Cardiac output normal value

The principal mechanism of the hypotensive effect of diuretics (qv) is salt and fluid depletion, leading to reduction in blood volume (200,240). Acute effects lead to a decrease in cardiac output and an increase in total peripheral resistance. However, during chronic adrninistration, cardiac output and blood volume return toward normal and total peripheral resistance decreases to below pretreatment values. As a result, the blood pressure falls. The usual reduction in blood volume is about 5%. A certain degree of sustained blood volume contraction has to occur before the blood pressure decreases. The usual decrease in blood pressure achieved using a diuretic is about 20/10 mm Hg (2.7/1.3 kPa) (systoHc/diastoHc pressures. 

Failure Draw this curve below and to the right of the normal curve. Highlight the fall in cardiac output at high LVEDP by drawing a curve that falls back towards baseline at these values. This occurs when cardiac muscle fibres are overstretched. The curve demonstrates that, at any given LVEDP, the cardiac output is less and the maximum cardiac output is reduced, and that the cardiac output can be adversely affected by rises in LVEDP which would be beneficial in the normal heart. 

Actions Thiazide diuretics, such as hydrochlorothiazide [hye droe klor oh THYE a zide], lower blood pressure, initially by increasing sodium and water excretion. This causes a decrease in extracellular volume, resulting in a decrease in cardiac output and renal blood flow (Figure 19.6). With long-term treatment, plasma volume approaches a normal value, but peripheral resistance decreases. Spironolactone [spye row no LAK tone], a potassiumsparing diuretic, is often used with thiazides. (A complete discussion of diuretics is found on p. 223.)... 

Invasive hemodynamic monitoring usually is performed with a flow-directed pulmonary artery (PA) or Swan-Ganz catheter placed percutaneously through a central vein and advanced through the right side of the heart and into the PA. Inflation of a balloon proximal to the end port allows the catheter to wedge, yielding the PAOP, which estimates the pulmonary venous (left atrial) pressure and, in the absence of intracardiac shunt or mitral valve or pulmonary disease, left ventricular diastolic pressure. Additionally, cardiac output may be measured and systemic vascular resistance (SVR) calculated. Normal values for hemodynamic parameters are listed in Table 14—12. 

Although splanchnic blood flow and DO2 may increase with dopamine, there is no preferential increase in the splanchnic perfusion as a fraction of cardiac output and systemic increases in D02. One study found an inverse relationship between fractional splanchnic flow at baseline and the change in fractional splanchnic blood flow such that dopamine was effective in increasing the fractional splanchnic blood flow in those in whom it was normal but worsened it in those with high baseline values, such as occurs with redistribution of regional blood flow in septic shock. Clinically, it is difficult to distinguish prospectively either subset of patients. 

Pulmonary hypertension is characterized by a chronically elevated pulmonary artery pressure. As described in previous sections of this chapter, under normal conditions, the pulmonary artery pressure has a systolic value of 18 to 25 mm Hg, a diastolic value of 6 to 10 mm Hg, and a mean value ranging from 12 to 16 mm Hg. Pulmonary hypertension exists when the pulmonary artery systolic and mean pressures exceed 30 and 20 mm Hg, respectively. In the disease state, the pressure in the pulmonary artery may fluctuate widely and is often so high that it equals the blood pressure in the systemic arterial bed. As would be expected, pulmonary vascular resistance is also extremely high in patients with pulmonary hypertension. In addition, patients with this disease exhibit an enlarged right ventricle and an enlargement of the main pulmonary artery and its branches. Systemic hemodynamic parameters, however, such as cardiac output, cardiac index, systemic artery pressure, and pulmonary artery wedge pressure are usually not elevated. 

The signs of depth of anesthesia achieved with hal-othane that are of the most practical value are blood pressure, which is progressively depressed, and response to surgical stimulation (e.g., pulse rate, blood pressure, movement, or even awakening). Hypotension results from two main effects. First, the myocardium is depressed directly, and cardiac output is decreased second, the normal barore-ceptor-mediated tachycardia in response to hypotension is obtunded. 

Cardiac output is the amount of blood pumped by the right or left ventricle per unit of time. It is expressed in liters per minute (L/min) and normalized by division by body surface area in square meters (m ). The resulting quantity is called the cardiac index. Cardiac output is sometimes normalized to body weight, being expressed as mL/min per kilogram. A typical resting value for a wide variety of mammals is 70 mL/min per kg. 

Low muscle pH with normal blood pH, the most common cd>normality seen, occurs in patients with clinical problems which cause a decrease in tissue perfusion such as bleeding, extracellular fluid deficit, decreases in cardiac output, and any condition which causes peripheral vasoconstriction and/or vasculitis. In children with decreased tissue perfusion, muscle pH as low as 6.60 has been observed. The lowest values have occurred during massive hemorrhage. Often muscle pH decline in hemorrhage, a result of reflex peripheral vasoconstriction, occurs before a fall in central blood pressure. 

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