Stroke volume

Isoflurane is a respiratory depressant (71). At concentrations which are associated with surgical levels of anesthesia, there is Htde or no depression of myocardial function. In experimental animals, isoflurane is the safest of the oral clinical agents (72). Cardiac output is maintained despite a decrease in stroke volume. This is usually because of an increase in heart rate. The decrease in blood pressure can be used to produce "deHberate hypotension" necessary for some intracranial procedures (73). This agent produces less sensitization of the human heart to epinephrine relative to the other inhaled anesthetics. Isoflurane potentiates the action of neuromuscular blockers and when used alone can produce sufficient muscle relaxation (74). Of all the inhaled agents currently in use, isoflurane is metabolized to the least extent (75). Unlike halothane, isoflurane does not appear to produce Hver injury and unlike methoxyflurane, isoflurane is not associated with renal toxicity. 

Glonidine. Clonidine decreases blood pressure, heart rate, cardiac output, stroke volume, and total peripheral resistance. It activates central a2 adrenoceptors ia the brainstem vasomotor center and produces a prolonged hypotensive response. Clonidine, most efficaciously used concomitantly with a diuretic in long-term treatment, decreases renin and aldosterone secretion. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

MAINTAINING CARDIAC OUTPUT. The heart rate and stroke volume determine cardiac output. The stroke volume is determined in part by the contractile state of the heart and the amount of blood in the ventricle available to be pumped out. The interventions listed above help to support the cardiac output of the patient in shock. 

A basic grasp of normal cardiac function sets the stage for understanding the pathophysiologic processes leading to HF and selecting appropriate therapy for HF. Cardiac output is defined as the volume of blood ejected per unit of time (liters per minute) and is a major determinant of tissue perfusion. Cardiac output is the product of heart rate (HR) and stroke volume (SV) CO = HR x SV. The following describes how each parameter relates to CO. 

Increased preload (through Optimize stroke volume via Pulmonary and systemic congestion... 

Vasoconstriction Maintain blood pressure and perfusion in the face of reduced cardiac output Increased MV02 Increased afterload decreases stroke volume and further activates the compensatory responses... 

Stroke volume index 30-65 mL/beat per square meter... 

Other symptoms are dependent on the degree to which cardiac output is diminished, which is in turn dependent on the heart rate and the degree to which stroke volume is reduced by the rapidly beating heart. 

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-... 

Cardiac output The volume of blood ejected from the left side of the heart per unit of time [cardiac output (L/minute) = stroke volume x heart rate]. 

Frank-Starling mechanism The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. 

Pulmonary artery catheter An invasive device used to measure hemodynamic parameters directly, including cardiac output and pulmonary artery occlusion pressure calculated parameters include stroke volume and systemic vascular resistance. 

Stroke volume The amount of blood ejected from the heart during systole. 

Discuss the factors that control stroke volume... 

The primary function of the heart is to deliver a sufficient volume of blood (oxygen and nutrients, etc.) to the tissues so that they may carry out their functions effectively. As the metabolic activity of a tissue varies, so will its need for blood. An important factor involved in meeting this demand is cardiac output (CO) or the volume of blood pumped into the aorta per minute. Cardiac output is determined by heart rate multiplied by stroke volume ... 

Cardiac output (CO) = heart rate (HR) x stroke volume (SV)... 

An average adult at rest may have a heart rate of 70 beats per minute and a stroke volume of 70 ml per beat. In this case, the cardiac output would be ... 

Many factors contribute to the regulation of stroke volume. Factors discussed in this section include ... 

It is this reduction in preload that, in some cases, is beneficial to patients experiencing heart failure or hypertension. Unlike a healthy heart, a failing heart is unable to pump all of the blood returned to it. Instead, the blood dams up and overfills the chambers of the heart. This results in congestion and increased pressures in the heart and venous system and the formation of peripheral edema. Because the failing heart is operating on the flat portion of a depressed cardiac function curve (see Figure 14.2), treatment with diuretics will relieve the congestion and edema, but have little effect on stroke volume and cardiac output. 

Hypertension (blood pressure >140/90 mmHg) may be caused by an elevation in cardiac output or excessive vasoconstriction. Diuretics are used in these patients to reduce cardiac output. Assume that the hearts of these individuals are operating on the ascending portion of the cardiac function curve. As the plasma volume is reduced in response to treatment with diuretic drugs, venous return and preload are reduced, as are ventricular filling and stroke volume, and cardiac output, thus bringing blood pressure back within the normal range. 

The contractility of the myocardium determines the ejection fraction of the heart, which is the ratio of the volume of blood ejected from the left ventricle per beat (stroke volume) to the volume of blood in the left ventricle at the end of diastole (end-diastolic volume) ... 

Under normal resting conditions in which the end-diastolic volume is 120 to 130 ml and the stroke volume is 70 ml/beat, the ejection fraction is 55 to 60% ... 

During exercise when sympathetic stimulation to the heart is increased, the ejection fraction may increase to more than 80% resulting in greater stroke volume and cardiac output. 

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