Print version ISSN 0103-507X
Rev. bras. ter. intensiva vol.24 no.1 São Paulo Jan./Mar. 2012
Eliane Regina Ferreira Sernache de FreitasI; Renata Serrou da Silva BersiII; Mariana Yuri KuromotoII; Silviane de Camargo SlembarskiII; Ana Paula Ayumi SatoII; Marcela Quadros CarvalhoIII
IIntensive Care Unit, Hospital Santa Casa de Londrina - Londrina (PR), Brazil; Course of Physiotherapy, Universidade Norte do Paraná - UNOPAR - Londrina (PR), Brazil
IICourse of Physiotherapy, Universidade Norte do Paraná - UNOPAR - Londrina (PR), Brazil
IIIIntensive Care Unit, Hospital Santa Casa de Londrina - Londrina (PR), Brazil
OBJECTIVE: To assess the effects of passive mobilization on acute hemodynamic responses in mechanically ventilated patients.
METHODS: This cross-sectional, quantitative, observational study enrolled patients who were admitted to the intensive care unit, sedated and mechanically ventilated. The infusion of sedative and analgesic drugs aimed to maintain a Ramsay scale sedation level of 4 to 6. Passive mobilization consisted of hip and knee flexion-extension movements for five minutes. After 10 minutes of rest, an additional five minutes of flexion-extension passive movements was performed for the shoulders. Hemodynamic assessments (heart rate and systolic, diastolic and mean blood pressure) were performed one minute before the mobilization protocol and one minute after each phase. The double product and myocardial oxygen consumption were calculated using appropriate formulas.
RESULTS: A total of 13 patients (69.2% male, with a mean age of 69.1 ± 15.8 years) were admitted from June to December, 2011. Passive mobilization led to statistically significant increases in heart rate, double product and myocardial oxygen consumption. However, mean blood pressure was not significantly altered.
CONCLUSIONS: Our results suggest that passive mobilization of mechanically ventilated and sedated patients is safe and provides beneficial effects on acute hemodynamic parameters, particularly heart rate, although mean blood pressure is not significantly altered.
Keywords: Hemodynamics; Intensive care unit; Artificial respiration
Critically ill patients who require sedation and mechanical ventilation are restricted to bed for long periods. This confinement is a risk factor for dysfunction in various organ systems, often becoming more severe than the underlying condition itself.(1) In the intensive care unit (ICU), patients' limbs are routinely mobilized by the unit's physiotherapists, aiming to preserve the range of motion, improve or preserve soft tissue length, maintain muscle condition and reduce the risk of thromboembolism.(2) Mechanical stress from limb mobilization may alter hemodynamic responses such as heart rate (HR), blood pressure (BP) and myocardial oxygen consumption (mVO2).(3) Cardiac output depends on the interaction between two main functions: 1) heart function, which is determined by HR, contractility and pre- and afterload, and 2) return function, which is determined by the volume of venous return, venous drainage resistance and right atrial pressure.(4,5) It has also been demonstrated that the distension and shortening of muscle fibers may activate mechanoreceptors, leading to cardiovascular adjustments via parasympathetic inhibition and sympathetic activation.(4-8)
The potential benefits of exercise for inactive ICU patients have been reported previously.(9,10) Passive lower limb mobilization in critically ill patients prevents muscle fibers atrophy,(11) increases oxygen consumption (VO2) and reduces venous blood oxygen saturation (SVO2), most likely due to an increased oxygen extraction rate (O2ER) and cardiac index.(12) However, the physiological mechanisms behind hemodynamic responses to passive mobilization in mechanically ventilated patients are not fully known.
This study aimed to assess the effects of passive mobilization on acute hemodynamic responses in mechanically ventilated patients.
The study protocol was approved by the ethics committee of Irmandade Santa Casa de Londrina (ISCAL) (project #380/11), and written informed consent forms were signed by designated family members for each patient. The study design was a cross-sectional, quantitative, observational format following the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) criteria.(13)
The patients included were aged over 18 years who were maintained on pressure-controlled-mode mechanical ventilation (MV) (Newport Wave E200, Newmed, CA, USA) for more than 48 hours with the following parameters: a positive end-expiratory pressure (PEEP) between 5 and 8 cmH2O, a tidal volume between 6 and 8 mL/kg and an inspired oxygen fraction (FiO2) of 21-50%. The infusion of sedative and analgesic drugs aimed at a sedation level between 4 (brisk response to stimulus) and 6 (no response to painful stimulus) on the Ramsay scale.(14) All patients were administered vasoactive drugs, and mean blood pressure (MBP) was maintained above 60 mmHg. The following subjects were excluded from the study: hemodynamically unstable patients (MBP < 60 mmHg), patients showing agitation during the maneuvers, and those with resistance to movement, dropping oxygen saturation (< 90%), an intra-aortic balloon, complex arrhythmias, neurologic and/or motor deficits or musculoskeletal limitations preventing the protocol-determined movements.
Passive mobilization (PM) protocol
The patients were maintained in a supine position, with the bed head raised at 30%. PM consisted of hip and knee flexion-extension movements for five minutes (90º flexion). After 10 minutes of rest, an additional five minutes of flexion-extension passive movements was performed for the shoulders (90º). PM was simultaneously performed by two physiotherapists alternating flexion and extension of the right and left limbs at a frequency of 30 movements/minute. To maintain a steady frequency, a metronome was used (KORG MA-30, Japan). Hemodynamic assessments (measurements of HR and systolic (SBP), diastolic (DBP) and mean (MBP) blood pressures) were performed one minute before the mobilization protocol and one minute after the end of each phase.
Clinical signs were continuously monitored using a multi-parameter monitor (Dixtal DX 2010 - Dixtal, Manaus, Brazil) to provide electrocardiogram (ECG), HR, SBP, DBP and MBP measurements. The variable double product (DP) was calculated as the product of SBP and HR (DP = SBP × HR), and myocardial oxygen consumption (mVO2) was calculated using the formula mVO2 = (DP × 0.0014) - 6.3.(15) Demographics and Acute Physiology Chronic Health Evaluation II (APACHE II) scores(16) were recorded for all patients. Drug infusions and mechanical ventilator settings were constant during the protocol.
The normality of the data was confirmed using the Kolmogorov-Smirnov test. Categorical variables are presented as absolute values and proportions, and continuous variables are reported as the means with standard deviations (±SD). The assessments before and after PM were compared using the pairwise samples parametric Student's t-test. A one-way ANOVA was used to compare pre- and post-PM assessments for the upper and lower limb mobilizations. Differences between categorical variables were compared using the Chi-squared test. The Statistical Package for Social Sciences (SPSS 17.0) software was used for the analyses, and a value of p < 0.05 was considered to be significant.
A total of 13 patients (69.2% male, with a mean age 69.1 ± 15.8 years) were enrolled from June to December, 2011. These patients had been admitted to the ICU of Hospital Santa Casa de Londrina - Paraná, Brazil. Table 1 lists the patients' baseline characteristics. The Ramsay scale was adopted to assess the level of consciousness. One patient was categorized as Ramsay 4, three as Ramsay 5 and nine as Ramsay 6.
Table 2 presents the patients' hemodynamic parameters according to the protocol applied to the upper and lower limbs. Statistically significant differences were found for HR (lower limbs, p = 0.015; upper limbs, p = 0.034), DP (lower limbs, p = 0.012; upper limbs, p = 0.025) and mVO2 (lower limbs, p = 0.011; upper limbs, p = 0.024). Immediately after PM, MBP showed a mild but not statistically significant increase.
When the responses to the lower and upper limb mobilizations were compared, no difference was found for the pre- and post-PM assessed variables (Table 3).
No adverse events, such as desaturation or agitation, were recorded during the PM maneuvers.
In this study, passive lower and upper limb mobilizations promoted significant increases in HR, DP and mVO2, but not in MBP. The physiological mechanisms of hemodynamic responses during passive mobilization are not fully known. Although HR increases with cardiac output (CO) during exercise, CO increase should not be interpreted as resulting only from increased HR but rather from the interaction of two main factors: 1) heart function, which is determined by HR, contractility and pre- and afterload, and 2) return function, which is determined by the volume of venous blood return, resistance to venous return and right atrial pressure.(4,5) Although passive mobilization produces no muscle contraction, Doppler tests conducted for the assessment of active and passive kinesiotherapy have shown an increased venous blood flow from the sural pump during passive kinesiotherapy that was well above the baseline.(17)
Muscle tension caused by passive movements can also lead to increased HR due to the activation of tendinous mechanoreceptors.(8,18) Prior studies have shown that simultaneous muscle stretching and shortening, as in typical passive mobilization, causes the activation of mechanoreceptors and type III fibers, which can induce vagal activation and stimulate baroreceptors, thereby contributing to the overall cardiovascular response.(19,20) The mobilization of large muscle groups (such as the hip, knee or shoulder) is another factor likely contributing to the increased HR observed in our study. A similar observation was recently reported by Farinatti et al.,(21) who assessed cardiovascular responses to static flexibility with passive movements in healthy subjects. Their results showed that HR was consistently higher with hip flexion (involving the ischiotibial muscles, a large group) than with ankle dorsal flexion (involving the gastrocnemius, a small group). Additionally supporting our findings, these authors(21) also reported that DP increased with the passive mobilization of both small and large muscle groups, concluding that passive stretching of muscle groups may affect cardiovascular responses. Gladwell and Coote(22) also assessed HR and SBP during one-minute passive and sustained sural triceps stretching, reporting significantly increased HR but not SBP, which are findings similar to our own.
Recently Magder (2012)(23) reviewed the physiological mechanisms regulating HR and the relevance of mobilizing critically ill patients, concluding that HR may be interpreted within the overall hemodynamic condition of the patient and that HR and CO regulation during exertion is reflected in a range of physiological responses, but that HR is the major cardiovascular system component responsible for adjusting CO.(24) Additionally, when the HR response is limited by underlying disease or pharmacological interventions, changes in the systolic volume may act to compensate for such limitations. However, this ability may in turn be limited by the passive filling of the left ventricle.
In our study, MBP was not observed to significantly increase in response to passive mobilization. This observation may be explained by noting that increased peripheral vascular resistance is also influenced by sustained muscle contraction, consequently increasing BP.(25) However, our protocol used a low cycle frequency, maintaining 30 movement cycles/minute for five minutes without active contraction.
Based on our findings, the increased DP may have been caused by increased HR, as no significant BP increase was observed,(26) shown by the MBP results. The DP is usually used to estimate cardiac workload during aerobic and strength exercises.(24) However, several authors have reported that during static flexibility exercises, DP may reach levels that are similar to the levels found during high-intensity, low-repetition resistance exercise.(27,28)
Comparative studies between upper and lower limb exertion tests have shown that at the same level of workload, the CO may be similar that for lower loads.(29-31) This difference may explain our results when comparing the responses for the mobilizations of the upper and lower limbs, where no differences was found for any of the variables, as the loads were the same for both the upper and lower limbs (30 movements/minute).
Cardiac metabolism is influenced both by chrono- and inotropisms, and both have an influence on myocardial overload and oxygen demand.(32) Myocardial oxygen demand may be measured as myocardial oxygen consumption (mVO2), which is determined by the interactions among myocardial tension, heart muscle contractility and HR. All of these factors change during physical exertion, increasing the myocardial requirements for nutrients and oxygen and causing increased coronary flow.(33) A linear correlation between mVO2 and coronary blood flow has been demonstrated, thus providing information on cardiac overload, i.e., the work performed by the heart to meet the body's demand. The product of HR and SBP, the DP, is highly correlated with mVO2 (r2=0.88).(32) Hellerstein & Wenger(15) described a mathematical function to convert DP into mVO2 (mVO2 = (DP × 0.00014) - 6.3), allowing the estimation of cardiac effort. This calculation was applied in our study; the results suggest that due to increased HR, which in turn influenced the DP, heart muscle overload occurred, with a consequently significant increase in mVO2. The hemodynamic and metabolic effects of cyclic passive lower limb mobilization in mechanically ventilated patients was previously assessed by Savi et al.,(12) who reported that all five assessed patients displayed increased oxygen consumption (VO2) concomitant with a drop in venous blood oxygen saturation (SVO2), most likely due to an increased oxygen extraction rate (O2ER) and cardiac index (CI). The authors additionally concluded that cyclic passive lower limb mobilization may influence the hemodynamic and metabolic conditions of sedated patients who are dependent on mechanical ventilation.(12) Additionally, aiming to assess exertion induced hemodynamic changes, Bittencourt et al. (2008) evaluated HR, DP, BP and mVO2 in 11 male subjects. In agreement with our findings, their results demonstrated that physical activity significantly changes HR, DP and mVO2.(34)
Our study had several limitations: 1) the small sample size may have influenced the lack of statistical significance for MBP and 2) the study included patients with Ramsay levels of 4 to 6. Ramsay 4 patients may have had a certain degree of active/assisted muscle activity; however, no comparative intergroup analysis was conducted due to the small sample size.
Our results suggest that passive mobilization of the lower and upper limbs produces acute hemodynamic effects in mechanically ventilated and sedated patients, particularly increasing HR; however, MBP was not significantly affected. It should be noted that considering the assessed variables, no changes were observed that may be considered dangerous according to the available literature. Our procedure resulted in beneficial heart muscle overload in critically ill mechanically ventilated patients.
This work was an initial study, and further studies will be necessary to explore this subject more deeply.
1. Krasnoff J, Painter P. The physiological consequences of bed rest and inactivity. Adv Ren Replace Ther. 1999;6(2):124-32. Review. [ Links ]
2. Koch SM, Fogarty S, Signorino C, Parmley L, Mehlhorn U. Effect of passive range of motion on intracranial pressure in neurosurgical patients. J Crit Care. 1996;11(4):176-9. [ Links ]
3. Rassier DE, MacIntosh BR, Herzog W. Length dependence of active force production in skeletal muscle. J Appl Physiol. 1999;86(5):1445-57. [ Links ]
4. Gladwell VF, Fletcher J, Patel N, Elvidge LJ, Lloyd D, Chowdhary S, Coote JH. The influence of small fibre muscle mechanoreceptors on the cardiac vagus in humans. J Physiol. 2005;567(Pt 2):713-21. [ Links ]
5. Fisher WJ, White MJ. Training-induced adaptations in the central command and peripheral reflex components of the pressor response to isometric exercise of the human triceps surae. J Physiol. 1999;520 Pt 2:621-8. [ Links ]
6. Drew RC, Bell MP, White MJ. Modulation of spontaneous baroreflex control of heart rate and indexes of vagal tone by passive calf muscle stretch during graded metaboreflex activation in humans. J Appl Physiol. 2008;104(3):716-23. [ Links ]
7. Fisher JP, Bell MP, White MJ. Cardiovascular responses to human calf muscle stretch during varying levels of muscle metaboreflex activation. Exp Physiol. 2005;90(5):773-81. [ Links ]
8. Hayes SG, Kindig AE, Kaufman MP. Comparison between the effect of static contraction and tendon stretch on the discharge of group III and IV muscle afferents. J Appl Physiol. 2005;99(5):1891-6. [ Links ]
9. Martin UJ, Hincapie L, Nimchuk M, Gaughan J, Criner GJ. Impact of whole-body rehabilitation in patients receiving chronic mechanical ventilation. Crit Care Med. 2005;33(10):2259-65. [ Links ]
10. Norrenberg M, De Backer D, Moraine JJ. Oxygen consumption can increase during passive leg mobilization. Intensive Care Med 1995;21(Suppl):S177. [ Links ]
11. Griffiths RD, Palmer TE, Helliwell T, MacLennan P, MacMillan RR. Effect of passive stretching on the wasting of muscle in the critically ill. Nutrition. 1995;11(5):428-32. [ Links ]
12. Savi A, Maia CP, Dias AS, Teixeira C. Efeitos hemodinâmicos e metabólicos da movimentação passiva dos membros inferiores em pacientes sob ventilação mecânica. Rev Bras Ter Intensiva. 2010;22(4):315-20. [ Links ]
13. Vandenbroucke JP, von Elm E, Altman DG, Gotzsche PC, Mulrow CD, Pocock SJ, Poole C, Schlesselman JJ, Egger M; STROBE Initiative. Strengthening the Reporting of Observational Studies in Epidemiology (STROBE): explanation and elaboration. Epidemiology. 2007;18(6):805-35. [ Links ]
14. Ramsay MA, Savege TM, Simpson BR, Goodwin R. Controlled sedation with alphaxalone-alphadolone. Br Med J. 1974;2(5920):656-9. [ Links ]
15. Hellerstein HK, Wenger NK. Rehabilitation of coronary patient. New York: John Willey; 1974. [ Links ]
16. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13(10):818-29. [ Links ]
17. Campos CC, Albuqerque PC, Braga IJ. Evaluation of venous flow volume of the calf muscle pump by Doppler ultrasound during active and passive kinesiotherapy: a pilot study. J Vasc Bras. 2008;7(4):325-32. [ Links ]
18. Drew RC, McIntyre DB, Ring C, White MJ. Local metabolite accumulation augments passive muscle stretch-induced modulation of carotid-cardiac but not carotid-vasomotor baroreflex sensitivity in man. Exp Physiol. 2008;93(9):1044-57. [ Links ]
19. Kaufman MP, Hayes SG. The exercise pressor reflex. Clin Auton Res. 2002;12(6):429-39. Review. [ Links ]
20. Baum K, Selle K, Leyk D, Essfeld D. Comparison of blood pressure and heart rate responses to isometric exercise and passive muscle stretch in humans. Eur J Appl Physiol Occup Physiol. 1995;70(3):240-5. [ Links ]
21. Farinatti PT, Soares PP, Monteiro WD, Duarte AF, Castro LA. Cardiovascular responses to passive static flexibility exercises are influenced by the stretched muscle mass and the Valsalva maneuver. Clinics (Sao Paulo). 2011;66(3):459-64. [ Links ]
22. Gladwell VF, Coote JH. Heart rate at the onset of muscle contraction and during passive muscle stretch in humans: a role for mechanoreceptors. J Physiol. 2002;540(Pt 3):1095-102. [ Links ]
23. Magder SA. The ups and downs of heart rate. Crit Care Med. 2012;40(1):239-45. [ Links ]
24. Simão R, Fleck SJ, Polito M, Monteiro W, Farinatti P. Effects of resistance training intensity, volume, and session format on the postexercise hypotensive response. J Strength Cond Res. 2005;19(4):853-8. [ Links ]
25. MacDonald JR, MacDougall JD, Hogben CD. The effects of exercising muscle mass on post exercise hypotension. J Hum Hypertens. 2000;14(5):317-20. [ Links ]
26. Barbosa P, Santos FV, Neufeld PM, Bernardelli GF, Castro SS, Fonseca JHP, et al. Efeitos da mobilização precoce na resposta cardiovascular e autonômica no pós-operatório de revascularização do miocárdio. ConScientiae Saúde. 2010;9(1):111-7. [ Links ]
27. DeBusk RF, Valdez R, Houston N, Haskell W. Cardiovascular responses to dynamic and static effort soon after myocardial infarction. Application to occupational work assessment. Circulation. 1978;58(2):368-75. [ Links ]
28. Longhurst JC, Stebbins CL. The power athlete. Cardiol Clin. 1997;15(3):413-29. Review. [ Links ]
29. Bevegard S, Freyschuss U, Strandell T. Circulatory adaptation to arm and leg exercise in supine and sitting position. J Appl Physiol. 1966;21(1):37-46. [ Links ]
30. Vokac Z, Bell H, Bantz-Holter E, Rodahl K. Oxygen uptake/heart rate relationship in leg and arm exercice, sitting and standing. J Appl Physiol. 1975;39(1):54-9. [ Links ]
31. Stenberg J, Astrand PO, Ekblom B, Royce J, Saltin B. Hemodynamic response to work with different muscle groups, sitting and supine. J Appl Physiol. 1967;22(1):61-70. [ Links ]
32. Miranda H, Rangel F, Guimarães D, Dantas EH, Novaes J, Simão R. Verificação da frequência cardíaca, pressão arterial e duplo-produto em diferentes posições corporais no treinamento de força. Rev Treinam Desport. 2006;7(1):68-72. [ Links ]
33. Fletcher GF, Balady GJ, Amsterdam EA, Chaitman B, Eckel R, Fleg J, et al. Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association. Circulation. 2001;104(14):1694-740. [ Links ]
34. Bittencourt PF, Sad S, Pereira R, Machado M. Effects of different intensities of resistance exercise on hemodynamic variations in young adults. Rev Port Cardiol. 2008;27(1):55-64. [ Links ]
Corresponding author: Submitted on January 11, 2012 Conflicts of interest: None. Study conducted in the Intensive Care Unit of Hospital Santa Casa de Londrina - Londrina (PR), Brazil.
Eliane Regina Ferreira Sernache de Freitas
Rua Belo Horizonte, 540 Apto 11
Zip Code: 86020-060 - Londrina (PR), Brazil.
Phone + 55 (43) 3324-0492
Accepted on March 13, 2012
Submitted on January 11, 2012
Conflicts of interest: None.
Study conducted in the Intensive Care Unit of Hospital Santa Casa de Londrina - Londrina (PR), Brazil.