Cardiovascular System Pdf Notes Download

[Patricia]

Zawnis a writer who covers medical, legal, and social justice topics. Her work has been published in dozens of publications and websites. She lives with her husband, daughter, six tortoises, a dog, and 500 orchids. In her spare time, she runs a local maternal health nonprofit.

Beth lives in London and works as a freelance writer on a range of projects. Along with writing regular articles for Medical News Today, she writes for the Horniman Museum, an anthropology museum in South London. This involves recording minutes for conferences, blogging for their website, and documenting their process of curating art exhibitions. She loves theatre, yoga, and cycling in her spare time.

Anna Smith Haghighi lives in Bangor, Northern Ireland, with her husband and their greyhounds Django and Zola. She found a passion for writing when creating content for various clients as part of an SEO company. Along the way, Anna has been a film and television extra, half of a singing duo, and a team member of the Belfast Eye. These days, Anna is more likely to be walking her dogs or playing a Zelda game for the millionth time.

Abnormalities or injuries to any or all parts of the cardiovascular system can result in serious health complications. Common conditions that can affect the cardiovascular system include coronary artery disease, heart attack, high blood pressure, and stroke.

There are two blood circulatory systems in the body. The first is the systemic circulatory system. This is the main blood circulatory system that transports blood to the organs, tissues, and cells throughout the body.

The second is the pulmonary circulatory system. This circulatory system moves blood between the heart and lungs. It is where oxygen enters the blood and carbon dioxide leaves the blood.

The heart pumps blood through closed vessels to every tissue within the body. The blood itself then delivers nutrients and oxygen to all cells in the body. Without blood, the cells and tissues would not function at their total capacity and would begin to malfunction and die.

The first phase is diastole, in which the ventricles fill with blood. It begins when the aortic or pulmonary valve closes and ends when the mitral or tricuspid valve closes. During diastole, blood vessels return blood to the heart in preparation for the next contraction of the ventricles.

The second phase is systole, in which the ventricles contract and eject blood. It begins when the mitral or tricuspid valve closes and ends when the aortic or pulmonary valve closes. The pressure inside the ventricles becomes greater than the pressure inside adjacent blood vessels, thereby forcing the blood from the ventricles to the vessels.

A heart attack happens when a part of the heart muscle does not receive enough blood. This can occur due to a blockage, a tear in an artery around the heart, or if the heart requires more oxygen than is available.

The treatment for stroke will depend on the type. A person who experiences ischemic stroke may receive medications to help break up the blood clot and restore blood flow to their brain. A person who experiences a hemorrhagic stroke may require surgery to fix the blood vessel that is bleeding out.

As a person ages, their heart begins to work less effectively than it used to. For example, it cannot beat as fast during physical activity, although the resting heart rate remains steady. Arrhythmias can also develop as the heart ages.

Another common condition of aging is more stiffness in the large arteries and stiffness of the heart muscle. This stiffness can cause high blood pressure, increasing the risk of heart attacks, stroke, and heart failure. Stiffness of the heart can also cause congestive heart failure.

The cardiovascular system consists of the heart, veins, arteries, and capillaries. These components make up two circulatory systems: the systemic and pulmonary circulatory systems. The cardiac cycle consists of two phases: systole (relaxation) and diastole (contraction).

As the body ages, the heart functions less effectively, especially during periods of high physical activity. The arteries also have a higher likelihood of becoming stiff with age, which increases the possibility of high blood pressure and associated cardiovascular issues.

Tobacco use is a leading global cause of death, accounting for more than 6 million deaths annually or at least 12 percent of deaths among people age 30 years and older (16 percent for men, 7 percent for women) (WHO 2012, 2013). It is the single most preventable cause of cardiovascular diseases (CVDs), which comprise a large number of conditions and are the leading cause of death globally, accounting for an estimated 17.3 million to 17.5 million deaths yearly (Naghavi and others 2015; WHO 2015a). Tobacco is also the leading cause of premature death from CVD (deaths before age 70 years), accounting for an estimated 5.9 million premature deaths in 2013 (Roth, Nguyen, and others 2015). Such deaths deprive families of productive members, and communities and economies of a productive workforce (Rigotti and Clair 2013). Tobacco use also causes substantial morbidity and results in tremendous health care costs related to CVD. Although tobacco use affects all countries regardless of their level of economic or health system development, the impact is most profound in low- and middle-income countries (LMICs), which shoulder the largest share of total and premature deaths from CVD globally (WHO 2015a). Future projections are alarming, with LMICs accounting for much of the future global burden of tobacco use and related CVD mortality and morbidity (Ezzati and Lopez 2003). China (with 301 million tobacco users) and India have the highest burden of tobacco use in the world (WHO n.d.).

Generally, high rates of tobacco use mean a higher burden of CVD. This association is compounded by population growth and aging, both of which are major contributors to the absolute number of CVD sufferers (Roth, Nguyen, and others 2015).

Reducing tobacco use is thus crucial to averting tobacco deaths, which are projected to increase to 10 million annually by 2030 if current trends continue (WHO 2013, 2015a). Premature deaths from CVDs are also projected to increase to 7.8 million in 2025 if business as usual continues, including in the approach to controlling tobacco use and preventing noncommunicable diseases (Roth, Nguyen, and others 2015). Urgent action is needed to halt and reverse this course.

Studies clearly show that reducing tobacco use is key to achieving these targets (Kontis and others 2014; Kontis and others 2015). Reducing tobacco use would offset some of the increase in the absolute number of cardiovascular deaths caused by population growth and aging, especially in LMICs (Roth, Forouzanfar, and others 2015). Indeed, several studies demonstrate the need to achieve more ambitious targets for reducing tobacco use (50 percent relative to 2010) if countries are to reach the 2525 target (Kontis and others 2014; Kontis and others 2015; Roth, Nguyen, and others 2015).

This chapter reviews the literature to synthesize key knowledge on the links between tobacco use and CVD. The introduction on burden of CVD attributable to tobacco is followed by a brief review of the main pathophysiological mechanisms by which tobacco use causes CVD. The third section highlights the role of tobacco and other CVD risk factors, and the fourth reviews tobacco-related CVDs that are most important from a public health and health systems perspective. The focus is on cigarette smoking, but other forms are also discussed in the fifth section. This is followed by a section on the socioeconomic dimensions of tobacco use. The seventh section highlights the cardiovascular health benefits of stopping tobacco use. The concluding section calls for enhanced engagement and cooperation of public health and health care providers to stem the rise of tobacco-related CVDs, especially in LMICs.

Tobacco use has myriad effects on the cardiovascular system that contribute to CVD pathophysiology. Box 4.1 reviews some of the terms used to explain the mechanisms by which tobacco use can cause CVD. The effects of cigarette smoking and exposure to secondhand smoke have been studied most, but many of the effects are common to other forms of use, including smokeless tobacco.

Burning tobacco products produce two forms of smoke: mainstream and sidestream. Mainstream smoke is inhaled and exhaled by the smoker, whereas sidestream smoke comes from the burning end of the cigarette (Ambrose and Barua 2004) and is even more toxic than mainstream smoke (Schick and Glantz 2005). Among the more than 7,000 chemicals in cigarette smoke, many components are known to mediate the pathophysiology of CVD (Borgerding and Klus 2005). Toxic chemicals such as carbon monoxide, polycyclic aromatic hydrocarbons, nicotine, and heavy metals and their oxides have profound effects on vascular endothelium (cells lining the blood vessels), blood lipids (fats), and clotting (thrombotic) factors causing atherosclerosis (plaque buildup). The latter affects arteries (vessels carrying oxygenated blood to organs across various vascular beds). These effects can lead to adverse cardiovascular events such as myocardial infarction (heart attack), stroke (brain attack), and aortic dissection (rupture of the aorta, the main artery emanating from the heart). Figure 4.1 illustrates the pathophysiological mechanisms implicated in tobacco-associated atherosclerosis.

The mechanisms by which cigarette smoking induces and promotes atherogenesis and, consequently, atherosclerosis and atherothrombosis are complex and interconnected. The key pathways are inflammation, endothelial dysfunction, prothrombosis, altered lipid metabolism, insulin resistance, and increased demand for but diminished supply of myocardial oxygen and blood (demand-supply mismatch) (U.S. Department of Health and Human Services 2014). Smoking is also known to be responsible for increased release of catecholamines, which exert cardiovascular effects such as increased heart rate, vasoconstriction, and increased cardiac output (Cryer and others 1976). Figure 4.2 displays the key constituents involved in some of these mechanisms.

3a8082e126