calcium channel blockers Flashcards
types of angina
1) “Classic”, “Stable”, or “EffortInduced”
• 2) “Unstable”
• 3) “Variant”, “Rest”, “Vasospastic”, or
“Prinzmetal”
• 4) “Acute Coronary Syndrome”
• 5) “Mixed
Classic Angina
Most common form of angina • Caused by a fixed coronary artery obstruction (generally atheromatous)Classic Angina • The pattern of pain remains stable. “It always starts to hurt on the 3rd or 4th fairway
Classic Angina
• Pain is relieved by
rest or NTG
UNSTABLE ANGINA
Pain at rest or with increasing frequency,
duration, severity, or as the result of less
exertion.
• Pain not relieved by NTG or prolonged
(>20 minutes) rest.
Prinzmetal Angina
Pain is episodic and unrelated to exertion.
• Although patient might have
atherosclerosis, angina is the result of
arteriospasm and unrelated to exertion or
rest. Treated with NTG or
Calcium Channel Blockers
Acute Coronary Syndrome
• Atheromatous plaque ruptures • Inflammatory cells and mediators are activated • “Lipid Pool” forms • Thrombus forms and propagates • Vasoconstriction occurs Vascular occlusion occurs • Cardiac muscle sickens and dies • Characteristic MI “biomarkers” are released
Characteristic MI “biomarkers
MYOGLOBIN, CKMB, TRPONIN 1, CK
Mixed Angina
Patients have angina during exertion
and at rest.• Caused by a fixed obstruction combined
with vasospasm &/or endothelial
disruptions
Two Angina Rx Strategies
1) Increase O₂ delivery
• 2) Decrease O₂ demand
The heart is already an 0₂ “sucker” and
extracts
75% of oxygen delivered to it
at rest.
• Arterial blood pressure determines how
much
myocardial wall stress is necessary to overcome that resistance and pump blood. So…arterial (overwhelmingly arteriolar) tone determines SVR ~~systolic wall stress.
Venous (capacitance) tone determines
how much blood can be “stored” in the
venous blood delivery system before it’s
returned to the heart. So venous tone determines
~~diastolic wall stress
Organic Nitrates and Nitrites
Cause rapid decrease in my0₂cardial demand and
prompt relief of stable,unstable, and variant
angina.
Organic Nitrates and Nitrites all work
similarly and differ in their onset
and duration of action.
most commonly used
nitrate/nitrite and one you will become
most comfy with.
NTG
Organic Nitrates and Nitrites
Side Effects
*Cyanide toxicity and Nipride (discussed earlier)
*Reflex tachycardia ( INCREASE myo₂cardial demand and
decrease coronary perfusion via diastolic filling)
* Reflex positive inotropy ( increase myo₂cardial
demand) *High sustained doses can cause
methemoglobinemia (huh?) particularly
in peds +/- Tylenol exposure.
methemoglobinemia
blood with an oxidized heme group. chocolate brown pee
what to do when you see methemoglobinemia
#1) Tell the physician #2) Prepare to give methylene blue at 1-2 mg/kg (up to 50 mg) IV over 3-5 minutes #3)…and ascorbic acid #4) …and lots of pure O₂
If the patient doesn’t respond to
these therapies for methemoglobinemia
they may be deficient in the enzyme glucose-6- phosphate dehydrogenase (G6PD)
G6PD-deficient patients who don’t
respond to methylene blue and
ascorbic acid require
1) Exchange transfusions take all blood out and put back in
2) Hyperbaric oxygen
dont give organic nitrates and nitrites with vasodilators
kill patient by hypovolemia
sodium channel blockers
Emerging class of drugs. • Effect the transmembrane sodium/calcium exchange. Less calcium enters the cardiomyocyte to relieve the cardiac workload.
ranolazine
ranexa. Sodium channel blocker. Also works by shifting cardiac metabolism from fatty acids …to carbs Which require less O₂ to metabolize
Cardiac ischemia decreases
he
transmembrane potential, increases the Ca⁺⁺ flow
into cells which activates ATP-consuming
systems which causes a positive feedback loop
contributing to even more profound ischemia. makes it easy to depolarize
calcium channel blockers work by
Smooth muscle is dependent on an inflow of Ca⁺⁺
to maintain ‘tone”…
-As those Ca⁺⁺ channels are “blocked”, those inner
circular and outer longitudinal vascular smooth
muscles relax.
Perhaps because there’s more sm. muscle in
arterioles than venules
Arteries are much more affected by Ca⁺⁺ channel blockade. …so arterial dilate, SVR drops, and arterial pressure falls.
calcium channel blockers effect on body
Consequently these agents
decrease afterload (which decrease myO₂cardial
consumption)
*And dilate coronary arteries (which increase
myO₂cardial delivery)
ca channel blocker can worsen HF by
negative inotrope
Calcium Channel Blockers
You only need to know three:
Verapamil (Calan, Isoptin)
2) Diltiazem (Cardizem)
3) Nifedipine (Procardia)
*They are differentiated by their ability to affect
the myocardium vs. vascular smooth muscle.
Nifedipine
procardia. A dihydropyridine derivative
(there are many “…ipines”)
-Almost exclusively a vasodilator with little
dromotropic or chronotropic effect.
*D.O.C. for variant angina (why?) caused by constriction
*Causes reflex tachycardia (why?
Verapamil
calan,isoptin. A diphenalkylamine derivative
-Strong negative dromotropic,
chronotropic, and inotropic effects.
-Weak vasodilatory effects.*Dramatically decreases impulse
conduction through the SA & AV nodes
which are rich in calcium pumps.
*D.O.C. for many supraventricular
tachyarrhythmias, such as SVT. because it slows down conduction times
Diltiazem
cardizem. Utilized extensively to prevent radial
artery spasm during harvest and postoperatively
to maintain patency.
beta blockers
Act as negative chronotropes and inotropes
to myO₂cardial consumption.
*Which adrenergic receptors are most related
to the heart???!!
*D.O.C. for exercise-induced angina
beta blockers
β-Blockers and Ca⁺⁺ Channel
Blockers are commonly
administered with
nitrates.
