Pathophysiology of Heart Failure Flashcards

1
Q

What is Starling’s Law?

A

As ventricular end diastolic volume increases, cardiac muscle fibes are subject to increased stretch. The more they stretch, the higher their contractility and therefore the higher the stroke volume.

  • This occurs up to a certain point, after which there is a decline in contractility despite increased cardiac myocyte stretch.
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2
Q

What increases contractility?

A
  • Exercise
  • Positive inotropes
  • Sympathetic stimulation:
    • Increases heart rate, contractility, rate force development and rest.
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3
Q

What factors affect stroke volume?

How is stroke volume calculated?

A

Stroke volume = EDV - ESV

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4
Q

Define net filtration pressure

A

Hydrostatic pressure - osmotic force

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5
Q

What facilitates filtration in the capillaries?

What facilitates absorption?

A

Positive net filtration pressure (hydrostatic pressure > osmotic force) facilitates filtration

Negative net filtration pressure (hydrostatic pressure < osmotic force) facilitates absorption

Loss from plasma in filtration should equal gain from plasma in absorption

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6
Q

What is the clinical definition of heart failure?

A

Clinically defined as a syndrome in which patients have classical symptoms (breathlessness, ankle swelling and fatigue) and signs (raised JVP, pulmonary crackles and displaced apex beat) resulting from abnormal cardiac structure or function.

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7
Q

What is the pathological definition of heart failure?

A

An abnormality of the cardiac structure or function leading to failure of the heart to deliver oxygen at a rate which is commensurate with the requirements of the metabolising tissues.

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8
Q

Name some common causes of heart failure

A
  • Hypertension (systemic and pulmonary)
  • Dilated, restrictive or hypetrophic cardiomyopathy
  • Intrinsic myocardial disease
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9
Q

How is heart failure classified?

A

HFrEF: Heart failure with reduced ejection fraction

  • Failure indicated by inabiity of the left ventricle to eject enough stroke volume to provide required oxygen to tissues.

HFpEF: Heart failure with preserved ejection fraction

  • Preserved ejection fraction, inefficiency of heart
  • Often caused by HTN
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10
Q

How is HFrEF diagnosed?

A

Must have all 3 symptoms of:

  • Typical symptoms of HF
  • Typical signs of HF
  • Reduced LVEF
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11
Q

How is HFpEF diagnosed?

A

Must have all 4 of:

  • Typical symptoms of HF
  • Typical signs of HF
  • Normal or mildly reduced LVEF, no LV dilation
  • Relevant structural heart disease (LV hypertrophy/LA enlargement and/or diastolic dysfunction)
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12
Q

In a failing heart, what will be the effect of increasing end diastolic volume? How does this compare to a normal heart?

A

In a normal heart, increasing the end diastolic volume will increase the stroke volume as it will increase ventricular contractility.

In a failing heart, increasing end diastolic volume will reduce the contractility and therefore stroke volume which reduces the ejection fraction.

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13
Q

What are echocardiograms used for?

What are the pros and cons?

What alternative imaging can be used?

A

To determine cardiac structure and function

Pros: cheap and robust

Cons: very subjective

CMR and nuclear can be used

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14
Q

What can cause HFrEF?

What can HFrEF lead to?

A

Can be caused by:

  • Regional damage (MI)
  • Global (cardiomyopathy)

Can lead to:

  • Myocardial injury
  • Myocardial overload (increased preload or afterload)
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15
Q

What is the effect of long term remodelling on the stroke volume and end diastolic volume?

A

As end diastolic volume increases, stroke volume increases very little and begins to decline earlier than in a normal heart.

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16
Q

What occurs in ventricular remodelling?

A

Chronic pressure overload = hypertrophy

Myocardial injury or chronic volume overload = ventricular dilation

17
Q

Describe the process of ventricular remodelling following an acute MI

A

Initial cardiac muscle infarction

Cardiac infarction spreads (over hours to days)

Global remodelling (days to months):

  • The remaining healthy myocardium compensates but cannot compensate completely
  • The ejection fraction reduces
  • Increased pressure on the left ventricle due to increased volume causes eventual dilation
  • This has additional complications such as stretching of the chordae tendinae.
18
Q

Describe the process of ventricular remodelling in diastolic and systolic heart failure

A
  • Hypertrophy caused by chronic hypertension leading to preserved ejection fraction heart failure.
  • Hypertrophied muscle compensates initially but eventually fails due to lack of extra vascularisation to cope with extra muscle mass.
  • This results in ischeamias and fibrosis of cardiac muscle.
  • Ventricle dilates.
19
Q

Describe the microscopic features of ventricular remodelling

A

Myocyte changes:

  • Cell thinning and lengthening
  • Hypertrophy
  • Necrosis
  • Apoptosis

Disorganised muscle fibre orientation

Extracellular matrix alterations and inflammatory changes

20
Q

Describe the macropscopic features of ventricular remodelling

A

Loss of muscle mass

Alteration in chamber size (dilation/hypertrophy)

Dys-synchronous contractions

21
Q

Describe the intracellular features of ventricular remodelling

A

Contractile protein structural and functional derangements

Disorganised cytoskeleton

Impaired cell-cell communication

Altered energy metabolism

Deranged excitation

22
Q

What are the signs and symptoms associated with left ventricular failure?

What are these caused by?

A

Decreased cardiac output causes:

  • Intolerance to exercise
  • Signs of poor tissue perfusion

Pulmonary congestion causes:

  • Pulmonary oedema leading to frothy sputum, orthopnoea, paroxysmal nocturnal dyspnoea.
  • Impaired gas exchange → cyanosis and signs of hypoxia
23
Q

What are the signs and symptoms associated with right ventricular failure?

What is the cause of these?

A

Right heart failure causes increase in venous pressure and congestion of peripheral tissues. This causes:

  • Liver congestion → impaired liver function, hepatomegaly
    • Reduced metabolism of certain hormones e.g. aldosterone → more sodium retention → increased intravascular volume
  • Gi tract congestion → anorexia, GI distress, weight loss
  • Dependent oedema and ascites
24
Q

How does acute heart failure present?

A
  • Dilated pupils (sympathetic)
  • Skin pale, grey or cyanotic
  • Dyspnoea
  • Orthopnoea
  • Crackles, wheeze
  • Cough (+/- frothy white sputum)
  • Low BP
  • Nausea and vomiting (decreased peristalsis)
  • Ascites
  • Dependent, pitting oedema in legs/sacrum
  • Anxiety
  • Low O2 sats
  • Confusion (decreased cerebral perfusion)
  • Raised JVP
  • Third heart sound (gallop)
  • Enlarged spleen and liver
  • Decreased urine output
  • Weak pulse
  • Cool, moist skin
25
Q

Why does oedema occur in heart failure?

A

Increased hydrostatic pressure causes filtration to exceed absorption therefore there is a net loss from plasma (loss from plasma does not equal gain from plasma) and fluid is retained in the extracellular space.

26
Q

Describe the compensatory mechanisms in heart failure

A

Fall in blood pressure from left ventricular failure leads to:

  • Activation of the sympathetic nervous system (vasoconstriction, increased heart rate and contractility)
    • SNS activates RAAS system
  • Decreased renal perfusion
    • Which activates RAAS system

RAAS system:

  • Aldosterone:
    • Increases sodium and water retention
      • Circulating volume increases, eventually inhibiting renin release from kidneys.
    • Causes myocardial fibrosis
    • Coronary vasculopathy
      • Angiotensin II causes:
    • Vasoconstriction
      • Which increases wall stress
    • Myocardial fibrosis

Hepatic congestion results in reduced metabolism of aldosterone therefore extra aldosterone is present so its effects are increased.

27
Q

How is acute decompensated heart failure treated?

A

Oxygen

Loop diuretics (fast acting)

  • E.g. furosemide, bumetanide

GTN (spray/infusion)

cPAP if necessary

Inotropes