CAD, Angina, And Acute Coronary Syndromes Flashcards
Factors affecting stroke volume
Preload, after load, contractility
CO
HR x SV
Preload
Volume and pressure inside ventricle at end of diastole
Determined by amount of venous blood returning to ventricle during diastole and amount left in ventricle after systole
After load
Resistance to ejection of blood from L ventricle
Affected by systemic vascular resistance
Contractility
Degree of myocardial fiber shortening
Affected by preload, myocardial O2 supply, inotropic stimuli
Arteriosclerosis
Thickening and hardening of the vessel wall
Atherosclerosis
Accumulation of lipid-laden macrophages within the arterial wall
Lesions progress from endothelial injury and dysfunction to fibrotic plaque
Desired lipid values
Cholesterol <200
LDL 100-129
Triglycerides <150
HDL > 40-60
LDL
Cholesterol and protein
Delivers cholesterol to tissues
Contributes to inflammatory and immune response
HDL
Phospholipids and protein
Reverse cholesterol transport brings to liver for bile elimination
Participated in endothelial repair and decreases thrombosis
Cholesterol
Used for bile acids and steroids
Obtained from foods
Some made by body cells
VLDL
Triglycerides
Myocardial Ischemia
Coronary arteries dilate with inc O2 demand
Coronary blood flow or oxygen content cannot meet the metabolic demands of myocardial cells
Factors for meeting cellular demands:
1. Amount of coronary perfusion
2. Myocardial workload
- heart rate
- preload
- after load
- contractility
Stable angina pectoris
Vessels cant dilate; generally predictable in frequency, intensity, and duration; elicited by similar stimuli each time and usually relieved by nitro and rest
S/S: discomfort heaviness, pressure, crushing on chest, may radiate down left shoulder or arm, or up to jaw, pallor, cyanosis, dyspnea, diaphoresis, tachycardia, high BP
ECG: ST depression, T wave inversion, ST elevation (STEMI)
Unstable angina
Transient/reversible ischemia due to unstable plaque occluding vessel x 10-20 minutes
ECG: ST depression or T wave inversion
Treat same as NSTEMI
Myocardial Infarction
Thrombus occludes vessel for prolonged period of time
Categorized as NSTEMI or STEMI
Can lead to heart attack
Necrosis of heart leads to troponin release
Can lead to Dec contractility, SV, CO and dysrythmias and cardiogenic shock
NSTEMI
ST depression or T wave inversion
Damages partial thickness of myocardium
STEMI
ST elevation
Damage to complete thickness of myocardium
Cardiogenic shock
Life threatening emergency
Occurs if left ventricular myocardium is severely damaged
Decreased perfusion to brain, kidney and all organs
S/S: confusion, LOC, rapid HR, SOB, pale, weak pulse, Dec urine output, cool hands and feet
Myocardial stunning
Temporary loss of contractile function that persists for hours to days after restoration of perfusion
Hibernating myocardium
Tissue that is persistently ischemic and undergoes metabolic adaptation to pro-long myocyte survival until perfusion can be restored
Myocardial remodeling
Myocyte hypertrophy and loss of contractility in the areas of the heart distant from the site of infarction
MI treatment
M- Morphine
O- O2
N- Nitrite
A- Aspirin
B- Beta blockers
