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

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

Dellinger, Crit Care Med, 2004

Treatment of septic shock
 Sedation:  Modified Ramsey 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)
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:  Bicarbonate: NOT

Maintain CBG<150 recommended for
(D), enteral feeding pH>7.15 (C)
preferable (E)  DVT
 Renal Replacement: prophylaxis:YES!!!
CVVH and (A)
intermittent HD are  Ulcer prophylaxis:
equivalent in YES!!! (A)`
hemodynamically
stable patients (B)
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!!