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OMSII BECOM Exam 2 > Ischemic heart disease I&II - Adje > Flashcards

Ischemic heart disease I&II - Adje Flashcards

1
Q

ischemic heart disease

A

-O2 supply is not meeting demand –> low perfusion of tissues

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2
Q

when does blood flow through the coronary arteries?***

A

-diastole**

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3
Q

autoregulation of coronary arteries***

A
  • vasodilate when there is need and vasoconstrict when there is no need**
  • vasodilation decreased resistance in vessels
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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
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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

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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

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7
Q

stable vs unstable plaque***

A
  1. stable
    - thick fibrous cap
    - less lipid core
    - less likely to rupture
  2. unstable
    - thin fibrous cap
    - more lipid core
    - more likely to rupture
    - macs release cytokines and MPs which destabilize cap tissue
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8
Q

ischemia vs infarction

A
  1. ischemia = reversible damage
    - <20 min occlusion
    - ST segment depression (subendocardial)
    - incomplete/partial occlusion
  2. infarction (MI) = irreversible damage
    - >20min occlusion
    - ST segment elevation (transmural)
    - complete occlusion
  • endocardium 1st to undergo ischemia** –> progresses to epicardium
  • order EKG to differentiate*****
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9
Q

stunned vs hibernating myocardium

A
  1. stunned
    - viable tissue that recovers function following a temporary reduction in blood flow
  2. hibernating
    - viable tissue in region of chronic CAD –> only improve contractile function with restoration of blood flow
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10
Q

sudden death in ischemic heart disease most commonly from what?*

A

-ventricular tachycardia

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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
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12
Q

types of angina***

A
  1. stable
    - predictable
    - brought on by exertion
    - pain goes away with rest***
  2. unstable
    - not predictable
    - plaque rupture
    - occurs at rest >10min or more prolonged/frequent
    - no relief with rest***
  3. prinzmetal
  4. microvascular damage
  5. ACS
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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)
  1. unstable angina
    - troponin NEG**
  2. STEMI
  3. NSTEMI
    - troponin POS**

-treat with aspirin and haparin

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14
Q

NSTEMI vs STEMI

A
  1. NSTEMI
    - not complete coronary occlusion **
    - myocardial necrosis and elevated troponin
    - ST segment depression***
  2. STEMI (acute MI)
    - COMPLETE coronary occlusion*
    - myocardial necrosis and elevated troponin
    - ST segment elevation    *
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15
Q

angina equivalents

A
  • symptoms of myocardial ischemia other than angina –> dyspnea, nausea, fatigue, faintness
  • more common in elderly and diabetics
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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
  1. 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)**
  2. 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)
  3. myoglobin MB
    - low specificity
    - O2 carrying molecule of muscle
    - used to examine reperfusion*
  4. 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**

  1. symptoms of ischemia
  2. EKG changes of new ischemia (ST-T or LBBB changes)
  3. see Q ways on EKG
  4. 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
  1. 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)
  2. 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
  3. heart failure (CHF)
    - LV function decreases 30% of normal –> loss of muscle and decrease in SV/EF*** –> cardiogenic shock
  4. 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
  5. 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
  1. Asystole
  2. Symptomatic bradycardia not responsive to atropine
  3. Complete Heart Block
  4. Second degree H.B ( Mobitz type II )
  5. New Bifasicular block
  6. Bilateral Bundle branch block
  7. Sinus pauses > 3 sec. , not responsive to atropine
  8. 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)

OMSII BECOM Exam 2 (24 decks)

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