Systole blood perfusion

Sepsis The systemic inflammatory response syndrome and documented infection (culture or Gram stain of blood, sputum, urine, or normally sterile body fluid positive for pathogenic microorganisms Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion, or hypotension (systolic blood pressure less than 90 mm Hg). Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or acute alteration in mental status. 

Septic shock Sepsis with hypotension (a systolic blood pressure of <90 mm Hg or a reduction of <40 mm Hg from baseline), despite adequate fluid resuscitation, along with the presence of perfusion abnormalities as seen by severe sepsis. Patients who are receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured. 

The integrated function of the vasculature and heart, as a closed circulatory system, supplies nutrients and oxygen to critical organs and removes metabolic wastes and carbon dioxide. This integrated system results from the careful control of cardiac output, arterial blood pressure (systolic and diastolic pressures integrated to derive mean arterial pressure), and systemic vascular resistance, thereby maintaining blood perfusion through... 

The specific mechanism of the losartan-induced improvement is not known. However, angiotensin II slows the rate of LV relaxation and increases LV diastolic pressures. In a 2-week period of time, there was no evidence of improved diastolic function. Losartan did slow the increase in systolic blood pressure during exercise and decreased the peak systolic blood pressure by a mean of 33 mm Hg. Although the patients had no evidence of myocardial ischemia, losartan may have improved endothelial function and coronary perfusion. 

Over the past decade, we (Sagawa, 1978) have measured the ventricular pressure (P)-volume (V) relationship in an isolated and blood perfused canine heart preparation and came to consider that the ventricular end-systolic P-V relationship (ESPVR) is (a) linear as opposed to the highly nonlinear P-V relationship of the frog s ventricle reported by Otto Frank a century ago, (b) rather insensitive to the preload and afterload and (c) changes its slope (E, ) sensitively with inotropic interventions without a significant shift in the volume intercept (Vq). This is to say that our model of the ventricle merely consists of a linear volume elastance E which varies with each heart beat from a smaller end-diastolic value to a larger... 

Stable angina pectoris Decreased myocardial oxygen consumption -decreased LV end-diastolic dimension -decreased LV filling pressure -decreased LV systolic pressure -decreased PVR Increased coronary blood flow -epicardial coronary artery dilation -stenotic segment dilation -coronary collateral vessel dilation -increased subendocardial perfusion... 

Thus, the nitrates enable myocardial flow resistance to be reduced even in the presence of coronary sclerosis with angina pectoris. In angina due to coronary spasm, arterial dilation overcomes the vasospasm and restores myocardial perfusion to normal. O2 demand falls because of the ensuing decrease in the two variables that determine systolic wall tension (afterload) ventricular filling volume and aortic blood pressure. 

Measurements possible in this model include end-diastolic and systolic pressure of the left ventricle, contractility of the heart (usually using peak positive LVdP/dt or LVdP/dt at a developed pressure of 40mmHg), heart rate, cardiac output and arterial blood flow in a given local perfusion bed. Test... 

Q1 Coronary arteries are the first to branch off the aorta. The heart has a large blood flow (200 ml min-1) but also has great metabolic needs and so has a relatively poor oxygen supply, with little in reserve when oxygen demands increase. At each heart beat (systole), the coronary arteries are compressed by cardiac contraction and blood flow diminishes to a low level. This effect is very marked in the left ventricle, and over 80% of coronary flow to the left ventricle occurs in the periods between beats (diastole). When heart rate increases (tachycardia), the duration of diastole decreases much more than the duration of systole, and the period available for perfusion of cardiac muscle diminishes. 

Cardiac muscle has a large oxygen requirement, and extraction of oxygen from coronary blood is high. The coronary arteries are compressed in systole, particularly in the left ventricle. Sympathetic stimulation, which increases heart rate and force, reduces the duration of diastole and increases myocardial oxygen consumption. A slow heart rate improves coronary perfusion, reduces oxygen demand and is beneficial for coronary perfusion. 

Blood flow to the coronary arteries arises from orifices located immediately distal to the aorta valve. Perfusion pressure is equal to the difference between the aortic pressure at an instantaneous point in time minus the intramyocardial pressure. Coronary vascular resistance is influenced by phasic systolic compression of the vascular bed. The driving force for perfusion therefore is not constant throughout the cardiac cycle. Opening of the aortic valve also may lead to a Venturi effect, which can slightly decrease perfusion pressure. If perfusion pressure is elevated for a period of time, coronary vascular resistance declines, and blood flow increases however, continued perfusion pressure increases lead, within limits, to a return of coronary blood flow back toward baseline levels through autoregulation. 

During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. " Within minutes, arterial systolic pressures may rise to values above 200 mm Hg, and heart rate may increase by 83 beats per minute. Although blood pressure returns to normal within 60 minutes, mean arterial pressure does not fall below 60 mm Hg hence cerebral perfusion pressure is not compromised. In animals, cerebral blood flow is also increased by 200% to 600%, thereby protecting neurons from hypoxic injury. 

Oxysparteine is formed by direct oxidation of sparteine and occurs naturally as isolupanine or aphyUine. Oxysparteine has been shown (75) to slow markedly the rate of the perfused frog heart, in addition to slowing both systole and diastole and resulting in an increased pulse pressure and pulse volume. Administered to a dog with low blood pressure (because of peptone shock), oxysparteine, 5 mg./kg., partly restored pressure and slowed the rate. 

An example of the calculated coronary perfusion flow based on the above relations, is shown in Figure 8. The coronary flow to the endocardial layers is seen to stop during systole (compression) while the flow in the epicardial layers, which are subjected to much lower compression values of P (y, t), is seen to reduce only slightly. The autoregulatory effect which adjusts the blood flow to the metabolic demand, is demonstrated by comparing curves A and B in Figure 8. Lower blood... 

WMe Eq, (7) indicates that the blood volume fractioii /is related to the RIS ratio, the thickness t can be shown to be related to the overall size S of the representative element. This blood-myocardium composite modei, ilso help explain the observations made by Hoffman (1978) regarding the transmuril. perfusion which are illustrated in Figure 7b and 7c. At end of systole of a cardiac cyCJe the myocardial fiber corcfraets but its cross section expands because of incompressibility. The spaces between fibers hence become narrower. At end of... 

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