Index
Module 11 • Cardiology
Cardiovascular Critical Care I
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Data Tables
Cardiovascular Critical Care I
Sajni V. Patel ~3 min read Module 11 of 20
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Cardiovascular Critical Care I

(4)Concentration-dependent protein binding includes about 25% bound to albumin and

about 50% bound to α1-acid glycoprotein (AAG).

(5)As AAG increases and decreases as an acute-phase reactant within the first 12–72

hours after certain stresses (e.g., acute MI, HF exacerbation, trauma), an unsuspected

variation can occur in free lidocaine concentrations. Because of the toxicity profile

and concentration-dependent efficacy, routine concentrations should be monitored in

most patients if lidocaine is to be continued beyond 24 hours (particularly in patients

with advanced age, HF, liver disease, and renal dysfunction).

Table 8. Lidocaine Concentrations and Toxicity Symptoms

Total Serum

Concentration (mg/L)

Toxicity

< 1.5–5

Typical therapeutic goal concentration

> 5–8

Increasing risk of light-headedness, confusion, dizziness, tinnitus, twitching,

tremor, blurred or double vision, hypotension, and bradycardia

> 8

High risk of seizures, respiratory depression, hypotension, bradycardia, AV nodal

blockade, decreased cardiac output

AV = atrioventricular.

(e)Procainamide
(1)Indicated for the treatment of hemodyanmically stable, sustained, monomorphic

VT and atrial fibrillation with pre-excitation (Circulation. 2017;138 (13):e272-391;

Circulation. 2024;149(1):e1-156)

(2)Compared to amiodarone, procainamide has been shown to be more effective

at terminating monomorphic VT with fewer cardiac complications (Eur Heart J

2017;38:1329-35).

(3)Procainamide should be avoided in patients with severe HF, acute MI, and end-stage

renal disease.

(4)Procainamide is a sodium channel blocking antiarrhythmic, so close monitoring

because of the QRS complex is necessary during treatment. Procainamide should be

discontinued if the QRS widens by more than 50%.

(5)Close monitoring of the QT/QTc is also important because both procainamide and

its active metabolite, N-acetyl procanamide, have potassium channel blocking

properties.

(f)Digoxin
(1)Digoxin may be considered to slow a rapid ventricular response in patients with ACS

and AF associated with severe LV dysfunction and HF or hemodynamic instability

(Circulation 2019;140:e125-51).
(2)Use for AF should be done with caution. Two published retrospective trials have

shown considerable evidence for increased hospitalization rates and risk of death.

71% increased risk of death (HR 1.71; 95% CI, 1.52–1.93) and 63% increased risk

of hospitalization (HR 1.63, 95% CI, 1.56–1.71) (Circ Arrhythm Electrophysiol

2015;8:49-58)

Digoxin-treated patients had higher mortality rates (95 vs. 67 per 1000 person-

years; p<0.001), and use was independently associated with mortality, despite

multivariate adjustment (HR 1.26; 95% CI, 1.23–1.29, p<0.001) (J Am Coll

Cardiol 2014;64:660-8).

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