ischemic hf case presentation

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ISCHEMIC HEART FAILURE TYPE 1V CASE PRESENTATION. Dr Asadullah Khan soomro E-mail; [email protected]

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Page 1: Ischemic hf case presentation

ISCHEMICHEART FAILURE

TYPE 1VCASE

PRESENTATION. Dr Asadullah Khan soomro

E-mail; [email protected]

Page 2: Ischemic hf case presentation

Case No 1 ( 100020548)Date &time of admission 17. 3. 2015, at 6.11

PmMode of Admission: Through ER.Date & time of Expiry: 8 . 4 . 2015 , at 10.50

Pm(Expired on 21th day of hospitalization)

DIAGNOSISPost CABG , haemorrhagic shock

severe diffuse 3 VD CAD Ischemic heart failure syndrome with severe LV systolic dysfunction ( type 1V) stage C ( Compensated) .Acute hypoxic

liver injury, cardio-renal syndrome. Syncope, moderate MR, Severe TR &

pulmonary hypertension. HTN & Smoker.

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Executive Summary50 year non saudi male hypertensive

& smoker ,presented to KFHH ER with history of progressive

breathlessness & fatigue for the last 6 months became severe at rest on the day of admission. No H/o chest pain suggestive of angina or

myocardial infarction.Evaluated by on call ,and admitted as

acute decompensated heart failure syndrome, echocardiogram showed

severe global LV systolic dysfunction EF < 20%.

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Cont, After HF stablization underwent Coronary angiogram and showed

severe diffuse 3VD CAD.Discussed in combined meeting and

was recommended for viability study, which showed dilated LV

prominent RV with increase lung uptake.

There were two totally reversible defect in LAD & LCX territory.

However RCA had irreversible ( non viable scar)

defect EF, 19%

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Cont, He was re discussed and was

accepted for high risk PCI. Later reviewed by

interventionalist team and deferred for PCI.

Again third time discussed in combined meeting and was

accepted for high risk CABG ( Euro-score 6.4 &

mortality around 5-10%)

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Cont,

Prepared for CABG IABP was inserted on 6th April, evaluated by pulmonologist and CT chest was done for pleural effeusion

prior to CABG.On 7 th April underwent CABG, all

arteries were deeply intramyocardial.

Had 4 grafts, LIMA to mid LAD, SVG to Diagonal & PDA of the RCA. OM was totally

occluded.

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Cont,

In recovery suddenly became hypotensive VT/Vib , re-opened again, bleeding

points were secured, another SV Grafting was done to LAD.

In view of his haemodynamic instability along with IABP ,ECMO was inserted and shifted to ICU in critical condition,

on multiple ionotropes .Bleeding continued through

drains ,platelets dropped to 42 along with HB% ,transfused various &

multiple blood products ( total 101, Rbc, Platelets, fresh frozen plasma &

Cryo precipitates) , all invain.

Page 8: Ischemic hf case presentation

Cont,

On 8th April again shifted to OR because of bleeding, re-thoracotomy done,

clots removed, areas of bleeding close to LAD were again sutured.

Chest packed with three large swabs, and shifted back to ICU.

On maximum haemodynamic support ( IABP ,ECMO & multiple

ionotrops) Dialysed through CRRT , subsequently developed hypoxic

hepatitis ( AST,ALT & LDH) in thousands. On the same day around 10 .20 pm developed bradycardia progressed to

asystole , resuscitation done but failed and expired at 10.50 Pm.

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PAST HISTORY6 months back was admitted to PSBJ H with

H/O progressive breathlessness FC11 & syncope .

Fell down from the bed while he was sitting alone ,recovered spontaneously after some time , sustained fascial injury with bleeding ,therefore went to hospital EKG & X-rays were done ,but prior to full evaluation left against medical advise ( LAMA).

Last time admitted to KFHH with worsening of symptoms of heart failure, however considered as suspected corona virus and remained in isolation ward untill cleared from dammam reports that corona is negative.

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Echocardiogram (26.3.15)

Moderately dilated LA /LV with severe global LV systolic

dysfunction EF < 20%. Normal RA/ RV size, and function.

Moderate Mitral Regurgitation. Severe TR, PASP= 50 – 55 mm. Intact septa , IVC mildly dilated.No pericardial effusion. No Clot.

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Coronary Angiogram

( 26.3.2015)LM: 30% plaque mid and at bifurcation.LAD: Type 3 vessel , mid 90% diffuse

disease, distally graftable .LCX: Non dominant . CTO proximally,

filling from RCA.

RCA: Dominant, diffuse disease, 50% proximal, 75% mid and 90% distal. PLVB diffusely diseased, PDA occluded filling from LCA .

Conclusion : Severe 3 VD diffuse disease for

discussion.

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CBC/Biochemistry (100020548)

8.4.2015

After CABG 7.4.2015

18.3.2015

50-100

Troponin

8.8 8.7 17.1 6.5 WBC

10.2 10 10 15.3 HEMOGLOBIN %

45,23,40 279 193 325 PLATELETS

1.8 PTT> 120

3.1 0.9 INR

21.8 5.2 4.6 GLUCOSE

8.1,6.9 9.1 7.7 BUN

170,171 113 87 CREATININE

840,947 493 99 CPK

Negative Sickling 315,313 125 17 CKMB

4.8 T3, 158,150 146 138 SODIUM

15.2 T4 4.8 , 5.2 3.9 3.9 POTASSIUM

2.4 TSH 1.5 2.1 CALCIUM

1.02 0.7 MAGNESIUM

420 564 URIC ACID

1.4 3.7 CHOLESTEROL

0.8 0.8 TRIGLYCERIDE

0.5 1.0 HDL

0.5 2.1 LDL

Troponin

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Liver function test (10020548)

8.4.2015 7.4.2015Post CABG

31.3.14 18.3.2015 Name of Test

B+Ve Bloodgroup

22.7 33.0 Total Bilirubin

5.1 19.0 Direct Bilirubin

Negative

HCV 1915 697 27 30 ALT

Negativ

Hbs 2784 695 47 36 AST

Negativ

HIV 2976 3185 299 354 LDH

18.4 / 9 14 ,13 32 72.4/22 T protein/

Albumin

190 117 Alpo4

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Transfusion ( total 101 units)

( Haemorrhagic shock)

Fresh FrozenPlasma

22Units

RBC

26Units

Cryo precipitate

23Units

Platelets

30Units

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