Cardiogenic shock

Cardiogenic shock

1. Prepared by SALMAN HABEEB CARDIOGENIC SHOCK

2. DEFINITION Cardiogenic shock (CS) is defined as persistent hypotension and tissue hypoperfusion due to cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure. Hemodynamically : persistent hypotension (systolic blood pressure <80 to 90 mm Hg or mean arterial pressure 30 mm Hg lower than baseline) with severe reduction in cardiac index (<1.8 L · min −1  · m −2  without support or <2.0 to 2.2 L · min −1  · m −2  with support) and adequate or elevated filling pressure ( eg , left ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to 15 mm Hg

3. ETIOLOGY COMMON- left ventricular failure due to extensive acute myocardial infarction ACCORDING TO SHOCK TRIAL REGISTRY

4. GENERAL ETIOLOGIC FACTORS Acute myocardial infarction Pump failure Large infarction Smaller infarction with preexisting left ventricular dysfunction Infarction extension Severe recurrent ischemia Infarction expansion Mechanical complications Acute mitral regurgitation caused by papillary muscle rupture Ventricular septal defect Free-wall rupture Pericardial tamponade Right ventricular infarction

5. Other conditions End-stage cardiomyopathy Myocarditis Myocardial contusion Prolonged cardiopulmonary bypass Septic shock with severe myocardial depression Left ventricular outflow tract obstruction Aortic stenosis Hypertropic obstructive cardiomyopathy Obstruction to left ventricular filling Mitral stenosis Left atrial myxoma Acute mitral regurgitation ( chordal rupture)

6. PATHOPHYSIOLOGY

7. CLINICAL PRESENTATION E vidence of hypoperfusion (low cardiac output ) manifested by sinus tachycardia , low urine output , and cool extremities patients who develop acute MI present with an abrupt onset of squeezing or heavy substernal chest pain; the pain may radiate to the left arm or the neck. The chest pain may be atypical, the location be in epigastric or only in the neck or arm. The pain quality may be burning, sharp, or stabbing.

8. History collection history of previous cardiac disease, use of cocaine, previous myocardial infarction (MI), or previous cardiac surgery A patient thought to have MI should be assessed for cardiac risk factors. associated symptoms are diaphoresis, exertional dyspnea, Presyncope or syncope, palpitations , generalized anxiety, and are other features indicative of poor cardiac function.

9. Physical Examination ashen or cyanotic , cool skin and mottled extremities Peripheral pulses are rapid and faint and irregular if arrhythmias are present Jugular venous distention and crackles peripheral edema also may be present . third and fourth heart sounds may be present The pulse pressure may be low, and patients are usually tachycardic signs of hypoperfusion , such as altered mental status and decreased urine output systolic murmer paradoxical thrill

10. DIAGNOSIS Laboratory Studies RFT, LFT, serum electrolytes to assess the functiong of vital organs (CBC) is helpful to exclude anemia Cardiac enzymes to diagnose MI creatine kinase- elevate within 10hrs, peaks at 24-48 hours troponin - Troponin levels peak at 14 hours after acute MI myoglobin- 4-fold rise of myoglobin over 2 hours LDH ABG

11. LDH- Elevated lactate values in a patient with signs of hypoperfusion BNP- indicator for heart failure IMAGING STUDIES echocardiography helps to deteremine mechanical causes of shock, such as acute ventricular septal defect, free myocardial wall rupture, pericardial tamponade , and papillary muscle rupture causing acute mitral regurgitation Assess the valvular and left ventricle function

12. CHEST X RAY HELP TO exclude other causes of chest pain tension pneumothorax , pneumomediastinum etc Manifest signs of LVF pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows the presence of Kerley B lines, cardiomegaly , and bilateral pleural effusions.

13. Ultrasonography Ultrasonography can be used to guide fluid management Coronary artery angiography A ssess the anatomy of the coronary arteries and need for revascularisation ECG A ssesss ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion

14. Invasive Hemodynamic Monitoring Help to precise measurement of volume status, left and right ventricular filling pressures, and cardiac output H elp guide fluid management and the use of inotropic agents and vasopressors Hemodynamic measurements can help guide fluid management and the use of inotropic agents and vasopressors

15. AHA) guidelines list pulmonary artery catheterization class I - patients with hypotension not responding to fluid administration or when mechanical complications of myocardial infarction are suspected and echocardiography is not available . class II recommendation for patients in CS who have persistent signs of hypoperfusion and in patients receiving inotropic and vasopressor drugs. (PCWP) of greater than 15 mm Hg and a cardiac index of less than 2.2 L/min/m 2

16. MANAGEMENT

17. PHARMACOLOGIC MANAGEMENT Inotropic Agents augments the coronary blood flow Dopamine Dopamine stimulates adrenergic and dopaminergic receptors Action depend upon the dose (low dose ): 1-5 mcg/kg/min IV- increase urine output and renal blood flow  (medium dose ): 5-15 mcg/kg/min IV ; increase renal blood flow, cardiac output, heart rate, and cardiac contractitlity (high dose ): 20-50 mcg/kg/min IV ; increase blood pressure and stimulate vasoconstriction; may not have a beneficial effect in blood pressure; may increase risk of tachyarrhythmias

18. Dobutamine a sympathomimetic amine with stronger beta effects than alpha effects produces systemic vasodilation and increases the inotropic state DOSAGE; 2-20 mcg/kg/min IV or IO not to exceed 40 mcg/kg/min Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia

19. Norepinephrine ( Levophed ) is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction There by increase bp and afterload Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia DOSAGE Initial: 8-12 mcg/min IV infusion; titrate to effect Maintenance : 2-4 mcg/min IV infusion

20. Milrinone It is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with positive inotropic and vasodilator effects; it has little chronotropic activity DOSAGE 50 mcg/kg loading dose by IV push over 10 minutes, then 0.375-0.75 mcg/kg/min IV  Maintenance : 1.13 mg/kg/day

21. Inamrinone Formerly known as amrinone , inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity DOSAGE Load: 0.75 mg/kg IV bolus over 2-3 minutes, THEN 5-10 mcg/kg/min IV  should not exceed 10 mg/kg/day likely to cause tachycardia than is dobutamine , and it may exacerbate myocardial ischemia

22. Vasodilators Vasodilators decrease preload and/or afterload. Nitroglycerin IV causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production intolerant of or unresponsive to SL NTG 5 mcg/min Increase by 5 mcg/min q3-5min up to 20 mcg/min, THEN   Increase by 10 mcg/min

23. DIURETICS to decrease plasma volume and edema and thereby decrease cardiac output and, consequently, blood pressure Furosemide (Lasix ) \ i nhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule. DOSAGE; Alternative: 20-40 mg IV/IM once

24. IntraAortic baloon pump(IABP )

25. IABP

26. Complications Bleeding Thrombocytopenia hemolysis, leg ischemia, aortic dissection, femoral artery injury, thromboembolism, and sepsis

27. Emergency Revascularization

28. many patients develop CS IN HSPITAL results from infarction extension, reocclusion of a previously patent coronary artery, recurrent ischemia, or decompensation of left ventricular function in the noninfarcted zone because of metabolic derangements FIBRINOLYTIC therapy as not much effective as primary coronary intervention

29. Ventricular Assist Devices (VADs ) Used for patients with CS refractory to IABP and reperfusion strategies very low cardiac output, less than 1.2 L/min/m2

30. What is a VAD? Mechanical circulatory device that is used to replace the pumping action of a failing human heart. Left ventricular failure is primarily treated using a VAD.

31. What is a VAD? Almost all VADs are made up of 3 parts: A pump that is implanted inside the body (an  implantable  VAD) or that is placed outside the body (an external or  paracorporeal  VAD) A system controller that stays outside the body and is used to program the settings of the VAD An outside energy source to power the pump—either a console or a battery pack.

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