RIGHT VENTRICULAR DYSFUNCTION

1. RIGHT VENTRICULAR DYSFUNCTION University of British Columbia October 15th, 2009

2. Case 1: 54 year old female referred from another institution with large pericardial effusion NYD and shock liver. The amount of fluid around the heart is large – enough to make her tachycardic with a soft blood pressure but she remains alert, mentating normally, pink, warm, dry. • Vital signs: HR: 100-110, BP: 100-110, RR: 24, SpO2: 93% on 4L • On the bedside monitor you notice both electrical alternans (on telemetry) and pulse pressure variation (on arterial line and SpO2 tracing).

3. What are the most sensitive and practical indicators of fluid responsiveness that we can derive from the bedside? ­- Rob

4. Sensitive and Practical Indicators of fluid responsiveness that we can derive from the bedside • Physical Exam • Capillary refill, blood pressure, heart rate, presence of peripheral cyanosis/skin mottling, extremity temperature, passive leg raising, JVP, urine output • Static Measures of Intravascular Volume • CVP • PAOP • RVEDV (PAC with thermistor) • LVEDA (TEE) • IVC Diameter (Subcostal echo) • Transpulmonary thermodilution (GEDV) • Dynamic Indices of Intravascular Volume • PPV (arterial waveform analysis) • SVV (Pulse contour analysis) • Aortic Flow Velocity/Stroke Volume (Esophageal Doppler) • Chest wall echo (LV) • Changes (dynamic) in IVC/SVC Diameter

5. Fluid Responsiveness assessment – Physical Exam • Physical Exam • Capillary refill • Blood pressure • Heart rate • Peripheral cyanosis/skin mottling • Extremity temperature • Passive leg raising • JVP • Urine output

6. Fluid Responsiveness Indicators – Static Measures of Intravascular Volume CVP PAOP RVEDV (PAC with thermistor) LVEDA (TEE) IVC Diameter (Subcostal echo) Transpulmonary thermodilution (GEDV)

7. Fluid Responsiveness Indicators – Dynamic Measures of Intravascular Volume PPV (arterial waveform analysis) SVV (Pulse contour analysis) Aortic Flow Velocity/Stroke Volume (Esophageal Doppler) Chest wall Echo (LV) Changes (dynamic) in IVC/SVC Diameter

9. 2009 Meta-analysisMarik et al., Crit Care Med 2009 in press • PPV and SVV measured during volume-controlled mechanical ventilation predicted with a high degree of accuracy those patients likely to respond to a fluid challenge as well as the degree to which the stroke volume is likely to increase • PPV: Sens 89% Spec 88% Thresold: 12% • SVV: Sens 82% Spec 86% Threshold: 13%

10. Limitations of SVV • Mechanical Ventilation • If not on 100% control with tidal volumes > 8cc/kg • Spontaneous Ventilation • Irregular rate and tidal volumes • Arrhythmias • PEEP • Increasing PEEP may cause an increase in SVV • Vasodilation therapy • Vasodilatory therapy may increase SVV

11. Esophageal Doppler Measures blood flow velocity in the descending aorta Cardiac output calculated based on diameter of aorta, distribution of the cardiac output (to the descending aorta) and the measured flow velocity of blood in the aorta. The duration of the aortic velocity signal corrected for HR (flow time corrected) is considered a static indicator of cardiac preload

12. Esophageal Doppler 1Dark and Singer Int Care Med 2004; 30: 2060-2066 2Sinclair et al BMJ 1997; 315: 909-912 3Chytra et al., Crit Care 2007; I 1: R24 • Cardiac output: 86% correlation with PAC and changes in cardiac output correlated with therapeutic interventions1 • Patients undergoing femur fracture repair randomized to intraoperative intravascular volume optimized with or without Doppler2 • Doppler: More rapid post-operative recovery and shorter hospital stays. • Similar study in trauma patients3 • Lower lactates • Lower incidence of infectious complications • Decreased ICU and hospital LOS

13. Esophageal Doppler • Disadvantages • Waveform is very much operator dependent • Steep learning curve • Not suitable for all patients • Inability to obtain continuous reliable meaurements • Correlation better in studies where the investigator was not blinded to the results of the cardiac output obtained with a PAC

14. 2. What is the role of bedside Intensivist-performed echo in this/similar settings (TTE and Esophageal Doppler)? - Marius

15. Assessing fluid responsiveness using TTE and esophageal doppler

16. TTE: Fully ventilated patients • Fluid responsiveness can be measured in patients being fully ventilated by measuring the change in IVC diameter (ΔDIVC)with inspiration. • Rationale: insufflation-induced changes in venous return are more marked in hypovolemic states.

17. Measuring IVC collapsibility

18. Performance of ΔDIVC • Feissel et al. Intensive Care Med (2004) 30:1834–1837 • ΔDIVC > 12% had a 93% PPV and 92% NPV for volume responsiveness. • Septic patients, sedated, on volume control with a Vt ≥ 8 cc/kg • Vol. responsiveness described an increase in CO ≥ 15% following an 8 cc/kg bolus of 6% hydroxyethylstarch over 20 min • IVC measured approx. 3 cm from RA • ΔDIVC = (Max DIVC – Min DIVC) / MeanDIVC

19. Performance of ΔDIVC • Barbier et al. Intensive Care Med (2004) 30:1740–1746 • ΔDIVC > 18% had a 90% sensitivity and 90% specificity for volume responsiveness • Fully ventilated ICU patients on volume control with a Vt of 8.5 ± 1.5 cc/kg • Vol. responsiveness defined as an increase in CO ≥ 15% following a 7 cc/kg bolus of 4% gelatin over 30 min • IVC examined just upstream of the origin of the suprahepatic vein • ΔDIVC = (Max DIVC – Min DIVC) / MinDIVC

20. Esophageal doppler and fully ventilated patients • Esophageal doppler measures aortic blood flow in the descending aorta. • Owing to various heart-lung interactions, volume responsive patients being fully mechanically ventilated tend to show variations in aortic blood flow related to inspiration. • These interactions are mediated by two factors: • An increase in pleural pressure leading to: • A decreased RV preload • An increase in transpulmonary pressure leading to: • An increased RV afterload • An increased LV preload • A decreased LV afterload

21. Hemodynamic effects of mechanical ventilation

22. Esophageal doppler • Monnet et al. Intensive Care Med (2005) 31:1195–1201 • A respiratory variation in aortic flow before volume expansion of at least 18% predicted fluid responsiveness with a sensitivity of 90% and a specificity of 94% • Fully mechanically ventilated patients (8±2 cc/kg) being considered for fluid bolus • Fluid responsiveness defined as an increase in aortic flow ≥ 15% with a 500 cc NS bolus given over 10 min. • ΔABF = (ABFmax – ABFmin) / ABFmean

23. Spontaneously breathing patients • Predicting fluid responsiveness in spontaneously breathing patients poses a greater challenge • Reasons: • Tidal volumes and respiratory rates are variable • Intrathoracic pressure is negative during inspiration • Intrathoracic pressure swings are lower than during mechanical ventilation • Options: • Measuring IVC diameter (no good studies) • Response to passive leg-raising

24. Measuring IVC diameter • Yanagawa et al. Journal of Trauma 2007; 63:1245–1248 • An expiratory IVC diameter < 1cm in spontaneously breathing trauma patients predicted recurrent hypotension after successful fluid resuscitation (SBP > 90)

25. Passive leg-raising • Given the increase in RV filling induced by passive leg raising does not depend on respiratory changes, it has been studied as a marker for fluid responsiveness in spontaneously breathing patients. • Leg raising is thought to “bolus” the patient without actually giving volume, the effects of which can be measured in real time by esophageal doppler or echo.

26. Spontaneously breathing patients

27. Passive leg-raising and TTE • Lamia et al. Intensive Care Med (2007) 33:1125–1132 • A PLR-induced increase in stroke volume ≥ 12.5% predicted volume responsiveness with a 77% sensitivity and a 100% specificity • Spontaneously breathing ICU patients (including PSV) • Volume responsiveness = 15% or more increase in stroke volume after a 500 cc NS bolus over 15 min. • Stroke volume = VTIAo x AVA

28. Passive leg-raising and TTE • Maizel et al. Intensive Care Med (2007) 33:1133–1138 • A PLR-induced increase in CO or SV ≥ 12% predicted volume responsiveness with a 69% sensitivity and 89% specificity • Spontaneously breathing patients with hypotension, acute renal failure, or clinical signs of volume depletion • Volume responsiveness = An increase in CO ≥ 12% following a 500 cc NS bolus over 15 min • SV = VTIAo x AVA

29. Passive leg-raising and esophageal doppler • Monnet et al. Critical Care Medicine (2006) 34:1402-1407 • PLR-induced increase of aortic blood flow ≥10% predicted fluid responsiveness with a sensitivity of 97% and a specificity of 94% • Spontaneously breathing and deeply sedated patients undergoing mechanical ventilation • Volume responsiveness = a rise in aortic blood flow ≥ 15% following a 500 cc NS bolus given over 10 min.

30. 3. Discuss the role of the PAC in the ICU. When is it useful? ­- ­Todd

31. What is the role of the pulmonary artery catheter in the ICU? • Who knows? • Everyone should have one. • Nobody should have one. • We should use them, but only use the information they provide if it confirms what we already think. • We should use them, but only for true mixed venous oxyhemoglobin values.

32. Some light bathroom reading… • BCMJ, vol. 51, No. 7, Sept 2009. 302-307 (3 UBC cardio fellows) • First right-heart cath by Forssman in 1929 (urethral catheter in his own arm…) • Further development (and Nobel Prize), with main limitation being the difficulty in passing the catheter without flouroscopy. • Swan’s major contribution was envisioning the balloon-tipped, flow-directed catheter, which he developed with Ganz in 1970.

33. Hemodynamic monitoring • Central venous pressure (directly measured) • Cardiac output (directly measured); Cardiac index (calculated) • Mixed venous O2 saturation (directly measured) • Pulmonary artery occlusion pressure (directly measured, but with caveats) • Systemic vascular resistance (calculated)

34. Controversy • Does routine use of this device in critically ill patients improve outcomes? • Apparently not.

36. JAMA meta-analysis • No clear benefit nor harm from routine PA catheter use in critically ill patients. • Many trials excluded patients in whom PA catheterization would be specifically indicated (i.e. lung transplant) • ESCAPE trial specifically looked at refractory CHF with reduced LVEF, and found that despite effectively reaching target hemodynamic values, outcomes didn’t improve.

37. Why? • Risks of insertion • Risks of catheterization of right heart/PA • Risk of “wedging” • Risks associated with interpretation of data… • Right Heart Cath as a marker for an aggressive (read: risky) style of care? • As a marker for sick patients who aren’t improving with less invasive hemodynamic monitoring • Timing?

38. When do you use it?

39. Over time the patient becomes less alert. Her respiratory effort is failing. You have to intubate her. • Outline your approach to the induction of a patient with a hemodynamically compromising pericardial effusion (assuming you can’t tap the effusion first). - Noemie • How would you change your approach if the hemodyamic compromise was, in fact, secondary to a submassive/massive pulmonary embolism? Or a large anterior mediastinal mass? - Noemie

40. Question 4 & 5 Approach to the induction of a patient with: • a hemodynamically compromising pericardial effusion. • a submassive/massive pulmonary embolism. • a large anterior mediastinal mass.

41. Pericardial Tamponade Physiology •  pericardial fluid   pericardial pressure •  End diastolic pressure • Early closure of AV valves •  SV and  CO

42. Concerns about intubation • Induction: • Medication used • Sympathetic drive • PPV: •  venous return   CO • PEEP

43. Induction • No right answer…Multiple case reports • Good IV access, Fluid bolus • Avoid hypotension! Pressors and inotrope ready • Awake intubation with topical anesthetic? • Medication • Ketamine ad etomidate suggested as drugs of choice b/c don’t cause significant SVR • Avoid propofol

44. Ventilation • Try to avoid intubation if possible • Pericardiocenthesis! • Avoid high PEEPs and can try spontaneous ventilation British journal of anesthesiology 1979;51:409-415

45. Massive PE • Complications of PPV •  RV afterload •  venous return • IV, pressors and inotrope at bedsie • Avoid hypotension to maintain good coronary perfusion

46. Massive PE • How to intubate? • Maintain spontaneous ventilation to avoid  RV afterload • Ketamine/midaz • Topical anesthetic with fibreoptic scope • Aggressive management of blood pressure to maintain coronary perfusion

47. Approach to the Mediastinal Mass • Possible Complications to think prior to intubation: • Progressive airway obstruction • Lung volume loss • PA and/or cardiac compression • SVC obstruction • POTENTIAL FOR CATASTROPHIC AIRWAY!

48. Canadian Journal of Anesthesia 1989;36(6):681-688

49. Approach to Induction • Positon: flat or sitting dpdg on pathology • Awake fibreoptic intubation with topical anesthesia • Avoid muscle relaxant!! • Maintain spontaneous ventilation during induction if possible Canadian Journal of Anesthesia 1989;36(6):681-688

50. Case 2: 43 year old female, smoker and on HRT, presents to the ED with shortness of breath and CP and diagnosed with “submassive PE”. • What is “submassive PE”, or what are the thresholds to treat with thrombolytics? What is the current standard treatment? - Rob