CHIEF COMPLAINT: Transfer from [**Hospital3 **] where she was admitted for
atypical chest pain and SOB

PRESENT ILLNESS: 62F with hx of severe of pulm HTN, CAD s/p DES to Lcx/LAD in
[**10/2177**], prior CVA s/p b/l CEA's, PVD, and COPD who was admitted
to OSH [**12-23**] 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 [**9-9**] 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 [**12-24**]
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.

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-[**Doctor Last Name **] bypass
-Rt CEA following CVA prior to [**2173**]
-Lt CEA following TIA [**2173**]
-Stenting of LCx DPromus [**Name Prefix (Prefixes) **]
-[**Last Name (Prefixes) **] of Prox/Mid LAD with Promus Stent

MEDICATION 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

ALLERGIES: No Known Allergies / Adverse Drug Reactions

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.

FAMILY HISTORY: Father had MI in his 50's and stroke in his 60's.  Siblings with

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
Acute on chronic diastolic heart failure,Acute kidney failure, unspecified,Primary pulmonary hypertension,Chronic airway obstruction, not elsewhere classified,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,Personal history of transient ischemic attack (TIA), and cerebral infarction without residual deficits
Ac on chr diast hrt fail,Acute kidney failure NOS,Prim pulm hypertension,Chr airway obstruct NEC,DMII neuro nt st uncntrl,Neuropathy in diabetes,Periph vascular dis NOS,Status-post ptca,Hx TIA/stroke w/o resid
Admission Date:  [**2178-12-25**]              Discharge Date:   [**2178-12-27**]

Date of Birth:  [**2116-2-19**]             Sex:   F

Service: MEDICINE

Allergies:
No Known Allergies / Adverse Drug Reactions

Attending:[**First Name3 (LF) 7055**]
Chief Complaint:
Transfer from [**Hospital3 **] 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
[**10/2177**], prior CVA s/p b/l CEA's, PVD, and COPD who was admitted
to OSH [**12-23**] 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 [**9-9**] 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 [**12-24**]
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-[**Doctor Last Name **] bypass
-Rt CEA following CVA prior to [**2173**]
-Lt CEA following TIA [**2173**]
-Stenting of LCx DPromus [**Name Prefix (Prefixes) **]
-[**Last Name (Prefixes) **] 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:
.
[**2178-12-25**] 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
[**2178-12-25**] 06:24PM BLOOD Neuts-77* Bands-0 Lymphs-18 Monos-4 Eos-0
Baso-0 Atyps-1* Metas-0 Myelos-0 NRBC-1*
[**2178-12-25**] 06:24PM BLOOD Hypochr-3+ Anisocy-1+ Poiklo-2+
Macrocy-NORMAL Microcy-2+ Polychr-NORMAL Ovalocy-OCCASIONAL
Target-OCCASIONAL Burr-2+
[**2178-12-25**] 06:24PM BLOOD PT-17.0* PTT-34.3 INR(PT)-1.5*
[**2178-12-25**] 06:24PM BLOOD Glucose-40* UreaN-45* Creat-1.8* Na-131*
K-3.6 Cl-93* HCO3-22 AnGap-20
[**2178-12-25**] 06:24PM BLOOD CK(CPK)-180
[**2178-12-26**] 05:17AM BLOOD ALT-81* AST-65* LD(LDH)-365* CK(CPK)-149
AlkPhos-88 TotBili-1.2
[**2178-12-25**] 06:24PM BLOOD CK-MB-13* MB Indx-7.2 cTropnT-0.37*
[**2178-12-25**] 06:24PM BLOOD Calcium-8.7 Phos-5.6* Mg-1.4*
.
PERTINENT LABS:
.
[**2178-12-25**] 06:24PM BLOOD CK-MB-13* MB Indx-7.2 cTropnT-0.37*
[**2178-12-26**] 05:17AM BLOOD CK-MB-11* MB Indx-7.4* cTropnT-0.31*
[**2178-12-26**] 08:54PM BLOOD CK-MB-9 cTropnT-0.35*
[**2178-12-27**] 04:23AM BLOOD CK-MB-29* MB Indx-10.1* cTropnT-1.00*
[**2178-12-27**] 04:23AM BLOOD Cortsol-32.8*
[**2178-12-27**] 04:23AM BLOOD TSH-2.1
[**2178-12-26**] 05:41AM BLOOD Lactate-1.7
[**2178-12-26**] 03:52PM BLOOD Lactate-2.5*
[**2178-12-26**] 11:26PM BLOOD Lactate-7.5*
[**2178-12-27**] 01:50AM BLOOD Lactate-8.7*
[**2178-12-27**] 04:24AM BLOOD Lactate-11.1*
[**2178-12-27**] 05:05AM BLOOD Lactate-10.3*
[**2178-12-27**] 11:38AM BLOOD Lactate-5.1*
[**2178-12-26**] 03:52PM BLOOD Type-ART pO2-52* pCO2-35 pH-7.42
calTCO2-23 Base XS
[**2178-12-27**] 01:50AM BLOOD Type-[**Last Name (un) **] pO2-40* pCO2-69* pH-7.02*
calTCO2-19* Base XS--15
[**2178-12-27**] 04:24AM BLOOD Type-CENTRAL VE pO2-53* pCO2-60* pH-7.10*
calTCO2-20* Base XS--11
[**2178-12-27**] 05:05AM BLOOD Type-CENTRAL VE pO2-52* pCO2-58* pH-7.16*
calTCO2-22 Base XS--8
[**2178-12-27**] 11:38AM BLOOD Type-[**Last Name (un) **] pO2-42* pCO2-73* pH-7.20*
calTCO2-30 Base XS--1
.
DISCHARGE LABS:
.
[**2178-12-27**] 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
[**2178-12-27**] 04:23AM BLOOD Glucose-506* UreaN-41* Creat-1.8* Na-131*
K-4.2 Cl-89* HCO3-19* AnGap-27*
[**2178-12-27**] 04:23AM BLOOD ALT-226* AST-262* LD(LDH)-905*
CK(CPK)-288* AlkPhos-89 TotBili-1.7*
[**2178-12-27**] 04:23AM BLOOD CK-MB-29* MB Indx-10.1* cTropnT-1.00*
[**2178-12-27**] 04:23AM BLOOD Albumin-3.4* Calcium-8.1* Phos-7.3*#
Mg-2.5
[**2178-12-27**] 11:38AM BLOOD Type-[**Last Name (un) **] pO2-42* pCO2-73* pH-7.20*
calTCO2-30 Base XS--1
[**2178-12-27**] 11:38AM BLOOD Lactate-5.1*
.
MICRO/PATH:
.
Blood Cultures x 2: Pending
MRSA Screen: Pending
.
IMAGING/STUDIES:
.
CXR Portable [**12-25**]:
IMPRESSION: Mild interstitial pulmonary edema is present, along
with a very small right pleural effusion, decreased since [**9-5**]. 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 [**Month (only) 216**] is difficult to assess but
probably has not worsened. No pneumothorax.
.
Aorta/Branches U/S [**12-25**]:
IMPRESSION: No evidence of abdominal aortic aneurysm.
Atherosclerosis.
.
CXR Portable [**12-25**]:
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 [**Month (only) 216**]
[**2178**], discussed with Dr [**First Name8 (NamePattern2) **] [**Last Name (NamePattern1) 30814**] at the time of dictation.
.
R LENI [**12-26**]:
IMPRESSION: Limited assessment of the right lower extremity due
to early
termination of the examination. No DVT seen in the examined
veins.
.
CXR Portable [**12-27**]:
FINDINGS: In comparison with the study of [**12-25**], 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 [**12-27**]: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.
[Intrinisic right ventricular systolic function is more
depressed given the severity of tricuspid regurgitation.] 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 [3+] 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 [**2178-10-16**],
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
[**10/2177**], prior CVA s/p b/l CEA's, PVD, and [**Hospital 2182**] 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[**Name (NI) **] 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-[**Doctor Last Name **] 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 [**Name Prefix (Prefixes) **] [**Last Name (Prefixes) **] 2 to LCx and LAD in
8/[**2177**]. 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. [**Known lastname **] 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



Completed by:[**2178-12-28**]
{'Acute on chronic diastolic heart failure,Acute kidney failure, unspecified,Primary pulmonary hypertension,Chronic airway obstruction, not elsewhere classified,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,Personal history of transient ischemic attack (TIA), and cerebral infarction without residual deficits'}


You are an AI assistant analyzing clinical admission notes from the MIMIC III dataset. Your task is to map symptoms mentioned in the notes to a list of provided ICD-9 LONG_TEXT.



### Clinical text :
CHIEF COMPLAINT: Transfer from [**Hospital3 **] where she was admitted for
atypical chest pain and SOB

PRESENT ILLNESS: 62F with hx of severe of pulm HTN, CAD s/p DES to Lcx/LAD in
[**10/2177**], prior CVA s/p b/l CEA's, PVD, and COPD who was admitted
to OSH [**12-23**] 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 [**9-9**] 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 [**12-24**]
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.

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-[**Doctor Last Name **] bypass
-Rt CEA following CVA prior to [**2173**]
-Lt CEA following TIA [**2173**]
-Stenting of LCx DPromus [**Name Prefix (Prefixes) **]
-[**Last Name (Prefixes) **] of Prox/Mid LAD with Promus Stent

MEDICATION 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

ALLERGIES: No Known Allergies / Adverse Drug Reactions

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.

FAMILY HISTORY: Father had MI in his 50's and stroke in his 60's.  Siblings with

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 

### Response:
{'Acute on chronic diastolic heart failure,Acute kidney failure, unspecified,Primary pulmonary hypertension,Chronic airway obstruction, not elsewhere classified,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,Personal history of transient ischemic attack (TIA), and cerebral infarction without residual deficits'}
