management of the rv in cardiogenic shock
TRANSCRIPT
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Management of the RV in cardiogenic shock
Susanna Price
Consultant Cardiologist & IntensivistRoyal Brompton & Harefield NHS Foundation TrustHonorary Senior Lecturer, NHLI, Imperial College, London
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Disclosures
• No disclosures/conflicts of interest
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Cardiogenic shock
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ICU
mort
alit
y
SCCM data, 2015. Parakh et al., Int Med J, 2015
0%
10%
20%
30%
40%
50%
60%
70%
80%
MOF Haem-onc RVI revasc Sepsis SARF ARF RVI no revasc
Lupi-Herrera et al., World J Cardiol, 2014
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Cardiogenic shock management
Cardiogenic shock/AHF
Improved
survival with
good QoL
✓ Revascularisation ✓ Device therapy✓ Structural
Oral
antiplatelets
GP IIb/IIIa
inhibitors
✓Inotropes
& pressors
✓ Electrolytes
Volume
Nutrition
Endocrine
Care bundles
Heparin Bivalirudin Beta blockers
& -ve inotropes
Death
Multi-organ failure
✓ Intubation
& ventilation
cardiology >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>> critical care
Medical treatment?
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Guidelines, 2016
Complex, management requires understanding of anatomy and mechanics,
Identification
Treat underlying causes
Support
Uncertainties remain
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CVP: +ve predictive value 47%
PCWP: +ve predictive value 54%
Volume?
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RV preload optimisation
• Initial studies: • Normal saline infusion, maintaining RAP <10mmHg
• Later clinical studies• Variable response reported
• Aim target PCWP 18-24 mmHg
• Berisha et al., 41 patients, electrocardiographic and haemodynamic criteria for RV infarction
– maximal RV SWI with filling pressure 10-14mmHg
- mean RAP >14mmHg associated with RV distension
- haemodynamic response variable - optimal PCWP (corresponding to maximum LVSWI) 16mmHg
Inohara et al., EHJ Acute Cardiovascular Care 2013
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RV preload optimisation
Smaller studies: Change in PCWP and CI
Wide variation in response
No linear association with higher mRAP target
Practically:
Aim transmural pressure 8-12mmHg
Measure CO and ScvO2/systemic organ perfusion
(not well-studied in acute RV failure)
Inohara et al., EHJ Acute Cardiovascular Care 2013
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Psyst reduced by
analgesia & sedatives
Hypovolaemia:
Sepsis/SIRS
Vascular permeability
Insensible loss
IPPV:
Increases ITP
1. Preload evaluation 3. RV afterload evaluationPVR normal: need increased RVEDP
PVR elevated: increase in RVEDP will shift septum
5. The pericardium2. Pressure-volume
4. Septal involvement
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Vasoconstriction
Noradrenaline
• Constrictor
• Antithrombotic
• Positive inotrope
Dopamine
• If >15mcg/kg/min is α-agonist
• Positive inotrope
• Elevation in PCWP
1678 patients with circulatory shock – 280 cardiogenic
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Systemic arterial pressure optimisation
• Perfusion RV free wall: difference in RV free wall tension and coronary artery pressure
• Volume resuscitation that increases RV free wall tension without increasing systemic pressure can decrease RV perfusion
• Ideal pressor: increase systemic arterial pressure – no change in PVR
Harjola et al., Eur J Heart Failure 2016
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Positive inotropic agents
• Diverse collection of pluripotent molecules
• Differing pharmacological properties
• Some shared activities – only one of which is positive inotropy• Will increase dP/dt with variable effects on cardiac output/index
• Alteration in myocardial oxygen demand
• Arrhythmia
Additional:
• Alteration in bacterial metabolism and translocation
• Alteration in inflammatory markers and ROS
• Immune-modulatory effects
• Coagulation
• Differential effects on macrocirculation & microcirculation
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Regional resistance:
• neurohumoral factors related to inflammation and the sympathetic nervous system
• local factors related to autoregulation
Key (neglected) organs:• GIT (gastric tonometry,
splanchnic/hepatic saturations, indocyanine green)
• Brain
Cardiac output: global vs regional perfusion?
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Each inotropic agent: efficacy vs toxicity
• Each inotropic agent
• Each organ system
•Cardiac
•Renal
•Hepatic
•Cerebral
•GIT
•Microcirculation
• Each pathological situation:
•Sepsis
•AMI+CS
•DCM+CS
•Haemorrhagic shock
• In context of different ICU interventions
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Which inotrope?
•No real evidence to support one over another
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Afterload reduction
• Critical illness frequently associated with increased PVR
• HPV – alveolar, pulmonary arterial/bronchial arterial hypoxaemia, worsened with acidemia
• Focus on:
• Reducing pulmonary vascular tone
• Judicious use of pulmonary vasodilators
• Awareness of the effects of positive pressure ventilation
RV FRC TLC
Aim: normoxia, normocarbia
Lung volumes near FRC
pH normal
Ventetuolo & Klinger, Ann Am Thorac Soc 2014
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Potentially injurious effects of ventilation
Spontaneous
Ventilated
Tavazzi G, ESICM 2014
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Effects of IPPV in RV restrictive physiology
• Inspiration increases E/A ratio
• Abolishes PA diastolic wave
• Relative contribution of “restrictive” antegrade a wave to forward flow:
• Inspiration: 7 +8%
• Expiration: 22 +10%
• 43% patients with SARF
• Inducible by IPPV
Cullen, Circulation. 1995 Mar 15;91(6):1782-
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Pulmonary vasodilators
• None approved for treatment of RV failure in critically ill
• All have systemic & pulmonary effects
• Systemic administration may alter V/Q mismatch, and worsen hypoxaemia
SpeakerHarjola et al., Eur J Heart Failure 2016
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Right heart afterload
Speaker
Pulmonary TAPSE
Maximal pulmonary vasodilatation
• iNO
+ Levosimendan
+ Nebulised prostacyclin
+ Low dose vasopressin
+ Nebulised milrinone
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Peripheral VA-ECMO
Cardiac (or cardiopulmonary) support
Percutaneous, rapid access
Awake or ventilated
Up to 8L/min – high, stable flow, 2-4 weeks
Better kit – transportation and monitoring
Cheaper than Tandem Heart and Impella
Expanding indications
23Fr venous, 19-21Fr arterial(Legmo: 10-12Fr)
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Guidelines?
??RV failure
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Transfemoral insertion
3D shaped cannula
22Fr motor housing
Pump on 1Fr catheter
4L/min @33,00rpm
ACT160-180
COHORT B: 58.3% survival (cohort predicted survival 40%)
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Statement from ESC
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Many interventions seem physiologically/intuitively sensible – but that doesn’t mean they are right
Sir Iain Chalmers, co-founder Cochrane collaboration, BBC Radio 4, 2013