Stroke volume contractility

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. 

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-... 

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) ... 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

Stroke volume is itself dependent on the prevailing preload, afferload and contractility. 

Secondary hypotension is a sign of an underlying disease that should be treated first. If stroke volume is too low, as in heart failure, a cardiac glycoside can be given to increase myocardial contractility and stroke volume. When stroke volume is decreased due to insufficient blood volume, plasma substitutes will be helpful in treating blood loss, whereas aldosterone deficiency requires administration of a mineralocor-ticoid (e.g., fludrocortisone). The latter is the drug of choice for orthostatic hypotension due to autonomic failure. A parasympatholytic (or electrical pacemaker) can restore cardiac rate in bradycardia. 

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-... 

Halogenated hydrocarbon inhalation anesthetics may increase intracranial and CSF pressure. Cardiovascular effects include decreased myocardial contractility and stroke volume leading to lower arterial blood pressure. Malignant hyperthermia may occur with all inhalation anesthetics except nitrous oxide but has most commonly been seen with halothane. Especially halothane but probably also the other halogenated hydrocarbons have the potential for acute or chronic hepatic toxicity. Halothane has been almost completely replaced in modern anesthesia practice by newer agents. 

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. 

Eor many years the prevailing view was that p-blockers are contraindicated in CHE. The physiological rationale for not using 3-blockers in heart failure was certainly well founded. Heart failure patients have a decrease in cardiac output. Since cardiac output is a function of stroke volume times heart rate (CO = SV xHR), an increased heart rate would be necessary to maintain an adequate cardiac output in the presence of the relatively fixed decrease in stroke volume observed in CHE. A rapid increase in heart rate does play an important role in the physiological response to acute hemorrhage. Thus, a decrease in heart rate, along with a depression in contractility produced by p-blockers, would be expected to precipitate catastrophic decompensation and this certainly can happen in the acute setting. 

Mechanism of Action Adirect-acting inotropic agent acting primarily on beta,-adrenergic receptors. Therapeutic Effect Decreases preload and afterload, and enhances myocardial contractility, stroke volume, and cardiac output. Improves renal blood flow and urine output. 

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. 

Cardiovascular effects. Anaesthetic concentrations of isoflurane, i.e. 1-1.5 MAC, cause only a slight impairment of myocardial contractility and stroke volume and cardiac output is usually maintained... 

The three factors that regulate the stroke volume are preload, afterload and contractility ... 

Dofetilide has a small positive inotropic effect in animal hearts (15,33). In a double-blind, placebo-controlled study of oral dofetilide 125, 250, or 500 mg bd for the maintenance of sinus rhythm after cardioversion of sustained atrial fibrillation or flutter in 201 patients, there were small changes in echocardiographic measures of atrial contractility, but no changes in stroke volume or cardiac output (34). 

The function of the cardiovascular system is to maintain adequate tissue perfusion. Cardiac output is the product of heart rate (rhythm) and cardiac contractility (giving rise to stroke volume). These factors are under neuronal, hormonal and mechanical control systems. Pharmacological manipulation of any of these contributors will result in changes in cardiovascular function and hence peripheral blood flow. In human medicine, the primary goal is to increase life expectancy, while maintenance of performance and quality of life are the main priorities in equine medicine. 

Intravenous administration of berberine (20 mg/kg) to anesthetized rats was observed to increase the cardiac index and stroke volume index. In the isolated guinea pig left atria, berberine (0.1 pmol/L) shifted the dose-response curve of ouabain to the left with an increase of the maximal effect. The alkaloid (10 pmol/L and 30 pmol/L) potentiated the maximal contractile force of ouabain and diminished the dose at which ouabain produced its peak effect. Berberine (30 pmol/L and 100 pmol/L) elevated the dose in which the toxicity of ouabain occurred. The investigators concluded that berberine might increase the cardiac output and widen the safety margin with ouabain-treatment [249]. 

Heart rate is controlled by the autonomic nervous system. Stroke volume, or the volume of blood ejected during systole, depends on preload, afterload, and contractility. As defined by the Frank-Starling mechanism, the ability of the heart to alter the force of contraction... 

Although -blockers and calcium chaimel blockers have taken a more prominent role in acutely controlling rate in patients with rapid atrial fibrillation or flutter, a cautionary note must be made. That is, most patients with these tachycardias also have concomitant symptoms of heart failure, and these two forms of drug therapy may worsen the situation initially. Usually, a prompt decline in rate and increase in stroke volume balances the decrease in contractility seen with p blockers or calcium chaimel blockers such that heart failure symptoms remain unchanged. However, occasionally, severe reactions and hypotension may occur one study implies that diltiazem may be safer than verapamil. ... 

Heart Four-chamber dilation atrophic degeneration with necrosis and fibrosis myofibrillar disruption QT prolongation, low voltage, bradycardia decreased cardiac output, stroke volume, and contractility preload intolerance diminished responsiveness to drugs... 

The a2-adrenergic agonists lower arterial pressure by an effect on both cardiac output and peripheral resistance. In the supine position, when the sympathetic tone to the vasculature is low, the major effect is to reduce both heart rate and stroke volume however, in the upright position, when sympathetic outflow to the vasculature is normally increased, these drugs reduce vascular resistance. This action may lead to postural hypotension. The decrease in cardiac sympathetic tone leads to a reduction in myocardial contractility and heart rate this could promote CHF in susceptible patients. 

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