week 13: multiple interacting systems Flashcards

(54 cards)

1
Q

shock

A

condition during which the cardiovascular system fails to perfuse the tissues adequately; causes general and widespread impairment of cellular metabolism.

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2
Q

common pathways in all types of shock

A

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

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3
Q

classes of shock

A

cardiogenic, neurogenic or vasogenic, anaphylactic, septic, hypovolemic

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4
Q

shock cm

A

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

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5
Q

shock tx

A

Oxygenation: Absolute necessity in all shock states
Correct or remove underlying cause
Provide supportive therapy

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6
Q

cardiogenic shock causes

A

myocardial ischemia, myocardial infarction

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7
Q

cardiogenic shock

A

Inability of the heart to pump adequate blood to tissues and end organs from any cause

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8
Q

as cardiac output decreases compensatory adaptive responses are activated:

A

Renin-angiotensin, neurohormonal, and sympathetic nervous system.

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9
Q

cardiogenic shock cm

A

Chest pain, dyspnea, and faintness, along with feelings of impending doom

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10
Q

cardiogenic shock hallmarks

A

Tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output

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11
Q

cardiogenic shock tx

A

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

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12
Q

hypovolemic shock

A

insufficient intravascular fluid volume

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13
Q

causes of hypovolemic shock include

A

hemorrhage, burns, emesis, diuresis, diaphoresis, diabetes

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14
Q

what compensates hypovolemic shock

A

compensatory vasoconstriction, increased systemic vascular resistance

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15
Q

hypovolemic shock clinical manifestations

A

poor skin turgor, thirst, oliguria
low systemic and pulmonary pressure
rapid heart rates

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16
Q

hypovolemic shock tx

A

prompt control of hemorrhage

fluid replacement

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17
Q

neurogenic shock

A

Widespread vasodilation occurs from an imbalance between parasympathetic and sympathetic stimulation.

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18
Q

neurogenic shock causes persistent

A

vasodilation, and creates relative hypovolemia

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19
Q

causes of neurogenic shock

A

trauma, severe pain and stress, anesthesia, and depressant drugs

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20
Q

neurogenic shock clinical manifestations

A

very low SVR, bradycardia

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21
Q

neurogenic shock tx

A

decrease pain level

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22
Q

anaphylactic shock

A

outcome of widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis

23
Q

widespread hypersensitivity rxn leads to

A

vasodilation, peripheral pooling, relative hypovolemia

24
Q

anaphylactic shock cm

A

Anxiety, difficulty breathing, gastrointestinal (GI) cramps, edema, hives (urticaria), sensations of burning or itching of the skin, fever, and hemolysis.

25
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.
26
septic shock most common infection sites
lungs, bloodstream, intravascular catheter, intraabdominal, urinary tract, and surgical wound.
27
septic shock progression
systemic inflammatory response syndrome sepsis severe sepsis septic shock
28
septic shock cm
Persistent low arterial pressure, low tissue perfusion, low SVR from vasodilation, and an alteration in oxygen extraction by all cells.
29
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.
30
macule
flat circumscribed area that is a change in the colour of the skin less than 1cm diameter
31
patch
flat, nonpalpable irregular shaped molecule more than 1cm diameter
32
papule
an elevated, firm, circumscribed area less than 1cm
33
plaque
elevated, firm, and rough lesion with flat top surface area greater than 1cm
34
benign skin tumours
seborrheic keratosis actinic keratosis nevi
35
malignant skin tumours
basal cell cercinoma squamous cell carcinoma malignant melanoma
36
first degree burns
A.K.A. partial (superficial) thickness injury involving only epidermis Skin maintains water vapor and bacterial barrier functions
37
first degree burns s&s
Local pain and erythema, no blisters for ~24hrs | Extensive burn may cause chills, headache, localized edema and N &
38
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)
39
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
40
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
41
severity of burns is affected by
age, medical hx, extent and depth of injury, involved body area
42
within several hours, capillar integrity is lost due to the release of
histamin and prostaglandin
43
burns exceeding 20% TBSA are considered
major
44
three main areas of burn patho
``` cardiovascular and systemic response cellular response - metabolic - immunologic evaporative water loss ```
45
fluid passes from intravascular system to
interstitial system
46
hallmark of burn shock
inadequate perfusion
47
basal fluid replacements per day
1500ml/day/m2 body surface area = | 24 hour requirement
48
evaporated water loss
(25 + % total body surface area burn) | X (2 m2 body surface area) = ml/hr
49
total hourly maintenance fluids
basal fluid requirements per day / 24 hours + evaporated water loss per hour = ml/hr
50
end point of burn shock
ndividual has adequate urine output for 2 hours + (30 ml/hr)
51
cellular effects of burns
altered cell membrane permeability, loss of normal electrolyte homeostasis - contributes to shock Transmembrane changes also occur in undamaged cells
52
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
53
three elements of burns survival
meticulous wound management adequate fluids and nutrition earlier surgical excision and grafting
54
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 ```