Congestive heart failure (CHF) results from any structural or functional cardiac disorder that impairs the ventricle's ability to fill with or eject blood. It is diagnosed based on history, physical exam, chest x-ray, EKG, and echocardiogram. Treatment focuses on restoring normal cardiopulmonary physiology by using ACE inhibitors, beta-blockers, diuretics, and addressing pulmonary complications. Management involves evaluating the patient's stage of CHF and functional classification to determine appropriate pharmacotherapy and monitoring according to guidelines from the American Heart Association.

1. Congestive Heart
Failure

2. Introduction
 Congestive heart failure (CHF) can result
from any functional or structural cardiac
disorder that impairs the ventricle’s ability
to fill with or eject blood.
 It remains a clinical diagnosis that is
largely based on a careful history and
physical examination and supported by
ancillary tests such as chest
radiograph, electrocardiogram, and
echocardiography.

3. Congestive heart failure (CHF)
 results in pulmonary vascular congestion and
reduced cardiac output.
 should be considered in the differential
diagnosis of any adult patient who presents
with dyspnea and/or respiratory failure.
 The measurement of serum brain natriuretic
peptide and echocardiography have substantially
improved the accuracy of diagnosis.

4. Therapy for CHF
 restoring normal cardiopulmonary physiology and
reducing the hyperadrenergic state.
 combination of an angiotensin-converting-enzyme inhibitor
and slow titration of a blocker.
 Patients with CHF are prone to pulmonary
complications, including obstructive sleep
apnea, pulmonary edema, and pleural effusions.
 Continuous positive airway pressure and noninvasive
positive-pressure ventilation benefit patients in CHF
exacerbations.

5. Congestive Heart Failure (CHF)
Latest Statistic (US)
 major and growing public health problem in the United States.
 Approximately 5 million patients in this country have HF, and
over 550 000 patients are diagnosed with HF for the first time
each year.
 The disorder is the primary reason for 12 to 15 million office
visits and 6.5 million hospital days each year.
 In 2001, nearly 53 000 patients died of HF as a primary cause.
The number of HF deaths has increased steadily despite
advances in treatment, in part because of increasing numbers
of patients with HF due to better treatment and “salvage” of
patients with acute myocardial infarctions (MIs) earlier in life.
(AHA,2005)

6. Latest Statistics (Phil population)
•In the Philippines, cardiovascular diseases are the most
common causes of mortality.
•About 77,060 in a 100, 000 populationhave died in the
Philippines due to diseases of the heart.
•The prevention of heart failure is an urgent public health need
with national and global implications. (DOH, 2005)

7. Pathophysiology Of Cardiac
Performance
Figure 1

8. Preload
 the amount of blood presented to the ventricle
just before systole. It increases the pressure in
the ventricle, which stretches the ventricular wall.
 Like a rubber band the ventricular muscle fibers
need to be stretched ( by blood volume) to
produce optimal ejection of blood. Too little or
too much muscle fiber stretch decreases the
volume of blood ejected.
 The major factor that determines the preload is a
venous return the volume of blood that enters the
ventricle during the diastole.

9. Afterload
 the amount of resistance to the ejection of
blood from the ventricle.
 Afterload inversely related to SV and an increase
in afterload causes the ventricle to work harder
and may decrease the amount of blood ejected.
 The major factors that determine afterload are
the diameter and distensibility of the great
vessels ( aorta and pulmonary artery) and the
opening and the competence of the semilunar
valves (pulmonic and aortic valves. When the
valves open easily the resistance is lower.

10. Contractility
 The force of contraction, is related to the
status of the myocardium.
 Catecholamines, released by sympathetic
stimulation during exercise or from
administration of positive inotropic
medications, can Increase contractility and
SV.

11. Pathophysiology of Congestive Heart Failure
 an abnormality in cardiac structure, function, rhythm, or
conduction.
 Degenerative valve disease, idiopathic cardiomyopathy, and
alcoholic cardiomyopathy are also major causes of heart
failure.
 elderly patients who have multiple comorbid conditions (eg,
angina, hypertension, diabetes, and chronic lung disease).
 Some common comorbidities such as renal dysfunction are
multifactorial (decreased perfusion or volume depletion from
overdiuresis), whereas others (eg, anemia, depression,
disorders of breathing, and cachexia) are poorly understood.

12. Pathophysiology of Congestive Heart Failure
CHF indicates not only an inability of the
heart to maintain adequate oxygen delivery;
◦it is also a systemic response attempting to
compensate for the inadequacy.
The determinants of cardiac output include
heart rate and stroke volume (Fig. 1)
stroke volume =preload (the volume that
enters the left ventricle), contractility, and
afterload (the impedance of the flow from the
left ventricle).

13. Pathophysiology of Congestive Heart Failure
 increased positive pleural pressure can
reduce right-atrial pressure (which equals
central venous pressure minus pleural
pressure), thus reduce ventricular filling.
 The cardiac pump is a muscle and will
respond to the volume it is given with a
determined output. If volume increases, so
will the amount pumped out in a normal
physiologic state, to a determined plateau;
this relationship is described by the Frank-
Starling law (Figs. 2 and 3).

14. Pathophysiology of Congestive Heart Failure
 Diastolic function is determined by 2 factors:
◦ the elasticity or distensibility of the left ventricle, which is a
passive phenomenon
◦ the process of myocardial relaxation, which is an active process
that requires metabolic energy
 Relaxation of the myocardium occurs in early diastole, and
the “untwisting” of the left ventricle is an active process
that produces a suction effect that augments left-
ventricular filling.
 Loss of normal lef tventricular distensibility or relaxation
by either structural changes (eg, left-ventricular
hypertrophy) or functional changes (eg, ischemia) impairs
ventricular filling (preload).

15. PATHOPHYSIOLOGY OF
CONGESTIVE HEART FAILURE
Fig. 2. The Frank-Starling law of the heart
states that as the ventricular
volume increases and stretches the
myocardial muscle fibers, the stroke volume
increases, up to its maximum capacity. After
that point, increasing volume increases
pulmonary capillary pressure (and
pulmonary congestion), without increasing
the stroke volume or cardiac output. The
mechanism is the length-force relationships
of muscle contraction.

16. PATHOPHYSIOLOGY OF
CONGESTIVE HEART FAILURE
Fig. 3. This series of Frank-Starling
curves demonstrates that at any given
preload (end-diastolic
volume), increases in contractility
will increase stroke volume (volume
of blood ejected from the ventricle
with each beat).

17. Pathophysiology of Congestive Heart Failure
 If cardiac output falls, either the heart rate or stroke
volume must change in order to maintain perfusion.
 If stroke volume cannot be maintained, then heart rate
must increase to maintain cardiac output.
 It also includes the cardiovascular response to poor
perfusion with the activation of the neurohumoral
system.

18. Pathophysiology of Congestive Heart Failure
 Activation of the renin-angiotensin system
attempts to increase preload by stimulating
retention of salt and water, increasing
vasoconstriction(and, thus, afterload), and
augmenting cardiac contractility.
 Initially, this response will suffice, but
prolonged activation results in loss of
myocytes and maladaptive changes in the
surviving myocytes and the extracellular
matrix.

19. Pathophysiology of Congestive Heart Failure
 The stressed myocardium undergoes
remodeling and dilation in response to the
insult.
 This process also has detrimental effects on the
functioning of the lungs, kidneys, muscles, blood
vessels, and probably other organs.
 Remodeling also results in additional cardiac
decompensation from complications, including mitral
regurgitation from valvular annulus stretching, and
cardiac arrhythmias from atrial remodeling

20. Pathophysiology of Congestive Heart Failure
 The respiratory care provider often
becomes involved with the CHF patient as
the elevated end-diastolic pressure leads to
pulmonary edema and dyspnea.
 The lung provides multiple mechanisms to
avoid the consequences of pulmonary
edema. Initially, as pressure
increases, pulmonary capillaries are recruited
and increase capacitance to deal with the
added volume.

21. Treatment includes the following:
 Nonpharmacologic therapy: Oxygen and noninvasive
positive pressure ventilation, dietary sodium and fluid
restriction, physical activity as appropriate, and attention
to weight gain
 Pharmacotherapy: Diuretics, vasodilators, inotropic
agents, anticoagulants, beta-blockers, and digoxin

22. A schematic diagram
PATHOPHYSIOLOGY
OF CHF

23. Non Modifiable factors: Modifiable factors:
Gender-female Sedentary Lifestyle
Age- 55 and above
Decreased elasticity of blood vessels and formation of
plaques on blood vessels
Narrowing of the blood vessels
Necrosis and scarring of the vascular endothelium
Impediment of blood flow to the body

24. Increased workload of the heart
Dilation of ventricles
Increased in preload
Increased stretching of myocardial muscle
Excessive stretching of myocardial muscle
Ineffective cardiac muscle and increase o2 demand of
cardiac muscle
Decreased contraction of cardiac muscle
Decreased cardiac output and
systemic perfusion

25. Activation of neurohormonal patways in order to increase circulating blood
vessel
Continued neurohormonal stimulation
Cardiac remodelling
Decreased blood filling
Increased stroke volume and decreased cardiac output
Inadequate perfusion Increased wall tension

26. Inadequate perfusion
Decreased perfusion of
pallor arteries
Decreased Increased
Deprivation of cardiac muscle cells of nutrients
blood flow pulmonary needed for survival
to the pressure
kidneys Normal balance between oxygen
supply and demand is disrupted
Fatigue and ischemia
Kidneys
weakness
produce Conversion of aerobic metabolism to
hormones anaerobic metalolism
Causes reduced contractility Decreased adenosine
Salt and water
retention Decreased heart Increased lactic acid
ability production
edema bradycardia Irritation of myocardial cells
Chest pain
Positive troponin t

27. Increased wall tension
Separation of mitral
leaflets
Increased pulmonary
pressure
Impaired left ventricular
relaxation
Increased diastolic pressure exceeding hydrostatic and
osmotic pressure in pulmonary capillaries
Fluid shifts from circulating blood into the
interstitium, bronchioles bronchi and alveoli
Pulmonary congestion
Decreased lung Fluid trapped in
expansion pulmonary trees
dyspnea Bilateral crackles

28. Figure 1. Stages in the Development of Heart Failure/Recommended Therapy by Stage ACEI
indicates angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker;
EF, ejection fraction; FHx CM, family history of cardiomyopathy; HF, heart failur...
2005 WRITING COMMITTEE MEMBERS et al. Circulation
2009;119:e391-e479
Copyright © American Heart Association

29. CONGESTIVE HEART FAILURE
GUIDELINE
Stages in the evolution of heart failure (HF) and recommended therapy
by stage. FHx indicates family history of cardiomyopathy; MI, myocardial
infarction; LV, left ventricular; and IV, intravenous.

30. CONGESTIVE HEART
FAILURE GUIDELINE

31. CONGESTIVE HEART
FAILURE GUIDELINE

32. CONGESTIVE HEART
FAILURE GUIDELINE

33. Initial Evaluation incudes the ff:
INITIAL EVALUATION
1. H&P, including hx of current &past
alcohol&drug use, orthostatic bp
changes, , weight&height&BMI
2. 2. Lab teting: CBC, UA, serum Determine type of heart failure based on:
electrolytes) BUN, serum >Clinical history
creatinine, FBS, lipid profile,liver >EKG and or echocardiogram results
fxn tests&TSH >2D echo
3. Assess ability to perform routine
&desired activities of daily living
4. 12L ECG
5. Chest x-ray (PA&lateral)
Determine stage and
Functional Classification
Therapy and Education per stage
based on AHA guidelines
Go back to Initial
no evaluation
Is patient stable?
yes
Follow-up at least Controllable as on
MANAGEMENT OF every 3-6 months outpatient
Admit to hospital
CHF
IN ACTUAL
Return to guideline after
discharge from hospital
to outpatient care
PRACTICE

34. Similarities of Actual Practice and
Standard of Care in CHF
 There is utilization of clinical guideline
based on American heart association in
managing Congestive Heart Failure. Their
management is based on the stage of CHF
as indicated in the standard of care.
 There is both a complete history
taking/documentation and rigorous
diagnostic procedures in detecting CHF.

35. Similarities of Actual Practice and
Standard of Care in CHF
 The diagnosis of HF is primarily based on signs
and symptoms derived from a thorough
history and physical examination.

36. Similarities of Actual Practice and
Standard of Care in CHF
 Effects of HF treatment were both monitored
with careful measurement of fluid intake and
output; vital signs; body weight, determined at the
same time each day; clinical signs (supine and
standing) and symptoms of systemic perfusion
and congestion. Daily serum electrolytes, urea
nitrogen, and creatinine concentrations should be
measured during the use of IV diuretics or active
titration of HF medications

37. Similarities of Actual Practice and
Standard of Care in CHF
 In end of life considerations, there are both
ongoing patient and family education regarding
prognosis for functional capacity and survival
for patients with. Most patients hospitalized
with severe HF indicate a preference that
resuscitation be performed in the event of a
cardiopulmonary arrest

38. Differences of Actual Practice from
Standard of Care in CHF
 Practice use of medications where not fully
explained in the actual practice

39. Differences of Actual Practice from
Standard of Care in CHF
 There is absence of exercise training in
actual practice. In the guideline, exercise
training should be considered for all
stable outpatients with chronic HF who
are able to participate in the protocols
needed to produce physical conditioning.
Exercise training should be used in
conjunction with drug therapy.

40. Differences of Actual Practice from
Standard of Care in CHF
 Alternative surgical and mechanical
approaches for the treatment of end-
stage HF are under development in actual
practice. Cardiac transplantation is
currently the only established surgical
approach to the treatment of refractory
HF, but it is available to fewer than 2500
patients in the United States each year.

41. Differences of Actual Practice from
Standard of Care in CHF
 In actual practice, method of treatment is
indicated for general population. Unlike in
the standard of care, there is a treatment
recommendation/ethical consideration for
special population
 In actual practice, still the management of
CHF depends on patient’s
cardiologist/general physician, decisions will
still be based on the patient. Standard of care
in CHF still serves as a guide or backbone of
management.

42. Applicability of the Standard of Care in the
actual hospital setting
It
is highly recommended to utilize this guidelines in
managing CHF for adult patients.
◦Since, the American College of Cardiology Foundation
(ACCF) and the American Heart Association (AHA) have
jointly engaged in the production of such guidelines in the
area of cardiovascular disease since 1980.
◦This effort is directed by the ACCF/AHA Task Force on
Practice Guidelines, whose charge is to develop and revise
practice guidelines for important cardiovascular diseases and
procedures.

43. Applicability of the Standard of Care in the
actual hospital setting
 The ACCF/AHA Task Force on Practice
Guidelines makes every effort to avoid any
actual, potential, or perceived conflicts of
interest that might arise as a result of an
outside relationship or personal interest of a
member of the writing committee.

44. Applicability of the Standard of Care in the
actual hospital setting
 All members of the writing committee, as
well as peer reviewers of the document, are
asked to provide disclosure statements of all
such relationships that might be perceived as
real or potential conflicts of interest. Writing
committee members are also strongly
encouraged to declare a previous
relationship with industry that may be
perceived as relevant to guideline
development.(AHA, 2009). Hence, we can
say that it is reliable and a correct practice
intended to improve patient care.

45. Applicability of the Standard of Care in the
actual hospital setting
•The practice guidelines produced are intended to assist healthcare
providers in clinical decision making by describing a range of
generally acceptable approaches for the diagnosis, management, or
prevention of specific diseases or conditions.
•These guidelines attempt to define practices that meet the needs of
most patients in most circumstances.

46. Applicability of the Standard of Care in the
actual hospital setting
 These guideline recommendations reflect a consensus
of expert opinion after a thorough review of the
available, current scientific evidence and are intended
to improve patient care.
 If these guidelines are used as the basis for
regulatory/payer decisions, the ultimate goal is quality
of care and serving the patient's best interests. The
ultimate judgment regarding care of a particular
patient must be made by the healthcare provider and
patient in light of all of the circumstances presented
by that patient. (AHA, 2009)

47. RECOMMENDATIONS HAVE
BEEN UPDATED WITH NEW
INFORMATION THAT HAS
EMERGED FROM CLINICAL
TRIALS OR OTHER ACCF/AHA
GUIDELINE OR CONSENSUS
DOCUMENTS

48.  2009 updated recommendation: Measurement of natriuretic
peptides (i.e., BNP and NT-proBNP) can be useful in the
evaluation of patients presenting in the urgent care setting in
whom the clinical diagnosis of heart failure is uncertain.
 Measurement of natriuretic peptides can be useful in risk
stratification. (Level of Evidence: A)
 The 2005 guidelines also recommended measurement of BNP
for evaluating patients who present in the urgent care setting
with possible heart failure; the 2009 update expanded this
recommendation to include the measurement of NT-proBNP.
 The 2009 update warns that, although elevated natriuretic
peptide levels may help confirm a suspected diagnosis of heart
failure, the results of this testing alone should not be used to
confirm or exclude a heart failure diagnosis.

49.  2009 updated recommendation: Use of ARBs is
recommended in patients with current or
previous symptoms of heart failure and reduced
LVEF who have an intolerance to angiotensin-
converting enzyme (ACE) inhibitors. (Level of
Evidence: A)
 2009 updated recommendation: Maximal exercise
testing with or without measurement of
respiratory gas exchange is reasonable to
facilitate prescription of an appropriate exercise
program for patients presenting with heart
failure. (Level of Evidence: C)

50. REFERENCE:
Hunt, S. et.al. 2013. ACCF/AHA Practice Guideline: Full
Text 2009 Focused Update Incorporated Into the
ACC/AHA 2005 Guidelines for the Diagnosis and
Management of Heart Failure in Adults.
Circulation.2009; 119: e391-e479.Published online before
print March 26,.2009. Retrieved from
http://circ.ahajournals.org/content/119/14/e391.full

51. TASK DISTRIBUTION
 Jaybee Bernandino-latest
statistics, pathophysiology
 Danielle Ann Santiago-actual
practice, clinical guideline
 Cathy Roxas- critique, similarities and
differences