Heart Failure Flashcards

1
Q

Define HF

A

An abnormality of cardiac structure/function leading to failure of the heart to deliver enough O2 to meet metabolic and physiological demands despite normal filling pressures

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2
Q

Define forward failure

A

reduced CO

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3
Q

When does forward failure occur?

A

When the LV contracts and cannot exert sufficient CO

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4
Q

Define backward failure

A

elevated A/V filling pressures

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5
Q

When does backward failure occur?

A

When either ventricles contract and are unable to reject all blood from chambers -> returning blood cannot refill due to no space

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6
Q

Describe HF-REF (systolic HF)

A
  • reduced LVEF <40%

- inability of the heart to contract effectively

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7
Q

Describe HF-PEF (diastolic HF)

A
  • normal LVEF > 40%

- inability of the heart to relax effectively

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8
Q

Describe the difference between acute and chronic HF

A
  • rapid onset (hrs/days)
  • sudden decline in cardiac function
  • potentially life threatening
  • chronic is slow onset (months/years)
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9
Q

State 4 causative factors of HF-REF

A
  • intrinsic myocardial damage
  • pressure overload
  • volume load
  • inadequate filling
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10
Q

Describe the pathophysiology of HF-PEF

A

Occurs a result of multiple comorbidites such as obesity, HPT, AF, Type 2 diabetes

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11
Q

State & describe 3 pathophysiological mechanisms of HF-REF

A
  • cardiorenal model - fluid retention secondary to forward failure & reduced renal BF
  • cardio-circulatory model - forward failure due to peripheral vasoconstriction & increases PVR
  • neurohormonal model - maladpative neurohormonal activation -> cardiac remodelling
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12
Q

Describe how the neurohormonal model works

A
  • Cardiac injury reduces CO output -> reduced BP & organ perfusion
  • reflex activation of several neurohormonal pathways which are initially beneficial but then become harmful
  • progressive deterioration of cardiac function
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13
Q

Describe the effects of the neurohormonal model on the sympathetic nervous system

A
  • Increase in catecholamines, myocardial contractility, HR, systemic & pulmonary vasoconstriction
  • Increased secretion of renin from juxtaglomerular apparatus of kidney activates RAAS
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14
Q

What effect do catecholamines (adrenaline & noradrenaline) have?

A

aggravates ischaemia, potentiate arrhythmias, directly toxic to myocytes, promote cardiac remodelling

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15
Q

Describe the renin-angiotensin-aldosterone system

A
  • increased angiotensin II increases systemic vasoconstriction and peripheral SNS activation
  • increased aldosterone increases Na & H2O retention, endothelial dysfunction, organ fibrosis
  • angiotensin II & aldosterone are directly toxic to cardiac myoctyes & promote cardiac remodelling
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16
Q

What happens as a result of increased ADH release?

A

Increased water retention & vasoconstriction

17
Q

describe the 2 symptom complexes of clinical features of HF

A

Reduced CO - hypoperfusion symptoms
- fatigue & decreased exercise tolerance

Impeded venous return - congestive symtpoms

  • pulmonary & systemic congestion
  • ankle oedema, cough, elevated JVP
18
Q

Describe the classification & staging of HF

A

classification Class I (asymptomatic) -> Class IV (severe)

staging stage A (high risk) -> Stage D (end/refractory)

19
Q

State the different drugs used to manage chronic HF and which model they apply to

A

Cardiorenal - diruetics, inotropes
Cardiocirculatory - inotropes, vasodilators
Neurohormonal - ACEIs, BBs, ARBs, ARNIs, aldosterone antagonists

20
Q

Describe the integrated approach for management of chronic HF

A

general measures:

  • Reduces cardiac workload
  • Restrict dietary salt & fluid intake
  • Smoking cessation & alcohol moderation

Drug therapy
Other - heart transplant

21
Q

List the treatment goals for CHF

A
  • improve CO (decrease forward failure)
  • reduce A/V filling pressures
  • stop/reverse cardiac remodelling
22
Q

State 3 treatment strategies of HF

A
  • myocardial stimulation
  • reduce cardiac workload
  • arrest/reverse cardiac remodelling
23
Q

Describe the treatment of myocardial stimulation

A

increases myocardial contractility with inotropic agents

24
Q

Describe treatment of reducing cardiac workload

A

reduces afterload/preload with diuretics/vasodilators

25
Q

Describe how cardiac remodelling is reversed

A

inhibits chronic neurohormonal activation with ACEIs, BBs, ARBs, ARNIs, aldosterone antagonists