Definition
Heart failure is defined as the condition where the heart is no longer able to pump enough blood to body tissues. Disorders of heart function can be either diastolic or systolic dysfunction, heart rhythm disorders, preload and afterload or discrepancies. Congestive heart failure (congestive heart failure) is a situation when there is a dam due to heart failure and circulatory mechanisms kompensatoriknya.
Etiology
Heart failure is a common complication of all types of congenital and acquired heart disease. Physiological mechanisms that cause heart failure include:
1. Increase the initial load
Circumstances that increase the initial burden include aortic regurgitation and ventricular septal defect.
2. Increase the load end
End load is increased in situations such as aortic stenosis and systemic hypertension.
3. Decrease myocardial contractility
Myocardial contractility can be decreased in the myocardial infarction and cardiomyopathy.
The third addition to the physiological mechanisms that lead to heart failure, there are other physiological factors that can cause the heart fails to work as a pump. Factors that interfere with ventricular filling (eg, atrioventrkularis valve stenosis) can lead to heart failure.
Factors that can lead to heart failure through the suppression of a sudden circulation can be:
1.Disritmia
Dysrhythmias would interfere with cardiac mechanical function by altering the electrical stimulus that initiates the mechanical response. Mechanical response of the synchronous and effective will not be generated in the absence of a stable cardiac rhythm.
2. Systemic infections and lung infections
Body's response to infection will force the heart to meet the increased metabolic needs.
3. pulmonary embolism
Pulmonary embolism is a sudden will increase the resistance to right ventricular ejection, the right trigger heart failure
Heart failure is defined as the condition where the heart is no longer able to pump enough blood to body tissues. Disorders of heart function can be either diastolic or systolic dysfunction, heart rhythm disorders, preload and afterload or discrepancies. Congestive heart failure (congestive heart failure) is a situation when there is a dam due to heart failure and circulatory mechanisms kompensatoriknya.
Etiology
Heart failure is a common complication of all types of congenital and acquired heart disease. Physiological mechanisms that cause heart failure include:
1. Increase the initial load
Circumstances that increase the initial burden include aortic regurgitation and ventricular septal defect.
2. Increase the load end
End load is increased in situations such as aortic stenosis and systemic hypertension.
3. Decrease myocardial contractility
Myocardial contractility can be decreased in the myocardial infarction and cardiomyopathy.
The third addition to the physiological mechanisms that lead to heart failure, there are other physiological factors that can cause the heart fails to work as a pump. Factors that interfere with ventricular filling (eg, atrioventrkularis valve stenosis) can lead to heart failure.
Factors that can lead to heart failure through the suppression of a sudden circulation can be:
1.Disritmia
Dysrhythmias would interfere with cardiac mechanical function by altering the electrical stimulus that initiates the mechanical response. Mechanical response of the synchronous and effective will not be generated in the absence of a stable cardiac rhythm.
2. Systemic infections and lung infections
Body's response to infection will force the heart to meet the increased metabolic needs.
3. pulmonary embolism
Pulmonary embolism is a sudden will increase the resistance to right ventricular ejection, the right trigger heart failure
Pathophysiology
Intrinsic abnormalities in myocardial contractility that are characteristic of heart failure due to ischemic heart disease, impairs the ability of effective emptying of the ventricles. Left ventricular contractility is decreased to reduce volume and increase the volume of residual sekuncup ventricle. With the increase in ventricular end-diastolic volume, an increase in left ventricular end-diastolic pressure. As a result, there is also an increase in left atrial pressure due to the atrium and ventricle during diastole directly related. Increased tekanana forwarded to the back of the left atrium into the pulmonary blood vessels, increase capillary pressure and pulmonary vein. If the hydrostatic pressure of the lung capillary matting exceeds oncotic pressure of blood vessels, will be transudation of fluid into the interstitial so that there was interstitial edema. Further improvement can lead to fluid leak into the alveoli and pulmonary edema occurs.
Pulmonary artery pressure may increase due to a chronic increase in pulmonary venous pressure. Pulmonary hypertension increased resistance to right ventricular ejection. A series of such events that occurred in the left heart, will also occur on the right heart, which eventually will happen systemic congestion and edema.
In response to heart failure, there are three primary mechanisms that can occur are:
1. Increased sympathetic adrenergic activity.
Sekuncup volume decreased in heart failure will evoke sympathetic response kompensatorik. Increased spending to stimulate the sympathetic adrenergic activity of catecholamines from cardiac adrenergic nerves and adrenal medulla. Heart rate and force of contraction will be increased to increase cardiac output. In addition, peripheral arterial vasoconstriction also occur to stabilize the arterial pressure and redistribution of blood volume by reducing blood flow to organs such as skin and low metabolism to maintain renal perfusion to the heart and brain. Venokonstriksi will increase venous return to the right side of the heart and increases the initial burden of heart which will increase the contraction and cardiac output.
2. Increased initial load through the activation of the renin-angiotensin-aldosterone system.
Decreased cardiac output in heart failure will result in decreased renal blood flow and glomerular filtration rate as a result there was the release of renin from the apparatus jukstaglomerulus. Interaction of renin with angiotensinogen in the blood will produce angiotensin I. Then will the conversion of angiotensin I into angiotensin II. Angiotensin II stimulates the secretion of aldosterone from the adrenal gland that increases the reabsorspi sodium in distal tubule and duct pengumpul.Natrium will attract water. In addition, angiotensin II vasoconstriction nevertheless produce effects that increase blood pressure.
3. Ventricular hypertrophy.
Kompensatorik last response in heart failure is myocardial hypertrophy or increased myocardial wall thickness. Hypertrophy will increase the number of sarcomeres in cells of the myocardium so as to increase the strength of ventricular contraction so that cardiac output increased aka.
The third response reflects an attempt to maintain cardiac output. This mechanism may be sufficient to maintain cardiac output at normal or nearly normal levels early in the course failed, and in a resting state. However, abnormalities of ventricular work and cardiac output decline usually appears during the move. With persistent heart failure, then the compensation will be increasingly less efektif.Klasifikasi
Heart failure heart failure can be divided into left and right heart failure. Heart failure can also be divided into acute heart failure, decompensated chronic heart failure, and chronic heart failure. Killip classification based on use in patients with acute myocardial infarction, with the division:
Grade I: No heart failure
Degree II: Heart failure with basal crackles in the lung wet smooth, S3 Galop and an increase in pulmonary venous pressure
Degree III: severe heart failure with pulmonary edema throughout the lung field.
Degree IV: Cardiogenic shock with hypotension (systolic blood pressure <90 mmHg) and peripheral vasoconstriction (oliguria, cyanosis, and diaphoresis)
Stevenson used the clinical classification by looking at the signs of congestion (the presence of orthopnea, distended veins juguler, wet crackles, hepato jugular reflux, peripheral edema, pulmonary heart sound that deviates to the left, or square wave to the Valsalva maneuver blood pressure) and the adequacy of perfusion (the pressure narrow pulse, pulsus alternans, symptomatic hypotension, cold extremities, and decreased consciousness). Patients who experience congestion so-called wet (wet) which is called the dry (dry). Patients with so-called reperfusion injury (cold) and are not called hot (warm). Based on the penderta divided into four classes, namely:
Class I (A): dry and warm (dry - warm)
Class II (B): wet and warm (wet - warm)
Class III (L): dry and cold (dry - cold)
Class IV (C): wet and cold (wet - cold)
Based on the New York Heart Association classification of heart failure:
Class I: No complaints - I can do daily physical activity without fatigue, shortness of breath, or palpitations.
Class II: Mild - mild physical activity / are causing fatigue, shortness of breath, or palpitations, but if the activity is stopped then the complaint is gone.
Class III: Medium - light physical activity / are causing fatigue, shortness of breath, or palpitations, but the complaint will be reduced if the activity is stopped.
Class IV: Heavy - can not do physical activity every day, even at rest any complaints still exist and more severe if the activity
Clinical Manifestations
Symptoms and signs of left heart failure backward:
Dyspnea (difficulty breathing)
Is the most common complaints. Dyspnea caused by an increase in respiratory work due to pulmonary vascular congestion had reduced lung elasticity and increased airflow resistance. Dyspnea on exertion (dyspnea d'effort) showed early symptoms of left heart failure.
Orthopnea
Orthopnea, which is defined as shortness of breath that occurs in a lying position, usually a further manifestation of heart failure compared dyspnea d'effort. This occurs due to redistribution of fluid from the circulation into the lower extremity splanchnik and central circulation during lying down, accompanied by an increase in pulmonary capillary pressure.
Nocturnal cough (cough experienced at night)
A symptom that often occurs in this process and often disguise other symptoms of heart failure.
Paroxysmal Nocturnal Dyspnea (PND)
This term means the presence of an acute episode of severe shortness of breath and a cough that usually occurs at night and wake the patient from sleep, usually 1-3 hours after the patient is sleeping. PND can manifest as coughing or wheezing, possibly because of increased pressure on the bronchial artery causing compression of the airways, accompanied by interstitial pulmonary edema that led to an increase in airway resistance. It is known that can relieve orthopnea after sitting up straight, while the PND patients often have a persistent cough and wheezing, although they claim to have sat up straight.
Rhonchi
Onset crackles caused by transudation of fluid from the lung is a hallmark of left heart failure. At first there was the bottom of the lungs due to the influence of gravity.
Hemoptysis
Bronchial veins are caused by bleeding caused by venous distention.
Dysphagia (difficulty swallowing)
Caused by distention of the left atrium or pulmonary veins causing compression of the esophagus and dysphagia.
Symptoms and signs of right heart failure backward:
Systemic venous congestion
Can be observed with increased jugular venous pressure (JVP), the veins of the neck have the dam. Central venous pressure (CVP) can paradoxically increase during inspiration if the right heart failure can not adjust to the increased venous return to the heart during inspiration.
Hepatomegaly (enlarged liver)
Liver tenderness may occur due to stretching of the liver capsule.
Gastrointestinal complaints.
Anorexia, nausea, and full of feeling associated with abdominal pain is often complained of symptoms and can be associated with edema of the intestinal wall and / or hepatic congestion.
Peripheral edema
Occur due to accumulation of fluid in the interstitial space. Edema first appears on the body that depends as palpebra in the morning. Edema noon will appear on the extremities, especially the legs due to gravity.
Nocturia (nighttime diuresis)
Nocturia is caused by fluid redistribution and reabsorption at the time lying down.
Ascites and edema anasarka
Heart failure that continues to cause ascites or generalized body edema.
Symptoms and signs of left heart failure in the future:
Hypoperfusion to nonvital organs
Decrease in cardiac output caused hypoperfusion to nonvital organs in order to maintain perfusion to the heart and brain so that the earliest manifestation of failure in the future is reduced perfusion to organs such as skin, skeletal muscle, and kidney.
- The skin is pale and cold
caused by peripheral vasoconstriction.
- Low-grade fever and excessive sweating
vaskonstriksi caused by the skin which can inhibit the body's ability to release heat.
- Weakness and fatigue
caused by a lack of perfusion to the skeletal muscle. Symptoms can also be exacerbated by an imbalance of electrolytes and fluids, or anorexia.
- Anuria
Due to lack of blood perfusion to the kidneys.
Cheyne-Stokes respiration
Also referred to as periodic breathing or cyclic breathing, Cheyne-Stokes respiration is common in severe heart failure and is usually associated with low cardiak ouput. Cheyne-Stokes respiration due to the reduced sensitivity of the respiratory center of pressure PCO2. There are apneu phase, which occurs when the decrease in arterial PO2 and arterial PCO2 increased. It changes the composition of arterial blood gases and lead to depression of respiratory center, resulting in hyperventilation and hypocapnia, followed by recurrence of apnea phase. Cheyne-Stokes respiration can be perceived by the patient's family as severe shortness of breath (severe) or breathing stops temporarily.
Symptoms of cerebral
Patients with heart failure can also come with cerebral symptoms, such as disorientation, sleep disturbances and mood, can also be observed in patients with severe heart failure, especially in elderly patients with cerebral arteriosclerosis and cerebral perfusion is decreased. Nocturia is common in heart failure and may contribute to insomnia
Intrinsic abnormalities in myocardial contractility that are characteristic of heart failure due to ischemic heart disease, impairs the ability of effective emptying of the ventricles. Left ventricular contractility is decreased to reduce volume and increase the volume of residual sekuncup ventricle. With the increase in ventricular end-diastolic volume, an increase in left ventricular end-diastolic pressure. As a result, there is also an increase in left atrial pressure due to the atrium and ventricle during diastole directly related. Increased tekanana forwarded to the back of the left atrium into the pulmonary blood vessels, increase capillary pressure and pulmonary vein. If the hydrostatic pressure of the lung capillary matting exceeds oncotic pressure of blood vessels, will be transudation of fluid into the interstitial so that there was interstitial edema. Further improvement can lead to fluid leak into the alveoli and pulmonary edema occurs.
Pulmonary artery pressure may increase due to a chronic increase in pulmonary venous pressure. Pulmonary hypertension increased resistance to right ventricular ejection. A series of such events that occurred in the left heart, will also occur on the right heart, which eventually will happen systemic congestion and edema.
In response to heart failure, there are three primary mechanisms that can occur are:
1. Increased sympathetic adrenergic activity.
Sekuncup volume decreased in heart failure will evoke sympathetic response kompensatorik. Increased spending to stimulate the sympathetic adrenergic activity of catecholamines from cardiac adrenergic nerves and adrenal medulla. Heart rate and force of contraction will be increased to increase cardiac output. In addition, peripheral arterial vasoconstriction also occur to stabilize the arterial pressure and redistribution of blood volume by reducing blood flow to organs such as skin and low metabolism to maintain renal perfusion to the heart and brain. Venokonstriksi will increase venous return to the right side of the heart and increases the initial burden of heart which will increase the contraction and cardiac output.
2. Increased initial load through the activation of the renin-angiotensin-aldosterone system.
Decreased cardiac output in heart failure will result in decreased renal blood flow and glomerular filtration rate as a result there was the release of renin from the apparatus jukstaglomerulus. Interaction of renin with angiotensinogen in the blood will produce angiotensin I. Then will the conversion of angiotensin I into angiotensin II. Angiotensin II stimulates the secretion of aldosterone from the adrenal gland that increases the reabsorspi sodium in distal tubule and duct pengumpul.Natrium will attract water. In addition, angiotensin II vasoconstriction nevertheless produce effects that increase blood pressure.
3. Ventricular hypertrophy.
Kompensatorik last response in heart failure is myocardial hypertrophy or increased myocardial wall thickness. Hypertrophy will increase the number of sarcomeres in cells of the myocardium so as to increase the strength of ventricular contraction so that cardiac output increased aka.
The third response reflects an attempt to maintain cardiac output. This mechanism may be sufficient to maintain cardiac output at normal or nearly normal levels early in the course failed, and in a resting state. However, abnormalities of ventricular work and cardiac output decline usually appears during the move. With persistent heart failure, then the compensation will be increasingly less efektif.Klasifikasi
Heart failure heart failure can be divided into left and right heart failure. Heart failure can also be divided into acute heart failure, decompensated chronic heart failure, and chronic heart failure. Killip classification based on use in patients with acute myocardial infarction, with the division:
Grade I: No heart failure
Degree II: Heart failure with basal crackles in the lung wet smooth, S3 Galop and an increase in pulmonary venous pressure
Degree III: severe heart failure with pulmonary edema throughout the lung field.
Degree IV: Cardiogenic shock with hypotension (systolic blood pressure <90 mmHg) and peripheral vasoconstriction (oliguria, cyanosis, and diaphoresis)
Stevenson used the clinical classification by looking at the signs of congestion (the presence of orthopnea, distended veins juguler, wet crackles, hepato jugular reflux, peripheral edema, pulmonary heart sound that deviates to the left, or square wave to the Valsalva maneuver blood pressure) and the adequacy of perfusion (the pressure narrow pulse, pulsus alternans, symptomatic hypotension, cold extremities, and decreased consciousness). Patients who experience congestion so-called wet (wet) which is called the dry (dry). Patients with so-called reperfusion injury (cold) and are not called hot (warm). Based on the penderta divided into four classes, namely:
Class I (A): dry and warm (dry - warm)
Class II (B): wet and warm (wet - warm)
Class III (L): dry and cold (dry - cold)
Class IV (C): wet and cold (wet - cold)
Based on the New York Heart Association classification of heart failure:
Class I: No complaints - I can do daily physical activity without fatigue, shortness of breath, or palpitations.
Class II: Mild - mild physical activity / are causing fatigue, shortness of breath, or palpitations, but if the activity is stopped then the complaint is gone.
Class III: Medium - light physical activity / are causing fatigue, shortness of breath, or palpitations, but the complaint will be reduced if the activity is stopped.
Class IV: Heavy - can not do physical activity every day, even at rest any complaints still exist and more severe if the activity
Clinical Manifestations
Symptoms and signs of left heart failure backward:
Dyspnea (difficulty breathing)
Is the most common complaints. Dyspnea caused by an increase in respiratory work due to pulmonary vascular congestion had reduced lung elasticity and increased airflow resistance. Dyspnea on exertion (dyspnea d'effort) showed early symptoms of left heart failure.
Orthopnea
Orthopnea, which is defined as shortness of breath that occurs in a lying position, usually a further manifestation of heart failure compared dyspnea d'effort. This occurs due to redistribution of fluid from the circulation into the lower extremity splanchnik and central circulation during lying down, accompanied by an increase in pulmonary capillary pressure.
Nocturnal cough (cough experienced at night)
A symptom that often occurs in this process and often disguise other symptoms of heart failure.
Paroxysmal Nocturnal Dyspnea (PND)
This term means the presence of an acute episode of severe shortness of breath and a cough that usually occurs at night and wake the patient from sleep, usually 1-3 hours after the patient is sleeping. PND can manifest as coughing or wheezing, possibly because of increased pressure on the bronchial artery causing compression of the airways, accompanied by interstitial pulmonary edema that led to an increase in airway resistance. It is known that can relieve orthopnea after sitting up straight, while the PND patients often have a persistent cough and wheezing, although they claim to have sat up straight.
Rhonchi
Onset crackles caused by transudation of fluid from the lung is a hallmark of left heart failure. At first there was the bottom of the lungs due to the influence of gravity.
Hemoptysis
Bronchial veins are caused by bleeding caused by venous distention.
Dysphagia (difficulty swallowing)
Caused by distention of the left atrium or pulmonary veins causing compression of the esophagus and dysphagia.
Symptoms and signs of right heart failure backward:
Systemic venous congestion
Can be observed with increased jugular venous pressure (JVP), the veins of the neck have the dam. Central venous pressure (CVP) can paradoxically increase during inspiration if the right heart failure can not adjust to the increased venous return to the heart during inspiration.
Hepatomegaly (enlarged liver)
Liver tenderness may occur due to stretching of the liver capsule.
Gastrointestinal complaints.
Anorexia, nausea, and full of feeling associated with abdominal pain is often complained of symptoms and can be associated with edema of the intestinal wall and / or hepatic congestion.
Peripheral edema
Occur due to accumulation of fluid in the interstitial space. Edema first appears on the body that depends as palpebra in the morning. Edema noon will appear on the extremities, especially the legs due to gravity.
Nocturia (nighttime diuresis)
Nocturia is caused by fluid redistribution and reabsorption at the time lying down.
Ascites and edema anasarka
Heart failure that continues to cause ascites or generalized body edema.
Symptoms and signs of left heart failure in the future:
Hypoperfusion to nonvital organs
Decrease in cardiac output caused hypoperfusion to nonvital organs in order to maintain perfusion to the heart and brain so that the earliest manifestation of failure in the future is reduced perfusion to organs such as skin, skeletal muscle, and kidney.
- The skin is pale and cold
caused by peripheral vasoconstriction.
- Low-grade fever and excessive sweating
vaskonstriksi caused by the skin which can inhibit the body's ability to release heat.
- Weakness and fatigue
caused by a lack of perfusion to the skeletal muscle. Symptoms can also be exacerbated by an imbalance of electrolytes and fluids, or anorexia.
- Anuria
Due to lack of blood perfusion to the kidneys.
Cheyne-Stokes respiration
Also referred to as periodic breathing or cyclic breathing, Cheyne-Stokes respiration is common in severe heart failure and is usually associated with low cardiak ouput. Cheyne-Stokes respiration due to the reduced sensitivity of the respiratory center of pressure PCO2. There are apneu phase, which occurs when the decrease in arterial PO2 and arterial PCO2 increased. It changes the composition of arterial blood gases and lead to depression of respiratory center, resulting in hyperventilation and hypocapnia, followed by recurrence of apnea phase. Cheyne-Stokes respiration can be perceived by the patient's family as severe shortness of breath (severe) or breathing stops temporarily.
Symptoms of cerebral
Patients with heart failure can also come with cerebral symptoms, such as disorientation, sleep disturbances and mood, can also be observed in patients with severe heart failure, especially in elderly patients with cerebral arteriosclerosis and cerebral perfusion is decreased. Nocturia is common in heart failure and may contribute to insomnia
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