Successful markers of resuscitation
Physiological characteristics of Renal Circulation
- Receives about 20% of CO, very active vasoregulation, very low oxygen consumption, but medulla very sensitive to hypoxia
- Extremely adaptive to circulating blood volume (from 16 mL to 300 mL/hr); activation of neurohormonal system (RAAS, ADH) will decrease diuresis in response to low GFR
- Even improvement in MAP with vasopressors may not improve renal function in setting of low blood volume
Detrimental effects of fluid therapy on renal function
- Excessive fluid therapy can increase MAP but decrease oxygen delivery
- https://www.ncbi.nlm.nih.gov/pubmed/19996951
- https://www.ncbi.nlm.nih.gov/pubmed/19215832
Should we use diuretics EARLY during shock?
https://www.ncbi.nlm.nih.gov/pubmed/28732314
Furosemide stress test to predict severity of AKI
https://www.ncbi.nlm.nih.gov/pubmed/25655065
Gattinoni
Oxygen delivery and consumption
SvO2 tells you there’s a problem with oxygenation, flow, carrying capacity, or consumption (not specific though)
Mixed vs central venous: not perfectly correlated, but decently so
If, ScVO2 is low; think CO, VO2, Hemoglobin, Oxygenation, Acidosis (Dissociation)
Monett
ETCO2 determinants: Alveolar ventilation, CO2 production, pulmonary blood flow
CO2 production:
- Aerobic: adrenergic stimulation, fever, shivering, agitation, sepsis
- R quotient: carbohydrate intake
- Anaerobic: buffering of anions
Washout:
- Increased minute ventilation
- Cardiac output
**If CO2 production is constant, then changes in ETCO2 reflect ventilation or cardiac output
The relationship between changes in CO/ETCO2 are not linear at extremes of output
During CPR, can help monitor cardiac output/efficacy of CPR and help determine patient viability
Monitoring of ETCO2 as evidence of volume responsiveness during passive leg raising
Marik
“Humans are not yeast and rarely become anaerobic.”
Lactate does not cause acidosis; it consumes H+ and actually causes alkalosis
Lactate is not produced by tissue hypoxia (mountain climbers with paO2 of 24 and lactate)
Muscles create lactate to use as fuel for heart/brain during exercise (no evidence of tissue hypoxemia)
Supply dependency/critical oxygen delivery happens at CO of 1 - why do septic patients develop hyperlactemia? Hyperadrenergic: creates more pyruvate than can be processed by Krebs cycle
Thiamine is essential for processing of pyruvate
Lactate administration during stress is beneficial, and removing it may be detrimental