Cardio Drugs Lecture-students' Copy

8/10/2019 Cardio Drugs Lecture-students' Copy

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Pharmacotherapy

Primary:

Diuretics

ACE Inhibitors

ARBs

Beta-blockers

Calcium channel

blockers

Alternate:

Alpha1-blockers

Alpha2-blockers

Direct-acting vasodilators

Peripheral adrenergic

antagonist


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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 H2

O from the

body and decreased BP


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Loop Diuretics

Mechanism of action:

Inhibits Na+and Cl-

resorption in theloop of Henle and

so H2O (water

follows sodium)

Dilates blood

vessels


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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 tohypotension

dose-related hearing loss (ototoxicity)


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Loop Diuretics

Specific Drugs

furosemide

Torsemide

bumetanideNursing actions:

Monitor I/O and BP

Monitor effects of Lanoxin (digoxin)

Baseline and close monitoring of K+ Assess for:

Dehydration

Hypotension

Hearing loss


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Thiazide

Mechanism of action: inhibit the sodium-chloride

transporter in the distal

tubule. Because this

transporter normally onlyreabsorbs about 5% of

filtered sodium, these

diuretics are less

efficacious than loopdiuretics in producing

diuresis and natriuresis.


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Thiazide

Therapeutic effects:

Excretion of Na+, Cl-, K+and H2O

without altering pH Treatment of edema

Side effects

Hypokalemia

Headache, dizziness


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ThiazideSpecific Drug

Hydrodiuril (hydrochlorthiazide)

Zaroxolyn (Metolazone)


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NCs: Thiazide

Nursing actions: Monitor I/O, BP and K+


Monitor electroytes

Adequate dietary K+

Monitor uric acid

Crosses placenta and into breastmilk


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Potassium Sparing Diuretics

contAdverse effects:

Electrolyte imbalance with potentialelevation in K+

Headache, dizziness

Prototype:

Aldactone (spironolactone)


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NCs: Potassium Sparing

DiureticsNursing actions:

Monitor I/O, BP and K+


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


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Calcium Channel Blockers


Inhibits transport of calcium intomyocardial and smooth muscle cells

Dilates peripheral arterioles, decreasingafterload

Decreases heart contractility (negativeionotrope)

Decreases SA node firing rate andconductivity of AV node (negativechronotrope)


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Calcium Channel Blockers cont.

Therapeutic Effects:

Lowers HR and BP- Depending on drug in

class Decreases myocardial O2demand

Decreases coronary artery spasm

Decreases angina and rhythmdisturbances


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Side effects:

Bradycardia, reflex tachycardia

Peripheral edemaInteractions:

Other antihypertensives and diuretics

(increased hypotensive effects)


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Prototypes:

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

Nursing considerations:

Monitor BP, HR, I/O, daily weight, sideeffects

Focus assessment-cardiac and pulmonary


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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


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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 indecreased vasoconstriction and decreased

afterload

Decreased aldosterone production results in

decreased Na and H2O reabsorption so

decreased BP


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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)


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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


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Angiotensin II Receptor Blockers

(ARBs)- 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


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Angiotensin II Receptor Blockers

(ARBs)- 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


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Beta Blockers- olols


Cardioselective: Bind to and block B1receptors

on the hearts conduction system and throughout

the myocardium Nonselective: bind to, and block, B1and B2

receptors (heart and lungs)

Decreases heart contractility (Negative

ionotrope) reducing O2requirements ofmyocardial cells

Decrease SA node firing rate (negative

chronotrope)


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Beta Blockers- olols cont.

Therapeutic Effects

Decreased heart rate and decreased

myocardial oxygen demand Decreased angina

Fewer rhythm disturbances

Decreased renin release


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Beta Blockers- olols cont.

Adverse effects:

Dysrhythmias (bradycardia), heartfailure

Bronchospasm / bronchoconstriction

Fatigue, depression, impotence

Interactions:

Other antihypertensives and diuretics(increased hypotensive effects)


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NCs: Beta-adrenergic Blockers

May take two weeks for optimal therapeuticresponse

Check BP and pulse prior to dose

Monitor cardiac function Assess for:

Respiratory distress

Bradycardia, heart block, fatigue, activityintolerance

DO NOT STOP SUDDENLY


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Alpha1-adrenergic Antagonists

Mechanism of action-selectively inhibits alpha-1 adrenergic

receptors. Blockages of the alpha-1adrenergic action on the vascular smooth

muscles lead to a decrease in vascular

resistance and antihypertensive activity.


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NCs: Alpha1-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


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Direct Vasodilators

Relaxes smooth muscle in arterioles

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