Contractility ventricular pressure—volume

FIGURE 17.10 Left ventricular pressure-volume work loops computed for the complete human circulation model (Figure 17.6) for control and varied inotropy, achieved by changing the contractile parameter c in Equation 17.8 for each heart chamber 25%. 

Several studies have indicated that n-butane sensitizes the myocardium to epinephrine-induced cardiac arrhythmias. In anesthetized dogs, 5000 ppm caused hemodynamic changes such as decreases in cardiac output, left ventricular pressure, and stroke volume, myocardial contractility, and aortic pressure. Exposure of dogs to 1-20% butane for periods of 2 minutes to 2 hours hypersen-... 

Fig. 1. Hemodynamic effects of anandamide in anesthetized mice. Representative recordings ofthe effects of anandamide [20 mg/kg i.v., W-arachidonoyl-ethanolamine (/1 4)] on mean arterial pressure (iW/iP, top panel, cardiac contractility (left ventricular systolic pressure LVSP and dP/df (dPdt) middle panel and pressure-volume relations (bottom panel in a pentobarbital-anesthetized C57BL6 mouse. The five parts of the and bottom panels represent baseline conditions (BI, phase I (/), phase II (//), and phase III (III ofthe anandamide response, and recovery 10 min following the injection. The arrow indicates the injection ofthe drug. The decrease ofthe amplitude of PV loops and shift to the right indicate decrease of cardiac contractile performance...

The most common sensor is the activity sensor, which uses any of a variety of technologies (e.g., piezoelectric crystals and accelerometers) to detect body movement. Systems using a transthoracic-impedance sensor to estimate pulmonary minute ventilation or cardiac contractility are also commercially available. Numerous other sensors (e.g., stroke volume, blood temperature or pH, oxygen saturation, and right ventricular pressure) have been researched or market-released at various times. Some systems are dual-sensor, combining the best features of each sensor in a single pacing system. 

Suga H, Sagawa K, Kostiuk DP (1976). Controls of ventricular contractility assessed by pressure-volume ratio, Emax. Cardiovasc Res 10 582-592. 

Recently, the relationship between pressure-volume or force-length at the end of systole has attracted a great deal of interest as a descriptor of the contractile state of the heart. This interest stems from a series of studies in isolated, canine left ventricular preparations (Taylor et al 1969 Suga et a/., 1973 Suga and Sagawa, 1974 Weber et /., 1976 Weber and Janicki, 1977), which demonstrated the end-systolic pressure-volume relation to be quite sensitive to variations in contractile state and relatively insensitive to variations in load. In addition, the relation is linear over a wide range of volumes so that its slope can be used to quantitate the contractile state. 

Figure 1. Steady state isovolumetric pressure-volume loops (vertical lines) are plotted for various ventricular volumes. Two contractile states are presented control (solid lines) and enhanced (broken lines, 6/Ltg/min Dobutamine). The linear regression lines for the peak isovolumetric pressure-volume points are also illustrated.

Grossman W, Braunwald E, Mann T, McLaurin LP, Green LH (1977) Contractile state of the left ventricle in man as evaluated from end-systolic pressure-volume relations. Circulation 56 845-852 Hunter WC, Janicki JS, Weber KT, Noordergraaf A (1979) Flow-pulse response A new method for the characterization of ventricular mechanics. Am J Physiol 237 H282-H292 Janicki JS, Reeves RC, Weber KT, Donald TC, Walker AA (1974) Application of a pressure servo system developed to study ventricular dynamics. J Appl Physiol 37 736-741 Mehmel HC, Stockins B, Ruffman K, Olshausen K, Schuler G, Kubler W (1981) The linearity of the end-systolic pressure-volume relation in man and its sensitivity for the assessment of left ventricular function. Circulation 63 1216-1222... 

Shroff SG, Janicki JS, Weber KT (1983a) The importance of internal resistance in the description of ventricular mechanics. Bull Philadelphia Phys Soc 2 32-43 Shroff SG, Janicki JS, Weber KT (1983b) Left ventricular systolic dynamics in terms of its chamber mechanical properties. Am J Physiol 245 H110-H124 Shroff SG, Weber KT, Janicki JS (1984) End systolic relations Their usefulness and limitations in assessing left ventricular contractile state. Int J Cardiol 5 253-259 Suga H, Sagawa K, Shoukas AA (1973) Load independence of the instantaneous pressure-volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ Res 32 314-322... 

Practitioners must have a good understanding of cardiovascular physiology to diagnose, treat, and monitor circulatory problems in critically ill patients. Eugene Braunwald, a renowned cardiologist, described the interrelationships between the major hemodynamic variables (Fig. 10-1).1 These variables include arterial blood pressure, cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR), stroke volume (SV), left ventricular size, afterload, myocardial contractility, and preload. While an oversim-... 

Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states). 

A clinically useful indirect estimate of Mvo2 is the double product (DP), which is HR multiplied by systolic blood pressure (SBP) (DP = HR xSBP). The DP does not consider changes in contractility (an independent variable), and because only changes in pressure are considered, volume loading of the left ventricle and increased MVo2 related to ventricular dilation are underestimated. 

Factors determining oxygen demand. The heart muscle cell consumes the most energy to generate contractile force. O2 demand rises with an increase in (1) heart rate, (2) contraction velocity, (3) systolic wall tension ( afterload ). The latter depends on ventricular volume and the systolic pressure needed to empty the ventricle. As peripheral resistance increases, aortic pressure rises, hence the resistance against which ventricular blood is ejected. O2 demand is lowered by 3-blockers and Ca-antago-nists, as well as by nitrates (p. 308). 

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little. 

The most prominent effect of halothane on the circulation is a dose-related decrease in arterial blood pressure. This is due mainly to reduced myocardial contractility and ventricular slowing. Cardiac output falls due to a decrease in stroke volume and bradycardia. Systemic vascular resistance also falls but this is less pronounced than with some other agents. Although halothane reduces myocardial oxygen consumption it also reduces oxygen demand and it is suitable for patients with myocardial ischaemia. 

Dobutamine is widely used to increase myocardial contractility, cardiac output, and stroke volume in the peri-operative period. It is less likely to increase heart rate than dopamine. There is evidence that dobutamine can increase both myocardial contractility and coronary blood flow. This makes it particularly suitable for use in patients with acute myocardial infarction. Dobutamine is also suitable for treating septic shock associated with increased filling pressures and impaired ventricular function. Owing to the competing a and 3 activity there is usually little change in mean arterial pressure. 

Decreased venous return to the heart and the resulting reduction of intracardiac volume are important beneficial hemodynamic effects of nitrate. Arterial pressure also decreases. Decreased intraventricular pressure and left ventricular volume are associated with decreased wall tension (Laplace relation) and decreased myocardial oxygen requirement. In rare instances, a paradoxical increase in myocardial oxygen demand may occur as a result of excessive reflex tachycardia and increased contractility. 

All three of the drug groups currently approved for use in angina (organic nitrates, calcium channel blockers, and 3-blockers) decrease myocardial oxygen requirement by decreasing the determinants of oxygen demand (heart rate, ventricular volume, blood pressure, and contractility). In some... 

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