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    Chapter 4: Preoperative

    Evaluation

    Screening ProceduresSummary of Perioperative Laboratory Testing

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    THE PREOPERATIVE EVALUATIONAn adequate pre-op preparation of the surgical patient is of the utmostimportance. The quality of pre-anesthetic care largely determines theoutcome, especially in patients with significant medical problems. What willconstitute proper pre-anesthetic screening will vary from patient to patientaccording to their physical status and chronological age. The anesthetic

    technique applicable to healthy patients for simple procedures will differ froma more complex technique for major procedures.

    Screening Procedures1. The History: Amedical history obtaining relevant information:a. DOES THE PATIENT HAVE AN M.D. AND IS HE/SHE PRESENTLY TREATINGTHIS PATIENTb. PRESENT or PAST MEDICAL PROBLEMSc. PREVIOUS HOSPITALIZATIONS/SURGERY & PROBLEMS WITH ANESTHESIAOR CLOTTING OR SCAR FORMATIONd. TAKING ANY MEDICATIONS FOR ANYTHING (RX OR OTC'S)

    e. ANY KNOWN ALLERGIESf. FAMILY HISTORY ( SICKLE CELL, DIABETES, HYPERTENSION, REACTION TOANESTHESIA, ETC.)g. SOCIAL HISTORY (SMOKING, DRINKING, DRUGS ETC.)h. REVIEW OF SYSTEMS

    2. The Physical Examination:a. Vital Signs: B.P., TEMP, PULSE, AND RESPIRATIONSb. Review of systems: HEAD AND NECK, LUNGS AND HEART (AUSCULTATION),ABDOMINAL, GI, GU, EXTREMITIES, NEUROLOGICAL, DERMATOLOGICAL,VASCULAR, AND ORTHOPEDIC/BIOMECHANICAL

    3.

    Laboratory Testing: BLOOD WORK, URINALYSIS, EKG AND CHEST XRAY(CXR)a. Complete Blood Count (Normal adult values):

    i. WBC- 4,800-10,800/mm3

    NOTE* ONCE THIS INFORMATION IS KNOWN THE PATIENT'S PHYSICALCONDITION CAN BE CATEGORIZED ACCORDING TO THECLASSIFICATION OF PHYSICAL STATUS ADOPTED BY THE AMERICANSOCIETY OF ANESTHESIOLOGISTS (ASA PHYSICAL STATUS)- Seesection Anesthesia

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    ii. WBC differential: allows for identification of the proportions of each type ofWBC for a more specific diagnosis of a disease entityDivided into 2 groups: Granulocytes (neutrophils, eosinophils, basophils) andNongranulocytes (lymphocytes, monocytes)

    NON-GRANULOCYTES:Lymphocytes (20-40%): involved in antibody production, function in cell-

    mediated immunity, delayed hypersensitivity, graft rejection, defense againstintracellular organisms such as tubercle bacillus, brucella, and neoplasms. AnIncrease can indicate VIRUSES (MOST COMMON), GERMAN MEASLES,BRUCELLOSIS, CONGENITAL SYPHILIS, THYROTOXICOSIS, PERTUSSIS, ANDMONONUCLEOSIS. A decrease can indicate HODGKIN'S DISEASE, DRUGS. ORIRRADIATION, AND IMMUNOLOGICAL DEFICIENCY DISORDERS.

    Monocytes (4-8%): transform into macrophages which destroy/ingestbacteria etc. An Increase can indicate RECOVERY FROM ACUTE INFECTIONS,

    SUBACUTE BACTERIAL ENDOCARDITIS, MYCOTIC/RICKETTSIAL/PROTOZOAL &VIRAL INFECTIONS, HEMATOLOGIC DISEASE, LEUKEMIA, AND HODGKIN'SDISEASE.

    GRANULOCYTES:Neutrophils (45-65%): same as PMN's (either SEGS 40-60% or Bands 0-

    5%). The first specific line of defense for the body, an increase being called aSHIFT LEFT (of immature neutrophils, called bands) usually indicating anacute bacterial infection. A decrease in neutrophils, NEUTROPENIA, may

    NOTE* A WBC GREATER THAN 11, 000= LEUKOCYTOSIS Leukocytosis dueto:a. AN ACUTE BACTERIAL INFECTION (Viral infection usually has normalWBC's)b. INTOXICATIONS (GOUT, HEAVY METAL POISONING, VACCINES)c. HEMOLYSIS

    d. HEMORRHAGEe. MYELOPROLIFERATIVE DISORDERSf. NORMAL VARIANTg. STRESSh. DEHYDRATION/ HEMOCONCENTRATION

    NOTE* A WBC LESS THAN 4, 400= LEUKOPENIA Leukopenia can be due to:a. SEVERE INFECTION OR SEPTICEMIAb. HEPATITISc. DRUGS (SULFA, ANALGESICS, BUTAZOLIDIN, THORAZINE)d. TRAUMA AND AIDSe. MYELOPROLIFERATIVE DISORDERS (MOST COMMON)

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    indicate an OVERWHELMING BACTERIAL INFECTION, SEVERE FUNGAL ORVIRAL INFECTION, BONE MARROW DEPRESSION, AUTOANTIBODIES, BONEMARROW REPLACEMENT, HYPERSPLENISM, AND MATURATION DEFECTS(VITAMIN DEFECTS)An Increase in neutrophils, NEUTROPHILIA, can indicate: INFECTION

    (TYPHOID), TOXIC AGENTS, PHYSICAL OR EMOTIONAL STIMULI, TISSUENECROSIS, HEMORRHAGE, HEMOLYSIS, AND HEMOLYTIC DISORDERS, ORRECENT STRAINED DEFECATION (VALSALVA MANEUVER).

    Eosinophils (1 -3%): contain histamine and transport alkalinephosphatase, an increase indicating INTESTINAL PARASITES, ALLERGICREACTIONS, URTICARIAL SKIN ERUPTIONS, LEUKEMIA, GI DISTURBANCES ORSCARLET FEVER. A decrease can indicate SEVERE INFECTIONS, CUSHING'SSYNDROME, ELECTRIC SHOCK THERAPY, AFTER INJECTION WITH ACTH OREPINEPHRINE.

    Basophils (0-1 %): contain heparin and transport alk phos and histamine,an increase is associated with POLYCYTHEMIA,LEUKEMIA, CHICKEN POX, SMALL POX. A decrease can be due to ACUTEINFECTIONS AND ACTH OR CORTICOSTEROIDS

    iii. PLATELET COUNT (150,000-400,000): Platelet disorders should besuspected in patients exhibiting PETECHIAE in the skin or mucosa.THROMBOCYTOPENIA: Decreased platelet count, is seen with

    THROMBOCYTOPENIA PURPURA, APLASTIC ANEMIA, OR SEPTICEMIA.

    THROMBOCYTOSIS: Increased platelet count seen with splenectomy,malignancy, and patient is prone to form clots with this conditioniv. RBC's: (Male, 4,700,000-6,100,000mm3) (Female, 4,200,000-5,400,000/mm3)

    NOTE* Usually with a shift left there is a characteristic relative fall inlymphocytes with neutrophil leukocytosis and increase in young forms.When the infection subsides and the fever drops, the total number ofleukocytes decreases

    NOTE* The most common cause of thrombocytopenia is chemotherapy

    Neutropenia may be the earliest clue to marrow failure

    Decreased platelet count increases the risk for hemorrhage. If the plateletcount is less than 60,000 give platelets (1 unit will raise the count

    5,000/cu mm. For any elective surgery the thrombocytopenic patientshould be postponed

    An increase may be due to POLYCYTHEMIA, METASTATIC CARCINOMAAFFECTING THE MARROW, THALASSEMIA, INCREASED ALTITUDE,EXERCISE OR EMOTIONAL STRAIN

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    v. RETICULOCYTE COUNT (.5-1.5% OF THE TOTAL RED COUNT):

    It is the best indicator to assess marrow activity

    Increases found with IRON DEFICIENCY AND MEGALOBLASTIC ANEMIA(recent bleeding/hemorrhage is the #1 cause)

    Decreases found with MACROCYTIC AND APLASTIC ANEMIAS

    vi. HEMATOCRIT (Males 43-53% Gm/dl) (Females 35-47% Gm/dl):

    That portion of the total blood volume occupied by red cells versusplasma

    Increased with POLYCYTHEMIA, DEHYDRATION OR ADDISON'S DISEASE

    Decreased with anemias and hemorrhage

    vii. HEMOGLOBIN (Males 12-17) (Females 11-16):

    Gives red cells their oxygen carrying capacity Increased with POLYCYTHEMIA, HEMOLYTIC ANEMIA, AND PORPHYRIAS

    Decreased with other anemias, HEMOGLOBINOPATHY and hemorrhage

    viii. MCV=HCT/RBC: Reflects the size of the red cell

    ix. MCH=Hb/RBC: Is an estimate of Hb in the average cell

    x. MCHC=Hb/HCT: An estimate of Hb In an average cell

    Decreased MCV Increased MCVIron deficiencies Pernicious anemiaThalessemia (B12 and Folate deficiency)

    Lead poisoning Liver diseaseSideroblastic anemia Hypothyroidism

    Hypernatremia Leukemia

    NOTE* THE HCT IS USUALLY 3 TIMES THE Hb

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    i.. Platelet count: for quantification purposesii. Prothrombin time: measurement of extrinsic blood coagulation pathway(normal 11-13 seconds)PT will be long with deficiencies of prothrombin, Factor V, Factor Il, or FactorX

    Affected by coumadin type anticoagulants

    iii. Partial thromboplastin time: measurement of intrinsic blood coagulationpathway (24-26 seconds is normal) and should be within 5 seconds of thecontrol (control is up to 45 seconds in some labs).iv. Bleeding time (Lee-White): a standard in vivo assay that measures theeffectiveness of platelet plug formation. This test is performed in patientswho are suspected of having a qualitative platelet disorder, such as patientshaving recently taken ASA or who have von Willebrand's disease

    c. Sequential Multiple Analyzer (SMA)SMA 12 has the following tests: ALBUMIN, ALKALINE PHOSPHATASE,BILIRUBIN, BLOOD UREA NITROGEN, CALCIUM, CHOLESTEROL, LACTATE

    NOTE* The mechanism for blood clotting may be divided into 3 stages:Stage 1: The production of plasma (extrinsic) or tissue (intrinsic)

    thromboplastin to form prothrombin activator.Stage 2: The conversion of fibrinogen to fibrin by the proteolytic action ofthrombin.Stage 3: The conversion of fibrinogen to fibrin by the proteolytic action ofthrombin. Calcium is required for all stages.

    NOTE* Coumadin prevents the conversion of vitamin K to its active form,thereby impairing the formation of vitamin K-dependent clotting factors.It is an anticoagulant indicated for the prophylaxis or treatment of

    venous thrombosis, pulmonary embolism, atrial fibrillation withembolization, and as a prophylaxis of embolism after myocardialinfarction.Coumadin therapy should be monitored by monthly internationalnormalized ratio (INR) testing. The test represents a standardized orcorrected prothrombin time since results for prothrombin time may varyby institution. The INR should be obtained preoperatively for anypatient on coumadin (Warfarin) and should range from 2 to 3.The dosing of the coumadin should be adjusted preoperatively so that theINR is maintained at the low end of of the therapeutic range. Holding thedose of coumadin for 2-3 days prior to elective surgery will provide

    protection against intraoperative bleeding without compromisingprophylaxis of the patient. If necessary, the coumadin effects on the INRmay be reversed by the administration of vitamin K1 or fresh frozenplasma

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    DEHYDROGENASE, SGOT, GLUCOSE, PHOSPHATE, TOTAL PROTEIN, AND URICACIDSMA 16 adds the following four electrolytes: NA, K, CL, AND C021. Albumin (3.6-5.2 Gm/dl): A blood protein from the liver-a good indicator ofhepatic health

    Reduced levels are a problem and can result in EDEMA Increased levels can cause dehydration

    Reduction due to: LIVER DISEASE, MALIGNANCY, MALNUTRITION, KIDNEYPATHOLOGY AND LARGE SKIN WOUNDS WITH SERUM LOSS SUCH ASBURNS

    ii. Alkaline Phosphatase (35-137 U/dl):

    Found in the liver, bone, placenta and lung as tissue-specific formsAnything that stimulates osteoblastic activity increases the Alk

    Phosphatase: METASTATIC BONE CANCER, GROWING CHILD, OSTEOGENICSARCOMA, PAGET'S DISEASE OF BONE, MONONUCLEOSIS, PREGNANCY,GROWTH AFTER FRACTURE

    iii. Bilirubin (less than 1.2 mg/dl):

    It is a pigment of bile from RBC breakdown in liver, spleen and marrow. Problems develop from abnormal production and decreased excretion

    Total bilirubin divided into direct and indirect fractions (direct increaseddue to direct hepatic obstruction- indirect due to liver disease.

    Bilirubin increased with: CIRRHOSIS, ACUTE VIRAL HEPATITIS, CHF,HEMOLYSIS AND SEPTICEMIA

    iv. Blood Urea Nitrogen (5-25 mg/dl):Isan end product of protein metabolism and produced only in the liver

    and excreted by the kidney.

    BUN increased with: DIABETES AND PROTEIN BREAKDOWN, KIDNEYPATHOLOGY, FEVER AND PROTEIN BREAKDOWN, CHF, RBC BREAKDOWNAND STARVATION (dehydration is #1 cause)

    BUN decreased with: HYDRATION, LIVER PATHOLOGY AND DECREASED

    PRODUCTION

    v. Calcium (4.5-5.5 mg/dl):Serum calcium increased with any disease of bony demineralization such

    as: MULTIPLE MYELOMA, CANCER OF BONE, EXCESSIVE CALCIUM INTAKE,HYPERPARATHYROIDISM AND HYPERVITAMINOSIS D.

    Serum calcium decreased with: RENAL FAILURE (#1), POOR ABSORPTION,MALNUTRITION, HYPOPARATHYROIDISM,PSEUDOHYPOPARATHYROIDISM AND DIARRHEA

    NOTE* The most common cause of elevated liver alkaline phosphataseis common duct obstruction, and the second most common cause is bedrest in the hospitalized patient

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    vi. Chlorides (98-110 meq/L): Usually lost from the urine or GI fluid which carry the chloride ion

    Chlorides decreased with: DEHYDRATION (#1), VOMITING, DIARRHEA,ULCER AND FLUID LOSS, EDEMA, DIURESIS, GI OBSTRUCTION ANDINFECTION.

    Rare to have elevated chloride, if so, can indicate CYSTIC FIBROSIS

    vii. Cholesterol (150-220 mg/dl): Produced from food and endogenous production (mostly in the liver) Used for membranes, STEROID hormones and bile acids.

    Increases: IDIOPATHIC, HYPOTHYROIDISM, DIABETES MELLITUS,PANCREATITIS

    Decreases: MALABSORPTION, LIVER DAMAGE AND POOR PRODUCTION

    viii. Creatinine (under 1.2 mg%):

    Produced from creatine in muscle tissue and excreted by the kidneys -Not

    elevated in the blood until 50% of renal function obliterated Any major reduction in creatinine clearance of urine indicates kidney

    impairment

    ix. Glucose (70-110 mg/dl):

    The liver produces glucose from protein (gluconeogenesis).

    Blood glucose is filtered through the kidney glomeruli and reabsorbed inthe proximal tubule, and if renal threshold is exceeded glucose is spilledinto the urine.

    Elevated with: DIABETES MELLITUS, CUSHING'S SYNDROME,ACROMEGALY, STRESS, BURNS, SHOCK, ACUTE PANCREATITIS, OBESITY,

    ACTH ADMINISTRATION AND AGE Decreased with: INSULIN SHOCK, ISLET CELL TUMOR, NUTRITION,

    GLUCAGON DEFICIENCY, ADDISON'S DISEASE AND HYPOTHYROIDISM(Hypoglycemia may be precursor to DM)

    x. Lactate Dehydrogenase (208-378U/L):

    This is a glycolytic enzyme that functions in carbohydrate metabolismwhich is found in the kidney, liver, heart, RBC's.

    Increased with any tissue damage, therefore it is NOT SPECIFIC

    xi. Total Protein (6.4-8.3 g/dI):

    Contains albumin and globulins and rarely is total protein increased sincemost disease states lower body reserves

    Increased with: DEHYDRATION caused by vomiting and diarrhea

    Albumin:Globulin Ratio= 1.5:1-2.5:1

    xii. Phosphate (8-12 mg/dl):

    it is absorbed in the intestine, stored in bone, and excreted by the kidneys

    Elevated with: RENAL FAILURE, HYPOPARATHYROIDISM, INCREASE VIT D

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    INTAKE, BONE DISEASE, FRACTURES, PAGET'S DISEASE OF BONE,MULTIPLE MYELOMA

    Decreased with: HYPOVITAMINOSIS D, DIABETES, HYPERPARATHYROIDISM(MOST COMMON IS POOR NUTRITION)

    xiii. Potassium (3.5-5.1 mEq/l): Very important element in the pre-opevaluation

    Decreased K produces muscle cramps and arrhythmias while increased Kproduces arrhythmias and cardiac pathology

    increased with: USE OF MINERALCORTICOIDS, RENAL FAILURE, ACIDOSIS,DIABETIC KETOACIDOSIS.

    Decreased with: ALKALOSIS, DIARRHEA, DIURETICS, INSULIN,MALABSORPTION AND STARVATION (#1 cause is with excess IV's)-Symptoms don't start until serum levels fall below 2.5 mEq/L -Cardiacstandstill can occur when levels exceed 7.5-8.0 mEq/L

    xiv. SGOT (AST 1-45 IU/L):

    The enzyme used in glycolysis and energy production and found mostly inthe liver, heart, and also in the muscle, kidney, and pancreas.

    Sudden increase seen with MI, also with liver and lung pathology

    Elevated in: CARDIAC DAMAGE, LIVER DAMAGE, SKELETAL PATHOLOGY,PANCREATIC PATHOLOGY.

    xv. Uric Acid (2.8-8.0 mg/dl): Manufactured from purine metabolism

    The pH of urine must be close to 7.4, as uric acid is poorly soluble as thepH decreases with crystals forming depositing in tissues across the cellmembrane. Therefore alkalinization of the urine increases uricosuricactivity.

    xvi. Serum Amylase: NOT USUALLY DONE PREOPERATIVELY

    Enzymes produced in the pancreas and used for the digestion of starch

    Elevation due to cellular destruction of amylase in the pancreas or poorrenal excretion, due to: PANCREATITIS, PERFORATED ULCER, PANCREATICDUCT OBSTRUCTION, AND RENAL FAILURE.

    Decreased due to CHRONIC PANCREATIC OBSTRUCTION.

    The SGOT parallels the SGPT AL , whose normal values = 1-60 IU/L,

    except the SGOT shows higher values with MI and the SGPT hashigher values with LIVER PATHOLOGY

    NOTE* Elevated SCOT (AST) seen in pulmonary embolism postoperatively

    NOTE* WHEN TREATING GOUT CHECK THE pH OF THE URINE

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    xvi. Acetone: Detected by dipstick urine test- should be negative

    ketone body from fat metabolism

    Elevated with: STARVATION, STRESS, DIABETES, LOW CARBOHYDRATEDIET

    xvii. Acid phosphatase: NOT USUALLY DONE PREOPERATIVELY

    Found in the male prostate, the male urine, RBC's and platelets (female).

    High levels consistent with METASTATIC CARCINOMA OF THE PROSTATE

    Can also be elevated with MULTIPLE MYELOMA AND PAGET'S DISEASE OFBONE

    4. URINE ANALYSIS:a. A multitest dipstick is used on the urine to get rough readings on glucose,acetone, bile, urobilinogen, protein and blood. The urine is then centrifugedand the solid matter goes to the bottom and is then examinedmicroscopically for red/white/epithelial cells, crystals and casts.

    b. Also checked is the color, clarity, pH and specific gravityc. The specific gravity range is 1.020-1.032. (when concentrated in the AM)

    A measure of the kidney's ability to concentrate and the SG is elevated byextra glucose (diabetes) and protein due to increased concentration in thefluid.d. All glucose in the urine is competely reabsorbed by the proximal tubules,therefore the appearance of glucose in the urine when the blood glucoselevels is below 180 (250 IN SOME TEXTS) may signify proximal tubuledamage.e. Small amounts of protein are found in the urine (albumin and globulins),however, large amounts in excess of 4gms daily indicate glomerular disease

    (mostly albumin)f. Ketone bodies accumulate due to altered lipid metabolism, most frequentlyas a consequence of diabetes mellitus or low carbohydrate dietg. OCCULT hematuria occurs from: EXCERCISE (#1), CYSTITIS,HEMORRHAGE, MENSTRUATION, GLOMERULONEPHRITIS, HYPERTENSION,POLYCYSTIC DISEASE AND RENAL THROMBOSISi. Microscopic hematuria seen with acute infection, sickle cell anemia,excercise, menses and SBE.h. GROSS hematuria associated with stones, tumors, TB, and acute

    NOTE*AS KETONES INCREASE pH DECREASES

    NOTE*: SERUM PROFILELIVER- BILIRUBIN, CHOLESTEROL, SGOT, SGPT, ALKALINE PHOSPHATASE,

    ALBUMINKIDNEY- CHLORIDE, CREATININE, BUN, PHOSPHOROUS, PROTEIN, TOTALPROTEIN, LDH, Na, K, C1, Co2CARDIAC- LDH, CPK, SGOT, ELECTROLYTES, BUNARTHRITIC- LATEX FIX, ESR, VDRL, ANA, ASO TITER, URIC ACID, LE PREP( RARELY DONE- ANA MORE ACCURATE)

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    glomerulonephritis.i. Normal urine is slightly acidic, pH usually below 5.3, is-altered by diet ormedicationsi. An alkaline urine in the presence of metabolic acidosis suggests RenalTubular Acidosis.

    j. Normal findings in the urinary sediment includes up to : 1 RBC, 5 WBC'S,AND AN OCCASIONAL CAST.k. Abnormal findings in the sediment include: RBC'S, WBC CASTS, YEAST,CRYSTALS OR EPITHELIAL CELLS.l. Casts are protein conglomerations in the shape of the renal tubule.Two types of casts:i. CELLULAR- RBC, WBC, EPITHELIAL CELLS, OR ANY COMBINATION IN APROTEIN MATRIX

    ii. PROTEIN- are composed entirely of proteinm. Crystals in the urine may indicate stones or certain metabolic diseasesn. Bile present indicates hepatic obstruction or constipationo. Urobilinogen can be present due to HEPATITISp. Catecholamines: elevation in the urine is indicative of pheochromocytomaor extramedullary chromaffin tumors, malignant hypertension, progressivems. dystrophy, myasthenia gravis, and drugs. (this is not usually donepreoperatively)

    5. Pregnancy testing:Should be performed on all women within childbearing years

    6. Chest x-ray:This compliments the H & P as a starting point for the diagnosis andevaluation of suspected pulmonary disorders. Abnormalities seen on the x-ray are: CHF, pulmonary masses, pleural effusions, pneumonia. Rememberthat the chest x-ray alone is not a good indicator for operative risk

    7. Electrocardiogram:Recommended that all patients over the age of 40 have this test done,

    NOTE* An alkaline urine is most commonly seen in a proteus UTI

    NOTE* With WBC casts, the cells become emulsified in the protein matrix andmay be found in pyelonephritis, acute glomerulonephritis, or SLE.The cells in RBC cell casts are emulsified in protein matrix and are indicative ofglomerulitis.Casts containing fat droplets are called fatty casts and are associated withnephrotic syndrome

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    however, a poor predictor of ischemic heart disease and perioperativecardiac morbidity and mortality. Electrocardiography is a graphicrepresentation of the electrical currents associated with the contraction ofthe heart muscle. The basic function of the electrocardiographic monitor is toamplify the small voltage formed by the depolarization of the heart so that itcan be presented on the screen for visual monitoring or so that a graphicrecord can be made.a. Conduction mechanism of the hearti. Sinoatrial node (SA): The electrical impulse is formed in the SA node, whichis the physiologic pacemaker of the heart, located at the junction of the rightatrium and superior vena cavaii. Atrioventricular node (AV): After the SA node the impulse speeds to the AVnode, at the junction of the atria and ventricles

    iii. Bundle of His: After the AV node fires, the impulse travels to the bundle ofHis, then the right and left bundle branches, Purkinje's fibers, and theventriclesb. The normal electrocardiogram:i. P wave: Indicates the results of the electrical activity during atrialdepolarization that initiates atrial contractions

    P-R interval: Represents the time it takes the impulse to spread from theSA node to the ventricles (normal time 0.12-0.20 sec)

    Normal EKG Tracing

    i. QRS complex: Is due to the depolarization of the ventricles, which triggerstheir contraction. It indicates the time it takes for ventricular depolarization

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    2. Urinalysis:a. Dipstick: Protein, blood, glucose, ketones, pHb. Microscopic exam: RBC's, WBC's, cellular casts, bacteria, crystals

    3. Pulmonary function tests:a. Static lung volumes: Total lung capacity, functional residual capacity,residual volume, vital capacityb. Dynamic volume measurement: Forced vital capacity (FVC), forced vitalcapacity in 1 second (FEV1), and FEV1 /FVC

    4. Arterial blood gas: Oxygenation, carbon dioxide, 02 saturation, pH5. Chest x-rays: Cardiac size, calcifications, lung masses, pleural effusions,infiltrates, interstitial patterns

    6. EKG:a. Rateb. Rhythmc. Intracardiac conduction times (PR interval, QRS interval, QT interval)d. Chamber enlargement (hypertrophy of myocardium)e. Myocardial infarction patterns (pathologic Q waves)f. ST segments of ischemia