Metabolic Acidosis
Diagnostic tests
ABG's serum electrolytes tests for underlying primary disorder
Implementation 6
Administer prescribed diuretics as ordered, monitor response. Loop and high-ceiling diuretics such as furosemide can lead to further electrolyte imbalances, esp. hypocalemia-significant risk in metabolic acidosis correction
Implementation 4
Assess hourly urine output, maintain accurate record of I & O, Note urine output <30 mL hr or positive fluid balance of 24 hour total I & O calculations. Heart failure and inadequate renal perfusion may lead to decreased urine output
Evaluation
Client maintains a pH w/in normal range Clients VS remain w/in personal normal range Client maintains adequate oxygenation of tissues Client is able to demonstrate measures to control the disease process to prevent further complications of pH balance.
Planning
Client will describe ad demonstrate preventitive measures related to chronic disease process pH will remain within normal range Disease process causing a/b imbalance will be controlled to reduce production of alkaline loss Client will maintain vital signs within normal range for age and condtion
Diagnosis for metabolic acidosis
Decreased Cardiac Output Risk for Excess Fluid Volume Risk for Injury
As metabolic acidosis is corrected
K shifts back into intercellular space. This shift can lead to hypokalemia and cardiac disrhythmias
Implementation 5
Obtain daily weight using same scale same time of day
Pathophys and etiology of MA
accumulation of metabolic acids excess loss of bicarbonate increase in Cl levels
Metabolic acidosis follows
acute lactic acidosis tissue hypoxia (shock cardiac arrest) Clients type 1 DM ketoacidosis acute renal failure impairs excretion of metabolic acids Diarrhea, intestinal suction or abdominal fistulas increase bicarbonate loss
if pH is less than 7.2
alkalizing solution given/IV sodium bicarbonate
Chronic acidosis skeletal problems
as Ca and phosphate are released from bone
Potassium is retained
as the kidneys excrete H+ in acidosis
Safety precations for acidosis
bed in lowest position, side rails up, keep personal items close and orient x3 as needed
Pancreas secretes
bicarbonate rich fluid into small intestine
Lactic acid is formed
buy lactate and H+
Cardiac dysrhthmias develop
cardiac arrest may occur
Acidosis depresses
cell membrane excitability, affecting neuromuscular function increases amount of free Ca in EFC by interfering with protein binding
Metabolic acidosis from diarrhea is treated
correcting underlying cause and providing fluid and electrolyte replacement.
Severe acidosis <7.0
depresses myocardial contactility leading to decreased cardiac output
Gastrointestinal functions cause
diminished appetite, N/V, abdominal pain
Acid-base balance effects
electrolyte balalance
Hyperchloremic acidosis
excess IV Cl infusion
Ketoacidosis (starvation, DM)
fatty tissues is broken down and fatty acids are released and converted to keytones
Lactic acidosis from decreased tissue perfusion (shock, cardiac arrest)
focuses on correcting .0 the underlying problem to increase tissue perfusion.
Potassium is displace
from inter-cellular space as H+ enters to maintain cations and anions in the cells in acidosis
Calcium is released
from its bonds with plasma proteins, increasing the amount of ionized (free) Ca in the blood in acidosis
Lactic acidosis results (exercise, MI)
from tissue hypoxia and a shift to anerobic metabolism by the cells
Decreased cardiac output and impaired tissue perfusion indicators
hypotension, diminished pulse strength, and slowed capillary refill
Monitor neurological function
including mental status, LOC, and muscle strength. As pH falls, the resulting decline in mental functioning leads to confusion, stupor, and decreased LOC.
Deep rapid respirations
known as Kussmaul respirations, shortness of breath, or dyspnea
Other alkalinizing solutions
lactate, citrate, and acetate solutions (which metabolize to bicarbonate)
LOC
may decline into stupor and coma
Magnesium levels
may fall in acidosis
Rapid correction of acidosis
may result in alkalosis and hypokalemia, possibly hypernatremia and hyperosmolarity leading to water retention and fluid overload
Risk for injury
mental status and brain function affected by acidosis
Implementation 3
monitor and maintain fluid replacement Monitor serum Na+ levels and osmolality Monitor heart and lung sounds, CVP, respiratory status. Report increased dyspnea, advantageous lung sounds, third heart sound (S3) due to volume of blood flow through the heart, and high CVP readings indicate hypovolemia
Implimentation
monitor vital signs, peripheral pulse, capillary refill.
Implamentation 2
monitory ECG pattern for disrhythmias and changes characteristic of hyperkalemia
Progressive ECG changes
such as widening of QRS compex indicates disrhythmias
Metabolic acidosis is rarely primary disorder
usually develops from another disease
General manifestations
weakness, fatigue, headache, general malaise
Diabetic ketoacidosis is treated
with intravenous insulin and fluid replacement
Alcoholic ketoacidosis is treated
with saline solution and glucose
