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Pharm 3 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

What is an arrythmia?

A

Alteration in normal impulse pathway b/c of:

  1. Alteration in pacemaker (SA node)→Ectopic focus is source of rhythm start (Standard reason)
  2. Alteration in transmission pathway

Single ectopic beat not an issue

Ppl can have arrythmias under GA

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2
Q

What is ventricular fibrillation

A

Life threatening unsynchronized contraction of muscle fibers

Leads to decreased CO and clots can form in heart

Ventricular arrythmias are the major cause of sudden cardiac death

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3
Q

Cardiac AP

A

-90mV resting potential

  1. Na influx→Rapid depolarization
  2. Ca influx→Plateau (prob. responsible for contraction of heart)
  3. K efflux→Repolarization
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4
Q

In most cases how do we treat arrythmias

A

No tx unless life threatening

Drugs can cause arrythmias

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5
Q

Types of non-drug tx for arrythmias

A

Note that non-drug tx is preferable

  • Pacemaker
    • Implantation
    • Very complex
  • Cardioversion
    • Global depol. of heart
    • Sends e- shocks to heart through electrodes on chest
  • Automatic defibrillator
    • Senses when rhythm is out of balance and gives global depol.
  • Ablation
    • Surgical removal of ectopic focus
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6
Q

Class I drugs for arrythmias

Characteristics and names

A

Na channel blockers

Local anesthetics→decreased rate of depol.

These drugs can cause arrythmias

These have a greater effect on ectopic foci vs AV node foci

1a drugs: “Double Quarter Pounder”

  • Disopyramide
  • Quinidine
  • Procainamide

1b drugs: “Lettuce+Mayo”

  • Lidocaine
  • Mexiletine
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7
Q

Quinidine

A

Tx: All arrythmias (Class Ia)

Mech: Na channel blocker

  • Depresses all mm fxn

SE:

  • Anti-cholinergic effects (antivagal effects)
    • Quinidine will direclty slow the heart, but it may indirectly speed up HR by suppressing the vagus nerve
    • Vagal innervation slows HR
    • May lead to arrythmias
  • GI
    • Nausea and vomiting
  • Anorexia
  • CNS
    • Tinnitus
    • Alterted color vision

With _Qu_inidine you feel _qu_easy and need _qu_iet (tinnitus)

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8
Q

Procainamide

A

Tx: All arrythmias (Class Ia)

  • Also LA

Mech: Na channel blocker

  • Like quinidine but does not get into CNS

SE:

  • Lupus like syndrome in slow acetylators
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9
Q

Disopyramide

A

Tx: Arrythmias (Class Ia)

Mech: Na channel blocker

SE:

  • Even stronger antivagal effects (than quinidine)
  • Antimuscarinic effects (opposite of DUMBBELS)
    • Wouldn’t use w/ glaucoma pts

Our mnemonic was Double Quarter Pounder

_D_isopyramide has double the antivagal effects as quinidine

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10
Q

Lidocaine

A

Tx: arrythmias (Class Ib)

*also LA

Mech: Na channel blocker

Route: Given IV

Kinetics: First pass effect

Toxicity: Low

Clinical use:

  • Emergency tx of ventricular arrythmias
  • Tx of ventricular tachycardia

SE:

  • Less likely to cause arrythmias but can enter CNS
    • Tremors
    • Seizures
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11
Q

Mexiletine

A

Tx: arrythmias (Class Ib)

Mech: Na channel blocker

Clinical use:

  • Emergency tx of ventricular arrythmias
  • Tx of ventricular tachycardia

Like lidocaine but can be given orally

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12
Q

Class II drugs for arrythmias

Names and characteristics

A

Beta1 receptor blockers in heart

“olol” drugs

Used to treat excessive symp. stimulation–slows HR

Drugs:

  • Esmolol
  • Propranolol
  • Metoprolol
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13
Q

Propranolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

Nonspecific B blocker

Decreases pacemaker firing rate

SE:

  • Bradycardia
  • Hypotension
  • B2 effects-asthma
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14
Q

Metoprolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

Specific B1 blocker

SE:

  • Bradycardia
  • Hypotension
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15
Q

Esmolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

Specific B1 blocker

More rapid onset of action

SE:

  • Bradycardia
  • Hypotension
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16
Q

Class III drugs for arrythmias

*Names *

A

K+ channel blockers

“-arone”s +sotalol

Drugs: “A Diet Soda”

  • Amiodarone
  • Dronedarone
  • Sotalol
17
Q

Sotalol

A

Tx: arrytmhias (Class III)

Mech: K+ channel blocker

Also a beta blocker

18
Q

Amiodarone

A

Tx: arrytmhias (Class III)

DOC for cardiac arrest–most effective anti-arrythmic

Mech: K+ channel blocker

Acts like all 4 classes of anti-arrythmic

SE:

  • Potentially fatal pulmonary fibrosis
    • Replaces lung tissue w/ fiber composites
  • Liver damage
  • Corneal deposits-optic neuritis
  • Deposits in skin-blue/gray skin coloration
  • GI upset

*Iodine responsible for some deposits

19
Q

Dronedarone

A

Tx: arrytmhias (Class III)

Mech: K+ channel blocker

Analog of amiodarone

Fewer SE-less efficacious

20
Q

Class IV drugs for arrythmias

A

Ca channel blockers→Increase refractory period

Tx: all arrythmias EXCEPT ventricular arrythmias

Most of the “ipine”s

Drugs: “Very Nifty Dildos”–put dont put that dildo in your ventricle (all arrythmias except ventricular)

Verapamil

Nifedepine

Diltiazem

21
Q

Verapamil

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

22
Q

Diltiazem

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

23
Q

Nifedipine

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

24
Q

Adenosine

A

Tx:

  • Arrythmias (Other class)
  • Adenosine for Atrial Tachycardia

Mech:

  • Binds to adenosine receptor
  • Decreases firing rate of AV node
  • Coronary vasodilator

Kinetics-Very short T1/2=10sec

25
Q

Angina definition and general tx methods

A

Not enough BF to heart

Causes chest pain (m becomes anoxic)

We usually have chest pain after we work out b/c we need more O2

But if at rest it is unstable angina

Tx by increasing BF or decreasing O2 demand

Tx:

  • Behavioral
    • Diet
    • Exercise
      • Creates collateral circulation (more blood vessels) in heart
    • Stop smoking
  • Drugs
26
Q

Glyceryl Trinitrate (nitroglycerin) (GTN)

A

Tx: Angina

Mech:

GTN→NO→Act. guanylate cyclase→cGMP→vasodilation

Rapidly dilates all blood vessels, including coronary art.

Route: Given sublingually–1st pass effect

Effects last 30-60min

Rapid tolerance so cannot take continuously

SE:

  • Hypotension
  • Skin flushing
  • Headache-opening blood vessels in brain, feel pulsing

*Nitroglycerin is unstable and explosive in some conditions

27
Q

Isosorbide dinitrate

A

Tx: Angina

Slow release nitrate formulation

Can be given orally

Slow enough that effects occur before 1st pass metabolism

28
Q

Other agents to treat angina

A

Agents that decrease heart work

  • B blockers-“olol”
  • Ca channel blockers- often “ipines”
29
Q

What is and what causes congestive heart failure

A

Heart m doesn’t contract strongly enough→Rest of body lacks BF

  • Tissues become anoxiated
  • Heart enlarges
  • Blood backs up in lungs→Pulmonary congestion→ decreased ability to breath
  • Kidney not well perfused
    • Not getting enough O2
    • Retention of Na fluid-leads to peripheral edema

Congestive-lot of fluid accumulation, pitting edema

Most common cause of hospitalization of ppl over 60

Cause=cardiac damage

Compensation is what kills pt– Don’t want fluid retention w/ increased HR

30
Q

How does our body adapt to CHF

A

In short, body thinks we are losing blood, but we are only losing O2

1) Apparent loss of blood b/c tissues underperfused

  • Release of E, NE, and Angiotension II
  • Lead to increase BP→Increase HR, vasoconstriction (peripheral)

2) Increase in BV

  • Make more blood
  • Angiotensin II causes increase in Na retention and aldosterone secretion→Na/K exchanger increase

3) Enlargement of heart
* Due to increase force of contraction

Initially this is okay but continued degradation of heart m→heart failure

31
Q

Tx of cardiac insufficiency

General scheme not drug names

A

Increase cardiac m contractility

Via inotropic agents to increase amount of Ca in heart m

32
Q

Digoxin

A

Tx: CHF

Class: Cardiac glycoside

  • Naturally occuring (foxglove and milk weed)
  • Produced as protection for plant

Route: orally

Kinetics: long T1/2

Mech:

  • When m stimulated, small influx of Ca→causes release of Ca into cell from SR→contraction
  • In order for m to relax after contraction, Ca must be removed (Na and Ca pumped out, K pumped in)
  • Digoxin inhibits NaK-ATPase
    • Na remains high in cell→prevents loss of Ca
    • High conc of Na inhibits the Na-Ca exchanger
  • Net result: Ca remains high
    • High Ca→greater contractility

Effects:

  • Increases duration of contractile response
  • Stimulates vagus n
  • Anti-arrythmic effects

SE:

  • Cardiac arrythmias
  • CNS effects
    • Yellow-green tinting of vision
    • Hallucinations
    • Activation of chemoreceptor trigger zone→severe nausea
  • Effects enhanced in hypokalemia
    • Bind K site
    • If less K outside of cell, more effective (less competition for K site)

Digoxin poisoning treated w/ anti-digoxin anti-bodies

33
Q

Dobutamine

A

Tx: CHF

Class: Inotropic agents

Mech: Beta1 agonist

Effects: Increase force of contraction

34
Q

Current best tx of CHF

A

Ace inhibitors→Decrease BP and fluid retention

Beta blockers→decrease HR

Vasodilators→Decrease BP

Diuretics too?

35
Q

“-afils”

A

Sildenafil

Vardenafil

Tadalafil

Avanafil

Tx: ED

Mech:

  • Inhibits type 5 cGMP phosphodiesterase
  • Nitrates→NO→cGMP→smooth m relax
  • cGMP degraded to 5’GMP via type 5 cGMP phosphodiesterase
  • Relaxes arteries in corpus cavernosum→increase BF

SE:

  • Slight drop in BP
    • Do not use w/ alpha 1 blockers or nitrates
    • Too much drop in BP
  • Stroke
  • MI (may be due to activity)
  • Visual disturbances
    • Impaired blue/green color discrimination
    • NAION-some potential for damage to retina induced by cGMP PDE inhibitors

Metabolism: P450

36
Q

Alprostadil

A

Tx: ED

Injectable prostaglandin (PGE1) leads to vasodilation when injected directly into penis

  • Think: Alprosta_dil_*
  • Prost=prostaglandin*
  • Dil=dilation*

Pharm 3 (6 decks)

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