The Breathing Rates in Standing and Supine Positions - Research Paper Example

Breathing paces on hemodynamic Breathing paces on hemodynamic Effects of different breathing paces on hemodynamic in human s:comparison of supine and standing positions Chapter 1: Introduction 1.1 General Background Rhythmic patterns analysis is a tool used in the assessment of the cardiac nervous activity balance. The variation of the heart rate determine the rhythmic patterns used to identify certain medical conditions. The medical conditions predicted include the myocardial infarction. The variability of heart rate has also been used in evaluation of the impacts of manipulated therapeutics (Hsia, 2009: 577). The concept has also been used in determining the link between body position and the cardiovascular system autonomic regulation. There have been several researches done that compare cardiovascular activity in prone and supine positions (Schulze, et al. 2013: 1). The main reason is because they are the commonly used positions during manual therapy. Comparison of the supine and standing positions have had deficiency in terms of research. The study therefore aims to redress the deficiency by comparing the breathing rates in standing and supine positions. 1.2 Autonomic Regulation of Cardiovascular System The autonomic nervous system help in the unconscious control of important organs like the blood vessels and the heart (Ellis and Thayer, 2010: 317). The autonomic control is due to the thin preganglionic fibers that are lightly myelinated. The fibers originate from central nervous system at the brainstem level or the sacral spinal cord (parasympathetic case) and lumbar or thoracic spinal cord (sympathetic case). The autonomic nervous system has a profound impact on the heart. The influence is based on its capability to change the cardiac rate that is known as chronotropy. The autonomic nervous system also has the modulation ability of the contraction (inotropy), relaxation (lusitropy) and conduction velocity commonly known as dromotropy. The dromotropic and chronotropic effects are controlled by both sympathetic and parasympathetic fibers from artrioventicular and sinoartrial nodes (Ma et al., 2009: 15950). The lusitropic and inotropic effects are caused mainly by the sympathetic fibers from ventricular and atrial myocytes. The parasympathetic fibers that travel in vagus nerve produce acetylocholine that activates the receptors (M2 Muscarinic acetylcholine). The receptors in return increase the conductance of the sinoartrial (SA) node and slow the conduction rate in the artrioventicular (AV) node. The effect of this is the slowing of the intrinsic rate of the heart. Sympathetic fibers produce norepinephrine that activates adenylate cyclase through binding with the β- adrenergic receptors. Other effects associated with it are intracellular cAMP increase and activation of PKA. The β- adrenergic receptors are in two forms: β1-adrenergic receptor and β2-adrenergic receptor. The β1-adrenergic receptor partners with the protein heterotrimeric G2 and is the main reason for the increase in cAMP concentrations. β2- adrenergic receptor role is more complex and it partners with both the G1 and G2 proteins. The β-adrenergic receptors activation leads to the increase of the diastolic depolarization slope in sinoartrial node. In return, the artrioventicular node conduction is increased thus increasing the heart rate (Liu and Wate, 2014: 403). For the case of myocytes, it increases the membrane’s Ca2+ currents and releases Ca2+ from the SR (sarcoplasmic reticulum) whenever there is an action potential. The result of this is increased force of production. The reuptake of the Ca2+ into the sarcoplasmic reticulum is increased therefore accelerating relaxation. The lusitropic and inotropic effects of the sympathetic stimulation brought together increases the volume of stroke. The autonomic nerves have therefore the ability to control both the stroke volume and cardiac rate. They provide vital remote mechanism that helps in the rapid adjustment of the cardiac output. The rapid adjustments help the heart to meet the short term dynamics to the needs of the body. Humans have more vagal discharge compared to the tonic sympathetic discharge amount. The effect of the tonic activities leads to the resting rate of the heart that is approximately 30% lower compared to intrinsic rate (90 to 100 beats per minute). The interplay also results in a cardiac output that is approximately 30% higher compared to when sympathetic discharge is absent (Thomas, 2011: 29). Increased vagal discharge further decreases the heart rate and reduces the cardiac output. However, increased sympathetic discharge increases stroke volume and heart rate and also increased the cardiac output. Conversely, reduction of the sympathetic discharge or tonic vagal has effects that are opposing to decrease or increase in cardiac output respectively. Figure 1: Autonomic Control of the Cardiovascular Function Source: Purves et al. 2001: 56 1.2.1 Baroreceptors, Pulmonary Receptors and Chemoreceptors Cardiovascular system is accurate when it comes to regulation of reflexes. Therefore, there is reliability in the supply of appropriate oxygenated blood supply in different circumstances. The homeostatic process is critically monitored by the mechanical information primarily (Kortepeter et al., 2011: 1000). The chemical information that is secondary in the system determines the level of carbon (iv) oxide and oxygen in the blood. The mechanical process is known as barosensory while the chemical process is known as chemosensory. Barosensory and chemosensory are determined by baroreceptors and chemosensory, respectively. The sympathetic and parasympathetic activities that are cardiovascular control relevant are determined by the data provided by the sensors. Baroreceptors are sensors found in the blood vessels of all vertebrates. They are located mainly in the medial wall of the carotid sinus connecting vagal nerves and the glossopharyngeal. Their role is to sense blood pressure and pass the information to the brain for the maintenance of the blood pressure (Condliffe et al., 2012: 21). They are mechanoreceptor sensory neuron kind that is made active by the blood vessel stretch. Increase in pressure in the blood vessels therefore triggers the generation of action potential thus providing information to the nervous system. The sensory data provided is used for autonomic reflexes primarily which in turn influences the cardiac output. The smooth muscles (vascular) are also influenced thus leading to total peripheral resistance. The baroreceptors in return act immediately in the form of negative feedback known as baroflex. It therefore takes the blood pressure levels to normal. The reflexes helps in the regulation of the blood pressure in short term. Baroreceptors can be categorized into two depending on the type of the blood vessel type. The categories are: low pressure and high pressure arterial baroreceptors that are also known as volume and cardiopulmonary receptors. The cardiopulmonary stretch receptors are located in the pulmonary vessels, ventricles atria and the lungs. Pulmonary (including lung) receptors influence the cardiovascular system during the abnormal circumstances (Geelhoed and Jaddoe, 2010: 678). Juxtapulmonary capillary receptors that are linked to non- modulated vagal afferents are normally influenced by the congestion at the pulmonary. The result is depression of somatic nervous system, reflex bradycardia and tachypnea. According to Shepherd (1989: 1), activation of the mechanoreceptotors found in pulmonary arteries by a pressure not above 60 mmHg cause occasional bradycardia and systematic hypotension. Increase in pressure increases the systematic pressure. Some of the mechanoreceptors that are found in the lung’s parenchyma have medullated fibers that pass to the spinal cord through the sympathetic nerves. Inflation of the lungs increases the discharge of the mechanoreceptors. The chemoreceptors can be divided into two: peripheral (aortic and carotid bodies) and central chemoreceptors that are medullary neurons. Their primary function is the regulation of the respiratory activity. Chemoreceptors help in the maintenance of the arterial blood PCO2, pH and PO2 at physical ranges that are appropriate (Abman et al., 2014: 424). For example, acute reduction of arterial PO2, known as hypoxemia, or increase in PCO2 (arterial) that is known as hypercapnia increases the depth and rate of respiration. The increase is due to the activation of chemoreceptor reflex. Chemoreceptor activities affect the function of the cardiovascular either indirectly or directly. The indirect effects are through the activity of the pulmonary stretch receptor. The direct effects are due to it interaction with the centers of the medullary vasomotor. Impaired exchange of gas in the lungs can be caused by respiratory arrest, hyperventilation, pulmonary embolism, and pulmonary edema among other causes. Its effects include decrease of the arterial pH and PO2 and increase on arterial PCO2. The changes stimulate the activities of the chemoreceptors thus improving the sympathetic outflow to the vasculature and heart. The outflow to these organs is made possible via the rostral ventolateral medulla. The cerebral ischemia role is to activate the central chemoreceptors in a way that vagal and sympathetic are simultaneously activated (Hansen, Sourjik and Wingreen, 2010: 17170). 1.2.2 Bainbridge Effects Similar to the baroreceptor reflex, Bainbridge reflex also controls the heart rate. Bainbridge reflex controls the heart rate through responding to blood volume. Experiments show that the Bainbridge effects are common among the primates. Evidence shows that it occurs among humans as well. Such a scenario can be explained through putting back the ulteroplacental blood to the mother’s circulation after delivery resulting in tachycardia. Increase in the venous return increases the inferior and superior vena cava pressures. It therefore results in the increase in right atrium pressure which in turn stimulates the receptor zones of low pressure (atrial stretch receptor). The receptors react through signaling the control centers of the medullary to increase heart rate, commonly known as Tachycardia. The sympathetic activity to SAN (sinoatrial node) mediates the tachycardia while the parasympathetic activity is maintained (Wu et al., 2009: 5972). Bainbridge reflex helps in the venous return. Heart rate increase helps by reducing the pressure at the inferior and superior vena cava through the drawing of extra blood out of right atrium. The action results in the decrease in the pressure that was in the venous. The process continues until the blood pressure at the right atrium returns to levels that are normal. The return of pressure to normal level ensures that the heart rate is decreased to the original level (Nicholls and Paton, 2009: 2447). Brainbridge reflex is also associated with the Respiartory Sinus Arrhythmia. The inhalation process leads to decrease in the intrathoracic pressure. It activates the increase of venous return which is detected by the stretch receptors. The stretch receptors via the Bainbridge reflex during inspiration increases momentarily the heart rate (Pelster et al., 2010: 775). 1.3 General Cardiovascular Responses to Breathing According to Laude et al (1993: 619), heart rate increases with during inspiration. The increase in heart rate is characterized by the delay of the breathing frequency and tidal volume by approximately 0.9 seconds. The respiratory sinus arrhythmia’s magnitude increases with the increase of tidal volume and decrease in breathing frequency. Systolic blood pressure increases with the increase in the tidal volume. Increase in the amplitudes of systolic blood pressure and respiratory sinus arrhythmia variation takes place at the lowest level of the breathing frequency. Systolic blood pressure decreases with decrease in inspiration. Respiratory effects on systolic blood pressure are caused by several mechanisms added to changes in the heart rate. 1.4 Changes in Breathing and Cardiovascular Function According to Turankar et al (2013: 916) slow breathing improves respiratory and cardiovascular functions and reduces the effects associated with stress. Breathing patterns change when we are asleep with it being more regular. The activities that we do when we are awake make the breathing system irregular. The activities include emotions, speech, posture, and exercise among others. Progress from the wakefulness state to non- REM sleeping stage is characterized by the breathing rate becoming more regular and decreases slightly. During the REM sleep, the breathing rate is normally increased with the pattern becoming more variable. During non- REM sleep stage, the heart has a chance to rest after vigorous activities done. In this stage blood pressure and heart rate decreases. REM sleep stage is characterized by increased variation in the cardiovascular activity thus increase in heart rate and blood pressure. The blood flow changes that cause erections among males and clitoris swell among females is caused by REM sleep (Bernardi et al, 2001: 1446). 1.5 Aims of the study The overall aim of the study is to determine the different breathing paces on the hemodynamic in human subjects by comparison of supine and standing positions. There are a number of specific objectives involved. The first one is investigate the breathing rate of hemodynamic in supine human subjects. The second one is determine the breathing rate of hemodynamic in human subjects at standing postures. The third one is compare the breathing rate between the standing and supine human subjects. The last one is identify the factors that lead to the difference in the breathing rate between the supine and standing human subjects. References Abman, S. H. et al. 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