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Advanced MedSurg > Shock (Final Exam) > Flashcards

Shock (Final Exam) Flashcards

1
Q

What is shock?

A

syndrome characterized by decreased tissue perfusion and impaired cellular metabolism, leading to an imbalanced supply of and demand for oxygen and nutrients

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2
Q

What are the 4 main categories of shock?

A

1) cardiogenic
2) hypovolemic
3) distributive: septic, anaphylactic, neurogenic shock
4) obstructive

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3
Q

Septic shock is characterized by _____ and caused by (3)

A
  • persistent hypotension (despite fluid resuscitation)

- caused by: virus, bacteria, fungal infection

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4
Q

Which patients are at highest risk for septic shock? (5)

A
  • immunocompromised
  • old age
  • diabetes
  • COPD
  • untreated infections (eg: UTI)
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5
Q

Sites of infection for septic shock (6)

A

1) RESPIRATORY (#1)
2) urinary
3) skin
4) intraabdominal (GI)
5) catheters
6) IV/PICC line site

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6
Q

signs and symptoms of septic shock (6)

A

1) brain: decreased LOC
2) lungs: tachypnea, hypoxia
3) cardiac: MAP <65, hypotensive
4) kidneys: oliguria (compensatory)
5) integ: warm (early/compensatory), cold (refractory)
6) lactate: severe > 4.0 (will rise very early on in sepsis infection)

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7
Q

Interventions for suspected sepsis (4)

A

1) obtain lactate lab values
2) blood draw for causative agents
3) start broad spectrum antibiotics (eg: cephalosporin, ceftriazone) within 1 hour
4) start fluids

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8
Q

What is the “give 3” and “take 3” treatment intervention for septic shock?

A

give 3:

1) start antibiotics within 1 hr of shock (after cultures are obtained)
2) oxygen: titrate O2 to sat 94-98%
3) fluids: minimum of 30 mL/kg of crystalloids

take 3:

1) obtain cultures
2) draw blood
3) collect urine output

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9
Q

Medication treatment for septic shock (3)

A

for hypotension: VASOPRESSORS:
epinephrine, phenylphrine, (inotropes: dopamine, dobutamine)

for refractory stage: NOREPINEPRHINE

If BP can’t be maintained, use IV corticosteroids

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10
Q

Acute care for septic shock (3)

A

1) stress ulcer: PPI (famotidine, omeprazole)
2) glucose: monitor for BS of 180 or below
3) VTE prophylaxis: heparin, enoxaparin

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11
Q

2 types of hypovolemic shock?

A

1) absolute hypovolemia

2) relative hypovolemia (aka third spacing)

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12
Q

What is absolute hypovelmia?

A

external loss of whole blood from hemorrhage of trauma, surgery, or GI bleeding

Other forms of loss of body fluids: vomiting, diarrhea, excessive diuresis, diabetes insipidus (increased excretion)

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13
Q

What is relative hypovolemia?

A

third spacing d/t internal bleeding (fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis) and fluid shifts (BURNS, ascites, SEPSIS)

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14
Q

signs and symptoms of hypovolemic shock? (4)

A

1) anxiety
2) increase in HR and CO
3) increased RR
4) decrease in SV, pulmonary artery wedge pressure (PAWP), urine output

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15
Q

Both absolute and relative hypovolemia can result in which compensation mechanisms? (2) and interventions (2)

A
  • increased HR, CO, RR depth
  • decreased excretion: oliguria, anuria
  • intervention: (1) administer crystalloids (lactated ringers, NS), (2) monitor hourly urine output
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16
Q

15-30% volume loss leads to baroreceptors activating _____. What is an intervention?

A
  • volume loss leads to baroreceptors activating fight-or-flight and increases HR
    intervention: give blood products
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17
Q

What is the #1 cause of cardiogenic shock? What are other causes?

A

1 cause: acute myocardial infarction

other: cardiomyopathy, blunt cardiac injury, severe hypertension

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18
Q

Pathophysiology of cardiogenic shock?

A

a PUMPING issue, the heart cannot pump enough blood to meet perfusion needs of the body = decreased CO, decreased perfusion leads to cell death

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19
Q

What is the formula for CO (amount of blood pumped per minute)

A

CO = HR x SV (stroke volume is the most important pumping chamber)

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20
Q

What is the goal of care for cardiogenic shock?

A

increase stroke volume (restore heart function and balance between O2 supply)

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21
Q

What are the three components of SV and what medications effect it?

A

1) preload: increased preload = increases SV; med: vasopressors (vasoconstricts)
2) afterload: decreased afterload = increased SV; med: vasodilator
3) contractility: increased contraction = increased SV; med: atropine

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22
Q

What are early signs of cardiogenic shock? (RSHF: 4 vs LSHF: 3)

A

left-sided HF:

1) crackle on auscultation = pulmonary edema
2) dyspnea
3) increased HR

right-sided HR:

1) JVD
2) peripheral edema
3) hepatomegaly
4) hypoperfusion

23
Q

signs and symptoms of cardiogenic shock?

A

1) tachycardia, hypotension
2) narrowed pulse pressure
3) tachypnea
4) cool, clammy skin; diaphoresis
5) pallor, cyanosis, decreased perfusion to extremities
6) cap refill <2 seconds (decreased cap refill)
7) hypoperfusion to kidneys = oliguria
8) anxiety, confusion, AGITATION

24
Q

Treatments for cardiogenic shock (5)

A

1) vasopressors: dobutamine, dopamine (assess IV site for extravasation)
2) vasodilators: nitroglycerin, sodium nitroprusside
3) DIURETICS (to reduce preload): IV furosemide (Lasix)
4) DEFINITIVE MEASURES: angioplasty with stenting, emergency revascularization, valve replacement
5) fluid replacement is CONTRAINDICATED (increases work of heart)

25
Q

Describe neurogenic shock

A

occurs within 30 minutes of the spinal cord injury at or above the 5th thoracic (T5) vertebrae

26
Q

signs and symptoms of neurogenic shock (3)

A

1) hypotension: from massive vasodilation
2) bradycardia: unopposed parasympathetic stimulation
3) poikilothermia: unable to regulate body temp

27
Q

Treatment for neurogenic shock (4)

A

for bradycardia: atropine (vasoconstrictor)

for hypotension: vasopressors (norepinephrine, phenylephrine, dopamine, dobutamine) MAP should be between 85-90

spinal cord injury treatment: spine precautions/stability

monitor for hypothermia

28
Q

What are 3 complications of neurogenic shock? (3)

A

1) massive vasodilation + no SNS response = pooling of blood, hypoperfusion = low BP and increased HR
2) impaired cell metabolism = irregular temperature (patient will be warm at first)
3) lasting paralysis

29
Q

Describe anaphylactic shock

A

allergic reaction caused by drug chemical, vaccine, food, inset venom

30
Q

Immediate reactions of anaphylactic shock are (3)

A

1) massive vasodilation
2) release of vasoactive mediators
3) increase in capillary permeability = fluid leaks into the vascular space

31
Q

signs and symptoms of anaphylactic shock? (7)

A

1) anxiety/confusion
2) dizziness
3) chest pain
4) incontinence
5) swelling of the lips and tongue
6) wheezing, stridor
7) flushing, pruritis, urticaria, angioedema

32
Q

What is the goal of treatment for anaphylactic shock?

A

maintain airway !! (major release of histamine = narrows airway)

33
Q

What is the drug of choice for anaphylactic shock? Other medications? Interventions to maintain a patent airway?

A

Epinephrine (drug of choice)

Other: diphenhydramine, ranitidine

Maintain patent airway:

  • bronchodilators
  • aerosolized epinephrine
  • ENDOTRACHEAL INTUBATION OR TRACHEOSTOMY

Aggressive fluid replacement (usually crystalloids)

34
Q

Describe obstructive shock

A

physical obstruction to blood flow occurs with a decreased CO

35
Q

Causes of obstructive shock (4)

A

1) restricted filling: cardiac tamponade, pneumothorax !!
2) pulmonary embolism: blood clot
3) superior vena cava syndrome
4) abdominal compartment: trauma to the abdomen !!

36
Q

signs and symptoms of obstructive shock? (4)

A

ribcage is constricted = oxygenation decreases = decreased perfusion

1) decreased CO
2) increased afterload
3) JVD
4) pulsus paradoxus: decrease of SBP by 10 mmHg or more

37
Q

treatment for obstructive shock? (4)

A

1) mechanical decompression (ie: pneumothorax = puncture of the lungs)
2) anticoagulants and pulmonary embolectomy for pulmonary embolism (thrombolytic therapy)
3) radiation, removal, debulking (shrink) for superior vena cava syndrome
4) decompressive for ABD compartment

38
Q

What are 2 main complications of all shock?

A

1) perfusion

2) cellular metabolism

39
Q

What are the 4 stages of shock?

A

1) initial
2) compensatory
3) progressive
4) refractory

40
Q

INITIAL stage of shock (3)

A
  • still reversible, no clinical s/s
  • lactic acid buildup (metabolized by the liver)
  • decreased CO
41
Q

COMPENSATORY stage of shock (types [3] and mechanisms [2])

A
  • types (3): neural, hormonal, biochemical
  • compensatory mechanisms:
    1) decreased BP, increased HR = increased CO
    2) blood pulls from non-vital organs to vital organs
42
Q

Non-vital organs that are hypoperfused in the compensatory stage of shock? (4)

A

1) kidneys: RAAS - decreased excretion - tachycardia, hypertension
2) lungs: V/Q mismatch - Kusmaul’s (hyperventilation)
3) GI: slowed peristalsis (risk for paralytic ileus)
4) Skin: cool and clammy (except septic shock = warm!!)

43
Q

PROGRESSIVE stage of shock (2)

A
  • irreversible = can lead to MODS (multiple organ dysfunction syndrome)
  • s/s: delirium, decreased CO and BP, anasarca (generalized full body edema)
44
Q

Effects of the PROGRESSIVE stage on different systems of the body (4)

A

lungs: decreased surfactant = crackles on auscultation

GI: ulcer, bleeding (bacteria can migrate to the lungs = infection)

GU: decreased blood flow to the kidneys = oliguria, acute kidney injury, increased BUN and creatinine

Liver: jaundice, Kupffer cells (liver cells) in the blood = disseminated intravascular coagulation (DIC) and abnormal blood clotting
- DIC: bleeding at the orifices

45
Q

REFRACTORY stage of shock (2)

- s/s (4)

A

irreversible, decreased perfusion from peripheral vasoconstriction and decreased CO

s/s:

  • profound hypotension and hypoxemia !!
  • mottled, cyanotic skin
  • decreased BP and HR
  • decreased RR and LOC
46
Q

ABGs seen in a patient with shock?

A

metabolic acidosis (normal HCO3: 22-28; if low, metabolic acidosis)

47
Q

Diagnostic tests for shock (2)

A

1) established from detailed hx and physical findings

2) SERUM LACTATE (elevated), base deficit (HCO3), 12-lead ECG, chest x-ray, pulse ox, hemodynamic monitoring

48
Q

What are the goals of treatment for shock? (2)

A

Drug therapy: correct the decreased tissue perfusion (vasopressor or vasodilation therapy = maintain MAP)

Nutrition: protein-calorie malnutrition (s/s of hypermetabolism in shock) = early enteral nutrition to decrease morbidity

49
Q

Emergency shock management (5)

A

1) high-flow O2 (100%) by non-rebreather mask, anticipate need for intubation
2) attempt IV access using large-bore 14- or 16-gauge) catheters/preparing for placement of central line
3) start fluid resuscitation with crystalloids and possible blood products
4) monitor chest tube drainage
5) insert catheters for intra arterial and central venous, urine output, NG drainage

50
Q

What is multiple organ dysfunction syndrome (MODS)

A

failure of 2 or more organ systems in an acutely ill patient such that homeostasis cannot be maintained with intervention

51
Q

What is the first system to show signs of dysfunction of MODS?

A

respiratory system = acute respiratory distress syndrome

52
Q

What assessments can be made to check for adequate tissue perfusion? (7)

A
  • LOC
  • urine output
  • capillary refill
  • peripheral sensation
  • skin color
  • extremity skin temp
  • peripheral pulses
53
Q

What tasks can be delegated to the UAP in shock management? (4)

A
  • measure/record urine output and NG drainage
  • aid with hygiene and repositioning
  • provide oral care, obtain weight, glucose monitoring
  • feeding assistance

Advanced MedSurg (11 decks)

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