Lactic Acidosis

what is the mortality rate if a patient has shock, severe lactic acidosis, and pH < 7.2

50%

where does metabolism of lactic acid occur mostly?

kidneys and liver under normal physiological

elevated lactate levels are typically the result of:

excess production or lower clearance

normal physiological levels of lactate:

< 2 mmol/L

hyperlactatemia level of lactate:

2-4 mmol/K

when is lactic acidosis considered?

at levels > 2 mmol/L with a pH < 7.35

how is lactic acid produced?

glycolysis —> pyruvate production —> anaerobic conditions —> cori/lactic acid cycle —> lactate and NAD+ production

what is type A lactic acidosis?

lactic acid production with the presence of hypoxia or tissue hypoperfusion

what is type B lactic acidosis

lactic acid production in the absence of hypoxemia or tissue hypoperfusion

what can cause type A LA:

septic shock, cardiogenic shock, obstructive shock, hypovolemic shock, regional hypoperfusion, muscle hyperactivity (seizures, exertion), severe anemia (< 4 g/dL), cardiovascular or pulmonary disorders, AIDS, cancer, kidney failure, respiratory failure

what substances cause type B lactic acidosis

alcohols, acetaminophen, HAART therapy, beta-adrenergic agents/cocaine, metformin, propofol, isoniazid, salicylates, valproic acid, sulfasalazine, linezolid

why does alcohol cause type B LA

increased NADH —> pyruvate to lactate

why does acetaminophen cause type B LA

increased NAPQI

how can HAART therapy cause type B LA

mitochondrial dysfunction

how can beta-adrenergic agents/cocaine cause type B LA

increased metabolic demand

how can metformin cause type B LA

mitochondrial dysfunction + renal/hepatic impairment

how can propofol cause type B LA

impaired fatty acid oxidation/mitochondrial dysfunction

how can isoniazid cause type B LA

seizures 2/2 pyridoxine depletion

how can salicylates cause type B LA

uncoupling oxidative phosphorylation

how can valproic acid cause type B LA

mitochondrial dysfunction

how can sulfasalazine cause type B LA

impairs tissue oxygenation and/mitochondrial dysfunction

how can linezolid cause type B LA

mitochondrial dysfunction

consequences of LA:

anaerobic metabolism, vasoconstriction, failure of pre-capillary sphincters, peripheral pooling of blood, efflux of potassium, influx of sodium and water

lab findings for LA:

pH < 7.35, lactate > 2 mmol/L, elevated SCr or BUN levels indicative of an AKI, decreased bicarbonate reserves

symptoms of LA

abdominal pain, anxiety, fatigue/weakness, irregular heart rate, lethargy, N/V, tachypnea, tachycardia, SOB

how to evaluate for LA?

CMP/BMP (electrolytes, renal function, anion gap), serial lactate levels, serial ABGs, if unknown etiology consider LFTs and other markers of liver injury

how to treat septic shock LA

broad spectrum antibiotics, stress-dose steroids, causes of infection

how to treat cardiogenic shock LA

Acute decompensated HF —> afterload reduction/inotropic support

MI/myocardial ischemia —> surgical or drug therapies

Cardiac tamponade —> fluid removal

how to treat hypovolemic shock LA

acute blood loss —→ replace blood

burn victims —> fluids and wound care

how to treat medication or toxin induced LA

stopping and removing the offending agent

what should be used for fluid resuscitation in LA

30 mL/kg bolus of balanced crystalloids assessing for response

when may vasopressors be needed?

to increase BP and improve perfusion in shock states - can help increase perfusion but may also “clamp” down patients

when can hemodialysis be used?

to correct acidosis or remove toxins causing acidosis such as alcohols, metformin, and salicylates

T/F: alkalotic therapy is not routinely recommended as it does not correct the underlying cause.

true

when to utilize isotonic sodium bicarbonate solutions?

to correct acidosis in unstable patients

treatment of lactic acidosis is usually by correcting ___________?

the underlying cause or reversing the effects of medications or toxins