Consider the following medical report that includes the patient's historical health records. Use it to predict the disease that the patient is high likely exposed to. 

 Medical Report: allergies: morphine / percocet attending: chief complaint: shortness of breath major surgical or invasive procedure: bipap endotracheal intubation cardiac catheterization w/ stent placement history of present illness: this is a 77 female with h/o atrial fibrillation (on coumadin), aortic stenosis (mod/severe), cardiomyopathy (lvef 40-50%), dm2, who presents from rehab hospital with several days of increasing shortness of breath. she was recently discharged from after a prolonged stay for a right psoas phlegmon s/p ct guided drainage. she was discharged 7 days pta, and reports initially feeling well upon discharge. beginning two days after arriving at rehab she began to get worsening lower back pain (same pain from abscess drain), that would cause her "bp to rise and hr to rise" and subsequently would get sob. she then began pt and was doing well. . on sunday (3 days pta) she became significantly more sob, and her family describes her as clamy. she had increasing orthopnea at this point, with worsening peripheral edema and wt gain. she the following day she was given 20 mg lasix twice, and had a cxr done. she continued to gain weight and feel increasingly sob, feeling as if "there was no more breath left." on the day of admission, be hospitalized. . she has not had any chest pain, cough, fever, chills ha, diarrhea, consitpation, urinary symptoms. she things her urine output was less at the rehab. she describes intermittent clamy feelings when getting sob. she has had no appetite and decreased po intake. . ros: as above . ed course: she was triaged with a requirement of 5l nc to maintain sats in mid 90s; she was afebrile, normotensive. she was found to be in af with rvr (to 150s - 160s). she was given 40mg iv lasix, and then subsequently given 80mg iv lasix, to which she put out ~1l. she was given dilt 5mg iv x 3, and subsequently dilt 15mg iv x 1, with only modest effect on her hr. a cxr showed worsening chf with pulm edema and a left pleural effusion. her ecg showed af at 115, no acute changes from prior. she was also given one dose of iv levaquin for presumed respiratory coverage. past medical history: as htn chronic af on coumadin djd with multiple joint replacements (r hip , r knee , l knee , r shoulder ) niddm s/p cholecystectomy social history: 5 children, very supportive. no tob/etoh/drugs. family history: nc physical exam: vs- 97 122/74 130 22 97% 2.5l gen- pale elderly female lying in bed with family at side heent- anicteric, dry mm, eomi, perrl, op clear, upper dentures, no lower teeth neck- supple, jvp to 9cm, no lad cv- irreg irreg, tachy, iii/vi sem at usb, hyperdynamic pmi chest- decreased bs at bases (l>r) with rales bilaterally, dullto percussion on left abd- soft, obese, nt, nd, +bs ext- 1+ pitting edema bilaterally, 1+ dp pulses bilaterally, scars over knees and right shoulder, well healed. picc line in right forearm neuro- aao x 3, moving all extremities skin- no lesions noted msk- palpable hardware right shoulder, nontender, no other joint effusions noted. pertinent results: 02:50pm blood wbc-6.3 rbc-3.24* hgb-10.6* hct-32.2* mcv-99* mch-32.8* mchc-33.0 rdw-14.9 plt ct-274 03:55am blood wbc-5.7 rbc-3.03* hgb-9.7* hct-29.9* mcv-99* mch-32.1* mchc-32.5 rdw-15.0 plt ct-264 09:14am blood wbc-6.6 rbc-3.48* hgb-11.1* hct-34.6* mcv-99* mch-31.7 mchc-32.0 rdw-15.6* plt ct-234 02:50pm blood hypochr-2+ poiklo-1+ macrocy-2+ 09:14am blood pt-24.4* ptt-32.3 inr(pt)-2.4* 02:50pm blood glucose-128* urean-21* creat-0.7 na-132* k-3.7 cl-87* hco3-39* angap-10 03:55am blood glucose-105 urean-22* creat-0.8 na-134 k-3.7 cl-88* hco3-40* angap-10 06:25am blood glucose-132* urean-20 creat-0.7 na-134 k-4.0 cl-86* hco3-45* angap-7* 09:14am blood glucose-176* urean-20 creat-0.7 na-134 k-3.4 cl-84* hco3-47* angap-6* 02:50pm blood ck(cpk)-69 03:55am blood ck(cpk)-59 02:50pm blood ck-mb-notdone probnp-* 03:55am blood ck-mb-notdone ctropnt-0.04* 03:55am blood calcium-9.2 phos-4.7* mg-1.5* 06:09am blood calcium-9.2 phos-3.0# mg-2.1 09:14am blood calcium-9.0 phos-2.6* mg-1.8 09:14am blood digoxin-1.5 11:42am blood type-art po2-115* pco2-90* ph-7.38 calhco3-55* base xs-22 05:17pm blood type-art po2-92 pco2-80* ph-7.43 calhco3-55* base xs-22-- studies: . chest ct: this non-contrast-enhanced study demonstrates interval increase in size of bilateral pleural effusions, left slightly greater than right which are moderate in size. mild basilar atelectasis. they are no pathologically enlarged nodes within the mediastinum, axillae, hila. stable cardiomegaly. coronary calcifications. no pericardial effusion. ground-glass opacities again noted bilaterally, appear more prominent with associated septal thickening, likely presenting pulmonary edema. again noted are few scattered nodules, less than 5 mm bilaterally. previously seen lesion in right psoas not clearly visualized on this study. probable dropped gallstone in hepatorenal recess. no evidence of pneumothorax. osseous structures are stable. impression: 1. interval increase in size of bilateral moderate pleural effusions with associated bibasilar atelectasis. 2. interval worsening of bilateral diffuse ground-glass opacity, likely representing pulmonary edema. no definite evidence of emphysematous change. 3. bilateral tiny pulmonary nodules, unchanged. recommend follow up to ensure stability. . mri l-spine: findings: again scoliosis of lumbar spine is seen. at t12-l1, increased signal is seen within the disc with some enhancement indicative of discitis. there is abnormal signal seen in the adjacent endplates indicative of marrow edema. again paraspinal soft tissue abnormalities with fluid collection are seen indicative of abscess. compared to the prior study, the paraspinal fluid collections have slightly decreased. the persistent signal changes and slight enhancement within the disc could be secondary to evolution of inflammatory change within the disc and not necessarily indicate worsening of discitis. further followup is therefore essential. there is no evidence of new inflammatory changes seen within the spinal canal. increased signal is seen within the l1-2 and l2-3 discs on the inversion recovery images which was not identified on the previous study. there is no enhancement seen in this region. this finding be secondary to technical differences or due to fluid within the disc from increased motion. further followup is recommended to exclude inflammation at this level. mild degenerative changes and bulging from l3-4 to l5-s1 level are again noted. the distal spinal cord shows normal signal intensities. no evidence of compression of the distal cord is seen. impression: 1. changes of discitis and osteomyelitis at t12-l1 level are noted with slightly increased endplate signal changes and subtle enhancement within the disc. this could represent evolution of inflammatory changes from discitis. no new soft tissue abnormalities are seen to suggest worsening of the inflammatory changes. 2. the paraspinal fluid collections are still noted indicating abscesses which are decreased in size from the previous study. 3. increased signal is seen within the l1-2 and l2-3 discs which is a new finding since the previous study and it could indicate fluid within the discs or early inflammatory changes. followup is recommended. . cxr: findings: there has been no significant change in the mild pulmonary edema from the comparison study. left retrocardiac opacity likely atelectasis and small left pleural effusion are unchanged. a left ij catheter is again identified unchanged in position. et tube is unchanged. ng tube projects below the diaphragm. impression: no significant change from . . - worsening chf. brief hospital course: this is a 77 female with h/o atrial fibrillation (on coumadin), aortic stenosis (mod/severe), cardiomyopathy (lvef 40-50% on tte), dm2, who presented from rehab hospital with several days of increasing shortness of breath. she had recently been discharged from after a prolonged stay for a paraspinal infection with multiple para-aortic retroperitoneal abscesses and right mssa psoas abscesses s/p ct guided drainage, with t12-l1 discitis. no evidence of dissection, endocarditis, intraspinal or epidural involvement. she also had sob during admission, with evidence of hypercapnia, and was found to have bilateral pleural effusions and mild pulmonary edema. she was treated with lasix with reasonable effect, but with residual sob, thought to be copd or pulmonary htn. she was discharged 7 days pta, and reportedly initially felt well upon discharge. beginning two days after arriving at rehab she began to get worsening lower back pain (same pain from abscess drain). she then began pt and was doing well. . on she became significantly more sob, and diaphoretic. she had increasing orthopnea, peripheral edema and wt gain, and was given 20mg lasix. of note, she had been maintained on lasix during her last hospitalization, but lasix was not continued as a standing order on discharge as she was felt to be euvolemic. the following day she was given 20 mg lasix twice, and had a cxr done. she continued to gain weight and feel increasingly sob, and was sent to the ed. . in the ed she was diuresed with 40mg and then 80mg iv lasix; she was found to be in rapid af and was give a total of 30mg iv dilt. this was not effective, and she was started on a dig load. on the medical floor, her afib was controlled with digoxin and metoprolol. she was cautiously diuresed, and was treated for her abscess pain with tylenol #3. the next morning, she was noted to be less responsive. abg at that time was 7.38/90/115. she was given lasix 20 mg iv with 800 cc uop over the next few hours, and her mental status improved. however at 5 pm she became unresponsive again and her abg was 7.43/80/92. she was tachypneic but not hypoxic. micu eval was called at that time for bipap, because per respiratory she needed bipap via mouth and not through her nose, and therefore could not get bipap on the floor. . in the micu she was felt to have a mixed acid base status, with metabolic alkalosis with superimposed respiratory acidosis. it was felt that the metabolic alkalosis could have been due to diuresis on the floor. her resp acidosis was thought to be due to obstructive disease of unclear etiology. she was given bipap overnight (), and her abg in am was 7.39/87/196. she subjectively felt better on 2l nc. she did not have any chest pain or fever. her diuresis was held, and her lytes were repleted. . over the next two days, intermittently on nc and bipap with mixed contraction alkalosis and hypercarbic respiratory acidosis, thought to be chroinic, possibly osa. cards consulted, who recommended l and r heart cath to evaluated filling pressures and to evaluate severity of as for possible avr. this was not possible at the time respiratory status and inability to lie flat. . on , neurology consulted to assess possible neuromuscular etiology of respiratory failure, which was thought unlikely normal respiratory pattern, ability to take deep breaths, overall normal neurological exam. emg demonstrated mild-mod generalized sensory polyneuropathy, but no findings suggestive of mg or proximal myopathy. snif test done, but uninterpretable in setting of pleural effusions. ent evaluated, confirmed no vocal cord paralysis. pfts done, which were incomplete pt fatigue, with mips decreased with each inspiratory effort, with fev1/fvc 167%, c/w restrictive pattern. . over the next couple of days, continued to have respiratory distress, with intermittent need for bipap, complicated by pt refusal to wear. pt was also gently diuresed. ct chest demonstrated moderate bilateral pleural effusions, ground glass opacities with associated septal thickening c/w chf, bibasilar atelectasis, old tiny pulmonary nodules. head ct obtained lethargy, demonstrated no evidence of acute bleed or mass effect. brain mri done, which demonstrated no significant abnormalities. consideration given to thoracentesis, but ip felt not indicated at that time. family discussion held , as pt not tolerating bipap, and would likely require either intubation with possible progression to trach, or comfort measures. family confirmed full code status, with intubation if necessary. acetazolamide also given decreased ph and hypercarbia. . pt was electively intubated somnolence and difficulty acheiving adequate oxygenation with intermittent bipap. she also experienced transient hypotension after intubation and sedatives, with no response to ivf, and was started on pressors. found to have uti, started on ctx . . repeat l-spine mri done , to evaluated previous psoas abscesses. mri demonstrated changes of discitis and osteomyelitis at t12-l1 level with slightly increased endplate signal changes and subtle disc enhancement, possibly representing evolution of inflammatory changes from discitis. no new soft tissue abnormalities seen to suggest worsening of the inflammatory changes. paraspinal fluid collections are still noted, but decreased in size from the previous study. crp increased from 14 on to 87 on . id consulted, reviewed mri with radiology. it was felt that new enhancement probably represent natural progression in setting of therapy. recommend continuing nafcillin therapy for 8 weeks total post abscess drainage, (end date ), at which point crp could be rechecked. urine culture grew e. coli, switched to cipro on . . as pt intubated, micu team proceeded with preparation for cardiac cath, as described above. coumadin reversed, lij placed, placed on heparin gtt. was slowly weaned off pressors by . stim test inappropriate, started on stress dose hydrocort/fludrocort on . pan-cultured to look for possible septic etiology for hypotension. blood cultures have been no growth. sputum cultures growing gnr at time of transfer. pt also had loose stools, c. diff x 3 sent, which were negative. . ms. cardiac cath on , while intubated. av area found to be 1.0cm2, with gradient of 20mmhg. cath demonstrated 80% mid-lad lesion, and 2 overlapping bms. placed on asa, plavix x 1 month, integrillin x 6 hours, after which heparin gtt was restarted to re-bridge to coumadin for af. pt had residual small intermedius and ostial rca disease that could be amenable to pci if pt had recurrent evidence of myocardial ischemia. ra 18, pcwp 18, map 75, ci 2.7. no complications post-cath. . ms. was successfully extubated on post-cath, and was called out to floor on . pt has appt with dr. in id on at 12pm. per id, should have qwk cbc, bun/cr checked and faxed to dr. . . on the floor, she continued to have episodes of afib with rvr with tachy-brady syndrome and has only been cautiously diuresed because of marginal bps on the floor. today, pt was triggered at 9am for relative hypotension and was given back 500ccns bolus. cardiology recommended increasing beta-blockade for hrs but might need pacer for possible tachy-brady syndrome. then, at 6:30 am, she became tachypneic to the 40's with labored breathing and complained of a "panic attack". o2 sat was noted to be 48% on 3l nc. she was temporarily placed on a nrb with increasing o2 sats to 94% and weaned off quickly on the floor to o2 sats 93% on 5l nc. her abg showed 7.30/85/67 with bicarb 38. she was triggered and micu consulted for further managment. she states that her breathing does feel shallow but denies any chest pain, nausea, vomiting. she has no other complaints now. she was transferred to icu for initiation of bipap therapy. . . micu course: ## respiratory: pt. was transferred to the micu for mental status changes in the setting of hypercarbia. the etiology of her hypercarbia is unclear - no history of copd. she most likely presented with a chf exacerbation. pt. has as, afib, and chf which have contributed to her dyspnea. her pleural effusions (l >r) could be limiting the expansion of her lung, causing a restrictive physiology. she also has evidence of pulmonary hypertension on last tte. however, given pt's difficulty w/ ventilation and normal oxygenation - chf is not the problem. concern for diaphragmatic dysfuction bilaterally during stay, but pt. unable to do sniff test to assess diaphragms pleural effusions. ent saw pt. - no vocal cord paralysis. neuro saw pt. and no neuromuscular disease appreciated. pfts unable to be completed to exhaustion, but pt. w/ restrictive pattern and mips decreased w/ each subsequent effort. overall, probably has a poor lv fx, poor forward flow. it was decided that pt. would be electively intubated to do a cardiac catheterizatio nwhere she was found to have an lad lesion that was stented. during intubation, pt's hypercarbia improved (pco2 in 60s which is probably her baseline). after cardiac cath, pt. was sucessfully extubated and did not have the feeling of dyspnea anymore. . ## acid/base: pt. w/ hypercarbia and high bicarb in micu. pt. w/ hypercarbia w/ co2 of 90s-100s. unclear what the cause was. twice during her micu stay she was found lethargic w/ high co2. she was placed on bipap w/ some improvement. pt. refused bipap when alert and oriented for the first few days, but then began using it with some regularity. pt. was then intubated and hypercarbia improved - 60s, which is likely her baseline. in the beginning of micu course, pt. give kcl aggressively to try to get rid of some bicarb - this improved somewhat. once, pt. intubated, pt's bicarb began to trend down. stable after extubation. . ## chf - pt. w/ diastolic chf w/ as - based on exam,labs, history, she most likely presented with a chf exacerbation, due to long standing tight as and diastolic failure. this is probably exacerbated by decreased diastolic filling with atrial fibrillation. pt. continued to be fluid overloaded w/ b/l effusions. at times hard to diurese pt. secondary to hypotension. goal was negative a liter a day. . ## cad - pt. w/ lad lesion s/p 2 bare metal stents. since cath, pt. has been breathing more comfortably so unclear if this is what was causing pt. to be so dyspneic. pt. will need to be on asa,plavix, and beta blocker. . ## hypotension - initially hypotension seemed to be in the setting of intubation and then it was found that pt. had adrenal insufficiency. pt. failed stim. test so is on of steroids (started 7 dday course on ). . ## anemia - pt. w/ progressively declining crits over micu stay, but no obvious source of bleeding. pt. will need a c-scope/egd as an outpatient or more urgently if crit does not increase . #afib: pt has a fib and has been going into afib w/ rvr a few times in micu. pt. was controllled w/ iv medications prn for rate control. will continue pt's beta blockade now that she is no longer on pressors. spoke to cards - no need for amio. pt. initially on coumadin and then switched to heparin for cath. after cath, pt. switched back to coumadin. inrs will have to be followed. . # uti - pt. w/ positive ua on w/ ctx that are growing 2 strains of e.coli - pt. on day of abx on . . ## abscess/discitis: had mssa bacteremia with spinal discitis, numerous psoas abscesses s/p drainage on a previous hospitalization. pt. had mri to evaluate spinal abscesses while in micu- stable abscesses, new l1-l2/l2-l3 increased signal in the disks indicate re-accumulating fluid in discs/early inflammatory changes. id reviwed mri w/ radiology and believe that pt. should have an 8 week course of abx total (first day ). pt. will likely have to have a follow mri per id recs and then f/u w/ id and possibly neurosurgery depending on mri. pt. will need to cont nafcillin day 21 (started on ). overall, pt. is on day 40/56 of abx (was previously on oxacillin) in order to finish an 8 week course. (first day of 8 week course was ). . ## dm2: at home, pt. on glipizide 5qd and pioglitazone 15 qd but will hold oral meds. pt. w/ good glycemic control on insulin sliding scale . ## hypercholesterolemia: cont lipitor 10 qd . ## fen: tf while intubated and then switched to heart healthy/diabetic diet. replete lytes prn . ## ppx: coumadin, ppi, bowel meds . ## code: full, discussed with pt and family. per discussion today, family still wants bipap and intubation as needed. . ## communication: with pt and daughters. . ## dispo: icu for compromised ventilation cc: micu call out after hypercarbic respiratory failure . hpi: this is a 77 female with h/o atrial fibrillation (on coumadin), aortic stenosis (mod/severe), cardiomyopathy (lvef 40-50% on tte), dm2, who presented from rehab hospital with several days of increasing shortness of breath. she had recently been discharged from after a prolonged stay for a paraspinal infection with multiple para-aortic retroperitoneal abscesses and right mssa psoas abscesses s/p ct guided drainage, with t12-l1 discitis. no evidence of dissection, endocarditis, intraspinal or epidural involvement. she also had sob during admission, with evidence of hypercapnia, and was found to have bilateral pleural effusions and mild pulmonary edema. she was treated with lasix with reasonable effect, but with residual sob, thought to be copd or pulmonary htn. she was discharged 7 days pta, and reportedly initially felt well upon discharge. beginning two days after arriving at rehab she began to get worsening lower back pain (same pain from abscess drain). she then began pt and was doing well. . on she became significantly more sob, and diaphoretic. she had increasing orthopnea, peripheral edema and wt gain, and was given 20mg lasix. of note, she had been maintained on lasix during her last hospitalization, but lasix was not continued as a standing order on discharge as she was felt to be euvolemic. the following day she was given 20 mg lasix twice, and had a cxr done. she continued to gain weight and feel increasingly sob, and was sent to the ed. . in the ed she was diuresed with 40mg and then 80mg iv lasix; she was found to be in rapid af and was give a total of 30mg iv dilt. this was not effective, and she was started on a dig load. on the medical floor, her afib was controlled with digoxin and metoprolol. she was cautiously diuresed, and was treated for her abscess pain with tylenol #3. the next morning, she was noted to be less responsive. abg at that time was 7.38/90/115. she was given lasix 20 mg iv with 800 cc uop over the next few hours, and her mental status improved. however at 5 pm she became unresponsive again and her abg was 7.43/80/92. she was tachypneic but not hypoxic. micu eval was called at that time for bipap, because per respiratory she needed bipap via mouth and not through her nose, and therefore could not get bipap on the floor. . in the micu she was felt to have a mixed acid base status, with metabolic alkalosis with superimposed respiratory acidosis. it was felt that the metabolic alkalosis could have been due to diuresis on the floor. her resp acidosis was thought to be due to obstructive disease of unclear etiology. she was given bipap overnight (), and her abg in am was 7.39/87/196. she subjectively felt better on 2l nc. she did not have any chest pain or fever. her diuresis was held, and her lytes were repleted. . over the next two days, intermittently on nc and bipap with mixed contraction alkalosis and hypercarbic respiratory acidosis, thought to be chroinic, possibly osa. cards consulted, who recommended l and r heart cath to evaluated filling pressures and to evaluate severity of as for possible avr. this was not possible at the time respiratory status and inability to lie flat. . on , neurology consulted to assess possible neuromuscular etiology of respiratory failure, which was thought unlikely normal respiratory pattern, ability to take deep breaths, overall normal neurological exam. emg demonstrated mild-mod generalized sensory polyneuropathy, but no findings suggestive of mg or proximal myopathy. snif test done, but uninterpretable in setting of pleural effusions. ent evaluated, confirmed no vocal cord paralysis. pfts done, which were incomplete pt fatigue, with mips decreased with each inspiratory effort, with fev1/fvc 167%, c/w restrictive pattern. . over the next couple of days, continued to have respiratory distress, with intermittent need for bipap, complicated by pt refusal to wear. pt was also gently diuresed. ct chest demonstrated moderate bilateral pleural effusions, ground glass opacities with associated septal thickening c/w chf, bibasilar atelectasis, old tiny pulmonary nodules. head ct obtained lethargy, demonstrated no evidence of acute bleed or mass effect. brain mri done, which demonstrated no significant abnormalities. consideration given to thoracentesis, but ip felt not indicated at that time. family discussion held , as pt not tolerating bipap, and would likely require either intubation with possible progression to trach, or comfort measures. family confirmed full code status, with intubation if necessary. acetazolamide also given decreased ph and hypercarbia. . pt was electively intubated somnolence and difficulty acheiving adequate oxygenation with intermittent bipap. she also experienced transient hypotension after intubation and sedatives, with no response to ivf, and was started on pressors. found to have uti, started on ctx . . repeat l-spine mri done , to evaluated previous psoas abscesses. mri demonstrated changes of discitis and osteomyelitis at t12-l1 level with slightly increased endplate signal changes and subtle disc enhancement, possibly representing evolution of inflammatory changes from discitis. no new soft tissue abnormalities seen to suggest worsening of the inflammatory changes. paraspinal fluid collections are still noted, but decreased in size from the previous study. crp increased from 14 on to 87 on . id consulted, reviewed mri with radiology. it was felt that new enhancement probably represent natural progression in setting of therapy. recommend continuing nafcillin therapy for 8 weeks total post abscess drainage, (end date ), at which point crp could be rechecked. urine culture grew e. coli, switched to cipro on . . as pt intubated, micu team proceeded with preparation for cardiac cath, as described above. coumadin reversed, lij placed, placed on heparin gtt. was slowly weaned off pressors by . stim test inappropriate, started on stress dose hydrocort/fludrocort on . pan-cultured to look for possible septic etiology for hypotension. blood cultures have been no growth. sputum cultures growing gnr at time of transfer. pt also had loose stools, c. diff x 3 sent, which were negative. . ms. cardiac cath on , while intubated. av area found to be 1.0cm2, with gradient of 20mmhg. cath demonstrated 80% mid-lad lesion, and 2 overlapping bms. placed on asa, plavix x 1 month, integrillin x 6 hours, after which heparin gtt was restarted to re-bridge to coumadin for af. pt had residual small intermedius and ostial rca disease that could be amenable to pci if pt had recurrent evidence of myocardial ischemia. ra 18, pcwp 18, map 75, ci 2.7. no complications post-cath. . ms. was successfully extubated on post-cath, and was called out to floor on . pt has appt with dr. in id on at 12pm. per id, should have qwk cbc, bun/cr checked and faxed to dr. . . on the floor, she continued to have episodes of afib with rvr with tachy-brady syndrome and has only been cautiously diuresed because of marginal bps on the floor. today, pt was triggered at 9am for relative hypotension and was given back 500ccns bolus. cardiology recommended increasing beta-blockade for hrs but might need pacer for possible tachy-brady syndrome. then, at 6:30 am, she became tachypneic to the 40's with labored breathing and complained of a "panic attack". o2 sat was noted to be 48% on 3l nc. she was temporarily placed on a nrb with increasing o2 sats to 94% and weaned off quickly on the floor to o2 sats 93% on 5l nc. her abg showed 7.30/85/67 with bicarb 38. she was triggered and micu consulted for further managment. she states that her breathing does feel shallow but denies any chest pain, nausea, vomiting. she has no other complaints now. she was transferred to icu for initiation of bipap therapy. . 77 f c mild as, diastolic chf atrial fibrillation, recent psoas abscess, admitted to the micu for hypercarbia and altered mental status s/p cardiac cath (lad lesion) w/ 2 bare metal stents who has been on the floor with worsening chf and afib with rvr. . ## respiratory: the etiology of her hypercarbia is unclear, but likely due to chf and copd (undx'd previously). there is likely a component of obesity hypoventillation syndrome also involved (will need sleep study w/u as outpt). she most likely presented with a chf exacerbation, in setting of af with rvr, diastolic failure. her pleural effusions (l >r) could be limiting the expansion of her lung, causing a restrictive physiology seen in pfts. she has evidence of mild pulmonary hypertension on cath. there was concern for diaphragmatic dysfuction bilaterally. pt. unable to do snif test to assess diaphragmatic strength 2/2 pleural effusions. ent saw no evidence of vocal cord paralysis. no evidence of neuromuscular disease contributing to sob. pfts unable to be completed to exhaustion, but c/w restrictive pattern. recently, she had acute respiratory acidosis for unclear reasons, xfered back to micu. overnight, gases on bipap and gases on nasal cannula seemed not to be different, but the patient's breathing seemed to be much more confortable on bipap. patient was diuresed as much as her blood pressure would allow, on standing lasix as well as lasix gtt. as above, the patient was made dnr/dni, after discussion with family, but bipap was allowed. patient was given intermittent breaks from bipap on nasal cannula, but her pco2 became much worse after being taken off bipap. on , the patient went to ir suite for picc line placement. she was required to be lying flat while getting the line placed and returned with significant respiratory distress. she was placed on bipap and her respiratory status and gas exchange improved significantly. however, later that night, the patient developed "agonal type" respirations despite being on bipap, with 2-8 second pauses between respirations. the patient's family was informed that the patient was not doing well and pass soon--and dnr/dni status was confirmed once again. the patient was given maximal non-invasive ventillatory support, but became progressively more somnolent and obtunted. within a short time, the patient's respiration suddely ceased, and staff coudl not arouse the patient even with sternal rubs. the patient then became bradycardic to 30s, then went into pea and passed shortly after with family by her side. . ## chf - pt. w/ likely diastolic chf with af with intermittent rvr. patient continued to be fluid overloaded during her stay despite maximum efforts to diurese her. . #afib: afib with rvr. frequent bursts into 160s/170s unresponsive to dilt and bb. patient was placed on amiodarone, since dc cardioversion was thought to be not indicated by cardiology consultants. sotalol was also suggested. after amiodarone, hr decreased to 120s-140s. please see above regarding the rest of hospital course and conditions around patient decompensating and eventually expiring. . ## abscess/discitis: had mssa bacteremia with spinal discitis, numerous psoas abscesses. pt. had mri to reevaluate spinal abscesses - stable abscesses, new l1-l2/l2-l3 increased signal in the discs. id favoring continuing 8 week course nafcillin, due to complete . patient was continued on iv abx, but expired as described above medications on admission: atorvastatin 10, colace, protonix 40, fluticasone 110/actuation aerosol , dulcolax prn, metoprolol 75 , acetaminophen-codeine q4 prn, oxacillin 2g q4, glipizide 5 qd, coumadin 2.5 qhs, pioglitazone 15 qd discharge disposition: expired discharge diagnosis: chf atrial fibrillation discitis osteomyelitis obesity hyperventillation syndrome hypercarbic respiratory failrue discharge condition: expired discharge instructions: n/a followup instructions: n/a procedure: venous catheterization, not elsewhere classified continuous invasive mechanical ventilation for 96 consecutive hours or more insertion of non-drug-eluting coronary artery stent(s) combined right and left heart cardiac catheterization coronary arteriography using two catheters injection or infusion of platelet inhibitor insertion of endotracheal tube enteral infusion of concentrated nutritional substances non-invasive mechanical ventilation transfusion of other serum cranial or peripheral nerve graft insertion of one vascular stent excision of lingual thyroid percutaneous transluminal coronary angioplasty [ptca] procedure on single vessel diagnoses: coronary atherosclerosis of native coronary artery urinary tract infection, site not specified congestive heart failure, unspecified unspecified essential hypertension diabetes mellitus without mention of complication, type ii or unspecified type, not stated as uncontrolled hyposmolality and/or hyponatremia chronic airway obstruction, not elsewhere classified atrial fibrillation aortic valve disorders acute respiratory failure hypotension, unspecified primary pulmonary hypertension other and unspecified disc disorder, lumbar region diastolic heart failure, unspecified mixed acid-base balance disorder 

Answer: The patient is high likely exposed to