Emergency Cardiovascular Care: EMT-Intermediate Treatment Algorithms Introduction to the Algorithms Cardiac Arrest Algorithms Prehospital Medication Profiles Perspective regarding the EMT- Intermediate algorithms The algorithms parallel AHA ACLS standards Frequent references are made to local standing orders in all of the algorithms The algorithms are patient-focused The EMT-I must decide whether the treatment algorithm is appropriate for the patient Causes for the dysrhythmia or presentation should be explored as the EMT-I works through the algorithm ACLS and the EMT-I ACLS is recognized as an international standard for cardiovascular care ACLS algorithms and treatments are based upon research Standards will change with new research studies The EMT-I should stay informed on cardiac care trends and recommendations Cardiac Treatment Algorithms Dead People Universal Treatment Algorithm Pulseless Electrical Activity Ventricular Fibrillation/Pulseless Ventricular Tachycardia Asystole Hypothermia Alive People Bradycardia Acute Pulmonary Edema and Shock Hypothermia What conditions are likely to cause cardiac arrest? Ischemic or infarcted cardiac tissue VF, pulseless VT, slow PEAs and asystole PVCs lead to VT/VF Slow rates with heart blocks Asystole with prolonged tissue hypoxia Trauma PEA that is fast and narrow Significant fluid loss Loss of red blood cells Pulmonary trauma and impairment of ventilation 1
Other causes of cardiac arrest Drug overdose Slow rhythms from depressant drugs Fast rhythms (narrow and wide) from stimulants PEA with antihypertensive overdoses Medical causes Renal failure Significant GI bleeds Cardiac Arrest Algorithms The Universal Algorithm for the Dead Emphasis early defibrillation when indicated VF/VT versus non- VF/VT approach Focus on rhythm ID and reversing the cause The Universal Algorithm (Tailored to the EMT-I) Primary ABCD A = Noninvasive management B = BVM (C = CPR) D = Defibrillation Secondary ABCD A = More invasive management B = Check placement C = Perfusion, Rx delivery, ECG leads D = Differentiate causes for the arrest Ventricular Fibrillation Ventricular Fibrillation Algorithm 2
V-Fib Flow Quick-Look, quick defib sequence! 200, 300, 360 Joules Keep the paddles on the chest If no conversion CPR, BVM, ET, IV, 3-lead Start differential diagnosis Start drug therapy Drugs are secondary to defibrillation! VF Drug Therapy Philosophies Pressor agents Epinephrine, vasopressin To prime the arteries for blood flow Vasoconstriction should raise blood pressure, cerebral blood flow in anticipation of successful defibrillation Antidysrhythmics Amiodarone, lidocaine To raise the fibrillation threshold Wipe out irritable electrical impulses V-Fib Flow First drug choices Epinephrine: 1mg every 3-5 minutes Vasopressin: 40 units One time only Resume defibrillation Shock Drug - CPR for 1 minute shock Antidysrhythmics Choose one and fit it into the above sequence Drug Profiles in Cardiac Arrest: Epinephrine and Vasopressin Epinephrine 1:10,000 Drug Class Sympathomimetic English, please!! Wide-spread stimulation of the sympathetic nervous system Increased vasoconstriction of peripheral arteries Vasodilation of coronary arteries Cardiac effects Post-conversion side effects. Vasopressin Synthetic anti-diuretic hormone (ADH) Responds to a drop in blood pressure or volume Secreted by the pituitary gland and the hypothalamus Actions Directly retains water at the kidneys Do you want to know more about this drug? (Click on one) Yes No 3
More on Vasopressin Vasoconstriction with high doses of the drug Direct stimulation of the muscular layer of the vessels No Beta properties Does not increase the workload on the heart Location of vasoconstriction Intense vasoconstriction of peripheral vessels Less intense in the cardiac and renal vessels Actual cerebral vasodilation seen! Go figure drugs can t be that easy to figure out! Vasopressin Research, 2000 Research on repeated administration Maintains cardiac perfusion and correlates with more successful resuscitations than epinephrine Not currently recommended, though Epinephrine and Vasopressin together Some better coronary blood flow Major decrease in brain perfusion, though Vasopressin Side effects Can you guess, now that you know it s mechanism of action?? Increased BP may indirectly increase the workload on the heart CO = SV x HR SV influenced by preload, contractility and afterload Cardiac patients may experience angina or acute episodes of pulmonary edema Theoretical Vasopressin Administration Indication Ventricular fibrillation Not currently recommended for asystole or PEA No research was performed for these applications Addition of the drug to these algorithms may occur in the future with further research Typically packaged in single-dose vials Vials of 20mg in 1mL of fluid Already in liquid form Give as a rapid IV bolus Back to the Action Potential Drug Profiles in Cardiac Arrest: Lidocaine and Amiodarone 0 1 2 3 4 Each drug manipulates a piece (or pieces) of the action potential Primary actions and locations for each drug will differ Lidocaine muscle tissue Amiodarone electrical tissue with some overlap on the muscle tissue 4
Lidocaine Makes it harder for the cell to fire Especially in ischemic heart muscles! Sodium-blocker Works on Phases 4 and 0 Prevents sodium from getting inside Lidocaine Side Effects Alters sodium movement in all nerve cells, to a point Side effects tend to reflect this fact: Ringing in the ears Blurred vision Drowziness Tremors or twitching Bradycardia/asystole Lidocaine Side Effects Mild Toxicity Drowsiness Tinnitus N/V Blurred vision Tremors/twitching Severe Toxicity Dyspnea Fainting Bradycardia Convulsions Coma Lidocaine Indication Pulseless VT and VF Administration Packaged as a pre-load, 100mg in 5mL Initial dose: 1-1.5mg/kg Subsequent doses: 0.5-0.75mg/kg every 5-10 minutes Exactly half of your initial bolus! Total dose of 3mg/kg Lidocaine Contraindications EMT-Intermediate Anything except pulseless VT or VF! Slow ventricular rhythms in cardiac arrest These rhythms are usually escape rhythms, that are trying to keep the heart alive Lidocaine will effectively eliminate these rhythms, leaving the EMT with asystole Amiodarone Protects both ends of the cell! Major inhibition of Na+ and K+ channels Keeps an irritable cell from firing (phase 0 and 4) Lengthens the refractory period (phase 3) Prevents other irritable impulses from moving in on the cell! 5
Amiodarone s Actions Effects on the conduction system Lengthens the P-R Interval Potentially lengthens the QRS interval and the T wave It also blocks alpha and beta receptors Slows sinus rate of firing May reduce contractility of the heart It will also drop blood pressure How potent is this drug? Can you guess some of it s side effects? Amiodarone Side Effects Acute worsening of CHF New-onset dysrhythmias, postconversion AV blocks, bradycardias, etc. Bradycardia, hypotension Dizziness 40-60 day half life of the drug! Amiodarone Administration Packaged as ampules and vials 150mg in 3mL Drug is suspended in a thicker solution Polysorbate 80 Dosage for cardiac arrest 300mg in 20-30ml of NS rapid IVP Repeat doses of 150mg every 3-5 min. The Logistics of Amiodarone Administration Ampules and vials Do NOT inject air into them prior to drawing up the drug The drug and solution will foam up and be unusable Instead, draw up 20-30mL of saline first, then draw up the amiodarone into the syringe Amiodarone Contraindications Any rhythm other than pulseless VT/VF! Any bradycardia Ventricular or otherwise Patients in cardiogenic shock Too Many Choices??!! Follow the guidelines of your standing orders Base your decisions on the patient s recent/past history and on the drug s side effects Vasopressin will cause less complications post-arrest for the MI patient or in the patient with a significant cardiac history 6
Too Many Choices??!! Epinephrine may be a better choice for non-cardiac related arrest Overdose Trauma Respiratory causes Amiodarone v. lidocaine Amiodarone is more global in its effects Lidocaine works well for ischemic hearts Take a breath the hard part is over!! PEA: Any rhythm without a pulse Organized rhythms should not cause cardiac arrest! Primary goal for this algorithm is to find the cause and treat it as specifically as possible The EMS drugs will not reverse the causes! PEA Philosophies The 5 Hs and 5 Ts Primary ABCD Manual airway maneuvers BVM ventilations Start CPR Quick-look for VF/VT Secondary ABCD Combitube Confirm placement IV Rhythm determination Find the cause PEA Algorithm Flow Some Causes of PEA Slow and Narrow Complexes Overdose Slow and Wide Complexes Severe acidosis Hypothermia Overdose Hypoxia Fast and Narrow Complexes Severe hypovolemia Trauma Medical causes Drug overdose Stimulants 7
PEA Drug Focus Epinephrine - Sympathomimetic Vasoconstrictor Stimulates contractility and heart rate Dose: 1mg every 3-5 minutes Atropine Parasympatholytic Only used for slow rates!! Stimulates heart rate at the sinus node Stimulates conduction through the AV node Dose: 1mg every 3-5 minutes to a maximum dose of 0.04mg/kg (average 3mg) Last of the rhythms: Asystole Forms of Asystole Asystole Algorithm Philosophies The presence of asystole should be viewed more as a confirmation of death than an aggressive treatment algorithm Make an early effort to confirm POLST, DNR, obvious signs of death Asystole Algorithm Flow Primary and secondary ABCDs are similar to PEA Drugs are the same as a slow PEA Consider termination of efforts Special Considerations of Cardiac Arrest 8
Pediatrics Common causes of cardiac arrest Respiratory arrest Congenital abnormalities Blunt trauma Head injury Chest trauma Abdominal trauma Pediatrics Algorithm flow is similar to adults Specific pediatric algorithms will be discussed in the pediatrics section High priorities of care Find the cause and make attempts to reverse it Effective airway and breathing management Pediatric Code Management Defibrillation Must have a defibrillator that is adaptable to kids Pediatric defibrillation patches should be used Start with 2 joules/kg Subsequent shocks increase to 4 joules/kg Drug-CPR-shock sequence is similar to adults Pediatric Code Management Drug doses PEA and asystole Epinephrine 1:10,000 0.01mg/kg, repeat every 3-5 minutes Atropine 0.02mg/kg, repeat only once Drug doses Pulseless VT/VF Lidocaine 1mg/kg Amiodarone 5mg/kg Hypothermia Primary ABCD is similar to the pulseless VT/VF algorithm Further treatments are determined by core temperature Drug intervals are lengthened or ceased due to poor systemic absorption Hypothermia Give more time for pulse checks Minimum of 30 seconds Hypothermia will slow the heart rate significantly Active rewarming for severe hypothermia should be avoided Protection from further cold exposure is appropriate, though 9
Cardiac Arrest Summary Attempt to find the cause for the arrest and direct your care accordingly Tailor your drug selection to provide the best action with the least side effects for the patient This may avoid further headaches for you in the post-resuscitation period Care for the family is as important as your care of the patient! 10