Complete description of haemodynamic changes in heart failure and the ways to treat this condition and improve the outcome of patients who are suffering from heart failure.Dealt beautifully with basics.

1. HAEMODYNAMIC
CHANGES IN
HEART FAILURE
DR ARINDAM KARGUPTA
3RD YEAR PGT , UNIT 4
CHAIRPERSON – PROF P .K. SINHA

2. Definition of Heart Failure
▪ A pathophysiologic state in which an abnormality of cardiac function is responsible for the
failure of the heart to pump blood at a rate commensurate with the requirements of the
metabolizing tissues.
▪ Complex clinical syndrome and can result from either structural or functional cardiac
disorder.
▪ Global problem with almost 20 million people affected.
▪ Prevalence is about 2% among adult population in developed countries.
▪ Viewed as a progressive disease that starts with an index event.

3. Progressive model of Heart Failure

4. Classification
Heart
Failure
HFpEF HFrEF

5. Etiologies of Heart Failure

6. Cardinal Features of Heart Failure
▪ Dyspnoea
▪ PND
▪ Orthopnoea
▪ Fatigue
▪ Exercise intolerance
▪ Pedal oedema
▪ Nocturia

7. Haemodynamic changes in a Failing Heart
▪ Cardiac output – It is the amount of the blood pumped into the aorta in each minute by
the heart.
▪ Normal value is 5.6 L/min for male and 4.9 L/min for female.
▪ It is dependent on the heart rate and stroke volume.
C.O = H.R S.V
 Heart rate is mainly under neural control.
 Stroke volume is determined by preload , afterload and inotropic state of Heart.

9. Role of preload in cardiac output regulation
▪ Preload is the load present before heart has started contracting.
▪ EDV is commonly used index for measurement of preload.
▪ Under normal circumstances it is the chief regulator of cardiac output.
▪ According to Frank-Starling’s law , within physiological limit , greater the preload , greater
the force of contraction . Accordingly cardiac output will also increase.
▪ This relationship is altered in heart failure.

10. NAUGHTY BOY

11. Role of afterload in regulation of cardiac output
▪ It is the load that the left ventricle does work against during ejection.
▪ The simplest index is the aortic pressure.
▪ Under physiologic circumstances afterload does not influence cardiac output much unless
there is failure.
▪ Heart can usually overcome any acute increase in afterload.
▪ But in case of chronically increased afterload , ventricle undergoes compensatory
hypertrophy to overcome the pressure.

12. Aortic pressure vs Wall stress
Aortic pressure Wall stress

13. ▪ More exact definition of afterload is LV wall
stress during ejection.
▪ According to Laplace’s law T = (P.R) / 2h .
▪ Larger the LV size ( radius ) and LV pressure ,
greater will be the wall stress.
▪ Increased wall thickness helps to reduce
cardiac wall stress.

14. Consequences of cardiac hypertrophy
Step 1 • Compensatory hypertrophy of heart
Step 2 • Reduced ventricular cavity size
Step 3 • Diastolic dysfunction
Step 4
• Myocyte loss due to hypertrophy and nutrient supply-demand mismatch
Step 5
• Ventricle thinned out
Step 6
• Systolic dysfunction

15. Relation between preload and afterload
Increased LV volume
Increased LV
contractility
Increased SBP
Increased afterload

17. Changes in Heart Failure

18. Influence of peripheral resistance on cardiac output
▪ Cardiac output varies inversely with
total peripheral resistance.
▪ Cardiac Output = Arterial Pressure /
Total Peripheral Resistance.
▪ Cardiac output increased in Beriberi ,
Thyrotoxicosis , Paget’s disease ,
anaemia.
▪ Output decreased in hypothyroidism.

19. Pressure – volume curve of LV
▪ D – A = diastolic filling.
▪ A – B = Isovolumic contraction.
▪ B – C = cardiac output.
▪ C – D = Isovolumic relaxation

20. Systolic dysfunction Diastolic dysfunction

21. Changes in the Kidney in Heart Failure
▪ From the Heart – ANP , BNP
▪ From the Kidney – RAAS activation
▪ ANP & BNP promote natriuresis and
decompression of the overloaded heart.
▪ RAAS promotes salt and water retention
and vasoconstriction.

22. Cardiorenal syndrome
▪ Disorders of the heart and kidneys
whereby dysfunction of one organ may
induce dysfunction in the other organ.
▪ Complex and multifactorial mechanism.
▪ Associated with poor prognosis.
▪ Treatment is dependent on the underlying
cause.

24. Changes in the lung in heart failure
Step 1
• Failing heart
Step 2
• Increased capillary hydrostatic pressure
Step 3
• Injury to alveolo-capillary membrane
Step 4
• Pulmonary capillary stress failure
Step 5
• Increased transudation of fluid

26. Impairment of
gas exchange
hypoxaemia

27. Changes in chronic heart failure
Chronically
increased
PCWP
Capillary
membrane
fibrosis
Reduced
capillary
permeability
Muscularization
of small
arteriole
Development of
PAH
Protection from
pulmonary
oedema

28. Changes in pulmonary function tests
▪ Reduced lung volume
▪ Reduced lung compliance
▪ Increased residual volume
▪ FEV1/FVC ratio maintained
▪ Reduction in DLCO

29. Take Home Messages
▪ Heart failure is a progressive disease.
▪ Cardiac output is dependent on preload , afterload and inotropic state of
heart.
▪ Under normal circumstances preload is the main determining factor of cardiac
output and afterload in a failing heart.
▪ Heart tries to adapt different compensatory mechanisms to maintain output.
▪ Heart failure leads to hemodynamic changes in different organs like kidney
and lung.

30. LOVE YOUR HEART…