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Emergency Medicine > Shock and Resuscitation > Flashcards

Shock and Resuscitation Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

Characteristics of hypovolemic shock?

A

CVP: low
PCWP: low
SVO2: low or normal
SVR: increased
CO: low
pp: decreased
cold, clammy b/c increased SVR, slow cap refill
- think trauma and hypovolemia - hemorrhagic until proven otherwise, don’t transfuse until Hgb less than 7, unless deteriorating quickly
- give warm fluids, blankets, correct coag (give PRBCs, platelet,s FFP)

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2
Q

Characteristics of cardiogenic shock?

A 
CVP: high
PCWP: high
SVO2: low
SVR: high
CO: low 
pp: decreased, cold clammy
- have to figure out underlying cause, don't overload w/ fluids
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3
Q

Characteristics of distributive shock?

A
  • CVP: low (+/-)
  • PWCP: low (+/-)
  • SVO2: high (+/-)
  • SVR: really low
  • CO: high (+/-)
  • PP: wide (diastolic typically goes down), warm extremities (SVR low)
  • can be sepsis: tx w/ fluids and empiric abx
  • anaphylaxis: fluid bolus asap, epi
  • adrenal crisis: fluids, steroids
  • neurogenic: dx of exclusion, tx bradycardia
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4
Q

Characteristics of obstructive shock?

A
  • CVP: +/-
  • PWCP: +/-
  • SVO2: +/-
  • SVR: high
  • CO: low
  • want echo, ekg, CXR to dx underlying cause
  • give IV fluids to raise pressure, desat quickly
    etiology:
    cardiac tamponade
    tension pneumo - thoracostomy
    PE
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5
Q

DDx for crashing pt?

A 
shock:
hypovolemic
cardiogenic
distributive
obstructive
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6
Q

Indicators of shock?

A
  • can’t always base off of BP
  • are tissues perfusing? skin changes
  • hypotension, tachycardia
  • AMS
  • oliguria/anuria
  • tachypnea early indicator
  • ## metabolic derangements: lactic acid, AGMA, BUN/Cr, transaminasess, coag factors, changes in SVO2, ScVO2
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7
Q

Cause of hypovolemic shock? H and P findings?

A
  • someone left the valve open
  • loss of intravascular vol:
    hemorrhage, GI/GU losses, dehydration, decreased filling pressures/CO, high SVR (reflex vasoonstriction), decreased SVO2/ScVO2
  • H and P:
    diarrhea, polyuria, poor intake, obvious volume loss (exsanguination), flat, non-distended neck veins
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8
Q

Effects of 15% loss of blood?

A
  • HR minimally elevated or normal, no change in BP, PP, or RR
  • orthostatic hypotension
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9
Q

Effects of 15-30% loss of blood?

A
  • tachycardia (100-120)
  • tachypnea (RR 20-24)
  • decreased PP
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10
Q

effects of more than 40% blood loss?

A
  • sig depression in BP and mental status
  • hypotensive
  • PP narrowed less than 25 mmHg
  • tachycardia over 120
  • urine output: minimal or absent
  • skin cold, pale, cap refill is delayed
  • will have supine hypotension
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11
Q

The triad of death?

A
  • coag leads to metabolic acidosis (lactic acidosis) - leads to hypothermia (decreased myocardial performance - leads to halt coag cascade - coag and repeat
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12
Q

What is recommended for severe ongoing hemorrhage?

A
  • immediate transfusion of blood products in 1:1:1 ratio of PRBC, FFP and platelets.
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13
Q

What is cardiogenic shock, H and P findings?

A
  • pump is broken
  • failure of heart to provide forward flow:
    ischemia, cardiomyopathy, mechanical, arrythmia
  • High SVR, high filling pressures, low CO
  • low SVO2/ScVO2
  • H and P:
    chest pain, orthopnea/PND, EKG
    JVD, periph/pulm edema, S3 gallop
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14
Q

Tx of cardiogenic shock?

A
  • goal: improve CO while reducing myocardial workload
  • be careful w/ IV fluids
  • consider inotropic and/or vasopressor support
  • management of underlying causes:
    revasc, rhythm conersion, HF optimization
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15
Q

What is distributive shock? H and P findings?

A
  • pipes are the wrong size
  • decrease in syst. vascular tone:
    -loss of fluid into extravascular 3rd space
    -sepsis, neurogenic injury, anaphylaxis, adrenal crisis
    -low SVR (vasodilation)
    -low filling pressures, high CO initially (hyper dynamic)
    -SVO2/ScVO2 nomal or high
  • H and P:
    known allergy, spinal injury, fever/infectious sxs, warm, edematous extremities
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16
Q

Tx of anaphylactic shock?

A

Can be rapidly fatal
- IV fluid boluses, IV antihistamines, IV corticosteroids
- actively search for/remove offending allergen
- IM epi (1:1000) in 0.3-.5 mg doses necessary to maintain perfusion
refractory pts: 0.3-0.5 mg doses of IV epi (1:10,000) given over 2-3 min

17
Q

Tx of adrenal crisis caused distributive shock?

A
  • difficult to determine appropriateness of cortisol levels in seriously ill pt
  • support hemodynamics w/ IV fluids, pressors as necessary
  • stress dose steroids (hydrocortisone)
18
Q

Neurogenic shock?

A
  • dx of exclusion
  • IV fluid resuscitation
  • pressor support for failed response
  • atropine, dopamine, transcutaneous pacing necessary for bradycardia
19
Q

What is obsructive shock?

A
  • stopped pipe
  • impaired cardiac filling:
    -absence of pressure gradient in R heart
    -decrease in venous return
    -cardiac tamponade, pericarditis, tension pneumo, PE
    -high filling pressures, low CO, high PVR/SVR
  • H and P:
    becks triad, asymmetric breath sounds, friction rub
  • pulsus paradoxus
20
Q

Causes of obstructive shock?

A
  • cardiac tamponade:
    IV fluid, emergent pericardiocentesis
  • PE: IV fluid, vasopressor support (NE), avoid inubation if possible, thrombolytics (CIs?)
  • tension pneumo: IV fluid, emergent needle thoracostomy followed by chest tube
21
Q

General principles of resuscitation?

A
  • ABCs
  • hemodynamic/ventilatory support:
    improve components of O2 delivery/consumption
  • decrease tissue metabolic demands: consider early mechanical ventilation, hyperactive resp muscles can steal up to 50% of cerebral blood flow
  • primary need is to restore normal cellular fxn
22
Q

Monitoring for pts in shock?

A

need to be admitted to ICU:

  • high risk of decompensation
  • telemetry
  • BP (invasive)
  • pulse ox
  • CVP
  • ScVO2
  • mental status
  • UOP
  • lactate
23
Q

How can we max O2 delivery? When should we transfuse?

A
  • supp O2, positive pressure ventilation:
    allows for improved oxygenation, also reduces O2 demand by reducing WOB
  • transfusion parameters:
    at 7 unless cardiac ischemia
24
Q

Describe the inability to match metabolic demands?

A
  • O2 delivery/consumption mismatch
  • under normal circumstances:
    O2 consumption is 250 cc/min
25
Q

What should be given if pt’s hypotension is refractory to IVF?

A
  • inotropes and vasopressors
26
Q

Receptors and fxns?

A
  • B1: increases cardiac contractility/chronicity
  • B2: induces smooth muscle vasodilation
  • a1: arterial vascular smooth muscle contraction
  • D1/D2: vasodilation of renal/splachnic vasculature
  • most affect a mult. of receptors
27
Q

MOA of NE?

A
  • primarily a1 agonist (some inotropic effects as well)
  • vasoconstriction w/o impacting CO or HR
  • 1st line for septic shock, also recommended in undiff shock states
  • can be toxic to cardiac myocytes (apoptosis)
28
Q

MOA of Vasopressin?

A
  • ADH
  • acts on V1(vasc)/V2(renal) receptors:
    V1 stim smooth muscle contraction, V2 increases water resorption at collecting ducts
  • improves sensitivity to NE
  • not affected greatly by acidosis/hypoxia
29
Q

MOA of dopamine?

A
  • natural precursor to NE
  • affects diff receptors at diff doses:
    3-10 micrograms/kg/min: B1 (promotes NE release)
    10-20micrograms: a1 (vasoconstriction)
  • assoc w/ higher risk of tachyarrhythmias
30
Q

MOA of dobutamine?

A
  • B1 and B2 receptor agonist
  • also binds a1 so results in mild net vasodilation
  • used in cardiogenic shock and sepsis induced cardiogenic dysfxn
  • increases myocardial O2 demand
  • potentially pro-arrhythmic (esp ventricular)
  • subject to tachyphylaxis
31
Q

MOA of epi?

A
  • high affinity for B1, B2, a1 receptors:
    B at low doses, a at high doses
    recommended primarily for cardiac arrest, improves coronary blood flow
  • can cause cardiac toxicity: apoptosis and contraction band necrosis
32
Q

Frank starling principle?

A
  • stroke vol of heart increases in response to increase in volume of blood filling the heart (end diastolic vol)
  • as larger vol flows into ventricle, the blood will sretch the walls, causing a greater expansion during diastole, which in turn increases the force of contraction and thus quantity of blood that is pumped into the aorta during systole
33
Q

IV access pearls?

A
  • when tx shock from any cause: 2 large bore 16 g or greater periph lines should be started
  • rate of infusion is directly proportional to catheter length
  • never place IV distal to cellulitis, burns or when there is potential vascular disruption proximal to insertion site
  • attempt IV in most distal upper extremity vein you can access
  • cephalic vein good choice
  • veins in hands are accessible but short and tortuous
  • antcubital fossa good in emergencies but need armboard to prevent kinking
34
Q

When should IO access be used?

A
  • initially suggested in kids under 5yo
  • shown to be safe in kids and adults
  • easily est and more rapidly accessed
  • manual insertion w/ force
35
Q

When should central access be done?

A
  • IJ, subclavian, femoral vein (don’t do this)
  • rapid delivery of meds
  • periph veins inadequate
  • measurement of CVP, ScVO2, SVO2
36
Q

What should be done in 1st 30 seconds of a code blue?

A
  • backboard and high quality CPR
  • pads on
  • timer
37
Q

What should be done in the next 90 sec of a code blue?

A 
- assign jobs:
access
meds
defib
compressors (3)
airway
recorder
family
  • get hx, Hs/Ts, meds, repeat, pulse and rhythm check no longer than 10 sec
38
Q

Vascular access during a code?

A
  • should be obtained at largest vein w/o disrupting resuscitation
  • dont try to get central access during cardiac arrest
  • get IO access and then place CVL once ROSC obtained

Emergency Medicine (22 decks)

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