Cause Slower Heart Rates On Diabetes

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

Parkinson 's disease is a progressive neurologic degenerative disease of the Central Nervous system. The brain produces Dopamine and Norepinephrine, which are chemicals needed for smooth muscle movement and coordination, heart rate, and blood pressure. Dopamine and Norepinephrine are released by basal ganglions that are produced in a bundle of nerve cells in the brainstem called substantia nigra. In Parkinson 's patients, the substantia nigra are destroyed and neither of the chemicals can be released into the body. (3) The decrease in Norepinephrine causes heart arrhythmia and low blood pressure, causing the person to get dizzy upon standing or tire easily. The lack of Dopamine, the smooth muscle movement and coordination controller is now gone, or significantly decreased, resulting in the first signs of Parkinson’s disease, pill-rolling, a one handed tremor and a decreased appetite. (2)

Uncontrolled diabetes can affect nearly every organ of the body; of which, heart disease and kidney failure are most commonly impacted. Known as diabetes mellitus, a collective term for various blood abnormalities, the term diabetes refers to either a scarcity of insulin in the body or the body’s inability to accept insulin. Though the symptoms of diabetes are manageable, many are unaware as to having it. According to the CDC report “2011 Diabetes Fact Sheet,” approximately 6 million people in the United States have undiagnosed diabetes. Undetected, diabetes can become deadly. In a recent World Health Organization report “Diabetes Action Now: An Initiative of the World Health Organization and the International Diabetes Federation,” it

Though data from vagal stimulation was disregarded, it is still important to mention the responses that should have been elicited had the vagus nerve been stimulated properly. The vagus nerve (cranial nerve X) is a part of the parasympathetic nervous system and reduce heart rate when given enough electrical stimulation. Vagal escape occurs when the vagus nerve has been stimulated to the point of the nerve ceasing to repolarize, and then resuming sending action potential for heartbeat. The result is a cease or slowing of heart rate temporarily, and then heart rate starting up again. When atropine is applied to the heart along with vagal stimulation, the atropine blocks any response the vagus nerve should send (Sarnoff et al,

The major causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia-induced ventricular transformation (coronary artery disease). Hypertrophy and ischemia cause a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation. Some of the other causes are aortic valvular disease and cardiomyopathies. Diabetes can also lead to diastolic heart failure (Huether and McCune 2012). Other risk factors for this disease are chronic kidney disease, obstructive sleep apnea, and older age. There are two types of the heart failure: systolic heart failure and diastolic heart failure. In systolic heart failure, the left ventricle has difficulty contracting and ejecting blood into the circulation, which causes reduced left ventricular fraction. On the other hand, diastolic heart failure has a slow and delayed relaxation and increased chamber rigidity, which then causes inadequate filling of blood and

Patients with acute unstable bradycardia may present various signs and symptoms, including fatigue, dizziness, exercise intolerance, syncope, and congestive heart failure. Treatments for the patients with bradycardia are determined by the patient’s overall condition and existing co-morbidities. In cases where the heart rate drops to a rate of 30-40bpm the patient may not tolerate this situation due to reduced cardiac output, decreased myocardial function which will lead to poor perfusion to vital organs (Swift, 2013). In severe cases, bradycardia may lead to asystole, which is why early recognition and treatment of the acute bradycardia is paramount to achieving a good outcome for the patient.

I now know that the hypotension is caused by vasodilatation because the sympathetic nerves that control tone are blocked. Peripheral

It affects the nerves that control the heart, regulate blood pressure, and control blood glucose levels (Callaghan, 2012). Autonomic neuropathy interferes with the body's ability to adjust blood pressure and heart rate, resulting in blood pressure to drop sharply after sitting or standing, causing light-headed or even to fainting. Damage to the nerves that control heart rate can mean that the heart rate stays high, instead of rising and falling in response to normal body functions and physical activity. Nerve damage to the digestive system commonly causes constipation, causing the stomach to empty too slowly (Callaghan, 2012). This can lead to persistent nausea and vomiting, bloating, and loss of appetite, making blood glucose levels fluctuate widely, due to abnormal food digestion. Nerve damage to the esophagus makes swallowing difficult, while nerve damage to the bowels can cause constipation alternating with frequent, uncontrolled diarrhea (Callaghan, 2012). Autonomic neuropathy often affects the control of urination, which can prevent the bladder from emptying completely, allowing bacteria to grow in the bladder and kidneys and causing urinary tract infections. Urinary incontinence may result due to not being able to sense when the bladder is full or control the muscles that release urine. It can also gradually decrease sexual response in both

Intro- Heart Failure is a multifactorial disease due to significant diminishing of heart pumping action. This is occurs in response to many underlying disease such as diabetes, hypertension, myocardial infarction and cardiac myopathies. These conditons lead to hemodynamic instability, neuroendocrine imbalances and structural remodeling of cardiac myocytes. Early less sever hf allows for compensatory mechanisms such as neuroendocrine stimulation- (beta adrenbergic r endothelin norepinephrine r), and hypertrophy which allow for sufficient left ventricular pumping action. However as hf develops these mechanisms become unable to compensate for the progressive underlying disease which results in further loss of contraction and relaxation efficiency and loss of regulation.

Smooth muscle cells of the ileum spontaneously contract due to the presence of pacemaker cells, called Cajal cells (Widmaier et al., 2014d). However, these smooth muscle they are also innervated by autonomic nerves, which can be stimulated to change contraction rates by stimulating. Figure 1, shows the effect of nerve stimulation of 17volts on isolated ileum tissue. Stimulating sympathetic (sympathetic nerves was stimulated for this particular tissue), causes release of noradrenaline, which inhabits contraction of smooth muscle cells. Furthermore, according to table 1, there is a -58.83% change in contraction amplitude. It can be extrapolated that fewer smooth muscles are contracting. At lower voltages, a weaker response was observed, as voltage is increased a stronger response was observed. Increasing the voltage, means more neurons are being recruited (Widmaier et al., 2014b). In this particular experiment, stimulation of nerves around the mesenteric artery caused an inhibitory response, therefore at higher voltages, more smooth muscles are being inhibited.

Wolff-Parkinson-White syndrome (WPW) is a conduction disorder of the heart that is caused by pre accessory pathway resulting in tachyarrhythmias. Kesler & Lahham (2016) state, “Approximately 0.07% of the population often presents with the chief complaint of palpitations”. A diagnosis of WPW is made in conjunction with certain characteristics. Characteristics of WPW include: a short PR interval < 0.12 second caused by a faster electrical conduction through the accessory pathway than the atrioventricular node, upsloping of the QRS and a delta wave. The delta wave is indicative of rapid ventricular depolarization caused by the rapid conduction through the accessory pathway (Kesler & Lahham, 2016, p. 469).

Diabetes has a huge impact on men and women higher in women who have cardiac disease problems or may lead to having cardiac problems. No matter the type of diabetes you have whether it be type 1 where you are insulin resistant or type 2 and you are not secreting enough insulin increases your risk for cardiac disease. Women with either type of diabetes not only increases their risk for cardiac problems but they are at risk for vascular problems such as having an MI and increased mortality rate. The factors that can contribute to these problems is poor glycemic control, elevated blood pressure and lipids, obesity, socioeconomic factors and depression.

According to the Merriam-Webster dictionary (“Physiology,” n.d.), physiology is defined as a branch of biology that deals with the functions and activities of life or of living matter and of the physical and chemical phenomena observed. Compared to physiology, pathophysiology is a much more specific section of physiology that deals specifically with the functional changes that accompany a particular syndrome or disease (“Pathophysiology,” n.d.). Braun and Anderson (2011) discuss that

Abnormalities in diastolic function mostly manifest as impaired relaxation of the ventricles which can affect the filling of the left ventricle during exercises. This rarely happens during resting period. The dysfunction occurs during the initial stage of left ventricle hypertrophy and can fail to show symptoms for a long period. Progression of disease in a patient with diastolic dysfunction leads to increased filling pressure during normal physical activities and exercises as well. Further progression of the disease causes elevation of filling pressure even at rest, abnormal enlargement of the left atrial and atrial fibrillation as well as reduced exercise tolerance with symptoms of congestive heart failure. During extreme physical activities,

Current drugs designed for the treatment of systolic HF act to block the neurohumoral response by inhibition of the RASS, adrenergic block and aldosterone antagonism, however non are focused on improving the contractile function of the heart (McMurray, 2010). In theory improving the contractile function of the heart would reduce the neurohumoral activation and improve or stabilise the decline in cardiac function. Previous attempts to increase cardiac function by using inotropes, such as β-adrenergic receptor agonists and phosphodiesterase inhibitors, which work by activating secondary messenger pathways that increase intracellular calcium, have been unsuccessful. In clinical trials they have resulted in arrhythmias, increased heart rate and oxygen consumption and have increased mortality (Cohn et al., 1998; Cuffe et al., 2002; Packer et al., 1991; Petersen and Felker, 2008).