Pathophysiology of Cardiac disease and congestive heart failure

Question 1

Define a heart failure.

Answer 1

• A clinical syndrome caused by heart diseases resulting in systolic and / or diastolic function severe enough to overwhelm the normal compensatory mechanisms, resulting in:
  Poor cardiac output and reduced peripheral perfusion (FORWARDS
  failure)
  and / or
  Elevated filling pressures, resulting in oedema and effusions
  (BACKWARDS, CONGESTIVE failure).

Question 2

What are the 4 major consequences of CHF?

Answer 2

• Oedema and Effusions
• Peripheral vasoconstriction
• Tachycardia / Arrhythmias
• Remodelling and Fibrosis of the Myocardium

Question 3

What are endogenous counteractions to the RAAS system?

Answer 3

Natriuretic peptides
* Atrial natriuretic peptide, ANP.
released due to atrial stretch
* Brain natriuretic peptide, BNP
released from ventricles, due to increased ventricular pressure
* Other natriuretic peptides:
CNP, Urodilatin, Adrenomedullin

Question 4

How does oedema and effusions occur?

Answer 4

*Excessive Na+ and H2O retention
-try to increase preload to increase CO

Question 5

Why does peripheral vasoconstriction occur?

Answer 5

• Homeostatic priority of the body, to maintain blood
  pressure, even at expense of increased filling pressures.
• Arterioconstriction maintains blood pressure.
• Venoconstriction increases pre-load, so venous return to
  heart, and utilisation of the Frank-Starling mechanism.

Question 6

What are the mediators of peripheral vasoconstriction?

Answer 6

• Sympathetic nervous system: 1 receptors (noradrenaline).
• Angiotensin II
• Reduced bradykinin levels (ACE = Kininase II)
• Vasopressin (ADH)
• Endothelin

Question 7

What is the effect of angiotensin ii on the kidney?

Answer 7

*Causes greater efferent arteriole constriction than afferent arteriole constriction
= increased glomerular capillary pressure

Question 8

ACE inhibitors counteract adverse effects of angiotensin ii. What does ACE inhibitors do?

Answer 8

• Balanced vasodilators
• Reduce aldosterone release, so reduced Na+ & H2O retention
• Reduce glomerular capillary pressure
• Prevent Angiotensin II mediated myocardial fibrosis and remodelling
• Permissive anti-adrenergic effects
• Reduce vasopressin release
• Reduce endothelin release

Question 9

What does increased aldosterone result in?

Answer 9

*Increased Na+ & H2O retention
*Myocardial remodelling and fibrosis

Question 10

What is an aldosterone antagonist?

Answer 10

Spironlactone

Question 11

What hormones can cause remodelling of myocardium and vascular smooth muscle cells?

Answer 11

• Angiotensin II
• Aldosterone
• Endothelin
• Catecholamines

Question 12

What is eccentric hypertrophy, what is it caused by, what happens, and what is an example where is occurs?

Answer 12

*Dilation of the ventricle
*Caused by volume overload
*E.g Mitral regurgitation

Question 13

What is concentric hypertrophy, what is it caused by, what happens, and what is an example where is occurs?

Answer 13

*Increased thickness of ventricular wall
*Caused by pressure overload
*E.g Aortic stenosis

Question 14

What can cause volume overload?

Answer 14

*Exercise - isotonic (marathon)
*Anaemia
*Valvular incompetence

Question 15

What can cause pressure overload?

Answer 15

*Exercise - isometric (Sprint/weightlifting)
*Aortic/pulmonary stenosis
*systemic hypertension (LV)
*Pulmonic hypertension (RV)

Question 16

What causes tachycardia / arrythmias?

Answer 16

• Mediated via elevated catecholamine levels, increased
  sympathetic drive, reduced vagal tone. (Parasympathetic)

Question 17

What are the so called ‘bad’ hormones involved with heart failure?

Answer 17

Adrenaline
Noradrenaline
Angiotensin II
Aldosterone
Vasopressin
Endothelin

Question 18

What are the ‘good’ hormones of heart failure?

Answer 18

Vagal tone
ANP / BNP
Bradykinin
PGE, PGI
Nitric oxide (NO.)