Pathophysiology of cardiac disease and congestive heart failure Flashcards

1
Q

Congestive heart failure is also known as?

A

Backwards heart failure

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2
Q

What is backwards HF associated with?

A

Elevated filling pressures and extravasation of fluid (e.g. pulmonary oedema in L-CHF).

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3
Q

Define preload and how does this affect stroke volume?

A

Venous return to the heart – stretches sarcomeres – more returned the higher the SV

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4
Q

Define afterload

A

Force of ejection from the heart (of the ventricles) – arterial resistance/pressure

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5
Q

Describe how preload influences cardiac output by the Frank Starling mechanism

A

Increased the endo diastolic ventricular volume
Sarcomere lengths are increased
Stroke volume of the heart is increased

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6
Q

What are the major consequences of CHF?

A
  • Oedema and Effusions
  • Peripheral vasoconstriction
  • Tachycardia / Arrhythmias
  • Remodelling and fibrosis of the myocardium
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7
Q

How does an increased afterload affect CO?

A

Increased afterload causes a decreased SV making it harder for the heart to pump

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8
Q

Define 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

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9
Q

What are the consequences of forwards HF?

A

Poor cardiac output and reduced peripheral perfusion

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10
Q

What are the consequences of backwards/congestive HF?

A

Elevated filling pressures, resulting in oedema and effusions

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11
Q

What is the role of neuro-hormonal activation in the consequences of CHF?

A

Baroreceptors – increase sympathetic drive in response to a decrease in BP
Sodium and water retention is trying to increase preload but can lead to oedema and effusions if too much

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12
Q

What is endothelin?

A

potent vasoconstrictor and causes myocardial remodelling and fibrosis

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13
Q

What are the 3 immediate consequences of an increased sympathetic drive in response to decreased blood pressue?

A
  • Increased HR (contractility)
  • Vasoconstriction
  • Renin release (RAAS)
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14
Q

What is the function of cardiac beta-1 adreno-receptors?

A

Increased HR - tachycardia
- The aim is to increase cardiac output (CO = SV x HR), but this is detrimental in the
long term, as it increases myocardial oxygen consumption and reduces coronary
perfusion.

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15
Q

What is the function of cardiac alpha-1 adreno-receptors?

A

Lie on vascular smooth muscle cells and cause vasoconstriction –> increases BP –> increases venous return (preload)

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16
Q

What is the role of angiotensin II within cardiac myocytes?

A

Results in hypertrophy and fibrosis (cardiac remodelling)

17
Q

What is the function of vasopressin (ADH)?

A

Results in water retention

Excessive Sodium and water retention results in Oedema and Effusions.

18
Q

In heart failure what is released during atrial stretch?

A

Atrial natriuretic peptide (ANP)

19
Q

In heart failure what is released due to increased left ventricle pressues?

A

Brain natriuretic peptide (BNP)

20
Q

What is used to diagnostically test for HF?

A

ANP and BNP can be assayed to demonstrate the presence of heart failure, but have a short half-life.
Dogs with CHF have sig. higher levels than normal dogs.

21
Q

In patients with oedema and effusions what is the aim of treatment?

A

To increase preload - venous return to the heart

22
Q

Give examples of mediators of peripheral vasoconstriction

A
  • Alpha-1 receptors in the peripheral NS
  • Angiotensin II
  • Reduced bradykinin levels
  • Vasopressin
  • Endothelin
23
Q

How does Angiotensin II affect filtration pressure in the kidney?

A
  • Angiotensin II causes greater EA constriction than AA.

- This increases glomerular capillary pressure (filtration pressure).

24
Q

What is the overall function of ACE inhibitors?

A

Counteract adverse effects of angiotensin II

25
Q

Which drug can be used to stop aldosterone escape (increased aldosterone levels despite adequate ACE inhibition)?

A

Spironolactone

26
Q

Compensatory hypertrophy due to volume overload is an example of … hypertrophy?

A

Eccentric

27
Q

What is volume overload of the heart?

A

One or more chambers of the heart “see” an increased volume of blood. This leads to
chamber dilation and usually compensatory hypertrophy

28
Q

In which situations would eccentric hypertrophy be seen?

A
  • Mitral regurgitation
  • Ventral septal defects
  • Patent ductus arteriosus
  • Tricuspid regurgitation
29
Q

What is pressure overload of the heart?

A

There is increased impedance or increased resistance to outflow of blood from a particular heart chamber (usually a ventricle).
Relative wall thickness increases (walls thick; chamber may be small).

30
Q

Pressure overload results in … hypertrophy?

A

Concentric

31
Q

Examples of pressure overload conditions on the left and right ventricles are:

A
  • Aortic stenosis
  • Systemic hypertension
  • Pulmonic stenosis
  • Pulmonary hypertension
32
Q

A pressure overload will lead to increased wall stress, how is this compensated for?

A

By increasing wall thickness (which lowers the chamber radius)

33
Q

What is the difference in adaptive and maladaptive modelling

A
Adaptive = initially compensatory 
Maladaptive = long term compensatory, more harmful than helpful
34
Q

Myocardial remodelling is associated with?

A

Fibrosis
Increased wall stress
Myocardial ischaemia