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NUR 230 > Shock > Flashcards

Shock Flashcards

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1
Q

shock

A

Life‐threatening condition in which tissue perfusion is inadequate to
deliver oxygen and nutrients to support cellular function
* Affects all body systems
* May develop rapidly or slowly
* Any patient with any disease state may be at risk for developing
shock
* Regardless of the initial cause of shock, certain physiologic responses
are common to all types of shock: hypoperfusion of tissues,
hypermetabolism, and activation of the inflammatory response
central perfusion problem

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2
Q

patho of shock

A

Decreased effective
tissue perfusion
(hypoperfusion, low
MAP)
Oxygen delivery less
than oxygen demand
Cells switch from
aerobic to anerobic
metabolism to make ATP
Leads to a buildup of
lactic acid and metabolic
acidosis
Acidosis and decreased
ATP causes cellular
dysfunction and cell
death
Without
treatment/intervention,
result is organ failure
and death

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3
Q

what is map

A

Average
blood pressure in a person’s blood vessels during a
single cardiac cycle (MAP= CO x SVR)

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4
Q

map goal

A

> or equal to 65 mm Hg

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5
Q

vasodilation makes map….

A

decrease

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6
Q

vasoconstriction makes map….

A

increase

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7
Q

factors affecting map

A

Total Blood Volume
* Cardiac Output Pump
* Size and Integrity of the vascular bed
(capillaries) Blood vessels

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8
Q

effects of low map

A

lack of perfusion
low 02 in blood
low bp

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9
Q

How does the
body sense and
respond to a low
MAP?

A

baroreceptors and chemoreceptors

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10
Q

what are the kidneys doing in shcok

A

fluid retention
retaining na
vasoconstriction…angiotensin

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11
Q

nsg assesment of shock

A

Head‐to‐Toe Assessment for Perfusion Status
* Mean Arterial Pressure (MAP)
* Pulse Pressure
* Passive Leg Raising (PLR)
* Invasive hemodynamic monitoring
* Central venous pressure (CVP)
* Central venous oximetry (ScvO2)
* Pulmonary artery (PA) monitoring
* Arterial line (A‐line)

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12
Q

what is pulse pressure

A

diastolic-systolic
diastolic increases
narrowed pulse pressure
<30-40
early stage of shock

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13
Q

compensatory stage

A

Switch from aerobic to anerobic metabolism
*Compensatory mechanisms effective to
maintain cardiac output
*Shunting of blood from non‐vital to vital
organs
*BP normal; pulse pressure may be narrow

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14
Q

progressive stage

A

Hypotension; MAP < 65 mm Hg
*Compensatory mechanisms fail
*Hypoperfusion to all organs
*Organ systems decompensate

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15
Q

irreversable (refractory) stage

A

Persistent hypotension and hypoperfusion
*Multiple Organ Dysfunction Syndrome
(MODS)
*Multiple Organ Failure
*Client will ultimately die

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16
Q

compensatory management

A

Treat underlying cause
* Fluid replacement
* Supplementation oxygen,
decrease patient anxiety
* Maintain BP and tissue perfusion
* Frequent assessment (subtle
changes)
* LOC, I&O, respiratory and heart
rate, BP (MAP of 65 mm Hg or
less, narrowing or decreased
pulse pressure)
* Promote safety (advanced
directives)

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17
Q

progressive management

A

Treat underlying cause
* Restore tissue perfusion with fluid
management
* Respiratory support
* Nutritional support for energy
* Assessment (subtle changes)
including ABGs, hemodynamic
monitoring, ECG monitoring,
mental status changes, and serum
electrolytes
* Oral care if on ventilator to
prevent VAP
* Promote rest and comfort to
reduce stress, decreased chance
of postintensive care syndrome

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18
Q

irreversable management

A

Treat underlying cause
* Respiratory support
* Circulatory support
* Nutritional support
* Experimental treatments
* Simple comfort measures
(palliative care)
* Support and education for the
friends and family
* Be honest regarding prognosis

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19
Q

what do inotropic meds do

A

improve contractility, increase stroke volume, increased co

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20
Q

disadvantages to inotropes

A

increase o2 demand of heart`

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21
Q

common inotrope

A

dobutamine

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22
Q

vasodilators

A

reduce preload and afterload
reduce o2 demand of heart

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23
Q

disadvantage to vasodilators

A

cause hypotension

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24
Q

common vasodilator used

A

nitroglycerin

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25
vasopressor agents
increased bp by vasoconstriction
26
disadvantags to vasorpressors
increase afterload therby increasing cardiac workload: compromise perfusion to skin, kidneys, gi tract
27
common vasopressor
norepi
28
what is hypovolemic shock
lack of volume (due to volume lost)
29
what is cardiogenic shock
heart itself not pumping effectively (pump failure)
30
distributive shock
volume displaced (vasodilation)q
31
neurogenic shock
loss of sympathetic response, volume pools in periphery
32
anaphylactic shock
antigen‐antibody reaction, vasodilatation and increased capillary permeability, volume pools in periphery
33
septic shock
systemic infection, inflammatory response causes vasodilation and capillary leakage, volume pools in periphery
34
external risk factors hypovolemic shock
Trauma, surgery, vomiting, diarrhea, diuresis, DKA, diabetes insipidus
35
internal risk factors hypovolemic shock
Hemorrhage, burns, ascites, peritonitis, dehydration
36
initial s/s hypovolemic shock
 HR *  diastolic BP *  pulse pressure *  pulses
37
s/s progressive hypovolemic shock
Orthostatic changes * decreased UO * decreased BP; SBP, pp & increased DBP * decreased pulse ox * Pale, cool skin * Delayed capillary refill * increased RR * Thirst * ∆ LOC
38
diagnostic tests for hypovolmeic shock
decreased HCT, HGB if caused by hemorrhage * increased HCT, HGB if caused by dehydration or fluid shift * increased K+, Na+, Cr, BUN * increased lactic acid * ABG * Radiology/x-rays/scans to identify source of bleeding (if hemorrhage) * Hemoccult, gastroccult * decreased CO, decreased preload
39
treatment hypovolemic shock
Control bleeding * Possible surgery * Fluid resuscitation * Large bore IVs/Central line * Crystalloids & Colloids * Transfusions PRBCs, FFP, platelets * Use warmer/warm fluids * Prevent complications of ischemia * Supplemental Oxygen * Mechanical Ventilation * Drug therapy * Vasoconstrictors (vasopressors) * Treat underlying cause- (ex: insulin for DKA; antidiarrheals/antiemetics for N/V/D)
40
what to monitor during hypovolemic shock treatment
LOC * VS * Hemodynamics * Pulses, cap refill, skin * I&O * Labs * Watch for S&S of fluid overload
41
causes of cardiogenic shock
Coronary * Acute MI * Noncoronary * Stress on myocardium * Ineffective myocardial function
42
s/s of cardiogenic shock
increased HR * Narrowed pulse pressure * Orthostatic Hypotension * decreased O2 sat * Pale, cool, clammy skin * Cyanosis * Delayed cap refill * increased RR, dyspnea, rales * decreased UO * ∆ LOC
43
diagnostic tests for cadiogenic shock
EKG * Cardiac enzymes * CXR * Hemodynamic monitoring * Electrolytes, BUN/Cr, liver enzymes * CBC, coagulation tests * ABG, lactic acid * Echo * Cardiac cath
44
cardiogenic shock treatment
Oxygen or ventilation support * Depends on overall client condition/signs & symptoms * Cautious administration of small fluid boluses * Monitor for fluid overload * Positive Inotropes (dobutamine) * Vasodilators (nitroglycerin) * Vasopressors (epi/norepi, vasopressin) * Diuretics (furosemide) * PTCA/Revascularization * IABP * LVAD
45
nsg management of cardiogenic shock
identify at risk pts promote adequate perfusion of heart muscle conserve to energy promptly relieve chest pain administer o2 monitor hemodynamics anticipate meds, iv fluids, and equipment report abnormal labs quickly assess cardiac and resp status often assess cardiac rhythm often report changes immediatly
46
patho of distributive shock
precipitating event vasodilation active inflammatory resonse maldistribution of intravascular volume decreased venous return decreased co decreased tissue perfuison
47
risk factors for sepsis and septic shock
Immunosuppression * Extremes of age (<1 y and >65 y) * Malnourishment * Chronic illness * Invasive procedures * Emergent and/or multiple surgeries * Medical devices
48
sirs criteria
Temperature >38.3°C or 101°F, < 36°C or 96.8°F * Tachycardia * Tachypnea * WBC’s >12 00/mm3 or <4000/mm3 or >10% immature bands * Short duration of this phase, may be missed
49
initial clinical manifestations of septic shock
Hyperthermia, warm flushed skin * Tachycardia * Bounding pulses * Hypotension with decreased urine output * Nausea, vomiting, decreased GI motility * Hepatic dysfunction‐ increased bilirubin, decreased platelets * Hypercoagulability‐ DIC * Hypermetabolism‐ increased glucose and insulin resistance * Subtle changes in mental status
50
later clinical manifestations in septic shock
BP continues to drop; cool, mottled skin; no urine output; multiple organ dysfunction with no response to treatment; bleeding due to DIC
51
septic shcok treatment
SEPSIS RESUSCITATION BUNDLE * AFTER CULTURES DRAWN- blood cultures + urine/sputum cultures * Broad Spectrum IV Antibiotics * Serum Lactate levels (increased) * Procalcitonin level (increased) * IV crystalloids- 30mL/kg bolus * Hypotension * IV vasopressors (norepinephrine) * Colloids * Clotting problems * (increase)D-dimer, FSP, PT/PTT * (decrease )fibrinogen, platelets * Heparin * Blood replacement * PRBCs, FFP, clotting factors, platelets * Nutritional support * Stress ulcer prevention * SEPSIS MANAGEMENT BUNDLE * Low dose steroids * Insulin drip * Mechanical ventilation * SEPSIS is a rapidly progressing emergency!
52
neuogenic shock risk factors
Spinal Cord Injury * Spinal Anesthesia * Depressant action of medications
53
neurogenic shock patho
disruption of sns loss of sympathetic tone...pns response venous and arterial vasodilation decreased venous return decreased stroke volumne decreased co....decreased hr decreased cellular o2 supply dedcreased tissue perfusion impaired cellular metabolism
54
neurogenic shock
Cardiovascular effect due to loss of autonomic function * Peripheral vasodilation and venous pooling * Bradycardia * Hypotension * Decreased CO * Core Hypothermia (with warm, dry skin below level of injury)
55
treatment for neurogenic shock
Spinal immobilization * C‐ Spine Precautions * Surgery * Hypotension * IV volume replacement * IV vasoconstrictors * Oxygen therapy * Ventilatory Support * Bradycardia * IV Atropine * Pacer * DVT Prevention * Warm blankets * Monitor for hypo/hyperthermia
56
risk factors for anaphylactic shock
History of medication sensitivity * Prescription of new medication * Transfusion reaction * History of reaction to insect bites/stings * Food allergies * Latex sensitivity
57
patho of anaphylactic shcok
antigen antibiody compliment, histamine, kinins, prostaglandins increased cap refill, peripheral vasodilation, constriction of extravascular smooth muscle extravascular fluids, decreased svr edema, relative hypovolemia decreased co decreased tissue perfusion impaired cellular metabolism
58
anaphylactic shock s/s
Itchy, urticaria, skin rash * Swelling lips & tongue * Wheezing or stridor * Tightness in chest – SOB * Bronchospasm * GI distress- pain, N/V * Headache, lightheadedness, feeling of impending doom, decreased LOC * Hypotension * Tachycardia & arrhythmia; can progress to cardiac arrest
59
treamtnet anaphylactic shock
Airway/Breathing * High flow O2 via NRB mask * High Fowler’s position * Intubation & mechanical ventilation * Epinephrine IM- 1:1000 concentration * Diphenhydramine (Benadryl) IV * H2 receptor antagonist (famotidine) IV * Steroids IV * Hydrocortisone * Methylprednisolone * Albuterol nebulizer * Cardiac arrest- CPR
60
invasive hemodynamic monitoring
Indicated for critically ill clients * Requires informed consent * Nurse prepares pressure monitoring system * Catheter with infusion system * Transducer * Monitor
61
nsg considerations central lines
Post‐insertion‐ CXR, auscultate lung sounds Record and trend values; Observe waveforms Assess that sutures are intact
62
complications with central lines
Infection * Cover with sterile, occlusive dressing * Assess for redness, swelling, drainage, firmness (induration) * Ventricular Arrythmias * Thrombus/ embolus at catheter site * Bleeding to site * Pulmonary Infarction/ rupture * Air emboli‐ position client on L side + head down
63
arterial catheter complications
Bleeding * Infection * Pain * Arterial spasms * Obstruction * Distal infarct * Air emboli
64

NUR 230 (16 decks)

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