3-1: 9/6: Ischemic Heart Disease And Myocardial Infarction

Front 1

Myocardial cell relaxation requires _________.

Back 1

Oxygen (energy!)

Front 2

This vessel type makes up the major resistance to flow in the normal state.

Back 2

Small, distal arterioles

Front 3

Atherosclerosis affects this vessel type.

Back 3

Proximal, large epicardial arteries

Front 4

Resistance to blood flow increases when _________.

Back 4

Distal, small arterioles are unable to dilate to compensate for stenotic arteries

Front 5

What factors determine myocardial oxygen demand?

Back 5

Heart Rate (linear relationship)
Contractility
Wall Tension (due to increased pre/afterload)

Increases in all of these increase oxygen demand--more energy required!

Front 6

MVO2 AKA?

Back 6

Myocadial Oxygen Demand

Front 7

What factors determine coronary blood flow?

Define each factor.

Back 7

Coronary blood flow = Pressure/Resistance

Thus, depends on coronary perfusion pressure and coronary vascular resistance

Front 8

What factors determine O2 carrying capacity?

Back 8

O2 saturation of blood
Hemoglobin content of blood

Front 9

What factors determine myocardial oxygen supply?

Back 9

Coronary Blood Flow
O2 Carrying Capacity

Front 10

Most of coronary blood flow occurs in [diastole/systole] because ___________.

Back 10

Diastole

During systole, aortic valve opens up, less blood flow into coronary arteries. Mechanical contraction of LV makes it difficult for blood to flow into muscle of the heart.

Front 11

Formula for coronary perfusion pressure.

Back 11

Coronary perfusion pressure = Diastolic BP - LVEDP

Front 12

What is coronary vascular resistance and how is it regulated?

Back 12

Coronary Vasc Resistance = external compression with local regulation (local metabolites, endothelial factors, neural factors--esp symp NS)

Front 13

Describe the process of autoregulatory resistance.

Back 13

Myocardial muscle cell produces byproducts of aerobic metabolism (lactate, adenosine)

Vascular endothelial cell (arteriole) responds by signaling endothelial SM cels to contract or relax

Front 14

Oxygen vs Adenosine as autoregulators of consriction

Back 14

O2:
Vasoconstrictor; as O2 levels fall during ischemia; pre-capillary vasodilation and inc'd myocardial blood supply

Adenosine (byproduct of metabolism):
Vasodilator; mediator of coronary vascular tone, binds to vascular SM and prevents Ca2+ entry

Front 15

When is adenosine produced in the body?

What are its effects?

Back 15

During hypoxemia, aerobic metabolism in mitochondria is inhibited, ADP/AMP accumulates, and adenosine produced

Adenosine vasodilates arterioles and increases coronary blood flow

Front 16

What is coronary flow reserve?

How is it influenced by progressive stenosis?

Back 16

Arteriolar autoregulatory vasodilatory CAPACITY in response to increased oxygen demand

Stenosis in epicardial vessel-->decreased perfusion pressure-->arterioles dilate to maintain normal flow

As stenosis progresses, arteriolar dilation becomes chronic, decreasing potential to augment flow (thus decreasing coronary flow reserve)

Front 17

What does a Coronary Flow Reserve of 1 mean?

Back 17

Coronary Flow Reserve = Maximum Flow/Baseline Flow

If Max Flow = Baseline Flow, reserve is maxed out and any further decrease in perfusion pressure or increase in oxygen demand will result in ischemia

Front 18

A [hard/soft] atherosclerotic plaque is most vulnerable to hemorrhage.

Back 18

Soft

Front 19

Stable Angina:
Symptoms
Treatment (Pharmacologic and Surgical)

Back 19

Stable angina
Syx:
mid-substernal chest pain, pressure-like quality, closed fist (LEVINE'S SIGN)
Builds to peak, lasts 2-20 mins
Radiates to left arm, neck, jaw, back


Assoc w/SOB, sweating, nausea

RELIEVED BY REST

Tx:
Statins (HMG CoA Reductase Inhibitors)
ASA
Decrease Oxygen Demand (nitrates, beta-blockers, ca2+ channel blockers, ACE-inhibitors)

Sx Tx:
Mechanical dilation (angioplasty, stent)
CABG

Front 20

What is Levine's Sign? What is it indicative of?

Back 20

Levine's Sign = clenched fist; indicative of stable angina

Front 21

What are three types of acute coronary syndromes?

How would you tell them apart on EKG and bloodwork?

Back 21

Unstable Angina (ST depression, T wave inversion or normal; no enzyme release)

Non-ST elevation MI: ST depression, T wave inversion or normal, no Q waves; CPK, LDH, troponin release

ST-Elevation (transmural) MI:
ST elevation, Q waves present, CPK, LDH, troponin release

Front 22

Describe the pathophysiology of acute coronary syndrome.

Back 22

Plaque vulnerability and extrinsic triggers result in plaque rupture

Platelet adherence, aggregation, and activation of coagulation cascade with polymerization of fibrin

Thrombosis with sub-total or total coronary artery occlusion (if total, usually causing a STEMI)

Note: this is the pathophysiology for STEMI, non-STEMI, and Unstable Angina!!!

Front 23

Unstable angina/non-STEMI:
Symptoms
Treatment

Back 23

New onset angina

Inc in frequency, duration or severity

Decrease in exertion required to provoke

Onset at REST or awakening from sleep

Tx:
ASA
Heparin
Dec O2 demand with nitrates, beta-blockers, Ca channel blockers, ACE-inhibitors

Front 24

This receptor is required for all pathways leading to platelet activation/aggregation.

Back 24

GPIIb/IIIa receptor!

Front 25

What is the wavefront phenomenon?

Back 25

The finding that prolonged coronary artery occlusion results in the expansion of small subendocardial infarcts into a larger transmural MI (encompasses area supplied by occluded artery)

Front 26

In acute myocardial infarction:
Limited area of infarction will lead to __________
>20% LV infarction will lead to ________
>40% LV infarction will lead to ________

Back 26

Limited area of infarct-->homeostasis

>20%LV-->CHF

>40%LV-->hemodynamic collapse

Front 27

Acute MI:
Non-transmural vs Transmural

Back 27

Non-transmural:
Non-occlusive thrombus or spontaneous reperfusion
ST depression
Some enzymatic release (troponin i most sensitive)

Transmural:
Total, prolonged occlusion
ST elevation
Need thrombolytic tx or cath lab

Front 28

What are causes of troponin elevation?

Back 28

Any cause of prolonged (>15-20 mins) subendocardial ischemia:
Prolonged angina
Prolonged tachy in setting of CAD
CHF
Hypoxia

Front 29

What cardiac enzymes are elevated within a few hours following acute MI/

A day following MI?

2 days following MI?

Back 29

Early CPK-MB within few hours

CPK-MB peaks within a day

Cardiac troponin peaks 1.5-2 days later

Front 30

What effect does ischemia have on the autonomic nervous system?

Back 30

Stimulation of Symp NS with subsequent catechol release--increased heart rate, inc'd bp, inc'd O2 demand

Front 31

MI:
Treatment

Back 31

ASA, heparin, analgesia, O2

Reperfusion tx (stent, thrombolytic tx, thrombectomy)

Decrease O2 demand (nitrates, beta block, ACE-i)