Following open-heart surgery, air travel is generally recommended no earlier than 10–14 days postoperatively, even in uncomplicated cases. The rationale for this recommendation is that residual intrathoracic air—such as asymptomatic pneumothorax, pneumopericardium, or pneumomediastinum—may remain trapped after surgery and can expand at higher altitudes due to reduced ambient pressure, potentially leading to clinically significant consequences.

For similar reasons, after implantation of any type of pacemaker or other cardiac electronic device, air travel should be postponed for at least two weeks, if complicated by pneumothorax. In uncomplicated cases, patients may fly as early as two days after the procedure, provided that adequate pain control has been ensured.

Following invasive electrophysiological procedures, air travel is generally recommended after seven days, even in uncomplicated cases, due to the risk of thromboembolic events—particularly after left-sided cardiac catheterization. In exceptional and well-justified circumstances, patients may be permitted to fly as early as two days after the procedure. Similarly, following structural cardiac interventions, air travel may be recommended after seven days in the absence of complications.

For patients with implanted cardiac devices, it is generally recommended that they carry their device identification card along with relevant medical documentation, including a recent electrocardiogram. Patients should inform airport security personnel about the presence of the implanted device, avoid placing handheld metal detectors directly over the device, and minimize the time spent in close proximity to metal detection systems (9).

All forms of passive heat exposure lead to an increase in core body temperature, which in turn initiates a range of hemodynamic changes. In the case of the Finnish sauna, esophageal temperature may reach 39°C within 10 minutes (18). Despite the lower ambient temperature, infrared sauna use may result in a 1.0–1.2°C increase in core body temperature within 15 minutes (19, 20). During warm-water bathing, shoulder-level immersion in 41°C water for 10 minutes induces a similar 1.0–1.2°C rise in core temperature. This effect is attributable both to the approximately 24-fold greater thermal conductivity of water compared with air and to the absence of evaporative cooling through sweating (20).

As core body temperature rises, skin temperature increases, leading to peripheral vasodilation and the onset of sweating, which typically occurs when core temperature increases by approximately 0.4°C (21). Owing to the nature of heat exposure, the Finnish sauna induces a greater degree of sweating than other modalities at comparable levels of core temperature elevation. In sauna-acclimatized individuals, sweat-induced fluid loss may reach up to 1.3 L/hour (22).

An increase in body temperature of 1°C is associated with an approximate rise of 30 beats per minute in heart rate. During Finnish sauna exposure, heart rate may reach 120–150 beats per minute, whereas the increase observed with infrared sauna use and warm-water bathing is generally less pronounced (22–25). Heat exposure also leads to an increase in cardiac output. During warm-water bathing, cardiac output may increase by 60–140%, while Finnish sauna use results in variable increases depending on exposure duration and temperature, ranging from mild elevations up to approximately 75%. Infrared sauna use increases cardiac output by 30–50% (26).

Passive heat exposure results in modality-specific changes in intracardiac pressures and stroke volume. Redistribution of the circulation occurs in all cases as body temperature rises. In Finnish and infrared saunas, where hydrostatic pressure does not play a role, right atrial pressure and left ventricular filling pressures decrease (27, 28). In contrast, during warm-water immersion, hydrostatic pressure increases venous return, leading to elevations in all intracardiac pressures. Based on this key difference, sauna use may be safer for patients with heart failure compared with warm-water bathing (20). However, the hemodynamic changes induced by warm-water immersion are comparable to those observed during moderate-intensity physical exercise, suggesting that warm-water bathing may be more effective in promoting cardiovascular adaptation (26). Stroke volume does not change significantly in response to heat exposure, and no meaningful differences have been observed when comparing sauna use with warm-water bathing (20).

Heat-induced peripheral vasodilation reduces systemic vascular resistance, resulting in a decrease in systolic and diastolic blood pressure during Finnish and infrared sauna use. During warm-water bathing, however, the hydrostatic pressure partially counteracts the reduction in diastolic blood pressure (20). The blood pressure–lowering effect of passive heat exposure may persist for up to 60 minutes after cessation of heat exposure, similar to the post-exercise hypotensive response observed following physical activity (25). Table 4 summarizes the hemodynamic changes induced by different heat modalities.

Among the passive heat modalities discussed, traditional Finnish sauna is the most extensively studied. The beneficial cardiovascular effects of sauna bathing are well established; however, concerns may arise regarding potential adverse effects in individuals with pre-existing cardiovascular disease. Finnish investigators have examined the safety of sauna bathing in a wide range of populations and have reported no adverse effects in patients with stable coronary artery disease, heart failure, or hypertension (29-31). It is important to note that the Finnish population studied typically engage in sauna bathing regularly, often several times per week, which likely results in significant hemodynamic adaptation.

Importantly, studies conducted in less sauna-acclimatized populations have likewise not demonstrated adverse events associated with sauna use when performed within safe limits (32, 33). In patients with coronary artery disease, myocardial ischemia may theoretically occur as a consequence of heat-induced increase in heart rate, similar to the physiological response observed during physical exertion. Therefore, the application of heart rate control during sauna bathing may be advisable. Adherence to the heart rate ranges determined and applied during structured cardiac rehabilitation exercise programs may reduce the risk of angina or latent myocardial ischemia.

Concerns are also frequently raised regarding the risk of arrhythmias and sudden cardiac death. In a study involving 98 patients with a history of acute myocardial infarction, arrhythmic events were observed in only 8% of participants during sauna bathing, compared with an incidence of 18% during submaximal physical exercise (26). In the majority of reported cases of sauna-associated sudden cardiac death, alcohol consumption was identified as a contributing factor. Alcohol intake in conjunction with sauna use increases the risk of hypotension, cardiac complications, and accidental injuries (24).

In individuals who have not previously engaged in regular sauna use, unexpected adverse reactions may occur. Therefore, the implementation of specific safety measures is advisable in sauna-naïve individuals, including shorter sauna sessions, longer recovery periods between sessions, adequate fluid replacement, and avoidance of cold-water immersion. Additionally, unsupervised sauna use or sauna bathing without a companion should be discouraged in this population.

Sauna bathing in any form, as well as the use of warm-water baths, is clearly contraindicated in the following conditions (26):