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CRRAB I > Antianginal Drugs > Flashcards

Antianginal Drugs Flashcards

1
Q

most common cause of angina

A

coronary artery disease

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2
Q

angina that occurs at night due to increase in venous return. Can be vasospastic.

A

Prinzmetal angina

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3
Q

angina due to imbalance when oxygen demand increases and coronary blood flow doesn’t increase proportionally, especially during exercise leading to pain

A

classic angina

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4
Q

angina where episodes occur at REST. Increases severity, frequency, duration of chest pain.

A

Unstable angina

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5
Q

causes of unstable angina

A

reduced blood flow due to partially occlusive thrombi or fissured/ulcerated plaque.

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6
Q

How do we treat classic angina?

A
  • decrease cardiac work
  • shift myocardial metabolism
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7
Q

angina where oxygen delivery decreases as a result of reversible coronary vasospasm

A

Variant angina

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8
Q

How do we treat variant angina?

A
  1. reverse spasm
  2. treat the atherosclerosis

* these affect the supply**

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9
Q

How do we treat unstable angina?

A

Treat the SUPPLY (increase)

  • reverse spasm
  • threat the atherosclerosis

treat the demand (reduce)

  • decrease cardiac work
  • shift myocardial metabolism
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10
Q

what determines ventricular wall stress?

A
  • intraventricular pressure - increases wall stress
  • radius of the ventricle - more filling = increased wall stress
  • ventricular wall thickness (h) - hypertrophied heart has LESS wall stress

T=P x r/2h

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11
Q

4 factors that affect myocardial oxygen demand

A
  1. ventricular wall stress - influenced by pressure, radius, and wall thickness
  2. heart rate - increases = increased O2
  3. contractility - greater force requires more oxygen
  4. basal metabolism
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12
Q

What determines coronary blood flow?

A
  • perfusion pressure - aortic diastolic pressure SHOULD BE HIGH (flow is ZERO during systole in coronary arteries)
  • duration of diastole - limiting factor for perfusion expecially during tachycardia
  • resistance
    • ​determined by:
      • metabolic products
      • autonomic activity
        • damage - alters ability to dilate (increases R)
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13
Q

What does arteriolar tone influence and does it control it?

A
  • controls peripheral vascular resistance and arterial BP
    • influences systolic wall stress
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14
Q

What does venous tone determine and influence?

A
  • determines the capacity of venous circulation and the location of blood sequestration
  • Controls diastolic wall stress
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15
Q

4 factors that influence the supply of the heart tissue=

A
  1. total coronary blood flow
    1. aortic diastolic pressure - increases increases coronary blood flow
    2. duration of diastole - increase for increase flow
  2. Left ventricular end diastolic P
    1. ejection fraction
  3. pAO2
    1. hematocrit, saturation, etc. (anemia)
  4. Membrane diffusion
    1. vascular wall thickness
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16
Q

2 factors that affect the demand on the heart :

A
  1. Heart rate
  2. Intraventricular wall stress
    1. ​preload
    2. afterload
    3. contractility
    4. wall thickness
17
Q

all drugs used for angina pain help to decrease myocardial oxygen demand by:

A
  1. decrease HR
  2. decrease ventricular volume
  3. decrease BP
  4. decrease contractility
18
Q

How do nitrates and nitrites work and what is a side effect?

A
  • Venodilation > arterial dilation (increases venous capacitance)
    • decreases preload (demand component)
    • decreases pulmonary vascular resistance
    • decrease left ventricular end-diastolic pressure (supply component) - favors distribution of coronary blood flow to endocardium
  • MINIMAL CHANGE in coronary blood flow
  • REFLEX increase in heart rate & contractility - could actually increase the demand on the heart
19
Q

Nitroglycerin

  • MOA
  • Effects
  • Applications
  • Toxicity
  • Interactions
A
  • MOA: release NO in smooth muscle –> activates gCyclase –> increases cGMP –> dephosphorylates myosin –> relaxation
  • Effects
    • relaxation –> vasodilation –> decreased venous return & heart size
    • may increase coronary flow in some areas (but doesn’t change total, just redistributes)
  • Used for angina
    • sublingual = acute
    • oral = prophylaxis
  • Tox: hypotension, reflex tachycardia, headache
  • Interactions = phosphodiesterase type 5 inhibitors - Viagra, Cialis, Levitra
    • due to synergistic hypotension
20
Q

2 other forms of nitroglycerin

A
  1. Isosorbide dinitrate
    1. ​slighltly longer duration of action
  2. isosorbide mononitrate
    1. ​active metabolite of dinitrate
    2. used orally for prophylaxis
21
Q

Metbolism of calcium channel blockers

A
  1. high first pass effect
  2. high plasma protein binding
  3. extensive metabolism
22
Q

How do calcium channel blockers affect supply and demand?

A
  • blockade of calcium influx –> muscle relaxation since calcium is needed for contraction of smooth muscle
  • Demand
    • ​decrease heart rate
    • decrease contractility
  • Supply
    • increase coronary blood flow
    • decrease left ventricle EDP
      • could cause REFLEX increase in HEART RATE
23
Q

Verapamil, Diltiazem

  • MOA
  • Effects
  • Application
  • Tox
  • interactions
A
  • MOA
    • blocks L type Ca2+ channels in heart and vessels
  • Effects
    • reduced vascular resistance, heart rate, contractility
      • –> reduced o2 demand
  • Applications
    • prophylaxis of angina, hypertension, arrythmias
  • Tox - AV block, acute heart failure, constipation, edema
  • INT - cardiac depressants & hypotensive drugs
24
Q

Nifedipine

  • MOA
  • Effects
  • Clinical
  • Tox
  • INt
A
  • MOA - blocks vascular L type channels
  • eff - decreased contractility, HR –> reduced o2 demand
  • App - prophylaxis of angina + hypertension
  • Tox - excessive hypotension, baroreceptor reflex tachycardia
  • INt - all other vasodilators
25
Q

B-adrenoreceptor blockers effect on supply and demand

A
  • Demand
    • decrease HR
    • decrease contractility
  • Supply
    • decrease aortic diastolic pressure (BP)
  • overall lowers myocardial oxygen demand
    • useful for CLASSIC ANGINA
  • Reflex
    • INCREASE in left ventricular EDP (ejection fraction)
    • INCREASE in coronary artery resistance
    • DECREASE total coronary blood flow
26
Q

most commonly used B-blocker for angina

A
  • Propranolol
    • ​nonselective antagonist
    • decreases HR, CO, BP –> reduces demand
    • prophylaxis of anigna
    • tox = asthma, AV block, acute HF, sedation
  • Atenolol, Metoprolol
    • B1 selective
    • less risk of bronchospasm
27
Q

4 newer drugs for angina and how they work

A
  1. Targets Na/Ca exchanger to reduce intracellular calcium –> reduces contractility (Ranolazine)
  2. Targets metabolism of ischemic tissue (Trimetazidine)
  3. inhibits funny current Na+ channels to inhibit hyperpolarization and reduce rate (Ivabradine)
  4. inhibits Rho kinase an inhibitor of MLCP that prevents relaxation (Fasudil)
28
Q

How do nitrates alone affect each:

  • heart rate
  • arterial pressure
  • EDV
  • contractility
  • ejection time
A
  • heart rate - reflex increase
  • arterial pressure - decrease
  • EDV - decrease
  • contractility - reflex incease
  • ejection time - decrease through baroreceptor reflex
29
Q

How do beta blockers or calcium channel blockers affect:

  • heart rate
  • arterial pressure
  • EDV
  • contractility
  • ejection time
A
  • heart rate - DECREASE
  • arterial pressure - DECREASE
  • EDV - unwanted increase
  • contractility - DECREASE
  • ejection time - unwanted increase

CRRAB I (8 decks)

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