Unusual case of Heart Failure
- 1. A CASE OF HEART FAILURE Dr.SRIRAM.S PROF.Dr.P.CHITRAMBALAM’S M5 UNIT
- 2. PATIENT PROFILE 35 years female Admitted for swelling of both legs-6 months Breathlessness-4months Decreased urine output-1month
- 3. Swelling of both legs-insidious onset,slowly progressive,painless,initially subsided with rest,but not relieved by rest at present Breathlessness-grade 2 initially,now progressed to grade 4,not associated with chest pain No h/o palpitations,syncope h/o oliguria+ h/o swelling of both hands+ h/o puffiness of face+
- 4. h/o early morning stiffness+ associated with pain over small joints of hands and feet h/o intermittent abdominal distension+ No h/o abd pain,bleeding tendencies No h/o hair fall,oral ulcers,rashes anywhere,fever,photosensitivity No h/o dysphagia Bowel habits normal
- 5. No past h/o similar illness No h/o HT,DM,PT,IHD,RHD,BA in the past Family h/o-nil sig Menstural h/o-normal
- 6. G/E Pt conscious,oriented,afebrile Dyspnoeic,tachypnoeic Tender and swollen small joints of both hands and feet+ Taut skin over the face+ b/l pitting pedal edema+ Puffiness of face+ JVP elevated BP-130/80mmHg PR-106bpm,reg RR-26cycles/min,reg Temp-normal
- 7. SYSTEMS CVS-S1 S2+, S3+ no murmur RS-NVBS+,b/l basal crepts+ ABD-soft,tender hepatomegaly+ 2cm below RCM CNS-no FND
- 8. CLINICAL DIAGNOSIS CCF ? Secondary to underlying CTD
- 9. INVESTIGATIONS Hb-9.2 TC-5200 DC-P52 L42 E6 ESR-12/25 PCV-30% PLT-1Lakh MCV-65.2 MCH-24.4 MCHC-28.6
- 10. URINE Alb-neg,sugar-nil, RBS-85mg% Bl urea-22 Sr creat-0.8 Sr sodium-140meq/l Sr potassium-3.8meq/l ECG-low voltage complexes,IVCD+ Chest x-ray-cardiomegaly+ Echo-global LV hypokinesia+ severe LV systolic dysfn+ EF-22%,MR,TR-mild,PHT-moderate no pericardial effusion PFT-Restrictive pattern
- 11. ANA-POSITIVE,1:100 DIL,SPECKLED PATTERN RA factor,ASO-neg; CRP-+VE;6mg/l Anti CCP-NEG Anti SCL 70-NEG 24 hours urine protein-280mg/day LFT-sr bilirubin-1mg%;sr total proteins-6.8 TFT-T3-130ng/dl(60-200) T4-7.7micg/dl(4.5-12) TSH-4.46(0.3-5.5) aPTT 31.2 PT-18.2,INR-1.9 HRCT chest-features s/o ILD PFT-restrictive pattern Anti U1RNP- 1:100 POSITIVE Sr.CPK-24
- 12. Cardiologist opinion-severe lv dysfunction Dermatology opinion-skin biopsy s/o scleroderma Rheumatologist opinion-to r/o MCTD,To do ENA PROFILE
- 13. TREATMENT GIVEN Antifailure measures Antiplatelet agents Chloroquine Prednisolone Pt developed dry gangrene of rt index finger in hospital.she was started on heparin and warfarin.gangrene didn’t spread and few days later there was autoamputation of gangrenous part
- 14. FINAL DIAGNOSIS DCMP/CCF/RLD-SECONDARY TO OVERLAP SYNDROME
- 15. PLASMA AUTOANTIBODIES RA FACTOR 1.sjogrens-100% 2.felty’s-nearing 100% 3.RA-70% 4.Infections(endocarditis,hepatitis)<50% 5.MCTD-50% 6.SLE-<40% 7.Systemic sclerosis-30% 8.normal-2 to10%
- 16. Rheumatoid Factor Positive in 75% RA (range 26 – 90%) Negative RF dose not exclude diagnosis of RA Should order only if inflammatory joint symptoms or signs of RA Low specificity in general population (positive predictive value of less than 20%) False positives in 2-25% over 75 (Low titre) Not used to monitor response to therapy
- 17. Anti-citrullinated peptides (antiCCP) Auto-antibodies that react with citrullinated proteins (post-translational modification of arginine residues) Sensitivity 60-80% Specificity >90% (RF specificity 70%) Present 70% cases RA, 5% controls Associated with erosive disease May predict RA in cases of early inflammatory arthritis
- 18. ANA Homogenous,peripheral-SLE Speckled-MCTD Nucleolar-systemic sclerosis Centromere-limited systemic sclerosis
- 19. CAUSES SLE->95% Autoimmune hepatitis-75% Sjogrens syndrome-68% Systemic sclerosis-64% RA -30% JIA-1% Normal-0 to 2%
- 20. Anti histone antibody-drug induced SLE Anti ds DNA-SLE(60%,more specific than ANA) Anti phospolipid Ab-APLA,SLE ANTI CENTROMERE Ab-limited syst sclerosis
- 21. ANTI ENA ANTIBODIES Anti Ro(SSA)- SLE,sjogrens,systemic sclerosis Anti La(SSB)-sjogrens,SLE(15%) Anti SM-SLE(20-30%) Anti RNP-SLE,MCTD Anti Jo,anti Mi2-polymyositis,dermatomyositis Anti scl 70- diffuse systemic sclerosis
- 22. AFFECTION OF HEART IN LUNG DISEASE Lung disease causes hypoxia with cyanosis and polycythemia Hypoxia is sensed by kidneys and via carotid body,generating increases in sympathetic activity and renal vasoconstriction Increased sympathetic activity leads to salt and water retention This extra salt and water is mainly held in capacitance vessels with raised JVP If vascular permeability raises(particularly when PaCO2 rises producing peripheral vasodilation and increase in capillary pressure)etra fluid accumulates independent tissues mainly ankles
- 23. A raised JVP and ankle edema in this setting are not due to impaired right ventricular function,but fluid overload and increased vascular permeability
- 24. LEFT VENTRICULAR CHANGES IN ILD pulmonary hypertension may be the reason for changes in left ventricular (LV) geometry due to an enlarged and overloaded right ventricle However,ventricular overload may be caused by an increase in pressure or volume, or a combination of both. Resting LV systolic function is more severely depressed in patients with right ventricular (RV) volume overload compared with patients with RV pressure overload.
- 25. Most studies have demonstrated that the underfilled left ventricle found in RV pressure overload conditions, such as idiopathic pulmonary fibrosis (IPF), has relatively preserved systolic function Increasing RV pressure by pulmonary artery constriction caused regional changes in systolic shortening in the anterior, posterior, and lateral walls of the left ventricle and the septum. Similar to RV volume overload, RV pressure overload distorts left ventricular end-diastolic geometry.
- 26. In contrast to RV volume overload, with RV pressure overload,the left ventricle does not return to its normal shape in systole Angiographic and echocardiographic data from patients with chronic pulmonary hypertension have also shown abnormalities in septal geometry and motion LV systolic dysfunction, rarely present, is often due to coexisting severe right-sided heart failure with pulmonary vascular disease
- 27. THANK YOU