A Prospective Observational Study of Plethysmograph Variability Index and Perfusion Index in Predicting Hypotension with Propofol Induction in Noncardiac Surgeries.

Context: Propofol induction is associated with hypotension due to changes in intravascular volume, tone of vessels and cardiac output. Plethysmograph variability index (PVI) and perfusion index (PI) are derived indices from pulse oximeter, used for assessing fluid responsiveness and vessel tone, respectively. We studied the utility of these indices in predicting hypotension due to propofol. Aims: The aim of the study is to test the baseline cutoff values of PVI > 15% and PI <1.05 in predicting hypotension with propofol induction. Settings and Design: This is a prospective double-blind observational study in tertiary care hospital.
Methods: Institutional ethical committee approval was obtained. 106 surgical in-patients as per inclusion and exclusion criteria were randomly allotted by computer-generated random numbers. All patients were nil by mouth for 6 h. Injection midazolam and fentanyl were used as premedicants. Propofol at dose of 2 mg.kg-1 was used for induction. Masimo Radical 7® monitor was used for recording of PVI and PI from the upper limb. Baseline values of PVI and PI were recorded every minute from preinduction period till intubation. Standard monitors of noninvasive blood pressure, pulse oximeter, and electrocardiography were used. As per the occurrence of hypotension, patients were grouped as Group H (hypotension) and Group NH (no hypotension). Statistical Analysis: Data were analyzed with SPSS version 20. Quantitative data were analyzed using mean, standard deviation, interquartile range as per distribution. Shapiro-Wilk test with P < 0001 was used descriptive parameters. Scatter plot and Spearman correlation were used to find correlation between the two variables. Mann-Whitney U test was used to compare the two groups in terms of PVI and PI at different time points. Receiver operator characteristic curve was plotted for PI and PVI against hypotension, and cutoff value was calculated. Sensitivity, specificity, positive predictive value, negative value, and diagnostic accuracy of PI and PVI were calculated. P <0.05 was considered statistically significant.
Results: Eighty-one patients (76.4%) who had hypotension were grouped into Group H and 25 patients (23.6%) without hypotension as Group NH. There was no difference between groups with respect to doses of midazolam (P = 0.28), fentanyl (P = 0.54), and propofol (P = 0.28). Baseline cutoff of PVI >15 had sensitivity of 58% and specificity of 56%, respectively. PI cutoff value of < 1.05 had sensitivity of 30.9% and specificity of 48%. The risk ratio of PVI cutoff and PI cutoff were 1.41 and 0.43, respectively. There was poor agreement between mean arterial blood pressure (MAP) estimation and prediction of hypotension by PVI (Cohen's kappa = 0.106, P = 0.218) and PI values (Cohen's kappa = -0.133, P = 0.054). Area under the receiver operator curve was 0.596 and 0.511 for PVI >15% and PI < 1.05, respectively. New cutoff values PVI >17.5% and PI > 0.76 were found. PVI and PI had poor diagnostic performance. There was no significant correlation of PVI and PI with hemodynamic variables such as heart rate, MAP, SBP, DBP, and PP.
Conclusion: Baseline values of PVI >15% and PI < 1.05 are not good tools for predicting hypotension with propofol induction. New values of baseline cutoff of PVI >17.5% have high specificity, and PI > 0.76 has high sensitivity and positive predictive value. Copyright:

INTRODUCTION

Propofol induction is often associated with hypotension.[1] Sympatholytic effect of propofol causes hypotension which is exaggerated in elderly, hypovolemic and cardiac patients, thus risking the occurrence of myocardial ischemia.[2] Prediction of hypotension in the preinduction period with noninvasive monitors can prevent the complications in high-risk cardiac patients.[3]

Hypotension following induction is partly due to changes in intravascular volume, cardiac output and vascular tone.[23] Plethysmograph variability index (PVI) and perfusion index (PI) are new indices derived from pulse oximetery in Masimo Radical 7® monitor, Masimo SET® Pulse Oximeter and Rainbow® Pulse Co-Oximeter from Masimo Corporation, Irvine, CA, USA.[4]

PVI is a noninvasive, dynamic measure of fluid responsiveness, and PI is a measure of vascular tone.[4] Studies have shown that preanesthesia value of PVI >15% and PI value of <1.05 in normotensive patients predicts hypotension with propofol induction.[56] There are no studies that compare the performance of PVI and PI as screening tools.

We aimed to study the baseline values of PVI and PI in predicting the occurrence of hypotension with propofol induction. We used both indices to find a better screening tool among PVI and PI. Primary objective was to compare the standard cutoff values of PVI >15% and PI <1.05 in predicting hypotension.[6] Secondary objectives were to test the sensitivity and specificity of PVI and PI, to find the new cutoff values for PVI and PI, to find the correlation of PVI, PI with heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP).

METHODS

Institutional Ethical Committee approval was obtained.

Patients were enrolled for study with written informed consent from willing patients. Sample size calculation was based PVI changes in normal patients (16 ± 5.5) and PI changes a minimum difference as 3, the effective size was 106.

Patients were randomized according to computer-generated random numbers [Figure 1].

Figure 1

Study design

The prospective randomized double-blind study was conducted in tertiary care hospital over 6 months from November 2018 to May 2019. 106 surgical inpatients in age group of 18–60 years, American Society of Anesthesiologists physical status Classes I and II, requiring general anesthesia were included for the study. Emergency surgeries, pregnant ladies, difficult airway, diabetic, hypertensive, ischemic heart disease, valvular heart disease patients, and patients with arrhythmias were excluded.

Preanesthetic evaluation was conducted on previous day of surgery. All patients were preloaded with 10 mL.kg − 1 of intravenous normal saline after 6 h of nil per oral status in preoperative holding area. Masimo Radical 7® Oximetry from Masimo Corporation, Irvine, CA, USA was used in all patients.

In operating room, preinduction monitors such as electrocardiography, noninvasive blood pressure (NIBP), and Masimo Radical 7® pulse oximeter was placed. Masimo® pulse oximeter probe was placed on the upper limb free from NIBP cuff. Patients and interpreter were blinded for the study. Data were collected by anesthesia resident who was not involved in the study. The readings from Masimo® were checked on all fingers and placed on finger with maximum signal strength. Baseline values of HR, SBP, DBP, PP, Mean arterial blood pressure (MAP), PI, and PVI were noted. The value of PVI and PI after 5 min in operation room before administration of premedication was taken as baseline value. Fentanyl 2 μg.kg −1 and midazolam 0.02 mg.kg −1 were administered intravenously (i.v.) as premedication and the readings were repeated. Postadministration PVI and PI values were taken as after premedication values. Patients were preoxygenated for 5 min. Propofol 2 mg.kg −1 i.v. was injected slowly over 30 s till loss of verbal response. Vecuronium 0.1 mg.kg −1 i.v. was used for muscle relaxation. All patients were mask ventilated with synchronized intermittent mandatory ventillation–pressure control mode with peak inspiratory pressure of 10 cm of H2O and zero positive end-expiratory pressure (PEEP). Parameters were recorded every minute until 5 min from completion of propofol injection before intubation. Patients were intubated after recording of 5th min with appropriate sized endotracheal tube. Maintenance of anesthesia was established with air: oxygen mixture at 50:50% along with isoflurane to maintain minimum alveolar concentration of 1.

Hypotension was defined as a drop in mean arterial blood pressure (MAP) by 20% of the baseline or absolute MAP fall to <60 mmHg. MAP below 55 mmHg was considered as severe hypotension which was treated with rapid intravenous fluid administration (10 mL.kg −1) and mephentermine 6 mg i.v. bolus. Bradycardia was be defined as HR <60 beats per minute (bpm) or decrease by 20% below the baseline value. Bradycardia was treated with atropine 0.6 mg i.v. Any occurrence of hypotension within 5 min after induction was recorded in both groups. Recordings for the study purpose were considered only for 5 min after induction. Recordings during intubation and mechanical ventilation were not considered for study. Intraoperative management was continued as per case requirements. All patients were followed up postoperatively for 24 h for complications of myocardial ischemia.

HR, SBP, DBP, PP, MAP, PI, PVI, and saturation of oxygen were the parameters studied. Correlation between SBP, DBP, MAP, PP with preinduction PVI and PI was assessed for the defined cutoff values. Maximum value of PVI and PI in the 5 min and maximum fall in SBP, DBP, and MAP within 5 min period after induction from baseline value were taken as efficacy parameters.

The data were collected and tabulated into Group H with hypotension (H) and Group (NH) without hypotension as per mean arterial blood pressure criteria. The standard cutoff values of PVI >15 and PI <1.05 were used as new tools in predicting hypotension. The correlation between cutoffs of baseline PVI and PI values was found with MAP, SBP, DBP, and PP. The sensitivity and specificity of the traditional cutoffs were studied.

Statistical analysis

The collected data were entered in Microsoft Excel. Data were analyzed and statistically evaluated using IBM SPSS Statistics for Windows, Version 20.0. Armonk, NY: IBM Corp.2012. Quantitative data were expressed in mean ± standard deviation or median with interquartile range depending on normality distribution. Receiver operator characteristic (ROC) curve was plotted using PI and PVI to predict hypotension, and cutoff value was calculated. Sensitivity, specificity, positive predictive value, negative value, and diagnostic accuracy of PI and PVI were calculated. P <0.05 was considered statistically significant.

Shapiro–Wilk test with P < 0001 was used for describing the distribution of descriptive parameters. Scatter plot and spearman correlation were used to explore the correlation between the two variables. Mann–Whitney U test was used to compare the two groups in terms of PVI and PI at different time points. Friedman test was used to explore the change in PVI and PI over time within each group. Generalized estimating equation method was used to explore the difference in change in PVI and PI between the two groups over time.

RESULTS

The descriptive parameters are as mentioned in Table 1.

Table 1

Descriptive parameters

Parameters	Mean±SD/n (%)
Age (years)	41.52±14.36
Gender
Male	53 (50.0)
Female	53 (50.0)
Weight (kg)	59.67±11.14
ASA class
I	78 (73.6)
II	28 (26.4)
Midazolam dose (mg)	1.07±0.22
Fentanyl dose (mcg)	106.23±14.89
Propofol dose (mg)	113.58±17.83
Hypotension by MAP (present)	81 (76.4)

MAP=Mean arterial blood pressure, SD=Standard deviation, ASA=American Society of Anesthesiologists

As per MAP criteria, 81 patients (76.4%) had hypotension grouped into Group H and 25 patients (23.6%) did not have hypotension as Group NH following induction with propofol. There was no difference observed between the study groups with respect to dose of midazolam (p= 0.28), fentanyl (p = 0.54), and propofol (p = 0.28) [Table 2].

Table 2

Comparison of parameters between Groups

Parameters	Group H Hypotension by MAP: Present (n=81)	Group NH Hypotension by MAP: Absent (n=25)	P
Age (years)	42.22±15.11	39.24±11.57	0.3921
Gender, n (%)
Male	40 (49.4)	13 (52.0)	0.8192
Female	41 (50.6)	12 (48.0)
Weight (kg)	60.72±11.36	56.28±9.84	0.1021
ASA class, n (%)
I	55 (67.9)	23 (92.0)	0.0172
II	26 (32.1)	2 (8.0)
Midazolam dose (mg)	1.08±0.24	1.02±0.10	0.2811
Fentanyl dose (mcg)	106.30±13.82	106.00±18.26	0.5411
Propofol dose (mg)	114.44±18.15	110.80±16.81	0.2811

MAP=Mean arterial blood pressure, ASA=American Society of Anesthesiologists

The Mean arterial blood pressure changed significantly (Friedman test: X2 = 303.7, P = <0.001) from baseline values [Table 3]. The MAP decreased from the time of induction and remained below the baseline values. 26.7% change was observed in overall trend. The steepest fall in MAP was observed at 3rd min. Statistically significant decrease from baseline values was noted for SBP, DBP, PP, and HR.

Table 3

Assessment of change in mean arterial blood pressure (mmHg) over time (n=106)

Time point	MAP (mmHg)			Friedman test
	Mean±SD	Median (IQR)	Range	χ 2	P
Baseline	105.07±76.53	96.15 (18.18)	66.00-873.00	253.9	<0.001
1 min	80.57±13.70	80.65 (18.05)	56.60-121.30
2 min	73.82±14.39	70.30 (14.75)	40.00-117.30
3 min	71.89±13.86	70.00 (18.69)	48.00-109.30
4 min	76.80±15.73	74.15 (25.00)	43.00-123.00
5 min	78.28±17.34	74.85 (25.45)	51.00-154.00

MAP=Mean arterial blood pressure, SD=Standard deviation, IQR=Interquartile range

In study population, 58 patients had baseline PVI >15% and 48 patients had PVI <15. Among 58 patients who had PVI >15%, the incidence of hypotension was 81.03% whereas in patients with PVI <15%, the incidence was 66.6% [Table 4]. The risk ratio as per PVI cutoff was 1.41. The two testing methods – MAP and PVI – for diagnosing hypotension agreed in 57.5% of the cases and disagreed in 42.5% of the cases. There was poor agreement between MAP and PVI method which was not statistically significant (Cohen's kappa = 0.106, P = 0.218).

Table 4

Hypotension as per plethysmograph variability index and mean arterial blood pressure criteria

Hypotension as per PVI	Hypotension by MAP			Cohen’s kappa
	Group H, n (%)	Group NH, n (%)	Total, n (%)	k	P
PVI >15%	47 (44.3)*	11 (10.4)┼	58 (54.7)	0.106	0.218
PVI <15%	34 (32.1)┼	14 (13.2)*	48 (45.3)
	81 (76.4)	25 (23.6)	106 (100.0)

The *cells on the diagonal represent cases where both the methods agreed. The ┼cells represent cases where the two methods disagreed. MAP=Mean arterial blood pressure, PVI=Plethysmograph variability index

The mean PVI values decreased in Group H whereas it increased in Group NH. PVI changed significantly in both group from baseline values (Friedman Test: X2 = 20.5, P = 0.002) [Table 5]. The maximum change in Group H was 9.3% whereas in Group NH, the change was 33.1%. There was significant change in PVI over time of 5 min between two study groups as estimated by generalized estimating equation method (p = 0.008).

Table 5

Assessment of change in plethysmograph variability index over time

Time point	PVI (%)			Friedman test
	Mean±SD	Median (IQR)	Range	χ 2	P
Baseline	17.65±9.97	15.00 (11.00)	5.00-59.00	20.5	0.002
1 min	15.75±6.81	15.00 (8.00)	6.00-39.00
2 min	16.57±6.70	16.00 (8.00)	2.00-39.00
3 min	17.00±6.64	17.00 (7.00)	6.00-39.00
4 min	15.89±6.13	15.00 (7.00)	6.00-39.00
5 min	15.65±6.30	15.00 (6.00)	6.00-50.00

PVI=Plethysmograph variability index, SD=Standard deviation, IQR=Interquartile range

In our study, 38 patients had PI value <1.05 and 68 patients had PI >1.05. In patients with PI <1.05, the incidence of hypotension was 65.9% and in patients with PI >1.05, the incidence was 82.24% [Table 6]. The risk ratio as per PI cutoff was 0.43.

Table 6

Comparison of hypotension by perfusion index (baseline, cutoff <1.05) with hypotension by mean arterial blood pressure

Hypotension as per PI	Hypotension by MAP			Cohen’s kappa
	Group H, n (%)	Group NH, n (%)	Total, n (%)	k	P
PI <1.05	25 (23.6)‡	13 (12.3)§	38 (35.8)	0.133	0.054
PI >1.05	56 (52.8)§	12 (11.3)	68 (64.2)
Total	81 (76.4)	25 (23.6)‡	106 (100.0)

‡Represent results where methods agreed. §Results where tests disagreed. MAP=Mean arterial blood pressure, PI=Perfusion index

The criteria of hypotension by MAP and PI <1.05, agreed in 34.9% of the cases and disagreed in 65.1% of the cases. There was a weak disagreement between the two methods which was not statistically significant (Cohen's kappa = −0.133, p = 0.054).

The mean PI increased from baseline values in both groups [Table 7]. The percentage change was 175.4% and 235.9% in Group H and Group NH, respectively. These changes from baseline were statistically significant within groups (Friedman test: X2 = 166.5, P ≤ 0.001). There was no statistically significant difference in PI values between the groups as estimated by generalized estimating equation method (P = 0.057).

Table 7

Assessment of change in perfusion index over time

Time point	PI			Friedman test
	Mean±SD	Median (IQR)	Range	χ 2	P
Baseline	2.18±2.58	1.20 (1.79)	0.23-15.00	166.5	<0.001
1 min	2.40±2.53	1.60 (1.92)	0.12-12.60
2 min	3.08±3.71	2.25 (2.60)	0.12-30.00
3 min	3.85±5.87	2.90 (2.95)	0.24-56.00
4 min	3.65±2.97	3.10 (2.40)	0.16-19.00
5 min	3.90±2.58	3.50 (2.45)	0.15-11.50

PI=Perfusion index, SD=Standard deviation, IQR=Interquartile range

The diagnostic performances of standard baseline cutoff values are represented in Table 8.

Table 8

Diagnostic performance of plethysmograph variability index and perfusion index as per standard cutoff values

Parameter	Cutoff	Sensitivity (%)	Specificity (%)	PPV (%)	NPV (%)	DA (%)	P
PVI, baseline	≥15%	58.0	56.0	81.0	29.2	57.5	0.218
PI, baseline	<1.05	30.9	48.0	65.8	17.6	34.9	0.054

PVI=Plethysmograph variability index, PI=Perfusion index, PPV=Positive predictive value, NPV=Negative predictive value, DA=Diagnostic accuracy

The area under the ROC curve (AUROC) for PVI was 0.596 (95% confidence interval [CI]: 0.472–0.719) at cutoff of PVI > 15, thus demonstrating poor diagnostic performance and statistically not significant (P = 0.150) [Figure 2 and Table 9].

Figure 2

Receiver operator curve analysis for plethysmograph variability index, perfusion index, and hypotension

Table 9

Diagnostic performance as per receiver operator curve analysis

Predictor	AUROC	95% CI	P
PVI (baseline) >15%	0.596	0.472-0.719	0.150
PI (baseline) <1.05	0.511	0.363-0.66	0.867

ROC=Receiver operator curve, AUROC=Area under ROC, CI=Confidence interval, PVI=Plethysmograph variability index, PI=Perfusion index

The AUROC for PI was 0.511 (95% CI: 0.363–0.66), thus demonstrating poor diagnostic performance. The cutoff and the diagnostic parameters recorded in our study point were not statistically significant [Table 9].

As per the ROC curve for the recordings in our cases, the new cutoff values achieved for PVI-baseline cutoff is 17.5% and for PI–baseline cutoff is PI > 0.76. The diagnostic performance is as shown in Table 10.

Table 10

Diagnostic performance of new cutoff of plethysmograph variability index and perfusion index

Parameter	Cutoff	Sensitivity (%)	Specificity (%)	PPV (%)	NPV (%)	DA (%)	P
PVI %	>17.5	38.3	84.0	88.6	29.6	49.1	0.038
PI	>0.76	81.5	36.0	80.5	37.5	70.8	0.068

PVI=Plethysmograph variability index, PI=Perfusion index, PPV=Positive predictive value, NPV=Negative predictive value, DA=Diagnostic accuracy

In our study of cutoff values, PVI > 15%, baseline showed weak positive correlation between and MAP (rho = 0.17, p = 0. 077), SBP (rho = 0.06, p = 0. 539), DBP (rho = 0.13, p = 0.192); PP (rho = 0.03, p = 0.741), HR (rho = 0.09, p = 0.377). The correlation was not statistically significant.

Baseline PI < 1.05 had weak positive correlation between the readings of HR (rho = 0.02, P = 0.838), Mean arterial blood pressure, SBP (rho = 0.08, P = 0.44); weak negative correlation with DBP (rho = −0.01, P = 0.888); and weak positive correlation with PP (rho = 0.03, P = 0.767). The correlation between PI and with changes in HR, MAP, SBP, DBP, or PP was not statistically significant at any time point in the study.

DISCUSSION

PVI and PI are derived indices from peripheral pulse oximeter signal which measure fluid responsiveness and tone of blood vessels. They are used as screening monitors in predicting the occurrence of hypotension during induction. Screening tests ideally should have high sensitivity to include all the susceptible subjects and help plan the management. Preinduction PVI and PI values were used in our study as screening tools to predict the occurrence of hypotension with standard cutoff values. High specificity will pick true negatives and help eliminate the nonrisky candidates. We found that preinduction values of PVI and PI were not sensitive tools to predict hypotension with propofol induction.

Preexisting fluid deficits can alter the intravascular volume and increase the incidence of hypotension with induction.[6] In our study, 58 patients had PVI >15% of whom 47 patients presented with hypotension. The traditional cutoff values of PVI >15% predicted hypotension with sensitivity of 58% and specificity of 56%. Tsuchiya et al.[6] recorded higher sensitivity of 79% with the same cutoff value. In study by Tsuchiya et al.,[6] NPO was for 11 h and preloading with intravenous fluids were not performed. This could have affected the severity and incidence of hypotension. We maintained NPO for 6 h which was followed by fluid administration. Tsuchiya et al.[6] recorded at frequency of 30 s for 3 min; and in our study, values recorded after induction at 1 min intervals. The difference in sensitivity and specificity may be due to different sample size, duration of NPO, and time points of recording.

Tsuchiya et al.[6] found positive correlation of MAP and moderate negative correlation between SBP and DBP with baseline PVI value of >15%. In our study, baseline PVI values were higher in patients who presented with hypotension, but there was no significant correlation of PVI with MAP, PP, SBP, and DBP. Our results differ from Tsuchiya et al.,[6] due to different time points and preoperative preparation, though the same cutoffs were used.

PEEP and mechanical ventilation affect PVI. PEEP alters the venous return in patients with low intravascular volume. Mechanical ventilation with positive pressure also alters the venous return. In our study, the baseline values were recorded in spontaneously breathing patients without PEEP. Cannesson et al.[7] studied fluid responsiveness on mechanically ventilated patients and effect of PEEP in general anesthesia cases where propofol was used for induction. The recordings were throughout the procedure in postintubation period. Cannesson et al.[7] used PVI value >14% as cutoff and recorded sensitivity of 81% and specificity of 100%. Our results differed in both sensitivity and specificity. We did not study fluid responsiveness as all patients were preloaded before induction with propofol. The data collection was in the first 5 min before intubation, during mask ventilation with zero PEEP. Hence, the results differ with that of Cannesson et al.[7]

Kuwata et al.[8] studied preprocedure PVI and PI in LSCS cases under spinal anesthesia. Spinal block leads to sympatholysis and venous pooling in lower limbs within minutes of intrathecal drug administration. Kuwata et al.[8] recorded high sensitivity of 78.1% and specificity of 83% with preprocedure PVI > 18% as compared to our study. We differ with results due to different set of study participants. We excluded obstetric cases and regional anesthesia.

PVI and PI also change in spontaneously breathing patients from mechanically ventilated patients. The differences observed with Kuwata et al.[8] could be due to different mechanisms for the occurrence of hypotension, which is primarily due to sympatholysis in spinal anesthesia and vasodilation and cardiac suppression in general anesthesia. As we studied patients on general anesthesia with intravenous induction, the occurrence of hypotension varies which in turn changes sensitivity and specificity of the study.

The incidence of hypotension in our study was 76.8%. Mehandale and Rajasekhar[9] noted a similar incidence of hypotension for propofol induction with the same cutoff value of PI. Mehandale and Rajasekhar[9] observed that preinduction PI was an independent predictor of fall in SBP following propofol induction. Preinduction PI value of < 1.05 was used for predicting fall in SBP with sensitivity of 93% and specificity of 71%. In our study, baseline PI < 1.05 could predict hypotension with sensitivity of 69% and specificity of 52%. Although the baseline cutoff values in our studies were comparable, SBP criteria were used for diagnosing hypotension whereas MAP was used in ours. We recorded changes within 5 min after drug administration without inhalational agent during mask ventilation. The effects of inhalational agents, mechanical ventilation in their study could have achieved different sensitivity and specificity. We considered only MAP criteria for its significance in achieving tissue perfusion. Mehandale and Rajasekhar[9] used SBP and absolute MAP changes for defining hypotension.

Tsuchiya et al.[6] found that PI had positive correlation with MAP. We did not find statistically significant correlation of PI with HR, SBP, DBP, MAP, or PP. Tsuchiya et al.[6] recorded values for 3 min following induction; measurements were made every 30 s and longer period of NPO was followed. Inhalation agent used during study period could have altered the values of PI and MAP which might have led to different results.

Cannesson et al.[7] also observed positive correlation of PVI and PP in normotensive patients. The PI is inversely related to vascular tone. Lesser the value at preinduction phase-greater the fall in blood pressure occurs in postinduction phase which is due to loss of vascular tone with GA drugs. Kuwata et al.[8] noted higher values in PI during hypotension. In our study, baseline PI was lower in patients who presented with hypotension and the PI values increased constantly in postinduction period. Tsuchiya et al.,[6] Kuwata et al.,[8] and Mehandale and Rajasekhar[9] noted significant difference in PI changes from baseline value. We observed similar findings in our study. We did not find correlation between baseline PI values and changes in MAP.[6] Kuwata et al.,[8] Mizuno et al.,[10] and Duggappa et al.[11] found weak positive correlation between PI and MAP with PI values >3. In our study, we considered the cutoff PI <1.05 and differed from other studies in NPO, duration of recording and fluid management in study cases.

The vasomotor tone is affected by drugs such as anxiolytics, opioids, inhalational agents, and induction agents due to vasodilation. Mizuno et al.[10] studied the changes in P I and PVI before and after induction of anesthesia. It was observed that PI increased from baseline values, whereas PVI decreased from baseline values. We recorded significant changes in PI and PVI from baseline values but the trend was not statistically significant between patients who had hypotension. The difference could be due to different time points in measurement. Mizuna et al.[10] recorded values from preinduction period values before induction till postintubation period. In our study, inhalational agents were avoided during mask ventilation and recording ended before intubation. The PVI is affected by intravascular volume, blood pressure, pulsations at peripheries, and respiratory dynamics. Induction agent and intubation response alter the peripheral circulation and affect the pulse signal strength. This possibly explains the differences observed in PVI in studies.

Kuwata et al.[8] observed that PI values increased throughout LSCS patients under spinal anesthesia. Higher PI values were noted hypotensive patients. We observed significant change from baseline till 5 min after induction. Our study was conducted on GA, nonobstetric patients where the mechanism of hypotension is different. We did not find correlation with PVI and PI as in Kuwata et al.[8] Duggappa et al.[11] found that parturients posted for LSCS with PI value >3.5 could predict the incidence of hypotension following spinal anesthesia with a sensitivity and specificity of 69.84% and 89.29%, respectively. The mechanisms that cause hypotension in subarachnoid blockade and general anesthesia and cutoff values used in our study could be the reason for difference in findings observed.

Limitations noted in our study – recordings were noted only till intubation, NIBP was used for correlation. We note this as a drawback as invasive blood pressure would accurately record blood pressure and reflect instant changes. We did not study the trends of PVI and PI in postintubation period.

Further studies are needed to find the cutoff values for PVI and PI in different patients and with different induction agents.

CONCLUSION

The standard baseline PVI >15% and PI <1.05 values did not predict the occurrence of hypotension in general anesthesia cases induced with propofol. There was no correlation between baseline PVI >15% and PI <1.05 with the occurrence of hypotension and hemodynamic parameters such as HR, SBP, DBP, and PP. PVI >17.5% has higher specificity and PI values < 0.76 has higher sensitivity than studied cutoff values. PVI and PI are not diagnostic tool for hypotension but are clinically useful tools in identifying hypovolemia in high-risk patients. PVI and PI are simple, noninvasive, sensitive, and dynamic monitors which ensure safety in anesthesia practice.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.