Shock VT

Slide 1
SHOCK
DOOMSDAY
1
A Free sample background from www.powerpointbackgrounds.com
Slide 2
Vicken Y. Totten
Shock lecture
Thanks to David Cheng MD
And all who taught me
Slide 3
Definition
SHOCK:
inadequate organ
perfusion to meet
the tissues
oxygenation
demand
Slide 4
PATHOPHYSIOLOGY OF SHOCK
SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & cells swell
membranes becomes more permeable
electrolytes & fluids seep in & out of cell
Cells Die in Many Organs Death
Slide 5
Stages of shock
Compensated /Early Shock

Vasoconstriction (renin & carotid sinus baroceptor
Increase in HR and RR <- sympthatic activation)
Normotensive usually <- (aldosterone/ADH Na+/h20
retention)
Decompensated / late Shock
Cool, clammy , hypotenisve.
Vital organ preservation
Worsening LOC
Continued increase in HR and RR <-----(Chemreceptor
respose to metabolic acidosis)
Irreversible HR and RR drop Multi Organ Failure Impending death)
Slide 6
Symptoms of Shock
General Symptoms
Anxious
Dizziness
Weakness
Faintness
Thirsty
I am sick
Specific Symptoms
Fevers / Rigors
(sepsis)
SSCP (cardiogenic)
Wheezing
(anaphylaxis)
Trauma pain
(hypovolemia)
Slide 7
Early Signs of Shock in

Non Complicated Patients
WARM EARLY STAGE / PRESHOCK
Need high index of suspicion b/c lack of signs

+/- tachycardia
+/- orthostatics (HR more sensitive than BP)
+/- pulse pressure narrowing
+/-restless
Slide 8
Hypoperfusion can be
present in the absence of
significant hypotension.
(Dont only relay on BP for
diagnosisng shock)
-fccs course
8
Slide 9
Signs of Late Shock

Hypotension
COLD LATE STAGE
Cold, clammy and pale skin
Rapid, weak, thready pulse
Rapid breathing (blow off CO2 met acidosis)
Cyanotic
AMS->Coma
Anuria
Slide 10
End Stage Clinical effects
Cardiovascular
Myocardial
depression
Vasogenic effects
Pulmonary
Ischemic bowel
Hematologic
Neutropenia,
Thrombocytopenia
DIC (Gm- > Gm+)
Renal
ARF
Hepatic
Increased LFTs, liver failure
ARDS
GI
CNS
coma
Slide 11
Multiple Organ Dysfunction Syndrome

Number of
Organs
Mortality (%)
0.8
6.8
26.2
48.5
68.8
83.3
*Adapted from Irwin and Rippes Critical Care Medicine 5th Edition, pg 1837
Slide 12
Circumferential
Subendocardial
Infarction due
to Shock
Slide 13
Shock
Lung
Slide 14
Acute congestion of liver due to shock
Slide 15
Acute tubular necrosis of the kidney due to shock
Slide 16
Intestinal mucosal hemorrhages due to shock
Slide 17
Adrenal gland hemorrhage due to shock
Slide 18
Remember
History and Physical often limited by patients

condition
Patient presentation can be variable secondary

to
Severity of the perfusion defect
Underlying cause
Prior organ dysfunction
Exam should be tailored to be performed

quickly with highest yield for uncovering the
cause of shock.
Slide 19
Components (fluids, pump,

pipes)
Slide 20
Components:
Blood (fluid)
Heart (pump)
Blood Vessels
(pipes)
Slide 21
Types of Shock
Hypovolemic (fluids)
Cardiogenic (pump)
Redistributive (pipes)
(septic, neurogenic, anaphylactic)
Slide 22
Adequate circulating blood

volume depends on 3
components;
A minor impairment in one
can be compensated for by
the other 2 for a limited time.
Prolonged or severe
impairments will lead to
SHOCK.
22
Slide 23
An Approach to Shock Know

this!
BP = SVR x CO
BP = blood pressure
CO = cardiac output (pump & fluids)
SVR = systemic vascular resistance (pipes)
Slide 24
An Approach to Shock
If the blood pressure is low, then either the:
CO is low
or
SVR is low
or
BOTH
Slide 25
Low SVR
There are only a few causes of low SVR.
They ALL cause vasodilation:
Septic shock
Neurogenic (spinal cord injury) shock
Anaphylaxis Shock
Vasodilator (antihypertensive) Posioning
Slide 26
How do you assess SVR?

Look at and feel the patient!
Low SVR has the features:
warm !!!
pink
Bounding pulses
hyperdynamic heart (fast and
pounding)
Slide 27
What if the SVR is high?
Pale
Poor cap refill (>2 seconds)
Cool arms/legs (>2 degree C difference)
Thready pulses (narrow pulse pressure (incr DBP))
Cause of shock (low BP) is then:
low CO
Slide 28
What are factors of CO?
CO = HR x SV
CO = cardiac output
HR = heart rate
SV = stroke volume
Slide 29
HR Problems
Heart Rate problems are easy to diagnose
Rate: bradycardia versus tachycardia
Slide 30
Low SV (stroke volume)
Most difficult to diagnose

and manage
Slide 31
Stroke Volume depends on

Preload--is the ventricle full?
Hypovolemic Shock
Obstructive Shock (ie Tension PTX, Tamponade)
Cardiac function
SqueezeContractility can the ventricle contract?
Can blood get out? Valve function:
normal?
regurgitation?
stenosis?
Slide 32
Perfusion (blood pressure) depends on:

BP = CO x SVR
CO = HR x SV
SV = preload & cardiac contractility-valve
Slide 33
Components of BP summary
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Slide 34
Why Monitor?
Essential to understanding their disease
Describe the patients physiologic status
Facilitates diagnosis and treatment of shock
Serial monitoring
Slide 35
Monitoring clinical shock parameter

Noninvasive
Blood pressure (SBP, MAP)
Urine output
Heart rate
Shock index
Invasive
Pulmonary artery catheter: CVP,
PAWP, CO, SVR, DO2I, VO2I,
SvO2
Arterial catheter: ABP, Serum
lactate,
Base deficit
Slide 36
Diagnosis of Shock
MAP < 60 or decrease

of 20 from baseline
systolic BP 90
systolic BP > 40 mm
Hg from the patients
baseline pressure
Shock index (HR>SBP)
Clinical s/s of
hypoperfusion of vital
organs
Slide 37
Mean Arterial Pressure
MAP is the mean perfusion pressure for the tissues

Most require a MAP of 60 or greater!
Dependent only on the elastic properties of the

arterial walls and the mean blood volume in the
arterial tree
MAP = (2 x DBP) + SBP

3
Slide 38
Pulse Pressure=SBP-DBP
The difference between the systolic (fxn of
ejection fraction) and diastolic pressures (function of
SVR and distensibility (elastic recoil) of the aorta
Wide
Normal 30-50 mmHg

Commonly seen with fever,
anemia, exercise and
hyperthyroidism
AR (aortic regurgitation) is
also a cause
Narrow
May indicate an increase

in vascular resistance with
decreased stroke volume
(ie aortic stenosis or
decreased intravascular
volume)
Slide 39
Invasive Markers
Global Markers
Regional Markers
Base Deficit
Lactate
Gastric pH
Sublingual CO2
Slide 40
Base Deficit
Inadequate tissue perfusion leads to tissue
acidosis
Amount of base required to titrate 1 L of
whole arterial blood to a pH of 7.4
Normal range +3 to 3 mmol per L
Elevated base deficit correlates with the
presence and severity of shock
Slide 41
Base Deficit
Inadequate tissue perfusion leads to tissue
acidosis
Amount of base required to titrate 1 L of
whole arterial blood to a pH of 7.4
Normal range +3 to 3 mmol per L
Elevated base deficit correlates with the
presence and severity of shock
Slide 42
Initial Lactate
Weil and Afifi. (Circulation 1970)
Slide 43
Lactate and Outcomes

A peak blood
Adult Patients
lactate level
of >4.0 mmol/L
was identified as a
strong
independent
predictor of
mortality
and morbidity
and suggests that
tissue
hypoperfusion
Demmers Ann Thorac Surg 70:2082-6:2000

Slide 44
Slide 45
Gastric Intramucosal pH
Blood flow is not uniformly distributed to all tissue
beds
Regions with inadequate tissue perfusion may exist
while global markers are normal
Gut mucosa among the first to be affected during
shock and the last to be restored to normal
Intramucosal pH falls when perfusion becomes
inadequate
Slide 46
Sublingual capnometry:
A new noninvasive measurement for diagnosis and
quantitation of severity of circulatory shock
hypercarbia is a universal indicator of critically reduced

tissue perfusion.
Slide 47
Sublingual CO2
Decrease gut perfusion
Gastric tissue = esophagus = sublingual tissue
Non-invasive, hand held monitor

Rapid measurement
Sensitive marker of decreased blood flow
Slide 48
Sublingual capnometry:
A new noninvasive measurement for diagnosis and
quantitation of severity of circulatory shock
P SL CO2
provides a
prompt
indication of the
reversal of
tissue
hypercarbia
when
circulatory
shock is
reversed
Slide 49
Direct arterial pressure

A-line
Slide 50
Pulmonary Artery Catheter
INDICATIONS
COMPLICATIONS
volume status
cardiac status
technical
anatomic
physiologic
Slide 51
Swan-Ganz Catheter
Slide 52
PLACEMENT
Slide 53
Correct PA-C Position
From the RIJ approach, the RA is entered at

approximately 25 cm, the RV at
approximately 30 cm, and the PA at
approximately 40 cm; the PCWP can be
identified at approximately 45 cm.
Slide 54
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
Slide 55
Why Index?
Body habitus and size is individual
Indexing to patient with BSA allows for

reproducible standard
PATIENT A
60 yo male
50 kg
CO = 4.0 L/min
BSA = 1.86
CI = 2.4 L/min/m2
PATIENT B
60 yo male
150 kg
CO = 4.0 L/min
BSA = 2.64
CI = 1.5 L/min/m2
Slide 56
Slide 57
PA Insertion
20
15
10
5
RA = 5
RV = 22/4
0
PA 19/10
PAOP(wedge) = 9
Slide 58
CVP
CVP of SVC at level of right atrium

pre-load assessment
normal 4 - 10 mm Hg
Slide 59
PAOP (wedge)
End expiration
Wedge adjustment with positive pressure
Measured PAOP - PEEP = real PAOP
Slide 60
Vascular Resistance
SYSTEMIC (SVR)
MAP - CVP
x 80
C0
SVR = vasoconstriction
SVR = vasodilation
PULMONARY (PVR)
MPAP - PAOP
CO
PVR = constriction
PE, hypoxia
Vascular resistance = change in pressure/blood flow

x 80
Slide 61
Cardiac Cycle
PVR
MPAP
RVSW
pulmonary
Right ventricle
CVP
Left ventricle
systemic
SVR
PCWP
MAP
LVSW
Slide 62
Swan Ganz interpretation

Etiology
CO
PCWP
SVR
cardiogenic
decreased
increased
increased
hypovolemic
decreased
decreased
increased
distributive
increased
decreased
decreased
Slide 63
Too Many Numbers
Slide 64
Definitions
O2 Delivery - volume of gaseous O2
delivered to the LV/min.
O2 Consumption - volume of gaseous O2
which is actually used by the tissue/min.
consumption > demand = anaerobic metabolism
Slide 65
Mixed venous oxygen saturation

Reflects difference between oxygen delivery
and consumption
Normal 65-75%
Measurement taken from the distal port of a
PA catheter
Slide 66
SvO2: Low Values (< 60%)
CO/CI
Hgb
SaO2
O2 consumption
SV/SVI
Slide 67
SvO2: High Values (> 75%)
Sepsis
AV shunts/fistulae
Slide 68
Oxycalculations
Slide 69
Break Time
Slide 70
Goals of Shock
Resuscitation
Restore
blood pressure
Normalize
Preserve
systemic perfusion
organ function
Slide 71
Parameters of Adequate
Resuscitation
Urine output (0.5 - 1.0 ml/kg/hr)
acceptable renal perfusion
Reversal of lactic acidosis (nl. pH)
improved perfusion
Normal mental status
adequate cerebral perfusion
Slide 72
SHOCK: an EMERGENCY !!!

Goal RAPIDLY RESTORE TISSUE PERFUSION
Recognize
it !!!
Immediate stabilization: ABC
. SHOTGUN approach
Normalization of BP, pulse, UOP
Hemodynamic parameters
Restoration of aerobic
metabolism, elimination of tissue
acidosis, repayment of O2 debt
Treat the cause

Slide 73
Shock is a symptom of its

cause.
-fccs course
73
Slide 74
In general, treat the

cause...
Slide 75
Management
ABCs
Maintain airway
Decrease work of breathing & Optimize 02
Circulation & Control Hemorrhage includes:
Direct pressure
Pressure points
Fluids & Drugs
Must address and treat:

PRELOAD
AFTERLOAD
PUMP
Re-assess every 5-15 minutes

(the sicker the patient, the shorter the interval
Slide 76
Management priorities
in hypoperfused states
Priority # Physiology to Intervention
improve
1
Volume
Fluids
Pressure
Vasopressor
Flow
Inotrope
Parameter to target
CVP 10-15
PAC
targets
DO2
Low Sao2
See CXR
Low SV, DO2
High HR,
Resistances
DO2
Low BP, SV,

Resistances
SBP? 100 or within 20-25

torr
MBP ? 80 of patient's Nl
Signs of perfusion
BP potency: Dopamine...NEVasopressin/Phenylephrine
When in doubt, try a little more volume

Avoid
Slide 77
Hypovolemia
Slide 78
Time
Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV)
allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal
Slide 79
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
Slide 80
Clinical Signs of Acute

Hemorrhagic Shock
% Blood loss
< 15
Clinical Signs
Slightly increased heart rate
15-30
Increased HR, increased DBP (narrow pp),

prolonged capillary refill, flat neck veins
30-50
Above findings plus: hypotension,

confusion, acidosis, decreased urine output
> 50
Refractory hypotension, refractory

acidosis, death
Slide 81
Hypovolemic Shock
Causes
hemorrhage
vomiting
diarrhea
dehydration
third-space loss
burns
Signs
cardiac output
PAOP/CVP
SVR
Slide 82
Treatment - Hypovolemic
Reverse hypovolemia & hemorrhage control

Crystalloid vs. Colloid
1 L crystalloid 250 ml colloid
Watch for fluid overload by reassessing lung sounds

3:1 Rule (3cc crystalloid for 1cc bld loss)
Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused
Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus
Colloids: (ex: albumin)

Will increase osmotic pressure, watch for pulm edema
Remain in vascular space longer (several hrs)
NOT increase survival
prbc sooner than later
500 ml whole blood increases Hct 2-3%, 250ml PRBCs increases Hct 3-4%
Increases oxygen carrying capacity
Used with acute hemorrhaging (mntn Hct 24% and Hgb 8g/dL)
NOT FOR VOLUME
FFP for coagulopathy (all factors)

Factor vii
PLT for thrombocytopenia
Pressors?
Slide 83
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.
Slide 84
Role of PASG?
Higher mortality rate in penetrating thoracic, cardiac

trauma
Role undefined in rural, blunt trauma
Splinting role
Slide 85
Cardiogenic Shock
Mech
Signs
defect in cardiac function (lost > 40% Fxn)

cardiac output
PAOP/CVP
SVR
left ventricular stroke work (LVSW)
Slide 86
Cardiogenic Shock
Myocardial failure (MI)
Severe Arrhythmia
Severe Valvular dysfunction
Reduction in cardiac output:

>Decreased oxygen delivery
Slide 87
Symptoms of Cardiogenic
Shock
Skin: progressive peripheral vasoconstriction

results in cool, moist, pale skin with mottling
CHF Sx
JVD, HJR, APE, pedal edema
Heart:
Sounds: d/t enlargement and congestion you can

hear murmurs or S3 or S4
Pulse: rapid rate and thready/weak pulse
BP: decreased BP and MAP

UO: decreases early d/t decreased renal
perfusion
Slide 88
Cardiogenic Shock
Assess for:
Signs of heart failure
Signs of tamponade
Cardiac dysrrhythmia
Myocardial infarction
Tachycardia
Muffled heart sounds or third heart sound
Engorged neck veins with hypotension
Dyspnea
Edema in feet and ankles
Slide 89
Coronary Perfusion
Pressure
Coronary PP = DBP - PAOP
coronary perfusion = P across coronary a.
GOAL - Coronary PP > 50 mm Hg

Slide 90
Treatment of Cardiogenic
Shock
Increase oxygen supply to the heart
Decrease O2 consumption (pain meds/sedation)

Increase O2 delivery (Mech vent, reperfusion of the
coronary arteries)
Maximize the cardiac output
Mntn normal rhythm (dysrhythmics, pacing,

cardioversion)
Diastolic Vasopressors (dopamine, epi, norepi,
vasopressin)
Improve myocardial contractility--Inotropes
dobut and amrinone
Decrease the afterload (workload of the LV)

IABP
LVAD
Slide 91
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 & LV assist devices
Slide 92
Intra-Aortic Balloon Pump
Slide 93
Distributive Shock
Types
Sepsis
Anaphylactic
Acute adrenal insufficiency
Neurogenic
Signs
cardiac output
PAOP
SVR
Slide 94
Anaphylaxis
Slide 95
Anaphylactic Shock
Rapid onset
Diffuse vasodilation mechanism from
histamine & bradykinin
Edema from increased capillary permeability
Bronchoconstriction
Slide 96
Symptoms
Onset within seconds and
progression to death in minutes
Cutaneous manifestations
urticaria, erythema, pruritis,
angioedema
Respiratory compromise
stridor, wheezing, bronchorrhea, resp.
distress
Circulatory collapse
tachycardia, vasodilation,
hypotension
CNS
apprehension->ams->coma
Slide 97
Diagnosis
History and physical alone make the
diagnosis
Lab values serve no role
Histamine levels are elevated for about 30 min,

tryptase for several hours.
Slide 98
Treatment
Remove the antigen

ABCs
IV Fluids, O2, cardiac monitor, pulse ox
First line Rx:
Epinephrine
For severe bronchospasm, laryngeal edema, signs
of upper airway obstruction, respiratory arrest or
shock: IV epi
100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in
10 mL of NS, give over 5-10 min)
If less severe, can give 0.3-0.5 mL 1:1000 SC
Slide 99
Treatment
2nd line:
H1 blocker: Diphenhydramine 25-50 mg IV
H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)
Steroids (Methylprednisolone 125 mg IV or Prednisone
40-60 mg po)
Albuterol
For patients taking Beta-blockers with refractory
hypotension, think about glucagon
Slide 100
Septic Shock
Slide 101
SEPSIS
Systemic Inflammatory Response (SIRS)

manifested by two or > of following:
Temp > 38 or < 36 centigrade

HR > 90
RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or > 10% Bands (immature
wbc)
Slide 102
Risk factors of Sepsis
Extreme age: <1 and >65 years

Surgical / invasive procedures
Malnutrition
Chronic illness
DM, CRF, Hepatitis
Compromised immune status
Drug resistant organisms
AIDS, immunosuppressives, EtOH, malignancies
Slide 103
What is Sepsis?
SIRS Sepsis Severe Sepsis Septic

Shock
Sepsis is the combination of the Systemic

Inflammatory Response Syndrome (SIRS) & a
confirmed or presumed infectious etiology.
Severe Sepsis: SIRS criteria, source of infection and
infection-induced organ dysfunction or hypoperfusion
abnormalities (sepsis + lactic
acidosis/oliguria/AMS/etc.)
Septic Shock: SIRS criteria, source of infection, and
hypotension not reversed with fluid resuscitation and
associated with organ dysfunction or hypoperfusion
abnormalities
Slide 104
Septic Shock
Bacterial, viral, fungal infection
Warm shock is early stage

Fever, tachycardia, tachypnoea,
leucocytosis,
inadequate oxygen extraction (High
SvO2, Metabolic acidosis) in infected
tissues
Cold shock is late stage
Slide 105
Septic/Inflammatory Shock
Signs:
Early warm w/ vasodilation, often adequate urine

output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Earlyhyperglycemia, respiratory

alkylosis, hemoconcentration,
WBC typically normal or low.
Late Leukocytosis, lactic acidosis
Very Late Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.
Slide 106
Septic Shock TX
Prompt volume replacement - fill the tank
Early antibiotic administration - treat the cause
If MAP < 60
Dopamine = 2 - 3 g/kg/min
Norepinephrine = titrate (1-100 g/min)
Slide 107
Neurogenic shock
Slide 108
Neurogenic Shock
Essential derangement:
paralysis of the
sympathetic chain which
controls vascular tone from
injury to thoracic or
cervical level spinal cord
injury.
Produces decreased SVR
from loss of vascular tone
and bradycardia from
unopposed
parasympathetic input to
SA node.
Slide 109
Neurogenic (Vasogenic) Shock
Caused by:
Spinal cord injury loss of SNS
Massive venous pooling & arteriolar dilatation

Signs and Symptoms:
Hypotension without tachycardia

Warm pink skin from cutaneous vasodilation
Low BP w/ minimal response to fluids
Accompanying Neurologic deficit
Spinal shock is not Neurogenic shock

Spinal Shock: the temporary loss of spinal reflex activity
that occurs below a total or near total spinal cord injury
Slide 110
Treatment of Neurogenic
Shock
Increase vascular tone and improve CO

Increase preload with fluids
CVP
PAWP
Increase vascular tone

Vasopressors
Maintain heart rate

Treat bradycardia if symptomatic
Maintain adequate oxygenation

Watch with SCI because of the disruption of O2 to the medulla
Initiate therapy to prevent DVT
Sluggish venous flow will increase risk factors

Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then
5.4 mg/kg/hr x 23 hours)
There are contradicting studies, all of which have flaw
The symptoms of neurogenic shock typically last 1-3 weeks
Slide 111
Obstructive Shock
Causes
Cardiac Tamponade
Tension Pneumothorax
Massive Pulmonary Embolus
Signs
cardiac output
PAOP/CVP
SVR
Treatment
Needle decompression
Embolectomy / TPA
Slide 112
Adrenal Crisis
Distributive Shock
Causes
Autoimmune adrenalitis
Adrenal apoplexy = B hemorrhage or infarct
This is suspected when patient is nonresponsive to fluids, vasopressors and

antibiotics.
Electrolytes may reveal hypoNa+ & hyperK+
Steroids may be lifesaving in patient who is
unresponsive to fluids-inotropic-vasopressor
(hydrocortisone 100mg IV)
Slide 113
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
Slide 114
Vasopressors & Inotropic

Agents
Dopamine
Dobutamine
Norepinephrine
Epinephrine
Amrinone
Slide 115
Dopamine
Low dose (0.5 - 2 g/kg/min) = dopaminergic
Moderate dose (3-10 g/kg/min) = -effects
High dose (> 10 g/kg/min) = -effects
SIDE EFFECTS
tachycardia
> 20 g/kg/min to norepinephrine
Slide 116
Dobutamine
-agonist
5 - 20 g/kg/min
potent inotrope, variable chronotrope
caution in hypotension (inadequate volume)

may precipitate tachycardia or worsen
hypotension
Slide 117
Norepinephrine
Potent -adrenergic vasopressor
Some -adrenergic, inotropic, chronotropic
Dose 1 - 100 g/min
Unproven effect with low-dose dopamine to protect

renal and mesenteric flow.
Slide 118
Epinephrine
- and -adrenergic effects
potent inotrope and chronotrope
dose 1 - 10 g/min
increases myocardial oxygen consumption

particularly in coronary heart disease
Slide 119
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
Slide 120
vasopressin
V1 vascular smooth muscle receptor
vasoconstriction
0.01-0.04 units/min
Risk: coronary, mesenteric ischemia,
hyponatremia, skin necrosis
Slide 121
Calcium Sensitisation by
Levosimendan
Enhanced contractility of myocardial cell

by amplifying trigger for contraction with
no change in total intracellular Ca2+
Clinical trials
status
Slide 122
Endpoints?
ACS / ATLS - restoration of vital signs and

evidence of end-organ perfusion
Swan-guided resuscitation
C.I. 4.5, DO2I 670, VO2I 166
Lactic Acid clearance
Gastric pH
Slide 123
Dont forget...
Shock: rude unhinging of the
machinery of life.
-Samuel D. Gross, 1872
123
Slide 124
??????????? For the human

speaker

Shock VT

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Slide 1

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Compensated /Early Shock

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Early Signs of Shock in

WARM EARLY STAGE / PRESHOCK

Need high index of suspicion b/c lack of signs

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Signs of Late Shock

Cold, clammy and pale skin

Rapid, weak, thready pulse

Rapid breathing (blow off CO2 met acidosis)

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End Stage Clinical effects

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Multiple Organ Dysfunction Syndrome

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Acute congestion of liver due to shock

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Acute tubular necrosis of the kidney due to shock

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Intestinal mucosal hemorrhages due to shock

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Adrenal gland hemorrhage due to shock

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History and Physical often limited by patients

Patient presentation can be variable secondary

Exam should be tailored to be performed

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Components (fluids, pump,

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Adequate circulating blood

An Approach to Shock Know

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How do you assess SVR?

What if the SVR is high?

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What are factors of CO?

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Heart Rate problems are easy to diagnose

Rate: bradycardia versus tachycardia

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Low SV (stroke volume)

Most difficult to diagnose

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Stroke Volume depends on

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Perfusion (blood pressure) depends on:

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Essential to understanding their disease

Describe the patients physiologic status

Facilitates diagnosis and treatment of shock

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Monitoring clinical shock parameter

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MAP < 60 or decrease

Mean Arterial Pressure