Hypotension

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.