Pathophysiology
CHF occurs due to complex interactions between the factors that affect contractility, after-load, preload, or function lusitropik (relaxation function), heart, and neurohormonal and hemodynamic response that is required to create compensation circulation. Although the hemodynamic consequences of heart failure respond to standard pharmacological interventions, there is a critical neurohormonal interactions that aggravate and prolong the combined effects of existing syndrome.
Reniniangiotensinfaldosteron system (RAA): In addition to increased peripheral resistance and blood volume circulation, angiotensin and aldosterone have implications for the structural changes seen in injured myocardium ischemic and hypertensive hypertrophic cardiomyopathy. These changes include the remodeling sarkomer infarction and death, loss of normal collagen matrix, and interstitial fibrosis. The occurrence of myocytes and sarkomer that can not transmit power, cardiac dilatation, and formation of scar tissue with loss of normal myocardial compliance also give an idea on hemodynamic and symptomatic CHF.
Sympathetic nervous system (SNS): Epinephrine and norepinephrine cause an increase in peripheral resistance with increased cardiac work, tachycardia, increased oxygen consumption by the myocardium, and increased risk of arrhythmia. Catecholamines also contribute to ventricular remodeling through direct toxicity to myocytes, induction of apoptosis of myocytes, and increased autoimmune response.
Endogenous vasodilators, such as endothelin and nitric oxide, cardiac peptide and natriuretic peptide: Its role in CHF is under investigation and the intervention being tested.
- Immune and inflammatory cytokines: tumor necrosis factor alpha (TNFa) and interleukin 6 (IL-6) causes ventricular remodeling with apoptotic myocytes, ventricular dilatation, and decreased contractility. Furthermore, they also play a role in systemic effects such as weight loss and weakness seen in CHF brat (kakheksia heart).
• Genesis etiology myocardium early influences initial response, but in line with the development of the syndrome, a common mechanism began to emerge so that patients with advanced CHF show the same symptoms and response to pharmacological intervention is the same no matter the cause of his early CHF.
• Although many patients have left ventricular systolic dysfunction and diastolic, this category should be regarded as different things in order to understand their effects on circulatory homeostasis and response to various interventions.
Left ventricular systolic dysfunction
1) Decrease in cardiac output due to reduced contractility, increased afterload, or increased preload resulting decrease in ejection fraction and increased end diastolic left ventricular volume (LVEDV). This increases pressure on left ventricular end diastolic (I-VEDP) and cause pulmonary venous congestion and pulmonary edema.
2) Decrease in contractility (inotropi) occurred due to inadequate myocardial function or uncoordinated schingga left ventricular ejection can not perform more than 60% of diastoliknya final volume (LVEDV). This causes a gradual increase in LVEDV (also called preload), resulting in increased LVEDP and pulmonary venous congestion. The most common causes of decrease in contractility is ischemic heart disease, which not only causes a real myocardial tissue necrosis, but also cause ischemic ventricular remodeling. Ischemic remodeling is a process that is partly mediated by angiotensin II (ANG II) that causes scarring and dysfunction in the heart sarkomer surrounding area of ischemic injury. Cardiac arrhythmias and cardiomyopathy primers such as those caused olch alcohol, infections, hemakromatosis, hyperthyroidism, drug toxicity and amyloidosis also cause a decrease in contractility. Decrease in cardiac output resulting in lack perfusion on systemic circulation and the activation of the sympathetic nervous system and RAA system, causing increased peripheral resistance and increased afterload.
3) Increased afterload means there is increased resistance to LV ejection. Usually caused by increased peripheral vascular resistance commonly seen in hypertension. Could also be caused by aortic valve stenosis. The left ventricle responds to increased workload with myocardial hypertrophy, a response which increases the left ventricular muscle mass but at the same time increasing the need for coronary perfusion in the left ventricle. An energy famine conditions are created so that combined with ANG II and other neuroendocrine response, causing adverse changes in myocytes, such as fewer mitochondria for energy production, changes in gene expression with an abnormal production of contractile proteins (actin, myosin, and tropomiosin), interstitial fibrosis, and decreased survival of myocytes. With time, contractility began to decline with reduced cardiac output and ejection fraction, increased LVEDV, and pulmonary congestion.
4) Increasing the preload means an increase in LVEDV, which can be caused directly by excess intravascular volume similar to those seen in intravenous infusion fluids or kidney failure. In addition, the decrease in ejection fraction caused by changes in contractility or afterload causes an increase in LVEDV thus increasing the preload. At the time of LVEDV increased, he will stretch the heart, mechanical positioned menjadikansarkomer unfavorable resulting in decreased contractility. The decrease contractility, which causes a decrease in ejection fraction, causing a further increase in LVEDV, thus creating a vicious cycle worsening heart failure.
5) So, the patient can enter the circle of decreased contractility, peningkatanafterload, and increased preload due to various reasons (eg, myocardial infarction [MI], hypertension, excess fluid) and then finally having all of hemodynamic conditions and neuro-hormonal CHF as a mechanism that led other mechanisms.
Left ventricular diastolic dysfunction
1) The cause of 90% of cases
2) Defined as a condition with classic findings of congestive failure with diastolic function abnormalities but normal systolic function, diastolic dysfunction, the mummy will be characterized by resistance to ventricular filling with increased LVEDP LVEDV without an increase or decrease in cardiac output.
3) Prisoners of left ventricular filling due to abnormal relaxation (lusitropik) left ventricle and can be caused by any condition which makes such stiff ventricular myocardial ischemic heart disease that causes scarring, hypertension resulting in hypertrophic cardiomyopathy, restrictive cardiomyopathy, valve disease or illness pericardium .
4) Increased heart rate causes a decreased diastolic filling time and aggravate the symptoms of diastolic dysfunction. Therefore, the intolerance towards sports has become common.
5) Because the treatment usually requires real changes in myocardial compliance, effectiveness of medications available today are still very limited. Management's most recent success with beta insulation which increases lusitropik function, lowering heart rate, and dealing with the symptoms. ACE inhibitors can help improve hypertrophy and assist the structural changes in tissue levels in patients with ischemic remodeling or hypertension.
CHF occurs due to complex interactions between the factors that affect contractility, after-load, preload, or function lusitropik (relaxation function), heart, and neurohormonal and hemodynamic response that is required to create compensation circulation. Although the hemodynamic consequences of heart failure respond to standard pharmacological interventions, there is a critical neurohormonal interactions that aggravate and prolong the combined effects of existing syndrome.
Reniniangiotensinfaldosteron system (RAA): In addition to increased peripheral resistance and blood volume circulation, angiotensin and aldosterone have implications for the structural changes seen in injured myocardium ischemic and hypertensive hypertrophic cardiomyopathy. These changes include the remodeling sarkomer infarction and death, loss of normal collagen matrix, and interstitial fibrosis. The occurrence of myocytes and sarkomer that can not transmit power, cardiac dilatation, and formation of scar tissue with loss of normal myocardial compliance also give an idea on hemodynamic and symptomatic CHF.
Sympathetic nervous system (SNS): Epinephrine and norepinephrine cause an increase in peripheral resistance with increased cardiac work, tachycardia, increased oxygen consumption by the myocardium, and increased risk of arrhythmia. Catecholamines also contribute to ventricular remodeling through direct toxicity to myocytes, induction of apoptosis of myocytes, and increased autoimmune response.
Endogenous vasodilators, such as endothelin and nitric oxide, cardiac peptide and natriuretic peptide: Its role in CHF is under investigation and the intervention being tested.
- Immune and inflammatory cytokines: tumor necrosis factor alpha (TNFa) and interleukin 6 (IL-6) causes ventricular remodeling with apoptotic myocytes, ventricular dilatation, and decreased contractility. Furthermore, they also play a role in systemic effects such as weight loss and weakness seen in CHF brat (kakheksia heart).
• Genesis etiology myocardium early influences initial response, but in line with the development of the syndrome, a common mechanism began to emerge so that patients with advanced CHF show the same symptoms and response to pharmacological intervention is the same no matter the cause of his early CHF.
• Although many patients have left ventricular systolic dysfunction and diastolic, this category should be regarded as different things in order to understand their effects on circulatory homeostasis and response to various interventions.
Left ventricular systolic dysfunction
1) Decrease in cardiac output due to reduced contractility, increased afterload, or increased preload resulting decrease in ejection fraction and increased end diastolic left ventricular volume (LVEDV). This increases pressure on left ventricular end diastolic (I-VEDP) and cause pulmonary venous congestion and pulmonary edema.
2) Decrease in contractility (inotropi) occurred due to inadequate myocardial function or uncoordinated schingga left ventricular ejection can not perform more than 60% of diastoliknya final volume (LVEDV). This causes a gradual increase in LVEDV (also called preload), resulting in increased LVEDP and pulmonary venous congestion. The most common causes of decrease in contractility is ischemic heart disease, which not only causes a real myocardial tissue necrosis, but also cause ischemic ventricular remodeling. Ischemic remodeling is a process that is partly mediated by angiotensin II (ANG II) that causes scarring and dysfunction in the heart sarkomer surrounding area of ischemic injury. Cardiac arrhythmias and cardiomyopathy primers such as those caused olch alcohol, infections, hemakromatosis, hyperthyroidism, drug toxicity and amyloidosis also cause a decrease in contractility. Decrease in cardiac output resulting in lack perfusion on systemic circulation and the activation of the sympathetic nervous system and RAA system, causing increased peripheral resistance and increased afterload.
3) Increased afterload means there is increased resistance to LV ejection. Usually caused by increased peripheral vascular resistance commonly seen in hypertension. Could also be caused by aortic valve stenosis. The left ventricle responds to increased workload with myocardial hypertrophy, a response which increases the left ventricular muscle mass but at the same time increasing the need for coronary perfusion in the left ventricle. An energy famine conditions are created so that combined with ANG II and other neuroendocrine response, causing adverse changes in myocytes, such as fewer mitochondria for energy production, changes in gene expression with an abnormal production of contractile proteins (actin, myosin, and tropomiosin), interstitial fibrosis, and decreased survival of myocytes. With time, contractility began to decline with reduced cardiac output and ejection fraction, increased LVEDV, and pulmonary congestion.
4) Increasing the preload means an increase in LVEDV, which can be caused directly by excess intravascular volume similar to those seen in intravenous infusion fluids or kidney failure. In addition, the decrease in ejection fraction caused by changes in contractility or afterload causes an increase in LVEDV thus increasing the preload. At the time of LVEDV increased, he will stretch the heart, mechanical positioned menjadikansarkomer unfavorable resulting in decreased contractility. The decrease contractility, which causes a decrease in ejection fraction, causing a further increase in LVEDV, thus creating a vicious cycle worsening heart failure.
5) So, the patient can enter the circle of decreased contractility, peningkatanafterload, and increased preload due to various reasons (eg, myocardial infarction [MI], hypertension, excess fluid) and then finally having all of hemodynamic conditions and neuro-hormonal CHF as a mechanism that led other mechanisms.
Left ventricular diastolic dysfunction
1) The cause of 90% of cases
2) Defined as a condition with classic findings of congestive failure with diastolic function abnormalities but normal systolic function, diastolic dysfunction, the mummy will be characterized by resistance to ventricular filling with increased LVEDP LVEDV without an increase or decrease in cardiac output.
3) Prisoners of left ventricular filling due to abnormal relaxation (lusitropik) left ventricle and can be caused by any condition which makes such stiff ventricular myocardial ischemic heart disease that causes scarring, hypertension resulting in hypertrophic cardiomyopathy, restrictive cardiomyopathy, valve disease or illness pericardium .
4) Increased heart rate causes a decreased diastolic filling time and aggravate the symptoms of diastolic dysfunction. Therefore, the intolerance towards sports has become common.
5) Because the treatment usually requires real changes in myocardial compliance, effectiveness of medications available today are still very limited. Management's most recent success with beta insulation which increases lusitropik function, lowering heart rate, and dealing with the symptoms. ACE inhibitors can help improve hypertrophy and assist the structural changes in tissue levels in patients with ischemic remodeling or hypertension.
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