Download Heart Failure

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1
Outlines
 Introduction & Epidemiology.
 Pathophysiology.
 Classifications.
 Signs & Symptoms.
 Diagnosis.
 Treatment.
 Key points.
2
Introduction
 Heart Failure ( HF ) : a
progressive , complex clinical
syndrome caused by the inability of the heart to
pump sufficient blood to meet the metabolic needs
of the body.
 Heart failure is the final common pathway for
numerous cardiac disorders including those
affecting the pericardium, heart valves, and
myocardium.
3
Introduction ( cont.)
 The primary manifestations of the syndrome
are dyspnea, fatigue, and fluid retention.
 Diseases that adversely affect ventricular
diastole (filling , relaxation), ventricular
systole (contraction), or both can lead to heart
failure.
 The leading causes of heart failure are
coronary artery disease and hypertension.
4
Introduction ( cont.)
 For many years it was believed that reduced
myocardial contractility, or systolic dysfunction (i.e.,
reduced left ventricular ejection fraction [LVEF]),
was the sole disturbance in cardiac function
responsible for heart failure.
5
Introduction ( cont.)
 However, it is now recognized that large numbers
of patients with the heart failure syndrome have
relatively normal systolic function (i.e., normal
LVEF).
 This is now referred to as heart failure with
preserved LVEF and is believed to be primarily
caused by diastolic dysfunction of the heart.
( 20% to 60% of patients with heart failure )
6
Introduction ( cont.)
 However, regardless of the etiology of heart failure,
the underlying pathophysiologic process and
principal clinical manifestations (fatigue, dyspnea,
and volume overload) are similar and appear to be
independent of the initial cause.
7
Introduction ( cont.)
 Historically, this disorder was commonly referred to
as congestive heart failure; the preferred
nomenclature is now heart failure because a
patient can have the clinical syndrome of heart
failure without having symptoms of congestion.
8
Introduction ( cont.)
 These disorders activate a number of cardiac and
peripheral neurohormonal compensatory adaptive
responses which with continued stimulation
become maladaptive and ultimately affect fluid
retention , mortality , disease progression.
 However, a subgroup of patient with LV dysfunction
are asymptomatic ( HF without symptoms ).
9
Epidemiology

Approximately 5 million Americans have heart
failure with an additional 550,000 cases diagnosed
each year. (1)
 Unlike most other cardiovascular diseases, the
incidence, prevalence, and hospitalization rates
associated with heart failure are increasing and are
expected to continue to increase over the next few
decades as the population ages.
1. Gheorghiade M, Sopko G, De Luca L, et al. Navigating the crossroads of
coronary artery disease and heart failure. Circulation 2006;114:1202–1213..
10
Epidemiology (cont.)
 A large majority of patients with heart failure are
elderly, with multiple comorbid conditions that
influence morbidity and mortality.
 The incidence of heart failure doubles with each
decade of life and affects nearly 10% of individuals
older than age 75 years.(2)
2. Rosamond W, Flegal K, Friday G, al. Heart disease and stroke statistics—2007 update: A report
from thet e American Heart Association Statistics Committee and Stroke Statistics
11
Subcommittee. Circulation 2007;115:e69–e171
Epidemiology (cont.)

Heart failure is more common in men than in
women until age 65 years.
 Current estimates suggest annual expenditures
for heart failure of approximately $33 billion,
with the majority of these costs spent on
hospitalized patients. (2)
12
Epidemiology (cont.)
 Although the mortality rates have declined over the
last 50 years, the overall 5-year survival remains
approximately 50% for all patients with a diagnosis
of heart failure, with mortality increasing with
symptom severity.(2)
13
Etiology
Impaired cardiac function
Excessive work demands
Loss of myocardial tissues (Myocardial diseases) :
Increased pressure work :
Cardiomyopathies
Systemic hypertension
Coronary insufficienc
√ Myocarditis
√ Myocardial infarction
Pulmonary hypertension
Coarctation of the aorta
Valvular diseases :
Increased volume work :
Stenotic valvular diseases
Arteriovenous shunt
Regurgitant valvular diseases
Excessive administration of
intravenous fluids
 Congenital pericarditis :
 Increased perfusion work :
Thyrotoxicosis
Constructive pericarditis
Anemia
14
Pathophysiology
 To understand the pathophysiologic processes in
heart failure, a basic understanding of normal
cardiac function is necessary.
 The relationship between CO and mean arterial
pressure (MAP) is
MAP = CO × systemic vascular resistance (SVR)
15
Pathophysiology (cont.)

Cardiac output (CO) is defined as :
the volume of blood ejected per unit time (L/min)
and it is the product of heart rate (HR) and stroke
volume (SV): CO = HR × SV
 Heart rate is controlled by the autonomic nervous
system.
16
Pathophysiology (cont.)
 Stroke volume, or the
volume of blood ejected
during systole, is equal to :
the difference between the
ventricular end-diastolic
volume (EDV) and the endsystolic volume (ESV).

SV = EDV – ESV
17
Pathophysiology (cont.)
 The EDV is :
the filled volume of the ventricle prior
to contraction.
 The ESV is :
the residual volume of blood
remaining in the ventricle after ejection.
 In a typical heart, the EDV is about 120 ml of blood
and the ESV about 50 ml of blood.
18
Pathophysiology (cont.)
 The difference in these two volumes, 70 ml,
represents the SV.
 Therefore, any factor that alters either the EDV or
the ESV will change SV.

SV depends on :
Afterload, preload, and contractility.
19
Pathophysiology (cont.)
 Afterload :
Pressure that the chamber or ventricle has to
generate to eject the blood out.


It is affected by : arterial blood pressure.
Systemic vascular resistance is the primary
determinant of Afterload load.
20
Pathophysiology (cont.)
 Preload :
Pressure on ventricle after contraction during filling

It is affected by :
1) venous blood pressure ( volume of blood )
2) Rate of venous return ( vein tone )
21
Pathophysiology (cont.)
 Left ventricular end-diastolic pressure (LVEDP) is
the primary determinant of preload (used in the
clinical setting to estimate preload ), estimated
clinically by measuring the pulmonary capillary
wedge pressure ( PCWP ) with a Swan-Ganz
catheter, normal level : 5-15 mmHG
22
Pathophysiology (cont.)
 The decrease in the heart’s pumping capacity results
in the heart having to rely on compensatory
responses ( hemodynamic and neurohormonal
changes ) to maintain an adequate cardiac output.
 These compensatory responses include :
23
Pathophysiology (cont.)
(1) Preload through the Frank-Starling mechanism,
whereby an increase in venous return to the heart
will increase the EDV of the ventricle, which
stretches the muscle fibers thereby increasing
their preload, This leads to an increase in the force
of ventricular contraction and CO.
24
Pathophysiology (cont.)
(2)
Tachycardia and increased contractility through
sympathetic nervous system (SNS) activation,
primarily due to release of norepinephrine (NE)
(3) Vasoconstriction: A number of neurohormones
likely contribute to the vasoconstriction, including
NE, angiotensin II, endothelin-1, and arginine
vasopressin (AVP).
25
Pathophysiology (cont.)
(4) Venricular hypertrophy & remodeling :
 Ventricular hypertrophy is a term used to describe
an increase in ventricular muscle mass.
 Cardiac or ventricular remodeling is
a broader term
describing changes in both myocardial cells and
extracellular matrix that result in changes in the
size, shape, structure, and function of the heart.
26
27
Key elemnts involved in
ventricular remodeling
28
29
Pathophysiology (cont.)
 These compensatory responses are intended to be
short-term responses to maintain circulatory
homeostasis after acute reductions in blood
pressure or renal perfusion.
 However, the persistent decline results in long-
term activation of these compensatory responses,
resulting in initiation and progression o fHF.
30
Pathophysiology (cont.)
 In addition to neurohormones, several
proinflammatory cytokines such as TNF-α have a
role in heart failure pathophysiology.

TNF-α produces multiple deleterious actions,
including negative inotropic effects, increasing
myocardial cell apoptosis, and stimulating
remodeling via several mechanisms.
31
Classifications
HF may be classified based on
Cardiac
Function
CO
Low
output
HIGH
OUTPUT
Side of
The Heart
Rt. Sided
HF
Onset of
Symptom
NYHA &
ACC/AHA
Lt. sided
HF
Acute
HF
Diastolic
HF
Systolic
HF
Chronic
HF
32
Classifications (cont.)
 According
to Cardiac output :
1)- High output HF : It is uncommon type of HF , The
function of the heart may be supranormal but
inadequate owing to excessive metabolic need for
cardiac output.
 Causes :
1) Severe anemia. 2) Thyrotoxicosis.
33
Classifications (cont.)
 2)-Low output HF :
The function of the heart is inadequate to
meet tissues needs of blood.
 caused by :
 disorder that impair the pumping ability
of the heart such as : IHD ,
Cardiomyopathy.
34
Classifications (cont.)
 In term of function :
 1)- Systolic dysfunction
:
There is impaired
ejection of blood from
the heart during systole
& cardiac contractility
35
Classifications (cont.)
 ejection fraction : It's the Percent of the total
amount of LV volume expelled during systole ,
normal EF ≥ 50 %
 EF misleading may occurred with mitral stenosis ,
aortic regurgitation.
 Causes :
 Conditions that impairs the contractile
performance of the heart ex. IHD, Cardiomyopathy.
 Increase pressure work on the heart ex. HTN ,
Valvular stenosis.
36
Classifications (cont.)
 2)- Diastolic dysfunction :
it account for 40% of all
cases of HF.
 There is impaired filling of
the ventricles during
diastole, characterized by
decreased the ability to
stretch during filling, so
the congestive symptoms
are predominate in
diastolic dysfunction.
37
Classifications (cont.)
 Causes :

Conditions that increase ventricular wall thickness
( ex. Myocardial hypertrophy ), conditions that
delay diastolic relaxation ex. IHD , aging
( ventricular stiffness )
38
Classifications (cont.)

According to the side of the
heart :

1)- Right sided HF :
Impairs the ability to move
deoxygenated blood from the
systemic circulation into
pulmonary circulation,
consequently, a dam back
of blood occurs, leading to its
accumulation in the systemic
venous system.
39
Classifications (cont.)

A major effect of Rt.sided HF is peripheral edema.

Causes :

Persistence left sided heart HF.

Acute or chronic pulmonary diseases ex. pulmonary
HTN.

Conditions that weaken the heart muscle or restrict
blood flow into lung ex. tricuspid or pulmonary valve
regurgitation.
40
Classifications (cont.)
 2)- Left sided HF :
Impairs the pumping of
blood from pulmonary
circulation into arterial
side of the systematic
circulation, as a results :
There is a decrease in CO,
Increase in LVEDP,
Congestion in the
pulmonary circulation.
41
Classifications (cont.)
 Pulmonary edema symptoms often occur at night
after the person has been reclining & gravitational
force has been removed from the circulatory
system, the edema fluid that had been sequestered
in lower extremities is redistributed into the
pulmonary circulation.
42
Classifications (cont.)
 Based on onset of symptoms :
 Acute HF : sudden onset of
signs and symptoms
of HF.
 Chronic HF : secondary to slow structural changes
occurring in the stressed myocardium.
 Acute decompensation : sudden exacerbation or
worsening of symptoms in chronic HF.
43
ACC/AHA HF stage
A
NYHA functional class
At high risk for HF but without
None
structural heart disease or symptoms
B
Structural disease but without HF
I
Asymptomatic
II
C
D
Structural heart disease with prior or
current HF symptoms
Refractory HF requiring specialized
interventions
Symptoms with minimal
exercise
III
Symptoms with moderate
exercise.
IV
Symptomatic at rest
44
SIGNS & Symptoms
 Although most patients initially have LVF, and
because LVF increases the workload of the right
ventricle, both ventricles eventually fail and
contribute to the heart failure syndrome.

Because of the complex nature of this syndrome, it
has become exceedingly more difficult to attribute
a specific sign or symptom as caused by either RVF
or LVF.
45
SIGNS & Symptoms
Rt. Sided HF
Systemic or peripheral tissues
congestion
Jugular venous distension
Ascites
Lt. Sided HF
Pulmonary congestion & CO
Impaired gas
exchange
Hepatomegaly
Splenomegaly
Lower limb edema
Cyanosis
Activity intolerance
Signs of hypoxia
Pulmonary
edema
Orthpnea
Paroxismal
nocturnal
dyspnea
Bibasilar rales
46
Diagnosis (cont.)
 No single test is available to confirm the diagnosis
of heart failure.
 Heart failure often is suspected initially in a patient
based on the symptoms & history.
 Measurement of B-type natriuretic peptide (BNP)
may assist in differentiating dyspnea caused by
heart failure from other causes.
47
Diagnosis (cont.)
 BNP is elevated in patients with heart failure and
thought to balance the effects of the RAA system by
causing natriuresis, diuresis, vasodilation,
decreased aldosterone release, decreased
hypertrophy.
48
Diagnosis (cont.)
 There are no specific ECG findings associated with
heart failure.
 The echocardiogram
can determine the presence
of systolic and/or diastolic dysfunction and the left
ventricular ejection fraction (LVEF).
49
Goals of treatment
 Improve the patient’s quality of life.
 Reduce symptoms & hospitalizations.

Slow progression of the disease process.
50
Goals of treatment (cont.)
 Prolong survival.
 Identification of risk factors for heart
failure and preventing the development
of this disorder.
51
Treatment ( non pharmacological )
 The first step in the management of
chronic heart failure is to determine the
etiology and/or any precipitating factors.
 Treatment of underlying disorders such as
anemia or hyperthyroidism may avoid the
need for treatment of heart failure.
52
Treatment ( non pharmacological )
 Restriction of fluid intake and dietary
sodium is an important intervention.
 Restriction of physical activity reduces
cardiac workload and it is recommended
for virtually all patients with acute
congestive symptoms.
53
Treatment ( non pharmacological )
 However, once the patient’s symptoms
have stabilized and excess fluid is removed,
restrictions on physical activity are
discouraged.
54
Treatment
( pharmacological )
 Although dietary sodium and water
restriction should be instituted in all heart
failure patients, pharmacologic therapy is
required for slowing disease progression
and prolonging survival and usually is
necessary for control of symptoms.
55
Treatment ( pharmacological )
 Current
American College of Cardiology/
American Heart Association(ACC/AHA)
treatment guidelines are organized around the
four identified stages of heart failure.
 This staging system emphasizes the progressive
nature of the disorder and targets treatment to
prevent or slow the progression of heart failure.
56
Stage
Description
Treatment
No structural heart disease
and no symptoms but risk
factors: CAD, HTN, DM,
cardiotoxins, familial
cardiomyopathy
Lifestyle modification, smoking
cessation; treat hyperlipidemia and
use ACEI for HTN
B
Abnormal LV systolic
function, MI, valvular heart
disease but no HF symptoms
Lifestyle modifications, β- blockers
adrenergic blockers, ACEI.
C
Structural heart disease and
HF symptoms
Lifestyle modifications, ACEI,
β-blockers, diuretics, digoxin
Refractory HF symptoms
to maximal medical
management
Therapy listed under A, B, C and
mechanical assist device, heart
transplantation, continuous IV inotropic
infusion, hospice care in selected
patients
A
D
57
Treatment ( pharmacological )

STANDARD FIRST-LINE
THERAPIES :

Alternative or for
selected patients :

Angiotensin Converting
Enzyme Inhibitors ( ACEI )

Angiotensin II- Receptor
Blockers ( ARB )

β- blockers


Diuretic

Digoxin
Vasodilators:
(Hydralazine/Nitrate)
58
Treatment
( pharmacological )
ACE Inhibitors
 ACE inhibitors are the cornerstone of
pharmacotherapy of patients with heart failure.
 MOA :
 By blocking the production of angiotensin II and, in
turn, aldosterone is decreased.
59
Treatment ( pharmacological )
ACE Inhibitors
 This attenuates many of the deleterious effects
including reducing ventricular remodeling
myocardial fibrosis, cardiac hypertrophy, and Na &
H2O retention.
60
Treatment ( pharmacological )
ACE Inhibitors
Vasodilatation
( arterio dilatation & venodilatation) :
The endogenous vasodilator bradykinin, which is
inactivated by ACE, is also increased by ACE
inhibitors,along with the release of vasodilatory
PG & histamine.

61
Treatment ( pharmacological )
ACE Inhibitors
 The beneficial effect of ACE inhibitors on mortality
has been documented conclusively, with numerous
trials showing a 20% to 30% relative reduction in
mortality with ACE inhibitor therapy compared with
placebo.
62
Treatment ( pharmacological )
ACE Inhibitors
 In addition to improving survival, ACE inhibitors also
reduce the combined risk of death or hospitalization,
slow the progression of heart failure, and reduce the
rates of reinfarction.
 The benefit occurs within the first few days
of
therapy and persists during long-term treatment.
63
Treatment ( pharmacological )
ACE Inhibitors
 The benefits are independent of the etiology of
heart failure and are observed in patients with
mild, moderate, or severe symptoms.
 ACE inhibitors clearly are superior to vasodilator
therapy with hydralazine-isosorbide dinitrate.
64
Treatment ( pharmacological )
ACE Inhibitors
 ACE inhibitors also are effective for prevention of
heart failure.
 No dose-dependent differences in mortality have
been reported for ACEinhibitors.
65
Treatment ( pharmacological )
ACE Inhibitors
 Side effects :
 Contraindications :

Dry cough.

Pregnancy.

First dose
hypotension.

Bilateral renal artery
stenosis.

Hypotension.

Hyperkalemia.

Acute renal failure.

Angioedema.
66
Treatment ( pharmacological )
Initial dose
Target dose
67
Treatment ( pharmacological )
ARB
 The current ACC/AHA
guidelines recommend the
use of ARBs in patients who are unable to tolerate
ACE inhibitors.
 The primary clinical trials supporting the use of
these agents in heart failure used either valsartan
or candesartan.
68
Treatment ( pharmacological )
ARB
 ARBs are not an alternative in patients with
hypotension, hyperkalemia, or renal insufficiency
secondary to ACE inhibitors because they are as
likely to cause these adverse effects.
 For patients who are unable to tolerate an ACE
inhibitor because of cough or angioedema, an ARB
is recommended as the first-line alternative.
69
Treatment ( pharmacological )
70
Treatment ( pharmacological )
β-blockers
 β-blockers have been shown to prolong survival,
decrease hospitalizations reduce morbidity and
mortality , and cause “reverse remodeling”.

Many studies show improvements in NYHA functional
class,
 β-blockers should be used in all stable patients with
heart failure and a reduced left ventricular ejection
fraction in the absence of contraindication.
71
Treatment ( pharmacological )
β-blockers
 MOA :

It seems likely that the mechanisms of benefit
include antiarrhythmic effects, slowing or reversing
the detrimental ventricular remodeling caused by
sympathetic stimulation, Up-regulation of β 1
receptors , decreased myocyte death from
catecholamine-induced necrosis or apoptosis.
72
Treatment ( pharmacological )
β-blockers
 In addition, there is evidence that response to
β-blockers is dose dependent.
 Therapy must be instituted
at low doses, with
slow upward titration to the target dose.
73
Treatment ( pharmacological )
β-blockers
 1/10 the final dose is typically starting dose,
with doses doubling no more frequently than
every 2 weeks until the target dose is reached.
 Therapy is generally limited to either carvedilol
or metoprolol and there is no compelling
evidence that one drug is superior to the other.
74
Treatment ( pharmacological )
β-blockers
 Side effects :



Bronchspasm.
Bradycardia.
Impaired glycemic
control.
 Contraindications :

Bradycardia.

AV Block .

Hypotension.

Acute exacerbation of
HF.
75
Treatment ( pharmacological )
Initial dose
Target dose
76
Treatment ( pharmacological )
Diuretics

Diuretic therapy is recommended in all patients
with clinical evidence of fluid retention.

Among the drugs used to manage heart failure,
diuretics are the most rapid in producing
symptomatic benefits.
77
Treatment ( pharmacological )
Diuretics
 Because
diuretics do not alter disease progression
or prolong survival, they are not considered
mandatory therapy.

Thus patients who do not have fluid retention
would not require diuretic therapy.
78
Treatment ( pharmacological )
Diuretics
 The primary goal of diuretic therapy is to reduce
symptoms associated with fluid retention, improve
exercise tolerance and quality of life, and reduce
hospitalizations from heart failure.
 They accomplish this by decreasing pulmonary and
peripheral edema through reduction of preload.
79
Treatment ( pharmacological )
Diuretics
 Diuretic therapy is usually initiated in low doses
with dosage adjustments based on symptom
assessment and daily body weight.

Change in body weight is a sensitive marker of fluid
retention or loss.
80
Treatment ( pharmacological )
Diuretics
 Thiazide Diuretics:

MOA :

Thiazide diuretics such as hydrochlorothiazide block
sodium and chloride reabsorption in the distal
convoluted tubule .

Consequently, the thiazides are relatively weak
diuretics and infrequently are used alone in heart
failure.
81
Treatment ( pharmacological )
Diuretics
 Thiazide diuretics may be preferred in patients with
only mild fluid retention and elevated blood
pressure because of their more persistent
antihypertensive effects compared to loop
diuretics.
82
Treatment ( pharmacological )
Diuretics
 Loop Diuretics:
 MOA :

They act by inhibiting a Na-K-2Cl transporter in the loop
of Henle, where 20% to 25% of filtered sodium normally
is reabsorbed.

Loop diuretics also induce a prostaglandin-mediated
increase in renal blood flow, which contributes to their
natriuretic effect.
83
Treatment ( pharmacological )
Diuretics
 Unlike thiazides, loop diuretics maintain their
effectiveness in the presence of impaired renal
function.
 doses above the recommended ceiling doses
produce no additional diuresis & thus, once the
ceiling dose is reached, it is recommended to give
the diuretic more frequently for additional effect
rather than to give progressively higher doses.
84
Treatment ( pharmacological )
Diuretics
 Side effects :

Hypokalemia

Hypomagnesamia.

Hyperlipidemia

Hyperglycemia
 Contraindications


:
Pregnancy
Renal failure
(only thiazide)
85
Treatment ( pharmacological )
86
Treatment ( pharmacological )
Diuretics
 Aldosterone
antagonist :
 Spironolactone and eplerenone are aldosterone
antagonists that work by blocking the
mineralocorticoid receptor, the target site for
aldosterone.
 Although the diuretic effects are minimal, the
potassium-sparing effects can have significant
consequences.
87
Treatment ( pharmacological )
Diuretics
 Recent evidence suggests that it may improve
survival in CHF patients because aldosterone
antagonists inhibit cardiac extracellular matrix and
collagen deposition, thereby attenuating cardiac
fibrosis and ventricular remodeling.
88
Treatment ( pharmacological )
Diuretics
 Side effects :

Hyperkalemia.

Gynecomastia.

Metabolic acidosis.
 Contraindications :

Hyperkalaemia
Concurrent use of other
potassium-sparing
products.

Renal failure

89
Treatment ( pharmacological )
Digoxin
 A number of clinical trials have shown that digoxin
improves LVEF, quality of life, exercise tolerance,
and HF symptoms.
 MOA :

+Ve inotropic effect by ↑ intracellular Ca.

Vagotonic effect.

Antrrhythmogenic effect.
90
Treatment ( pharmacological )
Digoxin
 Most of the benefits
from digoxin is achieved at
low plasma concentrations and little additional
effect is achieved with higher doses.
 Thus, for most patients, the target digoxin plasma
concentration should be 0.5 to 1.0 ng/mL.
91
Treatment ( pharmacological )
Digoxin
 This plasma concentration range can be achieved
with a daily dose of 0.125 mg.
 This target would also be expected to decrease the
risk of adverse effects from digoxin toxicity.
92
Treatment ( pharmacological )
Digoxin
 digoxin should not be used in patients with a
normal LVEF, sinus rhythm, and no history of heart
failure symptoms, because the risk is not balanced
by any known benefit.
93
Treatment ( pharmacological )
Digoxin
 Side effects & toxicity:
 Contraindications :

Vomiting.

Renal disease.

Bradycardia.

Ventricular arrythmia.

Heart block.

Heart block.

Visual disturbance.
94
Treatment ( pharmacological )
Vsodilators

Preload :
By Venodilators , ex:
Nitrate

Afterload :
By arteriodilators, ex:
Hydralazin
“ Isosorbide dinitrate, ISDN”
( GMP )
(direct arteriodilator)
95
Treatment ( pharmacological )
Vsodilators
 ISDN and hydralazine were combined originally in
the treatment of heart failure because of their
complementary hemodynamic actions.
 It is suggested that African Americans have less
nitric oxide than do non- African Americans, and
thus, may derive particular benefit from therapy
that enhances nitric oxide bioavailability.
96
Treatment ( pharmacological )
Vsodilators
 Hydralazine and ISDN is appropriate as first-line
therapy in patients unable to tolerate either an
ACE inhibitor or ARB because of renal
insufficiency, hyperkalemia, or possibly
hypotension.
97
Treatment ( pharmacological )
Vasodilators
 Side effects :

headache, dizziness, and gastrointestinal
distress
98
Treatment ( pharmacological )
 Anticoagulant : ( Warfarin )

It is used in case of :

Biventricular dysfunction ( Systole & Diastol ).

Sever LV dilatation.

Atrial fibrillation.

History of embolic episodes.
99
 Antiarrythmics :

Calcium channel blockers with negative inotropic
effects, such as verapamil or diltiazem, should be
avoided.

Amiodarone is a reasonable alternative for rate
control in those patients who are not responding to
digoxin and/or β-blockers or who have
contraindications to these agents.
100
Treatment ( pharmacological )
 Treatment of acute decompansated HF :
Goals of tratment : relieve congestion well as treat symptoms of
low cardiac output


IV Positive inotropic agents: the drugs that improve
myocardial contractility .
(β adrenergic agonists, dopaminergic agents,
phosphodiesterase inhibitors),
dopamine, dobutamine, milrinone, amrinone,
nitroglycerin.
IV fuerosemide
101
Treatment ( pharmacological )

Nesiritide :
 Nesiritide is the first new drug approved for the
treatment of decompensated heart failure since
milrinone.
 Manufactured by recombinant techniques, it is
identical to the endogenous human BNP.
102
Treatment ( pharmacological )
 MOA :

Mimics the vasodilatory and natriuretic actions of
the endogenous peptideby stimulating the
natriuretic peptide receptor A which leads to
increased levels of cyclic guanosine
monophosphate in target tissues.
103
Treatment ( pharmacological )

Nesiritide produces dose-dependent venous and
arterial vasodilation, increases in cardiac output,
natriuresis, and diuresis, and decreases cardiac
filling pressures, SNS and RAAS activity.
104
Key Points

Heart failure is a clinical syndrome caused by the
inability of the heart to pump sufficient blood to
meet the metabolic needs of the body.

Heart failure can result from any disorder that
reduces ventricular filling (diastolic dysfunction)
and/or myocardial contractility (systolic
dysfunction).
105
Key Points (cont.)

There are many classifications for HF.

The primary manifestations of the syndrome are
dyspnea, fatigue, and fluid retention.

The leading causes of heart failure are coronary
artery disease and hypertension.
106
Key Points (cont.)

Heart failure is a progressive disorder that begins
with myocardial injury.

In response to the injury, a number of
compensatory responses are activated which are
responsible for the symptoms of heart failure and
contribute to disease progression.
107
Key Points (cont.)

Most patients with symptomatic heart failure
should be routinely treated with
ACE inhibitor, β-blocker, and diuretic.

The benefits of these medications on slowing heart
failure progression, reducing morbidity and
mortality, and improving symptoms are clearly
established.
108
Key Points (cont.)

Patients should be treated with a diuretic if there is
evidence of fluid retention.

Treatment with digoxin may also be considered to
improve symptoms and reduce hospitalizations.
109
Key Points (cont.)

The combination of hydralazine and nitrates
improves the composite end point of mortality,
hospitalizations for heart failure, and quality of life
in African Americans who receive standard therapy.

Treatment goals for acute decompensated heart
failure are directed toward restoration of systemic
oxygen transport and tissue perfusion.
110
References

Joseph T. DiPiro, et al. Pharmacotherapy :
A Pathophysiologic Approach . The McGraw-Hill Companies.
Seventh Edition , 2008, Chapter 16, page : 173- 244

Frederic S. Bongard, Darryl Y. Sue, Janine R. E. Vintch, Current
Critical Care Diagnosis and Treatment, McGraw-Hill
Professional,Third edition , 2008, page:197-198

Mary Anne Koda-Kimble, Lloyd Yee Young , et al .Hand Book Of
Applied Therapeutics.Lippincott Williams & Wilkins. Eighth edition,
2007, Chapter 18 ,
page : 153-170

Daniel H. Cooper, et al. Washington Manual of Medical
Therapeutics. Therapeutics. Lippincott Williams & Wilkins.
32ed Edition, 2007, Chapter 6, page:168-177
111
Parameter
Value
end-diastolic volume (EDV)
120 ml
end-systolic volume (ESV)
50 ml
stroke volume (SV)
70 ml
ejection fraction (Ef)
58%
heart rate (HR)
70 bpm
cardiac output (CO)
4.9 L/m
112

For example:
EDV=120 , ESV= 50
EF = 120 - 50 / 120
= 0.58
= 58 %
113