Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FNA > Fluids and electrolytes > Flashcards

Fluids and electrolytes Flashcards

1
Q

What are the components of total body water?

A

ICV = 2/3 (main electrolytes = potassium, magnesium, and phosphate)
ECV = 1/3 ( main electrolytes = Sodium, calcium, bicarb, and Chloride)
TBW ~ 60% of lean body mass ~60L (if patient wt 100kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What function helps maintain resting membrane gradient?

A

Na + K + ATPase pump - transport sodium into ECV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What components make up ECV?

A

1) plasma (1/4 of ECV = 5L)

2) Interstitial (3/4 of ECV = 15L) - 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What factors affect fluid absorption?

A

Increased in these factors:

1) Interstitial fluid hydrostatic pressure (Pif)

2) Plasma oncotic pressure (TTc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does glycocalyx affect inflammatory processes?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the main electrolytes of ECV?

A

Sodium and Chloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the main electrolytes of ICV?

A

Potassium and Phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

RAAS

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happen to ANP in hypotension?

A

atrial receptors inhibit ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the percentage of daily water fluctuation?

A

0.2% of TBW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why give isotonic crystalloid?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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
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

**Albumin binds to calcium –> hypocalcemia

**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
Q

What effects do Cortisol have?

A

-Anti-inflammatory effect by inhibiting production, release, vascular aggregation of inflammatory mediators

51
Q

What occurs when patient is hypovolemic?

A
  • Decreased plasma hydrostatic pressure –> favor absorption –> fluids move from interstitial into intravascular space
52
Q

What are the disadvantages of Laparoscopic surgery?

A

1)pneumoperitoneum causes mechanical SPLANCHNIC ischemia –> GI epithelium ischemia, during insufflation >12-15mmHg –> vagal response, increased CVP d/t shunting blood from splanchnic circulation into the thorax –> ANP release

2)Increased abdominal pressure –> decreased preload by decreased venous return, increased pressure compress IVC, which leads to increased preload, increased SVR–> increased MAP, DECREASED SV

53
Q

What affects do laparoscopic surgery have on hemodynamics?

A

1) Increased CVP
2) Decreased preload/venous return
3)Decreased SV
4) increased preload
5) increased SVR
6) increased MAP

54
Q

What are the appropriate anesthesia considerations for laparoscopic surgery?

A

1) Opioid
2) Dexmedetomidine
3) neuraxial anesthesia

**All of these tx to reduce HPA response

55
Q

how to calculate fluid deficit for 3rd spacing?

A

THERE IS NO 3rd space!!!!

56
Q

what is the recommended fluid replacement ratio?

A

Crystalloid: blood loss 3:1 evidence show 2:1

57
Q

How to calculate IVF maintenace rate?

A

4:2:1 (restrictive)
1-4 ml/kg/hr (liberal)

E.g: pt wt 80kg, with restrictive plan

1st 10kg (out of 80kg) x 4 = 40
2nd 10 kg (of 80kg) x 2 = 20
(80kg-20kg) = 60 kg x 1 = 60

40+ 20+ 60 = 120ml/hr (IVF rate)

or quick way is to add pt’s wt with 40
80+40 = 120ml

58
Q

How does Frank-Starling Curve apply to fluid replacement plan?

A
  • it is the relationship between LVEDV + SV (or myocardial contractility)
    -with bolus IVF–> increased in LV preload –> increased in SV–> stretch cardiac sarcomeres to compensate for increased in preload (only effective until sarcomeres cannot compensate anymore)
59
Q

How to interpret the Flank-Starling Curve?

A

The ascending curve (left side) = preload dependence, favor more fluid bolus

The plateau = preload independence, does not respond to more fluid

60
Q

what elements affect post-op outcomes according ERAS?

A

1) fluid therapy
2) pain management

61
Q

How does sodium or solutes affect brain tissue?

A

-BBB has limited permeability to ionic solutes (sodium) –> important to maintain balance of concentration of plasma sodium in relation to water content in brain tissue

62
Q

What component transport sodium across the cell membrane?

A

Na-K-ATPase pump that requires energy (ATP)

63
Q

why is hyponatremia is bad?

A

-Causes cerebral edema (fluids shift from plasma to cells)

64
Q

Who is at risk for hyponatremia?

A

Na <130 mEq/L
1)Menstruating women are increased risk of brain damage due to hyponatremia d/t estrogen and progesterone inhibiting Na-K-ATPase pump
2) facilitate water into the brain due to ADH

65
Q

What are the treatments for hyponatremia?

A

1) fluid restriction
2) diuresis
3) IV convivaptan or PO tolvaptan

66
Q

What is the concern of correcting sodium?

A

Correct slowly, no more than 1-2 mEq/L/hr or no more than 10 - 15 mmol/L in 24hours

**Rapid correction –> osmotic demyelination

67
Q

How to treat hypernatremia?

A

Na> 145
for ACUTE hypernatremia: hypotonic solutions
for CHRONIC hypernatremia: isotonic solution

**slow correction, no more than 1-2mEq/hr

68
Q

What is the normal concentration of sodium?

A

ECV = 140 mEq/L

ICV = 25mEq/L

69
Q

What effect does potassium have?

A

Responsible for:
1) resting membrane potential
2) K is absorb in GI tract
3) K is excreted and reabsorb into renal tubules

70
Q

What is the normal concentration of potassium?

A

ECV = 3.5-5.0 mEq/L

ICV = 150-160 mEq/L

71
Q

Who is most at risk for hypokalemia?

A
  • patients on Thiazide (11 times more likely)
  • Men
72
Q

What the common cause of hypokalemia?

A

1) Renal losses: diuresis, steroid, metabolic ACIDOSIS, hyperaldosteronism (increased aldosterone–> increased K excretion), DM KETOacidosis, alcohol

2) Increased nonrenal losses: sweating, diarrhea, vomiting, laxative use

3) Decreased intake: Ethanol, malnutrition

4) HYPERVENTILATION, metabolic alkalosis, drugs (albuterol)

5) Cushing disease, Bartter syndrome, insulin

73
Q

What are the causes of hypertonic hypernatremia?

A

Serum osmolality >300 mOsm/kg

Causes
1) hyperglycemia
2) mannitol excess glycerol therapy

74
Q

What are the sx of hyponatremia?

A

N/V
Cramps
Weakness
Confusion
Agitation
Headache
Anorexia
Cerebral edema
Seizures
Coma

75
Q

What will EKG look like with hypokalemia?

A

1) prolonged QT
2) ST depression
3) U wave
4) flat T wave

76
Q

what s/sx of hypokalemia?

A

K < 3.5: palpitation, skeletal weakness, muscle pain

K< 2.5: paresthesia, decreased deep tendon reflexes, fasciculations, muscle weakness, decreased LOC, dysrhythmias (AVBs, VF, asystole)

77
Q

what are the causes of hyperkalemia?

A

-Impaired renal excretion
-high intake of K
-shift of K from ICV to ECV (Insulin deficiency)
-Hypoaldoesteronism
-Addison disease
-Drugs: ACEIs, ARBs, BBs (reduced angiotensin and renin –> reduced aldosterone–> hypocalcemia and hyPERkalemia)
-Succinylcholine
- Digoxin
*take away point: reduced Aldoesterone leads to HYPERkalemia and hypocalcemia

78
Q

How does hyperkalemia affects ECG?

A

1)Peaked T wave
2)P wave flatten
3)PR prolongation
4)QRS prolongation
5) QRS degrades to sine wave –> VF–> asystole

79
Q

Treatments for hyperkalemia

A

Loss of P wave and widening QRS

1) IV calcium - 10ml of calcium chloride over 10 mins
Onset 1-3mins
Duration: 30-60mins
(calcium chloride yields 27mg/ml)
or

10ml of calcium gluconate over 3-5 mins —-onset 1-3 mins
Duration: 30-60mins
(calcium gluconate yields 9mg/ml of ionized calcium)

**MOA: membrane stabilzation

2) IV of sodium bicarb 50-100mEq over 10-20mins
Onset 5-10 mins
Duration 1-2hrs

MOA: shift potassium intracellularly

80
Q

With Peaked T wave due to hyperkalemia, how to treat?

A

1) Glucose and insulin infusion:
IV 50ml of D5W and 5 units of regular insulin
On set 30 mins
Duration 4-6hrs

MOA- shift potassium intracellularly

2) Dialysis

81
Q

Treatments for hyperkalemia without ECG changes

A

1) potassium binding resins in the GI
onset: 1-2 hr
duration: 4-6 hr
MOA - GI excretion

2) Promotion of renal excretion diuretics —LASIX
on set: 15-30mins
duration 2-3hours

MOA: renal excretion

FNA (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions