BMS 561 - Acid Base Imbalance

what does the conc of H+ affect

distribution of other ions, muscle contraction, cognition, activity of enzymes involved in atp prod

what is the function of kidneys in terms of acid base balance

eliminate H+ and bicarb

how does tissue perfusion affect acid base balance

prevents accumulation of acids and subsequent acid base imbalance, H+ alters the ability of hb to bind and transport o2

describe strong acids

dissociate greater than weak acids and release large amts of H+

volatile vs nonvolatile acids

volatile = eliminated by lungs
nonvolatile = nongas, eliminated mainly by kidneys

describe the strength of a base in terms of binding H+

stronger the base, greater the affinity for binding H+

what ph range is compatible with life

7.8 to 6.8

how is acid base balanced in the body

plasma buffers, resp, renal

describe chemical buffers

converts strong acids/bases to weak ones
reacts immediately to changes in pH
contains: bicarb buffer system, phosphate buffer system, intra and extra cellular proteins

how do you calculate the pH of a buffer system

henderson hasselbach equation

how is co2 eliminated via the resp system

co2 interacts with water → forms carbonic acid via carbonic anhydrase

how does the resp system monitor ph

in the brainstem through chemoreceptors
most sensitive to ph

how long does it take for resp compensation for metabolic alterations to begin?

within minutes but can take hours to reach max effectiveness
slight delay due to time for transport of altered blood to resp center and to initiate reflex

why does resp compensation for metabolic alterations never finish?

ph is not returned all the way back to normal because as the ph approaches normal, the stimulus that is driving the resp center diminishes and the compensatory effort stops

how long is resp compensation effective for

a few days
most forms of metabolic acidosis are acute

who is at a dec capacity for resp compensation?

those with lung disease or neuromuscular disease (MS/ALS)

describe renal regulation of acid base balance

regulates bicarb and nonvolatile acids
mechanisms: conservation of bicarb, secretion of H+ into urine/synthesis of new bicarb, excretion of H+ buffered by ammonia
less effective in presence of kidney disease

describe renal compensation during resp acidosis

-upregulate Na/H+ antiporter and H+-ATPase in PCT and collecting ducts = inc HCO3- (bicarb) reabs
- upregulate H+-ATPase and H+/K antiporter activity in DCT and collecting ducts = inc H secretion in urine
result: urine becomes more acidic and plasma bicarb rises

describe renal compensation during resp alkalosis

-downregulate Na/H+ antiporter and H+-ATPase = dec HCO3- (bicarb) reabs
result: more bicarb lost in urine

describe renal compensation during metabolic acidosis

-upregulation H+-ATPase and H+/K antiporter activity in DCT and collecting ducts = more H+ secreted in urine
-inc glutaminase activity in PCT = converts glutamine to ammonium and bicarb (NH4 is excreted and HCO3- enters bloodstream)
result: urine becomes more acidic and plasma bicarb rises

describe renal compensation during metabolic alkalosis

-downregulate H+-ATPase and H+/K antiporter activity in distal nephron = less H+ secreted in urine
-downregulate Na/H+ antiporter activity in PCT and collecting ducts = less bicarb reabs
result: urine becomes more alkaline

describe the process of conservation of bicarb ions

• co2 combines with water to form h2co3

• h2co3 is split, forming H+ and hco3-

• H+ is secreted into the filtrate

• for each H+ secreted a hco3- enters the peritubular capillary blood via symport with na or antiport with cl-

• secreted H+ combines with hco3- in filtrate and forms carbonic acid

• hco3- disappears from filtrate at the same rate as it enters the peritubular capillary blood

• h2co3 formed in filtrate dissociates to release co2 and water

• co2 diffuses into the tubule cell where it triggers more H+ secretion

describe the secretion of H+ in the urine and synthesis of new hco3-

• co2 combines with water to form h2co3

• h2co3 splits forming H+ and hco3-

• H+ is secreted into the filtrate by an H+-ATPase pump

• for each H+ secreted, a hco3- enters the peritubular capillary blood via an antiport carrier with Cl-

• secreted H+ combines with HPO4(2-) in tubular filtrate forming H2PO4-

• H2PO4 is excreted in urine

describe the process of excretion of H+ buffered by ammonia

• PCT cells metabolize glutamine to NH4+ and hco3- via glutaminase

• nh4+ is a weak acid and is secreted into the filtrate taking the place of H+ on a Na/H+ antiport carrier

• for each nh4+ secreted, a bicarb ion enters the peritubular capillary blood via symport carrier

• nh4+ is excreted in urine

what is the acid base mnemonic ROSE

R O = respiratory opposite
ph inc = pco2 dec = alkalosis
ph dec = pco2 inc = acidosis
M E = metabolic equal
ph inc = HCO3 inc = alkalosis
ph dec = HCO3 dec = acidosis

what are the effects of acidosis and alkalosis on neuromuscular function

acidosis:
- more H+ binds to proteins with fewer sites available for ca
- inc free ca = blocks na channels in nerves and muscles and causes muscle weakness
alkalosis:
- inc neuromuscular activity
- positive symptoms

what are the effects of acidosis and alkalosis on the CNS

due to changes in ph and cerebral blood flow
acidosis:
- vasodilation of cerebral blood vessels
- inc cerebral blood flow
- intracranial pressure
alkalosis:
- vasoconstriction of cerebral blood vessels
- dec blood and o2 delivery to brain

what are the effects of acidosis and alkalosis on contractility

acidosis: dec in cardiac contractility due to more extracellular ca
alkalosis: inc in contractility up to ph of 7.7 and dec in contractility with ph levels above 7.7

what are the effects of acidosis and alkalosis on ion levels

• metabolic acidosis caused by excess of inorganic acids: excess H+ enters cells and K exits cells = results in hyperkalemia

• metabolic acidosis caused by excess organic acids = H+ and anion move into cell

• resp and metabolic alkalosis = some H+ move out of cells and K moves into cells = results in hypokalemia

how does acidosis and alkalosis effect the oxygenation curve

acidosis: hb-o2 curve shifts to the right
alkalosis: hb-o2 curve shifts to the left

what is a normal ph range

7.35-7.45

what is a normal PaCO2 range

35-45

what is a normal PaO2 range

80-100 in adults and 60-70 in newborns

what is a normal HCO3- range

22-26

describe a base excess test

detects excess of base or deficit of base
positive number greater than 2 = metabolic alkalosis or renal compensation for resp acidosis
negative number less than 2 = metabolic acidosis or renal compensation for resp alkalosis

describe the lab test anion gap

detects inc amount of anions
calc by subtracting sum of ion Cl- and bicarb from conc of Na+ cation

what is a normal anion gap

8 plus or minus 4
albumin is not accounted for and why the gap is not closer to zero
albumin is normally 4 mg/dL
if a patients albumin level is abnormal their expected anion gap wont be accurate (cirrhosis)

what are the predominant unmeasured anions for 20-24 mEq/L

phosphate, sulfate, various negatively charged proteins and organic acids

what are the predominant unmeasured anions for 11-12 mEq/L

potassium, calcium, magnesium

what does a high anion gap indicate

usually metabolic acidosis, hyperalbuminemia and uremia, hypocalcemia or hypomagnesemia

what can cause a normal anion gap despite metabolic acidosis

resp compensation

if measured pco2 is higher than expected pco2, then what is occuring

resp acidosis
if theyre the same then resp compensation is occurring

what does a low anion gap indicate

hypoalbuminemia, hypercalcemia, hypermagnesemia, lithium toxicity, hypergammaglobulinemia

what are the characteristics of resp acidosis

elevated PaCO2 = hypercapnia
blood ph less than 7.3
ratio of bicarb to carbonic acid 20:1

what are the causes of resp acidosis

impaired elimination of CO2 by lungs = resp disease, cns dysfunction, ion imbalances, metabolic conditions

what are the clinical manifestations and treatement of resp acidosis

renal compensation = inc bicarb reabs, inc renal H+ excretion
- dec neuromuscular excitability
treatment: improve alveolar ventilation of eliminate co2

what are the characteristics of resp alkalosis

inc blood ph
dec pCO2 = hypocapnia
raio of bicarb to carbonic acid is greater than 20:1

what are the causes of resp alkalosis

hyperventilation, cns dysfunction, emotions, meds, mechanical vent

what are the clinical manifestations and treatments for resp alkalosis

renal compensation = dec bicarb reabs, dec H+ excretion
inc neuromuscular excitability and impaired cell oxygenation
treatment: restoration of ventilation to normal and reversal of underlying cause

what are the characteristics and causes of metabolic acidosis

dec blood ph, dec hco3-, normal PaCO2
causes: categorized according to effect of anion gap

what are the clinical manifestations and treatments for metabolic acidosis

inc rate and/or depth of breathing and dec neuromuscular excitability
treatment: reversal of underlying cause and sodium bicarb for life-threatening situations

what are the characteristics and causes for metabolic alkalosis

inc blood ph, inc HCO3-, normal PaCO2
causes: excessive loss of hydrogen ions (vomiting), excessive intake of base, excessive renal retention of bicarb

what is a patient with chronic diarrhea at risk for

metabolic acidosis due to losing bicarb

what are the clinical manifestations and treatments for metabolic alkalosis

dec rate and/or depth of breathing, inc neuromuscular excitability, impaired cell oxygenation
treatment: reversal of underlying cause and correction of any fluid, potassium, or cl deficits