Presentation on theme: "RIGHT VENTRICULAR DYSFUNCTION University of British Columbia October 15 th, 2009."— Presentation transcript:
RIGHT VENTRICULAR DYSFUNCTION University of British Columbia October 15 th, 2009
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, SpO 2 : 93% on 4L On the bedside monitor you notice both electrical alternans (on telemetry) and pulse pressure variation (on arterial line and SpO 2 tracing).
1.What are the most sensitive and practical indicators of fluid responsiveness that we can derive from the bedside? - Rob
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
2009 Meta-analysis Marik 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%
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
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
Esophageal Doppler Cardiac output: 86% correlation with PAC and changes in cardiac output correlated with therapeutic interventions 1 Patients undergoing femur fracture repair randomized to intraoperative intravascular volume optimized with or without Doppler 2 – Doppler: More rapid post-operative recovery and shorter hospital stays. Similar study in trauma patients 3 – Lower lactates – Lower incidence of infectious complications – Decreased ICU and hospital LOS 1 Dark and Singer Int Care Med 2004; 30: 2060-2066 2 Sinclair et al BMJ 1997; 315: 909-912 3 Chytra et al., Crit Care 2007; I 1: R24
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
2. What is the role of bedside Intensivist- performed echo in this/similar settings (TTE and Esophageal Doppler)? - Marius
Assessing fluid responsiveness using TTE and esophageal doppler
TTE: Fully ventilated patients Fluid responsiveness can be measured in patients being fully ventilated by measuring the change in IVC diameter (ΔD IVC ) with inspiration. Rationale: insufflation-induced changes in venous return are more marked in hypovolemic states.
Measuring IVC collapsibility
Performance of ΔD IVC Feissel et al. Intensive Care Med (2004) 30:1834–1837 – ΔD IVC > 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 ΔD IVC = (Max D IVC – Min D IVC ) / MeanD IVC
Performance of ΔD IVC Barbier et al. Intensive Care Med (2004) 30:1740–1746 – ΔD IVC > 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 ΔD IVC = (Max D IVC – Min D IVC ) / MinD IVC
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
Hemodynamic effects of mechanical ventilation
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 = (ABF max – ABF min ) / ABF mean
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
Measuring IVC diameter Yanagawa et al. Journal of Trauma 2007; 63:1245–1248 – An expiratory IVC diameter 90)
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.
Spontaneously breathing patients
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
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
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.
3. Discuss the role of the PAC in the ICU. When is it useful? - Todd
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.
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.
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)
Controversy Does routine use of this device in critically ill patients improve outcomes? – Apparently not.
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.
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?
When do you use it?
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
Question 4 & 5 Approach to the induction of a patient with: 1. a hemodynamically compromising pericardial effusion. 2.a submassive/massive pulmonary embolism. 3.a large anterior mediastinal mass.
Pericardial Tamponade Physiology pericardial fluid pericardial pressure End diastolic pressure Early closure of AV valves SV and CO
Concerns about intubation Induction: – Medication used – Sympathetic drive PPV: – venous return CO – PEEP
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
Ventilation Try to avoid intubation if possible Pericardiocenthesis! Avoid high PEEPs and can try spontaneous ventilation British journal of anesthesiology 1979;51:409-415
Massive PE Complications of PPV – RV afterload – venous return IV, pressors and inotrope at bedsie Avoid hypotension to maintain good coronary perfusion
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
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!
Canadian Journal of Anesthesia 1989;36(6):681-688
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
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
Submassive PE Hemodynamic stable patients with evidence of right ventricular strain or dysfunction – 40-50% of those with acute PE 1,2,3 – Higher mortality - those with RV hypokinesis, even in the presence of normal SBP had a 2x mortality 1 – Another study described a 5% mortality rate in those with RV hypokinesis (those without RV dysfunction had a 0% rate) 35 162 patients 31% had RV dysfunction 1 Goldhaber et al Lancet 1999 353: 1386-1389 2 Grifoni et al Circulation 2000; 2817-2822 3 Ribiero et al., Am Heart J 1997; 479-487
Submassive PE Konstantinides 1 – 256 hemodynamically stable patients – Proven PE + RV hypokinesis or PHT – Got either r-tPA + heparin or placebo + heparin – 30 day follow up – End points: In-hospital death or “escalation of care” Vasopressor requirement Embolectomy Thrombolytics Intubation CPR 1 Konstantinides et al NEJM 2002
Konstantinides 1 Results 11% vs. 25% deterioration rate favouring lytic group RR reduction: 55% (NNT: 8) No difference in all cause mortality (3.4% vs. 2.2%) Significant Criticism – Allowed treating MD to administer rescue lytics which could have driven the composite end point to statistical significance 2008 ACCP Recs 2 : – Selected high –risk patients without hypotension, judged to have a low risk of bleeding should get thrombolytic therapy 1 Konstantinides et al NEJM 2002 2 Kearon et al Chest: 2008 454S-545S
Case 3: 27 year old male presents with massive hemoptysis to MSJ ER. Brutal CT chest with TB – there is significant burden of disease with consolidative process, cavitation/necrosis, and what appears to be only ~ 25% “healthy” or aerating lung. His right sided pressures are through the roof. Outline an approach to PHTN. - Neil What are the current therapies available in the ICU setting? And in this patient what are the risks:benefits of inhaled vs systemic pulmonary vascular vasodilators? - Neil