Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be acute or chronic. Acute decompensated heart failure is a life-threatening condition characterized by increased filling pressures, pulmonary edema, reduced cardiac output, and organ dysfunction. Heart failure is determined by factors like contractility, heart rate, preload, and afterload. Preload refers to the stretch of heart muscle fibers before contraction and depends on factors like ventricular relaxation and compliance. Diastolic dysfunction can increase preload but also cause pulmonary congestion. Elevated natriuretic peptide levels help diagnose heart failure.

1. PATHOPHYSIOLOGY
OF HEART FAILURE

2. “
A clinical syndrome arising when
abnormal cardiac structure or function
prevents oxygen delivery meeting tissue demand.
The demand met is usually only at the expense of
elevated filling pressures.

3. SYMPTOMOLOGY

4. NYHA CLASS

5. CHRONICITY
acute
acutely
decompensated
chronic

6. YOU HAD ONE JOB
Many present with ADHF (acute decompensated heart
failure), a life-threatening condition.
× escalating left ventricular filling pressure
× resulting pulmonary edema / peripheral edema
× and/or inadequate cardiac output
× and/or organ hypo-perfusion and dysfunction
× can lead to cardiogenic shock and dysrhythmias

7. DETERMINANTS
contractility
and
heart rate
preload afterload

8. PRELOAD

9. What is preload?
The stretch of cardiomyocytes
(or distention of ventricle) at
end-diastole.
This depends on:
 Active ventricular relaxation
 Passive ventricular compliance
 Contribution from late atrial
contraction
PRAY THAT IT FILLS
Normally
LV is compliant enough that
adequate preload is achieved
with end-diastolic pressure
(LVEDP) is low enough to
preserve PCWP of <12 mm Hg,
so no congestion occurs.

10. DIASTOLIC DYSFUNCTION
Them wall thic
LVH, MI, remodeling and
aging can reduce passive
compliance.
So, LV is no longer
adequately filled by
normal left atrial
pressure (LAP).
The compensation…
Upstream accumulation
of venous blood plus
neurohumoral response*
can elevate the LAP,
restoring the gradient for
LV filling.
Everything has a price
Preload is achieved BUT
at the cost of pulmonary
congestion.
How do we evaluate the
double D?
× PCWP >16 mm Hg
× NT-pro-BNP
Treatment?
× diuretics
× nitrates
× beta-blockers, ACEIs and
ARBs (in Grade I and II
diastolic dysfunction only)

11. LVH and MI can also reduce
isovolumetric relaxation and this
delays mitral valve opening.
This with reduced passive
compliance, means that adequate
LV filling will depend more on:
 Adequate diastolic duration
(reduced by tachycardia)
 Atrial contraction (reduced by
atrial fibrillation)
 Competent mitral valve
THERE IS MORE TO THIS
Sub-endocardial ischemia
The reduced LV compliance also
makes heart vulnerable to sub-
endocardial ischemia.
This can be provoked by acute
epsidoes of decompensation.
So the cardiac markers for ischemia
might be raised.

12. BNP FAMILIA
× Useful to differentiate ADHF from other causes of
dyspnea, to guide treatment and prognosis
× BNP is secreted by heart ventricles in repsonse
to excessive stretching of cardiomyocytes:
PreproBNP  ProBNP  BNP + NT-proBNP
× Physiologic actions of BNP are:
- vasodilation (decreases SVR)
- natridiuresis (reduced blood volume and preload)
Sensitivity 94 %
Specificity 85 %
Half life BNP 20 m
Half life of
NT-proBNP
120 m
Cutt-off
<75 years
125
pg/ml
Cutt-off
>75 years
450
pg/ml

13. AFTERLOAD

14. LaPlace’s Law
Systolic wall stress is:
S = P x R / 2*W
P = systolic pressure
R = radius
W = wall thickness
AFTERLOAD ME THIS
Pressure that must be generated to eject
blood is determined by arterial impedance
which increases with:
× increased arterial pressure
× increased vascular resistance
Radius increases with valvular incompetence
and ischemic cardiomyopathy.
Wall thickness actually decreases this stress.
But don’t forget that it decreases the preload.

15. Why increased SVR?
ADHF frequently presents with
hypertension.
Why? Because dyspnea and low CO
drives a catecholamine surge.
This reduced forward flow can cause
increased filling pressures (LVEDP).
This further increases pulmonary
congestion, dyspnea and low CO.
In HF, catecholamine reserves
eventually deplete.
VISCIOUS CYCLE
Oh MI MI
Increased SVR and tachycardia also
means increased metabolic demand
of myocardium.
This can result in myocardial
ischemia of the thickened LV.
Reduced preload and increased
afterload will decrease stroke
volume and CO, resulting in organ
hypo-perfusion.

16. CONTRACTILITY
AND HEART RATE

17. What is contractility?
It is intrinsic ability of the
myocardium to pump in the absence
of changes in preload or afterload.
It is related to:
× the rate of myocardial muscle
shortening dependent on
intracellular Ca2+ concentration
× increases in heart rate can also
enhance contractility, perhaps
because of increased availability of
intracellular Ca2+
INOTROPY
Sympathetic activity
SANS innervates atrial, ventricular
and nodal tissues.
Epinephrine and norepinephrine
increase contractility primarily β1-
receptor activation, in addition to
positive chronotropic effects.
Myocardial contractility is depressed
by hypoxia, acidosis, depletion of
catecholamine stores and loss of
functioning muscle mass as a result
of ischemia or infarction.

18. Bradycardia
× Reduces CO directly
× Increases EDV can ↑ ventricular
radius, hence ↑ afterload
(LaPlace’s law)
× Exacerbates MR
× Accumulates upstream venous
pressure and pulmonary
congestion/edema
CHRONOTROPY
Tachycardia
× Decreases ventricular filling and
preload, and therefore, CO
× Increases myocardial oxygen
demand and cause ischemia
× Decreases coronary perfusion
(which occurs during diastole)

19. STROKE VOLUME AND
CARDIAC OUTPUT

20. FRANKLY A
STARLTLING CURVE
× Y axis = stroke volume (SV)
× X axis = end-diastolic volume (EDV)
In a normal heart during exercise:
× SV will increase with increased
EDV and myocardial stretch.
In a failing heart:
× SV will not increase with
increasing SDV due to decreased
contractility
× increasing afterload will result in
rapid decompensation and
pulmonary edema

22. X axis = LV pressure; Y axis = LV volume
Red line - Ventricular
stiffness
× Steeper line shows
↑ contractility
Blue line - Effective
arterial elastance
× Steeper line shows
↑ afterload
Box B = ↓ preload
× ↓ ventricular
compliance
× EDV and SV are ↓ or
maintained
Box C = ↑ afterload
× ↑ arterial impedance
× ↑ contractility and
myocardial work
Box D = ↓ contractility
× ↓ SV and CO

23. Thanks!
Any questions?

24. MCQ 1
1) In a normal heart:
a. Pre-load is the same as left ventricular end-systolic volume
b. Increase in pre-load has no effect on the force of the next contraction
c. Systemic vasoconstriction reduces afterload
d. Isovolumetric ventricular contraction ends when the aortic valve opens
e. Ejection fraction of a normal left ventricle is approximately 40%

25. MCQ 2
2) Regarding heart failure:
a. The failing ventricle is invariably more compliant than normal
b. Central venous pressure should be kept to a minimum if diastolic failure is
suspected
c. Allowing tachycardia is an effective way of maintaining cardiac output
d. Vasodilation can help restore cardiac output in the failing ventricle
e. Inotropes should never be used

26. MCQ 3
3) Regarding the management of patients with heart failure:
a. ACE inhibitors should normally be continued throughout the perioperative period
b. Beta-blockers should be normally be continued throughout the perioperative
period
c. Arrhythmias should only be treated if blood pressure is compromised
d. Spinal anesthesia reduces perioperative risk in total knee replacement surgery