Congestive Heart Failure Abstract The primary function of the heart is to pump blood to all organs of the body, delivering oxygen and nutrients to the tissues and at the same removing waste products. At rest, organs need a certain amount of blood for this function. During activity, there are greater demands on the heart and more blood perfusion is required. To meet this varying demands, the heart rate and force of contraction of the heart may change and the blood vessels vasodilate to deliver more blood to the organs. In an individual with congestive heart failure (CHF), the heart is not able to meet these demands or is not able to work efficiently as it should. There are many causes of CHF some of which are reversible. However, heart failure can be sudden and present with a variety of symptoms such as dyspnea. Over time the architecture of the heart changes as it enlarges-this also alters the geometry of the valves leading to mitral valve regurgitation which makes heart failure worse. Overall, the prognosis of patients with heart failure is guarded and they have a poor quality of life. Introduction Heart failure is a pathological medical disorder where there is an abnormality of heart function, which results in an inability to pump blood to the rest of the body resulting in poor perfusion of the organs (Dumitru & Ooi, 2015). Heart failure may be due to systolic dysfunction where the pumping action of the hart is reduced or it may be diastolic where the heart chambers do not fill adequately because of stiffness in the walls. The clinical signs of heart failure depend on whether there is right or left heart failure. Heart failure is classified by the New York Heart Association based on presence of symptoms and the degree of effort needed to trigger them as follows: · Class I patients have no limitation of physical activity · Class II patients have slight limitation of physical activity · Class III patients have marked limitation of physical activity · Class IV patients have symptoms even at rest and are unable to carry on any physical activity without discomfort Pathophysiology The pathophysiology of heart failure is complex because of presence of compensatory mechanisms at all levels of the organization of the heart and other systemic influences. It is only when these network of organizations become overwhelmed that heart failure occurs. In summary the inefficient heart pumping results in back-up of fluids to lungs (Left sided failure) or peripheral tissues (Right sided failure). Compensatory mechanisms that occur include changes in myocyte size (ie hypertrophy) and activation of various neurohumoral systems. There is release of catecholamines by the sympathetic nerves to enhance myocardial contractility, activation of the activation of the renin-angiotensin-aldosterone system and other vasoregulating adjustments to maintain mean arterial pressure and perfusion of vital organs (Urso et al, 2015). Etiology The majority of patients who present.

1. Congestive Heart Failure
Abstract
The primary function of the heart is to pump blood to all organs
of the body, delivering oxygen and nutrients to the tissues and
at the same removing waste products. At rest, organs need a
certain amount of blood for this function. During activity, there
are greater demands on the heart and more blood perfusion is
required. To meet this varying demands, the heart rate and force
of contraction of the heart may change and the blood vessels
vasodilate to deliver more blood to the organs. In an individual
with congestive heart failure (CHF), the heart is not able to
meet these demands or is not able to work efficiently as it
should. There are many causes of CHF some of which are
reversible. However, heart failure can be sudden and present
with a variety of symptoms such as dyspnea. Over time the
architecture of the heart changes as it enlarges-this also alters
the geometry of the valves leading to mitral valve regurgitation
which makes heart failure worse. Overall, the prognosis of
patients with heart failure is guarded and they have a poor
quality of life.
Introduction
Heart failure is a pathological medical disorder where there is
an abnormality of heart function, which results in an inability to
pump blood to the rest of the body resulting in poor perfusion
of the organs (Dumitru & Ooi, 2015). Heart failure may be due
to systolic dysfunction where the pumping action of the hart is
reduced or it may be diastolic where the heart chambers do not
fill adequately because of stiffness in the walls. The clinical
signs of heart failure depend on whether there is right or left
heart failure. Heart failure is classified by the New York Heart
Association based on presence of symptoms and the degree of
effort needed to trigger them as follows:
· Class I patients have no limitation of physical activity
· Class II patients have slight limitation of physical activity

2. · Class III patients have marked limitation of physical activity
· Class IV patients have symptoms even at rest and are unable
to carry on any physical activity without discomfort
Pathophysiology
The pathophysiology of heart failure is complex because of
presence of compensatory mechanisms at all levels of the
organization of the heart and other systemic influences. It is
only when these network of organizations become overwhelmed
that heart failure occurs. In summary the inefficient heart
pumping results in back-up of fluids to lungs (Left sided
failure) or peripheral tissues (Right sided failure).
Compensatory mechanisms that occur include changes in
myocyte size (ie hypertrophy) and activation of various
neurohumoral systems. There is release of catecholamines by
the sympathetic nerves to enhance myocardial contractility,
activation of the activation of the renin-angiotensin-aldosterone
system and other vasoregulating adjustments to maintain mean
arterial pressure and perfusion of vital organs (Urso et al,
2015).
Etiology
The majority of patients who present with CHF have an
inadequate cardiac output. The causes of heart failure include
the following:
· Cardiomyopathies, congenital heart disease, Coronary artery
disease, valvular heart disease
· Dysrhythmias, hypertension
· Sepsis
· Pulmonary embolus
· Medications-doxorubicin
Precipitating Causes of Heart Failure
In some stable patients, there are clinical factors that can
increase myocardial oxygen consumption and demand beyond a
critical level and precipitate heart failure. Some of the more
common conditions these include:
· Profound anemia
· Multiple myeloma, Paget disease of bone

3. · Myxedema, thyrotoxicosis
· Obesity, Nutritional deficiencies (eg, thiamine deficiency,
beriberi)
· Polycythemia vera
· Pregnancy
Epidemiology
Based on data released by the American Heart Association
(AHA), nearly 5.7 million Americans (2% of the population) of
all ages have been diagnosed with CHF. As survival of patients
improves, CHF will continue to be a major health problem in
the US.
· CHF accounts for nearly 1/3rd of cardiac deaths (277,000
patients) each year.
· There are nearly 670,000 new cases of CHF diagnosed
annually.
· The average hospital stay is about 6 days and the cost of
care/year is nearly $40 billion (Sperry et al, 2015).
The prevalence and incidence of CHF is greater in African
Americans, Native Americans and Hispanics compared to
Caucasians. In this population the higher prevalence is directly
related to the higher incidence of diabetes and hypertension.
The problem is exacerbated by lack of access to care and
substandard preventive care. While men and women have the
same incidence, women tend to develop CHF later in life
compared to men. Overall women with CHF survive longer than
men
Prognosis
Patients admitted with CHF have a 10% mortality rate at 30
days and 22% at 1 year. Each admission increases mortality by
about 20%. Mortality is markedly increased in patients with
NYHA class IV and in those with an acute MI, atrial fibrillation
and cardiogenic shock.
History of Presentation
The following factors should be determined

4. · History of heart disease, family history of heart disease
· Alcohol and/or substance abuse
· Diabetes
· Dyslipidemia
· History of chemotherapy or radiation to chest area
· Hypertension
· Peripheral vascular disease
· Sleep apnea
· Thyroid disease
Determine presence of symptoms like:
· Bloating
· Chest pain, cough, palpitations
· Diaphoresis
· Dyspnea at rest, orthopnea, exertional dyspnea, paroxysmal
nocturnal dyspnea
· General symptoms like fatigue, weakness,
· CNS symptoms like confusion, anxiety, insomnia, headache,
memory impairment and nightmares
· Oliguria, nocturia
· Weight loss
Physical Exam:
Individuals with mild CHF may have no symptoms at rest but
may become dyspnea after activity. Most patients with CHF will
become dyspnea when lying supine and also exhibit air hunger.
Patients with chronic CHF may be cachectic and malnourished.
Examination may reveal:
- Ascites, edema
- Central and peripheral cyanoses
- Cold and pale extremities
- Elevated JVP, visible pulsation of neck and eye veins
- Hepatomegaly, icterus, malar flush
- Pulses may be weak, rapid and thready
- Rales over lung bases
- Presence of S3

5. - Wheezing and or expectoration of blood tinged sputum
Diagnosis
To make the diagnosis of CHF, the Framingham criteria plus the
presence of 2 major criteria or I major and 2 minor criteria are
needed:
Major criteria include the following:
· Acute pulmonary edema and X-ray features of cardiomegaly
· Hepatojugular reflux and neck vein distention
· Paroxysmal nocturnal dyspnea, pulmonary edema, visceral
congestion, or cardiomegaly at autopsy
· Rales and S3 gallop
· Weight loss of 4.5 kg in five days following diuretic treatment
Minor criteria are as follows:
· Decreased vital capacity
· Bilateral ankle edema
· Dyspnea on ordinary exertion
· Nocturnal cough
· Pleural effusion
· Tachycardia (rate equal to or > 120 bpm)
Testing
· Complete blood count (CBC), urinalysis and electrolyte level
· B-type natriuretic peptide levels (Roberts et al, 2015).
· Fasting blood glucose levels and Lipid profile
· Renal and liver function studies
· Thyroid stimulating hormone (TSH) levels
· ECG, chest x-ray and echocardiography
· Pulse oximetry & arterial blood gas
Treatment
General
· Admission to hospital for telemetry monitoring or ongoing
therapy
· Immediate evaluation and treatment of ABCs
· Cardiac monitoring

6. · Administration of nitrates and diuretic
· Initiate fluid and sodium restrictions
· Evaluate for need for CPAP or Bi-PAP if severe respiratory
compromise
Activity
· Bed rest with HOB elevated during exacerbations
· Anti-embolism stockings if lower extremity edema
· Walking to maintain strength
Diet
· Appropriate fluid restrictions based upon symptoms
· Sodium restriction
· Low-cholesterol
· Weight reduction when necessary
Medications
· Analgesics administered as prescribed when necessary
· Digoxin
· Angiotensin II receptor blockers (ARB)
· Aldosterone antagonists
· Beta blockers
· Hydralazine
· ACE Inhibitors (to decrease afterload of cardiac cycle)
· Diuretics:
· Furosemide (Lasix) 10-20mg IV for symptomatic CHF patients
not currently treated with diuretics, 40-80mg Iv for patients
using diuretic therapy, 80-120mg IV for those refractory to
treatment after 1 hour
· Nitrates:
· Nitroglycerin: 1-2 inches Nitro paste to chest wall, IV
therapy: 20mcg/min IV with titration 5-10mcg q 5 minutes until
effective
· Nitroprusside sodium (Nitropress): 10-15mcg/min IV with
titration 30-50mcg/min to acquire SBP > 90mmHG
· Inotropic agents:
· Dobutamine (Dobutrex): 2.5mcg/kg/min IV titrating to effect
· Dopamine (Intropin): 5mcg/kg/min IV increasing 5mcg/kg/min
to a maximum of 20mcg/kg/min dose

7. The latest guidelines for congestive heart failure treatment
divide patients into four stages, A/B/C/D, depending on the
severity of disease and the need for multidrug or specialized
therapy (Fergenbaum et al, 2015). The use of the various drug
classes including beta blockers, ARBs, aldosterone antagonists,
hydralazine, and nitrates are governed by specific algorithms
(Kaldara et al, 2015).
Surgery
· Possible valvular replacement and coronary artery bypass
· Intra-aortic balloon pump or ECMO
· Possible heart transplantation based upon pathological cause
of CHF
References
1. Dumitru, I., Ooi, H.H. (2015). Heart Failure.
http://emedicine.medscape.com/article/163062-overview.
Accessed on Sept 21, 2015.
2. Fergenbaum, J., Bermingham, S., Krahn, M., Alter, D.,
Demers, C. (2015). Care in the Home for the Management of
Chronic Heart Failure: Systematic Review and Cost-
Effectiveness Analysis.J Cardiovasc Nurs. 30(4 Suppl 1):S44-
51.
3. Kaldara, E., Sanoudou, D., Adamopoulos, S., Nanas, J.N.
(2015). Outpatient management of chronic heartfailure.Expert
Opin Pharmacother. 16(1):17-41.
4. Roberts, E., Ludman, A.J., Dworzynski, K., et al. (2015).
NICE Guideline Development Group for Acute HeartFailure.
The diagnostic accuracy of the natriuretic peptides in heart
failure: systematic review and diagnostic meta-analysis in the
acute care setting.BMJ.350:h910. doi: 10.1136/bmj.h910.
5. Sperry, B.W., Ruiz, G., Najjar, S.S. (2015). Hospital
readmission in heartfailure, a novel analysis of a longstanding
problem.Heart Fail Rev. 20(3):251-8
6. Urso, C., Brucculeri, S., Caimi, G. (2015). Acid-base and
electrolyte abnormalities in heartfailure: pathophysiology and
implications.Heart Fail Rev. 20(4):493-503