Fluid Resuscitation

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Transcript Fluid Resuscitation

Fluid Resuscitation
2013 NH
Which fluid?
Assessing volume status
Preload/Volume Status
Afterload/ Vascular tone
Predicting Responsiveness
Monitoring Response
Plan B
The setting
The environment is bad
- time and pressure are monumentally against the considered
diagnosis of shock
The patient is often bad
More often than not there are multiple comorbidities conspiring to
undermine our efforts to maintain homeostasis – small vessel disease,
immune dysregulation,
Clinical indices of the adequacy of
tissue/organ perfusion
Mean arterial pressure
Cerebral and abdominal perfusion pressures
Urine output
Capillary refill
Skin perfusion/mottling
Cold extremities (and cold knees)
Blood lactate
Arterial pH, BE and HCO3
Mixed venous oxygen saturation SmvO2 (or ScvO2)
Mixed venous pCO2
Tissue pCO2
Skeletal muscle tissue oxygenation (StO2)
Ideal Fluid Volume
Balance between optimum CO and avoidance of complications
(decreased lung compliance, Increased I Abdo pressure, ICP,
BP, HR are surrogate markers for CO and have limited correlation
Increase afterload
Cardiac Output may improve temporarily
Potential benefits of fluid
Preload – haemodynamic parameters
Perfusion and oxygenation of organs
Problems - End Organ damage
secondary to resuscitation
Lungs – ARDS/ APO
Kidneys – ATN
Liver – transaminaemia/ impaired gluconeogenesis
GUT – Compartment syndrome
Brain – Cerebral oedema
Fluid volume
Only about 50% of patients with circulatory failure will respond to a fluid challenge.[13,16]
Important to determine:
Preload (LVEDV)
Fluid responsiveness, - whether the patient will increase his/her stroke volume or cardiac
output with fluid
Overall fluid balance - interstitial fluid volume (third space volume).
13. Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived variables and
fluid responsiveness in mechanically ventilated patients. A systematic review of the literature. CritCare
Med 2009; 37: 2642–7.
14. Braunwald E, Sonnenblick EH, Ross J. Mechanisms of cardiac contraction and relaxation. In:
Braunwald E (ed.).HeartDisease. W.B.Saunders Company: Philadelphia, PA, 1988, pp. 383–425.
15. Nixon JV, Murray RG, Leonard PD, et al. Effect of large variations in preload on left ventricular
characteristics in normal subjects. Circulation 1982; 65: 698–703.
16. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the
evidence. Chest 2002; 121: 2000–8.
Volume Overload
Excessive fluid resuscitation with an accumulating positive fluid
balance is associated with worse clinical outcomes.
Radiographic and clinical signs of pulmonary edema and clinical
evidence of peripheral oedema are late signs of volume overload
Extravascular lung water (EVLW) as determined by lung ultrasound,
transpulmonary thermodilution are two techniques that 'measure'
interstitial fluid volume (tissue edema) and may aid in the assessment of
volume overload.
Vincent JL, Sakr Y, Sprung CL, et al. Sepsis in European intensive care units: results of the SOAP
study. Crit Care Med 2006; 34: 344–53.
Assessing fluid volume status
Clinical parameters
Preload surrogates:
IVC collapsibility
Problem = static
60-70% sepsis have cardiac dysfunction
CVP responders 8.7 +/- 2.32, non responders 9.7 +/- 2.32
Static Measures:
Dynamic Measures:
IVC collapsibility (>20% valid if intubated)
>50% valid if non intubated
ETC02 - Increase >5% after PLR 75% sens 100% spec for fluid responsiveness (ventilated)
Pulse Pressure Variation – ventilated, large Vt etc
Stroke Volume (echo)
Cardiac Output (Most valid measure)
Passive Leg Raise V Fluid challenge
CHEST 2008; 134;172-178
ANNALS 2010 March 55(3):290-295
Other techniques:
Predictive value of techniques used to determine fluid responsiveness
Pulse pressure variation
Arterial waveform 0.94 (0.93–0.95)
Systolic pressure variation Arterial waveform 0.86 (0.82–0.90)
Stroke volume variation Pulse contour analysis 0.84 (0.78–0.88)
Left ventricular end-diastolic area Echocardiography 0.64 (0.53–0.74)
Global end-diastolic volume Transpulmonary thermodilution 0.56 (0.37–0.67)
Central venous pressure Central venous catheter 0.55 (0.18–0.62)
*AUC = area under the curve with 95% confidence intervals.
nb: Ventilated patients
Ref: Hemodynamic Parameters to Guide Fluid Therapy
Bedside Ultrasound (E-FAST)
Good for diagnosing causes of shock:
RV dilatation ?PE
Free fluid in P.O.D ?ectopic
Cardiac Output (cardiac probe)
You have to fill the tank if its empty..
If CVP v low (1-4) – give fluid
>50% change with respiration = CVP<8
>20% change if ventilated
Which fluid
N Saline
Awaiting too long for initiation of vasopressors in patients with overt
shock (or awaiting for the patient to be transferred from the ward to
ICU to start vasopressors).
Slow titration of vasopressors
If the patient is persistently hypotensive (i.e., MAP < 65 mm Hg) start
vasopressors while continuing IV volume resuscitation
It is usually clear within the first 10-15 minutes or less of properly
administered IV fluid bolus, whether the blood pressure is properly
The washup…
Our tools, on the whole, taken in isolation, are fairly appalling for
identifying shock.
Measures of intravascular volume are all unreliable, particularly in
the spontaneously ventilating patient
IVC filling on ultrasound
lung ultrasound
End-tidal carbon dioxide (ETCO2) levels depend on cardiac output. Increasing
cardiac output with a fluid challenge or PLR increases ETCO2,as long as
ventilatory and metabolic conditions remain stable. In a recent small study, a
PLR-induced increase in ETCO2 ≥ 5 % predicted a fluid-induced increase in
cardiac index ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %)
and specificity of 100 (82-100) %(3). The maximal effects of PLR on CI and
ETCO2 were observed within 1 min.
In summary, differentiating fluid responders from non-responders in the ED
remains a challenge. The method used depends on available equipment and
expertise, and whether the patient is spontaneously breathing or mechanically
ventilated. The NICOM(TM) shows great promise but until your department can
afford one, ultrasound is the way to go; small collapsing IVCs suggest fluid
responders. Learning to measure a VTI on transthoracic echo or carotid Doppler
flow will help you assess the response to a PLR in spontaneously ventilating
patients. If they’re mechanically ventilated, then looking for an ETCO2 rise after
PLR could be a simpler alternative.