That would include thalamic hemorrhage. Since the stroke volume increased then the cardiac out put would increase, pumping out more blood with the same amount of heart beats. A 'cerebral hemorrhage' means bleeding within the brain. A myocardial infarction is a heart attack; during this, the heart's beat effectively stops and the heart is no longer pumping blood in any useable amount. Therefore, a myocardial infarction causes cardiac output to drop significantly and possibly drop to zero depending on the severity.
Cardiac output CO is roughly equal to stroke volume x heart rate. Stroke volume is related to preload, contractility, and afterload. As you can see, the only variables you have not controlled for is cardiac contractility. The frequency would decrease the gain and increase the output voltage. A cerebral hemorrhage is a type of stroke, and occurs in the brain.
Medically its the stroke volume times the heart rate, or just the amount of blood that the heart pumps in a minute. At rest, not at all. BUT there would be less of an increase in cardiac output during exertion - which results in quick fatigue and lowered maximum activity. The less blood in the system means that there will be less to be pumped out.
This can be a dangerous situation where someone has lost a lot of blood. Some way to stop the loss is immediately necessary and a transfusion may be also required when it can be done. Hemorrhage means to lose a lot of something. Typically, in medicine, hemorrhage is used to denote a huge loss of blood. Loss of blood can be caused by any number of reasons, so there is not going to be any one condition that would cause a patient to hemorrhage.
Log in. They increase the arterial pressure mainly by increasing the total peripheral resistance, which has no beneficial effect on cardiac output; however, the sympathetic con-striction of the veins is important to keep venous return and cardiac output from falling too much , in additionto their role in maintaining arterial pressure.
Especially interesting is the second plateau occur-ring at about 50 mm Hg in the arterial pressure curve of Figure 24—1. This results from activation of the central nervous system ischemic response, which causes extreme stimulation of the sympathetic nervous system when the brain begins to suffer from lack of oxygen or from excess buildup of carbon dioxide. A special value of the maintenanceof normal arterial pressure even in the presence of decreasing cardiac output is protection of blood flow through the coronary and cerebral circulatory systems.
The sympathetic stimulation does not cause significant constriction of either the cerebral or the cardiac vessels. In addition, in both these vascular beds, local blood flow autoregulation is excellent, which prevents moderate decreases in arterial pressure from signifi-cantly decreasing their blood flows.
Therefore, blood flow through the heart and brain is maintained essen-tially at normal levels as long as the arterial pressure does not fall below about 70 mm Hg, despite the fact that blood flow in some other areas of the body might be decreased to as little as one third to one quarter normal by this time because of vasoconstriction.
Eventually, the respiratory centers fail as well. Many other factors contribute to the accelerating decline characterizing progressive shock, most not as powerful as the effects of the failing heart and neurological centers. The vascular endothelium suffers damage from underperfusion either as a direct metabolic consequence or due to reactive oxygen species released from activated white blood cells.
The impacted endothelial cells release additional cytokines, many of which have vasodilator effects or stimulate white cell activity. With extreme states of low cardiac output and tissue underperfusion, some capillaries may experience prolonged periods when flow ceases completely. The stasis together with the damaged endothelium leads to platelet aggregation, initially as platelet clumping that can disaggregate if flow resumes.
However, with extended periods of stasis, clotting will develop, permanently occluding the vessel. Crowell termed this process, which can develop throughout the body, diffuse intravascular coagulation [ 50 , 51 ]. It may result in lasting deficits in functions of the brain and other organs even if the patient does not succumb. If the progressive phase of shock continues for an extended period, irreversible shock will develop, a condition that cannot be corrected regardless of therapeutic attempts.
The transition point between progressive but still reversible and irreversible shock is correlated with the total oxygen debt the difference between the basal oxygen consumption rate and that measured during the period following hemorrhage accumulated by the patient during the period of reduced cardiac output. Closely correlated with severe oxygen debt is depletion of cellular adenosine and high-energy adenosine compounds such as adenosine triphosphate ATP.
During periods of inadequate oxygen supply to the heart and other tissues, cells do not have adequate ability to generate high-energy phosphate bonds through oxidative metabolism due to low oxygen levels or through glycolysis due to inhibition of glycolitic enzymes by low pH.
Consequently, the cells deplete all high-energy compounds available, first ATP, then adenosine diphosphate, finally adenosine monophosphate AMP. The adenosine formed from the hydrolysis of AMP readily diffuses out of the cells and is converted to uric acid that cannot reenter the cells. If cells of critically important organs, such as the heart, become depleted of adenosine during a period of prolonged underperfusion, they will be unable to restore their adenosine supply for many hours.
Cardiac adenosine depletion can be a significant contributor to development of irreversible shock [ 54 ]. Even massive transfusions of blood during the irreversible phase cannot salvage the patient, even though it may temporarily improve cardiac output.
Mean systemic and atrial pressures may be elevated to very high levels by infusion of large volumes of blood, yet cardiac output may rise for only a short period, suggesting that the heart, not the peripheral vasculature, is the element of the system responsible for the ultimate failure.
Crowell and Guyton repeatedly recorded cardiac function curves during development of irreversible shock in anesthetized dogs. As the time during which the heart was underperfused progressed, the myocardium suffered more and more damage, eventually reaching a point at which its condition was irreversible. Therapy directed to improve cardiac function can delay the point at which shock becomes irreversible. But even with all available interventions, there is a degree of cardiac impairment that can accumulate during prolonged circulatory shock that precludes recovery.
After approximately 30 min, compensatory mechanisms respond with reverse stress relaxation, increased sympathetic nervous system reflex stimulation of the heart and vasculature, and fluid movement into the capillaries from the interstium throughout the body. As a result, the venous return curve and cardiac function curves are shifted to those illustrated as the yellow lines.
The cardiac function curve has moved to the left, whereas the venous return curve is shifted upward by the increase in mean systemic pressure, resulting in an intersection at a cardiac output value of 2.
The equilibrium point now with the unchanged venous return curve shown in yellow is at a reduced value of 1. From this condition, the system will deteriorate rapidly to the function curve shown as the blue line. If a massive transfusion of blood is given at this point, raising mean systemic pressure to 14 mm Hg, the heart retains insufficient strength to significantly increase output, even at extremely high atrial pressure. The new equilibrium point is at 1. The condition of the cardiovascular system will continue to deteriorate at an accelerating rate from this point until death.
If the heart is unable to pump enough blood to meet the demands of the tissues of the body, the condition is referred to as heart failure. The causes can be related to coronary artery occlusion with infarction of portions of the myocardium, myocardial ischemia associated with diffuse small artery disease throughout the myocardium, cardiomyopathy, valvular insufficiency or restriction, or cardiac tamponade due to fluid accumulation in the pericardium.
Failure to pump a sufficient rate of blood flow may be associated with inadequate contractile force or with inability of the myocardium to relax adequately during diastole.
The condition can develop suddenly after coronary artery thrombosis or over a period of months or years due to progressive myocardial ischemia or cardiomyopathy. The causes of the condition cannot be considered here, but the responses of the cardiovascular system to heart failure will be analyzed in detail. In response to an acute reduction in heart strength after an acute coronary artery occlusion, sympathetic nervous system reflexes act within seconds to increase strength of contraction and heart rate and increase mean systemic pressure.
The reflexes are initiated initially by reductions in arterial pressure sensed by the arterial baroreceptors, and if blood pressure falls below 50—60 mm Hg, the central nervous system ischemic reflex is activated as well.
The reflexes shift the cardiac function curve to the left and upward, whereas the increase in mean systemic pressure shifts the venous return curve to the right. Expected responses of venous return and cardiac function to an acute coronary artery occlusion resulting in compensated heart failure. Shown are responses at the moment of the event, at 0. Long-term compensation for heart failure includes renal sodium and water retention, which increases extracellular fluid and blood volume.
The sympathetic nervous system reflexes act in the kidneys to reduce renal blood flow and glomerular filtration rate, reducing sodium and water excretion as well. In addition, the sympathetic innervation of the afferent arterioles and juxtaglomerular apparatus of the renal cortex stimulate renin release.
The elevated renin levels generate higher concentrations of angiotensin I and II. Angiotensin II, in addition to being a powerful vasoconstrictor that significantly contributes to elevation of blood pressure and mean systemic pressure in the minutes following an acute cardiac event, also has a strong antinatruetic effect, increasing tubular reabsorption of sodium and water.
Furthermore, angiotensin II stimulates aldosterone secretion from the adrenal cortex, which also has a significant sodium-retaining effect on the renal tubules. While the sympathetic reflexes, angiotensin II, and aldosterone all are significant sodium- and water-retaining factors that act on the kidneys after acute cardiac impairment, reduction in arterial pressure associated with reduced cardiac output is the most powerful antinatriuretic influence.
Even reductions of a few mm Hg in renal perfusion pressure reduce sodium and water excretion significantly [ 35 , 56 — 58 ]. The combination of all sodium- and water-retaining mechanisms acting simultaneously can strongly reduce excretion even down to levels that approach complete retention in severe heart failure. The yellow curves in Figure 6. The beginnings of this process are reflected in the upward shift of the cardiac function curve drawn as the yellow line. If the responses to the initial impairment of cardiac pumping ability return cardiac output to near the normal resting level, the condition is referred to as compensated heart failure.
This is the situation depicted by the yellow function curves intersecting at a cardiac output value of 4. In this condition, the patient has a limited ability to increase his metabolic rate and demand for cardiac output since the plateau of his function curve is only slightly greater than his resting cardiac output.
However, since he is able to maintain enough cardiac output to provide for resting conditions and limited exertion, as long as he does not place additional demands on his heart, he will be comfortable. The condition is characterized by stable fluid and electrolyte balance with little or no edema, near-normal blood pressure and blood gases under sedentary, resting conditions, but little cardiac reserve.
In addition, his right atrial pressure, mean systemic pressure, blood volume, and extracellular fluid volume will remain elevated, but stable. Decompensated heart failure is the condition that results when cardiac output remains below the level required to maintain adequate blood flow to the body at rest. Heart failure may progress gradually to the decompensated condition in many chronic cardiac conditions, or it may develop suddenly as a consequence of a severe myocardial infarction associated with a major coronary artery occlusion.
Regardless of the cause, if cardiac output is significantly below normal for an extended period after the sympathetic reflexes and hormonal systems have achieved their maximum compensatory effects, fluid and electrolyte excretion will be severely restricted resulting in cumulative positive fluid and electrolyte balances.
The sodium- and water-retaining mechanisms described above continue to act on the kidneys as long as cardiac output is below the minimum level required for normal tissue metabolism. Consequently, persistence of the condition for several days or more leads to a large positive fluid balance that may give rise to peripheral edema, which is free fluid accumulation in the tissues. If right atrial pressure rises excessively, free fluid may also collect in the abdominal cavity as ascites.
Predominant left-sided heart failure may lead to left atrial pressure levels high enough to produce pulmonary edema before peripheral edema forms, although pulmonary edema may occur in severe bilateral failure as well. Decompensated failure is an unstable condition that may deteriorate progressively toward death unless intervention can salvage the pumping ability of the heart.
Sustained positive fluid and electrolyte balance in heart failure can expand blood volume to levels that result in very high right atrial pressure, approaching even 15 mm Hg. Associated with these very high levels of cardiac preload is a progressive deterioration of cardiac function.
As the atrial pressure increases, ventricular end diastolic radius increases, which, according to the law of Laplace, increases ventricular wall stress in proportion to the increase in radius. To develop pressure to eject blood from the ventricle, the myocardium must perform work to overcome wall stress. In severe heart failure, the heart has insufficient metabolic energy to perform the workload required of it and suffers progressive damage as a result.
The critical situation associated with high atrial pressures is undoubtedly exacerbated by the concomitant occurrence of inadequate coronary blood flow and arterial hypoxia that may develop from pulmonary edema. Clearly, such a condition has the features of a positive feedback cycle that can accelerate into a rapidly fatal vicious cycle. The progression of decompensated failure can be analyzed graphically, as presented in Figure 6. The normal function curves are drawn in black lines.
In this example, the patient suffers a serious coronary artery occlusion that suddenly shifts his cardiac function curve downward and to the right drawn in red , reaching an intersection with the momentarily unchanged venous return curve at 1.
With compensation from the reflex mechanisms, after approximately 10 min, the cardiac function curve may be improved to that illustrated in purple that reaches an equilibrium with the compensated venous return curve at 2.
Over the ensuing hours, cardiac function remains stable but cannot improve significantly, although fluid retention begins to increase blood volume and mean systemic pressure, shifting the venous return curve to the right shown in yellow. Although the new equilibrium point is on the same cardiac function curve, cardiac output is now 2. Several more days of positive fluid balance continues to shift the venous return curve to the right, although the cardiac function curve remains unchanged.
Once the venous return curve has shifted rightward to a degree that the intersection with the cardiac function curve is on the plateau blue venous return curve at a cardiac output 3. However, fluid retention continues, shifting the venous return curve and raising right atrial pressure still higher green venous return curve ; as a result, the heart weakens, shifting the cardiac function curve downward and to the right green cardiac function curve so that the new equilibrium value is at cardiac output of 2.
Fluid retention continues unabated, even more avidly as arterial pressure falls, shifting the venous return curve farther to the right, raising atrial pressure, further weakening the heart so that the subsequent equilibrium points are at progressively lower values of cardiac output and higher right atrial pressures.
The cycle of deterioration usually progresses rapidly to death. Responses expect in venous return and cardiac function following a severe coronary artery occlusion leading to decompansated heart failure are illustrated in the figure. The immediate change and subsequent responses over the next 20 hours are presented. The most common cause of postpartum hemorrhage is when the uterus does not contract enough after delivery.
ICH is most commonly caused by hypertension, arteriovenous malformations, or head trauma. Treatment focuses on stopping the bleeding, removing the blood clot hematoma , and relieving the pressure on the brain. Hemorrhage most commonly occurs after the placenta is delivered. The average amount of blood loss after the birth of a single baby in vaginal delivery is about ml or about a half of a quart.
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