Ischemic Heart Disease

Question 1

leading causes of death in US adults

Answer 1

• heart dz (all industrialized nations)
• Cancer
• Copd
• CVA

Question 2

risk for ischemic heart DZ

Answer 2

1. age - men >45, women >55
2. family hx
3. lipid abnormalities - Ldl >160 associated with heart dz; HDL <35 is cardioprotective
4. smoking tobacco
5. HTN
6. DM - causes vascular damage

Question 3

ischemia

Answer 3

• multiple etiologies, all involving imbalance in O2 supply and demand
• MCC atherosclerotic disease, also arterial thrombi, spasm, and rarely coronary emboli

Question 4

arteriosclerosis

Answer 4

hardening of the arteries - stiffening and scarring of the vessel wall

Question 5

artherosclerosis

Answer 5

plaque buildup within the vessle - can lead to stiffening of the vessel wall

Question 6

oxygenation of the myocardium

Answer 6

• myocardium extracts high and relatively fixed amount of oxygen
• myocardial blood flow modulated by varying vascular resistance of the coronary arteries
• 25% of cardiac muscle cell volume is mitochrondria

Question 7

What parts of the heart are supplied by the LAD

Answer 7

• anterior portion of left ventricle
• anterior two thirds of interventricular septum
• right bundle branch
• anterior division of left bund

Question 8

what parts of the heart are supplied by the RCA (right coronary)

Answer 8

• right ventricle
• posterior and inferior part of the left ventricle
• posterior third of the interventricular septum
• both SA and AV node
• His bundle
• posteriod division of the left bundle

Question 9

coronary artery blood flow

Answer 9

-fill in diastole

HR > 180 decreases filling time of coronary arteries which can lead to ischemia

Question 10

pathophysiology of atherosclerosis

Answer 10

• response to injury
• inflammatory response to endotheliual injury - tissue growth and deposition leading to occlusion
• causes: cholesterol/TG, HTN, smoking, glycolated substances

Question 11

endothelial dysfunction and atherosclerosis

Answer 11

• loss of NO (vasodilator dysfunction), inability of small vessels to vsodilate
• less capable of vasodilation = more susceptible to vascular damage

Question 12

dyslipidemia and atherosclerosis

Answer 12

• high cholesterol diets correlated with rapid development of atherosclerosis
• LDL is involved in plaque formation
• LPa is involved in thrombus formation
• TG + C3 has been linked causally to atherosclerosis

Question 13

CRP dysmorphisms

Answer 13

LP-PLA2 from macrophages may increase rupture risk

Question 14

how does smoking affect atherosclerosis

Answer 14

• decreases NO, increases inflammation, and causes oxidation of LDL
• oxidized LDL is like a free radical - causes more vascular damage

Question 15

pathophysiology of endothelial injury

Answer 15

• platelet adherence and aggregation at site of injury
• monocyte recruitment via cytokines released from damage to try to fix the damage
• smooth muscle proliferation within tunica media and invasion of intima
• foam cells and fatty streak formed - macrophages that have eaten the fats

Question 16

Fibromuscular plaque

Answer 16

• muscle fibers and cholesterol core
• combination of new muscle fibers and growth of tunica media with a cholesterol based core
• on the surface, thats referred to as a fatty streak

Question 17

which fat should you look at in order to begin treatment

Answer 17

LDL!! we look at elevated LDL

-decreased HDL by itself is NOT an indication for drug therapy

Question 18

tx for patients with two risk factors

Answer 18

• LDL > 130 = diet therapy

- LDL > 160 = drug therapy

Question 19

tx for patients with one or no risk facotrs

Answer 19

• LDL >160 = diet therapy

- LDL > 190 = drug therapy

Question 20

stable angina and sxs

Answer 20

• atherosclerosis of cornoary artery
• narrowing the lumen over 75% can lead to a subendocardial ischemia
• sxs: exercise/emotional induced chest pain lasting 1-5 mins. Also induced by cold or stress
• relieved by resting or nitroglycerine
• ST segment depression (subendocardial ischemia

Question 21

silent myocardial ischemia

Answer 21

• painless episodes of ischemia related to same pathophysiology as anginal pain
• pt may have defect in pain sensation or transmission of pain signals
• increased incidence in DM

Question 22

Prinzmetal variant angina pathogenesis and clinical findings

Answer 22

Pathogenesis:
 Coronary artery spasm, typically with arterial stenosis

Clinical findings:
 Episodic chest pain often occurring at rest, minimal exercise
 Frequently occurs in women, and at night (12-8AM)
 EKG: transient ST segment elevation (transmural ischemia), peaked T waves, inverted U waves, rhythm disturbances
• Inverted u waves can be a sign of a previous cardiac event
 Relieved by nitroglycerin

Question 23

how to evaluate for angina

Answer 23

o History and Risk Factors
o R/O other occupants of the thorax
o Evaluate ECG, ECHO, EST (exercise stress test), Angiogram

Question 24

angina treatment

Answer 24

o Disease maintenance, prevention of MI
o Lifestyle modification to lower RF
o Rx: antiplatelets, B-blockers, CCB, Nitrates, lipid control

Question 25

unstable angina pathogenesis and clinical findings

Answer 25

o Pathogenesis:  Caused by nonocclusive thrombus in an area of coronary atherosclerosis o Clinical findings:  Pain more persistent or severe than stable angina • 1) Pain at rest, >20 min • 2) Severe pain of new onset • 3) Progression from stable angina  High risk for acute myocardial infarction (MI) o The OBSTRUCTION is unstable  has a risk of traveling and obstructing the vessel completely

Question 26

NSTEMI

Answer 26

o Non-ST (segment) Elevation MI | o Increased severity over unstable angina signified by presence of serum markers of cardiac muscle damage.

Question 27

STEMI pathogenesis and types of myocardial infarction

Answer 27

o Pathogenesis:  Coronary artery atherosclerosis with plaque rupture and superimposed thrombus formation  Coronary artery spasm  Less common causes: vasculitis, cocaine use, embolization of plaque material o Types of myocardial infarction:  Transmural infarction (most common): Q wave infarction • Ischemic necrosis of > 50% of myocardial wall  Subendothelial infarction: non-Q wave infarction • Ischemic necrosis of < 50% of myocardial wall

Question 28

tombstones

Answer 28

o Distribution of coronary artery thrombosis  LAD: 45%  RCA: 35%  LCA (left circumflex artery): 15% o Names as such because people with this don’t typically survive – widespread ST elevation

Question 29

clinical presentation of STEMI

Answer 29

o Sudden onset of severe “crushing” substernal chest pain o Often radiate to the left arm, jaw and neck  this is claudication – muscular pain from hypoxia o Chest heaviness, tightness, and shortness of breath o Pain is prolonged, unrelieved by rest OR NITRO  if it is relieved by these, its rest or nitro o Diaphoresis, nausea, vomiting o Anxiety o Note: MI with little or no chest pain is seen most frequently in the  Elderly patient  Diabetics  Women  presents without chest pain, looks like GI issues  Postsurgical patients

Question 30

enzymes to look for during MI

Answer 30

o CK = CK-MB | o Troponin is TnI and TnT

Question 31

sudden cardiac death and etiology

Answer 31

``` o Definition: death within 1 hour of the onset of symptoms o Pathophysiology:  Fatal cardiac arrhythmia (usually, VF) o Etiology: 1. Coronary artery disease (80%) 2. Hypertrophic cardiomyopathy 3. Mitral valve prolapse 4. Aortic stenosis 5. Congenital heart abnormalities 6. myocarditis ```