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Perf tech II > test 4 > Flashcards

test 4 Flashcards

1
Q

Ischemia

A
  • Conventional: Imbalance between oxygen supply and demand
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2
Q

Anoxia

A
  • blood flow to tissue but no oxygen delivery

- problem with the release of O2 to the tissues

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3
Q

Hypoxia

A

-blood flow to tissue with inadequate oxygen delivery

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4
Q

Reperfusion

A
  • Restoration of blood flow after ischemic episode

- after cross clamp and every time you deliver cardioplegia

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5
Q

reperfusion injury

A
  • Reperfusion Injury extends or accelerates the damage from ischemia
  • Potential to increase infarct size
  • Ischemia sets the stage
  • Rate and long-term extent of ischemic injury may be altered by reperfusion conditions/therapy
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6
Q

cardiac myocytes (victim of reperfusion injury)

A
  • metabolic / functional center of heart
  • highest level of oxidative metabolism
  • highest rate of ATP turnover
  • doesn’t tolerate anaerobic metabolism
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7
Q

coronary vascular endothelium (victim of reperfusion injury)

A
  • active tissue
  • release bunch vasoactive substances
  • interface between blood and myocytes
  • arterioles / capillaries very sensitive to injury
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8
Q

good activators that the vascular endothelium produces

A
  • nitric oxide
  • adenosine
  • prostacyclin
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9
Q

bad activators that the vascular endothelium produces

A
  • platelet activating factor
  • endothelin-1
  • superoxide anion
  • histamine
  • RECRUITMENT OF NEUTROPHILS TO THE AREA (inflammatory process)
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10
Q

what factors determine what our myocardial oxygen demand is

A
  • Work done by appropriate chamber(s)
  • Passive stretch of myocardial cells
  • Heart rate
  • Inotropic state
  • Basal metabolic state
  • Reestablishment of ionic homeostasis
  • Oxidative energy diverted to myocyte repair
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11
Q

how are the concentrations of the ions effected by ischemia

A

-ischemia breaks everything down and doesn’t allow ATP therefore you can’t maintain the ion balance disrupting the ion concentrations

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12
Q

how does CPB Affect Myocardial Oxygen Demand?

A
  • decrease demand 50% or more
  • Myocardial cooling decrease demand by 50% for each 7oC decrease in temperature
  • Ventricular decompression
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13
Q

Global Myocardial Ischemia (GMI)?

A
  • the cross clamp
  • No flow to entire heart
  • Clamping aorta during bypass (controlled onset)
  • 45 min ischemia followed by unmodified reperfusion (reversable damage)
  • Right and Left coronary disease
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14
Q

Regional Myocardial Ischemia (RMI)?

A
  • No flow to part of the heart
  • “Off-pump” cases / Coronary blockage (uncontrolled onset)
  • 45 min ischemia followed by unmodified reperfusion
  • substantial damage
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15
Q

Consequences of Myocardial Ischemia?

A
  • Decreased global/regional contractile function
  • Increased endothelial damage
  • Decreased endothelial function
  • Decreased global/regional myocardial blood flow
  • Neutrophil accumulation
  • Apoptosis
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16
Q

Apoptosis

A

-Genetically programmed cell death

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17
Q

What Determines The Magnitude of Ischemic Injury?

A
  • Duration of ischemia
  • Collateral blood flow
  • Baseline health of tissue
  • Influx of calcium
  • Intracellular accumulation of sodium and loss of potassium
  • Stimulation of other activators
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18
Q

What Determines The Time To Onset of Irreversible Damage?

A
  • Severity of ischemia
  • Myocardial temperature
  • Tissue energy demands
  • Collateral blood flow
  • Appear after 30 minutes of occlusion in working heart
19
Q

what damage can reperfusion injury do?

A
  • Potential to extend postischemic injury
  • Myocardial stunning
  • No-reflow phenomenon
  • Reperfusion arrhythmias
  • Lethal reperfusion injury
20
Q

Myocardial Stunning

A

-Mechanical dysfunction after reperfusion

21
Q

No-Flow Phenomenon

A

-Inability to reperfuse previously ischemic area

22
Q

Reperfusion Arrhythmias treatments

A
  • pacing wires

- drugs

23
Q

Lethal Reperfusion Injury

A
  • Several abrupt biochemical and metabolic changes occur – compound injury created by ischemia
  • Mitochondrial reenergization
  • Generation of reactive oxygen species
  • Intracellular calcium overload
  • Rapid restoration of physiologic pH
  • Inflammation
  • Cell death results from opening of mitochondrial permeability transition pore (mPTP) and induction of cardiac myocyte hyper-contraction
24
Q

What Are The Mediators of Lethal Reperfusion Injury?

A

-oxygen-derived free radical
formation (reactive oxygen species (ROS))
-Hugh influx of calcium into the cell
-pH moves from acidic to normal – potentiates many of the changes
-neutrophil activation
-myocradial edema

25
mitochondrial permeability transition pore (mPTP)
- when open, it messes up ion homeostatis | - results in cell death
26
why do we use blood cardioplegia
-you are not increasing the amount of dissolved oxygen available and blood offers proteins to keep volume in resulting in less edema
27
When Are Oxygen Free Radicals Generated?
- Myocardial ischemia favors oxygen free radical generation - Tissue stores of endogenous antioxidants depleted during ischemia - Oxygen not available until reperfusion - GREATEST RISK (i.e. greatest production) occurres when oxygen returned to myocardium - hotshot
28
what is in endothelial cells that creates hydrogen peroxide
-xanthine oxidase
29
what two ways to create hydrogen peroxide
- mitochondria | - NADPH oxidase
30
What Factors Determine The Amount of Oxygen Free Radicals Produced?
- Severity of ischemic injury (duration) - Activation and recruitment of neutrophils to myocardium - Level of oxygen in the cardioplegic solution
31
What Changes Are Caused By Oxygen Free Radicals?
-destroys cell membrane
32
What do the oxygen free radicals do?
- Induce opening mitochondrial permeability transition pore - Act as neutrophil chemoattractants - Mediate dysfunction of sarcoplasmic reticulum - Contribute to intracellular calcium overload - Damage cell membrane by lipid peroxidation - Induce enzyme denaturation - Cause direct oxidative damage to DNA
33
What is the Mitochondrial Permeability Transition Pore?
- Nonselective channel (protein) of inner mitochondrial membrane - When open increases permeability of molecules <1500 Dalton - When open mitochondrial membrane potential collapses and oxidative phosphorylation is uncoupled - Closed during ischemia / open during reperfusion - Opens in response to mitochondrial calcium overload, oxidative stress, restoration of physiologic pH, and ATP depletion
34
How Can We “Attack” The Oxygen Free Radical Problem?
- Administer pharmacological agents that inhibit the formation of oxygen free radicals - Administer pharmacological agents that scavenge / remove oxygen free radicals - Administer anti-neutrophil agents
35
What Changes Are Caused | By Myocyte Calcium Influx?
- Depletion of high-energy phosphate stores - Accumulation in mitochondria kills ability to produce ATP - Activation of catalytic enzymes - Alteration of excitation-contraction coupling of actin-myosin-troponin
36
neutrophil products that act on endothelium
- platelet activating factor - O2 free radicals - hypoclorous acid - proteases - cytokines
37
What Causes Myocardial Edema?
- Increased intracellular osmotic pressure - Disruption of electrical potential across cell membrane - Increased microvascular permeability - Increased interstitial osmotic pressure - High cardioplegia delivery pressure - Hypothermia induced changes to sodium-potassium pump
38
How Can We Target The Perpetrators During Bypass?
- IV administration | - Cardioplegia
39
How Do We Target The Perpetrators During Off-Pump Cases?
- IV administration - NO cardioplegia - NO hypothermia - MINIMAL cardiac work-load reduction
40
What Clinical Results Do We See As a Result of RPI?
- Dysrhythmias - Systolic dysfunction - Diastolic dysfunction (compliance / relaxation) - Myocardial necrosis - Endothelial dysfunction - No reflow phenomenon
41
When Can Myocardial Injury Occur?
- Before bypass - During cardioplegic arrest - During reperfusion
42
Pre-bypass / before delivery of cardioplegia – “prebypass window” (myocardial injury)
- Period of unprotected ischemia - coronary artery or other disease process - hypotension due to dysrhythmia and/or cardiogenic shock - coronary spasm - Reperfusion injury also possible
43
Cross-clamp applied / cardioplegia delivered (myocardial injury)
- Period of protected ischemia - unresolved coronary stenosis - obstruction within vascular graft (kink, tight anastomosis, emboli) - maldistribution of cardioplegia - inadequate cardioplegia delivery (inadequate pressure or volume, inappropriate composition) - between infusions of intermittent cardioplegia - unintentional interruption of continuous cardioplegia - Reperfusion injury also possible
44
Reperfusion (myocardial injury)
- coronary blood flow restored with unmodified blood after clamp removal - Ischemic injury also possible - hypotension post clamp release - during weaning/termination CPB - vascular graft thrombosis or mechanical obstruction - dysrhythmias - vasospasm of grafted vessel

Perf tech II (16 decks)

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