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SHOCK

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Septic, Addison's, Anaphylactic, Neurogenic, Thyrotoxicosis, Beriberi, Paget's, ... If CARS reaction is severe it will manifest as anergy and infection susceptibility ... – PowerPoint PPT presentation

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Title: SHOCK


1
SHOCK
  • September 6, 2005
  • Andrew Filiatraut

2
In General
  • Shock
  • Clinical syndrome defined as hypoperfusion
  • Hypotension and Cellular Hypoxia
  • Elevated lactate
  • Oliguria
  • Hepatic/GI dysfunction
  • Mental status changes

3
In General
  • Four Classifications
  • Hypovolemic
  • Cardiogenic
  • Obstructive
  • Distributive
  • Septic, Addisons, Anaphylactic, Neurogenic,
    Thyrotoxicosis, Beriberi, Pagets, Cirrhosis,
    Chroinc Anemia, Osler-Weber-Rendu

4
Hemodynamic Profiles
TYPE BP C.O. PCWP SVR
? Vol. ? ? ? ?
Cardio ? ? ? ?
Tmpnad ? or N ? or N ? or N ?
P. E. ? ? ? or N ?
Distrib ? ? ? ?
5
Septic Shock
6
Epidemiology
  • 751,000 cases of severe sepsis /year
  • Up to half develop shock
  • Overall mortality rate of 45
  • Cause
  • Gram 35-40
  • Gram- 55-60
  • Slightly higher incidence in men, older adults
    (55-60 yrs)

7
Definitions
  • Infection
  • Inflammation against microorganism
  • Bacteremia
  • Viable bacteria in blood

8
Definitions
  • SIRS
  • Evidence of inflammation NOT necessarily
    infection
  • 2 or more of the following
  • Tempgt38 or lt36
  • HR gt90bpm
  • RR gt20 or PaCo2 lt32
  • WBCs gt12,000 or lt4000 or gt10 bandemia

9
Definitions
  • Sepsis
  • systemic inflammatory response as a result of
    infection
  • Severe Sepsis
  • sepsis associated with organ dysfunction
  • Lactic acidosis, oliguria, mental status change
  • Septic shock
  • sepsis-induced hypotension with presence of
    perfusion abnormalities

10
Definitions
  • Sepsis-induced hypotension
  • SBPlt90 or reduction of 40mm Hg from baseline
    without other cause
  • Multiple Organ Dysfunction Syndrome
  • Altered organ dysfunction in acutely ill patient
    requiring intervention to maintain homeostasis

11
(No Transcript)
12
Pathophysiology
13
Pathophysiology
  • Focus of infection
  • Pneumonia, UTI, cellulitits, abscess, indwelling
    device
  • ICU catheters, sinusitis, acalculus
    cholecystitis, C. diff, resistant organism,
    fungal infection
  • Blood stream invasion or proliferation of
    organism at site
  • Exogenous toxin release
  • Activation of endogenous mediators

14
Molecular Mediators in Pathophysiology
  • Three phases
  • Induction
  • Cytokine synthesis secretion
  • Cascade

15
(No Transcript)
16
Molecular Mediators in Pathophysiology
  • Induction
  • Interaction of microbial molecules with host
  • Mediators activated that amplify transmit the
    microbial signal to other cells
  • Ex LPS binds to LPS binding protein which is
    detected by CD14 releasing TNF-alpha
  • Peptidoglycan lipoteichoic acid of gram ()
    induce similarly

17
Molecular Mediators in Pathophys
  • Cytokine cascade
  • Activation release of central mediators
  • TNF-alpha and IL-1
  • Release of secondary mediators
  • IL-6, IL-8, PAF, PGs, leukotrienes
  • Activation of neutrophils, complement system,
    vascular endothelial cells
  • Synthesis of acute phase reactants

18
Molecular Mediators in Pathophys
  • Parallel to SIRS is CARS
  • Compensatory Anti-inflammatory Response System
  • Attempts to down regulate the SIRS response
  • IL-4, IL-10, transforming growth factor beta,
    CSF, soluble receptors to TNF, antagonists to
    TNF-alpha and IL-1
  • If CARS reaction is severe it will manifest as
    anergy and infection susceptibility

19
Vasoactive Mediators in Pathophys
  • Nitric Oxide
  • Produced by endothelium
  • Increased levels during shock
  • Actions at high levels
  • Mediator of vasodilation hypotension
  • Direct cellular toxicity
  • Myocardial depression
  • Increased permeability

20
Clinical Features
21
Clinical Features
  • Constitutional
  • Hyper/hypothermia
  • Tachycardia
  • Tachypnea
  • Wide pulse pressure
  • Mental status change
  • Most likely obtunded

22
Clinical Features
  • Cadiovascular
  • Early, vasodilators predominate
  • Cardiac output is increased with tachycardia
  • COSV x HR
  • i.e. Initially patients will have warm
    extremities
  • If not treated aggressively decompensation ensues
  • Typically hypotension is not reversible with
    fluids alone

23
Clinical Features
  • Pulmonary
  • Sepsis is most common condition associated with
    ARDS
  • Lung edema from increased permeability
  • Alveolar edema? dyspnea, hypoxemia, opacities on
    CXR
  • B/L infiltrates, wedge pressure lt18
  • Endotoxin, TNF-alpha, IL-1, IL-6, IL-8,
    bactericidal/permeability-increasing (BPI) protein

24
Clinical Features
  • Pulmonary
  • ARDS
  • B/L pulmonary infiltrates
  • PCWP lt18 (non-cardiogenic pulm edema)
  • PaO2/FiO2 lt200
  • If PaO2/FiO2 gt200, but lt300 then ALI

25
Clinical Features
  • Renal
  • Acute renal failure w/ azotemia, oliguria, active
    urinary sediment
  • Hypotension/Dehydration, aminoglycosides,
    pigmenturia (e.g. myoglobinuria)
  • Immune complex deposition
  • IgG, IgM,C3, bacterial antigens antibodies
  • Tubulointersitial disease
  • S. pneumoniae, S. pyogenes, Legionella,
    salmonellosis, brucellosis, diptheria

26
Clinical Features
  • Gastrointestinal
  • Accelerated apoptosis of GI epithelial cells
  • Can lead to blood loss anemia
  • Cholestatic jaundice (most frequent abnormality)
  • Transaminase/Alkaline phosphatase 1-3x normal
  • Bilirubin concentrations, usually not gt10mg/dL
  • Hemolysis of RBCs, hepatocellular dysfunction
    due to endotoxin

27
Clinical Features
  • Hematologic
  • Minor blood loss secondary to erosions in mucosal
    layer of stomach/duodenum
  • Accelerated apoptosis of lymphocytes
  • Possibly due to elevated glucocorticoids
  • Most frequent changes are neutrophilia or
    neutropenia, thrombocytopenia, DIC

28
Clinical Features
  • Hematologic
  • Neutrophilia
  • Most common
  • Left shift
  • Demargination release of less mature
    granulocytes from BM
  • C3a causes release of neutrophil releasing
    substance
  • Sustained neutrophilia is secondary to CSFs

29
Clinical Features
  • Hematologic continued
  • Neutropenia
  • Increases mortality
  • Increased peripheral use of cells, damage to
    cells by bacterial byproducts, depression of
    marrow by inflammatory mediators
  • Morphological changes of WBCs in sepsis
  • Toxic granulations, Dohle bodies, vacuolization
  • Functional changes of WBCs
  • Increased phagocytic/cytotoxic activities

30
Clinical Features
  • Hematologic continued
  • RBC production survival are decreased
  • Usually does not cause anemia unless infection is
    prolonged
  • Low serum Fe concentrations
  • Decrease by 50
  • Influx into liver other reticuloendothelial
    cells

31
Clinical Features
  • Hematologic continued
  • Thrombocytopenia
  • Usual a consequence of DIC
  • May be early sign of bacteremia
  • Inhibition of thrombopoiesis, increased platelet
    turnover, increased endothelial adherence,
    increased destruction

32
Clinical Features
  • DIC
  • Clotting fibrinolytic systems activated
  • Consumption of coagulation factors platelets
  • Clotting system activated through the extrinisic
    clotting system by bacteria, viruses, fungi,
    endo/exotoxins
  • Gram(-) precipitate DIC more readily than gram
    ()
  • Fibrinolytic system is activated by tissue type
    plasminogen activator
  • As sepsis progresses, increase release of
    plasminogen activator inhibitor type 1

33
Clinical Features
  • DIC continued
  • Two forms
  • Compensated
  • slower generalized activation
  • Bleeding prevented by increasing coagulation
    factor production in liver, release of platelets
    from reserve, synthesis of inhibitors at
    accelerated rate
  • Decompensated
  • Clinical bleeding and/or thrombosis
  • Thrombocytopenia, prolonged PT/PTT, decreased
    fibrinogen antithrombin III, increased fibrin
    monomer/fibrin split products/D-dimer

34
Clinical Features
  • Endocrine
  • Hyperglycemia
  • Increased catecholamines, cortisol, glucagon,
    peripheral insulin resistance, impaired glucose
    use, decreased insulin secretion
  • Significant risk for adverse outcome
  • Must maintain tight control w/insulin infusion to
    keep b/w 80-100 mg/dl (NEJM Nov 8, 2001 vol 345,
    19)
  • Hypoglycemia
  • Assoc. w/S. pneumoniae, S. aureus, S. pyogenes,
    Listeria, Neisseria meningitidis, H. flu,
    Enterobacteriaceae

35
Clinical Features
  • Acid/Base
  • Early in sepsis ? resp alkalosis
  • Metabolic acidosis suggests inadequate perfusion,
    impaired hepatic clearance of lactate/pyruvate,
    increased glycolysis
  • Hypoxemia often present due to vent/perfusion
    mismatch

36
Clinical Features
  • Cutaneous
  • Direct bacterial involvement
  • Cellulitis, erysipelas, fasciitis
  • Lesions as a consequence of sepsis/hypotension/DIC
  • Acrocyanosis necrosis of peripheral tissue
  • Lesions secondary to intravascular infection
  • Microemboli /or immune complex vasculitis

37
Diagnosis
38
Diagnosis
  • Pt presents with
  • Hypotension not responsive to fluid bolus
  • Inadequate perfusion
  • Complaints attributable to a serious infection
  • Hot flushed skin
  • Mental obtundation or agitation
  • Widened pulse pressure
  • Hyperventilation
  • Dysthermia
  • beware of the old, young, immunocompromised

39
Diagnosis
  • Differential Diagnosis
  • Other causes of shock
  • Cardiogenic
  • Neurogenic
  • Hypovolemic
  • Anaphylactic
  • Obstructive (PE, tamponade)
  • Endocrine (adrenal insufficiency, thyroid storm)

40
Diagnosis
  • H P
  • Basic lab and x-rays are usually successful in
    identification of source
  • CNS
  • Meningitis (nuchal rigidity, MS change,
    petechiae)
  • Brain abscess, sub/epi dural empyemas
  • Viral CNS infections

41
Diagnosis
  • Pulmonary
  • Acute bacterial pneumonia
  • Intra-abdominal processes
  • Most common source of infection leading to sepsis
  • Acute pancreatits
  • Cholangitis
  • Septic abortion/endometritis/myometritis
  • Pyelonephritis
  • Occult Abscess
  • Skin
  • Cellulitis (S.aureus, S.pyogenes)
  • Decubitus ulcer(s)

42
Diagnosis
  • No obvious source
  • Endocarditis
  • Primary bacteremia
  • S.aureus, S.pneumoniae, N.meningitidis
  • Asplenia
  • Salmonella, H flu, S pneumo, N. meningitidis
  • IVD users, Pseudomonas gram(-) bacteria
  • Skin abscess from popping

43
Diagnosis
  • Ancillary Studies
  • CBC
  • DIC panel (PT,PTT,fibrinogen,D-dimer, ATIII)
  • CMP (include Mag, Ca, Phosphate)
  • Lactate level
  • ABG
  • UA
  • CXR
  • Cultures (blood, urine)
  • If HP suggest
  • LP, CT (abd . . .)
  • Consider
  • CRP, pro-calcitonin, IL-6 level

44
Standard Treatment
45
Standard Treatment
  • ABCs!
  • Maintain O2 sats above 90
  • Hemodynamic Stabilization
  • Rapid fluid administration
  • Rate of 0.5L of NS every 5-10min
  • May require 2-6L in initial stabilization phase
  • Be careful with heart failure patients
  • Monitor response with BP, HR, RR, mental status,
    urine output (1cc/kg/hr), CVP, skin perfusion

46
Standard Treatment
  • ? Inotropic support
  • If no response to fluids or signs of fluid
    overload present
  • Goal is to keep MAP above 65 mm Hg
  • Dopamine 5-20 micrograms/kg/min
  • Beta-1, dopaminergic and alpha adrenergic
    activity
  • Norepinephrine
  • Beta-1 and alpha adrenergic stimulation
  • Short term vasopressin infusion (0.04 units/min
    for 4-16h)
  • Vasodilatory septic shock

47
Standard Treatment
  • End points
  • Early goal directed therapy provides significant
    benefit improves outcome
  • Rivers et al. NEJM vol. 3451368, 2001
  • Maintain CVP b/w 8-12
  • Hct 30
  • SVO2 gt70
  • Reduction in mortality from 44 in control group
    to 29 in intervention group

48
Standard Treatment
  • Empiric Antimicrobial Therapy
  • Start ASAP
  • Try to get culture samples before
  • Select based on adequate coverage of potential
    pathogens
  • Should cover gram /-
  • Give maximum dose allowed
  • Give IV

49
Empiric Antibiotics in Sepsis
  • Table 32-3

50
Standard Treatment
  • Removal of Source of Infection
  • Indwelling catheters ? send tip for culture
  • Replace Foley catheters
  • Intra-abdominal or soft tissue sites of pus
    require urgent drainage

51
Standard Treatment
  • Initial Baseline Assessment Continued
    Monitoring (again goal directed)
  • Some use serum lactate to monitor response
  • ABGs to monitor ventilation perfusion
  • 2 large bore IVs
  • Consider central line early
  • If requiring vasoactive drugs consider pulm
    artery thermal-dilution catheter
  • Other monitoring gadgets
  • Sublingual capnography, gastric pH tonometry,
    muscle oximetry, bioimpedance determination of CO

52
New Innovative Therapies
53
Innovative Therapy
  • Based in premise that neutralizing bacterial
    toxins, cytokines, other mediators could stop
    or slow the syndrome

54
Innovative Therapies
  • Corticosteroids
  • Meta-analysis has shown physiologic doses of
    hydrocortisone improves outcomes
  • (200-300mg/d) for 5-7 days
  • Then tapered for 5-7 days
  • Early studies (proir to 1989) used high doses and
    had increased mortality
  • Those published after 1997 (5)used lower doses
    and reported improved survival similar to that of
    Activated Protein C
  • Annal of Internal Med 200414147-56

55
Innovative Therapy
  • Activated Protein C (Xigris)
  • Inactivates Factors Va and VIIIa
  • Inhibits thrombin (decreases inflammation)
  • Inhibits platelet activation, neutrophil
    recruitment, and mast cell degranulation
  • Blocks cytokine production
  • Inhibits cell adhesion
  • Anti-apoptotic actions
  • Apoptosis (i.e. GI epithelial cell) induces anergy

56
Innovative Therapy
  • Summary
  • To date the only treatments shown to produce
    benefit
  • Early goal directed hemodynamic stabilization
  • Tight control of blood glucose with insulin
  • Activated protein C
  • Efficacy and Safety of Recombinant Human
    Activated Protein C for Severe Sepsis NEJM 2001,
    vol. 344 699-709

57
Cardiogenic Shock
58
Cardiogenic Shock
  • A state of decreased cardiac output(CO) producing
    inadequate tissue perfusion despite adequate or
    excessive circulating volume

59
Cardiogenic shock
  • Etiology
  • AMI
  • Pump failure (40 of LV involved)
  • Mechanical complications (MR,VSD,free wall
    rupture)
  • RV infarction
  • Depression of contractility
  • Sepsis, myocarditis, contusion
  • Mechanical obstruction
  • AS, hypertrophic CM, MS, LA myxoma
  • Regurgitation of LV output
  • AI, chordal rupture

60
Pathophysiology
  • AMI cell death loss of
    contractile function
  • Decreased CO/SV tachycardia/hypotension
    decreased coronary perfusion/diastolic
    filling time
  • Further ischemia SNS/Renin-Angiotension
    System activation
  • Increased SVR and myocardial O2 consumption


61
Cardiogenic Shock
  • Clinical Features
  • PE
  • Hypoperfusion
  • Skin mottling, obtunded
  • /-hypotension (SBPlt90)
  • May be compensated (pulse pressure lt20, ST) or
    pre-existing hypertension
  • Tachypnea, rales (clear if RV), JVD
  • Murmur
  • MR (chordae tendinea rupture) holosystolic at
    apex going to axilla
  • VSD holosystolic at L parasternal

62
Cardiogenic Shock
  • Ancillary Studies
  • ECG ischemia/infarction,electrolyte
    abnormality,drug toxicity
  • CXR helps r/o other causes (pneumonia, aortic
    dissection, pericardial effusion)
  • Labs BNP, cardiac enzymes, ABG, lactate,
    electrolytes, serum drug levels
  • Echo ventricular/valve dysfunction
  • HD monitoring (table 33-3) invasive vs
    bioimpedance

63
Cardiogenic Shock
  • Differential Diagnosis
  • AMI
  • PE
  • COPD
  • Pneumonia
  • Aortic dissection
  • Tamponade
  • Acute valvular insufficiency
  • Hemorrhage
  • Sepsis
  • Drug OD of negative inotropic/chronotropic agent

64
Cardiogenic Shock
  • Treatment
  • ABCs first
  • IV access/cardiac monitor/art line/foley
  • Correct hypoxia/hypovolemia/rhythm
    disturbance/electrolyte abnormalities/acid-base
    alterations
  • Hypotension
  • Dopamine,dobutamine
  • Fluid bolus if RV involved
  • Acute MR consider dobutamine and nitroprusside
  • IABP

65
Cardiogenic Shock
  • Treatment continued
  • Thrombolytic therapy
  • Better outcomes if followed by revascularization
  • Intraaortic balloon conterpulsion
  • Decreases afterload, increases diastolic BP
  • Early revascularization
  • Most important life saving intervention

66
Cardiogenic Shock
  • Treatment continued
  • Inotropic agents
  • Dopamine
  • First line agent
  • 2.5-5 micrograms/kg/min beta-1
  • 5-10 alpha beta-1
  • 10-20 alpha
  • Dobutamine
  • Use for signs of poor perfusion when SBPgt90
  • 2-20micrograms/kg/min
  • Norepinephrine
  • Use only when inadequate response to other
    pressors
  • 2 micrograms/min and titrate to response
  • Milrinone
  • 50 microgram/kg bolus followed by
    0.5microgram/kg/min infusionwatch BP!

67
Anaphylactic Shock
68
Anaphylactic Shock
  • Severe systemic hypersensitivity with multisystem
    involvement
  • Life-threatening release of mediators by mast
    cells and basophils

69
Anaphylactic Shock
  • Pathophysiology
  • 4 classic mechanisms
  • 1. cross-linking of 2 IgE molecules on a mast
    cell or basophil by a multivalent antigen
  • 2. reaction of IgM IgG to cell surface
    antigens
  • 3. soluble antigen-antibody complexes activating
    complement
  • 4. activation of T lymphocytes

70
Anaphylactic Shock
  • Pathophysiology
  • Classic anaphylaxis
  • 2 separate exposures
  • First the antigen or hapten-protein complex is
    processed by macrophage dendritic cells
  • Presented externally with MHC-2
  • T helper cells recognize and stimulate plasma
    cells to produce IgE
  • Second exposure recognized by these IgE
    antibodies triggers degranulation of mast cells
    and basophils

71
Anaphylactic Shock
  • Pathophysiology
  • Complement mediated reaction
  • Occur after administration of blood products
    secondary to immune complexes
  • C3a C5a cause degranulation
  • Non-immunologic anaphylaxis (anaphylactoid)
  • Exogenous substances directly degranulate mast
    cells
  • Radiocontrast dye, opiates, depolarinzing drugs,
    dextrans

72
Anaphylactic Shock
  • Pathophysiology
  • ASA/NSAIDS
  • Non-mast cell process
  • Modulate cyclooxygenase-arachidonic acid
    metabolism
  • Idiopathic anaphylaxis
  • Diagnosis of exclusion

73
Anaphylactic Shock
  • Clinical Features
  • Diffuse urticaria angioedema
  • /- abd pain or cramping, N/V, diarrhea,
    bronchospasm, rhinorrhea, conjunctivitis,
    dysrhythmias, hypotension
  • c/o lump in the throat heralds life-threatening
    laryngeal edema
  • Usually begin w/in 60 minutes of exposure
  • Faster the onset the more severe the reaction
  • Biphasic phenomenon
  • Second release of mediators clinically evident
    3-4h after the initial manifestations clear

74
Anaphylactic Shock
  • Diagnosis
  • History and physical
  • 2 or more body systems involved
  • Differential
  • Vasovagal reaction, status asthmaticus, seizure,
    epiglottitis, hereditary angioedema, FB airway
    obstruction, carcinoid, mastocytosis, non-IgE
    drug reactions, AMI, dysrhythmias

75
Anaphylactic Shock
  • Treatment
  • First Line
  • ABCs
  • Epinephrine, oxygen, fluids (NS 1-2L)
  • Epi 0.1mg in 10cc NS over 5-10minutes IV if signs
    of CV collapse
  • If refractive start infusion 1mg in 500ccD5W at
    1-4 micrograms/min
  • Less severe, give 0.3-0.5 mg IM in the thigh
  • decontamination

76
Anaphylactic Shock
  • Treatment
  • Second Line
  • Corticosteroids
  • Methylprednisolone 125mg IV
  • 2mg/kg in children
  • Antihistamines
  • Diphenhydramine (H1) 25-50mg IV
  • Ranitidine or cimetidine(H2)
  • Avoid cimetidine in elderly, renal/hepatic
    failure, or if patient is on beta blocker

77
Anaphylactic Shock
  • Treatment
  • Second Line
  • Agents for bronchospasm
  • Albuterol
  • Ipratropium bromide
  • Magnesium 2g IV over 20-30minutes
  • 25-50mg/kg in children
  • Glucagon
  • 1 mg IV q 5min until response followed by
    infusion 5-15 micrograms/min if patient on beta
    blockers with refractive hypotension

78
Anaphylactic Shock
  • Disposition
  • Unstable patients admit to ICU
  • If patient received epi-observe for 4h
  • Consider distance from care, someone to go home
    with, comorbidities, age
  • Good discharge instructions is a must
  • Send with epipen, short course of antihistamines
    and steroids

79
Neurogenic Shock
80
Neurogenic Shock
  • Acute spinal cord injury
  • Disruption of sympathetic outflow
  • Hypotension bradycardia
  • Majority caused by blunt trauma
  • MVA, falls, sports
  • Cervical region most commonly injured
  • Penetrating injury (10-15 of cases)
  • GSWs and stab wounds

81
Neurogenic Shock
  • Pathophysiology
  • 33 bony vertebrae
  • Anterior body, posterior arch, sup/inf articular
    processes, pedicles, laminae
  • Spinal cord is cylindrical arising from base of
    brain covered by 3 layers of meninges CSF
  • 31 pairs of spinal nerves exit the canal via
    intervertebral foramen
  • Spinal nerves are formed by ant/post nerve roots

82
Neurogenic Shock
  • Pathophysiology
  • Spinal cord contains white gray matter
  • White nerve fibers running up down in cord
    tracts
  • Gray nerve cells
  • Autonomic Nervous System
  • Sympathetic
  • Outflow tracts in lateral gray horns of 1st
    thoracic to 2nd lumbar
  • Controlled by hypothalamus
  • Lateral horn?anterior nerve root?ganglia of
    paraspinal sympathetic trunk?travel throughout
    the body

83
Neurogenic Shock
  • Pathophysiology
  • Autonomic Nervous System
  • Parasympathetic
  • Cranial Nerves 2-4th sacral segments
    (splanchnic nerves)

84
Neurogenic Shock
  • Clinical features
  • Hypotensive with warm,dry skin
  • Bradycardic ususally
  • Hypothermic
  • These symptoms last 1-3 weeks

85
Neurogenic Shock
  • Treatment
  • ABCDEs
  • Investigate all other possible sources of
    hypotension bradycardia
  • Infuse crystalloids rapidly
  • Attempt to keep MAP 85-90mm Hg for the first 7
    days to minimize secondary cord injury
  • Dopamine dobutamine may be helpful
  • Severe bradycardia can be treated with atropine
    or pacing
  • Steroids are not indicated in the treatment of
    neurogenic shock per se
  • Indicated in blunt injury with neuro deficits if
    started within 8h (30mg/kg bolus then 45 mins
    later infuse at 5.4mg/kg/h for 23h)

86
Questions
  • 1. In cardiogenic shock the PCWP is
  • A. Decreased
  • B. Increased
  • C. Normal

87
Questions
  • 2. SIRS is defined as inflammation secondary to
    infection
  • A. True
  • B. False

88
  • 3. Which is not a parameter used to define ARDS
  • A. Bilateral infiltrates on CXR
  • B. PCWPgt18
  • C. PaO2/FIO2 lt200

89
  • 4. What is considered the first line inotrope in
    cardiogenic shock
  • A. Dopamine
  • B. Dobutamine
  • C. Milrinone

90
  • Which is not considered a first line agent in
    treatment of anaphylaxis
  • A. Epi
  • B. Oxygen
  • C. albuterol

91
Answers
  • 1. B
  • 2. B
  • 3. B
  • 4. A
  • 5. C
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