Heart failure

Heart failure is a complex clinical syndrome that result in the inability of the heart to provide
sufficient blood to meet the oxygen needs of tissue and organ. It is chronic and progressive
condition characterized by sign and symptoms of fluid overload or of inadequate tissue
perfusion.

The term heart failure indicate myocardial disease which there is a problem with contraction
of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) that may or
may not cause pulmonary or systemic congestion. Basically, the heart can’t keep up the
normal mechanism regulating cardiac output.

Incidence

 More than 5 million people in the United States have HF.

 There are 550, 000 cases of HF diagnosed each year according to the American
Heart Association.
 HF is most common among people older than 75 years of age.
 HF is now considered epidemic in the United States.
 HF is the most common reason for hospitalization of people older than 65 years of
age.
 IN Nepal, mean age of the patients was 56.48 ±19.44 years, with 45.9% males.
Etiology
Primary cause
 Hypertension
 Coronary artery disease
 Rheumatic heart disease
 Congenital heart disease (ventricular septal defect)
 Pulmonary hypertension
 Cardiomyopathy
 Hyperthyroidism
 Valvular heart disease (mitral stenosis, mitral regurgitation, aortic stenosis)
 Myocarditis
Precipitating causes of heart failure
 Anemia
 Thyrotoxicosis
  Hypothyroidism
 Dysrhythmias
 Bacterial endocarditis
 Obstructive sleep apnea
 Pulmonary embolism
 Paget’s disease
 Nutritional deficiency
 Hypervolemia
In Nepal, the commonest cause of heart failure was rheumatic heart disease (25.1%),
followed by cardiomyopathy (22.8%) and coronary artery disease (18.1%) [ CITATION Sha17 \l
1033 ]

Pathophysiology

Left sided heart failure: result either from the inability of the left ventricle to empty
adequately during systole or fill adequately during diastole.

The hallmark of systolic failure is a decrease in EF. Normal EF is 55%-60%. It can be low as
55 to 10%. It is caused by impaired contractile function (MI), increased afterload
(hypertension), cardiomyopathy and mechanical abnormalities (Valvular heart disease).

Diastolic failure is the inability of ventricle to relax and fill during diastole. Hypertension is
the most common cause of diastolic failure. Other risk factor include older age, diabetes and
obesity.in diastolic failure, the LV is generally stiff and noncompliant. So it is characterized
by high filling pressure. It is diagnosed by sign and (1) symptom of heart failure (2) normal
EF (3) LV diastolic dysfunction by echocardiography.

Backward effect

Decrease emptying of the left ventricle

Increase volume and end diastolic pressure

Increase volume

Increase volume in pulmonary vein

 Transduction of fluid from capillaries to alveoli
Increase volume in pulmonary capillary
bed
Rapid filling of alveolar

Pulmonary edema

Forward effect

Decrease cardiac output

Decrease body tissue

perfusion
Decrease blood flow to kidney

Release renin and convert angiotensin to angiotensin I

Angiotensin I convert to Angiotensin II and release aldosterone

Sodium and water retention

Increase extracellular fluid volume

Increase total blood volume and increase BP

BPBBsystemic BO

Right sided heart failure: occur when RV fail to pump effectively. When RV fails, fluid
back up into the venous system. This causes movement of fluid into tissue and organ. The
most common cause of right sided heart failure is left sided HF.
Backward effect
Decrease emptying of the right ventricle

Increase volume and end diastolic pressure

Increase volume and pressure in great veins

Increase volume in systemic venous pressure

Increase volume in distensible organ (hepatomegaly, splenomegaly, ascites)

Increase pressure in capillary line

Peripheral edema
Forward effect

Decrease volume from the right

Decrease return to left atrium and subsequent decrease cardiac

output

All forward effects of left heart

failure
Compensatory mechanism

Renin- angiotensin aldosterone system: as CO fall, blood flow to the kidney decrease. This
is sense by the juxtaglomerular apparatus in the kidney as decreased volume. In response, the
kidney release renin, which convert angiotensin to angiotensin I and is next converted to
angiotensin II by converting enzyme made in lung. Angiotensin II causes (1) activation of
SNS to increase BP and HR (2) release of aldosterone from the adrenal cortex (3) increase
peripheral vasoconstriction (4) stimulation of the pituitary gland which release ADH. The
outcome of the cascade result in further water and sodium retention in and already
overloaded state and increased workload of the failing heart.

Sympathetic Nervous system: in response to an inadequate stroke volume and CO, the SNS
is activated, resulting in the release of the catecholamine (epinephrine and norepinephrine).
The circulating catecholamine enhances peripheral peripheral vasoconstriction and cause
increase in HR and myocardial contractibility

In HF continuous response of neuroharmonal response leads to elevated level of

norepinephrine, angiotensin II, aldosterone, ADH, endothelin. Together these factor result in
an increase in heart’s workload, ventricular dysfunction and ventricular remodeling.

Clinical manifestation

Right sided heart failure Left sided heart failure

RV heaves LV heaves
Murmurs Pulse alteration
Jugular vein distension Increase HR
Edema ( pedal sacrum, scrotum) Decrease Pa o2, increase Paco2
Weight gain Crackle ( pulmonary edema)
Increase heart rate Pleural effusion, confusion
Ascites, anasarca, hepatomegaly Change in mental status, restlessness ,
Fatigue anxiety depression Weakness, fatigue, anxiety depression,
dyspnea, orthopnea, nocturia
Dependent bilateral edema Shallow respiration up to 32 to 40 / min
Rt upper quadrant pain Dry hacking cough
Anorexia , GI bloating, nausea Frothy, pink tinged sputum

The American College of Cardiology and American Heart Association have

classifications of heart failure.

 Stage A. Patients at high risk for developing left ventricular dysfunction but
without structural heart disease or symptoms of heart failure.

 Stage B. Patients with left ventricular dysfunction or structural heart disease that
has not developed symptoms of heart failure.

 Stage C. Patients with left ventricular dysfunction or structural heart disease with
current or prior symptoms of heart failure.

 Stage D. Patients with refractory end-stage heart failure requiring specialized

interventions.
Diagnosis
History and physical examination

ECG: Ventricular or atrial hypertrophy, axis deviation, ischemia, and damage patterns may
be present. Dysrhythmias, e.g., tachycardia, atrial fibrillation, conduction delays, especially
left bundle branch block, frequent premature ventricular contractions (PVCs) may be present.
Persistent ST-T segment abnormalities and decreased QRS amplitude may be presen

Chest x-ray: May show enlarged cardiac shadow, reflecting chamber dilation/hypertrophy, or
changes in blood vessels, reflecting increased pulmonary pressure. Abnormal contour, e.g.,
bulging of left cardiac border, may suggest ventricular aneurysm.

Sonograms (echocardiography, Doppler and transesophageal echocardiography): May

reveal enlarged chamber dimensions, alterations in Valvular function/structure, the degrees
of ventricular dilation and dysfunction.

Positron emission tomography (PET) scan: Sensitive test for evaluation of myocardial

ischemia/detecting viable myocardium.

Cardiac catheterization: Abnormal pressures are indicative and help differentiate right-

versus left-sided heart failure, as well as valve stenosis or insufficiency. Also assesses
patency of coronary arteries. Contrast injected into the ventricles reveals abnormal size and
ejection fraction/altered contractility. Transvenous endomyocardial biopsy may be useful in
some patients to determine the underlying disorder, such as myocarditis or amyloidosis.

Liver enzymes: Elevated in liver congestion/failure

Electrolytes: May be altered because of fluid shifts/decreased renal function, diuretic

therapy.

Pulse oximetry: Oxygen saturation may be low, especially when acute HF is imposed

on chronic obstructive pulmonary disease (COPD) or chronic HF.

Arterial blood gases (ABGs): Left ventricular failure is characterized by mild respiratory

alkalosis (early) or hypoxemia with an increased Pco2 (late).

Complications

 Pleural effusion
  Dysrhythmias
 Heft ventricular thrombus
 Hepatomegaly
 Renal failure

Management

Medical management
Medical management based on the type, severity and cause of HF. The overall goal of
management is to relieve symptoms, to improve functional status, quality of life and to
extend survival.

Pharmacologic Therapy

 ACE Inhibitors. ACE inhibitors slow the progression of HF, improve exercise
tolerance, decrease the number of hospitalizations for HF, and
promote vasodilation and diuresis by decreasing afterload and preload.

 Angiotensin II Receptor Blockers. ARBs block the conversion of angiotensin I

at the angiotensin II receptor and cause decreased blood pressure, decreased
systemic vascular resistance, and improved cardiac output.

 Beta Blockers. Beta blockers reduce the adverse effects from the constant

stimulation of the sympathetic nervous system.

 Diuretics. Diuretics are prescribed to remove excess extracellular fluid by

increasing the rate of urine produced in patients with signs and symptoms of fluid
overload.

 Calcium Channel Blockers. CCBs cause vasodilation, reducing systemic

vascular resistance but contraindicated in patients with systolic HF.
 Morphine : it reduce preload and afterload, it dilate both pulmonary and systemic
blood vessels. Result include a decrease in pulmonary pressure and myocardial
oxygen needs and improvement in gas exchange
 Positive inotropes: increase myocardial contractibility.
Nutritional Therapy

 Sodium restriction. A low sodium diet of 2 to 3g/day reduces fluid retention and
the symptoms of peripheral and pulmonary congestion, and decrease the amount
of circulating blood volume, which decreases myocardial work.
 Patient compliance. Patient compliance is important because dietary indiscretions
may result in severe exacerbations of HF requiring hospitalizations.

Additional Therapy

 Supplemental Oxygen. The need for supplemental oxygen is based on the degree
of pulmonary congestion and resulting hypoxia.
 Cardiac Resynchronization Therapy. CRT involves the use of a
biventricular pacemaker to treat electrical conduction defects.
 Cardiac Transplant. For some patients with end-stage heart failure, cardiac
transplant is the only option for long term survival.

Nursing management

Nursing diagnosis

 Impaired gas exchange related to increase preload and alveolar – capillary membrane
change
 Altered cardiac output related to altered contractibility, preload and stroke volume.
 Excess fluid volume related to increase venous pressure and decrease renal perfusion
heart failure.
 Activity intolerance related to imbalance between oxygen supply and demand
secondary to cardiac insufficiency and pulmonary congestion.

Intervention

1. Health promotion:
 Encourage patient to obtain the flu and pneumococcal vaccine.
o Coronary revascularization procedure should be considered in patient with
CAD
 o Develop plan to deduce risk factor ( blood pressure control, tobacco cessation,
weight reduction)
2. Regular assessment of patient level of fatigue dyspnea heart rate and chest congestion
edema, shortness of breath.
3. Record daily weight in same time (prefer in morning), clothes and scale and inform if
weight gain 1.4kg in 2days or 2.3 kg in a week.
4. Record daily fluid intake and output.
5. Assess oxygen saturation by using pulse oximetry.
6. Provide oxygen supplement (8-10 l/minute) by mask to relieve dyspnea and hypoxia.
7. Position propped up to facilitate breathing
8. Provide emotional, physical rest and reduction of anxiety. Since anxiety may increase
SNS response and further increase myocardial work load.
9. A total of 30 minutes of physical activity every day should be encouraged to promote
activity intolerance.
10. Teach the patient how to take pulse rate. Pulse should take always foe full minute
because less than 50 beat /min is contra indicate to the patient with beta blocker and
digitalis
11. Teach the patient the symptoms of hyper – hypokalemia (weakness, fatigue,
constipation and muscle cramp) if the diuretic that deplete or spare potassium as
ordered.
12. Explain all procedure to patient in understandable term and provide calm
environment
13. Encourage the patient to verbalize their concerns and provide the patient with
decision-making opportunities.

References
Shareef, m., BahadurKC, M., Hirachan, A., KC, B., Agarwal, A. K., Shah, R. K., &
Adhikari, C. M. (2017). etiology of heart failure in the emergency depatment of a
tertiary cardiac centers of Nepal. Nepalese Heart Journal, 14(2), 1-4.
doi:doi.org/10.3126/njh.v14i2.18494
Lewis, Bucher, Heitkemper, Kwong, Harding, & Robert. (n.d.). Lewis's Medical Surgical Nursing
assessment and management of clinical problems (3rd south Asia edition ed., Vol. 1).
Elsevier.
sharma, M., Paudel, K., & Gautam, R. (2017). Essential testbook of Medical Surgical Nursing (2nd
edition ed.). Samikha.
Smeltzer, S., Bara, B., Hinkle, J., & Cheever, K. (n.d.). Brunner & Suddarth's Texbook of Medical
Surgical Nursing (11th edition ed., Vol. 1).

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