Transcript Shock

Slide 1
SHOCK
DOOMSDAY
1
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Slide 2
Vicken Y. Totten
Shock lecture
 Thanks to David Cheng MD
 And all who taught me

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Slide 3
Definition
SHOCK:
inadequate organ
perfusion to meet
the tissue’s
oxygenation
demand
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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
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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)
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Slide 6
Symptoms of Shock
General Symptoms






Anxious
Dizziness
Weakness
Faintness
Thirsty
“I am sick”
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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
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Slide 8
“Hypoperfusion can be
present in the absence of
significant hypotension.”
(Don’t only relay on BP for
diagnosisng shock)
-fccs course
8
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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
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Slide 10
End Stage Clinical effects

Cardiovascular
– Myocardial
depression
– Vasogenic effects

Pulmonary

– Ischemic bowel


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Hematologic
– Neutropenia,
Thrombocytopenia
– DIC (Gm- > Gm+)
Renal
– ARF
Hepatic
– Increased LFT’s, liver failure
– ARDS

GI

CNS
– coma
Slide 11
Multiple Organ Dysfunction Syndrome
Number of
Organs
Mortality (%)
0
0.8
1
6.8
2
26.2
3
48.5
4
68.8
5
83.3
*Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837
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Slide 12
Circumferential
Subendocardial
Infarction due
to Shock
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Slide 13
Shock
Lung
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Slide 14
Acute congestion of liver due to shock
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Slide 15
Acute tubular necrosis of the kidney due to shock
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Slide 16
Intestinal mucosal hemorrhages due to shock
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Slide 17
Adrenal gland hemorrhage due to shock
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Slide 18
Remember

History and Physical often limited by patient’s
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.
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Slide 19
Components (fluids, pump,
pipes)
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Slide 20

Components:
– Blood (fluid)
– Heart (pump)
– Blood Vessels
(pipes)
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Slide 21
Types of Shock
Hypovolemic (fluids)
Cardiogenic (pump)
Redistributive (pipes)
(septic, neurogenic, anaphylactic)
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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
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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)
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Slide 24
An Approach to Shock
If the blood pressure is low, then either the:
CO is low
or
SVR is low
or
BOTH
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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
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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)
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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
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Slide 28
What are factors of CO?
CO = HR x SV
CO = cardiac output
HR = heart rate
SV = stroke volume
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Slide 29
HR Problems
•
Heart Rate problems are easy to diagnose
•
Rate: bradycardia versus tachycardia
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Slide 30
Low SV (stroke volume)
Most difficult to diagnose
and manage
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Slide 31
Stroke Volume depends on
Preload--is the ventricle full?
Hypovolemic Shock
Obstructive Shock (ie Tension PTX, Tamponade)
Cardiac function
SqueezeContractility– can the ventricle contract?
Can blood get out?  Valve function:
normal?
regurgitation?
stenosis?
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Slide 32
Perfusion (blood pressure) depends on:
BP = CO x SVR
CO = HR x SV
SV =preload & cardiac contractility-valve
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Slide 33
Components of BP summary
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P
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Slide 34
Why Monitor?

Essential to understanding their disease

Describe the patient’s physiologic status

Facilitates diagnosis and treatment of shock
– Serial monitoring
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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
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Slide 36
Diagnosis of Shock
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MAP < 60 or decrease
of 20 from baseline
systolic BP  90
 systolic BP > 40 mm
Hg from the patient’s
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
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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
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
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
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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

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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

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Slide 42
Initial Lactate
Weil and Afifi. (Circulation 1970)
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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
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Slide 44
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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

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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.
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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

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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
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Slide 49
Direct arterial pressure
A-line
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Slide 50
Pulmonary Artery Catheter

INDICATIONS

COMPLICATIONS
– volume status
– cardiac status
– technical
– anatomic
– physiologic
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Slide 51
Swan-Ganz Catheter
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Slide 52
PLACEMENT
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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.
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Slide 54
Standard Parameters

Measured
– Blood pressure
– Pulmonary A.
pressure
– Heart rate
– Cardiac Output
– Stroke volume
– Wedge pressure
– CVP
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
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
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



PATIENT B
60 yo male
150 kg
CO = 4.0 L/min
BSA = 2.64
CI = 1.5 L/min/m2
Slide 56
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Slide 57
PA Insertion
20
15
10
5
RA = 5
RV = 22/4
0
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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
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Slide 59
PAOP (wedge)

End expiration
 Wedge adjustment with positive pressure
– Measured PAOP - ½ PEEP = “real PAOP”
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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
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x 80
Slide 61
Cardiac Cycle
PVR
MPAP
RVSW
pulmonary
Right ventricle
CVP
Left ventricle
systemic
SVR
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PCWP
MAP
LVSW
Slide 62
Swan Ganz interpretation
Etiology
CO
PCWP
SVR
cardiogenic
decreased
increased
increased
hypovolemic
decreased
decreased
increased
distributive
increased
decreased
decreased
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Slide 63
Too Many Numbers
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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
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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

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Slide 66
SvO2: Low Values (< 60%)

 CO/CI

 Hgb

 SaO2

 O2 consumption
– SV/SVI
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Slide 67
SvO2: High Values (> 75%)

Sepsis

AV shunts/fistulae
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Slide 68
Oxycalculations
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Slide 69
Break Time…
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Slide 70
Goals of Shock
Resuscitation
 Restore
blood pressure
 Normalize
 Preserve
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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
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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
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Slide 73
“Shock is a symptom of its
cause.”
-fccs course
73
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Slide 74
In general, treat the
cause...
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Slide 75
Management

ABC’s
– 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
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Slide 76
Management priorities
in hypoperfused states
Priority # Physiology to Intervention
improve
1
Volume
Fluids
2
Pressure
Vasopressor
3
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...NE…Vasopressin/Phenylephrine
When in doubt, try a little more volume
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Avoid
Slide 77
Hypovolemia
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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
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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
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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
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Slide 81
Hypovolemic Shock

Causes
– hemorrhage
– vomiting
– diarrhea
– dehydration
– third-space loss
– burns
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
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 PRBC’s 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?
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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.
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Slide 84
Role of PASG?

Higher mortality rate in penetrating thoracic, cardiac
trauma

Role undefined in rural, blunt trauma

Splinting role
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Slide 85
Cardiogenic Shock

Mech

Signs
– defect in cardiac function (lost > 40% Fxn)
–  cardiac output
–  PAOP/CVP
–  SVR
–  left ventricular stroke work (LVSW)
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Slide 86
Cardiogenic Shock

Myocardial failure (MI)

Severe Arrhythmia

Severe Valvular dysfunction

Reduction in cardiac output:
– >Decreased oxygen delivery
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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
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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
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Slide 89
Coronary Perfusion
Pressure
Coronary PP = DBP - PAOP
coronary perfusion =  P across coronary a.
GOAL - Coronary PP > 50 mm Hg
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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
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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
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Slide 92
Intra-Aortic Balloon Pump
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Slide 93
Distributive Shock

Types
–
–
–
–

Sepsis
Anaphylactic
Acute adrenal insufficiency
Neurogenic
Signs
– ± cardiac output
–  PAOP
– SVR
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Slide 94
Anaphylaxis
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Slide 95
Anaphylactic Shock

Rapid onset

Diffuse vasodilation mechanism from
histamine & bradykinin

Edema from increased capillary permeability

Bronchoconstriction
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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
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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.
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Slide 98
Treatment

Remove the antigen
 ABC’s
 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
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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
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Slide 100
Septic Shock
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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)
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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
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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
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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
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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: Early—hyperglycemia, respiratory
alkylosis, hemoconcentration,
WBC typically normal or low.
Late – Leukocytosis, lactic acidosis
Very Late– Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.
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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)
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Slide 107
Neurogenic shock
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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.
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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
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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
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Slide 111
Obstructive Shock

Causes
– Cardiac Tamponade
– Tension Pneumothorax
– Massive Pulmonary Embolus

Signs
–  cardiac output
–  PAOP/CVP
–  SVR

Treatment
Needle decompression
Embolectomy / TPA
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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)
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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
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Slide 114
Vasopressors & Inotropic
Agents


Dopamine
Dobutamine
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
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
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Slide 116
Dobutamine

-agonist

5 - 20 g/kg/min

potent inotrope, variable chronotrope

caution in hypotension (inadequate volume)
may precipitate tachycardia or worsen
hypotension
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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.
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Slide 118
Epinephrine

- and -adrenergic effects

potent inotrope and chronotrope

dose 1 - 10 g/min

increases myocardial oxygen consumption
particularly in coronary heart disease
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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

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Slide 120
vasopressin
V1 vascular smooth muscle receptor
vasoconstriction
 0.01-0.04 units/min
 Risk: coronary, mesenteric ischemia,
hyponatremia, skin necrosis

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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
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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
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Slide 123
Don’t forget...
Shock: “rude unhinging of the
machinery of life.”
-Samuel D. Gross, 1872
123
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Slide 124
??????????? For the human
speaker
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