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WATER AND ELECTROLYTES DISTURBANCES

University of Medicine and Pharmacy, IasiSchool of MedicineANESTHESIA and INTENSIVE CAREConf. Dr. Ioana Grigoras

MEDICINE4th year

English ProgramSuport de curs

PHYSIOLOGY

Body water= 55-60% of body weight

Water distribution:– Intracellular water – 66% of total (2/3)

– Extracellular water – 33% of total (1/3)

– Intracellular water – 40% of body weight– Extracellular water – 20% of body weight

• Intravascular water (volemia) - 5% of body weight

• Interstitial water - 15% of body weight

WATER DISTRIBUTION Variation according to gender

PHYSIOLOGY Electrolytic composition of water compartments

~ 300~ 300

66

214Proteins

11Phosphat

2727HCO

110103Cl

11Mg

2,52,5Ca

55K

142142Na

Interst CIntravasc C

~ 300~ 300

-6Org. acids

8014Proteins

551Phosphat

1027HCO

0-5103Cl

131Mg

-2,5Ca

1505K

15142Na

Intracell CExtracell C.

Org. acids

WATER AND ELECTROLYTES BALANCE Evaluation

CLINICAL EVALUATION :– History

• Water and salt ingestion• Losses• Thurst

– Skin and mucous membranes examination • Oral mucosae humidity• Skin humidity• Skin colour and temperature• Cutaneous turgor

– Body weight– Respiratory system clinical exam

• Polypneea• Crackles at lung bases

– Clinical examination of peripheral veins– Haemodynamic parameters

• Arterial blood pressure • Pulse wave amplitude• Orthostatic challenge• CVP,...

– Urinary outflow– Evaluation of the counscience level

Clinical evaluation of

the intravascular compartment:– thurst

– BP, heart rate, orthostatic challenge

– central venous pressure

– pulmonary capillary wedge pressure, cardiac output

– organ function:• conscience

• urinary flow

• tissue perfusion

WATER AND ELECTROLYTES BALANCE

Evaluation

Clinical evaluation of

interstitial space:

unreliable– skin and mucous membrane examination

• colour

• humidity

• turgour

• edema


Evaluation

Clinical examination of intracellular compartment:

unreliable

– thurst– mental status disturbances– neurological signs


Evaluation

LABORATORY EVALUATION– Hematocrit and total proteins

– Blood and urinary electrolytes measurement

– Blood and urinary osmolarity

– ECG


Evaluation

OSMOLARITY• Plasma osmolarity =

the sum contributions of all osmotic active substances

• The main plasma osmotic active substances: Na, glucose, ureea

• Plasma osmolarity– measured osmolarity– estimated (calculated) osmolarity

• Calculated osmolarity = Na-mia x 2 + blood glucose/18 +ureea/2,8

Intracellular volume disturbances are the consequences of

effective osmotic pressure variation


Classification (Shires şi Baxter)

• Volume disturbances• Volume contraction• Volume expansion

• Concentration disturbances• Hyponatremia• Hypernatremia• Other hyperosmolar states

• Composition disturbances• Hypo/hyperpotasemia• Hypo/hypercalcemia• Hypo/hypermagnesemia• Hypo/hyperphosphatemia• Hydrogen ion disturbances (acid-base disturbances)

VOLUME CONTRACTION

CLASSIFICATION OF HYPOVOLEMIC SHOCK

Class I Class II Class III Class IV

Blood loss- ml < 750ml 750-1500ml 1500-2000ml >2000ml

Blood loss-% <15% 15-30% 30-40% >40%

Pulse rate <100/min < 100/min 120-140/min >140/min

TA N N

Plus wave amplitude

N

Capillary refill N + + +

Respiratory rate 14-20/min 20-30/min 30-40/min >40/min

Urinary output >30ml/oră Oliguria Oligoanuria Anuria

Mental status Mild anxiety Anxiety Confused Lethargy

PRINCIPLES of TREATMENT• Treatment of causative disease • STOP THE LOSSES• Volume replacement

• Volume replacement– Routes of volume administration

– Solutions for volume replacement

– Rhythm of administration

– Monitorization of volume replacement efficiency

VOLUMEEXPANTION

VOLUME EXPANTION

VOLUME EXPANTION

PRINCIPLES of TREATMENT

• Treatment of causative disease

• Limitation of water intake

• Diuretics

SODIUM DISTURBANCES

• Plasma sodium concentration =

extracellular water – sodium ratio

• Na-mia is not a predictor of intravascular volume

SODIUM DISTURBANCES

HYPERNATREMIANa-mia > 145mEq/l

• Physiological effects– Extracellular hyperosmolarity– Water movement out of the cell– Preservation of extracellular volume despite losses– Intracellular volume contraction


• Clinical picture– Clinical signs of intracellular volume contraction –

neurological signs– Restlessness, iritability, letargia, hyporeflexia,

coma, convultions– High mortality, neurological sequelae


• Treatment – Water administration in order to correct

hyperosmolarity– When clinical signs of extracellular volume

contraction (hypovolemia) are present, isotonic solution should be given untill correction of intravascular volume

– Calculation of water deficit0,6 x kg x (Na actual / 140 – 1)

– Speed of correction NO > 2mEq/hour


CLASSIFICATION– HYPOVOLEMIC

• Water and Na deficit• Deficit of water > Na • Body total amount of Na

False hypernatremia– ISOVOLEMIC

• Water deficit • Body total amount of Na - normal

– HYPERVOLEMIC• Water and Na excess• Excess of Na > water • Body total amount of Na ↑

True hypernatremia

HYPOVOLEMIC HYPERNATREMIA Total body Na

MECHANISM- Water and Na deficit; deficit of water > Na; body total amount of Na

CAUSES– Extrarenal losses

• Skin losses (profuse sweating)• Digestive losses (cholera, infant diarrheea)

– Renal losses• osmotic diuresis• excess of diuretics• polyuria

DIAGNOSTIC– Clinical signs of extracellular volume contraction – Na urinary < 10mEq/l – extrarenal losses– Na urinary > 20mEq/l – renal losses

TREATMENT– Water and sodium administrationin isotonic proportions until correction of

hypovolemia; hypotonic solution (NaCl 0,45%)

ISOVOLEMIC HYPERNATREMIA total body Na normal

MECHANISM– water deficit; total body Na normal


• Skin losses (profuse sweating)• Respiratory losses (tachypnea, mechanical ventilation)

– Renal losses • Central diabetes insipidus • Nephrogenic diabetes insipidus • Hypodipsia (decreased water intake)

DIAGNOSTIC– Signs: fever, oliguria, azotemia, drowsiness, coma, convultions– hypotension (late finding)– variable urinary Na

TREATMENT– Increased water intake (NaCl 0,45%,)

ISOVOLEMIC HYPERNATREMIA

HYPERVOLEMIC HYPERNATREMIA total body Na ↑

MECHANISM– water excess; total body Na ↑

CAUSES– excess administration of hypertonic saline (NaCl 7,5%)

– Na bicarbonate administration

– Salt water drowning

DIAGNOSTIC– Signs of extracellular volume expansion

– Signs of intracellular volume contraction

TREATMENT– Diuretics

– Increased water intake

HYPONATREMIANa-mia < 135mEq/l

• Physiological effects– Extracellular hypoosmolarity– Water movement towards the cell– Signs of intracellular volume expansion


• Clinical picture– Dominated by neurological signs (cerebral edema)– Letargy, apatia, drowsiness, anorexia, nausea,

agitation, hyporeflexia, hypothermia, convulsions– Signs severity depends upon:

• severity of hypoNa-miei (Na < 120mEq/l)

• speed of hypoNa-mia occurrence (acute/chronic)

HYPONATREMIA

Speed of hypoNa-mia occurrence

HYPONATREMIA

• Treatment – Correction of extracellular osmolarity and water

excess removal– Speed of correction depens upon:

• severity of hypoNa-mia• prezence/absence of symptoms• speed of occurrence (acute/chronic)

– Rapid correction of chronic hypoNa-mia – pontine mielinolysis (irreversible sequelae)

– In the prezence of symptoms, rapid correction until Na-mie 120mEq/l, than slow correction

HYPONATREMIA


CLASSIFICATION– Hypovolemic

• Water and Na deficit• Deficit of Na > water• Total body Na

True hyponatremia

– Isovolemic • Water excess of extracellular compartment• Total body Na - normal

Dilutional hyponatremia / Pseudohyponatremia

– Hypervolemic• Water and Na excess• Excess of water > Na• Total body Na ↑

Dilutional hyponatremia

HYPOVOLEMIC HYPONATREMIA total body Na

MECHANISM– water and Na deficit; deficit of Na > water; total body Na


• Digestive losses (vomiting, diarrheea)• Skin losses (profuse sweating)• Third space formation (pancreatitis, burns, crush syndrome, intestinal

oclusions, etc.)– Renal losses

• osmotic diuresis, excess of diuretics, polyuria

DIAGNOSTIC• Signs of extracellular volume contraction (hypovolemia)• Na urinary < 10mEq/l – extrarenal losses• Na urinary > 20mEq/l – renal losses

TREATMENT– Correction of extracellular volume– Isotonic solutions

ISOVOLEMIC HYPONATREMIA total body Na normal

MECHANISM– water excess of the extracellular space; total body Na normal

CAUSES– Syndrome of inappropiate antidiuretic hormone secretion (SIADH)

– Fear, excitement, pain, drugs, surgical procedures

– Hyperosmolar states (hyperglycemia, intoxications)

DIAGNOSTIC– Extracellular water excess; no clinical signs

– Na urinary > 20mEq/l

TREATMENT– Water restriction

ISOVOLEMIC HYPONATREMIA

HYPERVOLEMIC HYPONATREMIA total body Na ↑

MECHANISM– Excess of water and Na; excess of water > Na; total body Na ↑

CAUSES– Edematous syndromes (cardiac failure, liver cirhosis, nephrotic

syndrome)– Acute and chronic renal failure

DIAGNOSTIC– Signs of extracellular volume expansion (edema)– Na urinary < 10mEq/l in edematous syndromes– Na urinar > 20mEq/l in renal failure

TREATMENT– Water (and salt) restriction

POTASIUM• Body K distribution

• 98% intracellular – 150-160mEq/l• 2% extracellular – 3,5-5mEq/l

The main intracellular cation• Intracellular functions

» Cell volume regulation» Intracellular pH regulation» Proteins and glycogen synthesis» Cell grow regulation» Cell enzymes activation» Rest potential of cell membrane

The main function membrane potential

POTASIUM DISTURBANCES

• Factors which influence K intercompartmental distribution:

– Serum K

– pH: acidosis or alcalosis

– Hyperosmolarity

– Hormons: insulin and catecholamines

• Factors which influence K urinnary excretion:– Serum K level

– Aldosteron

– Urinay flow

Factors which influence K intercompartmental distribution

POTASIUM

Intercompartmental K movements according to pH

– Acidosis → extracellular H+ ↑ → H+ moves into cell

K+ moves out of cell

hyperpotasemia

– Alcalosis → extracellular H+ → H+ moves out of cell K+ moves into cell

hypopotasemia

HYPERPOTASEMIA

• Frequent causes of pseudohyperpotasemia:– Blood drawing: thin needles, intense negative

pressure (erythrocytes hemolysis, K release), garou, fist “pumping” (K muscle release), blood storage (erythrocytes K release);

– Leucocytosis / thrombocytosis - hyperpotasemia;

HYPERPOTASEMIACAUSES

– Increased K+ intake• enteral intake• parenterală intake

– K+ movement out of the cells• Metabolic acidosis• Hyperglycemia• Excessive excercise• Hypercatabolism• Drugs: β-blockers, succinilcholine, digitalis

– Decreased urinnary K+ ellimination• Hypovolemia• Hypoaldosteronism• Renal failure• Drugs: spironolactone, AINS, heparine

HYPERPOTASEMIA

CLINICAL PICTURE– Muscle signs

• paresthesia

• muscle weakness

• paralysis

– Cardiac signs• EKG signs

• Rhythm disturbances

• Dyastolic cardiac arrest

HYPERPOTASEMIA

HYPERPOTASEMIA

• mild/moderate (K+= 6-8mEq/l) – no clinical signs– limited ECG changes (peaked T waves, no changes of P or

QRS)– need for monitoring and treatment.

• severe (K+= >8mEq/l) – severe signs– severe ECG changes (peaked high T waves, no p waves,

wide QRS complexes)– need for emergency ECG monitoring and emwergency

treatment – risk of cardiac arrest.

HYPERPOTASEMIA

• ECG changes in hyperpotasemia:

• K+= 6-7mEq/l - peaked high T waves

• K+ =8-9mEq/l - absent P wave

• K+ =10mEq/l - wide QRS complex

• K+= 10-11mEq/l – biphasic QRST

• K+ =10-12mEq/l – ventricular fibrillation / dyastolic stillstand

ECG changes in hyperK-mie

HYPERPOTASEMIA

• Mild/modarate forms:• limitation /stop K intake • resins (ion chelation)• diuretics

• Severe forms:– emergency treatment – antagonization of membrane effects

and decreased plasma level by redistribution• calcium gluconate / chloride • Na bicarbonate• glucose + insulin

– K removal• resins• diuretics• hemodialysis

– stop K intake

HYPOPOTASEMIA

CAUSES– Normal total K – changes of intercompartmental distribution

• Respiratorie / metabolic alcalosis

– Low total K • Deceased intake

• Poor nutrition (alcoholics)

• Digestive losses– Vomiting, gastric fistulae, naso-gastric tube, …

– Diarrheea, laxatives

• Renal losses– Excess of mineralocorticoids – primary/secondary

– Diuretics

– Osmotic diuresis

HYPOPOTASEMIACLINICAL PICTURE

Changes of membrane potential • Neuro-muscle effects

– Parestesia– Muscle weakness– Hyporeflexia– Paralitic ileus

• Cardio-vascular effects – Changes of cardiac excitability– ECG changes– Enhancement of digoxin toxicity – Rhythm disturbances– HTA

• Vegetative effects– orthostatic hTA

• Hepatic effects– Aggravation of encephalopathy in liver cirhosis patients

HYPOPOTASEMIA

ECG ABNORMALITIES• Flat T wave

• U wave

• wide QRS complex

• ST depresion

• Atrial and ventricular rhythm disturbances

HYPOPOTASEMIA

HYPOPOTASEMIA

PROPHYLAXIS• Administration of K daily needs – 1mEq/kg day

TREATMENT• Correction of causative disease• K amount– depends upon severity of hypo-K

– K-mia > 3mEq/l – oral

– K-mia 2-3mEq/l – 10-20mEq/h

– K-mia < 2mEq/l – 20mEq iv + than 20mEq/h

ECG monitoring - mandatory

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