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: no known allergies / adverse drug reactions attending: chief complaint: transfer from where she was admitted for atypical chest pain and sob major surgical or invasive procedure: -central venous line insertion into r ij -multiple attempts at securing arterial access history of present illness: 62f with hx of severe of pulm htn, cad s/p des to lcx/lad in , prior cva s/p b/l cea's, pvd, and copd who was admitted to osh for atypical chest pain and sob. she ruled out for acs with by enzymes (mb 8 -> 7 -> 5; trop 0.06 -> 0.07 -> 0.06) and ekg without acute ischemic changes but was found to have a bnp of 11k on admission. she was assessed as having severe decompensated r-sided chf and was diuresed with 40mg iv lasix in the ed but later that day experienced back pain with desat to the 50's and was transferred to the ccu for close monitoring with hr in the 60's and bp's in the 90's. she had echo on which showed severe pulmonary hypertension, rv pressure overload, modestly depressed rv function, and lvef of 55-65%. . here in the ccu she describes feeling gradually more short of breath over the past 2 months which has become acutely worse in the past 1-2 weeks. interestingly, about 1 month ago she was started on sildenafil for treatment of her pulm htn but felt she became more short of breath when taking that medication and stopped taking it about 2 weeks ago when she started feeling acutely more short of breath. she states that she has only gained about 2-3lbs in the past two weeks but noticed increased ankle swelling, increasing need for oxygen (she is usually at 88-92 on 3lnc at home but prior to these past 2 weeks she has only used oxygen at night). she has 2 pillow orthopnea, but denies pnd. she denies dietary indiscretion, recent illnesses, fevers, chills, cough, sputum production, or other symptoms. according to her family she has never had low back pain as a problem before but the patient states her back pain gets better with positional changes and rubbing. also, her baseline daily function has decreased as she is normally able to move around the rooms of house but has not been able to walk more than 10 feet due to shortness of breath in addition to her basleine vascular claudication. . on review of systems, s/he denies any prior history of stroke, tia, deep venous thrombosis, pulmonary embolism, bleeding at the time of surgery, myalgias, joint pains, cough, hemoptysis, black stools or red stools. s/he denies recent fevers, chills or rigors. all of the other review of systems were negative. . cardiac review of systems is notable for absence of chest pain, paroxysmal nocturnal dyspnea, palpitations, syncope or presyncope. past medical history: 1. cardiac risk factors: + diabetes, + dyslipidemia, + hypertension 2. cardiac history: cad s/p lad cypher stenting - cabg: n/a - percutaneous coronary interventions: - pacing/icd: n/a 3. other past medical history: -occult sbe with aortic valve vegetation -severe phtn -severe pvd s/p multiple vascular surgeries -rt fem- bypass -rt cea following cva prior to -lt cea following tia -stenting of lcx dpromus - of prox/mid lad with promus stent social history: pt livers with two daughters at home. tob: 0.5ppd x40years (since age 17) etoh: social - 2 beers every 2 weeks illicit drug use: denies family history: father had mi in his 50's and stroke in his 60's. siblings with dm. physical exam: admission physical exam: vs: t=96.7 bp=103/66 hr=72 rr=10 o2 sat= 93% non-rebreather general: nad. oriented x3. mood, affect appropriate. heent: ncat. sclera anicteric. perrl, eomi. conjunctiva were pink, no pallor or cyanosis of the oral mucosa. no xanthalesma. neck: supple with jvp to the earlobes cardiac: pmi located in 5th intercostal space, midclavicular line. rr, normal s1, loud s2. no m/r/g. s3 at apex. no thrills, lifts. lungs: rales halfway up bases abdomen: soft, obese, ntnd. no hsm or tenderness. abd aorta not enlarged by palpation. no abdominial bruits. extremities: 2+ pitting to mid shin, several old scars from prior vascular surgery procedures. no femoral bruits. skin: mild stasis dermatitis changes. pulses: right: carotid 2+ femoral 2+ popliteal 1+ dp 2+ pt 2+ left: carotid 2+ femoral 2+ popliteal 1+ dp dopplerable, pt dopplerable . discharge physical exam: patient expired. pertinent results: admission labs: . 06:24pm blood wbc-12.5* rbc-4.46 hgb-11.4* hct-35.8* mcv-80* mch-25.5* mchc-31.7 rdw-17.5* plt ct-348 06:24pm blood neuts-77* bands-0 lymphs-18 monos-4 eos-0 baso-0 atyps-1* metas-0 myelos-0 nrbc-1* 06:24pm blood hypochr-3+ anisocy-1+ poiklo-2+ macrocy-normal microcy-2+ polychr-normal ovalocy-occasional target-occasional burr-2+ 06:24pm blood pt-17.0* ptt-34.3 inr(pt)-1.5* 06:24pm blood glucose-40* urean-45* creat-1.8* na-131* k-3.6 cl-93* hco3-22 angap-20 06:24pm blood ck(cpk)-180 05:17am blood alt-81* ast-65* ld(ldh)-365* ck(cpk)-149 alkphos-88 totbili-1.2 06:24pm blood ck-mb-13* mb indx-7.2 ctropnt-0.37* 06:24pm blood calcium-8.7 phos-5.6* mg-1.4* . pertinent labs: . 06:24pm blood ck-mb-13* mb indx-7.2 ctropnt-0.37* 05:17am blood ck-mb-11* mb indx-7.4* ctropnt-0.31* 08:54pm blood ck-mb-9 ctropnt-0.35* 04:23am blood ck-mb-29* mb indx-10.1* ctropnt-1.00* 04:23am blood cortsol-32.8* 04:23am blood tsh-2.1 05:41am blood lactate-1.7 03:52pm blood lactate-2.5* 11:26pm blood lactate-7.5* 01:50am blood lactate-8.7* 04:24am blood lactate-11.1* 05:05am blood lactate-10.3* 11:38am blood lactate-5.1* 03:52pm blood type-art po2-52* pco2-35 ph-7.42 caltco2-23 base xs 01:50am blood type- po2-40* pco2-69* ph-7.02* caltco2-19* base xs--15 04:24am blood type-central ve po2-53* pco2-60* ph-7.10* caltco2-20* base xs--11 05:05am blood type-central ve po2-52* pco2-58* ph-7.16* caltco2-22 base xs--8 11:38am blood type- po2-42* pco2-73* ph-7.20* caltco2-30 base xs--1 . discharge labs: . 11:16am blood wbc-26.6*# rbc-4.37 hgb-11.3* hct-36.8 mcv-84 mch-25.8* mchc-30.6* rdw-16.9* plt ct-335 04:23am blood glucose-506* urean-41* creat-1.8* na-131* k-4.2 cl-89* hco3-19* angap-27* 04:23am blood alt-226* ast-262* ld(ldh)-905* ck(cpk)-288* alkphos-89 totbili-1.7* 04:23am blood ck-mb-29* mb indx-10.1* ctropnt-1.00* 04:23am blood albumin-3.4* calcium-8.1* phos-7.3*# mg-2.5 11:38am blood type- po2-42* pco2-73* ph-7.20* caltco2-30 base xs--1 11:38am blood lactate-5.1* . micro/path: . blood cultures x 2: pending mrsa screen: pending . imaging/studies: . cxr portable : impression: mild interstitial pulmonary edema is present, along with a very small right pleural effusion, decreased since . heart size is top normal, and the main pulmonary artery is substantially dilated, as before indicating persistent pulmonary arterial hypertension. previous mediastinal adenopathy documented on the chest ct in is difficult to assess but probably has not worsened. no pneumothorax. . aorta/branches u/s : impression: no evidence of abdominal aortic aneurysm. atherosclerosis. . cxr portable : tip of the new right internal jugular line ends in the region of the superior cavoatrial junction. no pneumothorax or increase in small right pleural effusion. interval increase in mediastinal caliber due to vascular engorgement, and due to elevated central venous pressure, probably a function of biventricular heart failure, reflected mild increase in the heart size, moderate increase in pulmonary edema. severe pulmonary atrial enlargement, an indication of marked pulmonary arterial hypertension, aortic valvular calcification, which could be hemodynamically significant (particularly in setting of decreased lv filling), and severe, global coronary calcification were shown on a chest ct in , discussed with dr at the time of dictation. . r leni : impression: limited assessment of the right lower extremity due to early termination of the examination. no dvt seen in the examined veins. . cxr portable : findings: in comparison with the study of , there has been placement of an endotracheal tube with its tip at the upper clavicular level, approximately 6.5 cm above the carina. nasogastric tube extends into the upper stomach, though the side hole is within the lower portion of the esophagus. continued enlargement of the cardiac silhouette with substantial pulmonary arterial enlargement consistent with pulmonary artery hypertension. there is moderate pulmonary edema as well. . tte :the left atrium is mildly dilated. the estimated right atrial pressure is at least 15 mmhg. left ventricular wall thicknesses and cavity size are normal. there is severe global left ventricular hypokinesis. the basal inferolateral wall contracts best (lvef = 25%). the right ventricular cavity is moderately dilated with severe global free wall hypokinesis. there is abnormal septal motion/position consistent with right ventricular pressure/volume overload. the aortic valve leaflets are mildly thickened (?#). no aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. there is no mitral valve prolapse. mild (1+) mitral regurgitation is seen. moderate to severe tricuspid regurgitation is seen. there is no pericardial effusion. impression: suboptimal image quality. normal left ventricular cavity size with extensive systolic dysfunction c/w diffuse process (multivessel cad, toxin, metabolic, etc.). marked right ventricular cavity dilation with free wall hypokinesis and abnormal septal motion c/w marked pulmonary artery hypertension (not quantified). moderate to severe tricuspid regurgitation. mild mitral regurgitation. compared with the prior study (images reviewed) of , biventricular systolic function has deteriorated and the heart rate is much higher. biventricular cavity size is similar. brief hospital course: 62f with hx of severe of pulm htn, cad s/p des to lcx/lad in , prior cva s/p b/l cea's, pvd, and transferred from osh for evaluation and management of right-sided diastolic chf exacerbation with background of severe pulmonary hypertension who rapidly decompensated and passed away despite maximal medical therapy. . active diagnoses: . # right-sided diastolic chf exacerbation: pt with clinical evidence of rales halfway up lung fields, jvd, and peripheral edema on admission with cxr evidence of pulmonary edema and bnp 11,000 at osh, and echo demonstrating fluid overloaded rv with s3 gallop on exam. she was ruled out for acs at osh with negative enzymes and non-ischemic ekg's and was transferred on dopamine drip for pressure support with max o2 on venturi mask in moderate respiratory distress satting in the low 90's. on arrival to the ccu, r ij was placed without complications and she was started on sildenafil 20mg qid with the hope that pressor support and vasodilatation of the pulmonary vasculature would increase cardiac output and allow for gentle diuresis. unfortunately she was found to be anuric despite these measures with a cr of 1.8 on transfer up from 0.8-0.9 the days prior at osh. in the late morning the day following transfer, dobutamine was added in an attempt to improve ionotropy but after this medication was started her bp began to drop and over the next few hours norepinephrine had to be added to maintain maps >65. these medications were up and down titrated to try to achieve a stable blood pressure but this kept ranging from 70/40-140/50. no stability could be reached. at the same time her hr was between 100-130's. the ccu team (including the ccu attending) attempted to place an arterial line for better bp monitoring given very severe peripheral vascular disease but this was unsuccesful via the radial aproach. anesthesia was contact to attempt an axial arterial line but this was not deemed feasible. the anesthesia attending attempted to obtain a l femoral arterial line without success. the right side was not attempted given her previous fem- bypass. through all of this her oxygenation was worsening and she had to be switched to 100% non-rebreather. at around 1600 dobutamine was stopped as this was felt to be contributing to her persistently low bp's. she remained stable until around 2100 when her bp again began to decrease. a 250 ml ns bolus was given without response and phenylephrine was started at this point. also at around this time her oxygen saturation began to drop and bipap was started. at this point the patient was on dopamine, norepinephrine and phenylephrine for bp support and bipap for respiratory support with bp in the 79/55-101/57 and o2 sat of 90%. at 2300 (after ~3 hrs on bipap) given her tenious state with persistently low bp, persistnently low o2 sat and tachypnea a discussion was held with the patient and the family regarding endotracheal intubation. given her worseining cardiopulmonary status the ccu team recommended intubation to try to achieve better oxygenation, prevent respiratory colapse and to allow us to manage her worsening heart failure while maintaing a patent airway with adequate oxygenation. anesthesia was called at 0000 for non-emergent intubation. this was performed succesfully and the patient tolerated it well. at ~0030, milrinone was added in an attempt to improve ionotropy. at this point the anesthesia attending was asked for assistance in placing an arterial line given the need for better blood pressure and oxygenation parameters. right radial was attempted as well as left femoral without success. at around 0100-0130 her bp began to drop, milrinone was stopped and vasopressin added. despite these 4 pressors her bp continued to drop. at this point she was given 4 amps of bicarb, 1 mg epinephrine and 1 amp of calcium carbonate. her family was updated of her condition. despite all of these additions her bp continued to drop and at this point a bicarb drip and an epinephrine drip were started. after this she stabilized at around 0200 and remained with hr 120-130's and sbp 80-100's for the next several hours. at around 0500 the ventilator began alarming due to high peak/plateau pressures. this was thought to be due to pulmonary edema as repeated succitioning brought up frothy fluid. she was continued on max doses of 5 pressors throughout the day with maximal respiratory settings for the sake of oxygenation. her condition continued to deteriorate despite maximal medical support. her family was made aware of her grave circumstances and started to carefully consider her code status. she coded in the later morning 2 days following transfer for pulseless electrical activity and was coded briefly until resuscitative efforts were halted per family request. the cause of her rapid decline was unclear but hypothesis of the team included possibly a pe (with suboptimal leni which was negative). she has an abdominal ultrasound to look for possible ruptured aaa given report of acute onset low back pain at osh but this was negative. . # anuric acute kidney injury: cr 1.8 on admission with oliguria/near anuria, 0.6-0.7 at baseline. was 0.9 yesterday at osh and making urine. thought to be due to her brief hypotensive episode after receiving bolus of 40mg iv lasix at osh. # severe chronic pulmonary hypertension/cor pulmonale: unclear etiology. perhaps related to her mild-moderate copd on ct (although re-assuring spirometry in records) or possibly recurrent embolic phenomena. she was treated aggressively as above but unfortunately had a poor outcome. . chronic diagnoses: . # copd/hypoxia: pt with mild-moderate copd changes on most recent ct chest but with essentially normal pft's. she requires 3lnc at home often worn during sleep but more recently during the day and even when at rest. has a 20-40 pack-year smoking history. not on any home copd medications. she ended up ventilated for respiratory support as above. . # cad: pt with severe 3vd with prior 2 to lcx and lad in 8/. non-ischemic ekg here on admission and at osh. enzymes unimpressive x 3. no chest pain or discomfort. she was continued on aspirin, plavix, and a statin. . # hld: stable. continued on her statin. . # severe pvd: stable. continued on her statin. . # niddm complicated by neuropathy: stable. managed on hiss while in-house as well as lyrica and gabapentin prior to her hemodynamic compromise. . transitional issues: -to the deep regret of the ccu team, mrs. did very poorly over her hospital course. her team took solace in the fact that she was surrounded by her large, loving family and hopefully felt little pain or suffering in her final hours. medications on admission: - plavix 75mg po daily - gabapentin 200mg po qhs - aspirin 81mg po daily - metoprolol succinate 100mg po daily - ativan 1mg po tid prn - metformin 100mg po bid - glyburide 2.5mg po daily - lisinopril 2.5mg po daily - torsemide 40mg po daily - lyrica 100mg po bid - tylenol pm 1 tab qhs - simvastatin 40mg po daily - prilosec 20mg po daily - niacin 500mg po bid discharge medications: n/a discharge disposition: expired discharge diagnosis: -severe pulmonary hypertension/cor pulmonale -biventricular diastolic congestive heart failure -severe peripheral vascular disease -chronic obstructive pulmonary disease discharge condition: deceased discharge instructions: patient was transferred from osh for acute decompensated biventricular heart failure complicated by severe pulmonary hypertension. she was managed aggressively with pressors (5 at max doses) with the goal to optimize her cardiac function with the hope of inducing diuresis. unfortunately her hemodynamics declined rapidly. code was called for pea with initiation of chest compressions and epi x 1 at which time code was called off per family preference. followup instructions: n/a procedure: venous catheterization, not elsewhere classified non-invasive mechanical ventilation diagnoses: congestive heart failure, unspecified acute kidney failure, unspecified chronic airway obstruction, not elsewhere classified acute on chronic diastolic heart failure diabetes with neurological manifestations, type ii or unspecified type, not stated as uncontrolled polyneuropathy in diabetes peripheral vascular disease, unspecified percutaneous transluminal coronary angioplasty status primary pulmonary hypertension personal history of transient ischemic attack (tia), and cerebral infarction without residual deficits 

Answer: The patient is high likely exposed to