� Summary
� Composition
� Ionic effects
� Fluid effects
� Metabolic effects
� Cardiovascular effects
� Neuroendocrine effects
� Metabolic effects
� Significant initial plasma expansion, subsequent distribution to ISF > plasma > ICF
� Distribution and excretion may depend upon hydration status
� Multi-system response restores plasma volume to normal
� Causes less electrolyte derangement than normal saline
|
Concentration in Hartmann�s (mM) |
Concentration in plasma (mM) |
Na+ |
131 |
140 |
Cl- |
111 |
100 |
HCO3- |
29 (as lactate) |
24 |
K+ |
5 |
4 |
Ca2+ |
2 |
2 |
Osmolality |
278 |
290 |
Oncotic pressure |
0 |
25 |
pH |
5-7 |
7.4 |
|
Distribution |
Effect |
Cause |
Na+ |
ECF |
Mild ↓[Na+] |
Active membrane transport (Na+K+ATPase) |
Cl- |
ECF |
Mild ↑Cl- |
Preservation of electrical neutrality |
K+ |
ICF |
Mild ↓ |
↑Distal nephron flow -> ↑Activity ENaC and ROMK -> ↑K+ excretion Active membrane transport (Na+K+ATPase) |
Ca2+ |
ECF |
↔ |
Active membrane transport (ATPases, exchangers) |
HCO3- |
ECF=ICF |
↔ |
- |
Immediate distribution |
� Entire 2L into plasma � t1/2α ~5 minutes � i.e. immediate distribution |
Steady state distribution |
� 479mL in plasma (10% ↑ volume) � 1438mL in ISF (14% ↑ volume) � 83mL in ICF (minimal %↑ volume) |
Excretion |
� Glomerulotubular imbalance o ↓Oncotic pressure -> ↑GFR + ↓prox tubule reabsorption -> ↑urine flow rate � Pressure diuresis o ↑mAP -> ↑urine output (? mechanism) � Hormonal response � ↓ADH � ↓RAAS � ↑ANP (Note excretion of both water and Na+ is faster than for normal saline) |
Energy |
� 58mmol lactate -> 29mmol glucose = 5g � i.e. minimal nutritive effect |
Acid-base |
� Metabolic alkalosis (wins) o 58mmol lactate infused -> 58mM H+ consumed o Lactate + H+ -> CO2 + H2O o 58mmol lactate infused -> 58mmol H+ consumed (≈ 58mmol HCO3- produced) � Metabolic acidosis (loses) o ↑[Cl-] -> ↓strong ion difference -> ↑dissociation of H2O -> ↑[H+] |
Temperature |
� Effect: ↓core temp and skin temp (? >1�C) � Response: vasoconstriction, shivering, heat conservation behaviour |
Osmolality |
� ↓2mM -> ↓<1% -> no response (ADH sensitivity ∆2%) |
Direct effects |
� ↑Blood volume -> distension of capacitance vessels -> ↑MSFP -> ↑venous return -> ↑preload -> ↑cardiac output � Minimal change in the healthy, euvolaemic subject when infused over 1h |
Response |
� Low pressure baroreceptors o ↑CVP -> ↑stretch -> ↑afferents to NTS -> ↓SNS output, ↑PSNS output, ↓HR, ↓contractility, vasodilatation � High pressure baroreceptors o Minimal ↑mAP -> minimal effect |
RAAS |
� ↑mAP -> ↑renal baroreceptor stretch -> ↓renin release -> ↓angiotensin 2 � Vasodilatation � ↓Na+/H+/H2O reabsorption from proximal tubule |
ADH |
� ↑Venoatrial stretch -> ↓ADH release (sensitivity ~∆10%) � Vasodilatation � AQP2 downregulation -> ↓H2O reabsorption from collecting ducts � Ureaporin downregulation -> ↓medullary interstitial osmolality -> ↓H2O reabsorption |
ANP |
� ↑CVP -> ↑venoatrial stretch -> ↑ANP release � Dilatation of afferent arterioles -> ↑GFR, ↑vasa recta flow, washout of medullary interstitium � Inhibit NCC in distal tubule -> ↓Na+Cl- reabsorption � Inhibit ENaC in collecting ducts -> ↓Na+ reabsorption |
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