INVITED EDITORIAL
European Journal of Heart Failure (2015) 17, 466–467 doi:10.1002/ejhf.265
Understanding cardiogenic shock Alain Rudiger*
This article refers to ‘Clinical picture and risk prediction of short-term mortality in cardiogenic shock’† by Veli-Pekka Harjola et al., published in this issue, European Journal of Heart Failure (2015); 17: 501–509. Cardiogenic shock is the most severe form of acute heart failure.1 It is defined as pump failure despite adequate preload, leading to tissue hypoxia and organ dysfunction. In particular, low mixed venous oxygen saturations and elevated lactate levels are surrogates for tissue hypoxia, while encephalopathy and low urine output indicate organ dysfunction. Using this definition, Harjola and co-workers identified 220 patients with cardiogenic shock in a multicentre observational study.2 Coronary artery disease was the most common underlying cardiac disease, and myocardial ischaemia was the most important trigger for decompensation. In-hospital survival of 63% was better than in other registries, in which mortality was greater than 50%.3 The authors created the CardShock risk score including information on patient characteristics (age), underlying cardiac disease (coronary artery disease), trigger for decompensation (myocardial ischaemia), cardiac function (left ventricular ejection fraction), surrogates of tissue hypoxia (elevated lactate levels), and evidence of organ dysfunction (encephalopathy, renal dysfunction). Not surprisingly, mortality increased with a higher score. Potentially, the CardShock risk score will allow better patient selection for particular therapies, for example early admission to an intensive care unit. It will also help to better characterize patients in future studies on cardiogenic shock. There is one aspect of this study that I would like to highlight, as I think it is of great clinical relevance. Twenty-four per cent of the study patients had shock at presentation to the hospital, whereas 76% developed shock after hospital admission. This information is in line with results from the Swiss AMIS plus registry, in which 72% of patients with acute coronary syndromes complicated by cardiogenic shock developed their haemodynamic instability after hospital admission.4 While shock might evolve from a worsening cardiac disease such as ongoing myocardial ischaemia, haemodynamic deterioration will develop, at least in some patients with acute heart failure, because of inappropriate medical treatment. Tables 1 and 2 list drugs commonly used and interventions frequently performed in patients with acute heart failure, which can potentially contribute to the shock state and promote organ dysfunction. I can recall several patients who rapidly improved from ‘cardiogenic shock’ with
............................................................................................................................
Cardio-surgical Intensive Care Unit, Institute of Anaesthesiology, University Hospital Zurich, Raemistrasse 100, CH–8091 Zurich, Switzerland
Table 1 Adverse drug effects contributing to shock and organ dysfunction in patients with acute heart failure (Adverse) effects Risks ......................................................................... Diuretics
Hypovolaemia
Insufficient preload Pre-renal kidney dysfunction Hypokalaemia, Arrhythmia (e.g. atrial hypomagnesaemia fibrillation) Beta-blockers Negative chronotrope action Insufficient heart rate Negative inotrope action Decrease in cardiac contractility ACE-inhibitors Vasodilation Hypotension Worsening kidney function Opioids Vasodilation Hypotension Nausea Aspiration with respiratory failure Anticoagulants Bleeding (e.g. Haemorrhagic shock retroperitoneal) Contrast media Allergic reactions Anaphylactic shock Renal toxicity Worsening kidney function ACE, angiotensin-converting enzyme.
Table 2 Interventional complications contributing to shock and organ dysfunction in patients with acute heart failure Pulmonary artery catheter Arrhythmia (atrial fibrillation, ventricular tachycardia) Perforation → pericardial tamponade → obstructive shock (Tension) pneumothorax → obstructive shock Bleeding → haematothorax → hypovolaemic shock Catheter infection/sepsis → distributive shock Mechanical ventilation Sedation → vasodilatation, hypotension Positive intrathoracic pressure → increased RV afterload → RV dysfunction Coronary angiography: Coronary perforation → pericardial tamponade → obstructive shock Bleeding (e.g. retroperitoneal) → hypovolaemic shock Anaphylactic reactions caused by contrast media → distributive shock Cardiac surgery Myocardial injury → pump failure, arrhythmia Bleeding → hypovolaemic shock Hypervolemia → respiratory failure, renal dysfunction Activation of SIRS → distributive shock, renal dysfunction RV right ventricular; SIRS systemic inflammatory response syndrome.
fluid administration, as shock was a consequence of insufficient preload resulting from the excessive use of diuretics.
The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology. †doi:10.1002/ejhf.260 *Corresponding author: +41 442559621; Fax: +41 442553181; E-mail: [email protected]
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
467
Figure 1 The evolution from acute heart failure to cardiogenic shock to multi-organ failure. Malperfusion of tissues triggers an inflammatory reaction, most likely by the release of damage associated molecular patterns (DAMPs) from the damaged cells. These DAMPs are recognized by pattern recognition receptors from immune cells, and a consecutive intracellular cascade is activated leading to the activation and/or suppression of particular genes. These genes encode for pro- and anti-inflammatory cytokines, which activate adaptive mechanisms and enable local repair. At sufficient concentrations, however, these cytokines trigger a systemic inflammatory response (SIRS), which contributes to vascular leakage, vasodilation, and consecutive hypotension. Shock and SIRS can induce multiple organ failure (MOF), which eventually might cause death, if the condition cannot be reversed promptly by adequate treatment.
So, how to best manage patients with cardiogenic shock? First, the underlying cardiac disease and the trigger for decompensation must be identified, as understanding the pathophysiology at play is crucial for the correct treatment. In particular, reversible causes of heart failure must be looked for and treated adequately, which in many circumstances will require prompt interventions
.........................................................................................................................................................
Invited Editorial
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
(e.g. balloon angioplasty in acute myocardial ischaemia resulting from coronary artery disease) or emergency cardiac surgery (e.g. mitral valve replacement in acute mitral regurgitation caused by papillary muscle rupture). Patients with a treatable underlying disease causing cardiogenic shock usually have a better prognosis than patients without.5 Second, cardiogenic shock must be reversed within hours, which includes optimization of cardiac preload and afterload, control of heart rate and the use of inotropes to increase contractility. While the condition is reversible in the early phase with adequate treatment, prolonged cardiogenic shock will cause multiple organ failure and eventually death (Figure 1). Hence, if cardiogenic shock cannot be reversed with the measures mentioned above, mechanical extracorporeal life support (ECLS) should be evaluated before irreversible organ damage has established.6 The ECLS treatment will buy some time for decision-making. In some patients care will have to be redirected to palliation because of futility of further treatment. In others, ECLS will bridge to recovery (e.g. acute myocarditis) or bridge to other types of assist devices and/or heart transplantation.7 Third, failing organs (kidneys, lungs) must be supported by intensive care with the caveat of first doing no harm.8 As soon as the patient can be stabilized, early rehabilitation must be started. The patient should be enrolled in a specialized heart failure follow-up programme, offering the full spectrum of pharmacological and non-pharmacological treatment options. In summary, a multi-disciplinary (cardiologists, intensivists, cardiac surgeons, and many more) and multi-professional (doctors, nurses, physiotherapists, and many others) approach is necessary to save the lives of critically ill patients with cardiogenic shock.
References 1. Rudiger A, Harjola V-P, Müller A, Mattila E, Säila P, Nieminen M, Follath F. Acute heart failure: clinical presentation, one-year mortality and prognostic factors. Eur J Heart Fail 2005;7:662–670. 2. Harjola VP, Lassus J, Sionis A, Kober L, Tarvasmäki T, Spinar J, Parissis J, Banaszewski M, Silva-Cardoso J, Carubelli V, Di Somma S, Tolppanen H, Zeymer U, Thiele H, Nieminen MS, Mebazaa A. Clinical picture and risk prediction of short-term mortality in cardiogenic shock. Eur J Heart Fail 2015;17:501–509. 3. Zannad F, Mebazaa A, Juillière Y, Cohen-Solal A, Guize L, Alla F, Rougé P, Blin P, Barlet M-H, Paolozzi L, Vincent C, Desnos M, Samii K, for the EFICA Investigators. Clinical profile, contemporary management and one-year mortality in patients with severe acute heart failure syndromes: The EFICA study. Eur J Heart Fail 2006;8:697–705. 4. Jeger RV, Radovanovic D, Hunziker PR, Pfisterer ME, Stauffer JC, Erne P, Urban P, Investigators APR. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med 2008;149:618–626. 5. Rudiger A, Businger F, Streit M, Schmid ER, Maggiorini M, Follath F. Presentation and outcome of critically ill medical and cardiac-surgery patients with acute heart failure. Swiss Med Wkly 2009;139:110–116. 6. Thiele H, Ohman EM, Desch S, Eitel I, de Waha S. Management of cardiogenic shock. Eur Heart J 2015; pii:ehv051 [Epub ahead of print]. 7. Sommer W, Marsch G, Kaufeld T, Rontgen P, Beutel G, Tongers J, Warnecke G, Tudorache I, Schieffer B, Haverich A, Kuhn C. Cardiac Awake Extracorporeal Life Support-Bridge to Decision? Artif Organs 2015; doi:10.1111/aor.12396 [Epub ahead of print]. 8. Singer M, Glynne P. Treating critical illness: The importance of first doing no harm. PLoS Med 2005;2:e167.
Copyright of European Journal of Heart Failure is the property of John Wiley & Sons, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
European Journal of Heart Failure (2015) 17, 466–467 doi:10.1002/ejhf.265
Understanding cardiogenic shock Alain Rudiger*
This article refers to ‘Clinical picture and risk prediction of short-term mortality in cardiogenic shock’† by Veli-Pekka Harjola et al., published in this issue, European Journal of Heart Failure (2015); 17: 501–509. Cardiogenic shock is the most severe form of acute heart failure.1 It is defined as pump failure despite adequate preload, leading to tissue hypoxia and organ dysfunction. In particular, low mixed venous oxygen saturations and elevated lactate levels are surrogates for tissue hypoxia, while encephalopathy and low urine output indicate organ dysfunction. Using this definition, Harjola and co-workers identified 220 patients with cardiogenic shock in a multicentre observational study.2 Coronary artery disease was the most common underlying cardiac disease, and myocardial ischaemia was the most important trigger for decompensation. In-hospital survival of 63% was better than in other registries, in which mortality was greater than 50%.3 The authors created the CardShock risk score including information on patient characteristics (age), underlying cardiac disease (coronary artery disease), trigger for decompensation (myocardial ischaemia), cardiac function (left ventricular ejection fraction), surrogates of tissue hypoxia (elevated lactate levels), and evidence of organ dysfunction (encephalopathy, renal dysfunction). Not surprisingly, mortality increased with a higher score. Potentially, the CardShock risk score will allow better patient selection for particular therapies, for example early admission to an intensive care unit. It will also help to better characterize patients in future studies on cardiogenic shock. There is one aspect of this study that I would like to highlight, as I think it is of great clinical relevance. Twenty-four per cent of the study patients had shock at presentation to the hospital, whereas 76% developed shock after hospital admission. This information is in line with results from the Swiss AMIS plus registry, in which 72% of patients with acute coronary syndromes complicated by cardiogenic shock developed their haemodynamic instability after hospital admission.4 While shock might evolve from a worsening cardiac disease such as ongoing myocardial ischaemia, haemodynamic deterioration will develop, at least in some patients with acute heart failure, because of inappropriate medical treatment. Tables 1 and 2 list drugs commonly used and interventions frequently performed in patients with acute heart failure, which can potentially contribute to the shock state and promote organ dysfunction. I can recall several patients who rapidly improved from ‘cardiogenic shock’ with
............................................................................................................................
Cardio-surgical Intensive Care Unit, Institute of Anaesthesiology, University Hospital Zurich, Raemistrasse 100, CH–8091 Zurich, Switzerland
Table 1 Adverse drug effects contributing to shock and organ dysfunction in patients with acute heart failure (Adverse) effects Risks ......................................................................... Diuretics
Hypovolaemia
Insufficient preload Pre-renal kidney dysfunction Hypokalaemia, Arrhythmia (e.g. atrial hypomagnesaemia fibrillation) Beta-blockers Negative chronotrope action Insufficient heart rate Negative inotrope action Decrease in cardiac contractility ACE-inhibitors Vasodilation Hypotension Worsening kidney function Opioids Vasodilation Hypotension Nausea Aspiration with respiratory failure Anticoagulants Bleeding (e.g. Haemorrhagic shock retroperitoneal) Contrast media Allergic reactions Anaphylactic shock Renal toxicity Worsening kidney function ACE, angiotensin-converting enzyme.
Table 2 Interventional complications contributing to shock and organ dysfunction in patients with acute heart failure Pulmonary artery catheter Arrhythmia (atrial fibrillation, ventricular tachycardia) Perforation → pericardial tamponade → obstructive shock (Tension) pneumothorax → obstructive shock Bleeding → haematothorax → hypovolaemic shock Catheter infection/sepsis → distributive shock Mechanical ventilation Sedation → vasodilatation, hypotension Positive intrathoracic pressure → increased RV afterload → RV dysfunction Coronary angiography: Coronary perforation → pericardial tamponade → obstructive shock Bleeding (e.g. retroperitoneal) → hypovolaemic shock Anaphylactic reactions caused by contrast media → distributive shock Cardiac surgery Myocardial injury → pump failure, arrhythmia Bleeding → hypovolaemic shock Hypervolemia → respiratory failure, renal dysfunction Activation of SIRS → distributive shock, renal dysfunction RV right ventricular; SIRS systemic inflammatory response syndrome.
fluid administration, as shock was a consequence of insufficient preload resulting from the excessive use of diuretics.
The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology. †doi:10.1002/ejhf.260 *Corresponding author: +41 442559621; Fax: +41 442553181; E-mail: [email protected]
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
467
Figure 1 The evolution from acute heart failure to cardiogenic shock to multi-organ failure. Malperfusion of tissues triggers an inflammatory reaction, most likely by the release of damage associated molecular patterns (DAMPs) from the damaged cells. These DAMPs are recognized by pattern recognition receptors from immune cells, and a consecutive intracellular cascade is activated leading to the activation and/or suppression of particular genes. These genes encode for pro- and anti-inflammatory cytokines, which activate adaptive mechanisms and enable local repair. At sufficient concentrations, however, these cytokines trigger a systemic inflammatory response (SIRS), which contributes to vascular leakage, vasodilation, and consecutive hypotension. Shock and SIRS can induce multiple organ failure (MOF), which eventually might cause death, if the condition cannot be reversed promptly by adequate treatment.
So, how to best manage patients with cardiogenic shock? First, the underlying cardiac disease and the trigger for decompensation must be identified, as understanding the pathophysiology at play is crucial for the correct treatment. In particular, reversible causes of heart failure must be looked for and treated adequately, which in many circumstances will require prompt interventions
.........................................................................................................................................................
Invited Editorial
© 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology
(e.g. balloon angioplasty in acute myocardial ischaemia resulting from coronary artery disease) or emergency cardiac surgery (e.g. mitral valve replacement in acute mitral regurgitation caused by papillary muscle rupture). Patients with a treatable underlying disease causing cardiogenic shock usually have a better prognosis than patients without.5 Second, cardiogenic shock must be reversed within hours, which includes optimization of cardiac preload and afterload, control of heart rate and the use of inotropes to increase contractility. While the condition is reversible in the early phase with adequate treatment, prolonged cardiogenic shock will cause multiple organ failure and eventually death (Figure 1). Hence, if cardiogenic shock cannot be reversed with the measures mentioned above, mechanical extracorporeal life support (ECLS) should be evaluated before irreversible organ damage has established.6 The ECLS treatment will buy some time for decision-making. In some patients care will have to be redirected to palliation because of futility of further treatment. In others, ECLS will bridge to recovery (e.g. acute myocarditis) or bridge to other types of assist devices and/or heart transplantation.7 Third, failing organs (kidneys, lungs) must be supported by intensive care with the caveat of first doing no harm.8 As soon as the patient can be stabilized, early rehabilitation must be started. The patient should be enrolled in a specialized heart failure follow-up programme, offering the full spectrum of pharmacological and non-pharmacological treatment options. In summary, a multi-disciplinary (cardiologists, intensivists, cardiac surgeons, and many more) and multi-professional (doctors, nurses, physiotherapists, and many others) approach is necessary to save the lives of critically ill patients with cardiogenic shock.
References 1. Rudiger A, Harjola V-P, Müller A, Mattila E, Säila P, Nieminen M, Follath F. Acute heart failure: clinical presentation, one-year mortality and prognostic factors. Eur J Heart Fail 2005;7:662–670. 2. Harjola VP, Lassus J, Sionis A, Kober L, Tarvasmäki T, Spinar J, Parissis J, Banaszewski M, Silva-Cardoso J, Carubelli V, Di Somma S, Tolppanen H, Zeymer U, Thiele H, Nieminen MS, Mebazaa A. Clinical picture and risk prediction of short-term mortality in cardiogenic shock. Eur J Heart Fail 2015;17:501–509. 3. Zannad F, Mebazaa A, Juillière Y, Cohen-Solal A, Guize L, Alla F, Rougé P, Blin P, Barlet M-H, Paolozzi L, Vincent C, Desnos M, Samii K, for the EFICA Investigators. Clinical profile, contemporary management and one-year mortality in patients with severe acute heart failure syndromes: The EFICA study. Eur J Heart Fail 2006;8:697–705. 4. Jeger RV, Radovanovic D, Hunziker PR, Pfisterer ME, Stauffer JC, Erne P, Urban P, Investigators APR. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med 2008;149:618–626. 5. Rudiger A, Businger F, Streit M, Schmid ER, Maggiorini M, Follath F. Presentation and outcome of critically ill medical and cardiac-surgery patients with acute heart failure. Swiss Med Wkly 2009;139:110–116. 6. Thiele H, Ohman EM, Desch S, Eitel I, de Waha S. Management of cardiogenic shock. Eur Heart J 2015; pii:ehv051 [Epub ahead of print]. 7. Sommer W, Marsch G, Kaufeld T, Rontgen P, Beutel G, Tongers J, Warnecke G, Tudorache I, Schieffer B, Haverich A, Kuhn C. Cardiac Awake Extracorporeal Life Support-Bridge to Decision? Artif Organs 2015; doi:10.1111/aor.12396 [Epub ahead of print]. 8. Singer M, Glynne P. Treating critical illness: The importance of first doing no harm. PLoS Med 2005;2:e167.
Copyright of European Journal of Heart Failure is the property of John Wiley & Sons, Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
![[Cardiogenic shock].](/assets/img/hold.png)
