Applied cardiovascular physiology

Abstract

Maintaining an equilibrium between oxygen supply and demand is a principal function of the cardiovascular system. In times of altered metabolic demand, mechanisms exist to maintain the balance between supply and demand. Exercise, haemorrhage and pregnancy all lead to changes in oxygen demand and subsequently modification of cardiac output. During isotonic exercise, metabolic demands of muscle are greatly increased. Sympathetic stimulation and inhibition of the parasympathetic system lead to increases in heart rate and venous return, increasing cardiac output. This allows a proportional increase in blood flow to the exercising muscle. Cardiac output increases throughout pregnancy. In the first and second trimesters this rise is mainly due to an increase in stroke volume; however, during the later stages of pregnancy stroke volume reaches a plateau and further increase in cardiac output is mediated by a rising heart rate. In contrast, during haemorrhage, decreased venous return leads to a reduction in cardiac output, with a baroreceptor response due to the drop in arterial blood pressure. The tachycardia and vasoconstriction which follows are compensatory mechanisms in an attempt to preserve blood pressure. The Valsalva manoeuvre illustrates several aspects of reflex control of the cardiovascular system and allows non-invasive assessment and quantification of control mechanisms. Changes in stroke volume during the respiratory cycle can be used to predict fluid responsiveness and can be measured as pulse pressure variation or stroke volume variation.

Learning objectives

After reading this article, you should be able to:
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explain the mechanisms controlling cardiac output during isotonic and isometric exercise
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describe the changes in cardiovascular physiology which occur during pregnancy
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discuss the cardiovascular response seen in acute haemorrhage
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contrast the physiological mechanisms used to increase cardiac output during haemorrhage and exercise
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explain the Valsalva manoeuvre and draw the physiological responses in heart rate and blood pressure corresponding to each phase
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understand how the heart and lungs interact during the respiratory cycle to change stroke volume and predict fluid responsiveness

The autonomic nervous system effects cardiac output, primarily via heart rate modulation. At rest, sympathetic and parasympathetic nervous systems are in balance. The vagus nerve originates in the medulla and innervates the sinoatrial (SA) and atrioventricular (AV) nodes. Acetylcholine acts as the neurotransmitter. Parasympathetic stimulation leads to decreased activity of the SA and AV nodes, decreasing heart rate. This baseline parasympathetic activity is known as vagal tone. The sympathetic nerves arise from the thoracolumbar spinal cord and innervate the SA node and ventricular muscle mass. The nerves release norepinephrine as the neurotransmitter. The response is an increase in heart rate and an increased force of contractility of the ventricles.

Stroke volume is governed by end-diastolic volume (preload), afterload and the strength of ventricular contraction. When end-diastolic volume (the preload) increases, the stroke volume increases. With this increased end-diastolic volume, a slight stretching of the cardiac muscle fibres also occurs, which increases the force of contraction. This is the Frank–Starling law.

Afterload is left ventricular wall stress during ejection, which in most circumstances is a measurement equivalent to the blood pressure (BP) in the aorta. The stroke volume has an inversely proportional relationship to the aortic BP.

Exercise

During exercise there is an increased metabolic load in the exercising muscles. In order to maintain the balance between oxygen supply and demand, several physiological mechanisms exist and sympathetic activity predominates. Initially, in anticipation of increased physical activity, there is a cortically mediated ‘central command’ response. This causes activation of the sympathetic nervous system and decreased parasympathetic outflow leading to an increase in heart rate prior to commencement of exercise. The next phase of the cardiovascular response is dependent upon whether the exercise is isometric (static) or isotonic (dynamic). In isometric exercise (when muscle fibre length remains static, such as during weight lifting), there is minimal change in stroke volume. Muscle contraction is sustained, causing occlusion of its own arterial supply and consequently, a marked increase in peripheral vascular resistance. This increase in vascular resistance raises both systolic and diastolic arterial blood pressures. Because BP is a major determinant of afterload, the left ventricular wall stress, and thus the cardiac workload, is significantly higher during static exercise compared with the cardiac workload achieved during dynamic exercise. In comparison, during isotonic exercise (when repeated shortening and lengthening of muscle occurs, for example in running or swimming), there is a marked increase in cardiac output via increases in heart rate and stroke volume ( Figure 1 ). Activation of the muscle pump greatly enhances venous return to the heart, which compensates for the reduced diastolic filling time resulting from the rise in heart rate. A decrease in oxygen concentration sensed by chemoreceptors located in the arch of the aorta and the carotid arteries and escalation of temperature leads to further sympathoactivation to allow increased oxygen delivery and reduction of internal core temperature. Epinephrine and norepinephrine released during exercise increase contractility via increased calcium influx through calcium channels in cardiac muscle membranes. This allows for greater myosin and actin interaction, increasing inotropy. During exercise, the afterload is reduced, which allows for an increase in stroke volume and therefore increased cardiac output.

Active skeletal muscle releases locally vasoactive substances such as adenosine, K ⁺ and acid metabolites which cause vasodilatation, capillary recruitment and redistribution of blood flow. Blood flow to the exercising muscle may increase more than tenfold. The resultant reduction in muscle vascular resistance is offset by an increased sympathetic drive to other vascular beds. Splanchnic, renal and initially skin blood flow are all decreased. As exercise progresses, cutaneous blood flow increases in order to facilitate heat loss and then falls again as exhaustion is approached. Blood flow to the myocardium is also increased to match metabolic demands ( Table 1 ).

Table 1

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