Pathophysiology of Cardiac disease and congestive heart failure Flashcards

1
Q

Define a heart failure.

A
  • 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).
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2
Q

What are the 4 major consequences of CHF?

A
  • Oedema and Effusions
  • Peripheral vasoconstriction
  • Tachycardia / Arrhythmias
  • Remodelling and Fibrosis of the Myocardium
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3
Q

What are endogenous counteractions to the RAAS system?

A

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

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4
Q

How does oedema and effusions occur?

A

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

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5
Q

Why does peripheral vasoconstriction occur?

A
  • 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.
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6
Q

What are the mediators of peripheral vasoconstriction?

A
  • Sympathetic nervous system: 1 receptors (noradrenaline).
  • Angiotensin II
  • Reduced bradykinin levels (ACE = Kininase II)
  • Vasopressin (ADH)
  • Endothelin
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7
Q

What is the effect of angiotensin ii on the kidney?

A

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

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8
Q

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

A
  • 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
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9
Q

What does increased aldosterone result in?

A

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

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10
Q

What is an aldosterone antagonist?

A

Spironlactone

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11
Q

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

A
  • Angiotensin II
  • Aldosterone
  • Endothelin
  • Catecholamines
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12
Q

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

A

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

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13
Q

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

A

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

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14
Q

What can cause volume overload?

A

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

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15
Q

What can cause pressure overload?

A

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

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16
Q

What causes tachycardia / arrythmias?

A
  • Mediated via elevated catecholamine levels, increased
    sympathetic drive, reduced vagal tone. (Parasympathetic)
17
Q

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

A

Adrenaline
Noradrenaline
Angiotensin II
Aldosterone
Vasopressin
Endothelin

18
Q

What are the ‘good’ hormones of heart failure?

A

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