Fluids & Monitoring Flashcards
Extracellular ⅓ 20%
sodium, ca, chloride, hco3
Intracellular ⅔ 40%
potassium phosphate and magnesium
Extracellular compartments are composed of
80% interstitial fluid 11L
20% plasma 3L
Hormone system that regulates blood pressure & fluid balance
RAAS
effect of aldosterone from adrenals in RAAS
causes kidneys to reabsorb Na and H2O
how RAAS regulates BP
Hypotension
Increased tubular chloride
Sympathetic stimulation
posterior pituitary releases
ADH
ADH effect on V1 and V2
V1: vasoconstriction
V2: decrease UO by causing reabsorption in distal tubules.
PH of 3 cryalloids
NS: 5.5
LR: 6.5
Plasmalyte: 7.5
The oSMolality of 3 crystalloids
Standard: 280-295
NaCl: 310
LR: 275
Plasmalyte: 298
benefits of LR
helps maintain electrical neutrality
Contraindications of LR (mildly hypotonic)
TBI, neurovascular insult (cerebral edema), blood transfusion,
Theoretical insult to renal patients due to lactate to bicarb
Plamalyte effect on renal function
the most isotonic. preserve pH and renal perfusion best.
compatible with blood
What is a colloid
High MW molecules in electrolytes solution. doesn’t pass intact glycocalyx (hyperglycemia)
Dextrans side effects
1 renal failure
2 impairs vWF and plt aggregation
3 no longer used in clinical practice.
Albumin in endothelial injuries
Pulmonary edema in patients with hyperglycemia/diabetics
How does anesthesia impact MV flow and organ perfusion?
- Opioid and dex decrease HPA stress response
- Neuralaxia anesthesia decreases SNS stim
3 Goal-directed fluid therapy (GDFT)
- supports O2 balance
- suports neuroendocrine response
- euvolemia preserves glycocalyx and MV flow
What activates HPA
autonomic and somatic stimulation
CNS activation causes the release of hormones
corticotropin-releasing hormone –>
anterior pituitary releases ACTH –>
cortisol from adrenals –> increase energy
sympathetic stimulation release of catecholamines from adrenals
increase SVR, HR, MV vasoconstriction = increased metabolic rate and O2 consumption
Tissue injury causes the endothelium to release
cytokines and inflammatory cells = hyperthermia, increase O2 demand, alters MV circulation
Prolonged tissue injury may cause
vasodilation, endothelial damage, edema, insulin resistance, vascular loss, hypotension, DECREASED ORGAN PERFUSION
angiotensin 2 causes:
- vessel vasoconstriction
- kidneys reabsorb NaCl and H2O
ANP pathway
atrial stretch –>
ANP release by cardiac myocytes –>
increase GFR –>
drop renin and ADH release –>
increase UO
Hydrostatic vs oNCotic pressure
Starling Forces –> dilute blood stops Na reabsoption
blood flow through capillaries depends on 4 things
1 BP in capillaries
2 hydrostatic pressure in interstitium
3 oncotic pressure
4 subglycocalyx
Atrial Natriuretic Peptide
Released by atrium in response to increased stretch
advantages of crystalloid
replacement ratio 3:1
Expands the ECF
Restores 3rd space loss
disadvantages of crystalloid
–>Limited ability to expand plasma volume (lasts 20-30min)
–>edema
–> Large volume of NaCL –> hyperchloremic metabbolic acidosis
–>dilutes albumin (decrease cap onc pressure)
–>dilutes coags
Colloid Advanatges
replacement 1:1
increases plasma vol 3-6 hours
small vol
less edema
anti-inflammatory
dextran 40 decreases blood viscosity & improves microcirculatory flow in vascular surgery
Dextran
no longer used in clinical practice due to renal failure, impairing vWF and platelet aggregation
females
45 % solids, 55% fluids
males
40% solids 60% fluids
Fluid exchange between extracellular compartments is dependent on
Starling Forces
daily fluid volume required to maintain TBW
25-35 ml/kg per day
intravasuclar blood pressure driven by CO and impacted by vascular tone
capaillary hydrostatic pressure Pc
hydrostatic pressure of the interstitial space
interstital fluid pressure Pif
osmotic force of
colloidal proteins within the vascular space
plasma oncotic pressure
3 effects of RAAS system
1 ADH release from posterior pituitary
2 Aldosterone release adrenal cortex
3 Renal efferent arteriolar vasoconstriction increases GFR
Atrial Natriuretic Peptide
Released by atrium in response to increased stretch
5 effects of ANP
1 Increase GFR (Kidneys release Na and Water)
2 Systemic vasodilation
3 Inhibit renin release
4 Opposed production & action of angiotensin 2
5 Decreases aldosterone secretion
Historical Fluid Management 4 Steps
- 4 2 1 rule
- NPO time hours x maintenance rate
- surgical loss
- Blood Loss
HPA –> cortiocoreleasing hormone –>
–> ant pit releases ACTH –> cortisol from adrenals
4 effects of cortisol from adrenals
- protein breakdown
- hepatic release of glucose
- Glycogenolysis
- anti-inflammatory
ultimately increase energy levels and preserve intravascular volume
Increase catecholamine from adrenal medulla –>
Increased HR, SVR, and microcirculatory vasoconstriction (bad). Causes increased metabolic rate and O2 consumption
Anesthetic Considerations of GDFT
dex/opiods/neuralaxia supports O2 balance, neuroendocrine response, and euvolemia preserves glycocalyx and MV flow
CI <2.5 after 250cc bolus
inotrope