Coronary Artery Disease Flashcards
Cardiac output
Cardiac output = Amount of blood pumped out of the heart per minute
= HR x SV
= 3-6 L/min
Factors
- Cardiac contractility
- HR (SNS)
- Preload
- Afterload
- Blood volume
Preload
Preload/stretch - volume of blood in ventricles at end of diastole
- Left ventricular end diasoltic volume - LVED
Includes frank-sterling mechanism = recall it has limits
Increases in hypovolemia, regurgitation, HF
Afterload
Afterload/Squeeze - resistance left ventricles must overcome to eject and circulate blood
Increases in HTN, vasoconstriction
High afterload increases cardiac workload
Electrical properties
Regulate HR/rhythm
Excitability, conductivity, contractility, refractiorness
Dysrhythmias can occur if heart muscle cells die, which is life threatening
SA node is pacemaker
Coronary circualtion
1) Right coronary artery (RCA)
- Supplies RA, RV, part of LV, SA/AV/Bundle of his
- Blockage = RV failure, bradycardia
2) Left anterior descending (LAD)
- Supplies LV, heart valves
- Blockage - LV failure, dysrhythmia
3) Circumflex
- Supplies - LA, LV, SA
- Blockage - LV failure, dysrhythmia
Collateral circulation
- Arterial connections in areas o focclusion when chronic ischemia occurs
- Not enough time to create it is rapid tho
Factors = genetics, chronic ischemia
Coronary artery disease
Most common heart disease, usually due to atherosclerosis
Atherosclerosis - formation of fatty, fibrous plaque
Risk factors
- Age
- Male
- FmHx
- Elevated serum lipid
- HTN above 140/90
- Tobacco
- Sedentary
- Obesity
- DM
- Homocysteine
= Framingham risk factor can help predict risk of IM in next 10 yrs
Stages of artherosclerosis
1) Endothelium damage
- Triggered by HTN, Tobacco, hyperlipidema, diabetes, homocysteinemia, viruses/toxins
2) Fatty streaks
- LDL initiate inflammation, macrophages ingest LDL and die, becoming foam cells that create fatty streak
3) Fibrous plaque
- Platelets and LDL release growth fraction that thick arterial wall
- Collagen and elastin create cap over the fatty streak
= Harden and stiffen
4) Complicated lesions
- As fibrous cap grows, it damages artery
- Can break off and become a embolism
Clinicals manifestations of CAD
1) Stable angina pectoris
- Cardiac pain from ischemia
- Can b esilent ischemia in diabetic
- Atypical = referred such as indigestion, jaw pain, fatigue, SOB, dizzy (common in women and older adults)
- 75% occlusion, stable plaque with 3-5 minute duration
- Meds help
2) Vasospastic angina
- Aka prinzmetal/variant
- Rare from vasospasm of coronary artery
- Triggered by cocaine, eds, magnesium deficiency, allergy
Ischemia clinical manifestations
1) Angina pectoris
2) Diastolic and systolic dysfunction - SOB
3) ECG changes = ST depression
Acute coronary syndrome (ACS)
Prolonged ischemia - require immediate hospitalization
1) Unstable angina
- 90% occlusion
- Worst chest pain, unpredictable pattern for 15-20 min
- Not elevated by meds
2) Non-ST segment elevation/NSTEMI MI
- Fully occluded, with partial thickness damage
- ST depression, T inversion
3) ST segment elevation/STEMI MI
- Full thickness
- ST elevation
-> cardiac cells can tolerate 20 min of ischemia before death
Myocardial infarction - clinical manifestation
- Chest pain - usually in the morning for longer than 20 minutes, radiate to left arm etc
- Dyspnea
- Atypical = weakness, fatigue, anxious, dizzy
- Older pt - sudden delirium, atypical
- Skin - ashen, cool, diaphoretic (SNS)
- CVS - Tacky/hypertension then hypotension with loss of CO
- Resp - dyspnea, RR, crackles
- GI - N/V
- Fever up to 38 from inflammation of myocardial cell death
Serum cardiac enzymes
1) Troponin
Cardiac enzyme, most realiable as long duration
Elevated in STEMI/NSEMI but not unstable
2/3) Creatinine kinase MB and Myoglobin
Unspecific to the heart
MI Healing
Inflammation -> neutrophils/macrophages remove necrotic tissue in 2-3 days, leaving thin, unstable wall
- Collateral circulation may occur
- 2-3 mobths, scar tissue replaces and cannot contract
- Necrotic zone can be identified by EKG chanfes
= Cardiac remodelling occurs when healthy myocardium hypertrophies to compensate, which leads to heart failure
Atorvastatin (Lipitor)
HMG-CoA Reductase inhibitors
MOA - Increase LDL receptor in hepatocytes allowing for removal of LDL
Drugs that lower lipoprotein production (lower LDL, increase HDL)
AE (Well-tolerated)
- HA, rash, memory loss, GI
- Myopathy/Rhabdomyolysis
- Hepatoxicity
NC
- Significant reduction in 2 week, but goes away if drug stopped
- Evening dose
- Monitor urea/creatinine, LFT, creatinine kinase, muscle pain, GI
Colesevelam (Welchol)
Bile-acid Sequestrants
MOA - Non-absorbable resin that binds bile acid preventing reabsorption
Decrease LDL by 20% in first month
AE - Not absorbed systemically, only GI - constipation, bloating, indigestion
Can be used with statins
