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Transcript of 1256784_634575635597512500
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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 )