When patients are admitted at an emergency room, the first priority is to stabilize the patient. Next, the cause for the emergency room visit must be discovered and addressed at the root causes. For example, a patient whose arm is bleeding due to a compound fracture is not simply treated by a splint for the bone and pressure applied to stop the bleed; but rather, the patient is scheduled for surgery to re-align the bones and to close the wound. If a patient arrives with a stab wound to the chest, there are a number of issues to consider in his treatment. Here, we will consider more specifically a patient who was stabbed in the chest, arrives with a cyanotic appearance, and who is unconscious due to lack of blood delivery to his brain. Drawing upon symptoms, it can be concluded that the patient is suffering from cardiac tamponade, and treatment can begin to move forward to stop or reverse any negative side effects.
Cardiac tamponade can most clearly be defined as an excessive buildup of fluid in the pericardial cavity that limits the ability of the heart to function as a pump for blood. The pericardial cavity is the small space between the visceral and parietal serous membranes, the double-layered tissues that surround the heart; it is typically filled with an amount of fluid that is sufficient to lubricate the two tissues layers as they rub together during heart contraction and relaxation. A buildup of excess fluid in the pericardial cavity will cause an inward pressure to be applied to the heart. This buildup of pressure is due to the fibrous layer just superficial to the serous membranes, a dense, tough connective tissue that will not expand outward. Under normal circumstances, this fibrous layer has a protective purpose, disallowing the heart from overexapnding as it fills with blood; this protective function is lost, however, during the extreme pressures suffered during cardiac tamponade.
The compressive pressure of the fluid buildup during cardiac tamponade has a negative effect on the heart’s ability to pump blood throughout the cardiovascular system. The first reason for this is that the two superior atria and the two inferior ventricles have smaller internal volumes due to the compression. As the fluid in the pericardial cavity increases, the heart chambers are forcibly shrunk; the decreasing amount of blood volume that is allowed into the chambers directly limits the amount of blood that can be expelled from the chambers. While a normal ventricle can hold approximately 120 milliliters of blood and expel approximately 70 milliliters with each systolic contraction, a compressed ventricle may be able to hold only 80 milliliters of blood and expel only 40 milliliters of blood. A single cardiac cycle that is 30 milliliters shy of ideal may not seem important; however, during cardiac tamponade, the decreased blood volume is a prolonged event, and a resulting propulsion of just over half of the normal volume of blood can have disastrous effects on a patient. Our hypothetical patient has already become bluish in his skin coloring as there is a lack of oxygenated blood being delivered to his body, and has gone unconscious as there is a similar lack of oxygenated blood, with its vital nutrients, being delivered to his brain.
In addition to the decreased internal volume of its four chambers, a heart that is compressed during cardiac tamponade will not have the ability to contract as forcefully as a heart that is not compressed. Cardiac muscle has been shown to have a positive relationship between its degree of stretch and the amount of force it is able to contract with. While cardiac cells at rest are typically shorter than optimal length for maximum force production, they are often stretched during atrial or ventricular filling to produce stronger contractions. The Frank-Starling law of the heart claims that this precontractile stretching is the most important factor in the amount of blood that the heart is able to expel. If stretching of the myocardial cells increases the volume of blood expulsion, then we can assume that the inversion is true as well, so that compression of the myocardial cells decreases the volume of blood expulsion. Just as the fluid in the pericardial cavity presses the internal walls of the heart closer together, it also presses the cells of the myocardium more tightly. As the contractile cardiac cells are thus forcibly shortened, they will be less able to eject their already lowered blood volume. Again, this will have such effects as cyanotic skin and unconsciousness in a patient suffering from cardiac tamponade.
While the entire heart will be affected by cardiac tamponade, it may be interesting to examine further how each of the four chambers will be affected, and the results of these consequences on the patient, in more detail. Following the standard model of blood flow through the heart, we can start such an examination in the right atrium. As blood flows into the right atrium passively from the superior and inferior vena cava and the coronary sinus, the compression of this chamber could potentially cause peripheral congestion as less blood would be allowed to enter the heart. While the contractile force of the right atrium would be diminished, this may have less of an effect on the resulting amount of blood flow into the right ventricle. It has been shown that approximately eighty percent of the blood flows passively into the right ventricle from the right atrium during diastole, when the atrial pressure is greater than the ventricular pressure and the tricuspid atrioventricular valve hangs open; only about twenty percent of the blood flow results from atrial contraction.
After flowing from the right atrium through the tricuspid valve, the blood would be in the now-compressed right ventricle. As the excess pericardial fluid presses into the right ventricle, the smaller internal volume would allow less blood to enter the right ventricle. In the ventricle, as opposed to the atrium, the decreased force of contraction may play a larger role in the patient’s declining state of health. The right ventricle must have a forceful enough contraction to create an internal pressure higher than that of the backflowing blood in the pulmonary trunk in order to open the pulmonary semilunar valve and send blood flowing to the lungs. If the lower blood volume and the lower contractile force allow for a shorter expulsion of blood into the pulmonary circuit of the pulmonary trunk and arteries, then less blood will travel to the lungs to be re-oxygenated in the lung capillaries. Blood that is lacking oxygen in its hemoglobins is a deeper red color, and appears blue under the skin; this is why our patient appears cyanotic.
Leaving the lungs and traveling through the pulmonary veins returns to the left atrium of the heart. Here, the results of cardiac tamponade will be much like they are in the right atrium. The decreased contraction forces will be seen, but may be less of a factor than the decreased volume capacity. Again, this is because approximately eighty percent of the flow of blood from the left atrium to the left ventricle occurs passively when the mitral atrioventricular valve drops into the low-pressure left ventricle during diastole.
During left atrial systole, blood would be less forcibly ejected through the mitral valve to the left ventricle where the greatest effects of cardiac tamponade may be taking place. As seen in the right ventricle, the compressed left ventricle would hold less blood volume and have a lower systolic contraction force. The left ventricle’s ability to create enough pressure to force open the aortic semilunar valve would be impaired, and the systemic circuit of blood circulation would be in jeopardy. Although it may seem that the left ventricle would be able to make up for some of the decreased contractibility because of its larger size in comparison to the right ventricle, this is not the case. In a normal heart, the left ventricle must be larger as is serves the systemic circuit, pumping blood from the heart to the entire body; this longer circuit of blood flow equates to about five times the resistance felt by the circuit, and so requires a stronger pump. When the left ventricle is compressed by excess fluid in the pericardium, its sheer size advantage over the right ventricle is not enough to overcome this still increased pressure resistance, and so there will be an equally lowered blood flow throughout the periphery of the patient’s body. This impaired systemic blood circulation is seen in the decreased blood supply to our patient’s brain which has caused him to become unconscious.
Finally, we must also look at the coronary circulation as well. Although the heart is filled with blood at all times, it is not able to meet its own oxygen and nutrient demands through mere diffusion and so has its own circuit of arteries and veins to deliver blood to its cells. The coronary circulation begins at the base of the aorta, just superior to the left ventricle. If the left ventricle is not able to create a high enough pressure to open the aortic semilunar valve to serve the systemic circuit, there would then also be a limited blood supply to the right and left coronary arteries. This could be a quickly down spiraling event as the limited blood supply would mean a limited oxygen supply to the myocardial cells and could lead to myocardial infarction, leading to less forceful or no contractions, leading to less oxygenated-blood delivery, continuing the cycle until the patient either dies or there is clinical intervention.