Pedal Edema

Diff. Diagnosis
Heart Failure: LV Systolic - Arteriosclerotic Heart Disease - Hypertensive CV Disease - Cardiomyopathies LV Diastolic

- PMH Hypertension RV Cor Pulmonale

- COPD - Sleep Apnea - 1o Pulmonary Hypertension

Biventricular - Longstanding all the above

 Drugs:

Renal Failure: Nephrotic Syndrome Glomerulonephritis Liver Failure: Cirrhosis Nutritional: Calorie Deficiency Protein Deficiency Thiamin Deficiency (Beri Beri)

Vasodilators Calcium Channel Blockers -Blockers all of them -Blockers all of them Thiazolindinediones NSAIDs all of them Corticosteroids Anabolic Steroids

Venous Obstruction Lymphagitic Obstruction

Other:
Angioedema Allergic Reactions Bacterial or Viral Infections Myxedema or Hyperthyroidism Idiopathic Edema Pregnancy & Pre-eclampsia

Etiology
Causes Related to Increased Venous Pressures1:
Congestive Heart Failure (CHF)

Thromboembolism
Lymphedema Cirrhosis of the Liver

Causes Related to Decreased Intravascular

Colloid Oncotic Pressure

Nephrotic Syndrome Nutritional Edema Refeeding Edema Protein Losing Enteropathy

Causes Related to Vasodilatation or Diminished

GFR

Beri-Beri Heart Disease Vasodilating Drugs Idiopathic Edema Premenstrual Edema Nonsteroidal Anti-inflammatory Drugs & Cyclosporine

Causes Related to Water & Sodium Retention

Acute Glomerulonephritis
Exogenous Corticosteroid Heat Edema Diuretic Withdrawal Edema Hypothyroidism

Causes Related to Capillary Endothelial Damage

- Trauma, bacterial or viral infections or allergic or immune responses are common

Pathophysio pedal Edema

Fluid Retention

Circulating Fluid Volume

Heart Failure
Heart failure is a clinical syndrome characterized by

symptoms of breathlessness and fatigue, with signs of fluid retention and supported by objective evidence of cardiac dysfunction (systolic and/or diastolic). The severity of the symptoms may be graded according to the New York Heart Association (NYHA) Functional Class

THE NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION CLASS I CLASS II No limitation. Ordinary physical activity does not cause undue fatigue, dyspnoea or palpitation Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina.

Class 1 Year Mortality . 5 10%

10 15%

CLASS III

Marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary activity will lead to symptoms.

15 20%

CLASS IV

Inability to carry on any physical activity without discomfort. Symptoms of congestive failure are present at rest. With any physical activity, increased discomfort is experienced.

20 50%

Clinical sign
Breathlessness, Ankle swelling, and Fatigue (common)

difficult to interpret, particularly in the elderly, obese, and in women. Peripheral edema, elevated jugular venous pressure and hepatomegaly characteristics signs of congestion of systemic veins. Other important clinical signs of HF tachycardia, a gallop third heart sound and pulmonary crepitations

Classification
right vs left vs biventricular heart failure, forward vs backward failure, low output vs high output heart failure, volume overload vs pressure overload, acute vs chronic heart failure, systolic vs diastolic HF.

For practical purposes, it may be sufficient to classify

HF into - acute heart failure (AHF) - chronic heart failure (CHF)

Congestive Heart Failure

Congestive Heart Failure Common Causes

Chronic CAD Hypertensive HD Rheumatic Heart Dis Congenital Heart Dis Cor pulmonale Cardiomyopathy Anemia Bacterial endocarditis Valvular disorders Acute Acute MI Dysrhythmias Pulmonary emboli Thyrotixicosis Hypertensive crisis Rupture of papillary muscle VSD Myocarditis

Etiology CHF
Patients with CHF may occasionally develop acute

decompensation. The more important causes are:

Acute myocardial infarction/ myocardial ischemia Arrhythmias (e.g. atrial fibrillation) Uncontrolled Blood Pressure Infections (e.g pneumonia) Non-compliance to medications Excessive fluid and salt intake Anemia Development of renal failure Adverse effects of drug therapy (e.g. Non Steroidal Anti

Inflammatory Drugs)

Congestive Heart Failure Pathophysiology

Systolic Failure
Defect in ventricular contraction Left Ventricle loses ability to generate enough pressure to eject blood forward through the high pressure aorta Decreased ejection fraction Afterload hypertension, cardiomyopathy, and valvular heart disease

Diastolic Failure
Impaired ability of ventricles to fill

Decreased filling = decreased stroke volume

Pulmonary congestion, pulmonary hypertension, with normal

ejection fraction

Congestive Heart Failure

Pathophysiology

Algorithm for the diagnosis of Heart Failure or LV dysfunction

Basic Investigation
ECG for ischaemia/infarction, left atrial overload, LV hypertrophy and arrhythmias
Chest X-ray to look for cardiac size and

shape, pulmonary congestion Blood test FBC, renal function, liver function, glucose, lipid profile Urinalysis proteinuria, glycosuria

Other important Ix
Echocardiogram to identify structural

abnormalities and assess LV systolic and diastolic dysfunction Natriuretic peptides or their precursors (especially BNP and NT-proBNP) If available useful in the evaluation of patients presenting with acute dyspnoea in the urgent care setting in whom the clinical diagnosis of HF is uncertain. A low-normal concentration of this marker in an untreated patient makes the diagnosis of HF unlikely. Thus it is a useful ruleout test in doubtful cases.

Additional investigations when indicated

Blood tests: cardiac biomarkers, thyroid

function tests, C-reactive protein (to look for inflammation)

Tests for myocardial ischemia and/or -

viability: treadmill exercise test stress echocardiography (exercise or pharmacological) radionuclide studies cardiac magnetic resonance imaging (CMR)

 Invasive tests:
- coronary angiography - cardiac catheterization - endomyocardial biopsy Others: - Holter electrocardiography, loop recorders and

long-time ECG recording pulmonary function tests

ACUTE HEART FAILURE (AHF)

Acute Heart Failure may present de novo or as acute

decompensation of CHF. The clinical manifestations may vary from mild decompensation to Acute Cardiogenic Pulmonary Edema and Cardiogenic Shock.

Investigations in Acute Cardiogenic Pulmonary Edema

The principles of management are:

Rapid recognition of the condition Stabilization of hemodynamics Adjust Heart Rate Decrease Preload Decrease Afterload Increase Contractility Increase Oxygenation

Improvement in clinical symptoms and signs

Identification and treatment of the underlying cause precipitating / aggravating factors.

Treatment of CHF
Oxygen nasal, BiPAP, intubation
Morphine Preload Reduction Loop diuretics Nitrates ACEi / ARB Morphine

Treatment of CHF
Afterload Reduction IV NTG, Nitroprusside Hydralazine ACEi / ARB Ionotropic Support Dopamine / Dobutamine Amrinone / Milrinone Digoxin (chronic) Mechanical (ABP)

 Beta-Blockers
Chronic > Acute Carvedilol (Coreg), Metoprolol (Toprol XL), prior to discharge Probably not acutely

Fluid Balance
Restrict fluid / salt intake Monitor I/Os and daily weight Dialysis if needed (Critical renal failure patients)

Aspirin Digoxin
Probably not acutely Titrate to effective dose prior to discharge

IABP
Cardiogenic shock unresponsive to above tx

 Patients with AHF should be hospitalized. The more ill patients

should be managed in the intensive care or high dependency unit. They should have their pulse, blood pressure (BP), oxygen saturation, respiratory rate and ECG monitored continuously. Given the urgent nature of the illness, history, examination, investigations, treatment and resuscitation should be performed simultaneously. When indicated, early access to diagnostic procedures such as echocardiography and coronary angiography is important.

Therapy
Oxygen 5 to 6 liters/minute, by mask with the aim of achieving oxygen saturation of more than 95% in order to maximize tissue oxygenation and to prevent end organ dysfunction or multi organ failure. Elective ventilation using non invasive positive pressure ventilation (Continuous Positive Airway Pressure [CPAP] or Bilevel Positive Airway Pressure [BiPAP]) should be considered early if necessary Should the oxygen saturation be inadequate or the patient develop respiratory muscle fatigue, then endotracheal intubation and mechanical ventilation is necessary

 Frusemide Intravenous (i.v.) frusemide 40 100mg. The dose should be individualized depending on the severity of the clinical condition Morphine sulphate i.v. 3 5 mg bolus (repeated if necessary, up to a total maximum of 10mg). It reduces pulmonary venous congestion and sympathetic drive. It is most useful in patients who are dyspnoeic and restless. Intravenous anti-emetics (metoclopramide 10mg or prochlorperazine 12.5mg) should be administered concomitantly. Care must be exercised in patients with chronic respiratory diseases.

 Nitrates If the BP is adequate (SBP > 100 mmHg), nitrates are indicated as first line therapy in AHF. It should be administered sublingually or intravenously. The i.v. route is more effective and preferable. Patients should be closely monitored for hypotension. This commonly occurs with concomitan diuretic therapy. Studies have shown that the combination of i.v. nitrate and low dose frusemide is more efficacious than high dose diuretic treatment alone Extreme caution should be exercised in patients with aortic and mitral stenosis. Nitrates are contraindicated in severe valvular stenosis

Drugs Commonly Used in AHF

Response to drug therapy should be assesse continuously. Parameters to assess during treatment include: Symptoms and signs Vital signs oxygen saturation heart rate blood pressure respiratory rate urine output body weight Investigations renal function tests Invasive haemodynamic monitoring (if necessary) pulmonary capillary wedge pressure, cardiac index

Cardiogenic Shock
Cardiogenic shock carries a very high mortality rate.

Features include:
SBP<90mmHg not improved with fluid administration Signs of hypoperfusion-cold extremities, altered mental

status, restlessness Reduced urine output (<20cc/hour) Cardiac index of <2.2 L/min/m2

Important considerations are: Ventricular Function

acute valve regurgitation, acute septal rupture, cardiac

tamponade

Intra Vascular Volume Status Excessive diuretic or vasodilator therapy, concomitant GI bleed or RV infarction. In the absence of signs of LV failure, fluid challenge with normal saline should be administered (usual recommended volume : 200 500mls) Arrhythmias Cardioversion, pacing, anti-arrhythymic drug therapy

In the presence of cardiogenic shock or near shock (hypoperfusion with adequate blood pressure) treatment would include Inotropic support Mechanical device support
Intra-aortic balloon pump or LV assist device

Identifying correctable causes: pump failure, ventricular septal rupture and acute mitral regurgitation

NON PHARMACOLOGICAL MEASURES

Education
Diet & Nutrition Lifestyle

Exercise