1. RIGHT CORONARY SUPPLIES:SINUS NODE: BRADYCARDIAAV NODE: CHB, 3RD HB, AV DISSOCIATIONRA & RV: RV INFARCTIONMITRAL VALVE: MITRAL INSUFFICIENCYINFERIOR WALL  2. LEFT ANTERIOR DECENDING SUPPLIES: BUNDLE OF HIS:  MOBITZ IIBUNDLE BRANCHES:  RBBBVENTRICULAR SEPTUM:  VSDANTERIOR-SEPTAL WALL

3. CARDIAC TRAUMAMYOCARDIAL CONTUSIONST ELEVATION IN LEADS LOOKING AT THE INJURYWORSE THAN PERICARDITISBROKEN BLOOD VESSELS THAT BLEED INTO THE HEART MUSCLEDEAD TISSUEPERICARDITIS ST ELEVATION IN ALL LEADSRISK OF CARDIAC TAMPONDE

4. PERICARDITIS CAUSES:VIRALMIPOST-OPRADIATIONIDIOPATHICTRAUMA 5. PERICARDITIS WATCH FOR:CARDIAC TAMPONADEHYPOTENTIONELEVATED JVDPULSUS PARADOXUS 6. DRESSLER'S SYNDROME - WHAT IS ITSHARP, STABBING PAININCREASES WITH INSPIRATIONLOW GRADE FEVERDYSPNEACOUGH

7. PACEMAKERSSPIKES ON T-WAVES = FAILURE TO SENSESENSITIVITY TOO HIGH, BATTERY FAILURE, CATHETER MALPOSITIONFAILURE TO CAPTURE = SPIKES BUT NO BEATLEAD DISLODGEMENT, BATTERY FAILURE, FAULTY CONNECTION

8. SHOCK STAGESCOMPENSATORY STAGEPROGRESSIVE STAGEREFRACTORY STAGE

9. COMPENSATORY STAGE OF HYPOVOLEMIC SHOCKBODY TRYING TO MAKE SHOCK BETTERDECREASE IN CO = STIMULATES SYMPATHETIC NERVOUS SYSTEM= ADRENALIN WHICH INCREASES CO, BP, ADH AND VASOCONSTRICTIONANXIOUS AND IRRITABLETACHYCARDIA, COOL AND PALE, DECREASED UO 10. PROGRESSIVE STAGE OF HYPOVOLEMIC SHOCKVASODIALATION DUE TO LACTIC ACIDOSISDECREASE IN CO & BP HYPOTENSIONOBTUNDED AND STUPORUSDECREASED CVP, PCWP, CO. INCREASED SVR  11. TREATMENTS FOR HYPOVOLEMIC SHOCK:REPLACE VOLUMECRYSTALLOIDS FFPRBCS 12. CARDIOGENIC SHOCK ETIOLOGY:MICHFARRHYTHMIASCARDIAC TAMPONADEPAPILLARY MUSCLE RUPTURE 13. CARDIAC SHOCK ASSESSMENT:CONFUSED, RESTLESSRAPID RESPIRATIONRALESRAPID THREADY PULSENECK VEIN DISTENTIONNARROW PULSE PRESSURES3 AND S4HYPOTENSIONOLIGURIADECREASED COELEVATED CVP, SVR, PCWP 14. CARDIOGENIC SHOCK TREATMENTSEARLY REPERFUSION PTCATHROBOLYTICSCABGIABPINOTROPIC DRUGS 15. INTRA AORTIC BALLOON PUMP IABP - WHAT IT DOESDECREASES AFTERLOADDECREASEES MYOCARDIAL O2 DEMANDINCREASES CORONARY PERFUSIONIMPROVE CARDIAC OUTPUT

16. IABP INFLATES DURING - DIASTOLE - WHEN BALLOON INFLATES IT PUSHES BLOOD DOWN. THIS IS WHEN HEART MUSCLE RECEIVES BLOOD SUPPLY. DEFLATES DURING - SYSTOLE - LV BLOOD PUSHES THROUGH AORTA 17. IABPPT MUST LAY FLATALWAYS CHACK PULSESMONITOR FOR BLEEDING 18. USES OF IABPSUPPORT ACUTE MI WITH CHOCKCIRCULATORY SUPPORT CABG PTSSUPPORT HIGH RISK CARDIAC CATHS 19. CONTRAINDICATIONS OF IABP:AORTIC INSUFFICIENCYPERIPHERIAL VASCULAR DISEASE

20. COMPLICATIONS OF IABP:ISCHEMIA OF LIMBDISSECTION OF AORTAINFECTION 21. SEPTIC SHOCKSEPSIS USUALLY CAUSED BY GRAM-NEGATIVE BACTERIA:E.COLIKIEBSIELLAENTEROBACTERPSEUDOMONASSERRATIA MARCESCENS 22. PREDISPOSING FACTORS:OLD AGEGRANULOCYTOPENIASEVERE BURN INJURYALCOHOL & DRUB ABUSERECENT SURGICAL PROCEDURESIMMUNOSUPPRESSION (HIV, CHEMO)PROLONGED INTENSIVE CARE UNIT STAY 23. SEPTIC SHOCK GRAM NEGATIVE BACTERIA --->ENDOTOXIN --->VASOACTIVE SUBSTANCES: CYTOKINES, BRADYKININS, INTERLEUKINS, HISTAMINES, SERATONINS, TNF--->VASODILATION  24. TWO STAGES OF SEPTIC SHOCK: WARM STAGECOLD STAGE 

25. WARM STAGE OF SEPTIC SHOCK:CONFUSIONINCREASED CO INCREASED RRBEST ABG GOOD BPINCREASED UONEEDS FLUIDS  26. COLD STAGE OF SEPTIC SHOCK:STUPORUS & OBTUNDEDDECREASED CO DECREASED UOPOOR ABGMETABOLIC ACIDOSIS HYPOTENSION -----> ARDS, ATN, MSOF, DIC 27. SHOCK CHART SHOCK                  PRELOAD          AFTERLOAD      CARDIAC OUTPUT     CARDIOGENIC        INCREASED    INCREASED          DECREASEDHYPOVOLEMIC      DECREASED    INCREASED          DECREASEDSEPTIC (WARM)    DECREASED    DECREASED          INCREASEDSEPTIC (COLD)      DECREASED    INCREASED          DECREASED ANAPHYLACTIC  DECREASED    DECREASED        DECREASED         28. WHICH OF THE FOLLOWING PRESSURES ARE WITHIN NORMAL LIMITS?

A. PAP 34/24  PCWB 12B. PAP 30/20  PCWB 10C. PAP 28/18  PCWP 20D. PAP 24/14  PCWP 12

 29. WHICH OF THE FOLLOWING WOULD CAUSE AN ELEVATED PULMONARY ARETERY PRESSURE AND NORMAL WEDGE PRESSURE?

A. PULMONARY HYPERTENSIONB. PULMONARY EDEMAC. LEFT VENTRICULAR FAILURED. CONSTRICTIVE PERICARDITIS

30. A LARGE V WAVE APPEARS ON THE PCWP TRACING OF A PATIENT WITH AN INFERIOR WALL MYOCARDIAL INFARCTION. THIS FINDING IS CONSISTENT WITH:

A. CARDIOGENIC SHOCKB. CONGESTIVE HEART FAILUREC. MITRAL REGURGITATIOND. PERICARDITIS

31. ST ELEVATION AND ABSENCE OF AN "R" WAVE IN V1-V4 WOULD BE INDICATIVE OF: A. ANTERIOR-SEPTAL WALL INFARCTION B. INFERIOR WALL ISCHEMIAC. ANTERIOR - SEPTAL WALL ISCHEMIAD. ANTERIOR - LATERAL WALL INFARCTION

 

32. WHICH OF THE FOLLOWING HEMODYNAMIC PARAMETERS WOULD INDICATE LEFT VENTRICULAR FAILURE IN A PATIENT WITH COPD?

A. PAP 54/22  PCWP 14  CVP 8B. PAP 48/26  PCWP 16  CVP 6C. PAP 22/12  PCWP 26  CVP 16D. PAP 48/26  PCWP 20  CVP 16

 33. THE RECIPROCAL CHANGES THAT OCCUR WITH AN INFERIOR WALL MI ARE SEEN AS ST DEPRESION IN LEADS:

A. II, III, AVFB. V1-V4C. II, AVL D. I, AVL

 34. WHICH OF THE FOLLOWING COMPLICATIONS IS MOST LIKELY TO OCCUR IN ACUTE INFERIOR MYOCARDIAL INFARCTION?

A. MOBITZ TYPE I HEART BLODK (WENCHEBACH)B. PAROXYSMAL ATRIAL TACHYCARDIA (PAT)C. RIGHT BUNDLE BRANCH BLOCK (RBBB)D. CARDIOGENIC SHOCK

 35. YOUR PATIENT WITH AN INFERIOR WALL MI ALSO HAS A RIGHT VENTRICULAR INFARCTION & DEVELOPS RIGHT VENTRICULAR FAILURE. WHICH DATA OBTAINED WOULD CORRELATE WITH THIS PATIENT'S CONDITION

A. PAP 28/10  PCWP 10  CVP 18B. PAP 38/22  PCWP 20  CVP 6C. PAP 54/28  PCWP 14  CVP 14D. PAP 23/8  PCWP 19  CVP 20 

36. THE TREATMENT MODAILITY FOR A PATIENT WITH RVF FROM AN INFERIOR WALL MI WOULD INCLUDE:

A. NIPRIDE AN DLOW DOSE DOPAMINEB. NORMAL SALINE FLUID CHALLENGEC. LASIX AND PRELOAD REDUCERSD. LIDOCAINE AND AFTERLOAD REDUCERS

2 INCREASING PRELOAD TO OVERSTRETCH THE RV TO GUARENTEE GETTING BLOOD TO THE LEFT SIDE OF THE HEART.  37. ASYSTOLE - TEATRANSCUTANEOUS PACINGEPINEPHRINE ATROPINE 38. BRADYCARDIA - ALL TRAINED DOGS EAT IAMSATROPINETRANSCUTANEOUS PACINGDOPAMINEEPINEPHRINE ISOPROTERENOL  

39. A PATIENT IWTH A HR OF 45 COMPLAINS OF DIZZINESS AND COOL CLAMMY EXTREMITIES. WHAT IS THE FIRST DRUG OF CHOICE?

A. ATROPINE 0.5MG - 1MG B. EPINEPHRINE 1MG IV PUSHC. ISUPREL INFUSION 2-10MCG/KG/MIND. ADENOSINE 6 MG IV PUSH 

 40. YOU ARE TREATING A PATIENT WITH A SLOW HEARTBEAT. FOR WHICH OF THE FOLLOWING PATIENT SWOLD ATROPINE BE EFFECTIVE?

A. A 55 Y/O MALE WITH SEVERE CHEST PAIN AND SINUS BRADYCARDIA AT 35 BPMB. A 55 Y/O MALE WITH WEAKNESS AND 3RD DEGREE HBC. A 55 Y/O MALE WITH FATIGUE AND A HEART TRANSPLANT 6 MONTHS AGOD. A 55 Y/O MALE WITH WEAKNESS AND ACUTE SYMPTOMS OF NAUSEA/VOMITING WITH A

SINUS HR OF 35NOT WITH CPATROPINE WONT WORK WITH 3RD DEGREE HBATROPINE WONT WORK WITH HEART TRANSPLANT BECAUSE VAGUS NERVE CUT 41. PEA  PULSELESS ELECTRICAL ACTIVITYREVIEW CAUSES: 5 "H" S 5 "T" SH - HYPOVOLEMIA, HYPOXIA, HYDROGEN IONS, HYPOTHERMIA, HYPERKALEMIAT - TENSION PNEUMOTHROAX, THROMBOSIS, TAMPONADE, TOXINSTREATMENTS: PEAPROBLEM EPINEPHRINE ATROPINE

42. VF/ PULSELESS VT TREATMENT: SHOCK 3XEPINEPHRINE OR VASOPRESSIN SHOCK X1AMIODARONE, LIDOCAINE, MAGNESIUM, PROCAINAMIDESHOCKBUFFERS (BICARB) PLEASE, SHOCK SHOCK SHOCK, EVERYBODY SHOCK AND LET'S MAKE PATIENTS DANCE.... BETTER  43. WHICH OF THE FOLLOWING THERAPIES IS THE MOST IMPORTANT INTERVENTIONS FOR VF/PULSELESS VT, WITH THE GREATEST EFFECT OF SURVIVAL TO HOSPITAL DISCHARGE?

A. EPINEPHRINEB. DEFIBRILLATIONC. OXYGEN D. AMIODARONE

 44. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIAVAGAL STIMULATIONADENOSINE PRESERVED HEART FUNCTIONAMIODARONEBETABLOCKERCA CHANNEL BLOCKERSDIGOXIN

PROCAINAMIDESOTALOLDC CARDIOVERSIONEF <40%, CHF - NO BETA BLOCKERS OR CCBDC CARDIOVERSIONAMIODARONEDILTIAZEM

45. WIDE COMPLEX TACHYCARDIAS OF UNKNOWN TYPEDRUGS: AMIODARONE & PROCAINAMIDEHX HF: AMIODARONE & LIDOCAINE 46. WIDE COMPLEX TACHYCARDIAS OF UNKNOWN TYPE CONTRAINDICATED: VERAPAMIL AND ADENOSINECCB, BETA BLOCKERS, DIGOXIN 47. STABLE VTCARDIOVERSION  48. A 75Y/O PATIENT WITH RAPID AF, APPROXIMATELY 160 PER MINUTE AND IRREGULAR C/O PALPITATIONS FOR A WEEK. NO EVIDENCE OF CARDIC OR CIRCULATORY FAILURE. WHICH WOULD BE INCLUDED IN THE INITIAL ORDERS?

A. OXYGEN, IV, MONITORB. IMMEDIATE CARDIOVERSIONC. NO THERAPY IS INDICATED D. EPINEPHRINE 1MG IV EVERY 3-5 MIN

 49. SAME PATIENT. HIS VITALS SIGNS REMAIN UNCHANGED, BP 100/70, IRREGULAR HR OF 160. WHICH OF THE FOLLOWING WOULD BE THE MOST APPROPRIATE TREATMENT FOR AF?

A. IV DIGOXINB. IV DILTIAZEM TO SLOW VENTRICULAR REPSONSEC. IV AMIODARONE TO CONVERT AF TO SRD. SYNCHRONIZED CARDIOVERSION

A,C,D MAY CONVERT. BEEN IN AF FOR A WEEK WILL SEND CLOTS FLYING 50. 25 Y/O WOMAN IS WITH PSVT, PRIOR MEDICAL HX CONFIRMED REENTRY TACHYCARDIA, NO WPW. HR 180BPM, SHE IS SOB AND REPORTS PALPITATIONS. WHICH WOULD BE THE NEXT MOST APPROPRIATE INTERVENTION?

A. DC CARDIOVERSIONB. IV DILTIAZEMC. IV PROPRANOLOLD. IV ADENOSINE

 51. 55 Y/O M WITH HX CHF & LBBB DEVELOPS SUSTAINED WIDE COMPLEX TACHYCARDIA AFTER AN EPISODE OF CP RELIEVED BY NTG. WHICH OF THE FOLLOWING IS THE MOST APPROPRIATE INITIAL MED?

A. IV LIDOCAINEB. IV ADENOSINEC. IV AMIODARONED. IV VERAPAMIL

52. CLINICAL MANIFESTATIONS OF CARDIOGENIC SHOCK FOLLOWING AN ANTERIOR WALL MI INCLUDE ALL OF THE FOLLOWING EXCEPT:

A. DISTENDED NECK VEINSB. PULMONARY CONGESTION, RALESC. PRESENCE OF AN S3 D. LOW CVP READING

 

53. "UNLOADING" THERAPY BY NITROPRUSSIDE IS BENEFICIAL BECAUSE IT: A. ENHANCES VENTERICULAR EMPTYINGB. DIMINISHES PERIPHERAL VASCULAR RESISTANCE OR "AFTERLOAD"C. RELIEVES PULMONARY CONESTION BY PROMOTING VENOUS POOLING OF BLOODD. ALL OF THE ABOVE

 54. WHICH OF THE FOLLOWING IS AN EXPECTED OUTCOME FROM IABP?

A. DECREASED MEAN SYSTEMIC BPB. INCREASED CARDIAC OUTPUTC. INCREASED PCWPD. ALL OF THE ABOVE

 55. UNSTABLE TACHYCARDIA TREATMENT: SYNCHRONIZED CARDIOVERSION  56. WHICH OF THE FOLLOWING GROUPS OF  HEMODYNAMIC DATA REFLECTS CARDIOGENIC SHOCK AS OPPOSED TO HYPOVOLEMIC SHOCK?

A. BP 88/60  PA 18/8  PCWP 12B. BP 70/40  PA 30/20  PCWP 22C. BP 90/60  PA 24/18  PCWP 25D. BP 94/56  PA 40/22  PCWP 20

PCWP HIGH, PAP HIGH, IN 2 WEDGE IS HIGHER THAN PAD 57. TO BE OPERATING CORRECTLY, THE IABP IS TIMED TO WORK IN WHICH MANNER?

A. INFLATE DURING SYSTOLE, DEFLATE DURING DIASTOLEB. INFLATE WHEN THE MEAN AORTIC PRESSURE FALLS BELOW A PRESET LIMITC. INFLATE WHEN THE HEART RATE FALLS BELOW A PRESET LIMITD. INFLATE DURING DIASTOLE DELFATE DURING SYSTOLE

58. ABSOLUTE CONTRAINDICATIONS TO INTRA-AORTIC BALLOON COUNTERPULSATION INCLUDE:

A. MITRAL INSUFFICIENCY B. AORTIC INSUFFICIENCY C. SEPSISD. FEMORAL ARTERY ANEURYSM

 59. ALL POSTOPERATIVE CARDIAC SURGERY PATIENTS DEVELOP:

A. PERICARDITIS B. ELECTROLYTE IMBALANCESC. HYPOXIA D. ATELECTASIS 

 60. WHICH OF THE FOLLOWING KINDS OF SHOCK IS CHARACTERIZED BY INCREASED VENOUS CAPACITANCE AND POOLING?

A. HYPOVOLEMIC SHOCK B. CARDIOGENIC SHOCK C. DISTRIBUTIVE SHOCK (SEPTIC)D. OBSTRUCTIVE SHOCK

61. EARLY STAGES OF SEPTIC SHOCK ARE CHARACTERIZED BY: A. VASOCONSTRICTION WITH THE RELEASE OF HISTAMINEB. INCREASED CARDIAC OUTPUT WITH PERIPHERAL VASOCONSTRICTIONC. VASODILATION WITH FLUID LOSS AND THE RELEASE OF LEUKOCYTESD. INCREASED CARDIAC OUTPUT WITH DECREASED VASCULAR RESISTANCE

 62. THE SIGNS OF HYPERVENTILATION, DIMINISHED SENSORIUM, AND INCREASED CO ARE OFTEN FOUND IN WHICH FORM OF SHOCK?

A. NEUROGENICB. SEPTICC. HYPOVOLEMICD. CARDIOGENIC

 63. A PATIENT ADMITTED TO THE ICU IN THE EARLY STAGES OF SEPTIC SHOCK PRESENTS WITH:

A. WEAK THREADY PULSES AND LOW BPB. DECREASED UOC. WARM, FLUSHED SKIND. HYPERNEA WITH PULMONARY CONGESTION 

 64. WHICH OF THE FOLLOWING SIGNS IS NOT CHARACTERISTIC OF CARDIAC TAMPONADE?

A. WIDENING PULSE PRESSUREB. RISING CVPC. WIDE MEDIASTINUM ON XRAYD. A FALL IN SYSTOLIC BP OF MORE THAN 10MMHG DURING INSPIRATION

 65. THE PLACEMENT OF MCL, ELECTRODES IS:

A. + ELECTRODE, 4TH ICS, R STERNAL BORDER, - ELECTRODE, BELOW OUTER 3RD OF L CLAVICLE

B. + ELECTRODE, 5TH ICS, R STERNAL BORDER, - ELECTRODE L LOWER ABDC. + ELECTRODE, L SHOULDER, - ELECTRODE, R SHOULDER D. + ELECTRODE, L MIDAXILLARY LINE, 5TH ICS; - ELECTRODE, BELOW OUTER 3RD OF

LEFT CLAVICLE 66. THE MOST SERIOUS EKG FINDING ASSOCIATED WITH ANTERIOR WALL MI IS:

A. FASCICULAR BLOCKS AND TACHYCARDIAB. RBBB AND SECOND DEGREE BLOCKSC. FEW VENTRICULAR ECTOPIC BEATSD. RAPID SUPRAVENTRICULAR RHYTHMS

67. THE HEMODYNAMIC PARAMETER THAT CLINICALLY MEASURES AFTERLOAD IS:A. CVPB. MAPC. SVRD. LEFT VENTRICULAR END-DIASTOLIC PRESSURE

 68. ALL OF THE FOLLOWING SUPPORT THE DIAGNOSIS OF CARDIAC TAMPONADE EXCEPT:

A. WIDENING PULSE PRESSUREB. PULSUS PARADOXUSC. ENLARGED HEART ON XRAYD. EQUALIZATION OF RIGHT AND LEFT HEART PRESSURES

69. A PATIENT WITH BP OF 200/142 WOULD HAVE WHICH OF THE FOLLOWING FORMS OF HTN?A. ESSENTIAL HTNB. ACCELERATED HTNC. MALIGNANT HTND. HYPERTENSIVE ENCEPHALOPATHY

 

70. ABGS NORMALS:                    PHACID <---- 7.35 - 7.45 ------> ALKA                  CO2          RESPIRATORYALKA<---- 35 - 45 -----> ACID                  HCO3              METABOLIC ACID <-----23 -27 ------>ALKA 71. ABGS - BABYS FIRST NAMEPH                                  CO2-RESPIRATORY                            HCO3-METABOLIC7.12 UNCOMP ACIDOSIS            7.55UNCOMP AKLALOSIS7.01UNCOMP ACIDOSIS7.23UNCOMP ACIDOSIS 72. ABGSCOMPENSATED ABG 7.35-7.45ACIDOSIS                                            ALKALOSIS7.35                          7.40                    7.45

73. ABGS - BABYS FIRST NAMEPH                              CO2-RESP                          HCO3-METABOLIC7.36COMP. ACIDOSIS7.45 COMP ALKALOSIS  74. ABG - LAST NAME MR. RESP MR. METABOLIC (MUST BE THE SAME AS BABYS FIRST NAME)PH          CO2-MR. RESP    HCO3-MR. META7.12                    28              11        UNCOMP META ACIDUN ACID    ALKA            ACID7.55                  29              20        UNCOMP RESP ALKAUN ALK    ALKA              ACID 75. ABG - LAST NAME MR. RESP MR. METABOLIC (MUST BE THE SAME AS BABYS FIRST NAME)PH          CO2-MR. RESP    HCO3-MR. META7.36                61                  34        COMP RESP ACIDCOM ACID  ACID              ALKA7.45                  22                20          COMP RESP ALKACOM ALKA  ALKA          ACID

76. ABG - LAST NAME MR. RESP MR METABOLIC (MUST BE THE SAME AS BABYS FIRST NAME)7.01                51                10        UNCOMP RESP ACIDUN ACID    ACID          ACID7.23                50                29      UNCOMP RESP ACIDUN ACID    ACID          ALKA                                                

77. CAUSES OF ACID-BASE IMBALANCESRESPIRATORY ACIDOSISDRUGS, CARDIAC ARREST, MUSCLE WEAKNESS (MG, ALS, GB), PULMONARY DISEASE (COPD)RESPIRATORY ALKALOSISHYPOXEMIA, CNS DISORDERS, SALICYLATE INTOXICATION, CIRRHOSIS, SEPSIS 78. CAUSES OF ACID-BASE IMBALANCES

METABOLIC ACIDOSIS KETOACIDOSIS, LACTIC ACIDOSIS, GI LOSS (DIARRHEA), RENAL FAILURE

METABOLIC ALKALOSISBLOOD TRANSFUSIONS, HYPOKALKEMIA, GI LOSS (GASTRIC ACIDS), CONTRACTION ALKALOSIS (TOO MUCH LASIX) 79. ACUTE REPIRATORY FAILURE TYPE 1 HYPOCAPNIC FAILURE DECREASED OXYGEN LEVEL WITH A NORMAL OR LOW CO2VENTILATION - PERFUSION IMBALANCEPULMONARY EDEMA, PULMONARY EMBOLISM, ASPIRATION PNEUMONIA, ASTHMA, ARDS  80. ACUTE RESPIRATORY FAILURETYPE 2 HYPERCAPNIC FAILUREDECREASED OXYGEN LEVEL WITH A HIGH CO2 LEVEL RESPIRATORY MECHANICAL PERFORMANCEDRUG OVERDOSE, COPD, CVA, SPINAL CORD: ALS, GB, MG, PNEUMOTHORAX, DECREASED PHOS 81. OXYHEMOGLOBIN DISSOCIATION CURVESHIFT TO R = LOWER SAT, LOWER O2 SAT, RBC RELEASING O2 ONTO TISSUEDECREASED PH, INCREASED CO2, HYPERTHERMIC (COPD)SHIFT TO L = HIGHER SAT, HIGH O2 SAT, RBC HOLDING ONTO O2INCREASED PH, DECREASED CO2, HYPOTHERMIC, LOW LEVELS OF 2,3 DPG  82. V/Q MISMATCHVENTILATION-PERFUSION IMBALANCECOPDASTHMAATELECTASISEMPHYSEMAHYPOVENTILATIONPULMONARY EDEMAPULMONARY EMBOLISMASPIRATION PNEUMONIA  83. SHUNTNO CONTACT BETWEEN BLOOD & ALVEOLIARDS 

84.WHICH OF THE FOLLOWING STATMENTS REGARDING VESICULAR BREATH SOUNDS IS TRUE?

A. THESE ARE MEDIUM INTENSITY SOUND HEARD OVER THE LARGE MAIN-STEM BRONCHIB. THEY ARE HEARD LONGER ON EXHALATIONC. THEY ARE DECREASED OR ABSENT WHEN AIRFLOW TO THE AREA OF LUNG IS

DIMINISHED D. THEY ARE AUSCULATED OF THE TRACH

85. WHICH OF THE FOLLOWING CHEST AUSCULTATION FINDINGS IS ABNORMAL?A. VESICULAR BREATH SOUNDS OVER LUNG PERIPHERY B. BRONCHIAL BREATH SOUNDS HEARD OVER LARGE AIRWAYC. VESICULAR BREATH SOUNDS HEARD DURING INSPIRATION AND EXPIRATION D. BRONCHOVESICULAR SOUNDS ADJACENT TO THE STERNUM

 86. PATIENT IN CCU POST CARDIAC ARREST: FIO2 0.8, PH 7.31, PCO2 42, PO2 60, O2 SAT 85% AND HCO3 18:

A. COMPENSATED METABOLIC ACIDOSISB. UNCOMPENSATED RESPIRATORY ACIDOSISC. UNCOMPENSATED METABOLIC ACIDOSISD. UNCOMENSATED METABOLIC ACIDOSIS

 87. PATIENT PRESENTS WITH AGITATION AND TINGLING OF THE FINGERS: FIO2 RA, PH 7.49, PCO2, O2 SAT 98%, HCO3 22:

A. NORMAL ACID-BASE BALANCEB. UNCOMPENSATED RESPIRATORY ALKALOSISC. UNCOMPENSATED RESPIRATORY ACIDOSISD. UNCOMPENSATED METABOLIC ALKALOSIS

 88. NEWLY ADMITTED MI PATIENT ON THIAZIDE DIURETICS AT HOME FOR HYPERTENSION HAS AN ABG: FIO2 0.6, PH 7.58, PCO2 36, PO2 70, O2 SAT 90%, HCO3 34

A. UNCOMPENSATED METABOLIC ALKALOSISB. UNCOMPENSATED RESPIRATORY ALKALOSIS C. UNCOMPENSATED METABOLIC ACIDOSIS D. COMPENSATED METABOLIC ALKALOSIS

 89. WHICH OF THE FOLLOWING PATIENT FINDINGS WILL CONTRIBUTE A SHIFT TO THE LEFT WITH IMPAIRED TISSUE UNLOADING OF OXYGEN?

A. PH 7.58B. TEMP 103FC. PACO2 50MMHGD. INCREASED HEMOGLOBIN 2, 3, DPG

  90. WHICH OF THE FOLLOWING PATIENT FINDINGS WILL CONTRIBUTE TO A SHIFT TO THE RIGHT WITH IMPROVED UNLOADING OF OXYGEN AT THE TISSUES?

A. PH 7.46B. TEMP 96FC. PACO2 54D. DECREASED HEMOGLOBIN 2, 3 DPG

 

91. PULMONARY CONSOLIDATION (LOBAR PNEUMONIA) WILL CAUSE WHICH OF THE FOLLOWING PHYSICAL FINDINGS OVER THE DISEASED AREA?

A. DULL PERCUSSION NOTEB. DECREASED TACTILE FREMITUSC. BRONCHIAL BREATH SOUNDSD. BOTH A AND C

92. A NOTABLE CHARACTERISTIC OF MUCUS WILL OFTEN BE PRESENT IN PATIENTS WITH STATUS ASHTMATIC ATTACT IN ITS:

A. COLORB. TENACIOUSNESSC. COPIOUS NATURED. ABSENCE

 93. AN OMINOUS FINDING IN THE PATIENT WITH STATUS ASTHMATICUS WOULD BE:

A. A RESPIRATORY RATE OF 34 B. LOUD EXPIRATORY WHEEZING C. A CO2 OF 55D. USE OF ACCESSORY MUSCLES 

94. A PATIENT WITH STATUS ASTHMATICUS IS ADMITTED. HIS BREATH SOUNDS ARE DIMINISHTED THROUGHOUT HIS LUNG FIELDS. RR=40. AFTER GIVING YOUR PATIENT AN AEROSOL BRONCHODILATOR, YOUR PATIENT SOUNDS WORSE AS THEY ARE NOW LOUDER. THIS INDICATEDS:

A. THE PATIENT HAS GOTTEN WORSEB. THE NEED FOR ANESTHEISIA TO BE PRESENT STATC. THE PATIENT IS GETTING BETTERD. THE PATIENT DOES NOT HAVE ASTHMA 

 95. WHEN ADJUSTING THE INITIAL SETTINGS ON A VOLUME VENTILATOR FOR AN ADULT IN RESPIRATORY FAILURE, THE TIDAL VOLUME IS USUALLY SET AT:

A. AT LEAST 10ML PER KG OR TWICE NORMALB. 15-20 ML PER KG OR TWICE NORMALC. 500 ML FOR ALL PATIENTSD. 300-500 ML

 96. A 70 KG PATIENT VENTILATED WITH FIO2 OF 45%, VT OF 800, IMV OF 8. PATIENTS RESPIRATIONS ARE 10/MIN. ABG RESULTS: O2 85%, CO2 55, WHAT VENTILATOR PARAMETER SHOULD BE CHANGED?

A. FIO2B. IMVC. VTD. ALL OF THE ABOVE

97. ADMINISTRATION OF 100% O2 WILL NOT IMPROVE THE PAO2 IN HYPOXIA CAUSED BY: A. V/Q IMBALANCEB. RIGHT TO LEFT SHUNTINGC. ALVEOLAR HYPOVENTILATIOND. IMPAIRED DIFFUSION

 

98. WHICH OF THE FOLLOWING DISEASES STATES DOES NOT CAUSE HYPOXIA DUE TO A PRIMARY MECHANISM OF V/Q MISMATCHING?

A. BRONCHOSPASTIC DISEASEB. PULMONARY EMPHYSEMAC. ADULT RESPIRATORY DISTRESS SYNDROMED. PULMONARY EMBOLIZATION

99. THE ADMINISTRATION OF OXYGEN ALONE WILL NOT IMPROVE HYPOXIA DUE TO:A. V/Q MISMATCHB. SHUNTING C. HYPOVENTILATIOND. DECREASED FIO2

100. WHICH OF THE FOLLOWING STATEMENTS REGARDING ARDS IS TRUE?A. THERE IS DECREASED CAPILLARY PERMEABILITYB. THERE IS DAMAGE TO TYPE II PNEUMOCYTES WITH A DECREASED OF SURFACTANTC. THERE IS AN INCREASE IN LUNG COMPLIANCED. THERE IS AN INCREASE IN FUNCTIONAL RESIDUAL CAPACITY

 101. ASSESSMENT FINDINGS INDICATIVE OF ARDS IN THE EARLY STAGE, WOULD INCLUDE ALL OF THE FOLLOWING EXCEPT:

A. TACHYPNEAB. NORMAL PCWPC. RESPIRATORY ALKALOSISD. HYPERCAPNIA

 102. THE HALLMARK OF ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) IS:

A. REFRACTORY HYPERCAPNIAB. REFRACTORY HYPOXEMIAC. LOW FUNCTIONAL RESIDUAL CAPACITYD. INCREASED COMPLIANCE SECONDARY

 103. THE NURSE CONSIDERS WHICH INTERVENTION TO BE INAPPROPRIATE WHILE CARING FOR THE PATIENT WITH ARDS?

A. ADMINISTER SMALL DOSES LASIX AS ORDERED BY MDB. INFUSION OF NORMAL SALINE RAPIDLY IN ORDER TO MAINTAIN HYDRATIONC. PULMONARY TOILETINGD. FREQUENT POSITION CHANGES.  

104. THE PLAN OF THERAPEUTIC ATTACT IN THE CARE OF ARDS PATIENTS MAY INCLUDE: A. USE OF VENT WITH  HIGH PRESSURE AND HIGH FLOW CHARACTERISTICSB. DIURETICS AND FLUID RESTRICTION C. USE OF PEEP D. ALL OF THE ABOVE

105. PALPATION OF TRACHEAL SHIFT TO THE LEFT MAY INDICATE:A. A TENSION PNEUMOTHORAX ON THE RIGHTB. MASSIVE ATELECTASIS TO THE RIGHTC. A TENSION PNEUMOTHORAX ON THE LEFT D. DIFFUSE AIRWAYS OBSTRUCTION

    

106. INITIAL NURSING ASSESSMENT FINDINGS IN THE PATIENT WITH AN ACUTE PULMONARY EMBOLISM INCLUDES:

A. CHEST PAIN, ST CHANGES, PULMONARY EDEMAB. RALES, RHONCI, TACHYCARDIA, C. CHEST PAIN, DYSPNEA, COUGHD. TACHYPNEA, BRADYCARDIA, RALES

 107. WHICH ASSESSMENT FINDING WOULD NOT BE PRESENT IN THE PATIENT WITH A MASSIVE PULMONARY EMBOLISM?

A. INCREASED CVP READINGB. PULMONARY RALESC. DISTENDED NECK VEINSD. LIVER ENLARGEMENT

108. BURNSFLUID SHIFTS FROM BLOOD TO INTERSTIAL AND INTRACELLULAR SPACESMAY CAUSE INCREASE TISSURE PRESSURE, LEASING TO COMPARTMENT SYNDROMEHEMOCONCENTRATION, INCREASED HEMATOCRIT AND BLOOD VISCOSITY RESULTS 109. BURNSDECREASE INTRAVASCULAR VOLUME - DECREASE BLOOD FLOW TO KIDNEYSDECREASE CARDIAC OUTPUT FURTHER DECREASES ORGAN PERFUSIONRESULTS IN HYPOVOLEMIC SHOCK, METABOLIC ACIDOSIS AND HYPERKALEMIAMICROVASCULAR LEAK WITH PULMONARY EDEMA, ARDS, ATN AND MYOGLOBINURIA 110. BURNSSMOKE INHALATION: OBSERVE FOR SIGNS OF OBSTRUCTION, STRIDOR, HOARSENESS, RESLESSNESS, BEHAVIORAL CHANGES AND DECREASED LOC 111. POISIONINGIN COMATOSE PATIENT BE PREPARED TO GIVE: DEXTROSE 50% 100ML THIAMINE 100MG IVNARCAN 2MG IVACTIVATED CHARCOAL 1 GRAM/KG OF WEIGHTPROVIDE ANTIDOTE 112. TYLENOL OVERDOSEANTIDOTE: NAC (MUCOMYST)140MG/KG LOADING DOSE70 MG/KG EVERY 4 HOURS FOR 17 DOSESGIVE ACTIVATED CHARCOAL IF LESS THAN 4 HOURS SINCE INGESTION (WAIT 1 HOUR BEFORE GIVIENG NAC IF CHARCOAL GIVEN) 113. ASA OVERDOSEANTIDOTE: LAVAGE OR INDUCE EMESISACTIVATED CHARCOAL URINARY ALKALINIZATION - SODIUM BICARBHEMODIALYSIS OBSERVE FOR: RENAL TUBULAR ACIDOSIS  

114. COCAINE OVERDOSEMONITOR FOR SEIZURE ACTIVITY

115. MASSIVE BLOOD TRANSFUSIONS =LOW CALCIUM LEVEL 116. TPN CAUSESHYPOPHOSPHATEMIA(MUSCLE WEAKNESS) 117. AMPHOGEN REDUCES HYPERPHOSPHATEMIA 118. WHAT IS A VVI PACEMAKER?V- CHAMBER PACEDV- CHAMBER SENSEDI - MODE THE PACER IS IN  119. HOW DO YOU DRAIN THE LEFT LOWER LUNG LOBE?LEFT SIDE, HEAD DOWN  120. LEFT VENTRICULAR ASSIST DEVICE BLOOD IS DIVERTED FROM THE LEFT ATRIUM AND RETURNED TO THE PATIENT VIA ASCENDING AORTA(BYPASS LEFT VENTRICLE) 121. IABP AUGMENTS THE CO BY 15% 122. TOUSADES DE POINTES TREATMENT: MAGNESIUM 123. MVA BROKEN LEG IS AT RISK FOR: FAT EMBOLI 124. COMPLICATION OF PEEP IS BARATRAUMA  125. RENAL TRANSPLANT ACUTE REJECTION OCCURS WITHIN: 1-2 WEEKS  126. A-LINE, DICROTIC NOTCH =CLOSURE OF THE AORTIC VALVE

127. MAP =DIASTOLIC PULSE + 1/3 OF PULSE PRESSURE 150/90 90 +1/3 PP (60)90+20 = 120 128. CARDIAC TROPONIN t AND i, MYOGLOBIN ARE SENSITIVE CARDIAC MARKERS, RISE IN LESS THAN 6 HOURS 129. ACIDOSIS CAUSES POTASSIUM TO RISE

130. ARDS KEEP PATIENT: DRY (DECREASE FLUIDS) 131. SIADH - WHAT IS IT?SYNDROME OF INAPPROPRIATE ADHTOO MUCH ADH 132. ADH MAKES YOUR KIDNEYS DO WHAT?HOLD ONTO WATER 133. DILUTIONAL HYPONATREMIA IS USUALLY ... SIADH 134. SIADH CAUSES WHATDECREASED OSMOLARITY. SODIUM LEVEL X2DECREASED SODIUM 135. WHAT ARE CAUSES OF SIADHOAT CELL CARCINOMA VIRAL PNEUMONIAHEAD PROBLEMSANESTHESIA, ANALGESIC, STRESS 136. COMPLICATION OF SIADH IS SEIZURE ACTIVITYBECAUSE WITH DILUTIONAL HYPONATREMIA WATER GOES INTO CELLS (BRAIN CELLS) CAUSING SEIZURES 137. TREATMENT FOR SIADHFLUID RESTRICTION AND HYPERTONIC SOLUTION 3% NS, D5NS, D5 1/2 NSNO HYPOTONIC SOLUTIONS!! 2.5 DEXTROSE, D5W, 0.33 SALINE 138. DIABETES INSIPIDUSNO ADH LOSES WATER 139. DI CAUSESINCREASE IN NA LEVELINCREASE IN OSMOLARITY 140. CAUSES OF DIHEAD PROBLEMSDILANTIN 141. PTS WITH DI NEED TO BE WATCHED FOR: SHOCK 142. TREATMENTS FOR DI GIVE ADH (PITRESSIN)GIVE FLUIDS MONITOR CARDIAC MONITOR MONITOR URINE SPECIFIC GRAVITY 

143. HYPOGLYCEMIC CVS                                  CNSTACHY                              CONFUSIONPALPITATIONS                  LETHERGYDIAPHORESIS                    SLURRED SPEECHIRRITABLE                          SEIZURESRESTLESS                            COMA 144. IF ON A BETA BLOCKER AND HYPOGLYCEMIC WILL NOT HAVE CARDIOVASCULAR SYMPTOMS 145. INITIAL SIGNS OF HYPOGLYCEMIA ARE CAUSED BY ADRENALIN RELEASE 146. DKA DIABETIC KETOACIDOSIS BLOOD SUGARS ARE BETWEEN:400-900 147. HHNK HYPERGLYCEMIC HYPEROSMOLAR NON-KETOTIC COMA. WHO GETS IT?OLD AGEDIET CONTROLLED DIABETICTPNPANCREATITIS

148. HHNK BLOOD SUGARS ARE BETWEEN:1000-2000 149. DKA CAUSES DEHYDRATION 4-6 L

150. HHNK CAUSESDEHYDRATION 6-8 L

151. IN DKA YOUR BODY IS DOING WHAT WITH INSULIN?NOT MAKING ANY INSULIN 152. IN HHNK YOUR BODY MAKES INSULIN BUTNOT ENOUGH  153. PEOPLE WHO HAVE DKA USUALLY ARE RECOGNIZED BECAUSE THEY ...GO IN A COMA 154. PEOPLE WITH HHNK CAN LIVE A COUPLE OF WEEKS WITH HHNK, THATS WHY THE BS GETS SOO HIGH 155. DKA CAUSES ACIDOSIS AND KUSSMAUL BREATHING 156. HHNK CAUESNO ACIDOSIS AND LITTLE TINY BABY BREATHS 157. TREATMENT FOR DKA INSULIN THEN GIVE FLUIDS

 158. TREATMENT FOR HHNKGIVE FLUIDS FIRST THEN INSULIN BECAUSE THEY ARE SO DEHYDRATED 159. WHAT TYPE OF FLUIDS DO YOU GIVE PEOPLE WITH DKA AND HHNKSTART WITH NSTHEN GIVE 0.45% NSTHEN GIVE D5 1/2 160. WHEN PEOPLE WITH DKA COME IN, WHAT DO YOU WANT THEIR POTASSIUM TO BE?NORMAL OR HIGH POTASSIUM LEVEL 161. POTASSIUM AND PH ARE REOCIPROCALHYDROGEN WILL MOVE INTO THE CELL, THEN POTASSIUM WILL MOVE OUT OF THE CELL

162. AS YOU BECOME MORE ACIDOTIC, YOUR POTASSIUM INCREASES. THAT’S WHY IN DKA, YOU’RE ACIDOTIC AND YOUR POTASSIUM WILL BE HIGH.PH 7.45            K 4.5PH 7.35            K 5.1PH 7.25            K 5.7PH 7.15              K 6.3PH 7.05            K 6.9

163. BICARB GIVEN TO DKA PT WITH PH 7.05 AND K 4.0 IT INCREASES YOUR PH BUT DECREASES YOU POTASSIUM

164. WHAT IS THE AFFECT OF ADH ON URINE FORMATION?A. RETENTION OF SODIUM AND WATER, EXCRETION OF POTASSIUMB. EXCRETION OF SODIUM AND WATER, EXCRETION OF POTASSIUMC. RETENTION OF WATER, CONCENTRATION OF URINED. EXCRETION OF WATER, DILUTION OF URINE

165. THE RELEASING STIMULUS FOR ADH IS NORMALLY: A. DECREASED SERUM WALL MYOCARDIAL INFARCTION?B. INCREASED SERUM OSMOLARITYC. AN ELEVATED CIRCULATING CORTISOL LEVELD. INCREASED SERUM POTASSIUM LEVELS

166. THE NORMAL RANGE OF SERUM OSMOLARITY IS: A. 145-155B. 200-250C. 275-295D. 325-375

167. SIADH IS MANIFEST CLINICALLY AS A:A. HYPEROSMOLAR STATEB. LOW OUTPUT STATEC. MYXEDEMA STATED. WATER INTOXICATION STATE

168. IN ADDITION TO ITS AFFECT ON BODY WATER EQUILIBRIUM, ADH IS ALSO A:A. VASOPRESSORB. CARDIOTONICC. BETA STIMULATORD. CARBONIC ANHYDRASE INHIBITER

169. THE SYMPTOMATOLOGY YOU WOULD ASSESS IN THE PATIENT WITH SIADH RESULTS FROM:A. ELEVATED POTASSIUM LEVELSB. WATER INTOXICATION C. INCREASED SERUM OSMOLALITYD. PRECIPITATING FACTORS OF SIADH

170. THE "CARDINAL SIGN" OF SIADH IS: A. DILUTIONAL HYPONATREMIAB. URINARY OUTPUT OF 10L PER DAYC. HYPOTENSION D. SYSTEMIC EDEMA

171. WHICH OF THE FOLLOWING LABORATORY FINDINGS WOULD BE PRESENT IN A PATION WITH SIADH?A. LOW SERUM SODIUMB. SERUM OSMOLALITY OF 350C. URINE SPECIFIC GRAVITY OF 1.003D. DECREASED URINARY OSMOLARITY

172. THE PATIENT WITH SIADH MAY PRESENT WITH: A. INCREASED URINARY OUTPUTB. SEIZURESC. HYPERTENSIOND. INCREASED POTASSIUM LEVELS

173. AS A STAFF NURSE IN ICU YOU ARE ASSIGNED TO A PATIENT RECENTLY ADMITTED WITH DI. WHICH OF THE FOLLOWING PATIENTS WOULD BE LIKELY TO DEVELOP DI?A. AN ELDERLY PATIENT RECEIVING THIAZIDESB. A YOUNG WOMEN WITH SEVERE PNEUMONIAC. A 50 YO MAN WITH ESOPHAGEAL VARICES ON PITRESSIND. A HEAD TRAUMA PT WITH A SKULL FRACTURE

174. DURING YOUR ASSESSMENT, WHICH OF THE FOLLOWING FINDINGS WOULD BE PRESENT IN A PATIENT WITH DI?A. SERUM OSMOLALITY OF 250B. SERUM SODIUM LEVEL OF 165C. URINARY OUTPUT OF LESS THAN 600CC IN 24 HOURSD. URINE SPECIFIC GRAVITY OF 1.025

175. THE NURSE UNDERSTANDS A MAJOR COMPLICATION OF DI IS:A. HYPOVOLEMIC SHOCKB. SEIZURESC. COGESTIVE HEART FAILURED. CARDIAC ARRHYTHMIAS

176. EVALUATION OF LABORATORY FINDINGS IN A PATIENT WITH DI WOULD SHOW: A. INCREASED URINE OSMOLALITYB. URINE SPECIFIC GRAVITY BETWEEN 1.001 TO 1.005C. DECREASED SERUM SODIUMD. DECREASED SERUM OSMOLARITY

177. THE MOST DANGEROUS COMPLICATION OF DI IS: A. DILUTIONAL HYPONATREMIAB. HYPOVOLEMIAC. CONGESTIVE HEART FAILURED. WATER INTOXICATION SYNDROME

178. DIABETES INSIPIDUS IS CHARACTERIZED BY ALL BUT WHICH OF THE FOLLOWING?A. URINE SPECIFIC GRAVITY OF 1.015B. TACHYCARDIAC. URINARY OUTPUT OF 2000 CC IN THREE HOURSD. BP 90/40

179. WHICH OF THE FOLLOWING IS CHARACTERISTIC OF DI?A. LOW URINARY OSMOLARITY B. SERUM OSMOLARITY INCREASED C. SERUM SODIUM ELEVATEDD. ALL OF THE ABOVE

180. A 66 YO IS ADMITTED WITH A BLOOD SUGAR OF 1200, SHE IS SEVERLY DEHYDRATED, RESPIRATIONS ARE 18 PER MINUTE AND SHALLOW: YOU WOULD FIRST SUSPECT?A. HYPEROSMOLAR COMAB. DIABETIC KETOACIDOSISC. EITHER OF THE ABOVED. NEITHER A OR B

181. IT IS IMPORTANT FOR THE NURSE TO IDENTIFY THOSE PATIENTS AT RISK FOR DEVELOPING HHNK. WHICH CONDITION WOULD NOT PREDISPOSE A PATIENT TO DEVELOP HHNK?A. PANCREATITISB. THIAZIDEOF SEROID THERAPYC. TPN THERAPYD. CEREBROVASCULAR ACCIDENT

182. NONKETOTIC HYPEROSMOLAR COMA (HHNK) IS NOT USUALLY ASSOCIATED WITH: A. DEFECTS IN ADH SECREATIONB. MILD DIABETES OF RECENT ONSETC. OLDER AGED. USE OF DIURETICS, STEROIDS AND HYPERTONIC SOLUTIONS

183. THE NURSE UNDERSTANDS THAT THE PRIMARY CAUSE OF THE CLASSICAL MANIFESTATIONS IN HHNK IS: A. RAPID DECREASE IN PLASMA OSMOLARITYB. MARKEDLY ELEVATED SERUM GLUCOSEC. INTRAVASCULAR DEHYDRATIOND. SERUM ELECTOLYTE ABNORMALITY

184. THE ALTERED MENATL STATUS IN A PATIENT IN HHNK RESULTS FROM: A. HYPEROSMOLAITY OF PLASMAB. INTRACEREBRAL DEHYDRATIONC. SEVERE OSMOTIC DIURESIS FROM HYPERGLYCEMIAD. INTRAVASCULAR DEHYDRATION

185. WHICH OF THE FINDINGS WOULD NOT BE PRESENT IN HHNK?A. KUSSMAUL'S RESPIRATIONS OF 28/MINB. SERUM GLUCOSE LEVEL ABOVE 650 AND OFTEN GREATER THAN 1000C. SERUM OSMOLARITY ABOVE 350D. SEVERE DEHYDRATION AND THE ABSENCE OF KETOACIDOSIS

186. EVALUATION OF A PATIENT'S LABORATORY VALUES WITH HHNK WOULD INCLUDE: A. A SERUM SODIUM OF 123B. A SERUM OSMOLARITY OF 340C. A URINARY SODIUM OF 60D. A BICARBONATE LEVEL OF 12 187. WHICH OF THE FOLLOWING LABORATORY FINDINGS IS NOT LIKELY TO BE SEEN IN PATIENTS WITH DKA?A. PH 7.19B. PCO2 45C. BASE DEFICIT -14D. SERUM K 5.5