Fluid, Electrolyte and Acid-Base Physiology: A Problem-Based Approach, Fourth Edition

✍ Scribed by Mitchell L. Halperin MD FRCPC, Marc B. Goldstein MD FRCPC, Kamel S. Kamel MBBCh FRCP

• Publisher: Saunders
• Year: 2010
• Tongue: English
• Leaves: 615
• Edition: 4th
• Category: Library

✦ Synopsis

The revised and updated fourth edition of Fluid, Electrolyte and Acid-Base Physiology continues to offer expert advice on the bedside management of acid-base and electrolyte disorders. Distinguished authors synthesize key theoretical and clinical information in a way that is easy to understand and apply. Discussions on the latest science, as well as new cases, new discoveries, and new approaches in intensive care are just a few of the updates you'll find to help you make the best management decisions. Clinical information is presented in an easy-to-understand style, and the integration of color offers increased visual guidance. What's more, diagnostic flow charts and critical questions challenge your problem-solving skills and reinforce your decision-making expertise.Incorporates relevant information on energy metabolism and endocrine, gastrointestinal, respiratory, and cardiovascular physiology.Features a consistent, user-friendly format with diagnostic algorithms and helpful margin notes.Includes numerous case studies that illustrate how key management principles are applied in practice.Presents questions and explanations throughout that let you test your knowledge and hone your skills. Features entirely new cases with discussions that keep you on the cusp of current clinical dilemmas and standards of practice.Discusses new treatment options to help you provide optimal care. Presents new discoveries to bring you up to date on the latest findings in science and clinical practice.Offers new approaches in critical care keeping you current in this emerging area of nephrology.

✦ Table of Contents

Cover......Page 1
ISBN 9781416024422......Page 2
Copyright
......Page 3
Dedication
......Page 4
Preface......Page 8
How to Use This Book......Page 11
Interconversionof Units......Page 12
List of Abbreviations......Page 13
List of Cases......Page 16
List of Flow Charts......Page 18
chapter 1
Principles of Acid-Base Physiology......Page 22
Uncoupling of oxidative phosphorylation......Page 24
PRODUCTION AND REMOVAL OF H......Page 25
HPO......Page 27
Base balance......Page 28
Binding of H to proteins......Page 29
Bicarbonate buffer system......Page 30
Venous Pco......Page 31
Failure of the bicarbonate buffer system......Page 32
Reabsorption of NaHCO3 in the proximal convoluted tubule......Page 34
Regulation of proximal H+ secretion......Page 36
Renal threshold for reabsorption of HCO3−......Page 37
Net acid excretion......Page 38
Biochemistry of NH production......Page 39
Diffusion of NH3 in the renal medulla: A more detailed examination......Page 44
Secretion of H+ in the distal nephron......Page 45
Urine pH and the excretion of NH4+......Page 46
High urine pH and CaHPO4 kidney stones......Page 47
WHY IS THE NORMAL BLOOD pH ...0?......Page 48
Acid-base changes in a sprint......Page 50
The alkaline phase of ischemic exercise......Page 51
Recovery from the sprint, an important rolefor the bicarbonate buffer system......Page 52
INTRODUCTION......Page 58
Questions......Page 59
PART A
DISORDERS OF ACID-BASE BALANCE......Page 60
Respiratory alkalosis......Page 61
MAKING AN ACID-BASE DIAGNOSIS......Page 62
LABORATORY TESTS USED TO MAKE ACID-BASE DIAGNOSeS......Page 63
An example......Page 64
Issues related to PAlbumin......Page 65
The osmolal gap in plasma......Page 66
The urine net charge......Page 67
The urine pH......Page 68
The Pco2 in alkaline urine......Page 69
The fractional excretion of HCO3–......Page 70
4Determine the quantitative relationship between the fall in PHCO3 and the rise in the PAnion gap......Page 71
5Detect the “tissue” form of respiratory acidosis......Page 72
Reliance on the arterial Pco2......Page 73
Correction for the PAlbumin......Page 74
Correlating the clinical and laboratory information.......Page 75
Does the patient have respiratory acidosis?......Page 76
What is the most likely basis for the respiratory acidosis?......Page 77
chapter 3
Metabolic Acidosis:
Clinical Approach......Page 79
PART A
CLINICAL APPROACH......Page 81
EMERGENCIES IN THE PATIENTWITH METABOLIC ACIDOSIS......Page 82
Toxin-induced metabolic acidosis......Page 83
Dangers related to overly aggressive administration of saline......Page 84
ASSESS THE EFFECTIVENESS
OF THE BICARBON......Page 86
DETERMINE THE BASIS OF METABOLIC ACIDOSI
......Page 87
Assess the renal response to metabolic acidosis......Page 88
What dangers might be created by therapy?......Page 89
Is metabolic acidosis present?......Page 90
What is the basis of the metabolic acidosis?......Page 91
chapter 4
Metabolic Acidosis due to a Deficit of NaHCO3......Page 94
DEFINITIONS OF METABOLIC ACIDOSIS......Page 95
PATHOGENESIS OF METABOLIC ACIDOSIS DUE TO NaHCH03 LOSS
......Page 97
DIRECT LOSS OF NaHCO3
......Page 98
Secretion of HCO3− by the late small intestine and the colon......Page 99
The patient with NaHCO3 loss via the GI tract......Page 100
Treatment......Page 102
PART C DISEASES WITH LOW RATE OF EXCRETION OF NH4+
......Page 103
PROXIMAL RENAL TUBULAR ACIDOSIS
......Page 104
Possible basis of the findings in isolated proximalrenal tubular acidosis......Page 105
Intracellular defect......Page 106
Diagnostic issues in the patient with proximal renaltubular acidosis......Page 107
Questions......Page 108
Clinical approach: Initial steps......Page 109
Subtype with low NH......Page 110
Subtype with low net distal H secretion......Page 112
Background physiology......Page 117
Patients with true “incomplete renal tubular acidosis”......Page 118
METABOLIC ACIDOSIS IN RENAL FAILURE
......Page 120
Generate new HCO3− by dissolving the alkaline salts in bone
......Page 121
Mechanisms......Page 122
Strategy used: Raise the osmolality at the tip of the villus......Page 124
CHOLERA: FROM BACTERIA TO DISEASE......Page 125
Reducing the incidence of cholera......Page 126
What is the basis of the metabolic acidosis?......Page 127
What is the cause of the low rate of excretion of NH4+?......Page 128
chapter 5
Ketoacidosis......Page 130
METABOLIC PROCESS ANALYSIS......Page 132
Hormonal signals......Page 133
Hierarchy of fuel selection in a metabolic process......Page 134
Formation of acetyl-CoA in the liver......Page 135
The metabolic fates of acetyl-CoA......Page 136
Production of acetone from ketoacids......Page 138
Clinical messages......Page 139
CLINICAL ASPECTS OF KETOACIDOSIS......Page 140
DIAGNOSIS OF DIABETIC KETOACIDOSIS......Page 141
Natural history......Page 142
Changes in body composition owing to the osmotic diuresis......Page 143
Laboratory findings in a patient with diabetic ketoacidosis......Page 144
Cautions in the laboratory diagnosis of diabetic ketoacidosis......Page 145
Cerebral edema during treatment of diabetic ketoacidosisin children......Page 146
Goals of intravenous therapy......Page 150
BIOCHEMISTRY OF ALCOHOLIC KETOACIDOSIS......Page 154
Removal of ketoacids in the patient with alcoholic ketoacidosis......Page 155
Associated biochemical findings......Page 156
Classification......Page 157
Importance of the PGlucose......Page 158
Nutritional deficiencies......Page 159
TREATMENT OF ALCOHOLIC KETOACIDOSIS......Page 160
Nutritional deficiencies......Page 161
CONTROL OF KETOGENESIS: A MOREDETAILED ANALYSIS......Page 162
Control by extrahepatic substrates......Page 163
Control by the supply of intrahepatic substrates(ADP and NAD+)......Page 164
Control of intrahepatic substrates by uncoupled respiration......Page 166
QUANTITATIVE ASPECTS OF ETHANOLMETABOLISM......Page 170
What makes ketoacidosis due to starvation or hypoglycemia an unlikely diagnosis?......Page 171
How may the patient’s intake of sweetened soft drinks contribute to the development of ketoacidosis?......Page 172
What are the major threats to Andy’s life?......Page 173
What are the issues for therapy?......Page 174
chapter 6
Metabolic Acidosis: Acid Gain Types......Page 179
MAJOR THREATS IN THE PATIENTWITH METABOLIC ACIDOSIS......Page 181
Causes of a rise in the concentration of l-lactate− and H+
......Page 182
Metabolic processes involved in the production of l-lactic acid......Page 183
Metabolic processes involved in the production of l-lactic acid during ethanol oxidation......Page 184
Rate of anaerobic glycolysis......Page 185
Clinical implications of these principles of biochemistry......Page 187
Treatment......Page 188
Ethanol......Page 189
Thiamin deficiency......Page 190
Riboflavin deficiency and the use of tricyclic antidepressants......Page 191
Uncoupling of oxidative phosphorylation......Page 192
QUESTIONS......Page 193
ORGANIC ACID LOAD FROM THE GASTROINTESTINAL TRACT (d-LACTIC ACIDOSIS)......Page 195
Diagnosis and treatment
......Page 194
Methanol......Page 196
Ethylene glycol (antifreeze) intoxication......Page 197
QUESTION......Page 198
Reference......Page 201
Clinical manifestations......Page 199
Treatment......Page 200
Biologic effects of reactive oxygen species......Page 202
Why does his blood pressure fall so precipitously?......Page 203
What is the basis for metabolic acidosis?......Page 204
What is the role of the patient’s low PUrate in causing his exercise-induced acute renal failure?......Page 205
DISCUSSION OF QUESTIONS
......Page 206
Reference......Page 207
chapter 7
Metabolic Alkalosis......Page 212
OVERVIEW......Page 214
Deficit of HCl......Page 216
Deficit of KCl......Page 218
Deficit of NaCl......Page 220
Input and retention of NaHCO......Page 221
How large was the deficit of HCl?......Page 223
Why did the deficit of......Page 224
What is the therapy for metabolic alkalosis at this stage?......Page 225
Why did metabolic alkalosis develop on days 3 and 4?......Page 226
Questions......Page 227
Effect of metabolic alkalosis on ventilation......Page 228
Vomiting or nasogastric suction......Page 230
Conditions with high mineralocorticoid activity......Page 231
Metabolic alkalosis associated with the intakeof nonreabsorbable anions......Page 232
Patients with metabolic alkalosis due to deficits of Cl– salts......Page 233
Patients with metabolic alkalosis due to retention of NaHCO3......Page 234
CHRONIC K+ DEFICIENCYAND HYPERTENSION......Page 235
Input of calcium from the gastrointestinal tract......Page 236
Output of calcium......Page 237
chapter 8
Respiratory Acid-Base Disturbances......Page 241
Which Pco2 should be used to assess buffering of H+by bicarbonate buffer in skeletal muscle?......Page 243
OVERVIEW OF CO2 HOMEOSTASIS......Page 244
Removal of CO2......Page 245
PHYSIOLOGY OF CO2 TRANSPORT......Page 246
RENAL RESPONSE TO A CHRONICCHANGE IN Pco2......Page 247
Tissue type......Page 248
Permissive hypercapnia......Page 249
RESPIRATORY ALKALOSIS......Page 250
PHYSIOLOGY OF O2......Page 254
Pitfalls in the use of the alveolar-arterial difference......Page 255
CONTROL OF THE RELEASEOF ERYTHROPOIETIN......Page 256
Is the patient able to buffer H+ appropriately using hisbicarbonate buffer system in skeletal muscle?......Page 258
chapter 9
Sodium and Water Physiology......Page 264
Question......Page 265
Distribution of water across cell membranes......Page 266
Defense of cell volume......Page 268
Distribution of water in the extracellular fluid compartment......Page 270
Work performed in the kidney......Page 272
What is a “normal” extracellular fluid volume?......Page 273
Sequestration of Na+ in an osmotically inactive form......Page 274
Control of the excretion of Na+......Page 275
Tubular reabsorption of Na+; general principles......Page 276
Initial functional unit of the nephron; the proximalconvoluted tubule......Page 278
Nephron segments in the renal medulla......Page 280
Integrative physiology of Na+; cerebral salt wasting......Page 290
CONTROL OF WATER BALANCE......Page 293
Sensor......Page 294
Excretion of a large volume of dilute urine......Page 295
Desalination of luminal fluid in the medullary thick ascending limb of the loop of Henle during a water diuresis......Page 296
Desalination of luminal fluid in the third functional nephron unit of the nephron during a water diuresis......Page 297
Retain “nondangerous” water for future sweat......Page 298
Excretion of concentrated urine......Page 300
Overview of the renal concentrating process......Page 301
Reabsorption of water and electrolytes......Page 303
Regulation of the urine concentrating processin the inner medulla......Page 307
RETENTION OF INGESTED WATER......Page 312
The majority of the descending thin limbsof the loop of Henle lack AQP1......Page 314
A more detailed analysis of the concentrating process......Page 315
Major dangers for the renal medulla......Page 316
Prevent the precipitation of calcium salts deeperin the renal medulla......Page 317
Resolution......Page 320
Critique of the countercurrent multiplier model......Page 326
What is the basis for the acute rise in his PNa?......Page 327
Introduction......Page 333
The plasma Na+ concentration......Page 335
Renal response to a deficit or a surplus of water......Page 336
Regulation of brain volume......Page 337
BASIS OF HYPONATREMIA......Page 338
PART B
ACUTE HYPONATREMIA......Page 339
Deal with emergencies......Page 340
Diagnostic issues......Page 341
Cautions......Page 342
Perioperative hyponatremia......Page 343
Hyponatremia due to retained lavage fluid......Page 344
Negative balance for NaCl......Page 347
Risk factors after the race......Page 348
IMPORTANT FACTS......Page 349
Identify emergencies on admission......Page 350
CLASSIFICATION......Page 351
Low distal delivery of filtrate......Page 352
Questions......Page 355
Discussion of Mini-Case 10-1......Page 356
Water......Page 360
Design of therapy for the second admission......Page 361
Create a positive balance for Na+......Page 362
Are there emergencies present on admission?......Page 363
Discussion of Mini-Case 10-3......Page 366
Administer NaCl and KCl......Page 367
Autonomous release of vasopressin......Page 368
Other possible causes......Page 369
Questions......Page 370
Background to understand why water restrictionmay raise the PNa......Page 371
Increase the excretion of water without electrolytes......Page 372
Use of aquaretics......Page 373
Discussion of Mini-Case 10-4......Page 374
Distal delivery of filtrate......Page 376
Residual water permeability......Page 377
“ESCAPE” FROM THE RENAL ACTIONSOF VASOPRESSIN......Page 378
Conclusions......Page 379
Is this acute hyponatremia?......Page 380
What is your therapy for this patient?......Page 381
chapter 11
Hypernatremia......Page 387
The plasma Na+ concentration......Page 390
Responses to hypernatremia......Page 391
PATHOPHYSIOLOGY OF HYPERNATREMIA......Page 395
Hypernatremia due to a deficit of water......Page 392
Hypernatremia due to Na+ gain......Page 393
IDENTIFY EMERGENCIES PRIOR TO THERAPY......Page 397
Induce a positive balance for water......Page 398
ACUTE HYPERNATREMIA......Page 401
Assess the renal response to hypernatremia......Page 402
Nephrogenic diabetes insipidus......Page 404
Low water intake......Page 409
TREATMENT OF PATIENTS WITH HYPERNATREMIA......Page 410
Chronic hypernatremia......Page 411
Control of water excretion in the newborn......Page 413
Maternal/fetal integrative physiology......Page 414
What are the changes in his ECF and ICFcompartment volumes?......Page 415
What is the basis for the high urine flow rate in this patient?......Page 416
What are the options for therapy?......Page 417
Why does he have such a severe degree of hypernatremia?......Page 418
What is the therapy of hypernatremia in this patient?......Page 419
Introduction......Page 422
SYNOPSIS OF THE PHYSIOLOGY......Page 423
FLUX THROUGH AQP2 WATER CHANNELS......Page 424
DEFINITION OF POLYURIA......Page 425
Osmole excretion rate......Page 426
Effective osmoles in the urine......Page 427
PRECAUTIONS TO AVOID MISINTERPRETATIONS......Page 428
What dangers related to Na+ and water may develop in this patient?......Page 429
CLINICAL APPROACH......Page 430
Step 3......Page 431
ISSUES IN THERAPY......Page 432
DIAGNOSTIC ISSUES......Page 433
Step 2. Assess which solute is likely to be the cause of the polyuria......Page 434
Postobstructive diuresis......Page 435
CREATININE AS A MARKER OF CATABOLISMOF BODY PROTEIN......Page 436
Metabolism of dietary arginine......Page 437
What is the major aim of therapy with respect to urea excretion?......Page 439
Introduction......Page 444
PART A
PRINCIPLES OF PHYSIOLOGY......Page 446
Driving force to shift K+ across cell membranes......Page 447
Pathways for the movement of K+ across cell membranes......Page 448
ALTERING THE NEGATIVE VOLTAGE IN CELLS......Page 449
Raise the intracellular concentration of Na+......Page 450
Activate preexisting Na-K-ATPase by hormones......Page 451
Acids that can be transported by the monocarboxylicacid transporter......Page 453
Acids that cannot be transported by the monocarboxylicacid transporter......Page 454
Low intake of K+ and HCO3−......Page 455
A much larger input of K+ and HCO3−......Page 456
COMPONENTS OF THE EXCRETION OF K+IN THE CORTICAL COLLECTING DUCT......Page 457
Overview......Page 458
K+ channels......Page 459
Generation of a lumen-negative voltage......Page 460
Mechanism of action of aldosterone......Page 461
Aldosterone paradox......Page 463
FLOW RATE IN THE LATE CORTICALDISTAL NEPHRON......Page 465
CONTROL OF THE EXCRETION OF K+:A PALEOLITHIC ANALYSIS......Page 466
Control of K+ excretion in Paleolithic times......Page 467
Mechanism to raise the distal delivery of Na+......Page 468
WNK KINASE SIGNAL SYSTEM......Page 469
Period when retention of NaCl is required......Page 470
Effects of stopping the intake of K+......Page 471
MEDULLARY RECYCLING OF K+: IMPLICATIONS FOR KIDNEY STONE FORMATION......Page 472
Stimuli for the release of insulin......Page 473
After the laboratory results were examined, were there any clues to suggest what the cause of acute hypokalemia might be?......Page 474
What tests should be performed in the emergency room if she has another episode of acute hypokalemia to reveal the correct diagnosis?......Page 475
chapter
14 Hypokalemia......Page 479
Introduction......Page 480
Questions......Page 481
Questions......Page 482
Negative voltage inside cells......Page 483
Secretion of K+ in the late cortical distal nephron......Page 484
Basis of a high [K+]CCD......Page 485
DEALING WITH EMERGENCIES ON ADMISSION......Page 486
What is the emergency therapy for acute, severehypokalemia in this patient?......Page 487
DIAGNOSIS......Page 488
Steps in the clinical approach to a patient suspectedof having acute hypokalemia......Page 490
Clinical approach to patients with chronic hypokalemia......Page 491
Clinical picture......Page 496
Therapy......Page 497
Pathophysiology......Page 498
DIARRHEA......Page 499
Secretory diarrhea type......Page 500
Diminished reabsorption of Na+ and Cl− in the colon......Page 501
Pathophysiology......Page 502
Differential diagnosis......Page 503
Pathophysiology......Page 504
Pathophysiology......Page 505
Molecular basis......Page 506
Therapy......Page 507
Antenatal Bartter’s syndrome......Page 508
Pathophysiology......Page 509
Molecular basis......Page 510
Therapy......Page 511
Pathophysiology......Page 512
Clinical picture......Page 513
Molecular basis......Page 514
Diagnosis......Page 515
Clinical picture......Page 516
Diagnosis......Page 517
Clinical picture......Page 518
General issues in treatment of the patient with hypokalemia......Page 519
K+ DEPLETION AND THE PATHOPHYSIOLOGYPATHOPHYSIOLOGY OF KIDNEY STONE FORMATIONFORMATION......Page 521
What are the features that affect the diffusion of ionizedcalcium from the interstitial compartment of the heart toplasma in this patient?......Page 522
What are the implications of this pathophysiologyfor the formationof kidney stones?......Page 523
Is there a medical emergency in this patient?......Page 524
What effects cause a prolonged shift of K+ into cells?......Page 525
Is there a danger to anticipate during therapy?......Page 526
Is there a danger to anticipate during therapy?......Page 527
Why is antenatal Bartter’s syndrome not a lethal abnormality?......Page 528
Introduction......Page 531
PART A BACKGROUND
......Page 532
SYNOPSIS OF THE PHYSIOLOGY......Page 533
K+ channels in cell membranes......Page 534
PART B CLINICAL APPROACH
......Page 535
Secretion of K+ in the late cortical distal nephron......Page 536
STAGES IN THE DEVELOPMENT OF HYPERKALEMIA......Page 537
Is the time period short and/or has the intake of K+ been low?......Page 538
Are there laboratory or technical problems?......Page 539
Basis for the low [K+]CCD......Page 540
PART C
SPECIFIC CAUSES
OF HYPERKALEMIA
......Page 541
ADDISON’S DISEASE......Page 543
Autosomal dominant form......Page 544
PSEUDOHYPOALDOSTERONISM TYPE II(GORDON’S SYNDROME)......Page 545
Group 2: Patients with low stimulus to produce renin......Page 546
Drugs that affect cellular redistribution of K+......Page 547
Drugs that interfere with renal K+ excretion......Page 548
EMERGENCY SETTING......Page 551
Induce a shift of K+ into the intracellular fluid......Page 552
Cation exchange resins......Page 553
IN-DEPTH ANALYSIS OF K+ EXCRETION DURINGCHRONIC HYPERKALEMIA......Page 554
Application of these principles to the management of chronic hyperkalemia in patients taking ACE inhibitors, angiotensin II receptor blockers, or direct renin inhibitors......Page 556
What could be the basis for the high PK, but onlywhile the patient was on the ward?......Page 557
Why is hyperkalemia present?......Page 558
If trimethoprim must be continued, what measurescan be taken to minimize its ability to block ENaC?......Page 559
chapter 16
Hyperglycemia......Page 562
Introduction......Page 563
Question......Page 564
Brain fuels......Page 565
Hierarchy of fuel oxidation......Page 566
Pool size for glucose......Page 567
Glycogen in skeletal muscle......Page 568
Removal of glucose via metabolism......Page 569
RENAL HANDLING OF GLUCOSE......Page 570
GLUCOSE-INDUCED OSMOTIC DIURESIS......Page 571
Fall in the PGlucose during therapy of hyperglycemia......Page 572
Glucose and the intracellular fluid volume......Page 573
Add an iso-osmotic solution of glucose......Page 574
Impact of an osmotic diuresis on body fluid composition......Page 575
Na+ and Cl–......Page 576
CLASSIFICATION OF HYPERGLYCEMIA......Page 577
Polyuric group......Page 578
Administration of Na+ and water......Page 579
Treat a hemodynamic emergency only if it is present......Page 580
Avoid a large fall in the PEffective osm......Page 581
Potassium therapy......Page 582
Discussion of Mini-case 16-1......Page 583
Luminal transport of glucose......Page 586
Kidneys......Page 587
Why did her PGlucose fail to fall in the first 100 minutes?......Page 588
In what way did a severe degree of hyperglycemia“help” this patient?......Page 589
Why did she have such a severe degree of acidemia, a PGlucose that was not very high, a modest degree of contraction of the effective arterial blood volume, and a lower than expected PK?......Page 590
The very low PHCO3 on admission......Page 591
The very low PK on admission......Page 592
Acid Base......Page 594
Hyperglycemia......Page 599
Index......Page 602