cardiac output it's determination by eficks
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Answer:
Cardiac output (CO) is defined as the amount of blood ejected by the heart per minute and is calculated as the product of heart rate (beats per minute) and stroke volume (mL).
Systemic Vascular Resistance
CO at peak effort in the sedentary subject reaches nearly 18 l min−1 (Table 1), a greater than threefold increase above basal CO. The trained 70 kg 40-year-old subject, by comparison, with a maximal VO2 increasing from around 40 to 50 ml kg−1 min−1 – a 25% increase – would attain a CO of 22 l min−1. Elite athletes have attained a CO at peak effort of up to 40 l min−1. Most of this increase in CO is distributed to exercising muscle beds. Despite these large relative increases in maximal CO after training, the MAP of blood during maximal effort is unchanged. MAP is a product of CO (blood flow) and SVR. Consequently, if maximal CO has increased with no change in MAP, SVR has decreased. Although the precise mechanism for this is unknown, it requires modification of arteriolar resistance, and to some extent reflects alterations in sympathetic tone, at least at matched submaximal work rates. But at peak effort, reduction in resistance is independent of sympathetic activation, and may reflect increased metabolic vasodilation.
Monitoring of patients
Cardiac patients require careful monitoring of clinical, hematologic, cardiac, radiographic, and hemodynamic variables. It is important to tabulate and establish the trend of important clinical signs: body temperature, respiratory rate and depth (in hospital and at home), breath sounds, heart rate, heart rhythm, mucous membrane color and refill time, pulse strength, attitude, and noninvasively determined arterial blood pressure (Box 21-7). Frequent determination of such simple variables as water and food intake, estimated urine output, body weight, and diuretic dosage provides the clinician with useful information about fluid dynamics and the need for fluid therapy. Home respiratory rates exceeding 35 to 40 in resting dogs correlates well with radiographic evidence of pulmonary edema. Serial determination of serum creatinine, BUN, sodium, and potassium concentrations is useful for monitoring fluid, diuretic, and cardiac therapy. Physical and radiographic signs of fluid accumulation may indicate a need to reduce fluid volume in hospitalized patients and to increase diuretic dosage or to consider additional treatments. For critically ill dogs, more accurate hemodynamic information can be obtained using a percutaneously placed pulmonary arterial catheter, as described in the following section. The effect of fluid therapy on CVP and pulmonary venous pressure is a prime concern in patients with heart failure and can be a major determinant of the rate of fluid administration. Insufficient venous pressure reduces cardiac output, whereas very high pressure promotes formation of edema. In heart failure, an optimal venous pressure is necessary to maintain cardiac output, but pulmonary venous pressure greater than 20 mm Hg and CVP greater than 10 to 12 cm H2O may be associated with formation of edema.
The CVP is simple to measure using an indwelling jugular venous catheter, and its determination quantifies and indicates the directional changes of right heart filling pressures. More practically, the inspection and estimation of jugular venous pressure provides similar qualitative information. A CVP line is useful in guiding fluid management of seriously ill patients without heart disease, but CVP is not an accurate reflection of pulmonary venous pressure in those with left-sided CHF. The ability of the left and right ventricles to accept and pump blood may be different in CHF. Accordingly, the effects of a volume infusion on the left ventricle and pulmonary circulation may not be accurately gauged by measuring the filling pressures of the right ventricle.44,45,163 It is common to observe animals with high pulmonary venous pressure but relatively low CVP. This is especially true after diuretic therapy. Even in animals with right-sided CHF, ascites may continue to develop despite a relatively low CVP, possibly as a result of avid sodium retention, hypoproteinemia, or the development of cardiac cirrhosis and portal hypertension secondary to chronic hepatic congestion. Noninvasive estimation of cardiac filling pressures can be accomplished using advanced Doppler echocardiographic techniques that record transmitral filling, pulmonary venous flow, and tissue ventricular movements during diastole, but these are not widely available and require advanced training to apply with any consistency. Experienced clinicians also recognize that a ventricular (S3) gallop sound typically corresponds to elevated filling pressures and as such will be diminished or eliminated with effective diuresis or management of heart failure.
Explanation:
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Explanation:
cardiac output expressed in litre and minutes is the amount of blood the heart pump in 1 minutes