acids and bases and ABG interpretation Flashcards Preview

Principles II > acids and bases and ABG interpretation > Flashcards

Flashcards in acids and bases and ABG interpretation Deck (77)
Loading flashcards...

how can mechanical ventilation alter the acid/base balance?

its effect on PCO2


how can blood loss effect acid/base balance?

potential to impact the pH buffering ability because of lost hemoglobin


what is homeostasis of acid base balance based on?

a balance between....
-intake and production of H+
-removal and elimination of H+


why is H+ concentration essential?

-it is essential for proper functioning of enzymatic reactions
-cell functions are altered when H+ changes
-requires more precision regulation compared to other ions since it is lower than other ions in the body
ex: Na+ over 3.5 million times greater than H+


what is an acid?

a molecule that releases H+ ion
-proton donators

HA - H+ + A-


what are some examples of acids?

-H2CO3 (Carbonic acid): dissociates to form H+ and HCO3- (bicarbonate ions)
-HCL (hydrochloric acid): dissociates to form H+ and Cl- (chloride ions)
-Phosphoric and sulfuric acids


what is considered the most important acid/base reaction in the body?

H2CO3 - H+ + HCO3-
-the dissociation of carbonic acid into H+ and bicarbonate ions or vice versa


what is a base?

molecule or ion that accepts H+ ion
-proton acceptor
-HCO3-, ammonia, and proteins are the body's bases

B + H+ - BH+


what are some examples of bases?

-HCO3- (bicarbonate ion): accepts/combines with H+ to form H2CO3 (carbonic acid)
-HPO4-: accepts/combines with H+ to form H2PO4-
-net negatively charged proteins (amino acids) also accept H+ (ex: Hgb)


what are the most important acid and base in the body?

carbonic acid and bicarbonate


what is the most important protein base?



describe strong acids and bases

acid: releases H+ rapidly and in large amounts
base: rapidly reacts with and quickly removes H+


describe weak acids and bases

acid: slow to dissociate and release H+
base: binds to H+ much slower and weaker bond


which type of acids and bases does acid base regulation involve?

weak acids and bases


what is the pH of solution related to ?

the ratio of the undissociated to the dissociated acid
-acidosis: ratio of HCO3- to CO2 decreases
-alkalosis: ratio of HCO3- to CO2 increases


how are pH and H+ concentration related?

inversely related


what determines the pH of the blood?

ratio of HCO3- to H2CO3 (or PCO2)
*PCO2 determines the amount of H2CO3 formed
*at a normal pH of 7.4 ratio of bicarb to carbonic acid is 20:1


what is seen with respiratory acidosis primarily?

increased PaCO2


what is seen with compensated respiratory acidosis?

increased PaCO2 and increased HCO3-


what is seen with respiratory alkalosis primarily?

decreased PaCO2


what is seen with compensated respiratory alkalosis?

decreased PaCO2 and decreased HCO3-


what is seen with metabolic acidosis primarily?

decreased HCO3-


what is seen with compensated metabolic acidosis?

decreased HCO3- and decreased PaCO2


what is seen with metabolic alkalosis primarily?

increased HCO3-


what is seen with compensated metabolic alkalosis?

increased HCO3- and increased PaCO2


what is normal arterial and venous blood pH?

arterial blood: 7.4
venous blood: 7.35


what is considered acidosis?

arterial pH less than 7.35


what is considered alkalosis:

arterial pH > 7.45


what pH range is compatible with life?

approx. 6.8-7.8


how does CO2 effect amount of H2CO3?

CO2 released from tissues combine with H2O via carbonic anhydrase to form H2CO3


what is the first H+ regulation mechanism to respond to acid/base imbalance?

buffering systems


describe buffering systems

-reversibly combine with acids or bases to prevent excess changes in H+
-reacts within seconds
-does not eliminate H+; keeps it bound up until balance can be re established


how do buffering systems work?

-buffers bind with free H+ to form a weak acid (H buffer)

Buffer + H+ HBuffer
-when H+ concentration increases the reaction is forced right and H+ binds to buffer
-when H+ concentration decreases the reaction is forced left and H+ releases from buffer (mass action)


describe the bicarbonate buffer system

*most powerful and most important extracellular buffer system in the body
-effective for metabolic acidosis (NOT respiratory)
-HCO3- changes very little in response to increased pCO2


describe the phosphate buffer system (HPO4-)

-strong acids such as HCl are buffered
ex: HCl + Na2HPO4 => NaH2PO4 + NaCl
-strong bases such as OH are buffered
ex: NaOH + NaH2PO4 => Na2HPO4 + H2O


describe the protein buffer system

-protein are anions (negative charge) that easily accept H+ proton
-most abundant intracellular buffers in the body
-hemoglobin is an effective buffer
ex: H+ + Hgb HHgb


what is the second H+ regulation mechanism for acid/base balance?

*reacts within minutes


how do the lungs help balance acid/base?

-regulates removal of CO2 which effectively eliminates H2CO3
-regulate pCO2
-chemoreceptors in the brainstem respond to CO2 "indirectly" but "directly" to H+ after CO2 crosses the BBB and chemical reaction occurs that liberates H+


how do central chemoreceptors assist the lungs in acid/base regulation?

respond to changes in the H+ concentration of CSF
-increased H+ (decreased pH) = increased ventilation
-decreased H+ (increased pH) = decreased ventilation
*although the BBB is impermeable to H+, CO2 easily diffuses across and liberates H+ ions from another ion that stimulates the receptors


how does CO2 lead to acidosis?

-aerobic cellular respiration process produces CO2 and H2O
ex: C6H12O6 + 6O2 => 6CO2 + 6H2O + 36 or 38 ATP
-CO2 reacts with H2O through carbonic anhydrase to form H2CO3
ex: CO2 + H2O H2CO3
-H2CO3 then easily donates H+ through carbonic anhydrase, leaving HCO3-
ex: H2CO3 H+ + HCO3-
*carbonic anhydrase inhibitors (diuretics) cause metabolic acidosis


where is carbonic anhydrase found?



what is the 3rd H+ regulation mechanism?

kidneys: eliminate acids and bases from the body
*last compensatory mechanism to respond
*reacts in hours and days (slowest)


describe the renal acid/base regulatory system

-kidneys regulate HCO3-
-most effective regulatory system for controlling H+ (since its actually eliminating rather than shifting)
-regulate extracellular fluid H+ using three mechanisms:
1) secretion of H+
2) reabsorption of filtered HCO3-
3) production of new HCO3-


describe renal secretion of H+ to balance acid/base

-usually a 1:1 ratio; for every H+ secreted an HCO3- enters the blood; approx. 4320 meq HCO3- filtered and 4320 meq of H+ secreted daily
-if a greater amount of one is lost then the blood becomes more acid or alkaline
-both excretion of H+ and the reabsorption of HCO3- are controlled by the H+ secretion process
-filtered HCO3- must react with H+ to form H2CO3 before it can be reabsorbed
*when H+ concentration is low, the kidneys cant reabsorb all of the filtered HCO3- which results in increased secretion of HCO3- (lost in urine), balancing the decrease in H+


describe renal production of new HCO3-

1)secreted H+ combines with phosphate and ammonia buffers to yield new HCO3-
*ammonia is the more important, most used system
2)glutamine, formed by amino acid metabolism, is changed to ammonium (NH4-) by renal tubular cells
* 1 glutamine form 2 NH4- and 2 HCO3-
**NH4- excreted in urine and the HCO3- is reabsorbed into the blood as new HCO3-


describe renal correction of acidosis

-increased H+ stimulates glutamine metabolism, resulting in increased production of NH4-
-NH4- causes increased secretion of H+ and addition of new HCO3-
*excess H+ is eliminated through urine
*newly produced HCO3- enters the blood
**most effective, but slowest, way to correct acidosis


describe renal correction of alkalosis

-ratio of HCO3- to CO2 (H+) increases (more HCO3-)
-HCO3- cant be reabsorbed (needs to be bound with H+)d/t the decrease secreted H+
-this process results in an overall decrease in plasma HCO3- and correction of alkalosis


what factors may increase H+ secretion and HCO3- reabsorption?

-increased PCO2
-increased H+ w/ decreased HCO3-
-decreased extracellular fluid volume
-increased angiotensin II
-increased aldosterone


what factors may decrease H+ secretion and HCO3- reabsorption

-decreased PCO2
-decreased H+ w/ increased HCO3-
-increased extracellular fluid
-decreased angiotensin II
-decreased aldosterone


what is the anion gap?

gap b/w anions and cations from a practical medical evaluation standpoint in which only certain cations and anions are measured (so looks like a gap)
*no "true" plasma anion gap
*concentration of anions and cations must be equal to maintain neutrality electrically


what is the normal plasma anion gap range?

7-14 mEq/L
= [Na+] - [HCO3-] - [Cl-]
= 144 - 24 - 108
=12 mEq/L


what cations and anions are measured?



what is the diagnostic purpose of anion gap?

-differentiating causes of metabolic acidosis
-movement of HCO3- or other anions up or down causes a compensatory up or down movement of Cl-
*hyperchloremic metabolic acidosis (normal anion gap metabolic acidosis): if decreased in HCO3- and Na+ is unchanged, then Cl- must increase to maintain electric neutrality


what are causes of metabolic acidosis associated with an increased anion gap (normal Cl-)?

-DM (ketoacidosis)
-lactic acidosis
-chronic renal failure
-aspirin (salicylate acid) poisoning
-methanol poisoning
-ethylene glycol poisoning


what are causes of metabolic acidosis associated with a normal anion gap (hyperchloremia)?

-increased GI loss (diarrhea, ingestion of CaCl2, MgCl2, fistulas)
-renal tubular acidosis
-carbonic anhydrase inhibitor
-Addison's disease (hyperaldosteronism)
-increased intake of chloride containing acids (ammonium chloride, lysine hydrochloride, arginine hydrochloride)
-TPN (Cl- salts of amino acids)
-dilutional (large amount of bicarb free fluids, i.e. NS)


what are physiological effects of alkalosis?

-increased affinity of hemoglobin for O2: harder for hgb to release form O2 to tissues; Oxyhgb curve shifts left
-plasma proteins have increased affinity for ionized Ca++ causing increased binding: hypocalcemia, CV/circulatory depression and collapse; NM irritability (tetany; laryngospasm?)
*H+ moves out of the cell while K+ moves into the cell, resulting in HYPOkalemia


what are side effects seen d/t alkalosis?

-CNS: decreased CBF, seizures, lethargy, delirium, tetany
-CV: arteriolar vasoconstriction, decreased coronary blood flow, decreased threshold for angina, predisposition to refractory dysrhythmias
-Resp: hypoventilation, hypercarbia, arterial hypoxemia
-metabolism: hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, stimulation of anaerobic glycolysis


describe respiratory alkalosis

-decrease in pCO2, which decreases H+
-d/t increased alveolar ventilation: CO2 eliminated more rapidly than produced
-tx: correct the cause of increased ventilation; during GA, reduce Vt and RR or if spontaneously breathing, give fentanyl or something to calm down


what are common causes of respiratory alkalosis?

-central: pain, anxiety, ischemia, stroke, tumor, infection, fever, drug-induced (salicylates, progesterone [pregnancy], analeptics [doxapram])
-peripheral: hypoxemia, high altitude, pulmonary disease (CHF, noncardiogenic pulmonary edema, asthma, PE), severe anemia
-metabolic encephalopathies


describe metabolic alkalosis

-excess HCO3- or loss of H+
-less common than metabolic acidosis
-causes: HCl loss; Na+ reabsorption and HCO3- secretion
-sx: hypokalemia (alkalosis causes K+ to shift intracellular)
-tx: PPIs (keep acid out of GI tract); K+ sparing diuretics (increases excretion of HCO3-


what are common causes of metabolic alkalosis?

-GI: vomiting, NG suction, choride diarrhea
-renal: diuretics, posthypercpanic, low Cl- intake
-sweat: cystic fibrosis
-increased mineralocorticoid activity: hyperaldosteronism, cushing's syndrome, licorice ingestion, bartter's syndrome
-severe hypokalemia
-massive blood transfusion
-acetate-containing colloid solutions
-alkaline administration w/ renal insufficiency (antacids)
-sodium PCNs
-glucose feeding after starvation


what are physiological effects of acidosis?

-decreased affinity of hgb for O2: easier for hgb to release O2 to the tissue
-sympathoadrenal activation
-CNS depression/lethargy: CO2 narcosis (CO2, not H+, penetrates BBB)
-cardiac and vascular smooth muscle less responsive to catecholamines
-H+ moves into cell while K+ move out of cell, resulting in Hyperkalemia
*K+ increases 0.6 mEq for every 0.1 decrease in pH


what are side effects seen with acidosis?

-CNS: obtundation, coma
-CV: impaired myocardial contractility, decreased CO, decreased arterial BP, sensitization to reentrant dysrhythmias, decreased threshold for V fib, decreased responsiveness to catecholamines
-Resp: hyperventilation, dyspnea, fatigue of resp. muscles
-metabolism: hyperkalemia, insulin resistance, inhibition of anaerobic glycolysis


describe respiratory acidosis

-increase in PCO2, which increases H+
-d/t decreased alveolar ventilation (worse when renal function poor)
-tx: normalize alveolar ventilation
*correct chronic CO2 SLOWLY to allow renal elimination of HCO3- (correcting too fast can lower CO2 faster than kidneys can excrete excess compensatory HCO3- and cause metabolic alkalotic state)
*correct chronic CO2 retainers back to their baseline (correcting to normal value results in respiratory alkalosis)


what are common causes of respiratory acidosis?

-CNS depression: drug-induced, sleep disorders, OHS, cerebral ischemia, cerebral trauma
-NM disorders: myopathies, neuropathies
-chest wall abnormalities: flail chest, kyphoscoliosis
-pleural abnormalities: pneumothorax, pleural effusion
-airway obstruction: upper (foreign body, tumor, laryngospasm, sleep disorders), lower (severe asthma, COPD, tumor)
-parenchymal lung disease: pulmonary edema, PE, pneumonia, aspiration, interstitial lung disease
-ventilator malfunction
*increased CO2 production
-large caloric loads
-malignant hyperthermia
-intensive shivering
-prolonged seizure activity
-thyroid storm
-extensive thermal injury (burns)


describe metabolic acidosis

-acidosis not caused by excess CO2
-d/t renal failure, excess production of acids, ingestion of acids, loss of HCO3- (diarrhea, intestinal vomiting), DM
-tx: correct the cause; if chronic conditions (resp. or renal failure) then neutralize acid (Bacitra, oxidizes to NaHCO3-)


what are common causes of metabolic acidosis?

*increased anion gap
-increased production of nonvolatile acids: renal failure, ketoacidosis (DM and starvation), lactic acidosis, alcoholic, inborn errors of metabolism
-ingestion of toxin: salicylate, methanol, ethylene glycol, paraldehyde, toluene, sulfur
*normal anion gap (hyperchloremic)
-increased GI losses of HCO3-: diarrhea, anion exchange resins (cholestyramine), ingestion of CaCl2 & MgCl2, fistulas (pancreatic, biliary, or small bowel), ureterosigmoidostomy or obstructed ileal loop
-increased renal losses of HCO3-: renal tubular acidosis, carbonic anhydrase inhibitors, hypoaldosteronism
-dilutional: large amount of bicarb free fluids, i.e. NS
-TPN: Cl- salts of amino acids
-increased intake of chloride-containing acids: ammonia chloride, lysine hydrochloride, arginine hydrochloride


how does acidosis effect K+ and Ca++?

-increased K+: H+ shifts into cell and K+ out of cell; increased excitation and depolarization; high T waves
*high serum K+ moves resting membrane potential higher which depolarizes
-increased Ca++: albumin less bound to Ca++ and releases easier causing an increase; depressed sensation of nerves, NM junctions, and reflexes; hypotonia
*raises the threshold potential moving it further from resting potential


how does alkalosis affect K+ and Ca++?

-decreased K+: H+ shifts out of cell and K+ moves in; muscular weakness, cramps, PVCs, U wave, flat T wave
*low K+ moves resting potential lower which hyperpolarizes
-decreased Ca++: albumin get more negatively charged in alkalosis; more ionized Ca++ to bind to albumin causing a drop; oversensitization of nerves and NM junction causing spasm
*lowers threshold potential closer to resting potential


what are normal ABG values?

-pH: 7.35-7.45
-pCO2: 35-45 mmHg
-pO2: 80-100 mmHg
-HCO3-: 22-26 mEq/L
-BE: 0 + or - 2 mEq/L
-SaO2: > 97%


what are the steps to ABG interpretation?

1) arterial pH: acidosis, alkalosis, normal
2) arterial pCO2: does it explain the pH?
3) arterial HCO3-: does it explain the pH?
4) any compensation: did non-contributing factor react and correct the pH?


how does temperature affect ABG measurement?

-affects pO2, pCO2, and pH, NOT HCO3-
-pO2 and pCO2 (gas tensions) decrease with hypothermia bc it lowers the partial pressure of gas in solution (total CO2 content unchanged, but partial pressure decreased)
*gas solubility indirectly proportional to temperature (gas solubility increases as temperature decreases)
-pH increases with hypothermia (pCO2 decreases but HCO3- unchanged)


describe ABG temperature correction

-uncorrected: regardless of temp, ABGs are typically warmed to 37 degrees for measurement (alpha stat management) when the patient is hypothermic
-corrected: table or program estimates what gas tension and pH would be at patient's actual temperature (pH stat management) when the pt. is hypothermic
*goal: practitioner to maintain pCO2 40 mmHg, pH 7.4 when patient is hypothermic


why is temperature correction important?

-pt. having CABG on CPB pump temp 25 degrees C
-uncorrected (alpha stat): pCO2 40, pH 7.40 at 37 C
-corrected (pH stat): pCO2 23, pH 7.60
*cerebral vasoconstriction reduces CBF; decreased K+, coronary vasospasm, increased SVR may occur
*perfusionist adds CO to oxygenator on CPB pump
-evidence shows that alpha stat preserves CBF autoregulation
*no appreciable differences in outcomes except in children b/w the two strategies


describe ABG use in determining A-a gradient

PAO2 - PaO2
-ABGs provide a PaO2: can determine V/Q mismatch, shunt, blood-gas barrier such as pulmonary edema, CHF, ARDS, atelectasis
-normal youth adult on room air = 5-10 mmHg
-increases 1 mmHg for every decade lived


what is base excess?

-amount of excess or insufficient level of bicarb
-positive number = metabolic alkalosis
-negative number = metabolic acidosis


describe mixed acid/base disorders

-mixed acid base disorders characterized by abnormal compensatory response
-two or more causes of acid/base imbalance
ex: pH low = acidosis, both pCO2 increased and HCO3- decreased (metabolic and respiratory component = mixed acidosis)
*diarrhea induced HCO3- loss in pt. with COPD