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Heart Failur - 2024-2025

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25 views26 pages

Heart Failur - 2024-2025

Uploaded by

negaag216
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Program of Pharm D

2rd year (2024-2025)


Block : CVS
Week : III

Heart Failure

DR. Warda Musbah

BALAGRAE
UNIVERSTY
By the end of this session you will be able to:

• Define heart failure


• Discuss Cardiac Hypertrophy: Pathophysiology and
Progression to Heart Failure
• List the causes of right and left heart failure
• Discuss the pathogenesis of systolic and diastolic left side
heart failure and its morphology
• Discuss right side heart failure: pathogenesis and morphology
The heart is unable to pump blood at a rate that meets
the requirements of the metabolizing tissues, or can
only do so only with filling pressures that are higher
than normal.
Cardiac Hypertrophy: Pathophysiology and
Progression to Heart Failure

• Sustained increase in mechanical work of either ventricle due to


pressure overload, volume overload, or trophic signals (e.g.,
those mediated through the activation of β-adrenergic receptors)
causes myocytes to increase in size (cellular hypertrophy);

• Hypertrophy requires increased protein synthesis to form


additional sarcomeres, as well as increasing the numbers of
mitochondria. Hypertrophic myocytes also have multiple or
enlarged nuclei,
The pattern of hypertrophy reflects the nature of the stimulus.

 pressure-overload hypertrophy (e.g., due to hypertension or aortic


stenosis).

 volume-overload hypertrophy (e.g., due to valvular regurgitation)


• In pressure-overload hypertrophy (e.g., due to
hypertension or aortic stenosis), new sarcomeres are
predominantly assembled in parallel to the long axes of cells,
expanding the cross-sectional area of myocytes in ventricles
and causing a concentric increase in wall thickness.
• volume-overload hypertrophy (e.g., due to valvular
regurgitation) , characterized by new sarcomeres being
assembled in series within existing sarcomeres, leading
primarily to ventricular dilation.
Cardiac Hypertrophy: Pathophysiology and
Progression to Heart Failure
Important changes at the tissue and cell level occur with cardiac
hypertrophy.
 Increase in myocyte size is not accompanied by a proportional
increase in capillary numbers.
 Supply of oxygen and nutrients to the hypertrophied heart, is
more tenuous than in the normal heart.
 Oxygen consumption by the hypertrophied heart is elevated due
to the increased workload that drives the process.
 Hypertrophy is also often accompanied by deposition of fibrous
tissue .
 Molecular changes include the expression of immediate-early
genes (e.g., FOS, JUN, MYC, and EGR1).
Figure 12.1 Left ventricular hypertrophy. (A) Pressure hypertrophy due to left ventricular outflow obstruction. The left ventricle is on the lower right in
this apical four-chamber view of the heart. (B) Left ventricular hypertrophy with and without dilation, viewed in transverse heart sections. Compared with
a normal heart (center), the pressure-hypertrophied hearts (left and in A) have increased mass and a thick left ventricular wall, and the hypertrophied,
dilated heart (right) has increased mass and an apparently normal wall thickness. (C) Normal myocardium. (D) Hypertrophied myocardium (C and D are
photomicrographs at the same magnification). Note the increases in both cell size and nuclear size in the hypertrophied myocytes, and the interstitial cells
remain small..)
There are many different ways to categorize heart failure,
including:
 left heart failure versus right heart failure
 systolic dysfunction or diastolic
 backward vs. forward failure
 low-output heart failure vs. high-output heart failure
Left-Sided Heart Failure

Left-sided heart failure is most often caused by the following:

i) Systemic hypertension
ii) Mitral or aortic valve disease (stenosis)
iii) Ischaemic heart disease
iv) Myocardial diseases e.g. cardiomyopathies, myocarditis.
v) Restrictive pericarditis.
Systolic dysfunction results Diastolic dysfunction refers to
from inadequate myocardial an inability of the heart to
contractile function, usually as a adequately relax and fill, which
consequence of ischemic heart may be a consequence of
disease massive left ventricular
hypertrophy, or constrictive
pericarditis.
Left sided failure leads to pulmonary venous congestion
Left-Sided Heart Failure
Morphology
Lungs.
Pulmonary congestion and edema produce heavy, wet lungs.
Pulmonary changes—from mildest to most severe—include
(1) Perivascular and interstitial edema, particularly in the interlobular
septa
(2) progressive edematous widening of alveolar septa
(3) Accumulation of edema fluid in the alveolar spaces.
(4) Extravasated red cells and plasma proteins in the alveoli are
phagocytosed and digested by macrophages; the accumulated iron
is stored as hemosiderin.
These hemosiderin-laden macrophages (also known as heart failure
cells)
heart failure cells
• Pleural effusions (typically serous) arise from elevated pleural
capillary and lymphatic pressure and the resultant
transudation of fluid into the pleural cavities
Right-Sided Heart Failure

Right-sided heart failure is most often caused by the following:


Right-sided heart failure occurs more often as a consequence of
left-sided heart failure.
However, some conditions affect the right ventricle primarily,
producing right-sided heart failure. These are as follows:
i) As a consequence of left ventricular failure.
ii) Cor pulmonale in which right heart failure occurs due to
intrinsic lung diseases (
iii) Pulmonary or tricuspid valvular disease.
iv) Pulmonary hypertension secondary to pulmonary
thromboembolism.
v) Myocardial disease affecting right heart.
vi) Congenital heart disease with left-to-right shunt.
Right sided failure
Right-Sided Heart Failure
Liver and Portal System.
• The liver is usually increased in size and weight (congestive
hepatomegaly) producing the characteristic “nutmeg liver”
• Centrilobular hypoxia produces centrilobular necrosis.
cardiac cirrhosis.

• Portal venous hypertension also causes :


congestive splenomegaly and chronic congestion and edema of the
bowel wall.
Pleural, Pericardial, and Peritoneal Spaces.

Systemic venous congestion can lead to fluid accumulation


(effusions) in the pleural, pericardial, or peritoneal spaces

(a peritoneal effusion is also called ascites).


Subcutaneous Tissues.

• Edema of the peripheral and dependent portions of the body,


especially foot/ankle (pedal) and pretibial edema, is a hallmark
of right-sided heart failure.
• Presacral edema.
• Generalized massive edema (anasarca)
CHF is characterized by variable degrees of decreased cardiac
output and tissue perfusion (forward failure), as well as pooling
of blood in the venous capacitance system (backward failure)
References

• Robbins and Cotran pathologic basis of disease 10th edition


(2020).
• Harsh Mohan, Text Book of Pathology, 7th edition , 2015

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