Cardiogenic shock is literally shock of cardiac origin. It is also the physiologic end point of all other causes of shock. Cardiogenic shock can therefore, regardless of its etiology, be thought of as shock caused by failure of the heart as a forward pump. Modern advances in medical care have made cardiogenic shock less common than it once was, but it is still a life-threatening reality. For example, in the 1970s, approximately 15% of all patients suffering from acute myocardial infarcts developed cardiogenic shock; today, the incidence of cardiogenic shock has dropped to about 5%.
There are several causes, some permanent and some temporary, that lead to failure of the heart as a forward pump. The most common etiology for cardiogenic shock is amyocardial infarction. Some of the less common causes of cardiogenic shock include infectious cardiac disease processes, such as acute myocarditis or endocarditis; induced heart failure from drugs/medications (i.e., cocaine, beta-blockers, tricyclic antidepressants); trauma-related, such as a myocardial contusion; or metabolic derangements that result in cardiac arrhythmias, such as sustained tachycardias or bradycardias. A massive pulmonary embolism may also produce cardiogenic shock by impeding blood flow in the pulmonary vessels, leading to volume overload of the right ventricle and a drastic reduction in left ventricular filling volume. In addition, the large pulmonary embolism produces a ventilation disorder by causing a perfusion/ventilation mismatch, which leads to hypoxemia. Arterial hypoxemia coupled with reduced coronary blood flow and subsequent systemic acidosis will have a deleterious effect on cardiac pump function.
The heart is comprised of specialized muscle fibers known as cardiac muscle. Myocardial fibers are unique in that they have the ability not only to initiate an impulse that will lead to contraction, but they are able to alter the speed of conduction as it travels between fibers. The cardiac muscle is divided into three distinct tissue layers: the endocardium, myocardium and pericardium (sometimes referred to as the epicardium). The endocardium is the innermost layer and is constantly surrounded by the blood that flows through the heart. The myocardium, or middle layer of the heart, tends to be the thickest due to the bulky muscle mass. The muscle cells that comprise the myocardium are unlike other muscles in the body because they are very strong and possess the ability to maintain constant stretch-like skeletal muscle while simultaneously being stimulated by self-generated electrical impulses. The overall strength of contraction comes from within the myocardium. The ability of the myocardium to be in constant use is largely due to the vast amount of capillary blood flow that is networked within the myocardial muscle bed. This provides the required oxygen and nutrient delivery, and equally important, waste removal, which is mandatory in order to sustain the ongoing workload. The pericardium is the layer commonly referred to as the “pericardial sac” because it is made up of a tough fibrous sac that surrounds the heart to provide protection and lubrication for the heart as it contracts.
The heart contains four distinct chambers: the left and right atria and left and right ventricles. The ventricles are the larger of the chambers and have the primary function of squeezing blood out of the heart into either the pulmonary circulation (to the lungs) or the systemic circulation (throughout the body). The walls of the ventricles are much more muscular than the atria and, as a result, have the ability to generate a greater force and pressure during contraction, as compared with the atria.
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.
Afterload is a measure of the pressure at which the ventricle must exert its force to eject the blood. The afterload is directly related to the pressure in the aorta that must be overcome with each cardiac contraction. As blood circulates through the body, it does so by means of pressure that is created within the vessels (vascular resistance). This pressure is greatest in the arterial system. One of the most significant concerns of an elevated arterial pressure is at the site of the aorta. If the overall pressure within the aorta is higher than normal, the ventricle must work harder to overcome the higher pressure to eject the blood, thus creating an increase in afterload. Because an increase in afterload requires a greater contractile force to eject the blood out of the ventricle, it creates an increase in myocardial workload, which, again, translates into an increase in myocardial oxygen demand and consumption. If there is a drastic reduction in arterial pressure, the afterload is reduced, since it will take less force to overcome the pressure in the aorta. If the patient’s arterial pressure is decreased, the patient’s heart may have to compensate by increasing the rate and strength of myocardial contractions to generate an adequate arterial pressure and maintain an adequate circulation. An increase in myocardial rate and contractile force will cause an increase in oxygen demand and consumption, potentially further exacerbating an already ischemic heart.
The progression of cardiogenic shock starts with an impaired cardiac muscle. It is important to note that a myocardial infarction in itself is not cardiogenic shock. Cardiogenic shock only develops after a minimum of 40% of the cardiac muscle has been affected by tissue death and no longer contributes to the ventricular contraction. Suppose, for example, you have a patient who has suffered a significant right ventricular infarction with a resultant reduction in right ventricular contractile force. A reduction in contractile force may lead to reduction in the amount of blood being effectively ejected by the right ventricle, with subsequent stagnation of blood. A reduction in blood volume being ejected from the right ventricle will lead to a reduction in preload of the left ventricle. The reduction in blood volume and preload will reduce the arterial pressure in the aorta and systemic arteries. A decrease in arterial pressure will be sensed by baroreceptors in the carotid bodies and aortic arch. The arterial baroreceptors will trigger the sympathetic nervous system (the fight-or-flight nervous system) via the hypothalamus. Upon stimulation, the sympathetic nervous system will promote vasoconstriction, increase the heart rate and contractile force, and stimulate renal fluid retention in an attempt to increase preload and arterial pressure for the purpose of restoring blood flow.
In cardiogenic shock, these compensatory mechanisms may actually work against the patient’s condition and worsen cardiac compromise. Increases in heart rate and force of contraction will increase myocardial oxygen demand and consumption, and may actually lead to or exacerbate myocardial ischemia. Fluid retention, coupled with the inability of the ventricles to completely fill in the presence of significant tachycardia, may lead to pulmonary congestion and a more severe state of hypoxia. Vasoconstriction will most likely increase pressure in the aortic root and create a need for a greater myocardial afterload, further increasing myocardial oxygen demand and consumption in an already hypoxic heart muscle.
As the amount of cardiac tissue necrosis and ischemia increases, the patient’s cardiovascular reserve becomes inadequate, and cardiac output and tissue perfusion are compromised. As the ventricular volume continues to decrease, the amount of blood available for coronary artery perfusion is decreased, leading to further myocardial ischemia and failure. The failure of cardiac compensatory mechanisms occurs, in part, because the degree of vasoconstriction is not sufficient enough to maintain the necessary pressure to support blood flow through the core organs, including the coronary arteries of the heart. Initially, assuming the patient can compensate well enough, the pressures will begin to increase systemically, leading to increased pressure on the right side of the heart and eventually on its left side. Increases in right heart volume will promote further right ventricular failure, which will lead to peripheral venous congestion and a consistently high right ventricular preload.
The systemic increases in pressure will exacerbate pump failure and further reduce blood flow through the coronary vessels. Additionally, the increase in pressures will promote greater stress on the internal walls of the myocardium, which, in turn, elevates myocardial oxygen demand and consumption, further worsening ischemia. The result is decreased cardiac output, which leads to ischemia. Prolonged states of cellular ischemia eventually lead to lactic acid accumulation in the myocardial cells (lactic acidosis), which will cause irreversible cellular membrane damage and, ultimately, complete and irreversible loss of pump function.
Cardiogenic shock is often difficult to effectively diagnose in the field, but suspicion for cardiogenic shock is not difficult to diagnose. Cardiogenic shock should be considered in the patient who presents with unexplained hypotension or cardiac output, unexplained impaired mental function and unexplained pulmonary vascular congestion. These unexplained clinical signs should be used as differential diagnosis criteria, not definitive measures of the presence of cardiogenic shock. The single greatest differential for cardiogenic shock versus any other form of shock is the presence of pulmonary edema. Do not, however, assume that because a patient does not have pulmonary edema he/she is not in cardiogenic shock. The shock state may have just begun to develop and the patient has not deteriorated enough to have developed pulmonary edema. Other signs or symptoms include dyspnea, tachycardia, cyanosis, peripheral edema, altered mental status, tachypnea and reduced urine output.
First and foremost, because the primary problem with the cardiogenic shock patient is related to ischemia, oxygen must be provided. A non-rebreather mask may be adequate in managing a patient in the early stages of cardiogenic shock. Once the patient develops pulmonary edema, however, the non-rebreather will not be effective, and the patient will require an oxygenation device such as CPAP or endotracheal intubation with positive end-expiratory pressure (PEEP). Just like pulmonary edema in the CHF patient, fluid is trapped between the alveoli and capillaries, and simple oxygenation without supplemental pressure will not be successful. Pressure will be needed to increase arterial oxygen tension and force oxygen through the fluid, and subsequently across the alveolar and capillary membranes.
In addition to ensuring the patient is adequately oxygenated, there are several pharmacological agents currently used in the prehospital care arena that may be considered when managing a cardiogenic shock patient. It should be understood that the primary goals in pharmacologic management of cardiogenic shock are restoration of oxygenated blood flow in conjunction with a reduction of cardiac workload and cardiac oxygen consumption. The most commonly used cardiogenic shock drugs are detailed below. Standard delivery of infusions in the field is difficult, because most ambulances do not carry infusion pumps and therefore cannot guarantee exact dosing of the infusion drug.
Dopamine is an ideal inotrope (inotropes deal with contractile force) for the patient in whom rate is not an important factor. Dopamine, when used at higher doses (10–20mcg/kg/min), has been shown to have significant effects on increasing the patient’s heart rate, which increases the amount of oxygen utilization and need. The ideal dose of dopamine, which delivers predominantly beta properties that increase inotrope, should be at around 5mcg/kg/min.
Dobutamine, a synthetic amine, has strong inotropic properties and is ideal for managing cardiogenic shock. It is not uncommon to infuse dobutamine in conjunction with low doses of dopamine. Dobutamine is a more potent inotrope than dopamine and has less influence on heart rate. However, dobutamine, when administered at high doses, may promote the production of norepinephrine, which will increase myocardial ischemia and cell death, thus worsening the degree of shock. This is why few ambulances without IV pumps carry dobutamine.
Nitroglycerin is a potent coronary vasodilator and a peripheral vasodilator that has proved to be highly beneficial when used in patients with cardiogenic shock. Nitroglycerin is beneficial because it dilates the coronary vessels, allowing for greater myocardial oxygenation. In addition, the peripheral vasodilatory effects lead to a reduction in preload and arterial pressure and subsequently to afterload, thus reducing the myocardial workload. A reduction in workload requires less myocardial oxygen and less coronary artery perfusion. In the patient with a confirmed right ventricular infarction, nitroglycerin should be withheld in the prehospital setting. The patient may already present as hypotensive due to an inadequate preload. Nitroglycerin will have little benefit in this patient and may lead to a further decrease in blood pressure by an additional reduction in preload. Instead of nitroglycerin, consider a fluid bolus in the right ventricular infarct patient. Nitroglycerin infusion in a hypotensive patient may be accomplished through simultaneous administration of an inotrope. At lower doses, inotropes like dopamine and dobutamine will help maintain adequate pressure through increasing the strength of cardiac contractile force, while the concurrent vasodilation will help in reducing the force at which the ventricle must eject the blood, thereby reducing myocardial workload.
Lasix is a diuretic that can be used in the patient with clinical signs of heart failure, including peripheral and/or pulmonary edema. Lasix may be used to help reduce edema by increasing fluid excretion through the kidneys and by reducing sodium reabsorption in the loop of Henle and the distal tubules. Again, like nitroglycerin, diuretics should be used with caution, because they promote water loss and, in the patient with a right ventricular infarct, further decrease preload, causing the patient to become more hypotensive.
Cardiogenic shock is a pathophysiologic cascade that often leads to death. Although there has been a dramatic decrease in the cases of cardiogenic shock since the 1970s, the mortality rate of those patients who are diagnosed with cardiogenic shock remains as high as 50% to 80%. As stated throughout the article, cardiogenic shock in its later stages cannot be reversed, but clinical signs and symptoms of the syndrome may be identified early enough to prevent a patient from developing irreversible end-stage cardiogenic shock.
As a prehospital care provider, you must be able to ensure the pre-shock patient has adequate oxygenation of the myocardium and can be effectively treated before it is too late.
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