Obesity Flashcards
(34 cards)
1
Q
What is metabolic syndrome?
A
- increased r/f cardiovascular disease events and are at increased risk for all-cause mortality
- up to 30% middle aged people in developed countries have metabolic syndrome
Diagnosis: Need 3 present
- Abdominal obesity
- Elevated fasting glucose
- HTN
- Low HDLs
- Hypertriglyceridemia
Metabolic syndrome:
- Abdominal obesity
- Atherogenic dyslipidemia
- ↑ TGs
- ↓ HDL-C
- ↑ ApoB
- ↑ small LDL particles
- Elevated blood pressure
- Insulin resistance ± glucose intolerance
- Proinflammatory state (↑ hsCRP)- inflammatory resp elevated
- Prothrombotic state (↑ PAI-1, ↓ FIB)
- Other
- endothelial dysfunction
- microalbuminuria
- polycystic ovary syndrome
- hypoandrogenism
- non-alcoholic fatty liver disease- 40% of NASH are obese
- hyperuricemia
2
Q
What is OSA?
A
- Recurrent episodes of partial or complete upper airway collapse occurring during sleep
- 70% pts obese
- Obstructive apneic event:
- complete cessation of airflow during breathing lasting > 10 seconds despite maintenance of neuromuscular ventilatory effort
- Dx: only by polysomnography
- Results of polysomnography are reported as the apnea-hypopnea index (AHI)
- total number of apneas and hypopneas divided by total sleep time
- (or) Respiratory disturbance index (RDI) → includes resp effort related arousals (RERAs)
- Results of polysomnography are reported as the apnea-hypopnea index (AHI)
- Apnea = 10 seconds or more of total cessation of airflow despite continuous respiratory effort against a closed glottis with decrease in SaO2 >4% (at least 5X/hr)
- Hypopnea = a 50% reduction in airflow that lasts at least 10 seconds or a reduction sufficient enough to cause a 4% decrease in arterial SaO2
3
Q
What is STOPBANG?
A
STOPBANG Assessment:
8 question survey
Score 5-8 → identify moderate/severe disease (KNOW)
- Snoring
- Tired
- Observed apnea
- Blood Pressure
- BMI >35
- Age >50
- Neck >40 cm
- Gender: Male
4
Q
What is the AHI index?
A
- Most sleep centers commonly use an AHI between 5 and 10 events per hour as a normal limit
- AHI categories:
- Mild Disease: 5-15 events/hr
- Moderate Disease: 15-30 events/hr
-
Severe Disease: > 30 events/hour
- Moderate/severe disease → tx w/ continuous positive airway pressure (CPAP) during sleep
- Additional measures:
- weight loss
- avoidance of ETOH
- side sleeping
*
5
Q
What are some risks of OSA?
A
- Systemic and pulmonary hypertension
- Left ventricular hypertrophy
- cardiac arrhythmias
- cognitive impairment
- persistent daytime somnolence
6
Q
What are some characteristics of the airway in obses OSA patients?
A
- increased amounts of adipose tissue deposited into oral and pharyngeal tissues
- inverse relationship exists between the degree of obesity and pharyngeal area
- Increased airway obstruction
- more difficult to maintain airway patency during mask ventilation
- more diff perform direct laryngoscopy
- Neuromuscular blockade should be fully reversed prior to extubation
- Airway obstruction following extubation is worse with use of opiate and sedative drugs
- these drugs tend to decrease pharyngeal dilator tone and increase the likelihood of upper airway collapse
7
Q
Respiratory pathophys in obese patient?
A
- Chest wall and lung compliance reduced
- Fat accumulation on thorax & abdomen
-
Increased pulmonary BV
- Needed to perfuse excess adipose tissue
- Polycythemia from chronic hypoxemia
- Add the supine position and anesthesia = situation worse
- increased work of breathing
- Increased RR with decreased Vt
- limited maximum ventilatory capacity = decreased respiratory muscle efficiency
-
PEEP is the only ventilatory parameter that has been shown to improve respiratory function in obese patients
- 10-12 cmH20 (watch BP)
- Increased PEEP → decrease VR (watch hypoTN)
- 10-12 cmH20 (watch BP)
- Increased oxygen consumption and carbon dioxide production
- High minute ventilation
- As obesity worsens you will see lung disease and pulm HTN
- PFTs remain normal until point of pulmHTN
8
Q
Effect of obesity on lung volumes?
A
- ↓ decreased ERV (60% of normal)
- ↓decreased FRC (80% of normal)
- FRC reductions with anesthesia are exaggerated
- 20% nml
- 50% obese
- FRC reductions with anesthesia are exaggerated
- ↓ decreased VC
- ↓ decreased TLC
- RV and CC: not changed
- relationship between FRC and CC: adversely affected
- FEV1 and FVC: w/in normal limits
9
Q
What are some airway changes in obesity?
A
- Upper thoracic and low cervical fat pads →
- Limited movement →
- TMJ
- atlanto-axial joint
- cervical spine movement
- Limited movement →
- Redundant tissue folds in the mouth and pharynx = narrowed upper airway
- Short, thick neck: measure neck circumference
-
Neck circ strongly predictive of diff w/ int, more so than some other msrs of assessing for diff with int
- 40 cm = 5% incidence difficult intubation
- 60 cm= 35% incidence difficult intubation (6 x increase)
-
Neck circ strongly predictive of diff w/ int, more so than some other msrs of assessing for diff with int
- Fat in suprasternal, pre-sternal, posterior cervical and submental regions → diff to position
- Use stubby laryngoscope
- Shortened distance between mandible & sternal fat pads
- OSA = INCREASE risk of excess pharyngeal tissue on lateral walls – why they obstruct
- Creates difficulty maintaining mask airway
- Creates difficult laryngoscopy and intubation
- “Ramp patient” to align sternum with ear → improve visualization
10
Q
CV alterations in obesity?
A
-
increase total BV –
- blood flow to fat: 2-3ml/100g tissue
- Obese pt: 50ml/kg
- Normal wt pt: 70ml/kg
- blood flow to fat: 2-3ml/100g tissue
- increase renal and splanchnic blood flow
- éincrease CO
- d/t ventricular dilation
- increase SV
- increase O2 consumption
- increase renin-angiotensin system (RAAS)
- increase SNS activity
- HTN:
- SBP: increase 3-4mmHg/10 kg wt gain
- DBP: increase 2mmHg/10kg wt gain
11
Q
Pathophysiologyc of OSA
A
- Altered functioning during the daytime:
- Sleepiness
- impaired concentration
- impaired memory
- headaches
- Ultimately lead to:
- Chronic hypoxia, hypercapnia
- pulmonary and systemic vasoconstriction (HTN)
- secondary polycythemia
- Chronic HPV → leads to right ventricular failure
12
Q
What is pickwickian/obesity hypoventilation syndrome
A
extreme consequence of obesity
- Extreme obesity with:
- Hypercapnia
- cyanosis induced polycythemia
- somnolence
- *right sided heart failure
- *pulmonary HTN
- Diagnosis:
- Obese pt w/ PCO2 >45 mm Hg w/o sig COPD
- Chronic daytime hypoxemia → better predictor of pulmHTN and cor pulmonale (‘pickwickian”) than the presence and severity of OSA
- A supine room-air SpO2 < 96% or increased Hct may merit further investigation (pulm HTN)
- Preop:
- PFTs
- ABGs
- CXR
- echo
- Preop:
13
Q
tCV complications of obesity?
A
- Need ECG
- left or right ventricular hypertrophy
- ischemia
- conduction defects
- Increased left ventricular wall stress →
- Hypertrophy
- reduced compliance
- impaired left ventricular filling (reflect diastolic dysfunction)
- increase left ventricular pressures
-
increase diastolic pressure
- → progresses to pulmonary edema
- Eventually LV wall thickening fails to keep pace with ventricular dilation and systolic dysfunction or “obesity cardiomyopathy”
- → results with eventual biventricular failure.
14
Q
What are some associated postoperative comp,ications related to CV changes in obesity?
A
- Limited mobility can mask significant cardiac disease and peri-op risk (difficult to calculate METS)
- CAUTION:
- Rapid IV fluids → result in ventricular failure
- Exaggerated negative inotropy with anesthetic agents
- Hypoxia and hypercapnia → may result in pulmonary HTN
- Careful with acute CO2 changes
- CAUTION:
- higher risk arrhythmias
- D/t: hypoxia, hypercapnia, CAD, OSA, increased circulating catecholamines, myocardial structural changes (hypertrophy, fatty infiltrates)
15
Q
What are some alterations in the pharmacology of obese patients?
A
- Volume of Distribution
- Central compartment is unchanged
- decrease Absolute total body water
-
increase Adipose and lean tissues
- Most altered VOD:
- Lipophilic
- polar drug
- Ex: barbiturates and benzos.
- Most altered VOD:
- increase Blood volume and CO
- Blood concentration of free fatty acids, triglycerides, cholesterol, and alpha 1 glycoprotein increased= decreased free drug concentration
- Organomegaly
16
Q
What are some alterations in drug metabolism in obese pt?
A
- Phase I (oxidation, reduction, hydrolysis)
- unaffected
- Phase II (glucuronidation, sulfation)
- enhanced
17
Q
Affect of obesity on drug clearance?
A
-
Hepatic clearance - unchanged
- despite histological and LFT alterations
-
Renal clearance of drugs - increased
- (increased GFR, RBF, and tubular secretion)
- Lipophilic drugs have an increased elimination half-life because of increased Vd but have normal clearance
18
Q
Generic principles for dosing of meds in obese patients?
A
- Weak or Moderate Lipophilicity dose on IBW or LBM (lean body mass)
- Adding 20% to IBW with hydrophilic medications (i.e. muscle relaxants) will include the extra LBM associated with obesity
- Miller 8th provides this formula for LBM- do not need to know
- Male: 1.1 × TBW − 128 × (TBW ÷ Ht) 2
- Female: 1.07 × TBW − 148 × (TBW ÷ Ht) 2
-
Loading dose
- drug distributed to lean tissue dose on LBW
- Drug even distribution b/w adipose and lean- use TBW
-
Maintenance
- drug similar clearance in obses and nonobese, use LBW
- Drug has clearance increased with obesity should have maintenance dose based on TBW
19
Q
Considerations for propofol dosing in obese pt
A
- Induction dose
- *LBW (no difference in initial VD between obese and non-obese patients)
- Maintenance dose
- *TBW
- Increased Vd (high affinity for fat and other well perfused organs) at steady state parallels increased clearance (high hepatic extraction and conjugation rate) = no change in E ½ life
20
Q
Benzodiazepine dosing in obese pt?
A
- Highly lipophilic drugs with larger Vd in obese patients
- Initial doses → LBW – may titrate to TBW (need larger doses to reach adequate serum concentrations)
- Infusions → LBW
- Prolonged duration of action though secondary to larger Vd and need higher loading doses
21
Q
Considerations of NMB drugs in obesity?
A
- Pseudocholinesterase activity increases as weight and ECF increases (linear relationship)
- Dose: Succinylcholine → TBW
- Vecuronium and Rocuronium –LBW
- Atracurium and Cisatracurium –LBW (Miller 8th TBW)
- General trend= exhibit prolonged DOA and recovery
22
Q
Sugammadex dosing in obesity?
A
- Dose → TBW
- Some have hypothesized that low Vd at steady state (estimated at 0.16 L/kg) indicates we should consider dosing on the lean/ideal body weight
- Studies indicate that this might not be adequate
- Controversial… follow drug insert for now
23
Q
Dosing of opioids in obesity?
A
- Fentanyl and Sufentanil = both are highly lipid soluble so – increased Vd and elimination ½ life
- Fentanyl → LBW (Miller 8th says TBW)
- Sufentanil → TBW
- then decrease maintenance to LBM
- Remifentanil → LBW
- pharmacokinetics are similar in obese and non-obese patients.
- High risk bc OSA → reducing dose anyway
- Barash 6th says dose sufentanil on TBW in text and LBW in chart 1237. Increased body fat increases the VOD of sufentanil and slows its elimination. Miller 8th presents very complex modeling that is very difficult to follow and remember for dosing in the obese pts. It also involves the definition of multiple “scaling” formulas… better summary in chapter p. 2212 but some contradiction with barash.
24
Q
Dexmedetomidine dose in obesity?
A
- Nice adjunct to consider when respiratory depression avoidance is priority
- Dose: 0.2-0.7 mcg/kg/hr
- reduce analgesic and anesthetic requirements
- Dose: TBW
25
VA effect in obesity?
* Metabolism is greater in obese patients = greater increase in inorganic fluoride
* **Greater** incidence of **halothane hepatitis**
* Some evidence suggests recovery more reliable after desflurane (i.e. fat:blood partition coefficient) compared to sevo or iso ; other evidence contradicts this???
* **N20 often avoided to maximize PaO2\***
* Even though obese pts have a greater increase in inorganic fluoride there is **no significant differences in post op** liver or renal function comparing obese and non-obese individuals with Sevo. Greater incidence of halothane hepatitis because obese pts use a hepatotoxic metabolic pathway to metabolize halothane.
* VA distribute so slowly to lipid stores that increasing the fat reservoir has little clinical effect on wake-up time even w/ long sx
26
Preop considerations of obese pt?
* Population w/ High incidence of:
* HTN, pulmonary HTN, right/left ventricular failure, CAD
* Excess adipose tissue may hide signs of cardiac failure
* Pulmonary HTN signs = dyspnea, fatigue, syncope, tricuspid regurgitation on echo, ECG (RVH, tall precordial R waves, right axis deviation), prominent pulmonary artery on CXR
* Nutritional deficiencies in **repeat bariatric surgery patients**:
* B12, iron, calcium, folate deficiencies
* Severe vitamin deficiencies can lead to acute postgastric reduction surgery neuropathy (APGARS)
* APGARS → S/S:
* protracted N&V
* hyporeflexia
* muscle weakness
* → careful dosing of NMB if s/s present
* Chronic vitamin K deficiency – coagulation studies
* Pre-medications:
* Anxiolysis- small doses (bc lead to resp depression)
* Tx as full stomach → aspiration pneumonitis precautions
* Ex: H1/2, nonparticulate, reglan
* IM injections unreliable – thickness overlying adipose tissue
* DVT prophylaxis
* Morbid obesity is a major independent risk factor for sudden death from PE. SQ heparin 5000u before surgery and repeated Q8-12hours, early mobilization
* OSA/OHS increased risk difficult airway – pre-op ABG
* **Airway assessment = neck circumference most important factor!**
27
Positioning considerations in obese patients
* Regular OR tables max weight ~ 200kg
* Newer tables can hold up to 300-455 kg, with greater width or side accessories
* High incidence of pressure sores and nerve injuries in this group
* A documented association between ulnar neuropathy and increasing BMI – 33% incidence of ulnar neuropathy in patients with a BMI of \> or + 38kg/m2 compared with 1% control group
* “Stacking” or ramped position for intubation to align ear with sternum
* **Supine-** decreased FRC, oxygenation, and ICV/aorta compression
* **Reverse Trendelenburg-** longest safe apnea period VS decreased cardiac output
* **Prone-** – free abdomen essential, increased intra-abdominal pressure
* **Lateral Decubitus-** better than supine if possible – improved diaphragmatic excursion.
28
What are some considerations of monitoring in the obese patient?
* Monitors – appropriate sized BP cuff
* Cuffs with bladders that encircle a minimum of 75% of the upper arm circumference or preferably the entire arm should be used. Forearm measurements with a standard cuff overestimate both SBP and DBP in obese patients.
* *remember cuff too small or put on too loose= falsely high BP*
* *cuff too big= falsely low BP*
* IV/arterial line access may be challenging
* Consider CVP or PAP catheter
1. Significant CV or pulmonary disease
2. When large fluid shifts expected
29
Prevention of thromboembolism in obese pt?
* Most mortality in the 30-day perioperative period after bariatric surgery is due to PE (at least 3 X more frequent than anastomotic leak with subsequent sepsis)
* LMW heparin (limit postop pain tx options)
* Pre-op aspirin and subsequent warfarin to INR= 2.3
* Decrease the risk : preoperative exercise, antithrombotic drugs, stocking prophylaxis, nonpolycythemic HCT, increased CO, and early ambulation
30
Induction considerations of obese patient?
* Pre-oxygenation = most important step!
* 30 degree RT position
1. Decreased FRC
2. Increased O2 consumption
3. +/- Higher incidence of difficult airway
* Induction drug dosing altered
* Consider awake intubation with minimal sedative – hypnotics
* RSI? Aspiration concerns
* May need two handed mask – extra help!
* Breath sounds difficult → Diff confirming ETT placement to hear
* PEEP 10 cm H20 can be helpful intra-op (if BP tolerates…)
31
Emergence of obese patient?
* Respiratory failure # 1 problem
* **Prompt extubation**
* fully awake
* NMB fully reversed
* adequate MV confirmed
* Semirecumbent position with 100% O2
* CPAP and Bi-PAP to combat post-operative atelectasis/ airway obstruction
* Analgesia to promote pulmonary toilet
* But caution
* Pulse oximetry and arterial blood gas monitoring often indicated
32
Regional anesthesia in obese patient
* Avoidance of intubation challenges VS technically challenging landmark identification
* Central neuraxial blockade easier in the lumbar region
* Longer needles may be required
* Ultrasound and fluoroscopy have been used to place catheter in epidural space
* **Local anesthetic doses reduced 20-25% in obese patients**
* epidural vascular engorgement and fatty infiltrates decrease volume of epidural space\*
* Subarachnoid block height can be **unpredictable** – **high** spinal possible
* **Hypotension** common in this population IVC compression etc.
33
Postop pain control considerations in obesity?
* Epidural anesthesia
* *prevent DVT, improved analgesia, GI motility, decreased O2 consumption, decreased LV stroke work*
* PCA with opioid
* (multi-modal opioid sparing should be attempted)
* Local anesthetic infusion to incision site
* Non-opioid analgesics and adjuvants
* Obesity significant risk factor for postop hypoxemia
* partially remedied by placing the patient in the semirecumbent (rather than the supine) position for 1st 48 - 72 hrs post-op
* Consider monitored bed/ICU + CPAP post-op
* *POD #1, 75% obese pt have PaO2 \<60*
34
ACLS in obese patients?
* Adequate chest compressions difficult
* may need mechanical compression device
* Use 400 joules of energy on defibrillator and be prepared to complete several attempts to overcome higher transthroacic impedence
* LMA and Combitube useful emergency supraglottic airway devices
