Tic Tac Toe Method- determining acid base imbalance Flashcards
Step #1 Determine nml range:
pH 7.35-7.45 (> 7.45 means alkaline)
PCO2 35-45* ACIDIC (>45 means acidic)
HCO3 22-26
Step #2 Make grid;
Acid/NML/Base
PH
PCO2
HCO3
Step #3 Put X in grid for pt results for each value:
Ex: Patient Results:
ph 7.47: base; PCO2 31: base; HCO3 24: nml
Acid/NML/Base
PH X
PCO2 X
HCO3 X
Pt has Respiratory Alkalosis!Acid/NML/Base PH PCO2 HCO3 * Pt values: pH 7.46; PO2 86; HCO3 24
Acid/NML/Base PH PCO2 HCO3 Pt has:
Acid/NML/Base PH PCO2 HCO3 Patient values: pH 7.57; PO2 88; PCO2 36; HCO3 30
Acid/NML/Base PH PCO2 HCO3 Patient has:
Acid/NML/Base PH PCO2 HCO3 Patient values: pH 7.3; PO2 72; PCO2 50; HCO3 26
Patient has:
Acid/NML/Base PH PCO2 HCO3 Patient values: pH 7.14; PO2 70; PCO2 35; HCO3 19
Patient has:
Sources of Acid/Base in the Body:
Acids:
H+ ions Ketoacids carbon dioxide lactic acid Results: low K (hypokalemia)
Sources of Acid/Base in the Body:
Base:
Bicarbonate
Results: increased pH
Sources of Acid/Base in the Body:
Compensatory mechanism:
*chemical buffers on the scene- in seconds
*respiratory- retention OR elimination of CO2- in minutes
*renal- regulates bicarbs (HCO3) to combat hydrogen losses & gains- in hours, but > permanent when other 2 mechanisms fail.
(Renal system slowly gets to work & requires up to 5 days to complete healing.)
General ACIDOSIS sxs: “low, slow, & weak”
Neuro: confusion- 1st sxs
decreased DTRs
muscle weakness
CV: weak pulses
bradycardia
hypotensionGeneral ACIDOSIS sxs: “low, slow, & weak”
Causes:
Hypoventilation Drug overdose Pulmonary Edema Mechanical ventilation Mechanical NM Dz
Respiratory Acidosis
ph LOW
CO2 HIGH
Metabolic Acidosis
ph LOW
HCO3 LOW
Metabolic Acidosis
Causes:
DKA ASA (salicylic acid) overdose Renal failure severe diarrhea shock
Respiratory Acidosis
TXMT:
Meds:
(ex: naloxone, bronchodilators, mucolytics- thin secretions)
O2 (w/ caution! Use lowest art possible)
Mechanical ventilation
Tx the Cause
Metabolic Acidosis
Txmt:
Tx the cause (i.e., stop diarrhea, provide O2/insulin drip)
Give sodium bicarbs if pH < 7.2
Hyperventilation
Results in:
Respiratory Alkalosis
Respiratory Alkalosis
pH high
CO2 low
Respiratory Alkalosis
Causes:
initial stages of Pulmonary Emboli hypoxia fever pregnancy high altitudes anxiety
Metabolic Alkalosis:
pH high
HCO3 high
Metabolic Alkalosis:
Causes:
Overuse of antacids
K+ wasting diuretics
(Increased loss of H+)
Loss of gastric juices
General Alkalosis SXS “Excitable & Weak”
Dizziness Confusion Hyperreflexia Numbness/tingling (mouth/toes) Cramps/Twitching Tachycardia
Alkalosis
TXMT:
Tx the cause
Fall precautions
Rebreather mask (respiratory alkalosis)
ABG Interpretation Rules to Remember:
CO2= Respiratory & ACID HCO3= Metabolic (kidney) & base/alkaline
ABG Interpretation Rules to Remember:
Steps:
-Acid or Base? look at the pH
Respiratory or Metabolic? use ROME method
ROME:
Respiratory pH high; PCO2 low
Opposite pH low; PCO2 high
Metabolic pH high; HCO3-high (alkalosis)
Equal pH low; HCO3-low (acidosis)
Na+ Imbalance Electrolyte
Fx/indication of imbalance
- Na+ serves as primary determinant of blood osmolarity.
* It’s an important regulating acid/base balance & contributes to Fx of nervous system & other excitable tissue.
Na+ Imbalance Electrolyte
SXS of Hyponatremia:
Muscle cramps weakness HA depression apprehension feeling impending doom personality changes lethargy stupor coma anorexia N/V abd cramps diarrhea
Na+ Imbalance Electrolyte
SXS of HYPERnatremia:
- Polydipsia
- oliguria/anuria/high urine specific gravity
- dry skin/mucous membranes; decreased tissue turgor
- tongue- rough/fissured
- decreased salivation/tears
- agitation/restlessness
- HA/SZ/coma/decreased reflexes
- tachycardia; weak, thready pulse; low BP/vascular collapse
Cl- (chloride)
Fx/indications of imbalance
(extracellular)
Most often assoc w/ Na+
Plays role in reg of acid/base balance
Cl- (chloride)
LOW LEVELS: hypochloremia
SXS:
increased muscle tone twitching weakness tetany shallow breathing respiratory arrest mental confusion
Cl- (chloride)
HIGH LEVELS:
HYPERchloremia
SXS:
metabolic acidosis deep, rapid breathing weakness HA diminished cognitive ability cardiac arrest
Imbalance of K+
K+ is intracellular cation
Fx/indication of imbalance:
Distribution of K+ b/w intracellular & extracellular compartments regulates electrical membrane potentials, controlling excitability of nerve & muscle cells & contractility of skeletal, cardiac, & smooth muscle tissue.
Hypokalemia
sxs:
dizziness muscle weakness/leg cramps cardiac arrhythmias/hypotension nausea/anorexia/thirst poorly concentrated urine/polyuria
HYPERkalemia
sxs:
N/V/D/abd/intestinal cramps cardiac arrhythmias paresthesias/weakness muscle cramps EKG changes; R/F: cardiac arrest (w/ very elevated K+)
Mg++
(intracellular)
Fx/indication of imbalance:
Acts as a cofactor in many IC enzyme reactions; is essential to all reactions requiring ATP, for every step r/t replication & transcription of DNA; & for translation of mRNA & required for cellular energy metabolism.
Hypomagnesemia
sxs:
Usually occurs w/ hypocalcemia & hypokalemia
sxs: personality changes, athetoid or choreiform movts, nystagumus, tetany…tachcardia, HTN, & cardiac arrhythmias.
HYPERmagnesemia
sxs:
lethargy
hyporeflexia
confusion/coma
hypotension/cardiac arrhythmias/cardiac arrest
HCO3 bicarbonate (extracellular) fx/indication of imbalance:
One way the body maintains nml pH is via chemical buffers in the ICF & ECF. The most important is HCO3 buffer system.
- A reduction in pH d/t increased HCO3: metabolic acidosis
- An elevation in pH d/t increased HCO3 levels: metabolic alkalosis
Metabolic Acidosis
sxs:
anorexia/N/V/abd pain weakness/lethargy/general malaise confusion/stupor/coma depression of vital fx: peripheral vasodilation, decreased HR, cardiac arrhythmias skin- warm/flushed bone dz (e.g. chronic acidosis)
Metabolic Alkalosis
sxs:
confusion/increased DTRs/tetany/convulsions
hypotension/arrythmias
respiratory acidosis d/t decreased respiratory rate
Ca+
(extracellular)
Fx/indications:
Provides strength & stability for skeletal system & serves as exchangeable source to maintain EC calcium levels. It plays role in many metabolic processes, including activity of enzyme systems, generation of action potential, & muscle contraction.
Hypocalcemia
sxs:
paresthesias (esp numbness/tingling) skeletal muscle cramps abd spasms/cramps increased DTRs carpopedal laryngeal spasm tetany hypotension s/o cardiac insufficiency failure to respond to drugs that act by calcium-mediated mechanisms...osteomalacia, bone pain/deformities, & fx
HYPERcalcemia
sxs:
polyuria/polydipsia
flank pain
s/o acute renal insufficiency/ s/o kidney stones
anorexia/N/V/constipation
muscle weakness/atrophy/ataxia/loss of muscle tone
osteoporosis
lethargy/personality & behavioral changes/stupor/coma
HTN/shortening of QT interval * AV block on EKG
Na
values; nml/critical
Nml range 135-145 mEq/L
critical values <120 or >160 mEq/L
Hypernatremia
causes:
diabetes insipidus exc perspiration copious diarrhea impaired renal fx decreased fluid intake nephrotic syndrome
Hypernatremia
(early) sxs:
dry, red, sticky tongue/mouth
restless
irritable
Hypernatremia
(later) sxs:
delirium twitching sz coma increased muscle tone hyperactive DTRs metabolic acidosis death
Hypernatremia
txmt:
hypotonic saline solution (0.45%) NaCl
sodium restricted diet
lasix, HCTZ
Hyponatremia
causes:
<136 mEq/L extensive vomiting/diarrhea Addison's dz extensive burns low-sodium diets, diuretic tx increased water renal failure
Hyponatremia
(early) sxs:
thirsty anorexia abd cramping confusion lethargy muscle twitching
Hyponatremia
(late) sxs:
sz
loss of coordination
generalized weakness
coma
Hyponatremia
txmt:
nml saline infusion
serum Na 2-4 hrs
daily weights
K
values:
3.5-5 mEq/L
critical <2.5 or > 6.5 mEq/L
Hyperkalemia
causes:
renal failure acidosis cellular damage w/ crushing injury burns other causes
Hyperkalemia
sxs: (early)
cramps muscle twitching nausea weakness abd/genral
Hyperkalemia
sxs: (later)
apathy
confusion
paresthesias
low, ascending paralysis lead to respiratory arrest
EKG changes
severe bradycardia
arrhythmias lead to 3rd degree heart block asystole
Hyperkalemia
txmt:
monitor levels 4-6 hrs monitor HR/rhythm monitor I&O restrict this electrolyte in diet Kayexalate lasix- K+ depletion NaHCO3 (K+ moves into cells) - life threatening
Hypokalemia
causes:
<3.5; critical < 2.5 excessive v/d diuretics DKA TPN Meds: geocillin; diamox; garamyan w/ CHG & chronic HTN
Hypokalemia
sxs: (early)
muscle weakness cramps lethargy apathy drowsiness confusion irritability decreased bowel motility cardiac abnormalities
Hypokalemia
txmt:
IV or oral replacement
monitor this electrolyte lab q8 hrs
increase foods with this electrolyte
Mg++
values:
1.3-2.1 mEq/L
critical values < 0.5 mEq/L or > 3 mEq/L
Hypomagnesemia
causes:
alcoholism malabsorption d/t colitis cancer hyperthyroidism corticosteroid drugs massive blood transfusion
Hypomagnesemia
sxs: (early)
N/V/D/anorexia muscle tremors muscle twitches agitation irritability
Hypomagnesemia
sxs: (late)
hyperactive DTRs
ataxia
vertigo
Hypomagnesemia
sxs: (severe)
clonus hallucinations tetany hypotension nystagmus coma/sz delirium cardiac arrhythmias CHF
Hypomagnesemia
txmt:
increase this electrolyte in the diet use antacids with this electrolyte MgSulfate IM/IV serum level after q16 mEq keep supine handle pts gently
Hypermagnesemia
causes:
renal failure
heavy use of antacids/laxatives
dialysis or TPN
hypoaldosteronism
Hypermagnesemia
sxs: (early)
weak hypotensive flushed/hot absent DTRs slurred speech drowsiness lethargy cardiac arrthymias
Hypermagnesemia
sxs: (later)
flaccid muscle paralysis respiratory depression leading to coma apnea heart block cardiac arrest
Hypermagnesemia
txmt:
IV hydration
thiazide diuretics
calcium chloride or gluconate
Phosphate (PO4)
values/critical:
3-4.5 mg/dL
critical values < 1 mg/dL
Hypophosphatemia
causes:
malabsorption syndromes colitis shortened GI tract excess thiazide diuretics
Hypophosphatemia
sxs: (early)
weakness tissue hypoxia (disruption of cellular fx)
Hypophosphatemia
sxs: (late)
mental confusion
irritability
severe anemia
bone brittleness (stress fx)
Hypophosphatemia
txmt:
oral supplements
neutra soda
phospho-soda (now off-market bc contributed kidney issues)
Hyperphosphatemia
causes:
renal failure
usually hypocalcemia concurrently
Hyperphosphatemia
sxs:
sxs similar to hypocalcemia
Hyperphosphatemia
txmt:
phosphate binders
restrict increased phosphate foods
Calcium
values/critical
9-10.5 mg/dL
critical values < 6 (may lead to tetany)
critical values > 14 (may lead to coma/cardiac arrest)
Hypocalcemia
causes:
malabsorption
parathyroid hormone deficiency
burns
copies wound drainage
Hypocalcemia
sxs: early
numbness/tingling lips anxiety/irritiability twitching, cramps grimacing increased DTRs
Hypocalcemia
sxs: late
bruising impaired coagulation general muscle spasms gluconate convulsion cardiac arrhythmias
Hypocalcemia
txmt:
Trousseau’s Phenomenon
Chyostek’s sign
monitor serum levels of this electrolyte
monitor EKG
diet rich in foods w/ this electrolyte & Vitamin D
this electrolye-gluconate or chloride
+ Trousseau’s sign
carpopedal spasm that dev usually 2-5 min after applying & inflating BP cuff to ~20 mmHG higher than systolic pressure on upper arm. This spasm occurs as the blood supply to ulnar nerve is obstructed.
Hypercalcemia
causes:
excessive use of milk/alkali products for peptic ulcer multiple fx multiple myeloma renal failure prolonged immobilization malignant growths
Hypercalcemia
sxs: early
lethargy depression/apathy malaise/weakness constipation N/V anorexia diarrhea arrhythmias
Hypercalcemia
sxs: (later)
HA coma polydipsia abd pain flaccid paralysis renal failure renal calculi/polyuria clumsiness confusion/slurred speech/memory loss/stupor HTN EKG changes
Hypercalcemia
txmt:
IV fluids- isotonic saline 5-6 L 1st 24 hrs/3L/day thereafter lasix force fluids (cranberry neutra phos/fleets phospho-soda (may be off-market now d/t kidney issues)
