Last Updated on January 26, 2024
Ever wonder what exactly blood pressure means? Or physiologically speaking, how does the blood generate pressure? What causes it to develop, and what should we do to prevent it from rising? Put simply, there are several causative factors affecting the cardiac output and blood pressure within the vasculature. The key to the crux lies in this blog, covering every aspect of systemic vascular resistance, the primary culprit behind high blood pressure, and an understanding of what is systemic vascular resistance. Continue reading the blog to learn about effective treatment options for correcting abnormally high and low SVR.
In addition to standard medications, participation in cardiology clinical study trials investigating novel and effective alternatives for the management of vascular resistance might be an option most people don’t think of.
What is Systemic Vascular Resistance?
Systemic vascular resistance refers to resistance to the blood flow offered by the arteries and arterioles during its passage from the left ventricle before it enters systemic circulation. It includes all the blood vessels involved in systemic circulation except those in the lungs.
However, SVR is regulated by factors such as:
- Diameter and length of the blood vessels
- The viscosity of the blood
- Contractility of the heart
Other factors include:
- Cardiac output
- Hormonal influence
Moreover, the blood volume ejected from the left ventricle reflects changes in the SVR caused by vasoconstriction. For example, increased narrowing and constriction of the arterioles manifests in 3 ways:
- Increased SVR.
- Diminished ventricular compliance.
- Reduced stroke volume.
- Decrease in cardiac output.
Mechanism of Systemic Vascular Resistance
Blood vessels in the human body consist of one to three main layers: the outer tunica adventitia, middle tunica media, and inner tunica intima. Each layer has distinct properties and thickness variations in different types of vessels.
- The adventitia, made of fibrous connective tissue, prevents vessel rupture under high pressure.
- The tunica intima, composed of epithelial cells, plays a crucial role in vascular function by signaling smooth muscle in the tunica media, particularly in response to injury. Endothelial damage may reduce the release of substances like prostaglandins and nitric oxide, leading to vasoconstriction and increased systemic vascular resistance (SVR).
- The tunica media, consisting of elastic connective tissue and smooth muscle, is crucial for maintaining blood pressure through SVR. Elastic fibers in this layer withstand the force of blood being pumped out of the heart and exert it back during diastole, contributing to blood pressure regulation. Smooth muscle in this layer also manipulates vessel diameter, impacting blood pressure.
The renin-angiotensin-aldosterone system is another significant mechanism influencing SVR by altering blood vessel resistance and the volume of circulating blood. Angiotensin II, a key component, signals smooth muscle in arterioles to increase their strength. Changes in vessel caliber dramatically affect blood flow; a 1/2 reduction in diameter allows only 1/16 of previous blood flow. Arteries, with thick tunica media and adventitia, maintain high pressures needed for organ perfusion, while veins lack a significant smooth muscle layer.
Blood viscosity is also pivotal in SVR. Conditions like polycythemia, with elevated red blood cell levels, increase viscosity, raising SVR. Conversely, anemia, with fewer red blood cells, results in lower SVR due to decreased blood thickness.
Interlink between Cardiac Output and Systemic Vascular Resistance
In a state of increased physical activity or cardiac dysfunction affecting systemic vascular resistance, the blood flow adjusts according to the body’s needs. For example, with an increase in systemic vascular resistance, the cardiac output diminishes, reducing the amount of blood flow to the organs, thus producing clinically significant signs and symptoms, including:
- Systolic blood pressure < 90 mm Hg
- Low blood pressure
- Weak pulse
- Cool extremities
- Decreased urinary output
- Altered mental status or confusion
- Fatigue or lack of energy
- Chest pain
- Swelling or edema in legs, feet, or ankles
Cardiogenic shock (a consequence of decreased cardiac output) is a state of shock in which the heart does not supply a sufficient amount of oxygenated blood to the vital organs inside the body necessary for survival. It is evident in a cardiac index below 1.8 L/min/m2.
Calculating Systemic Vascular Resistance
The range of systemic vascular resistance varies, depending on the method used to measure it, influenced by the age or health of the individuals, and other factors. Generally, the normal range of SVR in adults lies between 700 – 1500 dynes/sec/cm.
A standard formula to calculate systemic vascular resistance (SVR) is to subtract the right atrial pressure (RAP) from the mean arterial pressure (MAP), divided by the cardiac output (CO), and multiply by 80. SVR = (MAP-RAP/CO) * 80
What causes Systemic Vascular Resistance (SVR)?
Several medical conditions may cause an increase or decrease in systemic vascular resistance. Some of these conditions include:
Hypertension is a chronic disease that increases vascular resistance by narrowing the blood vessels. When the blood vessels constrict, this makes it harder for the blood to flow through them, thereby generating high SVR.
This is a condition that involves plaque buildup inside the arteries, making them narrower and stiffer. This results in an increase in 22. and an increased risk of heart attack and stroke.
People with diabetes, a common endocrine condition, are at an increased risk of developing atherosclerosis, which increases systemic vascular resistance.
A condition narrowing or constricting the blood vessels inside the fingers and toes in response to cold or stress. This, however, results in increased systemic vascular resistance in these areas.
Peripheral artery disease:
This is a condition causing the narrowing of the blood vessels in the lower extremities and an increase in systemic vascular resistance. It reduces the amount of blood flow to the legs.
It is a type of high blood pressure affecting the blood vessels in the lungs, increasing vascular resistance, and making it harder for the heart to pump blood through the lungs.
Polycythemia (increased red cell count):
This condition involves an abnormally high number of red cells in the blood. An increase in cell count increases the viscosity, making it difficult for the blood to flow through blood vessels, leading to an increase in SVR.
Anemia with reduced red cell count dilates the blood vessels and lowers the blood pressure. This results in a decrease in systemic vascular resistance.
One of the effects of sepsis is a widespread inflammatory response throughout the body that constricts or dilates the blood vessels. This results in an increase or decrease in the systemic inflammatory response.
Treatment Options Available
The treatment for SVR depends on the underlying condition causing the increase in resistance.
In case of increased systemic vascular resistance (SVR) due to hypertension:
- Adapting certain lifestyle modifications, such as maintaining a healthy weight, regular exercise, and a low-sodium diet is suggested.
- Medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, calcium channel blockers, and diuretics are prescribed to control blood pressure.
To reduce fluid overload and improve cardiac function:
Medications such as ACE inhibitors, ARBs, beta-blockers, and diuretics are prescribed to reduce the risk of heart failure.
To relax the blood vessels and reduce (SVR):
Vasodilator medications such as nitroglycerin, hydralazine, or nifedipine are prescribed.
To open blocked blood vessels or correct structural abnormalities:
Surgical intervention such as balloon angioplasty or stenting is necessary.
The outlook for systemic vascular resistance and how to manage it depends on the underlying cause and changes produced by systemic vascular resistance. If SVR remains elevated for a long period, it can put a strain on the heart and lead to cardiovascular complications such as heart failure, stroke, or shock. To improve heart outcomes, clinical research organizations are working tirelessly, investigating novel potential options for treating vulnerable heart conditions.