Download RIGHT VENTRICULAR DYSFUNCTION ON THE ICU

Volume administration
Overload
Hypovolemia
Volume and the failing RV
Volume
overload
Increased
wall tension
Reduced
contractility
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41 acutely ill patients receiving 300 cc albumin
over 30 minutes
All patients had an RVEF-capable Swan-Ganz
catheter
Measurements included RVEDVI, calculated from
(CI/HR) / RVEF
Chest 1990;98:1450-4
Volume challenge and RV response
Findings
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Patients with high baseline RVEDVI did not benefit from
volume loading
In all other patients RVESVI and RVEDVI did increase
similarly with volume
CVP is a poor predictor of volume responsiveness
(Normal) RV output is preload-dependent
In the failing RV, judicious volume management is
necessary, and fluid removal may eventually help with
recovery
Volume status
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Gentle volume challenge in the early stage of RV
failure (only shown for acute PE)
Close monitoring of fluid status either with echo or using
the CVP waveform, trend(, and number)
Excessive volume loading may worsen RV performance
(RV distention, TR, ventricular interdependence)
Diuretics or ultrafiltration may be indicated, but have
not been studied in this population
Loop diuretic resistance in chronic heart failure
sometimes requires addition of a thiazide diuretic drug
Cardiac output
Contractility
Cardiac output
Tachyarrhythmia
Increased afterload
(Systemic hypotension)
Sympathomimetic inotropes
Epinephrine
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Dobutamine
Improves contractility
(RVSWI and RVEF)
despite an increase in
mPAP
Never studied in
patients with
pulmonary
hypertension
Intensive Care Med 1997;23:664-70
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Up to 5 mcg/kg/min
Increases CO, reduces
PVR and SVR
Less tachycardiac than
dopamine
Higher doses can
cause systemic
hypotension
Crit Care Med 2003;31:1140-6
Sympathomimetic inotropes
Isoproterenol
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Dopamine
Primarily chronotropic
agent
Described in the heart
transplant population
Can cause significant
arrhythmias
Crit Care Med 1991;19:60-7
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Dopamine increases
CO
Almost always causes
(at least) mild
tachycardia
Increases PVR/SVR
ratio
Br Heart J 1975;37:482-5
J Pediatr 2002;140:373-5
PDE inhibitors
PDE inhibitors
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They all augment contractility and produce
vasodilation
Mild tachycardia is common
Good human data exists for LV dysfunction, but is
somewhat scarce for RV failure
Potential advantage is pulmonary vasodilation,
which is via PDE3-receptors and not specific
Can cause significant systemic hypotension
Ann Thorac Surg 1997;63:814-21
Clin Transplant 2010;24:515-9
Cardiac output
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Dobutamine should be used for RV failure; the dose
should not be higher than 10 mcg/kg/min
Higher doses may cause tachycardia, arrhythmias,
and systemic hypotension
Epinephrine is probably preferred in the setting of
low arterial blood pressure
PDE inhibitors like milrinone are probably similar to
dobutamine, but act via a different receptor system
and are more potent pulmonary vasodilators
Pulmonary vascular resistance
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RV is a high-volume
low-pressure chamber
It has about 1/6 of
the LV’s muscle mass
There is little tolerance
to acute increases in
afterload
(From Braunwald, 1984)
Targets for reducing PVR
Inhaled agents are always
preferred in the acute setting
N Engl J Med 2004;351:1425-36
Nitric oxide
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Rapid half-life, inactivated by hemoglobin
Virtually no systemic vasodilation, need for
continuous application
Studied in a variety of perioperative settings, small
studies
NO improves hemodynamics, but has not been
shown to improve outcomes
High cost (for how long?)
Nitric oxide in LVAD patients?
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150 patients undergoing LVAD with increased
preoperative PVR
NO versus placebo, option of open-label NO in the
presence of RV failure
Primary endpoint: RV failure
Secondary endpoints:
 Length-of-stay
 RVAD
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rate
No significant differences
J Heart Lung Transplant 2011;30:870-8
Alternatives
Inhaled epoprostenol
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Safe and effective in
the setting of cardiac
surgery
Easy to administer
Potential cost-saver
NO = $3000
vs.
EPO = $150
J Thorac Cardiovasc Surg 2004;127:1058-67
Oral sildenafil
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PDE5 inhibitor
Relatively selective
As effective as NO
Synergistic effect
No differences in
systemic blood
pressure
Circulation 2002;105:2398-403
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58 patients with increased PVR
Comparison of hemodynamic effects
NO and prostacyclin equally lowered PVR, mPAP,
and TPG as well as they increased CO
Nitroprusside lowered PVR, but also SVR and had
to be discontinued in 62% of the cases due to low
systemic blood pressure
J Card Surg 2005;20:171-6
Circles = SaO2
Diamonds = MAP
Squares = FiO2
Am J Respir Crit Care Med 1996;153:1985-7
Importance of maintaining systemic
blood pressure
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RCA perfusion
throughout the cardiac
cycle
As PVR approaches
SVR, coronary perfusion
will decrease
Adequate perfusion
pressure needed to
prevent RV ischemia
Maintain positive
SVR/PVR or MAP/mPAP
ratio
Aortic pressure
Coronary flow
Which vasopressor?
Norepinephrine
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Vasopressin
Potential vasoconstriction,
but improved PVR/SVR
ratio in most studies
Additional positive
inotropic effect via betareceptor
Improved coronary blood
flow during exercise by
endogenous
norepinephrine
Anaesthesia 2002;57:9-14
Exp Biol Med 2002;227:238-50
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Some small, but
promising studies
Potent peripheral
vasoconstrictor
Potential pulmonary
vasodilation
Eur J Cardiothorac Surg 2006;29:952-6
Am J Physiol 1994;267:H2413-9
• In the presence of increased RV afterload, volume expansion causes deterioration of
ventricular function likely due to increased wall stress
• Distention imposes increased wall stress, this can cause RV ischemia
• Volume-induced RV dysfunction was reversed by norepinephrine
• Ventricular interdependence caused SV to decrease despite constant or slightly
increased LVEDP
Anesthesiology 1984;60:132-5
Summary I
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Pulmonary
hypertension is a
serious disease
associated with
increased
perioperative
mortality
Worsening RV
dysfunction
determines of
symptoms and
outcome
Important to
distinguish
pulmonary arterial
and pulmonary
venous hypertension
Summary II
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Treatment of
underlying disease
and influencing
factors is
mandatory
Supportive therapy
includes:
Careful ptimization
of volume status
Maintenance of RV
perfusion pressure
Enhancing RV
contractility
Reduction of RV
afterload
Thank you!