Pharm Flashcards by Samar Azzaidani

A patient comes in with HR of 35, BP 85/50, and AMS. How do you treat?

Atropine.
First dose: 0.5 mg
Repeat q 3-5 min.
Maximum: 3mg

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HR of 35, BP 85/50, and AMS. No improvement with first line treatment. What’s your next best step?

Transcutaneous pacing
Epinephrine
Dopamine

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You decide to use an antimuscarinic to treat a patient with __. What is this drug, its AE, MOA, and its indication?

Bradycardia

Drug: Atropine

MOA: Antagonizes parasympathetic vagal tone

AE:

Mouth dryness, - Blurred vision
Photophobia
Tachycardia

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Dopamine:

Indication
MOA
AE

Indication: Bradycardia

MOA: Beta-1 & alpha-1 agonist

AE: cardiac arrhythmias

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Epinephrine

Indication
MOA
AE

Indication: bradycardia

MOA: beta-1 & alpha-1 agonist

AE:
- cardiac arrhythmias, - excessive rise in BP

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A patient comes in with HR of 165, BP 85/50, and AMS. How do you treat?

Synchronized cardioversion

Consider adenosine if regular narrow complex

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A patient comes in with HR of 165 and a wide QRS greater than/equal to 0.12 seconds. How do you treat?

IV
12 lead ECG
If regular and monomorphic: adenosine
antiarrhythmic infusion

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A patient comes in with HR 0f 165. No hypotension, AMS, or wide QRS. How do you treat?

IV access
12 lead ECG
Adenosine (if regular)
Beta-blocker or CCB

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A patient comes in with regular narrow complex tachycardia. He is symptomatic but stable. What do you do prior to meds?

Valsalva maneuver.

MOA: increases vagal response by slowing AV node conduction

Converts SVTs to sinus rhythm

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A patient comes in with regular narrow complex tachycardia. He is symptomatic but stable. You give adenosine. MOA? CI? AE?

MOA: endogenous purine nucleoside

activates Ach-sensitive K+ current in SA and AV nodes
hyperpolarization and suppression of Ca2+ dependent AP
Transiently blocks conduction through AV node

CI: asthma

AE:

transient flushing
dyspnea
bronchospasm
chest pressure

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If adenosine fails to convert a regular narrow complex tachycardia, what should you consider?

Other etiologies for this rhythm, including A-flutter or a non-reentrant SVT

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A patient comes in with irregular narrow complex tachycardia. They are symptomatic but stable. What is your first step?

Rate control

Goal: HR <100 beats/min via BB or non-DNP CCB OR digoxin

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MOA of Beta blockers?

Reduce effects of circulating catecholamines

Reduce HR

Reduce AV node conduction and BP

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MOA of non-DNP CCB?

Slow AV node conduction

Increase AV node refractoriness

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MOA of digoxin?

Enhances parasympathetic tone in tachycardia.

Since it’s a positive inotrope, it is useful in those with decompensated HF with reduced EF

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A patient presents with A-fib and is hemodynamically unstable. What do you do?

Synchronized cardioversion

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A patient presents with hemodynamically stable A-Fib. What do you do?

Nothing - most AF spontaneously convert to sinus in 24-48 hours

A patient presents with ventricular tachycardia and has a pulse. After checking ABC and monitoring via ECG, BP, and oximetry, you determine the patient is stable and has a monomorphic VT. What do you do next?

Administer amiodarone IV 150 mg over 10 min

Max dose of 2.2 g/24 hours

A patient presents with ventricular tachycardia and has a pulse. After checking ABC and monitoring via ECG, BP, and oximetry, you determine the patient is stable and has a polymorphic VT/ torsades de pointes. What do you do next?

Defib

Correct electrolyte imbalances

Mg load

Overdrive pacing or isoproterenol

A patient presents with ventricular tachycardia and has a pulse. After checking ABC and monitoring via ECG, BP, and oximetry, you determine the patient is unstable. What do you do next?

Immediate direct-current cardioversion x 3 attempts

Then amiodarone IV 300 mg over 2 min –> repeat shock

What are some AEs of amiodarone?

Pulmonary fibrosis

Cornea & skin discoloration

Hypo/hyperT

Peripheral neuropathy

Photosensitivity

Vasodilation

Arrhythmias (rare)

A patient presents with ventricular tachycardia. Amiodarone does not work. What is the second line treatment for VT?

Procainamide - 20-50 mg/min until arrhythmia is suppressed.

Max dose: 17

What are the AEs of procainamide and what is its indication?

AE:

N/V
Anorexia
Rash
Granulocytosis
Torsades de Pointes
Lupus like reaction

Indication: SVT and VT

A patient comes in for VT. Both amiodarone and procainamide don’t work. What’s your next line treatment?

IV lidocaine 100-200 mg

What are some AEs of lidocaine and what is its indication?

AEs: - visual disturbances - tremor - seizure - drowsiness - hallucination - coma - asystole & hypotension - N/V Indication: VT and VFib

A patient comes in with palpitations and HR 255. Synchronized cardioversion was attempted but unsuccessful. Amiodarone and a repeat cardioversion was attempted, which was followed by a recurrence of a tachycardia determined to be pre-excited AFib. How is a hemodynamically stable patient with pre-excited Afib treated?

Use an AV nodal blocking agent to enhance conduction over the accessory pathway exacerbating tachycardia, collapsing ventricular fibrillation. Tx with Ibutilide or IV procainamide

MOA and indication for ibutilide.

Indication: AFib with accessory pathway - hemodynamically stable MOA: - class III antiarrhythmic drug - prolongs AV node refractoriness - prolongs His-Purkinje system refractoriness

MOA and indication for procainamide.

Indication: - AFib with accessory pathway MOA: - class 1A antiarrhythmic - decreases excitability & conduction velocity of atrial and ventricular myocardium without any AV nodal blocking effect

A patient presents with cardiac arrest. You start CPR. The AED determines that the rhythm is not shockable. What is the patient in and how do you proceed?

Asystole/PEA CPR 2 minutes & Epinephrine q 3-5 minutes

A patient presents with cardiac arrest. The AED determines that the rhythm is shockable. What is the patient in and how do you proceed?

VP/pVT 1. CPR 2 min 2. Shock if rhythm is shockable 3. Epinephrine q 3-5 min 4. Shock if rhythm is shockable 5. CPR 2 min + amiodarone or lidocaine

What receptors does epinephrine stimulate and how does this affect BP?

Increases systolic BP: - Beta-1 mediated: increases HR and ventricular contractility Increases diastolic BP: - alpha-1 and 2 receptor mediated: vasoconstriction Dilates skeletal muscle blood vessels by stimulating Beta-2 receptors.

If a patient is in hypovolemic shock, what would we expect to see in terms of preload, CO, and SVR? Treatment?

**Preload: down** CO: up SVR: up Tx: IVF

If a patient is in cardiogenic shock, what would we expect to see in terms of preload, CO, and SVR? Treatment?

Preload: up **CO: down** SVR: up Tx: Inotropes & revascularization

If a patient is in distributive shock (septic, neurogenic), what would we expect to see in terms of preload, CO, and SVR? Treatment?

Preload: down CO: up **SVR: down** Tx: vasopressors & IVF

When is a swan-ganz catheter used?

When congestion and perfusion can't be determined from a clinical assessment or when symptoms persist despite empiric adjustment of standard therapies. It's used for direct pressure measurments but is not a first line tool.

What are examples of inotropes and when are they used?

Ex: - dopamine - dobutamine - milrinone Used: - severe systolic dysfunction - symptomatic hypotension - worsening renal function

What is the MOA of dopamine and what is its indication?

Indication: hypotension MOA: Beta adrenergic agonist - increases adenylate cyclase - increases cAMP Vasodilation, increases contratility

What is the MOA of dobutamine and its indication?

Indication: hypotension MOA: - increases Ca2+ = increases contractility Decreases SVR

If a patient is cold and wet, what do we give them?

Inotropes Decreases SVR and PVR --> hypotension (rare)

What is the MOA of milrinone and what is its indication?

MOA: decreases PDE, which increases cAMP

If a patient presents as cardiogenic + significant hypotension, how do you treat?

High dose dopamine and NE These preserve end-organ perfusion but increase afterload