ANGINA MEDICATIONS

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Author:
ssilvis
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197483
Filename:
ANGINA MEDICATIONS
Updated:
2013-02-02 20:31:19
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MEDS
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ANGINA
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  1. Myocardial Ischemia-
    • *Usually from Atherosclerosis
    • PRIMARY-
    • 1.  results from myocardial demand exceeding oxygen supply.
    • 2.  Reversible ischemia
    • 3.  Narrowed blood vessels
    • MI-
    • 1.  Irreversible ischemia
  2. Myocardial demand is determined by:
     Amount of evergy required to support the heart.
  3. Factors that influence work of the heart include:
    • 1.  HR
    • 2.  BP
    • 3.  Ventricular volume
    • 4.  Cardiac contractility
    • 5.  Myocardial wall tension (which is the result of myocardial wall thickness).
  4. CO=
    Stroke volume (HR X volume per stroke) X TPR
  5. The hearts contractility:
    • Calcim stimulates shortening of myocardial fibers which increases contractility, velocity of fiber shortening and peak systolic muscle tension increases.
    • (Calcium influx causes systolic muscle tension to increase).
  6. Preload:
    Is the measure of ventricular filling pressure or the volume of blood in  the left ventricle at rest (prior to it filling up)
  7. Afterload:
    • -Is the pressure that the heart must pump against- the higher the BP the harder the heart has to work.
    • -Resistance to ventricular ejection.
    • -Increased BP results in INCREASED afterload.
    • -The thicker the walls the harder it has to work.
    • -Regulated by ejection  impedance, wall tensions and regional wall geometry.
  8. Preload/Afterload:
    • 1.  Ventricular diastolic pressure-(Preload)
    • Is decreased when veins are dilated and venous pressure and cardicac filling pressure decreases.
    • 2.  Ventricular systolic pressure- (Afterload)
    • Dilation of arteries decreases arterial and aortic pressure.  decreases.
  9. S/S of Angina-
    • 1. CP
    • 2. SOB
    • 3. Fatigue
    • 4. DOE- "angina equivalent"- experience instead of CP.
    • 5. Occurs with exertion, releived with rest.
  10. Hallmark symptom of Angina-
    Pain with exertion and releived at rest.
  11. Risk factors-
    • Modifiable-
    • 1.  Smoking
    • 2.  HTN
    • 3.  Dylipidemia
    • 4.  Obesity
    • 5.  Physical inactivity
    • Nonmodifiable
    • 1.  Age
    • 2.  Family history
    • 3.  Gender
  12. Types of Angina-
    • 1.  Stable- precipitated by exertion, releived by rest.
    • 2.  Unstable angina- minimal exertion produces s/s. (CAN LEAD TO MI)
    • 3.  Nocturnal- at HS
    • 4.  Angina decubitus
    • 5.  Variant angina- arteris vasospasm
  13. Angina treatment-
    • 1. History
    • 2. Physical examination
    • 3.  Tests
    • 4.  Treatment goals
    • *releiving anginal s/s
    • *Prevent additional anginal episodes
    • *Decrease r/f MI
    • *Improve functional capacity
    • *Prolong survival
  14. Prognosis determined by:
    The number and location  of coronary artery stnosis, the severity of ischemia, and the presence of other CAD r/f's.
  15. Angina treatment:
    • 1.  Nonpharmacological treatment
    • *dietary changes
    • *exercise
    • *modify r/f's
    • 2.  Pharmacologic treatement-
    • *increase cardiac oxygen supply to the heart (not really an option with drugs)
    • *decrease oxygen demand on the heart by decreasing HR, decreasing contractility, and decreasing afterload or preload with medications.
  16. Agents for treatment-
    • 1.  Organic nitrates
    • 2.  BB's
    • 3.  CCB's
    • 4.  ACE inhibitors
    • 5.  Antiplatelet drugs- ASA DAILY!
    • 6.  Antilipid agents
  17. NITRATES-
    • -act on smooth muscle!
    • -prevent anginal episodes
    • Action-
    • -vasodilation
    • -dilate the vasculature in peripheral arteries and veins which decreases oxygen demand on the heart.
    • -decrease blood return to heart (preload)
    • -decrease afterload
    • -rapidly absorbed
  18. NITRATES- SHORT ACTING PRODUCTS-
    • 1.  Nitro SL
    • 2.  Nitro spray
    • 3.  Ointment, patch, po, sl, IV
  19. NITRATES- LONG ACTING-
    • 1.  Isosorbide
    • 2.  Transdermal Nitroglycerin patches
    • *prophylaxis
    • *maintain vasodilation and continuosly decrease workload of the heart
    • *increases myocardial perfusion
    • *veous pooling of blood, decrease in benous blood return to the heart, decrease in ventricual volume, pressure and wall tension, decrease cardiac work and oxygen demand and releive angina
    • *results in increased transmyocardial gradient and increases myocardial perfusion
    • *peripheral vasodilation also decreases cardiac afterload
    • *decreases preload on the heart
    • *ALL PTS WITH ANGINA SHOULD HAVE SHORT ACTING AND A LONG ACTING NITRATE!
  20. Nitrate tolerance-
    • -loss of ability of smooth muscles to respond to nitrates both inperipheral and coronary arteries
    • -occurs as early as 7-10 days after administration
    • -SL, patches
    • -Nitrate-free interval- at hs due to less activity
    • -S/E's h/a, flushing, dizziness, weakness,orthostasis, reflex tachycardia
    • -Precautions with nitrates- Phosphodiestrase- 5 inhibitors, Sildenfil (VIAGRA), Levitra, Cialis- causes severe HYPOTENSION.
  21. BETA BLOCKERS-
    • -Decrease HR
    • -Cardio-protectors
    • -recommended as INITIAL therapy by all guidelines for all pts, with or without previous MI (unless contraindicated).
    • -decreased myocardial demand.
    • -main role is preventing recurrence of MI's in pts with CAD- decrease risk for reinfaction and improve survival in pts who have had an MI.
    • -especially useful in those with exertional angina and resting tachycardia.
    • -decreases workload of the heart
    • -decrease myocardial oxygen demand by antagonism of adrenergic receptors
    • -decreases myocardial contractility, decreased HR, decreases conduction velocity.
    • -Nonselective BB decreases systemic vascular resistance and BP (afterload)
    • -ALL BB decrease myocardial demand
  22. BETA BLOCKERS-
    1.  Atenolol-
    • -most cost-effective
    • -once-daily dosing
    • -low adverse reactions profile
    • -Beta 1 selectivity ****
    • -preferred in DM d/t  prolong recovery from hypoglycemia with nonselective BB's and blunting of hypoglycemic symptoms*****.
  23. BETA BLOCKS:
    • 1.  Cardioprective-
    • decrease incidence of ventricular arrhytmias that cause sudden death s/p MI
    • 2.  Contraindications-
    • If hx of bradycardia, decompensating CHG, DM, asthma(if severe)
    • 3.  Caution with drugs that depress AV conduction - DIGOXIN, verapamil, cardizem- increase risk of bradycardia and heart block.
  24. ACE's-
    Diuretics-
    Glycosides (Digoxin)-
    Women are at a higher risk when?
    • 1.  ACE's- decrease cardiac workload.
    • 2.  Diuretics- control excess fluid.
    • 3.  Glycosides (Digoxin)- improve myocardial contractility (inhibit Na, K, ATpase)
    • 4.  After menopause
  25. CCB's-
    • Two classes-
    • 1.  Dihydropyridines (amlodipine, nicardipine,and nifedipine)
    • 2.  Nondihydropyridines (beprodil, dilitazem, and verapamil)
    • *BOTH prevent calcium reflux into cells, produces smooth muscle relaxation of systemic and coronary arteries and suppresses cardiac activity....prevents CP
  26. CCB action in Angina-
    • -depress cardiac contractility by decreased conduction through SA and V node which decreases MOD. (Dihydropyridines do not have this action)
    • -decrease HR, conduction, and mediates antianginal effect
    • -relieve coronary constriction  with vasospastic angina
    • -decrease afterload
    • -vasodilation
    • -increase MOS, decrease MOD
    • -S/E's- constipation, decrease BP, h/a, increase CHF, can worsen GERD
    • -Indications- Angina, HTN, tachyarrhythmias, migraine, Raynauds, esophageal spasm.
  27. ACE's-
    • -recommended for pts with EF less than 40
    • -DO NOT USED IN PREGNANCY
    • -for symptomatic pts with chronic stable angina to prevent MI (reinfarction) or death, and to reduce s/s
    • -Increase MOS and decrease MOD
    • -prevent formation of angiotensin 2 (vasoconstrictor)
    • -decrease PVR and decrease MOD d/t decreased afterload
    • -decreases thickening of coronary artery walls which decreases MOS
    • -decreases secretion of aldosterone, decreases the retention of sodium and water which decreases extracellular fluid volume and preload
  28. ANTIPLATELET THERAPY-
    • -inhibits synthesis of thromboxane A2 in production of platelets which decreases platelet aggregation and vasoconstriction
    • -indicated with pt with acute/chronic HF, 20% decrease in reinfarction
    • -81- 325 mg qd
    • -adverse effects- dyspepsia, bruising, bleeding, EC helps!
    • 1.  ASA
    • 2.  Clodpidrogel- antiplatelet agent, used when ASA is contraindicated, recommended for post-stent placement, 8.7% reduction in M & M as compared to ASA, rare s/e's.
  29. LIPID LOWERING AGENTS-
    • -all CAD pts with LDL cholesterol levels greater than 100!!!!
    • -STATINS are the preferred agent
    • -are believed to also have anti-inflammatory and thrombetic properties

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