CHF

• Important terminologies
 Preload
– Refers to the amount of blood the heart must pump with each beat
– Determined by:
• Venous return to heart
• Accompanying stretch of the muscle fibers
– Increasing preload  increase stroke volume in normal heart
– Increasing preload  in impaired heart  decreased SV. Blood is
trapped (congestion) chamber enlargement
 Afterload
– Refers to the pressure that must be overcome for the heart to
pump blood into the arterial system
– Dependent on the systemic vascular resistance
– With increased afterload, the heart muscles must work harder
to overcome the constricted vascular bed  chamber
enlargement
 Stroke volume
– Refers to the fraction of blood the heart pumps out with each
beat
• Determined by preload, force of contraction & afterload
• Healthy heart pumps 60% or more of the blood it receives
• Failing heart pumps 40% or less of the blood it receives
 Cardiac output
– Refers to the amount of blood pumped out by the left ventricle
in a given period of time
– CO = heart rate x stroke volume
– Heart rate is controlled by:
• Autonomic nervous system
• Hormonal systems
• Heart failure
– The inability of the heart to pump adequate amounts
of blood that meets the metabolic requirements of the
body
– It doesn’t mean that the heart stopped working
– Characterized by:
- Impaired ventricular performance (right or left or both)
- Exercise intolerance
- Shortened life expectancy
Classification of HF
Diastolic dysfunction or diastolic heart failure:
- Results from hypertrophy and stiffening of the myocardium
- Leads to CO reduction but normal stroke volume
- There is no uniformly agreed upon therapy for CHF secondary to
diastolic dysfunction (difficult for treatment)
Systolic dysfunction or systolic CHF

• Reduced left ventricular contractile function & SV
reduces to <45%
• Inadequate blood flow to vital organs due to decreased
cardiac output
• Defined by large, dilated, and poorly contracting heart
 Acutely, these compensatory mechanisms help to sustain CO by:
– Allowing the heart to operate at higher preload which increases
the stroke volume
– Concomitant vasoconstriction allows for regional redistribution
of CO to vital organs
– Increasing the rate & force of myocardial contraction
 Unfortunately, each of these compensatory responses will also
promote disease progression
– Elevations of both the preload & afterload leads to increased
diastolic & systolic wall stress
• Impairs myocardial energetics & will induce hypertrophic
remodeling of ventricles
– Neurohormonal effectors such as NE, Ag II & aldosterone act
directly on the myocardium & cause unfavorable remodeling:
• Causing myocyte apoptosis, abnormal gene expression
Sign and symptoms
• Characterized by:
– Impaired ventricular performance
– Exercise intolerance
– A high incidence of ventricular arrhythmias
– Tachycardia
– Shortness of breath/dyspnea
– Peripheral and pulmonary edema
– Cardiomegaly
– Shortened life expectancy
…
 Congestive heart failure may involve the left or right side of
the heart or all of the cardiac chambers.
 The most common causes of left-sided cardiac failure are
systemic hypertension, mitral or aortic valve disease,
ischemic heart disease, and primary diseases of the
myocardium.
 The most common cause of right-sided heart failure is left
ventricular failure, with its associated pulmonary congestion
and elevation in pulmonary arterial pressure.
…
 Because a failing left ventricle would cause blood to back up
in the left atrium, and then to the pulmonary circuit, right
ventricle, and right atrium, it is apparent that left heart failure
can eventually lead to right heart failure. In fact, the main
cause of right heart failure is left heart failure.
 As blood is poorly pumped out of the right side of the heart, it
begins to pool in the peripheral venous system. The end result
is a further reduction in circulating blood volume and blood
pressure, and a worsening cycle of heart failure.
Treatment
…
C. phosphodiesterase inhibitors
– PDH III is found in myocardial and vascular smooth

muscle
– PDH inhibitors increase contractility and vasodilation
– E.g. amrinone, milrinone
– Are given for severe acute CHF resistant to other drugs

A. CARDIAC GLYCOSIDES
Drugs
◦ Digoxin
◦ Digitoxin
Mechanism of action
◦ Act by inhibiting the membrane Na+/K- ATPase pump,
indirectly promoting Ca++ accumulation with in cardiac
cells increase force of contraction
◦ The C.glycosides bind to the K+ binding site of the enzyme
◦ Removal of free cytosolic calcium: If free cytosolic calcium
levels were to remain high, the cardiac muscle would be in a
constant state of contraction rather than showing a periodic
contraction.
…
Mechanisms of removal include two alternatives.
◦ Na/Ca exchange: Calcium is removed by a Na/Ca exchange
reaction that reversibly exchanges calcium ions for sodium
ions across the cell membrane
This interaction between the movement of calcium and
sodium ions is significant, because changes in intracellular
sodium can affect cellular levels of calcium.
◦ Uptake of calcium by the sarcoplasmic reticulum and
mitochondria: Calcium is also recaptured by the
sarcoplasmic reticulum and the mitochondria. More than 99
percent of the intracellular calcium is located in these
organelles and even a modest shift between these stores and
free calcium can lead to large changes in the concentration
of free cytosolic calcium
…
• Relationship of k+ to inotropic action
– K compete with C.glycosides for binding to Na/K
ATPase
– when k+ levels are low , binding of C.glycosides
to Na+/K ATPase will increase excessive
inhibition  toxicity
– when K+ levels are high, inhibition is
decreased reduction in therapeutic response
– Hence, it is imperative that K+ levels be kept
within physiologic range(3.5-5meq/l)
Therapeutic uses of cardiac glycosides
For treating low output CHF
Supra-ventricular arrhythmias
◦ Atrial fibrillation
 Restore the myocardial efficiency
 Decreased ventricular rate by decreased AV conduction
velocity and prolongation of ERP
◦ Atrial flutter
 May change it to atrial fibrillation, but decrease conduction
through AV node and this slows heart rate and improves cardiac
function
◦ Paroxysmal atrial tachycardia
 Useful because of its vagal stimulant action
Adverse effects
• Have a low safety margin
Cardiac adverse effects
– Bradycardia (since it is vagotonic action)
– Partial or complete heart block
– arrhythmias
Predisposing factors
– Hypokalemia secondary to diuretics
– Elevated cardiac glycosides levels
– Intentional/ accidental over dosage
– Increased absorption and increased elimination
Management of digoxin induced arrhythmia
 Withdraw digoxin and K wasting diuretics
 Monitor serum K levels
 Some patients may require an anti arrhythmic drug (lidocaine,
phentoin)
 Patients who develop bradycardia or AV block can be treated
by atropine
 When an over dosage is severe, digoxin level can be lowered
using Fab antibody fragment bind and prevent it from binding
2. DIURTEICS
• by decreasing blood volume decreases preload and after
load →decreases pulmonary and peripheral edema
→ decreases cardiac distension

• is one of the First line drug combination for patients with CHF
…
Thiazide diuretics
◦ Moderate diuresis  For chronic CHF
◦ N.B: ineffective when GFR is low
Loop diuretics
◦ Profound diuresis ;can promote diuresis even when GFR is low
◦ Drugs of choice for treating patients with severe CHF
◦ Furosemide, 40-240mg, P.O. divided in to 2-3 doses QD
◦ Potassium chloride, 600 mg P.O. once QD OR BID
K+ sparing diuretics
◦ promote only scant diuresis
◦ employed to counteract K+ loss due to loop and thiazide diuretics
◦ if the first line combination drugs found not enough,
Spironolactone, 25 mg P.O.QD can be added.
3. Vasodilators
 Venodiators  preload  decrease cardiac
distension as well as pulmonary and peripheral edema
 Arteriolar dilators  decrease afterload SV
CO
 By increasing CO and dilating arterioles of the kidney
 increase renal perfusion  increase loss of fluid
 In skeletal muscle, increase local perfusion
Drugs:
◦ Nitroglycerine
◦ Sodium Nitroprusside
◦ Hydralazine
ACE inhibitors

CHF

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• Important terminologies

Systolic dysfunction or systolic CHF

– PDH III is found in myocardial and vascular smooth

– E.g. amrinone, milrinone

– Are given for severe acute CHF resistant to other drugs

→ decreases cardiac distension

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