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TABLE12.7 EXOGENOUS CLOTTING FACTORS
Coagulation Factor
Concentrates
IX Control or prevention of bleeding
VIIa Prevention of bleeding in invasive/
VIII Control or prevention of bleeding in
Prothrombin Complex
Concentrate
SOURCE:Micromedex® Healthcare Series [Internet database]. Greenwood Village, Colo.:Thomson Micromedex. Updated periodically.
the replacement of a patient’s entire blood volume within
24 hours.16 e goal of massive transfusion is to restore an
eective circulating blood volume and attenuate the coagulopathy associated with trauma.7 Intraoperative use of massive transfusion protocols (MTPs) have been extrapolated
Indication Dosing
Goal of 80%– 100% of normal
in patients with factor IX deciency
(hemophilia B)
surgical procedures for patients with
hemophilia Aor B
patients with factor VIII deciency
(hemophilia A)
Vitamin K antagonist reversal in
patients with acute major bleeding
factor IX level prior to major
surgery
15- 120 mcg/ kg IV bolus q2- 6
hours
Major surger y:40- 50 IU/ kg
loading then 20- 25 IU/ kg q8-
12 hours to maintain plasma
level VIII 80%- 100% if normal
Kcentra/ Octaplex:25- 50
units/ kg depending on initial
INR FEIBA:50- 100 units/ kg
when applied to nontrauma massive hemorrhage. Given the
dierences in underlying physiology and coagulopathy of
trauma versus nontrauma patients, more studies are needed
to more clearly dene the role of these ratios in the perioperative management of nontrauma patients.
Other
Hematology consult recommended for use of
factor IX concentrate
Often used off- label in nonhemophilic patients
with hemorrhage. May have a high incidence of
thrombotic events in this population.
Hematology consult recommended for use of
factor VIII concentrate
Kcentra/ Octaplex is nonactivated factors II, VII,
IX, and X with proteins C and S; FEIBA contains
nonactivated II, IX, X, and activated VII
from case reports arising from military medicine. In 2007,
Borgman et al. published their retrospective review of
over 240 trauma patients. In this landmark study, trauma
VISCOELASTICTESTS
patients undergoing massive transfusion were treated with
either a high plasma to red blood cell (RBC) ratio of 1:1.4,
medium plasma:RBC ratio of 1:2.5, or low plasma:RBC
ratio of 1:8.7 In this study, patients treated in the highratio group (1:1.4) demonstrated the lowest mortality
rates (p < .001).7 Based on these ndings, it was recommended that MTPs for coagulopathic patients incorporate
a plasma:RBC ratio of 1:17 in order to decrease mortality
secondary to hemorrhage.
Currently, most hospital MTPs use a plasma:
platelet:RBC ratio of 1:1:116 in order to most closely
resemble reconstituted whole blood.17 A recent randomized, prospective study comparing 1:1:1 to 1:1:2 transfusion ratios for trauma patients undergoing massive
transfusion resuscitation found no signicant dierence
in mortality rates at 24 hours or at 30days between the
two groups.17 However, death by exsanguination within
Viscoelastic tests are increasingly used to manage patients
with massive hemorrhage. romboelastography (TEG)
and rotational thromboelastometry (ROTEM) are
dynamic tests that allow for real- time assessment of the
kinetics and strength of clot formation. ese tests provide
information on both the intrinsic and extrinsic pathways
and on the amount of brinogen present, and can detect the
presence of brinolysis. e more traditional tests of coagulation:international normalized ratio (INR), activated partial thromboplastin time (aPTT), and prothrombin time
(PT), do not account for potential derangements in platelet
function or clot formation. When combined with hemoglobin, platelets, and brinogen values, viscoelastic tests can
play an integral role in goal- directed hemostatic therapy
where factor- specic products are administered based on
the deciency present.
18
24 hours was lower in the 1:1:1 group as compared with
the 1:1:2 group.17 Additionally, patients in the 1:1:1 group
also demonstrated earlier hemostasis at 24 hours.17 Based
TRANSFUSION TRIGGERS
on these results, early use of the current MTP ratio of 1:1:1
continues to be recommended for trauma patients presenting with signicant hemorrhage. It should be noted, that
few clinical studies have studied the ecacy of these ratios
e decision to transfuse during the perioperative period is
multifactorial and depends on patient comorbidities (i.e.,
coronary artery disease, anemia) and the clinical setting.
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Rising arterial lactate and decreased mixed venous oxygen
saturation (SvO2) can assess oxygen delivery. Oxygen delivery (DO2) to the tissues is dependent on cardiac output
(CO) and arterial oxygen content (CaO2). e latter takes
into account the oxygen bound to hemoglobin in addition
to the amount of oxygen dissolved in blood:CaO2=1.39×
(Hemoglobin) × SaO2 + PaO2 × 0.003. e majority of
oxygen is carried by hemoglobin, while only a small portion is dissolved in blood. Given the risks associated with
blood product administration (Table 12.8),19 the clinician
must determine whether the administration of appropriate
blood products will potentially improve clinical outcomes.
In the absence of clinical signs and/ or symptoms, including tachycardia not responsive to uid administration,
orthostatic hypotension, chest pain, shortness of breath,
and congestive heart failure, most societies advocate for
more restrictive blood- product- administration protocols.16 A systematic review by the American Association
of Blood Banks (AABB) recommends a restrictive transfusion protocol, hemoglobin 7 to 8 g/ dL, for hospitalized
patients who are hemodynamically stable and not showing
any signs or symptoms of impaired oxygen delivery.16 For
patients with preexisting coronary artery disease who are
hemodynamically stable and are asymptomatic, the AABB
also recommends following a restrictive transfusion protocol. Two of the major trials included in this analysis were
the transfusion trigger trial for Functional Outcomes in
Cardiovascular Patients Undergoing Surgical Hip Fracture
Repair (FOCUS) and the Transfusion Requirements in
Critical Care (TRICC) trial. e FOCUS trial included
patients who had either risk factors for or a history of
cardiovascular disease.7 For the liberal group, the goal
hemoglobin was 10 g/ dL while a goal of 8 g/ dL was
used in the restrictive group. e study found no dierence in in- hospital morbidity, mortality rates, or ability
to walk independently at 60days follow- up between the
two groups.7 While the restrictive group did have a higher
rate of in- hospital acute coronary syndrome (5.2% versus
4.3%), this dierence did not reach statistical signicance.7
In the TRICC trial, critically ill patients were randomized
to either a liberal transfusion strategy to maintain a goal
hemoglobin of 10g/ dL or a restrictive group to maintain a
hemoglobin of 7 g/ dL.17 ere was no dierence in overall
30- day mortality between the two groups. In a subgroup
analysis, 30- day mortality was lower in younger (less than
55years of age) and less acutely ill patients randomized to
a restrictive strategy.17 While 30- day mortality rates for
patients with clinically signicant cardiac disease were
lower in the restrictive group when compared with the
liberal group, this dierence was not statistically signicant.17 In- hospital mortality rates were lower in the restrictive group. e TRACS trial, a prospective, randomized,
controlled trial of patients who underwent cardiac surgery with cardiopulmonary bypass, investigated transfusion goals of a hematocrit (Hct) ≥30% versus a restrictive
strategy of a Hct ≥24% during the perioperative period.
Researchers found no increase in 30- day all- cause mortality in the restrictive versus the liberal group.
15
TABLE12.8 BLOOD PRODUCTS
Blood Product
Packed Red
Blood Cells
Fresh Frozen
Plasma
Platelets Quantitative or
Cryoprecipitate Low brinogen Factor VIII,
SOURCE:Circular of Information;AABB.
HYPOVOLEMICSHOCK 107
Hematologic
Abnormality Corrected
Anemia, decreased O2
carrying capacity
Coagulation
abnormality, elevated
INR
qualitative platelet
abnormality
Content of 1 Unit Expected Change with
Transfusion
~250 mL of red blood
cells, hematocrit ~75%
Coagulation
factors, albumin,
immunoglobulins, acute
phase reactants
platelets
vonWillebrand’s factor,
bronectin, factor XIII, and
brinogen
1 unit will increase
hemoglobin by 1 g/ dL
or hematocrit by 3%
Variable Infection, TRALI, TACO Used for warfarin
Increase of ~5- 10 ×
109/ L per unit of
platelets
1 bag/ 10kg
body weight
raisesbrinogen
50- 75mg/dL
Adverse Reactions
Transfusion
reactions:febrile, allergic,
hemolytic. TRALI, TACO,
infection, citrate toxicity,
hyperkalemia
Infection, allergic
reaction, platelet and
RBC alloimmunization
Same as FFP Compatibility testing
Other Considerations
Must be type specic,
immunomodulatory
effects, avoid diluting
with calcium- containing
solutions
reversal, heparin
resistance, takes time
to thaw
Do not need to be
type specic, stored at
room temperature
not necessary, ABOcompatible preferred
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INTRAOPERATIVE TRANSFUSION OFRED
BLOODCELLS
or as individual component therapy. Platelet levels and viscoelastic tests can also guide therapy intraoperatively. In
general, for patients with ongoing blood loss or patients
Intraoperative restrictive RBC strategies can be problematic in patients with ongoing blood loss. While large- scale,
receiving antiplatelet therapy, experts recommend main-
taining levels greater than 100 × 109/ L.
18
randomized controlled trials to guide clinical practice are
lacking, experts recommend maintaining a hemoglobin
concentration of 7– 9 g/ dL.18 When not contraindicated,
cell salvage strategies should also be employed.
PHYSIOLOGIC AND ELECTROLYTE
ABNORMALITIES ASSOCIATED WITHMASSIVE
TRANSFUSION
INTRAOPERATIVE TRANSFUSION OFFRESH
FROZENPLASMA
Massive transfusion is associated with multiple acute and
delayed complications that can manifest either in the
operating room or postoperatively in the ICU (Table
Fresh frozen plasma (FFP) is administered during the
perioperative setting to either reverse warfarin or replenish clotting factors. According to the American Society of
Anesthesiologists (ASA) task force on blood component
administration, the indications for FFP administrationare:
12.9). Because blood products are commonly stored at
1°C– 6°C,20 rapid transfusion without the use of a uid
warming device can cause hypothermia. Complications of
hypothermia include decreased hepatic metabolism and
clearance of drugs and metabolic products (i.e., citrate),
hypothermia- induced coagulopathy, and decreased pro-
1. Correction of microvascular bleeding in the presence
of abnormal coagulation, PT greater than 1.5 times
normal, INR greater than 2, aPTT greater than 2 times
normal.
duction of acute phase proteins.
of hypothermia is secondary to decreased production of
clotting factors in addition to a reduction in factor activ-
20,21
it y.
For every 1°C decrease in temperature, there is a
20,21
e coagulopathy
10% decrease in clotting factor activity, which is associ-
2. Correction of microvascular bleeding for patients in
whom more than one blood volume has been replaced
byRBCs.
3. Reversal of warfarin.
4. Replacement of known coagulation factor deciencies.
5. Heparin resistance.
ated with clotting time prolongation at temperatures
below 33°C.20 Hypothermia- induced platelet dysfunction
and sequestration also contribute to the observed coagu-
lopathy. Hypothermia can be mitigated by using forced
air warming devices, increasing the room temperature,
attaching a humidier to the ventilator circuit, and warm-
ing intravenous uids.
Derangements in potassium, calcium, magnesium, and
In institutions where viscoelastic tests are not readily available
to guide component therapy, traditional coagulation studies
(PT, aPTT, INR) are used. As discussed above, transfusion
ratios for acute hemorrhage are commonly employed. For
patients with persistent microvascular bleeding, the goal is to
restore factor levels to greater than 30%, which corresponds
to the minimum factor level necessary for clot formation.
In general, this can be achieved with the administration of
10– 15 mL/ kg of FFP. For patients needing warfarin reversal,
lower doses of 5– 8 mL/ kg of FFP are recommended.
pH can occur during massive transfusion. Hyperkalemia is
a common manifestation of rapid blood product administration and can be transient or manifest over several hours.
Packed red blood cells (PRBCs) are a common source of
exogenous potassium, with levels ranging from 7– 77 mEq/ L
depending on the duration of storage.20 Inactivation of the
RBC ATPase pump in addition to RBC lysis are common
causes of PRBC- storage- induced hyperkalemia.20 PRBC
infusion rates of 100– 150 mL/ min have been associated
with transient hyperkalemia.20 Patients at particular risk for
developing hyperkalemia during transfusion include those
INTRAOPERATIVE TRANSFUSION
OFPLATELETS
with crush injuries, myonecrosis, rhabdomyolysis, and renal
failure.20 If time allows, the potassium content can be lowered by washing PRBC before transfusion. Hyperkalemia
should be treated aggressively with hyperventilation and
Depending on the clinical scenario, platelets may be administered according to the transfusion ratios discussed above
treatment with calcium, insulin, and glucose and possi-
bly continuous renal replacement therapy to avoid cardiac
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TABLE12.9 TRANSFUSIONRISKS
Blood Transfusion Risks
Allergic/ Urticaria 1%- 3% plasma- containing
Febrile Nonhemolytic <1% leukocyte reduced
TransfusionAssociated Circulatory
Overload (TACO)
Transfusion- Related
Acute Lung Injury
(TRALI)
Anaphylactic 1:20,000 to 1:50,000 Hypotension, tachycardia,
Sepsis 1:50,000 for platelets,
Incidence Signs/ Symptoms Details
components
red cell components,
<5% leukocyte reduced
aphaeresis platelet
components
<1% Cardiogenic pulmonary edema Pulmonar y edema due to
<0.01% Hypoxemia and noncardiogenic
1:5million RBCs
Ranges from mild urticaria or
wheezing to more severe with
cardiovascular symptoms
Elevation of temperature ≥1 C
pulmonary edema within 6 hours
of transfusion (not cardiogenic)
bronchospasm, laryngeal edema,
dyspnea
Fever, tachycardia, hypotension Bacterial infection caused by
Caused by antigen- antibody
mediated reaction
Diagnosis of exclusion, usually
caused by release of cytokines
from nonleukoreduced
products
volume overload, often in
patients with underlying
cardiac dysfunction
Acute lung injury from
recipient neutrophil activation
by transfused blood product
Can occur in IgA- decient
administered products that
contain antibodies.
contaminated blood product
Treatment
If hives alone, okay to
continue transfusion,
consider antihistamine.
If allergic reaction,
stop and treat as
anaphylactic.
Supportive care, stop
transfusion
Diuresis, mechanical
ventilation as needed,
supportive care
Supportive care, lung
protective ventilation
if patient requires
intubation
Epinephrine,
antihistamines, steroids,
uids, pressors
Broad- spectrum
antibiotics and uids/
vasopressors as needed
Acute Hemolytic
Transfusion Reaction
Citrate Toxicity Variable Hypocalcemia, Hypomagnesemia Occurs when large volumes of
SOURCE:Circular of Information;AABB.
complications. Hypokalemia occurs less commonly during PRBC administration. It is associated with reactivation ofthe RBC ATPase pump, metabolic alkalosis, and
the release of aldosterone, antidiuretic hormone, and catecholamines. It also can be seen with the administration of
large amounts of uids with minimal to no potassium— to
include FFP, crystalloid, albumin, and platelets.
Hypocalcemia and hypomagnesemia oen occur secondary to the amount of citrate in transfused blood products, especially FFP. Citrate is an anticoagulant added to
PRBCs that is normally metabolized by the liver hepatic
citric acid cycle where 1 gram of citrate is converted to about
2grams of bicarbonate.22 In general, each unit of PRBCs
contains 3 grams of citrate and, under normal conditions,23
the liver is able to clear this amount of citrate in 5 minutes.20
In patients with impaired hepatic function, transfusion
rates that exceed one unit of PRBCs every 5 minutes can
1:76,000 (fatal
1:1.8million)
Increase temperature,
tachycardia, chills, dyspnea, pain,
shock
lead to citrate toxicity, with levels 40– 140 times the normal
limit.20 In these cases, excessive amounts of citrate bind calcium and magnesium, which can cause QT prolongation,
cardiac conduction abnormalities, muscle tremors, and
negative inotropy.
Transient derangements in pH oen ensue following
20
massive transfusion (MT) of PRBCs. During the processing of PRBCs, the anticoagulant citrate- phosphatedextrose- adenine leads to a pH of 7.0.20 With the storage of
PRBCs, the pH oen decreases to 6.6– 6.8 as carbon dioxide is produced during ATP metabolism.20 During a massive
transfusion, a transient metabolic acidosis can develop. e
more common occurrence, however, is metabolic alkalosis,
because citrate is metabolized to bicarbonate. In patients
with a persistent metabolic acidosis during MT, signs of
hypoperfusion and impaired oxygen delivery should also be
investigated.
Acute intravascular hemolysis
caused by administration of
ABO incompatible RBCs.
citrated pRBCs are transfused
20
Stop transfusion,
hydration, diuresis
Intravenous calcium
HYPOVOLEMICSHOCK 109
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SUMMARY
you transfuse PRBCs? What if her base decit were
6mmol/ L and her lactate 4mmol/ L? Her nurse is
Hypovolemic shock represents inadequate circulating
plasma volume that decreases cardiac preload, cardiac
concerned that she is “oozy” and asks if you want to give
FFP. Her INR is 1.5. Would you transfuse FFP?Why?
output, and oxygen delivery to tissues. Common causes
of perioperative hypovolemic shock include hemorrhage,
diuretics, and GI losses. Preoperative assessment of volume status should be undertaken to determine whether the
patient is relatively hypovolemic. is includes a history of
diuretic use, prolonged NPO status, vomiting, or diarrhea
that may predispose the patient to hypovolemia. Adequate
venous access should be obtained in surgical cases associated
with large blood loss. Prompt resuscitation is imperative
to restore blood ow and thus oxygen delivery to tissues.
Volume decits can be replaced with crystalloids, colloids,
blood products, or a combination of uids. Optimal intraoperative replacement uid and transfusion triggers have
not yet been fully elucidated.
CASE- BASED LEARNING DISCUSSION
1. In this case of a patient undergoing surgery with a high
risk of hemorrhage, what considerations must be taken
to ensure adequate intravenous access? Does the fact
that she has antibodies on a previous type and screen
change management? What blood products would you
order before starting thiscase?
2. Aer induction of general anesthesia, you have
decided to place an arterial catheter for hemodynamic
monitoring and an introducer catheter for uid
resuscitation. Aer delivery of the neonate, the
obstetrician tells you that there is a large amount
of bleeding that they are having a dicult time
controlling. What would be your initial resuscitation
uid? What if the estimated blood loss were
approximately 2 liters with ongoing blood loss? Is there
any role for albumin in this resuscitation?
3. e bleeding continues, and you have set up
a rapid transfuser and activated the massive
transfusion protocol. What ratio of blood products
(plasma:platelet:RBC) would you administer? What
electrolyte abnormalities would you be concerned
about? How would you treat these electrolyte
abnormalities?
4. e patient does well during surgery and is extubated
with a blood pressure of 100/ 50mmHg in the ICU
postoperatively. Her hemoglobin is 6.7 g/ dL. Would
REFERENCES
1. Gross JB. Estimating allowable blood loss: corrected for dilution.
Anesthesiology. 1983;58(3):277– 80.
2. Tavernier B, Makhotine O, Lebue G, Dupont J, Scherpereel P.
Systolic pressure variation as a guide to uid therapy in patients with
sepsis- induced hypotension. Anesthesiology. 1998;89(6):1313– 21.
3. Michard F, Boussat S, Chemla D, etal. Relation between respiratory changes in arterial pulse pressure and uid responsiveness in
septic patients with acute circulatory failure. American Journal of
Respiratory and Critical Care Medicine. 2000;162(1):134– 8.
4. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005;103(2):419– 28; quiz 449– 15.
5. Lal DS, Shaz BH. Massive transfusion: blood component ratios.
Current Opinion in Hematology. 2013;20(6):521– 5.
6. Finfer S, Bellomo R, Boyce N, etal. A comparison of albumin and
saline for uid resuscitation in the intensive care unit. New England
Journal of Medicine. 2004;350(22):2247– 56.
7. Annane D, Siami S, Jaber S, etal. Eects of uid resuscitation with
colloids vs crystalloids on mortality in critically ill patients presenting
with hypovolemic shock:the CRISTAL randomized trial. Journal
of the American Medical Association. 2013;310(17):1809– 17.
8. American College of Surgeons Committee on Trauma.
Advanced Trauma Life Support: Student Course Manual. 9th ed.
Chicago:American College of Surgeons;2012.
9. Guly HR, Bouamra O, Little R, et al. Testing the validity of
the ATLS classication of hypovolaemic shock. Resuscitation.
2010;81(9):1142– 7.
10. Guly HR, Bouamra O, Spiers M, etal. Vital signs and estimated
blood loss in patients with major trauma: testing the validity of
the ATLS classication of hypovolaemic shock. Resuscitation.
2011;82(5):556– 9.
11. Mutschler M, Nienaber U, Brockamp T, etal. A critical reappraisal
of the ATLS classication of hypovolaemic shock: does it really
reect clinical reality? Resuscitation. 2013;84(3):309– 13.
12. Davis JW, Shackford SR, Mackersie RC, Hoyt DB. Base decit as a guide to volume resuscitation. Journal of Trauma.
1988;28(10):1464– 7.
13. Davis JW, Parks SN, Kaups KL, Gladen HE, O’Donnell- Nicol S.
Admission base decit predicts transfusion requirements and risk of
complications. Journal of Trauma. 1996;41(5):769– 74.
14. Mutschler M, Nienaber U, Brockamp T, et al. Renaissance of base
decit for the initial assessment of trauma patients:a base decitbased classication for hypovolemic shock developed on data
from 16,305 patients derived from the Trauma Register DGU(R).
Critical Care. 2013;17(2):R42.
15. Hajjar LA, Vincent JL, Galas FR, et al. Transfusion requirements
aer cardiac surgery: the TRACS randomized controlled trial.
JAMA. 2010;304(14):1559– 67.
16. Carson JL, Grossman BJ, Kleinman S, etal. Red blood cell transfusion:a clinical practice guideline from the AABB. Annals of Internal
Medicine. 2012;157(1):49– 58.
17. Hebert PC, Wells G, Blajchman MA, etal. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators,
Canadian Critical Care Trials Group. New England Journal of
Medicine. 1999;340(6):409– 17.
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18. Gill R. Practical management of major blood loss. Anaesthesia.
2015;70(Suppl 1):54– 57, e19– 20.
19. AABB. Circular of Information for the Use of Human Blood
and Blood Components: American Association of Blood Banks.
November2013.
20. Sihler KC, Napolitano LM. Complications of massive transfusion.
Chest. 2010;137(1):209– 20.
21. Hayter MA, Pavenski K, Baker J. Massive transfusion in the
trauma patient: Continuing professional development. Canadian
Journal of Anaesthesia = Journal Canadien d’Anesthesie.
2012;59(12):1130– 45.
22. Schultheiss C, Saugel B, Phillip V, etal. Continuous venovenous
hemodialysis with regional citrate anticoagulation in patients
with liver failure:a prospective observational study. Critical Care.
2012;16(4):R162.
23. Guidelines for transfusion for massive blood loss. A publication
of the British Society for Haematology. British Committee for
Standardization in Haematology Blood Transfusion Task Force.
Clinical and Laboratory Haematology. 1988;10(3):265– 73.
HYPOVOLEMICSHOCK 111
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13.
OBSTRUCTIVESHOCK
Julia Sobol and JackLouro
CASE
either prevent blood from entering the right heart or pre-
vent blood from being ejected by the heart (Table 13.1).
A 23- year- old male with past medical history of asthma
presents for an intramedullary nail of his le femur and
debridement of an open right elbow wound one day aer
involvement in a motorcycle accident. e patient has
never had an anesthetic and was found to have a distal
femur fracture, open elbow wound, and two parasternal rib
fractures on his initial evaluation in the emergency room.
All laboratory values were normal, chest and pelvis x- rays
demonstrated only two rib fractures with a trace le apical
pneumothorax. e anesthetic plan is for general anesthesia
plus a le femoral nerve block for postoperative pain control. One hour aer an uneventful induction with less than
100 milliliters of blood loss, the patient becomes tachycardic with a heart rate of 130, hypotensive with a mean
arterial pressure of approximately 40mmHg, and hypoxic
by pulse oximeter.
Normal right heart lling is a result of the pressure dieren-
tial between the right atrium (RA) and the venous system.
Disease states that externally compress the RA or central
veins will increase RA pressure and decrease this pressure
dierential; thereby preventing lling of the right heart.2
One example of increased RA pressure is cardiac tampon-
ade. When a pericardial eusion accumulates to a large
volume or over a short period of time, the pressures of the
cardiac chambers equalize in diastole and increase to abnor-
mal levels.3 e RA pressure is normally less than 10mmHg
but can increase to over 20mmHg if uid in the pericardial
sac compresses the RA and the right ventricle (RV).3 Blood
from the venous system is unable to ow into the right
heart due to elevated RA pressures, resulting in an under-
lled heart despite high intracardiac pressures. Low end-
diastolic volume from insucient venous return decreases
cardiac output in the setting of tamponade.2 Tamponade
DEFINITION OFOBSTRUCTIVESHOCK
may occur with malignant pericardial eusions, chronic
kidney disease, or aer cardiac surgery.3 One study showed
that almost two- thirds of patients undergoing cardiac surShock is a state of insucient perfusion and oxygen delivery to the tissues. In obstructive shock, physical obstruction
of blood ow decreases cardiac output and causes tissue
hypoperfusion. Low cardiac output is from failure of the
heart to ll or move blood out of the heart due to a physical
obstruction rather than pump failure.
1
gery have a postoperative pericardial eusion and nearly
2% of all patients develop clinical tamponade requiring
intervention.
4
Other etiologies can obstruct venous return by compressing the central veins. In the setting of a tension pneumothorax, air entrapment with subsequent increased
intrapleural pressure collapses the lung, compresses the
PATHOPHYSIOLOGY OFDISEASE
is section will review the mechanisms, risk factors and
assessment of patients with obstructiveshock.
MECHANISMS
e underlying mechanisms of obstructive shock physically
impair blood ow through the heart. ese mechanisms
112
TABLE13.1 ETIOLOGIES OFOBSTRUCTIVESHOCK
Tamponade Pulmonary embolism
Tension pneumothorax Pulmonary hypertensive crisis
Auto- PEEP Cardiac myxoma
Intra- abdominal hypertension Hyper tensive obstructive
cardiomyopathy
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major vessels, and impairs ventricular lling and venous
return.2 Although pneumothoraces may occur spontaneously, they are also found in up to 15% of mechanically
ventilated intensive care unit (ICU) patients, from trauma,
iatrogenic procedures, or positive pressure ventilation.5
Central vein collapse and shock may also occur with auto–
positive end- expiratory pressure (auto- PEEP), a phenomenon seen with insucient mechanical ventilator expiratory
time or dynamic airway obstruction.6 Intra- abdominal
obstruct the le ventricular outow tract (LVOT) during
systole. Certain physiologic states, such as tachycardia and
low systemic vascular resistance can decrease cardiac output
by worsening the dynamic obstruction. Patients may be well
compensated with pharmacologic treatments for HOCM.
However, the vasodilatory eects of anesthetics and tachycardia from pain or sympathetic stimulation increase the
risk of an acute obstructive episode in the perioperative
13
period.
hypertension and abdominal compartment syndrome can
cause obstructive shock from decreased venous return.
Increased intra- abdominal pressure compresses the inferior
vena cava, decreases venous outow from the lower body,
and displaces the diaphragm cephalad, which increases
intrathoracic pressure.
7
Tamponade, tension pneumothorax, auto- PEEP, and
abdominal compartment syndrome decrease the pressure differential between the venous system and the RA, obstructing venous return to the heart. However, obstructive shock
may also occur due to physical obstruction to outow from
the heart. One cause of outow obstruction is acute pulmonary embolism (PE). Pulmonary embolism has a variable
hemodynamic presentation depending on the clot burden
and the extent of obstruction in the pulmonary vasculature.
Mortality ranges from approximately one- third of patients
who present with shock to more than three- quarters of those
who require cardiopulmonary resuscitation.8 Obstruction of
pulmonary vessels by thromboemboli increases RV aerload,
which dilates the RV, decreases RV stroke volume, and shis
the interventricular septum, which reduces le ventricular
(LV) stroke volume.8 While the cause of PE is oen embolism of deep vein thromboses (DVT) from pelvic or lower
extremity veins, other sources of emboli to the pulmonary
vasculature include air, fat, and amniotic uid.
9– 11
Similar to
PE, pulmonary hypertensive crisis in patients with chronic
pulmonary arterial hypertension can cause an acute increase
in right ventricular aerload and subsequent RV failure. In
the perioperative period, these patients are at increased risk
of RV failure and cardiac arrest in the setting of sedation, systemic hypotension, and highPEEP.
8
Other disease states can prevent blood from moving
forward within the heart chambers and cause obstructive
shock. Cardiac myxomas are very rare, with an incidence of
less than 0.2%. ey are usually pedunculated and arise from
the le atrium. Myxomas can move into the mitral valve
aperture, temporarily obstructing ow from the atrium into
the ventricle, leading to episodes of syncope or even sudden
death due to obstructive shock.12 Hypertrophic obstructive
cardiomyopathy (HOCM) with septal hypertrophy can
cause the anterior leaet of the mitral valve to dynamically
RISK FACTORS
Obstructive shock is a multifactorial process caused by a
wide variety of mechanisms, but there are certain risk factors that can predispose to obstructive shock. One risk factor for obstructive shock is blunt or penetrating thoracic
trauma that may ultimately lead to cardiac tamponade or
tension pneumothorax.14 Pneumothorax occurs in a signicant proportion of chest trauma patients with rib fractures.
Cardiopulmonary resuscitation with chest compressions
may also increase the risk of pneumothorax. Asimple pneumothorax in a mechanically ventilated patient has a high
risk of evolution to a tension pneumothorax.5 Tra um a
patients are also at higher risk for other sources of obstructive shock during their hospitalization. Trauma victims
who sustain traumatic brain injury have a three- to fourfold increased risk of DVT compared with trauma patients
without traumatic brain injury, regardless of pharmacologic
prophylaxis.15 Post- traumatic pelvic and lower extremity
fractures, burns, and spinal cord injury also increase the risk
for venous thromboembolism due to patient immobilization, endothelial injury, hypercoagulability, and diculty
with pharmacologic prophylaxis due to bleeding risks.16
With a higher incidence of DVTs in trauma patients, the
risk of obstructive shock from PE also increases.
Hypercoagulable states (i.e., malignancy, pregnancy,
surgery) predispose patients to the development of venous
thrombosis. Hereditary conditions including factor V
Leiden and protein C and S deciencies also increase the
risk of developing DVTs.17 Certain malignancies (breast,
hepatocellular, or renal cell carcinoma) may also form macroemboli that cause obstruction of the pulmonary vasculature.18 Renal cell carcinoma can invade into the inferior vena
cava (IVC), reach the RA, and obstruct venous return.
19
Some conditions and surgical procedures pose a higher
risk of nonthrombotic pulmonary embolism. Fat embolism
can occur during repair and intramedullary reaming of long
bone and pelvic fractures and during knee prosthesis placement.20 Amniotic uid embolism (AFE) is a rare event in
the peripartum period that cannot be predicted and carries
OBSTRUCTIVESHOCK 113
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signicant maternal mortality.11 Rupture of membranes
(as in cesarean delivery, placenta previa, or abruption) may
increase the risk of AFE by exposing the maternal circulatory system to amniotic uid, which can also provoke
an allergic- type reaction.21 Air may be entrained into the
venous system and cause embolism. Venous air embolism
(VAE) is more likely to occur when surgically entering noncollapsed veins, such as in a sitting craniotomy or in laparoscopic procedures,9 or when manipulating central venous
catheters.18 e morbidity of a VAE depends on the level of
air entrapment in relation to the heart during the event, the
rate of air entrainment, and the volume of entrainedair.
9
Other iatrogenic factors may impact the development
of obstructive shock. Insuation during laparoscopic procedures increases intra- abdominal pressure and may reduce
venous return and lead to low cardiac output.22 Inadequate
expiratory time with mechanical ventilation can contribute to auto- PEEP, especially in patients with asthma or
chronic obstructive pulmonary disease,6 while excessively
high peak airway pressures and set tidal volumes may cause
alveolar rupture and pneumothorax.23 Pneumothorax is
also a potential complication of central venous catheter
placement.24 While open- heart surgery is associated with
the risk of pericardial eusion and tamponade,3 especially
in the rst month aer cardiac surgery,25 even less invasive
percutaneous coronary artery interventions pose a risk of
coronary perforation that can cause tamponade.26 In cases
of sepsis or massive blood loss, over- resuscitation causes
bowel edema and intra- abdominal hypertension.
27,28
Specialized invasive monitors such as an arterial catheter, a CVC, or a pulmonary artery catheter (PAC) can provide important diagnostic information about the etiology
of shock beyond standard noninvasive monitoring data.
For example, in cardiac tamponade, an arterial line may
demonstrate pulsus paradoxus, and equalization of the central venous pressure and pulmonary artery diastolic pressure may be observed from PAC information.3 Increased
pulmonary artery pressures visualized via PAC may occur
in an acute PE or pulmonary hypertensive crisis.
8
Data from other sources can also assist in diagnosing
the underlying etiology. Abladder catheter can be placed to
trend hourly urine output and measure intravesicular pressures if there is concern for intra- abdominal hypertension.7
Elevated serum lactate levels from dysfunctional cellular
oxygen metabolism29 can occur in shock, and monitoring these levels in response to treatment may be helpful.33
Elevations in creatinine and liver function tests may indicate end- organ hypoperfusion due to RV dysfunction.8 An
electrocardiogram (ECG) with a pattern of PR depression
and low QRS voltage suggests pericardial eusion with
tamponade.34 Aprominent S wave in lead Iplus a Q wave
and T wave inversion in lead III (the S1Q3T3 pattern),35
sinus tachycardia, or T wave inversions in V1 to V4 occurs
with acute RV pressure or volume overload from a PE.32
A chest radiograph may show a large pneumothorax or
hemidiaphragm attening with contralateral mediastinal
deviation in a tension pneumothorax.
31
e ventilator oen displays pressure, ow, and volume
indices that could be helpful in determining the underly-
ASSESSMENT OFTHE PATIENT WITHSUSPECTED
OBSTRUCTIVESHOCK
Obstructive shock usually presents with hemodynamic alterations such as hypotension and clinical signs of end- organ
hypoperfusion, such as altered mental status or cool skin
from peripheral vasoconstriction.29 Physical exam ndings
are oen nonspecic but may help guide the performance
of more specic diagnostic studies in certain cases. Physical
exam ndings specic to dierent types of obstructive
shock might include jugular venous distention in cases of
cardiac tamponade,30 tension pneumothorax,31 or massive
PE.32 Unilateral breath sounds suggest a pneumothorax,31
and equal bilateral lung sounds with distant heart sounds
may indicate tamponade.30 Patients with cardiac myxomas
oen have detectable systolic or diastolic murmurs,12 and
patients with acute RV failure may have a tricuspid regurgitation murmur.8 Aunilateral swollen and painful lower
extremity may occur in patients with aDVT.
16
ing cause of shock. Apattern in which the expiratory ow
loop does not return to baseline (Figure 13.1) implies that
auto- PEEP with dynamic hyperination may be the cause
of decreased venous return and shock.6 Apneumothorax
may suddenly increase airway pressure or decrease tidal volume.5 Similarly, elevated peak inspiratory and mean airway
pressures with decreased compliance and tidal volume can
occur with intra- abdominal hypertension.
7
Ultrasonography is an invaluable diagnostic tool for
evaluating obstructive shock. Key ndings on focused
transthoracic echocardiography (TTE) in cardiac tamponade are a pericardial eusion and diastolic collapse of
the RA and/ or RV36 (Figure 13.2). e focused TTE in
acute RV strain associated with pulmonary hypertensive
crisis or PE could show an enlarged RV, a D- shaped septum in the parasternal short- axis view, or even thrombus
within the heart36 (Figure 13.3). A more comprehensive
TTE examination evaluates tricuspid annular plane systolic
excursion (TAPSE) in RV dysfunction,37 the presence of an
114 PART III.SHOCK
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115
Auto-peep
Figure13.1 Ventilator ow waveforms demonstrating
auto- PEEP in the setting of a short expiratorytime.
intracardiac myxoma,12 or ndings typical of patients with
HOCM (thickened septal wall, dynamic LVOT obstruction, systolic anterior motion of the mitral valve).
13,38– 40
oracic ultrasound ndings such as lack of lung sliding, the A- line sign (presence of A- lines without B- lines),
and the identication of a lung point (lung sliding that
vanishes with expiration) diagnose a pneumothorax.
Evaluation of the IVC may show increased diameter and
lack of respiratory collapse in cardiac tamponade and PE.43
Ultrasound can also be used to detect a DVT in the lower
extremity veins, which may raise the possibility of PE as the
etiology of shock.
MANAGEMENT OFOBSTRUCTIVESHOCK
is section reviews the initial approach to the patient with
44
subsequent treatment steps and follow up of the patient.
INITIAL APPROACH
Management of any patient with suspected shock includes
establishing the airway, assisting breathing, and restoring
or maintaining circulation.1 Controlled ventilation reduces
the work of breathing and delivers oxygen to vital organs.1
When there is obstruction to cardiac lling with low pre-
41,42
load, a uid bolus can increase systemic pressure, venous
return to the RA, and subsequently cardiac output.2 In contrast, in the case of RV dysfunction, excessive uid administration might exacerbate RV volume overload and shi the
interventricular septum leward to worsen LV lling and
output.
32,37
As with other types of obstructive shock (i.e.,
auto- PEEP, intra- abdominal hypertension, and HOCM),
judicious intravenous uid resuscitation in pulmonary
hypertensive crisis should allow for adequate preload conditions.
6,13,37,45
Shock associated with PE or pulmonary
hypertensive crisis might require vasopressors to maintain
Interventricular
Septum
Pericardial fluid
Figure13.2 Pericardial uid surrounding the RA in apical four- chamberview.
OBSTRUCTIVESHOCK 115
RA
Figure13.3 D- shaped septum from RV pressure overload in the setting of
acutePE.
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