Blood pressure management in cardiovascular emergencies: an evidence-based approach

Introduction

Cardiovascular emergencies are a common presenting pathology to emergency departments worldwide with millions of visits each year (1). Of those, about 50% are admitted to the hospital with a significant percentage of these requiring intensive care unit admission (1,2). The pathophysiology of these disease states is closely tied to blood pressure management. Hypertension alone has been shown to increase the risk for cardiovascular disease (3,4). In addition to that, mortality has been found to be higher with both hypertension and hypotension in a number of acute cardiovascular emergencies (1-4). Several of these cardiovascular emergencies have more robust, evidenced-based guidelines for the management of blood pressure, including hypertensive emergency, intracranial hemorrhage, ischemic stroke, pre-eclampsia, and eclampsia to name a few (3). For example, the European Society for Hypertension (ESH) recently published their 2023 guidelines that includes evidence and recommendations on the diagnostic and management approaches to hypertensive emergency (5).

There exists a paucity of evidence surrounding acute aortic dissection, hypertensive cardiogenic pulmonary edema, abdominal aortic aneurysm (AAA), and post cardiac arrest after return of spontaneous circulation (ROSC). The American College of Cardiology (ACC)/American Heart Association (AHA) practice guidelines for blood pressure management in these four conditions have a highest level of evidence of Level C-EO, or consensus of expert opinion based on clinical experience (3). Despite the lack of guideline directed management approaches, acute aortic dissection, hypertensive cardiogenic pulmonary edema, AAAs, and post cardiac arrest after ROSC carry a high degree of prevalence, morbidity, and mortality. According to a large study of 20.6 million cardiovascular emergency department encounters, these four conditions represented an estimated 10% of all cardiovascular emergency department visits and had a broad mortality ranging from 2–87% (2). As such, these patients require management strategies that are based upon the best evidence available. In this review, we aim to provide both a physiologic and evidence-based approach to the blood pressure management of these patients including literature that has emerged since the last updated guidelines for these conditions. Medications and dosing recommendations can be found in Table 1.

Acute aortic dissection

Acute aortic dissection is a cardiovascular emergency. The incidence has been estimated to be 2.6 to 3.5 cases per 100,000 person-years (20). Acute aortic dissections have a significant, yet variable, mortality ranging from 0–58% depending on the expediency of diagnosis, type and severity of dissection, and chosen therapeutic intervention (6,21,22). Type A dissections, or those involving the aortic arch, have a very high mortality with an estimated 1–2% increase in mortality per hour after symptom onset. This can reach to as high as 50% without surgical repair (6). Type B dissections, or those not involving the aortic arch, have an estimated mortality of 10% by day 30 with this increasing to as high as 25% if complications ensue, such as renal failure, visceral ischemia, malperfusion, and more (6). The pathophysiology behind acute aortic dissection starts with a tear in the aortic intima. After that, a false lumen can develop as pressurized blood travels through the tear separating the intima from the media or adventitia in an anterograde and or retrograde fashion (21,22). This can result in an expanding false lumen with an intimal flap anywhere along the aortic vessel wall with the potential for expansion into connected arterial vessels.

The mainstay of medical treatment is to reduce aortic wall stress, false lumen pressurization, and left ventricular ejection through blood pressure and heart rate lowering, as these are the main determinants of dissection extension and rupture (6,7,20-24). Most expert consensus and guidelines recommend reducing the systolic blood pressure to less than 120 mmHg or the mean arterial pressure (MAP) to less than 80 mmHg, and to reduce the heart rate to less than 70 beats per minute (7,22). Other expert consensus takes a more aggressive approach advocating aggressive blood pressure lowering to the lowest level tolerable while maintaining adequate vital organ perfusion, specifically cerebral, coronary, and renal perfusion (6,24). One study found a significant decrease in aortic dissection complications with aggressive heart rate reduction to less than 60 beats per minute as compared to more than 60 beats per minute (24).

To achieve the blood pressure and heart rate targets laid out, first line agents are intravenous beta blockers to reduce heart rate while also lowering blood pressure (6,7,20-24). Labetalol and esmolol are the most well-established choices titrated to the aforementioned heart rate goals. In those with a potential intolerance to beta blockade, often citing asthma exacerbations, borderline bradycardia, or heart failure exacerbations, esmolol may be a better first line beta blocker while gauging tolerability given it’s shortened duration of action being 10–30 minutes as compared to labetalol’s 2–6 hours (22). For a patient with a true intolerance to beta blockers, such as a significant allergy, intravenous non-dihydropyridine calcium channel blockers including verapamil and diltiazem are less well studied but generally considered acceptable second line agents (6,22). The feared sequelae with acutely lowering the blood pressure without adequate beta blockade is the sympathetic compensatory mechanism that occurs with vasodilation causing a reflex tachycardia, and thus increasing the aortic wall stress. Verapamil and diltiazem have a lower risk of this reflex tachycardia as compared to other blood pressure lowering agents (22,24).

If optimal blood pressure control does not ensue after adequate heart rate control with beta blockade, vasodilators are indicated and recommended to be added on in addition to the beta blocker (6,7,20-23). The most well studied and thus most often recommended vasodilator in these cases being nitroprusside (6,7). Nicardipine and clevidipine have been deemed safe and efficacious in this role as well and avoid the potentially significant adverse effect profile of nitroprusside (8). Specifically, clevidipine has less venodilatory properties decreasing the risk for reflex tachycardia.

These blood pressure and heart rate targets should be continued as tolerated upon discharge for uncomplicated aortic dissection that did not require acute surgical intervention (5,7). There are no high-quality randomized trials to guide which anti-hypertensives should be continued upon discharge. The ESH does state in their 2023 guidelines that the use of beta blockers, ace inhibitors, or angiotensin receptor blockers are preferred (5). This is based on a large retrospective study that found a lower risk of all-cause mortality on long term follow up in patients treated with these agents (25).

Hypertensive cardiogenic pulmonary edema

Hypertensive cardiogenic pulmonary edema, also commonly referred to as hypertensive heart failure with pulmonary edema, describes a syndrome within the confines of acute decompensated heart failure. The driving clinical findings of hypertensive cardiogenic pulmonary edema are dyspnea and hypertension rather than significant and gross fluid overload, albeit there can be overlap (26-30). Given that the incidence, morbidity, and mortality data is most often quoted for acute decompensated heart failure, rather than specifically for hypertensive cardiogenic pulmonary edema, the exact epidemiology of this condition is not well established. One study by Peacock et al. examined patients who required intravenous blood pressure lowering in the emergency department and found that 25% of these patients had hypertensive acute heart failure (27).

The pathophysiology of this syndrome is theorized to be driven by vascular redistribution in the setting of a rapidly increasing afterload. This leads to elevated cardiac filling pressures compounded by decreased venous capacitance which then leads to pulmonary edema (26,29,30). As such, it can be seen in patients with both a preserved ejection fraction and in those with systolic dysfunction (28-30). This is considered a distinct clinical entity from more traditional models of decompensated heart failure where fluid accumulates overwhelming the Frank-Starling curve and leading to gross fluid overload, including pulmonary edema (26). Those with acute decompensated heart failure with hypertension tend to have a mortality much lower after symptom control than those presenting with normotension or hypotension (30).

These patients often present in acute respiratory extremis requiring emergent intervention in the form of vasodilators. Decreasing MAPs by 15–25% has been demonstrated to significantly improve dyspnea and is recommended in many guidelines (11,30,31). Trials have demonstrated that intravenous nitroglycerin in the acute setting does improve respiratory status and also improves hemodynamics (26,30,32,33). In those with severe and persistent dyspnea, high dose nitroglycerin has been shown in case series to be both safe and effective (12). Others have used the rapid up titration of nitroglycerin infusions with similar results (34). Calcium channel blockers clevidipine and nicardipine are additional options for rapid blood pressure reduction, although they lack the beneficial venodilation nitroglycerin has (35). Clevidipine has been found to be safer and more efficacious than nicardipine for blood pressure reduction and improvement of dyspnea (11).

The overall effect of intravenous nitroglycerin or calcium channel blockers on morbidity and mortality remains unclear (32,33,36). A number of trials have detected a significantly higher risk for acute kidney injury in those who were treated with acute blood pressure reduction with proportional severity to the degree of acute blood pressure lowering, especially if the systolic blood pressure was lowered below 120 mmHg (27,31). In addition to this, a Cochrane Review found no evidence to support the use of nitroglycerin over other therapies and found an increased risk of adverse effects in those treated with nitroglycerin (36). The 2023 ESH suggests either nitroprusside or nitroglycerin with a loop diuretic as first line treatment, and urapidil and a loop diuretic with blood pressure goals of systolic blood pressure <140 mmHg (5/6). Despite this uncertainty, for those with respiratory extremis expert consensus continues to recommend acute blood pressure reduction utilizing the aforementioned agents.

The utility of intravenous diuretics in this population is often guided by expert consensus without identified high quality trials. As discussed, the pathophysiology of this condition is oftentimes driven by high afterload that does not always concurrently have significant hypervolemia. The ESH’s 2023 guidelines do include diuretics as a treatment option (5). Other expert consensus suggests diuretics should be reserved for those with overt volume overload on clinical exam or persistent pulmonary congestion after the optimization of the patient’s hemodynamics (28,29).

AAA

AAAs represent a heterogenous group of disorders dependent on the location of the aneurysm, type of dilatation, size of the aneurysm, and complications (16,17,31,37-39). In general, the prevalence of AAA ranges from 4–9% with significant increases in those >65 years old, male gender, and smokers (17,37,39). The most feared complication is aneurysmal rupture with a resulting mortality ranging from 50–90% (37,39). The pathophysiology of the development and expansion of AAAs is still debated but thought to be secondary to localized inflammation rather than poorly controlled blood pressure (39). There also seems to be a genetic component and a strong association with smoking (17,39). Definitive therapy for ruptured AAA is surgical repair (16,17,39). The conservative management preceding that though is dependent on the severity of the AAA, which is often based upon size, symptoms, and complications (16,17,31,37-39,40-43). The common adage aligned with previous studies is that an aneurysm >55 mm requires urgent surgical repair whereas <55 mm can be closely monitored (17,39). In the pre-, peri-, and immediately post-rupture period, there has been significant discussion on the most appropriate blood pressure targets and the utility of impulse control.

In a patient with a ruptured AAA, the lifesaving therapy is surgical repair. Acutely though, there has been attention paid to pre-operative resuscitation targeting either normotension, which is typically considered a systolic blood pressure >100 mmHg, versus permissive hypotension, which is typically considered a systolic blood pressure from 50–100 mmHg (16,17,31,37-39). The rational being that large volume resuscitation can lead to dilutional coagulopathy and clot disruption (16,17,37). Crawford et al. in 1991 found a survival benefit to targeting a systolic blood pressure 50–70 mmHg, but a follow up study known as the IMPROVE Trial found a worsened 30-day mortality for any patient that had a systolic blood pressure of <70 mmHg (31,38). The 2011 European Society for Vascular Surgery guidelines recommend targeting a systolic blood pressure between 50–100 mmHg as Level 4 Evidence (poor quality), while the Society for Vascular Surgery 2017 guidelines recommends restricting aggressive volume infusion and implementing permissive hypotensive with a systolic blood pressure target of 70–90 mmHg as grade C evidence (moderate quality) (16,17).

There has been a fair amount of debate on the utility of acutely or subacutely lowering the blood pressure in those patients with a AAA that has not yet ruptured. An association between chronic hypertension and the development of an AAA has been demonstrated in several studies, but persistent hypertension has not been firmly established as a causal factor for aneurysmal growth or rupture (17,39-42). Studies on angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and calcium channel blockers have not been shown to reduce progression or rupture (6,20,24). Beta blockade as a means to control wall stress has a more heterogenous pool of data. In vivo pathophysiologic studies have demonstrated that aneurysmal wall stress is significantly higher preceding rupture, even in smaller aneurysms that rupture (40). Larger clinical studies though have demonstrated that beta blockade does not seem to affect the growth rate or rupture rate of AAAs with smaller studies finding that beta blockade may limit expansion in larger AAAs (39,41-43).

The Society for Vascular Surgery expert consensus does recommend standard treatment for hypertension targeting normotension during outpatient surveillance of aortic aneurysms. They recommend against the initiation of a beta blocker for the sole purpose of reducing AAA expansion as a Level 1 recommendation with Quality B evidence (17). The 2023 ESH has similar recommendations targeting the normal blood pressure values for the outpatient treatment of chronic hypertension with no drug preference (5).

In those with symptomatic AAA or AAA’s with impending rupture, expert consensus would support the initiation of blood pressure control and impulse control similar to aortic dissection goals starting with esmolol given it’s fast acting potential and short duration of action. Some experts have suggested targeting a HR <70 and systolic blood pressure <100 mmHg in these patients, while others suggest that targeting normotension is adequate. The 2023 ESH suggests targeting a blood pressure <130/80 mmHg with systolic blood pressures around 110 mmHg as a low end cutoff if tolerated (5/6).

Cardiac arrest with ROSC

Cardiac arrest has an exceedingly high mortality rate with survivors facing a large burden of morbidity. Prehospital mortality in cardiac arrest, although regionally variable, has been estimated to be as high as 60% (44). Of those that have ROSC, in-hospital mortality estimates have ranged from 50–90% based upon variables including age, time to ROSC, definitions of ROSC, and more (45). The International Liaison Committee on Resuscitation (ILCOR) identified four different pathophysiologic components of post-cardiac arrest syndrome including brain injury, myocardial dysfunction, systemic ischemia/reperfusion syndrome, and the precipitating pathology (45). Myocardial dysfunction and the ischemia/reperfusion syndrome are often transient, whereas the neurologic dysfunction may not be. In one single center, prospective study done in the United Kingdom, they found 46% of in-hospital ROSC deaths were due to neurologic injury (46). A large degree of the morbidity associated with survival to hospital discharge is also a result of neurologic dysfunction. In one large database, more than 30% of those that survived to hospital discharge had a Cerebral Performance Category (CPC) of severe cerebral disability or worse (45). The neurologic injury that can result at times may be irreversible (44,47-49).

Post cardiac arrest management often focuses on several things including temperature management, addressing precipitating causes, and blood pressure support (44,50). Hemodynamic support strategies need to take into account several concomitant pathologies. A balance has to occur between supporting cerebral perfusion pressure (CPP), which equals MAP minus the intracranial pressure (ICP), and not unnecessarily increasing the afterload given the potential for myocardial ischemia and cardiomyopathy. In the hours after cardiac arrest, CPP is more reliant on the MAP as the ability for the brain to autoregulate becomes compromised (51). In addition to this, ICP is not often affected in the early post-cardiac arrest phase (45). There is variability in both recommendations and literature on the optimal MAP goal in the post cardiac arrest patient.

There have been a number of studies done assessing MAP targets post-cardiac arrest. Many of the earlier studies were observational and found no consistent and significant difference when targeting different elevated MAP goals (18,44,48,49,51-53). Based on this data, the AHA 2015 guidelines on post-cardiac arrest care specify that avoiding and immediately correcting hypotension defined as a systolic blood pressure less than 90 mmHg or a MAP less than 65 mmHg may be reasonable (class IIb recommendation) (19). Although they state that a specific MAP or blood pressure target could not be identified. Whereas ILCOR stated it was reasonable to target a MAP between 65–100 mmHg taking into account the patient’s normal blood pressure, cause of arrest, and degree of myocardial injury (45).

Since the publication of the AHA and ILCOR guidelines there have been several additional studies published related to this clinical question. The NeuroProtect study published in 2019 evaluated whether targeting a MAP of 85–100 mmHg and an venous oxygen saturation (SvO2) of 65–75% could improve outcomes as compared to a MAP of 65 mmHg. They found that it was safe and did improve cerebral oxygenation, but did not change overall neurologic outcomes (54). Another study published in 2020 by Grand et al. randomly assigned post-cardiac arrest patients to be maintained at either a MAP of 65 or 72 mmHg and found no difference in biomarkers of organ injury at 48 hours (55). Most recently, the BOX trial was published in 2022 demonstrating no difference in mortality, severe disability, or coma between those maintained at a MAP of 63 versus 77 mmHg (18).

Bearing in mind the AHA and ILCOR guidelines, as well as these more recent trials, there has been no consistent benefit demonstrated in patient centered outcomes to targeting a higher MAP goal of 72–100 mmHg. Avoiding hypotension as defined by a MAP <65 mmHg by utilizing intravenous fluids or vasopressors as needed should be central, while additional studies can be considered on higher MAP targets immediately following cardiac arrest with ROSC.

Conclusions

The appropriate management of blood pressure in cardiovascular emergencies, specifically acute aortic dissection, hypertensive cardiogenic pulmonary edema, AAA, and cardiac arrest with ROSC is critical to best care for these very ill patients. Although there is variable evidence surrounding these management strategies, the observational trial data, expert consensus, and more recent randomized trials can guide a structured and evidence-based approach. By doing so, these critically ill patients will get the highest level of care available. The birth of high-quality research studies on the acute medical management discussed continues to require attention and thoughtful research approaches to further inform management decisions.

Acknowledgments

Funding: None.

Footnote

Peer Review File: Available at https://amj.amegroups.com/article/view/10.21037/amj-23-190/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://amj.amegroups.com/article/view/10.21037/amj-23-190/coif). The authors have no conflicts of interest to declare.

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