WATER AND ELECTROLYTES DISTURBANCES

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

Extracellular water interstitial water (75%) intravascular water (25%)

Extracellular water interstitial water (75%) intravascular water (25%)

WATER DISTRIBUTION Variation according to gender

Total Body Water = 0.6 x (kg body weight) - for malesTotal Body Water= 0.5 x (kg body weight) - for females Total Body Water = 0.6 x (kg body weight) - for malesTotal Body Water= 0.5 x (kg body weight) - for females

newborns have the highest percentage of water (75%); older persons and females have relatively less water. newborns have the highest percentage of water (75%); older persons and females have relatively less water.

PHYSIOLOGY Electrolytic composition of water compartmentsOsmosis is the way water moves between these spaces.Solutes create the concentration gradients that promote osmosis. Sodium is the major extracellular cation. Magnesium and potassiumare the major intracellular cations. The Na+/K+ ATPase, an energy-consuming pump, maintains the concentrations across the cellular membrane. Vascular membranes and pumps are relatively permeable to water and to these cations.

~ 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

BP 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 in chronic hyper Na Na - 0,5-1mEq/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

Hypokalemia (<3.5mEq/L)

• Pathophysiology – – Decrease in K+ causes decreased excitability

of cells, therefore cells are less responsive to normal stimuli

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

WATER AND ELECTROLYTES DISTURBANCES

Documents

Transcript of WATER AND ELECTROLYTES DISTURBANCES