Exam (elaborations)
CARDIAC ACP (2)
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Exam of 25 pages for the course PMI Agile Certified Practitioner at PMI Agile Certified Practitioner (CARDIAC ACP (2))
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CARDIAC ACPNitrates mechanism of action - ANS-•Nitroglycerin activation requires enzymatic action resulting
in the release of free nitrite ion, which is then converted to nitric oxide.
•Nitric oxide combines with guanylyl cyclase, activating that enzyme and causing an increase in
cGMP.
•Increased intracellular cGMP inhibits calcium entry into the cell, thereby decreasing intracellular
calcium concentrations and causing smooth muscle relaxation.
•NO also activates K+ channels, which leads to hyperpolarization and relaxation.
•NO acting through cGMP can stimulate a cGMP-dependent protein kinase that activates
myosin light chain phosphatase, the enzyme that dephosphorylates myosin light chains, which
leads to relaxation.
Inotropes - ANS-Strengthen cardiac contraction
chromotropic - ANS-heart rate
Dromotropic - ANS-rate of electrical conduction through the AV node
Drug therapy of Angina has two goals: - ANS-(1) prevention of myocardial infarction (MI) and
death
(2) prevention of myocardial ischemia and anginal pain
Rapid acting forms of nitrates - ANS-•Used to treat acute anginal attacks
•Sublingual tablets, intravenous infusion
•Amyl nitrite, nitroglycerin
long-acting forms of nitrates - ANS-Used to PREVENT anginal episodes
Nitrates: different forms available - ANS-•Sublingual*, buccal*, chewable tablets, oral
capsules/tablets, intravenous solutions*, transdermal patches/paste.
•* Bypass the liver and the first-pass effect
True or false, all Nitrates bypass the liver and the first pass effect. - ANS-False; only sublingual,
buccal and IV,
Nitrates effects - ANS-•Vasodilation results in reduced myocardial oxygen demand (↓preload,
↓afterload).
•Nitrates cause dilation of both large and small coronary vessels. Venous and arterial dilation is
dose-dependent.
•Nitrates alleviate coronary artery spasms.
,Nitrates Adverse effects - ANS-•Headaches: Usually diminish in intensity and frequency with
continued use
•Tachycardia, postural hypotension
•Tolerance may develop:
•Occurs in patients taking nitrates around the clock or with long-acting forms
•Prevented by allowing a regular nitrate-free period to allow enzyme pathways to replenish
Nitroglycerin Mechanism of action. - ANS-Nitro forms free radical nitric oxide, in smooth muscle
this causes relaxation which causes a vasodilator effect on the peropheral veins and arteries.
reduces cardiac oxygen demand by decreasing preoad.
dilates coronary arteries and improves collateral flow to ischemic regions.
Beta blockers mechanism of action - ANS-•β1-receptors on the heart are blocked, preventing
the binding of epinephrine and norepinephrine.
•This prevents the activation of adenylyl cyclase to form cAMP, preventing the phosphorylation
of L-type calcium channels, and reducing the release of calcium by the sarcoplasmic reticulum.
•The result is a decrease in chronotropy and a decrease in inotropy, thus reducing myocardial
work.
•After an MI, a high level of circulating catecholamines irritate the heart, causing an imbalance in
supply and demand ratio and even leading to life-threatening dysrhythmias. β-blockers block the
harmful effects of catecholamines, thus improving survival after an MI
Beta blocker effects in angina and MI - ANS-•Decreased heart rate, blood pressure, and
contractility, which decrease myocardial oxygen requirements at rest and during exercise
•Lower heart rate is also associated with an increase in diastolic perfusion time that may
increase coronary perfusion
•May also be valuable in treating silent or ambulatory ischemia.
•Decrease mortality of patients with recent MI
Beta blocker adverse effects and contraindications - ANS-•Contraindications:
•Asthma and other bronchospastic conditions, severe bradycardia, atrioventricular blockade,
bradycardia-tachycardia syndrome, and severe unstable left ventricular failure.
•Adverse effects:
•Increase in end-diastolic volume ejection time, both of which tend to increase myocardial
oxygen requirement.
•Fatigue, impaired exercise tolerance, insomnia, unpleasant dreams, worsening of claudication,
and erectile dysfunction.
Ca Channel blockers MOA - ANS-•Bind to L-type calcium channels on vascular smooth muscle,
cardiac myocytes, reducing the influx of calcium into muscle cells. This causes a reduction in
the release of calcium from the sarcoplasmic reticulum, leading to smooth muscle relaxation.
•Block L-type Ca channels on cardiac nodal tissue (sinoatrial and atrioventricular nodes) which
are responsible for pacemaker currents and myocyte depolarization.
, •By blocking calcium entry into the cell, CCBs cause vascular smooth muscle relaxation
(vasodilation), decreased myocardial force generation (negative inotropy), decreased heart rate
(negative chronotropy), and decreased conduction velocity within the heart (negative
dromotropy), particularly at the atrioventricular node.
Ca channel blockers effects - ANS-•The anti-anginal effects of CCBs are derived from their
vasodilator and cardiodepressant actions. Systemic vasodilation reduces arterial pressure,
which reduces ventricular afterload thereby decreasing oxygen demand. The more
cardioselective CCBs (verapamil and diltiazem) decrease heart rate and contractility, which
leads to a reduction in myocardial oxygen demand, making them excellent antianginal drugs.
•CCBs can also dilate coronary arteries and prevent or reverse coronary vasospasm (as occurs
in Prinzmetal's angina), thereby increasing oxygen supply to the myocardium.
Ca Channel blockers contraindications and adverse effects - ANS-•Contraindications:
•Preexistent bradycardia, conduction defects, or heart failure caused by systolic dysfunction
•Concomitant administration with a beta blocker
•Adverse effects:
•Flushing, headache, excessive hypotension, edema, reflex tachycardia, bradycardia,
conduction blocks.
The betablocker we are required to know - ANS-anything ending in (olol)
The Ca Channel blockers we are required to know - ANS-Diltiazem, verapamil, amlodipine,
Aspirin MOA - ANS-•Irreversibly inhibits formation of prostaglandin derivative, thromboxane A2,
via acetylation of platelet cyclooxygenase, thus inhibiting platelet aggregation.
•Irreversibly inhibits cyclooxygenase-1 and 2 enzymes, via acetylation, which results in
decreased formation of prostaglandin precursors.
•Has antipyretic, analgesic, and anti-inflammatory properties.
Adenosine Diphosphate Receptor Antagonists MOA - ANS-•Irreversibly blocks the P2Y12
component of ADP receptors on the platelet surface, which prevents activation of the GP IIb/IIIa
receptor complex, thereby reducing platelet aggregation.
•Inhibition of platelet aggregation by clopidogrel is achieved through an active metabolite.
•Platelets are affected for the remainder of their lifespan (~7-10 days).
•Examples: Clopidogrel (Plavix), Ticagrelor.
Glycoprotein inhibitors - ANS-•Inhibits platelet aggregation by preventing the binding of
fibrinogen, von Willebrand factor, and other adhesive molecules to GP IIb/IIIa receptor sites on
activated platelets.
•Abciximab, a chimeric monoclonal antibody directed against the IIb/IIIa complex including the
vitronectin receptor, was the first agent approved in this class of drugs.
•Eptifibatide and tirofiban inhibit ligand binding to the IIb/IIIa receptor by their occupancy of the
receptor but do not block the vitronectin receptor.
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