Acid-Base Balance Flashcards
Acid Base Imbalances are named according to…
- Body system that is the primary cause of the disorder
- the resultant pH
*these are not diseases, they are conditions caused by a disorder of pathological processes
Lungs or CO2 problem?
Respiratory acidosis: elevation of PCO2 = ventilation depression
Respiratory alkalosis: depression of PCO2 = hyperventilation
Any other organ or HCO3- problem
Metabolic acidosis: depression of HCO3- or elevation of any noncarbonic acid
Metabolic alkalosis: elevation of HCO3- (usually caused by excessive lost of metabolic acids)
Normal Range of pH
7.35-7.45
Below 7.4 = acidosis
Above 7.4 = alkalosis
PaCO2
35-45
alkalemic –> acidic
the lower the CO2, the less acidic the blood will be
HCO3
22-26
acidic –> alkalemic
the lower the HCO3-, the more acidic blood will be
PaO2
80-100
usually not a concern unless it goes under 60, or COPD patients, or pt at high elevation
Metabolic Acidosis
Description and Cause
increased concentrations of noncarbonic acids OR loss of bicarb from ECF OR bicarb cannot be regenerated from kidney
may develop quickly: lactic acidosis from decreased perfusion
slowly: kidney failure, diabetic ketoacidosis, starvation
-diarrhea: GI HCO3- loss, loss of pancreatic juices
renal HCO3- loss: kidney failure
S/S of Metabolic Acidosis
if slow onset –> headache, lethargy, confusion, coma
deep and rapid breathing (Kussmaul respirations/hyperventilation)
Anorexia, nausea, vomiting, diarrhea, abdominal discomfort, cardiac dysrhythmias, decreased BP, death
Hyperkalemia and acidosis
High H+ concentration in blood –> H+ diffuses into ISF –> H+ enters cells and displaces K+ –> K+ diffuses into blood
Metabolic Acidosis
The compensation
Respiratory: reduce PaCO2 by breathing quickly and deeply
Metabolic Acidosis
Clinical Management
Address underlying disorder: improve perfusion, reverse hyperglycemia
Support compensation: observe for signs of fatigue, intubation may be necessary
Metabolic Alkalosis
Description and Potential Etiologies
excessive loss of metabolic acids OR increase in bicarb ion
Causes: Loss of H+ (vomiting, suction, renal loss) Gain of HCO3- Some diuretics Hyperaldosteronism
Metabolic Alkalosis
S/S?
varies w/ cause and severity
Leads to low ionized calcium levels –> excitable cells become HYPOpolarized –> easier generation of action potentials
-weakness, muscle cramps, hyperactive reflexes
-atrial tachycardia
irritablility, confusion, convulsions
-paresthesia
Respirations: may be shallow to RETAIN CO2
-HYPOkalemia
Metabolic Alkalosis
The compensation
Slowed ventilation = CO2 retained = increased PaCO2
Respiratory Acidosis
Description and Cause
alveolar hypoventilation = CO2 retention = PaCO2 increases
- suppression of medullary respiratory centers by drugs
- trauma (CVA)
- problems with breathing muscles
- thoracic deformaties
- lung problems
Respiratory Acidosis
S/S
slow, shallow, absent breathing
Respiratory Acidosis
The Compensation
increased H+ renal excretion
Increased generation of new HCO3-
Respiratory Acidosis
Clinical Management
increase ventilation
support compensation
do not try to remedy a high HCO3- level (if there is one)
Respiratory Alkalosis
Description and Cause
alveolar hyperventilation (deep, rapid breathing) = excess CO2 elimination = PaCO2 falls
Hypoxemia Hypermetabolic states latrogenic (over ventilation w/ chemical ventilator) Hypoxemia Trauma to medullary respiratory centers Anxiety, pain, hysteria
Respiratory Alkalosis
S/S
Dizziness,confusion, tingling of extremities
hyperventilating?
irritable?
cramps, tetany, Chovstek and trosseau sign
Respiratory Alkalosis
The compensation
increase H+ retention
(takes several days)
if chronic problem –> renal compensation lowers HCO3- to partially correct pH
Respiratory Alkalosis
Clinical Management
Address underlying disorder
reduce rate and or volume of ventilation, relieve anxiety, relieve pain
breathe in paper bag if anxiety attack
Concentration of H+ ions in blood
less than 0.0001 mEq/L
Changes of normal pH interferes with
changes shape and reduces function of hormones and enzymes
changes distribution of other electrolytes (causing fluid and electrolyte imbalances)
changes excitable membranes (making heart, nerves, GI tract and muscles more active than normal
decreases effectiveness of many drugs
changes in pH has PROFOUND effects on side chains of amino acids = all proteins are sensitive to pH
chemical buffer systems
Bicarbonate buffer system: most important system of ECF
Protein buffer system (ECF and ICF)
- hemoglobin
- amino acid buffers
- plasma protein buffers
Phosphate buffer system: ICF; buffers pH of ICF AND urine
physiological buffer systems
lungs, kidneys, bones
chemoreceptors of medulla oblongata
“central” chemoreceptors
monitor changes in pH (reflective of CO2 levels in blood)
chemoreceptors of carotid bodies
“peripheral” chemoreceptors
monitor pH, pCO2, and PO2
chemoreceptors of aortic arch
“peripheral” chemoreceptors
monitor pCO2 and PO2
The Carbonic Acid-Bicarbonate Buffer System and CO2 transport
70% of CO2 is transported as HCO3- in blood
- H+ stays inside RBC –> binds to hemoglobin (Hb)
- HCO3- diffuses in plasma to be used as a buffer
23% of CO2 stays in RBC and binds to Hb
7% of CO2 dissolves in plasma
When RBC’s reach alveoli
HCO3- returns to RBC –> reacts with H+ to form H2CO3 –> dissociates into Water and CO2 –> CO2 is exhaled
Renal Response to Acidosis w/ Ammonia
NH3 (ammonia) is formed in proximal convoluted tubule and secreted into tubular fluid
NH3 can serve as a buffer distally
H+ and secreted and bound to NH3 to be excreted in urine
Renal Response to Acidosis w/ Phosphate
H+ is secreted from Type A inctercallated cell of collecting duct
Secreted H+ combines with phosphate ion to be excreted in urine
Acid Elimination
respiratory elimination of CO2 (ventilation)
Urine
Gastric Suction/Emesis
Base elimination
Loss of intestinal/colonic fluid
Urine
