Pathophys

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optics
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6365
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Pathophys
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2010-02-11 13:31:57
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pathophys ch 18
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chapter 18, Alterations in Cardiac Function
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  1. Cardiovascular disease Overview—
    twice as many people die of cardiovascular disease as all cancers combined: nearly 1 million people each year in the US. ½ of these deaths are due to coronary heart disease.
  2. Coronary heart disease (CHD)—
    insufficient delivery of oxygenated blood to myocardium due to atherosclerosis or coronary arteries.
  3. CHD (coronary heart disease) Etiology—
    usually coronary artery atherosclerosis (coronary artery disease or CAD) More rare causes include:

    i. Abnormal microcirculation (doesn’t show up on angiography)

    ii. Respiratory failure (inadequate oxygenation of blood)

    iii. Coronary vasospasm (Prinzmetal angina)

    iv. Poor perfusion pressure
  4. CHD Mechanisms of coronary atherosclerosis
    i. Major risk factors—age, family history, abnormal lipids, cigarette smoking, hypertension, diabetes, obesity

    ii. Risk factors are the same for atherosclerosis of other vessels discussed in chapter 15.

    iii. When plaques narrow arterial lumen by 75% or so, symptoms begin to develop.

    • iv. Acute coronary syndromes (ACS)—are almost always associated with acute disruption of a vulnerable plaque and include:
    • 1. Unstable angina
    • 2. MI (myocardial infarction)
    • 3. Sudden cardiac death (unexpected death within 1 hour from the onset of symptoms)—usually (not always) due to CAD

    v. Coronary vasospasm—plays an important role in patients with anginal signs & symptoms but no significant atherosclerotic coronary disease: so-called Prinzmetal or variant angina.
  5. 2 types of MI exist:
    a. Transmural infarct—more serious, commonly causes Q-waves to appear on EKG.

    b. Non-Q-wave (subendocardial) infarct—inner 1/3 to 1/2 of myocardial wall.
  6. Stenosis—
    failure of a valve to completely open.
  7. Regurgitation (insufficiency)—
    failure to completely close, allowing blood to flow in a reverse direction.
  8. Mitral valve prolapse—
    present in 2-3% of population, mostly females 20-40 years old, usually asymptomatic, treatment usually not necessary EXCEPT antibiotic prophylaxis as in 3.iv above

    iv. Patients with valvular disorders are at an increased risk of infection, so some of these patients receive prophylactic antibiotics before dental and some surgical or medical procedures.
  9. Rheumatic heart disease—
    • possible consequence of rheumatic fever, which is a possible complication of Group-A β-hemolytic streptococcal pharyngitis.
    • i. Symptoms include—carditis, polyarthritis, Syndenham’s chorea, erythema marginatum subcutaneous nodules, elevated antibody levels against streptococcus.
  10. Infective endocarditis—involves a variety of organisms
    1. Acute infective endocarditis—frequently fatal, usually in patients with previously normal valves.

    • 2. Subacute—less virulent organisms, usually some pre-existing valvular abnormality.
    • ii. In both types—bulky vegetations hang off the valves, interfering with their function. Treatment is long-term IV antibiotics, valve replacement if necessary.
  11. Dilated cardiomyopathy (DCM)—
    • cardiac failure associated with dilatation of all 4 heart chambers.
    • 1. Factors suspicious in development include: alcohol, genetic abnormality, pregnancy, postviral.
    • 2. Only definitive treatment is heart transplantation.
  12. Hypertrophic cardiomyopathy (HCM)—
    often genetic, may predominantly involve interventricular septum thus called idiopathic hypertrophic subaortic stenosis (IHSS). Sudden death possible after physical exertion, so these patients turn into couch potatoes.
  13. Restrictive cardiomyopathy (RCM)—
    rarest form, stiff ventricle with impaired filling.
  14. Pericardial effusion—
    excessive fluid in the pericardial space of various compositions.
  15. Cardiac tamponade—
    externally compresses the heart chambers, impeding filling. Treat initially with pericardiocentesis.
  16. Pericarditis—
    • inflammation of the pericardium
    • i. Acute pericarditis—can be serous, fibrinous, purulent, hemorrhagic, or caseous.
    • 1. MI is a common cause, common symptoms are back or neck pain, dysphagia, or pain confused with angina pectoris.
  17. Chronic pericarditis—
    • usually from healed acute. 2 types:
    • 1. adhesive mediastinopericarditis—
    • from previous infection, cardiac surgery, or radiation. Pericardial sac is destroyed, so heart adheres to surrounding chest structures.
    • 2. Constrictive pericarditis—
    • either idiopathic or due to previous infection. Pericardium stiff, filling impeded.
  18. foramen ovale:
    allows blood to enter the left atrium from the right atrium. It is one of two fetal cardiac shunts, the other being the ductus arteriosus
  19. ductus arteriosus:
    • shunts a significant majority (80%) of the blood flow of the umbilical vein directly to the inferior vena cava. Thus, it allows oxygenated blood from the placenta to bypass the liver
    • For most people, it closes at birth.
  20. Atrial septal defect—
    usually at location of foramen ovale. Small defects well tolerated, but the increase in pulmonary blood flow in larger defects leads to pulmonary hypertension, so early repair done.
  21. Ventricular septal defect (VSD)—
    the most common congenital cardiac anomaly. Frequently associated with other defects. Most common high in septum, near Bundle of His. Shunt initially left to right, but as pulmonary hypertension develops, the shunt may reverse.
  22. Patent ductus arteriosus—
    left-to-right shunt, with possible reversal later. The ductus normally closes as prostaglandin E levels drop, so prostaglandin inhibitors may effect a medical closure.
  23. Coarctation of the aorta—
    males 3-4X more common affected (including my brother). Classically, the blood pressure in the upper extremities is REALLY high, while the BP in the LEs is almost undetectable. Femoral arterial pulses absent. Repaired surgically.

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