Hydralazine is a medication primarily prescribed to manage high blood pressure (hypertension) and is also used in the treatment of heart failure. The drug’s main purpose is to lower the force against which the heart must pump blood, easing the workload on the cardiovascular system. However, its specific action on the heart rate is often counterintuitive, as it typically does not slow the heart; instead, it can cause an increase. Understanding this unique response is important for anyone using the medication.
How Hydralazine Lowers Blood Pressure
Hydralazine functions as a direct-acting vasodilator, meaning it works immediately on the physical structure of the blood vessels. Its primary target is the smooth muscle within the walls of the arterioles, which are the small arteries that primarily determine blood pressure. By preventing the influx or release of calcium within these muscle cells, the drug causes the arterial walls to relax and widen, a process called vasodilation.
This widening of the arteries results in a reduction of peripheral vascular resistance. When this resistance decreases, the blood pressure drops significantly. This action is beneficial in conditions like hypertension because it reduces the afterload, which is the force the left ventricle must overcome to eject blood. This mechanism allows the heart to pump more efficiently, a desired effect in treating high blood pressure and heart failure.
The Effect on Heart Rate
Contrary to what might be expected from a blood pressure-lowering drug, hydralazine does not decrease heart rate; it frequently causes an increase. This increase is known as reflex tachycardia, a common side effect of direct vasodilators. The rapid drop in systemic blood pressure triggers a powerful compensatory mechanism in the body.
This acceleration of the heart is the body’s attempt to restore blood pressure to its pre-treatment level. This effect can manifest as noticeable palpitations or an uncomfortable sensation of a racing heart. For individuals with underlying coronary artery disease, this increased heart rate and the subsequent rise in cardiac output can increase the risk of angina or other cardiac events. The heart rate can typically increase by 10 to 20 beats per minute.
The Physiology of Reflex Tachycardia
The phenomenon of reflex tachycardia is a biological feedback loop governed by the autonomic nervous system. The process begins with specialized pressure sensors called baroreceptors, located in the walls of the carotid arteries and the aortic arch. These baroreceptors constantly monitor the stretch of the arterial walls, which corresponds directly to the current blood pressure.
When hydralazine causes the arterioles to dilate, the blood pressure falls quickly, reducing the stretch sensed by these baroreceptors. The baroreceptors interpret this sudden decrease in pressure as a sign of impending hypotension, or dangerously low blood pressure. This signal is rapidly transmitted to the medulla in the brainstem, which controls cardiovascular function.
In response, the brain immediately activates the sympathetic nervous system, often referred to as the “fight or flight” system. This activation releases catecholamines, such as norepinephrine, which act directly on the heart muscle. These hormones increase both the rate at which the heart beats and the force of each contraction, increasing cardiac output. The goal of this reflex is to compensate for the reduced resistance in the periphery, attempting to push the blood pressure back toward the set point. This sequence constitutes the reflex tachycardia, a protective mechanism that can undermine the therapeutic goal of the medication.
Combining Medications for Heart Rate Stability
Because hydralazine’s powerful blood pressure-lowering effect is often accompanied by the undesirable side effect of reflex tachycardia, it is rarely prescribed alone for chronic hypertension. Standard clinical practice involves combining hydralazine with a second medication specifically to stabilize the heart rate. The most common drug class used for this purpose is beta-blockers, such as metoprolol or propranolol.
Beta-blockers work by blocking the effects of the sympathetic nervous system’s hormones on the heart. By doing so, they effectively dampen the exaggerated increase in heart rate and contractility triggered by the baroreceptor reflex. This combination therapy allows the patient to reap the benefit of hydralazine’s potent vasodilation and reduced peripheral resistance without the negative symptoms and cardiac strain of a persistently elevated heart rate. Hydralazine is frequently administered alongside a beta-blocker and often a diuretic to manage fluid retention that can also accompany vasodilation.