Diagnosa Kerja

1. syok kardiogenik Suatu keadaan dimana terjadi penurunan cardiac output (curah jantung) dan perfusi secara sistemik dikarenakan disfungsi dari jantung dengan volume intravascular yg adekuat, menyebabkan hipoksia jaringan. 2. Kriteria Diagnostik -Tekanan darah sistolik < 90 mmHg persisten selama lebih dari 30 menit -Hipoperfusi ke sistem organ-organ utama ditandai : oligouria, kulit dingin dan lembab, terganggunya fungsi mental -Indeks jantung < 2,2 L/menit/m2 -Tekanan pengisian ventrikel kiri > 15mmHg 3. Manisfestasi Klinis -Nyeri dada hebat -Nafas cepat -Sesak nafas -Keringatan -Kulit pucat, dingin -Penurunan atau kehilangan kesadaran -Nadi cepat tapi kuat angkat lemah -Kebingungan, cemas, agitasi -Penurunan fungsi mental : konsentrasi turun, kewaspadaan turun -Penurunan produksi urin 4. 1. 2. 3. 4. Diagnosis Banding Syok Kardiogenik et cause emboli paru Syok Kardiogenik et cause Regurgitasi aorta Syok Kardiogenik et cause shock septic Syok Kardiogenik et cause hipovolemik

* cardiogenik shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI). Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure.1 Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both.

Whenever patients who present in shock have been exposed to medications that may cause hypotension. however. which leads to left ventricular dysfunction and decreased arterial pressure. . exacerbate the myocardial ischemia. Other pathophysiological mechanisms responsible for cardiogenic shock include papillary muscle rupture leading to acute mitral regurgitation (4. Dead myocardium does not contract. If these medications are the culprits. Myocardial ischemia causes a decrease in contractile function. Additional surprising findings included nonelevated systemic vascular resistance on vasopressors and that most survivors have only New York Heart Association (NYHA) class I congestive heart failure. The management of RV infarcts is discussed elsewhere but should be considered in the setting of inferior wall MI. cardiogenic shock may result. complement. Cardiac tamponade may result as a consequence of pericarditis. and classical teaching has been that when more than 40% of the myocardium is irreversibly damaged (particularly. and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic shock. angiotensin-converting enzyme inhibitors. Elevated levels of white blood cells. by itself. The SHOCK trial. Nitroglycerin. Pathophysiology The most common initiating event in cardiogenic shock is AMI. which may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. ejection fraction. therapy directed at these toxicities is beneficial. these. Hypotension can be seen with or without bradycardia. Calcium channel blockers may cause profound hypotension with a normal or elevated heart rate. iNOS leads to the expression of interleukins.For related information. opiate. These lead to increased ventricular filling pressures. body temperature. interleukins. Additionally.1%) as a consequence of AMI. a marked decrease in contractility reduces the ejection fraction and cardiac output. these drugs should be considered as possible culprits in the disease. and free wall rupture (4. or in rare cases systemic lupus erythematosus. Similarly. may lead to hypotension and shock because of reduced preload to the left ventricle. demonstrated that left ventricular ejection fraction is not always depressed in the setting of cardiogenic shock. the anterior cardiac wall).5%). cardiac chamber dilatation. in turn. and C-reactive protein are often seen in large myocardial infarctions. uremic pericardial effusion. A systemic inflammatory response syndrome–type mechanism has been implicated in the pathophysiology of cardiogenic shock. inflammatory nitric oxide synthetase (iNOS) is also released in high levels during myocardial stress.4%). Right ventricular (RV) infarct. The end result is a vicious cycle that leads to severe cardiovascular decompensation. and ventricular septal defect (1. decreased forward flow. and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. iNOS induces nitric oxide production. Beta-blocking agents may also cause hypotension. see Medscape's Cardiology Resource Centers. On a mechanical level. or AV node block can be seen with either of these types of medications. which may themselves cause hypotension.

Mortality/Morbidity Cardiogenic shock is the leading cause of death in acute myocardial infarction (AMI). Frequency United States Cardiogenic shock occurs in 8.5%. antiplatelet therapies. but they have been reported to be as low as 30-50%. For children. the causes of cardiogenic shock are vastly different. whites. and lipid-lowering agents in patients with acute coronary syndromes. drug toxicity. In the National Registry of Myocardial Infarction covering the period from 1995-2004. and Asians/others. see eMedicine's Pediatric Critical Care Medicine article on Shock.6% of patients with ST-segment elevation MI with 29% of those presenting to the hospital already in shock. congenital heart disease.3. Rates vary depending on the procedure (eg. in-hospital mortality declined from 60. It occurs only in 2% of patients with non–ST-segment elevation MI. the mortality rate is 39. and toxic ingestions. • • • • The overall in-hospital mortality rate is 57%. mortality rates approach 70%.Initiating events other than AMI and ischemia include infection. 56%.9%. the mortality rate is 64. For persons older than 75 years. Race-based differences in mortality disappear with revascularization.4 Race • • Race-stratified mortality rates are as follows: Hispanics. This has decreased the incidence of cardiogenic shock developing in the hospital due to acute coronary syndromes. Mortality rates attributable to cardiogenic shock are also thought to be due to the increased frequency of use of PCI. stent placement. and pulmonary embolus.3% to 47. 74%. The SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. African Americans.2 This improvement has been attributed to the increasing frequency of the use percutaneous coronary intervention (PCI) and other revascularization procedures. Mortality rates have declined over time. 41%.1%. When rapid revascularization is not attempted. The incidence of cardiogenic shock on arrival to the hospital has not changed significantly. percutaneous transluminal coronary angioplasty. For details. For those younger than 75 years. thrombolytic therapy). Sex . 65%. The 3 primary causes of cardiogenic shock in children and infants are viral myocarditis. Outcomes significantly improve only when rapid revascularization can be achieved.

medscape. For adults. Sumber 1. Judith hochman.magnus ohman. http://emedicine.AHA Clinical series.diagnosis. cardiogenic shock presents as a consequence of fulminant myocarditis or congenital heart disease. For children. E. Tugas.Women comprise 42% of all patients with cardiogenic shock.com/article/759992-diagnosis Author: Ethan S Brandler. MPH 2. MD.2009.cardiogenic shock(American heart association). PIOLITTA CYRENIA W (o7-005) Kelompok 6 . the median age ranges from 65-66 years. Age Median age for cardiogenic shock mirrors the bimodal distribution of disease.bab 1.

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