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    Shair Muhammad HazaraBSN, M Sc BE [DUHS]

    Cardiac Disorders

    Cardiac Drugs

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    Cardiac Disorders

    System = heart, blood vessels (arteries & veins),

    Blood

    Blood rich w/ O2 & nutrients moves throughvessels 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

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    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

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    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

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    Right Ventricle

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    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

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    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.

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    Cardiac Disorders

    Stroke Volume (SV) = amt. of bld ejected from the Lvent. 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

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    Cardiac Disorders

    Cardiac 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 = heartfailure (or pump failure)

    - peripheral & lung tissues become congested =

    CHF

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    Cardiac Disorders

    Cardiac 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) + inotropicaction (inc. myocard. contraction) 2) -

    chronotropic action (dec. HR) #) - dromotropic

    action (dec. conduction of the heart cells

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    Cardiac Disorders

    Cardiac 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)

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    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

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    Cardiac Disorders

    Digoxin (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

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    Cardiac Disorders

    Heart 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

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    Cardiac Disorders

    Antianginal Drugs Used to treat angina pectoris ( acute cardiac pain caused

    by inadequate bld flow resulting from plaque occlusion inthe coronary arteries of the myocardium or from spasmsof the coronary arteries) - described as tightness, pressurein center of chest, pain radiating down L arm - attacksmay 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

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    Cardiac Disorders

    Antianginal 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

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    Cardiac Disorders

    Antianginals 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

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    Cardiac Disorders

    Antianginals SE = Headaches - less frequent w/ continued use,

    hypotension, dizziness, weakness, faintness

    Beta Blockers - Block the beta receptor siteAtenolol (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

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    Cardiac Disorders

    Antianginals 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

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    Cardiac Disorders

    Calcium 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

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    Cardiac Disorders

    Antidysrhythmics Cardiac dysrhythmia (arrhythmia) = any deviation from

    the normal rate or pattern of the heartbeat. HRs too slow(bradycardia), fast (tachycardia), or irregular

    Electrocardiogram (ECG) identifies the type ofdysrhythmia

    - P wave = atrial activation

    - QRS complex = ventricular depolarization- T wave = ventricular repolarization

    - PR interval = atrioventricular conduction time

    - QT interval = ventricular action potential duration

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    Cardiac Disorders

    Antidysrhythmics Atrial dysrhythmias = prevent proper filling of the

    ventricles & dec. CO by 1/3

    Ventricular dysrhythmias = life threatening d/tineffective filling of the ventricle = dec. or absent

    CO

    Dysrhythmias can occur - after an MI, fromhypoxia (lack of O2 to body tissue), hypercapnia

    (inc. CO2 in the bld.), excess catecholamines (epi,

    norepi), or electrolyte imbalance

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    Cardiac Disorders

    Antidysrhythmic Drugs

    2 major classifications of dysrhythmias

    * Above bundle of HIS = supraventricular - A-flutter, a-fib., PACs

    * Below bundle of HIS = Ventricular - PVCs, 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 ofcardiac tissue, dec. likelihood of ectopic foci, inc.repolarization

    - 3 subgroups of fast channel blockers

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    Cardiac Disorders

    Antidysrhythmics Class 1A - Procainamide (Pronestyl, Procan),

    Quinidine Sulfate (Quinidex) - slows conduction &

    prolongs repolarization- Use = Control PVCs, vent. tachycardia

    - SE = Anorexia, headache, dizziness, weakness

    Class 1B - Lidocaine (Xylocaine), Mexiletine (Mexitil) -

    Slows conduction & shortens repolarization

    - Use = Ventricular arrythmias associated w/ acute MIs

    - IM & IV - IV bolus then a drip started (1 - 4 mg/min.)

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    Cardiac Disorders

    Antidysrhythmics 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

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    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)

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    Diuretics

    Every 11/2 hr. the total vol. of the bodys extracellularfluid (ECF) goes through the kidneys (glomeruli) forcleansing = 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 proximaltubules, 35 - 40% in loop of Henle, 5 - 10% in distal

    tubules,

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    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:

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    Action of Diuretics on Different Segments of Renal Tubules

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    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

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    Diuretics

    Thiazides

    * CI - renal failure

    * DI - Digoxin - if hypokalemia occurs, the action ofdigoxin is enhanced & dig. toxicity can occur

    * Considered potassium - wasting - K supplements arefrequently prescribed & serum K levels are monitored

    Loop Diuretics - Act on the ascending loop of Henle by

    inhibiting Cl transport of Na into the circulation (inhibitspassive reabsorbtion of Na)

    - Potent & cause marked depletion of H2O & electrolytes

    - Effect = dose related - dose & response

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    DiureticsLoop diuretics

    More potent than thiazides as diuretics, but less effective asantihypertensive agents

    Can renal bld flow up to 40%

    Have a great saluretic (Na-loosing) effect & can causerapid 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, renaldysfunction, cirrhosis; hypertension; pulmonary edema

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    DirueticsLoop Diuretics

    Lasix (cont) - used when other conservative measuresfail (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 Klevels closely

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    DiureticsPotassium-Sparing Diuretics

    Weaker than thiazides & loop diuretics

    Action - act primarily in the collecting distal duct

    renal tubules to promote Na & H2O excretion & Kretention

    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

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    DiureticsPotassium - Sparing

    Spironolactone (Aldactone), Triamterene (Dyrenium)

    Aldactone (an aldosterone antagonist) - Aldosterone = amineralocorticoid 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

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    DiureticsCombination

    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 isusually less than the dose of any single drug

    SE = hyperkalemia - caution w/ clients having poor renal

    f ti d NOT K l t ( l K l )