Physio_22.txt

any ailment that reduces the ability of the heart to pump blood

• 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,

failure of the heart to pump enough blood to satisfy the needs of the body

• reduced cardiac output
• damming of blood in the veins resulting in increased venous pressure

only a few seconds because sympathetic nerve reflexes occur immediately and compensate for the damaged heart

• baroreceptor reflex
• lesser contributors are the chemoreceptor reflex, CNS ischemic response, and reflexes from the heart
• All increases sympathetics and inhibit parasympathetics

• 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

• after the first few minutes
• fluid retention and varying degrees of recovery from the heart

• 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

• 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

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

• 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

• collateral circulation starts to penetrate infarcted areas
• undamaged portion of the heart will hypertrophy
• usually recovery is complete in 5-7 weeks

the partial recovery of the heart can elevate the cardiac output curve the same as sympathetic stimulation can

cold and pallor

• the instantaneous effect of cardiac damage
• sympathetic compensation within 30 seconds
• chronic compensation of heart recovery and fluid retention

• 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

• 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

failure of the heart to pump sufficient blood to make the kidneys excrete the necessary fluid

• 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

• progressive retention of fluid
• progressive elevation of mean systemic filling pressure
• progressive elevation of rt atrial pressure until the heart is overstretched

progressive edema, especially in the lungs which leads to bubbling rails and dyspnea ( air hunger)

• strengthening the heart with a cardiogenic drug such as digitalis
• giving diuretic drugs while reducing salt and water intake

• 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

• 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

• pulmonary vascular congestion and pulmonary edema
• can occur so rapidly that it can cause death by suffocation within 30 minutes

• 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%

• 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

• 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

• 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

• 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

• 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

pulmonary edema

• 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

• tourniquet arms and legs to sequester blood and decrease workload of left heart
• bleed the patient
• rapid acting diuretics
• breath pure O2
• give digitalis

• maximum percentage that the cardiac output can increase above normal
• 300-400% in a health heart
• In heart failure little to no 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

the fact that cardiac output curve never raises above 5 L/min to re-establish normal renal function to cause a balance of fluid

• 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

• overload of the heart due to excessive workload from AV fistula
• beriberi causes an increase in venous return due to vaso dilation

• 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

• 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