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Fluids, Electrolytes and Shock

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Title: Fluids, Electrolytes and Shock


1
Fluids, Electrolytes and Shock
  • Tom Archer, MD, MBA
  • UCSD Anesthesia

2
Outline
  • 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

3
Three fluid compartments
  • Intracellular fluid (ICF)
  • Interstitial fluid (ISF)
  • Intravascular fluid (IVF)

4
Fractions to remember2/3, 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.

5
Three membranes
  • Cell membrane
  • Non- brain capillary endothelium
  • Brain capillary endothelium (blood-brain
    barrier BBB)

6
Solutes
  • Ions Na , Cl-, K, PO4---
  • Sugars glucose, mannitol
  • Large molecules (colloids) albumin, hetastarch

7
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.

8
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.

9
Blood-brain barrier
  • Behaves just like the cell membrane a tight,
    lipid rich membrane which is impermeable to
    everything but water (and lipophilic drugs).

10
Osmosis
  • What is osmosis?
  • Answer diffusion of water down its concentration
    gradient.

11
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.

12
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).

13
Multi-modal approach to cerebral protection /
resuscitation after TBI Monitoring Normovolemia A
void hyperglycemia and hyperthermia Seizure
prophylaxis Artificial ventilation,
oxygenation ICP monitoring Sedation, analgesia,
posture, paralysis PaCO2 management Osmotic Rx
(serum mOsm 320) Furosemide Hyperventilation Bar
biturate coma Surgical decompression
14
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.

15
Intravenous fluids
  • Crystalloids
  • Normal saline (just NaCl).
  • Lactated ringers
  • Plasmalyte
  • Normosol
  • Last 3 have K and other stuff (acetate, Mg,
    etc.)

16
Practical aspects
  • Crystalloids enter entire ECF ISF (3/4 of ECF)
    and IVF (1/4 of ECF).
  • 3 or 41 for replacement of blood loss with
    crystalloid
  • Colloids only enter IVF (in short term 16 hour
    half-time for entrance into ISF)
  • 11 replacement of blood loss with colloid

17
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,
    glomerulo-tubular balance, macula densa).

18
Colson P Anesth and Analg 1999
19
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.

20
Schrier RW The American Journal of Medicine
(2006) Vol 119 (7A), S47S53
21
Juan A. Oliver and Donald W. Landry Curr Opin
Crit Care 13376382. 2007 Lippincott Williams
Wilkins.
22
Syndrome of Inappropriate ADHA 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.

23
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).

24
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,
    pre-eclampsia, DIC, ARDS, hyperglycemia, etc.)

25
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
Obesity, hyperglycemia, sepsis or pre-eclampsia
Platelet
Platelets
Protein (edema)
Archer TL 2006 unpublished
26
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!

27
Different recipes for optimizing macrocirculation
in sepsis. Early goal-directed therapy of
septic shock.
Rivers E et al N Engl J Med, Vol. 345, No.
19 November 8, 2001
28
Like the giant plant in Little Shop of Horrors,
body tissues say, Feed me!
29
Feed me!
Arteriole
Capillary
Hungry tissue says, Feed me! to pre-capillary
sphincter.
30
Case 1The patient is overloadedThe 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

31
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 10341928
32
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 10341928
33
Case 1The patient is overloadedThe 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 gt13 suggests fluid
    bolus will increase CO. CO is fluid responsive.

34
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).

35
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

36
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
Serum (combined) NaCl 123
Aqueous phase NaCl 135
Osmolarity (tonicity) normal
37
Hypertonic Hyponatremia-- causes
  • Due to hyperglycemia, mannitol or glycerol.
  • Decreased Na in serum, but osmolality is high
    (gt290), due to sugar in the blood.
  • Sugar has sucked water out of cells, into the
    ECF. Water dilutes Na.

38
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
39
Hypertonic Hyponatremia-- Rx
  • Insulin to slowly reduce blood glucose.
  • NS volume replacement.
  • Complications of rapid reduction of serum glucose
    and tonicity hypoglycemia, cerebral edema

40
Four causes of increased ADH
  • Normal osmotic ADH release osmoreceptors in
    hypothalamus release ADH via posterior pituitary
    in response to serum mOsm gt 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.

41
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
42
Hypotonic hyponatremia too much free water
compared to NaCl. (Volume deficit with
non-osmotic ADH release, or CHF, cirrhosis or
SIADH)
Free water
ADH
NaCl
NaCl
Osmolarity (tonicity) decreased
43
Stress- induced, non-osmotic ADH release
  • This is why we DONT give D51/4NS in surgery.
  • This is why we DO give NS, Normosol or LR.
  • We dont give free water because of kidneys
    reduced ability to excrete it (due to non-osmotic
    ADH release).

44
Hypotonic, Hypovolemic Hyponatremia-- Rx
  • Volume restoration with NS if hypovolemic (GI
    losses, diuretics).
  • Explanation Severe hypovolemia causes
    non-osmotic 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.

45
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
46
(No Transcript)
47
Case 2Perioperative 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.
  • 245 AM next day, pt. C/O headache, verbal order
    for Tylenol 3.
  • At 900 AM, nurse tells surgeon of a sodium of
    127 mEq/L. No
  • new orders, IV fluids were continued.
  • At 130 pm, pt. lethargic and pain medications,
    pain meds held.
  • At 330 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
48
Case 2Perioperative 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
49
How aggressively do we Rx hyponatremic
encephalopathy?
  • Depends on symptoms, not the Na.
  • In symptomatic hyponatremic encephalopathy, use
    3 saline until sx improve.

50
Case 3Hyponatremic 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?

51
Case 3Hyponatremic 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.

52
Case 4Hyponatremic 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.

53
Case 4Hyponatremic encephalopathy
  • Two days later patient becomes incoherent and
    lethargic.
  • Na 108 mEq / L.
  • What is going on?
  • What should we do?

54
Case 4Hyponatremic 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!

55
Case 5Hyponatremic 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?

56
Case 5Hyponatremic 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?

57
Rx of hyponatremiaBased on symptoms not
numbers.
58
Case 6Central Pontine Myelinolysis
  • 79 yo female with Hx of HBP Rxd 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 (gt2 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.
59
(No Transcript)
60
Hyponatremia clinical manifestations
  • Asymptomatic gt 125 mEq / L
  • 110 125 mEq / L MS changes (confusion,
    seizures, coma).
  • lt 110 mEq / L Medical emergency

61
Hypotonic Hyponatremia-- Rx
  • Slow correction (0.5 mEq / L / hr) to avoid
    central pontine myelinolysis.
  • Get consultation and go very slow!

62
Case 7Dialysis patient
  • 57 yo obese male, DM, HBP, CRF on dialysis. Needs
    AV shunt revision.
  • How do we evaluate this patient?
  • Be highly specific.

63
Case 7Dialysis patient
  • Airway, IV access. Dont 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?

64
Case 8Do 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?

65
Case 8Do 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.

66
Case 9Hyponatremic 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 ?

67
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).

68
Hypernatremia causes (1)
  • Free water loss
  • Evaporative loss of water (sweat, burns).
  • Lungs (insensible loss)
  • Renal (nephrogenic diabetes insipidus)
  • CNS (lack of ADH secretion).

69
Hypernatremia causes (2)
  • Limited water intake
  • Comatose or disoriented patients
  • Hypothalamic tumor / disordered thirst mechanism

70
Hypernatremia causes (3)
  • Increased body sodium content
  • Excessive salt intake
  • Decreased sodium excretion

71
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.

72
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.

73
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.

74
Hypokalemia
  • Inside of nerve / muscle cells are increasingly
    negative due to hyperpolarized cell membrane.
  • EKG changes, decreased contractility
  • Neuromuscular changes cramps, weakness,
    paresthesias

75
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).

76
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.

77
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-? V-tach-? V-fib-? asystole

78
Hyperkalemia--- causes
  • Renal failure (cant 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.

79
Hyperkalemia--- Rx
  • Short term-- minutes (temporizing)
  • 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)

80
The End
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