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Cardiovascular System > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Define heart failure

A

-A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolising tissues

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2
Q

What are some causes of heart failure?

A

IHD is the primary cause of Systolic HF.

Other causes of HF include:

  • Hypertension
  • Dilated Cardiomyopathy:
  • Bugs (Viral/ Bacterial / Mycobacteria)
  • Alcohol / Drugs / Poisoning
  • Pregnancy
  • Idiopathic
  • Valvular Heart Disease / Congenital
  • Restrictive Cardiomyopathy e.g. amyloidosis
  • Hypertrophic Cardiomyopathy
  • Pericardial disease
  • High-Output Heart Failure
  • Arrhythmias
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3
Q

What are the characteristics of class 1 heart failure?

A

– No symptomatic limitation of physical activity

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4
Q

What are the characteristics of class 2 heart failure?

A

– Slight limitation of physical activity
– Ordinary physical activity results in symptoms
– No symptoms at rest

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5
Q

What are the characteristics of class 3 heart failure?

A

– Marked limitation of physical activity
– Less than ordinary physical activity results in symptoms
– No symptoms at rest

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6
Q

What are the characteristics of class 4 heart failure?

A

– Inability to carry out any physical activity without symptoms
– May have symptoms at rest
– Discomfort increases with any degree of physical activity

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7
Q

What are some characteristics of systolic dysfunction?

A
  • Increased LV capacity
  • Reduced LV cardiac output
  • Thinning of the myocardial wall (Fibrosis and necrosis of myocardium and Activity of matrix proteinases)
  • Mitral valve incompetence
  • Neuro-hormonal activation
  • Cardiac Arrhythmias
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8
Q

What are some structural changes seen in heart failure?

A
  • Loss of muscle
  • Uncoordinated or abnormal myocardial contraction*
  • Changes to the ECM: – Increase in collagen (III>I) from 5% to 25% – Slippage of Myocardial fibre orientation

• Change of cellular structure and function
– Myocytolysis and vacuolation of cells
– Myocytehypertrophy
– Sarcoplasmicreticulum dysfunction
– Changes to Calcium availability and/or receptor regulation

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9
Q

What are the consequences of sympathetic nervous system activation in heart failure?

A

-Baroreceptor-mediated response is early compensatory mechanism to improve CO:

– Increased cardiac contractility
– Arterial and venous vasoconstriction
– Tachycardia

However there are long-term deleterious effects:

– β-adrenergic receptors are down-regulated/uncoupled
– Noradrenaline increased

This leads to:

  • cardiac hypertrophy / myocyte apoptosis and necrosis via α-receptors
  • up-regulation of the RAAS
  • Reduction in heart rate variability (reduced paraSNS and increased SNS)
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10
Q

How does angiotensin 2 play a key role in organ damage?

A

Angiotensin 2, acting via AT1 receptors:

  • damage vasculature and organs
  • cause LV hypertrophy and remodelling
  • cause aldosterone release and hypertension

RAAS commonly activated in HF. (see lecture slide for full detail)

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11
Q

What is the role of the natriuretic hormones in heart failure? (atrial, brain and c-type)

A

Atrial: stretch (A&V):

– Predominate renal action- constricts efferent and vasodilates afferent arterioles
– Decreases Na+ reabsorption in the collecting duct
– Inhibits secretion of renin and aldosterone
– Systemic arterial and venous vasodilatation

Brain: stretch (V) – similar effects

C-Type: CNS and endothelium – limited effects

These peptides balance the effects of the RAAS on the vascular tone and Na+ /H2O balance

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12
Q

What is the role of ADH in heart failure?

A

Hypo-natraemia results from H2O in excess of Na+ retention and can be due to:

– Increased H2O intake (thirst)
– Action of ADH on V2 receptors in the collecting duct

Normally hypo-natraemia / hypo-osmolality inhibits ADH release – but ADH is increased in HF:

– Increased H2O retention
– Tachycardia and reduced systemic resistance resulting in increased CO

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13
Q

What is the significance of endothelin in heart failure?

A

Secreted by vascular endothelial cells:

  • Potent system and renal vasoconstrictor acting via autocrine (local) activity thus activating RAAS
  • Evidence of increased levels in some patients with HF
  • Correlates with indices of severity (poor prognostic sign)
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14
Q

What is the significance of Prostaglandins (E2 and I2) in heart failure?

A
  • Stimulated by NA and RAAS
  • Act as vasodilators on afferent renal arterioles to attenuate effects of NA / RAAS
  • NSAID Rx blocks de novo PG synthesis
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15
Q

What is the significance of Nitric Oxide in heart failure?

A
  • Usually potent vasodilator produced by endothelial cells via NO synthase
  • NO synthase may be blunted in HF
  • Loss of vasodilatation balance
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16
Q

What is the significance of Bradykinin and TNF in heart failure?

A

Bradykinin:

– Promotes natriuresis and vasodilatation
– Stimulates production of PGs

Tumour Necrosis Factor (α-TNF):

– Increased in HF
– Depresses myocardial function
– ?? Stimulates NO synthase
– ? Role in cachexia

17
Q

Describe current treatment protocol for heart failure

A
  • ACEI’s
  • B-blockers
  • MRA
  • AT1 receptor blockers
  • CRT
18
Q

Why is pitting oedema often seen in HF?

A

-increased capillary hydrostatic pressure

19
Q

Why is breathlessness often seen in HF patients when put under stress?

A
  • reduced skeletal muscle blood flow
  • cachexia
  • affects diaphragm leading to breathlessness, fatigue and exercise intolerance
20
Q

What are the renal effects of heart failure?

A
  • GFR is maintained in early HF by haemodynamic changes at the glomerulus
  • Increased Na+ /H2O retention due to neuro- hormonal activation
  • However in severe HF, renal blood flow falls leading to reduced GFR and a subsequent rise in serum urea and creatinine.
  • This can be exacerbated by treatment inhibiting the actions of Angiotensin II
21
Q

How does anaemia affect heart failure?

A

Contributes to symptoms

• Common and easily treated

• Multi-factorial aetiology:
– Chronic inflammatory disease 
– Expanded plasma volume
– Drug therapy (ACEi / Aspirin) 
– Iron malabsorption
– Chronic renal failure
22
Q

What are key factors in diastolic dysfunction?

A

– Frequently elderly and female

– Often history of hypertension/diabetes/obesity

23
Q

Describe diastolic heart dysfunction

A
  • Normal LV function with concentric remodelling
  • Reduced LV compliance and impaired myocardial relaxation (thicker and shorter cardiac myocytes)
  • Impaired diastolic LV filling (with increased LA and PA pressures
  • Unable to compensate by increasing LV EDP (Frank Starling)
  • Low cardiac output results
  • Triggers neuro-hormonal activation as per systolic heart failure
24
Q

What is the aetiology of right sided heart failure?

A

– Chronic lung disease
– Pulmonary embolism/pulmonary hypertension
– Pulmonary/tricuspid valvular disease
– Left-to-right shunts (ASD/VSD)
– Isolated right ventricular cardiomyopathy

Cardiovascular System (12 decks)

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