Drugs in CPR

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Drugs in CPR By M.H.Farjoo M.D. , Ph.D. Shahid Beheshti University of Medical Science

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Transcript of Drugs in CPR

Page 1: Drugs in CPR

Drugs in CPR

By

M.H.Farjoo M.D. , Ph.D.Shahid Beheshti University of Medical Science

Page 2: Drugs in CPR

M.H.Farjoo MD, Ph.D

Cardiac Arrest

Epinephrine is a mixed α- and β-agonist that increases blood pressure, coronary perfusion pressure,and cerebral blood flow.

it is the mainstay of pharmacologic therapy in the pulseless patient, regardless of the underlying rhythm.

Epinephrine may be given through an endotracheal tube if IV access cannot be obtained. (2.0-2.5 mg in 10 cc of normal saline).

High-dose epinephrine in adults is no longer recommended.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Vasopressin (ADH) causes peripheral vasoconstriction

It also constricts coronary, cerebral, and renal vasculature.

vasopressin has no benefit over epinephrine in cardiac arrest.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Dopamine exhibits dopaminergic and both α- and β-adrenergic effects.

Doses > 20 μg/kg/min may have adverse effects on splanchnic perfusion and should be avoided.

If hypotension persists after optimization of filling pressures, norepinephrine or dobutamine should be considered.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Norepinephrine affects α-receptors in the vasculature and β1-receptors of the heart.

It causes peripheral vasoconstriction and increased heart rate and contractility.

It is used in severe shock and is recommended for management of hypotension when systolic pressures are less than 70 mm Hg.

The starting infusion rate is 0.5-1.0 μg/min and titrated to effect, with a maximal infusion rate of 30 μg/min.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Dobutamine has potent β1-agonist properties. it improves myocardial contractility and increase

cardiac output. It is the agent of choice in patients with systolic blood

pressure of 70-100 mm Hg. Paradoxically it can worsen hypotension in patients

with inadequate preload. In addition, it can provoke tachyarrhythmias. It is run as an IV infusion of 2-20 mg/kg/min.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Adenosine is a potent but short-lived AV nodal blocking agent.

Along with vagal maneuvers, it is considered first-line therapy in paroxysmal supraventricular tachycardia (PSVT) secondary to a reentrant-type conduction defect.

Adenosine should not be used as an aid in differentiating between PSVT with aberrant conduction and VT.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

It is associated with a prolonged sinus pause. The initial dose is 6 mg, given as a rapid bolus

which can be increased to 12 mg IV. If there is no response, this dose may be

repeated in 1-2 minutes

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Amiodarone is useful in treating both supra- and ventricular tachydysrhythmias.

For VF and pulseless VT, the initial dose is 300 mg IV, which can be followed with a second dose of 150 mg if the arrhythmia persists.

While amiodarone has been found to increase the rate of survival from cardiac arrest, it has not been shown to increase survival to hospital discharge.

Amiodarone is a second-line agent for PSVT and can be used when adenosine fails.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest Atropine is useful in the treatment of symptomatic

bradycardias that are due to increased parasympathetic tone.

Atropine should not be used when infranodal pathology is suspected such as with second-degree AV blocks.

Atropine is indicated in the setting of asystole and bradycardic.

Atropine is ineffective in the setting of previous heart transplant and may worsen ischemia during a myocardial infarction.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest β-Blockers are indicated for SVT for rate control in patients

with preserved left ventricular function. Atenolol and metoprolol are β1-blocking agents available in

both IV and oral formulations. Esmolol is a short-acting β1-agent that must be given in a

bolus and then maintained through a continuous infusion. this may be advantageous in patients who may respond

negatively to β2-blockade (e.g., patients with COPD). If an adequate response is not achieved after 5 minutes, the

loading dose may be repeated and the infusion rate doubled.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Calcium channel blockers (i.e., diltiazem and verapamil) are also indicated for rate control in SVT.

They slow AV nodal conduction and prolong the AV nodal refractory period.

they are contraindicated in atrial fibrillation or atrial flutter with rapid ventricular response when an accessory pathway such as Wolf-Parkinson-White syndrome exists.

Diltiazem is better tolerated in patients with impaired left ventricular function.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Lidocaine is commonly used for ventricular rhythms, both stable and unstable.

Its use has largely been replaced by amiodarone. The initial dose in VF and pulseless VT is 1.0-1.5

mg/kg. Half of this dose may be repeated every 5-10 minutes,

with a maximal total dose of 3 mg/kg. If successful in terminating the offending rhythm, a

maintenance infusion of 3-5 mg/min is administered.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest

Magnesium is indicated for: those suspected to have a low magnesium level recurrent ventricular dysrhythmias those with torsades de pointes.

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M.H.Farjoo MD, Ph.D

Cardiac Arrest Procainamide is capable of suppressing both atrial

and ventricular arrhythmias. It may be used in treatment of atrial fibrillation and

atrial flutter (even in the presence of WPW syndrome) in patients with preserved left ventricular function.

procainamide may be used in SVT when vagal maneuvers and adenosine are ineffective.

Its use should be avoided in patients with long QT intervals or when drugs that prolong the QT interval, such as amiodarone, have already been administered.

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Drug Name Adult Dose Pediatric Dose Indications Frequency Effects

Epinephrine 1 mg IVOR2-5 mg IV via ETT

0.01 mg/kg IV or 10OR0.1 mg/kg via ETT

Any pulseless rhythms

Every 3-5 min Increases perfusion to myocardium and to brain by increasing peripheral vascular resistance

Vasopressin 40 units IV Not indicated VF, pulseless VT Single dose, may be followed at 10 min by epinephrine

Increases peripheral vascular resistance

Amiodarone For VF or pulseless VT: 300 mg IV push

For VF or pulseless VT: 5 mg/kg IV push

VF, pulseless VT, VT with a pulse, SVT

May use second dose of 150 mg for recurrent VF/VT. In children may be repeated in 5 mg/kg doses to a total of 15 mg/kg

Predominately class III antiarrhythmic, but has sodium, potassium channel, and α and β receptor blockade

Lidocaine 1.0-1.5 mg/kg IV push

Same VF, pulseless VT, VT with a pulse

Second and subsequent doses of 0.75 mg/kg every 5 min to a total dose of 3 mg/kg

Class IB antiarrhythmic; suppresses ventricular automatically and electrical conduction

Magnesium 1-2 g IV slow push 25-50 mg/kg IV slow push

Torsade de pointes, known hypomagnesemia

Single dose Can cause cutaneous flush, apnea, and hyporeflexia, if given too quickly

ETT, endotracheat tube; IO, intraosseoulsy; IV, intravenously; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.*Agents are listed from most effective (and most commonly used) to least.

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Procainamide 17 mg/kg IV slow bolus at maximum rate of 50 mg/min

15 mg/kg IV load; 3-6 mg/kg over 5 min, not to exceed 100 mg/dose

VT with a pulse Continue infusion (4 mg/min) until QRS widening >50%, dysrhythmia terminated, onset of hypotension; or 17 mg/kg infused

Decreases myocardial excitability and conduction velocity

Atropine Perfusing patients: 0.5 mg IV push q 5 min, to maximum of 3 mgPulseless patients: 1.0 mg IV push q 5 min, to maximum of 3 mg

0.02 mg/kg: minimum dose of 0.1 mg

Bradycardia, asystole

May be repeated once up to maximum dose of 3 mg

Parasympatholytic, eliminates vagal tone

Adenosine 6 mg rapid IV push through proximal peripheral line; central line dose is one-half

0.1 mg/kg rapid IV push; maximum dose, 6 mg

SVT If needed, second dose of 12 mg (pediatric, double initial dose up to 12 mg); third dose of 12-18 mg

Endogenous nucleoside causing brief asystole allowing dominant pacemaker to resume function

Diltiazem 0.25 mg/kg to a maximum dose of 20 mg IV push over 2 min

Same SVT Second dose of 0.35 mg/kg, maximum dose of 25 mg, at 15 min; after conversion, start diltiazem drip at 5-15 mg/h

Calcium channel blocker

ETT, endotracheat tube; IO, intraosseoulsy; IV, intravenously; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.*Agents are listed from most effective (and most commonly used) to least.

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Esmolol 500 ug/kg bolus over 1 min

100-500 ug/kg bolus over 1 min

SVT May give another bolus if desired effect is not achieved; start drip 50 ug/kg/min

β-Blocker (short acting)

Atenolol 5 mg IV over 5 min

Not indicated SVT, myocardial infarction

Repeat in 10 min, then give 50-mg oral load

β-Blocker (β1 selective)

Metoprolol 5 mg IV push Not indicated SVT, myocardial infarction

Repeat twice at 5-min intervals, then give 50-mg oral load

β-Blocker (β1 selective)

Dopamine 2-20 ug/kg/min Same Hypotension Low doses are predominantly β; higher doses become predominantly α

Inotropic agent/vasopressor (combined α- and β-agonists)

ETT, endotracheat tube; IO, intraosseoulsy; IV, intravenously; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.*Agents are listed from most effective (and most commonly used) to least.

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Dobutamine 2-20 ug/kg/min Same Hypotension Titrate to effect Inotropic agent (β-agonist)

Norepinephrine

Start at 8-12 ug/min, then titrate to 2-4 ug/min for maintenance; maximum dose of 30 ug/min if hypotension unresponsive to lower doses

0.05-2 ug/kg/min Hypotension Titrate to effect Vasopressor (predominately an α-agonist)

Phenylephrine 100-500 ug bolus IV

0.1-0.5 ug/kg/min Hypotension Every 5 min until desired effect, then continuous infusion of 40-180 ug/min

Vasopressor (pure α-agonist)

ETT, endotracheat tube; IO, intraosseoulsy; IV, intravenously; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.*Agents are listed from most effective (and most commonly used) to least.

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M.H.Farjoo MD, Ph.D

Drugs for Intubation

Many patients in the emergency department can be intubated without the use of pharmacologic intervention other than oxygen.

By pharmacologic adjuncts may dramatically reduce the difficulty of intubation.

Local, topical, or regional anesthesias are usually not considered options for an emergently compromised airway.

Occasionally, sedation alone may be useful in preparing for intubation.

For a semiobtunded or combative patient, use of neuromuscular blockade with sedation, provides rapid control of the airway.

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Drugs for Intubation

Drugs that induce apnea must be used by or under the direct supervision of experienced clinicians.

They should be prepared to obtain a surgical airway in the event of failed intubation.

Equipment necessary for intubation and surgical airway must be prepared in advance

They must be available at the bedside before the patient is sedated or anesthetized

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Drugs for Intubation in awake or semiconscious patients a short-acting

sedative is given to decrease agitation. A rapid-acting neuromuscular blocker is given to

paralyze the patient. The patient is intubated immediately after paralysis.

Further sedation or paralysis may then be effected as indicated.

During the short period when the patient is paralyzed and not intubated, the airway must be protected from aspiration with cricoid pressure.

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Rapid-sequence intubation protocol.

Preoxygenate with 100% oxygen. (Use bag-valve-mask ventilatory assistance only as needed.)

Give rapid intravenous injection of sedative.*

For trauma patients: Maintain in-line cervical traction from induction and until cervical collar can be replaced after the endotracheal tube has been secured.

Give rapid intravenous injection of succinylcholine,+ 1-2 mg/kg (unless contraindicated).

Initiate cricoid pressure and stop bag-valve-mask ventilation.

Observe for fasciculations followed by apnea.

Immediately intubate upon onset of apnea.

Begin ventilation.

Inflate endotracheal tube cuff and release cricoid pressure.

Confirm tube position clinically to auscultate breath sounds, use end-tidal CO2 detector.

Secure tube.

Provide additional sedation and paralysis as indicated.*Sedative drug choices: Etomidate, 0.3 mg/kg; Methohexital, 0.5-1 mg/kg; Midazolam, 0.1-0.3 mg/kg; Fentanyl, 1-5 mg/kg; Ketamine, 1-2 mg/kg; Thiopental, 1-4 mg/kg.+Alternative neuromuscular blocker: Vecuronium, 0.1-0.25 mg/kg; Rocuronium, 0.6 mg/kg. (Use only when succinylcholine is contraindicated.)

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M.H.Farjoo MD, Ph.D

Succinylcholine Succinylcholine is a depolarizing neuromuscular blocking

agent. The dose is 1.0-1.5 mg/kg in adults, 1.5-2.0 mg/kg in children. Onset is 60 seconds to complete relaxation and duration is 5-

10 min. It is drug of choice for the RSI protocol under most

circumstances owing to rapid onset, complete muscular relaxation, and short duration.

One single dose suffices in emergency department setting and is well tolerated.

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M.H.Farjoo MD, Ph.D

Succinylcholine

It is contraindicated in : If there is risk factors for hyperkalemia. Hereditary pseudocholinesterase deficiency (1 in

2800 patients) Penetrating ocular trauma or glaucoma. Known family or personal history of malignant

hyperthermia. Hypersensitivity to succinylcholine.

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Succinylcholine

Adverse effects and precautions Causes arrhythmias, and hyper- and hypotension.

Use with care in setting of irritable myocardium. Fasciculations Hyperkalemia Pseudocholinesterase inhibition may occur in

pregnancy, in renal and hepatic insufficiency

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Succinylcholine

Adverse effects and precautions (Cont’d) Malignant hyperthermia (occurs in 1 in 50,000 patients) Histamine release (bronchospasm or anaphylactoid

reaction). IOP is elevated during fasciculations. ICP may increase. Intragastric pressure may increase; use cricoid pressure

until endotracheal tube cuff is inflated. Always use sedation with alert patients

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Vecuronium

Vecuronium is a nondepolarizing neuromuscular blocking agent.

Standard dose is 0.1 mg/kg. To achieve rapid intubating conditions, 0.25 mg/kg may be used.

Onset is dose dependent; standard doses achieve paralysis in 3-5 minutes, larger doses in 1-1.5 min.

Duration is dose dependent; standard doses last 20-40 minutes and larger dose prolong paralysis 2-3 times the usual duration.

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Drugs for Intubation Several agents may be added to the RSI protocol under

specific circumstances. Atropine, 0.01-0.02 mg/kg given immediately before the

sedative, attenuates the vagal bradycardia associated with succinylcholine.

Children, who tend to be more sensitive to the bradycardic and hypotensive effects of succinylcholine, benefit from pretreatment with atropine.

Therefore all children younger than 10 years should be pretreated with atropine before succinylcholine is administered.

Pretreat adults with bradycardia and those receiving a second dose of succinylcholine.

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Drugs for Intubation Lidocaine, 1.5 mg/kg given 1 minute before

intubation, may attenuate elevations in ICP associated with succinylcholine and intubation.

It may have some protective effect against laryngospasm and ventricular arrhythmias during intubation.

If pain control is important, morphine sulfate, 0.1 mg/kg or fentanyl, 1-2 μg/kg IV should be added after intubation

barbiturates have little analgesic effect and neuromuscular blockers have none.

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Thank youAny question?

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M.H.Farjoo MD, Ph.D

CARDIAC ARREST FIBRINOLYTIC THERAPY Most cases of sudden cardiac death are secondary to an

intravascular thrombosis, with the majority of these cases related to either an intracoronary thrombus or massive pulmonary embolus. The primary goal in treating these patients is restoring perfusion immediately. In the case of myocardial infarction, the two methods to restore coronary blood flow are fibrinolytic therapy and percutaneous coronary intervention (PCI). Multiple studies have found that in centers that can provide rapid PCI, there is improved outcome and a decreased rate of reocclusion when compared to fibrinolytic therapy. However, the presentation to PCI should occur within 90 minutes.

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CARDIAC ARREST FIBRINOLYTIC THERAPY : (edaneh) Most facilities are

unable to perform PCI, and many transfer the patient to centers with catheterization capabilities. If the patient is unable to undergo PCI in the 90-minute period, initiation of fibrinolytic therapy should be initiated if not contraindicated. Ideally, if fibrinolytic therapy is to be initiated, it should occur within 30 minutes of the patient's presentation. Maximum benefit is seen in those patients who present within 3 hours from the onset of symptoms. There are current trials in which thrombolytics are given by properly trained EMS personnel. However, there has been no demonstrated improvement in survival to hospital admission or discharge.

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Vecuronium 4. Indications and advantages— a. One of the NDNMBs that can be used when succinylcholine is

contraindicated. b. Relative short duration allows neurologic reevaluation and provides

satisfactory paralysis for procedures such as computed tomography scan in an emergency setting.

c. Minimal cardiovascular effects at usual doses. d. Reversible after partial recovery (evidence of head lift, respiratory

effort, or muscle twitch response) with neostigmine, 0.04 mg/kg intravenously. Atropine, 0.02 mg/kg intravenously, must also be administered to prevent muscarinic side effects.

e. Does not cause fasciculations or elevate intracranial pressure.

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Vecuronium 5. Contraindication—Know hypersensitivity to vecuronium. 6. Adverse effects and precautions— a. Reduce dosage in patients with myasthenia gravis to avoid

prolonged blockade. b. Maintain cricoid pressure until inflation of endotracheal

tube cuff. c. Must use sedation or anesthesia in awake patients. d. Block is prolonged by aminoglycosides, lithium,

quinidine, lidocaine, and propranolol and in hypermagnesemia, hyperkalemia, dehydration, hypothermia, and respiratory acidosis.

e. Use during pregnancy only if clearly indicated.

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Choking pic.