Physiology of Heart Failure

1. Cardiac Failure
Any heart condition that
reduces the ability of the
heart to pump enough blood
to meet the body’s needs.

2. CIRCULATORY DYNAMICS IN CARDIAC FAILURE

3. ACUTE EFFECTS OF MODERATE CARDIAC FAILURE
 TWO MAIN EFFECTS OF CARDIAC
FAILURE:
 (1) reduced cardiac output
 Blood stays in the heart  Increase RA Pressure
 (2) damming of blood in the veins
 resulting in increased venous pressure.

4. CO – 5L
RA Pres -
0
Point B
• Immediately after the heart become
damage
• CO= 2/L
• RA pressure = (+) 4
Compensatory Responses
 baroreceptor reflex,
 sympathetic stimulation
Point C
• heart become stronger due to
compensatory responses
• CO = 4.5
• RA pressure = (+) 5
Point D
• Chronic stage of failure – Fluid
retention and compensated cardiac
output
• CO = 5
• RA pressure = (+) 6

5. CHRONIC STAGE OF
FAILURE—FLUID
RETENTION AND
COMPENSATED CARDIAC
OUTPUT
CHARACTERIZED
MAINLY BY TWO
EVENTS:
1. Retention of fluid by the
kidneys
2. Varying degrees of
recovery of the heart itself
over a period of weeks to
months

6. Renal Retention of Fluid and Increase in Blood Volume
DAMAGE HEART
low cardiac output
Renal Hypoperfusion
Retention of salt and water
Increase in body fluid and
blood volume
Moderate Increase Excess Fluid Retention
Increased in mean
systemic filling pressure
Decreases venous
resistance
Increase Cardiac Output
Beneficial Effects
Detrimental effects
increasing the workload
overstretching of the heart
filtration of fluid into the
lungs, causing pulmonary
edema and consequent
deoxygenation of the blood
development of extensive
edema
DECOMPENSATED HEART FAILURE
COMPENSATED HEART FAILURE

7. Recovery of the Heart After Myocardial Infarction
Damaged Heart
Natural reparative
processes
new collateral blood supply begins to penetrate the
peripheral portions of the infarcted area of the heart,
undamaged portion of the heart musculature
hypertrophies,
causing much of the heart muscle in
the fringe areas to become functional
again
Offsetting much of the cardiac
damage
Partial or complete recovery in 5 to 7
weeks

8. Cardiac Output Curve After Partial Recovery.
PARTIALLY RECOVERED
HEART • Fluid retention
• Cardiac output returns to normal
• Renal perfusion returns to normal
• No further retention of fluid
• But fluid retention already existed
• moderate excesses of fluid
• Elevated right atrial pressure
• COMPENSATED HEART FAILURE
If the heart recovers to a significant extent and
if adequate fluid volume has been retained,
the sympathetic stimulation gradually abates
toward normal -- due to increased CO

9. SUMMARY OF THE CHANGES THAT OCCUR AFTER ACUTE
CARDIAC FAILURE—“COMPENSATED HEART FAILURE”
1. the instantaneous effect of the cardiac
damage

10. DYNAMICS OF SEVERE CARDIAC FAILURE
 Also known as decompensated cardiac failure
 Severely damaged heart
 Failure of the compensatory mechanism to increase Cardiac output
 Continuous Renal Hypoperfusion
 Failure of kidneys to excrete excess fluid
 EDEMA & DEATH

11. DYNAMICS OF SEVERE CARDIAC FAILURE
Represents the approximate state of the
circulation before any compensation has
occurred
After another day or so, the right atrial
pressure rises to 9 mm Hg,. Still, the cardiac
output is not enough to establish normal
fluid balance.
cardiac output now less than 2.5
L/min and the right atrial pressure
16 mm Hg. This state has
approached or reached
incompatibility with life

12. Severe heart failure
Failure of CO and BP to rise to the critical
level for normal renal function
progressive retention of more and more fluid
progressive elevation of the mean
systemic filling pressure
progressive elevation of the right
atrial pressure
heart is so overstretched or so
edematous
heart fails completely
Seen clinically as
• progressing edema
• Pulmonary edema
• bubbling rales (a
crackling sound) in
the lungs
• dyspnea (air
hunger)

13. Treatment of Decompensation
 Administering a cardiotonic drug, such as digitalis
 Strengthening the heart
 the heart becomes strong enough to pump adequate quantities of blood required to
make the kidneys function normally again
 Administering diuretic drugs
 to increase kidney excretion of water
 while at the same time reducing water and salt intake

14. Mechanism of Action of the Cardiotonic Drugs Such as Digitalis
 strengthen heart contractions
 by increasing the quantity of calcium ions in muscle fibers
 Inhibition of the sodium-potassium pump
 accumulation of sodium inside the cell
 the sodium-calcium exchange pump relies on a high sodium
gradient across the cell membrane
 slows the sodium-calcium exchange pump, which extrudes
calcium from the cell in exchange for sodium.

15. UNILATERAL LEFT HEART FAILURE
Blood strongly pumped to the lungs
Left sided heart Failure Blood dams up in the lungs
mean pulmonary filling pressure
rises
mean pulmonary filling pressure = plasma colloid oncotic pressure
PULMONARY EDEMA DEVELOPS

16. Unilateral Left Sided Heart Failure
 Among the most important problems
 pulmonary vascular congestion
 pulmonary edema
 Symptoms
 Rales
 Orthopnea – dyspnea which occur on recumbent position
 Paroxysmal Nocturnal Dyspnea
 Patient being awaken at night due to dyspnea
 2-Pillow orthopnea
 Patient has dyspnea or sensation of drowning on lying flat needs
“two” pillow to relieve symptoms

17. LOW-OUTPUT CARDIAC FAILURE—CARDIOGENIC
SHOCK
 Circulatory shock syndrome caused by inadequate cardiac
pumping
 Less than 30 percent survival rate - even with appropriate medical
care
 Vicious Cycle of Cardiac Deterioration in Cardiogenic Shock
 Low cardiac output
 low arterial pressure
ing
a
vicious
cycle
cardiogenic shock due to
MI - greatly compounded
by already existing
coronary vessel blockage.

18. Physiology of
Treatment of
Cardiogenic Shock
 Digitalis is often administered
immediately to strengthen the heart
 Infusion of whole blood, plasma, or a
blood pressure–raising drug to
elevate arterial pressure
 Surgical clot removal in the coronary
artery, often in combination with a
coronary bypass graft
 Infusion of either STREPTOKINASE or
TISSUE-TYPE PLASMINOGEN ACTIVATOR
ENZYMES that cause dissolution of the
clot.

19. EDEMA IN PATIENTS WITH CARDIAC FAILURE
 Acute Left Cardiac
Failure
 Rapid congestion
of the lungs, with
development of
pulmonary edema
 Does Not Cause
Immediate
Peripheral Edema
When the CO
output decreases
RA pressure
increases
Capillary
pressure
decrease to 13
Decrease capillary pressure rather increased in capillary pressure is not enough
to push fluid int the interstitial space thus peripheral edema does not developed

20. LONG-TERM FLUID
RETENTION BY THE
KIDNEYS CAUSES
PERIPHERAL EDEMA IN
PERSISTING HEART
FAILURE
 overall heart failure or of rightventricular heart failure
 CO decreases
 Renal Hypoperfusion
 Retention of Water
 Increases the mean systemic feeling
pressure
 Increase Venus return
 Elevate RA
pressure
 Increased CO
 Arterial Pressure
Normalizes
Capillary hydrostatic
pressure increases
Peripheral edema bag

21. Causes of
reduced urine
output during
cardiac failure
1. Decreased glomerular filtration rate
2. Activation of the renin-angiotensin
system and increased reabsorption of
water and salt by the renal tubules.
3. Increased aldosterone secretion
4. Activation of the sympathetic nervous
system

22. Causes of reduced urine output during cardiac failure
1. Decreased
glomerular
filtration rate
2. Activation of the renin-angiotensin
system and increased reabsorption of
water and salt by the renal tubules.
Reduced CO
Reduced GFR
b. intense
sympatheti
c afferent
arterioles
constrictio
n
a.
reduced
arterial
pressure
Renin
Angiotensin II
Vasoconstrict Renal
Arterioles
Reduced renal blood
flow
Reduced the pressure in the
peritubular capillaries
Salt & water retention
Stimulates the renal tubular
epithelial cells to reabsorption of salt
and water
promoting greatly increased
reabsorption of both water
and salt from the tubules

23. Causes of reduced urine output during cardiac failure
3. Increased
aldosterone secretion
Increased serum K due reduced renal function
Na reabsorption
Angiotensin II
Stimulates Adrenal cortex to produce aldosterone
1. Reduction osmotic
pressure in the renal tubules
but Increases the osmotic
pressure in the renal
interstitial fluids
promote osmosis of water from
the tubules into the blood
secondary increase in water reabsorption
2. Absorbed sodium and
anions increase the osmotic
concentration of the ECF
ADH secretion by the hypothalamic-
posterior pituitary gland system
4. Activation of the
sympathetic nervous system.
1. constriction
of renal
afferent
arterioles
which reduces the GFR
2. activation of alpha-
adrenergic receptors
on tubular epithelial
cells
3. stimulation of
renin release
and angiotensin
II formation
4. stimulation of
antidiuretic
hormone release
from the
posterior pituitary
promote tubular reabsorption of
water and Na

24. Role of Atrial
Natriuretic Peptide in
Delaying the Onset
of Cardiac
Decompensation
Cardiac Failure
increases both the right and left
atrial pressures
Stretching of the atrial walls
A NP level increases
direct effect on the kidneys to
increase greatly their excretion
of salt and water

25. Acute Pulmonary
Edema in Late-Stage
Heart Failure—
Another Lethal
Vicious Cycle
Long standing heart
failure
TEMPORARY CARDIAC
OVERLOAD
Triggered by:
• Emotional distress
• heavy exercise
• Illness
blood begins to dam up in the
lungs.
the pulmonary capillary pressure
increases
fluid begins to transude into the lung
tissues and alveoli
increased fluid in the lungs
diminishes the degree of oxygenation
of the blood
weakens the heart and also
causes peripheral vasodilation
further increases venous return
of blood from the peripheral
circulation
Further damming of
blood up in the lungs.
Vicious
cycle

26. Interventions
1. Rotating Tourniquet
• Putting tourniquets on both arms and legs to sequester much of
the blood in the veins and, therefore, decrease the workload on
the left side of the heart
4. Administering a rapidly acting cardiotonic drug, such as
digitalis
• To strengthen the heart
2. Administering a rapidly acting diuretic, such as
furosemide
• To cause rapid loss of fluid from the body
3. Giving the patient pure oxygen
• To reverse the blood oxygen desaturation, heart
deterioration, and peripheral vasodilation

27. CARDIAC RESERVE
The maximum percentage that the cardiac output
can increase above normal
CARDIAC RESERVE
Young Adults
 300-400%
Athlete
 500-600%
In severe heart failure
 No cardiac reserve
Any factor that prevents the heart from pumping
blood satisfactorily will decrease the cardiac
reserve

28. Diagnosis of Low Cardiac Reserve—Exercise Test.
• If the patient remains at rest  asymptomatic
• Diagnostic work up
• Cardiac Stress Test  greatly increased cardiac output.
3. An excessive increase
in heart rate because the
nervous reflexes to the
heart overreact in an
attempt to overcome the
inadequate cardiac output
OUTCOME OF STRESS IN PATIENTS WITH NO CARDIAC RESERVE
1. Extreme shortness of
breath (dyspnea)
reduced blood flow to
the tissues tissue
ischemia and creating
a sensation of air
hunger
2. Extreme muscle fatigue
resulting from muscle
ischemia, thus limiting the
person’s ability to continue
with the exercise

29. Graphical Analysis of Normal heart
normal
cardiac
output curve
The normal
venous return
curve
Point A
• Normal
• CO= 5
• RA = 0
Cardiac output
in acute MI
Normal venous
return

30. Graphical Analysis immediately after an Acute
Heart Attack
Normal venous
return curve
Point B
• Normal
• CO= 2
• RA = 4
Cardiac output
in acute MI
*venous return
curve still has not
changed because
the peripheral
circulatory system
is still operating
normally

31. Graphical Analysis within next 30 seconds of Acute Heart
Attack
venous return
curve
Shift upward & to
the right
Point C
• Sympathetic
Compensati
on
• CO= 4
• RA = 5
CO 30 seconds
after an acute
MI
*Sympathetic
stimulation
• can increase
cardiac output curve
as much as 30 to
100 percent
• increase the mean
systemic filling
pressure 

32. Graphical Analysis showing compensation During the Next Few Days of Acute
Heart Attack
venous return
curve
Shift upward & to
the right
Point D
• Further
Compensation
s
• CO= 5
• RA = 6 CO during the
next few days
after an acute
MI
*cardiac output and
venous return curves rise
further because of
 (1) some recovery of
the heart and
• (2) renal retention of
salt and water, which
raises the mean
systemic filling
pressure still further

33. POINT A - time zero
• normal venous return
curve
• cardiac output of about 3
L/min
POINT B – 30 seconds after MI
• stimulation of the
sympathetic nervous system
 increases the mean
systemic filling pressure from 7
to 10.5 mm Hg. shifts the
venous return curve upward
and to the right
• CO increases but did not
reach critical cardiac output
level
• RA Pressure – Increased (5)
Point C – Continuous renal retention of
water and salt
• cardiac output of 4 L/min is still too
low for the kidneys to function
normally.  fluid continues to be
retained and the mean systemic
filling pressure rises from 10.5 to
almost 13 mm Hg
• RA pressure  7
Succeeding days the cardiac
output never rises high enough to re-
establish normal renal function .
Fluid continuous Fluid retention
 the mean systemic filling
pressure continues to rise 
venous return curve continues to
shift to the right
Condition accelerates
and death occurs

34. Treatment of decompensated heart
At Point E – treatment with Digitalis is
started
Point G – Digitalized Heart
• Increased cardiac contractility  increase
the cardiac output curve
• The cardiac output is now 5.7 L/min, a
value greater than the critical level of 5
liters
• No immediate change in the venous return
curve.
Diuresis
Reduction in the mean systemic filling
pressure
Point H – the final steady-state condition
of the circulation
• defined by the crossing point of three
curves: the cardiac output curve, the
venous return curve, and the critical
level for normal fluid balance.
• Compensated Heart
Continuous Diuresis
Cardia
c
Output
Venous
return
curve

35. Graphical Analysis of High-Output Cardiac Failure- AV FISTULA
AV FISTULA
 the systemic vascular resistance
(the total peripheral vascular
resistance) becomes greatly
decreased
 venous return curve rotates
upward
 Increased CO
 12.5 L/min
 Right atrial pressure
 3 mm Hg.
Mild congestion
Exercise
little cardiac reserve heart is
already at near maximum capacity
to pump the extra blood through the
arteriovenous fistula.
Failure condition and is called high-
output failure but in reality, the heart
is overloaded by excess venous
return

36. Graphical Analysis of High-Output Cardiac Failure- Beriberi
decreased level of the cardiac output
curve is caused by weakening of the
heart because of the avitaminosis
(mainly lack of thiamine)
decreased Renal blood flow
Retention a large amount of
fluid
increased the mean systemic filling
pressure
shifted the venous return curve to the
right.
• right atrial pressure in
this instance of 9 mm
Hg a
• Cardiac output about 65
percent above normal

37. thank you