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Home , Cardiogenic shock, Coronary care unit, Dopamine (medication), Shock (circulatory)

Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 705-712 Emergency

Cardiogenic

Clive E. Handler Department ofCardiology, Guy's , London, SE] 9RT, UK.

Introduction is a syndrome characterized by a bolytic agents and beta blockade in recent acute low , elevated left ventricular filling . pressure (usually greater than 18 mm Hg) and arterial An imbalance between supply and demand (commonly less than 80 mm Hg systolic). in the ischaemic zone of the myocardium is currently The commonest cause is extensive left ventricular believed to be the chief pathogenetic mechanism in damage resulting from myocardial infarction and this infarct extension (Hillis & Braunwald, 1977). has a poor . Other causes, which may be to limit infarct size and to support the surgically correctable and so have a better prognosis, haemodynamic state in cardiogenic shock affect one include rupture of the and or more ofthe three principal determinants ofmyocar- papillary muscle dysfunction (Table I). Prompt and dial oxygen consumption which are: (1) rate, (2) accurate haemodynamic assessment of a with left ventricular contractility, and (3) left ventricular shock is important as this will characterize the type of wall tension - determined largely by ventricular copyright. shock and provide valuable information on the most radius, systemic pressure and filling pressure. appropriate treatment. Inotropic agents, vasodilators The pathophysiological response to acute infarction and diuretics are the main used in the treatment is mediated chiefly by the sympathoadrenal response. of cardiogenic shock but they have both potentially This tends to increase , contractility and beneficial and deleterious effects on myocardial and , all of which alter unfavourably the target organ function. balance between oxygen supply and demand with further deterioration in left ventricular function. Coronary falls as blood pressure decreases. Pathogenesis The resulting low cardiac output produces pulmonary http://pmj.bmj.com/ oedema which jeopardizes further the precarious In acute myocardial infarction, the severity of left metabolic balance in the myocardium. This vicious ventricular dysfunction is related principally to the circle leads to extension of the infarct and further left extent of myocardial damage (Alonso et al., 1973), ventricular damage. presumably because a critical mass of contractile The major determinant of prognosis after myocar- is necessary to sustain pump function of the dial infarction and in cardiogenic shock is left ven- heart. The syndrome of cardiogenic shock appears to tricular function (Dwyer et al., 1983) and this can be on September 24, 2021 by guest. Protected be a direct consequence of massive myocardial des- assessed clinically (Peel et al., 1962; Killip & Kimball, truction, involving at least 45% of the left ventricle 1967), or non-invasively with radionuclide ven- (Caulfield et al., 1972). triculography (Schulze et al., 1977) or echocardiogra- Scheidt and co-workers (1970), observed that car- phy (Nador et al., 1984). diogenic shock frequently occurred hours or sometimes days after the onset of symptoms and suggested that this delay reflected progressive myocar- Clinical features dial damage. Early intervention in acute myocardial infarction has been shown to limit myocardial damage The clinical signs of cardiogenic shock reflect the low and so prevent cardiogenic shock (Pantridge, 1970). cardiac output and poor tissue and organ perfusion This approach forms the basis for the use of throm- and depend chiefly on the severity of the left ven- tricular impairment and the presence of other cardiac Correspondence: C.E. Handler, B.Sc., M.B., M.R.C.P. pathology. Accepted: 27 February 1985 Co-existing confusion makes history taking difficult C) The Fellowship of Postgraduate Medicine, 1985 Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from 706 C.E. HANDLER but ifthe patient is able to give a history it may help to Table II Differential diagnosis of cardiogenic shock exclude other causes of shock, producing a similar clinical picture (Table II). Some may be (1) Hypovolaemia. comatose. In most patients the hands and feet will be (2) (). cold and with a venous tone. There (3) Massive . clammy high will (4) (septicaemic, haemorrhagic, be a with a low systolic blood pressure neurogenic, endocrine failure, toxic, anaphylactic (commonly less than 80 mm Hg) and or shock). anuria. The character of the carotid arterial upstroke may be of help in distinguishing causes of cardiogenic shock due to left ventricular outflow tract obstruction or aortic regurgitation. Thejugular venous pressure is tions. should be flushed continuously with commonly raised in severe right ventricular infarction heparinized . The can also be used for or with causes of pulmonary . A left arterial blood gas analysis. The arterial and venous ventricular aneurysm may be detected by a dyskinetic catheters should be clearly labelled so that drugs like . Evidence ofcardiac tamponade should also diazepam and barbiturates are not given into an be sought clinically. may point to serious . valvular or septal disorders but often the low cardiac In patients with heart disease, measurement of only output makes this difficult. the may provide misleading information as it is a poor guide to left ventricular function. Very often a patient may have been given Management diuretics or opiates before reaching the . These drugs reduce the left ventricular end- Haemodynamic measurements diastolic pressure by reducing the preload and alth- ough the patient may still have a third heart sound and The differential diagnosis of cardiogenic shock is clinical and radiographic features of pulmonary presented in Table II. oedema, the left ventricular end-diastolic pressure An accurate haemodynamic assessment is invalua- may be within normal levels. On the other hand, acopyright. ble in diagnosing the type and severity of circulatory proportion ofpatients without clinical evidence ofleft failure, selecting the optimum medical treatment and assessing the response to . Right and left ventricular filling pressures and cardiac output can be measured with a flow-directed, balloon-tipped ther- modilution catheter (Swan et al., 1970). Direct arterial catheterization allows an accurate assessment ofblood

pressure which may be otherwise inaccurate or un- http://pmj.bmj.com/ recordable when measured by a cuff sphygmoman- ometer in a patient who has peripheral vasoconstric- tion. For peripheral artery cannulation the is preferred as the hand usually has collateral circulation from the ulnar artery which should be tested before catheterization using Allen's test. Infec- tion and ischaemia are the main but rare complica- on September 24, 2021 by guest. Protected Table I Causes of cardiogenic shock (1) Left ventricular infarction. (2) After cardiopulmonary bypass and cardiac . (3) Acute mechanical disorders (septal or free wall rup- ture, mitral or aortic regurgitation, left ventricular aneurysm). (4) Tachyarrhythmias or bradyarryhthmias. (5) Left ventricular outflow tract obstruction (, hypertrophic obstructive ). (6) Left ventricular inflow tract obstruction (mitral sten- osis, left atrial myxoma, right ventricular infarction). (7) Chronic heart muscle disease (end-stage car- diomyopathy). deflated Swan-Ganz catheter in the right in a patient with resolving pulmonary oedema Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from

CARDIOGENIC SHOCK 707 ventricular failure may have wedge pressures exceed- ing 18mmHg Catheterization of the right heart using a balloon- tipped, flow-directed, Swan-Ganz catheter allows measurement of the pulmonary occluded (wedge) pressure and an estimate of left atrial pressure (left ventricular preload or end-diastolic pressure). It is indicated in all patients with severe circulatory failure. Cardiac output can also be measured if the catheter has a thermistor. Swan-Ganz catheters can be inserted at the bedside and the tip position ascertained by pressure measurements. It is, however, easier to position the Figure 3 Normal pressure trace (mm Hg) from a Swan- catheter using X-ray guidance and this is important in Ganz catheter withdrawn from the wedge position patients with cardiogenic shock who do not tolerate (PAW) (top left) to the pulmonary artery (PA), to the lying flat for long periods. Problems in inserting and right ventricle (RV) to the right atrium (RA) showing maintaining Swan-Ganz catheters and interpretation characteristically normal waveforms. of the pressure recordings have been well reviewed Wiedemann et al., 1984a,b). The catheter can be inserted in several sites for venous access to the In cardiogenic shock due to myocardial infarction, pulmonary artery (Figures 1 and 2) but the subclavian left ventricular compliance is decreased, the left ven- and internal jugular are the most widely used. tricular end-diastolic pressure is usually equal to or is a well recognized complication with greater than 18 mm Hg and the below subclavian puncture. 1.8 I/min/m2. Prognosis is related to haemodynamic The criteria for a true wedge position include a mean findings and worsens as the pulmonary wedge pressure pulmonary wedge pressure lower than or equal to the increases (Forrester et al., 1976). pulmonary artery diastolic pressure and a characteris- In cardiac tamponade the filling pressures will be copyright. tic left atrial pressure waveform (Figure 3). The main equal on both sides of the heart. Right ventricular complications ofpulmonary artery catheterization are infarction may be diagnosed with some certainty by infection, pulmonary artery rupture, pulmonary infar- electrocardiographic changes (Morgera et al., 1984) ction, balloon rupture, knotting of the catheter, and by pressure measurements (Dell'Italia et al., complications near the insertion site (pneumothorax, 1984). The right ventricular filling pressure is raised arterial puncture and air embolism) and and the patient will usually have a raised jugular which are usually transient (Civetta, 1983). venous and right atrial pressure which may be further elevated in the presence of tricuspid regurgitation. It is http://pmj.bmj.com/ important to diagnose right ventricular infarction because diuretic treatment may be dangerous as an increased and not decreased right ventricular filling pressure is required to maintain cardiac output. An elevated pulmonary wedge pressure with a normal left ventricular end-diastolic pressure may be due to mitral regurgitation or stenosis, or rarely to a

left atrial myxoma or . Sector and M-mode on September 24, 2021 by guest. Protected will usually be diagnostic. Low right heart filling pressures with relatively normal left heart filling pressures are found in hy- povolaemic, septic, neurogenic, toxic and anaphylac- tic shock. General management of cardiogenic shock Relief of pain and with adequate doses of opiates is an important part of the treatment. Hy- Figure 2 Portable AP X-ray showing the tip of a potension, respiratory depression and nausea may deflated Swan-Ganz catheter in the 'wedge' position. result and so care is required in their use. Anti-emetics N.B. The exact tip position is confirmed by the pressure are usually given simultaneously. reading. Oxygenation is important and this may need to be Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from 708 C.E. HANDLER given by depending on the be useful in the pre- and post-operative stabilization of clinical status of the patient and the blood gases. patients but generally has a limited place in the Positive pressure ventilation may depress cardiac treatment of a patient with cardiogenic shock (Scheidt output (Jardin et al., 1981). It decreases preload (Qvist et al., 1973). Recently, however, it has been shown to et al., 1975) and clears pulmonary oedema. Baseline be of some benefit (Weiss et al., 1984). The aim of haematology, biochemistry and arterial blood gases counterpulsation of blood is to improve coronary should be performed and any metabolic abnormalities filling during diastole and to reduce left ventricular corrected. Blood cultures and samples for bac- work by lowering aortic systolic pressure. The widely teriology should be taken if appropriate. varying results for the efficacy of this treatment in cardiogenic shock are probably explained by the Specific measures differing definitions of shock (Kuhn, 1978). Cardiac arrhythmias need specific treatment and Drugs electrical is required if antiarrhythmic drugs are ineffective. Cardiac pacing is required for Diuretics, inotropic agents and vasodilators are the atrioventricular block with associated three major classes of drugs used in the treatment of and low cardiac output. Although atrial synchronized cardiogenic shock. There is no convincing evidence, pacing improves haemodynamics significantly however, that long term survival is improved or that (Fowler et al., 1984; Love et al., 1984), long-term left ventricular myocardium is preserved with the use benefits are unclear. of any of these agents (Rude, 1983; Sobel, 1984). In cardiogenic shock, there is a risk of damage to other organs. Shock is quite common and Diuretics remains difficult to treat effectively. The subject has been recently reviewed (Stevens & Raffin, 1984a,b). Diuretics must be used cautiously in cardiogenic shock After the patient has been resuscitated as far as as they may cause severe ototoxicity in the presence of possible, surgically correctable causes of cardiogenic renal failure. They are most useful in less severe cases shock should be looked for clinically and also with of shock when the left ventricular filling pressurecopyright. echocardiography and measurements of oxygen 20 mm Hg is less than Frusemide and ethacrynic acid saturation from the Swan-Ganz catheter. Technical are the loop diuretics most commonly used. Frusemide advances in nuclear cardiac imaging and quantitation also reduces left ventricular end-diastolic pressure by may, in the future, allow useful measurements of reducing and dilating the venous vascular ejection fraction and left ventricular wall movement to bed. The consequent reduction in left ventricular end- be made at the bedside but these methods need further diastolic volume is beneficial as left ventricular wall evaluation and are not widely available. tension is also reduced thus decreasing myocardial

If haemodynamically important septal rupture, oxygen consumption. Diuretics are dangerous in http://pmj.bmj.com/ aneurysm, aortic or mitral regurgitation are suspected, hypovolaemic shock and in right ventricular infarc- coronary and left ventricular angiography may be tion as cardiac output may be further critically necessary as early correction of these disorders may reduced. Therefore a serial assessment of left ven- improve prognosis. The results of coronary revas- tricular filling pressure is imperative in hypotensive cularization alone, however, have been generally dis- patients being treated with these agents. appointing (Mundth, 1977). When diuretics are unhelpful in the treatment of The optimum filling pressure of the left ventricle shock, the remaining therapeutic approaches focus on after infarction is 14- 18 mm Hg (Crexells et al., 1973). enhancing myocardial contractility with inotropic on September 24, 2021 by guest. Protected Most patients are already at the top of their Starling agents and unloading the heart with vasodilator drugs. curve and will need a lowering of their left ventricular filling pressure. Further increases in preload provide little or no haemodynamic improvement and may Inotropic agents increase any existing pulmonary oedema. A small proportion ofpatients, however, may have pulmonary The majority of patients with cardiogenic shock will wedge pressures at the upper limit of normal need inotropic agents. A major drawback in their use (12 mm Hg) and others may have co-existing hy- is that they may, in certain doses, increase oxygen povolaemia. In these cases a fluid challenge such as requirements by the failing left ventricle where the low molecular weight dextran (50 ml increments) to energy balance may be jeopardized further by the increase the pulmonary wedge pressure to 20 mm Hg presence of pulmonary oedema. may improve the cardiac output (Rackley et al., 1975; Sympathomimetic may improve cir- Russel et al., 1976). culatory haemodynamics in cardiogenic shock in the Intra-aortic balloon pumping has been reported to short-term but long-term survival is rarely improved Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from CARDIOGENIC SHOCK 709

(Sobel, 1984). Driving the heart out offailure is rarely, unclear but has been advocated as the if ever, possible since the diseased myocardium is of first choice in patients with mild hypotension unable to respond for long periods to extra metabolic and in chronic low output states (Loeb et al., 1977). demands (Katz, 1973). may be required if the blood pressure remains low in spite of higher doses of dobutamine Digitalis glycosides (Rude, 1983). Digitalis has a very limited place in the current treatment of shock (Cohn et al., 1969). It confers no benefit in acute infarction (Balcon et al., 1968) and This has both beta-I and beta-2 agonism and no may increase infarct size (Varonkov et al., 1977). It significant vasoconstrictor effects. It increases heart may, however, be ofsome use in patients with mild left rate, myocardial contractility, cardiac output and ventricular failure as it may decrease filling pressure decreases vascular resistance (Smith et al., 1967). and increase cardiac output (Mason et al., 1977). Its Because it increases myocardial oxygen consumption arrhythmogenic activity is a major cause for concern and is arrhythmogenic, it is potentially dangerous in particularly in ischaemic myocardium (Morris et al., recent infarction (Gunnar et al., 1968). It may be 1969). The digitalis glycosides may also increase useful in shock occurring after surgery. impedance to left ventricular ejection (Marcus, 1980) with loss of any inotropic gain. Nevertheless, it is Noradrenaline useful in controlling supraventricular arrhythmias, particularly poorly controlled , where This has beta-I and alpha action and increases co-existing hypotension contra-indicates the use of arterial blood pressure by increasing myocardial con- or other anti-arrhythmic agents with similar tractility and peripheral . It produces negative inotropic activity (Mason et al., 1977). only minor changes in cardiac output. It may, like other sympathomimetic agents, damage the heart due Dopamine to the ischaemia resulting from the increased

afterload. In addition, it is arrhythmogenic and may copyright. Dopamine, an endogenous catecholamine and the also decrease renal blood flow. These disadvantages immediate precursor of noradrenaline has mainly usually offset any advantage from an increased sys- beta-I agonist activity. Its useful renal and coronary tolic blood pressure, although it may have a place in a vasodilator properties are probably mediated by severely hypotensive patient who has not responded to dopamine receptors. At low infusion rates of 2- 5 yg/ either (or both) dopamine or dobutamine. Neverthe- kg/min it produces increases in cardiac contractility, less the prognosis remains extremely poor in this cardiac output and renal blood flow with negligible patient group.

changes in heart rate (Kho et al., 1980; Timmis et al., http://pmj.bmj.com/ 1981), although the peripheral resistance may decrease Vasodilator drugs slightly. At higher doses (5-10 tg/kg/min) it increases the arterial pressure, peripheral resistance and heart The rationale for the use of vasodilators is that they rate but renal blood flow may fall (Mueller et al., decrease both afterload and preload, thereby reducing 1978). At even higher doses (greater than 20 iAg/kg/ left ventricular work and myocardial oxygen consum- min) it may provoke ventricular arrhythmias (Loeb et ption. al., 1974). It is particularly useful in patients with renal They are useful in but their hypotensive dysfunction as it also increases . effects restrict their role in cardiogenic shock where on September 24, 2021 by guest. Protected tissue perfusion is already critically reduced (Chat- Dobutamine terjee & Parmley, 1977). They are of greatest value in cardiogenic shock where forward failure is due to a Dobutamine, a synthetic catecholamine with surgically correctable problem like interventricular predominantly beta-I adrenoceptor agonist proper- septal rupture or severe mitral regurgitation rather ties, has a variable effect on peripheral vascular than primary muscle disease. They have been used in resistance although it is usually reduced. It is less combination with dopamine and other inotropes inotropic than dopamine but in contrast to dopamine, to counteract sympathomimetic-induced peripheral may produce a beneficial fall in pulmonary vasoconstriction. Cardiac arrhythmias are not a wedge pressure (Leier et al., 1978). Both dobutamine problem with vasodilators as they have no direct and dopamine are arrhythmogenic and dobutamine cardiac effects. may be more so (Loeb et al., 1974). Nitroprusside is of some value in acute myocardial Any clear superiority of one of these agents in infarction because its short half-life makes control of cardiogenic shock complicating acute infarction is arteriolar and venous dilatation fairly easy. In acute Postgrad Med J: first published as 10.1136/pgmj.61.718.705 on 1 August 1985. Downloaded from 710 C.E. HANDLER infarction it has been shown to decrease left ven- Future directions tricular filling pressure and increase cardiac output in patients with moderate or severe left ventricular Reduction in mortality from cardiogenic shock failure (Chatterjee, 1976). Theoretically, nitroprus- ultimately lies in the prevention of coronary disease. side, in common with agents with a similar mode of Limitation ofinfarct size may improve prognosis after action (Hillis et al., 1981), may increase myocardial infarction and this subject is currently ofconsiderable ischaemia by coronary 'steal' and should not be given interest (Kubler & Doorey, 1985). Various interven- to patients in whom cardiogenic shock is due to tions including beta blockers (Peter et al., 1978), ischaemic heart disease (Rude, 1983). Cyanide toxicity intravenous nitroglycerin (Bussman et al., 1981), is a dose-related complication and can be a serious hyaluronidase (Maroko et al., 1977) and coronary hazard during prolonged administration although thrombolysis (Taylor et al., 1984; Mathey et al., 1981; hydroxocobalamin may provide some protection. It Kasper et al., 1984) and surgical has also been reported to produce ventilation-per- (DeWood et al., 1979) have been tried but large fusion mismatch (Bencowitz et al., 1984). controlled studies with adequate follow up are re- The major effect of nitroglycerin is to reduce quired to establish their efficacy. preload. It also reduces left atrial pressure in acute Cardiogenic shock is a very difficult condition to myocardial infarction (Borer et al., 1975) and in- treat and has a bad prognosis. An accurate haemodyn- creases coronary flow directly. It produces no sig- amic assessment is important to distinguish other nificant increases in cardiac output (Chatterjee, 1976) forms of shock where the management is different and but is probably the vasodilator of choice in car- the prognosis may be good. diogenic shock due to ischaemia. Of other vasodilators isosorbide dinitrate is availa- ble for intravenous use but there is at present little information on its value in cardiogenic shock. Phen- tolamine is a weak alpha- and beta-adrenoceptor Acknowledgements blocking agent but is a potent vasodilator. It is of I am very grateful to Dr Edgar Sowton, Dr Adam Timmis greatest value in patients with severe left ventricular and Dr Jonathan Crick for their constructive criticism of the copyright. impairment complicating myocardial infarction. manuscript.

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