Mkgrady8 Mos2 Low Cardiac Output

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

cardiac factors are heart rate and myocardial contractility; integrated factors are preload and mean arterial pressure

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

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;

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

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)

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

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

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

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

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

normal regulatory mechanisms that maintain cardiac output and mean arterial pressure

these compensatory mechanisms

vascular perfusion and if unresolved will eventually lead to death