Description

Hemorrhage is a major cause of hypovolemic shock. However, plasma loss/

dehydration and interstitial fluid accumulation (third spacing) adversely
reduce circulating volume by decreasing tissue perfusion. The primary defect
is decreased preload.

Four classifications of hypovolemic shock based on the amount of fluid and

blood loss:

 Class I: <750 ml, or ? 15% total circulating volume.

 Class II: 750 to 1000 ml, 05 15% to 30% total circulating volume
 Class III: 1500 to 2000 ml, or 30% to 40% total circulating volume
 Class IV: >2000 ml, or > 40% total circulating volume. The patient’s
compensatory response intensifies as the percent of blood loss is
increases.
Signs And Symptoms
 Depends on the degree of blood loss and compensatory response.
Physical Examination
Appearance
 Anxiety progressing to coma
Vital signs
 Blood pressure normal to unobtaionable
 Palpable radial pulse reflects systolic blood pressure of 80 mm Hg
 Palpable femoral pulse reflects systolic blood pressure of 70 mm
Hg
 Palpable carotid pulse reflects systolic blood pressure of 60 mm Hg
 HR normal to > 140 beats/min
 RR normal to > 35 breaths/ min
Cardiovascular
 Weak
  Thready pulse
Pulmonary
 Deep or shallow rapid respirations
 Lungs usually clear
Skin
 Cool, clammy skin, pale color
 Delayed/ absent capillary refill
 Lips cyanotic (late sign)
Acute Care Patient Management
Nursing Diagnosis: Ineffective tissue perfusion related to blood loss and
hypotension.
Outcome Criteria
 Patient alert and oriented
 Skin warm and dry
 Peripheral pulses strong
 Urine output 30 ml/hr or 0.5 to 1 ml/kg/hr
 Hct – 32%
 Systolic blood pressure 90 to 120 mm Hg
 Mean arterial pressure 70 to 105 mm Hg
 Cardiac index 2.5 to 4 l/min/m2
 O2 sat ?95 %
Patient Monitoring
1. Monitor BP continuously via arterial cannulation because cuff
pressures are less accurate in shock states.
2. Obtain cardiac output and cardiac index at least every 8 hours or
more frequently to evaluate the patient’s response to changes in
therapy.
3. Monitor peripheral artery pressures and central venous pressure
hourly or more frequently to evaluate the patient’s response to
treatment.
4. Continuously monitor ECG to detect life-threatening dysrythmias of
HR > 140 beats/min, which can adversely affect SV.
5. Monitor hourly urine output to evaluate renal perfusion.
6. Measure blood loss if possible.