oldies adv prin1
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| how many people over the age of 65 | 37 million and counting
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| if you make it to 65 you live on average | 18.4 years 20 for females 18 for males
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| aging is viewed as what and not what | physiological and not chronologic
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| is there a definition for geriatic? | no
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| cellular aging has to do with | apoptosis, DNA and RNA replication errors, cellular demise
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| 30 year old vs 70 year old | younger person has ten times the the reserve, and older a 40 percent decrease in organ function
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| geriatric and pediatric | everything is decreased in both. lung, arterial tension, cough, renal, hypothermia both population have less compensetory mechs
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| blood volume in elderely | 20-30 percent less
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| fat in oldies | fat increases
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| contracted state of vasculature give rise to | higher inital plasma concentration of anesthetic drug
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| increases body fat means what | lipid solubale drugs stick around longer
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| thermoregulations and oldies | hypothermia begins sooner, decreased BMR, high surface area to body mass
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| temps of shivering for young and old | 36 for young, 35 for old
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| shivering and oxygen demand | 400% increase in demand, acidosis, cardiovascular demise, protein catabolism
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| most common dysfunction in oldies | diastolic dysfunction. eval with echo
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| max heart rate decreases how as you get old | decrease one beat per min per year after 50
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| most cardiac issues are due to what changes | conduction issues due to fibrosis
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| what is pathological change in cardiovascular and what is not | atherosclerosis is pathological, arteriolsclerosis is not.
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| what causes decreased resting heart rate | increase vagal tone and less sensative to adrenergic resting rate
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| SA node fibrosis causes | dysrythmia,
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| systolic funtion in a healthy patient | healthy pt should be ok regardless of age
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| if afterload increases due to what what happens | due to stiff arteries can develop cardiomyapathy
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| what is the most common dysfunction | diastolic dysfunction evaluated by color flow echocardiogram
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| 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
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| in an oldie to increases Cardiac output what makes this happen | increase in end diastolic volume and not so much for heart rate
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| more prone to what if sudden increase in intravascular volume | more prone to chf
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| so CO is lower then why HTN | due to poor vessel compliance
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| why does diastolic dysfunction happen | CAD, cardiomyopathy, aortic stenosis, systemic HTN
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| atrial kick is how much of the LVEDV | 20% and even more important with stiff vessels
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| lost of artrial kick from what can cause what | afib or nodal rhythm may cause hypotension
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| oldies are diminishes responses to catecholamines so what | normally Ca ion transport improves cardiac function, this is less responsive in older generations
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| 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
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| forced expiratory volune 1second FEV1 and FVC decrease due | to loss of elastic tissue,
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| alveoli remain more distended at rest and less likely to fully exapand on | inspiration
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| closing volume | the volume that the small airway colapse increases, ie air trapping
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| under anesthesia closing capacity is greater than FRC so what | more small airway close, more vent to reduces perfusion, ie atelectasis in dependent lung.
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| as you get old, you shrink by 70 how much lung capacity due to physical changes has declined | 10%
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| as you get old you chest | stiffen goes up and anterior, increase in AP diametere and restrict chest expansion
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| resting PaO2 | PaO2=100-(0.4xage)
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| if given PCO2 how do you find PaO2 | PaO2=150mmHg-PCO2/0.8
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| what happens to PaO2 by 30 | decreases 5mmHg and 5 every 10 years ie old people hypoxia and hypercarbia much more quickly
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| alveolar to arterial gradient increases | normally 8 to 65. the larger the gradient the more serious the diffusion defect
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| A-a gradient equals | (age+10)/4 is equal to A-a gradient
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| airway reflex deminished ie | risk of aspiration, loss of laryngeal and pharygeal response
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| how much of your brain did you lose | 30% by 80, nueron density is decreased, CBF decreased, transmitter and receptor decreaed.
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| post op delerium vs impairment | delerium is transient 1-3 days, can use haldol. dysfunction is decrease cognitive performance-need neurologist
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| need less MAC for oldies | true
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| cognitive impairment is also attributed to | how much you use and continue to use your brain.
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| renal and aged | GFR down 8% every decade up to 50% by 65 for renal blood flow. CO down so renal down.
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| renal and CO decrease make the aged | more susceptible to fluid overload
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| NDMBA metabolism and excretion | reduced. can result in prolonged anesthesia
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| endocrine and aged | impaired ability to metabolize insulin, frequent glucose
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| pharmacokintetic consideration of oldies | vascular volume, protein binding, less lean body mass, metablism impaired so is elimination all can affect anesthesia
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| initial plasma of drug in oldies | higher
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| reduced plasma protein means | higher free drug in body. so is the fat so more stored.
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| pharmacodynamics and oldies | less brain mass, blood flow, ie MAC drops 4% per decade after age 40
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| how much propfol you need for oldie | half the amount for regular
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| renal elimination of NMBD | impaired and longer block, except for cisatriacuruium hauffman, succs longer in men than woman.
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| 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
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| preop ask about patients | eyedrops, antihypertensive and cardiac meds should be continued the day of but NOT ACE and diuretics.
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| versed and oldies | result in confusion agitation, hlaf life 6 hours and 2 in younger. can cause post op cog dysf in oldies
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| 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
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| anesthetic management | be careful, short acting, benzo spareingly, dont want post op cog dys, MAC REGIONAL AND GEN are ALL acceptable case by case.
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| oldies need what | TLC start low go slow...reorient, thermoregulation, maintain airway, maintain VQ
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| abnormal expiratory flow that does not change over months | COPD
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| physiologic event that shunts blood away from less oxygenate part of lung during anesthesia | hypoxic pulmonary vasoconstriction
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| pulses paradoxis is common in copd | true
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| asthma represents it self as | hyper irritable airway, bronchoconstriction, treated with B2 agonist, steroid and humid
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| eosinophillic inflamation and broncho constriction is | asthma
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| abnormal permanant enlargement of air space, disruption of alveoli without fibrosis | COPD
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| another term for COPD | COLD
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| cyclogeanse inhibition promostes increase in leukotriene via arachidonic acid pathway, this causes | aspirin induced asthma so no Toradol either
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| a form of emphysema, air containing spaces greater than 1cm result from lung tissue destruction | Bullae
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| Blebs are not form of emphesyma, because blebs have no involvement with alveoli | true
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| obstructive disease ie | no fibrosis
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| expiraroty flow abnormal, no fibrosis, enlargement of air spaces | obstructive
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| COPD = | emphysema with chronic bronchitis AKA COPD aka COLD
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| emphysema effects | 20 million americans, kills 60k
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| predominant feature of emphysema | progressive airflow obstruction, ie DECREASED forced expirartory volume in one second FEV1.
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| cause of obtstructive | small bronchial lumen, increase in collapsibilty of walls, loss of elastic recoil of lung
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| COPD and COLD | used interchangable emphysema and bronchitis
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| 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
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| exhale and COPD | need more positive pressure
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| COPD and right side return | reduces it, pulses paradoxis see in 2/3 of COPDers, increase in lung volume decreases venous return
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| COPD and circulation | HR increases, CO increases due to catecholamines, renal GFR reduced, renal plasma flow decrased
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| what is pulses parodoxis | 10 point drop in sys bp during inspiratioin
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| FEV1 and FVC decrease on spirometry is charateristic of | COPD, less than 70-80% can be ALSO restrictive lung disease
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| obstructive disease has decrease in FEV1 and FVC but also | increase in reserve volume and in crease in FRC
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| how to differentiate between obstructive and restrictive | look at reseves if high its obstructive, cant let air out
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| 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.
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| cynaosis is present in blood if | 5g of deoxygenated blood is present
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| xray and obstruction | hyperinflation flat diapharm evidence of bullae, hyperlucency ie decrease tissue density. all suggestive of COPD
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| chronic bronchitis is best found how | XRAY
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| 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%
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| what is cor pulmonale | right sided heart failure
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| normal FEV1 is 5L if less than 1.5 then do | ABG, give treatment, recheck.
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| continous FEV1 around 1.5L may be indicative of | CAD and Cor pulmonale and increased mortality
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| what is FVC | forced vital capacity ie how much can you blow after exhale.
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| what is FEV1 | forced expiratory volume in one second ie how much can you blow out in one second
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| ratio of FEV1 / FVC in healthy person | should be 80%
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| 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
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| closing capacity= | closing volume + residual volume
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| closing volume | at the point which dynamic compression of airways begins
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| factor that affect closing volume | age, smoking, lung disease, body position
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| residual volume | air remaining in the lungs following VC breath
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| preop evaltuation | hypercarbia can not be corrected too quickly. sudden decrease in PCO2 may result in alkalosis, kidney need time to excrete excess bicarb
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| what controls broncho constrictions | parasympathetic
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| anesthesia can be given to COPDers extubation is a concern | true
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| any block above T6 is | not recommended
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| VAA and COPD | bronchial dilitation, slow cillia,
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| give less than 100% to COPD why | absorptive atelectasis, provide intermittent vital capaticy maneuvers ie valsalvo
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| in presence of bullae what is contraindicated | N2O
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| remember bullae are | emphesemic changes
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| Blebs are | NOT emphesymic and are out side of the lung
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| GA and COPD | careful with PEEP, only 5cmH2O, expiration should be prolonged in order to decrease intrinsic peep. ie no breath stacking
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| arterial hypoxemia represent a very advanced stage of the disease manifested by | pulmonary vsoconstriction ie late sign
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| COPD vs Asthma | asthma is characterized by eosinophilic response, inflamation of airway except for lung parenchyma.
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| 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.
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| COPD and lung connective tissue | destruction of connective tissue and collapse of airways, exchange of CO2 and O2 between blood and alevoli impeded
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| COPD and lung compliance | lung becomes more compliant BUT shorter quicker breaths, less force. diaphram ineffective
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| COPD and intercostal muscles | thorax is misaligned used of accessory muscle is used, and assume the position of comfort, ie tripod
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| COPD with asthma attach | the inflimation of COPD allows foreign bodies to enter lung causing the asthma attack
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| 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
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| intra op COPD reminder | these pts have cardiac dysfunction, CVP with pulmonary HTN is reflective of RV rather than intravascular volume
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| early extubation of COPD | case by case, FEV1 less than 50% need post op vent
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| in a PFT if effort is low and reserves or capacity are high chances are | is a obstructive disease
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| what is a good predictor of small airway disease | FEF ie mid expratory force
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| FEV1 is a good predictor of | obsctructive disease
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| FEF is a good predictor of | early small airway disease
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| emphysema PFT | non reverisible obstruction, high lung volumes, low diffusing capacity, and positive smoking history.
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| chronic bronchitis | excessive mucus, at least 3 months of the year for at least 2 successive years, obstructive limits expiratory airflow
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| Bullae | form of emphysema, space greater than 1cm with air, deep elastic layer of visceral pleural avoid N2O
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| pulm HTN should i give N2O | NO
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| blebs | collection of air within the pleura, NOT emphysema, DO NOT involve asinus ie alveoli, cadidate for Pleurodesis ie glue together the two pleura
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| Pleurodesis | ie glue together the two pleura
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| 25% of all COPD have enhanced airway reactivity but | muscles thicken and contribute to narrowing, excessive mucus but cillia is impaired.
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| Asthma | chronic inflamation of airway, involves mast cells, neutrophills, eosingophils and T lymphocytes. serotonin can induce asthma
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| what is a potent broncho constrictor and found to be active in asthmatic respnse | serotonin
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| asthma is stimulated by messing with | parasympathetic system
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| parasympathetic maintains normal bronchial tone, vagal afferent are sensetive to | histamine, noxious stimuli cold air and irritants
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| reflex vagal activation results in | bronchoconsctriction caused by cGMP
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| pousile law talks of | flow and diameter
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| extrinsic asthama or allergic asthma | most common in children and young, IgE, infectious, psychological enviromental or physical
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| intrinsic asthma or idiosyncratic asthma | middle age happens without provoking
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| what is the most common chronic disease of childhood | asthma
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| asthma is a disease of | bronchoconstriction, airway inflammation hyper irritability
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| asthma and inflamation | irritant cause cause release of lymphocyte, histamine, mast cells, cytokine
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| the potent chemical mediatior promost vasoconstriction and what else | inscrase smooth muscle tone, enhance mucus production, airway edema, vascular permeability and infamematory cell chemotaxis
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| cyclooxygenase inhibition can cause | increase in leukotrien via arachidonic acid pathyway ie asthma attach. NO NSAIDS, this is not IgE,
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| ASA asthma is clinically associated with | nasal polyps
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| when prostaglandin production is blocked with NSAIDS then | laukotrienes cause over production of LT4 and produce severe allergy like effects.
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| can alcohol cause ASA asthma? | yes
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| asthma attack and tachypnea | causes hypocapnia, but if PaCO2 is norm and or high then resp failure is coming
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| signs of advanced pulmonary disease | pulses paradoxous, EKG change of right vent strain, ST changes, right axis deviation, RBBB
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| treatment of asthma | Beta2 agonist, methyxantheine ie theophyline, glucosteroids, anticholinergics to block muscurinic
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| how do Beta 2 agonist work for reversal of bronchoconstriction | B2 stimulated adenylate cyclase results in formation of cyclic AMP ie bronchial dilatation
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| name some beta 2 agonist with less beta 1 effects | albuterol or terbutaline
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| 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
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| anticholinergic and asthma | ipatropium bromide ie atrovent is a good one with no sympathomimetic effect
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| cimetadine or ranitidine and asthma | can cause asthma or severe interaction if pt on theophylline
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| fix asthma before surgery | FEV1 greater than 2-3L, FEV1/FVC should be greater than 70%, PEF 200-500ml, do xray
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| 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!
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| avoid histamine releasing drugs such as | atracurium, mivacurium, demerol, morphine, thiopental,
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| ketamine good for patient with asthma? | yea and no, yea if not on theophylline or else seizure city
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| 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
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| 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
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| restrictive pulmonary diease is | interference of inspiration, incrase inward elastic recoil, intrinsic and extrinsic varieties
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| restrictive and PFT | decrase lung volume, FEV1 and FVC reduces, TLV is reduced, HOWEVER FEV1/FVC ratio is NORMAL may have VQ mismatch
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| intrinsic pulmonary | edema, ARDS, infectous pneumonia, aspiration pneumonitis, low lung compliance due to extra vascular lung water
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| 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
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| obstructive and restrictive when it comes to residual volume | obstructive increased residual volume and restrictive low residual volume
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| volume related resp disease ie intrinsic restrictive lung | sarcoidosis, TB, pnuemonectomy, infectious pneumonia, pulm fibrosis, autoimmune disease
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| extrinsic restrictive lung | may be acute or chronic include: scoliosis, kyphosis, pectus, ankylosing spondylitis,, PL effusion, prego/obese, tumor, ascites, rib fx, pneumothorax
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| intersitial lung disease with enough damage to air sacs | disease is not reverible, impaired blood flow in lungs, causes SOB
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| Sarcoidosis | interstitial lung disease, multisys disorder, lungs skins and eyes. normal elastic tissue stiffens, looks like honeycomb, cause unknown
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| 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
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| ABG norms | ph 7.35-7.45, PaCO2 35-45, HCO3 25,
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| DO NOT treat resp acidosis with bicarb why | bicarb becomes more carbon dioxide makes acidosis worse.
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| total body bicarb deficit=base deficit and correction of _____is indicated not total correction. | correction of 1/2
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| acidemia in renal pts | use dialysis
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| correct hypoxemia via | incrase FIO2, PEEP, correct other resp issues ie suction, correct atelectasis etc...
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