IN CASE OF SHOCK STATE IN GENERAL AND IN SEPTIC SHOCK PARTICULARLY, YOUR PRIORITY IS TO REACH GOOD RESUSCITATION TO THE PATIENT HOW TO GUIDE YOUR RESUSCITATION?

1. RESUSCITATION AND
PERFUSION
DR.MAGDY KHAMES ALY
CRITICAL CARE MEDICINE
ZMH AL BATAYEH

2. INTRODUCTION
 Volume replacement remains the cornerstone of resuscitation in the
critically ill and injured patient.
 The initial therapeutic intervention in hypotensive patients, oliguric
patients, and patients with evidence of poor organ/tissue perfusion is
volume resuscitation.
 However, both underresuscitation and volume overload increase
morbidity and mortality in critically ill patients.
 Uncorrected hypovolemia, leading to inappropriate infusions of
vasopressor agents, may increase organ hypoperfusion and ischemia.
 Fluid management is one of the most important (and difficult) issues
in the critically ill patient.
 However, the volume status of each and every ICU patient needs to
be assessed on an ongoing basis.

3. PHYSIOLOGICAL RESERVE
 The human body is a complex system that adapts to a multitude of
external stressors; however, senescence or illness can reduce inherent
adaptive mechanisms, reducing complexity and reducing the
threshold for decompensation (i.e. acute illness or injury). This
theoretical critical threshold can be considered ‘physiologic
reserve’.
 The phenotypic expression of this process is frailty. Frailty is a
condition in which small deficits accumulate which individually may
be insignificant but collectively produce an overwhelming burden of
disease and heightened vulnerability to adverse events.
 Frail patients expend a greater proportion of their reserve simply to
maintain homeostasis, and seemingly trivial insults can contribute to
catastrophic decompensation.

4. SHOCK PATHOPHYSIOLOGY

5. Critically ill patients may have an expanded
extracellular, extravascular compartment (tissue
edema) with a contracted intravascular
compartment. It is important to distinguish
between these forms of volume depletion as the
management may differ

6. VOLUME DEPLETION
 Volume Depletion with Depleted Extravascular Compartment:
 Acute blood loss
– Trauma
– GI bleed
 Gastrointestinal tract losses (diarrhea, vomiting, fistula)
 Decreased fluid intake due to acute medical conditions
 Diabetic ketoacidosis
 Heat exhaustion
 Dehydration

7. VOLUME DEPLETION
 Volume Depletion with Expanded Extravascular
Compartment:
 Sepsis
 Pancreatitis
 Trauma
 Surgery
 Burns
 Liver failure
 Cardiac failure

8. ORGAN PERFUSION
 BEDSIDE ASSESSMENT:
– Mean arterial pressure
– Urine output
– Mentation
– Capillary refill
– Skin perfusion/mottling
– Cold extremities
– Pulse pressure variation (PPV) and/or stroke volume
variation(SVV)
– Echocardiography

9.  PERFUSION MARKERS:
– Blood lactate
– Arterial pH, BE, and HCO3
– Mixed venous oxygen saturation (SmvO2) or central
venous
oxygen saturation (ScvO2)
– Mixed venous pCO2
– Tissue pCO2 (sublingual capnometry or equivalent)
– Gastric impedance spectroscopy
– Skeletal muscle tissue oxygenation StO2

10. PERFUSION ADEQUACY
PvO2 and SvO2
 PvO2 of SVC and IVC
PO2 from IVC is normally higher (SO2 77%) than from SVC (SO2 71%)
=> because kidney takes 25% of cardiac output but use only 7-8% of
body's O2 consumption
=> IVC receives blood more oxygen rich.
=> PO2 from SVC may be higher because of renal vasoconstriction with
severe haemorrhage.

11. PERFUSION ADEQUACY
 Fick's principle
"Amount of O2 extracted from respired gases equals the amount added to the
blood that flows through the lung"
i.e. "O2 consumption per unit time = O2 taken up by pulmonary blood flow per
unit time"
 Fick equation
=> VO2 = Q (CaO2 - CvO2)
• VO2 = O2 consumption per minute (mL O2/time)
• Q = pulmonary blood flow (mL/time)
• CaO2 = O2 concentration in blood leaving lung (mL/100mL)
• CvO2 = O2 concentration in mixed venous blood (mL/100mL)

12. PERFUSION ADEQUACY
PvO2 and SvO2
A true PvO2 (normally 40 mmHg) measurement must come from a mixed
venous blood sample containing venous drainage from the SVC, IVC, and the
heart. Thus, the sample should be obtained from a pulmonary artery catheter.
There are several factors that determine PvO2, which can be remembered using
the mnemonic COALS:
 Cardiac output
 Oxygen consumption
 Amount of hemoglobin
 Loading of hemoglobin
 Saturation of hemoglobin

13.  Are PvO2 and SvO2 good markers of adequacy of
perfusion?
They are easy to measure markers but may NOT always
related to adequate tissue perfusion.
 If PvO2 or SvO2 are become normal, does it mean that
the patient adequately resuscitated? NO because may be
the patient’s tissue can’t extract the O2 (cytotoxic
hypoxia).
 In the other hand if SvO2 is decreased, does it mean that
the patient not resuscitated? No because SvO2 depends
on many changeable variables during resuscitation e.g:
Hb% which may be diluted by resuscitation fluids

14. PERFUSION ADEQUACY
A-V PCO2 Gradient (DPCO2)
Similar to Fick's principle
Production of CO2 = Elimination of CO2
VCO2 = Q (CaCO2-CvCO2)
CvCO2 = CaCO2 - VCO2/Q
 When CO2 dissociation curve is fixed
 CvCO2 is increased when
 CaCO2 is increased => heavily influenced by alveolar ventilation
 CO2 output is decreased
 Cardiac output is increased
 NB. CO2 output and production are the same in steady state, but different in
dynamic state because much of CO2 produced is diverted into body stores.
 DPCO2 = PvCO2 – PaCO2

15. PERFUSION ADEQUACY
A-V PCO2 Gradient (DPCO2)
Can the PCO2 gradient between arterial and venous blood gas
samples (DPCO2) represent adequacy of perfusion?
 In healthy tissues, decreases in oxygen delivery (QO2 = cardiac
output X arterial O2 content) do not lower oxygen consumption
(VO2) because tissue O2 extraction increases proportionately.
When delivery is reduced below a critical threshold, VO2 falls
because tissue extraction exceeds a critical threshold, and cannot
compensate for the reduction in delivery.
 The critical oxygen delivery point is when consumption (VO2) is
dependent on delivery (DO2)
 The DPCO2 is an index to identify the critical oxygen delivery
point (VO2/DO2).

16. PERFUSION ADEQUACY
A-V PCO2 Gradient (DPCO2)
critical oxygen delivery point is associated with an abrupt increase of
blood lactate levels and a significant widening in DPCO2.

17. PERFUSION ADEQUACY
A-V PCO2 Gradient (DPCO2)
It is logical that DPCO2 may serve as an excellent measurement
of adequacy of perfusion.

18. PERFUSION ADEQUACY
Lactate

19. Lactate
 PATHWAYS OF LACTATE PRODUCTION AND
HYPERLACTATEMIA :
 IN TISSUE HYPOXIA, lactate is overproduced and underutilized because of
impaired mitochondrial oxidation, largely through anaerobic glycolysis.
 Hyperlactatemia can also result from aerobic glycolysis, independent of tissue
hypoxia.
 In the hyperdynamic stage of sepsis, epinephrine-dependent stimulation of the
b2-adrenoceptor augments glycolytic flux both directly and through
enhancement of sarcolemmal Na+/K+-ATPase.
 Other conditions associated with elevated epinephrine levels, such as severe
trauma and cardiogenic shock, can cause hyperlactatemia through this
mechanism.
 In inflammatory states, aerobic glycolysis can also be driven by cytokine-
dependent stimulation of cellular glucose uptake

20. Lactate
Lactic acidosis refractory to standard resuscitation
is frequently caused by increased aerobic glycolysis
in skeletal muscle instead of anaerobic glycolysis
from hypoperfusion. Continued resuscitation
attempts targeting lactate levels may thus lead to
unnecessary blood transfusion and use of inotropic
agents.

21. Lactate
 LACTATE AND ITS CLEARANCE ARE USEFUL PROGNOSTIC
MARKERS:
 The clinical relevance of lactate and its clearance have
been repetitively evaluated. Lactate clearance greater than
10% from the initial value is predictive of survival from
septic shock, and targeting 10% clearance provided similar
survival rates to targeting central venous oxygen
saturation
 In patients with sepsis, lactate clearance greater than 20%
during the initial 8 h showed a 22% decline in mortality
risk relative to clearances less than 20%

22. LACTATE
 CONCLUSIONS REGARDING LACTATE:
 Because hyperlactatemia can be simultaneously related to,
and unrelated to, tissue hypoxia, physicians should
recognize that resuscitation to normalize plasma lactate
levels could be over-resuscitation and worsen the
physiological status.
 Thus, lactate is a reliable indicator of sepsis severity and a
marker of resuscitation, but is not a reliable marker of
tissue hypoxia/hypoperfusion.

23. KEY POINTES
 It is important to distinguish between the forms of volume
depletion as the management may differ.
 PvO2 and SvO2 they are easy to measure markers but may
NOT always related to adequate tissue perfusion.
 A-V PCO2 Gradient (DPCO2) It is logical that DPCO2 may
serve as an excellent measurement of adequacy of
perfusion.
 lactate is a reliable indicator of sepsis severity and a marker
of resuscitation, but is not a reliable marker of tissue
hypoxia/hypoperfusion

24. THANK YOU