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Abdominal Aortic Aneurysm Medication

  • Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Sep 28, 2015
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Antihypertensive agents are used to reduce tension on the vessel wall in patients with abdominal aortic aneurysms (AAAs) who have elevated blood pressure (BP). Analgesics are also an important element of care.

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Antihypertensives

Class Summary

Antihypertensives are used to reduce the rate of rise of the aortic pressure (dP/dt). For acute reduction of arterial pressure, the potent vasodilator sodium nitroprusside is very effective. To reduce dP/dt acutely, administer a beta blocker intravenously (IV) in incremental doses until a heart rate of 60-80 beats/min is attained. When beta blockers are contraindicated, as in second- or third-degree atrioventricular block, consider using calcium-channel blockers.

Esmolol (Brevibloc)

 

An ultrashort-acting beta1 blocker, esmolol is particularly useful in patients with elevated arterial pressure, especially if surgery is planned. It can be discontinued abruptly if necessary. This agent is normally used in conjunction with nitroprusside. It may be useful as a means of testing beta-blocker safety and tolerance in patients with a history of obstructive pulmonary disease who are at uncertain risk for bronchospasm from beta blockade. The elimination half-life of esmolol is 9 minutes.

Labetalol (Trandate)

 

Labetalol blocks alpha1-, beta1-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Propranolol (Inderal LA, InnoPran XL)

 

A class II antiarrhythmic nonselective beta-adrenergic receptor blocker, propranolol has membrane-stabilizing activity and decreases the automaticity of contractions. It is not suitable for emergency treatment of hypertension; it should not be administered IV in hypertensive emergencies.

Metoprolol (Lopressor, Toprol-XL)

 

Metoprolol is a selective beta 1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and electrocardiograms. When considering conversion from IV to oral (PO) dosage forms, use the ratio of 2.5 mg PO to 1 mg IV.

Nitroprusside (Nitropress)

 

Nitroprusside causes peripheral vasodilation by acting directly on venous and arteriolar smooth muscle, thus reducing peripheral resistance. This agent is commonly used IV because of its rapid onset and short duration of action. It is easily titrated to the desired effect.

Because nitroprusside is light-sensitive, both bottle and tubing should be wrapped in aluminum foil. Before initiating nitroprusside therapy, administer a beta blocker to counteract the physiologic response of reflex tachycardia that occurs when nitroprusside is used alone. This physiologic response will increase the shear forces against the aortic wall, thus increasing dP/dt. The objective is to keep the heart rate between 60 and 80 beats/min.

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Analgesics

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevents exacerbation of tachycardia and hypertension.

Morphine sulfate (Astramorph, Infumorph, Duramorph)

 

Morphine is the drug of choice for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Like fentanyl, morphine sulfate is easily titrated to the desired level of pain control. Morphine sulfate administered IV may be dosed in a number of ways. It is commonly titrated until the desired effect is obtained.

Fentanyl citrate

 

Fentanyl citrate is a synthetic opioid that has 75-200 times more potency of and a much shorter half-life than morphine sulfate. It has fewer hypotensive effects than morphine and is safer in patients with hyperactive airway disease because of minimal or no associated histamine release. By itself, fentanyl citrate causes little cardiovascular compromise, although the addition of benzodiazepines or other sedatives may result in decreased cardiac output and blood pressure.

Fentanyl citrate is highly lipophilic and protein-bound. Prolonged exposure to it leads to accumulation of the drug in fat and delays the weaning process. Consider continuous infusion because of the medication's short half-life.

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Contributor Information and Disclosures
Author

Saum A Rahimi, MD, FACS Interim Chief, Assistant Professor of Surgery, Division of Vascular Surgery, Rutgers Robert Wood Johnson Medical School

Saum A Rahimi, MD, FACS is a member of the following medical societies: American College of Surgeons, Society for Vascular Surgery, Eastern Vascular Society, Vascular Society of New Jersey

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Acknowledgements

Suman Annambhotla, MD Fellow in Vascular Surgery, Northwestern University, The Feinberg School of Medicine

Suman Annambhotla, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

Jeffrey Lawrence Kaufman, MD Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine

Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Pearce, MD Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University, The Feinberg School of Medicine

William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, andWestern Surgical Association

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Radiograph shows calcification of abdominal aorta. Left wall is clearly depicted and appears aneurysmal; however, right wall overlies spine.
On radiography, lateral view clearly shows calcification of both walls of abdominal aortic aneurysm, allowing diagnosis to be made with certainty.
CT demonstrates abdominal aortic aneurysm (AAA). Aneurysm was noted during workup for back pain, and CT was ordered after AAA was identified on radiography. No evidence of rupture is seen.
Arteriography demonstrates infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation for endovascular repair of aneurysm.
Lateral arteriogram demonstrates infrarenal abdominal aortic aneurysm. Demonstration of superior mesenteric artery, inferior mesenteric artery, and celiac artery on lateral arteriogram is important for complete evaluation of extent of aneurysm.
Arteriogram after successful endovascular repair of abdominal aortic aneurysm.
Ultrasonogram from patient with abdominal aortic aneurysm (AAA). This aneurysm was best visualized on transverse or axial image. Patient underwent conventional AAA repair.
MRI of 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, abdominal aortic aneurysm was discovered.
Age is risk factor for development of aneurysm.
Inflammation, thinning of media, and marked loss of elastin.
Pulsatile abdominal mass.
Aneurysm with retroperitoneal fibrosis and adhesion of duodenum.
Aortic endoprosthesis (Cook aortic and aortobi-iliac endograft).
Endoaneurysmorrhaphy
Endovascular grafts.
Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of feet (ie, blue toe syndrome).
Enhanced spiral CT scans with multiplanar reconstruction and CT angiogram.
Angiography is used to diagnose renal area. In this instance, endoleak represented continued pressurization of sac.
Table 1. Operative Mortality Risk of Open Repair of Abdominal Aortic Aneurysm
Lowest Risk Moderate Risk High Risk
Age < 70 y Age 70-80 y Age 80 y
Physically active Active Inactive, poor stamina
No clinically overt cardiac disease Stable coronary disease; remote MI; LVEF >35% Significant coronary disease; recent MI; frequent angina; CHF; LVEF < 25%
No significant comorbidities Mild COPD Limiting COPD; dyspnea at rest; O2 dependency; FEV1 < 1 L/sec
... Creatinine 2.0-3.0 mg/dL ...
Normal anatomy Adverse anatomy or AAA characteristics Creatinine >3 mg/dL
No adverse AAA characteristics ... Liver disease (↑ PT; albumin < 2 g/dL)
Anticipated operative mortality, 1%-3% Anticipated operative mortality, 3%-7% Anticipated operative mortality, at least 5%-10%; each comorbid condition adds ~3%-5% mortality risk
AAA—abdominal aortic aneurysm; CHF—chronic heart failure; COPD—chronic obstructive pulmonary disease; FEV1 —forced expiratory volume in 1 second; LVEF—left ventricular ejection fraction; MI—myocardial infarction; PT—prothrombin time.
Table 2. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture
AAA Diameter (cm) Rupture Risk (%/y)
< 4 0
4-5 0.5-5
5-6 3-15
6-7 10-20
7-8 20-40
>8 30-50
AAA—abdominal aortic aneurysm.
Table 3. Factors Affecting Risk of Abdominal Aortic Aneurysm Rupture
  Low Risk Average Risk High Risk
Diameter < 5 cm 5-6 cm >6 cm
Expansion < 0.3 cm/y 0.3-0.6 cm/y >0.6 cm/y
Smoking/COPD None, mild Moderate Severe/steroids
Family history No relatives One relative Numerous relatives
Hypertension Normal blood pressure Controlled Poorly controlled
Shape Fusiform Saccular Very eccentric
Wall stress Low (35 N/cm2 Medium (40 N/cm2 High (45 N/cm2)
Sex ... Male Female
COPD—chronic obstructive pulmonary disease.
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