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oldies adv prin1

QuestionAnswer
how many people over the age of 65 37 million and counting
if you make it to 65 you live on average 18.4 years 20 for females 18 for males
aging is viewed as what and not what physiological and not chronologic
is there a definition for geriatic? no
cellular aging has to do with apoptosis, DNA and RNA replication errors, cellular demise
30 year old vs 70 year old younger person has ten times the the reserve, and older a 40 percent decrease in organ function
geriatric and pediatric everything is decreased in both. lung, arterial tension, cough, renal, hypothermia both population have less compensetory mechs
blood volume in elderely 20-30 percent less
fat in oldies fat increases
contracted state of vasculature give rise to higher inital plasma concentration of anesthetic drug
increases body fat means what lipid solubale drugs stick around longer
thermoregulations and oldies hypothermia begins sooner, decreased BMR, high surface area to body mass
temps of shivering for young and old 36 for young, 35 for old
shivering and oxygen demand 400% increase in demand, acidosis, cardiovascular demise, protein catabolism
most common dysfunction in oldies diastolic dysfunction. eval with echo
max heart rate decreases how as you get old decrease one beat per min per year after 50
most cardiac issues are due to what changes conduction issues due to fibrosis
what is pathological change in cardiovascular and what is not atherosclerosis is pathological, arteriolsclerosis is not.
what causes decreased resting heart rate increase vagal tone and less sensative to adrenergic resting rate
SA node fibrosis causes dysrythmia,
systolic funtion in a healthy patient healthy pt should be ok regardless of age
if afterload increases due to what what happens due to stiff arteries can develop cardiomyapathy
what is the most common dysfunction diastolic dysfunction evaluated by color flow echocardiogram
cardiac functions declines by how much and so what 50% between 20 and 80 and increased circ time, slow iv induction, smaller reserve. faster gas induction
in an oldie to increases Cardiac output what makes this happen increase in end diastolic volume and not so much for heart rate
more prone to what if sudden increase in intravascular volume more prone to chf
so CO is lower then why HTN due to poor vessel compliance
why does diastolic dysfunction happen CAD, cardiomyopathy, aortic stenosis, systemic HTN
atrial kick is how much of the LVEDV 20% and even more important with stiff vessels
lost of artrial kick from what can cause what afib or nodal rhythm may cause hypotension
oldies are diminishes responses to catecholamines so what normally Ca ion transport improves cardiac function, this is less responsive in older generations
lungs and geri less elastic, gas exchange diminished by 15 percent by 70, Pa02 drops from 90-100 as the norm, alveolar mem thickens, can even have V/Q mismatch without disease
forced expiratory volune 1second FEV1 and FVC decrease due to loss of elastic tissue,
alveoli remain more distended at rest and less likely to fully exapand on inspiration
closing volume the volume that the small airway colapse increases, ie air trapping
under anesthesia closing capacity is greater than FRC so what more small airway close, more vent to reduces perfusion, ie atelectasis in dependent lung.
as you get old, you shrink by 70 how much lung capacity due to physical changes has declined 10%
as you get old you chest stiffen goes up and anterior, increase in AP diametere and restrict chest expansion
resting PaO2 PaO2=100-(0.4xage)
if given PCO2 how do you find PaO2 PaO2=150mmHg-PCO2/0.8
what happens to PaO2 by 30 decreases 5mmHg and 5 every 10 years ie old people hypoxia and hypercarbia much more quickly
alveolar to arterial gradient increases normally 8 to 65. the larger the gradient the more serious the diffusion defect
A-a gradient equals (age+10)/4 is equal to A-a gradient
airway reflex deminished ie risk of aspiration, loss of laryngeal and pharygeal response
how much of your brain did you lose 30% by 80, nueron density is decreased, CBF decreased, transmitter and receptor decreaed.
post op delerium vs impairment delerium is transient 1-3 days, can use haldol. dysfunction is decrease cognitive performance-need neurologist
need less MAC for oldies true
cognitive impairment is also attributed to how much you use and continue to use your brain.
renal and aged GFR down 8% every decade up to 50% by 65 for renal blood flow. CO down so renal down.
renal and CO decrease make the aged more susceptible to fluid overload
NDMBA metabolism and excretion reduced. can result in prolonged anesthesia
endocrine and aged impaired ability to metabolize insulin, frequent glucose
pharmacokintetic consideration of oldies vascular volume, protein binding, less lean body mass, metablism impaired so is elimination all can affect anesthesia
initial plasma of drug in oldies higher
reduced plasma protein means higher free drug in body. so is the fat so more stored.
pharmacodynamics and oldies less brain mass, blood flow, ie MAC drops 4% per decade after age 40
how much propfol you need for oldie half the amount for regular
renal elimination of NMBD impaired and longer block, except for cisatriacuruium hauffman, succs longer in men than woman.
ACE inhibitor are held before surgery SURE for the TEST yes for real life apparently NOT. hypotension, refractory and need great amount of volume to fix
preop ask about patients eyedrops, antihypertensive and cardiac meds should be continued the day of but NOT ACE and diuretics.
versed and oldies result in confusion agitation, hlaf life 6 hours and 2 in younger. can cause post op cog dysf in oldies
oral antacids have ups and down what about monitoring all non invasive are a good idea, and invasive has shown to reduce morbidity and mortality when for BIG surgeries
anesthetic management be careful, short acting, benzo spareingly, dont want post op cog dys, MAC REGIONAL AND GEN are ALL acceptable case by case.
oldies need what TLC start low go slow...reorient, thermoregulation, maintain airway, maintain VQ
abnormal expiratory flow that does not change over months COPD
physiologic event that shunts blood away from less oxygenate part of lung during anesthesia hypoxic pulmonary vasoconstriction
pulses paradoxis is common in copd true
asthma represents it self as hyper irritable airway, bronchoconstriction, treated with B2 agonist, steroid and humid
eosinophillic inflamation and broncho constriction is asthma
abnormal permanant enlargement of air space, disruption of alveoli without fibrosis COPD
another term for COPD COLD
cyclogeanse inhibition promostes increase in leukotriene via arachidonic acid pathway, this causes aspirin induced asthma so no Toradol either
a form of emphysema, air containing spaces greater than 1cm result from lung tissue destruction Bullae
Blebs are not form of emphesyma, because blebs have no involvement with alveoli true
obstructive disease ie no fibrosis
expiraroty flow abnormal, no fibrosis, enlargement of air spaces obstructive
COPD = emphysema with chronic bronchitis AKA COPD aka COLD
emphysema effects 20 million americans, kills 60k
predominant feature of emphysema progressive airflow obstruction, ie DECREASED forced expirartory volume in one second FEV1.
cause of obtstructive small bronchial lumen, increase in collapsibilty of walls, loss of elastic recoil of lung
COPD and COLD used interchangable emphysema and bronchitis
cause of emphysema protease and anti-protease imbalance ie alpha 1 antitrypsin defecency, oxidant burden from smoke and all chem classes, hyperplasia of mucus glands ie goblets too much mucus
exhale and COPD need more positive pressure
COPD and right side return reduces it, pulses paradoxis see in 2/3 of COPDers, increase in lung volume decreases venous return
COPD and circulation HR increases, CO increases due to catecholamines, renal GFR reduced, renal plasma flow decrased
what is pulses parodoxis 10 point drop in sys bp during inspiratioin
FEV1 and FVC decrease on spirometry is charateristic of COPD, less than 70-80% can be ALSO restrictive lung disease
obstructive disease has decrease in FEV1 and FVC but also increase in reserve volume and in crease in FRC
how to differentiate between obstructive and restrictive look at reseves if high its obstructive, cant let air out
ABG and COPD ie pink puffers vs blue bloaters pink PaO2 greater than 60 and PCO2 is normal. have emphysema. blue bloaters are PaO2 less than 60 and PCO2 greater than 45 and have cor pulmonale, bronchitic.
cynaosis is present in blood if 5g of deoxygenated blood is present
xray and obstruction hyperinflation flat diapharm evidence of bullae, hyperlucency ie decrease tissue density. all suggestive of COPD
chronic bronchitis is best found how XRAY
pre op eval with COPD severity, clear secretions, treat infections ,dialate, if PaCO2 is less than 60 give O2, or if cor pulmonale or HCT greater than 55%
what is cor pulmonale right sided heart failure
normal FEV1 is 5L if less than 1.5 then do ABG, give treatment, recheck.
continous FEV1 around 1.5L may be indicative of CAD and Cor pulmonale and increased mortality
what is FVC forced vital capacity ie how much can you blow after exhale.
what is FEV1 forced expiratory volume in one second ie how much can you blow out in one second
ratio of FEV1 / FVC in healthy person should be 80%
PEF peak expiratory flow ie speed of air moving out of your lungs begining of the expiration, measured in liter per second 200 to 500
closing capacity= closing volume + residual volume
closing volume at the point which dynamic compression of airways begins
factor that affect closing volume age, smoking, lung disease, body position
residual volume air remaining in the lungs following VC breath
preop evaltuation hypercarbia can not be corrected too quickly. sudden decrease in PCO2 may result in alkalosis, kidney need time to excrete excess bicarb
what controls broncho constrictions parasympathetic
anesthesia can be given to COPDers extubation is a concern true
any block above T6 is not recommended
VAA and COPD bronchial dilitation, slow cillia,
give less than 100% to COPD why absorptive atelectasis, provide intermittent vital capaticy maneuvers ie valsalvo
in presence of bullae what is contraindicated N2O
remember bullae are emphesemic changes
Blebs are NOT emphesymic and are out side of the lung
GA and COPD careful with PEEP, only 5cmH2O, expiration should be prolonged in order to decrease intrinsic peep. ie no breath stacking
arterial hypoxemia represent a very advanced stage of the disease manifested by pulmonary vsoconstriction ie late sign
COPD vs Asthma asthma is characterized by eosinophilic response, inflamation of airway except for lung parenchyma.
COPD vs asthma copd is COPD neutrophilic inflamation,parenchymal destruction, and irreversible ie dynamic compression. steroids will not really help in COPD like they do in asthma.
COPD and lung connective tissue destruction of connective tissue and collapse of airways, exchange of CO2 and O2 between blood and alevoli impeded
COPD and lung compliance lung becomes more compliant BUT shorter quicker breaths, less force. diaphram ineffective
COPD and intercostal muscles thorax is misaligned used of accessory muscle is used, and assume the position of comfort, ie tripod
COPD with asthma attach the inflimation of COPD allows foreign bodies to enter lung causing the asthma attack
REVIEW of asthma and COPD COPD not reversible, asthama is. ABG good idea for long abdom cases or chest. CO2 measurements help vent cause increased dead space widens the normal arterial venous ETCO2 gradient
intra op COPD reminder these pts have cardiac dysfunction, CVP with pulmonary HTN is reflective of RV rather than intravascular volume
early extubation of COPD case by case, FEV1 less than 50% need post op vent
in a PFT if effort is low and reserves or capacity are high chances are is a obstructive disease
what is a good predictor of small airway disease FEF ie mid expratory force
FEV1 is a good predictor of obsctructive disease
FEF is a good predictor of early small airway disease
emphysema PFT non reverisible obstruction, high lung volumes, low diffusing capacity, and positive smoking history.
chronic bronchitis excessive mucus, at least 3 months of the year for at least 2 successive years, obstructive limits expiratory airflow
Bullae form of emphysema, space greater than 1cm with air, deep elastic layer of visceral pleural avoid N2O
pulm HTN should i give N2O NO
blebs collection of air within the pleura, NOT emphysema, DO NOT involve asinus ie alveoli, cadidate for Pleurodesis ie glue together the two pleura
Pleurodesis ie glue together the two pleura
25% of all COPD have enhanced airway reactivity but muscles thicken and contribute to narrowing, excessive mucus but cillia is impaired.
Asthma chronic inflamation of airway, involves mast cells, neutrophills, eosingophils and T lymphocytes. serotonin can induce asthma
what is a potent broncho constrictor and found to be active in asthmatic respnse serotonin
asthma is stimulated by messing with parasympathetic system
parasympathetic maintains normal bronchial tone, vagal afferent are sensetive to histamine, noxious stimuli cold air and irritants
reflex vagal activation results in bronchoconsctriction caused by cGMP
pousile law talks of flow and diameter
extrinsic asthama or allergic asthma most common in children and young, IgE, infectious, psychological enviromental or physical
intrinsic asthma or idiosyncratic asthma middle age happens without provoking
what is the most common chronic disease of childhood asthma
asthma is a disease of bronchoconstriction, airway inflammation hyper irritability
asthma and inflamation irritant cause cause release of lymphocyte, histamine, mast cells, cytokine
the potent chemical mediatior promost vasoconstriction and what else inscrase smooth muscle tone, enhance mucus production, airway edema, vascular permeability and infamematory cell chemotaxis
cyclooxygenase inhibition can cause increase in leukotrien via arachidonic acid pathyway ie asthma attach. NO NSAIDS, this is not IgE,
ASA asthma is clinically associated with nasal polyps
when prostaglandin production is blocked with NSAIDS then laukotrienes cause over production of LT4 and produce severe allergy like effects.
can alcohol cause ASA asthma? yes
asthma attack and tachypnea causes hypocapnia, but if PaCO2 is norm and or high then resp failure is coming
signs of advanced pulmonary disease pulses paradoxous, EKG change of right vent strain, ST changes, right axis deviation, RBBB
treatment of asthma Beta2 agonist, methyxantheine ie theophyline, glucosteroids, anticholinergics to block muscurinic
how do Beta 2 agonist work for reversal of bronchoconstriction B2 stimulated adenylate cyclase results in formation of cyclic AMP ie bronchial dilatation
name some beta 2 agonist with less beta 1 effects albuterol or terbutaline
how do methylxanthines work theophylline inhibits phsphodiesterase, so no break down of cyclicAMP , blocks histamine, stimulate diaphram and catecholamine stim. narrow therapeutic 10-20mcg/ml
anticholinergic and asthma ipatropium bromide ie atrovent is a good one with no sympathomimetic effect
cimetadine or ranitidine and asthma can cause asthma or severe interaction if pt on theophylline
fix asthma before surgery FEV1 greater than 2-3L, FEV1/FVC should be greater than 70%, PEF 200-500ml, do xray
if high spinal is done and T1-T4 is compromised what happens cardiac accelators and sympathetic innervation is compromised ie parasymp runaway and asthma GLORE!
avoid histamine releasing drugs such as atracurium, mivacurium, demerol, morphine, thiopental,
ketamine good for patient with asthma? yea and no, yea if not on theophylline or else seizure city
VAA and asthma vaa is a bronchodialtator, steal is a constrictor, atropine and glyco can help but cause tachycardia, succs is usually safe even though releases histamine
anesthetic management in asthma vT less than 10ml/kg, prolong IE, treat with beta agonist, disconnect gas sample with giving MDI, 1-2mg/kg hydrocortisone. give glyco then neostyg, consider deep extubation consider lidocaine
restrictive pulmonary diease is interference of inspiration, incrase inward elastic recoil, intrinsic and extrinsic varieties
restrictive and PFT decrase lung volume, FEV1 and FVC reduces, TLV is reduced, HOWEVER FEV1/FVC ratio is NORMAL may have VQ mismatch
intrinsic pulmonary edema, ARDS, infectous pneumonia, aspiration pneumonitis, low lung compliance due to extra vascular lung water
intrinsic pulmonary disorder aka interstitial lung distease characterized by pulmonary fibrosis, insidous onset, chronic progression, pulm fibrosis, gas exchange and vent compromised many causes occupation, envir, autoimmune, O2 toxic
obstructive and restrictive when it comes to residual volume obstructive increased residual volume and restrictive low residual volume
volume related resp disease ie intrinsic restrictive lung sarcoidosis, TB, pnuemonectomy, infectious pneumonia, pulm fibrosis, autoimmune disease
extrinsic restrictive lung may be acute or chronic include: scoliosis, kyphosis, pectus, ankylosing spondylitis,, PL effusion, prego/obese, tumor, ascites, rib fx, pneumothorax
intersitial lung disease with enough damage to air sacs disease is not reverible, impaired blood flow in lungs, causes SOB
Sarcoidosis interstitial lung disease, multisys disorder, lungs skins and eyes. normal elastic tissue stiffens, looks like honeycomb, cause unknown
acid base balance with resp issues VAA are converted to carbonic acid and exhaled at rate of 24kmeg per day, non VAA acids are excreted via kidney 50meq
ABG norms ph 7.35-7.45, PaCO2 35-45, HCO3 25,
DO NOT treat resp acidosis with bicarb why bicarb becomes more carbon dioxide makes acidosis worse.
total body bicarb deficit=base deficit and correction of _____is indicated not total correction. correction of 1/2
acidemia in renal pts use dialysis
correct hypoxemia via incrase FIO2, PEEP, correct other resp issues ie suction, correct atelectasis etc...
Created by: Rooz