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562 - Perfusion Technology II > Exam 3 - Ultrafiltration & Endocrine Response To CPB > Flashcards

Exam 3 - Ultrafiltration & Endocrine Response To CPB Flashcards

1
Q

How does volume overload lead to mortality

A

Overload -> increase pre/afterload -> increase LV hypertrophy -> increase CHF -> Mortality

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2
Q

Ultrafiltration

A
  • hemoconcentration (increase [RBC])
  • removes water and low weight solutes
  • uses transmembrane CONVECTION pressure gradient across membrane
  • high to low pressure (positive pressure side to negative pressure side)
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3
Q

Advantages of hemoconcentration

A
  • Increase [protein] and [RBC]
  • Remove inflammatory mediators
  • Decrease lung water
  • Improve operative homeostasis
  • Reduced postop vent support
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4
Q

Hemoconcentrator design

A
  • hollow fiber
  • blood on inside
  • Dialysate on outside
  • can be used with or without vacuum
    - blood side generates pressure that pushes body water out
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5
Q

Hollow fiber bundle diameter

A

180-200 um

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6
Q

Microporous membrane thickness

A

5-10 um

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7
Q

Convection

A
  • fluid flow through membrane driven by pressure gradient
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8
Q

Diffusion

A
  • movement across membrane due to differences in solute concentration on each side (concentration gradient)
  • Blood side has high [solute]
  • Ultrafiltration uses both diffusion AND convection
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9
Q

Overall change in [solute] using ultrafiltration

A
  • There is none
  • removes water and diffusable solutes in equal concentrations
  • BUT protein / cells / protein bound solutes not removed
    - so concentration of blood side goes up
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10
Q

Principles of ultrafiltration

A
  • need blood flow and pressure gradient
  • sieving coefficient (pore size vs weight of solute)
  • rate of filtration based on flow rate and transmembrane pressure
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11
Q

Transmembrane pressure (TMP)

A
  • gradient between blood and ultrafiltrate compartment

- TMP should not exceed 500-600 mmHg

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12
Q

Ultrafiltration coefficient

A
  • Kuf
  • how efficient filtration is
  • typical rates 2-50 ml/hr/mmHg
  • increase blood flow / TMP = increase removal
  • decrease Hct / plasma protein = increase removal
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13
Q

Sieving coefficient

A
  • [ultrafiltrate solute] to [blood solute]
  • 0 to 1.0
  • 1 = solute will pass
  • 0 = solute will not pass
  • ease at which given solute will travel across filter membrane
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14
Q

CUF

A
  • Conventional Ultrafiltration
  • basic type normally used using pressure gradient
  • will increase Hct
  • level in reservoir will drop
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15
Q

Z-BUF

A
  • Zero balanced ultrafiltration
  • Equal input and output
  • replaces ultrafiltrate volume with electrolyte solution
  • can use normosol, plasma-lite, LR, etc
  • used to reduce cytokines / compliment levels (reduce inflammatory response)
  • used during re-warming (peak of inflammatory response)
  • treats hyperkalemia
  • need to add bicarb
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16
Q

MUF

A
  • Modified ultrafiltration
  • used following termination of CPB
  • volume from circuit back to patient
  • mainly used on pediatrics
  • brings down CVP
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17
Q

Where can ultrafiltration filters go in circuit?

A
  • O2 recirculation line

- Cardioplegia circuit

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18
Q

Post-CPB pump blood

A
  • residual blood is hemoconcentrated

- reduce need for bank blood transfusion

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19
Q

Parameters to think of w/ ultrafiltration

A
  • Flow
  • Pressure
  • Volume
  • may need to increase flow to keep pressure up since filter is another shunt
  • can add vacuum to [hemo] to increase removal rate
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20
Q

Things to be wary of w/ [hemo]

A
  • volume level
  • pink effluent means too high TMP (hemolysis)
  • vacuum increase removal but also hemolysis
  • [Hemo] is a shunt and must be off if pump is off
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21
Q

Dialysis

A
  • mainly uses diffusion but also convection
  • runs countercurrent
  • concentration gradient made by using dialysate solution
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22
Q

Dialysate solution

A
  • contains chemicals in [ ] ‘s similar to blood
  • flows countercurrent
  • substances that need to stay in blood are in same [ ] as blood in dialysate solution
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23
Q

Purpose of dialysis

A
  • treat renal failure
  • remove waste products from blood
  • return blood chemistry values back to normal
24
Q

ARF

A
  • acute renal failure
  • kidney may recover
  • CPB is cause of injury
  • can be put on dialysis to recover
25
Q

CKD

A
  • chronic kidney disease

- long/slow process where kidneys lose function

26
Q

ESRD

A
  • end stage renal disease
  • kidneys shut down permanently
  • permanent dialysis
27
Q

Renal failure

A
  • decrease in GFR (how well kidneys are filtering)
  • elevated BUN and Creatinine levels
  • GFR goes down with age
28
Q

Dialysis access

A
  • AV fistula (connection of artery to vein)
  • made by vascular surgeon
  • used to remove and return blood during dialysis
  • safer for patient
29
Q

Heart and lungs on CPB

A
  • not perfused
  • not able to secrete hormones
  • not part of normal drug metabolism
30
Q

Exposure to circuit on CPB

A
  • trauma to cellular components
  • removal of plasma proteins
  • stimulation of immune response
31
Q

Hemodilution and CPB

A
  • altered [ ] of electrolytes, hormones, serum proteins
32
Q

Hypothermia and CPB

A
  • decreased rate of all reactions

- disruption of hormonal responses

33
Q

Non-pulsatile flow and CPB

A
  • may change flow distribution to organs

- may change flow distribution within organs

34
Q

CPB and stress hormones

A
  • stimulate release
  • cortisol
  • increased levels of hormones post CPB
35
Q

Vasopressin

A
  • ADH
  • Hold onto water volume
  • Very potent
  • If high [ ]:
    • increase PVR
    • increase renal vascular resistance (less filtration / renal volume)
    • decrease coronary blood flow
    • decrease contractility
    • stimulate releases of von Willebrand factor (clotting)
36
Q

What stimulates ADH release

A
  • increased plasma osmolarity
  • decrease in blood volume / pressure (CPB)
  • hypoglycemia
  • stress / pain
  • angiotensin
  • anesthesia / surgery
  • ACE inhibitors
  • SIADH = syndrome of inappropriate ADH release
37
Q

ADH and CPB

A
  • Greatly increases release
  • persists hours post-op
  • caused by:
    • drop in blood volume on initiation
    • drop in LA pressure (vent)
    • hypotension
38
Q

Prevention of ADH on CPB

A
  • pulsatile flow (not really)
  • anesthesia w/ synthetic opioids (not completely)
  • regional anesthesia (only on non-cardiac)
  • THESE all decrease ADH but doesn’t stop completely on CPB
39
Q

Catecholamines

A
  • Epi (x10 on CPB) - peak at target temp
  • NE (x4 on CPB) - peak at clamp removal / rewarm
  • increase on CPB
  • from adrenal medulla
  • from sympathetic / central nerve terminal (NE only)
  • potent vasoconstrictor
40
Q

Prevention of Epi and NE on CPB

A
  • “just enough” anesthesia (deeper is better)
  • proposal infusion
  • opioid plus epidural versus opioid alone
  • anesthesia plays big role in prevention of catecholamines
  • magnitude of increase can be dropped but not eliminated
41
Q

Adrenal cortical hormones

A
  • Cortisol
    • stress hormone
    • corticosteroid
    • increases blood sugar
  • Adrenocorticotropic hormone
    • corticotropic
    • increases cortisol release
  • Both increased during CPB
42
Q

Prevention of adrenal cortical hormones on CPB

A
  • deeper levels of anesthesia
  • add epidural
  • not clear if increased levels good or bad
43
Q

Glucose and CPB

A
  • regulated by insulin / glucagon
  • [ ] altered w/ CPB
  • increase at initiation (hyperglycemia)
  • insulin levels drop (hypoinsulinemia)
  • insulin resistance (bad in DMII)
  • PRBC add a ton of glucose (400-700 g/dL)
44
Q

Atrial Natriuretic factor (ANF)

A
  • Reduces blood volume
  • release triggered by atrial distention (should be none)
  • cause:
    • increase GFR
    • inhibits renin
    • reduce atrial BP
    • inhibits aldosterone
45
Q

ANF and CPB

A
  • [ ] reduced during … no volume in heart
  • [ ] rise during rewarm and post-op… heart fills
  • normal values lost during bypass and early post-op
46
Q

Renin-angiotensin-aldosterone

A
  • regulates BP / volume
  • Kidneys release renin when:
    • drop in Na
    • drop volume
    • low renal flow
  • Sympathetic release during pain / stress / emotion
47
Q

Renin-Angiotensin-Aldosterone pathway

A
  • Renin converts angiotensinogen to angiotensin I (in blood)

- ACE converts angiotensin I to angiotensin II (in lungs)

48
Q

Angiotensin II

A
  • increase BP
  • vasoconstrictor
  • increase release of aldosterone
49
Q

Aldosterone

A
  • increase absorption of H2O / Na
  • increases BP
  • CPB increases hypertension which increases all these levels
50
Q

Eicosanoids

A
  • prostaglandin-thromboxane

- metabolized by lungs

51
Q

Prostaglandin H2

A
  • produces PGEs (vasodilator)

- produces TXA2 (vasoconstrictor)

52
Q

Prostaglandin and Thromboxane and CPB

A
  • levels increase during and drop shortly after

- no consistent effect found

53
Q

Histamine

A
  • inflammatory response
  • vasodilator
  • triggered by:
    • opioids
    • muscle relaxers
    • antibiotics
    • heparin
    • protamine
  • increased during CPB
54
Q

Calcium

A
  • maintained by bones/kidney
55
Q

Ca and CPB

A
  • changes caused by:
    • blood products (deplete Ca)
    • prime (few contain Ca)
    • albumin (drops ionized Ca)
  • Give extra Ca when:
    • termination
    • ionized Ca reduced
    • need to increase contractility and BP
    • NOT too much… stone heart
56
Q

Mg

A
  • need to actually administer Mg to increase levels
  • needed as factor for enzymes and membrane stability
  • Albumin binds Mg and drops levels
  • hemodilution drops levels
  • takes a while to come back up (no native hormone)
  • Supplemental Mg is GOOD…suppresses arrhythmias
57
Q

K

A
  • changes caused by:
    • cardioplegia
    • anesthesia
    • prime
    • renal function
    • pH
    • hypothermia (drop when cool…up when warm)
  • hyperkalemia not uncommon
  • albumin may help reduce decrease in [ ]
  • Normal is 3.5-5…..shoot for 4.5

562 - Perfusion Technology II (9 decks)

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