Cardio Megali

23
CARDIO MEGALI 16 Desember 2013 ~ wagekarsana Pengertian Kardiomegali adalah sebuah keadaan anatomis (struktur organ) di mana besarnya jantung lebih besar dari ukuran jantung normal, yakni lebih besar dari 55% besar rongga dada. pada Kardiomegali salah satu atau lebih dari 4 ruangan jantung membesar. Namun umumnya kardiomegali diakibatkan oleh pembesaran bilik jantung kiri (ventrikel kardia sinistra) Pada kardiomegali dapat oto-ototnya yang membesar atau rongganya yang membesar, manapun itu semua adalah adaptasi

description

cardiomegali

Transcript of Cardio Megali

Page 1: Cardio Megali

CARDIO MEGALI16 Desember 2013 ~ wagekarsana

Pengertian

Kardiomegali adalah sebuah keadaan anatomis (struktur organ) di mana besarnya jantung lebih besar dari ukuran jantung normal, yakni lebih besar dari 55% besar rongga dada. pada Kardiomegali salah satu atau lebih dari 4 ruangan jantung membesar. Namun umumnya kardiomegali diakibatkan oleh pembesaran bilik jantung kiri (ventrikel kardia sinistra)

Pada kardiomegali dapat oto-ototnya yang membesar atau rongganya yang membesar, manapun itu semua adalah adaptasi jantung utnuk menghaapi perubahan dalam tuntutan kerjanya.

Cara menentukan ukuran jantung adalah sebagai berikut:CTR = a + b  x 100%               c

Page 2: Cardio Megali

Pada foto dada PA standar, ukuran jantung dapat dihitung melalui rasio kardiotorasik. Secara umum rasio yang melebihi 50% antara ukuran jantung denbgan diameter internal maksimal dada mengindikasikan adanya pembesaran jantung.Penyebab

Penyebabnya ada banyak sekali, hampir semua keadaan yang memaksa jantung untuk bekerja lebih keras dapat menimbulkan perubahan-perubahan pada otot jantung sehingga jantung akan membesar. analoginya adalah misalnya pada binaragawan otot-otonya membesar karena seringnya mereka melakukan aktivitas beban tinggi. jantung juga demikian.

Penyebab penyakitnya apa saja??? Hmmm. banyak sekali… kalau di buku Hurst’s Heart Disease saja bisa sampai 20 bab lebih… dan bukunya hapir 2000 halaman…

Singkatnya saya akan beritahu penyebab yang terbanyak…

1. Penyakit Jantung Hipertensi

Pada keadaan ini terdapat tekanan darah yang tinggi sehingga jantung dipaksa kerja ekstra keras memompa melawan gradien tekanan darah perifer anda yang tinggi…

2. Penyakit Jantung Koroner

Page 3: Cardio Megali

Pada keadaan ini sebagain pembuluh darah jantung (koroner) yang memberikan pasokan oksigen dan nutrisi ke jantung terganggu sehingga otot-otot jantung berusaha bekerja lebih keras dari biasanya menggantikan sebagian otot jantung yang lemah atau mati karena kekurangan pasokan darah.

3. Kardiomiopati (Bisa karena diabetes)

Yakni penyakit yang mengakibatkan gangguan atau kerusakan langsung pada otot-otot jantung. Hal ini dapat bersifat bawaan atau karena penyakit metabolisme seperti diabetes. Akibatnya oto jantung harus kerja ekstra untuk menjaga pasokan darah tetap lancar.

4. Penyakit Katup Jantung

Di jantung ada 4 katup yang mengatur darah yang keluar masuk jantung. Apabila salah satu atau lebih dari katup ini mengalami gangguan seperti misalnya menyempit (stenosis) atau bocor (regurgitasi) akan mengakibatkan gangguan pada curah jantung (kemampuan jantung untuk memopa jantung dengan volume tertentu secara teratur). Akibatnya jantung juga perlu kerja ekstra keras untuk menutupi kebocoran atau kekurangan darah yang dipompanya.

5. Penyakit Paru Kronis

Page 4: Cardio Megali

Nah loh.. Pasti bingung… mengapa penyakit paru kronis juga bisa menyebabkan kardiomegali… Karena pada penyakit paru kronis dapat timbul keadaan di mana terjadi perubahan sedemikian rupa pada struktur jaringan paru sehingga darah menjadi lebih sulit untuk melewati paru-paru yang kita kenal dengan nama “HIPERTENSI PULMONAL”. Karena itu bilik jantung kanan yang memompa darah ke paru-paru perlu kerja ekstra keras, sehingga tidak seperti kebanyakan kardiomegali bukan bilik kiri yang membesar tapi bilik kanan, tapi jika sudah berat bahkan bilik kiri pun akan ikut membesar.

Nah kardiomegali itu sering kali disertai dengan keadaan gagal jantung… Oleh karena itu kardiomegali seringkali menunjukkan bahwa jantung telah lama mengalami kegagalan fungsi yang sudah berlangsung cukup lama dan berat. selain itu kardiomegali cenderung membuat jantung mudah terkena penyakit hjantung koroner karena jantung yang besar perlu pasokan darah dan oksigen yang besar sedangkan pasokan darah belum tentu lancar…Kardiomegali berpotensi berbahaya tapi yang lebih berbahaya adalah penyakit yang menyebabkannya karena seringkali timbul gejala-gejala klinis lain yang berpotensi fatal seperti gagal jantung dan stroke.

Gejala

1. Tergantung dari derajat keparahannya. Tampak gejala yang berhubungan dengan kegagalan pompa jantung untuk bekerja dengan baik

Page 5: Cardio Megali

2. Dapat disertai nggeliyer, pusing, atau sensasi mau jatuh. Orang awam menyebutnya “vertigo”. Dalam istilah asingnya disebut “dizziness”.

3. Sesak nafas, seperti orang yang terengah-engah.4. Terdapat cairan di rongga perut (ascites)5. Kaki (tungkai, pergelangan kaki) membengkakTerapi kardiomegali:

1. Sesuai dengan penyebab yang mendasarinya (underlying causes).

2. Obat golongan diuretik3. Obat golongan ACE inhibitor4. Obat golongan beta blocker5. Golongan nitrat6. Mengurangi/menurunkan berat badan7. Diet rendah garam8. Pembatasan (asupan) cairan9. BerolahragaPengobatan

Pengobatannya adalah kita obati penyakit dasarnya, tapi jantung yang membesar tidak serta merta akan mengecil kembali (seringkali permanen) yang perlu kita cegah adalah komplikasi yang mungkin timbul dari kardiomegali tersebut.

Jadi yang kita obati bukan kardiomegalinya tapi penyakit yang menyebabkannya, tapi kata mengobati juga tidak tepat karena rata-rata penyebabnya tidak dapat diobati. kata yang tepat adalah mengontrol keadaan yang menyebabkannya.

Page 6: Cardio Megali

Jikalau anda curiga kardiomegali, anda dapat memeriksakan diri ke dokter spesialis jantung dan pembuluh darah terdekat di kota anda…

Pemeriksaan Penunjang

Idealnya, pemeriksaan laboratorium pada penderita kardiomegali meliputi: hitung darah lengkap, sedimentation rate, ANA, chemistry panel, tes VDRL, profil tiroid, EKG, dan rontgen dada (chest x-ray).

Pemeriksaan dengan echocardiogram akan membantu menegakkan diagnosis valvular disease, myocardiopathies, congestive heart failure, dan pericardial effusion. Jika curiga gagal jantung kongestif (congestive heart failure), maka perlu diukur waktu sirkulasi, tekanan vena, dan perlu tes fungsi paru-paru. Jika disertai demam, maka penderita kardiomegali perlu melakukan tes streptozyme, ASO titer, dan kultur darah serial.

Kesimpulan

Faktor kardiomegali saja tidak menyebabkan kematian, terutama bila masih ringan. Biasanya kematian disebabkan oleh penyakit yang menyertai atau komplikasi yang dialami penderita kardiomegali.

Page 7: Cardio Megali

Nah, untuk mencegah agar tidak berlanjut atau menjadi parah, sebaiknya tekun beribadah dan bersedekah, rajin berolahraga, berpola hidup sehat dan seimbang, dan teratur kontrol ke dokter atau rumah sakit terdekat untuk melakukan general check-up, minimal sebulan sekali. Jika dinyatakan baik oleh dokter, perlu cek lagi setiap 2-3 bulan sekali, tergantung waktu dan kesempatan.OverviewCongestive heart failure (CHF) is a clinical syndrome in which the heart fails to pump blood at the rate required by the metabolizing tissues or in which the heart can do so only with an elevation in filling pressure. Signs of CHF are demonstrated in the image below.

Chest radiograph shows signs of congestive heart failure (CHF).The heart's inability to pump a sufficient amount of blood to meet the needs of the body's tissues may be a result of insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanisms increase blood volume, as well as the cardiac filling pressure, heart rate, and cardiac muscle mass, to maintain the pumping function of the heart and to cause a redistribution of blood flow. Despite these compensatory mechanisms, the ability of the heart to contract and relax declines progressively, and heart failure (HF) worsens.

The clinical manifestations of HF vary enormously and depend on a variety of factors, including the age of the patient, the extent and rate at which cardiac performance becomes impaired, and which ventricle is initially involved in the disease process. A broad spectrum of severity of impairment of cardiac function is ordinarily included in the definition of HF. These impairments range from the mildest forms, which are manifest clinically only during stress, to the most advanced forms, in which cardiac pump function is unable to sustain life without external support.[1]

Page 8: Cardio Megali

Echocardiography

Echocardiography is the preferred examination in CHF. Two-dimensional and Doppler echocardiography may be used to determine systolic and diastolic LV performance, the cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures.[2] Echocardiography also may be used to identify clinically important valvular disease.

Radiography

In cardiogenic cases, radiographs may show cardiomegaly, pulmonary venous hypertension, and pleural effusions. Pulmonary venous hypertension (PVH) may be divided into 3 grades. In grade I PVH, an upright examination demonstrates redistribution of blood flow to the nondependent portions of the lungs and the upper lobes. In grade II PVH, there is evidence of interstitial edema with ill-defined vessels and peribronchial cuffing, as well as interlobular septal thickening. In grade III PVH, perihilar and lower-lobe airspace filling is evident, with features typical of consolidation (eg, confluent opacities, air bronchogram and the inability to see pulmonary vessels in the area of abnormality). The airspace edema tends to spare the periphery in the mid and upper lung.

In noncardiogenic cases, cardiomegaly and pleural effusions are usually absent. The edema may be interstitial but is more often consolidative. No cephalization of flow is noted, though there may be shift of blood flow to less affected areas. The edema is diffuse and does not spare the periphery of the mid or upper lungs.

In cases of large, acute myocardial infarction (MI) and infarction of the mitral valve, support apparatus may produce atypical patterns of pulmonary edema that may mimic noncardiogenic edema in patients who in fact have cardiogenic edema.

Computed tomography scanning

In cases that are clinically troublesome, multidetector-row gated computed tomography (CT) scanning may provide excellent analysis of the heart and reveal the nature of the pulmonary edema.[3]

Electrocardiography

In cardiogenic cases, the electrocardiogram (ECG) may show evidence of MI or ischemia. In noncardiogenic cases, the ECG is usually normal.

The ECG image below depicts biventricular pacing.

Page 9: Cardio Megali

ECG shows biventricular pacing (double ventricular pacing spikes).Limitations of techniques

Although echocardiography is simple and noninvasive, it proves to be inadequate in 8-10% of cases; in addition, the results are difficult to interpret in patients with lung disease.

RadiographyTwo principal features of the chest radiograph are useful in the evaluation of patients with congestive heart failure: (1) the size and shape of the cardiac silhouette, and (2) edema at the lung bases. (see the image below).[4]

Chest radiograph shows signs of congestive heart failure (CHF).The size and shape of the cardiac silhouette provide important information concerning the precise nature of the underlying heart disease. The cardiothoracic ratio and the heart volume, as determined on plain film, are relatively specific but insensitive indicators of increased LV end-diastolic volume. There is a weak inverse correlation between the cardiothoracic ratio and LV ejection fraction (LVEF) in patients with HF; the relationship is not clinically useful in the individual patient.

In the presence of normal pulmonary capillary and venous pressures, the lung bases are better perfused than the apices when the patient is in the erect position, and the vessels supplying the lower lobes are significantly larger than those supplying the upper lobes. With elevation of left atrial and pulmonary capillary pressures, interstitial and perivascular edema develops; such edema is most prominent at the lung bases because hydrostatic pressure is greater there.

When pulmonary capillary pressure is slightly elevated (13-17 mm Hg), the resultant compression of pulmonary vessels in the lower lobes causes

Page 10: Cardio Megali

equalization in the size of the vessels at the apices and bases (early grade I PVH). With greater pressure elevation (18-23 mm Hg), actual pulmonary vascular redistribution into nondependent portions of the lung occurs (ie, with the patient in an upright patient, there is further constriction of the vessels that lead to the lower lobes, and there is dilatation of the vessels that lead to the upper lobes).

When pulmonary capillary pressures exceed 20-25 mm Hg, interstitial pulmonary edema occurs (grade II PVH). With grade II PVH, there is evidence of interstitial edema, with ill-defined vessels and peribronchial cuffing, as well as interlobular septal thickening. The interlobular septal thickening is referred to as Kerley B lines. Early blunting of the lateral and posterior costophrenic angles may occur; such blunting indicates the presence of pleural fluid.

When pulmonary capillary pressure exceeds 25 mm Hg, images may show large pleural effusions and grade III PVH, with consolidative alveolar edema in a perihilar and lower-lobe distribution.

With elevation of the systemic venous pressure, the azygos vein, brachiocephalic veins, and superior vena cava may become enlarged.

In patients with chronic LV failure, higher pulmonary capillary pressures may be accommodated with fewer clinical and radiologic signs, presumably because of enhanced lymphatic drainage. In a study of 22 patients with advanced HF who were referred for cardiac transplant evaluation and whose pulmonary capillary wedge pressure measurements were 25 mm Hg or greater, 68% had no or minimal pulmonary congestion, as shown on chest radiographs.

In summary, the typical findings of CHF on the plain radiograph are cardiomegaly; grade I, II, or III PVH; and increased central systemic venous volume, with enlargement of the mediastinal veins (including the azygous vein) and pleural effusions.

Degree of confidence

The degree of confidence is low. The weak negative correlation between the cardiothoracic ratio and the ejection fraction does not permit accurate determination of systolic function in the absence of radiographic evidence of PVH or pleural effusions in individual patients with HF. For this reason, a chest radiograph may not be very useful for determining the type of LV dysfunction. During the treatment phase of CHF, chest radiographic findings often lag behind clinical improvement.

Page 11: Cardio Megali

False-negative findings are frequent.

Computed TomographyCT scanning of the heart is usually not required in the routine diagnosis and management of congestive heart failure.

Multichannel CT scanning is useful in delineating congenital and valvular abnormalities; however, echocardiography and magnetic resonance imaging (MRI) may provide similar information without exposing the patient to ionizing radiation.

The degree of confidence in CT scanning is moderate, and the rates of false-positive and false-negative findings in the modality are low.

Magnetic Resonance ImagingBecause of the widespread acceptance of echocardiography, MRI is used only infrequently in the workup of patients with congestive heart failure. Its main use involves delineation of congenital cardiac abnormalities and assessment valvular heart disease; it is also used in patients with other conditions.[5]

The degree of confidence in MRI is high, and the rates of false-positive and false-negative findings are low.

UltrasonographyTwo-dimensional echocardiography is recommended as an initial part of the evaluation of patients with known or suspected congestive heart failure. Ventricular function may be evaluated, and both primary and secondary valvular abnormalities may be accurately assessed.[6]

Doppler echocardiography may play a valuable role in determining diastolic function and in establishing the diagnosis of diastolic HF.

HF in association with normal systolic function but abnormal diastolic relaxation affects 30-40% of patients presenting with CHF. Because the therapy for this condition is distinctly different from that for systolic dysfunction, establishing the appropriate etiology and diagnosis is essential. The combination of 2-dimensional echocardiography and Doppler echocardiography is effective for this purpose.

Two-dimensional and Doppler echocardiography may be used to determine systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures.

Page 12: Cardio Megali

Echocardiography may also be used to identify clinically important valvular disease.[4]

The degree of confidence in echocardiography is high, and the rates of false-positive and false-negative findings are low.

Nuclear ImagingNuclear imaging can be used in the assessment of heart function and damage in CHF.

ECG-gated myocardial perfusion imaging

The high photon flux of compounds labeled with technetium-99m (99m TC) makes it feasible to acquire myocardial perfusion images in an ECG-gated mode. ECG-gated myocardial perfusion images may be displayed as an endless-loop cine on the computer screen. ECG-gated single-photon emission CT (SPECT) images allow for assessment of global LVEF, regional wall motion, and regional wall thickening.

Regardless of whether the injection of radiopharmaceutical was performed during peak stress or at rest, because the acquisition is performed at rest, ECG-gated SPECT images reveal resting global function and wall motion and resting wall thickening in areas with defects of exercise-induced myocardial perfusion.

On ECG-gated SPECT images, regional wall thickening may be quantified as a percentage of wall thickening in comparison to end-diastole. Commercially available and validated software packages are available for the automatic calculation of resting global LVEF, LV volume, and regional wall thickening from ECG-gated SPECT sections.

In general, LVEF from gated SPECT agrees well with resting LVEF, as determined with other modalities. Quality assurance is important. Determinations of LVEF with gated SPECT may be less accurate, even invalidated, in the presence of an irregular heart rate, low count density, intense extracardiac radiotracer uptake adjacent to the LV, or a small LV.

Combined interpretation of perfusion and function on ECG-gated images substantially increases the confidence of interpretation. Taillefer and associates reported that the interpretation of stress and rest end-diastolic section, rather than summed ungated sections, may enhance the overall sensitivity for the detection of mild coronary artery disease (CAD).

ECG-gated images are useful for recognizing artifactual defects caused by

Page 13: Cardio Megali

attenuation (breast and diaphragm) and thus are useful in the quality control of SPECT imaging. ECG-gated SPECT imaging is presently considered the state of the art of radionuclide myocardial perfusion imaging.

Assessment of myocardial viability

For patients with angina, known CAD, previous infarction, and LV dysfunction, a reliable method for assessing the presence, extent, and location of viable myocardium is of considerable clinical importance. It is well established that global or regional ischemic LV dysfunction is not always an irreversible condition. Approximately 25-40% of patients may experience improvement in function after adequate revascularization.

Two important practical issues need to be addressed in the evaluation of patients with presumed ischemic dysfunction: (1) One should consider assessment of the relative regional myocardial uptake of thallium-201 (201 Tl; often after rest reinjection),99m Tc-sestamibi, or99m Tc-tetrofosmin (often after rest administration of nitroglycerin). When the resting uptake of radiotracer is greater than 50% of normal, one may expect recovery of function after revascularization. (2) One should consider assessment of the presence of demonstrable ischemia (eg, partially reversible defect) in a myocardial segment with decreased uptake, even if the resting uptake is less than 50%.

Equilibrium radionuclide angiocardiography

Equilibrium radionuclide angiocardiography (ERNA) uses ECG events to define the temporal relationship between the acquisition of nuclear data and the volumetric components of the cardiac cycle.

Sampling is performed repetitively over several hundred heartbeats, with physiologic segregation of nuclear data in accordance with their occurrence within the cardiac cycle.

Data are quantified and displayed in an endless-loop, cinegraphic format for additional qualitative visual interpretation and analysis. Equilibrium blood-pool labeling is achieved by use of99m Tc. The intravascular label is affixed to the patient's own red blood cells by use of an in vitro or modified in vitro technique. Unlabeled stannous pyrophosphate is used to facilitate this reaction. Conventional Anger scintillation cameras are used for these studies. Data are analyzed by use of a computer, generally with some operator interaction.

Analysis may be obtained in either the frame or list mode. Radionuclide

Page 14: Cardio Megali

data are collected and segregated temporally. The process generally requires 3-10 minutes for completion of each view. Following data acquisition, data from the several hundred individual beats are summed, processed, and displayed as a single representative cardiac cycle.

Data from the left anterior oblique (LAO) view are also used for qualitative analysis of global LV function. On this view, overlap of the 2 ventricles is minimal. In a count-based approach, LVEF and other indices of filling and ejection are calculated from the LV radioactivity preset at various points throughout the cardiac cycle.

Right ventricular function is best evaluated by first-pass techniques. The LAO view provides qualitative information concerning contraction of the septal, inferoapical, and lateral walls. The anterior view provides data concerning regional motion of the anterior and apical segments. The left lateral or left posterior oblique view provides optimal qualitative information concerning contraction of the inferior wall and posterobasal segment.

Ventricular aneurysm may be best assessed in the lateral views as well. Each segment is generally graded on a 5-point scale, with specific numerical grades assigned for dyskinesis, akinesis, mild and severe hypokinesis, and normal function.

ERNA may easily be combined with additional physiologic stress testing or provocation, which may be in the form of either physiologic stress, such as exercise; pharmacological stress, with the use of positive inotropic agents such as dobutamine or isoproterenol; or psychological stress.

Degree of confidence

The degree of confidence is moderately high.

False positives/negatives

False-positive and false-negative findings are infrequent.

AngiographyCardiac catheterization and coronary angiography have a useful role in patients with congestive heart failure, those with valvular heart disease, and those with congenial heart disease, as well as patients with other conditions.

For patients with CHF, cardiac catheterization and coronary angiography are clearly indicated in the following situations:

Page 15: Cardio Megali

6.CHF caused by systolic dysfunction in association with angina or regional wall motion abnormalities and/or scintigraphic evidence of reversible myocardial ischemia when revascularization is being considered

7.Before cardiac transplantation 8.CHF secondary to postinfarction ventricular aneurysm or other

mechanical complications of MI For these patients, the procedures are frequently indicated when systolic dysfunction of unexplained cause is present on noninvasive testing or when normal systolic function with episodic HF suggests ischemically mediated LV dysfunction.

In patients with valvular heart disease, cardiac catheterization and coronary angiography are clearly indicated in the following situations:

10. Before valve surgery or balloon valvotomy in an adult with chest discomfort, ischemia by noninvasive imaging, or both

11. Before valve surgery in an adult who is free of chest pain but who has many risk factors for CAD

12. Infective endocarditis with evidence of coronary embolization In patients with congenital heart disease, cardiac catheterization and coronary angiography are clearly indicated in the following situations:

• Before surgical correction of congenital heart disease when chest discomfort or noninvasive evidence is suggestive of associated CAD

• Before surgical correction of suspected congenital coronary anomalies such as congenital coronary artery stenosis, coronary arteriovenous fistula, and anomalous origin of the left coronary artery

• The patient has a form of congenital heart disease that is frequently associated with coronary artery anomalies that may complicate surgical management

• Unexplained cardiac arrest in a young patient For these patients, the procedures are frequently indicated before corrective open heart surgery for congenital heart disease in an adult whose risk profile is associated with an increased risk of coexisting CAD.

In patients with other conditions, cardiac catheterization and coronary angiography are clearly indicated in the following situations:

• Diseases affecting the aorta when knowledge of the presence or extent of coronary artery involvement is necessary for management (eg, aortic dissection or aneurysm with known CAD)

• Hypertrophic cardiomyopathy with angina despite medical therapy when knowledge of coronary anatomy might affect therapy

Page 16: Cardio Megali

• Hypertrophic cardiomyopathy with angina when heart surgery is planned For these patients, the procedures are frequently indicated in the following situations:

• There is a high risk of CAD when other cardiac surgical procedures are planned (eg, pericardiectomy or removal of chronic pulmonary emboli)

• Prospective immediate cardiac transplant donors have a risk profile that increases the likelihood of CAD

• Asymptomatic patients with Kawasaki's disease have coronary artery aneurysms on echocardiography

• Before surgery for aortic aneurysm/dissection in patients without known CAD

• Recent blunt chest trauma and suspicion of acute MI, without evidence of preexisting CAD

Degree of confidence

The degree of confidence is moderately high.

False positives/negatives

The rates of false-positive and false-negative findings are low.