotension: too much dilation from central core to peripheries

reflex tachycardia: fluid back into tissue, response to dropping HR

expansion of bl.
DI - vasodilators
other antihypertensive meds: diuretics since don't want volume back into heart
MOA - ACE Inhibitors
blocks the enzyme (angiotensin converting enzyme, kinase II) that converts angiotensin I to angiotensin II -> therefore dec vasoconstriction and aldosterone production.
Results in ACE Inhibitors
1. vasodilation
2. dec bl. volume
3. prevent or reverse pathological changesi n heart, vessels
IND - ACE Inhibitors
left ventricular dysfunction
AE - ACE Inhibitors
1. dry cough
2. first dose syncope: when first taken, BP can dec rapidly/dizziness, but later on no problems
3. hyperkalemia
4. renal failure
5. angioedema: edem in vessels of heart
DI - ACE Inhibitors
1. other anti HTN: potassium
2. potassium sparing diuretics or drugs that raise K
3. diuretics
MOA - Angiotensin II Receptor Blockers (ARBS)
ARBs competes with angiotensin II at tissue binding sites.

Blocks effects of angiotensin II.

Effects similar to ACE Inhibitors:
1. vasodilation
2. Red. bl. volume.
3. Reverses pathological changes in the heart
Types - Angiotensin II Receptor Blockers (ARBS)
end in "sartan"
AE - Angiotensin II Receptor Blockers (ARBS)
renal failure
less hyperkalemia - not as bad as ACE Inhibitors
Results for ACE Inhibitors & ARBs
Results in dec SVR (afterload) & vasodilation (dec BP)
Diuretics - def
drugs that inc renal excretion of water, Na, and other e-lytes - results in inc UO
Indications, general - diuretics
Remove edematous fluid
Prevent renal failure - stimulates kidneys
Classifications (2)
1. High-ceiling: Loop
2. Thiazides
3. Potassium - Sparing
4. Osmotic
MOA - High-ceiling: Loop - diuretics
inhibits Na and Cl reabsorption in ascending loop of Henle. Gets more fluid out.
IND - High-ceiling: Loop - diuretics
multiple uses - HTN, heart failure, PE, renal disease

Ex. Furosemide/Lasix - most common
AE - High-ceiling: Loop - diuretics
1. denydration
2. e-lyte imbalances esp K and Na
3. hypotension
4. ototoxicity - affects the ears - temporary, reverses when off.
DI - High-ceiling: Loop - diuretics
MOA - Thiazides
dec reabsorption of Na, H2O, Cl, bicarbonate in distal convoluted tubule.
IND - Thiazides
edematous states
Diabetes Insipidus (DI) - inc amt of UO/regulate.

Ex. HCTZ - hydrochlorothiazide: most common BP drug used for HTN or diuretic. Very effective & less AE.
AE - Thiazides
similar to loop diuretic, risk for hypokalemia, no ototoxicity
DI - Thiazides
similar to loop diuretics
MOA - Potassium - Sparing Diuretics
blocks aldosterone in distal nephron/tubules - dec Na reabsorption and K excretion
IND - Potassium - Sparing Diuretics
severe heart failure

Ex. spironolactone/aldactone
AE - Potassium - Sparing Diuretics
DI - Potassium - Sparing Diuretics
do not take w/ other agents that inc K levels or with other K sparing diuretics
MOA - osmotic
creates somotic forces in lumen of nephron - draws water into renal tubule. Drug isn't metabolized, just an osmotic force.

Used in emergencies to prevent failure. VERY RAPID!!!
IND - osmotic
prophylaxis of renal failure, reduction of intracranial pressure w/ cerebral edema, reduction of intraocular pressure

Ex. mannitol/osmitrol
AE - osmotic
HTN Drug Therapy - Selecting Meds (2)
1. Initial drug selection: w/ no compelling med hx and w/ compelling med hx

2. Step down therapy
1. Initial drug selection
a. w/ no compelling med hx:
first choice: thazide diuretic
add: beta blocker
if not responding: CCB, ACEI, ARB

b. w/ compelling med hx:
DM: diuretic, BB, ACEI, ARB, CCB
CHF: ACEI, diuretic
Kidney disease: ACEI, ARBs
2. Step down therapy
after BP controlled for 1 year, dec dosage and # of drugs
Nursing considerations - HTN drug therapy
1. acute
2. chronic
Acute - Nursing considerations for HTN drug therapy
1. take BP & HR before giving med
2. monitor BP & HR frequently
3. monitor lab values
Chronic - Nursing considerations for HTN drug therapy
1. check BP at home
2. T/L - med use
3. compliance
4. report any AE
CHF - def
heart unable to pump enough bl. to meet metabolic needs.

Manifestation related to inadequate pumping ability of heart.

Ventrical dysfunction causes: red CO, inadequate perfusion, fluid retention.
CHF - etiology
Major causes are HTN, MI.

Others: valve, disease, lung disease, CAD, cardiomyopathy.
Clin. Man. - CHF
1. fatigue
2. pale, cool skin
3. reduced exercise tolerance
4. peripheral edema, ascites
5. pulmonary edema, SOB
6. confusion
7. hepatomegaly - enlarged liver
Meds - CHF (4)
1. Inotropic agents
2. Diuretics
4. Beta Blockers
Inotropic agents
most common - digoxin/lanoxin.

Inc contractility, dec afterload = diuretics
MOA - Inotropic agents
inc contractility.

Inhibits enzyme - sodium potassium ATPase -> promotes Ca accumulation, inc contractility -> inc CO.

HR dec, ventric filling inc.
IND - Inotropic agents

Serum levels: therapeutic range very narrow!!
AE - Inotropic agents
predisposing factor: hypokalemia. Dig and K bind at same sites.

If K levels high, dig won't be effective & vice versa.

Digoxin toxicity:
Early S/Sx: visual changes, anorexia, n/v, fatigue.
Late S/Sx: dysrhythmias. Dig dec HR -> block AV node -> cardiac arrest or vfib

Antidote: digibind
DI - Inotropic agents
diuretics: K loss
Quinidine: causes Dig levels to double
Verapamil: CCB, inc Dig levels
Nursing considerations - Inotropic agents
monitor apical HR for 1 min before giving.

Don't give if HR <60.

Monitor serum K level, digoxin level

T/L how to monitor own pulse
Diuretics - CHF
inc renal excretion of water, Na, other e-lytes.

Inc UO, dec fluid overload - dec pulmonary and peripheral edema.

Loop, thiazide diuretics. Lasixs. Loops are more effective/stronger but inc K loss so supplement
can't use w/ kidney failure. Dec aldosterone levels

1. Vasodilation - dec BP
2. dec bl. volume since it reduces retention of Na nad H20.
3. reverses pathological changes in heart and bl. vessels. Prevents further damage.
block beta1 receptors in heart, dec sympathetic effects. This causes:

1. dec in HR
2. dec in force of contraction but w/ dig, it balances out.
3. reduced velocity of impulse conduction.
Dysrhythmias - def
abnormal heart rates and rhythms caused by disturbance of impulse formation (automaticity) or disturbances in the conduction system.

Most common causes: MIs, e-lyte imbalances (Ca & K), meds (dig), acid-base imbalances.
Types of dysrythmias (2)
1. supraventricular
2. ventricular
Supraventricular dysrhythmias
Outside ventricals

a. atrial flutter: causes a dec in vent filling, dec in CO. Atria contracting rapidly. Leads to CHF & atrial fib.

b. atrial fibrillation: atria quiver, no contraction, pooling of bl. Causes dec in CO, CHF, bl. clots.
Ventricular dysrhythmias
a. ventricular tachycardia: CO dec
b. ventricular fibrillation: HR not measurable. No contraction, no CO.
Classification of Anti-dysrhythmic drugs: Vaughan Williams Classification
1. Class I: Na channel blockers - IA, IB, IC
2. Class II: BB
3. K Channel blockers
Class I: Na Channel Blockers
block cardiac sodium channels.

Slows impulse conduction in atria, ventricles and the His-purkinge system.
Class 1A
quinidine (most common)
Class 1B
lidocaine/Xylocaine (most common)
Class 1C
not used as often

MOA - Class 1A
slows impulse conduction in atria, ventricles and the His-purkinge sys. Delays repolarization. Blocks Na channels. Slows recovery -> rate
IND - Class 1A
ssupraventricular and ventricular dysrhythmias
AE - Class 1A
cinchonism: tinnitus, HA, nausea, vertigo - syndrome of Sx
cardiotoxicity at [high] -> cardiac arrest or blockage of AV node. Slows down heart too much
DI - Class 1A
digoxin - doubles effect of dig

warfarin: intensifies effects of coumadin/warfarin
MOA - Class 1B Lidocaine
slows impulse conduction in atria, ventricles and His-purkinge system. Reduces automaticity in ventricles, accelerates repolarization.
IND - Class 1B Lidocaine
ventricular dysrhythmias following an MI b/c prevents vents from taking over.
AE - Class 1B Lidocaine
given IV - few AE.

High doses: drowsiness, confusion, numbness, tingling.

Toxic doses: resp failure.
Class II: BB
reduce sympathetic effects on heart.

a. dec automatically in SA node
b. slows impulse conduction in AV node
c. reduces contractility of atria and ventricles
IND - Class II BB
any type of tachycardia.

BB = "-ol"
Most common one used in propanolol.
Class III: K channel blockers
block K channels. Delays repolarization of heart, reducing conduction velocity and dec contractility.
MOA - Amiodarone/cordarone
causes reduced conduction velocity, dec contractility.

Also acts on coronary and peripheral bl. vessels -> promote dilation.

IND - Amiodarone/cordarone
life-threatening ventricular dysrhythmias

Half-life: ~120 days, so stays in body & toxic effects for long time.
AE - Amiodarone/cordarone
pulmonary toxicity
ocular effects
thyroid dysfunction
DI - Amiodarone/cordarone
grapefruit juice - changes in metabolis inc levels
digoxin, warfarin, quinidine - inc effects
BB, verapamil, diltiazem - inc risk of bradycardia
Class IV CCB
same effects as BB

a. dec automaticity in SA node
b. slows impulse conduction in AV node
c. reduces myocardial contractility
IND - Class IV CCB
supraventricular dysrhythmias
Only 2 that are effective:
1. diltiazem/Cardizem
2. verapamil/isoptin, calan
Class V Others (2)
reduce automaticity of SA node, dec impulse conduction in AV.

1. digoxin: all supraventricular dysrhythmias
2. Adenosine/adenocard: only for supraventricular tachycardia
Meds - Angina (3)
Purpose of meds: reduce myocardial demand for O2, inc O2 delivery to heart

1. organic nitrates
2. CCB
3. BB
Organic nitrates
cause vasodilation.

MOA - organic nitrates
NTG acts directly on vascular smooth muscle, veins, causing vasodilation -> dec venous return to heart, dec ventricular filling, dec preload -> dec in O2 demand.
Routes of administration - organic nitrates for rapid acting for acute attacks(3)
1. sublingual tablet (nitrostat): absorbed easily, bypass liver. If pain continues, q 5 mins but no more than 3 tablets.
2. ligual spray (nitrolingual): also on tongue
3. IV (tridil)
Routes of administration - organic nitrates for long acting for prevention (3)
1. nitroglycerin patches (Nitro-dur) to chest/arm. Slow release
2. nitroglycerin ointment (Nitropaste): acute care, apply on paper to chest
3. po: sustained released, thick coating
AE - organic nitrates
orthostatic hypotension
reflex tachycardia
DI - organic nitrates
antihypertensive meds: NTG can intensify effects. Risk of hypotension.

ED meds (viagara/levitra) intensify vasodilation
Nursing consideration - organic nitrates
monitor BP b/c risk of hypotension - get up slowly

pt T/L: use/administration/storage

Other nitrates: prevent Isosorbide dinitrate (isordil_, Isosorbide mononitrate(Imdur).
CCB - angina
affect bl. vessels and/or heart. Reduce demand of O2 and inc supply of O2 to heart by causing

a. vasodilation
b. dec force of contraction
c. dec HR
d. dec velocity of contraction/strength
BB - angina
dec sympathetic effects on heart, reduce demand of O2 by:

a. dec HR
b. dec force of contraction
c. reduced velocity of impulse conduction
Meds used for MI (9)
Help manage pain, inc O2 delivery o heart, dec demand of O2, restore bl. flow thru coronary arteries

1. morphine
2. NTG - dec demand, vasodil for O2
3. ACE I
4. CCB - inc O2 delivery dec demand
5. lidocaine - prevent ventricular dysrhythmias
6. lipid lowering agents - some sort of statin
7. antiplatelets - aspirin
8. anticoagulants (heparin) - break down bl. clots, restores coronary arteries
9. thrombolytics

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