Cardiac Cardiac MedicationsMedications

HypertensionHypertension

Learning ObjectivesLearning Objectives

Students will be able to:Students will be able to: Discuss the major categories of drugs as Discuss the major categories of drugs as

they relate to the treatment of Cardiac they relate to the treatment of Cardiac Disease. Disease.

Describe the major effects of various Describe the major effects of various medications on cardiac function.medications on cardiac function.

Discuss major nursing implications when Discuss major nursing implications when administering above medications.administering above medications.

New Zealand Statistics:New Zealand Statistics:

Maori die almost a decade earlier than Maori die almost a decade earlier than non-Maori in New Zealand. non-Maori in New Zealand.

Cardiovascular disease is a major Cardiovascular disease is a major contributor to this statistic (NZGG, 2003).contributor to this statistic (NZGG, 2003).

Maori should therefore be assessed for Maori should therefore be assessed for risk 10 years earlier than non-Maori. risk 10 years earlier than non-Maori.

HypertensionHypertension

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

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

Two types hypertensionTwo types hypertension Primary: no known causePrimary: no known cause Secondary: consequence of underlying Secondary: consequence of underlying

disease or conditiondisease or condition

Goal with hypertension:Goal with hypertension: Two primary regulatory factors:Two primary regulatory factors:

Blood flow (volume)Blood flow (volume) Peripheral Vascular Resistance (PVR)Peripheral Vascular Resistance (PVR)

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

Primary groups of drugs are used:Primary groups of drugs are used: DiureticsDiuretics Adrenergic inhibitors (Beta-blockers)Adrenergic inhibitors (Beta-blockers) VasodilatorsVasodilators ACE inhibitorsACE inhibitors Calcium antagonistsCalcium antagonists

Diuretics: to reduce overall Diuretics: to reduce overall volume of bloodvolume of blood

ThiazidesThiazides - block sodium - block sodium reabsorption in nephron’s reabsorption in nephron’s distal segmentdistal segment Water is excreted with Water is excreted with

sodium, producing decreased sodium, producing decreased blood volumeblood volume

Loop diureticsLoop diuretics – potent loop – potent loop diuretic that inhibits sodium diuretic that inhibits sodium and chloride reabsorption at and chloride reabsorption at proximal and distal tubules proximal and distal tubules and ascending loop of Henleand ascending loop of Henle Indicated for acute Indicated for acute

pulmonary oedemapulmonary oedema

MedlinePlus Medical Encyclopedia

Diuretics Cont’dDiuretics Cont’d Nursing Interventions:Nursing Interventions:

Monitor K+ routinely (depleted here)Monitor K+ routinely (depleted here) Monitor weight daily and intake/outputMonitor weight daily and intake/output Give in am so avoid nocturiaGive in am so avoid nocturia

Potassium-sparing diureticsPotassium-sparing diuretics(Aldactone or Spironolactone)(Aldactone or Spironolactone)

Potassium sparing diureticPotassium sparing diuretic Antagonises aldosterone in the distal tubules Antagonises aldosterone in the distal tubules

which increases sodium and water excretionwhich increases sodium and water excretion Need to watch for hyperkalemia and don’t give Need to watch for hyperkalemia and don’t give

potassium supplementspotassium supplements Monitor electrolytes and fluid intake/outputMonitor electrolytes and fluid intake/output Monitor blood pressure and daily weightsMonitor blood pressure and daily weights Less potent than thiazide and loop diuretics but Less potent than thiazide and loop diuretics but

useful as an adjunct to other diuretic therapyuseful as an adjunct to other diuretic therapy

VasodilatorsVasodilators

Hydralazine hycrochloride (Apresoline)Hydralazine hycrochloride (Apresoline) Dilate peripheral blood vessels by directly Dilate peripheral blood vessels by directly

relaxing arteriolar smooth musclerelaxing arteriolar smooth muscle Usually used in combination with other Usually used in combination with other

antihypertensives as they increase antihypertensives as they increase sodium and fluid retentionsodium and fluid retention

Calcium AntagonistsCalcium Antagonists

Felodipine, Nifedipine, DiltiazemFelodipine, Nifedipine, Diltiazem Inhibit the influx of calcium into muscle Inhibit the influx of calcium into muscle

cells; act on vascular smooth muscle cells; act on vascular smooth muscle (primary arteries) to reduce spasms and (primary arteries) to reduce spasms and promote vasodilatationpromote vasodilatation

May enhance serum Digoxin levelsMay enhance serum Digoxin levels

Cardiac MedicationsCardiac Medications

Coronary Coronary ArteryArtery

DiseaseDisease

New Zealand StatisticsNew Zealand Statistics Cardiovascular disease is the leading Cardiovascular disease is the leading

cause of death in New Zealand (NZGG, cause of death in New Zealand (NZGG, 2003).2003).

1998 N.Z. had age-standardised mortality 1998 N.Z. had age-standardised mortality rate from CAD of 111/100,000 peoplerate from CAD of 111/100,000 people

CAD death rates for Maori less than 75 CAD death rates for Maori less than 75 yrs old are 2-3X higher than non-Maori yrs old are 2-3X higher than non-Maori and 2X as high for Pacific peoples.and 2X as high for Pacific peoples.

So what is the overall goal So what is the overall goal in managing CAD?in managing CAD? To reduce 5-year cardiovascular risk to To reduce 5-year cardiovascular risk to

less than 15% with medications less than 15% with medications (NZGG, 2003).(NZGG, 2003).

Ensure individuals with total Ensure individuals with total cholesterol greater than 8mmol/L cholesterol greater than 8mmol/L undergo risk assessment and lipid undergo risk assessment and lipid modifying treatment.modifying treatment.

Ensure BP less than 170/100 drug Ensure BP less than 170/100 drug treatmenttreatment

Different drug effects:Different drug effects:

InotropicInotropic: relating to or : relating to or influencing the force of influencing the force of contractioncontraction

ChronotropicChronotropic: : influencing the rate; influencing the rate; especially the heart beatespecially the heart beat

DromotropicDromotropic: affecting : affecting the conductivity of the conductivity of cardiac muscle -- used cardiac muscle -- used of the influence of of the influence of cardiac nervescardiac nerves Jarvis, 2000, Figure 17-8. p. 505.

Figure 17-1. p. 498.

Overview of Pulmonary/Systemic CirculationOverview of Pulmonary/Systemic Circulation

Carolyn Jarvis, Physical Exam and Health Assessment 3rd Ed. 2000. Copyright by W.B. Saunders

So what is the goal of medical So what is the goal of medical management of heart management of heart disease?disease? Dissolve clots (save muscle)Dissolve clots (save muscle) Maximize blood flow to heart muscleMaximize blood flow to heart muscle Maximize preload Maximize preload Minimize the afterload Minimize the afterload Maximize cardiac contractility (inotropic effect)Maximize cardiac contractility (inotropic effect) Reduce chances clot formation Reduce chances clot formation Reduce overall blood volume if overloadReduce overall blood volume if overload Heart rate between 60-80 beats/min to maximize Heart rate between 60-80 beats/min to maximize

cardiac output and filling pressurescardiac output and filling pressures Treat arrhythmiasTreat arrhythmias

Preload/Afterload in HeartPreload/Afterload in Heart

Carolyn Jarvis, Physical Exam and Health Assessment 3rd Ed. 2000. Copyright by W.B. Saunders

So what drugs help meet So what drugs help meet these goals?these goals? Dissolve existing clots quickly—TPA, UrokinaseDissolve existing clots quickly—TPA, Urokinase Maximize preload— I.V. fluids, volume expandersMaximize preload— I.V. fluids, volume expanders Minimize afterload—Ace inhibitors, IABPMinimize afterload—Ace inhibitors, IABP Maximize cardiac contractility—Digoxin, Maximize cardiac contractility—Digoxin,

DopamineDopamine Decrease preload, increase coronary circulation, Decrease preload, increase coronary circulation,

and reduce pulmonary congestion—Nitratesand reduce pulmonary congestion—Nitrates Reduce chances clot formation—ASA or other Reduce chances clot formation—ASA or other

anti-platelet medicationsanti-platelet medications Reduce overall fluid volume in overload--diureticsReduce overall fluid volume in overload--diuretics Keep heart rate between 60-80/min (Beta Keep heart rate between 60-80/min (Beta

blockers and Calcium-channel blockers)blockers and Calcium-channel blockers) Arrhythmias—Atropine, Lidocaine, etc.Arrhythmias—Atropine, Lidocaine, etc.

Fibrolytic DrugsFibrolytic Drugs

TPA-tissue TPA-tissue plasminogen plasminogen activatorsactivators

StreptokinaseStreptokinase

Image from site http://www.americanheart.org/presenter.jhtml?identifier=4751

NitratesNitrates GTNGTN Cause vasodilatation reducing the amount of Cause vasodilatation reducing the amount of

blood returning to the heart from the venous blood returning to the heart from the venous system, thus decreasing preload.system, thus decreasing preload.

This decreases the work of the heart and the This decreases the work of the heart and the demand of the myocardium for oxygen.demand of the myocardium for oxygen.

Also dilate the peripheral arteries, decreasing Also dilate the peripheral arteries, decreasing the resistance against which the left ventricle the resistance against which the left ventricle must pump (decreases afterload).must pump (decreases afterload).

Increases coronary vasodilationIncreases coronary vasodilation Reduces lung congestionReduces lung congestion

ACE InhibitorsACE Inhibitors (pril)(pril) Used to treat both hypertension and ACSUsed to treat both hypertension and ACS Inhibit the conversion of angiotension I to Inhibit the conversion of angiotension I to

angiotension II, thus blocking the release angiotension II, thus blocking the release of aldosterone, thereby reducing sodium of aldosterone, thereby reducing sodium and water retentionand water retention

Potassium-sparing so watch for Potassium-sparing so watch for hyperkalemiahyperkalemia

Reduce afterload of heartReduce afterload of heart

InotropesInotropes DigitalisDigitalis Inhibits the sodium-potassium pump, causing Inhibits the sodium-potassium pump, causing

an increase in intracellular an increase in intracellular sodium sodium levelslevels Increased sodium levels force sodium out of Increased sodium levels force sodium out of

the cell in exchange for the cell in exchange for calciumcalcium Higher intracellular calcium levels increase the Higher intracellular calcium levels increase the

force of contraction, increasing cardiac outputforce of contraction, increasing cardiac output Digoxin also blocks the slow calcium channels Digoxin also blocks the slow calcium channels

of the AV nodes, slowing the HRof the AV nodes, slowing the HR

Antiplatelet AgentsAntiplatelet Agents

Low dose AspirinLow dose Aspirin Aspirin blocks the formation of Aspirin blocks the formation of

thromboxane Athromboxane A2 2 , inhibiting platelet , inhibiting platelet aggregationaggregation

A single daily dose of around 80mg can A single daily dose of around 80mg can effectively sustain the desired antiplatelet effectively sustain the desired antiplatelet effecteffect

AnticoagulantsAnticoagulants

Heparin (Clexane)Heparin (Clexane) Binds to anti-thrombin, inactivating Binds to anti-thrombin, inactivating

coagulation factors and thrombin, coagulation factors and thrombin, thereby blocking the conversion of thereby blocking the conversion of

fibrinogen to fibrinfibrinogen to fibrin

Side Effects: Side Effects: Anticoagulants, Fibrolytics and Anticoagulants, Fibrolytics and

AntiplateletsAntiplatelets

BleedingBleeding

What symptoms would you see?What symptoms would you see?

INRINR

Beta-blockersBeta-blockers

Block beta-adrenergic receptors of CNSBlock beta-adrenergic receptors of CNS Blockage of beta-1 receptors causes a Blockage of beta-1 receptors causes a

decrease in the force of contraction, a decrease in the force of contraction, a slowing heart rate, and a slowing of impulse slowing heart rate, and a slowing of impulse of conduction (negative inotrope, of conduction (negative inotrope, chonotrope, dromotrope)chonotrope, dromotrope)

These 3 mechanisms of action combine to These 3 mechanisms of action combine to decrease myocardial oxygen demanddecrease myocardial oxygen demand

Calcium-channel blockersCalcium-channel blockers Action: thought to inhibit calcium ion influx Action: thought to inhibit calcium ion influx

across cardiac and smooth muscles, across cardiac and smooth muscles, decreasing contractility and oxygen decreasing contractility and oxygen demand. May also dilate coronary arteries.demand. May also dilate coronary arteries.

Nursing implication: monitor for rapid drop Nursing implication: monitor for rapid drop in BP (especially if given intravenously). in BP (especially if given intravenously).

Cholesterol Lowering Cholesterol Lowering Agents: hypolipidaemic Agents: hypolipidaemic

drugsdrugs StatinsStatins Reduce plasma lipids and lipoproteinsReduce plasma lipids and lipoproteins Block the production of LDLs and increase Block the production of LDLs and increase

receptor activity that removes LDLsreceptor activity that removes LDLs Take other drugs 1 hour before or 4-6 hours Take other drugs 1 hour before or 4-6 hours

after Questran to avoid blockage of after Questran to avoid blockage of absorptionabsorption

Cardiogenic shock: Inability of the impaired ventricle to perfuse and

oxygenate body tissues Common in MI that damages 40% or more of

the left ventricle. Signs:

Systolic BP less than 90 mmHg Anxiety, restlessness, confusion, coma Cool, moist, clammy skin Rales in lungs, decreased (<30ml/hour) urine output S3 and S4 heart sounds Coma and death

Cardiac MedicationsCardiac Medications

Congestive Heart Failure

Table 17-10. p. 548.

Congestive Heart FailureCongestive Heart Failure

What can cause CHF?What can cause CHF?

CAD multiple heart attacksCAD multiple heart attacks High BPHigh BP Faulty heart valvesFaulty heart valves CardiomyopathyCardiomyopathy MyocarditisMyocarditis Congenital heart defectsCongenital heart defects Cardiac arrhythmiasCardiac arrhythmias

Aims of treatment CHF:Aims of treatment CHF:

Relieve symptomsRelieve symptoms Improve quality of lifeImprove quality of life Prevent readmission to hospital, and/or Prevent readmission to hospital, and/or

recurrent ischaemic eventsrecurrent ischaemic events Reduce mortalityReduce mortality

(Lonn & McKelvie, 2000)(Lonn & McKelvie, 2000)

ACE InhibitorsACE Inhibitors Beta BlockersBeta Blockers DiureticsDiuretics VasodilatorsVasodilators Inotropes (e.g. Dopamine)Inotropes (e.g. Dopamine) DigitalisDigitalis

Drugs used to treat CHF

InotropesInotropes DigitalisDigitalis Inhibits the sodium-potassium pump, causing Inhibits the sodium-potassium pump, causing

an increase in intracellular an increase in intracellular sodium sodium levelslevels Increased sodium levels force sodium out of Increased sodium levels force sodium out of

the cell in exchange for the cell in exchange for calciumcalcium Higher intracellular calcium levels increase the Higher intracellular calcium levels increase the

force of contraction, increasing cardiac outputforce of contraction, increasing cardiac output Digoxin also blocks the slow calcium channels Digoxin also blocks the slow calcium channels

of the AV nodes, slowing the HRof the AV nodes, slowing the HR

DopamineDopamine

Stimulates dopamine receptors in the Stimulates dopamine receptors in the renal vessels, increasing renal blood renal vessels, increasing renal blood flow, increasing diuresisflow, increasing diuresis

Net result is an increase in cardiac outputNet result is an increase in cardiac output Increase in systemic arterial pressureIncrease in systemic arterial pressure

Anti-arrhythmicAnti-arrhythmic DrugsDrugs

Ventricular arrhythmias Ventricular arrhythmias AmiodaroneAmiodarone

Treatment of tachyarrhythmias –Treatment of tachyarrhythmias –supraventricular nodal and ventricular supraventricular nodal and ventricular tachycardias, atrial flutter and fibrillation. tachycardias, atrial flutter and fibrillation.

LignocaineLignocaine

Decreased the depolarisation and excitability Decreased the depolarisation and excitability in the ventricles.in the ventricles.

PotassiumPotassium ChlorideChloride

Intracellular ionIntracellular ion Transmission of nerve impulsesTransmission of nerve impulses Contraction of cardiac musclesContraction of cardiac muscles Levels 4.0-4.5Levels 4.0-4.5 Hypokalaemia=potassium deficitHypokalaemia=potassium deficit

Nursing implications CHF:Nursing implications CHF: Daily weightsDaily weights Strict intake/output recordsStrict intake/output records May be on fluid restriction (1500ml/24hrs)May be on fluid restriction (1500ml/24hrs) Teaching regarding medications Teaching regarding medications Elevate feet to avoid stasis ulcersElevate feet to avoid stasis ulcers Oxygen on at all timesOxygen on at all times Monitor BP, heart rate, respiratory rate, pulse Monitor BP, heart rate, respiratory rate, pulse

oximetry frequently (every 2-4 hours)oximetry frequently (every 2-4 hours) Monitor labs (electrolytes, troponin-T)Monitor labs (electrolytes, troponin-T) Auscultate lung fields to assess for change every Auscultate lung fields to assess for change every

4 hours!4 hours!