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Title: Chapters 37


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 lt 60),
    anorexia, diarrhea, NV, 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.
    HRs 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., 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 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 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.)

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 bodys
    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, lt3 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, NV

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 (cont) - used when other conservative
    measures fail (Na restriction less potent
    diuretics)
  • May be given IV or PO
  • SE - Electrolyte imbalance ( esp.
    hypokalemia K lt 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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