Shock

Scott G. Sagraves, MD, FACS

Assistant Professor
Trauma & Surgical Critical Care
Associate Director of Trauma
UHS of Eastern Carolina
Objectives
Define & classify shock
Outline management principles
Discuss goals of fluid resuscitation
Understand the concepts of oxygen
supply and demand in managing shock.
Describe the physiologic effects of
vasopressors and inotropic agents
Goals
Review hemodynamic techniques in the ICU
Introduce the concept of the cardiac cycle
Review of the pulmonary artery catheter
parameters

Utilize the presentation to analyze clinical
cases and to feel comfortable with pa-c
parameters.
Shock:
A momentary pause in the act of
death.

-John Collins Warren, 1800s
Hypotension
In Adults:
systolic BP s 90 mm Hg

mean arterial pressure s 60 mm Hg

systolic BP > 40 mm Hg from the
patients baseline pressure
Definition
SHOCK: inadequate organ perfusion
to meet the tissues oxygenation
demand.
Hypoperfusion can be
present in the absence of
significant hypotension.
-fccs course
Pathophysiology
ATP + H
2
O ADP + P
i
+ H
+
+ Energy

Acidosis results from the accumulation of acid
when during anaerobic metabolism the
creation of ATP from ADP is slowed.

H
+
shift extracellularly and a metabolic acidosis
develops

Pathophysiology
ATP production fails, the Na
+
/K
+
pump
fails resulting in the inability to correct
the cell electronic potential.
Cell swelling occurs leading to rupture
and death.
Oxidative Phosphorylation stops &
anaerobic metabolism begins leading to
lactic acid production.
Why Monitor?
Essential to understanding their disease

Describe the patients physiologic status

Facilitates diagnosis and treatment of
shock
History
1960s
low BP = shock; MSOF resulted after BP
restored
1970s
Swan & Ganz - flow-directed catheter
thermistor cardiac output
1980s
resuscitation based on oxygen delivery,
consumption & oxygen transport balance.
Pulmonary Artery Catheter
Pulmonary Artery Catheter
INDICATIONS
volume status
cardiac status

COMPLICATIONS
technical
anatomic
physiologic
PLACEMENT
Wests Lung Zones
Zone I - P
A
> P
a
> P
v

Zone II - P
a
> P
A
> P
v

Zone III - P
a
> P
v
> P
A




P
A
= alveolar
Pa = pulmonary artery
Pv = pulmonary vein
Correct PA-C Position
Standard Parameters
Measured
Blood pressure
Pulmonary A.
pressure
Heart rate
Cardiac Output
Stroke volume
Wedge pressure
CVP
Calculated
Mean BP
Mean PAP
Cardiac Index
Stroke volume
index
SVRI
LVSWI
BSA
Why Index?
Body habitus and size is individual

Inter-patient variability does not allow
normal ranges

Indexing to patient with BSA allows for
reproducible standard
Index Example
PATIENT A
60 yo male
50 kg
CO = 4.0 L/min
BSA = 1.86

CI = 2.4 L/min/m
2

PATIENT B
60 yo male
150 kg
CO = 4.0 L/min
BSA = 2.64

CI = 1.5 L/min/m
2

PA Insertion
0
5
10
15
20
RA = 5 RV = 22/4
PA 19/10
PAOP = 9
CVP
CVP of SVC at level of right atrium
pre-load assessment
normal 4 - 10 mm Hg
limited value
PAOP
End expiration
Reflection changes with positive pressure
Waveforms change ~ every 20 cm
Waveform Analysis
A wave - atrial systole
C wave - tricuspid valve closure @
ventricular systole
V wave - venous filling of right atrium
Cardiac Cycle
pulmonary
Left ventricle
systemic
Right ventricle
RVSWI
PVRI
LVSWI
SVRI
CVP
MPAP
PCWP
MAP
Hemodynamic Calculations
Parameter Normal
Cardiac Index (CI) 2.8 - 4.2

Stroke Volume Index (SVI) 30 - 65

Sys Vasc Resistance Index (SVRI) 1600 - 2400

Left Vent Stroke Work Index (LVSWI) 43 - 62
Cardiac Index
C.I. = HR x SVI

SVI measures the amount of blood ejected by the
ventricle with each cardiac contraction.
Total blood flow = beats per minute x blood volume ejected per beat
Vascular Resistance Index
SYSTEMIC (SVRI)

MAP - CVP
CI

| SVR = vasoconstriction
+ SVR = vasodilation
PULMONARY (PVRI)

MPAP - PAOP
CI

|PVR = constriction
PE, hypoxia
x 80
x 80
Vascular resistance = change in pressure/blood flow
Stroke Work
LVSWI = (MAP-PAOP) x SVI x 0.0136

normal = 43 - 62
VSWI describe how well the ventricles
are contracting and can be used to
identify patients who have poor
cardiac function.
ventricular stroke work = A pressure x vol. ejected
Too Many Numbers
Definitions
O
2
Delivery - volume of gaseous O
2
delivered to the LV/min.
O
2
Consumption - volume of gaseous
O
2
which is actually used by the
tissue/min.
O
2
Demand - volume of O
2
actually
needed by the tissues to function in an
aerobic manner
Demand > consumption = anaerobic metabolism
Rationale for Improving
O
2
Delivery
Insult
Tissue Hypoxia
Increased Delivery
Increased Consumption
Demands are met
Critical O
2
Delivery
V
O
2
I

DO
2
I
The critical value is
variable
& is dependent upon the
patient, disease, and the
metabolic demands of the
patient.
Oxygen Calculations
Arterial Oxygen Content
(CaO
2
)
Venous Oxygen Content
(CvO
2
)

Arteriovenous Oxygen
Difference (avDO
2
)

Delivery (O
2
AVI)

Consumption (VO
2
I)
Efficiency of
the
oxygenation
of blood and
the rates of
oxygen
delivery and
consumption
Arterial Oxygen Content

CaO
2
= (1.34 x Hgb x SaO
2
) + (PaO
2
x 0.0031)



If low, check hemoglobin or pulmonary gas
exchange

Arteriovenous Oxygen
Difference
avDO
2
= CaO
2
- CvO
2


Values > 5.6 suggests more
complete tissue oxygen
extraction, typically seen in
shock



Oxygen Delivery (DO
2
I)
O
2
AVI = CI x CaO
2
x 10

Normal values suggests that the heart
& lungs are working efficiently to
provide oxygen to the tissues.

< 400 is bad sign
Oxygen Consumption
VO
2
I = CI x (CaO
2
- CvO
2
)

If VO
2
I < 100 suggest tissues are not
getting enough oxygen
SvO
2

SvO
2
= 1-
VO
2

DO
2

Oxycalculations
Resuscitation Goals
CI = 4.5 L/min/m
2

DO
2
I = 600 mL/min/m
2

VO
2
I = 170 mL/min/m
2

NOT ALL PATIENTS CAN ACHIEVE THESE GOALS
Critically ill patients who can respond to their disease states by
spontaneously or artificially meeting these goals do show a
better survival.
Break Time
Shock is a symptom of
its cause.
-fccs course
Signs of Organ
Hypoperfusion

Mental Status Changes

Oliguria

Lactic Acidosis
Components
Categories of Shock
HYPOVOLEMIC

CARDIOGENIC

DISTRIBUTIVE

OBSTRUCTIVE
Goals of Shock
Resuscitation
Restore blood pressure

Normalize systemic perfusion

Preserve organ function
In general, treat the cause...
Hypovolemic Shock
Causes
hemorrhage
vomiting
diarrhea
dehydration
third-space loss
burns
Signs
cardiac
output
PAOP
SVR
Classes of Hypovolemic Shock

Class I Class II Class III Class IV
Blood Loss < 750 750-1500 1500-2000 > 2000
% Blood Vol. < 15% 15 30% 30 40% > 40%
Pulse < 100 > 100 > 120 > 140
Blood Pressure Normal Normal Decreased Decreased
Pulse Pressure Normal Decreased Decreased Decreased
Resp. Rate 14 20 20 30 30 40 > 40
UOP > 30 20 30 5 15 negligible
Mental Status sl. Anxious mildly anx confused lethargic
Fluid crystalloid crystalloid blood blood
Treatment - Hypovolemic
Reverse hypovolemia vs. hemorrhage
control

Crystalloid vs. Colloid

PASG role?

Pressors?
Resuscitation
Transport times < 15 minutes showed
pre-hospital fluids were ineffective,
however, if transport time > 100 minutes
fluid was beneficial.

Penetrating torso trauma benefited from
limited resuscitation prior to bleeding
control. Not applicable to BLUNT
victims.
Fluid Administration
1 L crystalloid ~ 250 ml colloid
crystalloids are cheaper
blood must supplement either
FFP for coagulopathy, NOT volume

Watch for hyperchloremic metabolic acidosis
when large volumes of NaCl are infused

NO survival benefit with colloids
Role of PASG?
Houston - Higher mortality rate in penetrating
thoracic, cardiac trauma

No benefit in penetrating cardiac trauma

Role undefined in rural, blunt trauma

Splinting role
Cardiogenic Shock
Cause
defect in cardiac function

Signs
cardiac output
PAOP
SVR
left ventricular stroke work (LVSW)
Coronary Perfusion
Pressure
Coronary PP = DBP - PAOP

coronary perfusion = A P across coronary a.
GOAL - Coronary PP > 50 mm Hg
The Failing Heart
Improve myocardial function, C.I. < 3.5 is a risk
factor, 2.5 may be sufficient.

Fluids first, then cautious pressors

Remember aortic DIASTOLIC pressures drives
coronary perfusion (DBP-PAOP = Coronary
Perfusion Pressure)

If inotropes and vasopressors fail, intra-aortic
balloon pump
Distributive Shock
Types
Sepsis
Anaphylactic
Acute adrenal insufficiency
Neurogenic

Signs
cardiac output
PAOP
SVR
SIRS - Distributive Shock
Prompt volume replacement - fill the tank

Early antibiotic administration - treat the cause

Inotropes - first try Dopamine

If MAP < 60
Dopamine = 2 - 3 g/kg/min
Norepinephrine = titrate (1-100 g/min)
R/O missed injury
Adrenal Crisis
Distributive Shock
Causes
Autoimmune adrenalitis
Adrenal apoplexy = B hemorrhage or infarct
heparin may predispose

Steroids may be lifesaving in the patient
who is unresponsive to fluids, inotropic,
and vasopressor support. Which one?
Obstructive Shock
Causes
Cardiac Tamponade
Tension Pneumothorax
Massive Pulmonary Embolus

Signs
cardiac output
PAOP
SVR
Endpoints?
ACS CoT ATLS - restoration of vital signs and
evidence of end-organ perfusion

Swan-guided resuscitation
C.I. > 4.5, DO
2
I > 670, VO
2
I > 166

Lactic Acid clearance

Gastric pH
Summary
Type PAOP C.O. SVR

HYPOVOLEMIC + + |

CARDIOGENIC | + |

DISTRIBUTIVE + or N varies +

OBSTRUCTIVE | + |
Vasopressor Agents?
Augments contractility, after preload
established, thus improving cardiac output.

Risk tachycardia and increased myocardial
oxygen consumption if used too soon

Rationale, increased C.I. improves global
perfusion
Vasopressors & Inotropic
Agents
Dopamine

Dobutamine


Norepinephrine

Epinephrine

Amrinone
Dopamine
Low dose (0.5 - 2 g/kg/min) = dopaminergic

Moderate dose (3-10 g/kg/min) = |-effects

High dose (> 10 g/kg/min) = o-effects

SIDE EFFECTS
tachycardia
> 20 g/kg/min A to norepinephrine
Dobutamine
|-agonist

5 - 20 g/kg/min

potent inotrope, variable chronotrope

caution in hypotension (inadequate volume)
may precipitate tachycardia or worsen
hypotension
Norepinephrine
Potent o-adrenergic vasopressor

Some |-adrenergic, inotropic, chronotropic

Dose 1 - 100 g/min

Unproven effect with low-dose dopamine to
protect renal and mesenteric flow.
Epinephrine
o- and |-adrenergic effects

potent inotrope and chronotrope

dose 1 - 10 g/min

increases myocardial oxygen consumption
particularly in coronary heart disease
Amrinone
Phosphodiesterase inhibitor, positive inotropic
and vasodilatory effects

increased cardiac stroke output without an
increase in cardiac stroke work

most often added with dobutamine as a second
agent

load dose = 0.75 -1.5 mg/kg 5 - 10 g/kg/min
drip
main side-effect - thrombocytopenia
Dilators
+ inotropes
- inotropes
Pressors
Summary `pressors & inotropes







- inotrope
+ inotrope
dilator
pressor
Dobutamine
Milrinone/Amrinone
|-dopamine
Isuprel
Digoxin
Calcium
epinephrine
o-dopamine
neosynephrine
norepinephrine
|-blocker
Labetalol
Ca
+2
blocker
ACE inhibitor
hydralazine
nitroglycerine
Nipride
Case Studies
GSW
24 year old male victim of a
shotgun blast to his right lower
quadrant/groin at close range.

Hemodynamically unstable in the
field and his right lower extremity
was cool and pulseless upon arrival
to the trauma resuscitation area.
Shotgun Blast
Post-op
Patient received 12 L crystalloid, 15
units of blood, 6 units of FFP, and 2 6
packs of platelets.
HR 130, BP 96/48, T 34.7 C
PAWP 8, CVP 6, CI 4.2, SVRI 2700,
LVSWI 42.

Diagnosis? Treatment?
SHOCK/HYPOVOLEMIA
FLUIDS FLUIDS FLUIDS
BLOOD & PRODUCTS TRANSFUSION
CORRECT
ACIDOSIS
COAGULOPATHY
HYPOTHERMIA
MVC
38 year old
female restrained
driver who was
involved in a
high speed MVC.

She sustained a
pulmonary
contusion and
fractured pelvis.
ICU Course
Intubated and monitored with PA-C
PCWP = 22, CI = 3.5, SVRI = 2400,
LVSWI = 39.8
HR = 120, BP = 110/56, SpO
2
= 91,
UOP = 25 cc/hr

What do you think...
HYPOVOLEMIA
ADJUST YOUR WEDGE FOR THE
PEEP
Wedge Adjustment
Measured PAOP - PEEP = real
PAOP
PEEP = 28, therefore real wedge = 8
Auto-Pedestrian Crash
Thrown from the
rear bed of pick up
truck during a MVC
at 60 mph.
Hemodynamically
unstable
Pain to palpation of
the pelvis
Hematuria with
Foley

insertion
ICU Course
Pelvis closed
QID Dressings, intubated, PA-C
inserted

PCWP = 20, CI = 5.2, SVRI = 280,
LVSWI = 24.5, PEEP = 8

Diagnosis? Treatment?
Sepsis
Fluids
Correct the cause
Antibiotics
Debridement
Vasopressors
Phenylephrine
Levophed
Initial Resuscitation
CVP: 8- 12 mm Hg
MAP > 65 mm Hg
UOP > 0.5 cc/kg/hr
Mixed venous Oxygen Sat > 70%
Consider:
Transfusion to Hgb > 10
Dobutamine up to 20 g/kg/min
Vasopressors
Assure adequate fluid volume
Administer via CVL
Do not use dopamine for renal
protection
Requires arterial line placement
Vasopressin:
Refractory shock
Infusion rate 0.01 0.04 Units/min
Steroid Use in Sepsis
Refractory shock 200-300 mg/day of
hydrocortisone in divided doses for 7
days
ACTH test
Once septic shock resolves, taper
dose
Add fludrocortisone 50 g po q day
Geriatric Trauma
70 year old female

MVC while talking on
her cell phone

ruptured diaphragm
and spleen s/p OR

Intubated and PA-C
ICU Course
PCWP = 28, CI = 1.8, SVRI = 3150,
LVSWI = 20.7

Diagnosis? Treatment?
Cardiogenic Shock
Preload augmentation - Consider Fluids
Contractility
dopamine
dobutamine
phosphodiesterase inhibitor
Afterload reduction
nitroglycerin
dobutamine
Dont forget...




-Samuel D. Gross, 1872
Shock: rude unhinging of the
machinery of life.