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CRAAB 5 > Nordgren: Anti-anginal drug theory > Flashcards

Nordgren: Anti-anginal drug theory Flashcards

1
Q

What causes angina pectoris?

A

Myocardial ischemia>
metabolites accumulate>
chest pain

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2
Q

How is angina pectoris often described? Is it a disease or a symptom?

A 
Squeezing
pressure
heaviness
tightness
pain in the chest

SYMPTOM

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3
Q

What is the most common cause of angina?

A

Atheromatous obstruction of large coronary vessels (CAD)

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4
Q

What is the primary cause of angina pectoris?

A

O2 supplied by the coronary vessels doesn’t meet O2 demand of the heart

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5
Q

What is classic angina?

A

EFFORT angina

Inadequate blood flow in the presence of CAD

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6
Q

What is Prinzmetal Angina?

A

VASOSPASTIC or variant angina

TRANSIENT SPASM of a localized portion of vessel. D/t underlying ATHEROMAS.

Can cause MI and pain.

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7
Q

What is prinzmetal angina often nocturnal?

A

Recumbent increase in venous return triggers neurogenic alpha adrenergic coronary vasospasm.

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8
Q

What type of angina is often associated with exercise?

A

Classic

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9
Q

What happens to coronary flow reserve in classic angina?

A

It’s IMPAIRED.

Endothelial dysfunction>
impaired vasodilation>
ischemia at LOW levels of demand

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10
Q

What happens to blood flow in varian angina?

A

O2 delivery DECREASES d/t reversible coronary vasospasm

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11
Q

Unstable angina is also known as…

A

Acute Coronary Syndrome

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12
Q

What is unstable angina?

A
  1. Episodes of angina occur at REST

2. Increased severity, frequency, duration of chest pain in pts w/ previously STABLE angina

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13
Q

What causes unstable angina?

A

OCCLUSIVE THROMBI>
increased epidcardial coronary artery resistance>
platelets clot in vicinity of atherosclerotic plaque>
reduced blood flow

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14
Q

Is unstable angina considered a medical emergency?

A

YA–it’s associated w/ high risk of MI and death.

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15
Q

What is the theory behind treating angina?

A

You want to INCREASE supply and DECREASE demand.

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16
Q

How do you decrease demand in classical angina?

A
  1. decrease cardiac WORK

2. Shift myocardial metabolism

17
Q

How do you increase supply in variant angina?

A
  1. Reverse SPASM

2. Treat the atherosclerosis

18
Q

How do you treat unstable angina?

A

BOTH
1. Supply: reverse spasm, treat athero

  1. Demand: decrease cardiac work, shift myocardial metabolism
19
Q

What are determinants of myocardial O2 demand?

A
  1. ventricular wall stress
  2. HR
  3. Contractility
  4. Basal Metabolism
20
Q

What is ventricular wall stress?

A

TANGIBLE FORCE that acts on myocardial fibers and PULLS them apart.

Energy has to be expended to OPPOSE the force.

21
Q

What is the formula for ventricular wall stress?

A

σ = (P x r) / 2h

σ= VWS
P= intraventricular pressure (preload and afterolad)
r= radius of the ventricle
h= ventricular wall thickness
22
Q

What conditions increase PRESSURE in the LV and with that increase WALL STRESS and MYO O2 consumption?

A
  1. Aortic stenosis
  2. Hypertension
  3. Augmenting LV filling (increase radius)
23
Q

How happens to wall stress in a hypertrophied heart?

A

LOWER wall stress and O2 consumption/g of tissue

  1. If it develops chronic pressure overload, serves as a compensatory role in reducing O2
24
Q

How does HR relate to O2 requirements?

A

Increased heart rate>
INCREASE in O2 demand

  • more contractions per min
  • more ATP consumed per minute
25
Q

What is contractility?

A

A measure of the force of contraction

26
Q

How does contractility relate to O2 demand?

A

A greater force requires GREATER O2 consumption.

27
Q

What are the determinants of coronary blood flow and myocardial O2 supply?

A
  1. Coronary flow = perfusion pressure (aortic diastolic pressure) and DURATION of diastole
  2. Coronary flow- inversely proportional to coronary vascular resistance.
28
Q

What happens to flow during systole?

A

Drops to near zero

29
Q

What is the limiting factor for perfusion during tachycardia?

A

Duration of diastole

30
Q

What determines coronary vascular resistance?

A

Metabolic products, autonomic activity

2. DAMAGE to endothelium alters ability to dilate and INCREASES resistance

31
Q

What are determinants of vascular tone?

A

Peripheral arteriolar and venous tone contribute to myocardial wall stress

32
Q

What determines systolic wall stress?

A

Arteriolar tone directly controls peripheral vascular resistance and arterial BP

33
Q

What determines diastolic wall stress?

A

Venous tone determines the capacity of the venous circulation and location of blood sequestration

34
Q

What determines O2 consumption in terms of demand?

A
  1. HR

2. Intraventricular wall stress (preload, afterload, contractility, wall thickness)

35
Q

What determines O2 consumption on the supply side?

A
  1. Total coronary blood flow (aortic diastolic P, duration of diastole)
  2. Left ventricular end diastolic P (ejection fraction)
  3. pAO2 (hematocrit, saturation, anemia)
  4. Membrane diffusion (vascular wall thickness)
36
Q

What drugs are used as antianginals?

A
  1. organic nitrates
  2. Ca channel blockers
  3. beta adrenoceptor antagonists (blockers)

CRAAB 5 (9 decks)

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