This episode of CRACKCast covers Rosen’s Chapter 014, Cyanosis. Here are some tips for the next time someone comes in to the Emergency Department looking a little blue.
Shownotes – PDF Link
Rosen’s in Perspective:
- oxygenated vs. deoxygenated hemoglobin = saturated vs. desaturated hemoglobin
- SaO2 (arterial oxygen saturation measured/calculated by ABG) SpO2 (peripheral oxygen saturation measured by pulse oximetry)
- PaO2 PAO2 (partial pressure of O2 in the blood (measured by ABG) vs. partial pressure in the alveolus)
Cyanosis = imbalance between oxy/deoxy hemoglobin
- cyanosis is specific for hypoxia but not sensitive (can be hypoxic without cyanosis!)
- normal adults that is when deoxyhemoglobin >5g/dl
- cyanosis is about absolute amount of deoxygenated hemoglobin – anemic individuals turn blue only at lower levels of PaO2 and SaO2
1) What is the differential diagnosis for cyanosis?
- acute heart failure
- acute coronary syndrome
- hypovolemic or cardiogenic shock
- acute respiratory failure
- massive PE
- congenital heart disease
- methemoglobinemia (consider when no hx/physical suggesting underlying respiratory/CVS disease)
- rare cause of cyanosis
- most common after exposure to hydrogen sulfide from organic sources
- also from medications (sulfonamide derivatives)
- GI sources (bacterial overgrowth)
- consider when cyanotic and methemoglobin on CO-oximetry, but does not respond to methylene blue treatment
- polycythemia (elevated RBC mass)
- three main causes:
- polycythemia vera – bone marrow stem cell disorder with increase RBC mass, cyanosis, and splenomegaly
- secondary polycethmia – increase in erythropoietin (appropriate or not) in response to chronic hypoxemia
- e.g. congenital heart disease, cigarette smoking, high altitude exposure
- relative polycethemia – result of reduced plasma volume
- e.g. dehydration
- three main causes:
- Raynaud’s phenomenon
- may cause a cyanotic appearance
- 15% of the population
2) List the common causes for methemoglobinemia
Common causes of methemoglobinemia.
Rosen’s 8th Edition. Box 14-1. Chapter 14 – page 130.
3) Describe the mechanism for methemoglobin formation, treatment, and indications for methylene blue
- normally hemoglobin binds O2 via iron in its reduced state (Fe2+)
- if iron is oxidized it forms methemoglobin (Fe3+) – “ferric state”
- this new oxidized state cannot bind O2 and thus cannot transport O2 to tissues or remove CO2 leading to hypoxia and acidosis
- normally methemoglobin is only ~1% of total hemoglobin stores (cyanosis when greater than 10-25%)
- the body can use NADH to reduce methemoglobin back to Fe2+ (major pathway)
PEARL 1: pathognomonic sign of methemoglobinemia is dark-purple-brown or chocolate looking blood when exposed to room air
PEARL 2: second pathway to reduce methemoglobin exists using glutathione and G6PD. This is the MOA of methylene blue.
If cutaneous exposure, first don appropriate PPE and then decontaminate patient.
Urgent treatment with oxygen and methylene blue indicated for:
- symptomatic hypoxia (dysrhythmias, angina, respiratory distress, altered LOC, seizures)
- OR methemoglobin levels >30%
If patient does not respond to methylene blue but has elevated methemoglobinemia consider sulfhemoglobinemia
1) Explain the oxygen-hemoglobin dissociation curve
2) What is the hyperoxia test?
Bedside test to determine the cause of cyanosis (broad categories): poor oxygenation from lung dysfunction vs. presence of R to L shunt
Official test is using a baseline ABG, and then repeating ABG after high flow O2 for 10min
- if PaO2 increases to above 150mmHg problem is with their lungs
- if PaO2 stays below 100mHg problem is likely a R to L shunt
- lots of caveats and imprecise, but potentially useful tool
Can use SpO2 instead of PaO2 and see whether patients sat improves from 88% to 100% after 10 min of high flow oxygen. If so then likely V/Q cause of hypoxia.
This post was copyedited and uploaded by Sean Nugent (@sfnugent)