Geriatrics Flashcards
What % of the population is over 65 in 2030 and 2050
By 2030, 20% of US > 65 y/o
By 2050, 2 billion people worldwide over 60 y/o
What is aging (4)
Universal and progressive physiologic process
Decreasing end-organ reserve
Decreased functional capacity
Increased homeostatic imbalance
Increasing incidence of pathophysiologic processes
Memory and aging
Memory decline
40% of people > 60 y/o have some sort of memory decline
Not inevitable
Relates to ability to complete ADL’s
NS structure changes with aging
Cerebral atrophy; brain size shrinks. White matter shrinks more than gray matter. Don’t loose neurons but we lose functioning
Decrease grey matter;
Neuronal shrinkage (only a small neuron loss)
Decrease white matter;
Increases in ventricular size between the atrophy and decreases in gray/white matter leads to-> Progressive loss of memory, balance, mobility
NS and aging changes with nerve transmission
of synapses or amount of neurotransmitters decrease/ don’t work aswell because in decrease in number of synapses or a decrease in nt release or decrease amount built.
Animal studies;
Significant decrease in Dopamine, Ach, norepi and serotonin (all not)
No change in glutamate
Coupling of CMRO2, CBF, EEG unchanged
Neuraxial changes with Aging
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
Elderly more sensitive to Neuraxial blocks and Peripheral nerve blocks
Cardiac changes with aging (8)
Myocyte number decreases
LV wall thickens
SA node cells decrease
Conduction velocity decrease
Thickened and calcific aortic valve
Decreased contractility
Increased ventricular stiffness…higher filling pressure
Less Beta-adrenergic sensitivity
Tachy/brady syndrome
SA node cells decrease; don’t have as regular rhythm= more susceptible to a fib or brady tachy syndrome where the SA node doesntk now how to be regular so it speeds up and then slows down; put on Beta blocker to keep tachycardia at bay and they will have a pacemaker inserted for safety baselin.
Response of decrease beta adrenergic sensitivity
↓ maximal heart rate and ejection fraction during stress= decreased max rate
Vessel changes with aging
Vascular stiffness;
Due to Breakdown of collagen and elastin
Less NO related vasodilation; cant stretch and bound back
Early wave deflection…increased afterload, diastolic dysfunction
What is early wave deflection
As stroke volume is ejected = have arterial wave to periphery and to return back to the heart because of increased afterload it causes some diastolic dysfunction = stiff vessels that cant relax and we get the wave deflected back to the heart.
Pulmonary-Structural chagnes with aging
Loss of elastic recoil and loss of surfactant
Enlarged bronchioles and alveolar ducts
Early collapse of small airways during exhalation
Loss of vertebral height and calcification of vertebra
Loss of elastic recoil and loss of surfactant results in ……
Increased lung compliance
Enlarged bronchioles and alveolar ducts
Early collapse of small airways during exhalation causes……(3)
Increased anatomic dead space
Increased closing capacity
Impaired gas exchange
Loss of vertebral height and calcification of vertebra results in…..
Barrel chest
Diaphragmatic flattening
Chest wall stiffness….increased work of breathing
Changes to pulmonary function with aging
Decrease fev 1 by……
total lung capacity about the same
↓ vital capacity
↑ closing capacity
↑ residual volume
Decrease muscle mass and ↑ closing capacity
Decrease FEV1 by 6-8% per decade
Weaker pharyngeal muscles
Weaker pharyngeal muscles results in …….. (4)
Decreased clearance of secretions
Less efficient coughing
Decreased esophageal motility
Less protective upper airway reflexes
VQ matching with aging
Relationship between FRC and closing capacity;
Mismatch increases
Most important MOA for alveolar-arterial oxygen gradient
Shunt increases , arterial oxygenation declines
Renal changes with aging
GFR decreases;
Comorbidities may exacerbate. less IVP dye excretion
Blunted responses to aldosterone, vasopressin, renin;
Trouble adjusting Fluid &Electrolyte
Retention and UTI’s more common; difficult to contract because of decreased muscle
GI and Hepatic changes with aging
Liver function declines
Less PONV!
Avoid prochlorperazine, promethazine, metoclopramide (because of increased sensitivity to side effects)
What medications are okay and not okay for an aged liver
drugs that have Phase I metabolism are not OK… (oxidation, reduction, hydrolysis via CYP450)
drugs that use Phase II metabolism are OK…(acetylation and conjugation)
muscloskeletal changes with aging (4)
Muscle mass and strength declines
Subcutaneous fat thins
Impaired wound healing
Osteoarthritis
Thermoregulation changes with aging
Vasoconstriction threshold
Comparable in infants, children, adults/ elderly are likely to be 1 degree C less for adults 60-80 y/o
Operative risks with elderly
Ideas;
high mortality 90 y/o and up
ASA status predicted mortality (>4)
uncorrectable comorbidity in SICU; 100% mortality
high mortality from nursing home residents
Significant Predictors of 6 month-1 year Mortality (6)
Impaired cognition
Recent fall
Hypoalbuminemia
Anemia
Functional dependence
Comorbidities
surgery and anesthesia on vulnerable brain
Surgery and anesthesia causes peripheral inflammatory response crosses BBB and results in neuro inflammatory response = release of pro inflammatory mediators and in normal and healthy brain; the body takes care of the TNF/ WBC/ Interleukin and may have short term cognitive decline and may not be as sharp for a few days but you get over it and go back to normal.
If we have a neuroinflammatory releases of mediators to a vulnerable brain then that causes a greater anti inflammatory response / greater release of the mediators and the body cant recover from = long term cognitive decline.
Neurotoxicity Factors
Amyloid β
Tau
Calcium
Neuroinflammation (TNF, interleukin)
Anesthesia and Amyloid β
First studied with Halothane/mice
Significant increases in amyloid plaque
Young mice had improvement in learning/memory
Old mice accelerated onset of AD
… unclear translation to humans; other factors clearly involved
Amyloid-β
Fragment of synaptic origin
Unknown function
Accumulates extracellularly to form plaques
Originally thought to be toxic
Now? Less so…labile…aggregate then eliminated
Plaques May disrupt cell membranes over time
Tau
Neurofibrillary tangle (NFT);
Phosphorylated and aggregated 𝜏 protein
Destabilizes microtubules; Tau can be aggregated to large chunks that destabilizes microtubules in the cells so they don’t function as well.
Decreases in temperature 2-3 degrees C increases amount of 𝜏
(tauopathy)
Repeated exposure to Halothane, Isoflurane, Sevoflurane;
Increased phosphorylated 𝜏
Relationship of Amyloid and Tau to Symptoms
Both increase cognitive impairment the more accumulation you have
Calcium Release and Anesthesia and dantrolene
Exaggerated release from endoplasmic reticulum; Specifically ryanodine and IP3 receptors
Volatile anesthetics; known to cause malignant hyperpyrexia
Less dramatic release causing neurotoxicity???
Inhibition of release delay/decrease neurotoxicity???
Dantrolene;
Doesn’t cross BBB; so wont treat neurotoxicity/ confusion
Significant skeletal muscle weakness
Neuroinflammation mediators and modulators
Contributes to cognitive decline Through release of inflammatory factors
Cytokines
IL-6
TNF⍺
some Anesthesia drugs capable of modulating inflammation; dexamethasone, lidocaine, toradol
Anesthesia and the brain
General anesthetics alter cognitive state While they are in CNS
Alteration outlasts surgery
Depends on drug, duration of exposure and magnitude of exposure;
causes of cognitive decline;
Isoflurane > Desflurane > Propofol
Risk factors for cognitive decline with anesthesia
Increasing age,
duration of anesthesia, lesser education,
a second operation,
postoperative infection and
respiratory complications….
Anesthesia Implications for elderly (7)
- Using neuraxial/regional anesthesia when possible
- Avoid long-acting NMBD and reverse adequately
- Opioid sparing strategies
- Neutralization of stomach acid with non-particulants
- Consider using EEG based titration
- Avoid hypotension
- Pad skin and nerves
Goal Bis for elderly
60
Drug Challenges r/t Heart in the elderly
⬇️ Cardiac Output;
slower distribution to initial site of action
slower redistribution
slower distribution to metabolic organs
Drug Challenges r/t Neuromuscular Junction in elderly
⬆️ distance between axon and motor end plate
⬇️ concentration of Ach receptors
⬇️ amount of Ach in presynaptic vesicle
⬇️ release of Ach upon neuronal impulse
Kidney/Liver Dependent Metabolism vs Not
Kidney/Liver dependent metabolism drugs causes;
Prolongation of effect
Decreased need during maintenance phase
Delayed recovery phase for non-depolarizers
Not kidney/liver dependent causes;
No significant prolongation of effect
Essentially same requirements during maintenance
Essentially no delay in recovery phase
Pulmonary Resection in elderly mortality rate
Mortality 80-92 y/o 3%
Lobectomy mortality acceptable
Pneumonectomy mortality excessive
Pulmonary resection and respiratory and cardiac complications in elderly compared to younger pop
Respiratory complications 40% (2x younger pop.)
Cardiac complications 40% (3x younger pop.)
Predicted Postoperative FEV1 with lung resection
ppoFEV1 = Preop FEV1 % x (1-% lung tissue removed/100)
R lung and L llung segments (42)
R; 6,4,12
L; 10, 10
Algorithm for Preoperative Assessment:Thoracic (non-cardiac) Surgery
Tee to rule out Pulm htn-> exercise tolerance?-> perfusion scan? Echo? Coronary angiography
Three legged stool of prethoractomy respiratory assessment
Respiraotry mechanics; FEV1 (ppo >40%)
MVV, RV/TLC, FVC
Cardiopulmonary reserve;
VO2max (>15 ml/kg/min)
Stair climb > two flights, 6 min walk.
Exercise SpOx <4%
Lung parenchymal function;
DLCO
(PPO >40%)
PaO2 >60
PaCo2<45
PPO FEV1 >40% post thoracotomy
Extubate in OR if pt awake alert, warm and comfortable
PPO FEV1 30-40% post thoracotomy
Consider extubation beased on;
exercise tolerance
DLCO
VQ scan
Associated dz
PPO FEV1 <30% post thoracotomy
staged weaning for mech, ventilation consider extubation if >20% plus; thoracic epidural analgesia
What is Postoperative Cognitive Dysfunction (POCD)?
An objectively measured decline in cognitive function that persists beyond the period expected
