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- *Usually from Atherosclerosis
- 1. results from myocardial demand exceeding oxygen supply.
- 2. Reversible ischemia
- 3. Narrowed blood vessels
- 1. Irreversible ischemia
Myocardial demand is determined by:
Amount of evergy required to support the heart.
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).
Stroke volume (HR X volume per stroke) X TPR
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).
Is the measure of ventricular filling pressure or the volume of blood in the left ventricle at rest (prior to it filling up)
- -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.
- 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.
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.
Hallmark symptom of Angina-
Pain with exertion and releived at rest.
- 1. Smoking
- 2. HTN
- 3. Dylipidemia
- 4. Obesity
- 5. Physical inactivity
- 1. Age
- 2. Family history
- 3. Gender
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
- 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
Prognosis determined by:
The number and location of coronary artery stnosis, the severity of ischemia, and the presence of other CAD r/f's.
- 1. Nonpharmacological treatment
- *dietary changes
- *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.
Agents for treatment-
- 1. Organic nitrates
- 2. BB's
- 3. CCB's
- 4. ACE inhibitors
- 5. Antiplatelet drugs- ASA DAILY!
- 6. Antilipid agents
- -act on smooth muscle!
- -prevent anginal episodes
- -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
NITRATES- SHORT ACTING PRODUCTS-
- 1. Nitro SL
- 2. Nitro spray
- 3. Ointment, patch, po, sl, IV
NITRATES- LONG ACTING-
- 1. Isosorbide
- 2. Transdermal Nitroglycerin patches
- *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!
- -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.
- -Decrease HR
- -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
- -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*****.
- 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.
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
- 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
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
- -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.
- -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
- -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.
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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