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14 Cards in this Set
- Front
- Back
low cardiac output leads to |
circulatory shock; inadequate blood flow through the body; leads to cardiac failure and depressed venous pressure; we define circulatory shock as inadequate blood flow to the tissues of the body although as physicians you will associate shock with the variety of physiological responses evoked to compensate; inadequate blood flow implies that there is too little O2 and nutrients delivered to tissues to meet their metabolic demands; most of the time inadequate perfusion will originate from problems with heart function or from problems with the vasculature |
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factors controlling cardiac output |
cardiac factors are heart rate and myocardial contractility; integrated factors are preload and mean arterial pressure |
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physiological response to shock |
normal regulatory responses to low arterial pressure and cardiac output are the baroreceptors reflexes and CNS ischemic response that increase MAP, and the venoconstriction, decreased net filtration/increased fluid absorption, formation of angiotensin, and formation of vasopressin that increase the stressed volume; responses intended to increase mean arterial pressure are promoting tissue perfusion; responses intended to increase stressed volume are adjusting the preload on the heart to increase cardiac output; note that the compensatory responses have different time frames; the ANS can bring immediate help in the defense against shock because it can become activated within seconds; the release of circulating hormones and their effects require more time, on the order of minutes to hrs; finally the readjustment of blood volume by changes in renal filtration and fluid absorption can takes hrs to days |
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heart failure and cardiogenic shock |
anything that impairs cardiac function has the potential to cause shock; heart failure is defined as the inability of the heart itself to pump sufficient blood to satisfy the needs of the body; a common form of heart failure is caused by coronary artery occlusion which leads to acute myocardial infarction, in ischemic region within the heart that leads to necrosis; it is the form of failure most familiar to the lay pubic; the decrease in cardiac output is often accompanied by edema in response to the elevated venous pressure; this is particularly dangerous with pulmonary edema, a frequent complication of a left ventricular infarct; |
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progressive changes in cardiac failure |
immediately after the heart becomes damaged the cardiac function curve is compromised such that it shifts clockwise; for a given right atrial pressure it is capable of delivering less blood; at the initial right atrial pressure of 0 mmHg cardiac output would drop to nearly zero so over the next few beats blood begins to pool in the venous side of the system; this raises central venous pressure (and the right atrial pressure) so that at the new steady state a modest cardiac output is achieved; this low cardiac output might be sufficient to sustain life for a few hrs but it represents a transient state and lasts only a few seconds; all of this is the dramatic reduction in cardiac output that results in a decrease in arterial pressure |
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damaged heart and autonomic compensation |
the decrease in arterial pressure from the last slide is detected by the baroreceptors; in response to the baroreceptor reflex there is an increase in sympathetic discharge and a suppression of parasympathetic activity; within a few seconds contractility of the functional portions of the heart will be increased as well as heart rate; this autonomic regulation will also produce increases in venous tone, elevating mean systemic pressure; as a result of these compensatory changes, cardiac output is improved to a level that would be adequate in the absence of further demands; this response requires only seconds and a sudden moderate heart attack might go undetected producing temporary chest pain (angina) and a few seconds of fainting (syncope) |
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following these initial events |
a semi chronic state of compromised cardiac output follow that would be compensated slowly by additional responses; these would occur over a period of hrs to days; gradual healing of any recoverable myocardial damage would improve somewhat the functional status of the heart; in addition there would be increased retention of fluid by the kidneys that would support a more permanent elevation in mean systemic pressure; cardiac output may eventually improve to near initial levels if the myocardial damage were sufficiently modest; this condition can be maintained but notice that is comes at the cost of a much higher than normal right atrial pressure; this condition is described as compensated heart failure; notice also that there is very little cardiac reserve; in other words in the event of an increased demand it is not possible to increase cardiac output significantly |
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lab testing for myocardiac infarction |
markers of cardiac injury appear in the serum after myocardial infarction; myoglobin appears first in the blood but it is a relatively nonspecific marker and can also be released by damaged skeletal muscle; troponin I and troponin T are sensitive and specific markers that persist for several days after injury; myocardial creatine kinase isoenzyme (CK-MB) is also a good marker of myocardial injury; lactate dehydrogenase (LDH) is a relatively nonspecific marker of myocardial injury but the specificity of the test can be improved by measuring the LDH isozymes; with an infarction the circulating levels of the cardiac isozyme LDH should increase; necrosis causes changes in the QRS complex; ischemia causes T wave inversion |
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inadequate blood flow through the body due to the vasculature |
in this case the low cardiac output can be traced back to a loss of stressed volume (aka effective blood volume) that in turn compromises venous pressure |
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response to hemorrhagic shock |
hypotension which elicits a rapid baroreceptor response and activation of the sympathetic system as well as renal release of renin; these reactions adjust for the blood loss by increasing cardiac output despite the original decrease in central venous pressure; a series of gyton diagrams can be constructed that describe the regulatory changes associated with vasculature induced shock using logic similar to that employed for cardiac failure; one potentially unexpected consequence of the decreased net filtration in the cap is the reduction in hematocrit that accompanies hemorrhage; the shifts in fluid form the interstitium to the vasculature can restore partially the blood volume but it cannot replace the lost erythrocytes |
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stages of hemorrhagic shock |
in compensated shock the normal regulatory mechanisms are sufficient to maintain life; in irreversible shock the lack of adequate perfusion has caused tissue damage that simply cannot be revered by compensatory mechanisms or therapeutic intervention; in progressive shock compensatory mechanisms alone are not sufficient but timely therapeutic intervention can still allow the pt to recover |
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key concepts: the events that accompany cardiac failure and hemorrhage can be understood by application of the |
normal regulatory mechanisms that maintain cardiac output and mean arterial pressure |
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key concepts: guyton diagrams of the cardiac and vascular function curves can facilitate an analysis of |
these compensatory mechanisms |
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key concepts: both cardiac failure and circulatory shock compromise |
vascular perfusion and if unresolved will eventually lead to death |