Download phys chapter 22 [12-11

Phys Ch 22
Cardiac Failure
 Heart failure can result from any heart condition that reduces the ability of the heart to pump blood
o Usually decreased contractility of myocardium resulting from diminished coronary blood flow
o Can be caused by damaged heart valves, external pressure around heart, vitamin B deficiency, primary
cardiac muscle disease, or any other abnormality that makes heart hypoeffective pump
 Cardiac failure – failure of heart to pump enough blood to satisfy needs of body
Circulatory Dynamics in Cardiac Failure
 Progressive changes in heart pumping effectiveness at different times after acute MI
Points are operating points under these
conditions
Body does not remain at point B long
because of SNS takeover (if it didn’t, person
would faint from lack of blood pumping)
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When cardiac output falls precariously low, baroreceptor reflex is activated by diminished arterial pressure
Chemoreceptor reflex (CNS ischemic response) and some reflexes that originate in damaged heart contribute to
activating SNS
SNS reaction becomes strongly stimulated within a few seconds, and PNS signals to heart are inhibited
o If all of ventricular musculature is diffusely damaged but still functional, SNS stimulation strengthens
damaged musculature; if part of muscle is nonfunctional and part is normal, normal muscle is strongly
stimulated by SNS stimulation, partially compensating for nonfunctional muscle
o SNS stimulation also increases venous return because it increases tone of most blood vessels of
circulation, especially veins, raising mean systemic filling pressure to almost twice normal
o Damaged heart becomes primed with more inflowing blood than usual, and right atrial pressure rises,
which helps heart pump still larger quantities of blood
o SNS reflexes become maximally developed in about 30 seconds, so person with a sudden, moderate
heart attack might experience nothing more than cardiac pain and a few seconds of fainting
o SNS stimulated system stable, but person cannot undergo stress under these conditions
After first few minutes of acute MI, prolonged semichronic state begins, characterized mainly by retention of
fluid by kidneys an dvarying degrees of recovery of heart itself over period of weeks to months (light green curve
in graph above)
Low cardiac output has profound effect on renal function – urine output remains below normal as long as
cardiac output and arterial pressure remain significantly less than normal and will not return to normal levels
until cardiac output and arterial pressure rise to almost normal levels
Moderate increase in body fluid and blood volume is important factor in helping to compensate for diminished
pumping ability of heart by increasing venous return
o Increases mean systemic filling pressure, which increases pressure gradient for causing venous flow of
blood toward heart
o Distends veins, which reduces venous resistance and allows more ease of flow of blood to heart
If heart not too greatly damaged, increased venous return can often fully compensate for heart’s diminished
pumping ability (when heart is using 40-50% of normal pumping ability) without stress
o When heart’s pumping capability is reduced further, blood flow to kidneys becomes too low for kidneys
to excrete enough salt and water to equal salt and water intake – fluid retention begins and continues
indefinitely unless major therapeutic procedures used to prevent this
o Because heart is already pumping at maximum pumping capacity, excess fluid no longer has beneficial
effect on circulation because fluid retention increases workload on the already damaged heart and
severe edema develops throughout body, which can lead to death
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In severe failure, extreme excesses of fluid can cause
o Increasing workload on damaged heart
o Overstretching of heart, weakening heart still more
o Filtration of fluid into lungs, causing pulmonary edema and consequent deoxygenation of blood
o Development of extensive edema in most parts of body
 A week or so after MI, considerable fluid has been retained in body, increasing venous return and bringing heart
back to normal cardiac output rate, but with increased right atrial pressure
o Because cardiac output is normal, renal output of fluid returns to normal and no further fluid retention
occurs except that retention of fluid that has already occurred continues to maintain moderate excesses
of fluid, so person is normal except for increased right atrial pressure while they are at rest
o If heart recovers to significant extent and if adequate fluid volume has been retained, SNS stimulation
gradually abates toward normal because partial recovery of heart can elevate cardiac output curve by
itself and as heart recovers, fast pulse rate, cold skin, and pallor resulting from SNS in acute stage of
cardiac failure gradually disappear
 Compensated heart failure – heart failure compensated by SNS then eventual partial recovery (explained above)
o Maximum pumping ability of partially recovered heart is still depressed to less than ½ normal
o Many older people have normal resting cardiac outputs but mildly to moderately elevated right atrial
pressures because of various degrees of compensated heart failure
 If heart becomes severely damaged, no amount of compensation can make excessively weakened heart pump
normal cardiac output, so kidneys do not excrete enough (fluid retained), and person develops edema –
decompensated heart failure
o Increases right atrial pressure to try to get it to crucial cardiac output level to allow kidneys to release
fluid – eventually, cardiac function begins to decline because of this
 Decline caused by overstretching of heart and edema of heart muscle
o Because cardiac output starts to decrease because of increase of right atrial pressure, retention of fluids
accelerates and patient dies (arterial pressure drops and right atrial pressure rises, and circulation
cannot happen)
o Clinically, can be detected by progressing edema, especially edema of lungs (rales and dyspnea)
 Decompensation process can be stopped by strengthening heart by administration of cardiotonic drug (such as
digitalis) so that heart becomes strong enough to pump adequate quantities of blood required to make kidneys
functional normally again OR administering diuretic drugs to increase kidney excretion while at same time
reducing water and salt intake, which brings about balance between fluid intake and output despite low output
o Stops decompensation by reestablishing normal fluid balance so at least as much fluid leaves body as
enters it
 Cardiotonic drugs, such as digitalis, when administered to a person with a healthy heart, have little effect on
increasing contractile strength of cardiac muscle, but when administered to a person with chronically failing
heart, they can increase strength of failing myocardium by as much as 50-100%
o Strengthen heart contractions by increasing Ca2+ in muscle fibers due to inhibition of Na-K-ATPase in
cardiac cell membranes
o Inhibiting Na-K-ATPase increases intracellular Na+ and slows Na-Ca exchange pump because Na-Ca
exchange pump relies on high Na+ gradient across cell membrane
 In failing heart muscle, sarcoplasmic reticulum fails to accumulate normal quantities of Ca2+ and therefore
cannot release enough Ca2+ into free-fluid compartment of muscle fibers to cause full contraction of muscle
Unilateral Left Heart Failure
 In a large number of patients, especially those with early acute failure, left-sided failure predominates over
right-sided failure (rarely will right side fail without left side failure)
 When left side of heart fails without right side failure, blood continues to be pumped into lungs fine but not into
circulation – mean pulmonary filling pressure rises because of shift of large volumes of blood from systemic
circulation into pulmonary circulation
o As volume of blood in lungs increases, pulmonary capillary pressure increases, and if this rises above
colloid osmotic pressure of plasma, fluid begins to filter out of capillaries into lung interstitial spaces and
alveoli, resulting in pulmonary edema
 Most important problems of left-sided heart failure are pulmonary vascular congestion and pulmonary edema
Low-Output Cardiac Failure – Cardiogenic Shock
 After acute heart attack, heart becomes incapable of pumping blood flow required to keep body alive, so body
tissues begin to deteriorate, often leading to death in a few hours to a few days
 Cardiogenic shock (cardiac shock) – circulatory shock syndrome caused by inadequate cardiac pumping
 Once a person develops cardiogenic shock, survival rate often less than 30% even with appropriate medical care
 Low arterial pressure that occurs during shock reduces coronary blood supply even more, making heart weaker
still, which makes arterial pressure fall more (vicious cycle)
 In cardiogenic shock caused by MI, problem is greatly compounded by already existing coronary vessel blockage
o Because of blockage, arteries require more pressure to get through the block
o In treating MI, one must prevent even short periods of hypotension
 Often patient dies of cardiogenic shock before various compensatory processes can return cardiac output (and
arterial pressure) to life-sustaining level, so treatment of shock is one of most important problems in
management of acute heart attacks
 Immediate administration of digitalis often used for strengthening heart if ventricular muscle shows signs of
deterioration
 Infusion of whole blood, plasma, or blood pressure-raising drug used to sustain arterial pressure
o If arterial pressure can be raised high enough, coronary blood flow can increase enough to prevent
vicious cycle, allowing time for appropriate compensatory mechanisms to correct shock
 Some success has been used to save lives of patients with cardiogenic shock by
o Surgically removing clot in coronary artery, often in combination with coronary bypass graft
o Catheterizing blocked coronary artery and infusing either streptokinase or tissue-type plasminogen
activator enzymes that cause dissolution of clot
o Above are good if instituted within first hour of cardiogenic shock, but won’t do squat after 3 hours
Edema in Patients with Cardiac Failure
 Either left or right heart failure can cause slow peripheral edema
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When previously healthy heart acutely fails as a pump, aortic pressure falls and right atrial pressure rises
As cardiac output approaches zero, right atrial pressure and aortic pressure approach each other in
equilibrium around 13 mm Hg – capillary pressure will fall to this equilibrium value as well
o Because of capillary pressure fall, acute cardiac failure almost never causes immediate development of
peripheral edema
After first day or so of overall heart failure (or right-ventricular heart failure), peripheral edema begins to occur
because of fluid retention by kidneys
o Retention of fluid increases mean systemic filling pressure, resulting in increased tendency for blood to
return to heart, elevating right atrial pressure to still higher value and returning arterial pressure back
toward normal (capillary pressure rises), causing loss of fluid into tissues and development of edema
Causes of reduced renal output of urine during cardiac failure
o Decreased glomerular filtration rate – reduced arterial pressure and intense SNS constriction of afferent
arterioles of kidney cause lower glomerular filtration rate
 Even a slight decrease in glomerular filtration often markedly decreases urine output
o Activation of renin-angiotensin system and increased reabsorption of water and salt by renal tubules –
reduced blood flow to kidneys causes marked increase in renin secretion by kidneys, increasing
formation of angiotensin II
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Angiotensin has direct effect on arterioles of kidney to decrease further blood flow through
kidneys, which reduces pressure in peritubular capillaries around renal tubules, promoting
increased reabsorption of both water and salt from tubules
 Angiotensin acts directly on renal tubular epithelial cells to stimulate reabsorption of salt and
water
o Increased aldosterone secretion – results mainly from effect of angiotensin to stimulate aldosterone
secretion by adrenal cortex – some increase in aldosterone secretion results from increased plasma
K+(excess K+ is one of most powerful stimuli known for aldosterone secretion, and K+ rises in response to
reduced renal function in cardiac failure)
 Elevated aldosterone levels increase reabsorption of Na+ form renal tubules, leading to increase
in water reabsorption
 Elevated Na+ and Cl- elicit secretion of ADH, which further promotes reabsorption of water
o Activation of SNS – SNS stimulation of kidneys causes constriction of renal afferent arterioles, which
reduces GFR, stimulation of renal tubular reabsorption of salt and water by activation of alphaadrenergic receptors on tubular epithelial cells, stimulation of renin release and angiotensin II
formation, which increases renal tubular reabsorption, and stimulation of ADH release from posterior
pituitary, which then increases water reabsorption by renal tubules
 Atrial natriuretic peptide (ANP) – released by atrial walls of heart when they become stretched
o ANP has a direct effect on kidneys to increase excretion of salt and water, so it can help prevent extreme
congestive symptoms during cardiac failure
 When pulmonary edema occurs in a person without new cardiac damage, it usually is set off by some temporary
overload of the heart from stress (even severe cold can cause this) – results in vicious cycle (death in 20-60 min)
o Temporarily increased load on already weak left ventricle limits its pumping capacity, and blood begins
to dam up in lungs
o Increased blood in lungs elevates pulmonary capillary pressure and small amount of fluid begins to
transude into lung tissues and alveoli
o Increased fluid in lungs diminishes degree of oxygenation of blood
o Decreased oxygen in blood further weakens heart and also weakens arterioles everywhere in body,
causing peripheral vasodilation
o Peripheral vasodilation increases venous return of blood from peripheral circulation still more
o Increased venous return further increases damming of blood in lungs
 Types of measures that must be implemented if above circle has been initiated
o Putting tourniquets on both arms and legs to sequester much of blood in veins and decrease workload
on left side of heart
o Giving rapidly acting diuretic, such as furosemide, to cause rapid loss of fluid from body
o Giving pure oxygen to breathe to reverse blood oxygen desaturation, heart deterioration, and peripheral
vasodilation
o Giving patient rapidly acting cardiotonic drug, such as digitalis, to strengthen heart
Cardiac Reserve
 Cardiac reserve – maximum percentage that cardiac output can increase above normal (usually 300-400 in
young adults, and 500-600 in trained athletes)
 In cardiac failure, there is no cardiac reserve (any factor that prevents heart from pumping blood satisfactorily
will decrease cardiac reserve)
 Stress test – running on treadmill or walking up and down stairs – in those with low cardiac reserve
o Immediate and sometimes extreme dyspnea resulting from failure of heart to pump sufficient blood to
tissues, causing tissue ischemia and creating sensation of air hunger
o Extreme muscle fatigue resulting from muscle ischemia, limiting person’s ability to keep going
o Excessive increase in heart rate because nervous reflexes to heart overreact in attempt to overcome
inadequate cardiac output
Quantitative Graphical Method for Analysis of Cardiac Failure
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Cardiac output and venous return curves can be used
Red curve is normal
Blue curve is first few seconds after moderately severe MI
Lavender curve is next 30 seconds (SNS compensation)
Green curve is 1 week later (compensated)
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During first few seconds after MI, venous return curve has not changed because peripheral circulatory
system is still operating normally
o In next 30 seconds, SNS reflexes raise cardiac output and venous return curves (can also raise Psf, which
shifts venous return curve to right and up)
o During next week, cardiac output and venous return curves rise because of some recovery of heart and
renal retention of salt and water, which raises Psf – cardiac output is normal, and renal output is normal,
so new state of equilibrated fluid balance achieved – this is stable until some additional factor changes
either cardiac output curve or venous return curve
Decompensated venous return curves (with cardiac output curve of fully compensated heart failure)
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Graph on left represents venous return curves on successive days after acute fall of cardiac output curve
to the new low level
o Once cardiac output starts its downslope, further retention of fluid causes even more severe cardiac
edema, which hinders cardiac output more
o Graph on right shows patient at point E on graph on right – given digitalis to strengthen heart, which
increases cardiac output immediately, but not venous return (equates at point G)
o Because this gets cardiac output above critical value, kidneys excrete normal amounts of urine, so
kidneys eliminate more fluid than normally (built up edema excreted) causing diuresis
o Progressive loss of fluid over period of several days reduces mean systemic filling pressure back down
and new venous return curve becomes the blue curve on the right
High-output cardiac failure
AV fistula overloads heart because of excessive venous return, even
though pumping capability is not depressed
Beriberi – venous return greatly increased because of diminished
systemic vascular resistance and pumping capability of heart is also
depressed
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Mild signs of peripheral congestion with AV fistula – if person attempts to exercise, they will have little
cardiac reserve because heart is already near maximum capacity
o
Beriberi – decreased level of cardiac output curve caused by weakening of heart because of avitaminosis
(mainly lack of thiamine) that causes beriberi syndrome; weakening of heart decreases blood flow to
kidneys, so kidneys retain large amount of extra body fluid, which increases mean systemic filling
pressure, shifting venous return curve to right
 Venous return curve rotated upward because avitaminosis dilated peripheral blood vessels