Not infrequently, interventionalists are faced with a patient with increased blood pressure who is about to undergo a dialysis access intervention such as tunneled hemodialysis catheter, percutaneous balloon angioplasty, or declotting procedure for a clotted arteriovenous access. This can frequently create a dilemma as functional dialysis access is needed to provide dialysis therapy and delaying treatment could result in a life-threatening situation, particularly in the presence of hyperkalemia. This article investigates hypertension in patients undergoing percutaneous dialysis access interventions and provides guidance to their management.
J Vasc Access 2017; 18(5): 363 - 365
Article Type: EDITORIAL
AuthorsBhavika V. Gandhi, Tejas B. Patel, Eric J. Costanzo, Avais Masud, Sushil Mehandru, Loay Salman
- • Accepted on 14/06/2017
- • Available online on 27/07/2017
- • Published in print on 11/09/2017
This article is available as full text PDF.
Hypertension is a major cause of stroke, congestive heart failure, coronary artery disease and end-stage renal disease (ESRD). Because of volume overload, hypertension is particularly prevalent in the dialysis population. Interventionalists debate whether to postpone a case with high blood pressure (BP) until the pressure is within an acceptable range; however, this is one situation where dialysis access is absolutely required to provide life-sustaining therapy and to remove excess volume to make an impact on reducing pressure.
In general, it is stage II hypertension (BP ≥160/100 mmHg) that often draws particular attention prior to the procedure. At least one study has investigated patients undergoing percutaneous dialysis access interventions with a systolic BP ≥160 mmHg (1). In that study, 103 dialysis patients undergoing percutaneous interventions (tunneled hemodialysis catheter insertion and percutaneous balloon angioplasty, stent placement, and thrombectomy procedures) were included. All patients included in the study demonstrated an asymptomatic pre-procedure systolic BP of ≥160 mmHg (mean 185 ± 18 mmHg). The mean diastolic BP was 96 ± 14 mmHg. All patients were asymptomatic without any shortness of breath, chest pain, dizziness, blurring of vision or headache. All patients successfully underwent percutaneous interventions. The results disclosed a substantial reduction in BP with systolic BP decreasing from 185 ± 18 mmHg to 153 ± 25 mmHg (p<0.001). Similarly, diastolic BP decreased from 96 ± 14 to 87 ± 14 mmHg (p<0.001). Interestingly, antihypertensive medications were not used before, during or following the percutaneous interventions, yet nearly 30 mmHg decline in systolic and roughly 10 mmHg decrease in diastolic BP was observed in these patients. Importantly, the study demonstrated that none of the patients had an acute pulmonary edema, myocardial infarction or stroke before, during, or following the percutaneous procedures. Additionally, no patients had any of these complications during the 4-week follow-up period.
The above-cited study provides evidence that dialysis patients undergoing percutaneous interventions can successfully undergo procedures despite BP in a range that could potentially make an interventionalist nervous about undertaking an intervention (1). The procedures then allow for access to be available for dialysis therapy. A question which comes to mind is why did the BP go down without the administration of an antihypertensive agent? The investigators offered some explanation. The contribution of anxiety and sympathetic discharge is frequently downplayed and often ignored. Sympathetic stimulation is a powerful stimulus to raise BP. Despite dialysis patients frequently undergo dialysis access procedures, they are often anxious when they arrive to the procedure room. This can drive BP up. Sedatives, such as midazolam, can be used during a procedure to reduce anxiety. Both midazolam and fentanyl administered during the procedures can also lower BP (2).
Most non-ESRD procedures performed under conscious sedation can often be postponed for elevated BP to prevent/minimize procedure-related complications. Indeed, well-controlled procedures improve patient safety. However, ESRD patients presenting for vascular access procedures are unique. The luxury of postponing procedures is often not available, as the patient still needs to receive dialysis therapy through the vascular access. In this context, a thrombosed access needs to be treated and if the procedure is unsuccessful, an additional procedure is needed to place a central venous catheter (CVC). These patients create a unique set of challenges that the physician is forced with work with so that the patient can continue to receive life-sustaining dialysis therapy.
What target blood pressure to aim for before performing a dialysis access procedure? The importance of understanding “reasonable” BP control is vital for taking the decision to operate. Obtaining BP records and history from the dialysis unit to understand the baseline BP can help individualize the risk associated with the procedure. Non-adherence to BP medication is an important reason for uncontrolled BP and should be investigated prior to the procedures. It is important to point out that a uniform target of 140/90 mmHg may not be optimal for everyone. Such an approach may provide a target BP to aim for and improve safety.
Often, providers consider the use of medication to lower BP before dialysis access intervention. As such, among antihypertensive medications, clonidine is a commonly used drug. It is cost effective, frequently readily available and often used to decrease an acute rise in BP. However, this medication has multiple issues. Clonidine can cause a sudden and uncontrolled decreased in BP. This is particularly in patients undergoing percutaneous interventions, as many of these patients also receive midazolam and fentanyl, both of which can lower BP. Rebound hypertension is a common feature of clonidine and must be kept in mind when prescribing this medication during percutaneous interventions. The rebound could be magnified as the effects of midazolam and fentanyl wear off and hence, the use of clonidine is not without issues. Anxiety can raise BP and should be managed. Similarly, optimal pain control is vital to keep BP under control. Short-acting beta-blockers administered intravenously can be considered to lower BP. In addition, intravenous hydralazine titrated to the lowest dose and nitroglycerine paste may also be helpful. Finally, during the procedure interventionalists should monitor the patient for end-organ damage (neuro, visual, pulmonary, cardiac symptoms) to optimize patient care (
Table proposes steps that may be helpful in managing ESRD patients presenting for dialysis access procedure
|ESRD = end-stage renal disease; BP = blood pressure.|
|Step I||Evaluate for hypertensive emergency||Make appropriate arrangements to transfer the patient to the emergency department|
|Step II||Communicate with dialysis unit and obtain BP history and records||Individualize patient care. Do not categorically use a uniform target of 140/90 mmHg. Set a reasonable target for the given patient|
|Step III||Manage anxiety||Explain what to expect and use sedation appropriately|
|Step IV||Manage pain||Optimize pain control to better manage BP|
|Step V||Judicious use of anti-hypertensive medications||Avoid clonidine (see the text for details). Consider intravenous short-acting beta-blockers and hydralazine titrated to the lowest dose. Nitroglycerine paste may also be helpful|
|Step VI||Closely monitor the patient for end-organ damage during the procedure||Monitor the patient for neuro, visual, pulmonary and cardiac symptoms|
Reducing BP acutely in patients with chronically elevated BP can create a problem in patients. A substantial decrease in BP could deregulate cerebral circulation and create a catastrophe (3). To understand cerebral dysregulation, one needs to comprehend normal cerebral flow. It has been estimated that blood flow of 50-60 mL/100 gm of brain is needed to maintain normal cerebral functions. This blood flow is maintained by a mean arterial pressure (MAP) in the range of 50-150 mmHg (3). In this context, when MAP falls to 50 mmHg (BP = 70/50 mmHg), vasodilation of the intra-cerebral arteries occurs, which allows the cerebral blood flow to be maintained. This avoids cerebral hypoperfusion and irreversible ischemic damage to the brain. In contrast, when mean arterial BP exceeds 150 mmHg (BP = 190/130 mmHg), vasoconstriction of small intra-cerebral arteries ensues and protects against cerebral hyperperfusion and irreversible ischemic damage, increased intracranial pressure and hypertensive encephalopathy.
It is worth mentioning that a patient presenting with high BP and associated symptoms of chest pain, shortness of breath, mental status change, dizziness, visual disturbances, including blurring of vision and severe headache, should be referred to the emergency department in order to appropriately manage hypertensive emergency.
In conclusion, patients presenting with high BP before a percutaneous dialysis intervention do not categorically require antihypertensive medications to acutely reduce BP. A recent study conducted in chronic hemodialysis patients supported this notion and demonstrated a significant decline in systolic (nearly 30 mmHg) and diastolic (nearly 10 mmHg) BP. In this context, reducing BP acutely with antihypertensive medications can potentially decrease BP to a dangerously low level and cause cerebral dysregulation with its antecedent adverse effects.
- Gandhi, Bhavika V. [PubMed] [Google Scholar] 1
- Patel, Tejas B. [PubMed] [Google Scholar] 1
- Costanzo, Eric J. [PubMed] [Google Scholar] 1
- Masud, Avais [PubMed] [Google Scholar] 1
- Mehandru, Sushil [PubMed] [Google Scholar] 1
- Salman, Loay [PubMed] [Google Scholar] 2, * Corresponding Author (SalmanL@mail.amc.edu)
Department of Medicine, Jersey Shore University Medical Center, Seton Hall-Hackensack-Meridian School of Medicine, Neptune, NJ - USA
Department of Medicine, Albany Medical College, Albany, NY - USA