DEMOGRAPHICS
There was a total of 6 914 410 PhilHealth claims for hospitalization for either medical or surgical causes
during the time period of the study. Of these, 2 673 546 were claims for hospitalization due to medical causes. The
claims for medical causes, 44 046 were due to heart failure. This represented a prevalence rate of 1.6% or 1648
cases of CHF for every 100 000 patient claims for medical causes. The majority of these came from Region IV-A
(13.5%), National Capital Region (NCR) (10.7%), and Region III (10.3%). Patient claims without assigned regions
(0.9%) were attributed to those who were admitted in non-PhilHealth accredited hospitals who were probably
subsequently reimbursed in the local PhilHealth offices that may or may not have been the region where they were
confined. Also shown in 2010 Philippine population, the latest population count done before 2014, to demonstrate
the burden of the disease per region. The country's annual growth rate from 2010 to 2015 was 1.72%. The total
patient claims reported above represented individual unique claims or individual patients.
Number of patients who were hospitalized for CHF and the population in the Philippines and its regions in
2014
Region
N (%)*
Population†
Philippines
44 046
92 337 852
Ilocos
region (Region I)
3736 (8.5)
4 748 372
Cagayan Valley (Region II)
1229 (2.8)
3 229 163
Central Luzon (Region III)
4526 (10.3)
10 137 737
CALABARZON (Region IV-A)
5947 (13.5)
12 609 803
MIMAROPA (Region IV-B)
954 (2.2)
2 744 671
Bicol Region (Region V)
2686 (6.1)
5 420 411
Western Visayas (Region VI)
1677 (3.8)
7 102 438
Central Visayas (Region VII)
2163 (4.9)
6 800 180
Eastern Visayas (Region VIII)
1878 (4.3)
4 101 322
Zamboanga Peninsula (Region IX)
1939 (4.4)
3 407 353
Northern Mindanao (Region X)
3462 (7.8)
4 297 323
Davao Region (Region XI)
2692 (6.1)
4 468 563
SOCCSKSARGEN (Region XII)
2250 (5.1)
4 109 571
Caraga (Region XIII)
972 (2.2)
2 429 224
There were 16 cases of heart failure for every 1000 Filipino patients admitted due to a medical condition in 2014.
Hypertension was possibly the most common aetiologic factor. Compared to western and Asia-Pacific countries,
the local mortality rate was relatively higher.
INTRODUCTION
Heart Failure is a condition in which the heart loses its ability to pump blood. Right Heart Failure is most
commonly a result of left ventricular failure via volume and pressure overload. Clinically, patients will present
with signs and symptoms of chest discomfort, breathlessness, palpitations, and body swelling This condition is
evaluated using non-invasive techniques such as echocardiography, nuclear angiography, MRI, 64-slice CT, as
well as invasive hemodynamic measurements. Management is aimed at increasing right ventricular contractility,
reducing right ventricular afterload, and optimizing volume status. This activity reviews the evaluation and
management of right heart failure and highlights the role of the interprofessional team in improving care for
affected patients.
Congestive heart failure (CHF) is an important public health problem, with prevalence reported to range
from 1% to 12% in western countries, and 0.5% to 6.7% in Southeast Asian countries. It is defined as a clinical
syndrome resulting from any structural or functional cardiac disorder that leads to an impaired ventricular filling or
incomplete ejection of blood. The current three types of heart failure based on the recent revisions of the European
Society of Cardiology are: reduced with ejection fraction (EF) <40% (HFrEF); preserved with EF ≥50% (HFpEF);
and (3) mid-range with EF 40–49%. Although their clinical presentations are mostly the same, patients with HFrEF
are more likely to be male and have coronary artery disease (CAD), while HFpEF are more likely to be female,
elderly, and have hypertension. Patients with HFrEF have increased mortality and recurrent hospitalizations.
The DEAR HEART Registry, a 2-year study on CHF, described the demographic profile of patients
hospitalized for heart failure in six hospitals located in some urban areas in the Philippines. Another heart failure
registry, the ADHERE Asia-Pacific study, included 722 Filipino patients (7.1% of the study population). Despite
these studies, there are no data available regarding the prevalence of hospitalization for CHF in the Philippines.
Currently, the most comprehensive database regarding hospitalization claims in the country is with the
Philippine Health Insurance Corporation (PhilHealth). PhilHealth is a government corporation tasked with
administering the National Health Insurance Program of the country. Approximately nine out of 10 hospitals or
healthcare facilities accredited by the Department of Health are also accredited by PhilHealth. As of December
2014, 87% of the projected population of the country is either a member or a beneficiary of PhilHealth.
In view of the importance of CHF, this study was conducted to estimate the prevalence of hospitalization
for CHF in the Philippines. Because of PhilHealth's wide coverage, the study used its claims database to obtain a
representation of the overall hospitalization prevalence of CHF in the country.
The general objective of this study was to determine the prevalence of CHF among adult patients aged 19
years and above who were admitted to PhilHealth-accredited hospitals in 2014, with specific objectives as follows:
to determine the overall and regional prevalence of CHF in the country; to determine the demographic profile and
comorbid conditions of patients with CHF; to determine the etiology and type of CHF; to determine the duration of
hospitalization of CHF, as regard mean length of hospital stay, and length of hospital stay per region; and to
determine overall and regional mortality rates for all admissions of CHF.
(Heart Asia, 2017)
DEFINITION
Right-sided heart failure develops when the right side of the heart does not pump blood as well as it should
be, causing blood to back up into the venous system and limiting how much blood the heart can pump per minute.
Symptoms of right-sided heart failure, such as dyspnea (shortness of breath), edema (swelling of the limbs), and
fatigue can be severe. There are a multitude of reasons the right side of the heart might become weak and so
treatment, which can include lifestyle changes and medication, is determined based on the cause.
Heart failure is a clinical syndrome characterized by typical symptoms (e.g., dyspnea, ankle swelling,
fatigue) that may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles,
peripheral oedema) caused by a structural and/or functional cardiac abnormality, leading to a reduced
cardiac output and/or elevated intracardiac pressures at rest or during stress (definition according to the
European Society of Cardiology, ESC 2016). Heart failure is present only when symptoms are apparent.
The demonstration of an underlying cardiac dysfunction is essential for the diagnosis of heart failure.
This is usually a cardiac abnormality (e.g., myocardial infarction) causing systolic and/or diastolic
ventricular dysfunction. Abnormalities of the valves (stenosis, regurgitation), pericardium, endocardium,
heart rhythm/conduction or a combination of these alterations may also initiate heart failure. Identification
of the pathophysiological mechanism leading to heart failure is crucial to choose adequate t herapeutic
options i.e., valve repair, treatment of rhythm disorders, pharmacological treatment.
The clinical severity of heart failure is graded according to the New York Heart Association (NYHA)
on the basis of clinical symptoms at various degrees of physical activity of the patient. The American College
of Cardiology (ACC) and the American Heart Association (AHA) introduced a classification which combines
clinical symptoms and the concomitant disease and risk factors to develop heart failure.
The lifetime risk to develop heart failure is about one in five for a 40-year-old man in Europe or North
America and increases with age. Main risk factors are coronary heart disease, hypertension, diabetes
mellitus, a family history of heart disease, obesity, chronic pulmonary diseases, inflammation or chronic
infection, metabolic diseases, treatment with cardiotoxic agents (cocaine, anthracycline therapy in oncology
e.g., doxorubicin, trastuzumab in treatment of breast cancer) or alcohol abuse. Cardiotoxic agents may
induce cardiotoxicity acutely, early-onset chronically or late-onset chronically. Anthracycline-containing
therapy led to cardiotoxicity mostly within the first year and is associated with the given dose and the LVEF
at the end of treatment. Early detection (echocardiographic strain imaging; cardiac biomarker troponin) and
early treatment (ACE-I, ß Blocker, change in cancer treatment) of depressed cardiac function after
anthracycline induced cardiotoxicity is crucial for recovery of the heart function. Heart failure is a
progressive disease with an annual mortality rate of about 10%. The main causes of death are sudden
cardiac death (>50%) or organ dysfunction due to hypoperfusion.
ETIOLOGY
Right ventricular failure (RVF) is most commonly a result of left ventricular failure (LVF), via pressure and
volume overload.
In addition to LVF, there are other conditions of pressure overload that lead to RVF. These include transient
processes such as:
•
Pneumonia
•
Pulmonary embolism (PE)
•
Mechanical ventilation
•
Acute respiratory distress syndrome (ARDS)
Furthermore, chronic conditions of pressure overload may lead to RVF. These include:
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Primary pulmonary arterial hypertension (PAH) and secondary pulmonary hypertension (PH) as seen in
chronic-obstructive pulmonary disease (COPD) or pulmonary fibrosis)
•
Congenital heart disease (pulmonic stenosis, right ventricular outflow tract obstruction, or a systemic RV).
The following conditions result in volume overload causing RVF:
•
Valvular insufficiency (tricuspid or pulmonic)
•
Congenital heart disease with a shunt (atrial septal defect (ASD) or anomalous pulmonary venous return
(APVR)).
Another important mechanism that leads to RVF is intrinsic RV myocardial disease. This includes:
•
RV ischemia or infarct
•
Infiltrative diseases such as amyloidosis or sarcoidosis
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Arrhythmogenic right ventricular dysplasia (ARVD)
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Cardiomyopathy
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Microvascular disease.
Lastly, RVF may be caused by impaired filling which is seen in the following conditions:
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Constrictive pericarditis
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Tricuspid stenosis
•
Systemic vasodilatory shock
•
Cardiac tamponade
•
Superior vena cava syndrome
•
Hypovolemia.
PATHOPHYSIOLOGY
During fetal development, the RV accounts for approximately 66% of the cardiac output, and via the ductus
arteriosus and foramen ovale, shunts blood to the lower body and placenta. At birth, exposure to oxygen and nitric
oxide, as well as lung expansion, leads to a rapid decrease in pulmonary vascular resistance (PVR). The lungs,
which were bypassed in utero, become a low-pressure, highly distensible circuit. The thick-walled fetal RV
becomes thinner.
Anatomically the structures and resulting function of the RV and the LV are vastly different. For example:
•
The LV is elliptical and made of thick muscle fibers wrapped in two anti-parallel layers separated by a
circumferential band. This results in a complex contraction that involves torsion, thickening, and
shortening.
•
The RV, in contrast, takes a triangular and crescentic shape and is made up of both a superficial layer that
runs circumferentially and parallels to the atrioventricular groove and a deeper layer that runs longitudinally
from the base to the apex. Because of its structure, the contraction of the RV is limited to longitudinal
shortening of the tricuspid annulus towards the apex. The RV free wall is displaced inward toward the
septum and traction is created by the septum as it moves toward the LV in systole.
•
The RV is more heavily trabeculated and contains a circumferential moderator band at the apex.
•
The tricuspid valve (TV) is unique in that it has a large annulus and is tethered by greater than three
papillary muscles which make it vulnerable to structural deformation under sustained increased pressure or
volume loading.
•
Because the RV is substantially thinner than the LV with lower elastance, the RV is much more susceptible
to increases in afterload. A modest change in PVR may result in a marked decrease in RV stroke volume.
This is evident in patients with pulmonary arterial hypertension (PAH), pulmonary embolism (PE), mitral
valve disease with secondary pulmonary hypertension (PH), and the adult respiratory distress syndrome
(ARDS). The thinner RV is also more sensitive to the pericardial constraint.
Like the LV, contraction of the RV is preload dependent at normal physiologic filling pressures, and excessive
RV filling can result in a shift of the septum towards the LV and ventricular interdependence causing impaired LV
function.
Because of lower right-sided pressures and wall stress, the oxygen requirement of the RV is lower than that
of the LV. Coronary blood flow to the RV is lower, as is oxygen extraction. For this reason, the RV is less
susceptible to ischemic insults, and increases in oxygen demand are met via increases in coronary flow as is the
case in PAH or increased oxygen extraction which occurs with exercise.
RV function is affected by atrial contraction, heart rate, and synchronicity. Each of these has important
clinical implications, and RVF for any reason is a strong prognostic indicator. The response of the RV to a
pathologic load is complex. The nature, severity, chronicity, and timing (in utero, childhood, or adulthood) each
play a role in how the RV responds to an increased load. For example, in childhood, when confronted with
congenital pulmonic stenosis, fetal right ventricular hypertrophy (RVH) persists and allows the RV to compensate
for the increase in afterload.
In adulthood, however, the ability of RV to tolerate a chronic increase in afterload, such as that seen in
PAH, is poor. In the early stages of PAH, the RV responds to elevated pulmonary arterial pressures (PAP) by
increasing contractility, with little to no change in RV size. As PAP continue to rise, the RV myocardium begins to
hypertrophy, and RV stroke volume (SV) is maintained. This, however, is not enough to normalize wall stress, and
subsequently, dilatation occurs. This is accompanied by rising filling pressures, decreased contractility, loss of
synchronicity as the RV becomes more spherical, and dilatation of the TV annulus resulting in poor coaptation of
the valve leaflets and functional tricuspid regurgitation (TR). The TR worsens the RV volume overload, RV
enlargement (RVE), wall stress, contractility, and cardiac output.
This differs from the response of the RV to an acute increase in afterload, such as that seen with an acute
PE. In this case, the RV responds with an increase in contractility and end-diastolic volume but does not have time
for the adaptations that are seen in chronic RVF to occur, and quickly fails when unable to generate enough
pressure to maintain flow.
(Mandras and Desai, 2022)
CLINICAL MANIFESTATION
Right-sided heart failure is one type of heart failure. Right-sided heart failure is also called right ventricular (RV)
heart failure or right heart failure.
The right side of your heart pumps “used” blood from your body back to your lungs, where it refills with oxygen.
Right-sided heart failure means your heart’s right ventricle is too weak to pump enough blood to the lungs. As a
result:
•
•
•
•
Blood builds up in your veins, vessels that carry blood from the body back to the heart.
This buildup increases pressure in your veins.
The pressure pushes fluid out of your veins and into other tissue.
Fluid builds up in your legs, abdomen or other areas of your body, causing swelling.
Most right-sided heart failure occurs because of left-sided heart failure. The entire heart gradually weakens.
Often, left-sided heart failure results from another heart condition, such as:
•
•
•
Coronary artery disease.
High blood pressure.
Previous heart attack.
Sometimes, right-sided heart failure can be caused by:
•
•
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High blood pressure in the lungs.
Pulmonary embolism.
Lung diseases such as chronic obstructive pulmonary disease (COPD).
The main sign of right-sided heart failure is fluid buildup. This buildup leads to swelling (edema) in your:
•
•
•
Feet, ankles and legs.
Lower back.
Gastrointestinal (GI) tract and liver (causing ascites).
Other signs include:
•
•
•
Breathlessness.
Chest pain and discomfort.
Heart palpitations.
Where you accumulate fluid depends on how much extra fluid and your position. If you’re standing, fluid typically
builds up in your legs and feet. If you’re lying down, it may build up in your lower back. And if you have a lot of
excess fluid, it may even build up in your belly.
Fluid build up in your liver or stomach may cause:
•
•
•
Nausea.
Bloating.
Appetite loss.
Once right-sided heart failure becomes advanced, you can also lose weight and muscle mass. Healthcare providers
call these effects cardiac cachexia.
MEDICAL/SURGICAL MANAGEMENT
For patients with reversible RVF refractory to medical therapy, surgical options are indicated either as a
bridge to recovery or transplantation. Surgery may also be indicated for patients with RVF in the setting of valvular
heart disease, congenital heart disease, and chronic thromboembolic pulmonary hypertension (CTEPH). Adequate
preoperative diuresis is imperative, and the use of pulmonary vasodilators and inotropes peri-operatively may be
needed. In addition, the irreversible end-organ damage is a contraindication for surgical management.
Veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) may be indicated as salvage therapy in
patients with massive PE and refractory cardiogenic shock following systemic thrombolysis. ECMO may also be
used as a bridge to lung or heart-lung transplantation in patients with severe RVF due to end-staged PAH.
Mechanical support with a right ventricular-assist device (RVAD) may be an option for the patient with isolated
RVF awaiting transplant. However, ECMO may be a better treatment option for unloading the RV in the setting of
severely increased PVR as pumping blood into the PA may worsen PH and cause lung injury.
(Mandras and Desai, 2022)
Patients with RVF due to LVF may benefit from LVAD implantation, with improved PAP before heart
transplantation and possibly improved post-transplant survival. However, LVADs may worsen or lead to new RVF
due to alterations in RV geometry and flow/pressure dynamics and biventricular support may be required.
Pulmonary thromboendarterectomy (PTE) is the treatment of choice for patients with CTEPH and is often
curative. PTE has been shown to improve functional status, exercise tolerance, quality of life, gas exchange,
hemodynamics, RV function, and survival, particularly in patients with proximal lesions and minimal small vessel
disease., PTE is not recommended for patients with massively elevated PVR (greater than 1000 dyn/cm to 1200
dyn/cm). Outcomes with PTE have been shown to directly correlate with the surgeon and center experience,
concordance between the anatomic disease and PVR, preoperative PVR, the absence of comorbidities (particularly
splenectomy and ventricular-atrial shunt) and post-operative PVR. Operative mortality in an experienced center is
between 4% to 7%, and PTE should not be delayed in operative candidates in favor of treatment with pulmonary
vasodilator therapy.
Surgical embolectomy or percutaneous embolectomy may be used for acute RVF in the setting of massive
PE, but data comparing embolectomy with thrombolysis are limited.
Balloon atrial septostomy (BAS) is indicated for PAH patients with syncope or refractory RVF to
decompress the RA and RV and improve CO via the creation of a right-to-left shunt. BAS may be used as a bridge
to transplantation or as palliative therapy in advanced RVF/PAH and has a role in third world countries in which
pulmonary vasodilators are not available. Mortality associated with BAS is low (approximately 5%), particularly in
experienced centers, however spontaneous closure of the defect often necessitates repeating the
procedure. Contraindications of BAS include high RAP (greater than 20 mmHg), oxygen saturation less than 90%
on room air, severe RVF requiring cardiorespiratory support, PVRI greater than 55 U/m and LV end -diastolic
pressure greater than 18 mmHg.
Cardiac resynchronization therapy (CRT) restores mechanical synchrony in the failing LV, leading to
improved hemodynamics and reverse remodeling and improved morbidity and mortality in LVF. Animal studies
and small case series suggest that RV pacing results in acute hemodynamic improvement in patients with RVF in
the setting of PAH, however, no data show long-term clinical benefit in this population.
Ultimately, heart, lung, or combined heart-lung transplantation (HLT) is the treatment of last-resort for endstaged RVF. In patients with RVF due to PAH, RAP greater than 15 and CI less than 2.0 are poor prognostic
indicators and referral for transplantation is indicated. It remains unclear at which point the RV is beyond recovery,
however, in general, the RV is resilient, and most often lung transplant alone is sufficient with estimated 1 -yearsurvival of 65% to 75% and 10-year survival of 45% to 66%.
Congenital patients with RVF in the setting of Eisenmenger syndrome may undergo lung transplantation
with repair of simple shunts (ASDs) at the time of surgery or combined HLT, which has demonstrated a survival
benefit in this population.
Your healthcare provider will test your heart function using:
•
•
•
•
Chest X-ray.
Electrocardiogram (EKG).
Echocardiogram.
Blood tests, especially to measure substances called natriuretic peptides (NPs).
To confirm a diagnosis of heart failure or rule out other conditions causing your symptoms, you may need:
•
•
•
•
•
MRI.
CT.
Cardiac catheterization.
Stress test.
Nuclear exercise stress test.
NURSING INTERVENTION
Nurses greatly influence the outcomes of patients with heart failure through education and monitoring despite high
morbidity and mortality rates. Education empowers patients, improving adherence and preventing complications.
Vigilant monitoring enables early intervention, reducing risks. Nurses play a crucial role in reducing HF morbidity
and mortality.
Nursing assessment for patients with heart failure emphasizes evaluating the efficacy of treatment and the patient’s
adherence to self-management strategies. Monitoring and reporting worsening signs and symptoms of heart failure
are essential for adjusting therapy. Additionally, the nurse addresses the patient’s emotional well-being, as heart
failure is a chronic condition linked to depression and psychosocial concerns
Health History
•
•
•
Assess the signs and symptoms such as dyspnea, shortness of breath, fatigue, and edema.
Assess for sleep disturbances, especially sleep suddenly interrupted by shortness of breath.
Explore the patient’s understanding of HF, self management strategies, and the ability and
willingness to adhere to those strategies.
Physical Examination
•
•
•
•
•
•
•
•
Auscultate the lungs for presence of crackles and wheezes.
Auscultate the heart for the presence of an S3 heart sound.
Assess JVD for presence of distention.
Evaluate the sensorium and level of consciousness.
Assess the dependent parts of the patient’s body for perfusion and edema.
Assess the liver for hepatojugular reflux.
Measure the urinary output carefully to establish a baseline against which to assess the effectiveness
of diuretic therapy.
Weigh the patient daily in the hospital or at home.
Assess for the following subjective and objective data:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Increased heart rate (tachycardia)
ECG changes
Changes in BP (hypotension/hypertension)
Extra heart sounds (S3, S4)
Decreased urine output (oliguria)
Diminished peripheral pulses
Orthopnea
Crackles
Jugular vein distention
Edema
Chest pain
Weakness
Fatigue
Changes in vital signs
Presence of dysrhythmias
Dyspnea
Pallor
Diaphoresis
Weight gain
Respiratory distress
Abnormal breath sounds
Assess for factors related to the cause of congestive heart failure:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Altered circulation
Altered myocardial contractility/inotropic changes
Alterations in rate, rhythm, electrical conduction
Decreased cardiac output
Structural changes (e.g., valvular defects, ventricular aneurysm)
Poor cardiac reserve
Side effects of medication
Imbalance between oxygen supply/demand
Prolonged bed rest
Immobility
Reduced glomerular filtration rate (decreased cardiac output)/increased antidiuretic hormone (ADH)
production, and sodium/water retention.
Changes in glomerular filtration rate
Use of diuretics
Lack of understanding
Misconceptions about interrelatedness of cardiac function/disease/failure
Invasive procedures
Prolonged hospitalization
Alveolar edema secondary to increased ventricular pressure
Retained secretions
Increased metabolic rate secondary to pneumonia
CHANCE OF SURVIVAL
In general, more than half of all people diagnosed with congestive heart failure will survive for 5 years. About 35%
will survive for 10 years. Congestive heart failure (CHF) is a chronic, progressive condition that affects the heart’s
ability to pump blood around the body. Despite its name, CHF does not mean that the heart has completely failed.
However, it can be life threatening if left untreated. A person’s life expectancy with CHF will vary depending on
numerous factors, including their age, the stage of their condition, and the strength of their heart function.
Many disorders that weaken the heart can contribute to the development of CHF, including:
•
heart attacks
•
coronary heart disease
•
congenital heart disease
•
faulty heart valves
•
high blood pressure
•
inflammation or damage to the heart muscle
•
drug or toxin use
However, in some cases, a person can extend their life expectancy through lifestyle changes, medications, and
surgery.
(Johnson, 2022)