fluid and electrolyte disturbances

FLUID AND ELECTROLYTE DISTURBANCES

AGENDA• Physiology and pathophysiology of body fluid composition

• Disorders of the internal environment associated with normalECF effective tonicity

Isotonic hypohydrationThird spacingIsotonic hyperhydration

• Disorders of the internal environment associated with abnormalECF effective tonicity

Free water deficitFree water excess

• Differetial diagnosis of hyponatremia

• Differential diagnosis and treatment of hypokalemia

Composition of the body

solids 40%Transcelularcompartment P

LASMA

• Pericardialspace

• Pleural space

• Peritonealspace

• Intestinallumen

• Subcutaneoustissue (edema)

• Muscles

• Skin

Na-K-ATPase

Na+

K+

ECF

IFC ≈ 15%≈ 5%

ICF ≈ 40%Kg- Na≈ 2-3%- K≈97-98%

↓Oncoticpressure

↑Hydrostaticpressure

energy supply

Effectivetonicity

H2O

Concentrationof effective activemulecules

The basic requirement of the physiologicalcomposition of the internal environment

Isovolemia

Isotonicity

Electroneutrality

Maintanance of :

Preservation of blood pressureand circulation

Is determined by the amount of osmoles which are able to cause water transport between ICF a ECF

Electroneutrality is a balanced amount of positively and negatively charged solutes in body fluids. Disorders ofelectroneutrality influencedacid - base balance

Isovolemia is the superior law, becausemaintaining an effective circulating volume, so also functional blood circulation, allows in stress conditions fight or run away, so survive!!!

Na+ + K+ + Ca2+ + Mg2+ + H+ = OH- + Cl- + HCO3- + albumin- + Pi-

Electroneutrality is a balanced amount of positively and negatively charged solutes in body fluids

Osmolality- Osmolarity-TonicityOSMOLARITY (mmol/L),

OSMOLALITY (mmol/Kg)

is the concentration of all solutes

regardless of their ability to cause

water transport between ICF a ECF

Effective tonicity (mmol/L)

is determined by the amount of

osmoles which are able to cause water

transport between ICF a ECF

Natrium

Glukóza

Manitol

Glycin

Urea

Methanol

Ethanol

Ethylenglycol

OSMOLES

ENDOGENOUS EXOGENOUS

effective uneffective

Plasma osmolality and percentage portionof osmotic active particles

other

Osmolal gap

Effective tonicity = 2 x (Na+ + K+) + Sglucose

Osmolality = laboratory cryoscopic measurement of all

osmotic particles in ECF (plasma)

Osmolal gap = defference between measured

osmolality and calculated effective tonicity < 10

mosm/Kg. Effective tonicity determines water

trnasport between ECF and ICF.

Under conditions of hypotonichyponatremia(POsm<280 mOsm/kg H2O ), Uosm >100 mOsm/kg H2O confirms , that ADH plays an active role

Verbalis JG. Disorders of body water homeostasis. Clin Endocrin Metab 2003

Osmotic regulation of ADH releasedepends on the effective osmolality

Under conditions of effective osmolality < 280 mOsm/kg H2O release of ADH is totallysuppressed (Uosm je < 100 mOsm/kg H2O)

The main determinant of effective tonicity i ECF serum natrium concentration (S Na+)

Uosm is easy decetable laboratory marker of theADH activity under conditions of hyponatremie

ADH function in homeostasis of the internal environment

↑↑↑ADH

↑T ECF tonicity

Osmoreceptors Baroreceptors

EBV

Appropriaterelease

Inappropriaterelease

↑ADH

• ↑ADH release from

pituitry gland

• Ectopic ADH production

• ↑ ADH activity on

aquaporin-2-R

↑↑↑ADH







• Differential diagnosis of hypokalemia

Isotonic hypohydration

Isotonic dehydration: deficit of water and solutes in isotonic ratio (ECF volumedepletion)

ICF

IVC

• Plasma and ECF Na+ concentrationis unchanged

• No water transport betweenECF a ICF

• Plasma and ECF concentration K+

can be changed depending on thecause od dehydratation and acid-base disturbances

• Plasma and ECF Cl- concentrationdepends on causes and consequences of isotonic fluid loss

• ABB depends on causes and consequences of isotonic fluid loss

IFC

Causes of isotonic dehydration

• GI losses (vomiting, diarrhea, nasogastricsuction, fistula drenage, short bowel)

• Renal losses (salt lossing nephropathy, impairment of renal tubular function, primaryendocrinologic disorders)

• Sequestration of fluid (ileus, burns, peritonitis, pancreatitis)

Isotonic dehydration: etiology

GI losses:

Ethiopathogenesis

Primary loss of H+ a Cl-, retention HCO3- → matabolic alcalosis →renal

compensation → ↑NaHCO3 renal excretion→ Na+ loss → activation RAAS →

↑ aldosteron → ENAC: ↑Na+ tubular resorption and ↑ K+ and H+ secretion

vomiting,

nasogatric suction

H+ is neutralized by HCO3-

in equimolar ratio (1:1)

HCl

Isotonic dehydrataion + hypochloremia + hypokalemia + metabolic alkalosis


GI loss: small bowel fistula, surgical resection of the

small intestine: jejunostomy, ileostomy, ….

Ethiopathogenesis

Diet containing fatty acids → Diarrhea → primari GI loss of HCO3-

acompanied with Na+ →activation RAAS →

↑ aldosteron → ENAC: ↑Na+ tubular resorption and ↑ K+ and H+ secretion

Primary GI K+ loss

small bowel syndrome

jejunostomy Jejuno-colic an. jejun-ileo an.

Isotonic dehydratation, hyperchloremic metabolic acidosis, severe hypokalemia


GI Loss:

Ethiopathogesis

Diarrhea → primari GI loss of HCO3- acompanied with Na+ →activation RAAS

→ ↑ aldosteron → ENAC: ↑Na+ tubular resorption and ↑ K+ and H+ secretion

Primary GI K+ loss

Infection

Diverticulitis

Dysmicrobia

IBD

Ischemia

Malabsorption

Diarrhea

Izotonic dehydratation, hyperchloremic metabolic acidosis, hypokalemia

Isotonic dehydration: renal etiology

Urinary loss caused by „salt losin nephropathy“

DM complicated by ketoacidosis: loss of Na+ a K+ ketoacids salts

CSWS: Hyperproduction natriuretic peptides (brain trauma, brain tumor,

subarachnoid hemorrhage, apoplex)

Adrenal insufficiency

AIN, Chronic TIN, medullary kidney disease, ADPKD, SLE associated with

Sjoegren syndrome, ESRD)

Polyuric phase of ATN, post-obstructive natrium polyuria, secondary nephropathies

associated with hyporenin hypoaldosteronism, diuretics

Urinary loss caused by impairment of renal tubular function

Urinary loss caused by endocrinological disorders

Isotonic dehydration (clinical manifestation is

not apparent until 3-6 l isotonic fluid has been lost !)

Main symptoms ( ECF→hemodynamic : )1. Hypotension (ortostaticá hypotension !)

2. Invisible filling of jugular vein in horizontal position

3. HTC, serum protein, albumin, UA, PUREA (trends !)

4. Central blood pressure

5. BW (BW befor dehydratation has to be known !)

Unspecific symptoms1. Poor skin turgor

2. Sunken eyes

3. Oliguria

4. Absence of axillary sweat

5. Muscle cramps

6. thirst, anorexia

7. apathy, weaknes, confusion

Differencial diagnosisextrarenal vs renal losses

↓UNa+ < 30 mmol/L

↓EF Na+ < 0.4%

↓EFOsm < 2%

EFH2O < 1%

ABB metabolic acidosismetabolic alcalosis

UK+ > 20 mmol/L

↓EFK+

↑UNa+ > 30 mmol/L

↑EFNa+ > 1.2%

↑EF Osm > 3.5%

↑EF H2O > 2%

ABBmetabolic acidosismetabolic alcalosis

↑↓UK+

↓↑EFK+

Extrarenal (GI) loss Renal loss

Therapy od isotonic dehydration

1. i.v. substitution of isotonic volume

2. Choice of solute preparation depends on ABB (acidifying solution in pts. withalkalemia; alkalizing solutin in acidemia)

3. Amount of substituted solution and infusionrate depend on clinical status and underlying diseases

Na+

mmol/lCl-

mmol/lK+

mmol/lCH3COO-

ACETÁTC6H1107GLUKONÁT

C3H5O3LAKTÁT

Plasmalyte 140 98 5 27 23 0

Isolyte 137 110 4 34 0 0

Hartmann 131 111 5 0 0 29

F1/1 154 154 0 0 0 0

Ringer 147 156 4 0 0 0

Solute prepations for for therapyof izotonic dehydratation

Third spacing

Isotonic dehydration: sequetration of waterand solutes into the transcelularcompartment

Na + H2O

• Plasma and ECF Na+ concetration isunchanged

• No water transport between ECF a ICF

etiology• Intestinal lumen

• Sepsis: Subcutaneous tissue (edema)

• Muscles (rhabdomyolysis)

• Skin (burns)

Sequestration of water and solutes into the transcelular compartment(clinical manifestation is not apparent until 2-4 l

isotonic fluid has been retained !)

Clinical manifestation• BW gain• Edema• Dyspnea• Tachycardia• Clinical signes of pulmonary congestion

Diagnosis and treatment

• Diferencial diagnosis of edematous status

• Treatment of underlying disease

• Volum expansion volume expansion even though the patient is hyperhydratated

• CVVH

• artificial lung ventilation

Isotonic hyperhydration

Isotonic hyperhydration : excess of ECF

Na + H2O

• Plasma and ECF Na+ concetration isunchanged

• No water transport between ECF a ICF

etiology• Congestive hard failure

• Anuric renal failure

• Decompensated liver cirhosis

• Nephrotic syndrome

Isotonic hyperhydration

Clinical manifestation• BW gain• Edema• Dyspnea• Tachycardia• Jugular venous distention• Hepatojugular reflux • Clinical signes of pulmonary congestion

Diagnosis and treatment

• Diferencial diagnosis of hyperhydration status

• Treatment of underlying disease

• Diuretics (renal excretion = refill)

• CVVH

• Hemodialysis + ultrafiltration

Free water deficit =

hypertonic dehydration

Hypertonic dehydration : depletion of free water

H2OH2O

H2O

• Plasma and ECF Na+ concentrationincreasis

• water is transported into ECF • Plasma and ECF K+ concentration

remain stable• Plasma and ECF Cl- concentration

increasis• ABB remain stable

Hypertonic dehydration: Pathophysiology

• Insufficient oral intake of water (consciousness impairment )

• Decreased reactivity of osmoreceptor

in BG in very old patients

= loss of thirst

• insufficient home care

Auxiliary factors

Fever

Profuse perspiration

Diabetes insipidus

Hypertonic dehydrationClinical manifestation

• Tremulousnes

• Irritability

• Ataxia

• Spasticity

• Confusion

• Seizures

• Coma

Hypertonic dehydrationTreatment

• Intravenous 5% glucose infusion until SNa+ has been normalised

• Excesively rapid correction is dangerous !

• Infusion rate has to be so slow that SNa+

decrease das not exceed 0,5 mmol/L per 1 h

Relative free water excess=

hypotonic dehydration

Hypotonic dehydration : depletion ofsolutes < depletion of water

ADH

H2O

Free oral water inatake

H2O

PNa+ = ↓Na+

H2O

• Plasma and ECF Na+ concentrationdecreases

• water is transported into ICF • Plasma and ECF concentration K+

can be changed depending on thecause od dehydratation and acid-base disturbances

• Plasma and ECF Cl- concentrationdepends on causes and consequences of isotonic fluid loss

• ABB depends on causes and consequences of isotonic fluid loss

Patophysiology

Critical ECF volume depletion → ↑ baroreceptor-inducedactivation of ADH in order to maintaine isovolemia →thetonicity decreases

Auxiliary factors

• Free oral water intake

• GI loss of hypotonic fluid

• Farmacologic activation of ADH

Hypotonic dehydrationClinical manifestation

+

HYPONATREMIA

Main symptoms ( ECF→hemodynamic : )1. Hypotension (ortostaticá hypotension !)

2. Invisible filling of jugular vein in horizontal position

3. HTC, serum protein, albumin (trends !)

4. Central blood pressure

5. BW (BW befor dehydratation has to be known !)

Hypotonic dehydrationTreatment

• Re-expansion of ECF with isotonic saline

• Infusion rate has to be so slow that plasma Na rise das not exceed 10 mmol/L in 24 h (18 mmol/L in 18 h)

• Correction of underlyiing disorder

• Potassium deficit correction (it contributes to hyponatremia)

Isolated (absolute)excess of free water

Euvolemic hyponatremia: absolute excess offree water

↑↑↑ ADH releaze or activity

H2O

H2O

PNa+ = Na+

↑H2O

• Plasma and ECF Na+ concentrationdecreases

• water is transported into ICF

Euvolemic hyponatremia = absolute free water exces – clinical manifestation

+HYPONATREMIA

Symptoms of brain edema

Severity Symptom

Moderately severe Nausea witout vomitingConfusionHeadache

Sever VomitingCardiorespiratory distressAbnormal and deep somnolenceSeizuresComa (Glasgow Coma Scale ≤ 8)

Euvolemic hyponatremia = absolutefree water exces – treatment

• Correction of underlyiing disorder

• Infusion of 3% solution NaCl (150 mL/20-20 min)

AGENDA• Physiology and pathophysiology body fluid composition






• Differential diagnosis and treatment of hypokalemia

AGENDA• Physiology and pathophysiology body fluid composition







Disturbances of kalemia

Kalemia

Internal balance

External balance

ECF ICF

↑pH

pH↓

Intake Excretion

GI Renal

Hypokalemia (PK+ < 3.8 mmol/L)

Clinical manifestation (PK+ <2.5 mmol/L)• Malaise (nausea)

• Fatigue

• Neuromuscular disturbances (weakness, hyporeflexia, paresthesia, cramps, restless legs syndrome, paralysis, respiratory failure)

• GI symptoms (constipation, ileus, vomiting

• Cardiovascular abnormalities (arrhytmias, ECG changes – T wave flattening, prominent U waves, decreased QRS voltage, ST segment depression)

• Renal abnormalities (urinary concentrating defects, polyuria)

Hypokalemia

Causes

• Transcelular shift in alkalemia, insulin excess, hypothermia, anabolic states

• Inadequate intake over prolonged period

• Extrarenal losses

• Renal losses

Hypokalemia

Treatment

Oral therapy (KCl tablet = 13,5 /27 mmol)

Spironolacton

IV administration

7,45% KCl preparation ( 1 mL = 1 mmol)

Periferal vein: Maximal dose 40 mmol in 1000 mLsaline /1 h

Central vein: infusion dispenser 50 mL : 50 mL

7,45 %KCl (1 mL = 1 mmol)

Hyperkalemia (PK+ >5,3 mmol/L)

Clinical maifestation (PK+ >, mmol/L)

• Neuromuscular manifestation: weakness, paresthesias, areflexia, ascending paralysis

• Cardiac arrhytmias (bradycardia, asystol, prolongation of A-V conduction, A-V block, ventricular fibrilation

Hyperkalemia

Causes• Redistribution of K+ from ICF to ECF (acidosis, insulin

deficiency, hyperglycemia)• Decreased renal excretion

Acute and chronic oliguric failureImpairment of RAAS (hyporeninemichypoaldosteronism)Decreased aldosteron production (secondary to primary adrenal insufficiency)Impaired response to aldosteron (spironolacton)Inhibition of tubular secretion (Potassium sparing medicaments- amilorid, triamteren; distal renal tubularacidosis

Hyperkalemia

TreatmentAcute: calcium administration (protect the heart by

antagonizing the K+ effect on A-V conduction)

NaHCO3, insulin, glucose (to shift K+ from ECF to the ICF)

Cation exchange resisns

Hemodialysis

Chronic: treatment od underlying disorder

fluid and electrolyte disturbances

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