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Original Papers

Peri-operative dysrhythmias in patients undergoing major vascular surgery - a preliminary report

Shorten, G. D.; Comunale, M. E.; Cohen, M.; Robertson, L.; Darvish, A.

Author Information
European Journal of Anaesthesiology: January 1998 - Volume 15 - Issue 1 - p 16-20

Abstract

Introduction

In patients with coronary artery disease, episodes of myocardial ischaemia [1], acute myocardial infarction [2], ventricular tachycardia in acute myocardial infarction [3,4], and sudden death [5,6] are most likely to occur in the morning(06.00-12.00 hours) and least likely to occur at night. This pattern has been attributed at least in part, to physiological morning adrenergic stimulation [5]. In patients with chronic obstructive pulmonary disease, cardiac dysrhythmias are most likley to occur at night, the period during which arterial desaturation occurs most frequently [7]. Supplemental oxygen decreases the severity of arterial desaturation and the frequency of cardiac dysrhythmias in these patients [7]. Limited evidence exists to suggest a temporal relation between arterial desaturation and myocardial ischaemia in patients following elective aortic surgery [8]. Thus, it is likely that both nocturnal hypoxaemia and physiological morning adrenergic stimulation can be arrhythmogenic. We hypothesize that, during the post-operative course of patients with coronary artery disease, arterial desaturation is the more significant arrhythmogenic factor. As the first step in testing this hypothesis, we examined the frequency with which nocturnal dysrhythmias occur peri-operatively in such patients.

Methods

With approval of the institutional ethics committee, and having obtained their written informed consent, eight patients (five male, three female; 65-82 years) undergoing elective vascular surgery were studied. All patients had symptomatic coronary artery disease. Patients with unstable angina or recent (6 months) myocardial infarction, pulmonary disease, neurological disease or obstructive sleep apnoea were excluded. Patients who were not in sinus rhythm, who were receiving medications for treatment of dysrhythmias, or who had a history of previously documented ventricular tachycardia or ventricular fibrillation were also excluded.

Continuous Holter monitoring was performed on each patient from approximately 1 h pre-operatively until 2-5 days post-operatively (as determined by patient tolerance or duration of hospital stay). Cutaneous electrodes were placed after gentle skin abrasion approximately 1 h pre-operatively and tested for artifact elimination by changing body position. Lead II was monitored in all patients; lead V5 was monitored in patients undergoing carotid end-arterectomy and V2 in patients undergoing aortic or peripheral surgery. All Holter recordings were performed using a two-channel recorder (Marquette 8000D, Marquette Electronics Inc., Milwaukee, USA) and analysed semi-automatically using a Marquette Laser SXP(Marquette Electronics Inc., Milwaukee, USA). The reviewer was unaware of the purpose of the study. The frequencies of isolated supraventricular (SV i) and ventricular premature beats (Vi), and runs of three or more consecutive supraventricular (SV r) and ventricular premature beats (V r) were calculated for 6-h periods (00.00-06.00; 06.00-12.00; 12.00-18.00; 18.00-24.00 hours).

Supplemental oxygen (5 L min−1) was administered by a facemask during pre-operative insertion of venous and arterial cannulae. Midazolam (up to 0.07 mg kg−1) was administered pre-operatively to achieve anxiolysis. Anaesthetic management was not standardized. Intra-operative monitoring comprised an electrocardiogram (leads II and AVF), direct arterial pressure monitoring, pulse oximetry, and continuous nasopharyngeal temperature measurement(Merlin System, Hewlett Packard Co., Waltham, USA). Pulmonary artery catheters were inserted in two patients. All patients received fentanyl, nitrous oxide/oxygen, vecuronium, and isoflurane. Four patients received morphine intravenously (i.v.) during the operation and three had lumbar epidurals placed pre-operatively.

Post-operatively all patients were extubated either in the operating room or within 5 h of completion of surgery. Supplemental oxygen (2 L min−1 via nasal cannulae) was administered during the post-operative night and discontinued thereafter. Post-operative analgesia was provided either by epidural infusion of bupivicaine 0.1% with fentanyl (4 μg mL−1) at 5-14 mL h−1 or by patient controlled analgesia(PCA) with morphine sulphate.

The data obtained were analysed using analysis of variance. P<0.05 was taken to indicate significance.

Results

The intra-operative course was haemodynamically stable in all eight patients. Glyceryl trinitrate was administered by i.v. infusion for treatment of moderate hypertension in two patients, and phenylephrine administered in one patient to treat post-induction hypotension. No surgical complications occurred and no post-operative pulmonary complications were detected by clinical examination, arterial blood gas analysis, or chest radiography. Immediate post-operative haematocrit, axillary temperature, the surgical procedures and procedure durations are shown in Table 1.

Table 1
Table 1:
Individual patient data

Holter data for 696 patient hours were analysed. SV r and V r were identified, respectively, in seven and six of the eight patients studied. During the pre-operative period, isolated premature atrial contractions occurred more frequently than 1 min−1 in two patients and isolated ventricular ectopic beats occurred more frequently than 1 min−1 in one patient. Intra-operative dysrhythmias (Table 2) were not associated with haemodynamic instability. Table 3 summarizes the frequency of dysrhythmias on each post-operative day. The frequency of dysrhythmias was not significantly different on any two days studied.

Table 2
Table 2:
Intra-operative dysrhythmias (events per hour)
Table 3
Table 3:
Post-operative dysrhythmias: daily variation in frequency (events per hour)

Combined sample data for the post-operative period is summarized in Table 4. The frequencies of V r, SV i, and SV r were greater during the 00.00-06.00 hours interval than during any of the other 6-h periods studied, although this only achieved statistical significance for SV r. Three patients had significantly higher 6-h frequencies of all dysrhythmias in the 00.00-06.00 hours period on all days monitored.

Table 4
Table 4:
Frequency of post-operative dysrhythmias (events per 6-h period): variation with time of day

Discussion

These preliminary data suggest that, in patients with coronary artery disease undergoing major vascular surgery, ventricular and supraventricular dysrhythmias occur commonly; that a great inter-patient variability in frequency of dysrhythmias exists and that supraventricular tachycardia occurs most commonly between 00.00 and 06.00 hours.

In patients with stable angina, episodes of myocardial ischaemia are most likely to occur between the hours of 06.00 and 12.00 hours [1]. This relation is consistent whether or not the episodes are symptomatic. A parallel increase in ischaemia-related dysrhythmias occurs during these hours [1]. Similarly, acute myocardial infarction [2] and sudden cardiac death [5,6] occur with circadian variation with a peak incidence between 06.00 and 12.00 hours. The increased risk of these events during this 6-h period may be attributable to a physiological increase in sympathetic activity [9]. Such an increase can cause myocardial electrical instability and ventricular dysrhythmias [10]. In support of this hypothesis is the observation that this frequency pattern is not present when patients are studied in hospital, i.e. in a setting where daily autonomic cycles are disturbed [5].

A high prevalence of cardiac dysrhythmias exists in patients with chronic obstructive pulmonary disease[7]. In contrast with patients with coronary artery disease, premature ventricular contractions (PVC) occur more commonly at night than by day with peak incidences between 03.00 and 07.00 hours. In one study, ventricular tachycardia occurred only at night (21.00-09.00 hours) and only in patients not receiving supplemental oxygen [7]. The incidence of 'night time' PVCs was decreased by administration of supplemental oxygen, although this difference did not reach statistical significance. The authors concluded that arterial desaturation was an important arrhythmogenic factor [7].

A constant, moderate degree of hypoxaemia consistently occurs in patients who have undergone major surgery, particularly upper abdominal procedures [11]. It is greatest during the first post-operative day, but can persist for up to 2 weeks[12]. It is caused by a reduction in functional residual capacity (which also peaks on the first post-operative day) [12,13], which in turn is due to pain [14], reflex diaphragmatic inhibition [15] and the supine position [16]. A second distinct pattern of hypoxaemia has been reported in the post-operative period[17]. Episodes of severe arterial desaturation occur during sleep in patients who have received systemic opioids [17]. This episodic hypoxaemia can persist until the third post-operative day [18]. In a small study (of three patients after elective aortic surgery), Reeder et al. demonstrated a temporal relation between decreases in oxygen saturation and myocardial ischaemia detected using ST segment analysis [8]. In the early post-operative period, Gill et al. established a close correlation between the duration of hypoxaemia and myocardial ischaemia [19]. In that study, ischaemia was more likely to occur if an episode of hypoxaemia was prolonged (greater than 5 min) or severe (SpO2 <85%).

The data presented here suggest that the patients studied were most likely to have cardiac dysrhythmias between 00.00 and 06.00 hours (although statistical significance was achieved only for SV r). However, the evidence cited above indicates that, in patients with coronary artery disease, sudden cardiac death (which is frequently the result of a ventricular dysrhythmia) and ischaemia-related cardiac dysrhythmias are most likely to occur later (06.00-12.00 hours). We hypothesize that this apparent shift in the 'at risk for dysrhythmia' period is due to:

  1. Loss of the normal autonomic diurnal pattern because of admission to hospital.
  2. The presence of a second arrhythmogenic factor, nocturnal hypoxaemia, which is well documented in the post-operative period. Similarly, in another hypoxaemia-prone population, those with chronic obstructive pulmonary disease, the peak incidence of dysrhythmias occurs at night.

Because our patients received supplemental oxygen on the first post-operative night, one might expect a decrease in frequency of dysrhythmias on that night, if hypoxaemia were the main arrhythmogenic factor. Failure to demonstrate a difference may be attributable to the very large inter-patient variability in frequency of each category of dysrhythmia studied. For instance, on the second post-operative day, the mean hourly frequency of V i for patients 5 and 6 was 41.4 compared with 1.37 for the remaining 5 patients studied.

We conclude that:

  1. Patients with coronary artery disease have frequent post-operative dysrhythmias.
  2. In these patients, post-operative supraventricular tachycardia occurs most commonly between 00.00 and 06.00 hours.
  3. Post-operative hypoxaemia is likely to be a significant arrhythmogenic factor in these patients.

In order to reliably establish a causative or temporal relation between arterial desaturation and cardiac dysrhythmias in the post-operative period, it will be necessary to prospectively study a larger and high-risk sample of patients concurrently with Holter monitoring and continuous pulse oximetry. The data presented here indicate strongly that such a study is justified. If that relation is established, the effects of prolonged post-operative oxygen supplementation should be examined.

Acknowledgment

The authors acknowledge the financial support for this study provided by Nellcor Inc.

References

1 Hausmann D, Nikutta P, Trappe H-J, Daniel WG, Wenzlaff P, Lichtlen PR. Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease. J Am Coll Cardiol 1990;16: 49-54.
2 Muller JE, Stone PH, Turi ZGet al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985; 313: 1315-1122.
3 Lucente M, Rebuzzi AG, Lanza GA et al. Circadian variation of ventricular tachycardia in acute myocardial infarction. Am J Cardiol 1988; 62: 670-4.
4 Raeder EA, Hohnloser SH, Graboys TB, Podrid PJ, Lampert S, Lown B. Spontaneous variability and circadian distribution of ectopic activity in patients with malignant ventricular arrhythmias. J Am Coll Cardiol 1988; 12: 656-661.
5 Muller JE, Ludmer PL, Willich SN et al. Circadian variation in the incidence of sudden cardiac death. Circulation 1987; 75: 131-138.
6 Willich SN, Levy D, Rocco MB, Tofler GH, Stone PH, Muller JE. Circadian variation in the incidence of sudden cardiac death in the Framingham Heart Study population. Am J Cardiol 1987; 60: 801-806.
7 Flick MR, Block AJ. Nocturnal vs. diurnal cardiac arrhythmias in patients with chronic obstructive pulmonary disease. Chest 1979; 75: 8-11.
8 Reeder MK, Muir AD, Foex P, Goldman MD, Loh L, Smart D. Postoperative myocardial ischaemia: temporal association with nocturnal hypoxaemia. Br J Anaesth 1991; 67: 626-631.
9 Turton MB, Deegan T. Circadian variations of plasma catecholamines, cortisol and immunoreactive insulin concentrations in supine subjects. Clin Chim Acta 1974; 55: 389-394.
10 Corbalan R, Verrier R, Lown B. Psychological stress and ventricular arrhythmias during myocardial infarction in the conscious dog. Am J Cardiol 1974; 34: 692-697.
11 Knudsen J. Duration of hypoxaemia after uncomplicated upper abdominal and thoraco-abdominal operations. Anaesthesia 1970; 25: 376-380.
12 Craig DB. Post-operative recovery of pulmonary function. Anesth Analg 1981; 60: 46-52.
13 Ali J, Weisel RD, Layug AB, Kripke BJ, Hechtmann HB. Consequences of post-operative alterations in respiratory mechanics. Am J Surg 1974; 128: 376-382.
14 Wahba WM, Don HF, Craig DB. Post-operative epidural analgesia: effects on lung volumes. Can Anaesth Soc J 1975; 22: 519-527.
15 Dureuil B, Cantineau JP, Desmonts JM. Effects of upper or lower abdominal surgery on diaphragmatic function. Br J Anaesth 1987; 59: 1230-1235.
16 Craig DB, Wahba WM, Don HF, Couture JG, Becklake MR. Closing volume and its relationship to gas exchange in seated and supine positions. J Appl Physiol 1971; 31: 717-721.
17 Catley DM, Thornton C, Jordan C, Lehane JR, Royston D, Jones JG. Pronounced episodic desaturation in the post-operative period: its association with ventilatory pattern and analgesia regimen. Anesthesiology 1985; 63: 20-28.
18 Rosenberg J, Dirkes WE, Kehlet H. Episodic arterial desaturation and heart rate variations following major abdominal surgery. Br J Anaesth 1989; 63: 651-654.
19Gill NP, Wright B, Reilly CS. Relationship between hypoxaemic and cardiac ischaemic events in the perioperative period. Br J Anaesth 1992; 68: 471-473.
Keywords:

DYSRHYTHMIAS, supraventricular, ventricular; SURGERY, vascular

© 1998 European Academy of Anaesthesiology