Shock and its treatment
Jozsef Stankovics
Department of Paediatrics,
Medical University of Pécs
2008.
What is shock after all?
•circulatory failure?
•cardiac insufficiency?
•low blood pressure?
•etc.
Practical definition of shock
•A frightened look on a doctor's face: wehave a low blood pressure here, callsomeone to help me…..
Scientific definition of shock
•Is a condition where the perfusion of organsis too low to meet the metabolic demandsand leads to anaerobic metabolism
The simple truth of shock
VO2 > DO2
VO2 = oxygen consumption
DO2 = oxygen delivery
The basic triad of life
•functioning brain stem
•functioning respiratory system
•functioning circulatory system
Causes of shock I.
•Cardiogenic Shock
Causes
low contractility
valve malfunction
heart rate disturbances:
too fast
too slow
arrhythmias
Causes of shock II.
•Obstructive Shock
Causes
Tension pneumothorax
Massive pulmonary embolism
Cardiac tamponade
HOCM
Causes of shock III.
•Distributive Shock
Inappropriate vasodilatation of peripheralblood vessels
Causes
Septic shock
Neurogenic shock
Anaphylaxis
Adrenal insufficiency
High output failure (fistula,
pregnancy)
Causes of shock IV.
Hypovolemic Shock
Excessive blood loss (trauma)
Excessive plasma loss (burn)
Excessive fluid loss (diarrhea, vomiting)
Stages of shock
•Stages of shock - 1st and 2nd stages
1st stage = Initial phase.
The CO is insufficient to meet themetabolic needs of the body but not low enoughto produce symptoms (patient is anxious withtachypnoe).
2nd stage = Compensatory stage.
Due to catecholamine release BP isnormal/slightly reduced, but patient will have :
Increased HR.
Increase CO.
Vasoconstriction (cold periphery)
Stages of shock
3 rd stage = Progressive stage.
Unfavorable signs & symptoms moreapparent
Progressive fall in BP despite Thx.
Persistent tachycardia
Oliguria.
MOF
Shock to be reversed at this time,otherwise death results.
Stages of shock
4 th stage = Irreversible Stage
During this stage despite all efforts theoutcome is death
resistant myocardial depression
resistant capillary dilation/leak
blood remains pooled in the extremities
irreversible intracellular destruction
Clinical approach to assess tissueperfusion
•Pulse
•Pressure
•Perfusion
•Periphery (CRT < 2”)
•Pee ( 1 ml/kg/hr)
Physiologic approach to assesstissue perfusion
•DO2 = CO x 10 [(1.34 x Hb x SaO2) +(0.003 x PaO2)] ≈ CO x 13 x Hb x SaO2
•VO2 ≈ CO x Hb x 13 x (SaO2 – SvO2)
•O2ER = (VO2 / DO2) x 100
Treatment of shock
•Increase DO2
•Decrease VO2
•Then have a nice day
Treatment of shock
•A
•B
•C
•as always
How to increase DO2
•Perfusion: MAP – CVP
•MAP: CO X SVR
•CO: SV X Fr
•SV: preload, contractility, valve function
Practical approach I.
•SVR is low (few instances), extremities arewarm:
sepsis
anaphylaxis
spinal cord injury
vasodilator drugs
→ volume resuscitation, use of vasoconstrictors
Practical approach II.
•SVR is high: cold extremities
→ CO is low:
-preload ≈ CVP (fill up)
-contractility (inotropes)
-afterload („inodilatatores”)
-treat rhythm abnormalities
Volume replacement (≈ to manage CVP)
•crystalloid (normal saline or RL)
•colloid (gelatin or starch)
•human albumin (not preferred)
•blood (volumetric effect with increased O2delivery !!!)
•for sure: 20 ml/kg/20 min, until CVP isnormalized
Medical treatment ( to managecontractility and SVR)
Drug Receptor CO SVR Dose Range
Epinephrine
↑↑
↑
0.02 – 0.5
Norepinephrine
0 -↑
↑↑↑
0.05 – 0.5
Dopamine
DR
↑
↑
2 -12
Dobutamine
↑↑
↑
2 - 12
Dopexamine
DR
↑↑
0 -↑
0.9 - 5
Vasopressin
Angiotensin III
0 -
5 - 20
Amrinone
PDI
5 -10
(g/kg/min)
How to lower VO2 ?
•O2 supplementation
•pain management
•sedation
•temperature control
•mechanical ventilation (early considerationafter 2-3 fluid boluses)
Protocol for Early Goal
Directed Therapy in the ED:
(Adapted from NEJM 2001;345:1368-77, in which patientsreceiving this goal directly therapyhad improved in-hospital mortalitycompared to those with “standard”therapy, 31% to 47%.)