Shock
Julye N. Carew, M.D.
December 9, 2005

Shock
 Definition
 Clinical Evaluation
 Cardiogenic Shock
 Hypovolemia
 Sepsis
 Management of septic shock

Sepsis mortality
Dellinger, Crit Care Med, 2003

Definition
 Often misdefined as “hypotension”
 Multisystem end-organ hypoperfusion and
hypoxia with lactic acidosis commonly seen
 Hypotension
 Tachycardia
 Tachypnea
 Cool skin and extremities
 Altered mental status
 Oliguria/Anuria

Clinical Evaluation
 Patients are commonly hypotensive
 Initial evaluation should begin with identification
of adequate cardiac output (CO)
 DIMINISHED—narrow pulse pressure, cool
extremities and delayed capillary refill
 INCREASED– widened pulse pressure, warm
extremities, bounding pulses and rapid capillary
refill
 Pulse pressure is a surrogate for SV

Clinical Evaluation
 MAP= CO X SVR
 CO= SV X HR
 Pulse pressure is a surrogate for stroke
volume: Increased in high output states,
Reduced in hypovolemia and
cardiogenic shock

Clinical Evaluation
 Jugular venous pulse
 Cardiac gallop
 Edema
 Rales
 CXR—cardiomegaly, Kerley B lines,
pulmonary edema

CHF
Murray and Nadel, Textbook of Resp. Medicine, 4th ed

Clinical Evaluation
 Fever
 Leukocytosis/leukopenia
 Pancreatitis, hepatic failure, burns,
anaphylaxis, thyrotoxicosis
 Evidence of GI blood loss, diarrhea,
vomiting, polyuria

Resuscitation
 Few minutes to complete history and
physical examination
 Begin aggressive, early resuscitation to
establish perfusion and minimize end-
organ damage
 ABCs Ventilatory failure due to
increased load on respiratory system–
LA, pulmonary edema, inadequate
perfusion to RR muscles

Resuscitation
 Aggressive IVFs in patients with decreased
volume status, sepsis
 Crystalloid is preferred, may be increased
mortality with colloid
 Early administration of vasoactive drugs in
hypovolemic patient is not recommended
 Transfusion of PRBCs to hemoglobin of 7 g/dL
 GOAL IS OXYGEN DELIVERY AND END
ORGAN FUNCTION, not BP– mental status,
UOP

Resuscitation
 If evidence of hypoperfusion persists,
then consider vasoactive drugs and
invasive monitoring (PA catheter),
echocardiography, etc.

Cardiogenic Shock
 Cardiac output is low despite adequate
venous return (RAP) 50-80% mortality
 Systolic dysfunction
 Diastolic dysfunction
 Valvular disease
 Right heart failure
 “Other”

Systolic dysfunction
 Most common cause is acute coronary
ischemia
 Starling mechanism of compensation—and by
fluid retention and increase in sympathetic tone
 Cardiogenic shock reported to complicate 10%
of all acute MI
 Inotropes, intra-aortic balloon pump
 No data to suggest that lytics improve mortality
(Col, et al, 1994)

Cardiogenic Shock
 Improved mortality with early
revascularization—PTCA and CABG
 Hochman, et al. 1999 randomized 152
patients to revascularization (PTCA or
CABG) vs. medical therapy alone
 Six-month mortality was 50.3 vs. 63.1%
(P=0.027). Treatment benefit was only
achieved in those younger than 75 years

Diastolic dysfunction
 VERY common phenomenon, less likely
to cause frank shock
 LV chamber stiffness with impaired LV
filling
 May be difficult to treat
 Inotropes may be ineffective
 Aggressive management of tachycardia
with volume administration and negative
chonotropic agents. NSR very important

Valvular Disease
 AS– decrease HR, NSR, NO afterload
reduction
 AI– use of chronotropic agents to
decrease regurgitant filling time and
afterload reduction
 MR– NSR, afterload reduction
 MS—negative chronotropic agents to
maximize diastolic filling time
 ARRYTHMIAS

Right heart failure
Murray and Nadel, Textbook of Resp. Medicine

Right Ventricular Failure
 Most common cause is concominant LV
failure
 Elevated JVP with clear lungs, LE
edema
 PE, ARDS, RV infarction
 Volume administration, Dobutamine and
NE
 Treat underlying condition—eg., Lytic
therapy

“Others”
 Cardiac tamponade (Kussmaul’s
sign=increased JVP with inspiration,
pulsus and RAP=RVP=PCWP
 Pericardial effusion, tension
pneumothorax, ascites,
pneumopericardium, large pleural
effusions

Hypovolemia
 GI blood loss, trauma, coagulopathy
 Aggressive volume resuscitation with large
volumes of crystalloid and blood products
 “Wigger’s preparation”
 1. several hours of severe hypotension
produced “irreversible shock”
 2. ECF deficit could be corrected with
administration of crystalloid in volumes 2-3X
blood loss “3:1 rule”
Wiggers, NY Commonwealth Fund, 1950.

Hypovolemia
 More recent studies suggest that more
moderate volume repletion with
crystalloid is preferable (Kaweski,1990. Bickell, 1994)
 Mechanism? Interference of effective
thrombus and continued secondary
hemorrhage
 Bottom line: Volume resuscitate, correct
coagulopathy, fix the underlying problem

Septic shock
 Infection with state of hypoperfusion and end-
organ damage
 SIRS, sepsis, severe sepsis, septic shock
 High cardiac output state
 Widened pulse pressure, warm extremities,
brisk capillary refill
 Subgroup of patients with depressed cardiac
function (myocardial depressant factors)-- ?NE
and dobutamine

Septic shock
 Sepsis is the leading cause of death in
non-CCUs, 750,000 cases/year
 Unregulated inflammation and a
hypercoagulable state favoring
microvascular coagulation
 ARF carries a poorer prognosis
 >80% of patients will require mechanical
ventilation

D
e
l
Dellinger, Crit Care Med 2004.

Septic Shock
 Society of CC Medicine wrote consensus opinion on
recommendations treatment of septic shock, 2004
 Graded recommendations based upon available data
 Grade A- at least two level I studies (large, randomized
with clear results)
 Grade B- one level I study
 Grade C- level II investigations (small, randomized with
uncertain results)
 Grade D- at least one level III (nonrandomized)
 Grade E- level IV and V support (historical controls,
expert opinion; case series)
Dellinger,Crit Care Med, 2004

Reommendations for
treatment of septic shock
 Resuscitation (B): CVP 8-
12 mmHg MAP>65 mm
Hg UOP > 0.5 ml/kg/hr
Mixed venous> 70%
 Diagnosis (D):
Appropriate cultures prior
to ABX therapy
 Antibiotics (E and D):
Begun within 1 hour and
cover appropriate
organisms (eg.
Neutropenia)
 Source Control (E): drain
abscesses and removed
infected devices
 Fluids (C and E):
crystalloid or colloid, 1 L
over 30 minutes and
repeat if necessary
Dellinger, Crit Care Med, 2004

Treatment of septic shock
 Vasopressors:
 1. DA or NE (D)
 2. NO low-dose DA for “renal
protection”(B)
 3. Vasopressin in refractory patients(E)
Dellinger, Crit Care Med, 2004

Recommendations for
treatment of septic shock
 Inotropes (E and A): patients with low
CO—try dobutamine, a pre-defined CI is
not recommended
Dellinger, Crit Care Med, 2004

Treatment of septic shock
 Steroids:
 1. Stress-dose hydrocortisone in
refractory shock for 7 days
 2. ACTH stimulation test (E)
 3. DO NOT use doses >300 mg/day (A)
 4. In the absence of shock steroids
should not be used, except for usual
dose or if adrenal insufficiency is
suspected (E)
Dellinger, Crit Care Med, 2004

Treatment of septic shock
 rhAPC: for those at high
risk of death
(APACHE>25, MOFS,
shock) without
contraindication (B)
 Blood products:
1.Transfuse PRBCs only
when Hgb<7 (B)
2. No routine EPO (B)
3. No FFP (E) or AT3 (B)
4. PLT for PLT<5000 (E)
 Mechanical ventilation:
1. Low tidal volume (6
cc/kg), plateau
pressures<30 (B)
2. Hypercarbia is
acceptable to reduce
plateau pressure (C)
3. PEEP to lower
FiO2(E)
4. Keep patients at 45
degrees to prevent VAP
(C)
5. Weaning protocol and
spontaneous breathing
trials (A)
Dellinger, Crit Care Med, 2004

Treatment of septic shock
 Sedation:
 1. Sedation protocols and
scales should be used
(B)
 2. Bolus vs. continuous
with daily interruptions
(B)
 3. NM blockers should
be avoided, but if
necessary train of four
should be followed (E)
 Modified Ramsey Sedation
Scale.
1. Anxious, Agitated, Restless
2. Cooperative, Oriented,
Tranquil
Accepts mechanical ventilation.
3. Responds to commands only
4. Brisk response to light
glabellar tap or loud noise.
5. Sluggish response to light
glabellar tap or loud noise.
6. No Response.
Dellinger, Crit Care Med, 2004

Treatment of Septic Shock
 Glucose Control:
Maintain CBG<150
(D), enteral feeding
preferable (E)
 Renal Replacement:
CVVH and
intermittent HD are
equivalent in
hemodynamically
stable patients (B)
 Bicarbonate: NOT
recommended for
pH>7.15 (C)
 DVT
prophylaxis:YES!!!
(A)
 Ulcer prophylaxis:
YES!!! (A)`

Hydrocortisone
 Oppert, et al. (German) looked at 41
patients with septic shock
 18 received hydrocortisone 50 mg bolus
followed by 0.18 mg/kg/hr (70 kg would
receive 350 mg/24 hours), 23 placebo
 Primary endpoints: duration of shock,
reduction in pro-inflammatory cytokines

Hydrocortisone
Oppert, Crit Care Med, 2005

Hydrocortisone
Oppert, Crit Care Med, 2005

Hydrocortisone
Oppert, Crit Care Med, 2005

Hydrocortisone
 Not adequate power to determine
mortality benefit
 Showed a trend toward better outcome
with ACTH responders
 The jury is still out

Vasopressors
 Sharshar, et al. Looked at circulating
vasopressin levels in septic shock
 Found that plasma vasopressin levels were
almost always increased at the initial phase of
septic shock and decrease afterward.
Vasopressin deficiency was seen in 1/3 of late
septic shock patients
 I use vasopressin for patients who do not
initially respond to NE (dose .04 units/min)

The End!!