• Home Page
Main Index
1992
• Training/Info
• Drugs
LAS
• Drugs
Print
• Slide
Show
• Clipart
& gifs
• Mini
polls
• Poem
Learning
• ECG
To understand the process of shock, we must understand the basics of cardiovascular physiology. There are certain values which need be understood. The cardiac output (CO) is the volume of blood leaving the heart each minute. The stroke volume (SV) is the amount of blood ejected with each beat. By definition, the value of the cardiac output is equal to the stroke volume multiplied by the heart rate (HR). In the majority of patients, if the heart rate falls, the stroke volume will increase to maintain the cardiac output. In certain examples, however, the muscle of the ventricles is noncompliant and the stroke volume is unable to change, causing the cardiac output to fall when the heart rate falls. These examples include multiple myocardial infarctions, chronic cardiomyopathies in neonates. Therefore, neonates cannot tolerate bradycardia (a slowing of the heart rate) since it results in a precipitous fall in CO.
There are certain factors which affect the stroke volume. The three principal factors are preload, afterload and myocardial contractility. The definition of preload is the volume of blood that remains in the left ventricle at the end of diastole. The preload is equal to the left ventricular end diastolic volume (LVEDV). Preload is generally a reflection of the volume status of a patient. It is measured via the central venous pressure (CVP) or by the pulmonary capillary wedge pressure. Additionally, the LVEDV determines the cardiac output according to Starling's law. Clinically this means increasing precontraction muscle fibre length by increasing LVEDV through volume administration leads to an increase in the force of contraction. The afterload is defined as impedance or resistance to ventricular contraction. There are two factors that determine the afterload. They are vascular tone and changes in the intrathoracic pressure. Myocardial contractility is defined as the ability of the myocardial muscle to shorten itself. It is important in the treatment of shock states and in the use of fluids and inotropic agents.
Shock is defined as the acute disruption of circulatory function leading to inadequate delivery of nutrients to the tissues. It is a common misconception that shock is diagnosed solely on the basis of the blood pressure, but this is not true. For example, a decrease in the cardiac output can lead to activation of the renin-angiotensin and sympathetic nervous systems, which cause and increase in the systemic vascular resistance with a resulting normal blood pressure, even though the cardiac output was decreased. Therefore, a patient in shock can have decreased, normal or increased blood pressure. There are many types of shock. There are four which I will discuss in this article.
The first is cardiogenic shock, which is defined as shock resulting from a decline in cardiac output secondary to serious heart disease such as myocardial infarction. In cardiogenic shock, the preload and the afterload are increased, while myocardial contractility is decreased. There are many etiologies of cardiogenic shock, including congenital heart disease, arrythmias, ischemic heart disease, myocarditis, pericardial effusion and tamponade, myocardial contusion and/or traumatic injury, acute drug toxicities, chronic drug toxicities, late septic shock, infiltrative disease, thyrotoxicosis and pheochromocytoma. Some examples of ischemic heart disease include Kawasaki disease, anoxic injury and anomalous injury of the left coronary artery. Chronic drug toxicities include toxicities to chemotherapeutic agents and to radiation. The infiltrative diseases include mucopolysaccharidoses, and the glycogen storage diseases. What all of these etiologies have in common is that they all result in "pump failure" owing to myocardial damage.
The second type of shock is hypovolemic shock. Hypovolemic shock is caused by a reduction in the volume of blood. This is almost always caused by hemorrhage or dehydration (especially in young children). Volume depletion is usually caused by vomiting, diarrhea, diuretic over usage or ketoacidosis. Hypovolemic shock can also be found in cases of internal sequestration such as ascites, pancreatitis and intestinal obstruction. Hypovolemic shock can also be found in patients suffering from severe burns, who are at high risk for losing large amounts of plasma. In hypovolemic shock, preload is decreased, afterload is increased, and the myocardial contractility remains normal.
The third type of shock is septic shock. Septic shock is associated with sepsis which is the presence of pathogenic organisms in the blood or tissues. Septic shock is also associated with septicemia, usually by Gram-negative (endotoxic shock) bacteria, but also Gram-positive and rarely fungi. It is frequently associated with abdominal and pelvic infection complicating trauma or surgery. In early septic shock, the preload and afterload are decreased, and the myocardial contractility is increased. In late septic shock, the preload and afterload are increased and the myocardial contractility is decreased.
There
are three other possible causes of shock in neonates
and young infants. First, there is congenital adrenal hyperplasia.
This syndrome is usually recognized after birth, with virilization in
females, salt-wasting, hyponatremia, hyperkalemia, metabolic acidosis, and
cardiovascular collapse. This diagnosis should be considered in a
seriously ill child with metabolic acidosis and an increased serum
potassium.
The second possible cause is an inherited metabolic disorder with hyperammonemia. This usually results when there is a defect in the urea cycle, causing organic acidemias and an increased ammonia.
The third cause of shock in neonates is obstructive left heart syndromes, such as critical aortic stenosis, critical coarctation of the aorta, hypoplasic left heart, and interrupted aortic arch. This leads the neonate to be dependent on the ductus arteriosus for systemic circulation. In critical aortic stenosis and in hypoplasic left heart, blood can not be ejected from the left side of the heart. In critical coarctation of the aorta and interrupted aortic arch, the blood can not reach the lower part of the body.
SHAHIN
GHADIR, MS III
Universidad
Central del Caribe, School of Medicine
SHOCK
Anaphylactic
Spinal
Drug intoxication
Head injury