Acid Base Disorders Flashcards
acidemia
Acidemia is a decreased blood pH (normal is 7.36-7.44)
Acidosis
Acidosis is a clinical process in the body that decreases blood pH
Alkalemia
Alkalemia is an increased blood pH (normal is 7.36-7.44)
Alkalosis
Alkalosis a clinical process in the body that increases blood pH
Hyperkapnia and hypokapnia
Refers to increased or decreased pCO2in the blood
Ventilation
Process by which inhaled air (including O2) reaches the alveoli of the lungs where gas exchange occurs and exhaled air (including CO2) leaves the lungs
Minute Ventilation
Rate by which air reaches the alveoli.
Measured in Liters/minutes
Equal to Respiratory Rate (breaths per minute) x Tidal Volume (amount of air taken during one breath)
Hyperventilation vs. hypoventilation
Refers to increased or decreased minute ventilation rate respectively
Ventilation and pCO2
Hyperventilation leads to hypokapnia
Hypoventilation leads to hyperkapnia
Anion Gap is normally less than
10
Causes of Acid-Base Disorgers High Anion Gap Metabolic Acidosis
Mnemonics is MUDPILES Methanol Uremia (End Stage Renal Disease) Diabetic ketoacidosis Paraldehyde Infection, Iron, Isoniazide Lactic acidosis Ethylene glycol (antifreeze), alcohol Salicylates, starvation ketoacidosis
Uremic acidosis
Occurs when renal function is severely decreased (Creatinine clearance is less than 25ml/min)
Due to
decreased excretion of acids
decreased excretion of H+
Decreased reabsorption/synthesis of HCO3
Accumulation of organic and inorganic anions
Phosphates
Sulfates
Lactic Acidosis causes
anaerobic metabolism in the tissues from
Hypoxemia
Circulatory failure (hypotension, sepsis)
Peripheral vessels blockage
Anemia
Liver failure due to decreased clearance
Thiaminedeficiency
Hypophosphatemia
Sepsis (due to decreased perfusion of the tissues, impaired gluconeogenesis and poor clearance)
Seizures (due to release of lactate from muscles)
Short-lived
Lactic acidosis meds
Metformin
Some HIV meds
Isoniazide (toxic levels)
lactic acidosis diagnosed by
measuring arterial or venous level
Respiratory acidosis and alkalosis
are clinical processes that occur due to increase or decrease in ventilation and usually associated with pulmonary diseases
Metabolic acidosis and alkalosis
are clinical processes that are not due to ventilation problems
Henderson-hasselbach equation
pH = 6.1 + log HCO3-/0.03 x pCO2
Respiratory Acidosis
Hypoventilation > hyperkapnia > acidosis
Respiratory Alkalosis
Hyperventilation > hypokapnia >
alkalosis
Metabolic acidosis
Over-production or accumulation of acid
Loss of base (HCO3-)
Under-excretion of acid
All of the above will decrease HCO3and will decrease pH
Metabolic Alkalosis
Loss of acid
Under-excretion of base
Leads to increased HCO3and increased pH
Primary acid-base disorder
results from a pathological process
Secondary acid-based “disorder”
is a normal physiological compensation in response to a primary acid-base disorder
buffering
within minutes
Respiratory compensation (in metabolic disorders)
within hours
Metabolic compensation by kidneys
within 2-3 days
acute vs chronic acid-base disorders
Acute acid-base disorders results from the conditions that develop within hours of presentation
Chronic acid-base disorders are at least several days old
These terms are usually reserved to respiratory acid-base disorders
Acute respiratory disorders are compensated or not
uncompensated (resulting in acidemia or alkalemia).
Chronic respiratory disorders are compensated or not?
fully compensated (pH is close to normal) and developed more than 2-3 days before presentation,
Sub-acute resp disorders are compensated or not?
partially compensated (within 2 days frame)
metabolic disorders are compensated or not?
could be fully or partially compensated depending on the degree of the acidosis/alkalosis and on a lung function
mixed disorders
include combination of several acid-base disorders. They are very common
Metabolic acidosis and metabolic alkalosis
Respiratory acidosis and metabolic acidosis
Chronic respiratory acidosis and metabolic alkalosis
Etc.
Causes of resp acidosis
Decreased RR
Decreased TV
Causes of metabolic acidosis
High AG Mudpiles Normal AG Renal Loss (RTA) Extra-renal loss (diarrhea)
From Hypoventilation
From decreased RR Decreased respiratory drive Drugs Coma Stroke From decreased Tidal Volume Neuro-muscular disorders Severe kyphoscoliosis Airways obstruction COPD Obstructive sleep apnea/Obesity
Anion Gap
A.G.=Na+–HCO3–Cl-
Calculated from metabolic profile/electrolytes blood test
Represents unmeasured anions in the plasma
Anionic proteins (albumin)
Phosphate
Sulfate
Organic anions
Diabetic Ketoacidosis
Insulin deficiency >increased lypolysis increased fatty acid delivery to liver >production of ketones >acidosis
Associated with hyperglycemia
More often in Type I Diabetes Mellitus, but may happen in Type II as well
Usually part of the presentation of a new onset of type I DM
May be precipitated by patient’s non-compliance with insulin, infection, pancreatitis
Alcoholic Ketoacidosis
Large ethanol intake leads to altered hormonal and enzymatic activities leading to increase in ketones production
No hyperglycemia
High osmolal gap
Osmolal Gap
Alcoholic Ketoacidosis
OG (normal is less than 10)
Difference between measured serum Osmolality and calculated serum osmolality
Calculated Osmolality = 2 (Na+) + (Glucose/18) + BUN/2.8
OG should be equal to Ethanol level/4.6
If OG more than that, look for other alcohols
Ethylene Glycol poisoning
Found in antifreeze and in industrial solvents Metabolites are highly toxic Increased OG Calcium Oxalate crystals in urine Acute Renal Failure is common
Methanol poisoning
Found in wood alcohol and windshield fluid
Causes blindness and acute renal failure
Increased OG
Salicylates poisoining
Usually a result of accidental or intentional overdose
May cause metabolic acidosis and/or respiratory alkalosis
Symptoms Hemorrhage Fever nausea and vomiting, Diaphoresis Tinnitus Pulmonary edema
Causes of normal ag metabolic acidosis
Diarrhea or Ileal drainage with stoma/bypasses
Decrease reabsorption of HCO3 by renal tubules (therefore increased loss)
increase in anion intakes
large amount of nacl (expansion acidosis)
Diarrhea or Ileal drainage with stoma/bypasses
Due to loss of HCO3
Except for Chloride wasting diarrhea with villous adenoma
Decrease reabsorption of HCO3 by renal tubules (therefore increased loss)
Renal Tubular Acidosis
Due to diuretics ( carbonic anhydrase inhibitors [CAI])
Increase in anion intakes
Parenteral nutrition
Large amount of NaCl (expansion acidosis)
Due to dilution of the bicarbonate and to decreased renal bicarbonate reabsorption as a result of volume expansion
renal tubular acidosis
3 types
RTA Type I
RTA Type II
RTA Type IV
RTA type I
Decreased hydrogen ions excretion in the collecting ducts leading to alkaline urine and acidic serum
Increased calcium excretion and decreased citric acid concentration leading to kidney stone formation
Increased potassium loss leading to hypokalemia
RTA type II
Defect in bicarbonate reabsorption in proximal tubules, so more bicarbonate is excreted, lowering serum bicarbonate and leading to acidemia and elevation in urine bicarbonate concentration.
Increased Ca in the urine, but rarely leading to kidney stones due to normal citric acid concentration.
Because distal tubules work OK, ability to acidify urine in response to acidemia is intact, so urine pH is low.
High K loss also will lead to hypokalemia
RTA type IV
Occur in patient with moderate chronic renal failure
Due to insufficient aldosteroneproduction (hypo-reninemic) and/or aldosteronetubular resistance (due to renal failure)
Insufficient K excretion leads to hyperkalemia
RTA type I
Urine PH
Serum K
Kidney stones
> 5.5
low
yes
RTA type II
Urine PH
Serum K
Kidney stones
RTA type IV
Urine PH
Serum K
Kidney stones
Urinary Anion Gap
To differentiate between renal and extrarenal HCO3loss (RTA vs. diarrhea)
Urine (Na++ K+) -Cl-
Negative in extrarenal loss
Due to high level of unmeasured NH4+
Excretion of NH4+ by healthy kidneys is a compensatory mechanism for acidosis
Positive or non-existent in renal loss
Due to low level of NH4+ and increased level of HCO3
Respiratory Alkalosis list of causes
Usually acute Pain Anxiety Salicylates overdose Fever Sepsis Hypoxia from some pulmonary disorders CHF Pneumonia PE Mild asthma Mechanical ventilation
Metabolic alkalosis causes
Vomiting/NG suction
Due to lose of hydrochloric acid
Contraction alkalosis due to increased HCO3-reabsorption
Dehydration
Diuresis (with diuretics other than CAI)
Hypokalemia
Due to resulting increased mineralocorticoid secretion
Recent correction of chronic respiratory acidosis
Due to recent metabolic compensation.
Metabolic acidosis clinical manifestation
Kussmal respiration (sign of respiratory compensation) Nausea/vomiting Cardiac effects Arrhythmia Hypotension Neurological effects Confusion Lethargy Coma Symptoms of underlying disease
Respiratory Acidosis Clinical manifestation
Ineffective respiration/respiratory distress Cardiac effects Arrhythmia Hypotension Neurological effects Confusion Lethargy Coma (hypercapnic), CO2narcosis Symptoms of underlying disease
Metabolic alkalosis clinical manifestation
Decreased respiration (compensatory). This may lead to ineffective respiration and hypoxia Neurological Parasthesia Carpopedal spasm due to secondary hypocalcemia Confusion Seizures Dizziness Coma Weakness
Respiratory alkalosis clinical manifestations
Hyperventilation Neurological Parasthesia Dizziness Symptoms of underlying disease
Basic rules for interpreting ABG
Determine the predominate process by assessing blood pH
Differentiate between primary and secondary (compensatory) acid-base disturbances
Remember: BODY NEVER OVER-COMPENSATES
Determine if simple or mixed acid-base disorder presents
When math is about to fail you, pay attention at the clinical picture
Remember, you have a patient, not just the numbers.
Main ABG numbers
ph7.4
pco2 40
hco3 24
Step 1 for ABG
Look at pH: acidemia (7.4).
step 2 for abg
Look at HCO3-to determine if primary process is metabolic or respiratory
If HCO3 follows pH, process is metabolic. If goes in the opposite direction, process is respiratory.
Step 3 for abg
Determine if process is compensated (chronic), uncompensated (acute), or partially compensated (somewhere in between)
With metabolic disturbances, it’s easy. Look back at pH. If it’s normal, the process is compensated. If it’s abnormal, it’s uncompensated.
step 4 for abg
Calculate anion gap to classify the metabolic acidosis or to determine if there is a mixed disorder with other types of acid-base disturbances
step 5 for abg
If anion gap is present, Calculate delta-delta gap to find mixed disorders
D AG = (AG –10)/(24-HCO3)
If D AG is 1-1.6, pure high AG metabolic acidosis
If D AG is less than 1.0, concomitant non-AG acidosis
If D AG is more than 1.6, concomitant metabolic alkalosis is present
step 6 for abg
If metabolic disorder, look at pCO2 to determine if additional respiratory process exist.
If changed in the opposite direction from HCO3, additional respiratory acid-base disorder of the same polarity as metabolic one exists.
step 7 for abg
Refer back to clinical picture and see if your calculations make any clinical sense