Exposure to injurious

substance (fire, hot liquid via

splash)
Endocrine
Sensory

Thermoregulatory Massive stress

Cadiovascular response,
Respiratory sympathetic nervous
Integumentary Loss of skin causes Absence of the
Rapid changes in system activation
the inability to regulate protective covering
Massive stress skeletal muscle of the epidermis
Direct exposure to body temperature
response, Release of inflammatory Increased vascular Local inflammation in Destruction of mitochondrial function Inflammatory
Loss of epithelial Singed heat or steam in an
sympathetic nervous cytokine necrosis factor permeability respose to burn damage enclosed setting (inhalation tissue (skin, connective mediators induce
integrity nasal hairs Adrenal corticoid
system activation injury) and presence of tissue, bone) peripheral insulin
Dead and denatured hormones and
neck and face burns Increased Hypothermia in the Nerve endings are resistance
epidermal and dermal layers Skeletal muscle catecholamine release
Fluid is able to Systemic release of Edema vascular early hours after injury sensitized and exposed to
remain intact over bed of mitochondria from burn
Myocardial Loss of fluid through leak out of the blood inflammatory factors permeability stimulation
Vasodilation granulation tissue victims are more
Adrenal corticoid contractility may be evaporation circulation uncoupled
hormones and suppressed Increased vascular
catecholamine Particulate matter produced permeability Hypermetabolic
Increased blood Sooty during combustion (soot) can Fluid leak results in response resets core
release Leathery, Dry top Activation of key
Distributive vessel permeability sputum mechanically obstruct and Blisters edema between dermal Source for greater temperature
and epidermal layer waxy white layer enzymes involved in hepatic epinephrine and Altered release of
shock irritate the airways heat production within Norepinephrine has the
Upper airway is appearance Pain 10/10 gluconeogenesis and inhibition adipokines from
Red skeletal muscle norepinephrine stimulate hepatic added effect of increasing the
obstructed of glucose uptake in peripheral adipose tissue cause
Leakage of fluids appearance gluconeogenesis and supply of glycerol to the liver
Burn patients become
from intravascular space Thin epidermal layer tissues such as the skeletal glycogenolysis via lipolysis insulin resistance
Peripheral hyperthermic for
into interstitium and third Wet wound forming fluid-filled vesicle muscles
vasoconstriction Reflex bronchoconstriction much of the postburn period, even
space (lungs) caused by release of histamine, breaks open in the absence of infection
Low blood serotonin, and thromboxane,
pressure a powerful vasoconstrictor, as well as
Reduced total (90/50) Massive chest constriction secondary
blood volume pulmonary edema to chest burn
clogs up alveoli Fever
(38.9 C)
Blood
glucose: 10
Increased afterload Reduced cardiac Hypovolemic mmol/L
output shock

Decreased delivery of
O2/nutrients to different organs;
decreased CO2 removal/wastes Use of
Tachypnea
from tissues accessory Stridor
(32 cpm)
muscles
Tachycardia
(126 bpm) SPO2 of 80%
kidney brain
on high oxygen
concentration, 76%
Note: Chest excursion may be greatly restricted
in room air
Decreased in chest burns, causing decreased tidal volume
GFR Anoxic
brain injury

Low
urine
output