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Chapter 13 Fluid and Acid-Base Balance
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13.1 Introduction Crucial aspects of the regulation of ECF and ICF
Osmotic balance Total concentration of major solutes Total fluid volume Directly affects circulatory pressure Acid-base balance Crucial to the functioning of proteins Regulation of ECF and ICF composition is an integrative process not attributable to a single organ system 2
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13.1 Introduction Balance concept
The quantity of any substance in the ECF is considered a readily available internal pool. Substances are added to the pool by transferring more in from the external environment or producing them within the body. Substances are removed from the pool by loss to the outside or metabolic consumption. Substances may be transferred into or out of storage within cells or in extracellular structures. Input must be balanced by an equal output. 3
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13.1 Introduction 4
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Excretion to external environment (through kidneys, lungs, gills,
Inputs to internal pool Outputs from internal pool (Inside body) Excretion to external environment (through kidneys, lungs, gills, digestive tract, or body surface, e.g., sweat, tears, sloughed skin) Metabolically consumed in body (irretrievably altered) Metabolically produced by body Input from external environment (through ingestion, inhalation, absorption through body surface, or artificial injection) Storage depots within body (no function other than storage) Internal pool (extracellular fluid concentration) of a substance Reversible incorporation into more complex molecular structures (fulfills a specific function) Stepped Art Fig. 13-1, p.613
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13.1 Introduction Body water is distributed between the intracellular fluid (ICF) and extracellular fluid (ECF). ECF is hemolymph in animals with open circulatory systems ECF is divided into plasma and interstitial fluid in animals with closed circulatory systems Minor ECF compartments Lymph Transcellular fluids secreted into particular body cavities (e.g. cerebrospinal fluid, intraocular fluid) Digestive tract (technically part of the external environment) 6
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13.1 Introduction 7
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Exchange surfaces (e. g., gills)
Mouth Skin Exchange surfaces (e. g., gills) Cell Gut ECF ICF FIGURE A model of the major body compartments in an animal and exchange routes (arrows) between them. ECF, extracellular fluid; ICF, intracellular fluid. Kidney External environment Anus Transporting fluid system—“blood” Figure 13-2 p614
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13.1 Introduction Composition of fluid compartments
Plasma and interstitial fluid are nearly identical in composition Selectively permeable plasma membrane establishes differences between ECF and ICF composition Cellular proteins cannot leave cells Cellular organic osmolytes are higher in the ICF Sodium (Na+) is the primary extracellular cation Accompanied by chloride (Cl–) and bicarbonate (HCO3–) Potassium (K+) is the primary intracellular cation Accompanied by phosphate (PO43–) and negatively charged proteins 9
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13.1 Introduction 10
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Milliequivalents per liter of H2O
Plasma Interstitial fluid Intracellular fluid (skeletal muscle) 200 Na+ Capillary wall Plasma membrane 150 HCO3– HCO3– PO43– K+ Milliequivalents per liter of H2O 100 Na+ Cl– Na+ FIGURE Ionic composition of the major body fluid compartments in a mammal. Cl– 50 Protein anions Protein anions Other K+ Other Other K+ Other Other Cations Anions Cations Anions Cations Anions Figure 13-3 p616
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
Maintaining cell volume The major problem is the unequal distribution of Na+ in the ECF and ICF Na+ leaking into cells would raise the ICF solute concentration and attract water Na+/K+ ATPase pump exports Na+ at the rate it enters the cell Other potential problems: Salinity of the environment Evaporation of body water into air Ingestion and excretion Freezing concentrates ions in residual unfrozen water Pathologies such as diabetes, cystic fibrosis and hyponatremia 12
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
Strategies for maintaining osmotic balance Osmoconformers Body fluids and cells are equal in osmotic pressure to the environment Mainly found in the oceans, where osmolarity averages 1000 mOsm Osmoregulators Osmotic pressure of body fluids is homeostatically regulated and usually different from the external environment 13
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
ECF is similar to seawater (1000 mOsm), dominated by NaCl ICF has same osmotic pressure as ECF Universal solutes, e.g. K+ (400 mOsm) Organic osmolytes (600 mOsm) Common organic osmolytes include carbohydrates, free amino acids, methylamines, urea and methylsulfonium solutes Most organic osmolytes do not disturb macro-molecules and some stabilize macromolecules against denaturing forces 14
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
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FIGURE Examples of major organic solutes used as osmolytes by animals. Not shown are methylsulfonium solutes such as dimethylsulfoniopropionate (DMSP), which has the formula (CH3)2–S–CH2–CH2–COOH. Figure 13-5a p619
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FIGURE Examples of major organic solutes used as osmolytes by animals. Not shown are methylsulfonium solutes such as dimethylsulfoniopropionate (DMSP), which has the formula (CH3)2–S–CH2–CH2–COOH. Figure 13-5b p619
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FIGURE Examples of major organic solutes used as osmolytes by animals. Not shown are methylsulfonium solutes such as dimethylsulfoniopropionate (DMSP), which has the formula (CH3)2–S–CH2–CH2–COOH. Figure 13-5c p619
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FIGURE Effect of various solutes on the activity of an enzyme, lactate dehydrogenase, from a marine polychaete worm. Note that salts of Na and K are quite inhibitory, whereas the compatible organic osmolytes (glycine, betaine) are much less so, while the counteracting osmolyte TMAO is stimulatory except at high concentrations. Figure 13-6 p620
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
Types of osmoconformers Stenohaline osmoconformers Restricted to a narrow range of salinity Cannot regulate their osmolytes to compensate Euryhaline osmoconformers Tolerant of changes in salinity Successful in intertidal zones Regulate organic osmolytes in their cells 20
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
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Amino acid synthesis Amino acid loss Amino acid uptake
Na+ OC in external medium 1 OC in blood 2 Water enters cells Blood [Ions] OC in cells Cell 4 3 FIGURE Adjustments to changes in Na+ levels in a brackish-water nonvertebrate. A reduction in external Na+ and osmotic concentration (OC) causes a reduction in the blood (step 1), leading to osmosis of water into cells (step 2). This in turn triggers a reduction in cellular amino acid osmolytes (step 3), which enter the blood (step 4) to be broken down. Amino acid in blood Amino acid synthesis Amino acid loss Amino acid uptake Figure 13-8 p621
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
Types of osmoconformers Strict osmoconformers ECF composition closely resembles seawater ICF is dominated by organic osmolytes, mainly amino acids Marine nonvertebrates and hagfish Hypo-ionic osmoconformers Actively regulate ECF composition to maintain salt levels lower than seawater Produce and secrete organic solutes, urea and trimethylamine oxide (TMAO) to bring ECF and ICF osmolarity up to the level of seawater Marine chondrichthys and coelacanths 23
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13.2 Osmotic and Volume Balance: Overview and Osmoconformers
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FIGURE 13-4 Osmotic adaptations of marine animals
FIGURE Osmotic adaptations of marine animals. (a) Generalized osmotic contents of three different types of adaptation in marine animals. TMAO is trimethylamine oxide. Osmoconformers use primarily free amino acids as organic osmolytes in their cells, while osmoconforming hypo-ionic regulators use primarily urea and TMAO. In contrast, hypo-osmotic hypo-ionic regulators have very low levels of organic osmolytes. (b) General categories of responses of animal body fluids to variations in external concentrations, with (c) examples. Figure 13-4a p618 25
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FIGURE 13-4 Osmotic adaptations of marine animals
FIGURE Osmotic adaptations of marine animals. (a) Generalized osmotic contents of three different types of adaptation in marine animals. TMAO is trimethylamine oxide. Osmoconformers use primarily free amino acids as organic osmolytes in their cells, while osmoconforming hypo-ionic regulators use primarily urea and TMAO. In contrast, hypo-osmotic hypo-ionic regulators have very low levels of organic osmolytes. (b) General categories of responses of animal body fluids to variations in external concentrations, with (c) examples. Figure 13-4b p618
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FIGURE 13-4 Osmotic adaptations of marine animals
FIGURE Osmotic adaptations of marine animals. (a) Generalized osmotic contents of three different types of adaptation in marine animals. TMAO is trimethylamine oxide. Osmoconformers use primarily free amino acids as organic osmolytes in their cells, while osmoconforming hypo-ionic regulators use primarily urea and TMAO. In contrast, hypo-osmotic hypo-ionic regulators have very low levels of organic osmolytes. (b) General categories of responses of animal body fluids to variations in external concentrations, with (c) examples. Figure 13-4c p618
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13.3 Osmotic and Volume Balance: Osmoregulators
Osmoregulators maintain a steady ECF osmotic pressure regardless of osmotic changes in the external environment Marine osmoregulators are usually hypo-osmotic Some crustaceans and mosquito larvae in salty habitats, and most marine vertebrates Freshwater osmoregulators are hyperosmotic All freshwater animals 28
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13.3 Osmotic and Volume Balance: Osmoregulators
Hypo-osmotic osmoregulators Maintain ECF and cellular osmotic concentrations of mOsm Have low concentrations of organic osmolytes Marine animals must drink seawater and must absorb NaCl in order to absorb water, creating an excess of salt in the blood Gills use epithelial chloride cells to actively transport Na+ and Cl– outward Marine birds and reptiles remove excess salt using salt glands Marine mammals have efficient kidneys with long nephron loops 29
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13.3 Osmotic and Volume Balance: Osmoregulators
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Blood SW Accessory cell Chloride cell CFTR 0 mV Pavement cell
FIGURE Model for ion transport mechanisms in seawater teleost chloride cell. The process starts with active transport of Na+ and K+ (“pump” indicated by “ATP”). The resulting Na+ electrochemical gradient is used by an NKCC cotransporter (shown as the small blue membrane protein) to move one Na+, one K+, and two Cl− ions into the cell. The resulting high electrochemical gradient for Cl− (primarily due to the cell’s negative charge) allows those ions to exit into seawater via a CFTR channel. This creates a negative charge that helps draw Na+ across the tight junctions between cells (paracellular pathway, top green arrow) as well as some K+ from the cell. 0 mV Pavement cell Figure p625
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13.3 Osmotic and Volume Balance: Osmoregulators
Some osmoregulating vertebrates have high levels of organic osmolytes. Polar fishes have high concentrations of glycerol, which functions as an antifreeze. In deep-sea fishes, TMAO content increases with depth in the ocean Estivating animals build up large amounts of urea for waste storage, but also to help retain water in dry environments. 32
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13.3 Osmotic and Volume Balance: Osmoregulators
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Gills block loss of urea and TMAO
Medium 1,000 mOsm Gills block loss of urea and TMAO Most urea and TMAO retained by kidney Body fluids ca. 1,100 mOsm Divalent ions excreted in urine Water absorbed by gills and skin Salts lost via feces Ingests salts with food Sodium excreted by rectal gland FIGURE Diagrams of major osmotic gains, losses, regulation, and body fluid concentrations in marine vertebrates. (a) Cartilaginous fish Figure 13-9a p623
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Loses water through gills and skin Medium 1,000 mOsm
Removes salts via “chloride” cells in gills Body fluids ca. 400 mOsm Salts and little water lost via scant urine Gains water and salts by swallowing seawater and food Salts lost via feces FIGURE Diagrams of major osmotic gains, losses, regulation, and body fluid concentrations in marine vertebrates. (b) Bony fish Figure 13-9b p623
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Salt gland: hypertonic NaCI Gut Kidney
Medium 1,000 mOsm Salt gland: hypertonic NaCI Gut Kidney Body fluids ca. 300 mOsm Drinks seawater Isotonic urine 300 mOsm (slightly hyperosmotic in some birds) FIGURE Diagrams of major osmotic gains, losses, regulation, and body fluid concentrations in marine vertebrates. (c) Reptiles, birds Figure 13-9c p623
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Hypertonic urine (1,200–1,500 mOsm) Kidney
Medium 1,000 mOsm Gut Body fluids ca. 300 mOsm Na+ Hypertonic urine (1,200–1,500 mOsm) Kidney FIGURE Diagrams of major osmotic gains, losses, regulation, and body fluid concentrations in marine vertebrates. No drinking (d) Mammals Figure 13-9d p623
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13.3 Osmotic and Volume Balance: Osmoregulators
Hyperosmotic osmoregulators cope with the low osmolarity of fresh water. Valuable solutes are lost through the gills Mechanisms for regulating ECF osmolarity Active uptake of ions across gills and skin Hypotonic fluid excretion by kidneys or other structures Lower internal osmolarities Low permeability of integument 38
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13.3 Osmotic and Volume Balance: Osmoregulators
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Absorbs water through gills and skin Medium <5 mOsm
Body fluids ca. 300 mOsm Obtains salts through “chloride” cells in gills and with food Removes much water and some salt via dilute urine FIGURE Diagram of major osmotic gains, losses, regulation, and body fluid concentration in a freshwater bony fish. Salts lost via feces Figure p627
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13.3 Osmotic and Volume Balance: Osmoregulators
Salmon alternate between modes of osmotic adaptation Hypo-osmotic in the ocean, but hyperosmotic in rivers Acclimatization regulation coupled with an anticipation mechanism As salmon enter the ocean, cortisol triggers growth of seawater-type chloride cells in gills, which reverses the direction of ion transport, and increases Na+/K+ ATPase activity When returning to freshwater to spawn, prolactin stimulates return to freewater-type chloride cells, once again reversing the direction of ion transport 41
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13.3 Osmotic and Volume Balance: Osmoregulators
Terrestrial animals Must obtain water and solutes via dietary intake ECF osmotic concentrations are similar to freshwater osmoregulators NaCl is the dominant solute 42
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H2O lost via respiration
Terrestrial animals Dietary H2O NaCI H2O retention NaCI retention H2O lost via respiration FIGURE Diagram of major osmotic gains, losses, regulation, and body fluid concentration in a terrestrial vertebrate. H2O NaCI lost via excretion Figure p627
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13.4 Osmotic and Volume Balance in Mammals
ECF osmolarity must be closely regulated to prevent swelling or shrinking of the cells. Causes of ECF hypertonicity Insufficient water intake Excessive water loss Drinking hypertonic saline water (i.e. seawater) Alcohol consumption Retention of osmotically active solutes (e.g. urea in kidney failure) When ECF becomes hypertonic, cells will shrink Shrinkage can be reduced by transporting ions into the cell (regulatory volume increase) Some cells (e.g. neurons) can import or synthesize organic osmolytes 44
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13.4 Osmotic and Volume Balance in Mammals
ECF osmolarity must be closely regulated to prevent swelling or shrinking of the cells. ECF hypotonicity is due to low plasma Na+ (hyponatremia) Causes of ECF hypotonicity Intake of relatively more water than solutes (e.g. drinking too much water) Retention of excess water without solute (e.g. inappropriate secretion of vasopressin) When ECF becomes hypotonic, cells will swell Swelling can be reduced by transporting osmolytes out of the cell (regulatory volume decrease) 45
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13.4 Osmotic and Volume Balance in Mammals
Isotonic fluid gain or loss Disturbs blood volume without affecting cell volume Isotonic fluid gain is rare Consumption of isotonic brackish water Intravenous administration of an isotonic solution Isotonic fluid loss occurs in hemorrhage 46
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13.4 Osmotic and Volume Balance in Mammals
ECF volume must be closely regulated to maintain blood pressure A reduction in ECF volume lowers blood pressure by decreasing plasma volume Temporary relief of blood pressure disturbances is provided by: Baroreceptor reflex -- minimizes the impact of changes in circulating volume on blood pressure Fluid shifts between plasma and interstitial compartments 47
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13.4 Osmotic and Volume Balance in Mammals
To maintain water balance, water input must equal water output Sources of water input Food consumption Drinking water Metabolically produced water Sources of water output Urine excretion Insensible cutaneous and respiratory loss Sensible cutaneous and respiratory loss (e.g. sweating and panting) Loss in feces (additional losses due to diarrhea or vomiting) 48
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13.4 Osmotic and Volume Balance in Mammals
Water balance is regulated primarily by the kidneys and thirst. Free water reabsorption and excretion are regulated through vasopressin secretion Water input is regulated by thirst Vasopressin secretion and thirst are both stimulated by hypertonic blood and suppressed by hypotonic blood. Osmoreceptors, the thirst center and vasopressin-secreting cells are located in the same area of the hypothalamus. Left atrial volume receptors stimulate thirst and vasopressin secretion when blood pressure falls 49
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13.4 Osmotic and Volume Balance in Mammals
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ECF volume Relieves Arterial blood pressure Osmolarity Relieves
Hypothalamic osmoreceptors dominant factor controlling thirst and vasopressin secretion) Left atrial volume receptors (important only in large changes in plasma volume/ arterial pressure) Hypothalamic neurons Thirst Vasopressin Arteriolar vasoconstriction H2O FIGURE Control of increased vasopressin secretion and thirst during an H2O deficit (shown for a human). H2O intake H2O permeability of distal and collecting tubules H2O H2O reabsorption Urine output Plasma osmolarity Plasma volume Figure p632
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+ + Relieves Relieves ECF volume Osmolarity Arterial blood pressure
Hypothalamic osmoreceptors (dominant factor controlling thirst and vasopressin secretion) Left atrial volume receptors (important only in large changes in plasma volume/arterial pressure) + Hypothalamic neurons Thirst Vasopressin Arteriolar vasoconstriction H2O intake H2O permeability of distal and collecting tubules H2O reabsorption Urine output Plasma osmolarity Plasma volume Stepped Art Figure p632
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13.4 Osmotic and Volume Balance in Mammals
To maintain salt balance, salt input must equal salt output Sources of salt input Food consumption Salt hunger is stimulated by angiotensin II Sources of salt output Controlled excretion of salt in urine Loss in feces Sweating Total Na+ mass in the ECF is kept constant despite changes in dietary intake of salt 53
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13.4 Osmotic and Volume Balance in Mammals
Salt balance is regulated in the kidneys by glomerular filtration and tubular reabsorption GFR is decreased as part of the baroreceptor reflex response to a fall in blood pressure Control of Na+ reabsorption Renin-angiotensin-aldosterone system promotes Na+ reabsorption Stimulated by decreases in ECF Na+, plasma volume and arterial blood pressure Atrial natriuretic peptide antagonizes the RAAS when blood pressure is elevated 54
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Relieves Relieves 1 2 Na+ Na+ Na+ Na+ Na+ load in body
Arterial blood pressure 1 2 GFR Aldosterone Na+ filtered Na+ reabsorbed Excretion of Na+ and accompanying Cl– and fluid FIGURE Dual effect of a fall in arterial blood pressure on renal handling of Na+. See main text for details. See Figure for details of mechanism. See Figure for details of mechanism. Na+ Conservation of NaCl and accompanying fluid Na+ Na+ Na+ Figure p633
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Arterial blood pressure
Na+ load in body Arterial blood pressure b a Aldosterone GFR Na+ reabsorbed Na+ filtered Excretion of Na+ and accompanying Cl2 and fluid Conservation of NaCl and accompanying fluid Stepped Art Fig , p.633
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13.4 Osmotic and Volume Balance in Mammals
Consequences of hemorrhage Severe blood loss leads to reduced blood volume, decreased venous return, and a fall in cardiac output and arterial blood pressure. Baroreceptor reflex increases sympathetic activity and decreases parasympathetic activity. Sympathetic activity causes arteriolar vasoconstriction, increasing total peripheral resistance, and venous vasoconstriction, increasing venous return. Sympathetic activity increases heart rate and cardiac contractility, leading to increased cardiac output. Increases in cardiac output and total peripheral resistance produce a compensatory increase in arterial blood pressure. 58
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13.4 Osmotic and Volume Balance in Mammals
Consequences of hemorrhage Fluid shifts from interstitial fluid into capillaries (autotransfusion), enhanced by increased plasma protein synthesis by the liver Urine output decreases due to a fall in renal blood flow, increased vasopressin secretion, and activation of the RAAS Thirst is stimulated Red blood cells are gradually replaced 59
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13.5 Acid-Base Balance: General Concepts
Acids and Bases Acids are substances that dissociate when in solution to liberate free H+ and anions A strong acid (e.g. hydrochloric acid, HCl) has a greater tendency to dissociate in solution than a weak acid (e.g. carbonic acid, H2CO3) The extent of dissociation for a particular acid (A) in solution is constant: [H+][A–]/[HA] = Ka 61
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FIGURE 13-16 Comparison of a strong and a weak acid
FIGURE Comparison of a strong and a weak acid. (a) Five molecules of a strong acid. A strong acid such as HCl (hydrochloric acid) completely dissociates into free H+ and anions in solution. (b) Five molecules of a weak acid. A weak acid such as H2CO3 (carbonic acid) only partially dissociates into free H+ and anions in solution. Figure 13-16a p636
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FIGURE 13-16 Comparison of a strong and a weak acid
FIGURE Comparison of a strong and a weak acid. (a) Five molecules of a strong acid. A strong acid such as HCl (hydrochloric acid) completely dissociates into free H+ and anions in solution. (b) Five molecules of a weak acid. A weak acid such as H2CO3 (carbonic acid) only partially dissociates into free H+ and anions in solution. Figure 13-16b p636
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13.5 Acid-Base Balance: General Concepts
Acids and Bases Bases are substances that can combine with free H+ and remove them from solution A strong base can bind H+ more readily than a weak base The ability of a particular base (B) to associate with H+ is constant: [HB+][OH–]/[B] = Kb 65
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13.5 Acid-Base Balance: General Concepts
pH is used to express H+ concentration pH = log 1/[H+] High [H+] corresponds to a low pH Every pH unit represents a 10-fold change in [H+] The pH of pure water is 7.0 at 25o C and 6.8 at 37o C [H+] in typical mammalian ECF is 4.3 x 10-8 equivalents/liter or pH = 7.4 66
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Relative concentration
[OH–] [H+] Relative concentration Acidic Alkaline (basic) Neutral pH 7.0 14 (a) In chemistry 6.8 8.0 6.8 8.0 Venous blood Arterial blood FIGURE pH considerations in chemistry and physiology. (a) Relationship of pH to the relative concentrations of H+ and base (OH−) under chemically neutral, acidic, and alkaline conditions. (b) Blood pH range under normal, acidotic, and alkalotic conditions. Death Acidosis Normal Alkalosis Death Average 6.8 6.9 7.0 7. 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 8.0 pH range compatible with life (b) In the body Figure p637
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pH Hydrochloric acid (HCl) 1 Gastric fluid (1.0–3.0) 2 Lemon juice, cola drinks, some acid rain 3 Vinegar, wine, beer, oranges Acidic 4 Tomatoes Bananas Black coffee 5 Bread Typical rainwater 6 Urine (5.0–7.0) Milk (6.6) 7 Pure water [H+]=[OH–] Blood (7.35–7.45) 8 Egg white (8.0 Seawater (7.8–8.3) Baking soda 9 Phosphate detergents, bleach, antacids FIGURE Comparison of pH values of common solutions. 10 Soapy solutions, milk of magnesia Basic 11 Household ammonia (10.5–11.9) 12 Hair remover 13 Oven cleaner 14 Sodium hydroxide (NaOH) Figure p638
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13.5 Acid-Base Balance: General Concepts
Importance of blood pH Normal pH of mammalian arterial blood is 7.45; venous blood is 7.35 Acidosis is a blood pH less than 7.35 Alkalosis is a blood pH greater than 7.45 Consequences of fluctuations in blood pH Altered enzyme activity Disturbances of K+ levels Changes in excitability of nerve and muscle cells Depression of CNS in acidosis Hyperexcitability of CNS in alkalosis 71
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13.5 Acid-Base Balance: General Concepts
H+ ions are continually being added to body fluids Carbonic acid produced in metabolism Inorganic acids (e.g. sulfuric acid and phosphoric acid) produced during catabolism Organic acids (e.g. lactate) resulting from metabolism Defense against increasing [H+] Chemical buffer systems Respiratory mechanisms Excretory mechanisms 72
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13.6 pH Regulation: Buffers
Chemical buffer systems bind with or release free H+ A chemical buffer system is a mixture of two chemical compounds that minimize pH changes when an acid or a base is added to or removed from the solution Example: Carbon dioxide-bicarbonate buffer H+ + HCO3– <—> H2CO3 <—> CO2 + H2O HCO3– is abundant in ECF and closely regulated by the kidneys and respiratory system All chemical buffering systems act immediately 73
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13.6 pH Regulation: Buffers
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13.6 pH Regulation: Buffers
Buffer systems in vertebrates Carbon dioxide-bicarbonate buffer system Primary ECF buffer Peptide and protein buffer system Primary ICF buffer Hemoglobin buffer system Primary erythrocyte buffer for carbonic acid changes Phosphate buffer system Secondary ICF and primary urinary buffer 75
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13.6 pH Regulation: Buffers
Henderson-Hasselbalch equation describes the relationship between [H+] and the members of a buffer pair pH = pKa + log [HCO3–]/[CO2] The pKa for carbonic acid is 6.1 and the ratio of [HCO3–] to [CO2] is normally 20:1 pH = log (20) = = 7.4 76
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13.6 pH Regulation: Buffers
Peptide and protein buffering system Proteins are excellent buffers because they contain both acidic and basic groups and are abundant in ICF Histidine is the most important buffering amino acid, with a pKa close to 7 Hemoglobin in erythrocytes Most of H+ generated from CO2 becomes bound to histidines of reduced hemoglobin Phosphate buffering system Consists of an acid phosphate salt (NaH2PO4) and a basic phosphate salt (Na2HPO4) Can swap H+ for Na+ as needed Key role in buffering urine 77
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13.7 pH Regulation: Respiration and Excretion
Respiratory systems regulate [H+] through adjustments in ventilation Slower responses than buffering When arterial [H+] increases in air breathers, the respiratory center is stimulated to increase ventilation With increased CO2 excretion, less H2CO3 is added to body fluids and H+ decreases When arterial [H+] decreases, ventilation is reduced Metabolically produced CO2 is added to the blood to increase acid production Insects regulate H+ in a similar manner by changing ventilation through the spiracles 78
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13.7 pH Regulation: Respiration and Excretion
Excretory systems are the third line of defense of acid-base balance. Both [H+] and [HCO3–] are regulated Require hours to days to compensate Gill transporters can excrete both H+ and HCO3– Kidneys can simultaneously exchange H+ for HCO3– 79
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13.7 pH Regulation: Respiration and Excretion
Hydrogen ion excretion Filtration rate of H+ is very low H+ is secreted by primary active transport and by secondary Na+/H+ antiporters in the proximal tubule Type A intercalated cells in the distal and collecting tubules are H+-secreting, HCO3–-reabsorbing, K+-reabsorbing cells Active at normal pH and during acidosis Type B intercalated cells are HCO3–-secreting, H+- reabsorbing, K+-secreting cells More active during alkalosis 80
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FIGURE 13-20 Renal ion secretion
FIGURE Renal ion secretion. (a) Hydrogen ion secretion coupled with bicarbonate reabsorption in a Type A intercalated cell. The H+-secreting pumps are located at the luminal membrane, and the HCO3−-reabsorbing antiporters are located at the basolateral membrane. Because the disappearance of a fi ltered HCO3− from the tubular fluid is coupled with the appearance of another HCO3− in the plasma, HCO3− is considered to have been “reabsorbed.” (b) Bicarbonate secretion coupled with hydrogen ion reabsorption in a Type B intercalated cell. The HCO3−-secreting antiporters are located at the luminal membrane and the H+-reabsorbing pumps are located at the basolateral membrane. Figure 13-20b p644
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13.7 pH Regulation: Respiration and Excretion
Bicarbonate excretion Filtered HCO3– is not reabsorbed directly Converted to CO2, which enters tubular cell HCO3– formed in the tubular cell is then transported into capillary blood New HCO3– is reabsorbed in conjunction with H+ secretion 83
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FIGURE Hydrogen ion secretion and excretion coupled with the addition of new HCO3− to the plasma. Secreted H+ does not combine with filtered HPO42− and is not subsequently excreted until all the filtered HCO3− has been “reabsorbed,” as depicted in Figure 13-20a. Once all the filtered HCO3− has combined with secreted H+, further secreted H+ is excreted in the urine, primarily in association with urinary buffers such as basic phosphate. Excretion of H+ is coupled with the appearance of new HCO3− in the plasma. The “new” HCO3− represents a net gain rather than merely a replacement for filtered HCO3−. Figure p645
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13.7 pH Regulation: Respiration and Excretion
Renal response to acidosis When [H+] is elevated, proximal tubular cells and Type A intercalated cells secrete more H+ Filtration of HCO3– decreases; new HCO3– enters the plasma to buffer excess H+ Renal response to alkalosis When [H+] is low, Type B intercalated cells increase H+ reabsorption More HCO3– is filtered; Type B intercalated cells secrete HCO3– into the urine 86
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Plasma [H+] (or plasma [CO2]) H+ secretion HCO3– conservation
H+ excretion HCO3– excretion Plasma [H+] Plasma [HCO3–] Stepped Art Fig , p.645
![Plasma [H+] (or plasma [CO2]) H+ secretion HCO3– conservation](http://slideplayer.com./slide/10556672/36/images/88/Plasma+%5BH%2B%5D+%28or+plasma+%5BCO2%5D%29+H%2B+secretion+HCO3%E2%80%93+conservation.jpg "H+ excretion. HCO3– excretion. Plasma [H+] Plasma [HCO3–] Stepped Art. Fig , p.645.")
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13.7 pH Regulation: Respiration and Excretion
Buffers in urine HCO3– cannot buffer urinary H+ because HCO3– is not excreted in urine simultaneously with H+ Excess ingested phosphate (HPO42–) is filtered and binds with secreted H+ Phosphate buffering capacity is exceeded when H+ is high in urine Ammonia (NH3) from glutamine metabolism provides additional buffering capacity during acidosis Ammonia combines with free H+ to allow continuing secretion of H+ NH3 + H+ —> NH4+ Ammonium ion (NH4+) is excreted in the urine 89
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13.8 Acid-Base Imbalances: Respiratory, Environmental, and Metabolic Disturbances
An acid-base imbalance may have a respiratory, a metabolic, or an environmental source. A change in pH that has a respiratory cause is associated with an abnormal [CO2] Most environmental causes also involve abnormal [CO2] Causes other than abnormal [CO2] are metabolic In an acidosis, the ratio of [HCO3–]/[CO2] falls below 20:1 In an alkalosis the ratio exceeds 20:1 Chemical buffers have a limited capacity for restoring normal pH 90
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13.8 Acid-Base Imbalances: Respiratory, Environmental, and Metabolic Disturbances
Respiratory acidosis Abnormal CO2 buildup in body fluids, typically arising from hypoventilation To compensate, kidneys conserve HCO3– and secrete more H+ Respiratory alkalosis Excessive loss of CO2 from the body as a result of hyperventilation Hyperventilation can be a response to hypoxia at high altitude To compensate, kidneys conserve H+ and excrete more HCO3– 91
92
13.8 Acid-Base Imbalances: Respiratory, Environmental, and Metabolic Disturbances
Metabolic acidosis Reduction in plasma [HCO3–] with normal [CO2] Due to loss of fluids rich in HCO3– or accumulation of noncarbonic acids Common causes: Severe diarrhea -- loss of HCO3– Ketoacidosis in diabetes mellitus Strenuous activity -- excess production of lactate Uremic acidosis in severe renal failure To compensate, ventilation is increased and kidneys secrete more H+ and conserve more HCO3– 92
93
13.8 Acid-Base Imbalances: Respiratory, Environmental, and Metabolic Disturbances
Metabolic alkalosis Increase in plasma [HCO3–] with normal [CO2] Due to loss of fluids rich in H+ Most common cause is vomiting To compensate, ventilation is reduced and kidneys conserve H+ and excrete more HCO3– 93
94
13.7 pH Regulation: Respiration and Excretion
94
95
FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25). Figure 13-23a p648
![FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25).](http://slideplayer.com./slide/10556672/36/images/95/FIGURE+Relationship+of+%5BHCO3%E2%88%92%5D+and+%5BCO2%5D+to+pH+in+various+acid%E2%80%93base+statuses%2C+shown+visually+as+a+balance+beam+and+mathematically+as+a+solution+to+the+Henderson-Hasselbalch+equation.+Note+that+the+lengths+of+the+arms+of+the+balance+beams+are+not+to+scale.+%28a%29+When+acid%E2%80%93base+balance+is+normal%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+20%3A1.+Each+of+the+four+types+of+acid%E2%80%93base+disorders+has+an+uncompensated+state+and+a+compensated+state.+%28b%29+In+uncompensated+respiratory+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2820%3A2%29+because+CO2+has+accumulated.+In+compensated+respiratory+acidosis%2C+HCO3%E2%88%92+is+retained+to+balance+the+CO2+accumulation%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2840%3A2%29.+%28c%29+In+uncompensated+respiratory+alkalosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+increased+%2820%3A0.5%29+by+a+reduction+in+CO2.+In+compensated+respiratory+alkalosis%2C+HCO3%E2%88%92+is+eliminated+to+balance+the+CO2+de%EF%AC%81+cit%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2810%3A0.5%29.+%28d%29+In+uncompensated+metabolic+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2810%3A1%29+by+an+HCO3%E2%88%92+de%EF%AC%81cit.+In+compensated+metabolic+acidosis%2C+HCO3%E2%88%92+is+conserved%2C+which+partially+makes+up+for+the+HCO3%E2%88%92+de%EF%AC%81cit%2C+and+CO2+is+reduced%3B+these+changes+restore+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2815%3A0.75%29.+%28e%29+In+uncompensated+metabolic+alkalosis%2C+the+%5BHCO3%E2.jpg "Figure 13-23a p648.")
96
FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25). Figure 13-23b p648
![FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25).](http://slideplayer.com./slide/10556672/36/images/96/FIGURE+Relationship+of+%5BHCO3%E2%88%92%5D+and+%5BCO2%5D+to+pH+in+various+acid%E2%80%93base+statuses%2C+shown+visually+as+a+balance+beam+and+mathematically+as+a+solution+to+the+Henderson-Hasselbalch+equation.+Note+that+the+lengths+of+the+arms+of+the+balance+beams+are+not+to+scale.+%28a%29+When+acid%E2%80%93base+balance+is+normal%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+20%3A1.+Each+of+the+four+types+of+acid%E2%80%93base+disorders+has+an+uncompensated+state+and+a+compensated+state.+%28b%29+In+uncompensated+respiratory+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2820%3A2%29+because+CO2+has+accumulated.+In+compensated+respiratory+acidosis%2C+HCO3%E2%88%92+is+retained+to+balance+the+CO2+accumulation%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2840%3A2%29.+%28c%29+In+uncompensated+respiratory+alkalosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+increased+%2820%3A0.5%29+by+a+reduction+in+CO2.+In+compensated+respiratory+alkalosis%2C+HCO3%E2%88%92+is+eliminated+to+balance+the+CO2+de%EF%AC%81+cit%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2810%3A0.5%29.+%28d%29+In+uncompensated+metabolic+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2810%3A1%29+by+an+HCO3%E2%88%92+de%EF%AC%81cit.+In+compensated+metabolic+acidosis%2C+HCO3%E2%88%92+is+conserved%2C+which+partially+makes+up+for+the+HCO3%E2%88%92+de%EF%AC%81cit%2C+and+CO2+is+reduced%3B+these+changes+restore+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2815%3A0.75%29.+%28e%29+In+uncompensated+metabolic+alkalosis%2C+the+%5BHCO3%E2.jpg "Figure 13-23b p648.")
97
FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25). Figure 13-23c p648
![FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25).](http://slideplayer.com./slide/10556672/36/images/97/FIGURE+Relationship+of+%5BHCO3%E2%88%92%5D+and+%5BCO2%5D+to+pH+in+various+acid%E2%80%93base+statuses%2C+shown+visually+as+a+balance+beam+and+mathematically+as+a+solution+to+the+Henderson-Hasselbalch+equation.+Note+that+the+lengths+of+the+arms+of+the+balance+beams+are+not+to+scale.+%28a%29+When+acid%E2%80%93base+balance+is+normal%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+20%3A1.+Each+of+the+four+types+of+acid%E2%80%93base+disorders+has+an+uncompensated+state+and+a+compensated+state.+%28b%29+In+uncompensated+respiratory+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2820%3A2%29+because+CO2+has+accumulated.+In+compensated+respiratory+acidosis%2C+HCO3%E2%88%92+is+retained+to+balance+the+CO2+accumulation%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2840%3A2%29.+%28c%29+In+uncompensated+respiratory+alkalosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+increased+%2820%3A0.5%29+by+a+reduction+in+CO2.+In+compensated+respiratory+alkalosis%2C+HCO3%E2%88%92+is+eliminated+to+balance+the+CO2+de%EF%AC%81+cit%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2810%3A0.5%29.+%28d%29+In+uncompensated+metabolic+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2810%3A1%29+by+an+HCO3%E2%88%92+de%EF%AC%81cit.+In+compensated+metabolic+acidosis%2C+HCO3%E2%88%92+is+conserved%2C+which+partially+makes+up+for+the+HCO3%E2%88%92+de%EF%AC%81cit%2C+and+CO2+is+reduced%3B+these+changes+restore+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2815%3A0.75%29.+%28e%29+In+uncompensated+metabolic+alkalosis%2C+the+%5BHCO3%E2.jpg "Figure 13-23c p648.")
98
FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25). Figure 13-23d p648
![FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25).](http://slideplayer.com./slide/10556672/36/images/98/FIGURE+Relationship+of+%5BHCO3%E2%88%92%5D+and+%5BCO2%5D+to+pH+in+various+acid%E2%80%93base+statuses%2C+shown+visually+as+a+balance+beam+and+mathematically+as+a+solution+to+the+Henderson-Hasselbalch+equation.+Note+that+the+lengths+of+the+arms+of+the+balance+beams+are+not+to+scale.+%28a%29+When+acid%E2%80%93base+balance+is+normal%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+20%3A1.+Each+of+the+four+types+of+acid%E2%80%93base+disorders+has+an+uncompensated+state+and+a+compensated+state.+%28b%29+In+uncompensated+respiratory+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2820%3A2%29+because+CO2+has+accumulated.+In+compensated+respiratory+acidosis%2C+HCO3%E2%88%92+is+retained+to+balance+the+CO2+accumulation%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2840%3A2%29.+%28c%29+In+uncompensated+respiratory+alkalosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+increased+%2820%3A0.5%29+by+a+reduction+in+CO2.+In+compensated+respiratory+alkalosis%2C+HCO3%E2%88%92+is+eliminated+to+balance+the+CO2+de%EF%AC%81+cit%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2810%3A0.5%29.+%28d%29+In+uncompensated+metabolic+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2810%3A1%29+by+an+HCO3%E2%88%92+de%EF%AC%81cit.+In+compensated+metabolic+acidosis%2C+HCO3%E2%88%92+is+conserved%2C+which+partially+makes+up+for+the+HCO3%E2%88%92+de%EF%AC%81cit%2C+and+CO2+is+reduced%3B+these+changes+restore+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2815%3A0.75%29.+%28e%29+In+uncompensated+metabolic+alkalosis%2C+the+%5BHCO3%E2.jpg "Figure 13-23d p648.")
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FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25). Figure 13-23e p648
![FIGURE Relationship of [HCO3−] and [CO2] to pH in various acid–base statuses, shown visually as a balance beam and mathematically as a solution to the Henderson-Hasselbalch equation. Note that the lengths of the arms of the balance beams are not to scale. (a) When acid–base balance is normal, the [HCO3−]/[CO2] ratio is 20:1. Each of the four types of acid–base disorders has an uncompensated state and a compensated state. (b) In uncompensated respiratory acidosis, the [HCO3−]/[CO2] ratio is reduced (20:2) because CO2 has accumulated. In compensated respiratory acidosis, HCO3− is retained to balance the CO2 accumulation, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (40:2). (c) In uncompensated respiratory alkalosis, the [HCO3−]/[CO2] ratio is increased (20:0.5) by a reduction in CO2. In compensated respiratory alkalosis, HCO3− is eliminated to balance the CO2 defi cit, which restores the [HCO3−]/[CO2] ratio to a normal equivalent (10:0.5). (d) In uncompensated metabolic acidosis, the [HCO3−]/[CO2] ratio is reduced (10:1) by an HCO3− deficit. In compensated metabolic acidosis, HCO3− is conserved, which partially makes up for the HCO3− deficit, and CO2 is reduced; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (15:0.75). (e) In uncompensated metabolic alkalosis, the [HCO3−]/[CO2] ratio is increased (40:1) by excess HCO3−. In compensated metabolic alkalosis, some of the extra HCO3− is eliminated, and CO2 is increased; these changes restore the [HCO3−]/[CO2] ratio to a normal equivalent (25:1.25).](http://slideplayer.com./slide/10556672/36/images/99/FIGURE+Relationship+of+%5BHCO3%E2%88%92%5D+and+%5BCO2%5D+to+pH+in+various+acid%E2%80%93base+statuses%2C+shown+visually+as+a+balance+beam+and+mathematically+as+a+solution+to+the+Henderson-Hasselbalch+equation.+Note+that+the+lengths+of+the+arms+of+the+balance+beams+are+not+to+scale.+%28a%29+When+acid%E2%80%93base+balance+is+normal%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+20%3A1.+Each+of+the+four+types+of+acid%E2%80%93base+disorders+has+an+uncompensated+state+and+a+compensated+state.+%28b%29+In+uncompensated+respiratory+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2820%3A2%29+because+CO2+has+accumulated.+In+compensated+respiratory+acidosis%2C+HCO3%E2%88%92+is+retained+to+balance+the+CO2+accumulation%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2840%3A2%29.+%28c%29+In+uncompensated+respiratory+alkalosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+increased+%2820%3A0.5%29+by+a+reduction+in+CO2.+In+compensated+respiratory+alkalosis%2C+HCO3%E2%88%92+is+eliminated+to+balance+the+CO2+de%EF%AC%81+cit%2C+which+restores+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2810%3A0.5%29.+%28d%29+In+uncompensated+metabolic+acidosis%2C+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+is+reduced+%2810%3A1%29+by+an+HCO3%E2%88%92+de%EF%AC%81cit.+In+compensated+metabolic+acidosis%2C+HCO3%E2%88%92+is+conserved%2C+which+partially+makes+up+for+the+HCO3%E2%88%92+de%EF%AC%81cit%2C+and+CO2+is+reduced%3B+these+changes+restore+the+%5BHCO3%E2%88%92%5D%2F%5BCO2%5D+ratio+to+a+normal+equivalent+%2815%3A0.75%29.+%28e%29+In+uncompensated+metabolic+alkalosis%2C+the+%5BHCO3%E2.jpg "Figure 13-23e p648.")
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13.7 pH Regulation: Respiration and Excretion
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13.8 Acid-Base Imbalances: Respiratory, Environmental, and Metabolic Disturbances
Environmental acidosis Arises from increased CO2 or acids in the environment Increased CO2 in the Earth’s atmosphere as a result of human burning of fossil fuels Ocean acidification -- causes weakening of shells and coral skeletons Sulfuric acid from volcanoes and coal-burning power plants Environmental alkalosis Arises in highly alkaline bodies of water 101
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