Abdominal Aortic Aneurysm Medication
- Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD more...
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.
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.
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 blocks alpha1-, beta1-, and beta2-adrenergic receptor sites, decreasing blood pressure.
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 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 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.
Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevents exacerbation of tachycardia and hypertension.
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 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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|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.|
|AAA Diameter (cm)||Rupture Risk (%/y)|
|AAA—abdominal aortic aneurysm.|
|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|
|Family history||No relatives||One relative||Numerous relatives|
|Hypertension||Normal blood pressure||Controlled||Poorly controlled|
|Wall stress||Low (35 N/cm2||Medium (40 N/cm2||High (45 N/cm2)|
|COPD—chronic obstructive pulmonary disease.|