Hypotension

1.     Start with the ABC's and whether or not the patient is symptomatic. You determine this by looking for evidence of shock (i.e. inadequate tissue perfusion), tachycardia, tachypnea, pre-renal oliguria, altered mental status, etc. If shock is present, then evaluation should proceed sooner rather than later.

2.     Key questions if the patient is relatively stable:

  • Is this BP real? Measure the BP manually yourself with the correct sized cuff. Get all of the vitals and make sure they are current (never presume they were recently done).
  • Is it any different from prior values? If the patient usually lives around 80/40, then the acuity may be decreased somewhat.
  • Is the mean arterial pressure (MAP) < 60 mmHg?  MAP = (SBP + 2(DBP))/3.  MAP less than 60 signifies hypoperfusion to vital organs.
  • Is there associated hypoxemia?
  • Consider early on the need for central venous access or PA line.

3.     MAP = CO x SVR = HR x SV x SVR (where SV is a product of preload and contractility).  Therefore, hypotension can only be caused by one or more of the following:

  • Heart rate: look at ECG for pathologic tachycardia, bradycardia.
  • Decreased preload: assess JVP, volume status, and consider hypovolemia, tension pneumothorax, PE, tamponade, RV infarct, pulmonary hypertension.
  • Decreased contractility: listen for gallop, murmurs, rales and consider myocardial dysfunction, valvular dysfunction (AS, AI, MR), aortic dissection, drugs.
  • Decreased SVR: warm extremities, flushing; consider sepsis, anaphylaxis, spinal shock, adrenal insufficiency, drugs.

4.     Start with the hypotension algorithm as your initial approach in order to make a rapid empiric diagnosis of the cause of hypotension.  Once this is done, consider the following:

  • Overlap syndomes: get more data with a PA line or echocardiogram + CVP.
    • Sepsis + cardiogenic, sepsis + hypovolemia, cardiogenic + hypovolemia.
  • Consider other causes of hypotension as listed above and as follows:
    • Increased cardiac output without sepsis: ESLD or fulminant hepatic failure, severe pancreatitis, trauma with SIRS, thyroid storm, AV fistula.
    • Increased CVP without LV failure: pulmonary hypertension, PE, RV infarct, tamponade.
    • Nonresponsive hypovolemia: adrenal insufficiency, anaphylaxis, cold sepsis.

5.     Helpful hints:

  • Above all, stay calm. Crashing patients are scary. Don't try to manage shock by yourself.
  • Remember that the BP cuff can markedly underestimate BP in low flow states; therefore, an arterial line can be invaluable for better BP monitoring.
  • If BP is undetectable, palpate for pulses.  A palpable femoral pulse indicates systolic blood pressure (SBP) > 80 mmHg and a palpable carotid pulse indicates SBP > 60 mmHg.
  • For tamponade, you must call a cardiology consult to perform an echo and pericardiocentesis.
  • For pneumothorax, don't wait for a CXR. Insert a 14 or 16 gauge needle into the second intercostal space at the midclavicular line ASAP.
  • For anaphylaxis, give epinephrine 0.2-0.5 ml (0.2-0.5 mg) of 1:1000 SC/IM q20 minuntes (diluted dose, different from code blue dose), Benadryl 50 mg IV, hydrocortisone 100 mg IV. Consider nebulizers for bronchospasm or intubation for respiratory failure.
  • For sepsis, rapid administration of antibiotics and pressors will be crucial.

6.     If patient has evidence of shock (end-organ damage), act quickly. Some basic steps:

  • Treatment is aimed at the underlying cause, but almost all cases call for fluid resuscitation. If suspicion of CHF is low, then pour in the fluids.
  • Start O2, put patient in Trendelenberg, draw basic labs (CBC, lytes, BUN, creatnine, glucose, LFT's, blood cultures), get ECG, CXR, ABG.
  • Consider Foley to measure urine output.
  • Consider invasive monitoring (CVP or PA line, arterial line).

 

Principles of Criticle Care.  Hall JB, Schmidt GA, Wood LDH eds.  New York 1998: 277-301.