Ipapburke Pulm Test 2- Pulm. Embolism

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ESSENTIALS TO DIAGNOSIS OF A PULMONARY EMBOLISM

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PREDISPOSITION TO VENOUS THROMBOSIS, ABRUPT** ONSET OF DYSPNEA, CHEST PAIN, APPREHENSION, HEMOPTYSIS, AND SYNCOPE; ACUTE RESPIRATORY ALKALOSIS AND HYPOXEMIA IN MOST; CHAR. DEFECTS ON VENT/PERF LUNG SCAN; DIAGNOSTIC FINDINGS ON PULMONARY ANGIOGRAM OR SPIRAL CT

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SOURCES OF PULMONARY EMBOLISM

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FROM THROMBI IN VENOUS CIRCULATION OR RIGHT SIDE OF HEART (THROMBOEMBOLISM); FROM TUMOR THAT INVADED VENOUS CIRCULATION (TUMOR EMBOLI); FROM OTHER SOURCES- AMNIOTIC FLUID, AIR, FAT, BONE MARROW, AND IV MATERIAL

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WHAT DO MOST PE'S ORIGINATE AS?

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CLOTS IN DEEP VEINS OF LOWER EXTREMITIES, ESP. CALVES

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VIRCHOW'S TRIAD (DVT)

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VENOUS STATIS, VENOUS ENDOTEHLIAL INJURY, AND HYPERCOAGULABILITY

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WHAT TYPES OF THINGS LEAD TO HYPERCOAGULABILITY?

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ORAL CONTRACEPTIVES, CANCER, AND OTHER BLOOD DYSCRASIAS (DISORDER OF ONE OF THE FORMED ELEMENTS OF THE BLOOD)

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CLINICAL RISK FACTORS FOR DVT

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PROLONGED BED REST OR INACTIVITY, SURGERY, CHILD BIRTH, ADVANCED AGE, STROKE, MI CHF, OBESITY, FRACTURES OF HIP OR FEMUR

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MOST COMMON CAUSE OF DVT IN CAUCASIAN POPULATION

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FACTOR V LEIDEN --CAUSES RESISTANCE TO ACTIVATED PROTEIN C, PROTEIN S, AND ANTITHROMBIN III

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WHAT PERCENT OF P.E. PATIENTS DIE WITHIN THE FIRST HOUR?

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10%

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MOST COMMON CAUSE OF PE IN CAUCASIAN POPULATION

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FACTOR V LEIDEN

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WHAT IS THE RESULT OF A THROMBUS IN A PULMONARY ARTERY

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HEMODYNAMIC EFFECT WITH OBSTRUCTION OF VASCULAR BED AND REFLEX VASOCONSTRICTION; THE HEMODYNAMIC EFFECT RESULTS IN INCREASED PULMONARY VASCULAR RESISTANCE AND AT THE EXTREMES CAUSES PULMONARY HYPERTENSION AND RV FAILURE

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PULMONARY EFFECTS OF PE

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WILL GET REFLEX BRONCHOCONSTRICTION IN EMBOLIZED AREA; ALSO GET INCREASED DEAD SPACE AND LOSS OF ALVEOLAR SURFACTANT

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ABSOLUTE PULMONARY INFARCTION FROM A PE IS ________.

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UNCOMMON

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SIGNS AND SYMPTOMS OF A PE

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VERY PRONOUNCED OR SUBTLE DEPENDING ON SIZE OF PE AND PT'S CARDIOPULMONARY STATUS; CHEST PAIN, DYSPNEA, APPREHENSION, COUGH, HEMOPTYSIS, DIAPHORESIS, SYNCOPE IF MASSIVE PE; TACHYCARDIA, TACHYPNEA, CRACKLES, ACCENTUATION OF PULMONARY COMPONENT OF SECOND HEART SOUND

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MAY APPEAR LIKE PNEUMONIA, MI, PNEUMOTHORAX, AND EVEN RIB FRACTURE

Back 14

PE (LOOK FOR THROMBOPHLEBITIS)

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LAB FINDINGS IN PE (EVEN THOUGH NOT VERY HELPFUL SOMETIMES)

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ABGS NOTE RESPIRATORY ALKALOSIS SECONDARY TO HYPERVENTILATION, OFTEN WITH PAO2 UNDER 80 MM; EKG USUALLY ABNORMAL, BUT NOT SPECIFIC, PFTS ALSO NONSPECIFIC

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CXR IN PE

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OFTEN NONSPECIFIC WITH ELEVATION OF HEMIDIAPHRAGM AND PULMONARY INFILTRATES MOST COMMON; PROMINENCE OF PULMONARY ARTERY; HAMPTOM'S HUMP

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HAMPTOMS HUMP

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WEDGE SHAPED DENSITY POINTING TOWARD HILUM ON CXR INDICATIVE OF PE

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HOW IS PERFUSION SCAN PERFORMED?

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INJECTION OF RADIOACTIVE IV SOLUTION

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HOW IS VENTILATION SCAN PERFORMED?

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BY INHALING RADIOACTIVE XENON GAS

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LUNG SCANNING WILL BE ABNORMAL IN PE, BUT ALSO IN WHAT CONDITIONS?

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ASTHMA AND COPD

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HOW ARE LUNG SCANS INTERPRETED?

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NORMAL, LOW PROBABILITY, INTERMEDIATE PROBABILITY, AND HIGH PROBABILITY OF PE; A LOW PROBABILITY SCAN DOES NOT R/O PE

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THIS IS NOW THE IMAGING OF CHOICE WITH SUSPECTED PE

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HELICAL CT (FOLLOWED BY PULMONARY ANGIOGRAPHY)

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WHAT PATIENTS DO WE RESERVE PULMONARY ANGIOGRAPHY FOR?

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FOR PATIENTS WITH SUSPECTED EMBOLI, BUT OTHER STUDIES ARE INCONCLUSIVE; EXCELLENT FOR DIAGNOSIS BUT EXPENSIVE AND INVASIVE

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WHAT ARE THE TWO MAJOR CONCERNS WITH PULMONARY ANGIOGRAPHY?

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ACUTE RENAL FAILURE AND ALLERGIC REACTIONS

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WHY DO WE LOOK FOR DVT WHEN PE IS SUSPECTED?

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BECAUSE PE IS OFTEN A RESULT OF DVT

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WHAT TEST'S ARE DONE FOR DVT?

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MEASURE CALF, COMPARE TO OPPOSITE CALF, AND IF GREATER THAN 2 CM IT IS DVT; PERFORM HOLMAN'S TEST; USN

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IF DVT IS SUSPECTED AND THERE ARE NO CONTRAINDICATIONS, WHAT MEDICATION IS STARTED VIA IV?

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HEPARIN

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HOMAN'S SIGN

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PASSIVE DORSIFLEXION OF THE ANKLE BY THE EXAMINER ELICITS SHARP PAIN IN THE CALF

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PREVENTION OF DVT

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LOW DOSE HEPARIN GIVEN SUBC EVERY 8-12 HOURS, STARTING BEFORE SURGERY; EARLY AMBULATION AFTER SURGERY FOR LOW RISK PATIENTS; HIGH RISK PATIENTS- LOW DOSE HEPARIN, ELASTIC STOCKINGS, AND INTERMITTENT PNEUMATIC COMPRESSION; EXTREME HIGH RISK- PROPHYLATIC INFERIOR VENA CAVA FILTER

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TX OF PE

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ANTICOAGULATION, CLOTTING STUDIES WITH IV HEPARIN AND WARFARIN (MONITORING), MONITORING AFTER PT GOES HOME ON ORAL WARFARIN

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TX OF ACUTE DVT

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SC HEPARIN GIVEN FOR AT LEAST 6 DAYS AND UNTIL LONG TERM ANTICOAGULATION ESTABLISHED W/ WARFARIN OR ANOTHER AGENT (ENOXAPARIN)

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HOW DOES HEPARIN WORK?

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BY ACTIVATING ANTITHROMBIN III TO SLOW OR PREVENT PROGRESSION OF DVT AND TO REDUCE THE SIZE AND FREQUENCY OF PE

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HEPARIN DOES NOT ________ THE EXISTING CLOT.

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DISSOLVE

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GREATEST RISK WHEN USING ANTICOAGULANTS

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HEMORRHAGE

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WHAT IS THE ONLY AVAILABLE DEFINITIVE TREATMENT FOR PE

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LYSIS OF PULMONARY THROMBOEMBOLIA; STREPTOKINASE, UROKINASE, AND RECOMBINANT TISSUE PLASMINGEN ACTIVATOR (TPA) CAN BE USED

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WHY IS LYSIS CRITICIZED?

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BECAUSE OF HIGH COST COMPARED TO HEPARIN AND B/C OF POSSIBLE COMPLICATIONS

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WHEN IS SURGICAL INTERRUPTION OF THE INFERIOR VENA CAVA INDICATED?

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WHEN RECURRENT PE IS LIFE THREATENING AND MAJOR CONTRAINDICATIONS FOR ANTICOAGULATION OR FAILURE OF ANTICOAGULANTS IS PRESENT

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WHAT ARE FILTERS USED FOR?

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INFERIOR VENA CAVA INTERRUPTION

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PROGNOSIS FOR PE

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SUDDEN DEATH CAN HAPPEN, BUT IS RARE; MORTALITY RATE IS 30% IF UNTREATED; CHRONIC RECURRENT PE'S CAN CAUSE PULMONARY HYPERTENSION

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MUTATIONS IN THE F5 GENE CAUSE WHAT?

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FACTOR V LEIDEN THROMBOPHILIA

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WHAT DOES THE F5 GENE DO?

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PLAYS A CRITICAL ROLE IN THE FORMATION OF BLOOD CLOTS IN RESPONSE TO INJURY

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WHAT DOES ACTIVATED C PROTEIN DO?

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PREVENTS BLOOD CLOTS FROM GROWING TOO LARGE BY INACTIVATING FACTOR V

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IN PEOPLE WITH FACTOR V LEIDEN MUTATION, WHAT IS APC UNABLE TO DO?

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INACTIVATE FACTOR V NORMALLY; AS A RESULT THE CLOTTING PROCESS CONTINUES LONGER THAN USUAL INCREASING THE CHANCE OF ABNORMAL BLOOD CLOTS

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WHAT IS D-DIMER?

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PLASMA LEVEL OF A DEGRADATION PRODUCT OF A CROSS LINKED FIBRIN RELEASED WHEN THE ENDOGENOUS FIBRINOLYTIC SYSTEM ATTACKS THE FIBRIN MATRIX OF FRESH VENOUS THROMBOEMBOLIA; MEASURED BY ELISA AND TAKES SEVERAL HRS

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WHAT DOES THE ABSENCE OF A RAISED D- DIMER SUGGEST?

Back 45

THAT THERE IS NO FRESH THROMBOEMBOLIC MATERIAL UNDERGOING DISSOLUTION IN THE DEEP VEINS OR IN THE PULMONARY ARTERIAL TREE