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12 Surgical Intensive Care
383
Mode Uses Advantages Disadvantages
VVI Used for transvenous
pacing
VOO Used when sensing is
unreliable
DDD Common for
epicardial pacing
wires
DOO Used when sensing is
unreliable
Resistant to
interference
Maintains atrial kick Risk of endless loop
• Maintains atrial
kick
• Resistant to
interference
• Loss of atrial kick
• Difcult to assess ST
segment
• Loss of atrial kick
• Risk of R on T
tachycardia
Risk of R on T
phenomenon
Complications Description Treatment
Delivery of atrial pacing stimuli despite
Under- sensing
Oversensing
Non-capture
occurrence of spontaneous P waves or delivery
of ventricular pacing stimuli despite
occurrence of spontaneous QRS complexes
ECG that shows inappropriate inhibition of
atrial or ventricular output stimuli.
Oversensing in the atrial channel causes
earlier-than- expected ventricular pacing
stimuli
Pacing stimuli not followed by atrial or
ventricular depolarization
Place pacer wires in a different area of the
endocardium
Increase the ma (amount of electricity
delivered to the endocardium by the
pacemaker) or placement of the pacemaker
in a more sensitive endocardial location
Failure Absence of pacing stimulus outputs Change pacemaker generator or wires
Use of a debrillator in a patient with unstable arrhythmia
Mode Indications
Debrillation Pulseless ventricular tachycardia
Ventricular brillation
Synchronized cardioversion: timed (synchronized) with
the QRS complex
Supraventricular tachycardia, atrial brillation, atrial
utter, atrial tachycardia, and monomorphic VT with
pulses

384
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A. H. Sohail et al.
Hematology andBlood Products
Denitions
Factor VII Shortest half-life
Factor VIII Only factor not synthesized in liver (synthesized in endothelium)
Factor I (brin) Links platelets together (GpIIb/IIIa)
Factor II (thrombin) Thrombin converts brinogen into brin, activates multiple factors in the
coagulation cascade, and activates platelets
Vitamin K-dependent factors II, VII, IX, X, protein C and S
Von Willebrand factor (vWF) Von Willebrand factor is important in both primary and secondary
hemostasis
Primary hemostasis ➔it allows platelets, through glycoprotein Ib, to
adhere to the subendothelium of the injured vessel wall
Secondary hemostasis➔ prevents degradation of factor VIII
Links GpIb receptor on platelets to collagen
GpIIb/IIIa Fibrin links GpIIb/IIIa together
PT Partial thrombin time: Measures II, V, VII, X, and brinogen
PTT Partial thromboplastin time: Measures all factors except VII and XIII
Adhesion Gp1b attaches platelets to vWF
Aggregation GpIIb/IIIa allows platelets to aggregate
GPlb
GPllb-IIIa
complex
Fibrinogen
Platelet adhesion and aggregation
Gplb
Platelet
von Willebrand factor

Fibrin clot
Intrinsic pathway Extrinsic pathway
12 Surgical Intensive Care
Denitions
Warfarin
XII XIIa
XI
Apixaban
Rivaroxaban
Anticoagulation Antithrombin III inhibits thrombin and factor Xa
Vitamin K is required for the production of coagulation factors II, VII, IX, and X
Major causes of vitamin K deciency: inadequate dietary intake, decreased absorption (biliary tract obstruction), and hepatic disease (loss of storage sites)
XIa
Xa
IIa
VIIa
VII
Enoxaparin
Heparin
Dabigatran
XIIIa XIII
IX
IXa
XX
II
Fibrinogen Fibrin
Activated protein C and cofactor protein S degrade factors Va and VIIIa
blocking the amplication of the coagulation cascade
385
All coagulation factors are synthesized in the liver except for von Willebrand factor
Coagulation factors Components Uses
Highest
concentration of VWF- VIII
High brinogen
Cryoprecipitate
FFP
DDAVP
PCC-4 2, 7, 9, 10, C, S • Small volume
PCC-3
XIII
• All factors except C, S, AT-III
• Fibrinogen
Cause release of VIII and vWF
from endothelium
2, 9, 10
• Hemophilia A
• Von Willebrand’s disease
• No need to check Rh compatibility
• Hypobrinogenmia
• Reverses vitamin K antagonists
• ABO blood typing
• Risk of pathogen
• No need to check Rh compatibility
Uremic patients with bleeding
• Rapid
• Room temp
• Does not require cross match
• Virally inactivated

386
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Common anticoagulants
A. H. Sohail et al.
Anticoagulant
Dabigatran (Pradaxa)
Argatroban
Bivalirudin (Angiomax)
Apixaban (Eliquis) ➔
metabolized by liver
Rivaroxaban (Xarelto) ➔
metabolized by kidney
Route
Half-life
• PO
• T½=12–14h
• Increase PTT
• IV
• T½=50min
• IV
• T½=25min
• PO
• T½=5–9h
Characteristics Reversal
• Direct II (thrombin)
inhibitor
• Best test is ecarin clotting
time (ECT)
• Eliminated by kidneys
• Partially reversed by PCC
• Not approved as initial
mono DVT
• Used as an alternative to
warfarin for atrial
brillation
• Prolong PTT
• Direct II inhibitor
• Metabolized in liver
• Give if renal insufciency
• Used in HITT
• Follow PTT
• Direct II inhibitor
• Metabolized by proteinase
enzymes (blood)
• Give if liver problems
• Follow PTT
• Renal metabolism
• Direct Xa inhibitor
• Metabolized by liver/renal
excretion
• Decreased rates of
bleeding
• Approved for initial
monotherapy of DVT
• Not removed by dialysis
• Monitor anti-Xa levels
• Increase PT/PTT
Idarucizumab
Dialysis
PCC
Discontinue 24–48h
before surgery
• PCC
• Andexanet alfa
• Discontinue at least 24h
before a surgical
procedure
If reduced creatinine
clearance ➔discontinue
3–5days
• Indirect Xa inhibitor (bind
antithrombin III)
• Renal excretion
• Binds ATIII ➔ inhibits Xa
only
• Renal excretion
• Binds and activates
antithrombin III ➔inhibits
IIa/Xa
• Does not cross placenta
• Heparin resistance ➔ give
AT-III or FFP
• Given in patients with
renal failure
• Used for procedures
Protamine
Fondaparnix
LMWH (Lovenox)/
enoxaparin
Heparin
• Subcutaneous
• T½=17–21h
• Subcutaneous
• T½=4.5h
• IV
• T½=60–90min

12 Surgical Intensive Care
Common anticoagulants
387
Anticoagulant
Coumadin (warfarin)
Route
Half-life
• PO
• T1/2=40h
Characteristics Reversal
• Prevents vitamin
K-dependent factors
synthesis
• Warfarin-induced skin
necrosis: occur if warfarin
is started without heparin;
due to short t½ of protein C
& S; patients with protein
C deciency are affected
most
• Appropriate long-term
anticoagulation for patient
on dialysis
Antiplatelet
drugs
Drug Site of action Reversal
Aspirin Inhibits cyclooxygenase in platelets and
decrease TXA2
Clopidogrel
(Plavix)
Abciximab GpIIb/IIIa receptor inhibitor
ADP receptor antagonist Stop 7days before surgery
Stop 7days before surgery
Give platelets if bleeding
Give platelets if bleeding
FFP, PCC, vitamin K
Heparin-associated thrombocytopenia (HIT)
Pathophysiology
Diagnosis Platelet count decreases <100,000/microliter or by >50% of patient’s baseline when
Injection of heparin ➔ plasma concentration of PF4 increases ➔ PF4 binds to
heparin and forms a complex that continues to bind to platelet receptors and induces
platelet activation ➔ which releases more PF4
Platelets are also activated by the IgG antibodies formed against PF4 and PF4heparin complex
Activated platelets lead to shedding of membrane microparticles that trigger an
activation of the coagulation system ➔ prothrombotic state
the patient is on heparin therapy
Occurs typically between 5 and 7days from the initiation of heparin
(4Ts: Thrombocytopenia, timing, thrombosis, and no other thing)

388
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Heparin-associated thrombocytopenia (HIT)
Types Characteristic Management
A. H. Sohail et al.
Types and management
Type I Nonimmune and self-limited
drop in platelets within the rst
2days of heparin use
Immune-mediated life- and
limb-threatening disorder
involving antibodies against
platelet factor 4
Caused by IgG antibody
production against platelet
factor4
Type II
Thrombocytopenia 5–10days
after the initial exposure to
heparin
This diagnosis is conrmed with
enzyme-linked immunosorbent
assay (ELISA) testing for those
antibodies
Resolves without
discontinuation of heparin
Discontinuation all heparin
products
Started on a direct thrombin
inhibitor
Thromboelastography
Indication Useful in directing the use of blood products and resuscitation in the coagulopathic trauma
patient
Component Abnormal TEG
value
Treatment
Analysis
R time >10min FFP/PCC/Idarucizumab/Andexanet
Alpha angle <53 degrees Cryoprecipitate
K time >3min Cryoprecipitate
Maximum
amplitude
Lysis at 30min
(LY30)
<50mm Platelets and/or DDAVP
>3% Tranexamic acid

12 Surgical Intensive Care
Research
Reference Findings
389
Holcomb JB, Tilley BC, Baraniuk S, etal.; PROPPR
Study Group. Transfusion of plasma, platelets, and red
blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in
patients with severe trauma: The PROPPR randomized
clinical trial. JAMA. 2015;313(5):471–482
Using early balanced resuscitation for trauma patients
provides documented benets. Early balanced
resuscitation means giving equal amounts of platelets,
packed red blood cells, and fresh frozen plasma to
trauma patients who require transfusion. This means a
ratio of 1:1:1
Bleeding disorders
Disease Characteristic Treatment
Most common congenital bleeding disorder
Most common symptom is epistaxis
PT normal, PTT can be normal or abnormal
Elevated bleeding time
Diagnosis: Plasma vWF antigen
Von Willebrand’s
disease
Hemophilia A
Type I: Most common, autosomal dominant,
reduced quantity of vWF; only mild symptoms
Type II: Autosomal dominant, defect in vWF DDAVP, cryoprecipitate,
Type III: Autosomal recessive, complete vWF
deciency; causes most severe bleeding
Factor VIII deciency
Sex-linked recessive
Prolonged PTT and normal PT
Factor VIII crosses placenta ➔ newborn do not
bleed at circumcision
DDAVP, cryoprecipitate,
recombinant VIII-vWF
recombinant VIII-vWF
Cryoprecipitate or recombinant
VIII-vWF
Cryoprecipitate or recombinant
factor VIII
If patient develops Allo-antibodies
then give factor VII
Factor IX deciency
Hemophilia B
Factor VII deciency Prolonged PT and normal PTT FFP or recombinant factor VII
Hypobrinogenemia
Sex-linked recessive
Prolonged PTT and normal PT
Prolonged PT/PTT and decreased brinogen
levels➔
FFP or recombinant factor IX
Cryoprecipitate contains
vWF+factor VIII and brinogen
making it the most appropriate
therapy for hypobrinogenemia

390
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Platelets disorders: causes bruising, epistaxis, petechia, purpura
Disease Characteristic Treatment
Acquired thrombocytopenia Drug-induced thrombocytopenia
A. H. Sohail et al.
Continuous renal replacement therapy,
and chronic liver disease, septicemia,
recent cardiopulmonary bypass, and
venous limb gangrene
Uremia Inhibits platelets function by
inhibiting release of vWF, impaired
platelet adhesion, aggregation
Glanzman’s thrombocytopenia GpIIb/IIIa receptor deciency on
platelets
Bernard Soulier GpIb receptor deciency on platelets Platelets
Discontinue the cause
DDAVP
Hemodialysis
Cryoprecipitate
Platelets
Disseminated intravascular coagulation (DIC)
DIC is secondary to an underlying disorder
Pathophysiology
Diagnosis
Management
Ongoing activation of the coagulation system leads to brin deposition and thrombosis
Depletion of clotting factors from ongoing activation results in severe bleeding
Decreased platelets, low brinogen, high brin split products (D-dimer), prolonged PT, and
prolonged PTT
DIC associated with sepsis is the most common cause of digital necrosis
First line treatment is to treat underlying cause (sepsis) with antibiotics or source control,
supportive measures (uid administration)
Hypercoagulable disorders
Disease Characteristics Treatment
Most common congenital
Factor V Leiden mutation
Anti- phospholipid antibody
syndrome
Antithrombin III deciency Deciency in antithrombin
hypercoagulability disorder
Defect in factor V➔ resistance in
activated protein C
Presents with thrombosis or loss of
pregnancy
Caused by antibodies to phospholipids
(cardiolipin, lupus anticoagulant)
Prolonged PTT
Heparin
Warfarin
Heparin
Warfarin
Heparin does not work
Recombinant at-III concentrate or
FFP then heparin

the soft palate
the uvula
the uvula
only
The Mallampati Score
12 Surgical Intensive Care
Hypercoagulable disorders
Disease Characteristics Treatment
391
Deciency of protein C and protein S
Protein C or S deciency
results in the loss of these natural
anticoagulant properties
Prothrombin gene defect Mutation in prothrombin gene
Arterial and venous thrombi
Hyperhomocysteinemia
Caused by deciency in methylene
tetrahydrofolate reductase or
cystathionine beta synthase
Respiratory Failure andMechanical Ventilation
Intubation and difcult airway
• Inability to maintain airway (GCS<8 or Upper airway obstruction)
Indications for
Intubation
Evaluation of airway
• Acute respiratory failure
• Inadequate oxygenation or ventilation
• Airway protection in a patient with depressed mental status
• Neck immobilization in cases of suspected cervical spine trauma or previous spinal
surgery ➔ plan for a difcult intubation
• Optimize the glottic view using cricoid pressure or external laryngeal manipulation
(BURP: Push the larynx backwards, upwards, rightwards and then posterior)
Heparin
Warfarin
Heparin
Warfarin
Folic acid
B12
Mallampati
classication
• Mallampati classication and the 3–3-2 rule are used for evaluation of airway
The Mallampati classication refers to the proportion of hard and soft palates, uvula, and
pharyngopalatine arch visible when the patient sits upright and protrudes the tongue
Class I Class II Class III Class IV
Complete
visualization of
Higher Mallampati class ➔ increased difculty of intubation
Complete
visualization of
Visualization of
only the base of
Visualization of
the hard palate

392
Epiglottis
Epiglottis
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Intubation and difcult airway
The “3–3-2 rule” refers to certain distances (measured in ngerbreadths) in head and neck
anatomy that predict easier direct laryngoscopy
Distances less than those described ➔ difcult intubation
A. H. Sohail et al.
3–3-2 rule
ETT size
Intubation blades
The 3-3-2 rule is as follows:
• Three of the patient’s ngers can t into the patient’s mouth when open
• The distance from the tip of the chin to the anterior neck spans 3 of the patient’s
ngerbreadths (hyoid-mental distance)
• The distance from the mandible to the thyroid notch spans 2 of the patient’s
ngerbreadths (thyrohyoid distance)
• The average adult accommodates a 7.5–8.5-mm ETT
• ETT size for children can be determined a few different ways: The Broselow pediatric
emergency tape (age+4)/4 or by using the child’s little nger as a guide
Type Figure Characteristics Uses
Vallecule
Fits into a recess
at vallecula
Curved
Macintosch
blade
Retracts
hypoepiglotic
ligament ➔ lift
Minimize
stimulation of the
posterior
epiglottis
epiglottis
indirectly
Vallecule
Used when glottis
is deep or anterior,
Straight
miller blade
Inserted beneath
epiglottis and then
lift it directly
upper incisors are
prominent, or a
long, oppy
epiglottis
obscures the
glottis
Video laryngoscopy (glidescope)
Difcult intubation
Tracheal tube introducer (Bougie): is an adjunct to direct laryngoscopy
Laryngeal mask airway (LMA)
Conrmation of
intubation
End-tidal carbon dioxide (EtCO2) ➔is the most accurate means of conrming ETT
placement
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