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oldies adv prin1
| Question | Answer |
|---|---|
| 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... |
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Rooz
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