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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.
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
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
• INDICATIONS– volume status– cardiac status
• COMPLICATIONS– technical– anatomic– physiologic
West’s Lung Zones
• Zone I - PA > Pa > Pv
• Zone II - Pa > PA > Pv
• Zone III - Pa > Pv > PA
• PA = alveolar
• Pa = pulmonary artery
• Pv = pulmonary vein
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
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 ventricleRVSWI
PVRI
LVSWI
SVRI
CVP
MPAPPCWP
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 = pressure x vol. ejected
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
Increased Delivery
Increased Consumption
Demands are met
Critical O2 Delivery
VO
2I
DO2I
The critical value is variable& is dependent upon the patient, disease, and the metabolic demands of the patient.
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 ConsumptionVO2I = CI x (CaO2 - CvO2)
If VO2I < 100 suggest tissues are not getting enough oxygen
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 byspontaneously or artificially meeting these goals do show a better survival.
Goals of Shock Resuscitation
• Restore blood pressure
• Normalize systemic perfusion
• Preserve organ function
Hypovolemic Shock
• Causes
– hemorrhage
– vomiting
– diarrhea
– dehydration
– third-space loss
– burns
• Signs cardiac
output PAOP SVR
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 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, DO2I 670, VO2I 166
• Lactic Acid clearance
• Gastric pH
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
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
Dobutamine
-agonist
• 5 - 20 g/kg/min
• potent inotrope, variable chronotrope
• caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
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.
Epinephrine
- 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
Summary `pressors & inotropes
- inotrope + inotrope
dilator
pressor
DobutamineMilrinone/Amrinone
-dopamine
IsuprelDigoxinCalcium
epinephrine
-dopamine
neosynephrine
norepinephrine
-blocker
LabetalolCa+2 blocker
ACE inhibitorhydralazine
nitroglycerineNipride
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.
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...
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
Cardiogenic Shock
• Preload augmentation - Consider Fluids
• Contractility– dopamine– dobutamine– phosphodiesterase inhibitor
• Afterload reduction– nitroglycerin– dobutamine