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208 Cards in this Set

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What is the trick for remembering the extrinsic pathway?
The extrinsic pathway is initiated in response to damage outside the blood vessel.

The coagulation factors of the extrinsic pathway are III and VII “For 37 cents you get the extrinsic pathway"
what is the trick for remembering the intrinsic pathway?
The intrinsic pathway is initiated by damage within the blood vessel.

The coagulation factors of the intrinsic pathway are XII, XI, IX, and VII. "If you cannot buy the intrinsic pathway for $12 you can get it for $11.98."
What is the trick for remembering the final common pathways?
The coagulation factors for the final common pathway are X, V, II, I and XIII.

"The final common pathway can be purchased at the five and dime for 1 or 2 dollars on the 13th of the month"
What is the normal range for PT?
12 to 14.
what is the normal range for PTT?
20 to 30.
What 2 tests do we use to assess the pharmacodynamic effects of heparin?
PTT or ACT.
What is a test to check heparin concentration in the body?

how does it help us?
Hepcon.

it helps us determine how much protamine to give. It is more accurate than going by the ACT.
What relationship does the activated clotting time (ACT) have to heparin?
it is the dose response curve.
what happens during stopping clot formation with the clotting cascade?
antithrombin III (AT III) binds irreversibly to thrombin (IIa.)

AT III also binds to IXa, Xa, and XIIa of the intrinsic pathway.
Describe how heparin works and who it works with:
it binds to AT III. It increases the activity of AT III 1000 fold. This stops the clotting process, by preventing thrombin (IIa) from turning fibrinogen into fibrin.
What, chemically, does protamine do to heparin when it binds to it?
positive protamine neutralizes the charge of heparin.
Describe how protamine interacts with heparin chemically?
protamine is positively charged. It combines electrostatically with heparin, which is negatively charged. It reverses the action of heparin by neutralization.
How much protamine do we give for every 100 units of heparin?
1 mg.
How fast do we infuse protamine?
give it slowly.
What is the prevalence of people with antigens to protamine?
1%.
Who develops antigens to protamine?
diabetics on npH.
What happens when you give protamine to quickly?
hypotension is common.

if the patient is awake, it will complain of back spasms.

if given to quickly patient can go into cardiovascular collapse.

it can also cause massive pulmonary constriction and right ventricular failure.
what effect will heparin have if you have no antithrombin 3?
it won't do anything.
What is the most common reason people are heparin resistant?
antithrombin 3 deficiency.
How do we treat a patient who has antithrombin 3 deficiency and needs to be heparinized ?
we could give FFP, or you can pay the money and give synthetic antithrombin 3.
On which pathways does Coumadin act?
extrinsic and final common pathways. It also competitively inhibits vitamin K. clotting factors that are synthesized and the liver.
What is the function of endogenous antithrombin 3 in the body?
it inactivates thrombin that escapes from a local clot. This prevents clots in places elsewhere that we don't want clots.
Which products could you give to restore PT to normal if it is prolonged?
vitamin K, FFP, and cryo precipitate.
How much does one unit of packed red cells increase hematocrit and hemoglobin?
3%/1 g per deciliter.
Name six bad things that can happen with transfusion of blood products:
depressed erythropoesis

alloimmunization

allergic reactions

red blood cell alloimmunization

febrile reactions

delayed hemolytic reactions.
How does transfusion of 1 to 2 units of blood compare with 100% oxygenation with oxygen tissue delivery?
100% oxygen provides better oxygen tissue delivery, not the blood.
How much does 1 unit of platelets increase platelet count?
5000 to 10,000.
What does processing of RBCs require?
ABO and Rh matching.
What does processing of platelets require for testing?
only Rh matching.
How much does 1 unit of platelets increase platelet count by?
5000 to 10,000.
What are the signs and symptoms of citrate toxicity?
tingling around the mouth, hands, and feet. very rapid development of acute onset of tetany.
Describe the calcium issues when you take blood off of a patient and give it back to them later:
the citrate in the bag prevents the blood from clotting while you are holding it. When you give the blood back, however, you need to give some calcium as well.
What happens with the clotting cascade and preventing clot formation?
endogenous heparin acts as a catalyst for inactivation of thrombin by antithrombin III.

citrate and oxalate both chelate calcium. This is significant, because you need calcium to form a clot.
Why is it better to give fresh packed cells instead of old packed cells to liver and kidney patients?
There is less ammonia, citrate, and lactic acid.
Why do they add citrate to packed cells?
Addition of citrate phosphate dextrose preservative (cpda 1) increases storage time from 28 days to 35 days. Adenine allows the cells to make ATP. Dextrose allows glycolysis to continue.
How do you treat citrate toxicity?
intravenous calcium.
What happens to packed cells when they are stored for 35 days?
increased lactate, decreased pH, bioactive substances (cytokenes, histamine, lipids, soluble HLA.)

reduction in red blood cell surface area.

increased osmotic fragility.

loss of deformability.

meth hemoglobin.

decreased 23 DPG.
what is the "catecholamine?"
a sympathomimetic chemical compound derived from tyrosine. Released by the adrenal glands in times of stress.

epinephrine, norepinephrine, and dopamine are the catecholamines.
What do we need to know about epinephrine for the exam?
it increases SVR, cardiac output, and can also decrease renal blood flow by afferent decrease in flow with its vasoconstrictor properties.
What do we need to know about norepinephrine for the exam?
it increases SVR, can decreased cardiac output, heart rate by baroreceptor mediated decreases in heart rate.
What does stimulation of alpha 1 promote?
vasoconstriction.
what is the chief neurotransmitter that stimulates alpha 1 postsynaptic?
endogenous norepinephrine.
What effect does alpha 2 receptor have postsynaptically ?
vasoconstriction, Veno constriction, platelet aggregation.

this receptor, however, is not as significant.
Where are beta 1 receptors mostly found?
the heart.
What are beta 1 receptors responsible for?
myocardial chronotropy and inatropy.
Where are beta 2 receptors usually found?
lungs and blood vessels.
What does stimulation of Beta 2 receptors cause in heart and lungs?
vasodilation and bronchodilatation.
Where are beta 2 receptors usually found, presynaptic or postsynaptic?
both
with beta
blockers, what happens to selectivity when you go up on the doses?
you lose selectivity.
What does dopamine 1 receptor promote ?
it mediates vasodilation of the kidney, mesenteric, coronary, and cerebrum.
What enzyme does stimulation of dopamine 1 activate?
AC.
Where, synaptically, is dopamine 2 receptor found?
presynaptic.
What does stimulation of dopamine 2 receptor cause ?
it inhibits release of norepinephrine.
What effect does stimulation of dopamine 2 have on AC?
it inhibits it.

this is a negative feedback mechanism, just like presynaptic alpha 2.
How does dependent is dopamine?
it is extremely dose
dependent.
What type of receptor do dopamine and norepinephrine bind to?
G. protein.
When dopamine binds to the G. protein receptor, what effect does that have on cAMP?
it increases cAMP.
What happens in the vasculature when cAMP binds to the kinases?
a gene is modified and vasodilation occurs.
Is ephedrine direct or indirect?
it is direct.

its main method of action is direct effects on the beta receptor.
Does ephedrine have direct or indirect properties?
it has both. Its main method of action, however, is direct and binding to the beta receptor, promoting increased heart rate and increased myocardial contractility.
Where, synaptically, is dopamine 1 receptors found?
postsynaptically.
What does stimulation of dopamine 1 cause?
it mediates vasodilation of kidneys, mesenteric, coronary, and cerebral.

it activates AC.
What does dopamine 0.5 to 3 mcg per kilogram per minute promote?
renal vasodilation.
What does dopamine 3 to 10 mic/ kilogram per minute promote?
beta effects.

increased heart rate, increased cardiac output.

also, a little bit more of an "alpha" response.
What does dopamine greater than 10 mcg per kilogram per minute promote?
alpha response. It is a potent vasoconstrictor at this dose.
Why must we mix norepinephrine in 5% dextrose?
because alkaline solutions breakdown catecholamine drugs.
Describe how norepinephrine promotes baroreceptor mediated decreases in heart rate:
there is increased afterload which causes decrease in venous return and decrease in heart rate.
Why must we monitor ABGs when using norepinephrine?
there is decreased tissue perfusion because of intense peripheral vasoconstriction. Lactic acid builds up, and there can be metabolic acidosis.
How is norepinephrine primarily terminated?
by reuptake into the postganglionic sympathetic nerve endings.
Is ephedrine direct or indirect?
it is direct.

its main method of action is direct effects on the beta receptor.
Does ephedrine have direct or indirect properties?
it has both. Its main method of action, however, is direct and binding to the beta receptor, promoting increased heart rate and increased myocardial contractility.
What happens in the synapse when indirect acting sympathomimetics do their work?
the drug accumulates in the synapse, eliciting the release of norepinephrine, which then activates postsynaptic receptors.
What do alpha 2 antagonists promote?
inhibition of alpha 2 potentiates the release of norepinephrine, thereby activating alpha 1 and beta 1.
What happens to beta receptors when a patient is on a beta
blocker?
they are down regulated to some extent.
What is the story with beta blockers on day of surgery?
even though volatile agents depressed myocardial activity, we still need to give the morning dose. The reason why, is, if you held it, there would be up regulation of receptors combined with the stress response and increased catecholamines. The result would be tachycardia and hypertension, and possibly myocardial ischemia.
What is the Main method of action of beta antagonists?
to prevent catecholamines from binding to beta receptors.
What is the ratio of beta : alpha with labetalol?
7:1.

labetalol, primarily, is a nonselective beta antagonists.

it only has a little bit of alpha antagonism.
Why is reflux tachycardia attenuated with labetalol ?
it is attenuated by the beta 1 effects.

this, however, may cause symptomatic bradycardia.
What is the mechanism of action of hydralazine?
it is a direct systemic arterial vasodilator.

it activates guanylate cyclase, to produce vasorelaxation.
Describe reflux tachycardia with hydralazine:
arterial vasodilation may produce reflex sympathetic nervous system stimulation with increase in heart rate.
What is the mechanism of action of nitric oxide?
as a gas, it defuses to the target cells where it activates guanylate cyclase to increase the cyclic GMP concentration, which in turn results in vasodilation.
What is the mechanism of action of nitroprusside?
it is a direct acting, nonselective peripheral vasodilator that causes relaxation of arterial and venous vascular smooth muscle.

it interacts with oxyhemoglobin, dissociating immediately and forming meth hemoglobin while releasing nitric oxide and cyanide. Once released, the nitric oxide activates the enzyme guanylat cyclase which is present in vascular smooth muscle. This results in increased intracellular concentrations of cyclic GMP.

so, nitric oxide is the active mediator responsible for the direct vasodilator in effects of nitroprusside.
What is the bottom line regarding the mechanism of action of nitroprusside?
cyclic GMP inhibits calcium entry into vascular smooth muscle
What could you do to treat cyanide toxicity with nitroprusside?
first, recognize that it occurs in patients who exhibit tachyphylaxis with nitroprusside.

discontinue immediately and administer 100% oxygen, even if saturation is normal.

sodium thiosulfate 150 mg/kilogram over 15 minutes for treatment of cyanide toxicity (it acts as a sulfur donor to convert cyanide to thiocynate.
What is the mechanism of action of clonadine?
it is a centrally acting selective partial alpha 2 agonist.

it is an antihypertensive drug by virtue of its ability to decrease sympathetic nervous system output from the central nervous system.
What role does clonidine have intraoperatively?
it may be used as a preanesthetic to decrease intraoperative blood pressure.

it also decreases heart rate lability and plasma catecholamine concentration.
What effect would clonidine have on the pressor response to ephedrine?
it would augment it.
What role does clonidine have with smoking?
it may be used to treat symptoms associated with nicotine withdrawal.
What is the function of the renin angiotensin aldosterone system?
it plays a major role in the regulation of hemodynamics and water and electrolyte balance via its circulating hormone, angiotensin two.
What is renin?
it is an enzyme that limits angiotensin 2 production.

???NOT SURE OF THIS IS ACCURATE???
What effect does renin have on total peripheral resistance?
it increases it. It works as a direct vasoconstrictor, activating receptors on the vascular smooth muscle.
What effect does renin have on norepinephrine?
it enhances it, it augments norepinephrine release from sympathetic nerve terminals.

it also decreases norepinephrine reuptake to the presynaptic terminal.
What effect does the RAS have on the sympathetic nervous system?
it increases sympathetic outflow.

there is release of vasopressin (ADH), which increases vascular volume.

there is release of catecholamines from the adrenal medulla.
Regarding the RAS, what happens when there is low blood pressure to the kidneys?
1. Juxtaglomerular apparatus in the kidneys is stimulated.

2. Release of renin, which converts angiotensin to angiotensin 1.

3. Angiotensin converting enzyme converts angiotensin 1 to angiotensin 2 (this takes place in the lungs.)

4. Angiotensin 2 causes: a) aldosterone release (salt and water retention by the kidneys), and b) vasoconstriction of arterioles.

all of this results in increased blood pressure and increased blood volume, which in turn stimulates negative feedback which will shut renin off.
Which blood vessels does angiotensin 2 work on?
mostly arterial smooth muscle. A little bit on veins.
where are alpha 1 adrenergic receptors found?
vascular smooth muscle and glands.
What are the physiologic effects of alpha 1 stimulation?
mydriasis, vasoconstriction, release of red blood cells from the spleen, decreased renin release from the kidneys, relaxation of the stomach/intestines, increased insulin and glucagon secretion from the pancreas, contraction of the uterus.
Where are alpha 2 receptors found ?
presynaptic nerve terminals at sympathetic postganglionic neurons.
What are the effects of alpha 2 stimulation?
inhibition of norepinephrine synthesis and release.
What does stimulation of alpha 2 receptors in the substantia gelatinosa of a spinal cord cause?
analgesia. What drug is a selective alpha 2 adrenergic agonist?
In what 2 ways does clonidine produce its cardiovascular effects?
centrally, on alpha 2 receptors of vasomotor center of the medulla, as well as peripherally.
How much does clonidine decreased plasma catecholamine levels?
50%.
How does clonidine produce analgesia when administered into the epidural or subarachnoid space, without producing opioid side effects?
stimulation of alpha 2 receptors by clonidine in the substantia gelatinosa of a spinal cord inhibits the release of substance P, which decreases the transmission of pain action potentials.
Name 6 uses of clonidine:
preanesthetic medication, to prolong the effects of regional anesthesia.

diagnosis of pheochromocytoma.

treatment of opioid withdrawal.

to treat shivering.

attenuate the cardiovascular effects of ketamine.
What are the three common side effects of clonidine?
sedation, bradycardia, and dry mouth.
What is the mechanism of action of with rebound hypertension with clonidine withdrawal?
an increase in circulating catecholamines.
How should life threatening clonidine withdrawal be treated?
reinstitute clonidine therapy or administer the vasodilator such as hydralazine or nitroprusside.
What is the anesthetic concern, other than blood pressure, when a patient is abruptly taken off clonidine or dexmetomidine?
preoperative hypothermia.
What is the purpose of preoperative administration of clonidine ?
it blunts the sympathetic reflex response of direct laryngoscopy or surgical stimulation.

it decreases requirements for volatile agents and opioids.
By how might as does clonidine decrease the Mac of volatile agents ?
15 to 50%.
Why shouldn't beta blockers be given to someone withdrawing from clonadine?
because unopposed alpha vasoconstriction which can lead to heart failure.
What other groups of drugs can exaggerate the rebound hypertension of clonidine?
tricyclic antidepressants (by potentiate in pressor effects of norepinephrine.)
If a patient is on clonidine, what drugs may precipitate severe hypertension?
ephedrine and beta blockers.
Where are the peripheral alpha 2 receptors during clonidine administration?
presynaptic of sympathetic postganglionic neurons (norepinephrine cannot be found at alpha 1 receptors of blood vessels.)
Where are the central alpha 2 receptors ?
post synaptic receptors of the brain stem.
Phenylephrine stimulates what receptors?
alpha 1, alpha 2 receptors can produce vasoconstriction.
What are the physiological effects of phenylephrine?
vasoconstriction, which produces reflex bradycardia, decrease and cardiac output, increase in SVR, and increased myocardial oxygen requirement.
What are the side effects of phenylephrine administration?
increased SVR, decreased heart rate, decreased cardiac output, increased myocardial oxygen consumption.
Exam: what do we need to know about nitroglycerin?
it causes venodialation.

there is decreased LVEDP, RVEDP, and decreased venous return, SVR is usually unaffected, so the decrease in blood pressure is from decrease in preload, not after load.

it decreases pulmonary vascular resistance.

it dilates large conductance vessels of the coronary circulation.

there is dose
related prolongation of bleeding time that parallels the decrease in systolic blood pressure.

there is increased cGMP that inhibits platelet aggregation.
Exam: at which channels does amiodarone work?
potassium channels, sodium channels, calcium channels.

it also has some beta blockade and calcium channel blockade.
Exam: what are the pharmacological effects of calcium channel blockers?
decreased myocardial contractility.

decreased heart rate.

decreased rate of conductance of cardiac impulses through the AV node.

relaxation and vasodilation with reduction in blood pressure.
What are the 2 major cardiac actions of competitive alpha adrenergic antagonists?
decreased blood pressure secondary to vasodilation and reflux tachycardia.
What receptors are inhibited by Regitine?
alpha 1, and alpha 2.
What is the major pharmacologic action of Regitine?
it produces peripheral vasodilation and decreased blood pressure by inhibiting alpha 1 and alpha 2 receptors.
How does Regitine produce tachycardia?
it blocks alpha 2, which enhances the release of norepinephrine.
What kinds of drugs are phenoxybenzamine and prazosin?

how are they used in anesthesia?
phenoxybenzamine is a long acting nonselective alpha adrenergic receptor antagonist.

prazosin is a selective alpha 1 adrenergic receptor antagonist.

they are both used preoperatively to treat a patient with pheochromocytoma.
Why is prazosin a better choice for decreasing blood pressure than Regitine or phenoxybenzamine?
it is a selective alpha 1 antagonist, and does not cause tachycardia by inhibiting alpha 2 receptors.
What is yohimbime in what is it used for?
it is a selective alpha 2 antagonist is used to treat impotence.
Aside from hypertension emergencies, what else is Regitine used for ?
local infiltration when a sympathomimetic is infiltrated in an IV.
What are the clinical uses of phenylephrine?
hypotension, aortic stenosis, SVT (stable), to prolong spinal anesthesia.
Where are the beta 1 receptors found?
heart, kidneys, adipose tissue.
What does a beta 1 stimulation cause clinically?
increased heart rate (SA node.)

increased conduction velocity (AV node.)

increased contractility (heart muscle fiber.)

increased renin release.

lipolysis (breakdown of fat to fatty acids and ketones.)
Where are the beta 2 receptors found?
smooth muscle and glandular tissue.
What does stimulation of beta 2 receptor cause?
its actions are inhibitory, so vasodilation (decreased SVR) in skeletal muscles.

bronco dilation and increased secretion in the lung.

glycogenolysis.

gluconeogenesis (the formation of glucose from amino acids in the liver.)

uterine relaxation.

stimulation of sodium/potassium pump to decrease plasma potassium levels.
Drugs that stimulate what receptors have both positive inotropic and positive chronotropic properties?
beta 1 adrenergic receptors.
What are effects of selective beta 2 agonists?
reversal of bronchospasm and cessation of uterine contractions in premature labor.
What kind of drug is ritodrine (yutpar.)?
it is a selective beta 2 adrenergic receptor agonist used to relax the pregnant uterus.
Name 3 main side effects of ritodrine:
tachycardia.

hypokalemia.

hyperglycemia.
What are the clinical uses of beta blockers?
treatment of the central hypertension (by decreasing cardiac output in heart rate.)

decreased secretion of renin.

management of angina by decreasing myocardial oxygen demand.

treatment of post myocardial infarction.

suppression of cardiac arrhythmias by decreasing rate of spontaneous phase 4 depolarization.

blunting sympathetic nervous system response to direct laryngoscopy and tracheal intubation.

hypertrophic obstructive cardiomyopathy is.

pheochromocytoma.

hyperthyroidism.

cyanotic episodes in tetralogy of falot. – reflex baroreceptor mediated increase in heart rate with patients treated with vasodilators.

anxiety.
List 5 side effects of beta blockers:
heart block (secondary to decreased AV node conduction velocity.)

worsening of CHF.

bronchospasm.

coronary artery constriction and inhibition of insulin release.
What are the clinical uses for labetalol?
to decrease heart rate and what pressure during and after surgery.

treatment of rebound hypertension after withdrawal of clonidine.

prevention of hypertension and the patient with pheochromocytoma.

producing controled hypotension without increase in heart rate or inhibiting hypoxic pulmonary vasoconstriction or cardiac output.
What is the alpha: beta blockade ratio of labetalol?
1:7 (stronger beta blocking activities then alpha blocking activities.)
What are the clinical side effects of labetalol?
decreased heart rate.

decreased myocardial contractility.

decreased SVR.
Labetalol has some alpha 1 blocking. What attenuates the reflex tachycardia in this situation?
the fact that it has stronger beta 1 blockade.
Why do beta antagonists cause in heart block, heart failure, cold hands/feet and CHF?
because heart block because they block the beta 1 receptors in the SA node, decrease in heart rate.

they worsened CHF because of decreased myocardial contractility.

they produce vasoconstriction in skeletal blood vessels by blocking beta 2 receptors.
What is the risk of giving a nonselective beta blocker to someone with diabetes?
hypoglycemia.
What attenuates the reflex tachycardia with labetalol ?
the fact that it has stronger beta 1 blockade.
Which lab value regarding a electrolytes should we know prior to giving beta blocker?
potassium. This is because beta 2 blockade causes hyperkalemia due to inactivation of sodium/potassium pump.
What is the effect of beta blockade on myocardial function in a normal heart ?
a normal heart functions adequately, so long as SVR is not abnormally elevated.
What will happen if you beta block someone with high SVR?
you can send them into heart failure by unopposed vasoconstriction.
Why is ketamine undesirable in the presence of beta blockers?
high SVR can lead to heart failure with unopposed sympathetic stimulation.
Why are enflurane and halothane undesirable in the presence of beta blockers?
they both produce myocardial depression.
What mneumonic can be used for drugs that are undesirable in the presence of betablockers?
KEHO

ketamine, enflurane, halothane, opioids.
What is down regulation of cardiac beta receptors?
it is when the receptors are chronically exposed to the beta agonists, causing receptors that are very sensitive to beta blockade. This occurs in CHF, where the heart is desensitized to catecholamines.
What happens in up regulation of beta receptors?
there is chronic exposure of an antagonist (beta blocker), so receptors increase in numbers.

if you abruptly withdraw the medication, the receptors will be ultra sensitive to catecholamines. Tachycardia, increased cardiac output, hypertension, myocardial infarction can occur.
How is excessive beta blockade managed?
atropine 70 mcg/kilogram.

isoproterenol 2 to 25 mcg/minute.

dobutamine when excessive beta 1 antagonism is present.

calcium chloride 250 to 1000 mg.

glucagon 1 to 5 mg.
Where are the dopamine receptors found?
post synaptically, they mediate vasodilation in renal, mesenteric, coronary, and cerebral beds.
Where, synapyically, are dopamine 2 receptors found ?
presynaptically.
What does stimulation of presynaptic dopamine 2 receptors promote?
inhibition of the release of norepinephrine.
What are dopamine receptors mediated by?
adenylate cyclase.
At what dose of dopamine is renal vasodilation achieved?
0.5 to 3 mcg/kilogram/minute.
What are the renal effects of renal dopamine?
increased urine output, increased GFR, increased excretion of sodium.
Which receptors are stimulated with dopamine 3 to 10 mcg/kilogram/minute?
beta 1, causing increased heart rate, increased conduction velocity, increased contractility.
What receptors are stimulated with dopamine 10 mcg/kilogram/minute?
alpha 1. It is a potent vasoconstrictor at this dose.
What are the ventilatory effects of dopamine?
it interferes with ventilatory response to arterial hypoxemia.
What is the most common clinical use of dopamine?
positive inatropy in patients with poor myocardial contractility, especially in the presence of low urine output.
receptor wise, what is norepinephrine?
it is a mixed adrenergic agonists with alpha 1, alpha 2 and beta 1 stimulation.
What are the clinical effects of norepinephrine?
potent arterial and venous constriction, increased SVR, decreased venous return, decreased heart rate, decreased cardiac output.
Why does the decreased heart rate occur with norepinephrine?
although beta 1 stimulation is present, there is a baroreceptor mediated decrease in heart rate when you increase SVR.
Why does norepinephrine cause metabolic acidosis?
it promotes the decrease in tissue blood flow.
What must norepinephrine be mixed in?
5% glucose.
How is norepinephrine terminated?
by reuptake into the postganglionic sympathetic nerve endings.
By what mechanism does cocaine alter sympathetic function?
it blocks reuptake of norepinephrine.
Epinephrine and norepinephrine are metabolized by what enzymes?
MAO in nerve terminals. – catacol O methyl transferase (COMPT) on the postsynaptic neuron.
What is ephedrine?
it is a direct and indirect acting synthetic noncatecholamines that stimulates beta receptors and also the endogenous release of norepinephrine. (mostly, however, beta.)
What are the clinical uses of ephedrine?
treatment of hypotension associated with spinal or epidural regional anesthesia, especially in OB because uterine blood flow is not altered.

overdose of inhaled or injected anesthetics.

hyvolemia.
Ephedrine stimulates what adrenergic receptors?
it stimulates indirectly and directly all adrenergic receptors.
What are the cardiovascular effects of ephedrine?
vasoconstriction, venous constriction, increased cardiac output, increased venous return, stimulation of heart rate and stimulation of blood pressure.
What are 8 possible adverse reactions with ephedrine administration?
hypertension, tachycardia, arrhythmias, pulmonary edema, anxiety/tremor, hyperglycemia, hyperkalemia, necrosis at site of injection.
***The rest is tara’s stuff***
***The rest is tara’s stuff***
What are the 2 principal uses of digitalis?
treatment of CHF, control of supraventricular dysrhythmias like atrial tachycardia, atrial flutter, or atrial fibrillation.
What are the 3 cardiac effects of digitalis?
enhancement of contractility, decreased heart rate, slowing of impulse propagation through AV node.
How does digitalis slow the heart rate and conduction through the AV node?
it enhances parasympathetic nervous system activity.
How does digoxin increase calcium release?
it inhibits the sodium/potassium pump, so that high sodium is intracellularly. As intracellular sodium increases, calcium within the sarcoplasmic reticulum is exchange for sodium, which leads to increased intracellular calcium.

the shift in ventricular function is to the left, with decreased AV node conduction and prolonged refractory.
What effect does digoxin have on the QT interval?
it shortens it.
In what phase of the cardiac cycle does digitalis work to slow heart rate?
phase 4 depolarization.
What are the three signs of digitalis toxicity ?
atrial or ventricular cardiac dysrhythmias.

prolonged PR interval.

gastrointestinal disturbances like anorexia/nausea/vomiting.
What 3 electrolyte disturbances enhance digitalis toxicity?
hypokalemia.

hypercalcemia.

hypo magnesium.
Why does hypokalemia enhance digitalis toxicity?
it allows increased binding of digitalis to the sodium/potassium pump.
Why should hyperventilation be avoided during anesthesia for the patient who is taking digitalis?
because hyperventilation causes hypokalemia, which can increase the likelihood of digitalis toxicity.
What are the 2 phosphodiesterase inhibitors?
imamrinone (Inacor) and milrinone (primacor.)
How do phosphodiesterase inhibitors work?
inhibition of phosphodiesterase results in increased camp within cells which increases calcium at the sarcoplasmic reticulum.

this results in increased contractility and smooth muscle vasodilation.

in short, increased contractility with decreased SVR.
What potential side effects occur with inacor but not milrinone?
thrombocytopenia.
What class of antidysrhythmic is dose amiodarone belong to?
class three antidysrhythmics.
What is the mechanism of action of amiodarone?
it blocks sodium, calcium, and potassium channels. It also blocks beta adrenergic receptors, prolonging cardiac repolarization and increasing refractory.
What effect does amiodarone have on the EKG?
it slows heart rate and increases PR and QT intervals.
What is lidocaine used for in terms of cardiac dysrhythmias?
it is the drug of choice for ventricular dysrhythmias. It is also used to treat premature ventricular contractions.
In what phase of the ventricular action potential does lidocaine work to suppress ventricular ectopy?
phase 4 depolarization (Purkinje fibers.)
How does lidocaine slow phase 4 depolarization in Purkinje fibers?
it decreases potassium ion permeability during this phase.
How is lidocaine eliminated ?
in the liver.
What class does flecainide belong to?
class IC.
What is the mechanism of action of flecainide?
how do calcium channel blockers work?
they slow phase 4 depolarization of the SA node.

they also decreases ventricular contractility by blocking the entry of calcium during phase 2 depolarization of the ventricular action potential.
How do calcium channel blockers prolong the effect of neuromuscular blockers?
they inhibit sodium influx, which decreases the release of acetylcholine.
How do calcium channel blockers prolong the effects of local anesthetics?
they inhibit the sodium to prolong local anesthetic.
What is the interaction between calcium channel blockers and volatile anesthetics?
excessive vasodilation and myocardial depression.
What is the depolarization of vascular smooth muscle dependent on?
calcium influx.
What is responsible for the depolarization of the SA node and AV node tissue?
calcium movement during phase 2 of action potential.