Ch 13 part 3.docx

Ch 13 part 3 Control of Cardiac Output Since the cardiac output is determined solely by the heart rate and stroke volume, any change in either of these variables will highly impact the cardiac output. Like most organs, the heart is regulated by intrinsic and extrinsic control mechanisms, and these a...

Ch 13 part 3 Control of Cardiac Output Since the cardiac output is determined solely by the heart rate and stroke volume, any change in either of these variables will highly impact the cardiac output. Like most organs, the heart is regulated by intrinsic and extrinsic control mechanisms, and these are what produce the changes in cardiac output. Extrinsic control is the control exerted by something outside of the heart, such as the nervous system or hormones. Intrinsic control is a term for autoregulation, where the subject matter controls its own changes. For example, intrinsic control occurs when sarcomeres change their length. Remember that the heart is myogenic, so contractions are triggered from within, and not from the nervous system. However, the nervous system can influence the rate and force of contractions by altering the heart rate and stroke volume. Recall that the autonomic nervous system is divided into two components: The sympathetic nervous system, which is responsible for the body's "flight-or-fight" response. As part of this response, the sympathetic nervous system speeds the heart up. Sympathetic innervation of the heart comes from the cardiac accelerator nerves. The parasympathetic nervous system,which is responsible for the body's "rest and digest" response. As part of this response, the parasympathetic nervous system slows the heart down. Parasympathetic innervation of the heart comes from the vagus nerve. There is both sympathetic and parasympathetic innervation of the SA and AV nodes. The sympathetic nervous system innervates the myocardium and the pacemaker cells, whereas the parasympathetic nervous system only innervates the pacemaker cells. Therefore, the parasympathetic nervous system is only able to slow down heart rate because none of its cells innervate the muscle cells in the heart wall. This is unlike the sympathetic nervous system, which can impact both heart rate and stroke volume. At rest, the heart rate is under more parasympathetic control than sympathetic control because, at rest, the heart has higher vagal tone. If you were to remove all of the innervation of the heart, you would find that it beats faster than normal. For example, if the average adult resting heart rate is 72 beats per minute, removing both sympathetic and parasympathetic innervation might cause the heart to beat between 100 and 110 beats per minute. Recall that the heart's cardiac output depends on both heart rate and stroke volume. A change in either of these will cause a change in cardiac volume. Below, we will examine the factors that could affect heart rate or stroke volume. Factors that Affect Heart Rate The body's heart rate is regulated entirely by extrinsic factors. Both the parasympathetic nervous system and the sympathetic nervous system play a role in neural control of the heart rate; the sympathetic nervous system increases heart rate by depolarizing the pacemaker cells of the SA node, whereas the parasympathetic nervous system slows the heart rate by hyperpolarizing these same pacemaker cells. In addition to neural control, there is also a degree of hormonal control that affects heart rate. The heart rate increases when the heart is exposed to epinephrine (also called adrenaline), a hormone produced by the adrenal medulla. This explains the "adrenaline rush" experienced while riding a rollercoaster that results in a foster heart rate; your heart has been exposed to epinephrine, which serves much the same purpose as the sympathetic nervous system and speeds up the heart's rate of contraction. EXAM TIP: Heart rate is exclusively regulated via extrinsic mechanisms. Factors that Affect Stroke Volume There are three main factors that contribute to the ongoing regulation of stroke volume: 1. End diastolic volume is the maximum amount of blood that fills the heart during diastole. There is a very obvious, but important, rule associated with end diastolic volume: Starling's Law of the Heart, which states that when the rate at which blood flows into the heart from the veins changes, the heart automatically adjusts its output to match the inflow. Basically, this means the more that goes into the heart, the more it expels. This law is expressed in the Starling curve, which shows that an increase in end-diastolic volume will cause an increase in stroke volume, and vice versa. (The Starling curve is sometimes simply referred to as the length-tension curve for the myocardium.) Stroke volume increases when end-diastolic volume increases because the cardiac muscle fibers contract more forcefully when they are stretched out. Ventricular contraction is under both extrinsic and intrinsic control: o Extrinsic control - Innervation by the sympathetic nervous system affects ventricular contraction. Increased sympathetic activity increases stroke volume, shifting the entire Starling curve up. Decreased sympathetic activity decreases stroke volume, shifting the entire Starling curve down. Circulating epinephrine also affects ventricular contraction. Note that the parasympathetic nervous system is not involved in extrinsic control of stroke volume. Remember that only the sympathetic nervous system innervates the myocardium! o Intrinsic control - When the end-diastolic volume is greater, the myocardium stretches out. This increases contractility and thus increases the stroke volume. End diastolic volume is primarily determined by the end diastolic pressure (or preload). It is called preload because the load an the myocardium is increased as ventricular blood volume increases, and this all occurs before the contraction. Preload is affected by a couple of factors, including tilling time and atrial pressure. o Filling time, which is determined by the heart rate, affects the preload immensely. The faster a heart beats, the less time there is for ventricular filling, and the smaller is the preload (and end-diastolic volume). So, for example, at a heart rate of 60, diastole lasts 0.6 seconds. However, at a heart rate of 180, diastole will only last 0.1 seconds. o Atrial pressure affects preload because an increased atrial pressure will result in an increased atrial contractility, which will then cause an increase in ventricular filling. This is essentially an increased preload. 2. Ventricular contractility is the ventricle's capacity to generate force. Any factor which causes the ventricles to contract with more force will increase the stroke volume. Increased contractility, then, refers to the increased force at any given end diastolic volume. Obviously, increasing the amount of blood in the ventricle would stretch it out, putting the sarcomeres of their ideal length, and allowing them to contract with a greater force. When we talk about contractility, however, we are referring to the increased force generated for any given end diastolic volume. Without changing the end diastolic volume, how can we increase the force at contractions? We can do so through sympathetic innervation and circulating epinephrine. Epinephrine and norepinephrine (two catecholamines) bind to beta-1 adrenergic receptors in the heart, increasing cAMP (which, recall, is a second messenger) and the rate of crossbridge cycling. This enhances the presence of Ca2+ and results in an increased contractility at that end-diastolic volume. 3. Afterload is the pressure that the ventricles have to work against to expel blood from the heart. Stroke volume depends not only on the force-generating capacity of the ventricles, but also on the force that it has to work against. The pressure generated by the heart to pump blood out is impacted by the pressure of the arteries-this is the afterload. Afterload, therefore, increases as mean arterial pressure (MAP) increases. As MAP increases and vascular pressure rises, the heart has to work harder and harder to get the same amount of blood out and meet the demands of the body. To demonstrate the idea of afterload, think about someone pushing a boulder up a steep hill. In this analogy, the person is like the ventricles pushing blood through the blood vessels, and gravity is the afterload, which is opposing the force. Hypertension-high blood pressure - is sometimes called the "silent killer" because it has few visible symptoms before it causes a major problem, like a heart attack. Hypertension is so dangerous because it makes the heart pump harder to get the same volume of blood to the rest of the body. This puts stress on the heart, particularly during exercise or strenuous physical activity. Summary of Factors Affecting Stroke Volume and cardiac output At the end of the chapter, Dr. Nguyen provided a very useful chart detailing how factors affect stroke volume and cardiac output. Factors Affecting Stroke Volume An increased venous return will result in an increased end diastolic volume, which causes a rise in stroke volume. Also, an increase in sympathetic activity or epinephrine will stimulate an increased contractility, which will in turn cause an increase in stroke volume. Finally, a decreased arterial pressure or low afterload will cause an increased stroke volume. Factors Affecting Cardiac Output An increased activity of the sympathetic nervous system to the heart will cause both an increased stroke volume and heart rate (because of increased contractility), which will result in an overall increase in cardiac output. Likewise, a decrease in the activity of the parasympathetic nervous system will cause an increased cardiac output.

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