2016 updated acls handouts

8/15/2019 2016 Updated ACLS Handouts

1/24

S.A. Pulley, D.O., FACOEP ACLS ECG Rhythms

PCOM-EM

1

Electrocardiography: ACLS Rhythms

I. Objectives A. To establish a process for rhythm reviewB. To examine tachycardias and bradycardias

C. To highlight lethal rhythmsII. Electrical Conduction

A. PQRSIII. Systematic Approach

A. Rate1. Too Fast?2. Too Slow?3. Middle of the Road?

B. QRS1. Narrow?2. Wide?3. QRS (


2/24


PCOM-EM

2

1. Progressive prolongation P-R2. Then drops a QRS

G. Pearl1. Variable P-R interval can only be

a. 2nd Degree AVB-Mobitz Ib. 3rd Degree AVBc. To differentiate

i. Must check every P-P intervalii. Must check every R-R interval (or S-S)

d. Then look for the Wenckebach patternH. 3rd Degree AVB-Usually wide QRS, can be narrow

1. Variable P-R2. Constant P-P3. Constant S-S (or R-R )

a. Can be variable or absentI. 2nd Degree AVB-Mobitz II

1. Constant P-R Interval2. More P’s than QRS’s3. Described by ratio

a. 2:1, 3:1, 4:1, or Variable

VI. Lethal (or potentially lethal) A. Dead Rhythms-Rhythms without a pulse

1. Asystole2. Pulseless Electrical Activity (PEA)3. Ventricular Fibrillation (VF)4. Pulseless Ventricular Tachycardia (VT)

B. Asystole1. Confirm asystole in 2 leads

C. Pulseless Electrical Activity (PEA)1. Any organized rhythm without a pulse is PEA2. Except VT which gets treated as VF

D. VF/Pulseless VT (See below for VT)1. Priority is Defibrillation (if available)

E. Torsades de Pointes1. The impulse travels around the myocardium2. You are looking at it from the same spot (Lead II)3. Therefore, the amplitude changes rhythmically

VII. Tachycardias A. SVT (Narrow Complex)

1. Sinus Tachycardia (See above for ST)a. Normal P-R

2. Multifocal Atrial Tachycardiaa. P’s variably different

3. Atrial Tachycardia

a. P’s abnormal but non-variableb. Or too fast for Sinus Tachycardia

4. Paroxysmal-Start/Stop on own

5. Stable vs. Unstable (SVT or VT) a. Determined by physical signs, Not The Rate b. Stable

i. SBP > 90, Normal Mentation, No CP, Lungs Clear


3/24


PCOM-EM

3

c. Unstablei. SBP60 bpm)

B. Idioventricular1. Ventricular Escape (20-40 bpm)2. Idioventricular (>40 bpm)

X. Too Many P Waves A. Atrial Fibrillation

1. Irregularly irregular2. P waves are not well defined

B. Atrial Flutter1. Saw tooth pattern (Woodsman’s)2. Ratio: 2:1, 3:1, 4:1, Variable

C. Pearl

1. If a patient has a seemingly Sinus Tachycardia of 145-1552. And the patient is symptomatic in any way at all3. Consider that the patient may be in a 2:1 or 3:1 Atrial Flutter4. Because at that rate and ratio the extra p waves disappear into the QRS and T

waves


4/24


PCOM-EM

4

Let’s see if you were paying attention

1

2 3

4

5

6 7

8 9

10

11

12: A

D

B C


5/24

S.A. Pulley, D.O., FACOEP ACLS Pharmacology

PCOM-EM

1

ACLS Pharmacology

I. Snap Shot of Instability A. ABCDE’sB. Vital Signs

i. Heart Rate, Respiratory Rate, Blood Pressure

ii. Pulse Oximetry, Blood Sugariii. TemperatureC. Mental Status

i. Confusionii. Disorientation

D. Symptomsi. Chest Painii. Dyspneaiii. Lightheadedness

E. Physical Signsi. Respiratory Distressii. Palloriii. Diaphoresis

II. Initial Management A. Rapid Assessment

i. ABCDE’sii. Mental Statusiii. Gross Appearanceiv. Pulse/HR/RR

B. 12 Lead ECGC. Oxygen (O2) if Pulse Ox Brain Cellsii. Time => Resistance to Defibrillationiii. Time => Muscle

III. Drug Class Recommendations A. Class I

i. Always indicatedii. Solid proof of utility

B. Class IIai. Probably helpfulii. Most data support use

C. Class IIbi. Possibly helpfulii. Some supportive dataiii. Not harmful

D. Class Indeterminatei. Insufficient scientific evidence at this time

E. Class III-Contraindicated/Harmful


6/24


PCOM-EM

2

IV. PAY ATTENTION A. Time is Critical

i. Time=>Brain Cellsii. Time=>Resistance to Defibrillationiii. Time=>Cardiac Muscle

V. Do drugs make a difference? A. Not really

VI. What makes a difference? A. Optimal compressionsB. Avoid hyperventilationC. Early defibrillation

VII. Dead Rhythms (Rhythms without a pulse) Therapy A. Treatment

i. Oxygenii. Epinephrineiii. (Lidocaine/Amiodarone)iv. Defibrillationv. Magnesium Sulfate

B. Dead Box (Algorithm box)i. All dead rhythms (no pulse) have common elements of treatmentii. All get/continue AAA-CAB/CPRiii. All get an IV or IOiv. All get Epinephrine 1 mg IV (1:10,000)v. All get intubated/advanced airway when convenientvi. Elements added at beginning or end

C. Oxygeni. Always administer 100% FiO2 in Arrest statesii. Cardio-Respiratory distressiii. Class: Iiv. Contraindications-COPD

1. Never withhold Oxygen in hypoxic states2. Monitor ventilation (pCO2) and assist prn3. Intubate if necessary

v. However, in ischemic states once patient stabilized

1. Back off on FIO2 to keep pulse ox>94%Intraosseous recommended!

v. Indications-Class Ivi. V-Fib, Unstable V-Tach, Asystole, PEAvii. (Also, IM/SQ for Anaphylaxis or Status Asthmaticus)

1. 0.3 mg (0.3 ml of 1:1K)

CCAABB--DD//CCPPR R

IIVV//IIOO

EEppii 11 mmgg IIVV ((VVaassoopprreessssiinn 4400 uu IIVV))

I I nnt t uubbaat t ee

((WWhheenn CCoonnvveenniieenntt))


7/24


PCOM-EM

3

viii. Contraindications / Cautions1. Stable Vital Signs2. Caution in elderly

F. No IV?i. Preference is IV or IO (Intraosseous)ii. However, drugs that can be given via Endotracheal Tube (ETT)iii. True ACLS Drugs (A-L-E)

1. Atropine2. Lidocaine3. Epinephrine

iv. (N-A-V-E-L)1. Add Narcan and Vasopressin

G. Asystole-Check that leads are attached and check in more than one leadi. Recommend the same for VF

H. PEA (Pulseless Electrical Activity)-If bradycardic could consider transcutaneous pacingVIII. T’s and H’s

A. Anytime the patient is not doing welli. Do primary survey, ABCDEii. Check 6 vital signs (BP-HR-RR-T-PO-BS)

B. Consider the T’s and H’s (order reversed on purpose) (5 each)i. Tension Pneumo, Tamponade, Thrombosis-Pulmonary, Thrombosis-Coronary,

Toxins/Tabletsii. Hypoxia, Hypovolemia, Hyperacidemia, Hyperelectrolytemia, Hypothermia

C. PALS has 6 each adding Hypoglycemia and Trauma (for hemorrhage)IX. VF/Pulseless VT

A. Time => Resistance to DefibrillationB. Quick Look for and immediate Defibrillation if appropriateC. SHOCK at maximum for device

i. 360 J Monophasic or 120-200 (up to 360) J Biphasic depending on the machine.ii. Time to shock is criticaliii. Try to defibrillate as close to time 0 as possible

D. Dead Box Therapyi. CAB-D/CPRii. IV/IO

iii. Epinephrine 1mg IViv. Intubate/advanced airway when ready/convenient

E. 2 minute blocks for codei. CAB/CPR to Circulate drug for 2 minutesii. Drug at beginning of the block

1. (Every other 2 minute block is Epi step)iii. Reevaluate-TRIAD

1. Rhythm-if potentially perfusing check:2. Pulse-to see if it is perfusing:3. BP-to see how well it is perfusing4. If awake, don’t forget to ask how they are

iv. Shock-if shockable rhythmv. DO NOT PAUSE TO CHECK RHYTHM IMMEDIATELY AFTERWARDS

1. Wait for 2 minute mark due to myocardial stunningvi. Go back to i. to start next block and give next drug (if indicated)

F. Amiodaronei. Anti-Dysrhythmicii. Action:

1. Works @ AV Node, Bundles, & Ventriclesiii. Administration: IV

2 Minutes


8/24


PCOM-EM

4

iv. Dosage:1. VF / Unstable VT: 300 mg IVP

a. Repeat after 4 minutes once at ½ (150 mg IVP)2. Stable VT/SVT: 150 mg over 10 minutes3. Then administer @ 1 mg/min X 6 hrs4. Then @ 0.5 mg/min X 18 hrs

v. Indications

1. VF, Stable / Unstable VT & SVTvi. Contraindications / Cautions1. Caution in hypotension, Hypersensitivity

G. Lidocainei. Class: IIbii. Anti-Dysrhythmiciii. Action: works @ Bundles & Ventriclesiv. Dose:

1. Bolus: 1–1.5 mg/Kg IVP Max Dose 3 mg/Kg2. Repeat: 1/2 of bolus (0.5-0.75 mg/Kg)3. Infusion: 1 – 4 mg / min

v. Indications1. VF, VT

vi. Contraindications / Cautions1. Hypotension, Hypersensitivity

H. Magnesium Sulfatei. Action: Cardiac membrane stabilizationii. Administration: IViii. Dose

1. 1 – 2 grams IV over 5 – 60 min in 50 – 100 cciv. Indications

1. Torsades de Pointe => Class I2. Hypomagnesemia, Status Asthmaticus

v. Contraindications / Cautions1. Not recommended routinely in cardiac arrest

X. Too Fast (Tachycardic) Therapy A. Anti-dysrhythmics

i. Lidocaine, Amiodarone, Magnesium (done above)ii. Procainamide

1. Anti-dysrhythmic2. Action: AV Node, Bundles & Ventricles3. Dose

a. Code: 50 mg/mini. 1 gm in 100 cc @ 300 cc/h = 50 mg/min

b. Therapeutic: 20 – 30 mg/mini. 1 gm in 100 cc @ 150 cc/hr = 27 mg/min

c. Maximum 15 mg/kg (~1 gm)4. Indications

a. Atrial & Ventricular Dysrhythmias5. Contraindications / Cautions

a. Hypotensionb. Do not use with Amiodaronec. Avoid in Torsades

6. Reasons to Stopa. Hypotensionb. QRS width > 50% of baselinec. Reach maximum dose of 1 gm (15 mg/kg)d. Dysrhythmia suppression


9/24


PCOM-EM

5

B. Generally treatment of SVT is:i. Stable SVT: Vagal Maneuvers then Adenosine then Rate Control with Beta or

Calcium channel blockersii. Unstable SVT (See I below): Synchronized Cardioversioniii. Stable Tachycardia

1. SBP>902. Normal mentation

3. No chest pain4. Clear lungs/No dyspneaC. 1

st Vagal Maneuvers-Hands on-Remember you are an Osteopathic Physician!

i. Eyeballs-Ocular Pressure1. ***Caution in elderly

ii. Face-Surprise ice water immersioniii. Neck-Carotid sinus massage

1. ***Caution in elderlyiv. Belly-Valsalvav. Butt-Anal Massagevi. (Not in ACLS book: V-Spread)

D. Adenosinei. Action: AV node blockadeii. Half-Life: < 10 secondsiii. Administration: IV Rapid Push through at least proximal 18 ga.

1. With immediate slam IVP NSS bolus 10-20 ml2. And raise arm to enhance return

iv. Dose: 6 mg => 12 mg => 12 mg?v. Indications: SVT, PSVTvi. Contraindications / Cautions

1. May slow Atrial Fibrillation only2. Don’t use diagnostically in Wide Complex Tachycardia3. Effectiveness with Theophylline, Dipyridamole, Carbamazepine4. May cause bronchospasm

vii. WARN the patient as it transiently stops the heart (Don’t tell the patient THAT!)E. Verapamil

i. Action: Calcium Channel Blocker, AV Node Blockade

ii. Administration: IViii. Dose

1. 2.5 – 5 mg IV / 1 minute (0.075 – 0.15 mg / Kg)2. Re-dose 5-10 mg in 15-30 mg

iv. Indications1. Rate control of Narrow Complex Tachycardia

v. Contraindications / Cautions1. Wide Complex Tachycardia (re-entry)2. Hypotension (may result in hypotension)3. Calcium IV may be given if adverse effects

F. Diltiazemi. Action: Calcium Channel Blocker, AV Node Blockadeii. Administration: IV, PO

iii. Dose1. 1st Dose: 0.25 mg/Kg IV (5 – 10 mg)2. 2nd Dose: 0.35 mg/Kg IV (10 – 15 mg)3. Infusion: 5 – 15 mg/hr

iv. Indications1. Rapid Atrial Fibrillation, other SVT's

v. Contraindications / Cautions1. Hypotension2. Wide Complex Tachycardia

vi. May administer Calcium IV to reverse effects


10/24


PCOM-EM

6

G. Metoprolol/Atenolol and Labetololi. Action: Beta Blocker, AV Node Blockadeii. Dose

1. Labetalol: 10 – 20 mg IV over 1 – 2 mina. Double with each subsequent dose q10 minb. Infusion: 2 – 8 mg / min

2. Metoprolol: 5 mg IV over 2 – 5 min q 5 min (x 3 for ACS)

a. PO Dose given after IV loadingiii. Indications1. Hypertensive Emergency2. Heart Rate Control (esp. AMI) or SVT

iv. Contraindications / Cautions1. Hypotension, Bradycardia

H. Esmololi. Titratable Beta Blockerii. Short half life

iii. Little hypotension or bronchospasmiv. 250-500 mcg/kg IVB over 1 minutev. Then 25-50 mcg/kg/minvi. Re-bolus q 5 min PRN

vii. Increase in 50 mcg/kg/min steps to max of 200 mcg/kg/minI. Sotalol

i. Action:1. Blockade at AV Node, Bundles & Ventricles

ii. Dose1. IV: 1 – 1.5 mg/Kg @ 10 mg/min2. PO: 40 – 80 mg PO BID

iii. Indications1. Ventricular & Supraventricular Dysrhythmias

iv. Contraindications / Cautions1. Bradycardia2. Hypotension3. Pro-Dysrhythmic (Torsades)-So not used much

v. Limited by Slow infusion rate

J. If you use Calcium Channel or Beta Blocker be prepared to synchronized cardioverti. You can make them and Unstable Tachycardia mostly through hypotensionii. Because they all have antihypertensive properties

iii. Or, if they have a bypass tract tachycardia (e.g. WPW, LGL, etc.)1. Blocking the AV node pushes all the impulses to the bypass tract2. Which causes the HR to zoom up, and the BP crash

K. Synchronized Cardioversion for Unstable Tachycardiasi. When presented with a tachycardia, decision point as to whether stable or

unstableii. Unstable Electricity requires Electricity to fix itiii. SVT or VTiv. Unstable-Only need one of the following to be unstable

1. Hypotension (SBP


11/24


PCOM-EM

7

XI. Shock (Hypotension) Therapy A. Oxygen (Above)B. Normal Saline Solution

i. Crystalloidii. Preferred resuscitation solutioniii. First line treatment of hypotensioniv. 250 ml-1000 ml fluid bolus IV

1. Amount driven by clinical situationv. Caution (Doesn’t mean don’t give it)1. CHF (or History of CHF), Elderly2. Renal Failure

C. Dopaminei. Action:

1. Dopaminergic (Renal Artery Dilatation)2. Beta (Inotropic & chronotropic heart stimulation)3. Alpha (Peripheral arterial constrictor)

ii. Dose1. Dopaminergic: 3 – 5 ug/kg/min2. Beta: 5 – 10 ug/kg/min3. Alpha: 10 – 20 ug/kg/min (Shock Dose)

iii. Indications: HypotensionD. Dobutamine

i. Action: Inotropic beta stimulation, increases cardiac contractilityii. Dose: 5 – 20 ug/kg/miniii. Indications: Cardiogenic Shockiv. Adverse Effects: Hypotension due to arterial dilatationv. Do not administer unless SBP > 90 mmHg

E. Norepinephrinei. Action: Pure alpha stimulation, potent arterial constrictorii. Dose: 4 – 8 ug/miniii. Indications: Refractory Hypotensioniv. Very good for poor vascular tone shock such as neurologic or septic

F. Epinephrine (Above)XII. Too Slow (Bradycardia) Therapy

A. Atropinei. Action: AV Node stimulationii. Dose: IV

1. 0.02 mg/Kg IV (minimum dose = 0.1 mg)2. Bradycardia Dose: 0.5 mg IV (Don’t want to overshoot)

a. No longer indicated for Asystoleiii. Indications

1. Sinus Bradycardia with significant HypoTN (Class I)2. Other Symptomatic Bradycardia (Class IIb)3. Contraindications / Cautions

a. Use caution in Mobitz II and 3rd AV Blockb. May increase degree of block

B. Dopamine-Beta Property (Above)

C. Dobutamine-Beta Property(Above)D. Epinephrine-Beta Property (Above)E. Isoproteronol-Pure Beta-Just mentioning, rarely utilized

i. 2-10 mcg/minuteii. 2 mg in 250 ml starting at 15 ml/hriii. Sympathomimetic with pure betaiv. Potent inotropic and chronotropic effects


12/24


PCOM-EM

8

F. Symptomsi. Mild=>Perhaps no treatment, just monitoringii. Moderate=>Atropine and if it doesn't work a Beta drug

iii. Severe "Unstable"-SBPPacing

G. Pacemaker -i. Transcutaneous easiest to place

ii. Any symptomatic bradycardic rhythm1. Especially if with severe symptoms or perfusion issuesiii. Absolute consideration for Mobitz 2 and 3rd degree AVBiv. Downside is that TCP is uncomfortable

XIII. Too Wet (Fluid Overload) Therapy A. Oxygen (Above) B. Nitroglycerin

i. Coronary Artery Vasodilator1. Decreases preload first, Then afterload at higher doses

ii. Dosage:1. SL: 300–400ug (0.3–0.4mg) q5 min2. IV: 10–20 ug/min & titrate by 10ug q 5 min3. TC: ½ - 2 inch paste to chest wall

iii. Indications1. Ischemic Cardiac Chest Pain, CHF2. Hypertension (Including Hypertensive Emergency)

iv. Contraindications / Cautions1. Hypotension (SBP < 90)2. Viagra/Cialis/Levitra3. Revatio/Adcirca (used for pulmonary hypertension)

C. Positive Pressure Airway-CPAP, BiPAP, or VentilatorD. Furosemide

i. Loop Diureticii. Dose:

1. 0.5 - 1 mg/kg IV (~40 mg)2. Avoid over diuresing

iii. Indications:

1. Pulmonary Edema, Hypertensive Crisis2. Increased ICP

iv. Cautions:1. Low BP2. Hypovolemia3. Electrolyte lows

E. Dopamine-Beta Property (Above)F. Dobutamine-Beta Property (Above)

XIV. Too High (Pressure) Therapy A. Nitroglycerin-Afterload reduction (Above)B. Nitroprusside-Just mentioning, rarely utilized

i. Potent vasodilatorii. Indications:

1. High SVR cardiogenic shock, pulmonary edema, acute MVR or AVR2. Reduces afterload

iii. Indicated for severe hypertensioniv. Mix 50-100 mg in 250 D5W

1. Range 5-10 mcg/kg/min2. Begin 0.1 mcg/kg/min3. Light sensitive: Cover the IV bag

C. Beta Blockers-Afterload reduction (Metoprolol/Atenolol, Labetolol Above)


13/24


PCOM-EM

9

XV. Acute Coronary Drugs- (Covered in the ACS Lecture) A. Oxygen (Above)B. Nitroglycerin (Above)C. AspirinD. Heparin/LovenoxE. Beta Blockers (Above)F. Opiates

G. ThrombolyticsXVI. Miscellaneous DrugA. Calcium Chloride

i. Indications:1. Hyperkalemia, Hypocalcemia2. Antagonize Ca+ Channel Blockers

ii. Dose:1. 8 - 16 mg/kg (5 - 10 ml) IV

iii. Precautions:1. “Do not use routinely in cardiac arrest”2. Do not mix with Sodium Bicarbonate

B. Sodium Bicarbonatei. Action: Uncertainii. Dose

1. Initial: 1 meq/Kg IV Bolus2. Repeat: 0.5 meq/Kg q 10 min

iii. Indications1. Class I

a. TCA or Phenobarbital Overdoseb. Hyperkalemiac. Known pre-existent Metabolic Acidosis

2. Class II b =>Protracted Codeiv. Contraindications / Cautions

1. Avoid admixture or infiltration with Calcium or Epinephrine2. Use only after other Class I / Class II drugs


14/24


PCOM-EM

1

ACLS Pharmacology (List Only)

I. Dead Rhythms (Rhythms without a pulse) Therapy A. Asystole, Pulseless Electrical Activity, Ventricular Fibrillation,

Ventricular Tachycardia, Torsades De PointesB. Dead Box (Algorithm box)

i. All dead rhythms (no pulse) have common elements of treatmentii. All get/continue CAB-D/CPRiii. All get an IV/IOiv. All get Epinephrine 1 mg IVv. All get intubated/advanced airway when convenientvi. Elements added at beginning or end

C. Medicationsi. Oxygenii. Epinephrineiii. Lidocaine or Amiodaroneiv. Defibrillation (Non pharmacologic therapy)v. Magnesium Sulfate

II. Too Fast (Tachycardic) Therapy

A. Anti-dysrhythmicsi. Lidocaine, Amiodarone, and Magnesium (Covered earlier)ii. Procainamide

B. Stable SVTi. 1

st Vagal Maneuvers (Non pharmacologic therapy)

C. AdenosineD. Rate Control Calcium Channel Blockers

i. Verapamilii. Diltiazem

E. Rate Control Beta Blockersi. Metoprolol/Atenololii. Labetolol

F. Sotalol

G. Unstable Tachycardiai. Synchronized Cardioversion (Non Pharmacologic therapy)

III. Shock (Hypotension) Therapy A. Oxygen (Covered earlier)B. Normal Saline Solution

C. Dopamine-(β=>α ) D. Dobutamine-( β) (Cardiogenic Shock Only)

E. Norepinephrine-( α)

F. Epinephrine-( α & β) IV. Too Slow (Bradycardia) Therapy

A. AtropineB. Dopamine-( β) (Covered earlier)C. Dobutamine-( β) (Covered earlier)

D. Epinephrine-( β) (Covered earlier)E. Isoproteronol-( β) -Rarely utilizedF. Transcutaneous Pacemaker-(Non Pharmacologic therapy)-For Unstable

V. Too Wet (Fluid Overload) Therapy A. Oxygen (Covered earlier)B. NitroglycerinC. Positive Pressure-CPAP, BiPAP, or VentilatorD. FurosemideE. Dopamine-( β) (Covered earlier)F. Dobutamine-( β) (Covered earlier)


15/24


PCOM-EM

2

VI. Too High (Pressure) Therapy A. Nitroglycerin (Covered earlier)B. Nitroprusside-Rarely utilizedC. Beta Blockers (Metoprolol/Atenolol, Labetolol covered earlier)

VII. Acute Coronary Drugs (Covered in the ACS Lecture) A. Oxygen (Covered earlier)B. Nitroglycerin (Covered earlier)C. AspirinD. Heparin/LovenoxE. Beta Blockers (Covered earlier)F. NarcoticsG. Thrombolytics

VIII. Miscellaneous Drugs A. Calcium Chloride-Calcium Channel Blocker Toxicity, HyperkalemiaB. Na Bicarbonate-Hyperkalemia, TCA OD


16/24

S.A. Pulley, D.O., FACOEP Acute Brain Syndrome

PCOM-EM

1

Acute Brain SyndromeAcute Stroke

I. Objectives A. To identify symptoms and diagnostics

B. To establish priorities and treatmentsII. Brain Attack

A. Stroke has a similar pathogenesis as Acute Coronary SyndromeB. It also is very time sensitiveC. We are just starting to be able to treat Acute Stroke

III. Epidemiology A. 3rd Leading Cause of DeathB. Leading cause of disabilityC. 3.8 million stroke survivors

1. 10 % No deficits2. 48 % Hemiparetic3. 22 % Gait dysfunction4. 16 % Aphasic

IV. 8 D’s of Stroke Care A. Detection- Signs and SymptomsB. Dispatch- 9-1-1C. Delivery- Rapid transportD. Door- Urgent triageE. Data- Brain CTF. Decision (and Discussion)G. Drug- AdministrationH. Disposition

V. Pathophysiology A. Blockage causes cell death within minutes

1. We can not treat thisB. The goal is to prevent the ischemic penumbra from converting to cell death

1. This is the focus of therapies

VI. Cincinnati Stroke Scale-FAST Exam A. Facial Droop

i. Normal: Both sides of face move equallyii. Abnormal: One side of face does not move at all

B. Arm Drifti. Normal: Both arms move equally or not at allii. Abnormal: One arm drifts compared to the other

C. Speechi. Normal: Patient uses correct words with no slurringii. Abnormal: Slurred or inappropriate words or mute

VII. Los Angeles Prehospital Stroke Screen A. Look for obvious asymmetryB. Facial smile / grimace

i. Left and Rightii. Normal or Facial Droop

C. Grip Strengthi. Left and Rightii. Normal, Weak, No Grip

D. Arm weaknessi. Left and Rightii. Normal, Drifts Down, Falls Rapidly


17/24


PCOM-EM

2

VIII. Immediate Assessment-Within 10 minutes of arrival (Arrival to T+10 minutes) A. ABCs, Vital SignsB. Oxygen: If pulse ox110 (Until controlled)e. IC Neoplasmf. Active internal bleedingg. Coagulopathy/Thrombocytopenia


18/24


PCOM-EM

3

G. Some centers have extended 3 to 4.5 hours due to Evidenced-Based literature1. FDA is strongly against that2. Subgroups that did poorly and are thus exclusions:

a. BP >185/110 even if controlledb. DM with prior CVAc. NIHSS>25d. Age>80e. Any anticoagulant regardless of INR

A. < 3 hours you can correct warfarin to INR < 1.2B. Not so in the 3-4.5 hour timeframeC. Antiplatelet agents are OK

H. Intracerebral artery (invasive) TPA can be given to 6-8 hours (depends on location)XII. NIH Stroke Scale-NIHSS (Score of 0, 1, 2, 3…)

1A. LOC-Alert, Arousable, Repeated stimulation or pain, Not

1B. LOC Questions (2)-Month and Age

1C. Commands (2 tasks)-Open and close eyes and hands, or similar

2. Best Gaze

-Normal (EOMI), Palsy, Total paresis3. Visual

-Normal-Hemianopia: Partial, Complete Unilateral, Bilateral

4. Facial Palsy-Normal, Minor, Partial, Complete Paralysis

5. Motor Arm-Each Arm with own score-No Drift, Drift, Effort against gravity, No effort against gravity, No movement

6. Motor Leg-No Drift, Drift, Effort against gravity, No effort against gravity, No movement

7. Limb Ataxia (Finger-Nose, Heel-Shin)-Absent, Present in 1 limb, Present in 2 limbs

8. Sensory (Pinprick or Withdrawal)

-Normal, Mild to Moderate Loss, Severe to Total Loss9. Best Language (Aphasia)

-None, Mild/Moderate, Severe, Global10. Dysarthria

-None, Mild/Moderate, Severe11. Extinction/Inattention (Formerly Neglect)

-None, Inattention to stimulus, Profound Inattention XII. Permissive HTN

A. If TPA candidate, BP needs to be


19/24


PCOM-EM

4

XV. CT Scan A. Fast, widely available, cheaper than MRIB. Detects ICH/SDH/EDH about 100% of the timeC. Does not show CVAD. Misses about 3-6% of SAH

XVI. MRI A. Can show tissue that is dead and that at risk (penumbra)B. MRA shows the circulationC. Takes longer, not readily available, more expensive

XVII. Hemorrhagic CVA A. CT (+) For BleedB. ICH 10%, SAH 6% of CVA’sC. Requires Neurosurgical Consultation and Neuro ICU admission


20/24


PCOM-EM

5

Stroke DistributionsVascular Territories

XVIII. Anterior Cerebral Artery-2% A. Contralateral paresis, Legs>Arms

B. Sensory deficit in the same distributionC. Gait disturbance due to weakness, not cerebellar balance dysfunction

XIX. Middle Cerebral Artery-90% A. Contralateral paralysis, Face/Arms>LegsB. Sensory deficit in the same distributionC. Aphasia (if dominant hemisphere)D. Hemineglect (if nondominant hemisphere)E. Homonymous hemianopsia

1. Eyes look towards the side of the stroke2. Vision preserved on the side of the stroke

F. Right-handed=>Left hemisphere dominant=>Left MCA CVA1. Right hemiparesis & sensory deficit2. Aphasia

3. Right homonymous hemianopsia-(Looks to right)G. Right-handed=>Left hemisphere dominant=>Right MCA CVA1. Left hemiparesis & sensory deficit2. Left hemineglect3. Left homonymous hemianopsia-(Looks to left)

H. Reverse for opposite handedness and dominance I. Left-handed=>Right hemisphere dominant=>Right MCA CVA

1. Left hemiparesis & sensory deficit2. Aphasia3. Left homonymous hemianopsia-(Looks to left)

J.

Left-handed=>Right hemisphere dominant=>Left MCA CVA1. Right hemiparesis & sensory deficit

` 2. Right hemineglect3.Right homonymous hemianopsia-(Looks to right)

XX. Posterior Cerebral Artery-5% A. Supplies occipital cortex=>one of the following:

1. Homonymous hemianopsia on contralateral side2. Right artery looks left, Left artery looks right3. Visual agnosia-Can't recognize objects4. Cortical blindness5. Plus:

a. Confusionb. Paresthesiasc. Dizzinessd. Nauseae. Memory lossf. Language dysfunction

g. Minimal motor involvement in the form of a tremor


21/24


PCOM-EM

6

XXI. Vertebrobasilar Artery A. Supplies brainstem, cerebellum, visual cortexB. Mortality >85%C. Symptoms depend on the area of ischemia, can be variableD. Typically waxing/waning courseE. Up to 50% have TIA's days before the CVAF. ***Vertigo, Vomiting, HA, CN findings***G. Large number of manifestations

1. Abnormal oculomotor, dysarthria, dysphagia2. Face and tongue weakness, face and scalp sensory loss3. Decreased LOC, ataxia, contralateral weakness, incontinence

XXII. Cerebellar Artery-3% A. 3 vessels: Superior, Inferior, PosteriorB. ***Vertigo, Vomiting, HA, Ataxia***

1. Note similarity to the VBA CVA minus CN findingsXXIII. Lacunar Syndromes-15-25%

A. Small deep penetrating vesselsB. Microinfarctions in HTN/DM patientsC. Stuttering course, CT (-)D. Prognosis is better

E. 5 Types:1. Pure motor hemiparesis: Pons or Internal Capsule2. Pure sensory: Thalamus3. Dysarthria-Hemiparesis: Pons, Internal Capsule4. Ataxia-Hemiparesis: Pons, Internal Capsule5. Mixed Sensorimotor: Hemiparesis with Ipsilateral complaints

XXIV. Transient Ischemic Attack-TIA A. 2009 AHA/ASA:

1. A transient episode of neurological dysfunction caused by focal brain, spinal cord, orretinal ischemia, without acute infarction

B. Now a tissue based, not time based, diagnosisC. Requires imaging

1. Immediate neuroimaging is key

2. MRI is better3. CT is faster but is limited in the posterior circulation

D. Need to figure out why:1. ECG to look for A-fib that could be embolic cause2. MRA or CTA to look for stenosis3. Carotid doppler if MRA/CTA does not show the carotids well4. Echocardiography for clots and function5. Bubble test echocardiography to look for right to left shunts (e.g. PFO)

E. ABCD2 is not accurate enough for low riskF. All TIA's require urgent work-up within 48 hours

1.Usually accomplished through short admissionG. TIA=Warning signH. Risk of progression:

1. Within 2 days: 1 - 8% (=1/100-1/12 risk of CVA within 48 hrs)2. Within 7 days: 1.2 - 11%3. Within 90 days: 3 - 18%

XXV. Brain Attack A. TIA-warning sign=>Equate to USAB. Silent CNS Infarction=>Equate to NSTEMI

1. Damage without sxC. CVA-Damage with sx=>Equate to STEMI


22/24

S.A. Pulley, D.O., FACOEP Acute Coronary Syndrome

PCOM-EM

1

Acute Coronary SyndromeCardiogenic Chest Pain

I. Objectivesa. To discuss the epidemiology, pathogenesis and risk factors

b. To identify symptoms and diagnosticsc. To establish priorities and treatments

IIII.. Acute MI A. Time wasted is heart muscle lostB. TIME=MUSCLEC. Muscle=Quality of Life (or ability to live)

II. Scope of Problem A. 735K MI’s annuallyB. 47% die outside of hospitalC. Another 10-15% die within 12 monthsD. 318+ Billion dollar diseaseE. Approximately 600K annual cardiac deaths

1. ~370K are CAD related

III. Sudden Cardiac Death A. ~424K cases annually for SCDB. ~326K EMS cases annually for SCDC. Only 1/3 of victims get CPR in the fieldD. EMS intact save rate nationwide averages

a. Was 8%, Now up to 11%b. 31% for witnessed VF/VT

IV. Pathogenesis of AMI A. Interaction of multiple factors

1. Progressive artherosclerotic process2. Plaque fissuring and subintimal hemorrhage3. Platelet aggregation at site of existing narrowing

B. Coronary artery spasmC. Coronary artery embolismD. Spontaneous Inflammation

V. Chest Pain A. A patient presents to the Emergency Department with a complaint of chest painB. What do you do first?

VI. Screening for AMI A. Need a specific triage protocolB. Should be placed immediately in a treatment area so they can...C. Have a 12-lead ECG performed

VII. ECG Patterns of AMI A. Pattern of injury

1. ST elevation in only 50% of MI’s2. Nonspecific ST-T changes in about 25%3. About 25% have normal ECGs

B. “Old” Myocardial infarctionC. Non Q-wave infarctionD. New BBB

VIII. Pattern of Injury A. ST segment elevation (in 2 or more contiguous leads) leads

1. 2 mm in precordial leads2. 1 mm in limb

B. New LBBB


23/24


PCOM-EM

2

C. ECG Regions1. II, III, F: Inferior wall2. V1 - V2: Interventricular septum3. V3 -V4: Anterior wall4. I, L: High lateral wall5. V5 - V6: Low lateral wall6. R V3 - RV4: Right Ventricle7. Mirror V1 - V2 or V9: Posterior Wall

IX. Differential Diagnosis A. Acute Coronary Syndrome***(Short term life threat)B. Thoracic Aneurysm Dissection***(Short term life threat)C. Pneumothorax***(Short term life threat if Tension)D. Pulmonary Embolism***(Short term life threat)E. Booerhaves***(Short term life threat)F. TraumaG. Pleurisy/PneumoniaH. PericarditisI. GERD/Esophagitis

X. Risk Factors for AMI A. Not Modifiable

1. Prior disease (MI, bypass, angioplasty), Family history, Age/SexB. Modifiable

1. Sedentary, Obesity, HTN, Smoking, Hyperlipidemia, DMC. Other Modifiable

1. Stress, Poor nutrition, Excessive alcohol, Cocaine, MethamphetamineXI. Cardiogenic Chest Pain-Chest “Discomfort”

A. PressureB. TightnessC. HeavinessD. SqueezingE. Bricks or elephant sitting on chestF. Any discomfort from umbilicus to upper teeth, front or back, in the right patient, can be

considered cardiac related

G. The older the patient is, females, or the longer that the patient has had diabetes, the lesstypical the symptoms tend to be

XII. Cardiogenic Symptoms A. Chest discomfortB. “Levine” signC. Shortness of breathD. DiaphoresisE. Nausea/vomitingF. Radiation

XIII. Public Awareness A. 92% recognize chest pain as a symptoms of heart attackB. Only 27% were aware of all the major symptoms and knew to call 9-1-1C. With about 47% of people dying outside the hospital from cardiac arrest, it appears that most

do not heed the warning symptoms of heart attackXIV. Atypical Symptoms A. Any discomfort from umbilicus to upper teeth, front or back, in the right patient, can be

considered cardiac relatedB. The older the patient is, females, or the longer that the patient has had diabetes, the less

typical the symptoms tend to beXV. Decision Process

A. More likely to have1. Risk factors2. Suspicious story (Symptoms) which is the most important factor


24/24


PCOM-EM

B. Less likely to have1. Lack of risk factors2. Atypical story

C. Always err towards the conservative sideXVI. Management of Cardiac Chest Pain

A. Oxygen: If pulse ox less than 94%B. Aspirin: Chewable- 2-4 (162-324 mg)C. Nitroglycerin: 0.4 mg SL q 5 min until relief or HA/BP intoleranceD. Opiates: e.g. Morphine/Hydromorphone

XVII. Diagnostics A. ECGB. VS monitoring/Rhythm monitoring/Pulse Ox, IVC. CXRD. Cardiac lab markers

XVIII. Continuing Management of Cardiac Chest Pain A. Acute MI (ST Elevation-STEMI)

1. Choose reperfusion strategy-FIRST2. IV NTG3. IV Beta Blockers4. IV Heparin/SQ Enoxaprin

5. PO Clopidogrela. Normal 75 mg/dayb. Acutely 300-600 mg PO

B. NSTEMI (Non STEMI), USA, ACS1. Same initial medications as STEMI2. May add Glycoprotein IIb/IIa Inhibitor3. Serial ECG’s looking for STEMI conversion

C. Non-diagnostic ECG1. Topical or IV NTG2. ASA3. Others as above if intermediate to high risk4. On-going pain

a. Consider other causes (e.g. MSK or GERD)

1) Use caution as these can coexist with acute coronary syndromeb. Urgent Catheterizationc. And/or Double/Triple rule-out CT Angiogram of Chest

C. Coronary Artery Reperfusion1. PTCA/PCI2. Emergent Bypass (CABG)3. Thrombolytics

a. What do you think is the major determinant of the method chosen?b. Location Location Location

XIX. Thrombolytics A. Best within 4-6 hoursB. Door to needle time < 30 minutesC. Need teamwork

D. “Bleeding” history1. Stroke2. Clotting abnormalities3. Surgery

XX. Emergent Cardiac Catheterization A. PTCAB. Possible Emergent CABG

XXI. Summary-ED Management of Acute MI A. High index of suspicionB. Immediate 12 lead ECG and regular repeats if normalC. Know/Choose reperfusion strategy

2016 updated acls handouts

Documents