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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 ≤ 90 mm Hg
– mean arterial pressure ≤ 60 mm Hg
  systolic BP > 40 mm Hg from the
patient’s baseline pressure
Definition
SHOCK: inadequate organ perfusion
to meet the tissue’s oxygenation
demand.
“Hypoperfusion can be
present in the absence of
significant hypotension.”

-fccs course
Pathophysiology
ATP + H2O ⇒ ADP + Pi + 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 patient’s physiologic
status
• Facilitates diagnosis and treatment of
shock
History
• 1960’s
– low BP = shock; MSOF resulted after BP
restored

• 1970’s
– Swan & Ganz - flow-directed catheter
– thermistor → cardiac output

• 1980’s
– 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
West’s Lung Zones
• Zone I - PA > Pa > Pv
• Zone II - Pa > PA > Pv
• Zone III - Pa > Pv > PA

• PA = alveolar
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/m2

PATIENT B
•
•
•
•

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

CI = 1.5 L/min/m2
PA Insertion
20
15
10
5
RA = 5

0

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
PVRI

MPAP

RVSWI

pulmonary

Right ventricle

CVP

PCWP

Left ventricle

systemic
SVRI

MAP

LVSWI
Hemodynamic Calculations
Parameter
Cardiac Index (CI)

Normal
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

x 80

↑ SVR = vasoconstriction
↓ SVR = vasodilation

PULMONARY (PVRI)
MPAP - PAOP
CI

x 80

↑PVR = constriction
PE, hypoxia

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 = ∆ pressure x vol. ejected
Too Many Numbers
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.
• O2 Demand - volume of O2 actually
needed by the tissues to function in an
aerobic manner
Demand > consumption = anaerobic metabolism
Rationale for Improving
O2 Delivery
Insult
Tissue Hypoxia
Demands are met
Increased Delivery
Increased Consumption
VO2I

Critical O2 Delivery

The critical value is
variable
& is dependent upon the
patient, disease, and the
metabolic demands of the
patient.

DO2I
Oxygen Calculations
• Arterial Oxygen Content
(CaO2)
• Venous Oxygen Content
(CvO2)
• Arteriovenous Oxygen
Difference (avDO2)
• Delivery (O2AVI)
• Consumption (VO2I)

Efficiency of
the
oxygenation
of blood and
the rates of
oxygen
delivery and
consumption
Arterial Oxygen Content
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031)

If low, check hemoglobin or pulmonary gas
exchange
Arteriovenous Oxygen
Difference
avDO2 = CaO2 - CvO2
Values > 5.6 suggests more
complete tissue oxygen
extraction, typically seen in
shock
Oxygen Delivery (DO2I)
O2AVI = CI x CaO2 x 10
Normal values suggests that the heart
& lungs are working efficiently to
provide oxygen to the tissues.
< 400 is bad sign
Oxygen Consumption
VO2I = CI x (CaO2 - CvO2)
If VO2I < 100 suggest tissues are not
getting enough oxygen
SvO2

SvO2 =

1-

VO2
DO2
Oxycalculations
Resuscitation Goals
• CI = 4.5 L/min/m2
• DO2I = 600 mL/min/m2
• VO2I = 170 mL/min/m2
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
• Signs
  cardiac
– hemorrhage
output
– vomiting
  PAOP
– diarrhea
  SVR
– dehydration
– third-space loss
– burns
Classes of Hypovolemic Shock
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 = ∆ 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 µg/kg/min
– Norepinephrine = titrate (1-100 µg/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, DO2I ≥ 670, VO2I ≥ 166
• Lactic Acid clearance
• Gastric pH
Summary
Type

PAOP

C.O.

SVR

HYPOVOLEMIC

↓

↓

↑

CARDIOGENIC

↑

↓

↑

DISTRIBUTIVE

↓ or N

OBSTRUCTIVE

↑

varies
↓

↓
↑
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

• Norepinephrine

• Dobutamine

• Epinephrine
• Amrinone
Dopamine
• Low dose (0.5 - 2 µg/kg/min) = dopaminergic
• Moderate dose (3-10 µg/kg/min) = β-effects
• High dose (> 10 µg/kg/min) = α-effects
• SIDE EFFECTS
– tachycardia
– > 20 µg/kg/min ∆ to norepinephrine
Dobutamine
∀ β-agonist
• 5 - 20 µg/kg/min
• potent inotrope, variable chronotrope
• caution in hypotension (inadequate volume)
may precipitate tachycardia or worsen
hypotension
Norepinephrine
• Potent α-adrenergic vasopressor
• Some β-adrenergic, inotropic, chronotropic
• Dose 1 - 100 µg/min
• Unproven effect with low-dose dopamine to
protect renal and mesenteric flow.
Epinephrine
∀ α- and β-adrenergic effects
• potent inotrope and chronotrope
• dose 1 - 10 µg/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 µg/kg/min
drip
• main side-effect - thrombocytopenia
Dilators

- inotropes

+ inotropes

Pressors
Summary `pressors & inotropes
dilator
Labetalol
+2
Ca blocker

ACE inhibitor
hydralazine
nitroglycerine
Nipride

β-blocker - inotrope

Dobutamine
Milrinone/Amrinone
β-dopamine

+ inotrope

Isuprel
Digoxin
Calcium

epinephrine
α-dopamine

pressor
neosynephrine

norepinephrine
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, SpO2 = 91,
UOP = 25 cc/hr
What do you think...
HYPOVOLEMIA
ADJUST YOUR WEDGE FOR THE
PEEP
Wedge Adjustment
• Measured PAOP - ½ 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 µg/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 µg 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
Don’t forget...
Shock: “rude unhinging of the
machinery of life.”

-Samuel D. Gross, 1872
Shock

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Shock

  • 1. Shock Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina
  • 2. 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
  • 3. 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.
  • 4. Shock: “A momentary pause in the act of death.” -John Collins Warren, 1800s
  • 5. Hypotension • In Adults: – systolic BP ≤ 90 mm Hg – mean arterial pressure ≤ 60 mm Hg   systolic BP > 40 mm Hg from the patient’s baseline pressure
  • 6. Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand.
  • 7. “Hypoperfusion can be present in the absence of significant hypotension.” -fccs course
  • 8. Pathophysiology ATP + H2O ⇒ ADP + Pi + 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
  • 9. 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.
  • 10. Why Monitor? • Essential to understanding their disease • Describe the patient’s physiologic status • Facilitates diagnosis and treatment of shock
  • 11. History • 1960’s – low BP = shock; MSOF resulted after BP restored • 1970’s – Swan & Ganz - flow-directed catheter – thermistor → cardiac output • 1980’s – resuscitation based on oxygen delivery, consumption & oxygen transport balance.
  • 13. Pulmonary Artery Catheter • INDICATIONS – volume status – cardiac status • COMPLICATIONS – technical – anatomic – physiologic
  • 15. West’s Lung Zones • Zone I - PA > Pa > Pv • Zone II - Pa > PA > Pv • Zone III - Pa > Pv > PA • PA = alveolar
  • 17. 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
  • 18. 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
  • 19. Index Example 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
  • 20. PA Insertion 20 15 10 5 RA = 5 0 RV = 22/4 PA 19/10 PAOP = 9
  • 21. CVP • • • • CVP of SVC at level of right atrium pre-load “assessment” normal 4 - 10 mm Hg limited value
  • 22. PAOP • End expiration • Reflection changes with positive pressure • Waveforms change ≈ every 20 cm
  • 23. Waveform Analysis • A wave - atrial systole • C wave - tricuspid valve closure @ ventricular systole • V wave - venous filling of right atrium
  • 25. Hemodynamic Calculations Parameter Cardiac Index (CI) Normal 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
  • 26. 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
  • 27. Vascular Resistance Index SYSTEMIC (SVRI) MAP - CVP CI x 80 ↑ SVR = vasoconstriction ↓ SVR = vasodilation PULMONARY (PVRI) MPAP - PAOP CI x 80 ↑PVR = constriction PE, hypoxia Vascular resistance = change in pressure/blood flow
  • 28. 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 = ∆ pressure x vol. ejected
  • 30. 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. • O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner Demand > consumption = anaerobic metabolism
  • 31. Rationale for Improving O2 Delivery Insult Tissue Hypoxia Demands are met Increased Delivery Increased Consumption
  • 32. VO2I Critical O2 Delivery The critical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient. DO2I
  • 33. Oxygen Calculations • Arterial Oxygen Content (CaO2) • Venous Oxygen Content (CvO2) • Arteriovenous Oxygen Difference (avDO2) • Delivery (O2AVI) • Consumption (VO2I) Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption
  • 34. Arterial Oxygen Content CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031) If low, check hemoglobin or pulmonary gas exchange
  • 35. Arteriovenous Oxygen Difference avDO2 = CaO2 - CvO2 Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock
  • 36. Oxygen Delivery (DO2I) O2AVI = CI x CaO2 x 10 Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues. < 400 is bad sign
  • 37. Oxygen Consumption VO2I = CI x (CaO2 - CvO2) If VO2I < 100 suggest tissues are not getting enough oxygen
  • 40. Resuscitation Goals • CI = 4.5 L/min/m2 • DO2I = 600 mL/min/m2 • VO2I = 170 mL/min/m2 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.
  • 42. “Shock is a symptom of its cause.” -fccs course
  • 43. Signs of Organ Hypoperfusion • Mental Status Changes • Oliguria • Lactic Acidosis
  • 45. Categories of Shock • HYPOVOLEMIC • CARDIOGENIC • DISTRIBUTIVE • OBSTRUCTIVE
  • 46. Goals of Shock Resuscitation • Restore blood pressure • Normalize systemic perfusion • Preserve organ function
  • 47. In general, treat the cause...
  • 48. Hypovolemic Shock • Causes • Signs   cardiac – hemorrhage output – vomiting   PAOP – diarrhea   SVR – dehydration – third-space loss – burns
  • 50. Treatment - Hypovolemic • Reverse hypovolemia vs. hemorrhage control • Crystalloid vs. Colloid • PASG role? • Pressors?
  • 51. 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.
  • 52. 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
  • 53. 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
  • 54. Cardiogenic Shock • Cause – defect in cardiac function • Signs      cardiac output  PAOP  SVR  left ventricular stroke work (LVSW)
  • 55. Coronary Perfusion Pressure Coronary PP = DBP - PAOP coronary perfusion = ∆ P across coronary a. GOAL - Coronary PP > 50 mm Hg
  • 56. 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
  • 57. Distributive Shock • Types – – – – Sepsis Anaphylactic Acute adrenal insufficiency Neurogenic • Signs – ± cardiac output ± PAOP  SVR
  • 58. 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 µg/kg/min – Norepinephrine = titrate (1-100 µg/min) • R/O missed injury
  • 59. 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?
  • 60. Obstructive Shock • Causes – Cardiac Tamponade – Tension Pneumothorax – Massive Pulmonary Embolus • Signs   cardiac output   PAOP   SVR
  • 61. Endpoints? • ACS CoT 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
  • 63. 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
  • 64. Vasopressors & Inotropic Agents • Dopamine • Norepinephrine • Dobutamine • Epinephrine • Amrinone
  • 65. Dopamine • Low dose (0.5 - 2 µg/kg/min) = dopaminergic • Moderate dose (3-10 µg/kg/min) = β-effects • High dose (> 10 µg/kg/min) = α-effects • SIDE EFFECTS – tachycardia – > 20 µg/kg/min ∆ to norepinephrine
  • 66. Dobutamine ∀ β-agonist • 5 - 20 µg/kg/min • potent inotrope, variable chronotrope • caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
  • 67. Norepinephrine • Potent α-adrenergic vasopressor • Some β-adrenergic, inotropic, chronotropic • Dose 1 - 100 µg/min • Unproven effect with low-dose dopamine to protect renal and mesenteric flow.
  • 68. Epinephrine ∀ α- and β-adrenergic effects • potent inotrope and chronotrope • dose 1 - 10 µg/min • increases myocardial oxygen consumption particularly in coronary heart disease
  • 69. 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 µg/kg/min drip • main side-effect - thrombocytopenia
  • 71. Summary `pressors & inotropes dilator Labetalol +2 Ca blocker ACE inhibitor hydralazine nitroglycerine Nipride β-blocker - inotrope Dobutamine Milrinone/Amrinone β-dopamine + inotrope Isuprel Digoxin Calcium epinephrine α-dopamine pressor neosynephrine norepinephrine
  • 73. 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.
  • 75. 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?
  • 76. SHOCK/HYPOVOLEMIA • FLUIDS… FLUIDS… FLUIDS… • BLOOD & PRODUCTS TRANSFUSION • CORRECT – ACIDOSIS – COAGULOPATHY – HYPOTHERMIA
  • 77. MVC • 38 year old female restrained driver who was involved in a high speed MVC. • She sustained a pulmonary contusion and fractured pelvis.
  • 78. ICU Course • Intubated and monitored with PA-C • PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8 • HR = 120, BP = 110/56, SpO2 = 91, UOP = 25 cc/hr What do you think...
  • 80. Wedge Adjustment • Measured PAOP - ½ PEEP = “real PAOP” • PEEP = 28, therefore “real wedge” = 8
  • 81. 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
  • 82.
  • 83.
  • 84. ICU Course • Pelvis “closed” • QID Dressings, intubated, PA-C inserted • PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8 Diagnosis? Treatment?
  • 85. Sepsis • Fluids • Correct the cause • Antibiotics • Debridement • Vasopressors – Phenylephrine – Levophed
  • 86. 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 µg/kg/min
  • 87. 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
  • 88. 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 µg po q day
  • 89. Geriatric Trauma • 70 year old female • MVC while talking on her cell phone • ruptured diaphragm and spleen s/p OR • Intubated and PA-C
  • 90. ICU Course • PCWP = 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7 Diagnosis? Treatment?
  • 91. Cardiogenic Shock • Preload augmentation - Consider Fluids • Contractility – dopamine – dobutamine – phosphodiesterase inhibitor • Afterload reduction – nitroglycerin – dobutamine
  • 92. Don’t forget... Shock: “rude unhinging of the machinery of life.” -Samuel D. Gross, 1872