Lab Values and ICU Monitoring

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.

Lactic Acidosis

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 SepsisSymptoms 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

Lactic Acidosis

Patients will require high levels of Oxygen, often requiring mechanical ventilation. They will also demonstrate with increase VA to compensate

Lactic Acidosis

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.

Anion Gap

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−]

Anion Gap

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 acid-base balance. Calculating the anion gap is clinically useful, as it helps in the differential diagnosis of a number of disease states.

Anion Gap

"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

High Anion Gap

Another frequently used mnemonic is KARMEL.

K-Ketoacidosis A-ASA R-Renal failure M-Methanol E-Ethylene glycol L-Lactic acidosis

High Anion Gap

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

Metabolic ABGS

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.  

Answer

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

Metabolic Acidosis

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.

Answer

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

Base Excess

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)

Base Excess

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.

BUN

BUN 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

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

Renal Failure

BNP 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.

Typically associated with CHF, depending on the patient often requires positive pressure for associated pulmonary edema. Typically non-invasive ventilation

Increased BNP

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.

Cardiac Enzymes

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)

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.

Liver Enzymes

Liver FailureAcites, decreased sensorium

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.

Albumin

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).

INR/PT

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.

Metabolic encephalopathy

Patients will require intubation for airway protection

Risk for Sepsis

Metabolic encephalopathy

Disseminated intravascular coagulation (DIC)

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.

DIC