mashehabat@just.edu.

jo

Terminology
Heart Failure: The inability of the
heart to maintain an output adequate to maintain the metabolic demands of the body.

Pulmonary Edema: An abnormal

accumulation of fluid in the lungs.

CHF with Acute Pulmonary

Edema: Pulmonary Edema due to Heart

Failure (Cardiogenic Pulmonary Edema)

What is HF
Complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation.

Pathophysiology
Main Causes of Heart Failure: Ischemic Heart Disease (35-40%) Cardiomyopathy(dilated) (30-34%) Hypertension (15-20%) Other Causes: Valvular Heart Disease. Congenital Heart Disease. Alcohol and Drugs. Arrhythmias

Pathophysiological Changes in HF
Ventricular Dilatation. Myocyte Hypertrophy. Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction.

Signs & Symptoms

Symptoms: Exertional Dyspnoea Orthopnia Paraxysmal Nocturnal Dyspnoea Signs: Cardiomegaly Elevated Jugular Venous Pressure Tachycardia Hypotension Bi-basal crackles Pleural effusion Ankle Edema Ascites Tender hepatomegaly.

Classification of heart failure

No limitation. Normal physical exercise doesnt cause fatigue, dyspnea or palpitations. II. Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnea or palpitations. III. Marked limitation. Comfortable at rest but gentle physical activity produces marked symptoms of HF. IV. Symptoms of HF occur at rest and are exacerbated by any physical activity.
I.

Kussmauls Sign
This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also seen in right ventricular infarction, right heart failure, tricuspid stenosis, and restrictive cardiomyopathy. It is not seen in acute cardiac tamponadealthough it may be seen if tamponade occurs with a degree of constricive pericardiditis

PMI
The apex beat, also called the point of

maximum impulse (PMI), is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt. The cardiac impulse is the result of the heart rotating, moving forward and striking against the chest wall during systole. The normal apex beat can be palpated in the precordium left 5th intercostal space, at the point of intersection with the left midclavicular line. In children the apex beat occurs in the fourth rib interspace medial to the nipple. The apex beat may also be found at abnormal locations; in many cases of dextrocardia, the apex beat may be felt on the right side. Lateral and/or inferior displacement of the apex beat usually indicates enlargement of the

S1 The first heart sound - S1 - is in time with the pulse in your carotid artery in your

neck. The sound of the tricuspid valve closing may be louder in patients with pulmonary hypertension due to increased pressure beyond the valve. Non-heartrelated factors such as obesity, muscularity, emphysema, and fluid around the heart can reduce both S1 and S2. The position of the valves when the ventricles contract can have a big effect on the first heart sound. If the valves are wide open when the ventricule contracts, a loud S1 is heard. This can occur with anemia, fever or hyperthyroid. When the valves are partly closed when the ventricule contracts, S1 is faint. Beta-blockers produce a fainter S1. Structural changes in the heart valves can also affect S1. Fibrosis and calcification of the mitral valve may reduce S1, while stenosis of the mitral valve may cause a louder S1. S2 The second heart sound marks the beginning of diastole - the heart's relaxation phase - when the ventricles fill with blood. In children and teenagers, S2 may be more pronounced. Right ventricular ejection time is slightly longer than left ventricular ejection time. As a result, the pulmonic valve closes a little later than the aortic valve. Higher closing pressures occur in patients with chronic high blood pressure, pulmonary hypertension, or during exercise or excitement. This results in a louder A2 (the closing sound of the aortic valve). On the other hand, low blood pressure reduces the sound. The second heart sound may be "split" in patients with right bundle branch block, which results in delayed pulmonic valve closing. Left bundle branch block may cause aortic valve closing (A2) to be slower than pulmonic valve closing (P2). S3 During diastole there are 2 sounds of ventricular filling: The first is from the atrial walls and the second is from the contraction of the atriums. The third heart sound is caused by vibration of the ventricular walls, resulting from the first rapid filling so it is heard just after S2. The third heart sound is low in frequency and intensity. An S3 is commonly heard in children and young adults. In older adults and the elderly with heart disease, an S3 often means heart failure. S4 The fourth heart sound occurs during the second phase of ventricular filling: when the atriums contract just before S1. As with S3, the fourth heart sound is thought to be

Edema
Bilateral lower extremity edema

Hypertension
Hypertrophic Cardiomyopathy

Compensatory Mechanisms
Increased Heart Rate Sympathetic = Norepinephrine Dilation Frank Starling = Contractility Neurohormonal Redistribution of Blood to the Brain

Low Output

Increased Preload Norepinephrine

Increased Afterload

Increased Salt Flow

Vasoconstriction

Renal Blood

Renin Angiotension I Angiotension II Aldosterone

Infiltration of Interstitial Space

q

Normal Micro-anatomy

Micro-anatomy with fluid movement.

Acute Pulmonar y Edema

a true lifethreatening emergency

Treatment
Prevention. Control of risk factors Life style All Treat etiologic cause / aggravating factors Drug therapy Personal care. Team work Revascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator) Ventricular resyncronization Ventricular assist devices Heart transplant Artificial heart Neoangiogenesis, Gene therapy
Selected patients

Treatment Objectives Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms

(Cost)

Treatment Pharmacologic Therapy

Diuretics ACE inhibitors Beta Blockers

Digitalis Spironolactone Other

Diuretics Essential to control symptoms secondary to fluid retention

Prevent progression from HT to HF Spironolactone improves survival New research in progress

Diuretics Cortex
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

Medulla

Diuretics. Indications
1. Symptomatic HF, with fluid retention Edema Dyspnea Lung Rales Jugular distension Hepatomegaly Pulmonary edema (Xray)
AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weight Monitor serum K+ at frequent intervals
Reduce dose when fluid retention is controlled

Teach the patient when, how to change dose Combine to overcome resistance Do not use alone

Loop diuretics. Dose (mg)

Initial Bumetanide day Furosemide Torsemide 20 to 40 / 12-24h 400 / day 10 to 20 / 12-24h 200 / day 0.5 to 1.0 / 12-24h Maximum 10 /

AHA / ACC HF guidelines 2001

Thiazides, Loop Diuretics. Adverse Effects K+, Mg+ (15 - 60%) (sudden death ???) Na+

Stimulation of neurohormonal activity Hyperuricemia (15 - 40%)

Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic
Sharpe N. Heart failure. Martin Dunitz 2000;43 Kubo SH , et al. Am J Cardiol 1987;60:1322 MRFIT, JAMA 1982;248:1465 Pool Wilson. Heart failure. Churchill Livinston 1997;635

ACE-i. Mechanism of Action

VASOCONSTRICTION
ALDOSTERONE VASOPRESSIN SYMPATHETIC Angiotensinogen RENIN Angiotensin I

VASODILATATION
PROSTAGLANDINS Kininogen Kallikrein tPA

BRADYKININ

A.C.E.
ANGIOTENSIN II

Inhibitor

Kininase II
Inactive Fragments

ACE-I. Clinical Effects Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival

ACE-i. Indications
Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups
AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

ACE-I. Adverse Effects Hypotension (1st dose effect) Worsening renal function Hyperkalemia Cough Angioedema Rash, ageusia, neutropenia,

ACE-I. Contraindications
Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension

-Adrenergic Blockers Mechanism of action

Density of 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic

-Adrenergic Blockers Clinical Effects

Improve symptoms (only long term) Reduce remodelling / progression Reduce hospitalization Reduce sudden death Improve survival

-Adrenergic Blockers Indications

Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % After AMI
AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

-Adrenergic Blockers Adverse Effects

Hypotension Fluid retention / worsening heart failure Fatigue Bradycardia / heart block
Review treatment (+/-diuretics, other drugs) Reduce dose Consider cardiac pacing Discontinue beta blocker only in severe cases

Na-K ATPase
Na+ Na K+ K

Digitalis

Na-Ca Exchange
Na+ Ca++

Myofilaments

K+ Na+

Ca++

CONTRACTILITY

Digitalis. Mechanism of Action

Blocks Na+ / K+ ATPase => Ca+ +

Inotropic effect Natriuresis Neurohormonal control

Plasma Noradrenaline Peripheral nervous system activity RAAS activity Vagal tone - Normalizes arterial baroreceptors NEJM 1988;318:358

Digitalis. Clinical Effects

Improve symptoms Modest reduction in hospitalization Does not improve survival

Digitalis. Indications
When no adequate response to
ACE-i + diuretics + beta-blockers
AHA / ACC Guidelines 2001

In combination with ACE-i + diuretics

if persisting symptoms
ESC Guidelines 2001

AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day

Aldosterone Inhibitors

Spironolactone

Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney)

ALDOSTERONE

Retention Na+ Retention H2O Excretion K

+

Edema

Collagen

deposition

Arrhythmias

Fibrosis
- myocardium - vessels

Excretion Mg2+

Spironolactone. Practical use Do not use if hyperkalemia, renal insuf. Monitor serum K+ at frequent intervals Start ACE-i first Start with 25 mg / 24h If K+ >5.5 mmol/L, reduce to 25 mg / 48h If K+ is low or stable consider 50 mg / day New studies in progress

Angiotensin II Receptor Blockers (ARB)

RENIN Angiotensinogen Other pathways AT1 Receptor Blockers AT1 RECEPTORS AT2 Angiotensin I ACE ANGIOTENSIN II

Vasoconstriction

Proliferative Action

Vasodilatation Antiproliferative Action

NITRATES HEMODYNAMIC EFFECTS 1- VENOUS VASODILATATION Preload

Pulmonary congestion Ventricular size Vent. Wall stress MVO2

2- Coronary vasodilatation
Myocardial perfusion

3- Arterial vasodilatation
Afterload

Cardiac output Blood pressure

Nitrates. Clinical Use

CHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency)

Heart Transplant. Indications

Refractory cardiogenic shock Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity

Heart Failure and Myocardial Ischemia

Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia Angina coronary angio and revascularization

No angina Search for ischemia and viability in all ? Coronary angiography in all ?

HEART FAILURE MODELS

CONGESTIVE - Digoxin, Diurtics HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors

THANK YOU