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Transcript
CARDIOGENIC SHOCK William Harvey demonstrating his theory of the circulation of the blood to King Charles I. Oil on canvas, Robert Hannah, 1848, Royal College of Physicians, London. “…And now I may be allowed to give in brief my view of the circulation of the blood, and to propose it for general adoption. Since all things, both argument and ocular demonstration, show that the blood passes through the lungs, and heart by the force of the ventricles, and is sent for distribution to all parts of the body, where it makes its way into the veins and porosities of the flesh, and then flows by the veins from the circumference on every side to the centre, from the lesser to the greater veins, and is by them finally discharged into the vena cava and right auricle of the heart, and this in such a quantity or in such a flux and reflux thither by the arteries, hither by the veins, as cannot possibly be supplied by the ingesta, and is much greater than can be required for mere purposes of nutrition; it is absolutely necessary to conclude that the blood in the animal body is impelled in a circle, and is in a state of ceaseless motion; that this is the act or function which the heart performs by means of its pulse; and that it is the sole and only end of the motion and contraction of the heart”. William Harvey, Chapter XIV, “On the Motion of the Heart and Blood in Animals”, 1628 William Harvey made one of medicine’s most important discoveries when he deduced the circulation of the blood. For almost 1500 years, no one had challenged the doctrine established by the Roman physician Galen that venous blood “somehow” proceeded from the liver and that arterial blood “somehow” proceeded from the heart. Exactly were it was going seemed to be anybody’s guess. There was certainly no thought of a circulatory motion of the blood in Galen’s theory. In his Essay on “On The Motion of the Heart and Blood in Animals” in 1628, Harvey rejected Galen’s theories and for the first time fully explained the circulation of the blood and the central role played in this, by the heart. Difficult as it is to imagine now his new theory was considered very controversial at the time. His theory threw doubt onto the common practice of bloodletting (a “standard” medical practice by doctors from ancient times through to as recently as the Eighteenth century.) It was only after his death that his theory became widely accepted. Harvey would have been one of very few in the 17th century capable of understanding the 21st century concept of cardiogenic shock. CARDIOGENIC SHOCK Introduction Clinical Definition: Cardiogenic shock is an acute impairment of myocardial contractility presenting as a clinical syndrome of: 1 1. 2. A low systolic blood pressure: ● < 90 mmHg, or a value of greater than 30 mmHg below normal levels in a hypertensive patient ● For a period of at least 30 minutes Together with clinical evidence of decreased tissue perfusion, (such as peripheral vasoconstriction, altered conscious state and urine output below 20 mls / hr) Definition based on Hemodynamic Parameters: Cardiogenic shock may also be defined by the acute presence of all three of: 1. Systolic pressure less than 90 mmHg. 2. A cardiac index of less than 2.2 L / min / M2. 3. A pulmonary capillary wedge pressure of greater than 15 mmHg. Pathophysiology Causes: 1. Myocardial infarction, this is by far the commonest cause. ● Left ventricular, when there is critical loss (> 40%) of myocardium. The effects of recent and old infarcts will be additive. This scenario is seen with extensive anterior infarction. ● Right ventricular infarction. This is much less common. It is seen in association with inferior infarcts. 2. Drug and poison overdose. 3. Acute decompensation in patients with cardiomyopathies. Other causes are less common, but may include the following: 4. Severe myocarditis. 5. Severe myocardial contusion. 6. Myocardial failure secondary to acute structural lesions: 7. ● Severe mitral regurgitation. ● Acute aortic regurgitation. ● Rupture of the interventricular septum. ● Large left ventricular aneurysm. Severe outflow obstruction: ● Aortic stenosis. ● HOCM Note that there are many other cardiac causes of poor cardiac output and shock that are not due to intrinsic contractility problems. By convention these are not included in the strict definition of cardiogenic shock. These conditions include massive pulmonary embolism, cardiac tamponade, tension pneumothorax and arrhythmias. Reduced myocardial contractility due to severe sepsis is defined separately as septic shock. Prognostic Features 1. Worse with increasing age. 2. Underlying type and extent of pathology. 3. Associated medical problems. 4. A number of classifications have been developed to correlate the extent of pump failure with eventual mortality following an AMI. They include the Killip-Kimball and the Forrester-Diamond-Swan classifications. The Killip-Kimball Classification (based on clinical criteria) CLASS I No failure 5% mortality CLASS II Mild failure, basal creps & S3 15-20% mortality CLASS III Frank Pulmonary Edema 40% mortality CLASS IV Cardiogenic Shock 80% mortality The Forrester-Diamond-Swan classifications, (based on hemodynamic parameters): GROUP Cardiac Index (L/min/M2) PAWP (mmHg) Mortality I >2 <18 3% II >2 >18 9% III <2 <18 23% IV <2 >18 51% Investigations In patients with suspected cardiogenic shock, the following investigations will be needed: Blood tests ● FBE ● U&Es and glucose ● Troponin levels. ● ABGs CXR To look for: ● Associated pulmonary edema. If the lung fields are clear consider the possibility of a RV infarction, especially in the setting of an inferior myocardial ischemia. ● Other associated pathology. ECG To establish ● The rhythm ● The presence of any underlying ischemia or infarction. A normal ECG will virtually exclude a diagnosis of cardiogenic shock due to myocardial infarction. Anterior infarctions are much more commonly associated with cardiogenic shock than are inferior infarctions. If a patient appears to be in cardiogenic shock and the ECG shows an inferior infarction, then consider the possibility of RV infarction or other complicating pathology such as cardiac tamponade. Echocardiography The most important investigation, if available, is bedside echocardiography. It should ideally be done in all cases of suspected cardiogenic shock. It will: ● Confirm the diagnosis of cardiogenic shock. ● Establish the type (left versus right sided, systolic versus diastolic) and the severity of the myocardial failure. ● Rule out the presence of any potentially reversible “structural” causes, such as valvular lesions, free wall ruptures or interventricular septal ruptures. ● Help rule out other pathologies such as aortic dissection, massive PE, or cardiac tamponade. Management Management steps include the following: 1. General measures. 2. Optimizing fluid volume status. 3. Inotropic drug support. 4. Mechanical supports. 5. Specific measures. 5. Early consultation (ICU/ cardiology) General measures: 1. Immediate attention to any ABC issues, especially oxygenation. 2. Pain relief 3. Treat any arrhythmias. 4. Treat hyperkalemia or hypokalemia. 5. Continuous ECG monitoring and pulse oximetry. Optimizing fluid volume status 1. T o monitor volume status and “central” pressures insert an IDC and CVC. ● Insertion of a CVC should not delay inotropic support. Inotropes can be given via a cubital fossa vein in the first instance. ● Femoral lines can be relatively quickly placed and will also give a reasonable estimate of central pressures. 2. Fluid boluses can be given (100 - 250 mls) to optimize central pressures to a CVC of 10 cm water (15 mmHg PCWP) 3. In cases of right ventricular infarction with cardiogenic shock, fluid therapy needs to be somewhat more aggressive (up to 30 cms of water) Inotropic Drug Support Options for inotropic drug support include the following: Most commonly: 1. Adrenaline 2. Milrinone 3. Noradrenaline Inotropes will improve contractility but with the following adverse effects: ● Tachyarrhythmias. ● Increased myocardial oxygen demand ● Hyperglycemia and reduce glucose tolerance ● Lactic acidosis ● Vasocontriction-induced reduction in organ blood flow and ischaemia ● Aggravation of hypotension with some agents, (isoprenaline, dobutamine) Most commonly adrenaline will be the agent of choice for acute cardiogenic shock. If this proves insufficient then the addition of the phosphodiesterase inhibitor milrinone should be considered. Milrinone as well as being a good positive inotropic agent will also cause vasodilatation and so it is usually used in conjunction with noradreanaline. Therefore if adrenaline is not successful, it may be replaced with milnirone and noradrenaline infusions. Milrinone is primarily used in the ICU setting. Note that milrinone should only be commenced in the ED after discussion with ICU/ ED consultant. Less commonly other agents may be considered, (usually after cardiology consultation): ● Dobutamine ● Dopamine ● Isoprenaline Mechanical supports When pharmacological measures are insufficient some patients may be suitable for mechanical cardiac supports. These may include: ● The intraaortic balloon pump ● ECMO. Mechanical support devices, of which IABP is the most commonly used, have the major advantage compared pharmacologic agents of being able to improve coronary perfusion and cardiac performance, while at the same time reducing myocardial ischemia and cardiac work Indications for the Intraaortic balloon pump device include conditions that have a potentially reversible problem, including: ● Coronary occlusion. ● Severe mitral regurgitation, (AI is contra-indicated) ● Post trauma ● Drug overdose ● Patient’s on a wait list or those who may be suitable for cardiac transplantation. Specific measures 1. By far the commonest cause of cardiogenic shock is coronary artery occlusion and the best chance of survival is procedural intervention. ● Although not specifically contra-indicated, thrombolytic agents have not been shown to improve outcome in cardiogenic shock from coronary artery occlusion. ● Emergency PTCA or CABG surgery offer the best prognosis in acute cardiogenic shock due to myocardial infarction. 2. In some patients there may be a surgically correctable lesion such as severe mitral incompetence or septum rupture. 3. If facilities are available some patients may be suitable for emergency cardiac transplantation. Disposition: Early consultation should always be sought with: ● ICU ♥ ● Any patient with cardiogenic shock should be referred early to ICU. Cardiology ♥ Appendix 1 Any patient with cardiogenic shock due to myocardial infarction should be referred early to the on call cardiologist in order to plan for a possible PCI or emergency CABGs. Inotropic Agents Drug/Receptor a-1 a-2 ß-1 ß-2 ß-3 Noradrenaline ++ ++ ++ + + Adrenaline ++ ++ ++ ++ + Dopamine ++ ? ++ + ? Dobutamine ++ + ? Isoprenaline ++ ++ ++ - Increase: contractility, HR, renin &NA. vasodilate coronaries Increase HR contractility vasodilation bronchodilation Metabolic effects brochodilation vasodilation contractility fall Inhibit Na reabsorption vasodilate: renal, cerebral, splanchnic. Actions: Vasoconstriction, increase Postjunctional: contractility, vasoconstriction (decrease HR) prejunctional: decrease NA DA-1 & 2 ++ Dobutamine ● Useful in cases of mild hypotension (systolic pressures of 80-90 mmHg) ● Improves contractility and may reduce afterload, however may worsen hypotension Dopamine ● Useful in moderate hypotension (systolic pressures of 60-80 mmHg) ● Improves contractility and with alpha effects helps raise peripheral vascular resistance, however tachycardia may be problematic. Isoprenaline ● This is most useful as a chronotropic agent for patients with severe bradyarrhythmias. ● It has significant beta 2 effects, however which may worsen hypotension. Adrenaline ● Useful in cases of severe hypotension, (systolic pressures less than 60 mmHg) ● Improves contractility and maximally improves peripheral vascular resistance and diverts blood to vital organs. Milrinone ● This is a phosphodiesterase inhibitor with positive inotropic effects. ● It has some vasodilatory effects and so is usually used in conjunction with an agent that gives some vasoconstriction such as noradrenaline. References: 1. Robert M. Califf, James R. Bengtson: Cardiogenic Shock NEJM, vol 3330 no. 24. June 16 1994. Dr J Hayes Dr Graeme Duke Dr John Green. Reviewed 23 September 2006