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Advanced Pharm > Pharmacologic agents for Coronary Artery disease > Flashcards

Pharmacologic agents for Coronary Artery disease Flashcards

1
Q

How much coronary blood flow per minute?

With intense exercise?

How much O2 extracted?

A
  • Coronary blood flow is 70 ml/min/100g at rest
    • 5% of the CO
  • Coronary blood flow increases 2-4x with intense exercise
  • 70% of the oxygen is extracted from the blood
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2
Q

What are the physiological factors that regulate coronary flow?

A
  • Physical factors
  • Vascular control by metabolites
    • adenosine is released by myocardial cells in response to decreased PO2, causing coronary vasodilation
  • Neural and humoral control
    • sympathetic innervation
    • large vessels- Alpha; vasoconstriction effects
    • smaller vessels- Beta 2; dilator effects
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3
Q

What is the perfusion pressure to the left ventricle?

A

perfusion pressure to the left ventricle = DBP - LVEDP

Left ventricle only receives blood flow during diastole b/c systolic squeezing pressure closes arterioles and capillaries. This is not as much of an issue on the R side b/c the muscle mass is not as large

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4
Q

What factors increase myocardial demand?

A
  • tachycardia
  • high afterload
  • high preload
  • increased contractility
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5
Q

What factors increase myocardial supply?

A
  • hgb concentration
  • O2 saturation
  • bradycardia (within reason)
  • increased diastolic blood pressure
  • low-normal preload
  • decreased contractility
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6
Q

What is the treatment summary for stable angina?

(ABCDE)

A
  • A: ASA, antianginals (nitrates, CCB, BB)
  • B: Blood pressure (controlled)
  • C: Cholesterol (statin), Cigarettes (stop)
  • D: diet, diabetes
  • E: education, exercise
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7
Q

How do nitrates help with CAD?

A
  • Increase concentration of NO in smooth muscle cells
  • Relax venous capacitance vessels and large coronary arteries to decrease preload and ventricular wall tension
    • decrease demand and increase supply
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8
Q

Nitrate MOA?

A
  • Nitrates release NO after they are metabolized
  • NO activates soluble guanylate cyclase, increasing cGMP, which increases PKG
  • This prevents Ca from entering the cell and the smooth muscle relaxes
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9
Q

What are the organic nitrate drugs?

A
  • Nitroglycerin
  • Isosorbide dinitrate
    • DOA 6 hours
  • Isosorbide mononitrate
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10
Q

What are the different ways nitroglycerin can be delivered?

A
  • Sublingual- tablets or spray
  • Oral- has a huge first pass liver metab, not often used
  • Topical- ointment, patches
  • Intravenous
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11
Q

Nitroglycerin

E1/2t

SE

A
  • 90% degrated by the liver to inactive metabolites
  • E1/2t of IV = 1.5 minutes
  • SE
    • HA
    • postural hypotension
    • methemoglobinemia- usually only with high doses or liver disease
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12
Q

Whats the deal with Nitrate tolerance?

A
  • Nitrate-free intervals are necessary to prevent tolerance and/or adverse effects
  • Usually nitrate-free intervals are done at night when the person is at rest
    • removal of patch at night
  • Oral Isosorbide mononitrate has a long E1/2t so it can provide high levels followed by low levels and can be administered once/day
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13
Q

How are Beta antagonists helpful in treating CAD?

A
  • provide a more favorable O2 supply vs demand balance
    • used to prevent stable or unstable angina
  • decreases O2 demand by decreasing CO (more dramatic during activity than at rest)
    • decrease HR, decrease contractility
    • increase diastolic filling time (supply)
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14
Q

What kind of Beta antagonists are most used?

What should be avoided?

SE?

A
  • Use primarily beta-1 selective agents
    • metoprolol
    • atenolol
  • Improve survival in CAD
  • Avoid:
    • sudden d/c
    • in variant angina- can worsen shoch symptoms after MI if given within 8 hours of STEMI
  • SE
    • depression
    • insomnia
    • mask hypoglycemic warning signs in DM
    • exercise intolerance
    • bronchospasms
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15
Q

What is the MOA of CCB?

Where do they have their effect?

A
  • All bind to the alpha-1 subunit of the L-type calcium channel (at distinct sites)
    • Dihydropyridines are more selective for Ca channels in vasculature (arterial)
      • may cause reflex tachycardia
    • Non-Dihydropyridines are more selective for Ca channels on the SA & AV nodes
      • more at risk for heart block
      • avoid with BBs
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16
Q

What are the dihydropyridines CCBs?

What are the non-dihydropyridines?

A
  • Dihydropyridines:
    • Nifedipine
    • Amlodipine
    • Nicardipine
  • Non-dihydropyridine
    • Verapamil
    • Diltiazem
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17
Q

How is ASA used to treat CAD?

A
  • Antiplatelet activity of ASA prevents thrombus formation
  • Irreversible cox inhibition- lasts duration of platelet life (8-10 days)
  • 80 mg
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18
Q

What drugs are used to treat unstable angina or nonST elevation MI (partial occlusion)?

ST elevation MI (total occlusion)?

A
  • partial occlusion:
    • antianginal drugs
    • heparin, ASA
    • GPIIb/IIIa antagonists (eptifibatide)
    • Clopidogrel (plavix)
  • total occlusion
    • surgery
    • thrombolytics (streptokinase, tPA)
19
Q

Clopidogrel (plavix)

class

use

risks

A
  • Antiplatelet agent- irreversible platelet ADP-receptor antagonist
  • All acute coronary syndrome patients with ASA allergy take this
    • reduces coronary events
  • Risks:
    • combination with ASA or GPIIb/IIIa inhibitor increases risk of major bleeding
20
Q

GPIIb/IIIa inhibitors

names

use

A
  • Abciximab (ReoPro)
  • eptifibatide (Integrilin)
  • tirofiban (Aggrastat)
  • Reduce risk of MI in pts with unstable angina
  • reduce risk of recurrent MI and urgent revascularization in pts with NSTEMI
21
Q

What do you use to treat stable angina?

Unstable angina?

variant angina?

A
  • Stable angina:
    • Nitrates
    • BBs
    • CCBs
  • Unstable angina:
    • Nitrates
    • BBs
    • CCBs
    • Aspirin/clopidogrel
    • Heparin/thrombolytics
    • Glycoprotein IIb/IIIa receptor inhibitor
  • Variant angina
    • Nitrates
    • CCBs
22
Q

What is the viscious cycle of heart failure?

(pic)

A
23
Q

What are the different ventricular dysfunctions?

What causes them?

A
  • Systolic dysfunction (EF<40%)
    • Coronary artery disease
    • nonischemic cardiomyopathy
      • hypertension
      • valvular disease
      • alcohol
      • thyroid disease
      • cardiotoxic drugs
  • Diastolic dysfunction (impaired filling)
    • cardiomyopathies
    • incomplete relaxation of the LV during ischemia
24
Q

What are the major manifestations of HF?

A
  • Dyspnea
    • on exertion
    • orthopnea
    • paroxysmal nocturnal dyspnea
  • fatigue
  • fluid retention
25
Q

What are the physiologic goals of drug therapy for heart failure?

A
  • reduce preload
    • diuretics
    • aldosterone antagonists
    • venodilators
  • Reduce afterload
    • ACEIs
    • BBs
    • Vasodilators
  • Increase inotropu
    • cardiac glycosides
    • sympathomimetic amines
    • phosphodiesterase inhibitors
26
Q

What are the hemodynamic goals of CHF?

(table)

A
27
Q

How are diuretics used to treat HF?

most common diuretics used?

A
  • Alleviate congestive symptoms
    • use with caution, consider preload status (ideally it will remain normal)
  • No evidence of mortality benefit with thiazide or loop diuretics
  • Loop diuretics most commonly used
    • Furosemide, bumetanid, torsemide
    • Inhibit Na/K/Cl pump in loop on henle, promoting excretion of Na, K, H2O
28
Q

Which diuretics work on the distal tubule?

how much do they increase Na excretion?

A
  • Thiazides
  • Metolazone (thiazide-like)
  • K sparing (spirinolactone)
  • These diuretics lose effectiveness when creatinine clearance < 30 ml/min
  • Increase Na excretion 5-10%
29
Q

How much do loop diuretics increase Na excretion?

A

20-25%

30
Q

What is the aldosterone antagonist?

MOA?

What is RALES?

Can you with with ACEI?

A
  • Spirinolactone
    • K sparing diuretic that acts as a competative antagonist at aldosterone receptor
    • Decreases K/Na exchange in distal tubule and collecting duct of nephron
  • RALES study showed a 30% reduction in mortality of pts with HF treated with spironolactone
  • Must monitor K levels if given with an ACEI b/c both decrease K excretion
31
Q

What are some side effects of spironolactone?

Why?

What about Eplerenone?

A
  • Inhibits both androgen and mineralcorticoid receptors
    • Causing gynecomastia and impotence
  • Eplerenone is more selective and has fewer SE
32
Q

How does NTG work to improve HF?

A
  • Increases venous capacitance which reduces venous return to heart
  • decreases myocardial O2 demand
  • alleviates ischemia which improves diastolic relaxation
  • improved LV compliance in addition to preload reduction
  • Use with caution; don’t want to decrease preload too much, these pts need an adequate preload
33
Q

How do ACEIs treat HF?

A
  • Reverse vasoconstriction and volume retention that is caused by RAAS
  • Reduces afterload which increases SV
    • increases GFR, which increases natriuresis and diuresis
  • Reversal of aldosterone-related volume retention decreases preload
  • Statistically significant mortality benefit seen in multiple clinical trials
34
Q

How are ARBS used to treat HF?

A
  • Hemodynamic profile similar to ACEIs
  • lack of bradykinin related vasodilation means less of a preload reduction
  • Mortality benefit seen in studies
    • may be additive with ACEI
35
Q

How are Beta blockers used to treat HF?

A
  • **a little counterintuitife in CHF
  • Benefits are related to:
    • inhibition of Renin release
    • attenuation of cytotoxic and signaling effects of circulating catecholamines
    • prevention of ACS (acute coronary syndromes??)
  • Do not use in acute decompensated HF
36
Q

How are hydralazine and Isosorbide dinitrate used to treat HF?

A
  • Vasodilators
  • used when pt does not tolerate ACEIs
  • mortality benefit seen in african-american patients
  • use both agents together
    • hydralazine- pure arterial dilator
    • isosorbide dinitrate- venodilator
37
Q

How does digoxin work to treat HF?

A
  • Digoxin is an Na-K adenosine triphosphatase inhibitor
  • In vagal afferent fibers, it sensitizes cardiac baoreceptors to decrease sympathetic outflow
    • increases parasympathetic outflow
  • decreased conduction velocity; increased AV refractory period
  • decreases HR, preload and afterload
  • Increases intracellular calcium
  • decreased renal tubular absorption of Na
38
Q

What are the therapeutic levels of digoxin?

onset

half life

steady state?

metab?

SE?

A
  • Therapeutic levels 0.5-1.2 ng/ml
  • onset: 30-60 min
  • Half life 36 hours
    • steady state takes 7 days
  • 90% renally excreted
  • SE
    • hypokalemia
    • AV block
    • ventricular ectopy
39
Q

What is the antidote for digoxin toxicity?

A

digoxin immune Fab

40
Q

What are the pharmacodynamic interaction of Digoxin?

pharmacokinetic interactions?

A
  • Pharmacodynamic interactions:
    • increased risk of AV block with BBs
    • BBs and CCBs decrease contractility
  • Pharmacokinetic interactions
    • antibiotics increase absorption
    • verapamil, quinidine, amiodarone increase digoxin levels by affecting VD and/or renal clearance
41
Q

What other inotropic agent is used to treat HF?

A
  • Dobutamine
    • stimulation of B1 increases cardiac contractility
    • stimulation of vascular B2 causes arerial vasodilation and reduced afterload
42
Q

How do phosphodiesterase inhibitors work to treat HF?

A
  • Inhibit degredation of cAMP and cGMP in cardiac myocytes and vascular smooth muscle
    • “inodilators”
    • increased contractility (d/t increased intracellular Ca)
      • minimal increase in myocardial O2 demand
      • good choice for BB overdose
    • arterial and venous dilation decreases afterload and preload
    • mild bronchodilation
    • improved diastolic relaxation by increasing Ca removal from mycoplasm after action potential
43
Q

Amrinone

class?

effects?

SE?

A
  • Class: phosphodiesterase inhibitor
  • effects:
    • increased CO and LV EF
    • decreased LVEDP, pulmonary wedge pressures
    • slight increase in HR and slight decrease in BP
  • SE:
    • hypotension
    • thrombocytopenia
    • arrhythmias d/t increased intracellular Ca
44
Q

Milrinone

class?

effects?

A
  • phosphodiesterase inhibitor
  • effects: (similar to Amrinone)
    • increased CO and LV EF
    • decreased LVEDP and pulmonary wedge pressure
    • HR slightly increased, BP slightly decreased
  • long term use not proven to improve M&M
  • helpful in treating pulmonary hypertension

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