Furunculosis of the nasal vestibule: causes, diagnosis, complications, treatment

Heart failure, a serious disease , is discussed here regarding its definition, causes , compensatory mechanisms and precipitating factors .

Definition of  Heart failure

Failure of the heart to pump sufficient cardiac output to meet the demands of the body, with tissue hypoxia inspite of normal venous return and venous inflow to the heart (normal filling of the heart), this usually occurs with failure of the compensatory mechanisms.

Causes of Heart failure

I. Left sided Heart failure :

a. Pressure load:
- Aortic stenosis  - systemic hypertension.
- Coarctation of aorta .
b. Volume load:
- Mitral incompetence - Aortic incompetence.
- Ventricular septal defect.
c. Muscle disease:
Cardiomyopathy, diagnosed by exclusion, confirmed by echo.
d. Ischaemic heart disease.

II. Right sided failure:

a. Pressure load: 

- Pulmonary hypertension ( primary, cor pulmonale or secondary to left sided lesion , e.g MS of left sided failure) .

-Pulmonary stenosis.

-Pulmonary embolism.

b.Volume load: 

- Atrial septal defect - Tricuspid regurge.

c. Muscle disease:

Cardiomyopathy, diagnosed by exclusion, confirmed by echo.

d. Ischaemic heart disease.

The most frequent cause of right heart failure is secondary to left sided lesion e.g mitral stenosis or left heart failure.
Ventricular inflow obstruction can be caused by MS ,TS and constrictive pericarditis, so these lesions give picture of heart failure

Compensatory mechanisms in heart failure

When there is gradual impairment of cardiac function, (i.e in chronic heart diseases) a variety of compensatory changes may take place.

Aim: To maintain normal cardiac output.

i.e When the heart is subjected to any load ---> stimulation of compensatory mechanisms. as below to maintain sufficient COP.

1. Hypertrophy: "with pressure load"

i.e Increased thickness of cardiac muscle fibers , which will late lead to ischaemic heart disease.

2. Dilatation: "with volume load"

increased length of cardiac muscle fibers.

Starling law:

The force of contraction ex initial length of cardiac muscle fiber within limits.

3. Increased O2 extraction

i.e O2 dissociation curve shifts to the right -->> ++ O2 delivery to the tissues. 

4. Tachycardia: (Sympathetic drive)

The COP = stroke volume X heart rate,

Heart failure leads to Decrease in stroke volume so, this leads to reflex tachycardia to maintain normal COP.

5. Release of atrial naturetic peptide.

6. Activation of the renin angiotensin aldosterone system.

In ventricular remodeling there are changes in the size. mass and configuration of the ventricle as a consequence of hemodynamic changes triggered by myocyte growth, interstitial fibrosis, ischemia and apoptosis --> Thi leads to Decrease in the effectiveness of ejection .

 Mediators that lead to professive remodeling are angiotensin II, CA, TNF, growth hormone, while counter regulatory mediators are ANP, NO, Bradykinin. ACE inhibitors are helpful drugs to reduce the process of remodeling.

Precipitating factors :( Aggravating factors of chronic heart disease)

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