Physio_22.txt

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Author:
c_sopkovich
ID:
60094
Filename:
Physio_22.txt
Updated:
2011-01-16 14:49:31
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Physiology
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Cardiac Failure
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  1. Heart failure can result from
    any ailment that reduces the ability of the heart to pump blood
  2. Usual cause of heart failure
    • decreased contractility resulting from diminished coronary blood flow
    • can also be caused by valve problems, external pressure around the heart, Vitamin B deficiency, cardiac muscle disease,
  3. Definition of heart failure
    failure of the heart to pump enough blood to satisfy the needs of the body
  4. two acute effects of MI
    • reduced cardiac output
    • damming of blood in the veins resulting in increased venous pressure
  5. Length of acute stage of heart failure
    only a few seconds because sympathetic nerve reflexes occur immediately and compensate for the damaged heart
  6. What reflex is activated by diminished arterial pressure
    • baroreceptor reflex
    • lesser contributors are the chemoreceptor reflex, CNS ischemic response, and reflexes from the heart
    • All increases sympathetics and inhibit parasympathetics
  7. Two effects of sympathetic stimulation
    • increases the strength of the cardiac muscle
    • increases venous return by increasing vascular tone, raises mean systemic filling pressure shifting the venous return curve to the right
    • These both compensate for an acutly damaged heart
    • brings CO back toward normal but with an increased right atrial pressure
    • Maximally developed reflex within 30 seconds
  8. Characteristics of semi chronic failure
    • after the first few minutes
    • fluid retention and varying degrees of recovery from the heart
  9. Low CO affect on the kidneys
    • can cause anuria if the CO falls to one half to two thirds normal
    • urine output will stay diminished until the cardiac output and arterial pressure return to normal
  10. two ways in which increased blood volume increases venous return
    • increases mean systemic filling pressure, shifts venous return curve to the right. Increases the pressure gradient
    • distends the veins reducing the venous resistance, increasing the slope of the venous return curve
    • This return can fully compensate for the diminished CO if the heart is not to damaged
  11. When does fluid retention can become detrimental
    Fluid retention can fully compensate for a damaged heart but if the CO continues to decline more fluid will be retained. Since the heart is already pumping at its max ability the fluid no longer has a beneficial effect. severe edema can develop
  12. three detrimental effects of fluid retention
    • overstitching of the heart thus weakening it even more
    • filtration of fluid in the lungs causing pulmonary edema can deoxygenation of the blood
    • peripheral edema
  13. Normal reparative process of the heart
    • collateral circulation starts to penetrate infarcted areas
    • undamaged portion of the heart will hypertrophy
    • usually recovery is complete in 5-7 weeks
  14. Why does sympathetic stimulation gradually abate toward normal during heart recovery
    the partial recovery of the heart can elevate the cardiac output curve the same as sympathetic stimulation can
  15. Effects on the skin of high sympathetic stimulation
    cold and pallor
  16. Summary of acute compensated heart failure
    • the instantaneous effect of cardiac damage
    • sympathetic compensation within 30 seconds
    • chronic compensation of heart recovery and fluid retention
  17. Cardiac reserve in compensated heart failure
    • cardiac reserve is reduced in compensated heart failure
    • at rest a person can have a normal CO with an elevated rt atrial pressure
    • at exercise the symptoms of heart failure will return because the heart is not able to increase its CO to the required levels
  18. Decompensated heart failure
    • after severe damage no amount of sympathetic stimulation or fluid retention will cause a normal CO
    • as a consequence the CO will never raise high enough to stop the kidneys to stop retaining fluid
    • develop more and more edema which will eventually lead to death
  19. Main cause of decompensated heart failure
    failure of the heart to pump sufficient blood to make the kidneys excrete the necessary fluid
  20. Cause of decline of cardiac function days after damage
    • the overstitching of the heart , edema of the heart muscle, other factors that diminish CO
    • further retention of fluid will be more detrimental the beneficial
    • at this point fluid retention not only continues but accelerates due to reduces CO, this state is decompensated heart failure
  21. failure of the cardiac output to rise to critical levels results in, 3
    • progressive retention of fluid
    • progressive elevation of mean systemic filling pressure
    • progressive elevation of rt atrial pressure until the heart is overstretched
  22. CLinically decompensated heart failure is detected by
    progressive edema, especially in the lungs which leads to bubbling rails and dyspnea ( air hunger)
  23. Treatment of decompensated heart failure
    • strengthening the heart with a cardiogenic drug such as digitalis
    • giving diuretic drugs while reducing salt and water intake
  24. Mechanism of action of carditonic drugs such as digitalis
    • will not affect a healthy heart, increase the strength of a failing heart
    • increase the amount of calcium in the muscle fibers
    • digitalis depresses the calcium pump of the cell membrane of cardiac muscle fibers, this extra calcium increases strength of contraction
  25. affect of left heart failure on the lungs
    • blood is pumped into the lungs normally but not pumped out
    • result is increase in mean pulmonary filling pressure
    • as the pressure in the lungs increases the pulmonary capillary pressure increases and when it rises above 28mmHg pulmonary edema begins
  26. Most important problem of left heart failure
    • pulmonary vascular congestion and pulmonary edema
    • can occur so rapidly that it can cause death by suffocation within 30 minutes
  27. Cardiac shock
    • when the heart become incapable of pumping the minimal amount of fluid to keep the body alive
    • all tissue begins to deteriorate and eventually the heart starts to deteriorate
    • survival rate is 15%
  28. Vicious cycle in shock
    • the low arterial pressure that ossuaries during shock reduces the coronary blood flow even more
    • this makes the heart weaker, which makes the arterial pressure to fall even more
    • as the pressure falls the heart deteriates more and the pressure falls more until death
    • In a person with CAD the problem is compounded and the pressure does not need to fall as much for cardiac muscle death to occur. Very important to prevent period of hypotension
  29. Treatment of cardiogenic shock
    • administration of digitalis
    • infusion of whole blood, plasma or pressure raising drugs; if the blood pressure can be raised high enough the coronary blood supply is sufficient to stop heart muscle deterioration
  30. Peripheral edema in acute cardiac failure
    • almost never occurs because as pressure falls so does capillary pressure
    • peripheral edema will occur after a few days due to increased fluid retention by the kidneys, the increased fluid will cause an increase in cardiac output and arterial pressure raises increasing capillary pressure and edema
  31. Three causes of reduced renal output during cardiac failure
    • decreased glomerular filtrate; reduced arterial pressure and increased sympathetic constriction of the afferent renal arterioles
    • activation of the renin angiotensin system; caused by reduced blood flow
    • Increased aldosterone secretion; angiotensin stimulation of the adrenal cortex, also potassium increases due to reduced renal function stimulating aldosterone secretion. The increased osmotic concentration then in turn causes the release of antidiuretic hormone
  32. atrial natriuretic factor
    • hormone released by the atrial wall when it becomes stretched
    • increase almost five fold in severe heart failure
    • ANF directly effects the kidney by increasing the excretion of salt and water
  33. Frequent cause of death in heart failure
    pulmonary edema
  34. vicious cycle of pulmonary edema in late stage heart failure
    • temporary increase in load of a weak left ventricle
    • increased blood in the lungs and increases pulmonary capillary pressure, fluid begins to translude out
    • increased fluid in lungs caused deoxygenation
    • decreased oxygen further weakens the heart and causes peripheral vasodilation
    • vasodilator increases venous return
    • increased venous return increases the fluid in the lungs and desats even more
  35. Five heroic therapeutic methods to revers acute pulmonary edema in late stage heart failure
    • tourniquet arms and legs to sequester blood and decrease workload of left heart
    • bleed the patient
    • rapid acting diuretics
    • breath pure O2
    • give digitalis
  36. Definition of cardiac reserve
    • maximum percentage that the cardiac output can increase above normal
    • 300-400% in a health heart
    • In heart failure little to no reserve
  37. Diagnosis of low cardiac reserve
    • stress test with the following results
    • SOB resulting from failure of the heart to pump sufficient blood to the tissues causing tissue ischemia and air hunger
    • extreme muscle fatigue from muscle ischemia
    • excessive increase in heart rate from nervous reflex to attempt to overcome low CO
  38. Decomposition results from
    the fact that cardiac output curve never raises above 5 L/min to re-establish normal renal function to cause a balance of fluid
  39. With the use of digitalis in decompensated heart failure
    • will cause cardiac output to increase above the threshold for normal renal function
    • after this increase the kidneys will eliminate volume returning the mean systemic filling pressure toward normal and at the same time returning the increased CO toward 5 L/min
    • diuresis is a therapeutic effect of digitalis
    • causes the circulatory system to stabilize, decompensated heart failure has now been compensated
  40. High output cardiac failure
    • overload of the heart due to excessive workload from AV fistula
    • beriberi causes an increase in venous return due to vaso dilation
  41. AV fistula
    • decreases systemic resistance, no shift in venous return curve but an increase in slope
    • Get a large increase in CO with a small increase in rt atrial pressure along with mild signs of peripheral edema
    • Little cardiac reserve for exercise, heart is at max capacity
    • high output failure from overload of venous return
  42. Beriberi
    • decreased level of cardiac output curve from avitaminosis (thiamine)
    • weakening of the heart decreases blood flow to the kidneys, retention of fluid, increases systemic filling pressure (shift venous return curve to the right )
    • avitaminotsis also dilates vessels so venous return curve is shifted upward, increased slope
    • despite a weak heart you get high cardiac output from the increased systemic filling pressure and decreased venous resistance

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