Shock: Pathology review

Amina is a 42-year-old female who was brought to the emergency department after her car crashed into a tree. According to paramedics, part of the car was on fire upon arrival. During resuscitation, her vitals showed a blood pressure of 70 over 50 and a heart rate of 140. Upon examination, her extremities are cold and clammy and there were multiple first and second-degree burns on her neck, abdomen and lower extremities. Additionally, auscultation reveals decreased air entry on the left side of her chest, and this is Amina’s chest x-ray. Palpation of the pelvis produced significant tenderness, prompting the ED physician to order a pelvic x-ray. After resuscitating Amina, another individual is rolled into the emergency department. Anastasia, 77 years old, comes in with high fever and chills and a 5-day history of dysuria and flank pain. Her blood pressure is 80 over 40 and heart rate is 120 beats per minute. On examination, her extremities are warm and flushed.

Both people have a life threatening condition called Shock. Shock is defined as inadequate organ perfusion that results in hypoxia and cellular damage.. Perfusion of organs is normally maintained by the arterial blood pressure. The mean arterial pressure is equal to the cardiac output times the systemic vascular resistance. So, any alteration to the components of this equation can potentially lead to shock. On the exam, look for hypotension as an initial clue for shock. Others include tachycardia, decreased urine output and altered mental status.

Now we can classify shock into 2 major categories. There’s “cold” or low cardiac output shock, and “warm” or distributive shock where there’s decreased systemic vascular resistance. Okay, let’s start with “cold” shock. This includes cardiogenic, hypovolemic and obstructive shock. In cardiogenic shock, the cardiac output is compromised because of a problem with the heart. This could range from congestive heart failure, acute myocardial infarction, valvular dysfunction, to even a myocardial contusion from trauma, basically anything that could prevent the heart from pumping enough blood to the rest of the body. In response to the ensuing hypotension, the baroreceptors in the aorta and carotid arteries induce a sympathetic reflex that results in vasoconstriction of the peripheral arterioles, which increases the systemic vascular resistance. This vasoconstriction is good, as it redirects blood flow from non-vital organs like the skin, to more vital organs like the brain. As a result, the skin will feel cold and clammy on examination. Another clue is the pulmonary capillary wedge pressure, or PCWP for short, which is measured by inserting a catheter into a small pulmonary arterial branch. In cardiogenic shock, this is elevated because more blood remains in the left side of the heart and it prevents pulmonary venous return. The blood backs up into the pulmonary vessels, and the increase in pressure pushes fluid into the interstitium and alveoli of the lungs, resulting in acute pulmonary edema. This classically presents with shortness of breath and crackles on auscultation as a result of acute pulmonary edema. Now, SvO2, or Mixed Venous Oxygen Saturation, will be lower. This is measured in the right atrium and reflects the total amount of oxygen going back to the heart. In cardiogenic shock, blood flow is slower than normal, so any oxygen that remains in the blood is extracted furiously by the tissues, and so we'll see a lower content of oxygen when blood returns to the heart. Treatment of cardiogenic shock depends on the underlying cause and may include inotropic medications or mechanical support devices to improve cardiac contractility

Next is hypovolemic shock. In this type, intravascular volume is decreased, which decreases venous return to the heart, and ultimately cardiac output. So similarly to cardiogenic shock, hypovolemic shock makes the skin feel cold and clammy due to peripheral vasoconstriction. This also increases systemic vascular resistance. Now, since intravascular volume is decreased, pulmonary capillary wedge pressure will also be low, and tissues will be pulling out as much oxygen as they can, leaving the SvO2 much lower. Hypovolemic shock has two subtypes; hemorrhagic, which is the most common, and non-hemorrhagic. Hemorrhagic shock usually results from blunt or penetrating trauma, such as injury to the liver, spleen, or long bone fractures, like femur fractures. Other causes of hemorrhagic shock that are non-traumatic include variceal bleeding or postpartum hemorrhage. Non-hemorrhagic causes of hypovolemic shock include anything that results in fluid loss, like diarrhea or vomiting. Also, burns increase capillary permeability, causing a tremendous amount of fluid to shift from the plasma to the interstitial space, which is called “third-spacing”. And this is why fluid replacement is crucial in the management of burns. Hypovolemic shock is treated with intravenous fluids and blood transfusions if it’s hemorrhagic.

Next is obstructive shock, which from the name, involves something that obstructs the heart and prevents it from pumping out enough blood. That blood builds up in the heart, so PCWP will be elevated, but it can't be pushed out, resulting in decreased cardiac output. Now the blood vessels will try to compensate by squeezing tighter in order to increase systemic vascular resistance. And tissues are trying to pull out oxygen from the limited blood supply soSvO2 will be lower. Now, a high-yield cause of obstructive shock is a tension pneumothorax, in which there is air in the pleural cavity that can push against the superior vena cava. This decreases venous return and ultimately, the stroke volume. For treatment, the air needs to be removed right away by inserting a needle or a chest tube in the space between the second and third rib of the affected side, on the midclavicular line, which provides an escape route for the trapped air. Also when blood collects in the pericardial sac, the resulting cardiac tamponade can limit the heart’s ability to fill up with blood. Treatment is pericardiocentesis. That’s where a needle is inserted into the pericardium to drain the excess pericardial fluid. Finally, a large pulmonary embolus can occlude the pulmonary trunk, compromising the right heart’s ability to pump blood to the lungs. Treatment is anticoagulation or thrombolysis.

Moving on to warm or distributive shock. The problem here is that the systemic vascular resistance is decreased due to peripheral vasodilation. Because of this vasodilation, the classic feature on physical exam is warm and flushed skin. To compensate for this, the heart tries to pump faster, so cardiac output can be elevated. The fluid load on the heart and the pulmonary capillary wedge pressure will be a little bit lowered. Intuitively, one would think that vasodilation increases blood flow, and therefore should actually increase the delivery of oxygen to tissues. Well, the thing is that, blood flow, in this case, is too fast, and tissues aren’t given enough time to extract the necessary oxygen. The exam will test you on this by asking what the mixed venous oxygen saturation would be in distributive shock. Because tissues aren’t extracting as much oxygen, the SvO2 would be high. And that’s unique for distributive shock! Another feature of distributive shock is an increased cardiac output. See, vasodilation increases venous return to the heart, which increases the stroke volume and therefore the cardiac output.