Abstract
Background:
Physiological responses to propofol may defer in class 1 obesity compared to patients of normal weight. To aid decision-making and ensure safety in patients with class 1 obesity, it is important to study their haemodynamic and respiratory responses to propofol.
Aim:
We aimed to evaluate the haemodynamic and respiratory responses to propofol induction in patients with class 1 obesity in comparison to those with normal weight.
Patients and Methods:
Seventy patients aged 18–60 years scheduled for surgery under general anaesthesia were recruited and assigned equally to two groups based on the body mass index. All patients received intravenous propofol at 40 mg every 10 s until loss of consciousness. The mean dose of propofol was 132.71 ± 19.30 mg in the obese group and 128.57 ± 27.24 mg in the normal weight group. The blood pressure, oxygen saturation, heart rate, and end tidal carbon dioxide were documented at a 2-min interval.
Results:
At loss of consciousness, mean systolic blood pressure increased significantly in group O (P = 0.03) but decreased in group N (P = 0.31). The mean heart rate increased in both groups, P = 0.04 in group O and 0.14 in N. Mean end tidal carbon dioxide decreased in group O (P = 0.04), but increased in group N (P = 0.15).
At loss of consciousness, group O had significantly higher arterial oxygen saturation and diastolic blood pressure, and the mean arterial pressure did not differ in both groups. Two minutes after induction of anaesthesia, mean blood pressures increased in both groups. There was no significant difference in the end tidal carbon dioxide, occurrence of apnoea, and shallow breathing within 10 min of induction between both groups.
Conclusion:
Haemodynamic and respiratory parameters remained comparable and within desirable limits following propofol induction in patients with class 1 obesity and normal weight patients.
Keywords: General anaesthesia, haemodynamic, obesity, propofol, respiratory
INTRODUCTION
Obesity is a chronic complex disease defined by excessive fat deposition that can impair health.[1] Obesity influences the quality of living and is defined by body mass index (BMI) ≥30. The BMI is the relationship between a person’s height and weight expressed as a number. A BMI of 18.5 to 24.9 is considered normal, while 30.0 to 34.9 is considered class 1obesity.
The prevalence of obesity has been on the increase worldwide, with the figure reported as 16% by the WHO in 2022.[2] In Nigeria, it has been reported as 14.5%.[3] Consequently, the number of surgeries performed on obese patients is expected to increase. Obesity is associated with several cardiovascular, respiratory, endocrinal, and gastrointestinal comorbidities.[4,5] In obese patients, hypertension, increased cardiac output and cardiac workload, and arrhythmia may increase morbidity under anaesthesia. Reduced functional residual capacity, atelectasis, increased work of breathing, and oxygen demand may cause a rapid decrease in arterial oxygen levels during apnoea. Obesity increases the risk of obstructive sleep apnoea, obesity hypoventilation syndrome, wheezing, and pulmonary hypertension and may increase morbidity under anaesthesia. Endocrine diseases, metabolic syndrome, gall bladder disease, degenerative joint disease, thromboembolic phenomenon, and reduced wound healing may occur.
Propofol is an intravenous (IV) anaesthetic indicated for sedation, induction, and maintenance of anaesthesia at a dose of 1.5–2.5 mg/kg in healthy adults.[6] It is known to have systemic effects including decreasing the cerebral metabolic rate of oxygen, cerebral blood flow and intracranial pressure, reduction of airway responsiveness, and incidence of cough and laryngospasm, and it also has anti-emetic effects at sub-hypnotic concentrations.[7] It is a respiratory and cardiovascular depressant; shallow breathing and apnoea may occur as a result, which may require respiratory support.[7,8] Propofol depresses cardiac contractility and venous and arteriolar systemic vascular resistance, causing decreases in preload, afterload, and systemic blood pressure. It decreases mean arterial pressure, cardiac index, myocardial blood flow, and oxygen consumption.[7]
Understanding the impact of obesity on the pharmacokinetic and pharmacodynamics of propofol is important as the drug is commonly used for the induction of anaesthesia in many centres. Body fat has minimum metabolic activity and may have an indirect influence on metabolic and renal clearance.[9] In obesity cases, the pharmacokinetics of drugs is influenced by differences in the tissue distribution, haemodynamics, and blood flow to various organs.[10]
Considering the cardiovascular and respiratory effects of propofol, which may be aggravated during anaesthesia, it is important to ensure patient safety when the drug is used for induction of anaesthesia in obese people. The influence of obesity on the pharmacokinetics and pharmacodynamics of anaesthetic agents makes it even more desirable to study haemodynamics and respiratory changes during the use of propofol in these patients. These effects are even more pronounced when excessive doses are administered; hence, it is important to study these effects when sleep-inducing doses of propofol are used.
This study evaluated the haemodynamic and respiratory responses to propofol induction among class 1 obese patients compared to normal weight patients. Our findings will be valuable in decision-making during the safe conduct of anaesthesia in class 1 obese patients.
MATERIALS AND METHODS
The sample size was determined using data from a study by Lam et al.[11]
Using the formula[12]: M (sample size per group) = (2c)/δ +1
Where δ = (μ₁–μ₂)/σ
δ is the standardized effect, μ₁ and μ₂ are the means of the two treatment groups, and σ is the standard deviation.
Allowing for 10% attrition, a sample size of 35 patients per group was observed, with the total number of patients in both groups being 70 patients.
Approval for the study was obtained from the ethics review board of the Nnamdi Azikiwe University Teaching Hospital. Inclusion criteria included patients with American Society of Anesthesiologists (ASA) Physical Status I and II and those of both sexes aged 18–60 years scheduled for surgical procedures requiring general anaesthesia. Exclusion criteria were patients with cardiovascular disease, neurological conditions, pulmonary disease, and patients with known allergy to propofol. Written informed consent was obtained from all the study participants.
A preoperative evaluation was carried out for each patient, and weights and heights of all patients were measured using the Su Hong RGZ-120/ZT-120, model 120 stadiometer (manufactured by Jiangsu Kangjian Medical Apparatus Co. Ltd China), recorded in kilograms and metres, respectively, and their BMI calculated. No sedative premedication was prescribed. Patients were allotted to either of two groups (35 per group) based on their BMI. Patients with BMI 18.5–24.9 (normal weight patients) were assigned to group N, while those with BMI 30.0–34.9 (class 1 obese patients) were assigned to group O. Each patient was given an identification number, and the investigator was blinded to the patients’ identity and group. Routine standard monitoring was applied to all the patients.
An intravenous access was secured with an 18G cannula, and an intravenous fluid consisting of 0.9% normal saline was commenced for fluid management. All patients received IV paracetamol 15 mg/kg and morphine 0.1 mg/kg in 2-mg aliquots with 0.004 mg/kg glycopyrolate. All patients were pre-oxygenated for 3 min with 100% oxygen. Induction of general anaesthesia was achieved using IV propofol given at 40 mg (4 mL) every 10 s, until a clinical endpoint of loss of both verbal response to command and eyelash reflex was observed. Time to loss of consciousness was noted using a stopwatch. The total induction dose of propofol was documented for each patient. The data on systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), respiratory rate (RR), and oxygen saturation (SpO₂) were obtained 2 minutes before induction of anaesthesia, immediately after induction, every 2 minutes for 10 minutes, and every 5 minutes until the end of surgery. End tidal carbon dioxide was recorded after endotracheal intubation at 5-minute intervals.
Neuromuscular blockade for laryngoscopy and endotracheal intubation was achieved using IV suxamethonium 100 mg, administered at loss of consciousness. Following endotracheal intubation, IV atracurium 0.25 mg/kg was used for maintenance of muscle relaxation function.
The primary outcome measures evaluated the effect of propofol on haemodynamic and respiratory parameters in class 1 obesity and normal weight patients at loss of consciousness and within 10 min of induction of anaesthesia.
The secondary outcome measures evaluated the occurrence of side effects including apnoea, shallow breathing, bradycardia, and hypotension in class 1 obesity and normal patients following administration of propofol for induction of anaesthesia.
Statistical analysis
The IBM Statistical Package for the Social Sciences Statistics software version 23.0 (IBM Corp. Armonk, NY) was used for data storage and analysis. All continuous variables (age, weight, height, BMI, and haemodynamic responses and drug doses) were expressed as mean ± standard deviation (SD). The Z test (unpaired) was used to compare the mean age, weight, height, BMI, dose of propofol, and time to loss of consciousness between the two groups. The Z test (paired) was also used to compare data within the same group. The chi -square test was used to compare gender and ASA status. The level of statistical significance was set at P < 0.05.
RESULTS
Seventy patients met the inclusion criteria. Group O had a mean age of 38.37 ± 8.57 years, while that of group N was 43.31 ± 12.48 years (P = 0.14). The mean BMI was 32.09 ± 1.31 and 23.11 ± 2.04 for group O and group N, respectively [Table 1]. Group O had more females [26 (74.29%)] than males [9 (25.71%)] (P = 0.04), and group N also had more females [23 (65.71%)] (P = 0.05) than males [12 (34.29%)]. Group O had a mean total body weight of 84.37 ± 6.23 kg, while group N had a mean total body weight of 61.57 ± 11.16 kg. All patients in group O were classified as ASA II, whereas group N had more patients of ASA II status (62.86%) compared to ASA I (37.14%). The mean induction doses of propofol in groups O and N were 132.71 ± 19.30 mg and 128.57 ± 27.24 mg, respectively (P = 0.13). The estimated dose of propofol administered to group O is 1.57 mg/kg, while that for group N is 2.09 mg/kg.
Table 1.
Patient demographic characteristics
| Variable | Group O | Group N | P value |
|---|---|---|---|
| Age (Years) | 38.37 ± 8.57 | 43.31 ± 12.48 | 0.14 |
| Weight (kg) | 84.37 ± 6.23 | 61.57 ± 11.16 | 0.22 |
| Height (m) | 1.62 ± 0.07 | 1.66 ± 0.07 | 0.19 |
| BMI (kg/m2) | 32.09 ± 1.31 | 23.11 ± 2.04 | 0.32 |
BMI: Body Mass Index, kg: kilogram, m: metre
Trends in vital signs over time are as shown in Tables 2 and 3. The mean preoperative SBP was significantly less in group O than in group N (P = 0.03). There was no statistically significant difference between the preoperative HR of group O and that of group N (P = 0.25). In the preoperative period, the mean SBP was significantly less in group O than in group N (P = 0.03), and there was no significant difference in the mean DBP of the two groups (P = 0.22).
Table 2.
Comparison of vital signs between both groups within the first 10 min after induction
| Parameter | Group (O) | Group (N) | Mean diff | P value |
|---|---|---|---|---|
| Preoperative | ||||
| HR (bpm) | 78.17 ± 11.29 | 80.69 ± 11.44 | −2.51 | 0.25 |
| SBP (mmHg) | 119.03 ± 13.30 | 120.77 ± 11.80 | −1.74 | 0.03* |
| DBP (mmHg) | 74.09 ± 10.60 | 78.69 ± 8.24 | −4.60 | 0.22 |
| Baseline | ||||
| SpO₂ | 98.43 ± 1.04 | 98.26 ± 1.03 | 0.17 | 0.11 |
| ETCO2 | 30.39 ± 5.46 | 30.83 ± 4.29 | −0.44 | 0.14 |
| HR | 85.34 ± 13.72 | 89.86 ± 13.19 | −4.54 | 0.14 |
| SBP | 113.34 ± 14.02 | 134.91 ± 14.36 | −1.57 | 0.15 |
| DBP | 79.06 ± 10.18 | 85.26 ± 8.47 | −6.20 | 0.06 |
| MAP | 97.29 ± 12.18 | 101.91 ± 10.81 | −4.62 | 0.88 |
| At loss of consciousness | ||||
| SpO2 | 99.66 ± 0.79 | 99.34 ± 0.76 | 0.31 | 0.006* |
| ETCO2 | 30.00 ± 5.33 | 30.95 ± 4.18 | −0.95 | 0.06 |
| HR | 92.89 ± 20.13 | 92.51 ± 15.23 | 0.37 | 0.13 |
| SBP | 133.17 ± 18.67 | 126.06 ± 18.18 | 7.11 | 0.16 |
| DBP | 81.26 ± 13.79 | 81.37 ± 14.84 | −0.11 | 0.07 |
| MAP | 97.31 ± 14.72 | 96.20 ± 15.28 | 1.11 | 0.14 |
| AT 2 min | ||||
| SpO2 | 99.46 ± 1.29 | 98.86 ± 2.17 | 0.60 | 0.12 |
| ETCO2 | 31.75 ± 5.09 | 31.63 ± 3.92 | 0.12 | 0.06 |
| HR | 92.37 ± 16.02 | 98.89 ± 20.56 | −6.51 | 0.06 |
| SBP | 139.00 ± 26.87 | 130.91 ± 20.23 | 8.08 | 0.29 |
| DBP | 84.03 ± 20.28 | 84.06 ± 1.60 | −0.29 | 0.17 |
| MAP | 100.97 ± 21.03 | 102.49 ± 21.43 | −1.51 | 0.09 |
| At 4 min | ||||
| SPO2 | 99.66 ± 0.64 | 99.26 ± 0.74 | 0.40 | 0.13 |
| ETCO2 | 32.92 ± 4.37 | 31.60 ± 4.25 | 1.32 | 0.18 |
| HR | 91.29 ± 16.27 | 98.00 ± 20.00 | −6.71 | 0.02* |
| SBP | 132.46 ± 24.39 | 130.06 ± 21.70 | 2.40 | 0.36 |
| DBP | 81.91 ± 26.41 | 82.03 ± 11.91 | −0.11 | 0.07 |
| MAP | 96.26 ± 20.51 | 97.17 ± 13.18 | −0.91 | 0.02* |
| At 6 min | ||||
| SpO2 | 99.63 ± 0.49 | 99.31 ± 0.67 | 0.31 | 0.01* |
| ETCO2 | 33.08 ± 4.34 | 31.19 ± 4.32 | 1.89 | 0.25 |
| HR | 92.03 ± 14.62 | 97.17 ± 19.03 | −5.14 | 0.13 |
| SBP | 126.23 ± 21.57 | 126.74 ± 15.94 | −0.51 | 0.03* |
| DBP | 74.34 ± 22.19 | 79.86 ± 12.25 | −5.51 | 0.01* |
| MAP | 90.00 ± 19.86 | 95.03 ± 14.58 | −5.02 | 0.20 |
| At 8 min | ||||
| SpO2 | 99.46 ± 0.70 | 99.11 ± 0.96 | 0.34 | 0.14 |
| ETCO2 | 33.46 ± 4.95 | 30.58 ± 4.37 | 2.88 | 0.33 |
| HR | 89.96 ± 12.78 | 96.20 ± 9.21 | −6.23 | 0.16 |
| SBP | 125.49 ± 16.59 | 129.77 ± 24.30 | −4.28 | 0.15 |
| DBP | 73.51 ± 16.91 | 80.57 ± 14.82 | −7.05 | 0.12 |
| MAP | 89.20 ± 15.44 | 96.51 ± 18.14 | −7.31 | 0.18 |
| At 10 min | ||||
| SpO2 | 99.34 ± 1.11 | 99.26 ± 0.95 | 0.08 | 0.27 |
| ETCO2 | 33.96 ± 5.45 | 30.42 ± 4.97 | 3.54 | 0.15 |
| HR | 91.40 ± 13.58 | 96.14 ± 17.89 | −4.74 | 0.04* |
| SBP | 122.49 ± 17.07 | 124.43 ± 13.80 | −1.94 | 0.04* |
| DBP | 72.00 ± 16.65 | 78.97 ± 10.29 | −6.97 | 0.06 |
| MAP | 87.14 ± 14.65 | 92.54 ± 11.36 | −5.40 | 0.12 |
Statistically significant
Table 3.
Comparison of heart rate and mean arterial pressure within each group
| Parameter | Baseline | Loss of consciousness | P value |
|---|---|---|---|
| Group O | |||
| HR (bpm) | 85.34 ± 13.72 | 92.89 ± 20.13 | 0.04* |
| MAP | 97.31 ± 14.72 | 97.89 ± 12.18 | 0.43 |
| Group N | |||
| HR | 89.86 ± 13.19 | 92.51 ± 15.23 | 0.14 |
| MAP | 101.91 ± 10.80 | 96.20 ± 15.28 | 0.23 |
| Parameter | Loss of consciousness | At 2 min | P value |
| Group O | |||
| HR (bpm) | 92.89 ± 20.13 | 92.37 ± 16.02 | 0.59 |
| MAP | 97.31 ± 14.72 | 100.97 ± 21.03 | 0.15 |
| Group N | |||
| HR | 92.51 ± 15.23 | 98.89 ± 20.56 | 0.66 |
| MAP | 96.20 ± 15.29 | 102.49 ± 21.43 | 0.31 |
| Parameter | 2 min | 4 min | P value |
| Group O | |||
| HR (bpm) | 92.37 ± 16.02 | 91.29 ± 16.27 | 0.85 |
| MAP | 100.97 ± 21.03 | 96.26 ± 20.51 | 0.51 |
| Group N | |||
| HR | 98.89 ± 20.56 | 98.00 ± 20.00 | 0.68 |
| MAP | 102.49 ± 21.43 | 97.17 ± 13.18 | 0.21 |
| Parameter | 4 min | 6 min | P value |
| Group O | |||
| HR (bpm) | 91.29 ± 16.27 | 92.03 ± 14.62 | 0.61 |
| MAP | 96.26 ± 20.51 | 90.00 ± 19.86 | 0.90 |
| Group N | |||
| HR | 98.00 ± 20.00 | 97.17 ± 19.03 | 0.94 |
| MAP | 97.17 ± 13.18 | 95.03 ± 14.58 | 0.21 |
| Parameter | 6 min | 8 min | P value |
| Group O | |||
| HR (bpm) | 92.03 ± 14.62 | 89.96 ± 12.78 | 0.92 |
| MAP | 90.00 ± 19.86 | 89.20 ± 15.44 | 0.15 |
| Group N | |||
| HR | 97.17 ± 19.03 | 96.20 ± 9.21 | 0.76 |
| MAP | 95.03 ± 14.58 | 96.51 ± 18.14 | 0.78 |
| Parameter | 8 min | 10 min | P value |
| Group O | |||
| HR (bpm) | 89.96 ± 12.78 | 91.40 ± 13.58 | 0.79 |
| MAP | 89.20 ± 15.44 | 87.14 ± 14.65 | 0.83 |
| Group N | |||
| HR | 96.20 ± 9.21 | 96.14 ± 17.89 | 0.88 |
| MAP | 96.51 ± 18.14 | 92.54 ± 11.36 | 0.61 |
Statistically significant, bpm: beats per minute, HR: heart rate, MAP: mean arterial pressure
The mean baseline SPO2 for group O was 98.43 ± 1.04%, which increased to 99.66 ± 0.79% at loss of consciousness (P = 0.06). Group N had an increase in mean SPO2 from the baseline value of 98.26 ± 1.03% to 99.34 ± 0.76% at loss of consciousness (P = 0.23). The mean baseline SPO2 between both groups was not significantly different (P = 0.11). There was a significant difference in the SPO2 of both groups at loss of consciousness, group O had mean SPO2 of 99.66 ± 0.79%, while group N had an SPO2 of 99.34 ± 0.76% (P = 0.006).
Group O had a mean baseline ETCO2 of 30.39 ± 5.46 mm Hg, which decreased significantly to 30.00 ± 5.33 mm Hg at loss of consciousness (P = 0.04). Group N had a mean baseline ETCO2 of 30.83 ± 4.29 mm Hg, which increased to 30.95 ± 4.18 mm Hg at loss of consciousness (P = 0.15). There was no significant difference in mean baseline ETCO2 and ETCO2 at loss of consciousness between group O and group N (P = 0.14 and 0.06, respectively). The ETCO2 at loss of consciousness was lower in group O (30.00 ± 5.33 mm Hg) compared to group N (30.95 ± 4.18 mm Hg) (P = 0.06).
Group O had a statistically significant increase in mean baseline HR from 85.34 ± 13.72 bpm to 92.89 ± 20.13 bpm at loss of consciousness (P = 0.04). In group N, there was also an increase in the mean HR from the baseline value of 89.86 ± 13.19 bpm to 92.51 ± 15.23 bpm at loss of consciousness (P = 0.14). However, there was no significant difference in mean baseline HR values in both groups (P = 0.14), nor at loss of consciousness (P = 0.13).
Group O had a statistically significant increase in mean SBP from the baseline value of 113.34 ± 14.02 mm Hg to 133.17 ± 18.67 mm Hg at loss of consciousness (P = 0.03), whereas group N had a decrease in mean SBP from the baseline value of 134.91 ± 14.36 mm Hg to 126.06 ± 18.18 mm Hg at loss of consciousness (P = 0.31). At loss of consciousness, the mean SBP was higher in group O than in group N (P = 0.16), and the mean difference in mean baseline SBP and mean SBP at loss of consciousness between both groups was not significantly different (P = 0.15 and 0.16, respectively). At loss of consciousness, DBP was lower in group O compared to group N (P = 0.07).
In group O, the mean baseline DBP increased from 79.06 ± 10.18 mm Hg to 81.26 ± 13.79 mm Hg at loss of consciousness (P = 0.41), while in group N, it decreased from baseline value of 85.26 ± 8.47 mm Hg to 81.37 ± 14.84 mm Hg at loss of consciousness (P = 0.21).The mean difference in mean baseline DBP and DBP at loss of consciousness between both groups was not significantly different (P = 0.06 and 0.07, respectively).
In group O, the mean baseline MAP increased from 97.31 ± 14.72 mm Hg to 97.89 ± 12.18 mm Hg at loss of consciousness (P = 0.43), while in group N, it decreased from 101.91 ± 10.81 mm Hg to 96.20 ± 15.28 mm Hg at loss of consciousness (P = 0.23).), and the mean MAP was higher in group O than in group N (P = 0.14).
The mean baseline MAP and MAP at loss of consciousness between both groups was not significantly different (P = 0.88 and 0.14, respectively).
Group O had a higher HR 92.89 ± 20.13 bpm at loss of consciousness than group N 92.51 ± 15.23 bpm (P = 0.13).
Group O had a statistically significant increase in mean HR from 85.34 ± 13.72 bpm at baseline to 92.89 ± 20.13 bpm at loss of consciousness (P = 0.04).
There was a significant difference in the SpO2 of both groups at loss of consciousness, group O had mean SpO2 of 99.66 ± 0.79%, while group N had SpO2 of 99.34 ± 0.76% (P = 0.006).
Group O had a mean baseline ETCO2 of 30.39 ± 5.46 mm Hg, which decreased significantly to 30.00 ± 5.33 mm Hg at loss of consciousness (P = 0.04).
Two minutes after induction, there was no significant difference in HR, SBP, DBP, MAP, SpO2, and ETCO2 between the two groups.
Group N had a significant increase in mean ETCO2 from 30.95 ± 4.18 mm Hg at loss of consciousness to 31.63 ± 3.92 mm Hg at 2 min (P = 0.04).
Group N had a decrease in mean DBP from 84.06 ± 16.60 mm Hg at 2 min to 82.03 ± 11.91 mm Hg at 4 min (P = 0.03).
Three patients in group O (8.57%) had 30% or higher decrease in mean SBP at loss of consciousness compared to 14 patients (40%) in group N (P = 0.39). Two patients in group O (5.71%) had 30% or higher decrease in mean DBP at loss of consciousness, compared to eight patients (22.86%) in group N (P = 0.45). Three patients in group O (8.57%) had 30% or higher decrease in mean MAP at loss of consciousness compared to five patients (14.29%) in group N (P = 0.75). More patients in group N had ≥30% drop in SBP, DBP, and MAP than group O, at loss of consciousness, which is reflected in the decrease in the mean values of these variables in group N [Figure 1].
Figure 1.
Number of patients with ≥30% decrease in the value of the mean systolic blood pressure, diastolic blood pressure, and mean arterial pressure from baseline to loss of consciousness
Fifteen patients in group O (43%) had apnoea at induction, compared to twelve patients in group N (34%) (P = 0.83). Five patients in group O (14%) had shallow breathing at induction, compared to two patients in group N (6%) (P = 0.60). Two patients in each group (6% per group) had hypotension (P = 0.80), whereas 19 patients in group O (54%) had tachycardia, compared to 17 patients in group N (49%) (P = 0.89). Bradycardia was not recorded in either group. No statistically significant difference was, however, found in the occurrence of the above side effects between both groups [Figure 2].
Figure 2.
Number of patients with side effects in both groups
DISCUSSION
There was no difference in the mean age of patients in both groups (P = 0.14), and the demographic characteristics of both groups were comparable [Table 1]. The mean induction dose of propofol was higher in group O at 132.71 ± 19.30 mg compared to 128.57 ± 27.24 mg in group N; this difference was not statistically significant (P = 0.13). This may be because less body weight, body fat and volume of distribution of propofol is increased in obesity and also due to the use of sleep-inducing doses of propofol and not calculated doses. This contrasts with findings by Ismail et al,[13] who reported a significantly higher mean induction dose of propofol in obese patients than in non-obese patients.
The mean heart rate (HR) increased at loss of consciousness from baseline values in both the obese and normal patients. This increase was not statistically significant and contrasts with the those observed in the study by Ismail et al,[13] in which the HR post-induction was found to be significantly lower in obese patients compared to normal patients. The increase in HR at loss of consciousness in this study also contrasts with findings by Dutta et al[14] in which the HR decreased after induction with propofol in patients who received no drug or fluid preload before induction and those who received preload with Ringer’s lactate. Our findings may differ from those of Ismail et al.[13] and Dutta et al.,[14] possibly because the former premedicated their patients with IV midazolam, which depresses HR and used propofol doses of 2 mg/kg, while the latter premedicated their patients with fentanyl and used propofol doses of 2.5 mg/kg. The dosing of propofol and use of midazolam and fentanyl may have contributed to the reduction in HR seen in both studies.
Billota et al.,[15] on the other hand, found that propofol induction at 2.5 mg/kg, at an infusion rate of 10 mg/second, significantly reduced HR, while a lower infusion rate of 2 mg/s did not significantly change the HR. Both the higher propofol infusion rate and the lower infusion rate significantly reduced the MAP. The rate of drug administration is, therefore, a factor that influences HR. Claeys et al.[16] did not find any significant change in HR in patients who received 2 mg/kg of IV propofol injected over 30 s; they however found a rapid and significant decrease in the SBP (by 28%) and DBP (by 19%) among these patients (P < 0.001). The HR of patients in our study may have been dependent on the rate of injection of propofol. In contrast to our findings, Belekar[17] reported a mean HR below baseline value after induction of anaesthesia with 2 mg/kg of propofol. Belekar[17] did not observe any bradycardia among his study participants, as was the case in our study. Unlike the aforementioned study, the HR in both groups in our study increased at loss of consciousness. This may be because of the use of glycopyrolate. The use of sleep doses may result in administration of smaller quantities of drugs compared to when calculated doses are used. Propofol is known to cause bradycardia when given in standard doses.
The increases in SBP, DBP, and MAP observed in group O at loss of consciousness may be because of the sleep-inducing dose of propofol, as they may not cause a decrease in these haemodynamic parameters as would be caused by doses calculated using body weights. This finding contrasts with that of Lam et al,[11] in which patients experienced a decrease in blood pressure with the administration of higher doses of propofol, at 2 mg/kg.[11]
Our finding of increased MAP in the class 1 obesity group at loss of consciousness contrasts with findings by Ismail et al,[13] where MAP was lower in the obese patients. Differences in dosing of the drug may account for this. Ismail et al.[13] used propofol at 2 mg/kg.
The difference in dose of drug administered and the rate of drug administration may account for the contrast between blood pressure variables at loss of consciousness in group N and results from other studies. At this period, group N had a decrease in the mean SBP, DBP, and MAP, which was not statistically significant. Rabadi et al.[18] reported a significant drop in the MAP following induction with 2–2.5 mg/kg of propofol given over 30 s.[18] Unlike Rabadi et al,[18] our study found a decrease in MAP, which was not statistically significant. Similar to results in group N, Dutta et al.[14] found a decrease in SBP, DBP, and MAP at induction following propofol injection at 2.5 mg/kg, the decrease in SBP was similar in patients who received preload with Ringer’s lactate and those who received no drug but was less in patients who received ephedrine injection. In contrast, none of these drugs were used in our study. Unlike our findings in both groups, Belekar et al,[17] found a significant decrease in SBP, DBP, and MAP at induction.[17] They administered propofol at 2 mg/kg, but did not analyse BMI and did not report the rate of injection; however, their patients were premedicated with IV midazolam, unlike our study where no sedative premedicant was used.
More patients in group N had 30% or higher decrease in SBP 14 (40%), DBP 8 (22.86%), and MAP 5 (14.29%) at loss of consciousness than in group O. In group O, three patients (8.57%), two patients (5.71%), and three patients (8.57%) had 30% or higher decrease in mean SBP, DBP, and MAP at loss of consciousness, respectively. This contrasts with findings in Belekar’s study[17] in which no hypotension was recorded. It also contrasts with findings by Wani et al[19] in which only 0.8% of participants had hypotension, requiring fluids and vasopressors. There was no difference in the need for vasopressors between the obese patients and the non-obese patients (P = 0.254). In our study, hypotension was managed effectively by administration of intravenous fluid. In the study by Lam et al.,[11] 83% of all patients experienced hypotension, of which 44% experienced marked hypotension. There was no significant difference in SBP and DBP values in both groups. Most of these studies that reported significantly higher doses of propofol had smaller sample sizes than the present study in which the higher dose of propofol was not significant.
The mean SBP, DBP, and MAP increased in both groups at 2 min following induction; this is similar to findings in Belekar’s study[17] in which the SBP, DBP, and MAP increased from post-induction values. This may still be as a result of other events following loss of consciousness like laryngoscopy and intubation. At the same period, group O had a drop in the HR, while the HR increased in group N. This difference may be accounted for by differences in drug metabolism. In Belekar’s study[17] the HR increased significantly a minute after induction but decreased at the 3rd min and the 5th min.
We found the mean SpO2 values to be within normal limits in both treatment groups throughout the study. This is in contrast with the results from Edomwonyi et al,[20] in which the oxygen saturation was within normal limits in both treatment groups. Our patients were pre-oxygenated and received oxygen throughout induction of anaesthesia. In contrast, findings by Wani et al[19] showed hypoxemia in 74 patients (7.3%) out of 1016 patients who received either propofol or propofol combined with either benzodiazepines or opioids for sedation; they found that increased BMI was associated with increased frequency of airway manoeuvres (P < 0.001) and hypoxaemia (P = 0.001).[19] Hypoxaemia occurred in 9.4% of patients with BMI 30–35 (n = 159[16%]), 13.4% of patients with BMI >35 (n = 127[12%]), and 5.3% of patients with BMI<30 (n = 730[72%]). Their use of a combination of propofol and either benzodiazepines or opioids in most of the obese patients (62%) may account for the significantly higher incidence of hypoxaemia, placing them at greater risk of airway collapse during sedation and development of significant alveolar-to-arterial oxygen gradients.[19] However, the induction dose of propofol and total dose of propofol were lower in patients who received a combination of drugs for induction.
The reduced ETCO2 observed at loss of consciousness in group O may be because obese patients have a higher risk of airway obstruction under anaesthesia compared to normal patients. We came across few studies that discussed the respiratory effects of propofol under general anaesthesia. Of these, Ismail et al[13] monitored the end tidal carbon dioxide in patients, but did not discuss their observations on changes in this parameter. Kim et al[21] reported that the frequency of airway obstruction and carbon dioxide concentration in arterial blood increased as the target effect site concentration of propofol increased. Unlike our study which assessed end tidal carbon dioxide values, Kim et al[21] studied arterial partial pressure of carbon dioxide at increasing plasma concentrations of propofol. Unlike their study, none of our patients had airway obstruction prior to endotracheal intubation following propofol administration.
Group O had a higher frequency of apnoea (15[43%]), shallow breathing (5[14%]), and tachycardia (19[54%]) after injection of propofol than group N, in which 12 (34%) patients had apnoea, two (6%) patients had shallow breathing, and 17 (49%) patients had tachycardia.
The respiratory effects observed in our study are comparable to observations by Kim et al[21] and Lee et al[8] in which the frequency of respiratory complications induced by propofol increased with increased effect site concentration (EC); however, unlike these other studies, our study did not investigate the effect site concentration of the study drug. Lee et al[8] studied the effect site concentration of propofol that could cause respiratory depression in 5% (EC5), 10% (EC10), and 50% (EC50) of the population to which the drug was administered. In Lee’s study, the EC5 of propofol for respiratory depression was 3.09 mcg/ml (95% CI: 2.60–3.58), the EC10 was 3.18 mcg/ml (95% CI: 2.57–3.80), and the EC50 was 3.99 mcg/ml (95% CI: 2.36–5.61).[8] In the present study, the obese group received a higher mean induction dose of propofol and thus were more likely to have a higher number of patients with apnoea and shallow breathing.
In the study by Claeys et al,[16] 8 (80%) patients had apnoea at induction of anaesthesia with a mean duration of 90 ± 28 s. Their patients were elderly and were not classified based on BMI. They were also not intubated, and arterial blood gas analysis at 45 min indicated moderate respiratory impairment. Our study, unlike in the study by Claeys et al,[16] did not assess the duration of apnoea and arterial blood gases. Apnoea and shallow breathing were managed by manual ventilation using breathing circuits, while the tachycardia did not require pharmacological intervention.
In contrast to our study in which 38.57% of patients developed apnoea, Edomwonyi et al[20] found that 80% of the normal weight adult patients had this side effect. Unlike our study in which propofol was administered until loss of consciousness was achieved, Edomwonyi et al[20] used a dosage of 2–2.5 mg/kg of propofol. Edomwonyi et al[20], however, had a smaller sample size of 40 patients compared to our study.
The strength of this work lies in the comparability of most of the outcomes in both groups of patients, possibly due to the dosing of propofol, which did not result in undesirable exaggerated responses in the respiratory and cardiovascular systems. However, our study was limited by the difficulty in ensuring blinding, as patients who were obviously obese would have been recognised by the investigator.
CONCLUSION
There were mostly no significant differences in haemodynamic and respiratory parameters following induction of anaesthesia using sleep-inducing doses of propofol within the first 10 min of administration of the drug between patients with class 1 obesity and normal weight. There was also no significant difference in the occurrence of apnoea, shallow breathing, hypotension, and tachycardia between both groups.
We therefore recommend the use of IV propofol for induction of anaesthesia in class 1 obesity as it is safe and effective. However, more studies on depth of anaesthesia and occurrence of awareness under anaesthesia during such use of the drug for induction of anaesthesia in this class 1 obesity are needed.
Conflict of interest
There are no conflict of interest.
Author contributions
Concept and design of study: ORANUSI Ifeatu Ogochukwu, OGBOLI-NWASOR Elizabeth, EZEMA Evaristus Chino. Literature search: ORANUSI Ifeatu Ogochukwu, EZEMA Evaristus Chino.
Acknowledgement
We are grateful to all the patients who accepted to be part of this study.
Funding Statement
Equipment was provided by the Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria. Drugs were paid for by the authors.
REFERENCES
- 1.World Health Organisation. [Last accessed March 6, 2024]. Obesity and Overweight. Available from https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight .
- 2.World Health Organisation. [Last accessed March 8, 2024]. Media Centre: Obesity and Overweight 2024. Available at: https://www.who.int/en/news-room/fact-sheets/detail/obesity-and-overweight .
- 3.Chukwuonye II, Ohagwu KA, Ogah OS, John C, Oviasu E, John C, et al. Prevalence of overweight and obesity in Nigeria: Systematic review and meta-analysis of population-based studies. Plos Glob Public Health. 2022;2:e0000515. doi: 10.1371/journal.pgph.0000515. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Waheed Z, Amatul-Hadi F, Kooner A, Afzal M, Ahmed R, Pande H, et al. General anesthetic care of obese patients undergoing surgery: A review of current anesthetic considerations and recent advances. Cureus. 2023;15:e41565. doi: 10.7759/cureus.41565. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Sikka N, Wegienka G, Havstad S, Genaw J, Carlin AM, Zoratti E. Respiratory medication prescriptions before and after bariatric surgery. Ann Allergy Asthma Immunol. 2010;104:326–30. doi: 10.1016/j.anai.2009.12.009. [DOI] [PubMed] [Google Scholar]
- 6.Butt MN, Ahmed A. The Induction dose of propofol with ketamine-propofol and midazolam-propofol co-induction. J Anesth Clin Res. 2013;4:371–3. [Google Scholar]
- 7.Vuyk J, Sitsen E, Reekers M. Intravenous anesthetics. In: Gropper MA, Eriksson LI, Fleisher LA, Cohen NH, Leslie K, Johnson-Akeju O, editors. Miller’s Anesthesia. 10th ed. Philadelphia: Elsevier; 2024. pp. 512–554. [Google Scholar]
- 8.Lee MH, Yang KH, Lee CS, Lee HS, Moon SY, Hwang S, et al. The effect site concentration of propofol producing respiratory depression during spinal anesthesia. Korean J Anesthesiol. 2011;61:122–6. doi: 10.4097/kjae.2011.61.2.122. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Cortinez ZL, Anderson BJ, Penna A, Olivares L, Munoz HR, Holford NHG, et al. Influence of obesity on propofol pharmacokinetics: Derivation of a pharmacokinetic model. Br J Anaesth. 2010;105:448–56. doi: 10.1093/bja/aeq195. [DOI] [PubMed] [Google Scholar]
- 10.De Baerdemaeker LE, Mortier EP, Struys MM. Pharmacokinetics in obese patients. BJA Educ. 2004;4:152–5. [Google Scholar]
- 11.Lam F, Liao CC, Lee YJ, Wang W, Kuo CJ, Lin CS. Different dosing regimens for propofol induction in obese patients. Acta Anaesthesiologica Taiwanica. 2013;51:53–7. doi: 10.1016/j.aat.2013.06.009. [DOI] [PubMed] [Google Scholar]
- 12.Chan YH. Randomised controlled trials (RCTs)- Sample size: The magic number. Singapore Med J. 2003;44:172–4. [PubMed] [Google Scholar]
- 13.Ismail EA, Bakri MH. Evaluation of propofol dose based on total body weight in obese compared to non-obese patients guided by bispectral index. Int J Pharmaceut Med Res. 2016;4:1–5. [Google Scholar]
- 14.Dutta V, Ahmad M, Gurcoo S, Ommid M, Qazi SM. Prevention of hypotension during induction of anesthesia with propofol and fentanyl: Comparison of preloading with crystalloid and intravenous ephedrine. J Anaesthesiol Clin Pharmacol. 2012;1:26–30. [Google Scholar]
- 15.Billota F, Fiorani L, La Rosa I, Spinelli F, Rosa G. Cardiovascular effects of intravenous propofol administered at two infusion rates: A transthoracic echocardiographic study. Anaesthesia. 2001;56:266–71. doi: 10.1046/j.1365-2044.2001.01717-5.x. [DOI] [PubMed] [Google Scholar]
- 16.Claeys MA, Gepts E, Camu F. Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth. 1988;60:3–9. doi: 10.1093/bja/60.1.3. [DOI] [PubMed] [Google Scholar]
- 17.Belekar VR. A comparison of pressor response to induction and endotracheal intubation with thiopentone and propofol-prospective, randomised study. Int J Biomed Adv Res. 2012;3:708–13. [Google Scholar]
- 18.Rabadi D. Effect of normal saline administration on circulation stability during general anaesthesia induction with propofol in gynaecological procedures-Randomised-controlled study. Rev Bras Anestesiol. 2013;63:258–61. doi: 10.1016/S0034-7094(13)70227-7. [DOI] [PubMed] [Google Scholar]
- 19.Wani S, Azar R, Hovis CE, Hovis RM, Cote GA, Hall M, et al. Obesity as a risk factor for sedation-related complications during Propofol- mediated sedation for advanced endoscopic procedures. Gastrointest Endosc. 2011;74:1238–47. doi: 10.1016/j.gie.2011.09.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Edomwonyi NP, Okonofua BA, Weerasinghe AS, Dangnan F. A Comparative Study of induction and recovery characteristics of propofol and midazolam. Niger Postgrad Med J. 2001;8:81–5. [PubMed] [Google Scholar]
- 21.Kim KS, Kim K, Lee SS, Yoo BH, Lee Y, Yon JH, et al. The effect of cigarette smoking on propofol EC50 of airway obstruction during target controlled infusion of propofol. Korean J of Anesthesiol. 2005;49:25–9. [Google Scholar]