ACID BASE BALANCEPRESENTED BY

RAKHI S NAIR

INTRODUCTION

• PH denotes strength of hydrogen ions in solution

• Acid solution has more hydrogen ions than bicarbonate and hydroxyl ions.

• Basic solution has more bicarbonate ions or hydroxyl ions than hydrogen ions

Acids

• Act as electrolyte in water• Reacts with bases to form water and salt• High con;destroys body tissueCommon acids• Hcl-secreted by parietal cells of stomach converts

pepsinogen to pepsin (protein digesting enzyme of gastric juice)

• Carbonic acid-one form in which co2 transported in blood,part of bicarbonate buffer system ?(imptbuffer regulating body fluids)

• Acetic acid • Lactic acid

Acid base balance

• Stable hydrogen ion concentration in ecf(interstitial and intravascular compartments)fluid in narrow range bt 7.35-7.45

• Ph 7/less or ph of 7.8 can result in death

• State of uncompensated acidosis if bd ph decrease below 7.35

• Uncompensated alkalosis if ph above 7.45

Bases

• Contains no hydrogen ions acceptors

• Accept h+ from acids to neutralize acid

Common bases

• Magnesium hydroxide-milk of magnesia,antacid,mild laxative

• Aluminium hydroxide-cmpnt of antacids

• Ammonium hydroxide-house hold cleaners

Salt

• Compund formed when acid neutralized by base

• Crystalline in nature

• Salty taste

• Eg:

• Nacl

• Kcl

• Mag.sulphate.

Mechanism that maintains acid base

balance Buffers first line of defense (taken seconds)Primary buffer system in extracellular fluid• Hemoglobin system• Plasma protein system• Carbonic acid/bicarbonate system• Phosphate buffer systemSecond line of defense (taken minutes)lungs

Third line of defense(taken hours- days)kidneys Potassium

Hemoglobin system

• In the rbc

• Maiantain AB balance by chloride shift

• Chloride shift based on response to level of oxygen

• Each chloride leaves rbc 1 bicarbonate enters

• Each bicarbonate enters rbc chloride leaves

Plasma protein system

• Functions in conjunction with liver to vary amount of h+ in chemical structure of protein

• Pp has ability to attract /release h + ions

Carbonic acid/bicarbonate system

• Most impt buffer in body fluids

• Itz components base bicarbonate hco3- and carbonic acid h2co3 are actively and constantly regulated by action of respiratory and urinary system

• When body is in a state of ab balance ,blood contains 27 meq base bicarbonate /L and 1.35 meq carbonic acid /L

• Base bicarbonate ratio will be 20:1

Phosphate buffer system

• More important in intracellular fluids

• Especially active in kidneys

• Acts like bicarbonate and clears spare h+

Lungs –second line of defense

• Co2 is carried in d body in the form of carbonic acid and bicarbonate.

• Controls rate of co2 exhalation from lungs.• Whn increased co2 in body medulla stimulated to

increase rate and depth of respiration • Whn decreased co2 rate and depth of respiration

decrease.• During body metabolism co2 produced which reacts with

water and form carbonic acid ,resulting in decrease in ph • In lungs carbonic acid breaks down to co2 and h20 • Increased exhalation of co2 results in inc.ph (as acidity

decreases ph increases.

• Process of correcting a deficit takes 10-30 sec

• Lungs are capable of inactivating only h+ carried by h2co3 ,excess h+ created by other problems must be excreted by kidney.

Third line of defense (hrs to dayz )

kidneys• Ultimate correction of acid base disturbances is

dependent on kidneys.-even though renal excretnoccurs slowly

• Itz more thorough and selective than any other regulators

• In acidosis –ph goes down and excess h+ ions are secreted to tubules and combine with buffers for excretion in urine

• Alkalosis-ph goes up bicarbonate ions moves into tubules combine with sodium and excreted in urine

• Form ammonia and that combines with hydrogen ions and forms ammonium ions and excreted in urine in exchange for sodium ions which are reabsorbed into blood.

• When low level of h+ in body kidney retain hydrogen ion to form bicarbonate

Potassium

• Plays exchange role in maintaining ab balance• Body changes k level by drawing h+ into cell or

pushing them out to cell• K level changes to compensate hydrogen ions

changes• Acidosis-body protects from acid by moving h + into

cells and therefore k moves out to make room for h+,the serum k level goes up.

• Alkalosis-cells release h+ into blood in an attempt to increase acidity of blood and combat alkalinity .k moves into cells and serum k level goes down .

Normal blood gas values

• Ph- 7.35-7.45

• Pco2-35-45 mmhg

• HCO3-22-27 meq/L

• P02-80-100mmhg

Acid base imbalance

• Respiratory acidosis

• Metabolic acidosis

• Respiratory alkalosis

• Metabolic alkalosis

Respiratory acidosis

• Total conc:of buffer base lower than normal,withrelative increase H + con: thus greater no:of H+ in circulating blood than can be absorbed by buffer system.

• Ph BELOW 7.35

• PCO2 > 45MMHG

Cause –resp acidosis

• Due to primary defect in function of lungs/changes in normal resp.pattern

• Any condition that causes an obstruction of airway/depress resp.status can cause resp.acidosis.

• Hpoventilation-co2 retained h+ inc.acid state carbonic acid retained and ph goes down

• Medications-sedatives,narcotics,anestheticsdepress resp centre-leading to hypoventilation .co2 retained and H+ increases.

• Bronchitis

• Atelectasis

• Brain trauma

• Emphysema

• Asthma

• Pulmonary edema

• bronchiectasis

Clinical manifestations

• Rr and depth inc:• Head ache• Restlessness• Mental status changes –drowsiness and confusion • Visual disturbances• Diaphoresis• Cyanosis• Hyperkalemia• Rapid irregular pulse• Dysrhythmias leading to ventricular fibrillation

Management

• Administe o2• Semifowlers position unless contraindicated• Assist to turn,cough and deep breathe• Encourage hydration • Suction if needed• Reduce restlessness by improving ventilation

than by administering tranquillizers,sedatives or narciotics.

• Monitor electrolyte esp.k• Administer anti biotics if infection

Respiratory alkalosis

• Carbonic acid deficit hyperventilation blows off excessive co2

• Pco2 <35 mmhg

• A deficit of h2co3 and decrease in H+ con results from accumulation of base or from loss of acid with out comparable loss of base in body fluids.

Causes of resp ;alkalosis

• Due to conditions that cause overstimulation of respstatus

• Hyperventilation r/t anxiety /panic• Hysteria • Excessive mecahnical ventilation • Cond.inc metabolism-fever• Pain/brain trauma-causes overstimulation of

res.cntre in brain stem with resultant carbonic acid deficit

• Salicylates• Hypoxia

Clinical manifestations

• Initially hyperventilation and resp stimulation cause abnormal rapid respiration (tachypnea) in an attempt to compensate rr and depth then go down

• Head ache• Light headed ness• Vertigo• Mental status changes• Paresthesias such as tingling of fingers and toes• Hypokalemia ,hypocalcemia• Tetany• Convulsion

Management

• Emotional support• Reassurance• App.breathing patterns• Assist with breathing techniques• Voluntary holding of breath• Rebreathe exhaled co2• Rebreathing mask• Co2 breaths• Caution to ventilator clients –not forced to take

breath deeply or rapidly• Monitor elctrolyte value esp k and ca • Prepare to administer calcium gluconate

Metabolic acidosis

• Total con:of buffer base lower than normal with relative increase in H+ con:occurs as a result of loosing too many bases and holding too much acids with out sufficient bases.

• Base bicarbonate deficit; excess acid other than carbonic acid(a respiratory acid) accumulates beyond bodys ability to neutralize it

• Bicarb below 22 meq/l

• Ph below 7.35

Causes

• Diabetes mellitus/dka-insufficient supply of insulin causes increased fat metabolism leading excess acc.of ketones or other acids;bicarbonatethen ends up being exhausted .

• Renal insufficiency/failure

Inc.waste products of protein metabolism are retained

Excessive acid builds up and bicarbonates unable to maintain acid-base balance

• Insufficient metabolism of carbohydrate-whninsufficient supply of 02 is available for proper burning of carbohydrate,glucose and water lactic acid inc and lactic acidosis results.(anaerobic metabolism)

• Excessive ingestion of asa –increae H+ con

• Severe diarrhoea –intestinal or pancreatic secretions are normally alkaline so excessive loss of base leads to acidosis.

• Malnutrition –improper metabolism of nutrients cause fat catab olism leads to excess build up of ketones and acids.

• High fat diet-cuses too rapid accumulation of waste products of fat metabolism leading build up of ketones and acids.

Clinical manifestations

• Weakness

• Headache

• Cns depression-mental dullness,drowsinessstupor ,coma,Disorientation

• Deep and rapid breathing(kussmaul’s resp)

(in an attempt to blow off excess co2 and compensate for acidosis hypercapnea wit kr)

Nvd

Fruity smelling breath –improper fat metabolism

• Twitching

• Convulsions

• Hyperkalemia

Management

• Assess loc for cns depression

• Monitor I/O and assist with fluid and electrolyte replacement

• Iv ns,5 dextrose&1/2 ns,sodium lactate or bicarbonate to inc.buffer base.

• Safety and seizure precautions

• K monitr-whn acidosis terated k move back into cell and k serum level drop

Mgmnt in DKA

• Insulin given to hasten mvmt of serum glucose to cell and dec.concurrent ketosis

• When glucose being properly metabolized body stop converting fats to glucose

• Monitr circulatry collapse caused by polyurea-which result frm hyperglycemic state because polyurea or diuresis may lead to extracellular volume deficit.

Mgmnt in renal failure

• Dialysis-removing protein waste

• Low protein diet to dec protein waste products from protein catabolism

Metabolic alkalosis

• A deficit of h2co3 and dec.in hydrogen ion con results frm accu.of base /loss of acid with out comparable loss of base in body fluids.

• Base bicarb excess more than 26meq/l

• Ph above 7.45

Causes

• Loss of gastric juices(vomiting,ngdecompression,lavage)

• Excessive ingestion of alkaline drugs(sodium bicarbonate)

• Diuretics-loss of h+ and chloride causes inc in bicarb in blood

• (potent diuretics precipitate hypokalemia ,in the presence of hypokalemia kidneys conserve potassium and excrete hydrogen ,intracellular k moves into interstitial compt and hydrogen moves into cells as a result ,plasma hydrogen dec and base bicarb inc.)

• Hyperaldosteronism-inc renal tubular reabsorbtn of sodium occurs with loss of h+ ions

• Massive transfusion of whole blood-the citrate anticoagulant used for storage of blood is metabolized to bicarbonate .

Clinical manifestations

• In an attempt to compensate rr and depth go down to conserve co2

• Nvd

• Restlessness

• Numbness and tingling in extremities

• Twitching in extremities

• Hypokalemia

• Hypocalcemia

• Dysrhythmia,tachycardia

Management

• Monitr k and ca

• Safety precautions

• Adminster medications to promote kidney excretion of bicarbonate

• Prepare to replace kcl as prescibed

Arterial blood gases-gettng abg

specimen • Obtain vs

• Determine clt has arterial line

• Perform allen test

• Asssess factors that affect accuracy of result such as change in o2 settings,suctioning within last 20 minutes and clt activities

• Provide emotional support

• Assist with specimen draw by preparing a heparinized syringe

• Apply pressure to puncture site 5-10 min if clttaking anticoagulants

• Label specimen –transport it on ice to lab

• Lab form record clts temp and type of supplmntal o2 receiving