Exam 3 Flashcards
Average range for blood gases pH, PaO2 and PaCO2
pH 7.35 - 7.45
PaO2 80 - 100 mmHg
PaCO2 35-45 mmHg
Average range for blood gases, O2 saturation, Bicarbonate, total CO2, and base excess
O2 saturation >95%
Bicarbonate 22 - 26 mmol/L
Total CO2 23 - 27 mmol/L
Base excess -2 to +2 mmol/L
What does PaCO2 and pH tell us?
Acid/base status
What does PaO2 tell us?
oxygenation status
Hydrogen range in blood
38 - 42 nmol/L
Hydrogen survivable range
16 - 160 nmol/L
What is an acid?
A substance that can yield a hydrogen ion or hydronium ion when dissolved in water
What is a base?
A substance that can yirl hydroxyl ions or that can accept a proton
Dissociation constant
K, the relative strengths of acids and bases
pK
the negative log of the dissociation constant
buffer
combination of a weak acid or weak base and its salt is a system that resists changes in pH
pH equation
pH = -log[H+]
pH of draino
14
pH of battery acid
0
Normal blood pH
7.4
Gastric fluid pH
1.5
Buffer equation
HA = H+ + A-
HA is conjugate acid
A- is conjugate base
Henderson-Hasselbach equation
pH = pK + log [base]/[acid]
When pH = pK
[base] = [acid]
Dissociation constant equation
[H=] = Ka [HA]/[A-]
Body’s buffers
bicarbonate, proteins, phosphates, bone
Bicarbonate-carbonic system
CO2 + H2O = H2CO3 = H+ + HCO3-
Acid/Base balance in plasma
small amounts of Co2 remain as dissolved CO2 or combine with proteins to form carbamino compounds, most of the CO2 reacts with H2O to form H2CO3 which dissociates
CO2 in tissues
enters the RBC and reacts with H2O to form carbonic acid
Dissociation of H2CO3
causes the HCO3- concentration to increase in the RBCs and diffuse into plasma, followed by chloride diffuses into the RBCs to maintain neutrality
H+ and HbO2
react and form HHb and release O2 into plasma and tissues
Acid/Base regulation by lungs
H= carried on reduced hemoglobin in venous and released to react wit HCO3- to form H2CO3, which converts to H2O and CO2, CO2 diffuses into alveoli and exhaled
If CO2 is not exhaled at rate of production
CO2 accumulates in blood, increasing H+ concentration
If CO2 is exhaled too fast
H+ concentration decreases
Acid/Base regulation by kidneys
HCO3- is reabsorbed in proximal tubules, exchange of Na+ for H+ in the tubular cell, combining H+ with HCO3 in filtrate to form H2CO3, converted to H2O and CO2. CO2 diffuses into tubule and reacts with H2O to form H2CO3 and then HCO3 which is reabsorbed.
Diuretics
favor excretion of HCO3-
Bicarbonate equation
Bicarbonate = total CO2 - 0.03 x PaCO2
Henderson-Hasselbach for bicarbonate system
pH = 6.1 + log [HCO3-]/[0.03 x PaCO2]
respiratory acidosis
Increases PaCO2, so bicarbonate is increased as compensation
Respiratory alkalosis
Decreases PaCO2, so bicarbonate is decreased as compensation
Metabolic acidosis
decreases bicarbonate, so PaCO2 is increased as compensation
Metabolic alkalosis
increased bicarbonate, so PaCO2 is increased as compensation
Respiratory acidosis causes
decreased central drive, pulmonary issues
Respiratory alkalosis causes
sepsis, liver disease, salicylate intoxication, anxiety, high altitudes
Metabolic acidosis causes
GI loss of bicarbonate, metabolic derangements, exogenous intoxicants, renal disease
Lactic acidosis causes
circulatory failure, acute hypoxemia, carbon monoxide, malignancies, liver disease
Ketoacidosis causes
increased lipolysis and FA as seen in diabetes, starvation and alcoholism
renal failure
Decreased ammonium ion excretion due to renal tubular drop out
Type 1 renal tubular acidosis
Distal tubule
Type 2 renal tubular acidosis
Proximal tubule
Type 4 renal tubular acidosis
reduced aldosterone secretion
Metabolic alkalosis causes
loss of gastric fluid, diuretics, hypokalemia, aldosterone excess, volume depletion
Air at sea level
pressure: 760 mmHg
N2: 79%
O2: 21%
CO2: 0%
CO: 0%
Oxygen range for 2 day old to 60 year old
83 - 108 mmHg
> 90 year old oxygen range
> 50 mmHg
Oxygen saturation for adults
94 - 98%
Hypoxia
low oxygen in tissues
Hypoxemia
low pressure of oxygen in blood
O2 diffusion gradient
PaO2 - PaO2 <= 10 mmHg
Alveolar arterial diffusion gradient
Aa = (BP-pH2O) x FiO2 - (1.25 x PaCO2) - PaO2
What is needed for adequate tissue oxygenation?
available atmospheric oxygen, adequate ventilation, gas exchange between the lungs and arterial blood, loading of O2 onto hemoglobin, adequate hemoglobin, adequate transport, release of O2 to the tissues
Factors influencing the PO2 in the alveoli
% of O2 concentration inspired, the amount of PCO2 in the expired air, ratio of the volume of inspired air to the volume of the dead space air
Factor affecting the amount of O2 that reach the tissues
Destructi9on of alveoli, pulmonary edema, airway blockage, inadequate blood supply
O2 in arteria blood
transported to tissues by hemoglobin
Amount of O2 loaded onto hemoglobin
depends on availability of O2, concentration and types of hemoglobin, presence of CO, pH and T, and levels of PCO2 and 2,3-DPG
100% saturated hemoglobin
increase in O2 to the alveoli serves only to increase the concentration of dissolved O2 in arterial blood, may cause O2 toxicity and decreased ventilation and increased PCO2
HHb
reduced hemoglobin
O2Hb
oxygenated hemoglobin
COHb
carboxyhemoglobin
MetHb
methemoglobin
SulfHb
sulfhemoglobin
Oxygen saturation equation
SO2 = cO2Hb/(cO2Hb + cHHb) x 100%
Fractional or % oxyhemoglobin
FO2Hb = cO2Hb/(cO2Hb + cHHb + dysHb)
dysHb
COHb, MetHb, SulfHb, etc
Right shift
Causes increased CO2, increased temp, increased [H+], and increased 2,3-DPG
Left shift
Causes decreased CO2, decreased temp, decreased [H+], and decreased 2,3-DPG
Carbon Dioxide normal range
35 - 45 mmHg
Hypercapnea
High level of CO2
Hypocapnea
low level of CO2
Carbon monoxide normal ranges
Normal: <0.5%
Smokers: <6%
10% CO
shortness of breath
40-50% CO
headache, confusion, fainting
> 80% CO
rapidly fatal
Methemoglobin normal range
< 1.5%
1.5% to <20% methemoglobin
cyanosis
20 - 50% methemoglobin
weakness, fainting
> 70% methemoglobin
lethal
Na+
Major cation of extracellular fluid with serum concentration of 136-145 mmol/L, gradient across membrane maintained by ATPase pumps
Regulation of Na+
Intake of water in response to thirst, stimulated by high serum osmolality, excretion of water affected by ADH level
Hyponatremia
Serum Na+ < 130 meq/L
Isotonic hyponatremia
Serum Na+ <130 meq and normal osmolality
Hypotonic hyponatremia
serum Na+ <130 meq/L and osmolality < 280 mosm/kg
Hypertonic hyponatremia
Serum Na+ < 130 meq/L and osmolality > 295 mosm/kg
Hypernatremia
Excess water loss accompanied by impaired thirst mechanism, sodium excess greater than water
K+
Major intracellular cation, regulates neuromuscular excitability, contraction of skeletal and cardiac muscles
K+ regulation
Initially reabsorbed by proximal tubules, excretion regulated by aldosterone in distal tubules and collecting ducts, distribution between cells and extracellular fluid affected by Na-K ATPase and Insulin
Hypokalemia
serum K+ concentration < 3.5 mmol/L, may present with muscle weakness and cardiac arrhythmias
Causes of hypokalemia
therapy with thiazide diuretics, GI loss through vomiting, diarrhea and gastric suction and discharge
Hyperkalemia
Serum K+ concentrations > 5 mmol/L, renal insufficiency, diabetes, metabolic acidosis, drugs, enhanced tissue breakdown or acute oral load of K+
Cl-
major extracellular anion, shifts second to a movement of sodium or bicarbonate ions, filtered out by glomerulus and passively reabsorbed with sodium by proximal tubules, maintain osmolality, blood volume and electro-neutrality with sodium and through chloride shift
Hyperchloremia
Due to excess loss of bicarbonate ion
Hypochloremia
Due to excess loss of chloride from prolonged vomiting, diabetic ketoacidosis and salt-losing renal diseases
HCO3-
2nd most abundant anion in the ECF, account for 90% of total CO2, major component of the buffering system in the blood, converts CO2 in plasma to an effective buffer and buffers excess H ion by combining with acid to form CO2 which is eliminated in the lungs, reabsorbed by proximal and distal tubules, plasma level changes based on acid-base imbalance
Osmolality
2 [Na+] + [glucose]/20 + BUN 3
Ca++
Found in the skeleton 99%, soft tissues and ECF 1%, 3 physiochemical states in plasma: Free or ionized 50%. Plasma protein (albumin) bound 40%, and complexed with small diffusible anions 10%
0.5% in ECF is the plasma protein, 0.5% in ECF is complexed
Metabolism of Ca++
Absorbed by specific calcium-binding proteins controlled by vitamin D, deposited in bone regulated by PTH, excreted mainly through the kidneys under the control of PTH
Physiological functions of Ca++
Bone mineralization, muscle contraction, hormone secretion, glycogen metabolism, cell division, coag cascade, plasma membrane potential
Regulation of Ca++ by PTH
Stimulate osteoclasts to reabsorb bone and release calcium, increase renal tubular reabsorption of Ca++, promote renal production of active Vitamin D
Fundamental of bone physiology
Function in support and maintenance of mineral homeostasis, achieved by continuous bone remodeling, balance between reabsorption and formation is affected by many factors
Osteoblasts
Bone forming cells
Osteoclast
Reabsorb bone through a degradation process
Osteocytes
Bone cells
Activation of Vitamin D
Obtain in diet or from exposure of skin to sunlight, transported to liver by Vitamin D binding protein, converted to 25-Vit-OH-D2 or 25-Vit-OH-D3 in the liver and to 1,25-(OH)2-D2 or 1,35-(OH)2-D3 in the kidney
Functions of Vitamin D
Facilitate calcium and phosphate absorption in the intestine, increase bone reabsorption by increasing osteoclast activity, enhance the renal reabsorption of calcium and phosphorous
Vitamin D testing
Measured by RIA, HPLC, and LC-MS, most tests don’t differentiate D2 and D3, 25-hydroxyvitamin D is recommended marker for determining vitamin D deficiency
Regulation of calcium by calcitonin
Secreted from the medullary cells of the thyroid glands in response to increased calcium, decreases the flux of calcium and phosphorus from bone into the circulation, down-regulate the renal reabsorption of calcium, phosphorous, sodium, potassium and magnesium, elevated calcitonin seen in medullary thyroid carcinoma
Hypercalcemia
Serum total calcium > 10.0 mg/L, presented with neurologic, GI and renal symptoms or asymptomatic, treatment depends on cause byt biphosphates are the main class of drug
Primary hyperparathyroidism
Most common cause of hypercalcemia in out-patient population, caused by hypersecretion of PTH due to adenoma or carcinoma of the parathyroid gland, seen frequently in elderly females, may show clinical signs or be asymptomatic, characterized by elevated PTH secretion with hypercalcemia
Secondary hyerparathyroidism
Seen in patients with chronic renal disease, show elevated serum calcium level with altered levels of others like phosphate, magnesium and creatinine, secondary increase of PTH level
Malignant diseases
Most common cause of hypercalcemia in in-patient population, have hypercalcemia as a common complication, more prevalent in breast cancer, multiple myeloma and squamous cell carcinomas of the lung and renal carcinoma, may be caused by PTHrP
Hypocalcemia
Serum total calcium level < 8.5 mg/dL, present with irritability and cardiac irredularities, muscle cramps and seizures in serum calcium level less than 7.5 mg/mL, treat with oral or parenteral calcium therapy
Hypermagnesemia
Caused by renal failure, result from magnesium sulfate therapy
Hypomagnesemia
Caused by magnesium loss (GI), malabsorption and bypass surgery for obesity, renal tubular loss, dialysis, hyperaldosteronism, alcohol, diabetes, aminoglycoside antibiotics
Osteoporosis
Usually in older men and women after menopause, characterized by gradual loss of bone mass, which renders less dense bone, due to increased bone reabsorption and decreased bone formation, present with pain, skeletal deformity and fractures, featured by normal serum calcium, phosphorous, magnesium, alkaline phosphatase and PTH levels
Paget’s disease
Individuals older than 40 and increases with advancing age, excessive reabsorption of bone in a random fashion, causing irregular pattern of bone deposition, elevated serum ALP activity due to stimulation of the osteoblasts
Osteolytic phase of Paget’s disease
Osteoporosis circumscripta
Bone softening
Bowing, protrusion acetabuli or greenstick fracture
Mixed phase
Generalized bone enlargement
Sclerotic phase
Increased density, trabeculae and cortical thickening
Rickets/Osteomalacia
Result of vitamin D deficiency, associated with deposition of uncalcified bone matrix in rickets (children) and osteomalacia (adults), increase in serum ALP, low calcium, high PTH
Phosphate
Major intracellular anion, 80% in bone, absorbed in the intestine from diet, important for synthesis of DNA, RNA, ATP, creatine phosphate and 2,3-BPG, mostly regulated by PTH which overall lower blood phosphate by increasing renal excretion and Vit D which increases blood phosphate
Hyperphosphatemia
Caused by a decrease in renal phosphate excretion, increased breakdown of cells, neoplastic disorders, intravascular hemolysis and lymphoblastic leukemia
Hypophosphatemia
Seen in transcellular shift, nutritional recovery syndrome, use of antacids that bind phosphate and alcohol withdrawl
Anion gap
The difference between unmeasured anion and unmeasured cations, useful in indicating an increase in one or more of the unmeasured anions in serum, may serve as a form of quality control for the analyzer used to measure these electrolytes
AG calculation
AG = (Na+ + K+) - (Cl- + HCO3-)
Low anion gap
Rare but seen in multiple myeloma or instrument error
High anion gap
Seen in ketoacidosis, uremia causing PO4-3 and SO4-3 retention, ingestion of methanol, ethylene glycol, salicylate, lactic acidosis, and severe dehydration
Sodium determination
Chemical method, atomic absorption spectrophotometry, flame emission spectrophotometry, ion selective electrode
Ion selective electrode
Use a semipermeable membrane, glass membrane to develop a potential produced by having different ion concentrations on either side of membrane, have 2 electrodes with 1 having constant potential and make it the reference electrode and the other indicator electrode. Use the difference in potential to calculate concentration of ion
Potassium measurement
With ISE as the current method of choice, liquid ion-exchange membrane that incorporates valinomycin that selectively binds K+, can use serum, plasma and urine as long as not hemolyzed
Total calcium determination
Use orthocresolphthalein complexone or arsenazo III dye to form complex with calcium which can be measured through color reaction, affected by serum albumin concentration, use either serum or lithium heparin plasma
Ionized calcium determination
Use membranes impregnated with special molecules that selectively bind calcium ions, measure electric potential developed across the membrane to calculate the ionized calcium concentration, affected by pH, may use whole blood or serum collect anaerobically
Chloride determination
With ISE as most common where an ion-exchange membrane is used to selectively bind chloride ions, may use serum or plasma, other methods are amperometric-coulometric titration, mercurimetric titration and colorimetry
