Question Answer
What do we call a condition of low arterial pH, reduced plasma HC03 concentration, and usually compensatory alveolar hyper-ventilation resulting in decreased PCO2? Metabolic Acidosis
Metabolic acidosis can be due to increased acid production, decreased acid elimination, or ? Aspirin overdose – acetylsalicylic acid poisoning (accidental or otherwise).
This is estimated by subtracting the sum of the Cl and HC03 concentrations from the plasma Na concentration. Anion Gap . [Na]-([Cl]+[HCO3])
What accounts for most of the normal anion gap of 12 ± 4 mEq/L, and why? Negatively charged plasma proteins such as albumin
Why doesn’t hyperchloremic metabolic acidosis result in an increased anion gap? Because Chloride is part of the formula for the anion gap. [Na]-([Cl]+[HCO3])=Anion Gap
Why do renal or extrarenal losses of HC03 produce hyperchloremic (non-anion gap) metabolic acidosis? Kidney retention if chloride – to preserve extra cellular fluids.

Acid – donates a proton; releases H+ H+ + Cl- = Hydrochloric acid Too much H+ Acidemia – blood Acidosis-overall condition in body fluids When acid meets base…they neutralize! When acid meets base…they neutralize!
Base accepts or combines with a proton Na++ OH- = Sodium Hydroxide Too much base Alkalemia – blood Alkalosis- overall condition in body fluids
Clinical Manifestations of alkalosis Death convulsions arrhythmia irritability
Clinical Manifestations of acidosis drowsiness lethargy coma
Blood Buffers Acids are carried by Hb and HCO3 (88%) Bicarb system is open, primary system Due to loss of CO2 through breathing HC03 + H+ = H20 + CO2 (exhaled) Nonbicarb systems are closed Nothing is “lost” Hemoglobin, phosphates, proteins
Henderson-Hasselbach Equation Allows you to calculate pH, CO2, or HCO3 if you know 2 of the 3 variables in the formula Use: to check if pH, PCO2, and HCO3 in an ABG report are compatible, and to predict what happens when you change one component in the ABG
CO2 excretion depends on: Perfusion Diffusion Ventilation Think heart, lungs or CNS
Respiratory Acidosis Clinical signs hypoxemic manifestations, warm flushed skin, bounding pulse, arrhythmias, > ICP, headaches, <Cl-
Respiratory Acidosis Causes acute airway obstruction massive PE drugs (sedatives, narcotics) neuromuscular disease trauma (brain, spinal cord, chest wall) obesity kyphoscoliosis COPD cardiac arrest
Respiratory Alkalosis Terms: excess CO2 elimination, hypocapnia, hyperventilation Compensation: kidneys excrete HCO3 acute: -PaCO2 by 5 = HCO3 – by 1 (24-48 hrs) chronic: -PaCO2 by 10 = HCO3 – by 5
Respiratory Alkalosis Clinical signs tachypnea, dizziness, light-headedness, sweating, paresthesia
Respiratory Alkalosis Causes hypoxemia anxiety fever stimulant drugs pain brain tumor sepsis exercise early onset asthma pneumonia, pulmonary edema, CHF iatrogenic (vent, IPPB
Metabolic Acidosis Clinical signs hyperpnea, Kussmaul’s severe diabetic ketoacidosis, dyspnea, headache, N/V, lethargy, coma (severe)
Anion Gap Helps indicate the cause of metabolic acidosis Anion gap = Na+ – (Cl- + HCO3) Normal: 9 to 14 mEq/L Increased (>14) = metabolic acidosis is caused by an increase in fixed acids Normal anion gap = metabolic acidosis is caused by loss of HCO3
Anion Gap Metabolic Acidosis Due to increased fixed acids Causes: Diabetic ketoacidosis Lactic acidosis Alcoholic ketoacidosis Advanced renal failure Ethylene glycol intoxication Methanol intoxication (formic acid) Salicylate intoxication (aspirin)
Metabolic Alkalosis Usually accompanied by hypokalemia -Common in ICU; difficult to treat Compensation: hypoventilation but usually uncompensated : lower RR, apnea, cyanosis, N/V, confusion, headache, lethargy, tetany in severe cases
Metabolic Alkalosis Causes NG suction Diuretics Vomiting Steroids Hypokalemia Hypochloremia Hypovolemia NaHCO3 infusion Excessive antacids or alkali for peptic ulcers Posthypercapnic met. alkalosis Massive blood transfusion (>8 units)

Question Answer
S/Sx of FVE? Edema, JVD, anorexia, V&N, dyspnea, orthopnea couch, moints sounds. increased BP, bounding pulse, pitting
S/Sx of FVD? chng in LOC, thirst, headache, v&N, dry skin, decreased turgor, diarrhea, soncstipation, muslce weakness, parathesias, tetany. postural hypotention, change in rate of resp, pulse and depth of resp.
When edema is great it is called______. Anasarca
ABG’s give infor about what 3 things? oxygenation, ventilation and acid base.
When drawing blood for an ABG what should you note? Temperature
Level of HCO3 ? 22-26
Level of pH? 7.35 – 7.45
Level of PaCO2? 35-45
Acids release what? H
Bases bind what? H
As H increases pH does what? Decreases
Lungs excrete carbonic acid as what? CO2
When pH decreases ( becomes acidic) the rate and epth of resp does what? Increases to create greater excretion of CO2.
When pH increases ( alkalosis), the rate of resp does what? Decreases to retain CO2 (which will join with H2O to create carbonic acid.)
CO2 is constantly being formed by what? metabolism so the resp system is contantly balancing the amount of CO2 in the ECF
The kidney usually excretes______ urine and retains _______ acidic, bi-carbonate
What is the main point of excretion of CO2? The lungs
With Alkalosis, what is the kidney going to do? Bi-carb will be combined with Na in the tubules and excreted
With Acidosis, what will the kidneys do? Excrete excess H
What is the major effect of acidosis? CNS depression
What does Alkalosis do to the CNS? Over excites it
When ventilation decreases, what heppens? The amont of CO2 and H increases creating resp acidosis.
Hypercapnia ( too much CO2) causes what? CO2 Narcosis
Acidosis makes ______move out of cells, creating _______. K, creating hyperkalemia of the blood
what happens if you have too much blood K? Ventricl fibrilation.
What are the basic causes of Resp acidosis? Anything blocking airway, poor ventilation, decression of respirations(COPD most common), COPD, pneumothorax, atelectasis, pneumonia
What causes respiratory alkalosis? Excessive ventilation.
What is the common cause of resp alkalosis? Hyperventilation from anxiety, pain, hypozia, brain lesions, over ventilation on mechanical ventilator
Metabolic Acidosis is a deficit of what? Bi-Carbonate
What does metabolic acidosis come from? Losing bi-carb or too much organic acid is added to the body.
What are common causes of Metabolic Acidosis? DM and starvation.
Why idoes DM create metabolic acidosis problems? If glucose can’t be used (or there is none) the body uses fat creating ketone acids. Plasma bi-carb is used to try to buffer the ketones acids so you get metab. acidosis or keto acidosis.
Metabolic acidosis also can be created by lactic acid? Excess lactic acid is caused by prolonged exercise or oxidation without O2 from heart failure, shock, or a bicarb deficit from diarrhea or draining fistula.
What is the relationship between metabolic acidosis and kidney failure? The acids accumulate because they cannot be filtered out of the blood.
In a normal Kidney with acidosis, what happens? The excess H will be released, retain K and create hyper K along with the acidosis.
Metabolic Alkalosis is an excess of what? Bi-carb or lactate
What are some common causes of Metabolic alkalosis? loss of acids from vomit, suction, drainage, loss of K from fistulas and diarrhea, iinjestion of sodium bicarb, antacids, bicarb or lactate IV infusion, diuretics.
In metabolic acidosis, what happens with the K? It enters the cell and HypOkalemia results.
What do you assess for with Metabolic Alkalosis? HypOkalemia, dizziness and tingling.
What is the Tx for Resp Acidosis? enhance ventilation, TCDB, remove blockage
What is the Tx for Resp Alkalosis? treat cause, watch for dysrythmias, Ca gluconate for tetany, help renal function to help compensation
What is the Tx for metabolic acidosis? Treat Cause ( Dm, Starvation, lactic acid) give Na bi-carb, dialysis if from renal failure, beware hypo K as K moves back into cell.
What is the Tx for metabolic alkalosis? Treat cause(vomit, suction, drainage, antacids, fistualas, diarrhea) dc NGtube, dc antacids, give Na Cl or amonium Cl, diuretics to excrete excess bi-carb. keep resp function going to help compensation.
Elderly and COPDers are at an increased risk for______? Acid Base disorders
Acid Base disorders in elderly may lead to? Respiratory depression.
Normal pH distrubances are due to? Aging
Name some ore-existing conditions that can lead to Acid Base disorders? Renal, cardiac, endocrine and pulmonary.
Once an acid base disorder has occured, elders are less able to compensate because of what? Age related changes to the kidney.
the amount of diuresis produced is in direct proportion to.. The amont of Na and Cl blocked from reabsorption.
High ceiling diuretics produce the most and work even when… Glomerular filtration is low.
High ceiling diuretics can cause? dehydration, hypOtension, hearing loss ( ototoxity) and hypOkalemia
Thiazides produce les and are ineffective with…. lower glomerular filtration rate but aren’t ototoxic.
K sparing diuretics cause what rate of diuresis? Modest
K sparing diuretics are use to counteract what? K loss from high ceiling / thiazide diuretics
K sparing can cause what electrolyte disorder? HyperKalemia
Don’t comine K sparing diuretics with what? K supplements or with each other.
High ceiling and Thiazide diuretics are used for? HTN and Edema associated with CHF, cirrhosis and renal disease.,
Name a high ceiling diuretic. Furosimide / Lasix
Name some Thiazide diuretics. HCTZ and HydroDiuril
Name a K sparing diuretic. Spironolactone
When is comes to electrolyte, what is is really all about? Shrinking and swelling of the brain.
Aldosterone is a ______secreted by the ________. Hormone, Adrenal cortex.
Aldosterone secretion is stiumlated by____ FVD
Aldosterone site of action is.. Kidney
Aldosterone reabsorbs____ and secretes _____ Na, K
If a patient has hypo-aldosteroneism what will happen to BP and volume status? Low BP and dehyration
ADH is produced by the ? Hypothalamus
ADH is secreted by the ? Posterior Pituitary.
ADH is released in response to FVD or high osmolarity and thirst.
The site of ADH action? Kidney
ADH re-abropbs what? H2O
ADH allows for the excretion of what? concentrated urine
Three conditions that can trigger ADH are? stress, anasthesia and narcotics.
What is SIADH Syndrome of Inappropriate ADH
If a pt has SIADH what would you expect the volume status to be? FVE or normal. Na will be low, water is trying to move back into the cell.
What is the Tx for SIADH with a head injury? monitor I and O, fluid restriction, any fluid should be hypertonic to draw fluid away from brain, and check LOC
What is diabetes insipidus? Too little ADH
What happens with diabetes insipidus? H2O moves out of the cell, volume status is low, frequent urination.
Tx for diabetes insipidus? Give ml for ml urinated, replace with hypotonic fluids, give vasopressin,
What is vasopressin? Synthetic ADH
Types of Dehydration Isotonic, Hypotonic, Hypertonic
What is Isotonic dehydration? Fluid has the same osmolarity as plasma, from bleeding. Lose fluid and electros in equal amounts.
What is Hypotonic dehydration? Fluid has fewer solutes than plasma, from heatstroke
What is Hypertonic dehydration? Fluid has more solutes than plasma, Dm, DKA, hyperglycemia and DI
What are neuro manifestations of FVD? decreased lov , restless, dissy from low circulating blood vol. and confusion.
Whare are the cardiovascular manifestations of FVD? decreased BP and tachycardia
What are the Pulmonayr manifestations of FVD? increase respirations trying to pump blood around
What is the renal manifestation of FVD? increased specific gravity
what is the manifestation of FVD in the extremities? poor turgor, muscle cramps, dry skin, cold, clammy
What are the “general” manifestations of FVD? weight loss, shrunken eyeballs, thirsty
What are some causes of FVD? diuretics, third spacing, vomiting
What are neuro manifestations of FVE? confusion, seizures ( from increased ICP and decreased Na)
What are cardios signs of FVE? increase dystolic, decreased diastolic (widening pulse pressure)
What are pulmonary signs of FVE? crackles, SOB
What are some abdominal signs of FVE? aceites and enlarged liver
what are some signs in the extremities of FVE? edema, dependant or sacral
What are some general signs of FVE? weight fain, prone to bed sores
What are some causes of FVE? Disease processes or overhydration.
What are some causes of Hyper natremia? DI ( not enough ADH), excessive Na intake, fever, heatstroke, pulmonary infections, burns, diarrhea.
Hypernatremia may come from ____in the elderly? Decreased thirst response so they do not drink enough water.
The basic symptom rule of hyperNatremia? Everything is jacked up. Reflexes, blood pressure, CNS, thirst, heart rate
S/Sx of Hyper Natremia? Hyper reflexes, thirst, low urine output, HTN seixures, increased HR
Nsg Interventions Hyper Na? treat cause, monitor I & O, Hypotonic fluids ( D5), monitor labs ( blood sugar and Osmo), watch LOC , seizure precautions.
Why do you infuse IV slow with hyper Na? to avoid a rapid shift in fluid which will swell cells and create cerebral edema
What is the most important Nsg intervention for Hyper Na? Monitor I and O
What does hypO Na do? Pulls H2O from intravascular into the intracellular
HypO Na creates a potential for what? Cerebral Edema
What are some causes of HypO Na? Diuretics, vomiting sweating renal failure, over admin. of hypotonic fluids
S/Sx of Hyponatremia? Confusion, headache, nausea, vomit, muscle weakness, fatique, apathy, anorexia.
What are late s/sx of HypO Na? shock and coma
What are the Nsg Interventions for HypO Na? I & O, weigh daily, vital signs, check for postural hypotension.
Why do you need to correct the HypO Na before giving fluids? Use Isotonic to raise the Na level without the fluid so the cells don’t draw the H20 in first.
Kidneys excrete K in echanges for___, controlled by ________. Na, Aldosterone
The cause of HyperK is? use of supplements, , movement of K due to hypoxia or acidosis, sepsis, trauma, crushing
S/sx of Hyper K? Diarrhea, apathy, confusion, brady cardia and cardiac arrhythmias, cardiac arrest, numbness hands/feet.
Nsg Interventions for Hyper K? Cardiac monitor, Kayexalate, Ca gluconate, IV insulin and IV D50, sodium Bicarb.
why do you use Calcium gluconate Iv in hyperK? Offsets the effects of K on the heart.
Why do you use insulin and dextrose for Hyper K? Promotes the uptake of K into the cells. K follows the insulin/dextrose.
If a patinet has refractory hyperkalemia what do you do? Dialysis. It means that nothing else is working.
What happens with K and acidosis? K move out of the cell where K and H are xchanged and H goes into the cell.
If you are using K in a peripheral line what do you use with it? Lidocane for the pain.
What is the Iv rage for K in a peripheral line? 10 mEq / hr, no more.
What are the s/sx of Hypo K N&V, weak, hypOtension, elevated HR, dysrythmias, lethargy, confusion,( constipation and paralytic ileus with GI losses)
What happens with K and the kidney during metabolic alkalosis? K is lower as K is moving into the cells during the alkaline state, then excreted by kidneys which hold onto the K because of the alkalitic state.
What are common causes of HypO k? Starvation, increased aldosterone ( re-sorbs Na and rids of K), GI loss, laxatives and diuretics.
Most common causes of Hypo K? Diuretics and laxatives.
What are some Nsg Interventions for HypO K? Cardiat monitor, watch for dig toxicity, make sure you have urine output b/4 giving K, oral supplements
How do you administer intravenous K? Dilute K, add lidocane and give no faster than 10mEq/hr. ( perpiheral line)
What does digitalis do? Slow down the heart and increases contractility.
Why do you need to watch digitalis with K? Potentiates the Digitalis and risk of toxicity.
What is Mag use for? Protects against over excitability of muscles.
Mag has a sedative effect on?? the neuromuscular junction by inhibiting acetylcholine (ATC) release and diminishes nmuscle cell excitability
Mag also helps with? nerve conduction, DNA and PRO synthesis, ATP production, vasodilation.
have Torsseauds? Need more______> Magnesium
What are causes of HypO Mag? Malnutrition, alcoholism ( don’t eat) steriods, diuretics ( lose K lose mag) diarrhea.
If you have HypO Mag you probably also have_______. HypO Ca, mag effects parathyroid hormone.
S/Sx of Hypo Mag? Tachycardia , Toursedes, paresthesis, muscle spasm, tremors, tetany, loc changes, seizures
What is Toursedes ? Life Threathening cardia dysrymthias.
Low magnesium makes for muscular irritability. What are some signs of that? Tetany, muscles spasms, tremors.
What are some Nsg Interventions for HypOMag? Watch Dig ( mag enhances), cardiac monitor, seizure prec. replacement.
How do you administer IV Mag? 1 gm to 20 ml of NS to dilute.
What is a common side effect of IV Mag admin? Flushed, sweating, bradycardia, hypOtension.
What do you need to have before administering Mag? A urine output.
S/Sx of Hyper Mag? Bradycardia, hyporeflexia, resp. depress. lethary leading to coma
What are Nsg interventions for Hyper Mag? Volume admin, diuretics, insulin and glucose admint, hemodialysis, seizure precautions, watch loc
Why use unsuling and glucose admint with hyper mag? Mag follows K into the cells which is drawn there by the insulin/gluc.
why use diuretics with Hyper Mag? K wasting diuretics ( loops especially) will take the mag with the K.
Ca is for…. Transmission of nerve pulses, cardiac contractility, activation of clotting mech.
HypO Ca is related to what acid base problem? Alkalosis
Hyper Ca is rrelated to what acid base problem? Acidosis
HypO Ca is relate to _____Phosphate? Hyperphosphate = HypO Ca
Causes of HypO Ca? Multiple blood transfuions, dkined diseas and draining fistufals, diet, decrease GI absorb, decrease bone reabsorb, alkalosi, alcholism
Why does blood transfusion contribute to Hypo Ca? the citrate binds with the Ca
Why does kidney disease contribute to Hypo Ca? the kidney loses it’s ability to excrete phos and retain Ca
The S/Sx of HypO Ca is caused by.. increased muscle irritability.
The s/sx of HypO Ca are? Numbness, tingling, muscle weakness, twitching tetan seizures.
What are two nsg tests you can do for HypO Ca? Chvostek’s sign and Trousseau’s.
What are nsg interventions for HypO Ca? cardia montior, seizure precaution, replacement.
What are the IV Ca replacements Emerg- Ca Chloride, non emerg- Ca gluconate
What type of line is used for Ca chloride? Central line
What is the rate that Ca Chloride is given? 1gm/hr.
S/Sx of Hyper Ca? depressed deep tendon reflex, lethary coma, decrease GI motility, dysrythmias, fractures.
Interventions for Hyper Ca? cardia monitor, watch lOV, increase volume, diuretics, drugs calcitono and mithrimycin
Causes of Hyper Ca? bone loss, immobilization, intake, antacids, increase PTH and Vit D.
Everywoman will be slightly ______Calcemia? HypOcalcemic.
Phosphorus has an inverse relationship with? Calcium
Phosphorus is absorbed where? Jejunem of the intestine
S/sx of HypO phos? Muscle weakness, low energy, confusion, memory loss, slurred speech, HTN and decreased C.O.
What are the cardiac effects of HypO Phos? decreased contractility so they are HTN and decreased cardiac output, anemia, resp failure.
What are the resp effects of HypO Phos? weak muscles lead to resp failure
Phos effects the structure and functino of what? RBCs and Leukocytes, creating anemia
What does CHEMO stand for ( in hyperphophatemis?) Cardiac irregularites, Hyperreflexia, Eat poor, Muscle weakness, Oliguria
PaO2 tells you about.. Oxygenation
SaO2 tells you about Hemoglobin. Giving O2 doesn’t help if you don’t have the hemoglobin to carry it.
PaCO2 tells you about if they are breathing effectively.
HCO3 reflects the _______component of ABGs Renal
Causes of Hyperphosphatemia? Impaired renal function, acid base imbalance, thyroid or parathyroid surgery.
Tx of Hyper-Phospate Drug therapy, Iv therapy, diuretics and Hemodialysis
What type of drug therapy is used for Hyper Phos? Aluminum, Mag and Ca all will bind Phos
Fo Iv and Diuretic therapy for hyper phos what do you need? Functioning kidneys so you can promote renal excretion.
What are the three chemical buffer systems? Carbonic acid/bi-carb, Phosphate buffer and protein buffer.
How do you assess Resp Acidosis? 1. headache then2. confusion, then hyperkalemia
If CO2 is high what signs will the pt exhibit? Obtunded, sleepy, difficulty arousing.
What does compensation tell you? That the problem has been around long enough for the body to want to compensate.
Resp Alkalosis is always due to?? Hyperventilation, blowing off too much CO2
Who is at risk for Resp Alkalosis? those with anxiety, fear, asthma, head injury, pulmonary edema due to hypervent trying to get O2

Question Answer
At rest, the metabolizing tissue cells consume and produce what? Consume 250mL of O2 & produce 200mL of CO2.
How many ways does Plasma transport CO2? 1. Carbamino compound bound to Protein, 2. Bicarbonate, 3. Dissolved CO2.
Carbamino compound bound to protein in Plasma 1% of CO2 transport
Bicarbonate in Plasma 5% of CO2 transport
Process of bicarbonate in plasma (very slow process) CO2 + H2O (Hydrolysis) -> H2CO3 (carbonic acid) -> HCO3- + H+ (ionized ions)
Dissolved in Plasma 5% of CO2 transport
Dissolved CO2 in plasma is used to determine what? Pts. Pco2 (in venous blood) Pco2 x .03 = Pco2 mEq/L
How many ways does RBC transport CO2? 1. Dissolved CO2, 2. Carbamino-Hb, 3. Bicarbonate.
Dissolved in RBC 5% of CO2 transport
Carbamino-Hb in RBC 21% of CO2 transport
O2 that is released from the carbamino-Hb reaction is available for what? Tissue metabolism
Bicarbonate in RBC 63% of CO2 transport
Process of bicarbonate in RBC (very fast process) CO2 + H2O (Hydrolysis) ->(*see Carbonic Anhydrase) H2CO3 (carbonic acid) -> H+ + HCO3- (ionized ions, H+ are buffered by Hb)
Carbonic Anhydrase = CA An enzyme (or catalyst) that greatly enhances the bicarbonate reaction in the RBC causing the RBC to saturate with HCO3- & the excess to diffuse into the plasma.
The HCO3- overflow into the plasma does what? Combines with Na+ to form NaHCO3 and transports HCO3- to the lungs via venous blood.
What happens to the Cl from the NaCl in the plasma that the Na left for the HCO3-? The Cl- movies into the RBC to maintain electric neutrality. Known as the Chloride Shift, or the Hamburger Phenomenon, or as an Anionic Shift to Equilibrium.
What happens secondary to the chloride shift? Some H2O moves into the RBC to preserve osmotic equilibrium causing the RBC to slightly swell in the venous blood.
Homeostasis balance ratio in the plasma 20:1 or HCO3- (20): HcCO3 (1) or Base (20): Acid (1)
pH & the plasma ratio 20:1 keeps pH level w/in normal 7.35 – 7.45 range. Ratio increase = >pH & blood is more alkaline. Ratio decrease =
What helps maintain the pH balance and the H+ and HCO3- ion concentrations in blood regulated? 1. Chemical buffer systems (the 1st line of defense), 2. respiratory system (lungs – regulates CO2), & 3. renal system (kidneys – regulates HCO3- or H+).
pH > 7.45 alkaline, alkalosis, or alkalemia
pH < 7.35 acid, acidosis, or acidemia
Buffer is what? A substance that will neutralize the acids and bases w/out changing the pH.
Strong acid does what? Dissociates completely and irreversibly in water, i.e. HCL -> H+ + Cl-.
Weak acid does what? Does NOT dissociate completely, i.e. H2CO3 -> H+ + HCO3.
Strong bases do what? Dissociates easily and quickly ties up H+, i.e. NaOH -> Na + OH.
Weak bases do what? Dissociate incompletely and reversibly and are slower to accept protons, i.e. NaHCO3- -> Na+ + HCO3-.
pH means what? The negative logarithm, to the base of 10, of the hydrogen ion concentration (H+) in moles per liter, or -log H+.
Electrolytes are what? Compounds, mainly sodium, potassium, magnesium, calcium, chloride, and bicarbonate, that dissociates in fluid into ions capable of conducting electrical currents and is a major force in controlling fluid balance w/ the body.
Chemical buffer system Responds w/in a fraction of a second to resist pH change. It is composed of 1. the carbonic acid-bicarbonate buffer system, 2. the phosphate buffer system, and 3. the protein buffer system.
How does the chemical buffer system work? It inactivates the H+ ions and frees HCO3- ions in response to acidosis. In response to alkalosis it generates more H+ ions and decreases the concentration of HCO3- ions.
Respiratory System It acts w/in 1 to 3 minutes.
How does the respiratory system work? By increasing or decreasing the breathing depth and rate to offset acidosis or alkalosis, i.e. acidosis = inc in depth and rate = body COC2 dec and pH inc, or, alkalosis = dec in depth and rate = body CO2 inc and pH dec.
Renal System Requires a day or more to correct abnormal pH concentrations. It is the body’s MOST effective acid-base balance monitor and regulator.
How does the renal system work? When extracellular fluids become acidic it retains HCO3- and excretes H+ ions into the urine causing blood pH to inc. When the fluids become alkaline the system retains H+ and excretes primarily HCO3- into the urine causing blood pH to dec.
Henderson-Hasselbalch (H-H)equation pH = pK + log[HCO3-]/[H2CO3] (base/acid)
H-H equation shows what? How the pH of a solution is influenced by the HCO3- TO H2CO3 ratio. Decrease in ratio (12:1) is a dec in pH. Increase in ration (33:1) is an inc in pH. They are directly related.
Values in H-H equation pH (norm is 7.4) = pK (6.1 is constant) + log[HCO3-] (norm is 24mEq/L)/[H2CO3] (norm is Pco2 x .03 = 40 x .03 = 1.2mEq/L)