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Lactic acidosis is a physiological condition characterized
by low pH in body tissues and blood accompanied by the
buildup of lactate
Considered a distinct form of metabolic acidosis.
The condition typically occurs when cells receive too little
oxygen
For example during vigorous exercise. In this situation,
impaired cellular respiration leads to lower pH levels.
Simultaneously, cells are forced to metabolize glucose
anaerobically, which leads to lactate formation.
Therefore, elevated lactate is indicative of tissue hypoxia,
hypoperfusion, and possible damage.
Lactic acidosis is characterized by lactate levels
>5 mmol/L and serum pH <7.35.
Causes, incidence, and risk factors
 The most common cause of lactic acidosis is intense exercise.
However, it can also be caused by certain diseases, such as:
 AIDS
 Cancer
 Kidney failure
 Respiratory failure
 Sepsis
Symptoms
 Nausea
 Weakness
 Signs and tests
 Blood tests to check electrolyte levels
 Treatment
 The main treatment for lactic acidosis is to correct the
medical problem that causes the condition. Oxygen
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Patients will require high levels of Oxygen,
often requiring mechanical ventilation. They
will also demonstrate with increase VA to
compensate
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The anion gap is the difference in the
measured cations and the measured anions in
serum, plasma, or urine.
The magnitude of this difference (i.e. "gap")
in the serum is often calculated in medicine
when attempting to identify the cause of
metabolic acidosis. If the gap is greater than
normal, then high anion gap metabolic
acidosis is diagnosed.
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With potassium
It is calculated by subtracting the serum
concentrations of chloride and bicarbonate
(anions) from the concentrations of sodium and
potassium (cations):
= [Na+] + [K+] − [Cl−] − [HCO3−]
Without potassium (Daily practice)
However, the potassium is frequently ignored
because potassium concentrations, being very
low, usually have little effect on the calculated
gap. This leaves the following equation:
= [Na+] − [Cl−] − [HCO3−]
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In normal health there are more measurable
cations compared to measurable anions in the
serum; therefore, the anion gap is usually
positive.
Because we know that plasma is electro-neutral
we can conclude that the anion gap calculation
represents the concentration of unmeasured
anions.
The anion gap varies in response to changes in
the concentrations of the above-mentioned
serum components that contribute to the acidbase balance. Calculating the anion gap is
clinically useful, as it helps in the differential
diagnosis of a number of disease states.
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"Mudpiles"
The mnemonic MUDPILES is commonly used to remember
the causes of increased anion gap metabolic acidosis
M-Methanol
U-Uremia (chronic renal failure)
D-Diabetic ketoacidosis
P-Propylene glycol ("P" used to stand for Paraldehyde but
substance is not commonly used today)
I-Infection, Iron, Isoniazid
L-Lactic acidosis
E-Ethylene glycol (Note: Ethanol is sometimes included in
this mnemonic as well, although the acidosis caused by
ethanol is actually primarily due to the increased
production of lactic acid found in such intoxication.)
S-Salicylates
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Another frequently used mnemonic is
KARMEL.
K-Ketoacidosis
A-ASA
R-Renal failure
M-Methanol
E-Ethylene glycol
L-Lactic acidosis
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A 23-year-old woman with gastroenteritis
experiences nausea and vomiting. Aterial
blood gas analysis is done 1 hour after the
onset of symptoms. Which of the following
sets of blood gases is most likely.
A pH 7.30; PCO2 50; HCO3- 24
B pH 7.28; PCO2 40; HCO3- 18
C pH 7.56; PCO2 40; HCO3- 35
D pH 7.51; PCO2 50; HCO3- 35
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Choice D is the best answer.
1. Vomiting causes loss of stomach acid
leading to metabolic alkalosis.
The rise in pH will inhibit the peripheral
chemoreceptor for pH located in the carotid
bodies leading to hypoventilation (increased
PCO2), which is compensatory.
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A 35-year-old man with type 1 diabetes is admitted
to the emergency department after being found
unconscious and unresponsive at home. His breath
has a "fruity" odor. His wife told the EMTs that his
diabetes had been "out of control" lately and that he
has no other medical problems. His breathing is
deep and rapid. An arterial blood sample is taken for
analysis. Which of the following sets of arterial blood
gases is most likely.
A pH 7.00; PCO2 50; HCO3- 12
B pH 7.22; PCO2 30; HCO3- 12
C pH 7.56; PCO2 40; HCO3- 35
D pH 7.51; PCO2 45; HCO3- 35
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Choice B is the best answer. The presentation is
consistent with ketoacidosis (ketones are volatile
acids that are eliminated via both kidneys and
lungs). The overutilization of fats for metabolism
leads to ketoacidosis, a metabolic acidosis. The
low pH stimulates the carotid pH receptor leading
to hyperventilation (lower PCO2) which is
compensatory. recall that according to the
Henderson-Hasselbalch equation, pH = 6.1 + log
[HCO3]/PCO2 x αlpha. Compensation is always
aimed at restoring the ratio HCO3/PCO2 back to
a normal value, so if HCO3 decreases, PCO2 must
decrease via hyperventilation to provide
compensation.
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Base excess is defined as the amount of strong
acid that must be added to each liter of fully
oxygenated blood to return the pH to 7.40 at a
temperature of 37°C and a pCO2 of 40 mmHg
A base deficit (i.e., a negative base excess) can
be correspondingly defined in terms of the
amount of strong base that must be added.
A further distinction can be made between actual
and standard base excess: actual base excess is
that present in the blood, while standard base
excess is the value when the hemoglobin is at 5
g/dl. The latter gives a better view of the base
excess of the entire extracellular fluid
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The predominant base contributing to base
excess is bicarbonate. Thus, a deviation of
serum bicarbonate from the reference range
is ordinarily mirrored by a deviation in base
excess. However, base excess is a more
comprehensive measurement, encompassing
all metabolic contributions.
metabolic alkalosis if too high (more than +2
mEq/L)
metabolic acidosis if too low (less than −2
mEq/L)
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A blood urea nitrogen test measures the amount of urea
nitrogen that's in your blood. Your liver produces
ammonia — which contains nitrogen — after it breaks
down proteins used by your body's cells.
The nitrogen combines with other elements, such as
carbon, hydrogen and oxygen, to form urea, which is a
chemical waste product.
The urea travels from your liver to your kidneys through
your bloodstream. Healthy kidneys filter urea and other
waste products from your blood. The filtered waste
products leave your body in urine.
If a blood urea nitrogen test reveals that your urea
nitrogen levels are higher than normal, it probably
indicates that your kidneys aren't working properly. Or it
could point to high protein intake, inadequate fluid intake
or poor circulation.
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Typical Ref. Range: 5-25 mg/DL
Optimal Range: 12-20 mg/DL
Causes of Increased ("Azotemia")
Renal dysfunction (creatinine increases proportionately)
Pre-renal Azotemia (less proportional creatinine elevation)
Diabetes mellitus, uncontrolled
Starvation/dehydration/diarrhea
Congestive heart failure (decreased renal circulation)
GI hemorrhage and obstruction
Shock/Tissue necrosis/ Third degree burns
Renal Artery Stenosis (with hypertension)
Post-Renal
Renal vein thrombosis
Urinary tract obstruction
Non-Renal
Gout
Increased protein catabolism (Tetracycline, Addison's, excess glucocorticoids)
High protein diet
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Patients with high BUN/Creatine associated
with renal failure may develop pulmonary
edema from fluid overload.
They will produce with increase WOB,
decreased SaO2. often require intubation
Chronic anemia also associated with CRF,
carrying capacity of O2 will be decreased
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BNP is a substance secreted from the
ventricles or lower chambers of the heart in
response to changes in pressure that occur
when heart failure develops and worsens. The
level of BNP in the blood increases when heart
failure symptoms worsen, and decreases
when the heart failure condition is stable. The
BNP level in a person with heart failure – even
someone whose condition is stable – is higher
than in a person with normal heart function.
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Typically associated with CHF, depending on
the patient often requires positive pressure
for associated pulmonary edema. Typically
non-invasive ventilation
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Cardiac enzyme studies measure the levels of the
enzyme creatine phosphokinase (CPK, CK) and the
protein troponin in the blood.
Low levels of these enzymes and proteins are
normally found in your blood, but if your heart
muscle is injured, such as from a heart attack, the
enzymes and proteins leak out of damaged heart
muscle cells, and their levels in the bloodstream rise.
Because some of these enzymes and proteins are also
found in other body tissues, their levels in the blood
may rise when those other tissues are damaged.
Cardiac enzyme studies must always be compared
with your symptoms, your physical examination
findings, and electrocardiogram (EKG, ECG) results.
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Elevated liver enzymes may indicate inflammation or
damage to cells in the liver. Inflamed or injured liver
cells leak higher than normal amounts of certain
chemicals, including liver enzymes, into the
bloodstream, which can result in elevated liver
enzymes on blood tests.
The specific elevated liver enzymes most commonly
found are:
◦ Alanine transaminase (ALT)
◦ Aspartate transaminase (AST)
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Elevated liver enzymes may be discovered during
routine blood testing. In most cases, liver enzyme
levels are only mildly and temporarily elevated. Most
of the time, elevated liver enzymes don't signal a
chronic, serious liver problem.
Acites, decreased
sensorium
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Albumin is a protein made specifically by the
liver, It is the main constituent of total
protein; the remaining fraction is called
globulin (including the immunoglobulins).
Albumin levels are decreased in chronic liver
disease, such as cirrhosis. It is also decreased
in nephrotic syndrome, where it is lost
through the urine.
Poor nutrition or states of impaired protein
catabolism, may also lead to
hypoalbuminaemia.
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Since the Prothrombin time test or PT test evaluates the
ability of blood to clot properly, it can be used to help
diagnose bleeding. When used in this instance, it is often
used in conjunction with the PTT to evaluate the function
of all coagulation factors.
Occasionally, the test may be used to screen patients for
any previously undetected bleeding problems prior to
surgical procedures.
The International Normalized Ratio (INR) is used to
monitor the effectiveness of blood thinning drugs such as
warfarin (COUMADIN®).
These anti-coagulant drugs help inhibit the formation of
blood clots. They are prescribed on a long-term basis to
patients who have experienced recurrent inappropriate
blood clotting. This includes those who have had heart
attacks, strokes, and deep vein thrombosis (DVT).
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Metabolic encephalopathy is temporary or permanent damage to
the brain due to lack of glucose, oxygen or other metabolic
agent, or organ dysfunction. Most cases occur when the liver
cannot act normally to remove toxins from the bloodstream
during an acute illness, but it can also be caused by a toxic
overdose, or other systemic disease.
Causes
Metabolic encephalopathy occurs during significant metabolic
derangements, after some types of poisoning, and during
diseases such as cirrhosis or hepatitis that slow or stop liver
function, or diabetes, heart or renal failure.
It can also happen during medical conditions that cause blood
circulation to bypass the liver. These problems keep the liver
from removing toxins like ammonia, which build up in the blood
as part of normal metabolism. High levels of these toxins can
temporarily or permanently damage the brain, causing metabolic
encephalopathy.
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Patients will require intubation for airway
protection
Risk for Sepsis
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Disseminated intravascular coagulation (DIC) is not a
specific diagnosis, and its presence always indicates
another underlying disease.
Disseminated intravascular coagulation (DIC) is
characterized by a systemic activation of the blood
coagulation system, which results in the generation
and deposition of fibrin, leading to microvascular
thrombi in various organs and contributing to the
development of multiorgan failure.
Consumption and subsequent exhaustion of
coagulation proteins and platelets, due to the
ongoing activation of the coagulation system, may
induce severe bleeding complications, although
microclot formation may occur in the absence of
severe clotting factor depletion and bleeding.