United States Department of Transportation

National Highway Traffic Safety Administration

Paramedic:  National Standard Curriculum

(Reprinted with permission)

http://www.nhtsa.dot.gov/people/injury/ems/

 

Trauma: 4

Hemorrhage and Shock: 2

 

UNIT TERMINAL OBJECTIVE

4-2        the completion of this unit, the paramedic student will be able to integrate pathophysiological principles and assessment findings to formulate a field impression and implement the treatment plan for the patient with shock or hemorrhage.

 

COGNITIVE OBJECTIVES

At the completion of this unit, the paramedic student will be able to:

 

4-2.1     Describe the epidemiology, including the morbidity/ mortality and prevention strategies, for shock and hemorrhage. (C-1)

4-2.2     Discuss the anatomy and physiology of the cardiovascular system. (C-1)

4-2.3     Predict shock and hemorrhage based on mechanism of injury. (C-1)

4-2.4     Discuss the various types and degrees of shock and hemorrhage. (C-1)

4-2.5     Discuss the pathophysiology of hemorrhage and shock. (C-1)

4-2.6     Discuss the assessment findings associated with hemorrhage and shock. (C-1)

4-2.7     Identify the need for intervention and transport of the patient with hemorrhage or shock. (C-1)

4-2.8     Discuss the treatment plan and management of hemorrhage and shock. (C-1)

4-2.9     Discuss the management of external hemorrhage. (C-1)

4-2.10   Differentiate between controlled and uncontrolled hemorrhage. (C-3)

4-2.11   Differentiate between the administration rate and amount of IV fluid in a patient with controlled versus uncontrolled hemorrhage. (C-3)

4-2.12   Relate internal hemorrhage to the pathophysiology of compensated and decompensated hemorrhagic shock. (C-3)

4-2.13   Relate internal hemorrhage to the assessment findings of compensated and decompensated hemorrhagic shock. (C-3)

4-2.14   Discuss the management of internal hemorrhage. (C-1)

4-2.15   Define shock based on aerobic and anaerobic metabolism. (C-1)

4-2.16   Describe the incidence, morbidity, and mortality of shock. (C-1)

4-2.17   Describe the body's physiologic response to changes in perfusion. (C-1)

4-2.18   Describe the effects of decreased perfusion at the capillary level. (C-1)

4-2.19   Discuss the cellular ischemic phase related to hemorrhagic shock. (C-1)

4-2.20   Discuss the capillary stagnation phase related to hemorrhagic shock. (C-1)

4-2.21   Discuss the capillary washout phase related to hemorrhagic shock. (C-1)

4-2.22   Discuss the assessment findings of hemorrhagic shock. (C-1)

4-2.23   Relate pulse pressure changes to perfusion status. (C-3)

4-2.24   Relate orthostatic vital sign changes to perfusion status. (C-3)

4-2.25   Define compensated and decompensated hemorrhagic shock. (C-1)

4-2.26   Discuss the pathophysiological changes associated with compensated shock. (C-1)

4-2.27   Discuss the assessment findings associated with compensated shock. (C-1)

4-2.28   Identify the need for intervention and transport of the patient with compensated shock. (C-1)

4-2.29   Discuss the treatment plan and management of compensated shock. (C-1)

4-2.30   Discuss the pathophysiological changes associated with decompensated shock. (C-1)

4-2.31   Discuss the assessment findings associated with decompensated shock. (C-1)

4-2.32   Identify the need for intervention and transport of the patient with decompensated shock. (C-1)

4-2.33   Discuss the treatment plan and management of the patient with decompensated shock. (C-1)

4-2.34   Differentiate between compensated and decompensated shock. (C-3)

4-2.35   Relate external hemorrhage to the pathophysiology of compensated and decompensated hemorrhagic shock. (C-3)

4-2.36   Relate external hemorrhage to the assessment findings of compensated and decompensated hemorrhagic shock. (C-3)

4-2.37   Differentiate between the normotensive, hypotensive, or profoundly hypotensive patient. (C-3)


4-2.38   Differentiate between the administration of fluid in the normotensive, hypotensive, or profoundly hypotensive patient. (C-3)

4-2.39   Discuss the physiologic changes associated with the pneumatic anti-shock garment (PASG). (C-1)

4-2.40   Discuss the indications and contraindications for the application and inflation of the PASG. (C-1)

4-2.41   Apply epidemiology to develop prevention strategies for hemorrhage and shock. (C-1)

4-2.42   Integrate the pathophysiological principles to the assessment of a patient with hemorrhage or shock. (C-3)

4-2.43   Synthesize assessment findings and patient history information to form a field impression for the patient with hemorrhage or shock. (C-3)

4-2.44   Develop, execute and evaluate a treatment plan based on the field impression for the hemorrhage or shock patient. (C-3)

 

AFFECTIVE OBJECTIVES

None identified for this unit.

 

PSYCHOMOTOR OBJECTIVES

At the completion of this unit, the paramedic student will be able to:

 

4-2.45   Demonstrate the assessment of a patient with signs and symptoms of hemorrhagic shock. (P-2)

4-2.46   Demonstrate the management of a patient with signs and symptoms of hemorrhagic shock. (P-2)

4-2.47   Demonstrate the assessment of a patient with signs and symptoms of compensated hemorrhagic shock. (P-2)

4-2.48   Demonstrate the management of a patient with signs and symptoms of compensated hemorrhagic shock. (P-2)

4-2.49   Demonstrate the assessment of a patient with signs and symptoms of decompensated hemorrhagic shock. (P-2)

4-2.50   Demonstrate the management of a patient with signs and symptoms of decompensated hemorrhagic shock. (P-2)

4-2.51   Demonstrate the assessment of a patient with signs and symptoms of external hemorrhage. (P-2)

4-2.52   Demonstrate the management of a patient with signs and symptoms of external hemorrhage. (P-2)

4-2.53   Demonstrate the assessment of a patient with signs and symptoms of internal hemorrhage. (P-2)

4-2.54   Demonstrate the management of a patient with signs and symptoms of internal hemorrhage. (P-2)

 


DECLARATIVE

 

I.          Pathophysiology, assessment, and management of hemorrhage

A.         Hemorrhage

1.         Epidemiology

a.         Incidence

b.         Mortality/ morbidity

c.         Prevention strategies

2.         Pathophysiology

a.         Location

(1)        External

(a)        Controlled

(b)        Uncontrolled

(2)        Internal

(a)        Trauma

(b)        Non-trauma

i)          Common sites

ii)          Uncommon sites

(c)        Controlled

(d)        Uncontrolled

b.         Anatomical type

(1)        Arterial

(2)        Venous

(3)        Capillary

c.         Timing

(1)        Acute

(2)        Chronic

d.         Severity

(1)        Amounts of blood loss tolerated by

(a)        Adults

(b)        Children

(c)        Infants

e.         Physiological response to hemorrhage

(1)        Clotting

(2)        Localized vasoconstriction

f.          Stages of hemorrhage

(1)        Stage 1

(a)        Up to 15% intravascular loss

(b)        Compensated by constriction of vascular bed

(c)        Blood pressure maintained

(d)        Normal pulse pressure, respiratory rate, and renal output

(e)        Pallor of the skin

(f)         Central venous pressure low to normal    

(2)        Stage 2

(a)        15-25% intravascular loss

(b)        Cardiac output cannot be maintained by arteriolar constriction

(c)        Reflex  tachycardia

(d)        Increased respiratory rate

(e)        Blood pressure maintained

(f)         Catecholamines increase peripheral resistance

(g)        Increased diastolic pressure


(h)        Narrow pulse pressure

(i)         Diaphoresis from sympathetic stimulation

(j)         Renal output almost normal

(3)        Stage 3

(a)        25-35% intravascular loss

(b)        Classic signs of hypovolemic shock

i)          Marked tachycardia

ii)          Marked tachypnea

iii)         Decreased systolic pressure

iv)         5-15 ml per hour urine output

v)          Alteration in mental status

vi)         Diaphoresis with cool, pale skin

(4)        Stage 4

(a)        Loss greater than 35%

(b)        Extreme tachycardia

(c)        Pronounced tachypnea

(d)        Significantly decreased systolic blood pressure

(e)        Confusion and lethargy

(f)         Skin is diaphoretic, cool, and extremely pale

3.         Assessment

a.         Bright red blood from wound, mouth, rectum or other orifice

b.         Coffee ground appearance of vomitus

c.         Melena

d.         Hematochezia

e.         Dizziness or syncope on sitting or standing

f.          Orthostatic hypotension

g.         Signs and symptoms of hypovolemic shock                                

4.         Management

a.         Airway and ventilatory support

b.         Circulatory support

(1)        Bleeding from nose or ears after head trauma

(a)        Refrain from applying pressure

(b)        Apply loose sterile dressing to protect from infection

(2)        Bleeding from other areas

(a)        Control bleeding

i)          Direct pressure

ii)          Elevation if appropriate

iii)         Pressure points

iv)         Tourniquet

v)          Splinting

vi)         Packing of large gaping wounds with sterile dressings

vii)        PASG

(b)        Apply sterile dressing and pressure bandage       

(3)        Transport considerations

(4)        Psychological support/ communication strategies

 

II.          Shock

A.         Epidemiology

1.         Mortality/ morbidity

2.         Prevention strategies


3.         Pathophysiology

a.         Perfusion depends on cardiac output (CO), systemic vascular resistance (SVR) and transport of oxygen

(1)        CO = HR X SV

(a)        HR - heart rate

(b)        SV - stroke volume                                                        

(2)        BP = CO X SVR

(3)        Hypoperfusion can result from                                                    

(a)        Inadequate cardiac output

(b)        Excessive systemic vascular resistance                         

(c)        Inability of red blood cells to deliver oxygen to tissues

b.         Compensation for decreased perfusion

(1)        Occurrence of event resulting in decreased perfusion, e.g., blood loss, myocardial infarction, loss of vasomotor tone or tension pneumothorax

(2)        Baroreceptors sense decreased flow and activate vasomotor center

(a)        Normally stimulated between 60-80 mm Hg systolic (lower in children)

(b)        Located in carotid sinuses and aortic arch                       

(c)        Arterial pressure drop decreases stretch

i)          Nerve impulse through Vagus and Hering's nerve to glossopharyngeal nerve

ii)          Impulse transmitted to vasomotor center

iii)         Frequency of inhibitory impulses decreases        

iv)         Increase in vasomotor activity

v)          Sympathetic nervous system stimulated

(iv)        Decrease in systolic less than 80 mmHg stimulates vasomotor center to increase arterial pressure

(3)        Chemoreceptors are stimulated by decrease in PaO2 and increase in PaCO2

(4)        Sympathetic nervous system

(5)        Adrenal medulla glands secrete epinephrine and norepinephrine

(a)        Epinephrine

i)          Alpha 1

a)         Vasoconstriction

b)         Increase in peripheral vascular resistance

c)         Increased afterload from arteriolar constriction

ii)          Alpha 2 regulated release of alpha 1

iii)         Beta 1

a)         Positive chronotropy

b)         Positive inotropy

c)         Positive dromotropy

iv)         Beta 2

a)         Bronchodilation

b)         Gut smooth muscle dilation

(b)        Norepinephrine

i)          Primarily alpha 1 and alpha 2

a)         Vasoconstriction

b)         Increase in peripheral vascular resistance

c)         Increased afterload from arteriolar constriction 


(6)        Arginine vasopressin (AVP)

(a)        Also known as antidiuretic hormone (ADH)

(b)        Released from anterior pituitary gland

(c)        Effects

i           Increases free water absorption in distal tubule and collecting ducts of kidney

ii           Decreases urine output

iii          Splanchnic vascular constriction

(7)        Renin-angiotensin system

(a)        Renin released from kidney arteriole

(b)        Renin and angiotensinogen combine in renal arteriole to produce angiotensin I

 (c)       Angiotensin I converted to angiotensin II by angiotensin converting enzyme

(d)        Effects of angiotensin II

i           Potent vasoconstrictor

ii           Sodium reabsorption decreases urine output

iii          Positive inotrope and chronotrope

(8)        Aldosterone

(a)        Defends fluid volume

(b)        Secreted by cells of adrenal cortex in response to stress

(c)        Promotes sodium reabsorption and water retention in kidney

(d)        Reduces urine output

(9)        Insulin

(a)        Secretion is diminished by circulating epinephrine

(b)        Impaired effect on peripheral tissue

(c)        Contributes to hyperglycemia seen following injury and volume loss

(10)       Glucagon

(a)        Stimulated to be released by epinephrine