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ischemic heart dz Flashcards

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1
Q

Leading cause of death in U.S in adults

A

a. Heart disease (All industrialized nations)
b. Cancer
c. COPD
d. CVA

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2
Q

Risk factors for ischemic heart dz

A

i. Age:
Men>45,
Women>55 (non-modifiable)

ii. Family history: CAD or stroke (non-modifiable)

iii. Lipid abnormalities: (modifiable)
1. LDL>160 mg/dL
2. HDL<35 mg/dL
iv. Smoking tobacco (modifiable)

v. HTN (modifiable)
vi. DM (controllable) vascular z

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3
Q

ischemic heart disease has multiple etiologies but they all involve

A
  • Multiple etiologies, all involving imbalance in oxygen supply and demand
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4
Q

MCC of ischemia in all tissues is

A

MCC in all tissues: ATHEROSCLEROSIS.

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5
Q

other than atherosclerosis what can cause ischemia

A

arterial thrombi, vascular spasms, and rarely coronary emboli, anemia

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6
Q

hardening of the arteries
scarring specific to the artery seen as a physical change to the vessel wall regardless of what is going on in the lumen of the vessel

A

Arteriosclerosis

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7
Q

buildup of plaque within the vessel

A

atherosclerosis

can lead to stiffening (arteriosclerosis)

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8
Q

LAD

A

left anterior descending = anterior interventricular artery

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9
Q

L coronary artery

A

o Left circumflex aa.

o Left anterior descending aa. (LAD) aka anterior interventricular artery

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10
Q

● R coronary artery

A

o Marginal aa.
o R circumflex aa.
o Nodal aa. The feed SA and atrial nodes

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11
Q

skeletal muscle is ___ by volume of the myocardium

A

skeletal muscle is 2% by volume of the myocardium

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12
Q

_ of the myocardium is mitochondria

A

25%

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13
Q

o Myocardium extracts high and relatively fixed/constant amount of O2 from blood d/t

A

mitochondrial need

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14
Q

Myocardial blood flow modulated by _______

A

Myocardial blood flow modulated by varying vascular resistance of the coronary arteries.

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15
Q

_____O2 offloaded from HGB as it travels thru the myocardium –> keeps O2 levels very low in interstitium

A

75% O2 offloaded from HGB as it travels thru the myocardium keeps O2 levels very low in interstitium

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16
Q

there is variability to the vasculature of the heart but typically we think of the LAD of feeding

A

▪ Anterior portion of LV.
▪ Anterior two third of the interventricular septum.
▪ Right bundle branch.
▪ ANTERIOR DIVISION OF LEFT BUNDLE.

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17
Q

if you have a right bundle branch block is is probably because of occlusion of the

A

LAD artery

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18
Q

if you have a nodal block it is due to an occlusion

A

RCA

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19
Q

RCA provides blood to the

A

▪ RV.
▪ Posterior and inferior part of LV.
▪ Posterior third of the interventricular septum.
▪ Both SA and AV nodes
● Therefore, if you have an occlusion in RCA, can expect to see a heart block
▪ Bundle of His

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20
Q

coronary blood vessels fill in diastole or systole

A

diastole

only vessels that fo this

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21
Q

how does a HR greater than 180 lead to ischemia

A

▪ HR > 180 decreases filling time of ventricles AND coronary arteries, leading to ischemia.

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22
Q

why would we tolerate higher blood pressures in elderly especially with CAD

A

blood flow into the coronary vessels is going to be determined by the pressures in the aorta

would need higher systemic pressure to overcome and profuse coronary arteries against the ressitance from arteriosclerosis

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23
Q

Inflammatory response to __________ results in tissue growth and deposition leading to occlusion

A

▪ Inflammatory response to endothelium injury (inner lining) results in tissue growth and deposition leading to occlusion

usually endothelium does not clot but when it is damaged this exposure leads to bad stuff

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24
Q

endothelium is anti-thrombotic because

A

clotting is triggered when tissues are exposed on the outside of the endothelium and trigger clotting cascade

the wall itself can’t promote clotting

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25
what are factors that promote atherosclerosis
1. Cholesterol/TG (?) (cannot truly call it causative, can call it contributory) 2. HTN: cause tears that lead to atherosclerosis 3. Smoking 4. Glycolated substances (byproduct of having high blood sugar is that they attach to everything and cause cardiovascular disease) --> by product is ketones. promote unusual growth in blood vessel wall
26
Factors in atherosclerosis development
Endothelial dysfunction Loss of NO Dyslipidemia Inflammatory/Immunologic factors Smoking
27
why do we worry about genetic predisposition to inflammation
CRP dysmorphism inflammation softens plaques throwing clots is BAD LP-PLA2 from macrophages may also be indicated in plaque rupture
28
how does smoking impact atherosclerosis
decreases release of NO, increases inflammation, causes oxidation of LDL
29
stress vessels wall --> releases NO and leads to....
causes vasodilation and relieves stress
30
endothelial damage cascade that leads to atherosclerosis
platelet adherence and aggregation Monocyte recruitment - gobble up debris including fat Smooth muscle proliferation within tunica media and invasion of intima
31
what are foam cells
macrophages that have gobbled up fat
32
what is a fibromuscular plaque
combination of new muscle fibers from growth of tunica media (muscular part) with a cholesterol based core
33
what is a fatty streak
what a fibromuscular plaque looks like on the surface precursor to atherosclerotic plaque (forms in your teens and 20s)
34
Treatment for lipids in almost all cases is predominantly based on what factor?
a. Treatment for lipids in almost all cases is predominantly based on the LDL component of the lipid panel
35
All patients with coronary artery disease of any kind should receive drug therapy if their LDL _______ with the goal of reducing it to ______
All patients with coronary artery disease of any kind should receive drug therapy if their LDL >130 mg/dL with the goal of reducing it to <100mg/dL
36
when should Pts with two risk factors start drug tx
LDL > 130 = lifestyle changes therapy: diet + exercise (be specific!) LDL > 160 = drug therapy.
37
when should pts with only one or no risk factors start drug tx for high LDL
● Pts. with only one or no risk factors: o LDL > 160 = diet therapy. o LDL > 190 = drug therapy
38
Chronic Ischemic DZ
o Angina- stable and consistent o Variant angina o Silent MI
39
Acute coronary syndrome (ACS)
o Unstable angina o MI STEMI- ST elevation MI NSTEMI- non ST elevation MI
40
Angina Pectoris is characterized by
Paroxysmal (episodic) CP or pressure.
41
Angina Pectoris is associated with
transient cardiac ischemia
42
difference between ischemia and infarction
infarction= cell death ischemia= lack of oxygen
43
most common manifestation of CAD
angina More common than MI d/t being the step before a MI
44
stable angina is thought to be associated with
Stable angina associated with a fixed obstruction.
45
MOST COMMON FORM OF ANGINA.
Stable Angina.
46
pathogenesis of stable angen
▪Atherosclerosis of coronary artery → narrowing lumen >75% → Subendocardial ischemia. ▪Supply and demand problem: demand goes up and cant meet myocardial oxygen demand --> get chest pain
47
when do you see symptoms with stable angina
when demand goes up exercise emotionality cold
48
what EKG findings are associated with stable angina
``` ▪ ST-segment depression (subendocardial ischemia) ●ST segment drops down when they are ischemic ●Segment goes up when they are infarcted ```
49
o Painless episode of ischemia.
● Silent Myocardial Ischemia.
50
why would we see silent Myocardial Ischemia vs stable angina?
area affected too small for pain or defect in pain sensation can be see in DM because of vagus nerve neuropathy
51
Coronary artery spasm, typically with arterial stenosis.
● Prinzmetal Variant Angina.
52
Prinzmetal Variant Angina why do we see this
valvular issues arterial stenosis this can occur at rest or with minimal exercise
53
Prinzmetal Variant Angina most prevalent in ____at what time of day?
in women and night
54
EKG findings indicative of prinzmetal variant angina
``` ● Transient ST-segment elevation o transmural ischemia; ischemia all the way thru the wall of the heart ● Peaked T-waves. ● Inverted U-waves. ● Rhythm disturbances. ```
55
how do you evaluate of angina
``` o History and Risk factors o R/O other possible causes in the thorax Lungs, esophagus (GERD), aorta, nerves, chest wall muscles (infl, muscle strain) ``` oEvaluate ECG, Echo, Echo Stress Test, Angiogram. **DON'T give EST to pts with ACTIVE sx**
56
when would you not want to do a exercise stress test
in pts with active sxs don't want pt to have a heart attack on the treadmil
57
● Angina Treatment.
o Disease maintenance. o Prevention of MI. o . Lifestyle modification to lower risk factors. Rx: antiplatelets, B-Blockers, CCB, Nitrates, lipid control.
58
NSTEMI stands for...
Non-ST Elevation MI (NSTEMI)
59
NSTEMI Increased severity over unstable angina signified by
serum markers of cardiac muscle damage.
60
Caused by nonocclusive thrombus in an area of coronary atherosclerosis
Unstable angina (crescendo angina)
61
crescendo angina aka
Unstable angina
62
Unstable angina CM
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
63
MC STEMI
Transmural infarction (most common) ischemic necrosis of more than 50% of the wall
64
angina ST segments are
depressed because they are sad
65
in MI ST segments are
excited (screaming at you)
66
tombstones
widespread ST segment elevation
67
coronary artery thrombosis location
LAD: 45% RCA: 35% LCA (left circumflex artery): 15%
68
MI with little or no chest pain is seen most frequently in what population
Elderly patient Diabetics Women Postsurgical patients
69
Subendothelial infarction is seen with what EKG
non-Q wave infarction | Ischemic necrosis of < 50% of myocardial wall
70
Q wave infarction | Ischemic necrosis of > 50% of myocardial wall
Transmural infarction (most common
71
CM of heart attack
Sudden onset of severe “crushing” substernal chest pain (elephant) Often radiate to the left arm, jaw and neck (claudication) Chest heaviness, tightness, and shortness of breath Pain is prolonged, unrelieved by rest OR NITRO Diaphoresis, nausea, vomiting Anxiety (SNS) denial
72
women heart attack presents as
GI without chest pain back pain
73
markers in cell INFARCTION
o troponins rise first (12 hours later ) Takes time for LDH to rise hold pt w/ recent MI event in ED for 24hrs troponin rises first, stays elevated 7-10d hold pt >6 hrs for troponin LDH stays elevated 6-9d
74
why do you keep people in the emergency with suspected mi
B/c traponins rise over time (12 hrs) need serial hold pt >6 hrs for troponin
75
0-18 hrs what do we see after MI
no gross changes
76
vague pallor and softening is seen how long after MI
18-24 hrs
77
No changes or wavy myocyte fibers seen associated with and what survival time
0-4 hrs arrhythmia (most common cause of death w/in 24hrs)
78
Coagulation necrosis in the ventricular wall associated with what survival time
4-24 hrs
79
Neutrophilic infiltrate
1-4days
80
Macrophages infiltrate at the end of the first week seen with what survival rate
4-7d
81
Granulation tissue (spindle shape fibroblast + capillary)
7-28d
82
Fibrotic scar follow MI leads to death w/in
Ventricular aneurysm in scar area (within 1-2 months)
83
Pathophysiology of sudden cardiac death
Fatal cardiac arrhythmia (usually, VF)
84
Sudden cardiac death is defined as
death within 1 hour of the onset of symptoms i. Important family hx
85
Etiology of sudden cardiac death
i. Coronary artery disease (80%) ii. Hypertrophic cardiomyopathy iii. Mitral valve prolapse iv. Aortic stenosis v. Congenital heart abnormalities vi. Myocarditis

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