Cardiovascular Emergencies
Robert S. Kiken DDS Ocean Oral and Maxillofacial Surgery Santa Barbara, CA
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Management of Office Anesthetic and Medical Emergencies – a Systems Approach
Cardiovascular emergencies involving the conducting system Cardiovascular emergencies involving the vascular system Endocrine/Diabetic emergencies
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Deliver Oxygen & Prevent Hypoxia Deficiency in the amount of oxygen reaching the tissues. Can cause dysrhythmias, cardiac arrest, brain damage, and death. We must have: Adequate Circulation pump and conducting system An unimpaired Airway Uncompromised Breathing
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1 The Foundation
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Cardiovascular emergencies involving the conducting system - EKG Interpretation
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Conduction System: Basic Anatomy
SA Node: Bundle of primary His pacemaker
Internodal Bundle pathways branches and atria
Purkinje AV fibers Node
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2 SA Node Basic Electrophysiology Depolarization of the Ventricles
AV Node Repolarization of the Ventricles
Relationship of EKG to Anatomy of Cardiac Conduction system P QRS T
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The Electrocardiogram
Repolarization of Depolarization of the Ventricles the Ventricles
Depolarization of the Atria Hypokalemia or other metabolic disturbance
What does the EKG tell us?
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Rules Of EKG Interpretation Look For:
Rate
Rhythm
Regularity
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3 Rate How fast is the heart beating?
80 beats per Start where an R wave minute falls on a heavy line
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Another approach to find the rate is to divide 300 by the number of large boxes between R waves. 1 2 3 4 5 6
In this case we’ll divide 300 by 6: 300 ÷ 6 = 50 1 2
In this case we’ll divide 300 by 2: 300 ÷ 2 = 150
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Automaticity Foci (Ectopic Foci)
Foci throughout the heart have the property of “automaticity” i.e. they can initiate an action potential and become the heart’s pacemaker Automaticity foci may be located either:
In the atria
In the AV Junction
In the ventricles
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4 Automaticity Foci Foci in each of these areas has an inherent discharge rate SA Node 60-100/min INHERENT LEVEL RATE RANGE
Atria 60 - 80/min.
AV Junction 40 - 60/min.
Ventricles 20 - 40/min.
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As You Count The Boxes, Consider If The Rate Is A Problem.
2 Boxes
When there are less than two boxes between R waves
or 8 Boxes
When there are more than five boxes between R waves (in this example 8 boxes)
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Rhythm Do all the beats look the same?
Is it like wallpaper?
And, can you dance to it?
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5 Rhythm
If the beats all look the same…
…do they look worrisome?
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Rhythm Disturbances Arrhythmias may be either:
Supraventricular Arrhythmias - above the level of ventricles
Combined Arrhythmias -above and within the ventricles
Ventricular Arrhythmias - within the ventricles
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Regularity Are the beats evenly spaced?
A ==B C = D { { { {
1
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6 Principles of EKG : Helpful Hints
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1. Identify the QRS Complexes
Start 150 75
300 100
Can you identify them?...and • What is their rate?
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2. Is the QRS complex width normal?
½
Normal is < 0.11 sec (no more than ½ large block)
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7 3. Is there a P wave in front of each QRS?
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4. Is the P-R interval normal?
3-5 small blocks
Normal is 0.12 - 0.20 sec (3-5 small blocks)
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EKG Interpretation of Cardiac Dysrhythmias
Bradycardia Sinus tachycardia Stable tachycardias Unstable tachycardias Arrest rhythms: Ventricular fibrillation & pulseless ventricular tachycardia Asystole & PEA
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8 Normal Sinus Rhythm and Sinus Dysrhythmias
Normal Sinus Rhythm (NSR)
Sinus Arrhythmia (Sinus Dysrhythmia)
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Vagus Normal Sinus Rhythm (NSR) SA Defining characteristics: • All components present i.e. P, QRS and T waves • Regular rate and rhythm of AV 60 -100 bpm • PR = 0.12 – 0.20, QRS = < 0.12
Start 150 75 P QRS T 300 100
PR =.12 - .20 QRS < .11 83 26
Normal Sinus Rhythm (NSR) Rate
Defining characteristics: • All components present i.e. P, QRS and T waves • Regular rate and rhythm of 60 -100 bpm • PR = 0.12 – 0.20, QRS = < 0.12
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9 Sinus Arrhythmia Defining characteristics: • Similar to NSR except for irregular rate • Rate varies somewhat with inspiration and expiration • Decrease in PNS on inhalation results in an increase in heart rate • Usually a normal finding
Start Start 48 150 75 60 150 75 50 300 100 60 300 100 60
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Sinus Arrhythmia Rate
Defining characteristics: • Similar to NSR except for irregular rate • Rate varies somewhat with inspiration and expiration • Usually a normal finding
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Premature Atrial Contraction (PAC) Rate
Defining characteristics: • Overall NSR except for isolated early P waves • Beat with early P wave usually followed by a beat containing a compensatory pause
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10 Bradycardia
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Sinus Bradycardia Defining characteristics: • Like NSR, but with rate < 60 • May be due to increased parasympathetic tone • Seen as a normal finding in athletes
Start 150 75 50 50 300 100 60
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Sinus Bradycardia RATE
Defining characteristics: • Like NSR, but with rate < 60 • May be due to increased parasympathetic tone • Seen as a normal finding in athletes 33
11 78 year old medically compromised patient with bradycardia
Pre-Op
QRS Wider
No P Intra-Op PVC 34
Persistent Bradycardia
• Causing: • Hypotension • Altered mental status • Signs of shock • Ischemic chest discomfort • Acute heart failure • Treat…
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Treat Persistent Bradycardia Causing: Symptoms Signs • Chest discomfort • Hypotension • Shortness of breath • CHF • Decreased level of • Ventricular consciousness arrhythmia related • Weakness to the bradycardia • Fatigue • Dizziness • Syncope
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12 Bradycardia - Treatment
Atropine effect takes “foot off of Vagus Nerve the brake” X
Dopamine effect – puts “foot on the gas”
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Diagnosis: Pulse < 60 is “bradycardia,” but treat patient, not monitor Position: Semi-seated, comfortable Initial Management:
Observe, ABC’s, 02, IV, Monitor If Stable:
• Continue to observe, ABC’s, 02, IV, Monitor
If Unstable, Treat With: • Atropine • If atropine ineffective: • Transcutenous pacing • Dopamine • Epinephrine
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Bradycardia - Atropine
• Atropine 0.5 mg IV every 3-5 minutes to total dose of 3 mg. • A dose less than 0.5 mg may further decrease heart rate. • May worsen ischemia or increase infarction size. • Ineffective in cardiac transplant patient. • If type II/2 or 3rd degree block, atropine will likely be ineffective.
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13 Bradycardia - Dopamine
• Dopamine 2-10 mcg/kg/minute. • Has both α- and β-adrenergic actions. • Titrate to target heart rate or vasoconstriction. • Lower dose: inotropy and heart rate. • Higher dose: (>10) vasoconstriction. • Good choice if bradycardia and hypotension. • Adequate intravascular volume.
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Bradycardia - Epinephrine • Epinephrine 2-10 mcg per minute. • α- and β-adrenergic actions. • Good choice if bradycardia and hypotension.
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Tachycardia
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14 Cardiac Dysrhythmias -Tachycardias
• Sinus Tachycardia • Atrial Tachycardias - usually “Narrow Complex” • Ventricular Tachycardias - usually “Wide Complex”
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SA Sinus Tachycardia Defining characteristics: • Similar to NSR except for increased rate of > 100 bpm AV • Frequently seen during adrenergic stimulation 115 Start 150 300 100
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Sinus Tachycardia Rate
Defining characteristics: • Similar to NSR except for increased rate of > 100 bpm • Frequently seen during adrenergic stimulation 45
15 Atrial Dysrhythmias – Usually “Narrow Complex”
• Premature Atrial Contraction (PAC) • Paroxysmal Supraventricular Tachycardia (PVST) • Atrial Fibrillation (A. Fib.) • Atrial Flutter (A. Flutter) • Multifocal Atrial Tachycardia (MAT)
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Ectopic focus Premature Atrial within the Contraction (PAC) atrium Defining characteristics: • Overall NSR except for isolated early P waves • Beat with early P wave usually followed by a beat containing a compensatory pause
2X Y + Z = 2X
X X Y Z
Compensatory Pause 47
An atrial pacemaker takes over Paroxysmal Supraventricular Tachycardia (PSVT)
Defining characteristics: • Regular, narrow complex tachycardia (150- 250 bpm) • Sudden (paroxysmal) onset • Merged P-T waves
Merged P-T waves Rate increased from 83 to187
Normal sinus beats 48
16 Paroxysmal Supraventricular Tachycardia (PSVT) Rate
Defining characteristics: • Regular, narrow complex tachycardia (150-250 bpm) • Sudden (paroxysmal) onset • Merged P-T waves
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Atrial Fibrillation (A. Fib.) Defining characteristics: • Multiple ectopic foci within the atria create a wavy baseline consisting of small erratic spikes • An ectopic focus near the AV node may conduct into the ventricles and generate a QRS. • Irregular ventricular rate
Ventricular rate highly variable
R R R
Wavy baseline with small erratic spikes 50
Atrial Fibrillation (A. Fib.) Rate
Defining characteristics: • Multiple ectopic foci within the atria create a wavy baseline consisting of small erratic spikes • An ectopic focus near the AV node may conduct into the ventricles and generate a QRS. • Irregular ventricular rate
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17 An ectopic circular conduction loop Atrial Flutter (A. Flutter) Defining characteristics: • A chaotic circular conduction path creates a “saw tooth” baseline of “flutter waves.” • Slower ventricular rate, usually in a 3:1 or 4:1 ratio to flutter waves
A “saw tooth” pattern of F waves
F F F F
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Atrial Flutter (A. Flutter) Rate
Defining characteristics: • A chaotic circular conduction path creates a “saw tooth” baseline of “flutter waves.” • Slower ventricular rate, usually in a 3:1 or 4:1 ratio to flutter waves
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Multifocal Atrial Tachycardia
• Irregularly irregular • Distinguished from atrial fibrillation by the presence of P waves. • Pulmonary disease or multi-system issue (sepsis, shock, electrolyte abnormalities)
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18 Ventricular Dysrhythmias – Usually “Wide Complex” (i.e. the QRS Complex is Wide )
• Premature Ventricular Contractions (PVC’s) • Ventricular Tachycardia (VT)
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Premature Ventricular Contractions (PVC’s)
• Unifocal PVC’s • Bigeminal PVC’S • Trigeminal PVC’S • Couplet PVC’s • Runs of Paroxysmal Ventricular Tachycardia (PVT) – “Salvos” • Multiform PVC’S • R on T PVC’s
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An ectopic focus in the ventricles Unifocal Premature takes over Ventricular Contractions (PVC’s) Defining characteristics: • An ectopic focus in the ventricles fires prematurely before the normal impulse through the SA node and atria – No P Wave • The QRS complex is wide and often merges with the T wave • The cycle following a PVC usually contains a compensatory pause • Occasional PVC’s are seen in many healthy young people Y + Z = 2x 2x
y z x x
Compensatory Pause
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19 Unifocal Premature Ventricular Contractions (PVC’s) Rate
Defining characteristics: • An automaticity focus in the ventricles fires prematurely before the normal impulse through the SA node and atria – No P Wave • The QRS complex is wide and often merges with the T wave • Compensatory pause after the PVC • Occasional PVC’s are seen in many healthy young people
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A focus at a lower level SA (e.g. AV node) escapes to Bigeminal Premature pace the ventricle Ventricular Contractions (Bigeminal PVC’S)
Defining Characteristics: • Normal sinus beats alternate with PVC’s from a single ventricular focus with a 1:1 ratio
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An irritable focus fires Trigeminal Premature in the ventricle Ventricular Contractions (Trigeminal PVC’S)
Defining Characteristics: • Normal sinus beats alternate with PVC’s from a single ventricular focus with a 2:1 ratio
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20 Couplet PVC’s
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Run of Paroxysmal Ventricular Tachycardia (PVT) An irritable focus fires in the ventricle Defining characteristics: • An ectopic focus takes over and generates multiple PVC’s • Three or more PVC’s in a row constitute ventricular tachycardia • A warning sign calling for identification of etiology such as hypoxia
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Run of Paroxysmal Ventricular Tachycardia (PVT)
Rate
Defining characteristics: • An ectopic focus takes over and generates multiple PVC’s • Three or more PVC’s in a row constitute ventricular tachycardia • A warning sign calling for identification of etiology such as hypoxia
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21 Multiform Premature Ventricular A 2nd irritable An irritable Contractions (PVC’S) focus fires in focus fires in the ventricles the ventricles Defining characteristics: • Normal sinus rhythm is interrupted by periodic firing of two or more irritable ventricular foci • Usually considered a more ominous sign than unifocal PVC’s
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Multiform Premature Ventricular Contractions (PVC’S)
Rate
Defining characteristics: • Normal sinus rhythm is interrupted by periodic firing of two or more irritable ventricular foci • Usually considered a more ominous sign than unifocal PVC’s
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During the T wave R on T Premature Ventricular an irritable ectopic focus fires in the Contraction (PVC) ventricles Defining characteristics: • An irritable ectopic focus fires during a vulnerable period of the cycle • Often associated with hypoxia or decreased K+ • May lead to a dangerous arrhythmia such as VT or VF
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22 Ventricular Tachycardia (VT) An irritable ectopic Defining characteristics: ventricular focus • There is a wide, blunt, rapid wave takes over form consisting of merged QRS and T waves • No P waves present and individual QRS and T waves often can not be discerned. • Due to rapid ventricular rate, this rhythm can only support life for a short time. • Important to correlate with pulse, if no pulse consider as if VF
Merged QRS and T 136 Start QRS T 150 300
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Ventricular Tachycardia (VT) Rate
Defining characteristics: • Wide, blunt, rapid wave form consisting of merged QRS and T waves • No P waves present and individual QRS and T waves often can not be discerned. • Due to rapid ventricular rate, this rhythm can only support life for a short time. • Important to correlate with pulse, if no pulse consider as if VF
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Sinus Tachycardia
• Signs / Symptoms: Diagnosis: • As related to the • Pulse > 100 with underlying cause sinus rhythm Causes: • Treatment: • External influences • Treat underlying – Non-cardiac cause condition • Anxiety • Never attempt • Fever cardioversion, • Hypovolemia avoid cardiac drugs • Exercise • Hyperthyroidism
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23 Tachycardia With Pulses - Stable Diagnosis: Pulse > 150
• ABCs, give 02, start IV, monitor; identify and treat reversible causes Stable:
Narrow QRS Wide QRS
Regular Irregular Regular Irregular • • Vagal maneuver (A. Fib., A. Flut., (VT or uncertain) A.Fib. w/aberrancy) •Pre-excited A. Fib. • Adenosine 6 mg MAT) •Amiodarone • Avoid IV/1-35. • Diltiazem or • 150 mg IV/m., Adenosine, diltiazem, • After 1-2 min., • β blockers repeat to: 2.2 g verapmil Adenosine q/24h • Consider amiodarone 12 mg x2 No Conversion • Prepare for 150 mg IV/10 min. (A. Flut., Ectopic, synchronized cardioversion •Recurrent A. Tach., Junct. Tach) polymorphic VT Conversion = SVT • Diltiazem or β •Torsades de pointes, • Observe for blocker Magnesium, 1-2 g/ recurrence • Treat cause 5-60 min. • Adenosine or •Turf to Cards diltiazem
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Updates- since 2010
• ACLS algorithms have been simplified. • Greater importance placed on high- quality CPR. • Adequate rate and depth (1.5”-2”). • Complete chest recoil. • Minimize interruptions in chest compressions. • Avoid excessive ventilations. • De-emphasis of devices, drugs, and other distracters.
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Search For The Underlying H’s & T’s
H’s T’s • Hypovolemia • Toxins • Hypoxia • Tamponade (cardiac) • Hydrogen Ion • Tension (acidosis) pneumothorax • Hyper/Hypokalemia • Thrombosis (coronary • Hypoglycemia & pulmonary) • Hypothermia • Trauma
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24 Tachycardia With Pulses - Stable Wide QRS? > 0.12 second
No Yes •IV access and 12-lead ECG •IV access and 12-lead ECG •Vagal maneuver •Consider adenosine if regular and monomorphic •Adenosine (if regular) •Consider antiarrhythmic •β-blocker or calcium channel infusion blocker •Expert consultation •Expert consultation
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Why Vagal Maneuver?
• Increase parasympathetic tone and slow conduction through the AV Node • Methods: • Valsalva maneuver • Carotid sinus pressure • Facial immersion in ice water • Complications: • Dysrhythmias • Asystole • Stroke • Terminates 20 – 25% of SVT
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Why Adenosine? • Transient heart block at the AV Node • Terminates about 90% of re-entry arrhythmias • Contraindications: • Second or third degree heart block • Atrial fibrillation or flutter • VT
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25 Why Diltiazem or β-Blocker?
• Diltiazem: calcium channel blocker
• Metoprolol: selective β1-blocker • Decreases heart rate, decreases contractility, slows conduction at the AV Node • Control ventricular rate • Rapid ventricular response: > 120 bpm • Controlled ventricular response: 70-110 bpm • Slow ventricular response: < 60 bpm
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Tachycardia With Pulses - Stable Wide QRS? > 0.12 second
No Yes
•IV access and 12-lead ECG •IV access and 12-lead ECG •Vagal maneuver •Consider adenosine if regular and monomorphic •Adenosine (if regular) •Consider antiarrhythmic •β-blocker or calcium channel infusion blocker •Expert consultation •Expert consultation
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Wide-QRS-complex tachycardias
• Most commonly: • VT or VF • SVT with aberrancy • Pre-excited tachycardia • Ventricular paced rhythms • Torsades de pointes
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26 Consider adenosine if regular and monomorphic
• Why Adenosine? • Transient heart block at the AV Node • Terminates about 90% of reentry arrhythmias
Mitchell J, Lazarenko G (November 2008). "Wide QRS complex tachycardia. Diagnosis: Supraventricular tachycardia with aberrant conduction; intravenous (IV) adenosine". CJEM 10 (6): 572–3, 581.
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Infusions for Stable Wide-QRS Tachycardia
• Procainamide • 20-50 mg/minute until arrhythmia is suppressed or hypotension ensues • Amiodarone • 150 mg over 10 minutes • Repeat if VT recurs • Maintenance: 1 mg/min first 6 hours • Sotalol • 100 mg over 5 minutes • Avoid if prolonged QT
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SVT With Aberrancy
• Supraventricular impulse reaches the His-Purkinje system while one of its branches are still in the relative or absolute refractory period. • Abnormal conduction results in a widening of the QRS. • Difficult diagnosis in the office setting • Mimic bundle branch block • Mimic VT
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27 Pre-Excited Tachycardias
• Ventricles depolarized (excited) before (pre-) the normal conduction system • Conductive pathway other than AV Node • Wolff-Parkinson-White syndrome • Consider amiodarone • Do not use: adenosine, diltiazem, or verapamil
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Why Amiodarone?
• Mechanism of action unknown • Affects sodium, potassium, and calcium channels • α-adrenergic and β-adrenergic block • Prolongs action potential duration • Prolongs refractory period • Increases survival rates to hospital admission
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Dilution of Amiodarone for Treatment of Wide Complex Tachycardia
Preparation of Amiodarone: • As illustrated at left, 3 mL of amiodarone is drawn up in a 60 mL syringe. • The syringe is filled to 60 mL with IV fluid from the IV bag. • The diluted amiodarone is delivered slowly over 10 minutes through the continuous IV infusion. The rate of delivery is 3mL Draw up 3 mL of Fill the syringe to 60 amiodarone (150mg) mL with IV fluid from every 30 sec. (6mL/min.) in a 60 mL syringe the IV bag 84
28 Torsades de Pointes
• “Twisting of the points” • Specific type of VT • Contributory factors: long QT syndrome, hypomagnesemia, hypokalemia, R-on-T PVC • Treatment • Magnesium sulfate: 1-2 grams over 5-60 minutes
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Tachycardia With Pulses - Unstable
Diagnosis: Pulse > 150
• ABC’s, give 02, start IV, monitor; identify and treat reversible causes
Unstable: Chest pain, SOB, altered mental status, hypotension CALL 911 – The EMT’s will consider synchronized cardioversion as follows: • Consider sedation. • Synchronized cardioversion (monophasic) - V.T.: 100 J, A. Fib.: 200 OR PSVT, A. Flutter 50J. If failure to convert, can increase dose. • If regular narrow complex, consider adenosine.
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Ventricular Tachycardia Ventricular Fibrillation Asystole PEA
These Rhythms Will Kill
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29 Ventricular Tachycardia (VT) An irritable ectopic ventricular focus takes over When you see this on your monitor… ...check your pulse… …check your patient for a pulse.
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Ventricular Tachycardia (VT) Rate
When you see this on your monitor + There is no pulse Pulseless Ventricular tachycardia
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Ventricular Fibrillation (VF) Defining characteristics: • Rhythm consists of a rapidly vacillating baseline representing discharge from multiple irritable ventricular foci. • There are no discernable P, QRS or T waves • Rhythm results in no depolarization of the ventricles, hence no pumping of blood. • Rhythm often precedes asystole • Must be treated by electrical defibrillation immediately.
Rapid rate discharge from multiple irritable ventricular foci
No well-defined wave forms
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30 Ventricular Fibrillation (VF) Rate
Defining characteristics: • Rhythm consists of a rapidly vacillating baseline representing discharge from multiple irritable ventricular foci. • There are no discernable P, QRS or T waves • Rhythm results in no depolarization of the ventricles, hence no pumping of blood. • Rhythm often precedes asystole • Must be treated by electrical defibrillation immediately.
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Ventricular Fibrillation (VF) to Asystole Defining characteristics • In cardiopulmonary arrest situations, VF frequently precedes asystole • When the rhythm degenerates into asystole, defibrillation can no longer be an effective treatment modality
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REMEMBER: CPR and defibrillation of VF/pulseless VT are the only proven treatments Other ACLS interventions not proven to increase survival to discharge home
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31 Diagnosis: VF / Pulseless VT • Call 911 and call for defibrillator • Check Pulse - If no pulse proceed to treatment Treatment: • CPR until defibrillator is available • Check monitor for rhythm – If shockable, defibrillate 360 J. • CPR (2 minutes) while defibrillator charging, check rhythm • Defibrillate 360 J • CPR until IV/IO access is available • Establish IV/IO access • Epinephrine 1:10,000 1.0 mg IV/IO push, repeat q 3-5 min., or • Vasopressin 40 units IV/IO as first or second dose • CPR (2 minutes) while defibrillator charging, check rhythm • Defibrillate 360 J • CPR (2 minutes) and consider anti-arrythmic • Amiodarone 300 mg IV/IO push, then 150 mg q 3-5 min. or • CPR (2 minutes) • To paramedics and hospital 94
Asystole Defining characteristics: • No discernable wave form of any type i.e. no P, QRS or T waves • No rapid spiked oscillations such as those seen in ventricular fibrillation. • Cannot be successfully treated with defibrillation
• No P, QRS, T waves • No rapid spiked oscillations
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Asystole Rate
Defining characteristics: • No discernable wave form of any type i.e. no P, QRS or T waves • No rapid spiked oscillations such as those seen in ventricular fibrillation • Cannot be successfully treated with defibrillation
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32 Asystole - Treatment
Atropine Effect
Vagus N. x
ABC’s of CPR with ventilations and chest compressions
Epinephrine – sympathetic Adrenergic stimulation Effect
Atropine – no longer recommended for routine use
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If your patient’s EKG strip looks like this, …
Start CPR, give …but he has no pulse. epinephrine By definition, he has and P.E.A. determine P.E.A. the cause (Pulseless Electrical Activity) 98
Cardiac Arrest – Asystole / PEA Diagnosis: • Absent heart sounds, BP, pulse, patient ashen-gray, pupils dilated and fixed, patient flaccid, gasping followed by no respiration Position: Supine, feet slightly elevated Treatment: • Check responsiveness, call 911 and call for defibrillator • CPR for 5 cycles • Start IV/IO • Epinephrine 1:10,000 1.0 mg (10 cc’s) IV push, repeat q 3-5 min. • CPR for 5 cycles • Confirm asystole and assess for VF / Pulseless VT; shock prn • Transfer to hospital
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33 Cardiac Arrest - Summary
Treatment:
• 911
• BLS
• Defibrillate ?
• ACLS
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Dysrhythmia Summary
Normal Sinus Rhythm for comparison
Bradycardia
Tachycardias:
Supraventricular – “narrow complex”
Ventricular – “wide complex”
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Terminal Dysrhythmias Normal vs. Abnormal Normal Sinus Rhythm for comparison
Ventricular Fibrillation and Pulseless VT
No Pulse
Asystole (Cardiac Arrest)
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34 Management of Office Anesthetic and Medical Emergencies – a Systems Approach
• Emergencies of the respiratory system • Cardiovascular emergencies involving the conducting system • Cardiovascular emergencies involving the vascular system • An important emergency of the endocrine system - insulin shock
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Cardiovascular Problems Related To Vasculature
• Acute coronary syndromes • Hypertensive crisis • Hypotension
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Coronary Artery Disease (CAD) • Acute Coronary Syndrome: AHA definition: any group of clinical symptoms compatible with acute myocardial ischemia. • Each year 1.1 million people have a MI, almost half of which die. • Atherosclerosis is the underlying condition of CAD. • Accounts for 35% of all deaths among those 65 years of age and older.
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35 Coronary Artery Disease (CAD)
• Stable angina • Unstable angina • Myocardial infarction (MI)
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Acute Coronary Syndromes
• All have similar pathophysiology • All have similar presentation and early management • STEMI requires evaluation for acute reperfusion intervention
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Unstable Angina NSTEMI STEMI
Occluding thrombus sufficient to cause Complete thrombus Non occlusive occlusion thrombus tissue damage & mild myocardial necrosis ST elevations on Non specific ECG or new LBBB ECG ST depression +/- T wave inversion on Elevated cardiac Normal enzymes cardiac ECG enzymes Elevated cardiac More severe enzymes symptoms
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36 Angina • Stable • Precipitated by stress or exertion and rapidly resolves with rest or nitrates • Unstable • Occurs without precipitating factor, at rest, or if increasing in frequency or severity • Often initially indistinguishable from NSTEMI • Ischemia is fully reversible: no elevated levels of serum biomarkers
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Myocardial Infarction
• Old definition: symptoms, ECG abnormalities, and serum enzyme levels • 2007 Consensus Document: • Rise and/or fall of cardiac biomarker (troponin) • At least one of the following: • Symptoms of ischemia • New ST-T changes or new left bundle branch block • Pathologic Q wave • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
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Cardiac markers • CK-MB • Troponin ( T, I) isoenzyme • Very specific and more • Rises 4-6 hours after sensitive than CK injury and peaks at 24 • Rises 4-8 hours after hours injury • Remains elevated 36-48 • May remain elevated hours for up to two weeks • Positive if CK/MB > 5% • Can provide of total CK and 2 times prognostic information normal • Troponin T may be • Elevation can be elevated with renal predictive of mortality disease, • False positives with poly/dermatomyositis exercise, trauma, muscle disease, diabetes mellitus, pulmonary embolis 111
37 Timing of Release of Various Biomarkers After Acute Myocardial Infarction
Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
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Symptoms of Acute Coronary Syndrome • Chest pain • Most commonly reported symptom • 10 to 30% of patients report no chest pain • “Classic” chest pain: diffuse pain or pressure in the substernal or epigastric areas that may radiate to the neck, jaw, or left arm • Shortness of breath • Weakness • Diaphoresis • Nausea • Lightheadedness
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ACS: Patient History
• Traditional risk factors • Increasing age (>45 years old male, post- menopause), male gender, family history, cigarette smoking, hyperlipidemia, hypertension, obesity/overweight, sedentary lifestyle, diabetes • Emerging risk factors • Systemic lupus erythematosus, rheumatoid arthritis, HIV infection • 70 to 75% of patients hospitalized for suspicion of ACS are ultimately found not to have an MI • Given the sensitivity/specificity of the patient’s symptoms and risk factors, what should we do?
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38 Choose Your Patients Wisely
•Young •Old •Thin •Overweight •Athletic •Hypertensive •Non smoker •Hyperlipidemic •Sedentary lifestyle
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Estimation of Cardiac Risk in Our Patients
• Identify patients at high risk • Minimize risk • Appropriate testing • Therapeutic measures • Preoperative Evaluation • Patient specific clinical variables • Exercise capacity • Surgery-specific risk
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Preoperative Evaluation: Patient Variables
• Major predictors • Unstable coronary syndromes including unstable or severe angina or recent MI • Decompensated, worsening, or new heart failure • Significant arrhythmias • High grade AV block • Symptomatic ventricular arrhythmias • Symptomatic bradycardia • Ventricular tachycardia
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39 Preoperative Evaluation: Patient Variables
• Minor predictors • Greater than 70 years of age • Abnormal ECG • Rhythm other than sinus • Uncontrolled systolic hypertension
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Preoperative Evaluation: Patient Variables
• Other predictors that warrant careful assessment • Ischemic heart disease • History of cerebrovascular disease • History of compensated or prior heart failure • Diabetes mellitus • Renal insufficiency
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Preoperative Evaluation: Exercise Capacity • Metabolic equivalent • Take care of self (eat, dress, toilet) = 1 MET • Walk up a flight of stairs or hill = 4 METs • Heavy house work = 4 – 10 METs • Strenuous sports > 10 METs • Claudication Goldman L Hashimoto B et al. Comparative reproducibility and validity of systems for assessing • Other causes of poor cardiovascular functional class: Advantges of a new exercise tolerance specific activity scale. Circulation. 1981. 120
40 Preoperative Evaluation: ACC/AHA guideline summary • High risk (cardiac death or nonfatal MI > %5) • Aortic and other major vascular surgery • Peripheral artery surgery • Intermediate risk (1 - 5%) • Carotid endarterectomy • Head and neck surgery • Intraperitoneal/intrathoracic surgery • Orthopedic surgery • Prostate surgery • Low risk (<1%) Generally do not require preoperative cardiac testing • Ambulatory surgery • Endoscopic procedures • Superficial procedures • Breast surgery
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Angina Pectoris Treatment MONA Terminate surgery, suction, pack surgical site – call 911
100% 02 by mask, semi- recumbent position, loosen clothing 0 – the “O” of MONA 2 Nitroglycerin sublingually (tablet or spray) Monitors: BP, HR, EKG, Pulse Ox Nitroglycerin 2nd and 3rd dose every 5 min if needed Nitroglycerin – If no relief, assume MI the “N” of MONA
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Myocardial Infarction DIAGNOSIS: • Usually heavy, squeezing chest pain which does not respond to nitroglycerin, 20% of patient’s have no pain but exhibit nausea, vomiting, weakness, anxiety, cardiac dysrhythmia and hypotension often seen POSITION: • Semi-seated, loosen tight clothing
TREATMENT: “MONA” (morphine, oxygen, nitroglycerin and ASA) • Call 911.
• 02 by face mask. • Start IV. Monitor vital signs. • If nitroglycerine not given, 1 dose sublingually (spray or tablet) with 2nd in 5 minutes. • Aspirin – chew 1adult non-enteric coated or 2 low-dose “baby”. • Morphine Sulfate 1-3 mg increments every 5 minutes. • Monitor for bradycardia, hypotension, dysrhythmia and be prepared to treat. • Transfer to hospital.
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41 Use nitroglycerin cautiously or not at all in patients with inadequate ventricular preload…
•Inferior MI and RV infarction •Hypotension, bradycardia, or tachycardia •Recent phosphodiesterase inhibitor use (Viagra, Cialis, etc.)
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Blood Pressure Issues
• Hypertensive crisis • Hypotension
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Basic Relationships of Cardiovascular Parameters
Blood Pressure
Cardiac Output Systemic Vascular Resistance
Heart Stroke Rate Volume
Preload Contractility Afterload
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42 Hypertensive Crisis
• Hypertensive Crisis: BP > 240-250 / 140
• Precipitating factors: pain, anxiety, decreased 02, increased C02 or cardiopulmonary compromise • Cause: • Pump problem - Increased cardiac output • Treatment: decrease heart rate and/or stroke volume • Adrenergic blocker (e.g. Labetalol)
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Why Labetalol?
• Nonselective β-receptor antagonist • Blocks α-receptor mediated vasoconstriction • Dose-related decrease in SVR and blood pressure without reflex tachycardia • Particularly good for excess circulating catecholamines • Hypertension in the early post- operative period
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Hypertensive Crisis
• Hypertensive Crisis: BP > 240-250 / 140
• Precipitating factors: pain, anxiety, decreased 02, increased C02 or cardiopulmonary compromise • Cause: • Pump problem - Increased cardiac output • Treatment: decrease heart rate and/or stroke volume • Adrenergic blocker (e.g. Labetalol) • Vascular problem - Increased systemic vascular resistance • Treatment: vasodilate • Adrenergic blocker (e.g. Labetalol) Or Vasodilator (e.g. hydralazine)
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43 Hypotension BP decreased > 20%
Weakness - may Skin-pallor lead to loss of consciousness
Nausea
Tachycardia
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Hypotension Etiology: • Apprehension, dehydration, infection, postural change, allergic reaction, drug overdose, hypoxia, cardiovascular compromise Position: • Supine with legs above level of heart, may need to consider Trendelenburg position
Treatment:
• 100% 02, stop surgery, adjust anesthetic prn • Monitor BP, pulse (rate, rhythm, character), EKG • Check level of consciousness • Etiology? Check BP, HR, rhythm. Treat arrhythmia prn • Administer a bolus of IV fluids • If hypotension persists, administer either: Adrenergic agents • Ephedrine Sulfate – dilute 50 mg vial in 10 cc ( 5 mg/cc). Titrate to effect with 2.5 – 5.0 mg (0.5 – 1.0 ml) increments • Phenylephrine HCL – dilute 1 mg from 10 mg vial in 10 cc. Titrate to effect with 0.1 mg (1.0 ml) increments
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44 Diabetes
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Management of Diabetes
Affects about 8% of the US population Complex glycemic control Operative procedure, anesthesia Sepsis, disrupted meal schedules, altered nutritional intake, emesis Goals: surgery as early as possible in the morning Avoid hypoglycemia Prevent ketoacidosis/hyperosmolar states Maintain fluid and electrolyte balance Avoid marked hyperglycemia
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Management of Diabetes: Preoperative Evaluation
History Type I: risk of ketoacidosis; need basal insulin supply Long-term complications Glycemic control Hypoglycemia Medications Laboratory Blood glucose A1C Serum creatinine (renal function) ECG 135
45 Management of Diabetes
Target: glucose between 140 – 200 mg/dL Perioperative near normal glucose not associated with: Reductions in infectious complications Cardiovascular events Mortality BUT, was associated with increased risk of hypoglycemia
Buchleitner AM, Martinez-Alonso M, Hernadez M., et al. Perioperative glycemic control for diabetic patients undergoing surgery. Cochrane Database Syst Rev 2012
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Management of Diabetes: The Categories
Type 2 treated with diet alone Type 2 treated with oral hypoglycemic/noninsulin injectables Type 1 or insulin treated Type 2
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Management of Diabetes: Type 2 Treated With Diet Alone
Usually do not require any therapy Insulin if needed
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46 Management of Diabetes: Type 2 Treated With Oral Hypoglycemic/noninsulin Injectables
Morning of surgery: hold oral hypoglycemic and noninsulin injectables Most patients with good glycemic control undergoing a short procedure need no therapy Insulin if needed
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Management of Diabetes: Type 1 or Insulin Treated Type 2
Short procedures breakfast just delayed Delay usual morning insulin until after surgery and before eating Breakfast and lunch missed Omit short or rapid-acting insulin morning of surgery Give ½ intermediate or long-acting insulin morning dose Insulin pump give basal rate
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Management of Office Anesthetic and Medical Emergencies – a Systems Approach
• Emergencies of the respiratory system • Cardiovascular emergencies involving the conducting system • Cardiovascular emergencies involving the vascular system • An important emergency of the endocrine system - insulin shock
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47 Diabetic Emergencies
• Hypoglycemia – Rapid onset • By far the more common emergency situation • Mismatch between insulin dose and serum glucose • Hyperglycemia – Slow onset
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Hypoglycemia
Diminished serum glucose levels: • Increased administration of insulin • Poor glucose intake - • Normal insulin - inadequate diet • NPO - Fasting which can be either Intentional / unintentional • Increasing metabolic utilization: • Exercise • Infection • Emotional stress • ETOH ingestion
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Hypoglycemia – Signs & Symptoms (50-60 mg/dL)
Dizziness Confusion / Headache Hunger
Slurred Tachycardia speech
Sweating Lethargy
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48 Hypoglycemia: Early Treatment
Always treat as hypoglycemic until otherwise proven • Conscious patient - supine position • Monitor BP/Pulse • Check blood glucose levels • Treat blood glucose < 60 mg/dL (even with no symptoms) • High sugar content substitute: • Orange juice • Soft drink • Candy / Cake frosting 145
Hypoglycemia – Signs/Symptoms
• Moderate (<50 mg/dL) • Increased anxiety, confusion, restlessness, dizziness, headache, lack of energy, slurred speech • Severe (<30 mg/dL) • Lethargy, decrease in cerebral function – headache, seizures, hypothermia, loss of consciousness, coma
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Hypoglycemia - Treatment
Conscious: • Juice or candy Unconscious patient: • Activate EMS • 50% Dextrose IV solution – (50ml) over 2-3 minutes • IV solution – 5% - 20% dextrose solution • No IV – give Glucagon 1mg IM/IV • Recheck blood glucose in 15 minutes • Remain in office – 1 hour • Patient escorted home
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49 Why Glucagon? • Increases blood glucose levels by promoting hepatic glycogenolysis and gluconeogenesis • Dose: 1 mg IV / IM
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Hypoglycemia - Prevention
• Careful medical history • Determine the severity of disease • Hospitalization • Frequency of hypoglycemic events • Check patient’s blood sugar – AM glucose level • Reduce AM dose of insulin (usually ½ of AM dose) or keep basal level and D/C prandial insulin • Intravenous – continuous infusion of D5W • NPO considerations
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DON’T FORGET! YOU ARE A TEAM
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50 Fair winds and following seas
Dr. Robert S. Kiken Santa Barbara CA 151
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