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42 PART I PATIENT EVALUATION
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Figure 3-25. Second-degree atrioventricular (AV) block type I. (From Aehlert B: ECGs made easy, ed 5, St Louis, 2013,
Elsevier.)
Lead II
Figure 3-26. Second-degree atrioventricular (AV) block type II. (From Aehlert B: ECG study cards, St Louis, 2004, Mosby.)
PPPP
Figure 3-27. Third-degree atrioventricular block. (From Monahan FD, Sands JK, Neighbors M et al: Phipps’ medicalsurgi-
cal nursing: health and illness perspectives, ed 8, St Louis, 2006, Mosby.)
45. What rhythm is shown in Figure 3-28?
Premature ventricular contractions. The overall rate is normal. However, the fourth and sixth beats do
not have preceding P waves, and a PR interval cannot be measured. The QRS complexes are wide
(>0.12 seconds).
46. What rhythm is shown in Figure 3-29?
Ventricular tachycardia. P waves and PR intervals are not seen. The rate is usually greater than
100 beats/min, and the QRS complexes are 0.12 seconds or greater (wide).
47. What rhythm is shown in Figure 3-30?
Ventricular fibrillation. The rate cannot be determined, and there are no discernible P waves, PR
interval, or QRS complexes.
48. What rhythm is shown in Figure 3-31?
Asystole. No discernible waves present. It is a total absence of ventricular activity. There is no ven-
tricular rate or rhythm, no pulse or cardiac output. It may also be known as cardiac standstill or flat
line.
CHAPTER 3 ELECTROCARDIOGRAM 43
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1
Figure 3-28. Sinus rhythm with premature ventricular complexes (PVCs). The fourth and sixth complexes are very different in appearance from the normally conducted beats. They are PVCs and are not preceded by P waves. (From Grauer K: A
practical guide to ECG interpretation, ed 2, St Louis, 1998, Mosby.)
Figure 3-29. Venticular tachycardia. (From Aehlert B: ECGs made easy, ed 5, St Louis, 2013, Elsevier.)
Figure 3-30. Ventricular fibrillation. (From Aehlert B: ECGs made easy, ed 5, St Louis, 2013, Elsevier.)
2
3
4
5
6
Figure 3-31. Asystole. (From Goldberger AL, Goldberger ZD, Shvilkin A: Goldberger’s clinical electrocardiography: a simpli-
fied approach, ed 8, Philadelphia, 2013, Saunders.)
44 PART I PATIENT EVALUATION
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BiBliography
Aehlert B: ECGs made easy, ed 5, St Louis, 2013, Elsevier.
Baker WA, Lowery CM: Cardiac dysrhythmias. In Duke J, editor: Anesthesia secrets, ed 4, Philadelphia, 2011, Mosby
Elsevier.
Baker WA, Lowery CM: Electrocardiography. In Duke J, editor: Anesthesia secrets, ed 4, Philadelphia, 2011, Mosby Elsevier.
Becker DE: Fundamentals of electrocardiography interpretation, Anesth Prog 53:53–64, 2006.
Berul CI, Seslar SP, Zimetbaum PJ, Josephson ME: Acquired long QT syndrome. From UpToDate, Post TW, editor: Waltham.
Accessed on July 25, 2014.
Bickley LS: Bates’ guide to physical examination and history taking, ed 11, Philadephia, 2013, Wolters Kluwer Health.
Bisognano JD, Beck GR, Connell RW: Manual of outpatient cardiology, London, 2012, Springer.
Davies A, Scott A: Starting to read ECGs: the basics, London, 2014, Springer.
Dubin D: Rapid interpretation of EKG’s, ed 6, Fort Myers, 2000, Cover.
Gomella L, Haist S: Clinician’s pocket reference, ed 11, New York, 2007, McGraw-Hill.
Khan MG: Rapid ECG interpretation, ed 3, Totowa, 2008, Humana Press.
Longo D, Fauci A, Kasper D, Hauser S: Harrison’s principles of internal medicine, ed 18, New York, 2012, McGraw-Hill.
Podrid P, Ganz LI: Approach to the diagnosis and treatment of wide QRS complex tachycardias. From UpToDate, Literature
review current through: July 2014.
Strauss R: Interpretation of the electrocardiogram. In Laskin DM, editor: Clinician’s handbook of oral & maxillofacial
surgery, Hanover Park, 2010, Quintessence.
MCH = Hgb/RBC
LABORATORYTESTS
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Joel M. Friedman, Emery Nicholas
1. What is included in a complete blood count (CBC), and how are the results
charted?
The CBC, or heme 8, typically includes the items described in Table 4-1 and Figure 4-1.
2. What information does a white blood cell (WBC) differential provide?
The total WBC count is made up of neutrophils (50% to 70%), lymphocytes (20% to 40%), mono-
cytes (0% to 7%), eosinophils (0% to 5%), and basophils (0% to 1%). Most labs provide the absolute
number of each cell type as well as percentage. Differentials for alterations in the WBC fractions are
described in Box 4-1.
3. What is a left shift, and how is it significant?
Polymorphonuclear neutrophils (PMNs) are subdivided morphologically on the blood smear into segmented
neutrophils (segs or polys) and band forms (bands), based on the nuclear lobes and their chromatin
connections. The segs are more mature neutrophils, having two to five nuclear lobes and thin strands of
chromatin and comprising 50% to 70% of total PMNs. The bands are immature neutrophils, make up 0%
to 5% of total PMNs, and have a thick band of chromatin connecting one to two nuclear lobes. On the early
manual neutrophil counting machines, the keys that represented the bands were on the left side and the
keys representing segs were on the right. If the bands increased to more than 20% of the WBC total, or the
PMNs were more than 80% of the WBC total, the result was said to have a left shift. This shift increases
the likelihood of bacterial infection, sepsis, or hemorrhage as the etiology of an elevated WBC count.
4. How are the red blood cell (RBC) indices used clinically?
The indices are used to diagnose and classify anemia, which is defined as either a decreased RBC
mass or hemoglobin (Hgb) content below physiologic needs. The mean corpuscular volume (MCV) and
mean corpuscular hemoglobin concentration (MCHC) are the most useful in determining the etiology
of the anemia.
• MCV=(Hematocrit[Hct]×unitconstant)/RBC
• Macrocytic(>100fL):megaloblastic(pernicious)anemia(B12orfolatedeciency),chronicliver
disease, alcoholism, reticulocytosis, physiologic in the newborn
• Microcytic(<80fL):irondeciency,thalassemia,chronicdisease(cancer,renal,infection),orlead
toxicity
CHAPTER 4
The mean corpuscular hemoglobin (MCH) helps to diagnose chromaticity of cells because cells with
increased Hgb content will have more pigment (hyperchromic) and will be hypochromic in the reverse situation. Increased MCH suggests hyperchromic cells while decreased MCH suggest hypochromic cells. This
parallels changes in MCV in that macrocytic cells are hyperchromic and microcytic cells are hypochromic.
The MCHC increases with prolonged severe dehydration, heavy smoking, intravascular hemolysis, and spherocytosis. It will be decreased in over-hydration, iron deficiency anemia, thalassemia, and
sideroblastic anemia.
5. What does the reticulocyte count mean?
Reticulocytes are immature RBCs. These cells are larger, continue Hgb synthesis, and are bluer in color on
smears than mature erythrocytes. Reticulocytes constitute approximately 1% of total RBCs but can increase
when the need for erythrocytes rises. A corrected count is made by multiplying the reticulocyte count by
themeasuredHctdividedby45;theresultshouldbe<1.5%.Ifthecountisincreased,thenerythropoiesis
is usually caused by bleeding, hemolysis, and correction of iron, folate, or B12 deficiencies. Decreased
reticulocyte counts are often the result of transfusions or aplastic anemia.
45
46 PART I PATIENTEVALUATION
WBC
Hgb
Hct
Plt
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Table 4-1. Complete Blood Cell Count
DEFINITION NORMAL RANGE
White blood cell count 4-11×103cells/mm
RBC count 4.5-6×106cells/mm
Hgb Men:14-18g/dL
Women:12-16g/dL
Hematocrit Percentage of RBC mass in blood volume Men:40%-54%
Women:37%-47%
Platelets 150-400×103/mm
RBCindices:
Mean corpusclular volume AverageRBCvolumeinfL 80-100fL
Mean corpuscular hemoglobin EstimatesweightofHgbinaverageRBC 27-31pg
Mean corpuscular hemoglobin
concentration
fL, Femtoliters; Hgb, hemoglobin; RBC, red blood cell.
EstimatesaverageconcentrationofHgb
in average RBC
32%-36%
3
3
3
Figure 4-1. Demonstrates method of recording values in patient chart. The charting method allows universal communication with the patient progress notes.
Box 4-1. Differentials for Alterations in the White Blood Cell Fractions
Polymorphonuclear Neutrophils (PMNs)
Increased Decreased
Bacterial infection Aplastic anemia
Tissue damage (myocardial infarction, burn, or crush injury) Viral infection drugs
Leukemia Radiation
Uremia Kidney dialysis
Diabetic ketoacidosis (DKA)
Acute gout
Eclampsia
Physiologic:
Severeexercise
Latepregnancy
Labor
Surgery
Newborn
Lymphocytes (Lymphs)
Increased (lymphocytosis) Decreased
Viral infections Uremia
Acute or chronic lymphocytic leukemia Stress
Tuberculosis (TB) Burns
CHAPTER 4 LABORATORYTESTS 47
Hgb ×
*
=
RBC
Hgb
RBC × 9 = Hct
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Box 4-1. Differentials for Alterations in the White Blood Cell Fractions —(Continued )
Increased (lymphocytosis) Decreased
Mononucleosis Trauma
Monocytes
Increased (monocytosis) Decreased
Subacutebacterialendocarditis Aplasia of bone marrow
TB
Protozoal infection
Leukemia
Collagen disease
Basophils
Increased (basophilia) Decreased
Chronic myeloid leukemia Acute rheumatic fever
Polycythemia Lobarpneumonia
After recovery of infection or hypothyroidism (rarely) Steroidtreatment
Eosinophils
Increased (eosinophilia) Decreased
Allergy Steroids
Parasite Stress(infection,trauma,andburn)
Malignancy Increased adrenocorticotropic hormone (ACTH)
Drugs Cushing’s syndrome
Asthma
Addison’s disease
Collagen vascular diseases
Steroids
Normal in 20% of population
Stress
Thyrotoxicosis
6. What information is obtained from the Hgb and Hct values?
The Hgb concentration is an indicator of oxygen-carrying capacity of blood. It is dependent primarily
on the number of RBCs and much less significantly (or treatably) on the amount of Hgb per cell. Addi-
tionally,Hgbisknowntovarybyasmuchas1g/dLdiurnally,withpeaksinthemorning.Studieshave
alsoshowna1g/dLvariationbetweenHgbvaluesdrawnonadmissionandthosetakenfollowingone
nightofbedrest.TherelationbetweenHgbandHctisgivenby:
Increased Hgb and Hct values may result from polycythemia, dehydration, heart disease, increased
altitude, heavy smoking, or birth physiology. Decreased levels may indicate anemia, hemorrhage, dilution, alcohol, drugs, or pregnancy.
*Thisvariesbetween2.7and3.2basedontheMCHC.
7. Are Hgb and Hct primary indicators of blood loss and the need for transfusion?
No! These are poor early measures of bleeding because plasma and RBCs are lost in equal measures.
Ittakes2to3hoursafteruidresuscitationforHgb/Hcttoreectbloodloss.Todaymostpatients
aretransfusedforHgb<7g/dL,butthebestguidelinesarethevitalsignsandsymptomssuchas
shortness of breath and exercise intolerance. Initially low Hct values suggest chronic blood loss, which
should be supported by low MCV and a high reticulocyte count.
3
Hct
(millions) × 3 =
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8. What are some common terms and significant morphologic changes on smears?
• Poikilocytosis:IrregularlyshapedRBCs
• Anisocytosis:IrregularRBCsize
• Sickledcells:Crescentorsickle-shapedRBCsseenwithdecreasedoxygen(O2) tension
• Howell-Jollybodies:LargeRBCbasophilicinclusions(megaloblasticanemia,splenectomy,
hemolysis)
• Basophilicstippling:SmallRBCblueinclusions(leadpoisoning,thalassemia,heavymetals)
• Spherocytes:SphericalRBCs(autoimmunehemolyticanemia,hereditary)
• Burrcells:SpinyRBCs(liverdisease,anorexia,↑ bile acids)
• Schistocytes:HelmetRBCs(severeanemia,hemolytictransfusionreaction)
• Döhle’sinclusionbodies:PMNs(burns,infection)
• Toxicgranulation:PMNs(burns,sepsis,fever)
• Auerbodies:Acutemyelogenousleukemia
• Hypersegmentation:PMNswithsixtosevenlobes(megaloblasticanemia,liverdisease)
9. What is clinically useful about the platelet count?
• Anormalplateletcountis150,000to440,000/mm3. Thrombocytopenia is defined as a count of
<150,000/mm3 and is a quantitative platelet disorder. Intraoperative bleeding can be severe with
countsof40,000to70,000/mm3,andspontaneousbleedingusuallyoccursatcounts<20,000/mm3.
Theminimalrecommendedplateletcountbeforesurgeryis75,000/mm3 and it is safe to operate
providedplateletfunctionisnormal.Thrombocytopenia(lowplateletcount)thatis<50,000/mm3 is
an absolute contraindication to elective surgical procedures because of the possibility of significant
bleeding.
• Possibleetiologiesforlowplateletcountsareidiopathicthrombocytopenicpurpura(ITP),dissemi-
nated intravascular coagulation (DIC), marrow invasion or aplasia, hypersplenism, drugs, cirrhosis,
transfusions, and viral infections (mononucleosis).
• Althoughprophylacticpreoperativeplatelettransfusionisgenerallyadvocatedtotreatpreexisting
thrombocytopenia, the methods of evaluating clinical need are imprecise. Qualitative differences
in platelet function make it unwise to rely on platelet number as the sole criterion for transfusion.
Thrombocytopenic patients with accelerated destruction but active production of platelets have
relatively less bleeding than patients with hypoplastic disorders at a given platelet count.
10. How are platelet abnormalities categorized?
Plateletdisorderscanbeeitherquantitativeorqualitativeinnature:
• Quantitative platelet disorders:Inthese,theplateletcountisdecreased(thrombocytopenia)or
increased (thrombocytosis). They can be hereditary or, more often, acquired and include thrombocytopenia; dilution, as after massive blood transfusion; decreased platelet production as a result of malignant
infiltration (aplastic anemia, multiple myeloma); drugs (chemotherapy, cytotoxic drugs, ethanol, hydrochlorothiazide); radiation exposure; or bone marrow depression after viral infection. Other examples are
increased peripheral destruction due to hypersplenism, DIC, extensive tissue and vascular damage after
extensive burns, or immune mechanisms (ITP, drugs such as heparin, autoimmune diseases).
• Qualitative platelet disorders:Inthistypeofabnormality,theplateletcountmaybenormal,but
the platelets do not function normally. Therefore, increased bleeding can result. This abnormality
canalsobeaninherited(e.g.,vonWillebranddisease)and/oracquired(uremia;cirrhosis,particularlyafterethanol;drugs,suchasaspirin,NSAIDs)disorder.
11. What is bleeding time, and how does it assess platelet function?
Bleedingtimeisascreeningtestthatassessesplateletfunction.Thetestisperformedbyinatinga
blood pressure cuff to 40 mm Hg, making a standard incision in the patient’s forearm, and recording
the time until the bleeding stops (Ivy method). Normal bleeding time ranges from 4 to 9 minutes, and a
bleedingtime>1.5timesnormal(>15minutes)isconsideredsignicantlyabnormal.Ithasbeenrecommended that this test be used to diagnose specific hemorrhagic diseases and to monitor therapy of these
diseases, but not to screen preoperative patients who have no history of bleeding or abnormal coagulation studies. Assessment of preoperative platelet function is complicated by a lack of correlation between
bleeding time and any other test of platelet function and a tendency to increase intraoperative bleeding.
Thebleedingtimeisincreasedbyplateletcounts<100,000;bythepresenceofdrugssuchas
aspirin,NSAIDs,andantibiotics(syntheticpenicillins);andconditionssuchasuremia,alcoholism,
chronicliverdisease,vasculitis,Ehlers-Danlossyndrome,andvonWillebranddisease.Thereisan
undefined risk of bleeding with elevated test times until about double the control time.
CHAPTER 4 LABORATORYTESTS 49
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12. How do aspirin and NSAIDs affect platelet function and bleeding time?
Primary hemostasis is controlled by the balance between the opposing actions of two prostaglan-
dins:thromboxaneA2andprostacyclin.Dependingonthedose,salicylates(aspirin)produceadifferentialeffectonprostaglandinsynthesisinplateletsandvascularendothelialcells.Lowerdoses
preferentially inhibit platelet cyclooxygenase, impeding thromboxane A2 production and inhibiting
platelet aggregation irreversibly; as platelets lack a cell nucleus and cannot produce protein, the
effect lasts for their 7- to 10-day life span. The effect begins within 2 hours of ingestion. Because
approximately10%ofplateletsarereplacedeachday,ittakesanaverageof2to3daysfor
bleeding time to normalize, but most experts recommend allowing 7 days without aspirin before
surgery.
Othernonsteroidalantiinammatorydrugs(NSAIDs)reversiblyinhibittheactivityofcyclooxygenase,andthereforetheywillalterplateletfunctiononlytemporarily,usually<24hours.
NSAIDshaveasimilarbutmoretransienteffectthanaspirin,lastingforonly1to3daysafter
cessation of use.
13. Which clotting factors are synthesized in the liver?
Fourclottingfactorsaresynthesizedintheliver:factorsII,VII,IX,andX.
14. Which vitamin deficiency can affect coagulation and extrinsic pathway coagulation lab values?
VitaminKdeciency.VitaminKisrequiredforthesynthesisofcoagulationfactorsII,VII,IX,andX,as
wellasanticoagulantsproteinCandproteinS.
15. What are the differences between the coagulation tests?*
The basic difference between the intrinsic and extrinsic pathways is the phospholipid surface on
whichtheclottingfactorsinteractbeforeunionatthecommonpathway.Eitherplateletphospholipid (for the intrinsic pathway) or tissue thromboplastin (for the extrinsic pathway) can be added
tothepatient’splasma,andthetimetakenforclotformationismeasured.Lessthan30%of
normal factor activity is required for the tests to be sensitive enough to detect decreased levels.
Thetestsarealsoprolongedincasesofdecreasedbrinogenconcentration(<100mg/dL–1)and
dysfibrinogenemias.
Measurement of the Intrinsic and Common Pathways
1. Partial thromboplastin time (PTT)
• PTTmeasurestheclottingabilityofallfactorsintheintrinsicandcommonpathwaysexceptfactor
XIII.
• Partialthromboplastinissubstitutedforplateletphospholipidandeliminatesplateletvariability.
• NormalPTTisabout40to70seconds.
2. Activated PTT (aPTT)
• Anactivatorisaddedtothetesttubebeforeadditionofpartialthromboplastin;thisactivatorspeeds
up the clotting time, and a smaller and more consistent range of values results.
• NormalaPTTis25to35seconds.
• ThistestismoresensitivethanthePTTandthereforeusedoftentomonitorpatientsonheparin
therapy.
3. Activated clotting time (ACT)
• Freshwholeblood(providingplateletphospholipid)isaddedtoatesttubealreadycontainingan
activator.
• TheautomatedACTiswidelyusedtomonitorheparintherapyintheoperatingroom.
• Normalrangeis90to120seconds.
Measurement of the Extrinsic and Common Pathways
1. Prothrombin time (PT)
• Tissuethromboplastinisaddedtothepatient’splasma.
• TestvariesinsensitivityandresponsetooralanticoagulanttherapywhethermeasuredasPTinseconds
orsimplePTratio(PTpatient/PTnormal)(normal=themeannormalPTvalueofthelabtestsystem).
• NormalPTis11to13seconds.
*ReprintedfromKatzJJ:Coagulation.InDukeJ,editor:Anesthesia secrets, ed 2, Philadelphia, 2000, Hanley & Belfus.
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2. International normalized ratio (INR)
• Itwasdevelopedtostandardizetheinterpretationofcoagulationtests,whichcanvarywidely
based on testing method.
• ThisconvertsthePTratiotoavaluethatwouldhavebeenobtainedusingastandardPTmethod.
• INRiscalculatedas(PTpatient/PTnormal)ISI.(ISIistheinternationalsensitivityindexassignedto
the test system.)
• Therecommendedtherapeuticrangesforstandardoralanticoagulanttherapyandhigh-dose
therapy,respectively,areINRvaluesof2.0to3.0and2.5to3.5.
16. What are the most common indications of use of warfarin?
Themostcommonindicationsofwarfarintherapyare:
• Prophylaxisandtreatmentofdeepvenousthrombosisanditsextension,pulmonaryembolism(PE)
• Prophylaxisandtreatmentofthromboemboliccomplicationsassociatedwithatrialbrillation(AF)
and/orcardiacvalvereplacement
• Reductionintheriskofdeath,recurrentmyocardialinfarction(MI),andthromboembolicevents
such as stroke or systemic embolization after myocardial infarction, and congestive heart failure
17. What are the current indications for transfusion of fresh frozen plasma (FFP)?*
AtaskforceoftheAmericanSocietyofAnesthesiologists(ASA)recommendstheuseofFFPinthe
followingcircumstances:
• Urgentreversalofwarfarintherapy
• Correctionofknownanticoagulationdecienciesforwhichspecicconcentratesareunavailable
• Correctionofmicrovascularbleedinginthepresenceofelevated(>1.5timesnormal)PTorPTT
• Correctionofmicrovascularbleedingsecondarytocoagulationfactordecienciesinpatientstrans-
fused with more than one blood volume, when a PT or PTT cannot be obtained in a timely fashion
Thedosegivenshouldbecalculatedtoachieveaminimumof30%ofplasmafactorconcentration
(usuallyabout10to15mL/kgofFFP).
18. What are the indications for the use of platelets?*
TheASArecommendsthefollowing:
• Prophylacticplatelettransfusionisineffectiveandrarelyindicatedwhenthrombocytopeniais
caused by increased platelet destruction.
• Forsurgicalpatientswiththrombocytopeniacausedbydecreasedplateletproductionandsurgical
and obstetric patients with microvascular bleeding, platelet transfusion is rarely indicated when the
countis>100×109/Landusuallyindicatedifthecountis<50×109/L.Withintermediatevalues,
platelet therapy should be based on the risk of bleeding.
19. What is DIC?*
DIC is not a disease entity, but rather a manifestation of disease associated with various well-defined
clinicalentities:
• Obstetricconditions(amnioticuidembolism,placentalabruption,retainedfetussyndrome,
eclampsia, saline-induced abortion)
• Intravascularhemolysis(hemolytictransfusionsyndromes,minorhemolysis,massivetransfusion)
• Septicemia(gram-negative:endotoxin;gram-positive:mucopolysaccharides)
• Viremias(cytomegalovirus,hepatitis,varicella,HIV)
• Disseminatedmalignancy
• Leukemia
• Burns
• Crushinjuryandtissuenecrosis
• Liverdisease(obstructivejaundice,acutehepaticfailure)
• Prostheticdevices(LeVeenshunt,aorticballoon)
DIC usually is seen in clinical circumstances in which the extrinsic or intrinsic coagulation pathway (or
both) is activated by circulating phospholipid, leading to generation of thrombin; however, the usual
mechanisms preventing unbalanced thrombus formation are impaired. After systemic deposition of
intravascular fibrin thrombi, consumption of factors V and VIII, and loss of platelets, the resulting cir-
culating level of clotting factors and platelets represents a balance between depletion and production.
The fibrinolytic system is activated, and plasmin begins to cleave fibrinogen and fibrin into fibrinogen
and fibrin degradation products (FDPs). Recognition and understanding of the syndrome are made
difficult by the occurrence of both acute and chronic forms and by a clinical spectrum varying from
diffuse thrombosis to diffuse bleeding or both.
CHAPTER 4 LABORATORYTESTS 51
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20. What tests are used for the diagnosis of DIC?*
There is no one pathognomonic test for the diagnosis of DIC. In acute DIC, the PT is elevated in about
75% of patients, whereas PTT is prolonged in 50% to 60%. Platelet count is typically greatly reduced
and hypofibrinogenemia is common. The D-dimer test is a newer diagnostic test. The D-dimer is
a neoantigen formed by the action of thrombin in converting fibrinogen to cross-linked fibrin. It is
specific for fibrin degradation products formed from the digestion of cross-linked fibrin by plasmin.
In85%to100%ofpatientswithDIC,FDPsareelevated.ElevatedlevelsarenotdiagnosticofDICbut
indicate the presence of plasmin and plasmin degradation of fibrinogen or fibrin.
21. What is the treatment for DIC?*
The treatment for DIC is case-dependent and controversial. The triggering process should be identified
and treated accordingly. Heparin is the first-line treatment used to stop bleeding and the consumption
process before administration of specific coagulation products. If these measures fail, specific blood
components may be depleted and should be replaced after identification. If bleeding still continues,
antifibrinolytic therapy with epsilon aminocaproic acid should be considered, but only if the intravas-
cular coagulation process is shown to have stopped and residual fibrinolysis to continue.
22. What factors increase and decrease PT?
PT will be increased by warfarin, vitamin K deficiency, fat malabsorption, liver disease, DIC, and
artificially increased tourniquet time. Warfarin blocks vitamin K use, whereas broad-spectrum antibiot-
icselevatePTbykillingnormalbowelora,whichdecreasesvitaminKabsorption.Heparininhigh
dosesalsowillincreasePTbyalteringfactorX.FFPwillreversewarfarineffectsimmediately,whereas
vitamin K requires 12 to 24 hours to begin decreasing the PT. For most minor oral surgical procedures,
INR<3.5isunlikelytoproducesignicantperi-operativebleedingepisodes.
23. How does heparin work?
Heparin’s primary effect is to activate antithrombin III, which blocks coagulation by inhibiting mostly
factorsIXandX.AntithrombinIIIamountsaresignicantlydecreasedinseveremalignancy,severeliver
disease, nephrotic syndrome, deep venous thrombosis (DVT), septicemia, major surgery, malnutrition,
andDIC.Lowmolecularweightheparin(enoxaparin)alsoworksonantithrombinIII.Heparin’speak
effectisat30minutesto1hourafterintravenoususeand3to4hoursaftersubcutaneousdose;its
durationofeffectisapproximately3to4hourswhengivenintravenouslyand6hourssubcutaneously.
24. Why are FDPs and fibrin split products (FSPs) important?
The result of the clotting cascade is an insoluble polymeric fibrin meshwork. Naturally occurring
fibrinolysin (plasmin) attacks and breaks down fibrinogen and fibrin, leaving split products behind.
Physiologically, this occurs after trauma or surgery and is quickly regulated. Pathologically, plasmin may
be activated in DIC, DVT, malignancy, emboli, infections (especially gram-negative sepsis), necrosis, or
infarctions. This will result in an elevated fibrin split product assay. Fibrinogen assays will be decreased
(<150mg/dL)inDIC,burns,surgery,neoplasia,severeacutebleeding,snakebites,andsomehemato-
logicdiseases.ProtaminesulfateandD-dimer(aspecicFSP)areotherteststhatlookforabnormal
clotting activity. Though not very specific, the D-dimer assay is used to screen for DVT in the emergency
department because a normal value virtually excludes the possibility of this clotting problem.
25. What is measured in a blood chemistry test (also called basic metabolic, chem 7,
or SMA 7), and how is it charted?
The basic electrolytes, renal function evaluation, and blood glucose are tested (Fig. 4-2).
Normal Ranges
1. Sodium(Na) 136-145mEq/L
2. Potassium (K) 3.5-5.2mEq/L
3. Chloride (Cl) 95-108mEq/L
4. Carbon dioxide (CO2) 24-30mEq/L
5. Bloodureanitrogen(BUN) 6-20mg/dL
6. Creatinine 0.7-1.4mg/dL
7. Glucose 65-110mg/dL(fasting)
*ReprintedfromKatzJJ:Coagulation.InDukeJ,editor:Anesthesia secrets, ed 2, Philadelphia, 2000, Hanley & Belfus.
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