| Definition of Heart failure | Cardiac output is unable to meet the metabolic requirements of the body despite adequate filling pressure |
| What are some causes of Heart failure | Hypertension
Valvular stenosis → pressure overload
Valvular regurgitation → volume overload
Arrhythmias
Coronary artery disease → MI
Fibrosis → Diastolic dysfunction leading to restriction of filling |
| What are the 2 types of heart failure | Systolic Failure → Impaired Ventricular function --> Left Ventricular Ejection Fraction is less than 45%
Diastolic Failure → Impaired filling --> Left Ventricular Ejection Fraction is more than 50% |
| What is congestive heart failure | Left heart failure leads to right heart failure |
| What are the different classes of New York Association Classification | Class I → No symptomatic limitation of physical activity
Class II → Slight limitation of physical activity, Ordinary physical activity results in symptoms but no symptoms at rest
Class III → Marked Limitation of physical activity, Less than ordinary physical activity results in symptoms but no symptoms at rest
Class IV → Inability To carry out any physical activity without symptoms and symptoms at rest |
| What are some conservative management plans | Patient Education
Lifestyle modification
Reduce excess salt
Reduce Alcohol
Increase in aerobic exercise
Optimise CV risk factors: decrease BP, statin, stop smoking |
| What drugs can you give for a heart failure patient | Beta blockers reduce heart rate by decreasing beta receptor activation and sympathetic drive
Diuretics decrease fluid retention
Angiotensin converting enzyme inhibitor decreases angiotensin II formation
Angiotensin receptor blockers also stop the activation of the RAAS system
Aldosterone antagonist decreases sodium and water retention |
| Surgical Managements for Cardiac failure | Implantable cardiac defibrillators
Cardiac resynchronisation therapy
Implantable pacemaker
Left ventricular assist devices (LVAD)
Heart transplant |
| What are the 2 compensatory mechanisms of the heart during LV failure | Decrease cardiac output leads to an increase in LVEDP which according to Starling Law leads to increase stretching of the myocytes and increase in cardiac output and also can lead to hypertrophy
Neurohumoral compensation also takes place, and increases cardiac output which leads to increase in fluid retention and increase in central venous pressure which according to Starling Law leads to increase in cardiac output |
| What is the neurohumoral compensation | Myocardial damage leads to reduced CO and BP which activates the sympathetic NS
This leads to the activation of the RAAS system , vasoconstriction, increase heart rate and contractility
Vasoconstriction increases TPR which increases BP
RAAS leads to increase fluid retention which leads to increase in cardiac output
However in the long term the wall stress and increase oxygen demand leads to hypertrophy and decreased contractility |
| Briefly explain what the kidney does to compensate for decrease in CO | Sympathetic stimulation leads to vasoconstriction of the renal artery which leads to sodium and water retention
This leads to increase in release of renin hence leading to production of angiotensin I and angiotensin II ( Angiotensin converting enzyme )
Angiotensin II causes more vasoconstriction and increases the TPR which increases blood pressure
Angiotensin II also leads to release of Aldosterone which increases sodium and water retention
This leads to increase in volume so it increases central venous pressure
This hence leads to increase in end diastolic pressure
And according to Starling's Law it leads to increase in CO
Angiotensin II also leads to further sympathetic stimulation |
