Cardiopulm Cad

Front 1

CAD is a balance between ____ and _____.

Back 1

myocardial oxygen supply AND demand placed on the heart (workload).

Front 2

****Four components of supply and four components of demand****

Back 2

Supply =
1. Coronary artery patency
2. blood (volume, #RBC, O2, anemia)
3. cardiac mm pump fxn/shock (MI in ventricle, not pumping blood out well)
4. exercise/SNS

Demand =
1. drugs/metabolic condition (meds change demand)
2. HTN/LVH (LV hypertrophy, workload will be increased) (with HTN, LV has to do more work, afterload is higher-working against a greater afterload).
3. fever/SNS (being sick can change demand, raises metabolic rate)
4. excercise

Front 3

what is patency

Back 3

how much are they occluded, what is the diameter of the vessel. if its open = good supply

Front 4

prevalence of CAD

Back 4

deaths from CAD is more than all the cancers combined.
Leading killer of americans

Front 5

CAD define

Back 5

progressive, chronic dz process that is closely aligned with certain epidemiologically documented risk factors. where we have narrowing, supply doesnt meet the demands. it involves a steady buildup of atherosclerotic plaques in the coronary aa's leading to decreased myocardial blood flow

Front 6

CAD vs. CHD

Back 6

CAD- (coronary artery disease): presence of an obstruction that limits coronary blood flow but does not significantly limit heart muscle function. Synonym-Atherosclerotic Heart Disease (ASHD)

CHD- (coronary heart disease): an obstruction that causes permanent damage to heart muscle distally, decreasing heart muscle function.

difference: whether or not it has gotten bad enough to impact the heart

Front 7

***What happens when supply<demand (3 things)***

Back 7

Angina - chest pain (not everyone experiences chest pain. if they do it is a very describable pattern. symptoms will tell you what type of angina)

arrhythmias - tissue that is not getting enough oxygem. ischemic tissues causes arrythmias (how many PVC's per min. multifocal PVC's?)

myocardial infarction (heart attack) - tissue not enough oxyten, dies, get necorsis

Front 8

rules of fluid dynamics

Back 8

All fluids flow according to a pressure gradient
All fluids follow the path of least resistance
What If there is an obstruction?
fluid tends to follow another path, decreasing the volume of fluid crossing the obstruction
pressure driving the fluid distal to the obstruction is decreased.

Front 9

when does myocardial perfusion occur

Back 9

occurs primarily during diastole

normal person - diastole is longer. if the myocardium doesnt relax, it will decrease diastole

Front 10

myocardial perfusion

Back 10

assisted by collateral circulation. branches sprouted off arteries.

perfusion - blood is passing through, have an obstruction, have poor perfusion.

Front 11

what supplies the lateral wall of the LV?
what supplies the anterior wall of the LV and some of the interventricular septum?
What supplies the posterior wall of the LV

Back 11

L circumflex

LAD occlusion

R coronary artery

Front 12

What are the 4 determinants of myocardial blood flow

Back 12

1. Diastolic BP - drives blood into myocardial tissue
2. Vasomotor tone - regulates the diameter of the aa's
3. Resistance to blood flow - most commonly caused by atherosclerosis. can be reduced by collateralization (dehydrated = greater resistance, harder to pump).
4. LV End diastolic pressure - Pressure within the LV causes and occlusive force on the capillary beds of the mm closest to the pumping chamber, the endocardium

F (impact on blood flow) = DBP + VMT - R - LVEDP

Front 13

atherogenesis

Back 13

Development of fibrotic, fatty plaques in the walls of the arteries.

Can occur anywhere in the body
heart ---> myocardial infarction
brain ---> cerebral vascular accident
extremity ---> peripheral vascular disease

Front 14

3 layers of arteries

Back 14

adventitia - outer layer, contains collagenous elastic fibers and small blood vessels

Media - middle layer contains smooth muscle cells

tunica - inner layer, lined with endothelial cells which are supporsted by connective tissue (aka intima)

Front 15

***Process of atherosclerosis formation***

Back 15

1. Injury to endothelium --> inflammation --> scar tissue formation

2. Platelet aggregation - platelets release a substance called platelet derived growth factor (Responsible for cholesterol synthesis in smooth muscle and production of smooth muscle cells and migration of smooth muscle to the imtima) This is influenced by hyperlipidemia, smoking & glucose intolerance.

3. LDL proliferation - Increased LDL in muscle and increased number of smooth muscle cells, the lesion begins to grow in size. This is accelerated by hyperlipidemia & HTN

4. Calcium deposits = hardening of the artery. Ca2+ is deposited at the site of the lesion. This is the finished product--an atherosclerotic plaque.

Front 16

what can cause damage to the endothelial lining

Back 16

Cigarette smoke
HTN
Catecholamines
Genetics--weak spots in the arteries
Lipid accumulation
Bacterial toxin or virus

Front 17

components of an atheroma

Back 17

LDL
intrinsic vascular wall cells (endothelial and smooth muscle cells)
inflammatory cells (macrophages, T-lypmphocytes, mast cells)

Front 18

what is cholesterol

Back 18

1. An essential compound – keeps integrity to the cell wall
2. transporter of fatty acids
3. Most circulating cholesterol is LDL (delivers lipids to tissue, “The Bad” cholesterol)
4. HDL “the scavenger” (transports lipids from tissue to liver)

Front 19

what is the role of HDL

Back 19

"Good" Cholesterol

Protects Against the Formation of Plaques

removes cholesterol from smooth muscle in arterial walls.

blocks the effects of LDL’s on sm. muscle cells, i.e., proliferation, increased collagen formation.

Front 20

***what is prinzmetal's angina***

Back 20

Associated with ST elevation

Occurs at rest (typically in early morning)

Not associated with a preceding increase in myocardial demand

Relieved with nitroglycerin or other vasodilators
that Encourage the smooth muscle to relax.

Front 21

what is the mechanism of vasospasm

Back 21

Intimal smooth muscles proliferate in the intima of ASHD affected arteries, which makes the arteries more prone to spasm.

In normal arteries, a substance known as Endothelial Derived Relief Factor causes arterial smooth muscles to relax.

When the endothelium of the coronary artery is damaged (as in CAD), the intimal smooth muscle contracts instead of relaxes when stimulated by acetylcholine, which normally causes release of EDRF.

Front 22

***risk factors CAD - which are modifiable(7) and nonmodifiable (3)***

Back 22

HTN
Smoking
Hyperlipidemia
Obesity
Diabetes
Sedentary Lifestyle
Psychological fators
Family History *
Age *
Sex *

* = unalterable risk factors

Front 23

how does family Hx influence CAD

Back 23

A person with a close male relative (Father or Grandfather) who dies from an MI before age 60 has a 3-6X greater risk for developing CAD.

Risk increases with family history of hypercholesterolemia (50% die before age 60).

There is some genetic link toward HTN, diabetes & obesity, but many of these risk factor patterns are learned (eating habits, stress, exercise).

New study from Framingham Study (follow-up) indicates that presence of sibling CAD is an even stronger predictor than father or grandpa.

Front 24

how does gender influence CAD

Back 24

Premenopausal women have less risk than men.

Development of CAD is delayed 10 years in women compared to men. Incidence levels after menopause

Estrogen is thought to have a cardioprotective effect--
Reduces total cholesterol
Reduces LDL
Increases HDL
Lowers levels of lipoprotein a

HRT increases risk for CAD

Front 25

how does age influence CAD

Back 25

As we get better at battling the infectious diseases that used to kill so many people, chances are now that if you live longer, you will die from CAD.

Front 26

how does hyperlipidemia influence CAD

Back 26

2/3 of dietary fat is transported to the liver to form VLDL & LDL.

Key indicators:
Total Chol: HDL --> 4.5*... Triglycerides> 150mg/dl.... HDL <35

2002 AHA Recommendations
LDL < 160 - 130 if >2 RF present
TG < 150
HDL > 40-50

Front 27

how does cholesterol influence CAD

Back 27

Total cholesterol < 200 mg/dL desirable
Total cholesterol 200-239 mg/dL borderline
Total cholesterol > 240 mg/dL High

HDL > 45 mg/dL men > 55 mg/dL women desirable

LDL <130* mg/dL desirable

Front 28

how do we manage Hyperlipidemia

Back 28

Aim at decreasing LDL, increasing HDL

Endurance training: (Increases HDL LCAT, Decreases LDL, TG)
Diet: (Reduce saturated fat, Increase fiber, fish, garlic, alcohol)

Front 29

role of HTN in atherogenesis

Back 29

indirectly involved in damage to the endothelium

pressure forces infiltration of lipids into intimal cells

Effect on myocardial VO2:
increases afterload on the heart--this causes LVH, which increases myocardial VO2. When combined with atherosclerosis, LVH increases risk for ischemia.

Effect on myocardial efficiency: chronic afterload causes myofibril disorganization, and aggregation/swelling of mitochondria. Efficiency is decreased.

HTN with exercise as an indicator for CAD
Sieps et al: 83% of subjects that demonstrated an increase in DBP with exercise had significant CAD.

Front 30

management of HTN

Back 30

Lifestyle: (maintain/reach ideal body weight, decrease dietary fat and sodium, increase fiber, don't smoke/quit, increase activity, decrease stress producing behaviors)

Medication

Goal:<140/90; 130/85 if renal insufficiency or CHF present; <130/80 if DM present

Front 31

role of smoking on atherogenesis

Back 31

decreases HDL
Increases Platelet Aggregation/fibrinogen levels
Alters estrogen metabolism
Increases BP
Mobilizes FFAs

Direct cardiac effect--may be involved in the development. of fatal cardiac arrhythmias by decreasing the V. Fib threshold. May cause coronary vasospasm.

Risk for MI:
2-4x higher for heavy smokers (> 20 cigarettes/day)
may be as high as 5-21x higher for those that smoke >25 cigarettes/day
Risk no different with low tar/nicotine cigarettes

Front 32

management for smoking

Back 32

Risk begins to decline within months after quitting
After 2-3 years, risk decreases to approximately the levels found in those that have never smoked, regardless of the amount smoked, duration of the habit, or the age at cessation.

Avoid exposure to 2nd hand smoke

Front 33

define obesity

Back 33

having a very high amount of body fat in relation to lean body mass, or body mass index of 30 or higher

Front 34

what is BMI

Back 34

provides comparative weight for height information that is significantly correlated with total body fat

Front 35

effects of exercise no CAD

Back 35

Atherogenesis-- exercising monkeys fed an atherogenic diet had substantially reduced overall atherosclerotic involvement, lesion size and collagen accumulation than did sedentary controls.

Exercising monkeys had larger hearts and wider coronary arteries which decreased luminal narrowing.

increased myocardial efficiency
Improved metabolic capacity
Increased thyroid function/ increased metabolism
Coronary collateral circulation
increased fibrinolytic capacity
increased tolerance to stress ( BP, SNS)
increased HDL & LCAT, decreased LDL & TG
decreased DM/obesity
decreased platelet stickiness

Front 36

how much exercise is necessary for CAD

Back 36

aerobic exercise
3-5x/wk
60-90% max HR reserve (HRmax - HR rest) + HR rest OR 50-85% VO2 max
15-60 mins (continuous or cumulative)
at least 30 mins of moderate intensity exercise on most if not all days of the week

Front 37

role of atherogenesis in diabetes

Back 37

often associated with hyperlipidemia (31% people with DM also have increased lipids.
In obese people with hyperlipidemia, 75% have high TG's, 25% high chol, 50% both. Glucose intolerance is associated with increased tendency for platelet aggregation.
Management--exercise, dietary and pharmaceutical.
Aim for BG: <110, HgbA1c <7%

Front 38

role of alcohol and heart disease

Back 38

1-2 drinks/day has been demonstrated to reduce risk for CAD by 30-50%
1 drink = 12-ounce bottle of beer, a 4-ounce glass of wine, or a 1 1/2-ounce shot of 80-proof spirits

Front 39

Plasma homocysteine levels

Back 39

The effect of increased plasma levels of homocysteine and related molecules such as homocystine and homocysteine thiolactone are associated with accelerated atherosclerosis.
The magnitude of the plasma elevation is positively correlated with the severity of the atherosclerosis.
Markedly elevated levels resulting from documented mutations of relevant genes are rare, but mild elevations occur in 7% of the general population.
The mechanism responsible for the accelerated vascular damage is unsettled, but homocysteine is a significant source of H2O2 and other reactive forms of oxygen, and this may accelerate the oxidation of LDL.