A heat and moisture mask attenuates cardiovascular stress during cold air exposure

Abstract

Background:

Exposure to cold has been shown to cause cardiovascular stress and increased morbidity and mortality. Inhalation of cold, dry air can increase blood pressure and induce myocardial ischemia, particularly in people with preexisting hypertensive cardiovascular disease. Face masks that can warm and humidify inhaled cold air may reduce these cold air pressor effects.

Method:

We compared blood pressure measurements using a heat and moisture exchange mask (HME), a placebo mask (PL), and no mask (NM) in 53 patients with hypertension exposed to a cold chamber environment at −5°C for 1 h. Blood pressure and heart rate were recorded at baseline, and at 15 min intervals from 0 to 60 min of chamber exposure. All patients were taking antihypertensive medications with drug and dosage determined by their own physicians. Data were analyzed by a one-way analysis of variance test with repeated measures, and significant interactions were analyzed by Fisher’s least significant differences tests. A post hoc subgroup analysis for the effect of age was performed using Wilcoxon matched-pair rank tests.

Results:

Wearing the HME resulted in significantly lower systolic and mean arterial blood pressures than the PL and NM conditions. Diastolic blood pressures were significantly lower for the HME than the NM, but not the PL condition.

Conclusion:

Subgroup analyses suggested that the effect of the HME in mitigating systolic blood pressure increase from inhalation of cold air was significantly greater for patients aged 60 years or over than for those under 60 years.

Keywords

cold exposure hypertension blood pressure heat and moisture exchange mask

Introduction

Exposure to cold imposes stress upon the cardiovascular system. It has been well documented that a decrease in ambient temperature is associated with increased cardiac morbidity and mortality [Boulay et al. 1999; Bull and Morton, 1975; Douglas et al. 1995; Gyllerup et al. 1991; Ornato et al. 1996; Sheth et al. 1999], stroke [Sheth et al. 1999; Hong et al. 2003], and all-cause mortality rates [Keatinge et al. 1989; Mackenbach et al. 1992]. This hypothermic-induced morbidity and mortality appears to center on an increase in blood pressure (BP), particularly in people with preexisting hypertension or ischemic heart disease [Brennan et al. 1982; Giaconi et al. 1989; Jehn et al. 2002; Korhonen et al. 2006; Kunes et al. 1991; Psaty et al. 2001; Woodhouse et al. 1993; Flack et al. 1995; Rabkin et al. 1978].

Our upper airway serves to warm and humidify inspired cold dry air, but at a physiologic cost [Regnard, 1992; Latvala et al. 1995]. At rest in a cold ambient environment, almost 10% of the body’s heat is lost via our respiratory system [Brebbia et al. 1957]. In addition, studies directed at exposure of the tracheobronchial tree to cold air have shown an increase in BP with the potential to induce episodes of angina [Lassvik and Areskog, 1980]. Furthermore, inhalation of cold air has been shown to produce myocardial ischemic diagnostic changes on single-photon emission computed tomography and thallium scanning, as well as a release of endothelin 1, a potent vasoconstrictor that notably has proved to be a marker in exercise-induced ischemia [Petersen et al. 1994; Lubov et al. 2001]. With decreasing temperatures of inspired air, this cooling effect can further potentiate the release of vasoconstrictors [Jaeger et al. 1980; Petersen et al. 1994; McFadden, 1983; McFadden et al. 1985; Zawadski et al. 1988; Watt et al. 1989]. Warming of inspired air might reduce these untoward effects [Petersen et al. 1994; Romet et al. 1988].

A heat and moisture exchange mask (HME) captures heat lost, as well as trapping water vapor upon exhalation. This trapped heat and water vapor can then be used to warm the cold dry inspired air via latent heat transfer. This state of exhaled heat and water vapor could help to achieve less cardiovascular stress by mitigating the effects of breathing cold and dry air. Besides the effect on cardiovascular diseases, the use of an HME in people with cold-induced asthmatic symptoms has been shown to be effective in reducing forced expiratory volume in 1 s, which some studies have reported to be more effective than inhaled albuterol treatments [Millqvist et al. 1995; Beuther and Martin, 2006]. To warm and humidify inspired air, a mask must contain an exchange medium that is freeze resistant. To date, no studies have reported findings using an HME, specifically assessing cold-air-induced increases in BP. Therefore, the purpose of this study was to evaluate the effect of an HME mask on BP during cold air inhalation in patients with hypertension.

Materials and methods

This study enrolled 53 patients with hypertension (30 women and 23 men) between 18 and 80 years of age (mean 56.7 ± 13.4 years for women, 57.2 ± 12 years for men) without evidence of pulmonary, cardiac or peripheral vascular disease. Current hypertensive therapy was established pre enrollment by their personal physician and was controlled with either a single agent (n = 36) or a combination of pharmaceuticals (n = 17). This study was approved by St Cloud State University’s Institutional Review Board and each patient provided signed informed consent prior to participation.

Per protocol, the elapsed time between taking their hypertensive medication in the morning and data collection in the afternoon was standardized for all patients based on their procedural schedule. Three different treatment conditions during an exposure to cold inhalation were tested: the use of an HME (CT Mask, Airguard Medical Products, Memphis, TN, USA), a placebo mask without heat and moisture exchange capabilities (PL), and no mask (NM). Three separate assessments were performed for each patient with a minimum of 3 days between evaluations. The experimental design entailed 15 min of seated rest at an ambient room temperature of 23°C. During this rest interval, baseline BP, heart rate and peripheral oxygen saturation (SpO₂) were measured. BP was measured with a calibrated Welch Allyn/Tycos TR-2 aneroid sphygmomanometer (Skaneateles Falls, NY, USA) and standard adult-sized arm cuff by an experienced technician of the Human Performance Laboratory. Duplicate measurements were obtained at each evaluation. Mean arterial pressure (MAP) was calculated. Heart rate and SpO₂ were measured with a Nonin Medical pulse oximeter, model 8000H (Plymouth, MN, USA). Patients, dressed in winter clothing to minimize the convective and radiant cooling, then entered the cold chamber at −5°C and the same parameters were recorded in duplicate at 0, 15, 30, 45, and 60 min.

Statistics

Data were analyzed by a one-way analysis of variance with repeated measures. When a significant interaction was observed, comparative testing for significant F ratios was performed using Fisher’s least significant difference test. The α level of significance was established at 0.05. Subgroup analyses using Wilcoxon matched-pair tests were conducted to evaluate the relationship between age and the effects of the HME, PL, and NM treatment conditions on BP changes [LaVange and Koch, 2006]. These subgroup analyses were considered as exploratory and descriptive in accordance with accepted experimental design principles [Ellis et al. 2008].

Results

All 53 patients completed the study without experiencing any adverse events during the testing sessions. Baseline evaluation revealed no significant differences in mean systolic BPs or MAP between the HME, NM, and PL. However, during the cold exposure testing, there were significant differences between the groups. Systolic BPs, as well as MAP, were significantly lower for the HME than for the NM (p < 0.0001) and PL (p < 0.01) conditions (Table 1). There were no statistical differences in the MAP analysis between NM and PL conditions (p = 0.07). The lower systolic BP with the HME compared with either no mask or a placebo mask was immediate upon cold exposure. At 60 min, the difference was 12–13 mm, and the mean systolic pressure of HME wearers remained at or below 140 mm, not observed in either NM or PL evaluations.

Table 1.

Systolic and mean arterial blood pressure measurements during cold air inhalation.

	No mask	Placebo mask	HME
Mean systolic blood pressure (SD)
0 min	131 (20)	128 (18)	127 (17)
15 min	144 (20)	139 (17)	137 (19)
30 min	143 (18)	140 (18)	136 (18)
45 min	144 (17)	143 (17)	138 (17)
60 min	147 (18)	146 (19)	138 (18)
p value versus HME*	<0.0001	<0.01
Mean arterial blood pressure (SD)
0 min	96 (13)	95 (12)	96 (12)
15 min	107 (13)	104 (12)	103 (12)
30 min	107 (11)	105 (12)	103 (12)
45 min	108 (12)	107 (13)	104 (11)
60 min	110 (12)	108 (13)	104 (11)
p value versus HME*	<0.001	<0.006

One-way analysis of variance and Fisher’s least significant difference tests.

HME, heat/moisture exchange mask; SD, standard deviation.

Mean diastolic BP using HME was significantly lower than the findings in the NM condition (p < 0.0001), but did not differ from the PL condition (p = 0.15). Further data analysis revealed that the HME mask, in mitigating cold air induced systolic BP increases, may have a greater effect in older patients (Table 2). Post hoc subgroup comparisons of patients greater than 60 years of age demonstrated a significantly lower systolic BP effect with HME than with the NM and PL conditions at all measured time intervals. In patients under the age of 60 years, the HME was superior to the NM and PL treatment conditions only at 60 min. Tables 3 and 4 present the Wilcoxon matched pair results. No significant differences in heart rate or SpO₂ were observed between any treatment conditions.

Table 2.

Systolic blood pressure during cold air inhalation: aged 60 years or over and aged less than 60 years.

	0 min	15 min	30 min	45 min	60 min
Age ≥ 60 years
BP (+SD)
No mask	135 (21)	147 (22)	148 (20)	149 (18)	152 (19)
Placebo mask	127 (18)	146 (17)	146 (17)	149 (18)	151 (19)
HME mask	127 (17)	137 (21)	136 (19)	138 (17)	138 (20)
Age < 60 years
BP (SD)
No mask	128 (19)	140 (17)	138 (14)	140 (15)	143 (16)
Placebo mask	124 (16)	135 (18)	134 (16)	137 (15)	141 (18)
HME mask	126 (16)	137 (17)	137 (17)	138 (16)	138 (16)

BP, blood pressure; HME, heat/moisture exchange mask; SD, standard deviation.

Table 3.

Wilcoxon matched-pair two-tailed test for systolic blood pressure increase on cold air inhalation in treated patients with hypertension (aged 60 years and over; n = 25).

		0 min	15 min	30 min	45 min	60 min
HME versus PL	W statistic	88	71	69.5	57.5	41
	p value	<0.05	<0.02	<0.02	<0.01	<0.01
HME versus NM	W statistic	58	72	34.5	26.5	21
	p value	<0.02	<0.02	<0.01	<0.01	<0.01

HME, heat/moisture exchange mask; NM, no mask; PL, placebo mask; W, Wilcoxon.

Table 4.

Wilcoxon matched-pair two-tailed test for systolic blood pressure increase on cold air inhalation in treated patients with hypertension (aged < 60 years; n = 28).

		0 min	15 min	30 min	45 min	60 min
HME versus PL	W statistic	151	170	183.5	144	104.5
	p value	NS	NS	NS	NS	<0.05
HME versus NM	W statistic	134	129	139.5	139	72.5
	p value	NS	NS	NS	NS	<0.01

HME, heat/moisture exchange mask; NM, no mask; PL, placebo mask; NS, nonsignificant; W, Wilcoxon.

Discussion

Cold air exposure can pose significant health risks [Boulay et al. 1999; Bull and Morton, 1975; Douglas et al. 1995; Gyllerup et al. 1991; Ornato et al. 1996; Sheth et al. 1999; Hong et al. 2003; Keatinge et al. 1989; Mackenbach et al. 1992]. Our findings support this premise and support the results of Petersen and colleagues, reporting that cold air inhalation led to cardiovascular constriction [Petersen et al. 1994]. We observed that patients with known hypertension and treated effectively, in temperate environments, can experience significant elevations in systolic BP when inhaling cold air. Furthermore, we found a beneficial effect on BP when using an inhalation mask during exposure to the cold. The use of the HME mask significantly mitigated cold air induced increases in systolic BP, diastolic BP, and MAP in patients with hypertension. We found that the placebo condition exhibited a negligible effect on BP, such as using a scarf. A scarf can at least reduce the direct cold air effect on one’s face and may at best try to minimize the level of bronchoconstriction, but it does not provide the necessary warming and humidification of cold inspired air, which can be achieved with an HME mask.

A persistent elevation in systolic BP is associated with an increase in mortality due to events such as acute myocardial infarction and stroke. However, diastolic hypertension does not appear to have comparable risks or acute life-threatening events [Psaty et al. 2001; Lee et al. 1999]. Lassvik and Areskog reported that, during submaximal exercise, the inhalation of cold air can independently produce an elevation in BP [Lassvik and Areskog, 1980]. We found similar findings in our study population at rest. It is likely that if our study had used exercise, the positive findings might have been intensified, possibly due to an increase in minute volume ventilation with a subsequent increase in heat loss with vasoconstriction [Jaeger et al. 1980; McFadden, 1983; McFadden et al. 1985; Watt et al. 1989].

Inspired cold air directly affects our pulmonary airway. As cold air is inspired, levels of endothelin 1 are produced and released. Endothelin 1 stimulates peripheral vasoconstriction, as well as myocardial vasoconstriction with resultant ischemia [Petersen et al. 1994; Lubov et al. 2001]. Hemodynamically, peripheral vasoconstriction causes an increase in total peripheral resistance, placing increased stress on the heart with potentially elevating BP [Petersen et al. 1994; Jehn et al. 2002]. Millqvist and colleagues reported improvement in BP in patients wearing an HME mask during cold exposure [Millqvist et al. 1995]. An HME mask warmed inhaled cold air and significantly reduced pulmonary stress and heat loss, unlike the use of no mask or the use of a wool scarf. It is noteworthy that while a scarf may help minimize the level of bronchoconstriction, provided the dead air space is sufficient, the scarf does not offer the protection an HME mask provides. However, the problem with the HME mask that was used in the Millqvist study is that the thermal medium was made of a cellulose material which can absorb moisture and then has the potential to freeze as the environmental temperature drops below the freezing point or during prolonged exposure periods. Therefore, a mask should have a thermal medium resistant to freezing conditions.

The possibility of a greater benefit of the HME mask in patients over the age of 60 years definitely has additional clinical significance. The lower systolic BP with the HME versus the no mask and placebo mask conditions appeared rapidly on cold exposure. At 60 min, the difference was 12–13 mm, and the mean systolic BP of HME wearers remained at or below 140 mm, which was not the case for the NM and PL treatments. Post hoc analyses by Wilcoxon matched-pair rank tests revealed that for subjects older than 60 years, the HME was superior to the NM and PL conditions throughout the entire treatment session. For younger subjects the HME superiority was statistically significant at the 50 min time period. The incidence and degree of cardiovascular disease increases with age, therefore measures to minimize cardiopulmonary stress should be strongly considered. Subjecting an aging individual to cold situations has the potential to further stress an already compromised clinical condition. The use of an HME may have additional benefits beyond reduction in BP. Studies have reported that cold air inhalation in patients with coronary artery disease can precipitate myocardial vasoconstrictor peptide release, potentially precipitating ischemia [Dodds et al. 1995]. However, from a review of the literature and the findings in this initial study, the use of an HME should be strongly considered in individuals living in a cold climate and most importantly in those older than 60 years.

In another consideration, cold exposure may also lead to increased oxidative stress which, may lead to further complications in the clinical patient [Blagojevic et al. 2001; Marek et al. 2013]. Besides wearing an HME, one could argue that the use of nutraceutical supplements, such as various antioxidants and D-ribose, could offer a theoretical benefit to tissues subjected to ischemia or oxidative stress [Seifert et al. 2009; Jeserich et al. 1999; Ergonul et al. 2007]. Measured parameters of high-energy phosphates and oxidative stress metabolites may help in supporting this added dietary supplement premise. However, further research on this hypothesis is warranted.

Conclusion

An HME mask for cold exposure conditions can provide significant mitigation of cold air-induced increases in systolic BP, diastolic BP and MAP compared with NM and PL mask conditions in patients with diagnosed hypertension. While not isolating any certain pharmaceutical class, it is apparent that pharmaceuticals alone were not effective in minimizing hypertension during cold air inhalation. The benefit was greater in patients aged 60 years or over than in those under 60 years. Published reports centering on the increase in cardiovascular morbidity and mortality from cold, dry air inhalation would suggest that consideration in the use of an HME mask may provide a significant preventive benefit to people with hypertension, and the magnitude of this benefit may be more significant for those aged 60 years or over.

Footnotes

Funding

The study was funded by Polar Wrap, LLC, Memphis TN. Polar Wrap, LLC was not involved in the study design, data collection, analysis or interpretation of data, or in the preparation and writing of this manuscript.

Conflict of interest statement

The authors declare no conflicts of interest in preparing this article.

References

Beuther

Martin

(2006) Efficacy of a heat exchanger mask in cold exercise–imduced asthma. Chest 129: 1188–1193.

Blagojevic

Grubor-Lajsic

Spasic

(2011) Cold defence responses: the role of oxidative stress. Front Biosci (Schol Ed) 3: 416–427.

Boulay

Berthie

Sisteron

Gendreike

Gibelin

(1999) Seasonal variation in chronic heart failure hospitalizations and mortality in France. Circulation 100: 280–286.

Brebbia

Goldman

Buskirk

(1957) Water vapor loss from the respiratory tract during outdoor exercise in the cold. J Appl Physiol 11: 219–222.

Brennan

Greenberg

Miall

Thompson

(1982) Seasonal variation in arterial blood pressure. Br Med J (Clin Res Ed) 285: 919–923.

Bull

Morton

(1975) Seasonal and short-term relationships of temperature with deaths from myocardial and cerebral infarction. Age Aging 4: 19–31.

Dodds

Bellamy

Muirhead

Perry

(1995) Vasoconstrictor peptides and cold intolerance in patients with stable angina pectoris. Br Heart J 73: 25–31.

Douglas

Dunnigan

Allen

Rawles

(1995) Seasonal variation in coronary heart disease in Scotland. J Epidemiol Community Health 49: 575–582.

Ellis

Tendera

de Balder

van Boven

Widimsky

Janssens

. (2008) Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med 358: 2205–2217.

10.

Ergonul

Erdem

Balkanci

Kilinc

(2007) Vitamin E protects against lipid peroxidation due to cold-SO2 coexposure in mouse lung. Inhal Toxicol 19: 161–168.

11.

Flack

Neaton

Grimm

Jr Shih

Cutler

Ensrud

. (1995) Blood pressure and mortality among men with prior myocardial infarction. Multiple Risk Factor Intervention Trial Research Group. Circulation 92: 2437–2445.

12.

Giaconi

Ghione

Palombo

Genovesi-Ebert

Marabotti

Fommei

. (1989) Seasonal influences on blood pressure in high normal to mild hypertensive range. Hypertension 14: 22–27.

13.

Gyllerup

Lanke

Lindholm

Schersten

(1991) High coronary mortality in cold regions of Sweden. J Intern Med 230: 479–485.

14.

Hong

Rha

Lee

Kwon

Kim

(2003) Ischemic stroke associated with decrease in temperature. Epidemiology 14: 473–478.

15.

Jaeger

Deal

Roberts

Ingram

Jr McFadden

Jr (1980) Cold air inhalation and esophageal temperature in exercising humans. Med Sci Sports Exerc 12: 365–369.

16.

Jehn

Appel

Sacks

Miller

III (2002) The effect of ambient temperature and barometric pressure on ambulatory blood pressure variability. Am J Hypertens 15: 941–945.

17.

Jeserich

Schindler

Olschewski

Unmüssig

Just

Solzbach

(1999) Vitamin C improves endothelial function of epicardial coronary arteries in patients with hypercholesterolaemia or essential hypertension–assessed by cold pressor testing. Eur Heart J 20: 1676–1680.

18.

Keatinge

Coleshaw

Holmes

(1989) Changes in seasonal mortalities with improvement in home heating in England and Wales from 1964 to 1984. Int J Biometeorol 33: 71–76.

19.

Korhonen

(2006) Blood pressure and heart rate responses in men exposed to arm and leg cold pressor tests and whole-body cold exposure. Int J Circumpolar Health 65: 178–184.

20.

Kunes

Tremblay

Bellavance

Hamet

(1991) Influence of environmental temperature on the blood pressure of hypertensive patients in Montreal. Am J Hypertens 4: 422–426. Erratum in Am J Hypertens 4: 794.

21.

Lassvik

Areskog

(1980) Angina pectoris during inhalation of cold air reactions to exercise. Br Heart J 43: 661–667.

22.

Latvala

Reijula

Clifford

Rintamaki

(1995) Cold-induced responses in the upper respiratory tract. Arctic Med Res 54: 4–9.

23.

LaVange

Koch

(2006) Rank score tests. Circulation 114: 2528–2533.

24.

Lee

Rosner

Weiss

(1999) Relationship of blood pressure to cardiovascular death: the effects of pulse pressure in the elderly. Ann Epidemiol 9: 101–107.

25.

Lubov

Marmor

Gorenberg

(2001) Endothelin release: a marker for the severity of exercise-induced ischemia. Int J Cardiol 79: 19–24.

26.

Mackenbach

Kunst

Looman

(1992) Seasonal variation in mortality in The Netherlands. J Epidemiol Community Health 46:261–265.

27.

Marek

Volke

Mückenhoff

Platen

Marek

(2013) Exercise in cold air and hydrogen peroxide release in exhaled breath condensate. Adv Exp Med Biol 756: 169–177.

28.

McFadden

Jr (1983) Respiratory heat and water exchange: physiologic and clinical implications. J Appl Physiol 54: 331–336.

29.

McFadden

Jr Pichurko

Bowman

Ingenito

Burns

Dowling

. (1985) Thermal mapping of the airways in humans. J Appl Physiol 58: 564–570.

30.

Millqvist

Bake

Bengtsson

Lowhagen

(1995) Prevention of asthma induced by cold air by cellulose-fabric face mask. Allergy 50: 221–224.

31.

Ornato

Peberdy

Chandra

Bush

(1996) Seasonal pattern of acute myocardial infarction in the National Registry of myocardial infarction. J Am Coll Cardiol 28: 1684–1688.

32.

Petersen

Hansen

Frandsen

Strange

Jonassen

Nielsen

. (1994) Endothelin release and enhanced regional myocardial ischemia induced by cold-air inhalation in patients with stable angina. Am Heart J 128: 511–516.

33.

Psaty

Furberg

Kuller

Cushman

Savage

Levine

. (2001) Association between blood pressure level and the risk of myocardial infarction, stroke, and total mortality; the cardiovascular health study. Arch Intern Med 161: 1183–1192.

34.

Rabkin

Mathewson

Tate

(1978) The relation of blood pressure to stroke prognosis. Ann Intern Med 89: 15–20.

35.

Regnard

(1992) Cold and the airways. Int J Sports Med 13(Suppl. 1): S182–S184.

36.

Romet

Frim

Allen

Shephard

Goode

(1988) The effects of breathing warm air during cold exposure. Arctic Med Res 47(Suppl. 1): 272–276.

37.

Seifert

Subudhi

Riska

John

Shecterle

. (2009) The role of ribose on oxidative stress during hypoxic exercise: a pilot study. J Med Food 12: 690–693.

38.

Sheth

Nair

Muller

Yusuf

(1999) Increased winter mortality from acute myocardial infarction and stroke: the effect of age. J Am Coll Cardiol 33: 1916–1919.

39.

Watt

Baker

Thurston

(1989) Vasoconstrictor actions of endothelin-1 in human resistance vessels. J Hypertens Suppl 7: S134–S135.

40.

Woodhouse

Khaw

Plummer

(1993) Seasonal variation of blood pressure and its relationship to ambient temperature in an elderly population. J Hypertens 11: 1267–1274.

41.

Zawadski

Lenner

McFadden

Jr (1988) Comparison of intraairway temperatures in normal and asthmatic subjects after hypernea with hot, cold, and ambient air. Am Rev Respir Dis 138: 1553–1558.