DECOMPENSASI CORDIS PDF

Decompensasi cordis adalah kegagalan jantung dalam upaya untuk mempertahankan peredaran darah sesuai dengan kebutuhan tubuh. Ahmad ramali. Dekompensasi kordis adalah suatu keadaan dimana terjadi penurunan kemampuan fungsi kontraktilitas yang berakibat pada penurunan fungsi pompa jantung Tabrani, ; Price, Mekanisme fisiologis yang menyebabkan timbulnya dekompensasi kordis adalah keadaan-keadaan yang meningkatkan beban awal, beban akhir atau yang menurunkan kontraktilitas miokardium. Keadaan yang meningkatkan beban awal seperti regurgitasi aorta, dan cacat septum ventrikel. Beban akhir meningkat pada keadaan dimana terjadi stenosis aorta atau hipertensi sistemik.

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In , William Harvey first described the circulation. Before this time, there was very little understanding of the nature of heart failure HF. There are, however, accounts of a disease that now would be called heart failure, and herbal medicines such as the ancient boiled bulb of squill, or, later on, the broom plant Cytisus scoparius and the foxglove Digitalis purpura were used as diuretics to treat heart failure or dropsy edema.

Foxglove was described as a diuretic by William Withering in In the s, thiazide diuretics were introduced, and in the s furosemide became available. For a long time, diuretics and digitalis were the main treatment options for HF.

Vasodilator therapy for HF was introduced around , and the first randomized trial showing a mortality benefit with nitrates and alphablockers for HF was published in In , the first ACE inhibitor, captopril, was developed and it was approved for human use in , with data from the first randomized trial being published in Spironolacton, introduced in , was used in low dose for HF only after the introduction of ACE inhibitors.

Beta blockers were hardly used in heart failure even though they were shown to beneficial in the s. It was only in that data from the first randomized trial demonstrated a mortality benefit with beta blocker therapy. In , the Framingham heart study was launched.

At its start, residents of the town Framingham in the USA, aged between 30 and 62 years, were included in the study in an attempt to determine risk factors for cardiac disease. The study is still in progress today and long term data from the lengthy follow up have been published. This study is considered to be the most important longitudinal source of data on the epidemiology of heart failure[ 2 ].

According to the guidelines of the European Society of Cardiology, HF is defined as a syndrome in which the patient has the following triad of features: 1 symptoms typical of HF; 2 signs typical of HF; and most importantly 3 objective evidence of a structural or functional abnormality of the heart at rest Table 1.

Coronary heart disease at a young age is more prevalent in men than women, and so the prevalence of HF is also higher in this group compared to age matched women. In older age groups, the prevalence of HF is equal between the sexes. Heart failure may become a chronic condition, in which HF is persistent either with recurrences or with slow progression. A patient may be described as decompensated when chronic stable HF deteriorates. Acute HF has traditionally been used to describe the nature of the clinical presentation, as severe or of recent onset.

Different clinical presentations fall under this definition. Heart failure patients may be broadly classified into one of two groups, or a combination of both, depending on the left ventricular ejection fraction LVEF.

LF diastolic dysfunction may be present in asymptomatic patients, and it is considered an important precursor of heart failure. The term heart failure is not limited to a failing left ventricle; the right ventricle may also be involved in the process and there may also be isolated right ventricular heart failure. HF is caused by a loss of cardiac pump function, which can be due to a structural abnormality of the heart muscle e. The relationship between loading the ventricle by filling it and its output was described by Frank and Starling in and has become the cornerstone in understanding heart failure and how to treat it.

The relationship states that as a result of loading the heart increasing its filling or its pressure , the output increases Figure 1. A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens LV dilatation and increased filling pressure when the heart does not pump out enough volume, and, in the first phase of disease, compensates for the loss of contractility. It takes more energy from the heart to work at an increased loading, but the heart has a reasonable energy reserve.

In a chronic situation, remodeling of the heart progresses by hypertrophy of the myocytes and dilatation by increasing myocyte length and matrix changes , which, in the long term, leads to a further loss in function. The result of this dysfunction is further increased loading pressures in the heart and, by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded and leak water into the lungs.

Hemodynamic explanations the heart as a pump use the concept of preload filling and afterload workload of the heart, which is wall tension and arterial pressure or vascular resistance. In this way, the progression of left sided heart failure towards right sided heart failure is explained as follows: prolonged left ventricular failure increases pressures in the left atrium preload , which in time leads to a subsequent increased resistance in the pulmonary vascular system which is the afterload of the right ventricle and eventually may also lead to right ventricular failure.

Another relevant issue is afterload of the left ventricle influencing the output of the heart: as the afterload of the aortic pressure also influences the timing of closure of the aortic valve, a high aortic pressure will close the aortic valve early and will, therefore, diminish the output.

Decreasing theoretically diastolic, but more practically systolic aortic pressure will increase the stroke volume by latter closure of the aortic valves. Figure 2. A decreased cardiac output leads to diminished renal perfusion and release of hormones in the RAA-system: renin is released into the circulation by the renal juxtaglomerular apparatus, which stimulates the cleavage of angiotensinogen into angiotensin I and II during its passage through the lungs.

Angiotensin II stimulates vasoconstriction in the kidneys, and in other vascular systems, increasing blood pressure; the second effect of angiotensin is to stimulate the release of aldosterone from the adrenals into the plasma, which retains sodium from the kidney tubules in the blood and thereby water. The RAA —system, which works as a compensatory mechanism for heart failure to increase blood pressure and blood volume, also stimulates hypertrophy of muscle cells and the formation of fibrosis, which in the long term are detrimental to heart failure.

The other compensatory mechanism for heart failure, stimulation of the sympathetic nervous system, increases heart rate to increase cardiac output, which is a powerful compensatory mechanism.

However, chronic stimulation of the sympathetic nerves to the heart, leading to higher heart rates, is toxic to the heart, because of continuous release of norepinephrine to the myocyte. In addition, as a result of their continued stimulation, the betareceptors for norepinephrine are downregulated in heart failure, which further diminishes the function and functional reserve of the heart.

When a patient presents with symptoms of heart failure, it is worthwhile to have a dedicated diagnostic and therapeutic plan, in the order as indicated below Figure 3. Clinical aspects are important for diagnosis, but the final diagnosis is only made after objective evidence of heart dysfunction.

A careful history of the patient is important for the diagnosis and in order to identify the cause of HF. The history and physical examination can be used to differentiate between the abovementioned potential causes of HF refer to Etiology of heart failure. Family history of HF, smoking status, hyperlipidaemia, hypertension and diabetes mellitus are factors that should be taken into account during the assessment of the patient history in order to draw a risk profile of the patient.

Finally, the history should include previous events and the response to therapy. HF can manifest with a multitude of different symptoms and signs, but shortness of breath and tiredness are the most characteristic. Minor criteria are acceptable only if they cannot be attributed to another medical condition such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome. Diagnosis of HF requires the simultaneous presence of at least 2 major criteria or 1 major criterion in conjunction with 2 minor criteria.

In general, correlation between the severity of symptoms and the severity of HF in terms of loss of maximal oxygen consumption is weak. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnoea. Comfortable at rest, but less than ordinary activity results in fatigue, palpitation, or dyspnoea. There are several key features in the clinical examination of a patient presenting with HF.

The physical examination should focus on the general appearance of the patient, pulse and blood pressure, signs of fluid overload increased jugular venous pressure, peripheral edema, ascites and hepatomegaly , the lungs, and the heart apex, Gallop rhythm, third heart sound, murmurs. In order to assist in the diagnosis of HF and to differentiate between possible causes of HF, the following tests are available.

A chest X-ray is a part of the standard examination in potential HF patients. It is also important to rule out other causes of dyspnea. Echocardiography is the cornerstone in the diagnosis of HF, and should be performed routinely, because ventricular function can be evaluated accurately with this technique. It can provide objective evidence of a structural or functional abnormality of the heart at rest, besides signs and symptoms that are typical of heart failure. Important parameters that can be assessed include, but are not limited to, wall motion, valve function, left ventricular ejection fraction and diastolic function.

Diastolic dysfunction might be an important finding in symptomatic patients with a preserved ejection fraction. Refer to Table 3 for common echocardiographic findings in HF. Transesophageal echocardiography is indicated in patients with an inadequate transthoracic echo window, suspected endocarditis, complicated valvular disease or to exclude a LV thrombus.

If echocardiography provides inadequate information or in patients with suspected coronary artery disease, additional imaging includes CT scanning, cardiac magnetic resonance imaging or radionuclide imaging. A standard blood assessment includes a complete blood count, electrolytes, renal function, glucose and liver function.

Furthermore, urinalysis and other tests, depending on the clinical condition of the patient, complete the laboratory assessment. For example, cardiac troponins must be sampled if an ACS is in the differential diagnosis.

Natriuretic peptides are enzymes, secreted by the atria or ventricles in response to myocardial wall stress. The most commonly used tests are BNP and NT-proBNP measurements, which despite their different half-lives in the plasma, do not differ substantially in terms of diagnostic ability.

Cut-off values are different in acute settings with acute dyspnea compared to chronic settings. An exercise test is not diagnostic for HF, but may be used to identify ischemia as the cause of heart failure, or it can be used to assess the severity of HF, usually in conjunction with maximal oxygen uptake VO 2max measurement.

This test is performed on a treadmill or on a bicycle ergo meter. The patient is asked to give maximal effort while the workload gradually increases. During the test, the ECG is monitored for ischemia. When possible, oxygen consumption should also be measured during the test.

Not only is an oxygen consumption test a good tool to discriminate between lung- peripheral- or heart problems, but the obtained value for maximal oxygen uptake VO 2max has an important prognostic value. Heart catheterization is not always part of the routine diagnosis and work-up of patients with HF.

It should be considered however to exclude coronary heart disease Class of recommendation IIa, level of evidence C, see Table 4. Coronary angiography is recommended in patients at high risk of coronary artery disease Class of recommendation I, level of evidence C and in HF patients with significant valvular disease Class of recommendation IIa, level of evidence C. These patients mainly suffer from systolic HF due to wall motion abnormalities of the affected area and re-modeling of the non-affected parts of the myocardium.

In patients with a high systolic blood pressure BP , the left ventricle faces an increased afterload a higher workload pumping the blood against the increased vascular resistance. Over a certain period of time, this will lead to hypertrophy of the cardiac myocardium, and longer term remodeling may lead to pump function disorders diastolic or systolic.

Atrial fibrillation is a common rhythm disorder in the elderly. With this condition, the atria do not contract in the coordinated fashion as they would in normal sinus rhythm, and therefore the atria never optimally empty.

The absence of the atrial kick during atrial fibrillation can contribute to a reduced LVEF. However, atrial fibrillation is seldom the cause of heart failure, but more often a trigger of heart failure in already existing structural heart disease. Valvular disease, especially mitral- or aortic, can cause volume and pressure overload of the left ventricle of the heart.

Dilated cardiomyopathy DCM is characterized by dilatation of one or both of the ventricles of the heart, with a general decrease in contractility and consequently a decreased pump function.

Hypertrophic cardiomyopathy see also Hypertension is characterized by hypertrophy, which may be concentric or asymmetric. The asymmetric form is usually hereditary. Restrictive cardiomyopathy is characterized by a primary diastolic dysfunction of one or more of the ventricles, leading to increased filling pressures and hypertrophy, and initially a preserved systolic function. Arrhythmogenic right ventricular cardiomyopathy is characterized by fatty infiltration and fibrosis of the right ventricle or the left ventricle or both and is usually hereditary.

Restriction of ventricular filling by a tight inflamed or constrictive pericardium or by pericardial effusion and tamponade can be the cause of diastolic HF. The therapeutic management of HF involves both pharmacological and non-pharmacological treatment.

The goal is reduction in mortality and morbidity, prevention of the progression of HF, and the treatment of non- cardiovascular co-morbidities.

KABULIWALA RABINDRANATH TAGORE PDF

Decompensasi Cordis

Embed Size px x x x x MEDIS 1. Kegagalan fungsi pompa jantung dalam mencukupi kebutuhan darah nutrient dan oksigen secara adekuat sesuai dengan kebutuhan jaringan. Suatu keadaan dimana jantung tidak mampu lagi memompa darah yang cukup untuk memenuhi kebutuhan metabolisme jaringan. I Wayan sudarta. Gagal serambi kiri dan atau kanan dari jantung mengakibatkan ketidak mampuan untuk memberikan keluaran yang cukup untuk memenuhi kebutuhan jaringan dan menyebabkan terjadinya kongesti pulmonal dan sistemik. Doengoes, E Marilynn.

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Pathway Decompensasi Cordis

Congestive heart failure CHF has a substantial impact on care utilisation and quality of life. It is crucial for patients to cope with CHF adequately, if they are to live an acceptable life. Self-management may play an important role in this regard. Previous studies have shown the effectiveness of the 'Chronic Disease Self-Management Program' CDSMP , a group-based cognitive behavioural programme for patients with various chronic conditions.

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