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Cardio II > Phys-ischemia & HF > Flashcards

Phys-ischemia & HF Flashcards

1
Q

What is ischemia?

A

Reduced arterial blood flow, such that O2 demand is not met

*reduced washout is also a key feature of ischemia

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2
Q

What determines severity of ischemic damage?

A
  1. Tissue resistance to perfusion (kidney>skeletal muscle>liver, Brian, heart, intestine)
  2. Completeness of blockage
  3. Inmate resistance of tissue to ischemia (skeletal muscle>liver>kidney>brain, heart, intestine)
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3
Q

Global vs. Low-Flow ischemia

A
  • Global: complete interruption of flow (ex thrombosis). Least common, but most damaging
  • Low-Flow: reduction or partial interruption of flow (esp vasospasm). Most common, least damaging
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4
Q

Causes of flow interruption in the heart:

A
  1. Thrombosis
  2. Atherosclerotic plaque
  3. Catastrophic vascular accident
  4. Damaged endothelium
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5
Q

Intracellular anoxia generated a shift from ___ to ____ metabolism.
What happens?

A

Aerobic to anaerobic

  1. Krebs cycle decreases, less ATP is produced
  2. Glycolysis rates increase to cover ATP shortage
  3. Increased glycolysis and depressed oxidative phosphorylation cause accumulation of metabolites (lactic acid, inorganic P, free fatty acids, fatty acyl CoA)
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6
Q

Lack of Krebs cycle causes the rapid degradation of ___

A 
Nucleoside triphosphates (NTPs)
*5' nucleotides are degraded and exported as nucleosides, esp adenosine and inosine
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7
Q

endothelial cells further degrade nucleosides to ___.

____ appear in blood

A

Nucleobases and uric acid.

Hypoxanthine, inosine, and uric acid

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8
Q

___ attempts to restore energy poise by making ____ from ____

A

Myokinase reaction

1 ATP and 1 AMP from 2 ADP

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9
Q

Effects of decreased Krebs cycle activity

A
  1. Decreased ATP=increased glycolysis, decreased cell work and contraction, loss ion gradients, Na retention
  2. Decreased GTP=decreased protein synthesis, G-protein activity, and cytoskeletal stability
  3. Decreased CTP=decreased phospholipid synthesis
  4. Decreased UTP=decreased glycogen synthesis
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10
Q

Low pH , lack of high energy phosphates allow ___ to accumulate.

A

Cytosolic Ca

*mitochondria scavenge the extra Ca and are damaged in the process

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11
Q

The ___ is located in the mitochondrial inner membrane and is responsible for transporting ATP to the cytosol by exchanging ___ for ___

A
  1. Adenine nucleotide translocase protein
  2. Cytosolic ADP
  3. Matrix ATP
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12
Q

What happens when the mitochondria accumulate Ca?

A
  1. The AN translocase begins to dissociate

2. A large pore forms in the inner membrane (MPTP=mitochondrial permeability transition pore)

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13
Q

Consequences of significant numbers of MPTPs

A
  1. Swelling
  2. Loss of ionic gradients
  3. Accelerated loss of ATP
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14
Q

Summary of events from the onset of ischemia to cell death

A

⬇️flow - ⬇️O2 - ⬇️ATP - ⬆️Na - ⬆️Ca in - ⬆️MPTP - ⬆️cell death

  • ⬆️ATP also leads to ⬆️glycolysis - ⬆️lactate, H+ AND ⬇️NTPs (both of these lead to ⬆️Na)
  • ⬇️NTPs also leads to ⬆️membrane fragility and thus ⬆️cell death
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15
Q

Cell death causes certain enzymes to now be outside of the cell, which can be used as a diagnostic tool.

*which are cardiac specific?

A
  1. Myoglobin
  2. Myosin light chain
  3. Troponin I
  4. CK-MB (creatine kinase, MB form)
  5. Lactate dehydrogenase (LDH)
    * 3 and 4, 5 can be evaluated in a cardiac specific way
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16
Q

LDH evaluation

A

In myocytes and RBCs LDH1»LDH2

  • cell disruption releases LDH1 into the blood
  • normal LDH1/LDH2 <1
  • ischemia LDH1/LDH2 >1 (LDH “flip”)
17
Q

Timeline of ischemic events

A
  1. Early- 5 min: metabolic shifts
    * 20 min: metabolite buildup
  2. Transition- 20 min-1 hr: cell injury
  3. Intermediate- 1-6 hrs: cell death
  4. Late- After 6 hrs: repair
18
Q

Timeline of ischemic events:

Clinically observable features?

A
  1. Void areas on angiography, arrhythmia?
    * ST elevation?
  2. MRI becomes effective, loss/spreading of R wave, definite ST elevation, inverted T wave (V2-V6)
  3. Observable enzyme release, appearance of Q wave
  4. Reentrant arrhythmias, decreased plasma enzymes, spreading of QRS
19
Q

Early phase contractile changes

A
  1. Shortening of AP
  2. ⬆️extracellular K
  3. ⬆️conduction velocity
  4. Impaired contractility
20
Q

Transition phase contractile changes

A
  1. Continued loss of contractility

2. Impairment of relaxation

21
Q

Intermediate phase contractile changes

A
  1. Progressive infarction

2. ventricular stiffness

22
Q

Late phase contractile changes

A
  1. Ventricle is prone to reentrant arrhythmias

2. Replacement fibrosis produces collagen scar

23
Q

Consequences of ischemia and it’s compensations:

CO and venous return

A 
Initially: pump efficiency is decreased
-CO decreased, RAP elevated 
-mostly preload overload
1st Compensation: Frank-Starling effect
2nd Compensation: increased symp tone 
3rd Compensation: increased fluid retention 
-increased renin release due to reduced BP and increased symp tone, increases volume relative to container size, further increase in RAP 
4th compensation: hypertrophy
24
Q

Remodeling of tissues in the heart happens where?

A

“Remote zones” = non-ischemic zones

  • systems involved in signal transduction are overexpressed
  • huge inflammatory response
  • growth factor genes are overexpressed
25
Q

Tissue changes during remodeling:

Enzymatic isoform shifts

A
  1. Myosin heavy chain shifts from alpha to beta isoform (slower contraction means more efficient)
  2. LDH shifts from H4 to M4 isoform (more efficient)
  3. CPK shifts to a higher MB/MM ratio (Fetal situation)
  4. Increased collagen expression, more parallel elastic elements, stiffer heart
26
Q

Remodeling ___ wall stress

What changes?

A

Reduces

*LV systolic pressure, radius, and wall thickness all increase in compensatory hypertrophy

27
Q

Remodeling;

The good news

A
  1. Hemodynamics restored
  2. Collagen deposition results in greater contractile force
  3. Myosin isoform shifts cause slower, more efficient contractions
  4. CK and LDH shifts cause more efficient energy production in a less aerobic environment
28
Q

Remodeling;

The bad news

A
  1. Hemodynamics: reduced coronary vascular reserve lessens ability to increase coronary flow on demand
  2. Collagen deposition results in stiffer heart which impairs relaxation and filling is energetically more costly.
  3. Myosin isoform shifts cause reduced contractility of the fibers themselves, makes them less responsive
  4. OVERALL ENERGETICALLY COSTLY AND DIFFICULT TO MAINTAIN

Cardio II (16 decks)

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