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Introduction to

applications
 Haemodynamic monitoring is crucial in A basic haemodynamic monitor, which Unlike technologies that require external
surgical and critically ill patients. It can provides only the values of heart rate, calibration or the use of anthropometric
help physicians and nurses in identifying blood pressure and indirect preload (e.g. data to calculate Z (t) or impedance, Most-
the cardiovascular and pathophysiologi- CVP), does not allow the clinician to de- CareUp uses high definition 1000Hz mea-
cal status of a patient, allowing operators fine in detail the variations of individual surement of the arterial pressure wave to
to choose the most appropriate therapy cardiovascular profiles that follow one calculate Z(t), making MostCareUp ideal
(e.g. vasopressor, fluid, or inotropic drugs). another, for example in the septic patient. for any patient who requires constant or
Also, haemodynamic monitoring allows However a monitor that provides conti- occasional haemodynamic monitoring. Es-
pre-emptive therapy to be initiated early, nuous and advanced haemodynamic pecially those high-risk patients with hae-
before a deterioration of clinical condi- variables including cardiac output and modynamic instability or the presence of
tions can occur (e.g. detection of low out- oxygen delivery, systemic vascular resis- acute clinical variations.
put state or hypovolemia). tances, arterial elastance, indicators of
Standard monitoring procedure in ope- myocardial contractility and efficiency of
rating theatres and intensive care units the cardiac cycle, allows the clinician to
includes the measurement of heart rate, use the haemodynamic information
blood pressure and oxygen saturation. and, adapt therapy to reflect the diffe-
However, these variables are not suffi- rent haemodynamic requirements of the
ciently sensitive to drive treatment pro- septic patient.
tocols. For managing patients using goal
directed therapy, an advanced and conti-
nuous haemodynamic monitor, which pro-
vides additional, sensitive and predictive
haemodynamic parameters, is required.

26

Do & Check
15

7.7

function FiO2
45
PEEP
4
R.R.
15
T.V.
500

45°

PR PR
120 PR 105

CO CO
CO (+23%)

3.1 3.8
CCE
CCE CCE
-0.19 0.07
PPV

PPV 12.20 12.30 12.40 12.50 PPV

18% PLR
12%

Img. 1 – MostCareUp Do&Check function

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Perioperative haemodynamic optimisation
One of the important factors influencing (reactive approach). On the contrary, the move the risk of oxygen depletion from
the preoperative outcome is surgical use of a "goal directed therapy" proto- surgical stress. The above has proved to
stress, which leads to increased oxygen col allows a "proactive" strategy that be particularly important in patients with
demand. An unfavourable outcome is res- provides monitoring and optimisation of a moderate to high surgical risk.
ponsible for increased patient stay time haemodynamic variables and early inter-
and cost for the hospital. vention in order to prevent haemo-
Usually therapeutic intervention is a func- dynamic impairment. The final aim is
tion of actual haemodynamic impairment to improve tissue oxygen delivery and re-

hypovolemia hypervolemia

• Tissue and
• Hypoperfusion pulmonary
COMPLICATIONS

• Reduced DO2 oedema

LOW PRELOAD INTERMEDIATE PRELOAD HIGH PRELOAD

PRELOAD
(volume)

Img. 2 – Classic U-curve

One of the most frequent causes of tis- put. Hypovolaemia may be harmful to pa- SVV and SPV which are based on heart
sue hypoperfusion is linked to hyper or tients and excessive fluid administration lung interactions during mechanical ven-
hypovolemia. In the first case, tissue and may also be harmful. tilation have been shown to be accurate
pulmonary oedema, in the second case, predictors of fluid responsiveness. Fluid
reduced oxygen delivery, are responsible GDT-based guidelines recommend responders are patient’s whose CO
for organ damage, expressed by the clas- the use of functional haemodynamic mo- (or SV) increases > 10-15% after a fluid
sic U-curve. Adequate venous return to nitoring and do not recommend the use challenge or passive leg raising.
the heart is essential to support optimal of static variables (CVP, PAOP) to guide
Stroke Volume and hence Cardiac Out- fluid therapy. Dynamic variables PPV,

PPV
NORMAL VENTRICLE

% ∆SV
STROKE VOLUME

Fluid Challenge 2

% ∆SV FAILING VENTRICLE

% ∆SV
Fluid Challenge 1
Fluid Challenge 2

% ∆SV

Fluid Challenge 1

PRELOAD
Img. 3 – Frank-Starling curve

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 The increase in intrathoracic pressure with no spontaneous breathing and who When PPV is in the grey zone (9-13%)
induced by a positive pressure breath are in normal sinus rhythm. response to fluid administration cannot
during mechanical ventilation induces a be predicted.
When the PPV value is less than 9%
change in Pulse Pressure, Stroke Volume
administration of fluid is
and Systolic Pressure when the healthy
unlikely to lead to an in-
heart is working in the ascending part
crease in cardiac output
of the Frank-Starling Curve. PPV is often
(i.e. not fluid responsive).
preferred to SVV because it is measured
When the PPV is greater
and not calculated. It is important to ap-
than 13% administration
preciate that PPV, SVV and SPV are only
of fluid is likely to lead to
validated for use as predictors of fluid
an increase in CO. (i.e. pa-
responsiveness in specific conditions, in-
tient is fluid responsive e).
cluding mechanically ventilated patients

Tissue hypoperfusion
(reduced DO2, arterial hypotension, oliguria, hyperlactatemia, reduced SvO2, skin mottling, …)

Hypovolemia/Hypervolemia?

<9% PPV >13%

Normo/hypervolemia 9%< PPV <13% Fluid responsiveness check

grey zone**

PLR or Fluid
Check other (when Challenge
Consider
reasons of possible)
PLR test
hypoperfusion

<10%
SV, CO >10%
dP/dt, SVR, Ea, … along Increase?
with Echocardiographic
examination • Stop fluid load • HR reduction
• Check other variables • BP increase

* However, there is no agreement on the cut off (from 10 to 15%, Toscani et al.
CritCare 2017).
** 50% of the patients in the grey zone might respond to fluid challenge

Img. 4 - A typical algorithm of perioperative GDT focused on fluid responsiveness

1. Bellamy MC.Wet, dry or something else? British Journal of Anaesthesia 2006; 97:755-7
2. Jhanji S,Thomas B, Ely A,Watson D, Hinds CJ, Pearse RM. Mortality and utilisation of critical care resources amongst high-risk surgical patients in a large NHS
trust. Anaesthesia. 2008 Jul;63(7):695-700
3. M ichard F, Chemla D,Teboul JL. Applicability of pulse pressure variation: how many shades of grey? Crit Care 2015; 19(1): 144.
4. G iglio M, Manca F, Dalfino L, Brienza N. Perioperative haemodynamic goal-directed therapy and mortality: systematic review and meta-analysis with meta
regression. Minerva Anestesiol 2016. 82 (11): 1199-1213
5.Toscani L, Aya HD, Antonakaki D, Bastoni D,Watson X, Arulkumaran N, Rhodes A, Cecconi M.What is the impact of the fluid challenge technique on diagnosis
of fluid responsiveness? A systematic review and meta-analysis. Crit Care 2017 Aug 4;21(1):207.
6. B rienza N, Biancofiore G, Cavaliere F, Corcione A, De Gasperi A, De Rosa RC, Fumagalli R, Giglio MT, Locatelli A, Lorini FL, Romagnoli S, Scolletta S,Tritapepe L.
Clinical guidelines for perioperative hemodynamic management of non cardiac surgical adult patients. Minerva Anestesiol. 2019.

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Cardiac failure: cardiovascular function
evaluation and optimisation
Cardiac failure leads to a reduction in oxy- in filling pressures (LVEDP and CVP). The require experience, is not always instantly
gen delivery resulting in tissue hypoper- clinical consequences may be pulmo- available and is not designed for conti-
fusion, multi-organ dysfunction (MODS) nary oedema, venous stasis and increased nuous monitoring.
and multi-organ failure (MOF). There can afterload as a compensatory mechanism.
be many causes for cardiac failure, inclu- Also, poor cardiac contractility may be Continuous haemodynamic moni-
ding ischaemia and myocardial infarction, accompanied by unsuccessful weaning toring has the advantage of allowing the
arrhythmias, myocarditis, valvopathies and from mechanical ventilation and organ clinician to obtain information on the
idiopathic cardiomyopathies. hypoperfusion. These comorbidities are cardiovascular status of the patient on
responsible for a prolonged stay in inten- a continuous basis and thus facilitating
Left ventricular systolic insufficiency, is sive care. control of the effectiveness of the-
characterized by a reduction in contrac- rapy over time; using trending variables,
tility resulting in a reduction in stroke vo- Whilst echocardiography allows us to dia- thereby reducing the risk of a deteriora-
lume, arterial hypotension and an increase gnose the nature of heart failure, it does tion in the patient clinical condition.

Tissue hypoperfusion
(low SV and CO, reduced DO2, arterial hypotension, oliguria, hyperlactatemia, reduced SvO2, skin mottling,…)

Cardiac failure?

Reduced myocardial
contractility?

Hypokinesia with
Echocardiography Check other
NO
Low dP/dt, low CPO, determinants
low CCE of cardiac
failure
Inotropes
IABP YES

Check of

Preload and Filling

Afterload
pressures
SVR, Ea
PAOP, CVP

High Normal High Normal

Vasodilators
or low Vasodilators
or low
Diuretics Careful Careful
Fluid restriction Fluid treatment* Vasoconstriction
therapy **

*aim to keep normovolemia and avoid overload and pulmonary oedema

** aim to keep adequate afterload and optimal A_V coupling

Img. 5 - A typical example of haemodynamic monitoring-based therapy

1. Cecconi M, Reynolds TE, Al-Subaie N, Rhodes A. Haemodynamic monitoring in acute heart failure. Heart Fail Rev. 2007 Jun;12(2):105-11
2.Vincent JL, De Backer D. Circulatory shock.N Engl J Med. 2013 Oct 31;369(18):1726-34.
3. Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, Jaeschke R, Mebazaa A, Pinsky MR,Teboul JL,Vincent JL, Rhodes A. Consensus on circulatory
shock and hemodynamic monitoring.Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014 Dec;40(12):1795-815
4. De Backer D, Bakker J, Cecconi M, Hajjar L, Liu DW, Lobo S, Monnet X, Morelli A, Myatra SN, Perel A, Pinsky MR, Saugel B,Teboul JL,Vieillard-Baron A,Vincent JL.
Alternatives to the Swan-Ganz catheter. Intensive Care Med. 2018 Jun;44(6):730-741.

5
 Septic patient: haemodynamic derangement
and assessment
Sepsis is a complex syndrome that repre- The most evident clinical and haemodyna- plex mechanisms and slower to establish
sents a major challenge for the intensi- mic manifestation of the septic patient is (e.g. mitochondrial dysfunction, metabolic
vist, as it is quite frequent in intensive care arterial hypotension, often resistant to and autonomic alterations, ....) and which
leading to multiple organ complications pharmacological treatment. It is linked to involves a reduced cardiac output and a
and mortality. the three cardiovascular alterations pre- low tissue oxygen delivery.
viously reported: When microcirculatory dysfunction pre-
The clinical complexity of this syndrome a) hypovolaemia, mainly linked to fluid vails over macrodynamic alterations, the
derives mainly from the profound hae- shift due to increased vascular permea- oxygen delivery can be increased due to
modynamic changes that characterise bility (absolute hypovolemia), and de- the high cardiac output, although oxygen
sepsis itself and septic shock.These altera- termined by reduced vascular tone and peripheral extraction is decreased.
tions include a typical triad: hypovolemia, increased venous capacity (relative hypo-
decrease of vascular tone and myocardial volemia);
depression. These conditions are also ac-
b) decrease in vascular tone, linked to
companied by abnormal redistribution of
reduced or loss of adrenergic response by
blood flow between the various organs
smooth muscle cells of the vascular wall;
due to multiple microcirculatory deran-
gement. c) myocardial depression, which may
appear later because it recognizes com-

Tissue hypoperfusion
(arterial hypotension, oliguria, hyperlactatemia, increased/reduced SvO2, skin mottling,…)

Sepsis/Septic shock?

Posivive Biomarkers
Documented Infection
Microcirculatory alterations
A-V decoupling

YES
Hyperdynamic state Hypodynamic state

High SvO2 Low SvO2

High CO & DO2 Low CO & DO2

altered CCE* Low CCE* Inotropes

High PPV & SVV Fluids Low dP/dt

Arterial hypotension Arterial hypotension

Vasoconstrictors Vasoconstrictors
Low SVR Ea Low SVR Ea

* CCE in hyperdynamic state is expected to be low due to A-V decoupling. When high, it represents low energy exediture due to low SVR

Img. 6 - A typical example of haemodynamic monitoring-based therapy in a septic patient

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These complex haemodynamic altera- In other cases, the haemodynamic profile variations are characterized by a decou-
tions mean that sepsis can occur, for exa- of the septic patient may be characterized pling between vascular tone and ventricu-
mple, with a haemodynamic state called by a "hypodynamic" state, which mani- lar contractility (A-V decoupling).
"hyperdynamic". This condition of fests itself with low vascular resistance,
hyper-dynamism (high flow rate) is cha- arterial hypotension and low cardiac out-
racterized by low systemic vascular resis- put, the latter resulting from myocardial
tance, reduced arterial elastance, arterial dysfunction. In both cases, the tissue use
hypotension and high cardiac output. of oxygen is very low and haemodynamic

1. De Backer D, Scolletta S. Clinical management of the cardiovascular failure in sepsis. Curr Vasc Pharmacol. 2013 Mar 1;11(2):222-42.
2. Guarracino F, Ferro B, Morelli A, Bertini P, Baldassarri R, Pinsky MR.Ventriculoarterial decoupling in human septic shock. Crit Care. 2014 Apr 24;18(2):R80
3. P erner A, Gordon AC, De Backer D, Dimopoulos G, Russell JA, Lipman J, Jensen JU, Myburgh J, Singer M, Bellomo R,Walsh T. Sepsis: frontiers in diagnosis, resusci-
tation and antibiotic therapy. Intensive Care Med. 2016 Dec;42(12):1958-1969.
4. L esur O, Delile E, Asfar P, Radermacher P. Hemodynamic support in the early phase of septic shock: a review of challenges and unanswered questions. Ann
Intensive Care. 2018 Oct 29;8(1):102.

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