RIGHT VENTRICULAR DYSFUNCTIONUniversity of British Columbia

October 15th, 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, 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).

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

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

Fluid Responsiveness Indicators – Static Measures of Intravascular Volume

• CVP• PAOP• RVEDV (PAC with thermistor)• LVEDA (TEE)• IVC Diameter (Subcostal echo)• Transpulmonary thermodilution (GEDV)

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

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%

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 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

1Dark and Singer Int Care Med 2004; 30: 2060-20662Sinclair et al BMJ 1997; 315: 909-9123Chytra 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 (ΔDIVC) with inspiration.

• Rationale: insufflation-induced changes in venous return are more marked in hypovolemic states.

Measuring IVC collapsibility

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

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

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 = (ABFmax – ABFmin) / ABFmean

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 < 1cm in spontaneously breathing trauma patients predicted recurrent hypotension after successful fluid resuscitation (SBP > 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 PE1,2,3

– Higher mortality - those with RV hypokinesis, even in the presence of normal SBP had a 2x mortality1

– 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

1Goldhaber et al Lancet 1999 353: 1386-13892Grifoni et al Circulation 2000; 2817-28223Ribiero et al., Am Heart J 1997; 479-487

Submassive PE

• Konstantinides1

– 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

1Konstantinides et al NEJM 2002

Konstantinides1 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 Recs2:– Selected high –risk patients without hypotension, judged to have a low

risk of bleeding should get thrombolytic therapy

1Konstantinides et al NEJM 20022Kearon 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