Lecture 19.1 Cardiac Output & Sympathetic Activation PDF

Summary

This document provides an overview of cardiac output, the autonomic nervous system, and shock. It covers the conduction system of the heart, sympathetic and parasympathetic nervous system functions, and factors affecting stroke volume. The document is well-structured for educational purposes.

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Lecture 19.1: Cardiac output, the autonomic nervous system, and shock Introduction This review document will highlight some previously taught material about the heart’s conduction system, how the sympathetic and parasympathetic nervous systems modify cardiac output, and how cardiac output...

Lecture 19.1: Cardiac output, the autonomic nervous system, and shock Introduction This review document will highlight some previously taught material about the heart’s conduction system, how the sympathetic and parasympathetic nervous systems modify cardiac output, and how cardiac output is related to blood pressure. We will begin this discussion with a short overview of the autonomic nervous system. Autonomic nervous system Recall the central nervous system is the integration, interpretation, and coordination system of the NERVOUS SYSTEM; it includes the brain and spinal cord. The peripheral nervous system includes the cranial nerves and spinal nerves coming off the brain and spinal cord, respectively. The peripheral nervous structures are those that: - carry sensory signals to the brain and spinal cord and - carry motor signals from the brain and spinal cord to the body’s effectors (skeletal muscle, cardiac muscle, smooth muscle, glands, etc.). For this reason, the peripheral nervous system is divided into the afferent nervous system (which deals with ALL sensory signals) and the efferent nervous system (which deals with ALL motor signals). The efferent nervous system is further divided based on which effectors are being stimulated, voluntary effectors (i.e. skeletal muscles) or involuntary effectors (i.e. every other effector); hence, it is further categorized as the somatic nervous system and the autonomic nervous system, respectively. Peripheral nervous system Afferent: Sensory Efferent: Motor Voluntary: somatic involuntary: autonomic 1 The autonomic nervous system is continually active, and it is the antagonizing activity of its two subdivisions that set much of the activity of our involuntary effectors; heart, diameter of our respiratory passageways, blood vessel tone, level of alertness, digestive and urinary activity, salivary and lacrimal secretion, and mobilization of energy reserves.out of control The parasympathetic nervous system is more active when we are at rest. The nerves that control the rest-and-digest processes, namely salivation, lacrimation, urination, digestion, and defecation, come off the brain (cranial nerves III, VII, IX, and X) and the sacral portion of the spinal cord. The sympathetic nervous system is mostly active when we are experiencing a stressful or dangerous situation. The nerves that control the fight-or-flight processes, namely increasing the heart rate, increasing our ventilation rate, elevating muscle tone, mobilizing our energy reserves, and secreting adrenaline and noradrenaline, come off the thoracic and lumbar portions of the spinal cord. The nerves that send signals to the heart to increase its rate of contraction (heart rate) and strength of contraction (stroke volume) come off the thoracic spinal cord. To increase heart rate, these nerves communicate with the sinoatrial node and atrioventricular node, and to increase contraction strength, these nerves communicate with the atrial and ventricular cardiac muscle cells. 2 Cardiac output Cardiac output is defined as the volume of blood moved per minute. You can calculate cardiac output by multiplying heart rate (beats per minute; HR) by stroke volume (milliliters per beat; SV). Our body is constantly adjusting cardiac output to maintain our blood pressure. Changes in osmolarity cause water to move between the extracellular and intracellular compartments, and these changes are easily compensated for by adjusting HR or SV to ensure blood pressure remains stable. Large changes in blood pressure not only require large changes in HR and SV but also endocrine compensation (i.e. renin-angiotensin-aldosterone or natriuretic peptides). How does the heart maintain its rhythmic contractions? The sinoatrial node depolarizes on its own (at a rate of ~80 beats per minute); this causes an electrical signal to travel along the walls of the atria via the internodal pathways to reach the atrioventricular node. At this node, the signal is delayed, as these cells depolarize at a slower rate (this delay is necessary to allow the atria to finish contracting before the ventricles begin their contraction event). The signal continues along the atrioventricular (AV) bundle and bundle branches along the interventricular septum and up the walls of the ventricles along the Purkinje fibers. How do the nerves of the sympathetic nervous system stimulate an increase in heart rate via the SA and AV nodes? By transmitting norepinephrine onto the cells of these nodes, thereby increasing their rate of self-depolarization. What factors affect stroke volume and how can they be manipulated to increase or decrease stroke volume? Stroke volume is the amount of blood pushed out of the ventricle during systole, and it depends on end diastolic volume (i.e. the volume of blood in the ventricles at the end of diastole) and end systolic volume (i.e. the volume of blood leftover in the ventricles after systole); stroke volume is the volume measured by subtracting these two volumes. Manipulating end diastolic volume is primarily responsible for influencing stroke volume. What physiological factors affect end diastolic volume? Adequate venous pressure ensures the ventricles fill with enough blood, while inadequate venous pressure causes a decrease in this volume. Ventricular hypertrophy (as during heart failure) thickens the walls of the heart and shrinks the available space in the ventricles, limiting this volume. What physiological factors affect end systolic volume? Contractility of the ventricles ensures as much blood is pushed out of the heart during systole; this means greater contractility ensures less end systolic volume. Increased arterial pressure can make it difficult for blood to enter the aorta after ventricular contraction, thereby increasing this volume, so maintaining an appropriate arterial pressure ensures this volume remains low. An interesting heart reflex is the ventricular blood reflex which triggers an increase in contractility as end diastolic volume increases; this ensures that stroke volume is maximized. How is blood pressure related to cardiac output? Blood pressure is positively correlated to heart rate, stroke volume, and vascular resistance; this means increasing any of these factors will increase blood pressure, and decreasing any of these factors will decrease blood pressure. 3 Introduction to shock Shock is defined as a failure of the circulatory system to supply the tissues and organs with an adequate supply of blood. The complications of shock manifest from hypoxia, while its signs and symptoms commonly include hypotension and hypoperfusion. Initially, vital signs may appear normal as the body compensates; cardiac output, blood pressure, and tissue perfusion are maintained. However, when heart rate can no longer maintain blood pressure, and thus tissue perfusion, decompensation occurs. The complications of shock are determined by the severity and duration of hypoxia on the cells, as this will influence the development of morbidities (i.e. sequelae) and the survival rate. Recall that when tissues are properly perfused, oxygen and nutrients are adequately supplied, so pyruvate is metabolized aerobically in the mitochondria. When hypoperfusion occurs, oxygen and nutrients are inadequately supplied, and pyruvate is metabolized anaerobically; producing lactic acid. In severe forms of shock, metabolic acidosis occurs and ATP insufficiency impairs the Na+/K+ ion pump. Sodium becomes concentrated in the cells, and this causes cellular edema. The inability of other active pumps to work causes lysosomes to rupture and spill their contents, and cell death from necrosis triggers inflammatory cascades, while the production of reactive oxygen species damages other cells. How does the body compensate during shock? The two most prominent responses include activation of 1) the sympathetic nervous system and 2) the renin-angiotensinogen-aldosterone (RAA) system. Sympathetic activation is an acute response to increase cardiac output to maintain blood pressure, while the RAA system is a chronic response to increase blood pressure by retaining sodium and water retention and peripheral vasoconstriction. Sympathetic activation is common for three of the four types of shock, as distributive shock occurs due to a lack of blood vessel tone or loss of sympathetic activity. Shock progresses when the patient decompensates. We will examine shock further in lecture. 4 Review questions 1. Which divisions of the nervous system are responsible for the following events: You’re experiencing some anxiety while reviewing your anatomy notes, and your glossopharyngeal nerve monitors blood pressure in your aortic sinus, resulting in the contraction of smooth muscle in the walls of your blood vessels? 1. Afferent system sensory 2. Somatic efferent system 3. Sympathetic system fight or flight 4. Parasympathetic system A. 1 and 2 B. 1 and 3 C. 1 and 4 D. 2 and 4 E. 3 and 4 2. Which divisions of the nervous system are responsible for the following events: as you prepare lunch in your kitchen, your vestibulocochlear nerve detects a buzzing sound, resulting in you voluntarily turning your head towards the sound? 1. Afferent system 2. Somatic efferent system 3. Sympathetic system 4. Parasympathetic system A. 1 and 2 B. 1 and 3 C. 1 and 4 D. 2 and 4 E. 3 and 4 3. Blood reflexes, hormones, and neural centers can modify cardiac output (CO) when necessary. Modifying CO is important under different circumstances, and our body does so by manipulating our heart rate (HR) and stroke volume (SV). Which of the following conditions would ultimately DECREASE your CO? A. The cardiac reflex centers send signals along parasympathetic nerves. B. Sympathetic nerves stimulating the pacemaker cells C. More blood entering the ventricles to cause the ventricular reflex. D. A patient is administered a positive chronotrope. E. Norepinephrine release from the adrenal glands. 4. The conducting system of the heart includes some modified structures that allow the propagation of an electrical signal throughout the heart. Which of the following statements below is FALSE about this system? A. The cells of the SA node are self-excitatory as they gradually repolarize on their own, causing contraction. B. The signal arriving at the AV node is delayed in order to provide time for the atria to contract. C. The AV node sends signals down the AV bundle to the bundle branches towards the apex of the heart. D. The Purkinje fibers cause depolarization of the ventricular muscle cells to cause contraction. E. None of the above. 5 Answer key: B, A, A, A 6

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