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Lecture 8

Lecture 8. Chapters 37 & 38 Cardiac Disorders. Cardiac Disorders. System = heart, blood vessels (arteries & veins), Blood

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Lecture 8

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  1. Lecture 8 Chapters 37 & 38 Cardiac Disorders

  2. Cardiac Disorders • System = heart, blood vessels (arteries & veins), Blood • Blood rich w/ O2 & nutrients moves through vessels called arteries to narrower arteriols to capillaries where the rich blood is absorbed by bodies cells & waste products are absorbed (CO2, urea, Cr, ammonia) deoxygenated blood returned to circulation via venules to veins for elimination through lungs & kidneys

  3. Cardiac disorders • Heart = * 4 chambers - R & L atria, R & L ventricles * Blood from circulation to R atrium to R ventricle to pulmonary artery to lungs for gas exchange (CO2 & O2) to L atrium to L ventricle to aorta to systemic circulation • Heart muscle = myocardium & surrounds the atria & ventricles

  4. Cardiac Disorders • Pericardium = fibrous covering around the heart that protects it from injury & infection • Endocardium = 3-layered membrane that lines the inner part of the heart chambers • Valves = 4 - two atrioventricular (tricuspid & mitral) & 2 semilunar (pulmonic & aortic) - control blood. flow between atria & ventricles & pulmonary artery & the aorta

  5. Right Ventricle

  6. Cardiac disorders • Conduction = Generated & conducted by the myocardium - usually * Originates in sinoatrial (SA) node - pacemaker atrioventricular (AV) node bundle of HIS purkinje fibers ventricular muscle tissue contraction from apex upward forcing blood to lungs & circulatory system

  7. Cardiac disorders • Blood flow & Heart Rate (HR) * Ave. HR = 60 - 80 beats/min. (adult) * Ave. BP = 120/80 mm/Hg - resistance to blood flow through systemic arterial circulation • Arterial BP determined by Cardiac Output (CO) = the volume of bld. expelled form the heart in 1 min. - calculated by mult. HR by stroke volume - Ave. CO = 4 - 8 l/min.

  8. Cardiac Disorders • Stroke Volume (SV) = amt. of bld ejected from the L vent. w/ each heart beat - Ave. = 70ml/beat - SV determined by 3 factors: -Preload - blood flow force that stretches the ventricle - Contractility - force of ventricular contraction - Afterload - Resistance to vent. ejection of blood caused by opposing pressures in aorta & systemic circulation • Specific drugs can or preload & afterload, affecting both SV & CO - most vasodilators dec. preload & afterload a dec. in arterial pressure & CO

  9. Cardiac DisordersCardiac Glycosides • Digitalis - One of the oldest drugs (1200 AD) - Effective in treating congestive heart failure (CHF) - CHF = when the heart muscle weakens & enlarges loss of ability to pump blood through the heart & into the systemic circulation = heart failure (or pump failure) - peripheral & lung tissues become congested = CHF

  10. Cardiac DisordersCardiac Glycosides • CHF can be left sided or right sided • Cardiac glycosides = digitalis glycosides - inhibits the Na - K pump inc. intracellular Ca cardiac muscle fibers contract more efficiently - Digitalis = 3 effects on the heart 1) + inotropic action (inc. myocard. contraction) 2) - chronotropic action (dec. HR) #) - dromotropic action (dec. conduction of the heart cells

  11. Cardiac DisordersCardiac Glycosides • The inc. in myocardial contractility = inc. card., peripheral, & kidney function by inc. CO, dec. preload, improving bld flow to periphery & kidneys, dec. edema, & inc. fluid excretion fluid retention in lung & extremities is decreased • Digitals also used to correct atrial fibrillation & atrial flutter (cardiac dysrhythmias)

  12. Cardiac Disorders Cardiac Glycosides • Digoxin (Lanoxin) - Protein binding - low, t1/2 = 36 hrs - drug accumulation can occur - monitor SE & serum levels closely - metabolized by liver & excreted by kidneys - kidney dysfunction can affect excretion of dig. - Do not confuse digoxin & digitoxin - digitoxin = highly protein bound w/ a long t1/2 - seldom prescribed

  13. Cardiac DisordersDigoxin (Lanoxin) • Action = inc. myocardial contraction (+ inotrophy), and slows HR (- chronotropy), therefore regulating the rate & rhythm of the heart - Therapeutic serum levels = 0.5 - 2.0 ng/ml • Use = moderate/severe systolic CHF, arrythmias • SE = Dig. toxicity - bradycardia (pulse < 60), anorexia, diarrhea, N&V, blurred vision, lethargy - older adults more prone to toxicity • DI - Other heart meds

  14. Cardiac DisordersHeart Failure • Other drugs = * Vasodilators - dec. venous blood return to the heart & dec. cardiac filling, ventricular stretching & O2 demand * Angiotensin-converting enzyme (ACE) inhibitors - dilate venules & arterioles & improves renal bld flow & dec. bld fluid volume * Diruetics - first-line = reduces fluid volume

  15. Cardiac DisordersAntianginal Drugs • Used to treat angina pectoris ( acute cardiac pain caused by inadequate bld flow resulting from plaque occlusion in the coronary arteries of the myocardium or from spasms of the coronary arteries) - described as tightness, pressure in center of chest, pain radiating down L arm - attacks may lead to an MI • 3 Types of angina pectoris 1. Classic (stable) - stress or exercise 2. Unstable (preinfarction) - frequently over day, severity 3. Variant (Prinzmetal, vasospastic) - during rest

  16. Cardiac DisordersAntianginal Drugs • Action - Inc. blood flow by inc. O2 supply, or by dec. O2 demand by the myocardium • Nitrates, beta-blockers, calcium channel blockers • Nitrates & calcium channel blockers effective in treating variant or vasospastic angina (not beta blockers) • beta blockers effective in treating stable angina • Non-pharm Rx = avoid heavy meals, smoking, extremes in weather changes, strenuous exercise, stress - Proper nutrition, moderate exercise, adequate rest & relaxation techniques

  17. Cardiac DisordersAntianginals • Nitrates - First agents used - Nitroglycerine (NTG) - Action - acts directly on the smooth muscle of blood vessels = relaxation & dilation. - Dec. cardiac preload & afterload & reduces O2 demand - dilation of veins = less blood return to the heart - dilation of arteries = less vasoconstriction & resistance - Onset of Action - sublingual (under the tongue) & IV = 1 - 3 min. - transderm nitro patch = 30 - 60 min

  18. Cardiac DisordersAntianginals • SE = Headaches - less frequent w/ continued use, hypotension, dizziness, weakness, faintness • Beta Blockers - Block the beta receptor site Atenolol (Tenormin), Metoprolol tartrate (Lopressor), Nadolol (Corgard), Propranolol HCL (Inderal) - Action - Dec. the effects of the sympathetic nervous system by blocking release of epi. & norepi dec. HR & BP reduce the need for O2 & the pain of angina - Nonselective (beta-1 & beta-2) - Inderal, Corgard, Visken - Selective (beta -1) - Tenormin, Lopressor

  19. Cardiac DisordersAntianginals • SE - Dec. in HR & BP - Closely monitor vital signs • Calcium Channel Blockers (Calcium Blockers) - Newest Amlodipine (Norvasc), Diltiazem HCL (Cardizem), Nifedipine (Procardia, Adalat), Verapamil (Calan, Isoptin) - Action - Ca activates myocard. contraction; inc. workload of heart. Calcium blockers dec. cardiac contractility (- inotropic) & the workload of the heart = dec. O2 need

  20. Cardiac DisordersCalcium Blockers • Use - long - term Rx of angina • SE - Headache, Hypotension, dizziness, flushing of the skin - Bradycardia w/ verapamil (Calan) - Hypotension esp. w/ Nifedipine (most potent) - promotes vasodilation of coronary & peripheral arteries • Calcium blockers can cause changes in liver & kidney function - Check liver enzymes periodically • Can be given w/ nitrates to prevent angina

  21. Cardiac DisordersAntidysrhythmics • Cardiac dysrhythmia (arrhythmia) = any deviation from the normal rate or pattern of the heartbeat. HR’s too slow (bradycardia), fast (tachycardia), or irregular • Electrocardiogram (ECG) identifies the type of dysrhythmia - P wave = atrial activation - QRS complex = ventricular depolarization - T wave = ventricular repolarization - PR interval = atrioventricular conduction time - QT interval = ventricular action potential duration

  22. Cardiac DisordersAntidysrhythmics • Atrial dysrhythmias = prevent proper filling of the ventricles & dec. CO by 1/3 • Ventricular dysrhythmias = life threatening d/t ineffective filling of the ventricle = dec. or absent CO • Dysrhythmias can occur - after an MI, from hypoxia (lack of O2 to body tissue), hypercapnia (inc. CO2 in the bld.), excess catecholamines (epi, norepi), or electrolyte imbalance

  23. Cardiac DisordersAntidysrhythmic Drugs • 2 major classifications of dysrhythmias * Above bundle of HIS = supraventricular - A-flutter, a-fib., PAC’s * Below bundle of HIS = Ventricular - PVC’s, Vent. tachycardia, V-fib. • Desired action = restoration of normal cardiac rhythm • 4 Classes: • 1. Fast (sodium) Channel Blockers- dec. the fast Na influx to the cardiac cells, so - dec. conduction time of cardiac tissue, dec. likelihood of ectopic foci, inc. repolarization - 3 subgroups of fast channel blockers

  24. Cardiac DisordersAntidysrhythmics • Class 1A - Procainamide (Pronestyl, Procan), Quinidine Sulfate (Quinidex) - slows conduction & prolongs repolarization - Use = Control PVC’s, vent. tachycardia - SE = Anorexia, headache, dizziness, weakness • Class 1B - Lidocaine (Xylocaine), Mexiletine (Mexitil) - Slows conduction & shortens repolarization - Use = Ventricular arrythmias associated w/ acute MI’s - IM & IV - IV bolus then a drip started (1 - 4 mg/min.)

  25. Cardiac DisordersAntidysrhythmics • Class 1C - Flecainide (Tambocor) - Prolongs conduction w/ little to no effect on repolarization - Use - Life-threatening vent. dysrhythmias, supraventricular tachycardia, a-fib or flutter • Beta Blockers - dec. conduction velocity • Prolong Repolarization - Amiodarone (Cordarone) - emergency Rx of ventricular dysrhythmias. Inc. refractory perios & prolong action potential duration • Calcium Channel Blockers - inc. refractory period of the AV node, dec. vent. response

  26. Diuretics • Used for 2 main purposed: decrease hypertension (lower BP), & decrease edema (peripheral & pulmonary) in CHF and renal or liver disorders * Other uses = Dec. cerebral edema (Mannitol), dec. intraocular eye pressure (glaucoma), dec. ascities (liver disease) • Used either singly or in combo to dec. BP & dec. edema • Diuretics produce inc. urine flow (diuresis) by inhibiting Na & H2O reabsorption from the kidney tubules. Act on the kidneys in diff. locations to enhance excretion of Na (pg. 678)

  27. Diuretics • Every 11/2 hr. the total vol. of the body’s extracellular fluid (ECF) goes through the kidneys (glomeruli) for cleansing = 1st process for urine formation - sm. particles (electrolytes, drugs, glucose & waste) filtered in the glomeruli • Normally 99% of filtered Na passing through glomeruli reabsorbed. 50 - 55% Na reabsorbtion in proximal tubules, 35 - 40% in loop of Henle, 5 - 10% in distal tubules, <3% in collecting tubules • Diuretics that act on tubules closest to glomerule have greatest effect in causing natriuresis (Na loss in urine) - Mannitol

  28. Diuretics • Diuretics have an antihypertensive effect by promoting Na & H2O loss by blocking Na/Cl reabsorption = a dec. in fluid vol. & a dec. of BP • With fluid loss - edema should decrease. When Na is retained, H2O also retained & BP increases • Many diuretics cause loss of other electrolytes (K, Mg, Cl, bicarb) • 5 categories of diuretics:

  29. Action of Diuretics on Different Segments of Renal Tubules

  30. DiureticsThiazides/Thiazide-like Diuretics • Hydrochlorothiazide (Hydrodiuril, HCTZ), Metolazone (Zaroxolyn) * Action - Distal tubules of the kidney to promote Na, Cl, & H2O excretion; acts directly on arterioles, causing vasodilation & BP; preload & CO = dec. vascular fluid & dec. in BP * Use - Rx of hypertension & peripheral edema * SE - Electrolyte imbalance (hypokalemia), hyperglycemia (inc. bld sugar), hyperlipidemia (inc. bld lipid level), dizziness, headaches, N&V

  31. DiureticsThiazides * CI - renal failure * DI - Digoxin - if hypokalemia occurs, the action of digoxin is enhanced & dig. toxicity can occur * Considered potassium - wasting - K supplements are frequently prescribed & serum K levels are monitored Loop Diuretics - Act on the ascending loop of Henle by inhibiting Cl transport of Na into the circulation (inhibits passive reabsorbtion of Na) - Potent & cause marked depletion of H2O & electrolytes - Effect = dose related - dose & response

  32. DiureticsLoop diuretics • More potent than thiazides as diuretics, but less effective as antihypertensive agents • Can renal bld flow up to 40% • Have a great saluretic (Na-loosing) effect & can cause rapid diuresis vascular fluid vol. dec. in CO & BP • Bumetanide (Bumex), Furosemide (Lasix) - derivatives of sulfonamides • Furosemide (Lasix) - * Use - Rx fluid retention/overload due to CHF, renal dysfunction, cirrhosis; hypertension; pulmonary edema

  33. Diruetics Loop Diuretics • Lasix (con’t) - used when other conservative measures fail (Na restriction & less potent diuretics) * May be given IV or PO * SE - Electrolyte imbalance ( esp. hypokalemia K < 3.5) & dehydration, orthostatic hypotension * DI - digitalis preparations - dig. toxicity can result * Nursing - Strict I & O, daily weights, vital signs, hydration status of client * Clients should be on K supplements, monitor serum K levels closely

  34. DiureticsPotassium-Sparing Diuretics • Weaker than thiazides & loop diuretics • Action - act primarily in the collecting distal duct renal tubules to promote Na & H2O excretion & K retention • Use - mild diuretics or in combo w/ antihypertensive drugs • K supplements not used - serum potassium excess (hyperkalemia) results if K supplement taken w/ potassium - sparing diuretics

  35. DiureticsPotassium - Sparing • Spironolactone (Aldactone), Triamterene (Dyrenium) • Aldactone (an aldosterone antagonist) - Aldosterone = a mineralocorticoid hormone that promotes Na retention & K excretion; Aldosterone antagonsits inhibit the Na-K pump (K retained & Na excreted) • Amiloride (Midamor) - antihypertensive agent • Triamterene - Rx of edema caused by CHF or cirrhosis • K - sparing diuretics used alone = less effective than when combined with reducing body fluid & Na - Usually combine w/ a potassium wasting diuretic

  36. Diuretics Combination • Combine a potassium sparing & potassium wasting diuretic = intensifies the diuretic effect & prevents K loss • spironolactone & hydrochlorothiazide (Aldactazide) • amiloride & hydrochlorothiazide (Moduretic) • triamterene & hydrochlorothiazide (Dyazide, Maxide) • When diuretic combinations are used, either combined in one tablet or as separate tablets, the dose of each is usually less than the dose of any single drug • SE = hyperkalemia - caution w/ clients having poor renal function; do NOT use K supplements (unless K low)

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