1. ACLS Medications and Their Use
Billy Haynes, RN, BSN, CEN, EMT-P
Coordinator, Life Support Education

2. Objectives Discuss indications and dosages for:
Medications for Cardiac Arrest
Medications for Post arrest Care
Medications for Bradycardia
Medications for Tachycardia
Medications for Acute Coronary Syndromes
Medications for Acute Stroke

3. Routes of Administration
Medications should be given IV or IO
Avoid obtaining Central line access
ET Tube administration ONLY if unable to gain IV or IO Access

4. ENDOTRACHEAL TUBE MEDICATIONS
N arcan
A tropine
V asopressin
Epinephrine
L idocaine
x normal dose
4/16/2017

5. Medications for Cardiac Arrest

6. Two Types of Agents “Pressor” Agents (increased blood flow)
Epinephrine and Vasopressin
Antidysrhythmics (suppression of dysrhythmia)
Amiodarone, Lidocaine, Magnesium Sulfate

8. Pressor Agents

9. EPINEPHRINE + inotrope, + chronotrope, SVR, BP automaticity
force of contraction
 coronary and cerebral blood flow
Bronchial dilation
Some studies have raised doubts about the benefits of Epinephrine, pending more conclusive data or a formal change in ACLS guidelines, administer Epinephrine in accordance to current ACLS guidelines.
In general, pure beta-adrenergic agonists have the opposite function of beta blockers. Agonist aggravate the receptors. Adrenergic receptors are the targets of catecholamines (norepinephrine and epinephrine) and the binding of an agonist will generally cause a sympathetic response (flight or fight response)
Indications:
Hypoglycemia - epi as an alternative to glucogon
Bradycardia- flight or fight
Hypotension that is refractory to dpa/dba
Asthma- inhaled
COPD- B2 effects
Heart failure + inotrope
Allergic- anaphylaxis has two immediate dangers: a) loss of blood pressure and b)constriction of the air ways. Epinephrine relaxes the breathing passages so that the patient doesn't choke to death and also raises the blood pressure by peripheral vasoconstriction and accelerating the heart rate. B1 and B2 agonist.
Antidote to BB poisoning - Complications following beta blocker overdose are related to excessive beta adrenergic blockade, and occasionally the proarrhythmic (membrane-stabilizing) activity of these agents on cardiac conduction. Ingestion of other cardioactive agents in association with beta blockers increases mortality following overdose. Common and potentially dangerous coingestions include calcium channel blockers, cyclic antidepressants, and neuroleptics. Membrane stabilizing agents (eg, propranolol, acebutolol) inhibit myocardial fast sodium channels, which can result in a widened QRS interval and may potentiate other dysrhythmias. Overdose c MSA can cause significant cardiovascular morbidity. Beta blockers with high lipid solubility (eg, propranolol) rapidly cross the blood brain barrier into the central nervous system, predisposing to neurologic sequelae such as seizures and delirium. Beta Blockers with this characteristic are more amenable to treatment with 20 percent lipid emulsion therapy in the setting of a clinically significant overdose. Acebutolol , a cardioselective agent with partial agonist activity and significant MSA, is one of the most toxic beta blockers in overdose. Acebutolol toxicity may predispose the patient to ventricular repolarization resulting in arrhythmias. Sotalol  combines class III antidysrhythmic properties with beta adrenergic antagonism. Sotalol prolongs the action potential duration and increases the refractory period by blocking delayed potassium channels. This leads to prolongation of the QTc interval, and can contribute to the development of Torsades de Pointes
Calcium channel blocker OD- Dopamine is effective in increasing blood pressure and heart rate, and has been successfully used to treat ingestions of all three classes of calcium channel blockers.5 An epinephrine continuous infusion may also be effective in improving hemodynamic parameters. Like calcium administration, vasopressors are not always effective. Glucagon may improve cardiac contractility and increase heart rate by acting through stimulation of adenylate cyclase and the resultant increase in intracellular concentrations of cyclic adenosine monophosphate (cAMP). Animal studies of verapamil overdose show that glucagon can increase heart rate and arterial blood pressure as well as decrease the PR interval. adrenergic receptor-stimulating (vasoconstrictor) properties. Initial dose is 2-5 mg IV over seconds for an adult and 50 mg/kg in children. This may be repeated in five minutes if no response is seen. Responders should have a continuous infusion begun that consists of the initial
“response dose” given per hour.
The ∂-adrenergic effect of Epinephrine can increase CPP during CPR.
The value and safety of the ß adrenergic effects of epinephrine are controversial because they increase myocardial work and reduce subendocardial perfusion.
Although epinephrine has been used universally in resuscitation, there is a paucity of evidence to show that it improves outcome in humans.
The “standard” dose of epinephrine (1.0 mg) is not based on body weight.
Up to 0.2mg/kg may be considered (eg. Beta blocker/Calcium Channel Blocker overdose) but not recommended and may be harmful
4/16/2017

10. EPINEPHRINE Dosage IV/IO: Cardiac Arrest-1 mg q 3-5 min
Note: Higher Doses or more frequent doses do not increase survival and may contribute to myocardial dysfunction

11. VASOPRESSIN Dosage IV/IO: Potent peripheral vasoconstrictor
Cardiac Arrest- 40 U IV x 1 only
May replace either 1st or 2nd dose of epinephrine
Vasopressin may be effective in patients with asystole or pulseless electrical activity as well. However, as of 2000 we lack sufficient data to support an active recommendation to use vasopressin (Class Indeterminate: not recommended; not forbidden). Vasopressin should be effective in patients who remain in cardiac arrest after treatment with epinephrine, but there is inadequate data to evaluate the efficacy and safety of vasopressin in these patients (Class Indeterminate).
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12. VASOPRESSIN SPECIAL NOTE
May be especially helpful for prolonged down time without ventilation, because Epinephrine response in severe acidosis is blunted.
Vasopressin-not affected by acidosis.
Vasopressin is an effective vasopressor and can be used as an alternative to epinephrine for the treatment of adult shock-refractory VF (Class IIb: acceptable; fair supporting evidence).
Vasopressin is the naturally occurring antidiuretic hormone. In unnaturally high doses—much higher than those needed for antidiuretic hormone effects—vasopressin acts as a nonadrenergic peripheral vasoconstrictor. Vasopressin acts by direct stimulation of smooth muscle V1 receptors. This smooth muscle constriction produces a variety of effects, including pallor of the skin, nausea, intestinal cramps, desire to defecate, bronchial constriction, and in women, uterine contractions. Vasopressin, given intra-arterially, is an approved treatment for bleeding esophageal varices, because it causes vasoconstriction. Vasopressin also dispels bowel gas shadows during abdominal angiography by causing gastrointestinal smooth muscle constriction.
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13. Antidysrhythmics

14. AMIODARONE Dosage: VF/pulseless VT = 300mg IVP/IO
may repeat one time at 150mg IVP/IO
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15. LIDOCAINE Indication:
Consider using if amiodarone not available or allergy to Amiodarone
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16. LIDOCAINE Dosage: 1-1.5 mg/kg/dose x 1
then 0.5 – 0.75 mg/kg q 5-10 min (max. 3 doses or 3mg/kg)
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17. MAGNESIUM SULFATE Dosage: Indications: Torsades de pointes
(Hypomagnesaemia may lead to development of Torsades)
Dosage:
Pulseless arrest w/ Torsades,
= 1 – 2 grams
Epsom Salts
Two observational studies showed that IV Magnesium sulfate can facilitate termination of Torsades de Pointes (irregular/polymorphic V associated with prolonged QT interval). Magnesium sulfate is not likely to be effective in terminating irregular /polymorphic VT in patients with a normal QT interval. The use of group IA antidysrhythmic drugs, which tend to prolong the QT interval, can have disastrous consequences in torsade. Differentiating between these entities, therefore, is critically important.
Sodium channel blockers (group IA) have a local anesthetic-like action on ventricular muscle and on the rapid conduction system. Conduction is slowed and ectopic pacemaker discharge rate is reduced. Group IA agents produce a dose- dependent prolongation of the QRS duration, reflecting slowing of intraventricular conduction even in normal myocardium. They also increase the QTc duration.
Sodium-channel blockers comprise the Class I antiarrhythmic compounds according to the Vaughn Williams classification scheme. These drugs bind to and block the fast sodium channels that are responsible for the rapid depolarization (phase 0) of fast response cardiac action potential. This type of action potential is found in non-nodal, cardiomyocytes (e.g., atrial and ventricular myocytes; purkinje tissue). Because the slope of phase 0 depends on the activation of fast sodium-channels and the rapid entry of sodium ions into the cell (Figure: Na+ in), blocking these channels decreases the slope of phase 0, which also leads to a decrease in the amplitude of the action potential. In contrast, nodal tissue action potentials (SA and AV nodes) do not depend on fast sodium channels for depolarization; instead phase ) depolarization carried by calcium currents. Therefore, sodium-channel blockers have no direct effect on nodal tissue, at least through the blockade of fast sodium-channels.
The direct effect of Class IA antiarrhythmic drugs on action potentials is significantly modified by their anticholinergic actions. Inhibiting vagal activity can lead to both an increase in sinoatrial rate and atrioventricular conduction, which can offset the direct effects of the drugs on these tissues. Although a IA drug may effectively depress atrial rate during flutter, it can lead to an increase in ventricular rate because of an increase in the number of impulses conducted through the atrioventricular node (anticholinergic effect), thereby requiring concomitant treatment with a beta blocker or calcium channel blocker to slow AV nodal conduction. These anticholinergic actions are most prominent at the sinoatrial and atrioventricular nodes because they are extensively innervated by vagal efferent nerves. Different drugs within the IA subclass differ in their anticholinergic actions
A number of doses of magnesium sulfate have been used clinically, and an optimal dosing regimen has not been established.
Three RCT’s did not identify a significant benefit from use of magnesium compared with placebo among patients with VF arrest in the prehospital, intensive care unit and emergency department setting, respectively. Thus, routine use of magnesium sulfate in cardiac arrest is not recommended unless Torsades is present.
4/16/2017

18. Administration in Cardiac Arrest
Follow each medication with a 20 ml flush and elevate arm 1-20 seconds
Anticipate the next medication and have it ready to administer
If we administer medications at the beginning of the cycle of CPR, we can circulate them for 2 minutes

19. Administer Medications at beginning of cycle

20. Interventions NOT Recommended for Cardiac Arrest

21. Atropine
Atropine is only administered in the Bradycardia algorithm, NOT in the Cardiac Arrest Algorithm.
Evidence suggests that use of atropine during asystole or PEA is unlikely to have a therapeutic benefit.
For the treatment of the adult with symptomatic and unstable bradycardia, chronotropic drug infusions are recommended as an alternative to pacing.

22. SODIUM BICARBONATE
Not shown to improve defibrillation success or increase survival rate during cardiac arrest
Rapid ROSC is the key to restoring acid-base balance during cardiac arrest.
Adverse effects:
↓ CPP by ↓ Systemic Vascular Resistance
Creates extracellular alkalosis that will shift the oxyhemoglobin saturation curve and inhibit oxygen release
Produces excess CO2 that contributes to myocardial and cerebral intracellular acidosis
Bicarbonate may compromise CPP by reducing SVR. It can create extracellular alkalosis that will shift the oxyhemoglobin saturation curve and inhibit oxygen release. It can produce hypernatremia. And therefore hyperosmolarity. It produces excess CO², which freely diffuses into myocardial and cerebral cells and may paradoxically contribute to intracellular acidosis.

23. SODIUM BICARBONATE There are some Indications: hyperkalemia
pre-existing metabolic acidosis eg. DKA,
phenobarbital / TCA / aspirin overdose
Dosage: 1 meq/kg
Tissue acidosis and resulting acidemia during cardiac arrest and resuscitation are dynamic processes resulting from no blood flow during arrest and low blood flow during CPR. These processes are affected by the duration of cardiac arrest level of blood flow, and arterial oxygen content during CPR.
In cases of respiratory acidosis, the infused bicarbonate ion drives the carbonic acid/bicarbonate buffer of plasma to the left and, thus, raises the pH. It is for this reason that sodium bicarbonate is used in medically supervised cardiac resuscitation. Infusion of bicarbonate is indicated only when the blood pH is marked (<7.1–7.0) low.
It is used as well for treatment of hyperkalemia. Since sodium bicarbonate can cause alkalosis, it is sometimes used to treat aspirin overdoses. Aspirin requires an acidic environment for proper absorption, and the basic environment diminishes aspirin absorption in the case of an overdose. Sodium bicarbonate has also been used in the treatment of tricyclic antidepressant overdose. Rapid ROSC are the mainstays of restoring acid-base balance during cardiac arrest.
Two studies demonstrated increased ROSC, hospital admission, and survival to hospital discharge associated with the use of bicarbonate, however, the majority of studies show no benefit or found a relationship with poor outcome.
There is little data to support therapy with buffers during cardiac arrest. There is no evidence that bicarbonate improves the likelihood of defibrillation or survival rates in animals with VF arrest.
Sodium bicarbonate may be used in an oral form to treat chronic forms of metabolic acidosis such as chronic renal failure and chronic renal stones. It is used as the medicinal ingredient in gripe water for infants.

24. Calcium
No trial has found Calcium to have a beneficial effect on survival in cardiac arrest
Routine administration is not recommended

25. Also NOT Recommended in Cardiac Arrest:
Fibrinolysis
IV Fluid boluses (except hypovolemic arrest)
Pacing

26. Medications for Post Arrest Care

28. Post Arrest Hypotension Not Responsive to Fluid Bolus
Vasopressor Infusions:
Epinephrine mcg/kg/min
Dopamine 5-10 mcg/kg/min
Norepinephrine mcg/kg/min

29. Medications for Bradycardia

31. ATROPINE Class-anticholinergic or anti-parasympathetic. INDICATION:
Symptomatic Bradycardia (HR< 50 bpm and inadequate for clinical condition)
Dosage:
0.5 mg q 3-5 min
Maximum dose 3 mg
A receptor is cholinergic if it uses acetylcholine as its neurotransmitters
The sympathetic division are the police responders and the parasympathetic division as the court system. The sympathetic division typically functions in actions requiring quick responses. The parasympathetic division functions with actions that do not require immediate reaction.
Chronotropic effects (from chrono-, meaning time, and tropos, "a turn") are those that change the heart rate.
Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate. A dromotrope affects atrioventricular (AV node) conduction. A positive dromotrope increases AV nodal conduction, and a negative dromotrope decreases AV nodal conduction. A lusitrope is an agent that affects diastolic relaxation. Many positive inotropes affect preload and afterload.

32. Atropine for Heart Blocks?
Do not rely on atropine in second degree Mobitz type II - or third-degree AV block.
Use Atropine cautiously in the presence of acute coronary ischemia or MI. An atropine- mediated increase in heart rate may worsen ischemia or increase infarct size.
dilates pupils

33. Transcutaneous pacing
Atropine
If Atropine ineffective: (define ineffective)
Transcutaneous pacing or
Epinephrine infusion
Dopamine infusion
Atropine is a parasympatholytic, we can also call it a parasympathetic antagonist or parasympathetic blocker or an anticholinergic medication.
Blocking the muscarinic receptors causes the heart rate and contractility to increase, dilation of the bronchioles and less production of secretions in the body.
This is the exact effect of atropine, a drug we use to counteract too much parasympathetic activity such as from over-stimulation of the vagus nerve or the effects of certain chemical warfare nerve agents and organophosphate poisoning.

34. Transcutaneous pacing
HR X SV = CO
Infusion of beta adrenergic agonist with rate accelerating effects [dopamine or epinephrine] is now recommended as an equally effective alternative to external transcutaneous pacing when Atropine is ineffective.
Transcutaneous pacing or
Epinephrine infusion
Dopamine infusion
Pacing will increase HR and therefore CO the quickest. Even though Epi and Dopamine are alternatives, the time it takes to get a therapeutic effect makes them less attractive than pacing.

35. EPINEPHRINE Infusion for Bradycardia Dosage: 2-10 mcg/min
Remember: 3 different Epinephrine dosages
Cardiac arrest: 1 mg q 3-5 minutes
Post arrest: mcg/kg/min
Bradycardia: 2-10 mcg/min

36. DOPAMINE Bradycardia Dose: 2-10 mcg/kg/min
Remember 2 Dopamine Dosages:
Bradycardia: 2-10 mcg/kg/min
Post Arrest: 5-10 mcg/kg/min
Adrenaline (epinephrine) reacts with both α- and β-adrenoreceptors, causing vasoconstriction and vasodilation, respectively. Although α receptors are less sensitive to epinephrine, when activated, they override the vasodilation mediated by β-adrenoreceptors. The result is that high levels of circulating epinephrine cause vasoconstriction. At lower levels of circulating epinephrine, β-adrenoreceptor stimulation dominates, producing an overall vasodilation.
α receptors have several functions in common, but also individual effects. Common (or still unspecified) effects include:
Vasoconstriction of arteries to heart (coronary artery).
Vasoconstriction of veins
β1 receptor functions include:
Increase cardiac output, by raising heart rate (positive chronotropic effect), increasing impulse conduction (positive dromotropic effect), and increasing contraction (positive inotropic effect), thus increasing the volume expelled with each beat (increased ejection fraction). β² and β³ little to no cardiac impact.
Beta-1 vs Beta-2 receptor location "You have 1 heart and 2 lungs“
Beta 1 receptors - heart muscle contraction Beta 2 receptors - smooth muscle relaxation - bronchodilator Alpha 1 receptors - smooth muscle contraction Alpha 2 receptors - smooth muscle contraction and neurotransmitter inhibition Beta-1 are therefore primarily on heart Beta-2 primarily on lungs
All these terms mean the same; it means they block the action of acetylcholine at the parasympathetic receptors. The effect of blocking any receptor causes the opposite effect we would expect from stimulating the receptor.
Ipratroprium is another example of a parasympathetic blocker medication but this one is inhaled so most of the effect occurs in the lungs, and when we block parasympathetic receptors in the lungs we cause the bronchioles to dilate and decrease production of secretions like mucus. That makes ipratroprium useful in the patient with COPD who produces excessive pulmonary mucous and in combination with albuterol for any wheezing patient.
But remember that the primary rescue medication for bronchospasm is a Beta 2 agonist such as albuterol although ipratrorium is often added and is available as a combination inhaler with albuterol called Combivent.
It is important to remember that it is the balance between the sympathetic and parasympathetic nervous system that keeps our automated body functions in balance and working properly. Outside forces, including drugs, medications or poisons can change the functioning of the autonomic nervous system. And it is wise to keep in mind that all medications are potential toxins that have some beneficial side effects.
In summary, if you are familiar with the actions of the autonomic nervous system receptors then you can easily recall the therapeutic actions of many commonly used medications and their overdose presentation as well as certain poisons and frequently abused drugs.
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37. Medications for Tachycardia

39. Narrow Regular Rhythms

40. ADENOSINE
Chemically converts any re-entry arrhythmias that require the AV or SA node for the re-entry
Indications:
- PSVT
- diagnosing other supraventricular tachycardia (A-Flutter)
Do not use Adenosine for irregular rhythms- May cause V-Fib
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41. ADENOSINE Dosage: 6mg Rapid IVP (IV Site close to heart)
May Repeat once at 12 mg
Follow each dose w/ 20 ml flush (stopcock)
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42. ADENOSINE Side Effects: - flushing - chest pain
- brief asystole / bradycardia
- malaise
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43. ADENOSINE Considerations:  dose to 3mg if:
- Administration through Central Line
- Heart transplant patient- more sensitive to adenosine
- Taking Dipyridamole or Tegretol
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44. Narrow Irregular Tachycardia

45. Calcium Channel Blockers
Common Calcium Channel Blockers Diltiazem (Cardizem) Verapamil
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46. ß-Blockers Common ß-Blockers Propranolol Metoprolol Atenolol 4/16/2017
Beta blockers (e.g. metoprolol) or combined alpha and beta adrenergic blocking agents(e.g. laetalol) should be avoided in patients with a history of cocaine abuse. They can cause an unopposed alpha-adrenergic mediated coronary vasoconstriction, causing the worsening of myocardial ischemia and hypertension.
4/16/2017

47. Wide Complex Regular Tachycardia

48. ADENOSINE
Adenosine can now be considered in the initial assessment and treatment of stable, undifferentiated regular, monomorphic wide-complex tachycardia.
If arrhythmia is not due to reentry adenosine will not terminate arrhythmia and VT Confirmed
Do not use with wide complex tachycardias that are unstable, irregular, or polymorphic – may cause VF.
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49. AMIODARONE Wide Complex Stable Tachycardia's Dose:
- 150mg IV over 10 min. diluted in 100ml D5W
Refractory VF or pulseless VT may be caused by an acute coronary syndrome, in which case percutaneous coronary intervention can be performed if the patient is successfully resuscitated and the procedure is feasible. Following cardiac arrest the ECG may be insensitive for ACS; cardiology consultation is needed for patients with ROSC.
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50. PROCAINAMIDE Indications: - Stable wide complex tachycardia
Dose: 15 mg/kg over minutes
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51. PROCAINAMIDE Stop infusion of bolus when: 1. Arrhythmia suppressed
2.  BP
3. QRS complex widened by 50% of original width
4. 17 mg/kg has been administered
The loading dose is 100 mg IV bolus given slowly over five minutes. The maximum dose is 17 mg/kg. Use is discontinued when dysrhythmia is suppressed, or if hypotension ensues, the QRS complex widens by 50% or more, or the maximum dose is achieved.
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52. Medications for Acute Coronary Syndromes

54. MONA
Oxygen
Start at 4 LPM and Titrate to maintain O2 saturation <94%
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55. MONA Aspirin – 160mg – 325 mg (absorbed better if chewed)
- Aspirin (non-enteric coated) should be administered to ALL patients suspected of acute coronary syndromes, unless there is a true aspirin allergy or recent GI bleed.
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56. MONA Nitroglycerin SL 0.4mg tab q5min x 3 Dosage: Strong Cautions:
Right Ventricular infarct Phosphodiestrace inhibitors in last hours
RV infarction or ischemia may occur in up to 50% of patients with inferior wall MI. Be suspicious of patients with inferior wall infarction, hypotension, and clear lung fields. Patients with RV dysfunction and acute infarction are dependent on maintenance of RV filling pressure ( RVEDP) to maintain cardiac output. Thus nitrates, diuretics, and other vasodilators should be avoided because severe hypotension may result (treat with IVF bolus)
NTG contraindicated with phosphodiesterase inhibitor use (causes profound hypotension that is refractory to pressors) RV infarct (preload dependent) or bradyarrhythmias.
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57. MONA Morphine – Chest pain unresponsive to nitrates Dosage:
2-4 mg repeat PRN -
Side Effects: respiratory depression  BP
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58. USE of PCI
PCI is treatment of choice when it can be performed < 90 minutes door to balloon time
PCI is treatment of choice If facility not capable of PCI, but transfer to PCI facility can still accomplish door to balloon time of < 90 minutes

59. Fibrinolytic Therapy
Breaks up the fibrin network that binds clots together
Indications: ST elevation >1 mm in 2 or more contiguous leads or new LBBB or new BBB that obscures ST
Time of symptom onset must be <12 hours
Caution: fibrinolytics can cause death from brain hemorrhage
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60. Adjunctive Treatments
IV Nitroglycerin
Heparin
Clopidogrel (Plavix)
Beta Blockers
ACE Inhibitors
Statin Therapies

61. Medications for Stroke

63. Fibrinolytic Therapy
Breaks up the fibrin network that binds clots together
Indications: Stroke symptoms > 1hour with normal CT Scan
Time of symptom onset must be < 3 hours (now 4 ½)
Caution: fibrinolytics can cause death from brain hemorrhage
TPA is the only current approved medication
4/16/2017

64. Questions?