CAD Pathology Flashcards
Chronic Endothelial Injury
-HTN
-Tobacco use
-Hyperlipidemia
-Diabete
-Infection
_Toxins
How many % of occlusion shows signs of ischemia with exertion
75%
How many % of occlusion shows signs of ischemia at rest
90%
Collateral Circulation
Additional arterial connections found around areas of increasing occlusion
Body response to chronic, long-standing ischemia
When arterial occlusion is rapid there is no time for collateral circulation
When does atherosclerosis begin to cause symptoms
75% at exertion and 90% at rest
What are foam cells?
Cells with accumulated lipids
How do lipids enter the intima adventitia?
The lipids ruptures endothelium to enter the tubule
What are the three manifestations of cardiac chest pain?
Diastolic and systolic dysfunction
Electrical disturbances
Angina pectoris
Diastolic and systolic dysfunction
Failure of heart to relax and fill properly
Results in SOB
Electrical disturbances
ECG changes (ST depression)
Angina Pectoris
Chest squeeze
Result from ischemia
Silent ischemia
Ischemia that does not cause angina
Atypical symptoms for Angina
Indigestion, aching jaw, fatigue, SOB, dizziness, generalized anxiety, weakness, flu-like symptoms (Often experienced by Women, Older adults)
Adults over 80 may experience disorientation or confusion
Chronic stable Angina
Prolonged exertion
Pattern predictable
Frequency, duration and intensity constant
only slight limitation of activity
Associated with a stable plaque
Chronic stable Angina duration
3-5 minutes
can be managed with nitrates
Vasospastic Angina
Angina due to vasospasm
Triggers for vasospastic angina
Triggers include cocaine, meds (migraine, chmo), mg deficiency, allergic reaction
Treatment for vasospastic angina
Treat with nitrate and calcium channel blockers
Acute Coronary Syndrome
Myocardial ischemia and not immediately reversible
Associated with unstable plaque which ruptures
How many % is occluded with Acute coronary syndrome
90% so patient with ACS need immediate hospitalization
Acute Coronary Syndrome: Unstable Angina (USA)
Chest pain that is new, occurs at rest, or is worsening, usually 15-20 minutes and pattern changes
often not responsive to rest or medication
Rupture of stable atherosclerotic plaque and partial occlusion by thrombus
Acute Coronary Syndrome: Myocardial Infarction
Plaque rupture and thrombus formationNecrosis begins on the endocardial surface (inside) and progresses to the pericardial surface (outside)
How long can cardiac cell tolerate ischemia for until cell death begin
20 minutes before cell death begins
STEMI vs NSTEMI
STEMI - full thickness infarction of ventricle
NSTEMI -partial thickness infarction ventricle
Myocardial Infarction Clinical Manifestations
Chest pain
Dyspnea
Atypical symptoms: weakness, fatigue, anxious, dizziness
Skin: ashes, cool, and diaphoretic
CVS: increase HR BP but with decrease CO, BP decrease
Increase RR
Fever up to 38 degrees and last for a week
Inflammation caused by myocardial cell death
Serum Cardiac Enzymes
Troponin
CK-MB: stays elevated for 6 days after MI
Myoglobin
The Healing Process of MI
Neutrophils and macrophages remove all necrotic tissue
Collateral circulation limit area of injury
6 weeks after, scar tissue has replaced necrotic tissue
Complications of MI
Arrythmias
Pericarditis
HF
Valve disorder
Arrthymias
Most common complication
irregular heart rhythms
life threatening rhythms can occur
HF
Loss of pump
Mild dyspnea, restlessness, agitation, tachycardia, pulmonary congestion
Pericarditis
Inflammation can spread to pericardium and exudate fill pericardial cavity
Cause friction rub over pericardium
Valve disorder
Damage to the muscle can cause AV valve disorder
