1. Cardiac Medications Hypertension

2. Learning Objectives  Students will be able to:  Discuss the major categories of drugs as they relate to the treatment of Cardiac Disease.  Describe the major effects of various medications on cardiac function.  Discuss major nursing implications when administering above medications.

3. New Zealand Statistics:  Maori die almost a decade earlier than non-Maori in New Zealand.  Cardiovascular disease is a major contributor to this statistic (NZGG, 2003).  Maori should therefore be assessed for risk 10 years earlier than non-Maori.

4. Hypertension  Defined as a consistent elevation of the systolic or diastolic blood pressure above 140/90mm Hg  On two elevated readings (sitting and supine) on separate office visits  Two types hypertension  Primary: no known cause  Secondary: consequence of underlying disease or condition

5. Goal with hypertension:  Two primary regulatory factors:  Blood flow (volume)  Peripheral Vascular Resistance (PVR)  Goal is to optimise these two in order to get pressure below 140/90 mm Hg  Primary groups of drugs are used:  Diuretics  Adrenergic inhibitors (Beta-blockers)  Vasodilators  ACE inhibitors  Calcium antagonists

6. Diuretics: to reduce overall volume of blood  Thiazides - block sodium reabsorption in nephron’s distal segment  Water is excreted with sodium, producing decreased blood volume  Loop diuretics – potent loop diuretic that inhibits sodium and chloride reabsorption at proximal and distal tubules and ascending loop of Henle  Indicated for acute pulmonary oedema MedlinePlus Medical Encyclopedia

7. Diuretics Cont’d  Nursing Interventions:  Monitor K+ routinely (depleted here)  Monitor weight daily and intake/output  Give in am so avoid nocturia

8. Potassium-sparing diuretics (Aldactone or Spironolactone)  Potassium sparing diuretic  Antagonises aldosterone in the distal tubules which increases sodium and water excretion  Need to watch for hyperkalemia and don’t give potassium supplements  Monitor electrolytes and fluid intake/output  Monitor blood pressure and daily weights  Less potent than thiazide and loop diuretics but useful as an adjunct to other diuretic therapy

9. Vasodilators  Hydralazine hycrochloride (Apresoline)  Dilate peripheral blood vessels by directly relaxing arteriolar smooth muscle  Usually used in combination with other antihypertensives as they increase sodium and fluid retention

10. Calcium Antagonists  Felodipine, Nifedipine, Diltiazem  Inhibit the influx of calcium into muscle cells; act on vascular smooth muscle (primary arteries) to reduce spasms and promote vasodilatation  May enhance serum Digoxin levels

11. Cardiac Medications Coronary Artery Disease Disease

12. New Zealand Statistics  Cardiovascular disease is the leading cause of death in New Zealand (NZGG, 2003).  1998 N.Z. had age-standardised mortality rate from CAD of 111/100,000 people  CAD death rates for Maori less than 75 yrs old are 2-3X higher than non-Maori and 2X as high for Pacific peoples.

13. So what is the overall goal in managing CAD?  To reduce 5-year cardiovascular risk to less than 15% with medications (NZGG, 2003).  Ensure individuals with total cholesterol greater than 8mmol/L undergo risk assessment and lipid modifying treatment.  Ensure BP less than 170/100 drug treatment

14. Different drug effects:  Inotropic: relating to or influencing the force of contraction  Chronotropic: influencing the rate; especially the heart beat  Dromotropic: affecting the conductivity of cardiac muscle -- used of the influence of cardiac nerves Jarvis, 2000, Figure 17-8. p. 505.

15. Figure 17-1. p. 498.  Overview of Pulmonary/Systemic Circulation Carolyn Jarvis, Physical Exam and Health Assessment 3 rd Ed. 2000. Copyright by W.B. Saunders

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

17.  Preload/Afterload in Heart Carolyn Jarvis, Physical Exam and Health Assessment 3rd Ed. 2000. Copyright by W.B. Saunders

18. So what drugs help meet these goals?  Dissolve existing clots quickly—TPA, Urokinase  Maximize preload— I.V. fluids, volume expanders  Minimize afterload—Ace inhibitors, IABP  Maximize cardiac contractility—Digoxin, Dopamine  Decrease preload, increase coronary circulation, and reduce pulmonary congestion—Nitrates  Reduce chances clot formation—ASA or other anti-platelet medications  Reduce overall fluid volume in overload--diuretics  Keep heart rate between 60-80/min (Beta blockers and Calcium-channel blockers)  Arrhythmias—Atropine, Lidocaine, etc.

19. Fibrolytic Drugs  TPA-tissue plasminogen activators  Streptokinase Image from site http://www.americanheart.org/presenter.jhtml?identifier=4751

20. Nitrates  GTN  Cause vasodilatation reducing the amount of blood returning to the heart from the venous system, thus decreasing preload.  This decreases the work of the heart and the demand of the myocardium for oxygen.  Also dilate the peripheral arteries, decreasing the resistance against which the left ventricle must pump (decreases afterload).  Increases coronary vasodilation  Reduces lung congestion

21. ACE Inhibitors  (pril)  Used to treat both hypertension and ACS  Inhibit the conversion of angiotension I to angiotension II, thus blocking the release of aldosterone, thereby reducing sodium and water retention  Potassium-sparing so watch for hyperkalemia  Reduce afterload of heart

22. Inotropes  Digitalis  Inhibits the sodium-potassium pump, causing an increase in intracellular sodium levels  Increased sodium levels force sodium out of the cell in exchange for calcium  Higher intracellular calcium levels increase the force of contraction, increasing cardiac output  Digoxin also blocks the slow calcium channels of the AV nodes, slowing the HR

23. Antiplatelet Agents  Low dose Aspirin  Aspirin blocks the formation of thromboxane A 2, inhibiting platelet aggregation  A single daily dose of around 80mg can effectively sustain the desired antiplatelet effect

24. Anticoagulants  Heparin (Clexane)  Binds to anti-thrombin, inactivating coagulation factors and thrombin,  thereby blocking the conversion of fibrinogen to fibrin

25. Side Effects: Anticoagulants, Fibrolytics and Antiplatelets  Bleeding  What symptoms would you see?  INR

26. Beta-blockers  Block beta-adrenergic receptors of CNS  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)  These 3 mechanisms of action combine to decrease myocardial oxygen demand

27. Calcium-channel blockers  Action: thought to inhibit calcium ion influx across cardiac and smooth muscles, decreasing contractility and oxygen demand. May also dilate coronary arteries.  Nursing implication: monitor for rapid drop in BP (especially if given intravenously).

28. Cholesterol Lowering Agents: hypolipidaemic drugs  Statins  Reduce plasma lipids and lipoproteins  Block the production of LDLs and increase receptor activity that removes LDLs  Take other drugs 1 hour before or 4-6 hours after Questran to avoid blockage of absorption

29. 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

30. Cardiac Medications Congestive Heart Failure

31. Table 17-10. p. 548.  Congestive Heart Failure

32. What can cause CHF?  CAD multiple heart attacks  High BP  Faulty heart valves  Cardiomyopathy  Myocarditis  Congenital heart defects  Cardiac arrhythmias

33. Aims of treatment CHF:  Relieve symptoms  Improve quality of life  Prevent readmission to hospital, and/or recurrent ischaemic events  Reduce mortality (Lonn & McKelvie, 2000)

34.  ACE Inhibitors  Beta Blockers  Diuretics  Vasodilators  Inotropes (e.g. Dopamine)  Digitalis Drugs used to treat CHF

35. Inotropes  Digitalis  Inhibits the sodium-potassium pump, causing an increase in intracellular sodium levels  Increased sodium levels force sodium out of the cell in exchange for calcium  Higher intracellular calcium levels increase the force of contraction, increasing cardiac output  Digoxin also blocks the slow calcium channels of the AV nodes, slowing the HR

36. Dopamine  Stimulates dopamine receptors in the renal vessels, increasing renal blood flow, increasing diuresis  Net result is an increase in cardiac output  Increase in systemic arterial pressure

37. Anti-arrhythmic Drugs  Ventricular arrhythmias  Amiodarone Treatment of tachyarrhythmias – supraventricular nodal and ventricular tachycardias, atrial flutter and fibrillation.  Lignocaine Decreased the depolarisation and excitability in the ventricles.

38. Potassium Chloride  Intracellular ion  Transmission of nerve impulses  Contraction of cardiac muscles  Levels 4.0-4.5  Hypokalaemia=potassium deficit

39. Nursing implications CHF:  Daily weights  Strict intake/output records  May be on fluid restriction (1500ml/24hrs)  Teaching regarding medications  Elevate feet to avoid stasis ulcers  Oxygen on at all times  Monitor BP, heart rate, respiratory rate, pulse oximetry frequently (every 2-4 hours)  Monitor labs (electrolytes, troponin-T)  Auscultate lung fields to assess for change every 4 hours!