If you’re learning about advanced Med Surg concepts or even working in the clinical setting, you’ve no doubt heard of pulmonary embolism and might initially think the main consequence is impaired gas exchange. However, another significant complication of a large pulmonary embolism is impaired cardiac function which can lead to decreased cardiac output, significant hypotension and even cardiovascular collapse. 

In order to fully grasp this concept, it’s important to have an underlying understanding of cardiopulmonary circulation, the pathology that occurs in a pulmonary embolism, and the factors that contribute to blood pressure.

Cardiopulmonary circulation review

The first thing to ensure you understand is cardiopulmonary circulation and the best way to do that is to review the blood flow pathway. 

  • Deoxygenated blood travels through the superior vena cava and inferior vena cava and into the right atrium.
  • Blood flows from the right atrium, through the tricuspid valve and into the right ventricle.
  • Blood flows through the pulmonary valve into the pulmonary artery.
  • Blood flows through the pulmonary artery into the pulmonary vasculature.
  • Deoxygenated blood flows past the alveoli where it participates in gas exchange. It offloads carbon dioxide and picks up oxygen. It is now oxygenated!
  • Oxygenated blood returns to the heart via the pulmonary veins.
  • Blood enters the left atrium.
  • Blood flows from the left atrium, through the mitral valve and into the left ventricle.
  • Blood is pumped from the left ventricle up through the aortic valve into the aorta.
  • This oxygenated blood is sent into systemic circulation and it delivers oxygen to the tissues.

The key thing to pay attention to here is the right side of the heart. When blood is in the right side of the heart it is pumped forward into the pulmonary vasculature. Hold on to that concept as we dive further into understanding the connection between pulmonary embolism and hypotension.

Pulmonary embolism pathophysiology review

A pulmonary embolism occurs when a blood clot travels to the lungs and becomes lodged in the pulmonary vasculature. This clot impedes forward blood flow and disrupts gas exchange at the alveoli. Subsequently, hypoxia causes chemical mediators to be released which leads to vasoconstriction throughout the pulmonary vasculature. The combination of blocked vessel(s) and hypoxic vasoconstriction throughout the lungs leads to increased pulmonary vascular resistance (PVR).

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Blood pressure review

Blood pressure is a measurement of the force exerted on the vessel wall, and it has several contributing factors:

  • Cardiac output – Cardiac output is a influenced by heart rate and stroke volume
  • Stroke volume – Stroke volume is determined by preload, afterload, and contractility
  • Preload – Preload is the amount of stretch at the end of diastole and is dependent on blood volume. More volume leads to more stretch, and more stretch leads to greater contractility. Greater contractility leads to higher stroke volume and higher cardiac output. The opposite is also true. Lower preload leads to lower contractility and lower cardiac output.
  • Afterload – Afterload is the force the ventricles must work against.
  • Contractility – The ability of the muscle fibers to shorten and contract. Contractility is closely associated with preload.

How do these elements connect to cause hypotension in pulmonary embolism?

Now that you’ve reviewed the underlying concepts, it makes perfect sense how a pulmonary embolism causes hypotension. Let’s put all the pieces together step-by-step: 

  1. A blood clot travels to the lungs and becomes lodged in the pulmonary vasculature. 
  2. Blood flow downstream of the embolus is impeded. Those alveoli are not able to participate in gas exchange and the blood does not get adequately oxygenated, which leads to hypoxia.
  3. Chemical mediators are released in response to hypoxia, causing blood vessels in the lungs to constrict. 
  4. Vasoconstriction of the pulmonary blood vessels and the blockage caused by the embolism lead to increased pulmonary vascular resistance (PVR). 
  5. Increased PVR increases afterload of the right ventricle (remember afterload is the force the ventricle must work against).
  6. With increased afterload, outflow from the right ventricle is reduced, the right ventricle dilates, and the septum bows or flattens. 
  7. Decreased right ventricular outflow and dilation of the right ventricle lead to reduced filling of the left ventricle.
  8. With less filling in the left ventricle, you have less preload on that ventricle. With less preload, you have less stretch. And with less stretch you have reduced contractility. With reduced contractility you have reduced stroke volume and reduced cardiac output.
  9. Reduced cardiac output leads to hypotension and poor tissue perfusion.
  10. If severe enough, the right ventricle fails, the cardiovascular system collapses and death occurs. 

Signs and symptoms of pulmonary embolism

Now that you see how serious a pulmonary embolism can be, it’s clear that early recognition is vital. Some key signs and symptoms of pulmonary embolism include: 

  • Dyspnea
  • Tachypnea
  • Cough (with or without blood)
  • Pleuritic chest pain (pain that is worse with breathing)
  • Decreased SpO2
  • Tachycardia
  • Lightheadedness or syncope

Did you find this concept fascinating? Then you might enjoy learning about pulmonary hypertension here.

Take this topic on the go by tuning in to episode 341 of the Straight A Nursing podcast. Listen from any podcast platform, or straight from the website here.


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References:

Vyas, V., & Goyal, A. (2024). Acute Pulmonary Embolism. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK560551/