Download now
Fluid Compartments
Water occupies two main fluid compartments
Intracellular liquid (ICF) ” about two thirds by volume level, contained in cells Extracellular liquid (ECF) ” consists of two major neighborhoods Plasma ” the liquid portion of blood
Interstitial fluid (IF) ” liquid in areas between cellular material
Different ECF ” lymph, cerebrospinal fluid, eyesight humors, synovial fluid, serous fluid, and gastrointestinal secretions Extracellular and Intracellular Fluids
Normal water is the widespread solvent
Solutes are broadly labeled into:
Electrolytes ” inorganic salts, all stomach acids and angles, and some protein Electrolytes identify the chemical substance and physical reactions of fluids
Electrolytes possess greater osmotic power than nonelectrolytes Water moves relating to osmotic gradients
Nonelectrolytes ” for example glucose, lipids, creatinine, and urea Each fluid area of the body has a special pattern of electrolytes Extracellular fluids are very similar (except to get high protein content of plasma) Salt is the chief cation
Chloride is the key anion
Intracellular liquids have low sodium and chloride
Potassium may be the chief cation
Phosphate is the primary anion
Proteins, phospholipids, cholesterol, and neutral excess fat account for: 90% of the mass of solutes in sang
60% of the mass of solutes in interstitial fluid
97% in the mass of solutes in the intracellular inner compartment
Fluid Movement Among Compartments
Compartmental exchange is controlled by osmotic and hydrostatic pressures Net leakage of fluid from your blood can be picked up simply by lymphatic ships and delivered to the bloodstream Exchanges among interstitial and intracellular essential fluids are complicated due to the picky permeability from the cellular walls Two-way normal water flow is usually substantial
Ion fluxes happen to be restricted and move selectively by energetic transport Nutrients, respiratory smells, and toxins move unidirectionally Plasma is definitely the only smooth that flows throughout the human body and backlinks external and internal environments Osmolalities of all body fluids are equivalent; changes in solute concentrations will be quickly accompanied by osmotic changes
Water Balance and ECF Osmolality
To stay properly hydrated, water intake must equal water output Water intake sources
Ingested substance (60%) and solid foodstuff (30%)
Metabolic drinking water or water of oxidation process (10%)
Water end result
Urine (60%) and feces (4%)
Duro losses (28%), sweat (8%)
Improves in plasma osmolality result in thirst and release of antidiuretic junk (ADH) Dangerous Water ” Homeostaisis
Intake ” Hypothalmic Being thirsty Center
Thirst is definitely quenched the moment we begin to drink water
Reviews signals that inhibit the thirst centers include:
Moistening in the mucosa of the mouth and throat
Activation of stomach and intestinal stretch out receptors
Effect and Dangerous ADH
Water reabsorption in collecting ducts is proportional to ADH release Low ADH levels produce water down urine and reduced volume of body fluids High ADH levels create concentrated urine
Hypothalamic osmoreceptors bring about or hinder ADH relieve
Elements that especially trigger ADH release contain prolonged fever; excessive sweating, throwing up, or diarrhea; severe blood loss; and distressing burns Disorders of Water Balance:
Dehydration
Water loss exceeds water intake and the body is in negative fluid stability Causes contain: hemorrhage, extreme burns, long term vomiting or diarrhea, profuse sweating, drinking water deprivation, and diuretic abuse Signs and symptoms: cottonmouth, thirst, dried flushed skin area, and oliguria Prolonged dehydration may lead to weight loss, fever, mental confusion Various other consequences include hypovolemic shock and lack of electrolytes Hypotonic Hydration
Suprarrenal insufficiency or perhaps an extraordinary amount of water ingested quickly can lead to cell phone overhydration, or water intoxication ECF can be diluted ” sodium articles is normal nevertheless excess normal water is present The resulting hyponatremia promotes net osmosis into tissue cellular material, causing inflammation These events must be quickly reversed in order to avoid severe metabolic disturbances, especially in neurons Edema.
Atypical accumulation of fluid in the interstitial space, leading to tissue swelling Caused by anything that increases flow of fluids out of the bloodstream or hinders their return.
Factors that accelerate fluid lossinclude: Increased blood pressure, capillary permeability
Incompetent venous valves, localized blood vessel blockage
Congestive heart failure, hypertension, high blood volume
Hindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia ” low levels of plasma proteins
Forces fluids out of capillary beds at the arterial ends
Fluids fail to return at the venous ends
Results from protein malnutrition, liver disease, or glomerulonephritis Blocked (or surgically removed) lymph vessels:
Cause leaked proteins to accumulate in interstitial fluid
Exert increasing colloid osmotic pressure, which draws fluid from the blood Interstitial fluid accumulation results in low blood pressure and severely impaired circulation Sodium in Fluid and Electrolyte Balance
Sodium holds a central position in fluid and electrolyte balance Sodium salts:
Account for 90-95% of all solutes in the ECF
Contribute 280 mOsm of the total 300 mOsm ECF solute concentration Sodium is the single most abundant cation in the ECF
Sodium is the only cation exerting significant osmotic pressure The role of sodium in controlling ECF volume and water distribution in the body is a result of: Sodium being the only cation to exert significant osmotic pressure Sodium ions leaking into cells and being pumped out against their electrochemical gradient Sodium concentration in the ECF normally remains stable
Changes in plasma sodium levels affect:
Plasma volume, blood pressure
ICF and interstitial fluid volumes
Renal acid-base control mechanisms are coupled to sodium ion transport Regulation of Sodium Balance:
Aldosterone
The renin-angiotensin mechanism triggers the release of aldosterone This is mediated by juxtaglomerular apparatus, which releases renin in response to: Sympathetic nervous system stimulation
Decreased filtrate osmolality
Decreased stretch due to decreased blood pressure
Renin catalyzes the production of angiotensin II, which prompts aldosterone release Adrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECF Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly
Cardiovascular System Baroreceptors
Baroreceptors alert the brain of increases in blood volume (hence increased blood pressure) Sympathetic nervous system impulses to the kidneys decline
Afferent arterioles dilate
Glomerular filtration rate rises
Sodium and water output increase
This phenomenon, called pressure diuresis, decreases blood pressure Drops in systemic blood pressure lead to opposite actions and systemic blood pressure increases Since sodium ion concentration determines fluid volume, baroreceptors can be viewed as “sodium receptors Atrial Natriuretic Peptide (ANP)
Reduces blood pressure and blood volume by inhibiting:
Events that promote vasoconstriction
Na+ and water retention
Is released in the heart atria as a response to stretch (elevated blood pressure) Has potent diuretic and natriuretic effects
Promotes excretion of sodium and water
Inhibits angiotensin II production
Influence of Other Hormones on Sodium Balance
Estrogens:
Enhance NaCl reabsorption by renal tubules
May cause water retention during menstrual cycles
Are responsible for edema during pregnancy
Progesterone:
Decreases sodium reabsorption
Acts as a diuretic, promoting sodium and water loss
Glucocorticoids ” enhance reabsorption of sodium and promote edema Regulation
of Potassium Balance
Relative ICF-ECF potassium ion concentration affects a cell’s resting membrane potential Excessive ECF potassium decreases membrane potential
Too little K+ causes hyperpolarization and nonresponsiveness Hyperkalemia and hypokalemia can:
Disrupt electrical conduction in the heart
Lead to sudden death
Hydrogen ions shift in and out of cells
Leads to corresponding shifts in potassium in the opposite direction Interferes with activity of excitable cells
Influence of Aldosterone
Aldosterone stimulates potassium ion secretion by principal cells In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted Increased K+ in the ECF around the adrenal cortex causes:
Release of aldosterone “>Potassium secretion
Potassium controls its own ECF concentration via feedback regulation of aldosterone release Regulation of Calcium
Ionic calcium in ECF is important for:
Blood clotting
Cell membrane permeability
Secretory behavior
Hypocalcemia: Increases excitability, causes muscle tetany
Hypercalcemia: inhibits neurons and muscle cells; cause heart arrhythmias Calcium balance is controlled by parathyroid hormone and calcitonin PTH promotes increase in calcium levels by targeting:
Bones ” PTH activates osteoclasts to break down bone matrix
Small intestine ” PTH enhances intestinal absorption of calcium Kidneys ” PTH enhances calcium reabsorption and decreases phosphate reabsorption Calcium reabsorption and phosphate excretion go hand in hand Influence of Calcitonin
Released in response to rising blood calcium levels
Calcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible Acid Base Balance
Introduction to Acids and Bases
Strong acids ” all their H+ is dissociated completely in water Weak acids ” dissociate partially in water and are efficient at preventing pH changes Strong bases ” dissociate easily in water and quickly tie up H+ Weak bases ” accept H+ more slowly (e.g., HCO3 and NH3)
Normal pH of body fluids
Arterial blood is 7.4
Venous blood and interstitial fluid is 7.35
Intracellular fluid is 7.0
Alkalosis or alkalemia ” arterial blood pH rises above 7.45
Acidosis or acidemia ” arterial pH drops below 7.35 (physiological acidosis) Sources of Hydrogen Ions ” Most hydrogen ions originate from cellular metabolism Breakdown of phosphorus-containing proteins releases phosphoric acid into the ECF Anaerobic respiration of glucose produces lactic acid
Fat metabolism yields organic acids and ketone bodies
Transporting carbon dioxide as bicarbonate releases hydrogen ions Hydrogen Ion Regulation
Concentration of hydrogen ions is regulated sequentially by: Chemical buffer systems ” act within seconds
Physiological buffer systems
The respiratory center in the brain stem ” acts within 1-3 minutes Renal mechanisms ” require hours to days to effect pH changes Chemical Buffer Systems
Bicarbonate Buffer System
A mixture of carbonic acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates work as well) If strong acid is added:
Hydrogen ions released combine with the bicarbonate ions and form carbonic acid (a weak acid) The pH of the solution decreases only slightly
If strong base is added:
It reacts with the carbonic acid to form sodium bicarbonate (a weak base) The pH of the solution rises only slightly
This system is the only important ECF buffer
Phosphate Buffer System
Nearly identical to the bicarbonate system
Its components are:
Sodium salts of dihydrogen phosphate (H2PO4), a weak acid
Monohydrogen phosphate (HPO42), a weak base
This system is an effective buffer in urine and intracellular fluid Protein Buffer System
Plasma and intracellular proteins are the body’s most plentiful and powerful buffers Some amino acids of proteins have:
Free organic acid groups (weak acids)
Groups that act as weak bases (e.g., amino groups)
Amphoteric molecules are protein molecules that can function as both a weak acid and a weak base Physiological Buffer Systems
Respiratory Buffer System
The respiratory system regulation of acid-base balance is a physiological buffering system There is a reversible equilibrium between:
Dissolved carbon dioxide and water
Carbonic acid and the hydrogen and bicarbonate ions
CO2 + H2O “>H2CO3 “>H+ + HCO3
During carbon dioxide unloading, hydrogen ions happen to be incorporated in to water Once hypercapnia or rising plasma H+ arises:
More deeply and more speedy breathing expectorates more carbon dioxide
Hydrogen ion focus is decreased
Alkalosis causes slow, more shallow breathing, causing H+ to boost Respiratory system disability causes acid-base imbalance (respiratory acidosis or respiratory alkalosis) Renal Components of Acid-Base Balance
Launch
Chemical buffers can easily tie up excessive acids or bases, however they cannot remove them in the body The lungs may eliminate carbonic acid through the elimination of carbon dioxide The particular kidneys can rid the body of metabolic acids (phosphoric, uric, and lactic stomach acids and ketones) and prevent metabolic
acidosis The ultimate acid-base regulatory internal organs are the kidneys
The most important renal mechanisms for regulating acid-base balance are: Conserving (reabsorbing) or generating new bicarbonate ions
Excreting bicarbonate ions
Losing a bicarbonate ion is the same as gaining a hydrogen ion; reabsorbing a bicarbonate ion is equivalent to losing a hydrogen ion Hydrogen ion secretion arises in the PERCENTAGE
Hydrogen ions range from dissociation of carbonic chemical p
Reabsorption of Bicarbonate
CO2 combines with water in tubule cellular material, forming H2CO3
H2CO3 splits in to H+ and HCO3-
For each H+ secreted, a Na+ and a HCO3- are reabsorbed by the PCT cells Secreted H+ contact form H2CO3; thus, HCO3- vanishes from filtrate at the same price that it goes in the peritubular capillary bloodstream H2CO3 formed in filter dissociates to release CO2 & H2
LASER then diffuses into tubule cells, where it acts to trigger further H+ release Hydrogen Ion Excretion
Dietary H+ must be counteracted by making new HCO3-
The excreted H+ must bind to buffers in the urine (phosphate buffer system) Intercalated cells positively secrete H+ into urine, which is buffered and passed HCO3- produced is:
Moved into the interstitial space via a cotransport system
Passively came into the peritubular capillary blood vessels
Reacting to acidosis:
Kidneys generate HCO3-and add these to the blood
An equal volume of H+ are put into the urine
Ammonium Ion (NH4+) Excretion
This method uses NH4+ made by the metabolic rate of glutamine in PERCENTAGE cells Every glutamine metabolized produces two ammonium ions and two bicarbonate ions HCO3- moves to the blood and ammonium ions are excreted in urine Respiratory Acidosis and Alkalosis
Result from failure of the respiratory system to harmony pH
PCO2 is the single most important indicator of respiratory insufficiency PCO2 amounts ” typical PCO2 changes between thirty-five and forty five mm Hg Values over 45 logistik Hg transmission respiratory acidosis
Beliefs below thirty-five mm Hg indicate respiratory alkalosis
Respiratory acidosis is the most prevalent cause of acid-base imbalance Takes place when a person breathes shallowly, or gas exchange can be hampered by simply diseases just like pneumonia, cystic fibrosis, or perhaps emphysema Respiratory alkalosis is a frequent result of hyperventilation Metabolic Acidosis
All pH imbalances besides those brought on by abnormal blood carbon dioxide amounts Metabolic acid-base imbalance ” bicarbonate ion levels previously mentioned or below normal (22-26 mEq/L) Metabolic acidosis is definitely second most usual cause of acid-base imbalance Common causes will be ingestion of too much liquor and extreme loss of bicarbonate ions Other causes include accumulation of lactic acidity, shock, ketosis in diabetic crisis, starvation, and renal failure Metabolic Alkalosis
Increasing blood ph level and bicarbonate levels reveal metabolic alkalosis Typical causes are:
Vomiting from the acid items of the belly
Intake of excess basic (e. g., from antacids)
Constipation, in which excessive bicarbonate can be reabsorbed
Respiratory and Renal Settlements
Acid-base disproportion due to insufficiency of a physical buffer product is compensated pertaining to by the different system The respiratory system attempt to correct metabolic acid-base unbalances The kidneys will work to improve imbalances caused by respiratory disease Respiratory Compenstaion
In metabolic acidosis:
The rate and depth of breathing happen to be elevated
Blood pH is listed below 7. 35 and bicarbonate level is usually low
As co2 is eliminated by the respiratory system, PCO2 is catagorized below typical In metabolic alkalosis:
Compensation demonstrates slow, short breathing, allowing for carbon dioxide to
accumulate in the bloodstream Correction is definitely revealed by:
High pH (faster than 7. 45) and elevated bicarbonate ion levels
RisingPCO2
Renal Compensation
To fix respiratory acid-base imbalance, renal mechanisms are stepped up Acidosis provides high PCO2 and high bicarbonate levels
The high PCO2 s the main cause of acidosis
The excessive bicarbonate levels indicate the kidneys are retaining bicarbonate to counteract the acidosis Alkalosis offers Low PCO2 and large pH
The kidneys eliminate bicarbonate from the body system by declining to reclaim it or perhaps by definitely secreting this
you
