Transcript SHOCK Phil Ukrainetz, MD, PGY5 Jeff Plant, MD, FRCPC Core

SHOCK
Phil Ukrainetz, MD, PGY5
Jeff Plant, MD, FRCPC
Core Rounds, August 9, 2002
Shock talk outline
In the trenches approach
 What’s the evidence
 What is on the horizon

Shock definition
A condition of the circulatory system
whereby there is inadequate tissue
nourishment and removal of toxic
metabolites
Better shock definition
Inadequate blood flow secondary to
decreased cardiac output or maldistributed output that results in
irreversible tissue damage
Why is my sphincter tone so
high?
Shock is the transition between life and
death
 Cornerstone of emergency medicine
 You need to know it cold

Shock:assert yourself and know
your team
Preparation:
 Who’s the boss
 Know names of staff
 Assign tasks including reinforcing that you
are running the code (AKA: shut-up or
leave)
Shock: the set up
T: Triage
 V: Vitals including C/S and O2 sat
 M: Pulse-ox, ACF IV x 2, cardiac monitor,
O2 NRB

Your role as code leader
Your position is at the foot of the bed with
your hand on the pts femoral artery and
your eyes on the monitor
 Do not get roped into procedures
 Direct specific people for specific tasks
 Close the loop - “Please intubate the patient
and let me know when it is done” - then
check that tasks have been completed.

Shock: it is as simple as ABC’s
C: quick look because early defibrillation
makes such a difference
 A: if they will take a tube give it (have sux
on hand), confirm tube
 B: adequate vent and ox
 C: fluids then pressors
 S: sugar and temp

Shock: you want a directed
history
Do not wait for the info - ask these questions:
 A: Allergies
 M: Medications - cardiac CCB/BB/Dig
 P: PMHX - surgery?
 L: Last meal - who cares but it makes
AMPLE a word
 E: Events leading up
Shock: how do I know they are in
shock?
Confirm shock
 Encephalopathic - MAP of 50 before decr
CBF - do not rely ALOC to diagnose shock
 Hypotense
 Tachypnea
 Oliguria - sensitive at < 0.5cc/kg/hr
 Cold skin
Shock:how do I diagnose the
etiology
Head to toe etiologic clues:
 Head: pupils, neck stiffness, JVD
 Chest: muffled HS, S3, murmur, crackles
 Abdo: peritonitis, tense
 Skin: warm, cold, purpura fulminans
Shock:how should I remember it?
S: Sepsis/distributive - warm skin?
 H: Hypovolemic - hemorrhage/third space
 O: Obstructive
 C: Cardiogenic - pump, rhythm, valve
 K: Anaphylactic - red, laryngospasm or
wheeze?

Shock: when can I call the code
Have I done everything?
 Confirm ABC’s
 ACLS and fluid / pressor resuscitation)

When can I call a code? - confirm
5 H’s and their treatment
H: Hypovolemic
 H: Hypoxia
 H: H+ ions/acidosis
 H: Hyperkalemia
 H: Hypothemia

Fluids and pressors
 Tube / ox / vent
 HCO3 crapola
 Get I stat K+
Peaked T’s, sine
wave?
 Rectal temp

When can I call a code? - confirm
5 T’s and their treatment
T: Tablets
 T: Tension ptx
 T: Tamponade
 T: Thrombo
coronary
 T: Thrombo pulmo

Digibind, glucagon
 Needle, tube
 Pericardiocentesis
 PTCA, lyse
 TPA 100mg?

Remember shock is a spectrum recognize its early symptoms
Confused
 Tachypnea
 Pulse pressure
change
 Oliguria
 Anion gap
 Coagulopathy

Coma
 ARDS
 Hypotension
 Anuria
 Metabo;ic acidosis
 DIC

Shock classifications: how to
rally in an exam
Simplest: vasogenic, cardiogenic,
hypovolemic
 Quantitative vs qualitative
 SHOCK mnemonic
 It doesn’t matter how you do it just be
comprehensive and be able to rattle it off

Shock classifications: how to
rally in an exam

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 shock: circulatory
defect
Quantitative: large area of decreased tissue
perfusion secondary to a circulatory defect
 Vasogenic, hypovolemic and cardiogenic in
origin
 Compensate with hyperdynamic state; HR,
CO increased and clamp down
 Correct the circulatory defect

Qualitative shock: altered milieau
Affects the metabolic milieau from the getgo
 Sepsis, hemoglobinopathies, crush, heat,
cell poisons
 Do not necessarily have a compensatory
period
 Identify the toxin and customize
management

Shock unifying features:
Disrupted cellular homeostasis
 Think failed anaerobic metabolism
 Acidosis
 Calcium influx, SR pukes
 Failed ion gradients and cellular pumps
 Cell edema and death

Some other $25 cent words to
throw around
Membrane lipid peroxidation
 Free radicals
 Nitric oxide damage
 Enzymatic denaturation
 “Inflammatory mediators”

How does our body compensate?
Counter-regulatory mediators
 Catecholamines, glucocorticoids,
angiotensin, vasopressin, insulin
 Increased substrates: glucose, TG and FFA
 Anaerobic metabolism: incr CO2:02 ratio

Oxygen metabolism
Shock is a state of oxidative
phosphorylative failure
 Loss of autoregulation
 Inability to match demand
 Paralyze paradoxers: 50-100% increase in
02 demands, 50% decrease in CBF
 DELIVER 02!!!!!!!!!!!!!

Hemorrhagic shock
Case

50 year old male MVA victim, HR is 120,
BP is 100/75, RR is 20 complaining of
abdominal and chest pain. What is the
likely blood loss?
What is the utility of the
Hemorrhagic Shock Classification?
Class I
Class II
Volume
<750ml
750 – 1500 1500-2000 > 2000
%
< 15%
15-30%
30-40%
> 40%
HR
< 100
100 - 120
120 – 140
> 140
PP
N or incrd decreased
decreased
decreased
BP
normal
normal
decreased
decreased
LOC
anxious
anxious
confused
lethargic
Class III
Class IV
Classification utility
It makes you consider the signs of shock
 It makes you aware that you can have
significant blood loss with very little signs
or symptoms
 It tells you that patients become
hypotensive late so don’t wait

Compensatory mechanisms for
blood loss
Cardiac: increase rate to 150 then
diminished returns
 Resistance: catecholamines increase
diastolic pressure, narrowed pulse pressure
 Capacitance: shunt from catechol receptor
rich gut and skin, decreased renal function
means increased vascular colume

Case

14 year old male MVA victim, weighing 50
kg has a fractured femur, seat belt sign and
a GCS of 14. The accident happened right
outside ACH only minutes ago. His heart
rate is 95, BP is 95/65, RR is 20. Do these
vitals make you sweat?
Supine vitals sensitivity
I would sweat, supine vitals are:
 Not very sensitive
 15% loss has no change in vitals
 30% loss before hypotense
 Act early and aggressively - especially in
kids. They crump late and fast.
Case

Nurse comes to you saying “The girl
involved in the slow speed (5km/hr) rear
end MVC, the one who is complaining of
abdominal pain has an orthostatic increase
of 20 BPM”. Is this useful information?
Orthostatic vitals
Consider the context, however in the
absence of concerning trauma they are not
sensitive
 Normal euvolemic patients average an
orthostatic increase of 15 BPM, therefore an
orthostatic increase of 20 BPM is not
helpful
 A meaningful orthostatic increase is 30
BPM and this requires a 20% loss of blood
volume.

Hemorrhagic shock management

Management
– ABCs, vascular access, crystalloid bolus X 2,
blood transfusion prn
– Search for the cause of blood loss: CXR, abdo
and pelvis
– controversies




crystalloid versus colloid
immediate versus delayed
small versus large volume resuscitation
Optimal endpoints of resuscitation
Case

An ICU nurse gawks at you when you ask
to give the hemorrhagic shock patient NS.
She remarks you should pull up your MAST
pants and start giving pentaspan, albumin or
something useful - is she right?
Colloids
Albumin, protoplasm protein fraction,
hydroxyethylstarch, gelatin, dextran
 Advantages

– less fluid required, more volume in vascular
space, potential to draw fluid in from tissues

Disadvantages
– expensive, allergic reactions, coagulopathies
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
Colloids

Cochrane Database 2000. 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 albumins reduce
risk of death in trauma, burns, or surgery
Colloid summary
There is NO evidence that colloids decrease
mortality in the resuscitation of critically ill
patients.
 There IS evidence that colloids increase
mortality in the resuscitation of critically ill
patients.

Hypertonic saline

Advantages
– less volume, stays in vascular space, draws
fluid

Disadvantages
– hypernatremia, hyperosmolarity, seizures,
coagulopathy, anaphylactoid rxns with dextran
Hypertonic saline

Animal evidence
– improved hemodynamics and mortality

Human evidence
–
–
–
–
Wade et al 1997: HS and HSD in trauma
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 saline

Cochrane Database 2001. Alderson P.
–
–
–
–
Objective: effect on mortality
Study: metanalysis of 8 RCTs
Results: pooled RR of 0.88 (0.74, 1.95)
Conclusion: there is a trend toward reduction
in mortality with HSD although not statistically
significant
Hypertonic saline summary
There is evidence of TRENDS toward lower
mortality in resuscitation with hypertonic
saline but statistical significance has not
been demonstrated …………
 More RCTs are needed………..

Case

A 20 year old male comes in with a knife
wound to his abdomen. He is bleeding
profusely. The trauma surgeon will be here
in 10 minutes. The patients systolic is 70.
How much and what fluid would you like
Doctor?
Controlled fluid resuscitation
ATLS recommends 2 litres then switch to O
negative blood.
 Newer research suggests minimal fluids if
there is a short time to the OR
 Rationale: early, aggressive fluid
resuscitation with large volume dislodges
soft clots and dilutes clotting factors leading
to increased hemorrhage and mortality

Bickell et al 1990
The 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
Hemorrhage
Controls
0/8
783 ml
RL tx grp
8/8
2142ml
Bickell et al 1992. HSD vs RL after Aortotomy
HSD tx grp
5/8
1340ml
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%)
ARR 8%, NNTT 12
Statistically significant p = 0.04
Conclusion: delayed fluid resuscitation reduces
mortality in hypotensive patients with penetrating
trauma
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
Controlled Fluid Resuscitation Conclusions
There is evidence (limited) that early, large
volume aggressive fluid resuscitation
increases mortality in penetrating trauma.
 Further study needed on penetrating trauma
without immediate access to OR and for
blunt trauma and CHI

Case

You can’t get an IV in your exsanguinating
patient. A med student whips out a sternal
intraosseus infuser - Is it safe? Does it
work? Do people use these?
Sternal Intraosseus Infusion
Rationale:
 Average IV times are 1.5 to 10 min
 Too many outright failures to start IV’s
 Sternum easy to locate and access
 High red marrow content
Sternal Intraosseus Infusion
FAST system (First Access for Shock and
trauma, Pyng Medical Corp., Vancouver,
BC)
 Intraosseus infusion system with depth
control

A new system for sternal
inraosseus infusion in adults
Macnab et al, Prehospital Emerg Care 2000;4
Report the first 50 uses of the new system
 Adult patients, urgent need for fluids or
meds, unacceptable delay or inability to
achieve IV access
 Mean time to IV access was 77 seconds
 Overall success rate 84%
 First time users 74%
 Experienced 95%

Macnab et al, Prehospital Emerg
Care 2000;4, 173-177
Only 44% success in obese patients
 Flow rates of 80ml/min IV and 150 ml/min
by syringe
 No complications or complaints at 2 month
follow up
 Rapid and safe alternative

Macnab et al, Prehospital Emerg
Care 2000;4, 173-177
Still misses our hardest to start group obese, shocky patient
 Will it make a difference in outcome?
 Shouldn’t you compare to IM
administration of drugs or central access in
the ED?
 What about a pediatric unit?

Case

80 yr old male comes in with a leg cellulitis,
you start him on IV ancef and go to see
more patients. Two hours later you are
called back. The patient pressure is 70/50
he is stuporous, has paradoxical breathing
and his cellulitis is now up to his groin.
What has happened and what are you going
to do?
Sepsis
Microbiologic cause of shock. Typically
secondary to gram negative endotoxins but
also due to gram positive, parasitic and
fungal infections
 Gram positive infxn ~ 35 – 40%
 Gram negative infxn ~ 55 – 60%
 Most common sites

– Lung, abdomen, urinary tract
Hemodynamic changes with
sepsis
Compensating:
 Endotoxin decreased SVR with
 Compensatory increase in cardiac output.
 Presents as hyperdynamic, warm patient.
Hemodynamic changes with
sepsis
Decompensating:
 Can appear like cardiogenic shock
 Bacterial myocardial depressant
 Increased pulmonary pressures (ARDS)
 Pump failure and decreased forward flow
 Presents as cold patient in failure. Poor
prognosis
Sepsis general treatment
TVM
 ABC’S
 2 litres crystalloid
 Pressors Levo>dopamine
 Early empiric antibiotics

Fluid resuscitation
Important in septic shock
 Initially relative hypovolemia/fluid defecits
 Low CO and filling pressures which may
respond to volume
 Increased blood and plasma volumes
associated with enhanced survival and
increased CO

– Weil MH et al., AM J Med 1978
Vincent J-L, et al., Intensive Care
Medicine (2001)
Colloids and Crystalloid each work well
 Colloids in Europe, Crystalloids in NA
 Uncertain if one superior
 Need 2-4 x more volume with crystalloid
for same filling pressures

Fluids and sepsis summary

Aggressive fluid challenge important
– Dx clue
– Important physiologically

Will improve myocardial performance and
O2 delivery
Vasopressors

Cornerstone of Rx together with fluids and
antibiotics

Goal: increase MAP and therefore end
organ perfusion

First line agents:
– Dopamine or levophed
Most common choices

Dopamine:
– 1-5 ug/kg/min ~ dopaminergic
– 5-10 ug/kg/min ~ beta activity
– >10 ug/kg/min ~ alpha activity

Levophed:
– Potent alpha agonist
– Some beta properties
Structurally very similar
Dopamine
In past/and still with many, dopamine
preferred agent
 Effects well established
 Physicians comfortable with use

Norepinephrine
Concern with levophed worsening end
organ hypoperfusion
 Based on limited evidence
 Older studies on pressors, levophed used as
last resort and thus poor outcomes

– Hesselvik JF, et al., Crit Care Med 1989
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
Martin et al., Chest 1993
 Marik et al., JAMA 1994
 Small studies (n=20), surrogate markers
 Levophed has favourable effect on
hemodynamics and end organ perfusion as
compared to dopamine

Pressor summary
Dopamine/Levophed first line agents
 Levophed may be the superior agent in
septic shock
 Make sure the pump is full first
 Avoid supranormal restoration of MAP
 Invasive monitoring req’d

Bochud et al., Intensive Care
Medicine 2001

4 retrospective studies of gram neg
bacteremia
–
–
–
–
McCabe et al., Arch Intern Med 1962.
Bryant et al., Arch Intern Med 1971.
Freid et al., Arch Intern Med 1968.
Young et al., Ann Intern Med 1977.
Four studies combined
N=1190
 Appropriate Abx mort rate~28%
 Inappropriate Abx mot rate~49%
 P<0.001

Intensive Care Medicine 2001

Early appropriate antimicrobial Rx
improves the outcome of patients with
blood borne infections and severe sepsis or
septic shock..in patients with both gram
negative and positive bacteremia
Empirical antibiotic choices
Carbapenem
 B-lactam + aminoglycoside
 3rd/4th generation cephalosporin
 ? Extended spectrum penicillin

La message

Initial rapid appropriate antibiotics in
patients with severe sepsis/septic shock can
be life saving
Case

Despite Dop at 20 u/min/kg and Levo at
4ug/min the cellulitic patient still only has a
pressure of 80 systolic. He is tubed and has
no urine output by foley. What else is in
your arsenal?
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
Interest in Roids
Interest since the 1940’s
 Known beneficial in

– Pediatric bacterial meningitis
– Typhoid fever
– PCP pneumonia
Early mega-dose steroid trials
1930s mega-dose steroids
(methylprednisolone 30/mg/kg x 3-4 doses)
 Trend towards increased mortality with
corticosteroids
 No beneficial effect in septic shock patients
 Increase incidence of GI bleeding
 Trend towards increased mortality from
secondary infections

Newer steroid trials in the 1990’s
Revisited the steroid issue except at small
doses
 They aimed to replace steroids for a
“Relative adrenal insufficiency”
 Researchers hoped get catecholamine
sensitivity and anti-inflammatory effects
still

Bollaert et al.,Critical Care Medicine
1998
Double-blind, placebo controlled
 Septic shock pts according to ACCP criteria
or pressors >48hrs
 Solu-cortef 100mg IV q 8hrs x 5days vs.
placebo with tapering
 Baseline pt characteristics similar

Results

Shock reversal by day 7:
– 15/22 (68% Rx group)
– 4/19 (21% placebo group)
– P=0.007

Trend in Rx group of decrease mortality
– 63% vs 32% p=0.09

No increase adverse outcomes
Briegel et al., Crit Care Med
1999.
Double blind, randomized, placebo
controlled (n=40)
 Pts in septic shock
 Pts included if on vasopressors less than 72
hrs
 Randomized to solu-cortef 100mg IV then
low dose infusion
 Primary end point = time to shock reversal

Results
Shock reversal 2 days in Rx group vs. 7
days in placebo (p=0.005)
 Mortality unaffected by Rx
 1 GI bleed in Rx group

Annane et al., Crit Care Med,
2001
Review of the steroid literature
 Conclusions
– NO ROLE FOR HIGH DOSE
STEROIDS
– Growing evidence for replacement
steroids in pressor dependent septic shock

Case

A 10 year old tubed patient comes into
PICU with febrile status epilepticus.. You
astutely start him empirically on vanco and
cefotaxime. Two hours later the child is
coughing up blood, hypoxemic despite your
best efforts and has a BP of 70/40 on
maximum pressors? What is the latest
agent for septic shock?
Activated Protein C
Rationale:
 Pro-fibrinolytic
 Anti-thrombotic
 Anti-inflammatory

Bernard et al., NEJM 2001
Randomized, double blind(phase 3 trial)
 N=1690 severe sepsis
 Placebo vs. APC
 End point 28 day mortality

Bernard et al., NEJM 2001

Mort rate;
– 30.8% placebo
– 24.7% Rx group
Absolute risk reduction 6.1% (p=0.005)
 NNTT 16 (CI NNTT 10-50)
 Serious bleeding 3.5% vs 2%(p=0.06)
 NNTH 67

Commentary
Study results have been criticized
 Some of the investigators have left the
group
 Cost-effectiveness study of APC in CHR
hopefully to make it in Lancet … we ain’t
going to be using it

Case

A 28 year old women is found at home by
friends she is obtunded, hypotensive and
has purpura fulminans. After maximal
pressor support and the ravages of
meningococcemia her toes and fingers are
black. Your staff intensivist is at a loss.
Because you went to Phil’s talk you are
going to suggest?
Vasopressin
Known to be potent vasoconstrictor via V1
receptor smooth muscle
 Evidence that in septic shock there is a
relative lack of vasopressin

Vasopressin
Malay et al., J Trauma 1999
 Tsuneyoshi et al., Crit Care Medicine 2001
 Studies limited by design and small
numbers (N=10)
 Surrogate markers not mortality used as
end-points

Vasopressin
Vasopressin does increase MAP in pts with
septic shock
 ? Improved mortality
 Larger studies required
 ? Consider in ED as alternative to high dose
pressors

Sepsis management summary
Don’t forget fluids
 Levophed works better than dopamine
 Don’t delay giving appropriate ABX
 Increasing evidence for steroids in
refractory septic shock
 ? Activated protein C/vasopressin in future

Obstructive shock
Case

28 year old female, known breast cancer
comes in in extremis. She is cyanotic, has a
JVD to her ear, lungs are dry and she is
hypotense with a systolic BP of 70. You are
positive she has a PE and you have TPA in
hand - are you going to lyse her?
PE and shock
Needs to take out 50% of lung surface area
 Increase pulmonary pressures to 40mmHG
 Cause backflow and septal shift
 Hypotense, JVD +/- cyanosis

Lysis and massive PE
Not been studied enough to prove lysis
improves survival in PE induced shock
 Lysis does improve RV dilation, tricuspid
regurgitation and cardiac output in submassive PE
 I would treat with 02, fluids and pressors
and get a CT or echo
 If TPA is to be given: 100mg bolus? Over
30min? 2 hours? - no consensus

Case

25 yr old male, left sided anterior chest
wound. Two hypotensive episodes where
patient almost passes out. In between he is
alert and talking and says his chest just
hurts. There is no Beck’s triad - he has two
IV’s in. What do you want to do?
Pericardial tamponade stats
2% of penetrating chest trauma
 Stab > GSW
 Beck’s triad only in 1/3
 CXR will often reveal a globular heart, ED
ultrasound will typically confirm clinically
significant tamponade

Case

42 year old male comes in c/o crushing
retrosternal chest pain and is hypotensive at
80/60. The patient is having an
anterolateral infarct by EKG. How would
you manage the patient?
Cardiogenic shock

Management
– small fluid boluses
– invasive monitoring
– vasopressors



norepinephrine
dopamine
dobutamine
Cardiogenic shock approach
AMI +shock?
|
RV infarct?
YES /
\ NO
Volume resuscitate<<<----------------------Pulmonary congestion present?
|
NO
| YES
|
|
Response adrquate---------------------->>>> Pressor
| YES
NO
|
|
|
Revascularize<<<----------------------------Response adequate
YES
| NO
|
IABC and PTCA
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

Pathologically
– Will have lost 40% of myocardium
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
Why use pressors in cardiogenic
shock?
Increase your diastolic pressure or coronary
artery filling pressure
 They do however increase your LVEDP
which decreases coronary perfusion
 Dobutamine and IABP will increase
diastolic pressure and drop LVEDP

What is mortality in patient who
present with AMI andpump
dysfunction?
Killip Classification of Pump Dysfunction and
Mortality in AMI
Class Exam
Mortality
 I
No crackles, clear
5%
 II Crackles, S3
20%
 III Pulmonary edema
30%
 IV Cardiogenic shock
80%
So what should I do with my
patients in cardiogenic shock?
Ideally PTCA
 If there is a CCU with IABP capabilities get them there
 Second line would be to get systolic BP to
90 and lyse
 If you cannot get BP to 90 then treat
conservatively or lyse (the evidence would
say there is no difference between the two but a bleeding risk with TPA)

PTCA indications: CATHD’
JACC 1996; 28:1328-1428
C: Cardiogenic shock
 A: Anterior MI (STE >= 4 leads)
 T: Thrombolytic contra-indications
 H: Hemodynamic instability/dysrhythmias
 D: Duration less than 60 minutes

Don’t lyse in cardiogenic shock

Thrombolysis in cardiogenic shock
– GISSI (N=280)
– streptokinase
– medical mx
30day mortality
70.1%
69.6%
– NO trial has shown reduction mortality with
cardiogenic shock with thrombolysis
Temporize with IABC and then
lyse or preferably do PTCA

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%
– ongoing research
Cardiogenic: the SHOCK trial
Hochman JS et al. Early revascularizationin AMI +
cardiogenic shock: 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 mort
46.7%
56%
p=.11
– 6mo mort
50.3%
63.1%
p=.027
Cardiogenic Shock:
the SHOCK trial

Hochman JS. One year survival following
early revascularization for cardiogenic
shock. JAMA 2001.
–
–
–
–
Early revascularization survival 46.7%
Initial medical mx survival
33.6%
Statistically significant p<0.03
NOTE: sub group analysis only shows
mortality difference in age < 75yo
Case

76 year old female had an inferior MI 3
days ago. You are called to assess her in
CCU. She is hypotense, c/o of new chest
pain and has an impressive holosystolic
murmur. What is on your differential and
how are you going to manage her?
Holosystolic murmur
Loss of mechanical cardiac function
 Anteroseptal MI: acute VSD - thrill
 Inferior MI: papillary muscle rupture - no
thrill
 Both need urgent echo
 Cardiac surgical consultation - “Like
sewing moonbeams to flatus”

Case

A 20 year old male roofer comes in within
30 minutes of his accident. He cannot move
or feel anything below his shoulders. He is
arreflexic, hypotense and bradycardic. Is
this spinal shock or neurogenic shock?
How are you going to treat him?
Neurogenic shock
Cervical spine transections that result in
transection of sympathetic fibres
 Loss of sympathetic tone and unopposed
vagal tone
 Patients present bradycardic and
hypotensive
 Spinal shock can present identically

Neurogenic shock
Still give fluids
 Give dopamine, phenylephrine or ephedrine
 Use atropine for bradycardia and intubation
 T4 transections are the lowest lesions that
will give you neurogenic shock

Case

28 year old female comes in post bee sting.
She is glowing red, hypotense and
stridorous. How are you going to manage
her? What is your epi approach?
Anaphylaxis - only take home
ABC IV’S
 A: Adrenaline
 B: Benadryl
 C: Corticosteroids
 I: IV fluids
 V: Ventolin
 Severe: epinephrine IV

– 1ml of 1:10,000 q 30seconds to effect
Thanks
Simon Bartley
 Idan Khan
 Rob Hall
 Jeff Plant
 Morad Hameed

Keep the dream alive….