DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS

04/20/23Winter 20131

DRUGS AFFECTING THE CARDIOVASCULAR and RENAL

SYSTEMS

CARDIAC PROBLEM AREAS

Winter 20132

PUMP

CIRCULATION TO MUSCLE

ELECTRICAL SYSTEM

CARDIAC A&P REVIEW

04/20/23Winter 20133

CARDIAC A&P REVIEW

04/20/23Winter 20134

CARDIAC A&P REVIEW

Winter 20135

HEART FAILUREChapter 22

04/20/23Winter 20136

LEFT SIDED HEART FAILURE (CHRONIC HEART FAILURE)

RESTLESSORTHOPNEASOB (SHORTNESS OF BREATH)DOE (DYSPNEA ON EXERTION)

Common Causes for Heart Failure

Inadequate ContractilityMyocardial Infarction

Inadequate FillingAtrial fibrillation

Pressure OverloadHypertension

Volume OverloadHypervolemia

Complete list on pg. 336

04/20/23Winter 20137

DRUG CLASSES FOR HEART FAILURE

04/20/23Winter 20138

ANGIOTENSIN – CONVERTING ENZYME INHIBITORS

ANGIOTENSIN II RECEPTOR BLOCKERSBETA-BLOCKERSB-TYPE NATRIURETIC PEPTIDEPHOSPHODIESTERASE INHIBITORSCARDIAC GLYCOSIDES

ANGIOTENSIN –CONVERTING ENZYME INHIBITORS

ACE InhibitorsPrevents vasoconstriction, sodium and water

resorptionLisinopril

Indicated for heart failure, hypertension, acute Myocardial Infarction

04/20/23Winter 20139

ANGIOTENSIN II RECEPTOR BLOCKERS

ARBsvalsartan (Diovan)

Potent vasodilating effectsDecreases systemic vascular resistanceUsed in combination with diuretics to treat Heart

Failure and Hypertension

04/20/23Winter 201310

BETA-BLOCKERS

Block sympathetic nervous system stimulation of the heartReduce heart rate, delayed AV node conduction,

reduced myocardial contractility and decreased myocardial automaticity.

metoprololDecreased workload of the heart

04/20/23Winter 201311

Synthetic human B-type natriuretic peptide

Nesiritide (Natrecor)Vasodilating effect on both arteries and veins

Treatment of patients with acutely decompensated CHF who have dyspnea at rest or with minimal activity.

Treatment for severe life-threatening heart failureCauses diuresis, urine sodium loss and vasodilation

04/20/23Winter 201312

PHOSPHODIESTERASE INHIBITORS

inamrinone and milrinonePositive inotropic and vasodilating effectsDecrease cardiac work load Parenteral onlyShort-term management of CHF

04/20/23Winter 201313

CARDIAC GLYCOSIDES(aka: digitalis glycosides)

04/20/23Winter 201314

INCREASE THE EFFICIENCY OF THE HEART BY IMPROVING THE CONTRACTION OF THE HEART MUSCLEPOSITIVE INOTROPIC ACTION

INCREASING THE FORCE OF MYOCARDIAL CONTRACTION

Negative chronotropic effect – reduced heart rateNegative dromotropic effect – decreased automaticity at the

SA note, AV node and bundle of HIS

digoxin (Lanoxin)Not first line drug in Heart Failure

WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY??

04/20/23Winter 201315

INADEQUATE CONTRACTILITYMI (MYOCARDIAL INFARCTION)CORONARY ARTERY DISEASECARDIOMYOPATHY

INADEQUATE FILLINGATRIAL FIBRILLATION

Atrial Fibrillation

04/20/23Winter 201316

NORMAL SINUS RHYTHM (NSR)

A FIB

WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY??

04/20/23Winter 201317

PRESSURE OVERLOADHYPERTENSION

VOLUME OVERLOADHYPERVOLEMIA

DIGOXIN (LANOXIN)

04/20/23Winter 201318

DIGITALIZATIONThe administration of digitalis or one of its glycosides in a

dosage schedule designed to produce and then maintain optimal therapeutic concentration

CARDIAC GLYCOSIDES HAVE BEEN USED TO TREAT HEART FAILURE FOR OVER 200 YEARS

DIGOXIN (LANOXIN)

04/20/23Winter 201319

WHAT DOES IT DO???

INCREASES CARDIAC CONTRACTILITY BY INHIBITING THE K+/Na+ PUMP AND INFLUENCING CALCIUM MOVEMENT

STIMULATES THE VAGUS NERVE = SLOWING THE HEART RATE NEGATIVE CHRONOTROPIC EFFECT

POSITIVE INOTROPIC EFFECT – Increases the squeeze!

ADVERSE EFFECTS OF CARDIAC GLYCOSIDES MEDICATIONS

04/20/23Winter 201320

DYSRYTHMIASHEADACHEFATIGUE

ANOREXIAN, V, D

NURSING CONSIDERATIONS

04/20/23Winter 201321

APICAL PULSE FOR ONE MINUTE PRIOR TO GIVING DIGOXIN “HOLD” IF <60

ANTACIDS INTERFERE WITH ABSORPTION

AVOID GIVING DIGOXIN WITH HIGH-FIBER FOODS (FIBER BINDS WITH DIGITALIS)

TEACH S&S OF TOXICITY

TRACK BLOOD LEVELS FOR DIG AND ELECTROLYTES

DIGOXIN LEVELS MUST BE MONITORED 0.5 TO 2 ng/ml

DIGITALIS TOXICITY

04/20/23Winter 201322

SIGNS AND SYMPTOMSN, VANOREXIAVISUAL DISTURBANCES

MAY SEE YELLOW, GREEN, BLUE HALOSCONFUSIONBRADYCARDIAEKG CHANGES

TREATMENT FOR DIG TOXICITY

04/20/23Winter 201323

STOP TAKING THE DRUGDIGOXIN IMMUNE FAB (DIGIBIND)

WHAT CAUSED THE PROBLEM?HYPOKALEMIA R/T DIURETIC DRUGSLIVER FAILURE

ANTIDYSRHYTHMIC DRUGSChapter 23

04/20/23Winter 201324

DYSRHYTHMIA (ARRHYTHMIA)

ANY DEVIATION FROM THE “NORMAL” RHYTHM

“NORMAL” ELECTRICAL PATTERN OF THE HEART

04/20/23Winter 201325

04/20/23Winter 201326

Vaughan Williams Classification

System commonly used to classify antidysrhythmic drugs

Based on the electrophysiologic effect of particular drugs on the action potential

04/20/23Winter 201327

Vaughan Williams Classification (cont’d)

Class IClass IaClass IbClass Ic

Class IIClass IIIClass IVOther

04/20/23Winter 201328

Vaughan Williams Classification:Mechanism of Action

Class IMembrane-stabilizing drugsFast sodium channel blockersDivided into Ia, Ib, and Ic drugs,

according to effects

04/20/23Winter 201329

Vaughan Williams Classification:Mechanism of Action and Indications

Class I: moricizineGeneral class I drugHas characteristics of all three subclassesUsed for symptomatic ventricular and

life-threatening dysrhythmias

04/20/23Winter 201330

Vaughan Williams Classification:Mechanism of Action and Indications (cont’d)

Class Ia: quinidine, procainamide, disopyramide

Block sodium (fast) channelsDelay repolarizationIncrease APD (action potential duration)

Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome

04/20/2331 Winter 2013

04/20/2332 Winter 2013

04/20/23Winter 201333


(cont’d)

Class Ib: phenytoin, lidocaine

Block sodium channelsAccelerate repolarizationIncrease or decrease APDUsed for ventricular dysrhythmias only

Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation

04/20/23Winter 201334


(cont’d) • Class Ic: flecainide, propafenone ▫ Block sodium channels (more pronounced

effect)▫ Little effect on APD or repolarization▫ Used for severe ventricular dysrhythmias▫ May be used in atrial fibrillation/flutter, Wolff-

Parkinson-White syndrome, supraventricular tachycardia dysrhythmias

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04/20/2336 Winter 2013

04/20/2337 Winter 2013

04/20/23Winter 201338


Class II: beta-blockers: atenolol, esmolol, metaprolol, propranololReduce or block sympathetic nervous system

stimulation, thus reducing transmission of impulses in the heart’s conduction system

Depress phase 4 depolarizationGeneral myocardial depressants for both

supraventricular and ventricular dysrhythmiasAlso used as antianginal and antihypertensive drugs

04/20/23Winter 201339


Class III: amiodarone, sotalol*, ibutilide, others Increase APDProlong repolarization in phase 3Used for dysrhythmias that are difficult to treat

Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs

Sustained ventricular tachycardia

*Sotalol also exhibits Class II properties

04/20/23Winter 201340


Class IV: verapamil, diltiazem

Calcium channel blockersInhibit slow-channel (calcium-dependent) pathways

Depress phase 4 depolarizationReduce AV node conductionUsed for paroxysmal supraventricular

tachycardia (PSVT); rate control for atrial fibrillation and flutter

04/20/2341 Winter 2013

04/20/23Winter 201342

Vaughan Williams Classification: Other Antidysrhythmics

Digoxin, adenosine Have properties of several classes and are

not placed into one particular class

04/20/23Winter 201343

Unclassified Antidysrhythmic

adenosine (Adenocard)Slows conduction through the AV nodeUsed to convert paroxysmal supraventricular

tachycardia to sinus rhythmVery short half-life—less than 10 secondsOnly administered as fast IV pushMay cause asystole for a few secondsOther adverse effects minimal

ADVERSE REACTION TO ANTIDYSRHYTHMICS

04/20/23Winter 201344

N, V, DDIZZINESSHEADACHEBLURRED VISIONCAN CAUSE DYSRHYTHMIAS !!


04/20/23Winter 201345

MONITOR PULSE RATEIF SENDING PT HOME – TEACH THEM HOW TO

MONITOR THEIR PULSE

ALWAYS CHECK ALL VS BEFORE ADMINISTERING THE MEDICATION


04/20/23Winter 201346

MONITOR FOR FLUID RETENTION

DO NOT STOP DRUGS ABRUPTLY

AVOID ALCOHOL

CHAPTER 24CHAPTER 24

Antianginal DrugsAntianginal Drugs

04/20/2347 Winter 2013

Angina Pectoris (Chest Pain)

When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches”

The heart requires a large supply of oxygen to meet the demands placed on it

04/20/2348 Winter 2013

IschemiaIschemia

Poor blood supply to an organIschemic heart disease

Poor blood supply to the heart muscleAtherosclerosisCoronary artery disease

Myocardial infarction (MI)Necrosis, or death, of cardiac tissueDisabling or fatal

04/20/2349 Winter 2013

04/20/23Winter 201350

04/20/23Winter 201351

Types of Angina

Chronic stable angina (also called classic or effort angina)

Unstable angina(also called preinfarction or crescendo angina)

Vasospastic angina(also called Prinzmetal’s or variant angina)

04/20/2352 Winter 2013

Drug Classifications for Angina

Nitrates/nitritesBeta-blockersCalcium channel blockers

04/20/2353 Winter 2013

Therapeutic Objectives

Increase blood flow to ischemic heart muscle

and/or

Decrease myocardial oxygen demand

04/20/2354 Winter 2013

Therapeutic Objectives (cont’d)

Minimize the frequency of attacks and decrease the duration and intensity of anginal pain

Improve the patient’s functional capacity with as few adverse effects as possible

Prevent or delay the worst possible outcome: MI

04/20/2355 Winter 2013

Nitrates/Nitrites

Available formsSublingual*Buccal*Chewable tabletsOral capsules/tabletsIntravenous solutions*

*Bypass the liver and the first-pass effect

Transdermal patches* Ointments* Translingual sprays*

04/20/2356 Winter 2013

Nitrates/Nitrites (cont’d)

Cause vasodilation because of relaxation of smooth muscles

Potent dilating effect on coronary arteries

Used for prevention and treatment of angina

04/20/2357 Winter 2013


Vasodilation results in reduced myocardial oxygen demand

Nitrates cause dilation of both large and small coronary vessels

Result: oxygen to ischemic myocardial tissue

Nitrates alleviate coronary artery spasms

04/20/2358 Winter 2013


Rapid-acting formsUsed to treat acute anginal attacks

Sublingual tabletsIntravenous infusion

Long-acting formsUsed to PREVENT anginal episodes

04/20/2359 Winter 2013


NitroglycerinPrototypical nitrateLarge first-pass effect with oral forms

Used for symptomatic treatment of ischemic heart conditions (angina)

IV form used for BP control in perioperative hypertension, treatment of HF, ischemic pain, pulmonary edema associated with acute MI, and hypertensive emergencies

04/20/2360 Winter 2013

Nitrates

Isosorbide dinitrate (Isordil, Sorbitrate, Dilatrate SR)

Isosorbide mononitrate (Imdur, Monoket, ISMO)Used for:

Acute relief of anginaProphylaxis in situations that may provoke anginaLong-term prophylaxis of angina

04/20/2361 Winter 2013

Nitrates (cont’d)

Adverse effectsHeadaches

Usually diminish in intensity and frequency with continued use

Tachycardia, postural hypotensionTolerance may develop

04/20/2362 Winter 2013

Tolerance

Occurs in patients taking nitrates around the clock or with long-acting forms

Prevented by allowing a regular nitrate-free period to allow enzyme pathways to replenishTransdermal forms: remove patch at bedtime for 8

hours, then apply a new patch in the morning

04/20/2363 Winter 2013

Beta-Blockers

atenolol (Tenormin)metoprolol (Lopressor)propranolol (Inderal)nadolol (Corgard)

04/20/2364 Winter 2013

04/20/23Winter 201365

Beta Adrenergic Blockers: Mechanism of Action

Block beta1 Adrenergic -receptors on the heart

Decrease HR, resulting in decreased myocardial oxygen demand and increased oxygen delivery to the heart

Decrease myocardial contractility, helping to conserve energy or decrease demand

04/20/2366 Winter 2013

Beta Adrenergic Blockers: Mechanism of Action (cont’d)

After an MI, a high level of circulating catecholamines irritate the heart, causing an imbalance in supply and demand ratio and even leading to life-threatening dysrhythmias

Beta Adrenergic Blockers block the harmful effects of catecholamines, thus improving survival after an MI

04/20/2367 Winter 2013

Beta Adrenergic Blockers (cont’d)

IndicationsAnginaAntihypertensiveCardiac dysrhythmiasCardioprotective effects, especially after MISome used for migraine headaches,

essential tremors, and stage fright

04/20/2368 Winter 2013


Adverse effectsBody System Adverse EffectsCardiovascular Bradycardia, hypotension,

second- or third-degree heart block; heart failure

Metabolic Altered glucose and lipidmetabolism

04/20/2369 Winter 2013


Adverse effects (cont’d)Body System Adverse Effects

CNS Dizziness, fatigue, mental depression, lethargy,

drowsiness, unusual dreams

Other Impotence, wheezing, dyspnea, constipation

04/20/2370 Winter 2013

04/20/23Winter 201371

Calcium Channel Blockers

verapamil (Calan, Isoptin)diltiazem (Cardizem)nifedipine (Procardia)amlodipine (Norvasc)Others

04/20/2372 Winter 2013

04/20/23Winter 201373

Calcium Channel Blockers (cont’d)

Mechanism of actionCause coronary artery vasodilationCause peripheral arterial vasodilation,

thus decreasing systemic vascular resistance

Reduce the workload of the heartResult: decreased myocardial oxygen

demand

04/20/2374 Winter 2013


IndicationsFirst-line drugs for treatment of angina, hypertension,

and supraventricular tachycardia

Coronary artery spasms (Prinzmetal’s angina)

Short-term management of atrial fibrillation and flutter

Several other uses

04/20/2375 Winter 2013


Adverse effectsVery acceptable adverse effect and safety

profile

May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea, other adverse effects

04/20/2376 Winter 2013

Nursing Implications – All Antidysrhythmic Drugs

Before administering, perform a complete health history to determine presence of conditions that may be contraindications for use or those that may call for cautious use

Obtain baseline VS, including respiratory patterns and rate

Assess for drug interactions

04/20/2377 Winter 2013


Patients should not take any medications, including over-the-counter medications, without checking with their physician

Patients should be encouraged to limit caffeine intake

04/20/2378 Winter 2013


Patients should report blurred vision, persistent headache, dry mouth, dizziness, edema, fainting episodes, weight gain of 2 pounds in 1 day or 5 pounds in 1 week, pulse rates less than 60, and dyspnea

04/20/2379 Winter 2013


Alcohol consumption and spending time in hot baths or whirlpools, hot tubs, or saunas will result in vasodilation, hypotension, and the possibility of fainting

Teach patients to change positions slowly to avoid postural BP changes

Encourage patients to keep a record of their anginal attacks, including precipitating factors, number of pills taken, and therapeutic effects

04/20/2380 Winter 2013

Nursing Implications

NitroglycerinInstruct patients in proper technique and

guidelines for taking sublingual nitroglycerin for anginal pain

Instruct patients never to chew or swallow the sublingual form

Instruct patients that a burning sensation felt with sublingual forms indicates that the drug is still potent

04/20/2381 Winter 2013


Nitroglycerin (cont’d)Instruct patients to keep a fresh supply of

sublingual medication on hand; potency is lost in about 3 months after the bottle has been opened

To preserve potency, medications should be stored in an airtight, dark glass bottle with a metal cap and no cotton filler

04/20/2382 Winter 2013


Nitroglycerin (cont’d)Instruct patients in the proper application of

nitrate topical ointments and transdermal forms, including site rotation and removal of old medication

To reduce tolerance, the patient may be instructed to remove topical forms at bedtime and apply new doses in the morning, allowing for a nitrate-free period

04/20/2383 Winter 2013


Nitroglycerin (cont’d)Instruct patients to take prn nitrates at the first hint of

anginal pain

Monitor vital signs frequently during acute exacerbations of angina and during IV administration

If experiencing chest pain, the patient taking sublingual nitroglycerin should lie down to prevent or decrease dizziness and fainting that may occur because of hypotension

04/20/2384 Winter 2013


Nitroglycerin (cont’d)If anginal pain occurs:

Stop activity and sit or lie downTake a sublingual tablet, if no relief, call

911/Emergency Services immediately!If no relief in 5 minutes, take a second sublingual

tabletIf no relief in 5 minutes, take a third sublingual

tabletDo not try to drive to the hospital

04/20/2385 Winter 2013


Nitroglycerin (cont’d) IV forms of nitroglycerin must be given with

special non-PVC tubing and bags

Discard parenteral solution that is blue, green, or dark red

Follow specific manufacturer’s instructions for IV administration

04/20/2386 Winter 2013


Calcium channel blockersConstipation is a common problem; instruct

patients to take in adequate fluids and eat high-fiber foods

04/20/2387 Winter 2013


Beta-blockersPatients taking beta-blockers should monitor

pulse rate daily and report any rate lower than 60 beats per minute

Instruct patients to report dizziness or fainting

Constipation is a common problem; instruct patients to take in adequate fluids and eat high-fiber foods

04/20/2388 Winter 2013


Beta-blockers (cont’d)Inform patients that these medications should

never be abruptly discontinued because of risk of rebound hypertensive crisis

Inform patients that these medications are for long-term prevention of angina, not for immediate relief

04/20/2389 Winter 2013


Antianginal drugsMonitor for adverse reactions

Allergic reactions, headache, lightheadedness, hypotension, dizziness

Monitor for therapeutic effectsRelief of angina, decreased BP, or both

04/20/2390 Winter 2013


Antihypertensive DrugsAntihypertensive Drugs

04/20/2391 Winter 2013

ATHEROSCLEROSIS

04/20/23Winter 201392

DEPOSITS OF CALCIUMLIPIDSCHOLESTROL

ON THE WALLS OF THE ARTERIES

04/20/23Winter 201393

04/20/23Winter 201394

The plaque deposited in your arteries is hard on the outside and soft and mushy on the inside. Sometimes the hard outer shell cracks. When this happens, a blood clot forms around the plaque. If the clot completely blocks the artery, it cuts off the blood supply to a portion of the heart. Without immediate treatment, that part of the heart muscle could be damaged or destroyed.

Blood Pressure

Blood pressure = CO × SVR CO = cardiac outputSVR = systemic vascular resistance

Hypertension = high blood pressure

04/20/2395 Winter 2013

04/20/23Winter 201396

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of

High Blood Pressure (JNC-7)*

Four stages, based on BP measurements Normal Pre-hypertension Stage 1 hypertension Stage 2 hypertension

*New guidelines pending

04/20/2397 Winter 2013

Compelling Indications

Post-MI

High cardiovascular risk

Heart failure

Diabetes mellitus

Chronic kidney disease

Previous stroke

04/20/2398 Winter 2013

JNC-7: Significant Changes

High diastolic BP (DBP) is no longer considered to be more dangerous than high systolic BP (SBP)

Studies have shown that elevated SBP is strongly associated with heart failure, stroke, and renal failure

04/20/2399 Winter 2013

JNC-7: Significant Changes (cont’d)

For those older than age 50, SBP is a more important risk factor for cardiovascular disease (CVD) than DBP

“Prehypertensive” BPs are no longer considered “high normal” and require lifestyle modifications to prevent CVD

04/20/23100 Winter 2013

JNC-7: Significant Changes (cont’d)

Thiazide-type diuretics should be the initial drug therapy for most patients with hypertension (alone or with other drug classes)

The previous labels of “mild,” “moderate,” and “severe” have been dropped

04/20/23101 Winter 2013

Cultural Considerations

Beta-blockers and ACE inhibitors have been found to be more effective in white patients than in African American patients

CCBs and diuretics have been shown to be more effective in African American patients than in white patients

04/20/23102 Winter 2013

Primary Hypertension

Hypertension can also be defined by its cause

Unknown cause Essential, idiopathic, or primary hypertension 90% of casesGenetic (hereditary) – 30%

African-AmericanObesityRenal failureAdvanced ageAny of the above factors complicated by lifestyle

04/20/23103 Winter 2013

Secondary Hypertension

Known cause Secondary hypertension 10% of cases

Causes such as Pheochromocytoma, pre-eclampsia, renal artery disease

04/20/23Winter 2013104

Take the Salt quiz

04/20/23Winter 2013105

http://www.medicinenet.com/salt_quiz/quiz.htm



Antihypertensive Drugs

Medications used to treat hypertension

CategoriesAdrenergic drugsAngiotensin converting enzyme (ACE) inhibitorsAngiotensin II receptor blockers (ARBs)Calcium channel blockers (CCBs)DiureticsVasodilators

04/20/23106 Winter 2013

Adrenergic Drugs: Centrally Acting Alpha2-Receptor Agonists

clonidine (Catapres)methyldopa (Aldomet)

Can be used for hypertension in pregnancy

04/20/23107 Winter 2013

Adrenergic Drugs: Peripherally ActingMechanism of Action

Peripheral alpha1-blockers/antagonistsBlock alpha1-adrenergic receptors

doxazosin (Cardura)terazosin (Hytrin)

Results in decreased blood pressure

04/20/23108 Winter 2013

Adrenergic Drugs:Mechanism of Action (cont’d)

Beta-blockersReduce BP by reducing heart rate through

beta1-blockadeCause reduced secretion of reninLong-term use causes reduced peripheral vascular

resistancePropranolol, atenolol, othersNewest: nebivolol (Bystolic)—beta1-selectiveResult: decreased blood pressure

04/20/23109 Winter 2013

Adrenergic Drugs:Mechanism of Action (cont’d)

Dual-action alpha1- and beta1-receptor blockersBlock alpha1-adrenergic receptors

Reduction of heart rate (beta1-receptor blockade)Vasodilation (alpha1-receptor blockade)

carvedilol (Coreg) and labetalolResult in decreased blood pressure

04/20/23110 Winter 2013

Adrenergic Drugs: Adverse Effects

High incidence of orthostatic hypotension Most common

Dry mouth Drowsiness, sedation Constipation

Other Headaches Sleep disturbances Nausea Rash Cardiac disturbances (palpitations), others

04/20/23111 Winter 2013

04/20/23Winter 2013112

Adrenergic Drugs (cont’d)

Beta1 Adrenergic blockers

Act in the peripheryReduce heart rate owing to 1-blockadeExamples: nebivolol (bystolic), propranolol (Inderal),

atenolol (Tenormin), others

04/20/23113 Winter 2013

Angiotensin Converting Enzyme (ACE) Inhibitors

Large group of safe and effective drugs

Often used as first-line drugs for HF and hypertension

May be combined with a thiazide diuretic or calcium channel blocker

04/20/23114 Winter 2013

ACE Inhibitors:Mechanism of Action

Renin-Angiotensin-Aldosterone System

Inhibit angiotensin-converting enzyme, which is responsible for converting angiotensin I (through the action of renin) to angiotensin II

Angiotensin II is a potent vasoconstrictor and causes aldosterone secretion from the adrenal glands

04/20/23115 Winter 2013

ACE Inhibitors:Mechanism of Action (cont’d)

Aldosterone stimulates water and sodium resorption

Result: increased blood volume, increased preload, and increased BP

04/20/23116 Winter 2013

ACE Inhibitors:Mechanism of Action (cont’d)

Block angiotensin-converting enzyme, thus preventing the formation of angiotensin II

Prevent the breakdown of the vasodilating substance, bradykinin

Result in decreased systemic vascular resistance (afterload), vasodilation, and therefore decreased blood pressure

04/20/23117 Winter 2013

ACE Inhibitors:Indications

Hypertension

HF (either alone or in combination with diuretics or other drugs)

Slow progression of left ventricular hypertrophy after MI (cardioprotective)

Renal protective effects in patients with diabetes

04/20/23118 Winter 2013

04/20/23Winter 2013119

ACE Inhibitors: Indications (cont’d)

Drugs of choice in hypertensive patients with HF

Drugs of choice for diabetic patients

04/20/23120 Winter 2013

ACE Inhibitors (cont’d)

captopril (Capoten) Very short half-life

enalapril (Vasotec)Available in oral and parenteral forms

lisinopril (Prinivil and Zestril) and quinapril (Accupril), othersNewer drugs, long half-lives, once-a-day dosing

Several other drugs available

04/20/23121 Winter 2013

ACE Inhibitors (cont’d)

Captopril and lisinopril are NOT prodrugs

Prodrugs are inactive in their administered form and must be metabolized in the liver to an active form so as to be effective

Captopril and lisinopril can be used if a patient has liver dysfunction, unlike other ACE inhibitors that are prodrugs

04/20/23122 Winter 2013

ACE Inhibitors: Adverse Effects

Fatigue Dizziness Headache Mood changes Impaired taste Possible hyperkalemia Dry, nonproductive cough, which reverses when

therapy is stopped Angioedema: rare but potentially fatal

NOTE: First-dose hypotensive effect may occur!

04/20/23123 Winter 2013

04/20/23Winter 2013124

Angiotensin II Receptor Blockers

(A-II blockers, or ARBs)

Newer class

Well tolerated

Do not cause a dry cough

04/20/23125 Winter 2013

Angiotensin II Receptor Blockers: Mechanism of Action

Allow angiotensin I to be converted to angiotensin II, but block the receptors that receive angiotensin II

Block vasoconstriction and release of aldosterone

04/20/23126 Winter 2013

Angiotensin II Receptor Blockers

losartan (Cozaar, Hyzaar)

valsartan (Diovan)

eprosartan (Teveten)

irbesartan (Avapro)

Others

04/20/23127 Winter 2013

Angiotensin II Receptor Blockers: Indications

Hypertension

Adjunctive drugs for the treatment of HF

May be used alone or with other drugs such as diuretics

Used primarily in patients who cannot tolerate ACE inhibitors

04/20/23128 Winter 2013

Angiotensin II Receptor Blockers: Adverse Effects

Upper respiratory infections

Headache

May cause occasional dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigue

Hyperkalemia much less likely to occur

04/20/23129 Winter 2013

Calcium Channel Blockers:Mechanism of Action

Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction

Results inDecreased peripheral smooth muscle toneDecreased systemic vascular resistanceDecreased blood pressure

04/20/23130 Winter 2013

Calcium Channel Blockers

Benzothiazepinesdiltiazem (Cardizem, Dilacor)

Phenylalkaminesverapamil (Calan, Isoptin)

Dihydropyridinesamlodipine (Norvasc), bepridil (Vascor),

nicardipine (Cardene)nifedipine (Procardia), nimodipine (Nimotop)

04/20/23131 Winter 2013

Calcium Channel Blockers: Indications

Angina

Hypertension

Dysrhythmias

Migraine headaches

Raynaud’s disease

04/20/23132 Winter 2013

Calcium Channel Blockers:Adverse Effects

CardiovascularHypotension, palpitations, tachycardia

GastrointestinalConstipation, nausea

OtherRash, flushing, peripheral edema, dermatitis

04/20/23133 Winter 2013

DIURETICS AND DRUGS THAT EFFECT THE RENAL SYSTEM

04/20/23Winter 2013134

Diuretics

Decrease plasma and extracellular fluid volumes

ResultsDecreased preloadDecreased cardiac output Decreased total peripheral resistance

Overall effectDecreased workload of the heart, and decreased

blood pressure

04/20/23135 Winter 2013

CARBONIC ANHYDRASE INHIBITORS (CAIs)

04/20/23Winter 2013136

INHIBIT THE ENZYME ACTIVITY OF CARBONIC ANHYDRASE

CA RECEPTORS ARE LOCATED IN THE PROXIMAL RENAL TUBULE

CAIs PREVENT THE RESORPTION OF SODIUM = ELIMINATION OF WATER AND SODIUM

04/20/23Winter 2013137

WHEN TO USE CAIs?

04/20/23Winter 2013138

ACETOZOLAMIDE (DIAMOX)

USED IN THE TREATMENT OF:

GLAUCOMAEDEMAEPILEPSY

HIGH ALTITUDE SICKNESS (PULMONARY EDEMA)

LOOP DIURETICS

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Have renal, cardiovascular, and metabolic effects

Act along the ascending limb of the loop of Henle.

Blocks chloride and sodium resorption

Chemically related to sulfonamides antibiotics

WHEN DO WE USE LOOP DIURETICS?

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Heart Failure

Liver failure

Hypertension

Renal failure

Increase renal excretion of calcium

FUROSEMIDE (LASIX)

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BLOCK SODIUM AND CHLORIDE RESORPTION

USEFUL FOR RAPID DIURESIS

HYPOKALEMIA IS OFTEN A SIDE EFFECT

OSMOTIC DIURETICS

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PRODUCES OSMOTIC PRESSURE IN THE GLOMERULUS

PULLS WATER INTO THE RENAL TUBULES FROM THE SURROUNDING TISSUE

DECREASING CELLULAR EDEMA!

WHEN TO USE AN OSMOTIC DIURETIC?

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CEREBRAL EDEMA

INCREASED INTRAOCULAR PRESSURE

NOT USED FOR PERIPHERAL EDEMA – NOT ENOUGH SODIUM LOSS

MANNITOL (OSMITROL)

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PRODUCES OSMOTIC PRESSURE IN THE GLOMULAR FILTRATE

PULLS WATER FROM THE RENAL TUBULES AND SURRONDING TISSUE

USED IN ACUTE RENAL FAILURE AND CEREBRAL EDEMA

POTASSIUM SPARING DIURETICS

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WORK IN COLLECTING DUCTS AND DISTAL CONVOLUTED TUBLES

INTERFERE WITH SODIUM + POTASSIUM EXCHANGE

RELEASE Na+ AND H2O –> RETAIN K+

WHEN TO USE POTASSIUM SPARING DIURETICS?

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HYPERTENSIONCHF (CHRONIC HEART FAILURE)

SPIRONOLACTONE (ALDACTONE)

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INTERFERES WITH SODIUM AND POTASSIUM EXCHANGE

NURSE MUST BE AWARE OF THE DANGER OF HYPERKALEMIA

THIAZIDE AND RELATED DIURETICS

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RELATED TO SULFONAMIDE ANTIBIOTICS (ALSO

CAIs)

PREVENT RESORPTION OF SODIUM (Na) POTASSIUM (K) AND CHLORIDE (Cl) IN THE DISTAL CONVOLUTED TUBULE

WHEN TO USE THIAZIDE DIURETICS?

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CAN BE USED ALONE OR IN COMBINATION WITH OTHER DIURETICS TO TREAT:

EDEMAHYPERTENSION

CRONIC HEART FAILURERENAL FAILURE

HYDROCHLORTHIAZIDE (HCTZ) (ESIDRIX)

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INHIBIT RESORPTION OF SODIUM, POTASSIUM AND CHLORIDE

COMMONLY USED WITH OTHER ANTIHYPERTENSIVES

MAJOR SIDE EFFECTS ARE RELATED TO ELECTROLYTE BALANCE

Diuretics (cont’d)

Thiazide diuretics are the most commonly used diuretics for hypertension

Listed as first-line antihypertensives in the JNC-7 guidelines

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Vasodilators:Mechanism of Action

Directly relax arteriolar and/or venous smooth muscle

Results in:Decreased systemic vascular responseDecreased afterload (PVR)Peripheral vasodilation

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Vasodilators

diazoxide (Hyperstat)

hydralazine HCl (Apresoline)

minoxidil (Loniten)

sodium nitroprusside (Nipride, Nitropress)

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Vasodilators: Indications

Treatment of hypertension

May be used in combination with other drugs

Sodium nitroprusside and intravenous diazoxide are reserved for the management of hypertensive emergencies

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Vasodilators: Adverse Effects

hydralazineDizziness, headache, anxiety, tachycardia, nausea

and vomiting, diarrhea, anemia, dyspnea, edema, nasal congestion, others

sodium nitroprussideBradycardia, hypotension, possible cyanide toxicity

(rare)

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Vasodilators: Adverse Effects (cont’d)

diazoxideDizziness, headache, anxiety, orthostatic hypotension,

dysrhythmias, sodium and water retention, nausea, vomiting, hyperglycemia in diabetic patients, others

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Remind patients that medication is only part of therapy. Encourage patients to watch their diet, stress level, weight, and alcohol intake

Instruct patients to avoid smoking and eating foods high in sodium

Encourage supervised exercise

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Nursing Implications (cont’d)

Teach patients to change positions slowly to avoid syncope from postural hypotension

Instruct patients to report unusual shortness of breath; difficulty breathing; swelling of the feet, ankles, face, or around the eyes; weight gain or loss; chest pain; palpitations; or excessive fatigue

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Male patients who take these drugs may not be aware that impotence is an expected effect, and this may influence compliance with drug therapy

If patients are experiencing serious adverse effects, or if they believe the dose or medication needs to be changed, they should contact their physician immediately

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Hot tubs, showers, or baths; hot weather; prolonged sitting or standing; physical exercise; and alcohol ingestion may aggravate low blood pressure, leading to fainting and injury; patients should sit or lie down until symptoms subside

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Coagulation Modifier DrugsCoagulation Modifier Drugs

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Hemostasis

The process that halts bleeding after injury to a blood vessel

Complex relationship between substances that promote clot formation and either inhibit coagulation or dissolve a formed clot

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Coagulation System

“Cascade”

Each activated factor serves as a catalyst that amplifies the next reaction

Result is fibrin, a clot-forming substance

Intrinsic pathway and extrinsic pathway

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Coagulation Modifier Drugs

AnticoagulantsInhibit the action or formation of clotting factorsPrevent clot formation

Antiplatelet drugsInhibit platelet aggregationPrevent platelet plugs

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Coagulation Modifier Drugs (cont’d)

Hemorheologic drugsPentoxifylline(Trental) changes the shape of red blood

cells in your blood. This makes it easier for these blood cells to fit into small arteries (blood vessels). Pentoxifylline is used to improve blood flow. Improved blood flow helps to reduce leg cramps and other symptoms of vascular disease

Thrombolytic drugsLyse (break down) existing clots

Hemostatic or antifibrinolytic drugsPromote blood coagulation

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Anticoagulants

Also known as antithrombotic drugs

Have no direct effect on a blood clot that is already formed

Used prophylactically to preventClot formation (thrombus)An embolus (dislodged clot)

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Anticoagulants:Mechanism of Action

Vary depending on drug

Work on different points of the clotting cascadeDo not lyse existing clots

Heparin and low–molecular-weight heparinsTurn off coagulation pathway and prevent clot

formation

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Anticoagulants:Mechanism of Action (cont’d)

All ultimately prevent clot formationHeparinLow–molecular-weight heparinswarfarin

(Coumadin)Anti-Thrombin (Inhibit thrombin molecule)

fondaparinux (Arixtra) dabigatran (Pradaxa)

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Pradaxa channel 7 and FDA

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http://www.thedenverchannel.com/news/call7-investigators/pradaxa-maker-sued-over-claims-company-didnt-inform-doctors-about-dangers-of-blood-thinning-drug

Anticoagulants (cont’d)

Prevention of clot formation also prevents:StrokeMyocardial infarction (MI)Deep vein thrombosis (DVT)Pulmonary embolism (PE)

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Anticoagulants: Indications

Used to prevent clot formation in certain settings where clot formation is likely

Myocardial infarctionUnstable anginaAtrial fibrillationIndwelling devices, such as mechanical heart valvesMajor orthopedic surgery

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Anticoagulants:Adverse Effects

BleedingRisk increases with increased dosagesMay be localized or systemicHeparin-induced thrombocytopenia (HIT)

May also cause:Nausea, vomiting, abdominal cramps,

thrombocytopenia, others

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HeparinMonitored by activated partial thromboplastin times

(aPTTs)Parenteral (IV or SC)Short half-life (1 to 2 hours)Effects reversed by protamine sulfate

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Low–molecular-weight heparinsenoxaparin (Lovenox) and dalteparin (Fragmin)More predictable anticoagulant response

o Do not require laboratory monitoringGiven subcutaneously

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warfarin sodium (Coumadin)Given orally onlyMonitored by prothrombin time (PT) and International

Normalized Ratio (INR) (PT-INR)Vitamin K can be given if toxicity occurs

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Antiplatelet Drugs

Prevent platelet adhesionaspirindipyridamole (Persantine)clopidogrel (Plavix) and ticlopidine (Ticlid)

ADP inhibitorstirofiban (Aggrastat), eptifibatide (Integrilin), abciximab

(ReoPro)New class, GP IIb/IIIa inhibitors

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Antiplatelet Drugs: Indications

Antithrombotic effects Reduce risk of fatal and nonfatal strokesAcute unstable angina and MI

Adverse effectsVary according to drug

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Antifibrinolytic Drugs

Prevent the lysis of fibrinResult in promoting clot formation

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Antifibrinolytic Drugs (cont’d)

Enhance blood clottingaminocaproic acid (Amicar)desmopressin (DDAVP)

Similar to ADHAlso used in the treatment of diabetes insipidus

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Antifibrinolytic Drugs:Indications

Prevention and treatment of excessive bleedingHyperfibrinolysisSurgical complicationsExcessive oozing from surgical sites such as chest

tubesReducing total blood loss and duration of bleeding

in the postoperative periodTreatment of hemophilia or von Willebrand’s

disease

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Antifibrinolytic Drugs:Adverse Effects

Uncommon and mildRare reports of thrombotic eventsOthers include:

Dysrhythmia, orthostatic hypotension, bradycardia, headache, dizziness, fatigue, nausea, vomiting, abdominal cramps, diarrhea, others

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Thrombolytic Drugs

Drugs that break down, or lyse, preformed clots

Older drugsstreptokinase and urokinase

Newer drugsTissue plasminogen activator (t-PA)Anisoylated plasminogen-streptokinase activator

complex (APSAC)

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Thrombolytic Drugs (cont’d)

anistreplase (Eminase)alteplase (t-PA, Activase)reteplase (Retavase)tenecteplase (TNKase)

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Thrombolytic Drugs: Mechanism of Action

Activate the fibrinolytic system to break down the clot in the blood vessel quickly

Activate plasminogen and convert it to plasmin, which can digest fibrin

Reestablish blood flow to the heart muscle via coronary arteries, preventing tissue destruction

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Thrombolytic Drugs: Indications

Acute MIArterial thrombolysisDVTOcclusion of shunts or cathetersPulmonary embolusAcute ischemic stroke

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Thrombolytic Drugs: Adverse Effects

BleedingInternalIntracranialSuperficial

Other effectsNausea, vomiting, hypotension, anaphylactic

reactionsCardiac dysrhythmias; can be dangerous

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Assess: Patient history, medication history, allergiesContraindicationsBaseline vital signs, laboratory valuesPotential drug interactions—there are MANY! History of abnormal bleeding conditions

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Heparin: Nursing ImplicationsIntravenous doses are usually double-checked with

another nurse

Ensure that SC doses are given SC, not IM

SC doses should be given in areas of deep subcutaneous fat, and sites rotated

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Heparin: Nursing Implications (cont’d)

Do not give SC doses within 2 inches of: The umbilicus, abdominal incisions, or open wounds,

scars, drainage tubes, stomas

Do not aspirate SC injections or massage injection siteMay cause hematoma formation

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Heparin: Nursing Implications (cont’d)

IV doses may be given by bolus or IV infusions

Anticoagulant effects seen immediately

Laboratory values done daily to monitor coagulation effects (aPTT)

Protamine sulfate can be given as an antidote in case of excessive anticoagulation

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LWMHs: Nursing Implications

Given subcutaneously in the abdomen

Rotate injection sites

Protamine sulfate can be given as an antidote in

case of excessive anticoagulation

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Warfarin Sodium:Nursing Implications

May be started while the patient is still on heparin until PT-INR levels indicate adequate anticoagulation

Full therapeutic effect takes several days

Monitor PT-INR regularly—keep follow-up appointments

Antidote is vitamin K

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Warfarin:Nursing Implications

Many herbal products have potential interactions—increased bleeding may occur

Capsicum pepperGarlicGingerGingkoGinsengFeverfew

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Anticoagulants:Patient Education

Education should include:Importance of regular lab testing

Signs of abnormal bleeding

Measures to prevent bruising, bleeding, or tissue injury

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Anticoagulants:Patient Education (cont’d)

Education should include (cont’d):Wearing a medical alert bracelet

Avoiding foods high in vitamin K (tomatoes, dark leafy green vegetables)

Consulting physician before taking other meds or over-the-counter products, including herbals

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Antiplatelet Drugs:Nursing Implications

Concerns and teaching tips same as for

Anticoagulants

Dipyridamole should be taken on an empty stomachDrug-drug interactionsAdverse reactions to reportMonitoring for abnormal bleeding

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Thrombolytic Drugs:Nursing Implications

Follow strict manufacturer’s guidelines for preparation and administration

Monitor IV sites for bleeding, redness, pain

Monitor for bleeding from gums, mucous membranes, nose, injection sites

Observe for signs of internal bleeding (decreased BP, restlessness, increased pulse)

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Coagulation Modifier Drugs:Nursing Implications

Monitor for therapeutic effects

Monitor for signs of excessive bleedingBleeding of gums while brushing teeth, unexplained

nosebleeds, heavier menstrual bleeding, bloody or tarry stools, bloody urine or sputum, abdominal pain, vomiting blood

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Coagulation Modifier Drugs:Nursing Implications (cont’d)

Monitor for adverse effectsIncreased BP, headache, hematoma formation,

hemorrhage, shortness of breath, chills, fever

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DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS

Documents

heart failurewinter

heart failurechapter

heartreduce heart rate

heart failurecauses

myocardial contractility

myocardial automaticity

cardiac ap review

cardiac glycosidesaka