Download Congestive Heart Failure

Prepared By Dr.Mustafa Alshehabat
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 doesn’t
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.
Kussmaul’s 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 tamponade- although 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 heart.
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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-heart-related 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 caused by the vibration of
valves, supporting structures, and the ventricular walls. An abnormal S4 is heard in people with conditions
that increase resistance to ventricular filling, such as a weak left ventricle.
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
Increased Afterload
Increased Salt
Flow
Vasoconstriction
Norepinephrine
Renal Blood
Renin
Angiotension I
Angiotension II
Aldosterone
Infiltration of Interstitial
Space

Normal
Micro-anatomy

Micro-anatomy
with fluid
movement.
Acute
Pulmonar
y Edema
a true lifethreatening
emergency
Treatment
Selected patients
• 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
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
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
Medulla
Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle
Loop of Henle
Collecting tubule
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
Maximum
Bumetanide
0.5 to 1.0 / 12-24h
10 / day
Furosemide
20 to 40 / 12-24h
400 / day
Torsemide
10 to 20 / 12-24h
200 / day
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
VASODILATATION
ALDOSTERONE
PROSTAGLANDINS
Kininogen
VASOPRESSIN
SYMPATHETIC
tPA
Kallikrein
Angiotensinogen
RENIN
Angiotensin I
A.C.E.
ANGIOTENSIN II
Inhibitor
BRADYKININ
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
ß-Adrenergic Blockers
Mechanism of action
• Density of ß1 receptors
• Inhibit cardiotoxicity of catecholamines
• Neurohormonal activation
• HR
• Antiischemic
• Antihypertensive
• Antiarrhythmic
• Antioxidant, Antiproliferative
ß-Adrenergic Blockers
Clinical Effects
• Improve symptoms (only long term)
• Reduce remodelling / progression
• Reduce hospitalization
• Reduce sudden death
• Improve survival
ß-Adrenergic Blockers
Indications
• Symptomatic heart failure
• Asymptomatic ventricular dysfunction
- LVEF < 35 - 40 %
• After AMI
AHA / ACC HF guidelines 2001
ESC HF guidelines 2001
ß-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
Digitalis
Na-K ATPase
Na+
K+
Na-Ca Exchange
Na+
Myofilaments
K+ Na+
Ca++
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
ALDOSTERONE
-
Competitive antagonist of the
aldosterone receptor
(myocardium, arterial walls, kidney)
• Retention Na+
• Retention H2O
• Excretion
K+
• Excretion Mg2+
• Collagen
Edema
deposition
Fibrosis
Arrhythmias
- myocardium
- vessels
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
Angiotensin I
Angiotensinogen
ACE
Other pathways
ANGIOTENSIN II
AT1
Receptor
Blockers
AT1
Vasoconstriction
RECEPTORS
Proliferative
Action
AT2
Vasodilatation
Antiproliferative
Action
NITRATES
HEMODYNAMIC EFFECTS
1- VENOUS VASODILATATION
Pulmonary congestion
Preload
Ventricular size
Vent. Wall stress
MVO2
2- Coronary vasodilatation
Myocardial perfusion
3- Arterial vasodilatation
Afterload
4- Others
• 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, Diurétics
HEMODYNAMIC - Vasodilators
NEUROHUMORAL - ACE inhibitors,
- Blockers, Spironolactone
IMMUNOLOGICAL - Cytokine inhibitors
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