Acute coronary syndrome -MI Flashcards
Abouthalf of Americans(49%) have at least one of these three risk factors for ACS
HTN
hyperlipidemia
smoking
symptoms of MI
Chest pain Shortness of Breath Diaphoresis Nausea / Vomiting Fatigue Anginal Equivalents Fear and AnxietyIndigestion, heartburn Dyspnea, weakness, anxiety Feeling of doom Syncope Decreased LOC
MI (d)
Occurs with myocardial tissue is abruptly and severely deprived of oxygen
ACS –Myocardial Infarction can result from
a total occlusion (STEMI)
a partial occlusion leading to ischemia and cellular oxygen debt.
the lack of oxygen associated with ACS / MI leads to:
anaerobic metabolism and lactic acid accumulation → severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
Angina Pectoralis (Pain)
Described as heaviness, constriction, tightness, burning, pressure, or crushing
Common locations: substernal, retrosternal, or epigastric areas; pain may radiate
ACS / MI –CM
Sympathetic nervous system is stimulated due to circulating catecholamines resulting in
Release of glycogen (elevated blood sugar)
Diaphoresis
Vasoconstriction of peripheral blood vessels
Skin: ashen, clammy, and/or cool to touch
ACS / MI –CMCardiovascular – responds due to catecholamines and increased work load
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
CM- large list of ACS / MI
Angina SNS stimulation Cardiovascular response N/V Fever Atypical variants
Total occlusion
STEMI
partial occlusion
non stemi- ischemia and cellular oxygen debt
Myocardial infarction (d) occurs when?
occurs when myocardial tissue is abruptly and severely deprived of oxygen
SNS is stimulated in ACS / MI due to circulating catecholamines and _____
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
Why is N/V caused during ACS / MI?
Can result from vasovagal reflex stimulation of the vomiting center by the severe pain
Epigastric pain
Why is Fever caused during ACS / MI?
Systemic manifestation of the inflammatory process caused by cell death
Atypical variants of ACS / Mi are more common in who?
what are they?
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
Signs of MI
ECG changes Dysrhythmia Syncope Pallor, cyanosis, coolness of extremities Diaphoresis
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?
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
What is the most common cause of CAD
Atherosclerosis
Atherosclerosis (d)
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
Development of Atherosclerosis:
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.
Atheroma (d)
advanced fibrous lesion in the development of atherosclerosis
The core (middle) of these atheroma lesions contains:
lipid filled macrophages,
dead or dying cells,
cellular debris,
extracellular lipid
in more advanced stages calcification.
Protein Synthesis of Lesion
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,
