Cardiogenic Shock

Cardiogenic shock is literally shock of cardiac origin.


Blood flow through the heart originates in the right atrium, where unoxygenated blood from the venous circulation is delivered to the heart via the superior and inferior venae cava. Once the unoxygenated blood enters the right atrium, it is ejected into the right ventricle with the next contraction. Upon contraction of the right ventricle, the blood is pumped out into the pulmonary artery and into the pulmonary capillaries in the lungs, where alveolar/capillary gas exchange occurs. This process leads to arterial oxygenation and removal of carbon dioxide. Upon leaving the pulmonary capillaries, the oxygenated blood enters the pulmonary veins and is transported back to the left atrium of the heart. The blood filling the left atrium generates pressure on the atrial walls and eventually causes the mitral valve to open and allows blood to passively enter the left ventricle Approximately 70% of the blood from the right and left atria will flow passively into the right and left ventricles, respectively, as a result of gravity. The remaining 30% of the blood volume is ejected into the ventricle during atrial contraction. Upon contraction of the left ventricle, the blood is ejected through the aortic valve and into the aorta for distribution to organs and cells throughout the body.

The vessels of most importance when talking about cardiogenic shock are the coronary blood vessels. It is important to note that, although the chambers of the heart may have a full blood volume, it is the coronary vessels that are responsible for delivering the oxygenated blood throughout the heart and providing cardiac oxygenation. When a patient experiences ischemic chest pain or a myocardial infarction, it is because blood supply through the coronary vessels has been compromised. The coronary arteries originate at the base of the aorta. The roots of the coronary vessels are known as the coronary sinuses, which provide blood flow through the left and right coronary arteries. The left coronary artery supplies the left ventricle, the intraventricular septum, part of the right ventricle and part of the heart’s electrical conduction pathways. The right coronary artery supplies a portion of the right atrium and right ventricle, and the other part of the heart’s electrical conduction pathways. Another important aspect of cardiac physiology is that the coronary vessels receive their blood supply at the end of diastole. As the left ventricle contracts, the coronary vessels are occluded by the opened leaflets of the aortic valve. When the heart relaxes, the leaflets are pulled away from the opening of the coronary sinuses and the oxygen-rich residual blood in the aorta is drawn into the coronary sinuses. Thus, the volume of blood in the left ventricle at the end of diastole is an important determinant of coronary blood flow. A reduction in left ventricular blood volume will lead to a reduction in coronary artery perfusion, which may lead to myocardial ischemia.

Two important attributes that play a direct role in a patient’s cardiac output (overall cardiac function) are preload and afterload. An understanding of preload and afterload will allow an EMS provider to understand the complications potentially facing a patient suffering from a cardiac pump- or volume- related problem.

Preload is the tension on the ventricular wall when it begins to contract. Preload is determined primarily by the pressure created in the ventricle by the amount of blood volume at the end of diastole (end-diastolic filling volume). The amount of blood volume at the end of diastole is primarily determined by venous volume and blood flow from the right side of the heart through the pulmonary vasculature. Any patient, but specifically cardiac patients, can suffer from either an increased or decreased preload. Patients with an increase in preload are in danger due to an overload state in the ventricle. The increased blood flow exceeds the heart’s ability to effectively eject all of the volume before the next contraction, resulting in an overly stressed myocardium. The increased workload of the heart results in an increased need for oxygen. In other words, too much preload will result in undue myocardial stress and ultimately may lead to myocardial ischemia. Conversely, if preload volume is grossly diminished, the patient will not have enough blood volume to eject from the ventricles upon contraction, causing the patient to fall into a relative state of hypovolemia. This condition is dangerous because all of the core organs may be affected, including the heart. The reduction in circulating volume will be problematic because the residual volume that is used to perfuse the coronary vessels will be reduced and, as such, flow through the coronary sinuses will be impaired.