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Avon and Central Wheatbelt Primary Health provides health promotion services to Goomalling.
Health promotion officers support communities to improve their health by increasing knowledge and skills, creating opportunities for behavioural change, increasing social support and making changes to environments in our community.
Health promotion officers plan, deliver and assess the effectiveness of health promotion strategies working with local government, non-government organisations, businesses and community groups. Health includes mental, social, physical and spiritual wellbeing rather than simply the lack of disease.
The above percentages show that over 70% of our health is influenced by our lifestyle behaviours including what we eat and the environment in which we live, work and socialise.
For example, research has confirmed smoking cigarettes increases people’s risk of developing cardiovascular disease, type 2 diabetes, cancer, asthma and arthritis. For example, research shows people who drink excessive amounts of alcohol, are more likely to have poor mental health. Complete and send a Health Promotion Request Form, via fax or post to your local health promotion officer who will then contact you. If you have any difficulties completing the form, contact a local health promotion officer via phone to discuss your request. The autorhythmicity inherent in cardiac cells keeps the heart beating at a regular pace; however, the heart is regulated by and responds to outside influences as well. Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute.
SV is normally measured using an echocardiogram to record EDV and ESV, and calculating the difference: SV = EDV – ESV. SVs are also used to calculate ejection fraction, which is the portion of the blood that is pumped or ejected from the heart with each contraction. Maximum HRs are normally in the range of 200–220 bpm, although there are some extreme cases in which they may reach higher levels. Heart: Abnormal Heart Rates For an adult, normal resting HR will be in the range of 60–100 bpm. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. Initially, physiological conditions that cause HR to increase also trigger an increase in SV.
Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata ([link]).
Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart. Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The cardiovascular center receives input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria.
Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. Extreme stress from such life events as the death of a loved one, an emotional break up, loss of income, or foreclosure of a home may lead to a condition commonly referred to as broken heart syndrome. Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over HR. The catecholamines, epinephrine and NE, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. In general, increased levels of thyroid hormone, or thyroxin, increase cardiac rate and contractility.
Calcium ion levels have great impacts upon both HR and contractility; as the levels of calcium ions increase, so do HR and contractility. Although it is the world’s most widely consumed psychoactive drug, caffeine is legal and not regulated.
HR can be slowed when a person experiences altered sodium and potassium levels, hypoxia, acidosis, alkalosis, and hypothermia (see [link]). Acidosis is a condition in which excess hydrogen ions are present, and the patient’s blood expresses a low pH value. With increasing ventricular filling, both EDV or preload increase, and the cardiac muscle itself is stretched to a greater degree. The relationship between ventricular stretch and contraction has been stated in the well-known Frank-Starling mechanism or simply Starling’s Law of the Heart. Otto Frank (1865–1944) was a German physiologist; among his many published works are detailed studies of this important heart relationship.
Any sympathetic stimulation to the venous system will increase venous return to the heart, which contributes to ventricular filling, and EDV and preload. It is virtually impossible to consider preload or ESV without including an early mention of the concept of contractility.
Not surprisingly, sympathetic stimulation is a positive inotrope, whereas parasympathetic stimulation is a negative inotrope. Several synthetic drugs, including dopamine and isoproterenol, have been developed that mimic the effects of epinephrine and NE by stimulating the influx of calcium ions from the extracellular fluid.
Negative inotropic agents include hypoxia, acidosis, hyperkalemia, and a variety of synthetic drugs. Afterload refers to the tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system. SV is regulated by autonomic innervation and hormones, but also by filling time and venous return.
In a healthy young adult, what happens to cardiac output when heart rate increases above 160 bpm? Increasing EDV increases the sarcomeres’ lengths within the cardiac muscle cells, allowing more cross bridge formation between the myosin and actin and providing for a more powerful contraction.
Afterload represents the resistance within the arteries to the flow of blood ejected from the ventricles.
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Chronic conditions include cardiovascular disease, type 2 diabetes, cancers, asthma, mental illness, arthritis or becoming injured. It provides Nicotine Replacement Therapy advice, Fresh Start Groups and out-of-session motivational SMS or email messages. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by heart rate (HR), in contractions per minute (or beats per minute, bpm). SV can also be measured using a specialized catheter, but this is an invasive procedure and far more dangerous to the patient. Remember, however, that these numbers refer to CO from each ventricle separately, not the total for the heart.
SV can also increase from 70 to approximately 130 mL due to increased strength of contraction. Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above 100 bpm. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system. The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X.
The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles.
Some cardiac medications (for example, beta blockers) work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles.
Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances. During periods of stress, it is not unusual to identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol.

This condition may also be called Takotsubo cardiomyopathy, transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, Gebrochenes-Herz syndrome, and stress cardiomyopathy. The impact of thyroid hormone is typically of a much longer duration than that of the catecholamines. High levels of calcium ions (hypercalcemia) may be implicated in a short QT interval and a widened T wave in the ECG. Both of these nonregulated drugs have an excitatory effect on membranes of neurons in general and have a stimulatory effect on the cardiac centers specifically, causing an increase in HR. While precise quantities have not been established, “normal” consumption is not considered harmful to most people, although it may cause disruptions to sleep and acts as a diuretic. While legal and nonregulated, concerns about nicotine’s safety and documented links to respiratory and cardiac disease have resulted in warning labels on cigarette packages. The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Hypoxia (an insufficient supply of oxygen) leads to decreasing HRs, since metabolic reactions fueling heart contraction are restricted. Alkalosis is a condition in which there are too few hydrogen ions, and the patient’s blood has an elevated pH. Elevated body temperature is called hyperthermia, and suppressed body temperature is called hypothermia. While a number of variables are involved, SV is ultimately dependent upon the difference between EDV and ESV. At rest, there is little stretch of the ventricular muscle, and the sarcomeres remain short. This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. Ernest Starling (1866–1927) was an important English physiologist who also studied the heart. While much of the ventricular filling occurs while both atria and ventricles are in diastole, the contraction of the atria, the atrial kick, plays a crucial role by providing the last 20–30 percent of ventricular filling. Sympathetic stimulation triggers the release of NE at the neuromuscular junction from the cardiac nerves and also stimulates the adrenal cortex to secrete epinephrine and NE. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood.
Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation. Hemoglobin is the oxygen carrying pigment in the blood which is also responsible for its red color.
The table below outlines lifestyle behaviours that increase the risk of developing chronic conditions and injury. In addition, the heart is sensitive to several environmental factors, including electrolytes. This may be estimated by taking the maximal value of 220 bpm and subtracting the individual’s age. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction.
Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR.
Individuals experiencing extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. The recognized effects on the heart include congestive heart failure due to a profound weakening of the myocardium not related to lack of oxygen. After reading this section, the importance of maintaining homeostasis should become even more apparent. Epinephrine and NE have similar effects: binding to the beta-1 receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. The physiologically active form of thyroid hormone, T3 or triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. The QT interval represents the time from the start of depolarization to repolarization of the ventricles, and includes the period of ventricular systole. Caffeine works by increasing the rates of depolarization at the SA node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.
Its consumption by pregnant women is cautioned against, although no evidence of negative effects has been confirmed.
One of the primary factors to consider is filling time, or the duration of ventricular diastole during which filling occurs. With increased ventricular filling, the ventricular muscle is increasingly stretched and the sarcomere length increases.
This means that the greater the stretch of the ventricular muscle (within limits), the more powerful the contraction is, which in turn increases SV. Contractility refers to the force of the contraction of the heart muscle, which controls SV, and is the primary parameter for impacting ESV. In addition to their stimulatory effects on HR, they also bind to both alpha and beta receptors on the cardiac muscle cell membrane to increase metabolic rate and the force of contraction. Early beta blocker drugs include propranolol and pronethalol, and are credited with revolutionizing treatment of cardiac patients experiencing angina pectoris. Damage to the valves, such as stenosis, which makes them harder to open will also increase afterload. There are several feedback loops that contribute to maintaining homeostasis dependent upon activity levels, such as the atrial reflex, which is determined by venous return. In order for the heart to maintain adequate flow to overcome increasing afterload, it must pump more forcefully. There are several important variables, including size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload or EDV, and afterload or resistance.
So a 40-year-old individual would be expected to hit a maximum rate of approximately 180, and a 60-year-old person would achieve a HR of 160.
If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting (syncope). Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE) at the neuromuscular junction of the cardiac nerves. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. This may lead to acute heart failure, lethal arrhythmias, or even the rupture of a ventricle.
The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. It also impacts the beta adrenergic response similar to epinephrine and NE described above. Tolerance and even physical and mental addiction to the drug result in individuals who routinely consume the substance. Initially, both hyponatremia (low sodium levels) and hypernatremia (high sodium levels) may lead to tachycardia. Recall that enzymes are the regulators or catalysts of virtually all biochemical reactions; they are sensitive to pH and will change shape slightly with values outside their normal range.
The more rapidly the heart contracts, the shorter the filling time becomes, and the lower the EDV and preload are. As the sarcomeres reach their optimal lengths, they will contract more powerfully, because more of the myosin heads can bind to the actin on the thin filaments, forming cross bridges and increasing the strength of contraction and SV. This combination of actions has the net effect of increasing SV and leaving a smaller residual ESV in the ventricles. The drug digitalis lowers HR and increases the strength of the contraction, acting as a positive inotropic agent by blocking the sequestering of calcium ions into the sarcoplasmic reticulum. There is also a large class of dihydropyridine, phenylalkylamine, and benzothiazepine calcium channel blockers that may be administered decreasing the strength of contraction and SV.

However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues.
Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. While tachycardia is defined as a HR above 100 bpm, there is considerable variation among people. However, as HR continues to increase, SV gradually decreases due to decreased filling time.
Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm.
As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.
Meditation techniques have been developed to ease anxiety and have been shown to lower HR effectively. The exact etiology is not known, but several factors have been suggested, including transient vasospasm, dysfunction of the cardiac capillaries, or thickening of the myocardium—particularly in the left ventricle—that may lead to the critical circulation of blood to this region. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions. These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR. This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged. This effect can be partially overcome by increasing the second variable, contractility, and raising SV, but over time, the heart is unable to compensate for decreased filling time, and preload also decreases. If this process were to continue and the sarcomeres stretched beyond their optimal lengths, the force of contraction would decrease. In comparison, parasympathetic stimulation releases ACh at the neuromuscular junction from the vagus nerve. The fact is that anemia is a manifestation or complication of some other disease and not a diagnosis in itself. An average resting HR would be approximately 75 bpm but could range from 60–100 in some individuals. The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest.
Further, the normal resting HRs of children are often above 100 bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV.
It opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. The cardiac centers monitor these increased rates of firing, and suppress parasympathetic stimulation and increase sympathetic stimulation as needed in order to increase blood flow.
Doing simple deep and slow breathing exercises with one’s eyes closed can also significantly reduce this anxiety and HR.
While many patients survive the initial acute event with treatment to restore normal function, there is a strong correlation with death. If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. However, due to the physical constraints of the location of the heart, this excessive stretch is not a concern. Factors that increase contractility are described as positive inotropic factors, and those that decrease contractility are described as negative inotropic factors (ino- = “fiber;” -tropic = “turning toward”).
The membrane hyperpolarizes and inhibits contraction to decrease the strength of contraction and SV, and to raise ESV. In addition to the catecholamines from the adrenal medulla, other hormones also demonstrate positive inotropic effects.
Various infections, inflammations and malignancies show anemia as one of its complications. Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen.
Careful statistical analysis by the Cass Business School, a prestigious institution located in London, published in 2008, revealed that within one year of the death of a loved one, women are more than twice as likely to die and males are six times as likely to die as would otherwise be expected. Hypokalemia (low potassium levels) also leads to arrhythmias, whereas hyperkalemia (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail. In this case, the patient’s blood is normally diverted to an artificial heart-lung machine to maintain the body’s blood supply and gas exchange until the surgery is complete, and sinus rhythm can be restored.
Since parasympathetic fibers are more widespread in the atria than in the ventricles, the primary site of action is in the upper chambers. To speed up, one need merely remove one’s foot from the break and let the engine increase speed. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system. Parasympathetic stimulation in the atria decreases the atrial kick and reduces EDV, which decreases ventricular stretch and preload, thereby further limiting the force of ventricular contraction. Anemia is also associated with conditions such as hemorrhage, ulcers, menstrual problems or cancers. Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery. As HR increases from 120 to 160 bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Stronger parasympathetic stimulation also directly decreases the force of contraction of the ventricles. As HR continues to rise above 160 bpm, CO actually decreases as SV falls faster than HR increases. It can also be accompanied by headache and temporary blurring of vision.One of most common complains of children is decreased concentration. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between 120 and 160 bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age.
Causes of Anemia There are various causes of Anemia that can range from family history to infections. Men are not that easily affected though they too have a tendency to develop it in the form of a disorder.
Some of the most common forms of anemia are thalassemia, hemoglobinopathies, Rh null disease, enzyme abnormalities of the glycolytic pathways and hereditary xerocytosis.Nutritional- people who do not have a balanced diet are more prone to such diseases as they could be suffering from deficiency in their daily intake.
The most common forms of nutritional anemia are iron deficiency, Vitamin B-12 deficiency, folate deficiency and malnutrition due to starvation.Hemorrhage- this is the term that is used to describe the loss of blood in from the body due to some form of cuts or injury. Hemorrhage is one of the most common causes of anemia in men.Immunologic- this is one of the rare forms of anemia in which the body tends produce antibody mediated abnormalities. These can affect production and circulation of red blood cells in the body, ultimately leading to anemia.Physical trauma- certain physical traumas and weather conditions can lead to this form of injury due to which the body my lose blood and become anemic.
Among these, the most common are burns, frostbite and prosthetic calves and surfaces.Medications- consuming certain medications for a long time can also lead to anemia. Some of the most common forms of anemia that occurs as a reaction to drugs is aplastic anemia and megaloblastic anemia.Chronic diseases and cancer- certain chronic diseases can result in loss of blood or hamper the rate at which red blood cells are produced.
The most common among them are renal diseases, hepatic diseases, neoplasia and collagen vascular diseases.Infections- microbial infections can also destroy red blood cells, thus causing anemia. Hepatitis, gram-negative sepsis, malaria, toxoplasmosis, clostridia and cytomegalovirus are some of the most common infections.Conditions- certain medical conditions such as thrombotic thrombocytopenic purpura and hemolytic uremic syndrome can also cause anemia.

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