Cardiodrugs

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Information about Cardiodrugs
Health & Medicine

Published on June 2, 2009

Author: tozki

Source: slideshare.net

Cardiovascular Drugs Ma. Tosca Cybil A. Torres, RN, MAN

Learning Objectives Students will be able to: Discuss the major categories of drugs as they relate to the treatment of Cardiac Disease. Describe the major effects of various medications on cardiac function. Discuss major nursing implications when administering above medications.

Students will be able to:

Discuss the major categories of drugs as they relate to the treatment of Cardiac Disease.

Describe the major effects of various medications on cardiac function.

Discuss major nursing implications when administering above medications.

Antihypertensive

Hypertension Defined as a consistent elevation of the systolic or diastolic blood pressure above 140/90mm Hg On two elevated readings (sitting and supine) on separate office visits Two types hypertension Primary: no known cause Secondary: consequence of underlying disease or condition

Defined as a consistent elevation of the systolic or diastolic blood pressure above 140/90mm Hg

On two elevated readings (sitting and supine) on separate office visits

Two types hypertension

Primary: no known cause

Secondary: consequence of underlying disease or condition

CLASSIFICATION OF HYPERTENSION Hypertension is classified as follows: Prehypertension: BP 120 to 139 / 80 to 89 mm Hg Hypertension , Stage 1: BP 140 to 159 / 90 to 99 mm Hg Hypertension , Stage 2: systolic BP greater than or equal to 160 or diastolic BP greater than or equal to 100 mm Hg.

CLASSIFICATION OF HYPERTENSION

Hypertension is classified as follows:

Prehypertension: BP 120 to 139 / 80 to 89 mm Hg

Hypertension , Stage 1: BP 140 to 159 / 90 to 99 mm Hg

Hypertension , Stage 2: systolic BP greater than or equal to 160 or diastolic BP greater than or equal to 100 mm Hg.

Goal with hypertension: Two primary regulatory factors: Blood flow (volume) Peripheral Vascular Resistance (PVR) Goal is to optimise these two in order to get pressure below 140/90 mm Hg

Two primary regulatory factors:

Blood flow (volume)

Peripheral Vascular Resistance (PVR)

Goal is to optimise these two in order to get pressure below 140/90 mm Hg

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Pharmacotherapy Primary: Diuretics ACE Inhibitors ARBs Beta-blockers Calcium channel blockers Alternate: Alpha 1 -blockers Alpha 2 -blockers Direct-acting vasodilators Peripheral adrenergic antagonist

Primary:

Diuretics

ACE Inhibitors

ARBs

Beta-blockers

Calcium channel blockers

Alternate:

Alpha 1 -blockers

Alpha 2 -blockers

Direct-acting vasodilators

Peripheral adrenergic antagonist

 

Diuretics Therapeutic Effects (overall) General site of action is the nephron structure in the kidney (exact area depends on drug) Increases urine formation and output resulting in a net loss of H 2 O from the body and decreased BP

Therapeutic Effects (overall)

General site of action is the nephron structure in the kidney (exact area depends on drug)

Increases urine formation and output resulting in a net loss of H 2 O from the body and decreased BP

Loop Diuretics Mechanism of action: Inhibits Na + and Cl - resorption in the loop of Henle and so H 2 O (water follows sodium) Dilates blood vessels

Mechanism of action:

Inhibits Na + and Cl - resorption in the loop of Henle and so H 2 O (water follows sodium)

Dilates blood vessels

Loop Diuretics Therapeutic effects: Potent diuresis resulting in substantial fluid loss Treats edema associated with CHF and hepatic or renal disease Adverse effects: hypokalemia metabolic alkalosis dehydration (hypovolemia), leading to hypotension dose-related hearing loss (ototoxicity)

Therapeutic effects:

Potent diuresis resulting in substantial fluid loss

Treats edema associated with CHF and hepatic or renal disease

Adverse effects:

hypokalemia

metabolic alkalosis

dehydration (hypovolemia), leading to hypotension

dose-related hearing loss (ototoxicity)

Loop Diuretics Specific Drugs furosemide Torsemide bumetanide Nursing actions: Monitor I/O and BP Monitor effects of Lanoxin (digoxin) Baseline and close monitoring of K+ Assess for: Dehydration Hypotension Hearing loss

Specific Drugs

furosemide

Torsemide

bumetanide

Nursing actions:

Monitor I/O and BP

Monitor effects of Lanoxin (digoxin)

Baseline and close monitoring of K+

Assess for:

Dehydration

Hypotension

Hearing loss

Thiazide Mechanism of action: inhibit the sodium-chloride transporter in the distal tubule . Because this transporter normally only reabsorbs about 5% of filtered sodium, these diuretics are less efficacious than loop diuretics in producing diuresis and natriuresis.

Mechanism of action:

inhibit the sodium-chloride transporter in the distal tubule . Because this transporter normally only reabsorbs about 5% of filtered sodium, these diuretics are less efficacious than loop diuretics in producing diuresis and natriuresis.

Thiazide Therapeutic effects: Excretion of Na + , Cl - , K + and H 2 O without altering pH Treatment of edema Side effects Hypokalemia Headache, dizziness

Therapeutic effects:

Excretion of Na + , Cl - , K + and H 2 O without altering pH

Treatment of edema

Side effects

Hypokalemia

Headache, dizziness

Thiazide Specific Drug Hydrodiuril (hydrochlorthiazide) Zaroxolyn (Metolazone)

Specific Drug

Hydrodiuril (hydrochlorthiazide)

Zaroxolyn (Metolazone)

NCs: Thiazide Nursing actions: Monitor I/O, BP and K + Monitor effects of Lanoxin (digoxin) Monitor electroytes Adequate dietary K+ Monitor uric acid Crosses placenta and into breastmilk

Nursing actions:

Monitor I/O, BP and K +

Monitor effects of Lanoxin (digoxin)

Monitor electroytes

Adequate dietary K+

Monitor uric acid

Crosses placenta and into breastmilk

Potassium Sparing Diuretics Mechanism of action: antagonize the actions of aldosterone ( aldosterone receptor antagonists ) at the distal segment of the distal tubule. This causes more sodium (and water) to pass into the collecting duct and be excreted in the urine. Therapeutics effects: Diuresis Decreased K + excretion

Mechanism of action:

antagonize the actions of aldosterone ( aldosterone receptor antagonists ) at the distal segment of the distal tubule. This causes more sodium (and water) to pass into the collecting duct and be excreted in the urine.

Therapeutics effects:

Diuresis

Decreased K + excretion

Potassium Sparing Diuretics cont Adverse effects: Electrolyte imbalance with potential elevation in K + Headache, dizziness Prototype: Aldactone (spironolactone)

Adverse effects:

Electrolyte imbalance with potential elevation in K +

Headache, dizziness

Prototype:

Aldactone (spironolactone)

NCs: Potassium Sparing Diuretics Nursing actions: Monitor I/O, BP and K + Monitor effects of Lanoxin (digoxin) No salt substitutes or K+ rich foods Contraindicated: Pregnancy, lactation Initial and follow-up uric acid levels Monitor CBC Watch for s/s of infection Spironalactone Gynecomastia Testicular atrophy Hirsutism

Nursing actions:

Monitor I/O, BP and K +

Monitor effects of Lanoxin (digoxin)

No salt substitutes or K+ rich foods

Contraindicated:

Pregnancy, lactation

Initial and follow-up uric acid levels

Monitor CBC

Watch for s/s of infection

Spironalactone

Gynecomastia

Testicular atrophy

Hirsutism

Calcium Channel Blockers Mechanism of action: Inhibits transport of calcium into myocardial and smooth muscle cells Dilates peripheral arterioles, decreasing afterload Decreases heart contractility (negative ionotrope) Decreases SA node firing rate and conductivity of AV node (negative chronotrope)

Mechanism of action:

Inhibits transport of calcium into myocardial and smooth muscle cells

Dilates peripheral arterioles, decreasing afterload

Decreases heart contractility (negative ionotrope)

Decreases SA node firing rate and conductivity of AV node (negative chronotrope)

Calcium Channel Blockers cont. Therapeutic Effects: Lowers HR and BP- Depending on drug in class Decreases myocardial O 2 demand Decreases coronary artery spasm Decreases angina and rhythm disturbances

Therapeutic Effects:

Lowers HR and BP- Depending on drug in class

Decreases myocardial O 2 demand

Decreases coronary artery spasm

Decreases angina and rhythm disturbances

Calcium Channel Blockers cont. Side effects: Bradycardia, reflex tachycardia Peripheral edema Interactions: Other antihypertensives and diuretics (increased hypotensive effects)

Side effects:

Bradycardia, reflex tachycardia

Peripheral edema

Interactions:

Other antihypertensives and diuretics (increased hypotensive effects)

Calcium Channel Blockers cont. Prototypes: Calan (verapamil), Cardiazem (diltiazem) and Norvasc (amlodipine) Nursing considerations: Monitor BP, HR, I/O, daily weight, side effects Focus assessment-cardiac and pulmonary

Prototypes:

Calan (verapamil), Cardiazem (diltiazem) and Norvasc (amlodipine)

Nursing considerations:

Monitor BP, HR, I/O, daily weight, side effects

Focus assessment-cardiac and pulmonary

NCs: Calcium Channel Blockers Baseline ECG, HR, BP Frequent assessment of VS Contraindicated: complete heart block Pregnancy Category C No grapefruit juice May worsen Heart Failure Evaluate any c/o chest pain

Baseline ECG, HR, BP

Frequent assessment of VS

Contraindicated:

complete heart block

Pregnancy Category C

No grapefruit juice

May worsen Heart Failure

Evaluate any c/o chest pain

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RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS) Angiotensinogen in plasma Juxtaglomerular cells-kidney ↓ Serum Sodium ↓Blood volume Angiotensin I Kidney tubules Angiotensin II Adrenal Cortex ↑ Sodium resorption (H2O resorbed with sodium); ↑ Blood volume RENIN Angiotensin-converting enzyme ALDOSTERONE Intestine, sweat glands, Salivary glands Via vasoconstriction of arterial smooth muscle

Angiotensin Converting Enzyme Inhibitors (ACE-I)- “prils” Mechanism: Blocks interaction between Angiotensin I and Renin, preventing production of Angiotensin II Angiotensin II not produce resulting in decreased vasoconstriction and decreased afterload Decreased aldosterone production results in decreased Na and H 2 O reabsorption so decreased BP

Mechanism: Blocks interaction between Angiotensin I and Renin, preventing production of Angiotensin II

Angiotensin II not produce resulting in decreased vasoconstriction and decreased afterload

Decreased aldosterone production results in decreased Na and H 2 O reabsorption so decreased BP

Angiotensin Converting Enzyme Inhibitors (ACE-I)- “prils” cont. Adverse Effects Most common: dry, nonproductive cough Dizziness, increased potassium levels Interactions: Other antihypertensives and diuretics (increased hypotensive effects) Prototypes: Vasotec (enalapril) and Zestril (lisinopril)

Adverse Effects

Most common: dry, nonproductive cough

Dizziness, increased potassium levels

Interactions: Other antihypertensives and diuretics (increased hypotensive effects)

Prototypes:

Vasotec (enalapril) and Zestril (lisinopril)

 

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NCs: ACE Inhibitors Baseline VS Captopril- oral dose 1 hour pc First dose phenomenon IV: monitor BP carefully Monitor for Angioedema Monitor K+, CBC Assess for S/S infection Pregnancy Category D Assess for minor side effects

Baseline VS

Captopril- oral dose 1 hour pc

First dose phenomenon

IV: monitor BP carefully

Monitor for Angioedema

Monitor K+, CBC

Assess for S/S infection

Pregnancy Category D

Assess for minor side effects

Angiotensin II Receptor Blockers (ARB’s)- “sartans” Mechanism of action: Blocks binding of Angiotensin II to its receptor sites Therapeutic effects Decreased BP: Decreased vasoconstriction, decreased vascular resistance, decreased afterload Major use is afterload reduction in CHF and MI Frequently a second line treatment for patients who do not tolerate ACE-I

Mechanism of action: Blocks binding of Angiotensin II to its receptor sites

Therapeutic effects

Decreased BP: Decreased vasoconstriction, decreased vascular resistance, decreased afterload

Major use is afterload reduction in CHF and MI

Frequently a second line treatment for patients who do not tolerate ACE-I

Angiotensin II Receptor Blockers (ARB’s)- “sartans” cont. Adverse effects Most common is headache Interactions: Other antihypertensives and diuretics (increased hypotensive effects) Prototype: Cozaar (losartan) and Diovan (valsartan)

Adverse effects

Most common is headache

Interactions: Other antihypertensives and diuretics (increased hypotensive effects)

Prototype:

Cozaar (losartan) and Diovan (valsartan)

Angiotensin II Receptor Blockers (ARB’s)- “sartans” cont Nursing considerations Monitor BP, I/O, daily weight, side effects Monitor Potassium levels and renal function Reinforce patient education Contraindicated to pregnant women Can be taken without regard to food First Dose Phenomenon Orthostatic BP checks Monitor renal, hepatic, and electrolyte level

Nursing considerations

Monitor BP, I/O, daily weight, side effects

Monitor Potassium levels and renal function

Reinforce patient education

Contraindicated to pregnant women

Can be taken without regard to food

First Dose Phenomenon

Orthostatic BP checks

Monitor renal, hepatic, and electrolyte level

Beta Blockers- “olols Mechanism of action: Cardioselective: Bind to and block B 1 receptors on the hearts conduction system and throughout the myocardium Nonselective: bind to, and block, B 1 and B 2 receptors (heart and lungs) Decreases heart contractility (Negative ionotrope) reducing O 2 requirements of myocardial cells Decrease SA node firing rate (negative chronotrope)

Mechanism of action:

Cardioselective: Bind to and block B 1 receptors on the hearts conduction system and throughout the myocardium

Nonselective: bind to, and block, B 1 and B 2 receptors (heart and lungs)

Decreases heart contractility (Negative ionotrope) reducing O 2 requirements of myocardial cells

Decrease SA node firing rate (negative chronotrope)

Beta Blockers- “olols cont. Therapeutic Effects Decreased heart rate and decreased myocardial oxygen demand Decreased angina Fewer rhythm disturbances Decreased renin release

Therapeutic Effects

Decreased heart rate and decreased myocardial oxygen demand

Decreased angina

Fewer rhythm disturbances

Decreased renin release

Beta Blockers- “olols cont. Adverse effects: Dysrhythmias (bradycardia), heart failure Bronchospasm / bronchoconstriction Fatigue, depression, impotence Interactions: Other antihypertensives and diuretics (increased hypotensive effects)

Adverse effects:

Dysrhythmias (bradycardia), heart failure

Bronchospasm / bronchoconstriction

Fatigue, depression, impotence

Interactions:

Other antihypertensives and diuretics (increased hypotensive effects)

Beta Blockers- “olols cont. Prototypes: Inderal (propranolol), Lopressor (metoprolol) and Tenormin (atenolol) Nursing Actions: Monitor BP, HR, I/O, daily weight, side effects Focus assessment-cardiac and pulmonary Contrindicated with some dysrhythmias, CHF and some lung diseases

Prototypes:

Inderal (propranolol), Lopressor (metoprolol) and Tenormin (atenolol)

Nursing Actions:

Monitor BP, HR, I/O, daily weight, side effects

Focus assessment-cardiac and pulmonary

Contrindicated with some dysrhythmias, CHF and some lung diseases

NCs: Beta-adrenergic Blockers May take two weeks for optimal therapeutic response Check BP and pulse prior to dose Monitor cardiac function Assess for: Respiratory distress Bradycardia, heart block, fatigue, activity intolerance DO NOT STOP SUDDENLY

May take two weeks for optimal therapeutic response

Check BP and pulse prior to dose

Monitor cardiac function

Assess for:

Respiratory distress

Bradycardia, heart block, fatigue, activity intolerance

DO NOT STOP SUDDENLY

 

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Alpha 1 -adrenergic Antagonists Mechanism of action -selectively inhibits alpha-1 adrenergic receptors. Blockages of the alpha-1 adrenergic action on the vascular smooth muscles lead to a decrease in vascular resistance and antihypertensive activity.

Mechanism of action

-selectively inhibits alpha-1 adrenergic receptors. Blockages of the alpha-1 adrenergic action on the vascular smooth muscles lead to a decrease in vascular resistance and antihypertensive activity.

NCs: Alpha 1 -adrenergic Blockers First dose phenomenon Assess BP prior to and during RX Persistent orthostatic hypotension Assess for: Weakness, dizziness, headache, GI complaints Closely monitor elderly

First dose phenomenon

Assess BP prior to and during RX

Persistent orthostatic hypotension

Assess for:

Weakness, dizziness, headache, GI complaints

Closely monitor elderly

 

Direct Vasodilators Relaxes smooth muscle in arterioles  < PVR Highly effective but many side effects (some serious) Reflex tachycardia Sodium/water retention Not a first choice drug Primary use: emergency situations where immediate ↓ in BP is needed

Relaxes smooth muscle in arterioles  < PVR

Highly effective but many side effects (some serious)

Reflex tachycardia

Sodium/water retention

Not a first choice drug

Primary use: emergency situations where immediate ↓ in BP is needed

NCs: Direct Vasodilators Monitor: VS, ECG, SpO 2 during RX Assess for increased HR BP q 5 min if not continuous monitor Contraindicated: hypersensitivity, CAD, rheumatic mitral valve disease, CVA, renal insufficiency, SLE Priapism- medical emergency

Monitor: VS, ECG, SpO 2 during RX

Assess for increased HR

BP q 5 min if not continuous monitor

Contraindicated: hypersensitivity, CAD, rheumatic mitral valve disease, CVA, renal insufficiency, SLE

Priapism- medical emergency

Direct Vasodilators IV Nitroprusside (Nitropress): Continuously monitored Only dilute in D 5 W Brown color; protect from light Minoxidil (Loniten): BP & pulse both arms, three positions Assess for orthostatic hypotension Diazoxide (Hyperstat): For hypetensive crisis in L&D

IV Nitroprusside (Nitropress):

Continuously monitored

Only dilute in D 5 W

Brown color; protect from light

Minoxidil (Loniten):

BP & pulse both arms, three positions

Assess for orthostatic hypotension

Diazoxide (Hyperstat):

For hypetensive crisis in L&D

Cardiac Glycosides, Antianginals, Antidysrhythmics

Cardiac Glycosides, Antianginals, Antidysrhythmics

Cardiac Glycosides AKA digitalis glycosides Group of drugs that inhibit the sodium-potassium pump, thus increasing intracellular calcium which causes cardiac muscle fibers to contract more efficiently

AKA digitalis glycosides

Group of drugs that inhibit the sodium-potassium pump, thus increasing intracellular calcium which causes cardiac muscle fibers to contract more efficiently

Action Potential

Cardiac Glycosides Therapeutic Effects Positive Inotropic action Negative Chronotropic action Negative Dromotropic effect

Therapeutic Effects

Positive Inotropic action

Negative Chronotropic action

Negative Dromotropic effect

Inotropes

Inotropes Agents that affect myocardial contraction Positive Inotropes Cardiac glycosides Catecholamines Negative Inotropes BB CCB Class IA & IC anti-arrhythmics

Agents that affect myocardial contraction

Positive Inotropes

Cardiac glycosides

Catecholamines

Negative Inotropes

BB

CCB

Class IA & IC anti-arrhythmics

Class Participation Which of the following is an example of a positive inotrope? Docusate Digoxin HCTZ Propranolol Nitroglycerin

Which of the following is an example of a positive inotrope?

Docusate

Digoxin

HCTZ

Propranolol

Nitroglycerin

Class Participation Which of the following is an example of a positive inotrope? Docusate Digoxin HCTZ Propranolol Nitroglycerin

Which of the following is an example of a positive inotrope?

Docusate

Digoxin

HCTZ

Propranolol

Nitroglycerin

Cardiac Glycosides Prototype: Digoxin (Lanoxin ® , Digitek ® , Lanoxicaps ® )

Prototype: Digoxin (Lanoxin ® , Digitek ® , Lanoxicaps ® )

Digoxin MOA

Digoxin (cont’d) Nursing Responsibilities Assess heart rate before administration; if below 60 bpm withhold the drug. Monitor serum potassium Assess for signs of Digitalis toxicity Bradycardia GI manifestations (anorexia, nausea, vomiting and diarrhea) Dysrhythmias Altered visual perceptions In males: gynecomastia, decreased libido and impotence

Nursing Responsibilities

Assess heart rate before administration; if below 60 bpm withhold the drug.

Monitor serum potassium

Assess for signs of Digitalis toxicity

Bradycardia

GI manifestations (anorexia, nausea, vomiting and diarrhea)

Dysrhythmias

Altered visual perceptions

In males: gynecomastia, decreased libido and impotence

Chronotropes

Chronotropes Agents that change heart rate affects the nerves controlling the heart changes the rhythm produced by the SA node

Agents that change heart rate

affects the nerves controlling the heart

changes the rhythm produced by the SA node

Chronotropes (cont’d) Positive Chronotropes Atropine Quinidine Dopamine Dobutamine Epinephrine Isuprel Negative Chronotropes Beta-blockers Acetylcholine Digoxin Diltiazem Verapamil Ivabradine Metoprolol

Positive Chronotropes

Atropine

Quinidine

Dopamine

Dobutamine

Epinephrine

Isuprel

Negative Chronotropes

Beta-blockers

Acetylcholine

Digoxin

Diltiazem

Verapamil

Ivabradine

Metoprolol

Positive Chronotrope Prototype: Atropine belladonna alkaloid d,l -hyoscyamine Anticholinergic Uses Symptomatic bradycardia Aspiration prophylaxis Produces mydriasis Organophosphate toxicity Adjunct nerve agent & insecticide poisoning

Prototype: Atropine

belladonna alkaloid

d,l -hyoscyamine

Anticholinergic

Uses

Symptomatic bradycardia

Aspiration prophylaxis

Produces mydriasis

Organophosphate toxicity

Adjunct nerve agent & insecticide poisoning

Atropine (cont’d) MOA competitive inhibitor at autonomic postganglionic cholinergic receptors Clinical effects “ anti-SLUD” S alivation, L acrimation, U rination, D igestion, D efecation ↓ in salivary bronchial, & sweat gland secretions; mydriasis; changes in heart rate; contraction of the bladder detrusor muscle and of the GI smooth muscle; ↓ gastric secretion; and ↓ GI motility

MOA

competitive inhibitor at autonomic postganglionic cholinergic receptors

Clinical effects

“ anti-SLUD” S alivation, L acrimation, U rination, D igestion, D efecation

↓ in salivary bronchial, & sweat gland secretions; mydriasis; changes in heart rate; contraction of the bladder detrusor muscle and of the GI smooth muscle; ↓ gastric secretion; and ↓ GI motility

Nursing Responsibilities Monitor HR---note rhythm, quality, and rate Monitor I&O Assess for dryness or mucus membranes Monitor GI function

Monitor HR---note rhythm, quality, and rate

Monitor I&O

Assess for dryness or mucus membranes

Monitor GI function

Anti-anginal Drugs

Antianginal Drugs Prototype: Nitrites & Nitrates BB Calcium Channel Blockers (CCBs)

Prototype: Nitrites & Nitrates

BB

Calcium Channel Blockers (CCBs)

Angina Pectoris Definition: Angina: Choking or suffocation. Pectoris: Chest. Angina pectoris, is the medical term used to describe acute chest pain or discomfort. Angina occurs when the heart’s need for oxygen increases beyond the level of oxygen available from the blood nourishing the heart. It has 3 types Stable Angina Un stable angina & Variant Angina (Prinzmetal’s or resting angina) :

Definition:

Angina: Choking or suffocation.

Pectoris: Chest.

Angina pectoris, is the medical term used to describe acute chest pain or discomfort.

Angina occurs when the heart’s need for oxygen increases beyond the level of oxygen available from the blood nourishing the heart.

It has 3 types

Stable Angina

Un stable angina &

Variant Angina (Prinzmetal’s or resting angina) :

Types of Angina Stable angina : People with stable angina have episodes of chest discomfort that are usually predictable. That occur on exertion or under mental or emotional stress. Normally the chest discomfort is relieved with rest,   nitroglycerin (GTN) or both. It has a stable pattern of onset, duration and intensity of symptoms.

Types of Angina

Stable angina :

People with stable angina have episodes of chest discomfort that are usually predictable. That occur on exertion or under mental or emotional stress.

Normally the chest discomfort is relieved with rest,

  nitroglycerin (GTN) or both.

It has a stable pattern of onset, duration and intensity of symptoms.

Unstable angina: It is triggered by an un predictable degree of exertion or emotion. (progressive), more severe than stable. Characterized by increasing frequency & severity. Provoked by less than usual effort, occurring at rest & interferes with pt lifestyle.

Unstable angina:

It is triggered by an un predictable degree of exertion or emotion.

(progressive), more severe than stable. Characterized by increasing frequency & severity. Provoked by less than usual effort, occurring at rest &

interferes with pt lifestyle.

Variant Angina (Prinzmetal’s or resting angina) : occur spontaneously with no relationship to activity. Occurs at rest due to spasm. Pt discomfort that occurs rest usually of longer duration. Appears to by cyclic & often occurs at about the same time each day (usually at night). Thought to be caused by coronary artery spasm

Variant Angina (Prinzmetal’s or resting angina) :

occur spontaneously with no relationship to activity. Occurs at rest due to spasm. Pt discomfort that occurs rest usually of longer duration. Appears to by cyclic & often occurs at about the same time each day (usually at night). Thought to be caused by coronary artery spasm

Symptoms of Angina

Nitrites/Nitrates Previously known as “coronary dilators” Main effect: to produce general vasodilation of systemic vein & arteries ↓ preload & ↓afterload ↓ cardiac work & oxygen consumption 2 main uses Angina attacks Angina prophylaxis

Previously known as “coronary dilators”

Main effect: to produce general vasodilation of systemic vein & arteries

↓ preload & ↓afterload

↓ cardiac work & oxygen consumption

2 main uses

Angina attacks

Angina prophylaxis

Class Participation Which is the PREFERRED route for nitroglycerin during angina attacks? Topical (ointment 2%) IV infusion Transdermal SL Extended release tablets/capsules

Which is the PREFERRED route for nitroglycerin during angina attacks?

Topical (ointment 2%)

IV infusion

Transdermal

SL

Extended release tablets/capsules

Class Participation Which is the PREFFERED route for nitroglycerin during angina attacks? Topical (ointment 2%) IV infusion Transdermal SL Extended release tablets/capsules

Which is the PREFFERED route for nitroglycerin during angina attacks?

Topical (ointment 2%)

IV infusion

Transdermal

SL

Extended release tablets/capsules

Drug (Trade Name) Common Dosage Onset Duration Amyl nitrate (Vaporole ® ) 0.3 ml inhalation 30-60 sec 10 min ISDN (Isordil ® ) 2.5 - 10 mg SL 5 - 30 mg po qid 2-5 min 2 - 4 hr Nitroglycerin ( Nitro-bid ® ) 2% ointment 15 min 4 - 8 hr ( Nitrostat ® ) 0.3 - 0.6 mg SL 1-3 min 10 - 45 min ( Nitrogard ® ) 1,2,3 mg XR tab 30 min 8 - 12 hr ( Transderm-Nitro ® ) 2.5 - 15 mg/day Transdermal patch 30-60 min 24 hr

MOA Direct relaxation of arterial and venous smooth muscle Venodilation predominates at therapeutic doses which reduces preload Arteriodilation at high doses (high therapeutic/toxic) which produces hypotension compensated by sympathetics (heart/vascular)to produce tachycardia

Direct relaxation of arterial and venous smooth muscle

Venodilation predominates at therapeutic doses which reduces preload

Arteriodilation at high doses (high therapeutic/toxic) which produces hypotension compensated by sympathetics (heart/vascular)to produce tachycardia

Nitroglycerin (NG) Indications Angina Acute MI HF HTN Hypertensive emergency Hypotension induction Peri/postoperative HTN Pulmonary edema Pulmonary HTN

Indications

Angina

Acute MI

HF

HTN

Hypertensive emergency

Hypotension induction

Peri/postoperative HTN

Pulmonary edema

Pulmonary HTN

NG (cont’d) Dosing 1 tablet (0.3 mg, 0.4 mg, or 0.6 mg strength) SL, dissolved under the tongue or in buccal pouch immediately following indication of anginal attack During drug administration, the patient should rest, preferably in the sitting position Symptoms typically improve within 5 minutes. If needed for immediate relief of stable angina symptoms, SL nitroglycerin may be repeated every 5 minutes as needed, up to 3 doses

Dosing

1 tablet (0.3 mg, 0.4 mg, or 0.6 mg strength) SL, dissolved under the tongue or in buccal pouch immediately following indication of anginal attack

During drug administration, the patient should rest, preferably in the sitting position

Symptoms typically improve within 5 minutes. If needed for immediate relief of stable angina symptoms, SL nitroglycerin may be repeated every 5 minutes as needed, up to 3 doses

NG (cont’d) Adverse Effects dizziness or fainting flushing of the face or neck headache, this is common after a dose, but usually only lasts for a short time irregular heartbeat, palpitations nausea, vomiting Contraindication: sildenafil (Viagra®) tadalafil (Cialis®) vardenafil (Levitra ®) Lab monitoring not necessary

Adverse Effects

dizziness or fainting

flushing of the face or neck

headache, this is common after a dose, but usually only lasts for a short time

irregular heartbeat, palpitations

nausea, vomiting

Contraindication:

sildenafil (Viagra®)

tadalafil (Cialis®)

vardenafil (Levitra ®)

Lab monitoring not necessary

Antidysrhythmics Antiarrhythmics

What are Arrhythmias? Cardiac disorder of Rate Rhythm Impulse generation Conduction of electrical impulses in the heart Causes May develop from a diseased heart Consequence of chronic drug therapy Symptoms Mild palpitations  cardiac arrest Treatment goal Covert arrhythmia to a normal rhythm

Cardiac disorder of

Rate

Rhythm

Impulse generation

Conduction of electrical impulses in the heart

Causes

May develop from a diseased heart

Consequence of chronic drug therapy

Symptoms

Mild palpitations  cardiac arrest

Treatment goal

Covert arrhythmia to a normal rhythm

Antidysrhythmics/Antiarrhythmics Uses restore normal cardiac rhythm Successful conversion of an arrhythmia depends on the type of arrhythmia present

Uses

restore normal cardiac rhythm

Successful conversion of an arrhythmia depends on the type of arrhythmia present

Antidysrhythmics/Antiarrhythmics 4 major classes Class I Class IA Class IB Class IC Class II Class III Class IV

4 major classes

Class I

Class IA

Class IB

Class IC

Class II

Class III

Class IV

Cardiac Action Potential 4: resting membrane potential; steady K+ flux 0: Na+ influx into cell 1: K+ efflux 2: K+ efflux & Ca+ influx 3: K+ efflux

4: resting membrane potential; steady K+ flux

0: Na+ influx into cell

1: K+ efflux

2: K+ efflux & Ca+ influx

3: K+ efflux

Antiarrthymics: Class I Na channel blockers Common features Local anesthetic activity Interferes with movement of Na ions Slow conduction velocity Prolong refractory period Decreases automaticity of the heart

Na channel blockers

Common features

Local anesthetic activity

Interferes with movement of Na ions

Slow conduction velocity

Prolong refractory period

Decreases automaticity of the heart

Class I A Quinidine (Quinidine sulfate ® , Quinaglute ® , Quinidex ® , Cardioquin ® ) Disopyramide (Norpace ® ) Procainimide (Procainimide HCI ® , Procan ® , Procanabid ® , Pronestyl ® )

Quinidine (Quinidine sulfate ® , Quinaglute ® , Quinidex ® , Cardioquin ® )

Disopyramide (Norpace ® )

Procainimide (Procainimide HCI ® , Procan ® , Procanabid ® , Pronestyl ® )

Class 1A – Quinidine Derived from cinchona tree Depresses both the myocardium & conduction system Overall effect: slows heart rate Pharmacokinetics Well absorbed in GI tract after po administration Metabolized to several active metabolites Primarily excreted by urinary tract Cardiac poison when large amounts are present in blood

Derived from cinchona tree

Depresses both the myocardium & conduction system

Overall effect: slows heart rate

Pharmacokinetics

Well absorbed in GI tract after po administration

Metabolized to several active metabolites

Primarily excreted by urinary tract

Cardiac poison when large amounts are present in blood

Class 1A – Quinidine (cont’d) Adverse Effects N/V, diarrhea, weakness, fatigue, cinchonism Drug Interactions Hyperkalemia Digitalis propranolol Monitoring CBC ECG serum quinidine concentrations (target range 2-6 µg/ml or higher) CI: AV block

Adverse Effects

N/V, diarrhea, weakness, fatigue, cinchonism

Drug Interactions

Hyperkalemia

Digitalis

propranolol

Monitoring

CBC

ECG

serum quinidine concentrations (target range 2-6 µg/ml or higher)

CI: AV block

Class I B prototype: Lidocaine (Xylocaine®) Tocainide (Tonocard®) Mexiletene (Mexitel®) Phenytoin (Dilantin®)

prototype: Lidocaine (Xylocaine®)

Tocainide (Tonocard®)

Mexiletene (Mexitel®)

Phenytoin (Dilantin®)

Lidocaine – Class IB MOA: blocks influx of Na fast channel Indication: ventricular arrhythmias

MOA: blocks influx of Na fast channel

Indication: ventricular arrhythmias

Lidocaine – Class IB (cont’d) Common Adverse Effects anxiety, nervousness dizziness, drowsiness feelings of coldness, heat, or numbness; or pain at the site of the injection N/V Monitoring serum lidocaine concentrations (target range 2-6 µg/ml): parenteral use

Common Adverse Effects

anxiety, nervousness

dizziness, drowsiness

feelings of coldness, heat, or numbness; or pain at the site of the injection

N/V

Monitoring

serum lidocaine concentrations (target range 2-6 µg/ml): parenteral use

Class I C prototype: Flecainide (Tambocor®) Propafenone (Rhythmol®)

prototype: Flecainide (Tambocor®)

Propafenone (Rhythmol®)

Flecainide – Class IC MOA Blocks fast Na channels depresses the upstroke of the action potential, which is manifested as a decrease in the maximal rate of phase 0 depolarization. significantly slow His-Purkinje conduction and cause QRS widening shorten the action potential of Purkinje fibers without affecting the surrounding myocardial tissue. Indications Afib Atrial flutter Ventricular tachycardia prophylaxis

MOA

Blocks fast Na channels depresses the upstroke of the action potential, which is manifested as a decrease in the maximal rate of phase 0 depolarization.

significantly slow His-Purkinje conduction and cause QRS widening

shorten the action potential of Purkinje fibers without affecting the surrounding myocardial tissue.

Indications

Afib

Atrial flutter

Ventricular tachycardia prophylaxis

Flecainide – Class IC Adverse Reactions visual impairment, dizziness, asthenia, edema, abdominal pain, constipation, headache, fatigue, and tremor, N/V, arrhea, dyspepsia, anorexia, rash, diplopia, hypoesthesia, paresthesia, paresis, ataxia, flushing, increased sweating, vertigo, syncope, somnolence, tinnitus, anxiety, insomnia, and depression. Avoid in CHF Acute MI Hx of MI (LVEF < 30%) Monitoring ECG serum creatinine/BUN: baseline

Adverse Reactions

visual impairment, dizziness, asthenia, edema, abdominal pain, constipation, headache, fatigue, and tremor, N/V, arrhea, dyspepsia, anorexia, rash, diplopia, hypoesthesia, paresthesia, paresis, ataxia, flushing, increased sweating, vertigo, syncope, somnolence, tinnitus, anxiety, insomnia, and depression.

Avoid in

CHF

Acute MI

Hx of MI (LVEF < 30%)

Monitoring

ECG

serum creatinine/BUN: baseline

Class II – Beta Blockers Propranolol (Inderal®) Acebutolol (Sectral®) Atenolol (Tenormin®) Betaxolol (Kerlone®) Bisoprolol (Zebeta®) Carvedilol (Coreg®) Esmolol ( Brevibloc®) Metoprolol(Toprol®, Lopressor®) Nadolol (Corgard®) Timolol (Blocadron®)

Propranolol (Inderal®)

Acebutolol (Sectral®)

Atenolol (Tenormin®)

Betaxolol (Kerlone®)

Bisoprolol (Zebeta®)

Carvedilol (Coreg®)

Esmolol ( Brevibloc®)

Metoprolol(Toprol®, Lopressor®)

Nadolol (Corgard®)

Timolol (Blocadron®)

Propranolol Warning 2 situations in which propranolol requires extreme caution AV block CHF Asthma or emphysema

2 situations in which propranolol requires extreme caution

AV block

CHF

Asthma or emphysema

Class III K+ channel blockers Drugs: Prototype: Amiodarone (Cordarone) Bretylium (Bretylol) Sotalol (Betapace)

K+ channel blockers

Drugs:

Prototype: Amiodarone (Cordarone)

Bretylium (Bretylol)

Sotalol (Betapace)

Amiodarone – Class III MOA noncompetitively inhibits alpha- and beta-receptors, possesses both vagolytic and calcium-channel blocking properties relaxes both smooth and cardiac muscle Indications Vfib Vtach

MOA

noncompetitively inhibits alpha- and beta-receptors,

possesses both vagolytic and calcium-channel blocking properties

relaxes both smooth and cardiac muscle

Indications

Vfib

Vtach

Amiodarone – Class III (cont’d) Monitoring CBC chest x-ray ECG ophthalmologic exam thyroid function tests (TFTs)

Monitoring

CBC

chest x-ray

ECG

ophthalmologic exam

thyroid function tests (TFTs)

Class IV Ca channel blockers Drugs Adenosine (Adenocard ® ) Diltiazim (Cardizem®, Tiazac®) Verapamil (Dovera®, Isoptin®, Calan®) Clinical Effects widen the blood vessels may decrease the heart’s pumping strength

Ca channel blockers

Drugs

Adenosine (Adenocard ® )

Diltiazim (Cardizem®, Tiazac®)

Verapamil (Dovera®, Isoptin®, Calan®)

Clinical Effects

widen the blood vessels

may decrease the heart’s pumping strength

Sympathomimetics

Sympathomimetics 2 classes: α - agonist Phenylephrine Clonidine Oxymetazoline Tetrahydralazine Xylometazoline β -agonist Prototype: Epinephrine Norepinephrine Dopamine Dobutamine Isoproterenol SE: hypertension, excessive cardiac stimulation cardiac arrhythmias Long-term use increases mortality in heart failure patients. CI CAD  

2 classes:

α - agonist

Phenylephrine

Clonidine

Oxymetazoline

Tetrahydralazine

Xylometazoline

β -agonist

Prototype: Epinephrine

Norepinephrine

Dopamine

Dobutamine

Isoproterenol

SE:

hypertension,

excessive cardiac stimulation

cardiac arrhythmias

Long-term use increases mortality in heart failure patients.

CI

CAD  

Epinephrine “ fight or flight “hormone Aka “adrenaline” increases heart rate and stroke volume dilates the pupils constricts arterioles in the skin and gastrointestinal tract while dilating arterioles in skeletal muscles

“ fight or flight “hormone

Aka “adrenaline”

increases heart rate and stroke volume

dilates the pupils

constricts arterioles in the skin and gastrointestinal tract while dilating arterioles in skeletal muscles

Epinephrine MOA

Epinephrine (cont’d) Indications Vfib Ventricular asystole Cardiac arrest Pulseless electrical activity IV Dosage IV: 1 mg (10 ml of a 1:10,000 solution) IV; may repeat every 3-5 minutes Each dose may be given by peripheral injection followed by a 20 ml flush of IV fluid.

Indications

Vfib

Ventricular asystole

Cardiac arrest

Pulseless electrical activity

IV Dosage

IV: 1 mg (10 ml of a 1:10,000 solution) IV; may repeat every 3-5 minutes

Each dose may be given by peripheral injection followed by a 20 ml flush of IV fluid.

Epinephrine Common Adverse Effects anxiety or nervousness dry mouth drowsiness or dizziness headache increased sweating nausea weakness or tiredness Monitoring ECG: in patients receiving IV therapy

Common Adverse Effects

anxiety or nervousness

dry mouth

drowsiness or dizziness

headache

increased sweating

nausea

weakness or tiredness

Monitoring

ECG: in patients receiving IV therapy

Vasopressors

Vasopressors Vasoconstrictors vs. Vasodilators 2 Vasoconstrictor Classes Sympathomimetics Vasopressin Analogs Vasodilators Alpha-adrenoceptor antagonists (alpha-blockers) Angiotensin converting enzyme (ACE) inhibitors Angiotensin receptor blockers (ARBs) Beta2-adrenoceptor agonists (b2-agonists) Calcium-channel blockers (CCBs) Centrally acting sympatholytics Direct acting vasodilators Endothelin receptor antagonists Ganglionic blockers Nitrodilators Phosphodiesterase inhibitors Potassium-channel openers Renin inhibitors

Vasoconstrictors vs. Vasodilators

2 Vasoconstrictor Classes

Sympathomimetics

Vasopressin Analogs

Vasodilators

Alpha-adrenoceptor antagonists (alpha-blockers)

Angiotensin converting enzyme (ACE) inhibitors

Angiotensin receptor blockers (ARBs)

Beta2-adrenoceptor agonists (b2-agonists)

Calcium-channel blockers (CCBs)

Centrally acting sympatholytics

Direct acting vasodilators

Endothelin receptor antagonists

Ganglionic blockers

Nitrodilators

Phosphodiesterase inhibitors

Potassium-channel openers

Renin inhibitors

Vasoconstrictor any agent that produces vasoconstriction and a rise in blood pressure (usually understood as increased arterial pressure) Drugs Prototype: Vasopressin Epinephrine Dobutamine Dopamine Norepinephrine

any agent that produces vasoconstriction and a rise in blood pressure (usually understood as increased arterial pressure)

Drugs

Prototype: Vasopressin

Epinephrine

Dobutamine

Dopamine

Norepinephrine

Vasopressin aka : “ADH” MOA ↑ the resorption of water at the renal collecting ducts Vasoconstrictive property: stimulates the contraction of vascular smooth muscle in coronary, splanchnic, GI, pancreatic, skin, and muscular vascular beds

aka : “ADH”

MOA

↑ the resorption of water at the renal collecting ducts

Vasoconstrictive property: stimulates the contraction of vascular smooth muscle in coronary, splanchnic, GI, pancreatic, skin, and muscular vascular beds

Vasopressin (cont’d) Indications: Cardiac arrest Cardiogenic shock Cardiopulmonary resuscitation Hypotension Septic shock Diabetes Insipidus

Indications:

Cardiac arrest

Cardiogenic shock

Cardiopulmonary resuscitation

Hypotension

Septic shock

Diabetes Insipidus

Vasopressin (cont’d) Dosage for cardiac arrest including ventricular asystole and pulseless electrical activity (PEA) during cardiopulmonary resuscitation (CPR) IV or intraosseous dosage: Adults: A single dose of 40 units IV (or intraosseous) may be given one time to replace the first or second dose of epinephrine during cardiac arrest Do not interrupt cardiopulmonary resuscitation to administer drug therapy.

Dosage for cardiac arrest including ventricular asystole and pulseless electrical activity (PEA) during cardiopulmonary resuscitation (CPR)

IV or intraosseous dosage:

Adults: A single dose of 40 units IV (or intraosseous) may be given one time to replace the first or second dose of epinephrine during cardiac arrest

Do not interrupt cardiopulmonary resuscitation to administer drug therapy.

Vasopressin (cont’d) Adverse Effects Cardiovascular: Cardiac arrest; circumoral pallor; arrhythmias; decreased cardiac output; angina; myocardial ischemia; peripheral vasoconstriction; and gangrene CNS: Tremor; vertigo; “pounding” in head Dermatologic: Sweating; urticaria; cutaneous gangrene GI: Abdominal cramps; nausea; vomiting; passage of gas Hypersensitivity: Anaphylaxis (cardiac arrest and/or shock) has been observed shortly after injection Respiratory: Bronchial constriction. Monitoring serum osmolality serum Na

Adverse Effects

Cardiovascular: Cardiac arrest; circumoral pallor; arrhythmias; decreased cardiac output; angina; myocardial ischemia; peripheral vasoconstriction; and gangrene

CNS: Tremor; vertigo; “pounding” in head

Dermatologic: Sweating; urticaria; cutaneous gangrene

GI: Abdominal cramps; nausea; vomiting; passage of gas

Hypersensitivity: Anaphylaxis (cardiac arrest and/or shock) has been observed shortly after injection

Respiratory: Bronchial constriction.

Monitoring

serum osmolality

serum Na

Anticoagulants

Antiplatelets/Anticoagulants Prevents/interferes with coagulation Uses deep vein thrombosis (DVTs), pulmonary embolism, myocardial infarctions & strokes in those who are predisposed

Prevents/interferes with coagulation

Uses

deep vein thrombosis (DVTs), pulmonary embolism, myocardial infarctions & strokes in those who are predisposed

Types of Antiplatelets/Anticoagulants Antiplatelets Aspirin Dipyridamole Thienopyridines Clopidogrel (Plavix) Ticlopidine (Ticlid) Glycoprotein IIb/IIIa antagonists Abciximab (ReoPro) Eptifibatide (Integrelin) Tirofiban (Aggrastat )

Antiplatelets

Aspirin

Dipyridamole

Thienopyridines

Clopidogrel (Plavix)

Ticlopidine (Ticlid)

Glycoprotein IIb/IIIa antagonists

Abciximab (ReoPro)

Eptifibatide (Integrelin)

Tirofiban (Aggrastat )

Antiplatelets/Anticoagulants Anticoagulants Heparin LMWH Enoxaparin (Lovenox ® ) Dalteparin (Fragmin ® ) Tinzaarin (Innohep ® ) Factor Xa inhibitors Fondaparinux (Arixtra ® ) Direct Thrombin Inhibitors Argatroban Lepirudin (Refludan ® ) Oral Anticoagulants Prototype: Warfarin

Anticoagulants

Heparin

LMWH

Enoxaparin (Lovenox ® )

Dalteparin (Fragmin ® )

Tinzaarin (Innohep ® )

Factor Xa inhibitors

Fondaparinux (Arixtra ® )

Direct Thrombin Inhibitors

Argatroban

Lepirudin (Refludan ® )

Oral Anticoagulants

Prototype: Warfarin

Coagulation Cascade

Warfarin – Oral Anticoagulant MOA: Warfarin inhibits the synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S

MOA: Warfarin inhibits the synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S

Warfarin (cont’d) Indications Stroke DVT Post MI Afib Cardiomyopathy

Indications

Stroke

DVT

Post MI

Afib

Cardiomyopathy

Warfarin Warnings Bleeding Risk! Warfarin can cause major or fatal bleeding Risk factors for bleeding 65 years of age and older history of GI bleeding Hypertension cerebrovascular disease anemia, malignancy Trauma renal function impairment long duration of warfarin therapy. Pregnancy Category X

Bleeding Risk!

Warfarin can cause major or fatal bleeding

Risk factors for bleeding

65 years of age and older

history of GI bleeding

Hypertension

cerebrovascular disease

anemia, malignancy

Trauma

renal function impairment

long duration of warfarin therapy.

Pregnancy Category X

Warfarin (cont’d) SE Hemorrhage: Signs of severe bleeding resulting in the loss of large amounts of blood depend upon the location and extent of bleeding. Symptoms include: chest, abdomen, joint, muscle, or other pain; difficult breathing or swallowing; dizziness; headache; low blood pressure; numbness and tingling; paralysis; shortness of breath; unexplained shock; unexplained swelling; weakness Nursing responsibilities Patients should be instructed about prevention measures to minimize risk of bleeding and to report immediately to health care provider signs and symptoms of bleeding prothrombin time (PT) stool guaiac bleeding DDIs NSAIDs 3 G’s Garlic Ginger Ginsing Vitamin K intake

SE

Hemorrhage: Signs of severe bleeding resulting in the loss of large amounts of blood depend upon the location and extent of bleeding. Symptoms include: chest, abdomen, joint, muscle, or other pain; difficult breathing or swallowing; dizziness; headache; low blood pressure; numbness and tingling; paralysis; shortness of breath; unexplained shock; unexplained swelling; weakness

Nursing responsibilities

Patients should be instructed about prevention measures to minimize risk of bleeding and to report immediately to health care provider signs and symptoms of bleeding

prothrombin time (PT)

stool guaiac

bleeding

DDIs

NSAIDs

3 G’s

Garlic

Ginger

Ginsing

Vitamin K intake

Class Participation Question #5: Which foods are high in vitamin K?

Class Participation Question #5:

Which foods are high in vitamin K?

Class Participation Question #5: Which foods are high in vitamin K?

Class Participation Question #5:

Which foods are high in vitamin K?

Fibrinolytic Enzymes

Fibrinolytic Enzymes “ clotbusters” MOA: stimulate the synthesis of fibrinolysin which breaks the clot into soluble products Drugs Urokinase (Abbokinase ® ) Anistreplase (Eminase ® ) Alteplase (Activase ® ) Reteplase (Retevase ® ) Prototype: Streptokinase (Strepase ® )

“ clotbusters”

MOA: stimulate the synthesis of fibrinolysin which breaks the clot into soluble products

Drugs

Urokinase (Abbokinase ® )

Anistreplase (Eminase ® )

Alteplase (Activase ® )

Reteplase (Retevase ® )

Prototype: Streptokinase (Strepase ® )

Streptokinase (cont’d) Indications Acute MI Acute ischemic stroke Pulmonary embolism Lysis of DVT Dose Administration Parental infusion (usually IV) Deep vein or arterial thrombosis IV: 250,000 IU over 30 min followed by 100,000 IU per hour up to 72 hours

Indications

Acute MI

Acute ischemic stroke

Pulmonary embolism

Lysis of DVT

Dose Administration

Parental infusion (usually IV)

Deep vein or arterial thrombosis

IV: 250,000 IU over 30 min followed by 100,000 IU per hour up to 72 hours

Streptokinase (cont’d) Adverse Effects Hemorrhage Concomitant use of heparin, oral anticoagulants, NSAIDs is NOT recommended because of the increased risk of bleeding Allergic reactions

Adverse Effects

Hemorrhage

Concomitant use of heparin, oral anticoagulants, NSAIDs is NOT recommended because of the increased risk of bleeding

Allergic reactions

Streptokinase (cont’d)

Antilipidemics

Antilipidemics Drugs that lower down abnormal blood lipid levels.

Drugs that lower down abnormal blood lipid levels.

Types of antilipidemics Statin drugs work by inhibiting the synthesis of cholesterol in the liver. Liver enzymes must be regularly monitored. (ex. Simvastatin) Niacin , a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs.(Ex. Niacin SR) Fibric acid derivatives work by accelerating the elimination of VLDLs and increasing the production of apoproteins A-I and A-II. (ex. Lipofen, Tricor) Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol content. The primary effect is a decrease in total cholesterol and LDLs. (ex. Questran)

Statin drugs work by inhibiting the synthesis of cholesterol in the liver. Liver enzymes must be regularly monitored. (ex. Simvastatin)

Niacin , a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs.(Ex. Niacin SR)

Fibric acid derivatives work by accelerating the elimination of VLDLs and increasing the production of apoproteins A-I and A-II. (ex. Lipofen, Tricor)

Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol content. The primary effect is a decrease in total cholesterol and LDLs. (ex. Questran)

Side effects Constipation Peptic ulcer Flushing Headache

Constipation

Peptic ulcer

Flushing

Headache

Nursing responsibilities Monitor client’s lipid levels Observe for signs of GI upset Instruct to take with sufficient fluids or meals Low fat diet Instruct not to abruptly stop intake

Monitor client’s lipid levels

Observe for signs of GI upset

Instruct to take with sufficient fluids or meals

Low fat diet

Instruct not to abruptly stop intake

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