Cardiac Medications #4 08

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  • Cardiac Medications #4 08

    1. 1. Cardiac Medications Hypertension
    2. 2. Learning Objectives <ul><li>Students will be able to: </li></ul><ul><ul><li>Discuss the major categories of drugs as they relate to the treatment of Cardiac Disease. </li></ul></ul><ul><ul><li>Describe the major effects of various medications on cardiac function. </li></ul></ul><ul><ul><li>Discuss major nursing implications when administering above medications. </li></ul></ul>
    3. 3. New Zealand Statistics: <ul><li>Maori die almost a decade earlier than non-Maori in New Zealand. </li></ul><ul><li>Cardiovascular disease is a major contributor to this statistic (NZGG, 2003). </li></ul><ul><li>Maori should therefore be assessed for risk 10 years earlier than non-Maori. </li></ul>
    4. 4. Hypertension <ul><li>Defined as a consistent elevation of the systolic or diastolic blood pressure above 140/90mm Hg </li></ul><ul><li>On two elevated readings (sitting and supine) on separate office visits </li></ul><ul><li>Two types hypertension </li></ul><ul><ul><li>Primary: no known cause </li></ul></ul><ul><ul><li>Secondary: consequence of underlying disease or condition </li></ul></ul>
    5. 5. Goal with hypertension: <ul><li>Two primary regulatory factors: </li></ul><ul><ul><li>Blood flow (volume) </li></ul></ul><ul><ul><li>Peripheral Vascular Resistance (PVR) </li></ul></ul><ul><li>Goal is to optimise these two in order to get pressure below 140/90 mm Hg </li></ul><ul><li>Primary groups of drugs are used: </li></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><li>Adrenergic inhibitors (Beta-blockers) </li></ul></ul><ul><ul><li>Vasodilators </li></ul></ul><ul><ul><li>ACE inhibitors </li></ul></ul><ul><ul><li>Calcium antagonists </li></ul></ul>
    6. 6. Diuretics: to reduce overall volume of blood <ul><li>Thiazides - block sodium reabsorption in nephron’s distal segment </li></ul><ul><ul><li>Water is excreted with sodium, producing decreased blood volume </li></ul></ul><ul><li>Loop diuretics – potent loop diuretic that inhibits sodium and chloride reabsorption at proximal and distal tubules and ascending loop of Henle </li></ul><ul><ul><li>Indicated for acute pulmonary oedema </li></ul></ul>MedlinePlus Medical Encyclopedia
    7. 7. Diuretics Cont’d <ul><li>Nursing Interventions: </li></ul><ul><ul><li>Monitor K+ routinely (depleted here) </li></ul></ul><ul><ul><li>Monitor weight daily and intake/output </li></ul></ul><ul><ul><li>Give in am so avoid nocturia </li></ul></ul>
    8. 8. Potassium-sparing diuretics <ul><li>(Aldactone or Spironolactone) </li></ul><ul><ul><ul><li>Potassium sparing diuretic </li></ul></ul></ul><ul><ul><ul><li>Antagonises aldosterone in the distal tubules which increases sodium and water excretion </li></ul></ul></ul><ul><ul><ul><li>Need to watch for hyperkalemia and don’t give potassium supplements </li></ul></ul></ul><ul><ul><ul><li>Monitor electrolytes and fluid intake/output </li></ul></ul></ul><ul><ul><ul><li>Monitor blood pressure and daily weights </li></ul></ul></ul><ul><ul><ul><li>Less potent than thiazide and loop diuretics but useful as an adjunct to other diuretic therapy </li></ul></ul></ul>
    9. 9. Vasodilators <ul><li>Hydralazine hycrochloride (Apresoline) </li></ul><ul><li>Dilate peripheral blood vessels by directly relaxing arteriolar smooth muscle </li></ul><ul><li>Usually used in combination with other antihypertensives as they increase sodium and fluid retention </li></ul>
    10. 10. Calcium Antagonists <ul><li>Felodipine, Nifedipine, Diltiazem </li></ul><ul><li>Inhibit the influx of calcium into muscle cells; act on vascular smooth muscle (primary arteries) to reduce spasms and promote vasodilatation </li></ul><ul><li>May enhance serum Digoxin levels </li></ul>
    11. 11. Cardiac Medications Coronary Artery Disease
    12. 12. New Zealand Statistics <ul><li>Cardiovascular disease is the leading cause of death in New Zealand (NZGG, 2003). </li></ul><ul><li>1998 N.Z. had age-standardised mortality rate from CAD of 111/100,000 people </li></ul><ul><li>CAD death rates for Maori less than 75 yrs old are 2-3X higher than non-Maori and 2X as high for Pacific peoples. </li></ul>
    13. 13. So what is the overall goal in managing CAD? <ul><li>To reduce 5-year cardiovascular risk to less than 15% with medications (NZGG, 2003). </li></ul><ul><li>Ensure individuals with total cholesterol greater than 8mmol/L undergo risk assessment and lipid modifying treatment. </li></ul><ul><li>Ensure BP less than 170/100 drug treatment </li></ul>
    14. 14. Different drug effects: <ul><li>Inotropic : relating to or influencing the force of contraction </li></ul><ul><li>Chronotropic : influencing the rate; especially the heart beat </li></ul><ul><li>Dromotropic : affecting the conductivity of cardiac muscle -- used of the influence of cardiac nerves </li></ul>Jarvis, 2000, Figure 17-8. p. 505.
    15. 15. <ul><li>Overview of Pulmonary/Systemic Circulation </li></ul>Figure 17-1. p. 498. Carolyn Jarvis, Physical Exam and Health Assessment 3 rd Ed. 2000. Copyright by W.B. Saunders
    16. 16. So what is the goal of medical management of heart disease? <ul><li>Dissolve clots (save muscle) </li></ul><ul><li>Maximize blood flow to heart muscle </li></ul><ul><li>Maximize preload </li></ul><ul><li>Minimize the afterload </li></ul><ul><li>Maximize cardiac contractility (inotropic effect) </li></ul><ul><li>Reduce chances clot formation </li></ul><ul><li>Reduce overall blood volume if overload </li></ul><ul><li>Heart rate between 60-80 beats/min to maximize cardiac output and filling pressures </li></ul><ul><li>Treat arrhythmias </li></ul>
    17. 17. <ul><li>Preload/Afterload in Heart </li></ul>Carolyn Jarvis, Physical Exam and Health Assessment 3rd Ed. 2000. Copyright by W.B. Saunders
    18. 18. So what drugs help meet these goals? <ul><li>Dissolve existing clots quickly—TPA, Urokinase </li></ul><ul><li>Maximize preload— I.V. fluids, volume expanders </li></ul><ul><li>Minimize afterload—Ace inhibitors, IABP </li></ul><ul><li>Maximize cardiac contractility—Digoxin, Dopamine </li></ul><ul><li>Decrease preload, increase coronary circulation, and reduce pulmonary congestion—Nitrates </li></ul><ul><li>Reduce chances clot formation—ASA or other anti-platelet medications </li></ul><ul><li>Reduce overall fluid volume in overload--diuretics </li></ul><ul><li>Keep heart rate between 60-80/min (Beta blockers and Calcium-channel blockers) </li></ul><ul><li>Arrhythmias—Atropine, Lidocaine, etc. </li></ul>
    19. 19. Fibrolytic Drugs <ul><li>TPA-tissue plasminogen activators </li></ul><ul><li>Streptokinase </li></ul>Image from site http://www.americanheart.org/presenter.jhtml?identifier=4751
    20. 20. Nitrates <ul><li>GTN </li></ul><ul><li>Cause vasodilatation reducing the amount of blood returning to the heart from the venous system, thus decreasing preload. </li></ul><ul><li>This decreases the work of the heart and the demand of the myocardium for oxygen. </li></ul><ul><li>Also dilate the peripheral arteries, decreasing the resistance against which the left ventricle must pump (decreases afterload). </li></ul><ul><li>Increases coronary vasodilation </li></ul><ul><li>Reduces lung congestion </li></ul>
    21. 21. ACE Inhibitors <ul><li>(pril) </li></ul><ul><li>Used to treat both hypertension and ACS </li></ul><ul><li>Inhibit the conversion of angiotension I to angiotension II, thus blocking the release of aldosterone, thereby reducing sodium and water retention </li></ul><ul><li>Potassium-sparing so watch for hyperkalemia </li></ul><ul><li>Reduce afterload of heart </li></ul>
    22. 22. Inotropes <ul><li>Digitalis </li></ul><ul><li>Inhibits the sodium-potassium pump, causing an increase in intracellular sodium levels </li></ul><ul><li>Increased sodium levels force sodium out of the cell in exchange for calcium </li></ul><ul><li>Higher intracellular calcium levels increase the force of contraction, increasing cardiac output </li></ul><ul><li>Digoxin also blocks the slow calcium channels of the AV nodes, slowing the HR </li></ul>
    23. 23. Antiplatelet Agents <ul><li>Low dose Aspirin </li></ul><ul><li>Aspirin blocks the formation of thromboxane A 2 , inhibiting platelet aggregation </li></ul><ul><li>A single daily dose of around 80mg can effectively sustain the desired antiplatelet effect </li></ul>
    24. 24. Anticoagulants <ul><li>Heparin (Clexane) </li></ul><ul><li>Binds to anti-thrombin, inactivating coagulation factors and thrombin, </li></ul><ul><li>thereby blocking the conversion of fibrinogen to fibrin </li></ul>
    25. 25. Side Effects: Anticoagulants, Fibrolytics and Antiplatelets <ul><li>Bleeding </li></ul><ul><li>What symptoms would you see? </li></ul><ul><li>INR </li></ul>
    26. 26. Beta-blockers <ul><ul><li>Block beta-adrenergic receptors of CNS </li></ul></ul><ul><ul><li>Blockage of beta-1 receptors causes a decrease in the force of contraction, a slowing heart rate, and a slowing of impulse of conduction (negative inotrope, chonotrope, dromotrope) </li></ul></ul><ul><ul><li>These 3 mechanisms of action combine to decrease myocardial oxygen demand </li></ul></ul>
    27. 27. Calcium-channel blockers <ul><li>Action: thought to inhibit calcium ion influx across cardiac and smooth muscles, decreasing contractility and oxygen demand. May also dilate coronary arteries. </li></ul><ul><li>Nursing implication: monitor for rapid drop in BP (especially if given intravenously). </li></ul>
    28. 28. Cholesterol Lowering Agents: hypolipidaemic drugs <ul><li>Statins </li></ul><ul><li>Reduce plasma lipids and lipoproteins </li></ul><ul><li>Block the production of LDLs and increase receptor activity that removes LDLs </li></ul><ul><li>Take other drugs 1 hour before or 4-6 hours after Questran to avoid blockage of absorption </li></ul>
    29. 29. Cardiogenic shock: <ul><li>Inability of the impaired ventricle to perfuse and oxygenate body tissues </li></ul><ul><li>Common in MI that damages 40% or more of the left ventricle. </li></ul><ul><li>Signs: </li></ul><ul><ul><li>Systolic BP less than 90 mmHg </li></ul></ul><ul><ul><li>Anxiety, restlessness, confusion, coma </li></ul></ul><ul><ul><li>Cool, moist, clammy skin </li></ul></ul><ul><ul><li>Rales in lungs, decreased ( <30ml/hour) urine output </li></ul></ul><ul><ul><li>S3 and S4 heart sounds </li></ul></ul><ul><ul><li>Coma and death </li></ul></ul>
    30. 30. Cardiac Medications Congestive Heart Failure
    31. 31. <ul><li>Congestive Heart Failure </li></ul>Table 17-10. p. 548.
    32. 32. What can cause CHF? <ul><li>CAD multiple heart attacks </li></ul><ul><li>High BP </li></ul><ul><li>Faulty heart valves </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Myocarditis </li></ul><ul><li>Congenital heart defects </li></ul><ul><li>Cardiac arrhythmias </li></ul>
    33. 33. Aims of treatment CHF: <ul><li>Relieve symptoms </li></ul><ul><li>Improve quality of life </li></ul><ul><li>Prevent readmission to hospital, and/or recurrent ischaemic events </li></ul><ul><li>Reduce mortality </li></ul><ul><li>(Lonn & McKelvie, 2000) </li></ul>
    34. 34. <ul><li>ACE Inhibitors </li></ul><ul><li>Beta Blockers </li></ul><ul><li>Diuretics </li></ul><ul><li>Vasodilators </li></ul><ul><li>Inotropes (e.g. Dopamine) </li></ul><ul><li>Digitalis </li></ul>Drugs used to treat CHF
    35. 35. Inotropes <ul><li>Digitalis </li></ul><ul><li>Inhibits the sodium-potassium pump, causing an increase in intracellular sodium levels </li></ul><ul><li>Increased sodium levels force sodium out of the cell in exchange for calcium </li></ul><ul><li>Higher intracellular calcium levels increase the force of contraction, increasing cardiac output </li></ul><ul><li>Digoxin also blocks the slow calcium channels of the AV nodes, slowing the HR </li></ul>
    36. 36. Dopamine <ul><li>Stimulates dopamine receptors in the renal vessels, increasing renal blood flow, increasing diuresis </li></ul><ul><li>Net result is an increase in cardiac output </li></ul><ul><li>Increase in systemic arterial pressure </li></ul>
    37. 37. Anti-arrhythmic Drugs <ul><li>Ventricular arrhythmias </li></ul><ul><ul><li>Amiodarone </li></ul></ul><ul><ul><li>Treatment of tachyarrhythmias –supraventricular nodal and ventricular tachycardias, atrial flutter and fibrillation. </li></ul></ul><ul><ul><li>Lignocaine </li></ul></ul><ul><ul><li>Decreased the depolarisation and excitability in the ventricles. </li></ul></ul>
    38. 38. Potassium Chloride <ul><li>Intracellular ion </li></ul><ul><li>Transmission of nerve impulses </li></ul><ul><li>Contraction of cardiac muscles </li></ul><ul><li>Levels 4.0-4.5 </li></ul><ul><li>Hypokalaemia=potassium deficit </li></ul>
    39. 39. Nursing implications CHF: <ul><li>Daily weights </li></ul><ul><li>Strict intake/output records </li></ul><ul><li>May be on fluid restriction (1500ml/24hrs) </li></ul><ul><li>Teaching regarding medications </li></ul><ul><li>Elevate feet to avoid stasis ulcers </li></ul><ul><li>Oxygen on at all times </li></ul><ul><li>Monitor BP, heart rate, respiratory rate, pulse oximetry frequently (every 2-4 hours) </li></ul><ul><li>Monitor labs (electrolytes, troponin-T) </li></ul><ul><li>Auscultate lung fields to assess for change every 4 hours! </li></ul>

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