Blood Pressure Regulation: Hypotension - Easy as 1-2-3
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Example Case
A female patient presents from a nursing home with altered mental status. She is unable to provide sufficient history due to her confusion.
Per nursing home report, the patient has become increasingly more altered the past 24 hours and developed a fever today. The report also states she has a history of recurrent urinary tract infections.
Upon arrival, the patient is febrile with a temperature of 38.9 C, tachycardic with a heart rate of 120, and hypotensive with a blood pressure reading of 88/62. You know you must take action to stabilize her before her vital signs worsen.
Blood Pressure Regulation
Hypotension may cause inadequate perfusion of oxygenated blood to vital tissues and organs.
If left untreated, this can result in tissue hypoxia, cell death, and organ failure.
The body has 2 main compensatory mechanisms in place to regulate blood pressure when hypotension is present: the sympathetic nervous system and the renin angiotensin aldosterone system.
These 2 systems work synergistically to improve blood pressure and perfusion, and we will be walking through the steps the body takes to make this happen.
As with every EZmed post, you will be provided with a simple way to remember the content.
Blood Pressure Basics
To better understand how the body regulates blood pressure to improve hypotension, it is important to first consider what variables are involved.
The blood pressure equation should be committed to memory, as much of the body’s physiology relies on this core principle.
BP = CO X SVR
The 2 main variables that control blood pressure are cardiac output (CO) and systemic vascular resistance (SVR), or sometimes referred to as total peripheral resistance (TPR).
Increasing cardiac output and/or systemic vascular resistance will increase blood pressure.
The 2 main variables that influence cardiac output are heart rate (HR) and stroke volume (SV).
CO = HR X SV
Increasing heart rate and/or stroke volume will increase cardiac output, which will in turn increase blood pressure.
BP = Blood Pressure; CO = Cardiac Output; SVR = Systemic Vascular Resistance; HR = Heart Rate; SV = Stroke Volume
Hypotension Detection
Now that we understand blood pressure, how does the body detect hypotension?
Baroreceptors
The body has arterial baroreceptors located at the aortic arch and at the bifurcation of the external and internal carotid arteries, known as the carotid sinus.
The aortic and carotid baroreceptors are stretch receptors stimulated by changes to the arterial wall as blood pressure varies.
Arterial walls will stretch when blood pressure is adequate or high.
The stretch of the blood vessel wall causes sodium ion channels to open on the baroreceptors, leading to an influx of sodium.
The increased intracellular sodium levels will generate an action potential through afferent sensory fibers, which sends information from the baroreceptor to the central nervous system.
The aortic baroreceptors deliver information to the central nervous system via afferent sensory fibers of the vagus nerve (CN X).
The carotid baroreceptors deliver information to the central nervous system via afferent sensory fibers of the glossopharyngeal nerve (CN IX).
If blood pressure is low, then arterial walls will not stretch as much.
As a result, the sodium ion channels on the baroreceptors will not open, and the number of action potentials generated to the central nervous system will be reduced.
The central nervous system will increase sympathetic activity as a result of the reduction of action potentials received from the baroreceptors.
The sympathetic nervous system can directly simulate the renin angiotensin aldosterone system (RAAS) through beta1 adrenergic receptor activation on renal juxtaglomerular cells that release renin, the first step of the RAAS.
Kidneys
The kidneys are also able to detect decreased renal perfusion, decreased glomerular filtration rate, and/or decreased sodium and chloride levels.
If any of the above are present, then the kidneys will signal the juxtaglomerular cells to release renin to activate the renin angiotensin aldosterone system as well.
Decreased blood pressure reduces the stretch of a blood vessel wall.
This will decrease the number of action potentials generated by the aortic and carotid baroreceptors to the central nervous system (CN X and CN IX respectively).
The central nervous system will increase sympathetic activity as a result.
The sympathetic nervous system can directly act on juxtaglomerular (JG) cells to release renin, the first step of the RAAS.
Decreased renal perfusion, glomerular filtration rate (GFR), and/or sodium and chloride levels detected by the kidneys can activate the renin angiotensin aldosterone system as well.
Sympathetic Nervous System
We learned in the autonomic nervous system post that the sympathetic nervous system is involved in the fight or flight response.
Situations that provoke danger, fear, anxiety, or stress can increase sympathetic activity.
During a fight or flight response, we want adequate perfusion of vital tissues and organs.
Sympathetic activity will increase catecholamine levels, such as norepinephrine and epinephrine.
These catecholamines will bind to alpha adrenergic receptors on blood vessels and beta adrenergic receptors in the heart and kidneys to increase blood pressure.
So it makes sense in a hypotensive state that sympathetic activity will be increased.
How exactly does the sympathetic nervous system increase blood pressure?
Let’s go back to the blood pressure equation: BP = CO X SVR.
The sympathetic nervous system acts on both cardiac output and systemic vascular resistance to increase blood pressure.
Here’s how, starting with cardiac output.
Cardiac Output (CO = HR X SV)
Remember that cardiac output is influenced by heart rate and stroke volume.
Heart Rate (HR)
First, the sympathetic nervous system can improve cardiac output by increasing heart rate - one of the variables of cardiac output.
The conduction system of the heart contains beta1 adrenergic receptors in which epinephrine and norepinephrine can bind.
This will shorten phase 4 (the “resting” phase) of pacemaker cell action potentials, and increase the frequency of depolarization and firing.
The automaticity of the SA node and conduction velocity through the AV node will be increased as a result.
This will increase heart rate, which will increase cardiac output, which will increase blood pressure.
Increased sympathetic activity will increase SA node automaticity and AV node conduction velocity resulting in increased heart rate.
The increase in heart rate will increase cardiac output, which will increase blood pressure.
Stroke Volume (SV)
Second, the sympathetic nervous system can improve cardiac output by increasing stroke volume - the second variable of cardiac output.
Beta-1 adrenergic receptors are not only located on pacemaker cells discussed above, but they are also located on non-pacemaker cardiac myocytes.
The non-pacemaker cells are the cardiac muscle cells that lead to cardiac contraction.
We discussed in the beta receptor post that beta receptors are coupled with Gs proteins which ultimately increase intracellular calcium.
What happens when calcium levels increase in muscles? They contract.
The cardiac action potential post demonstrated this. During phase 2 of the non-pacemaker cell action potential, the calcium ion channels are open, leading to an influx of calcium that results in contraction.
Sympathetic activity will act on beta receptors to further augment the rise in intracellular calcium levels leading to increased cardiac contraction.
Increased cardiac contraction will increase stroke volume, which will increase blood pressure.
Increased sympathetic activity will increase cardiac contraction, which will increase stroke volume, which will increase cardiac output, which will increase blood pressure.
Systemic Vascular Resistance
Not only does the sympathetic nervous system uses cardiac output to increase blood pressure, it also uses systemic vascular resistance - the second variable of blood pressure.
There are alpha-1 adrenergic receptors located on blood vessels.
We learned in the alpha receptor post that alpha receptors are coupled with Gq proteins which also increase intracellular calcium levels.
We know that increased intracellular calcium will lead to muscle contraction.
Therefore, the activation of alpha receptors on blood vessels will lead to smooth muscle contraction and vasoconstriction.
Vasoconstriction will decrease the radius of the blood vessel leading to an increase in systemic vascular resistance and blood pressure.
*Of note, there are alpha1 receptors located on the veins as well that will lead to venoconstriction. This will increase venous return to the heart and improve stroke volume.
Increased sympathetic activity will lead to vasoconstriction which will increase systemic vascular resistance (SVR) and blood pressure.
Renin Angiotensin Aldosterone System
We learned in the renin angiotensin aldosterone system (RAAS) post that activating the system ultimately led to renin release from the juxtaglomerular cells of the kidneys.
Renin was used to convert angiotensinogen into angiotensin I, followed by the conversion of angiotensin I into angiotensin II using angiotensin converting enzyme.
Angiotensin II has many downstream effects to improve blood pressure including: vasoconstriction, antidiuretic hormone/vasopressin release, aldosterone release, sodium and water reabsorption from the kidney, and further augmentation of sympathetic outflow.
Similar to the sympathetic nervous system, the RAAS can act on both cardiac output and systemic vascular resistance to improve blood pressure.
BP = CO X SVR
Here’s how, starting with cardiac output.
Cardiac Output (CO = HR X SV)
We know that cardiac output is influenced by heart rate and stroke volume.
Heart Rate (HR)
Unlike the sympathetic nervous system which increases heart rate to improve cardiac output, the RAAS does not have specific receptors on the heart to affect heart rate.
Stroke Volume (SV)
However, the RAAS can improve cardiac output by increasing intravascular volume, which will increase stroke volume.
This is slightly different than the sympathetic nervous system in which stroke volume was increased mainly by increasing cardiac contraction.
The RAAS increases intravascular volume through 4 main mechanisms:
Angiotensin II stimulates the Na+/H+ channels in the proximal convoluted tubule to reabsorb sodium back into the vasculature, and water follows sodium.
Angiotensin II also constricts efferent arterioles in the kidney in order to maintain adequate GFR. This will lead to decreased plasma fluid downstream of the efferent arterioles thus further augmenting sodium and fluid reabsorption from the renal tubules.
Angiotensin II causes vasopressin/antidiuretic hormone (ADH) release from the posterior pituitary gland. Vasopressin will act on V2 receptors in the collecting duct of the renal tubule to reabsorb water back into the vasculature.
In addition to the release of vasopressin from the posterior pituitary gland, angiotensin II also causes aldosterone release from the adrenal cortex. Aldosterone acts on the distal convoluted tubule to reabsorb water and sodium.
All of the above effects lead to water and/or sodium reabsorption from the kidneys into the vasculature which increases intravascular volume.
This increase in intravascular volume will increase venous return to the heart, which will increase stroke volume, which will increase cardiac output, which will increase blood pressure.
Increased renin angiotensin aldosterone system activity will increase sodium and water reabsorption from the kidneys into the vasculature which increases blood volume, which increases stroke volume, which increases cardiac output, which increases blood pressure.
Systemic Vascular Resistance
The RAAS can also increase systemic vascular resistance like the sympathetic nervous system can.
Angiotensin II is a potent vasoconstrictor.
There are angiotensin receptors located on smooth muscle cells of blood vessels that lead to vasoconstriction when activated.
As mentioned above, angiotensin II also stimulates the release of vasopressin/ADH from the posterior pituitary gland.
There are vasopressin (V1) receptors located on blood vessels in which vasopressin can bind and cause vasoconstriction as well.
As we learned above, vasoconstriction will increase systemic vascular resistance which will increase blood pressure.
Increased renin angiotensin aldosterone system activity will lead to vasoconstriction from the effects of angiotensin II and vasopressin on blood vessels. This will increase systemic vascular resistance and blood pressure.
EZ as 1-2-3
Here is the EZmed simplification.
Blood pressure is influenced by heart rate (1), stroke volume (2), and systemic vascular resistance (3).
Simply remember HR, SV, SVR in alphabetic order and that they have 1, 2, and 3 effects on blood pressure respectively.
BP = CO X SVR or BP = HR X SV X SVR
Heart Rate
Sympathetic nervous system acts on beta1 adrenergic receptors in the cardiac conduction system to increase SA node automaticity and AV node conduction.
Stroke Volume
Sympathetic nervous system acts on beta1 adrenergic receptors on contractile cardiac myocytes to increase cardiac contraction.
RAAS acts on nephrons to increases sodium and water reabsorption from the kidneys to increase intravascular volume.
Systemic Vascular Resistance
Sympathetic nervous system acts on alpha1 adrenergic receptors on blood vessels that will lead to vasoconstriction.
RAAS acts on angiotensin receptors on blood vessels that will lead to vasoconstriction.
RAAS acts on vasopressin V1 receptors on blood vessels that will lead to vasoconstriction.
Practical Application
Increasing sympathetic and RAAS activity becomes clinically relevant when managing different types of shock.
If these compensatory mechanisms are not sufficient on their own, then the patient may require pressor medications to help augment their effects.
Alpha and beta agonists can be used to activate alpha and/or beta adrenergic receptors that will lead to the downstream effects discussed above.
Vasopressin can also be used to activate vasopressin receptors that will lead to the downstream effects discussed above.
Conclusion
Hopefully that helped you understand the 2 main mechanisms the body has to regulate blood pressure in a hypotensive state: the sympathetic nervous system and the renin angiotensin aldosterone system.
The sympathetic nervous system will act on beta1 adrenergic receptors in the heart to increase heart rate and cardiac contractility (stroke volume) thereby augmenting cardiac output.
The sympathetic nervous system also acts on alpha1 adrenergic receptors on blood vessels that will lead to vasoconstriction to increase systemic vascular resistance and blood pressure.
Activation of the renin angiotensin aldosterone system will lead to vasoconstriction and increased sodium/water reabsorption from the kidneys through the effects of angiotensin II, aldosterone, and antidiuretic hormone/vasopressin.
These effects will increase cardiac output and systemic vascular resistance to improve blood pressure.
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