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CCRN > MULTISYSTEM > Flashcards

MULTISYSTEM Flashcards

1
Q

shock is a CELLULAR DISEASE due to…

A
  • inadequate perfusion (oxygen demand > oxygen delivered) or

- inability of cells to utilize the delivered oxygen (oxygen utilization, consumption)

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2
Q

during the compensatory phase of shock, the BP is maintained due to what 2 mechanisms?

A
  • stimulation of the sympathetic nervous system –> vasoconstriction –> increased HR & contractility
  • activation of renin-angiotensin-aldosterone system (RAAS) –> increased renin secretion —> angiotensin I –> angiotensin II –> vasoconstriction; aldosterone release –> Na & H2O retention
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3
Q

what are the S/S of compensatory phase of shock? (BP maintained)

A

tachycardia, tachypnea, respiratory alkalosis, normal PaO2, oliguria, cool/pale skin, restlessness, anxiety, thirsty, BP MAINTAINED

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4
Q

what are S/S of progressive phase of shock? (compensatory mechanisms failing)

A

HYPOTENSION, worsening tachycardia/tachypnea/oliguria, metabolic acidosis, decreased PaO2, clammy/mottled skin, change in LOC, nausea

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5
Q

what are S/S of refractory phase of shock?

A

not responsive to interventions, severe systemic hypoperfusion, MULTISYSTEM ORGAN DYSFUNCTION, may survive shock but die from failure of one or more organs

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6
Q

what are the 2 most common types of hypovolemic shock?

A
  • internal - 3rd spacing, pooling in intravascular compartments
  • external - hemorrhage, GI or renal losses, burns, excessive diaphoresis
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7
Q

what happens hemodynamically in hypovolemic shock?

A
  • NARROW PULSE PRESSURE (SBP decreases, DBP maintains or elevates)
  • decreased: BP, CVP (RA), CO, O2 delivery, PAOP (LA), SvO2
  • increased systemic vascular resistance
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8
Q

how would you treat hypovolemic shock?

A
  • identify cause and correct if possible
  • volume! use fluid warmer if >2L/hr
  • goal is to maintain O2 delivery and uptake into tissue and sustain aerobic metabolism
  • use NS/LR
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9
Q

what is NS, how long do effects last, disadvantages, contraindications?

A
  • isotonic crystalloid
  • 40min, then leaves vascular space
  • large volumes may lead to hyperchloremic acidosis
  • don’t give to those with hypernatremia or renal failure
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10
Q

what is LR, how long do effects last, disadvantages, contraindications?

A
  • isotonic crystalloid; best mimic extracellular fluid, minus proteins, recommended resuscitation fluid
  • 40 min, then leaves vascular space
  • has potential to correct lactic acidosis; yet in severe hypo perfusion may promote lactic acidosis duet lactate accumulation
  • don’t give t those who shouldn’t receive K or lactate
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11
Q

should you give pressers for hypovolemic shock?

A

NO, SVR is already high r/t compensatory mechanisms

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12
Q

what is hemorrhagic shock class I? how to treat?

A
  • blood loss < 750ml
  • blood loss <15%
  • HR <100
  • BP normal
  • pulse pressure normal or decreased
  • capillary refill normal
  • RR 14-20
  • UO >30ml/hr
  • slightly anxious
  • treat with crystalloids
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13
Q

what is hemorrhagic shock class II?

A
  • blood loss 750-1500ml
  • blood loss 15-30%
  • HR >100
  • BP normal
  • pulse pressure decreased
  • capillary refill decreased
  • RR 20-30
  • UO 20-30ml/hr
  • mildly anxious
  • treat with crystalloids
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14
Q

what is hemorrhagic shock class III?

A
  • blood loss 1.5-2L
  • blood loss 30-40%
  • HR >120
  • BP normal
  • pulse pressure decreased
  • capillary refill decreased
  • RR 30-40
  • UO 5-15ml/hr
  • anxious, confused
  • treat with crystalloids + blood
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15
Q

what is hemorrhagic shock class IV?

A
  • blood loss >2L
  • blood loss >40%
  • HR >140
  • BP decreased
  • pulse pressure decreased
  • capillary refill decreased
  • RR >35
  • UO scant
  • confused, lethargic
  • treat with crystalloids + blood
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16
Q

why should blood products be warmed?

A
  • to prevent hypothermia: impairment of red cell deformability, platelet dysfunction, increase in affinity of hgb to hold onto O2
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17
Q

how can blood transfusion cause hypocalcemia and hypomagnesemia?

A

citrate in transfused blood binds ionized Ca and Mg

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18
Q

banked blod doens’t have adequate 2,3-DPG. What is the consequence?

A

shifts oxyhemoglobin-dissociation curve to the LEFT, increases affinity of hemoglobin to hold onto O2

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19
Q

what are massive transfusion protocols?

A

provide rapid infusion of large quantities of blood products to restore oxygen delivery, oxygen utilization, and tissue perfusion
10 units of RBCs in 24hrs, or 5 units in <3hrs

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20
Q

when is a massive transfusion protocol indicated?

A
  • traumatic injuries, ruptured abdominal aortic or thoracic aneurysm, liver transplant, OB emergencies
  • prevent TRIAD OF DEATH: hypothermia, acidosis, coagulopathy
  • > 50% mortality
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21
Q

what is systemic inflammatory response syndrome? (SIRS)

A

2 or more of the following:

  • T >/= 38C or <36C
  • HR >90
  • RR >20 or PaCO2 <32mmHg
  • WBC >12K or <4K or bands >10% (shift to left)
  • MAY HAVE SIRS W/O SEPSIS
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22
Q

what is sepsis?

A
  • systemic inflammatory response to a documented infection
  • clinical manifestations would include 2 or more of the SIRS criteria plus a documented infection or suspected infection
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23
Q

what is a suspected infection?

A

presence of one or more of the following:

    • cx results from blood, sputum, urine, etc
  • receiving abx anti fungal, or other anti-infectives
  • AMS in elderly
  • possible PNA
  • nursing home pt w/ foley
  • presence of pressure ulcers
  • acute ab
  • infected wounds, esp w/ hx of DM
  • immunosuppression
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24
Q

what is severe sepsis?

A
  • sepsis plus markers of organ dysfunction

- EX: hypotension, acute hypoxemia, acute drop in UO, lactate >2mmol/kg, change in LOC, plt <100K, coagulopathy

25
Q

what is septic shock?

A

severe sepsis plus one or both of the following:

  • systemic MAP <65mmHg despite adequate fluids
  • maintaining systemic MAP >65mmHg requires a PRESSOR
26
Q

what organisms can cause severe sepsis/septic shock?

A
  • gram +/- bacteria, fungi, viruses, Rickettsia, parasites
27
Q

what are some S/S of early septic shock?

A

tachycardia, bounding pulse, BP normal/low, skin warm/flushed, RR deep/fast, irritability, confusion, mental changes, oliguria, fever

28
Q

what are some S/S of progressive, later, septic shock?

A

hypotension, tachycardia, pulse weak/thready, skin cool/pale, RR fast/slow, lethargy, coma, anuria, hypothermia

29
Q

what are the hemodynamics of septic shock?

A

increased: CO/CI, SvO2, O2 delivery
decreased: RA, PA, PAOP, SVR, O2 consumption

30
Q

what are the hemodynamics of progressive, late, septic shock?

A

increased: RA, PA, PCWP,
decreased: CO/CI, O2 delivery, O2 consumption
variable: SVR, SVO2

31
Q

what are the diagnostic test results for septic shock?

A
  • mild resp alkalosis, combined respiratory alkalosis and metabolic acidosis
  • increased: PT/PTT, bands, glucose, lactate, troponin
  • decreased: PaO2, plt
    WBC up/down
32
Q

what are the diagnostic test results for progressive, late septic shock?

A
  • metabolic acidosis
  • very high: PT/PTT, bands
  • increased: BUN, creatinine, liver enzymes, lactate, troponin
  • very low: PaO2, plt
  • decreased: WBC, glucose
33
Q

what is the treatment for septic shock?

A
  • fluid challenge: 30ml/kg of crystalloid in first 3 hrs
  • pressers prn (NOREPI/LEVO, EPI, VASO)
  • ABX asap after blood cx X2 from different sites
  • inotropes (DOBUTAMINE) - for pts with cardiac dysfunction
  • SpO2 >95%; SvO2>65% when CVP and MAP goals met or ScvO2 >70%
  • if ScvO2 or SvO2 not achieved, consider further fluids, dobutamine infusion, or PRBC transfusion if hgb <7
34
Q

what are the therapeutic endpoints for septic shock?

A
  • CVP 8-12mmHg
  • MAP >65mmHg
  • UO >0.5ml/kg/hr
  • ScvO2>70% or SvO2>65%
  • normalization of HR
  • warm extremities
  • normal mental status
  • decreased lactate/improved base deficit
35
Q

what happens in anaphylactic shock?

A
  • IgE MEDIATED immediate hypersensitivity reaction to PROTEIN substances
  • usually occurs after previous exposure to substance
  • hives, angioedema in 88%, respiratory tract involvement in 50%, shock in 30%
36
Q

what is the pathophysiology of anaphylactic shock?

A

antigen antibody reaction–> histamine released–>increase capillary permeability, massive dilation, decreased CO, bronchospasm, laryngeal edema, urticaria–>hypotension

37
Q

how is anaphylactic shock treated?

A
  • removal of causative agent, if able
  • O2
  • epi IM to decrease dilation, bronchospasm
  • fluids 1-4L for hypovolemia
  • Benadryl 25-50mg IV to decrease allergic response
  • inhaled B-adrenergic agents to decrease bronchospasm
  • steroids (high dose) IV asap to decrease inflammatory response
38
Q

what is multiple organ dysfunction syndrome (MODS)?

A
  • progressive insufficiency of 2 or more organs in an acutely ill patient such that homeostasis can’t be maintained without intervention
  • may be due to any type of shock
39
Q

what is the trauma 1st and 2nd line assessment?

A

Airway - ensure patent/intubate
Breathing - 100% O2
Circulation - 2 large bore IVs with warm LR
Disability - neuro exam
Exposure/Environmental - remove clothes; warm/cool prn

Full set VS
Give comfort measures - pain
Hx
Inspect posterior

40
Q

the patient who is agitated should first receive analgesia-first sedation or anxiolytic? light/moderate/heavy level?

A

analgesia-first sedation; light bc improved clinical outcomes

41
Q

what should you know about Benzo reversal with Flumazenil (Romazicon)?

A

reversal effects of flumazenil may were off before effects of benzos; therefore, monitor for return of sedation, respiratory depression for at least 2 hrs and until the pt is stable and resedation is unlikely

42
Q

what are some adverse effects of Diazepam (valium)?

A

respiratory depression, hypotension, phlebitis

43
Q

what are some adverse effects of lorazepam (Ativan)?

A

respiratory depression, hypotension, propylene glycol-related acidosis/renal failure

44
Q

what are some adverse effects of midazolam (versed)?

A

respiratory depression, hypotension

45
Q

what are some adverse effects of propofol (diprivan?

A

pain on injection, respiratory depression, hypotension, hypertriglyceridemia, pancreatitis, allergic reactions, propofol-related infusion syndrome
*give loading dose if hypotension unlikely to occur

46
Q

what are some adverse effects of dexmedetomidine (precedex)?

A

bradycardia, hypotension; hypertension with loading dose; loss of airway reflexes

*avoid loading dose of hemodynamically unstable

47
Q

fentanyl (sublimaze) has more/less hypotension than morphine? accumulation with what organ impairment(s)?

A

less; hepatic

48
Q

what should you give to patients tolerant to morphine/fentanyl? accumulation with what organ impairment(s)?

A

dilaudid; hepatic/renal

49
Q

morphine has what kind of release? has the potential for what adverse effect? accumulation with what organ impairment(s)?

A

histamine; potential hypotension; hepatic/renal impairment

50
Q

when should remifentanil (ultiva) be used?

A

use IBW if body weight > 130% IBW

no accumulation in hepatic/renal failure

51
Q

What is Therapeutic hypothermia?

A

Treatment that lowers the patient’s core body temp in order to prevent neurological effects of ischemic injury to the brain of survivors of sudden cardiac death

52
Q

What is the inclusion criteria for use of therapeutic hypothermia?

A
  • cardiac arrest with ROSC
  • unresponsive or not following commands after cardiac arrest
  • witnessed arrest with downtime of <60min
53
Q

What is the exclusion criteria for use of therapeutic hypothermia?

A

Pregnancy, core temp <35C, age <18 or >85, existing DNR or terminal, CKD, sustained refractory ventricular arrhythmias, active bleeding, shock, hemodynamic instability, drug intoxication

54
Q

what is the induction phase?

A
  • 33C; initiate w/i 90min of arrest, may go out to 6hrs of arrest
  • goal SBP >90mmHg and MAP >70mmHg
  • CBC, CMP, coags, Mg, Phos, ABG, glucose
  • 12 lead ECG
  • deep sedation
  • paralytic for shivering
  • monitor/manage systemic effects of hypothermia
55
Q

what are systemic effects of hypothermia?

A
  • insulin resistence –> hyperglycemia
  • electrolyte and fluid shifts
  • shivering
  • skin breakdown
  • decreased CO; up to 25%
  • alteration in coagulation; plt dysfunction
  • increased risk for infection - neutrophil and macrophage functions decrease at temps <35C
56
Q

what is the maintenance phase (24hrs at 33C)?

A
  • continuous temp
  • monitor VS qhr
  • bedside glucose; insulin gtt prn
  • monitor train of 4 qhr if paralytic used with goal twitch 1-2 to prevent prolonged paralyzation
  • labs q8h until rewarmed
57
Q

what is the rewarming phase?

A
  • passive rewarming to 36.5C
  • increase target temp by 1C/hr
  • stop all K administration 8 hrs prior to rewarming; rewarming causes rebound hyperkalemia
  • d/c paralytics (if used) after pt is warmed to 36.5C
  • repeat labs when pt rewarmed
  • close neuro assessment
58
Q

what should you do during toxic ingestion?

A

ABCs FOR INITIAL MANAGEMENT

  • if comatose, give 50% dextrose 50mL, thiamine 50-100mg, narcan 2mg IV
  • activated charcoal 1gm/kg via gastric lavage; contraindicated with hydrocarbon or corrosive ingestions, not necessary with iron, lithium, EtOH
  • facilitate removal of drug - urine alkalization, HD
  • monitor for arrhythmias
  • monitor UO

CCRN (10 decks)

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