· Ropivacaine’s action
· Calculations
· CNS
· CVS
Class |
· Amide local anaesthetic |
Target |
· Voltage-dependent Na+ channel (VDNaC) · (less active at VDKC, VDCaC) |
Entry |
· From ICF: unionised form diffuses into axoplasm, ionised form enters active receptor · From ECF: ionised form enters active receptor (less common) |
Binding |
· Rate ∝ time spent in active state ∝ rate of cycling ∝ nerve activity · Affinity ∝ Inactive > resting > activated |
Effect |
· ↓Rate of cycling -> no action potential propagation · Initial: incomplete blockade, tonic · Repeated stimulation: complete blockade, phasic · No change to resting potential
|
Toxic thresholds |
· Subcut dose: 3mg/kg · Plasma concentration: 4mcg/mL · CC:CNS ratio 5:1 (c.f. lignocaine 7:1); hence ‘warning shot’ is late |
Amount given |
· 10mg/mL x 20mL = 200mg |
Cardiac output |
· 70mL/kg/min x 60kg = 4200mL · In 15 seconds: 1050mL |
Estimated plasma concentration |
· 200mg / 4200mL ≈ 50mcg/mL · Way above toxic threshold of 4mcg/mL |
Consequences |
· Coma and cardiac arrest almost certain · Rx intralipid · Likely prolonged CPR +/- CPB; long duration of action, t1/2β 120 mins |
Mechanism |
· Inhibition of neuronal VDNaC · Highly lipid soluble (300x procaine), easy passage across BBB |
Effects |
· Initial excitatory effects o Inhibition of inhibitory interneurons o Peri-oral tingling, tinnitus, vertigo, slurred speech, inattention, twitching, seizures · Then inhibitory effects o Inhibition of excitatory interneurons and others o Coma, apnoea |
Mechanism |
· Inhibition of cardiac VDNaC (very high affinity) · Inhibition of VDKC and VDCC (lower affinity) · ?↓cAMP |
Effects |
· First phase: ↑HR, ↑mAP · Second phase: myocardial depression, ↓mAP · Terminal phase: peripheral vasodilatation, ↓↓mAP, arrhythmia, arrest |
ECG |
· “As if being pulled apart” ↑QTC, ↑QRS duration · Arrhythmias: sinus bradycardia, AV block, ventricular tachyarrhythmia, asystole |