Test 2 Flashcards
Stats for Geriatric Population in 2003, 2030, and 2050:
-By 2030, 20% of US will be >65 y/o
-By 2050, 2 billion ppl worldwide will be >60 y/o
-Compare to 2003: 12% US was >65 y/o
What % of hospitalizations do old ppl make up?
-1/3 of hospitalizations
-44% of hospital charges
-2-3x more surgeries
-longer hospitalizations
Memory Decline and Aging:
-present in 40% of ppl >60 y/o
-not inevitable, can be slowed by things like working out, reading, family connection, etc.
Brain Structure and Aging:
-cerebral atrophy
-decreased gray matter
-neuronal shrinkage (not much actual loss of neurons)
-decreased white matter
-INCREASE in ventricular size
-progressive loss of memory, imbalance and mobility
True or false: there is a decrease in glutamate.
-False! There is no change in glutamate.
-may be some decrease in NTM like dopamine, Ach, norepi, and serotonin based on animal studies
Why is EEG unchanged in old ppl?
-CRMO2 and CBF decrease in parallel fashion so the EEG remains unchanged
Neuraxial changes with aging:
^^Things that decrease LA dose
-decreased epidural space
-increased permeability of dura
-decreased volume of CSF
-decreased diameter/number of myelinated fibers in dorsal and ventral nerve roots
Peripheral Nervous System changes with aging:
-Inter-Schwann cell distance decreased
-Conduction velocity decreased due to reduction in myelination across the nerve fibers
-so, elderly more susceptible to neuraxial blocks and peripheral nerve blocks
Heart changes with aging:
-decreased number of myocytes
-LV wall thickens
-SA node cells decrease
-conduction velocity decreases
-thickened and calcified aortic valve
-decreased contractility
-increased ventricular stiffness-HIGHER LV filling pressures
What are the implications of their being less beta-adrenergic sensitivity in the elderly?
-decreased maximal heart rate and EF during stress…more prone to decompensation during these periods and with neuraxial anesthesia
-so HR doesn’t spike up as much in times of need to aid in maintaining adequate CO
Cardiac Vessel changes with aging:
-vascular stiffness
-breakdown of collagen and elastin
-less endogenous NO (less vasodilation of coronaries)
-early wave deflection-increased afterload along with diastolic dysfunction
Pulmonary: Structural changes with aging:
-LOSS of ER and Surfactant
-increased lung compliance (think COPD)
-enlarged bronchioles and alveolar ducts
What does the early collapse of small airways during exhalation for elderly cause?
-increased anatomic dead space
-increased closing capacity
-impaired gas exchange
-lower baseline sats, increased arterial CO2
What does the loss of vertebral height and calcification of vertebra and intercostal cartilage in the elderly cause?
-barrel chest
-diaphragmatic flattening
chest wall stiffness…increased work of breathing-contribute to dyspnea on exertion
Pulmonary: functional changes with aging:
-decreased vital capacity
-increased closing capacity
-increased residual volume
-TLC stays the same due to compensation
-decreased muscle mass and increased closing capacity
-weaker pharyngeal muscles
How much does FEV1 decrease per decade?
-decreases by 6-8% per decade
What is closing capacity again?
Combination of closing volume and RV
What are the implications of the elderly having weaker pharyngeal muscles?
-decreased clearance of secretions
-less efficient coughing
-decreased esophageal motility
-less protective upper airway reflexes
ASPIRATION RISK
VQ mismatch with aging:
-gap between FRC and closing capacity WIDENS
-FRC increases slightly, but CC increases much more
-this is the MOST important MOA for alveolar-arterial oxygen gradient mismatch
-shunt increases and arterial oxygenation declines
Renal changes with aging:
-GFR decreases (10 per decade)
-blunted responses to ALDO, vasopressin, and renin
-urinary retention and UTIs become more common
GI and Hepatic changes with aging:
-liver function declines
-drugs cleared via phase 1 are not ok: oxidation, hydrolysis via CYP450, reduction
-drugs cleared via phase 2 are ok: acetylation and conjugation
-LESS PONV!! so, avoid drugs like prochlorperazine, promethazine, and metoclopramide (not needed)
MSK changes with aging:
-muscle mass and strength declines
-subcutaneous fat thins
-impaired wound healing
-osteoarthritis
Thermoregulation changes with aging:
-temp is comparable in infants, children, and adults
-1 degree less for adults 60-80 y/o
Studies on old age and surgery risk:
-Denney/Denson: high mortality rate with pts 90 y/o and up
-Djokovi/Hedley-Whyte: ASA status predicted mortality
-Del Guercio/Cohn: uncorrected comorbidity in SICU: 100% mortality
-Finlayson: high mortality from nursing home residents
Significant Predictors of 6 month-1 year mortality:
-impaired cognition
-recent fall
-hypoalbuminemia
-anemia
-functional dependence
-comorbidities
Vulnerable brain chart:
-vulnerable brain (elderly) have a dysfunctional anti-inflammatory response and can have exaggerated neuro-inflammation and acceleration of AD pathology, leading to Long-term cognitive decline
What does POCD stand for?
-Post-operative Cognitive Dysfunction
-can last months to years after surgery, or be indefinite
What are neurotoxicity factors?
List examples.
-factors that play a role in the pathogenesis of dementia-vulnerable brains
-Amyloid, Tau, Calcium, and Neuroinflammation factors
Tell me about amyloid:
-fragment of synaptic origin-so develop when synapses break down
-unknown function, but accumulates extracellularly to form PLAQUES
-these can aggregate but can also be eliminated
-may disrupt cell membranes over time
How might amyloids affect anesthesia?
-first studied in halothane and mice
-with amyloid plaque build up, the older mice have accelerated onset of alzheimers disease and dementia
Tell me about Tau:
-a protein
-neurofibrillary tangle (NFT)
-Phosphorylated and aggregated Tau protein
-DESTABILIZES microtubules
-decreases in temp of 2-3 degrees C INCREASES amount of Tau (Taupathy)
How do repeated exposures to Halothane, Isoflurane, and Sevoflurane affect Tau levels?
-Increased phosphorylated Tau
-can then aggregate into plaques and destabilize microtubules
-More Tau, more dementia
What’s the idea behind Dantrolene treating neurotoxicity?
-It could decrease calcium release b/c CCB, but doesn’t cross BBB so cant mitigate neurotoxicity
-significant skeletal muscle weakness with this drug
How does neuroinflammation contribute to cognitive decline?
What drugs do we give that could modulate this?
-through release of inflammatory factors like cytokines, IL-6, and TNFa
-Dexamethasone, lidocaine, and Toradol
They gave 3 drugs that can alter CNS and ordered them based on how much they can cause cognitive decline. What were they and what was the order?
-Isoflurane > Desflurane > Propofol
-so propofol is LEAST associated with cognitive decline
-may be reason we TIVA elderly patients
Bedford 1955 Study:
-out of 1193 patients >50 years old receiving GETA, 10% have mental deterioration (long-term or permanent)
International Study of Postoperative Cognitive Dysfunction:
-1998
-non-cardiac patients >59 years old
-POCD in these pts
-22% higher at 1 week
-7% higher at 3 months
-p value 0.04% :)
-risk factors: increasing age, duration of anesthesia, lesser education (lower SEC), second operation, post op infection, respiratory complications
True or false: surgery by itself can cause short term decline
-true!
-anesthesia alone is also causative so surgery is additive to it
-remember that pts have unknown vulnerabilities person to person
What are the issues with studies of anesthesia and surgery?
-underpowered
-poorly designed
-controversial
What would be ideal for studies looking at anesthesia and surgery?
-long, longitudinal surgeries
-biomarkers…CSF
-imaging like PET scans
Anesthesia implicants for cognitive decline and elderly:
-use neuraxial/regional when I can to avoid drugs affecting CNS
-avoid long-acting NMBD and REVERSE completely!! (sugammadex DOC)
-opioid sparing strategies
-neutralize stomach acid with non-particulates
-EEG based titration (BIS)
-avoid hypotension
-pad skin and nerves
Drug challenges in elderly related to the ehart:
-decreased CO and increase in circulatory time-takes longer for things to set in
-slower distribution to initial site of action
-slower redistribution
-slower distribution to metabolic organs: kdineys and liver
Drug challenges to NMJ in elderly:
-increased distance b/w axon and motor end plate
-decreased concentration of ACh receptors, amount of ACh in presynaptic vesicle, and release of ACh upon neuronal impulse
What’s true for elderly patients if drugs are kidney/liver dependent for metabolism?
-prolongation of effect, decreased need for redosing during maintenance phase, delayed recovery phase for non-depolarizers (ROC)
Whats true in ther elderly pop if drugs are NOT kdiney/liver dependent for metabolism?
-no prolonged effect, same requirements during maintenance, no delay in recovery phase (think Nimbex good for elderly)
Pulmonary resection in elderly:
-mortality in 80-92 year olds: 3%
-respiratory complications: 40% (2x younger ppl)
-cardiac complications: 40% (3x younger ppl)
-lobectomy mortality is not as bad, and less invasive techniques
-pneumonectomy mortality is excessive
Algorithm for Preoperative Assessment: Thoracic (non-cardiac) surgery:
exercise tolerance affects decision
-TTE can be done to rule out pulmonary HTN
Predictive Postoperative FEV1:
-predictor of postop outcomes
-there are 42 lung segments total, 20 on left and 22 on right side
-ppoFEV1= PreopFEV1% x (1-%lung tissue removed/100)
-ex: if preopFEV1 was 70% and RLL removed:
-70 x (1-(.29)/100))=50%
Triad of Pre-op Assessment:
-3 legged stool of pre-thoracotomy
-We want VO2 max >15 mL/kg/min
-PaO2 >60
-PaCO2 <45
Post-thoracotomy Anesthesia Management:
-FEV1 values let you know when to extubate
-<30%, don’t extubate yet!
Types of surgical site infections:
-Superficial incisional: just in incisional area
-Deep incisional: beneath the incision area in muscles and tissues surrounding the muscle
-organ or space: any area other than skin muscle: includes organs or space b/w organs
