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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
Q

mitochondrial permeability transition pore (mPTP)

A
  • when open, it messes up ion homeostatis

- results in cell death

26
Q

why do we use blood cardioplegia

A

-you are not increasing the amount of dissolved oxygen available and blood offers proteins to keep volume in resulting in less edema

27
Q

When Are Oxygen Free Radicals Generated?

A
  • 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
Q

what is in endothelial cells that creates hydrogen peroxide

A

-xanthine oxidase

29
Q

what two ways to create hydrogen peroxide

A
  • mitochondria

- NADPH oxidase

30
Q

What Factors Determine The Amount of Oxygen Free Radicals Produced?

A
  • Severity of ischemic injury (duration)
  • Activation and recruitment of neutrophils to myocardium
  • Level of oxygen in the cardioplegic solution
31
Q

What Changes Are Caused By Oxygen Free Radicals?

A

-destroys cell membrane

32
Q

What do the oxygen free radicals do?

A
  • 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
Q

What is the Mitochondrial Permeability Transition Pore?

A
  • 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
Q

How Can We “Attack” The Oxygen Free Radical Problem?

A
  • 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
Q

What Changes Are Caused

By Myocyte Calcium Influx?

A
  • 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
Q

neutrophil products that act on endothelium

A
  • platelet activating factor
  • O2 free radicals
  • hypoclorous acid
  • proteases
  • cytokines
37
Q

What Causes Myocardial Edema?

A
  • 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
Q

How Can We Target The Perpetrators During Bypass?

A
  • IV administration

- Cardioplegia

39
Q

How Do We Target The Perpetrators During Off-Pump Cases?

A
  • IV administration
  • NO cardioplegia
  • NO hypothermia
  • MINIMAL cardiac work-load reduction
40
Q

What Clinical Results Do We See As a Result of RPI?

A
  • Dysrhythmias
  • Systolic dysfunction
  • Diastolic dysfunction (compliance / relaxation)
  • Myocardial necrosis
  • Endothelial dysfunction
  • No reflow phenomenon
41
Q

When Can Myocardial Injury Occur?

A
  • Before bypass
  • During cardioplegic arrest
  • During reperfusion
42
Q

Pre-bypass / before delivery of cardioplegia – “prebypass window” (myocardial injury)

A
  • 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
Q

Cross-clamp applied / cardioplegia delivered (myocardial injury)

A
  • 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
Q

Reperfusion (myocardial injury)

A
  • 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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