1. Circulatory Failure 6 th November 2013

2. Physiology and pathophysiology of the heart and circulation Pathophysiological effects of altered intravascular volume Pathophysiology and treatment of cardiac failure Theoretical advantages and disadvantages of crystalloid and colloid solutions Indications for, contraindication, risks and alternatives to blood transfusion shock states (anaphylactic, cardiogenic, hypovolaemic, septic); Pathophysiology, detection and management of shock states according to aetiology and in response to physiological data Effect of circulatory failure and its treatment on other organ systems Indications and contraindications for treatment; circumstances when treatment is unnecessary or futile Use of fluids and vasoactive / inotropic / anti-arrhythmic drugs to support the circulation (see 4.4) Complications of specific therapies, their incidence and management Fluid therapies: components, physical properties, distribution and clearance of commonly used fluids; indications, contraindications and complications of their administration Mechanisms of assessment of response to fluid Indications and contraindications, limitations and complications of inotropic / vasoactive drug therapy Interactions between inotropic agents and concomitant therapies and/or co-morbid diseases (eg. ischaemic heart disease) Principles of haemodynamic monitoring - invasive and non invasive methods, indications and limitations, physiological parameters and waveform interpretation Invasive and non-invasive systems available for measuring cardiac output and derived haemodynamic variables, the principles involved and the type and site of placement of the monitoring device Indications and limitations of transthoracic / transoesophageal echocardiography in shocked patient Indications, limitations and complications of techniques of measurement of cardiac output (e.g. pulmonary artery catheter, oesophageal Doppler, PiCCO, LiDCO) and action to prevent them Integration of data from clinical examination and haemodynamic monitoring to characterise haemodynamic derangements Receptor-specific effects of inotropic and vasopressor agents; effects of critical illness and concomitant therapies on receptor function (e.g. down-regulation)

4. Cardiac Output CO = HR x SV preload contractility afterload

5. Preload What is it? What does it depend on?

6. Normal RAP (CVP), LAP

7. Preload (cont.) What determines it? Venous return …which depends on – Intravascular volume – Venous tone – ….which depends on ANS Circ catecholamines Local factors

8. or ?

10. Afterload Ω

11. Afterload and/or contractility

12. + or

13. Laplace’s Law

14. Physiology and pathophysiology of the heart and circulation Pathophysiological effects of altered intravascular volume Pathophysiology and treatment of cardiac failure Theoretical advantages and disadvantages of crystalloid and colloid solutions Indications for, contraindication, risks and alternatives to blood transfusion shock states (anaphylactic, cardiogenic, hypovolaemic, septic); Pathophysiology, detection and management of shock states according to aetiology and in response to physiological data Effect of circulatory failure and its treatment on other organ systems Indications and contraindications for treatment; circumstances when treatment is unnecessary or futile Use of fluids and vasoactive / inotropic / anti-arrhythmic drugs to support the circulation (see 4.4) Complications of specific therapies, their incidence and management Fluid therapies: components, physical properties, distribution and clearance of commonly used fluids; indications, contraindications and complications of their administration Mechanisms of assessment of response to fluid Indications and contraindications, limitations and complications of inotropic / vasoactive drug therapy Interactions between inotropic agents and concomitant therapies and/or co-morbid diseases (eg. ischaemic heart disease) Principles of haemodynamic monitoring - invasive and non invasive methods, indications and limitations, physiological parameters and waveform interpretation Invasive and non-invasive systems available for measuring cardiac output and derived haemodynamic variables, the principles involved and the type and site of placement of the monitoring device Indications and limitations of transthoracic / transoesophageal echocardiography in shocked patient Indications, limitations and complications of techniques of measurement of cardiac output (e.g. pulmonary artery catheter, oesophageal Doppler, PiCCO, LiDCO) and action to prevent them Integration of data from clinical examination and haemodynamic monitoring to characterise haemodynamic derangements Receptor-specific effects of inotropic and vasopressor agents; effects of critical illness and concomitant therapies on receptor function (e.g. down-regulation)

15. Shock Definition? “Shock is a clinical state that occurs when an imbalance of oxygen demand and supply leads to the development of tissue hypoxia” Classification – Cardiogenic – Hypovolaemic – Septic – Anaphylactic – Neurogenic

16. Oxygen delivery What is D0 2 Equation: D0 2 = CO x Ca0 2 Ca02= (1.3 x Hb x Sa02) + (0.003 x Pa02)

17. Oxygen uptake/extraction V0 2 is oxygen extraction/uptake V0 2 = CO x (Ca0 2 – Cv0 2 )

19. Physiology and pathophysiology of the heart and circulation Pathophysiological effects of altered intravascular volume Pathophysiology and treatment of cardiac failure Theoretical advantages and disadvantages of crystalloid and colloid solutions Indications for, contraindication, risks and alternatives to blood transfusion Pathophysiology, detection and management of shock states according to aetiology and in response to physiological data Effect of circulatory failure and its treatment on other organ systems Indications and contraindications for treatment; circumstances when treatment is unnecessary or futile Use of fluids and vasoactive / inotropic / anti-arrhythmic drugs to support the circulation (see 4.4) Complications of specific therapies, their incidence and management Fluid therapies: components, physical properties, distribution and clearance of commonly used fluids; indications, contraindications and complications of their administration Mechanisms of assessment of response to fluid Indications and contraindications, limitations and complications of inotropic / vasoactive drug therapy Interactions between inotropic agents and concomitant therapies and/or co-morbid diseases (eg. ischaemic heart disease) Principles of haemodynamic monitoring - invasive and non invasive methods, indications and limitations, physiological parameters and waveform interpretation Invasive and non-invasive systems available for measuring cardiac output and derived haemodynamic variables, the principles involved and the type and site of placement of the monitoring device Indications and limitations of transthoracic / transoesophageal echocardiography in shocked patient Indications, limitations and complications of techniques of measurement of cardiac output (e.g. pulmonary artery catheter, oesophageal Doppler, PiCCO, LiDCO) and action to prevent them Integration of data from clinical examination and haemodynamic monitoring to characterise haemodynamic derangements Receptor-specific effects of inotropic and vasopressor agents; effects of critical illness and concomitant therapies on receptor function (e.g. down-regulation)

20. Fluids

21. Definitions: Crystalloid a substance that in solution can pass through a semipermeable membrane Colloid a suspension of small particles dispersed in another substance

22. Which fluid? Colloids versus crystalloids for fluid resuscitation in critically ill patients. Alderson P, Schierhout G, Roberts I, Bunn F Cochrane Database Syst Rev. 2000; REVIEWER'S CONCLUSIONS: There is no evidence from randomised controlled trials that resuscitation with colloids reduces the risk of death compared to crystalloids in patients with trauma, burns and following surgery. As colloids are not associated with an improvement in survival, and as they are more expensive than crystalloids, it is hard to see how their continued use in these patient types can be justified outside the context of randomised controlled trials. Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta-analysis. Zarychanski R, Abou-Setta AM, Turgeon AF, Houston BL, McIntyre L, Marshall JC, Fergusson DA JAMA. 2013 Feb;309(7):678-88. CONCLUSION AND RELEVANCE: In critically ill patients requiring acute volume resuscitation, use of hydroxyethyl starch compared with other resuscitation solutions was not associated with a decrease in mortality. Moreover, after exclusion of7 trials performed by an investigator whose research has been retracted because of scientific misconduct, hydroxyethyl starch was associated with a significant increased risk of mortality and acute kidney injury. Clinical use of hydroxyethyl starch for acute volume resuscitation is not warranted due to serious safety concerns.

23. Which fluid? The appropriate one – Replace what has been lost – Keep Hb >70 g/l (?>10 g/l cardiac) – No starch – ?albumin

24. How much?

25. Physiology and pathophysiology of the heart and circulation Pathophysiological effects of altered intravascular volume Pathophysiology and treatment of cardiac failure Theoretical advantages and disadvantages of crystalloid and colloid solutions Indications for, contraindication, risks and alternatives to blood transfusion Pathophysiology, detection and management of shock states according to aetiology and in response to physiological data Effect of circulatory failure and its treatment on other organ systems Indications and contraindications for treatment; circumstances when treatment is unnecessary or futile Use of fluids and vasoactive / inotropic / anti-arrhythmic drugs to support the circulation (see 4.4) Complications of specific therapies, their incidence and management Fluid therapies: components, physical properties, distribution and clearance of commonly used fluids; indications, contraindications and complications of their administration Mechanisms of assessment of response to fluid Indications and contraindications, limitations and complications of inotropic / vasoactive drug therapy Interactions between inotropic agents and concomitant therapies and/or co-morbid diseases (eg. ischaemic heart disease) Principles of haemodynamic monitoring - invasive and non invasive methods, indications and limitations, physiological parameters and waveform interpretation Invasive and non-invasive systems available for measuring cardiac output and derived haemodynamic variables, the principles involved and the type and site of placement of the monitoring device Indications and limitations of transthoracic / transoesophageal echocardiography in shocked patient Indications, limitations and complications of techniques of measurement of cardiac output (e.g. pulmonary artery catheter, oesophageal Doppler, PiCCO, LiDCO) and action to prevent them Integration of data from clinical examination and haemodynamic monitoring to characterise haemodynamic derangements Receptor-specific effects of inotropic and vasopressor agents; effects of critical illness and concomitant therapies on receptor function (e.g. down-regulation)

26. Haemodynamic Monitoring Pulmonary Artery Catheter

28. Oesophageal Doppler

30. PiCCO Pulse Contour Analysis – Derives SV by area under the systolic curve

31. LiDCO Pulse power analysis Uses lithium dilution

32. ICON measurement of the changes of electrical conductivity within the thorax

33. ICON During diastole, the RBCs in the aorta assume a random orientation, which causes the electrical current to meet more resistance, resulting in a lower measure of conductivity. During systole, pulsatile flow causes the RBCs to align parallel to both the blood flow and electrical current, resulting in a higher conductivity state. By analyzing the rate of change in conductivity before and after aortic valve opening, or in other words, how fast the RBCs are aligning, EC technology derives the peak aortic acceleration of blood and the left ventricular ejection time (flow time). The velocity of the blood flow is derived from the peak aortic acceleration and used within our patented algorithm to derive stroke volume.

34. Transoesophageal echocardiography (TOE) Fick principle CO= oxygen consumption arteriovenous oxygen content difference

35. Assessing Haemodynamic Status

36. Inotropes and Vasopressors