Pharmacological Management of Hypotension
Context-Dependent Treatment Selection
The appropriate tablet for increasing blood pressure depends entirely on the clinical context—acute versus chronic hypotension, and the underlying etiology.
For Acute Hypotension (Septic Shock, Anesthesia-Related)
Intravenous vasopressors are required, not oral tablets, as acute hypotension demands immediate intervention. 1, 2
- Norepinephrine is the first-choice vasopressor for septic shock and acute vasodilatory hypotension, targeting a mean arterial pressure (MAP) of 65 mmHg 1
- Phenylephrine hydrochloride (IV) is indicated for increasing blood pressure in adults with clinically important hypotension resulting primarily from vasodilation, such as septic shock or anesthesia 2
- Epinephrine can be added to norepinephrine when an additional agent is needed to maintain adequate blood pressure 1
- Vasopressin (0.03 units/minute) may be added to norepinephrine to raise MAP or decrease norepinephrine dosage 1
For Chronic Orthostatic Hypotension
Midodrine is the primary oral tablet for treating chronic symptomatic orthostatic hypotension. 3, 4, 5
Midodrine Mechanism and Dosing
- Midodrine forms an active metabolite (desglymidodrine) that is an alpha-1 agonist, producing increased vascular tone and elevation of blood pressure 3
- Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10 mg dose, with effects persisting for 2 to 3 hours 3
- Typical dosing is 10 mg three times daily, with the last dose not later than 6 PM to avoid supine hypertension 3
- Peak blood concentrations of the active metabolite occur about 1 to 2 hours after dosing, with a half-life of 3 to 4 hours 3
Alternative Pharmacological Options
- Fludrocortisone provides volume expansion and is often used in combination with midodrine for orthostatic hypotension 4, 5
- Droxidopa is a short-acting vasoactive agent that can be used as an alternative to midodrine 6
For Heart Failure with Low Blood Pressure
In patients with heart failure and reduced ejection fraction (HFrEF), the goal is NOT to raise blood pressure with vasopressors, but rather to optimize guideline-directed medical therapy (GDMT) carefully. 1
- Start SGLT2 inhibitors and mineralocorticoid receptor antagonists first, as they have the least effect on blood pressure but rapid beneficial effects 1
- Subsequently consider low-dose beta-blockers (if heart rate >70 bpm) or very low-dose sacubitril/valsartan (25 mg twice daily) 1
- Selective β₁ receptor blockers are preferred due to lesser blood pressure-lowering effects than non-selective beta-blockers 1
- If beta-blockers are not well tolerated hemodynamically, ivabradine may be a viable alternative 1
Critical Diagnostic Steps Before Treatment
Confirm true hypotension by measuring blood pressure both supine and standing—a drop of 20 mmHg systolic and/or 10 mmHg diastolic within 3 minutes of standing suggests orthostatic hypotension. 1, 4
- Identify and discontinue aggravating medications: calcium channel blockers, centrally acting antihypertensives, alpha-blockers, NSAIDs 1, 6
- Rule out transient medical conditions causing dehydration (diarrhea, fever, overtreatment with diuretics) 1
- Assess for secondary causes: adrenal insufficiency, autonomic neuropathy (diabetes, Shy-Drager syndrome), hypovolemia 7, 8
- Verify medication adherence, as non-adherence is the most common cause of apparent treatment resistance 6
Non-Pharmacological Interventions (Always First-Line)
Education and non-pharmacological strategies are critical, as drug therapy alone is never adequate for chronic orthostatic hypotension. 5
- Patient education regarding triggering situations and physiological countermaneuvers 4, 5
- Increase fluid intake (2-3 liters daily) and salt intake (6-10 grams daily) unless contraindicated 5
- Compression stockings (waist-high, 30-40 mmHg) to reduce venous pooling 5
- Physical countermaneuvers: leg crossing, squatting, muscle tensing 5
- Elevate head of bed 10-20 degrees to reduce nocturnal diuresis and supine hypertension 5
Treatment Goals
The goal is to improve postural symptoms, standing time, and function—NOT to achieve upright normotension, which can lead to supine hypertension. 5