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How To Calculate Mean Arterial Pressure (MAP)

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What Is Mean Arterial Pressure

The concepts of blood pressure and mean arterial pressure are among the most important ones in cardiac physiology and medicine in general. Almost any patient, regardless of their complaint, get their blood pressure measured during any visit to the physician.

Why blood pressure is so important? Maybe because high mean arterial blood pressure (hypertension) is the #1 silent killer worldwide?

Blood pressure and mean arterial pressure calculation seem to be easy. However, the issue with them is not the calculation. Instead, it is the complex physiology of how the body regulates blood pressure and how high blood pressure can lead to serious pathophysiologic consequences.

 How To Calculate Mean Arterial Pressure?

The classic equation used to calculate mean arterial pressure (MAP) is the following:

MAP = Cardiac output  × Total peripheral resistance

However, in real life, mean arterial pressure is not determined by this equation since it is very hard to calculate a patient’s total peripheral resistance or cardiac output. Mean arterial pressure can be approximated by the following equation:

MAP = ⅓ Systolic blood pressure + ⅔ Diastolic blood pressure

Example

If systolic pressure is 110 mmHg and diastolic pressure is 80 mmHg, then MAP can be calculated as the following:

(1/3 x 110) + (2/3 x 80) = 36.6 + 53.3 = 90 mm Hg.

Have you ever wondered why we use 1/3 of systolic blood pressure and 2/3 of diastolic pressure? Why don’t we just average them?

This is because, during the cardiac cycle, the diastole is much longer than systole. Therefore, it would be inaccurate if we calculated their average.

Mean arterial blood pressure determinants

Systolic vs. Diastolic blood pressure

Our cardiac cycle is divided into two phases: systole and diastole. During systole, blood is pumped from the heart, and during diastole, the heart relaxes and fills with blood.

During states of increased heart rate as in exercise, the duration of diastole decreases. This makes the mean arterial pressure close to the arithmetic average of systolic and diastolic pressure.

In real life, we want to ensure that a patient has at least a mean arterial pressure (MAP) of 60 mm Hg. In cases of shock, for instance, we know that our resuscitation has been successful if the patient’s blood pressure is greater than 60 mm Hg.

Below that, perfusion to vital organs is at risk, and more serious steps need to be taken.

Cardiac output (CO)

Cardiac output is the product of stroke volume and heart rate. Stroke volume is determined b the contractility and ventricular preload. Ventricular preload can be altered by changes in blood volume and venous compliance.

Blood volume is controlled by renal function via the action of the Renin-Angiotensin-Aldosterone system and other hormones like ADH. Venous compliance is determined by constriction or dilation of veins. For example, in patients taking nitrates (a vein dilator), the blood pools in veins, and there is a decrease in the amount of blood returning to the heart and, thus, stroke volume.

There are so many other details regarding cardiac output and stroke volume. We highly encourage you to read our article on cardiac output if this isn’t enough for you.

Total peripheral resistance (TPR)

Total peripheral resistance is the resistance the circulatory must overcome to create blood flow.

If we increase TPR as in vasoconstriction → ↑ afterload → ↓ CO

If we decrease TPR as in vasodilation → ↓ afterload and ↑ venous return → ↑ CO

Figure-1

https://en.wikipedia.org/wiki/Vasodilation

However, the control of systemic vascular resistance is much more complex than this. To learn more about vascular resistance, we need to understand Poiseuille’s law. It states that the resistance is inversely related to the fourth power of the vessel radius (Resistance to flow: R = 8ηL/(πr 4).

Vascular factors like nitric oxide have an important influence on vessel diameter. Also, tissue factors like adenosine, histamine, and potassium ions can alter the vessel diameter. These factors are released by parenchymal cells (as in muscles) surrounding blood vessels.

Finally, neurohormonal mechanisms are vital in regulating vascular resistance and blood pressure. Neural refers to the autonomic nervous system regulation, while humoral refers to the hormones. Neural mechanisms like the sympathetic nervous system can lead to constriction of blood vessels.

For hormones, many hormones like renin-angiotensin-aldosterone system, atrial natriuretic peptide, and vasopressin (ADH) can alter the vascular function and mean arterial pressure.

Figure-2

Created with birender.com

Regulation of mean arterial pressure

Now, after we have learned how to calculate mean arterial pressure and what are some factors controlling it, it is time to learn how our body regulates blood pressure.

Sensors of blood flow regulation

Baroreceptors (Diagram here)

Baroreceptors are stretch-sensitive nerve endings that detect and regulate blood pressure in systemic circulation via signaling to our autonomic nervous system. They are located in the wall of the carotid sinus, aortic arch, and atria.

When there is a decrease in blood pressure, there is a decrease in the firing frequency of these baroreceptors. This decreases signaling to the vasomotor center in the brainstem, and increases sympathetic innervation, leading to vasoconstriction, increased heart rate, increased stroke volume, and of course, mean arterial pressure.

↓BP à  ↓ activity of baroreceptors à ↓ signaling to the vasomotor center à ↑ sympathetic tone à vasoconstriction à  ↑ HR, SV, and BP.

↑BP à ↑ activity of baroreceptors à activation of the vasomotor center à ↓ sympathetic tone→ vasodilatation → ↓ HR, SV, and BP.

Chemoreceptors

Chemoreceptors are specialized receptors that detect changes in blood pH and regulate O2, CO2, and pH levels through respiration.

There are 2 types of chemoreceptors: Peripheral and central.

Peripheral chemoreceptors are located in the carotid body and aortic body. They measure the concentration of oxygen, CO2, and pH.

Central chemoreceptors are located in the medulla oblongata. They measure the concentration of CO2 and pH of the cerebral intertrial fluid. Central chemoreceptors are less sensitive to O2 levels compared to peripheral ones.

How do they work? Any increase in CO2 or decrease in O2 or pH leads to increased sympathetic tone. In addition, they modulate breathing via the respiratory center in the medulla.

Central blood pressure regulation

It is time to put it all (the baroreceptors and chemoreceptors). What exactly happens in response to the activation of any of these receptors?

The central blood pressure regulation location is at the solitary nucleus in the medulla oblongata.

Afferent: It receives information via the glossopharyngeal nerve (IX) from the carotid sinus baroreceptors and carotid body chemoreceptors. It also receives information via the vagus nerve from the aortic chemoreceptor, aortic baroreceptor, and atrial volume receptors.

 Efferent: It sends signals via the sympathetic cervical chain and sympathetic fibers to blood vessels, SA node, and AV node. It also sends parasympathetic output via the vagus nerve to the AV and SA nodes. Note that the sympathetic and parasympathetic are never activated simultaneously. Activation of either of them depends on whether it occurred in response to a decrease or increase in mean arterial pressure. Here is a nice summary of central blood regulation:

   
 Sympathetic activationParasympathetic activation
ArteriesVasoconstriction à ↑ vascular resistanceVasodilation through the release of nitric oxide (NO) only in coronary arteries and vessels of the penis (erection)
VeinsVenous constriction à ↑ preload à ↑ stroke volumeVenous dilatation → ↓ preload → ↓ stroke volume
HeartIncreased contractility Increased heart rateDecrease heart rate (The parasympathetic supplies on the conduction system, not the myocardium. Therefore, contractility decreases by a decrease in sympathetic tone only)

Figure-3

Created with birender.com

The atrial reflex

The atrial reflex is a physiologic reflex characterized by increased heart rate in response to atrial stretch (increase in venous return). This reflex is mediated by stretch receptors in the atria.

Here is the mechanism: Increased venous return → Increased atrial stretch receptors stimulation → activation of stretch receptors in the atria → Increased sympathetic innervation, and no change in parasympathetic innervation → increased heart rate.

Atrial natriuretic peptide (ANP) secretion pathway

Similar to the atrial reflex, this pathway is activated through the stretch of the atrium. However, this time, the response is the production of ANP, not sympathetic activation.

Increased preload → Increased atrial stretch receptors stimulation→ release of ANP from atrial cardiomyocytes. This results in:

  1. Decreased Na+ reabsorption at the renal collecting tubules
  2. Increased excretion of sodium and water excretion by the kidneys via efferent arteriole constriction and afferent dilation
  3. Inhibition of renin
  4. Vasodilation of veins and arteries, leading to decreased afterload and preload.

As you see, the overall response is to lower blood pressure.

Diuresis reflex (Gauer-Henry reflex)

The diuresis reflex is a physiological reflex that leads to ADH release from the hypothalamus in response to low blood pressure. How does it work?

Increased blood pressure à Atrial stretch receptors inhibit ADH release via afferent vagal fibers → ↑ water excretion by the kidneys

And the reverse is true.

Figure-4

Created with birender.com

Renal regulation

Renin-angiotensin-aldosterone system (RAAS)

Now comes the master! The RAAS is the most important system in regulating blood pressure. Among all described mechanisms in regulating blood pressure, the RAAS is the most important. If you want to remember only one regulatory mechanism, please remember this one.

If there is a drop in blood pressure, this leads to decreased renal perfusion. If the pressure in the renal artery falls by more than 10-15 mmHg, renin is released from the juxtaglomerular apparatus.

Renin converts angiotensinogen to angiotensin I → ACE cleaves C-terminal peptides on angiotensin I, converting it to angiotensin II (ATII). ATII increases blood pressure via multiple mechanisms:

  1. Vasoconstriction à increased blood pressure
  2. Increases ADH secretion from the posterior pituitary à increased water reabsorption in the collecting ducts à increased blood volume à increased preload à increased cardiac output à increased mean arterial pressure
  3. Stimulates thirst in the hypothalamus à increased blood volume (same as ADH)
  4. Activates the release of aldosterone by the adrenal cortex à increased sodium and water reabsorption

Figure-5

https://en.wikipedia.org/wiki/Renin%E2%80%93angiotensin_system

Conclusion

In this article, we have learned a lot about the concept of mean arterial pressure. We also learned the mean arterial pressure equation (MAP = ⅓ Systolic blood pressure (SP) + ⅔ Diastolic blood pressure) and the normal mean arterial pressure range (>60 mmHg).

We also learned about the different neurohumoral mechanisms by which our body regulates blood pressure. Feel free to go through the article multiple times if you feel that was so much to learn. We know it is not easy!

How To Calculate Mean Arterial Pressure (MAP)

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