Copy of Cardiac

DRUGS AFFECTING the

CARDIOVASCULAR SYSTEM

Prepared and Presented by:

Ivy Monteclaro-Cornelia, RN

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THE HIGH RISK GROUPS

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Overview on Cardiovascular Drugs

Anti – Hypertensive Drugs

DiureticsAnti – Arrhythmic

AgentsAnti – Anginal AgentsCardiotonic AgentsDrugs Used to Treat

Anemia

http://www.avert.org/aids-picture.php?photo_id=530

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Anatomy and Physiology

HeartArteries Veins

Capillaries

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The Cardiovascular System:HEART

• located in the MEDIASTINUM• Enclosed by PERICARDIAL MEMBRANES parietal & visceral layer pericardial fluid : 50 ml • 3 layers:1. Epicardium2. Myocardium3. Endocardium

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Heart

• 4 chambers: 2 atria 2 ventricles

right atrium : receives deoxygenated blood

left atrium: receives oxygenated blood

right ventricle: pumps blood for pulmonary circulation

left ventricle: pumps blood for systemic circulation

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Heart

4 valves: 2 atrioventricular valves: tricuspid and

mitral 2 semilunar valves: pulmonic and aortic

prevent backflow or regurgitation

closing of the valves produces heart sounds

thus: S1 : closing of AV valves S2: closing of semilunar valves

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Heart

STARLING’s LAW OF THE HEART

- the farther the cardiac muscle is stretched, the stronger it springs back to its normal size

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THE HEART

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The Cardiac Cycle

• Diastole – period of cardiac muscle relaxation

• Systole - period of cardiac muscle contraction

• Cardiac Cycle – each period of systole followed by diastole

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The Cardiac Cycle

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The Cardiac Cycle

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The Cardiac Cycle

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The Cardiac Cycle

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Arteries, Capillaries and Veins

• resistance system : constrict and dilate

(arterial system)

• capillary system: connects the arterial and venous systems

• capacitance system: veins have the

capacity to hold large quantities of fluids as they distend with fluid volume

(venous system)

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Structure of arteries and Veins

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Structure of arteries and Veins

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ANTI – HYPERTENSIVE DRUGS

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Hypertension vs Hypotension

• Hypertension= pressure is above the normal limits for a sustained period= types:1. Primary/idiopathic/essential2. Secondary= Risk Factorssmoking, DM, high cholesterol level, >60 yrs old, genetic predisposition, gender ,alcohol

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HypertensionCategories Rating the Severity of

Hypertension

target organ damage:stroke or TIA, kidney disease, retinopathy, CHF,CAD

Classification Systolic (mmHg) Diastolic (mmHg)

Normal <120 and < 80

Pre-hypertension 120 – 139 Or 80 – 89

Stage 1 140 – 159 Or 90 – 99

Stage 2 >/= 160 Or >/= 100

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Hypotension• becomes too low, the vital centers in the brain as

well as the rest of the tissues of the body may not receive enough oxygenated blood to continue functioning

• Possible cause:1. When the heart muscle is damaged and unable

to pump effectively2. With severe blood loss, when volume drops

dramatically3. When there is extreme stress and the body’s

level of norepinephrine are depleted, leaving the body unable to respond to stimuli to raise the blood pressure

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Blood Pressure Control

The pressure in the cardiovascular system is determined by three elements:

• Heart Rate• Stroke Volume• Total Peripheral Resistance

Blood Pressure = cardiac output x peripheral resistance

Cardiac output = stroke volume x heart rate

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Renin-Angiotensin System

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Factors affecting BP

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Venous ReturnHeart Rate

Peripheral ResistanceElasticity of large arteries

Viscosity of the bloodLoss of Blood

Hormones

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Drug Therapy

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Lifestyle Modification

Blood Pressure Still Elevated

Start Drug Therapy

Uncomplicated Hypertension- Diuretics

- Beta Blocking Agents

If Complications are Present Recommended Tx- DM w/ proteinuria -ACE inhibitors

- CHF -ACE inhibitors

Diuretics

- Isolated Systolic HPN in older adults - Diuretics (preferred)

- Calcium antagonist

- MI - Beta antagonist

ACE inhibitors

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Procedure: 1) Start with low dose of long acting drug and titrate.

2) May consider use of low dose drug combinations.

Inadequate Patient Response

If no response or with S/E or A/E Drug tolerated but inadequateresponse

Substitute drug from other classificationAdd second drug from otherclassification

Response still inadequate

- Add another antihypertensive agents from other classification- May need to refer to a cardiologist or hypertensive specialist

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DIURETICS

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ACE INHIBITORS

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1. Therapeutic Actions and Indications

prevent ACE from converting angiotensin I to angiotensin II

leads to a decrease in blood pressure and in aldosterone secretion

to decrease the inactivation of bradykinin

increase synthesis of prostaglandin E

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2. Phamacokinetics

metabolized in the liver and excreted in the urine and feces cross the placenta

detected in the breast milk

3. Contraindications and Cautionsallergy impaired renal function pregnancy.caution CHF

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4. Adverse Effects • reflex tachycardia, chest pain, angina, CHF and

cardiac arrhythmias; GI irritations, ulcers, constipation and liver injury; renal insufficiency, renal failure and proteinuria and rash, alopecia, dermatitis and photosensitivity

• unrelenting cough• fatal pancytopenia and MI.

5. Clinically Important Drug – Drug Interaction• allopurinol• taken on an empty stomach, 1 hour before or 2

hours after meals

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Patient Teaching

1. Not to abruptly discontinue the drug.2. Teach how to take blood pressure.3. Explain that dizziness and lightheadedness

are expected during the first week of treatment (CAPOTEN).

4. If drug is taken SL, not to take anything PO for 30 minutes.

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Example of Drugs:

• Captopril (Capoten)• Enalapril (Vasotec)• Lisinopril (Prinivil, Zestril)• Quinalapril (Accupril)

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ANGIOTENSIN II RECEPTOR INHIBITORS

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1. Therapeutic Actions and Indications

binds with angiotensin II receptors sites in the vascular smooth muscle and in the adrenal gland

indicated to be used alone or in combination therapy for the treatment of hypertension and for treatment of CHF in patients who are intolerant to ACE inhibitors

2. Pharmacokineticsmetabolized in the liver by cytochrome P450 system

excreted in feces and urinecross the placenta

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3. Contraindications and Cautions• Allergy • Pregnancy and lactation• Caution : hepatic and renal dysfunction

4. Adverse Effects• associated with decrease in blood pressure • Cough

5. Clinically Important Drug to Drug interactions• decreased serum levels and loss of effectiveness

increases taken in combination with Phenobarbital

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Example of Drugs:

• Candesartan (Atacand)• Eprosartan (Teveten)• Irbesartan (Avapro)• Losartan (Cozaar)• Olmesartan (Olmetec)• Temisartan (Micardis)• Valsartan (Diovan)

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CALCIUM CHANNEL BLOCKERS

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1. Actions and Indicationsinhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells

a. depresses the myocardial contractilityb. slows cardiac impulse formation in the

conductive tissuesc. relaxes and dilates arteries

2. Pharmacokinetics

metabolized in the liver excreted in the urinecross the placenta and enter breast milk

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3. Contraindications and Cautions• Allergy • with heart block or sick sinus syndrome• with renal and hepatic dysfunction • pregnancy and lactation.

4. Adverse Effects• associated with effects on cardiac output and

smooth muscle• CNS effects include: dizziness, light headedness,

headache and fatigue• Cardiovascular effects include: hypotension,

bradycardia and heart block

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5. Clinically Important Drug to Drug Interactions

Drug to drug interactions vary with each of the calcium channel blockers used to treat hypertension

Note!!!!

interact with GRAPEJUICE

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Example of Drugs

• Amlodipine (Norvasc)• Diltiazem (Cardiazem)• Felodipine (Plendil)• Nicardipine (Cardene)• Nifedipine (Adalat) (strongest

peripheral smooth muscle dilator effect)

• Verapamil (Calan SR)

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SYMPATHOLYTICS

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Sympatholytics

5 groups:

1. Beta – adrenergic blockers2. Centrally acting alpha 2

agonists3. Alpha – adrenergic blockers4. Adrenergic neuron blockers

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Beta – Adrenergic BlockersSubclasses :

Beta1 and Beta 2 blockers

Location of Beta Receptors:

Beta 1 Beta 2

Compete with beta adrenergic agonists for available receptor site located on membrane of cardiac muscle, smooth muscle of bronchi and smooth muscles of blood vessels

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Beta – Adrenergic Blockers

Classification according to site of action:

1.Selective

Beta1 Selective, also known as CARDIOSELECTIVE

decrease BP and PR

2.Non – Selective

inhibit both Beta1 and Beta2 cause bronchospasm and impotence (inderal)

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Beta1 antagonists Effects:

a.Atenolol (Tenormin)b.Esmolol (Brevibloc)c.Metoprolol (Lopressors, Betaloc)d.Acebutolol (Sectral)

Beta1 and Beta2 antagonits effects:e.Labetolol (Normodyne)f. Propanolol (Inderal)g.Timolol (Blocadren)h.Cardeviol (Coreg)

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1.Action

decrease COreduce release of renin, impede outflow of sympathetic impulses from

brain stem control center to peripheral , retard release of norepinephrine

2 Pharmacodynamics

metabolized in the liver, excreted in urine

cross placenta and breast milk


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Beta – Adrenergic Blockers Contraindications and Cautions

• Sinus bradycardia• 3rd degree heart block• CAUTION: asthma, hepatic & renal problem,

type 1 diabetes

Adverse EffectsDizziness, drowsiness, hypotension

ALERT!!!!HypoglycemiaBronchospasmBradycardia

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NURSING IMPLICATIONS!

Take apical pulse 1 full minuteMonitor for side/adverse effects

PATIENT TEACHING!!!!

Take radial pulse before administering the drug

Avoid alcoholic beveragesChange position slowly

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Centrally Acting Alpha Agonist

decrease sympathetic response from brainstem to peripheral vessels

decrease sympathetic activityincrease vagus activity

decrease C.O.decrease epinephrine and norepinephrine and

renin release

reduced peripheral resistance

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for mild to moderate HPN

CAUTION:

CVD, hx of depression, pregnant, CRF, peripheral vascular disease (REYNAUD’S PHENOMENON), blood disorders

Common:

CLONIDINE (catapress)METHYLDOPA (aldoment)

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CLONIDINE (catapress)

available in TRANSDERMAL PREPARATION : 7 day duration of action

may be left with bathing

Note! ASSESS SKIN IRRITATION

PO: administer 1 hour before or 2 hours after meals

NO ABSOLUTE CONTRAINDICATIONS

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CLONIDINE (catapress)Patient Teaching!

• Advice the importance of periodic examination.

• NO ABRUPT WITHDRAWAL!• Take the last dose before bedtime to reduce daytime drowsiness.

• Move slowly• For long term tx: periodic eye exam (RETINAL DEGENERATION)


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METHYLDOPA (aldomet)

not to be used with impaired LIVER FUNCTIONmay cause BLOOD DYSCRASIAS

NOTE!!!

both can retain sodium and water

thus: given with DIURETICS

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Alpha Adrenergic Blockers

prevent norepinephrine from activating alpha1 receptors on vascular smooth muscle to produce

vasoconstriction

VASODILATATION AND DECREASED BP

useful in treating those with lipid abnormalitiesSafe for patients with DM

Common: PRAZOSIN (minipress)

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Alpha Adrenergic Blockers

PRAZOSIN (minipress) can slightly increase HR

Common S/E:Drowsiness, headache,

malaise

NO ABSOLUTE CONTRAINDICATIONS

CAUTION: in people who drive and operate heavy machinery

ALERT!!!Can cause SYNCOPE if taken with nitroglycerin

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Adrenergic Neuron Blockers

block norepinephrine release from sympathetic nerve endings

= decrease BP

can retain SODIUM and WATER

common: RESERPINE and GUANETHIDINE

NOTE!!

Use of RESERPINE can cause vivid dreams, nightmares and suicidal ideation

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Direct Acting Arteriolar Vasodilators

Relax the smooth muscles of blood vessels

Promote blood flow to brain and kidneys

Decreased BPSodium and Water are retained

S/E: REFLEX TACHYCARDIA (treated with Beta Blockers)

Common: HYDRALAZINE MINOXIDIL NITROPUSSIDE DIAZOXIDE

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HYDRALAZINE (Apresoline)

given in HYPERTENSIVE EMERGENCIES

Given IVTT: onset of action : 10 – 20 minutes peak : 15 – 30 minutes

A/E: headache, dizziness, depression, tachycardia,

SLE symptoms

NOTE!!!If with S/S of infection, DISCONTINUE: blood dyscrasias

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NITROPRUSSIDE (nipride)given in HYPERTENSIVE EMERGENCIES

Given IVTT: onset of action: 30 – 60 seconds peak : 1 - 2min

administered through an INFUSION PUMP with container WRAPPED in aluminum foil

S/E is due to rapid infusion: GI and CNS

Note!!! Metabolized first to CYANIDE then to THIOCYANATE

DISCONTINUE if with cyanide toxicity:Coma, dilated pupils, pink color, shallow respirations, imperceptible PR, distant heart sounds, hypotension, absent reflexes

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Discharge Instructions for all anti-hypertensive Agents

1.Advice all possible adverse effects of the drug.

2.Do not abruptly discontinue or skip doses of medications.

3.Change position gradually.4.Avoid alcohol and hot bath/showers.5.Do not take OTC without consulting

physician.6.Monitor weight and eat low-sodium food.7.Take BP and have a diary.8.Do no drive or operate heavy machinery

until drug effects are established.

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ANTI – ARRHYTHMIC AGENTS

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Conduction System of the Heart

1.Automaticity= refers to the cell’s ability to spontaneously initiate an impulse

2. Excitability= results from ion shifts across cell membrane and indicates how well a cell responds to an electrical stimulus

3. Conductivity= ability of a cell to transmit an electrical impulse to another cardiac cell

4. Contractility= refers to how well the cell contracts after receiving a stimulus

4 characteristics of CARDIAC CELLS

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ACTION POTENTIAL Phase O

DepolarizationSodium gates open and sodium ion rushes in

Phase 1When sodium ion concentration are equal inside and outside the cell

Phase 2Cell membrane becomes less permeable to sodiumCalcium goes in and potassium begins to leave

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ACTION POTENTIAL

Phase 3

Rapid repolarization as the gates close and potassium rapidly moves out of the cell

Phase 4

Cell comes to rest

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AUTONOMIC INFLUENCES

influence the heart rate, rhythm and strength of contraction

PARASYMPATHETIC SA node, atrial muscles, AV junction

slows the heart rate and decrease the speed of conduction at the AV node

SYMPATHETIC

stimulates the heart to beat speeds up conduction at AV node

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CARDIAC ARRHYTHMIAS

disruption in the cardiac rate or rhythm

DYSRHYTHMIA

interfere work of the heart affecting C.O.arise due to changes in the automaticity/conductivity

influencing factors:

Drugs, acidosis, hypoxia, electrolyte imbalances

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DRUG THERAPY

Class I : SODIUM CHANNEL BLOCKERS

Class II : BETA – ADRENERGIC BLOCKERS

Class III: POTASSIUM CHANNEL BLOCKERS

Class IV: CALCIUM CHANNEL BLOCKERS

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DRUG THERAPY

CLASS I: SODIUM CHANNEL BLOCKERS

Blocks the influx of SODIUM into the cell during rapid depolarization (phase O)

For life-threatening VENTRICULAR ARRHYTHMIASHas pro-ARRHYTHMIC EFFECT

CATEGORIES:

1.Class Ia2.Class Ib3.Class Ic

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DRUG THERAPY


PHARMACOKENITECSAbsorbed at GITMetabolized in LIVER and excreted in URINECross placenta, breast milk

CONTRAINDICATIONS and CAUTIONS

AllergyBradycardia or heart blockCHF/shock

CAUTION! Pregnant , liver and kidney dysfunction

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DRUG THERAPY


Class Ia : Bind to sodium channels ad interfere with sodium influx Depression of CONDUCTION VELOCITY

Class Ib: either INCREASE or NO EFFECT on conduction velocity

Class Ic: can cause SINUS ARREST, AV block and LIFE –THREATENING VENTRICULAR ARRHYTHMIAS

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DRUG THERAPY


ADVERSE EFFECTS:Associated with membrane stabilizing effects on action potentialCNS: dizziness, drowsiness, slurred speech, tremors – convulsionGIT : metallic taste, n/vCARDIO: PROARRHYTHMIA, hypotensionRESPI: respiratory depressionOTHERS: bone marrow depression

INTERACT w/!!!Digoxin, beta blockers, oral anticoagulants(quinidine) avoid food that alkalinize urine (citrus juice)

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DRUG THERAPY


QUINIDINEfor atrial fibrillation/flutter, PVC, paroxysmal supraventricular tachycardia

stabilizes cell membrane by preventing ready movement of Na and K

A/E:With indirect ANTICHOLINERGIC EFFECTPeripheral VASODILATION

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DRUG THERAPY


NURSING IMPLICATION• Monitor ECG, VS, eletrolytes, CBC, kidney & liver

function.• Monitor quinidine serum: 3 – 6 mcg/ml• Take apical pulse.• Taken with food if with GI upset.• Clients taking DIGOXIN with quinidine is at risk for

DIGOXIN TOXICITY.PATIENT TEACHING

• Regular dental check-up.• Adverse effects (ex. bleeding gums, s/s of

hypotension)• Not to discontinue without DR’s advice.

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DRUG THERAPY


PROCAINAMINDE (Pronestyl)Action is similar with quinidine, EXCEPT:

• Less effective in controlling abnormal ectopic pacemaker activity

• Few anticholinergic effects• More potent positive INOTROPIC effects

NURSING IMPLICATIONS:• Given through infusion pump.• ECG monitoring.• VS• Serum level 4 – 8 mcg/ml

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DRUG THERAPY

CLASS Ib: SODIUM CHANNEL BLOCKERS

LIDOCAINE HYDOCHLORIDEDOC for suppressing ventricular arrhythmias (before)Given with loading dose then an infusion thereafter

A/E:CNS stimulation: SEIZURE!!!

NURSING IMPLICATIONS:1.Monitor VS, ECG, neurologic status.2.Monitor serum level : 1.5 – 5mcg/ml.

Other Drug:Tocainide Hcl (Tonocard)

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DRUG THERAPY

CLASS Ic: SODIUM CHANNEL BLOCKERS

FLECAINIDE (Tambocor)NO anticholinergic effects

A/E:Bradycardia, chest pains, heart failure, constipation, headaches

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DRUG THERAPY

CLASS II: BETA ANDRENEGICS

ANTAGONISTS

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DRUG THERAPY

CLASS III: POTASSIUM CHANNEL BLOCKERS

Blocks K+ channels prolonging phase 3, which prolongs repolarization and slows rate and conduction of heart

PHARMACOKINETICSMetabolized in liver and excreted in urine. With little information regarding pregnancy and lactation.

CONTRAINDICATIONS and CAUTIONSNo absolute contraindications!CAUTIONS: shock, hypotension, respiratory depression

Note! Can increase digoxin, & oral anticoagulants

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DRUG THERAPY


ADVERSE EFFECTS:n/v and GI distress, weakness & dizziness, hypotension, CHF and arrhythmia

Common Drugs:

Bretylium tosylate (Bretylate)Amniodarone (Cordarone)Ibutilide fumarateDofetilide (Tikosyn)Sotalol (Betapace, Betapace AF)

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DRUG THERAPY


AMNIODARONE (cordarone)Decrease automaticity, prolongs AV conductionBlocks Ca2+, K+, Na+ and beta receptors (complex effects on heart, therefore limited use)

DOC for VENTRICULAR FIBRILLATION or pulse less VENTRICULAR TACHYCARDIA

NOTE!it can cause PHOTOSENSITIVITYIncrease level of phenytoin, theophylline, digoxin

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DRUG THERAPY

CLASS III: CALCIUM CHANNEL BLOCKERS

blocks calcium channel in the cell membrane leading to depression of depolarization and a

prolongation of phases 1 and 2 slowing automaticity and conduction

with effect on heart muscle;

DILTIAZEM (cardizem)VERAPAMIL (calan)

indicated for: SUPRAVENTRICULAR TACHYCARDIA

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DRUG THERAPY

CLASS III: CALCIUM CHANNEL BLOCKERS

PharmacokineticsMetabolized in the liver and excreted in the urineCan cross the placenta

CONTRAINDICATIONS & CAUTIONSAllergyPregnancy and lactation

Caution!!! CHF and hypotension, liver/kidney disease

Adverse Effects are related to changes in the ACTION POTENTIAL

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DRUG THERAPYANTI – ARRHYTHMIC AGENTS

NURSING PROCESS1.Assessment - Baseline Data (present sickness,

laboratory and diagnostics exams2. Nursing Diagnoses - Decreased cardiac output - Risk for activity intolerance - Poor tissue perfusion3. Planning - Client will no longer experience

abnormal sinus rhthym - client will comply

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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.

5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco

ANTI – ANGINAL DRUGS

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BLOOD SUPPLY TO THE MYOCARDIUM

provided by RIGHT and LEFT CORONARY ARTERIES arising from the BASE of AORTA

Right Atrium and Ventricle = right coronary artery

Left Atrium and Ventricle = left coronary artery (anterior branch and circumflex branch

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BLOOD SUPPLY TO THE MYOCARDIUM

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CORONARY ARTERY DISEASE

Coronary Atherosclerotic Heart Disease

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PathophysiologyRISK FACTORS

Non- Modifiable age

Genderrace

heredity

ModifiableStress, diet, sedentary

livingSmoking, alcohol, HPN,

Obesity, DM, OCP

Endothelial Injury

Desquamation of Endothelial Lining

Increased Permeability / Adhesion Molecules

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Lipids and Platelets Assimilate into the Area

Oxidized Lipids attracts Monocytes & Macrophages to the site

Plaques begin to form and imbed into the endothelium

Lipids are engulfed by the cells and smooth muscle cells develop


Decreased Coronary Tissue Perfusion

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Coronary Ischemia

Decreased Myocardial Oxygenation

Angina PectorisMyocardial Infarction

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What is ANGINA/ANGINA PECTORIS?

• acute cardiac pain caused by inadequate blood flow to the myocardium

• Paintransient, paroxysmal substernal or precordial

described as HEAVINESS or TIGHTNESS , INDIGESTION

radiates in one or both arms, left shoulder, jaw, neck, back

precipitated by activity / exertion

relieved by REST and NITROGLYCERIN

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PAIN PATTERN IN ANGINA

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ANGINA PECTORIS

Pathophysiology

Reduced Coronary Tissue Perfusion

Diminished Myocardial Oxygenation

Anaerobic Metabolism

Increased Lactic Acid Production (Lactic Acidosis)

PAIN

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ANGINA PECTORIS

Associated S/S:Pallor

Diaphoresis

Dyspnea

Faintness

Palpitations

Dizziness

Digestive Disturbance

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DRUG THERAPY

The IDEAL Anti – Anginal Drugs:

1.Establish a balance between coronary blood flow and metabolic demands of the heart.

2.Have a local effect rather than systemic.

3.Promote oxygen extraction by the heart from the arterial flow.

4.Be effective when taken orally and have sustained action.

5.Have an absence of tolerance.

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DRUG THERAPY

NITRATES

caused generalized vascular and coronary vasodilation thus increasing blood flow

Directly acts on the smooth muscle

Common Drugs:

Nitroglycerin (Transderm Patch, Nitro – Bid)Isosorbide dinitrate (Isordil)Isosorbide mononitrate (Imdur)

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DRUG THERAPYNitroglycerin

Vascular Smooth Muscle Interacts w/ sulfhydryl groups

Nitric Oxide (active form)Activates guanylate cyclase

GTP to GMP

Decrease Intracellular Calcium

VASODILATATION

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DRUG THERAPY

NITROGLYCERIN

SL: rapidly absorbed in JUGULAR VEIN & RIGHT ATRIUM

Common S/E: HEADACHE

Note!!!!should be tapered if discontinuedshould be given slowly if through IV push to

prevent REFLEX TACHYCARDIA

Other S/E: hypotension, dizziness, rashes (using ointment/patch)

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DRUG THERAPYNITROGLYCERIN

Route Onset Duration

IV 1 – 2 min 3 – 5 min

SL 1 – 3 min 30 – 60 min

Translingual Spray

2 min 30 – 60 min

Transmucosal Tablet

1 – 2 min 3- 5 min

Oral, SR Tablet 20 – 45 min 8 – 12 min

Topical Ointment

30 – 60 min 4- 8 H

Transdermal 30 – 60 min 24 H

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DRUG THERAPY

NURSING DIANOSIS!!!

• Decreased cardiac output related to hypotensive effects.

• Risk for injury related to CNS or cardiovascular effects.

• Ineffective tissue perfusion (total body) related to hypotension or change in cardiac output.

* Deficient knowledge regarding therapy.

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DRUG THERAPY

NURSING IMPLICATIONS!!!

Check V/S especially blood pressure.

For SL and transbuccal, check the oral mucosa.

Let the patient assume sitting/supine position.

No more than 3 tablets should be taken in 15 – minute period.

Ointment / Patch should be applied in hairless areas.Nitro – Patch usually applied in the morning, rotate site.

Offer sips of water before giving SL nitrates.

Observe for side effects.

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DRUG THERAPYDISCHARGE TEACHING!!!!!

Take maximum of 3 doses only at five minute interval.

Change position slowly.

Avoid alcohol.

Carry 3 tablets always in the pocket.

Store in cool, dry, dark colored, airtight container.

“Fizzles” or burns under the tongue indicates potency.

Stored tablets should be discarded after 3 months.

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DRUG THERAPY

Beta Adrenergic Blockers

block the stimulatory effect of sympathetic nervous system

block the beta adrenergic receptors (in the heart and juxtaglomerular apparatus) and vasoconstriction and prevent increase in heart rate and increased intensity of myocardial contraction

Common Drugs:

Metoprolol (Betaloc)Propanolol (Inderal)Nadolol (Corgard)

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DRUG THERAPY

CONTRAINDICATIONS

bradycardia, asthma, COPD

CAUTION

DM and Thyrotoxicosis

ADVERSE EFFECTS

related to blockage of SNSRespiratory System: bronchospasm

and cough

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DRUG THERAPYADVERSE EFFECTS

CNS : Headache, dizziness, weaknessGI : N/VCardio : Hypotension and Reflex tachycardia

COMMON DRUGS

Atenolol (Tenormin)Metoprolol tartrate (Lopressor)Nadolol (Corgard)Propanolol (Inderal)

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DRUG THERAPY

Calcium Channel Blockers

Calcium

activates myocardial contraction, increasing workload and the need for more oxygen

Indications:

Angina (Prinzmetal’s angina)Hypertention

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DRUG THERAPY

Therapeutic ActionsCalcium movement(inhibited)

action potential altered & muscle cell contraction blockage

Myocardial contractility depresses

Decrease cardiac workload and O2 consumption

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DRUG THERAPY

Common Drugs:

Amlodipine (Norvasc)Diltiazem (Cardizem)Verapamil (Calan)Nifedipine (Adalat)

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CARDIOTONIC AGENTS

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BASIC ACTION OF CARDIOTONIC AGENTS

affect INTRACELLULAR CALCIUM

increased contractility

increased cardiac output

increased renal blood flow

increased urine output

decreased blood volume

DECREASED CARDIAC WORKLOAD

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CARDIAC MUSCLE

sarcomere

action and myosin

Contraction process requires:

1.Oxygen2.Energy3.Calcium

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CONGESTIVE HEART FAILURE

LEFT SIDED HEART FAILURE

causes:MI, HPN, Aortic/ Mitral

StenosisReduced myocardial

contractilityIncreased cardiac workloadDecreased diastolic filingObstruction of left atrial

emptyingIncreased left atrial pressure

Left Sided CHF

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Blood goes back to Pulmonary beds

Increased pressure in

Pulmonary beds

Fluid shift into intraalveolar

and interarveolar

spaces

Pulmonary edema

Decreased stroke volume

Decreased tissue perfusion

Increased cellular hypoxia

S/S of PULMONARY PROBLEMS

Decreased blood

Flow to the kidneysRAAS

activation

Vasoconstriction & Na &

water reabsorption

Increased ECF volume

Increased total volume

Increased systemic BP

04/22/2023 124

RIGHT SIDED HEART FAILURE

causes:LSCHF

Pulmonary EmbolismRight Ventricular InfarctionCongenital Septal Defect

Reduced Myocardial Contractility

Increased Cardiac WorkloadDecreased Diastolic FillingObstruction of Right Atrial

EmptyingIncreased Right Atrial Pressure

Blood goes back from RV to RA

S/S of RSCHF

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DRUG THERAPY

VASODILATORS

decrease the workload of the heart

relaxes the vascular smooth muscle decreasing the

afterload

decreases venous return thus decreasing preload

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DRUG THERAPY

VASODILATORS

Nitroprusside (Nipride)Hydralazine (Apresoline)

Nifedipine (a calcium channel blocker)

Captopril (Capoten)

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DRUG THERAPY

DIURETICS

to decrease the circulating blood volume thereby

decreasing the preload

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DRUG THERAPY

BETA ADRENEGIC AGONISTS

stimulate the beta receptors in the SNS increasing calcium

flow thereby increasing contraction

INOTROPIC EFFECT

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DRUG THERAPY

BETA ADRENERGIC AGONISTS

Dobutamine

with direct activation of BETA 1 increasing contraction but

induce less heart rate and less decrease in peripheral vascular

resistance

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DRUG THERAPY

CARDIAC GLYSCOSIDES (digitalis glycosides)

DIGOXIN (LANOXIN)

Action:

increase intracellular calcium during depolarization

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DRUG THERAPY

CARDIAC GLYCOSIDES

1. Positive inotropic effect2. Negative Chronotropic

effect3. Diuretic Effect

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DRUG THERAPY

CARDIAC GLYCOSIDE

with narrow therapeutic margin:

0.5 – 2ng/mlAdverse Effects:

ArrhythmiasBradycardia

Visual disturbance

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DRUG THERAPY

CARDIAC GLYCOSIDES

NURSING IMPLICATIONS:

1. Half life is longer in elderly.2. Monitor CBC, electrolytes,

liver & kidney functions.3. Hold if apical heart rate is:

<60 or > 120 adults<90 or infants<70 children and adolescents

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DRUG THERAPY

CARDIAC GLYCOSIDES

4. Encourage food high in POTASSIUM.5. Give after meals.6. Avoid IM injections.7. S/S of TOXICITY:

bradycardia GI manifestations

halo vision8. ANTIDOTE:

Digoxin Immune Fab (Digi-bind)

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DRUG THERAPY

CARDIAC GLYCOSIDES

ALERT!!!!

increase toxicity with HYPOKALEMIA

serum level increases with QUINIDINE

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DRUG THERAPY

PHOSPHODIESTERASE INHIBITORS

Inotropic agents

blocks phosphodiesterase

increase cAMP

Increase intracellular calcium

Increase contraction

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DRUG THERAPY


Inamrinone (Inocor)Milrinone (Primacor)

Adverse Effects:

HypotensionVentricular arrhythmias

Thrombocytopenia (Inamrinon)

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DRUG THERAPY


ALERT!!!!!

give solution separatelyit PRECIPITATES…….

Drug Used to Treat Anemia

Blood

Slide 10.1b

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 10.1

Anemia

Deficiency in the number of ERYTHROCYTES, quantity of Hgb, & volume of Hct

Not a specific disease, manifestation of pathologic process

Grouped according to:

MORPHOLOGIC

ETIOLOGIC

Anemia

Anemia

ETIOLOGIC CLASSIFICATION1. Decreased Erythrocyte Production

=IDA=Thalassemia

2. Defective DNA Synthesis= Cobalamin (Vitamin B12) Deficiency= Folic Acid Deficiency

3. Decreased Number of Erythrocyte Precursors= Aplastic Anemia= Anemia of Myeloproliferative Disease= Chronic Disease or Disorders

Anemia

ETIOLOGIC CLASSIFICATION

4. Chemotherapy

5. Blood Loss (Acute or Chronic)

6. Increased Erythrocyte Destruction= Intrinsic= Extrinsic

MORPHOLOGIC CLASSIFICATION

Normocytic, Normochromic(normal size & color)

Macrocytic, normochromic(large size, normal color)

Microcytic, hypochromic(small size, pale color)

Anemia

Iron Supplement

Mechanism of Action:

Replaces iron stores needed for RBC development, energy, and O2 transport, utilization

Therapeutic Indications:

Prevention & Correction of IDA

Contraindications:

hypersensitivity

Adverse Effects:

Nausea, epigastric pain, constipation, black stools

http://rds.yahoo.com/_ylt=A0S020vQVVRL.g4A0zOJzbkF;_ylu=X3oDMTBpY2Y5NXNiBHBvcwM2BHNlYwNzcgR2dGlkAw--/SIG=1lldrbcu6/EXP=1263904592/**http:/images.search.yahoo.com/images/view?back=http://images.search.yahoo.com/search/images?p=%22ferrous+sulfate%22&ei=UTF-8&fr=yfp-t-701&w=350&h=400&imgurl=www.healthwarehouse.com/media/catalog/product/cache/1/image/5e06319eda06f020e43594a9c230972d/f/e/ferroussulfate-100ct-front2.jpg&rurl=http://www.healthwarehouse.com/diet-nutrition/ferrous-sulfate-325mg-100-tablets.html&size=13k&name=Ferrous+Sulfate+...&p=%22ferrous+sulfate%22&oid=f49ebf81a96f1f20&fr2=&no=6&tt=532&sigr=12kejcm17&sigi=140opktjq&sigb=12qpo5rs8

ALERT for Oral Iron Therapy!!!

• Enteric Coated or sustained release (SR) should not be used

• Iron should be taken about 1 hour after meals• Vitamin c enhances Iron absorption• Increase fluid and fiber intake• Avoid consumption of milk, tea, coffee with Oral Iron

• Liquid preparation to be administered using straw

• Warn client that it can change color and consistency of stool

Iron Supplement

THANK YOU!!!

questions???clarifications???

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