BASIC ACLS

DRUG DOSE “CHEAT SHEET” PLEASE COMPLETE THE WORKSHEET AS WE GO OVER EACH MED YOU CAN USE THIS FOR YOUR PRACTICAL SCENARIOS SORRY ! CAN’T USE IT FOR THE WRITTEN TEST RED IS VERY IMPORTANT

ADENOSINE ADENOCARD TREAT STABLE FAST RHYTHMS 6MG –”SLAM” 12 MG “SLAM” 10 SEC HALF LIFE

ASPIRIN TREAT CHEST PAIN UP 325 MG BABY ASA 81 MG

AMIODARONE USED TO TREAT VENTRICULAR DYSRHTHYMIAS V-FIB AND V-TACH 300 MG CARDIAC ARREST/REFRACTORY V-FIB 150 MG FOR “LIVE” PT CAN BE USED IN PLACE OF LIDO

ATROPINE USED FOR STABLE SLOW RHYTHM .5 MG MAX DOSE 3 MG NOT FOR CARDIAC ARREST

CARDIAZEM DIALTIAZEM SECOND LINE FOR STABLE FAST SVT .25 MG/KG .35 MG /KG SECOND DOSE

DOPAMINE INCREASE BP IN HYPOTENSIVE PT TREAT HYPOVOLEMIA FIRST 2-10 MCG/KG/MIN 5 MCG/KG/MIN

EPI FIRST LINE DRUG FOR CARDIAC ARREST 1MG NO MAXIMUM EPI DRIP FOR BRADYCARDIA BEST GIVEN BY PERIPHERAL IV IN CARDIAC ARREST

LIDOCAINE TREAT VENTRICULAR DYSRHYTHMIAS V-FIB OR V TACH 1-1.5 MG/KG NO DRIP REQUIRED

MAGNESIUM SULFATE TREAT –TORSADES OR HYPOMAGNESIA REFRACTORY V-FIB 1-2 GM IN 50cc ADMINISTERED OVER 5-10 MINUTES

MORPHINE USED FOR CHEST PAIN 2-6 MG

NARCAN USED TO TREAT NARCOTIC OVERDOSE 2MG FOR CARDIAC ARREST

NITRO USED TO TREAT CHEST PAIN 4 MG UP TO 3X 5 MINUTES APART BP >90 MM/HG NO ED NO RVI

NORMAL SALINE FLUID REPLACEMENT HYPOVOLEMIA 1-2 LT

SODIUM BICARBONATE USED TO TREAT KNOWN ACIDOSIS 1MEQ/KG

VERSED MIDAZOLAM USED AS PREMEDICATION FOR ELECTRICAL THERAPY AMNETIC 5 MG

DEFIBRILLATION V-FIB OR PULSE LESS V-TACH DEFIBRILLATE THE DEAD 200 JOULES FOR BIPHASIC 360 JOULES FOR MONOPHASIC KNOW YOUR EQUIPMENT

CARDIOVERSION SYNCHRONIZED DEFIBRILLATION 100/200/300/360 CARDIOVERT 100 J– CENTURY 100 YEARS ROMAN NUMERAL FOR 100 ?

Hs and Ts Hypovolemia Hypoxia Hypothermia Hypo-/Hyperkalemia Hydrogen ion n (acidosis) Hypomagnesia Hypoglycemia Tamponade, cardiac Tension pneumothorax Thrombosis: lungs Thrombosis: heart Tablets/toxins: drug overdose The 5 Hs and 5 Ts is another memory aid that may be used to recall possible treatable causes of cardiac emergencies.

WORKBOOK SLIDES WITH THE BLUE BACKGROUND WILL BE IN YOUR WORK BOOK FILL IN THE BLANKS AS WE GO THRU THE SLIDES IT WILL BE VERY HELPFUL !!!

Components of Basic Life Support Recognition of signs of: Stroke Heart Attack Cardiac arrest FBAO How to perform: Abdominal thrust CPR Early Defibrillation with an AED Until recently, resuscitation guidelines for an infant referred to a child less than 1 year of age. A child was considered 1 to 8 years of age and adult resuscitation guidelines applied to individuals more than 8 years of age. The 2005 resuscitation guidelines redefined the age of a child for healthcare professionals. Child resuscitation guidelines apply to victims from 1 year of age to the onset of puberty (about 12 to 14 years of age).

TEAM CONCEPT ALL MEMBERS NEED TO BE PROFICIENT IN THEIR SKILLS EVERY MEMBER NEEDS TO BE ABLE TO OPERATE/TROUBLESHOOT THEIR EQUIPMENT CONSTRUCTIVE INTERVENTIONS OUR PURPOSE AS MEMBERS OF M.E.T. IS TO PREVENT PT DETERIORATION BY EARLY INTERVENTIONS

STABLE VS. UNSTABLE STABLE –A & OX3 SKIN WARM DRY COLOR GOOD NORMAL V.S. UNSTABLE – A.M.S. / PALE OR CYANOTIC/ SWEATY/ABNORMAL V.S. UNSTABLE PT IS IN SHOCK

IMPORTANT !! STABLE PATIENTS ARE TREATED WITH MEDS UNSTABLE PATIENTS ARE TREATED WITH ELECTRICITY DEFIB/ PACER/ CARDIOVERSION

CABD SEQUENCE

WHAT DO AEDS AND EASTER EGGS HAVE IN COMMON ? POWER UP ATTACH ELECTRODES ANALYZE RHYTHM SHOCK/NO SHOCK

Emergency Action Steps Assess-Alert-Attend to ABCDs D=DEFIBRILLATION SHOCK/NO SHOCK. If AED instructs “shock indicated” yell “CLEAR” or something similar. Press shock button. Immediately resume chest compressions. If no shock is indicated, immediately resume chest compressions. Then follow instructions as given by AED

TROUBLESHOOTING AED USUALLY PROBLEM LIES WITH POOR PADS ADHESION OR CABLE NOT CONNECTED ANY MALFUNCTION WITH THE AED IMMEDIATELY START CPR

Emergency Action Steps Assess-Alert-Attend to ABCDs D=DEFIBRILLATION (Summary) SHOCK advised CLEAR and give 1 shock. Immediately resume CPR. Continue 30:2 x 5 cycles (2 min.). Reassess rhythm. NO SHOCK advised Immediately resume CPR AEDS that have not been reprogrammed to 2005 recommendations may repeat charging sequence for a second and third shock. During series of 3 shocks, rescuer should not interrupt or interfere. These AEDS are programmed to allow 1 minute (as opposed to 2 minutes) for CPR between shocks. In all cases, listen to and follow AEDS voice/visual prompts. Do your best to minimize interruptions in chest compressions. For an unwitnessed cardiac arrest, local protocol may instruct EMS providers to provide a couple minutes of CPR to oxygenate heart and brain before attempting defibrillation.

CRITICAL THINKING AFTER PULSE CHECK –START CPR 30:2 AND A RATE OF 100 COMPRESSIONS PER MINUTE INTERRUPTIONS IN CPR SHOULD BE KEPT TO LESS THAN 10 SECS HIGH QUALITY CPR IN PT WITH ADVANCED AIRWAY UNINTERRUPTED CHEST COMPRESSIONS AND 10 VENTILATION PER MINUTE

For high quality CPR SWITCH COMPRESSORS EVERY 5 CYCLES (2 MINUTES) HIGH QUALITY CPR HARD FAST UNINTERRUPTED AND ALLOW FOR COMPLETE CHEST RECOIL INTERRUPTIONS TO LESS THAN 10 SECS

CRITICAL THINKING NO PULSE = CHEST COMPRESSIONS IF YOU ARE NOT SURE IF PT HAS PULSE- START CPR

SUCTIONING SELECT PROPER SIZE/TYPE CATHETER SUCTION ON THE WITHDRAWAL NO MORE THAN 10 SECS WATCH O2 SATS AND HEART RATES

VENTILATION RATES VENTILATION RATE WITH PULSE –EVERY 5-6 SECS WITH ADVANCED AIRWAY- ONE EVERY 6-8 SECONDS DELIVER OVER 1 SEC. JUST ENOUGH TO MAKE CHEST RISE

Capnography

Exhaled Carbon Dioxide Detection Capnography is the continuous analysis and recording of carbon dioxide concentrations in respiratory gases. Capnometry is the measurement of CO2 concentrations without a continuous written record or waveform. A capnometer is a device used to measure the concentration of CO2 at the end of exhalation. An end-tidal CO2 (ETCO2) detector is a capnometer that provides a noninvasive estimate of alveolar ventilation, the concentration of exhaled CO2 from the lungs, and arterial carbon dioxide content. ETCO2 monitoring is currently used for assessment of conscious sedation safety, evaluation of mechanical ventilation, verification of endotracheal tube placement, continuous monitoring of endotracheal tube position, and monitoring of exhaled CO2 levels in patients with suspected increased intracranial pressure. Because the air in the esophagus normally has very low levels of CO2, capnometry is considered a rapid method of preventing unrecognized esophageal intubation. The presence of CO2 (evidenced by a color change on the colorimetric device or number/light on the electronic monitor) suggests tracheal tube placement. A lack of CO2 (no color change on colorimetric detector or indicator on the electronic monitor) suggests tube placement in the esophagus, particularly in patients with spontaneous circulation. Because CO2 may inadvertently enter the stomach, ventilate the patient at least six times before evaluating ET tube placement using an exhaled CO2 detector to quickly wash out any retained CO2. In animals, false-positive results (CO2 is detected despite tube placement in the esophagus) have been reported when large amounts of carbonated beverages were ingested before a cardiac arrest. False-negative results (lack of CO2 detection despite tube placement in the trachea) may occur in cardiac arrest or in a patient who has a significant pulmonary embolus because of reduced delivery of CO2 to the lungs.

CONFIRMATION ….. Monitor for changes in color (colorimetric device) or number (digital device) on an exhaled CO2 detector CONTINUOUS WAVEFORM MOST RELIABLE METHOD OF VERIFYING ET TUBE PLACEMENT CAUTIOUSLY SECURE ET TUBE –CIRCUMFRENTIAL TIES AROUND NECK CAN RESTRICT BLOOD FLOW

What is capnography? Capnography measures exhaled PETCO2. Used to determine the effectiveness of respiration and/or ventilation. CO2 is measured in mmHg Normal is defined as 35-45mmHg Post ROSC we want 35-40 mmHg

What’s the Difference SpO2 = Pulse oximetry – measures oxygenation EtCO2 = Capnography – measures ventilation

Devices used for Capnography Measured using qualitative and quantitative devices Qualitative gives you a color change (purple to yellow) Quantitative gives you a number value(EtCO2 and Respirations) Most effective is Waveform Capnography

What does it mean in ACLS? CO2 measures the effectiveness of our compressions, ventilations and overall patient care in resuscitation Compressions only 25-35% as effective as heart beating on its own Therefore CO2 during cardiac arrest may drop as low as 10mmHg

What does it mean in ACLS? CO2 less than 10mmHg means something is wrong PETCO2 >10mmHg=Good CPR CO2 should never drop below 10mmHg in Cardiac Arrest

Troubleshooting Low CO2 Check compressions and confirm carotid pulse with compressions Confirm tube placement Check equipment WHEN IN DOUBT PULL ENDOTRACHEAL TUBE AND GO BACK TO BASICS.

What does no CO2 Mean? CO2 readings of 0 or straight-line mean no CO2 is being registered. Access tube placement Check ventilator WHEN IN DOUBT PULL ENDOTRACHEAL TUBE

CRITICAL THINKING COMMON FATAL MISTAKE IS PROLONGED INTERRUPTIONS IN CHEST COMPRESSIONS- USUALLY FOR AIRWAY COMPONENT OF HIGH QUALITY CPR IS ALLOWING COMPLETE CHEST RECOIL

EKG RECOGNITION

12 Lead EKG Except for unstable pt –any pt with chest pain/pressure/ discomfort gets 12 lead immediately Looking for STEMI – ST elevation MI

Six Steps in Analyzing a Rhythm Strip Assess the rate Assess rhythm/regularity Identify and examine P waves Assess intervals Evaluate overall appearance of rhythm Interpret rhythm/evaluate clinical significance

Rate Measurement Six-second method Most ECG paper in use today is printed with 1-second or 3-second markers on the top or bottom of the paper. To determine the ventricular rate, count the number of complete QRS complexes within a period of 6 seconds and multiply that number by 10 to find the number of complexes in 1 minute. This method may be used for regular and irregular rhythms and is the simplest, quickest, and most commonly used method of rate measurement. 5 large boxes = 1 second 15 large boxes = 3 seconds 30 large boxes = 6 seconds

Large Box Method Count the number of large boxes between two consecutive waveforms (R-R interval or P-P interval) and divide into 300 To determine the ventricular rate, count the number of large boxes between two consecutive R waves (R-R interval) and divide into 300. To determine the atrial rate, count the number of large boxes between two consecutive P waves (P-P interval) and divide into 300. This method is best used if the rhythm is regular; however, it may be used if the rhythm is irregular and a rate range (slowest and fastest rate) is given.

Sinus Rhythm

TWO PARTS TO A BEATING HEART ELECTRICAL –ALL RHYTHMS (EXCEPT ASYSTOLE ) HAVE ELECTRICAL ACTIVITY MECHANICAL- ALL PERFUSING RHYTHMS ARE SUPPORTED BY ELECTRICAL COMPONENT AND MECHANICAL. MEASURED BY BLOOD PRESSURE

Ventricular Fibrillation (VF) SQUIGGLY LINE-LOOKS LIKE A KID DRAWING ON A WALL !!

Ventricular Fibrillation (VF) Coarse VF Fine VF Ventricular fibrillation (VF) is a chaotic rhythm that begins in the ventricles. In VF, there is no organized depolarization of the ventricles. The ventricular muscle quivers. As a result, there is no effective myocardial contraction and no pulse. Since no drugs used in cardiac arrest have been shown to improve survival to hospital discharge, the priorities of care in cardiac arrest due to pulseless VT or VF are CPR and defibrillation.

Monomorphic Ventricular Tachycardia Ventricular tachycardia exists when three or more PVCs occur in immediate succession at a rate greater than 100 beats per minute. VT may occur as a short run lasting less than 30 seconds (non-sustained) but more commonly persists for more than 30 seconds (sustained). VT may occur with or without pulses and the patient may be stable or unstable with this rhythm. Ventricular tachycardia, like PVCs, may originate from an ectopic focus in either ventricle. In VT, the QRS complex is wide and bizarre. P waves, if visible, bear no relationship to the QRS complex. The ventricular rhythm is usually regular but may be slightly irregular. When the QRS complexes of VT are of the same shape and amplitude, the rhythm is termed monomorphic VT. When the QRS complexes of VT vary in shape and amplitude, the rhythm is termed polymorphic VT (see irregular tachycardias).

Polymorphic Ventricular Tachycardia In polymorphic VT, the QRS complexes appear to twist from upright to negative or negative to upright and back. Polymorphic VT that occurs in the presence of a long QT interval is called Torsade de Pointes. Polymorphic VT that occurs in the presence of a normal QT interval is simply referred to as polymorphic VT or polymorphic VT resembling torsades de pointes. Symptoms are usually related to the decreased cardiac output that occurs because of the fast ventricular rate. Signs of shock are often present. The patient may experience a syncopal episode or seizures. The rhythm may occasionally terminate spontaneously and recur after several seconds or minutes, or it may deteriorate to ventricular fibrillation. If the rhythm is polymorphic VT, it is important to determine if the patient’s QT interval just before the tachycardia is normal or prolonged. If the QT interval is normal and the patient is symptomatic due to the tachycardia, treat ischemia if present, correct electrolyte abnormalities, and proceed with electrical therapy or antiarrhythmic medications if necessary. If the QT interval is prolonged and the patient is symptomatic due to the tachycardia, discontinue any medications the patient may be taking that prolong the QT interval, correct electrolyte abnormalities, and proceed with electrical therapy or antiarrhythmic medications if necessary. If the rhythm is sustained polymorphic VT and the patient is unstable or has no pulse, defibrillate. ALSO CALLED TORSADES

Ventricular Tachycardia (VT) Treat the following as VF: Pulseless monomorphic VT Pulseless polymorphic VT Monomorphic VT and polymorphic VT have already been discussed. If either of these rhythms presents without a pulse, the rhythm is treated as VF.

Asystole (Cardiac Standstill)

Asystole “P-wave” Asystole Asystole is a total absence of ventricular electrical activity. There is no ventricular rate or rhythm, no pulse, and no cardiac output. Some atrial electrical activity may be evident. If atrial electrical activity is present, the rhythm is called “P-wave” asystole or ventricular standstill. Confirm there is no pulse, begin immediate CPR, and confirm the rhythm in two leads. If the rhythm is confirmed as asystole, additional care includes starting an IV, considering the possible causes of the arrest, possible insertion of an advanced airway, epinephrine, and atropine.

Asystole Check leads Long down time 25 minutes or greater 2 rounds of drugs with no rhythm change indicates death CONSULT MED CONTROL TO TERMINATE EFFORTS

Sinus Bradycardia If the SA node fires at a rate slower than normal for the patient’s age, the rhythm is called sinus bradycardia. The rhythm starts in the SA node and then heads down the normal pathway of conduction through the atria, AV junction, bundle branches, and ventricles. This results in atrial and ventricular depolarization. In adults and adolescents, a sinus bradycardia has a heart rate of less than 60 bpm. The term severe sinus bradycardia is sometimes used to describe a sinus bradycardia with a rate of less than 40 bpm. Assess how the patient tolerates the rhythm at rest and with activity. If the patient has no symptoms, no treatment is necessary. If the patient is symptomatic because of the slow rate, initial treatment may include O2, starting an IV, giving IV atropine, and/or transcutaneous pacing.

Second-Degree AV Block, Type II The conduction delay in second-degree AV block type II occurs below the AV node, either at the bundle of His or, more commonly, at the level of the bundle branches. This type of block is more serious than second-degree AV block type I and often progresses to third-degree AV block. Preparations should be made for pacing when this rhythm is recognized. The use of atropine should be avoided. In this situation, atropine will usually not improve the block but will increase the rate of discharge of the SA node. This may trigger a situation in which even fewer impulses are conducted through to the ventricles and the ventricular rate is further slowed.

Second-Degree AV Block, 2:1 Conduction (2:1 AV Block) In 2:1 AV block, two P waves occur for every one QRS complex (2:1 conduction). Since there are no two PQRST cycles in a row from which to compare PR intervals, the decision as to what to term the rhythm is based on the width of the QRS complex. A 2:1 AV block associated with a narrow QRS complex (0.10 sec or less) usually represents a form of second-degree AV block, type I. A 2:1 AV block associated with wide QRS complexes (greater than 0.10 sec) is usually associated with a delay in conduction below the bundle of His—thus it is usually a type II block.

Third-degree AV Block Third-degree AV block associated with an inferior MI is thought to be the result of a block above the bundle of His. It often occurs after progression from first-degree AV block or second-degree AV block type I. The resulting rhythm is usually stable because the escape pacemaker is usually junctional (narrow QRS complexes) with a ventricular rate of more than 40 bpm. Third-degree AV block associated with an anterior MI is usually preceded by second-degree AV block type II or an intraventricular conduction delay (right or left bundle branch block). The resulting rhythm is usually unstable because the escape pacemaker is usually ventricular (wide QRS complexes) with a ventricular rate of less than 40 bpm. The patient’s signs and symptoms will depend on the origin of the escape pacemaker (junctional vs. ventricular) and the patient’s response to a slower ventricular rate. If the QRS is narrow and the patient is symptomatic due to the slow rate, initial management consists of atropine and/or transcutaneous pacing. If the QRS is wide and the patient is symptomatic due to the slow rate, transcutaneous pacing should be instituted while preparations are made for insertion of a transvenous pacemaker.

BRADY IS A BRADY WIDE OR NARROW –STABLE GETS MEDS UNSTABLE GETS PACED ASYMPTOMATIC-LEAVE IT ALONE

Sinus Tachycardia

Monomorphic Ventricular Tachycardia Ventricular tachycardia exists when three or more PVCs occur in immediate succession at a rate greater than 100 beats per minute. VT may occur as a short run lasting less than 30 seconds (non-sustained) but more commonly persists for more than 30 seconds (sustained). VT may occur with or without pulses and the patient may be stable or unstable with this rhythm. Ventricular tachycardia, like PVCs, may originate from an ectopic focus in either ventricle. In VT, the QRS complex is wide and bizarre. P waves, if visible, bear no relationship to the QRS complex. The ventricular rhythm is usually regular but may be slightly irregular. When the QRS complexes of VT are of the same shape and amplitude, the rhythm is termed monomorphic VT. When the QRS complexes of VT vary in shape and amplitude, the rhythm is termed polymorphic VT (see irregular tachycardias).

NARROW VS WIDE NARROW QRS USUALLY IS SUPRAVENTRICULAR WIDE COMPLEX ORIGINATES IN THE VENTRICLES

Sinus Tachycardia—Causes Fever Pain Anxiety Hypoxia CHF Acute MI Infection Shock Hypovolemia Exercise Fright Dehydration Medications Epinephrine Atropine Caffeine, nicotine Cocaine

Pulseless Electrical Activity (PEA) PEA exists when organized electrical activity (other than VT) is present on the cardiac monitor, but the patient is apneic and pulseless Pulseless electrical activity is a clinical situation, not a specific dysrhythmia. PEA exists when organized electrical activity (other than VT) is observed on the cardiac monitor, but the patient is unresponsive, not breathing, and a pulse cannot be felt. PEA was formerly called EMD – electromechanical dissociation. The term was changed from EMD to PEA because research using ultrasonography and indwelling pressure catheters revealed that the electrical activity seen in some of these situations is associated with mechanical contractions – the contractions are simply too weak to produce a palpable pulse or measurable blood pressure. PEA has a poor prognosis unless the underlying cause can be rapidly identified and appropriately managed. Treatment includes CPR, O2, IV access, possible insertion of an advanced airway, IV access, giving epinephrine (and atropine if the rate is slow), and an aggressive search for possible causes of the situation.

Critical Resuscitation Tasks Airway management Chest compressions Monitoring and defibrillation Vascular access/medication administration

Defibrillation—Indications Pulseless ventricular tachycardia Ventricular fibrillation

Paddles/Electrodes Hand-held paddles or combination pads are used to deliver current from the defibrillator to the patient. Combination pads consist of a flexible metal “paddle,” a layer of conductive gel, and an adhesive ring that holds them in place on the patient’s chest. If available, use combination pads instead of hand-held paddles for electrical therapy. Combination pads are disposable and have multiple functions. They are applied to a patient’s bare chest for ECG monitoring and then used for defibrillation and synchronized cardioversion (and in some cases, pacing) if necessary. Not all combination pads are alike. Some pads can be used for defibrillation, synchronized cardioversion, ECG monitoring, and pacing. Others can be used for defibrillation, synchronized cardioversion, and ECG monitoring, but not for pacing. Combination pads enhance operator safety by physically separating the operator from the patient. Instead of leaning over the patient with hand-held paddles, the operator delivers a shock to the patient by means of discharge buttons (one for each pad) located on a remote cable, an adapter, or on the defibrillator itself. Combination pads have multiple names including “combo pads,” “multi-purpose pads,” “combination electrodes,” “therapy electrodes,” and “self-adhesive monitoring/defibrillation pads.”

Paddle/Pad Position Hand-held paddles or combination pads should be placed on the patient’s bare chest according to the manufacturer’s instructions. Paddles or pads may be labeled according to their position on the chest (sternum/apex, front/back) or according to their polarity (positive, negative). When preparing the skin for paddle or pad placement, do not use alcohol, tincture of benzoin, or antiperspirant. When positioning paddles or pads, be sure that they do not overlap bone (such as the sternum, spine, or scapulae) because bone is not a good conductor of current. The typical paddle/pad position used during resuscitation is the sternum-apex position (also called the anterolateral or apex-anterior position). This position is often used because the anterior chest is usually easy to get to and placement of the paddles/pads in this position approximates ECG electrode positioning in lead II. Place the right (sternum) paddle/pad to the right of the sternum, just below the clavicle. Place the center of the left (apex) paddle/pad in the midaxillary line, about level with the V6 ECG electrode position (about the fifth intercostal space).

HANDS FREE SAFER ALLOWS FOR MORE RAPID DEFIBRILLATION CONTINUE CPR DURING CHARGING OF DEFIBRILLATOR

CRITICAL THINKING CPR IMMEDIATELY AFTER DEFIB SIGNIFICANTLY INCREASES THE CHANCES OF CONVERSION

VAGAL MANEUVERS USED TO SLOW FAST HEART RATES Gagging. Holding your breath and bearing down (Valsalva maneuver). Immersing your face in ice-cold water (diving reflex). Coughing.

Synchronized Cardioversion—Indications Unstable supraventricular tachycardia Unstable atrial fibrillation with rapid ventricular response Unstable atrial flutter with rapid ventricular response Unstable wide-complex tachycardia Unstable ventricular tachycardia with a pulse

Electrical Therapy—Safety Remove supplemental oxygen sources from area before defibrillation and cardioversion attempts Place them at least 3½-4 feet away from the patient’s chest Remove supplemental oxygen sources from the area of the patient’s bed before defibrillation and cardioversion attempts and place them at least 3 1/2 to 4 feet away from the patient’s chest. Examples of supplemental oxygen sources include masks, nasal cannulae, resuscitation bags, and ventilator tubing. Case reports exist that describe instances of fires ignited by sparks from poorly applied defibrillator paddles/pads in the presence of an oxygen-enriched atmosphere (Theodorou 2003). Severe fires have resulted when ventilator tubing was disconnected from an endotracheal tube and then left next to the patient’s head while defibrillation was attempted.

Transcutaneous Pacing — Procedure Set initial rate at 100 pulses/min. Increase the output (mA) until pacer spikes are visible before each QRS complex. Verify capture. The final mA setting should be slightly above where capture is obtained to help prevent the loss of capture.

Transcutaneous Pacing (TCP) Set the output (milliamps) setting Increase current slowly until capture achieved Watch monitor closely for electrical capture

Transcutaneous Pacing (TCP) Mechanical capture occurs when pacing produces a measurable hemodynamic response Pulse Measurable blood pressure greater than 90 systolic Assess mechanical capture by checking the patient’s right upper extremity or femoral pulses. Avoid assessment of pulses in the patient’s neck or on the patient’s left side. This helps minimize confusion between the presence of an actual pulse and skeletal muscle contractions caused by the pacemaker. Once capture is achieved, continue pacing at an output level slightly higher (about 2 mA) than the threshold of initial electrical capture. For example, if capture is achieved at 90 mA, set the output level at 92 mA. Assess the patient’s BP and level of responsiveness. Monitor the patient closely and record the ECG rhythm.

CPR SHOCK-200 J (BIPHASIC) EPI – 1MG or VASOPRESSEN 40 UNITS SHOCK DRUG-LIDO (1MG/KG) OR 300 MG AMIODARONE EPI-1MG SHOCK LIDO/AMIODARONE EPI EVERY 3-5 MIN 5H &5 T

PULSE LESS –TREAT LIKE V-FIB STABLE ADENOSINE 6MG “SLAM” REPEAT AT 12 MG AMIODARONE -150MG LIDOCAINE 1MG/KG UNSTABLE CARDIOVERT 100J DRUGS VERSED 5MG CARDIOVERT 200J

STABLE OXYGEN AND AIRWAY IF O2 SATS >93% ATROPINE .5MG DOPAMINE 2-10 MCG/KG/MIN EPI DRIP 1MG IN 100CC OVER 10 MINUTES UNSTABLE OXYGEN AND AIRWAY TCP-PACER ATROPINE – IF PACER IS DELAYED

STABLE VAGAL MANEUVERS ADENOSINE 6MG ADENOSINE 12 MG CARDIAZEM-.25MG/KG UNSTABLE CARDIOVERT 100J VERSED 5MG CARDIOVERT 200

PEA-NO PULSE BUT SHOULD BE ONE ! CPR/EPI/5H’S-5T’S HYPOVOLEMIA-FLUID HYPOKALEMIA-K+ HYPOXIA-O2 HYPOGLYCEMIA-D50 HYPOTHERMIA-TEMP HYDROGEN ION-BICARB 1MEQ/KG TAMPONADE-STEEL TOXIN-NARCAN 2MG TENSION PNEUMO-SURGEON TRAUMA-SURGEON THROMBOSIS-FIBRO

TREAT LIKE PEA CONSIDER TERMINATING EFFORTS AFTER EXTENDED TIME ( GREATER THAN 25 MIN ) AN 2 OR MORE ROUNDS OF DRUGS

POST ROSC MAINTAIN BP>90 SYSTOLIC PETCO2 > 35-40 MMhG O2 SAT > 93 % OPTIMIZE VENTILATIONS AND OXYGENATION THERAPEUTIC HYPOTHERMIA- NOT NECESSARY IF PT A&OX3

ACS-HEART ATTACK 12 LEAD ASAP MORPHINE – 2-6 MG MONA 12 LEAD EKG REALLY- OANM ASA-325 MG NITRO -.4 MG UP TO 3 TIMES- NO RVI/NO E.D. / BP > 90 SYSTOLIC MORPHINE – 2-6 MG 12 LEAD EKG FIBRONYLITICS

STROKE/CVA/BRAIN ATTACK SUDDEN ONSET NEUROLOGICAL PROBLEM HEADACHE UNILATERAL WEAKNESS = CINCINNATI OR OTHER STROKE ASSESSMENT NEEDS HEAD CT ASAP FIBRONOLYTICS WITHIN 3 HRS

CRITICAL THINKING WHAT IS THE ONE DRUG USED IN ALL ARRESTS ? DOSE ??BEST ROUTE TO ADMINISTER WHY IS ATROPINE USED IN HYPOTENSIVE PTS W/ SLOW RHYTHMS WHAT IS THE WINDOW FOR THROMBOLYTICS 12 LEAD AS SOON AS POSSIBLE FOR CHEST PAIN “RACING HEART” OR “INDIGESTION”

CRITICAL THINKING VENTRICULAR PROBLEMS NEED EITHER LIDO OR AMIODARONE GOAL IS TO HAVE BREATHING PULSED PT WITH BP >90/ CO2 35-40mm/hg THERAPEUTIC HYPOTHERMIA