Hypertension: Nursing pathophysiology

Hypertension occurs when the force of the blood pushing against the artery walls is too high, causing damage to organs.

Okay, so, as the heart pumps blood throughout the body, it creates pressure against the walls of the arteries, which is referred to as blood pressure, or BP.

Blood pressure is expressed as a fraction, where the top number, called the systolic pressure, represents the pressure in the arteries when the heart is contracting and pumping blood; and the bottom number, called the diastolic pressure, represents the pressure in the arteries when the heart is relaxed and filling with blood. Normal blood pressure is less than 120 mmHg systolic and less than 80 mmHg diastolic.

Factors that impact blood pressure include cardiac output, or CO, and systemic vascular resistance, or SVR. First, cardiac output is the quantity of blood pumped by the heart and is measured in L/min. The two components of cardiac output are stroke volume, or SV, and heart rate, or HR. Stroke volume is the amount of blood leaving the heart with each contraction, and heart rate is the number of contractions in one minute.

The higher the stroke volume and heart rate, the higher the cardiac output.

Next, systemic vascular resistance is determined by the radius and elasticity of blood vessels. If blood vessels are narrow or stiff, systemic vascular resistance increases, which then increases blood pressure.

Now, blood pressure is regulated by short-term and long-term mechanisms. Short-term regulation is mainly controlled by the autonomic nervous system, or ANS. For example, when changing from a lying to a standing position, blood pressure tends to drop.

When this happens, baroreceptors, which are pressure-sensitive receptors located mostly in the aortic arch and carotid sinuses, respond by sending signals to the vasomotor center in the medulla. The medulla activates the sympathetic nervous branch of the autonomic nervous system, which increases heart rate, systemic vascular resistance, and cardiac contractility. Together, these actions increase blood pressure.

On the other hand, long-term regulation is mainly controlled by the renin-angiotensin-aldosterone system, or RAAS, which begins in special cells in the kidneys, called juxtaglomerular cells. When blood pressure is low, these cells release an enzyme called renin into the circulation. Renin converts angiotensinogen, an inactive protein made by the liver that’s always floating around in the blood, into angiotensin I, which is then converted into angiotensin II by angiotensin-converting enzyme, primarily in the lungs.

Angiotensin II then increases blood pressure by causing vasoconstriction and increased systemic vascular resistance. It also increases stroke volume by triggering the release of aldosterone, which causes the kidneys to retain sodium and water. And lastly, it acts on the hypothalamus, stimulating thirst and the production of antidiuretic hormone, which increases water reabsorption by the kidneys.

Finally, the RAAS is a negative feedback system, so once blood pressure is normalized, the kidneys stop releasing renin, and RAAS activity is essentially turned off.

Now, hypertension can be categorized as primary or secondary. Primary hypertension has no clear, identifiable cause. There are both modifiable and non-modifiable risk factors for primary hypertension. Modifiable risk factors include obesity, sedentary lifestyle, tobacco use, and a diet high in sodium and saturated fats. Non-modifiable risk factors include increasing age and a genetic predisposition for hypertension.