**8. Cardiopulmonary effects of tramadol**

Acute pulmonary hypertension and right heart failure are the uncommon presentations reported in a young tramadol-overdosed patient [86]. Cardiopulmonary arrest was reported in some cases that had ingested more than 5 g of tramadol [8]. Higher doses of tramadol can block sodium channels and cause Brugada pattern in the ECG [11,47] which can be accompa‐ nied by ventricular dysrhythmias including ventricular fibrillation [11]. In a study on 479 tramadol-poisoned patients, up to 73% of the patients had ECG changes due to blockage of the sodium channels. Almost one-thirds of the patients had terminal 40 msec frontal plane axis deviation and one-fourth had QT prolongation (more than 0.44 sec) [47]. Some cases of right heart failure, resistant shock, asystole, hypotension (especially systolic), and sinus tachycardia have also been recorded [6,35,44,49]. Hypertension has also been reported. The least tramadol dose that has resulted in hypertension and agitation is 500 mg [49].

Eleven suspected cases of tramadol-related angioedema have been reported from Sweden. Involvement of the mouth/pharynx and upper respiratory system can progress to acute respiratory distress and airway obstruction [87]. Tramadol causes respiratory depression with less frequency in comparison with other opioids [28,57,88]. Renal failure is a probable risk factor for respiratory depression [28,89]. Tramadol overdose can cause respiratory depression; but in therapeutic oral doses, it does not cause respiratory complications. In a study on IV administration of 50 to 75 mg of tramadol, no significant changes were detected in the respiratory rate, respiratory volume per minute, and arterial PaO2 [90].
