current clinical strategies - critical care medicine (lb. englezĂ)

8/2/2019 CURRENT CLINICAL STRATEGIES - CRITICAL CARE MEDICINE (LB. ENGLEZ)

1/153

Current Clinical Strategies

Critical Care Medicine

2002-2003 Edition

Matthew Brenner, MDAssociate Professor of MedicinePulmonary and Critical Care DivisionUniversity of California, Irvine

Michael Safani, PharmDAssistant Clinical ProfessorSchool of Pharmacy

University of California, San Francisco

Georgina Heal, MDRyan M. Klein, MDScott T. Gallacher, MDGuy Foster, MD

Michael Krutzik, MD

Farhad Mazdisnian, MDRoham T. Zamanian, MDHans Poggemeyer, MDH. L. Daneschvar, MD

S. E. Wilson, MD

Division of Pulmonary and Critical Care MedicineCollege of MedicineUniversity of California, Irvine

Current Clinical Strategies Publishing

www.ccspublishing.com/ccs


2/153

Digital Book and Updates

Purchasers of this book may download the digital book and updates of thistext at the Current Clinical Strategies Publishing Web site:www.ccspublishing.com/ccs.

Current Clinical Strategies Publishing

www.ccspublishing.com/ccs

27071 Cabot RoadLaguna Hills, California 92653Phone: 800-331-8227E-Mail: [email protected]

Copyright 2003 Current Clinical Strategies Publishing. All rights reserved. This book, orany parts thereof, may not be reproduced or stored in an information retrieval networkwithout the written permission of the publisher. The reader is advised to consult the drugpackage insert and other references before using any therapeutic agent. No liability exists,expressed or implied, for errors or omissions in this text. Current Clinical Strategies is aregistered trademark of Current Clinical Strategies Publishing Inc.


3/153

Contents

Advanced Cardiac Life Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Critical Care Patient Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Critical Care History and Physical Examination . . . . . . . . . . . . . . . . . . . 15Critical Care Physical Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Admission Check List . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Critical Care Progress Note . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Procedure Note . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Discharge Note . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Fluids and Electrolytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Blood Component Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Total Parenteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Enteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Radiographic Evaluation of Interventions . . . . . . . . . . . . . . . . . . . . . . . . 20Arterial Line Placement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21Central Venous Catheterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21Normal Pulmonary Artery Catheter Values . . . . . . . . . . . . . . . . . . . . . . . 24

Cardiovascular Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Myocardial Infarction and Unstable Angina . . . . . . . . . . . . . . . . . . . . . . . 25Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36Hypertensive Emergency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44Torsades de Pointes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Acute Pericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Pulmonary Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49Orotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49Nasotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50Ventilator Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51Inverse Ratio Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

Ventilator Weaning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52Pulmonary Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Chronic Obstructive Pulmonary Disease . . . . . . . . . . . . . . . . . . . . . . . . 62Pleural Effusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Tension Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68Cardiac Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69Pericardiocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

Hematologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71Transfusion Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71Disseminated Intravascular Coagulation . . . . . . . . . . . . . . . . . . . . . . . . . 72Thrombolytic-associated Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73


4/153

Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Bacterial Meningitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79Pneumocystis Carinii Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83Antiretroviral Therapy and Opportunistic Infections in AIDS . . . . . . . . . . 85Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

Peritonitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91

Gastroenterology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93Upper Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93Variceal Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94Lower Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96Acute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99Hepatic Encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105Poisoning and Drug Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105Toxicologic Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106Acetaminophen Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106Cocaine Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108Cyclic Antidepressant Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109Digoxin Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

Ethylene Glycol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110Gamma-hydroxybutyrate Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111Iron Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111Isopropyl Alcohol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112Lithium Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112Methanol Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113Salicylate Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113Theophylline Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114

Warfarin (Coumadin) Overdose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117Ischemic Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117Elevated Intracranial Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120Status Epilepticus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122

Endocrinologic and Nephrologic Disorders . . . . . . . . . . . . . . . . . . . . . 125Diabetic Ketoacidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125Acute Renal Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127Hyperkalemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130Hypokalemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133Hypomagnesemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134Hypermagnesemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135Disorders of Water and Sodium Balance . . . . . . . . . . . . . . . . . . . . . . . 136Hypophosphatemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140Hyperphosphatemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141

Commonly Used Formulas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142

Commonly Used Drug Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144


5/153

Advanced Cardiac Life Support

EMERGENCY CARDIAC CARE

If wi tnessed arrest, give

precord ial thump andcheck pulse. If absent,continue CP R

As sess Re spo nsiveness

UnresponsiveCall for code team and De fibr illato rAssess breathing (op en the airway, look,liste n an d feel for breathing)

If Not Bre ath ing,give two slow b reaths.Assess Cir cula tion

PULSE NO PULSE

Initia te CPRGive oxygen by bag maskSecure IV access

Dete rmine proba ble e tiol ogy of arrestbased on histo ry, physical exam, car diacmonitor, vital signs, and 12 lead ECG.

Ven tricularfibrillation/tach ycardia

(VT/VF) p rese nt onmonitor?Hypo ten sion /shock,

acute p ulmonaryedema .

Go to fig 8

NO YES

Intu bateConfirm tube pla ceme ntDete rmine rhythm and

cause.

VT/VFGo to Fig 2

Arrh ythmia

Brad ycardiaGo to Fig 5

Tachycardia

Go to Fig 6

Electrical A ctivity?

YES NO

Pulseless e lectrical activityGo to Fig 3

AsystoleGo to Fig 4

Fig 1 - Algorithm for Adult Emergency Cardiac Care


6/153

VENTRICULAR FIBRILLATION AND PULSELESSVENTRICULAR TACHYCARDIA

Con tinue CPR

Pe rsist ent orrecu rr en t V F/VT

Ep i nep hrine 1 mgIV pu sh, re pe atq3 -5m in o r 2 m g in10 ml NS via ET t ubeq3 -5m in or

Vasopressin 40 U I VP x1 do se o nly

Def ibrillate 360 J

A miodarone (Cordarone) 300 mg IV P orL ido ca in e 1. 5 m g /k g IV P , a n d rep e a t q 3 -5 m in , u p t o to ta l m a x o f 3 mg/ kg orMagnesiu m s ulf at e (if Tors ade de poin te s or hypo ma gn es emic ) 2 gms IV P orP rocaina mide (if ab ove are in ef fec tive ) 3 0 mg/min I V inf u sion to ma x 17 mg/kg

Continue CPRSecure IV accessIn tub at e i f no re spo nse

Def ib ril late im m edia tely, u p to 3 tim es at 20 0 J, 20 0-30 0 J, 36 0 J.Do n ot de la y d efibril lation

Return ofspo nt ane ou scirculation

Pu lseless E lectri calAct ivityGo to Fig 3

Monit or vital sign sSu pp or t a irwaySu pp or t b re ath ingProvide me dications appropriate for bloo d

pre ssure, hea rt rate, and rhythm

Asse ss Airway, B reath ing, Circulation, Diffe rent ial DiagnosisAdminister CPR until defibrillato r is ready (p recordial thump if witn esse d arrest )Ve ntricular Fib rillation or Ta chycardia p resen t on d efibrillator

Asyst oleGo to Fig 4

Check pu lse and Rhythm

Co nt inue CP RDe fibrilla te 36 0 J, 30-60 seconds af te r ea ch dose of me dication

Re pe at a m io d aro ne ( Cord ar o ne ) 15 0 m g IV P pr n (if re ur ren t VF/ VT) , up to m a xcu m ul a tive do se o f 2 2 00 m g in 24 h o ur s

Cont in ue CP R. Ad minist er s odium bicarbo nate 1 mE q/k g I VP if long arres t periodRe pe at p att ern o f d rug -sho ck, dr u g-sh o ck

Note: Ep inephrine, lidocaine, atropine may b e given via endotracheal tube at2-2.5 t imes the IV d ose. Dilute in 10 cc of saline.

After each intravenous dose, give 20-30 mL bolus of IV fluid and elevateextremity.

Fig 2 - Ventricular Fibrillation and Pulseless Ventricular Tachycardia


7/153

PULSELESSELECTRICALACTIVITY

PulselessElectricalActivity Includes:

Electromechanical dissociation (EMD)Pseudo-EMDIdioventricular rhythmsVentricular escape rhythmsBradyasystolic rhythmsPostdefibrillation idioventricular rhythms

Epinephrine 1.0 mgIVbolus q3-5min, or highdoseepinephrine0.1 mg/kg IVpushq3-5min; maygiveviaETtube.

ContinueCPR

If bradycardia (


8/153

ASYSTOLE

Continue CPR. Confirmasystolebyrepositioning paddlesor bychecking2leads.IntubateandsecureIVaccess.

Consider underlyingcause, suchashypoxia,hyperkalemia, hypokalemia, acidosis, drug

overdose, hypothermia. myocardial infarction.

Consider transcutaneous pacing(TCP)

Atropine1 mgIV, repeat q3-5minuptoatotal of0.04 mg/kg; maygivevia ET tube.

Epinephrine1.0mgIVpush, repeat every 3-5 min;maygivebyETtube; highdoseepinephrine 0.1mg/kg IVpushq5min(1:1000sln).

Considerbicarbonate1mEq/kg(1-2amp)ifhyperkalemia,acidosis,tricyclicoverdose.

Consider terminationof efforts.

Fig4-Asystole


9/153

BRADYCARDIA

No Yes

YesNo

Assess Airway, Breathing, Circulation, Assess vital signs

Differential Diagnosis ReviewhistorySecure airway andgive oxygen Perform brief physical examSecureIVaccess Order 12-leadECGAttach monitor,pulse oximeter and

automaticsphygmomanometer

Tooslow(


10/153

No or borderline

Atrial fibrillationAtrial flutter

TACHYCARDIA

Paroxysmalsupraventricularnarrow complextachycardia(PSVT)

Wide-complextachycardia ofuncertain type Ventriculartachycardia (VT) Torsade de pointes(polymorphic VT)

Determine Etiology: Hypoxia, ischemia,MI, pulmonary embolus,hyperthyroidism, electrolyte abnomality,theophylline, inotropes.

If uncertain if V tach,give Adenosine 6mg rapid IV pushover 1-3 sec

Amiodarone 150-300 mg IV over 10-20 min

Adenosine12 mg, rapid IVpush over 1-3 sec(may repeat oncein 1-2 min)

1-2 min

Adenosine6 mg, rapid IVpush over 1-3 sec

1-2 min

Cardioversion of atrial fibrillation to sinus rhythm:If less than 2 days and rate controlled:

Procainamide or amiodarone, followed bycardioversion

If more than 2 days: Coumadin for 3 weeks;control rate, start antiarrythmic agent, thenelectrical cardioversion.

Control Rate: Diltiazem,verapamil, digoxinesmolol, metoprolol

Yes

Assess Airway, Breathin g, Circulation, Differential DiagnosisAssess Vitals, Secure AirwayReview his to ry and examine patien t.Give 100 % oxygen , secure IV access.Attach ECG m onitor, pulse oximeter , blood pressure monitor.Order 12-lead ECG, portable chest x -ray.

Correct underlyingcause: Hypokalemia, drug over-dose (tricyc lic,phenothiazine,antiarrhythmicclass Ia, Ic, III)

UNSTABLE, with serious signs or symptoms?Unstable includes, hypotension, heart failure, chest pain, myocardial

infarction, decreased mental status, dyspnea

IMMEDIATE CARDIOVERSIONAtrial flutter 50 J, paroxysmal supraventricular tachycardia

50 J, atrial fibrillation 100 J, monomorphic ventriculartachycardia100 J, polymorphic V tach 200 J.

Premedicate with midazolam (Versed) 2-5 mg IVP whenpossible.

Vagal maneuvers:Carotid sinus

massage if nobruits

Fig 6 Tachycardia


11/153

Ad eno sine 12 m g , ra pid IVp ush o ver 1 -3 se co nd s ( m ayrep eat o n ce in 1-2 m in ); m a xto ta l 30 m g

Lidoca ine1-1 .5 m g/ kg IV pu sh .R ep ea t 0.5 -0. 75m g /kg IV P q 5-1 0m into m a x to ta l 3 m g/ kg

M ag nesium 2-4 gm IVo ver 5 -1 0 m in

Ove rdrive pa cing(c ut an eo us or ve n ou s)

Iso pro te re no l 2 -2 0 m cg/ m inOR

Ph e nyto in 15 m g /kg IV at 5 0

m g/m in ORLidoca ine 1 .0-1 .5 m g /kg IV PC ard io ve rsi o n 20 0 J

Pro cainam ide 30m g /m in IV to m axto ta l 17 m g /kg

Lidoca ine 1 .0-1 .5 m g /kg IV P

C om p lex wid th ?

Nar row Wide

If W o lf -Pa rkin son -W hit esy n dr om e , gi ve am io da r on e(C or da r on e) 1 5 0-30 0 m g IVover 1 0-20 m in

Pr o cain am id e2 0-30 m g /m in, m a x to ta l 1 7 m g /kg ;fo llow ed b y 2 -4 m g /m in in fu sion

If W P W , a void a de nos ine , b et a-b lo cke rs, ca lc iu m -blo cker s, an ddigoxin

Syn ch ro nize d car d io ve rsio n 10 0 J

N or m a l or e leva te d press ure L ow -un sta ble

Ve rap am il2.5-5 m g IV

15-30 m in

Ve rap am il5 -1 0 m g I V

Con side rDigo xinBe ta b lo cke rsD ilt iaze mOve rdr ivepacing F i g 6 - T a c h y c a r d ia

Blo od Pressure ?


12/153

STABLE TACHYCARDIA

If ventricular rate is >150 beats/min, prepare for immediate cardioversion.Treatment of Stable Patients is based on Arrhythmia Type:

Ventricular Tachycardia:Procainamide (Pronestyl) 30 mg/min IV, up to a total max of 17 mg/kg,orAmiodarone (Cordarone) 150-300 mg IV over 10-20 min, orLidocaine 0.75 mg/kg. Procainamide should be avoided if ejection

fraction is


13/153

HYPOTENSION, SHOCK, ANDACUTEPULMONARY EDEMA

Sy s t o l i c B P7 0 - 1 0 0 m m H g

D o p a m in e 2 . 5 - 2 0: g /k g p e r m in I V( a d d n o r e p in e p h r in e

if d o p a m in e i s > 2 0: g /k g p e r m in)

N o r e p in e p h r in e 0. 5 -3 0 : g / m in IV or

D opam in e 5-2 0 : g / kgp e r m in

B ra d yc a r d iaG o t o F ig 5

Syst oli c B P > 100 m m H gan d dia sto lic BP n orm al

S y s to li c B P< 7 0 m m H g

Diasto lic B P > 11 0 mm Hg

D o b u t a m in e 2 .0 -2 0: g / k g p e r m in I V

F u r o s e m id e IV 0 .5 -1 .0 m g /kgM o r p h i ne I V 1- 3 m gN it r o g ly c e r in S L 0 .4 m g t a b

q3 -5 m in x 3O xy g e n

T a c h y ca r d iaG o to F ig 6

D e te rm in e bl o o d p r es s u re

D e t e r m in e u n d e r ly ing c aus e

H y p o v o l e m ia P u m p F a i lu r eB ra d y car d i a o r T a c h y c a r d ia

A d m in is te r F lu id s, B lo o dC ons ide r v a s op re s s o r sA p p l y h e m o s ta s is ; t re a t

u n d e r ly in g p r o ble m

I f is c h em ia an d h ype rte n s ion :N itr og ly c er in 10 -20 :g / m i n

IV , an d t i t ra te to e ff ec t a n d /o r

N itr o p r u s s id e 0. 1- 5 .0: g/k g / m in I V

Signsand symptoms of congestiveheart failure, acute pulmonary edema.Assess ABCD's, secure airway, administer oxygen; secure IVaccess. Monitor ECG, pulse oximeter,

bloodpressure, order 12-lead ECG, portable chest X-rayCheck vital signs, review history, and examine patient. Determine differential diagnosis.

Fig8 - Hypotension,Shock, and AcutePulmonaryEdema


14/153


15/153

Critical Care History and Physical Examination 15

Critical Care Patient Management

T. Scott Gallacher, MD, MS

Critical Care History and Physical Examination

Chief complaint: Reason for admission to the ICU.History of present illness: This section should included pertinent chronological

events leading up to the hospitalization. It should include events during

hospitalization and eventual admission to the ICU.Prior cardiac history: Angina (stable, unstable, changes in frequency),

exacerbating factors (exertional, rest angina). History of myocardial infarction,heart failure, coronary artery bypass graft surgery, angioplasty. Previousexercise treadmill testing, ECHO, ejection fraction. Request old ECG, ECHO,impedance cardiography, stress test results, and angiographic studies.

Chest pain characteristics:A. Pain: Quality of pain, pressure, squeezing, tightness

B. Onset of pain: Exertional, awakening from sleep, relationship to activitiesof daily living (ADLs), such as eating, walking, bathing, and grooming.C. Severity and quality: Pressure, tightness, sharp, pleuriticD. Radiation: Arm, jaw, shoulderE. Associated symptoms: Diaphoresis, dyspnea, back pain, GI symptoms.F. Duration: Minutes, hours, days.G. Relieving factors: Nitroclycerine, rest.

Cardiac risk factors: Age, male, diabetes, hypercholesteremia, low HDL,hypertension, smoking, previous coronary artery disease, family history ofarteriosclerosis (eg, myocardial infarction in males less than 50 years old,stroke).

Congestive heart failure symptoms: Orthopnea (number of pillows), paroxys-mal nocturnal dyspnea, dyspnea on exertional, edema.

Peripheral vascular disease symptoms: Claudication, transient ischemicattack, cerebral vascular accident.

COPD exacerbation symptoms: Shortness of breath, fever, chills, wheezing,sputum production, hemoptysis (quantify), corticosteroid use, previous

intubation.Past medical history: Peptic ulcer disease, renal disease, diabetes, COPD.

Functional status prior to hospitalization.Medications: Dose and frequency. Use of nitroglycerine, beta-agonist, steroids.Allergies: Penicillin, contrast dye, aspirin; describe the specific reaction (eg,

anaphylaxis, wheezing, rash, hypotension).Social history: Tobacco use, alcohol consumption, intravenous drug use.Review of systems: Review symptoms related to each organ system.

Critical Care Physical Examination

Vital signs:Temperature, pulse, respiratory rate, BP (vital signs should be given inranges)Input/Output: IV fluid volume/urine output.


16/153


17/153

Critical Care Progress Note 17

Critical Care Progress Note

ICU Day Number:

Antibiotic Day Number:Subjective: Patient is awake and alert. Note any events that occurred overnight.Objective: Temperature, maximum temperature, pulse, respiratory rate, BP, 24-hr input and output, pulmonary artery pressure, pulmonary capillary wedgepressure, cardiac output.Lungs: Clear bilaterallyCardiac: Regular rate and rhythm, no murmur, no rubs.Abdomen: Bowel sounds normoactive, soft-nontender.

Neuro: No local deficits in strength, sensation.Extremities: No cyanosis, clubbing, edema, peripheral pulses 2+.Labs: CBC, ABG, chem 7.ECG: Chest x-ray:Impression and Plan: Give an overall impression, and then discuss impressionand plan by organ system:

Cardiovascular:Pulmonary:

Neurological:Gastrointestinal:Infectious:Endocrine:Nutrition:

Procedure Note

A procedure note should be written in the chart when a procedure is performed.Procedure notes are brief operative notes.

Procedure Note


18/153

18 Discharge Note

Date and time:Procedure:Indications:

Patient Consent: Document that the indications, risks and alternatives tothe procedure were explained to the patient. Note that the patient wasgiven the opportunity to ask questions and that the patient consented tothe procedure in writing.Lab tests: Relevant labs, such as the INR and CBCAnesthesia: Local with 2% lidocaineDescription of Procedure: Briefly describe the procedure, includingsterile prep, anesthesia method, patient position, devices used, anatomic

location of procedure, and outcome.Complications and Estimated Blood Loss (EBL):Disposition: Describe how the patient tolerated the procedure.Specimens: Describe any specimens obtained and labs tests which wereordered.Name of Physician: Name of person performing procedure and supervis-ing staff.

Discharge Note

The discharge note should be written in the patients chart prior to discharge.

Discharge Note

Date/time:Diagnoses:Treatment: Briefly describe therapy provided during hospitalization,including surgical procedures and antibiotic therapy.Studies Performed: Electrocardiograms, CT scans.Discharge medications:Follow-up Arrangements:

Fluids and Electrolytes

Maintenance Fluids Guidelines:70 kg Adult: D5 1/4 NS with 20 mEq KCI/Liter at 125 mL/hr.

Specific Replacement Fluids for Specific Losses: Gastric (nasogastric tube, emesis): D5 NS with 20 mEq/L KCL.

Diarrhea: D5LR with 15 mEq/liter KCI. Provide 1 liter of replacement foreach 1 kg or 2.2 lb of body weight lost.Bile: D5LR with 25 mEq/liter ( amp) of sodium bicarbonate.Pancreatic: D5LR with 50 mEq/liter (1 amp) sodium bicarbonate.


19/153

Blood Component Therapy 19

Blood Component Therapy

A. Packed red blood cells (PRBCs). Each unit provides 250-400 cc of

volume, and each unit should raise hemoglobin by 1 gm/dL andhematocrit by 3%. PRBCs are usually requested in two unit increments.

B. Type and screen. Blood is tested for A, B, Rh antigens, and antibodiesto donor erythrocytes. If blood products are required, the blood can berapidly prepared by the blood bank. O negative blood is used when typeand screen information is not available, but the need for transfusion isemergent.

C. Type and cross match sets aside specific units of packed donor red

blood cells. If blood is needed on an urgent basis, type and cross shouldbe requested.D. Platelets. Indicated for bleeding if there is thrombocytopenia or platelet

dysfunction in the setting of uncontrolled bleeding. Each unit of plateletconcentrate should raise the platelet count by 5,000-10,000. Platelets areusually transfused 6-10 units at a time, which should increase the plateletcount by 40-60,000. Thrombocytopenia is defined as a platelet count ofless than 60,000. For surgery, the count should be greater than 50,000.

E. Fresh Frozen Plasma (FFP) is used for active bleeding secondary toliver disease, warfarin overdose, dilutional coagulopathy secondary tomultiple blood transfusions, disseminated intravascular coagulopathy, andvitamin K and coagulation factor deficiencies. Administration of FFPrequires ABO typing, but not cross matching.1. Each unit contains coagulation factors in normal concentration.2. Two to four units are usually required for therapeutic intervention.

F. Cryoprecipitate1. Indicated in patients with Hemophilia A, Von Willebrand's disease, and

any state of hypofibrinogenemia requiring replacement (DIC), orreversal of thrombolytic therapy.

2. Cryoprecipitate contains factor VIII, fibrinogen, and Von Willebrandfactor. The goal of therapy is to maintain the fibrinogen level above100 mL/dL, which is usually achieved with 10 units given over 3-5minutes.

Total Parenteral Nutrition

Infuse 40-50 mL/hr of amino acid dextrose solution in the first 24 hr; increasedaily by 40 mL/hr increments until providing 1.3-2 x basal energy requirementand 1.2-1.7 gm protein/kg/d (see formula, page 142)Standard Solution per Liter

Amino acid solution (Aminosyn) 7-10% 500 mLDextrose 40-70% 500 mLSodium 35 mEqPotassium 36 mEqChloride 35 mEqCalcium 4.5 mEqPhosphate 9 mMolMagnesium 8.0 mEqAcetate 82-104 mEq


20/153

20 Enteral Nutrition

Multi-Trace Element Formula 1 mL/dRegular insulin (if indicated) 10-20 U/LMultivitamin 12 (2 amp) 10 mL/dVitamin K (in solution, SQ, IM) 10 mg/weekVitamin B 12 1000 mcg/week

Fat Emulsion:-Intralipid 20% 500 mL/d IVPB infused in parallel with standard solution at 1

mL/min x 15 min; if no adverse reactions, increase to 20-50 mL/hr. Serumtriglyceride level should be checked 6h after end of infusion (maintain100 mL. Flush tube with 100 cc of water after each bolus.

Special Medications:


21/153

Radiographic Evaluation of Interventions 21

-Metoclopramide (Reglan) 10-20 mg PO, IM, IV, or in J tube q6h.-Famotidine (Pepcid) 20 mg J-tube q12h OR-Ranitidine (Zantac) 150 mg in J-tube bid.

Symptomatic Medications:-Loperamide (Imodium) 24 mg PO or in J-tube q6h, max 16 mg/d prn OR-Diphenoxylate/atropine (Lomotil) 5-10 mL (2.5 mg/5 mL) PO or in J-tube q4-

6h, max 12 tabs/d OR-Kaopectate 30 cc PO or in J-tube q6h.

Radiographic Evaluation of Interventions

I. Central intravenous linesA. Central venous catheters should be located well above the right atrium,

and not in a neck vein. Rule out pneumothorax by checking that the lungmarkings extend completely to the rib cages on both sides. Examine forhydropericardium (water bottle sign, mediastinal widening).

B. Pulmonary artery catheter tips should be located centrally andposteriorly, and not more than 3-5 cm from midline.

II. Endotracheal tubes. Verify that the tube is located 3 cm below the vocalcords and 2-4cm above the carina; the tip of tube should be at the level ofaortic arch.

III. Tracheostomies. Verify by chest x-ray that the tube is located halfwaybetween the stoma and the carina; the tube should be parallel to the longaxis of the trachea. The tube should be approximately 2/3 of width of thetrachea; the cuff should not cause bulging of the trachea walls. Check forsubcutaneous air in the neck tissue and for mediastinal widening secondaryto air leakage.

IV. Nasogastric tubes and feeding tubes. Verify that the tube is in the stomachand not coiled in the esophagus or trachea. The tip of the tube should not benear the gastroesophageal junction.

V. Chest tubes. A chest tube for pneumothorax drainage should be near thelevel of the third intercostal space. If the tube is intended to drain a free-flowing pleural effusion, it should be located inferior-posteriorly, at or aboutthe level of the eighth intercostal space. Verify that the side port of the tubeis within the thorax.

VI. Mechanical ventilation. Obtain a chest x-ray to rule out pneumothorax,subcutaneous emphysema, pneumomediastinum, or subpleural air cysts.Lung infiltrates or atelectasis may diminish or disappear after initiation ofmechanical ventilation because of increased aeration of the affected lunglobe.

Arterial Line Placement

Procedure1. Obtain a 20-gauge 1 -2 inch catheter over needle assembly (Angiocath),

arterial line setup (transducer, tubing and pressure bag containingheparinized saline), arm board, sterile dressing, lidocaine, 3 cc syringe, 25-gauge needle, and 3-O silk suture.


22/153

22 Central Venous Catheterization

2. The radial artery is the most frequently used artery. Use the Allen test to verifythe patency of the radial and ulnar arteries. Place the extremity on an armboard with a gauze roll behind the wrist to maintain hyperextension.

3. Prep the skin with povidone-iodine and drape; infiltrate 1% lidocaine using a25-gauge needle. Choose a site where the artery is most superficial anddistal.

4. Palpate the artery with the left hand, and advance the catheter-over-needleassembly into the artery at a 30-degree angle to the skin. When a flash ofblood is seen, hold the needle in place and advance the catheter into theartery. Occlude the artery with manual pressure while the pressure tubing isconnected.

5. Advance the guide wire into the artery, and pass the catheter over the guide

wire. Suture the catheter in place with 3-0 silk and apply dressing.

Central Venous Catheterization

I. Indications for central venous catheter cannulation: Monitoring of centralvenous pressures in shock or heart failure; management of fluid status;insertion of a transvenous pacemaker; administration of total parenteralnutrition; administration of vesicants (chemotherapeutic agents).

II. Location: The internal jugular approach is relatively contraindicated inpatients with a carotid bruit, stenosis, or an aneurysm. The subclavianapproach has an increased risk of pneumothorax in patients with emphysemaor bullae. The external jugular or internal jugular approach is preferable inpatients with coagulopathy or thrombocytopenia because of the ease ofexternal compression. In patients with unilateral lung pathology or a chesttube already in place, the catheter should be placed on the side of predomi-

nant pathology or on the side with the chest tube if present.III. Technique for insertion of external jugular vein catheter

1. The external jugular vein extends from the angle of the mandible tobehind the middle of the clavicle, where it joins with the subclavian vein.Place the patient in Trendelenburg's position. Cleanse skin with Betadine-iodine solution, and, using sterile technique, inject 1% lidocaine toproduce a skin weal. Apply digital pressure to the external jugular veinabove the clavicle to distend the vein.

2. With a 16-gauge thin wall needle, advance the needle into the vein. Thenpass a J-guide wire through the needle; the wire should advance withoutresistance. Remove the needle, maintaining control over the guide wireat all times. Nick the skin with a No. 11 scalpel blade.

3. With the guide wire in place, pass the central catheter over the wire andremove the guide wire after the catheter is in place. Cover the catheterhub with a finger to prevent air embolization.

4. Attach a syringe to the catheter hub and ensure that there is free back-

flow of dark venous blood. Attach the catheter to an intravenous infusion.5. Secure the catheter in place with 2-0 silk suture and tape. The catheter

should be replaced weekly or if there is any sign of infection.6. Obtain a chest x-ray to confirm position and rule out pneumothorax.

IV. Internal jugular vein cannulation. The internal jugular vein is positionedbehind the stemocleidomastoid muscle lateral to the carotid artery. Thecatheter should be placed at a location at the upper confluence of the twobellies of the stemocleidomastoid, at the level of the cricoid cartilage.


23/153

Central Venous Catheterization 23

1. Place the patient in Trendelenburg's position and turn the patient's headto the contralateral side.

2. Choose a location on the right or left. If lung function is symmetrical and nochest tubes are in place, the right side is preferred because of the directpath to the superior vena cava. Prepare the skin with Betadine solutionusing sterile technique and placea drape. Infiltrate the skin and deepertissues with 1% lidocaine.

3. Palpate the carotid artery. Using a 22-gauge scout needle and syringe,direct the needle lateral to the carotid artery towards the ipsilateral nippleat a 30-degree angle to the neck. While aspirating, advance the needleuntil the vein is located and blood flows back into the syringe.

4. Remove the scout needle and advance a 16-gauge, thin wall catheter-

over-needle with an attached syringe along the same path as the scoutneedle. When back flow of blood is noted into the syringe, advance thecatheter into the vein. Remove the needle and confirm back flow of bloodthrough the catheter and into the syringe. Remove the syringe, and use afinger to cover the catheter hub to prevent air embolization.

5. With the 16-gauge catheter in position, advance a 0.89 mm x 45 cm springguide wire through the catheter. The guidewire should advance easilywithout resistance.

6. With the guidewire in position, remove the catheter and use a No. 11scalpel blade to nick the skin.

7. Place the central vein catheter over the wire, holding the wire secure at alltimes. Pass the catheter into the vein, remove the guidewire, and suturethe catheter with 0 silk suture, tape, and connect it to an IV infusion.

8. Obtain a chest x-ray to rule out pneumothorax and confirm position of thecatheter.

V. Subclavian vein cannulation. The subclavian vein is located in the angle

formed by the medial 1/3 of the clavicle and the first rib.1. Position the patient supine with a rolled towel located between the

patient's scapulae, and turn the patient's head towards the contralateralside. Prepare the area with Betadine iodine solution, and, using steriletechnique, drape the area and infiltrate 1% lidocaine into the skin andtissues.

2. Advance the 16-gauge catheter-over-needle, with syringe attached, intoa location inferior to the mid-point of the clavicle, until the clavicle bone

and needle come in contact.3. Slowly probe down with the needle until the needle slips under theclavicle, and advance it slowly towards the vein until the catheter needleenters the vein and a back flow of venous blood enters the syringe.Remove the syringe, and cover the catheter hub with a finger to preventair embolization.

4. With the 16-gauge catheter in position, advance a 0.89 mm x 45 cmspring guide wire through the catheter. The guide wire should advanceeasily without resistance.

5. With the guide wire in position, remove the catheter, and use a No. 11scalpel blade to nick the skin.

6. Place the central line catheter over the wire, holding the wire secure at alltimes. Pass the catheter into the vein, and suture the catheter with 2-0silk suture, tape, and connect to an IV infusion.

7. Obtain a chest x-ray to confirm position and rule out pneumothorax.


24/153

24 Pulmonary Artery Catheter Values

VI. Pulmonary artery catheterization1. Using sterile technique, cannulate a vein using the technique above. The

subclavian vein or internal jugular vein is commonly used.2. Advance a guide wire through the cannula, then remove the cannula, but

leave the guide wire in place. Keep the guide wire under control at alltimes. Nick the skin with a number 11 scalpel blade adjacent to the guidewire, and pass a number 8 French introducer over the wire into the vein.Remove the wire and connect the introducer to an IV fluid infusion, andsuture with 2-0 silk.

3. Pass the proximal end of the pulmonary artery catheter (Swan Ganz) toan assistant for connection to a continuous flush transducer system.

4. Flush the distal and proximal ports with heparin solution, remove all

bubbles, and check balloon integrity by inflating 2 cc of air. Check thepressure transducer by quickly moving the distal tip and watching themonitor for response.

5. Pass the catheter through the introducer into the vein, then inflate theballoon with 1.0 cc of air, and advance the catheter until the balloon is inor near the right atrium.

6. The approximate distance to the entrance of the right atrium is deter-mined from the site of insertion:

Right internal jugular vein: 10-15 cm.Subclavian vein: 10 cm.Femoral vein: 35.45 cm.

7. Advance the inflated balloon, while monitoring pressures and wave formsas the PA catheter is advanced. Advance the catheter through the rightventricle into the main pulmonary artery until the catheter enters a distalbranch of the pulmonary artery and is stopped (as evidenced by apulmonary wedge pressure waveform).

8. Do not advance the catheter while the balloon is deflated, and do notwithdraw the catheter with the balloon inflated. After placement, obtain achest X-ray to ensure that the tip of catheter is no farther than 3-5 cmfrom the mid-line, and no pneumothorax is present.

Normal Pulmonary Artery Catheter Values

Right atrial pressure 1-7 mm HgRVP systolic 15-25 mm HgRVP diastolic 8-15 mm Hg

Pulmonary artery pressurePAP systolic 15-25 mm HgPAP diastolic 8-15 mm HgPAP mean 10-20 mm Hg


25/153

Acute Coronary Syndromes 25

Cardiovascular Disorders

Roham T. Zamanian, MDFarhad Mazdisnian, MDMichael Krutzik, MD

Acute Coronary Syndromes (Acute MyocardialInfarction and Unstable Angina)

Acute myocardial infarction (AMI) and unstableangina are part of a spectrumknown as the acute coronary syndromes (ACS), which have in common aruptured atheromatous plaque. These syndromes include unstable angina,nonQ-wave MI,and Q-wave MI. The ECG presentation of ACS includes ST-segmentelevation infarction, ST-segment depression (including nonQ-waveMIand unstable angina), and nondiagnostic ST-segment and T-wave abnormalities.Patients with ST-segment elevation will usually developQ-wave MI. Patients with

ischemic chest discomfort who do not have ST-segment elevation will developQ-waveMI and nonQ-wave MI or unstable angina.

I. Clinical evaluation of chest pain and acute coronary syndromesA. History. Chest pain is present in 69% of patients with AMI. The pain may

be characterized as a constricting or squeezing sensation in the chest.Pain can radiate to the upper abdomen, back, either arm, either shoulder,neck, or jaw. Atypical pain presentations in AMI include pleuritic, sharp or

burning chest pain. Dyspnea, nausea, vomiting, palpitations, or syncopemay be the only complaints.

B. Cardiac Risk factors include hypertension, hyperlipidemia, diabetes,smoking, and a strong family history (coronary artery disease in early ormid-adulthood in a first-degree relative).

C. Physical examination may reveal tachycardia or bradycardia, hyper- orhypotension, or tachypnea. Inspiratory rales and an S3 gallop areassociated with left-sided failure. Jugulovenous distention (JVD),

hepatojugular reflux, and peripheral edema suggest right-sided failure. Asystolic murmur may indicate ischemic mitral regurgitation or ventricularseptal defect.

II. Laboratory evaluation of chest pain and acute coronary syndromesA. Electrocardiogram (ECG). The initial ECG reveals diagnostic ST

elevations in only 40% of patients with a confirmed AMI. ST-segmentelevation (equal to or greater than 1 mV) in two or more contiguous leadsprovides strong evidence of thrombotic coronary arterial occlusion andmakes the patient a candidate for immediate reperfusion by thrombolysisor angioplasty.

B. Laboratory markers1. Creatine phosphokinase (CPK) enzyme is found in the brain, muscle,

and heart. The cardiac-specific dimer, CK-MB, however, is presentalmost exclusively in myocardium.


26/153

26 Acute Coronary Syndromes

Common Markers for Acute Myocardial Infarction

Marker Initial Eleva-

tion After MI

Mean Time to

Peak Eleva-tions

Time to Re-

turn to Base-line

Myoglobin 1-4 h 6-7 h 18-24 h

CTnl 3-12 h 10-24 h 3-10 d

CTnT 3-12 h 12-48 h 5-14 d

CKMB 4-12 h 10-24 h 48-72 h

CKMBiso 2-6 h 12 h 38 h

CTnI, CTnT = troponins of cardiac myofibrils; CPK-MB, MM = tissueisoforms of creatine kinase.

2. CK-MB subunits. Subunits of CK, CK-MB, -MM, and -BB, aremarkers associated with a release into the blood from damaged cells.Elevated CK-MB enzyme levels are observed in the serum 2-6 hoursafter MI, but may not be detected until up to 12 hours after the onsetof symptoms.

3. Cardiac-specific troponin T (cTnT) is a qualitative assay and cardiactroponin I (cTnI) is a quantitative assay. The cTnT level remainselevated in serum up to 14 days and cTnI for 3-7 days after infarction.

4. Myoglobin is the first cardiac enzyme to be released. It appearsearlier but is less specific for MI than other markers. Myoglobin is mostuseful for ruling out myocardial infarction in the first few hours.

III. Initial treatment of acute coronary syndromesA. Continuous cardiac monitoring and IV access should be initiated.

Morphine, oxygen, nitroglycerin, and aspirin ("MONA") should beadministered to patients with ischemic-type chest pain unless contraindi-cated.

B. Morphine is indicated for continuing pain unresponsive to nitrates.Morphine reduces ventricular preload and oxygen requirements byvenodilation. Administer morphine sulfate 2-4 mg IV every 5-10 minutesprn for pain or anxiety.

C. Oxygen should be administered to all patients with ischemic-typechestdiscomfort and suspected ACS for at least 2 to 3 hours.

D. Nitroglycerin1. Nitroglycerin is an analgesic for ischemic-type chest discomfort.

Nitroglycerin is indicated for the initial management of pain andischemia unless contraindicated by hypotension (SBP


27/153


(maximum, 3 mcg/kg/min). Titrate to decrease the mean arterialpressure by 10% in normotensive patients and by 30% in those withhypertension. Slow or stop the infusion if the SBP drops below 100mm Hg.

E. Aspirin1. Aspirin should be given as soon as possible to all patients with

suspected ACS unless the patient is allergic to it. Aspirin therapyreduces mortality after MI by 25%.

2. A dose of 160-325 mg of aspirin should be chewed and swallowed onday 1 and continued PO daily thereafter. If aspirin is contraindicated,clopidogrel (Plavix) 75 mg qd should be administered.

IV. Risk stratification, initial therapy, and evaluation for reperfusion in

the emergency department

Risk Stratification with the First 12-Lead ECG

Use the 12-lead ECG to triage patients into 1 of 3 groups:1. ST-segment elevation

2. ST-segment depression($1 mm)

3. Nondiagnostic

or normal ECG

A. Patients with ischemic-type chest pain and ST-segment elevation $1mmin 2 contiguous leads have acute myocardial infarction. Reperfusiontherapy with thrombolytics or angioplasty is recommended.

B. Patients with ischemic-type pain but normal or nondiagnosticECGs orECGs consistent with ischemia (ST-segment depressiononly) usually donot have AMI. These patientsshould not be given fibrinolytic therapy.

C. Patients with normal or nondiagnostic ECGs usually do not have AMI, andthey should be evaluated with serial cardiac enzymes and additional teststo determine the cause of their symptoms.

V. Management of ST-segment elevation myocardial infarctionA. Patients with ST-segment elevation have AMI should receive reperfusion

therapy with fibrinolytics or percutaneous coronary intervention.

B. Reperfusion therapy: Fibrinolytics1. Patients who presentwith ischemic pain and ST-segment elevation ($1

mm in $2 contiguous

leads) within 12 hours of onset of persistent painshould receive fibrinolytic therapy unless contraindicated. Patients witha new bundle branch block (obscuring ST-segment analysis) andhistory suggesting acute MI should also receive fibrinolytics orangioplasty.


28/153


Treatment Recommendations for AMI

Supportive Care for Chest Pain

All patients should receive supplemental oxygen, 2 L/min by nasal canula, for aminimum of three hours Two large-bore IVs should be placed

Aspirin:

Inclusion Clinical symptoms or suspicion of AMI

Exclusion Aspirin allergy, active GI bleeding

Recommendation Chew and swallow one dose of160-325 mg, then orally qd

Thrombolytics:

Inclusion All patients with ischemic pain and ST-segment elevation ($1 mm in $2 contiguousleads) within 12 hours of onset ofpersistent pain, age


29/153


Beta-Blockade:

Inclusion All patients with the diagnosis of AMI. Within 12 hours of

diagnosis of AMI

Exclusion Severe COPD, hypotension, bradycardia, AV block, pulmo-nary edema, cardiogenic shock

Recommendation Metoprolol (Lopressor), 5 mg IV push every 5 minutes forthree doses; followed by 25 mg PO bid. Titrate up to 100mg PO bid ORAtenolol (Tenormin), 5 mg IV, repeated in 5 minutes, fol-lowed by 50-100 mg PO qd.

Nitrates:

Inclusion All patients with ischemic-type chest pain

Exclusion Nitrate allergy; sildenafil (Viagra) within prior 24 hours;hypotension; caution in right ventricular infarction

Recommendation 0.4 mg NTG initially q 5 minutes, up to 3 doses or nitroglyc-

erine aerosol, 1 spray sublingually every 5 minutes. IVinfusion of NTG at 10-20 mcg/min, titrating upward by 5-10mcg/min q 5-10 minutes (max 3 mcg/kg/min). Slow or stopinfusion if systolic BP 100 mm hg

C. Thrombolytics1. ECG criteria for thrombolysis

a. ST Elevation (>1 mm in two or more contiguous leads), time totherapy 12 hours or less, age younger than 75 years.

b. A new bundle branch block (obscuring ST-segment analysis) andhistory suggesting acute MI.

2. Alteplase (t-PA, tissue-plasminogen activator, Activase) andReteplase (Retavase) convert plasminogen to plasmin. Both agentsare clot-specific and bind to new thrombus. Activase is superior tostreptokinase. The alteplase thirty-day mortality rate of 6.3% is the

lowest of the fibrinolytics, compared with 7.3% for streptokinase.Alteplase provides the earliest and most complete reperfusion.3. Streptokinase (SK, Streptase) provides greater benefit in older

patients with a smaller amount of myocardiumat risk who presentlater and those with a greater risk of ICH. The dose of IV SK is 1.5million units given over 60 minutes.

D. Reperfusion therapy: Percutaneous coronary intervention


30/153


1. PCI is preferable to thrombolytic therapy if performed in a timelyfashion by individuals skilled in the procedure. Coronary angioplastyprovides higher rates of flow than thrombolytics and is associated withlower rates of reocclusionand postinfarction ischemia than fibrinolytictherapy.

2. Patients at high risk for mortality orsevere LV dysfunction with signsof shock, pulmonary congestion,heart rate >100 bpm, and SBP


31/153


Heparin and ST-Segment Depression and NonQ-Wave MI/UnstableAngina

! IV heparin therapy for 3 to 5 days is standard for high-risk and someintermediate-risk patients. Treat for 48 hours, then individualizedtherapy.

! LMWH is an acceptable alternative to IV unfractionated heparin.-Enoxaparin (Lovenox) 1.0 mg/kg SQ q12h OR-Dalteparin (Fragmin) 120 IU/kg (max 10,000 U) SQ q12h.

C. Nitrates should be given for recurrent angina. Sublingual nitroglycerin

(NTG) , initially, give up to three doses of 0.4 mg sublingual NTG everyfive minutes or nitroglycerine aerosol, 1 spray sublingually every 5minutes. Nitroglycerin patch 0.2 mg/hr qd. Allow for nitrate-free period toprevent tachyphylaxis. Isosorbide dinitrate (Isordil) 10-60 mg PO tid -[5,10,20, 30,40 mg], or isosorbide mononitrate (Imdur) 30-60 mg qd.

D. Beta-blockers. A beta-blocker should be initiated for patients with ST-segment depression.1. Beta-blockers reduce the size of the infarct in patientswho do not

receive fibrinolytic therapy. A significant decrease in death andnonfatal infarction has beenobserved in patients treated with beta-blockers after infarction.Contraindications to beta-blockers: severe LVfailure and pulmonary edema, bradycardia (heart rate


32/153


VII. Management of patients with a nondiagnostic ECG


33/153

A. Patients with a nondiagnostic ECG who have an indeterminate ora lowrisk of MI should receive aspirin while undergoing serial cardiac enzymestudies and repeat ECGs.

B. Treadmill stress testing should be considered for patients with asuspicion of coronary ischemia.

Heart Failure

Congestive heart failure (CHF) is defined as the inability of the heart to meet themetabolic and nutritional demands of the body. Approximately 75% of patientswith heart failure are older than 65-70 years of age. Approximately 8% of patientsbetween the ages of 75 and 86 have heart failure.

I. EtiologyA. The most common causes of CHF are coronary artery disease, hyperten-

sion, and alcoholic cardiomyopathy. Valvular diseases such as aortic

stenosis and mitral regurgitation, are also common.B. Coronary artery disease is the etiology of heart failure in two-thirds ofpatients with left ventricular dysfunction. Heart failure should be presumedto be of ischemic origin until proven otherwise.

II. Clinical presentationA. Left heart failure produces dyspnea and fatigue. Right heart failure leads

to lower extremity edema, ascites, congestive hepatomegaly, and jugularvenous distension. Symptoms of pulmonary congestion include dyspnea,orthopnea, and paroxysmal nocturnal dyspnea. Clinical impairment iscaused by left ventricular systolic dysfunction (ejection fraction of less than

40%) in 80-90% of patients with CHF.B. Patients should be evaluated for coronary artery disease, hypertension,

and valvular dysfunction. Use of alcohol, chemotherapeutic agents(daunorubicin), negative inotropic agents, and symptoms of a recent viralsyndrome should be assessed.

C. CHF can present with shortness of breath, dyspnea on exertion, paroxys-mal nocturnal dyspnea, orthopnea, nocturia, and cough. Exertionaldyspnea is extremely common in patients with heart failure.

Precipitants of Congestive Heart Failure

Myocardial ischemia or infarc-tion

Atrial fibrillation Worsening valvular disease Pulmonary embolism Hypoxia Severe, uncontrolled hyperten-

sion

Thyroid disease Pregnancy Anemia Infection Tachycardia or bradycardia Alcohol abuse Medication or dietary noncompli-

ance

D. Physical examination.Lid lag, goiter, medication use, murmurs, abnormalheart rhythms may suggest a treatable underlying disease. Patients withCHF may present with resting tachycardia, jugular venous distension, athird heart sound, rales, lower extremity edema, or a laterally displaced


34/153

34 Heart Failure

apical impulse. Poor capillary refill, cool extremities, or an altered level ofconsciousness may also be present.

New York Heart Association Criteria for Heart Failure

Class I AsymptomaticClass II Symptoms with moderate activityClass III Symptoms with minimal activityClass IV Symptoms at rest

E. Laboratory assessment1. Patients with symptoms suggestive of CHF should have a 12-lead

ECG.2. Impedance cardiography (ICG) is a noninvasive, reliable method of

measuring cardiac index and stroke volume. It should be done on thefirst day of hospitalization and repeated to assess response to drugtherapy.

3. A chest x-ray should be performed to identify pleural effusions,pneumothorax, pulmonary edema, or infiltrates.

4. If cardiac ischemia or infarction is suspected, cardiac enzymes shouldbe drawn. A complete blood count, electrolytes, and digoxin level, ifapplicable, also are mandatory. Patients with suspected hyper-thyroidism should have thyroid function studies drawn.

F. Echocardiography is recommended to evaluate the presence ofpericardial effusion, tamponade, valvular regurgitation, wall motionabnormalities, and ejection fraction.

Laboratory Workup for Suspected Heart Failure

Blood urea nitrogenCardiac enzymes (CK-MB,troponin, or both)Complete blood cell countCreatinine

ElectrolytesLiver function tests

MagnesiumThyroid-stimulating hormoneUrinalysisEchocardiogramElectrocardiography

Impedance cardiography

III. Management of chronic heart failureA. Patients should also be placed on oxygen to maintain adequate oxygen

saturation. In patients with severe symptoms (ie, pulmonary edema),continuous positive airway pressure (CPAP) or endotracheal intubation(ETI) may be employed.

B. Angiotensin-converting enzyme inhibitorssignificantly reduce morbidityand mortality in CHF. Side effects include cough, worsening renal function,hyperkalemia, hypotension, and the risk of angioedema. ACEIs should bestarted at a very low dose and titrated up gradually to relieve shortness ofbreath. Renal function and electrolytes should be monitored.


35/153

Heart Failure 35

ACE Inhibitors Used for Heart Failure

Benazepril (Lotensin) start 10 mg po bid, target 20-40 mg po bid

Captopril (Capoten) start 6.25-12.5 mg po tid, target dose 50-100 mg tidEnalapril (Vasotec) start 2.5 mg po qd/bid, target 2.5-10 mg tidFosinopril (Monopril) start 10 mg po qd, target 20-40 mg/dLisinopril (Prinivil, Zestril) start 5 mg po qd, target 5-20 mg/dQuinapril (Accupril) start 5 mg po bid, target 20-40 mg/dRamipril (Altace) start 2.5 mg po bid, target 10 mg/dTrandolapril (Mavik) start 1 mg po qd, target 2-4 mg qd

C. Angiotensin II receptor blockers (ARBs). In patients who cannot tolerate

or have contraindications to ACE inhibitors, ARBs should be considered.ARBs are as effective as ACE inhibitors with a lower incidence of coughand angioedema.

Angiotensin II Receptor Blockers for Heart Failure

Candesartan (Atacand)start 4-8 mg qd bid, target 8-16 mg qd bid

Irbesartan (Avapro)start 75-150 mg qd, target 150-300 mg qdLosartan (Cozaar)start 25-50 mg qd, target 50 mg bidValsartan (Diovan)start 80 mg qd, target 160-320 mg qd

D. Hydralazine/Isordil combination may be used in patients who areintolerant to ACE-inhibitors and ARBs; however, this combination is lesseffective in reducing mortality. Hydralazine can cause reflex tachycardiaand increase ischemic pain. Reflex tachycardia due to hydralazine may be

beneficial in patients with bradycardia caused by beta-blockers. Thedosage of hydralazine is 10-50 mg qid, combined with isosorbide dinitrate(Isordil) 10-40 mg qid, OR isordil mononitrate (Imdur) 30-60 mg qd.

E. Diuretics induce peripheral vasodilation, reduce cardiac filling pressures,and prevent fluid retention.Loop diuretics are the most potent agents inCHF. Diuretics should be prescribed for patients with heart failure whohave volume overload.

Diuretic Therapy in Congestive Heart Failure

Loop diuretics

Furosemide (Lasix) 20-200 mg IV/PO daily or bid, or 10-20 mg/hr IVinfusion

Bumetanide (Bumex) 0.5-4.0 mg IV/PO daily or bid Torsemide (Demadex) 5-100 mg IV/PO dailyLong-acting thiazide diuretics

Metolazone (Zaroxolyn) 2.5-10.0 mg qd PO bid Hydrochlorothiazide 25 PO mg qdAldosterone Antagonists Spironolactone (Aldactone) 12.5-25 mg PO qd

F. Beta-Blockers are beneficial in heart failure, improving contractility andsurvival. Beta-blockers should be started at low doses and advanced


36/153

36 Heart Failure

slowly. Beta-blockers should not be used in acute pulmonary edema ordecompensated heart failure, and they should only be initiated in thestable patient. Beta-blockers are an add-on therapy for patients beingtreated with ACE inhibitors.

Carvedilol, Metoprolol, and Bisoprolol Dosages and Side Effects

Carvedilol (Coreg) start at 1.625-3.125 mg bid; target dose 25-50 mgbid

Metoprolol (Lopressor) start at 12.5 mg bid; target dose 100 mg bid Bisoprolol (Zebeta) start at 1.25 mg qd; target dose 10 mg qd

Digoxin Dosing

Start at 0.250 mg/d with near normal renal function; start at 0.125 mg/dif renal function impaired.

Maintain serum digoxin level of 0.8-1.2 ng/mL.

G. Digoxin does not improve survival in CHF (as do ACE-inhibitors andbeta-blockers). Digoxin may be added to a regimen of ACE-inhibitors anddiuretics if symptoms of heart failure persist. Digoxin can increaseexercise tolerance, improve symptoms, and decrease the risk ofhospitalization.

H. Spironolactone improves mortality in severe CHF and should be usedin addition to an ACE-inhibitor or ARB. A dosage of 25 mg qd should beconsidered in patients with severe CHF. It can cause hyperkalemia, rash,

and gynecomastia.I. Nonpharmacologic treatments

1. Salt restriction (a diet with 2 g sodium or less), alcohol restriction,water restriction for patients with severe renal impairment, and regularaerobic exercise as tolerated.

2. Synchronized biventricular pacing in patients with an ejection fractionof 150 msec may improve symp-toms and the overall clinical course.

J. Inotropic support1. Positive inotropic agents improve quality of life and reduce need for

hospitalization but increase mortality. Parenterally positive inotropictherapy increases cardiac output and decreases symptoms ofcongestion.

2. Parenteral inotropic agents can be administered continuously inpatients with exacerbations of heart failure. These agents may beadministered continuously or intermittently at home. Impedance

cardiography is used to assess clinical response before and duringtreatment.


37/153

Atrial Fibrillation 37

Inotropic Agents for Cardiogenic Shock

Milrinone (Primacor) start at 0.375 mcg/kg/min and titrate to 0.75

mcg/kg/min Dobutamine (Dobutrex) start at 2-3 mcg/kg/min and titrate 5

mcg/kg/min Dopamine (Intropin) start at 2-5 mcg/kg/min and titrate to 10

mcg/kg/min

K. Natriuretic peptides1. Atrial and brain natriuretic peptides regulate cardiovascular homeosta-

sis and fluid volume.2. Nesiritide (Natrecor) is structurally similar to atrial natriuretic peptide.

It has natriuretic, diuretic, vasodilatory, smooth-muscle relaxantproperties, and inhibits the renin-angiotensin system. Nesiritide isindicated for the treatment of moderate-to-severe heart failure.

3. The initial dose of nesiritide is 0.015 mcg/kg/min IV infusion slowlytitrated to max 0.03 mcg/kg/min. Hypotension occurs frequently with amild increase in heart rate.

Treatment of Acute Heart Failure/Pulmonary Edema

Oxygen therapy, 2 L/min by nasal canula Furosemide (Lasix) 20-80 mg IV (patients already on outpatient dose

may require more) Nitroglycerine start at 10-20 mcg/min and titrate to BP (use with cau-

tion if inferior/right ventricular infarction suspected) Sublingual nitroglycerin 0.4 mg Morphine sulfate 2-4 mg IV. Avoid if inferior wall MI suspected or if

hypotensive or presence of tenuous airway Potassium supplementation prn

Atrial Fibrillation

Atrial fibrillation (AF) is the most common arrhythmia. The median age of onsetis 75, and the incidence and prevalence increase dramatically with age. Forpatients older than 80 years, the incidence of AF is 9%. For patients aged 80-90,nearly one-third of strokes that occur are related to AF.

I. Pathophysiology. The cardiac conditions most commonly associated withAF are coronary artery disease, hypertension, rheumatic heart disease, mitral

valve disease, cardiomyopathies, and open-heart surgery. Hypertension andcoronary artery disease are the most frequent risk factors, accounting for 65%of AF cases. The most common noncardiac causes are pulmonary diseases(including COPD), hypoxia, and hyperthyroidism.

II. Clinical evaluation


38/153

38 Atrial Fibrillation

A. Patients with AF often experience dyspnea and palpitations, althoughsome may be asymptomatic. AF may be associated with palpitations,dizziness, dyspnea, chest pain, syncope, fatigue, or confusion.

B. The most common physical sign of AF is an irregular pulse. Otherphysical exam findings include a pulse deficit, absent a wave in the

jugular venous pulse, and a variable intensity of the first heart sound.

Causes of Atrial Fibrillation

Structural Heart Disease Absence of Structural Heart Disease

HypertensionIschemic heart diseaseValvular heart disease: Mitral stenosis,

aortic stenosis, mitral regurgitationPericarditisCardiac tumorsSick sinus syndromeCardiomyopathiesCongenital heart disease

Wolf-Parkinson-White syndrome

Pulmonary diseases: COPD, hypoxia,pneumonia, pulmonary embolus,metabolic disorders, thyrotoxicosis,electrolyte imbalance

Acute ethanol intoxicationMethylxanthine derivatives:

Theophylline, caffeineSystemic illnessSepsis, malignancyLone atrial fibrillation

III. Diagnostic studiesA. Laboratory studies should include chemistries, CBC, INR/PTT, and a

TSH. A chest x-ray may uncover COPD, pneumonia, CHF, orcardiomegaly.

B. Ambulatory 24-hour (Holter) ECG monitoring should be performed todetermine both the frequency and duration of AF.

C. Echocardiogram provides information on cardiac dimensions (left atrialsize), LV systolic function, valvular disease, and LV hypertrophy.

IV. Initial managementA. If the duration of AF is less than 48 hours, the initial goals are either

cardioversion or ventricular rate control and observation. If the patient isnot hemodynamically compromised and the AF is of new onset, an initialperiod of observation using medications for rate control andanticoagulation with heparin are initiated. If AF persists despite rate

control, restoration of sinus rhythm is the usual goal if the patient issymptomatic during AF, requires AV synchrony for improved cardiacoutput, or wants to avoid lifelong anticoagulation. Sinus rhythm can beachieved with either external cardioversion and/or pharmacologicalagents.

B. Initial treatment of atrial fibrillation1. Anticoagulation in patients with nonvalvular AF reduces the incidence

of embolic strokes.

2. Oral anticoagulation therapy with warfarin (Coumadin), with an INRgoal between 2.0-3.0, should be considered in all AF patients withone or more risk factors, as described below, regardless of age.

3. In patients without rheumatic heart disease who are younger than 75years of age, warfarin therapy should be initiated if risk factors arepresent, including previous transient ischemic attack or stroke,hypertension, heart failure, diabetes, clinical coronary artery disease,mitral stenosis, prosthetic heart valves, or thyrotoxicosis. In patients


39/153


younger than 65 and without these risk factors (lone AF), aspirinalone may be appropriate for stroke prevention.

4. Patients between the ages of 65 and 75 with none of these riskfactors could be treated with either warfarin or aspirin.

5. In patients older than 75 with AF, oral anticoagulation with warfarin isrecommended. In patients with major contraindications to warfarin(intracranial hemorrhage, unstable gait, falls, syncope, or poorcompliance), a daily aspirin is a reasonable alternative.

6. If the duration of AF is unknown or more than 48 hours, then ratecontrol and anticoagulation therapy should be initiated first. Thepatient should be evaluated for the presence of an intracardiacthrombus with a transesophageal echocardiography (TEE). If the TEE

demonstrates a clot, the patient is anticoagulated for three weeksbefore a scheduled cardioversion. If no left atrial thrombus isidentified by TEE, heparin is started and the patient is cardioverted.Following successful cardioversion, the patient is placed on warfarinfor an additional four weeks.

C. Rate control1. Patients with AF of greater than one year duration or a left atrial size

greater than 50 mm may have difficulty in converting to sinus rhythm.

In these patients, rate control, rather than conversion to sinus rhythmmay, be beneficial. A controlled ventricular rate in AF is less than 90bpm at rest.

2. The pharmacological agents used for rate control are calcium channelblockers (diltiazem, verapamil), beta-blockers (metoprolol, esmolol)and digoxin. Calcium channel blockers should be used first becauseof rapid onset of action compared to digoxin, which takes 4-6 hoursto show pharmacological effect. Digoxin is the first drug of choice in

significant left ventricular dysfunction.3. Calcium channel blockers can slow AV node conduction and arefirst-line agents for rate control therapy.

4. Beta-blockers slow AV nodal and sinoatrial nodal conduction. Themost commonly used beta-blockers are metoprolol and atenolol.

5. Digoxin has numerous drug interactions, an unpredictable doseresponse curve, and a potentially lethal toxicity. Digoxin is is reservedfor patients with systolic dysfunction and heart failure.

Agents Used for Heart Rate Control in Atrial Fibrillation

Agent Loading

Dose

Onset of Ac-

tion

Maintenance

Dosage

Major Side

Effects

Diltiazem(Cardizem)

0.25 mg perkg IV over 2minutes, mayrepeat dosewith 0.35mg/kg after 15min x 1

2-7 minutes 5-15 mg perhour IV or 120-360 mg PO ev-ery day in div-ided doses

Hypotension,heart block,heart failure

Verapamil(Calan,Isoptin)

0.075-0.15 mgper kg IV over2 minutes

3-5 minutes 240-360 mg POevery day individed doses

Hypotension,heart block,heart failure


40/153

40 Atrial Fibrillation

Agent Loading

Dose

Onset of Ac-

tion

Maintenance

Dosage

Major Side

Effects

Esmolol(Brevibloc)

0.5 mg per kgIV over oneminute

5 minutes 0.05-0.2mg/kg/minuteIV

Hypotension,heart block,bradycardia,asthma, heartfailure

Metoprolol(Lopressor)

2.5-5 mg IVbolus over 2minutes, up to3 doses

5 minutes 50-200 mg POevery day in 2daily doses


Propranolol(Inderal)

0.15 mg perkg

5 minutes 40-320 mg POevery day individed doses


Digoxin

(Lanoxin)

0.25 mg IV or

PO every 4hours, up to1.0-1.5 mg

4-6 hours 0.125-0.25 mg

PO/IV qd

Digitalis toxic-

ity, heartblock, brady-cardia, ven-tricular fibrilla-tion

Agents Used for Heart Rate Control in Atrial Fibrillation

Drug Mechanism

of Action

ECG

Changes

Dose Adverse Re-

action

Class la Agents

Quinidine Decrease NainfluxReduce

upstrokevelocity,Prolongrepolariza-tion

QRS wid-ens, QTlengthens

Sulfate 300-600mg po q6-8hrsQuinaglute 324-

628 mg po q8-12 hrs

GI, cinchonismVT/VF/Torsade de

Pointes

Procain-amide


Load: IV 13-17mg/kg over 30-60 minMaintenance: IV2-4 mg/min orProcan SR 750-1500 mg poq6hr

SLE-like syn-drome, confu-sion


41/153


Class Ic Agents

Flecainide Reduction in

upstrokevelocity

QRS wid-

ens, QTlengthens

Start 50-100 mg

po q12hr; max.200 bid

Dizziness,

headaches

Propa-fenone


Start 150 mg poq8hrs; max. 300mg po q8hr

Dry mouth, GI,dizziness

Class III Agents

Amio-darone

Blocks Kefflux, pro-longsrepolar-ization

Dose-depend-ant QTprolonga-tion

Load 400 mg potid x 7-14 days,then 400 mg poqd x 1 month;Maintenance:100-400 mg/day

Ataxia, trem-ors pulmonaryfibrosis, pneu-mon-itis/alveolitis,skin discolor-ation, thyroidand LFTabnormalities

Sotalol Potent beta-blocking ac-tivity

80 mg po bid;max. 160 mg bid

Bradycardia,Torsade dePointes.

Ibutilide Prolong ac-tion potentialand refrac-tory period

1 mg IV infusionover 10 min,may repeat onceafter 10 min

Torsade in 3-8%

Dofetilide 125-500 mcgbid, dependingon renal function

0.5-10% tor-sade

D. Antiarrhythmics. Restoration of sinus rhythm is the optimal goal, as itmay relieve symptoms and improve cardiac output.

1. Class Ia. These medications act by blocking the fast sodiumchannel, reducing the impulse conduction through the myocardium.a. Quinidine can be used for acute conversion as well as to

maintain of sinus rhythm.b. Procainamide can also be used for both acute conversion and

maintenance. It is slightly less effective than quinidine.c. Disopyramide has negative inotropic properties. Disopyramide

is infrequently used in the treatment of AF due to poor efficacyand frequent side effects.

2. Class lc. This class of medications acts by prolongingintraventricular conduction.a. Flecainide can cause acute conversion to sinus rhythm in 50-

55%. Due to its negative inotropic action, flecainide should beused cautiously in patients with AF and hypertrophiccardiomyopathy. It should not be used in patients with structural


42/153

42 Hypertensive Emergency

heart disease. It is reserved for patients with normal LV functionand refractory AF.

b. Propafenone may have fewer side effects and is better toleratedthan the Ia agents. It is available only in an oral form and can alsobe given as a single bolus dose for AF of less than 24 hours.Proarrhythmia can occur but is reported less frequently than withthe other Ic medications. Propafenone is useful for patients whoare hypertensive and have a structurally normal heart with AF.Propafenone should be avoided in patients with structural heartdisease.

3. Class III. The medications in this class act by blocking outwardpotassium currents, resulting in increased myocardial refractoriness.

All class III agents cause a dose-dependent QTc prolongation,resulting in Torsades de Pointes. These agents are contraindicatedif the QTc is >0.44 seconds.a. Amiodarone (Cordarone) has sodium, calcium, and beta-

blocking effects. Amiodarone has a low proarrhythmia profile. It issafe and efficacious in patients with CHF and AF. Side effectsinclude pulmonary fibrosis, pneumonitis, skin discoloration, thyroidand liver abnormalities, ataxia, and tremors (33%).

b. Sotalol (Betapace) has a beta-blocking effect. It is less effectivethan quinidine, with a conversion rate of 20%. It is most appropri-ate for sinus maintenance in patients with AF and coronary arterydisease. Sotalol should be avoided in patients with severe LVdysfunction and COPD.

c. Ibutilide(Corvert) is highly effective for the conversion of recentonset AF (30%) and atrial flutter (70%). Polymorphic ventriculartachycardia occurs in about 6%. Pretreatment with magnesium

may prevent polymorphic ventricular tachycardia.d. Dofetilide (Tikosyn) is indicated for acute conversion andmaintenance of atrial fibrillation. The success rate in acuteconversion is 30%.

E. Nonpharmacologic strategies. Due to drug intolerance, possibleproarrhythmic effects, and disappointing long-term efficacy of theantiarrhythmic agents, non-pharmacological therapies have an importantrole in the management of AF.1. Electrical cardioversion is rapid and highly effective, with success

rates greater than 80%.2. Radiofrequency catheter ablation/atrial defibrillators. The

delivery of radiofrequency current through a catheter tip advanced tothe atrium is highly effective and safe.

Hypertensive Emergency

Hypertensive crises are severe elevations in blood pressure (BP) characterizedby a diastolic blood pressure (BP) higher than 120-130 mm Hg.

I. Clinical evaluation of hypertensive crisesA. Hypertensive emergency is defined by a diastolic blood pressure >120

mm Hg associated with ongoing vascular damage. Symptoms or signs of


43/153

Hypertensive Emergency 43

neurologic, cardiac, renal, or retinal dysfunction are present. Hypertensiveemergencies include severe hypertension in the following settings:1. Aortic dissection2. Acute left ventricular failure and pulmonary edema3. Acute renal failure or worsening of chronic renal failure4. Hypertensive encephalopathy5. Focal neurologic damage indicating thrombotic or hemorrhagic stroke6. Pheochromocytoma, cocaine overdose, or other hyperadrenergic

states7. Unstable angina or myocardial infarction8. Eclampsia

B. Hypertensive urgency is defined as diastolic blood pressure >120 mm

Hg without evidence of vascular damage; the disorder is asymptomaticand no retinal lesions are present.

C. Causes of secondary hypertension includerenovascular hypertension,pheochromocytoma, cocaine use, withdrawal from alpha-2 stimulants,clonidine, beta-blockers or alcohol, and noncompliance withantihypertensive medications.


44/153

44 Hypertensive Emergency

II. Initial assessment of severe hypertensionA. When severe hypertension is noted, the measurement should be repeated

in both arms to detect any significant differences. Peripheral pulses shouldbe assessed for absence or delay, which suggests dissecting aorticdissection. Evidence of pulmonary edema should be sought.

B. Target organ damage is suggested by chest pain, neurologic signs,altered mental status, profound headache, dyspnea, abdominal pain,hematuria, focal neurologic signs (paralysis or paresthesia), or hyperten-sive retinopathy.

C. Prescription drug use should be assessed, including missed doses ofantihypertensives. History of recent cocaine or amphetamine use shouldbe sought.

D. If focal neurologic signs are present, a CT scan may be required todifferentiate hypertensive encephalopathy from a stroke syndrome.

III. Laboratory evaluationA. Complete blood cell count, urinalysis for protein, glucose, and blood; urine

sediment examination; chemistry panel (SMA-18).B. If chest pain is present, cardiac enzymes are obtained.C. If the history suggests a hyperadrenergic state, the possibility of a

pheochromocytoma should be excluded with a 24-hour urine for catechol-

amines. A urine drug screen may be necessary to exclude illicit drug use.D. Electrocardiogram should be completed.E. Suspected primary aldosteronism can be excluded with a 24-hour urine

potassium and an assessment of plasma renin activity. Renal arterystenosis can be excluded with captopril renography and intravenouspyelography.

Screening Tests for Secondary Hypertension

Renovascular Hyper-

tension

Captopril renography: Renal scan before and after 25 mgPO

Intravenous pyelographyMRI angiography

Hyperaldosteronism Serum potassium24-hr urine potassium

Plasma renin activityCT scan of adrenals

Pheochromocytoma 24-hr urine catecholaminesCT scanNuclear MIBG scan

Cushing's Syndrome Plasma ACTHDexamethasone suppression test

Hyperparathyroidism Serum calciumSerum parathyroid hormone

IV. Management of hypertensive emergenciesA. The patient should be hospitalized for intravenous access, continuous

intra-arterial blood pressure monitoring, and electrocardiographicmonitoring. Volume status and urinary output should be monitored.


45/153


46/153

46 Ventricular Arrhythmias

G. Nicardipine (Cardene IV) is a calcium channel blocker. It is contrain-dicated in presence of CHF. Tachycardia and headache are common.The onset of action is 10 min, and the duration is 2-4 hours. The doseis 5 mg/hr continuous infusion, up to 15 mg/hr.

H. Fenoldopam (Corlopam) is a vasodilator. It may cause reflex tachycar-dia and headaches. The onset of action is 2-3 min, and the duration is 30min. The dose is 0.01 mcg/kg/min IV infustion titrated, up to 0.3mcg/kg/min.

I. Phentolamine (Regitine) is an intravenous alpha-adrenergic antagonistused in excess catecholamine states, such as pheochromocytomas,rebound hypertension due to withdrawal of clonidine, and drug ingestions.The dose is 2-5 mg IV every 5 to 10 minutes.

J. Trimethaphan (Arfonad) is a ganglionic-blocking agent. It is useful indissecting aortic aneurysm when beta-blockers are contraindicated;however, it is rarely used because most physicians are more familiar withnitroprusside. The dosage of trimethoprim is 0.3-3 mg/min IV infusion.

Ventricular Arrhythmias

I. Ventricular fibrillation and tachycardia-If unstable (see ACLS protocol page 5), defibrillate with unsynchronized

200 J, 300 J, then 360 J.-Oxygen 100% by mask.-Procainamide loading dose 10-15 mg/kg at 20 mg/min IV or 100 mg IV

q10min, then 2-4 mg/min IV maintenance OR-Also see other antiarrhythmics below.

II. Torsades de Pointes-Correct underlying cause and consider discontinuing drugs that cause

Torsades de Pointes (dofetilide, ibutilide, sotalol, amiodarone, quinidine,procainamide, disopyramide, moricizine, bepridil, phenothiazines, tricyclicand tetracyclic antidepressants, vasopressin, imidazoles, pentamidine);correct hypokalemia and hypomagnesemia.

-Defibrillate with 360 J.-Magnesium sulfate (drug of choice), 2 gm IV push.-Isoproterenol (Isuprel) 2-20 :g/min (2 mg in 500 mL D5W, 4 :g/mL) OR-Phenytoin (Dilantin) 100-300 mg IV given in 50 mg increments q5min.

III. Other antiarrhythmicsClass Ib

-Lidocaine 50-100 mg (1 mg/kg) IV, then 2-4 mg/min IV.-Mexiletine (Mexitil) 100-200 mg PO q8h, max 1200 mg/d.-Tocainide (Tonocard) loading 400-600 mg PO, then 400-600 mg PO q8-12h;

max 1800 mg/d.-Phenytoin (Dilantin), loading dose 15 mg/kg at 50 mg/min, then 100 IV q8h.

Class Ic-Flecainide (Tambocor) 50-100 mg PO q12h, max 400 mg/d.-Propafenone (Rythmol) 150-300 mg PO q8h, max 1200 mg/d.

Class III-Amiodarone (Cordarone) PO loading 400-1200 mg/d in divided doses x 5-14

days, then 200-400 mg PO qd OR 150 mg slow IV over 10 min, then 1mg/min IV infusion x 6 hours then 0.5 mg/min IV infusion thereafter.


47/153

-Sotalol (Betapace) 40-80 mg PO bid, max160 mg bid.Labs: SMA 12, Mg, calcium, CBC, cardiac enzymes, LFTs, ABG, drug

levels, thyroid function test. ECG, electrophysiologic study.

Acute Pericarditis

Pericarditis is the most common disease of the pericardium. The most commoncause of pericarditis is viral infection. This disorder is characterized by chestpain, a pericardial friction rub, electrocardiographic changes, and pericardialeffusion.

I. Clinical featuresA. Chest pain of acute infectious (viral) pericarditis typically develops in

younger adults 1 to 2 weeks after a viral illness. The chest pain is ofsudden and severe onset, with retrosternal and/or left precordial pain andreferral to the back and trapezius ridge. Pain may be preceded by low-grade fever. Radiation to the arms may also occur. The pain is oftenpleuritic (eg, accentuated by inspiration or coughing) and may also berelieved by changes in posture (upright posture).

B. A pericardial friction rub is the most important physical sign. It is oftendescribed as triphasic, with systolic and both early (passive ventricular

filling) and late (atrial systole) diastolic components, or more commonlya biphasic (systole and diastole).

C. Resting tachycardia (rarely atrial fibrillation) and a low-grade fever may bepresent.

Causes of Pericarditis

IdiopathicInfectious: Viral, bacterial, tubercu-lous, parasitic, fungalConnective tissue diseases Meta-bolic: uremia, hypothyroidism Neo-plasm, radiation

Hypersensitivity: drugPostmyocardial injury syndromeTraumaDissecting aneurysmChylopericardium

II. Diagnostic testingA. ECG changes. During the initial few days, diffuse (limb leads and

precordial leads) ST segment elevations are common in the absence ofreciprocal ST segment depression. PR segment depression is alsocommon and reflects atrial involvement.

B. The chest radiograph is often unrevealing, although a small left pleuraleffusion may be seen. An elevated erythrocyte sedimentation rate andC-reactive protein (CRP) and mild elevations of the white blood cellcount are also common.

C. Labs: CBC, SMA 12, albumin, viral serologies: Coxsackie A & B,measles, mumps, influenza, ASO titer, hepatitis surface antigen, ANA,rheumatoid factor, anti-myocardial antibody, PPD with candida, mumps.Cardiac enzymes q8h x 4, ESR, blood C&S X 2.

D. Pericardiocentesis: Gram stain, C&S, cell count & differential,cytology, glucose, protein, LDH, amylase, triglyceride, AFB, specificgravity, pH.


48/153


49/153

Pacemakers 49

Generic Pacemaker Codes

Position 1

(chamberpaced)

Position 2

(chambersensed)

Position 3

(response tosensing)

Position 4

(programma-ble functions;

rate modula-

tion)

Position 5

(anti

current clinical strategies - critical care medicine (lb. englezĂ)

Documents