When assessing your patient, you are going to be looking at myriad factors to determine if s/he is stable or not…and one of the most important data points you are looking at is blood pressure. What is blood pressure, how does it play into your patient’s overall picture and what factors cause it to go up, or (more importantly) go down?

What is blood pressure?

Blood pressure is a measurement of the amount of force the blood exerts on the vessel wall. This force is a product of the amount of volume in that vessel, the size of the vessel and the resistance to blood flow present in the vessel. The two big determinants of blood pressure are cardiac output and total peripheral resistance (TPR).

What is cardiac output?

You may recall from your physiology course that cardiac output is a component of stroke volume (SV) and heart rate (HR).

CO = HR X SV

  • Stroke volume is determined by preload, afterload and the contractility of the heart itself
    • Preload is the amount of stretch placed on the cardiac muscle fibers at the end of diastole. This stretch is caused by the amount of blood volume present…more volume equals more stretch. More stretch leads to higher contractility and higher cardiac output. Note that the opposite is also true…less stretch leads to less contractility and lower cardiac output.
    • Afterload refers to all those things that oppose the ventricles’ ability to eject and empty during the contraction phase. In other words, it’s the force the ventricles have to work against in order to eject blood during contraction. The big things that come into play here are the valves (pulmonic and aortic), blood volume, blood viscosity, the elasticity of the pulmonary artery and aorta, and something called metarteriole vasoactivity. It’s a big term that simply refers to the ability of those short vessels that link arterioles and capillaries (the metarterioles) to dilate and constrict.
    • Contractility is the heart muscle’s ability to shorten the fibers which creates tension…it is essentially the contractile force of the heart muscle.
  • Heart rate can be too fast, too slow or juuuuuust right (that’s an easy one!)

What is total peripheral resistance (TPR?)

Total peripheral resistance is determined by the length of the vascular bed, the viscosity of the blood and vascular tone.

  • Of these, vascular tone is the most variable. We see this come into play when the arterioles constrict and dilate. When they dilate, TPR goes down; when they constrict, TPR goes up. Think about your garden hose with your thumb partially occluding the spout…when you constrict that opening the TPR goes up and the water spews out of the hose at much greater force!
  • When we talk about viscosity of the blood, think about someone with polycythemia or really high blood sugar levels…that blood is going to be “thick” and viscous, which can cause an increase in TPR.

Regulation of blood pressure

Recall that the body is always trying to achieve and maintain hemostasis, so several different mechanisms come into play when regulating blood pressure:

  • Chemoreceptors in the carotid sinus and aortic arch sense increased carbon dioxide, increased hydrogen ions and decreased oxygen which triggers the SNS to increase BP
  • Baroreceptors located in the carotid sinuses and aortic arch sense changes in mean arterial pressure (MAP) and send messages to the brain. When MAP is high, these baroreceptors send more and more signals, the SNS is suppressed and the PNS takes over causing decreased BP and HR…in other words, the baroreceptors tell the SNS to back off and tell the PNS to “put on the brakes.” When MAP is low and these baroreceptors are triggered less, it sends signals to the SNS to say, “Hey! Blood pressure is low, do your thang!”
  • The SNS causes vasoconstriction, faster respiratory rate, faster heart rate and increased contractility. All of these things are going to play a role in increasing blood pressure.
  • The endocrine system sends chemical messengers (hormones) that affect the diameter of the arterioles (dilate or constrict) and blood pressure.
    • Hormones that increase BP: vasopressin, angiotensin II, and some prostaglandins; antidiuretic hormone and aldosterone work to maintain fluid balance to maintain optimal blood pressure levels
    • Hormones that decrease BP: nitric oxide, histamine and some prostaglandins

So now that we got that cleared up…

Now that you understand the components of blood pressure, let’s talk a bit about how you’ll use this information to assess your patients and understand their risk for experiencing hypotension. Here are a few of the most common causes for hypotension that you’ll see in the clinical setting:

  • Bradycardia: Since cardiac output is a component of stroke volume and heart rate, a rate that is too slow can often cause a low blood pressure. When the blood pressure cannot be maintained at safe levels (typically a MAP > 65, then we say the patient is “unstable.” Note that many athletes are technically in a sinus bradycardia at rest, but because their heart is so strong, their stroke volume makes up for the slow rate and their cardiac output is juuuuust fine. However, let’s say you’ve got a patient with known heart failure and big ol’ floppy ventricles. If he suddenly becomes bradycardic, how nervous are you going to be? Probably pretty darn nervous!
  • Tachycardia: When the heart is beating too fast, ventricular filling times and preload are reduced. And what do you think happens to cardiac output? It goes down, too.
  • Atrial fibrillation or flutter: In atrial fibrillation or flutter, the atria are not contracting adequately and ventricular filling is reduced. We call this the loss of “atrial kick” and it is estimated to reduce cardiac output by about 20%. If your patient’s BP has been borderline and they suddenly go into a-fib (especially a rapid a-fib), you’re going to want to watch their BP like a hawk!
  • Cardiac dysrhythmias: A pretty safe bet when your patient is having any kind of cardiac dysrhythmia is to expect it to affect their blood pressure in unpleasant ways.
  • Heart failure: When the pump doesn’t work well, cardiac output is decreased and…well, you can guess the rest.
  • Shock states: We could do a whole big long thing about shock states (and we definitely will), but for now just know that shock states are going to cause BP to be low. And yes, this includes sepsis and septic shock.
  • Volume depletion: Your dehydrated patient will try to compensate for the decreased volume in the vasculature by increasing the heart rate. Ditto for your patient who is bleeding. However, note that some patients cannot compensate…maybe their heart isn’t working optimally or they’re taking a beta blocker. Restoring volume typically does the trick for getting these patients back in balance (oh, and if they’re bleeding, you’re gonna want to do something about that!)
  • Acidosis causes hypotension through some very complicated pathways (which you can read about here in all their glory). The short version is that acidosis contributes to decreased cardiac contractility, smooth muscle relaxation and increased nitric oxide production (which we already mentioned causes vasodilation and drops in BP).
  • Endocrine disorders can cause low blood pressure when the hormones that help regulate BP are affected.
  • Medications that cause hypotension include diuretics, some antidepressants, levodopa, meds for pulmonary hypertension or erectile dysfunction, and (of course) meds used to therapeutically treat hypertension (patients can easily take too many!)

What happens when blood pressure is low

When blood pressure is low we worry about end organ perfusion…in other words, we worry about the organs getting the oxygen they need to survive.

  • Neuro:  Low blood pressure can cause your patient to have a decreased level of consciousness or feel dizzy when moving from a supine to standing/sitting position. Exceptionally low blood pressure essentially causes anoxic brain injury due to decreased oxygen delivery.
  • Cardiac: If the heart isn’t getting enough oxygen then very bad things can happen, including cardiac arrest. And, don’t be surprised if your hypotensive patient has angina…a heart hungry for oxygen is painful and should get you very, very concerned.
  • Lungs: In cases of blood loss (and thus less oxygen-carrying capacity), gas exchange is compromised which leads to lower PaO2 and SpO2.
  • Kidneys: The kidneys DO NOT LIKE hypotension at all. Many patients go into acute renal failure from even brief episodes of hypotension. Decreased urinary output (less than 0.5ml/kg/hr) is one of the key indicators of decreased organ perfusion, which is why we watch output so closely in the critical care setting.
  • Liver: A condition known as ischemic hepatitis (or you may hear it called “shock liver”) occurs when the liver does not receive adequate blood flow. If your patient is already sick (namely with sepsis) and they suddenly develop liver failure, things definitely can get real complicated real fast.

Hopefully this helps you understand the complexities of blood pressure regulation and why it’s so important to keep your patient’s blood pressure optimized. Did we miss any key information or examples you commonly see in the clinical setting? Let us know in the comments below!


References:

Hemodynamic Consequences of Arrhythmias. (n.d.). Retrieved May 21, 2018, from http://www.cvphysiology.com/Arrhythmias/A011
Kimmoun, A., Novy, E., Auchet, T., Ducrocq, N., & Levy, B. (2017). Erratum to: Hemodynamic consequences of severe lactic acidosis in shock states: From bench to bedside. Critical Care,21(1). doi:10.1186/s13054-017-1624-2
Schell, H. M., & Puntillo, K. A. (2008). Critical care nursing secrets. New Delhi: Mosby.