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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
CKD
- chronic kidney disease | - long/slow process where kidneys lose function
26
ESRD
- end stage renal disease - kidneys shut down permanently - permanent dialysis
27
Renal failure
- decrease in GFR (how well kidneys are filtering) - elevated BUN and Creatinine levels - GFR goes down with age
28
Dialysis access
- AV fistula (connection of artery to vein) - made by vascular surgeon - used to remove and return blood during dialysis - safer for patient
29
Heart and lungs on CPB
- not perfused - not able to secrete hormones - not part of normal drug metabolism
30
Exposure to circuit on CPB
- trauma to cellular components - removal of plasma proteins - stimulation of immune response
31
Hemodilution and CPB
- altered [ ] of electrolytes, hormones, serum proteins
32
Hypothermia and CPB
- decreased rate of all reactions | - disruption of hormonal responses
33
Non-pulsatile flow and CPB
- may change flow distribution to organs | - may change flow distribution within organs
34
CPB and stress hormones
- stimulate release - cortisol - increased levels of hormones post CPB
35
Vasopressin
- 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
What stimulates ADH release
- increased plasma osmolarity - decrease in blood volume / pressure (CPB) - hypoglycemia - stress / pain - angiotensin - anesthesia / surgery - ACE inhibitors - SIADH = syndrome of inappropriate ADH release
37
ADH and CPB
- Greatly increases release - persists hours post-op - caused by: - drop in blood volume on initiation - drop in LA pressure (vent) - hypotension
38
Prevention of ADH on CPB
- 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
Catecholamines
- 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
Prevention of Epi and NE on CPB
- "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
Adrenal cortical hormones
- Cortisol - stress hormone - corticosteroid - increases blood sugar - Adrenocorticotropic hormone - corticotropic - increases cortisol release - Both increased during CPB
42
Prevention of adrenal cortical hormones on CPB
- deeper levels of anesthesia - add epidural - not clear if increased levels good or bad
43
Glucose and CPB
- 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
Atrial Natriuretic factor (ANF)
- Reduces blood volume - release triggered by atrial distention (should be none) - cause: - increase GFR - inhibits renin - reduce atrial BP - inhibits aldosterone
45
ANF and CPB
- [ ] reduced during ... no volume in heart - [ ] rise during rewarm and post-op... heart fills - normal values lost during bypass and early post-op
46
Renin-angiotensin-aldosterone
- regulates BP / volume - Kidneys release renin when: - drop in Na - drop volume - low renal flow - Sympathetic release during pain / stress / emotion
47
Renin-Angiotensin-Aldosterone pathway
- Renin converts angiotensinogen to angiotensin I (in blood) | - ACE converts angiotensin I to angiotensin II (in lungs)
48
Angiotensin II
- increase BP - vasoconstrictor - increase release of aldosterone
49
Aldosterone
- increase absorption of H2O / Na - increases BP - CPB increases hypertension which increases all these levels
50
Eicosanoids
- prostaglandin-thromboxane | - metabolized by lungs
51
Prostaglandin H2
- produces PGEs (vasodilator) | - produces TXA2 (vasoconstrictor)
52
Prostaglandin and Thromboxane and CPB
- levels increase during and drop shortly after | - no consistent effect found
53
Histamine
- inflammatory response - vasodilator - triggered by: - opioids - muscle relaxers - antibiotics - heparin - protamine - increased during CPB
54
Calcium
- maintained by bones/kidney
55
Ca and CPB
- 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
Mg
- 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
K
- 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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