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SHOCK. Core Rounds August 7, 2003 Dr. Rob Hall PGY4 Dr. Gil Curry MD, FRCPC. JOHN-WEST. Shock Talk: outline. A few cases Approach to and ddx of shock Detailed review of major causes Focus on septic, hypovolemic, cardiogenic shock for literature review

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shock

SHOCK

Core Rounds August 7, 2003

Dr. Rob Hall PGY4

Dr. Gil Curry MD, FRCPC

shock talk outline
Shock Talk:outline
  • A few cases
  • Approach to and ddx of shock
  • Detailed review of major causes
  • Focus on septic, hypovolemic, cardiogenic shock for literature review
  • Controversies in management of sepsis, hypovolemic shock, cardiogenic shock
definitions of shock
Definitions of Shock
  • Clinical manifestations of the inability of the circulatory system to adequately supply tissues with nutrients and remove toxic waste
  • Inadequate blood flow secondary to decreased cardiac output or mal-distributed output that results in irreversible tissue damage
rosen s empiric cirteria for the diagnosis of shock 4 out of 6 criteria
Ill appearance or decreased LOC

HR > 100

RR > 22 or PC02 < 32

Base deficit < -5 or lactate > 4

Urine output < 0.5 ml/kg/hr

Hypotension > 20 minute duration

NOTES

Can be in shock without being hypotensive

Base deficit = amount of base required to neutralize the pH (normal is > -2)

Rosen’s Empiric Cirteria for the Diagnosis of Shock: 4 out of 6 criteria
classification of shock find your own way to classify shock and remember the ddx
Pre - heart

hypovolemia, venous pooling

Heart

contractility, arrythmias, mech obstruction

Post - heart

loss of vascular tone, inability to deliver to tissues, inability of tissues to utilize

Quantitative

hypovolemic, hemorrhagic, obstructive, myocardial dysfunction

Qualitative

sepsis, anaphylaxis, neurogenic, dyshemoglobinemia, cellular poisons

Classification of Shock: find your own way to classify shock and remember the ddx
etiological classification man this guy looks sshhoccke
Etiological Classification: man this guy looks SSHHOCCKE…
  • S - septic
  • S - spinal (neurogenic)
  • H - hypovolemic
  • H - hemorrhagic
  • O - obstructive (PE, pthrx, hthrx, ct)
  • C - cardiogenic (rate, contractility, obstruction, valve)
  • C - cellular toxins (CN, CO, HS, ASA, Fe)
  • K - anaphylaCTic
  • E - endocrine/adrenal crisis
pathophysiology
Pathophysiology
  • Common final pathway = cellular injury
  • FIVE unifying features of shock
    • intracellular calcium overload
    • intracellular hydrogen ion
    • cellular and interstitial edema
    • catabolic metabolism
    • inflammation
slide10
Undifferentiated Shock: Thorough history, complete physical, shot gun investigations………ya, but what are some tips?
  • History
    • Paramedics, caregivers, witnesses, family, and old chart are keys to give you historical clues
    • Get someone on the phone EARLY (ie: in resusc bay) who can tell you what was going on
  • Physical
    • Don’t forget the chemstrip, rectal, AAA exam
  • Investigations
    • STAT echo can be very useful
    • Emerg ultrasound will soon be available
shock trivia
Shock Trivia
  • Patient in shock but is bradycardic: why?
    • Elderly, medications, neurogenic shock, intraabdominal pathology (vagal tone)
  • Shock index
    • HR/SBP > 0.9 suggest shock
  • Lactate clearance index
    • Patient is under – resuscitated if lactate has not decreased by 50% since last measurement
  • Gastric/Rectal Tonography
    • Balloon probe measure mucosal pH as an indicator of gut perfusion
slide13
Definitions:Consensus conference on definitions for sepsis: Critical Care Medicine 2000. Volume 28 (1): 232 - 235
  • SIRS (Systemic Inflammatory Response Syndrome)
    • temp > 38 or < 36
    • HR > 90
    • RR > 20 or PaC02 < 32
    • wbc > 12, < 4, or > 10% bands
  • Sepsis = SIRS + documented infection
  • Severe Sepsis = Sepsis + MODS (Mulitorgan dysfuntion)
  • Septic Shock = Sepsis + Hypotension refractory to volume resuscitation (requiring vasopressors)
management of septic shock
Management of Septic Shock
  • Intubate/ventilate
    • Control airway
    • Decrease work of breathing
  • Fluids
    • Boluses of NS or RL
    • Adults: bolus 1-2 L and repeat
    • Peds: bolus 20 ml/kg and repeat
    • Pressors after 2-3 boluses but keep fluids running
    • Require a lot of fluid
      • Absolute hypovolemia: increase incensibles, poor intake
      • Relative hypovolemia: vasodilation and decreased SVR
vasopressors most common choices
Dopamine:

1-5 ug/kg/min ~ dopaminergic

5-10 ug/kg/min ~ beta activity

>10 ug/kg/min ~ alpha activity

Preferred agent for many

Effects well established

Physicians comfortable with use

Levophed:

0.01 – 3 ug/kg/min

Potent alpha agonist

Some beta propertiesConcern with levophed worsening end organ hypoperfusion

Older studies: levophed used as last resort and thus poor outcomes

Hesselvik JF, et al., Crit Care Med 1989

Vasopressors:Most common choices
norepinephrine
Norepinephrine
  • Norepinephrine improves renal blood flow and tissue oxygenation in patients with septic shock:
    • Desjars et al., Crit Care Med 1989
    • Rendl-Wenzel et al., Intensive Care Med 1993.
    • Meadows et al., Crit Care Med 1988
    • Martin C., et al., Crit Care Medicine 2000
dopamine versus norepinephrine
Dopamine versus norepinephrine
  • Martin et al., Chest 1993 and Marik et al., JAMA 1994
    • Many small studies (n=20) like these two that showed a benenfit in physiological markers with norepinephrine
  • Levophed has favourable effect on hemodynamics and end organ perfusion as compared to dopamine
  • A mortality benefit for levophed over dopamine has never been shown
pressor summary
Pressor summary
  • Make sure the pump is full first
  • Dopamine/Levophed first line agents
  • Levophed may be the superior agent in septic shock
  • Titrate up doses fast (q 5-10 min to effect)
  • Add second agent if needed
  • Invasive monitoring required
sepsis and antibiotics
Sepsis and Antibiotics
  • Bochud et al., Intensive Care Medicine 2001: reviewed 4 retrospective studies of septic patients and abx choice
    • N=1190
    • Appropriate Abx mort rate~28%
    • Inappropriate Abx mot rate~49%
    • P<0.001
  • Early ED antibiotics have also shown to decrease mortality in many disease subgroups (pneumonia, meningitis, urosepsis)
slide20

EARLY and APPROPRIATE initiation of antibiotic coverage are CRUCIAL emergency department interventions in the patient with septic shock

empirical antibiotic choices
Empirical antibiotic choices
  • Target suspected source of infection
  • Refer to SANDFORD’s recommendations
  • Use maximum doses of antibiotics
  • Broad spectrum = grm +ves, grm –ves, anaerobes
  • Amp + Gent + Flagyl
  • Piperacillin/Tazobactam being used more often
  • Imipenum as monotherapy (big gun)
  • Neutropenic: cover pseudomonas (ceftazidime, cipro, tobramycin)
newer approaches to septic shock
Newer approaches to septic shock:
  • Vasoactive mediators
    • vasopressin, nitric oxide
  • Coagulation Cascade
    • protein C, protein S, antithrombin III
  • Inflammatory mediators
    • anti TNF antibodies, anti LPS, TFPI, interleukins, IVIG
question how to get an intensivist talking at a wine and cheese party

Question: how to get an intensivist talking at a wine and cheese party?

Answer: just say……

There is NO evidence for steroid use in septic shock

Recombinant activated Protein C is killing patients

steroids in septic shock
Steroids in septic shock

Rationale:

  • Anti-inflammatory
  • Relative adrenal insufficiency in many of cases of refractory shock
  • Upregulates catecholamine receptors
  • Hopefully immunosuppression and bleed risk did not counter benefits
steroids and sepsis
Early mega-dose steroid trials

“supraphysiologic” doses

Solumedrol 30/mg/kg x 3-4 doses

Trend towards increased mortality

Increase incidence of GI bleeding

Increased incidence of secondary infections

1990’s trial’s with lower dose steroids

“physiologic doses”

aimed to replace steroids for a “Relative adrenal insufficiency”

Researchers hoped get catecholamine sensitivity and anti-inflammatory effects still

Steroids and Sepsis
steroids and sepsis bollaert et al critical care medicine 1998
Steroids and Sepsis:Bollaert et al.,Critical Care Medicine 1998
  • Double-blind, placebo controlled, small study
  • Solu-cortef 100mg IV q 8hrs x 5days vs. placebo
  • Outcome Steroid group Placebo
    • Shock reversal @7d: 68% 21% p=.007
    • Mortality 32% 63% p=.09
  • No increase adverse outcomes
  • Showed more shock reversal at 7 days with low dose steroids
steroids and sepsis briegel et al crit care med 1999
Steroids and Sepsis: Briegel et al., Crit Care Med 1999.
  • Another small RCT (n=40)
  • Randomized to solu-cortef 100mg IV then low dose infusion vs placebo
  • Outcome Steroid group Placebo
    • Time to shock reversal 2 days 7 days (p=.005)
  • No increase adverse outcomes, no diff in mortality
  • Showed earlier shock reversal with low dose steroids
steroids and sepsis annane jama 2002
Steroids and Sepsis:Annane. JAMA 2002.
  • Largest prospective trial of low dose steroids
  • RCT, blinded, N = 300
  • Randomized to low dose hydrocortisone (50 mg iv q6hr) + fluticasone vs placebo
  • Did ACTH stim test on everyone
  • Mortality decreased 10% in “non-responders”
    • 63% -> 53% (p = 0.02)
  • Criticisms of their definitions of non-responders and how they did the stim test exist
steroids and sepsis review article in chest may 2003
Steroids and Sepsis:Review article in Chest May 2003
  • High dose steroids clearly shown to increase mortality
  • There is some evidence for benefit from low dose steroids in sepsis
  • Current debate over low dose steroids unresolved and needs further study
steroids and sepsis take home message
Steroids and Sepsis:Take home message
  • There is no current indication for the ED initiation of low dose steroids in sepsis unless adrenal crisis is suspected
  • You should be aware that ICU will likely do an ACTH stim test and may give steroids
activated protein c and sepsis
Antithrombotic

Profibrinolytic

Anti-inflammatory

Activated Protein C and Sepsis
activated protein c and sepsis drotrecogion zigris
Activated Protein C and Sepsis:drotrecogion (Zigris)
  • PROWESS TRIAL (Bernard. NEJM 2001)
  • Multicentered RCT, N = 1690
  • Mortality 30.8% in placebo, 24.7% in treatment group (p= 0.005)
  • ARR 6.1% for NNT 16
  • RRR of 19%
  • Serious bleeding 3.5% vs 2.0% (p=0.06)
  • Enrollement criteria changed ½ way through!
activated protein c and sepsis33
Activated Protein C and Sepsis
  • The FDA is confused
    • Study stopped early because of “remarkable effect”, FDA approved the drug
    • Further discussion and controversy: FDA limited its use to only sicker patients (based on APACHE score) and asked for further study
  • Critical Care Medicine. 31(1). S85-96
    • Recent review on rhAPC
    • Highlights problems with PROWESS study and FDA approval --------- calls for further study
activated protein c and sepsis34
Activated Protein C and Sepsis
  • Take home messages:
    • rhAPC is expensive (10,000 per course)
    • rhAPC has been shown to decrease mortality although the effect is modest (ARR 6%)
    • There is NO role for ED initiation of rhAPC
    • May be used in ICU
slide35
15 yo male

Attempted hanging

Cut down from tree

HR 75, BP 85/30

Why is he in shock?

Case
neurogenic shock definitions
Neurogenic Shock:Definitions
  • Spinal Shock
    • initial loss of spinal cord function following SCI including motor, sensory, and sympathetic function
  • Neurogenic Shock
    • loss of sympathetic autonomic function due to spinal cord injury
neurogenic shock pathophysiology
Neurogenic Shock: Pathophysiology
  • Hypotension
    • Due to loss of sympathetic tone thus vasodilation and decreased SVR
    • Usually only occurs with lesions at or above T6 because lower lesions leave enough of the body with intact sympathetics that the BP doesn’t drop
  • Bradycardia (absolute or relative)
    • Due to unopposed parasympathetic (VAGAL) tone to the heart
    • Usually only occurs with lesions at or above T4 because sympathetic innervation to heart is at T4
neurogenic shock management
Neurogenic Shock:Management
  • Fluids
  • Atropine 0.5 mg – 1.0 mg iv
    • NOTE: may see bradycardia or bradyasystolic arrest due to stimulation from laryngoscopy so have atropine ready if intubating
  • Vasopressors
    • Epinephrine 1:10,000 (1ml prn to effect)
    • Phenylephrine: 10 mg in 100ml NS (1ml is 100 ug)
    • Ephedrine
hemorrhagic shock definition
Hemorrhagic Shock:Definition
  • Hemorrhage vs Hemorrhagic shock?
  • Rosen’s definition of hemorrhagic shock = Requires 4 out of 6 empiric criteria for shock
      • Ill or decreased LOC
      • U/o < 0.5 ml/kg/hr
      • HR > 100
      • RR > 22 or PC02 < 32
      • BD < -5 or lactate > 4
      • Hypotension > 20 minutes
hemorrhagic shock management
Hemorrhagic Shock: Management
  • V: vascular access, crystalloid bolus X 2, blood transfusion prn, identify and treat cause
  • Controversies
      • Which fluid?
      • When to fluid resuscitate?
      • How fast should fluid be given?
      • Optimal endpoints of resuscitation?
      • Blunt versus penetrating trauma
hemorrhagic shock43

Hemorrhagic Shock

Which fluid to give?

colloids
Colloids
  • Albumin, protoplasm protein fraction, hydroxyethylstarch, pentastarch, gelatin, dextran
  • Advantages
    • less fluid required, more volume in vascular space, potential to draw fluid in from tissues
  • Disadvantages
    • expensive, allergic reactions, coagulopathies
colloids45
Colloids
  • Cochrane Database of Systematic Reviews. BMJ 1998: 317:235-40.
    • Objective: effect of albumin on mortality
    • Study: 30 RCTs total 1419 patients
    • Results: RR of death 1.46 hypovolemia, 2.40 burns, 1.69 hypoalbuminemia
    • Pooled RR of death 1.68 (1.26,2.23)
    • Conclusion: albumin increases mortality
colloids46
Colloids
  • Cochrane Database 2003. Colloids versus crystalloids for fluid resuscitation.
    • Albumin: 18RCTs RR1.52 (1.08,2.13)
    • HES: 7 RCTs RR 1.16 (0.68,1.96)
    • Gelatin: 4 RCTs RR 0.50(.08,3.03)
    • Dextran: 8 RCTs RR 1.24 (.94,1.65)
    • Conclusion: No evidence that colloids reduce risk of death in trauma, burns, or surgery
colloids summary
Colloids:Summary
  • There is NO evidence that colloids decrease mortality in the resuscitation of critically ill patients.
hypertonic saline
Hypertonic Saline
  • Advantages
    • less volume, stays in vascular space, draws fluid
  • Disadvantages
    • hypernatremia, hyperosmolarity, seizures, coagulopathy, anaphylactoid rxns with dextran
  • Details
    • Hypertonic saline (7.5% NaCl) +/- 6% dextran
    • Most often given as a 250 cc bolus (~ 4ml/kg) over 5-10 min
hypertonic saline49
Hypertonic Saline
  • Animal evidence
    • improved hemodynamics and mortality
  • Human evidence: Wade et al 1997:
    • HS and HSD in trauma patients
    • Metanalysis of 8 RCTS of HSD and 6 HS
    • HS (7.5% saline): no difference in mortality
    • HSD (+6%dextran): decreased mortality in 7/8 trials overall 3.5%; trend only ---> Not stat sign
hypertonic saline50
Hypertonic Saline
  • Cochrane Database 2003. Alderson P. Colloids vs crystalloids for fluid resuscitation.
    • Part of this systemic review looked at Hypertonic Saline + Dextran and effect on mortality
    • Study: metanalysis of 8 RCTs
    • Results: pooled RR of 0.88 (0.74, 1.05)
    • Conclusion: there is a trend toward reduction in mortality with HSD although not statistically significant
hypertonic saline51
Hypertonic Saline
  • Cochrane Database: 2003. Bunn F. Hypertonic vs Isotonic Crystalloid
    • 17 RCTs with total N = 869 (small trials!)
    • 12/17 reported on mortality rates
    • Trauma: RR death 0.84 (.61 – 1.16)
    • Trend that favors hypertonic saline
hypertonic saline conclusions
Hypertonic Saline:Conclusions
  • There is evidence of TRENDS toward lower mortality in resuscitation with hypertonic saline but statistical significance has not been demonstrated in large studies
  • More RCTs are needed………..
hemorrhagic shock53

Hemorrhagic Shock

When to give fluids?

How much?

How fast?

controlled fluid resuscitation rationale
Controlled Fluid Resuscitation:Rationale
  • Also called hypotensive resuscitation or permissive hypotension
  • Elevation of BP before hemorrhage control may be harmful
  • Reasons
    • Hydraulic pressure
    • Dislodgement of soft clots
    • Dilution of clotting factors
controlled fluid resuscitation evidence
Controlled Fluid Resuscitation:Evidence
  • Early anmimal studies of fluid replacement were in CONTROLLED hemorrhage models showed benefit for fluids
  • Recent animal studies of fluid replacement in UNCONTROLLED hemorrhage models show increased mortality with early and aggressive fluids (especially if BP is elevated)
controlled fluid resuscitation evidence56
Controlled Fluid Resuscitation:Evidence
  • Review articles:
    • Emerg Med Clinics: 123(4). Nov 2002
    • Journal of Trauma supplement Vol 54(5S). May 2003.
slide58
Bickell et al 1990The Detrimental Effects of Intravenous Crystalloid after Aortotomy in Swine. Surgery 110: 529-36.
  • Objective: does rapid volume replacement inc mortality?
  • Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg )
  • Results Mortality
  • Controls 0/8
  • RL tx grp 8/8
  • Then repeated the study with hypertonic saline + dextran
  • Bickell et al 1992. HSD vs RL after Aortotomy
  • HSD tx grp 5/8
slide59
Bickell et al. NEJM 1994.Immediate versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Trauma
  • Study: 598 patients SBP<90, odd/even day randomization, immediate fluids vs none until OR
  • Immediate fluids - mortality 110/303 (38%)
  • Delayed fluids - mortality 86/289 (30%)
  • Statistically significant p = 0.04
  • Concln: delayed fluid resuscitation reduces mortality in hypotensive patients with penetration
  • Comments: even/odd day randomization, significant cross over between groups, note short transport times
controlled fluid resuscitation what about blunt trauma
Controlled Fluid Resuscitation:What about blunt trauma?
  • Turner. Health Technol Assess 2000. Prehospital fluid replacement in serious truama.
    • RCT, immediate resuscitation vs no prehospital fluids in blunt trauma
    • N = 1309
    • No diff in mortality, complications
    • Hard to draw conclusions -> MAJOR protocol violations
controlled fluid resuscitation what about blunt trauma61
Controlled Fluid Resuscitation:What about blunt trauma?
  • Sampalis. J Trauma 1997
    • Retrospective evidence of increased mortality with IV therapy (? Due to longer scene time)
  • Dutton. Resuscitation 1996
    • Retrospective evidence of increased mortality of rapid iv infusion compared to historical controls
controlled fluid resuscitation what about blunt trauma62
Controlled Fluid Resuscitation:What about blunt trauma?
  • Dutton RP. J. Trauma 2002. Hypotensive Resuscitation During Active Hemorrhage: Impact on in Hospital Mortality
    • RCT, N=40, target SBP >70 or > 100
    • ½ penetrating and ½ blunt trauma
    • No difference in survival
    • Small study, heterogenous patients, low mortality
controlled fluid resuscitation
Controlled Fluid Resuscitation
  • Cochrane Database 2001. Kwan I. Timing and volume of fluid administration for patients with bleeding following trauma.
    • 3 RCTs for early vs delayed fluids
    • 3 RCTs for large vs small volume
    • NO evidence for early or large volume fluid replacement and trends toward increased mortality
    • But only 6 studies thus not a valid systemic review
controlled fluid resuscitation take home messages
Controlled Fluid Resuscitation: Take home messages
  • Early, aggressive fluid resuscitation increases mortality in penetrating trauma.
  • Controlled fluid resuscitation probably better (target SBP 70 – 90)
  • Delayed fluid resuscitation (until hemmorrhage controlled) may be better
  • Further study needed especially in blunt trauma
  • Unknown if this applies to long transport times
  • Pour it in for arrested or near-arrested patients
where will trauma resuscitation be in 2010

Where will trauma resuscitation be in 2010?

My prediction: small volume of hypertonic saline + dextran for target SBP 90 and to OR ASAP!

cardiogenic shock67
Cardiogenic shock
  • Definition
    • decreased cardiac output and evidence of tissue hypoxia in presence of adequate intravascular volume
  • Criteria
    • hypotension (SBP < 90) x 30 min, or 30mmHG below baseline, cardiac index < 2.2 L/min/m2, PCWP > 15 mmHg
    • Rosen’s: 4 out of 6 criteria for empiric shock
  • Pathologically
    • Will have lost 40% of myocardium
cardiogenic shock approach
Cardiogenic Shock:Approach
  • Stabilize the ABCs
  • Identify etiology of cardiogenic shock
  • Small fluid bolus (250cc)
  • Don’t be shy on fluids if RV infarct
  • Ionotropic/vasopressor support
  • Manage infarct
cardiogenic shock pressor choices
Cardiogenic shock: Pressor choices
  • Dobutamine: beta adrenergic
    • positive B1 ionotrope; may drop BP b/c of vasodilation
    • SBP 70 - 100 without signs of hypoperfusion a/f fluids
  • Dopamine: dopaminergic, beta , alpha adrenergic
    • SBP 70 - 100 with signs of hypoperfusion after fluids
  • Norepinephrine: alpha agonist
    • SBP < 70 after fluids
  • Others
    • Amrinone, milrinone
mi cardiogenic shock how to manage the mi
MI + Cardiogenic shock:How to manage the MI?
  • Options
    • Thrombolysis
    • Get BP up with ionotropes then thrombolyse
    • Stabilize with IABP then thrombolyse
    • PTCA
    • Emergency CABG
  • What does the literature tell us?
mi cardiogenic shock how to manage the mi72
MI + Cardiogenic shock:How to manage the MI?
  • Thrombolysis in cardiogenic shock
    • GISSI (N=280) 30day mortality
    • streptokinase 70.1%
    • medical mx 69.6%
    • NO trial has shown reduction mortality with cardiogenic shock with thrombolysis
mi cardiogenic shock how to manage the mi73
MI + Cardiogenic shock:How to manage the MI?
  • Intra-Aortic Balloon Pump
    • Gusto I: early IABP + lysis showed trend towards lowered 30d and one year mortality
    • SHOCK trial: IABP + lysis mortality 17% versus medical mx alone 32%
  • Temporizing with IABP then lysis is an option
cardiogenic the shock trial hochman js nejm 1999 vol 341 9 625 34
Cardiogenic: the SHOCK trial Hochman JS. NEJM 1999; vol 341 (9): 625-34.
  • RCT of AMI + cardiogenic shock
    • 152 early revascularization (PTCA or CABG) or 150 initial medical mx only (lysis initially, some had PTCA/CABG after 52hrs)
    • End Point early revasc. Med Mx stats
    • 30d mortality 46.7% 56% p=.11
    • 6m mortality 50.3% 63.1% p=.027
cardiogenic shock the shock trial
Cardiogenic Shock:the SHOCK trial
  • Hochman JS. One year survival following early revascularization for cardiogenic shock. JAMA 2001.
  • End Point early revasc. Med Mx stats
  • 1yr survival 46.7% 33.6% p=.03
mi cardiogenic shock how to manage the mi76
MI + Cardiogenic shock:How to manage the MI?
  • Conclusions …….
    • Patients with AMI complicated by cardiogenic shock, especially those < 75yo, should undergo emergent revascularization (PTCA or CABG)
anaphylactic shock
Anaphylactic Shock
  • You’d better know this!
    • Airway management
    • Epinephrine
    • Benadryl
    • Fluids
    • Steroids
    • Racemic epinephrine and ventolin nebs
    • Ranitidine
    • Glucagon
etiology of adrenal crisis
Etiology of Adrenal Crisis

Underlying Adrenal Insufficiency

(Addision’s and Chronic Steriods)

Acute Precipitant

Adrenal

Crisis

acute adrenal crisis
Underlying Adrenal insufficiency

Addison’s disease

Chronic steroids

No underlying Adrenal insufficiency

Adrenal infarct or hemorrhage

Pituitary infarct or hemorrhage

Precipitants of Adrenal crisis

Surgery

Anesthesia

Procedures

Infection

MI/CVA/PE

Alcohol/drugs

Hypothermia

Acute adrenal crisis?
key features of adrenal crisis
Nonspecific

Nausea, vomiting, abdominal pain

Shock

Distributive shock not responsive to fluids or pressors

Laboratory (variable)

Hyponatremia, hyperkalemia, metabolic acidosis

Known Adrenal insufficiency

Features of undiagnosed adrenal insufficiency

Weakness, fatigue, weight loss, anorexia, N/V, abdo pain, salt craving, hyperpigmentation

Key Features of Adrenal Crisis
adrenal crisis
Adrenal Crisis
  • Consider on the differential diagnosis of SHOCK NYD
management of adrenal crisis
Management of Adrenal Crisis
  • Corticosteroid replacement
    • Dexamethasone 4mg iv q6hr is the drug of choice (doesn’t affect ACTH stim test)
    • Hydrocortisone 100 mg iv is an option
    • Mineralocorticoid not required in acute phase
  • Other
    • Correct lytes, fluid resuscitation (2-3L)
    • Glucose for hypoglycemia
    • Pressors
conclusions
Conclusions
  • Shock is the transition between illness and death
  • Shock has many different causes but the end result is the same
  • The diagnosis and management of shock is essential knowledge in emergency medicine