Hypotension

I. Problem/Condition.

Hypotension is defined as abnormally low blood pressure (BP) or a significant decrease in BP. Hypotension will lead to inadequate perfusion of organs and over time, organ dysfunction. Often, hypotension will result in signs and symptoms due to low flow of blood to the arteries and veins. In general, normal healthy adults’ BP range from systolic 90-120 and diastolic 60-80mmHg.

Contrary to hypertension, hypotension is defined by signs and symptoms of low blood flow, not by a specific number. For example, a person who lives with persistently elevated BPs (i.e. sys 180’s) may develop dizziness and not tolerate a sudden drop to ‘normal’ pressures. As such, that person would be deemed hypotensive. Conversely, there are some healthy adults that may live at systolic BPs below 90. It is therefore important to identify the person’s baseline BP and assess for symptoms before concluding the person is hypotensive.

II. Diagnostic Approach

A. What is the differential diagnosis for this problem?

It is helpful to construct a differential diagnosis for hypotension by thinking about the problem from a physiologic standpoint. BP is dependent upon the product of 2 factors: cardiac output and systemic vascular resistance. Cardiac output is then determined by the stroke volume and heart rate. Stroke volume is a function of preload, afterload and contractility.

Medications

When reviewing causes of hypotension, it is useful to first review the medication list if no apparent cause is evident. Consider holding or lowering dosage of medications that may cause hypotension.

Anti-hypertensives:

1. Diuretics: lower BP by decreasing body sodium stores

a. Thiazide (i.e. hydrochlorothiazide, metolazone)

b. Loop diuretic (i.e. furosemide, bumetanide)

c. K sparing diuretic (i.e. spirinolactone)
2. Sympatholytic agents

a. Central acting agents (i.e. clonidine): This is an alpha-2 agonist and works centrally to reduce sympathetic tone and increases parasympathetic tone, this results in decreasing BP and decreased heart rate.

b. Peripheral acting agents

i. Beta-blockers (i.e. Metoprolol, Carvedilol, Labetalol, Atenolol): Labetalol (alpha/beta-blocker) is considered the most potent beta-blocker.

ii. Alpha-blockers (i.e. Doxazosin, Tamsulosin, Terazosin): Block alpha-receptors in smooth muscle of peripheral arteries throughout the body. Often these drugs are used to treat benign prostatic hyperplasia (BPH).

3. Direct vasodilators

a. Hydralazine

b. Minoxidil

c. Nitroprusside

4. ACE-I inhibitors (i.e. Lisinopril): Block conversion of angiotensin I to II. Angiotension II lead to increased BP.

5. ARB (i.e. Losartan): Angiotensin receptor blockers block angiotensin II.

6. Calcium channel blocker

a. Dihydropyridine (i.e. amlodipine, nifedipine): reduce systemic vascular resistance.

b. Non-dihydropyridine (i.e. diltiazem, verapamil): reverse coronary spasm and treat angina; much less effect on BP.

7. Nitrates (i.e. Nitropaste, Isosorbide mononitrate, dinitrate): nitropaste is an effective agent used for hypertensive urgency/emergency because of its potent quick lowering of BP. As such, it can also cause hypotension. In such cases, one can quickly terminate the drug effects by removing the patch and wiping off the nitropaste.

Benign prostatic hyperplasia (i.e. Tamsulosin, terazosin)
Anti-Parkinsonian9
Combination: Nitrates & sildenafil (Viagra)
Tricyclic anti-depressants
Narcotics

Systemic vascular resistance

Anaphylaxis

Sepsis/SIRS

Adrenal insufficiency

Spinal shock

Toxic shock syndrome

Hyperthyroidism

Cardiac output

Stroke volume

1. Contractility
a. Congestive heart failure (CHF)
b. Right heart failure
2. Preload
a. Hemorrhage b. Fluid depletion c. Acute mitral regurgitation
d. Acute aortic regurgitation
3. Afterload a. Severe aortic stenosis

Heart Rate

1. Bradycardias
2. Tachycardias

Extracardiac (obstructive)

Massive pulmonary embolism
Cardiac tamponade

1. Historical information important in the diagnosis of this problem.

1. Is there a change in the mental status of the patient? If so, see chapter on Shock.
2. Do any of the medications taken cause hypotension? Any new medications recently added?
3. Any new foods or medications that may cause anaphylaxis?
4. Take a focused cardiac history: chest pain, shortness of breath, leg edema.
5. Any recent procedures or surgery that may result in significant loss of blood or tamponade? i.e. cardiac catheterization, coronary artery bypass graft (CABG)
6. Does the patient chronically take steroids? Sudden stoppage of steroids may cause adrenal insufficency and hypotension. Alternatively, a patient who is chronically on steroids and has a significant infection may develop adrenal insufficiency.
7. Any use of tampons recently? This may result in atoxic shock syndrome which manifests as high fever diffuse rash, malaise, confusion, hypotension and multi-organ failure.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

1. Tamponade – evaluating for pulsus paradoxus is useful to rule out tamponade. Inflate cuff to known systolic blood pressure. Slowly deflate cuff until you first hear Korotkoff sounds. At that point, clamp the cuff, note the blood pressure and watch for chest expansion and deflation. The first Korotkoff sounds are heard with only chest deflation (expiration). Now slowly unclamp cuff until you hear Korotkoff sounds with both chest expansion (inspiration) and deflation (expiration). This is your second pressure. If the difference of pressures is greater than 12mmHg, there is an abnormal pulsus paradoxus and this is suggestive of possible tamponade.
2. Aortic stenosis – classically described by a harsh diamond shaped murmur at right upper sternal border; however, the severity of AS is not characterized by the intensity of the murmur and in some cases of severe AS a murmur is difficult to detect; best way to characterize severity is by assessing for late peaking murmur during systole.
3. Acute mitral regurgitation – usually holosystolic and best heard at apex; no correlation between intensity and severity of MR.
4. Septic shock – early sepsis usually presents with warm extremities and bounding pulses. Late sepsis will reveal cool, pale cyanotic extremities with mottling.
5. Cardiogenic shock – This presents as cool extremities, faint pulses, and jugular venous distention.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

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1. Assessment of BUN/Cr ratio may be helpful to identify volume depletion. However, CHF can also result in a pre-renal picture.
2. Chest X-ray (CXR) is useful to rule in/out CHF, pneumonia.
3. Brain naturetic peptide is a pretty good marker, if normal, ruling out CHF. However, understand that it can be falsely elevated in cases of renal failure, pulmonary embolism, mitral regurgitation or any conditions that cause atrial stretching.
4. Bedside echo can be done to assess the cardiac ejection fraction, valvular function, tamponade.
5. Cultures of blood, urine, sputum, feces and/or any other potential sites of infection if sepsis is suspected.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

1. Medications- diagnosed by history and ruling out other causes.
2. Anaphylaxis – history and exam with swelling of lips, tongue and difficulty breathing.
3. Sepsis/SIRS – suspected infection with elevated white blood cell count, tachycardia and tachypnea.
4. Adrenal insufficiency – history of chronic steroid use with sudden stoppage and further exacerbated by infection; 5AM cortisol level less than, or equal to, 3 meets the criteria.
5. Spinal shock – severe autonomic dysfunction, hypotension, relative bradycardia, peripheral vasodilation and hypothermia.
6. Toxic shock syndrome – sudden onset of high fever, severe hypotension, multiorgan failure. Other features include a diffuse rash and desquamation of palms and soles that occurs 1-2 weeks later. Classic history is a woman who uses a tampon for longer periods of time. Other clinical settings include surgical wound infections, postpartum infections, deep abscesses, osteomyelitis, empyema, peritonsillar abscess, and sinusitis.
7. CHF – history, physical exam findings, CXR, BNP level, or echo.
8. Right heart failure – physical exam findings with JVD, hepatojugular reflux, leg edema but clear lungs.
9. Hemorrhage – usually in patients post-cath with retroperitoneal hemorrhage and significant amount of abdominal or groin discomfort.
10. Fluid depletion – history of BUN/Cr – a normal one likely rules out fluid depletion.
11. Acute mitral regurgitation – history of sudden, severe shortness of breath with flash pulmonary edema, recent MI or infective endocarditis, history of mitral valve prolapse; echo.
12. Acute aortic regurgitation – history of sudden, severe shortness of breath with flash pulmonary edema, chest pain may also be complaint if due to aortic dissection; echo.
13. Severe aortic stenosis – history and exam.
14. Bradycardias – electrocardiography (EKG) shows complete or high degree heart block; these are the only bradycardias that cause hypotension.
15. Tachycardias – EKG to assess if it is ventricular tachycardia or atrial tachyarrhythmia.

III. Management while the Diagnostic Process is Proceeding

A. Management of Hypotension.

1. Is there a change in the mental status of the patient?
2. Get the history from the patient. History will most likely help you diagnose the cause of hypotension.
3. If patient develops symptomatic hypotension, consider stopping all anti-hypertensive medications, removing patches like clonidine, a nitroglycerin patch.
4. If the hypotension is from CHF, assess if patient is compensated (warm extremities) or uncompensated (cool extremities). If patient is compensated, only diuretics are required. However, if the patient is uncompensated and hypotensive, he/she will need diuretics plus inotropes. Consult with cardiology.
5. If the hypotension is from sepsis/SIRS, start giving fluids generously to replete losses and treat with broad spectrum antibiotics. Patient may need pressors if blood pressure does not respond to fluids.
6. If there is concern of adrenal insufficiency as above, start stress dose steroids but remember to add on a cortisol level, if possible AM cortisol.
7. If there is concern of acute MR or AR by history, call cardiology for a stat bedside echo.
8. If there is severe AS, try to avoid afterload reducers (i.e. ACEI) and preload reducers (i.e. nitrates, diuretics). Call cardiology and CT surgical consult.
9. If there is complete or high degree heart block, call cardiology immediately and have atropine by bedside. Hold all beta-blockers, calcium channel blockers, and digoxin. Patient needs to have a monitored bed.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

1. Septic Shock: Pitfalls that physicians often encounter is insufficient or excess fluid. Patients can be given a multiple fluid boluses of normal saline ranging from 250cc to 1000cc. In general, it is safe to give 1000cc of fluid unless the patient is on dialysis or has CHF, in which case one can consider 250cc bolus.

After each bolus, one should reassess the patient for fluid overload by auscultation of lungs and assessing for jugular venous distension. There is no contraindication to aggressive fluids in the face of oliguria and hypotension. Monitoring of urine output is useful for evaluating adequate renal perfusion. During and after the bolus, one needs to ensure MAP greater than 60mm Hg for brain perfusion. Also, consider transfusion with packed red blood cells if patient is significantly anemic i.e. hgb less than 10.

2. Congestive heart failure: Another pitfall occurs where care providers may want to withhold all anti-hypertensives in patients with low blood pressure (i.e. systolics of 100) who have systolic heart failure. In general, if a patient is otherwise asymptomatic and generally has low blood pressure, one should not withhold all anti-hypertensives unless patient is symptomatic. As such, one should either consider decreasing the dose of certain anti-hypertensives or withholding certain anti-hypertensives.

What's the evidence?

Hollenberg, Steven, M., Parrillo, Joseph E.. “Chapter 38: Shock".”. Harrison's Principles of Internal Medicine. pp. 214-222.

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