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PHARMACOLOGY > Unit 6 - Cardiovascular Drugs > Flashcards

Unit 6 - Cardiovascular Drugs Flashcards

1
Q

What is the CVS purpose?

A

transport system for the body: moves nutrients, O, hormones and picks up waste products and moves them to organs of removal

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2
Q

What could happen when the heart stops working?

A

poor O of tissues = exercise intolerance, fatigue, weakness
Fluid build up - especially problematic if in lungs = wheezing, coughing, orthopnea

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3
Q

What is the formula for cardiac output?

A

strove volume x heart rate

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4
Q

What are the compensatory mechanisms to help maintain CO?

A

inc HR, inc SV thru inc force of contraction
cardiac muscle hypertrophy
fluid retention to maintain BP

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5
Q

What happens if there is an excessive amount of compensatory mechanisms to maintain CO?

A

HR can get too fast to allow chambers to fill
Hypertrophy can result in making the chamber volume smaller
High BP makes it harder for heart to push blood around the system

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6
Q

What is preload?

A

volume of venous blood returned to the heart

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7
Q

What is afterload?

A

arterial resistance the heart must pump against

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8
Q

When are cardiac drugs used?

A
  1. treating heart failure: goals to slow down HR to work effectively, correct arrhythmias, reduce preload and afterload to lighten work load, dec hypertrophy, allows time to fill, prevents exhaustion
  2. CPR - increase CVS function by inc HR and contractility, and speed of electrical conduction
    Epinephrine does all of this
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9
Q

What are the two major types of cardiac drugs?

A
  1. drugs that affect the heart thru the ANS
  2. Drugs that affect ion channels
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10
Q

What type of ANS drugs do we give with decreased vs increased heart function?

A

Decreased: cholinergic drugs to inc PNS activity. Ex. Adrenergic blockers like b1 blockers
Increased: Anti-cholinergic drugs dec PNS activity. Ex. Adrenergic drugs (especially b1 adrenergics)

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11
Q

What are ion channel drugs?

A

depolarization and repolarization of cardiac muscle cells due to movement of Na, K, Ca in and out of cells thru specific ion channels
some cardiac drugs target function of these ion channels
Can inc, dec or co-ordinate movement of ions into cardiac cells
Drugs that block Ca and Na channels to dec heart function
Drugs that block K channels to increase heart function

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12
Q

How do we classify CVS drugs?

A

According to effect on heart.
1. Inotropes - alter STRENGTH of contractions. Pos inotropes inc contractility, neg dec contract
2. Chronotropes - Alter the RATE of contractions: pos inc HR, ned dec HR
3. Dromotropes - Alter SPEED OF ELECTRICAL CONDUCTION thru the heart: Pos in speed ex. epinephrine. Neg dec speed. ex. Bblockers

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13
Q

What are anti-arrhythmics used for?

A

used to correct abnormal heart rhythms
majority slows down the heart (neg chronotropes) to allow better filling time, works less > dec hypertrophy and wearing out
Some also affect conductivity (dromotropes)
Some decrease contractility (ned inotropes
3 classes

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14
Q

What are the 3 classes of anti-arrhythmics?

A
  1. Sodium channel blockers
  2. Calcium channel blockers
  3. Bblockers
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15
Q

What are sodium channel blockers?

A

bind to and decrease the flow of Na ions into the cardiac cell - slows down rate of depolarization, extends the refractory period
Resul: dec HR (neg chronotrope)
also, by slowing any spontaneous cell depolarization occurring abnormally in heart, SA node can regain control of the overall heart rhythm
Ex. lidocaine

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16
Q

How might lidocaine work as a CVS drug?

A

local anesthetic
also has anti-arrhythmic properties when given systemically; partially blocks Na channels in the ventricles
Considered an emerg cardiac drug
if using as a local anesthetic caution regarding total dose administered
used to treat PVCs and ventrical arrhythmias (incl. V-fib)
given as a CRI (metabolized very quickly)
slight overdose causes sedation, ataxia
larger OD’s can excitement/seizure/collapse
Systemic OD = sinus arrest, paralysis of cardiac and resp muscles = death
cats more sensitive
only use LIDOCAINE NEAT for IV admin - other form used as local anesthtic only (lido + epi, which if given IV can cause acute heart failure)

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17
Q

What are calcium channel blockers

A

Block CA influx into cardiac cells
Result is dec rate of cell depolarization; but dec heart contractility (ned inotrope and chronotrope)
most common vet use is for treating cats with HCM > dec HR > to heart works less > muscle does not thicken as much
Ex. Amlodipine, diltiazem, verapamil

18
Q

What are beta blockers?

A

drugs that bind to and selectively block B1 receptors (ex. atenolol) or non-selective which block B1 and B2-receptors (ex. propranolol) on cardiac muscle cells so there is no SNS stimulation
Blocking B1-receptors results in dec HR (neg chronotrope) and neg contractility (neg inotrope)
allows time for ventricles to fill completely

19
Q

What are the side effects of beta blockers?

A
  1. bronchoconstriction - due to some B2 blocking activity by non-selective blockers
  2. Neg inotrope activity can dec CO so less blood is being moved by the heart > hypotension risk
    Symptoms of dec BP: weak, lethargic, syncope
    Inc risk if: heart is slowed too much, on other drugs that also slow heart and cause vasodilation, dehydration
20
Q

What is unique to b1 blockers

A

drugs become less effective over time
cardiac cells start to prod more B1 receptors over time; may inc dose
also means that suddenly stop the drug may cause a heightened sympathetic response ew/ severe arrhythmias
wean off slowly

21
Q

What are positive inotropes

A

drugs that inc force of myocardial contraction - used on a weakened heart, work by inc amount of CA that enters the cardiac cell; and enhances the binding of CA to contractile fibers

22
Q

What are some commonly used pos inotropes?

A
  1. adrenergic drugs (epinephrine, ephedrine)
  2. cardiac glycosides (digoxin)
  3. Pimobendan (vetmedin)
  4. Anticholinergic (atropine)
23
Q

What are adrenergics?

A

Sympathomimetics
Older name is catecholamines
Epinephrine, ephedrine, dobutamine
Turn on the SNS
bind to and stim B1 receptors on cardiac cells to inc force and rate of myocardial cell contraction (pos ino and chronotrope), very strong and short acting
only used short term
emerg use in CRP (epinephrine) and acute heart failure (dobutamine) and hypotension (ephedrine)

24
Q

What do we need to be aware about with cardiac glycosides

A

digoxin and digitoxin
produced from digitalis found in the foxglove plant
plant considered poisonous > causes cardiac toxicity > severe bradycardia > heart block > death

25
Q

What are some cardiac glycosides?

A

digotoxin, digitoxin
inc strength of cardiac contractions by causing release of Ca from intracellular stores
Also has PS activity bc it binds the ACh receptors and dec HR
Requires renal elimination
therapeutic druc monitoring is advised

26
Q

What are some benefitical effects and s/e of cardiac glycosides?

A

beneficial: slows HR while increasing contractility
S/e due to high serum lvls - first see anorexia, V/D, if not managed, can lead to various arrhythmias

27
Q

What is pimobendan?

A

Vetmedin
Most commonly prescribed heart drug in SA
Functions by 1. sensitizes cardiac cells to Ca (CA binds better to myosin fibers); inc force of contraction
2. neg chronotrope (inc ventricular filling time)
3. Vasocilation to reduce hypertension
S/e:a norexia, V/D (give 1hr before food), risk of hypotension if dehydrated

28
Q

What cardiac drugs used in CPR to treat ventricular fibrillation?

A

lidocaine - NA channel blocker; slows the heart in V-fib

29
Q

What cardiac drugs used in CPR is used to tx asystole?

A

atropine - anticholinergic; turns down PS response to inc HR
Epinephrine - adrenergic agonist (beta 1 and a2 agonist activity); inc HR, contractility and BP

30
Q

What is high blood pressure and what does it cause?

A

high BP is a result of heart failure, renal failure or hyperthyroidism
A compensatory mechanism in heart failure
Not enough blood moved by heart > dec blood flow to kidney signals body to undergo vasoconstriction and water retention (renin-angiotensin system) > inc BP > inc preload (fluid volume) and afterload (arterial pressure) which makes more work for an already poorly functioning heart

31
Q

What might high BP cause?

A

pleural effusion, pulomary edema, ascites
retinal detachment, cerebral edema

32
Q

How might we treat high BP?

A
  1. tx underlying problems (hyperT4 in cats)
  2. Vasodilators: dilate veins and/or arteries to dec preload/afterload to prevent flooding (arteriole dilators like hydralazine, amlodipine and venous dilators like nitroglycerine < wear gloves, plus mixed vasodilators like ACE-inhibitors (enalapril, benazepril, captopril), a1 blockers - prazocin, and nitroprusside
  3. diretics: remove fluid volume
  4. Decrease salt intake to reduce water retention
33
Q

What are ACE-inhibitors?

A

work by inhibiting angiotensi-convertign enzyme (ACE)
ACE is part of the renin-angiotensin system which 1. turns on antidiuretic hormone > water retention and vasoconstriction, 2. turns on aldosterone > Na retention and 2nd water retention, 3. Overall effect: inc BP
inhibition of ACE turns off the above and results in mild-mod vasodilation
S/e of drug: hypotension, weakness, syncope

34
Q

How does the renin-angiotensin system normally works?

A

Decreased blood flow to kidneys > kidney prods renin > angiotensin > AGTI > ACE (ACE inhibits this enzyme) > AGTII > 1. adrenal gland >aldosterone > Na retention, 2. Pituitary > anti-diuretic hormone (ADH; AKA vasopressin)+Na rention to > water retention
Anti-diretic hormone to > vasoconstriction to all of it inc BP

35
Q

What are diuretics?

A

drugs to promote fluid loss thru inc urination
used in congestive heart failure to dec total body water volume; to treat high BP; to treat fluid retention: to treat cerebral edema, pulmonary edema, pleural effusion

36
Q

What are the 4 classes of diuretics. Which ones work in the kidneys and blood vessels?

A
  1. Loop diuretics - furosemide (Lasix)
  2. Thiazides - very mild, seldom used
  3. Potassium-sparing diuretics - spironolactone
    ^^ works in kidneys
  4. Osmotic diuretics - in blood vessels
37
Q

What does furosemide do?

A

commonly used diuretic in ALL vet species
causes water loss via kidneys by acting at loop of henle and inhibits Na reabsorption @ the loop so Na is lost into urine, water will follow the Na and at the convoluted tubule, NA is exchanged for K (Na is reabsorbed, K is excreted; water stays in tubule)
ultimately, causes loss of Ka nd water into urine

38
Q

How is furosemide given, what is the s/e and contraindications?

A

can be given IV, IM, SQ, PO (fastest to slowest)
IV acts in 5-15m, IM and SQ, act in 10-30m
very potent, very safe
part of emerg drug kit for cerebral edema, pleural effusion, pulmon edema and drug toxicity
s/e: dehydration, hypovolemia, avoid if already dehydrated
can cause hypokalemia w/ long term use
avoid in renal failure

39
Q

What are osmotic diuretics

A

mannitol, glycerin
large sugards that stay in vessels and draw water out of the interstitial spaces > then readily secreted into urine (not not reabsorbed) > inc osmotic pressure in urine which also results in more water being retained in the urine

40
Q
A

PHARMACOLOGY (12 decks)

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