Shock

Cardiac Physiology

CO = SV X HR

Preload Contractility Afterload

Venous Vascular
dp / dt
Capacitance Tone
Pathophysiology
Cellular Alteration in shock
Recognition of Shock State
1. Tachycardia
2. Vasoconstriction
2. ↓ Cardiac output
Narrow pulse pressure
3. ↓ Map
3. ↓Blood Flow

Caution : Compensatory mechanisms

Pitfalls in shock Recognition
 Extremes of age
 Athletes
 Pregnancy
 Medications
 Hematocrit/hemoglobin concentration
Etiology of Shock
Hemorrhagic
 Most common
Nonhermorrhagic
 Tension
 Clinical clues
pneumothorax
•H&P
 Cardiogenic
• Selected
 Neurogenic
diagnostic tests
 Septic
Hemorrhagic Shock
 Loss of circulating blood volume
 Normal blood volume
• Adult 7% of ideal weight
• Child: 9 % of ideal weight
Classification of Hemorrhage
 Class I-IV
 Not absolute
 Only A clinical guide
 Subsequent treatment determined by
patient response
Class I Hemorrhage
750 mL BVL
Class II Hemorrhage
750 – 1500 ml BVL
Class III Hemorrhage
1500 – 2000 ml BVL
Class IV Hemorrhage :≥ 2000 ml
≥ 2000 ML BVL
Fluid Shifts : Soft – tissue Injury

Blood loss into Tissue

injury site edema

Compounds
intravascular loss.
Assessment and Management
 Recognize shock
 Stop the bleeding !
 Replenish intravascular volume
 Restore organ perfusion
Assessment and Management
 Airway and Breathing
• Oxygenate and ventilate
• Pao₂ > 80 mm hg (10,6 kpa)
 Circulation
• Assess
• Control
• Treat
Assessment and Management
 Disability – cerebral perfusion
 Exposure/Environment
• Associated injuries
• Prevent hypothermia
 Gastric and bladder decompression
 Urinary output
Management : Vascular Access
 2 large – caliber, peripheral IV s
 Central access
• Femoral
• Jugular
• Subclavian
 Intraosseous
 Obtain blood for croossmatch
Management : Fluid Therapy
 Warmed crystalloid solution
 Rapid fluid bolus ringer,s lactate
• Adult: 2 Liters, Riger’s Lactate
• Child :20 ml /kg ringer,s lactate
 Monitor response to initial therapy
Reevaluate Organ perfusion
Monitor
 Vital signs

 CNS status

 Skin perfusion

 Urinary output

 Pulse oximetry
Resuscitation Evaluation
Hourly Urinary Output
Inadequate output suggests
inadequate resuscitation
Acid –Base Abnormalities
 Monitor with ABGs
 Usual etiology
• Adult : Acidosis due to inadequate
perfusion
• Child : Acidosis due to inadequate
ventilation
Acid –Base Abnormalities
 Treatment
• Oxygenate and ventilate
• Stop the bleeding !
• Consider inadequate volume
restoration
 Bicarbonate rarely indicated
Therapeutic Decisions
 Patient response determines
subsequent therapy
 Hemodynamically “normal” vs

hemodynamically “stable”
 Recognize need to resuscitate in

operating room
Therapeutic Decisions
Rapid Response
 <20 % blood loss

 Responds to fluid replacement

 Surgical consultation evaluation

 Continue to monitor
Therapeutic Decisions
Transient Response
 20% -40% blood loss

 Deteriorates after initial fluids

 Surgical consultation evaluation

 Continued fluid plus blood

 Continued hemorrhage : Operation

Therapeutic Decisions
Minimal to No Response
 > 40% Blood loss

 No Response to fluid resuscitation

 Immediate surgical consultation

 Exclude nonhemorrhagic Shock

 Immediate operation
Volume Replacement

Warmed fluids
 Crossmatched PRBCs

 Type – specific

 Type O, Rh negative

 Autotransfusion

 Coagulopathy
Pitfalls

 Equating Bp  Athletes
with cardiac  Pregnancy

output  Medications

 Extremes of
 Pacemaker
age
 Hypothermia
Avoiding Complications
 Continued hemorrhage
 Fluid overload

 Invasive monitoring (ICU)

• CVP
• Pulmonary artery catheter
 Other problems
Keys to Successful Treatment
 Early control of hemorrhage
 Euvolemia
 Continuous reevaluation