Nordgren: Anti-anginal drug theory

Question 1

What causes angina pectoris?

Answer 1

Myocardial ischemia>
metabolites accumulate>
chest pain

Question 2

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

Answer 2

Squeezing
pressure
heaviness
tightness
pain in the chest

SYMPTOM

Question 3

What is the most common cause of angina?

Answer 3

Atheromatous obstruction of large coronary vessels (CAD)

Question 4

What is the primary cause of angina pectoris?

Answer 4

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

Question 5

What is classic angina?

Answer 5

EFFORT angina

Inadequate blood flow in the presence of CAD

Question 6

What is Prinzmetal Angina?

Answer 6

VASOSPASTIC or variant angina

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

Can cause MI and pain.

Question 7

What is prinzmetal angina often nocturnal?

Answer 7

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

Question 8

What type of angina is often associated with exercise?

Answer 8

Classic

Question 9

What happens to coronary flow reserve in classic angina?

Answer 9

It’s IMPAIRED.

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

Question 10

What happens to blood flow in varian angina?

Answer 10

O2 delivery DECREASES d/t reversible coronary vasospasm

Question 11

Unstable angina is also known as…

Answer 11

Acute Coronary Syndrome

Question 12

What is unstable angina?

Answer 12

1. Episodes of angina occur at REST

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

Question 13

What causes unstable angina?

Answer 13

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

Question 14

Is unstable angina considered a medical emergency?

Answer 14

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

Question 15

What is the theory behind treating angina?

Answer 15

You want to INCREASE supply and DECREASE demand.

Question 16

How do you decrease demand in classical angina?

Answer 16

1. decrease cardiac WORK

2. Shift myocardial metabolism

Question 17

How do you increase supply in variant angina?

Answer 17

1. Reverse SPASM

2. Treat the atherosclerosis

Question 18

How do you treat unstable angina?

Answer 18

BOTH
1. Supply: reverse spasm, treat athero

2. Demand: decrease cardiac work, shift myocardial metabolism

Question 19

What are determinants of myocardial O2 demand?

Answer 19

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

Question 20

What is ventricular wall stress?

Answer 20

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

Energy has to be expended to OPPOSE the force.

Question 21

What is the formula for ventricular wall stress?

Answer 21

σ = (P x r) / 2h

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

Question 22

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

Answer 22

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

Question 23

How happens to wall stress in a hypertrophied heart?

Answer 23

LOWER wall stress and O2 consumption/g of tissue

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

Question 24

How does HR relate to O2 requirements?

Answer 24

Increased heart rate>
INCREASE in O2 demand

• more contractions per min
• more ATP consumed per minute

Question 25

What is contractility?

Answer 25

A measure of the force of contraction

Question 26

How does contractility relate to O2 demand?

Answer 26

A greater force requires GREATER O2 consumption.

Question 27

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

Answer 27

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

Question 28

What happens to flow during systole?

Answer 28

Drops to near zero

Question 29

What is the limiting factor for perfusion during tachycardia?

Answer 29

Duration of diastole

Question 30

What determines coronary vascular resistance?

Answer 30

Metabolic products, autonomic activity | 2. DAMAGE to endothelium alters ability to dilate and INCREASES resistance

Question 31

What are determinants of vascular tone?

Answer 31

Peripheral arteriolar and venous tone contribute to myocardial wall stress

Question 32

What determines systolic wall stress?

Answer 32

Arteriolar tone directly controls peripheral vascular resistance and arterial BP

Question 33

What determines diastolic wall stress?

Answer 33

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

Question 34

What determines O2 consumption in terms of demand?

Answer 34

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

Question 35

What determines O2 consumption on the supply side?

Answer 35

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)

Question 36

What drugs are used as antianginals?

Answer 36

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