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NR 283 / NR283 Unit 4 Chapter 12 Outline Cardiovascular (Latest 2021 / 2022):, Study Guides, Projects, Research of Nursing

NR 283 / NR283 Unit 4 Chapter 12 Outline Cardiovascular (Latest 2021 / 2022): Pathophysiology - Chamberlain College of Nursing

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2020/2021

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NR283 Pathophysiology

Unit 4 – Chapter 12 Outline

Cardiovascular

  1. How does blood flow through the heart? (p. 227-228)
    1. The two atria are relax and are filled with blood (from the inferior and superior venae cavae into the right atrium, and from the pulmonary veins into the left atrium).
    2. AV valves open as the pressure of the blood in the atria increases and the ventricle are relaxed.
    3. Blood flows into the ventricles, almost emptying the atria.
    4. The conduction system stimulates the atrial muscle to contract, forcing any remaining blood into the ventricles.
    5. Atria relaxes
    6. The two ventricles begin to contract, and pressure increase in the ventricles.
    7. AV valves close
    8. For a brief moment, all valves are closed, the ventricular myocardium continues to contract, building up pressure in this isovolumetric phase (no change in blood volume in the ventricles).
    9. The increased pressure opens the semilunar valves; blood is forced into the pulmonary artery and aorta.
    10. At the end of the cycle, the atria have begun to fill again, the ventricles relax, and the aortic and pulmonary valves close to prevent backflow or blood, and the cycle repeats.
  2. What determines cardiac output? (p. 228-230)
    • Cardiac output is the volume of blood ejected by the ventricle in one minute and depends on the heart rate and stroke volume, the volume pumped from one ventricle in one contraction. This means that at rest, the heart pumps into the system an amount equal to the total blood volume in the body every minute, which is remarkable feat. When necessary, the normal heart can increase its usual output by four or five times the minimum volume.

Cardiac output = Heart Rate x Stroke Volume Amount of blood pumped Number of contractions Amount of blood ejected by each ventricle in min. of the ventricles each from each ventricle with minute each contraction.

  1. Define preload, afterload, and contractility. (p. 228)
    • Preload: refers to the mechanical state of the heart at the end of diastole with the ventricles at their maximum volume.
    • Afterload: Is the force required to eject blood from the ventricles and is determines by the peripheral resistance to the opening of the semilunar valves. o Example: Afterload is increased by a high diastolic pressure resulting from excessive vasoconstriction. - Contractility:
  2. Describe the process of atherosclerosis? (Understand how a fatty streak and plaque develops). (p. 235-237) - Process begins with endothelial injury in the artery, often at a very young age. - The endothelial injury causes inflammation in the area, which leads to elevated C- reactive protein (CRP) levels. - Monocytes, macrophages, and lipids accumulate in the intima or inner lining of the artery and in the media or muscle layer. - Smooth muscle cells proliferate or multiples; a plaque forms and inflammation persists. - Platelets adhere to the rough damage surface of the arterial wall, which forms a thrombus and a partial obstruction of the artery. - Lipids continue to build up at the arterial injury site, along with fibrous tissue. - Platelets adhere and release prostaglandins, which precipitate inflammation and vasospasm. This draws more platelets to aggregate at the site, enlarging the thrombus. - Arterial flow becomes more turbulent, promoting thrombus formation. - The cycle persists, whereas the blood flow decreases as the lumen narrows. - Plaque ulcerate and break open, which can precipitate more inflammation or a thrombus may form at the site resulting in total obstruction in a very short time. - Precipitating factor for myocardial infarction. - Atheroma damages the arterial wall, weakening the structure and decreasing elasticity. - In time atheromas may calcify, causing rigidity of the wall. - This can lead to aneurysm, a bulge in the arterial wall or a rupture and hemorrhage of the vessel.
  • The atheroma manifest as a yellowish fatty streak in the wall, then becomes larger, and eventually becoming a large firm mass with an irregular surface which a thrombus forms.
  • Atheroma increases size over time and the coronary arteries are partially obstructed, angina may occur.
  • Total obstruction leads to myocardial infarction. Atheromas are also a common cause of strokes, renal damage, and peripheral vascular disease, which affects the legs and feet.
  1. What is dyslipidemia? Which lipids are protective and which lipids are harmful? (p. 235)
  • Dyslipidemia: Abnormality in or abnormal amounts of lipids and lipoproteins in the blood.
  • Low density lipoproteins, which have a high lipid content and transports cholesterol from the liver to cells, is the dangerous component of elevated serum levels of lipids and cholesterol. It’s a major factor that contributes to the formation of atheroma. o Example: LDL bind to receptors; on the membranes of vascular smooth muscle cells and enters them; it is consider the “bad” lipoprotein that promotes atheroma formation.
  • High density lipoproteins is the “good” lipoprotein. It’s a low lipid content and is used to transport cholesterol away from the peripheral cells to the liver, where it undergoes catabolism and excretion.
  1. Define myocardial ischemia. (define in mayo clinic)
  • Occurs when blood flow to your heart is reduced, preventing it from receiving enough oxygen. The reduced blood flow is usually the result of a partial or complete blockage of your heart’s arteries (coronary arteries).
  • Myocardial ischemia can damage your heart muscle, reducing its ability to pump efficiently. A sudden or severe blockage of a coronary artery can lead to a heart attack. It can also cause serious abnormal heart rhythms.
  1. Define angina. What is unstable angina? What does unstable angina lead to? (p. 239-
  • Angina : or chest pain, occurs when there is a deficit of oxygen to the heart muscle. This occurs when the blood or oxygen supply to the myocardium is impaired, when the heart is working harder than usual and needs more oxygen.
  • Unstable angina refers to prolonged pain at rest and of recent onset, perhaps the result of a break in an atheroma. This may precede a myocardial infarction.
  1. What is myocardial infarction? What are the classic symptoms? (p. 240- 241)
  • Myocardial infarction or heart attack occurs when a coronary artery is totally obstructed, leading to prolonged ischemia and cell death, or infarction, of the heart wall.
  • The most common cause is atherosclerosis, usually with thrombus attached.
  • Classic symptoms : o Pain: Sudden substernal chest pain that radiates to the left arm, shoulder, jaw, or neck is the hallmark of myocardial infarction. The pain is usually described as severe, steady, and crushing, and no relief occurs with rest or vasodilators. In some cases, pain is not present (silent myocardial infarction) or is interpreted as gastric discomfort. Women often report a milder pain, more like indigestion. o Pallor and diaphoresis, nausea, dizziness and weakness, and dyspnea o Marked anxiety and fear o Hypotension is common, and the pulse is rapid and weak as cardiac output decreases and shock develops. o Low-grade fever
  1. What is an arrhythmia?
  2. What is heart failure?
  3. What causes left-sided heart failure? What does that put the patient at immediate risk

for?

  1. What causes right-sided heart failure? What symptoms will the patient exhibit?
  1. What are the risk factors for a DVT?
  2. What are the risk factors for primary HTN?
  3. Why is HTN damaging to the cardiovascular system?
  4. How does the RAAS system contribute to HTN?