HYPOTENSION

Introduction

Hypotension is a decrease in systemic blood pressure below accepted low values. While there is
not an accepted standard hypotensive value, pressures less than 90/60 are recognized as
hypotensive. Hypotension is a relatively benign condition that is under-recognized mainly
because it is typically asymptomatic. It only becomes a concern once pumping pressure is not
sufficient to perfuse key organs with oxygenated blood. This leads to symptoms impacting the
quality of life of a patient.  Hypotension is classified based on the biometric parameters of the
blood pressure measurement. It may be absolute with changes in systolic blood pressure to less
than 90 mm Hg or mean arterial pressure of less than 65 mm Hg. It may be relative to a decrease
in diastolic blood pressure to less than 40 mm Hg. It may be orthostatic with a decrease in
systolic pressure or 20 mm Hg or greater or a decrease in diastolic pressure of 10 mm Hg or
greater on positional change from lying to standing. It may be profound which is defined as
being medication-dependent. In acute conditions, the hypotensive shock is a possible and life-
threatening condition. Blood pressure is defined as:

 Blood Pressure = Cardiac output x Total peripheral vascular resistance

 The mean arterial pressure is an average blood pressure over the course of one cardiac
cycle. It is calculated as:

 Mean arterial pressure = 2/3 diastolic pressure + 1/3 systolic pressure

Etiology

Blood pressure is modulated via 2 primary mechanisms: cardiac output and total peripheral
vascular resistance.

Therefore, any disease of pathology that impacts one or more of these parameters will induce
hypotension.[1][2][3][4][5]

The heart functions as a pump system to generate a pressure gradient for the distribution of blood
throughout the body. This pumping potential is referred to as the cardiac output. Cardiac output
is mathematically determined via an equation where:

 Cardiac output = Stroke Volume x Heart Rate

Disease states that reduce stroke volume or heart rate will decrease the total cardiac output of the
heart, functionally decreasing the ability to generate blood pressure. Various medications are also
capable of inducing hypotension via augmenting these biologic parameters. Most notorious for
decreasing heart rate are the beta-blockers and calcium channel blocker classes of medicines.
Diuretic medications are also possible sources that decrease cardiac stroke volume. Disease
states include arrhythmias, valvular regurgitation, valvular stenosis, diastolic or systolic heart
failure, large volume losses of blood, and cardiac tamponade.
Total peripheral vascular resistance is the resistance to blood flow through the terminal arterioles
of the various organ sites in the body.  This mathematically equals:

 Systemic Vascular Resistance = 80 x (Mean Arterial Pressure - Mean Venous Pressure) /

Cardiac Output

or

 Systemic Vascular Resistance = (8 X L x n) / (3.14 x radius of a vessel^ 4) 

Where L equals the length of the vessel and n equals the viscosity of blood. Functionally, vessel
length is not subject to change in the body and viscosity does not rapidly adjust and can be
accepted as standard value in most cases. Therefore, the only modifiable physiological value is
the radius of the vessel. A decrease in arteriolar caliber increases the resistance to blood flow,
thus increasing blood pressure. Conversely, increasing the diameter of terminal arterioles will
decrease resistance to blood flow, thus decreasing blood pressure. Total peripheral vascular
resistance is primarily controlled via autonomic neuronal responses to modulate fluctuations in
blood pressure. The natural state for arteriolar smooth muscle tone is to be relaxed with dilated
arterioles. Therefore, the absence or blunting of autonomic input by medications or disease states
will lead to hypotension. In orthostatic hypotension, a combination of the blunting of the
autonomic nervous system and mild hypovolemia from dehydration is the culprit. When lying
flat, there is even distribution of fluid throughout the body. However, on standing heart rate fails
to increase appropriately and peripheral resistance fails to increase appropriately leading to a
rapid, transient decrease in blood pressure that improves with postural changes. This is
classically symptomatic with dizziness and syncope.

Both cardiac output and total peripheral vascular resistance function as feedback compensation
mechanisms for the other in healthy individuals. When cardiac output decreases, peripheral
resistance should increase via constriction of terminal arterioles to decrease vessel caliber to
maintain blood pressure. When peripheral resistance decreases, cardiac output will increase via
increased heart rate to maintain blood pressure.
Acute disease processes that are life-threatening are possible and are classified depending on
etiology as distributive shock, cardiogenic shock, hypovolemic shock, obstructive shock, or a
combined-type hypotensive shock. 

Distributive shock occurs as a failure of the ability to maintain total peripheral resistance with
maintained cardiac function attempting to compensate. This classically presents with warm
extremities and skin, edema, increased mucous secretions, and tachycardia. This is classically
associated with anaphylactic allergic reactions and septic shock.

Cardiogenic shock is a failure to achieve sufficient cardiac output with maintained total
peripheral resistance. Classically these patients present with cool, dry extremities and skin with
bradycardia.

Hypovolemic shock is a loss of total blood volume such that blood pressure is not
maintained. Both cardiac output and total peripheral vascular resistance are maintained. This is
possible via trauma with massive loss of blood or overuse of diuretic medications with fluid
volume loss via urine. Cortisol deficiency as seen in Addison disease leads to a loss of fluid via
urine and a relative cortisol deficiency. Sheehan syndrome is postpartum pituitary necrosis
leading to a loss of many pituitary hormones as a result of postpartum shock or hemorrhage.

Obstructive shock occurs with the obstruction, constriction, or compression of the cardiovascular
system such that blood flow does not efficiently occur or there is a decrease in stroke volume of
the heart. This leads to a relative drop in blood pressure systemically. Obstruction may occur
secondary to pulmonary embolism, tension pneumothorax, cardiac tamponade, constrictive
pericarditis, or some other restrictive cardiomyopathy. These will classically present with signs
of congestive failure including distended jugular veins, peripheral edema, pulmonary crackles,
quiet heart sounds, or pulsus paradoxus.

Hypotensive shock is also possible via any combination of the above pathologies occurring
simultaneously. One example is Waterhouse-Friderichsen syndrome, which is an adrenal-gland
failure to produce mineralocorticoids, glucocorticoids, and sex steroids due to frank hemorrhage
into the adrenal glands secondary to bacterial infection by Neisseria. This leads to a host of
hypovolemic and distributive shock symptoms.

Epidemiology

The precise epidemiology of hypotension is highly variable and depends on the exact etiology. In
general, elderly patients are more prone to non-traumatic, symptomatic hypotensive episodes.
Also, more physically active and healthy patients will have lesser resting asymptomatic blood
pressures.

Pathophysiology

Blood pressure is continuously regulated via the autonomic nervous system as a balance of the
sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous
system acts to raise blood pressure by increasing heart rate and constricting arterioles. The
parasympathetic nervous system lowers blood pressure by decreasing heart rate and relaxing
arterioles to increase vessel diameter.
History and Physical

Hypotension is most commonly asymptomatic. However, if symptoms become apparent, the

most common is lightheadedness or dizziness.  In extremely low pressures, syncope may occur.
Other symptoms are possible which typically begin from the underlying etiology rather than
hypotension itself. They may include chest pain, shortness of breath, irregular heartbeat, fever
higher than 101 degrees Fahrenheit, headache, stiff neck, severe upper back pain, cough with
sputum, diarrhea, vomiting, dysuria, acute allergic reactions, fatigue, or vision aberrations.

Evaluation

Evaluation is dependent on the suspected cause. Basic lab work including complete blood count
(CBC) with differential, thyroid-stimulating hormone (TSH), free t4, cortisol levels can be
ordered. If a patient is in shock STAT echocardiogram with inferior vena cava (IVC) variability
can be done along with stabilizing measures. An echocardiogram will determine left ventricle
ejection fraction, right ventricle pressures, and presence or absence of pericardial effusion. If
left-ventricular ejection fraction (LVEF) and right ventricular function are adequate and the
patient is in distributive shock, then the inferior vena cava (IVC) variability test will help in
managing fluid resuscitation. Pulse pressure variation is used to determine the best fluid
resuscitation plan. Saddle embolus pulmonary embolisms are a possible source of frank
hypotension as well and can be ruled out via computed tomography (CT) angiogram of the chest.

Treatment / Management

Asymptomatic hypotension should not receive drastic interventions. However, if symptoms are

present, the treatment of hypotension should focus on reversing the underlying etiology.
Noninvasive imaging or hemodynamic indices of low cardiac output or systemic vascular
resistance are not diagnostic but may help to classify hypotension. Therefore electrocardiogram,
echocardiogram, and chest X-ray may assist in the workup. In a trauma case with hypotension
and no apparent blood loss, an extended focused assessment with sonography in trauma (e-
FAST) exam may be beneficial to identify the presence of intracavitary bleeding. It is important
to monitor urine output to verify those fluid resuscitation efforts are sufficient with an output of
0.5 to 1.0 mL/Kg per hour. Along with fluid resuscitation, it is important to monitor fluid
electrolytes and replace them as appropriate to avoid inducing an abnormality. Orthostatic vital
signs may be beneficial to diagnosis also. If a medication is suspected to be the source,
discontinue the medicine. In acute shock conditions, rapid fluid resuscitation with the cessation
of bleeding is key. Vasopressors may be indicated if the mean arterial pressure is less than 65
mm Hg. If sepsis is suspected, serial blood cultures and early antibiotics are essential. If
anaphylaxis is suspected, intramuscular epinephrine is essential. Adding steroids for treatment of
distributive shock when a patient's vasopressor requirement is continually increasing, and
appropriate fluid resuscitation has been done will assist in maintaining blood pressure as well.[6]
[7][8][9][10]

Differential Diagnosis

 Benign hypotension
  Distributive shock

 Cardiogenic shock

 Hypovolemic shock

 Obstructive shock

 Combined-type hypotensive shock

Prognosis

The prognosis of benign hypotension is very good. Symptomatic hypotension has a variable
prognosis depending on the etiology and severity.

Complications

Complications of untreated hypotension with poor cardiac output are severe and can ultimately
lead to death. In impending shock or fulminant shock, untreated hypotension can lead to multi-
organ failure. Current guidelines on treating patients with shock or impending sepsis are focused
on aggressive and adequate fluid resuscitation to avoid these outcomes. 

Enhancing Healthcare Team Outcomes

The diagnosis and management of hypotension are best managed with an interprofessional team
that consists of an internist, intensivist, endocrinologist, emergency department physician, and
nurse practitioner. Outpatients with asymptomatic hypotension do not need treatment. However,
if symptoms are present, the treatment of hypotension should focus on reversing the underlying
etiology. Some patients may need vasopressor support in addition to intravenous fluids to reverse
the hypotension. If bleeding is the cause, then blood transfusions may be required. Vasopressors
may be indicated if the mean arterial pressure is less than 65 mm Hg. If sepsis is suspected, serial
blood cultures and early antibiotics are essential. If anaphylaxis is suspected, intramuscular
epinephrine is essential. Adding steroids for treatment of distributive shock when a patient's
vasopressor requirement is continually increasing, and appropriate fluid resuscitation has been
done will assist in maintaining blood pressure as well. The outcomes for outpatients with
asymptomatic hypotension are good but in the hospital, the prognosis depends on the cause. [10]
[11][12](Level V)

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References
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ORTHOSTATIC HYPOTENSION
DEFINITION
Orthostatic hypotension is defined as a sustained reduction of systolic blood pressure (SBP) of at
least 20 mm Hg or of diastolic blood pressure (DBP) of at least 10 mm Hg within 3 minutes of
standing or head‐up tilt to at least 60° on a tilt table. Current European Society of Cardiology
(ESC) syncope guidelines propose that SBP reduction of <20 mm Hg from the supine to the
erect position, but with standing SBP values <90 mm Hg, should also be considered as OH. In
hypertensive subjects, a cut‐off of 30 mm Hg fall in SBP may be more appropriate, since blood
pressure (BP) fall after standing up largely depends on baseline BP. This is the classical form of
OH. If BP fall occurs following standing of more than 3 minutes, OH is characterized as delayed.
The situation where a more pronounced BP reduction, that is at least 40 mm Hg in SBP or at
least 20 mm Hg in DBP, is observed immediately after standing (within 15 seconds) is called
initial OH; in this OH type, BP values are quickly restored (within <40 seconds).5

PATHOPHYSIOLOGY
Normally, transition from supine to upright position is accompanied by redistribution of
intravascular volume, with 300‐800 mL of blood pooling in lower extremities and splanchnic
veins due to gravity. This causes a transient reduction in venous return, a decrease in stroke
volume and cardiac output (up to 40%) and finally in BP levels. As a consequence, activation of
BP regulating reflexes that rise from baroreceptors located in the carotid sinus and the aortic arch
results in stimulation of the sympathetic system and diminished activity of the parasympathetic
system that increase heart rate, venous return, cardiac contractility, and vascular tone. Thus, BP
levels are restored. Increase in peripheral vascular resistance is the major contributor to BP
restoration, while an increase in heart rate may act supplementary. These compensatory
responses stabilize BP within seconds and are generally capable to maintain BP within normal
values in the short‐term. In case of prolonged upright posture, additional mechanisms are
activated, that is activation of the renin‐angiotensin‐aldosterone system (RAAS) and increased
secretion of vasopressin.
Orthostatic hypotension occurs in patients with inadequate autonomic nervous system (ANS)
adjustment and can be divided into three major categories: drug‐induced, related to depletion of
(total or effective) intravascular volume and neurogenic, while in many patients, such as the
elderly, multiple causes may coexist.
DIAGNOSIS

Orthostatic hypotension may be asymptomatic or symptomatic.4 Dizziness, lightheadedness,

pain in the neck and shoulder, sweating, hearing and visual disturbances, weakness, and nausea
are the most common symptoms, while, in more severe cases, OH may result in loss of
consciousness due to excessive hypotension and cerebral hypoperfusion. OH is considered a
major cause of syncope.

Diagnosis of OH is typically determined through consecutive BP measurements in supine and

erect position, a testing known as “active standing.”Patient should be in supine position for at
least 5 minutes. After standing, multiple BP measurements within 3 minutes may be necessary to
detect a BP fall that satisfies the criteria for OH Heart rate should be assessed, since blunted
chronotropic compensatory response (<10‐15 bpm) is supportive of autonomic impairment and
may be a practical tool to identify neurogenic OH.
When OH is suspected but not detected with “active standing,” ambulatory blood pressure
monitoring (ABPM) for 24 hours (or more if necessary) can be used. This test is useful for
diagnosing OH only if patient's posture during each BP measurement is recorded. In this case,
assessment of fluctuations between supine and standing BP values could unmask previously
undetected OH, especially in presence of relevant symptoms.

Alternatively, head‐up tilt testing can be helpful to diagnose OH. This test is mainly indicated in
patients with a high probability of OH when previous tests are inconclusive, usually due to
delayed onset of OH. Patient is tilted in 60‹‐70° angle for 20‐45 minutes in order to detect BP
fall, increase or decrease in heart rate, and reproduction of symptoms.

Once OH diagnosis has been established, basic laboratory tests should be performed in all
patients with OH (either neurogenic or non‐neurogenic), including electrocardiogram, complete
blood count, fasting glucose, electrolytes, renal function blood tests, and thyroid‐stimulating
hormone. Levels of B12 should also be measured, as B12 deficiency can cause OH. Liver
function blood tests and serum albumin can be useful, especially for patients with weight loss,
constitutional symptoms, and increased burden of comorbidities.

TREATMENT