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NRSG 331 > Shock > Flashcards

Shock Flashcards

1
Q

meds for shock

A

VIVA
vasoconstrictors, inotropes, vasodilators, antidysrhythmics

  • vasoconstrictors: V PANE: vasopressin, phenylphrine, alpha-range dopamine, norepi, epi
  • inotropes: BEN MD: beta-range dopamine, epi, norepi, milrinone, dobutamine
  • vasodilators: NN Hy Lol: nitroprusside, NTG, hydralazine, labetalol
  • antidysrhythmics: PALED VA Lol: procainamide, amiodarone, lidocarine, esmolol, diltiazem, verapamil, adenosine, labetalol
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2
Q

tx for shock

A

major focus on improving tissue perfusion (meds), supporting O2 delivery and Hgb levels (give blood if Hgb very low, intubate and MV, give O2), give crystalloid or colloid if intravascular volume depletion, give enteral therapy within 24-48 hrs or TPN if can’t do enteral but should delay it for 7 days, keep glucose in 140-180, identify and correct cause of lactic acidosis, don’t give sodium bicarb for acidosis.

Assess response to therapy, prevent and maintain surveillance for complications, and provide emotional/comfort support.

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3
Q

consequences of shock

A
  • cardiovascular: ventricular failure and microvascular thrombus
  • neuro: SNS dysfunction, cardiac/resp depression, thermoregulatory failure, coma
  • pulm: ARDS, acute lung failure
  • renal: AKI
  • hematologic: DIC
  • GI: GI tract failure, liver failure, pancreatic failure
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4
Q

causes of hypovolemic shock (internal vs external)

A

internal causes: hemothorax, 3rd spacing, hemorrhagic pancreatitis, ruptured spleen/liver, dissecting aneurysm, ascites, peripheral edema

external losses: loss of blood, plasma, body fluids (surgery, obstetric delivery, burns, gi loss)

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5
Q

classes/stages of hypovolemic shock

A

Class I: loss up to 15%, or up to 750 mL
Class II: loss up to 15-30%, or 750-1500 mls
Class III: loss of 30-40%, or 1500-2000 mL
Class IV (severe and usually refractory): loss >40% or loss >2000 mL

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6
Q

how much fluid and what type to give in hypovolemic shock?

A

can give blood or isotonic crystalloids (NS/LR)

  • 3:1 ratio (300 mLs for every 100 mLs of fluid lost)
  • hemodynamic monitoring monitors fluid replacement
  • fluid challenge
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7
Q

evaluating effectiveness of fluid volume resuscitation

A
  • BP arterial pressure 65-70 (map??)
  • CVP 6-8
  • UO 0.5 ml/kg/hr
  • normal BUN/Cr
  • serum lactate returning to normal
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8
Q

S/S of cardiogenic shock (initial vs later)

A

initial:

  • decline in CO
  • chest pain
  • tachycardia
  • ABGs: resp alkalosis and hypoxemia
  • pulm edema

later as compensation fails:

  • continued increased HR
  • chest pain
  • dysrhythmias
  • deteriorating pulm function, resp distress
  • ABGs: resp acidosis, metabolic acidosis, hypoxemia
  • renal failure
  • decreased LOC from cerebral hypoperfusion
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9
Q

diagnosis of cardiogenic shock

A
  • CI less than 2.2 l/min/m2 in presence of elevated PAOP >15 mm Hg
  • echo confirms diagnosis by giving noninvasive estimate of PAOP and EF and clarifies etiology
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10
Q

tx of cardiogenic shock

A

-mechanical: IABP and VAD
-pharm approach:
diuretics and venous vasodilators to decrease preload, positive inotropes to increase CO, arterial vasodilators to decrease afterload

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11
Q

complications of IABP, LVAD, ECMO

A
  • infection
  • bleeding
  • thrombocytopenia
  • hemolysis
  • embolus
  • stroke
  • device malfunction
  • circulatory compromise of a cannulated extremity
  • sirs
  • sepsis
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12
Q

causes of obstructive shock

A
  • impaired diastolic filling (cardiac tamponade, tension pneumo, constrictive pericarditis, compression of great veins)
  • increased right ventricular afterload (PE, severe pulm HTN, increased intrathoracic pressures)
  • increased left ventricular afterload (aortic dissection, systemic embolism, aortic stenosis)
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13
Q

s/s of cardiac tamponade

A
  • muffled heart sounds
  • hypotension
  • pulsus paradoxus (decrease in SBP during inspiration)
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14
Q

s/s of tension pneumo

A
  • decreased breath sounds on affected side

- tracheal shift away from affected side

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15
Q

tx of obstructive shock

A
  • pericardiocentesis
  • thoracentesis
  • surgical reduction of long bone fx (preventing PE)
  • intermittent pneumatic compression devices
  • ROM
  • prophylactic anticoagulants
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16
Q

hemodynamic changes that occur in distributive types of shock

A
  • decreased BP
  • decreased SV
  • decreased CO
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17
Q

types of distributive shock

A
  • neurogenic
  • anaphylactic
  • septic
18
Q

causes of neuro shock

A
  • sci (most common)
  • spinal anesthesia
  • nervous system damage
  • vasomotor depression
19
Q

what does the loss of sympathetic tone in neuro shock lead to?

A

-massive peripheral vasodilation, inhibition of baroreceptor response, and impaired thermoregulation.
The massive vasodilation (arterial and venous) causes decreased SVR and decreased BP and relative hypovolemia with blood pooling in the venous circuit leading to decreased preload.
Loss of baroreceptor response causes bradycardia which worsens CO.
Loss of vasomotor tone results in inability for blood vessels to dilate/constrict for temp maintenance which leads to loss of thermoregulation

20
Q

s/s of neuro shock

A
  • bradycardia with hypotn
  • warm dry flushed skin
  • decreased CO/CI
  • declining RAP and pAOP (venous vasodilation decreasing preload)
  • decreased SVR (arterial vasodilation causing decreased afterload)
  • hypothermia (unable to thermoregulate)
21
Q

tx of neuro shock

A
  • immobilize spine and positioning
  • IV fluids carefully, watch for overload
  • vasopressors if pt doesnt respond to fluid
  • slow rewarming to prevent more vasodilation
22
Q

how does anaphylactic shock occur

A

-antigen-antibody response causes cellular breakdown and the release of powerful vasoactive mediators from the mast cells and basophils –> vasodilation causes decreased BP, relative hypovolemia, fluid shifts

23
Q

s/s of anaphylactic shock

A
  • upper airway: laryngeal edema
  • lower airway: bronchial constriction
  • excessive mucus production
  • angioedema (swelling of eyes, lips, tongue, hands, feet, genitalia)
  • tachycardia and hypotension
  • skin: itching, pain, pruritis, urticaria
24
Q

tx of anaphylactic shock

A

-remove trigger
-establish airway
-meds:
Epi for bronchodilation and vasoconstriction
Histamine blockers like ranitidine and benadryl as secondary agents
Corticosteroids to reduce inflammation
IV fluids to counteract hypotn

25
Q

sepsis vs septic shock definitions

A

sepsis: presence (probable or documented) of infection together with systemic manifestations of infection
vs
septic shock: sepsis-induced hypotension that persists despite adequate fluid resuscitation

26
Q

causes of septic shock

A
  • immunosuppression (extremes of age, malnutrition, alcoholism, drug abuse, malignancy, hx of splenectomy, chronic health problems, immunosuppressive therapies)
  • bacteremia (invasive procedures, invasive devices, traumatic wounds or burns, GI infection, untreated disease, peritonitis, food poisoning, prolonged hospitalization, translocation of GI bacteria)
27
Q

s/s of septic shock

A
  • metabolic acidosis
  • acute encephalopathy
  • oliguria
  • hypoxemia
  • coagulation disorders
  • hypotension
  • decreased skin perfusion/mottling
  • petechiae
28
Q

tx of septic shock

A
  • prevention (hand hygiene, asepsis)
  • ABX (Empirical then change to specific once c&s results available)
  • iv fluids to keep CVP >8 and HR <110
  • maintain MAP >65 with vasopressors (dopamine/norepi) and vasopressin if needed
  • give blood to keep SCVO2 >70% , can use dobutamine and or PRBCs
  • give ACTH for low cortisol
  • keep glucose <180
  • temp control
  • treat cause
  • minimize o2 consumption
29
Q

sepsis diagnosis

A

2 or more of the following are present after an infection:

  • temp >38 or <36 (100.4 and 98.6)
  • HR >90
  • RR >20 or PaCO2 <32
  • WBC >12k, <4k, or > 10% immature band forms
30
Q

early sepsis manifestations

A
  • tachycardia
  • bounding pulse
  • warm flushed skin
  • change in mental status
  • oliguria
  • hyperthermia
  • inc CO/CI, svo2
  • decreased RAP, PAOP, SVR
  • respiratory alkalosis with hypoxemia
  • increased WBC and glucose
31
Q

late sepsis s/s

A
  • tachycardia
  • weak thready pulse
  • cold pale skin
  • lethargy/coma
  • anuria
  • hypothermia
  • decreased CO/CI, SVO2
  • variable RA/PAWP/SVR
  • metabolic acidosis with hypoxemia
  • decreased WBC and glucose
32
Q

surviving sepsis campaign bundles: within 3 hours do what?

A
  • measure lactate
  • obtain blood cx before administration of ABX
  • administer broad spec ABX
  • administer 30 ml/kg crystalloid for hypotension or lactate greater than or equal to 4
33
Q

sepsis campaign bundle: within 6 hrs do what?

A
  • apply pressors (for hypotn that does not respond to initial fluids) and maintain MAP > or = 65
  • reassess volume status and tissue perfusion
  • remeasure lactate if initial lactate was elevated
34
Q

vasopressin: when to use it and what effects does it have

A

-can be added to norepi
It’s synthetic ADH that sensitizes arterioles to catecholamines, increasing the release of cortisol and ACTH. gives vasoconstriction without the effects of other drugs (tachycardia, dysrhythmias)

35
Q

sepsis continuum

A

microorganism invasion –> SIRS + infection –> sepsis + hypotension despite fluid resuscitation –> septic shock –> MODS

36
Q

mortality rates of MODS

A
  • 45-55% with 2 failed systems
  • 80% with 3/more
  • 100% with 3/more for more than 4 days
37
Q

organs severely affected in MODS?

A
  • lungs (the first affected)
  • liver
  • kidneys
  • splanchnic bed
38
Q

causes of MODS

A
  • can be primary or can be from shock, trauma, burns, infections impairing perfusion
  • most common causes are sepsis and septic shock
39
Q

s/s of MODS

A
  • tachypnea, hypoxemia
  • petechiae/bleeding
  • jaundice
  • abd distention
  • oliguria –> anuria
  • tachycardia
  • hypotension
  • change in LOC
40
Q

tx of MODS

A
  • control infection: ABX
  • provide adequate tissue oxygenation: maintain 88-92% o2 sat and maintain Hgb >7-9
  • restore intravascular volume: aggressive fluids with isotonic crystalloids
  • support organ functions
41
Q

splanchnic bed

A

blood supply to the GI tract, liver, spleen, pancreas

NRSG 331 (3 decks)

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