EDEMA due to Cardiac Cause

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EDEMA due to Cardiac Cause

• Prof. A. George Koshy

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Anatomy and pathophysilolgy

• 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)

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EDEMA

• Edema is defined as a clinically apparent
  increase in the interstitial fluid volume
• Weight gain precedes overt 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.

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Edema
Pitting edema
Non-pitting edema
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• Five factors contribute to the formation of
  edema
• by increased hydrostatic pressure
• reduced oncotic pressure within blood vessels
• by increased blood vessel wall permeability as in
  inflammation
• by obstruction of fluid clearance via the
  lymphatic system
• by changes in the water retaining properties of
  the tissues

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Approach to the patient with Edema
Generalized
HeartLiver Kidney Nutritional
or

Localized
Venous obstructionLymphatic obstruction
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Systemic EdemaCongestive heart failure
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Congestive heart failure

• 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.

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Differential diagnosisHeart Failure

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

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Heart Failure

• Elevated JVP
• Tender hepatomegaly

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Heart Failure

• Systolic HF
• Diastolic HF/ HF with preserved LV systolic
  function. Near normal LVEF.
• Combination

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Edema in CHF

• Multi factorial
• Renal vasoconstriction
• Increased aldosterone vasopressin activity
• Increased sympathetic tone
• Increased venous pressure
• Even with asymptomatic LVD, renal avidity
• for Na H2O is enhanced

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Thiazides Inhibit active exchange of Cl-Na in
the cortical diluting segment of the ascending
loop of Henle
Cortex
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
Medulla
Loop of Henle
Collecting tubule
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Loop diuretics preferred

• More powerful natriuretic agents.
• Effective even with renal impairment
• High ceiling diuretics
• Increase in vasodilatory ANP

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Loop diuretics

• Furosemide
• Bumetanide
• Torsemide
• Ethacrynic acid

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Loop diuretics

• Furosemide
• Oral
• Bioavailability-50, Onset- 30-60 mts
  Peaks-1-2 hrs, Half life 50 mts
• LAsts for SIX hrs.
• Intravenous Onset 15 mts, Peaks 30-60 mts
  Duration 2 hrs . Transient venodilatation in
• acute pulmonary edema - vasodilator
  prostaglandins

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Loop diuretics

• Torsemide
• Longer duration of action
• IV dose 10 to 20mgms in HF
• 80 hepatic metabolism, 20 excreted unchanged
  in urine
• 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

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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
• Braking phenomenon increase in sodium
  reabsorption by the distal tubule that occurs
  with chronic diuretic therapy

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Diuretics. Indications

• Symptomatic HF, with fluid retention
• Edema
• Dyspnea
• Lung Rales
• Jugular distension
• Hepatomegaly
• Pulmonary edema (Xray)

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Diuretic Resistance

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

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Managing Resistance to Diuretics

• Restrict sodium and water intake
• Increase dose (individual dose, frequency, i.v.)
• Combine furosemide thiazide/spironolactone/meto
  lazone
• Dopamine (increase cardiac output)
• Reduce dose of ACEI
• Ultrafiltration

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Sequential Nephron Blockade

• Combination of diuretics acting at different
  sites, by differing modes of action provides
  synergistic benefits

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Aldosterone Inhibitors
ALDOSTERONE
Spironolactone
-
Competitive antagonist of the aldosterone
receptor (myocardium, arterial walls, kidney)

• Retention Na
• Retention H2O
• Excretion K
• Excretion Mg2

• Collagen
• deposition
• Fibrosis
• - myocardium
• - vessels

Edema
Arrhythmias
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Spironolactone
Annual Mortality Aldactone 18 Placebo 23
RALES NEJM 1999341709
Survival
Aldactone
p lt 0.0001
N 1663 NYHA III-IV Mean follow-up 2 y
Placebo
months
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Spironolactone. Indications

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

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EPHESUS
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Special precautions

• Elderly
• Diastolic dysfunction
• RVMI
• Pregnancy
• Electrolyte abnormalities
• Combination therapy

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Digitalis
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DIGOXINHEMODYNAMIC EFFECTS
Cardiac output LV ejection fraction LVEDP Exer
cise tolerance
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DIGOXIN NEUROHORMONAL EFFECTS
Plasma Noradrenaline Natriuresis RAAS
activity Vagal tone Normalizes arterial
baroreceptors
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N6800 NYHA II-III
Mortality
Placebo n3403
p 0.8
Digoxin n3397
0
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12
24
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DIG NEJM 1997336525
Months
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Death or hospitalization due to worsening HF
DIG NEJM 1997336525
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Only inotropic agent than does not increase
HROnly inotropic agent that does not increase
mortality
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Indications

• 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

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Bat wing appearance
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Doppler evaluation MV inflow
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The Past

• Haemodynamic hypothesis Damaged pump causes low
  blood pressure. Back pressure causes oedema.
• Liberal use of diuretics and Digoxin.

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• Hemodynamic Neurohormonal
• approach --gt approach
• Diuretics RAAS
• Inotropes SNS
• Vasodilators

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Drugs improving Survival

• Drugs acting on RAAS.
• ACEI.
• ARB.
• ARA Spironolactone, Eplerenone.
• Beta blockers.
• ISDN Hydralazine.
• Amiodarone ?
• Statins ?

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Major Trials of Beta-Blockade in HF
CIBIS Investigators and Committees. Circulation
1994 90 1765-1773. CIBIS-II Investigators and
Committees. Lancet 1999 353 9-13. MERIT-HF
Study Group. Lancet. 1999 35320012007. Packer
M, Bristow MR, Cohn JN et al. US Carvedilol Heart
Failure Study Group. N Eng J Med 1996 334
1349-1355. Poole-Wilson PA et al Lancet 2003
362 7-13. Capricorn Investigators. Lancet 2001
357 1385-1390.
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Major Trials of ACE-Inhibitors in HF
The CONSENSUS Trial Study Group. N Eng J Med
1987 316 1429-1435., The SOLVD Investigators. N
Eng J Med 1991 325 293-302. The SOLVD
Investigators. N Eng J Med 1992 327 685-691.,
Pfeffer MA, Braunwald E, Moye LA et al. The SAVE
Investigators. N Eng J Med 1992 327 669-677.,
The Acute Infarction Ramipril Efficacy (AIRE)
Study Investigators. Lancet 1993 342 821-828.,
Køber L, Torp-Pedersen C, Carlsen JE et al.
Trandolapril Cardiac Evaluation (TRACE) Study
Group. N Eng J Med 1995 333 1670-1676.
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THANK YOU