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Pharm > Cardiac drugs > Flashcards

Cardiac drugs Flashcards

1
Q

Associated symptoms of angina

A
  • Shortness of breath
  • belching indigestion nausea vomiting
  • diaphoresis
  • dizziness and lightheadedness
  • cold and clamminess
  • fatigue
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2
Q

Types of angina drugs

A
  • Nitrates9short and long acting
  • beta blockers(target Beta1 receptors in heart)
  • calcium channel blockers
  • Ranolazine
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3
Q

How does nitrate therapy work?

A
  • metabolized to NO, which produces SM relaxation and vasodislation
  • Most of the effect is from systemic vasodilation.
  • Primary venodilators and result in reduced venous return and reduction of preload
  • higher dose can cause aterial vasodilation and drop in BP associated with reflex tachycardia.
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4
Q

NItrate perp and different types

A
  • Adimistered orally, sublingually, transdermally and intravenously
  • short acting 2-5min OOA and 15-30 min duration
  • longer acting oral, OOA=30 min, duration of up to 8 hrs. tid
  • Longest acting OOA=30-60min, 12-24hr duration
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5
Q

Side effects of nitrates

A

Most of the symptooms go away with continued use

  • headache
  • flushing
  • lightheadedness
  • blurred vision
  • edema
  • nausea
  • tachycardia
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6
Q

how do beta blocker work

A

_redce oxygen demand and increase oxygen supply

  • **reduction in HR
  • Reduction in BP-reduced AL
  • reduction in left ventricular contractility
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7
Q

Properties of beta blockers

A

-Cardioselectiveity
–nonselective or selective to beta1(metaprolol)
Beta 1 in heart
beta 2 in bronchial and peripheral vasculature
-alpha blocking activity- block alpha receptor

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8
Q

Cardiac side effects of beta blockers

A
  • negative ionotropy- may worsen heart failure in patients with decompensated heart failure
  • negative chronotrophy- sinus bradycardia, sinus node dysfunction
  • AV nodal blockade- complete heart blck
  • Beta blocker withdrawal- precipitation of angina, myocardial infarction, sudden death
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9
Q

NONCARDIAC SIDE EFFECTS OF BETA BLOCKERS

A

Increased airway resistance/bronchospasm
CNS – fatigue, hallucinations, insomnia, depression,
mood alteration
Sexual dysfunction/impotency
Potential adverse reactions – include hypoglycemia
and exacerbation of peripheral vascular disease
Drug interactions – e.g., calcium channel blocker
(verapamil, diltiazem) and digoxin

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10
Q

how do CALCIUM CHANNEL BLOCKERS for angina work?

A

Calcium channel blockers block the initial influx of calcium into the myocyte and vascular smooth muscle cell
-Reduction in calcium available for binding to actin and myosin.
Results in vasodilation and reduced myocardial contractility (inotropy)
Some calcium channel blockers (verapamil, diltiazem) affect pacemaker tissue that generates a slow action potential mediated by calcium currents (chronotropy)

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11
Q

PROPERTIES OF CALCIUM CHANNEL BLOCKERS(dihydropyridines/

-ipine)

A

Have a greater selectivity for vascular smooth muscle than for the myocardium; more potent vasodilators
(arterial and venous) than the nondihyrdopyridine

Reduce vascular resistance, increase coronary (and other arterial) blood flow

Elicit a strong reflex beta-adrenergic response (often with reflex tachycardia)

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12
Q

PROPERTIES OF CALCIUM CHANNEL BLOCKERS(Nondihydropyridines)

A

Verapamil – much less potent vasodilator than
dihydropyridines; has more direct myocardial effects,
decreasing myocardial contractility; depresses
sinus node rate and slows AV nodal conduction

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13
Q

SIDE EFFECTS OF CALCIUM CHANNEL BLOCKERS

A

Headache
Dizziness/lightheadedness
Flushing
Peripheral edema
Cardiac – decreased inotropy, bradycardia, AV block
Increased mortality post MI/increased MI in severely hypertensive patients – short acting nifedipine
Severe hypotension

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14
Q

how does RANOLAZINE work

A

Ranolozine inhibits inward sodium current in cardiac muscle, reduces intracellular Ca+ - reduces oxygen demand

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15
Q

RANOLAZINE side effects

A

Dizziness, constipation, headach
Contraindicated in patient with liver disease due to impact on QT in this patient population

Metabolized by CYP3A & inhibits CYP2D6. Need to monitor other drugs for interactions with these enzymes

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16
Q

Antiarrhythmics what exactly are the yused to treat?

A

Supraventricular

       - Premature atrial complexes
- Atrial fibrillation - Atrial flutter - Atrial tachycardia - Supraventricular tachycardia

Ventricular

 - Premature ventricular complexes
 - Ventricular tachycardia
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17
Q

describe the phases of saction potentials

A

Phase 0: Depolarization- Mediated largely by influx of Ca++
Phase 2 and 3: Repolarization - Largely mediated by efflux of K+
Phase 4: Slow Depolarization - Widely believed to be due to If (K+ and Na+), although controversial.

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18
Q

VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class I

A

Class I (local anesthetic agents) - All these agents
block the Na+ channel, slowing the upstroke of
phase 0 and slowing impulse conduction velocity
and the rate of depolarization

19
Q

VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class Ia

A

– (quinidine) – moderate effect on prolonging phase 0 upstroke. Also block K+ efflux during repolarization (class 3 activity), which causes QT prolongation

20
Q

VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class Ib

A

lidocaine) – slight effect on phase 0 upstroke

21
Q

VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class Ic

A

propafenone) – marked effect on prolonging phase 0 upstroke

22
Q 
VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS 
class II
A

Beta blockers
All work by blocking effect of sympathetic stimulation on the heart. They have no direct antiarrhythmic effects. Major action is on the sinus and AV nodes.

23
Q 
VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS 
class III
A

All these agents block the efflux of K+ during phase 2 and 3 repolarization, resulting in prolongation in refractoriness.
amiodarone

- Amiodarone and dronedarone also have 
  class I, II, and IV antiarrhythmic effects.
24
Q 
VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS 
class IV
A

Calcium channel blockers, primarily verapamil and diltiazem. No direct antiarrhythmic effect. Major action is on the sinus and AV nodes.

25
Q

NON-VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

A

Digoxin, adenosine (actions are outside of Vaughan-Williams classification)

26
Q

Lidocaine

A

Local anesthetic agent
Class 1B antiarrhythmic drug prototype
Is administered IV only
Onset of action 45-90 sec
Bolus for loading, continuous IV infusion thereafter
Half life 15-20 min single dose; 90-120 min with IV infusion
Side effects – GI, neurologic, respiratory

27
Q

AMIODARONE

A

Prototype antiarrythmic agent with multiple class effects
Primarily a class III antiarrhythmic agent – K+ channel blocker prolonging action potential duration and repolarization. Also has class I, II, and IV antiarrhythmic activity
Every 200 mg of amiodarone contains 80 mg of iodine; accounts for many of the side effects
Pharmacology – only 50% bioavailable with oral therapy, requires prolonged loading period (up to 3 months) as the drug is highly lipophilic and binds to all adipose tissue and these stores are saturated before therapeutic effect noted. Metabolized by liver to active metabolite. Half life is 26-107 days.
Indicated for supraventricular and ventricular arrhythmias

28
Q

AMIODARONE minor SIDE EFFECTS

A 
Minor and asymptomatic
	- corneal microdeposits
	- elevated LFTs
	- thyroid function abnormalities
	- blue-gray skin discoloration
Minor and symptomatic
   	- skin rash, photosensitivity
	- CNS – ataxia, temors, headache, paresthesias
	- GI – nausea, anorexia, constipation
	- visual complaints
 	- hair loss
	- epididymitis
29
Q

AMIODARONE major SIDE EFFECTS

A

Major side effects (require dose reduction or drug
discontinuation)
Hypothyroidism/hyperthyroidism
Pulmonary complications
Bradycardia – sinus node dysfunction, AV node blockade
Arrhythmia aggravation (rare)
Hepatic injury
Drug interactions – warfarin, digoxin, beta blockers, calcium channel blockers, other drugs that prolong QT interval (eg antibiotics)

30
Q

ELECTROPHYSIOLOGIC EFFECTS OF DIGOXIN

A

Enhances vagal tone (vagal innervation primarily to sinus and AV nodes)
- reduces sinus node automaticity and rate
- prolongs refractoriness of AV node and slows
conduction through this structure

At toxic doses also increases sympathetic outputs from central nervous system. The increase in the peripheral vagal tone and central sympathetic outputs results in digoxin toxic arrhythmias
31
Q

PRELOAD REDUCTION

A

REDUCTION IN VENOUS RETURN
Diuretics - thiazide, loop, aldosterone antagonist
Venodilation (capacitance vessels)
- nitrates (IV, SL, transdermal, oral)
- nitroprusside (IV)

32
Q

DIURETICS IN HEART FAILURE

A

Reduce venous congestion
improve shortness of breath
improve lower extremity edema
Reduce preload, reducing end-diastolic volume and wall stress and increasing stroke volume
Thiazide vs. loop diuretics
Loop diuretics (e.g. furosemide) more efficacious and commonly used in patients with congestive heart failure

33
Q

DIGOXIN IN HEART FAILURE

A

Prototypic inotropic drug
Increase in intracellular Ca++
Increase in myocardial contractility
Increase stroke volume and cardiac output; reduces LV preload
Directly and indirectly reduces sympathetic nervous system activity
Decrease in heart rate (withdrawal of sympathetic activity and increased vagal tone)

34
Q

DIGOXIN PHARMACOKINETICS

A

75% of dose rapidly absorbed; rest inactivated in lower gut by bacteria
Half life 36 hour
Binds to tissue receptors in heart as well as skeletal muscle
Is lipid soluble, penetrates the brain
Is excreted unchanged in urine
Dose adjustment necessary in chronic renal failure
Dose reduction in patients with reduced skeletal muscle mass (thin patients, elderly)

35
Q

DIGOXIN SIDE EFFECTS

A

Cardiac
bradycardia, AV block, asystole, supraventricular arrhythmias, junctional arrhythmias, ventricular arrhythmias

Noncardiac
- GI (nausea, vomiting, abdominal pain, anorexia)
- Neurologic (visual disturbances, abnormal dreams,
headache, dizziness, apathy, confusion, mental
disturbances, anxiety, depression, delirium,
hallucinations)
- Weakness

36
Q

PHARMACODYNAMICS OF VASODILATORS (AFTERLOAD REDUCTION)

A

Reduction in arterial vascular tone or resistance (afterload)
Reduction in venous tone- increase in venous capacitance, decrease in venous return (preload
Reduction in myocardial wall stress
Improved ventricular systolic function (inotropy)-increase in stroke volume and cardiac output
Enhanced myocardial relaxation (lusitrophy) - improved diastolic function

37
Q

AFTERLOAD REDUCTION(VASODILATION)

A

Direct acting – smooth muscle dilatation
Alpha receptor blockade
Angiotensin converting enzyme (ACE) inhibition
Angiotensin II receptor blockade (ARB)
Calcium channel blockade
Nitric oxide generation – endothelium derived relaxing factor

38
Q

HYDRALAZINE

A

Direct smooth muscle relaxation and arterial vasodilation via inhibition of calcium influx
Can be administered IV or orally (three times per day)
When used for heart failure therapy is combined with long acting nitrate (isosorbide mononitrate or dinitrate)

39
Q

HYDRALAZINE SIDE EFFECTS

A

Cardiovascular – tachycardia (which can precipitate angina), hypotension
Drug induced lupus-like syndrome
Headache
Dizziness
Flushing
Increased renin secretion- salt and water retention and edema
GI – anorexia, nausea, vomiting

40
Q

(ACE) INHIBITORS

A 
Hemodynamic effects mediated by:
Reduction in angiotensin II levels
    - reduction in arterial vascular resistance 
      (afterload)
Prevention of aldosterone secretion
    - reduced salt and water retention
    - reduced preload
Blockade of bradykinin metabolism
    - arterial vasodilation
Reduction in sympathetic activity
41
Q

ACE INHIBITOR SIDE EFFECTS

A 
Hypotension 
Weakness
Dizziness, lightheadedness
Syncope
Acute renal failure – primarily in patients with renal artery stenosis, heart failure, chronic renal disease, hypertensive kidney disease
Cough
Hyperkalemia
-for ACEI with sulfhydryl group
Neutropenia
Altered taste
Angioedema
42
Q

(ARB) (-sartin)

A

Blocks the binding of angiotensin II to the AT1 receptor on the vascular smooth muscle
- reduction in arterial vascular resistance (afterload)
Reduces sympathetic activity
Blocks effect of angiotensin II on adrenal gland- inhibits secretion of aldosterone
Has no effect of bradykinin metabolism
Primarily used in patients intolerant of ACE inhibitors, as add-on therapy in patients treated with an ACE inhibitor, and in patients with preserved LVEF

43
Q

ARB SIDE EFFECTS

A

Side effect profile generally the same as that for ACE inhibitors
Hypotension
Dizziness, lightheadedness
Syncope
Weakness
Hyperkalemia
Acute renal failure – primarily in patients with renal artery stenosis, heart failure, chronic renal disease, hypertensive kidney disease
Less likely to cause cough, neutropenia, angioedema

44
Q

Dental Management Guidelines

A

For undiagnosed patients with symptoms of ischemia, heart failure, or arrhythmia
avoid elective care; refer to physician
For diagnosed patients with cardiac symptoms
Asymptomatic: routine care
Mild symptoms with exertion: elective care OK, recommend consultation with physician
Symptoms with minimal activity or at rest: avoid elective care; if treatment necessary, manage in consultation with physician; consider referral to a special patient care setting; avoid use of vasoconstrictors or epinephrine

Pharm (10 decks)

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