Cardiac Test 2

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nalonso
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64512
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Cardiac Test 2
Updated:
2011-02-06 22:11:19
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Cardiovascular Alterations
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Cardiovascular Alterations
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  1. Describe how this compensatory mechanism increases cardiac output as a result of heart failure, and indicate the long term effects.
    Sympathetic Nervous System—adrenergic receptors
    • Action: Increased heart rate (beta-adrenergic) and blood pressure from
    • vasoconstriction (alpha-adrenergic). There is also increased venous return to the heart, which stretches the myocardial fibers. This increased stretch is a preload that makes a more forceful contraction, increasing stroke volume and CO.
    • Long-term effects: Increased oxygen demand; increased afterload, which is the resistance against which the heart must pump; too much myocardial stretch (preload).
  2. Describe how this compensatory mechanism increases cardiac output as a result of heart failure, and indicate the long term effects.

    Cardiac hypertrophy
    • Action: The walls of the heart become thick, increasing muscle mass and
    • increasing the force of contraction.
    • Long-term effect: The heart cannot meet the increased oxygen demand that hypertrophied condition requires.
  3. Describe how this compensatory mechanism increases cardiac output as a result of heart failure, and indicate the long term effects.

    Hormonal response
    • Action: Activates the renin-angiotensin system, which raises the blood pressure by increasing fluid retention and vasoconstriction.
    • Long-term effect: This eventually increases the stretch (preload) and the
    • resistance (afterload). Ventricular remodeling may develop.
  4. Left ventricle is unable to contract
    forcefully. LV is unable to eject blood
    adequately into the circulation.
    • Systolic dysfunction (systolic
    • ventricular dysfunction)
  5. Effects of Systolic Ventricular Dysfunction
    • Cardiac output decreases. Symptoms
    • of inadequate tissue perfusion,
    • pulmonary and systemic congestion
    • occur.
  6. Left ventricle is unable to relax
    during diastole; this prevents the
    ventricle from filling.
    • Diastolic dysfunction (diastolic
    • ventricular dysfunction)
  7. Effects of Diastolic Ventricular Dysfunction
    • Diminished tissue perfusion
    • and decreased cardiac output.
    • Symptoms similar to those of systolic
    • dysfunction.
  8. Differentiate between the terms arteriosclerosis and atherosclerosis
    Arteriosclerosis is a thickening or hardening of the arterial wall resulting in a loss of elasticity.

    Atherosclerosis is a form of arteriosclerosis that involves the formation of plaque within the arterial wall, which leads to eventual interference with blood flow through the artery.
  9. List in order the development of atherosclerosis
    • Intimal layer of artery is injured
    • Fatty streak is deposited on intimal layer
    • Fibrous plaque develops
    • Calcification, thrombosis, ulceration of fibrous lesions occur
  10. Describe the characteristics of plaque in the development of atherosclerosis
    Plaque is white and fibrous, and partially or completely blocks the flow of blood in an artery
  11. List the causes of injury to the inner layer of the arterial wall that contributes to the development of atherosclerosis
    • Mechanical Injury: hypertension
    • Chemical Injuries: toxins from renal failure, carbon monoxide from smoking
    • Natural Causes: aging
    • Diseases: diabetes, hyperlipidemia
    • Others: stress (type A personality is uptight, type D personality is depressed), obesity, and sedentary lifestyle
  12. Describe the rate of progression and factors that influence the development of atherosclerosis
    • Rate of progression depends on factors that cause the injury and the number of risk factors that a patient has.
    • For example, if a patient is older, eats a high fat diet, and has diabetes, the rate of progression is high.
  13. Describe the characteristics of a fatty streak in the development of atherosclerosis
    A fatty streak is a fatty deposit on the inner lining of the arteries but not enough to affect the integrity of the arterial wall
  14. What are the waist measurements that determine risk for CVD?
    • Women with waists greater than 35in
    • Men with waists greater than 40in
  15. When a mature atherosclerotic plaque develops, it is not uniform and has a lipid liquid center filled with procoagulant factors. A connective tissue fibrous cap covers the top of the fluid lipid center.
    What happens when this cap abruptly ruptures?
    • The abrupt rupture allows procoagulant lipids to flood into the vessel lumen and rapidly form a coronary thrombosis.
    • As the enlarging clot blocks blood flow through the coronary artery, a "heart attack" will occur unless there is adequate collateral circulation from other coronary vessels
    • Symptoms associated with this cap rupture include chest pain not relieved by rest or Nitro.
    • This is considered an Acute Coronary Syndrom- unstable angina
  16. Type of atherosclerotic plaque that is prone to rupture has a weak fibrous cap and a large amount of liquid cholesterol within the core
    • Vulnerable plaque
    • As deep fissures in the cap expose the procoagulant factors to the blood plasma, an unstoppable cycle is put into motion.
    • As the liquid inner core travels through the cardiovascular system, it collects RBCs and other debris along the way forming a clot that can occlude the coronary artery(microembolism occulsion)
    • Vulnerable plaques are usually not obstructive like calcified plaques are
  17. Type of atherosclerotic plaque that can't rupture but can occlude the coronary arteries
    • Calcified Plaque
    • Although stable it can occlude
    • The part of the artery that is calcified can no longer constrict or dilate
    • Calcified plaque is related to the aging process where vulnerable plaque is related to lifestyle
  18. Will lowering cholesterol levels change the dimensions of the fibrous or calcified portions of the plaque?
    • No but, it can decrease the plaque size by decreasing the amount of liquid cholesterol within the plaque core.
    • Lower cholesterol levels also reduce vascular inflammation and make vulnerable plaque less likely to rupture
  19. Term used to describe the array of clinical presentations of coronary artery disease (CAD) that range from unstable angina to acute MI
    Acute Coronary Syndrome (ACS)

    • Stable manifestation of CAD is referred to as stable angina
    • Acute manifestations of CAD are described as an acute coronary syndrome and refers to unstable angina and acute MI
  20. Chest pain caused by myocardial ischemia and is a symptom of coronary artery disease
    Angina

    It is a symptom not a separate disease
  21. Angina is caused by a blockage or spasm of a coronary artery, leading to diminished myocardial blood supply. The lack of oxygen causes myocardial ischemia, which the patient describes as?
    • Chest discomfort, pressure or pain
    • Angina may occur anywhere in the chest, neck, arms, or back.
    • Most commonly described location is pain or pressure behind the sternum that radiates to the left arm but can also radiate down both arms and to the back, shoulder, jaw, or neck
    • Teach that angina does not always present in the dramatic scenarios seen on TV
  22. Many women experience a variety of different symptoms before and during an acute MI. It is important that all patients are made aware of angina symptom equivalents, such as?
    • Unexpected shortness of breath
    • Breaking out in a cold sweat
    • Sudden fatigue, nausea, or lightheadedness
    • More women die every year of cardiovascular disease than men
  23. What are the effects of the Parasympathetic Nervous System on: Automaticity, Contractility, Conduction velocity, and Rate?
    Parasympathetic Nervous System Decreases all functions
  24. What are the effects of the Sympathetic Nervous System on: Automaticity, Contractility, Conduction velocity, and Rate?
    Sympathetic Nervous System Increases all functions
  25. Type of angina that is predictable and caused by similar precipitating factors each time; typically, it is exercise induced
    Stable Angina
  26. Stable angina is the result of?
    • Fixed lesions (blockages) of more than75% of the coronary artery lumen
    • Ischemia and chest pain occur when myocardial demand from exertion exceeds the blood oxygen supply
    • Pain control should be achieved within 5 minutes by rest and by taking sublingual nitro
  27. Defined as a change in previously established stable pattern of angina, and is part of the continuum of acute coronary syndrome
    • Unstable Angina
    • More intense than stable angina, may awaken the person from sleep, or may necessitate more than nitrates for pain relief
    • A change in the level or frequency of symptoms requires immediate evaluation
    • Severe angina that persists for more than 5 minutes, is worsening in intensity, and is not relieved by one nitro tablet is a medical emergency
  28. Unstable angina is an indication of?
    • Atherosclerotic plaque instability
    • It can signal atherosclerotic plaque rupture and thrombus formation that can lead to MI
  29. Severe angina persisting longer than 5 minutes or worsening symptoms without relief from rest or sublingual nitro indicates?
    Preinfarction symptoms (Unstable Angina)
  30. Pathophysiology of Acute Coronary Syndrome
    AtherosclerosisACS
    • Chronic inflammation of arterial wall
    • Plaque formation
    • Atherosclerotic plaque ruptures
    • And/Or

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