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Shock: Pathology review
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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
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