Ischemic heart disease I&II - Adje Flashcards
1
Q
ischemic heart disease
A
-O2 supply is not meeting demand –> low perfusion of tissues
2
Q
when does blood flow through the coronary arteries?***
A
-diastole**
3
Q
autoregulation of coronary arteries***
A
- vasodilate when there is need and vasoconstrict when there is no need**
- vasodilation decreased resistance in vessels
4
Q
what is affected 1st during ischemia?*
A
- diastole***
- requires energy for the Na+/K+ pump, but don’t have ATP during ischemia**
- abnormal relaxation of the ventricle (EKG changes)
- systolic dysfunction follows
5
Q
what is the main cause of ischemia (reduced O2 supply) of the heart***
A
- atherosclerosis*** –> reduces the lumen of the coronary arteries due to plaque build up
- mainly affects right and left coronary arteries**
- right coronary artery supplies AV node
- left coronary artery supplies SA node
-usually don’t get ischemia until you have 80% blockage of coronary
6
Q
cells involved in atherosclerotic plaques***
A
-in epicardial coronary arteries usually
- endothelial damage –> collect fat, smooth muscle cells, fibroblasts, intercellular matrix**
- fat enters endothelial cells –> taken up by macs –> foam cells –> form plaque with addition of smooth muscle cells and MPs
- take decades to form
-untreatable with meds –> cannot penetrate vessel wall
7
Q
stable vs unstable plaque***
A
- stable
- thick fibrous cap
- less lipid core
- less likely to rupture - unstable
- thin fibrous cap
- more lipid core
- more likely to rupture
- macs release cytokines and MPs which destabilize cap tissue
8
Q
ischemia vs infarction
A
- ischemia = reversible damage
- <20 min occlusion
- ST segment depression (subendocardial)
- incomplete/partial occlusion - infarction (MI) = irreversible damage
- >20min occlusion
- ST segment elevation (transmural)
- complete occlusion
- endocardium 1st to undergo ischemia** –> progresses to epicardium
- order EKG to differentiate*****
9
Q
stunned vs hibernating myocardium
A
- stunned
- viable tissue that recovers function following a temporary reduction in blood flow - hibernating
- viable tissue in region of chronic CAD –> only improve contractile function with restoration of blood flow
10
Q
sudden death in ischemic heart disease most commonly from what?*
A
-ventricular tachycardia
11
Q
angina pectoris***
A
- syndrome due to transient myocardial ischemia (low blood/O2 supply)
- retro/substernal chest DISCOMFORT –> Levine’s sign*
- last 2-5 min.
- crescendo-decrescendo murmur
- radiate to shoulder, both arms, scap, neck, jaw, epigastic
12
Q
types of angina***
A
- stable
- predictable
- brought on by exertion
- pain goes away with rest*** - unstable
- not predictable
- plaque rupture
- occurs at rest >10min or more prolonged/frequent
- no relief with rest*** - prinzmetal
- microvascular damage
- ACS
13
Q
acute coronary syndrome (ACS)**
-type of angina
A
- partially occluding thrombus sitting on plaque on coronary artery*
- portion of myocytes deprived of O2 –> necrosis determined by time of reperfusion (pharmacologically or PCI)
- unstable angina
- troponin NEG** - STEMI
- NSTEMI
- troponin POS**
-treat with aspirin and haparin
14
Q
NSTEMI vs STEMI
A
- NSTEMI
- not complete coronary occlusion **
- myocardial necrosis and elevated troponin
- ST segment depression*** - STEMI (acute MI)
- COMPLETE coronary occlusion*
- myocardial necrosis and elevated troponin
- ST segment elevation*
15
Q
angina equivalents
A
- symptoms of myocardial ischemia other than angina –> dyspnea, nausea, fatigue, faintness
- more common in elderly and diabetics
16
Q
angina equivalents
A
- symptoms of myocardial ischemia other than angina –> dyspnea, nausea, fatigue, faintness
- more common in elderly and diabetics
17
Q
heart morphology changes in acute MI
A
- loss of blood supply –> necrosis –> WBCs and macs enter to clean up debris –> form fibrosis
1. 4-12 hr. –> coagulative necrosis
2. 12-24 hr. –> infiltrating neutrophils
3. 1 day –> dark mottling; damaged subendocardium
4. 3 day –> heavy neutrophil infiltrate –> inflammation/repair
5. 5 days –> neutrophils replaced with macs for phagocytosis
18
Q
ventricular wall post MI
A
- ventricular remodeling**
- infarcted areas are stretched bc can’t contract (slipping myocytes) –> LV dilation –> decrease contractility
- fibrosis with each MI
- prognosis depends on size of infarct
19
Q
cardiac biomarkers***
A
- troponin**
- released during damage/infarct
- TnT, TnI (specific, sensitive, preferred) –> have monoclonal Abs and can differentiate b/w skeletal and cardiac muscle damage
- peaks at 24 hr. then declines (lasts for 7 days)** - CK-MB
- less sensitive
- cannot differentiate b/w skeletal and cardiac muscle damage
- short duration –> used to test for reinfarction***
- peaks at 10-12hr. (lasts 2-3 days) - myoglobin MB
- low specificity
- O2 carrying molecule of muscle
- used to examine reperfusion* - LDH
- LDH1 in heart, LDH2 in serum
- peaks 72 hr. (lasts 10-14 days)
- also seen in cancer, meningitis, encephalitis, HIV (not specific)
20
Q
troponin assay use***
A
- POS troponin confirms diagnosis of NSTEMI***
- NEG troponin confirms unstable angina **
same chest discomfort in both cases
21
Q
criteria for diagnosis of MI***
A
-need evidence of myocardial necrosis with ischemia and rise/fall of biomarkers**
- symptoms of ischemia
- EKG changes of new ischemia (ST-T or LBBB changes)
- see Q ways on EKG
- imaging evidence of loss of myocardium
22
Q
what is the most common cause of death post MI?***
A
-cardiogenic shock*** and heart failure
23
Q
complications of MI***
A
- electrical complications
- Na+/K+ imbalance –> arrhythmias
- ventricular arrhythmias –> V-tach, Vfib, PVCs –> treat by correcting electrolyte imbalance, shock for sustained V-tach or Vfib, beta blockers for sinus tachycardia
- SVT –> sinus tachycardia, Afib, Aflutter
- bradyarrhythmias –> sinus bradycardia (inferior, posterior infarcts)
- 2nd degree AV block type II (temporary pacemaker)
- complete AV block (inferior, anterior infarcts) - mechanical complications
- acute mitral regurge –> due to papillary muscle dysfunction or rupture (loss of O2 from inferior infarct)
- ventricular septal rupture –> loud, holosystolic murmur** left sternal border –> heart failure –> emergency surgery
- free wall rupture –> syncope or sudden death (rarely saved by pericardiocentesis, thoracotomy)
- ventricular aneurysm –> pouch in heart wall, ST segment elevation - heart failure (CHF)
- LV function decreases 30% of normal –> loss of muscle and decrease in SV/EF*** –> cardiogenic shock - pericarditis
- 2-4 days post MI
- chest pain and friction rub that radiates to trapezius
- post MI syndrome (dressler’s syndrome)*** –> chest pain, friction rub 1 to several weeks post MI –> pericardial effusion, rarely have tamponade - Post infarct angina or re-infarction
24
Q
AV block infarcts***
A
- anterior infarct with AV block –> sudden and need permanent pacemaker***
- inferior infarct with AV block –> resolved on its own
25
Q
indications of temporary pacing in acute MI***
A
- Asystole
- Symptomatic bradycardia not responsive to atropine
- Complete Heart Block
- Second degree H.B ( Mobitz type II )
- New Bifasicular block
- Bilateral Bundle branch block
- Sinus pauses > 3 sec. , not responsive to atropine
- Incessant V- Tachycardia ( overdrive pacing)
26
Q
ventricular septal rupture***
A
- loud holosystolic murmur***
- higher pressure in LV and flows to RV
27
Q
cardiogenic shock***
A
-persistent hypotension SBP <80mmHg for >30min (no hypovolemia) when >/= 40% of myocardium is affected**
28
Q
sudden cardiac death (SCD)***
A
- abrupt cessation of cardiac mechanical function**
- reversible by prompt intervention (defibrillation, CPR, etc.)
- EKG patterns –> Vtach/Vfib, ventricular asysystole, pulseless electrical activity
29
Q
Q wave
A
-suggests complete infarction
30
Q
ACS management
A
- All hospitalized
- Immediate PCI/Thrombolytics for STEMI
- All ACS pts medical management ( mnemonic HOBANACS)
- Heparin (low-molecular-weight heparin→fewer MIs and deaths)
- Oxygen
- Beta-blocker
- Aspirin (initially 160–325 mg each day then 70–162 mg daily indefinitely)
- Nitroglycerin (for pain; stop if hypotension occurs)
- ACE inhibitor (within the first 24 hours if anterior-location infarct, heart failure, or ejection fraction of ≤40%, unless contraindicated)
- Clopidogrel (Other Antiplatelets)
- Statins (HMG-CoA-reductase inhibitors)
