Cardiology Pharmacology

Graduate Nursing 7550 with Cranwell-bruce at Georgia State University

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By: Stephanie Goetter
Created: 2011-09-10
Size: 91 flashcards
Views: 26

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Diuretics : Thiazide

Thiazides

Inhibit active exchange of Cl-Na

in the cortical diluting segment of the

ascending loop of Henle

Diuretics: K-sparing

K-sparing

K Inhibit reabsorption of Na in the

distal convoluted and collecting tubule

Diuretics: Loop

Loop Diuretics:

nhibit exchange of Cl-Na-K in

the thick segment of the ascending

loop of Henle

How to best use diuretics in HF:

• Start with variable dose, then titrate to

achieve dry weight‐dose by pt.

• Monitor serum K+ carefully

• Reduce dose when fluid retention is controlled

• Combine diuretics to overcome resistance

• Teach pt. when to and how to change

dose based on symptoms

We use diuretics in BP management bc they:

reduce plasma volume

In tx of HF, diuretics:

Decrease pre and after load

Improve contractility and decrease heart rate

Diuretics in HF:

Drug of Choice with Fluid overload

Can also help control HTN

Use thiazide early in treatment

May need to add or change to loop diuretic

Loop diuretics are _____acting; cause large_______.

short; natriuresis

Loop Diuretics:

• Liver primary site of metabolism

• All excreted by kidneys

• Use cautiously in electrolyte abnormalities,

diabetes, gout, hypotension

• Monitor creatinine clearance, electrolytes, BP,

Loop Diuretics:

• Bumetanide‐(Bumex), pregnancy C/D start 0.5

to 1mg qd to bid and max dose 10mg/day

• Furosemide (Lasix), pregnancy C, start 20‐

40mg qd to tid and max dose 600mg/day.

• Torsemide (Demadex), pregnancy B, 10‐20mg

in divided doses, max 200mg/day

• AHA/ACC guidelines

First line and monotherapy for mild-moderate

HTN.

Mild to moderate HF

Can be used in combination therapy with other

cardiac drugs

Thiazide Diuretics

• _______ lasting than loop

• _______ diuresis

• Still increases potassium excretion

Thiazide diuretics: longer; slower

• Well absorbed orally

• Monitor electrolytes, diabetes, gout,

hypotension, lipids

Thiazide diuretics

Thiazide Diuretics:

• Chlorthalidone (Thalitone), pregnancy D, dose 25‐

100mg/day, max 100mg for HTH, 200mg for HF

• Hydrochlorothiazide (Microzide), pregnancy D,

dose 12.5‐50mg/day for HTN, 25‐200mg/day for

Thiazide Diuretics

• Indapamide‐ pregnancy D, dose 1.25‐5mg/day for

HTN, 2.5‐5mg/day for edema

• Metolazone‐ (Zaroxolyn), pregnancy D, dose 2.5‐

5mg/day for HTN, 2.5‐10mg/day for edema

What are some adverse affects of diuretics

• ↓ K+ and Mg+ can cause sudden death

• ↓Na+

• ↑ Glucose

• Stimulation of neurohormonal activity

• Hyperuricemia (monitor gout patients)

• Hypotension, ototoxicity, gastrointestinal,

metabolic alkalosis

• Hyperlipidemia with thiazides

Aldosterone Inhibitors: How they work:

Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney)

*aldosterone saves sodium and wastes potassium

When to use spironolactone?

• Weak diuretic‐potassium sparing

• Recent or current symptoms despite use of

ACEI, diuretics, digoxin and β blockers I HF

patients (AHA/ACC guidelines)

• Recommended in advanced heart failure, in

addition to treatment with ACEI and diuretics

Do not use _______ (diurectic) in hyperkalemia or renal insufficiency

spironolactone

With Spironolactone, patient should always be on ____first. The starting dose for Spironolactone is ____mg/day.

ACEI; 25mg/day

If Kt is greater than 5.5 on Spironolactone, reduce the dose to

25mg/48 hours

If K+ is low or stable on Spironolactone, you can use how many mg per day?

50mg/day

Drugs that work in the RAAS

Angiotenisn Converting Enzyme Inhibitors (ACEI)

Angiotensive II receptor blockers (ARB)

Mechanism of Action of ARB:

• Molecular: Competitive inhibitor of AT1 receptors. Blocks

ability of angiotensins II and III to stimulate pressor and cell

proliferative effects

• Antihypertensive effects

• Cell growth effects

• Lack of “bradykinin” effects

Clinical indications for ARB:

• Hypertension

• Heart failure

• Prevention of restenosis

following angioplasty

List therapeutic uses of ARB and ACEI

• Anti‐hypertensive

• Prevent or reverse LVH

• Protect against sudden death and second myocardial

infarction after acute MI

List therapeutic uses of ARB and ACEI

• Improve survival and hemodynamics in patients with

congestive heart failure by improving symptoms,

reduce remodeling/progression and reduce

hospitalization

• Protect against progression of diabetic and nondiabetic

nephropathy

• Current research also looking at protection against the

progression of retinopathy

ARBS/ACEI Practical use in HF patients

•Start with very low dose

•Increase dose if well tolerated

•Renal function & serum K+ after 1 2 w

•Avoid fluid retention / hypovolemia (diuretic use)

•Dose NOT determined by symptoms

•Combine to overcome “resistance”

•Do not use alone

ACEI/ARBS in HTN: First line drug after ______. If patient is also DM, should be on ACEI or ARB as _________.

thiazides;

first line therapy

EBR have shown that ARBS/ACEI are highly beneficial--

Decrease BP

Improve O2 to heart

Decrease cardiac remodeling

kidney protective

ARBS/ACEI adverse effects:

• Hypotension‐worst with first dose‐give at

bedtime

• Worsening renal function

• Hyperkalemia‐monitor K+

• Angioedema and cough (ACEI) (higher in black

and Asian patients)

• Rash, neutropenia

• Antihypertensive response is reduced by NSAIDS

ARBS/ACE Contraindications:

• Intolerance‐angioedema, anuric renal failure

• Bilateral renal artery stenosis

• Pregnancy‐category D

• Renal insuffiency (creatinine >3mg/dl)

• Hyperkalemia (>5.5)

• Severe hypotension

B-Adrenergic Blockers: How do they work?

Beta blockers have effects on beta-1-cardiac and beta-2 bronchial and smooth muscle receptors

B-adrenergic blockers: How do they work?

Beta 1 blockade decreases heart rate and myocardial activity during periods of high sympathetic activity, which decreases cardiac output, which decreases BP. The blockade also suppresses automaticity resulting in decreased oxygen demand.

B-adrenergic blockers: how do they work?

Beta 2 blockade causes bronchospasms, hypoglycemia, peripheral vasoconstriction

B-blockers: Why do we use them?

HTN, angina, heart failure, asymptomatic ventricular dysfunction-- LVEF <35-40%, after acute MI, arrhythmias

Migraine headache prevention

Hyperthyroidism

Glaucoma-topical

Clinical Effects of Beta Blockers:

Improve symptoms-- long term

Reduce remodeling/progression

Reduce hospitalization

Reduce sudden death

Improve survival

B-blockers: When to start:

Patient must be stable

No physical evidence of fluid retention

No need for IV inotropic drugs

START ACEI/DIURETIC FIRST

No contraindications for therapy

While in hospital or at home

Types of Beta Blockers: Nonselective and Cardioselective

• Non selective

Prototype: Propranolol (others: nadolol, timolol, pindolol,

labetolol)

• Cardioselective

Prototype: Metoprolol (others: atenolol, esmolol, betaxolol)

Types of Beta Blockers: Nonselective and Cardioselective:

Non selective and cardioselective ß-blockers are

EQUALLY effective in reducing blood pressure

Remember Beta 2 affects the lungs-bronchospasm

Beta Blockers Contraindications:

Respiratory conditions with bronchospasms--can try a beta 1 selective drug

AV Blocker (except with pacemaker)

Symptomatic hypotension/bradycardia

Cocaine use

Limited cardiac and renal reserves

Hypoglycemia--monitor more frequently

Beta Blockers Contraindications:

Hyperthyroidism

Pregnancy category C/D

PVD- may worsen

Alpha-Adrenergic Blockers: Mechanism of action:

blockade of vascular a-adrenergic receptors

Non selective a-1 and a-2 blockers:

Phentolamine, phenoxybenzamine and dibenamine

Selective (a1) prototype:

prazosin (others: terazosin, doxazosin, trimazosin)

alpha-1 adrenoceptor blockers: USES

Treatment of pheochromocytoma

BPH--helpful if the man also has HTN

Because they block catecholamines and lower BP, they tend to cause hypotension both sitting and standing therefore limited use

First dose orthostatic hypotention--take at bedtime

Centrally Acting Sympatholytics:

a-methyldopa

clonidine

Alpha-2 Adrenoceptor Agonists Mechanisms of Action: Central Action:

Stimulation of a2 adrenoceptors in the brainstem reduces sympathetic tone, causing a centrally mediated vasodilitation and reduction in heart rate

Alpha-2 Adrenoceptor Agonists Mechanisms of Action: Prejunctional Action:

Prejunctional Action: Stimulation of a2 adrenoceptors located prejunctionally on peripheral neurons reduces norepinephrine release

Alpha-2 Adrenoceptor agonists mechanism of action: Vascular smooth muscle

a2 adrenoceptors located on vascular smooth muscle open Ca2+ channels and cause vasoconstriction. not evident clinically unless given intravenously.

Mechanisms of action: clonidine:

direct acting a2 adrenoceptor agonists

Mechanisms of action: a-methyldopa:

Prodrug taken up by central adrenergic neurons and converted to the a2 adrenoceptor agonist a-methylnorepinephrine.

Adverse effects of a2-Adrenoceptor Agonists:

Hypotension (esp. in volume depleted pts)

Sedation: more prominent for direct acting a2-adrenoceptor agonists--50% of pts

Nightmares and Insomnia-clonidine

Gynecomastia

Gastrointestinal

Withdrawal syndrome: HTN, tachycardia, nervousness and excitement

Calcium Channel Blockers: USES:

• Angina Pectoris

• Hypertension

• Treatment of supraventricular arrhythmias --atrial

flutter, artrial fibrillation, paroxysmal

SVT

• Migraine headache prophylaxis‐unlabeled

• Raynaud’s syndrome‐unlabeled

Three classes of CCBs:

Phenylalkylamines

Benzothiazepines

1,4‐dihydropyridines Nifedipine

Phenylalkylamines

Generic: Verapamil

Brand names :

Calan

Calan SR

Isoptin SR

Verelan

Benzothiazepines:

Generic: Dilitiazem

Brand Names:

Cardizem CD

Dilacor XR

1,4 dihydropyridines

Generic: Nifedipine

Nicardipine

Isradipine

Felodipine

Amlodipine

Brand names:

Adalat CC

Procardia XL

Cardene

DynaCirc

Plendil

Norvasc

CCBs Adverse effects:

• Hypotension

• Bradycardia

• Constipation‐100% of patients on verapamil

• Photosensitivity

• Edema, flushing, headaches, GI upset,

dizziness

Pathophysiology of Angina

Angina pectoris is caused by accumulation of metabolic byproducts

in myocardial tissue and results because oxygen demand by the

myocardium far exceeds the oxygen (blood) supply.

Patho of Angina

Oxygen supply and demand mismatch are primarily due to

atherosclerotic occlusion of coronary arteries (exertional, stable angina).

Angiospasms (variant angina) is also responsible for cardiac ischemia.

Theoretically the supply to demand mismatch can be corrected by:

- improving blood flow to the myocardium

- decreasing myocardial oxygen demand

Nitrates dilate _____ preferentially over ______ leading to decreased left

and right heart ______________ (decreased preload) with small

change in TPR.

Nitrates dilate veins preferentially over arteries leading to decreased left

and right heart end-diastolic pressure (decreased preload) with small

change in TPR.

Nitrate Therapy

heart rate _____or slightly ____ due baroreceptor

reflex mechanism.

- Cardiac output ____ due to lower ventricular enddiastolic

pressure.

heart rate unchanged or slightly increased due baroreceptor

reflex mechanism.

- Cardiac output decreases due to lower ventricular enddiastolic

pressure.

Nitrate Therapy; Lower doses VS higher doses

Lower doses dilate arterial vessels of skin, meninges – flushing,

headache

Higher doses (1) decrease systolic and diastolic pressure: decrease

TPR; (2) decrease C.O.; (3) cause venous blood pooling; (4) reflex sympathetic nerve activity

Nitrate Therapy: Appear to alleviate anginal pain by restoring myocardial oxygen

supply/demand via:

- decreasing myocardial work due to decreased afterload and

preload

- Ischemic regions of heart may have improved blood flow to

subendocardial regions due to decreased preload that decreases

ventricular wall tension.

Nitrate Therapy in Angina: Adverse Effects:

Adverse effects: (cardiovascular) headache, dizziness, weakness,

postural hypotension, flushed skin, tachycardia, rash.

Nitrate Therapy: Drug Interactions:

Drug Interactions

Nitrates are contraindicated in patients on sildenafil (Viagra®) due to

increased potential for hypotensive episode via PDE5 inhibition.

Nitrates: Therapeutic Use:

Used in exertional and variant angina to restore myocardial oxygen

supply/demand

Nitrates are used in congestive heart failure

Improve coronary blood flow after MI

Nitrate Therapy: Patient Teaching

• Patient teaching is critical for correct use for

prevention and acute relief.

• Removing patches, correct use of tablets,

sprays

• Storage of prn tablets

• Calling 911 if no relief with acute relief

medication

Other agents in Angina Therapy:

β-blockers: metoprolol, timolol, atenolol have been shown effective in

reducing anginal attacks by decreasing myocardial oxygen demand.

Calcium-channel blockers: amlodipine, bepridil, nicardipine improve

coronary BF to increase myocardial oxygen supply

Cardiac Glycosides / Intotropic Agents : increase the _____ of the heart.

Positive inotropic agents that increase the contractile

force of the heart, causing the ventricles to empty

more completely and thus improving cardiac output.

Cardiac Glycosides / Inotropic Agents:

– All cardiac glycosides are produced from a natural

source

– 10% of all hospitalized pts received cardiac glycosides.

– Many clients are rehospitalized for noncompliance

– Pt education is a must when clients are on these

medications

Cardiac Glycosides: Which is first line?

– Digoxin‐lanoxin‐ First Line

– Digitoxin‐crystodigin

Cardiac Glycosides: Action:

• Direct effect on cardiac muscle and the conduction system

• Indirect action on the cardiovascular system mediated

through the ANS

• The effects are dose related

• Digitalis glycosides have both a positive inotropic and

negative chronotropic effect on the muscle of the heart.

Cardiac Glycosides: Action: How does positive inotropic action work?

• Pos inotropic‐complete emptying of ventricles‐This in turn

increases CO and decreases SVR‐Alleviates symptoms of

CHF

Cardiac Glycosides: The positive inotropic effect is due to what? The negative chronotropic effect?

• Positive inotropic effect is due to inhibition of ATP.

• A negative chronotropic effect is due to the increase effect

of the neurotransmitter acetylcholine(from the vagus

nerve)

Positive inotropes ______the effect of muscular contraction

increase

• The primary site of chronotropic action of the digitalis

glycosides is the ________.

AV node

Digitalis glycosides also exhibit the following:

– decrease the heart size in pts. with cardiomegaly and

heart failure that occurs secondary to increase in work

load.

– Mild indirect diuretic effect.

– Effect the ECG‐Changes in the T wave, PR interval, ST

segment and U wave.

Uses for Digitalis glycosides:

– systolic heart failure

– dysrhythmias‐atrial fibrillation, atrial flutter, and SVT.

Digoxin level normals:

1-1.5ng/ml up to 2ng/ml for atrial fibrillation

Contraindications/precautions cardiac glycosides:

--keep in mind that renal function and client age may alter metabolism and excretion of digoxin.

--Infants and children have a larger volume of distribution than adults--larger doses are required to achieve similar concentrations of dig

Contraindications/precautions cardiac glycosides:

--idopathic hypertrophic subaortic stenossi

--diffuse cardiomyopathies

--constrictive pericarditis

--WPW

--cautious use in hyperthyroidism, impaired renal fx, preg, fluid electrolyte imbalances, elderly clients, acute MI.

Adverse Effects: Non cardiac (glycosides)

– GI‐nausea vomiting, anorexia, diarrhea

– GI effects are self‐limiting and disappear after

continued therapy.

– GI effects may reappear in digitalis toxicity

Adverse Effects: Non cardiac(glycosides)

– Visual disturbances‐Blurred vision, white dots, halos,

yellow or green tint to vision, double vision and

flickering.

– GI / CNS side effects not life threatening

– gynecomastia

– less common effects include‐depression, respiratory

depression, pruritis.

Cardiac Effects:(digitalis glycosides)

--Heart block due to slowing down conduction through AV node--expected effect

-- can be 1st degree or greater to complete block

• PVC’s, PAC’s, and other ventricular arrythymias

can occur due to disturbances in automaticity.

Cardiac Effects: (digitalis glycosides)

• Children may experience ectopic junction or atrial

beats(PAC’s or PJC’s)

• Because digitalis can produce many rhythm

disturbances assume all rhythm changes are a

result of digitoxin until proven otherwise

Digitalis Toxicity / Interactions:

• Interactions

– aluminum containing antacids

– kaolin‐pectin preparations

– bran

– Oral aminoglycosides(neomycin) also inhibit absorption of cardiac

glycosides

– Chemotherapy combined medicaitons

– quinidin‐increases serum dig levels

Digitalis Toxicity / Interactions:

Digitoxin immune Fag(Digibind)-- used in treatment of life threatening digoxin and digitoxin and digitoxin intoxications

About this deck

By: Stephanie Goetter
Created: 2011-09-10
Size: 91 flashcards
Views: 26

About StudyBlue

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis