1. Heart failure
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cardiac Failure

2. Definition Inability of the heart to pump blood
at a sufficient rate
to meet the body’s metabolic needs (forward failure)
or the ability to do so
only if the cardiac filling pressure are abnormally high (backward failure) or both.
HF may be the principal manifestation
of nearly every form of cardiac disease.
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3. Causes of HF Pressure overload Impaired contractility Volume overload
Aortic stenosis, uncontrolled hypertension.
Pulmonary stenosis, Pulmonary HT
Impaired contractility
MI, Dilated CMP, transient myocardial ischemia
Volume overload
Aortic regurgitation, Mitral regurgitation
Pulmonary regurgitation, Tricuspid regurgitation
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4. Causes of HF Ventricular diastolic dysfunction
ventricular hypertrophy,
Hypertrophic CMP
Transient myocardial ischemia
Obstruction of ventricular filling
Mitral stenosis,Tricuspid stenosis
Pericardial constriction or tamponade.
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5. Features of Heart failure
One possible consequence of HF is that
Blood may back up
on the atrial/venous side of the failing ventricle
Leading to engorgement and distension
of veins (and the organs they drain)
as the venous pressure rises.
Another consequence
poor tissue perfusion
Reduced CO
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6. Features of Heart failure
This can be limited to a single ventricle
Lt sided HF
Rt sided HF.
Commonly biventricular
Congestive cardiac failure (CCF)
Rt ventricle commonly fails
secondary to Lt VF
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7. Features of Lt sided HF Dyspnoea on exertion Orthopnea
? pulmonary venous congestion or decreased CO.
Orthopnea
sensation of laboured breathing on lying flat
Paroxysmal Nocturnal Dyspnoea (PND)
Cough
Hemoptysis
Fatigue and weakness
reduced skeletal muscle perfusion
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8. Features of Lt sided HF Signs Cold extremities, tachycardia, tachypnea
Rales , wheezes, Gallop rhythm.
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9. Features of Rt sided HF Peripheral edema
Rt upper quadrant abdominal discomfort
Anorexia and nausea
edema GIT.
Signs
Ascitis
Hepatomegally
Jugular venous distension
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10. Features of CCF Features of Lt sided & Rt sided HF 6/20/2018
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11. Compensatory Mechanisms
Frank- starling mechanisms
Neurohomornal activation
Myocardial hypertrophy
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12. Frank – Starling Mechanisms
Reduced SV results in incomplete
ventricular emptying during systole
Volume of blood accumulating
during diastole is higher than normal
Increased EDV/EDFL/preload
greater SV on subsequent contraction
Which helps to empty the enlarged ventricle
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13. Frank – Starling Mechanisms
There are limits
for this beneficial compensatory mechanisms
In severe CF
and marked depression of contractility
marked elevation of EDV&P
transmitted retrograde
to the atrium,veins &capillaries
Resulting in edema/pulmonary congestion
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14. Neurohormonal activation
In response to fall in CO
Sympathetic reflexes
Fluid retention by the kidneys
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15. Sympathetic reflexes In acute stage of cardiac failure
Sympathetic become strongly stimulated
within a few seconds (30seconds)
parasympathetic become reciprocally
inhibited at the same time.
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16. Sympathetic reflexes Baroreceptor reflex Chemoreceptor reflexes
operates when arterial pressure is diminished.
Chemoreceptor reflexes
CNS ischaemic response
All these activate the SNS
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17. Sympathetic reflexes Sympathetic stimulation Increases heart rate
Increases force of contraction
Increase the tone of most of the blood vessels.
Especially the veins
raising the Mean systemic filling pressure and VR
increasing cardiac output.
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18. Fluid retention by the kidneys
In Chronic stage of cardiac failure
Increase blood volume
for hours to days
Mechanisms
RAS
Renal body fluid system
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19. Renin Angiotensin system
Effects of Angiotensin II
vasoconstriction
Increase sodium reabsorption (directly)
Activate aldosterone secretion
Acts on brain to increase secretion of ADH
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20. Renal body fluid system
Decreased GFR in cardiac failure
Because of reduced renal blood flow
intense sympathetic constriction of afferent arterioles of the kidneys
Reduced urine output
when cardiac output and arterial pressure are significantly less than normal
Sometimes anuria when CO falls to ½ - 1/3 normal
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21. Fluid retention by the kidneys
Fluid retention leads to:
Increased blood volume
Increases venous return
by Increasing mean systemic filling pressure
Distending the veins which reduces venous resistance.
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22. Fluid retention by the kidneys
But excess fluid retention
in severe stage of HF
Overstretch the heart
causing ventricular dilatation
thus weakening the heart still more
Leads to filtration of fluid into the lungs
pulmonary edema
Development of extensive edema
all the peripheral tissues of the body
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23. Fluid retention by the kidneys
Note
Stretched atrial walls raises ANP level.
ANP has a direct effect on the kidneys
to increase greatly their excretion of salt and water.
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24. Decreased CO SNS RAS ADH contractility HR vasoconstriction
circulating volume
arteriolar
venous
VR to the heart
(preload)
Maintain BP
CO
Peripheral edema
&Pul. congestion
SV
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25. Ventricular hypertrophy
Due to sustained ventricular wall stress
Either due to volume overload
or high afterload.
Increased mass of muscle fibers
helps to maintain ventricular contractile force.
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26. Ventricular hypertrophy
However this compensation
may be at the expense of higher than normal
diastolic ventricular pressure
and therefore atrial pressures,
because of increased stiffness of the hypertrophied wall.
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27. Recovery from cardiac failure
There may be progressive recovery
of the heart itself
over a period of several weeks to month.
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28. Recovery from cardiac failure
eg HF caused by MI
New collateral blood supply
begins to penetrate the peripheral portions
of the infracted area of the heart.
Hypertrophy of undamaged portion
of the heart musculature
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29. Recovery from cardiac failure
A - Normal state of circulation
normal heart
B - acutely damaged heart
Few seconds
after heart attack
but before sympathetic reflexes have occurred 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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30. Recovery from cardiac failure
C - damaged heart &
sympathetic stimulation
Raise in CO
towards normal
caused by sympathetic reflexes 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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31. Recovery from cardiac failure
D - Final return of CO
to normal after several days to weeks
of cardiac recovery
and fluid retention.
partially recovered heart 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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32. Recovery from cardiac failure
This final state is called
compensated heart failure
The maximum pumping ability
of the heart is still depressed to less than a half normal 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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33. Recovery from cardiac failure
However one of the results of chronic cardiac weakness
is a chronic increase in Rt atrial pressure
( 6mmHg) 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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34. Recovery from cardiac failure
A patient with compensated heart failure
has a reduced cardiac reserve. 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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35. Recovery from cardiac failure
Has normal CO at rest,
but heavy exercises causes immediate return of the symptoms of Acute failure
because the heart is unable to increase its pumping capacity
to the level required to sustain the exercise 10 5
CO L/min A D C B –
Rt atrial pressure (mmHg)
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36. Cardiac reserve.
It is the maximum percentage that the CO can increase above the normal level.
In a heavy young adult the cardiac reserve is 300 – 400%
Athletically trained person occasionally up to 500 – 600%
In heart failure, no reserve
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37. Cardiac reserve Any factor that prevent the heart
From pumping blood satisfactorily
decreases cardiac reserve
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38. Precipitating factors:
Many patients with chronic HF
remain asymptomatic for extended periods,
either because impairment is mild
or because of compensatory mechanisms.
Often clinical manifestation occur
only in presence of precipitating factors
that increase the cardiac workload.
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39. Precipitating factors
Common precipitating factors are;
Increased metabolic demands
Fever, infection, anemia, tachycardia, hyperthyroidism, pregnancy.
Increased circulatory volume (preload)
Excessive sodium in diet
Excessive fluid administration
Renal failure.
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40. Precipitating factors
Conditions that increase afterload
Uncontrolled HT
Pulmonary emboli
↑Rt ventricular afterload
Conditions that impair contractility
Negatively inotropic drugs
Excessively slow HR
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41. Principles of Treatment in HF
Identification and correction
of the underlying condition causing HF
Elimination of the acute precipitating cause of CCF symptoms
MEDICATIONS
Diuretics
Inotropic drugs
Vasodilators.
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42. Principles of Treatment in HF
Diuretics
reduce the venous fluid overload.
Inotropic drugs
(eg. Digoxin)
improve myocardial contractility.
Afterload reducing agents (i.e arterial vasodilators)
reduce the load against which the ventricle must contract.
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43. NOTE:
Cardiac failure can lead to shock.
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