Fluids, Electrolytes and Shock
Tom Archer, MD, MBA
UCSD Anesthesia
Outline
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Three fluid compartments (ICF, ISF, IVF)
Three membranes
Osmosis– theory and clinical
Shock-- tissue needs and cardiac output
Water and electrolytes in general (3
overlapping systems)
• Hyponatremia– appropriate and
inappropriate secretion of ADH
• Hypernatremia and K+ disorders
Three fluid compartments
Intracellular fluid (ICF)
Interstitial fluid (ISF)
Intravascular fluid (IVF)
Fractions to remember:
2/3, 2/3, 3/4
• TBW (42 L) = 2/3 of body weight (70 kg).
• ICF (28 L) = 2/3 of TBW.
• ECF (14 L) = 1/3 of TBW.
• Interstitial fluid (ISF, 10.5 L) = ¾ of ECF
• Intravascular fluid (IVF, 3.5 L) = ¼ of ECF.
Three membranes
Cell membrane
Non- brain capillary endothelium
Brain capillary endothelium (“bloodbrain barrier– BBB”)
Solutes
Ions: Na+ , Cl-, K+, PO4--Sugars: glucose, mannitol
Large molecules (colloids): albumin,
hetastarch
Two types of membranes
• Non-brain capillary endothelium is
permeable to everything but colloid,
therefore, only colloid is osmotically active
at non-brain capillary membrane.
Two types of membranes
• Cell membrane and healthy BBB are only
permeable to water, therefore, all ions,
sugars and large molecules are
osmotically active at cell membrane and
BBB.
Blood-brain barrier
• Behaves just like the cell membrane– a
tight, lipid rich membrane which is
impermeable to everything but water (and
lipophilic drugs).
Osmosis
• What is osmosis?
• Answer: diffusion of water down its
concentration gradient.
For all osmosis questions:
• What is the solute?
• What is the membrane?
• Is the membrane permeable to the solute?
• If not, solute will "pull" water across the
membrane.
Clinical examples
of osmotic effects
• Brain trauma: mannitol to shrink normal brain to make room
for mass lesion.
• Brain trauma or blood loss: Hypertonic saline to shrink
normal brain or expand ISF and IVF.
• Hyperglycemia causes osmotic diuresis and hypovolemia.
• Hyperglycemia causes brain dehydration (with potential for
cerebral edema with rapid correction of hyperglycemia).
Multi-modal approach to cerebral protection
/ resuscitation after TBI:
Monitoring
Normovolemia
Avoid hyperglycemia and hyperthermia
Seizure prophylaxis
Artificial ventilation, oxygenation
ICP monitoring
Sedation, analgesia, posture, paralysis
PaCO2 management
Osmotic Rx (serum mOsm = 320)
Furosemide
Hyperventilation
Barbiturate coma
Surgical decompression
Edema vs. Osmotic effects
• Edema can be purely hydrostatic (6 hours
head down during surgery)
• Edema can be d/t low oncotic pressure
(hypoalbuminemia in cirrhosis)
• Can be due to both factors.
Intravenous fluids
• “Crystalloids”
– Normal saline (just NaCl).
– Lactated ringers
– Plasmalyte
– Normosol
– Last 3 have K+ and other stuff (acetate,
Mg++, etc.)
Practical aspects
• Crystalloids enter entire ECF: ISF (3/4 of
ECF) and IVF (1/4 of ECF).
• 3 or 4:1 for replacement of blood loss with
crystalloid
• Colloids only enter IVF (in short term– 16
hour half-time for entrance into ISF)
• 1:1 replacement of blood loss with colloid
Homeostatic systems for water,
electrolytes and circulation
• Renin-angiotensin-aldosterone system (RAAS)
• Osmoreceptors, thirst, ADH (V1 vasocon and V2 tubular)
• Sympathetic nervous system
• Aortic, carotid, atrial and ventricular stretch receptors-Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide
(BNP), vasogenic intestinal peptide… and others.
• Kidney (glomerulus, tubules, collecting duct, glomerulotubular balance, macula densa).
Colson P Anesth and Analg 1999
Fast and slow components of fluid
volume homeostasis.
• RAAS: angiotensin II is fast / aldosterone is
slow.
• ADH (“arginine vasopressin”): ADH in high
concentration is immediate vasopressor on V1
receptor.
• ADH in low concentration retains free water
(slowly) in collecting duct via V2 stimulation.
Schrier RW The American Journal of Medicine (2006) Vol 119 (7A), S47–S53
Juan A. Oliver and Donald W. Landry Curr Opin Crit Care 13:376–382. 2007
Lippincott Williams & Wilkins.
“Syndrome of Inappropriate ADH”
A Garbage Term?
• Seen in neurological disease or injury.
• Seen in pulmonary disease (tumors, TB, etc.)
• ADH release by pain, stress, opioids and nausea
is also “inappropriate.”
• Excessive and counter-productive ADH release
in CHF and cirrhosis is also “inappropriate.”
Big picture– Shock (1)
• Inadequate circulation and supply of nutrients to
tissues– either at the macro or micro level.
• Intravascular volume loss (hemorrhage, burns,
GI losses). Preload problem.
• Cardiogenic (pump failure).
• Spinal cord transection / anaphylaxis. Preload
and afterload problems.
• Microcirculatory failure by RBC sludging, stasis
or microcirculatory coagulation (sepsis, DIC).
Causes of shock
• Preload (How do we judge preload? CVP?,
PAOP?, LVEDP?, LVEDV?, SPV?, PPV?, SVV?)
• Pump (contractility, dP/dT)
• Afterload (SVR)
• Microcirculatory (endothelial) failure (sepsis, preeclampsia, DIC, ARDS, hyperglycemia, etc.)
Obesity, hyperglycemia, sepsis and pre-eclampsia all “activate”
(damage) endothelium, white cells and platelets, leading to
white cell adhesion and infiltration, thrombosis and edema
(inflammation).
WBC
WBC
Platelet
Obesity, hyperglycemia,
sepsis or pre-eclampsia
Platelets
Protein (edema)
Archer TL 2006 unpublished
Big picture– Shock (2)
• Hemodynamic manipulations of HR, SV, SVR,
preload, afterload, contractility, etc. may provide
limited help to microcirculation deranged by sepsis
(for example).
• Hemodynamic manipulations may simply “buy us
time” and support patient while we treat the
underlying cause of the shock.
• Endothelium must heal!
Different recipes
for optimizing
macrocirculation
in sepsis.
“Early goaldirected therapy
of septic shock.”
Rivers E et al
N Engl J Med,
Vol. 345, No. 19
·
November 8,
2001
Like the giant plant in “Little Shop of Horrors”, body tissues say,
“Feed me!”
“Feed me!”
Arteriole
Capillary
Hungry tissue says, “Feed me!”
to pre-capillary sphincter.
Case #1
“The patient is overloaded…”
“The patient is dry…”
• 24 yo male, previously healthy, 4 days s/p GSW
abdomen with shock, peritonitis, sepsis,
hypotension. Controlled ventilation. BP = 90/60,
HR = 130.
• Weight gain 4 kg since admission.
• Albumin = 1.9. BUN / creat = 48 / 1.9.
• PAOP = 5 mm Hg.
• Systolic pressure variation: 18%
Is the patient “dry”?
Systolic pressure variation
(together with pulse pressure
variation and stroke volume
variation) are new “dynamic”
indices of whether or not the
cardiac output will increase with a
volume bolus.
Michard F, Anesthesiology 2005; 103:419–28
Is the patient “dry”?
Positive pressure
ventilation sequentially
(1-2-3) reduces vena
cava blood flow, PA blood
flow and arterial pressure.
Michard F, Anesthesiology 2005; 103:419–28
Case #1
“The patient is overloaded…”
“The patient is dry…”
• Patient has low INTRAVASCULAR
volume, but also has excessive
INTERSTITIAL fluid (edema).
• This is totally consistent with the “leaky
capillary” picture of sepsis.
• Systolic pressure variation >13% suggests
fluid bolus will increase CO. CO is “fluid
responsive”.
The Three Hyponatremias
• Isotonic (proteins or lipids dilute Na+ on bulk
basis). Often called “artifactual.” “Watery” portion
of serum has normal tonicity.
• Hypertonic (osmotic agent “sucks” water out of
ICF, diluting Na+, but tonicity stays high).
• Hypotonic. By far the most common (and
hardest to understand).
Isotonic hyponatremia
• Hyperproteinemia or hyperlipidemia dilutes
out the Na+. [Na+] in the water portion of
the blood is normal.
• Glycine solution with TURP.
• Treatment is to work up and treat
underlying cause
Isotonic hyponatremia (“artifactual”). Protein or lipid takes up some of
the plasma volume. Aqueous “portion” of plasma has normal [NaCl].
Protein or lipid “phase”
[NaCl] = 0
Aqueous “phase”
Serum
(combined)
[NaCl] = 135
[NaCl] = 123
Osmolarity (tonicity)
normal
Hypertonic Hyponatremia-- causes
• Due to hyperglycemia, mannitol or
glycerol.
• Decreased [Na+] in serum, but osmolality
is high (>290), due to sugar in the blood.
• Sugar has “sucked” water out of cells, into
the ECF. Water dilutes Na+.
Hypertonic hyponatremia– osmotically active sugar “draws” water into
vascular space, diluting NaCl, but increasing overall osmolarity (tonicity).
Glucose,
mannitol,
glycerol
[NaCl] =
140
[NaCl] =
123
Osmolarity (tonicity)
increased
Water in ICF and
interstitial ECF
Hypertonic Hyponatremia-- Rx
• Insulin to slowly reduce blood glucose.
• NS volume replacement.
• Complications of rapid reduction of serum
glucose and tonicity: hypoglycemia,
cerebral edema
Four causes of increased ADH
• Normal osmotic ADH release: osmoreceptors in hypothalamus release
ADH via posterior pituitary in response to serum mOsm > 290. Makes
physiological sense.
Stress-related ADH release (pain, nausea, opioids, running a marathon).
• Non-osmotic increased ADH (in hypovolemia):
– “Defense of intravascular volume”-- severe volume contraction. Makes
physiological sense.
– Diuretics, GI losses, burns, hemorrhage, sweating, adrenal insufficiency.
• Non-osmotic increased ADH (causing hypervolemia):
– Pathological states (CHF, cirrhosis, pulmonary, CNS). These are
classically called “SIADH”.
All these conditions are associated with increased ADH
secretion.
Achinger, Moritz, and Ayus • Dysnatremias: Why Are Patients Still Dying?
Southern Medical Journal • Volume 99, Number 4, April 2006
Hypotonic hyponatremia– too much
free water compared to NaCl.
(Volume deficit with non-osmotic
ADH release, or CHF, cirrhosis or
SIADH)
NaCl
Free water
ADH
NaCl
Osmolarity
(tonicity)
decreased
Stress- induced, non-osmotic
ADH release:
• This is why we DON’T give D51/4NS in surgery.
• This is why we DO give NS, Normosol or LR.
• We don’t give free water because of kidney’s
reduced ability to excrete it (due to non-osmotic
ADH release).
Hypotonic, Hypovolemic
Hyponatremia-- Rx
• Volume restoration with NS if hypovolemic (GI
losses, diuretics).
• Explanation: Severe hypovolemia causes nonosmotic ADH release. Body tries to “defend
intravascular volume” by secreting ADH.
• Volume restoration suppresses non-osmotic
ADH release and cures hyponatremia by
allowing free water excretion.
Hypotonic, Hypervolemic
Hyponatremia-- Rx
• Fluid restriction if hypervolemic (CHF, liver
failure).
• Diuretics (causing Na+ and water loss) are
currently used for ECF overload. We want to get
rid of water, but we get rid of Na+ as well.
• Emerging Rx: “Aquaretics” are ADH V2 receptor
antagonists which prevent inappropriate free
water retention in CHF or cirrhosis.
Courtesy Dr. Jaydeep Shah
Case #2:
Perioperative hyponatremia
• 34 yo female, no significant past medical history.
• Elective L/S BTL 0900. During the surgery, D5 ¼ NS at 125 cc/ hr.
• Pt in PACU until afternoon. “Too sedated to go home.” Got IV
meperidine. No PO intake, IV D5 1/4 NS continued.
• 2:45 AM next day, pt. C/O headache, verbal order for Tylenol #3.
• At 9:00 AM, nurse tells surgeon of a sodium of 127 mEq/L. No
• new orders, IV fluids were continued.
• At 1:30 pm, pt. lethargic and pain medications, pain meds held.
• At 3:30 pm, she had sz and respiratory failure. The patient intubated
and ventilated. Serum sodium 122 mEq/L.
Achinger, Moritz, and Ayus • Dysnatremias: Why Are Patients Still Dying?
Southern Medical Journal • Volume 99, Number 4, April 2006
Case #2:
Perioperative hyponatremia
Stress, pain, nausea all cause increased ADH
secretion from posterior pituitary.
Free water administration with D5 1/4NS allows
free water retention.
Biggest danger in children, menstruating
females and patients having suffered hypoxic
episodes.
Achinger, Moritz, and Ayus • Dysnatremias: Why Are Patients Still Dying?
Southern Medical Journal • Volume 99, Number 4, April 2006
How aggressively do we Rx
hyponatremic encephalopathy?
• Depends on symptoms, not the [Na++].
• In symptomatic hyponatremic
encephalopathy, use 3% saline until sx
improve.
Case #3
Hyponatremic encephalopathy
• 31 yo female collapses 30 min after
running marathon. Disoriented and SOB.
• Crackles in all lung fields. CXR
pulmonary edema. [Na+] = 126 mEq / L.
• What is going on?
Case #3
Hyponatremic encephalopathy
• Patient had been told to “drink as much water as
possible to prevent dehydration.”
• Increased ADH with stress + free water leads to
hyponatremia.
• Pulmonary edema d/t cerebral edema.
• Rx is 3% saline both encephalopahy and pulmonary
edema resolved.
• Sports drinks are hypotonic. Athletes need to drink only
when thirsty.
Case #4
Hyponatremic encephalopathy
• 72 yo male in nursing home. S/P
neurogenic bladder followed by TURP.
• On nasal DDAVP HS to avoid
incontinence at night. [Na+] = 139 mEq / L.
• Staff requests increased DDAVP to BID, to
prevent incontinence during PT.
Case #4
Hyponatremic encephalopathy
• Two days later patient becomes
incoherent and lethargic.
• [Na+] = 108 mEq / L.
• What is going on?
• What should we do?
Case #4
Hyponatremic encephalopathy
• 3% saline given until sx improved at [Na+] = 122
mEq / L, then stopped. DDAVP was stopped.
• Patient diuresed promptly with a rapid rise in
serum [Na+].
• “Best management would have been to continue
DDAVP and restrict fluid to prevent excessively
rapid correction.”
• Get a consult!
Case #5
Hyponatremic encephalopathy
• 69 yo female for screening colonoscopy.
• Oral polyethylene glycol bowel prep the day
before (Go-lytely)
• Pt. gets nauseated and vomits repeatedly
along with having diarrhea. Gets HA.
• Husband finds her unresponsive next AM. Pt.
has tonic-clonic sz. Serum [Na+] = 114.
• What is going on?
Case #5
Hyponatremic encephalopathy
• Dehydration with bowel prep and vomiting thirst +
increased ADH.
• Free water retention hyponatremia.
• Rx: 3% saline until sz stop and mental status better.
Restore volume also with NS.
• Was patient also taking a thiazide diuretic?
Rx of hyponatremia
Based on symptoms– not numbers.
Case #6
Central Pontine Myelinolysis
• 79 yo female with Hx of HBP Rx’d with thiazides. Had elective
colonoscopy after bowel prep.
• Six hours after the examination of confusion followed by sz.
The patient stayed comatose. Serum [Na+] = 108.
• Brain-CT was normal. No signs of cerebral edema, but Rx with
IV dexamethasone was begun. (3% NS used to correct)…
hyponatraemia (>2 mEq/L/hr) up to 132.
• Pt. regained consciousness but was unable to speak and
swallow. This condition remained stable for 3 days, when …
neurological evaluation was… (requested).
Spengos K. Vassilopoulou S. Tsivgoulis G. Dimitrakopoulos A. Toulas P. Vassilapoulos D. Hyponatraemia
and central pontine myelinolysis after elective colonoscopy. [Letter] European Journal of Neurology.
12(4):322-3, 2005 Apr.
Hyponatremia– clinical
manifestations
• Asymptomatic > 125 mEq / L
• 110 – 125 mEq / L: MS changes
(confusion, seizures, coma).
• < 110 mEq / L: Medical emergency
Hypotonic Hyponatremia-- Rx
• Slow correction (0.5 mEq / L / hr) to
avoid central pontine myelinolysis.
• Get consultation and go very slow!
Case #7
Dialysis patient
• 57 yo obese male, DM, HBP, CRF on
dialysis. Needs AV shunt revision.
• How do we evaluate this patient?
• Be highly specific.
Case #7
Dialysis patient
• Airway, IV access. Don’t use IV dialysis
catheter.
• Exercise tolerance, chronic and recent.
• Has patient been getting dialyzed with a
venous catheter? If so, when was the last
time? Needs to be dialyzed day before
surgery.
• BP, lungs (rales?), can he lie flat?
• Do we need to recheck lytes AM of
surgery if patient was dialyzed day before?
Case #8
Do we discontinue ACEI and ARBs
before surgery?
• 48 yo male with DM and HBP, on insulin
and enalapril, for Whipple procedure,
(resection head of pancreas for CA).
• What are the advantages or
disadvantages of D/Cing the enalapril prior
to surgery?
Case #8
Do we discontinue ACEI and ARBs
before surgery?
• Worry is “refractory hypotension” due to vasodilatory
effect of anesthetics plus loss of angiotensin II
vasoconstriction.
• Controversial area.
• If we do not D/C ACEI and ARBs, we “go easy” with
the vasodilating anesthetics and have the
vasopressors ready.
• Big volume loss procedure would predispose us to
D/C enalapril.
Case #9:
Hyponatremic encephalopathy
• 78 yo female, incoherent, limping, bruise on face.
Bruise over L hip  L femur fx.
• Totally OK until recently. Started on new BP (thiazide
diuretic) med 2 weeks ago
• Serum Na+ = 104 mEq / L.
• What is going on ?
Case #9
Hyponatremic encephalopathy
• Thiazide diuretic blocks Na+ reabsorption
in distal tubule and cortical collecting duct. Causes
volume loss and trouble diluting urine.
• Free water retention (+ weight gain) from increased
ADH.
• Patients should be weighed 48 hrs. after starting
thiazide.
• Check lytes in patients on diuretics (we are checking
K+ AND Na+).
Hypernatremia– causes (1)
• Free water loss:
– Evaporative loss of water (sweat, burns).
– Lungs (insensible loss)
– Renal (nephrogenic diabetes insipidus)
– CNS (lack of ADH secretion).
Hypernatremia– causes (2)
• Limited water intake
– Comatose or disoriented patients
– Hypothalamic tumor / disordered thirst
mechanism
Hypernatremia– causes (3)
• Increased body sodium content
– Excessive salt intake
– Decreased sodium excretion
Hypernatremia– clinical
manifestations
• Intracellular dehydration
• CNS tissue volume loss (across BBB).
Possible tearing of cerebral vessels.
Mannitol sometimes used to increase
[Na+] to decrease ICP.
• Restlessness, tremor, ataxia, seizures,
death.
Hypernatremia– Rx
• Replace free water, orally or IV
• For every liter of free water deficit, [Na+] will
increase 3 mEq / L.
• As with hyponatremia, correct slowly. Brain cells
accommodate by increasing osmolarity. Too
rapid decrease in extracellular [Na+] can cause
brain cell swelling.
Potassium and Phosphate
• K+ and PO4--- are the most abundant
intracellular ions. MOST K+ AND PO4--ARE INSIDE CELLS!
• K+ gradient across cell membrane sets the
resting transmembrane potential.
• PO4--- essential for DNA, ATP, etc.
Hypokalemia
• Inside of nerve / muscle cells are increasingly
negative due to hyperpolarized cell membrane.
• EKG changes, decreased contractility
• Neuromuscular changes– cramps, weakness,
paresthesias
Hypokalemia-- causes
• GI losses (NG suction, diarrhea, vomiting, bowel
obstruction, fistulas, bowel prep)
• Renal losses (diuretics, mineralocorticoid
excess, nephropathy)
• Intracellular shifts (alkalosis, insulin, TPN,
catecholamine effect)
• Inadequate intake (diet, IV fluids).
Hypokalemia-- Rx
• Most of deficit is intracellular.
• Hyperkalemia is always a danger.
• Replace SLOWLY. Oral is best. 40 mEq q
6h. IV can replace up to 25 mEq / hr.
Hyperkalemia
• Transmembrane potential becomes less
negative- goes toward easy depolarization.
• EKG is most sensitive indicator: peaked T
waves- prolonged P-R interval- absent P
waves- widened QRS- sine wave- Vtach- V-fib- asystole
Hyperkalemia--- causes
• Renal failure (can’t excrete)
• Drugs (succinylcholine, K+ sparing diuretics,
ACE inhibitors.
• Hemolysis.
• Tissue breakdown (burns, crush injury)
• Acidosis
• Exogenous K+ (old blood).
• Factitious– hemolyzed blood sample,
contamination from K+ infusion.
Hyperkalemia--- Rx
Short term-- minutes (temporizing):
1) CaCl2 5-10 mg/kg. Stabilizes cardiac cell membrane.
2) Push K+ into cells:
–
–
Produce alkalosis (hyperventilation, NaHCO3)
Insulin and glucose administration
3) Beta agonist (albuterol, epi)
Longer term-- hours:
4) Increase K+ excretion (loop diuretics, dialysis, lactulose to
produce diarrhea-- Kayexelate enemas no longer used)
The End