Med School Basics: Your How-To Guide on Hypotension

  • /Reviewed by: Amy Rontal, MD
  • In working up hypotension, we often need to think and act fast. And in order to know how to best act, we need to figure out the cause of the hypotension. Like any medical problem, we start with a differential, and narrow it down based upon the data we have.

    Let’s get back to the very basics!

    First, the age old equation,

    P = Q * R

    Spelled out, it tells us that

    Pressure = Flow * Resistance

    In physiologic terms,

    MAP = CO * SVR

    As cardiac output is the product of heart rate and stroke volume, we get

    MAP = (Stroke volume * Heart Rate) * SVR

    Through this simple derivation, we see that blood pressure depends on Heart Rate and stroke volume (whose product gives us cardiac output), as well as systemic vascular resistance, or less technically, the level of tone in the vasculature.

    If we break things down even further, we recall that stroke volume is dependent on Preload (Left Ventricular filling), and contractility. Rhythm plays a role in stroke volume as well. Remember that some patients are dependent upon a normal sinus rhythm and atrial kick for adequate ventricular filling. An atrium that is fibrillating does a poor job filling the left ventricle, and will decrease blood pressure.

    Afterload, the last member of the party, plays a part in determining stroke volume and is a surrogate measure of SVR.

    We’ve done it! We’ve boiled hypotension into 5 simple to comprehend values –

    1. Heart Rate
    2. Rhythm
    3. Preload
    4. Afterload
    5. Contractility.

    By thinking in these terms, we can think more logically and systematically when we evaluate and treat hypotensive patients. This prevents us from empirically “giving fluids” or “stating pressors” when faced with hypotension. We step through the process, and have a reason for our intervention.

    Let’s walk through some examples:

    A patient in the ED is tachycardic, hypotensive, and complains of acute onset shortness of breath. She has a 20 year pack smoking history, hypertension, diabetes, and just back from a 6 hour interstate car trip. Why is she hypotensive?

    When you read acute shortness of breath, classic differentials should populate your mind: COPD exacerbation, MI, pulmonary embolism, pneumothorax.

    We go through the five categories and assess the patient across them:

    Rate – if too high, diastolic ventricular filling (and thus stroke volume) might be impaired. If too low, cardiac output will suffer. This tachycardic patient might suffer from the former.

    Rhythm – In a patient that is dependent on normal sinus rhythm for an adequate atrial kick and optimal LV filling, an arrhythmia might decrease cardiac output. Obviously, arrhythmias like ventricular tachycardia or ventricular fibrillation are not conducive to adequate stroke volumes, but they have their own algorithms to work through.

    Preload – What is the patient’s volume status? Are they hypovolemic from a week long bout with viral gastroenteritis? Are medications like nitroglycerin increasing the size of the venous reservoir of blood in the unstressed circulation? Are diuretics causing hypovolemia? Is a large pulmonary embolism preventing left ventricular filling?

    Afterload – Perhaps a heart failure patient in an acute decompensation is suffering from sympathetic overdrive, is clamped down, and has an SVR through the roof (thus decreasing stroke volume). Is your patient septic or in anaphylaxis, suffering from vasodilation, wide open pipes, and an SVR in the toilet? Is regional anesthesia causing a sympathectomy and vasodilation?

    Contractility – An ischemic heart in a patient suffering from acute coronary syndrome/myocardial infarction will have depressed contractility.

    You can tailor the questions you ask yourself to your clinical situation. Just think logically – postoperative patients are more likely to hemorrhage (decreased preload), have pulmonary emboli (decreased preload/left heart filling), have MIs (decreased contractility), and be taking medications that suppress the sympathetic nervous system (beta-blockers, opioids). Cardiac ICU patients are likely to have have increased sympathetic tone/SVR (decreased stroke volume), recent/current MI leading to heart failure (decreased contractility), and rhythm disturbances.  

    The beautiful thing about the framework is that it can be applied to any hypotensive patient. Did someone pass out in clinic with a blood pressure of 84/40? Did you walk into an ICU patient’s room and see 67/40 on the monitor? Or maybe during a surgical procedure, the A-line unexpectedly reads 77/52. No matter where you are, the framework and physiology is the same. Use it!