Hypertensive and Hypotensive Emergencies in Interventional Radiology

Abstract

Hyper- and hypotensive emergencies represent some of the most severe clinical issues that can occur during or around an interventional radiology procedure. While some patients are known to be more predisposed to cardiovascular collapse, nearly all patients are at risk for such an outcome. This is particularly true of patients undergoing moderate sedation, with the possibility of cardiovascular compromise occurring not just due to the underlying pathology for which the patient is being treated, but as a complication of sedation itself. Understanding the underlying cause of hyper- or hypotension is paramount to performing an appropriate and timely intervention. While the underlying cause is being corrected—if possible—the changes in blood pressure themselves may need to be intervened upon to maintain cardiovascular stability in these patients. Interventional radiologists must be familiar with measures taken to correct hyper- or hypotensive emergencies, including the most commonly used medications to treat these disorders. This article discusses the most common etiologies of such clinical scenarios, and the most common interventions performed for these settings.

Since many interventional procedures are performed with moderate sedation without the use of anesthesiologists and often in patients with multiple comorbidities and critical illnesses, trainees and interventionalists should be aware of the pharmacologic agents used to manage changes in blood pressure as well as understanding the etiology of hemodynamic changes in adult patients. Moderate sedation is defined by the American Society of Anesthesiologists as patients being in a state where they retain “purposeful response to verbal or tactile stimulation” with preserved spontaneous ventilation that does not require advanced airway management. Compared with general anesthesia, the patient's hemodynamic function is more likely to be well-preserved and postprocedural recovery is quicker, making this form of procedural sedation inherently less risky than general anesthesia. ¹ This review will discuss the management of hemodynamic changes in the periprocedural time frame in the scope of interventional radiology.

Preprocedural Management

The patient is assessed preprocedure for their risk of undergoing moderate sedation without the supervision of an anesthesia team. This includes evaluation of the Mallampati score as well as a preprocedural fasting time of 6 hours for solids and 2 hours for clear liquids. Preprocedure counseling also includes instructions for holding or continuing certain medications. This is usually done in the interventional (IR) clinic; however, a preprocedural evaluation with anesthesia can be requested more medically complex patients.

Typically, most antihypertensive medications including β-blockers, calcium channel blockers (CCBs), and α-2 agonists are continued on the day of the procedure. This helps in reducing blood pressure fluctuations during the procedure. ² The literature supports holding diuretics, direct renin inhibitors, and angiotensin-converting enzyme (ACE) inhibitors on the day of the procedure to avoid hypotension, though this can be evaluated on an individual basis. ³ A study examining associations with acute kidney injury (AKI) in patients undergoing vascular surgery found the number of antihypertensive agents on the day of surgery was associated with postoperative AKI, which suggests that in some patients at high risk for AKI the number of antihypertensive medications should be modulated on an individual basis. ⁴ During the day of the procedure evaluation, it should be confirmed which medications were held and which were continued the day of the procedure; this helps in the management of intra- and postprocedural hemodynamic changes as well as management of any other postprocedural complications.

Hypertension

Preprocedural Hypertension

Uncontrolled hypertension prior to elective surgeries has been demonstrated to increase the risk of cardiovascular and cerebrovascular complications as well as intraprocedural blood loss and overall mortality. ⁵ Some authors advocate for postponing elective procedures if preprocedural systolic blood pressure (SBP) is over 180 mm Hg and/or diastolic blood pressure (DBP) exceeds 100 mm Hg; in this setting, the risk of perioperative cardiovascular complications may be increased by 35%. ⁶

As with all definitions of peri- or intraprocedural hyper- or hypotension, it is vital to determine the degree of blood pressure changes in the setting of the patient's underlying normotensive state. For example, an SBP of 170 mm Hg is far more meaningful for a patient with a baseline SBP of 110 mm Hg than it is for a patient with a baseline pressure of 160 mm Hg. Most IR procedures are not done under general anesthesia, raising the question of the validity of these conclusions in the surgical and anesthesia literature. Such an improved safety profile is one of the distinct advantages of using local anesthesia and moderate sedation. There are limited data regarding cardiac risk with patients undergoing interventional procedures with moderate sedation. It has been shown, however, that there is a lower cardiac risk in patients undergoing endovascular versus open cardiac procedures. ^{6 7} For elective procedures in patients undergoing general anesthesia, interventionalists should weigh the urgency of the procedure versus the risk of complications associated with uncontrolled hypertension. While the exact time frame for achieving blood pressure correction is unknown, some authors advocate postponing procedures by at least 6 to 8 weeks to achieve blood pressure control and resultant improvement of cardiovascular status. ⁸

Intraprocedural Hypertension

The American Heart Association 2017 guidelines define perioperative hypertension as blood pressure ≥160/90 mm Hg or SBP ≥20% of the preoperative value that lasts for more than 15 minutes. ⁹ Common etiologies include inadequate analgesia, hypothermia, hypercarbia and hypoxemia, and hypervolemia. ¹⁰ Additionally, transient elevations in blood pressure can occur during the administration of anesthesia and tracheal manipulation during general anesthesia, which is not the case for the majority of interventional procedures. ¹⁰ The surgical anesthesia literature has reported adverse outcomes associated with intraoperative tachycardia and hypertension during long noncardiac surgeries. ¹¹ These transient elevations in blood pressure permit more controlled blood pressure management usually targeting the underlying etiology, as opposed to cases of hypertensive emergency with evidence of end-organ damage, which must be treated more rapidly (discussed later). ² Of note, during sedation, hypotension is more commonly encountered than hypertension. ¹⁰

Postprocedural Hypertension

The surgical and anesthesia literature regarding postoperative hypertension can be adapted to interventional procedures in some situations, such as procedures undergoing general anesthesia and certain vascular interventions. Definitions of postoperative/postprocedural hypertension vary, but is defined by some authors as an SBP > 160 mm Hg and/or a DBP > 90 mm Hg on two separate readings; another arbitrary definition in the anesthesia and surgical literature is two separate readings of SBP >190 mm Hg and/or DBP >110 mm Hg. ^{2 10} Typically postprocedural hypertension lasts less than 4 to 8 hours. Similar to periprocedural hypertension, causes include sympathetic activation, pain and anxiety, hypervolemia, urinary retention, hypothermia, and shivering. The most common cause of postprocedural hypertension is existing essential hypertension, which is why a patient's existing hypertensive regimen should be continued till the day of procedure. ¹² Long procedures may require a urinary catheter to avoid discomfort and associated hypertension secondary to urinary retention. Additionally, hypothermia can cause increased metabolic demands postprocedurally, which can lead to peripheral vasoconstriction and increased blood pressure. ^{13 14 15} In the surgical literature, postoperative hypertension has been suspected to cause an increase in postoperative bleeding, though a report in the cardiac literature did not find an association between peak SBP/MAP (mean arterial pressure) and increased bleeding, as measured by chest tube output, transfusion, or surgical reexploration. ^{6 16} Additionally, in patients with multiple comorbidities and chronic hypertension, aggressively decreasing the SBP/MAP can run the risk of relative renal hypoperfusion and AKI in patients with altered renal autoregulation, as well as a risk of relative cerebral hypoperfusion risking acute stroke. ¹⁶ Ultimately these risks should be balanced when considered postprocedural blood pressure management.

Specific Clinical Scenarios Requiring Treatment of Hypertension

Hypertensive Urgency and Emergency

A hypertensive crisis (urgency) is defined by the American Heart Association (AHA) as an SBP greater than 180 mm Hg and DBP over 120 mm Hg without evidence of end-organ damage. ⁹

Per the AHA 2017 guidelines, certain situations warrant ICU admission and signs of target-organ damage that is new or worsening, including conditions such as aortic dissection, pheochromocytoma crisis, and severe preeclampsia or eclampsia. A hypertensive crisis can also be precipitated by an invasive procedure. During an adrenal vein sampling procedure, for example, specific protocols can be performed to avoid this hypertensive crisis. If these situations arise postprocedurally and the interventionalist is managing the blood pressure, it is recommended to reduce the SBP by no more than 25% within the first hour, and then to 160/100 mm Hg within the next 2 to 6 hours, then to baseline within 24 to 48 hours. ⁹

Unlike hypertensive urgencies, a hypertensive emergency is the presence of systolic BP > 180 mm Hg and DBP > 120 mm Hg with signs of new or worsening target end-organ damage including intracerebral or subarachnoid hemorrhage, ischemic stroke, hypertensive encephalopathy, acute renal insufficiency, or cardiovascular events such as myocardial infarction or aortic dissection. ² Hypertensive emergencies require very aggressive blood pressure control and consultation with a critical care specialist should be strongly considered.

Acute Aortic Dissection

In patients with an acute aortic dissection, β-blockers such as esmolol and labetalol are preferred; these agents can rapidly lower the SBP to less than 120 mm Hg within 20 minutes. For this reason, β-blockers should be used first before vasodilators such as nicardipine or nitroprusside, which can also assist with blood pressure control and prevention of reflex tachycardia. ⁹

Adrenal Crisis

If there is concern for an undiagnosed pheochromocytoma in cases of paroxysmal hypertension with associated headache, diaphoresis, and palpitations, workup includes collecting plasma or 24-hour urinary fractionated metanephrines. ⁹ In addition to adrenal vein sampling, there is a risk of catecholamine surge resulting in a hypertensive crisis when performing an adrenal mass biopsy or ablation. ¹² Preprocedure endocrinology consultation and assistance by an anesthesiologist can mitigate this risk. Patients take α-adrenergic antagonist for 1 to 3 weeks prior to the scheduled procedure; an intraprocedural hypertensive crisis is treated with intravenous (IV) nitroprusside. ¹²

Intracranial Hemorrhage

Patients with intracranial hemorrhage (ICH) have more nuanced blood pressure regulation for two main reasons. Theoretically, patients with primary ICH secondary to small vessel ischemic disease or ICH secondary to ruptured aneurysm or arteriovenous malformation are at risk of worsening cerebral hemorrhage without blood pressure control, particularly with the latter condition. ^{2 17} In contrast, reduction of blood pressure may cause decreased cerebral perfusion pressure (CPP) which may jeopardize the ischemic penumbra. ¹⁷ While performing a procedure in a patient with ICH, such a central line insertion for hypertonic saline administration, it is best to confirm with the primary service the management of an appropriate blood pressure range since no specific threshold exists. The AHA 2017 guidelines emphasize that there are scant data supporting a specific blood pressure threshold, and that an SBP reduction to less than 160/90 mm Hg was associated with improved outcome within 6 hours. ¹⁷ Large-scale studies examining outcomes of ICH patients treated with SBP control in the ranges from 110 to 200 mm Hg are currently ongoing. ¹⁷

Pharmacologic Agents for Controlling Hypertension

Though the full range of antihypertensive is out of the scope of this article, what follows is a brief overview of commonly used oral and IV antihypertensives and their contraindications and potential side effects ( Table 1 ).

Table 1. An overview of commonly used IV antihypertensive agents, doses, and pharmokinetics ¹² .

Drug	Dose	Onset of action	Duration	Potential side effects
Nitroprusside	initial infusion 0.3 – 0.5 μg/kg/min, maximum rate of 10 μg/kg/min	Immediate	1–2 min	cyanide toxicity, coronary steal, increased intracranial pressure 19
Nitroglycerin	IV 5 μg/min titrated every 3–5 minutes to clinical response, maximum infusion rate of 20 μg/min 6	2–5 min	3–5 min	avoid in patients with increased ICP 20
Clevidipine	initiated at 0.2 μg/kg/min and titrated to a maximum of 8.0 μg/kg/min 21	2–5 min	5–15 min	Abrupt withdrawal may lead to rebound hypertension
Labetalol	10–20 mg IV bolus, then 40–80 mg every 10 min up to 300 mg dose	2–5 min	2–18 h	relatively well-tolerated, but can include postural dizziness 22
Hydralazine	10–20 mg IV administration every 4–6 h, up to 40 mg dose	5–20 min	1–4 h	tachycardia, headache 23
Nicardipine	initial IV rate of 5 mg/hr, titrated up to 15 mg/hr, decreased to 3 mg/hr when target rate reached 24	2 min	2–4 h	dizziness, avoid in patients with severe aortic stenosis

IV nitroglycerin, sodium nitroprusside, dihydropyridine CCB, and β-blockers are commonly used for procedural hypertension management. ⁶ The α-1 antagonist phentolamine can be used in certain circumstances such as pheochromocytoma crisis. ¹² Parenteral administration of the β-blocker esmolol has the advantage of onset within 1 minute and a short duration of less than 20 minutes. Hydralazine has the advantage of quick onset within a few minutes. ¹⁰ Clonidine is an α-2 agonist that is effective in reducing sympathetic activity, which can lower cardiac complications; however, it can also increase the risk of bradycardia and hypotension. ¹² This agent can reduce SBP within 2 to 4 minutes, however, a continuous infusion may not be the most convenient given the short duration of most interventional procedures. ^{10 18} Short-acting direct alpha-agonists like clonidine that can be administered either as continuous infusion or a bolus, onset of action of 5–15 minutes and range of 15–120 minutes. ²⁴ After infusion of a CCB, patients should be monitored for at least 8 hours to evaluate for rebound hypertension. ⁶ Nitroglycerin is a direct venodilator which decreases preload and has a short duration of action of 1 to 2 minutes with an immediate onset of activity and are indicated in cases of acute coronary syndrome or acute pulmonary edema. ⁹ Sodium nitroprusside decreases both preload and afterload as an arterial and venous dilator, with a similar immediate onset and short duration of less than 2 minutes. ¹⁰

Hypotension

Periprocedural hypotension has been variously described as an SBP lower than 20 to 30% of the baseline or absolute SBP < 80 – 90 mm Hg and/or a MAP < 65 mm Hg. ^{10 19} Common etiologies include excessive sedation, vasovagal syncope, or hypovolemia ( Fig. 1 ). ¹

Fig. 1.

An algorithm for common etiologies of periprocedural hypotension. Adapted from two studies. ^{25 28} SBP, systolic blood pressure; MAP, mean arterial pressure.

Patients undergoing interventional procedures using moderate sedation are typically performed with routine incremental noninvasive blood pressure monitoring with blood pressure cuff measurement obtained every 5 minutes. If there is concern for intraoperative hypotension or a need for more accurate real-time data, arterial catheter placement preprocedurally may be beneficial in better guiding management. ¹⁰ This may be placed intraprocedurally; however, consent must be obtained prior to administering sedation or under emergent conditions.

Periprocedural hypotension runs the risk of inadequate tissue perfusion, which can be done by the assessment of capillary perfusion, mentation, or urinary output; however, clinical signs may be difficult to assess during procedures. Studies demonstrate intraoperative hypotension during general noncardiac surgeries increases mortality, risks AKI, myocardial perfusion, and stroke. ^{25 26 27} As there is a paucity of studies reporting IR-specific blood pressure control and postprocedural outcomes, surgical data must be extrapolated for image-guided procedures which are often shorter in duration and performed under moderate sedation rather than general anesthesia.

Systolic blood pressure is a result of cardiac output, which in turn is a result of stroke volume multiplied by the heart rate. Stroke volume is dependent on the preload and myocardial contraction; so, the first step in improving SBP is usually increasing the preload by administering IV fluids. ^{28 29} The risk of increasing preload is that it may cause vascular congestion or volume overload in those with decreased cardiac function. Hypotension may otherwise be due to excessive anesthesia causing a decrease in the systemic vascular resistance, which can be countered with a reduction in the anesthesia agent administered. Otherwise, hypotension is treated with vasopressors including dopamine, dobutamine, norepinephrine, epinephrine, and phenylephrine ( Table 2 ). ³⁰ If there is any concern for continued hypotension, the basics of life support assessment should be undertaken with evaluation of airway, breathing, and circulation. ²⁸

Table 2. Common agents and doses for use during periprocedural hypotension ²⁴ .

Drug	Suggested dosage	IV onset of action	Duration of action	Mechanism of action	Indications	Potential side effects
Ephedrine	5–10 mg every 5 min up to 50 mg	1–3 min	15–20 min	Mixed agonist of α- and β-adrenergic receptors	First-line treatment during GA 10	Hypertension, ventricular arrhythmias, cardiac ischemia
Atropine	0.5–1 mg IV every 3–5 min (maximum dose 3 mg) (the ACLS algorithm for bradycardia starts with atropine 1 mg bolus every 3–5 min)	Immediate		Cholinergic antagonist	Bradycardia	Blurry vision
Phenylephrine	Bolus 0.1–0.5 mg IV every 10–15 min Infusion 0.4–9.1 μg/kg/min	1–3 min	10–20 min	Direct α-1 agonist	Hypotension	Administration with nonselective β-blocker risks hypertension
Epinephrine	Bolus 1 mg IV every 3–5 min (max 0.2 mg/kg) Infusion: 0.01–0.10 μg/kg/min (ACLS algorithm for bradycardia with hypotension recommends 2–10 μg/min infusion)	Immediate	5–15 min	Predominantly direct α-1 and α-2 agonist, β-1 and β-2 agonist	Hypotension and cardiac arrest	Ventricular arrhythmias, cardiac ischemia, sudden cardiac death, hypertension
Norepinephrine	0.01–3 μg/kg*min	Immediate	5–15 min	Predominantly direct α1 and α-2 agonist, β-1 >> β-2 agonist	Hypotension	Cardiac arrhythmias, peripheral digital ischemia, bradycardia
Dopamine 32	2–20 IV 2–5 μg/kg/min intially, titrated by 5 – 10 μg/kg/min, max dose of 20 mcg/kg/min (max of 50 μg/kg*min) (ACLS algorithm for bradycardia with hypotension recommends 5–20 μg/kg/min infusion)	5–10 min	10 min	Direct D1 and D2 agonist, β agonist > α agonist	Hypotension	Cardiac arrhythmias at high doses > 20 mcg/kg/minute
Vasopressin 32	Bolus: 40 U IV bolus Infusion: 0.01–0.1 U/min	Immediate	15–20 min	Direct V1 (vascular smooth muscle)	Cardiogenic and hypotensive shock and cardiac arrest	Skin necrosis

Abbreviations: ACLS, advanced cardiac life support; GA, general anesthesia; IV, intravenous.

Specific Clinical Scenarios Requiring Treatment of Hypotension

Vasovagal Syncope

Vasovagal syncope triggered by a Valsalva maneuver or stimuli such as fear or pain can be self-limiting, typically resolving without intervention. These etiologies should prompt monitoring but not necessarily intervention with pharmacologic agents. ²⁸ Use of sedation itself may depress innate sympathetic response controlling hemodynamic parameters, resulting in hypotension. ³¹

Hypovolemia

In cases of hypovolemic hypotension, several options are available for expanding intravascular volume. A fluid bolus may be an appropriate treatment if there is a concomitant increase in stroke volume. ²⁵ Another etiology of hypovolemic hypotension, blood loss, can occur in cases of high bleeding risk procedures such as gastrointestinal bleed embolization or transjugular intrahepatic portosystemic shunt (TIPS) creation. This may be evidenced by a decreased MAP (<60–65 mm Hg) with reflex tachycardia (> 90–100 beats per minute). Importantly, the reflexive increase in heart rate may be blunted in those taking β-blockers. Preprocedure evaluation of bleeding risk, as well as assessment of antihypertensive medications, is important to have requisite blood products readily available to administer during the procedure.

Aspiration

Given the loss of protective airway reflexes, aspiration pneumonitis is a risk of sedation. This risk is lower in those who have fasted, but present in emergent procedures where preprocedure fasting is not possible. Obesity, hiatal hernia or gastric reflux, diabetes, ileus or bowel obstruction, enteral feeds, and pregnancy are thought to be additional risk factors. ³³ In procedures not using general anesthesia, aspiration is more common in endoscopic procedures and in procedures using propofol. ³⁴ Clinically, patients who have aspirated will have shortness of breath, oxygen desaturation, tachypnea, and tachycardia. Severe cases may result in pulmonary edema and hypotension requiring intubation. Thus, minimizing the risk of aspiration is key, whether by delaying the procedure or performing tracheal intubation. ³⁵

Anaphylaxis

Preprocedure evaluation includes checking for drug allergies to avoid preventable complications such as allergic reactions. However, in the event of an unknown drug allergy, intraprocedural management is an emergency, especially in the cases of anaphylaxis. This severe reaction results in dyspnea and hypotension that can be life-threatening and progresses to anaphylactic shock. ³¹ Usually these occur soon after drug administration, often within 15 to 20 minutes, and fatal cases have been reported in 5 to 30 minutes. ^{36 37} For example, very small injection volumes can still produce anaphylaxis; there are reports of anaphylaxis after thrombin injection to treat femoral pseudoaneurysms, evidenced by pruritus, severe shortness of breath edema, and hypotension. ^{38 39} The first-line treatment is intramuscular epinephrine administered in the anterolateral thigh, using a 1:1,000 dilution (1 mg/mL), at a dose of 0.2 to 0.5 mL, every 5 to 15 minutes. ⁴⁰ This should not be confused with the dose for cardiac arrest, which is a 1:10,000 IV push. ³⁶ Administration of IV epinephrine (infused at a rate of 1 μg/min, and titrated to a maximum of 10 μg/min as needed) can be considered for anaphylaxis when several doses of intramuscular epinephrine have failed and the patient is severely hypotensive and/or in cardiac arrest. It is important to note that intravenous epinephrine administration is riskier, and can lead to arrhythmias or myocardial ischemia/ infarction. ³⁶ When available, administration of IV epinephrine should warrant invasive blood pressure monitoring. Additionally, IV fluids should be administered. In cases with shortness of breath, emergent airway management may be required and secondary medications including antihistamines and corticosteroids can be administered. ^{35 37} Although they may be additive, antihistamines have a longer time to onset and onset of action which is why they are typically administered only after epinephrine. ²⁹ Corticosteroids can be administered as 1mg/kg IV methylprednisone every 6 hours or an oral prednisone dose of 0.5 mg/kg for milder cases can be considered, though evidence is lacking in their efficacy in the treatment of anaphylaxis once it occurs. ^{36 41}

Bradycardia-Associated Hypotension

The American Heart Association Advanced Cardiovascular Life Support algorithm for bradycardia with a pulse, defined as less than 50 beats per minutes, recommends atropine 1 mg bolus, repeated 3 to 5 minutes for maximum dose of 3 mg. If there is persistent hypotension and bradycardia, they recommend either dopamine infusion or epinephrine infusion. Dopamine is dosed at 5 to 20 μg per minute titrated to patient response with a slow taper, and epinephrine is administered 2 to 10 μg per minute infusion, titrated to response. ⁴²

Pharmacologic Agents to Manage Hypotension

If reducing anesthesia or IV fluids administration has failed to improve SBP or MAP, additional adrenergic agents can be used to manage periprocedural hypotension. Ephedrine is an inotrope that acts by releasing norepinephrine and acts as a mixed α- and β-receptor agonist and can be administered 5 to 10 mg every 5 minutes up to 50 mg. ²⁸ The onset of action of ephedrine is 1 minute with a duration of 60 minutes. Ephedrine administration carries the risk tachycardia and has a longer duration than other agents. ⁴³ Phenylephrine is commonly a first-line adrenergic agent administered for sustained hypotension and acts as a selective α agonist. ²⁸ The recommended dose is 0.1 mg administered every 3 minutes up to 0.5 mg. ²⁸ A risk of phenylephrine administration is rebound hypertension and bradycardia. Administration of epinephrine , which is an α- and β-receptor agonist probably should be reserved for cases of anaphylaxis or cardiac arrest. The recommended dose is 10 μg/min concentration administered 5 to 20 μg every 2 to 5 minutes at a rate of 0.5 to 2 mL/minutes. ⁴³ As discussed earlier but worth repeating, in anaphylaxis epinephrine is best administered as an intramuscular dose in 1:1,000 dilution as 0.3 to 0.5 mg, while the concentration for cardiac arrest is IV 1:10,000, 0.1 mg every 3 to 5 minutes. ²⁸ The onset is 1 minute and duration is 5 to 10 minutes. For asystole/pulseless electrical activity, epinephrine is administered every 3 to 5 minutes at 1 mg. ⁴³ A complication of epinephrine is tachycardia and rebound hypertension. ⁴⁴ Table 2 lists some of the most commonly used pharmacologic agents in the treatment of hypertension.

Conclusion

Understanding common scenarios for managing hypertensive and hypotensive episodes in the periprocedural period is vital to patient safety and improved outcomes. Additional studies evaluating the risk factors for hypotension and hypertensive scenarios specific to interventional procedures and moderate sedation are warranted.