Acute coronary syndrome -MI

Question 1

Abouthalf of Americans(49%) have at least one of these three risk factors for ACS

Answer 1

HTN
hyperlipidemia
smoking

Question 2

symptoms of MI

Answer 2

Chest pain
Shortness of Breath
Diaphoresis
Nausea / Vomiting
Fatigue
Anginal Equivalents
Fear and AnxietyIndigestion, heartburn
Dyspnea, weakness, anxiety
Feeling of doom
Syncope 
Decreased LOC

Question 3

MI (d)

Answer 3

Occurs with myocardial tissue is abruptly and severely deprived of oxygen

Question 4

ACS
 –Myocardial Infarction can result from

Answer 4

a total occlusion (STEMI)

a partial occlusion leading to ischemia and cellular oxygen debt.

Question 5

the lack of oxygen associated with ACS / MI leads to:

Answer 5

anaerobic metabolism and lactic acid accumulation → severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration

Question 6

Angina Pectoralis (Pain)

Answer 6

Described as heaviness, constriction, tightness, burning, pressure, or crushing
Common locations: substernal, retrosternal, or epigastric areas; pain may radiate

Question 7

ACS / MI –CM

Sympathetic nervous system is stimulated due to circulating catecholamines resulting in

Answer 7

Release of glycogen (elevated blood sugar)
Diaphoresis
Vasoconstriction of peripheral blood vessels
Skin: ashen, clammy, and/or cool to touch

Question 8

ACS / MI –CMCardiovascular – responds due to catecholamines and increased work load

Answer 8

Initially, ↑ HR and BP,

then ↓ BP (secondary to ↓ in CO)

Irregular heart rhythm

Crackles, wheezes (left sided heart failure)

Jugular venous distention (rt sided heart failure)

Abnormal heart sounds
S3 or S 4

New murmur or Pericardial friction rub

Question 9

CM- large list of ACS / MI

Answer 9

Angina
SNS stimulation
Cardiovascular response
N/V
Fever
Atypical variants

Question 10

Total occlusion

Answer 10

STEMI

Question 11

partial occlusion

Answer 11

non stemi- ischemia and cellular oxygen debt

Question 12

Myocardial infarction (d) occurs when?

Answer 12

occurs when myocardial tissue is abruptly and severely deprived of oxygen

Question 13

SNS is stimulated in ACS / MI due to circulating catecholamines and _____

Answer 13

increased work load.

resulting in:Release of glycogen (elevated blood sugar)
Diaphoresis
Vasoconstriction of peripheral blood vessels
Skin: ashen, clammy, and/or cool to touch

Question 14

Why is N/V caused during ACS / MI?

Answer 14

Can result from vasovagal reflex stimulation of the vomiting center by the severe pain

Epigastric pain

Question 15

Why is Fever caused during ACS / MI?

Answer 15

Systemic manifestation of the inflammatory process caused by cell death

Question 16

Atypical variants of ACS / Mi are more common in who?

what are they?

Answer 16

Not all patients have the classic symptoms of an MI

Women may experience
Atypical discomfort
Shortness of breath
Fatigue
May present with vague symptoms and ECG changes 

Elderly 
Shortness of breath
Pulmonary edema
Dizziness
Altered mental status
Dysrhythmias
Syncope

Question 17

Signs of MI

Answer 17

ECG changes
Dysrhythmia
Syncope
Pallor, cyanosis, coolness of extremities
Diaphoresis

Question 18

Unstable Angina

is a CM of ACS: what is unstable angina?

How long does UA take to cause irreversible myocardial cell death (necrosis)

Necrosis of entire thickness takes how long?

Answer 18

New in onset

Occurs at rest

Has a worsening pattern

unpredictable

medical emergency.

Ischemia is currently happening

Result of sustained ischemia
(>20 minutes), causing irreversible myocardial cell death (necrosis)

Necrosis of entire thickness of myocardium takes 4 to 6 hours

Question 19

What is the most common cause of CAD

Answer 19

Atherosclerosis

Question 20

Atherosclerosis (d)

Answer 20

Complex process that results in narrowing of the lumen of the coronary arteries. (Fuel supply to the heart)

Causes a limitation of blood flow to the myocardium
Oxygen supply and demand mismatch

Question 21

Development of Atherosclerosis:

Answer 21

endothelial injury

inflammatory process started

Macrophages accumulate

More endothelial damage (from macrophages and other inflammatory mediators)

Oxygen free radicals oxidize the Low Density Lipoproteins.

Macrophages engulf the oxidized LDL and foam cells are formed.

Foam cells accumulate and form fatty streaks,

Macrophages stimulate the growth of smooth muscle cells

The combination of the foam cell accumulation, smooth muscle proliferation and collagen results in the development of fibrofatty lesions

Ultimately these can become complicated lesions called fibrous plaques

The fibrous plaques narrow the lumen of the arteries
Advanced fibrous lesion called atheroma are covered by a fibrous cap.

Question 22

Atheroma (d)

Answer 22

advanced fibrous lesion in the development of atherosclerosis

Question 23

The core (middle) of these atheroma lesions contains:

Answer 23

lipid filled macrophages,

dead or dying cells,

cellular debris,

extracellular lipid

in more advanced stages calcification.

Question 24

Protein Synthesis of Lesion

Answer 24

Cells within the core secrete proteins into the sub-endothelial space that stimulate thrombin and fibrin production, both of which contribute to development of clot formation,

Question 25

Plaque rupture occurs when strain is placed on the fibrous cap.

Characteristics of plaque likely to rupture:

Answer 25

Large soft lipid core

High macrophage count

Relatively few smooth muscle cells

A thin fibrous cap

Question 26

ACS results in response to plaque rupture causing limitation of blood flow to the myocardium

Answer 26

Ischemia
Acute coronary syndrome (ACS) develops if ischemia is prolonged or not immediately reversed. (Necrosis of myocardial tissue)

Question 27

ACS encompasses:

Answer 27

1. Unstable angina (UA) also known as Non ST segment elevation acute coronary syndrome (NSTE-ACS)
2. Non–ST-segment-elevation myocardial infarction (NSTEMI)
3. ST-segment-elevation (STEMI)