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
Slide 4
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
Slide 5
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
Slide 6
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
Slide 7
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
Slide 8
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
Slide 9
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
Slide 10
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. 10 1. Gheorghiade M, Sopko
G, De Luca L, et al. Navigating the crossroads of coronary artery
disease and heart failure. Circulation 2006;114:12021213..
Slide 11
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 statistics2007 update: A
report from thet e American Heart Association Statistics Committee
and Stroke Statistics Subcommittee. Circulation 2007;115:e69e171
11
Slide 12
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
Slide 13
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
Slide 14
Excessive work demands Impaired cardiac function Increased
pressure work : Systemic hypertension Pulmonary hypertension
Coarctation of the aorta Loss of myocardial tissues (Myocardial
diseases) : Cardiomyopathies Myocarditis Coronary insufficienc
Myocardial infarction Increased volume work : Arteriovenous shunt
Excessive administration of intravenous fluids Valvular diseases :
Stenotic valvular diseases Regurgitant valvular diseases Increased
perfusion work : Thyrotoxicosis Anemia Congenital pericarditis :
Constructive pericarditis 14 Etiology
Slide 15
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
Slide 16
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
Slide 17
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 end- systolic volume
(ESV). SV = EDV ESV 17
Slide 18
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
Slide 19
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
Slide 20
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
Slide 21
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
Slide 22
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
Slide 23
Pathophysiology (cont.) The decrease in the hearts 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
Slide 24
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
Slide 25
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
Slide 26
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
Slide 27
27
Slide 28
28 Key elemnts involved in ventricular remodeling
Slide 29
29
Slide 30
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
Slide 31
Pathophysiology (cont.) In addition to neurohormones, several
proinflammatory cytokines such as TNF- have a role in heart failure
pathophysiology. TNF- produces multiple deleterious actions,
including negative inotropic effects, increasing myocardial cell
apoptosis, and stimulating remodeling via several mechanisms.
31
Slide 32
Classifications HF may be classified based on CO Cardiac
Function Cardiac Function Side of The Heart Side of The Heart Onset
of Symptom Onset of Symptom NYHA & ACC/AHA NYHA & ACC/AHA
Low output Low output HIGH OUTPUT Diastolic HF Diastolic HF
Systolic HF Systolic HF Lt. sided HF Lt. sided HF Rt. Sided HF Rt.
Sided HF Acute HF Acute HF Chronic HF Chronic HF 32
Slide 33
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
Slide 34
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
Slide 35
Classifications (cont.) In term of function : 1)- Systolic
dysfunction : There is impaired ejection of blood from the heart
during systole & cardiac contractility 35
Slide 36
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
Slide 37
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.) 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
Slide 40
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
Slide 41
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
Slide 42
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
Slide 43
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
Slide 44
44 A A t high risk for HF but without structural heart disease
or symptoms B S tructural disease but without HF C Structural heart
disease with prior or current HF symptoms D Refractory HF requiring
specialized interventions IV Symptomatic at rest III Symptoms with
moderate exercise. II Symptoms with minimal exercise I A
symptomatic NYHA functional class ACC/AHA HF stage None
Slide 45
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
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
Slide 48
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
Slide 49
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
Slide 50
Goals of treatment Improve the patients quality of life. Reduce
symptoms & hospitalizations. Slow progression of the disease
process. 50
Slide 51
Goals of treatment (cont.) Prolong survival. Identification of
risk factors for heart failure and preventing the development of
this disorder. 51
Slide 52
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
Slide 53
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
Slide 54
Treatment ( non pharmacological ) However, once the patients
symptoms have stabilized and excess fluid is removed, restrictions
on physical activity are discouraged. 54
Slide 55
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
Slide 56
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
Slide 57
57 TreatmentDescriptionStage Lifestyle modification, smoking
cessation; treat hyperlipidemia and use ACEI for HTN No structural
heart disease and no symptoms but risk factors: CAD, HTN, DM,
cardiotoxins, familial cardiomyopathy A - blockers Lifestyle
modifications, adrenergic blockers, ACEI. Abnormal LV systolic
function, MI, valvular heart disease but no HF symptoms B Lifestyle
modifications, ACEI, -blockers, diuretics, digoxin Structural heart
disease and HF symptoms C Therapy listed under A, B, C and
mechanical assist device, heart transplantation, continuous IV
inotropic infusion, hospice care in selected patients Refractory HF
symptoms to maximal medical management D
Slide 58
Treatment ( pharmacological ) STANDARD FIRST-LINE THERAPIES :
Angiotensin Converting Enzyme Inhibitors ( ACEI ) - blockers
Diuretic Digoxin Alternative or for selected patients : Angiotensin
II- Receptor Blockers ( ARB ) Vasodilators: (Hydralazine/Nitrate)
58
Slide 59
Treatment ( pharmacological ) 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 ACE Inhibitors
Slide 60
Treatment ( pharmacological ) This attenuates many of the
deleterious effects including reducing ventricular remodeling
myocardial fibrosis, cardiac hypertrophy, and Na & H2O
retention. 60 ACE Inhibitors
Slide 61
Treatment ( pharmacological ) 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 ACE Inhibitors
Slide 62
Treatment ( pharmacological ) 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 ACE
Inhibitors
Slide 63
Treatment ( pharmacological ) 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 ACE
Inhibitors
Slide 64
Treatment ( pharmacological ) 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 ACE Inhibitors
Slide 65
Treatment ( pharmacological ) ACE inhibitors also are effective
for prevention of heart failure. No dose-dependent differences in
mortality have been reported for ACEinhibitors. 65 ACE
Inhibitors
Treatment ( pharmacological ) 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 ARB
Slide 69
Treatment ( pharmacological ) 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 ARB
Slide 70
Treatment ( pharmacological ) 70
Slide 71
Treatment ( pharmacological ) -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, -blockers should be used in
all stable patients with heart failure and a reduced left
ventricular ejection fraction in the absence of contraindication.
71 -blockers
Slide 72
Treatment ( pharmacological ) 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 1 receptors, decreased
myocyte death from catecholamine-induced necrosis or apoptosis. 72
-blockers
Slide 73
Treatment ( pharmacological ) In addition, there is evidence
that response to -blockers is dose dependent. Therapy must be
instituted at low doses, with slow upward titration to the target
dose. 73 -blockers
Slide 74
Treatment ( pharmacological ) 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
-blockers
Slide 75
Treatment ( pharmacological ) Side effects : Bronchspasm.
Bradycardia. Impaired glycemic control. Contraindications :
Bradycardia. AV Block. Hypotension. Acute exacerbation of HF. 75
-blockers
Treatment ( pharmacological ) 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 Diuretics
Slide 78
Treatment ( pharmacological ) 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 Diuretics
Slide 79
Treatment ( pharmacological ) 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 Diuretics
Slide 80
Treatment ( pharmacological ) 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 Diuretics
Slide 81
Treatment ( pharmacological ) 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 Diuretics
Slide 82
Treatment ( pharmacological ) 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 Diuretics
Slide 83
Treatment ( pharmacological ) 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 Diuretics
Slide 84
Treatment ( pharmacological ) 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 Diuretics
Treatment ( pharmacological ) 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
Diuretics
Slide 88
Treatment ( pharmacological ) 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 Diuretics
Slide 89
Treatment ( pharmacological ) Side effects : Hyperkalemia.
Gynecomastia. Metabolic acidosis. Contraindications : Hyperkalaemia
Concurrent use of other potassium-sparing products. Renal failure
89 Diuretics
Slide 90
Treatment ( pharmacological ) 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
Digoxin
Slide 91
Treatment ( pharmacological ) 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
Digoxin
Slide 92
Treatment ( pharmacological ) 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 Digoxin
Slide 93
Treatment ( pharmacological ) 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 Digoxin
Treatment ( pharmacological ) 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 Vsodilators
Slide 97
Treatment ( pharmacological ) 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 Vsodilators
Slide 98
Treatment ( pharmacological ) Side effects : headache,
dizziness, and gastrointestinal distress 98 Vasodilators
Slide 99
Treatment ( pharmacological ) Anticoagulant : ( Warfarin ) It
is used in case of : Biventricular dysfunction ( Systole &
Diastol ). Sever LV dilatation. Atrial fibrillation. History of
embolic episodes. 99
Slide 100
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 -blockers
or who have contraindications to these agents. 100
Slide 101
Treatment ( pharmacological ) Treatment of acute decompansated
HF : IV Positive inotropic agents: the drugs that improve
myocardial contractility. ( adrenergic agonists, dopaminergic
agents, phosphodiesterase inhibitors), dopamine, dobutamine,
milrinone, amrinone, nitroglycerin. IV fuerosemide 101 Goals of
tratment : relieve congestion well as treat symptoms of low cardiac
output
Slide 102
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
Slide 103
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
Slide 104
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
Slide 105
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
Slide 106
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
Slide 107
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
Slide 108
Key Points (cont.) Most patients with symptomatic heart failure
should be routinely treated with ACE inhibitor, -blocker, and
diuretic. The benefits of these medications on slowing heart
failure progression, reducing morbidity and mortality, and
improving symptoms are clearly established. 108
Slide 109
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
Slide 110
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
Slide 111
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
Slide 112
112 ParameterValue end-diastolic volumeend-diastolic volume
(EDV)120 ml end-systolic volumeend-systolic volume (ESV)50 ml
stroke volumestroke volume (SV)70 ml ejection fraction (E f )58%
heart rateheart rate (HR)70 bpm cardiac outputcardiac output
(CO)4.9 L/m
Slide 113
113 For example: EDV=120, ESV= 50 EF = 120 - 50 / 120 = 0.58 =
58 %
