Pharm Flashcards
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
HR of 35, BP 85/50, and AMS. No improvement with first line treatment. What’s your next best step?
- Transcutaneous pacing
- Epinephrine
- Dopamine
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
Dopamine:
- Indication
- MOA
- AE
Indication: Bradycardia
MOA: Beta-1 & alpha-1 agonist
AE: cardiac arrhythmias
Epinephrine
- Indication
- MOA
- AE
Indication: bradycardia
MOA: beta-1 & alpha-1 agonist
AE:
- cardiac arrhythmias, - excessive rise in BP
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
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
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
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
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
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
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
MOA of Beta blockers?
Reduce effects of circulating catecholamines
Reduce HR
Reduce AV node conduction and BP
MOA of non-DNP CCB?
Slow AV node conduction
Increase AV node refractoriness
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
A patient presents with A-fib and is hemodynamically unstable. What do you do?
Synchronized cardioversion
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
- CPR 2 min
- Shock if rhythm is shockable
- Epinephrine q 3-5 min
- Shock if rhythm is shockable
- 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
