Shock
Dr.Indubala Maurya MD,DNB
Assistant Professor
Dept of Aanesthesia & Critical Care
MGMCRI
Introduction
Shock can be defined as a state of inadequate
or inappropriate tissue perfusion resulting in
abnormal cellular metabolism.
Shock is associated with anaerobic metabolism,
oxygen debt and tissue acidosis.
Combination of hemodynamic parameters:
MAP< 60
SBP<90
Clinical feature
Abnormal lab value ( lactate > 4 mmol/L)
Types of shock
Hypovolemic shock
Distributive Shock
Cardiogenic Shock
Hypovolemic shock
Hypovolemic shock is related to decreased intravascular
volume, secondary to loss of:
Blood (e.g. trauma)---- > Hemorrhagic shock
Plasma (e.g. burns)
Water and electrolytes (e.g. vomiting, diarrhoea).
Hypovolemic shock
Clinical feature :
Hypovolemic shock
Management :
Establish vascular access ; large bore cannula , Send
sample for Hb
Start fluid resuscitation depending on clinical
presentation -----with crystalloid/Blood product
Hb > 9gm% ----> continue Fluid therapy
Hb < 9gm% --- > PRBC, correct coagulation abnormality
Search for source of bleeding : compression of visible
vascular injury, exposure and control of internal bleeding,
embolisation ,banding
Measure CVP and MAP
CVP < 8 --------> continue Fluid therapy
CVP > 8 and MAP < 60 -----> Administer Vasopressor ( NE,DA)
CVP > 8 and MAP > 60 ------> Resuscitation complete
Others
Airway control
Plt/FFP
Activated factor VII
Calcium/magnesium supplement
Rewarming
Antibiotics
look for other cause of shock
Distributive shock
e.g.
Septic shock
Anaphylactic shock
Septic shock
Surviving sepsis campaign 2012
Sepsis is defined as the presence of infection together with systemic
manifestations of infection.
Severe sepsis is defined as sepsis plus sepsis-induced organ
dysfunction or tissue hypo perfusion.
Sepsis-induced hypotension is defined as a systolic blood pressure
(SBP) < 90 mm Hg or mean arterial pressure (MAP) < 70 mm Hg or a SBP
decrease > 40 mm Hg or less than two standard deviations below normal
for age in the absence of other causes of hypotension
Septic shock
Clinical feature
SBP< 90
MAP < 70
Feature of severe sepsis :
Fever Hypothermia ,tachy,Tachypnea,Altered mental
status, Leukocytosis ,Leukopenia.
With one or more organ involvement ( lung ,liver ,kidney )
Septic shock
Management
Goals during the first 6 hrs of resuscitation:
a) Central venous pressure 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Central venous (superior vena cava) or mixed venous
oxygen saturation 70% or 65%, respectively
•Fluid Therapy of Severe Sepsis:
•Crystalloids as the initial fluid of choice in the resuscitation
•Vasopressors
•Norepinephrine as the first choice vasopressor
•Inotropic Therapy
•Dobutamine infusion
•myocardial dysfunction as suggested by elevated cardiac
filling pressures and low cardiac output.
•ongoing signs of hypoperfusion, despite achieving adequate
intravascular volume and adequate MAP
•Blood Product Administration
•Red blood cell transfusion if Hb <7.0 g/dL
•Platelets prophylactically when counts are <10,000/mm3 in the
absence of apparent bleeding
Diagnosis :
•Cultures as clinically appropriate before antimicrobial therapy
•imaging
•Antimicrobial Therapy
•Administration of effective broad spectrum intravenous
antimicrobials within the first hour of recognition of septic shock.
•
Not more than 5 days, De-escalate antibiotic therapy.
•Duration of therapy typically 7–10 days
•Source Control
•eg: abscess drainage
•Mechanical Ventilation of Sepsis-Induced ARDS
Anaphylactic shock
Suspected impending respiratory collapse ---->
intubate
IM epinephrine 0.3-0.5 mg to ant/ lat thigh
For severe symptoms poor response
Iv bolus epinephrine 0.1-0.2 mg
If hypotensive start fliud therapy
if no response to above
start iv epi infusion
Aggressive fluid therapy
Pt on beta blocker ----> Glucagon
Treat all patients with Histamine 1,2 blocker
Diphenhydramine (H1)
Ranitidine (H2)
Cardiogenic shock
Cardiogenic shock is related to ‘pump’
failure from many possible causes
myocardial infarct ( common)
valve dysfunction
papillae rupture
arrhythmias
tamponade
pulmonary embolus
Negative ECG finding :
Rule out mechanical cause of CS ( ECHO)
Cardiac monitoring ( confirm cardiac etiology )
Continued medical support (vasopressure, inotropic)
Cardiogenic shock
In case of refractory cardiac shock
Left venticular assist device
Transplant
Cradiac temponade :
Beck’s triad ( raised jvp,muffled hreart sound,hypotension)
Presence of pulsus paradox( insp fall in SBP>10)
Echo finding
Consider Subxiphoid Pericardiocentesis