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Heart failure can result from
any ailment that reduces the ability of the heart to pump blood
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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,
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Definition of heart failure
failure of the heart to pump enough blood to satisfy the needs of the body
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two acute effects of MI
- reduced cardiac output
- damming of blood in the veins resulting in increased venous pressure
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Length of acute stage of heart failure
only a few seconds because sympathetic nerve reflexes occur immediately and compensate for the damaged heart
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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
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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
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Characteristics of semi chronic failure
- after the first few minutes
- fluid retention and varying degrees of recovery from the heart
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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
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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
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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
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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
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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
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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
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Effects on the skin of high sympathetic stimulation
cold and pallor
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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
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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
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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
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Main cause of decompensated heart failure
failure of the heart to pump sufficient blood to make the kidneys excrete the necessary fluid
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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
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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
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CLinically decompensated heart failure is detected by
progressive edema, especially in the lungs which leads to bubbling rails and dyspnea ( air hunger)
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Treatment of decompensated heart failure
- strengthening the heart with a cardiogenic drug such as digitalis
- giving diuretic drugs while reducing salt and water intake
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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
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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
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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
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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%
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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
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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
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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
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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
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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
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Frequent cause of death in heart failure
pulmonary edema
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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
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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
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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
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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
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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
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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
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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
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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
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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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