UCARDS Survey

UCARDS: Use of CARdiovascular Drugs in Shock

In shock, organs are hypoperfused leading to dysfunction or death at a cellular level, as well as disruption in cardiovascular functions. Cardiovascular drugs are often used to manage patients in this state, despite the lack of consensus on their use. This survey from the Cardiovascular Dynamics Section aims to evaluate the indications, current practice, and therapeutic goals in European ICU‘s on the use of cardiovascular drugs in the treatment of shock states.

Thank you for participating in the survey,

Jean-Louis TEBOUL, Chair ESICM Cardiovascular Dynamics Section
Thomas SCHEEREN, Deputy for the Cardiovascular Dynamics Section

1.Country(Required.)

3.Experience

I am not specialized as an intensivist (yet)

I am an intensivist but work only part time on an ICU

I am an intensivist for less than 2 years and work full time on an ICU

I am an intensivist for more than 2 years but less than 5 years and work full time on an ICU

I am an intensivist for more than 5 years and work full time on an ICU

4.Type of ICU(Required.)

Medical ICU

Surgical ICU

Mixed ICU

Other (please specify)

5.Number of ICU beds:(Required.)

7.Type of institution(Required.)

University hospital

University affiliated hospital

Non-university public hospital

Private hospital

Other (please specify)

8.What is your main triggering factor(s) for initiating a vasopressor in a shock state?(Required.)

Insufficient mean arterial pressure response to the initial fluid resuscitation

Insufficient cardiac output response to the initial fluid resuscitation

Insufficient central venous oxygen saturation response to the initial fluid resuscitation

A low diastolic blood pressure whatever the correction of hypovolemia

Other (please specify)

9.What is your first line vasopressor in the treatment of hypotension?(Required.)

10.How do you dose your vasopressor? (several answers may apply)(Required.)

I dose my vasopressor in mg/h

I dose my vasopressor in mcg/kg/min

I have a maximum vasopressor dose that I never exceed

I have a target vasopressor dose that I apply most of the time

I titrate my vasopressor on the dose rather than a clinical (hemodynamic) endpoint

11.When do you use your vasopressor(Required.)

I use a vasopressor only after assessment of preload dependence

I use a vasopressor only after completed treatment of preload dependence

I use a vasopressor regardless of preload dependence

I use a vasopressor early, before volume resuscitation (despite preload dependence)

I try to avoid any use of vasopressors and stick to volume therapy

12.What is your main reason for increasing the dose of the vasopressor used?(Required.)

No arterial blood pressure response to current dose

Mean arterial pressure target not reached

Systolic arterial pressure target not reached

Diastolic arterial pressure target not reached

Signs of organ dysfunction despite reaching the arterial blood pressure target

13.What is your arterial blood pressure target for vasopressor therapy?(Required.)

A mean arterial pressure >60-65 mmHg

A mean arterial pressure >70-75 mmHg

A mean arterial pressure >80-85 mmHg

A systolic blood pressure >100 mmHg

A diastolic blood pressure >40 mmHg

14.How do you measure arterial blood pressure in shock?(Required.)

Always invasively and continuously via an arterial line

Invasively only in case of severe shock

Mostly non-invasively and discontinuously (arm cuff)

Mostly non-invasively but continuously using finger cuff

Mostly non-invasively but continuously using applanation tonometry

15.Which patient’s factor(s) may encourage you to increase your arterial blood pressure target?(Required.)

16.When the patient does not respond to your current vasopressor therapy, what is your main reason for adding another vasopressor agent to the current therapy?(Required.)

A pre-defined maximum dose of the 1st choice vasopressor has been reached

Although the pre-defined maximum dose of the 1st choice vasopressor has not been reached, previous increases in the dose of this vasopressor were ineffective

By adding a second vasopressor although the pre-defined maximum dose of the 1st choice vasopressor has not been reached, I want to limit/reduce the side-effects of the first vasopressor

I suppose that the mechanism of action of the first vasopressor is exhausted (e.g. adrenoceptors down regulation) and want to use of second one with an independent mechanism of action

I want to use synergistic effects of two different mechanisms of action

17.What is your main reason for reducing or stopping vasopressor therapy?(Required.)

Arterial blood pressure targets have been reached

I am concerned by potential side effects of current vasopressor therapy

Side effects of current vasopressor have occurred

The patient’s clinical situation is improving even if the arterial blood pressure target has not been reached

Vasopressor treatment is futile

18.Which of the following statements fits best your opinion on norepinephrine use in the treatment of shock?(Required.)

Restoring mean arterial pressure with norepinephrine is usually associated with a decrease in systemic blood flow

Restoring mean arterial pressure with norepinephrine is usually associated with no change in systemic blood flow

Restoring mean arterial pressure with norepinephrine is usually associated with an increase in systemic blood flow

Restoring mean arterial pressure with norepinephrine is usually associated with a reduction in microcirculatory blood flow and/or tissue oxygenation

Restoring mean arterial pressure with norepinephrine is usually associated with a deterioration of renal function

19.What is your first-line inotrope to increase cardiac pump function?(Required.)

20.What are your most important criteria for using an inotrope to increase cardiac pump function?(Required.)

I measure cardiac output and find it low (e.g. cardiac index <2.5 L/min/m2)

I measure left ventricular ejection fraction and find it low (< 45%)

I measure central venous oxygen saturation and find it low (< 70%)

There are persistent clinical signs of hypoperfusion (e.g. skin mottling, low urine output) or persistent hyperlactatemia despite a supposed adequate use of fluids and vasopressors

There are persistent clinical signs of hypoperfusion (e.g. skin mottling, low urine output) or persistent hyperlactatemia despite a supposed adequate use of fluids and vasopressors in the context of low left ventricular ejection fraction

21.What are your primary therapeutic targets when using an inotrope?(Required.)

22.When the patient does not respond to your current inotropic therapy, what is your main reason for adding another inotrope/vasoactive agent to the current therapy?(Required.)

The maximum dose of the 1st choice inotrope has been reached

Although the maximum dose of the 1st choice inotrope has not been reached, previous increases in the inotrope dose were ineffective

By adding a second inotrope although the maximum dose of the 1st choice inotrope has not been reached, I want to limit/reduce the side-effects of the first inotrope

I suppose that the mechanism of action of the first inotrope is exhausted (e.g. adrenoceptors down regulation) and want to use a second one with an independent mechanism of action

I want to use synergistic effects of two different mechanisms of action

23.Which of the following statements fits best your opinion on catecholamine use in the treatment of shock?(Required.)

Although adrenaline (ADR) has the same adrenoceptors profile than the combination of noradrenaline (NOR) plus dobutamine (DOB), ADR should be preferred because of its easiness to be used (single agent).

Although adrenaline (ADR) has the same adrenoceptors profile than the combination noradrenaline (NOR) plus dobutamine (DOB), the combination NOR/DOB should be preferred since either component can be titrated individually.

The combination NOR/DOB should be preferred over ADR due to a better patient outcome

The combination NOR/DOB should be preferred over ADR since ADR may decrease regional blood ﬂow, particularly in the splanchnic circulation.

The combination NOR/DOB should be preferred over ADR since ADR may increase blood lactate levels and cause cardiac arrhythmias

24.Which of the following statements fit(s) best your opinion on the use of phosphodiesterase (PDE)-inhibitors in the critically ill?(Required.)

Compared to ß-adrenoceptor agonists (e.g. dobutamine), PDE-inhibitors have similar effects on cardiac output but additionally decrease the cardiac filling pressures (CVP, PAOP)

Compared to pure vasodilators (e.g. nitroprusside), PDE-inhibitors cause larger increases in cardiac output and smaller decreases in arterial pressure

Because of their prominent vasodilatory effect on the pulmonary circulation, PDE-inhibitors should be preferred in the treatment of predominant right heart failure

PDE-inhibitors should be avoided in the treatment of cardiogenic shock since they are associated with increased mortality

PDE-inhibitors should be avoided in the treatment of cardiogenic shock since they may increase the incidence of atrial fibrillation or tachyarrhythmias

25.Which of the following statements fits best your opinion on the use of levosimendan in the critically ill?(Required.)

Levosimendan is the only inotrope that is not associated with an increased mortality

Levosimendan is the only inotrope that does not increase myocardial oxygen demand

Levosimendan is also a potent vasodilator in the systemic and pulmonary circulation

Levosimendan may be considered as cardioprotective, as it reduces troponin I release (pleiotropic effect)

Levosimendan is associated with an increased incidence of atrial fibrillation and ventricular ectopy

26.What do you think about the use of vasodilators in patients with shock?(Required.)

I never use vasodilators in septic shock even when arterial blood pressure has been maintained with a vasopressor

I do use in septic shock when arterial blood pressure has been maintained with a vasopressor in order to improve the microcirculatory blood flow

I do use vasodilators in cardiogenic shock to decrease left ventricular afterload

I do use vasodilators in cardiogenic shock to improve the microcirculatory blood flow

I have no experience or no opinion about the use of vasodilators in patients with shock

27.What do you think about the use of ß-adrenoceptor antagonists (ß-blockers) in patients with shock?(Required.)

ß-blockers are contraindicated in shock states

ß-blockers should be added to the cardiovascular management in order to decrease myocardial oxygen demand

ß-blockers should be used in septic shock since they can decrease mortality

I do use ß-blockers in septic shock only in case of excessive tachycardia (e.g. > 130 beats/min)

I have no experience or no opinion about the use of ß-blockers I shock states