Cardiovascular Considerations for Scuba Divers

Abstract

As the popularity of scuba diving increases internationally, physicians interacting with divers in the clinical setting must be familiar with the cardiovascular stresses and risks inherent to this activity. Scuba presents a formidable cardiovascular challenge by combining unique environmental conditions with the physiologic demands of underwater exercise. Hemodynamic stresses encountered at depth include increased hydrostatic pressure leading to central shifts in plasma volume coupled with cold water stimuli leading to simultaneous parasympathetic and sympathetic autonomic responses. Among older divers and those with underlying cardiovascular risk factors, these physiologic changes increase acute cardiac risks while diving. Additional scuba risks, as a consequence of physical gas laws, include arterial gas emboli and decompression sickness. These pathologies are particularly dangerous with altered sensorium in hostile dive conditions. When present, the appropriate management of patent foramen ovale (PFO) is uncertain, but closure of PFO may reduce the risk of paradoxical gas embolism in divers with a prior history of decompression sickness. Finally, similar to other Masters-level athletes, divers with underlying traditional cardiovascular risk should undergo complete cardiac risk stratification to determine “fitness-to-dive.” The presence of undertreated coronary artery disease, occult cardiomyopathy, channelopathy, and arrhythmias must all be investigated and appropriately treated in order to ensure diver safety. A patient-centered approach, facilitating shared decision-making between divers and experienced practitioners should be utilized in the management of prospective scuba divers.

Introduction

In the United States (US), scuba (self-contained underwater breathing apparatus) diving has increased in popularity among both recreational sporting enthusiasts and by trade.¹ Similar to other recreational sporting endeavors, increased participation rates have necessitated consideration of potential cardiovascular (CV) risks associated with scuba. In particular, there are now increased numbers of older individuals, many with known CV conditions, who are engaged in scuba.^1,2

Unique aquatic environmental stimuli may directly stress the CV, pulmonary, and autonomic nervous systems and lead to pathologic outcomes in divers.³ Further, the presence of common intracardiac shunts, namely patent foramen ovale (PFO), in combination with diving-related adverse sequelae may present downstream clinical management dilemmas. For cardiologists and sports cardiologists, there must be an understanding of the complex interplay between CV exercise physiology and physical gas laws when counseling and caring for divers. In this review, we will discuss the physiology associated with water immersion that may impact the CV system and specific pathologies unique to divers including immersion pulmonary edema (IPE), arterial air embolism, and decompression sickness (DCS). Specific emphasis will be placed on the relevant gas laws and the underlying pathophysiology of diving-related pathologies. Finally, we will guide practitioners in consideration of CV risk stratification for divers and diving „sports-eligibility‟ in those with underlying CV risk.

Physical Gas Laws

Understanding key dive-related pathologies requires an understanding of physical gas laws. Boyle‟s law states that assuming constant temperature, gas pressure and volume are inversely related (P₁V₁=P₂V₂).³ As a diver descends, for every 10 meters of seawater depth, pressure increases by 1 atmosphere, translating to 50% gas volume compared to the surface (Table 1).³ Injuries that result from depth-related gas expansion (diver ascension) are referred to as decompression illness (DCI). According to Henry‟s Law (C=kP), the concentration of dissolved gas (C) is proportional to partial pressure (P) and the dissolved gas constant (k), which translates to higher amounts of inert gasses (primarily nitrogen) dissolved in tissue as ambient pressure increases. During scuba, gases approach equilibrium in blood and tissue at increased pressure. Tissues become supersaturated and with ascension, dissolved gasses re-enter a free gas state with potentiation for vascular gas emboli. Bubbles formed are primarily venous as arterial pressure discourages spontaneous gas formation.⁴ However, right-to-left sided shunts, particularly when intracardiac, may result in arterialization of venous gas emboli (Figure 1).⁵

Table 1.

Pressure and Gas Volume Relationship in Seawater

Depth Sea Water (meters)	Ambient Pressure (atmospheres)	Ambient Pressure (mmHg)	Relative Gas Bubble Size
0 (sea level)	1	760	100%
10	2	1,520	50%
20	3	2,280	33%
30	4	3,040	25%
40	5	3,800	20%

Figure 1. Physiologic effects of scuba diving (Panels A and B) and potential pathophysiologic sequelae with rapid ascension (Panel C).

Panel A. Increased hydrostatic pressure leads to increased venous return from the extremities.

Panel B. Hemodynamic shifts and mixed autonomic response to depth and temperature lead to increased preload and afterload and decreased, then increased heart rate, all yielding a net increase in cardiac output.

Panel C. With rapid ascent, the formation of inert gas bubbles increases the risk of paradoxical arterial gas embolism, including in those with high-grade patent foramen ovale (PFO)

Effects of Immersion

Hemodynamic alterations while diving are driven by cold water exposure and external hydrostatic compression, which increases proportionally with water depth (Figure 1).^3,6 Hydrostatic compression increases venous return from the extremities and plasma volume increases as tissue pressure rises in relation to capillary hydrostatic pressue.^7,8 Physical activity concomitant with cold water immersion synergistically increase mean arterial pressure, pulmonary arterial pressure (PAP), and pulmonary artery wedge pressure (PAWP).⁷ In addition, the parasympathetic „diving-reflex‟ is triggered by temperature-sensitive facial receptors that increases venous return by constricting peripheral and visceral capillary beds.⁶ Despite early increases in parasympathetic activity, increased plasma volume and subsequent sympathetic activation results in augmented stroke volume and a 30–60% increase in cardiac output.^8,9 Importantly, however, hemodynamic changes have been inferred from head-out physiologic studies, thus scuba-specific intrathoracic physiology remains uncertain.¹⁰

Prolonged cold water exposure leads to dynamic autonomic effects.^9,11 Recent heart rate variability studies indicate that with cold water diving, parasympathetic activity dominates initially, but concurrent sympathetic activation occurs with prolonged exposure.⁹ Simultaneous parasympathetic and sympathetic activation places further demands on the CV system, increasing the risk of malignant arrhythmia provocation among at-risk divers.^11,12 Cold environments also impair normal metabolic regulation over time while increasing physiologic heat production to maintain normothermia.⁸ While subcutaneous adipose tissue, diver technique, and wetsuit use protect against heat loss, these measures become limited over time influencing energy costs.⁸

Immersion Pulmonary Edema

Hydrostatic and temperature stimuli associated with diving contribute to acute IPE in susceptible divers. While pathophysiologic mechanisms underlying IPE remain uncertain, it is believed that central redistribution of blood from hydrostatic compression and increased arterial afterload induced by cold water play a central mechanistic role in clinically manifest IPE.¹³ A rise in PAP or PAWP may affect pulmonary capillary pressure causing vascular congestion and pulmonary vascular trauma.¹⁴

IPE occurs in healthy, young and older individuals with underlying CV risk.^14,15 Symptoms include dyspnea, cough, hemoptysis, wheezing, and chest tightness.¹³ While typically self-limited, symptoms can be severe and there is risk for recurrence. To date, there are no randomized trials assessing IPE therapy, but diuretics, ß-2 agonists, and supplemental oxygen may be considered.^14,15 In one IPE study from Moon and colleagues, sildenafil was shown to reduce PAP and PAWP.¹³ However, at present, these hypothesis-driving data should not dictate clinical care standards.¹³

Underlying CV risk may be a common predisposing factor for IPE. In a study from Peacher and colleagues (N=36), 72% of subjects with IPE had preexisting medical conditions,¹⁵ suggesting that underlying hypertension and subclinical cardiac dysfunction increase risk in susceptible individuals.^3,15 Increased afterload and PAWP in those with impaired left ventricular (LV) function further increases risk of pulmonary congestion upon submersion,¹³ thus divers with a history of IPE warrant echocardiographic evaluation.

Arterial Gas Embolism (AGE)

If a diver breath holds during ascension, gas becomes trapped in alveoli and expands, which may lead to alveolar rupture causing mediastinal emphysema, pneumopericardium, pneumothorax, pneumoperitoneum, or subcutaneous emphysema.³ AGE occurs when air enters the pulmonary capillaries and crosses over to the systemic arterial circulation. Based on Boyle‟s law, AGE may occur at depths as shallow as one meter (Table 1).¹⁶ Although small emboli are generally tolerated by skeletal muscle and viscera, acute myocardial infarction or stroke are more dreaded AGE sequelae.¹⁷ Cerebral air embolization may result in motor dysfunction, immediate loss of consciousness, or cardiac arrest in 4% of cases.⁴ Symptoms of AGE typically present shortly after surfacing.⁵

Decompression Sickness

Bubble formation in vascular beds may lead to a systemic illness that varies in symptoms and severity and has been termed DCS. Common symptoms are non-specific and include fatigue, arthralgias and myalgias, rash, and mild neurological symptoms. More severe DCS is often associated with hemoconcentration due to diffuse endothelial leak.⁵ In contrast to AGE, DCS usually presents between 1–24 hours after diving, and up to several days later in those who fly soon after diving.¹⁸ While ultrasound studies have demonstrated that venous gas emboli are common after scuba, there is poor correlation between gas emboli quantity and clinical severity of DCS.⁵ DCS is associated with older age and high body-mass index, factors associated with significant changes in metabolism leading to increased bubble formation.¹⁹

Evaluation and Treatment of AGE and DCS

While AGE and DCS may have different temporal presentations, the clinical presentation for both is frequently indistinguishable and both result from the pressure-volume gas relationship.⁴ As such, AGE and DCS are frequently combined in clinical studies and referred to as DCI. Diagnosis of DCI is clinical, requiring a careful cardiopulmonary and neurologic exam. When pulmonary pathology is present, this should raise the suspicion for AGE.⁵ Central neurologic symptoms, regardless of severity, warrant immediate concern for DCI. Treatment for DCI begins with an emergency survey. 100% oxygen should be administered as primary first aid to clear inert gas from the lungs and establish a tissue gradient to clear bubbles while also treating ischemia.^3,5 Transfer for recompression in a hyperbaric chamber should be arranged immediately even in delayed DCI presentation cases.²⁰ Hyperbaric oxygen treatment effectively resolves bubbles and redistributes the gas obstructing microcirculation.²¹

Patent Foramen Ovale

The presence of PFO carries potential clinical relevance when detected in divers.^5,22 Physiologically, Valsalva maneuvers performed shortly after surfacing may explain the temporal presentation of AGE soon after diving in individuals with high-grade PFO.²³ However, the association between PFO and DCI and whether PFO closure reduces the risk of DCI remains controversial.²³

In an important study of experienced divers (N=230) by Torti and colleagues²⁴, the risk of significant DCI was 4.8–12.9 fold higher in those with PFO detected by trans-esophageal echocardiography, and risk was further increased with increasing PFO size. It is noteworthy, however, that the absolute risk of DCI was very low, at 2.5 events per 10,000 dives, a finding reproduced in other case-control studies.^24,25 Brain imaging studies have demonstrated a higher prevalence of cerebral lesions, suspicious for chronic AGE, in divers with PFO vs. those without.²² However, the clinical relevance of these lesions remains uncertain.²⁶

Several interventional studies of PFO closure in divers are available to inform practitioners on the efficacy of PFO closure in this population (Table 2).^27–31 In a study examining venous and arterial bubbles as a surrogate for DCI risk, Honěk and colleagues evaluated 47 divers, 20 of whom underwent percutaneous PFO closure. After simulated dives, only divers without PFO closure had arterial bubbles detected (88%), suggesting PFO closure is effective in reducing the risk of paradoxical embolism.²⁸ In a more recent prospective study from the same group (DIVE-PFO Registry), 702 divers were followed longitudinally (421 with no PFO, 55 with high-grade PFO closed percutaneously, 98 with high-grade PFO managed conservatively, and 128 with low-grade PFO managed conservatively). DCS incidence was highest in the conservative high-grade PFO group (HR: 26.2 [95% CI 5.8–118.2], P<0.0001) and no divers with PFO closure had DCS.³¹ However, clinical implications should be cautiously interpreted as incidence of DCS events were low and self-reported, and cases were non-randomized and vulnerable to selection bias.

Table 2.

Select Interventional Studies of Transcatheter Patent Foramen Ovale Closure in Divers

Study	Participants and Methods	Key Findings
• Honěk et al. 2021 [31]	• 702 divers followed over 6.5±3.5 years • 421 controls with no PFO; 55 with high-grade PFO and PFO closure; 98 with high-grade PFO (conservative); 128 with low-grade PFO (conservative)	• No divers in the PFO closure group had DCS events • DCS incidence was similar in the low-grade group vs. controls (HR: 3.97 [95% CI 0.56–28.2], P=0.17) • DCS incidence was highest in the high-grade group (HR: 26.2 [95% CI 5.8118.2], P<0.0001).
• Honěk et al. 2020 [30]	• 153 divers with high-grade PFO • 55 underwent PFO closure (7.1±3.8 years follow-up) vs. 98 with conservative dive management (6.5±3.2 years follow-up	• No divers in the PFO closure with DCS vs. 11 (11%) divers in the conservative group with DCS (P=0.01)
• Anderson et al. 2019 [29]	• 62 divers with PFO • 42 underwent PFO closure vs. 23 with conservative dive management (3 subjects in common) • Subjects followed for 56 years	• Divers in PFO closure group had reduced risk of confirmed DCS: 2.7 events vs. 13.1 events per 104 dives (RR: 0.3 [95% CI: 0.2–0.4], P<0.0001)
• Honěk et al. 2014 [28]	• 47 divers with high-grade PFO analyzed after hyperbaric chamber-simulated dive • 20 with prior PFO closure vs. 27 divers conservative with dive management • Venous bubbles assessed with echocardiography and arterial bubbles assessed with transcranial sonography	• 18m dive: Arterial bubbles more common in the conservative (32%) vs. PFO closure group (0%, P=0.02) • 50m dive: Arterial bubbles more common in the conservative (88%) vs. PFO closure group (0%, P<0.01) • Venous bubbles similar in both groups at both depths
• Billinger et al. 2011 [27]	• 65 divers with PFO vs. 39 divers without PFO • Divers with PFO (N=65): 26 underwent PFO closure vs. 39 conservative dive management • Cerebral MRI and DCI questionnaire at baseline and 1, 3, and 5 years after enrollment	• Major DCI events per 104 dives more common in the non-closure group (35.8±102.5 events) vs. the PFO closure (0.5±2.5 events) and no PFO (0 events) groups • Ischemic brain lesions per 104 dives more common in the non-closure group (104±246 lesions) compared to the PFO closure (6±13 lesions) and no PFO (16±42 lesions) groups

DCI: decompression illness; DCS: decompression sickness; MRI: magnetic resonance imaging; PFO: patent foramen ovale

Given the high prevalence of PFO in the general population and overall low absolute risk of DCI among divers,²⁴ indiscriminate PFO screening is not recommended in divers.^32,33 Further, percutaneous PFO closure carries a >1% peri-procedural risk of serious device-related complications and there is an additional association between PFO closure and incident atrial fibrillation,³⁴ suggesting the risks of prophylactic PFO closure in those without a history of DCI outweigh the potential benefits. Among divers with prior DCI, evaluation for PFO and downstream closure may be clinically reasonable, particularly for those with repeated DCI episodes.^3,30 In this clinical evaluation, bubble-contrast trans-thoracic echocardiography with provocative maneuvers is necessary,³³ and subsequent trans-esophageal echocardiography may be indicated if PFO closure is pursued.

The presence of PFO, particularly if detected incidentally, is not a contraindication to scuba diving.³² Conservative measures to decrease risks of DCI include: maximum depth 15m dives, extended safety stops, utilizing air with decreased nitrogen content, and slow ascension.²³ Thus, the decision to proceed with PFO closure, in most cases, presents an opportunity for appropriate shared decision-making (SDM), which includes discussion of the current rigor and limitations of contemporary data and the individual diver‟s goals and risk profile.

Cardiovascular Risk and “Fitness to Dive”

In the general population, recreational diving is safe with data from the US and Canada reporting only 1.8 deaths per million recreational dives.² Excluding scuba-specific issues, CV disease is a leading cause of diving-associated mortality.^2,35 In a seminal investigation from Denoble and colleagues, cardiac incidents were responsible for 26% of disabling diving injuries and the cause of death in 13% of cases with divers >60 years-old at increased risk of diving-associated death from CV disease.³⁵ Among US scuba divers, prior registry data (N=113,892) found 36% were >50 years-old, 39.6% reported prior tobacco use, and 47.9% were overweight.¹ Considering that symptoms of CV disease manifest while scuba diving may lead to dangerous or even fatal outcomes, the environmental demands associated with diving provide strong rationale for careful consideration of CV risk stratification in Masters-aged divers (>40 years-old) or those with inherent CV risk.^1,32

Most official scuba certifying associations require pre-participation health questionnaires, including assessment of CV symptoms and CV disease that may require a “fitness-to-dive” medical evaluation.³⁶ Consensus guidelines from the Recreational Diving Facilities Workshop Proceedings recommend that scuba divers with CV symptoms or risk greater than „intermediate‟ should be risk-stratified for functional capacity and evaluated for obstructive coronary artery disease (CAD), cardiomyopathy, Long QT syndrome (LQTS), or other arrhythmias.³² Ischemic CV risk can be estimated via methodologies endorsed by the American College of Cardiology (ACC) and American Heart Association (AHA).³⁷ Similar to Masters endurance athletes, it is our opinion that Masters-aged scuba divers with known CV risk factors should be rigorously risk stratified given the unique physiologic challenges and hostile environments encountered while diving. In this final section, we will provide a review of eligibility considerations for divers, based on updated ACC/AHA guidelines for sports eligibility in athletes with CV disease,³⁸ and our suggested approach to specific CV conditions in divers (Figure 2).

Figure 2. Evaluation and risk stratification of cardiovascular disease in scuba divers.

Recommendations based off American College of Cardiology / American Heart Association Eligibility and Disqualification Recommendations for Competitive Athletes³⁸

CAD: coronary artery disease; CT: computed tomography; EF: ejection fraction; MRI: magnetic resonance imaging; VT: ventricular tachycardia

Coronary Artery Disease

CAD is the most common cause of sports-related sudden cardiac death in Masters athletes.³⁹ Vigorous physical activity may induce malignant arrhythmias either through disruption of unstable plaque, creation of demand ischemia through a stenotic lesion,⁴⁰ or as a consequence of existing scar.³⁹ Divers with known CAD, symptoms suggesting ischemia, or those >45 years-old with risk factors such as smoking, early family history of myocardial infarction, hyperlipidemia, or diabetes should be aggressively medically managed and risk stratified with maximum effort exercise testing for inducible ischemia.³²

Exercise stress testing allows for simultaneous evaluation of ischemia, functional capacity, and provoked electrical instability. With abnormal exercise testing, CT coronary angiography may be useful to evaluate for the presence of obstructive CAD, however invasive angiography is preferred with higher pre-test probability.⁴¹ After revascularization or an acute coronary syndrome, a return to diving should be approached similar to competitive athletes (Figure 2). With normal LV systolic function (ejection fraction >50%) and no inducible ischemia or arrhythmias, it is reasonable to resume scuba diving.⁴²

Cardiomyopathy

In general, most patients with a clinical diagnosis of any inherited cardiomyopathy should be advised against scuba diving (Figure 2).^32,43 This contrasts somewhat with the evolving paradigm for sports eligibility in athletes with CV disease (ex. hypertrophic cardiomyopathy), in which guidance has shifted to more patient-centered SDM.⁴⁴ The rationale for a more conservative approach with divers is based on several key points. First, dependent on type of cardiomyopathy, symptoms may manifest unpredictably while underwater. As previously discussed, the environmental stressors while diving may increase the risk of physical impairment with underlying cardiac dysfunction.¹⁵ Second, risks of arrhythmia provocation while diving are also increased in those with cardiomyopathy.¹¹ Third, minor symptom impairments while diving can result in catastrophic outcomes in solo divers. Finally, for those who “buddy-dive”, the safety of the pair or group is dependent on all divers being fully functional in potentially hostile environments. Similar to considerations for the „occupational athlete‟,⁴⁵ one incapacitated diver may threaten the safety of their partner(s). As such, while SDM remains reasonable in the context of „fitness-to-dive‟, diving-specific factors must be included in this process that may favor a more conservative approach.

Long QT Syndrome

Patients with LQTS are generally advised against scuba diving.³² However, recent data from competitive athletes with LQTS suggest cardiac safety during vigorous physical exertion is preserved when these athletes are appropriately risk stratified and managed.⁴⁶ Indeed, the diagnosis of LQTS should be confirmed and cared for by a cardiologist with expertise in inherited arrhythmia syndromes.⁴⁷ A prolonged QT interval is a risk factor for syncope and sudden cardiac death because delayed ventricular repolarization, manifest as QTc prolongation, predisposes to malignant arrhythmias that may degenerate to ventricular fibrillation.⁴⁷ The autonomic response to increased hydrostatic pressure and cold water induces relative bradycardia that may further promote ventricular ectopy in those with an underlying pro-arrhythmic substrate.^9,11 Swimming may also precipitate cardiac events in those with cardiac channelopathies.⁴⁸ In a seminal case series, Ackerman and colleagues demonstrated swimming was an arrhythmic trigger in those with LQTS.⁴⁹ In consideration of scuba for divers with LQTS, environmental stresses and safety concerns for dive partners should be emphasized and a more conservative approach with scuba activities may be advisable. However, after appropriate risk stratification and implementation of clinical treatment strategies,⁵⁰ we advocate for ongoing patient-centered, SDM between patient and physician (Figure 2).

Arrhythmias

Divers with uncontrolled arrhythmias that impair exercise tolerance or consciousness should be advised against scuba and proceed with more intensive cardiac risk stratification.³² This includes malignant arrhythmias such as ventricular tachycardia, but also less malignant, symptomatic atrial arrhythmias such as atrial fibrillation (AF) and other supraventricular tachycardias (SVTs). Importantly, in those with significant symptoms from atrial arrhythmias, AF or SVT can be effectively controlled with medications or ablation.⁵⁰ We recommend that in individuals with a history of AF or SVT, exercise stress testing should be performed to assess the effects of arrhythmia on exercise tolerance. Exercise stress testing may also provoke arrhythmias in those with paroxysmal symptoms in presumed arrhythmia syndromes. Cardiac imaging, typically echocardiography, should be obtained to exclude structural pathology.⁵⁰ Ultimately, if structural or ischemic pathologies are excluded, the arrhythmic burden is controlled, functional capacity is adequate, no symptoms are elicited, and no ventricular arrhythmias develop during exercise testing, these individuals may be permitted back to scuba diving.⁵⁰

Functional Capacity

Dive fitness is optimal when divers achieve a maximum of 12–13 metabolic equivalents of task (METs).³² However, requiring 13 METs as standard functional capacity has been deemed too restrictive, especially for divers who do not plan to regularly navigate challenging environments.^3,32 Recreational scuba divers should be able to maintain a minimum of 6 METs of continuous activity.³² Some dive certification societies still suggest 13 METs of exercise tolerance, and if a diver can achieve this without symptoms, ischemia, or electrical instability, this higher level of fitness is viewed as an additional reassuring finding.³² Divers may benefit from referral to dedicated dive medicine centers for exercise testing when appropriate, but these centers are rare and universal referral for all Masters-aged divers is not practical.

CONCLUSIONS

As participation in scuba diving increases, practitioners charged in the care of divers must understand the inherent environmental stresses posed by diving and the importance of careful CV risk stratification in at-risk divers. Unique environmental factors may lead to dive-specific pathologies including IPE, AGE, and DCS, and increase risk of precipitating acute coronary syndromes or malignant arrhythmias in susceptible divers. CV disease in divers requires careful assessment as even minor symptoms may prove deadly in potential hostile dive conditions. With limited evidenced-based management strategies, treatment options often require SDM with the practitioner and diver fully engaged in individualized clinical management strategies.