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CV Perf Tech III > Renal Response to CPB- Exam 1 > Flashcards

Renal Response to CPB- Exam 1 Flashcards

1
Q

What does the kidney do?

A

Regulates fluid composition, intravascular volume and excretion of metabolic byproducts

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2
Q

What is the incidence of renal failure (i.e. requiring dialysis)

A

Decreasing; 1%

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3
Q

Why is the incidence of renal failure decreasing?

A

Better patient preparation
Improved perfusion techniques
better management cardiac performance post op

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4
Q

If renal dysfunction occurs, what is the mortality rate?

A

> 50% mortality rate

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5
Q

What is the function unit of the kidney?

A

Nephron

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6
Q

How many nephrons in each kidney?

A

More than 1 million

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7
Q

What are the two main parts of the nephron?

A

Glomerulus

Tubular system

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8
Q

What is the glomerulus?

A

Specialized capillary network

Allows filtration of fluid from plasma (no cellular components or proteins)

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9
Q

Glomerular membrane vs. normal capillaries

A

100x more permeable than normal capillaries

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10
Q

Tubular system

A

Collects filtered fluid

alters composition converting plasma filtrate to urine

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11
Q

What is the normal Glomerular Filtration Rate

A

100-200 mL/min in normal adult; preserved over a broad range of blood pressures

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12
Q

What percent of the volume filtered is reabsorbed (osmotic diffusion)?

A

99%

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13
Q

How is urine output related to arterial blood pressure?

A

Linear increase in output with increase in arterial blood pressure

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14
Q

If you increase pressure 100 to 200 mmHg urine output increases by factor of what?

A

7

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15
Q

Decrease blood pressure below 50 mmHg causes what?

A

Urine output to stop

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16
Q

What allows long term control of blood pressure?

A

Urine output

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17
Q

What determines how concentrated or dilute the urine is?

A

ADH

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18
Q

ARF Risk in patients with valve surgery vs. CABG

A

Patients undergoing valve surgery twice the risk compared to CABG patients

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19
Q

What is the most significant risk factor for acute renal failure?

A

Preoperative renal dysfunction

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20
Q

How can you determine preoperative renal dysfunction?

A

Elevated serum creatinine

Decreased creatinine clearance

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21
Q

What are some other risk factors for acute renal failure?

A

Impaired cardiac function
Complexity of procedure
Advanced age
genetics

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22
Q

ARF-D develops in what percent of patients?

A

1.2 to 13% of patients post CPB

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23
Q

Intraoperative Renal Risk Factors

A 
Low flow
Decreased blood volume
IABP
Prolonged CPB times with SIRS
Inappropriate hemodilution
Emboli
Avoiding hypothermia
Pulsatility
24
Q

High Hematocrit results in

A

Decrease in microcirculatory blood flow

25
Q

Low hematocrit results in

A

Decrease in renal oxygen-carrying capacity

26
Q

What lowers organ metabolic requirements?

A

Hypothermia

27
Q

What is hte most important target in hypothermia?

A

Brain

28
Q

Stroke & Renal failure at 37C vs 34C?

A

Strokes and renal failure occured more frequently at 37C than 34C; difference not statistically significant

29
Q

What is the difference in plasma renin activity or concentration of vasopressin?

A

No difference in plasma renin activity or concentration of vasopressin 37C vs 34C

30
Q

What happened to renal clearance and other indices of renal function while on bypass with warm heart surgery?

A

Transient increase in renal clearance returned to normal after bypass; temp had no lasting effect

31
Q

Pulsatile Perfusion

A 
Some studies say it is better
others show no idfference
no studies show it is harmful
Most cases not creating "true" pulse pressure
Adds significant degree of complexity
No significant advantage
32
Q

Incidence of emboli and their associated clinical problems greatly reduced when…

A

Stopped using bubble oxygenators

Started using arterial/cardiotomy filter

33
Q

Most patients who develop post op renal failure:

A

suffer form pre-existing renal disease

Have compromised renal perfusion secondary to low CO during perioperative period

34
Q

What on bypass can cause post op renal failure ?

A

Low renal perfusion pressure while on bypass

Low renal perfusion pressure off pump caused by renal vasoconstriction during low cardiac output states

35
Q

What is the goal of any pharmacological intervention?

A

Prevent acute renal failure that requires dialysis

36
Q

Calcium Channel Antagonists

A

Nifedipine
Felodipine
Diltiazem

37
Q

Anti-inflammatory/antioxidant drugs

A

Corticosteroids
Aspirin
N-acetylcysteine

38
Q

What is an indication of renal hypoperfusion?

A

Monitor urine output with decreased output

39
Q

Oliguria

A

U/O less than 0.25-0.33 ml/kg/hr

40
Q

What is the relationship between intraoperative urine volume and post op renal dysfunction?

A

No correlation

41
Q

Decreased urine output could be result of what?

A

Kinked or obstructed catheter or stress-induced ADH

42
Q

What is the most important counter to renal hypoperfusion?

A

Maintaining adequate perfusion

43
Q

Dopamine

A

MOA: Stimulate dopamine receptors in renal vasculature; vasodilation; inhibits sodium reabsorption in proximal tubule

Dose: 0.5 ug/kg/min

Problems: Post-Op A-fib, impairment of ventilatory drive in response to hypoxemia and hypercarbia, supress circulating levels of anterior pituitary-dependent hormones; renal effect is unpredictable

Current Research: No benefit, unpredictable

44
Q

Fenoldopoam

A

Type: Synthetic benzazepine derivation

MOA: Binds selectively to DA1 receptors, causes systemic and renal vasodilation; theoretically augments RBF during CPB

Dose: 0.1 ug/kg/min
0.5 ug/kg/min

Problems: Should not be used prophylactically, further research necessary

Current ResearcH: Improvement in creatinine clearance, less renal-replacement therapy, decreased time of mechanical ventilation and ICU stay; currently no difference in ARF-D incidence

45
Q

Dopexamine

A

Type: Synthetic sympathomimetic amine

MOA: stimulates B2 and dopaminergic DA1 receptors, exerting both systemic and renovasodilatory effect

Dose: 0.5 ug/kg/kim- 2.0 ug/kg/min

Problems: Only modest improvements in creatinine clearance; role is still speculative

Current Research: Potentially inhibits SIRS due to decrease in proinflammatory cytokines by B2 and DA1 receptor stimulation

46
Q

Furosemide (Loop Diuretics)

A

MOA: inhibits active transcellular transport of Cl and Na, produce natriuresis

Problems: Higher rate of renal impairment compared to LDD; worsens outcome when treating oliguria

Current Research: reducing active transport decreases cellular oxygen demand and decreases damange to mTAL. May increase clearance of necrotic cellular debris diminishing tubular obstruction; improvement in urine flow rates but no change in overall dialysis-free survival

47
Q

Mannitol (Osmotic Diuretic)

A

MOA: “Flushing” effect of necrotic tubular debris, oxygen-free radical scavenging and improevement in meduallary blood flow reducing endothelial edema

Dose: 0.25 - 1.0 g/kg before aortic XC

Problems: Unproven as a renal protectant

Current Studies: No greater renal protection

48
Q

Natriuretic Peptides

A

MOA: Dilates afferent arterioles, increases Pgc and GFR. Inibits the tubular reabsorption of chloride and sodium, redistributes medullary BF and bloods endothelin in renal vasculature

Problems: Worse in patients with nonoliguric ARF, due to hypotension from ANP; no role in perioperative renal dysfunction

Research: Increase in dialysis-free survival only in patients with oliguric ARF.

49
Q

Calcium Channel Antagonists

A

Nifedipine
Diltiazem
Felodipine

50
Q

Nifedipine

A

Research: improved GFR, enhance vasodilating protraglandin E2, supress the vasoconstricting prostaglandin Thromboxane B2, modulate vascular sythesis of endothelin, improvements in postop renal function measured by creatinine clearance

51
Q

Felodipine

A

Type: dihydropyridine calcium channel antagonist

MOA: preferential increase in regional blood flow to ischemic regions of hte kidneys

Research: in patients with baseline serum creatinine levels less than 1.3 mg% undergoing elective CABG with CPB. IV infusion of felodipine administered during the second half of hypothermic CPB nad discontinued before rewarming. GFR and active tubular transport improved

52
Q

Diltiazem

A

Reductions in urinary microenzyme excretion

Problems: Little protection against ARF

MOA: lowers blood pressure while possibly preserving renal function

53
Q

Anti-Inflammatory/Antioxidant Drugs

A

Corticosteroids
Aspirin
N-Acetylcysteine

54
Q

Corticosteroids

A

Problem: Induced renal injury as evidenced by increase in urinary N-acetylglucosaminidase levels

Research: Suggests no benefit, potential harm due to the effects of hyperglycemia

55
Q

Aspirin

A

Normally discontinued 7-10 days before open-heart surgery to minimize perioperative hemorrhage due to platelet dysfunction.

MOA: inhibition of thromboxane, a potent renovasoconstrictor

Dose: 100 mg until day of surgery

Potentially beneficial for preserving post op renal function.

Problems: increase in postop bleeding

Research: Significantly less postop renal insufficiency in aspirin-treated group

56
Q

N-Acetylcysteine

A

MOA: Attenuating radiocontrast-induced nephropathy

Problems: should not be considered as a prophylactic renoprotective drug

Research: failed to show any benefit of therapy in at-risk patients undergoing CABG with CPB

CV Perf Tech III (16 decks)

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