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NURS 671 - Intro to Anesthesia > Fluids and electrolytes COPY > Flashcards

Fluids and electrolytes COPY Flashcards

1
Q

What are the components of total body water?

A

ICV = 2/3 (main electrolytes = potassium and phosphate)
ECV = 1/3 ( main electrolytes = Sodium and Chloride)
TBW ~ 60% of lean body mass

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2
Q

What function helps maintain resting membrane gradient?

A

Na + K + ATPase pump - transport sodium into ECV

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3
Q

What is the daily fluid volume required to maintain TBW homeostasis for a normal healthy, normothermic adult?

A

25- 35ml/kg per day or 2-3L/day

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4
Q

What components make up ECV?

A

1) plasma (1/4 of ECV)

2) Interstitial (3/4 of ECV) - composed of extravascular fluid in the tissue spaces

3) transcellular fluids - include cerebrospinal fluid, synovial, GI secretions, and intraocular fluids (Isolated from fluid dynamics –> NON functional)

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5
Q

what pressures are account for in Starling forces?

A

1) Capillary Hydrostatic pressure (Pc)
2) Interstitial oncotic pressure (TTif)
3) Interstitial fluid Hydrostatic pressure (Pif)
4) Plasma oncotic pressure (TTc)

Oncotic forces PULL fluid in/out
Hydrostatic forces PUSH fluid in/out

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6
Q

Capillary hydrostatic pressure (Pc)

A

intravascular BP = force of CO and vascular tone

**Increases capillary hydrostatic pressure and interstitial oncotic pressure –> favor FILTRATION (fluids out to interstitial space)

Pc -> pushes fluid out into interstitium this is why it favors filtration
TTif -> pull fluid into the interstitium this is why it favors filtration

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7
Q

Interstitial fluid hydrostatic pressure (Pif)

A

-Hydrostatic pressure of the interstitial space

**Increases Interstitial fluid pressure and plasma oncotic pressure –> favor ABSORPTION (fluids goes into intravascular space)

Pif -> pushes fluid into the vascular space this is why it favors absorption
TTc -> pulls fluid into the vascular space this is why it favors absorption

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8
Q

Plasma oncotic pressure (TTc)

A

-Osmotic force of colloidal proteins (i.e. albumin)

***Increases Interstitial fluid pressure and plasma oncotic pressure —> favor ABSORPTION (fluids goes into intravascular space)

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9
Q

Interstitial oncotic pressure (TTif)

A

-Osmotic force of colloidal proteins (albumin) within interstitial space

***Increases plasma hydrostatic pressure and interstitial oncotic pressure –> favor INFILTRATION (fluids out to interstitial space)

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10
Q

What factors affect fluid filtration?

A

Increased in these factors

1) Capillary hydrostatic pressure (Pc)

2) Interstitial oncotic pressure (TTif)

3) filtration coefficient

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11
Q

What factors affect fluid absorption?

A

Increased in these factors:

1) Interstitial fluid hydrostatic pressure (Pif)

2) Plasma oncotic pressure (TTc)

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12
Q

What are the effects of net filtration?

A

-Positive net filtration = Fluid exudation into the tissues
-Negative net filtration = fluid absorb into vasculature

Pif of most tissues is slightly negative

Net filtration tends to be slightly positive at the arterial end of capillaries and slightly negative at venous end

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13
Q

What is the constant fluid filter rate?

A

2ml/min

Lymphatic system carries fluids back into the interstitial space –> under euvolemic conditions, net fluid filtration ~ equal to lymphatic flow

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14
Q

What is the difference of net filtration between arterial and venous capillary beds?

A

Positive at the arterial end

Negative at the venous end

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15
Q

What is glycocalyx ?

A

-composed of a matrix of

1) glycoprotein
2) polysaccharides
3) hyaluronic acid

-Binds to ionic side chains and plasma proteins to create physiologically barrier within vascular space

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16
Q

how and why glycocalyx repel blood components?

A

-Acts a barrier that repels negative charged polar compounds and blood components -> prevent blood component adhesion to the vascular wall and augmenting LAMINAR blood flow

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17
Q

How does glycocalyx affect net infiltration?

A
  • binds to Albumin
    -preserve capillary oncotic pressure and decrease capillary permeability to water —> effects plasma hydrostatic pressure on net filtration
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18
Q

How does glycocalyx affect inflammatory processes?

A

-contain inflammatory mediators –>prevent leukocyte adhesion excepts when acute inflammation or endothelial damage occurs

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19
Q

What are other function of the glycocalyx?

A

1) scavenging of free radicals
2) binding and activation of coagulation factors
3) signal transduction that regulate local vasoactive responses to mechanical stress

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20
Q

What are the main electrolytes of ECV?

A

Sodium and Chloride

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21
Q

What are the main electrolytes of ICV?

A

Potassium and Phosphate

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22
Q

the RAAS

A

Renin is released by juxtaglomerular cells from the kidneys when hypotension and systemic sympathetic stimulation detected by baroreceptors in the atria, aorta, and carotid and renal afferent arterioles

23
Q

RAAS

A
24
Q

what is the main function of Anti Diuretic Hormone?

A

-regulate water balance!!!

-When there is an increased in serum osmolality (detected by osmoreceptors in the hypothalamus), the posterior pituitary gland release ADH

***Hypothalamus also stimulate thirst

25
Q

What is the effect of ADH on the kidney?

A

ADH causes AQUAPORIN channels within the kidney to reabsorb water –> reserve volume–> increase urine concentration and osmolality

26
Q

How does ADH help to increase BP?

A

-ADH is a potent arterial vasoconstrictor

Stimulate when detected by baroreceptors in the atria, aorta, and carotids during hypotension conditions

27
Q

What stimulate the release of Atrial Natriuretic peptide (ANP)?

A

-Stretch receptors in the atrial walls stimulate the ANP from cardiac myocytes when there is increased in preload or hypervolemic states

28
Q

How does ANP affect the Blood volume?

A

1)ANP stimulates kidney to release sodium and water –> reduce blood volume, offloading the heart

2) Produce vasoactive responses in the afferent and efferent renal arterioles to increase GFR

3) inhibit release of renin and ADH

29
Q

What happen to ANP in hypotension?

A

atrial receptors inhibit ANP

30
Q

what is the percentage of daily water fluctuation?

A

0.2% of TBW

31
Q

Why give isotonic crystalloid?

A

1) hydration of ECV
2) restoring water and electrolyte homeostasis to both intravascular and interstitial spaces

32
Q

Why give crystalloids?

A

1) restoration of vascular volume
2) preservation of flow
3) decrease in hormone-mediated vasoconstriction
4) correction of plasma hyperviscosity d/t acute hemorrhage
5) Preferred for lack of allergenic potential

33
Q

why isotonic crystalloids are disadvantage?

A

-Evenly distributed –> expand plasma volume is transient
-low molecular weight –>hemodilution of plasma proteins and loss of capillary oncotic pressure —> 75-80% volumes goes into interstitial space

34
Q

What patients population are preferrable options using NS?

A

-0.9% saline is the least physiologic
-0.9% saline is preferred for patients at risk for cerebral edema
-NS is preferred for patients with anuria, and ESRD (NS does not have potassium)

  • NS contains equal parts of sodium and chloride = isotonic crystalloid
35
Q

What acid-base imbalance will occur when 0.9% NS for fluid resuscitation?

A

-Hyperchloremic metabolic acidosis

36
Q

What are the negative effects of hyperchloremia?

A

1) decreased GFR (due to increased reabsorption of chloride on renal arteriolar vascular resistance)

2) impair renal regulation of bicarbonate

3) causes increased in salt and water retention –> hemodilution –> interstitial edema

37
Q

when to use hypertonic solutions?

A

-Trauma/head injured patients –> promot volume expansion that draw fluids back into the intravascular space –> reduce intracranial HTN

38
Q

Risks when using hypertonic solutions

A

-vascular irritation
-sudden fluid shift into intravascular space –>dehydration of neural cells –> osmotic demyelination syndrome

39
Q

Why LR is not good for Diabetic patients?

A

LR contains sodium lactate as the buffer agent –> gluconeogenesis in diabetic patients due to byproduct metabolism of lactate

40
Q

Is LR hypo or hyperosmolar?

A

HyPOosmolar - Osmolality is 273 mosmol/L
-NO GOOD for TBI, can lead to CEREBRAL EDEMA
-contains potassium - not good for ESRD patients
-contains calcium - not good for blood products (has citrate in blood to prevent clotting)
-contains lactate - don’t give LR in patients with DM –lactate metabolism lead to gluconeogenesis
-LR large infusion can lead to metabolic alkalosis d/t lactate metabolism

41
Q

Is NS hypo or hyperosmolar?

A

HyPERosmolar
-Osmolality 308 mosmol/L
- good for patient who are at risk for cerebral edema

42
Q

Why use hypertonic 3%?

A

Hyperosmolality
- Good for trauma and TBI
-promote volume expansion that draw fluids back into intravascular space –> reduce swelling in the brain

**RISK for dehydration of neural cells –> osmotic demyelination syndrome

43
Q

What are colloids?

A

-high molecular weight
-expands plasma volume by increasing plasma oncotic pressure, decreased transcapillary filtration

E.g: RBCs and albuim

Classified by weight, concentration, and half life

44
Q

Why Dextran is not available in US?

A

-Derived from bacterial metabolism of sucrose
-cause AKI d/t hyperosmolar accumulation
-Coagulopathy effects d/t impaired vWF, activation of plasminogen, interference with platelet aggregation

-Dextran binds to platelet, RBCs –> interfere with cross-match, induce anaphylaxis

45
Q

why hydroxyethel starches (HES) has Black Box warning?

A

Made from starchy plants
-induce anaphylaxis
-difficult to metabolize
-prolonged plasma expansion
-Risk of AKI, dialysis requirements, coagulopathy, sepsis, increased mortality up to 90 days after HES administration

46
Q

When to give Albumin?

A

-Albumin is a rapid volume expander-colloid
-Albumin preserve renal perfusion in septic shocks and preserve integrity of glycocalyx in early sepsis

47
Q

Why Albumin is not the best option for fluid?

A

-Risk for anaphylaxis or immune response
-Costly
-Carrier for many protein bond ionic substances –> increased plasma osmolality, increased volume–> Donnan effect, can lead to mortality in neurotrauma

**Hyperglycemia and sepsis damage glycocalyx barrier –> albumin leaks to the interstitial space –> pulmonary edema and end organ complications

48
Q

How does surgical stimulation affect metabolic response?

A

1)Surgical incision/stress/surgery –> Stimulation of somatic and autonomic afferent nerves –> Hypothalamic pituitary axis (HPA) activated–> hypothalamus releases corticotropin-releasing hormone–> anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH) –> cortisol is created and released from adrenal cortex
2)Cortisol stimulates protein catabolism, hepatic gluconeogenesis, glucogenolysis, increased hepatic release of plasma proteins –> increased plasma oncotic pressure to preserve plasma volume, provide cellular energy in time of increased metabolic demand (surgery) –> hyperglycemia
3) SNS stimulation –> release of ADH, vasoconstriction, reabsorption of water and potassium excretion
4) Endothelial release cytokines –> hyperthermia, increased O2 demans, regional alteration in microvascular flow

49
Q

What effect do cytokines have ?

A

High cytokines :(= vasodilation, endothelial damage, increased filtration–> tissue edam, insulin resistance, intravascular loss, hypotension –> decreased organ perfusion

50
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51
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52
Q
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53
Q

Why 0.9% can cause acid-base imbalance?

A
  • Plasma concentration of sodium is higher than chloride
    -Using 0.9% NS as fluids resuscitation –> hyperchloremic state –> Metabolic acidosis

NURS 671 - Intro to Anesthesia (8 decks)

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