acids and bases and ABG interpretation 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?
hemoglobin
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?
Lungs
*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?
- lungs
- RBCs
- kidney
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
- hypokalemia
what factors may decrease H+ secretion and HCO3- reabsorption
- decreased PCO2
- decreased H+ w/ increased HCO3-
- increased extracellular fluid
- decreased angiotensin II
- decreased aldosterone
- hyperkalemia
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?
HCO3-
Na+
Cl-
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
- starvation
- rhabdomyolysis
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
- sepsis
- metabolic encephalopathies
- ventilator-induced
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)
- hyperkalemia
- 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?
- hypoventilation
- 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
- rhabdomyolosis
- 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
