week 13: multiple interacting systems Flashcards
shock
condition during which the cardiovascular system fails to perfuse the tissues adequately; causes general and widespread impairment of cellular metabolism.
common pathways in all types of shock
Impairment of cellular metabolism as a result of decreased delivery of oxygen and nutrients
Frequently coupled with an increased demand and consumption of oxygen and nutrients
Decreased removal of cellular waste products
classes of shock
cardiogenic, neurogenic or vasogenic, anaphylactic, septic, hypovolemic
shock cm
Weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath, and generally “feeling sick”
Decreased blood pressure, cardiac output, and urinary output
Increased respiratory rate
shock tx
Oxygenation: Absolute necessity in all shock states
Correct or remove underlying cause
Provide supportive therapy
cardiogenic shock causes
myocardial ischemia, myocardial infarction
cardiogenic shock
Inability of the heart to pump adequate blood to tissues and end organs from any cause
as cardiac output decreases compensatory adaptive responses are activated:
Renin-angiotensin, neurohormonal, and sympathetic nervous system.
cardiogenic shock cm
Chest pain, dyspnea, and faintness, along with feelings of impending doom
cardiogenic shock hallmarks
Tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output
cardiogenic shock tx
Intraaortic balloon counterpulsation (IABP) or percutaneous or ventricular assist devices (VADS)
Fibrinolytic therapies: To disintegrate coronary thrombus
Percutaneous interventions: Balloon angioplasty, stent placement, and thrombectomies
Surgery: Coronary artery bypass, ventriculoplasty, or heart transplantation
Cardiosupportive drug and fluid regimens
Continuous hemodynamic monitoring
hypovolemic shock
insufficient intravascular fluid volume
causes of hypovolemic shock include
hemorrhage, burns, emesis, diuresis, diaphoresis, diabetes
what compensates hypovolemic shock
compensatory vasoconstriction, increased systemic vascular resistance
hypovolemic shock clinical manifestations
poor skin turgor, thirst, oliguria
low systemic and pulmonary pressure
rapid heart rates
hypovolemic shock tx
prompt control of hemorrhage
fluid replacement
neurogenic shock
Widespread vasodilation occurs from an imbalance between parasympathetic and sympathetic stimulation.
neurogenic shock causes persistent
vasodilation, and creates relative hypovolemia
causes of neurogenic shock
trauma, severe pain and stress, anesthesia, and depressant drugs
neurogenic shock clinical manifestations
very low SVR, bradycardia
neurogenic shock tx
decrease pain level
anaphylactic shock
outcome of widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis
widespread hypersensitivity rxn leads to
vasodilation, peripheral pooling, relative hypovolemia
anaphylactic shock cm
Anxiety, difficulty breathing, gastrointestinal (GI) cramps, edema, hives (urticaria), sensations of burning or itching of the skin, fever, and hemolysis.
anaphylactic shock tx
Begins with the removal of the antigen, if possible.
Epinephrine: Decreases mast cell and basophil degranulation, causing vasoconstriction; reverses airway constriction.
Intravenous (IV) volume expanders (lactated Ringer solution): Reverses relative hypovolemia.
Antihistamines and steroids: Stops inflammatory reaction.
septic shock most common infection sites
lungs, bloodstream, intravascular catheter, intraabdominal, urinary tract, and surgical wound.
septic shock progression
systemic inflammatory response syndrome
sepsis
severe sepsis
septic shock
septic shock cm
Persistent low arterial pressure, low tissue perfusion, low SVR from vasodilation, and an alteration in oxygen extraction by all cells.
septic shock tx
Check lactate level; obtain blood cultures; start antibiotic and vasopressor medications; implement fluid challenge; and achieve goals for blood pressure, central venous pressure, and central venous oxygen saturation.
macule
flat circumscribed area that is a change in the colour of the skin less than 1cm diameter
patch
flat, nonpalpable irregular shaped molecule more than 1cm diameter
papule
an elevated, firm, circumscribed area less than 1cm
plaque
elevated, firm, and rough lesion with flat top surface area greater than 1cm
benign skin tumours
seborrheic keratosis
actinic keratosis
nevi
malignant skin tumours
basal cell cercinoma
squamous cell carcinoma
malignant melanoma
first degree burns
A.K.A. partial (superficial) thickness injury involving only epidermis
Skin maintains water vapor and bacterial barrier functions
first degree burns s&s
Local pain and erythema, no blisters for ~24hrs
Extensive burn may cause chills, headache, localized edema and N &
superficial partial sickeness second degree burns
fluid-filled blisters appear immediately, pain due to exposures of nerve endings to air if blisters break open
heal in 3-4 weeks if well nourished and no complications
usually no scar (depends on skin type)
deep partial thickness second degree burns
usually involves entire dermis (hair follicles are preserved)
looks waxy white surrounded by superficial partial-thickness injury
usually can’t distinguish between this burn and 3rd degree until day 7 when skin buds appear
take weeks to heal
tx. autograft
lots of scarring
potential for infection
third degree burns
A.K.A. full thickness burns
Destruction of entire epidermis, dermis & often underlying tissues (subcutaneous, muscle, bone)
Elasticity of dermis is destroyed (dry, leathery appearance)
Edema - distal circulation may be affected in areas of circumferential burns so…
Escharotomies to relieve pressure - painless d/t destroyed nerve endings
severity of burns is affected by
age, medical hx, extent and depth of injury, involved body area
within several hours, capillar integrity is lost due to the release of
histamin and prostaglandin
burns exceeding 20% TBSA are considered
major
three main areas of burn patho
cardiovascular and systemic response cellular response - metabolic - immunologic evaporative water loss
fluid passes from intravascular system to
interstitial system
hallmark of burn shock
inadequate perfusion
basal fluid replacements per day
1500ml/day/m2 body surface area =
24 hour requirement
evaporated water loss
(25 + % total body surface area burn)
X (2 m2 body surface area) = ml/hr
total hourly maintenance fluids
basal fluid requirements per day / 24 hours + evaporated water loss per hour = ml/hr
end point of burn shock
ndividual has adequate urine output for 2 hours + (30 ml/hr)
cellular effects of burns
altered cell membrane permeability, loss of normal electrolyte homeostasis - contributes to shock
Transmembrane changes also occur in undamaged cells
immunologic response to burns
result is immunosuppression with inc. susceptibility to potentially fatal systemic burn wound sepsis
Cytokines are identified in immed. postburn period which contribute to the immune response as well as healing
Cortisol is released as a stress response which can increase risk for infection
three elements of burns survival
meticulous wound management
adequate fluids and nutrition
earlier surgical excision and grafting
burns dx and tx
Rule of Nines BUN, creatinine clearance urine output CBC, electrolytes Narcotics for pain relief Remove rings and jewelry ASAP O2 administration Hydration
