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

(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

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

(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

(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

(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

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

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

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

(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

(d) Reduces urine output

(9) Insulin

(a) Secretion is diminished by circulating epinephrine

(b) Impaired effect on peripheral tissue

(10) Glucagon

(a) Stimulated to be released by epinephrine

(b) Promotes

i Liver glycogenolysis

ii Gluconeogenesis

iii Amino acid uptake for conversion into glucose

iv Transfer of fatty acid into mitochondria

(11) ACTH (adrenocorticotropic hormone)-cortisol system

(a) ACTH release stimulates the release of cortisol from the adrenal cortex of kidney

(b) Cortisol increases glucose production by inhibiting enzymes that break down glucose

(12) Growth hormone

(a) Secreted by anterior pituitary gland

(b) Early effects of growth hormone

i Promotes uptake of glucose and amino acids in muscle

ii Stimulates protein synthesis

(13) Failure of compensation to preserve perfusion

(14) Preload decreases

(15) Cardiac output decreases

(16) Myocardial blood supply and oxygenation decrease

(a) Myocardial perfusion decreases

(b) Cardiac output decreases further

(d) Myocardial ischemia

(17) Capillary and cellular changes

(a) Ischemia

i Minimal blood flow to capillaries

ii Cells go from aerobic to anaerobic metabolism

(b) Stagnation

a65535 Lactic acid

b65535 Vasomotor center failure

c65535 Increased carbon dioxide

i Postcapillary sphincters remain constricted

ii Capillaries engorge with fluid

iii Anaerobic metabolism continues, increasing lactic acid production

a65535 Aggregation of red blood cells and formation of microemboli

b65535 Potent vasodilator

c65535 Destroys capillary cell membrane

iv Plasma leaks from capillaries

v Interstitial fluid increases

a65535 Distance from capillary to cell increases

b65535 Oxygen transport decreases secondary to increased capillary-cell distance

vi Myocardial toxin factor released by ischemic pancreas

(d) Washout

i Postcapillary sphincter relaxes

ii Hydrogen, potassium, carbon dioxide, thrombosed - erythrocytes wash out

iii Metabolic acidosis results

iv Cardiac output drops further

c0 Stages of shock

(1) Compensated or nonprogressive

(a) Characterized by signs and symptoms of early shock

(b) Arterial blood pressure is normal or high

(2) Decompensated or progressive

(a) Characterized by signs and symptoms of late shock

(b) Arterial blood pressure is abnormally low

(3) Irreversible

(a) Characterized by signs and symptoms of late shock

(b) Arterial blood pressure is abnormally low

d0 Etiologic classifications

(1) Hypovolemic

(a) Hemorrhage

(b) Plasma loss

(d) Endocrine

(2) Distributive (vasogenic)

(a) Increased venous capacitance

(b) Low resistance, vasodilation

(3) Cardiogenic

(a) Myocardial insufficiency

(b) Filling or outflow obstruction (obstructive)

(4) Spinal neurogenic shock

(a) Refers to temporary loss of all types of spinal cord function distal to injury

i Flaccid paralysis distal to injury site

ii Loss of bladder and bowel control

iii Priapism

iv Loss of thermoregulation

(b) Does not always involve permanent primary injury

(5) Spinal shock

(a) Also called spinal vascular shock

(b) Temporary loss of the autonomic function of the cord at the level of injury which controls cardiovascular function

i Loss of sympathetic tone

ii Relative hypotension

a65535 Systolic pressure 80 - 100 mmHg

iii Skin is pink, warm and dry

a65535 Due to cutaneous vasodilation

iv Relative bradycardia

(d) Occurrence is rare

(e) Shock presentation is usually the result of hidden volume loss

i Chest injuries

ii Abdominal injuries

iii Other violent injuries

(f) Treatment

i Focus primarily on volume replacement

4 Assessment - hypovolemic shock due to hemorrhage

(1) Early or compensated

(a) Tachycardia

(b) Pale, cool skin

(d) Level of consciousness

i Normal

ii Anxious or apprehensive

(e) Blood pressure maintained

(f) Narrow pulse pressure

i Pulse pressure is the difference between the systolic and diastolic pressures, i.e., pulse pressure = systolic - diastolic

ii Pulse pressure reflects the tone of the arterial system and is more sensitive to changes in perfusion than the systolic or diastolic alone

(g) Positive orthostatic tilt test

(h) Dry mucosa

(i) Complaints of thirst

(j) Weakness

(k) Possible delay of capillary refill

(2) Late or progressive

(a) Extreme tachycardia

(b) Extreme pale, cool skin

(d) Significant decrease in level of consciousness

(e) Hypotension

(f) Dry mucosa

(g) Nausea

(h) Cyanosis with white waxy looking skin

a0 Differential shock assessment findings

(1) Shock is assumed to be hypovolemic until proven otherwise

(2) Cardiogenic shock

(a) Differentiated from hypovolemic shock by one or more of the following

i Chief complaint (chest pain, dyspnea, tachycardia)

ii Heart rate (bradycardia or excessive tachycardia)

iii Signs of congestive heart failure (jugular vein distention, rales)

iv Dysrhythmias

(b) Distributive shock

i Mechanism that suggests vasodilation, e.g., spinal cord injury, drug overdose, sepsis, anaphylaxis

ii Warm, flushed skin, especially in dependent areas

iii Lack of tachycardia response (not reliable, though, since significant number of hypovolemic patients never become tachycardic)

(d)) Obstructive shock

i Differentiated from hypovolemic shock by presence of signs and symptoms suggestive of

ii Cardiac tamponade

iii Tension pneumothorax

5 Management/ treatment plan

a0 Airway and ventilatory support

(1) Ventilate and suction as necessary

(2) Administer high concentration oxygen

(3) Reduce increased intrathoracic pressure in tension pneumothorax

b0 Circulatory support

(1) Hemorrhage control

(2) Intravenous volume expanders

(a) Types

i Isotonic solutions

ii Hypertonic solutions

iii Synthetic solutions

iv Blood and blood products

v Experimental solutions

vi Blood substitutes

(b) Rate of administration

i External hemorrhage that can be controlled

ii External hemorrhage that can not be controlled

iii Internal hemorrhage

a65535 Blunt trauma

b65535 Penetrating trauma

(3) Pneumatic anti-shock garment

(a) Effects

i Increased arterial blood pressure above garment

ii Increased systemic vascular resistance

iii Immobilization of pelvis and possibly lower extremities

iv Increased intra-abdominal pressure

(b) Mechanism

i Increases systemic vascular resistance through direct compression of tissues and blood vessels

ii) Negligible autotransfusion effect

i Hypoperfusion with unstable pelvis

ii Conditions of decreased SVR not corrected by other means

iii As approved locally, other conditions characterized by hypoperfusion with hypotension

iv Research studies

(d) Contraindications

i Advanced pregnancy (no inflation of abdominal compartment)

ii Object impaled in abdomen or evisceration (no inflation of abdominal compartment)

iii Ruptured diaphragm

iv Cardiogenic shock

v Pulmonary edema

(4) Needle chest decompression of tension pneumothorax to improve impaired cardiac output

(5) Recognize the need for expeditious transport of suspected cardiac tamponade for pericardiocentesis

c0 Pharmacological interventions

(1) Hypovolemic shock

(a) Volume expanders

(2) Cardiogenic shock

(a) Volume expanders

(b) Positive cardiac inotropes

(d) Rate altering medications

(3) Distributive shock

(a) Volume expanders

(b) Positive cardiac inotropes

(d) PASG

(4) Obstructive shock

(a) Volume expanders