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EDEMA due to Cardiac Cause Prof. A. George Koshy.

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Presentation on theme: "EDEMA due to Cardiac Cause Prof. A. George Koshy."— Presentation transcript:

1 EDEMA due to Cardiac Cause Prof. A. George Koshy

2 Anatomy and pathophysilolgy 1/3 of total body water is extracellular space, and 2/3 is intracellular space; 1/3 of total body water is extracellular space, and 2/3 is intracellular space; Extracellular space is composed of the intravascular plasma volume (25%) and the extravascular interstitial spaces (75%); Extracellular space is composed of the intravascular plasma volume (25%) and the extravascular interstitial spaces (75%);

3 EDEMA Edema is defined as a clinically apparent increase in the interstitial fluid volume Edema is defined as a clinically apparent increase in the interstitial fluid volume Weight gain precedes overt edema Weight gain precedes overt edema Anasarca refers to gross, generalized edema. Anasarca refers to gross, generalized edema. Ascites and hydrothorax refer to accumulation of excess fluid in the peritoneal and pleural cavities, respectively, and are considered to be special forms of edema. Ascites and hydrothorax refer to accumulation of excess fluid in the peritoneal and pleural cavities, respectively, and are considered to be special forms of edema.

4 Edema Pitting edema Non-pitting edema

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6 Five factors contribute to the formation of edema: Five factors contribute to the formation of edema:  by increased hydrostatic pressure hydrostatic pressurehydrostatic pressure  reduced oncotic pressure within blood vessels; oncotic pressureoncotic pressure  by increased blood vessel wall permeability as in inflammation; inflammation  by obstruction of fluid clearance via the lymphatic system; lymphatic system lymphatic system  by changes in the water retaining properties of the tissues

7 Approach to the patient with Edema Generalized Localized or Heart Liver Kidney Nutritional Venous obstruction Lymphatic obstruction

8 Systemic Edema Congestive heart failure

9 Congestive heart failure Left-sided heart failure: shortness of breath with exertion and when lying down at night (orthopnea) PND, pulmonary edema Left-sided heart failure: shortness of breath with exertion and when lying down at night (orthopnea) PND, pulmonary edema Right-sided heart failure: swelling in the legs and feet. Ascites. Right sided Pleural effusion. Right-sided heart failure: swelling in the legs and feet. Ascites. Right sided Pleural effusion.

10 Differential diagnosis Heart Failure Edema initially occurs at lower part of the Edema initially occurs at lower part of the body (lower extremities). body (lower extremities). Symmetric location. Symmetric location. Painless, Pitting Painless, Pitting The presence of heart diseases The presence of heart diseases Dyspnoea cardiac enlargement gallop rhythm Dyspnoea cardiac enlargement gallop rhythm basilar rales venous distention hepatomegaly basilar rales venous distention hepatomegaly Noninvasive tests may be helpf Noninvasive tests may be helpf CXR ECG echocardiography CXR ECG echocardiography

11 Heart Failure Elevated JVP Elevated JVP Tender hepatomegaly Tender hepatomegaly

12 Heart Failure Systolic HF Systolic HF Diastolic HF/ HF with preserved LV systolic function. Near normal LVEF. Diastolic HF/ HF with preserved LV systolic function. Near normal LVEF. Combination Combination

13 CME Cardio 2003 MCH Trivandrum

14 Multi factorial Multi factorial Renal vasoconstriction Renal vasoconstriction Increased aldosterone & vasopressin activity Increased aldosterone & vasopressin activity Increased sympathetic tone Increased sympathetic tone Increased venous pressure Increased venous pressure Even with asymptomatic LVD, renal avidity Even with asymptomatic LVD, renal avidity for Na &H 2 O is enhanced for Na &H 2 O is enhanced Edema in CHF

15 Cortex Medulla Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop of Henle Collecting tubule

16 Loop diuretics preferred … More powerful natriuretic agents. More powerful natriuretic agents. Effective even with renal impairment Effective even with renal impairment High ceiling diuretics High ceiling diuretics Increase in vasodilatory ANP Increase in vasodilatory ANP

17 Loop diuretics Furosemide Furosemide Bumetanide Bumetanide Torsemide Torsemide Ethacrynic acid Ethacrynic acid

18 Loop diuretics Furosemide Furosemide Oral Oral Bioavailability-50%, Onset mts Peaks-1-2 hrs, Half life 50 mts Bioavailability-50%, Onset mts Peaks-1-2 hrs, Half life 50 mts LAsts for SIX hrs. LAsts for SIX hrs. Intravenous –Onset 15 mts, Peaks mts Duration 2 hrs. Transient venodilatation in Intravenous –Onset 15 mts, Peaks mts Duration 2 hrs. Transient venodilatation in acute pulmonary edema - vasodilator prostaglandins acute pulmonary edema - vasodilator prostaglandins

19 Loop diuretics Torsemide Longer duration of action Longer duration of action IV dose 10 to 20mgms in HF IV dose 10 to 20mgms in HF 80 % hepatic metabolism, 20 % excreted unchanged in urine 80 % hepatic metabolism, 20 % excreted unchanged in urine 80-90% Bioavailability, Peaks in 2 hrs, HL in 3.3 hrs, prolonged in cirrhosis 80-90% Bioavailability, Peaks in 2 hrs, HL in 3.3 hrs, prolonged in cirrhosis In CHF, absorption is unimpaired and less variable than furosemide In CHF, absorption is unimpaired and less variable than furosemide

20 Loop diuretics Rebound phenomenon- a decrease in sodium excretion below baseline after the effect of the loop diuretic has worn off. Volume depletion activates the sodium retaining mechanisms Rebound phenomenon- a decrease in sodium excretion below baseline after the effect of the loop diuretic has worn off. Volume depletion activates the sodium retaining mechanisms Braking phenomenon –increase in sodium reabsorption by the distal tubule that occurs with chronic diuretic therapy Braking phenomenon –increase in sodium reabsorption by the distal tubule that occurs with chronic diuretic therapy

21 Diuretics. Indications Symptomatic HF, with fluid retention Symptomatic HF, with fluid retention  Edema  Dyspnea  Lung Rales  Jugular distension  Hepatomegaly  Pulmonary edema (Xray)

22 Diuretic Resistance Neurohormonal activation Neurohormonal activation Rebound Na + uptake after volume loss Rebound Na + uptake after volume loss Hypertrophy of distal nephron Hypertrophy of distal nephron Reduced tubular secretion (renal failure, NSAIDs) Reduced tubular secretion (renal failure, NSAIDs) Decreased renal perfusion (low output) Decreased renal perfusion (low output) Altered absorption of diuretic Altered absorption of diuretic Noncompliance with drugs Noncompliance with drugs

23 Managing Resistance to Diuretics Restrict sodium and water intake Restrict sodium and water intake Increase dose (individual dose, frequency, i.v.) Increase dose (individual dose, frequency, i.v.) Combine: furosemide + thiazide/spironolactone/metolazone Combine: furosemide + thiazide/spironolactone/metolazone Dopamine (increase cardiac output) Dopamine (increase cardiac output) Reduce dose of ACEI Reduce dose of ACEI Ultrafiltration Ultrafiltration

24 Sequential Nephron Blockade Combination of diuretics acting at different sites, by differing modes of action provides synergistic benefits

25 ALDOSTERONE Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Collagen deposition Fibrosis - myocardium - vessels Spironolactone Edema Arrhythmias Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Aldosterone Inhibitors -

26 Aldactone Placebo Survival months p < Annual Mortality Aldactone 18%; Placebo 23% N = 1663 NYHA III-IV Mean follow-up 2 y RALES NEJM 1999;341:709 Spironolactone

27 Spironolactone. Indications Recent or recurrent symptoms despite ACEI, diuretics, digoxin and  -blockers Recent or recurrent symptoms despite ACEI, diuretics, digoxin and  -blockers AHA / ACC HF guidelines 2001 AHA / ACC HF guidelines 2001 Recommended in advanced heart failure (III-IV), in addition to ACEI and diuretics Recommended in advanced heart failure (III-IV), in addition to ACEI and diuretics Hypokalemia Hypokalemia ESC HF guidelines 2001 ESC HF guidelines 2001

28 EPHESUS

29 Special precautions … Elderly Elderly Diastolic dysfunction Diastolic dysfunction RVMI RVMI Pregnancy Pregnancy Electrolyte abnormalities Electrolyte abnormalities Combination therapy Combination therapy

30 Digitalis

31 DIGOXIN HEMODYNAMIC EFFECTS Cardiac output LV  ejection fraction LVEDP Exercise  tolerance

32 DIGOXIN NEUROHORMONAL EFFECTS Plasma Noradrenaline Natriuresis RAAS activity Vagal tone Normalizes arterial baroreceptors

33 Placebo n=3403 Digoxin n= Mortality % DIG NEJM 1997;336:525 Months p = 0.8 N=6800 NYHA II-III

34 CME Cardio 2003 MCH Trivandrum Death or hospitalization due to worsening HF DIG NEJM 1997;336:525

35 Only inotropic agent than does not increase HR Only inotropic agent that does not increase mortality

36 Indications Out patient treatment of all patients who have persistent symptoms NYHA class 2 to 4 despite conventional therapy with diuretics, ACEI, beta blockers Out patient treatment of all patients who have persistent symptoms NYHA class 2 to 4 despite conventional therapy with diuretics, ACEI, beta blockers AF with fast ventricular response AF with fast ventricular response

37 Bat wing appearance

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39 Doppler evaluation – MV inflow

40 The Past Haemodynamic hypothesis –D amaged pump causes low blood pressure. Back pressure causes oedema. Liberal use of diuretics and Digoxin.

41 Hemodynamic Neurohormonal approach --> approach Diuretics RAAS Inotropes SNS Vasodilators

42 Drugs improving Survival Drugs acting on RAAS. Drugs acting on RAAS. ACEI. ACEI. ARB. ARB. ARA – Spironolactone, Eplerenone. ARA – Spironolactone, Eplerenone. Beta blockers. Beta blockers. ISDN + Hydralazine. ISDN + Hydralazine. Amiodarone ? Amiodarone ? Statins ? Statins ?

43 Major Trials of Beta-Blockade in HF HF Post-MI HF All-cause mortality:  23%(p=0.03)  40 N/A1.25yrs1959CAPRICORN All-cause mortality:  17%(p=0.0017) <35II-IV4.9yrs3029COMET All-cause mortality:  65% (p<0.001)  35 II–IV6.5mths1094 US Carvedilol HF Study All-cause mortality:  34% (p=0.0062)  40 II–IV1yr3991MERIT-HF All-cause mortality:  34% (p  )  35 III-IV1.3yrs2647CIBIS-II All-cause mortality:  20% (p=0.22) <40III-IV1.9yrs641CIBIS Effects on all-cause mortality LVEF (%) NYHA Class Mean Follow-up Patients CIBIS Investigators and Committees. Circulation 1994; 90: CIBIS-II Investigators and Committees. Lancet 1999; 353: MERIT-HF Study Group. Lancet. 1999; 353:2001–2007. Packer M, Bristow MR, Cohn JN et al. US Carvedilol Heart Failure Study Group. N Eng J Med 1996; 334: Poole-Wilson PA et al Lancet 2003; 362: Capricorn Investigators. Lancet 2001; 357:

44 Major Trials of ACE-Inhibitors in HF HF Post-MI HF All-cause mortality  8% (p=0.30)  35 N/A3.1yrs4228 SOLVD- Prevention All-cause mortality:  22%(p=0.001)  35 N/A2-4.2yrs1749TRACE All-cause mortality:  27%(p=0.002) N/AI–III1.25yrs2006AIRE All-cause mortality:  19%(p=0.019)  40 N/A3.5yrs2231SAVE All-cause mortality:  16% (p<0.0036)  35 II–III3.4yrs2569 SOLVD- Treatment All-cause mortality: At 6 months  40%(p=0.002) N/AIV188 days253CONSENSUS Effects on all-cause mortality LVEF (%) NYHA Class Mean Follow-up Patients (n) The CONSENSUS Trial Study Group. N Eng J Med 1987; 316: , The SOLVD Investigators. N Eng J Med 1991; 325: The SOLVD Investigators. N Eng J Med 1992; 327: , Pfeffer MA, Braunwald E, Moye LA et al. The SAVE Investigators. N Eng J Med 1992; 327: , The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Lancet 1993; 342: , Køber L, Torp-Pedersen C, Carlsen JE et al. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Eng J Med 1995; 333:

45 THANK YOU


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