Hemodynamic Monitoring

Emmy Pranggono

Internal Medicine Department, Pulmonary and Critical Care Division

Universitas Padjajaran

INTRODUCTION

Hemodynamic, make it easy

Hemodynamic management is

a very important

a corner stone of activity in high/care intensive care or emergency room, although it can be happened in the ward

Misleading of the treatment

increasing the morbidity and mortality

Understanding is mandatory.

One type of shock is circulatory shock which is

a complex clinical syndrome

if not corrected will be fatal

Hemodynamic, make it easy

Monitoring hemodynamic in shock as a guide and dictation of accurate clinical assessments

The issues raised in the new statements or recommendations for monitoring hemodynamic shock

individualization of blood pressure targets

prediction of fluid responsiveness

the use of echocardiography which is not invasive as the first means during the initial evaluation of circulatory shock. Bedside assessment of intravascular volume status in critically ill

to prevent the risk of organ failure and mortality.

Hemodynamic, make it easy

Clinicians often use invasive hemodynamic monitoring like Central venous pressure (CVP) is a hemodynamic parameter that is extensively used

CVP is a good indicator of right ventricular preloadbut the complication associated with CVP insertion includes

failure to place the catheter, arterial puncture, catheter malposition, pneumothorax, subcutaneous hematoma, hemothorax, asystolic cardiac arrest and catheter-related infection

Hemodynamic, make it save

There is a needs for a non-invasive and economical technique like ultrasound in the critically ill patient

helps to approach diagnosis and treatment of the critically ill patients.

to estimate the intravascular status by measuring IVC diameter uses the size

collapsibility of the inferior vena cava (IVC).

Fluid administration and pharmacological therapy with vasopressor or inotropes are used to maintain CO and improve organ perfusion while treating the underlying disease

Shock states

Initiated by inadequate tissue perfusion Impaired the oxygen supply to the mitochondria Resulting severe dysfunction of vital organs (cellular

dysoxia) Associated with elevated blood lactate levels.

Hypotension is no longer mandatory in defining a shock state (ESICMc-2014)

Shock can occur following either hypoperfusion or inadequate perfusion of end organs leading imbalance oxygen delivery (DO2) and oxygen

consumption (VO2) Elevated blood lactate

Definition and pathophysiological features of shock in the ICU

According to ESICM (ESICMc-2014)

Circulatory shock an acute clinical life-threatening generalized syndrome of acute circulatory

failure associated with inadequate oxygen utilization

by the cell

Critical Care Medicine 2016,The Diagnosis anHemodynamic Circulatory Shock: Monitoring Current and Future Trends Adham Hendy, Şerban-Ion Bubenek-Turconi,

The hemodynamic monitoringtechniques in shock

There are three main reasons for hemodynamic

monitoring in shock patients:

1. To identify the type of shock

2. To select the most appropriate therapy

3. To evaluate the response to that therapy

What is blood pressure?

As the heart contracts, blood is forced out of the left ventricle and into the aorta and distributing arteries

The force created by the heart's contraction generates pressure as blood pushes against the walls of the vessels

This is known as blood pressure and consists of two pressures readings: The maximum pressure (systolic) occurs as the heart contracts The minimum pressure (diastolic) occurs as the heart fills back

up with more blood

The normal blood pressure for an adult is 120/80 mmHg.

Blood Pressure

What is Mean Arterial Pressure (MAP)?

The average blood pressure during a single cardiac cycle

Necessary for adequate perfusion of the organs

A better indication of perfusion than systolic blood pressure

At least 60 mmHg to provide enough blood to

the coronary arteries, kidneys, and brain

The normal range is between 70 and 100 mmHg

MAP is directly affected by factors:

Amount of blood pumped out of the heart per minute (cardiac output)

Heart rate (beats per minute)

Blood pressure

Resistance to blood flow in the vessels

At normal resting heart rates, MAP can be approximated by the following equation:

MAP = (CO × SVR) + CVP

Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:

MAP ≈ CO × SVR which is

CO depend on Heart Rate (HR) and Stroke Volume (SV)

CO = Cardiac Output

SVR = Systemic Vascular Resistance

CVP = Central Venous Pressure

Approach management of hypotension

How to Calculate MAP

The most accurate MAP can only be determined through an invasive central line

However, it can be measured by another equation using the systolic blood pressure (SBP) and diastolic blood pressure (DBP)

Four types of hemodynamic shock

Hypovolemic shock:

A direct loss of effective circulating blood volume (internal and/or external) which primary leads to decreased cardiac preload, stroke volume and consequently impaired end-organ perfusion.

Cardiogenic shock

A decreased systemic circulatory blood flow due to an intrinsic defect in cardiac function either the heart muscle and/or valvular dysfunction.

Four types of hemodynamic shock

Obstructive shock

Intra-cardiac or extra-cardiac mechanical obstruction to cardiac filling that decreases the cardiac output and consequently decreases end-organ perfusion.

Distributive shock:

A peripheral vascular dilatation causing a decreased systemic vascular resistance (SVR) associated with increased cardiac output and compromised perfusion of vital organs.

However many patients with circulatory failure have a combination of more than one form of shock as is seen in cases of septic shock.

Sepsis previously was defined as

a systemic inflammatory response syndrome (SIRS) in response to an infectious process

Septic shock

severe sepsis with persistent signs of end organ damage, hypotension (systolic blood pressure <90mmHg) and elevated serum lactate (>4mmol/l).

Considering that there was a need to re-examine theclassical definition of sepsis to distinguish sepsis from uncomplicated infection

ESICM and the Society of Critical Care Medicine (USA) published in February 2016

“The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

“The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

They redefined sepsis as “a life-threatening organ dysfunction caused by a dysregulated host response to infection”.

Hence, they advocated a change in the way sepsisand septic shock is approached,

away from a focus on the reaction to a systemic inflammation and towards a consideration of organ dysfunction

The latter can be identified in ICU patients as an

acute change in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score>2 points, subsequent to the infection

Mortality septic shock vs sepsis alone

>40 % versus >10 %

The Sepsis-3 definition for the septic shock in adult patients is based on cumulative criteria

sepsis plus hypotension requiring the use of vasopressors to maintain MAP ≥ 65mm Hg

elevated blood lactate levels > 2 mmol/L

persisting after adequate fluid resuscitation

Diagnosis of shock

Patients should be assessed for the etiology of shock by an initial rapid clinical

evaluation based on a history taking

physical examination

appropriate initial laboratory tests.

Diagnosis of shock

Clinical signs and bedside observations

maintained arterial blood pressure

is still possible to find markers of inadequate tissueperfusion such as

increased blood lactate levels

low mixed venous oxygen saturation (SvO2)

low centralvenous oxygen saturation (ScvO2) values

Diagnosis of shock

For this reason, hypotension was excluded from themandatory definition of shock states, with the notable exception of septic shock

On the other hand, some early clinical findings such as

skin colour and skin temperature disturbances, heart rate, rhythm, electrocardiogram (ECG), capillary re-fill test, urineoutput, mental status, the effect of body position on the blood pressure, remain valuable signs of hemodynamicshock and pre-shock phases.

Diagnosis of shock

Clinicians should always check for clinical signs of ineffective tissue perfusion take into account the three “windows” (1) skin (cutaneous perfusion)

(2) kidney (urine output)

(3) brain (mental status)

2. Metabolic markers of regional and microcirculation

and the assessment of cellular function in shock

Arterial or venous blood lactate levels

The higher blood lactate level the higher mortality and morbidity Hyperlactatemia is a marker of

Imbalance between the oxygen consumption (VO2)and oxygen delivery (DO2) in any kind of shock

It is a much more precise indicator of ineffective perfusion than a base deficit or metabolic acidosis

the transition from aerobic to anaerobic metabolism

The new ESICMc-2014

Blood lactate levels > 2mEq/L should be consideredthe hallmark of an existing shock syndrome

Presence of hemodynamic shock plus hyperlactatemia > 4.0 mmol/L is associated with a mortality of 30% to 45%

Blood lactate levelel > 6 mmol/l predicts a mortality range between 80% and 90%

Obviously, the other circumstances associated withhigh lactate levels, are driven by ineffective localperfusion such as

local ineffective perfusion, drug effects, liver failure, malignancy, thiamine deficiency, seizures, or patients in bed struggling against restraints or shivering, have to be exclude.

Apart from blood lactate, SvO2 or ScvO2 values canoffer valid information about the balance between DO2 and VO2.

Inferior Vena Cava collapsibility Ultrasound for Volume Status Assessment

Echocardiography is an essential tool for guiding resuscitation in critically ill patients in an effort to reverse organ dysfunction

Intravenous fluid boluses can benefit the circulation but also cause harm of inappropriate use of fluid are becoming increasingly apparent

Although the purpose of fluid resuscitation is often to increase cardiac output, blood flow is not routinely used to guide resuscitation

Diameter Vena Cava Inferior

Vena cava inferior Atrium

kanan

Pressure of IntrathoracalIntraperikardial Intraabdominal,

Hipertensi Pulmonal

collapsibility

Ǿ 1,2 - 1,7 cm

1-8 mmHg

RAP 10-15 mmHg

collaps < 50%

RAP >15 mmg

No collaps

RAP 6-10 mmHg

collaps ≥ 50%

Ǿ VCI <1,2 cm

spontancolaps

Subcostal

view

M

mode

Inferior Vena Cava collapsibility Ultrasound for Volume Status Assessment

Although the purpose of fluid resuscitation is often to increase cardiac output, blood flow is not routinely used to guide resuscitation

Sufficient mean arterial pressure (MAP) is rightly targeted but is proportional to flow only for a given systemic vascular resistance (SVR)

Measurement of flow requires more equipment, time and expertise than standard parameters such as blood pressure and for an individual patient is not predictable

Mixed venous oxygen saturations and lactate are useful but only reveal a large mismatch between supply and demand, missing subtler shock states.

Inferior Vena Cava (IVC) collapsibility Ultrasound for Volume Status Assessment

The presence of signs that fluid delivery improves cardiac output does not mean that a greater cardiac output is necessary.

??? the patient improves with

fluid

additional vasopressors or inotropes

Echocardiography is an evidence-based approach and ideally suited to address this problem.

IVC and collapsibility

Conclusions

Hemodynamic monitoring is mandatory in critically ill patient

The superiority of the dynamic over the static parameter to predict fluid responsiveness

Echocardiography is an uninvasive methode and preferred technical method for the initial diagnosis and follow-up of patient in hemodynamic shock

Blood lactate is an important clinical bed-side biomarker during the follow-up of a patient in circulatory shock.

TERIMA KASIH