Bariatics And Robotics Flashcards
At what point does BMI become a problem?
Morbid obesity
> 40 is automatically ASA III
Endocrine function of adipose tissue
• A reserve energy source & insulates vital organs
• Produces cytokines, chemokines and steroids
-result is chronic inflammation
Two types of adipose distribution
Android- central/trunkal-associated with cardiovascular risk
Gynecoid- all in the legs
NO increased CV risk
Leptin
Hormone signaling to CNS/hypothalamus
Produced in adipose cells
-signals fullness-but you can become resistant with the high circulating levels found in obesity
Adiponectin
Hormone produced in adipose
Signals CNS
Modulates insulin sensitivity- levels are low in obesity
Ghrelin
Hunger hormone of the stomach
Arcuate nucleus
In the hypothalamus
Receives and transmits signals based on information received from adipocytes
3 components of the pathophysiology of obesity
-leptin/adiponectin/ghrelin
-arcuate nucleus
-efferent system
What do we do with extra calories?
Converted to triglycerides and stored in adiopocytes
Explain adipocytes accommodation of extra triglycerides in obesity
They EXPAND until a BMI of 40
Then the PROLIFERATE to accept more energy
Percentage of energy needed for resting metabolic rate
60%
Define hypopnea
50% reduction in airflow for >10 seconds
Differentiate central sleep apnea and obstructive sleep apnea
-lack of brain signaling to respiratory muscles-usually in presence of severe systemic illness
-partial or complete periodic obstruction of the upper airway
3 criteria in obesity hypoventilation syndrome
BMI >30
PaCO2 over 45 mmhg
No alternative explanation
How is OSA classified?
Number of hypopneic events in an hour
Mild- 5-14
Moderate- 15-29
Severe > 30
How common is OHS in the morbidly obese?
Only 5-10%
Main difference between OHS and OSA
OSA is transient at night and OHS results in chronic changes in PaCO2 and PAO2
Obesity airway concerns
DECREASED pharyngeal area
Excess hypopharyngeal tissue
Posteriorly displaced hyoid bone
Difficulty laying flat
High incidence of GERD/OSA
Pulmonary compliance in obesity
Decreases exponentially with increasing BMI
chest wall lung compliance DECREASES to 35% of predicted values
Most commonly reported respiratory issues in obese patients
Decreased FRC and ERV
Most sensitive indicator of obesity affects on pulmonary function
ERV
Change in cardiac output with obesity
Increases buy 20-30ml/kg of excess fat
Ex. 1kg of fat increases CO by 100ml/min
SO-increased blood volume and increased LV workload
Impact of obesity on cardiovascular plumbing
Accelerated atherosclerosis
-fat can infiltrate cardiac tissue and the conduction system
Fluid administration in obesity
Easy to overload with rapid administration
-can cause intraop ventricular failure