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Contents
Symptoms of chronic heart failure.......................................................................................................3
Pathophysiology of congestive heartfailure.........................................................................................3
Causes of congestive heart failure .......................................................................................................4
Left-Sided Heart Failure ......................................................................................................................6
Morphology....................................................................................................................................6
Clinical Features:.........................................................................................................................7
Right-Sided Heart Failure ....................................................................................................................7
Morphology....................................................................................................................................8
Liver and Portal System ...............................................................................................................8
Pleural andPericardial Spaces…………………………………………………………………………………………………….……8
SubcutaneousTissues………………………………………………………………………………………………………………………9
Clinical Features………………………………………………….……………………………………………………………………………9
Diagnosis ...........................................................................................................................................9
Treatment (Medication)......................................................................................................................9
DRUGS USED TO TREAT CONGESTIVE HEART FAILURE.........................................................................10
Treating Congestive Heart failure ......................................................................................................11
Patient counseling............................................................................................................................11
Patient counseling Lifestyle changes..................................................................................................12
References………………………………………………………………………………………………………………………………….…………13
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Congestive heart failure (CHF)
Chronic heart failure (CHF), also called congestive cardiac failure (CCF), is an ongoing condition
in which the heart muscle is weakened and can’t pump as well as it normally does. The main
pumping chambers of the heart (the ventricles) become larger or thicker, and either can’t
contract (squeeze) or can’t relax as well as they should. This triggers fluid retention, particularly
in the lungs, legs and abdomen.
The major causes of CHF include coronary heart disease, hypertension, cardiomyopathy and
other heart diseases. Of these, coronary heart disease (usually accompanied by a history of past
heart attacks) is by far the most common.
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Chronic heart failure is more common in elderly people. The survival rate for people with this
disorder depends on the severity of their condition. Treatments include medication, lifestyle
changes and (sometimes) surgery. (Better health channel, 2016)
Symptoms of chronic heart failure
Symptoms of chronic heart failure include:
new or worsening shortness of breath (particularly during physical activity or waking you up at
night)
weight gain
muscular fatigue, tiredness
swelling of ankles or legs
swelling of abdomen
dizziness
heart palpitations
chest pain or discomfort in parts of the upper body
unexplained coughing and wheezing
loss of appetite
constipation. (Better health channel, 2016)
Pathophysiology of congestive heart failure
Congestive heart failure is a syndrome that can be caused by a variety of abnormalities,
including pressure and volume overload, loss of muscle, primary muscle disease or excessive
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peripheral demands such as high output failure. In the usual form of heart failure, the heart
muscle has reduced contractility. This produces a reduction in cardiac output, which then
becomes inadequate to meet the peripheral demands of the body. The 4 primary determinants
of left ventricular (LV) performance are generally altered as follows:
(1) There is an intrinsic decrease in muscle contractility.
(2) Preload or left atrial filling pressure is increased, resulting in pulmonary congestion and
dyspnea.
(3) Although systemic blood pressure is often reduced, there is an increase in systemic vascular
resistance (afterload), which can further reduce cardiac output.
(4) Heart rate is generally increased as part of a compensatory mechanism associated with an
increase in sympathetic tone and circulating catecholamines. In patients with coronary disease,
there is often an imbalance between myocardial oxygen supply and demand. An increase in
heart size may be particularly deleterious by increasing wall tension because of the Laplace
relation and increasing myocardial oxygen consumption. (NCBI, 1985)
Causes of congestive heart failure
The heart is a double pump made up of four chambers. Deoxygenated blood from the
veins enters the right upper chamber (right atrium), is passed to the right lower
chamber (right ventricle), and then pumped to the lungs. Oxygenated blood from the
lungs enters the left upper chamber (left atrium) and then enters the left lower chamber
(left ventricle). The blood is then pumped around the body, under pressure, via arteries.
In a person with CHF, the left ventricle does not empty properly. This leads to increased
pressure in the atria (upper chambers) and the nearby veins. This backlog of blood
affects the kidneys – interfering with their function and leading to fluid retention
(oedema) in the lungs, abdominal organs and legs.
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In some people with heart failure, rather than failed pumping of the blood from the left
ventricle, there is failed relaxation of the left ventricle. This also leads to blood pooling under
back-pressure.
CHF can be caused by several conditions, including:
past heart attacks from coronary heart disease – this can lead to scarring in the heart muscle
and is the most common cause for CHF
high blood pressure (hypertension) – the high pressure in the arteries means that the heart
must keep pumping more forcefully. It may not be able to keep it up
heart valve disease – damaged heart valves may allow the blood to flow backwards or may
obstruct forward flow
congenital heart disease – heart abnormalities may be present from birth, such as defective
valves or abnormal communications between heart chambers
cardiomyopathy – this condition is characterised by enlargement of the heart muscle, where
the left ventricle enlarges to compensate for poor contraction
myocarditis – viruses or other infections may damage the heart muscle
heart arrhythmia – rapid heartbeat with irregularity, over a long period of time, can also lead to
inefficient contraction and heart failure
thyroid disease – the thyroid gland produces too much of its hormone, thyroxine. This increases
the work of the heart and can lead to heart failure. (American heart association, 2017)
Heart failure can affect predominantly the left side or the right side or both sides of the heart.
The most common causes of left sided cardiac failure are
1) IHD,
2) Systemic hypertension,
3) Mitral or aortic valve disease, and
4) Primary diseases of the myocardium.
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The most common cause of right-sided heart failure is left ventricular failure, with its associated
pulmonary congestion and elevation in pulmonary arterial pressure. Right sided failure can also
occur in the absence of left sided heart failure in patients with intrinsic diseases of the lung
parenchyma and/or pulmonary vascular and in patients with primary pulmonic or tricuspid
valve disease. It sometimes follows congenital heart disease, i.e., in the setting, of left to right
shunts with chronic volume and pressure overloads. ( Vinay Kumar; Abul K Abbas; Jon C Aster;
Stanley L Robbins, 2013)
Left-Sided Heart Failure
The morphologic and clinical effects of left-sided CHF primarily result from progressive
damming of blood within tie pulmonary circulation and the consequences of diminished
peripheral blood pressure and flow.
Morphology
Findings in the heart depend on the underlying disease process; for example, myocardial
infarction or valvular deformities may be present. Except in cases of mitral valve stenosis (or
other processes that restrict left ventricular size), the left ventricle is usually hypertrophied and
often dilated, sometimes quite massively. There are usually nonspecific changes of hypertrophy
end fibrosis in the myocardium. Secondary enlargement of the left atrium with resultant atrial
fibrillation (i.e., uncoordinated, chaotic contraction of the atrium) can reduce stroke volume or
lead to blood stasis and thrombus formation (particularly in the atrial appendage); a fibrillating
left atrium carries a substantially increased risk of embolic stroke. The extracardiac effects of
left-sided heart failure are manifested most prominently in the lungs.
Rising pressure in the pulmonary veins is ultimately transmitted retrogradely to the capillaries,
resulting in pulmonary congestion and edema. The lungs are heavy and boggy, and
histologically there are perivascular and interstitial transudate, alveolar septal edema, and intra
-alveolar edema. Moreover, capillary leakiness leads to the accumulation of erythrocytes
(containing hemoglobin) that are phagocytosed by macrophages. Within macrophages,
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hemoglobin is converted to hemosiderin and hence hemosiderin-containing macrophages in
the alveoli (called heart failure cells) are evidence of prior of pulmonary edema.
Clinical Features: Dyspnea (breathlessness) is usually the earliest and most significant complaint
of patients in left-sided heart failure; cough is also a common accompaniment of left heart
failure due to fluid transudation into airspaces. With further cardiac impairment, patients
develop dyspnea when recumbent (so-called orthopnea); this occurs because of increased
venous return from the lower extremities and by elevation of the diaphragm when in the
supine position. Orthopnea is typically relieved by sitting or standing, so that such patients
usually sleep while sitting upright. Paroxysmal nocturnal dyspnea is a particularly dramatic form
of breathlessness awakening patients from sleep with attacks of extreme dyspnea bordering on
suffocation.
Other manifestations of left ventricular failure include an enlarged heart (cardiomegaly),
tachycardia, a third heart sound and fine tales at the lung bases, produced by respiration
through edematous pulmonary alveoli. With progressive ventricular dilation, the capillary
muscles are displaced laterally, causing mitral regurgitation and a systolic murmur. Subsequent
chronic dilation of the left atrium it often associated with atrial fibrillation manifested by an
“irregularly irregular” heartbeat.
Right-Sided Heart Failure
Right-sided heart failure is usually the consequence of left-sided heart failure; any pressure
increase in the pulmonary circulation inevitably produces an increased burden on the right side
of the heart. Isolated right-sided heart failure is less common and it occurs in patients with
intrinsic disease of lung parenchyma and/or pulmonary vasculature that result in chronic
pulmonary hypertension. It can also occur in patients with pulmonic or tricuspid valve disease.
Congenital heart diseases with right-to-left shunt can cause isolated right-sided heart failure, as
well. Hypertrophy and dilation are generally confined to the right ventricle and atrium,
although bulging of the ventricular septum to the left can cause dysfunction of the left
ventricle.
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The major morphologic and clinical effects of pure right-sided heart failure differ from those of
left-sided heart failure in that pulmonary congestion is minimal, whereas engorgement of the
systemic and portal venous systems is typically pronounced.
Morphology
Liver and Portal System: The liver is usually increased in size and weight (congestive
hepatomegaly), and a cut section displays prominent passive congestion, a pattern referred to
as nutmeg liver: congested red centers of the liver lobules are surrounded by paler, sometimes
fatty, peripheral regions. In some instances, especially when left-sided heart failure is also
present, severe central hypoxia produces centrilobular necrosis along with the sinusoidal
congestion. With long-standing severe right-sided heart failure, the central areas can become
fibrotic, creating so-called cardiac cirrhosis.
Right-sided heart failure also leads to elevated pressure in the portal vein and its tributaries.
Congestion produces a tense, enlarged spleen (congestive splenomegaly). With long-standing
congestion, the enlarged spleen can achieve weights of 300 to 5009m (normal <160 gm).
Microscopically, there can be marked sinusoidal dilation. Chronic edema of the bowel wall may
interfere with absorption of nutrients. Accumulations of transudate in the peritoneal cavity can
cause ascites.
Pleural and Pericardial Spaces: Fluid may accumulate in the pleural space (particularly right)
and pericardial space (effusions).Thus, while pulmonary edema indicates left-sided heart
failure, pleural effusions accompany both right sided and left sided heart failure. Pleural
effusions (typically serous) can range from 100mL to well over 1L and can cause partial
atelectasis of the affected lung. Unlike inflammatory edema, the edema fluid in CHF has a low
protein content.
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Subcutaneous Tissues: Peripheral edema of dependent portions of the body, especially ankle
(pedal) and pretibial edema, is a hallmark of right sided heart failure. In chronically bedridden
patients, the edema may be primarily presacral. Generalized massive edema is called anasarca.
Clinical Features: While the symptoms of left-sided heart failure are largely due to pulmonary
congestion and edema, pure right-sided heart failure typically causes very few respiratory
symptoms. Instead, there is systemic and portal venous congestion, with hepatic and splenic
enlargement, peripheral edema, pleural effusion, and ascites. It is worth emphasizing, however,
that in most cases of chronic cardiac decompensation, patients present with biventricular CHF,
encompassing the clinical syndromes of both right-sided and left-sided heart failure. As CHF
progresses, patients can become frankly cyanotic and acidotic, as a result of decreased tissue
perfusion. ( Vinay Kumar; Abul K Abbas; Jon C Aster; Stanley L Robbins, 2013)
Diagnosis
Electrocardiogram (ECG, “EKG”)
Chest x-ray Echocardiography (“Echo”)
Heart catheterization Stress test Blood tests
Treatment (Medication)
• ACE Inhibitors
• Diuretics
• Inotropic Agents
• Beta Blockers
• Calcium Channel Blockers
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Nifedipine
Diltiazem
Verapamil
Treating Congestive Heart failure
Upright position
Nitrates
Lasix Oxygen
ACE inhibitors
Digoxin
Fluids(decrease)
After load (decrease)
Sodium retention
Test (Dig level, ABG’s, Potassium level)
Patient counseling
• Lifestyle changes
• Monitoring for changes
• Medications
• Surgery
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Patient counseling Lifestyle changes
• Stop smoking
• Lose weight
• Avoid or limit alcohol
• Avoid or limit caffeine
• Eat a low-fat, low-sodium diet
• Exercise
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References:
Vinay Kumar; Abul K Abbas; Jon C Aster; Stanley L Robbins. (2013). Hearrt failur. In
Robbins, Basic pathology (pp. 380-381). Philadelphia, PA : Elsevier/Saunders.
Vinay Kumar; Abul K Abbas; Jon C Aster; Stanley L Robbins. (2013). Heart failure. In
Robins, Basic Pathology (pp. 381-382). Philadelphia, PA : Elsevier/Saunders .
American heart association. (2017). Congestive heart failure (CHF). Retrieved April 17,
2018, from
http://www.heart.org/HEARTORG/Conditions/Heartfailure/Aboutheartfailure/Types-of-
Heart-Failure_UCM_306323_Article.jsp#.WtW9yZArLIU
Better health channel. (2016, December). Congestive heart failure (CHF). Retrieved April
17, 2018, from
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/congestive-
heart-failure-chf
Better health channel. (2016). Congestive heart failure (CHF). Retrieved April 17, 2018,
from https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/congestive-
heart-failure-chf
NCBI. (1985, jul). Pathophysiology of congestive heart failure. Retrieved April 17, 2018,
from https://www.ncbi.nlm.nih.gov/pubmed/4014051
