Practical Applications of Intravenous Fluids in Surgical Patients Shaila Shodhan Kamat
Page numbers followed by f refer to figure.
Abdominal distension 202
Abdominal tenderness 207
Abscess drainage 201
Acetate 63, 124
abnormalities 213
composition 69
disturbances 204
Acute renal failure, precipitation of 82
Adrenal insufficiency 239
Adrenaline 283, 284
Adverse drug reaction 111
Albumin 68, 7173, 76, 97, 127, 183, 239, 275
amount of 78
composition of 72
concurrently, bottle of 76
fluid evaluation 238
in blood 73
in critical illnesses 74
in health, functions of 73
influences coagulation 73
infusion 110
loss of 71
replacement, value of 74
solution 71, 76
stabilises 72
synthesis 71
types of 71
Aldosterone 23, 177
in water balance, role of 23, 25f
mechanism of action of 24, 24f
secretion 24, 25
Alkalaemia, severe 205
Alkalosis 211
Alveolar oedema 270
Amino acids 275
Amiodarone 284
Amphetamines 194
Anaesthesia 145
administering 198
in pre-eclamptic patients 253
regional 145
type of 156
Analgesia 253
Anaphylactic reaction 81, 111
reactions 90, 111, 120
shock 98
Angiotensin 19
in water balance, role of 22, 23
role of 22f
Angiotensinogen 22
Anticipated operative time 156
Antidiuretic hormone 10, 11, 162, 167, 177
concentrations 14f
formation of 11f
in pregnant patients, role of 15
in trauma, role of 16
in water balance, role of 10
on kidney, effects of 16, 16f
on vascular system, effects of 17
physiological effects of 16
release of 15
secretion of 14, 133, 163
syndrome of inappropriate 143
synthesis of 11f
Antipyretic therapy 245
Anuria 151, 171
Arrhythmias 195
Arterial baroreceptors, high pressure 7, 8, 9f
Arterial blood 188
gas analysis 210
Arterial pressure 209
mean 239
Atrial natriuretic peptide 27, 150, 254
in water balance, role of 27, 28f
production of 232
Atropine fever 199, 200f
Autonomic nervous system 9
Bacteria and toxins, source of 196
Bainbridge reflex 8f
Baroreceptor 7
in regulation of water balance, role of 7
reflex 9, 9f
Betaine 227
Bicarbonate 204
Blood 111, 183, 209
and blood substitutes 275
component therapy 175
cross-matching, interference with 82
in suction bottles 212
rheology 242
substitutes 137, 184
sugar level, random 209
transfusion 58, 275
urea nitrogen 195
Blood glucose
level 197
measurement 163
Blood loss 150, 153, 175, 206
allowable 169, 175
compensate for 181
estimated 169
replace 222
replacement 152
Blood pressure 187, 246, 251, 282
non-invasive 260
normal 209
variation 280
Blood volume 158, 175
estimated 175
increased 7
Blood-brain barrier 217, 220, 242
across 213
in head injury, changes in 220
intact 243
Bloodstream 22
Body fluid
compartment, solute composition of 45f
composition of 1
distribution of 38, 44, 44f, 157
Body spaces, resuscitation of 143
Body temperature 191
variation in 190
Body water
compartment 48f
sources of 4
Body weight loss 209
Bowel exposure 174
Bowel obstruction 154
Bowel preparation 145
quality of 156
Bowel wall oedema 150
Bradycardia 120
capillary, structure of 217, 217f
natriuretic peptide 27
in water balance, B-type 27
in water balance, role of 28f
oedema 233
regulation 235
swelling 213
water 221
content 213
Brainstem herniation 239
Bronchospasm 120
Bucket analogy, hole in 155
Burn 78, 143
therapy 75
Calcium 73, 275
Caloric expenditure 161
Capillary filtration coefficient 215
Capillary hydrostatic pressure 234
Capillary microcirculation 214f, 269f
Capillary refill pressure 279
Capillary tissue fluid dynamics 140
Caprylic acid 72
Carbohydrate 144
Carbonic anhydrase inhibitor 205
Cardiac arrest 81, 196
Cardiac function 143
Cardiac output 183
Cardiac surgery 122
patients 121
Cardiogenic shock, patient with 187
Cardiopulmonary and renal function 156
Cardiopulmonary bypass 75
Cardiopulmonary system, effects on 249
Cardiovascular function 153
Cardiovascular instability 171
Cardiovascular stabilisation 237
Cardiovascular stable 201
Cardiovascular system 161
effects on 110
Catabolism, patients with increased 74
Cell volume, packed 209
Central nervous system 194
effects on 250
Central pontine myelinolysis 226
Central venous
catheter 281
pressure 188, 233, 237, 254, 268, 279
applications of 273
Cerebral blood flow 230, 235, 238
Cerebral dehydration 225
Cerebral irritability, increased 196
Cerebral ischaemia 239
Cerebral oedema 57, 223, 225, 234, 241, 251
formation of 219
Cerebral pathology 213
Cerebral perfusion pressure 237
Cerebral salt wasting 240
Cerebral vasospasm, effects of 230
Cerebrospinal fluid 226
radiograph 279
tightness of 81
Chloride 63, 124
Circulatory disturbance 90
Circulatory dysfunction 276
Clear-fluid losses 126
Clostridium welchii 195
Cocaine 194
Cold extremities 151
Colloid 66, 128, 135, 181, 183, 239
accepted statements of 130
advantages of 64
and crystalloid in body compartments, distribution of 54f
artificial 176
characteristics of 126
constitute 218
disadvantages of 64
electrolyte content 69
fluid 155, 274
general characteristics of 66
in brain, effects of 218
in fluid resuscitation 98
in perioperative period, current consensus on 128
indications of 70
intravenous fluid 97, 127
size 67, 67f
weight 66
natural 77
pharmacology of 66
half-life 69
substitute 69, 137
substitute, functions of 70
substitute, types of 69
volume expansion 67
synthetic 113, 129
theories favouring 135
use of 259
volume replacement by 222
Colloid molecules
enter 135
removal of 130
Colloid osmotic pressure 41, 68, 68f, 72, 216
avoid decrease in 259
reduction of 218
Colloid solutions 66, 112, 128, 129, 141, 183, 241
contain colloid 55
Colloidal active molecules 219
Colloidal osmotic pressure 73
Colon 203
Coma 151, 171
Compounds, transport of 73
Congestive cardiac failure 119
Corticosteroids 244
use of 244
Critically ill
patients 275
surgical patient 187
Crush injury 184
Crystalline solids in water, solutions of 53
Crystalloid 53, 96, 98, 126, 130, 181, 277
accepted statements of 130
administration 131
decreases osmotic pressure 241
advantages of 64, 98
characteristic of 53
controversy 274
over 135
disadvantages of 64
favouring therapy 186
fluids 135, 155
in brain, effects of 218
in perioperative period, current consensus on 128
intravenous fluids 65
mechanism of action of 55
pharmacology of 53
plasma substitutes 137
solutions 75, 129, 141, 144, 183, 241
types of 55
use of 259
volume replacement by 222
catalyses 198
enzyme 199
blocking action of 199
Deficit patients, chronic 173
Dehydration 207, 225
with moderate 173
with severe 173
clinical signs of 208, 209
degree of 208
estimation of degree of 170, 209
mild 170
moderate 171
severe 172, 209
severity of 171
sign of 177
type of 169
Desmopressin acetate 231
Dexamethasone treatment 224
Dexmedetomidine 284
Dextran 68, 79, 183, 276
general properties 79
interferes 82
low doses of 82
solution of 88
types of 79
Dextran 40 84, 87, 127
clinical uses 85
excretion 84
metabolism of 84, 86
pharmacological basis 84
Dextran 70 85, 86, 127
dose of 87
metabolism of 86
pharmacological basis 85
Dextran administration
complications with 81
disadvantages with 81
Dextran-induced anaphylactoid reactions, severe 81
Dextrose 55, 61, 63, 65, 138, 196, 197
administration, lower 134
advantages 58
and water for bolstering 201
avoid 164
containing solutions 141, 148
avoid 242
contraindications 57
disadvantages 58
indications 57
management during surgery 164
pharmacological basis 56
precautions 59
properties 56
safe rate of administration 56
solutions, administering 163
Dextrose saline 61, 98
indications 61
pharmacological basis 61
precautions 61
properties 61
insipidus 230
mellitus 155
uncontrolled 58
Diarrhoea 196
chronic 153
Dihydroergotamine 235
Dilated pupil, unilateral 243
Dilutional hyponatraemia 134
Diminished sensorium 151
Diphtheria 195
Dipotassium hydrogen phosphate 63
Diuretic therapy and hypotension, avoid 258
Dobutamine 283, 284
Dopamine 283, 284
actions of 266, 267f
in water balance, role of 29, 29f
Dopaminergic renal vasodilatation 29
dilutions for infusions 283
interactions 79
protocol, infusion of 284
Drying agent, avoid 199
Dysarthria 226
Eclampsia 247, 248
Electrocardiogram 210
Electrolyte 213
abnormalities 231
after estimation, replace 201
contents 65, 97, 127
disturbances 181
correction of 210
solution, balanced 125
Elevated metabolic activity 194
Emesis 207
End-expiratory pressure, positive 189, 266
Endogenous pyrogen 191
Endothelial cell layer 140
Endothelial glycocalyx layer 140
Endothelial leucocyte adhesion molecule-1 122
Endothelial surface layer 140
Endotoxaemia 112
Epidural analgesia decreases 256
Esomeprazole 284
Examiner's thumb 171
Exhausted adrenal cortex 196
Extensive cellulites 201
Extensor posturing 243
Extracellular compartment 40
Extracellular electrolytes, concentrations of 23
Extracellular fluid 45, 46, 52, 139, 157, 158, 180, 263
deficits 150
signs of 151
non-functional 159
replace 149, 150
treatment of 151
volume, decreased 204
Extracellular space 47f, 53
resuscitations of 143, 144
Extracellular tonicity 40, 228
Extracellular water 44, 158
constitutes 158
Extracorporeal circulation 92
Fasting guidelines 144
Fat 157
diseases 191
reaction 60
Fentanyl 284
Fever 190, 194, 196
caused by brain lesions 193
clinical significance of 194
facts about 190
postoperative 194
reaction 192
two-thirds of 194
Filling space, priority of 146
Filtration fraction, decrease 22
Fluid 245
and electrolyte loss 196
and volume management, current controversies of 131
boluses 71
calculation of 283
drop rate calculation of 283
during aneurysmal surgery 229
for volume replacement, types of 137, 182
gelatins, modified 70
in infant and children 165
in intestinal obstruction 202
in neurointensive care units 231
in postoperative care units 231
in solid food 4
infusion of 212
ingested 4
intraoperative 180
load 132f
mechanism of action of 140f, 141
movement, basics of 215
overload, higher chances of 165
perioperative management of 221
preferred, types of 178
replacement 149, 274
required, smaller total volume of 165
requirement of 177
resuscitative 274
retention 154
selection of 201
shear stress 131
shifts, internal 154
types of 98, 172, 176, 241
with diabetes insipidus 230
within bowel lumen, sequestration of 203
Fluid administration 239
goals of 182
intraoperative 149
perioperative 168
route and rate of 187
Fluid balance 146, 261
influence of positive pressure ventilation on 266
Fluid calculation 172
for elective stable cases 173
Fluid deficit
assessment of 162
correction of 162
non-iatrogenic sources of 156
on physical examination, signs of 156
restoration, total 173
Fluid intake
remaining 272
typical 272
Fluid loss 178
intraoperative 174, 176
preoperative 207
typical obligatory 271
Fluid management
basic concepts in 237
decision pathway, perioperative 156
during surgery 164
goals of 210
in neurosurgery 221
in neurosurgical patients 213, 229
in postoperative period 177
in pregnant patients 256
with pre-eclampsia 259
in severe pre-eclampsia 258f
in surgery 153
in ventilated patient 263, 271
intermediate surgery 154
intraoperative 229
major surgery 154
minor surgery 153
of neurosurgical patients, intraoperative 222
of paediatric surgical patients 157
perioperative 166, 180
issues affecting 144
Fluid replacement
adequacy of 212
amount of 131
assessment of 212
principles of 145
surgical 152
Fluid requirement
assessment of daily 147
calculating 161
infants and older children maintenance 163
intraoperative 177
Fluid restriction
avoid 221
severe 221
Fluid resuscitation 236
adequate 222
standard or liberal 131
Fluid therapy
goals of intraoperative 174
in eclampsia 246
in fever 190
in infants and children 157
perioperative 157
in pre-eclampsia 246, 253
in trauma resuscitation 181
in traumatic brain injury 234
management of perioperative 166
monitoring 179, 278
perioperative 147
Fresh frozen plasma 67, 175
Furosemide 244
Gastric drainage 207
Gastric losses, chronic 153
Gastrointestinal fluid
composition of 203
loss of 152
volume of 203
Gastrointestinal loss 177
Gastrointestinal pathology 146
Gastrointestinal surgery 142
Gastrointestinal system 146
Gastrointestinal tract 205
Gelatin 69, 96, 277
administration, indications of 90
solutions 86
advantages of 89
clinical pharmacology 88
disadvantages 90
excretion 89
metabolism 89
pharmacokinetics 88
properties 88
undesirable side effects 92
type of 88, 96
Gelifundol 88
Gelofusine 88, 95, 96, 97
comparative effects of 96
indication 96
properties 95
unique benefits of 95
Glomerular filtration
decreased 21
rate 33, 159, 252, 263
Glucocorticoids 23
Glutamine 227
Glycerol 220
Goal directed therapy 181
Gut 195
H+ ion, loss of 205
Haemaccel 93, 97
contraindication 95
excretion 93
metabolism 93
mode of administration 93
pharmacological basis 93
properties 93
side effects 94
decrease of 111
risen 210
Haematological disturbances 247
in pre-eclampsia 251
Haemodilution therapy 117
Haemodynamic stabilisation 98
Haemodynamic support 238
Haemodynamically unstable, treatment of 181
Haemoglobin 209
concentration 235
Haemorrhage 183
Haemorrhagic shock 78, 183, 226
Haes-Steril, effects of 114, 115
Hartmann's solution 134, 173
Head injury 122
failure 266
rate 187, 188, 209, 279
Heat stroke 194
HELLP syndrome 248, 252
Heparin 284
Hepatic artery bringing blood 196
Hepatic reserve, narrowed 196
Herring body 12
Hetastarch 68, 113, 120, 172, 239
Homeostatic responses, long-term 265, 266f
in water balance, role of 2, 10
salt and water retaining 26
secretions 7
Human albumin 71
general properties 71
shelf-life and storage 71
Hydralazine injection 251
Hydrated, epidural analgesia 256
Hydrochloric acid, loss of 205
Hydrostatic forces 215, 218
Hydrostatic pressure 235
in capillary 270
Hydroxyethyl starch 70, 88, 99, 101, 106, 117, 172, 183, 276
advantages of 113
adverse reactions 120
balanced 125
clinical uses of 112, 119
concentration 99
contraindications 119
disadvantages 106
doses of 120
effects of 110
evaluation of 113
first-generation 113
general pharmacological properties of 99, 105
generations 127
indications 119
metabolism of 106
molecular weight 100
nomenclature of 104, 105f
on coagulation, effect of 109f
pharmacology of 99
plateau effect of 118f
saline 125
second-generation 114
solutions 110
special precautions 112
third-generation 117
type of 100, 120
warning and precautions 119
Hyperbilirubinaemia 254
mild to moderate 111
Hyperchloraemic acidosis 124
Hyperglycaemia 148, 164, 176, 224
augments 224
avoid 224
severe 58, 148
Hyperkalaemia 176
Hypernatraemia 58, 232, 278
Hypernatraemic extracellular fluid 227
Hyperoncotic renal injury 276
Hyperoncotic solution 115
Hyperosmolar fluid
newer 232
use of 225
Hyperosmolar therapy 242
Hyperosmolarity, acute 220
Hypertension 60, 248, 250
Hyperthermia, malignant 194
Hypertonic crystalloid solution 241, 277
Hypertonic saline 183, 220, 225, 226, 228, 242, 243
disadvantages of 226
dose of 228
therapy 226
Hypertonic solution 55
osmolality of 225
Hypertonicity 19
Hyperuricaemia 252
Hypervolaemia 229
Hypoalbuminaemia, patients with 74
Hypocalcaemia 176
Hypochloraemia 61, 205
Hypoglycaemia 197, 224
Hypokalaemia 204, 211, 232
aggravates 204
Hyponatraemia 37, 58, 134, 135, 167, 227, 231, 239, 240, 278
causes of 240
chronic 226
degrees of 219
severe 226
Hypo-oncotic solution 115
Hypoperfusion, severe 178
Hypotension 19, 81, 151, 171, 177, 222, 238, 250, 258
effects of 222
in pre-eclamptic parturients 250
severe 81
systemic 238
Hypothalamic neurosecretory neurones 10
Hypothalamic temperature controller 192, 193f
Hypotonic fluids 208
Hypotonic solutions 55
Hypovolaemia 13, 14, 19, 61, 91, 121, 142, 177, 185, 186, 188, 204, 213, 237
correction of 210
in antidiuretic hormone release, role of 14, 15f
preoperative 146
treatment of 245
Hypovolaemic patients 128
Hypovolaemic shock 57, 59
emergency treatment of 75
Hypoxaemia 142, 213, 249
Hypoxia 50, 274
avoid 199
Hypoxic ischaemic 251
Idiosyncratic drug reactions 194
Ileum 203
Immune system disorders 111
Impaired renal function 60
Infant, preterm 162
Infant's cardiopulmonary status 170
Infection 191
Inflammation 191
Influenza-like symptoms, mild 120
Infusion of albumin, indications for 74
Inositol 227
Inotropic drugs 181
Insensible loss 169
greater 165
Insensible water loss
abnormal 5
normal 4
Insulin 284
Intensive insulin therapy 232
Interleukin-I, role of 191, 192f
Interstitial compliance 218
Interstitial fluid 47, 51, 129, 168
acts 204
volume 158
loss of 208
Interstitial oedema 130, 150, 277
Interstitial pressure falls 216
Interstitial space
causes of over expansion of 50
constriction of 265
disadvantages of over expansion of 50
negative pressure in 49
Interstitium 219
Intestinal obstruction 207, 212
anaesthesiologist with 202
surgery 202
Intracellular dehydration 144
Intracellular fluid 45, 52, 157, 159
Intracellular gaps 217
Intracellular space 53
disadvantages of over expansion of 50
Intracellular tonicity 228
Intracranial hypertension 228, 237
Intracranial injury 234
Intracranial mass lesions 213
Intracranial pressure 220, 221, 223, 225, 226, 228, 234, 237
increase 236
lower 221
Intravascular fluid 46, 168
Intravascular persistence 98
Intravascular plasma volume 158
Intravascular pressure 218
Intravascular volume
deficiency 182
loss of 204
replacement 223
Intravenous fluid 133
composition of 166
replacement 254
start 197
Invoke delirium 199
Ionic solution 53, 55, 141
uses of 141
Ischaemic stroke, acute 58
Isolyte P 63, 65
contraindications 64
indications 64
pharmacological basis 63
precautions 64
Iso-oncotic solution 115
Isoprenaline 283, 284
Isotonic colloid solution 239
Isotonic crystalloid 239
amounts of 216
Isotonic electrolyte solution 124
Isotonic intravenous solutions 259
Isotonic saline 59
in body compartments 54f
Isotonic solutions 55
Isovolaemic haemodilution, acute 91, 116
Itching 111, 120
Jejunum 203
Juxtaglomerular apparatus 20f
nephron with 20f
Juxtaglomerular cells 19
Kidney 1, 20, 134, 195
in sodium reabsorption, role of 32, 33f
in water balance, role of 2, 30
supply blood flow to 160f
Kinins in water balance, role of 29
Labour 256
Lactate production, metabolic aspects of 236
Lactate-pyruvate ratio 236
Laparoscopic cholecystectomy patients 144
Laparotomy 5
Lasix (furosemide) 284
Leukocyte pyrogen 191
Levosimendan 284
Liberal fluid resuscitation 131
Liver 195
cirrhosis of 60
disease 73
effects on 251
enzymes, raised 248
failure 154
acute 75
surgery 142
transplantation, after 79
Lomodex 79
Loop of Henle
ascending 32
descending 32
Low glomerular filtration rate 159
Low osmolality outside cell 227f
Low plasma sodium, chronic 228
Low pressure
atrial baroreceptors 7
atrial stretch receptors 8f
stretch receptors 7
stimulation of 7
Lung 195
Lymphatic system disorders 111
Macrodex 79, 127
Macula densa 20
region 20
Magnesium 63, 73, 124, 152
chloride 63
Maintenance fluid 148, 162, 271
requirement 163
Mannitol 220, 225, 243
repeated administration of 244
use of 229
Maternal dehydration 16
Mechanical ventilation 175, 263
Medication, severe 178
Meningococcus 195
Mental status 188
Metabolic acidosis 155, 206
Metabolic alkalosis 205
aggravation of 205
correction of 211
Metabolic water 4
Metabolically generated water 272
Metabolism 56, 73, 86
and excretion 81, 114
Midazolam 284
Milrinone 284
Mineralocorticoids 23
Minimally invasive methods 279
Mitochondria 236
Molar substitution 101, 101f, 102f
Monodisperse 67
Motility, decreased 142
Mucous membrane 209
Multiple traumas complicate 234
Muscarinic receptor, acetylcholine for 200f
Myocardial depressant drugs, avoid direct 200
Myocardial efficiency, decreased 195
Myocardial irritability 195
N-acetyl-DL-tryptophan 72
aspiration 211
suction 205
tube 210
Nausea 81
cardiac output 161
hypoglycaemia 254
intensive care unit 167
maintenance fluid requirement 162
myocardium 161
Neurohypophysis 12
Neuroleptic malignant syndrome 194
Neurosurgery 143
Neurosurgical patients, management of 213
Neurosurgical procedures 57
Newer developments 232
Nitroglycerine 284
Non-cardiac pulmonary oedema 120
Non-haemorrhagic hypovolaemia 186
Non-ionic solution 53, 55, 141
uses of 141
Non-ketotic hyperglycaemia 17
Non-osmotic stimulus 15
Non-protein nitrogen 195
Noradrenaline 283, 284
Normal saline 59, 98, 222
advantages 60
contraindications 60
disadvantages 60
indications 59
pharmacological basis 59
precautions 60
properties 59
Normovolaemia 229
Normovolaemic haemodilution, acute 91, 116
Oedema 249
body for prevention of formation of 51
formation 218
producing 216
rebound 225
Oligaemic shock 91
Oliguria 151, 177
in labour for vaginal delivery 256
postoperative 177
Oncotic pressure 216
gradient 130
in interstitium 270
Operation, type of 156
Optimal fluid
management 222
resuscitation 133
Oral carbohydrates 144
Oral feed, start 179
Orchidopexy 166
Organ dysfunction, postoperative 154
Osmolality 38, 40, 68
in antidiuretic hormone release, role of 13, 13f
outside cell, high 227f
outside cell, normal 227f
role of 13
sensors 35
Osmolar therapy 225
Osmolarity 38, 39, 124
Osmoles 38
Osmolytes 227
fall 227
in water balance, role of 5, 6f
of hypothalamus 12, 12f
Osmosis 41, 42, 42f, 138
fundamental physiology of 42
Osmo-sodium receptors in water balance, role of 5
Osmotic activity, basic concepts of 38
Osmotic diuresis 146
Osmotic forces, equalisation of 43
Osmotic molecules 55
Osmotic pressure 41, 268
effective 41
Osmotic reflection coefficient 215
Otoneurological disorders, precautions in patients with 117
Overhydration 90
risk of 98
Oxygen 256
delivery 253
transport in high-risk 187
Oxypolygelatins 70, 88
Oxytocin drip 254
Paediatric intensive care unit 136, 163
Pancreas 203
Pantoprazole 284
Paradoxical aciduria 205
management of 205
Parsimonious fluid therapy 272
Pentastarch 126
Perfluorocarbons 184
Peripheral capillary, structure of 215, 216f
Peripheral oedema 50, 60
formation of 219
Peripheral perfusion 208
Peripheral pulse, poor 151
Peripheral tissue 221
Permeability pulmonary oedema 271
pH 124, 172
Pharmacodynamics 117
Pharmacokinetics 118
Phenylephrine 284
Phosphate 63, 152
Pituitary gland 230
posterior 10, 11f
Pituitary hormones, posterior 10
Placental changes 253
Plasma 46, 129, 168, 206, 239
bilirubin, effects on 111
colloid osmotic pressure 79, 98
derivative, naturally occurring 69
exchange 91
factors 206
normal 72
osmotic pressure, normal 268
substitute 137
tonicity 39
Plasma osmolality 14f, 39
factors influencing 239
in water balance, role of 264
Plasma protein 88
decrease of 111
fraction 67, 73
Plasma volume 155, 158, 203
comparative 98
decreased 195
expansion 77
homeostatic responses to maintain 264
loss of 208
substitutes 91
Plasmagel 88
Plasmion 88
contain 175
transfusion 175
Polydisperse 67
Polygeline 88, 96
comparative effects of 96
Positive end-expiratory pressure, effects of 267f
Positive pressure ventilation, effects of 267f
Postrenal oliguria 178
Potassium 63, 72, 124, 152
chloride 63, 178
content 96
Practical fluid balance 138
basic principles 138
Pre-anaesthetics consideration 207
Pre-eclampsia 246, 248
classification 247
incidence of 246
severe 247
Pre-eclamptic patients 256
after parturition, care of 262
mild 257
severe 257
Pregnancy induced hypertension 246
classification of 247
Prehydration 257
basic concepts of 254
with hypotonic fluid, avoid 167
Preload-central venous pressure, measure of 188
Prerenal oliguria 178
Pressure stretch receptors 7
Pressure ventilation, positive 266, 268
Preterm labour, women at risk for 16
Pro-inflammatory cytokines 122
Prophylactic crystalloid solution 147
Prostaglandins 22
in water balance, role of 29, 30f
membrane basic 238
molecules 47
rich fluids, sequestration of 75
Proteinuria 92, 246, 248
Pruritus 111, 120
Pulmonary artery
catheter 281
occlusion pressure 273, 279
wedge pressure 230
Pulmonary capillary wedge pressure 255
Pulmonary function 143
Pulmonary oedema 50, 60, 256, 260, 273
acute 273
management of acute 261
postobstructive 271
signs of impending 257
Pyrexia 207
Pyrogens 191
in causing fever, mechanism of action of 191
Randomized controlled trials 145
Red blood cells, packed 176
Refractory vomiting 205
Regional anaesthesia, prehydration before 255
Regional analgesia, precautions before initiation of 255
Rehydration 172
Rehydration therapy 172
before surgery, goals of 172
monitoring 174
Renal artery hypotension 21
Renal blood flow, low 159
Renal causes 177
Renal effects 84
Renal failure 83, 155, 165, 225
acute 155
avoid 83
incidence of 146
Renal filtration 31f
Renal function 110, 143, 153, 170, 261
effects on 110
test, abnormal 83
Renal insufficiency 123
Renal oliguria 178
Renal physiology 159
Renal sympathetic nerves 21
Renal system, effects on 252
Renal units, basic 160f
Renal water handling 31
factors influencing release of 21, 21f
in water balance, role of 19, 22
primary function 22
Renin-angiotensin-aldosterone system 26f, 265f
Respiratory acid-base disorder 206
Respiratory arrest 81
Respiratory muscles 195
Respiratory rate, increased 195
Respiratory system, effects on 252
Respiratory variation in systolic 279
Restricted fluid resuscitation 132
Resuscitation 210
fluids 182, 185, 274
in trauma patients 184
Reticuloendothelial system 106
Rhabdomyolysis, severe 178
Rheomacrodex 127
Ringer's lactate 61, 62, 98, 134, 141, 169, 173, 180, 223, 229, 233, 239
contraindications 63
indications 62
pharmacological basis 62
precautions 63
solution 241
Ringer's solution 61, 245
Saline 65, 180, 238
solution 125
Saliva 203
Salt solution
balanced 129, 149, 150
infuse balanced 211
Semisynthetic colloid 69
Sensible water losses 4
Sensorium changes 171
Septic shock 74
Serotonin syndrome 194
amylase, increase of 111
biomarker levels 238
electrolytes 179
oncotic level 78
osmolality 239
tonicity 226
Sex hormones 23
Shock 81, 171
bacteraemic 196
original 181
Short-term homeostatic responses 264, 265f
Sick newborn 176
Skin 171, 195
colour 209
disorder 111
turgor 209
decreased 171
Sodium 37, 46, 63, 72, 124, 218
accounts 6
acetate 63
and water
metabolism 37
retention 266
balance 213
chloride 117, 134
concentration 39
regulation of 3, 34f, 35, 35f
content 225
in antidiuretic hormone release, role of 36f
in controlling water balance, role of 264
in extracellular fluid 6
in hyponatraemia, correction of 228
nitroprusside 284
containing 141
without 141
Starch 97
Starling equation 213, 268, 269
Starling's forces 213, 269
Starling's hypothesis 39, 213, 214, 269
Steril 120
Stomach 203
Streptococcus 195
Subcutaneous tissue disorder 111
Succinylated gelatin 96
and stress response 142
moderate 174
superficial 174
types of 142
System organ class 111
adverse drug reaction 111
Systemic abnormalities, existing 170
Systemic derangements 202
with intestinal obstruction 202
Systemic inflammation, effects on 122
Systolic blood pressure 279
Tachycardia 120, 151, 171, 209
Tachypnoea 171
Temperature 175
controller 192
Tetrastarch 117, 118f, 121, 126
Thirst mechanism
absence of 165
factors influencing 18, 18f
Thrombocytopenia 248, 251
Thromboembolic complications 143
Thromboprophylactic effect 80
Thyroxin 275
oedema 98
oxygenation 121
Tonicity 40
clinical significance of 40
of solution 219
Tonsillectomy 166
Total body water 1, 51, 157, 158
childhood 43
compartmental distribution of 43
content 263
distribution of 1
females 43
males 43
newborn infant 43
regulation of 2, 3f
young adult
females 43
males 43
Toxaemia 206
of pregnancy 60
bacteria 191
shock 195
Transcapillary refill 204
Transcellular fluid 48, 168
losses 150
Transcellular water 48
Transfusion, complications of 189
Traumatic brain injury 230, 232, 234, 236, 237, 242
patient 237
salt and water balance in 244
severe 237
Traumatic shock 187
Traumatised brain 239
Units of measurement 38
anion 38
cation 38
ions 38
Urea 220
cross-linked gelatin 88, 96, 127
solutions 69
Urinary calcium excretion 252
Urinary excretion of water 30f
Urinary loss, greater 165
Urine 210
concentrating ability 161
low output of 177
osmolality 240
output 209, 279
production 35
hormonal control of 33, 33f
specific gravity 172, 208
Urosurgery 122
Urticarial, generalised 81
Vaginal delivery, labour for 256
Vasopressor drugs 181
Ventricular arrhythmias 204
Vicious cycle 218
Volulyte 120, 124
Volume expansion
acute 256
degree of 77, 104
therapeutic options in 98
Volume loading, benefits of 212
Voluven 117, 120, 122
Vomiting 81, 203
Water 196
and electrolyte
causes of deprivation of 203
disturbances 202
balance 6, 35, 263, 268
arginine vasopressin in 10
in body, control of 5
normal 1
role of thirst in 17
content of food 272
control in body 52
diffusion of 42
for injections 72
free permeability of 42f
homeostasis 1, 1f, 36f
regulation of 34f, 35, 35f
intake of 24
consumption of 3
intoxication 58
movement, principles of 213
output 2, 4, 4f
Wheezing 81
Whole blood and plasma 137
Wound surfaces, exposed 150
Chapter Notes

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Normal Water BalanceChapter 1

The kidneys are essential for regulating the volume and composition of body fluids. Hence key regulatory systems involving the kidneys for controlling volume, sodium and potassium concentration and the pH of body fluids should be understood thoroughly.
A most critical concept is to understand how regulation of water and sodium are integrated to defend the body against all possible disturbances in the volume and osmolality of body fluids. Simple examples of such disturbances include dehydration, blood loss, salt ingestion and plain water ingestion.
Water homeostasis (Fig. 1.1)
Normal day-to-day fluctuations in total body water (TBW) are small (< 0.2%) because of a fine balance between input (controlled by the thirst mechanisms) and output (controlled mainly by the kidneys), which is influenced by various hormonal factors.
zoom view
Figure 1.1: Water homeostasis
Distribution of total body water
Total body water (TBW)—60% of body weight in adults
  1. Two-thirds of total body water (TBW) is intracellular2
  2. One-third of total body water (TBW) is extracellular
    1. Two-thirds of extracellular fluid is interstitial
    2. One-third of extracellular fluid is intravascular.
Estimated blood volume ml/kg
Premature neonates
Term neonates
2 month – 1 year
1 year to adolescence
Regulation of total body water (Fig. 1.2)
The regulation of body water depends upon fine balance between intake and output orchestrated by several factors:
  1. Water intake
  2. Water output
    1. Sensible water losses
    2. Normal insensible water losses
    3. Abnormal insensible water losses.
  3. Sensors that are involved in control of water balance in the body
    1. Osmoreceptors or osmo-sodium receptors
    2. Baroreceptors
      1. Low pressure atrial baroreceptors or volume receptors
      2. High pressure aortic baroreceptors or mechanoreceptors
  4. Role of hormones in water balance
    1. Role of antidiuretic hormone (ADH) and thirst in water balance
    2. Role of renin in water balance
    3. Role of angiotensin II in water balance
    4. Role of angiotensin III in water balance
    5. Role of aldosterone in water balance
    6. Role of atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP) in water balance
    7. Role of kinins in water balance
    8. Role of dopamine in water balance
    9. Role of prostaglandin in water balance
  5. Role of the kidneys in water balance
    1. Renal filtration, reabsorption, and excretion of water
    2. Role of the kidneys in sodium excretion
    3. Physiology of urine production.3
  6. Regulation of sodium concentration by regulation of water homeostasis
    The central controller for water balance is the hypothalamus but there is no single anatomically defined ‘centre’ which is solely responsible for producing an integrated response to changes in water balance. The regulation of body water and sodium are closely inter-related.
I. Water Intake
Total body water content is regulated by the intake and output of water. Water intake can be considered to consist of two components: a non-regulatory component (all other fluid intake) and a regulatory component (due to thirst).
The consumption of water intake is regulated by behavioural mechanisms, including thirst and salt cravings. While almost a litre of water per day is lost through the skin, lungs and faeces, the kidneys are the major site for regulated excretion of water.
The principal sources of body water are ingested fluid, water present in the solid food and water produced as an end product of metabolism. Intravenous fluids are another common source in hospital patients.
Water intake includes ingested fluids (an adult averages 2300 ml) plus average 750 ml ingested in solid food and 300 ml generated metabolically from oxidation in food.
zoom view
Figure 1.2: Regulation of total body water
II. Water Output (Fig. 1.3)
Actual and potential outlets for water are classified conventionally as sensible and insensible losses. Normal insensible losses denote losses from the skin and lungs, sensible losses denotes mainly from the kidneys and gastrointestinal tract.
Intake of water
Output for water
Sources of body water
Normal insensible losses
Sensible losses
Ingested fluid
Fluid in solid food
Metabolic water
  1. Sensible water losses
    Sensible water losses are through the kidneys and the gastrointestinal tract. Approximately 60%, i.e. about 1400 ml of the normal daily intake of water is excreted as urine, and 100 ml is present in the stool.
  2. Normal insensible water losses
    Loss of water by evaporation through the respiratory tract and diffusion through the skin is known as normal insensible water loss as it is not perceived by the individual.
    • The cholesterol-filled, cornified layer of the skin shields against a greater insensible water loss through the skin. Indeed, when the cornified layer becomes denuded, as after burn injury, the outward diffusion of water is greatly increased.
    • Insensible water losses through the skin and respiratory tract are largely mandatory but are not fixed. Normally 700 ml is lost by evaporation through the respiratory tract and 300 ml is lost through sweat by diffusion through the skin. Hence, insensible losses are approximately one litre.
    • All gases that are inhaled are saturated with water vapour at 47 mmHg. This water vapour is subsequently exhaled, accounting for an average water loss through the lungs, approximately 700 ml every 24 hours.
      zoom view
      Figure 1.3: Water output
    • The water content of inhaled gases decreases with temperature, which is why more endogenous water is required to achieve a water vapour pressure of 47 mmHg as environmental temperature decreases. As a result, insensible water loss from the lungs is greatest in cold weather and least in warm environments. This is consistent with the sense of dryness perceived in the respiratory passages in cold weather.
  3. Abnormal insensible water loss
    Higher amount of water is lost during fever, exercise, burns, surgery, e.g. laparotomy.
    • During laparotomy if the exposed intestine is not covered adequately with moist packs, insensible water loss is around 750 ml to 1 litre for every one hour of exposed intestine.
    • At high ambient temperatures or with significant exercising, the amount of water lost through sweating increases and reflects most of the total body water loss. Heavy exercising can lead to 50 times more water loss, through sweating, than the normal rate.
    • Increased ventilation increases the insensible loss of water through the respiratory tract. Under these conditions, renal water loss decreases to compensate for the increased sweating and insensible water loss.
III. Sensors that are Involved in Control of Water Balance in the Body
The main sensors that are involved in control of water balance in the body are:
  1. Osmoreceptors or osmo-sodium receptors
  2. Baroreceptors
    1. Low pressure atrial baroreceptors or volume receptors
    2. High pressure arterial baroreceptors or mechanoreceptors.
Role of Osmoreceptors or Osmo-sodium Receptors in Water Balance (Fig. 1.4)
The osmoreceptors are specialized cells located in the hypothalamus which respond to changes in extracellular tonicity (rather than to changes in osmolality). The critical difference between osmolality and tonicity is that all solutes contribute to osmolality but only solutes that do not cross the cell membrane contribute to tonicity.
  1. Thus, tonicity expresses the osmotic activity of solute restricted to the extracellular compartment. Tonicity is the effective osmolality and is equal to the sum of the concentrations of the solutes which have the capacity to exert an osmotic force across the membrane.6
    zoom view
    Figure 1.4: Role of osmoreceptors in water balance
  2. Osmolality takes into account the total concentration of penetrating solutes and non-penetrating solutes; whereas tonicity takes into account the total concentration of only non-penetrating solutes.
  3. As sodium accounts for 92% of extracellular fluid tonicity, these osmoreceptors (during normal physiology) function essentially as monitors of sodium in extracellular fluid. These receptors have been also called ‘osmo-sodium’ receptors.
    • Osmoreceptors are very sensitive, which respond to changes as small as one to two per cent change in tonicity.
    • Water intake can vary greatly but plasma osmolality varies only one to two per cent because of the efficient and powerful control system coupled to these osmoreceptors.
  4. These osmoreceptors are monitoring ‘water balance’ indirectly because they look at the effect of an excess or deficit of water by its effect on tonicity. This could cause a problem, if both extracellular water and solute increased together so that sodium and tonicity remained constant, e.g. an intravenous infusion of normal saline (i.e. an isotonic expansion of the extracellular fluid). Fortunately the body has several mechanisms of recognising changes in intravascular volume e.g. baroreceptors.
  5. Sodium in extracellular fluid is an effective monitor of total body water.
    • Osmoreceptors effectively respond to the change in sodium concentration in extracellular fluid. This is the factor which effectively controls the distribution of water between intracellular and extracellular fluid.7
    • The sodium in extracellular fluid thus regulates the extracellular fluid volume and controls the ICF: ECF distribution of body water.
Role of Baroreceptors in Regulation of Water Balance
Baroreceptors are sensors (pressure stretch receptors) located in the blood vessels, which are less sensitive (but more potent) than the osmoreceptors. The threshold for the low pressure atrial stretch receptors to cause changes in ADH secretion is 8 to 10% change in blood volume. But when stimulated, they cause ADH levels to be increased much higher than that seen with osmoreceptors stimulation.
Hormone secretions that target the heart and blood vessels are affected by the stimulation of baroreceptors. Arterial baroreceptors convey information about arterial blood pressure, but other stretch receptors in the large veins and right atrium convey information about the low pressure parts of the circulatory system, i.e. venous blood pressure.
Baroreceptors (pressure stretch receptors) can be divided into two categories:
  • Low pressure atrial baroreceptors are present in the cardiac atria (right and left atrium) which are also called volume or cardiopulmonary receptors.
  • High pressure arterial baroreceptors which are present in the aortic arch and carotid sinus are also called mechanoreceptors.
Low Pressure Atrial Baroreceptors or Volume Receptors (Fig. 1.5)
  1. Low pressure stretch receptors or volume receptors are baroreceptors located in the right atrium, at the junction of the venae cavae and in the left atrium, at the junction of the pulmonary veins.
  2. Increased blood volume is detected by stretch receptors located in both atria at the veno-atrial junctions. These receptors respond to changes in the wall tension, which is proportional to the filling state of the low pressure side of circulation. It means effective intravascular volume can be independently assessed by the low pressure atrial baroreceptors.
  3. Stimulation of low pressure stretch receptors in the cardiac atria produces three effects:
    • They send inputs to osmoreceptors of hypothalamus, which in turn produces decrease in ADH, renin and aldosterone secretion. The decrease in ADH secretion results in an increase in the volume of urine excreted.
    • In addition, stretching of atrial receptors increases secretion of atrial and B-type or brain natriuretic peptide (ANP and BNP), which promotes increased water and sodium excretion through the urine.
    • Bainbridge or atrial reflex (Fig. 1.5)
      The Bainbridge reflex is also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure.8
      zoom view
      Figure 1.5: Low pressure atrial stretch receptors—Bainbridge reflex
      • As venous return increases, the pressure of the right atrium increases, which stimulates the atrial stretch receptors (low pressure receptor zones).
      • These receptors in turn signal the medullary control centres to increase the heart rate (tachycardia). Unusually, this tachycardia is mediated by increased sympathetic activity to the sino-atrial node with no fall in parasympathetic activity. This reflex is called Bainbridge reflex.
      • Increased heart rate serves to decrease the pressure in the superior and inferior vena cavae by drawing more blood out of the right atrium. This results in a decrease in atrial pressure, which serves to bring in more blood from the vena cavae, resulting in a decrease in the venous pressure of the great veins. This continues until right atrial blood pressure returns to normal levels, upon which the heart rate returns to its original level.
High Pressure Arterial Baroreceptors (Fig. 1.6)
High pressure arterial baroreceptors are a type of mechanoreceptors that detect the pressure of blood flowing through them, and can send messages to the central nervous system to increase or decrease total peripheral resistance and cardiac output.9
zoom view
Figure 1.6: High pressure arterial baroreceptors—Baroreceptor reflex
Baroreceptor Reflex (Fig. 1.6)
  1. Basically, baroreceptor reflex is initiated by stretch receptors, called either baroreceptors or pressor receptors which are located in the walls of the large systemic arteries, i.e. in the transverse aortic arch and the carotid sinuses of the left and right internal carotid arteries.
  2. The baroreceptors found within the aortic arch monitor the pressure of blood delivered to the systemic circulation, and the baroreceptors within the carotid arteries monitor the pressure of the blood being delivered to the brain.
    • A rise in pressure stretches the baroreceptors and sends input to the hypothalamus via adrenergic pathways. Aortic baroreceptors through the vagus nerve (cranial nerve X) and carotid baroreceptors through the glossopharyngeal nerve (cranial nerve IX) transmit signals into the central nervous system (the nucleus tractus solitarius in the medulla oblongata in brainstem). It stimulates vagal centre and decreases heart rate, decreases strength of contraction of myocardium and produces peripheral vasodilatation.
    • The volume receptors (low pressure baroreceptors) and the high pressure baroreceptors also send the input to the hypothalamus when there is a pressure rise.
  3. Baroreceptor reflex is the mechanism of arterial pressure control which acts immediately as a part of a negative feedback system. It is an example of a short-term blood pressure regulation mechanism. Feedback signals are then sent through the autonomic nervous system to the circulation to reduce arterial pressure towards the normal level.10
  4. The Bainbridge reflex increases the heart rate and the baroreceptor reflex decreases the heart rate. They act antagonistically to control heart rate.
    • When blood pressure increases, the baroreceptor reflex is dominant, and it decreases the heart rate.
    • When blood volume is increased, the Bainbridge reflex is dominant and it increases the heart rate. After delivery of an infant when a large volume (up to 800 ml) of uteroplacental blood is autotransfused into the mother's circulation it always results in tachycardia.
  5. Stimulation of both pressure stretch receptors (high and low) helps to decrease blood pressure with decrease in ADH and renin release and vice versa.
IV. Role of Hormones in Water Balance
One of the mechanisms that the body uses to control urine volume is through the action of hormones. Hormones are secreted by specialised glands in the body. The two endocrine glands that are concerned with the regulation of fluid balance within the body are the pituitary gland and the adrenal gland.
Roughly 60% of the weight of the body is water and despite wide variations in the amount of water taken each day, body water content remains incredibly stable.
Such precise control of body water and solute (sodium) concentrations is a function of several hormones acting on both the kidneys and vascular system, however there is no doubt that antidiuretic hormone (ADH) is a key player in this process. Several factors have been implicated in the control of sodium excretion but the renin-angiotensin-aldosterone system (RAAS) seems to play a key role.
1. Role of Antidiuretic Hormone (ADH) or Arginine Vasopressin (AVP) in Water Balance
Posterior pituitary (Fig. 1.7)
The pituitary is insignificant in appearance (about the size of a corn) but it packs an extremely powerful punch. The pituitary is actually two glands in one, posterior and anterior. Of the two, the posterior pituitary manufactures no hormones of its own, but stores two hormones that are initially secreted in a part of the brain known as the hypothalamus. These hormones are oxytocin (a hormone responsible for stimulating labour at the end of pregnancy), and antidiuretic hormone (ADH), which helps the body retain its fluids.
The posterior pituitary or neurohypophysis is an extension of the hypothalamus. It is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland. It is composed of bundles of axons from hypothalamic neurosecretory neurones intermixed with glial cells and other poorly-defined cells called pituicytes. Roughly 100,000 axons participate in this process to form the posterior pituitary. Infundibular stalk also known as the infundibulum or pituitary stalk, bridges the hypothalamic and neurohypophysis systems.
These axons have their cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. These neurones secrete oxytocin and antidiuretic hormone classically known as posterior pituitary hormones.11
zoom view
Figure 1.7: Posterior pituitary
Formation and storage of ADH (Fig. 1.8)
Antidiuretic hormone, also commonly known as arginine vasopressin, is a nine amino acid peptide. ADH is derived from a preprohormone precursor that is synthesised in the hypothalamus.
zoom view
Figure 1.8: Formation and synthesis of ADH
Herring bodies are dilated areas or bulges in the terminal portion of axons that contain clusters of neurosecretory granules. The granules contain oxytocin or antidiuretic hormone, along with a carrier protein called neurophysin. Both are transported slowly along the ‘hypothalamo-hypophyseal tract’ with carrier protein to the nerve endings in the posterior pituitary gland where they are stored.
The neurohypophysis contains abundant capillaries, particularly in its ventral portion where most hormone release occurs. Herring bodies often are seen in association with these capillaries. Many of these capillaries are fenestrated (contain holes), facilitating delivery of hormones into the blood.
Osmoreceptors of the hypothalamus (Fig. 1.9)
Osmoreceptors are special sensory receptors primarily found in the supraoptic and paraventricular nuclei of the hypothalamus that detect changes in extracellular osmolality. Osmoreceptors receive synaptic input from regions adjacent to the anterior wall of the third ventricle. They also receive input from ascending adrenergic pathways from the low and the high pressure baroreceptors.
ADH is released when the body is dehydrated. ADH will help the kidneys to conserve water, thus concentrating the urine and reducing urine volume.
zoom view
Figure 1.9: Osmoreceptors of the hypothalamus
Role of osmolality, hypovolaemia and non-osmotic stimuli in ADH release
  1. Role of osmolality in ADH release (Fig. 1.10)
    • The main stimulus for secretion of ADH is increased osmolality of plasma. Reduced volume of extracellular fluid also has this effect, but its a less sensitive mechanism (note that anything that stimulates ADH secretion also stimulates thirst).
    • Plasma osmolality is closely regulated by osmoreceptors in the hypothalamus. These specialised neurones control the secretion of the antidiuretic hormone (ADH) and the thirst mechanism. Plasma osmolality is therefore, maintained within relatively narrow limits by varying both, water intake and water excretion.
      As seen in the Figure 1.11, antidiuretic hormone concentrations rise steeply and linearly with increasing plasma osmolality.
    • When plasma osmolality is below a certain threshold, the osmoreceptors are not activated and secretion of antidiuretic hormone is suppressed. When osmolality increases above the threshold, the osmoreceptors recognise this as their cue to stimulate the neurones that secrete antidiuretic hormone.
      • ADH is secreted from the posterior pituitary gland in response to reductions in plasma volume and in response to increase in the plasma osmolality due to shrinkage of osmoreceptors.
        zoom view
        Figure 1.10: Role of osmolality in ADH release
        zoom view
        Figure 1.11: ADH concentrations and plasma osmolality
      • Conversely, a decrease in extracellular osmolality and increase in plasma volume causes osmoreceptors to swell and suppresses the release of ADH.
      • Feedback control: Increased ADH release in response to increased plasma osmolality allows reabsorption of water in the kidneys. This reduces plasma solute, i.e. sodium, which is detected by the osmoreceptors in the hypothalamus, allows sensitive feedback control of ADH secretion. Decreased ADH release allows a water diuresis, which tends to increase osmolality to normal.
        In response to changing plasma sodium, release of ADH changes, which can vary urine osmolality from 50 to 1200 mOsmol/kg and urinary volume from 0.4 to 20 L/day.
  2. Role of hypovolaemia in ADH release (Fig. 1.12)
    • Hypovolaemia is a more potent stimulus for ADH release than hyperosmolality. A hypovolaemic stimulus to ADH secretion will override a hypotonic inhibition and volume will be conserved at the expense of tonicity.
    • The maximum levels of ADH reached with significant volume depletion (20%) are about 40 pg/ml which is larger than the 12-15 pg/ml reached with a maximum isovolaemic increase in osmolality.
    • Secretion of antidiuretic hormone is also stimulated by decrease in blood pressure, conditions sensed by stretch receptors in the heart, large arteries and veins. Changes in blood pressure are not as sensitive stimulator as increased osmolality. Loss of 15 to 20% of blood volume by haemorrhage results in massive secretion of antidiuretic hormone.15
      zoom view
      Figure 1.12: Role of hypovolaemia in ADH release
    • Angiotensin II stimulates ADH secretion, in keeping with its general pressor and pro-volaemic effects on the body.
    • Atrial and B-type natriuretic peptide inhibits ADH secretion, by inhibiting Angiotensin II-induced stimulation of ADH secretion.
  3. Non-osmotic stimulus for release of antidiuretic hormone
    • Secretion of ADH is stimulated by pain, nausea, emotional stress, hypoxia and drugs such as morphine and barbiturates.
    • ADH is released by the posterior pituitary gland in response to positive pressure ventilation and surgical stimuli.
Role of ADH in pregnant patients
Osmoreceptors monitor the solute concentrations in the blood. When the osmoreceptors send excitatory messages to the “ADH secreting neurones”, less urine is produced, leaving more volume in the circulating blood. During pregnancy the osmoreceptors are “reset” to deal with the increased blood volume of pregnancy.
  1. The actions of the hormones of the posterior pituitary are important in the pregnant woman who is at risk for preterm labour especially if there is maternal dehydration.16
  2. Maternal dehydration may trigger the secretion of ADH by the posterior pituitary. It is thought that oxytocin may also be released at the same time, bringing about uterine contraction before the optimum time. These uterine contractions, or uterine “irritability” (low intensity, high frequency contractions) of preterm labour are often treated with maternal hydration.
  3. Women at risk for preterm labour are encouraged to drink abundant amounts of water throughout the day, and, if hospitalised for contractions, hydration with a bolus of intravenous fluid is often effective to “quiet” the uterus.
Role of ADH in trauma patients
In trauma patients, a great deal of ADH is released, to counteract blood loss. The result is constriction of smooth muscles of the blood vessels, in order to raise the arterial blood pressure. Very little blood is getting to the baby through the constricted blood vessels if patient is pregnant.
Physiological Effects of Antidiuretic Hormone
Effects of ADH on the Kidney (Fig. 1.13)
The single most important effect of antidiuretic hormone is to conserve body water by reducing the loss of water in urine. ADH initiates its physiological actions by combining with specific receptors of ADH (vasopressin receptors), i.e. V1 and V2 receptors.
  1. Antidiuretic hormone binds to the V2 receptors on cells in the distal renal tubules and collecting ducts of the kidney, which stimulates insertion of “water channels” or aquaporins 2 into the membranes of cells.
    zoom view
    Figure 1.13: Effects of ADH on the kidney
  2. Insertion of aquaporin-2 channels requires signalling by the antidiuretic hormone. These channels transport solute-free water through tubular cells. This allows water reabsorption and excretion of more concentrated urine, i.e. antidiuresis. It leads to a decrease in plasma osmolality and an increase osmolality of urine.
  3. Without ADH, little water is reabsorbed in the collecting ducts and dilute urine is excreted.
Effects of ADH on the Vascular System
Though the most important role of ADH is to regulate water in the body, in many species, high concentrations of antidiuretic hormone causes widespread constriction of arterioles, which leads to increased arterial pressure. It was for this effect that the name vasopressin was coined. In healthy humans, antidiuretic hormone has minimal pressor effects.
  1. The V1 receptors are located on blood vessels and are responsible for the vasopressor action by ADH. ADH increases peripheral vascular resistance (vasoconstriction) and thus increases arterial blood pressure.
  2. This effect appears small in healthy individuals; however it becomes an important compensatory mechanism for restoring blood pressure in hypovolaemic shock which occurs during haemorrhage.
  3. However, this response appears to be reset within 32 hours of sustained hypovolaemia.
Role of thirst in water balance
There is an interesting parallel between antidiuretic hormone secretion and thirst. Both phenomena appear to be stimulated by hypothalamic osmoreceptors, although probably not the same ones. The osmotic threshold for antidiuretic hormone secretion is considerably lower than for thirst, as if the hypothalamus is saying “Let's not bother him by invoking thirst unless the situation is bad enough that antidiuretic hormone cannot handle it alone.”
  1. Thirst is the primary mechanism of controlling water intake, is triggered by an increase in body fluid osmolality or by a decrease in extracellular volume (in response to a decrease in volume of the plasma).
  2. Thirst leads to drinking which is a powerful defense against serum hyperosmolality. Drinking stimulates mechanoreceptors in the mouth and pharynx. These peripheral receptors provide input to the hypothalamus and the sensation of thirst is attenuated. This occurs even before any reduction in plasma tonicity. This may safeguard against the over-ingestion of water as there is an inevitable delay before the ingested water is absorbed and available to decrease plasma osmolality.
  3. As long as access to water is unrestricted and the person is able to drink, then significant serum hyperosmolality will not develop. For example, elderly patients with non-ketotic hyperglycaemia do not become significantly hyperosmolar unless water intake becomes restricted for some reason.18
Factors influencing thirst mechanism (Fig. 1.14)
Both the thirst and the ADH mechanisms are regulated in the hypothalamus. The thirst centre is located in the lateral hypothalamus.
  1. Activation of osmoreceptors in the lateral pre-optic area of the hypothalamus by increase in extracellular osmolality stimulates thirst centre and causes the individual to consume water. Conversely, hypo-osmolality suppresses the thirst centre.
  2. Thirst is the major defense mechanism against hyperosmolality and hypernatraemia, because it is the only mechanism that increases water intake. Unfortunately, the thirst mechanism is only operative in conscious individuals who are capable of drinking.
    Stimulation of Thirst and ADH Secretion
    ECF hyperosmolality
    Aortic, carotid and atrial baroreceptors
    Emotional stress
    β agonists
    Cholinergic agents
    Renin-angiotensin stimulation
    zoom view
    Figure 1.14: Factors influencing thirst mechanism
  3. The threshold of thirst for osmotic stimuli has a higher set-point then that for ADH release. Some consider thirst as the ‘back up’ mechanism that acts only when the ADH release is insufficient to reduce the plasma osmolality to normal.
The four major stimuli to thirst are:
  1. Hypertonicity
    Cellular dehydration acts via an osmoreceptor mechanism in the hypothalamus.
  2. Hypovolaemia
    Low volume is sensed via the low pressure baroreceptors in the great veins and right atrium.
  3. Hypotension
    The high pressure baroreceptors in carotid sinus and aorta provide the sensors for this input.
  4. Angiotensin II
    This is produced consequent to the release of renin by the kidney in response to renal hypoperfusion.
2. Role of Renin in Water Balance
Renin is also known as an angiotensinogenase. It is an enzyme that participates in the body's renin-angiotensin system (RAS) is also known as the renin-angiotensin-aldosterone axis which regulates extracellular volume, and arterial vasoconstriction. Thus, it regulates the body's mean arterial blood pressure.
The capillary vascular supply of nephron consists of two distinct capillary beds, the glomerular capillary bed and the peritubular capillary bed. A vessel leading to and from the glomerulus is the glomerular capillary bed. The afferent arteriole feeds the bed while the efferent arteriole drains it. The glomerular capillary bed has no comparison elsewhere in the body.
Glomerular capillary bed is a high-pressure bed along its entire length. Its high pressure is a result of two major factors:
  1. The bed is fed and drained by arterioles (arterioles are high-resistance vessels as opposed to venules, which are low-resistance vessels).
  2. The afferent feeder arteriole is larger in diameter than the efferent arteriole draining the bed.
The high hydrostatic pressure created by these two anatomical features forces out fluid and blood components smaller than proteins from the glomerulus into the glomerular or Bowman's capsule. That is, it forms the filtrate which is processed by the nephron tubule.
  1. Juxtaglomerular (JG) cells are associated with the afferent arteriole while entering the renal glomeruli. They are the primary site of renin storage and release in the body (Fig. 1.15).20
    zoom view
    Figure 1.15: Nephron with juxtaglomerular apparatus
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    Figure 1.16: Juxtaglomerular apparatus
  2. In the kidney, the macula densa is an area of closely packed specialised cells lining the wall of the distal tubule, and it lies adjacent to the juxtaglomerular cells of the afferent arteriole. The cells of the macula densa are chemoreceptors that sense the tubular concentration of sodium and can help to regulate volume status. Macula densa region with juxtaglomerular cells of the kidney is called juxtaglomerular apparatus, which is another modulator of blood osmolality (Fig. 1.16).21
Factors influencing release of renin (Fig. 1.17)
Renin is a proteolytic enzyme that is released into the circulation primarily from juxtaglomerular cells of kidney, which is activated via signalling from the macula densa. Its release is stimulated by:
  1. Increased activity of renal sympathetic nerves
    Beta1 adrenoceptors located on the juxtaglomerular cells respond to renal sympathetic nerve stimulation by releasing renin. Increased activity of renal sympathetic nerve is seen when plasma volume decreases.
  2. Renal artery hypotension
    Renal artery hypotension is caused by systemic hypotension or renal artery stenosis. A reduction in afferent arteriolar pressure causes the release of renin from the juxtaglomerular cells, whereas increased afferent arteriolar pressure inhibits renin release.
  3. Decreased glomerular filtration
    When afferent arteriolar pressure is reduced, glomerular filtration decreases, and this reduces sodium and chloride in the distal tubule. A decrease in sodium and chloride concentration in distal tubule is sensed by macula densa that has following effects:
    • It increases renin release from the juxtaglomerular cells which are the major storage sites for renin.
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      Figure 1.17: Factors influencing release of renin
    • Decrease filtration fraction serves as an important mechanism contributing to the release of renin when there is afferent arteriole hypotension.
    • Renin's primary function is therefore eventually to cause an increase in blood pressure, leading to restoration of perfusion pressure in the kidneys.
When sodium and chloride is elevated in the tubular fluid, renin release is inhibited. Hyperkalaemia also releases renin. There is evidence that prostaglandins (PGE2 and PGI2) stimulate renin release in response to reduced sodium and chloride in the distal tubule.
Role of renin in water balance
Angiotensinogen is a glycoprotein synthesised and secreted into the bloodstream by the liver. Renin acts on angiotensinogen (gamma globulin from the liver) and converts it into angiotensin I. Angiotensin I plays role in water balance through angiotensin II and aldosterone.
Renin indirectly increases sodium reabsorption, and increase in blood volume and/or pressure, due to formation of angiotensin II and release of aldosterone.
3. Role of Angiotensin II in Water Balance (Fig. 1.18)
Angiotensin converting enzyme (ACE) is also known as kinase III is widely distributed in the small vessels of the body, but particularly concentrated in the pulmonary capillaries of the lungs. Angiotensin converting enzyme (ACE) converts angiotensin I to its active form angiotensin II (vasoconstrictor) and inactivates bradykinin (vasodilator).
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Figure 1.18: Role of Angiotensin II in water balance Patterned arrows shows action of angiotensin II
  1. Angiotensin II is a potent constrictor of all blood vessels.
    It acts on the smooth muscle and, therefore, raises the peripheral resistance, posed by these arteries to the heart. The heart, trying to overcome this increase in its ‘load’, by working more vigorously, causing the blood pressure to rise and restore blood pressure.
  2. Angiotensin II conserves blood volume, by reducing urinary loss through the secretion of vasopressin (ADH) from the posterior pituitary gland.
  3. Stimulates cardiac hypertrophy and vascular hypertrophy.
  4. The RAAS also acts on the CNS to increase water intake by stimulating thirst.
  5. Facilitates norepinephrine release from sympathetic nerve endings and inhibits norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic function.
  6. Angiotensin II is converted to angiotensin III. Angiotensin III acts on the adrenal glands and releases aldosterone.
4. Role of Angiotensin III in Water Balance
Angiotensin III stimulates aldosterone production without vasoconstriction.
5. Role of Aldosterone in Water Balance
So far we have discussed the role of the pituitary gland (through the release of ADH) and thirst in the regulation of body fluids. These are the two primary mechanisms that are responsible for making sure that there is an appropriate water and sodium level in the blood.
The second set of glands that participate in the regulation of body fluids are the adrenal glands. The adrenals sit on top of each kidney like a cap and, although they usually vary somewhat in size and shape, they generally look like pyramids. Like the pituitary, each adrenal gland is really two glands in one. The central portion is termed the adrenal medulla, and the outer part is the adrenal cortex. The two sections represent distinct glands that secrete different hormones.
All the hormones secreted by the adrenal cortex are “adrenocorticosteroids.” There are three groups of adrenocorticosteroids, each secreted by cells in a different layer of the cortex:
  1. Glucocorticoids, which influence the metabolism of carbohydrates, proteins, and fats.
  2. Sex hormones, which affect sexual characteristics.
  3. Mineralocorticoids, which helps to regulate the concentrations of extracellular electrolytes, e.g. aldosterone.24
Aldosterone secretion is controlled in various ways:
  1. Increased potassium levels or decreased sodium content are the most sensitive stimulators of aldosterone.
  2. The adrenal cortex also directly senses change in plasma osmolality. When the osmolality increases above normal and aldosterone secretion is stimulated.
  3. The stretch receptors located in the atria of the heart detect decreased blood pressure. The stimulated stretch receptors send impulses to the adrenal gland to release aldosterone.
Mechanism of action of aldosterone (Figs 1.19 and 1.20)
Angiotensin III acts on the adrenal glands and releases aldosterone. Aldosterone is a yellow steroid hormone (mineralocorticoid family) produced by the outer-section (zona glomerulosa) of the adrenal cortex in the adrenal gland.
Aldosterone acts primarily on the distal tubules and collecting ducts of the kidneys. Aldosterone increases permeability of sodium channel, potassium channel and activity of sodium potassium pump.
This hormone acts mainly through the kidneys to maintain the homeostasis of sodium and potassium ions. It causes the kidney to excrete potassium (K+) and to reabsorb sodium back into the bloodstream. More specifically, aldosterone causes the kidneys to conserve sodium ions (Na+) and to excrete potassium ions (K+). At the same time, it promotes water conservation and reduces urine output.
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Figure 1.19: Mechanism of action of aldosterone Note: Large Na+, K+ shows high concentration and vice versa
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Figure 1.20: Role of aldosterone in water balance
  1. The mechanism that controls the secretion of aldosterone is primarily responsive to the potassium ion (K+) concentration in body fluids. This mechanism operates as a negative feedback loop to detect high levels of K+ and to release aldosterone so that the K+ level can be reduced. Or, if the K+ level is too low, less aldosterone will be released so that K+ is allowed to accumulate.
    • As the K+ concentration rises, sensors in the body detect this increase and signal the adrenal cortex to release more aldosterone into the bloodstream.
    • The blood carries aldosterone to the kidneys which, in turn, stop reabsorbing the K+ back into the bloodstream, causing more K+ to be excreted in the urine.
  2. Aldosterone secretion is also stimulated in response to changes in the sodium ion (Na+) concentration in the blood. In this case, if low levels of Na+ are detected by the body, the adrenal cortex is stimulated to release aldosterone.
    • The presence of aldosterone stimulates the tubules to reabsorb sodium salts back into the blood at a faster rate so that it can remain in the body.
    • On the other hand, if high levels of Na+ are detected by the body, the adrenal cortex holds back on the release of aldosterone to decrease reabsorption of the salt back into the blood, allowing more to be excreted.26
  3. Finally, the presence of aldosterone tends to increase tubular water reabsorption (that is, water tends to flow out of the kidney tubules back into the blood).
  4. Aldosterone is a part of the renin-angiotensin system. Aldosterone is the final common pathway in a complex response to decreased effective arterial volume, i.e. hypovolaemia.
The term “salt- and water-retaining hormone,” therefore, is a descriptive nickname for aldosterone. Aldosterone can also be called the “potassium-eliminating hormone”.
Summary (Figs 1.21 and 1.22)
The net effect aldosterone on urine excretion is a decrease in the amount of urine excreted, with an increase in the osmolality of the urine. The lack of aldosterone causes less sodium to be reabsorbed in the distal tubule. The overall effect of aldosterone is to increase reabsorption of sodium and water in the kidney, expanding of intravascular fluid volume and, therefore, increasing blood pressure.
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Figure 1.21: Renin-angiotensin-aldosterone system
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Figure 1.22: Summary
6. Role of Atrial Natriuretic Peptide (ANP) and B-type Brain Natriuretic Peptide (BNP) in Water Balance (Fig. 1.23)
Two powerful hormonal systems regulate total body sodium. The renin-angiotensin-aldosterone pathway is regulated not only by the mechanisms that stimulate renin release, but it is also modulated by natriuretic peptides (ANP and BNP) released by the heart. These natriuretic peptides act as an important counter-regulatory system.
The natriuretic peptide defends against sodium overload and the renin-angiotensin-aldosterone can defend against sodium depletion and hypovolaemia.
  1. Atrial natriuretic peptide (ANP) is a polypeptide hormone involved in the homeostatic control of body water and sodium. ANP is released from the cardiac atria in response to increased atrial stretch.
  2. Brain natriuretic peptide, now known as B-type natriuretic peptide (BNP) secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes). Brain natriuretic peptide is named as such because it was originally identified in extracts of porcine brain, although in humans it is produced mainly in the cardiac ventricles.
Physiological action of ANP and BNP
ANP and BNP are released due to the increased atrial and ventricles stretch due to expanded extracellular volume and in response to high blood pressure. Both exert vasodilator effects and increase renal excretion of water and sodium.
ANP and BNP dilate the afferent glomerular arteriole, constrict the efferent glomerular arteriole, and relax the mesangial cells. This increases pressure in the glomerular capillaries, thus increasing the glomerular filtration rate (GFR), resulting in greater excretion of sodium and water.28
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Figure 1.23: Role of ANP and BNP in water balance
ANP and BNP inhibit renin secretion, thereby inhibiting the renin-angiotensin system. It also reduces aldosterone secretion by the adrenal cortex since angiotensin III formation is reduced. Reduced aldosterone decreases sodium reabsorption in the distal convoluted tubule and cortical collecting duct of the nephron. ANP and BNP antagonise vasoconstriction secondary to angiotensin II.
ANP and BNP are the predominant salt excreting hormone resulting in decreased sodium reabsorption producing dilute urine (300 mOsm/kg) and abundant urine sodium (80 mEq/L).
The physiological actions of BNP are similar to ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. Thus, the net effect of BNP and ANP is a decrease in blood volume which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction. ANP and BNP secretion is decreased during hypovolaemia.
Therapeutic manipulation of this pathway is very important in treating hypertension and heart failure. ACE inhibitors, angiotensin II receptor blockers and aldosterone receptor blockers are used to decrease arterial pressure, ventricular afterload, blood volume and hence ventricular preload, as well as to inhibit and reverse cardiac and vascular hypertrophy.29
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Figure 1.24: Role of dopamine in water balance
7. Role of Kinins in Water Balance
Kinins are converted from kininogens by kallikrein and are regulated by salt intake, renin release and hormone levels. They cause renal vasodilatation and natriuresis.
8. Role of Dopamine in Water Balance (Fig. 1.24)
Dopamine is produced in the kidneys following conversion from L-dopa under the action of the L-amino acid decarboxylase enzyme, present in the proximal tubules.
The conversion is controlled by a high salt diet, leading to increased urinary sodium loss, as dopamine inhibits sodium reabsorption in the proximal tubule and contributes to the increase in urine output. This is seen following the administration of a low dose of dopamine.
9. Role of Prostaglandins in Water Balance (Fig. 1.25)
The renal synthesis of prostaglandins, such as prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2), tends to maintain renal blood flow and GFR through vasodilatation and directly increases water and sodium excretion.
Dopaminergic renal vasodilatation in part acts through the release of PGI2. This administration of dopaminergic antagonists leads to reduced urinary prostaglandins and loss of dopaminergic vasodilatation.
Thereby, explaining why a low dose of dopamine appears to be ineffective in septic ICU patients who already have a prostaglandin-driven kidney.30
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Figure 1.25: Role of prostaglandins in water balance
V. Role of the Kidneys in Water Balance (Fig. 1.26)
Urine is produced not only in order to eliminate many of the cellular waste products, but also to control both the amount and the composition of the extracellular fluid in the body. Controlling the amount of water and chemicals in the body is essential to life, and our body does so by producing various amounts of urine so that we can either excrete the “extra” water and chemicals (mainly sodium) or conserve the water and chemicals when they are in short supply.
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Figure 1.26: Urinary excretion of water
Therefore, the volume of urine that we excrete everyday is a reflection of how much extracellular fluid and sodium our body has to spare. The kidney tubule regulation of the salt and water in our bodies is the most important factor in determining urine volume. Too much water and salt in our bodies is dangerous and too little water and salt in our bodies is also dangerous. Therefore, the level of water and salts excreted in urine and the urine volume is adjusted to the needs of the body. As a general rule, however, and under optimum conditions, the body produces urine at a rate of about 1 ml/min.
In other words kidneys are the major regulators of water output. The kidneys can directly control the volume of body fluids, by the amount of water excreted in the urine. Regulation of water balance by the kidneys is dependent on its ability to excrete urine with an osmolality that varies from maximal dilution to maximal concentration.
  1. Either the kidneys can conserve water by producing urine that is concentrated relative to plasma, or they can rid the body of excess water by producing urine that is dilute relative to plasma.
  2. ADH provides a mechanism for adjusting water output via the kidney.
  3. Reabsorption of filtered water and sodium is enhanced by hormonal factors such as antidiuretic hormone (ADH) and renin-angiotensin-aldosterone system and decreased by atrial and B-type natriuretic peptide (ANP and BNP).
Renal water handling has three important components (Fig. 1.27):
  1. Delivery of tubular fluid to the diluting segments of the nephron
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    Figure 1.27: Renal filtration, reabsorption, and excretion of water. The black arrows represent electrolytes and the patterned arrows represent water. Water and electrolytes are filtered by the glomerulus
    Note: The numbers (300, 600, 900 and 1200) between the descending and ascending loops of Henle represent the osmolality of the interstitium in mOsm/kg.
  2. Separation of solute and water in the segments
  3. Variable reabsorption of water in the collecting ducts.
Proximal Tubule (1)
In the proximal tubule, water and electrolytes are reabsorbed isotonically.
Descending and Ascending Loop of Henle (2)
  • In the descending loop of Henle, water is absorbed to achieve osmotic equilibrium with the interstitium while electrolytes are retained.
  • This concentrated fluid is diluted by the active reabsorption of electrolytes in the ascending loop of Henle and in the distal tubule, both of which are relatively impermeable to water.
    • The cells of the macula densa of distal tubule are chemoreceptors that sense the tubular concentration of sodium and can help to regulate volume status.
Medullary (3a) and Cortical (3b) Diluting Sites
  • The delivery of solute and fluid to the distal nephron is a function of proximal tubular reabsorption, as proximal tubular reabsorption increases, delivery of solute to the medullary (3a) and cortical (3b) diluting sites decreases.
  • In the diluting sites, electrolyte free water is generated through selective reabsorption of electrolytes while water is retained in the tubular lumen, generating a dilute tubular fluid.
Collecting ducts (in the absence of vasopressin—ADH) (4a) and collecting ducts (in the presence of vasopressin)(4b)
As fluid in the distal tubule enters the collecting duct, osmolality is approximately 50 mOsm/kg.
  • In the absence of vasopressin (ADH), the collecting ducts (4a) remain relatively impermeable to water and dilute urine is excreted.
  • When vasopressin (ADH) acts on the collecting ducts (4b), water is reabsorbed since the collecting duct becomes vasopressin responsive nephron segments, allowing the excretion of concentrated urine.
Role of the kidneys in sodium reabsorption (Fig. 1.28)
More than 99% of the filtered sodium is reabsorbed by the kidneys at four sites.
  1. Proximal Tubule ①
    50-70%, absorption is active iso-osmotic (having the same osmotic pressure or exhibiting equal osmotic pressure) reabsorption. (Isotonic is when a solution has the same salt concentration as the blood and cells of the human body).
  2. Ascending Loop of Henle ②
    10-20%, absorption is secondary to active reabsorption of chloride.
  3. Distal Tubule ③
    10% is active reabsorption under influence of aldosterone. Bulk reabsorption occurs at the proximal tubule but the eventual sodium concentration of the urine is dependent upon distal tubular nephron.33
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    Figure 1.28: Role of the kidneys in sodium reabsorption
  4. Collecting duct 1% ④
    1% absorption is active absorption.
Hormonal control of urine production (Fig. 1.29)
  1. Atrial and B-type natriuretic peptide (ANP and BNP) is released from the heart when extracellular volume is increased.
    • ANP and BNP increases glomerular filtration rate (GFR) by increasing blood pressure and the filtration fraction.
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      Figure 1.29: Hormonal control of urine production
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      Figure 1.30: Regulation of sodium concentration by regulation of water homeostasis
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      Figure 1.31: Regulation of sodium concentration by regulation of water homeostasis—Summary
    • Urine production is increased by ANP and BNP since it inhibits sodium reabsorption in the distal nephron.
  2. Urine production is reduced by the antidiuretic hormone (ADH), which works on the collecting duct.
VI. Regulation of Sodium Concentration by Regulation of Water Homeostasis—Summary (Figs 1.30 and 1.31)
Osmolality sensors (osmoreceptors) are neurones located in the hypothalamus, which stimulate thirst and antidiuretic hormone release (vasopressin) from posterior pituitary in the circulation. The osmoreceptors are by far more sensitive, enabling fine control over plasma volume. Strong release of ADH occurs in response to reduced plasma volume, irrespective of the tonicity of plasma.
ADH is stored as granules in the posterior pituitary and is released in response to an increase in serum osmolality. Under normal conditions, serum osmolality and therefore sodium concentration (which is predominant ion in ECF) is regulated by water homeostasis (Figs 1.32 and 1.33).
Water balance naturally fluctuates with the dictates of sodium balance (renin–angiotensin system). The urine sodium content can be used to differentiate oliguric states. Normal responses to hypovolaemia make urine sodium content low (<20 mmol/L) whereas in acute tubular necrosis it usually exceeds 40 mmol/L.36
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Figure 1.32: Role of sodium in ADH release
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Figure 1.33: Summary of water homeostasis
Water losses which are sufficient to cause ECF volume contraction, hypotension, and decrease in cardiac output stimulate ADH release, causing water retention and dilutional hyponatraemia.
Sodium and water metabolism are intimately related, although controlled by separate mechanisms. The movement of sodium is always accompanied by water to maintain osmotic equilibrium. Thus, in conditions of sodium depletion or accumulation, there is always an associated shift of water, which is the basis to understand intravenous fluid infusion in various circumstances.