ESICM Regional Conference Athens 2017: Pathophysiology of shock

Regulation of cardiac output (S Magder)

VO2 – normal physiology: CO increases in proportion to VO2
In young adult, can increase >12 fold i.e. from 0.25 to >3L/min
What regulates CO? ——> metabolism (assuming normal Hb and SpO2)
Normally DO2 does not determine VO2 —> determined by metabolism
DO2 = CO x Hb x k x SpO2
 
DO2 = CO * Hb * O2 sats (Hb and sats less amenable to intervention. Therefore, to increase DO2, need to increase CO)
CO has 2 components — cardiac function (LH/RH/Pulm circuit) and return function
  1. Cardiac function
Increase in cardiac function = Increase CO for same preload
  1. Return function?
Flow = Stressed volume/Venous compliance x Venous resistance
Needs to be a compliant region to have flow
SV out is what we normally focus on but also SV IN
Heart has a permissive function. Allows the veins to empty
Volume is not a physiological regulator of CO
  1. Cardiac Function
  2. Limit of return function
  3. Only stressed volume determines venous return
    1. Only about 1L
    2. Unlikely that a volume infusion >1L will increase stressed volume
  4. So….change in capacitance e.g. with vasopressor
  5. Can change by 10-15ml/kg – 700ml of stressed volume back again
  6. Increase capillary leak – increasing volume increased leak
Physiological approach
BP = CO x SVR
Measure:
  1. BP
  2. Estimated/measured CO (clinically or with device)
Is the CO decreased? or Is the CO normal/increased? in which case it’s the SVR
CO down?
  1. Heart not working
  2. Return not working

 

Volume and its relationship to cardiac output and venous return

 

Fluids after cardiac surgery: a pilot study of the use of colloids versus crystalloids.

 

Stressed vs. unstressed volume and its relevance to critical care practitioners

 

Vascular hyporesponsiveness (D Payen)

The unknown physiology when pt becomes critically unwell means that deciding on treatment is challenging

Blood pressure is not the same as cardiac output or flow

The Pressure Recording Analytical Method (PRAM): Technical Concepts and Literature Review

Vascular structure comprises of vascular smooth muscle and endothelium

Vascular Adaptation to Exercise in Humans: Role of Hemodynamic Stimuli

 

Interactions between fluids and vasoactive therapy (M Cecconi)

Occult hypoperfusion and mortality in patients with suspected infection

Unstressed volume does not generate a pressure.

Association Between US Norepinephrine Shortage and Mortality Among Patients With Septic Shock

Addition of vasopressors can increase cardiac output by altering the stress:unstressed volume relationship

Fluid administration in severe sepsis and septic shock, patterns and outcomes: an analysis of a large national database

Pharmacodynamic Analysis of a Fluid Challenge.

Association of arterial blood pressure and vasopressor load with septic shock mortality: a post hoc analysis of a multicenter trial

Dynamic arterial elastance predicts mean arterial pressure decrease associated with decreasing norepinephrine dosage in septic shock

Can one size fit all? The fine line between fluid overload and hypovolemia

Cardiac dysfunction and functional haemodynamics (M Pinsky)

Functional hemodynamic monitoring

Functional hemodynamic qns

  • Is my patient in compensated shock?
  • Will CO increase with fluids?
  • Is arterial tone increased, normal or decreased?
  • Is the heart able to maintain adequate output under pressure?

52% of pts who present in circulatory shock will not be fluid responders!

Comparison of Echocardiographic Indices Used to Predict Fluid Responsiveness in Ventilated Patients

Limitations of PPV or SSV to predict responsiveness

  • Arrhythmias
  • Constant TV
  • High RR
  • Spont ventilatory efforts

Microcirculation derangements (C Ince)

4 stages of shock:
  1. Cardiogenic
  2. Hypovolaemic
  3. Obstructive
  4. Distributive ——> vascular distribution
Amended by Ince:
  1. Cardiogenic
  2. Hypovolaemic
  3. Obstructive/reperfusion
  4. Distributive ——> vascular distribution
  5. Anaemic/hamodilutional
Sepsis is a disease of the microcirculation. All 5 present
Systemic variables are a surrogate for abnormalities in tissue perfusion
All drugs focused on systemic haemodynamics in expectations tissues will improve perfusion
If doesn’t work – unresponsive i.e. dont know what is going on!
Microciculation
  1. RBC
  2. Endothelium/glycocalyx
  3. Auto regulatory control
  4. O2 handling in mitochondria
Need ATP for Na-K pump
Shunting model of sepsis
Implication: That active recruitment of the microcirculation is an important component of resuscitation
Haemodynamic coherence: Resus concept that says that when you resuscitate a systemic variable you expect a parallel improvelemt in microcirculation and tissue perfusion
4 area:
  1. Heterogeneity e.g. sepsis
  2. Haemodilution
  3. Constriction
  4. Edema

The endothelium in sepsis

Hemodynamic coherence and the rationale for monitoring the microcirculation

A few of our favorite unconfirmed ideas